Overcoming Sex/Gender and Nature/Nurture - unipub

Overcoming Sex/Gender and Nature/Nurture

Anne Fausto-Sterling’s Dynamic Systems Theory

Masterarbeit

zur Erlangung des akademischen Grades

Master of Arts (MA)

an der Karl-Franzens-Universität Graz

vorgelegt von

Maximilian BURKARD

Am Institut für Philosophie

Begutachter:

Univ.-Prof. Dr. Marian David

Graz, 2018

Danksagung

Ich danke Professor Marian David für die Betreuung der Arbeit.

Ich danke meiner Familie für all das wohlmeinende und respektierende Verständnis und

besonders meinen Eltern dafür, dass sie mir ermöglicht haben zu tun, was ich gerne tue, und

vor allem meiner Mutter für die zahlreichen fruchtbaren und für mich lehrreichen Gespräche

zum Thema dieser Arbeit sowie natürlich allgemein.

Zusammenfassung

In der akademischen Tradition der Empirischen Sozialwissenschaften wurden studierte Phänomene häufig im Rahmen dessen interpretiert, was in der Literatur normaler Weise ‚Nature/Nurture‘-Konzept genannt wird. Dieses Konzept ist beispielsweise im Kontext von Geschlechtsunterschieden und deren Bedeutung in der Form ‚Sex/Gender‘ instanziiert und dessen ist die Behauptung der Möglichkeit einer empirischen Trennbarkeit von Nature- und Nurture-Kausalursachen. Dieser Text diskutiert die Arbeit der feministischen Wissenschaftlerin Anne Fausto-Sterling und ihren Vorschlag Nature/Nurture und Sex/Gender zu Gunsten von Dynamic Systems Theory (DyST) aufzugeben. Entsprechender Weise ist der erste (von zwei) Hauptteil(en) dieses Textes der Einführung und Kritik von Nature/Nurture- und Sex/Gender-Positionen gewidmet. Dies geschieht zunächst am Beispiel von Steven Pinker und Matt Ridley und später an Hand des Konzepts ‚Heritabilität‘, welches im Zuge der Nature/Nurture-Kontroverse über IQ und Intelligenz berüchtigt wurde, sowie an Hand relevanter Konzepte wie ‚Interaktion‘ und ‚Reaktionsnorm‘. Der zweite Teil richtet seine Aufmerksamkeit auf Anne Fausto-Sterling’s vorgeschlagene Alternative und führt DyST ausführlich ein, bevor das Argument herausgearbeitet, erklärt, und kritisiert wird, welchem die Überwindung von Natrure/Nurture und Sex/Gender zugeschrieben wird. Im Verlauf des gesamten Textes spielt außerdem die Frage der Kausalität in den empirischen Sozialwissenschaften explizit oder implizit eine wichtige Rolle. In diesem Kontext, schließt auch der Text mit der Folgerung, dass, während Fausto-Sterling’s DyST zwar Nature/Nurture und Sex/Gender überwinden kann und besprochenen Nature/Nurture-Ansätzen objektiver Weise deutlich überlegen ist, diesem Konzept aber die Kausalität ähnliche Probleme bereitet.

Abstract

Traditionally, explications of phenomena in the social sciences have often been embedded in what has come to be dubbed the nature/nurture framework (whose principal claim is that nature and nurture causes can be empirically separated) such that, for instance, the notion ‘sex/gender’ has been introduced in order to conceptualize the differences between men and women and why they exist. This text discusses the feminist researcher Anne Fausto-Sterling and her proposal of Dynamic Systems Theory (DyST) to replace this nature/nurture framework and its cognate sex/gender. Accordingly, Part One (of two) introduces and criticizes nature/nurture- and sex/gender-positions as instantiated by especially Steven Pinker and Matt Ridley through a critique of the associated concept ‘heritability’, which was a hot topic in the nature/nurture debate on IQ and intelligence starting around the 1960’s, and by disputing important associated concepts like ‘interaction’ and ‘reaction norm’. Part Two focusses on Anne Fausto-Sterling’s proposed alternative and thus provides a substantial introduction of DyST, before I work out, discuss, and criticize the argument, based on which Fausto-Sterling’s DyST is said to overcome nature/nurture and sex/gender. In addition, and quasi throughout this text, the question of causality is either implicitly or explicitly present. And in the end, this text concludes that, while Fausto-Sterling’s DyST can overcome nature/nurture as well as sex/gender and while it’s objectively superior to the nature/nurture accounts encountered, it has similar problems with causality.

Table of Contents

1. Introduction ........................................................................................................................ 7

1.1 Terminological note .................................................................................................................................. 8

1.2 The structure of the text ........................................................................................................................... 9

1.3 Introductory opinion piece ..................................................................................................................... 11

2. Part One: Nature/nurture and sex/gender ....................................................................... 14

2.1 The nature/nurture framework .............................................................................................................. 15

2.1.1 A brief introduction ......................................................................................................................... 16

2.1.1.1 What is nature, what is nurture? ............................................................................................................ 16

2.1.1.2 Why is it nature “versus” nurture? ......................................................................................................... 17

2.1.1.3 Conclusion .............................................................................................................................................. 18

2.1.2 Three case studies ........................................................................................................................... 19

2.1.2.1 Steven Pinker: ‘Truth cannot be sexist’ .................................................................................................. 19

2.1.2.2 The early Anne Fausto-Sterling ............................................................................................................... 24

2.1.2.3 Matt Ridley: Nature via nurture ............................................................................................................. 26

2.1.3 Conclusion ....................................................................................................................................... 29

2.2 Genes/environment: Can heritability separate nature and nurture? .................................................... 30

2.2.1 What is heritability? ........................................................................................................................ 30

2.2.1.1 Computing heritability: A statistic method ............................................................................................. 31

2.2.1.2 Heritability and IQ: A hot topic ............................................................................................................... 33

2.2.2 The causal irrelevance of heritability: Oscar Kempthorne’s critique ............................................... 35

2.2.3 Conclusion ....................................................................................................................................... 41

2.3 Introducing Anne Fausto-Sterling and concluding nature/nurture ........................................................ 42

2.3.1 On Fausto-Sterling’s work: A brief overview ................................................................................... 43

2.3.2 Fausto-Sterling on ‘reaction norm’ and ‘interaction’ ...................................................................... 44

2.3.3 Fausto-Sterling on ‘(standard) environment’ .................................................................................. 47

2.3.4 Conclusion ....................................................................................................................................... 50

2.4 Conclusion of Part One ........................................................................................................................... 51

2.4.1 Summary ......................................................................................................................................... 51

2.4.2 Main conclusions and final remarks ................................................................................................ 52

3. Part Two: Overcoming nature/nurture and sex/gender .................................................. 54

3.1 Systems approaches to biology .............................................................................................................. 56

3.1.1 Terminological preliminaries: DST, DeST, and DyST? ...................................................................... 57

3.1.2 What is DeST?.................................................................................................................................. 59

3.1.3 A taste of critique ............................................................................................................................ 61

3.1.4 Fausto-Sterling: DeST and DyST ...................................................................................................... 64

3.1.4.1 Fausto-Sterling (2000b) and DeST .......................................................................................................... 65

3.1.4.2 Fausto-Sterling (2003, 2007, 2014): DeST or DyST? ............................................................................... 66

3.1.5 Conclusion ....................................................................................................................................... 67

3.2 Fausto-Sterling and Dynamic Systems Theory (DyST) ............................................................................ 68

3.2.1 Three case studies of Fausto-Sterling applying DyST ...................................................................... 69

3.2.1.1 First case study: DyST and sexual orientation ........................................................................................ 69

3.2.1.2 Second case study: DyST and infant gender development ..................................................................... 72

3.2.1.3 Third case study: Differences in bones ................................................................................................... 75

3.2.1.4 Conclusion .............................................................................................................................................. 77

3.2.2 Systematic explication of Fausto-Sterling’s DyST of gender ............................................................ 78

3.2.2.1 DyST and (infant) gender development .................................................................................................. 78

3.2.2.2 Core concepts of DyST: Embodiment/experience and emergence/iteration ......................................... 81 3.2.2.2.1 Embodiment/experience ...................................................................................................................................... 82 3.2.2.2.2 Emergence/iteration ............................................................................................................................................. 85 3.2.2.2.3 Conclusion ............................................................................................................................................................ 87

3.2.3 Fausto-Sterling’s DyST: Framework and theory .............................................................................. 88

3.2.4 Overcoming nature/nurture and sex/gender .................................................................................. 91

3.2.4.1 Fausto-Sterling’s notion of ‘sex’ ............................................................................................................. 91

3.2.4.2 Dimorphic and non-dimorphic traits ...................................................................................................... 93

3.2.4.3 Non-dimorphic differences and DyST ..................................................................................................... 94

3.2.4.4 The essential argument and its justification ........................................................................................... 96

3.2.4.5 Ad hoc reproaches and their rebuttals ................................................................................................... 98

3.2.4.6 Conclusion ............................................................................................................................................ 100

3.2.5 A critical perspective: Kempthorne again ...................................................................................... 101

3.2.5.1 Comparative experiments .................................................................................................................... 102

3.2.5.2 Observation studies .............................................................................................................................. 105

3.2.5.3 A Kempthornian critique of Fausto-Sterling’s DyST and a defence ...................................................... 107

3.2.6 Conclusion ..................................................................................................................................... 110

3.3 Conclusion of Part Two ......................................................................................................................... 110

3.3.1 Summary ....................................................................................................................................... 110

3.3.2 Main conclusions and final remarks .............................................................................................. 113

4. Epilogue ........................................................................................................................... 114

4.1 Outro ..................................................................................................................................................... 114

4.2 Limits and further research .................................................................................................................. 117

5. References ...................................................................................................................... 121

Terminological note

7

1. Introduction

This text concerns research about differences between women and men, often-called ‘sex

differences’. This is a vast topic, because it has been studied in different disciplines and thus

from different perspectives. For instance and with respect to empirical research, there are

studies in Medical Science, Biology, Genetics, Sociology, and Psychology or studies in

Philosophy ranging from Metaphysics to Ethics with respect to theoretical research. Moreover

and as if the question of what differences exist was not vast enough a topic already, the closely

associated question, why these differences exist, has been considered equally.

Against the background of multi-disciplinarity just mentioned, I find it inadequate for me to

write a ‘purely philosophical’ text about the two questions just mentioned. This is also,

because the relevance of ‘purely philosophical’ texts is somewhat restricted in the sense that

there are a large number of philosophically un-schooled empirical researchers which ignore

‘purely philosophical’ texts as ‘unscientific’. But ‘cultural’ boundaries (cf. Snow 2012) between

disciplines are often arbitrary and their maintenance often as irrational as inadequate with

respect to the object studied. Therefore, I mean this text to be an honest attempt of

appreciating and of engaging with data driven sciences—even if from an external and in the

end overall philosophical perspective.

If I had to topologize this text in the disciplinary landscape, I would therefore characterize it

as an intersection between Empirical Methodology, (Philosophy of) Psychology, and

(Philosophy of) biology. Perhaps more informative is that I find myself again1 drawn to

theorize the relation between data and their interpretation in the social sciences, i.e., what

(else) does (not) follow under which condition from a given data set on some research object.

In my view, this question is of crucial importance given the pervasiveness and importance of

numbers (and statistics) not only in the (social) sciences but also in every-day life. Not only,

because the reflection of this relation immediately resonates with important societal issues

both in every-day life and science. But also because the degree of its reflection is, or so I

believe, an important indicator of rationality and an important protection against ideology.

Having provided a first glimpse of what this text will be about, let me now inform you that

section 1.2 will present the contents of this text in more detail. And this will be just after a

1 As in my other master’s thesis in musicology (cf. Burkard 2018).

Terminological note

8

brief note on terminology in section 1.1. In terms of content, the ‘real’ argument concerning

the nature/nurture, sex/gender, and differences between men and women will start in section

1.3, which purports to introduce the topic and to provide an idea the argument’s overall

direction of impact.

1.1 Terminological note

In this section, I explain, how I will apply the words ‘sex’ and ‘gender’ and their composed

derivatives. To begin with, the standard meaning of ‘sex’ and ‘gender’ is the following: ‘Sex’ is

said to refer to a (set of) biological entity (or entities), which quasi-universally and factually

distinguish(es) between females and males (via chromosomes, sexual organs, sex hormones,

sexed brains, etc.).2 On the other, ‘gender’ usually refers to culturally specific ways in which

the females and males enact themselves as men and women (hair style, clothing, jewellery,

certain behaviour, etc.).3 Briefly speaking, there are two semantical word-families: There is

{‘Gender’, ‘cultural’, ‘acquired’, …, ‘men/women’} on one hand and {‘sex’, ‘biological’, ‘innate’,

…, ‘male/female’} on the other. Thus, ‘sex’ and ‘gender’ are really thick concepts, because they

immediately imply for each trait a way of genesis (i.e. ‘innate’ vs. ‘acquired’).

The terminological problem is that ‘sex difference’ does not always refer to differences

regarding some biological entity, because the application of the words ‘sex’ and ‘gender’ in

combination with ‘difference’ ambiguous. One reason for this is, I figure, that basically all

mental differences between men and women (e.g. different character traits, cognitive

abilities, motivations, etc.) are hotly debated to be either essentially biological or fully cultural.

Therefore, and on one hand, just reading the title of a study on mental differences between

men and women carrying either ‘gender differences’ or ‘sex differences’ sometimes suffices

to anticipate its conclusion. On the other, however, it seems also to be the case that

oftentimes (e.g. feminist) scholars use ‘sex difference’, even if they are arguing in favour of

2 In its definition of ‘sex’, the Oxford Dictionary is not too much ‘up to date’ including only external genitals in the definiens (instead of biological features): “Either of the two main categories (male and female) into which humans and most other living things are divided on the basis of their reproductive functions.” (cf.: https://en.oxforddictionaries.com/definition/sex, last access: 27.05.2018) 3 In its definition of ‘gender’, the Oxford Dictionary is more ‘up to date’ (even if pretty much blurry in the second sentence, which is ‘glued’ to the first one): “Either of the two sexes (male and female), especially when considered with reference to social and cultural differences rather than biological ones. The term is also used more broadly to denote a range of identities that do not correspond to established ideas of male and female.” (https://en.oxforddictionaries.com/definition/gender, last access: 27.05.2018)

https://en.oxforddictionaries.com/definition/sex

https://en.oxforddictionaries.com/definition/gender

The structure of the text

9

them being cultural. For instance, this is clearly true of Anne Fausto-Sterling’s usage. Hence,

the ambiguity regarding ‘sex difference’ and what it implies.

In order to disambiguate the wording for this text, let me render transparent my own use of

words. I adopt the following terminologies:

1. I use ‘sex difference’ to denote a classically biological differences between men and

women (e.g. chromosomes, genitals, height, strength, bones, hormones, etc.).

2. I use ‘sex/gender difference’ to denote all sex differences (as defined in 1.) plus in

addition: mental differences between men and women (e.g. different character traits,

abstract reasoning, motivations, etc.), which are claimed to be essentially innate.

Depending on the context of usage, this expression might emphasize the one or the

other aspect of the defined meaning: Either its inclusion of mental differences or its

reference to what is thought to be classically biological sex differences.

In other words, I intend this notion to be descriptive, i.e., to represent the discursive

state of the art that (in addition to classic biological sex differences due to nature) also

mental differences are claimed to be sex differences and thus due to nature.

3. I don’t use ‘gender difference’ at all.

Against the background of these terminologies, it’s important to mention that this

terminological policy clearly differs from many of the policies of the authors cited in this text.

However, I chose to apply ‘sex/gender difference’ at any point I thought that the authors

actually mean ‘biological plus mental sex differences (i.e. as in 2.)’, even if they talk about ‘sex

differences’. Obviously, however, I didn’t change any of the citations, which read ‘sex

difference’ (even if I take them to mean to refer to sex/gender differences). But now you know

that the cooccurrence of ‘sex/gender difference’ and ‘sex difference’ should not be

interpreted as a terminological inconsistency.

Note that, in effect, I believe that my application of ‘sex/gender difference’ in the above

specified sense does not only create no ambiguity but also that there is rather a considerable

gain of clarity with respect to my ow discourse and the discourse of the authors’ cited.

1.2 The structure of the text

This section’s purpose is to provide the structure of the text’s content. In general the text is

divided into two main parts. The first part (i.e. section 2) introduces and criticizes the

The structure of the text

10

nature/nurture framework. The second part (i.e. section 3) introduces in general terms the

rival framework focussing on the specific instantiation defended by Anne Fausto-Sterling.

More precisely, the discussion in terms of content starts with the section 1.3, which is

supposed to be a trigger of the topic at hand. The main argument, however, starts in the first

subsection 2.1 of Part One, where I introduce what I understand the nature/nurture

framework to consist in. This is achieved via a brief systematic explication in section 2.1.1 and

via a casuistic study of three scholars’ held positions in section 2.1.2. It closes with a conclusion

in 2.1.3.

The next section 2.2 concerns the methodological critique of an instantiation of the

nature/nurture framework: Genes/environment. In 2.2.1, I introduce the closely associated

concept of heritability, its historical context (i.e. the IQ debate), and why it’s so contentious.

Next, I argue in section 2.2.2 that heritability coefficients cannot separate nature and nurture

in the case of social sciences and have no causal relevance at all, which, in my view, sheds

doubt on the gene/environment-framework as well as on its instantiating framework

nature/nurture as is stated in the conclusion in 2.2.3.

Finally, and as the last section of Part One, section 2.3 introduces the scholar Anne Fausto-

Sterling, whose approach stands I in particular focus of Part Two and who aims to replace the

nature/nurture framework and sex/gender. At this point, however, I only briefly introduce

Fausto-Sterling generally in 2.3.1 and then concern Fausto-Sterling’s reception of key ideas

from the IQ debate’s context in 2.3.2 and 2.3.3. The purpose is to clarify these key ideas further

but also to provide a smooth transition from Part One and Part Two as well as to render

nature/nurture even more implausible drawing form Fausto-Sterling. I finish Part One with a

substantive conclusion in 2.4, where I sum up the most important points and state my main

conclusions.

Part Two of this text is divided in essentially two main sections. Section 3.1 introduces the

framework in biology ‘DST’ (from which Fausto-Sterling’s is a variant), which has been

developed in critical response to nature/nurture. More precisely, I firstly clarify in 3.1.1 the

acronym DST, which is widely (but equivocally) used in the biological literature, by

distinguishing at least two related but different approaches, namely, DeST (Developmental

Systems Theory) and DyST (i.e. Dynamic[al] Systems Theory). In the following section 3.1.2, I

present the main ideas of DeST, which is argued to denote a framework (like nature/nurture)

Introductory opinion piece

11

in contrast to DyST, which is conceived of as a scientific theory in the ordinary sense. Finally,

section 3.1.3 provides a taste of critique against DeST and 3.1.4 localizes Anne Fausto-

Sterling’s work in the context of DeST and DyST. Section 3.1.5 concludes the section.

The maybe most important passage of this text, section 3.2, treats Fausto-Sterling’s adoption

of Dynamic Systems Theory (DyST). It starts ‘bottom up’ in section 3.2.1 by discussing three

case studies of Fausto-Sterling applying DyST to different topics: Sexual orientation, infant

gender development, and differences between men’s and women’s bones. Section 3.2.2 then

takes a ‘top down’ systematic perspective by explicating what I take to be the most important

concepts of Fausto-Sterling’s DyST (i.e. the connotations ‘experience/embodiment’ and

‘iteration/emergence’). Next, section 3.2.3 clarifies and justifies the status of Fausto-Sterling’s

DyST on the framework- as well as on the theory-level, which is an important presupposition

for Fausto-Sterling’s motivation to overcome nature/nurture. Finally, section 3.2.4 explicates

and defends Fausto-Sterling’s argument concluding to have overcome nature/nurture and

sex/gender. Having introduced Fausto-Sterling’s DyST, section 3.2.5 provides a taste of

critique by reconsidering Oscar Kempthorne and his theory of causation from Part One and by

examining an implicated critique of Fausto-Sterling’s DyST. Finally, section 3.2.6 concludes the

section.

To close Part Two section 3.3 provides a substantive summary of the most important points

argued (cf. 3.3.1) and states the main conclusions that I draw from the issues discussed (cf.

3.3.2).

Finally then, this whole text is concluded in section 4 with an Epilogue. This Epilogue contains

an outro in section 4.1, which purports to bring together the two argumentative strings of Part

One and Part Two and also to refer back to the Introductory opinion piece in 1.3. Finally,

section 4.2 takes a critical look at this very text and its limitations and in addition discusses

further suggestions of research, which far exceeded the scope of this text.

1.3 Introductory opinion piece

This section purports to introduce the topic at hand and to provide a notion of the content

and direction of my argument. To begin with, and as mentioned above, the main topic of this

text are differences between men and women and therefore why men and women have

become what they are. Differences between men and women obviously exist. For instance, I

surely agree with Marc Hauser writing that


12

“[i]t is hard to imagine anyone living today disagreeing […] that there are biological differences between the sexes. Even the staunchest cultural relativists have to acknowledge that there are differences in the sex chromosomes and hormonal titers that lead directly to differences in our anatomy.”

(Baron-Cohen et al. 2005)

In other words, (nearly) binary biological differences exist, even if their categorical character

is disputed, because some ‘male’ and ‘female’ traits are shared greatly by men and women

while others are not. And as we will see below, the case is relatively clear regarding

chromosomes, but it’s not so clear regarding hormones and the status of ‘male’ or ‘female’

anatomy in general. Besides, however, such biological differences between men and women

don’t display the core of the problem in my view. Rather, I think that the problem revolves

around mental sex/gender differences and their relation to biological ones.

That is it revolves around the question, if men and women really ‘come from different planets’

(the terrible Mars- and Venus- analogy). In other words, do they have different kinds of minds

manifesting in different motivations, preferences, and mental capacities? Granted, a quick

look around suffices of course to convince that women and men are vastly different not only

from a biological but also from a psychological and sociological perspective. While this is of

course true, we have not yet specified, why this is the case, i.e., why those differences obtain.

Let me draw an analogy here I deem to be relevant. With respect to the measured IQ

differences between races, Stephen Jay Gould stated in an interview in 1995: “It’s a fact whose

meaning is totally unspecified by the existence of the fact itself” (ibid., min. 01:15). And: “The

existence of the […] difference is thoroughly consistent with the two utterly extreme

interpretations, namely, nature and nurture” (ibid., min. 00:45). What I claim is that the same

is true for differences between men and women. It might right away be reproached that IQ

and sex/gender are phenomena too different for analogy.4 I agree that they are different but

I don’t think that this difference invalidates that Gould’s punch line, i.e. ‘the existence of the

difference is consistent with the nature and the nurture interpretation’, is valid also regarding

differences between men and women.5 Thus, and in yet other words, I take it that the

4 One might point out, for instance, that there are obvious biological features (e.g. sexual organs), which correlate with the differences between men and women and that this is just not the case of IQ (meaning that there is no comparatively obvious ‘IQ-organ’ correlating with IQ differences). 5 Gould’s statement resonates with Susan Oyama’s often cited more general statement that “[m]any nature-nurture debates, in fact, have arisen because interested parties have accepted this logic and then battled to haul phenomena back and forth across the biological border” (Oyama 2000, 190).


13

empirical fact of both types of differences is underdetermined by nature- and nurture-

explanations.

This is also the reason, I believe, why nature/nurture is widely received and conceived of as

the nature versus nurture debate or controversy. The underlying aim, I impute, is to find or to

approximate a yet undiscovered true proportion of nature/nurture (with respect to whatever

trait under study). As a consequence, “interested parties […] battled to haul phenomena back

and forth across the biological border” (Oyama 2000, 190). Presupposing such true proportion

and its approximation, arguments that diverge are said to stem just from political calculations

afflicting ‘pure’ science. With respect to mental sex/gender differences, such reasoning might

be read into Steven Pinker stating: “Truth cannot be sexist” (Pinker and Spelke 2005).6

But such true proportion between nature and nurture does not exist in the first place, or so I

claim. This claim might be counterintuitive on first sight, because there is an obvious

correlation between biological and mental differences between men and women. But the

point is that this intuition is reasonable really only on first sight, because of the radical

explanatory underdetermination that I claim to hold for mental differences between men and

women. To see this clearly, take a look at the following argumentative form on mental

sex/gender differences:

1st premise There are biological sex differences (chromosomes, anatomy, hormones, etc.) between men and women.

2nd premise There are mental sex/gender differences (e.g. in cognitive abilities, character traits, motivations, etc.) between men and women.

3rd premise The biological sex differences stand in a non-random relation to mental sex/gender differences in cognitive abilities.

Conclusion Biological sex differences (partially) cause the mental sex/gender differences.

Premise 1 and premise 2 are beyond doubt true, even if there are surely quarrels to how large

the empirically documented biological and mental sex/gender differences are. What makes

this argument dubious is not premise 1 or 2. It’s rather the leap to the conclusion via premise

3 and thus the inference of a directed causal link between biology and cognition based on

their correlation.

6 This is breath-takingly bold an assumption and, if Pinker is serious about this, it’s a telling one, too.


14

More precisely, whole argument just is ambiguous, because its conclusion is perfectly

interpretable in terms of nature as well as in terms of nurture. On one hand, and with respect

to ‘nature’, it’s possible to interpret the conclusion such that male or female biological

features have some sort of effect on the mind in the form of an innate and inner drive or

instinct or predisposition. This would then be, why our stereotypes about males and females

exist and why virtually all societies have some attributions of social roles to men and women

in common. On the other, and with respect to nurture, it’s also conceivable that there are

mental sex/gender differences, because they reflect the stereotypes that spring from partially

universal social organisation. In other words, biological differences cause us to perceive and

to treat different persons differently producing self-fulfilling prophecies. Hence, the

underdetermination of nature and nurture explanations visible in this argument.7

But if this radical claim about the radical underdetermination of nature/nurture explanation

is true, then there is no point in asking neither whether nature or nurture provides the right

explanation nor what is the right proportion of nature or nurture. Consequently (and this is

identical with the position of Fausto-Sterling discussed later), the conclusion of this text will

be that the very framework, which produces these questions, namely, the nature/nurture

framework, is faulty.

But Fausto-Sterling’s counter-suggestion will be we studied only later. Before concerning it,

it’s necessary to explicate in more detail what the nature/nurture framework is in the first

place and to discuss more precisely what speaks against it. This will be done in the following

Part One of this text.

2. Part One: Nature/nurture and sex/gender

As already indicated, the purpose of this section is, firstly, to introduce the nature/nurture

framework, which implies the mode of thinking of biological (or innate) sex and cultural (or

acquired) gender. Secondly, it aims to criticize and render implausible this same framework

especially by means of an attack of one of its methodologies, i.e. heritability coefficients, as

well as by means of conceptual criticisms of core notions.

7 Obviously, refuting this general argumentative form doesn’t automatically refute all the particular arguments, in which researchers do their best to separate the effects of nature-elements (e.g. hormones, genes, etc.) and nurture influences. But this is quite consistent with the pedagogical purpose of the discussion of the argumentative form.

The nature/nurture framework

15

More precisely, I start out in section 2.1 with an introduction to what the nature/nurture

framework is supposed to be in the first place. More precisely, and in section 2.1.1, I firstly

sketch what ‘nature’ and ‘nurture’ are generally said to refer to and why nature/nurture is

often put as nature versus nurture. Secondly, I present three scholars: Steven Pinker, Matt

Ridley, and the early Anne Fausto-Sterling and their positions, which I take to be instantiations

of the nature/nurture framework in section .2.1.2.

After that, I focus in section 2.2 on the gene/environment-framework, which I think to be an

instantiation of nature/nurture and which figured prominently in the positions of Steven

Pinker and Matt Ridley. The main concern of this section is the critique of this specific

instantiation via the critique of one of its important methodologies: The heritability

coefficient, which is supposed to separate nature and nurture causal influences. To this end, I

firstly introduce in section 2.2.1 the technical concept and (historical) significance of

heritability. Secondly, I rebut in 2.2.2 its often attributed effect of separating nature and

nurture in terms of a pretended causal analysis. Thirdly, and finally, section 2.1.3 provides a

conclusion.

In section 2.3, I provide a first contextualized and partial impression of the biologist and

feminist Anne Fausto-Sterling and her work in section 2.3.1, on which Part Two of this thesis

will focus especially. Moreover, I provide further argument in order to render implausible

nature/nurture and gene/environment, respectively, in section 2.3.2. More precisely, I discuss

in section 2.3.2 Fausto-Sterling’s reception (entailing a further explication) of ideas

encountered in the section about heritability, the IQ debate, and genes/environment. In

section 2.3.3, I provide a brief discussion of the notion ‘environment’, which somewhat

foreshadows the change of perspective in Fausto-Sterling’s approach work, which is

documented in the Part Two of the text. I briefly conclude in 2.3.4.

Finally, section 2.4 closes the whole argument of Part One of the text by providing substantial

summary in 2.4.1 and by stating the main conclusion drawn in 2.4.2 adding a number of

qualifications as final remarks.

2.1 The nature/nurture framework

Let’s start then with an introduction into what the nature/nurture framework is about. In

section 2.1.1, I firstly discuss nature/nurture from a somewhat systematic perspective by

introducing what ‘nature’ and ‘nurture’ means for different scholars. Next, I explicate why


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nature/nurture is often put in terms of nature versus nurture. In section 2.1.2, I present the

three positions of the three scholars: Steven Pinker, Matt Ridley, and the early Anne Fausto-

Sterling as case studies of manifestations of the nature/nurture framework and their views on

sex/gender differences.

2.1.1 A brief introduction

The purpose of this section is to sketch what the nature/nurture framework is about. More

precisely, I concern what scholars usually mean by ‘nature’ and by ‘nurture’ and discuss

afterwards, why this framework is usually restated as nature versus nurture, before

concluding.

2.1.1.1 What is nature, what is nurture?

As a starting point, let’s take a look at a few characterizations of what ‘nature’ and ‘nurture’

are usually said to refer to in the context of an organism and some trait under study.

To begin with, the psychologists Eagly and Wood (2013) invoke “the terms in their broadest

meaning, whereby nature refers to biological structures and processes and nurture refers to

sociocultural influences” (ibid., 1, their italics). They thematise “nature and nurture causation

of sex differences and similarities in traits, abilities, behavioural tendencies, and attitudes and

beliefs” (ibid., 2) and thus concern sex/gender differences between men and women.

Next, Harris (2009) means by ‘nature’ “things that are inherited” (ibid., 13)—more specifically:

genes and/or DNA (ibid., 1/50)—and by ‘nurture’ “things that are acquired through

experience” (ibid.). In her book, she aspires to make the point that “[p]arenting has been

oversold” (ibid., 331) and that parents “have been led to believe that [they] have more of an

influence on [their] child’s personality than [they] really do” (ibid.). Thus, Harris is interested

in the genesis of personality in general.

In addition, Fausto-Sterling (2000d) characterizes nature and nurture as “two kinds of

processes: one guided by genes, hormones, and brain cells (that is, nature), the other by the

environment, experience, learning, or inchoate social forces (that is, nurture)” (ibid., 25).

Similar to Eagly and Wood above, Fausto-Sterling is usually concerned with sex/gender

differences.

And, finally, and independent of a particular research focus, in Plomin et al. (2015) use nature

and nurture in their introduction to Behavioural Genetics, which denotes the application of


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genetics to the study of behaviour, as “broad categories representing genetic and

environmental influences, respectively” (ibid., 73).

In sum, we have ‘nature’ referring to biological entities (genes, hormones, brain cells) inside

the organism and ‘nurture’ to sociocultural influences, experiences, etc, which are external to

the organism. Elements of these two sides are studied with respect to their influence on the

manifestation of an organism’s traits: For instance, dispositions, preferences, behavioural

tendencies, personality features, etc.

2.1.1.2 Why is it nature “versus” nurture?

We have learned in the last section that, relative to some trait’s manifestation, ‘nature’ usually

refers to the influence of some biological entity belonging to an organism and that ‘nurture’

usually refers to the influence of anything outside of the perceiving organism.

There is a history of two parties with opposing positions, which are construed as ‘genetic

determinists’ on one hand and ‘postmodernists’ on the other. The former have been

conceived of as holding that ‘biology is destiny’ as well as that there is a ‘human nature’ and

the latter as holding that the mind is a ‘blank slate’. Very roughly, the core of this opposition

is identical with the conflict between a rationalistic viewpoint, if characterised only by

‘considering some things innate’, and a radically empirist viewpoint, if characterised by

‘everything comes from experience’: The only difference being that it doesn’t concern

necessarily knowledge (or ideas) in the sense of the classic philosophical debate (e.g.

concerning mathematics).

This was only a very rough depiction and it paints extreme positions, which are usually not

seriously held. This will become more transparent in the course of the case studies presented

in the following section. But note already that regarding ‘nature-scholars’, the cognitive

psychologist Steven Pinker, for instance, explicitly denies that genes or biology are destiny (cf.

e.g. ibid. 2004, 7), e.g., that women and men necessarily conform with the average woman

and man, respectively. Rather, Pinker emphasizes the consistency of biology and malleability

(cf. e.g. ibid. 2002, 48/9), even if he explicitly holds that some (aspects of) mental traits are

innate and that there is such thing as a human nature.8

8 Cf. also Ridley 2002, epilogue and/or Halpern 2011, 32 f.


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On nurture’s side, we find the general claim that biology doesn’t matter in the sense that there

are no innate mental traits, no genetic predispositions, no human nature. Obviously, however,

just like the nature-scholars reject the extreme view of biological determinism (i.e. biology is

destiny), the nurture of nature are threatened by biological determinism, the nurture

defenders reject cultural determinism, which means that an individuals is reduced to what it

experiences (cf. e.g. Pinker 2002, 156 ff.; Butler 2011, ix). But while they (should) reject the

extreme positions that gender is either forcibly and totally imposed by culture or changeable

at will, ‘postmodernists’ still attempt to refute claims of human nature and related essentialist

positions, which furnish men and women with special innate predispositions (cf. Butler 2010,

2011).

Since both extreme, determinist positions are unlikely to be held due to their implausibility,

“virtually all researchers pay lip service to interactionist positions” (Halpern 2011, 9), as Diane

Halpern puts it. That is, virtually everybody is granting that neither nature nor nurture ‘can

do the job alone’ but that both are necessary for the explication of traits such that “the better

question is how much do nature and nurture contribute” (ibid.). However, this doesn’t prevent

that there are highly contested ‘grey areas’, which are argued to be due to nature or due to

nurture, respectively.9 In other words, just what the exact proportion of nature and nurture is

represents an open question.

More precisely, and as already indicated in 1.3, mental features especially (from preferences

attitudes over empathy to IQ), whose differential manifestations in men and women are the

main topic of this thesis, are fiercely discussed with respect to ‘how much is nature’ versus

‘how much is nurture’.

2.1.1.3 Conclusion

The nature/nurture framework contrasts biological entities internal to an organism and

entities external to organism with respect to their causal influence on the manifestation of an

organism’s trait in question. The influence due to biology is said to connote ‘innateness’ and

the influences of nurture is said to connote ‘acquiredness’. Moreover, the former has been

simplistically taken to be imply ‘unchangeability’ and the latter ‘changeability’.

9 A vivid example is provided by the discussion between Steven Pinker and Elizabeth Spelke about the nature of sex/gender differences in mathematical abilities measured and in the same context the fact that less women than men are employed disciplines like maths, physics, etc (cf. Pinker and Spelke 2005).


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However, these extreme positions are in fact not defended. Rather, researchers argue that

nature and nurture contribute to trait manifestation, i.e. they interact, and the proportion of

their influence relative to a trait in question is the subject of study. Note that this precisely

implies the existence of a (un-)knowable true proportion of nature and nurture (for some

trait), which was already alluded to in section 1.3.

Generally speaking, it’s helpful, even if not quite often stated that explicitly, to think of the

thus conceived nature/nurture interaction in a following way: Given a normal environment a

nature influence on a trait X determines the main direction of the trait’s development, while

nurture influences, canalizes and/or modifies the trait’s development but normally without

changing the main direction, which the nature-influence determined for X.

2.1.2 Three case studies

After having provided a very general look on what nature/nurture is about, this section aims

to introduce three scholars and their positions about human nature (and nurture), which I

take to be manifestations of the nature/nurture framework. I firstly concern Steven Pinker,

cognitive psychologist at Harvard University, then the early Anne Fausto-Sterling, current

Nany Duke Lewis Professor Emerita at Brown University, and finally Matt Ridley, science

journalist and regular contributor to The Times newspaper.

2.1.2.1 Steven Pinker: ‘Truth cannot be sexist’

Steven Pinker seems to define human nature as follows: Something is an element of human

nature (or human condition) if and only if it’s ‘innate’ or manifested in a ‘predisposition’—

words, which both occur frequently in Pinker 2002, 2004, and 2015). More precisely, Pinker

believes that the human brain/mind has an ‘innate’ or ‘genetic’ organization (ibid. 2002,

2004).

But what seems especially important for Pinker is not the very specific content of human

nature in the first place, because this content seems not fixed. At least it’s not fixed apart from

language, which he considers to be part of human nature and a product of natural selection

(cf. Pinker and Bloom 1990).10 And I would even take this to be a non-contentious point, if not

10 “The paper [i.e. “Language Learnability and Language Development” and/or “Learnability and Cognition”, M.B.] shaped me not just professionally but intellectually, by sensitizing me to the importance of innate mechanisms in cognition. Innate mechanisms are important not because everything is innate and learning is unimportant, but because the only way to explain learning is to identify the innate mechanisms that make learning possible. It was


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Pinker (2004) argued that, curiously, not all languages are innate: “Japanese and Yoruba are

not” (ibid., 6). (I found nothing to further qualify this claim so far.) But generally, and beyond

this point, it seems that Pinker’s notion of human nature has no ultimately fixed (or fixable)

content.

The reason for this is that in his view it’s the empirical sciences like Cognitive sciences,

Developmental and Evolutionary Psychology, Behavioural Genetics, and Neurosciences that

reveal human nature.11 He states: “These discoveries not only have shown that the innate

organization of the brain cannot be ignored, but have also helped to reframe our very

conception of nature and nurture” (ibid., 6). In over words, human nature is empirically

discoverable and its content non-fixed by the inductive nature of empirical sciences. In

consistence with this view, Pinker (2002) argues that, contrariwise to the positive hypothesis

human nature, the claim that human nature is a blank slate, i.e., that no mental traits inborn

is an empirical hypothesis turning out as false.12

Pinker’s view of human nature’s discoverability is closely associated with the view that it’s in

general possible to separate nature and nurture. In other words, framing the nature/nurture-

debate as an empirical hypothesis, the question whether some measured phenomenon is due

to nature or due to nurture needs to be a testable claim and, by implication, nurture-causes

and nature-causes need to be separable. Accordingly, Pinker writes about the importance of

“disentangle[ing] the knot of biological and cultural causes” (ibid., 317) or of “disentangle[ing]

heredity and environment” (Pinker 2004, 8).

Accordingly, Pinker (2002) muses in the context of discussing sex/gender differences about an

ideal experiment “to separate biology from socialization” (ibid., 348/9). But what interests

here most is that for Pinker such an ideal experiment is not just a piece of fantasy: He goes on

to actually identify such a theoretical ideal with studies conducted including the John-Joan-

case by John Money (ibid., 349). This famous case involved an ultimately failing sex-

an appreciation of this logical point that began a lifelong fascination with the nature of human nature—not just the parts that make language possible, but those that underlie cognition, emotion, aesthetics, and violence.” (Pinker 2013, 2, his italics) 11 [I]t was inevitable that the debate [i.e. nature vs. nurture] would be transformed by the recent efflorescence of the sciences of mind, brain, genes, and evolution. One outcome has been to make the doctrine of the blank slate untenable.” (Pinker 2004, 6) What follows is a list of these findings which by Pinker’s definition lists all candidates for elements of human nature. 12 “Regardless of its good and bad effects, the Blank Slate is an empirical hypothesis about the functioning of the brain and must be evaluated in terms of whether or not it is true.” (Pinker 2004, 42)


21

reassignment of a boy, who lost his penis in an accident, as female. This case has sparked a lot

of discussion (cf. on Money’s studies also e.g. Fausto-Sterling 2000, 66-70; Butler 2001), also

because Money himself promoted the initially successful reassignment at the beginning as an

affirmation of the nurture-hypothesis of gender and sexuality. Having been unsuccessful after

all, Pinker on the contrary interprets the case now as a falsification of the nurture-hypothesis

of gender.13

Let’s exemplify Pinker’s view of human nature in terms of its relation to sex/gender

differences. Pinker argues that, in contrast to racial and ethnic differences, sex/gender

differences are part of the “human condition” and therefore of particular importance.14 Pinker

(2002) provides a list of stable sex/gender differences and cross-cultural similarities found and

promoted by special sciences from Neuroscience to Evolutionary Psychology (ibid., 243 ff., 246

ff.).15 And though he grants that not all of those differences and similarities will be rooted in

human nature he holds that some of them surely are (Pinker 2002, 245). More precisely, he

holds thus that some behavioural sex/gender differences and similarities (in addition to the

anatomical sex differences) are part of human nature implying consequently that men and

women have by nature different minds.16

13 It seems that Pinker’s own view is that sexual orientation and gender are largely due to prenatal hormone exposure (cf. Pinker 2002, 348/9). On this logic, little John had been exposed to male hormones during pregnancy, which determined its sexual orientation (and sort of as a corollary) his gender. Other scholars are more careful: Reiner et al. (2006) state in their review that “[i]n sum, gender identity, whether consistent or inconsistent with other sex characteristics, may be understood to be ‘much less a matter of choice and much more a matter of biology’” (ibid., section 44). But they are unable to really detail the relevant aspects of biology and remain vague: “The outcome in the John/Joan case was consistent with the evidence derived from the intersex studies that seem at least, to indicate that individuals are born with an innate sense of their gender identity, which does not necessarily accord with the genital appearance, and cannot necessarily be overridden by consistent socialisation supported by hormone administration” (ibid., section 29.). Besides and for your interest, here we witness the reception of a stereotype, which is usually attributed to feminists, namely, the claim that sexual orientation is a matter of choice implying changeability to the point of arbitrariness. However, no one can reasonably defend this against the abundance of empirical data, which suggest that sexual orientation is stable and only sometimes subject to change. 14 “But unlike other human divisions such as race and ethnicity, where any biological differences are minor at most and scientifically uninteresting, gender cannot possibly be ignored in the science of human beings. The sexes are as old as complex life and are a fundamental topic in evolutionary biology, genetics, and behavioural ecology. To disregard them in the case of our own species would be to make a hash of our understanding of our place in the cosmos” (Pinker 2002, 340) 15 Moreover, he exemplifies in Pinker and Spelke (2005) stable sex/gender differences listing priorities in life, interest in people vs. abstract rule systems, risk taking, three-dimensional mental transformations, and, finally, mathematical reasoning. 16 “For all we know, some of the current sex differences may be just ephemeral. But gender feminists argue that all sex differences, other than the anatomical ones, come from the expectations of parents, playmates, and society.” (Pinker 2002, 345/6). To drive home his point, Pinker next cites the early Fausto-Sterling from her book Myths of Gender where in fact she held this position. But ‘gender feminists’, including Fausto-Sterling have long


22

Let’s make Pinker’s way of conceiving things more concrete in concerning in more detail his

view on sex/gender differences in cognitive abilities. These differences include differences in

spatial and mathematical reasoning, for instance. But they do not concern general intelligence

or basic categories of cognition (Pinker and Spelke 2005).

In general, Pinker argues that these differences are also due to a fundamental sex/gender

difference in objects of interest between people (females) versus things (males), which also

influences career choice:

“And this difference in interests will tend to cause people to gravitate in slightly different directions in their choice of career. The occupation that fits best with the ‘people’ end of the continuum is ‘director of a community services organization.’ The occupations that fit best with the ‘things’ end are physicist, chemist, mathematician, computer programmer, and biologist.”

(ibid.)

Moreover, Pinker claims that the cognitive sex/gender differences are accountable from an

evolutionary perspective: “In many mammals a greater territorial range is accompanied by an

enhanced ability to navigate using the geometry of the spatial layout […]. More often it is the

male who has the greater range, and that is true of human hunter-gatherers. Men’s advantage

in using mental maps and performing 3-D mental rotation may not be a coincidence” (ibid.,

347). He also points to the importance of hormones stating that “[w]hen women preparing

for a sex-change operation are given androgens, they improve on tests of mental rotation and

get worse on tests of verbal fluency” (ibid., 348). Consequently, he argues that “[w]omen’s

cognitive strengths and weaknesses vary with the phase of their menstrual cycle. When

estrogen levels are high, women get even better at tasks on which they typically do better

than men, such as verbal fluency. When the levels are low, women get better at tasks on which

men typically do better, such as mental rotation” (ibid.; cf. also Baron-Cohen et al. 2003).

However, in Pinker and Spelke (2005), he relativizes the reliability of the literature on

hormones with respect to cognition arguing that “the literature is a bit messy” (ibid.) and it’s

possible that all claims of the effects of hormones on cognition will turn out to be bogus”

(ibid.).

since jettisoned the distinction between biological sex and social gender in favour of a more radical position—remind yourself just of Judith Butler’s Gender Trouble (1990). So this somewhat implies that Pinker (2002) is not particularly well informed regarding feminist positions.


23

Granted, Pinker is well aware of the (often pointed to) assumption’s fallacy that being an

element of human nature implies the unchangeability of this element.17 Rather, and

consistent with malleability, he conceptualizes innate organizations in terms of probability,

which has nothing to do with biological determinism or hardwiring in the sense of ‘biology is

destiny’ (cf. Pinker 2002, 48/49). Consequently, Pinker does not hold that for some

behavioural trait, its being rooted in human nature implies that it applies to all individuals,

who share this human nature. For instance, he states that “[n]o sex difference yet discovered

applies to every last man compared with every last woman, so generalizations about a sex will

always be untrue of many individuals” (Pinker 2002, 340). In other words, sex/gender

differences are statistical phenomena and such that the traits in males and females are

normally distributed (Pinker and Spelke 2005).18

To sum up the most important characteristics of Pinker’s position: Firstly, he holds that human

nature is accessible via the empirical sciences. This implies that what qualifies as human

nature is never irrevocable (due to the research’s empirical nature) and that nature and

nurture are measurable and thus separable. Secondly, Pinker assumes that human nature is

quasi-universal and probabilistic, which means that its laws know exceptions (in contrast to

laws of physical nature). Finally, and regarding sex/gender differences, he holds that

anatomical sex differences are part of human nature as well as mental differences and that

they are based on an genetically and/or innately organized brain/mind.

17 “[I]nnate organization cannot be equated with a lack of sensitivity to environment, and […] responses to the environment are often not specified by the stimulus but by the nature of the organism.” (Pinker 2004, 13) For instance, Gould (1996) charges Herrnstein’s and Murray’s The Bell Curve (1994), which concerns intelligence and class structure in the United States, to have committed the fallacy of “advocat[ing] ‘permanent and heritable differences’” (Gould 1996, 35; cf. also ibid., 367 ff. for a critique of The Bell Curve). 18 Still, there seem to be core-features of human nature which are universal in the strict sense: Pinker (2004) says that “cognitive science has shown that there must be complex innate mechanisms for learning and culture to be possible in the first place” (ibid., 6). Similarly, Pinker (2013) writes that “the only way to explain learning is to identify the innate mechanisms that make learning possible” (ibid., 2; his italics). This seems to me an element of human nature which is different in kind from elements like sex/gender differences, because learning is an constituting aspect (without specifying content), while sex/gender differences seem to be elements that specify content. But remember that I argued above that the content of human nature is dependent of empirical findings, hence notoriously non-fixed. It seems that we have to add therefore what might be called an constitutive element of human nature (i.e. learning) which is fixed and does not concern specific contents (even though it’s also been ‘discovered’ by cognitive sciences). I assume that Pinker concerns also this constitutive element of human nature, when he calls himself a “Hobbesian” (Pinker 2013, 228) because “the computational theory of mind was foreshadowed by Hobbes” (Pinker 2002, 33). (Besides, notably, his explicitly Hobbesian belief that persons are born as rather competitive and non-cohesive beings whose living together is secured only by a social contract of a governing body; cf. e.g. ibid., 318-332)


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2.1.2.2 The early Anne Fausto-Sterling

In a footnote of the former section, we have encountered Steven Pinker’s characterisation of

Fausto-Sterling’s view on sex/gender differences, namely, that

“[t]he key biological fact is that boys and girls have different genitalia, and it is this biological difference that leads adults to interact differently with different babies whom we conveniently color-code in pink or blue to make it unnecessary to go peering into their diapers for information about gender.”

(Fausto-Sterling 1992, 152/3 as cited in Pinker 2002, 345/6)

As far as I can see, Pinker (2002) correctly characterizes the view that the early Anne Fausto-

Sterling was committed to and which can be reformulated as follows: human beings are

dimorphically distinguished by their biological sex differences (in terms of body parts) based

on which all gendered behaviour is then culturally imposed. Pinker subsumes Fausto-Sterling

under the pejorative notion ‘gender feminist’ due to her claim that “all sex differences, other

than the anatomical ones, come from the expectations of parents, playmates, and society”

(Pinker 2002, 246).

I think, Pinker rightly represented Fausto-Sterling’s early view. In what follows, I claim that

Fausto-Sterling’s positions is actually similar to Pinker’s, because her position entails as well

as his that human beings’ sex (in terms of anatomical sex and as separate from gender) can

be in principal discovered (and might be characterised as an element of human nature). For

instance, Fausto-Sterling suggests in “The Five Sexes” (1993; even if explicitly “with tongue in

cheek”) that we are merely wrong in holding that there are only two sexes (representing the

nature of homo sapiens). This is wrong because nature confronts us with greater variability of

sexes which the dyadic male-female-system just cannot exhaustively account for: “[S]ex is a

vast, infinitely malleable continuum that defies the constraints of even five categories”

(Fausto-Sterling 1993, 2). In other words, the dimorphic description does not correspond to

the biological facts and it therefore needs to be reformulated in terms of an ultimately n-adic

spectrum or continuum of sex (ibid., 1).19

19 But this point and its epistemological implications are actually a minor point, because Fausto-Sterling (1993) actually concerns the surgical interventions performed on babies with the aim to normalize ambiguous bodies with regard to the male-female-system. She muses about a society where, for instance, “hermaphrodites [i.e. persons who possess one testis and one ovary (the sperm- and egg-producing vessels, or gonads; Fausto-Sterling’s definition in the same text] would be concerned primarily not about whether they can conform to society but about whether they might develop potential life-threatening conditions […]” (ibid., 5).


25

Note the larger context of the early Fausto-Sterling at least from 1993 till including 2000,

which was the question of intersexuality and especially its treatments in terms of medical

intervention, as discussed, for instance, in Fausto-Sterling (1993, 2000e).20 Therefore, Fausto-

Sterling (1993) can together with Fausto-Sterling (2000a) as well as with Fausto-Sterling et al.

(2000) be read as the attempt to render intersexuality natural or even as to make the

ultimately moral argument in favour of a strategy-change in intersex-persons’ treatment as

persons whose sex need to be corrected). By extension, it could be said that these texts

attempt to naturalize the continuum-notion of sex and to locate intersex as one of its ordinary

manifestations—and all this based on a fact-oriented argumentative style. This fact-

orientation becomes manifest in the article “How sexually dimorphic are we?” (Fausto-Sterling

et al. 2000), which explicitly studies the morphology (i.e. biology’s subdiscipline comprising

anatomy and physiology) of the human being and makes the point that about 1.7% of all

births are non-pathologically intersex. Thus, the authors argue that there is a significant

overlap between male and female, even if the validity of the article is conceptually but also

methodologically questioned (cf. Sax 2002, Hull et al. 2003). Hence, and in terms of

morphology, Fausto-Sterling conceives of herself as standing on the firm ground of

discoverable biological facts.

But in addition and just like Pinker does, it seems that the early Fausto-Sterling holds that

(beside anatomical sex differences) also absolute behavioural sex/gender differences can be

discovered in principle (and by implication as part of human nature). She argues that “[o]nly

as the separate cultures of men and women become more alike (a spectre that horrifies many)

will we be able to assess the possibility of unalterable sex differences” (Fausto-Sterling 1992,

270).21 What interests here, however, is not the question which behavioural sex/gender

differences these might be. The early Fausto-Sterling’s actual position is clearly that

sex/gender differences are socially constructed22 and that even non-mental sex differences

might be at least socially caused to a large degree (cf. ibid. 1992).23 What interests is rather

20 Intersex with respect to “sex chromosome composition, gonadal structure, hormone levels, and the structure of the internal genital duct systems and external genitalia” (Fausto-Sterling et al. 2000, 151). 21 Compare also the whole “Afterword for the second edition” in Fausto-Sterling (1992). 22 Cf. Fausto-Sterling 1987, 1995, 1997 and e.g. the title of ibid. 1987: Society writes Biology / Biology Constructs Gender. 23 For instance, sex differences in height and strength might largely be caused by socially instituted differences in treatment (nutrition, physical activities, etc.; cf. Fausto-Sterling 1992, 214 ff.). She suspects that “given widespread changes leading to equal physical activity for boys and girls in an environment with adequate


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the logic underlying Fausto-Sterling’s thinking and what it implies: Namely, nature and nurture

can in principle be separated and human nature is thus in principle measurable. In other

words, it’s in principle decidable and testable whether or not some sex/gender differences are

innate.

All this backs the assumption that Fausto-Sterling’s early position and Pinker’s position on

sex/gender differences are cognate in kind if yet differing in detail. It’s granted though that

Fausto-Sterling disagrees with Pinker under what circumstances human nature is measurable.

Remember that Pinker argued with regard to John Money’s studies and that ideal experiments

have incidentally been performed. In contrast, Fausto-Sterling seems to have a rather

unrealizable ideal experiment in mind to decide the question of absolute sex/gender

differences, because it’s not very realistic that men and women might be equal in terms of

any relevant aspect, in order to have no potential confounding variables. This would include

anything ranging from legal and educational aspects to equal nutrition, over equal appearance

on first sight (excluding some set of biological sex differences) over to equal stereotypes.

2.1.2.3 Matt Ridley: Nature via nurture

Pinker (2004) also cites repeatedly Matt Ridley who argues that nature operates via nurture.

Ridley’s account aspires to replace the nature/nurture framework in favour of nature via

nurture (cf. ibid., 3/4, 95/6, 277/8). This replacement suggests a qualitative change from

nature versus nurture towards nature via nurture. However, and as we will see, while Ridley’s

position seems different at first it turns out to be rather ordinary due to its defence of (genetic)

predispositions and to be actually quite similar to Pinker’s view.

Explaining his nature-via-nurture-framework, Ridley makes it quite clear that it consists in a

mapping of a certain (set of) gene(s) on one hand and a certain (set of) environment(s) on the

other. This becomes clear in the following citation, for instance24:

nutrition, the male/female height dimorphism will decrease by a few percentage points but will not disappear altogether” (ibid., 216). 24 Compare also Ridley (2003b): “The genes cannot be denied. And yet, of course, there are no genes for liking guns or dolls, there are only genes for channelling male instincts into imitating males and female instincts into imitating female behaviour. There are natures that respond to some nurtures and not others […]” (ibid. , 256; my italics). Or as well Ridley (2003a, 118, my italics): “It is another forceful reminder that bodies—and brains—are not made, like model airplanes. They are grown, and that growth is directed by genes. But the genes react to each other, to environmental factors, and to chance events. To say that genes are nature and the rest is nurture is almost certainly wrong. Genes are the means by which nurture expresses itself, just as surely as they are the means by which nature expresses itself.” Or compare Ridley (2003a, 205).


27

“Having a certain set of genes predisposes a person to experience a certain environment. Having ‘athletic’ genes makes you want to practice a sport; having ‘intellectual’ genes makes you seek out intellectual activities. The genes are agents of nurture”.

(Ridley 2003a, 92, my italics)

Ridley thinks of nature always in relation with nurture (i.e. with certain environments) and

implies a notion of human nature different from Pinker’s. He argues that it doesn’t matter

“whether human nature is more innate or more learned, but instead the precise way in which

it is both” (Ridley 2003a, 70). That is, Ridley seems to argue that what qualifies as knowledge

of human nature is only what yields knowledge about the interaction of certain genes in

relation with certain environments. By consequence, Ridley’s notion of human nature includes

heritable (i.e. genetic, innate) features (or aspects) of human nature (ibid., 76/7) as well as

non-heritable (i.e. learned, cultural) features (or aspects) of human nature.

This stands in contrast to Pinker’s notion of human nature, which is formulated differently and

in terms of rather absolute (and not environment-relative) terms (which of course does not

imply that Pinker does not acknowledge the importance of environmental effects). It seems

adequate to say in that in Ridley’s case the human nature is reduced to the problem not of

disentangling nature and nurture but of matching nature(s) and nurture(s), which implies,

however, that nature and nurture are presupposed.

Besides these initial differences, Ridley is more similar to Pinker in what follows: His discussion

of nature via nurture and of human nature seems to crystallize in the notions instinct (cf.

Ridley 2003a,b), predisposition (cf. Ridley 2003a), and preference (cf. Ridley 2003b) which I

take to be quite synonymous in effect. In the citation given above, Ridley (2003a) defines

‘predisposition’ as follows: “Having a certain set of genes predisposes a person to experience

a certain environment” (ibid., 92). Thus, predisposition, instinct, or preference manifests itself

in terms of genes and they are innate (e.g. ibid., chapter two).25 Such predisposing genes are

said to be necessary but not sufficient (which is actually a very strong claim) to result in

25 For the interrelation between ‘genes’, ‘disposition’, and ‘instinct’: “In fact, there is a way of acquired characteristics to come to be incorporated into genetic inheritance, but it takes many generations and it is blindly Darwinian. It goes by the name of the Baldwin effect. A species that over many generations repeatedly exposes itself to some experience will eventually find its offspring selected for a genetic predisposition to cope with that experience. Why? Because the offspring that by chance happen to start with a predisposition to cope with that circumstance will survive better than others. The genes can thereby come to embody the experience to the past Something that was once learned can become an instinct.” (Ridley 2015, 57, my italics)


28

schizophrenia (cf. ibid., 111 ff.). Something similar might hold for toy preferences26 (ibid., 253),

criminality (ibid.), and aggression (ibid., 245), and racism (ibid., 264)27.

Let’s take an explicit look at what Ridley says with respect to sex/gender differences. Ridley

thematizes especially toy preferences. I already indicated in the above paragraph that Ridley

(2003a) believes that toy preferences are partially due to a respective disposition. Ridley

(2015) reaffirms his position arguing that “it has now been conclusively shown that the aisles

of toy shops, with their rampant sexism, are responding to innate preferences in human

beings, not causing them” (ibid. 2015, 169). Moreover, he takes this to be additionally

supported on a level of Evolutionary Psychology citing (ibid.), for instance, the study Alexander

and Hines (2002) which claims to have found that “vervet monkeys […] show sex differences

in toy preferences similar to those documented previously in children.” (ibid., 467).28

Providing general reasons for his belief in sex/gender differences, Ridley (2003b) points, firstly,

towards evolutionary theory (and men’s and women’s different evolutionary pressures) and,

secondly, towards what he calls the ‘overwhelming’ empirical evidence from physiologists and

psychologists (ibid., 248). Ridley assumes just like Pinker that classically biological sex

differences as well as mental sex/gender differences are universal and therefore innate (cf.

Ridley 2003b, 247 ff.). Ridley points this out, for instance, regarding mating referencing the

cross cultural studies performed by David Buss (cf. Ridley 2003a, 53-55) and he holds of course

that homosexuality is innate as well (cf. Ridley 2000b, 263 ff.; ibid. 2003 160 ff.).29

We learned above that Ridley’s view of nature via nurture seems specific because it

theoretically frames predispositions (or preferences, or instincts) in terms of their connection

with specific environments. Remember also that for Ridley it’s the precise connection of

certain nature(s) with certain nature(s) that concerns human nature.30 This seems indeed

26 Ridley’s even thinking in the context of gender stereotypes that “the parental reaction itself is just as likely to be innate: parents could be genetically predisposed to perpetuate rather than fight gender stereotypes” (Ridley 2013, 253). 27 “By the end of the twentieth century, sociologists were gingerly hinting at a new and disturbing idea—that however unjustified the science of race might be, racism might be in the genes. There might be an inevitable human tendency to be prejudiced against people of a different ethnic origin. Racism might be an instinct.” That he endorses this general claim (even though if there might be difference between different instincts) is clear in the moral he draws: “Moral: The more we understand both our genes and our instincts, the less inevitable they seem.” (ibid., 266) 28 This study was criticized by Meynell (2012). 29 This study was criticized by Kitcher (2003a) 30 This might explain, why Ridley (just as Pinker: cf. ibid. 2002, 381 ff.) praises so much Judith Rich Harris’ books on development of children’s personality: Harris claims to firstly examine all that is inherited (Harris 2009) and


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different from Pinker’s view at least in formulation, since Pinker seems to talk rather in

absolute terms and without emphasizing knowledge of both nature and nurture. In other

word, it might be stated that Pinker relies covertly on a absolutized, but specific standard

environment, while Ridley sticks to this standard environment as well while thematizing it.

However, Ridley’s notion seems to have very similar consequences as Pinker’s theory does,

because it presupposes the separability and thus measurability of nature and nurture as well

as it sticks to the notion of human nature and its accessibility via the empirical sciences.

2.1.3 Conclusion

Let me wrap up what was argued and emphasize what I take to be the most important points

of this section. Remember that its purpose was to give an impression of what the

nature/nurture framework is about.

To begin with, discussing the nature/nurture framework in general, we found firstly that

‘nature’ usually refers to the influence on a given trait of some biological, innate entity interior

to a well individuated organism in question. In contrast, ‘nurture’ usually refers to the

influence on a trait of anything, which is exterior to the organism like culture and environment.

Secondly, nature/nurture is usually framed as nature versus nurture, due to the fact that, e.g.

with regard to sex/gender differences, there are certain differences between men and women

regarding which the question of how much is nature and how much is nurture is very

contested.

Thirdly, and given the innateness of the biological influences on traits, and considering the

case studies, we learned also that quasi-universality, i.e. high probabilities, with respect to

then to examine all that is environmental (Harris 2007). In her book The Nurture Assumption, she is said to argue that “[c]hildren get their personalities mostly from within themselves” (Ridley 2015, 162) and that what is not “from within” is due to peers instead of parents influence children (ibid., 161/2; cf. also Ridley 2003a, 251-7). In the follow up book No Two Alike, “Harris was able to address the really interesting mystery that the behaviour-genetics studies had revealed: what causes the 50 per cent of personality differences that cannot be caused directly and indirectly by genes?” (Ridley 2015, 162; cf. ibid. 154-169). For a view opposing Harris and arguing that “it seems highly unlikely that parents have no or little impact on their adolescents’ values, attitudes, and personality. Indeed […]: How could it be that adolescents’ development is influenced by the people with whom they interact—as Harris admits, by pointing to the importance of peer influence—but not affected by the people who have lived with them, raised, them, and tried to influence them since the moment they were born? Is it conceivable that evolution would have led to the development of human organisms that are influenced by the development of human organisms that are influenced by everyone other than their parents? Given what we know about modelling, observational learning, and social influence, this proposition is preposterous.” (Steinberg 2001, 11; compare also ibid., 10-12 and the review of Harris 1998 by Collins et al. 2000). Similarly critical is also Halpern (2011, 289 ff.).

Genes/environment: Can heritability separate nature and nurture?

30

trait similarities or differences (across cultures) are thought to allow the inference of a nature-

cause or as ‘being part of human nature’.

Fourthly, and more generally, all three scholars discussed above take nature, or specifically

sex/gender differences, to be measurable in principle and thus discoverable by the empirical

sciences. This measurability clearly implies a separability of nature and nurture. Hence, all

three scholars situated in the nature/nurture framework.31

Finally, we saw that Pinker and Ridley concerned nature/nurture especially in terms of genes

and genetic (and/or) ‘disposition’ or ‘organization’ (of the brain/mind). This leads us to the

discussion of the genes/environment-framework, which I take to be an instantiation of the

nature/nurture framework and which I treat in the following section.

2.2 Genes/environment: Can heritability separate nature and nurture?

As we have seen especially with respect to Matt Ridley’s and Steven Pinker’s notion of human

nature, one possibility to manifest the nature/nurture framework is the opposition: Genes

versus environment. This instantiation emphasizes the causal relevance and immediate

importance of genes with respect to all (complex) traits that a human being manifests. This

section has the purpose of criticizing this instantiation of nature/nurture by refuting the

effectivity to separate nature and nurture of one of its important methodologies: The

computation of heritability coefficients.

In what follows, I, firstly, introduce the notion of heritability, its historical context, why it

became a very contentious concept, and what is its link with sex/gender differences. The next

section 2.2.2 argues against the causal relevance of heritability and against its possibility to

separate nature and nurture in the context of social sciences. I close with a conclusion in 2.2.3.

2.2.1 What is heritability?

This section introduces the notion of heritability. More precisely, the first section presents

how heritability is calculated as based on the statistical inferential method of Analysis Of

Variance (ANOVA). The following section then introduces the historical context of heritability,

and why it became a contentious concept.

31 This is true, even we saw that Fausto-Sterling takes the ideal circumstance, under which absolute sex/gender differences (i.e. this knowledge of human nature) are knowable, is not achievable, while Pinker (and Ridley) see human nature practically discoverable.


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2.2.1.1 Computing heritability: A statistic method

The heritability coefficient32 is a statistical entity, which is based on the more general statistical

method of Analysis Of Variance (henceforth short: ANOVA). Heritability coefficients, which

range between 0 and 1 (or 0% and 100%), are defined to denote the proportion of total

phenotypic differences (i.e., for instance, of a trait X measured), which is ‘due to’ genotypic

variance (cf. Plomin et al. 2015, 87). They are based on a data set in the form of a reaction

norm, which is “a table of correspondence between phenotype, on one hand, and genotype-

environment combinations on the other” (Lewontin 2006a, 522).33

Heritability coefficients and their underlying data are often visualized by a graph. For instance,

figure 134 has an underlying data matrix featuring n factors (or columns) representing n

different environments and two rows with two

different genotypes.

On this graph, we see the continuous measurements

(P) of an organism’s trait on the y-axis and on the x-

axis a set of (not further specified) environments (E),

in which the trait has been measured. The two lines

represent two different genotypes (G1 and G2) of

organisms, whose reactions (in terms of P) on the different environments have been tested.

In the context of heritability, we’re now interested in the following question: To which factor,

‘environment’ or ‘genotype’, can more trait-variance be ascribed?

Statistically speaking we’re interested, firstly, in main effects.35 Regarding figure g, we would

argue that there is a main effect on G and on E, because, firstly, G1 is always higher than G2

and, secondly, because both Gs change relative to the environments. Importantly, however,

G1 and G2 are (pretty much) parallel, which means that there is (quasi) no interaction effect,

which in turn would be implied by non-parallelism of the lines.

32 For a nice introduction to heritability see Rose (2005) and Block (1995). 33 In other words, for each pairs genotype × environment, there is a phenotype-value and what interests in ANOVA (and heritability) are the variances that can be computed and compared. 34 Reproduced with permission from Lewontin, R. c. (2006). The analysis of variance and the analysis of causes. In: International Journal of Epidemiology, 25, 520-525, ©2006, Oxford University Press. 35 A simple main effect only on G would show on the graph two horizontal and parallel lines (G1 and G2), which would thus be equal in no matter which environment. A simple main effect only on E would show two lines G1 and G2, which were essentially merged to one line and which would not be horizontal (and change relative to the environment).

Figure 1: From Lewontin (2006a), 522.


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To compute those effects, ANOVA computes variances36 due to the two factors G and E (main

effects) and due to their interaction (G×E) and relative to the total data’s variance. That is, if

(relative to the whole data set’s variance) the trait values P of organisms with G1 differ strongly

from those of G2 (ignoring E), then there is a main effect of G. And if (relative to the whole

data set’s variance) the trait values for P of organisms in E1 differ strongly from E2, E3, En

(ignoring G), then there is a main effect of E. In figure 1, we can see that we have main effects

both for G and E but almost no interaction (due to almost parallelism between G1 and G2).37

Finally, and as already mentioned, the heritability coefficient then just is the proportion of the

computed ‘genetic variance’ (variance due to factor G) to the ‘total variance’.38

Note that the notion of statistical interaction and, generally speaking, the concept of

interaction in this context is problematized by Lewontin arguing against heritability (cf. section

2.2.2) and that I also reconsider interaction again as well as in a more vivid and less abstract

36 Variance is defined as the mean of the squared deviations of a set of values from their mean. What matters mathematically is the theorem that the total variance equals the row variance + the column variance + the error variance (cf. Serlin 2005). 37 There is a reason to include into one’s model of phenotypic variance not only G×E interaction but also what is called ‘genotype-environment correlation’. An instance of such a case is for example presented by Block (1995): In a world, where red haired persons would be hated and abused because of their hair colour, all red-haired children would score lower than all other children. But this would not be because of bad ‘genes for IQ’, but because of genes for red hair that happen to indirectly effect IQ (cf. Block 1995, 116 ff.). Similarly, if identical twins are treated more similarly like non-identical ones, because the former look more alike than the latter, then the former higher similarity regarding a trait P would not be due to more equal genes associated with P, but rather due to those genes that make them look so similar in the first place (which is not what is to be proven in the context of a study of a complex trait. 38 In formulae, this looks as follows. Firstly, we have our model of total phenotypic variance stating that it’s equal to the sum of the genotypic (1st factor) and the environmental variance (2nd factor).

𝑉𝑝 = 𝑉𝑔 + 𝑉𝑒

Next, heritability is defined as the proportion of the total genetic variance and total phenotypic variance:

𝐻𝑒𝑟𝑖𝑡𝑎𝑏𝑖𝑙𝑖𝑡𝑦 =𝑉𝑔

𝑉𝑝

Notably, Vg does not refer to additive genetic variance. In other words, we’re not concerning narrow heritability (h2), which models genetic influence stating that “underlying genes […] act to sum together […], so that one doe dose of the allele results in the addition of 1 unit of a trait, two doses of the allele yields 2 units, and so on […]” (Schaffner 2016, 25, his italics). Rather, we’re concerning broad heritability (H2), where Vg is defined as the addition of Vag, Vd, Vep, and Vam and the above formula looks as follows:

𝐻2 =𝑉𝑎𝑔 + 𝑉𝑑 + 𝑉𝑒𝑝 + 𝑉𝑎𝑚

𝑉𝑝

Consequently, broad heritability models Vg as the addition of additive genetic variance (Vag) plus variation due to gene-gene interaction (Vep; i.e. a gene covaries with a phenotype only in context of another (set of) gene(s)) plus variation due to dominant genetic influence (Vd; i.e. genetic interactions of different alleles at one gene locus), and, finally, plus variation due to assortative (i.e. non-random) mating (Vam).


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manner in section 2.3.2, which concerns Anne Fausto-Sterling’s reception of Lewontin’s

discussion of interaction (in case the reader wants to take a potentially instructional detour).

2.2.1.2 Heritability and IQ: A hot topic

Heritability coefficients were originally used in agriculture in order to find those genotype-

exemplars of plants, which have the best outcome on a certain soil (cf. Keller 2010, 59;

Wahlsten 1990, 119). But heritability only became a highly popular and contentious topic in

the debate about the relation between IQ and race-membership, where heritability was part

of the argument. More precisely, Arthur Jensen incited large criticism with his paper “How

much can we boost IQ and scholastic achievement?” (Jensen 1967), which is based on the

assumption

“that currently used IQ tests do indeed reflect innate, genetically determined aspects of intellectual ability in persons from the population on which the tests were standardized and validated.”

(ibid.)39

From then on, scholars like Richard C. Lewontin, Stephen J. Gould (and also Noam Chomsky)

amongst others participated in a heated and long debate on the side of Jensen’s critiques (cf.

Lewontin 2006a, 1970, 1976; Gould 1996; Chomsky 1972a,b). They we’re arguing and

polemizing against Jensen and his defenders like Richard J. Herrnstein and Charles Murray (cf.

Herrnstein and Murray 1995) or, more recently, Neven Sesardic (cf. Sesardic 2005) amongst

others.40

Since then, heritability was also adopted as an methodical element of Quantitative Genetics

(or Behavioural Genetics). Lots of data have been gathered and high percentages of

heritability have been attributed (non-contentiously) to numerous human non-complex but

39 What will have enraged Jensen-critiques are probably sentences like this one “One set of facts may be viewed as having potentially serious implications for the welfare of Negro Americans as well as of society in general. It appears that forces are at work which may create and widen the genetic aspect of the average difference in ability between the Negro and white populations, with the possible consequence that no amount of equality of opportunity or improvement of educational facilities will result in equality of achievement or in any improvement of the chances for the Negro population to compete on equal terms”. But to be fair, Jensen also states in the same context that “[t]he fact that social and cultural differences in fact exist among different races and social strata in our population is not in itself evidence that these cultural factors are important determinants of IQ differences. The evidence indicates that they are not. […] The reason I am not as alarmed by this conclusion and [sic] might be, is that I see the IQ as representing only a portion of the total spectrum of human abilities” (ibid.). Against this background, Jensen is also making the point that IQ just is not identical with scholastic achievement (relativizing importance of the former), which is much more complex and that “[t]he proper evaluation of such programs [i.e. compensatory education programs] should therefore be sought in their effects on school performance, not on how much they raise the child’s IQ” (ibid.). 40 A sober discussion with a systematic interpretation of this debate is provided by Taber (2014).


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also (and contentiously) complex human traits: That is, to height, weight, body mass index,

but also to intelligence, personality, schizophrenia, depression, political attitudes and

divorce.41 Besides, heritability has also been applied to sex/gender differences. In the list of

Chabris et al. (2013), one can find ‘sexed’ (and thus differing) heritability coefficients for

depression, smoking, alcohol use for adults men and women and with respect to non-adults:

externalizing problem behaviour and internalizing problem behaviour. In addition, heritability

coefficients have been also produced for atypical gendered behaviour and gendered beliefs

(cf. e.g. Knafo et al. 200542 as well as Knafo and Spinath 2011, respectively). A review of the

relevant literature concerning heritability and gender identity is Polderman et al. (2018; cf.

also Halpern 2011, 167 ff.).

However, in hindsight, computations of heritability have been found to be ‘too successful’

(Turkheimer 2011, 230; cf. Schaffner 2016, 45 ff.; Ridley 2002, 82/3). This is because it has not

been possible to identify specific (small sets of) genes in relation to the measured traits in

order to substantiate causally interpreted heritability claims, i.e., claims that a trait X’s

heritability is implicative with respect to the importance of the role of genes for the

development of X. This problem is labelled in the literature ‘missing heritability’43 (and it exists

also in its environmental version of missing environment44). This is then also, why Stephen

Downes could write in 2015 that

41 Cf. Chabris et al. 2013, table 1, for a list of traits and their coefficients. 42 Criticized in Fausto-Sterling (2015b), for your interest. 43 One aim of the Human Genome Project, which was launched in the 90s, was to identify precisely which genes (or set of genes) correlate with which complex human traits. However, the results of the attempts of identifying specific genes or small sets of genes with certain traits has been highly unsuccessful. From the beginning, HGP was largely advertised and hyped (cf. Lewontin 2000a), even if there were also critical voices arguing that causal interplay between genes and complex human traits would be too complicated to find replicable associations (Turkheimer 2000, 163/4). However, the scepticism had turned into disappointment, when Turkheimer (2011) wrote that “sometimes prediction is just prediction [and] [t]hat [this] is what the missing heritability problem is really about, and why it has not yet been solved” (ibid., 240). Moreover, Chabris et al. (2013) conclude that “[i]f we have learned that behavioural genetic variation is caused by many genes with effects that are too small to currently measures, then we have also learned something important about the physiology and evolutionary history of such traits” (ibid., 164). On missing heritability cf. also e.g. Bourrat and Lu (2017). 44 There is a discussion lead among behavioural geneticist concerning non-shared (external) environment in the

context of twin-studies (cf. Plomin et al. 2001, Plomin et al. 2011, Turkheimer 2000; for a quick overview see cf. Schaffner 2016, 26 ff.). In contrast to shared environment which makes twins more alike, non-shared environment is “defined as all those things that make the twins different” (ibid., 27, his italic). The problem is very clearly stated by Schaffner (2016) referencing a meta-analysis of influence of non-shared environment in general and independent of specific behavioural traits: “[T]he nonshared environment may help to explain about 50% of the phenotypic variance, but the specific factors that constitute the nonshared environment typically are not measured, so thus far they only seem to account for 2% of explained variance” (Schaffner 2016, 29). That is, strictly speaking, researchers don’t really know and cannot enumerate what exactly makes twins different and were confronted to a problem of ‘missing environment’ (Bleidorn et al. 2014)—remind yourself of the problem


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“[t]here is something of a consensus in most fields (e.g. philosophy of biology, evolutionary biology, psychology and behavioural genetics) that heritability measures […] only have a very limited use.”

(ibid. 2015)

Still, and as we saw in the last paragraph, the notion of heritability is to this day present in the

literature on complex human traits (including sex/gender differences) of a certain provenance.

And, there is still large potential for misunderstandings, as will be argued more clearly in what

follows. Therefore, I take the time to perform a refutation of heritability’s attributed causal

implications.

2.2.2 The causal irrelevance of heritability: Oscar Kempthorne’s critique

Up to this point, I did not concern in detail what heritability is claimed to achieve: Namely, to

provide information about the causal relevance of genes for the development of a complex

human trait and to separate nature and nurture. In what follows, I’m arguing that heritability

can achieve neither of these things.

The problem at hand is therefore what heritability claims actually mean. For instance, what

does it mean to say that ‘about half of the variance of IQ scores can be accounted for by genetic

factors’ (cf. Plomin et al. 2015, 88)? Or that: ‘the heritability of height is about 90%’ or ‘most

of the height differences among individuals are due to genetic differences among them’ (cf.

Plomin et al. 2015, 92)? Or what does the statement ‘heritability is a statistic that describes

the contribution of genetic differences to observed differences among individuals in a

particular population at a particular time’ (cf. ibid.) mean?45 Or more precisely, what denote

of missing heritability mentioned above. Schaffner (2016) locates part of the problem in the definition of non-shared environment stating that there is effective and objective non-shared environment. Effective non-shared environment is anything which has influence that differs from one sibling to the other (possibly being the same event!) and objective non-shared environment is anything which is objectively part of the one sibling’s environment but not part of the other’s (ibid., 28/9). He argues, finally, that shared and non-shared environments are highly relative context specific and to be specified in the very studies conducted (ibid., 28). Generally speaking, one can say that, while we have relative importance of environment from heritability measures, this cannot hide that there just is a lot of what one doesn’t know about environment. This stands corresponds to what Philip Kitcher argues. In Kitcher (1985), the author introduces a notion of normal environment relative to a trait in the context of ‘norm of reaction’, which is defined as a threefold relation and “a function that assigns a phenotypic value to each appropriate argument” (ibid., 25) continuing that “[a]n appropriate argument is some combination of the critical environmental variables” (ibid., 25, my italics). Kitcher emphasizes “critical environmental variables”, even if he grants that in the case of human behaviour “it would be rash to assume that we already know how to identify all the critical factors” (ibid., their italics). In the very same spirit, but more concrete, Kitcher (2003b) warns that documenting reaction norms for violent behaviour is likely to be deceptive, because the environmental causes of potentially very fine-grained environments are not very well understood (cf. ibid., 295 ff.). 45 Cf. also the definition of heritability in Plomin et al. (2015): “To the complex traits that interest behavioural sciences, it is possible to ask whether genetic influences are important but also how much genetics contributes


36

the expressions ‘due to’, ‘contribution’, and ‘account for’’? Even on the assumption that the

authors themselves exactly know what they are talking about in their texts and textbooks46,

the semantics of ‘heritability’ and related words is still critiqued as ambiguous (cf. e.g. Keller

2010, 10 f., 70 f.; Kempthorne 1978, 6)—as can apprehended, for instance, in Plomin et al.

(2015), chapter 6 and 7.

In terms of its meaning, there are roughly two sorts of interpretations of heritability: One does

assume heritability to imply causal relevance, the other doesn’t. That is, some have argued in

favour of heritability’s interpretation as implying something about the causal role of genes

with respect to (the development of) a trait in question (cf. Tabery 201447; Oftedal 200548;

Sesardic 200549). For instance, Polderman et al. (2018) write with respect to gender that

to the trait. […] The question about how much genetics contributes to a trait refers to effect size, the extent to which individual differences for the trait in the population can be accounted for by genetic differences among individuals. […]. The statistic that estimates the genetic effect size is called heritability. Heritability is the proportion of phenotypic variance that can be accounted for by genetic differences among individuals.” (ibid., 86/7). 46 For instance, Matt Ridley and Steven Pinker are relatively progressive and sceptical with regard to heritability

(cf. Ridley 2002, 75 ff., 82 ff.; Pinker 2002, 374 ff.). Ridley argues that “[h]eritability is usually highest for those features of human nature caused by many genes rather than by the action of single genes. And the more genes are involved, the more the heritability is actually caused by the side effects of genes rather than the direct effect.” (ibid., 87) Similarly, Pinker, who states that “heritability is a measure of correlation and cannot distinguish direct effects of the genes (proteins that help wire the brain or trigger hormones) from indirect effects that operate many links away.” (ibid., 387) Both scholars freely make this sceptical point implying that heritability coefficients are not so helpful with regard to finding causal information about the trait measured, just because there is too much ‘noise’ from indirect effects. Still, neither Ridley nor Pinker totally abandon heritability: Pinker argues, for instance, that “we know that the heritability of personality cannot, in fact, be reduced to genes for appearance” (ibid., 377). If this was true, then parent and offspring would be similar in personality not because of their genes (and due to ‘a force form the inside’) but rather because they are treated very similarly producing similar character (‘from the outside’). And, similarly, Ridley knows contexts, in which heritability says something about genes: “Yet in a sample of people who have all these advantages [i.e.: food, parental care, teaching, books], the variation between who does well in exams and who does not could indeed be a matter of genes. In that sense, variation in intelligence can be genetic” (ibid., 77). 47 Tabery (2014) systematized these two senses of causation this arguing that the variation-partitioning, “which ask[s] how-much questions about how much variation is caused by the different causes of variation” (ibid., 99 ff.) in contrast to Lewontin, who propagates mechanism-elucidation and seeks “to explain the developmental process. Tabery, notably, leans on Woodward (2003) and Waters (2007) and thus on a manipulationalist theory of cause in order to conceive of a causal notion for the variance-portioning approach. 48 Oftedal tried to mediate between Sesardic and Lewontin by applying the causal theory conceived by Fred Dretske agreeing that it has some causal relevance (cf. Dretske 1988, 2004, 2010). 49 “Indeed, heritability is supposed to give us causal knowledge, but it gives us no information about causal details or mechanisms underlying the process of development. […] The very purpose of heritability estimates is to give us some knowledge about causality precisely in those situations where we are ignorant of causal specifics “ (Sesardic 2005, 24). And similarly: “[…] [N]o researcher worth his salt ever thought that the partition of phenotypic variance into components exhausts all the relevant information about causality of trait development. The underlying complexity is fully recognized and taken for granted, but the claim is that even causally most convoluted situations still leave open the possibility of additivity of genetic and environmental influences” (ibid., 87).


37

“family and twin-based50 heritability studies provide the first evidence that genetic factors

contribute to the development of gender identity and gender-related constructs.”

(ibid., 5)

Similarly, Knafo and Spinath (2011) argue that

“[u]nderstanding genetic and environmental contributions in the context of gender and the gender relevance of [gendered or gender-neutral, M.B.] values has profound implications for understanding the development of values.”

(ibid., 731)

In other words, these authors apply heritability based on the motivation that it helps to

understand the importance of genes for a trait in question. And this naturally implies that it’s

possible to identify precisely which specific genes are important for developing the trait in

question. As mentioned in footnote 43 above, this was tried to achieve in the context of the

Human Genome Project (HGP). However, problems occurred, because (no small set of) gene(s)

would specifically correlate with complex human traits.

In contrast, others have argued against a causal interpretation of heritability (cf. e.g. Block

1995, Gould 1996) and the locus classicus51 here is clearly Lewontin’s 1974 paper “The analysis

50 A short digression about twin studies: This type of study is widely referred to as a “quasi-experimental gift of genetically identical and nonidentical twins” (Turkheimer 2000, 162), an “experiment of nature” (Schaffner 2016, 18). Its logic is simple: On one hand, we have monozygotic twins (MZ), which share almost 100% of their genes, and on the other dizygotic twins (DZ), which share almost 50% of their genes (like any other ordinary sibling). The reasoning now goes like that: if MZ twins are always more similar than DZ twins, then surely this similarity is caused by MZ twins being genetically more similar than DZ twins and this would be true no matter whether they have been reared apart or reared together. It’s widely acknowledged that twin studies presuppose the validity of the EEA stating that “environmentally caused similarity is roughly the same for both types of twins reared in the same family” (Plomin et al. 2015, 81). This assumption does not hold, if the environment treated MZ twins more similar than DZ twins, because the former do more look alike than the latter. Then, MZs’ twins scoring more similar on a measured trait ‘X’ than DZ twins would not be due to genes for X but rather indirectly because of genes for identical physical appearance and due to more similar treatment. If the EEA holds and to what extent is a contentious issue: Some think it does not hold at all (cf. e.g. Joseph 2004, 2016) and others think that it is at least not violated to an extent, which endangers the validity of twin studies (cf. Pinker 2002, 375 f.; Rutter 2006, 41 ff.; Segal 2012, 3; Schaffner 2016, 164, footnote 14; Harris 2007, chapter 2). Note that, I think, the EEA is an instantiation of an assumption that has been codified as one of “the three laws of behaviour genetics” (Turkheimer 2000, Chabris et al. 2015) stating that “[t]he effect of being raised in the same family is smaller than the effect of genes” (ibid., 160). In other words, shared environment influences, which are “defined as all those things that make […] twins [or siblings] alike” (Schaffner 2016, 27, his italics), e.g. parenting style, regarding two (biological or non-biological) siblings being raised in the same family is claimed usually to not make those siblings more similar than some two randomly picked people and thus to be in most cases negligible (cf. Harris 2009, 35). Cf. also Plomin et al. (2016, 12) and Plomin et al. (2015), pp. 96 ff. There are two common ways to claim the validity of the EEA (cf. Joseph 2015, 158 ff.). The first is just to claim that MZ twins actively create (due to their genetic similarity) more similar environment than DZ twins do. The other is to argue that the (in-)validity of the EEA needs to be empirically established for each studied trait separately (cf. e.g. Sesardic 2005, 107-15; cf. Plomin et al. 2016, 12/3). 51 Sesardic (2005), for instance, takes up the argument in Lewontin’s paper, which he takes to be “[t]he best known anti-hereditarian argument based on statistical interaction” (Sesardic 2005, 59) and to have “made a big


38

of variance and the analysis of causes” (Lewontin 2006a). But in my view, the most striking

argument against the causal relevance of heritability, which disambiguates the whole

discussion, has been launched by Oscar Kempthorne.52 And Kempthorne interestingly not only

criticizes the Jensen-style causal interpretation of heritability but also Lewontin’s

argumentative force by criticizing Feldman and Lewontin (1975), a paper very similar to

Lewontin’s vastly received classic.

More precisely then, Kempthorne attacks the authors’ understanding of the mathematical

nature of ANOVA (Kempthorne 1978, 11) and in addition states that it’s “grossly defective”

(Kempthorne 1978, 20; cf. also ibid., 11) with respect to the concepts ‘causality’ and

‘prediction’. Nonetheless, Kempthorne agrees in general with Lewontin denouncing as a

“fallacy […] that a knowledge of the heritability of some trait in a population provides an index

of the efficacy of environmental or clinical intervention” (Lewontin 2006a, 520). (Note this

conclusion’s strong allusion to the title of Jensen’s paper asking how much IQ can be boosted

and thus to the paper itself.) In his critique of Lewontin’s (and Feldman’s) argument,

Kempthorne doesn’t go into great detail, but its main thrust is discernible and interesting,

which is why I’m quickly reproducing Lewontin’s argument, before I’m presenting

Kempthorne’s critique of heritability.

Lewontin’s just mentioned conclusion (that heritability doesn’t predict success of

intervention) rests heavily on two assumptions: Firstly, the assumption of pervasive

interaction53, which basically claims that all linear effects between genotype and

environments for a trait X (as well as their causal interpretation) will turn out as non-linear if

tested under additional environments and more globally. And, secondly, the assumption that

ANOVA entails a necessarily local analysis54, because reaction norms for complex human traits

impact on later discussions of these issues” (ibid.).51 Cf. also ibid. 65, where Sesardic alludes to Lewontin’s ‘authority’. 52 Kempthorne was trained as a statistician and affiliated to the University of Iowa. His main areas of thought were experimental design, genetic statistics, and the philosophy and foundations of statistics (cf. Hinkelmann 2001). 53 For instance, Lewontin already begins his text proclaiming that “all individuals owe their phenotype to the biochemical activity of their genes in a unique sequence of environments and to developmental events that may occur subsequent to, although dependent upon, the intimal action of the genes” (ibid., 520). He grants that the really interesting question is not separation “by a line that separates environmental from genetic causation but by a line that separates two kinds of genetic basis: a single gene with major effect or many genes each with small effect” (ibid. 521). Compare also his example of interaction between genotype and environment in reaction norms of the fruit fly (ibid., 524). 54 “In man, measurements of reaction norms for complex traits are impossible because the same genotype cannot be tested in a variety of environments” (Lewontin 2006a, 524).


39

(involving many test-environments) are impossible to obtain, which is why the obtainable

graphs are necessarily only snippets of hypothetically (more) complete reaction norms. And

these snippets are insufficient for a causal analysis, which ought to be global and thus ought

to involve many test-environments (ibid. 524/5). Put briefly, pervasive interaction and

necessarily locality imply: No causal analysis is possible and hence no way to predict the

effectiveness of interventions.55

Note that Sesardic (2005), who tries to rehabilitate heritability in his revisionary book Making

sense of heritability, in fact reconstructs Lewontin’s argument quite adequately and utters

doubts that are not unjustified (ibid., 59 ff.). But beyond his negative critique, he’s far from

offering an alternative, because his arguments are spiked with absurd notions (cf. e.g. his

notion of ‘normal environment’) and weak arguments (cf. e.g. his argument concerning

monomorphic traits and PKU). Unfortunately, I lack the space to develop the critique of

Sesardic here (which might not have been developed in detail anywhere).56

What imports though is that Kempthorne (who is even briefly cited by Sesardic on p. 23!),

embeds his critique of ANOVA and heritability (cf. Kempthorne 1978; Kempthorne and Dupont

1978) in a wider context of causal theory (cf. Kempthorne 1977, 1979, 1992).57 In a nutshell,

he argues quite simply and intuitively that, in general, causality can only be established

experimentally and thus featuring at least a manipulation.58, 59 With respect to the IQ debate,

55 Both assumptions appear interlaced in the following main rationale of his text: Lewontin (2006a) argues that

“the amount of environmental variance that appears depends upon the genotypic distribution, while the amount of genetic variance depends upon the environmental distribution (ibid., 523)”. That this is the main rationale is affirmed by Lewontin’s commentary to his text, where he states that “[t]he reason why the portioning of variance does not partition causes is that changing the distribution of genotypes will also change the environmental variance, while changes in the distribution of environments will also change the genetic variance. Moreover, neither the magnitude nor the direction of these changes can be predicted from the analysis” (ibid. 2006b, 537). 56 Schaffner (2016) writes that “[m]ore recently, several philosophers have responded to Lewontin’s arguments, including Sesardic (2005) and Tabery (2014), but most philosophers have not read those responses as yet” (ibid.,16). This sort of implies that Sesardic (2005) still awaits a serious critique; there are to my knowledge just the book reviews Tabery (2006) and ibid. (2009), which are not exhaustive though. 57 I happily return to this later in section 3.2.5.3. 58 He argues: “Even if in our data we had random association of genome and environment [implying additivity, M.B.], we could perform our calculation without problems [i.e.: we could neatly partition the variances, M.B.], but we would still have a useless answer with respect to causation (Kempthorne 1978, 19, his italics). Why is that? Because there’s no intervention! 59 It should be noted that, on the first reading, Kempthorne’s theory might resemble Woodward’s manipulationist theory of causation (cf. Woodward 2003). As Waters (2007) summarizes, this theory says roughly that “[t]o say that there is a causal relationship between X and Y, on his account, is to say that X and Y are properties and that manipulating one property would change the other” (ibid., 561). While the inspiration from experimental science is something in common with Kempthorne, Woodward (2003) does not require actual manipulation (and thus actually performed experiments) in contrast to Kempthorne, I believe (cf. Woodward 2003, 10 ff.). Hence, a


40

Kempthorne criticizes consequently that virtually all literature is observational60 emphasizing

that

“a data analysis of an existent population cannot tell us about the potential effects of intervention unless that existent population has sub-populations which differ only in that intervention has been exercised by the observer, i.e., in a comparative experiment.”

(ibid., 13)

In the context of Behavioural Genetics’ study of (complex) human behaviour, he emphasizes

thus that “[t]he only intervention that is both available and acceptable to our society is

environmental, and this cannot determine genetic causation” (ibid., 22). Hence, no way for

ANOVA and heritability to have causal relevance even principle in the context of human

traits.61

Let me add two comments: Firstly, at the beginning of this section I talked about heritability

purporting to have causal relevance and to separate nature and nurture, while in the context

of Kempthorne and Lewontin only causal relevance was discussed. However, part of their

argument is that both scholars claim that separating nature and nurture is impossible, because

in the context of human beings, there is no additivity but pervasive interaction between genes

and environment (Lewontin) and/or no independence of genotype and environment

(Kempthorne)62. In contrast, and if genotype and environments could be combined at will (as

is quasi possible in plant studies where plants can be cloned), then nature and nurture could

potential difficulty for Woodward, because the above mentioned characterization of Woodward can characterize, I think, causation as well as correlation, whose distinction is the problem of social science. 60 “What, indeed, is the ‘grip’ on environment in the human IQ area? It is no more than ‘reared together’ versus

‘reared apart’, and what does ‘reared apart’ mean? Nothing more than at some age two related individuals, e.g., identical twins or full-sibs were separated by adoption, and then placed in homes that could be related familially and/or, of similar economic and social nature. I can only comment: Really, how naïve can one be? The Burt study was characterized in the literature as the ‘only experiment’. Some experiment!” (ibid., 18) And: “But to use so much time and money in areas where experimental studies are possible, is most unfortunate, is suggest. I reiterate my opinion that the few experiments on the effects of environmental intervention on achieved abilities, not on ‘intelligence’, are worth much more than all the observational studies and data analyses.” (Kempthorne and Dupont 1978., 714). Kempthorne—being close here to what Gould will argue in 1996’s The Mismeasure of Man—clearly rejects the concept of intelligence in the sense of the “reification of the IQ score” (Kempthorne 1978, 5) granting, however, that the abilities that IQ tests measure are of considerable importance to some of the activities of our society” (ibid. 1978, 5). 61 Kempthorne (1978) argues that heritability is totally justified (and useful) in plant studies and fairly justified (and useful) in animal studies, because these studies are usually experimental (cf. ibid., 17 ff.). He even seems to grant that a separation of the importance of nature and nurture is possible, because random assignment and additivity of genetic and environmental effects holds. 62 He puts this dependence of genes and environments as follows: “If we think of a deity giving at random to a soul a collection of chromosomes and an environmental mixture, and that this deity makes a random draw from a population of chromosomes and a random draw from a population of environment, then we can, I suppose that for that deity and for the souls, genotype and environment are independent. But we are not the deity” (ibid., 15).


41

be separated. Note, however, that to gain information about causal relevance, Kempthorne

requires in addition an experimental intervention, while Lewontin, it seems to me, accepts

that, if a relation between genes and environments were additive with respect to some human

trait (which, he claims, is never the case due to pervasive interaction), then analysis of variance

would in fact yield causal information.63

2.2.3 Conclusion

Let me conclude this section and state what I take to be its most important points. Remember

that its purpose was to criticize an instantiation of the nature/nurture framework, namely,

genes/environment, which we found to be implied Matt Ridley’s and Steven Pinker’s accounts

of human nature. This framework was (historically) and is still today closely associated with

the notion of heritability, which has traditionally been taken to provide information about the

causal importance of genes for some trait in question.

Remember that heritability is a statistical entity computed in the course of an Analysis Of

Variance (ANOVA). It concerns a population and the differences of trait-scores with respect to

the factors ‘genotype’ and ‘environment’. It’s defined as the proportion of genetic variance

and the total phenotypic variance. Remember also that heritability was used in the IQ debate

in order to support the claim of a genetic basis of intelligence and to imply something about

the range of interventional possibilities to ‘boost’ IQ. In addition, it’s still today widely used

and, as we saw, also in the context of the study of sex/gender (differences).

The most important point was that in fact heritability does not imply anything about the causal

role of genes with respect to (the development of) a given trait. I argued with Kempthorne

that this is because heritability coefficients have been applied in the context of observational

studies, which don’t involve any sort of intervention, while experimental theory à la

63 “There is one circumstance in which the analysis of variance can, in fact, estimate functional relationships. This is illustrated exactly in figure 1h and approximately in figure 1g. In these cases there is perfect or nearly perfect additivity between genotypic and environmental effects so that the differences among genotypes are the same in all environments and the differences between environments are the same for all genotypes” (Lewontin 2006a, 524). Moreover, Lewontin argues that “[i]f an event results from the joint operation of a number of causative chains and if these causes ‘interact’ in any generally accepted meaning of the word, it becomes conceptually impossible to assign quantitative values to the causes of that individual event. Only if the causes are utterly independent could we do so” (ibid., 521, his italics, my underlining). Therefore, Lewontin in principal accepts causal talk in association with ANOVA and observation studies the note his statement that “[t]he first thing to observe is that in every case the phenotype is sensitive to differences in both environment and genotype. That is, each genotype reacts to changing environment, and in no case are the two genotypes identical in their reactions. Thus in any usual sense of the word, both genotypes and environment are causes of phenotypic differences and are necessary objects of our study.” (ibi., 522)

Introducing Anne Fausto-Sterling and concluding nature/nurture

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Kempthorne implies that intervention is necessary for causal inference. In addition, it’s

impossible for heritability to separate nature from nurture, because—arguing again with

Kempthorne—genes and environments are not independent of each other (but highly

correlated). In contrast, separating nature and nurture would be possible (independent of the

causal relevance) in the study of plants (and maybe even in the study of animals), where genes

and environments can be assigned randomly.

To conclude, this section purported to render implausible the gene/environment-framework

as an instantiation of the nature/nurture framework in the context of complex human traits.

According to the story told, the framework’s logic cannot be retrieved in the object of study:

Nature and nurture cannot be separated in terms of genes and environment via heritability

and there is theoretical justification (i.e.: the dependence of genes and environments) that

such separation is generally impossible.

2.3 Introducing Anne Fausto-Sterling and concluding nature/nurture

The former section refuted the claim that nature and nurture can be separated in terms of

genes and environment via heritability, which was supposed to shed doubts both on

nature/nurture and genes/environment. This section argues in the same spirit; but this time

from the perspective of Anne Fausto-Sterling (whose work will be the main topic in the

remainder of this thesis).

Accordingly, this section should be read as another set of arguments countering

nature/nurture and genes/environment. But in addition, it should also be read as a first and

partial introduction to the work of Anne Fausto-Sterling. More precisely, it shows to what

extent Fausto-Sterling received Lewontin’s idea of pervasive interaction, which—as you will

remember—was an important assumption underlying his argument of ANOVA’s (and

heritability’s) causal irrelevance. Consequently, this is also a good occasion to further clarify

the notion of interaction, which remained a bit abstract during the heritability-discussion

above.

The structure of this section is then as follows. In section 2.3.1, I briefly provide some

contextual and introductory information about the researcher Fausto-Sterling herself. Next,

section 2.3.2 concerns Fausto-Sterling’s reception of Lewontin’s discussion of reaction norm

and interaction. Section 2.3.3 discusses Fausto-Sterling’s constructive critique of the concept


43

‘environment’ such that she takes it to figure in the nature/nurture framework. Finally, section

2.3.4 summarizes the argument.

2.3.1 On Fausto-Sterling’s work: A brief overview

This brief sketch of the researcher Anne Fausto-Sterling purports to contextualize the

arguments drawn from her work in what follows next and later in Part Two of this thesis.64

Fausto-Sterling is a trained biologist having graduated in Developmental Genetics at the

Brown University, Providence. Fausto-Sterling worked in a laboratory on the development of

model organisms and taught classes in embryology, before she got interested in Feminist

Theory and Science and Technology Studies (STS). Fausto-Sterling worked as a professor of

gender studies and biology and held the chair of the science and technology studies program

at Brown University, where she is Nancy Duke Lewis Professor Emerita since 2014.

The book Myths of Gender (1985) was the first manifestation of the merge of biological

interest with feminist theory, which characterizes Fausto-Sterling’s thinking. In 1993, she

published the widely read article “The Five sexes: Why Male and Female Are Not Enough”,

which is also why she revisited this article in 2000. The topics of these two articles, the natural

occurrence of intersex and the critique of its medical policy, were manifest also in her second

book Sexing the Body (2000b), which in addition carried already the mark of Fausto-Sterling

discovering the work of Esther Thelen and her Dynamic Systems Theory sometime in the 90s.

This book then was followed up in 2012 by Sex/gender: Biology in a social world, which is

clearly formulated against the theoretical background of Dynamic Systems Theory, however,

without providing a systematic introduction. Notably, Fausto-Sterling’s just mentioned third

book is associated with a set of empirical studies, which Fausto-Sterling (and colleagues)

published from 2011 on and which focussed on (infant) gender development explicitly

applying Dynamic Systems Theory. Thus, a systematic and extensive introduction into this

framework, which is absent from Fausto-Sterling (2012), can be said only to be distributed

across the introductions of her papers.

64 All information drawn from her official web-site: http://www.annefaustosterling.com/biography/, last access 20.05.2018.

http://www.annefaustosterling.com/biography/


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2.3.2 Fausto-Sterling on ‘reaction norm’ and ‘interaction’

This section concerns Fausto-Sterling’s reception of the idea of interaction, which we already

encountered in the context of the IQ debate and Lewontin’s argument against the causal

relevance of heritability and ANOVA.

Fausto-Sterling cites Lewontin (cf. e.g. Fausto-Sterling 2000; cf. also ibid. 2012c, 102 ff.) and

notes in 2005 the notion ‘norm of reaction’ as a historical precursor of the set of ideas she

calls “systems theory”, which includes her already mentioned own approach of Dynamic

Systems Theory (Fausto-Sterling 2005, 1512). She usually refers to ‘norm of reaction’ without

large discussion in her texts. But there are two texts, in which Fausto-Sterling (if yet not in a

too detailed way) concerns in association with ‘reaction norm’ Lewontin’s thesis that

‘interaction is pervasive’ (cf. Fausto-Sterling 1997; ibid. 2012, 102 f.). In what follows, I briefly

comment on her more extensive discussion in Fausto-Sterling (1997), where she comments

on two of Lewontin’s actual reaction norms; the one obtained from his model organism

‘fruitfly’ and the other from his model plant Achillea (cf. e.g. Lewontin 2000b). Besides her

reception of Lewontin, I then reproduce similar reflection of Fausto-Sterling based on her own

study of rat sexuality.

The reaction norm for the fruit fly, which she cites, depicts the eye size of wild type fruit flies

in comparison to fruit flies that carry the Infrabar or the Ultrabar genetic mutation that have

been found to reduce eye size (Lewontin 2000b, 30 ff.). Importantly, at ≈ 15°C both mutations

produce indistinguishable phenotypes, while at ≈ 30°C, they produce easily distinguishable

phenotypes. Therefore, Infrabar and Ultrabar, whose values look the same in one

environment, result in different phenotypes with rising temperature (and thus in different

environments), which clearly underlines the potential of false generalization based on only

one (standard?) environment. Consequently, Fausto-Sterling herself generalizes from this that

“most of the time there is no such thing as a fixed genetic trait. Genetic traits can only be

defined in a particular environment” (ibid., 247).

Next, Fausto-Sterling (1997) mentions Lewontin’s example regarding the plant Achillea (cf.

Lewontin 2000b, 20 ff.). In this example, a sample of 7 genetically different plants of the type

Achillea was cloned and a clone of each planted into three different environments, i.e., into

three soils with different elevations (low, medium, high). The phenotypical characteristic of

interest was their height, and it turned out that growth of the plants was kind of chaotic. In


45

other words, different plants had different (linear or non-linear) patterns of height in relation

to their environment (low, medium, high). Hence again, no way of predicting the heights of

the plants based only on the scores in one single test-environment. Accordingly, Fausto-

Sterling infers again generally that “[w]ith norms of reaction, there is no way to predict an

outcome. The question is entirely empirical” (Fausto-Sterling 1997, 248). Hence, Fausto-

Sterling clearly supporting Lewontin’s notion of pervasive interaction of genes and

environment (cf. also e.g. Fausto-Sterling 2016, 201).

However, Fausto-Sterling does not just followed blindly Lewontin’s authority, whose writing

had great influence, as we heard above (cf. footnote 51). Rather, she presented herself a case

from animal studies, which strongly implies pervasive interaction. In Fausto-Sterling (1995)

and ibid. (2000, chapter 8), the author reviews the experimental study of rats with respect to

their sexual behaviour. More precisely, she discusses a theory, which she calls ‘O/A theory’ of

sexuality, i.e., organisation-activation theory, formulated on the basis of these studies,

according to which

“[d]uring the pre- […] or peri- […] natal period, hormones (usually testosterone, but some believe estrogen will do the trick) permanently affect [i.e. organize, M.B.] brain development. Somehow […], neural structures in the brain become dedicated to future behaviors such as mounting [i.e. male sexual behaviour, M.B.] or lordosis [i.e.: female sexual behaviour of lifting the back to enable penetration, M.B.] […]. Puberty hits, activates the previously organized neural pathways, and the behaviour becomes visible.”

(Fausto-Sterling 2000, 226, my italics)

According to Fausto-Sterling, this theory is problematic, however, because “the effects of

prenatal hormone treatment were contingent on the experimental test situation” (ibid., 222).

They could be made to disappear changing the data based on which the theory was built in

the first place.

More precisely, Fausto-Sterling describes the standard laboratory set up (cf. ibid., 220 ff.) such

that researchers usually introduced the male rat into a cage letting it familiarize with its

environment. And only then, a female rat (unfamiliarised with what it will experience) was

added, who was treated with the ‘male’ hormone Androgen perinatally (i.e. approximately a

few weeks before birth), which resulted in ‘masculinized’ genitals (closed vaginas, enlarged

clitorises, etc.; ibid. 229). In the case of comparison, a non-treated female rat was added to

the male rat in its familiarized environment. The result was that the female rat treated with

‘male’ hormones was ‘masculinized’ by usually showing lordosis (i.e. copulative behaviour


46

enabling penetration) to a lower degree. This was taken to prove that the ‘male’ hormone

Androgen could masculinize the organisation of the female rat’s brain (ibid., 221/2).

However, once other researchers changed this standard experimental setup they made this

effect disappear: They created variations of the mentioned rat and hormone experiment, in

which the “female choice” (ibid., 221) was introduced, i.e., in which “females had to want to

mate” (ibid.). That is, female rats were allowed to familiarize with their environment, for

instance, and this made female rats, which were treated with Androgen (as above), show

lordosis to a high degree (just like untreated rats). Hence, “[t]he permanent organizing effects

of androgen on the female brain seemed to have disappeared” (ibid., 221/2).

Comparing these two experimental performances, we recognize (as we did in the context of

the fruit fly or Achillea) that the female rat’s phenotype in question is anything else but stable

over different environments. Therefore, we encounter again the predictive problem from one

to another environment implying the complexity of the behaviour measured. In other words,

we encounter “interaction between nature and nurture” (ibid., 227). The treated ‘standard’

female rat shows different sexed behaviour than the non-treated ‘standard’ female rat in one

environment than in another. Note in addition that (consistently) masculinized behaviour in

rats doesn’t at all necessarily cooccur with masculinized female genitalia.

Beyond Androgen, Fausto-Sterling discusses another example featuring rats and

Testosterone, a specific sort of Androgen. While she grants well that Testosterone affects the

genitalia, brain, and behaviour (ibid., 229), she emphasizes the non-directness of

Testosterone’s effects on sexed behaviour by establishing the following more detailed linkage

(associating Testosterone and sexed behaviour): Firstly, Testosterone levels in rat pubs

influence the smell they emit. Secondly, the smell of the rat pubs influences the mother’s

licking behaviour regarding the respective rat pubs. Thirdly, (the degree of) being licked affects

a pubs sexual behaviour: In males, licking speeds up ejaculation and shortens the length for

refractory period between ejaculations (ibid., 229). Briefly speaking, Testosterone is linked

with smell is linked with licking is linked with sexual behaviour.

Fausto-Sterling points out a number of factors affecting elements of the above mentioned

linkage. For instance, Testosterone level of female rats is influenced by prenatal litter

composition (i.e. the proportion of male and female pubs): That is, if a rat pub shares the rat


47

mother’s womb with many male rat pubs, then the female rat pub is likely to have higher than

average Testosterone level (cf. Fausto-Sterling et al. 2015, 9).

Next, the extent to which a pub is licked is dependent of “[s]alt and water balance, pup leg

extension, and urine release—each of which differs in male and female pups” (ibid. 2000, 230),

because all these affect the rat mother’s licking behaviour. In addition, the extent of licking is

dependent of the pub licking and grooming its own genitalia (ibid.). Finally, the extent to which

a pub is licked depends also on the postnatal litter composition (i.e. the proportion of male

and female pubs; cf. Fausto-Sterling et al. 2015, 9/10).

Fausto-Sterling (2000b) concludes her discussion of rat pubs’ sexed behaviour stating that

“[n]ature and nurture are not separate here” (ibid.) and that the “brain, it seems, is one among

several elements affected by early hormone exposure. Some elements are anatomical [e.g.

genitalia, M.B.], some physiological [e.g. hormones, M.B.], some behavioural [e.g. own

grooming behaviour, M.B.], and some social [e.g. litter composition, rat mother’s licking,

M.B.]. They all form part of a unitary system” (ibid.).

All this renders implausible the above stated theory of sexuality based on prenatal hormone

exposure (the A/O theory). But much more important, it demonstrates that Fausto-Sterling

accepts and contributes to the plausibility of Lewontin’s thesis of pervasive interaction and

developmental complexity and its implicative demand of global causal analysis.65 Moreover,

and more generally, it also renders more plausible the critique of nature/nurture and

sex/gender, which is manifest in the A/O theory.

2.3.3 Fausto-Sterling on ‘(standard) environment’

The former section concerned concrete instances of interaction between many variables

including genes and environment as well as behavioural, social, and physiological variables.

These were rendered thanks to testing in many environments. More precisely, we talked

65 It should be mentioned that Fausto-Sterling (2012, 102 ff.) makes a similar point. Citing from a study, Fausto-Sterling observes that “male-female difference in birth weight in developed countries was about three tenths of a pound. However, the sex difference in developing nations was only two tenths of a pound” (ibid., 102). She speculates that “relative birthweights vary when nutrition is better or worse, or mothers are more likely to be ill” (ibid.). In other words, the explanation is not that XX (i.e. girls) are lighter than XY (i.e. boys) in terms of a biological universal. Rather, she refers to ‘reaction norm’ arguing that XX and XY embryos might simply have different norms of reactions with respect to moderating factors of birth weight (like “improved nutrition, decreased maternal smoking, or other factors that increase fetal growth and birth weight”, ibid., 103). By implication (and here I am going beyond Fausto-Sterling), there is an environment, in which XX and XY tend to have very equal if not identical birth weights (on average).


48

about prediction on the basis of measurements gathered in just one environment such that it

(in the best case) for some reason is a justified base for generalization. Such environment has

been called traditionally ‘standard environment’ and it’s a contentious issue whether such an

environment exists in the first place.

Some argue that it doesn’t (cf. Lewontin 2000b), some that it does (Sesardic 2005), and others

that it does in a qualified way (cf. Kitcher 1995, 2003). According to Kitcher (1985), a standard

environment implies that for a trait studied, there is a crucial set of variables (cf. ibid., 25 ff.),

which (by implication) has to be identified and which dictates the design of laboratory

environments.66

For instance, and regarding rat sexuality, Fausto-Sterling clearly implies that there cannot be

such a thing as a standard test environment due to complexity, i.e., pervasive interaction of

nature and nurture. Moreover, Fausto-Sterling (2000b), in a traditionally feminist manner,

describes how sciences resonate with their embedding socio-cultural context. Thus, it was

held in America in the middle of the 20th century that “[a]ll males, be they rats, guinea pigs, or

humans, had to strive against an inner femininity” (ibid., 200). This fundamental notion of

‘female’ as standard entailed that females we’re understudied in general (cf. ibid., 220;

Fausto-Sterling 2012c, 16 ff.).

But beyond her critique of standard environment pointing to disappearance of effects in many

test-environment as well as to socially contingent belief sets, Fausto-Sterling critiques

‘environment’ also as a concept in itself (which can be read as a direct attack against the logic

at the heart of nature/nurture or gene/environment). More precisely, she argues that “we

need to become more imaginative and specific about what we mean by the word

environment” (Fausto-Sterling 2000, 246, her italics). She continues that with respect to

human sexual development “[a]t the moment […] we are pretty clueless about the

environmental components” (ibid.). Detailing further, she explicates that “[t]he term

environment could also refer to events in utero. […] The term environment can also refer to

post-birth effects resulting from parental reinforcement or modelling, peer interactions, and

the like” (ibid., footnote 59, 374). Briefly speaking, Fausto-Sterling is convinced of the “failure

66 Kitcher implies so much: “The norm of reaction of a genotype is a function that assigns a phenotypic value to each appropriate argument. An appropriate argument is some combination of the critical environmental variables […]” (Kitcher 1985, 25).


49

to specify ‘environment’ in much detail” (Fausto-Sterling 2012a, 412), a problem, we already

briefly encountered under the label of missing environment.67

Next, Fausto-Sterling (2007) urges to “use environment very broadly […] to include both a

cellular environment, say, in the developing embryo, and behaviors and experiences that

stimulate gene activity” (ibid., 56). She emphasizes this in order to make the point that genes

should not be conceived as blueprints or programs (implying activity independent of

environments) but rather as being themselves susceptible and dependent of their next (e.g.

intra-organismic) environment (ibid.; cf. also e.g. Fausto-Sterling 2014, 315; cf. also Kitcher

2003).

A more concrete instance of Fausto-Sterling’s critique beyond the reproach that “[o]ften

‘environmental influences’ are not clearly defined” (Fausto-Sterling 2015c, 13) is that often

“they are studied under the guise of socialization, which is itself often presented as an

external, disembodied concept” (ibid.). The keyword here is ‘disembodied’ (cf. also 2012b,

403) and Fausto-Sterling’s statement might make us think of a vulgar social constructionist

position, which posits the creation of ‘the world’ by linguistic discourse and based especially

on accounts of the performative, fact-creating force of language.

For your interest, this resonates with a criticism of Judith Butler’s Gender Trouble first

indicated in Fausto-Sterling (2003, 126) and explicitly (re-)stated in Fausto-Sterling (2016):

“[…] I balk at the phrase that sex is no longer understood as a reality of nature. I balk because

it seems to suggest that our discussion of sex is in no way constrained or shaped by the

materiality of the body. But material embodiment needs to be part of the theoretical

discussion” (ibid., 199). Even with regard to Butler’s Bodies that matter, whose aim precisely

is to underline materiality of the body, Fausto-Sterling (2000b) emphasizes that while Butler

is right that there cannot be neutral or objective theories of sexual development “we have to

acknowledge and use aspects of materiality ‘that pertain to the body’” (ibid., 23).

Having severely criticized the logic of nature/nurture and/or genes/environment, Fausto-

Sterling attempts to overcome these dichotomies. As we will see in the next part of the text,

67 This resonates with Kitcher (1985), who argues that studying human behaviour “we may speculate about environmental variables that may be relevant, but it would be rash to assume that we already know how to identify all the critical factors” (ibid., 26). Kitcher (2003) also implies so much, when he concerns “our pervasive ignorance of the causally relevant features of the extraorganismic environment” (ibid., 295) and “our massive ignorance about how to partition environments” (ibid., 297) in the context of the study of violent behaviour.


50

she achieves this also by substituting the ‘unspecified’ and ‘disembodied’ notion of

environment in favour of the rich notion ‘experience’ (cf. already Fausto-Sterling 2005,

footnote 8, 1495; Fausto-Sterling 2012b; ibid. 2015c). Having mentioned this, I postpone a

discussion in more detail to Part Two.

2.3.4 Conclusion

Let’s briefly wrap up the most important points of this section. Remember that its main

purpose was in general to provide a first impression of Anne Fausto-Sterling’s work as well as

reconsidering important concepts like ‘interaction’ from 2.2 and rendering more implausible

nature/nurture and sex/gender.

More precisely, it the provided discussions of experiments presented above, no matter if they

concerned fruit flies, plants, or rats, which demonstrated the complexity of organisms’ traits.

Be it on the level of genes/environment, where single genes that assumedly correspond to

traits might be stable only in specific environments (as in the case of the fruit fly) or where the

same set of genes might respond differently to supposedly linearly ordered environments (as

in the case of the Achillea). Or on the level of nature/nurture, where hormones correlate with

rats’ sexual behaviour, but only indirect and in dependence of other variables on different

levels: From anatomical, over neurophysiological, to social. This complexity defies simple

explanations in terms of single nature-elements with a general effect on no matter what

environment. In contrast, it was shown that the test of effects in many environments tended

to make disappear linear effects and to relativize their importance.

Part of this discussion was next the critique of ‘standard environment’, which would be

identical with a laboratory environment featuring the most important variables for a trait

studied. I read Fausto-Sterling as agreeing with Lewontin that no such standard environment

exists, just because there is organismic complexity. More importantly, however, I criticized

the logic of ‘environment’, which is according to Fausto-Sterling unspecified and disembodied

in theory and which has not been achieved researchers to be specified in detail by means of

empirical research.

In conclusion, I take to have rendered implausible further nature/nurture and

genes/environment not only by suggesting with Fausto-Sterling (and Lewontin) its

inadequateness to the objects studied in more than one environment but also critiquing its

logic as exemplified by the critique of ‘environment’.

Conclusion of Part One

51

2.4 Conclusion of Part One

Finally, let me provide a substantive conclusion of this Part One of the thesis. To begin with, I

wrap up the most important points in 2.4.1. Then I present my main conclusions in 2.4.2 drawn

from this Part One and close with a few qualifications and closing comments.

2.4.1 Summary

Remember that the purpose of this Part One of the thesis was to introduce and to criticize the

nature/nurture framework, where ‘nature’ usually refers to some biological entity (and its

causal influence on some trait) and ‘nurture’ usually refers to environmental causal influences

(on some trait). Against the background of the case studies discussed, I argued especially that

one of its most important assumptions is the measurability of human nature implying the

separability of nature and nurture by means of empirical methods. In close association, the

most important problem of study in this framework is the question to which degree (or ‘how

much’) some trait is ‘due to’ nature (e.g. genes) and due to nurture (environment), i.e., it’s

nature versus nurture. This is question of proportion is highly contentious for quasi each

cognitive sex/gender difference studied, for instance.

The critique of the nature/nurture framework was launched by discussing the framework’s

instantiation of genes/environment. The latter was attacked at first on the basis of a related

statistical method, the computation of heritability coefficients, which had been often said to

be able to separate nature and nurture as well as to provide information about the causal

importance of genes. However, I argued above referencing Oscar Kempthorne that heritability

cannot in principle tell us anything about the genetic causation, and thus nature-causation, of

complex human traits, because causal claims are justified only by experimental design and

because the data, which the coefficients are based on, are virtually all gathered from non-

experimental observational studies. Moreover, heritability is impotent also with regard to

separating nature’s and nurture’s (non-causal) importance, because in the context of human

beings genes and environments are not randomly associated.

Next, I introduced the biologist and feminist Anne Fausto-Sterling. I provided a brief

introduction of Fausto-Sterling, whose work is the main topic in the following Part Two, and

pointed out her reception of the concepts ‘interaction’ and ‘reaction norm’ mentioned in the

context of Lewontin and the IQ debate (which, I hope, also rendered those concepts more


52

clearly). More precisely, I argued that Fausto-Sterling accepts Lewontin’s claim of pervasive

interaction adding insights taken from studies about rats’ sexual behaviour of rats, which

suggest a complex interaction of variables at anatomical, physiological, behavioural, and social

level that, however, become only visible when the behaviour not in only one environment.

While this already supports the argument against nature/nurture, Fausto-Sterling’s passages,

which directly criticize the concept ‘environment’ as disembodied and empirically unspecified,

had the same consequence of rendering even more implausible the nature/nurture

framework.

2.4.2 Main conclusions and final remarks

I draw one main conclusion from this Part One of the thesis: The nature/nurture framework

has become quite implausible. And this for three reasons.

Firstly, one of its important tools, the heritability coefficients, can under no circumstance

separate nature and nurture in terms of genes and environments in the context of complex

human traits. Secondly, nature/nurture, no matter if it’s instantiated as genes/environment

or hormones/environment or sex/gender, does not provide the right framework for

conceptualizing the complexity of trait development, which empirical studies (e.g. about rat

sexuality) suggest so saliently. Thirdly, I hold that there is in principle no way to move from

the data available to the conclusion that there is something like genetic predispositions or

biological instincts and thus no way to rule out that alternative explanations alluding to

nurture or indirect genetic effects. This latter reason points in my view to an inherent

problematic within the framework of nature/nurture itself, which therefore should be

dumped.

But let me be more specific regarding what I reject and what not. I don’t want to be

misunderstood. On one hand’s it’s crystal clear that genes matter and that genetic

predispositions must exist. Most obviously, if this were untrue, then any animal could in

principle learn to talk as we do. But experiments have shown that this works not even with

apes, which are genetically quite similar to us. But unfortunately, and regarding this question,

Quantitative Genetics has not provided us with a (set of) genes that predispose for linguistic

competence, which would be really interesting and which should really exist. Instead, as we

have seen, we’re presented with (sets of) genes for whatever human trait no matter if physical

or complex.


53

While I think that there is prima face justification for genetic research about physical traits,

this is not the case for genetic research about complex human trait. On the contrary, the

narratives that flow from this are even counter-intuitive, in my view.

For instance, take a look at what Sam Harris, science activist and convinced atheist, states in

a podcast discussion concerning IQ with the co-author of The Bell-Curve Charles Murray:

“[Harris:] [Y]ou can think of the fact that genetic tendencies early in life can lead to changes in environment. So if we think about environment we can’t just think about environment that gets imposed on a child by the parents or by society. But you also have to think about the things, children choose to do with their lives and then increasingly do as a adults. So if you become obsessed with computers and then go and get a job at Google, well, then your environment has been shaped by what you have payed attention to and what you have payed attention to, and your aptitudes and the underlying aptitudes that caused you to do that were to a very significant degree of, it seems, at least 50% dictated by the genes you inherited of your parents. [Murray:] Ja, and all of that is true.”

(Harris and Murray 2017, min. 26:00)

But this claim just is not supported. If you’d continue to ask for some details, there would not

much else to be returned than maybe some heritability coefficient (which I diagnosed to be

uninformative). The reason is that either, no (set of) gene(s) has been identified with a trait

and/or that it’s many genes that each have little effect. Schaffner (2016) tells us so much

arguing that “these days behavioural geneticists are expecting that almost all genes that relate

to behaviors, including some of the major psychiatric disorders, are likely to be ones that have

small effect, and that there are likely to be many of them” (ibid., 41, his italics; cf. also ibid.

47). And even the geneticist Robert Plomin states that “[h]eritability is caused by many genes

of small effect” (Plomin and Deary 2015, 98; cf. also Chabris et al. 2015). In the worst cases,

genetic causation is therefore employed as a knock out argument relying only on inconclusive

heritability coefficients.

Against such background, and even if these results are taken at face value, I’m not even sure,

if a theory based on such evidence would have any predictive value and would be productive

in this sense. And if not, then what would distinguish it from a theory positing a force like

entelechy (cf. Carnap 1966, 13-16)? Granted, I don’t even take this evidence at face value,

because I (as already mentioned) assume the principle problem of underdetermination of

nature- and nurture-explications. For the case at hand, for instance, the posited genetic force,

which is posited to ‘cause’ the person’s computer love, can’t be distinguished at all from

potentially complex (un-)conscious environmental (nurture-)causes. To believe nevertheless

in genetic causation in a case like this is in my view a mere article of faith; and potentially


54

misleading in addition, because it all too often causes a blind eye for potential environmental

causes.

However, I hasten to add that what was said holds not for any trait studied, because I do not

think that that genetic research should be dumped totally (along with its associated

nature/nurture logic). More precisely, genetic research might be fruitful in the context of

(psycho-)pathology68 and with respect to non-complex physical traits (height, eye colour, etc.).

However, I follow Kitcher’s pragmatic attitude (cf. ibid. 1995, 2003) arguing, for instance, that

research for causally relevant violence-genes in decaying inner cities does not make a lot of

sense, because there are much more salient causes of violent behaviour (cf. ibid. 2003, 295

ff.). By extension, I think that genetic research would be justified best, if it implied means to

alleviate suffering (implicating certain medical treatments, for example).

But let’s stop here with the negative critique and instead continue with Part Two, which treats

first and foremost Anne Fausto-Sterling’s positive suggestion, how to replace nature/nurture

and sex/gender by means of her Dynamic Systems Theory and what the latter is supposed to

be in the first place.

3. Part Two: Overcoming nature/nurture and sex/gender

As just mentioned, this Part Two of the text positively constructive in contrast to Part One,

because its purpose is to introduce an alternative for the nature/nurture framework with

respect to gender development and sex differences as proposed by Anne Fausto-Sterling.

Such alternative is necessary, because as one consequence of Part One, we should be

convinced that there is just no point in conceptualizing, for example, sexual orientation in

terms of hormones. As we saw, this displays an in appropriate simplification already in the

case of rats and it’s therefore likely to be even more of a simplification in the case of speaking

human beings.

Besides Fausto-Sterling’s approach, which I’ll focus on in this Part Two, there are in fact also

other alternative approaches to the study of sex differences, which are less simplifying and

account better for the obvious complexity of (complex) human traits. For instance, Diane

Halpern adopts a framework in Sex Differences In Cognitive Abilities (2011), which explicitly

68 For instance, single-gene-defects like PKU or addictive attitudes involving chemical substances (cf. Kitcher 1995, 2003, Schaffner 2016).


55

integrates the complex interaction of variables on several levels (which has already been

indicated to be a more appropriate conceptualization of how traits work). More precisely, and

in her theorisation of cognitive sex differences, she explicitly rejects the separation of nature

and nurture via ANOVA and emphasises their inseparability (ibid., 8-10) as well as the

complexity and context dependency of (gendered) cognitive development (ibid., 86, 212, 363-

6). More concretely, she adopts what she calls a ‘biopsychososcial perspective’ in order to

make sense of sex/gender differences, which explicitly emphasises not only the interaction of

different variables but also of different levels, like the physical, the psychical, and the social

level (cf. ibid., chapter 8).

But note that, in contrast to Fausto-Sterling’s view discussed below, Halpern seems (on first

sight) to find the developmental perspective over time not particularly important. Rather,

Halpern emphasizes cross-sectional study design (‘observational studies’ in Kempthornian

jargon) and especially those, which study cross-cultural similarities between men and women

claiming that they can provide “strong support for the importance of sex-related biological

variables in the determination of cognitive abilities” (ibid., 356; cf. ibid. 355/6). Remember

that we have already encountered the inference of nature-causation from universal or cross-

cultural similarity or difference as an employed strategy in our discussion of Steven Pinker’s

and Matt Ridley’s positions. Moreover, but without wanting to exaggerate the importance of

this, she seems to deemphasizes longitudinal study design (cf. 86/7), which is covered only in

a tiny passage and concrete study instances of which are barely mentioned in her book.69

As we will see below, Halpern’s framework neatly fits into what will be called below a specific

systems approach to below, namely, an approach labelled Developmental Systems Theory

(later called ‘DeST’). Moreover, it seems that the deemphasis of the temporal dimension turns

out to be the criterion distinguishing DeST from the approach of Dynamic Systems Theory

(later called ‘DyST’), which is precisely the approach pursued by Anne Fausto-Sterling and

which is thus treated in this Part Two a potential substitute for nature/nurture and

sex/gender.

But before laying all this out in detail, let me introduce you to the structure of this Part Two.

It consists of two main sections 3.1 and 3.2 (and a conclusion 3.3). Section 3.1 is introductory

69 This might of course also reflect an objective lack of longitudinal studies in the domain of study of cognitive sex/gender differences and need not be a point of critique against Halpern herself.

Systems approaches to biology

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in nature and its main task to disambiguate. This is necessary, because Fausto-Sterling’s DyST

is also referred to as DST in the literature, which is an acronym that is, however, also employed

for DeST. But, while both DeST and (Fausto-Sterling’s) DyST share ideas, they are not at all

identical, for instance, with respect to their status of framework vs. theory and their emphasis

of the temporal dimension of trait development. Mindful of this (non-)overlap, I introduce the

main ideas of DeST but as well as its critiques in 3.1.2 and 3.1.3, respectively. Finally, I situate

Fausto-Sterling with respect to DeST and DyST in order to fully disambiguate the issue in 3.1.4.

I deem section 3.2 to be the most important part of this whole text, because it presents

Fausto-Sterling’s DyST approach to the study of gender and sex differences. To begin with, it

introduces Fausto-Sterling’s DyST from two perspectives. Section 3.2.1 takes a casuistic

perspective by providing a first bottom up impression of Fausto-Sterling’s DyST via the

discussion of its application to sexual orientation, gender infant development, and sex

differences in bones. Next, section 3.2.2 takes a systematic perspective focussing on what I

take to be the core concepts of Fausto-Sterling’s DyST in application to her theory of infant

gender development. Section 3.2.3 then argues that Fausto-Sterling’s DyST is no mere

scientific framework replacing nature/nurture but is situated also on the level of a scientific

theory. Afterwards, section 3.2.4 explains in more detail, how Fausto-Sterling in fact manages

to ‘overcome nature/nurture’ accounting for her main motivation of overcoming also

sex/gender. Finally, section 3.2.5 provides a critical perspective on (and a subsequent defence)

of Fausto-Sterling’s DyST, which is implied by the views of Oscar Kempthorne, whom I already

mentioned in Part One and whose views on causality I detail a bit more on this occasion. I

close in 3.3 with a substantive summary and the statement of the most important conclusions

I draw form this Part Two.

3.1 Systems approaches to biology

This section has the purpose of introducing and disambiguating two instantiations of what is

called ‘systems approach to biology’ (cf. Fausto-Sterling 2005, 1511 ff.). As already mentioned,

these are Developmental Systems Theory (DeST) and Dynamical Systems Theory (DyST),

which, however, are both referred to as DST in the literature. Therefore, section 3.1.1 draws

distinctions especially between DeST and DyST. Then, mindful of the fact that DeST and DyST

share certain basic assumptions in spite of their differences, section 3.1.2 introduces DeST and


57

3.1.3 provides a critical view. Finally, section 3.1.4 situates Fausto-Sterling in the context of

DyST as well as DeST and 3.1.5 concludes this section.

3.1.1 Terminological preliminaries: DST, DeST, and DyST?

In the respective literature ‘DST’ can mean both Developmental Systems Theory and Dynamic

Systems Theory. In this section, I discuss their relation. In order to keep the two apart, I dub

the former ‘DeST’ and follow Griffiths and Tabery (2013) in dubbing the latter ‘DyST’.

To begin with, Evelyn Fox Keller distinguishes DeST and DyST with respect to their different

history of idea development, i.e., with respect to different groups of researchers developing

and employing them (ibid. 2005). Keller even distinguishes as many as three different uses of

the acronym ‘DST’ and not two: She argues that there is DST as traditionally associated with

Russell Gray and Paul Griffiths (amongst others), secondly, of Donald Ford and Richard Lerner

(amongst others), and, thirdly, as associated with Esther Thelen (amongst others; cf. ibid.). In

what follows, you will see that I will be justified to transform Keller’s threefold typology

interpreting it as binary and only between DyST and DeST and its species DeST-1.

In terms of content similarities, all DST approaches are said to defend a ‘systems perspective’

of development (cf. Keller 2005, 414) or might be subsumed under the label

‘developmentalists’ (cf. Schaffner 2016, Longino 2013). That is, they are taken to share

influences from scholars like, for instance, Daniel Lehrman, Conrad Waddington, Susan

Oyama, and Richard Lewontin (cf. Keller 2005, 411/2; Griffiths and Tabery 2013; Schaffner

2016, chapter 3).

In terms of content-differences, there is agreement at least with regard to one very general

point. What distinguishes DeST from DyST is that the latter emphasizes especially the

temporal dimension of development. For instance, Griffiths and Tabery (2013) argue that DyST

“adds an additional [i.e. the temporal, M.B.] dimension” (ibid., 83) but they continue to argue

that “there is nothing about the basic idea of dynamical [i.e. temporal, M.B.] interaction that

requires the use of DyST” (ibid., 83) implying that also DeST can integrate this dimension. Thus,

what Keller (2005) treats typologically as a separate species, i.e., ‘DeST-1’ as denoting DeST

plus an incorporation of temporality is simply taken to be identical with DeST by Griffiths and

Tabery (2013). Finally, Longino (2013), who also cites Keller (2005), refers to DyST as

characterized by the ‘crucial difference’ of stressing the temporal dimension in comparison to


58

DeST scholars (cf. e.g. ibid., 84/110), which might be not so categorical after all as we just

learned.

While the just discussed criterion of individuation is not particularly helpful, there are two

other criteria with regard to which there is more agreement: Firstly, all three authors

mentioned agree in holding that DyST has been historically championed especially by Esther

Thelen (Griffiths and Tabery 2013, 82 ff.; Longino 2013, 84; Keller 2005, 413). Another

potential criterion individuating DyST (of which I don’t know if it’s a good one being able to

distinguish between DeST-1 and DyST) is that “[i]n contrast with the meticulous studies of

human infants or interactional patterns in the dynamic systems approach, there are no social

sciences conducted explicitly using the developmental systems approach” (Longino 2013, 89;

cf. also ibid., 109).

The second helpful criterion is that Keller (2005) holds that Thelen’s (and colleagues’) DyST

should be interpreted as a “theory in the sense of a specific model that produces predictions

to be tested against rival models” (ibid., 412, cited from Oyama et al. 2001b, 1)—a view which

seems also implied in the passages concerning DyST from Longino (2013, chapter 6).70 This

stands in contrast to DeST (and DeST-1), which is conceived by Griffiths, Gray, and Oyama as

a “theoretical perspective on development” (Keller 2005, 410, cited from Oyama et al. 2001b,

1).

More precisely, DeST is usually viewed as a conceptual framework, which is supposed to

substitute the conceptual framework of nature/nurture and not as a scientific theory

producing predictions (cf. Griffiths and Hochman 2015, 5; Griffiths and Tabery 2013, 75 ff.;

Godfrey-Smith 2001). Thus, it’s not on the level of a scientific theory that DeST is supposed to

make a difference, but rather on the level of Kuhnian scientific paradigm (in the wide sense

and not in the sense of exemplar) or, equivalently, as a disciplinary matrix (Kuhn 1996, 182

ff.).71 Such a paradigm renders (un-)sensible certain vocabularies, suggests metaphors,

contains certain metaphysical claims (ibid.), and, finally, suggest certain exemplary ‘ideas’

(paradigms in the narrow sense), which are then adopted as a strategy for normal research

(ibid., 187 ff.). For instance, DeST renders literally senseless concerning human nature and

70 And again on page 413, Keller (2005) write (my italics): “[F]or Kelso, as for Thelen and Smit, reference to dynamical systems theory is intended to be quite literal: the aim of these researchers is to construct detailed mathematical models of development in the conventional sense of the term theory.” 71 Both Oyama et al. (2001b) and Godfrey-Smith (2001) refer (even if only briefly) to Kuhn.


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genetic predispositions. In spite of this contrast between DeST as a framework and DyST as a

scientific theory, I feel that DyST somewhat implies DeST. Still, it will be interesting to test this

assumption in the course of discussing Fausto-Sterling’s concrete DyST.

As far as Anne Fausto-Sterling is concerned, she seems to know only the binary distinction

between DeST and DyST, however, without elaborating in detail what she takes to be the

relation between DyST and DeST in terms of content. In Fausto-Sterling (2005), she merely

refers to them as “two overlapping sets of ideas—developmental and dynamic systems

theory” (ibid., 1510; cf. also ibid., 1498). Similarly, in Fausto-Sterling (2014), she speaks of

“[t]wo overlapping arenas of thought—dynamic systems theory and developmental systems”

(ibid., 310).

From a purely linguistic point of view, we it’s quite clear that Fausto-Sterling has adopted

DyST, even if her employment of ‘DST’ meaning ‘DeST’ and ‘DyST’ is not at all consistent and

a bit confusing. She refers in her early texts rather to DeST (cf. ibid. 2003) or to both (cf. ibid.,

2000, 2005: employing a bit of a terminological mish-mash there; cf. Keller 2005, footnote 10).

But against what her terminology in Fausto-Sterling (2003) implies note that the references

notably of Esther Thelen in this text imply that she actually discusses DyST instead DeST. A bit

more consistently, Fausto-Sterling later switched to refer rather exclusively to DyST and

consistently adhered to this notion from then on (cf. 2007, 2012a,b, 2014, 2015a; Fausto-

Sterling et al. 2011a,b). In addition Fausto-Sterling explicitly refers to DyST on her web site,

even if in her recent note Against Dichotomy, she talks about having adopted a

“developmental systems approach” (ibid. 2017, 65).

3.1.2 What is DeST?

Before taking a closer look at Anne Fausto-Sterling’s DyST, let’s take a look at some basic

assumptions of DeST being also mindful of the fact that DyST and DeST do overlap in content.

To begin with, it should be noted that DeST is historically associated as opposing a gene-

centered view in biology72, the latter of which implies, for instance, that genes are the unit of

evolution and that organisms’ traits are programmed in their genes—a popular and

sophisticated defender of this view is Richard Dawkins, for instance. In what follows I sketch

72 Cf. e.g. the introduction of Oyama et al. 2001a.


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some major claims associated with DeST citing from Griffiths and Tabery (2013) and Griffiths

and Hochman (2015), which are both introductory articles to (the key concepts of) DeST.

Firstly, as one of its core features, DeST assume the importance of developmental systems

both for ontogenesis and phylogenesis (and thus evolution): ‘Developmental system’ is

defined as an epigenotype defined as “[t]he interaction of many genes produc[ing] an

emergent level of organization” (Griffiths and Tabery 2013, 79) plus “nongenetic factors that

influence development” (ibid.). Thus, the developmental system “a global expression of the

causal factors that influence[d] development” (ibid.). This, however, without determining “a

unique phenotype, both because development [is] a probabilistic process and because

development [is] plastic by design” (ibid., 79/80).

Moreover, the DeST authors adopt the concept ‘probabilistic epigenesis’ where “the course

of development [of a developmental system] depends on the interaction between each stage

in development and environmental factors at that stage” (Griffiths and Hochman 2015, 1;

Griffiths and Tabery 2013, 79/80). What is present here is, firstly, a notion of developmental

(temporal) dynamics, which just emphasizes that “development at each stage builds on the

results of development at an earlier stage” (Griffiths and Tabery 2013, 82) and thus

emphasizes differences and change (ibid., 82 ff.). In addition to this ‘horizontal’ dimension,

the complex, vertical interaction of many levels or (in Oyama’s words) interactants of a

developmental system is emphasized (cf. Oyama 2000, 72 ff.).

Next, there is the notion ‘developmental niche’ (or ‘ontogenetic niche’). Griffiths and

Hochman (2015) argue that

“[i]n developmental niche construction, organisms structure the environment in which their descendants will develop, and thus exert environmental as well as genetic influences on the phenotypes of their descendants. Niche construction in this sense is the same thing as extended inheritance.”

(ibid., 4)

The developmental niche is exactly to that to which is related the organism in a developmental

system. This notion emphasizes the non-passivity of the organism changing and altering its

environment and also passing it on to its descendants as conceived in the extended notion of

inheritance (cf. Griffiths and Tabery 2013, 80 ff.). The moral to draw is that “[t]he stability of

inheritance is not only explained by the insensitivity of development to context […], but also

by the active reproduction of context by the parental generation” (ibid., 81).


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While these explications might have been a little abstract, DeST might become clearer, when

its implications are considered. Firstly, the notion of a developmental system implies that

there is causal parity and thus equal importance between genes and other causes (and, in

other words, equal importance between different interactants at different levels).

Interestingly, this can be stated as the testable claim

“that if some role is alleged to be unique to nucleic acids and to justify relegating nongenetic factors to a secondary role in explaining development, it will turn out on closer examination that this role is not unique to nucleic acids, but can be played by other factors.”

(Griffiths and Hochman 2015, box 1)

That is, there are equally important and different levels of causal influence (Griffiths and

Tabery 2013, 82, 85 f.), just because DeST considers development on “multiple levels (genetic,

neural, behavioural, environmental)” (ibid., 85) such that each level interacts with each other.

Next, DeST implies a different notion of inheritance and by extension a modified account of

evolution (Griffiths and Hochman 2015, 4 ff.; Griffiths and Tabery 2013, 80 ff.). That is, it’s not

genes which are decisive in terms of phylogeny but also non-genetic factors. This negates that

natural selection works on the level of genes exclusively and proposes selection on the level

of developmental systems—which (as was defined above) just is the organism in relation to

its developmental niche (cf. Griffiths and Gray 2005a).

Finally, it might be helpful to mention that from a broader perspective DeST is actively

associated by its proponents with a philosophy of mechanism (Hochman and Tabery 2013, 84

ff.). In addition, Tabery (2014) distinguishes in his history of the nature/nurture debate the

two traditions of mechanism-elucidators (asking how questions) like Richard Lewontin and of

variance-partitioners (asking how much questions) like Arthur Jensen (cf. e.g. ibid., 99 f.). And

just as Tabery associates the philosophy of mechanism with the perspective of those

motivated to answer how questions (cf. ibid., 101 ff.), he obviously attributes the DeST

perspective to the mechanism-elucidators.

3.1.3 A taste of critique

This section has the purpose of providing a critical perspective on DeST. I chose to reproduce

the critique of Kenneth Schaffner (2016) and Philip Kitcher (2003), also because this critique

(besides being extensive and in my view substantial) concerns DeST as represented by


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Lewontin’s position, whose views were touched already in Part One, and for the sake of

continuity.73

Before beginning, it’s important to note that, when I respond to the critiques, I do this in the

name of DeST but from my own (more or less informed) perspective, which implies that strictly

speaking my responses are speculative and need not be what DeST specialists would respond.

To begin with, and as already mentioned both Kenneth Schaffner and Philip Kitcher launch

their critique against Richard Lewontin representing DeST positions. For instance, Kitcher

(2003b) is critical about the already in Part One mentioned classic “The Analysis of Variance

and the Analysis of Causes” (2006a) of Lewontin. The major reproach in Kitcher (2003b) is that

Lewontin abandons the concept ‘reaction norm’ (cf. Kitcher 2003b, 287/9), based on

Lewontin’s argument (holding at least for social sciences) that reaction norms cannot obtained

in principle.74

In addition to this, Kitcher concerns Lewontin’s assumption of an uncontrollable, stochastic or

random factor playing a role in development (cf. Lewontin 2000b, 35-8). More precisely,

Kitcher assumes that no such ‘developmental noise’ need to be assumed in the context of trait

development, because seemingly random development might simply require a more fine-

grained examination to enable causal reduction (cf. ibid., 289 ff.).75

Moreover, he argues against Lewontin and DeST in favour of a pragmatic focus on genes in

some cases (e.g. for research on alcohol addiction) demanding in general a case by case

73 However, it’s beyond the scope of this text to provide a wider selection of developmentalists’ critiques. This is not only, because DeST defends very general and partially metaphysical claims, but also because these claims have consequences for different subdomains of biology ranging from Organism Development Theory to Evolutionary Theory (cf. e.g. Griesemer et al. 2005, 523 ff.). This also, why I ignore, for instance, the sources mentioned in Barberousse (2010) and do not exploit the critical response papers contained in Oyama et al. (2001a). I leave out also the critique by Helen Longino (2013). 74 I’m not sure, if Lewontin genuinely abandons the concept ‘reaction norm’, because he argues even in the very same text that “[t]he real object of study, both for programmatic and theoretical purposes, is the relation between genotype, environment, and phenotype. This is expressed in the norm of reaction […]” (Lewontin 2006a, 522, his italics). In addition, the concept reappears in his later programmatic work as a tool for representing the complexity of phenotypical development (cf. e.g. Lewontin 2000b). 75 For instance, Kitcher argues with respect of the question whether there is a random developmental factor in the development of the trait ‘number of bristles’ in the model organism Drosophila (fruit fly) that “[i]t is quite possible that the differences in rates of cell division do account for the difference in bristle number and that these rate differences are remote effects of the inhomogeneity of the zygote. Although we could reasonably describe them as ‘random’ […] they are not irreducibly random. A fine-grained specification of the total environment of the DNA would provide a causal explanation of the asymmetry in bristle numbers. Thus, once again, the form of the phenotype can be viewed as fixed by the genotype and the environment provided that we conceive of the environment in the proper (total) fashion. There is no need to invoke developmental noise or to think that the notion of a norm of reaction breaks down here” (Kitcher 2003, 289/90).


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analysis (ibid., 295 ff.).76 Generally, however, he accepts the idea of causal parity, because its

in this very spirit that his principle of causal democracy should be evaluated: No cause is a

priori more important than another.77

In sum, Kitcher clearly and especially criticizes Lewontin’s DeST, because it aspires a

fundamental change on the framework-level, where Kitcher is in favour of sticking to a

received but reformed framework of interactionism. But all this does of course not hinder him

to sympathize with Lewontin’s (and DeST’s) ideas in general.

Next, Kenneth Schaffner launches in his book Behaving. What’s Genetic, What’s Not, and Why

Should We Care? (2016) a critique of what he takes to be five core concepts of a

developmentalist position as represented by Lewontin. These five concepts are ‘parity’,

‘nonpreformationism’, ‘contextualism’, ‘indivisibility’, and ‘unpredictability’ (ibid., 95) and he

explains them as follows:

“Basically, parity means genes are not special—not ‘master molecules.” Nonpreformationism implies that we do not find ‚traitunculi‘—little copies of the traits the genes determine—in the genes. Contextualism indicates that genes have little meaning (as ‘informational molecules’) per se, only in context with other genes, and in an environment that is cellular, extracellular, and extraorganismic. Indivisibility refers to the thesis that genes and environment cannot be identified by their effects on traits in any separable sense: the effects are a seamless unification—an amalgam. Unpredictability means that from total information about genes and environment, we cannot predict an organism’s traits: they are, accordingly, emergent.”

(ibid., 95, his italics)

In his book, Schaffner evaluates the validity of those claims with respect to a simple model

organism (similar to Lewontin’s fruit fly), the worm C. elegans. He concludes by accepting two

of the claims: nonpreformationism and contextualism while rejecting the other claims. More

precisely, Schaffner argues that, firstly, genetic causes can be separated from environmental

causes (‘indivisibility’), secondly, that the focus on genes is heuristically and pragmatically

defendable (‘parity’) and, thirdly, that there is no strictly uncontrollable random or stochastic

factor rendering phenotypes emergent (‘unpredictability’).

76 Kitcher (2003b) criticises also that developmentalists’ approaches for analysing human behaviour don’t “offer

anything that aspiring researchers can put to work” (ibid., 294). However, Kitcher reassessed this critique later stating that “the models Oyama, Lewontin, and Griffiths tried to elaborate are useful tools for explaining families of biological phenomena, and, by demonstrating that, it’s possible to destabilize the monocular fixation of genes. I should have recognized the potential worth of some vivid examples in action” (Kitcher 2016, 93). This statement implies Kitcher recognizing that developmentalists have in fact been successful in “putting their models to work”. 77 He argues that “[i]nteractionist ought to support a principle of causal democracy: if the effect E is the product of factors in set S, then, for any C ∈ S, it is legitimate to investigate the dependence of E on C when the other factors in S are allowed to vary” (ibid., 290).


64

You might have noted that Schaffner’s rejection of ‘unpredictability’ (meaning Lewontin’s

developmental noise, i.e., a random factor in development) as well as his rejection of

(metaphysical) ‘parity’ (in favour of pragmatic non-parity) are really close to Kitcher’s positions

mentioned above and this is explicitly addressed and acknowledged by Schaffner (cf. ibid., 220

ff.).

In addition to Kitcher, Schaffner cautions that developmentalists might involve too much

context and get lost in complexity, “unless it provides us with some form of prioritized

ontology” (ibid., 114). This reproach is echoed by the critique picked up in Griffiths and

Hochman (2015) about “replacing the clear boundaries of an organism […] with the vague and

indeterminate boundaries of a ‘system’” (ibid., 5).

Moreover, Schaffner argues that the claim of vast non-additivity which entails the indivisibility

of nature and nurture causes is empirically relative, i.e., in some cases true but in other cases

false (ibid., 164). This is a classic argument also found in Sesardic (2005) in the context of the

validity of the EEA (cf. ibid. 107-15; footnote 48).

Finally, and more generally, it should be noted that Schaffner draws these inferences based

on his study of the worm C. elegans as his model organism. This is as justified as what Lewontin

and others claim with regard to their model organism ‘fruit fly’ (cf. e.g. Lewontin, 2000,

2006a). Both make fundamental claims and far reaching and generalizing claims based on their

studies. On one hand, Lewontin infers the existence of developmental noise and inseparability

of gene. On the other, Schaffner claim that genes and environment are separable and that

there is no such thing as developmental noise. The underlying argument is obviously that, if

already this ‘simple’ organism’s development turns out to be complex, then this will be the

case for any comparatively simple and of course all the less simple organism as well.

3.1.4 Fausto-Sterling: DeST and DyST

The following two subsections continue in the introductory spirit of this section and pursue

further the goal of disambiguation. We already have an idea of what DeST is in the first place

and we have learned that Fausto-Sterling rather quickly positioned herself directly in the

tradition of Esther Thelen. While this is known now, we still need to examine Anne Fausto-

Sterling’s position in relation to DeST against the background of her adoption of DyST in terms

of content.


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Thus, in what follows I investigate, if Fausto-Sterling talking DeST versus talking DyST is just a

matter of words and less important in terms of content. More precisely, I fly, firstly, over some

passages from Sexing the Body (Fausto-Sterling 2000) and “The problem with sex/gender and

nature/nurture” (Fausto-Sterling 2003), which explicitly refer to DeST. Secondly, I concern the

close linkage between the texts Fausto-Sterling (2003), (2007), and (2014), which, from

linguistic point of view, suggests that Fausto-Sterling’s usage of ‘DeST’ versus ‘DyST’ is really

rather a matter of terminology than a matter of content.

3.1.4.1 Fausto-Sterling (2000b) and DeST

As already indicated above, one encounters DeST in Fausto-Sterling’s work as early as in Sexing

the Body (2000b). One important theme of this book is the overcoming of the nature/nurture-

logic, which, or so I think, had not yet been adopted in her earlier writings and especially her

book Myths of Gender (1985). It’s in this very context of overcoming nature/nurture and by

implication sex/gender that Fausto-Sterling discusses DeST (ibid., 25-7). She argues that

instead of there being “fundamentally two kinds of processes” (ibid., 25), i.e. nature and

nurture, phenotypic traits are neither determined, e.g., by genes nor by environment (ibid.,

26). Rather, she sees “nature and nurture as an indivisible, dynamic system” (ibid., 228). She

adopts (what we already encountered as) “the idea of a developmental system […] because

the idea of a system entails the concept of mutual interdependence of its parts” (ibid., 271

footnote 114).

Closely associating DeST with connectionism, as do Thelen and Bates (2003)78, Fausto-Sterling

(2000b) emphasizes non-linearity (‘interaction’) and complexity: “[A] single behaviour may

have many underlying causes, events that happen at different times in development” (ibid.,

27). Later, Fausto-Sterling mentions three general points motivating the applicability of “the

work on dynamic developmental systems” (ibid., 246) to sexual development and gender:

“First, we need to stop looking for universal causes of sexual behaviour and gender acquisition and instead learn more about (and from) individual difference. Second, we need to think harder about how to study sex and gender as part of a developmental system. Third, we need to become more imaginative and specific about what we mean by the word environment.”

(Fausto-Sterling 2000, 246, her italics)

78 They argues that “connectionism and dynamic systems are not competing theories of development. The two theories have somewhat different histories. […] Their practitioners continue to differ in their preferred methodologies and research questions. But at a more general theoretical level, there are far more shared assumptions than real differences.” (Thelen & Bates 2003, 390)


66

She provides as an interesting example of application the study of the human smile (ibid., 245

ff.), whose universality, importantly, need not imply its innateness. She grants well that,

“initially, a basic set of neural connections develops that enables a human to ‘smile’ as a reflex,

even in utero” (ibid., 245) but that this early smile “at first does not function as a mode of

emotional expression” (ibid.). It’s just in the course of development in relation to other

persons that the “physiological response becomes ‘socialized’” (ibid., 246) which is to say that

it’s integrated into complex communication.

The morale for Fausto-Sterling is that smiling is a relational phenomenon (not an individual

trait) and that it’s stable but changeable (as demonstrates early infant development (ibid.,

246). Hence, no universal (e.g. biological) cause, but rather a focus on development over time

and its stable and unstable phases, and a particular focus on environment and the organisms'

detailed interaction with it.

3.1.4.2 Fausto-Sterling (2003, 2007, 2014): DeST or DyST?

To begin with, the texts Fausto-Sterling (2003) and ibid. (2007) have more in common than

one might suppose prima facie, since there are no cross-references. On first sight, and firstly,

they concern the question of how to overcome the dichotomy of nature/nurture or

sex/gender, respectively. Secondly, they both deal with sexual orientation (or homosexuality),

even if Fausto-Sterling (2007) focusses more explicitly on this topic. Thirdly, and in terms of

their theoretical concepts under scrutiny, both texts focalize on terms like ‘embodiment’ as

well as sexuality ‘as a system’ with stable and unstable periods. Fourthly, they both draw

heavily from Thelen and Smith (1996): A Dynamic Systems Approach to the Development of

Cognition and Action, which Keller (2005, 413) characterizes as the “bible” of DyST. Yet,

officially, Fausto-Sterling (2003) concerns DeST, while Fausto-Sterling (2007) concerns DyST.

Due to this significant overlap, the discussion of Fausto-Sterling (2003) is postponed to the

discussion of Fausto-Sterling (2007) in the context of DyST in 3.2. But let me still say that in

terms of content, there is nothing in Fausto-Sterling (2003), which justifies Fausto-Sterling’s

repeated reference to DeST (and not to DyST) with the exception of a single reference to the

DeST pioneer Susan Oyama (ibid., 124; standing in contrast to substantial reproductions from

Thelen and Smith 1996).

The relation between the texts Fausto-Sterling (2003) and ibid. (2014) is more obvious,

because here Fausto-Sterling (2014) explicitly references Fausto-Sterling (2003). Just like


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Fausto-Sterling (2003) and ibid. (2007), the author concerns the outlook of overcoming

dichotomies like nature/nurture or sex/gender. But in 2014, she talks also about the “[t]wo

overlapping arenas of thought-dynamic systems theory and developmental systems” (ibid.,

310). And beyond that, she in fact and explicitly focusses on DyST reproducing DyST’s goals

according to Thelen and Smith (1996): A first aim is to “understand the origins of novelty”

(Fausto-Sterling 2003, 126), a second “is to reconcile global regularities with local variability”

(ibid.), a third “is to integrate developmental data at many levels of explanation” (ibid.), a

fourth “is to provide a biologically plausible yet non-determinist account of the development

of behaviour” (ibid.), a fifth “is to understand how local process […] can lead to global

outcomes” (ibid., 127), and a sixth, finally, “to establish a theoretical basis for generating and

interpreting empirical research that breaks out of the idea of adding up so much nature and

so much nurture to create a final outcome” (ibid.). Hence, this text clearly concerning DyST in

terms of content. And it’s these goals of DyST, which are cited both in 2014 and officially in

the name of DyST as well as in the 2003 and in the name of DeST.

3.1.5 Conclusion

Let me wrap, what was discussed and what should be kept in mind from this section for the

rest of the text, which is about Anne Fausto-Sterling’s application of DyST.

Firstly, and especially in the spirit of disambiguation, I discussed DeST, which (besides DyST) is

also referenced by the acronym DST that is widely spread in the literature. We found

specifically that DeST, which historically evolved as countering a gene-centered view, is

characterized as scientific framework containing basic assumptions with respect to biology

and its subdisciplines by introducing, for instance, the developmental system as the crucial

biological unit for ontogenesis and phylogenesis. This stands in contrast to DyST, which—while

sharing certain claims with DeST—is said to be situated on the level of a scientific theory.

Moreover, DyST is historically especially associated with Esther Thelen and is said to put

accord special importance to the temporal dimension of development (which, however, was

also said to be integrable with DeST).

Secondly, I argued that DeST has been criticized for their general assumptions, specifically, for

their claims that 1) nature and nurture can never be separated (just like organism and

environment are not separable), 2) there is no one cause more important than another, 3)

there is no way to predict an organism’s trait due to a developmental random factor.

Fausto-Sterling and Dynamic Systems Theory (DyST)

68

Moreover, doubts have been uttered, if DeST can have practical consequences disproving that

it’s either positing to much complexity or that it’s just ‘armchair philosophy’.

Finally, I argued that in the specific case of Fausto-Sterling, her reference to ‘DeST’ and ‘DyST’

seems not to make a large difference and represents rather a merely terminological matter,

because Fausto-Sterling perceives DyST and DeST as ‘overlapping’ areas or ideas mentioned.

However, it became clear that Fausto-Sterling is really much closer to DyST than to DeST due

to the fact that she has received Esther Thelen much more extensively than she has received

the texts of scholars associated with DeST.

3.2 Fausto-Sterling and Dynamic Systems Theory (DyST)

This section can be said to represent the heart of this Part Two and the text, because it aims

to answer the specific question what Fausto-Sterling’s concrete DyST is about, which is

supposed as an alternative for nature/nurture.

To meet this end, and in order to provide first impression of Fausto-Sterling’s DyST and some

important notions, section 3.2.1 analyses at first three cases of Fausto-Sterling applying DyST

to three different topics (sexual orientation, sex differences in bones, infant gender

development).

In contrasts to the non-systematic, bottom-up character of the former section, section 3.2.2

then changes the perspective to a more systematic, top down perspective. While the aim is

still the clarification of what DyST means for Fausto-Sterling, this second section, firstly,

reproduces Fausto-Sterling’s DyST theory of gender development and, secondly, it

systematically focusses on the discussion of what I take to be four core notions of Fausto-

Sterling’s DyST: embodiment/experience, and emergence/iteration.

In the following section 3.2.3, I then establish explicitly what was already foreshadowed

before (e.g. in 3.1.4), namely, that Fausto-Sterling’s DyST is situated on a framework- as well

as on a theory-level. This is important, because Fausto-Sterling’s DyST being situated also on

a framework level is, of course, presupposed for Fausto-Sterling’s aspired overcoming of


Section 3.2.4 then discusses one of the main interests of this text, namely, the question, if

(and, if yes, how) Fausto-Sterling succeeds to overcome the nature/nurture framework, which

was discussed in Part One, by adopting DyST. The core of this section is that I provide the

Fausto-Sterling and Dynamic Systems Theory (DyST)

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relevant argument, which I attribute to Fausto-Sterling, and the explication of its premises and

the rebuttal of a few ad hoc critiques.

Section 3.2.5 then reconsiders the view of Oscar Kempthorne, which was already touched in

Part One, in order to examine the critique of Fausto-Sterling’s DyST, which flows from it, in

more detail. And section 3.2.6 finally closes this section with a conclusion.

3.2.1 Three case studies of Fausto-Sterling applying DyST

As mentioned above, the aim of this section is to provide a first impression of what DyST

consists in from the perspective of Anne Fausto-Sterling. In what follows I discuss three

different instances, in which Fausto-Sterling applied DyST. This approach is rather non-

systematic by sticking to certain texts of Fausto-Sterling, even if I work out important ideas

mentioned there. I will not mind drawing the connections, but you might want to keep in mind

the key ideas of DeST discussed above, which are partially associated with what is discussed

in what follows.

More precisely, I firstly treat the case of Fausto-Sterling applying DyST to sexual orientation.

The second section concerns infant gender development and the third sex differences

between men and women with respect to bones. The whole section closes with a conclusion,

which reproduces and assembles some important ideas that crystallize in the different case

studies.

3.2.1.1 First case study: DyST and sexual orientation

As already mentioned above in section 3.1.4, we can take the texts Fausto-Sterling (2003) and

ibid. (2007) as being inspired by Thelen and Smith (1996) and thus DyST (even if Fausto-

Sterling 2003 speaks of DeST). In what follows, I examine Fausto-Sterling’s application of the

received DyST concepts to the subject of sexual orientation.79

In both texts, Fausto-Sterling clearly motivates her citation of Thelen and Smith with regard

to the promise of overcoming dichotomies and in particular sex/gender (cf. Fausto-Sterling

2007, 50 ff.). For instance, in Fausto-Sterling (2003), the author implies this motivation of the

adoption of DyST stating that “[f]rom the point of view of DST [for us: DyST, M.B.], neither

naked sex nor naked culture exist” (ibid., 125). This aim becomes but clearer, when Fausto-

79 In fact, Fausto-Sterling (2014) is in terms of content referring to DyST also quite close and sometimes literal with respect to Fausto-Sterling (2003).

Three case studies of Fausto-Sterling applying DyST

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Sterling references Judith Butler’s Gender Trouble, which pursued exactly the same goal (ibid.).

Note for your interest Fausto-Sterling’s claim that DyST is even ‘better’ than Butler’s attempt,

because “D[y]ST can provide accounts of how gender materializes in the body that will work

for all animals, not just humans” (ibid., 126, her italics). In both texts, Fausto-Sterling makes

clear that she proposes as replacement for nature/nurture an “analytical framework” (Fausto-

Sterling 2007, 48/52) or “intellectual framework” (ibid. 2003, 125). In contrast, she is not

concerning “technical strengths and weaknesses” (ibid.) implying a remaining inside the given

nature/nurture framework.

In what follows, I focus on a few concepts, which stand out as important in one or both texts.

A first concept is that of a ‘(dynamic) system’ and both Fausto-Sterling (2007) and ibid. (2003)

argue that sexual orientation should be perceived as such a system. According to Fausto-

Sterling (2007), a dynamic system has as characteristics that it’s complex, interactive, self-

organizing, and self-maintaining (ibid., 55). Fausto-Sterling (2003) supplements adds that a

“functional system [e.g. walking or sexual orientation, M.B.] emerges from a context-bound

system in which seemingly random activity [….] evolve[s] into more highly structured form and

function” (ibid., 128).

Next, both text concern (in-)stability of such a just mentioned dynamic system. Both texts

underline that a system like sexual orientation is stable in some periods of development and

unstable in others. It’s unstable, when “enough of the inter-supporting subunits are

disrupted” (Fausto-Sterling 2007, 55), but it re-gains stability such that “[t]he new stable state

can produce the same types of desire, or a new set of desires” (ibid.), which is when “someone

‘changes’ sexual preference” (ibid.). Fausto-Sterling (2003) properly characterizes the

system’s (i.e. sexual orientation’s) change of stable and unstable periods as ‘softly-assembled

states’: “Although relatively stable, such states can dissolve into chaotic periods out of which

new types of stability can emerge” (Fausto-Sterling 2003, 128/9).

The just mentioned DyST notions concerning system’s (in-)stability are according to Fausto-

Sterling appropriate to account for empirical facts about sexual orientation, for instance, that

it’s perceived as both stable (or even determined) and malleable at the same time (cf. ibid

2003, 125/9, 130; ibid. 2007, 53-56). Accordingly, Fausto-Sterling (2003) states that “[f]or

many homosexuals, same-sex attraction is a stable state of desire” (ibid., 129), but emphasizes

also that “it can sometimes become destabilized and after a period of disarray, some new


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quasi-stable form of desire can emerge” (ibid.). Fausto-Sterling (2007) emphasizes that DyST

enables an explanation of sexual orientation’s (relative) stability, without having to appeal to

a “hidden essence” (ibid.). Instead, conceiving sexual orientation as a system entails that

understanding its components implies understanding its stable states.80

The components that make up a the just mentioned system of sexual orientation are therefore

important. According to Fausto-Sterling (2007), these components are found on different

levels, because “[t]here are many levels of organization to consider, from the subcellular to

the sociocultural” (Fausto-Sterling 2007, 56). Importantly, this implies what was called above

the parity of causes, because genes are explanatorily not more important than other factors

(ibid.). In accordance, Fausto-Sterling relativizes the importance of genes stating that “[g]enes

don’t cause; they respond” (ibid.) and urges to conceive of “gene activity as a reaction to a

particular environment or experience” (ibid.).

Next, both Fausto-Sterling (2007) and ibid. (2003) concern the concept of embodiment. More

precisely, Fausto-Sterling (2007) argues that DyST can explain, “how we come to embody

desire” (ibid., my italics), while going into detail only by virtue of treating the neighboured

concept ‘incorporated knowledge’. Like knowing-how knowledge of riding a bike (ibid., 56),

incorporated knowledge is characterised as contextual, sedimented in the body (rather than

abstract), and habitual and by implication unconscious (ibid., 56). As a consequence of these

three characteristics, Fausto-Sterling argues that “it is possible, through the human capacity

to narrate our own lives, for it [i.e. the incorporated knowledge] to become a part of our

conscious thought as well” (ibid.). In contrast, Fausto-Sterling (2003) directly (even if briefly)

concerns embodiment, which “suggests a process by which we acquire a body rather than a

passive unfolding of some preformed blueprint” (ibid., 131; cf. also 129 f., her italics).

In conclusion, this case study underlined the concepts of a dynamic system, of its being soft

assembly of its components implying equally changeability and stability, and, finally, the

concept of embodiment. What should be emphasized about this case study is a remarkable

implication of DyST with respect to the study of sexual orientation: Heterosexuality (i.e. the

norm) becomes the object of study rather than homosexuality, which is the deviation of the

norm and has traditionally been the subject of study (cf. Fausto-Sterling 2007, 47/55). Thus,

80”If we are to understand desire as a dynamic system, we must learn more about the underlying components that produce a stable state (or become destabilized)” (ibid., 56).


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the question is not, why people become/are homosexual, but rather and more generally:

“[W]hat are the processes by which desire becomes inherent to the body” (ibid., 55)?

3.2.1.2 Second case study: DyST and infant gender development

Fausto-Sterling et al. (2011a,b) pursue the aim of clarifying how DyST can be applied to the

study of (infant) gender development. Before entering the texts, remember that Fausto-

Sterling is strongly influenced by the work of Esther Thelen. This is manifest in Fausto-Sterling

et al. (2011a,b)81, because the four core concepts of DyST, with respect to which Fausto-

Sterling et al. construe their text, are taken from Spencer et al. (2006), which is a synthetic

review of Thelen’s key ideas including the mentioned four core concepts (ibid., 1533 ff.). The

following paragraphs present these concepts as applied by Fausto-Sterling to her study of

infant gender development, which are: Focus on diachronicity, soft assembly of states,

cognition as embodied, and a focus on the individual.

First of all, Fausto-Sterling et al. mention “a new emphasis on timing” (ibid., 1693, her italics),

which is to mean nothing else but the emphasis of development over time and thus the

emergence of traits.82 Accordingly, Fausto-Sterling et al. (2011) elucidates the temporal

development, the ‘emergence’, of stable sex/gender differences at age 3, namely, motor

activity levels, toy preferences, vocalization, and sensory system behaviours (ibid., 1685 f.).

They do this by correlating ‘sex-related’ events already studied (anatomical, physical,

behavioural, and treatment differences; ibid., 1694 ff.). Amongst those events, the authors

stress the sex-related events that take place in the context of caregiver-infant dyad, i.e.

especially the mother infant relation (cf. also Fausto-Sterling 2012b, 408 ff.). They claim that

“a process by which the development of early sex differences is initiated might be identified”

(ibid. 2011a, 1696), which is here based on the assumption that the caregiver-infant dyad

looks differently for girls than for boys. Finally, the authors emphasize to have chosen “the

somewhat arbitrary cut-off point of 36 months, because by that time there are well-

81Cf. also ibid. (2014), 310 f. and ibid. (2003). 82 The word ‘timing’, which is used by Fausto-Sterling et al., might be a source of ambiguity: Intuitively, this associates (to me) to the idea of a system’s (here: gender’s) windows of development, which is a temporarily instable state against the background of the system’s normally stable state. More precisely, and regarding to gender, this system is rendered unstable by one of the components in the set that makes up the whole system and, importantly, what render gender unstable tends to be different at different periods in time. But this is just not what is meant here (but which is concerned as the 2nd core concept). Rather, ‘timing’ concerns emphasis on temporal development which is quite consistent with the fact that Spencer et al. (2006) write in the passage cited that “D[y]ST creates a new emphasis on time [sic]” (ibid., 1533).


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established sex-related differences” (Fausto-Sterling et al. 2011a, 1685, my italics) and

implying of course that ‘gender development’ does not ‘stop’ there. Moreover, the authors

stress also that the resulting time line and the associated sex-related events should not be

taken to be universally valid (ibid., 1695; cf. ibid. 2012b, 408/9).

Next, Fausto-Sterling et al. underline that „behaviors and other physiological states are softly-

assembled” (ibid. 2011a, 1969, her italics; cf. also ibid. 2012b, 407/8).83 Fausto-Sterling et al.

make this more precise stating that

“behaviour is temporarily stable and provides a platform for individual experimentation and future development” (ibid. 2011a, 1669) and it’s “an emergent property resulting from the interactions of several subsystems and the transition from one softly-assembled state to another involves a non-linear phase shift followed by a new period of stability.”

(ibid.)

This is really abstract, which is why in what follows I reproduce an exemplification provided

by Fausto-Sterling et al. (2011).

Fausto-Sterling et al. concern as an example boy-girl difference in infant activity level, which

is manifest already around birth. However, it “seems to disappear at three to four months,

[and, M.B.] reappears at five months and increases in size thereafter to a moderate level in

toddlers” (ibid, 1696/7). On the interpretation of DyST, however, this just means that the

system of motor activity passes from one stable state (different for boys and girls) to another

stable state (equal for boys and girls) to another stable state (different for boys and girls).

In more detail, the authors explain this change of states pointing to two different sub-systems

(or components) of the system ‘motor activity’, which are situated on different levels. Firstly,

they point out a correlation of motor activity with the caregiver-infant dyad’s (differences in)

boy and girl treatment (i.e. bodily vs. non-bodily stimulating and arousing infants; ibid., 1697)

and, secondly, a correlation “with different rates of prenatal neural development” (ibid.) in

little boys and girls. Based on these two aspects, they reason that the latter physiological

system might be responsible for the differences at birth. Differences, which, as mentioned

above, “even out by 4 months, leading to a decline in sex-related difference in activity levels”

(ibid.), before they reappear again. But, crucially, the reappearing differences are this time

due to the influence of gendered caregiver-infant relations. The effects of these relations build

83 Spencer et al. (2006) argue that “behaviour is multiply determined and softly assembled from the nonlinear interactions of multiple subsystems” (ibid., their italics).


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on the ‘stage’ as prepared by the physiological system creating the sex-related differences,

which are thus due to differences in treatment.

To conclude this, Fausto-Sterling et al. (2011a) sum up that therefore “activity level is not a

constant ‘thing’ but rather a semi-stable state” (ibid.) of the system ‘motor activity’ (one might

want to add). The authors emphasize that differences observed at two points in time (here:

after birth and after six months) “may have a different underlying genesis” (ibid.). Finally, and

importantly, the authors suggest not that the first system is nature and the second is nurture

but rather “an ongoing flow or process that is at once biological and experiential” (ibid.). The

point is that sub-components (here: neurophysiology and playing style) interact to produce

stable or unstable states.

The next concept presented in Fausto-Sterling et al. (2011a) is ‘embodiment’ and means that

“[t]he body integrates perception, action and cognition” (ibid.). The authors cite Thelen, who

“postulated the formation of neural maps connecting vision and proprioception to produce a

presumably pleasurable outcome” (ibid.). In other words, in any cognitive task in which a

person engages, he or she will connect her perceptions involved as well as the cognitive

contents reciprocally with his or her (bodily) performance.

In application to gender, the authors hold this reciprocity between cognitive contents,

perception, and (bodily) action to be clearly evidenced in that “[s]ocial interaction affects

neural development via chemical signalling including hormones […]” (ibid., 1697). With

respect to toy preference, they hypothesize that “toy preference in infants and young toddlers

is an emotional outcome of the play history of the caregiver-infant system” (ibid., 1698, their

italics). More precisely, they distinguish various stable periods of play in play history starting

with “face-to-face communications” (ibid.), continuing with a period were “mother

demonstrates, infants observes” (ibid.), and adding “stable endpoint in which the infant

explores the object while the mother observes” (ibid.). Here, of course, the concept of soft

assembly mentioned above resonates, because each move from stable to stable state is, as I

understand it, mediated by an instable state.

Finally, Fausto-Sterling et al. mention as last core concept or idea “a new respect for

individuality” (ibid. 2011a., 1698) implying that the supreme study object is not the child-on-


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average but “individual patterns of development” (ibid., 1699 f.).84 Based on this idea, Fausto-

Sterling et al. feel then enabled to “reframe the basic question of difference: how do larger

group differences emerge with time from a starting point of large individual variability but

small group differences?” (cf. ibid., 1698). This responds to what they take to be the

conundrum of most sex/gender differences, i.e., the fact that “[o]n the one hand, we make

verifiable claims about statistically significant group differences. On the other, the differences

are usually small enough that we are reluctant to apply policies or specific health care based

on the group to any particular individual” (ibid.).

3.2.1.3 Third case study: Differences in bones

The third case thematizes Fausto-Sterling (2005), where the author applies DyST to the study

of sex differences regarding bones. A salient difference to be thus explained is the fact that

bone-thinning (possibly entraining osteoporosis, i.e., bone-fracture or low bone-density)

“increases dramatically around the time of the menopause” (ibid., 1508; cf. also ibid. 1507,

1500 f.), an increase, which is unique for women and finds no correspondence in men.85

An often adopted explanation of this sex difference refers to the influence of hormones,

whose activity in the context of women’s menopause correlates with bone-thinning thus

manifesting the absolute sex difference (cf. ibid., 1505/7-10). Fausto-Sterling is unsatisfied

with this explanation “within the framework of sex versus gender” (ibid., 1503), which allows

nothing more but “probability statements about large and diverse categories of people” (ibid.,

1510). In contrast to this explanation, which is based on a non-diachronic (cross-sectional)

snapshot and the nature/nurture framework, Fausto-Sterling urges to “ask the development

question” (ibid., 1503) based on the hypothesis that “our bodies physically imbibe culture”

(ibid., 1495) and that “experience shapes the very bones that support us” (ibid.).

84 Spencer et al. (2006), on which Fausto-Sterling et al. (2011a) base their discussion, are again much clearer here: “Development happens in individual children solving individual problems in their own unique ways. […] We start with a child-in-context composed of multiple components at different levels of an integrated system” (ibid., 1533). 85 Independent of the DyST approach, Fausto-Sterling (2005) also relativizes the sex difference by contextualizing it (ibid., 1550): “The accuracy of the claim that osteoporosis occurs four times more frequently in women than in men […] depends on how we define osteoporosis, in which human populations (and historical periods) we gather statistics, and what portions of the life cycle we compare.”


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More precisely, applying DyST (cf. ibid., 1513 ff.) consists here in the effort to explaining the

sex difference mentioned above as being produced by “seven systems that contribute to bone

strength throughout the life cycle” (ibid., 1513).

“Each of the seven—physical activity, diet, drugs, bone formation in fetal development, hormones, bone cell metabolism, and biomechanical effects on bone formation—can be analysed as a complex system in its own right. Bone strength emerges from the interrelated actions of each (and all) of these systems as they act throughout the life cycle.”

(ibid.)

Fausto-Sterling adds that these subsystems, which interact to produce the emergent property

of bone strength, need to be examined with respect to how they interact (ibid., 1513 ff.).

Moreover, she emphasizes that “in a life course approach, prior events set the limits on later

ones. If girls and women enter into adulthood with weakened bones, therefore, they can

rebuild them, but their peak density may be less than if they had built stronger bones in

adolescence” (ibid., 1515, my italic). Finally, the system of bone density might be “dynamically

stable in mid-life but destabilize during old age”, while it’s not understood precisely “how the

transition from a stable to an unstable system of bone maintenance occurs” (ibid., 1513).

More concretely, Fausto-Sterling implies that the sex/gender differences in bones, which

becomes so clearly manifest in the comparative probabilities of osteoporosis in older age, is

but an extreme manifestation of the accumulation of many small effects of many (sexually

differential) influences over time. For instance, she specifies that sex/gender differences in

diet (ibid., 1515) as well as sex/gender differences in physical activity are two important

sources for the difference in bone density in older age.86

To conclude in a general manner and in comparison to the first two case studies, we encounter

in Fausto-Sterling (2005) similar key concepts: Emergence (cf. ibid., e.g. 1503, 1513 f.), self-

organization (ibid., 1511), a system’s stability and instability (ibid., 1512 f.), embodiment (ibid.,

1496 ff.), and relative development from (variable) states to the next states (ibid., 1515).

Similarly, Fausto-Sterling (2005) also mentions her motivation to replace nature/nurture or

sex/gender in favour of “the idea that we are always 100 percent nature and 100 percent

nurture” (ibid., 1510).

86 The dynamic system of bone density and the components it subsumes is helpfully displayed in a figure Fausto-Sterling (2005) on page 1511, which can be found online here: http://www.jstor.org/stable/pdf/10.1086/424932.pdf?refreqid=excelsior%3A150a061ef41e9efa9472ea021e25aa43, last access: 25.05.2018.

http://www.jstor.org/stable/pdf/10.1086/424932.pdf?refreqid=excelsior%3A150a061ef41e9efa9472ea021e25aa43

http://www.jstor.org/stable/pdf/10.1086/424932.pdf?refreqid=excelsior%3A150a061ef41e9efa9472ea021e25aa43


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But Importantly and in contrast to the other two case studies, Fausto-Sterling (2005) does not

apply DyST here in order to explain a behavioural or dispositional sex/gender difference, i.e.,

toy preferences, sexual orientation, or motor activity (which is nothing else than a disposition

to movement). Rather, she concerns “bone development—an area often accepted as an

irrefutable site of sex difference” (ibid., 1498).

3.2.1.4 Conclusion

Let me conclude by emphasizing the most important points of this section. Remember that its

goal was to provide a first and non-systematic introduction to Fausto-Sterling’s DyST by

presenting three applications of Fausto-Sterling’s DyST to three different subjects of study.

Firstly, let me point out three important core ideas that appeared in the discussion of the cases

and which are largely derived from the work of Esther Thelen. To begin with, there is the

notion of complexity, which is to say that a trait is modelled as a system with components on

different levels (e.g. psychic, biological, social, relational), which interact. Next, there is the

emphasis of temporality or ‘complexity over time’. This notion implies that in order to

understand a trait at a certain time, it’s necessary to study its emergence before it has been

present in the first place. Thirdly, there is the notion of a trait’s changeability and at the same

time its stability over time, which was captured under its being softly assembled. Importantly,

it’s implied that a trait (conceived of as a system) is differently sensible to different

components at different times. That is, a component, which might have large influence at time

t1 might have low influence at t2. Finally, and if you like, remember also the similarities that

associate with the few things that we learned about DeST and in particular the notion of a

developmental or dynamic system as the crucial biological unit (without that I want to go into

detail here).

Next, note that, in terms of content, the case studies concerned different sort of traits. On one

hand and referring to sex differences in bones, we treated a trait, which would have

traditionally been labelled as belonging to sex, i.e. on nature’s side, or as ‘biological’ or

‘innate’. On the other and thematizing motor activity, toy preferences, and sexual orientation,

we concerned traits, which are clearly connotated with ‘nurture’, i.e. on culture’s side and

characterized as (at least partially) acquired. In other words, Fausto-Sterling applies DyST to

explain the emergence of both classic gender-traits and classic sex-traits—a fact which is going

Systematic explication of Fausto-Sterling’s DyST of gender

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to be systematized in 3.2.4 and in the context of the argument, which overcomes

nature/nurture.

3.2.2 Systematic explication of Fausto-Sterling’s DyST of gender

In contrast to the bottom-up approach of the former section, which treated three case studies

of concrete application of Fausto-Sterling’s DyST, this section changes the perspective from

non-systematic to systematic or top-down. In other words, I concern what I take to be the key

elements of Fausto-Sterling’s DyST against the back ground of her total work. The main aim,

of course, remains the explication of Fausto-Stelring’s DyST and it holds here as it does above

that certain key ideas discussed in the context of DeST will reappear, but without that I will

concern this explicitly.

More precisely then, the first section attempts to provide a systematic account of Fausto-

Sterling’s theory of (infant) gender development, which (i.e. the theory) is of course work in

progress. The second section focuses on what I take to be at the heart of Fausto-Sterling’s

conceptual DyST thinking: The two connotations experience/embodiment and temporality/

iteration. The fourth section closes with the summary of the most important points.

3.2.2.1 DyST and (infant) gender development

In Fausto-Sterling (2012b), the author formulates a theory of gender development from birth

to age three. According to this theory, there are two different phases of gender development

(cf. ibid., 414). Firstly, a phase of presymbolic gender formation and, secondly, a phase of

symbolic gender formation and such that both phases are mediated by a transition. It should

be noted though that Fausto-Sterling has covered the presymbolic phase more in detail than

the symbolic phase up till now, which is also why the latter is discussed not so extensively in

what follows.

Let’s begin the discussion of those two phases and their transition by providing a well-put

summary of the presymbolic phase of gender formation:

“a) from the beginning (possibly even before birth) the dyadic interaction [between infant and caregiver, M.B.] shapes individual nervous systems in such a way that groups with overlapping but statistically differentiable behaviors start to emerge; b) at birth great individual variability in developmental parameters exists; some of which rises to the level of average group differences between male and female infants; c) from birth on, average sex-related differences in (parent-infant) communication take shape, developing into varied patterns of vocal, physical, and emotional interactions. Between 3 and 6 months other dyadic patterns emerge, some of which appear to be sex-differentiated.”


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(Fausto-Sterling 2012b, 409/10)

In other words, there is great individual variability between new born children and there is the

gendered interaction between children and caregiver, which is experienced by the children

and whose gendered structure is embodied and will produce group differences over time.

Important sex-related events, which are associated to the presymolic phase, are that “both

visual and auditory categories can be noted by 6-9 months (faces and voices) and by 12

months cross-modal abilities emerge including an association of male and female voices with

gender related objects (ibid., 411). For a more complete compilation of important sex-related

events compare the figure 1 and 2 in Fausto-Sterling (2011b) on page 1694/5.

Let me comment a bit on this first presymbolic phase of gender formation. A crucial point for

Fausto-Sterling is that new born infants differ especially individually and less in groups of male

vs. female (Fausto-Sterling et al. 2011a,b; Fausto-Sterling 2012c, 99 ff.).87 Fausto-Sterling

emphasizes that while “at birth enormous individual variability in developmental parameters

exists; some of this variability rises to the level of average group differences between male

and female infants” (Fausto-Sterling et al. 2011b, 1696). But the urge to play down group

difference at birth is clearly visible: With respect to verbal differences between male and

female infants, Fausto-Sterling et al. (2011b) “believe that initial variability [i.e.: at birth; M.B.]

can be analysed without regard to sex/gender differences, but that sex-related experience

initiate a process of embodiment in which group differences become more visible” (ibid.,

1699). In ibid. (2011a), they argue accordingly that “small variations […] begin as individual

differences” (ibid., 1690, my italics). By implication, assumed sex/gender differences between

boy and girls at birth might either be unimportant or no real sex differences at all. According

to Fausto-Sterling’s theory, they just become group differences in the course of time and

through their interaction with the gendered world (cf. ibid. 2012b).

Fausto-Sterling (2015c) underscores the importance of individual differences by considering it

in addition as a possibly direct causal factor in relation to gender formation. More precisely,

87 To be more precise with regard to the group differences: In terms of behavioural sex differences (e.g. toy preference, motor activity, vocalization), Fausto-Sterling et al. (2011b) notes that “neonatal starting points” (ibid., 1695) may also include “average differences in crying and fussing at birth, three months and six months” (ibid.). In terms of non-behavioural biological sex differences Fausto-Sterling (2011a) sums up as follows: “On average, boys are slightly heavier and have slightly larger brains at birth. They have been exposed to higher levels of testosterone prenatally and experience postnatal testosterone surge at three months, while girls have been exposed to higher levels of follicle stimulating hormone. Neonatal differences in motor activity level decline postnatally, but reemerge at 4 months” (ibid., 1690).


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she assumes that “initial differences that have no sex-related behavioural content might start

processes that produce later sex-related differences” (ibid. 5). These initial differences, which

show “small but significant neonatal sex differences” (ibid., 10), are birth weight, head

circumference, and Apgar scores (ibid., 8), where Apgar scores measure the robustness of the

infant at birth (ibid., 12).88 Fausto-Sterling speculates that these differences might produce

“non-gender-driven handling difference [which in turn, M.B.] might gradually produce average

related infant differences, first in motor or activity levels and later in more complex behaviors

and preferences” (ibid., 12). For instance, heavier and more robust boys and girls would

accordingly elicit a ‘rougher’ parenting style correlating with higher motor or activity levels in

the parented (ibid., 12). These higher levels are in turn are correlated with rough and tumble

play in toddlers (ibid., 7), which is gender-conform only for boys, of course. Hence, here we

encounter Fausto-Sterling relativizing the importance of caregivers’ gendered beliefs as a

cause for the emergence of group-differences (or at least adding another possible causal

factor), in favour of ‘objective differences’ in the babies Apgar scores, which are claimed to

elicit by themselves differences in parental treatment that built on differences at birth.

But let’s finally proceed to concern the second, i.e. the symbolic, phase of gender formation

and its transition.89 In terms of important sex-related events, Fausto-Sterling (2012b)

mentions for instance the fact that

“[a]t 18 months, children startled at culturally gender inappropriate images […] and have also developed a system of gender-related metaphors […]. Before 2 years of age, children learn to label others as boy or girl […]. They next develop the ability to self-label and can exhibit a nonverbal gender identity.”

(ibid., 412).

These are the sex-related events in the symbolic phase of gender formation, which have been

gathered to matter so far. For a fuller picture, compare again figure 1 and 2 in Fausto-Sterling

et al. (2011b) on pages 1694/5.90

88 In other words, boys and girls were ordered into three different clusters relative to birth weight, head circumference, and Apgar scores: “Cluster 1, characterized by the heaviest, largest head circumference children with Apgar scores averaging 9.0, has about 40% more boys than girls. […] Cluster 2, which contains the smallest children and mean Apgar scores of 8.4 has about 25% more girls. […] Cluster 3, containing intermediate sized infants with mean Apgar Scores of 9.4 is almost equally divided between males and females […]” (Fausto-Sterling 2015c, 10). 89 Curiously, the transition and the symbolic phase itself are not clearly separated. 90 This can be be found online here: https://ac.els-cdn.com/S0277953611003832/1-s2.0-S0277953611003832-main.pdf?_tid=c5492d0a-6185-4f5a-965d-fef980be5048&acdnat=1527254569_40d6400f85578b7cd3900e8ec0bb8b60, last access: 25.05.2018.

https://ac.els-cdn.com/S0277953611003832/1-s2.0-S0277953611003832-main.pdf?_tid=c5492d0a-6185-4f5a-965d-fef980be5048&acdnat=1527254569_40d6400f85578b7cd3900e8ec0bb8b60




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Having concerned the phases of gender formation and especially the first presymbolic phase,

it’s important to remember now that, generally, and just like in the case studies discussed

above, infant gender development is perceived here as a system of interacting components

(or subsystems/elements). There are the

“elements contributing to presymbolic gender embodiment and representation, indicating a period of transition—critically mediated by language development—to symbolic gender knowledge. Such knowledge builds on previous embodiment and enmeshes in a web of behaviour, self-labeling and preferences that are the subsystems of that dynamic web we call internalized gender identity. In each developmental phase, there are dynamically interacting subsystems; but the developmental time line is unidirectional.”

(ibid., 414/5, her italics)

The “interacting subsystems” for the first phase, in which gender is presymbolic and

embodied, are firstly notably external inputs (cloths, toys, faces, voices, gendered adults, i.e.

‘the gendered world’) as well as secondly in the context of the infant-caregiver dyad: Parental

touch, affects, and vocalization (i.e. the infant-caregiver dyad) as well as thirdly the infant’s

physiological regulation and brain development. For the second (i.e. the symbolic phase), in

which gender identity is said to be symbolically internalized, there is notably verbal labelling,

peer play preferences and playing style, toy preferences, notions of femininity and

masculinity.

In conclusion, gender is, firstly, and during a time, where the infant has no self-concept (and

maybe more animal than person), especially embodied. Then, secondly, and falling together

with language development (such that the acquisition of a symbolic self-concept is assumed

to presuppose language), gender is internalized and takes the status of knowledge (which is

no less cognitive than embodied). In total, gender is the above mentioned “dynamic web” of

the “subsystems” of behaviour, self-labelling, and preferences (which due to their nature of a

subsystems can be studied as system itself); it’s an ongoing process over time. And finally, it is

neither located in the individual (i.e. its body and mind), nor in the external world but only

thinkable in terms of the relation of the individual and the gendered world (and especially

salient in terms of the caregiver-infant dyad).

3.2.2.2 Core concepts of DyST: Embodiment/experience and emergence/iteration

Having gained an impression of Fausto-Sterling’s theory of (infant) gender development based

on a DyST perspective, this section has the purpose of systematically working out what I take

to be core ideas of Fausto-Sterling’s DyST: Namely, the connotating pairs of words


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embodiment/experience and temporality/iteration. As a corollary, this section purports to

establish that Fausto-Sterling’s DyST is really relevant on a framework level such that it differs

and is incommensurable with the nature/nurture framework due to its specifically introduced

DyST terminology.

3.2.2.2.1 Embodiment/experience

The first important concept is ‘embodiment’ and in its very context ‘experience’. Both

concepts are closely related. To begin with, let me concern ‘embodiment’.

To begin with, Fausto-Sterling et al. (2015) define ‘embodied gender’ as the following

mechanism:

“[E]ven nonconscious gender stereotypes held by a caregiver leads [sic!] to different patterns of touch and caregiver generated movement for male and female infants, and if these patterns differentially affect infant nervous system development, then caregiver gender-related behaviors might literally become embodied in an infant.”

(ibid., 1)

In other words, the infant ‘mirrors’ the gendered world as represented by the gendered

caregiver and mediated to the child in the context of the gendered caregiver-infant dyad. But

this ‘mirroring’ is to be understood not just as the infant superficially reflecting a caregiver’s

behaviour. Rather, the ‘mirroring’ implies bodily reactions, couplings, or maybe inscriptions,

and last but not least: Specific brain development. More generally, it implies a sedimentation

in the child on the long run of what is mirrored. And it’s just this ‘mirroring’ and its

sedimentation effect in the infant, which I take ‘embodiment’ to express.

Moreover, Fausto-Sterling (2012b), even if she’s not explicit, should in my view be taken to

characterize ‘embodiment’, when she writes that

“the brain/mind is integrated into the body. Through its sensory and motor abilities the exterior layers of the body bring the world into the central nervous system. Neural plasticity lies at the heart of the matter. A toddler’s mind emerges from experience in a particular body and particular world. The brain’s very synapses from, take shape, die back, or reconnect in response to the world and body that envelops it. The same is true of the forming neuromuscular connection—links from the central nervous system to the muscles that control motor ability and visceral responses. […] Gender identity is located in all three interacting networks [i.e.: the world, the body, the brain/mind], a product of the coupling of critical systems.”

(Fausto-Sterling 2012b, 405, my italics)

Here, Fausto-Sterling emphasizes three different levels: The brain (or: central nervous

system), which is identified with the mind, and the body and the world. But even if they can

be listed separately, Fausto-Sterling’s very point is that it’s all these three levels at once, which


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are in play when infants (or toddlers) experience. In her own words, it’s the central nervous

system, which (subsuming the brain and the nerves in the spinal cord) receives all the inputs

from the peripheral nervous system for processing and which is shaped. And the shaping

influences in turn manifest their effects on various loci from bodily development to psychic or

mental development to social and relational development of the infant.

This rich process of learning of a child is called ‘experience’ (cf. e.g. the last citation) and it’s

particularly its ‘multilevel’ aspect, which results in embodiment, which is emphasized. In this

spirit, Fausto-Sterling et al. (2011a) agree that

“Krieger considers embodiment as a multi-leveled process, arguing that good theory and research practice ought to integrate body and psyche within specific social, historical and ecological contexts […].”

(Fausto-Sterling et al. 2011a, 1684)

Again, studying gender based on the hypothesis that gender is embodied just means that all

three levels: the mind/brain/psyche, the body, and the world need to be considered, because

this is how especially children engage with the world via experiencing it.

To be more precise on ‘experience’, Fausto-Sterling (2005) writes in the context of her study

on bones that she uses “the term experience rather than the term environment […] to refer to

functional activity” (ibid., 1495, her italics).91 That is, and as already alluded to in 2.3.3,

‘experience’ replaces the nature/nurture concept ‘environment’. Moreover, she argues that

”[o]ne cannot easily separate bone biology from the experiences of individuals growing, living,

and dying in particular cultures and historical periods and under different regimens of social

gender” (ibid., 1510).

Moreover, and quite concretely, Fausto-Sterling et al. (2015) receive ‘experience’ “as a

process that ‘captures transactions between the organism at multiple levels of analysis’ […]

encompassing cellular, behavioural, and cultural features”92 (ibid., 2). Also, and in a very

precise way, Fausto-Sterling (2015c) explicates the concept of experience contrasting it again

91 ‘Functional activity’ is not meant in the sense of ‘activity, which bones are used for’. Rather, functional activity, which defines ‘experience’, is just activity different levels associated with a trait relative to the development of this trait: “Experience is synonymous with function or activity, and is construed very broadly to include the electrical activity of nerve cells and their processes: impulse conduction; neurochemical and hormonal secretion; the use and exercise of muscles and sense organs (whether interoceptive, proprioceptive, or exteroceptive); and, of course, the behaviour of the organism itself. Thus, the term experience, as used here, is not synonymous with environment, but rather stresses functional activity at the neural and behavioural levels of analysis.” (Gottlieb et al. 1998, 220) 92 The same definition is reproduced in Fausto-Sterling (2015c), page 7.


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with ‘environment’ or ‘socialization’, which tend to have a “disembodied” character (ibid., 7;

cf. also ibid. 2012c, 403).93 In contrast to the latter, she argues that “the concept of experience

casts a wider net than that of socialization, invoking the mutual interplay between the

physiological, the physical environment, and individual daily practices of child rearing”94 (ibid.,

7), while “[t]he latter, of course, are shaped by the wider culture in which they occur” (ibid.).

Thus, ‘experience’ intends to be a much richer concept than ‘environment’.

With respect to sex/gender differences, it follows from all this that an individuum experiences

the world and that it’s actually his or her “gendered experiences” (ibid. 2015b, 13), which it

embodies and which therefore produce to a large degree the differently sexed/gendered

individuals.

Before closing, let me point out some implications of what was discussed. Firstly,

experience/embodiment is not passive: It always implies experiencer’s (potentially

unconscious) activity on several experiential or modal levels (ibid., Fausto-Sterling 2003, 131;

Fausto-Sterling et al. 2011a,b,). This active aspect of experience stands out particularly clear,

when Fausto-Sterling concerns the caregiver-infant dyad and the high degree of true

interaction that takes place in this situation.

Secondly, it’s just those two concepts, embodiment/experience, which entail that the border

between organism and environment is seriously blurred, or so I believe. Investigating a trait

or some behaviour, this view implies that the behaving organism is continuous with the

stimulus it reacts to, because the stimulus is a culturally, socially, and psychologically rich

object and because those three properties are as much in the object as in the perceiving

‘organism’. The reason is that any experience so far has (quite literally) shaped ‘the organism’

as well as ‘the organism’ has shaped enriched and shaped its objects. Hence, the subsumption

of ‘organism’ and ‘environment’ under a developmental system (as already promoted by DeST

and discussed in 3.1).

93 Cf. also section 2.3.3 in this text. 94 In a similar way, Fausto-Sterling (2015c) speak about “the intertwined concepts of physical, social, and emotional experience” (ibid., 7).


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3.2.2.2.2 Emergence/iteration

The second core idea is in my view the dynamic character of a trait’s development, i.e.,

development over time (i.e., its emergence), which is closely associated with the notion of

iterative development.

To begin with, we already heard Fausto-Sterling arguing that to study “emergence of

difference […] means starting before a phenomenon of interest is measurable in order to

follow its appearance over time” (Fausto-Sterling et al. 2011a, 1685, her italics). In different

words: “Methodologically, we insist that to study difference we must begin before it exists

and observe its emergence” (ibid.).

For instance, and with respect to toy preferences, Fausto-Sterling et al. (2011a) state that

“[s]tudies of toy preference development need to detail the kinds and numbers of toys found in an infant’s environment from birth, how (and how often) specific toys are offered by caregivers, and what unprompted interest the infant exhibits.”

(ibid., 1698)95

Thus, what matters is the time before a trait, toy preference in this case, appears, which is

based on the assumption that are reasons to be found why the trait expresses the way it does.

A closely related aspect, which I want to emphasize, is Fausto-Sterling’s iterative concept of

development. She states that “[s]imply put, the state of the organism at developmental time

x is the platform on which the events of time x + 1 take place” (Fausto-Sterling 2017, 64). In

other words, differences build on differences; starting points of different individuals are never

equal, which is why same influences can have different effect. Or again in Fausto-Sterling’s

words: “[W]hat happens at one point builds on what has gone before” (ibid., 1515/6) and we

find similar statements spread out across her work (cf. also Fausto-Sterling 2012b, 405; ibid.

2012c, 113).

This has three important implications: Firstly, Fausto-Sterling’s theory is not a finished theory

of gender for the simple reason that it concentrates on gender development in infants from

birth to three years. It’s not complete in the sense that periods before birth and periods after

three years are suspended: “Although birth characteristics provide a moment to begin analysis

95 Cf. also Fausto-Sterling et al. (2015, 4): “Following in the theoretical footsteps of Thelen and her colleagues, we reasoned that gender-related processes that might lead to the embodiment of sex/gender would precede their actual emergence.”


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of developmental processes that lead to sex-related differences in behavior and preference,

this too, is an arbitrary starting point” (Fausto-Sterling 2015c, 13).96

And secondly, since different individuals are different and development takes place iteratively

and over time, not all individuals have the same ‘developmental windows’ (cf. Fausto-Sterling

2003, 128 f.; ibid. 2012c, 67), which means that dramatic changes of a variable v1 in the

complex system ‘gender’ might critically destabilize it at time t1, while it might not (or barely)

destabilize it at t2. Why this is precisely so is stated by Fausto-Sterling (2012b) arguing that,

for instance, what “we call gender identity in a 3 year old differs in important ways from that

which we call gender identity in a 7 year old” (ibid., 407). An immediate consequence thereof

is, of course, that there is no biologically normal program for gender: It’s the ‘timing’, which

here (in contrast to the usage in 3.2.1.2) does really mean ‘timing’ (cf. e.g. Fausto-Sterling

2012b, 407; Fausto-Sterling et al. 2011, 1693 ff.), which differs in differently individuals with

different histories (cf. e.g. Fausto-Sterling et al. 2011b, 1696; Fausto-Sterling 2012b,

399/408).97

Finally, all this implies and culminates in the thesis that “[n]ot a thing, gender identity is a

pattern in time” (ibid. 2012b, 405; cf. also 2015a), just as sexual orientation, or, “human desire

[is, M.B.] a developmental process rather than a typological state” (ibid.). This stands in

contrast with the view that gender is a static trait, which, once and somehow biologically or

culturally fixed (i.e. innate or acquired), is from then on ‘carried along’.98

96 See also: “As the developmental details and dynamic interactions of phase 1, the transition and phase 2 come into clearer focus, a supportable theory of gender identity development will emerge” (Fausto-Sterling 2012b, 416, my italics). 97 The point that an individual’s gender formation is relative to its own to developmental timing, which in turn is socio-culturally relative is also emphasized by the following citation: “The achievement of universal developmental task (e.g., dyad competence and physiological regulation) provides the skills needed to internalize and symbolize gender; these universal tasks, however, are always individually and culturally specific. The developmental state of the newborn, the emotional and skill states of the parents, their financial resources, the cultural accoutrements of parenthood structured by social gender norms all matter” (Fausto-Sterling 2012b, 408). By implication, “the processes for both gender variant and gender congruent kids are similar in kind, but differ in timing and or execution” (Fausto-Sterling 2012b, 407). In conclusion, there are only universal tasks (i.e.: to represent a stable system), but not universal biological programs. Or as Fausto-Sterling et al. (2011b) put it in the context of their “time line of sex -related events during the first 3 years” (ibid., 1694): “[T]he schemata are not intended as representations of universal developmental patterns” (ibid.) emphasizing that sex-related events and their distributions is likely to differ between different cultures. 98 Fausto-Sterling (2017) motivates this view arguing that “[b]elieving that traits are static creates methodological conundrums. Which times in the life cycle would be the ones that we analyse? Is the gender identity of a 3-year-old the same as that of a 13-ear-old, a 25-year-old, an 80-year-old?” (ibid., 64).


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3.2.2.2.3 Conclusion

Let me wrap up what was discussed and what were the most important insight from this

section. Remember that its aim was to provide a closer inquiry of what I took to be the two

most characteristic word pairs of Fausto-Sterling’s DyST.

Firstly, I concerned the connotation ‘embodiment/experience’. I argued that the notion of

experience is important, firstly, because it’s a feature, which clearly distinguishes DyST from

the nature/nurture concepts and their disembodied notions of environment. In contrast to

the latter, ‘experience’ is a much richer concept, especially because it connotates an actively

experiencing subject as well as an experience on multiple levels (from psychic, to physical, to

social). In close connection, embodiment denotes the fact that the central nervous system

(and, by implication, the body) of an experiencing subject is overtime shaped by the

experiences it makes. Just like ‘experience’, this notion connotates an active subject and thus

emphasizes the interaction between subject and world.

Secondly, I discussed the word pair ‘emergence/iteration’. ‘Emergence’ denotes the

methodological principle that, to understand the expression of a trait, it’s necessary to

examine the time until the trait’s first expression. It therefore emphasizes trait development

over time just like the notion ‘iteration’ does. However, ‘iteration’ underlines in addition that

the starting points of (the study of) trait development might be different for different

organisms and that differences build on differences implying, for instance, different effects of

same stimuli for different organisms (and at different times).

Briefly speaking, one might say that ‘embodiment/experience’ accounts for synchronic (or

vertical) complexity regarding the different ‘layers’ (psychic, physic, social) of an organism

studied by different disciplines (Psychology, Anatomy/Physiology, Sociology). In contrast,

‘emergence/iteration’ accounts for diachronic (or horizontal) complexity and enables the

thinking of different developmental timing and/or pathways.

Finally, remember that this section should also convince you from the fact that Fausto-

Sterling’s DyST is situated on a framework level. More precisely, the framework it instantiates

is critically different from the nature/nurture framework, which is clearly indicated by the

DyST concepts introduced in this section.

Fausto-Sterling’s DyST: Framework and theory

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If you’re not already convinced, then note that it’s not difficult to find respective passages in

her work (cf. e.g. Fausto-Sterling 2000, 2005, 2012b, 2017).99 Besides, we have since the

beginning been confronted with the fact that Fausto-Sterling motivates DyST in terms of

overcoming dichotomies like sex/gender, nature/nurture and thus in terms of arguments on

a framework level. Fausto-Sterling has also dedicated articles to directly making this point

“against dichotomies” (ibid., 2014, 2017; cf. also ibid. 2000, chapter 1).

3.2.3 Fausto-Sterling’s DyST: Framework and theory

Up till now, I have analysed both theoretical and empirical works by Anne Fausto-Sterling. On

one hand, we found Fausto-Sterling regularly concerning the nature/nurture framework and

calling for its replacement and at the same time promoting DyST. On the other, however,

Fausto-Sterling applied DyST for the expost interpretation of and the exante design of

empirical studies on the development of sex/gender (differences).

This reproduces the question already implied in the context of DyST’s and DeST’s relation to

each other. Namely, in what sense Fausto-sterling’s DyST is situated on the level of a scientific

theory and/or on the level of a scientific framework? Remember from the just mentioned

discussion above that, in contrast to DyST, its relative DeST has classically been conceived as

a framework and this perhaps in the sense of a Kuhnian paradigm (cf. Oyama et al. 2001b,

Griffiths and Hochman 2015). In contrast, Keller (2005) and (as it seems) also Longino (2013)

took DyST to function as a scientific theory (in the ordinary sense of a set of propositions

yielding empirically testable predictions).

Since we should be already convinced that Fausto-Sterling’s DyST is situated on the framework

level from the former section, which examined closer specific DyST concepts, I focus in what

follows on establishing that Fausto-Sterling’s DyST functions as well as a scientific theory

yielding predictions on the evidence of relevant passages.

A first indication that DyST has the status of a scientific theory is found in Fausto-Sterling

(2005). As we heard, this article concerns the application of DyST to sex differences in men’s

99 For instance, Fausto-Sterling (2012a), she argues that “[t]herefore, we still need theories of gender in early

development hat have sufficient intellectual force to displace the nature/genetics/nurture/environment paradigm […]” (ibid., 415). In addition, Fausto-Sterling (2007) and ibid. (2003) situate the application of DyST to sexual orientation on the level of an “analytical framework” (ibid. 2007, 48/52) and an “intellectual framework” (ibid. 2003, 125), respectively.


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and women’s bones. In it, and on one hand, the author pragmatically motivates the

application of DyST as helpful for finding better measures for prevention of health issues like

(in the concrete case) osteoporosis in bones.100 On the other, however, Fausto-Sterling also

states that (beyond all pragmatism), her approach provides better answers such that “better

includes an ability to predict outcomes for individuals, based on their particular life histories

and genetic makeups, rather than merely making probability statements about large and

diverse categories of people” (ibid., 1510). Moreover, Fausto-Sterling implies that her DyST

approach involves “a theoretical model, to be tested in part or whole and modified as needed”

(ibid., 1515). In other words, DyST is clearly conceived as an empirical theory and claimed to

be even epistemically superior to cross-sectional approaches.

Next, in Fausto-Sterling (2012b), it seems that the author concerns her own theory’s

falsifiability, which I take to be a clear characteristic of scientific theories in general:

“If the transformation [of gender identity, M.B.] really is a dynamic system, then we might expect this period to be chaotic and unstable relative to the stability of well-formed dyadic synchrony that precedes, and the relative rigidity of gender identity evidenced by, children by the time they are 4-5 years of age […]”

(Fausto-Sterling 2012b, 416)

This statement clearly implies that, by modus tollens, gender formation is maybe no dynamic

system (meaning that her theory has a problem), if gender (conceived as a system) of 4-5 year

old children is found to be stable.

Another indication that Fausto-Sterling’s theory is really a scientific theory in the ordinary

sense entailing empirically testable consequences represents the following citation:

“[W]e expect that similar studies [of infants’ gender development providing a time line of sex-related-events from birth to age three] conducted in other cultures will reveal variability of great interest to the topic of sex-related differentiation.”

(Fausto-Sterling et al. 2011b, 1694)

The general claim here is that sex-related events, which constitute gender formation, and their

distribution are likely to be different in different cultures. More precisely, the authors predict

that culturally relevant differences will be found in the “variation in the percentage of hours

each day that fathers spend holding their children” (ibid.) as well as regarding “social

happenstance (matrilocality vs. patrilocality, and availability of post-menopausal female

relatives)” (ibid.). Thus, this non-universality of gender of being “tailored to the specific culture

100 Regarding sex/gender differences and health issues regard also Fausto-Sterling et al. (2011a,b) and Fausto-Sterling (2012a).


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in which a child develops” (Fausto-Sterling 2012b, 399) is empirically testable. But—and this

is quite intriguing—not only difference but also similarity in gender formation is empirically

testable, because it’s manifested in sex-related events that different cultures have in common.

This stands in obvious contrast with the fact that (nearly) universal features have traditionally

been thought to indicate a universal in terms of a biological basis (cf. Halpern 2011, 48; Pinker

2004, 6; Ridley 2002, 52 ff.).

In addition, and again implying the DyST’s status of scientific theory, Fausto-Sterling (2015c)

says in her abstract that her paper’s “goal is primarily theoretical—to reframe existing

analyses with an eye toward designing and executing more predictive analyses in the future”

(ibid., 5, my italics). In the same text, but on a different matter she argues that

“even if it were possible to study the many influences on human fetal growth and development, prenatal hormones would most likely be decentered and we would still need to use a dynamic, non-linear framework to examine the development of these standard birth measurements [of weight, head circumference, and Apgar scores, which showed in this study three cluster, to of which were dominated by girls and boys, respectively, and the third of which was mixed; M.B.]”

(ibid., 13)

Reading this, we should keep in mind Fausto-Sterling’s work on rat sexuality concerned in 2.3,

where the theory that hormones explain rats’ sexual behaviour was argued to be too

simplifying. Rather, Fausto-Sterling implied that the ‘world’ to be modelled by data gathered

from experiments just calls for a much more refined, qualified, and especially less simplifying

picture. Thus, the hormone-theory of sexuality is implied to be false, and DyST just is a better

model of rat sexuality, because it can explain rat sexuality also in other than only standard

laboratory environment (where the effects posited by the hormone theory had disappeared).

If there was another argument in favour of DyST’s status of a scientific theory needed, then

you should take into account the following citation from Fausto-Sterling et al. (2015): They

argue that their

“findings that mothers in our sample engaged in significantly more instrumental and stimulatory touch with sons than with daughters suggests two testable hypotheses: First, the increasing sex differences in activity levels after 4 months […] might result from earlier gender-differentiated dyadic patterns of caregiver-infant interaction. Second, if there are, indeed, sex-related patterns of coregulation and unilateral behaviors, these might relate to emerging patterns of object play, specifically more sedate versus more motorically active patterns so often noted in toddlers. Using a more focused longitudinal design that follows development from birth to 2 or 3 years of age, it should be possible to empirically test these ideas”.

(ibid., 11)

Overcoming nature/nurture and sex/gender

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Here we have two very concrete predictions: The first says that sex/gender differences in

motor activity (i.e. boys are motorically more active) at month four are due to caregivers

different treatments of boys vs. girls from birth on. And the second prediction claims that

higher motor activity is correlated with certain play styles, especially, toddlers’ rough and

tumble play, a correlation, which is also hypothesized in Fausto-Sterling (2015c), as we noted

above. Both predictions can be tested and fail if the hypothesized correlations cannot be

found.

In conclusion, we can state that Fausto-Sterling’s application of DyST has both consequences

on the framework level and empirical consequences on the theory level. That is, interpreting

gender as a dynamic system both has empirically testable consequences on one hand. But on

the other, and as discussed in the former section, it also contains specific terminologies, which

entail its logical non-equivalence with the nature/nurture framework.

3.2.4 Overcoming nature/nurture and sex/gender

After having introduced non-systematically and systematically Fausto-Sterling’s DyST and

after having explicitly established that Fausto-Sterling’s DyST has the theoretical status both

of a scientific theory and of a scientific framework, the crucial question now is, of course, if

(and, if yes, how) Fausto-Sterling’s argument, which concludes that DyST can replace the

nature/nurture framework and by implication sex/gender, works in the first place.

This section presents therefore what I take to be Fausto-Sterling’s argument against

nature/nurture. More directly, the immediate background for the premises is discussed in the

first three sections. The fourth then concisely formulates the argument. It points out its

potential weaknesses and concerns how it’s justified in relation to Fausto-Sterling’s work.

Finally, the fifth section proposes ad hoc reproaches, which I can think of, and their rebuttals.

3.2.4.1 Fausto-Sterling’s notion of ‘sex’

An important presupposition in order to understand how Fausto-Sterling wants to overcome

nature/nurture and sex/gender concerns is to know her concept of sex, which is discussed in

this section via a brief detour concerning its development.

In her well-known text “The Five Sexes” (1993), Fausto-Sterling conceptualized sex as an

“infinitely malleable continuum” (ibid., 2) between male and female. The later Fausto-Sterling

(cf., for instance, ibid. 2000a) discarded this concept of sex as a continuum (ibid., 21).


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According to Fausto-Sterling (2016), one reason for this discard lies in the logic of the term

‘continuum’: “The term [i.e. ‘continuum’, M.B.] applies to a single trait or characteristic […]”

(ibid., 191) and not a set of traits. However, and this is Fausto-Sterling’s new suggestion

(pointed out in what immediately follows), it’s precisely as a set of traits that sex should be

conceived.

As just mentioned, Fausto-Sterling (2000a) disagrees with her older self. Instead, and in the

same text (whose title “The Five Sexes, Revisited” was precisely its program) Fausto-Sterling

proposes that sex should be rather conceptualized as

“points in a multidimensional space” (ibid., 21), such that one can distinguish “between sex at the genetic level and at the cellular level (sex-specific gene expression, X and Y chromosomes); at the hormonal level (in the fetus, during childhood and after puberty); and at the anatomical level (genitals and secondary sexual characteristics).”

(ibid., 22)

This very notion of sex as a multilevel property is the one that Fausto-Sterling defends till

today, I believe. For instance, it is picked up in her third book Fausto-Sterling (2012c, chapter

2), where sex is also said to have different layers (e.g. chromosomal, fetal, hormonal,

anatomical, …; ibid., 119). Moreover, Fausto-Sterling (2016) visibly sticks to this concept of sex

as well by concerning the different ‘organisational levels’ of sex (cf. ibid., 191/5).101

What is remarkable, however, is that Fausto-Sterling (2000a) continues the above cited

passage directly by putting the above-mentioned conceptualization of sex into relation with

gender. She adds:

“… (genitals and secondary sexual characteristics). Gender identity presumably emerges from all of those corporeal aspects via some poorly understood interaction with environment and experience.”

(ibid., 22, my italics)

This is remarkable, because, in effect, here we have a theoretical anticipation of the point that

Fausto-Sterling constantly reaffirms in her following works: That nature/nurture or,

sex/gender for that matter, can’t be separated. As a consequence, even nurture-thought

differences between men and women, e.g. (maybe) toy preferences, need to be studied with

respect to how they emerge biologically. And the mechanism, which links biology and mental

101 Note the parallel of Fausto-Sterling’s conceptualizations of sex with her conceptualizations of gender. As gender, also sex was at first proposed as a continuum such that it can be linearly modelled, before Fausto-Sterling argued sex to be points on a multiple space such that it can be orthogonally modelled. Both have the consequence in common that persons can be highly female and highly male as well as highly masculine and highly feminine, respectively, at the same time, which is not possible on a linear model of sex or gender.


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properties, of course, was exactly what we discussed above: (Un-)conscious gendered

treatment of boys and girls, respectively, which interacts with the boys and girls individual

differences and augments and/or canalizes them to group differences by means of their being

embodied by the experiencing children.102

3.2.4.2 Dimorphic and non-dimorphic traits

In addition to and at the background of this technical, multidimensional concept of sex, it’s

crucial to present how Fausto-Sterling details the logic of this concept or, more precisely, the

logic of its single dimensions (e.g. chromosomal, fetal, hormonal, etc.).

That is, she argues that these single dimensions (or: traits) can be dimorphic (i.e. discrete,

binary) or non-dimorphic (i.e. continuous; cf. also Fausto-Sterling et al. 2000; Daphna and

Fausto-Sterling 2016). For a trait to be dimorphic means that there are “large differences that

have little overlap” (ibid. 2012c, 34) with regard to all existing men and women. More

precisely, she argues that “anatomically and physiologically, humans are almost dimorphic

with regard to [external and internal, M.B.] genitalia and chromosomes” (ibid., 190; cf. also

Daphna and Fausto-Sterling 2016, 1). In other words, genitalia and chromosomes are really

(almost) universal differences between men and women.103

In contrast, the other dimensions that make up the multilevel sex are non-dimorphic (i.e.

continuous): That is, hormones, breast size, voice timbre, facial hair, and even height, for

instance (ibid. 2016). This means that there is substantial overlap, if the trait is examined with

respect to the total population of (genital and/or chromosomal and/or demographic)104

females is compared with the total population of the respective males. This overlap or non-

102 Finally, note that on a linguistic level, this non-separation of sex and gender is manifested, when Fausto-Sterling (2005) and ibid. et al. (2015), without adopting this usage definitively, however, refer only to ‘sex/gender’ with regard to what makes women out of the ones and men out of the others. 103 Fausto-Sterling (2016) emphasizes that “the language of sex, gender, continuum, and dimorphism is imperfect” (ibid., 192), for instance, due to the fact that there are no absolute dimorphisms, but rather “’good enough’ dimorphism[s]” (ibid., 1993). 104 Why this disjunction? See next section.


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universality is closely associated, for instance, to temporal (e.g. hormones)105 or local (e.g.

height)106 relativity.

Thus, we are presented with the differentiation of quasi non-overlapping and significantly

overlapping differences between men and women and I want to emphasize that this

distinction is really significant for Fausto-Sterling (and her argument). This is quite explicitly

indicated, besides already by the fact that it permeates various of Fausto-Sterling’s works as

we saw above, for instance, in Fausto-Sterling et al. (2011b):

“Most sex differences present a conundrum. On the one hand, we make verifiable claims about statistically significant group differences. On the other, the differences are usually small enough that we are reluctant to apply policies or specify health care based on the group to any particular individual. Women and men may, on average, have different symptoms for heart attacks. But we would not want to ignore a ‘male typical’ symptom because a woman is exhibiting it.”

(ibid., 1698)

That is, the size of difference, and therefore the dichotomy ‘dimorphic vs. non-dimorphic’

really matters. If another proof is needed, then you should note that Fausto-Sterling in what

follows defines ‘sex-related’ differences in terms of differences, which correlate with genital

(or demographic) sex and, therefore, with a (quasi) dimorphic trait.

3.2.4.3 Non-dimorphic differences and DyST

In fact, what was discussed in the two section before seems to be all that is needed to

understand Fausto-Sterling’s argument to overcome nature/nurture and sex/gender. I suggest

thus that Fausto-Sterling’s crucial move in overcoming nature/nurture and sex/gender is to

aspire an explanation of any non-dimorphic, nature- or nurture-thought trait differing

between men and women (e.g. in hormones, bones, and more ordinarily in mental

differences) in terms of its emergence over time and due to differently socio-culturally

structured experiences in the sense of DyST.

This is also, why Fausto-Sterling (and colleagues) concern(s) ‘sex-related’ differences (cf. also

Fausto-Sterling 2016, 203), where ‘sex-related’ is taken “to designate behaviors or

105 Fausto-Sterling (2016) argues that restriction of ‘sex’ to a discussion of what is involved in reproduction doesn’t work, “if you move beyond eggs and sperm to, say, consider reproductive hormones, since hormone levels are themselves influenced by environment—day length, temperature, behaviors of various sorts” (ibid., 192). Hence, reproductive hormones also potential sex-related differences. 106 Again, Fausto-Sterling (2016) argues that “features, which exhibit mean group differences between populations of similar geographical background, are clearly not dimorphic. For example, you have to compare Dutch men and women for height and Italian men and women for height, but not Dutch women to Italian men. They are sex-related averages for traits that are continuous in distribution” (ibid. 191).


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preferences that are often (but not always) linked to genital or demographic characteristics”

(ibid., 1). Similarly, Fausto-Sterling et al. (2011b) refer to

“group differences found in very young children as ‘sex-related’. These differences overlap greatly between boys and girls, are variable within each group, and are not clearly a primary of secondary sex characteristic. Statistically, they correlate with natal genital sex and some believe that their early appearance means that they have a clear biological origin.”

(ibid., 1693)

It should be noted, firstly, that we learn from both citations that sex-related differences just

are defined as differences between men and women, which are non-dimorphic. But, secondly,

it’s important to briefly comment on the notion ‘genital sex’, which equally figures, in order

to prevent misunderstandings. The term ‘genital sex’ has here merely the function of picking

out two sets of people. And this precisely against the background that genital sex (just like

demographic sex or chromosomal sex) is a (quasi) dimorphic trait. In other words, genital sex

is not to be confused with Fausto-Sterling’s multileveled notion of sex discussed above. It’s

rather a merely pragmatic tool presupposed by her essentially empirical approach.107

Coming back to the notion ‘sex-related’, it imports also to note that all non-dimorphic

differences between men and women (operationalized as any nature- or nurture-thought,

non-dimorphic difference correlating with genital sex) are a priori potential subjects for

reformulation in terms of Fausto-Sterling’s DyST: Fausto-Sterling (2016) consequently implies

a broad range of non-dimorphic differences, which—by consequence—should be re-

formulable in terms of her DyST, namely, “a huge variety—ranging from the physiological to

the psychological” (ibid., 193).

While we already know that, on a factual level, this reformulation corresponds to explaining

these differences as emerged over time and as caused by differentially gendered experiences,

something else requires emphasis: The fact that all non-dimorphic facts are candidates for

reformulation in terms of DyST means that, on one hand, and quite naturally, the

reformulation concerns (non-dimorphic) differences between men and women, which have

107 Speculating a bit, I’m tempted to argue that the task of ‘genital sex’ to fix the reference is even more obvious, because it’s accompanied by ‘demographic sex’ in the first citation, which is, firstly, a social category (if yet based on biological features) and, secondly, a trait which is dimorphic. In other words, I take Fausto-Sterling to imply that the study of two populations as picked out referring to genital sex is in a way socially contingent (e.g. with respect to the other dimorphic features). In the same way, I would treat Baron Cohen (2005) to merely fix the reference stating that “[y]our sex is either male or female, and in biology your sex is defined by whether you have 2 X chromosomes or an X and Y chromosomes” (ibid.). He says it (even though I don’t know if he means it): This is merely a definition.


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been traditionally thought to be acquired (due to ‘nurture’). But on the other, it concerns also

(non-dimorphic) differences between men and women, which have been traditionally

classified as innate or biological (due to ‘nature’), like differences in brains, hormones, bones.

3.2.4.4 The essential argument and its justification

From what was discussed, we can now extract Fausto-Sterling’s argument, according to which

nature/nurture as well as sex/gender are successfully overcome and contrasted with the

positive claim that “sex and gender are two sides of the same coin. As such they constitute

one another in a manner that makes them inextricable” (Fausto-Sterling 2016, 200).108 This

section states the argument explicitly and then defends its conclusiveness by defending its

premises.

But before we concern the argument concluding that nature/nurture and sex/gender are

overcome, note that there are two more ways to clearly recognize its conclusion, which,

however, tend to underrepresent the underlying complexity of the argument, which is actually

at work: Firstly, one might remark that the distinction ‘dimorphic vs. non-dimorphic’ totally

cuts across ‘sex vs. gender’ (being based on ‘nature vs. nurture’) and that Fausto-Sterling

literally replaces the latter in favour of the former. Secondly, and yet differently put,

nature/nurture and sex/gender might be said to be overcome by systematically proving the

local or temporal relativity of universal-thought and/or innate-thought sex/gender differences

and providing a DyST explication for their emergence.

Having said this, take a look at the argument, which I claim to overcome nature/nurture and

sex/gender and which I attribute to Fausto-Sterling:

1st premise There are dimorphic and non-dimorphic differences between men and women.

2nd premise Many nature- (or innate-thought) traits as well as gender-thought traits, which differ between men and women, are non-dimorphic and correlate with dimorphic sex differences (e.g. in terms of genitals).

3rd premise All non-dimorphic traits (from bones over hormones to cognitive abilities), which differ between men and women, can be fruitfully explained via application of DyST and its notions of embodiment/experience and emergence/iteration.

Conclusion Nature/nurture and sex/gender are rendered useless and are therefore overcome.

108 Or: “I don’t think we can define the concept of sex itself independently of gender because they are mutually constitutive. This does not take away from the importance of studying the body and sex/gender using the tools of biology” (Fausto-Stelring 2016, 200).


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Now the weak point of the argument is obviously premise 3. In contrast, premise 1 fails only,

if the distinction ‘dimorphic/non-dimorphic’ is rejected, which I find not quite probable,

because it seems rather sensibly referring to ‘biological facts’, which are probably accepted by

researchers (including particularly those defending nature/nurture), which have at least some

notion for the value of empirical sciences. Thus, premise 2 is very likely to be true, because, if

premise 1 is accepted, then premise 2 protocols just the empirical consequences of premise

1.

I therefore focus on premise 3 and its qualification. Premise 3 is supported, when Fausto-

Sterling’s DyST is successful in terms of its applications. Obviously, there is no absolute answer

to this and, in addition, the necessary presupposition for finding (successful) applications of

Fausto-Sterling’s DyST in the first place is having accepted its fundamental claims about

complexity, embodiment, and emergence. But as soon as these fundamental assumptions are

accepted, then we can of course concern whether Fausto-Sterling’s DyST is plausible and

predictively fruitful and thus being successfully applied, while bearing in mind that the

application of DyST is still work in progress.

However, some support can be drawn from Fausto-Sterling’s empirical(ly based) work that is

already done. In my view, for instance, that DyST is successfully applied in Fausto-Sterling

(2005) and ibid. et al. (2015).

Remember that (as was argued in the third case study above) in Fausto-Sterling (2005), the

author claimed that bone differences in men and women, which are “an area often accepted

as an irrefutable sex difference” (ibid., 1498) can be explicated by means of socio-culturally

differing experiences (in its DyST-sense) of men and women.

Similarly, Fausto-Sterling et al. (2015) performed a longitudinal study of differences in motor

activity (amongst others) in boys and girls from 3 to 12 months. While early appearance of

differences is often assumed to imply its biological causation or innateness (ibid., 10)109,

Fausto-Sterling et al. studied the infant-caregiver relation finding that “[m]others of boys

spent more time offering affectionate touch to their sons (not significant [i.e. statistically,

M.B.), but that mothers of daughters used more caretaking touch on their daughters

109 “[B]ecause there are few good theories of social causation for young infants, researchers often assume that sex-related differences found in early infancy (0- months) reflect a biological causation” (Fausto-Sterling et al. 2015, 10).


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(significant)” (ibid., 11). The authors imply that these difference in treatment might explain

the innate-thought differences in motor activity between boys and girls (ibid. 10/1) in addition

to objective individual differences (cf. Fausto-Sterling 2015c, 7).

There are also promising results with regard to explaining the emergence of different toy

preferences in boys and girls around year 2 and 3 (cf. e.g. Fausto-Sterling 2012a,b,c; Fausto-

Sterling et al. 2011a, 1685/6). As mentioned in the second case study of applied DyST above,

Fausto-Sterling (and colleagues) argue(s) that toy preferences emerge due to a combination

of influences due to playing style in the context of the caregiver-infant dyad and toy

availability.

Finally, Fausto-Sterling’s DyST is rendered plausible by the empirically localizable temporal or

local relativity of differences between genitally females and genitally males. For instance,

Fausto-Sterling (2015c, 13) and ibid. (2016, 192) argue that ‘male’ and ‘female’ hormones are

temporally relative. Fausto-Sterling (2017) even states that “[i]n fact, there is nothing in the

body that can be said to be permanent and unchanging” (ibid., 63) implying that quasi any

non-dimorphic difference can be reformulated in DyST-terms.

3.2.4.5 Ad hoc reproaches and their rebuttals

Let me provide a few ad hoc reproaches that I can think of and which I take to be rebuttable.

To begin with, one might reproach that Fausto-Sterling’s argument simply turns out to make

the claim that it’s all nurture after all. In my view, this is implied by Steven Pinker’s reading of

Fausto-Sterling and when he complains about her ‘radical feminist’ position that “all sex

differences, other than the anatomical ones, come from the expectations of parents,

playmates, and society” (Pinker 2002, 246, his italics). And: “The key biological fact is that boys

and girls have different genitalia, and it is this biological difference that leads adults to interact

differently with different babies whom we conveniently color-code in pink or blue to make it

unnecessary to go peering into their diapers for information about gender” (Fausto-Sterling

1992, 152/3 as cited in Pinker 2002, 345/6). So Pinker might conclude: Fausto-Sterling holds

that the mind is a blank slate, or, in other words: it’s all nurture after all.

But this reproach would be misguided, because it doesn’t take into account the conceptual

changes, which are implied by an adoption of DyST. As was emphasized above, ‘nurture’ and

its correlative ‘environment’ don’t figure as concepts anymore and turn out unthinkable. The

closest, we can get is by relying on the notion of experience. However, and as we learned


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above, this notion is fundamentally different from ‘nurture’ or ‘environment’, since it closely

associates the notion of embodiment, which is not formulable in terms of nature/nurture.

Hence, Fausto-Sterling’s argument not reducible to ‘it’s all nurture’.110

Next, and in close context to the former reproach, whose rebuttal emphasized Fausto-

Sterling’s framework character, one might follow up doubting that it would be possible for

Fausto-Sterling to disprove that traits are innate, where ‘innate’ implies nature as a

nature/nurture concept, given that Fausto-Sterling changes the framework. In other words,

can Fausto-Sterling’s argument refute innateness, a notion, based on nature/nurture and

which by this very fact has logically no connection to the argument, whose logic is based on

DyST?

My answer is, firstly, that nature/nurture and DyST might conceptually and on the framework-

level be different, but without having to be fully incommensurable. More precisely, I think that

‘innateness’ is a limiting case of DyST and is close to what is called ‘dimorphic traits’ in Fausto-

Sterling’s DyST. However, and strictly speaking, ‘innateness’, even if its formulable in DyST, is

a threatened notion: Even dimorphic differences have to temporally develop and require

certain environments. And it’s this emphasis of the interactive entity-environment/experience

coupling that is responsible for a refined and qualified conception of ‘innateness’.

Moreover, and independent of a conceptual level, it’s important to keep in mind that DyST

and nature/nurture (as represented by Pinker and Ridley, for instance) share their empirical

orientation including its main strategy of data mining for correlations and thus also the

associated scientific standards. In addition, remember also that DyST is situated as well on the

level of a scientific theory and might just be particularly successful. In effect, I claim that

Fausto-Sterling just is a ‘better’ empiricist (in comparison Pinker and Ridley), because she

gathers more data (in addition to the existing an data which are also taken in account), to find

for more correlations (by exploiting the time before traits are established), and all this in order

to have a more substantial empirical basis for DyST and to test its predictions (which will

hopefully not be contradicted by the data).

110 The same refutation works for a reproach, which points to the ‘inconsistency’ that Fausto-Sterling defines a notion of sex (cf. 3.2.4.1) in order to overcome nature/nurture and by implication ‘sex’. This is not inconsistent, because Fausto-Sterling’s notion of sex has nothing to do with the just mentioned framework and its logic.


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And actually, Fausto-Sterling herself makes a similar argument appealing to the ‘empirical

mindedness’ of her empirist colleagues in Psychology etc.: She criticizes the research on

sex/gender differences or gender development precisely on the grounds that data lack (cf.

also Fausto-Sterling 2012c, 13-26; Fausto-Sterling et al. 2011a). For instance, Fausto-Sterling

et al. (2015) argues that “analyses of gender and socialization, perhaps reflecting the available

literature, neglect potentially important processes occurring during the first year of life” (ibid.,

7). In addition, and with respect to one review of sex/gender differences, she criticises the

study’s adoption of “a lumped age category of 0-5 years, so that critical information on

infancy—if it existed—could not be teased out of their data” (ibid.).

A final ad hoc reproach, which I can think of, might allude to the fact that Fausto-Sterling, who

has not perfectly strictly adopted a fixed set of technical terms, continues to apply ‘sex’ as well

as ‘gender’, whose classic usage is definitely inconsistent with Fausto-Sterling’s notion of

inseparable sex/gender. This is true, but it’s necessary to emphasize that these two notions,

which Fausto-Sterling’s purports to refer traditionally, are again embedded in the totally

different concept of DyST such that therefore their logic (i.e. the set propositions they imply)

has radically changed.

3.2.4.6 Conclusion

Let me wrap up what was said above and what has most importantly been argued. Recall that

this section intended to discuss if (and if yes how) Anne Fausto-Sterling’s application of DyST

entails substitution of nature/nurture (and sex/gender) on the framework-level.

At first, I prepared Fausto-Sterling’s argument provided by discussing Fausto-Sterling’s notion

of sex, which she operationalizes as a set of dimorphic and non-dimorphic traits of men and

women such that ‘dimorphic’ refers to traits (like genitals and chromosomes), for which there

is practically no overlap between men and women, and such that ‘non-dimorphic’ refers to

traits, for which there is a good deal of overlap in contrast (i.e. quasi anything else).

I continued to argue that the most important aspect of the dichotomy ‘dimorphic vs. non-

dimorphic’ is that it totally cuts across the dichotomy ‘nature vs. nurture’, since many non-

dimorphic traits are (in addition to classic gender-traits) traditionally innate- or biological-

thought traits. This fact becomes significant in the context of Fausto-Sterling implying that any

non-dimorphic trait can reformulated in terms of DyST (including innate- or biological-thought

non-dimorphic traits). In contrast, I argued that dimorphic traits just serve to fix the reference,

A critical perspective: Kempthorne again

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without which there would be no population to study in the first place. Thus, and even, if one

might argue that dimorphic might just be the new ‘nature’, then this is not adequate because

‘dimorphic’ is a concept, which is much less thick than ‘nature’ used to be.

Thus, I concluded next that given DyST is successfully applied to non-dimorphic traits, then

nature/nurture and sex/gender are overcome. Remember my indication that this overcoming

can be also comprehended in terms of the dichotomy dimorphic/non-dimorphic substituting

sex/gender (or nature/nurture) and, in addition, that the exposure of a trait as temporally or

locally relative is an argument in favour of its being non-dimorphic and a potential subject for

reformulation in terms of Fausto-Sterling’s DyST. However, and this is important, this does

underrepresent the complexity of the actually underlying argument, whose understanding

just requires the understanding of DyST and its specific concepts (e.g. emergence, iteration,

embodiment, experience).

With reference to Fausto-Sterling’s argument, I pointed out that its depends especially on

whether or not DyST can in fact be successfully applied to non-dimorphic traits. While I argued

that Fausto-Sterling’s own work concerning differences between (genital) males and (genital)

females regarding bones, infant motor activity, and toy preferences suggests a successful

application of DyST, I granted also that further research via DyST is needed.

I closed the section by anticipating and refuting a number of ad hoc reproaches. Most of them

could be rebutted by reminding that Fausto-Sterling’s DyST is situated on the level of a

framework and of a scientific theory, respectively, and by underlining that her approach can

be conceived as a superior empiricism in comparison to the nature/nurture empiricists.

3.2.5 A critical perspective: Kempthorne again

In addition to my own ad hoc reproaches just discussed, this section intends to provide a

critical perspective from a third party on Fausto-Sterling’s DyST. Prior to this, I found in fact

no direct criticism of Fausto-Sterling, which is both substantive and which considers Fausto-

Sterling’s DyST, which is so important for and characteristic of her approach though. So, I

chose to focus on the critique that is implicated by Oscar Kempthorne and his theory of

causation, which we already encountered in Part One. I chose him not because there is any

direct, critical relation to DyST. Rather, I picked Kempthorne, for reasons of continuity with


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Part One, but especially because I think his thoughts are really interesting and disserve to be

concerned again and also a bit more detailed.111

In order to better understand the critique of Fausto-Sterling’s DyST, which is implied by

Kempthorne’s views, it will be helpful to say a little bit more about Kempthorne’s theory of

causation. As Kempthorne notes repeatedly (cf. e.g. ibid. 1979), these are (partially) often

somewhat basic issues, which are nonetheless not sufficiently considered often times. But in

my view, the basic character of these issues neither renders them less interesting nor less

difficile (at least for me).

Preliminarily, note that Kempthorne draws a line between three designs of empirical studies

implying different sorts of data-analytic inferences (cf. e.g. Kempthorne 1977, 3-6; ibid. 1979,

1992)112: Firstly, the survey-design and its sampling inference, secondly, the design of

observational studies and their observational inference, and, thirdly, the design of

comparative experiments and their experimental inference. I’m interested here only in what

Kempthorne says about experiments in contrast to observational studies, which will be

discussed in the first and in the second section, respectively, because these are most relevant

for this text at hand.113 Finally, the last section construes the relevant criticism implied by

Kempthorne’s view and how a defence from Fausto-Sterling’s perspective might look like.

3.2.5.1 Comparative experiments

To begin with, I concern the comparative experiment and the experimental inference at first

(cf. e.g. Kempthorne 1992, 14 ff.). Kempthorne explains that “[t]he experiment consists then

of a definition of a set of units and a set of treatments and the assignment of a particular

treatment to each of the units that will be used in the experiment” (ibid., 5). Its purpose is “to

determine the effects of treatment factors” (ibid. 1979, 129).

111 In other words, I preferred Kempthorne also over critiques, which directly or indirectly concern DyST.

Accordingly, I don’t review the critique against DeST, which is a priori also relevant for DyST and which was evoked in Part One through Schaffner (2016) and Kitcher (2003). Moreover, I ignore Helen Longino’s direct critique of DyST (cf. Longino 2013, 93 ff.; 111 ff.). Finally, I leave out the Andy Clark’s and Steven Shapiro’s indirect critique of DyST, which is ‘indirect’, because they criticizes the theory of embodied cognition (cf. Clark 1997, 1999; Shapiro 2007), which as we have learned is also adopted by Fausto-Sterling. 112 For concise characterizations of the three types, see Kempthorne (1979, 125) or ibid. (1977, 3 f.) or ibid. (1992, 13/4). 113 For a good introduction to observational studies cf. also Rosenbaum (2005) and for a less good one to clinical trials cf. Lesaffre and Verbeke (2005).


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The ideal and impossible case of an experiment would feature experimental units114 such that

the experiment would then “conjoin every treatment with every unit” (ibid. 1979, 125).

Clearly, if it were possible to do this, then one could infer the general treatment effect

(because one knew the treatment- and non-treatment effects for every single unit). In

contrast, an ideal and possible experiment would feature experimental units, which are strictly

identical (like it can happen in physical or chemical science, where such units can be

manufactured (cf. ibid. 1977, 6). Here an experiment can be conducted such that it’s just as if

one has tested the same unit with and without treatment, because the pairs of units are

identical (cf. ibid., 6).

However, for disciplines other than chemical sciences and physics, there is no availability of

such identical experimental units. Rather, in social sciences, for instance, the experimental

units (i.e. human beings) under study are ‘severely’ non-identical. They “occur naturally” (ibid.

1977, 5) as different and this creates the fundamental problem that “whatever mean

difference [between treatment and control group, M.B.] we observed can be equally well

attributed to difference of effects of treatment […] or the difference between the 2 sets of

units” (ibid. 1992, 20). The only way to handle this problem is according to Kempthorne by

randomly drawing samples to be tested from their respective population (cf. ibid. 1977, 1979,

1992).115 In my view, this makes sense because it minimizes the probability (and given that

not the whole population has a confounding trait) that a sample has been drawn whose

member happen to have another trait which is ‘confounding’ with the trait measured, because

both traits happen to be coextensive for just this particular sample.

114 An experimental unit is whatever is to be studied and thus depends of the disciplinary context. Kempthorne (1977) writes that “[i]t is difficult to give any general definition that will carry force to the whole spectrum of experimentation. All one can do, I think, is to attempt to convey the idea by examples and by pointing. In the case of human experimentation, the unit may be a single human being or it may be a time segment of a human being or a cluster of human beings such as household, a city, or a nation. In the case of a simple experiment to look at the gas law a unit is a short time interval or a particular piece of apparatus with its contents. In the case of a chemical rector, the unit may be a time interval of the reactor and its contents. In a genetical experiment with animals or plants, a unit may be an off-spring of a particular genetic cross. In agronomic experimentation, the unit may be a plot of land. And so on.” (ibid., 5) 115 For instance: „In a comparative experiment, because we can conjoin only one treatment to any one experimental unit, we can never determine the exact truth, and we surely have confounding of treatment effect and experimental unit effect. However, if we have a large experiment and have used randomization in conjoining treatments and units, we shall come close to the truth that would be achieved if we could conjoin every treatment with every unit. We shall obtain a causal conclusion of the type that imposing such and such a treatment on the set of units gives a certain response.” (Kempthorne 1979, 1259, my italics)


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But the randomness of a sample drawn, which is experimentally studied, just is what the

standard theory of statistical analysis presupposes by default and this presupposition just is

what Kempthorne (1979) criticizes:

“A specification of a population of possible experimental units can be made; for example, all infants of one year of age of the United States in 1975 who have symptoms of diabetes. But to use the notion of random sampling is quite impossible. We would have to make a complete enumeration of these individuals, and then we could draw a random sample. But then it would be practically impossible to conduct the experiment. In fact, we have to use a set of experimental units that are available and the hypothesis that the set of available units is a random sample from the population is ridiculous.”

(ibid. 1977, 16)

In other words, random sampling is just not possible in the social sciences (cf. also ibid. 1979,

123/136).116 Hence, no distinguishability, whether an effect due to the treatment or not. A

further complicating theoretical (without even mentioning practical and ethical) aspect(s) is

that randomization goes with the assumption of additivity, which—as I argued above—is

arguably invalid in the case of social science (cf. ibid. 1977, 7/17 ff.; ibid. 1979, 130 ff.).

In conclusion, however, it’s important to note that for Kempthorne all this still does not imply

that comparative experiments are impossible for to conduct in the social sciences. Even if it’s

true that their causal claims are less justified, he still prefers them over observational studies

(as we also heard already above; cf. Kempthorne and Dupont 1978, Kempthorne 1978). In

addition, Kempthorne proposes in fact a ‘fix’ called ‘finite random sampling’ for the design of

causal studies in social sciences, I believe (cf. ibid. 1977, 12 ff.; ibid. 1979, 126 ff. and 129 ff.),

even if I neither can nor want to go into this here.117 What matters for me is rather

Kempthorne’s claim generally valid claim “that causation can be inferred only by the

comparative experiment” (ibid. 1977, 4, his italics), even if we’re aware that there are

qualifications.118

116 Kempthorne (1979) says that it’s “[a] harsh, bare and elemental fact […] that without the use of randomizers in the collection of the data, or without the use of the assumption that Nature has randomized for us, the notion that we have a random sample is untenable. A second and related unpleasant fact is that we do not know the population from which we have the supposed sample.” (ibid., 140) 117 It’s not important to detail how this work. The important thing is that experiments in social sciences are possible. 118 And: “So I maintain that experimental inference is sui generis and cannot be incorporated in what is commonly discussed in texts on mathematical statistics and in Bayesian statistics under the name ‘inference’” (ibid., 138).


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3.2.5.2 Observation studies

As mentioned above, Kempthorne contrasts comparative experiments (besides surveys) with

observational studies. For instance, Kempthorne (1992) neatly defines what is the underlying

problem of observation studies:

“In the observation problem, we observe a whole population, but we hope and wish that this population that we observe is representative of a much larger population. […] So, then, in the observation problem, we must have a model that represents what we hypothesize about the unobserved world, unobserved because it is in the past or in the future, or at present and not looked at.”

(ibid., 14)119

Note that this really is different from what the comparative experiment consists. In the case

of an observational study “data that have been obtained not by a defined process of random

sampling form a finite population or by a defined process of experiment randomization” (ibid.

1979, 140, his italics).

In addition, there is no experimental treatment involved in observational studies. Comparing

observational study and experiment, Kempthorne (1977) makes this very clear:

“Is there a difference, for instance, in logical nature between the two-way classification and a randomized block experiment? It seems obvious that there is a huge difference. In the one case, one has a set of data that consists of triples {y(u), x1(u), x2(u)} in which, for a set of observational units indexed by u, the stance is taken that y(u) is a variable to be explained by two classificatory variables x1(u), x2(u) representing row and column classes. There can be in this case no unambiguous answer to the question of what variables ‘cause’ what other variables. One could turn things around and take the stance that x1(u), x2(u) are variables to be explained by the variable y(u). […] In any experiment, in contrast, the explanatory forces are chosen by the investigator and data are generated by applying levels of these explanatory forces to experimental units according to some experimental design.”

(ibid., 4)

In other words, this just says that a observational study can only obtain correlation but not

causal relation (cf. ibid. 1977, 4).

And granted again that this is a very basic point. But Kempthorne still complained that these

differences in study design (and their implications) were too often just forgotten in the context

of applied statistics (cf. Kempthorne 1979, 118 ff.). And 40 years later, I don’t know, if things

have radically changed, even if researchers of course mention the problem of causality (cf. e.g.

119 Kempthorne (1977) writes that the purpose of an observation study is “that one has ideas that a particular observation protocol will lead to data that can suggest a structure for a part of the real world” (ibid., 3‚). Protocol‘ is something with respect to which there is a subject-selection and which is done also, for instance, in clinical trials (e.g. for testing a drug): “The potential subjects for the experiment will be examined carefully with respect to a large number of attributes” (ibid. 1977, 9). In other words, we have something like a ‘controlled environment’ (cf. ibid., 5).


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Halpern 2011, 44 ff.). Thus, but without being able to prove its wide justification, as I’m happy

to concede, I adopt a sceptical attitude assuming that also today social sciences standardly

perform rather observational than experimental studies without paying sufficient attention to

the methodological implications until convinced of the contrary.120

Returning to the argument and being slightly repetitive, the characterizing feature of

observational inference is therefore to find a model, i.e. mathematical formula, which predicts

the data obtained. And this is a task identical to determining the frequency distribution from

which the data are obtained given that a randomized sample is not possible as in social science

studies (cf. ibid. 1979, .139 ff.).121

Finally, and while holding that there is no causal justification inherent to observational studies,

Kempthorne grants of course that observational studies are not irrelevant with respect to

causal claims. For instance, Kempthorne (1977) argues that it’s possible to make an “informed

judgement that certain variables represented in the data set are exogenous, i.e., determined

by extraneous forces, which then have a causal effect on the variable to be explained” (ibid.,

4). In my view, this is just what Halpern (2011) means stating that “[c]orrelational data with

nonrandom assignment can provide a stronger case for causation if the results are in accord

with a highly plausible theory and when other sorts of data provide converging evidence for

the relationship being studied” (ibid., 48).122 Still, Kempthorne remains sceptical and holds

that often observation studies might imply causal claims, which themselves, however, can and

should only be established experimentally (cf. Kempthorne and Dupont 1978, 714).

120 For instance in the case of a clinical trial (cf. Kempthorne 1977, 9 ff.). He argues that due to the non-identity of human beings as experimental units (which enters analysis as covariates) “we are in a position very much like the data analyser with purely observational, nonexperimental, data” (ibid., 9). 121 It’s illuminating to lay the finger on what differentiates observational studies from surveys is precisely the fact that in surveys randomization is possible, because the population is known, while in observational studies randomization is not possible (cf. e.g. Kempthorne 1977, 3). 122 Even if this invites the criticism applied in Fine (1990): “The usual remedy for this [i.e. the encountered underdetermination of correlations by causal interpretations in a concrete data set] prescribed by the causal theorists is to supplement the assumptions about what causal relations are sensible with even stronger assumptions about the completeness of the causal analysis. […] the difficulty is that although strong causal assumptions can indeed imply causal conclusions, one needs to investigate the soundness of the assumptions before those conclusions are detachable. Insofar as this is an empirical question it is a matter of gathering further correlational data which, once again, will be liable to various causal interpretations. Further causal assumptions will be needed to sort the new data. So as we go down the line we will need to make more causal assumptions, not less. This is not a procedure for narrowing down the class of models, but rather for expanding it. The remedy appears to be worse than the disease.” (ibid. 2010, 103)


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3.2.5.3 A Kempthornian critique of Fausto-Sterling’s DyST and a defence

The purpose of this section is to state a point of criticism against Anne Fausto-Sterling’s DyST,

which naturally flows from the Kempthornian view on causation, and then to propose a

defence.

From a Kempthornian perspective, the obvious problem with Fausto-Sterling’s account of

(infant) gender development, for instance, concerns—just like in the nature/nurture case of

IQ in Part One)—causation. This problem is manifested in my reading of Fausto-Sterling in that

she proposes essentially two different pathways, which cause (?) sex/gender differences in

children. Firstly, there are caregivers’ (un-)conscious gendered beliefs, which influence the

treatment of their children and which become visible in differently gendered caregiver-infant

dyads on one hand (cf. e.g. Fausto-Sterling et al. 2011a,b; ibid. 2015; 2012b). On the other,

there are objective individual differences between the new born children, which (independent

of caregivers’ gendered beliefs and the new born children’s sex) are said to cause (?) a

different treatment of robust and less robust children, whose effects eventually and for some

children merge into gender conform group-differences (Fausto-Sterling 2015c).

The point is that, even if I have the impression that Fausto-Sterling is really careful in her usage

of ‘cause’ and/or even rarely uses it in the first place, these two pathways almost call out for

a causal interpretation. However, the problem from a Kempthornian perspective is, of course,

that on the basis of Fausto-Sterling’s work, which is to my knowledge purely observational,

it’s not possible to prove the causal relevance of the one or the other of the just mentioned

pathways, because there is in principle no causation without experimentation.

Nor, is it strictly speaking possible to know whether differences are induced in the child from

outside or arise from the child and this is relevant, because even if DyST is applied, there will

always remain unstudied differences, because it’s impossible to include everything. In a way,

Fausto-Sterling et al. (2015) seem quite aware of this stating that

“[f]or now, though, our evidence suggests that the differences in maternal behavior are probably maternally motivated during the time period of our study. Still, the differential maternal behaviors we observed could have been conditioned by sex-related infant behavioural differences during the first 3 months after birth, a period not included in our data set.”

(ibid., 11)

In other words, there will always be starting points (i.e. initial differences) such they might in

theory be innate or not. But this invalidates not the fact that Fausto-Sterling’s approach is


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promising and superior to the views presented in Part One. This entails merely that Fausto-

Sterling needs to be careful as well with causal claims as long as she does not conduct

experiments. Still, there is of course a qualitative distinction between Fausto-Sterling’s

potentially causal claims above and claims about the causal force of Ridley’s and Pinker’s

genetic predispositions. In what follows, I defend that this surplus quality of Fausto-Sterling’s

approach is especially due to the following three methodological aspects (all of which we have

already encountered).

Firstly, Fausto-Sterling implies a methodological shift by adopting DyST entailing synchronic

(multilevel) complexity. The radicality of Fausto-Sterling’s methodological shift (alongside with

DeST and other systems approaches, of course) is clearly expressed, when we remember her

argument that, in the context of studying the emergence of differences in girls and boys,

individual differences in a sample of new born babies should not be viewed as potential

confounding factors but rather as meaningful developmental starting points (cf. Fausto-

Sterling 2015c). Generally speaking, Fausto-Sterling therefore appreciates the fact that in

social sciences, theorists do not have business with identical experimental units but with

complex, individually differing human beings (cf. e.g. Kempthorne 1977).

Secondly, and particularly, Fausto-Sterling’s DyST implies a methodological shift by focussing

on longitudinal studies of trait development implementing thus a diachronic perspective.

Granted, correlations, which are stable over time, neither imply causation: Remember the

classic example of correlation between ‘violent character’ and ‘consummation of violence in

media’ (cf. Aronson et al. 344-6). And also the elementary cautions, i.e. influence of a

measurement at tn-1 on the outcome at tn, dropping out of probands, and long duration, which

Diane Halpern expresses, are of course in principal justified (cf. Halpern 2011, 87).

Thirdly, and relevant to what I just argued, it seems that Fausto-Sterling’s methodological

assumption of the emergence of traits is important and which, it seems to me, implies the

impossibility of a creatio ex nihilo and therefore stands squarely against the old nature-

assumptions. But in the end, I concede that I don’t really have more left in terms of justification

than the naïve argument a complex study object like the human being requires appropriate

(specially in terms of non-simplifying) models.

Much hinges therefore on the complexity-claim. While, we cases for complex interaction

between nature and nurture (remember e.g. rat sexuality) were presented already before,


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there is another way of recognition: In my view, complexity is undeniable at least for human

beings, even if DyST is already claimed to be necessary due to animals’ complexity.123 The

complexity of human beings is clearly discerned relative to other animals, if the particularity

of human language (and it implicates) is concerned in contrast to other animals’

communication systems. One branch of science, where this language-based complexity shines

clearly through is psychoanalysis (cf. e.g. Lacan 1966) and, remarkably, Fausto-Sterling—even

if she’s not reading Lacan—shows awareness for the significance of psychoanalytic works by

citing them (cf. e.g. Fausto-Sterling 2000; ibid. 2012b; 2012c, 93).

Having available at the end only this concededly somewhat non-specific, naïve argument on

one hand, we have on the other alternative nature/nurture approaches, which were

concerned in this text. As we heard, these aspire to explain, why differences between men

and women exist, by relying on cross-sectional ‘snapshot’ studies, which in the best case find

cross-cultural differences (cf. Halpern 2011, 48; Pinker 2004, 6; Ridley 2002, 52 ff.), which,

however, turned out not to justify the inference of a universal biological cause: Remember

the phenomena of the human smile and heterosexuality, for instance. Alternatively, and/or in

addition, they might rely on computing heritability coefficients as we learned from the

respective discussion in Part One (cf. Polderman et al. 2018). But what these approaches have

in common is just that they jump to conclusions and unjustifiably simplify a more complex

world as well as that they are situated in a conceptual framework, which have grave inherent

problems (i.e. underdetermination).

In contrast and in conclusion, I hope to have convincingly argued that the leap to conclusions

is smaller in the case of Fausto-Sterling and that she is situated in a much more reasonable

conceptual framework. And even if I grant it follows from Kempthorne’s views that also

Fausto-Sterling cannot really make causal claims as long as there is no real experimental

testing to provide a less unstable fundament, I still defend that Fausto-Sterling is unjustified

to a lesser degree than are the competing approaches I mentioned to account for differences

between men and women and why they exist.

123I’m not saying that animals are not complex, but I want to emphasize the complexity of human beings as established warranting DyST’s application in any case, no matter how complex are animals.

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3.2.6 Conclusion

Let me summarize this section and point out the most important things. But this time rather

briefly, because the following section will provide another summary of the content of the

complete Part Two and thus will be somewhat repetitive.

Remember that the purpose of this section was to systematically and non-systematically

introduce Anne Fausto-Sterling’s DyST and to examine how it manages overcome


Amongst the most important points argued, was at first that Fausto-Sterling’s DyST has the

theoretical status both of a scientific theory and an epistemic framework, since it is empirically

fruitful on one hand and differs significantly in its conceptual underpinnings from

nature/nurture on the other hand. In favour of the latter, I pointed especially to the

connotations ‘embodiment/experience’ and ‘emergence/iteration’. Next, I provided what I

took to be Fausto-Sterling’s successful argument that nature/nurture and sex/gender can be

overcome: Namely, that there are dimorphic and non-dimorphic differences between men

and women, that all non-dimorphic ones can be successfully reformulated in terms of DyST

and that this reformulation entails that nature/nurture and sex/gender are rendered

superfluous and hence are overcome. Finally, I granted, however, that Fausto-Sterling cannot

strictly speaking provide a causal account but that there are virtues thanks to which Fausto-

Sterling’s DyST to gender development and, ultimately, the question why differences between

men and women exist, should be favoured over others.

3.3 Conclusion of Part Two

This section concludes Part Two of this thesis. Remember that the purpose of this part was to

introduce Anne Fausto-Sterling’s instantiation of Dynamic Systems Theory (DyST) as a

substitute for nature/nurture and sex/gender. In what follows, section 3.3.1 summarizes again

all the most important points made in the whole Part Two and section 3.3.2 states the main

conclusions I draw from it.

3.3.1 Summary

This Part Two was divided into two main sections 3.1 and 3.2. The first section identified DyST

(Dynamic[al] Systems Theory) as a systems approach to biology and invoked a binary typology

to distinguish it from DeST (Developmental Systems Theory), both of which are similar but

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non-identical and which are often both (and thus ambiguously) referred to as DST. More

precisely, and based on Anne Fausto-Sterling’s references, I situated Fausto-Sterling’s DyST in

the tradition of Esther Thelen’s DyST granting that Fausto-Sterling herself is not strict in

distinguishing DyST and DeST. In terms of content differences, I worked out that DeST is

usually thought of as a conceptual framework in contrast to DyST, which is usually identified

as a theory. Moreover, DyST is said to emphasize the temporal dimension of development to

a higher degree than DeST. Then, and mindful of the shared content of DyST and DeST, I

provided a selection of important background assumption of DeST, which seem to follow

largely from the central notion of a developmental system (instead of gene or organism) as

the crucial, biological unit of ontogeny and evolution. I closed by touching the critiques of

Philip Kitcher and Kenneth Schaffner, who—in spite of general sympathy for the approach—

especially doubt the claim that nature and nurture are never separable and argue in favour of

pragmatic focus on genes accepting causal parity in general.

While section 3.1 purported to disambiguate and to work out what DyST is in general, section

3.2 focussed on Fausto-Sterling’s DyST and had the purpose of providing a detailed

introduction to what it is and how it works. More precisely, in section 3.2.1, I provided a non-

systematic, bottom-up introduction of how Fausto-Sterling applied her DyST to the study of

differences between men’s and women’s bones as well as to sexual orientation and to infant

gender development. As an important characteristic of this bottom-up analysis I emphasized

that Fausto-Sterling applies DyST to classic and nature- or biological-thought differences in

bones, a characteristic, which was of course later explicitly conceptualized in terms of the

dichotomy of dimorphic/non-dimorphic difference.

In section 3.2.2, I attempted a systematic, top-down explication of Fausto-Sterling applying

DyST to gender development, in the course of which I pointed out two main mechanisms by

means of which sex/gender differences emerge in infants over time: Firstly, sex/gender

differences emerge, because girls and boys are (un-)consciously and according to gendered

stereotypes differently treated, which can be made visible in the caregiver-infant dyad. And

secondly, individual differences at birth cause differential treatment irrespective of genital sex

and the differential treatment’s effects eventually merge and conform with the gender

identity (based on genital sex). With respect to both mechanisms and to DyST in general, I

then emphasized the importance of the connotations ‘embodiment/experience’ and


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‘emergence/iteration’, which I explicated also as conceptualizing synchronic and diachronic

complexity. Moreover, I underlined that it’s thanks to such specific DyST terminology that

Fausto-Sterling’s DyST is to be conceived of as situated on the framework level (as

nature/nurture does).

The following section 3.2.3 then explicitly concerned the question of the theoretical status of

Fausto-Sterling’s DyST. While I had already argued that it’s situated on a framework level in

the former section, I established here by means of providing relevant passages as evidence

that Fausto-Sterling’s DyST can be thought as equally located on the level of an ordinary

scientific theory, because it yields empirically testable consequences and is falsifiable. The fact

that Fausto-Sterling’s DyST is situated on a framework level was a presupposition, which

directly concerned the next section concerning Fausto-Sterling’s argument realizing her

programmatic motivation of overcoming nature/nurture and sex/gender.

Consequently, the next section 3.2.4 focussed on what I took to be Fausto-Sterling’s argument

concluding that nature/nurture and sex/gender are overcome. More precisely, I presented the

argument and how it actually works by discussing and contextualizing what is presupposed in

its premises. Thus, I introduced at first Fausto-Sterling’s multilevel notion of sex in contrast to

the notion of genital sex. I claimed that the purpose of the latter just is to pick out a population

and that therefore ‘genital sex’ is a merely pragmatic notion built into the empirical approach.

Secondly, I discussed the notion of dimorphic vs. non-dimorphic traits such that, essentially,

the former (dimorphic) fulfil the just mentioned pragmatic task (because it subsumes genital

sex besides demographic or chromosomal sex) and such that non-dimorphic traits are the

primary explananda of DyST. I emphasized that it’s those non-dimorphic traits, which include

both classic nature- and nurture-thought traits and which are candidates for reformulation in

terms of DyST. Next, I underlined that Fausto-Sterling’s argument hinges on the question,

whether or not DyST can be successfully applied to classic nature/nurture topics. I argued in

response that Fausto-Sterling’s own work provides positive instances granting at the same

time that the question is still open to empirical refutation.

The following section 3.2.5 finally presented a critical perspective on Fausto-Sterling’s DyST.

More precisely, I picked up Oscar Kempthorne’s theory of causation, which was encountered

already in the critique of heritability in Part One and which I detailed a little bit more. More

precisely, I discussed Kempthorne’s methodological distinction of observational studies and


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comparative experiments and in particular what this distinction implies in terms of inferences.

Briefly put, it implies that causal inferences are only justified, if there’s an experiment

featuring an intervention and can therefore in principle not be based on the data of

observational studies. Applied to Anne Fausto-Sterling’s DyST, the critique that flows from

Kempthorne’s views states that also Fausto-Sterling cannot make causal claims, because her

studies are observational and not experimental in nature. While this critique cannot be

rebutted and is shared by Fausto-Sterling with the nature/nurture scholars discussed in Part

One, I emphasized also that Fausto-Sterling’s DyST is still preferable to nature/nurture

positions. Briefly speaking, I underlined that Fausto-Sterling is actually the ‘better empirist’ in

considering more data and that therefore her leap from data to conclusion is smaller and

better justified than the leap of nature/nurture scholars.

3.3.2 Main conclusions and final remarks

After having summarized what was argued in Part Two of this text, let me now state the three

main conclusions, which I draw from its discussion.

Firstly, Anne Fausto-Sterling’s DyST is a different but related thing than DeST. Standing in the

tradition of Esther Thelen’s approach, Fausto-Sterling’s DyST is importantly characterized

being at the same time situated on the level of a falsifiable scientific theory with empirically

testable consequences as well as on the level of scientific framework.

Secondly, Fausto-Sterling’s DyST has overcome nature/nurture and sex/gender. And this not

just by introducing the dichotomy dimorphic/non-dimorphic, which cuts across nature- and

nurture-thought traits, but also and especially by specifying DyST concepts like

embodiment/experience as well as emergence/iteration and reformulating classic nature- and

nurture-thought traits in terms of DyST.

Thirdly, even though Fausto-Sterling’s DyST has overcome nature/nurture and sex/gender and

even though she provides an objectively better empirical theory (than other approaches

mentioned in this text) of (infant) gender development (including sexual orientation,

sex/gender differences), also Fausto-Sterling’s DyST is not justified to make causal claims.

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4. Epilogue

This last section has the purpose of closing the whole text. It starts with an outro in section

4.1, which has the aim of synthesizing what was argued in Part One and in Part Two and to

conclude the topic. After that, section 4.2 takes a brief and critical look on the text itself and

its limits pointing out some implications and further research perspectives.

4.1 Outro

Let me end this text by synthesizing Part One and Part Two and provide some finalizing

comments. Before I do this, remember that this text concerned differences between men and

women and the closely associated question, why they exist, which essentially translates to the

question why the one become men and the others become women.

As we learned, one way to answer this question is to study how much of a trait is nature and

how much is nurture inside the nature/nurture framework. Remember Pinker’s and Ridley’s

reference to innate predispositions and the importance of the inference of innateness from

universality (or cross-culturality) of some trait. However, we found that this approach is

problematic, because it has problems pinning down (or at least detailing) nature factors as

well as (especially) nurture as was vividly clear in the context of (missing) heritability.

Moreover, empirical data suggest the disappearance of effects, if interpreted in terms of

nature/nurture theories and the fundamental threat of underdetermination looms.

More generally speaking, I claimed therefore that this approach is inherently dysfunctional.

As a consequence, the notion of human nature and the explication of sex/gender differences

as biological represents an unjustifiable inferential leap. It is empiricist in a vulgar way,

because it claims that factual differences between men and women wear their meaning

(namely, a probabilistic binary human nature of men and women) on their sleeves (remember

Pinker stating that ‘truth cannot be sexist’) instead of acknowledging the importance of

contingent structures.

As an alternative, I introduced another way to answer the question, why women and men

differ. Fausto-Sterling’s Dynamic Systems Theory (DyST) is much more effective, when it

comes to detailing relevant factors of its study object (gender development and sex/gender

differences) and thus accounts for an in fact interacting and complex world of human beings.

Fausto-Sterling’s approach is more responsive to this complexity because it has the conceptual

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means to accounts for its synchronic complexity (and thus between different levels, i.e., from

psychic to social) as well as to account for its diachronic complexity and thus over time. But

Fausto-Sterling’s theory does not only propose a better model of the world and is predictively

fruitful; it has also the power of substituting the nature/nurture framework and this without

any loss of scientific rigor as its dictated in the empirical sciences. I argued that rather and on

the contrary, Fausto-Sterling is a better and non-vulgar empiricist applying her DyST, because

her approach responds to the complexity of the study object and thus rejects a too strong and

too quickly generalizing interpretation of the data.

To see the two answers to the question of differences between men and women in condensed

form, let’s now reproduce the argumentative form from section 1.3, which I claimed to

represent nature/nurture reasoning about mental differences between men and women, and

then contrast it with a reinterpretation in terms of Fausto-Sterling’s DyST. But before

providing the reinterpretation, look at first at the nature/nurture argument:

1st premise There are biological sex differences (chromosomes, anatomy, hormones, etc.) between men and women.

2nd premise There are mental sex/gender differences (e.g. in cognitive abilities, character traits, motivations, etc.) between men and women.

3rd premise The biological sex differences stand in a non-random relation to mental sex/gender differences in cognitive abilities.

Conclusion Biological sex differences (partially) cause the mental sex/gender differences.

Remember that I argued that premise 3 is the weak spot here, because it infers causality from

correlation between biological and mental differences between men and women. Moreover,

this argument is notoriously ambiguous, because it can be interpreted in terms of nature- as

well as nurture causation, which renders visible the problem of underdetermination, which I

claim to exist for nature/nurture.

In contrast, take a look at the following argument, which is formulated in terms of Fausto-

Sterling’s DyST and which clearly shows its difference from the above nature/nurture

argument in that only premise 2 stays the same:

1st premise There are (nearly) dimorphic biological differences (chromosomes, genitals) between men and women.

2nd premise There are non-dimorphic differences between men and women (including mental sex/gender differences but as well classic nature- and nurture-thought differences).

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3rd premise The dimorphic differences of new born children correlate with differences in treatment (as visible e.g. in the caregiver-infant dyad) due to (un-)conscious gender bias and/or due to individual differences of the children in robustness.

4th premise Differences in treatment are experienced by the children and embodied over time.

Conclusion Non-dimorphic sex differences (including mental sex/gender differences) between men and women emerge over time being based on dimorphic differences after birth.

This argument provides in a very concentrated way all that is so distinctive of Fausto-Sterling’s

DyST. We have the dichotomy ‘dimorphic/non-dimorphic’ as well as the important concepts

of emergence, experience, and embodiment which take into account synchronic (multilevel)

complexity and diachronic complexity of trait development over time. As an important

consequence, this argument renders visible that strictly speaking the distinction between

mental and bodily differences (between men and women) has been blurred in the first place,

because mental traits are claimed to emerge systemically involving brain, body, and world

(especially as mediated by the caregiver-infant dyad).

While this argument is very strong, remember that it’s not strong enough to warrant causal

inference, because (similar to nature/nurture studies) Fausto-Sterling’s DyST is based on non-

experimental observational studies, a critique, which flows from Oscar Kempthorne’s views

on causation and which I find important. But even if this is true, I argued that Fausto-Sterling’s

DyST is preferable, the relation between data and interpretation is much less problematic in

causal interpretations by means of Fausto-Sterling’s DyST than in causal interpretations by

means of nature/nurture.

To conclude at last, let’s see where we have finally arrived at. Fausto-Sterling’s DyST provides

a theory of gender (development), which acknowledges that there are differences between

men and women. But she determines the meaning of these differences (i.e. why they exist)

not based on a dubious claim of some natural, biologically founded order of men and women.

Rather, her acknowledgment of these differences, and what they mean, is strictly and

throughout rationalized and illuminated.

On her picture, the human species differs dimorphically, ‘absolutely’ (i.e. cross-culturally or

universally) only in terms of genitals and chromosomes. In contrast, all traits that correlate

with those absolute features are in principle (and in this contingent world to a lesser or higher

degree) synchronically or diachronically relative. That is, these traits (when interpreted as

developmental systems) are relative to the relevant variables (e.g. psychic, physic, social,

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relational) that make it up, whose relevance and composition is itself subject to temporal

change. This is why on Fausto-Sterling’s account, sex/gender, ‘femininity’, ‘masculinity’, sexual

orientation, etc. are no fixed traits but rather multi-variable processes at specific times in the

life cycles of genital (or genetical or demographic) males and females.

A beautiful consequence of Fausto-Sterling’s view is then that it can account for similarities as

well as differences, i.e. for the content of the norm as well as its deviation, i.e. for the (cross

cultural) universality of a trait as well as for its distincitive particularity. It’s (amongst others)

this aspect that effectively renders Fausto-Sterling’s DyST superior to the nature/nurture

framework, because it enables to grasp the contingency of empirically stable features.

Finally, and to provide a very last clarification, reconsider Marc Hauser’s citation provided

already in 3.1, where he argued that

“[i]t is hard to imagine anyone living today disagreeing […] that there are biological differences between the sexes. Even the staunchest cultural relativists have to acknowledge that there are differences in the sex chromosomes and hormonal titers that lead directly to differences in our anatomy.”

(Baron-Cohen et al. 2005)

Fausto-Sterling would surely agree but she’d hasten to qualify, I surmise, that the normal

development from XX/XY to normal differences in hormones and to normal differences in

anatomy takes place in a standard environment and, in addition, that this development need

neither conform with other levels of (male and female) sex (respectively) nor with the person’s

developing gender (as a man or woman, respectively). And this qualification, even if it

describes the very same empirical phenomenon in this case, provides additional information,

which makes a difference that is large after all. Maybe, and with respect to this particular case

here, this difference is adequately captured stating Fausto-Sterling has entirely changed the

meaning of sex chromosomes.

4.2 Limits and further research

This section is finally the very last one in this text and it has the purpose of taking a brief and

critical look on this very text. Moreover, it aims to point out a few interesting aspects that

came up in the course of the discussion but whose treatment were beyond the scope of this

text.

To begin with, I concede well that this text covered a too large topic. It would have been

perfectly fine to devote a whole master’s thesis only to the work of Anne Fausto-Sterling and


118

I would have done so, if I’d had more time and if I had progressed faster in my understanding.

Therefore, and as it stands now, this text also reflects my learning curve, which sort of

vacillated between the complex ‘nature/nurture, IQ debate, heritability’ and ‘Anne Fausto-

Sterling, DyST, sex/gender differences’. This learning curve is also visible in the opposition of

non-systematic case studies and the attempt of systematic examinations in the context of the

nature/nurture position and Fausto-Sterling’s DyST. But even if the coverage of this text was

not ideal, because it was not focussed enough and thus resulted in a slippage of the

phenomenon studied (from IQ to sex/gender in general over to specific sex/gender

differences), the coverage was neither arbitrary nor unwarranted. The connections I drew on

the conceptual level between both thematic complexes are clearly there. I could have had it

more easily though.

Next, there are a number of aspects, which are connected to this text’s discussion, but which

I could not go into lacking the space. Firstly, I want to be clear that I take Fausto-Sterling’s

DyST to be anything else but exhausted in this text. While I’m sure that there are a few

valuable insights, which this text provides, I’m as convinced that there is lots of potential for

many other and especially much more fine-grained analyses of Fausto-Sterling’s DyST. For

instance, and very intuitively, it would surely be fruitful to focus on Fausto-Sterling’s

application of DyST to a specific trait (such as toy preference) and perform a much closer

analysis of how DyST works in comparison to alternative theories.

Secondly, it’s clear that DyST needs to be further applied, which means that (just like Fausto-

Sterling et al. 2011b demand) more empirical studies need to be performed. This would

reduce the lack of data specifically diagnosed by Fausto-Sterling et al. (2015) and further

warrant judgements of how well DyST works. On a theoretical level, it’s necessary to study

DyST applications, which have already been performed (e.g. on women’s sexuality by Diamond

2008a,b; 2012)124, and put different applications into comparative relation with each other. In

other words, DyST needs to be tested on a theory level in terms verifying its empirical

consequences and in terms of its data-interpretative value.

Thirdly, and because it’s difficult to detach the concrete study (e.g. on gender development)

in DyST on a theory level from the fundamental claims (or denials) of DyST as a framework,

it’s of course also necessary to further study the background assumptions that underlie DyST

124 Fausto-Sterling is aware of Lisa Diamond’s word (cf. e.g. Fausto-Sterling 2012c, 94-8).


119

and how they manifest in the context of the concrete empirical study (e.g. of gender

development). In any case, it might not correspond to a very familiar notion to be confronted

with a theoretical construct like Fausto-Sterling’s DyST, which is implied to be both situated

on the level of an empirical theory and on the level of a framework. I’m sure it would be

illuminating to take a second and much closer look at this hybrid theoretical status of Fausto-

Sterling’s DyST.

Fourthly, it was recognizable that there is a large problem of the concept ‘causality’ in the

context of social sciences in general, because of its non-experimental character. While I

argued that Fausto-Sterling’s DyST is better, basically because she studies complex subjects

with adequate means, Fausto-Sterling’s approach as well cannot provide a causal account of

gender development. As a consequence, it needs to be examined, either if the notion of

causality in the social sciences should be reconsidered and detached from experimental

theory or if the general purpose of social sciences should be reconsidered in terms of seeking

correlations and not causes. In this context, it might be interesting to return again to Oscar

Kempthorne’s views on causation, which were anything else but exhausted in this text.

Fifthly, I think it would be very fruitful to work out in much more detail the connecting points

between (in my view preferably Lacanian) psychoanalytic theory of sexuation and (Anne

Fausto-Sterling’s) DyST as applied to gender development. One reason why I think that this

would be illuminating is because there are prima facie shared aspects, which be deeper than

that. For example, Fausto-Sterling’s DyST as well as psychoanalytic theory theorize the genesis

of human desire itself instead of purporting to explain the deviation of some norm like, for

instance, homosexuality with respect to heterosexuality. In addition, Fausto-Sterling seems to

emphasize language, which plays an essential role in psychanalysis, in the context of her

theory of gender development to the point that she contrasts a presymbolic with a symbolic

phase of gender identity formation (cf. Fausto-Sterling 2012b).

Sixthly, it would be interesting to systematically examine whether the claim of

underdetermination of nature- and nurture-explanations by empirical data can be

conclusively supported. In this text, I sort of presupposed this without providing a discussion,

which is why this diagnosis is strictly speaking nothing more than an intuitive judgement based

on prima facie evidence and on statements from other authors like Stephen J. Gould and Susan

Oyama, which I take to imply this.


120

Finally, it would as well be interesting to take a closer look at Fausto-Sterling’s perspective on

sex/gender in relation to classically philosophical account of sex/gender. For instance, it would

be very illuminating to compare in much more detail Judith Butler’s account and point out

what they have in common and where they disagree. And last but not least, it would be helpful

to write a critique of the revisionary book of Neven Sesardic (2005), part of which I spelled out

in an earlier draft of this paper but which in the end had to be left out since it went beyond

the scope of this text.

121

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Overcoming Sex/Gender and Nature/Nurture - unipub

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