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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?

*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 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.

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.

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