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 article “The Soft Science of Dietary Fat,” which is available at www.diabetes-book.com/articles/ssdf.shtml or in the March 3, 2001, issue 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 be found at www.diabetes-book.com/cms/articles/3-advice-a-commentary/7416-what-if-its-all-been-a-big-fat-lie. I also recommend his book Good Calories, Bad Calories (Knopf, 2007), as well as the very informative Trick and Treat by Barry Groves (Hammersmith Press, 2008). Both books are available at Amazon.com.
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 explanations may at this moment represent more theory than fact, but they’re based on the latest information available to us.
Throughout the appendix I refer to the adverse effects of high serum insulin levels. This does not mean that insulin should not be injected to normalize blood sugars. It is the industrial doses of insulin commonly produced or injected to cover high-carbohydrate diets that cause problems. Furthermore, high blood sugars cause many more problems of much greater severity than do high insulin levels.
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 or touted by many (not all) dietitians and certified diabetes educators.
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 supposedly 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) and the New York Heart Association, later by the American Heart Association (AHA), and eventually by other groups around the world. On the new diet, most of us had much higher serum cholesterol and triglyceride 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.
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 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 (high-density lipoprotein), LDL (low-density lipoprotein), triglyceride, fibrinogen, homocysteine, C-reactive protein, ferritin (iron), and lipoprotein(a). High serum levels of dense, compact LDL particles, triglyceride, fibrinogen, homocysteine, C-reactive protein, ferritin, 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 considered 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 recent update of the very large Framingham Heart Study found no relationship between saturated fat and serum cholesterol and none between cholesterol and heart disease.
A large multicenter study (the Lipid Research Clinics Coronary Primary Prevention 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 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 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. 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 may 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, excessive serum insulin levels dictated by high-carbohydrate diets bring about increased production of the potentially hazardous small, dense LDL particles and enlargement of the cells lining the arteries. We now can measure the size distribution of these LDL subparticles as a routine laboratory test. Most labs report the benevolent large, buoyant LDL subparticles as “type A” and the small, dense LDL subparticles as “type B.”
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 can 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 be released 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 glycation end products. These AGEs accumulate in the blood, where they can become incorporated into the walls of arteries, forming fatty deposits called atherosclerotic 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 foam 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 or stroke.
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 for stroke, heart disease, and kidney disease. 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 a heart attack. 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, lipoprotein(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 abnormal 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 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 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 low-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. A long-term study of 7,321 “nondiabetics” in 2006 showed that for every 1 percent increase in HgbA1C above 4.5 percent, the incidence of coronary artery disease increased 2.5-fold. The same study also showed that for every 1 percent increase in HgbA1C above 4.9 percent, mortality increased by 28 percent. Yet the ADA still advocates a target HgbA1C of 6.5–7 percent for selected diabetics, and higher for many others. No wonder I call diabetes an “orphan disease.” The “authorities” who write the rules are not supporting our well-being.
The National Health and Nutrition 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 ages 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 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 several 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 forty 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 fibrinogen. 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 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 hormone(s)—frequently one pill daily. The best screening test is free T3, tested by tracer dialysis. 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.
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 Basic Food Groups,” 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 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 1 million microscopic blood filters, called glomeruli. Figure A-1 illustrates how blood enters a glomerulus through a tiny artery called the afferent (incoming) arteriole. This 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 efferent (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. 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 10 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).
Fig. A-1. The microscopic filtration unit of the kidneys.
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. However, studies by an Israeli group 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 Harvard study on diabetic rats showed the following: Rats with blood sugars maintained at 250 mg/dl rapidly developed diabetic nephropathy (kidney disease). If their dietary protein was increased, kidney destruction accelerated. 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 the 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 in slightly damaged kidneys 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 by some 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.
By the way, it’s been shown that dietary protein stimulates the production of the satiety hormone PYY, thereby inhibiting overeating.
Many diabetics have hypertension, or high blood pressure. Less than 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. In fact, a study published in the Journal of the American Medical Association in May 2011 (305:1777–1785) showed that among nondiabetic, nonhypertensive individuals, there was no difference in the incidence of new hypertension over 7.9 years between the highest and lowest salt eaters. Furthermore, this study showed that cardiovascular mortality in the lowest salt consumers was five times that in the highest consumers. Hypertension accelerates glomerulopathy (destruction of the glomerulus) in people with chronically elevated blood sugars, but in type 1 diabetics, hypertension usually appears after, not before, the appearance of kidney damage as indicated by significant amounts of albumin in the urine. A study in the March 2011 issue of Diabetes Care showed that for type 2 diabetics, for every extra 2.3 grams of sodium (from salt) consumed, the risk of dying from all causes dropped by 28 percent. The following month, Diabetes Care published another study showing that type 1 diabetics who ate more sodium (salt) were less likely to develop kidney failure. 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.
People with advanced glomerulopathy will inevitably develop hypertension, in part because GFR is severely diminished. These people cannot make enough urine, and therefore they 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 a 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 a 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.
Why don’t 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 (ANF). When 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 (my patients).
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 doctor’s office, then you should measure your own blood pressure at home in a similar fashion. Repeated measurements with low values just exceeding 120/70 suggest that your blood pressure is “borderline.” You then may or may not 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 here. 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. People with advanced kidney disease should not consume supplemental potassium. 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 or increase dietary calcium consumption. Those who advocate salt restriction for all humans should read the results of the National Health and Nutrition Examination Survey, which showed that cardiovascular morbidity in obese individuals was reduced with higher salt intake (Journal of the American Medical Association, 1999; 282:2027–2034), and the 2011 studies cited earlier in this section.
“Fiber” is a general term that has come to refer to the indigestible 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 thirty-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. When I finally met Dr. Jenkins in 2010, he explained that the guar gum should have been mixed with the flour before the bread was baked. 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.
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 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 some of 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 of diabetics 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. Studies discussed in the book Trick and Treat by Barry Groves report many adverse health effects caused by excessive fiber consumption.
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. It is true, however, that low-carbohydrate vegetables are usually composed mostly of insoluble fiber and therefore contain far less digestible carbohydrate than starchy vegetables. Thus if the options are either fiber or starch, there is great value in “high fiber.”
Another 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 here) was within the normal range and her ratio of total cholesterol to HDL was very low (meaning her supposed 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 rapid-acting insulin (as much as I used for an entire meal). After 3 hours, my blood sugar went up by about 100 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 here, raise blood sugar relatively 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.*
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 then repeatedly 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.
This term was, as I recall, first coined by the same Dr. Jenkins mentioned in the previous 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 percentage. Thus, if a food generates a 3-hour area one-fifth that of glucose, its glycemic index would be 20 percent.
So what’s wrong with that?
As attractive as it may seem, the concept is clearly flawed in four respects: First, diabetics show vastly 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. Third, the index is an average of values for a number of different people, 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 I’ve 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. Finally and 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. I’ve 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 of carbohydrate and 1 ounce of protein in a meal and cover it with injected rapid-acting insulin—but who can eat only one handful of peanuts?*
The carbohydrate foods that we recommend, salads and selected vegetables (see Chapter 9, “The Basic Food Groups”), have glycemic indexes much lower than peanuts and work more slowly. Furthermore, they are more filling. The issue here, though, is to understand that such indexes are unreliable and won’t help you keep your blood sugars normalized.
Actual results are the yardstick for an appropriate diet. We have 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 doctor’s 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, I’m referring to “diet” in the very simple sense of what you eat. I’m 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.