BMI Body Mind Inspiration

Weight Loss Surgery Preoperative Risk Reduction

The Obesity Action Coalition: The Voice of Those Affected by Obesity

Treatment Considerations for Osteoarthritic Knee Pain in Patients with Obesity

Hair Loss Among Weight Loss Surgery Patients

18

14

20

25

A peer-reviewed e-journal providing lifestyle and health information for weight loss surgery patients and candidates

WEIGHT LOSS

BEFORE

WEIGHT LOSS

SURGERY

WEIGHT LOSS

BEFORE

WEIGHT LOSS

SURGERY

What Do We Know About Dropping Those Preoperative Pounds?

Winter 2012

Volume 1, Issue 1

p8

LIKE us on Facebook • FOLLOW us on Twitter • CONNECT with us on LinkedIn

BMI: BODY • MIND • INSPIRATION

A peer-reviewed,

evidence-based e-journal

providing lifestyle and

health information for

individuals interested in

combating obesity,

diabetes, and metabolic

disorders and improving

their overall health and

well being.

w w w. b o d y m i n d i n s p i r a t i o n . c o mTo view the current issue, visit

Digital publishing sponsored by

Introducing a New e-Journal for Medical and SurgicalWeight Loss Patients and Candidates

• Exciting, New, FREERESOURCE covering avariety of topics in thefield of metabolic andbariatric surgery

• FOUR issues in 2012

Editor’s Message

BM

I

Copyright © 2012 MMC BMI Body • Mind • Inspiration—Winter 2012 3

Dear Readers:

On behalf of MatrixMedical Communications,I am very proud towelcome you to thefirst edition of Body •

Mind • Inspiration—or BMI.

Sadly, the obesityepidemic continues tothrive, not only inAmerica but around theglobe. As I am certainwe are all aware,

obesity is a multifactorial disease that is not yetclearly understood or easily controlled. Obesityseems to be determined, among other causes, by animbalance between an individual’s genotype andphenotype. Human genetic code has beendetermined by the struggle of human species tosurvive the lack of food. Thus, over the lastcenturies, the human body has evolved to include adefense mechanism against famine by protecting thehighest weight attained. The expression of genotypevaries among humans, thus making us susceptible tobecoming overweight. Conversely, human phenotypeis mainly determined by impacting environmentalfactors. One would imagine that these factors couldbe easily controlled. However, serious eating andpersonality disorders, as well as our economicreality, make such changes extremely difficult formany Americans. Sedentary lifestyles, whether bychoice or by necessity, as well as the abundance of apalatable and affordable food supply in industrializednations, are the main negative phenotypic influencespredisposing these populations to becoming obese.

Recent publications have clearly demonstratedthat obesity is indeed a serious medical conditionthat severely impacts health and shortens lifeexpectancy. BMI was primarily created as a forum inwhich to deliver the latest updates and importantinformation related to weight management, so that

Americans are educated in the fight against thisdebilitating disease.

The successful treatment of obesity andoverweight is primarily based on long-term lifestylechanges and commitment to these changes. New andhealthy eating habits must be preserved and routinephysical activities must be incorporated into dailylifestyle. Unfortunately, as we are all aware, this ismuch more easier said than done!

This month, Liz Goldenberg, MPH, RD, CDN,discusses the benefits of losing weight beforeundergoing weight loss surgery, including reductionof comorbid conditions and complications. AdrienneYoudim, MD, lists common comorbidities andprovides tips for patients on reducing the severity ofthese condition. James Choi, MD, and JonathanShaffer, MD, MBA, discuss osteoarthritic knee painin the patient with obesity and present operativeand nonoperative treatment modalities. Sylvia LeiteFaria, MS, et al present an extensive review ofcurrent literature on the causes and treatment ofhair loss in weight loss surgery patients. This month,we also highlight the Obesity Action Coalition, theonly nonprofit organization whose sole focus isrepresenting those affected by obesity througheducation, advocacy, and support. This articleoutlines membership benefits and providesinformation on how you can get involved.

In future issues, we will be bringing youinformation on a wide variety of topics, includingexercise, nutrition, body contouring, skin health, andmuch more. We hope that BMI will be a valuableresource to you in your efforts to become andremain fit and healthy.

Welcome and I hope you will enjoy this first issue.BMI

Sincerely,

Raul J. Rosenthal, MD, FACSClinical Editor, BMI

Raul J. Rosenthal, MD, FACS,Clinical Editor, Body,Mind,Inspiration, Program Directorof Minimally Invasive Surgery,Director of the MinimallyInvasive Fellowship Program,Director of the Bariatric andMetabolic Institute, andDirector of the GeneralSurgery Residency Program,Cleveland Clinic Florida—Weston, Fort Lauderdale,Florida.

Winter 2012

Volume 1, Issue 1

Publisher’s Message

BM

I

Copyright © 2012 MMC4 BMI Body • Mind • Inspiration—Winter 2012

Winter 2012

Volume 1, Issue 1

Dear Readers:

We are pleased to announce the launch of Body

• Mind • Inspiration or BMI, a journal inspired bynumerous calls and e-mails from individualsrequesting information from our company onmedical weight loss and weight loss surgicalprocedures, and health issues weight loss surgerypatients should be aware of two, five, and ten yearspost surgery.

BMI will be published quarterly in 2012,providing articles on lifestyle and health forindividuals seeking to loose weight, and for pre andpost weight loss surgical patients and candidates.Articles will be clear and concise and offerresources on a continual basis. As a community, weneed to stay informed and BMI will be a resourceavailable complimentary to assist individuals ontheir quest to combat obesity, diabetes, andmetabolic disorders.

The following is a sample of topics that you canexpect to see in future issues:

• Insurance Information• Nutrition• Patient Checklists• Body Contouring• Association Updates• Revisional Surgery• Skin Care• New Product Reviews• Patient Advocacy• Overview of Surgical Procedures• Exercise Physiology• Emotional Issues• Communicating with your physicians• Weight Regain• Programs and Resources• Motivational Tips and Techniques

As subscriber, you will receive a notification e-mail when each new issue is available for viewing.The BMI publishing platform automaticallydetermines the web-enabled device you are usingto access the journal and immediately formats theentire issue for reading on computers,smartphones, and tablets.

We are excited to provide a valuable resourcesuch as BMI to individuals interested in improvingtheir health and well being. Additional resourcesare in development and will be introduced in thecoming months. In the meantime, please share thesubscriber link with family, friends, coworkers, oranyone that you believe will benefit from theinformation BMI has to offer. BMI has beendesigned for readers such as yourself. Pleaseprovide feedback on BMI, comment on articles, andfeel free to suggest topics that you would like tosee featured in upcoming issues. BMI

All the best,

Robert L. DoughertyPublisher, BMI

Editorial Advisory Board

BM

I

CLINICAL EDITOR

Raul J. Rosenthal, MD, FACSProgram Director of Minimally InvasiveSurgery, Director of the Minimally InvasiveFellowship Program, Director of theBariatric Institute, and Director of GeneralSurgery Residency Program, ClevelandClinic Florida—Weston, Fort Lauderdale,Florida

EDITORIAL ADVISORY BOARD

Susan Gallagher Camden, RN PhD WOCN,CBN, HCRM CSPHPSenior Clinical Advisor, CelebrationInstitute, Inc., Houston, Texas

Tracy Martinez, RN, BSN, CBNProgram Director, Wittgrove BariatricCenter, La Jolla, California

Melodie K. Moorehead, PhD, ABPPBoard Certified in Clinical HealthPsychology, JFK Medical Center, BariatricWellness and Surgical Institute, Atlantis,Florida

Harry Pino, PhDDirector of Clinical Exercise PhysiologyProgram, RecoverHealth Center, New York,New York; Medical Center, Stony Brook, NewYork

Craig B. Primack, MD, FAAPMedical Bariatrician/Certified MedicalObesity Specialist/Co-Medical Director,Scottsdale Weight Loss Center PLLC,Scottsdale, Arizona

Wendy Scinta, MD, MS, FAAFP, FASBPMedical Director, Medical Weight Loss of NY,BOUNCE Program for Childhood Obesity,Manilus, New York; Clinical AssistantProfessor of Family Medicine, UpstateMedical University, Syracuse, New York

Kimberley E. Steele, MD, FACS,Assistant Professor of Surgery, The JohnsHopkins Center For BariatricSurgery,Baltimore, Maryland

Christopher D. Still, DO, FACN, FACPDirector, Center for Nutrition and WeightManagement, Geisinger Health System,Danville, Pennsylvania


Winter 2012 Volume 1, Issue 1

Table of Contents

The Obesity Action Coalition:

The Voice of Those Affected by Obesity 18

Treatment Considerations for Osteoarthritic

Knee Pain in Patients with Obesity 20

Hair Loss Among Weight Loss

Surgery Patients 25

Weight Loss Surgery Preoperative Risk

Reduction 14

BMI BODY MIND INSPIRATION EDITORIAL STAFF

Editor

Raul J. Rosenthal, MD, FACS

Program Director of Minimally Invasive Surgery,

Director of the Minimally Invasive Fellowship

Program, Director of the Bariatric and Metabolic

Institute, and Director of the General Surgery

Residency Program, Cleveland Clinic Florida—

Weston, Fort Lauderdale, Florida.

Vice President, Executive Editor

Elizabeth A. Klumpp

Matrix Medical Communications

West Chester, Pennsylvania

Associate Editor

Angela M. Hayes



Associate Editor

Kimberly B. Chesky



BMI BODY MIND INSPIRATION BUSINESS STAFF

President/Group Publisher

Robert L. Dougherty



Partner

Patrick D. Scullin



Vice President, Business Development

Joseph J. Morris



EDITORIAL CORRESPONDENCE should be directed to

Executive Editor, Matrix Medical Communications,

1595 Paoli Pike, Suite 103, West Chester, PA 19380.

Toll-free: (866) 325-9907; Phone: (484) 266-0702;

Fax: (484) 266-0726;

E-mail: [email protected]

ADVERTISING QUERIES should be addressed to Robert

Dougherty, President/Group Publisher, Matrix

Medical Communications,1595 Paoli Pike, Suite 103,

West Chester, PA 19380. Toll-free: (866) 325-9907;

Phone: (484) 266-0702; Fax: (484) 266-0726;

E-mail: [email protected]

1595 Paoli Pike

Suite 103

West Chester, PA 19380

BMI Body Mind Inspiration [ISSN TBD] is published

digitally four times yearly by Matrix Medical

Communications.Copyright © 2012 Matrix Medical

Communications. All rights reserved. Opinions

expressed by authors, contributors, and advertisers

are their own and not necessarily those of Matrix

Medical Communications, the editorial staff, or any

member of the editorial advisory board. Matrix

Medical Communications is not responsible for

accuracy of dosages given in the articles printed

herein. The appearance of advertisements in this

journal is not a warranty, endorsement, or approval

of the products or services advertised or of their

effectiveness, quality, or safety. Matrix Medical

Communications disclaims responsibility for any

injury to persons or property resulting from any

ideas or products referred to in the articles or

advertisements. This publication provides basic

information about a broad range or medical

conditions. It is not intended to serve as a tool for

diagnosing illness, in prescribing treatments, or as a

substitute for the physician/patient relationship. All

persons concerned about medical symptoms or the

possiblity of disease are encouraged to seek

professional care from an approprpiate healthcare

provider.

p8


mailto:[email protected]

mailto:[email protected]

Dear Editor:

This letter is in response to the an article published in The

Journal of the American Medical Association (JAMA) by

Ludwig and Murtagh entitled, “State intervention in life-

threatening childhood obesity.”1 As a frontline childhood

obesity physician, I strongly disagree with the premise of this

article.

Genetic predisposition, environment in utero, and birth

weight all affect obesity rates long before any active parenting

occurs.2 Race, ethnicity, poverty, infant feeding practices, and

the well-recognized cost disparity between healthy and less

healthy foods play a role.3 Children do not expend energy as in

the past, and school vending machines, poor-quality school

lunches, and the regrettable removal of physical education,

recess, and health education classes are also factors in this

issue.4,5

This is not to say that parents are completely defenseless to

our obesogenic environment.5 Simple changes, such as sitting

down to dinner as a family, decreasing fast food consumption,

controlling use of electronics, and modeling good behavior,

can have a significant impact on a child’s weight. But what

happens when an engaged family has made these changes and

the child remains severely obese (body mass index [BMI] at or

beyond the 99th percentile)?6 Are our only answers to put him

or her through surgery or remove the child from his or her

home?

Approximately two million children in the United States

have severe obesity,6 clearly more than an overburdened foster

care system can handle. Children with obesity are

discriminated against by peers and teachers and are bullied

relentlessly. The added insult of removing a child from his or

her home will, in most cases, do more harm than good. In

addition, with 75 percent of our society being overweight, the

chances that a child will be placed in a home where the family

members also struggle with a weight problem is more likely

than not.7

Choices do exist for a child with obesity besides

experimental surgery and state intervention. The 2007 Expert

Committee on Child and Adolescent Overweight and Obesity

(of which Dr. Ludwig was a member) developed an eloquent

algorithm that involves early identification and assessment by

primary care providers followed by prevention and treatment

by clinical obesity experts. Bariatricians and other childhood

obesity experts are in the process of rolling out these

recommendations nationally while simultaneously conducting

outcomes research, with initial results that look very

promising.

Certainly, the premise of turning a child with severe obesity

over to the state is thought provoking, but unless there are

clear signs of neglect or abuse in conjunction with the obesity,

it is unnecessary, unrealistic, and likely damaging to that child

long term.

References

1. Murtagh L, Ludwig DS. State intervention in life-threatening

childhood obesity. JAMA. 2011;306(2):206–207.

2. Zhao J, Grant SF. Genetics of childhood obesity. J Obes.

2011;2011:845148.

3. Van Cleave J, Gortmaker SL, Perrin JM. Dynamics of obesity and

chronic health conditions among children and youth. JAMA.

2010;303(7):623–630.

4. Rahman T, Cushing RA, Jackson RJ. Contributions of built

environment to childhood obesity. Mt Sinai J Med.

2011;78(1):49–57.

5. Eisenmann JC, Gundersen C, Lohman BJ, et al. Is food insecurity

related to overweight and obesity in children and adolescents? A

summary of studies, 1995–2009. Obes Rev. 2011;12(5):e73–83.

6. Skelton JA, Cook SR, Aulinger P, et al. Prevalence and trends of

severe obesity among US children and adolescents: what could

be better? Acad Peds. 2009;9(5): 322–329.

7. Hadfield SC, Preece PM. Obesity in looked after children: is

foster care protective from the dangers of obesity? Child Care

Health Dev. 2008;34(6):710–712.

With regards,

Wendy Scinta, MD, MS, FAAFP, FASBPMedical Director, Medical Weight Loss of NY, BOUNCEProgram for Childhood Obesity, Manilus, New York; Clinical Assistant Professor of Family Medicine, UpstateMedical University, Syracuse, New York BMI

Letters to the Editor

BM

I

Childhood/Adolescent Obesity

and State Intervention: Parents

Not Solely to Blame in the Battle


Weight loss surgery is growing in popularity.

According to the American Society for Metabolic

and Bariatric Surgery (ASMBS), there were

220,000 bariatric surgeries performed in 2008 and this

number is on the rise. Considering that approximately

five percent of American adults meet the criteria for

morbid obesity, a large pool of surgical candidates

remain.1 As more operations are being performed and the

morbidity and mortality statistics of these surgeries

remain favorable, older and sicker patients may be

finding their way to the bariatric surgeon’s office. These

patients are considered to be at higher risk for

complications, since age and the presence of medical

comorbidities, along with male gender, body mass index

(BMI), and fat distribution, have been identified among

the factors that negatively impact the safety of the

operation. Of these factors, few can be altered except

BMI and fat distribution.

Physicians can choose to operate on higher risk

patients by modifying the procedure, perhaps by

performing a sleeve instead of, or prior to, a Roux-en-Y

gastric bypass (RYGB).

Another option for bariatric programs to deal with

higher risk candidates is by recommending, or in some

cases mandating, weight loss prior to undergoing weight

loss surgery. Some surgery centers recommend

preoperative weight reduction for all of their patients, for

the reasons listed in Tables 1 and 2

BENEFITS TO PREOPERATIVE WEIGHT LOSSThe liver, operative time, and length of stay. A

number of studies have found benefits to preoperative

weight loss. Liu et al2 compared patients who did and

who did not lose weight before surgery and found that

those who lost weight were more likely to undergo

surgery that did not deviate from the standard RYGB

operation. Additionally, patients who did not lose weight

were more likely to have their surgeon comment that the

patients’ livers were enlarged. The authors did not find

differences in operative time, length of stay, major

complications, or wound infections between the groups.

There are a number of studies that look at the effects

of weight loss on the liver. Benjaminov et al3 found a

reduction in liver volume of 8.1 percent, as well as a

nonobjective observation by surgeons that this facilitated

surgery, in patients who lost weight in the four weeks

prior to surgery. In the six weeks prior to surgery, Lewis

et al4 accomplished an even greater reduction in mean

liver volume of 14.7 percent, as well as a 43-percent

decrease in mean liver fat. Both a reduction in liver size

Body • Mind • Inspiration

BM

I


Weight Loss before

Weight Loss

Surgery: What Do We

Know About Dropping

Those Preoperative

Pounds?

by Liz Goldenberg, MPH, RD, CDN

Ms. Goldenberg is from New-York Presbyterian Hospital, Weill Cornell College of Medicine of

Cornell University, Department of Surgery, New York, New York.

This article reviews the issues surrounding weight loss before surgical weight loss, and aims to answer the questions that

weight loss surgery centers might have when making decisions about including a preoperative weight loss component in their

surgical programs.


BM

I


and operative time was achieved in a small group of

patients who lost an average of 4.8kgs, also in a six-week

time frame prior to surgery.5 Operative times were found

to be a highly significant 36 minutes shorter in 62 out of

90 patients who were able to lose more than five percent

of their preoperative weight.6 Still et al1 calculated that

length of stay was less likely to be greater than four days

in high-risk patients who were able to lose 5 to 10

percent of their excess weight before undergoing RYGB.

It has been pointed out that high-risk patients may

experience a greater benefit from preoperative weight

loss.15

Overall complications. The overall major

complication and mortality rates of bariatric surgery are

quite low, less than 3.0 percent and 0.3 percent,

respectively. Studies have shown mixed results as to

whether preoperative weight loss lessens postoperative

complications. Not only have some studies been unable

to find fewer complications for those that lost,6,7 but in

one study8 even preoperative weight gain did not

negatively impact complication rates.

However, considering the low overall complication

rates of bariatric surgery, among the criticisms of these

studies are that they involved inadequate sample sizes of

200 patients or less. Benotti et al9 reviewed the records

of 881 RYGB patients for categories of complications

including the following: respiratory issues, bleeding,

gastrointestinal issues, feeding intolerance, cardiac

issues, leakage, infection, thromboembolism, acute renal

failure, urinary issues, wound issues, and stricture. The

reviewers found statistically significant trends that

confirmed a diminishing likelihood of any complication

with increasing preoperative weight loss.

Impact on postoperative weight loss. There has

been some conflicting data as to whether successful

weight loss preoperatively will translate into more

successful postoperative weight loss. In 2005, Alvarado

et al6 reported that preoperative weight loss was

associated with greater weight loss at one year

postoperatively, specifically an increase of one percent of

preoperative weight loss for a 1.8-percent increase after

surgery. This occurred despite the fact that 83 percent of

the patients in the study failed to achieve the

recommended 10-percent weight loss. In 2008, Alger-

Mayer et al10 described a more successful weight loss

achievement, as well as a significant correlation between

weight lost before and at three years after surgery. One-

hundred and fifty patients who were advised to lose 10

percent of their initial presenting weight were able to

realize a 9.5±6.8-percent loss before undergoing gastric

bypass. The authors attribute their positive results to the

implementation of physical activity and positive dietary

changes early, and they point out that their patients

credit their success to the same factors. Another possible

explanation is that those patients who were able to

achieve greater weight loss before surgery are the same

patients who are more likely to follow up and adhere to

the guidelines afterwards. A review article by Livhits et

al11 compiled data from 15 different papers comparing

weight loss before and after surgery. This large synopsis

came to the same conclusion that preoperative weight

loss results in greater total postoperative weight loss.

Contrary to the collection of studies mentioned

previously are papers by Jantz et al12 and Ochner et al.13

In 2009, Jantz et al12 failed to find a correlation between

the percentage of excess weight loss (EWL) at one year

postoperatively and the maximum amount of weight loss

achieved prior to surgery. However, this was looking at

self-reported weight loss and did not necessarily occur in

the short period of time prior to surgery. In an even more

recent paper published in Obesity in February 2010,

Ochner et al13 found that more weight gain was predictive

of more weight loss after surgery. This study only looked

at the three-month postoperative visit and, perhaps more

importantly, compared patients who were mandated to

undergo a six-month, physician-supervised weight loss

program prior to surgery to those who did have this

requirement. On average, more than 75 percent of

patients in both groups gained weight before surgery.

TABLE 1. Weight loss before weight loss surgery

WEIGHT LOSS BEFORE WEIGHT LOSS SURGERY HAS BEEN LINKED TO

Co-morbidity reduction

Improved patient selection• Those who cannot lose weight before will not be successful after?

• Those who comply with the program before will comply with the

after-surgery follow up, diet, and exercise guidelines?

More successful weight loss postoperatively

Technically easier, safer surgery with lower complication rates

TABLE 2. Questions that a center might ask

Are there benefits? What are they?

Are there drawbacks? What are they?

How do insurance carrier-mandated weight loss requirements impactour patients and our program?

How can the weight loss be accomplished?

How much weight should be lost?


BM

I


Surprisingly, at three months postoperatively, these same

“gainers” had lost more weight than those who has lost

weight prior to their operation. Authors propose that diet

fatigue or the “last supper syndrome,” which occurs

when patients intentionally over-eat, or binge on their

favorite foods for fear that they will miss this habit or

these foods after surgery, may be responsible. This

binge-eating behavior is squelched postoperatively by the

new, tiny pouch. Finally, the authors point out that the

biological set-point theory may play a role in why

patients who lose more weight prior to surgery lose less

after.

DRAWBACKS TO PREOPERATIVE WEIGHT LOSS ORPREOPERATIVE WEIGHT LOSS PROGRAMS

While there is some trepidation over the safety of

encouraging rapid weight loss in patients who are months

or weeks away from major surgery, this author is

unaware of any negative clinical outcome reports.

Nevertheless, there are a handful of drawbacks to

consider by a surgery center looking to implement this

type of program. One downside is the cost to the

program in staffing and other resources. The programs

are usually administered by registered dietitians,

physicians who are part of a medical weight loss arm of

the program, or, in some programs, surgeons or

gastroenterologists who may place a device, such as an

intragastric balloon. While programs usually include an

exercise component to them, few studies mention the

utilization of a trained exercise specialist.

Another possible deterrent may be the concern of

patients dropping out of the program. A well-designed

preoperative weight loss program may go on for as little

as two weeks or as long as six months, which is a

significant delay. Programs may argue that delaying

surgery may deter patients from ultimately having the

surgery. Alami et al7 discuss this fear but did not find a

delay; the times from consultation to operation

(approximately five months) were similar in the groups

that did and did not undergo a preoperative weight loss

program. One patient in this study left to have surgery at

a center that did not have this requirement.

Weight loss attempts required by insurance

carriers versus the surgeon. Insurance-mandated

preoperative weight loss programs have become a routine

delay. Preoperative weight loss interventions are

assumed to improve outcomes by increasing weight loss

and subsequently the positive aspects of weight

reduction. Many feel that these programs are meant to be

a test of patients’ motivation.

Two studies aimed to

challenge the merit of this

prerequisite by comparing

sets of patients who were

required to undergo an

insurance-mandated

preoperative program with

those who did not have this

requirement. Researchers in one study reported that 28

percent of patients commanded to follow the registered

dietitan-supervised 13-week program dropped out of the

program, as compared to only 19 percent of the group

free from this requirement.14 Both groups were more

likely to gain versus lose weight prior to surgery. Both

groups had similar total weight loss at one year, yet the

patients who did not have the mandated delay achieved a

greater percentage of EWL that was significant at the

one-year mark. The recent study in Obesity by Olchner

et al13 came to a similar conclusion when comparing

groups of patients with or without insurance

requirements.13 The 94 patients who had to fulfill the

requirement gained weight preoperatively; an average of

2.9±4.4 percent of their initial body weight.

Olchner et al propose that some patients fear that

successful weight loss may lead to insurance denial for

the surgery. Both studies accused insurance-required

programs of being obstacles to patient access to surgical

treatment of obesity, in addition to not being effective at

bringing about preoperative weight loss.

In contrast to the studies by Olchner et al13 and Jamal

et al,14 the 150 patients in the study by Alger-Mayer et

al10 were required by their surgeon and not by their

insurance carrier to undergo a diet and exercise

program. All patients that wished to undergo surgery at

this practice, regardless of presenting BMI, were

expected to follow the program and lose 10 percent of

their initial documented weight. Instead of a 28-percent

drop out rate, reportedly only one of their patients left to

go to another practice that did not require preoperative

weight loss.

PREOPERATIVE WEIGHT LOSS METHODSMany patients with obesity seeking weight loss surgery

are actually quite adept at losing weight. They are able to

take off the weight for a short period, usually through

diet and/or exercise, but then find themselves

rebounding, gaining back part, all, or even more weight

than they initially lost. Others find that the difficulty

occurs when they reach that plateau of 10, 20, or 50

pounds and the scale is at a stand-still. On the other

Insurance-mandated preoperative weight loss programs have

become a routine delay. Preoperative weight loss interventions

are assumed to improve outcomes by increasing weight loss and

subsequently the positive aspects of weight reduction.


BM

I

hand, some patients have never in their lives successfully

lost weight. Regardless of the history, patients who

appear in the surgeon’s office can become a highly

motivated bunch if told by the surgeon that they will not

be operated on unless they lose weight beforehand. As

described previously, aside from or in addition to

surgeons making these demands on patients, many

insurance providers place demands on doctors to

supervise their patients’ weight loss efforts in order for

them to get coverage. However, most health insurance

plans do not specify any particular type of program for

providers to follow. As surgical programs looking to

accomplish preoperative weight loss, what are the

options?

Diets, medication, and a device. Dieting is the

method of weight loss most often cited in studies that

look at weight loss prior to surgery. This could be

because most weight loss surgery programs already have

dietitians either as part of their team or as consultants

who carry out preoperative evaluations (as required to

fulfill National Institutes of Health [(NIH)] criteria, by

insurance companies, and for ASMBS Centers of

Excellence [(COE)] or American College of Surgeons

[(ACS)] Bariatric Surgery Center Network [(BSCN)]

certification). As pointed out previously, few programs

have exercise experts on their teams, probably because

they are not required by the above organizations. Yet

plenty of evidence backs the synergism of diet plus

exercise, or the effects of an entire multidisciplinary

team including these providers previously noted along

with psychologists or behavioral therapists, in bringing

about weight loss.

The diets that have reportedly been used for bringing

about preoperative weight loss range from a vague

“healthy balanced diet,” to a strict very low-calorie,

liquid diet,2,4 to a very low carbohydrate (30g) diet,3 to a

highly involved and resource-consuming, supervised 11-

week inpatient weight loss program.15

Which type of diet is the most effective is the topic of

another paper, but there are two common denominators

to be found among the conclusions to studies that

compare the efficacy of various weight loss diets. The

first is that those who stay on the diet lose the most

weight, and the second is that patients who have a say in

which diet they follow (versus having to follow a diet

that is chosen for them) will be more successful.16,17 One

can see how these two suggestions are interdependent. A

final point on choice of diet is that although these may

seem to be common-sense recommendations, they can be

easily overlooked by programs that routinely use

standard diet plans and thus fail to individualize plans

according to patients’ preferences.

One study5 looked at the effectiveness of sibutramine

(Abbott Laboratories, North Chicago, Illinois) in

preoperative weight loss. Twenty patients received 15mg

of this medication once daily for six weeks, while another

20 patients did not. The medication group lost 4.8kg

while the control group gained 7.0kg and spent an

additional 20 minutes in the operating room when

compared to the patients who took sibutramine.

There are two reports on the use of an intragastric

balloon for preoperative weight loss.18,19 Thirty-one and

75 patients achieved 22 and 16-percent EWL,

respectively, after the device was implanted for at least

six months. There was no operative mortality and only

two patients in each of the studies suffered from

intolerance and had to have the balloon removed soon

after implantation.

HOW MUCH WEIGHT SHOULD BE LOST?There is a scarcity of data comparing the pros and

cons of how much weight should be lost. Though

insurance companies often mandate that the attempt

must be made, they rarely make specific

recommendations as to the amount of weight loss.13 This

is likely because it is difficult to draw conclusions from

existing data. One reason for the difficulty is that a

standard definition for how to report weight loss is

lacking. Some studies report on total weight loss or

percentage of total weight loss, while others use EWL or

percentage of EWL, and still others use excess BMI loss.

Another issue is a lack of prospective, randomized trials;

most papers are retrospective reviews.20

Many papers support 5- to 10-percent total weight loss

or the same amount of excess weight loss as a desirable

goals.1,7,11 Evidence for this goal is seemingly derived from

studies that link this range of weight loss to significant

reductions in obesity-related comorbidities. Most would

agree that more quality data are needed in order to draw

evidence-based conclusions on the ideal amount of

weight loss that should be recommended.

Even if studies were forthcoming, realistic versus

optimistic weight loss is an important distinction in this

group. Patients who are typically 100 or more pounds


Many patients with obesity seeking weight loss surgery are actually quite adept at losing

weight. They are able to take off the weight for a short period, usually through diet and/or

exercise, but then find themselves rebounding, gaining back part, all, or even more

weight than they initially lost.

away from their ideal body weight and have a history of

“failed” dieting attempts will continue to be challenged

by the irony of trying to lose weight before undergoing

an operation that will give them help to achieve the same

result.

CONCLUSION

In summary, whether programs should suggest or

require weight loss before weight loss surgery and

whether it should be for all patients or only for select

groups, such as high-risk patients, will probably continue

to be a controversial decision to make. Barring any

mandates from insurance carriers or accreditation

programs, surgery centers will likely continue to decide

for themselves whether it is in theirs, and of course their

patients’ best interests to promote the dropping of those

preoperative pounds.

REFERENCES

1. Still CD, Benotti P, Wood GC, et al. Outcomes of

preoperative weight loss in high-risk patients undergoing

gastric bypass surgery. Arch Surg.

2007;142(10):994–998.

2. Liu RC, Sabnis AA, Forsyth C, Chand B. The effects of

acute preoperative weight loss on laparoscopic Roux-en-Y

gastric bypass. Obes Surg. 2005;15(10):1396–1402.

3. Benjaminov O, Beglaibter N, Gindy L, et al. The effect of

a low-carbohydrate diet on the nonalcoholic fatty liver in

morbidly obese patients before bariatric surgery. Surg

Endosc. 2007;21(8):1423–427.

4. Lewis MC, Phillips ML, Slavotinek JP, et al. Change in

liver size and fat content after treatment with Optifast

very low calorie diet. Obes Surg. 2006;16(6):697–701.

5. Aberle J, Freier A, Busch P, et al. Treatment with

sibutramine prior to Roux-en-Y gastric bypass leads to an

improvement of metabolic parameters and to a reduction

of liver size and operative time. Obes Surg.

2009;19(11):1504–1507.

6. Alvarado R, Alami RS, Hsu G, et al. The impact of

preoperative weight loss in patients undergoing

laparoscopic Roux-en-Y gastric bypass. Obes Surg.

2005;15(9):1282–1286.

7. Alami RS, Morton JM, Schuster R, et al. Is there a benefit

to preoperative weight loss in gastric bypass patients? A

prospective randomized trial. Surg Obes Relat Dis.

2007;3(2):141–145; discussion 145–146.

8. Harnisch MC, Portenier DD, Pryor AD, et al. Preoperative

weight gain does not predict failure of weight loss or co-

morbidity resolution of laparoscopic Roux-en-Y gastric

bypass for morbid obesity. Surg Obes Relat Dis.

2008;4(3):445–450.

9. Benotti PN, Still CD, Wood GC, et al. Preoperative weight

loss before bariatric surgery. Arch Surg.

2009;144(12):1150–1155.

10. Alger-Mayer S, Polimeni JM, Malone M. Preoperative

weight loss as a predictor of long-term success following

Roux-en-Y gastric bypass. Obes Surg.

2008;18(7):772–775.

11. Livhits M, Mercado C, Yermilov I, et al. Does weight loss

immediately before bariatric surgery improve outcomes: a

systematic review. Surg Obes Relat Dis.

2009;5(6):713–721.

12. Jantz EJ, Larson CJ, Mathiason MA, et al. Number of

weight loss attempts and maximum weight loss before

Roux-en-Y laparoscopic gastric bypass surgery are not

predictive of postoperative weight loss. Surg Obes Relat

Dis. 2009;5(2):208–211.

13. Ochner CN, Puma LM, Raevuori A, et al. Effectiveness of

a prebariatric surgery insurance required weight loss

regimen and relation to postsurgical weight loss. Obesity

(Silver Spring). 2010;18(2):287–292.

14. Jamal MK, DeMaria EJ, Johnson JM, et al. Insurance-

mandated preoperative dietary counseling does not

improve outcome and increases dropout rates in patients

considering gastric bypass surgery for morbid obesity.

Surg Obes Relat Dis. 2006;2(2):122–127.

15. Huerta S, Li Z, Anthony T, Livingston EH. Feasibility of a

supervised inpatient low-calorie diet program for massive

weight loss prior to RYGB in superobese patients. Obes

Surg. 2010;20(2):173–180.

16. Brehm BJ, D’Alessio DA. Weight loss and metabolic

benefits with diets of varying fat and carbohydrate

content: separating the wheat from the chaff. Nat Clin

Pract Endocrinol Metab. 2008;4(3):140–146.

17. Dansinger ML, Gleason JA, Griffith JL, et al. Comparison

of the Atkins, Ornish, Weight Watchers, and Zone diets

for weight loss and heart disease risk reduction: a

randomized trial. JAMA. 2005;293(1):43–53.

18. Frutos MD, Morales MD, Luján J, et al. Intragastric

balloon reduces liver volume in super-obese patients,

facilitating subsequent laparoscopic gastric bypass. Obes

Surg. 2007;17(2):150–154.

19. Mills S, Bassona S, Cornisha J, et al. Intragastric balloon

use to reduce weight before bariatric surgery. Surg Obes

Relat Dis. 2010;6(2):224.

20. Tarnoff M, Kaplan LM, Shikora S. An evidenced-based

assessment of preoperative weight loss in bariatric

surgery. Obes Surg. 2008;18(9):1059–1061. BMI


BM

I



BM

I


Obesity remains a growing and ongoing problem in

the United States. While recent reports have

shown obesity rates have stabilized, severe classes

of obesity are on the rise,1 having important implications

in regard to treatment. Weight loss surgery remains a

durable treatment for obesity, effectively resulting in

remission of many obesity-related conditions.2 In

addition, recent reports have

demonstrated a mortality benefit

in patients who have had

bariatric surgery.3 As a

result, weight loss

surgeries are on the rise.

Studies have shown a

five-fold increase in the

number of bariatric

surgeries between 1998

and 2003.4 The number

of weight loss surgeries

performed in the United

States has increased in all

groups despite age,

income, or insurance status

or type. However, this elective

surgery is not without

complications. Surgeon experience appears

to be a significant predictor of postoperative morbidity

and mortality,5 however, patient-inherent risks have also

been identified. While studies have been conflicting, age,

smoking history, superobesity, and certain comorbidities

are factors implicated in increasing morbidity and

mortality with bariatric surgery.6–8 One validated risk

score identified five perioperative variables that

predicted 30-day mortality. These variables include

superobesity, male gender, hypertension, age greater

than 45, and risk factors for pulmonary embolism,

including obstructive sleep apnea. Patients who had 4 to

5 of the above risk factors had a 12-fold greater (2.4%)

30-day mortality than patients who had none to one risk

factor (0.2%).8 Certain high-risk patient groups may

benefit from optimizing their medical status prior to

weight loss surgery through medical nutritional therapy

and preoperative weight loss.

DIABETESThe relationship between type 2 diabetes and obesity

is well documented as the incidence of diabetes

increases incrementally with rising body mass index

(BMI).9,10 Recent guidelines recommend long-term

glycemic control with HbA1c of 7.2 percent or less prior

to bariatric surgery.11 While pharmacotherapy is

appropriate, medical nutritional therapy remains the

mainstay of treatment. Studies have shown weight loss of

as little as 5 to 10 percent results in effective reduction

of fasting blood glucose and HbA1c. In one study,12

weight loss of up to 14 percent resulted in a two-point

Weight Loss

Surgery

Preoperative

Risk Reduction

by Adrienne Youdim, MD

The presence ofhypertension is asignificant risk factorfor perioperativecomplications.14

Validated risk scoreshave demonstratedhypertension to beassociated with higher30-day mortalityfollowing bariatricsurgery...8

Dr. Youdim is Medical Director, Comprehensive Weight Loss Center, Cedars Sinai Medical

Center, Los Angeles, California, and Assistant Clinical Professor of Medicine, David Geffen

School of Medicine, University of California Los Angeles, California.


BM

I

reduction in HbA1c, comparable to targets achieved by

pharmacotherapy.12 Given the favorable effect of modest

weight loss on glycemic control, preoperative weight loss

should be used to achieve glycemic targets in bariatric

surgery patients.

HYPERTENSIONObesity is associated with other cardiometabolic

conditions, including hypertension. Mechanisms of this

association are multifactorial and include secretion by

adipocytes of many proteins of the renin-angiotensin

system, the pathway that mediates hypertension through

sodium and water reabsorption and increased vascular

tone.13 The presence of hypertension is a significant risk

factor for perioperative complications.14 Validated risk

scores have demonstrated hypertension to be associated

with higher 30-day mortality following bariatric surgery,8

and guidelines recommend optimal hypertensive control

prior to bariatric surgery.11 Modest weight loss has been

shown to reduce both systolic and diastolic blood

pressure. Prior studies have shown reductions in blood

pressure of 1mmHg per kilogram weight loss.15 A more

recent systemic review16 suggests that for 10kg weight

loss there is a 4.6mmHg and 6.0mmHg reduction in

diastolic and systolic blood pressure, respectively.16

Moreover, change in macronutrient intake to reduce

sodium and increase fruits, vegetables, and limit

saturated fats can itself result in reductions in blood

pressure independent of weight loss.17 While

pharmacotherapy is often necessary to control

hypertension, medical nutritional therapy and

preoperative weight loss is a useful adjunct to optimize

hypertensive control in patients with morbid obesity.

OBSTRUCTIVE SLEEP APNEAConcomitant obstructive sleep apnea (OSA) is

frequently present in the patient population with morbid

obesity. Obesity is a leading cause of OSA, and a 10-

percent increase in BMI results in a 32-percent increase

in apnea-hypopnea index (AHI). A diagnosis of OSA is an

independent risk factor for 30-day morbidity and

mortality following bariatric surgery.18,19 Surgical patients

with OSA are vulnerable to the effects of sedation,

anesthesia, and analgesia. Patients with OSA have been

shown to have a higher number of postoperative

complications, including but not limited to respiratory

complications, and patients with more severe OSA

(higher AHI or more significant oxygen desaturations)

can be at greater risk for these complications.20 Modest

weight loss can result in significant improvements in

OSA. In one study,21 an average weight loss of 13.5

percent at 6 and 12 months resulted in reduction of the

oxygen desaturation index (desaturation events per hour

of sleep exceeding 4% from baseline) by 28 and 26

points, respectively. Modest weight reduction will

improve OSA and may optimize patient-inherent risk

related to OSA prior to bariatric surgery.

SUPEROBESITYSuperobesity, as defined by a BMI of 50kg/m2 or

greater, has consistently been implicated in increasing

surgical risk with bariatric surgery.6–8,18,22 In one study,22

BMI ?50kg/m2 was independently associated with higher

30-day mortality with an odds ratio of 3.6. Additionally,

preoperative weight loss of 5 to 10 percent has been

associated with more rapid postoperative weight loss and

greater one-year excess weight loss (EWL).23–24 This may

be particularly relevant to a patient with super obesity

who requires a greater overall weight loss to achieve

normal BMI.

PREOPERATIVE WEIGHT LOSSStudies have specifically evaluated the effect of

preoperative weight loss prior to bariatric surgery.

Studies25,26 have shown preoperative weight loss resulted

in reduced liver size and visceral fat. In one study,25 4.1-

percent weight loss resulted in 5.1-percent mean

reduction in liver size and fat. In another study,26 patients

who participated in a 12-week very low energy diet

(VLED) lost an average of 11 percent (80% of which

occurred in the first two weeks of the dietary

intervention) and achieved 28.7- and 24.1-percent

reduction in liver size and visceral adipose tissue,

respectively. Smaller liver size and reduced visceral

adiposity may improve technical feasibility of the

surgery. In a study by Liu et al,27 preoperative weight loss

resulted in a reduced likelihood to encounter an enlarged

liver and reduced likelihood of deviating from standard

operative procedure. Specifically, average weight loss of

3.3kg resulted in a 17-percent reduction in the number

of cases that deviated from standard operation, including

use of additional trocars and conversion to an open

procedure during laparoscopic Roux-en-Y gastric bypass

(RYGB) surgery.27

Preoperative weight loss has also been associated with

reduced probability of surgical complications after

gastric bypass surgery, particularly in open gastric

bypass. In one study,28 EWL of up to 10 percent resulted

A diagnosis of OSA is an independent risk factor for 30-day morbidity and mortality following bariatric

surgery.18,19 Surgical patients with OSA are vulnerable to the effects of sedation, anesthesia, and analgesia.



BM

I


in reduced major and minor complications. Statistically

significant trends revealed reduced likelihood of any

complication with increasing preoperative weight loss for

the entire cohort of 881 patients (p=0.004) and for those

who underwent open gastric bypass (p=0.02). This

relationship was preserved after adjusting for age, BMI,

number of comorbidities, and type of surgery. In

addition, the degree of weight loss was significant in the

reduction of complications. When compared to those who

lost 10 percent or more excess body weight (EBW),

those who gained five percent or more EBW had a two-

fold increased likelihood of a complication.28 Patients who

underwent preoperative weight loss have also shown

reduced intraoperative blood loss, shorter operative

times,27,29 and reduced length of hospital stay,23 which may

have important implications in resource utilization and

reducing cost of surgery.

CONCLUSIONS

Bariatric surgery remains safe and effective for the

treatment of obesity with recent studies placing 30-day

mortality at 0.03 percent.18 Determining patient-inherent

risk factors allows clinicians to appropriately advise

patients of individual surgical risk and to optimize that

risk when possible prior to surgery. Several studies have

identified patient-inherent variables that portend higher

morbidity and mortality with bariatric surgery.

Superobesity and certain comorbidities, including

diabetes, OSA, and hypertension, are factors implicated

in increasing surgical risk. Routine preoperative weight

loss may not be indicated in all weight loss surgery

patients given low overall complication rates, but may be

of benefit in the higher-risk patient population.

REFERENCES

1. Sturm R. Increases in clinically severe obesity in the United

States: 1986–2000. Arch Intern Med. 2003;163(18):2146–2148.

2. Sjöström L, Lindroos AK, Peltonen M, et al. Lifestyle, diabetes,

and cardiovascular risk factors 10 Years after bariatric surgery. N

Engl J Med. 2004;351:2683–2693.

3. Adams TD, Gress RE, Smith SC, et al. Long-term mortality after

gastric bypass surgery. N Engl J Med. 2007;357:753–761.

4. Santry HP, Gillen DL, Lauderdale DS. Trends in bariatric surgical

procedures. JAMA. 2005;294:1909–1917.

5. Flum DR, Dellinger EP. Impact of gastric bypass operation on

survival: a population-based analysis. J Am Coll Surg.

2004;199:543.

6. Livingston EH, Arterburn D, Schifftner TL, et al. National surgical

quality improvement Pprogram analysis of bariatric operations:

modifiable risk factors contribute to bariatric surgical adverse

Outcomes. J Am Coll Surg. 2006;203(5):625–633.

7. Lautz DB, Jackson TD, Clancy KA, et al. Bariatric operations in

veterans affairs and selected university medical centers. J Am

Coll Surg. 2007;204:1261–1272.

8. DeMaria EJ, Murr M, Byrne TK, et al. Validation of the obesity

surgery mortality risk score in a multicenter study proves it

stratifies mortality risk in patients undergoing gastric bypass for

morbid obesity. Ann Surg. 2007;246(4):578–582.

9. Chan JM, Rimm EB, Colditz GA, et al. Obesity, fat distribution

and weight gain as risk factors for clinical diabetes in men.

Diabetes Care. 1994;17:961–969.

10. Colditz GA, Willett WC, Rotnitzky A, Manson JE.. Weight gain as

a risk factor for clinical diabetes mellitus in woman. Ann Intern

Med. 1995;122:481–486.

11. Mechanick JI, Kushner RF, Sugerman HJ, et al. American

Association of Clinical Endocrinologists, The Obesity Society, and

American Society for Metabolic & Bariatric Surgery Medical

guidelines for clinical practice for the perioperative nutritional,

metabolic, and nonsurgical support of the bariatric surgery

patient. Endocr Pract. 2008;14 Suppl 1:1–83.

12. Wing RR, Koeske R, Epstein LH, et al. Long-term effects of

modest weight loss in type II diabetic patients. Arch Intern Med.

1987;147(10):1749–1753.

13. Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J

Clin Endocrinol Metab. 2004;89(6):2548–2556.

14. Watson K. Surgical risk in patients with metabolic syndrome:

Focus on lipids and hypertension. Curr Cardiol Rep.

2006;8(6):433–438.

15. Neter JE, Stam BE, Kok FJ, et al. Influence of weight reduction

in blood pressure: a metal-analysis of randomized controlled

trials. Hypertension. 2003;42:878–884.

16. Aucott L, Poobalan A, Smith WC, et al. Effects of weight loss in

overweight/obese individuals and long-term hypertension

outcomes: A systemic review. Hypertension. 2005;45:1035–1041.

17. Appel LJ, Sacks FM, Carey VJ, et al. Effects of protein,

monounsaturated fat, and carbohydrate intake on blood pressure

and serum lipids: results of the OmniHeart randomized trial.

JAMA. 2005;294:2455–2464.

18. Flum DR, Belle SH, King WC, et al. The Longitudinal Assessment

of Bariatric Surgery (LABS) Consortium. Perioperative safety in

the longitudinal assessment of bariatric surgery. N Engl J Med.

2009;361:445–454.

19. Flancbaum L, Belsley S. Factors affecting morbidity and mortality

of Roux en-Y gastric bypass for clinically severe obesity: an

analysis of 1,000 consecutive open cases by a single surgeon. J

Gastrointest Surg. 2007;11:500–507.

20. Chung SA, Yuan H, Chung F. A systemic review of obstructive

sleep apnea and its implications for anesthesiologists. Anesth

Analg. 2008;107:1543–1563.

21. Romero-Corral A, Caples SM, Lopez-Jimenez F, Somers VK.

Interactions between obesity and obstructive sleep apnea:

Implications for treatment. Chest. 2010;137(3):711–719.

22. DeMaria EJ, Portenier D, Wolfe L. Obesity surgery mortality risk

score: proposal for clinically useful score to predict mortality risk

in patients undergoing gastric bypass. Surg Obes Relat Dis.

2007;3:34–40.

23. Still CD, Benotti P, Wood GC, et al. Outcomes of preoperative

weight loss in high-risk patients undergoing gastric bypass


BM

I

surgery. Arch Surg. 2007;142(10):994–998.

24. Solomon H, Liu GY, Alami R, et al. Benefits to patients choosing

preoperative weight loss in gastric bypass surgery: New results of

a randomized trial. J Am Coll Surg. 2009;208:241–245.

25. Fris RJ. Preoperative low energy diet diminishes liver size. Obes

Surg. 14;1165–1170.

26. Colles SL, Dixon JB, Marks P, et al. Preoperative weight loss with

a very-low-energy diet: quantitation of changes in liver and

abdominal fat by serial imaging. Am J Clin Nutr.

2006;84(2):304–311.

27. Rockson CL. Pre-operative weight loss and intraoperative

outcomes. Obes Surg. 2005;15:1396–1402.

28. Benotti PN, Still CD, Wood GC, et al. Preoperative weight loss

before bariatric surgery. Arch Surg. 2009;144(12):1150–1155.

29. Alvarado R, Alami RS, Hsu G, et al. The impact of preoperative

weight loss in patients undergoing laparoscopic Roux-en-Y

gastric bypass. Obes Surg. 2005;15;(9):1282–1286. BMI


A MEMBERSHIP ORGANIZATIONThe Obesity Action Coalition (OAC) is a membership

organization. We have three levels of membership; one

for individuals and two for organizations and companies

that would like to support the OAC. Individual

membership benefits include the following:

• Official membership card and welcome letter

• A subscription to the OAC’s official publication titled,

Your Weight Matters

• Subscriptions to Obesity Action Alert and OAC

Members Make a Difference e-Newsletters

• Advocacy alerts

• “Bias Busters” alerts

• The ability to lend your voice to the cause of fighting

obesity

Membership in the OAC also qualifies you to purchase

one of our “educational add-ons.” These “educational

add-on” packages allow you to order OAC educational

resources in bulk. There are three different packages

available, based on the number of materials an individual

is interested in ordering. To learn more about OAC

membership, please visit www.obesityaction.org/

membership/overview.php.

EDUCATIONThe OAC offers a wide variety of free educational

resources on obesity, severe obesity, and childhood

obesity, as well as resources on the consequences and

treatments of the disease. One of our most popular

educational resources is our quarterly publication, Your

Weight Matters. This publication is geared toward

individuals affected by obesity and contains a wide

variety of educational and advocacy information. Each

issue features information on a broad range of weight-

related topics and includes features on weight-loss

surgery, obesity-related conditions, childhood obesity,

nutrition, current advocacy news, and much more. To

learn more about the OAC’s educational resources, please

visit www.obesityaction.org/educationaltools

/brochuresandguides.php.

Other educational materials available include the

following:

• Understanding Obesity brochure series

• Understanding Obesity

• Understanding Severe Obesity

• Understanding Childhood Obesity

• Understanding Obesity Stigma

• Understanding Childhood Obesity poster

• Understanding Obesity poster

• Understanding Excess Weight and Type 2

Diabetes brochure series

• Understanding Excess Weight and its Role in

Type 2 Diabetes

• Understanding Prediabetes and Excess Weight

• Understanding Excess Weight and Type 2

Diabetes

• OAC Insurance Guide: Working with Your

Insurance Provider


BM

I


THE OBESITY

ACTION COALITION:

The Voice of those

Affected by Obesity

by Joe Nadglowski

JOE NADGLOWSKI, President and CEO of the Obesity Action Coalition

The Obesity Action Coalition is a registered 501(c)3 nonprofit organization founded in 2005. The Obesity Action Coalition is the only nonprofit whose sole focus is representing thoseaffected by obesity through education, advocacy, and support.

http://www.obesityaction.org/educationaltools

http://www.obesityaction.org/membership/overview.php



BM

I


ADVOCACYThe OAC conducts a variety of advocacy efforts

throughout the United States on both the federal andstate level, and encourages individuals to becomeproactive advocates. The primary focus of our advocacyefforts is improving access to obesity treatments. Arecent advocacy victory that the OAC was involved inwas the state of Missouri restoring their bariatric surgerybenefit for state employees in 2012. Several OACmembers testified before the Missouri legislature insupport of this.

Currently, the OAC has been hard at work advocatingfor obesity treatments to be included in the EssentialHealth Benefits (EHB) package for the new state-basedhealth exchange plans under healthcare reform law.Toward the end of 2011, the United States Department ofHealth and Human Services (HHS) held a number ofregional listening sessions across the country to hearfrom local stakeholders about which services should beincluded in the EHB. OAC member advocates spoke ateach of these sessions about the “essential” nature ofobesity treatment and why it is important that HHSinclude these services in the EHB package. To learnmore about the OAC’s advocacy efforts, please visitwww.obesityaction.org/advocacy/overview.php.

SUPPORTThe OAC offers support to those affected by obesity

through everything we do. One of the biggest ways wesupport our members is by representing them in thebattle against weight bias. Recently, the OAC started our“Bias Busters” initiative to bring attention to weight biasand discrimination, as well as to activate our membershipon these issues and ask their help in speaking out against

bias. Weight bias issues addressed so far include thecreation of a petition directed at Facebook concerning“obesity hate” pages that were found on the popularsocial networking site, an Entertainment Tonight

segment where a reality TV star dressed up in a “fatsuit,” as well as targeting stock photography websites,asking them to remove offensive photos of individualsaffected by obesity. To learn more about “Bias Busters”please visitwww.obesityaction.org/gettinginvolved/biasbusters/overview.php.

HOW TO GET INVOLVEDWhether you are personally affected by obesity or just

passionate about the cause, membership in the OAC isone of the easiest ways that you can give back to thefight against obesity. Individual membership in the OACis just $20/year. You can learn more about the OAC atwww.obesityaction.org. BMI

LEARN MORE, GET INVOLVED

For more information on the OAC and how you can get involved, visit the following websites:

GENERAL INFORMATIONwww.obesityaction.org

MEMBERSHIPwww.obesityaction.org/membership/overview.php.

EDUCATIONAL RESOURCESwww.obesityaction.org/educationaltools/brochuresandguides.php.

ADVOCACY EFFORTSwww.obesityaction.org/advocacy/overview.php.

“BIAS BUSTERS”www.obesityaction.org/gettinginvolved/biasbusters/overview.php.

http://www.obesityaction.org/advocacy/overview.php

http://www.obesityaction.org/gettinginvolved/biasbusters/overvi

http://www.obesityaction.org

http://www.obesityaction.org


http://www.obesityaction.org/educationaltools/brochuresandguides.php

http://www.obesityaction.org/advocacy/overview.php

http://www.obesityaction.org/gettinginvolved/biasbusters/overview.php


BM

I


Knee pain is among the most common of health

concerns in the population, and the subset of

bariatric patients is no exception.1,2 Independently,

in the United States, obesity has prevalence in excess of

33 percent, and a 2006 Centers for Disease Control and

Prevention (CDC) survey of adults reported an 18-

percent incidence of knee pain within the past 30 days.3,4

Bariatric patients have a well-established positive

association with knee osteoarthritis, and it has been

previously noted that body mass index (BMI) in young

adulthood, a time when many patients are now choosing

to pursue bariatric surgical options, may be a good

predictor of subsequent osteoarthritis in later years.5–7

While the etiology of knee pain and treatment

modalities can be wide ranging, this article will focus on

existing medical knowledge of knee pain secondary to

osteoarthritis in the bariatric population, considerations

of the treatment options available for those afflicted with

that diagnosis, and a discussion of the “best questions to

address” in terms of future collaboration between and

treatment options available to primary care physicians,

orthopedic surgeons, and bariatric physicians and

surgeons.

ANATOMYThe knee is a modified hinge joint that experiences

high contact and shear forces during ambulation. There

are three alignments commonly observed in the knee:

neutral, valgus (knock-knee), and varus (bow-legged).8

Existing alignment of the knee can be exacerbated or

altered by degenerative changes, which can significantly

impact force distribution and wear patterns affecting the

three compartments of the knee: medial, lateral, and

patellofemoral. In level walking, the force experienced by

the knee with each step is approximately four times the

total weight of the body, and this increases to

approximately eight times when ambulating down an

incline.9 In effect, the average bariatric patient’s knees

will experience forces comparable to downhill walking at

baseline and much higher forces with additional activity.

The joint is stabilized by four primary ligaments—

anterior cruciate ligament, posterior cruciate ligament,

and medial and lateral collateral ligaments, as well as the

surrounding musculature. Additionally, the knee is

cushioned by synovial fluid and layers of cartilage and

meniscus.

Injury or degeneration of any of these components can

lead to knee pain. A history of prior injury and the

effects of advancing age can lead to degeneration of the

Treatment

Considerations for

Osteoarthritic Knee

Pain in Patients with

Obesity

by James Choi, MD; Jonathan Schaffer, MD, MBA

Dr. Choi, is from the Department of Orthopaedic Surgery, Massachusetts General Hospital, Boston,

Massachusetts. Dr. Schaffer is from the Orthopaedic and Rheumatologic Institute, Cleveland Clinc, Cleveland,

Ohio.

This article discusses treatment modalities for osteoarthritic knee pain in the patient with obesity. Nonoperative options include

physical therapy, orally administered analgesia, and knee injections. Operative intervention options include total knee arthroplasty as

definitive treatment.


BM

I


cartilage (osteoarthritis) with an unpredictable

expression of pain and level of functional impairment.

Previous studies have not correlated obesity with

radiographic progression of osteoarthritis. Notably, it has

been observed that obesity can increase the risk of

osteoarthritis progression in those patients with neutral

or valgus (knock-knee) alignment, but varus (bow-

legged) aligned knees did not show the same risk

progression.10,11

EVALUATION AND THERAPY OPTIONS FOR KNEEPAIN

Osteoarthritic pain characteristically worsens with

increased activity, particularly weight bearing, and

improves with rest. Generally, patients report no

systemic symptoms and on physical exam may have

decreased range of motion, crepitus, mild joint effusion,

and palpable osteophytic changes at the knee joint,

though these findings may be more difficult to elucidate

in patients with obesity.12 Pain that continues and

progresses warrants radiographic evaluation with joint

space narrowing representing cartilage degeneration,

characteristic of osteoarthritic changes. Unless there is

suspicion of soft tissue injury, there is generally no need

for further radiographic evaluation by computed

tomography (CT) or magnetic resonance imaging (MRI)

modalities.

Treatment for osteoarthritic knee pain is symptom

based and relies heavily on the patient’s report of

symptoms and functional limitations. There is not a

predictive correlation between a patient’s complaint of

symptoms to radiographic evaluation of osteoarthritis.

The dependence on patient-reported symptoms for

treatment action makes the understanding of pain

reporting especially helpful. The results of the Swedish

obese subjects study13 indicate that patients with a

higher BMI tend to have a higher prevalence of work-

restricting pain (including the knees) than their general

population counterparts. This same study also noted that

postoperative female bariatric patients reported a greater

level of improvement in their symptoms as compared to

their nonoperative peers and that work-restricting knee,

hip, and ankle pain was more responsive than axial

musculoskeletal complaints.13

At present, treatment of osteoarthritic knee pain is

based upon relief of symptoms beginning with

nonoperative options, and treatment modalities generally

do not differ for patients with obesity as compared to

their nonobese counterparts. Pharmacologic therapy is

primarily targeted at analgesia, and periodic use of

analgesics can be effective for intermittent and mild-to-

moderate symptoms. Nonsteroidal anti-inflammatory

drugs (NSAIDS) are often effective for osteoarthritis

pain.14 The use of NSAIDS is complicated in the gastric

bypass patient population due to an increased risk of

adverse gastrointestinal side effects, which include

development of marginal ulcers at the previously created

anastomosis sites. NSAIDs should be used with caution

and possibly with proton pump inhibitor therapy.15 In the

gastric bypass population, there has been little definitive

guidance on the most effective pharmacologic

alternatives given the risks of NSAID use in this patient

subset. Narcotics are generally considered a

pharmacologic last option for advanced osteoarthritis

pain that is refractory to other treatments, and systemic

corticosteroids have not been shown to be effective for

pain relief although localized injections that are

discussed later can be effective for relief of symptoms.14

Physical therapy targeted at the surrounding

musculature, specifically quadriceps strengthening, can

be effective in providing pain relief.16

Among more invasive interventions, knee injections

fall under two categories: corticosteroid and

viscosupplementation. Corticosteroid injections reduce

the inflammatory response within the knee joint and can

provide good relief of variable duration of weeks to

months, but rarely are more than two or three intra-

articular injections to the same joint administered per

year for concern of potentially progressive cartilage

damage.14 Additionally, recent studies have demonstrated

that bupivacaine, a commonly used intra-articular local

anesthetic often combined with a corticosteroid, has a

significantly increased in-vitro toxicity to human

articular chondrocytes when compared to ropivacaine,

and further research on long-term effects should be

followed closely.17 Viscosupplementation of hyaluronates

is intended to counteract the reduction of concentration

and size of hyaluronan, a key component of synovial

fluid, which occurs in osteoarthritis. Clinical trials of

viscosupplementation have yielded highly variable results

ranging from no effect to improvement in symptoms

lasting up to one year.

Physicians should also be aware of patient-directed

therapies as well. In the context of osteoarthritis, this

primarily consists of the nutritional supplements

glucosamine and chondroitin, and National Institute of

Health-sponsored research studies to date have not

shown significant efficacy in symptom relief.14,18

The end-stage therapy for osteoarthritic knee pain is

In effect, the average bariatric patient’s knees will experience forces comparable to

downhill walking at baseline and much higher forces with additional activity.


BM

I


surgical intervention, including arthroscopy, osteotomy,

partial knee arthroplasty, and total knee arthroplasty.19

Should this be required, total knee arthroplasty is the

definitive treatment. Other operative modalities that can

potentially be offered include a partial knee arthroplasty,

including patello-femoral arthroplasty for patients with

specifically isolated compartment osteoarthritis. Knee

arthroplasty is generally regarded as a highly successful

procedure with predictably good outcomes. Historically,

orthopedic surgery has been somewhat reticent to

embrace operative treatment for patients with high BMIs.

This is perhaps no better exemplified than by the

decision of the East Suffolk (UK) health board to

prioritize lower extremity arthroplasty for those patients

that are not overweight or obese. The two most cited

reasons for not proceeding with arthroplasty in the obese

patient set are a high rate of perioperative complications

(e.g., wound healing and infections) and concern for the

longevity and efficacy of the implant. Winiarsky et al20

showed a significantly increased postoperative infection

rate (26% vs. 2%) for patients with morbid obesity

undergoing a total knee arthroplasty. A review article by

Gillespie and Porteous21 showed a trend of increasing

complication rates with increasing BMI though no

definitive cutoff could be determined. A study by Amin

et al23 in 2006 showed that arthroplasty patients with

BMIs greater than 40kg/m2 had clinical outcome scores

significantly lower than the control group and a higher

rate of revision and perioperative complications. Amin et

al recommended that patients lose weight and maintain

that weight loss prior to arthroplasty and should be

counseled about the potential for inferior results without

weight loss.22 In 2000, Parvizi et al24 reported seeing

excellent hip and knee arthroplasty results in patients

who were postoperative from bariatric procedures with a

mean BMI change from 49kg/m2 to 29kg/m2.

DISCUSSION/CONCLUSIONSAlthough the connection between these two

morbidities is strong, the course of treatment is not well

defined. From the orthopedist’s perspective, a high BMI

may be viewed as potentially exclusionary from surgical

treatment of osteoarthritis, at least until the patient

achieves some degree of stable and sustained weight

loss. Looking from the bariatric surgeon’s perspective,

bariatric procedures have not historically promoted any

efficacy in improving musculoskeletal concerns to the

extent that has been the case for improving

cardiovascular and endocrine morbidities. In the

literature today, there is a paucity of publications

addressing the long-term outcomes of joint arthroplasty

in the context of osteopenia that is generated by the

malabsorptive state created by a gastric bypass

procedure. This leads us to a number of questions as to

the appropriate path of care for the patient with obesity

and progressive knee osteoarthritis.

1. For patients meeting criteria for both bariatric surgery

and knee arthroplasty, which procedure should be

performed first?

2. How do we best minimize the exposure of patients to

perioperative risk?

3. Can we better understand the outcomes of post-

bariatric procedure patients as compared to their

general population and conservatively treated obese

controls?

4. What is the appropriate timing of procedures? Should

there be absolute BMI cutoffs?

5. What are the cost benefits and comparisons as well as

quality of life considerations regarding bariatric and

arthroplasty procedures?

Some points for future consideration include the

following: 1) understanding noncongruence in age of the

typical bariatric versus arthroplasty patient; 2)

determining whether or not primary care physicians and

orthopedists who have patients with BMIs of greater than

35 presenting to their clinic with knee pain should

consider referring those patients for evaluation by a

bariatric clinic; and 3) determining when a “suboptimal”

arthroplasty procedure is in the best interest of the

patient. Bariatric patients tend to present at a younger

age than the typical arthroplasty candidate. The

youngest bariatric patients would generally not be

considered for arthroplasty; however, patients

progressing into their 40s to 50s may be a potential

subset for future outcomes studies. If weight loss

through invasive restrictive procedures or nonoperative

There is evidence that correlation exists between obesity and progression of knee

pain.5–7 In the patient population with BMI in excess of 40, research indicates that

these patients tend to have suboptimal postoperative arthroplasty results and a higher

incidence of perioperative complications than their knee pain control peers. A gray

area exists for patients with BMIs between 30 and 40 with a noted increasing trend to

suboptimal results and higher complication rates but no definitive cutoff mark.


BM

I


methods can improve symptoms and delay the need for a

primary orthopedic procedure, it may be worthwhile to

further investigate outcomes of each population group as

well as gain a better understanding of the pain response

and symptom reporting as compared to current weight

for bariatric patients. It may also be worthwhile to

consider the appropriateness of arthroplasty in specific

high BMI patients. Amin et al23 demonstrated a

significant difference in Knee Society Scores between

patients with obesity and control patients; however, an

additional consideration may be that the arthroplasty

patient with obesity may not need to generate the same

quantitative score to experience an improvement in

function and decrease in pain. Is it acceptable to expect

less than standard results from the surgeon’s perspective

as long as the patient is aware of the increased risks and

diminished benefits when compared to patients with

lower BMIs?

There is evidence that correlation exists between

obesity and progression of knee pain.5–7 In the patient

population with BMI in excess of 40, research indicates

that these patients tend to have suboptimal

postoperative arthroplasty results and a higher incidence

of perioperative complications than their knee pain

control peers. A gray area exists for patients with BMIs

between 30 and 40 with a noted increasing trend to

suboptimal results and higher complication rates but no

definitive cutoff mark. In limited studies, patients who

require knee arthroplasty after bariatric surgery have

done well, and long-term follow up of those patients will

yield useful information. Presently, it may be worthwhile

to consider a referral to a bariatric surgeon by a primary

care physician or orthopedic surgeon for patients with

obesity presenting with knee pain. After undergoing

bariatric surgery, these patients may see improvement in

the common comorbidities of high BMI patients as well

as improvement in their osteoarthritic knee pain

symptoms. This also generates the potential for delaying

the need for any orthopedic surgical intervention and

reducing the likelihood of perioperative complications

and need for revision surgery should there be a need for

arthroplasty in the future. Further study of outcomes of

bariatric patients with osteoarthritic knee pain would be

helpful to further delineate appropriate treatment

protocols in the future.

REFERENCES

1. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of

the prevalence of arthritis and other rheumatic conditions

in the United States. Part II. Arthritis Rheum.

2008;58(1):26–35.

2. Grotle M, Hagen KB, Natvig B, et al. Obesity and

osteoarthritis in knee, hip and/or hand: An

epidemiological study in the general population with 10

years follow-up. BMC Musculoskelet Disord. 2008;9:132.

3. United States Obesity Trends.

http://www.cdc.gov/obesity/data/trends.html. Accessed

October, 28, 2009.

4. Adults Reporting Joint Pain or Stiffness in the Past 30

Days, 2006. http://www.cdc.gov/Features/dsJointPain/.

Accessed October 28, 2009.

5. Stürmer T, Günther KP, Brenner H. Obesity, overweight

and patterns of osteoarthritis: the Ulm Osteoarthritis

Study. J Clin Epidemiol. 2000;53(3):307–313.

6. Felson DT, Zhang Y, Hannan MT, et al. Risk factors for

incident radiographic knee osteoarthritis in the elderly:

the Framingham Study. Arthritis Rheum.

1997;40(4):728–733.

7. Gelber AC, Hochberg MC, Mead LA, et al. Body mass

index in young men and the risk of subsequent knee and

hip osteoarthritis. Am J Med. 1999;107(6):632–633.

8. Hoppenfeld S. Physical Examination of the Spine and

Extremities. Prentice Hall, Upper Saddle River, NJ, 1976.

9. Kuster MS, Wood GA, Stachowiak GW, Gächter A. Joint

load considerations in knee replacement. J Bone Joint

Surg BR. 1997;79(1):109–113.

10. Felson DT, Goggins J, Niu J, et al. The effect of body

weight on progression of knee osteoarthritis is dependent

on alignment. Arthritis Rheum. 2004;50(12):3904–3909.

11. Niu J, Zhang YQ, Torner J, et al. Is obesity a risk factor

for progressive radiographic knee osteoarthritis?

Arthritis Rheum. 2009;61:329–335.

12. Evaluation of Patients Presenting with Knee Pain.

http://www.aafp.org/afp/20030901/917.html. Accessed

October 28, 2009.

13. Peltonen M, Lindroos AK, Torgerson JS. Musculoskeletal

pain in the obese: a comparison with a general population

and long-term changes after conventional and surgical

obesity treatment. Pain. 2003;104:549–557.

14. Klippel JH et al. Primer on Rheumatic Diseases, edition

12. Arthritis Foundation 2001: 295–296.

15. Wilson JA, Romagnuolo J, Byrne TK, et al. Predictors of

endoscopic findings after Roux-en-Y Gastric Bypass. Am

J Gastroenterol. 2006;101(10):2194–2199.

16. Fransen M, Crosbie J, Edmonds J. Physical therapy is

effective for patients with osteoarthritis of the knee: a

randomized controlled clinical trial. J Rheumatol.

2001;28(1):156–164.

17. Piper SL, Kim HT. Comparison of ropivacaine and

bupivacaine toxicity in human articular chondrocytes. J

Bone Joint Surg Am. 2008;90:986–991.

18. Clegg DO, Reda DJ, Harris CL, et al. Glucosamine,

chondroitin sulfate, and the two in combination for

painful knee osteoarthritis. N Engl J Med.

2006;354(8):795–808.

19. Gidwani S, Fairbank A. The orthopaedic approach to

managing osteoarthritis of the knee. BMJ.

2004;329(7476):1220–1224.

http://www.cdc.gov/obesity/data/trends.html

http://www.cdc.gov/Features/dsJointPain/

http://www.aafp.org/afp/20030901/917.html


BM

I


20 Winiarsky R, Barth P, Lotke P. Total knee arthroplasty in

morbidly obese patients. J Bone Joint Surg Am.

1998;80:1770–1774.

21. Mantilla CB, Horlocker TT, Schroeder DR, et al. Risk

factors for clinically relevant pulmonary embolism and

deep venous thrombosis in patients undergoing primary

hip or knee arthroplasty. Anesthesiology.

2003;99(3):552–560; discussion 5A.

22. Gillespie GN, Porteous AJ. Obesity and knee arthroplasty.

Knee. 2007; 14:81–86.

23. Amin AK, Clayton RA, Patton JT, et al. Total knee

replacements in morbidly obese patients. J Bone Joint

Surg Br. 2006;88(10): 1321–1326.

24. Parvizi J, Trousdale RT, Sarr MG. Total joint arthroplasty

in patients surgically treated for morbid obesity. J

Arthroplasty. 2000;15(8):1003–1008. BMI


BM

I


Morbid obesity is a refractory disease related to diets

and medication.1 Bariatric surgery is seen as the only

effective treatment in such cases.2,3 Currently, surgical

treatment of obesity is divided into the following two groups:

1) restrictive surgical procedures and 2) mixed surgical

procedures, with the restrictive factor described as having

more or less of a disabsorptive component. Malnutrition is a

risk associated with all bariatric procedures, and hair loss is a

frequent complaint that may be associated with nutritional

factors, such as lower caloric intake and/or lower absorption of

important nutrients for the maintenance and growth of hair.4

Hair loss can seriously impact the lives of individuals and

may lead to anxiety, low self-esteem, psychosocial problems,

and depression. As a consequence, hair loss can be a stress

factor for this population.5,6 The aim of this article is to provide

a comprehensive review of the literature on hair loss in

patients undergoing bariatric surgery and provide clinicians

with a description of the causes and recommended treatments.

LITERATURE SEARCHA broad review of the Medline and Pubmed databases for

articles published between the years 1983 and 2009 was

conducted, selecting articles related to humans. The key

words used in the electronic search included the following:

hair loss, bariatric surgery, alopecia, nutritional deficiencies,

biotin, zinc, iron, vitamin B12, and essential fatty acids.

A total of 41 articles were found, of which 30 were selected.

Among these, 15 were reviews, four compilations of guidelines,

eight original articles, two clinical case studies, and one

statement of the original article. Articles that addressed other

causes of hair loss, outside of the area of nutrition, were

excluded. Besides scientific articles, 10 chapters from books

and one monograph were also examined.

CAUSES AND TREATMENTS OF HAIR LOSSThe most likely causes of hair loss were found to be related

to age, sex, disease, and genetic factors. It is therefore

important to gather history of each patient who presents with

hair loss regarding any current illness, recent illnesses, auto-

immune diseases, family history of hair loss, food intake,

medications, and the use of cosmetics harmful to the hair.5

Hair follicles have two stages: the anagen (hair growth)

stage and the telogen (inactive) phase. All hairs begin their

cycle in the anagen phase, grow for a period of time and move

into the telogen phase, which lasts about 100 to 120 days.

Then the hair falls out. This process, if accelerated, is called

telogen effluvium and is the cause of hair loss in bariatric

patients.7

The causes for telogen effluvium are drugs, surgery, fever,

childbirth, diseases related to the thyroid, such as hyper- and

Hair Loss Among

Weight Loss

Surgery Patients

by Silvia Leite Faria, MS; Orlando Pereira Faria, MD;

Renato Diniz Lins, MD; and Heloisa Rodrigues de

Gouvea

Ms. Faria is a nutritionist from Gastrocirurgia de Brasília, Brasília, Brazil and is also in private

practice; Dr. Pereira Faria is a chief surgeon, Gastrocirurgia de Brasília, Brasília, Brazil; Dr. Lins is a

medical doctor from Gastrocirurgia de Brasília, Brasília; and Ms. Rodrigues de Gouvêa is a

nutritionist and trainee from Gastrocirurgia de Brasília, Brasília, Brazil.

Bariatric surgery may lead to nutritional deficiencies due to reduced food intake, the scope of the surgery itself, rapid weight

loss, inadequate absorption of nutrients, and the lack of adherence to supplement programs. This article provides an extensive

review of current literature relating to hair loss in bariatric patients. A description of current methods of treatments is included.


BM

I


hypothyroidism, rapid weight loss, anorexia, low proteinintake, iron and zinc deficiency, and toxicity of heavy metals.4–6

In bariatric surgery, telogen effluvium may be associated withpatients who are nonadherent to the supplement program orwho have had rapid weight loss, difficulty in feedingthemselves, or have poor dietary habits (e.g., foodintolerances, especially with protein sources).4

Hair loss after bariatric surgery often occurs between thethird and sixth month after surgery and can last 6 to 12months or more. In the first six months, this framework can bereversed without intervention, although there is no consensuson treatment for these cases.8 After six months postsurgery,nutritional causes are involved in hair loss.4 In both cases,there is no harm to the follicle, so the hair can grow back.9

The nutrients possibly related to hair loss are protein, iron,zinc, essential fatty acids, vitamin B12, and biotin.

Protein. Protein-energy deficiency is associated withincreased hair loss.4,5 A protein deficiency can manifest itselfthrough the reduction of hepatic proteins including albumin,loss of muscle mass, asthenia (weakness), and alopecia.10

Among the factors contributing to protein deficiency arethe following: insufficient chewing, since food needs to bebetter digested in order to compensate for the mechanicalbarrier imposed by the weight loss surgery (WLS);10 reductionof the availability of pepsin, renin, and hydrochloric acid due tothe isolation of the distal stomach, thus limiting proteindigestion;11 anorexia; frequent episodes of vomiting; diarrhea;food intolerances; depression; fear of weight regain; abuse ofalcohol or drugs; and socioeconomic status. Thus, all patientsafter surgery are at risk of developing protein deficiency inconnection with restrictive and disabsorptive procedures.10

Patients who undergo Roux-en-Y gastric bypass (RYGB)usually have a low-calorie diet of 500 to 800kcal per day.Despite a calorie-protein increase during the first year, suchintakes remain at insufficient levels.11

According to Marcason,12 the minimum recommendedprotein intake for bariatric patients is 60g per day, withemphasis on proteins of high biological value (HBV).12,13

However, in general, the recommended intake is 80g of proteinfor women and 100g for men per day or 1.5g/kg idealweight.11,14 In cases of more disabsorptive surgery, such asbiliopancreatic diversion (BPD), there is a raisedmalabsorption of protein. It is therefore recommended thatpatients intake at least 90g of protein.15

It is believed that a reduction in the availability of proteincan cause thinning of the hair, difficulty in the normal hairgrowth process, and diffuse alopecia.16 In relation to essentialamino acids, their deficiency can affect growth anddifferentiation of hair, since they compose 27 percent of the

protein content of hair.16

Among all essential amino acids, a deficiency of L-lysine, inparticular, can contribute to hair loss while “full body suppliesof L-lysine” improve hair growth after periods of decline andimprove the levels of iron in the body. Its bioavailable form isprimarily found in fish, meat and eggs and a decrease inconsumption of these foods may cause a negative balance ofthis amino acid affecting hair growt.17 Thus, a supplementationof 1.5–2g of L-lysine is recommended.4

Iron. Iron is the micronutrient most related to hair loss. Itsdeficiency, in cases without anemia, was related to hair loss forthe first time in the early 60s.18

In WLS, specifically RYGB, a decreased intake of foods richin iron occur. Decreased absorption also occurs, since ironabsorption is more efficient in the duodenum and adjacentparts of the jejunum, which are isolated in RYGB. Concomitantwith this is a decrease in the reduction process of iron to itsmost bioavailable form, due to lower production ofhydrochloric acid.10

For women, iron deficiency is more prevalent among thosewho are in a fertile age, and serum ferritin levels below 40Ìgare strongly associated with hair loss.4,10,19 Kantor et al20 relatedlow concentrations of serum ferritin and hemoglobin with hairloss. Researchers have observed in cases of telogen effluviumthat a significant number of people respond well when treatedwith iron. In a study by Rushton et al,21 researchers correlatedlow serum ferritin with hair loss among women treatment forsix months with daily supplementation of 72mg of iron, and

The nutrients possibly related to hair loss

are protein, iron, zinc, essential fatty

acids, vitamin B12, and biotin.

TABLE 1. Recommended supplements for specific

micronutrient deficiencies

NUTRIENT RECOMMENDATION

ProteinWomen: 80g/daya

Men: 100g/daya

Biotin 2,5 mg/day

Flaxseed oil 2 capsules/day

Multivitamin/Multimineral 200% DRIb

Vitamin B12(crystalline form)

350–500Ìg /day

Iron (ferrous fumarate orgluconate)c 320mg

320mg

Elemental iron 65mg

aWith adequate amounts of L–lysine: 1.5 to 2g/daybDietary Reference Intake (Daily Value)cWomen in their fertile age


BM

I


1.5g of L-lysine decreased the percentage of hairs in thetelogen phase as well as the hair loss in 39 percent andincreased levels of serum ferritin.

Iron supplementation recommended for patients with hairloss is 320mg of ferrous fumarate or gluconate or 65mg ofelemental iron twice a day, with a volume of approximately 25percent ingested being absorbed.18,22 Parenteral infusion mustbe prescribed for bariatric patients who are refractory to ironsupplementation or have anemia related to iron deficiency orhemoglobin serum levels below 11g/dL.23

Biotin. A biotin deficiency can cause depigmentation ofhair and diffuse alopecia, since this vitamin plays an importantrole in the development of the hair follicles.16,24 It is believedthat supplementation or topical use of biotin can prevent hairloss and accelerate growth after a period of decline.4

Such biotin deficiency related to hair loss was initiallyobserved in patients undergoing total parenteral nutrition(TPN) without prolonged biotin. After starting theirsupplementation of biotin, patients undergoing TPN improvedrapidly in terms of hair loss.9

In 2001, Bruginsky25 evaluated 118 patients and found that17 percent of women reported alopecia due to surgery. Also,these women presented with inadequate intake of severalnutrients, such as folic acid, retinol, fiber, vitamin C, and biotin.In a period of 30 days, the growth of hair in 100 percent ofcases was observed after supplementation of 100mcg of biotinand other nutrients, such as folic acid, inositol, choline, Bcomplex, that are known to boost the action of biotin.

One must consider that the daily 1 to 2mg of biotin mayprovide clinical support to cases of hair loss not responding toother types of treatment.17 Daily consumption of 2.5mg wasestablished as a safe limit of intake of biotin, the no observedadverse effects level (NOAEL).24

Zinc. Zinc has several functions and is an important factorfor growth and development of hair. Its uptake can be assistedby the presence of glucose and amino acids in the intestinaltract and its deficiency can cause growth retardation, diarrhea,alopecia, skin lesions, and loss of appetite, among othersproblems.26,27

In cases of hair loss, a supplementation of 15mg/day of zincchelate is recommended.28 The upper level is 40mg of zinc; asupplementation of 50mg over long periods can lead to copperdeficiency.10

Essential fatty acids. Some studies have observeddeficiency of essential fatty acids (linoleic and linolenic acids)

in patients after RYGB and adjustable gastric banding (AGB)since these procedures alter the digestion of lipids and, as aconsequence, the uptake of essencial fatty acids.10,15,29 Inrelation to BPD and duodenal switch (DS), only 28 percent ofingested fat is absorbed.29

In patients with biotin deficiency, levels of linoleic acidlower than normal were observed. In cases of functionaldeficiency of biotin (due to lack of carboxylase) associated tohair loss, supplementation with polyunsaturated fatty acidsmay reduce this symptom, suggesting that hair loss can becaused by impairment of elongation of polyunsaturated fattyacids as a result of reduced activity of acetyl-CoAcarboxylase.24

For patients post-RYGB, flaxseed oil (15mL) isrecommended.15 The recommended dose of linolenic acid is 0.5to 1.0 percent of energy intake and linoleic acid is from 3 to 5percent. These amounts can be reached with two capsules of1g of linseed oil and two tablespoons of extra virgin olive oil.22

Vitamin B12. It is known that the human body has storesof vitamin B12, on average, for 3 to 5 years dependent on one’sdaily intake. However, since patients undergoing RYGB havelower production of hydrochloric acid and of the intrinsicfactor, both of which are needed for its absorption in theterminal ileum, there may be deficiency of vitamin B12 if thesupplementation is not adequate. Thus, RYGB patients havedigestion, release, and absorption difficulties of vitamin B12.10

Brolin et al30 observed deficiency of vitamin B12 in patientssix months after bariatric surgery, becoming more commonafter one year.10 Deficiency in B12 may alter the pigmentationof hair. This alteration can be reversed with B12supplementation.16 The supplementation of vitamin B12 mustbe at least 350 to 500Ìg/day orally in its crystalline for, butpatients may need a monthly intramuscular supplement of1000Ìg.10,22

RECOMMENDATIONSPatients who present with hair loss six months postsurgery

should follow the following recommendation daily: intake 80gof protein for women and 100g for men (with sufficientamounts of L-lysine, 1.5 to 2g/day), add 15 mL of flaxseed oil,2.5g of biotin, one or two multivitamin capsules with minerals(thus providing 200 percent of DRIs), 350 to 500Ìg/day of B12in its crystalline form, and 320mg of ferrous fumarate orgluconate or 65mg of elemental iron twice daily. (Table 1) Thesupplementation of zinc recommended in this article is already

Patients undergoing WLS may have hair loss after surgery due to the lower intake and

inadequate absorption of protein, iron, biotin, zinc, vitamin B 12, and essential fatty

acids. These patients need an adequate supplementation in order to prevent

complications from evolving.

present in sufficient doses in multivitamins that contain

minerals.

CONCLUSION

Patients undergoing WLS may have hair loss after surgery

due to the lower intake and inadequate absorption of protein,

iron, biotin, zinc, vitamin B 12, and essential fatty acids. These

patients need an adequate supplementation in order to

prevent complications from evolving. Further randomized

studies on hair loss in bariatric patients are needed in order to

know, with accuracy, the adequate levels of supplementation

of these nutrients to be administered.

REFERENCES

1. Buchwald H, Avidor Y, Braundwald E, et al. Batritric surgery: a

systematic review and meta-analysis. JAMA.

2004;292(14):1724–37.

2. Sjostrom L, Lindroos AK, Peltonen M, et al. Lifestyle, diabetes,

and cardiovascular risk factors 10 years after bariatric surgery.

N Engl J Med. 2004;351:2683–2693.

3. Folli F, Pontiroli AE, Schwesinger WH. Metabolic aspects of

bariatric surgery. Med Clin N Am. 2007;91:393–414.

4. Jacques J. Micronutrition for the Weight Loss Surgery

Patient. Edgemont, PA: Matrix Medical Communications;

2006:146–147.

5. Beattie PE. The patient with hair loss. Practioner.

2003;247(1643):128–134.

6. Williamson D, Gonzalez M, Finlay AY. The effect of hair loss on

quality of life. JEADV. 2001;15:137–139.

7. Pereira JM. Analysis of spontaneously eliminated hair. Na Bras

Dermatol.1996;71(6):517–524.

8. Fujioka K. Follow-up of nutritional and metabolic problems

after bariatric surgery. Diabetes Care. 2005;28(2):481–484.

9. Innis SM, Allardyce DB. Possible biotin deficiency in adults

receiving long-term total parenteral nutrition. Am J Clin Nutr.

1983;37:185–187.

10. Aills L, Blankenship J, Buffington C, et al. ASMBS allied health

nutritional guidelines for the surgical weight loss patient. Surg

Obes Relat Dis. 2008;4(Supp):73S–108S.

11. Moize V, Geliebter A, Gluck ME, et al. Obese patients have

inadequate protein intake related to protein intolerance up to 1

year following Roux-en-Y gastric bypass. Obes Surg.

2003;13:23–28.

12. Marcason W. What are the dietary guidelines following bariatric

surgery? J Am Diet Assoc. 2004;104(3):487–488.

13. Jacques J. Protein basics. In: Rosenthal RJ, Jones DB, eds.

Weight Loss Surgery: A Multidisciplinary Approach. Edgemont,

PA: Matrix Medical Communications; 2008:437.

14. Woodward BG. A Complete Guide to Obesity Surgery. Victoria:

Trafford; 2001.

15. Scopinaro N, Adami GF, Marinari G, et al. Biliopancreatic

diversion: two decades of experience. In: Deitel M, Cowan

GSM, eds. Update: Surgery for the Morbidly Obese Patient.

Toronto: FD-Communications Inc; 2000:227–258.

16. Geiler CC, Blume-Peytavi U, Orfanos CE. Metabolic disorders

involving the hair. In: Camacho FM, Randall VA, Price VH, eds.

Hair and its Disorders. Biology, Pathology and Management.

London: Martin Dunitz; 2000:275–282.

17. Rushton DH. Nutritional factors and hair loss. Clin Exp

Dermatol. 2002;27:396–404.

18. Trost LB, Berfeld WF, Calogeras E. The diagnosis and

treatment of iron deficiency and its potencial relationship to

hair loss. J Am Acad Dermatol. 2006;54(5):824–844.

19. Kushner R. Managing the obese patient after bariatric surgery:

a case report of severe malnutrition and review of the

literature. JPEN J Parenter Enteral Nutr. 2000;24:126–132.

20. Kantor J, Kessler LJ, Brooks DG, et al. Decreased serum

ferritin is associated with alopecia in women. J Invest

Dermatol. 2003;121(5):985–988.

21. Rushton DH, Norris MJ, Dover R, et al. Causes of hair loss and

the developments in hair rejuvenation. Int J Cosmet Sci.

2002;24:17–23.

22. Mechanick JI, Kushner RF, Surgeman HJ, et al. American

Association of Clinical Endocrinologists, the Obesity Society,

and American Society for Metabolic and Bariatric Surgery

medical guidelines for clinical practice for the perioperative

nutritional, metabolic, and nonsurgical support of the bariatric

surgical patient. Surg Obes Relat Dis.

2008;4(Supp):109S–184S.

23. Malinowski SS. Nutritional and metabolic complications of

bariatric surgery. Am J Med Sci. 2006;331(4):219–225.

24. Vannucchi H, Chiarello PG. Biotin and Pantothenic Acid. In:

Cozzolino SM, ed. Bioavailability of Nutrients, 2nd Ed. São

Paulo: Manole; 2007:411.

25. Bruginsky A. Biotin supplementation as a treatment for

alopecia post gastroplasty. [Monograph]. Sao Paulo: Brazilian

Institute of Homeopathic Studies. Specialization in

Orthomolecular Nutrition and longevity. São Paulo, 2001:38.

26. Yuyama LKO, Yonekura L, Aguiar JPL, Rodrigues ML, Cozzolino

SM. Zinco. In: Cozzolino SM, ed. Biodisponibilidade de

Nutrientes. Second Edition. São Paulo: Manole; 2007:549.

27. Institute of Medicine (IOM). Dietary Reference Intakes for

Vitamin A, Vitamin K, Arsenic, Boron, Chomium, Cooper,

Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon,

Vanadium and Zinc. Washington, DC: National Academy Press;

2001:420–441.

28. Rhode BM, Maclean LD. Vitamin and mineral supplementation

after gastric bypass. In: Deitel M, Cowan GSM, eds. Update:

Surgery for the Morbidly Obese Patient. Toronto: FD-

Communications Inc; 2000:161.

29. Slater GH, Ren CF, Siegel N, et al. Serum fat-soluble vitamin

deficiency and abnormal calcium metabolism after

malabsorptive bariatric surgery. J Gastrointest Surg.

2004;8:48–55.

30. Brolin RE, Gorman JH, Gorman RC, et al. Are vitamin B-12 and

folate deficiency clinically important after Roux-en- Y gastric

bypass? J Gastrointest Surg. 1998;2:436–42. BMI

28 BMI Body • Mind • Inspiration—Winter 2012 Copyright © 2012 MMC

BM

I


Documents

BMI Body Mind Inspiration