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Obesity

What is obesity?

The Merck Manual defines obesity as “the excessive accumulation of body fat.” Thus obesity is not simply weight gain because a heavily muscled person may weigh more than average. Obesity is typically classified as mild (20-40% overweight), moderate (41-100% overweight) and severe (>100% overweight). These definitions however, are problematic in that they are simply indicative of the range in which obesity can manifest, and are not necessarily a classification of risk factors. The term ‘overweight’ refers to an excess of body fat between 10 and 20%. (Berkow 1992).

Physiology of fat

When we use the term ‘fat’ we are referring to lipids, a diverse group of chemicals that includes triglycerides, phospholipids, steroidal complexes, carotenoids, vitamins such as A, E and K and eicosanoids. As lipids are repelled by water, in order to travel in the blood they need to be bound to special water-soluble proteins, called lipoproteins. Although there are many kinds of lipids in the body, when we are dealing with obesity, we are generally referring to triglycerides, called such because they are composed of three carbon glycerol molecule and three (tri) fatty acids attached to each carbon in the glycerol molecule. Triglycerides are the most common lipid in the diet, and function as a highly concentrated source of energy, providing twice as much energy as proteins or carbohydrates, gram for gram. Fat, or adipose tissue, is a form of loose connective tissue in which certain kind of cells, called adipocytes, store dietary triglycerides. These adipocytes function to insulate the body and reduce heat loss through the skin, as well as to store nutrients for later usage.

When we talk of fat however, we need to understand that there are two primary forms of fat tissue in the body: white fat and brown fat. White fat is by far the most abundant form of adipose tissue, and when we speak of obesity it is this fat we are discussing. White fat stores triglycerides in large droplets and is poorly supplied with blood. In contrast, brown fat stores triglycerides in numerous small droplets within each cell, is highly supplied with blood and contains numerous energy-producing mitochondria. Because of this rich blood supply and the activity of the mitochondria, brown fat generates a considerable amount of heat, called thermogenesis. It is abundant in the fetus and in the newborn, but decreases with age, the ratio shifting in favour of white fat. There is still brown fat in the adult, typically found in the subcutaneous tissue between the shoulder blades, in the mediastinum (surrounding the heart, thymus and major blood and lymphatic vessels) and near the kidneys.

Epidemiology

The prevalence of obesity in the United States is about 30%, with a further 25% classified as overweight.¹ These figures are in stark contrast to the 1960 figure, when 13% of Americans were believed to be obese, or the 1994 figure when 22.5% of the population was obese. The prevalence of obesity varies considerably when one takes into account age, socio-economic status and race. There is a twofold increase in the prevalence of obesity between the ages of 20 and 50, and more than twice the prevalence of obesity among women of lower socio-economic class compared to those of upper socio-economic status. Among racial groups there is no significant difference between white and black men, but there is a significant difference in prevalence among black women, reaching upwards of 60% by middle age. (NIH 2000)

Measurement of obesity

In the past, obesity has been measured by comparing a patient’s weight with a "desirable" or "relative" weight. The criteria for desirable weight was developed by the life insurance industry, based on weights associated with the lowest mortality among the insured population. Unfortunately this population is not representative of all of members of society, and thus the data cannot be extrapolated to the population at large (no pun intended). Relative weight is calculated by dividing the patient's weight by a “standard” weight that is based on the patient's height, age and sex. Similar to the desirable weight, the relative has been found to be too arbitrary, and does not take into account individual factors.

To accommodate these complaints a newer, supposedly more useful measure has been developed, called the Body Mass Index (BMI). The BMI is calculated by dividing the weight (W, in kg) by height (H, in meters), squared (W/H²). The lowest morbidity and mortality for both sexes occur in persons with a BMI of more than 22-25 kg/m². According to the NIH criteria, “overweight” is defined as a body mass index (BMI) of 25 to 29.9 kg/m², and “obesity” is defined as a BMI ? 30 kg/m².

Risk factors and obesity

The major risk factors associated with obesity increase proportionally as the patient’s weight increases. The following is a listing of the various risk factors associated with diabetes:

Hypertension: In overweight young adults ages 20-45, the prevalence of hypertension is six times that of their normal-weight peers. Although classified as a disease, in truth hypertension is a symptom of cardiovascular disease. (Berkow 1992, 982-983; Kuczmarski and Flegal 2000; NIH 2000)

Cardiovascular disease and fat distribution: According to the Framingham data, for each 10% increase in body weight there is approximately a 20% increase in the incidence of coronary artery disease. For every 10% increase in relative body weight, systolic blood pressure increases 6.5 mm/Hg, plasma cholesterol 12 mg/dL and fasting blood glucose 2 mg/dL. (Berkow 1992, 982-983; Kuczmarski and Flegal 2000; NIH 2000)

Obesity and diabetes: Men who are 20% above the desirable weight have twice the risk of diabetes. Moderate obesity (41-100% overweight) increases the risk of non-insulin dependent diabetes mellitus by ten times. (Berkow 1992, 982-983; Kuczmarski and Flegal 2000; NIH 2000)

Obesity and women: Many woman are acutely conscious of their weight, but there needs to be a clear delineation between truncal-abdominal (apple-shape) and gluteal-femoral (pear-shape) weight gain: in the former, obesity is a reflection of excess stored energy, whereas in the latter extra weight serves as a storage organ for female sex hormones. If women strive to maintain a waist to hip ratio of 0.8 the risk associated with gluteal-femoral obesity is negligible. In premenopausal obesity there is often a decrease in sex hormone binding globulin (SHBG) and an increase in androgen levels, and in some women, the development of secondary male sexual characteristics such as hirsutism (facial hair) and alopecia (hair loss). A decrease in SHBG also promotes higher levels of free estrogen, which can be converted by adipose tissue in androgens. Both androgenization and hyperestrogenism are associated with a greater risk of menstrual abnormalities, and high serum levels of androgens specifically can inhibit progesterone secretion and ovulation. Elevated androgens also promote insulin abnormalities in a vicious cycle pattern, whereas elevated estrogen is thought to play a role in estrogen dependent cancers. Obese women also have more problems getting pregnant and sustaining pregnancy, with an increased frequency of toxemia and hypertension. (Berkow 1992, 982-983; Kuczmarski and Flegal 2000; NIH 2000)

• Obesity and cancer: Overweight men have a significantly higher mortality rate for colorectal and prostate cancer; men whose weight is 130% or more above average are 2.5 times more likely to die of prostate cancer. Menopausal women with truncal-abdominal obesity have an increased risk of developing breast, uterine and ovarian cancer. (Berkow 1992, 982-983; Kuczmarski and Flegal 2000; NIH 2000)
• Obesity and gall bladder disease: Obese women between the ages of 20 and 30 years have six times the risk of developing gall bladder disease compared to normal-weight women. By the age of 60, almost one-third of obese women can expect to have developed gall bladder disease. The typical gall bladder patient is comprised of the four ‘F’s: fat, forty, farting and female. Men who are 20% above the desirable weight show a 40% increase in gall bladder disease. (Berkow 1992, 982-983; Kuczmarski and Flegal 2000; NIH 2000)
• Obesity and respiratory abnormalities: As an individual becomes more obese the muscular effort required for breathing increases, and thus there is a commensurate decrease in lung volume. Obstructive sleep apnea (Pickwickian syndrome) is common in moderately to severely obese persons, with a narrowing of the upper airways and obstruction of the glottis eventually leading to pulmonary failure. (Berkow 1992, 982-983; Kuczmarski and Flegal 2000; NIH 2000)
• Obesity and arthritis: An increase in body weight adds trauma to weight bearing joints and in women especially is a good predictor of osteoarthritis of the knee. Persons aged 45-64 years old have a dramatically increased prevalence of gout when relative weight is greater than 130% above desirable. (Berkow 1992, 982-983; Kuczmarski and Flegal 2000; NIH 2000)
• Obesity and psychological disorders: Any severely obese person will experience a functional impairment in daily activities, and frequently complain of insomnia, shortness of breath, and joint problems, all of which can contribute to a feeling of dissatisfaction. Obese people are frequently ridiculed by their peers and the media, and experience varying degrees of discrimination, all of which can lead to a poor self-image and depression. (Berkow 1992, 982-983; Kuczmarski and Flegal 2000; NIH 2000)

Causative factors of obesity

Medical science declares that the specific cause of obesity is unknown but understanding the mechanism is simple enough: the consumption of more calories than are utilized through physical exercise. The science behind understanding obesity however is complex, with at least seven factors that contribute to obesity, apart from the obvious effects of diet:

• Genetic factors: Twin and adoption studies have shown that genetics is a critical factor in the development of obesity, but the role is unclear. Generally, the tendency towards asthenia or obesity appears to be an inherited trait, but why some who have a strong genetic predisposition to weight gain are able to remain free of obesity indicates behavioral and lifestyle factors are at play. (Berkow 1992, 982)
• Social factors: In the West, obesity is far more prevalent in people of a low socio-economic status, and wealth specifically is a good inverse predictor of obesity in women: for men however the relationship is less clear. Among populations in the developing world there is a direct link between increasing economic status and the prevalence of obesity, but only to a point, and then the prevalence is more or less similar to the West. With the rising affluence and emergence of the middle class in developing countries the wide acceptance of Western-style fast foods has promoted an explosion in obesity and diabetes in these countries. (Berkow 1992, 982)
• Endocrine and metabolic factors: Certain metabolic disorders are a cause of obesity. In Cushing’s syndrome the excess secretion of corticoids promotes increased gluconeogenesis, a commensurate increase in insulin secretion, resulting in lipogenesis. Obesity is also a common symptom of hypothyroidism. (Berkow 1992, 982)
• Psychological factors: Psychological problems occur with more or less the same frequency in obese and non-obese problems, and thus is not a useful indicator of poor mental health. However, the stigma of obesity does contribute to a psychological issues induced by social prejudice and discrimination. Bulimia is a disorder characterized by eating binges, and in obese persons does not progress to compensatory mechanisms such as vomiting found in anorexia nervosa – hence, there is a net gain in weight. It has been observed that many obese people consume the bulk of their calories during the evening (night-eating syndrome), with eating patterns characterized by morning anorexia (lack of appetite), afternoon hyperphagia (extreme hunger) and insomnia. (Berkow 1992, 982-83)
• Developmental factors: Obesity can relate to either an increase in the size of the fat cells (hypertrophic), an increase in the number of fat cells (hyperplastic), or both. It appears that the period from late childhood to puberty is a critical period when it comes to obesity, and is the major determinant of hyperplastic forms of obesity; in contrast, hypertrophic obesity is usually an adult manifestation. In very obese people there is usually a combination of factors, and such people can display up to as much as five times the number of fat cells as an average non-obese or adult-onset obese person. In these persons there may be biological limits upon the extent to which weight loss can be achieved. Childhood obesity is therefore a potentially serious condition, and much care should be taken to ensure the diet is suitably balanced. (Berkow 1992, 982-83)
• Physical activity: As obesity is defined as the accumulation of body fat due to the consumption of more calories than are utilized, it makes sense that a general societal trend towards decreased physical activity would play a role in obesity. Given modern conveniences such as cars and mass transportation, as well as working lives that has less to do with hard physical labor than with tapping away at a keyboard, it is not surprising that obesity has reached epidemic proportions. Since the turn of the last century the prevalence of obesity in industrialized nations has more than doubled despite a 10% decrease in daily caloric content. This suggests that while physical activity plays an important role, the whole notion of caloric intake is suspect. (Berkow 1992, 983)
• Brain damage: Brain damage and in particular damage to the hypothalamus can lead to obesity, although it is a very rare cause. I once had a patient with an astrocytoma of the third ventricle, and upon surgical excision part of the hypothalamus was damaged. His weight sky-rocketed from 65 kg to over 150 kg in a period of six months. Tumors of the hypothalamus or adjacent structures of the brain can also cause abnormalities in hypothalamic function.

Physiology behind obesity

As there are no sensory receptors to monitor one’s weight how then is food intake regulated? Although the answer is far from clear it seems that weight depends upon several factors. This includes the level of certain nutrients and hormones in the blood, psychological elements such as depression, signals from the gastrointestinal tract and the special senses, and neural connections between the hypothalamus and other parts of the brain.

Within the hypothalamus a cluster of neurons located in the lateral hypothalamic nuclei called the feeding centre, and when it is stimulated in experimental animals it causes a feeding frenzy, even if the animals are already full. A second cluster of neurons located in the ventromedial hypothalamic nuclei is the satiety centre, and when stimulated in experimental animals causes them to stop eating, even if they haven’t eaten for days. It seems that the feeding centre is always active, but is inhibited by the activity of the satiety centre. The hypothalamus serves as a rely unit that responds to and integrates stimuli from various parts of the brain, rather than being the penultimate controller of eating behaviour. The hypothalamus receives input from the brain stem, limbic system and cerebral cortex, as well as from a variety of other sensory receptors, including stretch receptors, chemoreceptors, photoreceptors, olfactory receptors and taste receptors.

One factor in regulating food intake is the composition of the blood after the consumption of food and while fasting. When glucose and/or amino acid levels are low, feeding is stimulated, perhaps by decreasing the activity of the satiety centre of the brain. When the level of glucose and amino acids are elevated in the blood the activity of the satiety centre increases. The amount of free circulating fatty acids in the blood released in proportion to the total stored body fat is also thought to have an inhibitory effect on appetite. Cold environments also seem to enhance the activities of the feeding centre. Stretch receptors in the gastrointestinal tract that indicate the presence of food stimulate the activity of the satiety centre when active. The hormone cholecystokinin (CCK) is secreted when triglycerides enter the small intestine, inhibiting stomach emptying and seems to have an inhibitory effect on appetite

Obesity according to Ayurveda

According to Ayurveda the cause of obesity is multifactoral, including a lack of physical exercise, sleeping during the day and consuming foods that increase kapha, which are preferentially stored as adipose tissue. This accumulation of kapha obstructs the nutrient channels of the other tissues of the body, and deprives them of nutrition. Thus there is an accumulation of fat tissue and a general depletion of all other tissues of the body. Ayurveda has observed that in obese persons fat tissue tends to accumulate around the abdomen. By this action vata becomes obstructed within the gastrointestinal tract and stimulates agni to excess, causing an excessive appetite and a craving for large amounts of food. This activity is further enhanced by a relative lack of nutrients to other tissues of the body, which call upon agni to nourish them. Ayurveda considers a person obese when his or her buttocks, abdomen and breast show disproportionate movement upon activity. Medo roga, or obesity, is considered to have many complications.

Calories and weight loss

Diet plays an enormous part in the development of obesity and decreasing the total caloric consumption seems to be the tool of choice of many popular weight loss regimens. This is based on an inaccuracy however, or rather, on an over-investment in the concept of calories. Calories quite simply are a measure of how much energy a given food contains. Because it is impossible to quantitatively measure how much energy a certain food will produce once it’s been digested in the body, a simpler method has been developed. A given food item is placed in an incinerator and is burned until it is reduced to inorganic material, and the amount of heat energy is recorded. This means that if you take two foods of equal caloric content they will generate the same amount of energy when incinerated. Unfortunately the processes of metabolism in the human body are much more complex than this, and thus a caloric measurement of any food should be regarded skeptically. A steak, a bowl of brown and a chocolate bar may have the same caloric content but almost certainly they will be metabolized differently. When we look at diet we need to include a complete assessment of vitamin, mineral, fiber, carbohydrate, protein and fatty acid content, as well as other nutrients that might not fit into the above categories.

Dietary strategies in weight loss

A variety of dietary therapies are used in the treatment of weight loss, but most boil down to either a high carbohydrate/low fat or a including high fat/high protein/low carbohydrate diet. In some respects this dichotomy is an oversimplification, and either extreme should be avoided for any significant period of time. The dietary approaches emphasized in Applied Phytotherapeutics course is that the diet should be based in the way humans have been eating for the last 400,000 years (or longer), as opposed to a fad diet that doesn’t take into account the myriad factors involved in proper nutrition.

High complex carbohydrate, low fat

This is the prototypical recommendation of conventional modern nutrition, based primarily upon experimental animal models and the insudation hypothesis still promulgated by conventional medicine, that fat consumption promotes vascular disease. This diet is outlined in the badly dated Food Guide Pyramid developed by the U.S. Department of Agriculture, consisting of the following:

• 6-11 servings of cereals and grains
• 3-5 servings of vegetables
• 3-5 servings of fruit
• 2-3 servings of low fat dairy products
• 2-3 servings of meat, eggs and/or legumes
• fats, oils, and sweeteners used sparingly

In total, the diet should yield no more than 1600-2800 calories per day, depending on size, sex, physical activity and body weight. To be fair, nutritionists admit that the Food Guide Pyramid is outdated, and recently, researchers have focused on the benefits of a Mediterranean-style diet that emphasizes fats such as olive oil. Nonetheless, the basic ratios of carbohydrate to protein and fat described in the Food Pyramid are preserved. Perhaps the most out-spoken proponent of this way of eating is Dr. Dean Ornish, who advocates an essentially low-fat vegetarian diet rich in fruit and vegetables and alternate source of proteins such as soy. Unfortunately, this diet does not address the underlying mechanism of acquired obesity, which is related to insulin-resistance, and in fact could be seen to worsen it, despite that it is rich in antioxidant compounds derived from an increase in fruit and vegetables. For obese and overweight patients weight loss can only be sustained when patients implement a reduction in their overall caloric intake and implement an aggressive regimen of physical activity, a combination that few can sustain for any significant period of time. Furthermore, the emphasis on a low fat increases the glycemic index of the diet (promoting the dynamic of insulin resistance and hyperinsulinemia) and potential fatty acid deficiencies. The particular fascination with soy products demonstrated by proponents such as Dr. Ornish, which have become an important commodity in the North American agriculture, is particularly worrying, due to their suppressive activity upon thyroid function (decreasing metabolism), chelating effect upon minerals, and lectin-mediated damage in the gut (increasing the likelihood of autoimmune disease).

High protein, high fat, low carbohydrate

These diets rely upon the consumption of high amounts of fat and protein with relatively little in the way of carbohydrate. Although popularized by Dr. Robert Atkins, this diet is has a long history, and in a recent Oxford Symposium paper, was first implemented as a dietary therapy in 1868 by William Banting (Groves 2003). Banting suffered from obesity and hearing loss, and tried many different treatments, avoiding fat and meats, and exercising regularly, all with no result. Upon the recommendation an ear, nose and throat specialist named Dr. William Harvey, Banting was taken off his carbohydrate-rich diet an placed on a low carbohydrate diet, consisting of the following:

• up to six ounces of bacon, beef, mutton, venison, kidneys, fish or any form of poultry or game
• fruit pudding, but no pastries
• any vegetable except potato

Within one year Banting records that he lost “…46 lbs in weight and 12 1/4 inches off his waist,” and had his hearing restored. Highly pleased with these results Banting published a prospectus on the diet in 1868 and endowed an institution called the Middlesex County Convalescent Hospital to treat obesity. Since then Banting has lent his name to the basis of a low-carbohydrate diet, such that it has become a verb: to “bant,” i.e. to eat a low carbohydrate diet. (Groves 2003).

The principle action behind the Banting or Atkins diet is the increased excretion of ketones that remove energy-containing substances away from the body. It obviously has psychological appeal because of the rich foods that can be consumed, and the initial rapid weight loss is often an incentive. There are however three primary arguments that are leveled against this diet:

• that the weight loss experienced on the diet is mostly water loss
• that the excess consumption of saturated fat and cholesterol through the increased consumption of animal protein promotes atherosclerosis
• that ketogenesis is dangerous

The basis of the argument that the weight loss experienced on a low carbohydrate diet is water loss is not substantiated by any study, only presumed. Other potential mechanisms could include the preservation of lean body mass, a reduction in metabolic efficiency (i.e. fats and proteins require more energy to metabolize), the excretion of energy-rich ketones in the urine, feces and sweat, and the partitioning of nutrients away from fat storage and towards the accumulation of lean tissue (Volek and Westman 2002).

Another argument is that these diets promote the risk of cardiovascular disease through the increased consumption of saturated fat and cholesterol. In fact, several studies have shown that such diets correct the HDL to LDL ratios, and reduce total triglycerides. In some subjects these diets are associated with a small increase in total serum cholesterol, a diagnostic finding that is of increasingly little value, and can usually be corrected by simply enhancing exercise (Volek and Westman 2002).

The last argument against the low carbohydrate diet is that it promotes the formation of ketones, and that ketones are dangerous. Although body cells typically use glucose as a source for ATP production, when the availability of glucose in the body is decreased it must rely upon the catabolism of fat and the production of ketones for energy. Triglycerides from body fat or from the diet are split into glycerol and fatty acid molecules, the glycerol molecules converted to glucose by gluconeogenesis, or into pyruvic acid, dependent upon the energy needs of the cell. Fatty acids undergo beta-oxidation in the mitochondria of the cell to form acetyl coenzyme A, which then goes on to enter the Krebs cycle to help generate ATP. Part of the normal process of fatty acid catabolism however is the generation of ketone bodies, substances that freely diffuse through plasma membranes. High levels of ketones keep plasma insulin levels low, which stimulates the release of fatty acids from adipose tissue and thus enhanced fat mobilization.

The theoretical problem with ketones is that that are highly acidic and when elevated in the blood they use up the blood’s pH buffers, such as bicarbonate ions. This elevation in acidity interrupts normal chemical processes in the body, disrupting homeostasis. Elevated levels of ketones in the blood is called ketosis, and prolonged ketosis is thought by some experts to lead to ketoacidosis, a life-threatening condition marked by a lowered blood pH, dehydration, lassitude, nausea and vomiting and circulatory shock. Ketoacidosis is a feature of uncontrolled diabetes in type 1 diabetics, which is characterized by ketoacidosis in conjunction with elevated blood sugar from pancreatic failure. In non-insulin dependent diabetics and normal obese persons however, the concern of ketoacidosis are more theoretical than actual, since the actual rate of ketogenesis in a low carbohydrate diet is actually quite low, compared to the ketogensis that occurs during starvation or in IDDM. Studies that have examined a ketogenic diet, such as those that have been used in epileptic children, have found no adverse effects except for calcium and urate kidney stones (0.5-5% incidence), vomiting, amenorrhea (21%), hypercholesterolemia and water-soluble vitamin deficiencies (Volek and Westman 2002). While there are potential issues with a ketogenic diet, given our hunter-gatherer evolution and the relatively infrequency of carbohydrates in the diet, humans are well adapted to ketogenesis as an alternate mechanism of energy production in the body.

The biggest problem with a low carbohydrate diet is that many patients forget to eat low-carbohydrate, antioxidant-rich, and high fiber plant foods. Such foods are potent source of water-soluble vitamins, antioxidants, and fiber, and contain alkalizing compounds that can offset any acidic change promoted in the blood by implementing a ketogenic diet. This problem is particularly true of patients that have not done their dietary research, and think that by eating a half a pound of bacon for breakfast with a couple eggs, and a T-bone steak for dinner is somehow healthy. In a diet that contains high amounts of protein and fat, leafy greens and other above-ground vegetables should constitute at least half the diet, gram for gram.

Food Allergies

Food allergies are thought to play a role in some forms of obesity, creating cycle of dependency upon an allergenic food substance to mask chronic allergy symptoms. If an allergenic food is consumed several times a day there may be a masking of the allergic reaction to this food item, characterized by an improvement in chronic symptoms that can last up to two hours, followed by a progressive worsening of symptoms. Such people learn to eat these allergenic foods to avoid dealing with the symptoms and thus are caught in a cycle of dependency. When these foods aren’t consumed there may be an extended period of extreme hunger, sinus congestion, poor concentration, difficulty breathing, fatigue, anger, or nervousness. Continued effort to avoid the allergenic food promotes diuresis, the disappearance of edema and a normalization of appetite. The most common allergenic foods include dairy, wheat, corn and sugar, but there may be others. Avoiding these foods can greatly aid a weight loss regimen

Medical management of weight loss

Apart from implementing the typical high carbohydrate-low fat diet with a commensurate increase in exercise, first line medical treatments for weight loss usually consist of amphetamine and chemically related compounds such as phenylpropanolamine (e.g. Acutrim®, Dexatrim®), diethylpropion (e.g. Tenuate®), phentermine (e.g. Fastin®), mazindol (e.g. Mazanor®, Sanorex®), phenmetrazine (e.g. Preludin®), phendimetrazine (e.g. Bontril®, Plegine®) and benzphetamine (e.g. Didrex®). In one way or another all these drugs exert their effect upon the hypothalamus and at best promote a 5-10% loss in total body weight while taking them. Common side effects include nervousness, irritability, headaches, sweating, dry mouth, nausea, and constipation, and must not be taken with monoamine oxidase (MAO) inhibitors. In the 1990’s some of the drugs in combination (i.e. “fen-phen,” phentermine + fenfluramine) caused severe problems and even death in many patients. Alternative to stimulants include drugs such as xenical (Orlistat®), which blocks fat absorption in the stomach and intestine, allowing people to eat fat but not absorb it. Much controversy surrounds the use of this drug, which could also promote fat-soluble nutrient deficiencies. There are also a number of new drugs which may hit the market soon, including leptins and cholecystokinin boosters which act on the brain to suppress appetite, but their safety is unclear. Another class of drugs commonly used in obesity are antidepressants, based on the belief that psychiatric illness can cause problems such as over-eating. One such commonly used drug is fluoxetine (Prozac®), the best-known member of a family of drugs called selective serotonin reuptake inhibitors (SSRIs). Although not specifically approved for weight loss, the latitude afforded doctors in prescribing drugs allows it to be used for weight loss. Typical side effects include fatigue, diarrhea, sweating, insomnia, thirst, nausea, and vomiting.

Holistic treatment of weight loss

The following is an overview of key nutrients, herbal remedies and natural regimens that are helpful in promoting weight loss. Dietary strategies however are key, and as a best bet for clinical results, a low carbohydrate diet with generous amounts of vitamin and antioxidant-rich vegetables and fruits should also be included. Exercise is another important component of weight loss, ad in severely obese patients, should be implemented after there is some initial weight loss, emphasizing low-impact, muscle-building exercise.

Supplements

• Vitamin B complex: stimulates metabolism, antioxidant; dose: 100 mg daily
• Vitamin C: may reduce obesity by increasing cellular energy consumption through increasing sodium pump activity; antioxidant; dose: 3 g daily
• Vitamin E: cardioprotective, inhibits lipid peroxidation; dose: 400 – 800 IU daily
• Magnesium: significantly low serum levels have been observed in obese persons compared to non-obese persons; used especially to treat the deficiency found in Syndrome X; dose 800 mg daily
• Zinc: significantly lower serum levels of Zinc have been observed in obese persons compared to non-obese persons; Copper serum levels are typically higher in obese patients; dose: 50 mg (citrate) daily
• Selenium: plays a role in the conversion of the thyroid hormone, T₄, into the metabolically active T₃. Thus, a selenium deficiency may be implicated in hypothyroidism, which is a cause of obesity; dose: 100 – 250 mcg daily
• Chromium: binds with GTF, enhancing the activity of insulin, normalizing serum glucose; enhances fatty acid and carbohydrate metabolism; dose: 400 – 800 mcg (chelate) daily
• Vanadium: mimics insulin, stabilizes serum glucose levels, suppresses cholesterol synthesis, encourages glycogen synthesis in muscle instead of lipogenesis; dose: 15 mg (vanadyl sulfate) daily taken with carbohydrates. NOT appropriate for low CHO diets.
• CoQ₁₀: serum levels may be reduced in obese persons, enhances metabolism; dose: 100 mg daily
• Eicosapentanoic acid (EPA) and docohexanoic acid (DHA) may help to increase brown fat activity, promoting thermogenesis; these oils also inhibit platelet stickiness, reduce inflammation and inhibit free radical formation; dose: 1000 mg each, daily
• Digestive enzymes: taken short term to enhance digestive effectiveness, which can combat craving associated with poor absorption
• Conjugated Linoleic acid (CLA): naturally occurring fatty acid found in the tissues and milk of ruminative animals such as cows; appears to regulate body fat accumulation and inhibit appetite; dose: 4000 mg daily
• L:arginine and L:lysine, equal parts: increases hGH and fatty acid metabolism, improves energy; dose: 1500 mg before bed
• Hydroxy citric acid (HCA): derived from Garcinia cambogia; inhibits lipogenesis by reducing the level of acetyl coenzyme A, the extra:mitochondrial precursor of fatty acid and cholesterol synthesis; dose: 1500 mg daily
• Antioxidants, to inhibit lipid peroxidation and free radical formation, including bioflavonoids (quercetin, rutin and catechin, 3 g daily), alpha:lipoic acid (300 : 900 mg daily) and N:acetylcysteine (1: 2 g daily)

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