Appendix
A: What About the Widely Advocated Dietary Restrictions
on Fat, Protein, and Salt, and the Current High-Fiber
Fad? /
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Most of this book
is instructional, of the how-to variety. The intent
of this appendix is to provide you with a little of
the science that surrounds the program described in
the rest of the book. I hope that I can cut through
some of the myths that cloud diet and the treatment
of diabetic complications so that you will have the
why that supports the how-to. We've already discussed
some of the myths. We'll look at the origins of those
myths to try to give you as many of the facts as are
available at this writing. If your only interest is
in the how-to, feel free to skip this chapter.
Once you've started to
follow a restricted-carbohydrate diet, you may find
yourself pressured by well-meaning but uninformed
friends or family, or even newspaper articles, to
cease penalizing yourself and eat more "fun"
foods, sweets, and treats. This chapter will provide
you with specific scientific information that underpins
my philosophy and will perhaps give you some ammunition
for responding to this pressure. Even if you skip
it now, you may want to come back to it later, or
show it to your loved ones to lay their concerns to
rest. As I don't expect most readers to be scientists,
I've tried to keep all these explanations relatively
simple. Some of the explanations may at this moment
represent more theory than fact, but they're based
on the latest information available to us.
How Did the Commonly Prescribed
High-Carbohydrate Diet Come About?
If, like me, you've
had diabetes for a while, you've probably been told
to cut way down on your dietary intake of fat, protein,
and salt, and to eat lots of complex carbohydrate.
You may even have read this advice in publications
circulated to diabetic patients.
Why is
such advice being promulgated, when the major cause
of such diabetic complications as heart disease, kidney
disease, high blood pressure, and blindness is high
blood sugar?
When I first developed
diabetes, in 1947, little was known about why this
disease, even when treated, caused early death and
such distressing complications. Prior to the availability
of insulin, about twenty-five years earlier, people
with Type I diabetes usually died within a few months
of diagnosis. Their lives could be prolonged somewhat
with a diet that was very low in carbohydrate and
usually high in fat. Sufferers from the milder Type
II diabetes frequently survived on this type of diet,
without supplemental medication. When I became diabetic,
oral hypoglycemic agents were not available, and many
people were still following very low carbohydrate,
high-fat diets. It was at about this time that diets
very high in saturated fats, with resultant high serum
cholesterol levels, were experimentally shown to correlate
with blood vessel and heart disease in animals. It
was promptly assumed by many physicians that the complications
of diabetes, nearly all of which related to abnormalities
of large or small blood vessels, were caused by the
high-fat diets. I and many other diabetics were therefore
treated with a high-carbohydrate, low-fat diet. This
new diet was adopted in the mid-1940s by the ADA,
the New York Heart Association, and eventually by
the American Heart Association (AHA) and other groups
around the world. On the new diet, many of us had
even higher serum cholesterol levels, and still developed
the grave long-term complications of diabetes. Seemingly
unaware of the importance of blood sugar control,
the ADA raised the recommended carbohydrate content
to 40 percent of calories, and then more recently
to 60 percent.
Recent Developments Regarding
Risk Factors for Heart Disease
In the past twenty
years, research studies have generated considerable
new information about heart disease and vascular (blood
vessel) disease in general, and their relationship
to diabetes in particular. Some of this more recent
information is summarized here.
A number of fatty substances
have been found in the blood which relate to risk
of heart attacks and vascular disease. These include
HDL (high-density lipoprotein), LDL (low-density lipoprotein),
triglyceride, fibrinogen, and lipoprotein(a). High
serum levels of LDL, triglyceride, fibrinogen,
and lipoprotein(a) tend to increase cardiovascular
risk, while high levels of HDL tend to protect
from cardiovascular disease. Cholesterol is a component
of both LDL and HDL particles. The fraction of total
cholesterol found in LDL particles is an index of
risk, while the fraction of cholesterol found in HDL
particles is an index of protection. Nowadays, when
we want to estimate the effects of lipids upon the
risk of coronary artery disease, we look at the ratio
of total cholesterol to HDL and also at fasting triglyceride
levels. Someone with high serum HDL can thus have
a high total cholesterol and yet be at low statistical
risk for a heart attack. Conversely, a person with
low total cholesterol and very low HDL may be at high
risk.
Recently a very large multicenter
study (the Lipid Research Clinics Trial) investigated
the effects of a low-fat, high-carbohydrate diet on
middle-aged men. The study followed 1,900 people for
seven years. Throughout this period, total cholesterol
had dropped 5 percent from baseline in the low-fat
group, but serum triglyceride went up about 10 percent!
(Serum triglyceride rises very rapidly after a high-carbohydrate
meal in nondiabetics, and moves up and down with blood
sugar levels in most diabetics.) As with prior studies,
no significant correlation was found between serum
cholesterol levels and mortality rates.
On average, diabetics with
chronically high blood sugars have elevated levels
of LDL (the "bad" cholesterol) and depressed
levels of HDL (the "good" cholesterol),
even though the ADA low-fat diet has now been in use
for many years. Of great importance is the recent
discovery that the forms of LDL that harm arteries
are small, dense LDL, oxidized LDL, and glycosylated
LDL. All of these increase as blood sugar increases.
In addition, independently of blood sugars, high serum
insulin levels caused by high-carbohydrate diets bring
about increased production of small, dense LDL particles
and enlargement of the cells lining and surrounding
arteries.
Under normal conditions,
receptors in the liver remove LDL from the bloodstream
and signal the liver to reduce its manufacture of
LDL when serum levels rise even slightly. Glucose
may bind to the surface of the LDL particle and also
to liver LDL receptors, so that LDL cannot be recognized
by its receptors. In people with high blood sugars,
many LDL particles thus become glycosylated, and are
therefore not cleared by the liver. They accumulate
in the blood, where they can become incorporated into
the walls of arteries, forming fatty deposits called
atherotic plaques. Since liver LDL production cannot
be turned off by the glycosylated LDL (and also the
presence of glycosylated LDL receptors), the liver
continues to manufacture more LDL, even though serum
levels may be elevated.
The proteins in the walls
of arteries can also become glycosylated, rendering
them sticky. Other proteins in the blood then stick
to the arterial walls, causing further buildup of
plaque.
Serum proteins also glycosylate
in the presence of glucose. White blood cells called
macrophages ingest glycosylated proteins and glycosylated
LDL. The loaded macrophages swell up, becoming very
large. These transformed macrophages, loaded with
fatty material, are called foam cells. The foam cells
penetrate the sticky arterial walls, causing disruption
of the orderly architecture of the artery, and narrow
the channel through which blood can flow.
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