A P P E N D I X A
What About the Widely Advocated Dietary Restrictions on Fat, Protein,
and Salt, and the Current High-Fiber Fad?
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. With respect
to a number of the issues raised in this section, I would also refer
you again to Gary Taubes’s award-winning Science article “The Soft Science
of Dietary Fat, ”which is available on the Web site for this book, www.diabetes-book.com/articles/ssdf.shtml,
or from the March 2001 edition of the journal Science. Another masterpiece
by Taubes, “What If It’s All Been a Big Fat Lie?,” appeared as the cover
article in the New York Times Magazine of July 2, 2002. It can also
be found on this book’s Web site.
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 appendix.
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, bread, pasta, and fruits. This chapter will provide
you with specific scientific information that underpins my approach
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 explana- tions 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 still 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 1946, 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 1 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. Most
sufferers from the milder type 2 diabetes 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 then-known complications
of diabetes, most 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 American Diabetes Association
(ADA), the New York Heart Association, and eventually by the American
Heart Association (AHA) and other groups around the world. On the new
diet, most of us had much 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 from 40 to 50 percent of calories, and then more
recently to 60 percent. The ADA’s most recent guidelines have backed
off by vaguely stating that some diabetics may do better with less carbohydrate.
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 substances have been found in the blood which relate to
risk of heart attacks and vascular disease. These include HDL (highdensity
lipoprotein), LDL (low-density lipoprotein), triglyceride, fibrinogen,
homocysteine, C-reactive protein, and lipoprotein(a). High serum levels
of LDL, triglyceride, fibrinogen, homocysteine, C-reactive protein,
and lipoprotein(a) tend to be associated with increased 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 (fatty substances)
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.
A large multicenter study (the Lipid Research Clinics Trial) investigated
the effects of a low-fat, high-carbohydrate diet versus a high-fat,
low-carbohydrate diet on nondiabetic middle-aged men with elevated cholesterol
levels. The study followed 1,900 people for seven years. Throughout
this period, total cholesterol had dropped only 5 percent from baseline
in the low-fat group, but serum triglyceride went up about 10 percent!
(Serum triglyceride rises very rapidly after a highcarbohydrate 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. Furthermore, a
study reported in the Journal of the American Medical Association in
1997 showed that a 20 percent increase in either saturated or monounsaturated
dietary fat lowered the risk of stroke to one-eighth of what it was
in individuals on lower-fat
diets. Unsaturated fats showed no such benefit.
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 glycated LDL. All of these increase as blood sugar increases. In
addition, independently of blood sugars, high serum insulin levels dictated
by high-carbohydrate diets bring about increased production of small,
dense LDL particles and enlargement of the cells lining the 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 become glycosylated, and are therefore not cleared by
the liver. This glycosylation is reversible if blood sugar drops. After
about 24 hours, however, a rearrangement of electron bonds occurs in
glycosylated proteins, so that the glucose can’t release even if blood
sugar drops. This irreversible glycosylation is called glycation, and
the affected protein molecules are said to be “glycated.” They are also
referred to as AGEs, or advanced glycosylation end products. These AGEs
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/
glycated LDL (and also the presence of glycosylated/glycated 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/
glycated, rendering them sticky.Other proteins in the blood then stick
to the arterial walls, causing further buildup of plaque. Serum proteins
glycosylate in the presence of glucose.White blood cells called macrophages
ingest glycosylated/glycated proteins and glycosylated/ glycated 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 now sticky arterial
walls, causing disruption of the orderly architecture of the artery,
and narrow the channel through which blood can flow.
The middle layer of the walls of large arteries contains smooth muscle
cells that can invade the fatty coating (plaque) that these cells create.
They then prevent the plaque from breaking loose. When the nerves that
control this smooth muscle die, as in diabetic autonomic neuropathy
(caused by high blood sugars), the muscle layer dies and calcifies.
It then cannot prevent plaque rupture. When a piece of ruptured plaque
enters the blood it can block narrow vessels upstream
and cause a heart attack.
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