by Joseph Brasco, MD
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Increased Saturated Fats
Of all our nutritional mantras, the one most widely and emphatically
proclaimed is the relationship between saturated fats and
coronary artery disease. One would think a "fact"
so ingrained in our social psyche would be supported by mountains
of evidence.
However, the reality is the data to support the "diet-heart
hypothesis" is flimsy at best - non existent at worst.
In an extensive review of existing studies, Ravnskov came
to the conclusion that, "Few observations agree with
the diet-heart idea, but a large number have falsified most
effectively.
Man's diet possibly includes factors of importance to the
vessels or the heart, but there is little evidence that saturated
fatty acids as a group are harmful or that polyunsaturated
fatty acids as a group are beneficial." In a similar
review, Dr. Mary Enig was also unable to find a solid relationship
between saturated fat consumption and coronary artery disease.
She instead came to the conclusion that the inordinate increase
in trans fatty acid consumption was more likely the causative
factor.
When discussing the "dietary heart hypothesis",
the work of Dean Ornish, M.D., is often cited as clinical
evidence for the efficacy of dietary fat reduction. However,
while Ornish is a major proponent of the "low fat diet",
in his studies a number of coronary artery risk factors are
addressed, in addition to the dietary changes.
In Ornish's work, study participants underwent vigorous
lifestyle changes, which included smoking cessation, stress
management, exercise and a low-fat (near vegan) diet (the
only animal products allowed were egg whites and one cup of
non-fat milk or yogurt per day).
After following these changes for one year, the experimental
group did show an overall regression of atherosclerotic plaque,
Ornish's study is extraordinarily important because he was
able to demonstrate, in quantifiable terms to the medical
community, that lifestyle changes could be as powerful as
drugs in managing a serious disease. However, to extrapolate
that this study proves the value of the low fat diet is fallacious.
Ornish manipulates four separate variables in his study,
all of which have purported association with cardiovascular
disease. To suggest that any one variable or combination of
variables is more important than the other cannot be concluded
from Ornish's data.
Even if diet alone is examined, there are multiple variables
within the diet, that in and of themselves could have significance.
Was it the omission of trans fatty acids (which have been
linked to cardiovascular disease)? Was it the increase of
antioxidants provided by the intake of fresh fruits and vegetables?
Was it the fact that the experimental group experienced an
average loss of 22 lbs?
Again, to conclude that it was the "low fat diet"
which was primarily responsible for the experimental group's
success (as the study is often interpreted), is quite disingenuous.
A factor often overlooked in Ornish's work is the effect of
low fat/high carbohydrate diets on lipid profiles. While it
is true, the experimental group had an overall reduction in
cholesterol, there was a concomitant reduction in HDL cholesterol
with an increase in triglycerides.
Numerous recent studies have verified this dietary effect.
Of these current studies, Berglund specifically looked at
the response of the reduction in dietary total and saturated
fats and HDL cholesterol subtypes. The study demonstrated
a decrease in dietary total and saturated fat resulted in
a significant decrease in HDL2 and HDL2b cholesterol concentrations.
The authors concluded that the dietary changes suggested to
be prudent for a large segment of the population will primarily
affect the concentrations of the most prominent antiatherogenic
HDL subpopulations.
Although definitive conclusions for the general population
may be premature, in individuals demonstrating evidence of
hyperinsulinemia and dyslipidemia (i.e. - Syndrome X) carbohydrate
restriction is imperative for improved lipid profiles. In
nutrition, as well as in life, balance is always the key.
Nowhere is balance more crucial than in the discussion of
dietary fats.
ANY diet, whether it be high fat - low fat (or anything in-between),
if it promotes imbalances in fatty acid profiles, will in
the long run have negative health consequences. In the mid
'50s, the biochemist, anthropologist, and explorer Hugh Sinclair
suggested an alternative explanation for the relationship
between dietary fat and cardiovascular disease.
Sinclair noted that several people groups existed that consumed
relatively high amounts of fat and yet were free of heart
disease. Sinclair detailed the dietary habits of the Eskimos
(previously discussed); the Masai people of Kenya who ate
large quantities of ruminant milk and meat; and Jamaicans
who ate large amounts of saturated fat in the form of coconut
oil. All three groups, all consuming high fat diets, were
relatively free from heart disease.
Sinclair suggested that the polyunsaturated profiles of these
diets were protective, and concluded that the rise in cardiovascular
disease was more related to their exclusion from the diet
rather than the inclusion of saturated fats or cholesterol.
Since Sinclair's day, our biochemical understanding of fat
has increased exponentially. We now realize it is not just
the polyunsaturated content of the diet, but the ratio of
N-6 to N-3 polyunsaturates that may ultimately determine health.
Both dietary extremes discussed fail to introduce balance
in this ratio. High carbohydrate diet due to their high grain
and plant content will ultimately be low in N-3 fats (especially
long chain N-3 fats - i.e. EPA/DHA), thus unbalancing the
N-6/N-3 ratio. Low carbohydrate diets, in their popular form,
rely heavily on commercially raised grain-fed meats and poultry
(the fatty acid profile of the meat from wild game, free range
beef and poultry have a significantly higher N-3 to N-6 ratio),
eggs (free range hens also make better eggs) and cheeses.
A diet based on these foods will also greatly unbalance the
N6/N3 ratio. Although the precise ratio remains controversial,
the N6/N3 ratio should probably be in the range of 4-3/1 to
optimize human health, western diets rich in vegetable oils,
cereal grains and grain fed live stock, drive this ratio to
an unprecedented 50-10:1. This imbalance may have implications
in a host of diseases, including hyperinsulinemia, artherosclerosis
and tumorgenesis.
When the diets of hunter-gatherer populations are studied,
authors have concluded that their N6/N3 ratio varied between
4:1 to 1:1. This ratio appears to be biologically optimal.
Based on these considerations, investigators, have advocated
a return to dietary ratios of ancestral humans. A diet based
on lean meats (wild game or free range livestock), fish, raw
nuts and seed, vegetables, low glycemic fruit (paleocarbs)
- "an evolutionary diet" - not only will be helpful
in the management of obesity, but in a host of other common
western diseases, including cardiovascular disease.
Dietary
Protein and Cardiovascular Disease
Multiple recent studies have demonstrated the benefit of
dietary fats (especially N-3 polyunsaturates and monounsaturates)
in cardiovascular disease and in the reduction of cardiovascular
risk factors. A more recent study trend has examined the possible
beneficial role of dietary protein.
Wolfe has published numerous articles demonstrating the positive
effects of the isocaloric substitution of protein for carbohydrate
on lipid profiles. His studies have demonstrated a decreased
LDL-C, an increased HDL-C, and reduction of triglycerides,
thus reversing the dietary effects of increased carbohydrates.
Wolfe states that substitution of carbohydrate for fat in
the diet results in a reduction in HDL apoprotein transport
rates along with increased catabolism of apolipoprotein A-1.
The decreases in plasma VLDL and LDL resulting from substitution
of protein for carbohydrate in the diet may relate to either
increased catabolism or decreased production. Thus, according
to Wolfe's work, the simple dietary substitution of protein
for carbohydrate could have profound health benefits.
Wolfe's data has recently been validated by Hu. In this study
the dietary habits of over 80,000 women were examined. After
controlling for variables, high protein intakes were associated
with lowered risk of ischemic heart disease. Both animal and
vegetable protein sources were protective. This inverse association
was noted in women on both low fat or high fat diets. Wolfe's
and Hu's work both indicate that dietary protein has cardioprotective
properties independent of those of dietary fat.
Given the multiple health benefits ascribed to N-3 polyunsaturates
and the evolving data regarding dietary protein - fish may
be one of the best foods for human consumption. In a fascinating
piece of epidemiological work, Marcovina compared 2 racially
homogenous Bantu populations from Tanzania. The only appreciable
difference between the groups was their dietary habits.
The Bantu living closer to the shore had a predominantly
fish based diet, while the inland Bantu consumed an essentially
vegan diet (a diet devoid of animal products ). When plasma
lipoprotein (a) (an independent cardiovascular risk factor)
levels were compared, those among the fish eating population
were 40% lower. This suggests another cardioprotective aspect
of fish consumption.
In a recent study by Mori, he demonstrated the inclusion
of fish in a weight loss program yielded greater results than
either fish consumption or weight loss alone in their obese
subjects. The experimental group in their study demonstrated
improved glucose, insulin and lipid metabolism, as well as
greater reductions in blood pressure, heart rate and weight
loss versus controls. This study suggests a novel approach
to the dietary management of obesity and NIDDM.
Perhaps the most influential of the studies looking at the
benefits of fish, was the Diet and Reinfarction Trial (also
known as the DART trial). In this study, the authors demonstrated
that the addition of a modest amount of fish (2-3g of EPA
per week or the equivalent of 300g of fatty fish per week)
reduced post myocardial infarction mortality by about 29%
when compared to controls.
One of the more interesting aspects of the study was that
the control group was instructed on the standard fat reduction
diet and on average had lower cholesterol levels than did
the experimental group. The authors theorized that the fish
oils had a favorable effect on clotting mechanisms and blood
platelets, as well as a potential anti-arrhythmic effect on
the ischemic heart. The results of this study are profound,
especially given the modest and otherwise innocuous interventions
undertaken.
Given the evidence of the benefit of N-3 polyunsaturates,
coupled with the potential benefits of dietary protein, fish
clearly is a biologically superior food source. The isocaloric
substitution of fish for dietary carbohydrates is not only
evolutionary appropriate, by may have untoward health benefits
from weight control to improved glucose homeostasis to cardiovascular
disease prevention.
Risk of Osteoporosis
Of all the potential negative side effects of dietary protein,
the issue of osteoporosis is perhaps the most difficult to
resolve. The literature is greatly divided on the topic, and
clear recommendations are hard to find. In a recent study,
Munger found that the intake of dietary protein, specifically
from animal sources was associated with a reduced incidence
of hip fractures in post menopausal women.
In the articles' discussion, a brief review of protein's
controversial role in osteoporosis was undertaken. In the
studies showing a potential benefit (as in the author's paper),
it has been theorized that dietary protein may strengthen
bone by its effect on the structure and function of bone-related
proteins.
In studies demonstrating a negative effect, it has been argued
that dietary protein (especially in the form of animal based
protein) is a primary source of acid ash, which results in
the acidification of urine. In order to buffer the urine and
maintain acid-base homeostasis, calcium salts are mobilized
from the skeleton, resulting in a net calciuria. Over time,
this buffering of endogenous acids may contribute to a progressive
decline in skeletal mass and, ultimately, lead to osteoporosis.
However, Wachman and Bernstein, the two authors who originally
postulated this mechanism for osteoporosis, theorized that
by increasing the dietary alkaline ash this process could
be halted.
In a study by Sebastian., he was able to reduce calicuria
and improve overall calcium/phosphorous balance by the administration
of potassium bicarbonate as a buffering agent to postmenopausal
women consuming an acid promoting diet. The authors suggest
that potassium bicarbonate could be administered long-term
as a novel means of preventing and treating postmenopausal
osteoporosis.
In a 4-year longitudinal study by Tucker, he was able to
demonstrate that a greater bone mineral density was associated
with increased dietary potassium and magnesium levels, as
well as increased consumption of fruits and vegetables. The
authors concluded that this positive association was due to
the beneficial effects of potassium and magnesium on calcium
balance and bone metabolism, as well as the buffering properties
of increased alkaline ash in the form of fruits and vegetables.
Given the divergent nature of the theories, it is highly
probable that both have merit. With respect to protein's beneficial
effects, protein is certainly necessary for proper bone matrix
formation and metabolism. It is likely a chronic suboptimal
intake will jeopardize this function. One could conjecture
that the studies finding a negative association between protein
and osteoporosis have somehow highlighted this aspect of the
equation. Those studies finding a positive association between
protein and osteoporosis are probably looking at the endogenous
acid production issue.
In an article by Remer, he calculated the potential renal
acid load (PRAL) of frequently consumed foods in order to
help dietitians design diets of varying urinary pH. On their
list, animal protein sources (as expected) were calculated
to increase PRAL.
However, grain products, legumes and dairy products (especially
hard cheeses) also increased PRAL. In fact , according to
Remer's data brown rice had a greater PRAL than any of the
meat products examined (with the exception of canned corned
beef - if you want to call that meat).
Perhaps the most ironic of all, was Remer's finding that
cheeses had the highest of the calculated PRALs. Parmesan,
cheddar, and processed American cheese had PRALs almost 2
times any meat product. In light of Remer's data, the relationship
of protein and osteoporosis cannot fully be determined without
addressing the total dietary PRAL. The type of protein being
consumed (lean meats vs. Processed meats vs. Cheese) and the
other foods in the diet are likely to significantly affect
the study's outcome.
The protein osteoporosis controversy was addressed in a review
article by Spencer. According to the author, numerous studies
have been published on the calcium-losing effect of protein.
However, several aspects of the study conditions have to be
considered in the interpretation of the results.
Some of these are the type of protein, such as purified
proteins (which seem not to promote calciuria): the duration
of the study (there may be a transient increase in calciuria
followed by a normalization or reduction); whether the phosphorous
(which has an independent calcium sparing effect) intake remained
the same, was increased, or decreased; whether the diets were
under strict control or with outpatient volunteers; whether
the protein intake was changed from a low to a high protein
intake or was changed from a normal to a high protein intake;
and whether excessively high protein intakes were used.
All these factors affect urinary calcium excretion during
high protein consumption. After reviewing the available data,
based on the aforementioned criteria, the authors concluded,
"to our knowledge, no convincing data have been published
showing that a high protein diet, using complex proteins for
prolonged periods of time under strictly controlled dietary
conditions, causes calcium loss."
It is quite obvious that the role of dietary protein in calcium
homeostasis is complex and multifactorial in nature. However,
given the work of Remer, it may actually be the net PRAL of
the diet that is most important in influencing the development
of osteoporosis, rather than the diet's absolute protein content.
Since most of the current low carbohydrate diets encourage
the ample consumption of vegetables, this is likely to offset
any potential acidifying effects of increased dietary protein.
In fact, given most individuals do not consume enough vegetables
and fruits, these diets are likely to promote better acid-base
balance then the average American diet. Unlike the more modified
low carbohydrate diets, modern ketogenic diets may pose a
risk for calciuria since they rely heavily on animal protein,
cheeses, and cured meats, and are usually not salt restricted
(the Cl ion- not the Nat ion - can also cause a renal acid
load and subsequently calciuria).
However, since most people are in ketosis for only a short
period of time (after which they are theoretically supposed
to transition into a modified low carbohydrate diet), it is
unlikely that these diets will significantly contribute to
an individual's overall risk for osteoporosis.
Kidney and Liver Damage
While it is generally accepted that people with pre existing
kidney and liver disease will benefit from some level of protein
restriction there is no data to support proposition that increased
dietary protein will actually cause kidney or liver damage.
In a study by Blum, he examined the kidney function of a
group of healthy individuals consuming an ad lib. high-protein
diet, as compared to a group of healthy vegetarians (Isn't
that an oxymoron?). At the study's end, the authors concluded
that protein does not affect kidney function in normal kidneys,
and it does not influence the deterioration of kidney function
with age.
The relationship of protein and the liver is somewhat more
complex. Although there is no evidence that increased dietary
protein will cause permanent liver damage, there is an actual
dietary "protein ceiling". According to Rudman there
is a lever at which dietary protein intake can exceed the
liver's ability to metabolize it to the urea, thus leading
to a build up of intermediary metabolites. These metabolites
can subsequently lead to a toxic state in the affected individual.
The level of protein at which this will occur varies, but
it is thought to be possible when protein makes up 30-40%
of the calories in an eucaloric diet (the percent calories
from protein can be higher in a hypocaloric diet).
"Rabbit Starvation" (a term coined by V. Stefansson
to describe the phenomenon of excessive dietary protein) often
occurred among explorers who would live for long periods of
time on extremely low fat small game animals (i.e. rabbits).
The condition was marked by nausea, vomiting, weight loss
and fatigue. "Rabbit Starvation" was reversible
when the percentage of daily calories from protein began to
drop. Although the "Rabbit Starvation" phenomenon
could effect an individual consuming a ketogenic diet, it
is highly improbable.
In general, if one is consuming commercially available meats
(even chicken), the percentage of calories from fat would
be too high to induce this condition. In the modified low
carbohydrate diets, due to the varied food sources, the risk
of protein toxicity, for all practical purposes, is non-existent.
Conclusion
A critical reading of the current literature certainly supports
the dietary trends of decreased carbohydrate intake (especially
of neocarbs), increased protein intake, and increased fat
intake (especially of monounsaturates and N-3 polyunsaturates).
The data that supports these contentions comes from a wide
spectrum of disciplines, including the basic sciences, medical
science, epidemiology, and anthropology.
The one dietary program that addresses these principles in
full, is the so called "evolutionary diet." The
modern inception of this prehistoric lifestyle would favor
the consumption of lean meats (preferably wild game or non-grain
fed, free-range domesticated animals), fish, seafood, vegetables,
fruits, raw nuts, and seed. Notably absent from this dietary
genre are dairy products, cereal grains, beans, legumes and
concentrated sweets (except for perhaps the occasional foray
into raw honey!).
Adherence to these dietary guidelines will not only address
obesity, but may also prove helpful in the management of everything
from NIDDM to diseases of autoimmunity to cardiovascular illnesses.
The guidelines are broad, but can be made quite specific depending
on the goals, lean body mass, activity level, and overall
health of the patient.
In the last few years, there has been a literal explosion
of data in the nutritional sciences. Sometimes when addressing
this data, we are put in the uncomfortable situation of realizing
that today's facts are rapidly becoming tomorrow's fiction.
However, by keeping an open mind and always questioning what
we think we know, we will be able to provide our patients
with the best and most innovative care possible.
Dr. Mercola's Comment:
My congratulations to Dr. Brasco for compiling such an
outstanding review of the concerns that some have when confronted
with the "low carb" diet. Dr. Brasco is a close
personal friend and is also the physician who covers for me
when I go out of town.
He is an internist and gastroenterologist and I believe
one of the best in the country. It is a strange paradox of
medicine that most GI specialist know virtually nothing about
nutrition. That is certainly not true of Dr. Brasco who is
clearly one of the leading nutritional GI specialists in the
country.
I typically warn my patients that the diet recommended
is NOT low carbohydrate but full of vegetables which are the
good carbohydrates. Dr. Brasco provides an incredible review
of the literature and some very sound scientific support for
what appears to be the diet most of us were designed to eat.
I frequently explain to patients that part of the reason
for the confusion on the carbohydrate issue is the fact that
not all carbohydrates are created equal. The glycemic index
mentioned above is one science tool that is used to explain
this, but most patients have a hard time with this concept.
I give them an analogy to think of grains and most below
ground vegetables as a simple train. Each car in the train
represents a simple sugar molecule which is easily broken
down once it reaches the digestive system.
I then ask them to visualize that same train but this
time stacked 20 to 50 high with other trains and each train
care interconnected to the cars above them. This is an accurate
representation of the much more highly complexed and branched
sugar molecules that are present in most above ground vegetables.
They have multiple bonds connecting each of the sugar
molecules and take the body a long time to break them down.
The extra time allows the body to slowly use the sugar and
thus not have to secrete large amount of insulin to store
the excess.
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