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Updated 7/24/2013   

         Dr. Bernard Presser D.C.

5696 Magnolia Woods Drive

Memphis, TN 38134


If you have any questions, please contact us at 901-417-7905

 More articles coming soon.


Anyone conscious knows that Americans are getting heavier and fatter.  The weight gain has been creeping up for decades. For example, compare these average weights

                                                                                           1963-1965                   1999-2002

                                 Women, age                20-74                   138                               164

                                 Men, age                     20-74                   165                               190

                                 Girls, age                     12-17                   118                               130

                                 Boys, age                    12-17                   125                               141

                                 Children, age                6-11                      65                                 74

In 2002, about 30% of the US population was obese and 35% was ‘just' overweight; that's 65% of all Americans!  The prevalence of obesity doubled in only two decades.  Overweight in adolescents tripled.  Not only are Americans gaining weight, they're getting fatter at younger ages.  About 27% are obese by age 37 and 34% are "merely" overweight. About 31% of 6- to 11-year old children and 12- to 19-year old adolescents are overweight or at risk of overweight.  The prevalence of morbid (extreme) obesity quadrupled from 1988 to 2003, meaning the number of people about 100 pounds overweight went from one in 200 to one in 50; the number roughly 150 pounds overweight climbed from one in 2,000 to one in 400.  The number of morbidly obese people is rising faster than any other group of overweight people.  To be severely obese, a 5'5" woman would have to weigh at least 240 pounds; a 6' man, at least 295 pounds.  Increases in obesity continue in both sexes, all ages, all races, all educational levels, all income categories.  Over two-thirds of US adults are overweight.  A larger percentage of the population is obese (23%) than are poor (14%), heavy drinkers (6%), or daily smokers (19%).  One researcher contends that, if the current trend continues, by the year 2040, 100% of Americans will be overweight and by 2100, 100% will be obese! i


As people get fatter, they become more prone to a number of diseases and unhealthy conditions.  Experts warn of an impending global epidemic of excess-weight-related diseases - from gout, arthritis, digestive disruptions, chronic headache, knee pain, respiratory complications, and sleeping disorders to diabetes, high blood pressure, heart disease, and cancer.  It is unhealthy to be overweight, especially to be obese.  The incidence of diabetes, gallstones, hypertension, heart disease, colon cancer, and stroke increases with the degree of overweight.  Obesity is "a significant and often underestimated risk factor" for coronary heart disease -- even minimal increases of weight are associated with increased risk.  Structural heart abnormalities are commonly found in obese persons.  An overweight person has a higher risk of heart failure, even if not obese.  Obesity is "the most important controllable risk factor in the development and maintenance" of high blood pressure.  Excess fat (particularly abdominal) is associated with insulin resistance, glucose tolerance imbalances, left ventricular hypertrophy (a heart valve problem), and disruption in plasma fibrinogen and blood lipids.  Overweight is a major risk factor for type 2 diabetes mellitus.  An estimated 41 million Americans are prediabetic and at risk of developing full blown type 2 diabetes unless they lose weight and increase physical activity.  At least 18.2 million Americans are already diabetic, including an increasing number of young people.  All these factors contribute to the spiraling incidence of metabolic syndrome.  The incidence of all types of stroke rises in direct proportion to weight grain, particularly in obesity.

Other complications include gastroesophageal reflux disease (GERD or severe heartburn); back pain; sleep disorders including disruptive sleep patterns and sleep-disordered breathing; higher risk of dementia; fatty liver; elevated liver enzymes and liver disorders; higher serum C-reactive protein concentrations (suggesting low-grade systemic inflammation); and lower libido (sexual desire).  Being overweight or obese increases the risk of all the leading types of cancer including cancers of the colon, breast, uterus, kidney, pancreas, and esophagus.  Even the moderately overweight have an increased risk of many kinds of cancer.  Overweight is generally associated with a loss of life expectancy, more so in the obese.  Younger adults will likely face a greater risk of mortality throughout life than previous generations.  Overweight people run a higher rate of premature death, even among people who don't smoke and are otherwise "healthy."  Obesity can kill.  Overall deleterious effects on quality of life are greater from obesity than from smoking and low income.  Obese people live a sicker life. ii


Researchers frequently use the body-mass index (BMI) as an indicator of overweight and obesity.  The BMI is defined as the weight of a person in kilograms divided by the square of the person's height in meters (kg/m2).  This is the method often used these days for statistics and epidemiological studies.  However, BMIs do NOT make allowance for body composition (differentiating between lean muscle mass and body fat), bone structure, or gender (women tend to have less muscle and bone than men and are generally shorter).  If a person exercises regularly or is very muscular, he/she may appear to be overweight or even obese on the standard BMI index chart.  So too with people who are genetically stocky with dense bones and large muscles.  Many professional athletes are classified as too fat even though their body fat may be extremely low.  Conversely, a person with a small frame who never exercises might have too much body fat and still have a low BMI.  Correlating weight (a volume-related measure) to height (a linear measure) is overly simplistic.  Taller people, for example, would have to be proportionally much thinner than shorter people to be in the ‘normal' range.  And the BMI rationale is not applicable to all racial or ethnic groups in the same manner.  For instance, lower BMI cutoffs are needed for Asians.  Thus, BMIs have "underlying uncertainty," do not give a true picture of overweight, and have very little to do with real health or lack thereof.  "In fact, the old [weight] charts may have been more useful for individuals, because they at least considered frame size."

Some researchers contend that body fat percentage is a better and more direct measure of healthy weight than the BMI.  Others say to measure your waist to find out if you are at risk for weight-related health problems as it reflects the accumulation of intra-abdominal fat better than the waist-to-hip ratio.  A number on a scale is not a great indicator either - muscle weighs more than fat, so an accurate assessment of body composition is not always possible.  The point is that BMIs, weight tables, measurements and other indices "serve only as an approximate guide" to what you should weigh.  The best judgment comes from how you look and how you feel. iii


There is no single cause for overweight and obesity.  They are "the result of numerous factors acting together over time."  Similarly, there is no single solution.  Can't people lose weight if they just eat fewer calories and exercise more?  This is an overly simplistic (and moralistic) dogma.  Actually, there is "considerable variation among individuals regarding their susceptibility to weight gain."  Some become obese despite a continuous struggle not to, whereas others stay lean without any conscious control.  A wide range of variables including biochemical individuality, endocrine/hormonal imbalances, digestive problems, blood sugar fluctuations, liver/gallbladder disruptions, psychological issues, toxic load, and others can contribute to weight gain and/or difficulty in weight loss.  No doubt the most ominous cause is the "toxic food environment" in which we live.  That's why the longer immigrants live in the US, the more likely they are to be obese.

Obesity is not like other epidemics.  Not an acute illness, it is responsible for a long list of chronic conditions and diseases that do not suddenly appear.  Like that little bit of "extra padding" that gradually expands, the fatigue, decreased circulation, mental sluggishness, sleep apnea, joint damage and pain, breathing difficulties, hormone imbalances, vision problems, bone fractures, angina, heart attack, stroke, diabetes, high blood pressure, and other complications develop over time.  But, like any other health problem, treating the symptoms is not as useful or beneficial as getting to the causes.  Some of these causes are: iv


Common medications can cause weight gain.  Some antidepressants (tricyclic drugs and selective serotonin reuptake inhibitors such as Prozac), some anti-psychotics, mood stabilizers (like lithium), steroids (such as prednisone), anti-epileptic drugs, beta-blockers, oral contraceptives, and type-2-diabetes medications can all contribute to weight gain.  (Prescribed medications should never be stopped suddenly; a doctor should be consulted before changing a drug regimen.)


An enormous amount of research has been done on the genetic influence on weight - genes that promote weight gain and genes that make it difficult to lose weight.  There is even a gene dubbed "OB" for obesity.  Many of the studies have been performed with laboratory mice or other animals, but it is admitted that obesity is not as simple in humans.  There may be some susceptibility to obesity in some individuals; genetics may play a role, though "the culprit genes have been difficult to identify" because obesity arises from the combined effects of multiple genes AND "environmental factors" - like diet and exercise.

Genetic researchers concede that "environmental changes" play an important role in reducing rates of obesity and that "environmental influences will probably predominate when it comes to getting fat."  Eating habits and physical activity play a greater role in determining obesity than genetic background.  So genes cannot be blamed for it all, though they MAY play a small role in an individual's tendency.  Besides, the gene pool has not changed significantly during the past few decades - or in even two or three generations - and cannot be responsible for the spiraling numbers of overweight and obese people.  "Fifty years ago, obesity as we know it didn't exist, but our biology hasn't changed."  Even IF you have a genetic tendency to be fat, you have a tremendous amount of control over whether the "fat genes" are expressed.  Genes do NOT condemn a person to being fat!  One reason why weight problems can run in families is that the food choices, amount consumed, and activity patterns all tend to be learned and passed along.  Patterns and routines can be changed! vi


Metabolism is the process by which our bodies burn calories (food "energy").  Some studies seem to indicate that, after losing weight, the body resists maintaining the loss - that its own metabolism defeats it.  Terms used for metabolism include Resting Metabolic Rate, Basal Metabolic Rate, and Resting Energy Expenditure.  Although scientific studies may not use the phrase "set point," that is often what they are about.  The theory contends that the brain has its own ideas about what you should weigh and imposes its will.  The "set point" gets set by the adipostat, a kind of biological ‘thermostat.'  It is a nerve center that keeps track of fat cells in the body and minimizes the difference between one's "programmed" weight and actual weight.  Therefore, the adipostat could influence your hunger level, eating habits, and level of physical activity.  After a range of five pounds or so (gain or loss), the adipostat supposedly adjusts your metabolic rate.  If your weight gets higher than your "set point," the furnace is turned up and you will burn slightly more calories with a given amount of work.  If you lose weight, you burn fewer calories.  Genes are considered keys to the adipostat's set point, determining the amount of fat stores you carry.  If the genes make errors or mutate, the set point is pushed too high and weight gain results.

Formerly obese people do have metabolic rates that are 3% to 5% slower on average than never-obese people.  But the set point fluctuates "according to the actual impact of factors influencing fat balance."  In other words, set point has been "over-rated."  Metabolic measurements DO NOT indicate a predisposition to obesity.  Other factors explain weight gain.  An individual who has lost weight will use up fewer calories than someone who has always been slim, BUT this drop in metabolic rate is TEMPORARY and usually small.  "Metabolic resistance" does not go on indefinitely.  Generally people are not "doomed to be fat."  They have a lot of control. However, a prolonged period of severe food deprivation - a very low calorie diet - puts the body into "starvation" mode to conserve energy (calories), and reduces metabolic rate.  This may take a longer time to overcome.  Very low-calorie diets lower core body temperature, adversely affect sleep patterns (with fatigue and less activity), and have other undesirable consequences, often involving lowered thyroid function.  Such diets are not a good idea!

If the thyroid gland is not functioning properly, the body cannot utilize energy from food as efficiently as it should.  Calories not burned can be stored as fat.  But an under-functioning thyroid tends to suppress appetite as well as slow down metabolism.  Hypothyroidism does not necessarily cause a big weight gain, perhaps 5 to 15 pounds.  The majority of overweight people do NOT have a thyroid problem.  Yet there are a minority of people who eat less than others but still cannot lose excess weight.  They may have an underactive thyroid.  The most common symptoms are fatigue (and less physical activity), depression and anxiety (which can lead to overeating), feeling too cold, and slowed digestion.  Overeating and reduced activity can result in significant weight gain.  Unfortunately, blood tests for hypothyroidism are imprecise and may show readings out of normal range only when thyroid function is badly awry.  In reality, the production of thyroid hormone gradually falls off, so a slight or mediocre reduction can cause symptoms in some people, even though blood tests appear normal.  TSH (thyroid stimulating hormone) is the first test to indicate imbalance, but ‘normal' is broadly defined (from 0.4 to 4.4 milliunits per liter) and the issue is really what is normal for that individual.  Symptoms can appear months or even years before TSH registers abnormal.  Metabolic rate should really be viewed in relation to calorie intake, thyroid function, hormonal balance, physical activity, food quality, and nutritional balance.  They all count. vii


Balancing insulin and glucagons can result in successful weight management for many people.  This involves avoiding refined carbohydrates, altered fats, and denatured proteins along with supplementing nutrients to support pancreatic and liver function.  Insulin resistance frequently results from obesity with increased fat formation and decreased fat breakdown.  Losing weight often lessens or eliminates insulin resistance.  But insulin disruption - particularly if due to excess consumption of refined and artificial sugars and other refined carbohydrates - can also predispose to weight gain.

Many women gain excess weight during periods of possible hormone imbalance such as puberty, after childbirth, and menopause.  This may be due to estrogen inadequately balanced by progesterone.  Estrogen dominance (often caused by estrogen replacement therapy or birth control pills) can activate a fat-storing enzyme as well as pull down the function of the thyroid gland and lower metabolic rate.  A chronic release of stress hormones such as cortisol, especially if combined with excess estrogen, can disturb blood sugar regulatory mechanisms, increase breakdown of lean body tissues, slow metabolic rate, impair digestion, and stimulate synthesis of fatty tissues.  High cortisol levels do not always make people fat, but supporting adrenal function with whole food nutrients may be of assistance.  Although hypothyroidism does not typically cause a lot of weight gain, this imbalance combined with other endocrine challenges can complicate the weight problem. viii


Sluggish sympathetic nervous activity may contribute to weight gain in some folks.  The sympathetic nervous system plays a key role in rousting stored fat so it can be converted to energy.  A dense array of nerve branches reaches throughout the digestive tract, and there is extensive communication to and from the brain.  Digestive tract nerve fibers can process data they collect so the brain receives integrated messages.  This processing results in local adjustments to the digestive tract to ensure maximum nutrient absorption.  Various biochemicals (including hormones and protein fragments) take part in the gut-brain communication and in regulation of food intake.  Thus, foods consumed are as much a neurobiological issue as a nutritional one.  Digestive problems, nerve disruptions, hormonal imbalances, poor food choices, and nutritional deficits can add to weight distortions.

Chronic stress can contribute to overweight, especially to abdominal fat.  A brain hormone signals the adrenal glands to release hormones (including cortisol) to help the body deal with stress.  Cortisol causes glucose and fatty acids (which provide energy to muscles) to be released.  If cortisol stays high or frequently becomes high, appetite increases (to replenish energy stores the body assumes have been spent in fight or flight), insulin is released, and fat storage is upped.  Anxiety, irritability, and other symptoms may appear.  When cortisol hits any fat cell, it activates fat-storing enzymes that cause the cell to plump up with fat.  Central fat cells (abdominal) act as a source of quick energy during stress and have more cortisol receptors than other fat cells.

People with psychological issues (such as a history of childhood physical, emotional, or sexual abuse) are at increased risk for obesity.  People with emotional problems often use food as a way to cope with or soothe uncomfortable feelings.  "One in four persons seeing a primary care physician about weight problems has an active psychiatric illness, usually depression."  Each person is unique, both physically and emotionally, so successful weight loss must address all the specific aspects.  For example, an individual needs to understand and work with any emotional causes for overeating patterns or food cravings.  These may include loneliness, boredom, anger, depression, seeking substitutes for love, a means of covering up feelings, seeking rewards, as a way to cope with circumstances such as domestic violence or unemployment, dislike of one's body, lack of needed support, using food as a means to take care of oneself, for gratification, or - for a variety of reasons - not being able to commit to the behavioral changes that would result in weight loss and improved health.  Such issues may not be entirely responsible for excess weight, but they certainly enter into the equation and need to be addressed.  Food is the universal drug of choice when moods inevitably push people to become "users."

Biochemical contributors must also be considered.  For instance, which came first, the depression or the weight gain?  Are nutritional deficiencies or imbalances contributing to the depression?  And is the stress of depression contributing to the deficiencies?  "Dysfunctional eating habits" have been shown to be related to energy and tension.  Negative moods are reflected in overeating.  Healthful foods, good nutrition, and exercise help individuals to maintain positive control over their moods - even debilitating depression and anxiety.

Researchers have found a strong connection between getting enough sleep and keeping off the pounds.  People who slept less than 7 hours a night had an increased risk for obesity.  The risk ranged from 23% among 6-hour sleepers to 73% for those getting only 2 to 4 hours of sleep.  Some people are particularly sensitive to light deprivation - whether due to shorter winter days or simply not getting enough exposure to natural sunlight.  About 5% of the population becomes markedly depressed with seasonal affective disorder (SAD).  About 20% are affected to some degree.  This can induce increased food cravings and weight gain in susceptible people. ix


Molecules of toxins and pollutants are often shunted to fat cells for storage.  When fat is ‘burned' off - as occurs with dieting or exercise - toxins from these fat cells are mobilized and make their way into the bloodstream.  This may reduce the amount of leptin (a natural hormone known to help the body reduce fat and regulate weight) in fat cells.  Modern-day pollutants may complicate the regulation of energy -- interfering with the thyroid gland and the mitochondria in cells where fuel is converted into energy, slowing metabolic rate.  Even if the body burns only 100 fewer calories a day, this can add up to significant weight gain over the period of a year.  

Effects of various synthetic chemicals in relation to weight control are being examined.  Legitimate and illicit use of chemical substances in the food industry is widespread.  A huge number of synthetic chemicals with the potential to disrupt the endocrine system and its hormones have been released into the environment.  Hormonal changes are associated with increases in body weight and are related to the distribution of fat tissue.  The body stockpiles environmental chemicals throughout life that damage metabolic enzymes, affecting the ability to ‘burn' calories.  The prime areas of fatty acid oxidation (inside mitochondrial and peroxisomes of cells) are poisoned by plastics or phthalates which are just about everywhere including food packaging.  EPA studies show plastic chemicals are the top pollutant in the human body.  Many practitioners find that supporting detoxification - cleaning out stored chemicals that damage normal chemistry and keep food addictions raging - is a huge help in weight control.  Many stored xenobiotics including PCBs, dioxins, phthalates, pesticides and other hydrocarbons that damage glands and hormone receptors on cell membranes can be reduced.  A good detoxification protocol can aid in reversing "a lifetime of bad fat-paralyzing chemistry."

"Accurate identification of food sensitivities is vital to a successful weight loss and healthy eating program."  Food intolerances may cause cravings for various things such as refined carbohydrates or for the ‘offending' foods.  Elimination of offending foods often helps restore biochemical balance.  People working night shifts may be more susceptible to weight gain - endocrine and other disruptions relating to the biological ‘clock' can contribute to appetite and weight changes.  Television viewing increases the risk of developing obesity.  This is often attributed to the sedentary nature of watching television, but it may also reflect the messages sent by TV contents (such as advertising and food cues).  It has been suggested that vivid television images can cause changes in human physiology and emotions, influencing decision making. x


By far, the most influential aspect in people's lives that affects the tendency for weight gain (or difficulty losing weight) is the food, or more pointedly, the non-food, going into their bodies.  Traditional diets of whole foods, locally-raised and consumed fresh, have been supplanted by diets of stripped, depleted, unbalanced, altered, denatured, artificial, highly processed, and embalmed poor performance foods.  The increased proliferation of high-calorie, low-nutrition foods - widely available, heavily promoted, cheap, and served in large portions - is creating what Yale psychologist Kelly Brownell calls a "toxic food environment."

Refined, distorted, degenerate, mutated non-foods crowd out nutritionally complete foods that provide essential components for health and balance.  The most heavily advertised foods tend to be of "dubious nutritional value" - candy, sugary cereals, soda, snack foods like chips, fast foods, etc.  Food marketers find new aggressive ways to advertise and promote their products.  Food purveyors have subtle ways of making people eat more than they intend or are even aware of.  People eat considerably more than they have in the past.  Increased variety of supermarket and restaurant offerings encourages sampling.  Portion sizes have been getting bigger.  Food is readily accessible in virtually every locale.  Food is often inexpensive and takes little or no time or energy to prepare.  People eat outside the home more than ever.  "Fast" food is available at home, at school, at work, and in restaurants and other venues.  Refined carbohydrates, partially hydrogenated fats, and questionably construed sugars now comprise a large portion of the standard American diet (SAD).  They are not healthy for anyone.  American women consume 335 more calories a day, men 170 extra calories a day, than they did 20 years ago.  Almost all the extra calories come from refined carbohydrates such as sugary snacks and soft drinks.  Fat intake has remained about the same.  But fat comprises a smaller percentage of daily calories now than it did 2 decades ago because of the rise in total calories - mostly depleted, decimated carbohydrates stripped of the nutrient-dense and fiber-rich portions.  And many fats are altered; more trans fatty acids are eaten which can block membrane hormone receptors from working, contributing to weight gain.

High-fructose corn syrup (HFCS) now constitutes 10% of total caloric intake.  It is 6 times sweeter than refined cane sugar and bypasses the complex bodily breakdown process that other sugars go through, arriving almost completely intact in the liver.  The liver releases a lot of fatty acids (triglycerides).  Muscle tissues develop insulin resistance, and decreased glucose tolerance results.  HFCS does NOT stimulate an increase in insulin the way most sugars do and does NOT cause an increase in the compound leptin - both of which signal the central nervous system to stop eating.  HFCS increases the level of ghrelin, a compound that enhances appetite.  It disrupts the natural ability to register satiety; you don't know when to stop eating.  Obviously this leads to weight gain.  HFCS "is about the furthest thing from natural that one can imagine, let along eat."  Yet it appears in sodas, pastries, candy, snacks, convenience foods, and essentially much of what Americans are eating more of.

Too many refined sugars (such as those in candy, pastries, sodas and artificial juices, for instance); too many refined starches (such as those in ‘white' breads, read-to-eat cereals, cakes, pastas, pizza, cookies, etc.); too many altered fats (such as partially-hydrogenated oils, refined oils, and ‘fake' fats); too many disrupting chemical additives; too many foods raised in toxic, unnatural, depleted, unbalanced, discomfiting ways; too many "empty" calories - all contribute to excess weight and obesity.  The body's ability of handle large amounts of non-foods or "dietary toxic waste" is overloaded.  Fat tissue may be used as a sort of toxic waste dump site.  And with so much non-usable ‘garbage' - almost or entirely void of nutrients in complex food forms - the body may shunt the end products to fat cells whence there is little else that can be done with them without their whole food collaborators.  In other words, people are eating too much of what they don't need and not nearly enough of what they do need to be healthy and lean.  They are eating but not feeding!  Combine this with increasingly urbanized, automated, and more sedentary lifestyles, and an ideal recipe for weight gain is created. xi

To be continued...

This website has excellent nutritional protocols for weight loss which are available in conjunction with the Symptom Survey.  Take the Symptom Survey to discover specifically what nutrition you need for your individual health problems.  I want to emphasize that the nutrition I recommend CANNOT be purchased in any retail store: so-called "health food" store, drug store, super market, etc.  The nutrition I recommend will help rebuild your body and help restore your health.  Those other products will only give you a pharmaceutical (drug) effect.  They will attempt to deal with your symptoms, which is the ONLY thing any drug can do, while leaving the state of your health unchanged.

i UC Berkeley Wellness Lttr, May 2005, 21(8): 8 & Feb 2004, 20(5): 1 & Sept 2002, 18(12): 1; H Butchko et al, Nutr Today, Nov/Dec 2004, 39(6): 235-44; JAMA, 9 Oct 2002, 288(14): 1723-32, 1758-61; Nutr Week, 9 May 2005, 35(10): 2 & 6 Jan 2003, 33(1): 6 & 16 Dec 2002, 32(23): 8 & 19 Aug 2002, 32(16): 8 & 18 Jun 2001, 31(23): 1; Tufts Univ Health & Nutr Lttr, Dec 2003, 21(10): 2; A Mokdad et al, JAMA, 1 Jan 2003, 289(1): 76-9; R Sturm, Arch Intern Med, 2003, 163: 2146-8; J Raloff, Sci News, 28 Feb 2004, 165(9): 139-40; P Abelson et al, Science, 4 Jun 2004, 304(5676): 1413; J Foreyt, Eating Well, Feb/Mar 2005, 3(3): 21-3; Acres USA, Oct 2004, 34(10): 37.

ii Eating Well, Feb/Mar 2005, 3(3):21-3 & Fall 2004, 3(2): 17; A Field et al, Arch Intern Med, 2001, 161:1581-6; Hlth News, Jun 2005, 11 (6): 13 & Feb 2003, 9(2):11; Nutr Week, 25 Apr 2005, 35(9):7 & 28 Mar 2005, 35(7):2 & 3 Jan 2005, 35(1):3 & 30 Sept 2002, 32(18):7 & 22 Oct 2001, 31(40):6 & 27 Aug 2001, 31(33):7; NEJM, 2002, 347:305, 358; JAMA, 9 Apr 2003, 289(14):1880; Arch Intern Med, 1998, 158: 1333-7; D Carmelli et al, Obesity Res, Dec 2000, 8(9):632-7; G Lam et al, Nutr Rev, Oct 2004, 62(10):394-9; C Meier et al, J Hepatol, 2002, 37:741-7; S Kojima et al, J Gastroenterol, 2003, 38:954-61; M Visser et al, JAMA, 8 Dec 1999, 282(22):2131-42; UC Berkeley Wellness Lttr, Jul 2003, 19(10):1 & Dec 2002, 19(3):1; K Fontaine et al, JAMA, 8 Jan 2003, 289(2):187-93; M St Onge et al, Nutr Rev, Sept 2003, 61(9):313-16; C Mann, Science, 18 Mar 2005, 307(5716):1716-17; R Rowens, Second Opin, Feb 2002, 12(2):3; Consumer Mag Digest, Apr 2005, 17(4): 5;Second Opin, Sept 2000, 10(9):6-7; NEJM , 7 Oct 1999, 341:1097-1105; Health & Healing, Oct 2003, 13(10):5 & Mar 2002, 12(3):5.

iii Consumer Mag Digest, Jul 2004, 16(7): 5 & Feb 2003, 15(2): 5 & Oct 2002, 14(10): 5; Sci News, 11 Jul 1998, 154(2): 19; Primary Care Reports, 7 Feb 2000, 6(3): 19-30; T Hudson, Townsend Lttr D&P, Aug/Sept 2002, 229/230: 184-7; W Pan et al, Am J Clin Nutr, Jan 2004, 79(1): 31-9; V Hubbard, Am J Clin Nutr, Nov 2000, 72(5): 1067-8; Lancet, 10 Jan 2004, 363(9403): 157-63; K Flegal et al, JAMA, 20 Apr 2005, 293(15): 1861-7; D Mark, JAMA, 20 Apr 2005, 293(15): 1918-9; J Curtis et al, Arch Intern Med, 2005, 165: 55-61; Health, Mar 2003, 17(2): 37; Nutr Today, Nov/Dec 2000, 35(6): 204; Nutr Week, 1 Sept 2000, 30(33): 3; UC Berkeley Wellness Lttr, Mar 1999, 15(6): 8; J Seidell et al, Am J Clin Nutr, Sept 2001, 74(3): 315-21; M Sperl, Health, Mar 2002, 16(2): 102-7.

iv Nutrition Week, 5 Apr 2004, 34(6): 4-5; H Bell, Tufts Univ Health & Nutr Lttr, Jul 2004, 22(5): 1, 4-6; UC Berkeley Wellness Lttr, Mar 2005, 21(6): 8; D Williams, Alternatives, Apr 2003, 9(22): 172-6; A Dulloo, Science, 2 Aug 2002, 297(5582): 780-1.

v Consumer Magazines Digest, Mar 2005, 17(3): 5 & Jan 2004, 16(1): 5 & Jan 2003, 15(1): 5 & Aug 2001, 13(8): 7.

vi S Roberts & A Greenberg, Nutr Rev, Reb 1996, 54(2): 41-9; Science, 4 Apr 2003, 300(5616): 21; D Allison & M Faith, Nutr Today, Jan/Feb 2000, 25(1): 18-21; B Heitmann et al, Am J Clin Nutr, Sept 1997, 66(3): 672-8; Consumer Mag Digest, Nov 2002, 14(11): 5 & May 2002, 14(5): 5 & Oct 2000, 12(10): 1; P Williams, Health, Jul/Aug 1996, 10(4): 18-9; Lancet, 21 Mar 1998, 351(9106): 88809; A Comuzzie & D Allison, Science, 29 May 1998, 280(5368): 1374-7; Let's Live, Aut 1998: 26; Health, Sept 1999, 13(7): 22; N Barnard, Veg Times, May 2005, 331: 13, 18-19; L Perosse & C Bouchard, Nutr Rev, May 1999, 57(5): S31-8.

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Originally published as an issue of Nutrition News and Views, reproduced with permission by the author, Judith A. DeCava, CNC, LNC.