Diabetes here refers to diabetes mellitus. Other uncommon forms of diabetes are not covered in this discussion.

People with diabetes cannot properly process glucose, a sugar the body uses for energy. As a result, glucose stays in the blood, causing blood glucose to rise. At the same time, however, the cells of the body can be starved for glucose. Diabetes can lead to poor wound healing, higher risk of infections, and many other problems involving the eyes, kidneys, nerves, and heart.

There are two types of diabetes mellitus. Adult-onset diabetes is also called type 2 or non-insulin-dependent diabetes. With type 2, the pancreas often makes enough insulin, but the body has trouble using the insulin. Type 2 responds well to natural therapies.

Childhood-onset diabetes is the other form of diabetes mellitus. It is also called type 1 or insulin-dependent diabetes. In type 1, the pancreas cannot make the insulin needed to process glucose. Natural therapies cannot cure type 1, but by making the body more receptive to insulin supplied by injection, it may help. It is particularly critical for people with type 1 to work carefully with the doctor prescribing insulin before contemplating the use of any herbs, supplements, or dietary changes mentioned in this section. Any change that makes the body more receptive to insulin could require critical changes in insulin dosage that must be determined by the treating physician.

People with diabetes have a high risk for heart disease. As a result, information in the section on atherosclerosis is also important to read.

Years ago, one researcher reported an increase in diabetes among Yemenite Jews who had migrated from a region where no sugar was eaten to one in which they ate a diet including sugar.⁵ However, other factors, such as weight gain, may explain the increased risk that occurred in this group.⁶ Other studies have found no independent relationship between sugar intake and the development of glucose intolerance.⁷

Eating carbohydrate-containing foods, whether high in sugar or high in starch (such as bread, potatoes, cold breakfast cereals, and rice), temporarily raises blood sugar and insulin levels.⁸ The blood sugar-raising effect of a food, called its "glycemic index," depends on how rapidly its carbohydrate is absorbed. Many starchy foods have a glycemic index similar to sucrose (table sugar).⁹ People eating large amounts of foods with high glycemic indices (such as those mentioned above), have been reported to be at increased risk of type 2 diabetes.^{10 11} On the other hand, eating a diet high in carbohydrate-rich foods with low glycemic indices is associated with a low risk of type 2 diabetes.^{12 13 14} Due mostly to the health-promoting effects of soluble fiber found in beans, peas, fruit, and oats, these foods have low glycemic indices despite their high carbohydrate content.

Diabetes disrupts the mechanisms by which the body controls blood sugar. Until recently, health professionals have recommended sugar restriction to diabetics, even though short-term high-sugar diets have been shown not to cause blood sugar problems in diabetics in some studies.^{15 16 17} Currently, the American Diabetic Association guidelines¹⁸ do not prohibit the use of moderate amounts of sugar, so long as the goals of normalizing blood levels of glucose, triglycerides, and cholesterol are being achieved.

Most doctors recommend that diabetics cut intake of sugar from snacks and processed foods, and replace these foods with high-fiber, whole foods. This tends to lower the glycemic index of the overall diet and has the additional benefit of increasing vitamin, mineral, and fiber intake. Other authorities also recommend lowering the glycemic index of the diet to improve the control of diabetes.¹⁹

High-fiber supplements, such as psyllium,^{20 21} guar gum (found in beans),²² pectin (from fruit),²³ oat bran,²⁴ and glucomannan,²⁵ have improved glucose tolerance in some studies. Good results have also been reported with the consumption of 1–3 ounces of powdered fenugreek seeds per day.^{26 27} A review of the research revealed that the extent to which moderate amounts of fiber help people with diabetes in the long term is still unknown, and the lack of many long-term studies has led some researchers to question the importance of fiber in improving diabetes.²⁸ Nonetheless, most doctors advise people with diabetes to eat a diet high in fiber. Focus should be placed on fruits, vegetables, seeds, oats, and whole-grain products.

Vegetarians have been reported to have a low risk of type 2 diabetes.³⁰ When people with diabetic nerve damage switch to a vegan diet (no meat, dairy, or eggs), improvements have been reported after several days.³¹ In one study, pain completely disappeared in 17 of 21 people.³² Fats from meat and dairy also cause heart disease, the leading killer of people with diabetes.

Vegetarians eat less protein than do meat eaters. Reducing protein intake has lowered kidney damage caused by diabetes^{33 34} and may also improve glucose tolerance.³⁵ However, in a group of 13 obese males with high blood-insulin levels (as is often seen in diabetes), a high-protein, low-carbohydrate diet resulted in greater weight loss and control of insulin levels, compared with a low-carbohydrate diet.³⁶ Switching to a high- or low-protein diet should be discussed with a doctor.

Diets high in fat, especially saturated fat, worsen glucose tolerance and increase the risk of type 2 diabetes,^{37 38 39 40} an effect that is not simply the result of weight gain caused by eating high-fat foods. Saturated fat is found primarily in meat, dairy fat, and poultry skins and dark meat. In contrast, glucose intolerance has been improved by diets high in monounsaturated oils,^{41 42} and these oils may be good for diabetics.⁴³ The easiest way to incorporate monounsaturates into the diet is to use olive oil. However, those who are overweight need to be careful—olive oil is high in calories.

Should children avoid milk to prevent type 1 diabetes? Countries with high milk consumption have a high risk of type 1.⁴⁴ Animal research indicates that avoiding milk affords protection from type 1.⁴⁵ Milk contains a protein related to a protein in the pancreas, the organ where insulin is made. Some researchers believe that children who are allergic to milk may develop antibodies that attack the pancreas, causing type 1 diabetes. Most studies indicate that children with type 1 drink cow’s milk at an earlier age than other children.⁴⁶ Children with type 1 may have high levels of antibodies that attack milk protein.⁴⁷

Immune problems in people with type 1 have been tied to other allergies as well,⁴⁸ and the importance of focusing only on the avoidance of dairy products remains unclear.⁴⁹ Preliminary studies have found that early introduction of cow’s milk formula feeding increases the risk of developing type 1 diabetes, although contradictory results have also been published.^{50 51} A study of 821 Finnish children (including 435 full-term diabetics) showed that early introduction of cow’s milk formula feeding (before 3 months of age vs. after 3 months of age) was associated with increased risk of type 1.⁵² This research supports abstaining from dairy products in infancy and early childhood, particularly for children with a family history of type 1. Recent research also suggests a possible link between milk consumption in infancy and an increased risk of type 2.⁵³

Increased weight gain in infancy has been associated with a 1.5-fold increase in the risk of developing type 1 in childhood.⁶² Being overweight also increases the need for insulin. Therefore, people with type 1 should achieve and maintain appropriate body weight.

Exercise helps decrease body fat⁶³ and improves insulin sensitivity.⁶⁴ Exercisers are less likely to develop type 2.⁶⁵ People with type 1 who exercise require less insulin.⁶⁶ However, exercise can induce low blood sugar or even occasionally increased blood sugar.⁶⁷ Moreover, a preliminary study showed that long-term physical activity was not associated with control of blood glucose in people with type 1.⁶⁸ Therefore, diabetics should never begin an exercise program without consulting a healthcare professional.

Moderate drinking in healthy people improves glucose tolerance.^{69 70 71 72} However, alcohol has been reported to worsen glucose tolerance in the elderly⁷³ and in diabetics⁷⁴ in some studies. Diabetics who drink have also been reported to have a high risk for eye⁷⁵ and nerve damage.⁷⁶

Questions remain about where the line should be drawn regarding alcohol intake. For healthy people, light drinking will not increase the risk of diabetes, but heavy drinking might and should be avoided. Until more is known, people with diabetes should also limit alcohol intake to two drinks per day. Total avoidance of alcohol in diabetics who are not suffering from alcoholism, liver disease, gastritis, ulcers, and other conditions made worse by alcohol might actually be counter productive. In one report, older people with type 2 diabetes who drank daily but moderately had a dramatically lower incidence of deaths from heart disease compared with non-drinkers.⁷⁷ This outcome is not surprising because moderate alcohol intake is associated with protection from heart disease in most other reports. This finding may be of particular importance because heart disease is the leading killer of people with diabetes.

Diabetics who smoke are at higher risk for kidney damage,⁷⁸ heart disease,⁷⁹ and other diabetes-linked problems. Smokers are more likely to become diabetic;⁸⁰ therefore, it is important to quit smoking.

In one of the few trials to not find vitamin E helpful with glucose intolerance in people with type 2, damage to nerves caused by the diabetes was nonetheless partially reversed by supplementing with vitamin E for six months.⁸

Vitamin E prevents blood from clotting too fast⁹ and has other actions that protect diabetics’ blood vessels from damage.¹⁰ Vitamin E has protected animals from diabetic cataracts.¹¹ In one double-blind trial, very high amounts of vitamin E (1,800 IU per day)—amounts considered excessive by some doctors—resulted in a normalization of kidney function and blood flow to the eyes in type 1 patients.¹² These changes signal possible protection against diabetic retinopathy (which can lead to blindness) and nephropathy (which can lead to kidney failure). No extended studies have yet explored whether vitamin E can provide long-term protection against these serious complications of diabetes.

Higher blood levels of vitamin E—a reflection of dietary intake—have been associated with a dramatically reduced risk of being diagnosed with type 1.¹³ The possibility that vitamin E supplementation might be protective has not yet been directly explored by researchers. The way vitamin E is thought to protect against type 1 (by reducing oxidative damage in the pancreas) appears unrelated to the possible protective roles vitamin E appears to play in type 2.

Glycosylation is an important index of diabetes. It refers to how much sugar attaches abnormally to proteins. Vitamin E reduces this problem in some,^{14 15 16 17} although not all studies.^{18 19 20}

In an isolated report, vitamin E was found to impair glucose tolerance in obese patients with diabetes.²¹ Why the outcome of this trial is so different from other published research is unclear.

People with type 1 appear to have low vitamin C levels.²² As with vitamin E, vitamin C may reduce glycosylation.²³ Vitamin C also lowers sorbitol in diabetics;²⁴ sorbitol is a sugar that can accumulate and damage the eyes, nerves, and kidneys of diabetics. Vitamin C may improve glucose tolerance in type 2,^{25 26} although not every study confirms this benefit.²⁷ Many doctors suggest that diabetics supplement with 1–3 grams per day of vitamin C. Higher amounts could be problematic. In one person, 4.5 grams per day was reported to increase blood sugar levels.²⁸

One study compared antioxidant supplement intake, including both vitamins E and C, with diabetic retinopathy (damage to the eyes caused by diabetes).²⁹ Surprisingly, several correlations were found between extensive retinopathy and greater likelihood of taking vitamin C and vitamin E supplements. The outcome of this trial, however, does not fit with most other published data and might simply reflect the fact that sicker people are more likely to take supplements in hopes of getting better. For the present, most doctors remain relatively unconcerned about the unexpected outcome of this isolated report.

Many diabetics have low blood levels of vitamin B6.^{30 31} Levels are even lower in diabetics with nerve damage.³² Vitamin B6 supplements improve glucose tolerance in women with diabetes caused by pregnancy.^{33 34} Vitamin B6 is also effective for glucose intolerance induced by birth control pills.³⁵ For other people with diabetes, 1,800 mg per day of a special form of vitamin B6—pyridoxine alpha-ketoglutarate—has improved glucose tolerance dramatically in some research.³⁶ Standard vitamin B6 has helped in some,³⁷ but not all, studies.³⁸

Vitamin B12 is needed for normal functioning of nerve cells. Vitamin B12 taken orally, intravenously, or by injection has reduced nerve damage caused by diabetes in most people studied.³⁹ In an uncontrolled trial, people with nerve damage due to kidney disease or to diabetes plus kidney disease received intravenous injections of 500 mcg of methylcobalamin (the main form of vitamin B12 found in the blood) three times a day for 6 months in addition to kidney dialysis. Nerve pain was significantly reduced and nerve function significantly improved in those who received the injections.⁴⁰ Oral vitamin B12 up to 500 mcg three times per day has also been used.

Biotin is a B vitamin needed to process glucose. When people with type 1 were given 16 mg of biotin per day for one week, their fasting glucose levels dropped by 50%.⁴¹ Similar results have been reported using 9 mg per day for two months in people with type 2.⁴² Biotin may also reduce pain from diabetic nerve damage.⁴³ Some doctors try 16 mg of biotin for a few weeks to see if blood sugar levels will fall.

High levels—several grams per day—of niacin, a form of vitamin B3, impair glucose tolerance and should not be taken by people with diabetes.^{44 45} Smaller amounts (500–750 mg per day for one month followed by 250 mg per day) may help some people with type 2,⁴⁶ though this research remains preliminary.

Preliminary studies have shown that niacinamide, the other form of vitamin B3, might be useful in the very early stages of type 1,⁴⁷ though not all trials support this claim.^{48 49 50} Although an analysis of all significant research published up to 1996 shows that niacinamide does help preserve some function of insulin-secreting cells in people recently diagnosed with type 1, the amount of insulin required for those given niacinamide has remained essentially as high as for those given placebo.⁵¹ Although the optimal amount of niacinamide remains somewhat unclear, recent evidence suggests that 25 mg per kg (2.2 pounds) body weight per day may be as effective as higher amounts.⁵²

Some,⁵³ but not all,⁵⁴ reports suggest that healthy children at high risk for type 1 may be protected by supplementing niacinamide. Parents of children with type 1 may discuss the possibility of protecting their other children through niacinamide supplementation with a doctor.

Years ago, blood levels of vitamin B1 were reported to be low in people with type 1.⁵⁵ Long before that, a trial using 10 mg of vitamin B1 per day for four weeks reported reduced blood sugar levels in six of eleven diabetics.⁵⁶ Recently, supplementation of both vitamin B1 (25 mg per day) and vitamin B6 (50 mg per day) by a group of people with diabetic neuropathy led to significant improvement in only four weeks.⁵⁷ However, this was a study conducted in a vitamin B1-deficient third world country. Therefore, these improvements might not occur in other diabetics. A recent German study also found that combining vitamin B1 (in a special fat soluble form) and vitamin B6 plus vitamin B12 in high but variable amounts led to improvement in some aspects of diabetic neuropathy in twelve weeks.⁵⁸ As a result, some doctors recommend that people with diabetic neuropathies supplement vitamin B1, though the optimal level of intake remains unknown.

Vitamin D is needed for adequate blood levels of insulin.⁵⁹ Vitamin D receptors have been found in the pancreas where insulin is made and preliminary evidence suggests that supplementation can increase insulin secretion for some people with type 2; prolonged supplementation might also help reduce blood sugar levels.⁶⁰ Not enough is known about optimal amounts of vitamin D for diabetics, and high levels of vitamin D can be toxic. Therefore, people with diabetes considering vitamin D supplementation should talk with, and have vitamin D status assessed by, a doctor.

Animal studies show that chromium improves glucose tolerance.⁶¹ Medical reports dating back to 1853 as well as modern research indicate that chromium-rich brewer’s yeast (9 grams per day) can be useful in treating diabetes.^{62 63} Double-blind research shows that chromium supplements improve glucose tolerance in people with both type 2⁶⁴ and type 1, apparently by increasing sensitivity to insulin.⁶⁵ Chromium improves the processing of glucose in people with pre-diabetic glucose intolerance⁶⁶ and in women with diabetes associated with pregnancy.⁶⁷ Chromium even helps healthy people,⁶⁸ although one such report found chromium useful only when accompanied by 100 mg of niacin.⁶⁹ Chromium may also lower total cholesterol, LDL-cholesterol and triglycerides (risk factors in heart disease).^{70 71} The typical amount of chromium used in research trials is 200 mcg per day, although as much as 1,000 mcg per day has been used.⁷² Some doctors recommend up to 1,000 mcg per day for diabetics.⁷³

Diabetes patients tend to have low magnesium levels.⁷⁴ Double-blind research indicates that supplementing with magnesium overcomes this problem.⁷⁵ Magnesium has led to improved insulin production in elderly people with type 2.⁷⁶ However, a double blind study found no effect of about 500 mg per day in people with type 2, although twice that amount led to some improvement.⁷⁷ Elders without diabetes can also produce more insulin as a result of magnesium supplements, according to some,⁷⁸ but not all, studies.⁷⁹ Insulin requirements are lower in people with type 1 who supplement with magnesium in some trials.⁸⁰ However, in people with adult-onset diabetes who nonetheless do require insulin, Dutch researchers have reported no improvement in blood sugar levels.⁸¹

Diabetes-induced damage to the eyes is more likely to occur to magnesium-deficient people with type 1.⁸² In magnesium-deficient pregnant women with type 1, the lack of magnesium may even account for the high rate of spontaneous abortion and birth defects associated with type 1.⁸³

The American Diabetes Association admits "strong associations...between magnesium deficiency and insulin resistance" but will not say magnesium deficiency is a risk factor.⁸⁴ Many doctors, however, recommend that diabetics with normal kidney function supplement with 300–400 mg of magnesium per day.

People with type 1 tend to be zinc deficient,⁸⁵ which may impair immune function.⁸⁶ Zinc supplements have lowered blood sugar levels in people with type 1,⁸⁷ though some evidence indicates that zinc supplementation in people with type 2 does not improve their ability to process sugar.⁸⁸ Nonetheless, people with type 2 also have low zinc levels, caused by excess loss of zinc in their urine.⁸⁹ Many doctors recommend that people with type 2 supplement with moderate amounts of zinc (15–25 mg per day) as a way to correct for the deficit.

Some doctors are concerned about having people with type 1 supplement with zinc because of a report that zinc supplementation increased glycosylation,⁹⁰ generally a sign of deterioration of the condition. This study is hard to evaluate because zinc increases the life of blood cells and such an effect artificially increases the lab test results for glycosylation. Until this issue is resolved, those with type 1 should consult a doctor before considering supplementation with zinc.

People with diabetes cannot adequately process carbohydrates. Coenzyme Q10 (CoQ10) is needed for normal carbohydrate metabolism. Animals with diabetes have been reported to be CoQ10 deficient. People with type 2 also appear to be CoQ10 depleted.⁹¹ In one trial, blood sugar levels fell substantially in 31% of people with diabetes after they supplemented with 120 mg of CoQ10 per day.⁹² In people with type 1, however, supplementation with 100 mg of CoQ10 per day for three months neither improved glucose control nor reduced the need for insulin.⁹³ The importance of CoQ10 supplementation for diabetics remains an unresolved issue, though some doctors recommend approximately 50 mg per day as a way to protect against possible effects associated with diabetes-induced depletion.

Inositol is needed for normal nerve function. Diabetes can cause nerve damage, or diabetic neuropathy. Some of these abnormalities have been reversed by inositol supplementation in preliminary research (500 mg taken twice per day).⁹⁴

Alpha lipoic acid is a powerful natural antioxidant. It has been used to improve diabetic neuropathy and to improve insulin sensitivity. A double-blind trial found that 600 or 1200 mg per day of lipoic acid taken for two years significantly improved nerve function and decreased symptoms of diabetic neuropathy.⁹⁵ Another study successfully used an oral intake of 800 mg per day to improve one type of diabetic neuropathy.⁹⁶ In an uncontrolled trial, 600 mg of lipoic acid twice daily improved glucose metabolism and increased sensitivity to insulin in people with diabetes.⁹⁷ In a controlled trial, oral lipoic acid was found to significantly improve insulin sensitivity in people with type 2 diabetes.⁹⁸ People who took 600 mg once, twice, or three times daily for four weeks had improved metabolism of glucose, regardless of the amount taken. Double-blind studies are needed to confirm these preliminary results.

L-carnitine is a substance needed for the body to properly use fat for energy. When diabetics were given L-carnitine (1 mg per 2.2 pounds of body weight), high blood levels of fats—both cholesterol and triglycerides—dropped 25–39% in just ten days in one trial.⁹⁹ In higher amounts (1 gram per day by injection), L-carnitine has been reported to reduce pain from diabetic nerve damage as well.¹⁰⁰

Taurine is an amino acid found in protein-rich food. People with type 1 have been reported to have low taurine levels, which leads to "thickened" blood—a condition that increases the risk of heart disease. Supplementing taurine (1.5 grams per day) has restored taurine levels to normal and corrected the problem of blood viscosity within three months.¹⁰¹ However, in a double-blind trial, taurine supplementation (2 grams per day for 12 months) failed to improve kidney complications associated with type 2.¹⁰²

Supplementing with 4 grams of evening primrose oil per day for six months has been found in double-blind research to improve nerve function and relieve pain symptoms of diabetic neuropathy.¹¹³

Doctors have suggested that quercetin might help people with diabetes because of its ability to reduce levels of sorbitol—a sugar that accumulates in nerve cells, kidney cells, and cells within the eyes of diabetics and has been linked to damage to those organs.¹¹⁴ Human trials have yet to explore whether quercetin actually protects people with diabetes from neuropathy, nephropathy, or retinopathy.

Vanadyl sulfate, a form of vanadium, may improve glucose control in individuals with type 2,^{115 116} though it may not help people with type 1.¹¹⁷ The long-term safety of the large amounts of vanadium needed to help people with type 2 (typically 100 mg per day) remains unknown. Many doctors expect that amounts this high may prove to be unsafe.

In a preliminary study, administration of fructo-oligosaccharides (FOS) (8 grams per day for two weeks) significantly lowered fasting blood-sugar levels and serum total-cholesterol levels in patients with type 2 diabetes.¹¹⁸ However, in another study, supplementing type 2 diabetics with FOS (15 grams per day) for 20 days had no effect on blood-glucose or lipid levels.¹¹⁹ In addition, double-blind studies of healthy individuals showed that supplementing with FOS or galacto-oligosaccharides (GOS) for eight weeks had no effect on blood-sugar levels, insulin secretion, or blood lipids.^{120 121} Because of these conflicting results, more research is needed to determine the effect of FOS and inulin on diabetes and lipid levels.

Are there any side effects or interactions? Refer to the individual supplement for information about any side effects or interactions.

Herbs that may be helpful: Gymnema may assist the pancreas in the production of insulin in people with type 2. Gymnema also improves the ability of insulin to lower blood sugar in people with both type 1 and type 2. So far, no double-blind studies have confirmed the benefit of gymnema for people with any type of diabetes. One uncontrolled study found that 400 mg daily of a gymnema extract could reduce or eliminate the need for oral blood sugar-lowering drugs in some people with type 2.¹²² Another uncontrolled study suggested the same amount of the extract could allow for use of less insulin in people with type 1.¹²³ Gymnema is not a substitute for insulin.

Asian ginseng is commonly used in traditional Chinese medicine to treat diabetes. It has been shown in test tube and animal studies to enhance the release of insulin from the pancreas and to increase the number of insulin receptors.^{124 125} Animal research has also revealed a direct blood sugar-lowering effect of ginseng.¹²⁶ A recent double-blind study in humans found that 200 mg of ginseng extract per day improved blood sugar control, as well as energy levels in type 2.¹²⁷

Bilberry may lower the risk of some diabetic complications, such as diabetic cataracts and retinopathy. One uncontrolled study found that a standardized extract of bilberry could improve signs of retinal damage in some people with diabetic retinopathy.¹²⁸ Ginkgo biloba extract may prove useful for prevention and treatment of early-stage diabetic neuropathy, though research is at best very preliminary in this area. Other herbs that may help are fenugreek seeds (discussed as a source of fiber in Part 2: Dietary and Lifestyle Changes) and eleuthero (Siberian ginseng).

Two single-blind studies have found that aloe vera juice helps lower blood sugar levels in people with type 2. One study found that 1 Tbsp (15 grams) twice daily notably improved the efficacy of the oral blood sugar-lowering drug glibenclamide.¹²⁹ The other study found the juice by itself was effective.¹³⁰

Preliminary studies have found that the whole, fried slices,¹³¹ water extracts,¹³² and juice¹³³ of bitter melon may improve blood sugar control in people with type 2. Double-blind studies are needed to confirm this potential benefit.

Topical application of creams containing capsaicin (the main active compound in cayenne) can help relieve symptoms of diabetic neuropathy according to double-blind studies.^{134 135} Four or more applications per day may be required to relieve severe pain.

Mistletoe extract has been shown to stimulate insulin secretion from pancreas cells,¹³⁶ and other research found that it reduces symptoms in diabetic mice.¹³⁷ No research in people has yet been published, however given mistletoe’s tradition around the world for helping diabetics and these promising pre-clinical results, studies are warranted. To use mistletoe, traditionally a cold water extract (cold infusion) is made by soaking 2–4 teaspoons of chopped mistletoe in two cups of water overnight. This is drunk first thing in the morning and can be sweetened with honey. Another batch is left to steep during the day and is drunk at bedtime.

Supplementing with psyllium has been shown to be a safe and well-tolerated way to improve control of blood glucose and cholesterol. In a double-blind study, men with type 2 who took 5.1 grams of psyllium per day for 8 weeks lowered their blood glucose levels by 11% -19.2%, their total cholesterol by 8.9% and their low-density-lipoprotein (LDL) cholesterol (the "bad" cholesterol) by by 13%, compared to placebo.¹³⁸

Olive leaf extracts have been employed experimentally to lower elevated blood-sugar levels in diabetic animals.¹³⁹ Unfortunately, these results have not been reproduced in human clinical trials and as such, no clear conclusions can be made from this animal study in the treatment of diabetes.

Animal studies and some very preliminary studies in humans suggest reishi may have some beneficial action in persons with diabetes.¹⁴⁰

Information about the effects of a particular supplement or herb on a particular condition has been qualified in terms of the methodology or source of supporting data (for example: clinical, double blind, meta-analysis, or traditional use). For the convenience of the reader, the information in the table listing the supplements for particular conditions is also categorized. The criteria for the categorizations are: "Primary" indicates there are reliable and relatively consistent scientific data showing a health benefit. "Secondary" indicates there are conflicting, insufficient, or only preliminary studies suggesting a health benefit or that the health benefit is minimal. "Other" indicates that an herb is primarily supported by traditional use or that the herb or supplement has little scientific support and/or minimal proven health benefit.

1. Salonen JT, Nyssonen K, Tuomainen T-P, et al. Increased risk of non-insulin dependent diabetes mellitus at low plasma vitamin E concentrations: a four year follow up study in men. BMJ 1995;311:1124–7.

2. Bierenbaum ML, Noonan FJ, Machlin LJ, et al. The effect of supplemental vitamin E on serum parameters in diabetics, post coronary and normal subjects. Nutr Rep Int 1985;31:1171–80.

3. Paolisso G, D’Amore A, Giugliano D, et al. Pharmacologic doses of vitamin E improve insulin action in healthy subjects and non-insulin dependent diabetic patients. Am J Clin Nutr 1993;57:650–6.

4. Paolisso G, D’Amore A, Galzerano D, et al. Daily vitamin E supplements improve metabolic control but not insulin secretion in elderly type II diabetic patients. Diabetes Care 1993;16:1433–7.

5. Tütüncü NB, Bayraktar M, Varli K. Reversal of defective nerve condition with vitamin E supplementation in type 2 diabetes. Diabetes Care 1998;21:1915–8.

6. Paolisso G, Di Maro G, Galzerano D, et al. Pharmacological doses of vitamin E and insulin action in elderly subjects. Am J Clin Nutr 1994;59:1291–6.

7. Paolisso G, Gambardella A, Galzerano D, et al. Antioxidants in adipose tissue and risk of myocardial infarction.Lancet 1994;343:596 [letter].

8. Tütüncü NB, Bayraktar M, Varli K. Reversal of defective nerve condition with vitamin E supplementation in type 2 diabetes. Diabetes Care 1998;21:1915–8.

9. Colette C, Pares-Herbute N, Monnier LH, Cartry E. Platelet function in type I diabetes: effects of supplementation with large doses of vitamin E. Am J Clin Nutr 1988;47:256–61.

10. Gisnger C, Jeremy J, Speiser P, et al. Effect of vitamin E supplementation on platelet thromboxane A2 production in type I diabetic patients: Double-blind crossover trial. Diabetes 1988;37:1260–4.

11. Ross WM, Creighton MO, Stewart-DeHaan PJ, et al. Modelling cortical cataractogenesis: 3. In vivo effects of vitamin E on cataractogenesis in diabetic rats. Can J Ophthalmol 1982;17:61.

12. Bursell SE, Schlossman DK, Clermont AC, et al. High-dose vitamin E supplementation normalizes retinal blood flow and creatinine clearance in patients with type I diabetes. Diabetes Care 1999;22:1245–51.

13. Knekt P Reunanen A, Marniumi J, et al. Low vitamin E status is a potential risk factor for insulin-dependent diabetes mellitus. J Intern Med 1999;245:99–102.

14. Ceriello A, Giugliano D, Quatraro A, et al. Vitamin E reduction of protein glycosylation in diabetes. Diabetes Care 1991;14:68–72.

15. Duntas L, Kemmer TP, Vorberg B, Scherbaum W. Administration of d-alpha-tocopherol in patients with insulin-dependent diabetes mellitus. Curr Ther Res 1996;57:682–90.

16. Paolisso G, D’Amore A, Galzerano D, et al. Daily vitamin E supplements improve metabolic control but not insulin secretion in elderly type II diabetic patients. Diabetes Care 1993;16:1433–7.

17. Jain SK, McVie R, Jaramillo JJ, et al. Effect of modest vitamin E supplementation on blood glycated hemoglobin and triglyceride levels and red cell indices in type I diabetic patients. J Am Coll Nutr 1996;15:458–61.

18. Reaven PD, Barnett J, Herold DA, Edelman S. Effect of vitamin E on susceptibility of low-density lipoprotein and low-density lipoprotein subfractions to oxidation and on protein glycation in NIDDM. Diabetes Care 1995;18:807.

19. Bursell S-E, Schlossman DK, Clermont AC, et al. High-dose vitamin E supplementation normalizes retinal blood flow and creatineine clearance in patients with type I diabetes. Diabetes Care 1999;22:1245–51.

20. Fuller CJ, Chandalia M, Garg A, et al. RRR-alpha-tocopheryl acetate supplementation at pharmacologic doses decreases low-density-lipoprotein oxidative susceptibility but not protein glycation in patients with diabetes mellitus. Am J Clin Nutr 1996;63:753–9.

21. Skrha J, Sindelka G, Kvasnicka J, Hilgertova J. Insulin action and fibrinolysis influenced by vitamin E in obese tpye 2 diabetes mellitus. Diabetes Res Clin Pract 1999;44:27–33.

22. Cunningham JJ, Ellis SL, McVeigh KL, et al. Reduced mononuclear leukocyte ascorbic acid content in adults with insulin-dependent diabetes mellitus consuming adequate dietary vitamin C. Metabolism 1991;40:146–9.

23. Davie SJ, Gould BJ, Yudkin JS. Effect of vitamin C on glycosylation of proteins. Diabetes 1992;41:167–73.

24. Will JC, Tyers T. Does diabetes mellitus increase the requirement for vitamin C? Nutr Rev 1996;54:193–202 [review].

25. Eriksson J, Kohvakka A. Magnesium and ascorbic acid supplementation in diabetes mellitus. Ann Nutr Metab 1995;39:217–23.

26. Paolisso G, Balbi V, Volpe C, et al. Metabolic benefits deriving from chronic vitamin C supplementation in aged non-insulin dependent diabetics. J Am Coll Nutr 1995;14:387–92.

27. Will JC, Tyers T. Does diabetes mellitus increase the requirement for vitamin C? Nutr Rev 1996;54:193–202 [review].

28. Branch DR. High-dose vitamin C supplementation increases plasma glucose. Diabetes Care1999;22:1218 [letter].

29. Mayer-Davis E, Bell RA, Reboussin BA, et al. Antioxidant nutrient intake and diabetic retinopathy. The San Luis Valley Diabetes Study. Ophthalmology 1998;105:2264–70.

30. Wilson RG, Davis RE. Serum pyridoxal concentrations in children with diabetes mellitus. Pathology 1977;9:95–9.

31. Davis RE, Calder JS, Curnow DH. Serum pyridoxal and folate concentrations in diabetics. Pathology 1976;8:151–6.

32. McCann VJ, Davis RE. Serum pyridoxal concentrations in patients with diabetic neuropathy. Aust N Z J Med 1978;8:259–61.

33. Spellacy WN, Buhi WC, Birk SA. Vitamin B6 treatment of gestational diabetes mellitus. Am J Obstet Gynecol 1977;127:599–602.

34. Coelingh HJT, Schreurs WHP. Improvement of oral glucose tolerance in gestational diabetes by pyridoxine. BMJ 1975;3:13–5.

35. Spellacy WN, Buhi WC, Birk SA. The effects of vitamin B6 on carbohydrate metabolism in women taking steroid contraceptives: preliminary report. Contraception 1972;6:265–73.

36. Passariello N, Fici F, Giugliano D, et al. Effects of pyridoxine alpha-ketoglutarate on blood glucose and lactate in type I and II diabetics. Int J Clin Pharmacol Ther Toxicol 1983;21:252–6.

37. Solomon LR, Cohen K. Erythrocyte O2 transport and metabolism and effects of vitamin B6 therapy in type II diabetes mellitus. Diabetes 1989;38:881–6.

38. Rao RH, Vigg BL, Rao KSJ. Failure of pyridoxine to improve glucose tolerance in diabetics. J Clin Endocrinol Metab 1980;50:198–200.

39. Yamane K, Usui T, Yamamoto T, et al. Clinical efficacy of intravenous plus oral mecobalamin in patients with peripheral neuropathy using vibration perception thresholds as an indicator of improvement. Curr Ther Res 1995;56:656–70 [review].

40. Kuwabara S, Nakazawa R, Azuma N, et al. Intravenous methylcobalamin treatment for uremic and diabetic neuropathy in chronic hemodialysis patients. Intern Med 1999;38:472–5.

41. Coggeshall JC, Heggers JP, Robson MC, Baker H. Biotin status and plasma glucose in diabetics. Ann NY Acad Sci 1985;447:389–92.

42. Maebashi M, Makino Y, Furukawa Y, et al. Therapeutic evaluation of the effect of biotin on hyperglycemia in patients with non-insulin dependent diabetes mellitus. J Clin Biochem Nutr 1993;14:211–8.

43. Koutsikos D, Agroyannis B, Tzanatos-Exarchou H. Biotin for diabetic peripheral neuropathy. Biomed Pharmacother 1990;44:511–4.

44. Molnar GD, Berge KG, Rosevear JW, et al. The effect of nicotinic acid in diabetes mellitus. Metabolism 1964;13:181–9.

45. Gaut ZN, Pocelinko R, Solomon HM, Thomas GB. Oral glucose tolerance, plasma insulin, and uric acid excretion in man during chronic administration in nicotinic acid. Metabolism 1971:1031–5.

46. Clearly JP. The importance of oxidant injury as a cause of impaired mitochondrial oxidation in diabetes. J Orthomolec Med 1988;3:164–74.

47. Clearly JP. Vitamin B3 in the treatment of diabetes mellitus: case reports and review of the literature. J Nutr Med 1990;1:217–25.

48. Lewis CM, Canafax DM, Sprafka JM, Bazrbosa JJ. Double-blind randomized trail of nicotinamide on early-onset diabetes. Diabetes Care 1992;15:121–3.

49. Chase HP, Butler-Simon N, Garg S, et al. A trial of nicotinamide in newly diagnosed patients with type 1 (insulin-dependent) diabetes mellitus. Diabetologia 1990;33:444–6.

50. Mendola G, Casamitjana R, Gomis R. Effect of nicotinamide therapy upon B-cell function in newly diagnosed type 1 (insulin-dependent) diabetic patients. Diabetologia 1989;32:160–2.

51. Pozzilli P, Browne PD, Kolb H. Meta-analysis of nicotinamide treatment in patients with recent-onset type 1. The nicotinamide trialists. Diabetes Care 1996;19:1357–63.

52. Visalli N, Cavallo MG, Signore A, et al. A multi-centre randomized trial of two different doses of nicotinamide in patients with recent-onsent type 1 diabetes (The IMDIAB VI). Diabetes Metab Res Rev 1999;15:181–5.

53. Elliott RB, Picher CC, Fergusson DM, Stewart AWAD. A population based strategy to prevent insulin-dependent diabetes using nicotinamide. J Pediatr Endocrinol Metab 1996;9:501–9.

54. Lampeter EF, Klinghammer A, Scherbaum WA, et al. The Deutsche Nicotinamide Intervention Study. An attempt to prevent type 1 diabetes. Diabetes 1998;47:980–4.

55. Haugen HN. The blood concentration of thiamine in diabetes. Scand J Clin Lab Invest 1964;16:260–6.

56. Vorhaus MG, Williams RR, Waterman RE. Studies on crystalline vitamin B1: observations in diabetes. Am J Dig Dis 1935;2:541–57.

57. Abbas ZG, Swai ABM. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East African Med J 1997;74:804–8.

58. Stracke H, Lindemann A, Federlin K. A benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes 1996;104:311–6.

59. Ref: Labriji-Mestaghanmi H, Billaudel B, Garnier PE, Sutter BCJ. Vitamin D and pancreatic islet function. 2. Time course for changes in insulin secretion and content during vitamin deprivation and repletion. J Endocrine Invest 1988;11:577–87.

60. Boucher BJ. Inadequate vitamin D status: does it contribute to the disorders comprising syndrome ‘X’? Br J Nutr 1998;79:315–27 [review].

61. Schroeder HA. Serum cholesterol and glucose levels in rats fed refined and less refined sugars and chromium. J Nutr 1969;97:237–42.

62. Herepath WB. Journal Provincial Med Surg Soc Apr 28, 1854:374.

63. Offenbacher EG, Pi-Sunyer FX. Beneficial effect of chromium-rich yeast on glucose tolerance and blood lipids in elderly subjects. Diabetes 1980;29:919–25.

64. Evans GW. The effect of chromium picolinate on insulin controlled parameters in humans. Int J Biosocial Med Res 1989;11:163–80.

65. Gaby AR, Wright JV. Diabetes. In Nutritional Therapy in Medical Practice: Reference Manual and Study Guide. Kent, WA: (gaby@halcyon.com), 1996, 54–64 [review].

66. Anderson RA, Polansky MM, Bryden NA, Canary JJ. Supplemental-chromium effects on glucose, insulin, glucagon, and urinary chromium losses in subjects consuming controlled low-chromium diets. Am J Clin Nutr 1991;54:909–16.

67. Jovanovic-Peterson L, Gutierrez M, Peterson CM. Chromium supplementation for gestational diabetic women improves glucose tolerance and decreases hyperinsulinemia. J Am Coll Nutr 1995;14:530 [abstract #26].

68. Anderson RA, Polansky MM, Bryden NA, et al. Chromium supplementation of human subjects: effects on glucose, insulin, and lipid variables. Metabolism 1983;32:894–9.

69. Urberg M, Zemel MB. Evidence for synergism between chromium and nicotinic acid in the control of glucose tolerance in elderly humans. Metabolism 1987;36:896–9.

70. Lee NA, Reasner CA. Beneficial effect of chromium supplementation on serum triglyceride levels in NIDDM. Diabetes Care 1994;17:1449–52.

71. Hermann J, Chung H, Arquitt A, et al. Effects of chromium or copper supplementation on plasma lipids, plasma glucose and serum insulin in adults over age fifty. J Nutr Elderly 1998;18:27–45.

72. Anderson RA, Cheng N, Bryden NA, et al. Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. Diabetes 1997;46:1786–91.

73. Gaby AR, Wright JV. Nutritional protocols: diabetes mellitus. In Nutritional Therapy in Medical Practice: Protocols and Supporting Information. Kent, WA: (gaby@halcyon.com), 1996, 10.

74. Paolisso G, Scheen A, D’Onofrio FD, Lefebvre P. Magnesium and glucose homeostasis. Diabetologia 1990;33:511–4 [review].

75. Eibl NL, Schnack CJ, Kopp H-P, et al. Hypomagnesemia in type II diabetes: effect of a 3-month replacement therapy. Diabetes Care 1995;18:188.

76. Paolisso G, Sgambato S, Pizza G, et al. Improved insulin response and action by chronic magnesium administration in aged NIDDM subjects. Diabetes Care 1989;12:265–9.

77. Lima M, Cruz T, Carreiro Pousada J et al: The effect of magnesium supplementation in increasing doses on the control of type 2 diabetes. Diabetes Care 1998;21:682–6.

78. Paolisso G, Sgambato S, Gambardella A, et al. Daily magnesium supplements improve glucose handling in elderly subjects. Am J Clin Nutr 1992;55:1161–7.

79. Smellie WS, O’Reilly D St J, Martin BJ, Santamaria J. Magnesium replacement and glucose tolerance in elderly subjects. Am J Clin Nutr 1993;57:594–5 [letter].

80. Sjorgren A, Floren CH, Nilsson A. Oral administration of magnesium hydroxide to subjects with insulin dependent diabetes mellitus. Magnesium 1988;121:16–20.

81. de Valk HW, Verkaaik R, van Rijn HJM, et al. Oral magnesium supplementation in insulin-requiring type 2 diabetic patients. Diabet Med 1998;15:503–7.

82. McNair P, Christiansen C, Madsbad S, et al. Hypomagnesemia, a risk factor in diabetic retinopathy. Diabetes 1978;27:1075–7.

83. Mimouni F, Miodovnik M, Tsang RC, et al. Decreased maternal serum magnesium concentration and adverse fetal outcome in insulin-dependent diabetic women. Obstet Gynecol 1987;70:85–9.

84. American Diabetes Association. Magnesium supplementation in the treatment of diabetes. Diabetes Care 1992;15:1065–7.

85. Nakamura T, Higashi A, Nishiyama S, et al. Kinetics of zinc status in children with IDDM. Diabetes Care 1991;14:553–7.

86. Mocchegiani E, Boemi M, Fumelli P, Fabris N. Zinc-dependent low thymic hormone level in type I diabetes. Diabetes 1989;12:932–7.

87. Rao KVR, Seshiah V, Kumar TV. Effect of zinc sulfate therapy on control and lipids in type I diabetes. J Assoc Physicians India 1987;35:52 [abstract].

88. Niewoehner CB, Allen JI, Boosalis M, et al. Role of zinc supplementation in type II diabetes mellitus. Am J Med 1986;81:63–8.

89. Pidduck HG, Wren PJJ, Price Evans DA. Hyperzincuria of diabetes mellitus and possible genetic implications of this observation. Diabetes 1970;19:240–7.

90. Cunningham JJ, Fu A, Mearkle PL, Brown RG. Hyerzincuria in individuals with insulin-dependent diabetes mellitus: concurrent zinc status and the effect of high-dose zinc supplementation. Metabolism 1994;43:1558–62.

91. Myake Y, Shouzu A, Nishikawa M, et al. Effect of treatment of 3-hydroxy-3-methylglutaryl coenzyme I reductase inhibitors on serum coenzyme Q10 in diabetic patients. Arzneimittelforschung 1999;49:324–9.

92. Shigeta Y, Izumi K, Abe H. Effect of coenzyme Q7 treatment on blood sugar and ketone bodies of diabetics. J Vitaminol (Kyoto) 1966;12:293–8.

93. Henriksen JE, Bruun Andersen C, Hother-Nielsen O, et al. Impact of ubiquinone (coenzyme Q10) treatment on glycaemic control, insulin requirement and well-being in patients with Type 1 diabetes mellitus. Diabet Med 1999;16:312–8.

94. Salway JG, Whitehead L, Finnegan JA, et al. Effect of myo-inositol on peripheral-nerve function in diabetes. Lancet 1978;ii:1282–4.

95. Reljanovic M, Reichel G, Rett K, et al. Treatment of diabetic polyneuropathy with the antioxidant thioctic acid (alpha-lipoic acid): a two year multicenter randomized double-blind placebo-controlled trial (ALADIN II). Alpha Lipoic Acid in Diabetic Neuropathy. Free Radic Res 1999;31:171–9.

96. Ziegler D, Schatz H, Conrad F, et al. Effects of treatment with the antioxidant alpha-lipoic acid on cardiac autonomic neuropathy in NIDDM patients. A 4-month randomized controlled multicenter trial (DEKAN Study). Diabetes Care 1997;20:369–73.

97. Konrad T, Vicini P, Kusterer K, et al. alpha lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with type 2 diabetes. Diabetes Care 1999;22:280–7.

98. Jacob S, Ruus P, Hermann R, et al. Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled pilot trial. Free Radic Biol Med 1999;27:309–14.

99. Abdel-Aziz MT, Abdou MS, Soliman K, et al. Effect of carnitine on blood lipid pattern in diabetic patients. Nutr Rep Int 1984;29:1071–9.

100. Onofrj M, Fulgente T, Mechionda D, et al. L-acetylcarnitine as a new therapeutic approach for peripheral neuropathies with pain. Int J Clin Pharmacol Res 1995;15:9–15.

101. Franconi F, Bennardini F, Mattana A, et al. Plasma and platelet taurine are reduced in subjects with insulin-dependent diabetes mellitus: effects of taurine supplementation. Am J Clin Nutr 1995;61:1115–9.

102. Nakamura T, Ushiyama C, Suzuki S, et al. Effects of taurine and vitamin E on microalbuminuria, plasma metalloproteinase-9, and serum type IV collagen concentrations in patients with diabetic nephropathy. Nephron 1999;83:361–2.

103. Zak A, Zeman M, Hrabak P, et al. Changes in the glucose tolerance and insulin secretion in hypertriglyceridemia: effects of dietary n-3 fatty acids. Nutr Rep Int 1989;39:235–42.

112. Okuda Y, Mizutani M, Ogawa M, et al. Long-term effects of eicosapentaenoic acid on diabetic peripheral neuropathy and serum lipids in patients with type II diabetes mellitus. J Diabetes Complications 1996;10:280–7.

113. Jamal GA, Carmichael H. The effect of gamma-linolenic acid on human diabetic peripheral neuropathy: a double-blind placebo-controlled trial. Diabet Med 1990;7:319–23.

114. Gaby A. Preventing complications of diabetes Townsend Letter 1985;#32:307 [editorial].

115. Halberstam M, Cohen N, Schlimovich P, et al. Oral vanadyl sulfate improves insulin sensitivity in NIDDM but not in obese nondiabetic subjects. Diabetes 1996;45:659–66.

116. Boden G, Chen X, Ruiz J, et al. Effects of vanadyl sulfate on carbohydrate and lipid metabolism in patients with non-insulin dependent diabetes mellitus. Metabolism 1996;45:1130–5.

117. Aharon Y, Mevorach M, Shamoon H. Vanadyl sulfate does not enhance insulin action in patients with type 1 diabetes. Diabetes Care 1998;21:2194 [letter].

118. Yamashita K, Kawai K, Itakura M. Effect of fructo-oligosaccharides on blood glucose and serum lipids in diabetic subjects. Nutr Res 1984;4:961–6.

119. Roberfroid M. Dietary fibre, inulin and oligofructose. A review comparing their physiological effects. Crit Rev Food Sci Nutr 1993;33:103–48 [review].

120. van Dokkum W, Wezendonk B, Srikumar TS, van den Heuvel. Effect of nondigestible oligosaccharides on large-bowel functions, blood lipid concentrations and glucose absorption in young healthy male subjects. Eur J Clin Nutr 1999;53:1–7.

121. Luo J, Rizkalla SW, Alamowitch C, et al. Chronic consumption of short-chain fructooligosaccharides by health subjects decreased basal hepatic glucose production but had no effect on insulin-stimulated glucose metabolism. Am J Clin Nutr 1996;63:939–45.

122. Baskaran K, Ahmath BK, Shanmugasundaram KR, Shanmugasundaram ERB. Antidiabetic effect of a leaf extract from Gymnema sylvestre in non-insulin-dependent diabetes mellitus patients. J Ethnopharmacol 1990;30:295–305.

123. Shanmugasundaram ERB, Rajeswari G, Baskaran K, et al. Use of Gymnema sylvestre leaf extract in the control of blood glucose insulin-dependent diabetes mellitus. J Ethnopharmacol 1990;30:281–94.

124. Zhang T, Hoshino M, et al. Ginseng root: Evidence for numerous regulatory peptides and insulinotropic activity. Biomed Res 1990;11:49–54.

125. Suzuki Y, Hikino H. Mechanisms of hypoglycemic activity of panaxans A and B, glycans of Panax ginseng roots: Effects on plasma levels, secretion, sensitivity and binding of insulin in mice. Phytother Res 1989;3:20–4.

126. Waki I, Kyo H, et al. Effects of a hypoglycemic component of ginseng radix on insulin biosynthesis in normal and diabetic animals. J Pharm Dyn 1982;5:547–54.

127. Sotaniemi EA, Haapakoski E, Rautio A. Ginseng therapy in non-insulin-dependent diabetic patients. Diabetes Care 1995;18:1373–5.

128. Scharrer A, Ober M. Anthocyanoside in der Behandlung von Retinopathien. Klin Monatsblatt Augenheilk 1981;178:386–9.

129. Bunyapraphatsara N, Yongchaiyudha S, Rungpitarangsi V, Chokechaijaroenporn O. Antidiabetic activity of Aloe vera L juice II. Clinical trial in diabetes mellitus patients in combination with glibenclamide. Phytomedicine 1996;3:245–8.

130. Yongchaiyudha S, Rungpitarangsi V, Bunyapraphatsara N, Chokeshaijaroenporn O. Antidiabetic activity ofAloe vera L juice I. Clinical trial in new cases of diabetes mellitus. Phytomedicine 1996;3:241–3.

131. Leatherdale BA, Panesar RK, Singh G, et al. Improvement of glucose tolerance due to Momordica charantia (karela). BMJ 1981;282:1823–4.

132. Srivastava Y, Venkatakrishna-bhatt H, Verma Y, et al. Antidiabetic and adaptogenic properties of Momordica charantia extract: An experimental and clinical evaluation. Phytother Res 1993;7:285–9.

133. Welihinda J, Karunanaya E, Sheriff MHB, Jayasinghe K. Effect of Momordica charantia on the glucose tolerance in maturity onset diabetes. J Ethnopharmacol 1986;17:277–82.

134. Capsaicin study group. Treatment of painful diabetic neuropathy with topical capsaicin. A multicenter, double-blind, vehicle-controlled study. The capsaicin study group. Arch Intern Med 1991;151:2225–9.

135. Capsaicin study group. Effect of treatment with capsaicin on daily activities of patients with painful diabetic neuropathy. The capsaicin study group. Diabetes Care 1992;15:159–65.

136. Gray AM, Flatt PR. Insulin-secreting activity of the traditional antidiabetic plant Viscum album (mistletoe). J Endocrinol 1999;160:409–14.

137. Swanson-Flatt SK, Day C, Bailey CJ, Flatt PR. Evaluation of traditional plant treatments for diabetes: Studies in streptozotocin-diabetic mice. Acta Diabetologica Latina 1989;26:51–5.

138. Anderson JW, Allgood LD, Turner J, et al. Effects of psyllium on glucose and serum lipid responses in men with type 2 diabetes and hypercholesterolemia. Am J Clin Nutr 1999;70:466–73.

139. Peirce A. Practical Guide to Natural Medicines. New York: William Morrow and Co., 1999:469–71.

140. Jones K. Reishi mushroom: Ancient medicine in modern times. Alt Compl Ther 1998;4(4):256–66 [review].