Editor's note. As we went to press with this issue the controversy over the death of Dr Atkins erupted upon the unauthorized release of documents indicating that he may have died not just of complication of a head injury from a fall, but from being overweight. To date this has not been confirmed,

but the cultural conversation surrounding the charge, has reintroduced a new level of doubt about the Atkins diet from nutrition experts. As always, we must turn to the science to answer the fundamental questions about all such low-carb diets. Patrick Johnson does so admirably within these page.

SINCE 1980, THE PERCENTAGE OF THE ADULT population in the U.S. that is obese has risen approximately 8 to 12%, and the prevalence of disease that is often associated with excessive body weight has increased correspondingly. In 1999, Americans spent about $60 billion on products that claim to aid in weight control. Some of the most popular products are diet plans with novel food restrictions. But scientific theory states that if an individual simply takes in more energy than he or she expends, the excess will be stored as fat. (1)

In the late 1990s the idea that obesity is caused by carbohydrates (sugars and starches) rather than overeating became popular and has been put forth in several diet books, such as Dr. Atkins' New Diet Revolution, Protein Power, Enter the Zone, Sugarbusters, and Neanderthin. (2) The specifies of these plans vary, but they all share the common claim that significantly reducing carbohydrates will lead to improved health and a reduction in body fat without an overall reduction in caloric intake. This, according to the authors, is due to the effect that reducing carbohydrates has on insulin levels and the subsequent availability of fat for use as an energy source.

After review of the basics of fat and carbohydrate metabolism, as well as the evidence for the efficacy of some of the common claims made by the respective authors, it becomes clear that, though theoretically plausible, these claims are not well supported. It is also apparent that the methods used by the authors to verify these claims are not scientific. At its simplest, weight loss still appears to involve the difficult task of increasing daily energy expenditure and lowering food intake. The authors who claim otherwise bear the burden of proof and, thus far, have not met that burden. (3)

An Introduction to Diet Science

In the body, carbohydrate breakdown occurs in what is known as the glycolytic pathway. The process, which is known as glycolysis, takes one sugar molecule and splits it into two pyruvate molecules (Figure 1). Pyruvate is further broken down in either an aerobic or an anaerobic fashion.

[FIGURE 1 OMITTED]

During aerobic metabolism (slow glycolysis), pyruvate is converted to a molecule called acetyl-coenzyme-A (acetyl-CoA), which then continues on to what is called the tricarboxylic acid (TCA) cycle. In anaerobic metabolism (fast glycolysis) acetyl-CoA is converted to lactate and does not go directly through TCA. (4)

Glycolysis, both fast and slow, is what allows mammals to perform high-intensity activity; when it is operating fat metabolism is slowed. If glycolysis is inhibited-- carbohydrate deprivation or metabolic dysfunction--fat metabolism becomes the prime source of energy, and the intensity level during activity becomes difficult to maintain at higher than about 50-60% of an individual's V[O.sub.2]max (aerobic capacity determined as a function of the volume of [O.sub.2] that one can consume in a given time period), an important physiological consideration for anyone who is trying to include regular moderate exercise in his or her lifestyle.

TCA and Oxidative Phosphorylatlon

The tricarboxylic acid (TCA) cycle (Figure 2), along with oxidative phosphorylation in the electron transport chain (ETC), is the body's primary means of adenosine triphosphate (ATP) generation. ATP is the principal molecule used by the body to generate free energy. In the TCA cycle, which takes place in the matrix of the mitochondria, acetyl-CoA combines with a molecule called oxaloacetate to form citrate, the first step in a series of reactions that subsequently generate one guanosine triphosphate (GTP)---the energetic equivalent of ATP--tree nicotinamide-adeninedinudeotide (NADH) and one flavin-adenine-dinucleotide (FAD[H.sub.2]), both of which are electron carriers that each lead to the production of three and two ATP respectively in the ETC. (5)

[FIGURE 2 OMITTED]

The ETC takes the electrons from NADH and/or FAD[H.sub.2] and moves them through another series of reactions that are ultimately responsible for converting adenosine diphosphate (ADP) into ATP at the expense of [O.sub.2]. This is the primary source of energy for animals (Table 1). Neither the TCA cycle nor ETC is initially affected by carbohydrate deprivation clue to the fact that fat breakdown also results in acetyl-CoA, which thus enters TCA.

Beta-Oxidation

Free fatty acids (FFAs) are broken down (oxidized) for energy two carbons at a time in the mitochondrial matrix via the beta ([beta])-oxidation cycle. The result of this cycle is also acetyl-CoA, which then enters the TCA cycle. The rate-limiting step in [beta]-oxidation is the last step, which is catalyzed by an enzyme called alpha ([alpha] ketothiolase; acetyl-CoA inhibits this enzyme. (6) It is logical then that if one consumes a high carbohydrate meal, which will elevate acetyl-CoA via glycolysis, that fat metabolism will be slowed, and that conversely, when acetyl-CoA is depleted through exercise, carbohydrate deprivation, or diabetes, that fat metabolism will be elevated.

Different tissues rely primarily on different types of metabolism. The heart and liver are well adapted to use fats whereas the brain and the red blood cells almost exclusively rely on glycolysis for energy. During carbohydrate deprivation, when fat metabolism is the predominant form of energy metabolism, glycolysis, though not eliminated, is severely inhibited, thus raising the risk of inadequate fuel to the brain and red blood cells. (7) Fortunately there is an indirect mechanism employed by mammals to use fats for energy in tissue that prefers glucose: the utilization of ketone bodies.

Ketone Bodies

Ketone bodies are formed in the liver when [beta]-oxidation of FFAs is in excess of what is required by the surrounding tissue. (8) Fat is converted to acetyl-CoA then the liver converts excess acetyl-CoA to ketone bodies: primarily acetoacetate, [beta]-hydroxybutyrate, and less significantly, acetone (Figure 3). During starvation or prolonged carbohydrate deprivation, ketone levels can get high enough that they can cross the blood-brain barrier and, after a series of reactions, subsequently generate two acetyl-CoA, which then enter the TCA cycle 21 (Figure 4).

[FIGURES 3-4 OMITTED]

High levels of blood ketones, a condition called ketosis and a consequence of carbohydrate deprivation that is also sometimes seen with poorly treated diabetes and other metabolic dysfunctions that disrupt carbohydrate metabolism, can change blood pH. Ketoacidosis is a potentially life threatening condition that occurs when blood pH levels drop substantially due to increased ketone levels. Despite some potential problems that can arise clue to ketosis, however, a mammal's ability to survive through periods of starvation depends on the ability to generate and utilize ketones as fuel.

Insulin and Fat Metabolism

Insulin is the hormone responsible for the transport of glucose from the blood to the cell. When levels rise, it is an indication that blood glucose levels are elevated, which, in a healthy individual, usually means that some type of carbohydrate has been ingested. Elevated insulin inhibits an enzyme called hormone-sensitive lipase (HSL), which is responsible for the release of FFAs into the blood. When this enzyme is inhibited, fat oxidation is limited and, if the amount of energy consumed is less than the amount expended, storage may increase. (9)

Nearly all of the popular diet authors claim that obesity is caused by elevated blood sugar and/or metabolic disorders that lead to excessive insulin production, and that this is a major factor in cardiovascular disease (CVD), hypertension (HTN), and noninsulin dependent diabetes (NIDDM), which appears to be true when insulin resistance is present. Insulin resistance is brought about by decreased glucose utilization in skeletal muscle and is highly correlated with obesity. (10) It is not, however, dearly established whether obesity is a cause or a consequence of insulin resistance.

According to Sievenpiper and colleagues, contrary to the claims of the low-carbohydrate diet authors, promising data have emerged showing that a high-fiber, high-carbohydrate, low-fat diet plus regular exercise programs maintained through intensive counseling can decrease the risk of NIDDM by over 40%. (11) Furthermore a link has been established between high-saturated fat, very-low-carbohydrate diets, and increased low density lipoprotein (LDD or Dad cholesterol levels, which can also lead to CVD and HTN. (12)

The Glucose-Fatty Acid Cycle

In 1963, Randle and coworkers proposed the glucose fatty acid (GFA) cycle. (13) Though it was intended to explain how animals maintain plasma glucose levels, it also provides a theoretical framework for the low-carbohydrate diet plans.

Randle postulated that increased FFA levels cause a greater oxidation and uptake of FFA that leads to inhibition of glycolysis and glucose uptake (Figures 5 and 6). (14) therefore, increased levels of FFA bought forth by carbohydrate deprivation should also lead to a similar increase in oxidation. This may support the idea that calories are not of central importance in weight loss when one is operating on a fat based metabolism, due to the possible increase in oxidation without an increase in energy expenditure, as well as the claim that elevated insulin is a prime factor in the reduction of fat oxidation that occurs in the presence of carbohydrates.

[FIGURES 5-6 OMITTED]

According to Randle, Garland, Hales, and Newsholme, the cycle works as follows:

   In the tissue phase, fatty acids and
   glycerol are released from glycerides
   in both muscle and adipose tissue
   (lipolysis): they may be reincorporated
   into glycerides by esterification
   with glycerolphosphate formed from
   glucose, but not by reaction with
   glycerol, which Ls released into extra-cellular
   fluid. Fatty acids may also be
   oxidized (both tissues), or transferred
   to plasma albumin (adipose tissue).
   In the blood phase, uptake of glucose
   by adipose tissue is depicted as
   inhibiting the flow of fatty acids from
   adipose tissue (and of ketone bodies
   formed from them in the liver) to
   muscle through the blood-stream; and
   the increased availability, for oxidation,
   of fatty acids (from muscle or
   adipose tissue glycerides) or of
   ketone bodies is depicted as inhibiting
   glucose uptake by muscle. The
   cycle thus provides a primitive mechanism
   which, quite independently of
   hormonal control, will tend to maintain
   a constant plasma-glucose concentration
   in animals that feed intermittently.
   Control by the cycle is
   modified by insulin, which enhances
   glucose uptake in muscle and adipose
   tissue, inhibits release of fatty
   acids in adipose tissue and increases
   esterification of tatty acids in adipose tissue and
   muscle. It may be noted that the effects of the hormone
   on glyceride metabolism may potentiate its
   effects on glucose uptake. (15)

The GFA cycle is conceptually important because it helps explain how high levels of one fuel source can influence the use of another. (16) There remains, however, some doubt as to whether it operates in human skeletal muscle during periods of rest.

Studies done on rat skeletal muscle have shown no effect on glucose uptake due to increased levels of the fatty acid, palmitate or to blood ketones. However the addition of oleate (another fatty acid) to the perfusion medium was found to inhibit glucose uptake during contraction. (17) In a study conducted by Hargreaves et al, no changes in muscle FFA uptake or oxidation, glucose-6-phosphate levels, or muscle citrate release were observed during one hour of knee extension exercise at 80% of the maximum amount of weight a person can lift at one time. (18) The investigators demonstrated that infusion of a 20% triglyceride emulsion and heparin resulting in a physiological elevation of FFA was associated with inhibition of high glucose uptake at rest and during exercise. They concluded, however, that the observed effect on glucose uptake might not have been due to the glucose-fatty acid cycle but rather to direct inhibition of glucose transport by FFA.

It is plausible that increased circulating FFA may inhibit glucose uptake and that the converse--increased blood glucose inhibiting circulating FFA levels--is also true due to the GFA cycle. Important to remember, however, is that alterations in FFA availability, the subsequent effects on fat oxidation and glucose metabolism, and the underlying mechanisms are not yet fully understood and require further investigation. (19) The GFA cycle, while conceptually important, has proven difficult to substantiate experimentally.

Potential Side Effects of Chronic Carbohydrate Deprivation

Limited carbohydrates in the diet can lead to ketosis, and possibly fatigue. (20) Although it has been found that human subjects can adapt to chronic ketosis over time, potassium depletion, elevated blood and urine calcium possibly due to the body using calcium to help neutralize the increased acidity of the blood, as well as other electrolyte disruptions are potential side effects that can occur. (21) Potassium is important for neural function through its role in fire propagation of action potentials, which allow neural synaptic transmissions to occur, and calcium plays a crucial role in muscular contraction. (22) Interference, therefore, with either of these two electrolytes can lead to difficulty during skeletal muscle contractions and, more significantly, to cardiac arrhythmia. (23) Furthermore, it is plausible that the increased blood calcium may be taken from bone, which could theoretically, over time, lead to osteoporosis. (24)

The Ketogenic Diet as a Medical Therapy

There does exist a medically supervised version of the low-carbohydrate diet, referred to as the ketogenic diet, which has been shown to be effective in the treatment of certain types of seizures. (25) This fact is often cited as verification of the safety of low carbohydrate diets. However, though it has been shown that humans can safely adapt to chronic ketosis, (26) the very fact that a diet that induces this condition works to treat a neurological disorder such as epilepsy allows one to conclude that it causes significant physiological change. It is important to remember that what is beneficial for the epileptic may not be so for an individual without a similar pathology.

Efficacy of Low Carbohydrate Diets as Treatment for Overweight and Obesity

After reviewing basic nutrient metabolism it becomes evident that reducing carbohydrate intake may, in fact, be helpful for individuals wishing to increase FFA levels. The claim by most of the popular low-carbohydrate diem, however--that it will help without a reduction in overall caloric intake--remains questionable. When an individual is using stored fat as enemy that individual will likely only burn as much as one needs to fuel the essential metabolic processes and the level of activity. Therefore, if one consumes more than one expends, even without carbohydrates present, one will likely gain weight. The notion that simply increasing FFA availability is enough to shed pounds over a long period of time is not well supported.

The assertion does have some theoretical substantiation in the GFA cycle and with the findings of Kekwick and Pawan, who placed five obese subjects on a 2000 Calorie per day (Cal/d) diet containing a normal amount of protein, carbohydrate, and fat. (27) Over the period of observation for the 2000 Cal/d, the investigators noted that subjects either maintained weight or gained a little. Over the next observation period, the same subjects were given a new diet in which the total calories were increased to 2600 Cal/d but the macronutrient content was changed to reduce the carbohydrate content and increase the protein and fat content. During this period four of the five patients lost weight despite the increase in caloric intake. The authors concluded from the results of this study that a reduction in carbohydrate intake could increase weight loss significantly even when caloric intake is elevated.

The aforementioned study appears, at first glance, to provide some compelling evidence in favor of the low carbohydrate authors' claims. There are, however, several flaws inherent in the study that hinder the credibility of the conclusions. First, there was no statistical analysis performed on any of the numbers. The results for the increased-calorie/reduced-carbohydrate diet and the balanced control am presented by Kekwick and Pawan in a single table (Table 2) and were not gathered in a way that is conducive to statistical comparison. (28) There is a total of five subjects, three of whom participated in three diet observations. Subjects one and three were observed first on the 2600 Cal/d diet, then on the 2000 Cal/d, then again on a 2600 Cal/d diet; subject two was first on the 2000 Cal/d diet, then the 2600 Cal/d diet, then again on the 2000 Cal/d diet. Subjects four and five were observed only twice, once on each diet. This inconsistency does not necessarily preclude statistical comparison if one compares all the 2600 Cal/d weight loss with all the 2000 Cal/d weight loss. The observation periods, however, were inconsistent, ranging from four days to 14 days, making it illogical to compare the numbers statistically. The greatest weight change during the reduced carbohydrate portion of the experiment was 2.6kg (5.72 lbs) and it occurred in the subject who was observed for 14 days. The authors estimated that 3%5@/o of the weight lost by the four subjects who lost weight was body water, which further reduces the significance of the numbers regarding fat loss. Finally, even the longest observation was probably not long enough to observe whether the change was effective on a permanent level.

In another study that kept nine lean, and apparently healthy men on a ketogenic diet for 35 days, Phinney and coworkers noted a mean weight loss of 0.7 kg (1.54 lbs.) within the lust seven days followed by a further drop of 0.4 kg (0.88 lbs.) throughout the second week. During the subsequent two weeks, however, subjects regained a mean weight of 0.6 kg (1.32 lbs.). The investigators found that none of the mean changes was significant by two-way ANOVA. (29)

The information obtained by Phinney et al. is consistent with the findings of Kekwick and Pawan. Despite a lack of statistical significance in both cases, each found that substantially reducing dietary carbohydrates could cause a slight drop in body weight. The study by Phinney, however, with its longer observation period, further indicates that once the body adapts to the change, weight will normalize back to an amount similar to the original. It is reasonable to conclude from the information in these two studies that the preliminary drop in weight is due to the body's initial adaptation to the metabolic change brought about by limitation of dietary carbohydrates; it appears, however, that once the body adapts to the change, weight loss is no longer affected.

A study conducted by Kennedy and coworkers evaluated the food consumption of approximately 10,000 adults from the 1994-1996 Continuing Survey of Food Intake by Individuals, and observed that people who habitually followed a lower carbohydrate eating pattern ([+ or -]30% of energy from carbohydrates) had a significantly higher body mass index (BMI)--an index of height to weight that often correlates with body fatness--than those who followed a high carbohydrate, low fat diet. This is likely because the higher carbohydrate, lower fat diets tend to be lower in energy. (30) The investigators concluded from this analysis that manipulation of nutrients is not associated with weight reduction in the long term, but rather that weight loss will occur when energy intake is less than the body needs to maintain its current weight. This conclusion is evidentially well supported. (31)

Methods Used by Popular Diet Authors

Despite some theoretical plausibility that may exist regarding the efficacy of low-carbohydrate diets, the methods used by the authors to verify their respective claims are clearly not scientific. Whereas with science one should start with a question and look for possible answers, these diet promoters appear to have started with their respective conclusions, then sought evidence to verify them. The danger of this practice is that it is very easy to notice evidence that supports what one already believes and to completely ignore any contradictory information.

Much of the evidence presented by the various authors as verification of their respective claims is based on testimonial or anecdotal evidence rather than replicable scientific research. Often suitable background information with appropriate references is given by the authors until they get to their statement of controversy at which point the referencing ceases or becomes inappropriate. A good example of this can be found in Protein Power where Drs. Michael R. and Mary Dan Eades explain that reduced insulin levels help to lower blood cholesterol:

   And when dietary fat and cholesterol do cause
   problems, it's usually because of carbohydrate
   eaten along with them. It is true that fat is the raw
   material from which the them makes cholesterol,
   and it is also true that if you add morn fat to your
   diet your cholesterol will increase, but only if you
   continue to eat a lot of carbohydrate at the ,same
   time you add the fat. Although fat is the raw material
   the body uses to make cholesterol, insulin runs
   the cellular machinery that actually makes it. If you
   reduce the level of insulin, the cells can't convert
   the fat to cholesterol, almost no matter how much
   fat is available. (32)

No references are given by the authors to support the assertions made in this paragraph (33) and, up to that point, the entire segment (entitled "What We Eat") in Chapter Three, is supported in a footnote by correlative information from a survey conducted in 1983 by the National Health and Nutrition Examination Survey (NHANES II) the results of which show that the number one food consumed by Americans is white bread and related products (rolls, crackers etc ...) but provide no insight as to how insulin or carbohydrates raise cholesterol levels.

It can be hypothesized from the information in the NHANES II that carbohydrates are causing obesity, elevated cholesterol, and several other related metabolic disorders. From the same information, however, one can also hypothesize that increased availability of convenience foods, a large portion of which are high in simple carbohydrates, leads to over-consumption, and that this is the ultimate cause of overweight and obesity and the subsequent metabolic dysfunction.

An analysis conducted by Heini and Weinsier (34) of information obtained from NHANES II and III, the USDA Nationwide Food Consumption Survey, the Behavioral Risk Factor Survey System, and the Calorie Control Council Report found that the prevalence of overweight in the U.S. population increased by 31% from the period of 1976-1980 to the period of 1988-1991. The analysis also found that, during the same period, the average fat intake decreased by 11%. Though this information could lend support to the claims of the Eades, Heini and Weinsier conclude that the paradoxical increase in the prevalence of obesity with the overall decrease in dietary fat intake may be due to a concurrent drop in physical activity related energy expenditure.

When one examines the different possible conclusions that can be drawn from correlative information, it becomes apparent that the ideas presented by the Eadeses in the excerpt above can only be treated as hypotheses that perhaps deserve further investigation, but not as scientifically supported facts.

Common Features of Spurious Nutrition and Fitness Claims

Some of the features common to spurious nutrition and fitness claims are that the claimant frequently purports to have found the secret to easy weight loss and wellness, and that a specific product or plan is the key to success. Many questionable claims take responsibility for obesity and poor fitness away from the consumer and place blame on the "uncaring" or "conspiratorial" scientific establishment. The factor common to nearly all of them, however, is that they rely heavily on testimonial evidence, which is not sufficient to verify a scientific claim. This is due to such factors as the placebo effect, the aptly-titled fallacy of false cause, the fallibility of personal recollection, and the subjective nature of what constitutes improvement in an uncontrolled setting. (35) When a controversial statement is made about something with little or inappropriate evidence to support it, reliability regarding the claim is threatened. A good example of this is the commentary made by the late Dr. Atkins about his diet plan during a televised interview on CNN:

   We've got real human beings who have been on
   this diet, and they'll tell you exactly what happens.
   They've never felt better in their life. If they have
   medical problems such as diabetes, their need for
   medication goes away. If they have high blood
   pressure, their need for medication goes away.
   Heart disease reversed. What more do you need?
   These are real people. And studies have been done
   and you [The American Heart Association] have
   ignored them. Studies have been done showing
   that the diet works and helps the risk factors. (36)

Atkins is making some big contentions about his diet plan, yet he offers no information to support them. Several reputable scientific organizations, such as The American College of Sports Medicine, The American Dietetic Association, The Cooper Institute for Aerobics Research, and The American Heart Association have all issued statements that high-protein, high-fat, low-carbohydrate diets are not effective for most people and can, in some cases, cause harm. (37) When there is a substantial body of evidence supporting a scientific theory it is up to the challenger(s) of that theory to provide verifiable evidence in rapport of the alternate ideas. (37)

While it will likely be helpful for those trying to lose weight to avoid sugary snacks that provide little nutrition, there is, thus far, little evidence that low-carbohydrate diets like those touted by the popular diet doctors are the magic bullet solution to the problem of obesity.

Conclusion

According to the U.S. Centers for Disease Control and Prevention, about 55% of the U.S. population is overweight. (37) The number of people working more than 50 hours per week has increased steadily since the 1970s. (38) According to the American College of Sports Medicine, 29% of men and 44% of women in the U.S. are trying to lose weight. However, only 22% of those men and 19% of those women who reported attempts at weight loss are reducing energy intake and exercising. (39) That a large number of people don't have the time or inclination to exercise and plan wise food choices, in addition to the fact that our culture places a high value on thinness, leaves a sizeable market to exploit. It is evident from the amount of money spent each year on weight-loss related products that Americans want to believe that there is an easy solution to achieving proper nutrition and fitness. Lamentably, there is a great disparity between the amount of money spent on these products and the number of people who are actually losing weight and getting healthier.

The bottom line is that what is known about nutrition is based on science, not intuition. There are many factors to consider regarding health and wellness. The had news is that at its physiological core weight loss still appears to involve the difficult task of increasing daily energy expenditure and lowering food intake. The idea that a single nutrient is to blame for the problem has proven erroneous; it turned out not to be true with fat, and it appears to be erroneous with carbohydrates as well. The authors who claim otherwise bear the burden of proof and thus far have nor sufficiently met that burden.

Table 1: Major energy sources--ATP yield from Glycolysis, the
TCA Cycle, and Oxidative phosphorylation.

Pathway          High energy      ATP yield    Subtotal
                                  molecule

Glycolysis          2 ATP                         2 **
                    2 NADH           --           8
Pyruvate            2 NADH          6 ATP        14
to Acetyl-CoA                       6 ATP
TCA Cycle            2 GTP                       16
                    6 NADH          2 ATP        34
                 2 FAD[H.sub.2]    18 ATP        38
                                    4 ATP

** The end total if glycolysis is anaerobic. (Adapted from Powers
& Howley, 2001)

Table 2: Possible evidence in favor of low carbohydrate diet claims--a
reproduction of Table VI from Kekwick and Pawan (1956).
Weight changes in 5 patients during periods on normal 2000
calorie diet and on high-fat, 2600-calorle diets of series 3.

Case     Daily      Initial body     Final body
no.     calories    weigh (kg.)     weight (kg.)

 1        2600          94.3            93.0
          2000          93.0            93.7
          2600          93.7            91.8
 2        2000          81.9            82.4
          2600          82.4            80.9
          2000          80.9            81.1
 3        2600         111.9           109.3
          2000         109.3           109.3
          2600         109.3           107.7
 4        2000         111.6           111.2
          2600         111.2           111.3
 5 *      2600          93.5            92.5
          2000         885.0            90.3

Case     Period of       Change In
no.     observation.    weight (kg.)
           (days)

 1           6              -1.3
             5              +0.7
             9              -1.9
 2           7              +0.5
             8              -1.5
             8              +0.2
 3          14              -2.6
             8              +0
             8              -1.6
 4           8              -0.4
             4              +0.1
 5 *        10              -1.0
             7              +1.8

* Intermediate period between 2 observations put on 2000 calorie
high-fat diet on which weight dropped from 92.5 to 88.5 kg.

References

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(2.) Atkins, R. 2002. Dr. Atkins' New Diet Revolution. New York: HarperCollins. Eades. M.R., Eades, M.D. 1996. Protein Power. New York: Bantam Books. Sears, B. 1995. Enter The Zone. New York: HarperCollins. Audette, R. 1999, Neanderthin. New York: St. Martin's Press. Steward, H.L., Bethea, M. Andrews. S., Balart, L. 1998. SugarBusters! New York: Ballantine Books.

(3.) The FDA now has to prove that a nutritional supplement is ineffective or causes harm before any imposition is made on the manufacturer by the courts, This shifting of the burden has allowed many unverified and ineffective Products to remain on the market.

(4.) Brooks. F., White B. 2000. Exercise Physiology. Human Bioenergetics and It's Applications (3rd ed.) Mountain View, CA: Mayfield.

(5.) Brooks, et al. op. cit., 2000.

(6.) Acheson K.J., Flatt J.P., Jequier E. 1982. "Glycogen Synthesis versus Lipogenesis After a 500 Gram Carbohydrate Meal in Man." Metabolism 3(12): 1234-40.

(7.) Randle, P. J. Garland. P.B. Hales C.N., Newsholme, E.A. 1963. "The Glucose-Fatty Acid Cycle: Its Role in Insulin Sensitivity and the Metabolic Disturbances of Diabetes Mellitus." Lancet. April 13: 785-89.

(8.) Zubay, G. 1998. Biochemistry (4th ed.). Dubuque, IA: Wm. C. Brown Publishers.

(9.) Nadler S., Attie A. 2001, "Please Pass the Chips: Genomic Insights into Obesity and Diabetes." Journal of Nutrition 131(8): 2078-2081.

(10.) Bell, D.S.H. 1993. "Insulin Resistance." Postgraduate Medicine 93(7): 99-103,107-107.

(11.) Sievenpiper J.L., Jenkins AL, Whitham D.L., Vuksan V. 2002. "Insulin Resistance: Concepts, Controversies. and the Rote of Nutrition." Canadian Journal of Dietetic Practice and Research 63(1): 20-32.

(12.) Liebman. B. 2000, "Diet vs. Diet. Battle of the Bulge Doctors." Nutrition Action Healthletter 27(4): 9-10.

(13.) Randle, et al. 1963, op. cit.

(14.) Hargreaves M. 1995. "Skeletal Muscle Carbohydrate Metabolism During Exercise." In M. Hargreaves (Ed.) Exercise Metabolism. Champaign, IL: Human Kinetics,

(15.) Randle, et al, 1963, op cit., 785.

(16.) Brooks, et al. 2000, op cit.

(17.) Hargreaves, 1995, op cit.

(18.) Hargreaves M., Kiens B,. Richter E.A., 1991. "Effect of Increased Plasma Free Fatty Acid Concentrations on Muscle Metabolism in Exercising Men." Journal of Applied Physiology 70: 194-201.

(19.) Hargreaves, 1995, op cit.

(20.) Phinney, S.D., Bistrian B., Evans W., Gervino E., Blackburn G. 1983. "The Human Metabolic Response to Chronic Ketosis Without Caloric Restriction; Physical and Biochemical Adaptation." Metabolism 32(8): 757-68

(21.) Furth S.L. Casey J.C., Pvzik P.L., Neu A.M., Docimo S.G., Vining E.P., Freeman J.M., & Fivush B.A. 2000. "Risk Factors for Urolithiasis in Children on the Ketoganic Diet." Pediatric Nephrology 15(1-2): 125-128.

(22.) Ichikawa, Lekuni (ed.). 1990. Pediatric Textbook of Fluids and Electrolytes. Baltimore MD: Williams and Wilkins, 8, 9, 26. Brooks, et al, 2000, op cit.

(23.) Ichikawa, 1990, op cit.

(24.) "The Atkins Diet." 2000. Medical Letter on Drugs & Therapeutics 42(1080): 52.

(25.) Freeman. J.M., Kelly, M.T., and Freeman. J.B. 1996. The Epilepsy Diet Treatment: An Introduction to the Ketogenic Diet (2nd ed).; New York: Demos Vermande. 5, 6, 27-8,

(26.) Phinney, et al, 1983, op cit.

(27.) Kekwick A., Pawan G.L.S. 1956, "Calorie Intake in Relation to Body-Weight Changes in the Obese," Lancet, July 28: 15, 5-6.

(28.) Ibid.

(29.) Phinney, et al, 1983. op cit.

(30.) Kennedy E. Bowman S., Spence J., Freedman M., King J. 2001. "Popular Diets: Correlation to Health. Nutrition, and Obesity," Journal of the American Dietetic Association 101: 411-420.

(31.) Astrup A, Grunwald R. 2000. "The Role of Dietary Fat in Body Fatness: Evidence From a Preliminary Metaanalysis of ad libitum Low-Fat Dietary Intervention Studies." British Journal of Nutrition 83: S-25-32.

Carmichael H., Swinburn B., Wilson M. 1998. "Lower Fat Intake as a Predictor of Initial and Sustained Weight Loss in Obese Subjects Consuming an Otherwise ad libitum Diet." Journal of the American Dietetic Association 98: 35-39.

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(32.) Eades and Eades, 1996, 39.

(33.) The authors opted not to include references at the end of their book, instead directing those readers interested in the book's bibliography to their website: http://www.eatprotein.com. This method makes it difficult to associate a reference with a particular assertion.

(34.) Heini A.F., Weinsier R.L. 1997. "Divergent Trends in Obesity and Fat Intake Patterns: The American Paradox." The American Journal of Medicine 102(3): 259-264.

(35.) Schick T., Vaughn L. 1995. How to Think About Weird Things. Mountain View, CA: Mayfield, 15, 8.

(36.) CNN. "Atkins Diet: Can We Have Our Turkey and Eat it too?" 1999. Transcript available:http://www, cnn.com/HEALTH/diet.fitness/ 9911/26/atkins.diet/index.html

(37.) "High Protein Diets Panned by Major Health Promoting Groups." 1997. Tufts University Health & Nutrition Newsletter, December: 6.

(37.) Shermer, M. 1997 Why People Believe Weird Things. New York: W.H Freeman, 50, 51, 56.

(37.) Putnam, J. 1999. "Food Consumption and Spending: U.S. Food Supply Providing More Food and Calories." Feed Review 22(3): 2-12.

(38.) Lardner. J. 1999. "World-Class Workaholics." U.S. News & World Report 127 (4): 42-53.

(39.) American College of Sports Medicine. 2001. Position Stand: Appropriate intervention strategies for weight loss and prevention of weight regain for adults. Medicine and Science in sports and Exercise 33(12): 2145-56.