The worldwide obesity epidemic: a review
(A 15,000 years' unsolved disease)

Author:
 Dr. Daniel Oscar Belluscio 1992-2009. ©All rights reserved

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Index to the article

• Combating the "yo-yo" syndrome
• Fighting their natural tendency to retain the weight
• The health risk of being overweight.
• Discrimination
• Loss of self esteem
• Weight control programs: Why did we not reach our goal?
• Adipose tissue metabolism: An overview (opens in a new window)

• Clinical and field methods to estimate obesity (opens in a new window)
  B. Obesity by fat content.
  C. Methods to estimate body fat content

• Metropolitan height-weight Tables NEW!

• BMI Calculator

• Nature vs. nurture.
• Physical activity and obesity.
• Prevalence of obesity.
• A multifactorial model to explain the genesis of obesity.
• The "villain" in our story: The hypothalamus as the end organ in the genesis of obesity.
• Autonomic Nervous System and Obesity.
• Endocrine system and Obesity.
• The treatment of obesity: Are we unjustly blaming obese subjects for their lack of will power to struggle against their disease?
• The hCG (Human Choriogonadotropin) method for weight loss: overcoming the "test of time" NEW! (opens in a new window)
• Bibliography

Obesity: A worldwide epidemic

"To say that obesity is caused by merely consuming too many calories is like saying that the only cause of the American Revolution was the Boston Tea Party."

Adelle Davis-American Nutritionist and Writer, 1904-1974

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Obesity has reached epidemic proportions in the industrialized world. Recently it has been declared a major health problem.(1- 7- 24- 29- 43- 76- 85- 104- 112- 117-118-131- 132- 140- 143- 157 -201- 225- 232- 238-239- 291- 338- 339-459-487-488).

At the same time, in today's body-conscious society, overweight individuals are subjected to diverse degrees of subjective and objective discrimination. This causes them social adjustment disorders that range from moderate to severe.

Motivated by the desire for career advancement and a better self-image, and/or to avoid health problems, overweight individuals flock to any weight control center offering a cure for the disease.

In addition to a lowered self-esteem that can lead to mental instability, obese individuals also must cope with external and internal threats (122).

Obese individuals struggle with:

The "yo-yo" syndrome"

Keeping a normal weight is a constant battle. They gain back the weight that they loose the minute they go off their diet  (86-173-339-364-421).

After many years of this back and forth, clinical complications arise. Relapses are very common, despite patients' continuous efforts to keep their weight down.

A natural tendency to maintain  the desired weight

A common affliction is that the weight increases with a near normal or slightly greater than normal food intake (5-68- 107-150-164- 208-214-220-243-370- 380- 429- 446- 450- 451). This common clinical complaint, scientifically ignored for many years, has now been accepted as the main cause for the difficulty obese people experience in maintaining a desirable weight after continuous dieting (set-point of body weight control) (254-255-256-323).

Despite in some cases their food intake is the nearly the same as normal weight individuals, obese patients have the tendency to gain weight well beyond than what would be expected for the number of consumed calories . They keep their set-point of body weight control at a higher level than the corresponding to their age, sex, or height (145-205-322-340-357-427-428)

• The health risk of being overweight.

•  

• Discrimination

Today's body conscious society tends to discriminate against obese individuals. This not only contributes to lowering self-esteem, but it causes obese individuals to be more prone to bouts of depression.(6-187-386-463-496).

Social discrimination and obesity: Two studies found that notwithstanding comparable scholastic performance, obese students are not accepted to prestigious colleges as often as their normal-weight counterparts (94-95-356).

Discrimination in the workplace: A study by Roe and Eichwort, reported that 16% of employers would not employ obese individuals under any circumstances, and an additional 44% would employ them only under special circumstances (390).

Another study revealed that only 9% of individuals who enjoyed incomes between $ 25,000 and $ 50,000 were more than 10 pounds overweight, whereas 39 % of those earning $ 10,000 to $ 20,000 were similarly overweight. Each pound of excess fat costs an executive $ 1,000 a year (512).

The Police, Army and Fire Departments do not enlist obese individuals.

Landlords are less likely to rent to overweight individuals (252).

Almost twice as many obese women experience bouts of depression as they rise in income class (compared to those who stay at the same social level. (390).

In every aspect of daily life, obese subjects are reminded they are not welcomed by their social milieu. Society dislikes fat as much as obese patients dislike themselves for being overweight. (271-405).

• Loss of self-esteem

Upper middle-class women are more affected, because sanctions against their overweight are very severe at this social level (441).

Adolescence may be the more delicate period for body image disorders (24).

Thus, constrained by a myriad of social and subjective factors; receiving no solution to their despair; subjected to many clinical complications, the strong become indignant and decide that modern medicine is a fraud and their representatives are fools. The weak just give up the struggle.

In either case, the result is the same: further weight gain, resignation to an abominable fate and a resolution to live a tolerable life during the short span allotted to them - a fight for doctors and Insurance Companies.

Obesity treatment: Why did we not reach our goal?

Weight control statistics display disappointing results. Treatment of the disease remains a mayor challenge for Clinical Medicine (1- 2-12-37-42-54-55- 73- 91- 108-116- 135- 136- 165- 176-184- 193- 195- 203- 219- 220-228- 235-247- 259- 269- 299 - 300- 334- 343-349- 363-364-388- 389- 422-431-434- 443- 445- 453- 455- 459- 461-486-495-507-509).

Since no effective treatment has been found so far, several Investigators have recently adhered to the nihilistic hypothesis that "no treatment is much better that any treatment at all".

In our opinion, we did not reach our goal because:

1. For centuries, obesity has been considered a minor health problem and has not been given proper attention by the Medical Community (179).

2. Highly refined foods are easily available today. With these foods the digestive system is spared of the natural and physiologic work that would otherwise be required to get rid of useless extra calories (358-360).

3. Tendency to inherit the genetic trait of obesity.

Looking back, looking forward

"Obesity problems are perhaps not so dramatic as the problems of cancer or polio, but often cause life-long suffering. How many promising careers have been ruined by excessive fat; how many lives have been shortened. If some way - however cumbersome - can be found to cope effectively with this universal problem of modern civilized man, our world will be a happier place for countless fellow men an women." (ATW Simeons 1966).

Obesity

The term Obesity derives from the Greek expression: ob-edere, which means overeating.

For centuries, it was considered a matter of gluttony, or craving for food, and women were preferred chubby, because chubbiness was erroneously linked to a proper motherhood.

No longer. Many obese patients are rejected by a society that tends to believe that the reason they are obese is because they are unable to control what they eat.

Obesity, like fever and anemia, is a symptom rather than single disease entity: a variety of causes for obesity have been identified in humans and laboratory animals, but in the overwhelming majority of patients the etiology of obesity cannot be determined .Since the underlying causes are poorly understood, it follows that no effective treatment has been developed so far.

This is unfortunate, because obesity is a very common disorder, shortening the life-span of millions of people around the world (421).

During the past fifty years, several treatments have been presented as the solution to this problem. Some could be classified as naïve, others almost useful, and several as health hazardous. Nevertheless, anxious to find relief, patients flock to Medical Centers, Clinics or any other entity that offers a cure to their long-lasting health problem.

Unlike a fever, where a rise in temperature to above 100.4º or 102.2º C indicates the possibility of an underlying clinical disease, obesity is more difficult to characterize. Several methods for assessing the disorder have been recently published .

According to classical height/weight tables, obesity can be broadly described as excess weight as per the usual Life Insurance Tables.

This method is not a good determination of body fat because it only estimates weight. Take two same weight individuals: the one who tends to gain weight around the abdomen may be at a greater risk for heart disease and diabetes mellitus than another whose fat accumulates in the femoral region.

Therefore, what method can we use to determine what makes an individual obese and another normal-weight?

Definitions

Obesity can be assessed from different perspectives:

A. According to body weight

The definition of obesity as an increase in body weight has prevailed for many years as the most common clinical tool. It is still being used, although it is not an accurate measure of obesity (230).

Recently, relative weight has become the most popular and convenient obesity indicator. Relative weight is calculated by dividing an actual weight by ideal weight according to and individual's height, age and sex. A relative weight of 1.20 or greater (i.e.,20% above ideal weight) defines obesity (National Institutes Consensus Development Panel on the Health implication of Obesity, 1985) (230).

However, there are some problems with real or relative weight. For example, a person may be overweight without being obese,
and,
the degree of overweight at which an individual develops a greater risk for cardiovascular complications remains subject of debate.

Besides, ideal weight indicators for specific populations have changed recently. We need to be aware of these limitations.

Years ago, the Metropolitan Life Insurance Company issued their Height-Weight Tables. According to these tables, the risk of mortality begins to substantially increase at weights 20 per cent above desirable. A desirable weight was considered a standard weight for any given age and height. Several oversimplified versions of these Height-Weight Tables have become popular throughout these years (318-319).

In these tables, the standard weight for a given age and height is based on the weight that is associated with the lowest rate of mortality for a given height. These tables have some limitations, however. For example, since a table of standard weight is required to determine relative weight, there is no single standard for all patients.

Another problem of these tables is that it is not know how closely an obese patient must approach the standard to satisfactory reduce health risks.

Despite some controversy regarding an index of 2 for the power function, a standard value of 2 is more practical, and studies suggested that a value of 2 for p was adequate for men, whereas a value of 1,5 for p was preferable for women.

Since these calculations need to be made every time that weight is estimated, nomograms have been published for this purpose.

However, as in any mathematical calculation relative to an indirect evaluation of body fat, BMI suffers from some inaccuracy (321).

All these methods - almost accurate as they may be - should be viewed with caution: normal-weight individuals may show all the clinical complications of obesity despite being of normal or less than normal weight according to the weight reported by the scale.

B. Obesity by fat content

This may be described as an excess of fat.

However, these are cumbersome procedures , time-consuming, require highly specialized settings and facilities and cannot be applied regularly to larger research studies or populations.

What the clinician needs is an inexpensive, precise, adequate method that can be used in routine consultation: Click here for clinical methods to estimate fat content

Nature Vs. nurture

Genetic influences determine whether an individual will become obese, but many other factors decide if that individual will actually be obese (240- 241-257- 275-289- 320- 392- 418- 521). There is a popular proverb says that no one becomes fat under starvation conditions .

As far as heredity is concerned, several studies on families from adopted children and twins, concluded that a predisposition to obesity may be genetically determined (14-202-508).

Family studies reported that rough heredity estimates ranging from 0.40 to 0.60, suggest that genes are responsible for approximately one-half of the total phenotypic variation in obesity (454).

However, both reports reflect only the common set of genes that influence obesity during the ages being considered, but do not reflect the impact of age-specific genetic effects. Thus, they may underestimate the total heredity of obesity at any given point in time (64-65).

Despite the fact that genotype is determined by genes, phenotype ( the genotype related to external factors) can be a determinant factor in the genesis of obesity (61-75-462-505).

Phenotype is strongly influenced by environmental factors (such as easy availability of refined foods), that can strongly influence the onset of the disorder.

The obese phenotype is a multifactorial trait, determined by genetic and non-genetic factors. Among non-genetic factors, we could include total caloric intake, composition of the diet, psychological factors, and habit-modifications (quitting smoking, drinking, etc.) (63).

It would be interesting, therefore, to consider two kinds of genetic effects: the additive effect of genetics and the result of the genotype-environment interaction.

Genotype account for a significant fraction of the individual differences in Resting Metabolic Rate, Thermic effect of Food (TEF) and Thermal effect of exercise (TEE)

Genotype-environment interaction accounts for the rest in this equation.

It would be reasonable to suppose that, given a fixed percentage of hereditary factors in the genesis of obesity, the environmental factors of contemporary society play a key role in the ever increasing number of obese individuals who live in industrialized nations (58-75-133-470).

Physical activity and obesity.

Despite claims that increased physical activity may be a useful method of weight control, several studies could not confirm that it is the key treatment for the disorder (244-412).

The decrease in physical activity observed in obese individuals could be related to adiposity level. Basically, the process of becoming obese requires an over-consumption of food and some basic regulatory disorder, but once obesity is established, physical inactivity may contribute to aggravate the disease.

That over-consumption of food is not the only cause for the genesis of obesity was clearly demonstrated in a series of research studies concluding that some volunteers maintained a fairly stable weight throughout the study, despite a food intake well over their daily requirement, whereas those prone to obesity gained weight (427).

However, physical exercise provides some benefits in the management of obesity: It limits the amount of muscle tissue that is lost during a weight reduction program; produces psychological benefits, including improvements in mood and self-esteem, and prevents the urge to snack that is more prevalent during periods of inactivity (120-379-414-466).

Prevalence of obesity

Obesity and overweight are highly prevalent at every age and in both sexes (67-186). Data derived from NHANES 11 suggest that 32.6 million American adults are overweight as per the BMI definition. Of these, 11.5 million are severely overweight (BMI of 31 or higher (188- 245- 246- 337- 338).

It is estimated that in the United States, about 300,000 deaths a year are caused directly or indirectly by obesity.

The frequency of overweight appears to increase in frequency in the older population. Fifty two percent of American women and 42 percent of American men ages 50 to 59 are overweight, whereas the percentage for Americans between the ages of 20 to 29 is 20. But the young are hardly exempt: 25 percent of children between the ages of 6 and 17 are now obese according to any standard (180).

Women have a higher tendency to be overweight and obese than men. The NHANES 11 survey concluded that 25.8 per cent of American women and 22.8 per cent of men are overweight, 24 percent of women and 22 percent of men are obese.

Therefore, the prevalence of obesity among adult Americans appears alarmingly high. Men's and women's body weights have progressively increased between 1960 and 1980 (469).

American adults have shown an average weight gain of nearly eight pounds per person, with 33.4 percent now considered obese, compared to 25.4 per cent in 1980 and 24.3 per cent in 1962 (469).

Although African American and Hispanic women remain the groups most prone to obesity (48,6 and 46,7 per cent respectively), the largest increases have been among white men and women: 7.8 percent and 9.1 percent respectively are now more overweight than a decade ago.

Many factors have helped to generate this epidemic of modern society: availability of highly refined foods that spares the human body of the additional work to digest foods; the misconception that during pregnancy there are two mouths to feed and a tendency to inactivity and heredity tending to perpetuate obesity in future generations .

For example, the American food Industry generates 3,700 calories a day for every man, women and child and spends $ 36 billion a year to advertise its products (469).

Up to 10,000 food commercials, specially designed for children, are displayed every year : Nearly all food ads on Saturday mornings are for sugary, fatty or salty foods (469).

Concerning our tendency to inactivity, Kelly Brownell concluded: "The amount of energy that people used to expend even a decade ago is enormous compared to what they expend today" (258-469).

While an increase in physical activity does not contribute to further weight loss, it elevates the body's aerobic capacity, increases the activity of plasmatic neuropeptides which creates a sense of well-being, and replaces body fat with muscle mass (which is lighter, but has better aerobic turnover rate (74).

A multifactor hypothesis to explain obesity

We ignore what metabolic processes lead otherwise healthy subjects develop and maintain obesity. Therefore, we have outlined a multifactor model encompassing all the known factors capable of causing the disorder.

Each contributes to or aggravates the condition and the condition becomes more or less severe, depending on the number of factors involved.

Thus, male subjects with hereditary obesity traits, living in an industrialized country, subjected to different psychological pressures and displaying the abdominal type of body fat distribution, face greater health risks than female subjects, with no hereditary obesity traits, and a gynoid type of body fat distribution.

As per the following diagram, all these factors lead to the same conclusion: They aggravate or generate a subtle modification at the hypothalamic neurotransmitter level, which in turn initiates an amount of stored fat greatly exceeding daily energy requirement.

The hypothalamus: The main organ responsible for the genesis of obesity

For those of us who refuse to be discouraged there is hope. Buried deep in the human brain, there is a part that humans have in common with all vertebrate animals, the diencephalon. It is a very primitive part of the brain that, in humans, is buried under masses of nervous tissue giving us the ability to think, reason and voluntarily move our body. The diencephalon is the part of the central nervous system that controls all spontaneous body functions, such as breathing, heart-beat, digestion, sleep, sex, urinary system, autonomous or vegetative nervous system and, via the pituitary, the whole network of endocrine glands (32-35-113-158-159- 249-273-274-326)

Thus, it is not unreasonable to assume that the complex operation of fueling the body might also be controlled by the diencephalon (105-169-182-199- 242- 290-297)

It has been known that the destruction of another diencephalic center produces a voracious appetite and rapid weight gain in animals that never become fat spontaneously (Simeons, Pounds and Inches) (213-233).

The hypothalamus is the most studied and best understood of all the Central Nervous System components regulating food intake and energy metabolism (70).

It has long been recognized that it plays a key role in the mechanisms regulating food intake and fat accumulation (9-10-213-260-324-355-372-410-511).

Electrical or chemical destruction of the hypothalamic region results in hyperphagia and obesity, or decreased hunger, depending on the anatomic area where damage has taken place (438-448-449).

A laboratory lesion of the Ventromedial hypothalamus (VMH) results in hyperphagia, hyperinsulinemia, decreased GH secretion, rapid weight gain and obesity that persist until a new plateau in body weight is achieved.

By contrast, verified cases of human hypothalamic obesity due to tumors, inflammations or injury due to surgery are extremely rare in the literature (71-101).

Therefore, as we have proposed in a previous report, slight changes at the hypothalamic neurotransmitters level might account for the weight gain that obese patients experience despite continued efforts at dieting.

In fact, some publications suggest that human obesity might be characterized by a subtle hypothalamic disorder, still not accessible to current diagnostic methods. Indirect evidence supporting this hypothesis can be presumed from several data: (36-169-410).

Amatruda et al. demonstrated that a group of obese males showed an abnormal response to 100 g. of GnrH (Gonadotrophin Releasing Hormone), indicating a dysfunction of the hypothalamus (15).

Jung et.al. concluded that women with hereditary obesity traits display a hypothalamic function disorder that is not totally corrected after weight loss (248).

Kopelman et al., after investigating the Prolactin response to insulin-induced hypoglycemia, concluded that hypothalamic function is severely altered in human obesity (273-264).

Although a hypothalamic regulation of energy metabolism might be crucial in the genesis of obesity, the food-intake regulatory process is a complex mechanism encompassing several CNS regions.

Destruction of various components of the limbic system (temporal and frontal lobes for example) has been shown to cause obesity, although these are very rare situations.

On the other hand, the hypothalamic region receives signals from different regions of the body. Many of these are mediated by neuropeptides (78-293-332).

Regulation of eating behavior, including receipt of the signal to begin and stop eating, is facilitated by a series of gastrointestinal humor factors including Cholecystokinin, bombesin, vasoactive inhibitory peptide, pancreatic polypeptide and gastrin (437-491).

The administration of Cholecystokinin has been shown to decrease food intake both in laboratory animals and humans (367). Parenteral administration of bombesin decreases eating in rats, an effect not eradicated by vagotomy (491).

Regarding metabolic modifications observed in obesity, changes in the concentration of plasmatic hormones might also send different signals to the hypothalamic region.Thus, an intracranial administration of insulin to rats and baboons has been reported to decrease food intake.

Hyperphagia and hyperinsulinemia appear to be two important factors in the development of hypothalamic obesity in experimental animals. The later (hyperinsulinemia) seems to be essential for the development of obesity in animals with a hypothalamic Ventromedial lesion (70).

Since insulin is a lipogenic hormone, an increased plasmatic level of this substance might account for the excessive fat that has been observed to accumulate in cases of obesity.

Substances such as norepinephrine, serotonin, Thyrotrophin Releasing Hormone, dopamine and neural peptides (b-endorphins, Cholecystokinin, dynorphin, enkephalins, bombesin, etc. act as intermediates in this complex network

These substances might play an important role also in the genesis of obesity: for example, several data suggest that a CNS opioid system regulates energy metabolism and ingestion of nutrients (204-270-308-310-311-313-409-515).

ß-endorphin has been one of the most investigated neuropeptides (56-189-200-227-276- 278-296-316-330- 331-332-333- 368- 406- 407-515).This molecule acts upon the mechanisms, eliciting eating through a food-rewarding system. For example, food ingestion might increase CNS opioids levels thus creating a feeling of self gratification. Obese subjects could, therefore, feel compelled to increase their food intake to maintain CNS an elevated neuropeptides concentration .

Gluttony, as observed in obese patients, would consequently be biochemically explained . Food addiction may be a recognizable CNS opioid disorder (308).

Gambert reported that fasting decreases the content of hypothalamic ß-endorphin in rats. Therefore, food restriction, as observed during dieting, might account for the feeling of weakness, hunger and physical distress associated with a low calorie diet (174).

Finally, some evidence suggests that the diencephalic region plays a regulatory role on the mechanisms that are responsible for the storage and release of fat (98). Research on hypothalamic neuropeptides may shed new light on the interpretation of obesity, i.e., subtle biochemical modifications in the hypothalamic opioids concentration may be the cause (or the indication) of an underlying neuromodulator disorder (99-109-406).

This would in turn initiate and perpetuate the metabolic changes leading to the obese condition (427).

Conversely, a persistent elevated food intake could lead to metabolic modifications in the diencephalic region, as observed in obesity. These modifications might be mediated by the Autonomic Nervous System (ANS), or the endocrine system.

Autonomic Nervous System and Obesity.

This system influences energy insulin secretion, which in turns affects the storage, uptake and expenditure of energy. Also acts upon catecholamines and other endocrine neural factors secretion, regulating energy utilization (79-80-181-183-236-237-287).

Endocrine system and Obesity.

For many years it was generally believed that the main cause for obesity was a glandular problem.

One of the suspected glands was the thyroid, because it was observed that hypothyroid patients showed, among other physical signs, moderate degrees of obesity. However, recent research demonstrates that thyroid tests are within normal limits in the vast majority of obese patients .

In the few cases where thyroid dysfunction appears to be associated with obesity, the condition may be easily corrected with the proper administration of thyroid hormones indicated for the management of hypothyroidism.

Therefore, it would appear that thyroid dysfunction plays a minor (or null) role in obesity and only when it is not properly treated.

Adrenal cortical hormones also have been associated with obesity. However, hypercorticism appears in a few cases of obesity, and nearly always in the context of an abdominal or android type of body fat distribution (402).

Modifications of growth hormone (GH) secretion were observed in some obese patients (57-77-156). But it appears that this is a consequence rather than the cause of obesity. Reports were published regarding obesity treatment with Growth Hormone (92). This approach should be viewed with caution, since prolonged administration of GH may provoke the onset of a Parkinsonian syndrome (342-381). Furthermore, with a recent publication demonstrating an approximate 2-fold increase in mortality in critically ill patients receiving large doses of GH, the use of GH should remain in the realms of replacement therapy and research, until there are significant advances in our understanding.

Gonadal steroids do not appear to play a role in the genesis of obesity. Rather, they are related to the peripheral conversion of estrogen and testosterone, since this conversion is carried out mainly in adipose tissue (375-377-378).

Metabolic gonadal steroids activity might account for the selective accumulation of fat in certain regions, as observed in gynoid (Estrogen), or android (Testosterone) obesity.

Are we unfairly blaming obese subjects for their lack of will power to fight the disease of obesity?

Some would believe that the only thing that obese individuals need to do to stop being obese is eating less.

After many years of experience on the subject and a careful review of all the information previously cited, I have concluded that this belief, reasonable as it may seem, is not the complete solution to the disorder.

First, several reported studies conclude that weight regain after dieting was the rule rather than the exception.

Next, it has been repeatedly demonstrated that, under very controlled conditions (same Hypercaloric Diet), some subjects failed to gain weight, or reported their weight remained stable despite broad changes in their food intake,

and,

Some obese patients failed to lose weight despite following a strictly controlled diet.

No patient is so enthusiastic as an overweight patient who is anxious to lose those unwanted pounds.

While some patients are grossly obese, the vast majority of these present a moderate overweight. The former are case problems for General surgeons (gastric bandage, etc.) , since the disease usually recurs or aggravates throughout the years.

Patients should discuss the problem of obesity with their physicians. Both need to understand what they are facing is a chronic problem like diabetes or hypertension, that ranges from moderate to severe, and they must treat the disease as a serious health hazard.

In any case, a pre-surgical weight management program is likely to yield better results, both from the patient's and surgeon’s viewpoint.

29/03/2009