Common Myths About Low Carbohydrate Diets

by Anthony Colpo

Myth 1: 'Low-carbohydrate diets cause heart-disease'

Proponents of the high-carbohydrate, low-fat diet repeatedly contend that saturated fat and cholesterol are the major dietary contributors to coronary heart disease (CHD). They claim that replacing these nutrients with carbohydrates will lower one's risk of cardiovascular disease. Research does not back this view - in fact it contradicts it.

The theory that saturated fat raises cholesterol levels, and that these elevated cholesterol levels lead to heart disease is known as the "lipid hypothesis". The origins of this theory can be traced back to the early 1900's, when Russian researcher M.A. Ignatovsky induced fatty deposit build-up in rabbit arteries by feeding them large amounts of animal foods. Protein was initially blamed, but a few years later the spotlight was cast on cholesterol (1). Animal experiments are frequently cited in support of the saturated fat/cholesterol CHD theory , but as most individuals wishing to avoid heart disease belong to the omnivorous human species, it should be pointed out that these artery clogging experiments are successful only in herbivorous animals. Feeding large amounts of fat and cholesterol to carnivorous animals fails to induce such pathological changes, except in dogs that have had their thyroids surgically removed or suppressed by pharmaceutical means (2). The lipid deposits seen in animals also bear little resemblance to the atherosclerotic plaques seen in humans, which are comprised not just of cholesterol and fatty acids, but also white blood cells, calcium and fibrous scar tissue. The relevance of animal cholesterol-feeding studies to humans ranks somewhere between zero and zip.

Nonetheless, in the 1950's a researcher named Ancel Keys, armed with the knowledge that fat and cholesterol produced lipid build-up in the arteries of certain animals, proposed that the same dietary constituents were causing heart disease in humans. Keys plotted the coronary heart disease (CHD) death rates from a mere six countries on a graph, and was able to show an almost perfect correlation between fat consumption and CHD mortality (3). However, Keys had hand-picked his countries; data was actually available for 22 countries at the time, and when another group of researchers later plotted the data from all these countries on a graph, Key's correlation vanished into thin air (4). Keys, however, was on the nutrition advisory committee of the powerful American Heart Association, and his erroneous theories were officially incorporated into AHA dietary guidelines in 1961 (5) A long tradition of selectively citing epidemiological research of questionable validity had begun in earnest.

Epidemiological research is the study of disease trends among certain populations. It can involve comparisons between inhabitants of different countries, or of those living in the same country, state, or city. Such population-based research can be useful in identifying potentially fruitful leads for further research, but epidemiological data should never be used as conclusive proof of anything. Due to the presence of so many other confounding factors, it is at best circumstantial. One of the arguments commonly used in support of the lipid hypothesis is that countries with high levels of saturated fat consumption have the highest levels of CHD. Sure they do - but they also have the highest consumption of sugar, refined carbohydrates, polyunsaturated vegetable oils, hydrogenated vegetable fats, uncultured milk products and the lowest levels of physical activity, all of which have been implicated in the pathogenesis of CHD. To conclusively prove that saturated fat causes CHD, we need to conduct randomized, clinical trials comparing low-saturated fat diets with saturated fat-rich diets, in which all other possible confounding variables are controlled. Then, and only then, are we in a position to come to conclusions about the role of saturated fat in CHD with any degree of confidence. Numerous dietary trials have indeed been performed over the years, but supporters of the lipid hypothesis rarely mention them, instead focusing on circumstantial epidemiological data. There's a reason for this, which we will discuss in a moment. But first, lets look at some of the notable exceptions to the supposedly strong epidemiological association between saturated fat and CHD.

The Masai are a warlike tribe residing in East Africa who for the last 10,000 years have existed as cattle-herding nomads. Their sustenance is derived from large amounts of high fat milk and meat, which may be supplemented by fresh cattle blood in the dry season. Thanks to their copious consumption of high fat animal foods, Masai males ingest a hefty 300g of mostly saturated fat on a daily basis. If the lipid hypothesis had any merit, the Masai should be riddled with obesity and CHD, but when Professor George Mann from Vanderbilt University visited the Masai in the 1960's he found a slim, robust population free of CHD. When given treadmill tests, several of the tribesmen achieved performances superior to those of Olympic champions. Autopsy examinations on deceased Masai males showed an almost complete absence of atheromas, the advanced atherosclerotic lesions implicated in coronary blockage. The Masai also recorded one of the lowest average cholesterol levels ever measured in any population (6-8). A few years later, another group of American researchers performed similar autopsy examinations on deceased Masai and confirmed "the paucity of atherosclerosis" documented by Mann (9).

Another east African tribe, the Samburus, have an even higher fat intake than the Masai. Whilst they eat less meat, the Samburus tend to consume far more milk than the Masai. Samburu warriors and elders may consume between 4.5 to 7 liters of high fat milk in a single sitting. During the wet season when grass is abundant and their cattle consequently produce more milk, they will do this twice a day. This amount may drop to a "mere" 2 to 3.5 liters daily during the dry season. As a result of their copious milk intake, the slender Samburu males consume up to a whopping 400g of animal fat daily. Again, if the lipid hypothesis had any merit, the record-breaking fat intake of the Samburus would be accompanied by sky-high cholesterol levels and astronomical rates of heart disease. Researchers found the exact opposite. Similar to the Masai, the slim, athletic Samburus displayed both low serum cholesterol levels and a notable absence of CHD (10).

The residents of Pukapuka and Tokeluau, two tiny Pacific atolls, were also examined in the 1960's. Due to the daily consumption of coconut, the Pukapukans and Tokelauans obtained 35% and 53% of their calories from fat, respectively. Only a few grams of their daily fat intake was in the form of unsaturated fats - the rest was saturated. "Despite" their high consumption of saturated fat, residents of both islands enjoyed a complete absence of CHD and a remarkably low incidence of other degenerative diseases (11).

Perhaps you are thinking that the Masai, Samburu and Pacific islanders are blessed with some sort of genetic protection against the allegedly harmful effects of saturated fat. Hardly. Studies show that when the Masai migrate to Nairobi where they are exposed to a more "refined" diet and sedentary lifestyle, their cholesterol levels rise, discounting the proffered notion that their low cholesterol levels were a manifestation of some sort of advantageous genetic aberration (12). When Pukapuka and Tokeluau residents moved to New Zealand, where they were similarly exposed to processed foods and a more sedentary lifestyle, they experienced a marked increase of gout, diabetes and other degenerative disorders (13-16).

You may also be thinking that a high level of physical activity was responsible for the low rate of CHD amongst the aforementioned populations. The Masai, for example, walk up to 30 miles a day. That no doubt helped, but not because it was countering any purported harmful effects of saturated fat. After all, heavy physical activity did not help the population of North Karelia, Finland in the 1960's. Despite a high proportion of lumberjacks and farmers, residents of this isolated community suffered one of the highest CHD rates in the world. The population of St. Helena, where motorized transport was rare and the residents were forced to transverse the hilly landscape by foot, was also observed to suffer from a high rate of CHD. Fat consumption was relatively low in St. Helena, but sugar consumption was high (17).

One of the more fashionable current dietary theories is that of the "Mediterranean Diet", which attributes the low rate of CHD in Southern Europe to the frequent intake of olive oil, fruits, vegetables, legumes - and a supposedly low level of saturated fat consumption. There's no arguing the benefits of fruit and vegetables, but there is a glaring contradiction to the theory that low saturated fat consumption contributes to the low rate of CHD in the Mediterranean. That contradiction is the population of France, which enjoys the lowest incidence of CHD in Southern Europe whilst simultaneously enjoying the highest saturated fat intake. Red wine intake has been posited as an explanation for this alleged "paradox", but does not satisfactorily explain the difference. After all, the per capita wine consumption of the Italians, fond of their "vino rosso", is virtually identical to that of the French yet they suffer from a notably higher rate of CHD (18).

Numerous other exceptions to the epidemiological link between saturated fat and CHD, while rarely mentioned in anti-cholesterol and anti-saturated fat propaganda, have been recorded in the scientific literature. But let's cut to the chase - has saturated fat restriction been shown to reduce the incidence of CHD in controlled, randomized, blinded clinical trials? If saturated fat is such a dangerous substance, the benefits from its restriction should be readily demonstrable in controlled experiments with human volunteers.

The gold standard of clinical research is the double-blind study, where both investigators and participants are unaware of who is receiving the placebo and who is receiving treatment. This acts as a safeguard against researcher bias and eliminates the possibility that a placebo effect is responsible for any improvement amongst those receiving treatment. When seeking to release a new drug that may eventually be used by thousands, even millions, of people, drug manufacturers must be able to demonstrate the efficacy and safety of the proposed pharmaceutical. A new drug application that sought approval simply on the basis of an allegedly "strong epidemiological association" would no doubt be greeted with hearty laughter by regulatory authorities. Pharmaceutical manufacturers must prove the efficacy of their wares with data from double-blind clinical trials. Let's see what happens when we demand the same standard of proof from those promoting the notion that saturated fat and cholesterol cause heart disease.

Numerous trials have been conducted since the early sixties, when the AHA began pushing the idea that saturated fat was involved in the pathogenesis of CHD. Only three of these trials were of the double-blind variety - the National Diet-Heart Study , the Los Angeles Veterans Administration Study and the Minnesota Survey (19-21). All of these trials involved the substitution of highly saturated animal fats with polyunsaturated vegetable fats (well-known for their ability to lower blood cholesterol levels) and all completely failed to show any benefit from the reduction in saturated fats. This was despite the fact that saturated fat restriction consistently lowered cholesterol levels among the treatment groups of these studies. The Veterans Administration Study did show a noteworthy decrease in CHD fatalities among the treatment group, but the results were biased by a significantly higher proportion of heavy smokers in the control group. Despite this advantage to the treatment group, they still suffered a significantly higher frequency of cancer deaths which neutralized the mortality reduction from CHD. Total mortality between the two groups after 8 years was virtually identical. One has to wonder what the result would have been had there been a similar proportion of heavy smokers in both treatment and control groups. The bottom line is that when the gold standard of proof from tightly-controlled, double-blind trials is demanded of those propagating the saturated fat and cholesterol myth, they cannot provide any - which, of course, is why they rely so heavily on notoriously unreliable, selectively-cited epidemiological studies.

It should be noted that the only CHD dietary intervention trials showing convincing benefits are those that involved an increase in omega-3 fatty acid intake (which can be obtained by eating fatty fish or taking fish oil capsules), fruit and vegetable consumption, or both (22-27). One of these, the DART trial, found a 30% reduction in mortality among men who were randomized to a group instructed to either eat more fish or supplement with fish oil. Another group told to replace saturated fats with polyunsaturated fats experienced no change in death rates, and a small mortality increase was observed among men told to increase their fiber intake. In a blatant contradiction of the lipid hypothesis, the fish advice group enjoyed the greatest decrease in mortality whilst simultaneously experiencing an increase in their average cholesterol levels (22). In the Lyon Diet Heart Study, the experimental group was advised to increase consumption of root vegetables, green vegetables, fish and fruit, and were supplied with a special canola-based margarine that was higher in monounsaturated and omega-3 fatty acids than regular margarines. The study was originally intended to follow the patients for 4 years, but death rates diverged so dramatically early on that researchers decided it would be unethical to continue and called an end to the trial. After an average follow-up of 27 months, the overall death rate of the control group was more than twice that of the experimental group. Again, the difference could not be explained by cholesterol-lowering; both total and LDL cholesterol levels of the treatment and control groups were virtually identical throughout the entire study. Those in the treatment group, however, did show significantly higher blood levels of omega-3 fatty acids and antioxidants (23). In the massive GISSI-Prevenzione study in Italy, subjects who were given modest doses of fish oil experienced a significant decrease in CHD deaths. The mortality benefits of fish oil appeared early on in the study - as did a small increase in LDL cholesterol levels (according to those that promote the lipid hypothesis, LDL is supposedly the "bad" cholesterol that should be the main focus of lipid-lowering efforts).

Even the reductions in CHD deaths seen in trials with cholesterol-lowering statin drugs occur independent of any cholesterol-lowering effect - in fact, in the recent PROSPER trial those with the highest LDL levels enjoyed the highest survival rate (28-36). If you have been brainwashed into believing that blood cholesterol reductions via saturated fat restriction will lower your risk of CHD, understand that there is no credible scientific evidence to support such a strategy - you would be far better off increasing the antioxidant content of your diet by upping your intake of fresh fruits and especially vegetables, and consuming omega-3-rich foods on a regular basis, in the form of either fatty fish or fish oil supplements (highly-hyped vegetable sources of omega-3 fats such as flax oil have not shown any ability to lower CHD mortality in randomized trials). Avoiding a diet with a high glycemic load is also paramount. Glycemic load is the combined product of both glycemic index and total carbohydrate intake (the glycemic index is a measure of how high and how quickly a particular food can raise blood glucose levels). Long-term adherence to a diet with a high glycemic load typically leads to chronically elevated blood sugar levels, and is a sterling way to develop disorders in blood sugar metabolism such as Type-2 diabetes. Even relatively brief spikes in blood sugar can lead to dramatic increases in glycation, a process in which both free radicals and highly-damaging protein-glucose "cross-links" are formed (37). Both of these agents damage vital organs and tissues, including those that comprise the cardiovascular system. It is no coincidence that diabetics have 2-4 times greater risk of suffering CHD than the rest of the population.

If you want to maximize your chances of avoiding CHD, a diet high in antioxidants and phytochemicals, a low glycemic load, and regular consumption of omega-3 fats, appears to be just what the (smart) doctor ordered. A low carbohydrate diet based on paleolithic food choices, that is, a diet based on free-range animal products and low carbohydrate, low-glycemic plant foods, fits the bill quite nicely. So go ahead, eat your steak and salad!

Myth 2: 'Low-Carbohydrate Diets Contain Too Much Fat, and Fat Makes You Gain Weight

Some folks have been so inculcated with the simplistic "fat makes you fat" theory that they just cannot believe a diet high in fat can lead to a loss of bodyfat. The fact is, high fat diets can result in spectacular fat loss - as long as carbohydrate intake is kept low. Eat a diet that is high in both fat and carbohydrate and your bodyfat percentages will head north real quick! (38)

On a high-carbohydrate diet the body will burn predominantly glucose for fuel. On a high-fat, low-carbohydrate diet, however, the body will burn mainly fat - both dietary fat and bodyfat, which is exactly what every aspiring dieter needs. This is not wishful thinking on the part of low-carb proponents - it is a basic physiological fact (39).

Some high-carb proponents, when faced with the fact that low-carbohydrate diets can indeed cause weight loss, resort to some rather ridiculous claims. One common claim is that the weight loss seen on low-carbohydrate diets is simply 'water loss'. Such critics want you to believe that when someone loses 30 pounds on a low-carb diet, the entire weight loss is purely water!

This claim is absurd, but seems to get a lot of mileage, so I'll address it quickly. When commencing a weight-loss regimen, the first few pounds lost are usually shed water. However this short-lived effect is by no means unique to low-carb diets. While the initial magnitude of this effect is stronger on low carb diets, it fails to account for the significant longer-term weight loss experienced by many low-carbohydrate dieters (40-44).

Another oft-repeated claim is that low-carb diets cause excessive muscle loss. I don't know where this myth began, but it could not have come from anyone familiar with the literature - most of the studies comparing low carb diets with high carb regimens have shown that a similar portion of the weight lost in both groups was from fat, and some have actually shown proportionately greater fat loss, and less muscle loss, on low carbohydrate diets.

Another common claim is that low-carb diets are only effective for weight loss because they contain less calories than your typical high-carb diet. That's a bit like saying they work, but only because they work. Some folks do find higher-fat foods more satiating, and consequently consume less calories (45). However other studies have found subjects on low-carb diets experienced greater fat loss at higher caloric intakes than those on high-carbohydrate diets.

The Standard Western Diet (SWD) is typically high in both fat and carbohydrate - and often leads to obesity. High-carb advocates immediately blame fat as the culprit responsible for body fat increases. Their argument seems to be re-inforced when some individuals lower their fat intake and lose weight. However, lowering fat in a high-fat, high-carbohydrate diet will reduce calories, which will go some way towards assisting weight loss.

Of course, we know there is another alternative to lowering fat intake - lowering carbohydrate intake! What happens when we directly compare weight loss on a low-carb, high-fat diet with a low-fat, high-carb diet? Studies comparing fat loss on calorie-restricted low carb diets with that from similarly-restricted high-carb diets show that low carb diets produce similar, and in many instances superior, body composition changes. Let's take a look at some of the more recent studies...

A 1999 study compared the effects of a high protein, low carbohydrate diet with that of a high carbohydrate, low protein diet in thirteen hyperinsulinemic obese men. Fat intake was kept at 30% on both diets, which were followed for four weeks. Average weight loss was higher in the low carbohydrate group. In addition, 71% of those in the low carbohydrate group achieved a weight loss of 7kg or more, compared to only 16% in the high carbohydrate group. Insulin levels dropped in both groups, but were reduced to within the normal range only among those following the low carbohydrate diet (46).

The effects of a low carbohydrate diet, similar to that popularized by the late Dr. Robert Atkins, in obese 12-18 year olds was examined by Sondike and colleagues. Sixteen adolescents ate a diet in which carbohydrates were restricted, but no limits were placed on protein and fat intake. A control group was instructed to eat a low fat diet emphasizing fat-free dairy, fruits, vegetables and whole grains. Subjects in both groups were recommended to take a multivitamin supplement and to exercise for 30 minutes 3 times per week. After 12 weeks, the sixteen subjects eating a low carbohydrate diet lost almost 2˝ times more weight than the fourteen eating a high carbohydrate control diet (9.9kg versus 4.1kg). This greater weight loss occurred despite the fact that those on the Atkins-style diet consumed two-thirds more calories than the low fat dieters (1830 versus 1100 calories per day). No abnormalities were seen in serum electrolytes or kidney and liver function in either group. Eight patients in the low carbohydrate group, but only 1 patient in the low fat group, completed 1 year of follow-up; none of these patients had gained back the weight they had lost (47).

Fifty-three obese women were randomized to either an Atkins-style low carbohydrate diet or a calorie-restricted high carbohydrate diet by Brehm and co-workers. The women in the low carbohydrate group were instructed to eat freely - no restriction on total caloric intake was imposed. The women in the low fat, high carbohydrate group were placed on a reduced-calorie diet consisting of 55% carbohydrate, 15% protein, and 30% fat. All the women participated in both individual and group counseling sessions to encourage compliance, and all were instructed to maintain their usual level of activity. Throughout the study, women in the low fat group consumed an average of 1707 calories daily. Despite no calorie-restriction being demanded of the low carbohydrate dieters, the women in this group averaged only 1608 calories per day. Both groups had reduced their daily energy intake by approximately 450 calories from initial levels, but the low carbohydrate subjects lost more than twice as much weight as those on the high carbohydrate diet. Fifty to sixty percent of the weight lost in both groups was comprised of fat, and neither group showed any change in bone mineral density (48).

In May 2003, the prestigious New England Journal of Medicine published the results of two randomized trials which directly pitted low carbohydrate diets against conventional low fat, high carbohydrate diets. One of these was a 12-month study in which thirty-three obese subjects were again placed on an Atkins-style low carb diet. No restrictions were placed on fat and protein intake, but Dr. Atkin's standard protocol for limiting daily carbohydrate intake was employed. The 30 subjects assigned to the high carbohydrate group followed a low fat, high carbohydrate diet in which daily caloric intake was restricted to 1200-1500 for women, and 1500-1800 for men. Unlike other dietary intervention studies that employed regular counseling sessions with dietitians, participants in this study received a bare minimum of professional contact to replicate the conditions experienced by the average dieter. This lack of support no doubt contributed to the high rate of attrition - 13 subjects from the low fat group and 13 from the low carbohydrate group failed to complete the study. After 3 months, the low carbohydrate dieters had lost significantly more weight, and at the six-month point the average bodyweight in this group had decreased 7%, compared to only 3.2% in the high carbohydrate group. At the 12 month point, however, the dieters had regressed; weight loss was 4.4% and 2.5% below baseline in the low and high carbohydrate groups, respectively (49).

The second study to appear in the New England Journal of Medicine was a 6-month trial headed by Frederick Samaha, M.D. One-hundred and thirty-two severely obese individuals participated. Thirty-nine percent of the subjects were diabetic, 77 were black and 23 were women. Sixty-four subjects were assigned to a diet in which carbohydrates were limited to 30g per day or less. No restriction was placed on their fat intake, and they were encouraged to eat fruits and vegetables that were high in fiber but low in carbohydrates. The 68 subjects in the low fat group were placed on a diet that restricted fat to 30% or less of calories, and total daily energy intake to 500 calories below maintenance levels. Attrition was higher in the low fat group throughout the study; after 6 months, 47% and 33% participants in the high and low carbohydrate groups, respectively, had dropped out of the study. Despite no limits being placed on the caloric intake of the low carbohydrate dieters, their daily intake was similar to those on the energy- restricted, low fat, high carbohydrate diet - 1630 versus 1576 calories per day, respectively. After 6 months, those in the low carbohydrate group had lost an average of 5.8kg; the high carbohydrate dieters, only 1.8kg. Nine of the low carbohydrate dieters, but only 2 of the high carbohydrate dieters, had lost 10% or more of their initial bodyweight. Improvements in insulin sensitivity and blood glucose levels were significantly greater amongst those in the low carbohydrate group. By six months, 7 subjects in the low carbohydrate group were able to reduce their dosage of diabetic medication. In the high carb group, one subject had their insulin dosage reduced, and another had to begin taking oral glucose-lowering medication (50).

Because they can obtain little solace from the results of clinical trials, opponents of low carbohydrate diets are fond of citing the National Weight Control Registry, which was set up by Brown University researchers to record individuals who had successfully lost 30lbs or more, and successfully maintained that weight loss for 1 year or more. According to these researchers, low carbohydrate dieters are poorly represented on the Registry's database. A number of commentators have suggested, in all seriousness, that this under-representation is proof that low carbohydrate diets are incapable of successfully inducing long-term weight loss. If the main goal of embarking on a weight loss diet was to increase one's willingness to register for national databases, then the National Weight Control Registry would certainly be of relevance. However, as a measure of the relative fat-loss efficacy of low and high carbohydrate diets, the Registry is about as scientifically valid as tarot card reading. There could be countless reasons why the names of low carbohydrate dieters appear infrequently on the Registry; to attempt to guess what these reasons might be would be just that - speculative conjecture. To cite the National Weight Control Registry, and ignore the data from randomized clinical trials that directly compare the effects of low and high carbohydrate diets reveals, not only a contemptuous disregard for the scientific method, but a new level of desperation by anti-low carbohydrate proponents as they attempt to discredit an eating pattern that directly challenges the validity of their closely-held low fat, high carbohydrate dogma.

The notion that fat is responsible for weight gain is true only if it occurs in the presence of a high carbohydrate intake. As numerous studies have shown low carb diets to produce, at worst, equal weight loss, and often superior weight loss than high carb diets, the laws of logic dictate that carbohydrates should also be blamed for causing weight gain. Unfortunately, reason and logic don't appear to hold much sway among those promoting the low fat, high carbohydrate theory.

Myth 3: 'Low-carbohydrate, High-Protein Diets cause Osteoporosis.'

The accusation is that high protein intakes cause calcium to 'leech' from bones, thus causing bone-thinning. A review of the research in this area shows that high protein intake, in the presence of alkalinising fruit and vegetable intake and adequate calcium intake, either has no adverse affect on bone mass or has a positive affect on bone mass (51).

High-carb advocates are quick to point out that meat increases the acid load in the body, claiming this will lead to bone thinning. They are strangely silent when it comes to pointing out that grains also increase the acid load in the body (57). Those attacking low-carb diets like to portray them as `unbalanced' diets, consisting of huge amounts of animal protein and little else.

Don't believe them! Alkalinising low-carbohydrate vegetables and small servings of low-glycemic fruits are a perfect compliment to animal protein in a low-carb diet. Dr. Robert Atkins, invariably mentioned by those attacking low-carb diets, repeatedly recommended the consumption of fruits and (especially) vegetables in his writings. Paleolithic nutrition (my favoured approach to low-carb eating) is by its very nature a diet high not only in animal protein but low-carbohydrate plant foods.

Studies have shown high levels of protein and calcium to act synergistically in increasing bone mineral density (BMD). Higher protein intake was significantly associated with a favorable change in total-body BMD in elderly subjects supplemented with calcium and vitamin D. In this 3 year study, a placebo group not receiving the supplements did not experience such favourable changes (52).

The message here is to consume a well-rounded diet that includes whole-food sources of protein, and alkalinising plant foods. A calcium and vitamin D supplement may well be warranted for those at risk of, and wishing to prevent, bone thinning.

A recent study from Denmark examined the effects of a six-month high-protein diet vs a low-protein diet in 65 overweight adults. No adverse effects on bone mineral content were seen in the high-protein group, who lost almost twice as much weight as the low-protein group (53).
A study with women 55-69 years of age showed that as the consumption of animal protein increased, the incidence of hip fracture decreased (54).

Another study showed significantly lower calcium absorption in women consuming the lowest-fat, highest-fiber diets, compared to those eating the highest-fat, lowest-fiber diets (55).
For over 2 million years, humans were hunter-gatherers. Through their research, paleontologists have determined what the hunter-gatherers ate - and it wasn't pasta, rice cakes and low-fat cookies! (56) The hunter-gatherers ate a diet rich in animal protein. Far from being delicate and fracture-prone, their remains show skeletal structures that were more robust than those of modern man.

The hunter-gatherers consumed mainly meat, and a wide variety of wild plant foods - nuts, seeds, and alkaline fruits and vegetables. Grain consumption was either non-existent or minimal. The widespread consumption of grains in the human diet is a relatively recent phenomenon, dating back 10,000 years. Grains and legumes contain 'anti-nutrients' such as phytates, which act to intefere with the body's absorption of vital minerals, particularly iron and zinc (which is essential for healthy bone formation) (58,59). As mentioned, grains also increase the acid load in the body.

We can see that a low-carbohydrate, high fat, high protein diet is a far better choice for building strong bones than a low-fat, high-carbohydrate diet. It ensures adequate intake of protein; it replaces acid-forming, phytate-containing grains and legumes with alkalinising fruits and vegetables; and the fat content of such a diet assists the absorption of fat-soluble bone-building vitamins like Vitamin D and K.

Myth 4: 'High-Protein Diets Cause Kidney Disease'

There is evidence that a high-protein intake may be harmful to people with pre-existing kidney damage. Protein metabolism results in the production of urea, which must be filtered through the kidneys. Damaged kidneys may not be able to safely process the increased amounts of urea on a high-protein diet. Some studies have shown protein-restricted diets to help those with kidney disease.High-carb proponents want us to believe that a protein intake that is harmful to damaged kidneys is also harmful to healthy kidneys.

There is no evidence to support such a claim.

A study with 20 bodybuilders and 18 other highly trained individuals examined the effects of high-protein diets on kidney function. Some of the subjects in the study were consuming up to 2.8g/kg of protein daily (210g protein daily for a 75kg individual). Such intakes would have a lot of orthodox nutritionists in a fit, but all measures of kidney function fell within normal ranges (60).

Bodybuilders and strength athletes have been consuming high-protein diets for decades. Given the widespread global participation in these activities, if the claims of kidney damage were true, by now there would be an enormous number of case studies of ex-bodybuilders and strength athletes afflicted with kidney disease. Needless to say, this is not the case.
A comparison of healthy subjects eating 100g or more of protein per day with long-term vegetarians eating 30g or less of protein per day concluded that both groups had similar kidney function. The subjects were aged 30-80 and both groups displayed similar progressive deterioration of kidney function with age (61).

Individuals with healthy kidney function have little to fear from higher levels of protein consumption.

Myth 5: 'Low-Carbohydrate Diets Put You In Ketosis, And Ketosis Is Dangerous!'

First of all, it should be pointed out that not all low-carbohydrate diets induce ketosis. Carbohydrates can be restricted, but not necessarily to the point where ketosis is induced (daily carbohydrate intake of 50g or less seems to be a reliable benchmark).

If carbohydrate intake is kept low enough however, one eventually enters a state known as ketosis, characterised by a measurable increase of ketones in the bloodstream. Ketones are an intermediate product of fat breakdown, and are an alternative source of energy to glucose. Ketosis indicates a heightened state of fat-burning.

Contrary to the alarmist claims of some critics, there is nothing dangerous about ketosis.
One of the more important functions of ketones is to serve as an alternative fuel source for the brain (62) - contrary to the claims of some that the brain can only use glucose for fuel.

Ketogenic diets do not cause rampant, life-threatening acidosis as some claim (63,64). These folks seem to be confusing ketoacidosis, which is a serious condition affecting diabetics, with ketosis. They are not the same thing! Ketoacidosis occurs when diabetics produce high levels of ketones in the presence of elevated blood sugar levels. Insufficient insulin, or inefficient insulin function, means this elevated blood sugar cannot be delivered to the cells for energy. Consequently ketones must be formed as an alternate energy source. Ketone bodies are slightly acidic, and excessive levels could decrease the blood's pH. Under normal circumstances the body can efficiently buffer against any decrease in pH. In diabetes the body is unable to efficiently cope with the increased acid load and ketoacidosis occurs, increasing the acidity of the blood (64).This abnormal state of affairs associated with diabetes (induced by high blood sugar levels from consumption of carbohydrates) has nothing to do with the benign ketosis induced by low-carbohydrate diets.

Despite the hype, healthy people have little to fear from ketosis - unless they have a strong aversion to losing fat!

Myth 6: 'Low Carbohydrate Diets Are An Unproven Fad!'

This has to be the most ridiculous criticism of all, especially when one considers its source. The human species has been eating a meat-based diet for 2.4 million years, and analysis of the diets consumed by recent hunter-gatherer societies (the best available surrogate for paleolithic nutrition) shows that plant foods comprised, on average, one-third of daily food intake - the rest was derived from animal products (56). What's more, the bulk of these plant foods were low-glycemic, low-carbohydrate items such as nuts, seeds, wild fruits and vegetables. Carbohydrate-rich cereal grains did not appear in any meaningful quantity in the human diet until the onset of the agricultural revolution some 10,000 years ago. Humans evolved on meat-based, low to moderate carbohydrate nutrition, meaning that low carbohydrate diets are far more in accordance with man's genetic evolution than the low-animal fat, high carbohydrate nonsense that is currently espoused by mainstream authorities. The anti-animal fat, high carbohydrate diet concept is a mere 4 decades old, nothing more than a speculative construct of mid-twentieth century researchers who were at a loss to explain the high prevalence of CHD in modernized countries. While the paleolithic diet kept the human species thriving for over two-million years, the track record of the high-carbohydrate, grain-based diet movement is atrocious - their persistent, fanatical rantings against animal fats have been remarkably successful in driving people towards vegetable fats and carbohydrate-rich foodstuffs, the increasing consumption of which has been accompanied by alarming increases in the incidence of obesity and Type-2 diabetes (despite an abundance of propaganda to the contrary, USDA food consumption data shows that animal fat consumption has changed little over the last century; FAO data also shows animal fat intake has remained constant over the last 40 years). For purveyors of a nutritional doctrine that is little more than 40 years old to denigrate a dietary pattern that has served humans well for millions of years is nothing short of ludicrous.

Conclusion

Those criticising low-carbohydrate diets often do so under false pretenses. They unfairly equate high-carb, high-fat diets with low-carb, high-fat diets, even though they have vastly different metabolic effects. Another tactic employed by such critics is to create fear of possible adverse effects, which upon closer inspection only concern individuals with certain metabolic defects. As we have seen, this tactic is applied to claims of kidney damage and ketoacidosis, even though there is no evidence that low-carbohydrate diets initiate these ailments. Indeed, hypertensive kidney damage and ketoacidosis are complications of diabetes, a disease associated with excessive carbohydrate intake.

Years ago, I believed the high-carbohydrate propaganda and followed a low-fat, high carbohydrate diet. When it became apparent that this diet was not conducive to optimal health and performance, I had no choice but to experiment. Through trial and error I adopted a paleolithic-style low-carbohydrate diet. The result has been a marked improvement in energy, mental focus, blood sugar control, and an ability to maintain year round single-digit bodyfat levels. I encourage all my personal training clients to follow low-carbohydrate nutrition, and those who take my advice invariably experience benefits similar to my own.

Best of health,

Anthony Colpo.

Related articles:

Low Carbohydrate FAQ

Just how low will the anti-low carb crowd go?

Did the Atkins Diet really kill Dr. Atkins?


Anthony Colpo is a certified fitness consultant with 20 years' experience in the physical conditioning arena. To contact Anthony, email contact@theomnivore.com

Disclaimer: This article is presented for information purposes only and is not intended as medical advice. Persons with medical conditions should institute dietary changes whilst being monitored by a competent medical practitioner.

© Anthony Colpo 2002. http://www.theomnivore.com

References

1 Kritchevsky D. Dietary Protein, cholesterol and atherosclerosis: A review of the early history. Journal of Nutrition, 1995; 125: 589S-593S.

2 Steiner A, Kendall FE. Atherosclerosis and arteriosclerosis in dogs following ingestion of cholesterol and thiouracil. Archives of Pathology, 42: 433-444. 1946.

3 Keys A. Atherosclerosis: a problem in new public health. Journal of Mount Sinai Hospital, 1953; 20:118-139

4 Yerushalmey J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodological note. The New York State Journal of Medicine, 1957; 57: 2343-2354

5 Page I. H., et al., Dietary fat and its relation to heart attacks and strokes. Circulation 1961; 23:133-136.

6 Mann GV, et al. Cardiovascular disease in the Masai. Journal of Atherosclerosis Research, 1964; 4; 289-312.

7 Mann GV, et al. Physical fitness and immunity to heart-disease in Masai. Lancet, 1965 Dec 25; 2 (7426): 1308-10.

8 Mann GV, et al. Atherosclerosis in the Masai. American Journal of Epidemiology, 1972 Jan; 95 (1): 26-37.

9 Biss K, et al. Some unique biological characteristics of the Masai of east Africa. New England Journal of Medicine, April 1, 1971; Vol. 284, No. 13: 694-699.

10 Shaper, AG. Cardiovascular studies in the Samburu tribe of Northern Kenya. American Heart Journal, 63 (4); 437-442, 1962.

11 Prior IA, et al. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies. American Journal of Clinical Nutrition, 1981 Aug; 34 (8): 1552-61

12 Day J, et al. Anthropometric, physiological and biochemical differences between urban and rural Masai. Atherosclerosis, 1976; 23: 357-361.

13 Stanhope JM, et al. The Tokelau Island Migrant Study: serum lipid concentration in two environments. Journal of Chronic Disease, 1981; 34 (2-3): 45-55.

14 Joseph JG, et al. Elevation of systolic and diastolic blood pressure associated with migration: the Tokelau island migrant study. Journal of Chronic Disease, 1983; 36 (7): 507-16.

15 Ostbye T, et al. Type 2 (non-insulin-dependent) diabetes mellitus, migration and westernisation: the Tokelau Island Migrant Study. Diabetologia, 1989 Aug; 32 (8): 585-90.

16 Prior IA, et al. Migration and gout: the Tokelau Island migrant study.
British Medical Journal (Clinical Research Edition), 1987 Aug 22; 295 (6596): 457-61.

17 Temple NJ. Coronary heart disease - dietary lipids or refined carbohydrates? Medical Hypotheses, 1983; 10: 425-435.

18 Food intake data from Food and Agriculture Organization of the United Nations, Statistical Database. CHD mortality data from World Health Statistics Annual, 1961, 1966 and 1997-1999 editions.

19 National Diet Heart Study. Final report. Circulation, 1968; 37: 1-428.

20 Dayton S, et al. A controlled clinical trial of a diet high in unsaturated fat in preventing complications of atherosclerosis. Circulation, 1969; XL: II-1-63.

21 Frantz Jr ID, et al. Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota coronary survey. Arteriosclerosis, 1989; 9: 129-135.

22 Burr ML, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet, 1989; 2: 757-761.

23 De Lorgeril M, et al. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet, 1994; 343: 1454-1459.

24 Marchioli R, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002; 105: 1897-1903.

25 Watts GF, et al. Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine, in the St Thomas' atherosclerosis regression study (STARS). Lancet, 1992; 339: 563-569

26 Singh RB, et al. Randomised controlled trial of cardioprotective diet in patients with recent acute myocardial infarction: results of one year follow-up. British Medical Journal, 1992; 304:1015-1019.

27 Singh RB, et al. Randomized, double-blind, placebo-controlled trial of fish oil and mustard oil in patients with suspected acute myocardial infarction: the Indian experiment of infarct survival-4. Cardiovasc Drugs Ther. 1997; 11: 485-491.

28 Bradford RH et al. Expanded Clinical Evaluation of Lovastatin (EXCEL) study results. I. Efficacy in modifying plasma lipoproteins and adverse event profile in 8245 patients with moderate hypercholesterolemia. Archives of Internal Medicine, 1991 Jan;151(1):43-9

29 Shepherd J, et al. Prevention of Coronary Heart Disease with Pravastatin in Men with Hypercholesterolemia. November 16, 1995. Volume 333, No. 20: 1301-1308

30 Sacks FM, et al. The Effect of Pravastatin on Coronary Events after Myocardial Infarction in Patients with Average Cholesterol Levels. New England Journal of Medicine, October 3, 1996. Vol. 335, No. 14: 1001-1009.

31 Sacks FM, et al. Relationship Between Plasma LDL Concentrations During Treatment With Pravastatin and Recurrent Coronary Events in the Cholesterol and Recurrent Events Trial. Circulation. 1998; 97: 1446-1452.

32 The Long-Term Intervention with Pravastatin In ischaemic Disease (LIPID) Study Group. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. New England Journal of Medicine, 1998. Vol. 339: 1349-1357.

33 Downs JR, et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels. Journal of the American Medical Association. Vol. 279, 1998: 1615-1622.

34 Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high risk individuals: a randomised placebo-controlled trial. Lancet 2002; 360: 7-22M.

35 Ravnskov U. Implications of 4S evidence on baseline lipid levels. Lancet, July 1995; Vol. 346: 181.

36 Shepherd J, et al. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. Lancet, 23 November 2002. Vol. 360, No. 9346: 1623-30.

37 Lyons TJ. Glycation and oxidation: A role in the pathogenesis of atherosclerosis. American Journal of Cardiology, Feb. 25, 1993; 71: 26B-31B.

38 Dreon DM, et al. Dietary Fat: Carbohydrate Ratio and Obesity in Middle-Aged Men. American Journal of Clinical Nutrition, 1988; 47: 995-1000.

39 Bisschop PH, et al. Dietary fat content alters insulin-mediated glucose metabolism in healthy men. American Journal of Clinical Nutrition, 2001; 73: 554-559.

40 Young CM, et al. Effect on Body Composition and Other Parameters in Obese Young Men of Carbohydrate Level of Reduction Diet," The American Journal of Clinical Nutrition, 24, 1971, pages 290-296.

41 Kasper H, et al. Response of Body Weight to a Low Carbohydrate, High Fat Diet in Normal and Obese Subjects. The American Journal of Clinical Nutrition, 1973; 26: 197-204.

42 Willi SM, et al. The Effects of a High-Protein, Low-Fat, Ketogenic Diet on Adolescents With Morbid Obesity: Body Composition, Blood Chemistries, and Sleep Abnormalities. Pediatrics, 1998; 101 (1): 61-67.

43 Golay A, et al. Weight-Loss With Low or High Carbohydrate Diet. International Journal of Obesity, 20 (12), 1996: 1067-1072.

44 Rabast U, et al. Loss of Weight, Sodium and Water in Obese Persons Consuming a High-or Low-Carbohydrate Diet. Annals of Nutrition and Metabolism, 1981; 25 (6): 341-349.

45 Yudkin J, Carey M. The Treatment of Obesity by the 'High-Fat' Diet: The Inevitability of Calories. The Lancet, October 29, 1960: 939-941.

46 Hwalla Baba N, et al. High protein vs high carbohydrate hypoenergetic diet for the treatment of obese hyperinsulinemic subjects. International Journal of Obesity, 1999; 23: 1202-1206.

47 Sondike SB, et al. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factors in overweight adolescents. Journal of Pediatrics, March 2003; 142: 253-258.

48 Brehm, et al. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. Journal of Clinical Endocrinology and Metabolism, 2003; 88 (4): 1617-1623.

49 Foster GD, et al. A randomized trial of a low-carbohydrate diet for obesity. New England Journal of Medicine, May 22, 2003; 348: 2082-2090.

50 Samaha FF, et al. A low-carbohydrate diet as compared with a low fat diet in severe obesity. New England Journal of Medicine, May 22, 2003; 348: 2074-2081.

51 Massey LK. Does Excess Dietary Protein Adversely Affect Bone? Symposium Overview. Journal of Nutrition, June 1998; 128 (6): 1048-1050

52 Dawson-Hughes B, Harris SS. Calcium intake influences the association of protein intake with rates of bone loss in elderly men and women. American Journal of Clinical Nutrition, April 2002; 75 (4): 773-779.

53 Astrup A., et al. The Effect of Protein Intake on Bone Mineralisation: A Randomised Controlled 6-Months Trial in Overweight Subjects. The American Journal of Clinical Nutrition 2002; 75 (2s): abstract 16.

54 Munger R.G, et al. Prospective study of dietary protein intake and risk of hip fracture in postmenopausal women. American Journal of Clinical Nutrition, 1999; 69: 147-152.

55 Wolf R.L, et al. Factors associated with calcium absorption efficiency in pre- and perimenopausal women. American Journal of Clinical Nutrition, 2000; 72: 466-471.

56 Cordain L, et al. Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets, American Journal of Clinical Nutrition, March 2000; 71 (3): 682-692.

57 Barzel US, K. Massey LK. Excess Dietary Protein Can Adversely Affect Bone. Journal of Nutrition. 128: 1051-1053.

58 Hallberg L, et al. Iron absorption in man: ascorbic acid and dose-dependent inhibition by phytate. American Journal of Clinical Nutrition; 49: 140-144.

59 Lönnerdal B. Dietary Factors Influencing Zinc Absorption. Journal of Nutrition, 2000; 130: 1378S-1383S.

60 Poortmans JR, Dellalieux O. Do regular high protein diets have potential health risks on kidney function in athletes? International Journal of Sports Nutrition and Exercise Metabolism, Mar. 2000; 10 (1): 28-38.

61 Blum M, et al. Protein Intake and Kidney Function in Humans: Its Effect on Normal Aging. Archives of Internal Medicine, 1989; 149 (1): 211-212.

62 Mitchell GA. et al. Medical Aspects of Ketone Body Metabolism. Clinical and Investigative Medicine, 1995; 18(3): 193-216.

63 Phinney SD, et al. The Human Metabolic Response to Chronic Ketosis Without Caloric Restriction: Physical and Biochemical Adaptation. Metabolism, 1983; 32 (8): 757-768.

64 Hoffer LJ. Metabolic Consequences of Starvation. Modern Nutrition in Health and Disease, Shils ME, et al. (editors), Lippincott Williams & Wilkens, 1999, 9th ed: 645-665.