Myths About Low Carbohydrate Diets
Over the last several years,
low-carbohydrate diets have experienced a substantial increase in
popularity. However, along with the ever-increasing popularity of these
diets, there has been an increase in the number, and virulence, of
attacks on them by advocates of the high-carbohydrate, low-animal fat
diet theory that came into vogue around 40 years ago. Nutrition
"experts", who should know better, repeat common myths about
low-carbohydrate eating that are clearly disputed by ample scientific
and empirical evidence. Let's look at some common attacks made on
Myth 1: 'Low-carbohydrate diets cause
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.
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.
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
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.
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.
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).
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).
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).
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
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).
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).
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).
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.
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.
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.
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
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
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
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
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
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)
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).
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
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
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
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
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...
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).
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).
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).
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).
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.
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
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
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
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
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
Ketogenic diets do not cause rampant, life-threatening acidosis as some
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!'
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.
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.
how low will the anti-low carb crowd go?
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 firstname.lastname@example.org
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
© Anthony Colpo 2002. http://www.theomnivore.com
1 Kritchevsky D. Dietary
Protein, cholesterol and atherosclerosis: A review of the early history.
Journal of Nutrition, 1995; 125: 589S-593S.
A, Kendall FE. Atherosclerosis and arteriosclerosis in dogs following
ingestion of cholesterol and thiouracil. Archives of Pathology, 42:
3 Keys A.
Atherosclerosis: a problem in new public health. Journal of Mount Sinai
Hospital, 1953; 20:118-139
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.
AG. Cardiovascular studies in the Samburu tribe of Northern Kenya.
American Heart Journal, 63 (4); 437-442, 1962.
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.
JM, et al. The Tokelau Island Migrant Study: serum lipid concentration
in two environments. Journal of Chronic Disease, 1981; 34 (2-3): 45-55.
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.
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.
IA, et al. Migration and gout: the Tokelau Island migrant study.
British Medical Journal (Clinical Research Edition), 1987 Aug 22; 295
NJ. Coronary heart disease - dietary lipids or refined carbohydrates?
Medical Hypotheses, 1983; 10: 425-435.
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:
S, et al. A controlled clinical trial of a diet high in unsaturated fat
in preventing complications of atherosclerosis. Circulation, 1969; XL:
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.
Lorgeril M, et al. Mediterranean alpha-linolenic acid-rich diet in
secondary prevention of coronary heart disease. Lancet, 1994; 343:
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.
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
J, et al. Prevention of Coronary Heart Disease with Pravastatin in Men
with Hypercholesterolemia. November 16, 1995. Volume 333, No. 20:
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.
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:
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.
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.
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.
U. Implications of 4S evidence on baseline lipid levels. Lancet, July
1995; Vol. 346: 181.
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:
PH, et al. Dietary fat content alters insulin-mediated glucose
metabolism in healthy men. American Journal of Clinical Nutrition, 2001;
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.
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.
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.
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.
J, Carey M. The Treatment of Obesity by the 'High-Fat' Diet: The
Inevitability of Calories. The Lancet, October 29, 1960: 939-941.
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.
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.
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.
GD, et al. A randomized trial of a low-carbohydrate diet for obesity.
New England Journal of Medicine, May 22, 2003; 348: 2082-2090.
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:
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):
61 Blum M, et al. Protein Intake and Kidney Function in Humans: Its
Effect on Normal Aging. Archives of Internal Medicine, 1989; 149 (1):
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.
[an error occurred while processing this directive]