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?
Whether your renal risk profile is normal or abnormal, your resting
blood pressure should also be measured. A proper measurement requires
that you be seated in a quiet room, without conversation, for 15–30
minutes. Blood pressure should be measured every 5 minutes, until it
drops to a low value and then starts to increase. The lowest reading
is the significant one. If you get nervous in the doctor’s office, then
you should measure your own blood pressure at home in a similar fashion.
Repeated measurements, with low values just exceeding 135/ 85, suggest
that your blood pressure is “borderline.” (The American Diabetes Association
suggests that 120/80 be considered borderline for younger diabetics.)
You then may benefit from dietary salt reduction. The only way to find
out is to check your blood pressure while on your current salt intake,
and again after following a low-salt (sodium) diet for at least two
months.* Your physician can give you guidelines for such a diet, and
you can consult nutritional tables such as those in the books listed
in Chapter 3. I would suggest that resting blood pressures be measured
several times a day, and at the same hours each day, throughout the
study. Each day’s blood pressures can then be averaged, and the averages
compared. If your blood pressure drops significantly on the low-salt
diet, your physician may urge you to keep the salt intake down. Alternatively,
he may want you to take small amounts of supplemental potassium, which
tends to offset the effects of dietary salt on blood pressure.Recent
studies suggest that as many as 40 percent of hypertensive patients
(the so-called low-renin hypertensives) may show lower blood pressures
when they take calcium supplements.
WHAT ABOUT DIETARY FIBER?
“Fiber” is a general term that has come to refer to the undigestible
portion of many vegetables and fruits. Some vegetable fibers, such as
guar and pectin, are soluble in water. Another type of fiber, which
some of us call roughage, is not water soluble. Both types appear to
affect the movement of food through the gut (soluble fiber slows processing
in the upper digestive tract, while insoluble fiber speeds digestion
farther down). Certain insoluble fiber products, such as psyllium, have
long been used as laxatives. Consumption of large amounts of dietary
fiber
is usually unpleasant, because both types can cause abdominal discomfort,
diarrhea, and flatulence. Sources of insoluble fiber include most salad
vegetables. Soluble fiber is found in many beans, such as garbanzos,
and in certain fruits, such as apples.
I first learned of attempts at using fiber as an adjunct to the treatment
of diabetes about twenty-five years ago. At that time, Dr. David Jenkins,
in England, reported that guar gum, when added to bread, could reduce
the maximum postprandial blood sugar rise from an entire meal by 36
percent in diabetic subjects. This was interesting for several reasons.
First of all, the discovery occurred at a time when few new approaches
to controlling blood sugar were appearing in the medical literature.
Second, I missed the high-carbohydrate foods I had given up, and hoped
I might possibly reinstate some. I managed to track down a supplier
of powdered guar gum, and placed a considerable amount into a folded
slice of bread. I knew how much a slice of bread would affect my blood
sugar, and so as an experiment, I used the same amount of guar gum that
Dr. Jenkins had used, and then ate the concoction on an empty stomach.
The chore was difficult, because once moistened by my saliva, the guar
gum stuck to my palate and was difficult to swallow. I did not find
any change in the subsequent blood sugar increase. Despite the unpleasantness
of choking down powdered guar gum (which is often used in commercial
products such as ice cream as a thickener), I repeated this experiment
on two more occasions, with the same result. Subsequently, some investigators
have announced results similar to those of Dr. Jenkins, yet other researchers
have found no effect on postprandial blood sugar. In any event, a reduction
of postprandial blood sugar increase by only 36 percent really isn’t
adequate for our purpose, since we’re shooting for the same blood sugars
as nondiabetics. This means virtually no rise after eating.
*To complicate things somewhat, a 1998 report in the Journal of Clinical
Endocrinology and Metabolism demonstrated that salt restriction in nonhypertensive
type 2 diabetics reduced insulin sensitivity by 15 percent. A prior
article in the American Journal of Hypertension found a similar effect
in hypertensive individuals. Another study of rats, published in the
journal Diabetes in 2001, found that this insulin resistance cannot
be reversed by the insulin-sensitizing agent pioglitazone.
Dr. Jenkins also discovered, however, that the chronic use of guar
gum resulted in a reduction of serum cholesterol levels. This is probably
related to the considerable recirculation of cholesterol through the
gut. The liver secretes some cholesterol into bile, which is released
into the upper intestine. This cholesterol is later absorbed lower in
the intestines, and eventually reappears in the blood. Guar binds the
cholesterol in the intestines, so that rather than being absorbed, it
appears in the stool. In the light of these very interesting results,
other researchers studied the effect of foods (usually beans) containing
other soluble forms of fiber. When beans were substituted for faster-acting
forms of carbohydrate, postprandial blood sugars in diabetics increased
more slowly, and the peaks were even slightly reduced. Serum cholesterol
levels were also reduced by about 15 percent. But subsequent studies,
reported in 1990, have uncovered flaws in the original reports, casting
serious doubt upon any direct effect of these foods upon serum lipids.
In any event, postprandial blood sugars were never normalized by such
diets. Many popular articles and books have appeared advocating “high-
fiber” diets for everyone—not just diabetics. Somehow, “fiber” came
to mean all fiber, not just soluble fiber, even though the only viable
studies had utilized such products as guar gum and beans.
In my experience, reduction of dietary carbohydrate is far more effective
in preventing blood sugar increases after meals. The lower blood sugars,
in turn, bring about improved lipid profiles.
A recent food to join the high-fiber trend is oat bran. This has gotten
a lot of play in the popular press. A patient of mine started substituting
oat bran muffins for protein in her diet. Before she started, her HgbA1C
(see Chapter 2) was within the normal range and her ratio of total cholesterol
to HDL was very low (meaning her cardiac risk ratio was low). After
three months on oat bran, her HgbA1C became elevated and her cholesterol-to-HDL
ratio nearly doubled. I tried one of her tiny oat bran muffins after
first injecting 3 units of fast-acting insulin (as much as I use for
an entire meal). After 3 hours, my blood sugar went up by about l00
mg/dl, to 190 mg/dl. This illustrates the adverse effect that most oat
bran preparations can have upon blood sugar. This is because most such
preparations contain flour. On the other hand, I find that certain bran
products, such as the bran crackers listed in Chapter 10, raise blood
sugar very little. Unlike most packaged bran products, they contain
mostly bran and little flour. They therefore have very little digestible
carbohydrate. You can perform similar experiments yourself. Just use
your blood glucose meter. Beware of commercial “high-fiber” products
that promise cholesterol reduction. If they contain carbohydrate, they
must at least be counted in your meal plan and will probably render
little or no improvement in your lipid profile.
Fiber, like carbohydrate, is not essential for a healthy life. Just
look at the Eskimos and other hunting populations that survive almost
exclusively on protein and fat, and don’t develop cardiac or circulatory
diseases.*
WHAT ABOUT THE GLYCEMIC INDEX?
For a number of years, the term “glycemic index” has popped in and
out of the popular press. It also has been a pet subject for many dietitians
and diabetes educators. I will explain why, but I think it’s important
to make clear that there is simply no way to determine objectively how
any given food at any given time is going to behave in any given individual,
unless blood sugar is tested before and for a number of hours after
its consumption. It sounds like an elegant idea—mashed potatoes do X;
table sugar does Y. As with a lot of elegant ideas, however, the reality
is far more complex.
*As the first edition of this book was going to press, a report appeared
entitled “Dietary Fiber, Glycemic Load, and Risk of Non-Insulin-Dependent
Diabetes in Women” (Jnl Amer Med Assoc 1997; 277:472–477). This study
of 65,173 nurses and former nurses found a strong association between
diets high in starch, flour, and sweet foods and the development of
type 2 diabetes. Furthermore, consumption of minimally refined grain
(such as bran without flour) lowered this risk. The combination of high
glycemic foods and low intake of unrefined insoluble fiber was associated
with a 2.5-fold higher incidence of diabetes. If you remember our discussion
of beta cell burnout (pages 39–42), this should come as no surprise.
This term was, as I recall, first coined by the same Dr. Jenkins mentioned
in the above section. The concept is more complicated than the popular
press would have you believe.
Imagine two graphs, each depicting a curve of a blood sugar increase
over a 3-hour time span. The first curve is after eating pure glucose,
the standard. The second is after eating any other food of equivalent
total carbohydrate content (20 grams glucose versus 20 grams carbohydrate
content of, say, rice).
Dr. Jenkins defined the glycemic index for a given food in terms of
how its curve related to that of the glucose curve.
So to arrive at the index for rice, for example, the area under the
3- hour curve of blood sugar increase caused by the rice would be divided
by the area under the curve for pure glucose. The measurement is usually
made on a number of nondiabetics and then averaged, and finally expressed
as a percent. Thus, if a food generates a 3-hour area one-fifth that
of glucose, its glycemic index would be 20 percent.
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