Too much weight gain, too little exercise, bad eating habits, etc. account for the preponderance of cases of diabetes in Western countries.

Most authorities argue that diabetes is largely lifestyle related. Too much weight gain, too little exercise, bad eating habits, etc. account for the preponderance of cases of diabetes in Western countries. Overall, the American diet is mineral-poor. We as a nation are not fond of green leafy vegetables or of whole grains and, as a result, a majority of all Americans consume, for example, inadequate amounts of magnesium. Supplementation with magnesium in a recent trial with overweight subjects for four weeks supported the hypothesis that dietary magnesium plays a beneficial role in the regulation of insulin and glucose homeostasis.1 Two other minerals of special importance for fending off diabetes are chromium and manganese.

Clinical studies have shown that obesity, particularly increased visceral fat, is associated with insulin resistance and hyperinsulinemia.2,3 If proper lifestyle modification is not enforced soon enough, this may progress to impaired glucose tolerance (IGT) and/or development of type 2 diabetes ( T2D) in some individuals. Thus, maintenance of an active lifestyle and healthy weight management are critical for the prevention of type 2 diabetes in both children and adults. In addition, early diagnosis of type 2 diabetes is important for those who have developed the disease in order to obtain adequate treatments, lifestyle changes, self-motivation, and family support.

Some components of the diet play especially important roles in the development of diabetes. Diabetes and the metabolic syndrome involve the liver in the majority of cases via inappropriate gluconeogenesis, meaning that the liver in diabetics usually continues to release glucose into the blood stream despite adequate insulin and blood sugar present to inhibit such actions in healthy individuals. Recovering normal liver regulation of gluconeogenesis is important for resolving the metabolic syndrome. Improving aspects of non-alcoholic hepatic liver disease also improves many aspects of diabetes, including not just blood sugar, but also lipid disorders.

Excessive consumption of the simple sugar fructose, by the way, is important as a cause of liver dysfunction.

Fructose is one of a handful of common nutrients not well regulated by the liver. Excessive consumption of fructose leads to the synthesis of fat in the liver and this, in turn, interferes with the liver’s response to signals from insulin.

Food is not the only cause of diabetes. Psychological stress and related factors long have been suspected of being causally related to cardiovascular disease, diabetes and similar health concerns. Stress that is not well controlled activates cortisol mechanisms that release glucose (gluconeogenesis) from the liver and lean tissues in preparation for “fight or flight” decisions. Surveys have found that being able to respond actively to stressors improves the ability to control their negative sides. In this light, a study in Sweden found that work stress and shift work may contribute to the development of T2D in women, whereas in men the risk was decreased by high work demands, high strain and an active job.4 Hence, it is not stress alone, but also the available responses to stress that help to determine whether work stress contributes to diabetes.

Recent Science
The arsenal of diabetes / blood sugar regulating nutrients has been pretty well picked over. Still, one interesting new alternative for blood sugar regulation is a wild genotype of bitter melon (Momordica charantia). Half a decade ago, the similarities between the mechanisms of action of bitter melon and metformin were recognized. These include reducing excessive hepatic glucose output and reducing serum insulin.5 In the traditional systems of India, East Asia, the Caribbean and elsewhere, bitter melon as either a fresh vegetable or freshly pressed juice is widely recognized for preventing and treating diabetes as well as preventing excessive weight gain. Animal studies have confirmed these traditional uses over and over again.6,7

In a new study, wild bitter melon was shown to rival metformin itself in regulating blood glucose in diabetic animals and also to be superior to two commercial extracts of cultivated bitter melon in areas such as nitric oxide generation and inhibition of the angiotensin-converting enzyme (ACE).8 These facts suggest that wild bitter melon, especially if properly extracted and preserved, may perform some of the other functions of metformin, as well, such as encouraging weight loss. Currently, the only Wild Bitter Melon ingredient available is Glycostat® from Glykon Technologies Group.

Other Supplements
Supplements for blood sugar support, for the most part, fall into a small number of categories. These include items that increase the output of insulin, those that improve the actions of insulin and those that inhibit the digestion of carbohydrates and/or their uptake into the bloodstream.

Gymnema sylvestre is the best known and best researched of the herbs that increase insulin release. Increasing insulin release can improve blood sugar regulation. However, inasmuch as insulin resistance—meaning reliance on elevated levels of insulin to regulate blood sugar—usually already is present in those who need help with blood sugar control, this herb likely is not a good choice as a standalone supplement, although it can be useful in formulations. Most prediabetics do not need to release more insulin, but rather to respond more appropriately to smaller amounts of the hormone.

Improving the response to insulin is always a better starting point than increasing the release of insulin. Wild Bitter Melon already has been mentioned and another useful item is green coffee bean extract. Both act as insulin sensitizers, especially for the liver. In recent years, a great deal of attention has been directed towards cinnamon extracts as insulin sensitizers. Cinnamon may improve insulin resistance by preventing and reversing impairments in insulin signaling in skeletal muscle and by increasing the expression of peroxisome proliferator-activated receptors including, PPARγ in adipose tissue. Another item that improves the actions of insulin is chromium. In an animal model, niacin-bound chromium also has been shown to increase life span.9

Not to be overlooked is a supplement with an extensive clinical track record for use in diabetes. That supplement is alpha-lipoic acid. The newer stabilized R-alpha lipoic acid likely is the supplement of choice.

Items that reduce the rate of digestion and uptake of carbohydrates and sugars are a third category for blood sugar regulation. Well known and well researched is the extract of white bean (Phaseolus vulgaris), often suggested as a carb blocker to reduce blood glucose levels. Perhaps more interesting and requiring lower intakes for efficacy is the polyphenol-rich extracts from two brown seaweeds sold as InSea2™, which reduced plasma glucose concentration, reduced insulin and increased insulin sensitivity. This seaweed extract inhibits both starch and sucrose digestion.10

Concluding Thoughts
Diabetes for about 90 percent of individuals is the result of issues of diet and exercise and usually is associated with weight problems. Nutritional approaches to blood sugar control usually take weeks or months to show their true results. However, once certain benefits are being realized, they are likely to be fairly stable. Readers should practice patience and as they pursue the promise of more even and consistent blood sugar regulation with the use of supplements that overcome deficiencies.

In the U.S. it is available in two products sold by Jarrow Formulas of Los Angeles: Pressure Optimizer and Glucose Optimizer.

References:

  1. Am J Clin Nutr. 2011 Feb;93(2):463 –73.
  2. N Engl J Med. 2004;346:802–10.
  3. Diabetes Care. 2002;2:1631– 6.
  4. Diabetes Care. 2013 Sep;36(9):2683–9.
  5. Med Hypotheses. 2004;63(2):340 –3.
  6. Br J Biomed Sci. 2005, 62:124– 6.
  7. J Nutr. 2005, 135:2517–23.
  8. J Med Food. 2011 Dec;14(12):1496 –504.
  9. J Inorg Biochem. 2011 Oct;105(10):1344 – 9
  10. Appl Physiol Nutr Metab. 2011 Dec;36(6):913 – 9.

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