If, like me, you’ve had diabetes for a while, you’ve probably been told to cut When I first developed diabetes, in 1946, little was known about why this …
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
Taubess award-winning Science article The Soft Science of Dietary Fat,
which is available on the Web site for this book, wwwdiabetes-
bookcom/articles/ssdfshtml, or from the March 2001 edition of the journal
Science Another masterpiece by Taubes, What If Its 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 books 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 Weve already discussed some of the myths Well 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 youve 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 dont expect most readers to be
scientists, Ive tried to keep all these explanations relatively simple
Some of the explana- tions may at this moment represent more theory than
fact, but theyre based on the latest information available to us
HOW DID THE COMMONLY PRESCRIBED HIGH-CARBOHYDRATE DIET COME ABOUT?
If, like me, youve had diabetes for a while, youve 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 ADAs 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 lipoproteina High serum levels of
LDL, triglyceride, fibrinogen, homocysteine, C-reactive protein, and
lipoproteina 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 cant 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 stickyOther proteins in the blood then stick to
the arterial walls, causing further buildup of plaque
Serum proteins glycosylate in the presence of glucoseWhite 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
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 This 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, lipoproteina,
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 bloodMost longterm,
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 middleaged 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
elevated 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]
Furthermore, research published in the journal Diabetes in 1990
demonstrated that elevated serum insulin levels cause excessive leakage of
protein from small blood vessels This is a common factor in the etiology
of blindness via macular edema and kidney disease in diabetics
Although the AHA and the ADA have been recommending lowfat, high-
carbohydrate diets for diabetics for many decades, no one had compared the
effects on the same patients of low- versus highcarbohydrate 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 22 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 Thats 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 didnt stop It
is only logical to look elsewhere, to elevated blood sugar and
hyperinsulinemia, for the causes 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 more than thirty years ago, when I
abandoned the high-carbohydrate, low-fat diet that I had been following
since 1946
Sometimes, months to years after a patient has experienced normal or near-
normal blood sugars and improvements in the cardiac risk profile, we will
see deterioration in the results of such tests as those for LDL, HDL,
homocysteine, and lipoproteina All too often, the patient or his
physician will blame our diet Inevitably, however, we find upon further
testing that his thyroid activity has declined Hypothyroidism is an
autoimmune disorder, like type 1 diabetes, and is frequently
inherited by
diabetics and their close relatives It can appear years
before or after the development of diabetes and is not caused by high blood
sugars In fact, hypothyroidism can cause a greater likelihood of
abnormalities of the cardiac risk profile than can blood sugar
elevation The treatment of a low thyroid condition is oral replacement of
the deficient hormones-usually one pill daily The best screening test is
free T3 If this is low, then a full thyroid risk profile should be
performed Correction of the thyroid deficiency inevitably
corrects the abnormalities of cardiac risk factors that it caused
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
If your physician finds all of this hard to believe, he or she might
benefit from reading the seventy articles and
abstracts on this subject
contained in the Proceedings of the Fifteenth International Diabetes
Foundation Satellite Symposium on Diabetes and Macrovascular
Complications,Diabetes 45, Supplement 3, July 1996 Also worth reading is
Effects of Varying Carbohydrate Content of Diet in Patients with Non-
Insulin Dependent Diabetes Mellitus, by Garg et al, Jnl Amer Med Assoc
1994; 271:1421-1428
By looking at how the kidney functions, one can better understand the
relative roles of glucose and protein in the 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 or tuft 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
Fig A-1 The microscopic filtration unit of the kidneys
The glomerular filtration rate GFR is a measure of how much filtering the
kidneys perform in a given period of time Many diabetics with frequent
high blood sugars and normal kidneys will initially 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 not uncommon 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 kidneys that were not fully functional 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
ammonium, 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 nondiabetic people on high protein meat-eating and very low
protein vegetarian diets,
disclosed no difference in GFRs 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 1
diabetics without discernible kidney disease were put on protein-restricted
diets, and experienced a very small reduction in GFR and no change in other
measures of kidney function As long ago as 1984, a study appeared in the
journal Diabetic Nephropathy demonstrating that elevated GFR is neither a
necessary nor a sufficient condition for the development of diabetic kidney
disease This evidence would suggest that the currently prevailing
admonition to all diabetics to reduce protein intake is unjustified
A 1995 article in the journal Nutritional Biochemistry, 6:411-437,
demonstrated that a higher protein diet enables the kidneys to increase
their capacity for net acid secretion as ammonium
Studies on diabetic rats have shown the following: Rats with blood sugars
maintained at 250 mg/dl rapidly develop diabetic nephropathy kidney
disease If their dietary protein is increased, kidney destruction
accelerates At the same laboratory, diabetic rats 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
Other studies have enabled researchers to piece together a scenario for the
causes of diabetic nephropathy, where glycosylation of proteins, abnormal
clotting factors, abnormal platelets, antibodies to glycosylated proteins,
and so on, join together to injure glomerular capillaries Early injury may
only cause reduction of electrical charge on the pores As a result,
negatively charged proteins such as albumin leak through the pores and
appear in the urine Glycosylated proteins
leak through pores much earlier than normal proteins High blood pressure,
and especially high serum insulin levels, can increase GFR and force even
more protein to leak through the pores If some of these proteins are
glycosylated or glycated, they will stick to the mesangium, the tissue
between the capillaries Examination of diabetic glomeruli indeed discloses
large deposits of glycated proteins and antibodies to glycated proteins in
capillary walls and mesangium As
these deposits increase, the mesangium
compresses the capillaries, causing pressure in the capillaries to increase
enlarging the pores and larger proteins to leak from the pores This
leads to more thickening of the mesangium, more compression of the
capillaries, and acceleration of destruction Eventually the mesangium and
capillaries become a mass of scar tissue Independently of this, both high
blood sugars and glycated proteins cause mesangial cells to produce type IV
collagen, a fibrous material that further increases their bulk Increase in
mesangial volume has been found to be commonplace in poorly controlled
diabetes even before albumin or other proteins appear in the urine
Many studies performed on humans show that when blood sugars improve, GFR
improves and less protein leaks into the urine When blood sugars remain
high, however, there is further deterioration There is a point of no
return, where a glomerulus has been so injured that no amount of blood
sugar improvement can revive it Although this seems to be true for humans,
blood sugar normalization has actually brought about the appearance of new
glomeruli in rats
Nowadays many diabetics who have lost all kidney
function are treated by
artificial kidneys dialysis machines that remove nitrogenous wastes from
the blood In order to reduce the weekly number of dialysis treatments,
which are costly and unpleasant, patients are severely restricted in their
consumption of both water and dietary protein Instead of using large
amounts of carbohydrate to replace the lost calories, many dialysis centers
now recommend olive oil to their diabetics Olive oil is high in
monounsaturated fats, which are believed to lower the risk of heart
disease
Because the survival rate of diabetics on dialysis is so much lower than
that of nondiabetics, some dialysis centers are now using low carbohydrate,
high-protein diets for their diabetic patients
In summary: Diabetic nephropathy does not appear if blood sugar is kept
normal Dietary protein does not cause diabetic nephropathy, but can
possibly still uncertain slightly accelerate the process once there has
been major, irreversible kidney damage Dietary protein has no substantial
effect upon the GFR of healthy kidneys, certainly not in comparison to the
GFR increase caused by elevated blood sugar levels
The May 1996 Journal of the American Medical Association
published a
summary of fifty-six studies demonstrating that in nondiabetics increased
protein consumption actually lowered blood pressure
RESTRICTIONS ON SALT INTAKE: ARE THEY REASONABLE FOR ALL DIABETICS?
Many diabetics have hypertension, or high blood pressure About half of all
people with hypertension will experience blood pressure elevations when
they eat substantial amounts of salt for at least two months This rarely
occurs in those who are not already hypertensive Hypertension accelerates
glomerulopathy destruction of the glomerulus in people with chronically
elevated blood sugars, but in type 1 diabetes, hypertension usually appears
after, not before, the appearance of kidney damage as indicated by
significant amounts of albumin in the urine Is it therefore appropriate to
ask all diabetics to lower their salt intake? Let us look at a few of the
mechanisms involved in the hypertension that some diabetics experience
Your physician might find informative the following articles on this
subject:
Molecular and Physiological Aspects of Nephropathy in Type 1 Diabetes
Mellitus, by Raskin and Tamborlane, Jnl Diabetes and Its Complications,
1996, 10:31-37; The Effects of Dietary
Protein Restriction and Blood
Pressure Control on the Progression of Chronic Renal Disease, by S Klahr
et al, New England Jnl Med, 1994, 330:877-884; also, in the same issue of
New England Jnl Med, the editorial
The Role of Dietary Protein Restriction in Progressive Azotemia pp 929-
930 Another study, in the journal Diabetes Care, 25:425-430, in the year
2000, showed that obese people on a high-protein diet lost more fat and
less muscle mass than those on a low-fat diet They also showed more than
double the reduction in LDL the bad cholesterol
People with advanced glomerulopathy will inevitably develop hypertension,
in part because GFR is severely diminished These people cannot make enough
urine, and therefore retain water Excessive water in the blood causes
elevated blood pressure There are many other ways hypertension can be
caused by high blood sugars The mere presence of high blood sugar will
cause water to leave tissues and enter the bloodstream, even experimentally
in nondiabetics
It is not unusual to observe reduction in blood pressure concomitant with
control of blood sugar Studies have shown that many, and possibly most,
hypertensive nondiabetics are insulin-resistant,
and therefore have high
serum insulin levels In addition to causing elevation of serum
triglycerides and reduction in serum HDL in nondiabetics, high serum
insulin levels have long been known to foster salt and water retention by
the kidneys Furthermore, excessive insulin
stimulates the sympathetic nervous system, which in turn speeds up the
heart and constricts blood vessels, causing further increase in blood
pressure Thus type 2 diabetics who eat lots of carbohydrate, and therefore
will tend to make excessive insulin, can readily develop hypertension Type
1 diabetics treated with the usual industrial doses of insulin to cover
high-carbohydrate diets are likewise more susceptible to hypertension One
dramatic study showed that in hypertensive individuals, blood pressure is
directly proportional to serum insulin level A report from Nottingham,
England, showed that a brief infusion of insulin and glucose would increase
blood pressure in normal men without changing their blood sugars A 1998
study in Glasgow, Scotland, demonstrated that salt restriction increased
insulin resistance in type 2 diabetics
A study of older individuals who were rotated between low-, moderate-,
and
high-salt diets demonstrated that those on low-salt diets experienced
significantly more sleep disturbances, and had more rapid heart rates and
higher serum norepinephrine adrenaline levels An international study
called Intersalt, covering 10,079 people in 32 countries, reported in 1988
that salt has only small importance in hypertension More recently,
another study showed that salt restriction
increases insulin resistance and thus can indirectly increase blood
pressure Large amounts of dietary salt can facilitate loss of calcium from
bones of post-menopausal women, who are already at high risk for
osteoporosis bone weakening
Why dont all diabetics on high-carbohydrate diets or all poorly controlled
diabetics have hypertension?
One reason is that the body has several very efficient systems for
unloading sodium a component of salt and water One of the more important
of these systems is controlled by a hormone manufactured in the heart
called atrial naturietic factor ANFWhen the heart is expanded by even a
slight fluid overload, it produces ANF The ANF then signals the kidneys to
unload sodium and water Hypertensive individuals, and the children of two
hypertensive parents,
tend to produce much lower amounts of ANF than do
normal people Nonhypertensive
diabetics apparently are able to produce enough ANF to control the blood
pressure effects of high blood sugars and high serum insulin levels,
provided they do not have moderately advanced kidney disease Indeed, a
study, in which some of my patients participated, showed that diabetics
with high blood sugars produce significantly more ANF than those with lower
blood sugars
How does all this apply to you? First, you and your physician should know
if you have glomerulopathy This is readily determined if the renal risk
profile tests suggested in Chapter 2 are performed If these tests are
abnormal, your physician may advise you to reduce your salt
intake because salt is much more likely to cause hypertension in people
with diminished GFR
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 doctors 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 days 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 pressureRecent 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 isnt adequate
for our purpose, since were 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 dont 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 its 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 25-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
So whats wrong with that?
As attractive as it may seem, the concept is clearly flawed in three
respects: First, diabetics show much higher blood sugar increases than
nondiabetics Second, digestion of the carbohydrate portion of a meal
typically takes at least 5 hours in the absence of gastroparesis, and the
index ignores effects upon blood sugar that last longer than 3 hours
Finally, the index is an average, and true numbers have been found to vary
considerably from one person to another, from one time to another, and from
one study to another As Ive pointed out, a food that makes my blood sugar
rise dramatically may have little or no effect on that of one of my
patients who still makes some insulin
Unfortunately, many dieticians and diabetes educators still recommend foods
that have been shown to have a low glycemic index in some study, and
assume that an index of 40 or 50 percent is low They may
thus select
apples, lima beans, and the like as appropriate for diabetics,
even though consumption of typical portions of these foods will cause
considerable blood sugar elevations in diabetics
A medium-sized apple, according to one table of food values, contains 21
grams of carbohydrate It will raise my own blood sugar by 105 mg/dl, and
much more rapidly than I can prevent with an injection of rapid-acting
insulin Peanuts usually have the lowest glycemic
index in many studies about 15 percent, yet 1 ounce contains 6 grams of
carbohydrate and close to 1 ounce of protein Ive found this portion to
raise my blood sugar by 80 mg/dl, albeit much more slowly than the apple
Since peanuts work so slowly more slowly than 3 hours, I can substitute 1
ounce for 6 grams carbohydrate and 1 ounce protein in a meal-but who can
eat only one handful of peanuts? The carbohydrate foods that we recommend,
salads and selected
vegetables Chapter 9, have glycemic indices lower than peanuts and work
more slowly Furthermore, they are more filling The issue here, though, is
to understand that such indices are unreliable and wont help you keep your
blood sugars normalized
WHAT DIET WILL WORK FOR
YOU?
Actual results are the yardstick for an appropriate diet We have the tools
for self-monitoring of blood sugar and blood pressure We have tests for
measuring kidney function, HgbA1C, thrombotic risk profiles, and lipid
profiles see Chapter 2 Under your doctors supervision, try
our diet recommendations for at least three months Then try any other diet
plan for three months and see what happens The differences may not be in
the direction that the popular literature would predict
Finally, in its most common usage, diet usually indicates some sort of
franchise The______Diet you can fill in the blank usually has a
particular name or marketing term associated with it and often comes with
products ready for your consumption When I use the
term, Im referring to diet in the very simple sense of what you eat Im
not selling a brand or products, but providing guidelines so that you can
understand how foods are likely to affect you You can then create your own
diet, one that will not only allow you to keep your blood sugars normalized
but also to satisfy yourself
By the way, natural peanut butter has a glycemic index much higher than
that of the peanuts from which it was created because
it is digested more
rapidly
