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History of childhood and causation of health. Are lives programmed?. What is a child?. UN: 0-18 years And what is health??. - PowerPoint PPT Presentation
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History of childhood and causation of health
Are lives programmed?
What is a child?
UN: 0-18 years
And what is health??
•WHO 1946:’Health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity’ (later added: ’ability to lead a socially and economically productive life’)
•Sigmund Freud: ’You have health if you are able to work and love’
•Peter F Hjort: ’…Health is to master everyday’s demands’
Helse?• Samme kategori ord som kjærlighet,
lykke, kultur, bærekraftig• Alle har et forhold til begrepene,
ingen er enige om hvordan de skal defineres Hva lykke er? Det er å gå på en gressgrodd
setervei i tynne, tynne sommerklær klø sine første myggestikk med doven ettertenksomhet og være meget ung og meget rik på uoppplevet kjærlighet
(Inger Hagerup)
How can we measure health?Proxies (health indicators)
• MortalityMortalitet
• Morbidity
• Infant mortality (IMR)
• Life expectancy
• Under-5 mortality
• Birth weight
• Body height
All endpoints are proxies for what we call health
Quality of life model the different spheres(Lindstrøm, Allhardt)
• Global:macroenvironment, human rights
• Outer sphere:Socioeconomi
• Humen relations: Family, friends
• Personal: physical, mental, spiritual, activity, selfconfidence
What is mental health?
• (Meriam Webster):
• A state of emotional and psychological well-being in which an individual is able to use his or her cognitive and emotional capabilities, function in society, and meet the ordinary demands of everyday life”.
The three circles of social determinants of health
Family
Friends
Neighbours
Home
Norms
Expectations
Community
AreaLocal services
Naturalresources
Pollution
LocaleconomySchools
Macrosocial influences
Government
Laws
Economic system
Nationalpriorities
Welfare model
Justice
Equality
CHILD=child health indicators for life and development (EU)
• Demographic and socioeconomic determinants
• Health and disease (mortality, morbidity)
• Health determinants (positive,negative)
• Health policy
Children’s health and quality of life
Globalchanges
Technical changes
Economicalchanges
Societal changes
Educational changes
Populationchanges
Life style changes
Nutrition
Changes in disease panorama
?
?
??
?
?
What is epidemiology?
Basicly: The study of the origin of diseases
• Epidemiologiske undersøkelser dreier seg om undersøkelser av grupper av befolkningen, ikke av enkeltindivider
• Epidemiologi er grunnlaget for helseovervåkning og for å foreslå forebyggende tiltak i befolkningen
Eilert Sundt: Om dødeligheden i Norge (1855)
…”der er intet blindt tilfælde (av dødsfall). Det lære vi, naar vi ikke alene saaledes med bevæget sind betragte de enkelte dødsfald, som kunne være inntruffet i den snevrere kreds, men tillige med sindigt overlæg samle en større mengde erfaringer ved at tælle alle de dødsfald, som i et længere tidsrum ere intrufne i i en by, en egn eller i et helt land.”
Helsediktet fra Salerno - ca. 1300 e.Kr.
Om årsakene til sykdom:Årsakene til øresting:
• Sno, byld, sult, støt og hete, flere ting er nevnt som grunn til øresting. Samme skade kan det gjøre at folk skriker i ens øre.
Årsakene til sukkersyke:
• Er nyrene tørre, og sterkt opphetes, vil du få diabetes; også elskov, hopping og kappløp gjør sitt, og at en har slitt.
Hvordan skal vi måle sykdom eller helse?
• Forekomst (antall tilfeller, andel) må ha en teller (antall tilfeller) og en nevner (hele befolkningen, deler av befolkningen, aldersgrupper, osv.
• Vi må ha en kilde for å få frem tallene: register (dødsregisteret, kreftregisteret hvor alle tilfeller blir meldt), eller vi må gjøre spesielle undersøkelser, surveys
Examples (mortality)
• Number of deaths per 100 000 inhabitants• Infant mortality (IMR): number of deaths in first year
of life per 1000 live born• Deaths per 100 000 inhabitants in a county• Deaths per 1000 among people in certain
employments• Number of deaths per 100 000 of a specific
diagnose(cause specific mortality)
Target population, everyone ”at risk” must be stated.
Two types of epidemiological studies
• DescriptiveDescriptions of prevaence of illness(disease) in a
population (group) – nothing about causes
• AnalyticalTry to look for causal factors
Typer av epidemiologiske undersøkelser
• Hypotesegenererende• pasient• serier av pasienter• tverrsnittsstudier av befolkningen
• Hypotesetesting
Observerende: • pasient-kontroll (case-control)
• cohort
Eksperimentelle• Randomiserte(RTC)
Måling av sykelighet
• Forekomst/prevalens egner seg vesentlig for tilstander som er noenlunde stabile gjennom en tid (kroniske?). Uttrykkes i antall tilfelle per (for eksempel) 100 000 av målpopulasjonen
• For noen sykdommer er dette et uegnet mål, for eksempel ved akutte infeksjonssykdommer. Da kan vi måle insidens: antall nye tilfeller per 100 000
Letalitet
Det er også hensiktsmessig å kjenne uttrykket letalitet, som er antall døde per antall som er blitt
syke
Lif expectancy at birth, Norway 1900 -94
0
10
20
30
40
50
60
70
80
90
1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 1994
boys girls
life
tim
e, y
ear
s
Cohort Studies – definition(R.Doll)
• ”…the delineation of a group of persons who are distinguished in some specific way from the majority of the population and observation of them long enough to allow any unusual morbidity or mortality to be recognised”.
”Case control”
• Compare exposure (risk factors) for people with a known endpoint (disease) with a control group without the disease
• The Norwegian Mother and Child Cohort Study studies cases and controls from the same set of data (”nested case control” )
Kohortdesignets fordeler:
• Man undersøker eksponeringsforhold (potensielle årsaksfaktorer) før utfallet er kjent
Assosiasjon mellom eksponering (risiko) og utfall
(sykdom)Risiko Sykdom
+ -
+ 201(a) 25(b)
- 20(c) 145(d )
Odds ratio= a x d/b x c
Association is not equivalent to causality!
• Criteria for associations= causes (Bradford-Hill):
• strength
• consistency
• specificity
• time sequence
• biological gradient (dose/response)
• plausibility
• coherence
• experimental proof
• analogy
Hvor kan vi hente data fra?Utfallsdata (sykdom,død): Registre (døds-,kreft-,fødsels-,diabetes-,pasi-entutskrivnings-)
Helseundersøkelser
(statens h.u.,CONOR, SSB, helsestasjonsdata, meldepliktige sykdommer)
Spesielle undersøkelser (surveys)
Hvor kan vi hente eksponeringsdata?
Eksempler:
• Kommunedata (luft,vann etc)
• Trafikketaten (trafikktetthet etc)
• Spesielle spørreundersøkelser til enkeltindivider
• Spesielle målinger (forurensning, støy etc)
• Biologiske prøver
• SSB (sosioøkonomi etc)
ER SYKDOMMEN ARVELIG?Design i genetisk epidemiologi
• Tvilling- og adopsjonsstudier• Segregasjonsstudier• Koplingsanalyse• ”Vanlig epidemiologisk design”: Ved
samspill mellom arv og miljø, behandler man de genetiske faktorene som en vanlig risikofaktor.
NB: de aller fleste sykdommer er styrt av mange gener, og av miljøpåvirkning!
IntervensjonsstudierVirker et tiltak?
• Randomiserte forsøk= RCT (randomized control trials
Ofte vanskelig design!
Alltid ved legemiddelutprøving
”Økologisk” (Ecological) design
Her sammenlignes hele grupper, ikke knyttet opp mot
enkeltindivider, eksempel er fra Forsdahl studie av hjerte-kar
dødsfall i Finnmark
New indicator for child health
(Student, Croatia):
”The proportion of children that smile to you when you meet them”
Health and Illness in Norwegian Childhood through 100 years-
from Poverty to Wealth
• Rannveig Nordhagen
• Norwegian Institute of Public Health
• Oslo, Norway
Ord om barn og barndom
• Barnets innebygde mål er å bli voksen, før dette eksisterer det bare som en mulighet, et potensial (Aristoteles)
• Barndommens historie er et langt mareritt, som vi bare langsomt holder på å våkne opp fra (Lloyd de Mause, am. psykoaanalytiker)
Scenario 1900:
Population 2,2 mill
Emigration 1901-10: 38 172
Infant mortality 1896-1900:
boys: 105,5/1 000,girls: 92/1000
Important diseases: Infections (Tbc)
Life expectancy:
0 år: 51,5
5 år: 55,5
20 år: 44,04
2007
• Folkemengde: 4 500 000
• Innvandrere: 8% (i 2060: 19-27%)
• Spedbarnsdødelighet: 3 per 1000
• Viktigste sykdommer: Hjerte-kar sykdommer, kreft (kroniske lidelser)
• Forventet gjenstående levetid (ved 0 år)
• Kvinner: > 82 år, menn: 78 år
Chr Krohg:Fighting for existence
Helene Scherfbeck
Spedbarnsdødeligheten
E.Munch: Fostermother
s in court
”Angel mothers”:
Fostermothers who starved the children to death
Infant mortality in Norway per 1 000 1905-1994
0
5
10
15
20
25
30
35
40
45
50
1905 1910 1915 1920 1925 1930 1935 1940 1945 1950 1950 1955 1960 1970 1975 1980 1985 1990 1994
boys girls
IMR and U5MR per 1 000 in some selected countries in 1960 and 2003
U5MR I MR
1960 2003 1960 2003
Niger 320 262 211 154
Pakistan 227 103 139 81
Turkey 219 39 163 33
Romania 82 20 69 18
US 30 8 26 7
UK 27 6 23 5
Norway 23 4 19 3
Life expectancy at birth, Norway 1900 -94
50
55
60
65
70
75
80
85
1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 1994
boysgirls li
fe ti
me
, ye
ars
Tbc mortality, Norway, 1900-65, age 15-19 years
050
100150200250300350400450
1900
1905
1910
1915
1920
1925
1930
1935
1940
1945
1950
1955
1960
1965
Girls
Boys
Year
BCGChemotherapy
Mortality per 100
000
Mortality of tbc per 100 000
Age -1900 -1915 -1940
M F M F M F
0-4 345 339 180 156 38 37
10-14 145 223 87 154 20 27
15-19 319 375 272 333 27 81
Causes of infant mortality, Norway 2002
All 3.5/ per 1000
Per 100 000:Birth/perinatal complications: 153 Malformations: 108SIDS 31
Rate of low birthweight (< 2 500g) in the Nordic countries (NOMESCO 1997, %)
Denmark Finland Iceland Norway Sweden
1980-82 5,73 - 3,64 4,21 4,33
1983-85 5,78 - 3,82 4,50 4,42
1986-88 5,58 - 3,51 4,68 4,67
1989-91 5,36 3,84 3,33 4,87 4,54
1992-94 5,31 4,06 3,96 4,81 4,48
1980-94 5,53 3,93 3,65 4,63 4,49
Rate ratio(RR) of children with social support at the age of 7 in relation to
birthweight (Norway 1998)
Cause Weight groups
500-999 1000-1499
1500-1999
2000-2500
> 2500
Mentaldisorder
11,5 4,2 3,8 2,9 1
Nevrologicdisorder
53,0 36,9 13,6 3,5 1
CP 94,2 67,6 22,5 4,9 1
Eye disease 155,2 50,5 4,4 4,0 1
Ear disease 14,7 9,3 3,5 2,8 1
Malformat. 6,7 4,9 3,7 3,8 1
Mortality of tbc, Norway, 1900-65, age 0-4 years
0
100
200
300
400
1900 1905 1910 1915 1920 1925 1930 1935 1940 1945 1950 1955 1960 1965
Mor
talit
y pe
r 10
0 00
0 Girls
Boys
Year
”Finsen-treatment” Hagavik hospital
Screening for tbc
Mortality rates and life expectancy (US)
1800 1850 1900 1950 2000
Infections
Chronic Disease
Life Expectancy
Tarlov 1996
Reported cases of invasive Hib infection, Norway, 1989-96
0
20
40
60
80
100
120
140
1989 1990 1991 1992 1993 1994 1995 1996Year
Nu
mb
er o
f re
po
rted
cas
es
3m-2years3-10 years>10 years
Vaccine
Kari Kveim Lie 1997
”The Oslo breakfeast”
Weight and hight screening
World war 2, 1940-45:
Food restrictions, undernutrition in towns
Mean hight for different age groups of girls, Oslo from 1920 to 1975. GH Brundtland et al 1980
Relation between height at the age of 7, and unemployment at age 22-32
0
0,5
1
1,5
2
2,5
3
3,5
114 119 122 124 126
Height at 7 years
Od
ds
ra
tio
fo
r u
ne
mp
loy
me
nt
crudeadjusted
Montgomery S et al. 1996
Parent reported overweight in Nordic children 1996,%
0
2
4
6
8
10
12
14
16
18
6 yrs 9 yrs 12 yrs 15 yrs 17 yrs
boys
girls
Chidren’s healthand quality of
life
Global changes
Technologicalchanges
Economical changes
Societalchanges
Educationalchanges
Changes inpopulation
Life stylechanges
Nutritionalchanges
Changes ofdiseasepattern
?
?
??
?
?
Infant mortality per 1 000 live born, Norway, 1901-63
0
20
40
60
80
100
120
140
160
Mor
tali
ty
MarriedUnmarried
Social class and infant mortality 1911-71, England & Wales
020406080
100120140160180
1911 1920 1931 1951 1971
Year
Infa
nt
mo
rtal
ity
per
100
0
IIIIIIIVV
Incidence of tye 1 diabetes in the Nordic countries 1995-2003, both
sexes, 0-14 yrs
0
10
20
30
40
50
60
1995 2000 2003
Inci
den
ce p
er 1
00 0
00
Denmark
Finland
Norw ay
Iceland
”Binge drinking” and problems associated with use of alcohol, both
sexes, 15-16 yrs
0
5
10
15
20
25
30
Denmark Faroe Islands Greenland Finland Iceland Norw ay Sw eden
Per
cen
t Binge drinking
Relationship problems
Delinquency problems
Mortality 1-17 years. Norway 2002,
per 100 000Total Infectious
diseases
Tumours Congenital
malformat.
21 0.9 3.4 2.4
The child’s century?(essay by RB, Norwegian school boy,
1999)
”…the developing countries seem to mirror the industrial countries a century ago, which should mean that the development goes in the right direction - which I believe. With an increased effort towards the developing countries towards year 2 000, I think we rightly might call this century the children’s century.”
The greatest threats for children in 2 000 (UNICEF):
• Wars
• AIDS/HIV infections
• Poverty
When are our lives determined?
Edvard Munch:Inheritance.
Why do we vaccinate against Rubella (German measels)?
Is this a clue??
Have we asked our questions at the right time?
Forsdahl/Bakketeig1991
Forsdahl/Bakketeig 1991
Anders Forsdahl :…”whereas the weaker of the cohort
die in infancy, the fit survive and carry with them a life-long
vulnerability”
Dødsårsaker, døde per 100 000, 2003
0 100 200 300 400
hjertekar
kreft
åndedrett
fordøyel
vold
trafikk
suicid
menn
kvinner
Standardised mortality ratios among men according to birthweight and weight at one year
Weight(lb)
Coronary All causes
Birth 5.5 102 93-7.5 82 80-9.5 56 68
1 year 18 105 89-22 85 82>26 42 62
Barker 1991
Hazard ratios for coronary heart disease in adult life among Finnish men according to birthweight and weight at 12
monthsBw (g) Hazard ratio (RR)
≤ 2500 3.63
-3000 1.83
-4000 2.08
>4000 1.00
P value for trend 0.006
Weight at 1 y (kg)
≤ 9 1.82
-10 1.17
-11 1.12
>12 1.00
P value for trend < 0.0001
Correlations of cause of death (SMRS) at ages 35-75 years and IMR
Cause of death Correlation coefficient
Ischaemic heart disease 0.73
Broncitis 0.82
Stomach cancer 0.79
Rheumatic heart disease 0.72
Stroke 0.54
Lung cancer 0.46
Barker 1986
Ethel Margaret Burnside, 17 yrs1877-1953
A pet child has many
namesForsdahl hypothesis??
Barker hypothesis?Fetal programming hypothesis?
Fetal origins hypothesis?
The concept of biological (fetal) programming (Lucas):
When an early stimulus or insult, operating at a critical or sensitive
period (infetal life), results in a permanent or long-term change in
the structure or function of the organism
Later programming hypothesis (Lucas 2):
If the fetus experiences undernutrition in fetal life, the fetus adopts to this state, and if a later
rapid overnutrition of the baby occurs, it can get out of balance- for instance what concerns the
tolerance of glucose (insulin resistence- diabetes 2).
”The growth accelaration hypothesis”
(Singhal & Lucas 2004)Hypothesis about rapid growth
very early in life
De viktigste assosiasjonene i de første Barker-studiene mellom fødselsvekt/vekt
ved ett år:• Hjerte-kar sykdommer,spesielt koronarlidelser• Diabetes II• Obstruktiv lungesykdom (KOLS)• Risikofaktorer for hjerte-kar sykdommer:
Hypertoni, koagulasjonsfaktorer, kolesterolnivå, overvekt
• Syndrom ”X”=diabetes2 +hypertoni+hyperlipidemi
Andre antropometriske mål ved fødselen som viser tilsvarende
assosiasjoner:Abdominal omkrets
HodeomkretsPlacental vekt/fødselsvekt
LengdePonderal index =kg/m³ (lengde³)
BMI =kg/m²(lengde²)
Low birthweight ”per se” is not the cause of later coronary
disease, but what has happened in intrauterine life
Three hypotheses (P. Magnus)
• The environmental model: Exposures, i.e. those related to poverty, have effects of the growing fetus, later leading to adult disease
• Genetic confounder model: the association between birth weight and later disease (coronary) is completely causes by genes influencing both factors
• Environmental confounder model: Same background factors can influence both early and late phenotypes, example is smoking..
”These diseases can best be focused on from a lifecycle
perspective(Erikson 2006)
Pathways from early life to later health
a)Programming
Programming in intrauterine life - Later illness/health (latency model)
b) Continuous life events
Parents’ SES - Childrens SES
Birth weight - Later illness
Foreslåtte mekanismer bark programmeringseffekten
(Lucas)
Cellulære mekanismer• Ernæringsforholdene (miljøet) endrer genetisk
ekspresjon permanent• Ernæringsforholdene virker inn på (reduserer) fosterets
cellemasse• Seleksjon av kloner av gener
• Ernæringsforholdet endrer organstrukturen• Ernæringsforholdene virker gjennom sensibilisering for
hormoner
Regression models (Lucas 1999)
- Early model: regression used simply to relate early size to later outcome
- Combined model: includes both early and later size, obtained by adding later size to the early model
- Interaction model: adds the interaction of early and later size to the combined model. The interaction terms
is calculated as the product of early and later size
- Late model: later size alone is related to outcome, which helps to interpret the relative importance of early
and later size separately and together
The fetal hypothalamic-pituitary- adrenal axis (DM Sloboda)
• …Programming of the fetal HPA axis during development appears to play a central role in the link between fetal growth and long-term disease in adulthood. Prenatal programming of HPA axis function may increase the the risk of developing cardiovascular and metabolic disease.Cognitive and behavioural modifications have also associated with fetal programming and linked to alterations in HPA axis activity ….
Mor Far
Barn
But what about genes??
• Single gene conditions (2% of the population in a life perspective)
• Chromosome anomalies (Down)
• Multifactorial conditions
Antenatal maternal anxiety and depression and infant development and
behaviour at 6 months
Rannveig Nordhagena Anne Inger Helmen Borgeb
aNorwegian Institute of Public Health, OslobInstitute of Psychology, University of Oslo
Leonardo da Vinci:Woomb
The hypothesis of fetal ”programming” (Forsdahl/Barker/Lucas)
• The intrauterin environment afforded by the mother at a critical period of development may permanently ”program” the structure and physiology of her offspring, and have a lasting or lifelong significance, for instance on the brain development.
Our hypothesis (slightly moderated from the title):
• Can the mother’s anxiety and depression in pregnancy affect the child’s behaviour at 6 months of age?
Rossetti: Ecce ancillaDomini(1850)
The Norwegian Mother and Child Cohort Study
• An ongoing cohort study starting in pregnancy, basicly a questionnaire study,but biological samples (blood, urine) are collected. Linking to health registries may be performed (Birth, Death,Cancer etc).
• Aim:
Recruitment of 100 000 pregnant women,
100 000 children, 80 000 fathers.
Status per 01012006: > 60 000 women included
Study progress:
• 1992: Project planned• 1995: Pilot project• 1999: Project start at first hospital• 2000: 2 752 women recruited• 2004: 40 000 women recruited• 2006: >60 000 women recruited• The participation rate is < 50% of all
invited women
Hospitals in Norway participating in the
MoBa Study
Time of questionnaires:
Q1: Week 17-18 of pregnancy (ultrasound)Q2: Week 24 of pregnancy (nutrition)Q3: Week 30 of pregnancyQ4: 6 months post partum Q5: 18 months post partum Q6: Child 3 yearsQ7: Child 7 years
Ca 100 Q in each questionnaire, and many subquestionsUsed in this study: Q1, Q3 and Q4 all reported by the mother
Included in this study:
• All mothers who had filled in Q1(week 17 in pregnancy), Q3 (week 30 in pregnancy) and Q4 (6 months post partum)
• Singleton births
All together: 37 011 women
Some missing on single questions!
Variables used in this study
• Outcome variable: Problematic child at 6 months
• Measure:
• 10 Q mainly from Infant characteristic questionnaire (ICQ) (Bates et al.)
• Items:crying, soothability, easily upset, intensity of protest, easy to get along with, smiles, very demanding, require attention, easy to put to sleep)
Exposure variables
• Mother’s general anxiety and depression week 30 in pregnancy and 6 months pp (short version of symptom check list (SCL). 8 questions: 4 for anxiety, 4 for depression)
• ”Specific” anxiety (week 30):Fear of giving birthWorries about the baby’s health
• Covariates/confounders:Maternal factors: Anxiety/depression 6 months pp, mother’s
education,mother’s age
Child factors: sex of baby, birth weight
E.Munch:Inheritance
Else Hagen: The Family
The results of this study cannot be published on the net, due to later
scientific publication.
Sorry!