30 August, 2004
Common Myths About Low Carbohydrate Diets
by Anthony Colpo,
Last updated 9th July 2003
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
Let's look at some common attacks made on low-carbohydrate diets...
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
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
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
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
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
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
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
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
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 2½ 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
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
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
A study with women 55-69 years of age showed that as the consumption
of animal protein increased, the incidence of hip fracture decreased
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
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
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
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 calorie 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
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.
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.
Anthony Colpo is a certified fitness consultant with 20 years'
experience in the physical conditioning arena. To contact Anthony,
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.
how low will the anti-low carb crowd go?
the Atkins Diet really kill Dr. Atkins?
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