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The Diet Zoo: Does Science Provide Guidance?

by William R. Ware, PhD


Dieting has a long history, initially associated with creating a desired image, e.g. the slender beauty, or dealing with a medical problem for which the conventional wisdom of the time used dietary modification as a therapy.

Bill Ware At the turn of the century, North Americans ate lots of meat and fat, some put thick layers of lard on their bread, and many ate fresh produce only when in-season, and yet cardiovascular problems and adult onset diabetes were relatively rare, and obesity was not the subject of constant comment in the press nor regarded as an epidemic of great public health concern. The French Paradox is approximately the modern- day equivalent. A big change occurred some 30-40 years ago when both the US government and the medical and nutritional authorities took the position that all fat was unhealthy and responsible for the growing incidence of heart disease and cancer. While this view was strongly opposed by a minority of scientists, it became the true dogma by which many chose to live. The oversimplified notion that all fat is bad was deeply embedded, both among layman, the medical profession and the nutritional scientists, and a low-fat diet was accepted as the answer to many health problems. Many health care professionals and much of the general public still hold this view. The net result was the replacement of fat by carbohydrate, in many cases rapidly digested carbohydrate, which constituted a significant change in the diet of North Americans. This subject was reviewed in International Health News (IHN) newsletters, November 2002 through January, 2003 [1]. It is also discussed in two widely quoted articles by Gary Taubes [2,3]

It was not until the early seventies that a contrary voice was loud enough to be heard by the general public, the voice of the late Robert Atkins, M.D., a cardiologist, who took a position diametrically opposed to The Establishment (the American Heart Association, the American Diabetes Association, the USDA, the American Medical Association, etc.) and promoted a diet high in fat and protein and low in carbohydrates with emphasis on slowly digested carbohydrates. Initially, his primary concern was weight loss. This diet flew in the face of the conventional wisdom and was vigorously and vehemently condemned by the government, the medical establishment, and nutrition experts. Atkins had to appear before a congressional committee to defend himself, as though he was some sort of public enemy. Nevertheless, his first book became a best seller, and subsequent editions have followed the same course, making books on the Atkins diet the most widely read diet guides in the history of man.

In the past decade a number of other similar low-carbohydrate diets have also become very popular. Most have been and are still labeled by their critics with the apparently intentionally derogatory term "fad diets," and this collection of diets defines one boundary of the great diet controversy that has arisen and now rages. A visit to a large book store like Boarders or Chapters or Barnes and Noble will reveal the present state of the popular diet book market, with hardcovers and paperbacks on every imaginable diet topic and philosophy, displayed typically in 10 to 20 linear feet of 6 to 8 foot high book shelves. This is the popular print version of the Diet Zoo.

The word "diet" has many connotations and a varied usage, but this review will be concerned with the meaning related mainly to changes in eating habits, either self-motivated or suggested by someone, generally a health care professional. Also, there is the very general question, what should I eat? Whatever the motivation, it is important to have clearly in mind the answer to the question, why am I dieting or why am I following a particular diet philosophy? While the following list is not complete, it covers the most common reasons.

  • Overweight or obese, or avoiding these conditions.
  • Bad lipid profile, e.g. high LDL cholesterol, low HDL cholesterol, high triglycerides.
  • Presence of the characteristics of the metabolic syndrome or insulin resistance.
  • Hypertension, and/or diabetes.
  • Primary prevention of coronary heart disease (CHD), cardiovascular disease (CVD) and diabetes.
  • Secondary prevention of CHD or CVD related adverse events, i.e. after a heart attack or stroke, or the existence of stable angina, transient ischemic attacks, etc.
  • The desire to become more beautiful and attractive or more closely resemble some idol. Includes the extreme and pathological disorders anorexia and bulimia.
  • Body building and training for sports.
  • Maintenance of good health, i.e. concern that the present diet may carry risks even in the absence of any evidence from symptoms or a physical exam. For example, deciding to adopt a so-called heart-healthy diet, and thus being confronted with the question of what in fact is a heart-healthy diet.

It would seem that diets undertaken in response to a health crisis must be judged by different criteria than those embarked upon for less pressing reasons. The main theme of most diet books and magazine articles on diet would suggest that weight loss is the primary motivation, although it appears likely that many individuals embarking on such an endeavor may be totally unaware of other aspects of their health that frequently accompany being overweight or obese and also respond to dietary intervention. In fact, the implication of the above list is that specific diets can be used as a therapeutic approach to health problems that transcend or accompany being overweight or obese. The flip side is that diet may be implicated in the same health problems. This is an important and fascinating area. For example, cardiovascular disease and diabetes are major health problems in the developed world which are now thought to be susceptible to dietary and lifestyle intervention, with the potential for sensational reductions in risk[4,5,6,7,8].

This review will attempt to probe the basic science involved in the issues that accompany the Diet Zoo and will attempt to evaluate the evidence, which allows a judgment call on questions of benefits and risks of various dietary approaches. This review will also examine selected popular fad-diet schemes as well as current recommendations from what will continue to be called The Establishment.

METABOLISM AND WEIGHT LOSS. To metabolize essentially means "to change" and it involves chemical processes that transform the nutrients (chemical substances) derived from food to chemical substances that can be used in the multitude of chemical transformations that occur in the body. Food enters the system via the mouth, and the digestion processes occur there, in the stomach and in the intestines. It is important to realize that this digestive system is outside the body, being continuous and "open at both ends," and that substances in the food must pass through the walls of this system to get into the body proper. Many chemical transformations are required for digestion and absorption of food, and undigested material, including fiber, is simply eliminated, never having really been "inside" the body. Proteins, carbohydrates and fats are each processed differently in the digestive system to yield amino acids, simple sugars, and emulsified fat subunits, respectively, which pass into the body and constitute the raw materials for metabolism.

Weight loss is a very common goal of dieting. Every day we take in a certain amount of liquid and solid material which includes considerable water, both in food and consumed separately. In addition, there are gases absorbed, mainly by the lungs. This then is the mass intake. Mass is lost through breathing, sweating, urinating and defecating. The "complete burning" of food fuel or body fat and muscle to produce energy yields water, carbon dioxide, and if necessary, certain nitrogen compounds. Carbon dioxide and some water are lost through the lungs, some water leaves via sweat, the remainder of the water and various waste chemicals are lost in urine and stool. It is important to understand that when chemical reactions occur during metabolism, mass is conserved, and that mass loss must occur via the routes just described. We are not like nuclear reactors where mass is converted directly into energy in a closed system. Also, many chemical reactions involved in metabolism do not involve "complete burning" but simply result in the generation of other chemicals that are then used by the body for a wide variety of purposes. Thus to loose weight one must have a mass loss greater than the mass gain that comes from eating, breathing and drinking. The calorie counting view is oversimplified and ignores both the complexities of metabolism, the ability of the body to metabolically adjust to reduced calorie intake, and the fact that mass loss (weight loss) is only accomplished by breathing, sweating and by liquid and solid waste elimination. Many of the processes associated with metabolism simply generate, from the point of view of mass, equivalent masses of other chemical species, some of which must be eliminated to yield a weight loss. In fact, when these chemical reactions have either a net heat energy gain or deficit, the energy comes almost entirely from differences in the chemical bond energies of reactants as compared to products of these reactions. Nevertheless, it is possible to incorporate these principles and generalize to the extent of having a rough, empirical number for the caloric intake required to maintain weight, based on body mass and activity or direct observation. When caloric intake falls below this level, then the deficit in energy is made up by utilizing non-food sources such as body fat and muscle, and some of the end products of the chemistry are eliminated to give one a weight loss.

The caloric intake required to maintain weight varies with body mass and activity at work and recreation. Typical values range from 2000 to 3000 calories (actually kcal) per day. The consensus opinion seems to be that eating less than 1200 calories per day is not a good idea, and that starvation diets can have serious health consequences including the loss of muscle mass, deleterious deficiencies in essential nutritional fats and potentially serious hormonal imbalances [9].

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METABOLIC SYNDROME X AND INSULIN RESISTANCE. Because dietary intervention can impact both the metabolic syndrome and insulin resistance, it is important to develop some background in these and related problems. This subject has recently been discussed in an IHN research report by Hans Larsen with the title Insulin Resistance and Diabetes. The metabolic syndrome was recently given a new, high profile by virtue of its inclusion in the latest position paper of National Cholesterol Education Program Adult Treatment Panel (ATP-III) as a risk factor for diabetes, CHD and CVD. The ATP-III [10] definition of the presence of the metabolic syndrome is the presence of three or more of the following:

  • Waist Circumference greater than 102 cm (M), 88 cm (F), i.e. excess abdominal fat or an "apple shape."
  • Triglycerides greater than 150 mg/dL (1.7 mmol/L)
  • HDL cholesterol less than 40 mg/ dL (1.03 mmol/L)
  • Hypertension. Blood Pressure equal or greater than 130 systolic, 80 diastolic mmHg
  • Fasting glucose equal to or greater than 110 mg/dL (6.1 mmol/L)

    Several studies indicate that this definition produces an incidence rate of about 24% in the U.S. population [11]. A similar definition by the World Health Organization produces 25% [12]. This average value is deceiving. A recent review [11] finds a strong variation of incidence with both age, body mass and ethnic background. For example, in white males, the prevalence goes from about 15% at age 30 to 40% at age 70, and with white men who are not overweight, prevalence ranges from about 7 to 10%, but if they are obese, the prevalence can reach 75%. It will be noted that the ATP-III definition includes commonly measured or observed parameters obtained during routine physical examinations. It is also important to recognize that there are individuals who are obese but metabolically healthy, i.e. they have none of the attributes of the metabolic syndrome aside from obesity. It may be important to identify this group to avoid inappropriate treatment, to lessen the psychological impact of obesity in these individuals, and to avoid confounding in research studies [13]. However, as discussed below, the health risks associated with obesity may go beyond those related to the metabolic syndrome.

    The metabolic syndrome, as defined above, is the latest incarnation of numerous descriptions of a collection of clinical attributes that, according to many studies, lead to greatly increased risks of heart disease and diabetes. Dr. Gerald Reaven [14] of Stanford University is acknowledged as the ground breaker in this fascinating area. The syndrome has also been called Syndrome X, the Metabolic Syndrome X, the Dismetabolic syndrome, and the Deadly Quartet, to name the principal variations on this theme. The importance lies in its association with a large increase in the risk of CHD, CVD, and diabetes. The presence of four or five of the above attributes further increases the risk. It is of interest that LDL cholesterol levels are not included in the ATP-III definition. Part of the reason is that the ATP-III committee is making the metabolic syndrome an independent risk factor over and above elevated LDL. It is interesting in this context that there are those who consider that an elevated triglyceride level coupled with a low HDL cholesterol level may confer at least as great a risk of CHD as an elevated LDL level alone [15,16]. The bottom line is simply that the metabolic syndrome is shockingly prevalent, appears to confer serious risk of CHD and diabetes, and should be taken very seriously by both individuals and their physicians. The relevance to this review is that the metabolic syndrome can be avoided or reversed in many individuals by diet and lifestyle [14].

    When the fasting blood glucose level is between 110 and 125 mg/dL (6.1-7.0 mmol/L), the condition is called impaired fasting glucose (IFG). Closely related to IFG is impaired glucose tolerance (IGT). Glucose tolerance is determined by measuring the serum glucose level after giving a fasting patient a drink containing 75 g of glucose, the so-called glucose challenge. At two hours, a blood glucose level of 140-199 mg/dL (7.8-11.0 mmol/L) is regarded as evidence of IGT. In all prevalence studies up to 2002, only half or less of the people with IFG have IGT, and an even lower proportion (20-30%) with IGT have IFG. It is argued that IGT and IFT represent different metabolic disturbances [17], but this is still not clear. The glucose tolerance test, also called the oral glucose tolerance test (OGTT), is not popular, presumably because it requires the patient to wait or revisit the office or clinical lab. Those in favor of the test feel it provides valuable additional information over the fasting glucose measurement [18], whereas those opposed [19] feel that combining the fasting glucose measurement with other clinical observations [20] allows the physician to adequately assess the risks of heart disease and diabetes without "inconveniencing" the patient! However, there is also evidence the OGTT is a better predictor of deaths from all causes as well as CVD as compared to fasting glucose values [21]. The reluctance to do an OGTT is curious considering the serious nature of the problems being investigated. IFG and/or IGT, even as isolated conditions, should be considered warning signals, taken very seriously, and hopefully the recognition would stimulate lifestyle and diet modifications.

    Individuals who have IFG or IGT may or may not have what is called insulin resistance, a malfunctioning of the insulin-glucose system wherein abnormally large amounts of insulin are required to maintain blood glucose under control both fasting and after eating. Reaven [14] considers insulin resistance to be at the root of the problems associated with the metabolic syndrome, and to be almost always present when patients present with high triglycerides, low HDL cholesterol, and abdominal obesity. Either the fasting or post glucose challenge insulin level can provide some indication of the presence of insulin resistance. Reaven et al [22] recently reported that an abnormally high fasting or two-hour post glucose challenge serum insulin levels are the best simple clinical indicators of insulin resistance. However, Reaven holds the position that no test easily used in normal clinical practice at present is really satisfactory for demonstrating the presence of insulin resistance, mainly due to the lack of standardization of serum insulin assays [23].

    In view of the close connection between the characteristic risk factors of diabetes and cardiovascular disease, as formalized in the concept of the metabolic syndrome, the hypothesis that diabetes and cardiovascular disease arise from a "common soil" has become attractive, i.e. adult onset diabetes should perhaps be viewed basically as a vascular disease. This point was recently made by Harvard's Frank Hu and Mier Stampfer in an editorial [24] concerning a study by Hunt et al [25] that linked the development of type 2 diabetes and the development and progression of atherosclerosis (as measured by elevated carotid artery intima-media thickness levels). This may well be a turning point in the matter of thinking about and preventing type 2 diabetes, since it emphasizes the need to reduce the risk of atherosclerosis and to treat the risk factors such as hyperlipidemia (elevated cholesterol and triglycerides) and hypertension aggressively, hopefully first with diet and lifestyle changes. A recently reported study on elevated CVD risk prior to the clinical diagnosis of type 2 diabetes also supports the "common soil" hypotheses [26]. In this follow-up study, women who went on to develop type 2 diabetes had a relative risk of 3.75 (3.17 after adjusting for BMI, smoking and other CVD risk factors) for a heart attack and 2.30 for stroke in the period prior to the diabetes diagnosis, as compared to women who did not go on to develop diabetes.

    WHY DO PEOPLE BECOME OVERWEIGHT AND OBESE? The answer depends on to whom one listens. Being overweight, incidentally, is generally defined as having a Body Mass Index (BMI) of between 25 and 30, whereas obesity involves a BMI of greater than 30. Thus the healthy range is generally considered to be below 25, although very low numbers, especially if they are decreasing, should prompt an investigation of pathological causes. A low BMI can also be related to smoking which dulls the appetite in some individuals. BMI is calculated by multiplying 703 (unit conversion factor) times weight in pounds and dividing by the square of the height in inches (kg/m2). Today it has largely replaced older "ideal weight" tables both in clinical practice and research.

    The conventional explanation for being overweight or obese is that simply not enough exercise or physical and metabolic activity occurs to compensate for the calories consumed, i.e. more calories are consumed than are required to maintain normal weight for a given level of physical activity. For any given level of physical activity, if more calories are consumed than needed, then the excess is stored as fat. Consumption of high levels of rapidly digested carbohydrates can produce high transient levels of insulin, and these high levels of insulin are thought to facilitate the storage of fat from carbohydrates converted into fat. This also fits in well with the theory [27] that the increase in overweight and obesity in the past 20-30 years is due in part to the replacement of dietary fat by sugar and starchy foods.

    However, there can be little doubt that the question posed at the beginning of this section is far from simple. Consider the so-called French Paradox. The French do not have the overweight or obesity problem nearly to the extent seen in North Americans. Their incidence of heart disease is dramatically lower (about one-third) than ours. They eat baguettes, greasy croissants, liver pate, butter, cheese, lots of olive oil, etc., i.e. lots of fat. Low- fat or fat-free foods are almost unknown on French grocery store shelves. It is estimated that they get 35-45% of their calories from fat. Their obesity rate is about 8% and constant compared to 30% and growing in North America. One company in the US that specializes in oversized coffins to accommodate the obese reports a 20% annual growth rate in sales (National Post, September 28)! Needless to say, this paradox has attracted considerable attention over a number of years. The French Paradox obviously goes against the thesis that fat makes one fat, which was discussed at in a review in IHN [1] with particular reference to the views and research of Dr. Walter Willett, who regards this notion as a fallacy [28,29]. Foreyt and Poston have recently presented a "symposium consensus " view on this subject [30] which emphasized the role of lifestyle, excessive caloric consumption from all sources, and decreased physical activity as causes of obesity.

    A very interesting view of the French Paradox is presented by Dr. Will Clower in the new book The Fat Fallacy [31]. Clower is a neurophysiologist on the faculty of the University of Pittsburgh. He spent two years as a research fellow in Lyon, France and availed himself of the opportunity to study in an informal way the French Paradox. The French have radically different eating habits as compared to North Americans. They eat smaller portions of a greater variety of food. Their meals tend to be, whenever possible, special occasions and extend, whenever time permits, over a much greater period of time than do ours. They take small bites, and rarely stuff their mouths' as do many North Americans. They prepare, eat and enjoy food with almost religious fervor. The idea of heaping plates and a quick, gobble-it-down-and-run meal are foreign to their eating philosophy. The French also have salad after the main meal. When there is vinegar in the dressing, this tends to slow down digestion, as does the cheese that generally follows. Desserts, if offered, are generally small and may well consist of fruit. Their meat consumption is lower than ours and their use of olive oil much greater. Between-meal snacking is uncommon, as is the heavy consumption of the standard fare of what we find in the local doughnut shop or they find in their boulangerie-patisserie, and their pastries incidentally tend to be very pricey. The consumption of what Cower calls "faux-foods", e.g. highly processed foods from the super market freezer, canned goods shelves or in the form of ready-to-eat dinners, is much lower. The drinking of wine with meals is almost universal, and starts at a fairly early age. Food is generally prepared with great care and much attention to flavor, taste and presentation. With many cooks, it comes close to being an art form. While there are fast food restaurants in France, they do not represent a significant aspect in French eating habits.

    An interesting and popular theory regarding the tendency to become obese or overweight, the "thrifty genotype" hypotheses, holds that many individuals are very efficient at metabolic pathways that lead to the storage of fat during times of feasting, since this would have had a big survival advantage tens of thousands of years ago when humans had to endure long periods of food shortages. We have essentially the same genetic makeup. Today the situation is one of feast rather than famine, every day, at least in North America, and this feast now has large portion sizes, low-fat foods, unknown until very recently, loaded with refined carbs, a fast-food industry making a big play on "super sizing," and all-you-can-eat buffets that are the rage.

    Finally there are familial and genetic predispositions to obesity, as well as endocrine causes. The latter include Cushing's syndrome, and some hypothalamic tumors, and as well, hypothyroidism can cause weight gain by reducing the metabolic rate. One would hope that physicians dealing with patients presenting with obesity problems would examine these possibilities.

    Thus stability of body weight or weight gain appears to involve a complex set of factors, such as the amount of daily exercise, the amount of food eaten and how it is eaten, the nature and content of meals and snacks, the amount of food that is required to produce satisfaction, the rate of return of hunger and the urge to eat again, and restraint regarding the portions offered or available. Willett's recent book Eat, Drink and be Healthy (Chapter 3) contains an interesting and relevant review of this subject [27].

  • BEING OVERWEIGHT OR OBESE CARRIES SERIOUS RISKS. The number of Americans that are overweight or obese has rapidly increased in the last two decades from 47% to about 60% of the population. Below are summarized some of the unfavorable health aspects associated with obesity or being overweight.

    • The risk of death from all causes increases throughout the range of moderate to severe overweight for both men and women in all age groups. The risk associated with a high BMI is greater for white as compared to black individuals [32]. Many attempts to correlate mortality with BMI show a U shaped curve, but the interpretation of the increased risk at low BMI is subject to much debate, is related to the inclusion of smokers, and is difficult to correct for long term effects of diseases that cause wasting and are ultimately fatal [33]. This also causes a problem when attempts are made to establish guidelines for a "healthy weight" [33].
    • Increased body weight is associated with increased death rates from all cancers combined and for cancers at specific sites, in particular esophagus, colon and rectum, liver, gallbladder, pancreas, kidney, non-Hodgkin's lymphoma and multiple myeloma. Significant trends of risk and higher BMI were seen for death from stomach and prostate cancer in men and breast, uterus, cervix and ovary cancer in women [34]. Thus avoidance of weight gain appears to be an important factor in cancer prevention [35].
    • Being elderly, female and overweight carries an enhanced risk of Alzheimer's disease, according to a study published in 2003 [36].
    • An interesting study just published indicates that abdominal obesity is an independent and potent risk factor for ischemic stroke in all race-ethnic groups, and is a stronger risk factor than BMI. Also a greater effect was observed among younger persons [37].
    • It has been theorized that insulin resistance and obesity are involved in a vicious circle, where once obesity occurs, basal lipolysis in the enlarged fat mass causes increased free fatty acid levels which tend to increase insulin resistance and hyperinsulinemia, and the hyperinsulinemia ultimately leads to fat storage and more obesity, and thus the cycle continues [38]. Unless steps are taken early to halt the weight increase and abdominal fat deposition, the patient may be "swept away in the morbidity and mortality of the metabolic syndrome" [38].
    • There seems little question that obesity is related to an elevated risk of hypertension, elevated plasma insulin and insulin resistance, adult-onset diabetes, and unfavorable blood lipid profiles, with the end result of increased risk of CVD as well as non-CVD complications associated with diabetes [39]. There is also growing evidence that emerging risk factors -- insulin resistance, a proinflammatory state, and a prothrombotic state are common in obese persons and are independent risk factors for the development of atherosclerosis [40].

    This is by no means a complete listing of the suspected or documented adverse aspects of being overweight or obese. For example, the adverse effects on joint health have been omitted. Also, space does not permit a detailed discussion of the influence of gender, age, or ethnic origin on the risks of obesity or being overweight, but there are definitely substantial differences observed. When risk factors are examined as a function of BMI, the relationship is frequently an increasing linear relationship, or one that curves upward, with increased risk having a threshold in what is considered the upper limit of the normal range, i.e. about 23-25 kg/m2 [33,34]. Thus adjusting diet to halt weight gain at its onset is easily justified. While with the obese, weight reduction to achieve a BMI in the normal range is in many cases unrealistic, studies consistently indicate substantial declines in risk for many health problems with only a 10 or 15% decrease in BMI, even though the patient is still overweight or obese [33].

    The implications are clear. The percentage of the population in North America that is overweight or obese is already very high and is growing at an alarming rate. Thus far the recommendations of The Establishment, followed by large numbers of individuals for several decades, have not resulted in a change in the bleak picture. Americans were told to decrease their fat consumption, which they did (as a percentage of total calories), but they only collectively got fatter [2,27]! This is clearly a crisis situation, and as we will see below, The Establishment is slowly changing its position. But unless dramatic changes occur in actual eating habits among the general public, some of whom have become highly skeptical or cynical regarding flip-flops in Establishment dietary recommendations, the implications as regards the coming impact on the heath care systems, the health care insurance industry, and the taxpayer are almost beyond comprehension. The situation is especially critical because of the impact of the obesity epidemic includes major areas of illness, i.e. cancer, CVD, and diabetes. The name of the game, so to speak, is to avoid or delay the onset of CVD, diabetes and other health problems by not being overweight or obese. Clearly, the related metabolic syndrome is something to avoid like the plague. There is considerable evidence suggesting that diet can play an essential role in avoiding the metabolic syndrome or at least significantly reducing the magnitude of the problems that characterize it, and insulin resistance appears to be reversible if caught early enough [14,9]. Interested readers may also wish to consult the book by Challem et al [41] for more information on reversing insulin resistance.

    While this review will not discuss such lifestyle aspects as exercise and stress reduction, these must be very seriously considered along with diet in context of achieving or maintaining health. The role of exercise in both weight control and weight reduction cannot be overemphasized. Recent studies suggest that between 50% and 70% reductions in the incidence of heart disease and diabetes can be achieved by diet and lifestyle alone [4,5,6,7,8]. By normal standards of risk reduction, these numbers are sensational.

    DIET AND CANCER IN GENERAL. Clearly an important question when judging diets. It is a difficult area since prospective cohort and case-control studies frequently disagree. This was discussed in the IHN review [1] in connection with cancer and fat. In terms of positive risk factors, large prospective studies have not supported the role of dietary fat. Instead, according to a recent review by Willett [42], positive energy balance, reflected in early age for the onset of menstruation and weight gain as an adult, appear to be the important determinants of the risk of both colon and breast cancer. Likewise, lack of physical activity has been shown to be associated with positive risk for these diseases. Thus diet enters indirectly when it contributes to being overweight or obese. In terms of decreasing risk, the role of fruits and vegetables appears to be overstated [42], but Willett emphasizes the potential role of folic acid in connection with both breast and colon cancer. The effects of folic acid consumption appear strongest among persons who regularly consume alcohol, which itself is associated with a risk of these cancers. A recent study by Terry et al [43] found from a large prospective study that individuals who consumed very low amounts of fruit and vegetables had an enhanced risk of colorectal cancer. The connection between dairy products and prostate cancer appears to be absent, but there is a modest risk associated with a large intake of calcium >2000 mg/day vs. <700 mg/day [44]. Willett's review ends with the following conclusions which are also similar to those given in his book [27]:

    • Weight control and regular physical activity should be high priorities for the prevention of cancer.
    • Decisions about dietary fat should be made primarily on it relationship with CVD, not cancer. The 2002 review by Moyad [45] takes essentially the same position.
    • Consuming an abundance of fruits and vegetables and eating grains in a minimally processed, high fiber form is desirable, but the benefits appear greater for CVD than for cancer.
    • Adequate folic acid intake appears important in reducing cancer risk, particularly if alcohol is consumed regularly. Taking a multiple vitamin is the most reliable approach.
    • Aside from the above, one must wait for the results of 30 large prospective studies that are underway in order to form additional significant conclusions regarding diet and cancer.

    Specific reference will be made in Part II to recent studies that also bear on this subject in the context of either fat and red meat or carbohydrate.

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    THE PROTEIN QUESTION. The amount of protein needed each day is the subject of much debate which unfortunately appears to occur in the absence of hard scientific data. There is no question that protein is an essential component of the human diet. The body gets the amino acids required for its own protein, enzyme and hormone synthesis from the amino acids derived from the protein in food. Some amino acids the body can make, others must come from food, which is a concern for pure vegetarians. The Establishment promotes a figure of 0.8 grams per day per kg of body weight (55 g for a weight of 150 lbs, 73 g for a weight of 200 lbs), but compelling evidence in favor of this number appears lacking. Most low-carb advocates feel this is too low and suggest 1 to 1.2 grams per day per kg or even higher.

    Low-carb diets generally involve increased protein consumption, and the critics almost always raise the spectre of serious health problems associated with bone loss, decreased bone mass density, increased rates of heart disease and the risk of kidney stones or kidney damage. While there is no question that individuals with kidney problems or a tendency to form stones should be careful of high protein intake and should work with their physicians if altering their diets in this direction, there appears to be very little modern scientific evidence that increasing the protein intake to 1.2 g/kg or even somewhat higher is associated with any of the risks to the general population that the critics enumerate. The following is a short list of recent studies that relate to these criticisms.

    • In a review of recent epidemiological studies, Kerstetter et al [46] found that reduced bone density and increased rates of bone loss were observed in individuals consuming low protein diets, not high protein diets.
    • In a study published in 2003, Layman et al [47] found that increasing the proportion of protein to carbohydrate in the diet of adult women had a positive effect on body composition, blood lipids, glucose homeostasis and satiety during weight loss.
    • In a study also published in 2003, Roughead et al [48] found that calcium retention was not reduced when subjects consumed a high protein diet from common dietary sources such as meat.
    • Layman et al [49] found in a recent study that a diet with increased protein and a reduced carbohydrate/protein ratio stabilizes blood glucose during non-absorptive periods and reduces the post-meal insulin response, both of which are generally viewed as desirable effects.
    • In a prospective study published in 1999 based on the Nurses' Health Study data, Hu et al [50] found no support for the hypothesis that high protein intake increases the risk of ischemic (occlusive) heart disease. In fact, their findings suggest that replacing carbohydrates with protein may be associated with lower risk of ischemic heart disease.
    • According to a study published in 2003, Farnsworth et al [51] found that replacing carbohydrate with protein from meat, poultry, and diary foods had beneficial metabolic effects and no adverse effects on markers of bone turnover or calcium excretion.
    • The importance of calcium intake in promoting the favorable effect of increased dietary protein intake is discussed in two recent papers. Dawson-Hughes and Harris discuss supplementation with calcium citrate and vitamin D [52]. Dawson-Hughes [53] reviews studies that also deal with this aspect.
    • Rapuri et al [54] found that the highest quartile of protein intake was associated with higher bone mass density in elderly women only when calcium intake exceeded about 400 mg/day. Over a three-year follow-up, no association was seen between protein intake and the rate of bone loss.
    • A study reported by Kerstetter et al [55] in 2000 concluded that for young healthy women consuming a well- balanced diet moderate in nutrients known to influence calcium metabolism, the recommended daily allowance (RDA) for protein of 0.8 g/kg body weight does not support optimal calcium nutrition. They suggest at least 0.9 g/kg are need to normalize calcium metabolism.
    • Appel [56] has recently reviewed the question of the effects of protein intake on blood pressure and CVD. His summary is of interest: "Recent evidence suggests that an increased intake of protein, particularly plant protein, may lower blood pressure and reduce the risk of cardiovascular disease"
    • Knight et al [57] in 2003 reported that high protein intake was not associated with renal function decline in women with normal renal function, but a high intake of non-dairy animal protein may accelerate renal function decline in women with mild renal insufficiency.

    With millions of people worldwide adopting the low-carb way of life and therefore eating more protein, if the critics were correct one might have expected a worldwide epidemic of kidney stones, but the critics of these diets appear unable to come up with evidence of such an epidemic.

    Those who advocate consuming only protein from plant sources on occasion argue that our ancestors during and prior to the Stone Age were vegetarians, but modern research suggests otherwise and indicates that they were hunter gatherers who derived 30-40% of their calories from lean meat, bone marrow and animal brain [58] . Cordain et al [59] estimates that the worldwide average protein consumption of hunter-gathers was in the range of 19-35% of total energy. The tentative conclusion from this research is that our genetic makeup, which is virtually unchanged since the Stone Age, is suited to a diet that includes considerable protein and fat from animal sources.

    Thus the criticism of low-carb diets that they contain too much protein does not appear justified except for individuals with special medical problems or who eat huge amounts of meat. Red meat and processed meats (bacon, ham, etc.) constitute a special case to be discussed below. However, no really long-term studies on the safety of very high protein diets are available (Willett's criticism, [27]), but the high score prudent diet quintile in the Nurses' study [60] had a daily consumption of 100 g, which for a 150 lb woman is about 1.5 g/kg, almost twice the Establishment number, and this was a long-term study.

    CARBOHYDRATES. Before the advent of agriculture, which originated about 10,000 years ago, humans obtained their carbohydrate principally from leaves, roots, berries, nuts, and occasionally honey. Cordain et al [59] estimate that our Stone Age ancestors obtained 22-40% of their energy from carbohydrates. These carbohydrates were mostly of the type that were slowly digested and presumably did not result in large swings in insulin and blood glucose. With agriculture came the cultivation of grains, which assumed an ever- increasing role as an important food source. Moving forward to the present, the treatment of grains has become highly sophisticated and commercialized. The fine grinding of grains along with the removal of the outer covering which contains many nutrients and fiber has resulted in flour that is rapidly digested, can produce huge swings in both blood sugar and insulin, and is mainly starch. The feeding of grain and corn to animals raised for meat has changed dramatically the distribution of the various types of fat in the meat, especially in animals fattened in feed lots, as compared to free range or wild animals. Today, the typical North American consumes 50-55% of total energy in the form of carbohydrates, which translates to over 200-300 grams per day. This is in total harmony with the USDA food pyramid. More about this pyramid later.

    The terms complex and simple are frequently used to describe carbohydrates, and those labeled complex have tended to be regarded as superior health-wise. Sugars such as sucrose and fructose were labeled simple, whereas the carbohydrates in bread and starchy foods such as potatoes are considered complex. In fact, starch is just sugar molecules strung together, and the digestive process rapidly breaks down these links to generate sugars, so the distinction between complex and simple is deceiving and misleading. The effect on blood glucose, the principal end result of carbohydrate digestion and absorption, is similar whether the source is sugar, white bread or potato. An average sized potato is equivalent to about 1/4 cup of sugar. Over the last century the consumption of sugar in North America has constantly increased, reaching about 150 pounds per person per year, which is an astounding figure considering many people eat far less. A lot of this sugar is hidden in prepared foods such as baked goods, canned food, low-fat foods, etc. There are those who consider this huge sugar consumption to be a serious health issue [61].

    Today the terms complex and simple have been largely replaced by a new nomenclature -- high and low glycemic index carbohydrates [62]. The glycemic index (GI) indicates the effect, for normal, healthy individuals, of a measured amount of the food on the rise and subsequent fall of blood sugar. This generates a scale which uses as a reference point for comparison the effect of either white bread or pure glucose. Another yardstick, which is also gaining popularity, especially in nutritional epidemiology, is the glycemic load (GL), defined as the glycemic index times the amount of carbohydrate. The basic idea is that eating a small amount of a high GI food can be equivalent to eating a large amount of a low GI food, and that the glycemic load is an appropriate measure of the influence of a typical serving of a carbohydrate containing food. The GI is a useful guide to food selection if the goal is to reduce swings in blood sugar and insulin, since eating significant amounts of high GI foods with a meal, even in the presence of fat and protein, will generally elevate the blood glucose levels more than will a low GI mix of carbohydrates with the same protein and fat meal.

    There is a growing consensus, even it would appear among the experts advising The Establishment, that it is wise to limit high GI foods and emphasize low GI foods. Thus the frequently and recently seen recommendation to eat vegetables, fruit, and whole grains, beans and legumes, and avoid potatoes, sugar, and foods made from refined flour such as bread, cookies, muffins, other baked goods, flour tortillas, and most pasta. This recommendation is inconsistent with the guidelines contained in the USDA food pyramid or in the standard recommendations from nutritional experts or even the American Diabetes Association a few years ago. Interested readers should consult Dr. Walter Willett's new book, Eat, Drink and be Healthy, the Harvard Medical School Guide to Healthy Eating [27], for a scathing criticism of the USDA pyramid and a discussion of the important question of what carbohydrates to eat. This book was reviewed in IHN, April 2003.

    Eating foods with a high GI or large amounts of foods with a low GI, i.e. a high GL, can result in significant blood glucose elevation after eating, so-called postprandial hyperglycemia, which is accompanied by elevated insulin levels. In the presence of insulin resistance, there may be what is called compensatory hyperinsulism, i.e. abnormally high insulin levels to compensate for the lack of insulin sensitivity as the body attempts to regulate the blood glucose levels. Thus questions have arisen as to the possibility of health problems associated with postprandial hyperglycemia and hyperinsulinemia. A number of studies have provided strong evidence that the consumption of high GI and GL meals contributes significantly to the risk of CHD, CVD and diabetes [63,64,65]. The other area of interest involves the connection with cancer. Both of these concerns have recently been reviewed in the journal Nutritional Reviews by Janette Brand-Miller [66]. There have been a number of case-control studies (See [1] for a discussion of the various types of epidemiologic study) of the question of a connection between cancer and a high dietary glycemic load and the consumption of high GI foods. Studies involving colorectal cancer [67], breast cancer [68] and endometrial cancer [69], have all indicated enhanced risk even after correcting for confounding factors. However, the evidence from large prospective studies of breast cancer [70] and colorectal cancer [71] have not confirmed these findings, although a prospective study based on the Nurses' Study data found that impaired glucose metabolism may play a role in pancreatic cancer [72]. Thus there remains considerable uncertainty regarding the GI-GL cancer connection [66]. In spite of this, the evidence regarding the enhanced risk of CHD, CVD and diabetes should be sufficient to raise real concerns about this aspect of diet, quite independent of the ultimate resolution of the cancer risk question.

    There is a certain irony in the fact that the widespread adoption of the low-fat dogma resulted in many cases in the substitution of fat with carbohydrates, many of which were from high GI foods. Dr. Gerald Reaven, in a recent paper regarding the effect of high-carb diets on triglyceride-rich lipoproteins, HDL cholesterol and the risk of CHD (Abbasi et al [73]), comments that "Given the atherogenic potential of these changes in lipoprotein metabolism, it seems appropriate to question the wisdom of recommending that all Americans should replace dietary saturated fat with carbohydrates." Dr. Walter Willett takes the same position [27] and recommends replacing saturated fat with unsaturated fat rather than carbohydrate.

    DIETARY FIBER. There seems little doubt as to the health benefits of consuming adequate amounts of dietary fiber [74], which consists of the structural and other polysaccharides and lignin in plants that are not digested in the human stomach and small intestine. An added benefit of a diet adequate in fiber containing foods is that they are usually rich in micronutrients in addition to nonnutritive components that have health benefits. It is common practice today to classify fiber as either insoluble or soluble. Foods rich in soluble fiber include oats, beans and psyllium, whereas wheat bran is rich in insoluble fiber. Prospective, case-control and intervention studies that have investigated the relationship between fiber consumption and various diseases have not always yielded consistent or statistically significant results. The early hope, kindled in the early 70s by the observation that a high fiber diet was protective against colorectal cancer in Africans, has not withstood the scrutiny of modern epidemiology, although the American Dietetic Association still holds that position [74], based on a 1992 meta-analysis of case control-studies. However, when this analysis was refined by restricting it to studies that used validated dietary questionnaires, the risk became nil [75]. This is consistent with the recent prospective study [75] based on the Nurses' Health Study data as well as five other large prospective studies where the inverse relationship between fiber intake in the risk of colon cancer was weak or nonexistent [75].

    On a more positive note, an inverse association between high fiber and whole-grain intake and the risk of diabetes has been recently reported [76], a result that is consistent with seven other prospective studies. Also, a higher intake of dietary fiber, particularly water-soluble fiber, has been associated with reduced risk of CHD [77]. In addition, Liu et al [78] found that higher intake of dietary fiber was associated with lower risk of both CVD and heart attacks, but the association was not statistically significant when adjusted for confounding. Nevertheless, the authors suggest that their data and that of others generally supports the current dietary recommendations to increase the consumption of fiber-rich whole grains, fruits and vegetables for the primary prevention of CVD. These recommendations typically suggest consuming amounts and types of foods that translate into >25 g/day of fiber which is about twice the current national average of 14-15 g/day [79]. A problem with some studies is that the cohort in question had a rather high level of overall fiber consumption, which makes it difficult to assess the risk as a function of fiber intake. For example, in [78] the median intake in the lowest quintile was 18 g/day and in the highest quintile 26 g/day, whereas in [77], which found a stronger association, the total fiber intake in the lowest quartile was only 5.9 g/day.

    The mechanism of the action of fiber in relation to health is no doubt complex, but dietary fiber has been shown to delay the absorption of carbohydrates after a meal and thus decrease the insulin response to carbohydrates, and higher insulin levels have been linked to blood lipid disorders, hypertension, abnormalities in clotting factors, and atherosclerosis. Water-soluble fiber decreases total and LDL cholesterol, but the effect is small unless huge amounts of fiber are consumed. Dietary fiber has also been associated with other CVD risk factors such as fasting insulin, and levels of triglycerides and fibrinogen [74,77].

    DIETARY FATS AND RED AND PROCESSED MEAT. In the great diet debate, fats get most of the attention and generate most of the controversy and animosity. It is clear from reading dietary recommendations in the popular press as well as in medical and nutritional journals that the notion is still common that fat is bad and low-fat diets are the way to go. This subject was reviewed recently in three issues of the IHN [1] and by Gary Taubs in two articles, one titled "The Soft Science of Dietary Fat" in the journal Science [2] and the other titled "What If It Has Been A Big Fat Lie," the cover story in a recent issue of the New York Times Magazine [3]. Dr. Walter Willett has a chapter devoted to this subject titled "The Surprising News About Fat" in his book Eat, Drink and Be Healthy. A very recent review in JAMA by Hu and Willett [4] is highly recommended in connection with the question of dietary fat and heart disease, as is the review by Hu et al on types of dietary fat and the risk of CHD [80]. For the past several decades, low-carb diets that were high in fat and protein were condemned because they violated the First Commandment of health, i.e. avoid all fat as much as possible because fat is bad for you. Since it was never possible for The Establishment, no matter how hard they tried [2,3], to provide an evidence based case against all fat, over the past decade or so the position has shifted to the condemnation of only saturated fat and trans-fat. The evidence that the mono- and polyunsaturated fats had many healthy attributes could no longer be ignored!

    Saturated fat increases LDL and HDL cholesterol in many individuals. Since LDL is considered bad and HDL good, one can argue that the outcome is more or less neutral rather than a bad mark against saturated fat. However, this is definitely not the Establishment view. And in addition, attention must be paid to the triglyceride (TG) levels. Elevated TG levels are considered to be an independent cardiovascular risk factor [81,82], and high TG levels coupled with low HDL levels are also a significant risk factor for CVD [83]. Elevated levels of triglycerides are also associated with increased blood viscosity, also a predictor of CVD [84]. There is also considerable evidence that elevated TG levels combined with high total or LDL cholesterol levels yield enhanced risk of CVD [85]. It is worth repeating that low-fat high-carb diets rich in rapidly digested carbs tend to elevate TG and reduce HDL in many individuals, but this is still an area with many unresolved issues [86]. This is one of the principle arguments used by opponents of low-fat diets [27]. Favorable changes in these two blood lipids are generally seen when individuals on low-fat diets switch to low-carb diets. This dietary change generally results in moderate to large decreases in fasting triglycerides, with only a small increase in total cholesterol which are prevented or reversed if significant weight loss occurs. Increases in HDL are also seen in some studies of low- carb diets.

    Epidemiologic studies aimed at determining the effect of saturated fat on the risk of CHD have been limited in number and inconsistent. In the most recent reviews of this question [4,80], only two studies are quoted where total fat and thus presumably saturated fat was reduced. One gave an increase, one a decrease in CHD risk. In a number of studies, however, where saturated fat was replaced by unsaturated fat, it was observed that there was a very significant decrease in the incidence of the first adverse coronary event or that there was protection from secondary adverse events. These studies are the principal basis for the commonly encountered recommendation today that saturated fat should be replaced by unsaturated fat rather than by carbohydrate, this latter action being the normal reaction to advice to reduce fat consumption. These studies, while providing important guidance, do not prove that saturated fat is bad, but merely that changing the ratio of saturated to unsaturated is important. Two variables were changed at once. The Lyon Heart Study [87] which addressed the question of diet and secondary prevention of adverse cardiovascular events, found a large increase in the consumption of omega-3 fatty acids plus a Mediterranean type diet relatively high in fat (~30% of energy) produced a 73% reduction in new events compared to the "prudent Western diet" which was significantly lower in omega-3 fats. Also, a study from Harvard published in October, 2003 reports finding no support for associations between intake of total fat, cholesterol, or specific types of fat and the risk of stroke in men [88].

    A 2001 paper from the Harvard School of Public Health by Hu et al [80] reviewed the relationship between the types of dietary fat and the risk of CHD. Their comment on the results from the Nurses' Study merits quoting. "The association between saturated fat and CHD observed in the Nurses' Health Study was much weaker than predicted by international comparisons, but is consistent with the possibility that the proportional increase in plasma HDL concentration produced by saturated fat somewhat compensates for its adverse effects on the LDL level." Note that the principal reason The Establishment condemns saturated fat is that it raises LDL. This review (free full text at contains an excellent discussion of the importance of omega-3 fatty acids and many other issues related to fat and heart disease. Their conclusion section includes the following statement. "It has been increasingly recognized that the widely promoted low- fat concept is too simplistic and not compatible with available scientific data." Hung et al [89] also provide a good review of the arguments in favor of diets higher in monounsaturated fatty acids, fiber and low GI foods in the context of insulin resistance, glycemic and blood lipid control.

    A recent study by Sacks and Katan [90] is directly related to the question of the level of dietary fat that is beneficial. They examine three diets which were compared with the standard Western diet: (a) the AHA step 1 diet with 30% fat, 55-60% carbohydrate, and 10% saturated fat; (b) a low-fat diet with 20% fat, 65% carbohydrate, 7% saturated fat and (c) the Mediterranean diet estimated at 38% fat and rich in unsaturated fats. The standard Western diet was taken to contain 38% fat, 42% carbohydrate, and 17% saturated fat. All numbers are percentages of total energy. These diets were analyzed on the basis of estimates of the effects of diet composition, including the intake of unsaturated fats, on HDL, LDL and TG levels, available from epidemiologic data, and the associated changes in the risk calculated. As compared to the Standard Western diet (38% fat), the 30% fat diet gave a 0% increase in CHD risk for men, and an 8% increase for women. The 20% fat diet yielded a 1% increase for men and a 21% increase for women. The Mediterranean diet with its high level of unsaturated fat gave a 19% decrease in risk for men and a 16% decrease for women as compared to the Western diet. Examination of their data reveals the interaction between the postulated changes in risk due to the elevation of TG, the decrease in HDL and the decrease in LDL as the fat content of the diet was reduced. The predicted effects in men suggest the futility of the low-fat intervention. The predicted adverse effect of low- fat intervention in women, in the words of the authors, "raises further questions about safety." The Mediterranean diet produced results that compare favorably with drug interventions for hyperlipidemia.

    The bottom line is that the case against saturated fat as being bad in the context of heart disease appears very weak, but that the advice to decrease saturated fat and increase unsaturated fat should be taken seriously because there is a reasonable amount of evidence based justification for such a dietary modification. Thus the criticism of the low-carb diets as regards saturated fat contains an element of "evidence based truth." The results of large prospective epidemiologic studies support the hypothesis that CHD risk depends on the type rather the quantity of dietary fat, and that the adverse effects of trans-fats extend beyond their adverse influence on the LDL/HDL ratio. Consumption of linoleic and particular a-linolenic acid (an omega-3 fatty acid) appear to reduce the risk of CHD [91].

    There are many health problems aside from the above mentioned elevation of TG and suppression of HDL that are associated with a very low-fat or "almost zero fat" diets which are heavy in high GI carbs. A good source for a discussion of low-fat diets based on modern endocrinology can be found in Dr. Diana Schwarzbein's book The Schwarzbein Principle. She has treated countless patients over a number of years suffering the ill and sometimes near fatal effects of such diets. For diabetics, Dr. R. K. Bernstein provides a modern discussion of fat in the context of blood sugar control [92].

    The connection between dietary fat and cancer and in particular meat and red meat and cancer has been a subject of great interest since early studies indicated a strong connection, even prompting the National Academy of Sciences to suggest in 1982 that decreased fat intake might result in decreased rates of breast, colorectal and prostate cancer. Since that time, analytic epidemiologic studies have generally failed to substantiate these early findings [93], and in the case of breast cancer it is now generally accepted that total dietary fat intake is not significantly related to risk. [93]. But a pooled analysis of prospective studies found a weak positive association between breast cancer risk and saturated fat among both pre- and postmenopausal women, but no association with other fats [94]. Also, in a very recently published prospective study [95] that concentrated on premenopausal women (age 25-33 at the start of the study, the Nurses' Health Study II), it was found that the intake of animal fat during the premenopausal years, mainly from red meat and high-fat dairy foods, was associated with an increased risk of breast cancer. Disagreement with other studies that found no association, especially with red meat, was attributed to the age distribution in the groups studied. Both cancer of the colon and prostate appear to carry positive risk associated with red meat intake [93]. It is unclear whether it is a fat component or some other factor related to drugs or chemicals present in the meat or to the method of preparation. In the case of colon cancer, studies suggest that fat intake per se is not a risk factor [93]. Also, not all studies are consistent. Hill [96] reviews a number of studies that suggest rejecting the connection between colorectal cancer and meat. Case-control studies related to pork consumption and colorectal cancer, for example, vary widely and are inconsistent with odds ratios ranging from 0.39 (very protective) to 3.3 (very risky) [93]! Processed meats such as ham and bacon are well known to contain chemicals that are transformed on cooking into chemicals that are carcinogenic in animals. Finally, there is no modern epidemiologic evidence implicating vegetable fats in the etiology of cancer.

    Frequently encountered advice encourages individuals to limit their intake of dairy products. Norat and Riboli [97] have recently reviewed studies that address the question of the connection of dairy products and colorectal cancer. Their findings indicate that cohort studies consistently found a protective effect of total dairy products and milk intake. No relationship was found with cheese or yoghurt intake. However, as mentioned above, a very recent study linked high-fat dairy products to breast cancer in premenopausal women.

    The role of fat in the etiology of diabetes has been the subject of much debate in recent years. Two recent studies, one based on the Nurses' Health Study [98], and the other on the Health Professionals Follow-up Study [99], find essentially no association between fat intake and the risk of developing diabetes. For women, neither total fat, saturated fat or monounsaturated fatty acids intakes were associated with an increased risk of type 2 diabetes, but trans-fatty acids increased the risk and polyunsaturated fatty acids reduced the risk. For men, the association between total and saturated fat intake and an elevated risk for type 2 diabetes was eliminated when BMI was taken into account. Frequent intake of processed meats was found to perhaps increase the risk. However, Schulze et al [100] have recently reported a large study that implicates diets high in processed meats as increasing the risk for type 2 diabetes in women. A relative risk of 1.91 was obtained when less than once a week consumption was compared with five times a week. The authors suggest nitrites and advanced glycation end products may be implicated.

    Therefore it appears prudent when considering sources of fat for a low-carb diet to limit the intake of red meat and processed meats, and high-fat dairy products, and to emphasize mono- and polyunsaturated fats over saturated fat. Thus there is some justification for the criticism leveled by the critics of low-carb diets and especially the Atkins Diet, as regards unlimited and indiscriminate meat and high-fat dairy food consumption. Also, the low-carb dieter has a wide choice of fat sources such as fish, poultry, and nuts, and oils. There is essentially universal agreement as to the potentially adverse effects of consuming trans-fats (See [1] for a review of this subject).

    DIETARY PATTERNS. We rarely eat individual macronutrients in isolation, but rather eat meals consisting of a variety of foods with complex combinations of nutrients, both macro and micro, that are quite possibly either interactive or synergistic. We are now seeing studies that attempt to address this problem by examining the relationship between whole dietary patterns and the incidence or risk of disease [101,102]. Dietary pattern analysis is viewed as complementary to more traditional analysis and as well can be used to determine if the effect of a specific nutrient is independent of overall dietary patterns, and the pattern approach can also be used to evaluate dietary guidelines. Most importantly, it can identify types of diets that carry low risk for particular diseases such as cancer, diabetes or CHD without dealing in detail with the relative merits of the individual components. Two popular methods, factor analysis and cluster analysis are by their very nature a posteriori, since the eating patterns are derived through statistical modeling of dietary data. The results so far have been quite interesting.

    • Two recent studies, one based on the Nurses' Health Study [60], the other on the Health Professionals' Follow-Up Study [103], identified two major dietary patterns. One, called the "prudent" pattern," was characterized by higher intake of fruits, vegetables, fish, whole grains and legumes. The other, called the "Western Pattern" was characterized by higher intake of red and processed meat, high-fat dairy products, refined grains, French fries, sweets and desserts. In both men and women, the prudent diet was associated with decreased risk of CHD whereas the Western diet provided increased risk. For example, when women in the highest prudent diet quintile and the lowest Western quintile were compared to those with the opposite extreme pattern, the relative risk of CHD was 0.64, a dramatic reduction. Similar results were obtained in the men's study.
    • A recent study, from Harvard [104] where no association was found for breast cancer risk when a Western diet (red and processed meat, refined grains, fat and sweets) was compared to a 'healthy" diet (fruit and vegetables, fish and poultry, low-fat dairy and whole grains). Alcohol was found to increase the risk. These results are consistent with a recent pooled analysis of cohort studies by Missmer et al [105]. It is interesting that the pattern analysis found no risk with the Western pattern in spite of the recent study [95] quoted above that linked animal fat and high-fat dairy food with breast cancer.
    • In another study from Harvard [106] based on the Nurses' Study data, which yielded on factor analysis the two major dietary patterns described above, the "Western" and the "Prudent," no significant positive association between the Western dietary pattern and the risk of colorectal cancer was observed, and the protective nature of the prudent pattern for colon cancer was not statistically significant.
    • The Harvard group [107] found that a "Western" type diet pattern was associated with a substantially increased risk of type 2 diabetes in men. This is particularly interesting in connection with the hypothesis discussed above that type 2 diabetes is a vascular disease, since the Western diet also carried a higher risk for CHD. When low physical activity and obesity were also included in the analysis, the relative risk was 11.2, a particularly high risk.

    The researchers at Harvard and their collaborators suggest that the relationship between CHD risk and dietary patterns, which appear to apply to both men and women, may act through biochemical factors. In an earlier study [108] they had found the prudent pattern in men was associated with lower levels of insulin, and the Western pattern was associated with higher levels of tissue plasminogen activator, fasting insulin, leptin and homocysteine, markers consistent with increased risk of CHD. Also, the women with the higher prudent-pattern score had higher intake of protein, folate (folic acid) and fiber. In connection with protein consumption and the "protein question" discussed above, Appel [56] in his review points out that in the prudent diet, the highest score went with the highest protein consumption (100g/day) whereas the highest Western diet pattern score had the lowest protein consumption of 90 g/day.

    COMBINING LIFESTYLE AND DIET. While such aspects of lifestyle as exercise and smoking have not been discussed, they are very important modifiable aspects of risk for both diabetes and heart disease. The following studies leave no doubt.

    • In a 16-year follow-up [7] over 84,000 women in the Nurses' Study, free at baseline of diagnosed CVD, diabetes or cancer, were studied to determine the incidence of type 2 diabetes. As compared to the rest of the cohort, women in the upper 40% of the dietary score who exercised 30 min/day, had a BMI <25, did not smoke but consumed alcohol had a risk factor of 0.09, that is, 91% of the cases of diabetes in this cohort could be attributed to habits and forms of behavior that did not conform to the low risk pattern. Just including diet, exercise and BMI gave a risk factor of 0.12, still sensationally low. The low risk diet was defined as low in trans- fats and GL and high in cereal fiber with a high ratio of polyunsaturated to saturated fat.
    • In a study [5] of men and women, average age 51, with IGT (impaired glucose tolerance) and IFG (impaired fasting glucose) and a BMI equal or greater than 24, diet and lifestyle modifications were introduced to determine the effect on the progression to type 2 diabetes. The modest goals were at least a 7% reduction in weight and at least 150 minutes of physical activity per week. The dietary recommendations involved a low- calorie low-fat diet. The result was a 58% reduction in the progression of IFG and IGT to diabetes, as compared to the placebo group (there was also a drug intervention arm of this study).
    • In a recent study [6] 522 men and women, mean age 55 with IGT were randomly assigned to an intervention or control group. The intervention group received individual guidance on increasing physical activity. The intervention diet had a weight reduction goal of only 5% minimum and involved a diet with less than 30% fat, l0% saturated fat, fiber intake of at least 15g/1000 cal, frequent ingestion of whole-grain products, vegetables, fruits, low-fat milk and meat products, soft margarines, and oils rich in monounsaturated fat. The risk of type 2 diabetes was reduced by 58% in the intervention group as compared to the control group.
    • In a study [8] of primary prevention of CHD in women using the Nurses' Study data, diets were scored according to a 'low risk" diet low in trans-fats and GL, high in cereal fiber, marine omega-3 fatty acids, and folate with a high ratio of polyunsaturated to saturated fat. During follow-up of 14 years, women in the upper 40% of the diet score, non-smoking, BMI<25, 30 minutes of exercise per day, and alcohol consumption of equal to or greater than 5 g/day had a sensational reduction in risk of CHD for a relative risk of 0.17. Eliminating alcohol raised the risk factor to 0.34, and in addition removing the BMI restriction, raised it to 0.43.

    CONCLUSION. The summary given in Chapter 11 of Walter Willet's book Eat, Drink and be Healthy nicely summarizes the conclusions that arise from the scientific studies discussed above. He suggests [27]:

    • maintaining a stable, healthy weight;
    • replacing saturated and trans-fats with unsaturated fats;
    • substituting whole-grain carbohydrates for refined-grain carbohydrates;
    • choosing healthier sources of proteins by trading red meat for nuts, beans, chicken and fish
    • eating plenty of vegetables and fruits; and
    • using alcohol in moderation.

    In other words, adhere to the "prudent diet" and avoid the "Western diet," as defined by the diet pattern studies from Harvard and supported by extensive prospective studies involving huge cohorts and long follow-up. It also seems clear that concerns over protein consumption exceeding the Establishment recommendation are unwarranted, that fat, except for trans-fat, is by and large good for one with the qualification that excessive saturated fat, especially at the expense of unsaturated fat, may not be healthy and that red and processed meats may carry some risk. Willett's recommendation of avoiding refined grains is equivalent to the emphasis of low-GI sources of carbohydrates, as is his recommendation regarding fruits and vegetables, although some fruits carry a rather high GI.

    So far, it seems that nutritional epidemiology has identified only a handful of macronutrients that it might be wise to minimize or avoid in making dietary decisions. These include red meat, processed meats such as bacon, ham, sausage etc, saturated fat, high-fat dairy products, as well as the high GI foods such as starchy foods and those made from highly refined grains, white rice, sugars, and of course anything containing any trans-fats. Considering the variety of foods available in this age of plenty, simply avoiding or limiting the consumption of these questionable food sources should not present a serious hardship, should not result in the failure to consume adequate amounts of important nutrients, and may well yield substantial health rewards.


    THE ATKINS DIET [110,111] The Atkins diet (AD) is the lowest carb diet in the menagerie. It will be discussed in more detail than similar diets because of its status as the poster child of the low-carb diets, and the low-carb diet that is most frequently compared in studies to Establishment diets and low-fat diets. The mere mention of the Atkins diet in some circles produces a vitriolic and totally irrational response with some of those taking up the argument risking a stroke or dangerous hypertension. It is doubtful that any other diet is seen in such black and white terms. The induction diet typically consists of 20 grams of low GI carbs per day for two weeks, which is indeed a very low amount. As the dieter moves from induction to eventual maintenance, the carb allowance increases to whatever the individual can tolerate while maintaining an ideal or target weight. Thus low GI fruits and vegetables are slowly introduced. The amounts of fat, protein and calories are more or less up to the individual, although this type of diet generally results in a calorie reduction. Contrary to the frequently heard statements of critics of the AD, there have indeed been recent studies that addressed the question of the efficacy and safety of this protocol, and as well there is a recent review suggesting that low carb diets such as this one deserve further and serious study and that the criticisms lack scientific evidence [112]. Highlights of five recent studies are as follows:

    • Brehm et al [113]. Fifty-three obese healthy women were randomized to either a low-carb or a slightly reduced fat diet (30% of energy, which is only 8-10% below normal Western diets) which the authors call a low- fat diet, for a period of 6 months. The low-carb diet started with the 20g of carb a day for two weeks and then progressed to 40 to 60 g/d if ketosis (ketones in the urine indicating fat metabolism) was maintained. Fat and protein were ad libitum. Each group reduced caloric intake by about 400 calories. The low-carb group lost 8.5 kg vs. 3.9 for the "low-fat" group, and as well the low carb group had twice the loss of body fat. There were no significant changes in either group in total cholesterol, or LDL cholesterol. The low-carb group has a significant decrease in triglycerides as well as a modest increase in HDL cholesterol, as compared to the low-fat group. The change in the ratio of TG/HDL in the low-carb group was in a direction and of a magnitude that was very favorable for CHD risk reduction.
    • Foster et al [114]. Sixty-three men and women were randomized into two groups, one consuming a low-carb (Atkins model) diet, the other a conventional diet. The low-carb group was started with 20g/day of carbs for the first two weeks, and then allowed to increase carbs until a "stable and desired weight was achieved." It is unclear what the desired weight was, since the subjects were all obese. The low-carb group was given a copy of Atkins' book and told to read and follow the diet described. The "conventional diet" group was encouraged to eat a diet with 25% energy from fat, 60% from carbs and 15% from proteins, with 1200-1500 cal/day for women, 1500-1800 for men. Subjects on the low-carb diet lost more weight, 7 vs. 3.2 kg at 6 months, but at 12 months the numbers were 4.6 vs 2.5 kg, which was not a significant difference. The decrease in TG and the increase in HDL concentrations were greater among subjects on the low-carb diet as compared to the conventional diet throughout most of the study. Both diets significantly decreased diastolic blood pressure and the serum insulin response to an OGTT. No information is provided as to the 6 or 12 month carb consumption of the low-carb group seeking their "desired weight." The low-carb diet was associated with greater improvement in some risk factors for CHD. These positive results were in spite of poor adherence, high attrition and apparently little control of carbs as the low-carb diet progressed.
    • Samaha et al [115]. Published simultaneously in the New England Journal of Medicine with Foster et al [114]. Seventy-nine severely obese men and woman completed this six-month study. The authors randomly assigned subjects to a low-carb diet or a calorie and fat-restricted diet, with the goal of comparing weight loss, changes in blood lipids and markers of glucose metabolism. However, examination of their Table 3 indicates the puzzling fact that the low-fat group consumed on average almost identical amounts of fat, protein and carbohydrate at six-months as compared to baseline, based on percent of energy. However, there was a decrease in calorie consumption in the low-fat group, but there was also a similar decrease in the low-carb group. The low-carb diet increased fat, decreased carbs and increased protein as a percentage of energy, as would be expected. In spite of these aspects of the study design, the low-carb group had a significant decrease in TG levels as compared to the low-fat group, but TC, HDL and LDL were little changed at six-months in both groups. The low-carb group, which included a high prevalence of diabetics and those with the metabolic syndrome lost more weight and experienced a relative improvement in insulin sensitivity, even after adjustment for weight loss, as compared to the low-fat group. Incidentally, the low fat group consumed 33% of their calories as fat, which is rather close to the Western diet average, and would not be considered by some as "low-fat."
    • Westman et al [116]. Fifty-one overweight healthy volunteers who wanted to lose weight were placed on a very low-carb diet (<25 g/day), with no limit on caloric intake. Carbohydrate intake was increased to about 50 g/day when the 40% of the subject's self determined target weight loss was achieved. This study included nutritional supplementation and recommendation to exercise. The average weight loss on an average daily caloric intake of about 1500 calories was about 20 pounds over 6 months. BMI dropped by 3.2 units, moving the group on average from obese to simply overweight. Changes in blood lipids were: Total cholesterol, 214 to 203; LDL, 136 to 126; HDL, 52 to 62, TG, 130 to 74 (all in mg/dL). These are clearly very favorable blood lipid changes. There were no serious adverse effects observed.
    • Sharman et al [117]. This study examined the effect of a ketogenic (producing ketosis) diet on serum biomarkers for CVD in normal weight men. The study lasted six weeks. Twelve men switched from their habitual diet (17% protein, 47% carb, and 32% fat) to a ketogenic diet of 30% protein, 8% carb and 61% fat. This would be close to the Atkins induction diet. Total and LDL cholesterol were unaffected, TG significantly decreased and HDL tended to increase. There were favorable changes in LDL particle size in subjects with small LDL particles. These results, according to the authors, suggest that a short-term ketogenic diet does not have a harmful effect on CVD risk factors and may improve lipid disorders characteristic of an unfavorable blood lipid profile.

    These studies, while short term, indicate that greater weight loss is obtained with the Atkins' protocol than less restrictive or high carb diets with beneficial or neutral changes in the blood lipid profile. These five studies, all reported in 2002 or 2003, fail to support some of the criticisms of low-carb diets (bad breath is not considered a serious adverse result), and in particular the very restrictive AD. The long-term picture for the AD can only be obtained from Atkins' own clinical records. His clinic has treated over 60,000 patients over several decades, many with weight, cardiovascular or blood sugar problems. He claims a high success rate. There is no reason to not believe this, unless one considers him to have been a charlatan, dedicated only to making money and selling books. Anyone who has met this man would have a hard time accepting such a negative view. His enemies even claim that he recently had a heart attack because of adherence to his own diet, which is not true - his heart problem stemmed from an infection. He recently died from cerebral complications following a head injury due to a fall on the sidewalk in New York City during icy conditions. The critics also point to the high protein content, the high fat content, the lack of fruits and vegetables, the dangers of ketosis, etc, but they neglect to take into account the fact that the diet they are criticizing is not the maintenance diet, which offers the patient ample choice of both fruits and vegetables, although not 200-300 grams of carbs per day, which the typical American eats. The protein and fat objections have been discussed in detail in Part II. There is reason for some to be concerned with his lax attitude about saturated fat and red meat, processed meat and high-fat dairy products, but the Atkins principles can be equally well applied while substituting more fish and poultry for the protein component. However, it should be mentioned that constipation is a common complaint associated with induction-phase type low-carb diets and it is generally suggested that soluble fiber such as psyllium be used, taken with large quantities of water, as a supplement to eliminate this problem.

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    THE SOUTH BEACH DIET [118]. This is a relatively new diet developed by Dr. Arthur Agatston, M.D, a cardiologist who lives in Miami Beach. He found that low-fat high-carb diets advocated by the AHA, while giving initial modest improvements in weight and cholesterol levels, invariably were followed by a return to the initial state, or even worse. With his patients, both the Pritikin and Ornish diets also failed, and these observations were not only based on his experience, but also that of some of his colleagues. Patients were unable to sustain cholesterol and/or weight reductions using low-fat high-carb diets. Agatston also had a weight problem himself and feared the development of insulin resistance and obesity. The South Beach Diet (SBD) is the result of his research, experimentation and clinical observations. It appears to be rapidly gaining popularity.

    Like the AD, the SBD has three phases. Phase one last two weeks and includes normal-size portions of meat, chicken, turkey, fish, shellfish, eggs, cheese, nuts and vegetables. Salads are made with olive oil dressing. Certain snacks and desserts are OK, as is coffee or tea. But, no bread, rice, potatoes, pasta, baked goods or fruit. No candy, cake, cookies, ice cream, or sugar. No beer or alcohol. That's it. No estimates of grams of carbs or calories. This sounds a lot like the AD except there is no quantitative limit on the grams of carbs per day. In Agatston's experience, there will be a weight loss of 8-13 pounds in phase 1, and some of this will be from fat loss. Phase 2 starts adding foods intelligently selected from the forbidden list as long as weight loss continues, albeit at a slower rate of one to two pounds per week - actually the generally recommended rate that is considered healthy. Wine is recommended. Phase 3 kicks in when one hits their target weight. Then the amounts of added foods are adjusted to stabilize weight and prevent weight gain.

    Agatston organized a small clinical study involving 60 patients. Almost all experienced weight loss, lowered TG, lowered LDL, raised HDL and an improved waist-to-hip ratio. The results were presented at a symposium at an annual AHA meeting. He also conducted a randomized study pitting the SBD against the AHA step 2 diet. The favorable results observed in the first study also appeared in this study when the two groups were compared. This work was presented at a meeting of the American College of Cardiology.

    Agatston's book contains chapters that guide the reader in the selection of good vs. bad fats and carbs. The philosophy is similar to that of most low-carb diets and follows in general the principles outlined above in the discussion of fats and carbohydrates. For example, he cautions against trans-fats and saturated fats, and high GI carbs. The book also contains case histories and is half recipes and meal plans.

    THE SCHWARZBEIN PRINCIPLE [9]. The subtitle of this book by Dr. Diana Schwarzbein, M.D. and Nancy Deville is The Truth About Losing Weight, Being Healthy and Feeling Younger. Dr.Schwarzbein is an internist specializing in endocrinology who founded the Endocrinology Institute of Santa Barbara in 1993. She sub-specializes in metabolism, diabetes, osteoporosis, menopause and thyroid conditions. The "principle" in question is "Degenerative diseases are not genetic but acquired. Because the systems of the human body are interconnected and because one imbalance creates another imbalance, poor eating and lifestyle habits, not genetics, are the cause of degenerative disease."

    When Schwarzbein first started practicing it was in a clinic where she saw only diabetics. This was in 1990 and she treated them according to the standard practice of the day, which included low-fat high-carbohydrate diets. When she actually experienced the phenomenon of making her patients sicker on the American Diabetes Association (ADA) diet, she began to study this undesirable outcome and experiment with alternatives, using her patients as subjects for diet variations. The ADA diet and the notion that low-fat high-carb diets were the gateway to health for everyone was so deeply imbedded in her training that it took a while to realize that "by recommending a high-carbohydrate diet we were giving sugar to diabetics (italics from original text)." Space does not permit a detailed discussion of her development of the diet, but suffice to say that over more than a decade of treating both diabetics and non-diabetics with weight, cholesterol, heart, glucose metabolism and other problems, the optimum diet was found to be a low-carb diet with emphasis on low GI foods, but which did not limit protein or fat. This sounds remarkably like Agatston's story, but in the context of diabetics rather than cardiac patients. But both this diet and the SBD apply in general, not just to the patient populations that led to their development.

    This diet is called the Schwarzbein Healing and Maintenance program. The basic guidelines are (a) Do not skip meals - five a day are OK; (b) Eat "real food" that you could in theory pick, gather, milk, hunt or acquire by fishing; (c) Choose from the four nutrient groups at each meal by eating as much good fat and protein as needed and a variety of non-starchy vegetables. Carb consumption (the fourth category, differentiated from non-starchy vegetables) should be in accord with metabolic and activity levels; (d) Avoid caffeine, alcohol and stimulants; (e) Make the elimination of over-the-counter and prescription medication a goal with the help of your physician. The healing phase is similar to Phase 1 of the SBD, since the emphasis is on low GI carb sources, the avoidance of starchy foods, and the consumption of ample fat and protein. This diet separates non-starchy vegetables, for which there is no limit on consumption, and what Schwarzbein terms carbohydrates, a category that includes starchy vegetables, legumes, grains, whole grain flour and meals, yogurt, fruit, bread and crackers. Tables of "carbohydrate foods" are presented giving the portions that contain 15 grams of carbohydrate, and a table is given that provides quantitative guidance as to consumption. This interesting table (pp 260, paperback edition) takes into account how active a person is, how overweight the person is, and how much fat has collected around the mid-section, which she calls the "insulin meter." The numbers range from 15 to 75 grams per meal, the latter for normal body composition and extreme activity. Thus this diet is quite low-carb, and the numbers, for overweight individuals, compare more or less to the AD ongoing and maintenance stages, but the non-starchy vegetables do not count in determining the grams of carb per meal. The healing phase lasts until the health problems have been rectified, e.g. a return to normal blood lipid profile, weigh loss, normal glucose metabolism, increased insulin sensitivity, etc. The Nutritional Maintenance program is simply intended to prevent the "cured" problems from recurring or new problems from developing. This diet also shares a basic philosophy with the AD and the SBD.

    Readers interested in Schwarzbein's approach should read the book. It also contains extensive justification of the approach based on elementary endocrinology and the role of high insulin levels in the development of health problems. The case histories are compelling. Some of her patients who were on nearly zero-fat diets were in fact slowly killing themselves, were prematurely aged, and could be frequently identified at a glance as they walked into the consulting room.

    THE PROTEIN POWER LIFEPLAN [119,120]. Developed by Michael and Mary Eades, two MDs who practice weight loss medicine in Boulder, Colorado. Their diet is described in two popular books. They examine questions of nutrition and lifestyle through the "Paleolithic lens", and are concerned not only with weight loss but with many other health problems including diabetes, cholesterol and triglyceride disorders, autoimmune syndromes, etc. The Eades belong to the low-carb school and have found through years of clinical practice that that dramatically decreasing the carbohydrate content of meals from the typical Western diet (50-60% of energy) frequently leads to a decrease in blood insulin and glucose, and improves the blood lipid picture, including the type of LDL present, and in general contributes to improved health. They emphasize that the decrease in insulin decreases the fat storage process and increases the fat utilization process, as the body burns fat to get energy. While the low-carbohydrate diet is a weight reducing diet, this can be thwarted by consuming too many calories, and thus from the point of view of the Eades, calories do count. According to their clinical experience, if you want or need to lose weight but still can't on a typical low-carb diet, then it is necessary to restrict calories or use more energy in physical or mental activity, or both. While they place no limits on fat consumption, calorie restriction is most easily done by fat restriction because of the large number of calories per gram in fat, but they hold that it is very important to get proper amounts of the essential fatty acids in the daily diet, and keep the omega-3 to omega-6 ratio near one to two. According the their clinical experience, for the vast majority of people, simply following a low-carb diet will create enough of a calorie deficit to result in significant weight loss. If a person has small caloric demands, then weight loss can become a problem. Once a weight goal has been reached, one should be able to increase the caloric intake to halt weight loss by eating more protein and fat, as well as additional carbohydrate, as long as the carbohydrate consumption keeps the insulin and blood sugar levels in the normal range. They use an in-office insulin response test based on the blood glucose response to a small IV dose of insulin.

    The Protein Power Lifeplan differs from those described above in that the diet involves setting a minimum for protein intake per meal. The calculation of minimum protein intake per meal takes into account an individual's weight, gender and height. For example, the following numbers have been taken from their table: 125 lb woman, 5' to 6' in height - 26 g/meal; 200 lb woman, 5' to 6' in height - 34 g/meal, 150 lb man, 5'4" to 6'6"in height - 34 g/meal, 200 lb man, 5'8" to 6'10" in height - 40 g/meal. Now examine the protein content of common foods: beef, poultry, pork and fish, 7 g/oz; eggs, 6 g/egg; hard cheese, 6-7 g/oz; cottage cheese, 7 g/1/2 cup.

    Obviously, breakfast is the only real problem, since two eggs provide only 12 grams of protein. One can make a cheese omelet and approach the numbers given. Other authors of diet plans suggest that the protein problem can be partly solved by using a protein concentrate such as whey in the form of a low carbohydrate protein drink, either alone or mixed with other things. Health food stores have whole walls devoted to displaying huge, half- empty containers of protein powders, but it is important to read the labels and select low-carb products. Certain products also contain aspartame, which some refuse to consume. This is an easy way to boost the protein content of snacks and especially breakfast without resorting to steak and eggs or a tuna melt at 7 or 8 AM while in a rush to get to work. To put these protein numbers in perspective, consider a maintenance diet with 30g carbs/meal or 90 g/day. If the person is on a 1500 calorie diet, then this is 24% of calories from carbs, leaving 76% from protein and fat. If we take 40% from fat, then the remaining 36% from protein translates into 135g/day, which is close to but above the minimum for a 200 lb man who is tall.

    Now the crux of the matter, carbohydrate limitation. The initiation level of their diet involves 7-10 grams per meal of carbohydrates, but they count only the non-fiber part of the carbohydrate that is convertible into glucose (the ECC, the effective carbohydrate content). The 7-10 grams per meal translates into about 20-30 grams of ECC per day, which is similar to the Atkins induction diet. Very small amounts of commonly consumed foods will meet or exceed this limit. The Eades set no specific time limit on the initiation phase. It depends on why one is on the diet. Their patients stay on it until the underlying health problems are solved, and this generally involves repeated blood tests for triglycerides, HDL, LDL, blood sugar, insulin etc., as well as the observation of weight loss and loss of body fat. Like the Atkins approach, one then increases the carbohydrate intake and watches to see what happens. The transition period involves 15 grams ECC per meal, and maintenance 20-30 ECC grams per meal if there are no undesirable effects. At this point their protocol becomes somewhat more complicated since they offer different approaches depending on the dieter's philosophy. Consulting their books is necessary at this point. While some critics call this simply a high-protein diet, it is really a low-carb diet with the balance of calories made up from protein and fat. They simply set what they consider to be the minimum on the protein content -- a different philosophy than some of the diets discussed which simply allow fat and protein amounts to be decided on an ad lib basis. However, in many instances, followers of other low carb diets will without knowing it meet their protein minimums.

    THE NEW SUGAR BUSTERS! [61]. Of the four individuals involved in the development and promotion of this diet, three are MDs, including a cardiovascular surgeon, an endocrinologist, and a gastroenterologist. The basic concepts are as follows. They encourage the reader to avoid refined sugar and processed grain products (i.e. made from flour), and instead select what they call "low-insulin producing carbohydrates," i.e. low GI carbs. They hold that most of the fat in our bodies comes from sugar or indirectly from sugar derived from starch, not fat. They recommend fruits, green vegetables, dried beans, and whole grains. Such action provides a high-fiber content. They recommend lean and well-trimmed meat, with "careful attention to saturated fats." Consumption of low fat milk and cheese is suggested, and trans-fats are to be avoided. Three meals a day are suggested, along with appropriate snacks, with attention to moderate portions sizes. Late night snacking is discouraged. The similarity between Sugar Busters and the diets described above cannot escape recognition. However, Sugar Busters does not spell out amounts, or require counting grams of carbs or calories. The chapter on "Acceptable foods and substitutes" does not give quantitative guidance as to amounts. They do, however, suggest 30-40% calories from fat if most of the fat is mono- or polyunsaturated, and see nothing wrong with 30% of calories from protein. Clearly, a lot is left up to the individual to adjust portion sizes to achieve slow but steady weight loss. Their point is that the main hurdle is passed when one switches to low GI carbs and eliminates sugar and starchy foods. By now this should sound familiar!

    DR. SINATRA'S MODIFIED MEDITERRANEAN DIET [121]. Dr. Stephen Sinatra is a board certified cardiologist and Assistant Clinical Professor of Medicine at the University of Connecticut School of Medicine. He is also in private practice at his New England Heart Center in Manchester, Connecticut. In his book Heart Sense for Women [121], published in 2000, he endorses only the Mediterranean diet for both heart health and weight loss. Like Schwartzbein and Agatston, a decade ago or more he recommended the standard low-fat high-carb diet to his cardiac patients. His comments are worth quoting: "Boy, was I off the mark! Many of my patients did initially lose weight on the no-fat, low-fat diets, but over time their HDL 'good' cholesterol decreased and their triglycerides shot up, and they often regained weight."

    The diet he now recommends involves decreasing intake of (a) processed foods containing white flour and sugar, such as breads, cereals, flour-based pastas, pastries and bagels; (b) foods containing trans-fats, especially commercially prepared crackers, cakes, candies cookies, doughnuts, chips and processed cheese; (c) starchy, high GI cooked vegetables such as potatoes and corn; (d) processed canned vegetables; (e) processed fruit juices which are generally high in sugar; (e) red meats and organ meats; (f) corn, safflower, sunflower, peanut and canola oil; (g) whole milk, high-fat cheese, and whole-milk yogurt.

    He recommends increasing the intake of (a) oatmeal and high fiber pastas; (b) low GI vegetables such as asparagus, broccoli, kale, spinach, cabbage, Brussels sprouts, and legumes such as lentils, soybeans and chickpeas; (c) onions and garlic; (d) herbs such as rosemary, basil and oregano; (e) fruits such as cherries, peaches, grapefruit, plums, dried apricots, rhubarb, pears, apples, cantaloupes, grapes and kiwi, although the latter three are somewhat high in sugar; (f) protein such as fish, especially fatty cold water fish like salmon, mackerel, sardines and shellfish, and eggs, up to 6 per week; (g) soy products like tofu, soybeans and soy milk; (h) extra-virgin olive oil on salads and vegetables; (i) nuts and seeds, including walnuts, almonds and flaxseed; (j) low-fat cottage cheese, feta cheese, and small amounts of parmesan grated.

    On his website ( Dr Sinatra estimates his Mediterranean diet has 20-25% protein, 30-35% healthy fats, and 45-50% low GI carbs, which includes some fruit. Thus this is not a low-carb diet, but approaches the low end of the high-carb type diets, with the qualification that the carbs suggested are mostly low GI. Nevertheless, the allowed and discouraged food items are very similar to the above diets. In many respects, it is like a maintenance diet of the low-carb school if the individual can maintain a desired weight on 45-50% energy from selected carbs. The principles can also be applied with reduced carb consumption. No detailed information is given as to amounts, calories, or what to do if this diet does not result in weight loss, although presumably one simply cuts down on portions. Sinatra also recommends supplements (as do most proponents of low-carb diets) to aid in weight loss (see his website). The website contains a good summary of the research backing up the healthful aspects of this type of diet. A whole review could be devoted to the Mediterranean diet.


    The following is presented as evidence that The Establishment is changing its views to some extent in the direction of the diets described above and the philosophy promoted by Willett and others. For example, mention of low-fat diets per se is now uncommon, and the National Cholesterol Education Program (NCEP) has set 35% as the upper limit for calories from fat, which by standards of a decade or two ago is revolutionary. As regards fat, all the AHA discusses is saturated and trans-fats, with no total fat limit.

    AMERICAN HEART ASSOCIATION. The AHA position as of 2002 regarding the primary prevention of CVD and stroke through the manipulation of macronutrients: Consume a variety of fruits, vegetables, grains, low- fat dairy products, fish, legumes, poultry and lean meats. Match energy intake with needs and make changes to achieve weight loss if needed. Reduce saturated fats to < 10% of calories, and reduce trans-fatty acids by substituting grains and unsaturated fats from vegetables, fish, legumes and nuts [122].

    NATIONAL CHOLESTEROL EDUCATION PROGRAM (ADULT TREATMENT PANEL III). Recommended distribution and sources of macronutrients (in the context of LDL lowering therapy): Saturated fat 7%; protein approximately 15% and carbohydrates 50-60% of total calories. Total fat is allowed to range from 25-35% of total calories provided saturated fats and trans-fats are kept low. "A higher intake of total fat, mostly in the form of unsaturated fat, can help reduce triglycerides and raise HDL cholesterol in persons with metabolic syndrome (italics not in original)." Carbohydrates should be obtained predominantly from foods rich in complex carbohydrates including whole grains, fruits and vegetables [123].

    AMERICAN DIABETES ASSOCIATION. Recommendations for the prevention of type 2 (adult onset) diabetes: Reduce the intake of total fat, particularly saturated fat. Increase the intake of polyunsaturated fat, keeping in mind the appropriate energy intake for weight management. Increase the intake of whole grains and dietary fiber. Author's note: examination of the source reference will reveal that each of these recommendations is carefully worded to indicate uncertainty in the connection between the indicated macronutrient and the risk of developing diabetes. No quantitative guidelines are given for fat or carbohydrates [124].

    US DIETARY GUIDELINES, USDA/US DEPARTMENT OF HEALTH AND HUMAN SERVICES. These are the recommendations from the 2000 Edition that relate to the choice of macronutrients (from [125]): Choose a variety of grains daily, especially whole grains. Choose a variety of fruits and vegetables daily. Choose a diet that is low in saturated fat and cholesterol and moderate in total fat. Choose beverages and foods to moderate your intake of sugars. Author's note: In the 1995 Edition, the fat recommendation was to choose a diet low in fat, saturated fat and cholesterol. The 2000 Edition recommendations also indicate that one should "let the pyramid guide your food choices." See [27] an alternative view on the pyramid, and [125] for a discussion of the deficiencies in these Guidelines.


    The so-called fad-diets selected to be reviewed were all developed by practicing physicians to meet what they considered to be a need for something that worked. The patients were probably followed as carefully or even more carefully than they would have been in formal studies, with attention to blood lipids, fasting glucose, blood pressure kidney function, etc. The record of success observed by these physicians is unfortunately not material acceptable to the major peer-reviewed journals. These were uncontrolled observations on non-randomized populations, what is generally painted with the term "anecdotal", and mainstream medicine has been taught to ignore, ridicule and even fight such "research" and regard the results as unproven, undeserving of their attention, and perhaps even dangerous. Historically, mainstream medicine listened to The Establishment, whose recommendations regarding both fat and carbohydrates they believed were based on sound science. This turned out by and large not be true, as both Gary Taubes and Walter Willett have taken pains to point out in a very public way. Meanwhile, the developers of the much-maligned fad-diets, it would appear, were in fact on the right track. In fact it now seems quite inappropriate to continue calling them fad-diets.

    All the reviewed diets are rather similar in their basic philosophy, which simply stated is that sugar, starchy foods, processed foods and baked goods containing refined grains and sugar, and high GI fruits and vegetables should be eaten in limited amounts or not at all, depending on the individual circumstances. This philosophy is similar to the prudent diet pattern discussed above. The extent to which the lost calories are replaced by fat and protein depends on why one is dieting, but in general, this substitution results in a lower calorie diet and may contribute to weight loss, better glucose metabolism, and a better blood lipid profile. In spite of the fact that the diets differ in detail, this common thread is important because this appears to be the same direction The Establishment is headed and as well corresponds with the general conclusions from the large nutritional epidemiology studies from Harvard and elsewhere which are so well summarized in Willett's book. One difference, however, is that the guidelines quoted above from Willett's book do not directly address the problem of weight loss. While the authors of the various diet books would no doubt be quick to point out their unique features, and the critics quickly state their favorite complaints, the common philosophy is nevertheless clear. In addition, to call the Atkins, South Beach, Schwarzbein, Protein Power, and Sugarbusters diets simply low-carb is an oversimplification, since in the maintenance phase they become what might be termed moderate carbohydrate diets, with the carb consumption geared to the individual's metabolic requirements so that weight is stabilized. Thus food selection and portion sizes become the central problem, both with regard to fruits and vegetables, but also with regard to fat and protein. Also, it is important to recognize that these diets in general address blood lipid and glucose metabolism problems as well as weight loss. There is a certain irony in the fact that the general public is being drawn closer to many of the current Establishment recommendations by following the very diets the Establishment was condemning a few years ago. The emphasis has dramatically shifted to a recognition of the importance of selecting types of fats and carbohydrates, rather than advocating a diet simply low in fat, which means in practice, high in carbohydrates, frequently indiscriminately selected.

    There is a huge variation in individual reactions to the macronutrient content of a diet, both with regard to weight gain or loss and the clinical parameters related to glucose metabolism and blood lipids. It is possible to take the general principles of the reviewed diets and manipulate the distribution of macronutrients, bearing in mind the considerations associated with the selection of each class, and experiment to determine if a successful, individually tailored formula can be achieved. In this scenario periodic glucose and blood lipid tests are as important for some as the number that appears on the scale.

    Some individuals like diets that are spelled out in detail, perhaps even meal by meal, whereas at the opposite extreme is Willett's book which puts forward an eating philosophy as a guide to selection of macronutrients -- those to emphasize, those to avoid or limit, and thus allows a creative and individualized approach consistent with the personal goals involved. What is important is the basic philosophy which relates to the question of what is a healthy diet, a subject that has been emphasized in this review. Readers interested in pursuing one of the discussed diets or making up their own unique diet are encouraged to purchase some of the diet books mentioned, if for no other reason than that they contain valuable lists of foods classified according to the type of fat or carbohydrate that predominates. Such food tables are very valuable in making up lists of acceptable foods, given a preconceived diet philosophy one has decided to follow.

    Nutritional epidemiology and nutritional science are difficult areas because of the extreme complexity of food on the one hand, and the individual variability on the other. After all, the adult population in North America consists of a grand mixture of the slim to the obese, a large racial mix, and there is a range from the really healthy to those with a assortment of ailments, some diet related, some not, some life threatening, some only offering the potential. However, it must be kept in mind that in the areas of cardiovascular disease and diabetes, diet plays a significant role both in prevention and treatment. When a healthy diet is combined with other lifestyle aspects such as exercise, not smoking, and stress reduction, the reduction in risk for both CVD and diabetes can be dramatic.

    This review has only touched on the highlights of the subject of popular diets. The fact that a number of popular diets have not been discussed should in no way be taken to indicate a positive or negative attitude of the author toward these omitted diets, but rather simply space limitations and selection criteria. Detailed discussion of important subjects such as the role of supplements and exercise has been omitted. This review should not be viewed in any way as providing medical advice, but rather a guide to a selected segment of the "popular" and peer reviewed literature. This review deals with various aspects of diet as they relate to adults, and should not be extrapolated to diet questions concerning children, since neither the literature quoted nor the diets reviewed deal with either pediatric nutrition or the problem of teenage obesity. Individuals embarking on significant dietary changes should consult with their health care provider, especially if they are on any medications or have health problems.


    The recent media furor over the physical condition of Dr. Robert Atkins at the time of his fall and subsequent death deserves a comment. The media have gone wild over a mistakenly released report from the New York Medical Examiners (ME) Office which passed through the hands of a Nebraska physician and on to an association called the "Physicians Committee for Responsible Medicine," or PCRM, a group known to actively promote vegetarian diets and to have a strong anti-Atkins agenda. They released the report to the media. While the dedicated vegetarian connection was pointed out in the New York Times article (Feb 11), as well in an article in the Wall Street Journal (Feb13), this aspect of the PCRM may not be generally known either in the medical or lay communities. The lead editorial in The Globe and Mail on February 16 failed to mention this connection. The PCRM have used their platform of apparent medical respectability to help create what appears to be a quite unnecessary and in fact a seemingly irresponsible furor. At issue is Atkins' reported weight at death, 258 lbs, and brief, scribbled notes by a medical examiner indicating a history of heart attack, congestive heart failure and hypertension. The ME's observations were not based on an autopsy -- one was not performed according to a spokesperson from the ME's office quoted in the Times. Hospital records provided by the family indicate that he weighed 195 pounds when admitted to hospital after the fall. In addition, Dr Patrick Fratellone, Atkins' personal cardiologist, is quoted in the WSJ (Feb 13) as saying that his weight fluctuated within 5 to 10 pounds of 195 during the three years that he cared for him until June 2002. At six-foot height, this puts him as just slightly overweight, not obese due to following his own diet, as his critics are now claiming. Dr. Fratellone commented that a viral infection had resulted in cardiomyopathy and thus heart weakness, and was quoted as saying that "Under my care, he never had a heart attack and I did not treat him for hypertension." The WSJ also reports that Fratellone indicated an angiogram in 2002 revealed only a minor narrowing of the arteries that did not cause any symptoms. Atkins was 72 at the time of his death. The public dissemination of medically confidential records presumably violates medical ethics. According to the New York Times article this release to the media was called, by the Atkins supporters, illegal and in violation of federal law. Some might have reason to question the word "Responsible" in the title "Physicians Committee for Responsible Medicine." The Atkins diet and the other related low-carb diets should be judged as best one can on scientific grounds rather than on speculation and innuendo and what is presented by the media.

    My favourite Supplements


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