Eating - Is Anything Reasonable?

by Bob Lombardi

Last revised 2/23/02

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It is my aim to show in this paper, based on as much hard evidence as I can find, that the best approach to a diet is to eat a variety of foods, without much preference to any one macronutrient group. Nothing is forbidden, but everything has a consequence. No food is perfect. If you search the web for any length of time, no matter what food or food additive you mention, someone will say it is worst thing that has ever hit the earth; someone else will say it is a veritable gift from God. I'm going to limit myself to things that are essentially all from peer-reviewed scientific journals. Even with this intent, it is easy for me to add opinions or personal bias to what I've written. My apologies if I've quoted someone incorrectly; I accept full responsibility for this article.

Intro

The problem with eating is that we need to. Down through all of human history, the biggest problem they had with food was that there wasn't any. In this time, and in the western world, this is no longer the problem. This is a land of plenty, and the free market assures that any food we may desire will be available. Unfortunately, we are continually bombarded with messages of what we should or shouldn't eat. They are often contradictory, and not often clear, even to many of the physicians who have to advise us. Even worse, scientists who should know better have gone well beyond the conclusions of their studies to recommend changes to the our diet - changes that have not all been proven.

It seems to me that there is an idea floating at large in our society, that if we just eat the one right way, we won't age, we won't develop cardiovascular disease, cancer, kidney disease, diabetes or any other debilitation. But the simple fact of nature is that, "we are all going to die; it's just a question of how and when" (to quote writer Joe Straczinksky - as his character Lennier on "Babylon5"). We might possibly be able to steer the odds away from one cause toward another, but we are all going to die. Since behaviors have been strongly linked to some health problems (the major example is smoking and the diseases linked to it), there has long been a temptation to try and link all health problems to behaviors. The multi-billion dollar "Health Food Industry" seems to this writer to be the result of people believing that if we eat right, or eat the one magic food (or take that one magic vitamin/mineral/herb), we'll avoid health problems. But children and even babies get cancer, and you can't blame it on a lifetime of poor eating or poor living. As my wife's oncologist says, "sometimes cells just freak out...".

My journey down this road of discovery starts out in a peculiar way. It all began when my wife, Pam, came down with breast cancer in her early 40s. At the oncologists office, we picked up a copy of a little booklet on "Eating for Cancer Patients". We had long been following a lowfat diet, doing our best to keep up with the recommendations of the dietary authorities. This book made our heads spin faster than Linda Blair's in the Exorcist! It said things like, "keep hard boiled eggs around the house - they make excellent quick snacks", "remember you can improve the flavor of the things you eat by adding butter". They also made the point that our entire immune system is made of protein, and to strengthen it, we need to get adequate protein in our diets. At that point I told myself, "you have the Internet, the greatest research tool in history. If the lowfat case is so strong you'll have no problem finding out". That's when my dietary world began to turn around.

The Lowfat Mantra - America's Official Fad Diet

Part I, Fat and Heart Disease

The "prevailing dietary wisdom" as expressed in the USDA Food Pyramid, says that we should get the vast majority of our caloric intake - up to 65% - from carbohydrate, with the remaining 35% split between protein and fat. This reflects the idea that one of the major macronutrient groups (in this case, fat) is "evil" and the cause of all problems. This is because of the particular association of one type of fat (saturated fat, most commonly found in animal products) with cardiovascular disease (CVD). I argue that this idea - that all health problems stem from dietary fat consumption - is not supported by current evidence. I'm going to spend a lot of time discussing dietary fat because Americans have been trained that fat is evil for a long time, and it will take a lot of evidence to counter this.

Let's stop for a minute and think about percent calories from fat in our diet. There's a big problem lurking under the surface here! The percentages of calories in your macronutrients can only come from three sources: protein, carbohydrates and fat. If you decrease the percentage of one, you increase the percentage of the others. If you ate a tablespoon of butter for a day, that would be very low calorie, but 100% calories from fat. Likewise, if you ate the same calories in sugar, it would be 100% carbohydrate. If you mixed sugar and butter but made sure the calories remained the same, it would be still be low calorie but you would have reduced your percentage of calories from fat. If you had one tablespoon of sugar and one of butter, you would have increased your calorie intake, but lowered your fat percent of calories. If you want to eat a lowfat diet (as percent of calories - what the FDA is saying), simply eat a lot of sugar! Protein is relatively safe, but since most sources of protein come with some built-in fat, the simplest thing to do, and the thing that the makers of the current flood of lowfat foods do, is fill them with sugar to make the percent of fat calories lower.

So what's so bad about sugar? Simply that overconsumption of sugar - refined carbohydrates - may be responsible for the surge in diabetes in America since lowfat diets started being pushed on the American people. Diabetes, in turn, brings a risk of heart disease - just what you're trying to avoid by going to the lowfat diet. "Between 1990 and 1998, a 70 percent increase in diabetes was found among individuals aged 30 to 39, followed by an increase of 40 percent among those aged 40 to 49, and a 31 percent increase among those aged 50 to 59. " (47) Other sources quote a doubling of the incidence of adult- onset diabetes between 1980 and 2000. The so-called "adult-onset" diabetes has become so endemic it is affecting children! Along with this has been an increase of what is referred to as Metabolic Syndrome X - characterized by insulin resistance, low HDL cholesterol/high triglyceride blood profiles, high blood pressure and overweight. All of these conditions have been linked to high-carbohydrate diets. "(Stanford University Endocrinologist Gerald) Reaven and Ron Krauss, who studies fats and lipids at Lawrence Berkeley National Laboratory in California, have shown that when men eat high-carbohydrate diets their cholesterol profiles may shift from normal to syndrome X. In other words, the more carbohydrates replace saturated fats, the more likely the end result will be syndrome X and an increased heart disease risk. "The problem is so clear right now it's almost a joke," says Reaven. How this balances out is the unknown. "It's a bitch of a question," says Marc Hellerstein, a nutritional biochemist at the University of California, Berkeley, "maybe the great public health nutrition question of our era."(40)

There's an old saying in physics that "Nature abhors a vacuum", to which one wag replied, "a vacuum is a hell of a lot nicer than a lot of what nature fills it with". Maybe fat is a hell of a lot nicer than what we replace it with in our diets!

Since I wrote the original version of this article, the American Heart Association, in their flagship publication "Circulation" issued a statement on very lowfat diets (which they define as 15% fat or less). (35). Their conclusion is that these diets have not been proven safe or effective. The studies that seem to back Very Low Fat (VLF) diets are confounded by other variables, notably exercise, stress reduction and weight loss. I can't do better than to quote from their conclusion: "Because very low fat diets represent a radical departure from the current prudent dietary guidelines, such diets must be proved both advantageous and safe before national recommendations can be issued. " They go on to say that until we know better, a "limited group of motivated, high-risk persons with high LDL cholesterol and/or preexisting cardiovascular disease may benefit from very low fat diets but only with support, careful supervision, and regular follow-up by the healthcare provider." In other words, this is a risky thing to do, and requires close attention by a doctor. They're especially concerned about "optimal substitutions of complex carbohydrates for fat while preserving protein intake" and getting enough micronutrients. They use the term "current prudent dietary guidelines" to mean 30% calories from fat (CFF). Yet certain "diet gurus", such as Dr. Dean Ornish and Dr. Gabe Mirkin have long recommended VLF diets. It should be noted that this 30% figure comes from biochemist Ancel Keys in 1952, long before such a precise number could be derived from any particular experiments. It has remained the "prudent" number because no one could come up with proof for why it should be lower, or higher. (40)

So here you have the American Heart Association saying that going to very lowfat diets is risky, requires close attention of a physician, and those eating this way need to be watched to make sure they get enough protein and micronutrients. And yet this is what many athletes and health-conscious people are eating - without the close supervision of a physician!

Now look at this from the perspective of the food pyramid. If you're eating what the AHA considers a prudent amount of fat, 30%, you must be eating 70% carbohydrate and protein. Assuming you need somewhere near 20% of your calories from protein, that leaves you with 50% carbs, 20% protein and 30% fat. This is lower percent calories from carbo than the 65% mentioned before, but it's the AHA "Prudent Diet". Stated another way, if you decreased your calories from fat (CFF) from (say) 40% to 30%, what are you eating now that you didn't eat before? What are you not eating now that you ate before? Did you replace butter with green vegetables? Or did you replace it with sugar?

The story of how fat became the bad boy of nutrition in the US is quite interesting (40) (43). Reference 40 is a fascinating look by an excellent science writer at the politics, business-interest and wishful thinking that led to the 50+ year national obsession with fat in the diet. Available online at: http://www.second-opinions.co.uk/taubes.html (and other places), you should read it. Briefly, in the early part of the 20th century, heart disease went from being unheard of in the average doctor's practice to a major cause of death. It was noted that this increase occurred at the same time as the increasing affluence in America led to increased consumption of butter, milk, dairy, eggs and meat. (It has not been widely noted, but this also occurred along with the growth of the vegetable oil business (44)). This led to the "Lipid Hypothesis", that blood levels of cholesterol were the cause of this epidemic and that dietary changes could reverse the epidemic. The only problem with the Lipid Hypothesis, as widely accepted as it is, is that has never been proven. This despite having had dozens of large studies aimed at proving it, at the cost of billions of dollars in taxpayer's money.

Saturated fat was an early emphasis when the earliest researchers found a correlation between saturated fat and atherosclerosis. It was found to raise serum cholesterol (both LDL - the "bad" cholesterol, and HDL - the "good"), although that distinction was not made until 30 years later. Risk studies gave saturated fat a "double whammy". Not only was it bad because it was a fat, the saturation somehow made it worse. In 1996, researchers showed that this is not the case. (1) If researchers correct for fiber in the diet, saturated fat's only contribution to CVD is this cholesterol raising effect. There is no other effect going on. (4) Let me be clear about this: blood levels of LDL are directly related to CVD risk. The questions are whether diet affects this risk, and whether the "normal, healthy" population needs to be concerned about such things, and whether a national change of diet will prevent disease and extend lives. That said, there are other indicators that are as strong or stronger, such as the Triglyceride/HDL ratio, a ratio notoriously degraded by a lowfat, high carbohydrate diet. (29) (33) (35) to name a few.

In fact, of the actual saturated fatty acids found in foodstuff, "only three saturated fats have this hypercholesterolemic property, C12:0, lauric, C14:0, myristic, and, C16:0, palmitic. There is also some discrepancy about how cholesterolemic each fatty acid is. Some investigators have not found C12:0 comparable to the other two. One explanation for this discrepancy is that C12:0 may be variably hypercholesterolemic depending on the level of dietary cholesterol. That is, the more cholesterol you consume, the easier it becomes for lauric (C12:0) to raise your serum cholesterol". (2) Other saturated fats, notably Stearic acid (C18:0) found in beef, are not all hypercholesterolemic (2). One paper (36) makes the point that, "Although stearic acid (C18:0) is typically considered neutral, exaggerated consumption of C18:0-rich fat (cocoa butter) lowers both LDL and HDL". In general, modern thought is that the best profile is to lower LDL and raise HDL. The short chain saturated fatty acids in butter, mostly butyric acid, are said to be metabolized quickly for energy, not easily incorporated into body fat, and to display other desirable properties. (43)

If dietary fat is the cause of CVD, then clearly reducing fat intake should result in improvements. In a survey of 26 available studies printed in the "European Heart Journal", UK researchers led by Dr. Laura Corr, one of Great Britain's leading cardiologists, concluded that "The Low Fat/Low Cholesterol Diet Is Ineffective." (3) The conclusion states, "The commonly-held belief that the best diet for prevention of coronary heart disease is a low saturated fat, low cholesterol diet is not supported by the available evidence from clinical trials. In primary preventions, such diets do not reduce the risk of myocardial infarction or coronary or all-cause mortality." They went on to state, "Similarly, diets focused exclusively on reduction of saturated fats and cholesterol are relatively ineffective for secondary prevention and should be abandoned. There may be other effective diets for secondary prevention of coronary heart disease but these are not yet sufficiently well defined or adequately tested. The circumstantial evidence of benefit from oils, particularly olive oil, vegetables, fruit and fish is strong." In other words, if you're trying to avoid a heart attack, don't try to avoid olive oil, or oily fish.

A common thread in studies of this subject is that the public doesn't know what it eats, or that they can't be objective reporters of what they eat. National statistics are argued over constantly, but they appear to show that at the urging of the authorities, Americans have cut their fat consumption. At the same time, adult-onset (non-insulin dependent, or "obesity") diabetes has skyrocketed, almost doubling since 1990. And while the rate of death from heart disease has indeed gone down, it appears to be more from better treatment than from diet.(40)

The European Heart Journal study (3) is not the only study to reach this conclusion. Ascherio et al (4), a study involving thousands of American men over a period of years, strongly suggests that there is no link between fat intake and heart disease in men and supports the contention that linolenic acid (a form of fat) is actually preventative against heart disease. The esteemed Harvard Nurses' Study published data in the New England Journal of Medicine (5) that shows that simply reducing fat is not the key: "Our findings suggest that replacing saturated and trans-unsaturated fats with unhydrogenated monounsaturated and polyunsaturated fats is more effective in preventing coronary heart disease in women than reducing overall fat intake". Trans-unsaturated fat are rare in nature, being essentially a man-made creation that date only to the beginning of this century. (Remember my remark in passing that the heart disease epidemic coincides with the rise of the food oil industry?) Health-food writers have long maintained what this study shows (44). Food makers are not required to list trans-fats on their labels, but if the label says "partially hydrogenated" or "shortening", that's the stuff you should be avoiding. Yes, "butter is better". For a variety of reasons (43), butter is preferable over margarine and trans-unsaturated fats for cooking and as a spread.

Several studies recently have pointed out the health benefits of eating fats. Matthew W. Gillman, M.D. studied the association of stroke incidence and consumption of fat in 832 men, aged 45 to 65, participating in the Framingham Heart Study over a 20-year period. (37) "The researchers found that increased intakes of total dietary fat and some types of fat (saturated and monounsaturated) were associated with a reduced risk of developing ischemic stroke. Polyunsaturated fat did not have the same association. For example, for each three percent increase in total fat as a percentage of total energy intake, there was a 15 percent decrease in stroke risk". In 1991, (38) Franceschini et al published a study in Metabolism that demonstrates that high intake of fats from the Omega-3 group increase HDL cholesterol levels, which is considered protective against heart disease. Laugharne, Mellor, and Peet published work (39) in 1996 showing correlation between schizophrenia and deficiencies in fats from both the omega-6 and omeaga-3 series. Supplementation with extra fats in these groups significantly improved symptoms of schizophrenia in most patients. I could go on, but I won't. The point here is that there are fats that are essential to health, and we shouldn't be skipping them out of some misguided idea that all fats are bad and we shouldn't eat any.

Perhaps the final word on dietary fat and heart disease ought to belong to the American Heart Association. In a paper presented in late 1997, and still contested by those who believe that fat is evil, Robert H. Knopp, M.D. said, "Moderately reducing the amount of fat intake in people with high cholesterol can help lower cholesterol levels. However, more extreme reductions in dietary fat do not provide further benefits and may be harmful to some people" (11) The editorials with the paper in JAMA imply that a low-fat diet will help some people, have no effect on some people, and hurt some people. This paper may well have marked the turning point in the AHA's support of a very lowfat diet for the American public.

The medical arm of the UN, the WHO, recommends 30 % - 35% calories from fat. That seems a reasonable number. But there is more here than simple percentages. Walter C Willett, considered by many to be the pre-eminent epidemiologist in America, wrote in an online publication directed at physicians (12): (note, he's using the term CHD - Coronary - Heart Disease - as I've used CVD).

"Conclusions:

1. CHD rates can be dramatically influenced by nutritional means, but consuming high carbohydrate diets instead of diets high in saturated fat will make little difference.

2. We should abandon recommendations regarding % of energy from fat and avoid pejorative references to fat or "fatty foods" because this is not supported scientifically and distracts from other more important goals.

3. Advice about dietary fat should focus on replacement of saturated and trans fat with vegetable oils, including sources of alpha-linolenic acid.

4. Advice about carbohydrate should focus on replacing refined grains, sugar, and potatoes with whole grain products.

5. Staying lean and active throughout life is extremely important.

6. Additional research is needed on vitamin E, folate, vitamin B6, fruits and vegetables, but weight of evidence strongly suggests that vitamin E and multiple vitamin supplements will substantially reduce risk of CHD."

So where does this leave the lipid hypothesis? In pretty bad shape, really. The U.S. Surgeon General's Office set off in 1988 to write the definitive report on the dangers of dietary fat. ... in June 1999, 11 years after the project began, they quietly killed the project.(41) If the case was so iron-clad and strong, would they have killed the project? While the usefulness of cholesterol lowering drugs has been demonstrated (it took a surprisingly long time to do that), the effectiveness of a lowfat diet has not. In the early 1970s, the NIH funded a half-dozen small studies which everyone hoped would be sufficiently persuasive to conclude that low-fat diets prolong lives. Four of these trials -- comparing heart disease rates and diet within Honolulu, Puerto Rico, Chicago, and Framingham--showed no evidence that men who ate less fat lived longer or had fewer heart attacks. A fifth trial, the Multiple Risk Factor Intervention Trial (MRFIT), tried to amplify the subtle influences of diet on health by persuading subjects to avoid fat while simultaneously quitting smoking and taking medication for high blood pressure. That trial suggested, if anything, that eating less fat might shorten life. (40) (43)

Part II, Fat and Cancer

Well, surely if fat isn't causing CVD, then it must be causing cancer, right? This is another commonly held idea. The idea behind this is that when cultures with typically lowfat diets (like the Japanese or rural Chinese) are compared to Americans, they have lower rates of some cancers. When they come to American and start eating the Standard American Diet they develop American rates of these diseases. A common example is breast cancer. Vast numbers of American women have started eating a lower fat diet in hopes of escaping of this terrible disease. Every time American researchers have looked at the numbers, dietary fat had no effect. In a seminal article (6), Willett's group published in the NEJM, "We found no evidence of a positive association between total dietary fat intake and the risk of breast cancer. There was no reduction in risk even among women whose energy intake from fat was less than 20 percent of total energy intake. In the context of the Western lifestyle, lowering the total intake of fat in midlife is unlikely to reduce the risk of breast cancer substantially." It has been noted that perhaps it is something else in the lifestyle, or environment, between the old country and America that causes the discrepancy in the cancer rates. Or, again, as the diet became more western it wasn't the fat that was added, it was something else they ate in the old country that was abandoned.

Another interesting point is that as Americans started eating a larger amount of polyunsaturated vegetable oils (as extracted oils - not in their natural state in nuts and other sources), the incidence of certain cancers has gone up. To quote one review article, "Several different dietary fats and oils have been compared with respect to carcinogen-induced tumorigenesis in animals and the results clearly show that polyunsaturated fats caused a significant increase in primary breast and colon tumors, whereas saturated fats had little effect". (22, 23) There are many factors to consider in answering this sort of question, and it isn't entirely clear that we can ever really know all relevant variables. In the case of breast or prostate cancer, for example, it might be more relevant to understanding any contribution of dietary fats to tumor development to know what the population ate during puberty rather than what they ate in the year or two before being diagnosed. (22) Polyunsaturated fats are so effective at suppressing the immune system that linoleic acid has been used to prevent the rejection of transplanted organs. Unfortunately, this led to cancer instead of organ rejection. (48) (49)

One of the characteristics of polyunsaturated fats (PUFA) is that they oxidize very quickly. Saturated fats don't oxidize, and mono-unsaturated fats are oxidized at an intermediate rate. It is thought that the oxidation of the PUFA is the cause of it becoming carcinogenic. If you eat the nuts or vegetables that contain the PUFAs, they're "packaged" with antioxidants that keep them safe. When they're extracted from the source, they're likely to oxidize. If you buy polyunsaturated oils, like flax oil, from a health food store, they need to be cold pressed and never out of refrigeration. One source says you should not let PUFAs exceed about 4% of your fat intake for this reason. Other sources say 3%, but we can't eliminate them. Linoleic acid is one of the essential fatty acids we need to survive.

Well, even if there is no gain to be had by switching to a low-fat diet, then it surely isn't hurting, right? It depends on what you're eating instead of the fat. If you're eating pasta, bread and other starches, Francheschi et al found that breast cancer correlated with starch consumption, but not fruits and vegetables. (7) "the highest intakes of total fat and saturated fat had no effect on the incidence of breast cancer. Of all the dietary factors considered, starch consumption had the greatest negative impact in predicting breast cancer incidence". It should be noted that pasta, bread and other starches are exactly what the prevailing wisdom says you should be eating. Prevention magazine, and others, continually recommend that we eat mounds of rice, pasta and other starches, using meat "as a condiment". Other researchers have correlated starch consumption with gastric cancers (9) (10).

One of the most frightening types of breast cancer is when it occurs in young, pre-menopausal women. Witte, Ursin, Siemiatycki et al studied just such cases (8) and found that "Monounsaturated fat, polyunsaturated fat, oleic acid, and linoleic acid intake was observed to decrease premenopausal breast cancer risk. Consumption of carbohydrates (and sweetened beverages) was associated with an increased risk of breast cancer." Low fat dairy products and tofu were associated with a decrease in risk. The protective effects of lowfat dairy and tofu was observed in a study of about 220 women, and were not noted in the larger Harvard Nurses' study. (6)

In the early '80s, dietary fat was thought to be easily linked to cancer risk. All that was needed was to just "do the studies". "Fifteen years and hundreds of millions of research dollars later, ... the World Cancer Research Fund and the American Institute for Cancer Research could find neither "convincing" nor even "probable" reason to believe that dietary fat caused cancer". (40)

Part III, Fat and Fat (overweight)

Since fat in the diet is a significant contributor to being satisfied with a meal, very lowfat diets leave dieters very hungry. So if the only way to loose weight is to cut calories while eating VLF then the experts want you to live your life very hungry most of the time. A moderate fat intake, 30%, will leave you feeling much less hungry on the same energy intake. (As we've just seen, Walter Willet, one of the leading researchers in the world on this subject says we shouldn't even keep track of the percent fat calories in our diet.) In the Women's Health Initiative study of 50,000 women, they found that those who ate a "draconian" 20% calories from fat had lost an average of one kilogram (around 2 pounds) after 3 years. (40)

The Golden Rule of treating overweight is what I call the thermodynamic model: calories in - calories out = weight change. There are countless good, solid, rigorous, clinical studies that support this idea. But that doesn't mean it is an easy principle to apply. The simple question "how many calories in this food item" is difficult to answer due to item to item variations. An early season peach, say, may be lower in sugar than one from the peak of the season. As anyone with fruit trees will tell you, the fruit from the same tree will vary greatly in sweetness between pieces. But the hardest thing to answer is how much energy you are burning doing anything. The American Journal of Clinical Nutrition study mentioned above (39) talks about how when someone changes to a lowfat diet in a metabolic ward experiment (typically less than two weeks duration), they lose some weight. After a few weeks to months, and here the subjects are free-living (not in a hospital ward), the regulatory systems in the body return the weight to the starting point. Has food intake gone up? Has energy usage changed? Covert Bailey, in his bestseller "Fit or Fat" makes note of observing fat people and thin people involved in various activities: he concludes that fat people move less in every activity, thereby burning fewer calories. So how do you know how much to eat, if you can't even know how much you're burning?

Another Golden Rule is "A calorie is a calorie is a calorie" - that no matter what you eat, if you eat a certain amount of extra calories, you'll gain the same amount of weight. The figure often used is that one pound of body fat represents around 3600 calories. An increasing amount of evidence says this is wrong. There have been researchers over the years that have presented apparently solid data that says it isn't true. The mainstream is apparently not believing it, although the research seems to be well done. In 1956, for example, Kekwik and Pawan of the UK examined the change in weight of a small number of subjects when eating diets of 90% protein, 90% fat and 90% carbohydrate. Their subjects lost 4.2 and 6.3 pounds in a week on protein and fat respectively. On 90% carbohydrate, they gained 1.2 pounds in a week. This was published in "The Lancet", one of the world's premier medical journals. (41) The usual objection to this kind of unconventional data is that it must simply be water weight loss. In answer to this, they did additional studies of water balance and detailed animal studies where they autopsied and did tissue analysis to determine just what was lost. Yes, it was fat that was lost, not just water. (personal aside - at one time I lost 65 pounds on a zero-carb diet (Atkins). If that were all water, I'd have been as shriveled up as a raisin with blood as thick as corn syrup. It wasn't water.) Note that there commonly is water weight loss when a low carbohydrate diet is started. The main storage of carbohydrate in mammals is glycogen, which requires about 4 times the weight stored as water for its use. When the dieter uses up their internal carbohydrate stores, they loose that water. But that only happens once, and it's only about 3 or 4 pounds.

A US DHEW publication seems to back up Kekwik and Pawan. (36) "On a high-fat diet, 4703 to 8471 excess calories were required for each kilogram of added weight. On a low carbohydrate VLCD (very low calorie diet), replacing fat calories with 8 g/day of equivalent carbohydrate calories reduced weight loss by 1.68 kg, corresponding to 3300 calories of carbohydrate/kilogram, possibly 2500 calories per kilogram for carbohydrate alone". (37) Read that again: 4700 to 8470 excess calories of fat were required to get the subjects to add a kilogram. Yet it only took 2500 - 3300 calories of carbohydrate to add the same weight.

Finally, in 2002, the Journal of the American College of Nutrition published a study that starts from the observed evidence that people on low carbohyrdate, higher protein/fat diets loose fat more effectively and shows that the level of metabolic burning goes up with these diets. In the paper, "Postprandial Thermogenesis Is Increased 100% on a High-Protein, Low-Fat Diet versus a High-Carbohydrate, Low-Fat Diet in Healthy, Young Women", (53) the authors fed a higher protein, low carb, low fat diet (they specifically used Barry Sears "Zone" diet) to their experimental group and showed they burned up 100% more (twice as much) energy sitting around as the control group that ate a high carbohydrate diet. So while a calorie of fat may be thermodynamically the same as a calorie of sugar, it seems that the body burns far more calories (twice as many) on the fat as on the sugar.

Regardless of whether or not "a calorie is a calorie", it seems apparent that the action in the body is not quite so simple. The variation between humans in their responses to nutrients seems to cover quite a range. While it may be difficult to find an American who has never thought about their weight, of friends who are not consciously dieting and are eating at will, they run the gamut from extremely low to extremely high percentage body fat. If you tend to put your weight on around your midsection (you're an "apple" rather than a "pear"), you likely have a problem with insulin resistance. The action of insulin and other hormones may account for the contradiction between the gross energy content of fat and carbohydrate compared with their dietary effects on human weight. Insulin has been called the main storage hormone in the body. In the presence of large amounts of insulin, produced by eating some carbohydrates, typically simple sugars and starches, the body is primed to store energy into fat. When insulin levels are lower, as would be common in a low carb, higher fat diet, the body would be reluctant to store energy into fat stores, but would be more likely to burn the fat.

Another personal observation. There appears to this writer to be at least two populations of overweight people in America. One population never goes more than a few pounds over their "ideal" weight, and they don't have any trouble getting rid of that weight, by cutting back a few treats, or perhaps taking short walks. Most of the time, they eat what they want when they want. If they put on a few pounds at Christmas, they loose it by Ground Hog's day. I call this "simple overweight". Then there's the population that has it harder. They can easily hit 50 or more pounds over their "ideal". They end up spending their lives trying everything to loose that weight. They've all been put on low calorie diets by well-meaning doctors (some researchers believe that dieting is the root cause of obesity) (42). When those diets didn't work, or they gained back the weight, they started trying more extreme approaches. I call this population "refractory overweight" (where refractory means 1. Obstinately resistant to authority or control. or 2. Resistant to treatment). The medical community insists on believing that treatments for refractory obesity are the same as for simple obesity. Whatever biochemical or hormonal differences are between the populations need to be understood. The experiences of the patients are routinely dismissed by the practitioner, bringing to mind the old saying that "the most important phrase in science isn't "Eureka!!", it's "that's funny...". It seems simplistic to believe that the same treatment that works for a 22 year old who put on a few extra pounds while in college will work for 50 year old who has been dieting for their entire life. Like it or not, if you're "refractory overweight", you probably have metabolic problems that will prevent you from loosing weight the way a "simple overweight" person would. My personal opinion is that you'd probably do better on a low or zero carbohydrate diet.

So do calories count? Of course they do. But they aren't the complete answer. Weight loss is a big, extensive topic, and if I emphasized that, I would miss many of the areas I'd like to cover. But, as in the case of the lipid hypothesis still being advocated by well-meaning workers despite no solid evidence that it's true, many practitioners are far behind the science. Genes responsible for obesity have been found in humans and other species. Metabolic pathways are being mapped. There is an emerging scientific consensus that weight control is highly complex topic and that the old ideas that overweight people are "lazy" or "out of control" are absurd and insulting. If weight loss is your main goal, there is no better introduction to the scientific thinking on the subject, written for the "intelligent layman" than "Adiposity 101", published on the web at: http://www.omen.com/adipos.html

Carbohydrates

Moving on to the other macronutrients, let's hit carbohydrates. We have seen from the Italian studies that eating simple starches is associated with increasing risk for breast, colon, rectal, and other gastric cancers. Sugars are found to be associated with the worst form of breast cancer: that found in pre-menopausal women. On the other hand, the high fiber content of whole grains has been seen to mitigate the effects of saturated fat in the diet. Low fiber carbohydrates are associated with increased risk of colon cancer. Cooked carbohydrates like fried or baked potatoes were recently (2002) found to have elevated levels of acrylamide, a known carcinogen, although the risk from eating it is unknown (46). Finally, just as your mother told you (if you're old enough), sugars and starches are a contributing factor in the start of diabetes (type II, or NIDDM) (40) (43) (50), if not the main factor, although some genetic determination seems to be involved.

Carbohydrate is unique of the three macronutrient classes in that there is no biochemical requirement for carbohydrate in the diet. This doesn't say that there is no requirement for carbohydrate in the body, only that we don't need to eat it. The main energy exchange in the body is via glucose. The brain, for one, runs largely on glucose. There is no requirement for dietary carbohydrate because the body can synthesize enough glucose to meet its needs via a process called gluconeogenesis. (My pet observation, not recognized by anyone, is that what the brain wants, the brain gets. Since the brain runs on glucose, we have this mechanism to ensure we have glucose even though none is in the diet). Note: I was challenged on the first sentence of this paragraph by an emailer years ago. This is first-course biochemistry stuff, but our society is so convinced we need sugar that some won't believe it. See (45) for information.

So while we don't need the glucose in carbohydrate foods, there are many essential nutrients found in fruits and vegetables packed along with carbohydrates that any sane person will say must be part of the diet. In one English study, the only food type found to be associated with longevity was fruit (13) In this article, researchers studied 11,000 health- conscious individuals for 17 years to see what, if any, food is associated with a decrease in mortality. The only food with a positive association was fruit. The subjects had a 24-percent reduction in death from heart disease, a 32-percent reduction in deaths from strokes, and a 21-percent reduction in deaths from all causes. There are no similar associations with the consumption of whole-grain bread, bran cereal, or other starches. In a recent paper published online by the American Chemical Society's Journal of Agricultural and Food Chemistry, berries were shown to inhibit the buildup of LDL cholesterol. (38) Blackberries had the highest effectiveness, "followed by red raspberries, sweet cherries, blueberries and strawberries, according to Edwin Frankel, Ph.D., of the University of California at Davis where the research was done."

Is this really the explanation for the apparent differences between countries with lowfat diets and highfat diets? Is this really what the experimenters are seeing?? As I've said many times, whatever you eat, no matter how much or how little, it's only calories from three things: fat, carbohydrate and protein. Is the difference that explains the low heart disease rates along the Mediterranean and the high rates of Scotland or Finland? Is it the abundant fresh vegetables in the Mediterranean versus the northern countries? (40) It has been said that "the only green leafy vegetable used in Scotland is tobacco". Meanwhile, while the southern Mediterranean peoples have increased the amount of meat and western foods in their diets, their CVD rates have remained low, while their rate of consumption of fresh vegetables and fruits has remained high. Their famously high consumption of fats has perplexed the anti-fat crowd for half a century.

If you are an athlete, or one of the estimated 25% of adults who work out regularly, you have been trained to think that carbohydrate is holy. It is certainly true that during peaks of anaerobic activity your body is fueled almost entirely by carbohydrate. It needs to be remembered, though, that you really cannot be anaerobic for long periods of time. In track events, for example, the 100 meter race is purely anaerobic. The 200 meters is stretching. By the time you hit 400 meters, you can't be entirely anaerobic and have fallen into the upper end of the aerobic range. No one can run a 1500 meter race, let alone a marathon, in a completely anaerobic pace. The human body simply cannot do this.

The question of substrate utilization in exercise is complex. At sedentary power output levels, the energy used (what little there is of it) comes virtually entirely from fat. Between sedentary and your aerobic threshold (AT) the source of the needed energy is a combination of fat and carbohydrate. There is ample evidence that you can train yourself to burn differing amounts of both at various exertion levels. Thus, carbohydrate doesn't have to be the only source of dietary energy used during exercise. Fats will do quite nicely, and amino acids from proteins (especially the branched chain amino acids - BCAAs) also enter the cell's main energy cycle, the tricarboxylic acid cycle (TCA) or Kreb's cycle. (15) French riders in the Tour de France were known a few years ago for eating buttery croissants while riding. The short fatty acids in butter (mostly butyric acid) burn quickly and are not easily turned into body fat. (43)

I would be remiss if I didn't address the concerns of weekend athletes (or real competitors) that eating fat will kill their performance. It will not. Several studies in the last couple of years have documented this. In one study, (24) Leddy, Horvath et al showed that increasing runner's dietary fat intake from 16 to 30 to finally 42% of calories had no effect other than to improve their cholesterol and other lipid profiles. Pendergast, Leddy, Horvath, and Venkatramna (25) showed that runners had more endurance with increasing fat in their diet: "Based on these factors, increasing the fat in the diet (while maintaining adequate intramuscular glycogen) increases VO2max and intramuscular stores of fat (presumably due to increased mitochondrial volume). These two factors result in a significant increase in the time to exhaustion at set levels of exercise (endurance)." In other words, higher dietary fat led to higher endurance. A more recent article (26) Venkatramna and Pendergast show that diets up to 41% calories from fat "....significantly increased endurance run time and had no adverse effects on the level of ..." some markers for inflammatory response they were studying. Although there are many studies that show that fats will not kill your abilities, runners still need to be convinced. Stephen Seiler, Ph.D., of Running Times magazine wrote in his column (27), "We endurance athletes have become preoccupied with carbohydrates. The pre-race carbo-loading prescription of 70 % carbohydrate / 10 % fat / 20 % protein has also become the training diet prescription. We treat dietary fat like a metabolic poison. Some of us act as if each gram of fat ingested will add 30 seconds to our marathon time. That attitude isn't appropriate. " He concludes, "What's the bottom line? Keep some fat in your training diet. Don't forgo an occasional bowl of ice cream, but don't eat like a husky."

Is it possible to produce enough glucose for extended endurance-type athletic events, while on a low or zero carb diet? Sure. I routinely do bike rides up to 50 miles without eating anything along the way, and with no more than around 18 grams of carb in any meal. Is it possible to compete at a world class level without eating carbohydrate? I don't know of enough evidence to say. Certainly, there have been elite-level athletes who competed and won on low carb diets. Triathlete Wendy Ingraham comes to mind. But there are very few competitors at these levels; only a tiny percentage of the population is capable of getting to this level regardless of how hard they train, and their metabolic responses are probably not the same as the rest of ours. When people ask me this, though, they really want to know if they can do better on low carb. Sources like the Gatorade Sports Nutrition Center, and the Powerbar folks put large ads in every athletic magazine telling you that you need carbohydrate (specifically, their carbohydrate), so that leads people to believe that they must eat pounds of carbs for any athletic event. If you're wondering, do the experiment. It will take you a few weeks to adapt to working out without gobbling carbs, so don't try a long event until you've adapted. Only you can tell.

An interesting question is why is there such a human craving for carbohydrate products. Obviously fruits, nuts and berries were energy-rich "easy pickin's" for our paleolithic ancestors, but the first person who ate wheat berries must have been very hungry indeed. Grasses (all grains are grasses) are not part of our natural diet - we are not ruminants and do not have the biological equipment required to digest raw grains. (no reference - if you question this one, I suggest a freshman biology course in any junior college). An interesting paper in the journal "Australian Biologist" suggests the reason may be addiction to compounds in grains (and dairy). To quote, "Indeed, an increasing array of arguments over recent years has suggested that agriculture, far from being a natural and upward step, in fact led commonly to a lower quality of life. Hunter-gatherers typically do less work for the same amount of food, are healthier, and are less prone to famine than primitive farmers (Lee & DeVore 1968, Cohen 1977, 1989)." Their article is long to include much from here, but is worth a read (51). It might explain how carbohydrates were eventually deemed the "holy" food while fat was deemed "evil". It has been my experience that if you question the low-fat "religion" in public, you're likely to be hammered by those who adamantly believe in eating carbohydrate. Is this like taking the drugs from an addict?

Protein

This leaves protein as the remaining macronutrient. If fat is the "bad boy" in conventional wisdom about nutrition, protein is a close second. The current US RDA for protein is a "one size fits all" number. It implies a sedentary, 100 pound housewife needs the same amount of protein as a 300 pound lineman in NFL training camps. Is this reasonable? According to the leading researchers in human protein requirements, such as PWR Lemon and MA Tarnopolsky, no, it is not reasonable. (16, 17, 18, 19) Physically active people need more protein in their diet than sedentary people. Lemon summarizes this work as follows, "'These studies indicate that the RDA (which was determined using subjects who were essentially sedentary) is insufficient for individuals who are involved in a heavy resistance training program.' Lemon goes on to show linear regression analysis to arrive at a protein intake of 1.7 - 1.8 grams of protein per kilogram of bodyweight per day to maintain nitrogen balance while working out with weights." and 1.2 - 1.4 grams of protein per kilogram of bodyweight per day for endurance athletes.(20). (For the metrically-challenged Americans, this is 0.77 - 0.82 g/lb and .54 - .64 g/lb). Presumably, those of us who do some weight work along with our endurance events should go somewhere between those two ranges. It should be noted that this is not extreme amounts of protein. In 1991, Fern (21) compared body mass gains in heavy weight lifters using 3.3 versus 1.3 grams of protein per kilogram of bodyweight per day. After 4 weeks, the 3.3 gram group had larger gains.

The fact that protein requirements go up with exercise (which is known to break down muscle) should be common sense, but it apparently isn't, at least aside from old coaches. This raises the interesting question of why modern writers are so opposed to protein. The best explanation I've come across (20) attributes it to several reasons. The one I would like to address is the commonly held belief that protein consumption leads to kidney disease. This is a bad reading of the experimental evidence which simply says that those with certain existing diseases can improve their health by reducing protein intake. It says nothing about healthy people needing to reduce their protein intake. The interested reader is referred to (20).

There are reports that protein is associated with certain cancers. Again, these tend to be population studies of vastly different cultures with vastly different lifestyles. The caveats mentioned above (re: Japanese breast cancer rates) apply equally. The flip side of this is that protein has been correlated with decreasing blood pressure (28), that is, as protein consumption as percent of calories goes up, blood pressure went down.

Since all of the amino acids that the body requires for protein synthesis can not be synthesized by the body, the 20 essential amino acids must be obtained from the diet. But there are complicating factors. The bioavailabilities of proteins are not all created equally. Vegetable sources are less available, and therefore more must be eaten (around 1/3 more, as a sloppy general rule). Lean meats, such as chicken, turkey and many types of fish, are the best protein sources. Eggs are also an excellent source of high quality protein (i.e., containing all the essential amino acids).

Conclusions - So What's to Eat?

This leads me to my conclusions on what and how to eat. This is going to ignore issues like food sensitivities and allergies, intolerances and other problems. First of all we need to get some things straight. Bacon double cheeseburgers are not on anyone's acceptable diet! (Anyone who would say it's okay to eat the burgers, cheese and bacon wouldn't allow the buns ...) Whole pizzas are not on anyone's acceptable list (anyone who would allow that much dough wouldn't allow the cheese and olive oil...). Candy isn't, either (although there is precious little difference, if any, between a candy bar and a rice cake after a few seconds of digestion). It needs to be said that many things that are widely available in our society, that taste wonderful (which is why they are widely available) should not be eaten regularly. Once in a while is okay; but "a while" is not every day or even every week.

My starting assumption is that there is only so much that we can eat. My next assumption (pretty obvious) is to eat only the things that are essential. Now essential means something specific to the biochemist. It means that we can't synthesize it and must get it in our diets. We need to make sure we get the essential fatty acids, the essential amino acids and then add carbohydrate sources for the fiber and micronutrients they bring. If we require a certain amount of protein, based on our activity, then we need to eat that. This is what "essential amino acids" means - we require them in our diet! The alternative is going into protein malnutrition, where your body literally digests itself. Complete proteins are easier to deal with than vegetarian sources, but vegetarian sources are fine. It may be better to consume lean meats, as close to fat free as possible, so that we can consume monounsaturated fats in the place of the meat fats. Turkey and chicken breasts come about as close to fat free as you will find. Still, dietary boredom can result, and other sources of protein are fine, if fiber intake is kept high.

So number one is to figure out how much protein you need to eat. If you're lean already, use Lemon's data for your protein requirements, above. If you're not lean (men over 20% body fat), figure your lean body mass (there are online calculators) and use that number to figure your protein requirements.

Next, we need to decide what percent of our diet will be fat, that is, if we even care (remember Willett's conclusions, above, found in (12)). If you do, there appears to be no backing for going much below 30 to 35% calories from fat, as recommended by the WHO, the AHA, and others. The fats should be mostly saturated and monounsaturated - found in olives, avocados, and nuts. Saturated fat like butter seems a safer alternative to margarines. Oily fish, like salmon, should be eaten regularly. We should avoid trans-unsaturated acids, often referred to as "partially hydrogenated" oils, as much as possible and strive for higher intakes of omega-3 fatty acids. These are found in oily fish, and flax seed oil, to name a couple. I know that a big deal has been made about margarines with monounsaturated oils and pine sterols, but I will avoid them until safety is a bit more established.

Now we're left with carbohydrates. Some would suggest we simply fill in the remainder of our required calories with carbohydrate. There is a problem with this, though. With the exception of starches and refined sugars, carbohydrates are very filling. I believe there is evidence to support staying away from starches and refined sugars; at the very least, they are not a benign food that can be eaten without regard to any possible consequences. There is ample evidence that carbohydrates alter lipid profiles in ways that are not good. (29-33) (more studies are listed in (35)). There is also ample evidence that starches and simple sugars link to certain cancers. Finally, starches and simple sugars tend to have high glycemic index values, that is, they tend to produce large spikes of blood sugar followed by large spikes of insulin. These have both been linked to causing diabetes. (50) If you are going to minimize the amount of starches you eat, it may not be possible to eat enough calories from carbohydrates. If you are trying to cut calories and loose weight, then you absolutely must get the most nutrient dense foods you can. If you find you can't get enough calories from non-starchy fruits and vegetables, extra monounsaturated fat may be the best choice.

So we are left with a diet that strives to provide adequate amounts of protein, for essential amino acids, essential fatty acids from nuts, olive oil, salmon, avocados and the like, all of which is balanced with nutrient dense fruits and vegetables. This ends up being essentially Barry Sears's Zone program. You eat the protein you require, add some monounsaturated fat, then add carbohydrates in a reasonable amount. My rule of thumb is to eat Sears recommended amount of protein - he is using Lemon's data and is consistent with the best peer-reviewed experiments. Eat Sears' recommended amount of fat for his diet. As for carbohydrates, in general, I eat all the fruits and vegetables I can, which can leave you short of carbohydrates if you follow a strict 40-30-30. If I feel like having bread, I'll only eat whole grain, and very little of it so I can still have some fruit. Same if I eat a sweet potato, or sweet corn. But these are foods I don't eat often. If you eat too much starch, you can't get the benefits of the fruits and vegetables. You can only eat so much. Nothing is forbidden, but everything has a consequence.

Let me Leave you with Some Thoughts

Finally, if I can leave you with one thought, keep the idea I stressed about proportions or percentages of calories in mind when you read stories about the health benefits of something. Are the results from eating what they're telling you to eat, or not eating something else? For example, if a report said that eating soy led to some improvement, was it from eating the soy or not eating something else? If a report says that a different population in a different country has a different rate of some disease and then says it's the fat, or the soy, or the green tea, or some other specific thing, how do they know that? What are they not eating or not drinking or not rubbing into their bellies? Is their explanation the only one that fits? Let's go back to the famous Japanese population studies that show breast cancer rates are lower than in the US - the reports immediately suggested it was their lower dietary fat. How did they know that? How do they know it wasn't the wasabi on their sushi, or a thousand other variables? Is the Japanese culture and population so homogeneous that the same rates apply to everyone? If not, what's the difference?

When I first started running about 25 years ago, much was made about a study that attempted to compare heart attack rates in marathon runners with the general population. The researchers discovered that no marathon runner had ever had a heart attack. The conclusion they reached was that marathon running made you immune to heart disease. This, as we now know, is rubbish. As more and more people, with their checkered pasts, started running, it wasn't too long before marathon runners started having heart attacks, too. Theirs wasn't the only explanation. This is a classic case of what statisticans call "selection effect", one of the most common mistakes in science. What they should have concluded was that the population of runners was different from the general population, and that something in this group's life prevented heart attacks. Think about it: running is pretty commonplace today, but this was in the early 1970s and the people they were studying were a self-selected group of dedicated runners who were in the sport long before it was a fad, and long before any doctor or medical group ever recommended activity. Can the same be said for other self-selected groups like vegetarians or vegans? When you read that vegetarians have a lower rate of some disease, think that not too long ago, this was a very, very marginal lifestyle. They still number only a few percent of the population. Is it the case that anyone that would become a vegetarian 30 years ago (and stay one) would have other characteristics that make them different from the general population?

When I read things like reference (40) on the history of the lowfat madness, it appears to me as the triumph of hope over science. Or - more correctly - the triumph of FDA politics over science. Time and time again, if researchers had just looked at their data, instead of explaining them away and trying more experiments to prove their notions were correct, the fad would have been stopped. We're talking about real lives, here. Real people have suffered from or died of cancers, or suffered from diabetes, osteoporosis and other real afflictions by altering their diet needlessly. Real lives have been ruined by these researchers' zealous pursuit of something that wasn't there. Gee, thanks.

Ya'll take care out there.

1. Willett, W. C. (1998). Nutritional Epidemiology, Oxford University Press, New York.

2. Kurilla, M. G., MD, Ph.D., (1998) Private communication

3. Dr. Laura A. Corr (MB, BS, MRCP, Ph.D., FESC, Consultant Cardiologist, Guy's and St. Thomas' Hospitals, London U.K.) and M.F. Oliver of the National Heart and Lung Institute in London. January (1997) (Vol. 18) European Heart Journal. Published online at http://www.omen.com/corr.html

4. Ascherio A, Rimm EB, Giovannucci EL, Spegelman D, Stampfer M, and Willett WC. "Dietary fat and risk of coronary heart disease in men." Brit J Med 313: 84-90 (1996)

5. Frank B. Hu, Meir J. Stampfer, et al, NEJM, November 20, 1997, Volume 337, Number 21, "Dietary Fat Intake and the Risk of Coronary Heart Disease in Women"

6. David J. Hunter, Donna Spiegelman, et al, "Cohort Studies of Fat Intake and the Risk of Breast Cancer -- A Pooled Analysis", (1996), N Engl J Med 1996;334:356-61.

7. Francheschi S, Favero A, Decarli A, et al, "Intake of macronutrients and risk of breast cancer." (1996) Lancet 347: 1351-1356

8. Witte JS, Ursin G, Siemiatycki J, Thompson WD, Paganini-Hill A, Haile RW. "Diet and Premenopausal Breast Cancer Risk", Breast Cancer Res Treat, 1997 Feb;42(3):243-251

9. La Vecchia C, Negri E, D'Avanzo B, and Franceschi S. "A Case-Control Study of Diet and Gastric Cancer in Northern Italy." Int J Cancer 40: 484-489 (1987)

10. Bidoli E, Franceschi S, Talamini R, Barra S, and La Vecchia C. "Food Consumption and Cancer of the Colon and Rectum in Northeastern Italy." Int J Cancer 50: 223-229 (1992)

11. Robert H. Knopp, M.D. JAMA, Nov 12, 1997, (1997;278:1509-1515)

12. Published online originally at: http://www.healthnet.org/programs/procor/procor-commentary-hma/msg00007.html Attempts to find it again in 2002 bring "Error 404".

13. Key T, Thorogood M, Appleby P, and Burr M. "Dietary Habits and Mortality in 11,000 vegetarians and Health Conscious people." Brit Med J 313: 775-779 (1996)

14. Kris-Etherton, Penny, Ph.D, Dist. Prof. of Nutrition at The Pennsylvania State University, and Sabate, Joan, Ph.D., Assoc. Professor and Nutrition Department Chair at Loma Linda University. "Nuts in a Healthful Diet," part of the 1998 Experimental Biology annual meeting of the Federation of American Societies for Experimental Biology - FASEB.

15. Kurilla, M. G., MD, PhD, (1996), ENERGY SUBSTRATE UTILIZATION DURING EXERCISE, web-published at http://www.zonehome.com/zlibstar.htm

16. Lemon, PWR. (1992). Effect of exercise on protein requirements. In Williamsc, JT Devlin (eds), Food, nutrition and sports peformance. E&FN Spon, London, pp65-86.

17. Lemon, PWR. (1996). Is increased dietary protein necessary or beneficial for individuals with a physically active lifestyle? Nutr Rev 54:S169-S175.

18. Tarnopolsky, MA, SA Atkinson, and JD MacDougall. (1992). Evaluation of protein requirements for trained strength athletes. J Appl Physiol. 73:1986-1995.

19. Tarnopolsky, MA, JD MacDougall, and SA Atkinson. (1988). Influence of protein intake and training on nitrogen balance and lean body mass. J Appl Physio l64:187-193.

20. Kurilla, M. G., MD, PhD, (1996), PROTEIN REQUIREMENTS IN HUMANS web-published at http://www.zonehome.com/zlibstar.htm

21. Fern, EB, RN Bielinski, and Y Schultz. (1991). Effects of exaggerated amino acid and protein supply in man. Experentia 47:168-172.

22. Erickson, Kent L, "Is There a Relationship Between Dietary Linoleic Acid and Cancer of the Breast, Colon or Prostate?", Am Jrnl of Clin. Nutr, 1998; 68:507

23. Erikson, KL and Hubbard, NE, "Dietary Fat and Tumor Metastasis", Nutr. Rev, 1990; 48:6-14

24. Leddy J, Horvath P, Rowland J,and Pendergast D., "Effect of a high or a low fat diet on cardiovascular risk factors in male and female runners." Medicine and Science in Sports and Exercise 29:17-25 (1997)

25. Pendergast DR, Horvath PJ, Leddy JJ, Venkatraman JT, "The role of dietary fat on performance, metabolism, and health". Am J Sports Med 1996;24(6 Suppl):S53-S58

26. VENKATRAMAN, J. T. and D. PENDERGAST. "Effects of the level of dietary fat intake and endurance exercise on plasma cytokines in runners". Med. Sci. Sports Exerc., Vol. 30, No. 8, pp. 1198-1204, 1998.

27. Seiler, Stephan, Ph.D. "PARTIAL ZONE DEFENSE -- Why your racing diet shouldn't be your training diet", Running Times Magazine, 9/96 (?) (found reprinted on the web at http://www.zonehome.com/zlibstar.htm)

28. D Chee, R Nichols, P Elliott, London, UK, The British Dietary and Nutritional Survey, "INVERSE RELATIONSHIP OF DIETARY PROTEIN WITH BLOOD PRESSURE OF INDIVIDUALS - FURTHER ANALYSIS OF THE DIETARY AND NUTRITIONAL SURVEY OF BRITISH ADULTS", 1996

29 Jeppeson, J., et. al. "Effects of low-fat, high-carbohydrate diets on risk factors for ischemic heart disease in postmenopausal women" . (American Journal of Clinical Nutrition, 1997;65:1027-33.) Shows that low-fat, high-carbohydrate diets (15% protein, 60% carbohydrate, 25% fat) increase risk of heart disease in post-menopausal women over a higher fat, lower carbohydrate diet (15% protein, 40% carbohydrate, 45% fat).

30. Olefsky JM; Crapo P; Reaven GM. "Postprandial plasma triglyceride and cholesterol responses to a low-fat meal". (American Journal of Clinical Nutrition, 1976 May, 29:5, 535-9). Says that low-fat, high-carbohydrate meals lead to increases in plasma triglyceride levels.

31. Ginsberg H et. al. "Induction of hypertriglyceridemia by a low-fat diet." J Clin Endocrinol Metab, 1976 Apr, 42:4, 729-35. Shows low-fat high-carbohydrate diets can induce hypertriglyceridemia.

32. Liu GC; Coulston AM; Reaven GM. "Effect of high-carbohydrate-low-fat diets on plasma glucose, insulin and lipid responses in hypertriglyceridemic humans". Metabolism, 1983 Aug, 32:8, 750-3. In which it was shown that in humans with existing trouble with high triglycerides, low-fat, high-carbohydrate diets significantly increased metabolic risk factors for coronary artery disease.

33. Coulston AM; Liu GC; Reaven GM. "Plasma glucose, insulin and lipid responses to high-carbohydrate low-fat diets in normal humans". Metabolism, 1983 Jan, 32:1, 52-6. In which it is shown that low-fat, high carbohydrate diets in normal human males caused changes in insulin, TG, and HDL-cholesterol concentrations which have been associated with an increase in incidence of coronary artery disease.

34. Letters to the editor following: Robert H. Knopp, M.D. (JAMA. 1997;278:1509-1515)

35. Lichtenstein, Alice H., DSc; Van Horn, Linda, Ph.D, R.D., "Very Low Fat Diets", Circulation. 1998;98:935-939. Currently on the web. Go to http://www.ahajournals.org/ and click on "Search". You can find it by the authors or the Volume and page (98, 935).

36. Department of HEW Pub NIH 75-708, GovernmentPrinting Office, 165-86

37. Am J of Clin Nutr 1992;56:217S-23S

both references 36, 37 and the supporting paragraph are in "Adiposity 101" at http://www.omen.com/adipos.html

38. Journal of Agricultural and Food Chemistry, online edition, 9/12/98

39. Walter C. Willett, "Is Dietary Fat a Major Determinant of Body Fat?" American Journal of Clinical Nutrition 67(Sup): 556S-562S 1998

40. Taubes, Gary, "The Soft Science of Dietary Fat", Science Magazine, American Association for the Advancement of Science, March 2001. A fascinating look by an excellent science writer at the politics, business-interest and wishful thinking that led to the 50+ year national obsession with fat in the diet. Available online at: http://www.second-opinions.co.uk/taubes.html

41. Kekwick, A., Pawan, G.L.S., "Calorie Intake in Relation to Body-Weight Changes in the Obese," The Lancet, July 28, 1956, pages 155-161.

42. "dieting may be the major cause of obesity", -Jean-Paul Deslypere, University of Ghent Professor of human nutrition, taken from http://www.omen.com/adipos.html

43. Byrnes, Stephen, ND, RNCP, "Diet and Heart Disease, It is not what you think", online source, "NursingCEU.com", June 11, 2000 http://www.nursingceu.com/NCEU/courses/diet/

44. Enig, Mary G. and Sally Fallon, "The Oiling of America", NEXUS Magazine, December 1998-January 1999 and February-March 1999; available at http://us.altnews.com.au/nexus/OilingAmerica.1.html

45. http://web.indstate.edu/thcme/mwking/gluconeogenesis.html The top level of this website has information on many different biochemistry subjects. It is not for the layman! It assumes some college-level expertise in organic chemistry.

46. Center for Science in the Public Interest, http://www.cspinet.org/new/200206251.html

47. Press Release, August 23, 2000, United States Center for Disease Control, online at http://www.cdc.gov/nccdphp/dnpa/press/archive/diabetes_increase.htm

48. Uldall PR, et al., the Lancet, 1974; ii: 514.

49. Pearce M L, Dayton S. "Incidence of Cancer in Men on a Diet High in Polyunsaturated Fat", the Lancet, 1971; i: 464.

50. An excellent reference on the glycemic index and why it's important is found on Rick Mendosa's web site at http://www.mendosa.com/gi.htm There are many other excellent resources on his pages for both the diabetic and those living with family members who are diabetic.

51. Wadley, Greg, and Martin, Angus, "The origins of agriculture - a biological perspective and a new hypothesis", Australian Biologist, 6:96-105, June, 1993, online at http://www.vegan-straight-edge.org.uk/GW_paper.htm

52. Taubes, Gary, "What if It's All Been a Big Fat Lie?", The New York Times Magazine, 07/07/2002

53. Carol S. Johnston, PhD, FACN, Carol S. Day, MS and Pamela D. Swan, PhD, "Postprandial Thermogenesis Is Increased 100% on a High-Protein, Low-Fat Diet versus a High-Carbohydrate, Low-Fat Diet in Healthy, Young Women", Journal of the American College of Nutrition, Vol. 21, No. 1, 55-61 (2002), Published by the American College of Nutrition. This study is at: http://www.jacn.org/cgi/content/full/21/1/55