Obesity: The Last Bastion of Prejudice

Introduction

For an obese woman living in today’s society, life can be made very hard. Seemingly simple tasks such as buckling a safety-belt, sitting in a chair, grocery shopping or standing in line are painful both physically and, even more so, psychologically. The obese are constantly ridiculed and prejudged as to their lifestyles, eating habits and personalities. For Leslie Lampert, a ‘normal’ weight woman who spent 1 week in a ‘fat suit,’ the changes in people’s behavior towards her were astounding.

One morning I gained 1501b, and my whole life changed. My husband looked at me differently, my kids were embarrassed, friends felt sorry for me, and strangers were shamelessly disgusted by my presence. The pleasures of shopping, family outings and going to parties turned into wrenchingly painful experiences. In truth, I became depressed by just the thought of running the most basic errands; a trip to the grocery store or the video shop was enough to put me in a bad mood. But mostly, I became angry. Angry because what I experienced in the week that I wore a ‘fat suit’–designed to make me look like a 250-plus-lb woman–was that our society not only hates fat people, it feels entitled to participate in a prejudice that at many levels parallels racism and religious bigotry. And in a country that prides itself on being sensitive to the handicapped and the homeless, the obese continue to be the target of cultural abuse.1

The preconceived notions that the majority of ‘normal’ weight people have toward the obese are mistaken. The image that enters most of our minds when envisioning a ‘fat person’ would most likely be an overweight woman, struggling down the street. Perhaps she is eating a donut. You probably think she smells bad. You pity her, you ridicule her for not being able to control her eating. You may even feel that she is a slob, lazy, stupid, and it is her fault she weighs so much; she should go on a diet. You are probably convinced that she has no will-power, and she represents your deepest fears of getting fat and not being to control yourself with eating. You might make fun of her, snickering behind her back as passes by, just loud enough for her to hear. Once she is out of earshot, you stop your snickering, feeling some sort of power over her, like you are suddenly better than she is. Or maybe for just moment you show some humanity and wonder why you did what you just did … did she really deserve that?

‘Fat people’ are not lazy, stupid, or uncaring anymore than a ‘normal’ weight person is. They have just as much willpower, more in some cases. In a personal letter sent to Dr. Latham Flanagan of the Oregon Center for Bariatric Surgery, the woman wrote, “A client once told me, ‘It’s easy to lose weight; just quit eating.’ Even though I quit smoking after 30 years, people assume I have no willpower.” Most of these ‘fat people’ are some of the kindest, most caring people I have ever met. They understand humiliation, pain, isolation, and the absolute cruelty of the human race, because they live with these phenomena every day of their lives.

What Is Obesity?

Obesity, defined as 20% over ideal body weight, is believed to affect as many as 30% of Americans, or over 75 000 000 people! Severe clinical obesity, or morbid obesity, defined as 75% over ideal body weight (45 kg or 90-100 lb excess weight for an average adult) is believed to affect over 5% of Americans, or about 12 000 000 people. The numbers are not entirely accurate because many severely obese people ‘hide’ from conventional sources of these statistics. Their reasons include fear of embarrassment or severe physical disability.

The cause of severe obesity has been, and continues to be, highly misunderstood. Traditionally, obesity has been considered to be a psychological or a social disease–a disease of sin and sloth. The obese person has been considered to be not quite normal, and often the sideshow freak of a traveling circus. In the last two decades, there have been extensive studies into the cause of obesity and the nature of obese persons. Medical science now understands morbid obesity to be primarily a genetic disease, an organic disease of abnormal fat metabolism. The mechanism, as experienced by the morbidly obese person, appears to be that an amount of food sufficient in calories to meet basal metabolic needs and energy expenditure of the muscles is not experienced as being ‘satisfying’. To feel satisfied, as any normal weight person would feel after a meal, the obese person must eat more than he/she requires.

But Are They Normal?

The severely obese suffer for something that they have little control over, as it largely a genetically determined metabolic disease of abnormal fat storage.2 A study completed in 1985 by Dr Stunkard and his Danish colleagues of 3580 adoptees found a strong correlation in weight between the biologic parents, but none with the adoptive parents. This is considered to be the definitive proof of the genetic origin of severe obesity.

An obese person is as normal, psychologically, as anyone else. “The long-standing belief that obese persons suffer disproportionately from emotional disturbances has been shown to be incorrect. In two of (Moore and colleagues) studies obese persons actually had lower levels of psychopathology than their non-obese counterparts (in a study of 1660 people in midtown Manhattan).”3

Further, medical science has been able to demonstrate that morbidly obese persons are psychologically normal in all respects except for some traits that are caused by social prejudices. “Emotional problems specific to obese persons do exist, but they are now seen as consequences of the prejudice and discrimination directed against obese persons.”3 Therefore, the seriously obese are mentally as normal as lean individuals and, where they behave otherwise, it is either a normal human response to prejudicial treatment or a reflection of a similar incidence of mental disorders which are experienced by the non-obese population. Their large size and related diseases are a manifestation, phenotype, of their genetic inheritance which all humanity is heir to.

The Beginnings of Prejudice

If a child is not told that it is wrong to discriminate, they will carry it into their adult lives, thinking that it is acceptable. From religious bigotry to ethnic hatred, racism to sexism, bigotry has been ingrained through generations of accepted hatred, and it is no different for ‘sizism’. The idle comments made by children are allowed to slip by, sometimes are even reinforced, and continue on into adulthood.

… children no more than 6 years of age describe silhouettes of an obese child as ‘lazy, dirty, stupid, ugly cheats and liars.’… black-and-white line drawings of a normal-weight child, an obese child, and children with various handicaps, including missing hands and facial disfigurement, (were shown) to a variety of audiences. Both children and adults rated the obese child as the least likable. This prejudice extends across races, across rural and urban dwellers, and, saddest of all, even to obese persons themselves.3,4

Unfortunately, it seems that societal acceptance of prejudice toward the severely obese has already occurred across the globe, and steps to rectify the situation are slow at best. The barriers to break down have been made strong through the years of letting this prejudice slip by the wayside unnoticed. The media, from MTV to the local newspaper, contributes to the stereotype of the skinny American woman. Over the last 30 years, as the weight of the average American woman has steadily increased, the models used by Playboy magazine have grown progressively thinner.5

But perhaps this discrimination is more deep-seated than it initially appears to be. “To many, obesity symbolizes an inability to control oneself or to maintain personal health.”1 In a society where control over oneself is so important to the individual, it is no wonder the obese are picked on so readily. They represent that part of all of us that we assume to be so dangerous–lack of self-control. Let us analyse a not atypical example of the types of treatment the obese often receive.

Pamela

Pamela (not her actual name) attended a Eugene high school between the fall of 1991 and the fall of 1992, her freshman and half of her sophomore years. At 155 cm (5’2″) and 180 kg (395 lb), each day of school met with constant harassment and threat of personal injury. She recalls being pushed down stairs, her hair being pulled out, being spat on, and of having numerous objects thrown at her. She would find pig snouts taped to her locker, jokes about her weight shouted out, such as “go to Jenny Craig/Weight Watchers,” and “she’s so fat she can’t fit through the front doors.” She became the school joke. On Valentine’s Day, students put up posters stating “if you’re fat and ugly like Pamela, you need Valentine’s Day Dating Service.”

On an extreme occasion, three boys followed her home from school and maced her; she had in no way provoked them. The boys were arrested, but released on bail. The following day she did go to school, where the boys were waiting for her at her locker. She went directly to the office where she called her mother to come pick her up. Pamela was dismissed from school for 3 months on the grounds that she had disrupted the learning processes of other students.

She attempted to talk with the administration and with school counselors. The principal told her to “deal with it” and that it was “her fault” and she should “go on a diet”. When she was harassed in the hallways, Pamela says that “the teachers would just stand and watch”.

Pamela began to skip school; she could not bear the thought of going and having to face the constant ridicule. Finally in late fall of 1992, she dropped out and began attending school at the Opportunity Center, a remedial high school. Conditions were much better there. She says that the teachers would not allow the harassment, and she was never made fun of or beaten up.

In 1993, Pamela had the gastric bypass surgery. Following this, and with her subsequent weight loss, Pamela noticed significant improvement in the way she was treated, and in the way she felt about herself. When returning to her previous high school to pick up her yearbook, those who had known her could hardly believe she was the same person. She then weighed 113.5 kg (250 lb) and remembers looks of admiration. She was in no way harassed.

She is now at 79.5 kg (175 lb) and beautiful. She is actively dating, has a good job and many friends.

Social Disadvantages of the Severely Obese

As a ‘normal’ weight person 177.5 cm, 65.9 kg (5’11”, 145 1b), I never think twice about using a public bathroom, going out to eat, flying, riding a bus, grocery shopping, sitting in class, buying clothes, applying for a job, or any number of daily activities. However, for an obese person, each of these tasks is a struggle. Personal hygiene is extremely difficult; when eating in public, everyone around the obese seems to become an expert in their diet, and often express an opinion. Some people check the contents of a grocery cart and make comments.7 The desks are not big enough in the classroom, the seats are not big enough in airplanes, no one will sit next to them on the bus, and special stores are needed for buying clothes. When recently attending a support group for bariatric surgery patients, one lady commented that she could not remember the last lime she had shopped in Meier & Frank, and was ecstatic for just having done so. Many employers will not even consider hiring an obese person; and if they do, the ‘fat person’ is kept out of sight. Everyday is a trial, filled with isolation.8

Fat people are frequently objects of public scorn and malicious ridicule … Their obese physiques are the antithesis of the lean, trim, and muscular body habitus so highly prized in today’s exercise-conscious Western society.9

When you are obese, no one wants to talk to you, no one wants to have you around because you are an embarrassment; of course no ‘normal’ weight person would ever stop to consider how much embarrassment an obese person feels daily. Even family members ostracize you.

America is a society that would like to think of itself as open-minded and liberal. However, I know of no one who is not guilty of ridiculing a person at least once for being fat. Everyone is guilty of it, and yet nothing is done about it. Racism, religious prejudice, sexual discrimination, class prejudice, these are all things that we hear and read about daily. These societal problems are topics for lunch-time or coffee-house talks, essays and articles. So where does this kind of bigotry fall in? Weight prejudice? Sizism?

This ‘sizism’ is the last place where people can discriminate openly without fear of reprimand. ‘We’re the last safe prejudice … The fat person is the last person you can safely kick around.”10 “Fat people (report) that they are accosted on the street by strangers who admonish them to lose weight. Often their own children are ashamed of them … even many doctors find fat people disgusting, and some refuse to treat them.”11

Prejudice in the Medical Community

It is not only high school students who behave in a prejudicial manner towards the obese. Young children can be brutally honest in their comments (e.g. “Mommy, look at the fat person!”). Adults are just as bad, but they are better at hiding their prejudice. Even doctors can be ignorant and cruel. In the obesity surgery patients’ support group, one lady remembered asking her family doctor if he had any advice on how best to lose weight; she says he stood back from her and replied “have you ever seen a fat person in a concentration camp?” Another woman reported that after having back surgery, her doctor had complained to her of having to cut through the two inches of ‘blubber’.

… all too often (health-care providers) share the prevailing contempt for the obese … one group of 77 physicians described their obese patients as ‘weak-willed … ugly … awkward.’… based on the belief that obese persons are self-indulgent and ‘hence at least faintly immoral and inviting retribution.’3

Many family and general practitioners do not even know of the existence of obesity surgery, or doubt its reasonability.

Anti-fat bias has been found among family physicians, medical students, nurses and nursing students, and nutritionists. A group of 438 Michigan family physicians ranked obesity as the fifth most negative patient characteristic … (another group) surveyed 324 members of the American Academy of Family Physicians and found that two-thirds of the respondents believed their obese patients lacked self-control, and 39% thought they were lazy; 34% characterized their obese patients as sad.12

Much of this type of anti-fat sentiment derives from the physician trainers who place such an emphasis on the need for an obese person to lose the weight. Physicians see obesity as a self-inflicted problem, for which, if the individual would only stick to a diet, they could cure themselves.12 “… the majority of surgeons I know do not seem to seek to understand or even tolerate the obese and their problems.” Coming from another surgeon, Dr George S.M. Cowan, a Professor of Surgery at the University of Tennessee at Memphis, this statement is particularly powerful.

Health Issues

Along with the psychological impact of such a disease, there are also significant medical health issues. Hypertension, strokes, heart failure, heart attacks, diabetes, cirrhosis of the liver, accident proneness, operative risks, osteoarthritis, gall bladder disease, sleep apnea, heartburn, urinary stress incontinence in women, benign brain swelling, cancer of the uterus, breast and ovaries in women, cancer of the prostate in men, cancer of the colon, and an increase of sudden death risk from unknown causes.13

Men aged 15-69 years, and who are 20% over ideal body weight, experience mortality rate increases of 30%. Excess mortality rate increases by 15% for cancer, 60% for stroke, 80% for nephritis, and 140% for diabetes.13 Although these figures are 17 years old, instances of obesity are on the rise in America, making the figures even more significant than they appear.

The National Institutes of Health Consensus Conference on Obesity concluded that morbid obesity is a serious, disabling, and common disease, and that morbid obesity, like other diseases, deserves treatment and insurance coverage for therapy.9

Unfortunately, many insurance companies do not cover the Gastric Bypass or Gastroplasty because they are seen as cosmetic surgeries, although, once surgery is completed, the patient is left with a scar from xyphoid to umbilicus. Also, once weight loss begins, the individual will develop large flaps of skin under the upper arms, inner-thighs, neck and a large apron of abdominal skin that may extend down to the thighs and even knees. Thus, despite some insurers’ claims that the gastric bypass and other related surgeries are cosmetic, it is quite the contrary; “if anything, it (bariatric surgery) is clearly ‘anti-cosmetic’ rather than enhancing the formerly-obese person’s appearance.”14

After surgery is performed on the obese individual, and subsequent weight loss occurs, most of the health issues associated with obesity, the ‘co-morbidities’, either disappear or are drastically reduced. The individual is more inclined to seek advancement, additional education, get off the welfare rolls and acquire a job (self-image has improved, and employers are more likely to hire a thinner person over the obese). The individual is able to sleep at night, fit into chairs, drive, move without constant physical discomfort, and has a mental outlook that is much brighter due to the fact that the constant ridicule is no longer tangible. Their self-confidence soars, and with the common case of employment, so do their bank accounts. They are no longer a ‘burden’ on society, for they no longer live off Welfare. Society actually reaps a double benefit from the successful treatment of the formerly obese: (1) no more medical or entitlement support costs; (2) they now pay taxes. To understand even more of the implications of this disease, we will take a closer look at the costs of serious obesity before treatment.

Economic Costs To the Individual

The costs to the individual are often enormous. The hundreds of different diets the obese person will try add up, and will be effective for only a short time until the weight returns. Medical costs for doctor bills, depression/sleeping pills, unemployment, and special clothing are all costs the obese person has to endure. Sleep apnea, a common problem, results in the individual falling asleep on the job, which usually concludes in their being fired.

As to obtaining a job initially, “employers usually consider the morbidly obese poor candidates because of their unfavorable appearance, their inability to fit into office furniture or into factory environments, and their high absenteeism due to illness.”9 Often a less qualified, but thinner applicant will be hired over an obese person.

Jane (not her actual name) graduated in the top 10% of her class from the Colorado Institute of Art and is highly skilled in various computer applications. She did not realize how wide-spread ‘sizism’ is until she and three cousins applied for a job together. “I knew I was qualified for a position and expected to be interviewed.” ‘Katy’ was also qualified for a position and had good references. ‘Jenny’ and ‘Pat’ had been “drawing public assistance” for several years.

‘Katy’ and I (both obese) went in first; there were kids in the car so we went in shifts, after completing the applications, ‘Katy’ and I were told that there were no available positions, but that our applications would be kept on file for future openings … ‘Jenny’ and ‘Pat’ (non-obese) went in to fill out applications so they could be in line for future openings. They were each interviewed, drug-tested, and hired on the spot.

‘Jane’ went home in a fury, called up the potential employer and demanded an interview, “but they had no record of our applications.”

Allan Cox surveyed more than 1000 middle and top managers about how 105 qualities and characteristics would affect executive success at their companies. More than 24% said even 15 lb (6.8 kg) of excess weight would have a ‘somewhat negative’ effect, and 4% said that the effect would be ‘very negative.’ Up the ante to 50 lb (22.7 kg) excess weight and 43% thought the effect would be ‘somewhat negative,’ while 27% said it would be ‘very negative.’15 “Employers feel they don’t have to give you good raises, because you’ll have a hard time getting a job elsewhere.”15

Only 9% of executives with salaries of $25 000-50 000 were more than 10 lb (4.5 kg) overweight, whereas 39% of those earning $10 000-20 000 were comparably overweight. Each pound of fat costs an executive $1000 a year.15

Stunkard reports that “twice as many obese women (22%) were downwardly socially mobile as were upwardly socially mobile (12%).” Also, overweight women are 20% less likely to be married,16 and felt inadequate in their parental roles (due in fact to the embarrassment of their children and other family members). For obese high school students, acceptance rates into college are lower, despite qualifications, high school performance or application rates.4

The average obese women has 4 months less schooling than a non-obese woman, and is 10% more apt to live in poverty.4 Whether the inclination towards poverty is a direct result of the lesser schooling, or from the social pressures and physical inabilities, has not been clearly defined. I am more prone, however, to believe the latter from my experience. Social pressures and prejudices can be so overwhelming as to push the obese individual out of public schooling, as in the case of Pamela. Taking into consideration that obesity is largely genetic, the parents are more likely to be obese themselves, possibly on welfare, and not able to afford alternative education. The child would most likely not attend college, most likely fall into the welfare program, or work menial jobs on low pay, and therefore be at or below the poverty-line. Beyond the individual, what does this mean to our society?

Economic Costs to the Society

Obesity not only costs the individual but also society as a whole.

The cost of treating various medical conditions due to or associated with severe obesity is estimated at 39 billion dollars per year, of which 17 billion is spent for musculoskeletal disorders. Additionally, US consumers spent an estimated 32 billion dollars a year on commercial weight control programs and products.17

The amount of money that is poured into weight-loss programs each year is incredible. “Americans spend over $33 billion a year to lose weight, most regain it quickly …”18 Severe obesity cannot be treated effectively with dieting, because the weight simply returns. The National Institutes of Health Technology Assessment Conference of 1992 ‘Voluntary Methods for Weight Loss and Control’ determined that in the best of available weight-loss programs using any combination of diet, behavior modification, exercise, or medication, two-thirds of any weight lost is regained in the first year after the program, and almost all within 5 years. Surgery is the only effective treatment.

Surgical Treatment of Severe Obesity

Surgery has often been considered a desperate last resort for treating severe obesity. However, results of current operative procedures in the last 15 years have improved to the point that the National Bariatric Surgery Registry reports a 0.3% mortality rate in over 15 000 patients.19

Lifestyles of the severely obese are quite altered following surgery. In a study by Rand and Macgregor, 57 consecutive patients who received obesity surgery reported drastic reductions in the amount of perceived prejudice connected with their weight.20,21 “Preoperatively, 40% … of patients answered ‘always’ or ‘usually’ to every item describing acts of prejudice or discrimination … (postoperatively) no patient reported the same degree of prejudice and discrimination …”

Conclusion

For severely obese individuals, surgical treatment is the most effective way to treat their disease, both physical and societal, if they are willing and able to have a major operation. For those who cannot undergo surgery or who do not qualify, there is as of yet no answer to their problem.

Ignorance is the driving force of prejudice and discrimination. Until society is awakened to the unjust treatment of the obese, the discrimination will continue. Just as racism, sexism and other prejudices have been out in the open and recognized by the majority as wrong, so must ‘sizism’. As ignorance is the cause, enlightenment through education is the cure. Organizations, such as the National Association to Aid Fat Americans, or NAAFA, have already begun the process of stopping the discrimination towards the obese in the work place, but it is a slow process. Individuals must be educated, laws enacted, and cultural norms changed so that the protective bastions which allow the devastatingly harmful prejudices against the obese cease to exist.

Obesity does not arise from lack of self-control. It is largely a genetic disease which contributes to severe physical health problems, as well as psychological distress from social pressures, and a lower socioeconomic status due in great part to prejudice. Obesity is a disease which afflicts one-third of all Americans, and is on the rise. Obesity will not go away; it is a growing epidemic in our society which needs to be recognized and effectively dealt with.

References

1. Lampert L. Fat like me. Ladies Home Journal May 1993: 154-215.

2. Stunkard AJ, Sorenson TIA, Harris C, et al. An adoption study of human obesity. N Engl J Med 1986; 314: 193-8.

3. Stunkard AJ, Wadden TA. Psychological aspects of human obesity. Human Obesity: General Aspects 1992: 352-8.

4. Wadden TA, Stunkard AJ. Social and Psychological Consequences of Obesity. Ann Intern Med 1985; 103: 1062-7.

5. Presentation to the American Society for Bariatric Surgery. New Orleans June 1991.

6. Interview of ‘Pamela’. 19 October 1995.

7. Anonymous. Personal letter.

8. Various Speakers. Oregon Center support group for Bariatric Surgery Patients, 15 October 1995.

9. Pories WJ. The surgical approach to morbid obesity. Textbook of Surgery. Philadelphia: W.B. Saunders 1991: 851-65.

10. Lampert W. Obese Workers Win On-the-Job Protection Against Bias. Wall Street Journal, 12 November 1993: B1+.

11. Kolata G. Are fat people last to beat bias? Eugene Register Gaurd. 23 November 1992: A1+.

12. Robinson BE, Gjerdingen DK, et al. Obesity: A move from traditional to more patient-orientated management. JABFP 1995; 8(2): 99-108.

13. Yudkin J. Nutritional, psychological and social aspects of obesity. Ruschlikon-Zurich: Somogyi, JC 1978: 146-50.

14. Cowan GSM Jr. Personal letter.

15. Zetlin M. Sizable problems. Savvy Manager, August 1988: 22-4.

16. Associated Press. Obese women suffer more than men. Eugene Register Gaurd, September 1993: A3.

17. Serdula M. Weight control practices in U.S. adolescents and adults: youth risk behavior survey and behavioral risk factor surveillance system. National Institutes of Health Technology Assessment Conference. Methods for voluntary weight loss and control. Bethesda, Maryland. March 30-April 1, 1992.

18. Associated Press. Experts urge disclosure in diet programs. Eugene Register Gaurd, 6 December 1994: A6.

19. National Bariatric Surgery Registry pooled report. Iowa City 52242-1086, USA.

20. Rand CSW, Macgregor AMC. Morbidity obese patient’s perceptions of social discrimination before and after surgery for obesity. South Med J 1990; 83: 1390-5.

21. Rand CSW, Macgregor AMC. Successful weight loss following obesity surgery and the perceived liability of morbid obesity. Int J Obes 1991; 15: 577-9.

IFSO Statement on Bariatric Surgeon Qualifications

This IFSO Statement is made with the intent to guide those surgeons interested in, or engaged in the practice of, bariatric surgery to understand what qualifications are considered acceptable to the international community of bariatric surgeons (IFSO). This is based upon the IFSO’s dedication to optimizing the overall safety and long-term effectiveness of bariatric surgical procedures for those patients who qualify for this surgery.

The IFSO acknowledges that an average, formally certified, general surgeon may be technically capable of performing most primary bariatric surgical procedures. However, like any other area of surgery, the techniques which improve each surgical procedure’s safety and effectiveness are exemplified by experienced and frequent practitioners of each particular type of bariatric surgery.

The IFSO also acknowledges that the proper patient selection and education as well as short-, intermediate- and long-term management of primary bariatric surgery patients is extremely complex. This requires considerable experience and judgement which should best be learned from a preceptor(s) with in-depth experience in bariatric surgery.

IFSO, therefore, strongly recommends that, prior to independently performing primary bariatric surgery, each surgeon meet the following minimal standards:

  1. Be a fully-trained, qualified, certified general or gastrointestinal surgeon who has completed a recognized general/gastrointestinal surgery program;
  2. Has completed a preceptorship in all aspects of bariatric surgery, including patient education, support groups, operative techniques and post-operative follow-up with an IFSO or IFSO Affiliate Society-designated bariatric surgeon or one who has performed at least 200 bariatric surgical procedures and has five or more years experience in the field of bariatric surgery;
  3. Has received a written approval from his preceptor of his/her satisfactory bariatric surgical abilities;
  4. Maintains a well-informed, up-to-date knowledge of bariatrics and bariatric surgery literature such as contained in the journal Obesity Surgery;
  5. Holds, or has applied for, membership in an Adhering Body of IFSO or, if no such national body is available to him or her, to IFSO directly;
  6. Has attended at least one meeting of IFSO or one of its Adhering Bodies or one of its bariatric surgery courses;
  7. Is personally committed to strongly encouraging the necessary education and life-long follow-up of his/her bariatric surgery patients;
  8. Performs bariatric surgery in institutions where he/she has made every reasonable effort to obtain equipment, facilities and support systems adequate for the comfort and safety of bariatric surgery patients.

IFSO also acknowedges that re-operative bariatric surgery is an even more complex and demanding area which requires considerable primary bariatric surgical experience, as well as knowledge of surgical options, precautions, risks, benefits, possible complications and implications. This requires considerable experience and judgement which should best be learned from one or more colleagues with in-depth experience of re-operative bariatric surgery. It therefore recommends that the bariatric surgeon, at least early in his/her re-operative bariatric surgical practice, refer back to, confer with or otherwise work with, one or more bariatric surgical colleagues who have extensive experience in re-operative bariatric surgery, ideally 60 or more such cases.

7 Tips For Healthy Living – Staying Fit and Eating Well

Healthy living is something we can all achieve with sensible food choices and by keeping active. It’s forgivable to eat treats sometimes and party on the weekend. But the majority of the time it is important to look after our bodies that we live in, and not poison them with tobacco, alcohol and excessive sugar and fat consumption. If you want to learn more, read the 7 tips for healthy living, below.

Healthy Living Tip #1 – Eat a Combination of at Least 5 Fruits and Vegetables a Day

Make sure you are eating enough fruit and vegetables every day. Most health departments recommend a combination of 5 fruit and vegetables a day, not weighing less than 400 grams. Fruit and vegetables contain many nutrients and minerals. One other important fact to note is that both fruit and vegetables contain daily fiber which is essential for gut health and being regular. Various fruit and vegetables contain nutrients for various body functions. E.g carrots are good for eye health, broccoli protects against cancer, oranges contain vitamin C which protects against cold and flu. You can buy vitamin C tablets, but tablets are sugar lolly-like tablets compared to the juicy and tasty, orange fruit.

Healthy Living Tip #2 – Ensure That You Include Omega 3 Fatty Acids In Your Diet

You can buy Omega 3 and 6 capsules and vitamins but is far healthier to eat oily fish that contain these nutrients. The best sources of Omega 3 are Salmon, sardines, and trout. If you are allergic to fish taking supplements is the next best thing. Certain vegetables contain Omega 3 fatty acids but not in large enough quantities to make a difference to your health. Omega 3 helps keep:

  • your heart healthy, prevent cardiovascular disease and helps prevent an irregular heartbeat otherwise known as arrhythmias, which can cause sudden death
  • lower blood pressure
  • prevent asthma in children
  • maintain healthy brain tissue
  • keep the retina of your eyes healthy
  • prevent stroke
  • lower the risk of dementia

Healthy Living Tip #3 – Reduce Saturated Fat and Sugar.

It’s important to eat less saturated fat, as saturated fat can increase cholesterol, which can cause heart disease. Many of the foods that are high sources of saturated fat are treat foods. These treat foods include cakes, donuts, chips, biscuits, hard cheese, sausages, cream, butter, lard, fried foods, pies, and oven foods from the supermarket.

Eating excessive amounts of sugar can cause weight gain and lead to obesity. It has been found that the human body can metabolize up to 6 teaspoons of sugar but beyond this figure, health problems begin to eventuate, including diabetes. From diabetes, a whole host of other diseases can begin, from heart disease to cancers. Excessive sugar can also damage your liver and cause scarring of liver tissue and liver failure.

Eating too much sugar and particularly drinking sugary sodas can also increase the rate at which your teeth will decay. Teenagers are particularly prone to drinking sodas as it becomes almost a staple in their diet.

Healthy Living Tip #4 – Limit Salt (Sodium) to 6 Grams a Day

A pinch of salt is healthy, but any more than 6 grams a day for adults can lead to heart problems and high blood pressure. To limit salt intake, read food labels thoroughly and buy salt reduced products where possible. Another idea is, that you could limit the number of processed foods which will get you closer to the goal of limiting your salt intake to 6 grams a day. But as many people eat snack foods and shelf foods, most people exceed this limit. Even with healthy choices like pasta and noodles, the sauces and flavor sachets have increased levels of sodium (salt). Over a day it adds up and most people eat more salt than recommended.

Healthy Living Tip #5 – Get Enough Exercise

With the widespread use of computers and video games, children and adults are much less active than past generations. People playing with their phones has become the norm. Some people even continue this as they walk along the street, and this can sometimes cause road accidents. Childhood obesity has increased, well beyond figures of previous generations. Many people will tell you that they don’t have time to exercise, but as with any event or activity, it is a matter of priorities.

Walking is good exercise and brisk walking is even better, which increases your heart rate and helps you burn fat. Exercising every day is beneficial, but many people take the weekends off. Cycling is also good exercise and good for fat burning. Rather than limit your exercising to the gym, try to get out and breathe fresh air while exercising.

Healthy Living Tip #6 – Eat Good Meals But Don’t Feast

Eat foods with the nutrients your body needs to ensure that you don’t need to supplement your diet with vitamins, as the foods containing the essential nutrients and minerals are a natural and healthier source. At meal times remember to only eat until you are full and not overeat. Everyone has a different set point to how much they can eat. Try to eat the recommended amount of calories or kilojoules that are correct for your sex. For men, this is 2,500 calories or 10,500 Kilojoules and for women, this is 2000 calories or 8,400 Kilojoules.

Healthy Living Tip #7 – Switch to a Low Glycemic Index Diet For Weight Management

Eat Low GI foods, as these keep you feeling full, whereas High GI foods give you a sugar rush but moments later you feel hungry. Unlike conventional diets, low GI foods that are best to eat are non-starchy foods. This means avoiding white potatoes, which like white flour and white bread, are high GI foods. Replace these foods with dried beans (these can be tinned), chickpeas, lentils, and multi-grain and sourdough breads.

Sugar is high GI which means that eating sweets and biscuits are not recommended. If you want to eat sweet foods replace these sweets with fruit and dried fruits and mix with plain yogurt. Fruit yogurts contain an increased amount of sugar. Choose the full-fat yogurt as the no fat yogurt’s fat is often replaced with sugar or artificial ingredients. The best low GI drink you can drink is water. If you need some flavor add a squeeze of lemon juice.

Conclusion

Healthy living means healthy choices. It is recommended to eat a diet with fresh fruit and vegetables, limited amounts of saturated fat, sugar, and salt. Preferably, eat a low GI diet to keep you from snacking on snack foods, and if you are overweight this option will help you lose weight. For good heart, brain and eye health eat oily fish twice a week, and if you are allergic to fish, fish supplements are the next best thing. Remember to exercise for at least 30 minutes, 5 times a week, and keep digital device usage down, to reduce the amount of time you are sedentary. As with anything balance is important. Eat a balanced diet, and eat good meals but don’t feast.

Review: Laparoscopic Bariatric Surgery

Background: According to the WHO, obesity and obesity with associated morbidity constitute a chronic, multi-factorial condition requiring treatment. Conservative treatment has been shown in long-term studies to be ineffective in morbid obesity. Surgical treatments break down into restrictive, malabsorptive, combined restrictive and malabsorptive or motility-reducing procedures.

Method and results: Laparoscopic implantation of an adjustable gastric band is an efficient restrictive measure for treating the majority of patients with this condition. The adjustable gastric band enables weight loss and food intake to be adapted to the individual patientrsquos need. Of these patients, 80–90% can expect to lose 55–70% of their excess weight. Vertical banded gastroplasty is losing ground among the restrictive options. Preliminary experiences are encouraging, but the long-term results are disappointing when assessed by the standard criteria. Gastric bypass is gaining ground in Europe and is a standard procedure in the USA. This operation is estimated to give a 70–80% loss in excess weight, and provides a better quality of life than do restrictive procedures. The biliopancreatic diversion with duodenal switch combines a sleeve gastrectomy with a duodeno-ileal switch to achieve maximum weight loss. Consistent excess weight loss of between 70% and 80% is achieved, with acceptable decreased long-term nutritional complications. The laparoscopic approach to this procedure has successfully created a surgical technique with optimum benefit and minimal morbidity, especially in the super-obese patient. Intra-gastric stimulation is the least invasive surgical procedure at present. However, the excess weight loss is lowest with this method, at only 32% in the first 2 years after the operation.

Conclusion: Provided that safety recommendations are observed, laparoscopic operations for obesity have a fairly low risk. The mortality rate in centres with experienced staff is less than 0.3%. The death rate due to untreated morbid obesity is significantly higher than in a comparable group of patients after surgery.

Introduction

Morbid obesity is a chronic lifelong, multi-factorial, congenital disorder, causing the patient to have excessive fat deposits and associated medical, psychological, physical, social and economic problems [1]. Aetiological factors include the involvement of hereditary, biochemical, hormonal, environmental, behavioural, health and cultural elements. Extreme forms of obesity are hardly likely to respond to diet, behavioural therapy or medication [1]. Obesity is directly correlated with type II diabetes and cardiovascular disease [2, 3]. Non-surgical treatments for morbid obesity have relapse rates of up to 90%, irrespective of the choice of conservative treatment [1, 3]. As early as 1991, the US National Institute of Health issued a statement recognising the known lack of success with conservative forms of treatment, noting that operations to constrict or bypass the stomach were justified for fully informed and consenting patients and constituted an acceptable risk [4, 5]. Safe and effective surgical treatment increases the life expectancy and quality of life for extremely obese individuals [6, 7].

Surgical operations

Minimally invasive surgery or laparoscopic procedures have made inroads into almost every surgical discipline, and they have shown a more marked increase since the beginning of the 1990s due to on-going improvements in operating techniques. Vertical banded gastroplasty, gastric bypass and biliopancreatic diversion are now performed laparoscopically (Chua and Mendiola [8], Wittgrove et al. [9], Cleator et al. [10]). The operations most amenable to laparoscopic techniques are adjustable gastric banding and Roux-en-Y gastric bypass.

Indication for surgery

A body mass index (BMI = body weight in kilogrammes divided by body height in metres squared) of 40 or over constitutes clinical obesity requiring medical treatment. Surgical treatment is considered to be justified if desired by the patient and accepted as indicated by the surgeon. Patients with a BMI of 35–40 should be considered for surgical treatment if they are suffering from associated conditions that would be likely to improve as a result of weight loss.

The patient should have a BMI of 40 kg/m2 or more, i.e. 45 kg or more above the ideal weight according to a body-weight table and depending on physical constitution (a BMI of 40 corresponds approximately to 45 kg overweight in relation to ideal weight and average height). If the BMI is between 35 and 40 kg/m2 (i.e. fewer than 45 kg above ideal weight), the risk of a proposed operation would need to be justified by a serious medical problem that could be substantially improved if the patient were to lose weight. A highly motivated patient and an interdisciplinary treatment approach are more influential on the outcome than strict exclusion criteria that are rejected repeatedly year after year. The follow-up to the fitting of an adjustable gastric band, including band adjustment, psychological care and dietary counselling, forms a major part of the treatment. The operation should never be performed unless proper follow-up is assured. Further recommendations issued by the American Society for Bariatric Surgery (ASBS) and the International Federation of Surgery for Obesity (IFSO) say that a centre should have sufficient experience in open and laparoscopic intestinal surgery. Furthermore, it should have access to a suitable infrastructure of trained dieticians, psychologists, well-motivated nursing staff and, if possible, a self-help group. The appropriate equipment such as examination couches, operating tables, hospital beds and instruments should be available in case it is necessary to switch from laparoscopy to open surgery. Peri-operative monitoring facilities are also necessary. That the surgeons should have appropriate training and experience goes without saying. Informed consent from the patient, i.e. the first interview with the patient, takes time and is extremely important. The success or failure of this type of operation depends, more than almost any other, on the patientrsquos co-operation and compliance. The patient needs to be fully informed about obesity as a disorder, laparoscopic gastric banding, possible complications, warning signs and symptoms and the post-operative follow-up.

Pre-operative procedure

The usual patient history is taken and a physical examination performed, and, additionally, endocrinological disorders need to be properly managed and treated. Internal examination by a specialist, an ultrasound scan of the abdomen and spirometry are recommended by the anaesthesiologist in our centre. If gallstones are present, they should be removed at the same time, because gallstone complications are frequent with intensive weight loss [11]. The patient sees the anaesthetist for the test results a few days before the operation. Dietary counselling and a psychological diagnosis of eating disorders are essential to determine which procedure should be appropriate for the patient. It is also highly advisable for the patient to have compressive stockings fitted by the ward nurse before admission to the ward, to prevent deep-vein thrombosis. On the day of admission to hospital, the patient should bring documents confirming that the cost will be reimbursed by the health insurance fund. In our department, we prefer to obtain informed consent from the patient well before the date for the operation.

Peri-operative care

Unlike many other types of surgical intervention, the operation for obesity represents the first stage of treatment. Regular check-ups and active patient compliance are essential for a successful outcome. A prophylactic single dose of antibiotics and low-molecular-weight heparin are recommended. On the day of the operation the patient is allowed to sip some tea or water. On post-operative day 1, the diet run-in phase begins after an oral Gastrografin X-ray has been taken. If possible, the patient should be given another dietary counselling session before the first band adjustment. Further checks may vary according to the particular operation; naturally, individual needs are taken into consideration.

Gastric bypass

The gastric bypass procedure was published as a treatment for morbid obesity as early as 1967 by Mason and Ito (see [1]). The introduction of laparoscopy surgery led to the development of many new procedures, although the principle of the gastric bypass remained the same. The concept of the gastric bypass is that the gastric pouch and the malabsorption effect of a Roux-en-Y anastomosis with an 80 to 120-cm length of the limb will cause a feeling of fullness. Between 1993 and 1999, Wittgrove and Clark [12] performed over 500 laparoscopic bypass procedures. The stomach is transected with a linear stapler (3.5-mm staples, 45 mm long) to form a proximal gastric pouch. The Roux-en-Y limb is brought to the upper abdomen either behind the colon and stomach, with an incision at the base of the mesentery of the transverse colon, or is placed in an ante-colic position. The end-to-side anastomosis of the remaining part of the stomach is made either with a circular stapler under percutaneous endoscopic control, or with an anastomosis technique that uses a linear stapler, side-to-side, as described by Lφnroth et al. [13]. The small-bowel anastomosis is also made with a linear stapler.(According to Lonroth)

The average weight loss resulting from a gastric bypass is 60–70% of the excess weight after 5 years and 55–60% after 10 years; 90% of patients can expect to achieve this result [14, 15]. A comparative study [16] at our hospital showed that higher weight loss and a better quality of life were obtained than with a vertical banded gastroplasty or the adjustable gastric band. The complications specific to this operation are anastomotic leakage 0.5 to 9%; marginal ulcer 4.5–16%; long-term micro-nutrient deficiencies in B12, folate and iron of up to 73%; weight regain in the long-term follow-up studies; and a mortality rate of 0.1–2.5% [9, 10, 11, 12, 13, 14, 15, 16, 17]. Higa et al. reported a total complication rate of 14.8% in a series of 1,500 consecutive patients [18]. The laparoscopic gastric bypass is a viable alternative to traditional open techniques. It is as safe and effective and can be performed with equal or greater efficiency. Vitamin (A, D, E and B12 and folic acid) and mineral (calcium) supplements are obligatory.

Biliopancreatic diversion/duodenal switch

The basic principle of the biliopancreatic diversion/duodenal switch (BPD/DS) procedure is similar to that of the biliopancreatic bypass. Scopinaro et al., who developed the procedure, report the largest experience with biliopancreatic bypass. The procedure, in a series of 2,241 patients operated on during a 21-year period, caused a mean permanent reduction of approximately 75% of the initial excess weight [19]. The authors report that during the first 3 to 4 months after the surgery, patients have decreased appetites related to the dumping syndrome. Scopinaro, Marinari, and Camerini reported similar early results with the laparoscopic technique [20].

The duodenum is divided between the stomach and the bile ducts, diverting pancreatic juice and bile. The duodenal stump is then closed. Ninety percent of the stomach is removed. The small intestine is divided. Using this separated section of small intestine, the surgeon makes a new connection to the open end of the duodenum. The remaining end of the small intestine is re-attached approximately 30 in. from the colon. This biliopancreatic segment now carries the digestive enzymes and bile. Food and digestive juices mix in the final short 30-in. section of the intestine. Baltasar et al. [21] and Feng and Gagner [22] described a laparoscopic variant of the biliopancreatic bypass, the duodenal switch procedure. Instead of performing a distal gastrectomy, the surgeon performs a ldquosleeverdquo gastrectomy along the vertical axis of the stomach, preserving the pylorus and initial segment of the duodenum, which is then anastomosed to a segment of the ileum, similar to the above procedure, to create the alimentary segment. Preservation of the pyloric sphincter is designed to be more physiological. The sleeve gastrectomy decreases the volume of the stomach and also decreases the parietal cell mass, with the intent of decreasing the incidence of ulcers at the duodeno-ileal anastomosis. However, the basic principle of the procedure is similar to that of the biliopancreatic bypass, i.e. it produces selective malabsorption by limiting food digestion and absorption to a short, common ileal segment. The potential for metabolic complications exists with this procedure. Patients undergoing the duodenal switch procedure require long-term medical follow-up and regular monitoring of fat-soluble vitamins, vitamin B12, iron and calcium.

Marceau et al. [23] reported on 465 patients with a duodenal switch procedure compared with 252 patients who underwent the biliopancreatic bypass. In addition to the preservation of the duodenum, the common segment was elongated to 100 cm. The authors noted similar weight loss in the two groups. In the duodenal switch group, a lower incidence of metabolic abnormalities such as protein malnutrition was noted, which prompted reversal of the procedure in 1.7% of those undergoing biliopancreatic bypass vs only 0.1% after the duodenal switch procedure. The excess weight loss varied between 70% and 90%, depending on the length of the common segment and alimentary limb. The biliopancreatic diversion with duodenal switch combines a sleeve gastrectomy with a duodeno-ileal switch to achieve maximum weight loss. Consistent excess weight loss of between 70% and 80% is achieved, with acceptable decreased long-term nutritional complications. With a higher entry weight, the super-obese patient (BMI >50 kg/m2) benefits the greatest from a procedure that produces a higher mean excess weight loss. The laparoscopic approach to this procedure has successfully created a surgical technique with optimum benefit and minimum morbidity, especially in the super-obese patient [24].

Vertical banded gastroplasty

Vertical banded gastroplasty (VBG) is a purely non-adjustable restrictive procedure and, recently, has been performed laparoscopically [25, 26]. In this procedure the upper stomach near the oesophagus is stapled vertically for about 2.5 in. (6 cm) to create a smaller stomach pouch. The outlet from the pouch is restricted by a band or ring that slows the emptying of the food and thus creates the feeling of fullness. Moreover, MacLean and colleagues reported staple-line perforations in 48% of patients, of whom 36% underwent re-operation [27]. Preliminary experiences are encouraging [26] but the long-term results of VBG are disappointing when assessed by the standard criteria [28].

In a prospective non-randomized 9-year follow-up study we could demonstrate an advantage of the adjustable restrictive procedure, namely the adjustable gastric band (AGB) [29]. The overall re-intervention rate for long-term complications in 1,011 patients was 15.6% for the VBG and 7% for the AGB group (P<0.0001). No statistically significant difference in outcome in terms of weight loss, reduction of co-morbidity and improvement in quality of life following AGB or VBG was observed. VBG was performed from 1977 but, therefore, was abandoned by our institute in 2001.

Adjustable gastric band

Early experience gained in Europe with the LAP-BAND system made by Bioenterics (Inamed Corporation, USA) led to repeated modification of the technique and resulted in great improvements in outcome [30, 31, 32, 33, 34, 35, 36, 37, 38, 39]. As with the adjustable band, the so-called Swedish band (SAGB, Obtech AG, ETHICON), which makes a smaller pouch, significantly reduced the post-operative complication rate [40, 41, 42, 43]. The AGB is a 12-mm-wide soft silicone band with an elastic balloon that can be inflated by injection according to individual need. The band is fitted around the upper part of the stomach, dividing it into two sections, the smaller of which is above the band and has a capacity of approximately 15–20 ml (pouch); the larger remaining part is below the band. The constriction is called a stoma. The following are the main differences in technique for gastric banding: by means of a calibration balloon positioned in the stomach, the site of incision is determined at the small curvature. At this site, a 0.5 to 1-cm window is placed close to the cardia. The fenestration is continued along the posterior wall of the gastro-oesophageal junction up to the angle of His. Another so-called pars flaccida technique starts at the medial edge of the right crus of the diaphragm after incision of the pars flaccida of the lesser omentum dissecting to the angle of HIS (Fig. 3). Tunnelled suturing is obligatory to prevent band slippage and to ensure that the fundus does not slide under the band. We also recommend gastropexy in addition to the stomach wall suture (fundus sutured to the left side of the diaphragm). The AGB makes it possible for the surgeon to alter the stoma diameter. Laparoscopic implantation of an AGB requires approximately the same level of skill as laparoscopic Nissen fundoplication. As with all laparoscopic procedures, there is a learning curve [44, 45] for banding that can vary quite substantially. Good surgical training, careful patient selection and inter-disciplinary follow-up management are some key factors. Trouble-free banding requires experience and practice. De Jong and van Ramshorst report a re-operation rate of 30% in their first 50 patients and a significant reduction of 13% for the next 47 [45]. Elmore et al. report that the largest number of complications occurred in the first 25 patients [46]. Angrisani and colleagues [47] report ldquodisappointing resultsrdquo in the early laparoscopic operations. Table 2 gives a summary of complications. Weight loss is given in the literature as BMI 43–46 pre-operatively to BMI 28–32 post-operatively. The target of a 50–60% reduction of excess weight is achievable [31, 47, 48, 49, 50, 51, 52]. Belachew et al. [31] have demonstrated that 80% of their patients reduced their excess weight by 60%. OrsquoBrian et al. [38] reported excess weight loss of 51% in the first year, 58% in the second, 61% in the third and 68% in the fourth year post-operatively. Studies with a follow-up of over 5 years confirm that the weight loss is long-term. A prospective study in our department, comparing the two bands, found no difference in weight loss and complication rate between LAP banding and SAGB after a 4-year follow-up [53]. Complications break down into peri-operative and late complications. Top priority is given to the prevention of complications, however. Thorough training and an inter-disciplinary approach to therapy are essential. We believe that the laparoscopically implanted AGB, both the LAP-BAND system and SAGB, is an efficient treatment method for patients with morbid obesity. It dispenses with the need for open surgery on the stomach or small intestine, which remain intact in terms of anatomy and digestive physiology. Long-term metabolic complications are not anticipated. Weight loss and food intake can be adapted to individual patient needs. Of the patients, 80–90% can expect to lose 60–70% of their excess weight. It is much easier with this method than with other procedures for the surgeon to remove the band and restore the original situation. The surgical technique is difficult in the learning phase, but it becomes easy with practice and is fairly low risk provided that the safety recommendations are observed. All these reasons make gastric banding a relatively safe and efficient treatment for morbid obesity, and it is likely to be an important surgical addition to the treatments available for most of these patients.

Gastric pacemaker

In 1995, Cigaina et al. discovered, when experimenting with pigs, that electrical stimulation of the stomach wall resulted in characteristic patterns of gastric peristalsis in both directions [54]. A further pig study demonstrated that stimulation of the stomach wall influenced the animalsrsquo eating habits. Animals whose stomach wall had been stimulated ate less. Weight loss is attributed to lower absorption of food or absorption in the gut [55].

In February 2000, a randomised, placebo-controlled double-blind trial was launched in the USA and Europe to check the clinical effectiveness and safety of the Transcend implantable gastric stimulator. The implantable gastric stimulation (IGS) system consists of two electrodes that are introduced into the stomach wall with a needle. A wire connects the electrodes to a 60Χ40Χ10.3-mm stimulator, which is implanted below the left costal arch in a subcutaneous pouch and can be programmed from outside. A suitable site is selected on the stomach wall in the gastro-oesophageal transition region, at which the electrodes can be placed in a strictly intra-mural position. The needle entry and exit points should be 2.5 cm apart and are marked with electrocautery. The electrodes are then introduced under gastroscopic control to prevent perforation of the stomach wall The probe is secured proximally with two PDS sutures and distally with a clip. The conductor wire is then taken to the outside and connected to the stimulator system. Forty-eight IGS systems have been implanted in patients throughout Europe in a clinical trial. There have been no serious complications, either post-operatively or later. Among the implants in Austria, two patients required tightening of the connection between the wire and the stimulator. This was done under local anaesthetic in day surgery. Current results of trials in all the centres show a significant excess weight loss of 32% after 15 months with a stimulator. All the implantations of IGS systems have been successful, and there have been no life-threatening or fatal complications [56, 57].

The principle of gastro-intestinal stimulation for weight loss in morbid obesity is currently one of the least invasive surgical techniques. Many more studies and examinations of eating habits and quality of life will be necessary before clear statements about the ranking of implantable gastric stimulation can be made in comparison with other treatment methods for morbid obesity. Whether the high costs (about five-times higher than the material cost of an AGB) will be justified in terms of outcome remains to be seen from further studies.

Weight loss and co-morbidity

Weight loss from BMIs of 43–46 pre-operatively to BMIs of 28–32 is reported in the literature. The target of a 50–60% reduction in excess weight is achievable. Studies with a long-term follow-up of over 5 years confirm that weight loss is maintained after obesity surgery. A prospective study in our department has shown that 80% of associated disease has either improved or resolved completely only 3 years after VBG, adjustable gastric banding and Roux-en-Y gastric bypass [16] have been performed. Morbid obesity is associated with a large number of health risks [58]. Studies have produced evidence of a significant reduction in blood sugar and cholesterol levels and blood pressure even with a modest weight loss of ldquoonlyrdquo 10% after surgical treatment. The improvement in co-morbidity is in direct proportion to weight loss after gastric banding. In 50% of patients with associated disease (diabetes, high blood pressure, dyslipidaemia), this had resolved after only 1 year, with significant improvement in a further 24% of patients [58]. Dixon and OrsquoBrien [59] describe 83% of patients with high blood pressure (78 out of 88), which was normal after 17 months (RR <140/90). Dixon and OrsquoBrien [59] documented the effects on 48 consecutive patients with reflux disease (GERD) and gastric banding. Of the GERD patients, 76% were found to be symptom free only 3 weeks after the operation. The effect was directly linked to the banding system rather than weight loss. Examination of 32 patients with bronchial asthma 12 months after banding noted a significant improvement of this condition in all of them (100%) based on the number of attacks, medication requirements, hospitalisation and physical stress [60]. Dixon et al. [60] reported a reduction of sleep apnoea and a significant reduction in obstructive airways disease in patients with the LAP-BAND system. Similar results were published by Alvarez-Cordero et al. [61]. Nine out of ten of his patients needed no medication for hypertension, and six out of 11 no longer needed medication by mouth for diabetes. Sleep apnoea resolved in all patients who had suffered from this disorder before their operation [60]. Improvement in co-morbidity as a result of significant weight loss due to adjustable gastric banding and gastric bypass is confirmed in many publications [58, 59, 60, 61, 62, 63, 64, 65]. If the patient fails to lose weight quickly enough, complications such as band slippage or leakage should be ruled out before the patient is referred to the psychologist and dietician.

Quality of life

Quality of life is significantly improved in morbid obesity patients [66, 67, 68, 69], both in terms of life expectancy [70] and physical activity, as well as satisfaction [66]. According to an analysis by Weiner et al. [67], quality of life improved significantly in 92% of patients. Our studies have shown a direct correlation between quality of life and BMI [7]. Moreover, statistically significant improvements in all areas of life (social contacts, physical activity, self-confidence, and sexuality, working and family life) were demonstrated after a BMI reduction of 5 [7]. The bariatric analysis and reporting outcome system (BAROS) has now become the accepted assessment method for quality of life and treatment outcome after AGB surgery. The BAROS assessment score covers weight loss (–1 for weight increase to +3 for 75–100% excess weight loss), co-morbidity (–1 for deterioration to +3 for completely resolution) and the quality of life questionnaire (self-esteem, physical activity, social contacts, job satisfaction, sexuality (+3, maximum and –3, minimum). Points are lost for complications (1 point) and re-operation (1 point). A score of 7–9 points is thus an excellent result, 4–6 points is good and 1–3 points is a satisfactory score, with –3 to 0 points indicating failed treatment. The health status and quality of life (QoL) assessment after surgery for obesity is summarised in Table 3 [16]. Favretti et al. report on 170 LAP-BAND-system patients, with excellent and good results in 48% [68]. The failure rate in this group is reported as 10%. Klaiber et al. reported the failure rate in their patients with the SAGB system as only 3.9% [50].

Because the band system is adjustable, the stoma can be adjusted in a female patient to assure a normal pregnancy if this occurs [71]. Patients rate the success of adjustable gastric banding very highly due to weight loss, reduction in co-morbidity and the improvement of quality of life it gives them. The positive assessment and laparoscopic implantation techniques result in a high level of acceptance among patients, GPs, specialists in internal medicine, psychologists, dieticians and sports researchers [69, 72].

The overall BAROS assessment of laparoscopically implanted gastric banding, band-assisted gastroplasty and stomach bypass shows a significantly higher rate of excellent results for the stomach bypass [16]. In terms of failure of a surgical procedure Orlistat (Roche) could be a good option as an adjuvant medical therapy [73].

Surgical treatment for obesity has proved that it is the best and most effective means of preventing the life-threatening complications and serious degenerative problems associated with pathological obesity. It is indicated by the ineffectiveness of non-surgical treatment methods and the high risk resulting from untreated obesity [70, 74]. Safe, effective surgical treatment methods increase life expectancy and quality of life for patients with extreme excess weight.

References

1.

Council on Scientific Affairs (1988) Treatment of obesity in adults. JAMA 260

2.

Segal L, Carter R, Zimmet P (1994) The cost of obesity, the Australian perspective, Pharmacoeconomics 5 [Suppl 1]

3.

Martin LF, Hunter S, Lauve R, OrsquoLeary JP (1995) Severe obesity: expensive to society, frustrating to treat, but important to confront. South Med J

4.

National Institute of Health (1985) Health implications of obesity, 59

5.

National Institute of Health Consensus Statement (1991) Gastrointestinal surgery for severe obesity. 9:1

6.

Finigan KM, Martin LF, Robinson AF, Roth N (1997) Improvement in quality of life one year after gastric Lap-Band. Obes Surg 7:281

7.

Miller K, Mayer E, Pichler M, Hell E (1997) Quality-of-life outcomes of patients with the LAP-BAND versus non-operative treatment of obesity. Preliminary results of an ongoing long-term follow-up study. Obes Surg 7:280

8.

Chua TY, Mendiola RM (1995) Laparoscopic vertical banded gastroplasty: the Milwaukee experience. Obes Surg 5:77–80

9.

Wittgrove AC, Clark GW, Schubert KR (1996) Laparoscopic gastric bypass, Roux-en-Y: technique and results in 75 patients with 3–30 months follow-up. Obes Surg 6:500–504

10.

Cleator IGM, Litwin D, Phang PT, Brosseuk DT, Rae AJ (1994) Laparoscopic ileogastrostomy for morbid obesity. Obes Surg 4:358–360

11.

Sugerman HJ, Brewer WH, Shiffman ML, et al. (1995) A multicenter, placebo-controlled, randomized, double-blind, prospective trial of prophylactic ursodiol for the prevention of gallstone formation following gastric-bypass-induced rapid weight loss. Am J Surg 169:91–96

12.

Wittgrove AC, Clark GW (2000) Laparoscopic gastric bypass: a five year prospective study of 500 patients followed from 3 to 60 months. Obes Surg 10:233–239
ChemPortPubMed

13.

Lφnroth H, Dalenbδck J, Haglind E, Lundell L (1996) Laparoscopic gastric bypass. Surg Endosc 10:636–638
SpringerLinkPubMed

14.

Pories WJ, MacDonald KG Jr, Morgan EJ, Sinha MK, Dohm GL, Swanson MS, et al. (1992) Surgical treatment of obesity and its effect on diabetes: 10-y follow-up. Am J Clin Nutr 55 [2 Suppl]:582–585

15.

Sugerman HJ, Kellum JM, Engle KM, Wolfe L, Starkey JV, Birkenhauer R, et al. (1992) Gastric bypass for treating severe obesity. Am J Clin Nutr 55 [2 Suppl]:560–566

16.

Hell E, Miller K, Moorehead MK, Samuels N (2000) Evaluation of health status and quality of life after bariatric surgery: comparison of standard Roux-en-Y gastric bypass, vertical banded gastroplasty and laparoscopic adjustable gastric banding. Obes Surg 10:214–219
CrossRefChemPortPubMed

17.

MacLean LD, Rhode B, Forse RA, Nohr C (1995) Surgery for obesity—an update of a randomized trial. Obes Surg:8:145–153

18.

Higa KD, Ho T, Boone KB (2001) Laparoscopic Roux-en-Y gastric bypass: technique and 3-year follow-up. J Laparoendosc Adv Surg Tech A 11:377–382
CrossRefChemPortPubMed

19.

Scopinaro N, Adami GF, Marinari GM, Gianetta E, Traverso E, Friedman D, Camerini G, Baschieri G, Simonelli A (1998) Biliopancreatic diversion. World J Surg 22:936–946
SpringerLinkChemPortPubMed

20.

Scopinaro N, Marinari GM, Camerini G (2002) Laparoscopic standard biliopancreatic diversion: technique and preliminary results. Obes Surg 12:362–365
CrossRefPubMed

21.

Baltasar A, Bou R, Miro J, Bengochea M, Serra C, Perez N (2002) Laparoscopic biliopancreatic diversion with duodenal switch: technique and initial experience. Obes Surg 12:245–248
CrossRefChemPortPubMed

22.

Feng JJ, Gagner M (2002) Laparoscopic biliopancreatic diversion with duodenal switch. Semin Laparosc Surg 9:125–129
CrossRefPubMed

23.

Marceau P, Hould FS, Simard S, Lebel S, Bourque RA, Potvin M, Biron S (1998) Biliopancreatic diversion with duodenal switch. World J Surg 22:947–954
SpringerLinkChemPortPubMed

24.

Kim WW, Gagner M, Kini S, Inabnet WB, Quinn T, Herron D, Pomp A (2003) Laparoscopic vs open biliopancreatic diversion with duodenal switch: a comparative study. J Gastrointest Surg 7:552–557
CrossRefPubMed

25.

Hess DW, Hess DS (1994) Laparoscopic vertical banded gastroplasty with complete transection of the staple-line. Obes Surg 4:44–46
CrossRefPubMed

26.

Natalini G, Breccolotto F, Carloni G, Calzoni L (1999) Laparoscopic adjustable vertical banded gastroplasty: a new method for treatment of morbid obesity: preliminary experience. Obes Surg 9:55–56
CrossRefChemPortPubMed

27.

MacLean LD, Rhode BM, Forse RA (1990) Late results of vertical banded gastroplasty for morbid and super obesity. Surgery 107:20–27
ChemPortPubMed

28.

Verselewel de Witt Hamer PC, Hunfeld MA, Tuinebreijer WE (1999) Obesity surgery: discouraging long term results with Masonrsquos vertical banded gastroplasty. Eur J Surg 165:855–860
CrossRefPubMed

29.

Miller K, Hφller E, Hell E (2002) Restrictive procedures in the treatment of morbid obesity—vertical banded gastroplasty vs adjustable gastric banding. Zentralbl Chir127:1038–1042
CrossRef

30.

Belachew M, Legrand M, Jaquet N (1993) Laparoscopic placement of adjustable silicone gastric banding in the treatment of morbid obesity: an animal model experimental study. Obes Surg 3:140

31.

Belachew M, Legrand M, Vincent V, Lismonde M, Le Docte N, Deschamps V (1998) Laparoscopic adjustable gastric banding. World J Surg 22:955–963
ChemPort

32.

Doherty C, Maher JW, Heitshusen DS (1997) Prospective investigation of complications, reoperations, and sustained weight loss with an adjustable gastric banding device for treatment of morbid obesity. Presented at the Digestive Disease Conference, Washington DC, May 1997

33.

Fox SR, Fox K, Hyun K (1998) The adjustable silastic gastric band versus the vertical banded gastroplasty: 7-year outcomes. Obes Surg 8:379

34.

Favretti F, Cadiere GB, Segato G, Bruyns G, De Marchi F, Himpens J, Foletto M, Lise M (1995) Laparoscopic adjustable silicone gastric banding: technique and results. Obes Surg 5:364–371
CrossRefPubMed

35.

Alvarez-Cordero R, Castillo-Gonzalez A, Ramirez-Wiella G, Aragon-Viruette E (1998) Lessons learned after 2 years LAP-BAND experience. Obes Surg 8:395

36.

Berrevoet F, Pattyn P, Hesse UJ, de Hemptinne B (1998) Retrospective analysis of laparoscopic gastric banding technique: short and mid-term follow-up. Obes Surg 8:361

37.

Chelala E, Cadiιre GB, Favretti F, Himpens J, Vertruyen M, Bruyns J, Maroquin L, Lise M (1997) Conversions and complications in 185 laparoscopic adjustable silicone gastric banding cases. Surg Endosc 11:268–271
SpringerLinkChemPortPubMed

38.

OrsquoBrian P, Brown W, Smith A, McMurrick PJ, Stephens M (1999) Prospective study of a laparoscopically placed, adjustable gastric band in the treatment of morbid obesity. Br J Surg 85:113–118
CrossRef

39.

Belva PH, Takieddine M, Lefebvre JC, Vaneukem P (1998) Laparoscopic LAP-BAND gastroplasty: European results. Obes Surg 8:364

40.

Forsell P, Hallberg D, Hellers G (1993) Gastric banding for morbid obesity: initial experience with a new adjustable band. Obes Surg 3:369–374
CrossRefPubMed

41.

Forsell P, Hellers G (1997) The Swedish adjustable gastric banding for morbid obesity—nine year experience and a four year follow-up of patients operated with a new adjustable band. Obes Surg 7:345–351
CrossRefChemPortPubMed

42.

Forsell P, Hellers G, Hell E (1998) The Swedish adjustable gastric banding (SAGB) for morbid obesity—weight loss, complications, pouch volume, and stoma diameter in a four-year follow up. Acta Chir Austriaca 30:161–165

43.

Catona A, La Manna L, Forsell P (2000) The Swedish adjustable gastric band: laparoscopic technique and preliminary results. Obes Surg 10:15–21
CrossRefChemPortPubMed

44.

Belva PH, Takieddine M, Lefebvre JC, Vaneukem P (1998) Laparoscopic LAP-BAND gastroplasty: European results. Obes Surg 8:364

45.

De Jong JR, van Ramshorst B (1998) Re-interventions after laparoscopic gastric banding. Obes Surg 8:386

46.

Elmore U, Restuccia A, Perrotta N, Polito D, De Leo A, Silecchia G, Basso N (1998) Laparoscopic adjustable silicon gastric banding (LASGB): analyses of 64 consecutive patients. Obes Surg 8:399

47.

Angrisani L, Lorenzo M, Santoro T, Nicodemi O, Da Prato D, Ciannella M, Persico G, Tesauro B (1998) Follow-up of LAP-BAND complications. Obes Surg 8:384

48.

Dargent J (1999) Laparoscopic adjustable gastric banding: lessons from the first 500 patients in a single Institution. Obes Surg 9:446–452
CrossRefChemPortPubMed

49.

Favretti F, Cadiere GB, Segato G, De Marchi F, et al. (1999) Lap-band for the treatment of morbid obesity. A 6-year experience of 509 patients. Obes Surg 9:327

50.

Klaiber C, Metzger A, Forsell P (2000) Laparoskopisches gastric banding. Chirurg 71:146–151
ChemPortPubMed

51.

Miller K, Hell E (1999) Laparoscopic adjustable gastric banding: a prospective 4-year follow-up study. Obes Surg 9:183–187
CrossRefChemPortPubMed

52.

Stieger R, Thurnheer M, Lange J. Morbid obesity: 130 consecutive patients with laparoscopic gastric banding. Schweiz Med Wochenschr 128:1239

53.

Miller K, Hell E (1999) The adjustable silicone gastric band (Lap-Band) versus the Swedish adjustable gastric band (SAGB)—a prospective randomized study. Obes Surg:9:329

54.

Cigaina V, Pinato GP, Rigo V, Bevilacqua M, Ferraro F, Ischia S, Saggioro A (1996) Gastric peristalsis control by mono situ electrical stimulation: a preliminary study. Obes Surg 6:247–249
CrossRefPubMed

55.

Cigaina V, Saggioro A, Rigo V, Pinato GP, Ischia S (1996) Long-term effects of gastric pacing to reduce feed intake in swine. Obes Surg 6:250–253
CrossRefPubMed

56.

Miller K (2002) Implantable electrical gastric stimulation to treat morbid obesity in the human: operative technique. Obes Surg 12:17S–20S
CrossRefPubMed

57.

Miller K, Hφller E, Hell E (2002) Intragastric stimulation (IGS) for the treatment of morbid obesity. Zentralbl Chir 127:1049–1054
CrossRefChemPortPubMed

58.

Gordon T, Kannel WB (1976) Obesity and cardiovascular disease: the Framingham study. Clin Endocrinol Metab 5:367–375
ChemPortPubMed

59.

Dixon JB, OrsquoBrien PE (1999) Gastroesophageal reflux in obesity: the effect of LAP-BAND placement. Obes Surg 9:527–531
CrossRefChemPortPubMed

60.

Dixon JB, Chapman L, OrsquoBrien P (1999) Marked Improvement in asthma after LAP-BAND surgery for morbid obesity. Obes Surg 9:385–389
CrossRefChemPortPubMed

61.

Alvarez-Cordero R, Ramirez-Wiella G, Aragon-Viruette E, Toledo-Delgado A (1998) Laparoscopic gastric banding: initial two year experience. Obes Surg 8:360

62.

OrsquoBrian P, Brown W, Smith A, Chapman L, Kotzander A, Dixon J, Stephens M (1998) The LAP-BAND provides effective control of morbid obesity—a prospective study of 350 patients followed for up to 4 years. Obes Surg 8:398

63.

MacGregor AMC (1999) Effect of surgically induced weight loss on asthma in the morbidly obese. Obes Surg 3:15–21
CrossRef

64.

Amaral JF, Tsiaris W, Morgan T, Thomson WR (1987) Reversal of benign intracranial hypertension by surgically induced weight loss. Arch Surg 122:946–949
ChemPortPubMed

65.

Pories WJ, MacDonald KG, Jr, Morgan EJ, Sinha MK, Dohm GL, Swanson MS, et al. (1992) Surgical treatment of obesity and its effect on diabetes: 10-y follow-up. Am J Clin Nutr 55 [2 Suppl]:560–566

66.

Miller K, Hell E, Schoen E, Ardelt E (1998) Quality of life outcome of patients with the LAP-BAND vs vertical banded gastroplasty: results of a long-term follow-up study. Obes Surg 8:359

67.

Weiner R, Wagner D, Datz M, Bockhom H (1999) Quality of life outcome after laparoscopic gastric banding. Obes Surg 9:336

68.

Favretti F, Cadiere GB, Segato G, Busetto L, et al. (1998) Bariatric analysis and reporting outcome system (BAROS) applied to laparoscopic gastric banding patients. Obes Surg 8:500–504
CrossRefChemPortPubMed

69.

Oria HE, Moorehead MK (1998) Bariatric analysis and reporting outcome system (BAROS). Obes Surg 8:487–499
CrossRefChemPortPubMed

70.

Drenick EJ, Bale GS, Seltzer F, Johnson DG (1980) Excessive mortality and causes of death in morbidly obese men. JAMA 243:443–445
CrossRefChemPortPubMed

71.

Martin LF, Finigan KM, Rabner JG, Greenstein RJ (1997) Adjustable gastric banding and pregnancy. Obes Surg 7:280

72.

Doldi SB, Micheletto G, Lattuada E, Zappa MA (1997) Surgical procedure for morbid obesity: our 20 yearsrsquo experience. Obes Surg 7:294

73.

Miller K, Hell E (1999) Orlistat treatment after failure of the adjustable gastric band system. Obes Surg 4:333

74.

Wadden TA (1993) Treatment of obesity by moderate and severe caloric restriction. Results of clinical research trials. Ann Intern Med 119:688–693
ChemPortPubMed

The Obese Are Victims Not Perpetrators

The lean are not “better” or superior persons because their weight appears “under control.” Their thinness is a biological gift. They are the lucky ones who have won the “Weight Sweepstakes.” Somehow, by a Monte Carlo roll of the dice, they received a biology which has kept their bodies within a range of weight our society regards as “normal.”
The human body controls the weight of the lean with the same basic mechanisms as it does that of the obese. They, therefore, do not deserve any more praise or blame than the obese for being driven by their own biology.

What is deserved, however, is our society coming to finally accept that the obese (as well as the lean) are powerlessness in voluntarily controlling their own weight. We all are truly powerless because we do not know the exact details, the “secrets,” of how our biology controls our weight. Someday, we will fully understand those “secrets” so that we may help develop medical treatments to keep or make everyone thin, at least if they want to be. Someday, we’ll know–not for a good while I expect, despite the hype about “cures” in animals and new treatments we frequently see, hear and read in the media.

But, for now, without possessing those “secrets” about how the body’s biology keeps a person thin or fat, and having little else practical to offer most morbidly obese persons for their greatly excess weight and associated co-morbidities, surgery is the appropriate weight control option to consider for those who meet the bariatric surgical standards.

If surgery is not acceptable or available for some reason, we should at least treat the obese with respect. We should regard them as victims of their disease which they are, because, once we see them as victims, not culprits, they have our sympathy, our hearts go out to them, we understand that their condition is something fundamentally beyond their control. We can at least help them to cope better with their disease and its co-morbidities instead of allowing them to be mocked, derided and scorned on a daily basis.

The fat cells of the obese progressively overgrow their bodies, gathering more and more fat like a huge enveloping overcoat, a gigantic tumor which, at the same time, is invading every body organ. These obese victims have greatly increased chances of a shorter life, heart disease, hypertension, diabetes, sleep apnea, cancer and many other conditions known to be associated with obesity, particularly morbid obesity.

Morbid obesity thus has a malignant nature which is often unremitting, punishing and lethal. To “politely” ignore it is as ludicrous as the courtiers in the children’s story saying the naked Emperor was well-clothed. In an analogous case, saying that the morbidly obese Emperor “has a little weight problem which he needs to control” totally denies the truth and enormity of the subject. Our society, likewise, remains largely in denial about the truly serious, basically involuntary, malignant nature of obesity.

This malignancy makes the obese victims of their own biology, the helpless products of chance associations between their genetics and their environment. How can they, in all honesty, be more “guilty” than the lung cancer victim who smokes heavily, the heart attack victim who chronically consumes a high fat diet or others who acquire sexually transmitted diseases? How can our society dare to deny the obese a share in this victimhood? All of these other victims may likewise possess genes which promote a specifically compulsive lifestyle which our exceptionally bountiful, permissive environment promotes. Yet, medical insurors and their ilk almost always support treatment for these other diseases but deny it to obesity. They draw the line, an unfair, stereotypical, highly visible one.
And, obesity is nothing if not highly visible. Superficially at least, you can hide your addiction if you are an alcoholic or drug addict or have somewhat different approaches to sex. But, unlike certain movie plots, the obese cannot magically shrink. Obesity is obvious; it is there for all to see, even at a glance. Their outsize skin and all of its contents make the obese walking billboards, highly visible targets. If you have a hang-up or need to “take it out” on someone, or even to help improve your medical insurance company’s bottom line, they are there, targets for abuse without penalty.

And, they are there almost all alone, most obese persons passively accepting the scorn and their “guilt” as well-founded. Their gross mistreatment is further supported by “political correctness” which freely punishes the obese since they have become the “last bastions of prejudice.” They are truly the undeserved victims of a cultural, as well as medical, disease, the modern medical-moral equivalent of lepers.

Our Society must come to understand that the obese deserve the same compassion and understanding as do other disease victims, regardless of how they came to be victims. A disease is a disease is a disease is obesity.

As a first step towards making amends for past damage, let us resolve to not add to the already tragic malignancy of their condition by heaping more abuse upon the obese victims. Rather, let’s resolve to treat others, and ourselves where indicated, better, to love and care for people regardless of their weight. And, as part of this respect for all people, we must deny weight harassment and fat-ism any place within the boundaries of our society. It should be made as illegal as sexual harassment and with at least as many penalties.

Bibliography

Cowan GSM Jr, MD Smalley, N Defibaugh, KB Cowan, ML Hiler, W Sehnert, S James. Obesity Stereotypes Among Physicians, Medical and College Students, Bariatric Surgery Patients and Families. Obesity Surgery 1(2):171-176, 1991.

Cowan GSM Jr. Bariatric Surgeons, Stereotypes and Paradigms. Obesity Surgery. 2(1):7-12, 1991. [Delivered as Presidential Address to American Society for Bariatric Surgery, June, 1991]

Plastic Surgery After Massive Weight-Loss Obtained From Bariatric Surgery

There is much knowledge to share between bariatric surgery and plastic surgery, which are close fields. There are also some misunderstandings, and a need to improve cooperation between them.

Plastic surgery can play a very important part relative to massive weight loss. It is already well known that fat pads can be removed either by aesthetic or plastic surgery. More recently, surgeons have been exploring methods of plastic reconstruction after massive weight-loss, such as that obtained after digestive surgery. Bariatric surgeons should be aware that some of their patients will need heavy and painful reconstructive procedures.

1. Key-points of the strategy in plastic surgery in an obese patient with massive weight-loss:

Successful weight-loss can be associated with two types of side-effects:

  • The skin is too loose: The tension and elasticity of the skin vary greatly from one person to another. A 25 kg weight-loss can be as troublesome as a 80 kg one, depending on the patient.
  • The quality of the skin will also vary on different parts of the body. Many patients find the abdomen to be their major area of concern, although the arms, the interior side of the thighs, or breasts can be just as troublesome.

  • Fat is still present in some areas of the body: This depends on the type of obesity (gynoid or android). The goal of plastic surgery is to re-harmonize the two parts of the body by removing excess fat and skin.

2. Therapeutic strategy

  • Scheduling the operation
  • There is a general consensus for scheduling the operation when the weight has stabilized and remained so for several months. As a rule, one counts at least one year after digestive surgery (or the successful outcome of an intensive diet).

    Notwithstanding, some patients are prepared to have surgery when they still have few kilograms to lose. This is not necessary a contra-indication, for the following reasons:

    Plastic surgery can reinforce the motivation for further weight-loss.
    The operation can remove kilos that would otherwise have been very difficult to lose, even with the most effective procedure or a very strong diet. An abdominoplasty can, for example, remove 2 to 3 kg, a bodylift 4 to 6 kg, a breast reduction 1 to 2 kg, and liposuction 3 to 4 kg.

  • Where to start?
  • One should start with the most troublesome area, which in most cases is the abdomen.

    Some patients prefer to start with a breast reduction because postoperative care is short, enabling them to return to work rapidly. For some, even if upset by a hanging abdomen, reshaping their face is a priority because of its obviousness.

    3. Parts of the body on which to have plastic surgery

  • Abdomen : Abdominoplasty is the most claimed operation (80%).
  • It aims at the following:

    1. To remove excess fat tissue.

    2. To remove excess skin above and beneath the umbilicus.

    3. To repair overdistended muscles resulting from pregnancy or the pressure formerly exerted by body fat before weight loss.

    The scar resulting from the abdominoplasty is situated very low, just above the pubis, going up slightly on either side, and can be hidden in the swimsuit. The pubic hair is repositioned as normal.

    An additional liposuction may also decrease the size of the “Venus mount”.

    Follow-up is generally simple. Hospitalisation lasts about one week. The main complications patients face are thrombo-embolism, and wound problems. The patient should remain off work for one month.

  • Breasts:
  • Both functions of the breasts, i.e. feeding and erotic, are important. The psychological role they play according to their shape is major, and any flaw in their shape or size can cause much distress. From of health point of view, they may cause lumbago if too heavy. Hence, the aim of surgery is to recreate a normal shape and volume. The procedure is relatively straightforward: a hospitalisation of 48 to 72 hours is enough.

    The only cause for concern is the scars left behind after surgery, but these are getting smaller and smaller thanks to rapidly improving techniques.

  • Inside part of the thighs
  • This is one of the areas of the body where skin is the thinnest. As the patient loses weight, the skin shrinks, creating a distressing roll of fat, which in turn leads to functional and aesthetic problems (“it rubs”).

    Surgery is effective (1,5 kg of skin is removed from each thigh) and discreet because the scar can be hidden at the root of the thigh.

    Scar healing does, however, take longer than usual because the scar is located in a fold which is very mobile and is also prone to steep.

  • Bodylift
  • This is a complete lift of the lower body, with a scar going right round the body, low enough to be hidden by the swimsuit.

    A bodylift is often performed in conjunction with liposuction of the fat on the buttocks.

    The bodylift is a relatively heavy procedure because of the amount of skin removed (20 to 30 cm in height of skin around the body), the weight of the tissues (4 to 6 kg in an average, sometimes more), the length of the intervention (4 to 5 hours). Also the fact that the abdomen, buttocks, hips, and thighs are all lifted at the same time adds to the seriousness of this intervention. The recovery period is often marked by extreme fatigue but the result can be very spectacular.

  • Arms
  • The excess of fat and skin on the arms can be a problem with clothing. Lifting of the arms is therefore very sought.

    The operation itself is relatively straightforward, and the scar is easily hidden under the arm. This operation can, for example, be combined with a breast reduction.

  • Face
  • Facial lift can decrease the ptosis of the skin on the face and the neck. Individual bone shape, heredity and quality of the skin all play an important role regarding the outcome, and to a certain extent how long the lift will be effective. The aim is to enable the patient to “look good for his age”, and to give the face a sharper outline and a brighter look. .
    The surgeon works on one side of the face, then the other, through small incisions made in the scalp, or in the natural creases around and at the back the ears. Incisions are designed to obtain the smallest possible scars. If necessary, excess fat is removed and distended muscles are tightened. The skin is then pulled and any excess skin is removed.
    The aim is to give the face a firm and fresh contour. The colour of the skin may temporarily change after the operation, and the patient may experience a feeling of tingling and hardening of the skin on the face and the neck. Healing is slow, and it can take weeks or even months before the final result is obtained.

    The scars can be hidden within the hair, and by appropriate make-up. The skin remains fragile for several weeks. It is therefore recommended to avoid exposure to the sun and to protect the skin with a total sunblock cream. The patient may use make-up very soon after surgery.

    General comments

    We would like to emphasize three points:

    1. A previous laparoscopic approach for bariatric surgery (such as the adjustable gastric banding) facilitates further plastic surgery. But let us not forget that the patient will hence deserve the best possible reconstruction.

    2. Although we know the main rules of timing and priorities for reconstruction , such topics should be investigated furthermore.

    3. Coordination between the two surgical fields should be upgraded, so that we could reach an integrated approach for each patient. This has been the goal of common meetings, such as those organized in Lyon in 1999 and 2000 in November.

The Physiology of Weight Change

INTRODUCTION

All professionals dealing with obese people, especially obesity surgeons who deal with extremely obese people, have observed the discrepancy existing between what many fat persons say and what are the common beliefs for both lay people and medical doctors. One example indicates what I mean. Practically all of the about 10,000 obese patients who came to my observation during the last 25 years told me a story of progressive lifelong weight gain, whereas no one of them ever told me of a progressive lifelong increase in food intake. The easier explanation for this apparently inexplicable phenomenon is that obese people lie. But, why should they lie to the bariatric surgeon, and, above all, is it possible that all of them lie?

Other common statements of the obese persons (especially women) which may be difficult to explain are: 1) that there are many other persons (especially men) of the same age and height who eat much more than them and still are much thinner than they are; 2) that they do not lose weight even staying on a diet; 3) that, after losing weight on a diet, when they go back to the previous food intake they stabilize at a higher weight than the previous one. Common sense teaches that when many people tell the same story they are probably telling the truth. So, the conclusion is that there must be something we have not understood.

The aim of this paper is to clarify the relationship between energy balance and body weight, in order to avoid grossly mistaken evaluations on which are based many false assumptions, beliefs and expectations that are today frequently accepted also, if not especially, among professionals dealing with obesity.

THE BALANCE BETWEEN BODY WEIGHT AND ENERGY INTAKE

Like any other natural entity, human body must obey physical laws, in this case represented by the first principle of thermodynamics, according to which energy cannot be created nor destroyed, but only transformed. Consequently, all excess energy introduced must necessarily modify the internal energy of the system, being retransformed in potential chemical energy. And, since our main energy store is fat, an energy intake greater than energy expenditure unavoidably causes an increase of adipose tissue, which is always accompanied by an increase of lean body mass, and thus an increase of body weight.

Starting from a condition of weight stability, a permanent increase of energy intake causes an increase of body weight. Since body energy expenditure is proportional to body weight, an increase of the latter also causes an increase of energy expenditure. The body weight will then stabilize when the energy expenditure of the weight gain will equal the increase of energy intake, the balance condition being reestablished. Exactly the opposite happens if the energy intake is permanently reduced. It may then be concluded that, under the same conditions (and then in each individual), to each definite energy intake corresponds a definite body weight, which is the one that produces an energy expenditure equal to that energy intake, and to each definite permanent change of energy intake corresponds a definite change of body weight, which is the one that produces a change of energy expenditure equal to that change of energy intake. For the same permanent change of energy intake, the size of weight change evidently depends on the energy expenditure of the weight that is gained or lost, which in turn depends on its composition and on the unit energy expenditure of its components.

The weight gained or lost by a person with normal body weight is composed of two-thirds adipose tissue and one-third lean body mass, which consume about 5 and 40 Cal/kg/day, respectively. One kilogram of such weight consumes then about 17 Cal/day. Therefore, if a normal weight person increases or decreases permanently his/her energy intake by 100 Cal/day, his her body weight will eventually increase or decrease by about 6 kilograms, which produce an energy expenditure equal to the variation of energy intake. Considering that 100 Calories represent more or less the energy content of a cappuccino, the corresponding weight change appears decidedly greater than what is commonly believed.

How long does it take to gain or lose the above 6 kilograms? It evidently depends on how many Calories are cumulatively necessary to build a new kilogram of body weight (energy cost of weight gain = energy content of the tissue + energy needed to build it) and, vice versa, on how many Calories are provided by the demolition of one kilogram of existing body weight (energy yield of weight loss = energy content of the tissue – energy needed to demolish it). The energy cost of adipose tissue and lean body mass correspond to about 10,000 and 2,000 Cal/kg, and the energy yield to about 7,500 and 800 Cal/kg, respectively. Therefore, energy cost and yield of one kilogram of weight with the above mentioned composition (two-thirds adipose tissue and one-third lean body mass) are equivalent to about 7,000 and 5,400 Calories, respectively. Since 6 kilograms are to be gained or lost, the overall cost or yield would amount to 42,000 and 32,000, and, as the positive or negative energy price paid per day is 100 Calories, one would be tempted to conclude that total gain or loss would be completed in 420 and 320 days, respectively. However, energy balance is positive or negative by 100 Cal/day only initially, then it gradually reduces because the body energy expenditure changes according to the consumption of the weight gained or lost. Times for gain or loss are consequently lengthened, with an asymptotic curve such as 99% of the total weight is gained or lost in about 4 and 3 years, respectively. However, due to this type of curve, 75% of the total weight is gained or lost in little more and little less than one year, respectively.

Interestingly, if the permanent change of energy intake, and thus the weight change, was smaller or greater (e.g., 200 Cal/day for 12 kilograms), the composition and consequently the cost and yield of the weight gained or lost being the same, the time for the total weight change would remain exactly the same. In fact, the quicker variation of body weight due to the greater energy imbalance would be exactly counterbalanced by the quicker variation of energy expenditure that accompanies the weight variation. Instead, if the composition of weight change was different, for the same variation of energy intake times for gain or loss would be the longer or shorter the greater or smaller the percentage of adipose tissue (and thus the cost or the yield) in the weight gained or lost.

Whereas there is no theoretical upper limit to body weight in humans, there is probably a limit to lean body mass size, as there is for stature, that may be indicated as 100 kg for men and 70 kg for women. The more the weight increases and the lean body mass approaches that limit the smaller is its increase in proportion to body weight increase, and thus the composition of weight gain or loss varies according to the starting body weight. Consequently, the weight gained or lost by a heavier individual, containing less lean body mass, consumes less and costs or yields more in comparison with the same weight gained or lost by a lighter individual. Therefore, a heavier person, for the same energy intake variation, gains or loses more weight and in a longer time than a lighter person. To give an example, one kilogram of weight gained or lost by a very lean person, composed of 50% lean body mass, consumes about 22.5 Cal/day and costs or yields about 6,000 or 4,000 Calories, whereas one kilogram gained or lost by a person so heavy that the percentage of lean body mass in his/her weight variation can be considered negligible consumes about 5 Cal/day and costs or yields about 10,000 or 7,500 Calories, respectively. A permanent change in energy intake of 100 Cal/day would cause the first person to gain or lose 4.5 kilograms in about 2.5 or 1.8 years, while the second person would gain or lose as much as 20 kilograms, even if in about 19 or 14 years, respectively.

Contrarily to what is generally believed, the heavier one is, the easier it is to gain further weight, and this occurs for smaller and smaller increases of energy intake, so small that it becomes practically impossible to perceive them; in addition, the long time necessary to reach the stabilization makes it very difficult to notice the weight variation.

This phenomenon explains the common clinical observation of the patient who reports a history of progressive lifelong weight gain with no progressive lifelong increase in food intake. Moreover, it is quite possible that the energy intake has actually remained the same, the progressive weight gain being caused by decreased energy expenditure due either to the progressive reduction of physical activity that generally accompanies weight gain or to the progressive reduction of lean body mass which inevitably occurs with aging.

In reality, the fact that weight gain, since the ratio fat/lean in what is gained is inverse to that of what exists, alters body composition at the advantage of adipose tissue, thus causing a progressive decreasing energy expenditure per unit of body weight, has been known for a long time. What is interesting to note is the extent that this phenomenon can reach considering that the composition of the weight gain is not constant, but containing a percentage of lean body mass which progressively decreases with the increase of body weight. As a consequence, with progression of weight gain, any further gain corresponds to smaller and smaller increases of energy expenditure, with a progressively greater discrepancy between the increase of body weight and the increase of energy expenditure. The obvious result is that the differences in energy expenditure/intake among subjects with relatively great differences in body weight is relatively small. And this explains another common clinical observation (especially in women) which is ignored or denied by many bariatric professionals.

The obese patient eats on the average more than the lean person, but not much more.

In our population, the difference in total energy expenditure, and thus of energy intake, between a group of 34 lean subjects with mean stable body weight of 65 kg (range 55-83 kg; mean TEE: 1,989 Cal/day, range 1,167-3,176) and a group of 86 obese patients with mean stable body weight of 124 kg (range 90-203 kg; mean TEE: 2,246, range 1,322-5,064) was little more than 250 Cal/day. Furthermore, due to the enormous interindividual variability, caused by many variables other than composition of weight change, the overlap between the two groups was such that it was well possible for a subject much heavier than another one to consume and eat much less than the latter.

THE BALANCE BETWEEN BODY WEIGHT AND ENERGY EXPENDITURE

We have dealt above with the variations of body weight consequent to a permanent variation of the energy intake. They also entail a variation of energy expenditure which is secondary to the variation of body weight and stops when the new energy expenditure reaches the balance with the new energy intake, with the ensuing stop of the body weight variation. Let us see now what happens in the opposite case, i.e. when the variation of energy expenditure is primitive, and, the energy intake remaining unchanged, it causes the variation of body weight.

Total energy expenditure (TEE) is composed about 70% of “resting energy expenditure” (REE), about 20% of “activity energy expenditure” (AEE), and about 10% of “diet-induced thermogenesis” (DIT), which represents the energy expenditure necessary for mastication, transit, digestion, absorption, and metabolism of food. What varies with body weight is essentially REE. Let us refer initially to the most common case, that is the variation of AEE due to decrease or increase of physical exercise. A permanent change of AEE, the energy intake remaining unchanged, obviously causes an energy imbalance, with consequent increase or decrease of body weight until the ensuing change of REE brings TEE back to its starting level, corresponding to the unchanged energy intake. Exactly the same occurs following a possible change of DIT in percent of energy intake which, the latter being unchanged, evidently results in a change of the DIT absolute value. Another very common case is the disappearance of the thermogenesis induced by cigarette smoking, which inevitably causes weight gain if the smoke cessation is not accompanied by a reduction of energy intake. In all these instances, where the energy intake is unchanged, the variation of one of the TEE components is counterbalanced by the variation of opposite sign of another component, namely REE, so the energy expenditure goes back to its starting value thanks to a variation of body weight.

Only apparently more complex is the case of energy expenditure change due to increase or decrease of REE per unit of body weight, i.e. a variation of REE not caused by a variation of body weight, and then of the consuming mass, but, the weight being unchanged, by the fact that the same mass consumes (in resting conditions) more or less than before. This simply occurs because of change of the ratios among the components of body mass, which, as we know, have very different unit resting consumption. The most common case is the variation of the fat/lean ratio, that, as said above, inevitably follows any body weight change, but can occur, body weight being unchanged, for instance after weight loss and regain for a drastic diet, or simply due to aging. However, let us remember that the two main components of lean body mass also have very different REE, that of viscera (about 360 Cal/kg/day) much greater than that of muscles (about 18 Cal/kg/day). Therefore, if for any reason, with body weight remaining unchanged, within lean body mass muscle/viscera ratio changes, REE of lean body mass increases or decreases because the proportions of tissues with very different REE have changed. And this also obviously results in a variation of REE per unit of body weight.

In case of variation of REE per unit of body weight, as a rule the energy balance is not reestablished by variation of opposite sign of another component of TEE (even if this is a possible eventuality), but by variation of REE itself which, by increasing or decreasing as absolute value with the variation of body weight, compensates the relative variation that had determined the energy imbalance, thus reestablishing the equilibrium. In other words, the energy intake being unchanged, if each kilogram of body weight consumes more or less than before, the number of kilograms must decrease or increase to produce an energy expenditure equal to the energy intake. This phenomenon is better understood if we think that the change of body composition that causes it does not occur contextually (even if generally the long time necessary to completion of the overall variation could make it believable), but first the loss or gain of a weight with a certain composition and thus a certain unit consumption, and subsequently the gain or loss of another weight with a different composition and unit consumption may be identified, the overall energy expenditure of the second being necessarily equal to that of the first.

The physiological loss of lean body mass that occurs with aging, if the energy intake remains the same, compulsorily causes the gain of a body weight which, as we know, is composed of lean and fat, and thus consumes less and must be gained in a greater amount to produce the same consumption of what was lost. To give another example, drastic diets cause a weight loss containing a percentage of lean body mass which may exceed 50%, whereas the composition of the weight that is subsequently regained, as we saw, depends on the starting weight and contains anyway less lean in comparison with the weight lost, thus consuming less than the latter. In both cases the result is a person who, eating as much as before, necessarily weighs more.

The size of the change in body weight which, with the energy intake remaining constant, is caused by a change of body composition depends on the different unit resting consumption of the tissues that were exchanged. And, since the unit resting consumption of the different body constituents are very different among themselves, small changes of body composition may cause great changes of body weight.

In conclusion, we first learned that each variation of energy intake must be counterbalanced by an equal variation of energy expenditure, which occurs through a variation of body weight, so that for each individual to a definite energy intake must correspond the body weight that produces the energy expenditure equal to that intake. However, we also learned that the same energy expenditure may be produced by very different body weights, as well as the same body weight may produce very different energy expenditures, depending on different body compositions. This explains how individuals with equal body weight may have different energy intakes, and individuals with the same energy intake may have different body weights, and how a very heavy individual may have an energy intake much smaller than that of another much lighter individual, and vice versa. In summary, certainly the energy intake determines body weight and its variations, but the size of body weight and of its variations is determined by body composition and by its variations.

THE REGULATION OF BODY WEIGHT CHANGE

There are many biological phenomena, which occur as a consequence of variations of body weight, or energy intake, or energy expenditure, or energy balance, that in turn influence body weight. Some of these phenomena produce a negative feed-back system, opposing any body weight variation in any direction, and then tending to maintain body weight at any level it is. Other phenomena, again at any level of body weight, act only opposing its reduction, and other only favoring its increase. All these phenomena are to be considered “physiological”, because they occur necessarily in all individuals, and, even if they favor the onset of obesity, they do it equally in all subjects. Finally, there are phenomena favoring weight increase, congenital or acquired, that can be considered frankly “pathological”, because they occur only in some individuals, who, independently of the fact that they become obese or not, are in a condition of greater vulnerability towards weight gain as compared to other people.

PHYSIOLOGICAL PHENOMENA TENDING TO LIMIT WEIGHT CHANGE

The simplest among the phenomena that create a negative feed-back mechanism tending to limit the weight change is the above described variation of energy expenditure that accompanies the weight change itself and stops it when the energy balance has been reached. Other phenomena that act by limiting the energy imbalance, causing increase of energy expenditure in the case of positive energy balance and vice versa, are the variation of DIT which accompanies increase or decrease of energy intake and the variation of AEE which accompanies increase or decrease of body weight according to the corresponding variation of the mass to be moved. The increased appetite consequent to the increased energy cost of physical activity acts in the same direction.

The most important and also the most debated among these phenomena is represented by the variation of resting energy expenditure per unit of fat-free mass (REE/FFM) consequent to a consistent increase or a drastic reduction of energy intake. This phenomenon, particularly investigated in the case of reduction of energy intake, is generally admitted and considered totally reversible with the resumption of previous energy intake, whereas its permanence in the case of energy intake permanently reduced is questioned. In six subjects who had kept for three to ten years a body weight steadily reduced by a drastic diet from a mean of 103 kg to a mean of 69 kg we found a mean REE and energy intake smaller by 30% in comparison with a group of controls with equal mean body weight, while the lean body mass was smaller only by 15%. The variation of REE/FFM consequent to the great variations of energy intake could be caused, rather than by an actual variation of resting consumption of the tissue unit (very difficult to be explained), by an alteration of the viscera/muscles ratio for increase or decrease of the first sector consequent to greater or smaller trophic stimulation of the GI tract by food. This explanation, referring to a change of body composition, would also account for the persistence of the phenomenon as long as its cause persists, which in this case would not be reduction of food intake but reduced food intake.

PHYSIOLOGICAL PHENOMENA OPPOSING WEIGHT REDUCTION

As we saw, if the energy intake is permanently reduced, body weight also reduces until it produces en energy expenditure equal to the intake, and the size of the reduction is inversely proportional to the consumption of the weight loss, which in turn depends on its composition that is determined by the starting weight. As already mentioned, a drastic diet, either in absolute terms (less than 1,200 Cal/day) or in relative (more than 500 Calories less than the starting TEE), causes the loss of a weight containing a percentage of lean body mass greater than what would be physiological for that definite starting weight. This phenomenon, which was proved in fertile women, while the clinical experience and the results of our studies suggest that it does not occur in postmenopausal women or in men, has two types of negative consequences. On one side, starting from the same body weight, since the weight loss consumes more, for a definite cumulative reduction of energy intake less weight is lost, even if in shorter time, than what would be if the weight loss composition was the physiological one. On the other side, with the weight attained being the same, since more lean than due was lost, body weight contains less lean and more fat, and then it consumes less. This means that to maintain any weight after a drastic diet one has to eat less than another person who has lost the same weight with the physiological composition, or a person with equal body weight who never lost weight. But the worst aspect of this phenomenon is that the alteration of body composition that it causes is permanent. In fact, in the case of weight regain after a drastic diet, the composition of the weight regain is the one physiological for the starting weight. Thus, less lean and more fat are regained in comparison with what was lost, and consequently also the maintenance of a weight equal to that prior to the diet entails an energy intake smaller than that before dieting. And, since the alternative is to go back to the previous energy intake stabilizing at a higher weight than that before dieting, it is easily understood how a series of such ups and downs (which is defined as “weight cycling”) may lead to a progressive weight gain progressively more difficult to control. Many young women with no genetic predisposition to obesity, misled by mass media and not protected by specialized surveillance, vainly pursue unrealistic beauty ideals and eventually condemn themselves to become obese or to stay on a diet all their life.

PHYSIOLOGICAL PHENOMENA FAVORING WEIGHT GAIN

As said above, with aging the lean body mass physiologically reduces, and, if this is not counterbalanced by an adequate reduction of energy intake, the obvious result is an increase of body weight. But the most perverse of the physiological mechanisms that favor weight gain can be identified with the already described variation of the composition of the weight gain or loss according with the starting weight. As we saw, the weight gained or lost contains the more lean the smaller is the body weight, and vice versa. Now, if the weight decreases this phenomenon opposes the weight loss (and, as to this aspect, it should have been described in the preceding paragraph). Actually, since the decrease of lean body mass is progressively increasing, the reduction of energy expenditure also progressively increases, and this obviously opposes further weight reduction. Indeed, due to the increasing lean/fat ratio in the weight loss, each kilogram successively lost consumes more and more, and then requires a negative variation of energy balance greater and greater to be lost. On the contrary, when body weight increases, the same phenomenon, instead of opposing the weight gain, favors it. In fact, the increase of lean body mass progressively decreases, and the same is true for the increase of energy expenditure. The lean/fat ratio in the weight gain decreases; each kilogram successively gained consumes less and less and is gained for a smaller and smaller positivity of energy balance. As we already saw, this explains how, especially in the already obese subject, relatively great increases of body weight are accounted for by relatively small increases of energy intake. Therefore, the variations of energy expenditure consequent to the modifications of body composition which accompany the weight changes produce effects that go in the same direction in both cases of weight gain and loss.

The sum of all the above physiological regulation mechanisms causes the human organism to tend not to the maintenance of body weight, even if at any level, as it is commonly believed, but on the whole to favor weight gain and to oppose weight loss, an aptitude that was selected during many thousands of centuries in conditions of food scarcity and that was certainly in other days providential for the preservation of our species.

PATHOLOGICAL PHENOMENA FAVORING WEIGHT GAIN

The word “thermogenesis” (improperly used, since all types of energy consumption eventually result in heat production) defines the increase of REE consequent to stimuli such as cold, anxiety, cigarette smoking, caffeine (as well as pharmacological agents able to reproduce their effects), but above all food. The diet-induced thermogenesis (DIT), differently than that produced by other stimuli, was found reduced in obese subjects in comparison to lean individuals, in a proportion that, according to different studies, varies from one-third to two-thirds of cases. This necessarily entails, for the same energy intake, a greater body weight. A genetically reduced lean body mass would evidently produce the same effect. However, it is practically impossible to demonstrate the primitivity of both these phenomena, because there are no studies in the preobese, and the results of those carried out in the postobese are conflicting and biased by other variables.

Other pathological phenomena, similarly only hypothetical so far, that could favor weight gain are congenital or acquired alterations of the composition of weight gain or loss, but above all of the visceral mass size. On the contrary, it is beyond doubt that any pathological reduction of AEE, of any type and due to any cause, favors weight gain.