Structure & Function: Support for Glucose Metabolism
Adult Alpha Lipoic acid 300 - 600 mg Beta carotene* Biotin 1 mg/d Brewer's yeast** 1 tbsp 3x/d Carnitine* Chromium** 200-400 mcg/d Copper 2 mg/d CoQ10* DHEA* Fiber 20-30 g/d Garlic* Ginkgo biloba* Lecithin* Magnesium 400 mg/d Quercetin 500 mg/d Selenium 200 mcg/d Vitamin A* Vitamin B-complex 25 mg/d Vitamin C 1 g/d Vitamin E 200 IU/d Zinc (preferably picolinate) 25 mg/d Luteolin*
* Please refer to the respective topic for specific nutrient amounts.
** if allergic to yeast - use chromium supplements instead, unless the diabetic also has gout.
Note 1: Under no circumstances should a person suddenly stop taking diabetic drugs, especially insulin. According to current information, an IDDM patient will never be able to stop taking insulin. In addition, since these therapies may change blood sugar levels significantly, those who are on insulin or blood sugar-lowering drugs must be carefully monitored by a physician to assure proper control of drug dosages.
Note 2: All amounts are in addition to those supplements have a Recommended Dietary Allowance (RDA). Due to individual needs, one must always be aware of a possible undetermined effect when taking nutritional supplements. If any disturbances from the use of a particular supplement should occur, stop its use immediately and seek the care of a qualified health care professional.
Note 3: Some authorities have stated that aloe vera is contra-indicated as a supplement in diabetes.
Note 4: All amounts are in addition to those supplements having a Recommended Dietary Allowance (RDA). Due to individual needs, one must always be aware of a possible undetermined effect when taking nutritional supplements. If any disturbances from the use of a particular supplement should occur, stop its use immediately and seek the care of a qualified health care professional.
Although the following discussion of specific nutrients documents their usefulness, they are not a panacea, proper and adequate treatment of diabetes requires much more than a bottle of supplements.
In general, diabetics should be on a heavy supplementation program to help prevent many of the major diabetic complications, particularly atherosclerosis and diabetic neuropathy.
Most other supplements have been tried, some of which provide alternatives to listed nutrients within the same category. Vitamin A is an antioxidant, although most authorities now recommend its precursor, Beta carotene.
The objectives are always to improve the metabolism of the diabetic, such that energy and endogenous insulin may, at least, approach a balance.
Digestion, elimination, the immune system and hormonal balance, primarily, are all addressed by different protocols.
Digestion and elimination may be considered together. Fiber is listed but a specific type often used is guar gum. Enzymes, which may also contribute to anti-oxidation, include CoQ10 and superoxide dismutase.
Several plant foods, or supplements, may contribute to boosting the immune system: garlic (500 mg q.i.d.), green barley and spirulina.
[Rumessen J.J., et al. Fructans of Jerusalem artichokes: Intestinal transport, absorption, fermentation, and influence on blood glucose, insulin, and C-peptide responses in healthy subjects. Am J Clin. Nutri 52 (1990): 675-68 I.]
Morbid obesity often precedes the development of NIDDM. Fatty acids are therefore important (such as fish oils) which, together with exercise, may also impact hormone production. Hormonal balance may be improved with DHEA.
Cerebral blood flow may benefit from supplementation with ginkgo biloba.
Several complications of diabetes, including neuropathies and retinopathies have improved with vitamin B6 supplementation, beyond the levels usually provided in a multiple B-complex formulation.
This B vitamin has been shown to work synergistically with insulin and independently in increasing the activity of glucokinase, an enzyme involved in regulating blood glucose levels. An inverse correlation has been shown to exist between serum biotin and fasting blood sugar levels in patients with insulin dependent diabetes. In one study patients with IDDM were removed from insulin therapy and treated with biotin (16 mg/d) or placebo for one week. The placebo group showed the expected elevation in blood sugar level while the treated group's glucose levels dropped significantly. Serum biotin levels reached during therapy were typically 100-times pretreatment levels.
Carnitine supplementation of diabetics has resulted in significantly decreased total serum lipid and increased HDL- cholesterol levels. In addition, it improves a-oxidation of fatty acids, possibly playing a role in preventing diabetic ketoacidosis.
Chromium is a critical nutrient in DM. Supplementation has been shown to improve almost every aspect of the disease.
Trivalent chromium (Cr+++) is the only form of chromium that exhibits biological activity, and is an integral component of the so-called "glucose tolerance factor" (GTF). Supplemental chromium, in the form of brewer's yeast or chromium chloride significantly improves glucose tolerance, decreases fasting glucose, cholesterol and triglyceride levels, and increases the HDL-cholesterol level by increasing insulin sensitivity in normal, elderly and NIDDM patients.
Exercise increases tissue chromium concentrations while the consumption of simple carbohydrates increases chromium excretion. All these effects appear due to increased insulin sensitivity.
It is not, however, a panacea for NIDDM patients, since double blind studies of chromium alone have yielded conflicting results. This may signify GTF as found in brewer's yeast is better absorbed than chromium salts (as has been demonstrated in rats) or some NIDDM patients lose their ability to incorporate chromium into GTF.
In some supplement combinations intended specifically for the large population of diabetics, chromium is combined with other exotic minerals e.g. vanadium.
Combinations with chromium and vanadium (as vanadyl sulfate) are also available.
Magnesium levels are significantly lowered in diabetics, and lowest in those with severe retinopathy. The degree of diabetic control affects serum magnesium levels; poorly controlled diabetics have significantly depressed magnesium levels.
Hypomagnesemia appears to be a significant risk factor in the development of cardiovascular disease, particularly coronary artery spasm. Magnesium is also an important cofactor in glycolysis and an important intracellular cell regulator.
Magnesium supplementation appears warranted in diabetics since it is a common deficiency, possibly prevents damage to the blood vessels of the eyes, increases HDL levels, decreases platelet aggregation, and prolongs clotting time.
Manganese is an important cofactor in key enzymes of glycogen metabolism. A deficiency results in hyperglycemia in guinea pigs and the frequent birth of offspring who develop pancreatic abnormalities or no pancreas at all. Diabetics have been shown to have only one-half the red blood cell manganese of normals.
Potassium supplementation yields improved insulin sensitivity, responsiveness and secretion in diabetics on a hypocaloric diet. Insulin administration induces hypokalemia. The recommended diet should supply adequate potassium.
Quercetin is a strong aldose reductase inhibitor (important in the prevention of the complications of DM). It is also an inhibitor of platelet aggregation, making it an important nutrient for DM. Quercetin's other physiological effects are also very useful for the diabetic since it has vitamin C-sparing effects, increases membrane integrity and is an anti-oxidant.
This trace element functions synergistically with vitamin E as an anti-oxidant and decreases platelet aggregation.
Diabetics with neurological damage have been shown to be deficient in pyridoxine, and benefit from its supplementation. Peripheral neuropathy is a known result of pyridoxine deficiency and is clinically indistinguishable from diabetic neuropathy. Pyridoxine is also important in preventing other diabetic complications because it is an important coenzyme in the cross-linking of collagen and inhibits platelet aggregation.
Vitamin B12 supplementation has been used with some success in treating diabetic neuropathy. It is not clear if this is due to the correcting of a deficiency state or the normalization of the deranged cobalamin metabolism seen in diabetics.
Clinically, diabetic neuropathy is very similar to that of classical cobalamin deficiency. Absence of megaloblastic anemia is not an adequate criteria for ruling out a deficiency, since a neural deficit will usually precede a hematological abnormality, often by several years. Serum levels are more reliable. Oral supplementation may be sufficient, but intramuscular vitamin B12 may be necessary in many cases.
The transport of ascorbic acid into cells is facilitated by insulin. It has been postulated that, due to impaired transport or dietary insufficiency, a relative scorbutic state exists in the diabetic which may be responsible for the blood vessel abnormalities of DM.
Diabetic patients appear to have an increased requirement for vitamin E. This results in increased free-radical-induced damage, particularly of the vascular endothelium. Supplemental vitamin E may help prevent diabetic complications through its anti-oxidant activity, the inhibition of platelet aggregation, increasing HDL-cholesterol levels, and its role in fatty acid metabolism.
A relative, or absolute, zinc deficiency has been suggested to play a role in the development of DM in humans. Zinc is involved in virtually all aspects of insulin metabolism: synthesis, secretion and utilization. Zinc also has a protective effect against pancreatic cell destruction, and has well-known anti-viral effects. Diabetics typically hyperexcrete zinc and therefore require supplementation until the renal abnormalities are corrected. Supplementation to obese hyperglycemic mice has improved all aspects of glucose tolerance.
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