Appendix
A: What About the Widely Advocated Dietary Restrictions
on Fat, Protein, and Salt, and the Current High-Fiber
Fad? /
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In recent years, the tendency of blood to clot has
come into focus as a major cause of heart attacks.
People whose blood clots too readily are at very high
risk. You may recall that one of the medical names
for a heart attack is coronary thrombosis. A thrombus
is a clot, and coronary thrombosis refers to the formation
of a large clot in one of the arteries that feed the
heart. People who have elevated levels of certain
clotting precursors or depressed levels of clotting
inhibitors in their blood are at high risk of dying
from heart attacks. The risk probably far exceeds
that caused by high LDL or low HDL. Some of the blood
factors that enhance clotting include fibrinogen and
factor VII. Another factor, lipoprotein(a)—abbreviated
Lp(a)—inhibits the destruction of small thrombi before
they become large enough to cause a heart attack.
All of these factors have been found to increase in
people with chronically high blood sugars. Platelets,
or thrombocytes, are particles in the blood that play
major roles in the blocking of arteries and the formation
of clots. These have been shown to clump together
and stick to arterial walls much more aggressively
in people with high blood sugars. What is exciting
is that all of these factors, including sticky platelets,
tend to normalize as long-term blood sugars improve.
Diabetics
die from heart failure at a rate far exceeding that
of people with normal glucose tolerance. Heart failure
involves a weakening of the cardiac muscle so that
it cannot pump enough blood. Most long-term, poorly
controlled diabetics have a condition called cardiomyopathy.
In diabetic cardiomyopathy, the muscle tissue of the
heart is slowly replaced by scar tissue over a period
of years. This weakens the muscle so that it eventually
"fails." There is no evidence linking cardiomyopathy
with dietary fat intake or serum lipids.
A fifteen-year study of
7,038 French policemen in Paris reported that "the
earliest marker of a higher risk of coronary heart
disease mortality is an elevation of serum insulin
level." A study of middle-aged nondiabetic women
at the University of Pittsburgh showed an increasing
risk of heart disease as serum insulin levels increased.
Other studies in nondiabetics have shown strong correlations
between serum insulin levels and other predictors
of cardiac risk such as hypertension, elevated triglyceride,
and low HDL. The importance of elevated serum insulin
levels (hyperinsulinemia) as a cause of heart disease
and hypertension has taken on such importance that
a special symposium on this subject was held at the
end of the 1990 annual meeting of the ADA. A report
in a subsequent issue of the journal Diabetes Care
quite appropriately points out that "there are
few available methods of treating diabetes that do
not result in systemic hyperinsulinemia" unless
the patient is following a low-carbohydrate diet.
Although the AHA and the
ADA have been recommending low-fat, high-carbohydrate
diets for diabetics for many decades, no one had compared
the effects on the same patients of low- versus high-carbohydrate
diets until the late 1980s. Independent studies performed
in Texas and California demonstrated lower levels
of blood sugar and improved blood lipids when patients
were put on lower-carbohydrate, high-fat diets. It
was also shown that, on average, for every 1 percent
increase in HgbA1C (the test for average blood sugar
over the prior four months), total serum cholesterol
rose 2.2 percent and triglycerides increased 8 percent.
The National Health Examination
Follow-Up Survey, which followed 4,710 people, reported
in 1990 that "in the instance of total blood
cholesterol, we found no evidence in any age-sex group
of a risk associated with elevated values." That's
right—they found no risk associated directly with
elevated total cholesterol. On the same page, this
study lists diabetes as by far the single most important
risk factor affecting mortality. In males aged 55–64,
for example, diabetes was associated with 60 percent
greater mortality than smoking and double the mortality
associated with high blood pressure.
The evidence is now simply
overwhelming that elevated blood sugar is the major
cause of the high serum lipid levels among diabetics
and, more significantly, the major factor in the high
rates of various heart and vascular diseases associated
with diabetes. Many diabetics were put on low-fat
diets for so many years, and yet these problems didn't
stop. It is only logical to look elsewhere, to elevated
blood sugar and hyperinsulinemia, for the cause of
what kills and disables so many of us.
My personal experience
with diabetic patients is very simple. When we reduce
dietary carbohydrate, blood sugars improve dramatically.
After about two months of improved blood sugars, we
repeat our studies of lipid profiles and thrombotic
risk factors. In the great majority of cases, I see
normalization or improvement of abnormalities. This
parallels what happened to me nearly thirty years
ago when I abandoned the high-carbohydrate, low-fat
diet that I had been following since 1947.*
Why Is
Protein Restriction So Common?
About 30 percent
of diabetics develop kidney disease (nephropathy).
Diabetes is the greatest single cause of kidney failure
in the United States. Early kidney changes can be
found within two to three years of the onset of high
blood sugars. As we discussed briefly in Chapter 9,
the common restrictions on protein intake by diabetic
patients derive from fear regarding this problem,
and ignorance of the actual causes of diabetic kidney
disease.
By looking at how the kidney
functions, one can better understand the relative
roles of glucose and protein in kidney failure of
diabetes. The kidney filters wastes, glucose, drugs,
and other potentially toxic materials from the blood
and deposits them into the urine. It is the urine-making
organ. A normal kidney contains about 6 million microscopic
blood filters, called glomeruli. Figure
A-1 illustrates how blood enters a
glomerulus through a tiny artery called the incoming
arteriole. The arteriole feeds a bundle of tiny vessels
called capillaries. The capillaries contain tiny holes
or pores that carry a negative electrical charge.
The downstream ends of the capillaries merge into
an outgoing arteriole, which is narrower than the
incoming arteriole. This narrowing results in high
fluid pressure when blood flows through the capillary
tuft. The high pressure forces some of the water in
the blood through the pores of the capillaries. This
water dribbles into the capsule surrounding the capillary
tuft. The capsule, acting like a funnel, empties the
water into a pipelike structure called the tubule.
The pores of the capillaries are of such a size that
small molecules in the blood, such as glucose and
urea, can pass through with the water to form urine.
In a normal kidney, large molecules, such as proteins,
cannot readily get through the pores. Since most blood
proteins carry negative electrical charges, even the
smaller proteins in the blood cannot easily get through
the pores, because they are repelled by the negative
charge on each pore.
The glomerular filtration
rate (GFR) is a measure of how much filtering the
kidneys perform in a given period of time. Anyone
with a high blood sugar and normal kidneys will have
an excessively high GFR. This is in part because blood
glucose draws water into the bloodstream from the
surrounding tissues, thus increasing blood volume,
blood pressure, and blood flow through the kidneys.
A GFR that is one-and-a-half to two times normal is
commonplace in diabetics with high blood sugars prior
to the onset of permanent injury to their kidneys.
These people may typically have as much glucose in
a 24-hour urine collection as the weight of 5 to 50
packets of sugar. According to an Italian study, an
increase in blood sugar from 80 mg/dl to 272 mg/dl
resulted in an average GFR increase of 40 percent
even in diabetics with severe kidney disease. Before
we knew about glycosylation of proteins and the other
toxic effects of glucose upon blood vessels, it was
speculated that the cause of diabetic kidney disease
(nephropathy) was this excessive filtration (hyperfiltration).
The metabolism of dietary
protein produces waste products such as urea and ammonia,
which contain nitrogen. It therefore had been speculated
that in order to clear these wastes from the blood,
people eating large amounts of protein would have
elevated GFRs. As a result, diabetics have been urged
to reduce their protein intake to low levels. Studies
by an Israeli group, however, of people on high-protein
(meat-eating) and very low protein (vegetarian) diets,
disclosed no difference in GFR. Furthermore, over
many years on these diets, kidney function was unchanged
between the two groups. A report from Denmark described
a study in which Type I diabetics without discernible
kidney disease were put on protein-restricted diets,
and experienced a very small change in GFR and no
change in other measures of kidney function. These
would suggest that the currently prevailing admonition
to all diabetics to reduce protein intake is unjustified.
Recent studies on diabetic
rats have shown the following: Rats with blood sugars
maintained at 250 mg/dl rapidly develop diabetic nephropathy.
If their dietary protein is increased, kidney destruction
accelerates. Diabetic rats at the same laboratory,
with blood sugars maintained at 100 mg/dl, live full
lives and never develop nephropathy, no matter how
much protein they consume. Diabetic rats with high
blood sugars and significant nephropathy have shown
total reversal of their kidney disease after blood
sugars were normalized for several months.
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