A new study by Kresge Eye Institute, Detroit, Michigan, which involved supplementation of a nutrient, R-Alpha Lipoic, “has produced a significant beneficial effect on the impaired mitochondria biogenesis and also on the continued progression of diabetic retinopathy”.

According to Warwick Medical School (UK), Nazionale Ricovero e Cura Anziani Diabetes (Italy) and the Department of Cell Biology, University of Oklahoma (USA), “metabolic memory” is defined as diabetic vascular stresses persisting after glucose normalization, which has been supported both in the laboratory and clinical studies, both in type 1 and type 2 diabetes. (1)

Constant elevated blood-glucose levels result in metabolism of glucose via cells independent of insulin and, at least in the retina and kidneys, it produces superoxides that accumulate in mitochondria and ultimately damage the mitochondria. The superoxides are neutralized through cellular production of anti-oxidants called superoxide-dismutase (SOD).

In animal studies, the production of retinal SOD was totally absent and the anti-oxidant capacity was sub-normal, up to six month after cessation of poor glycemic control, which translates to abnormally high activities of superoxides and the consequent stress, placed upon the cells. In another word, a persistent stress “metabolic memory”. (2)

Mitochondria are the major source of superoxide, which is considered to be a causal link between elevated glucose levels and the development of vascular complications in diabetes. (3)

In the Kresge study, supplementation of R-Alpha Lipoic (AKA Lipoic Acid) “produced a significant beneficial effect on the impaired mitochondria biogenesis”.

R-Alpha Lipoic is made and known to the human body. In the biologic processes, its reduced form is made in conjunction with the metabolism of glucose and is a vital co-enzyme.

Supplemental R-Alpha lipoic is water and fat-soluble and, thus, easily passes the cellular membranes and, due to its structure, in mitochondria receives a hydrogen (H) from an abundant co-enzyme “NADH” (thus, converting it to NAD) and, thereof, R-Alpha Lipoic converts to its anti-oxidant form. (4)

In 2007 Dr. David Sinclair, a professor of Pathology at Harvard medical School, published the result of a study, done in conjunction with National Institute on Aging, National Institutes of Health, whereas they stated Nutrient-Sensitive Mitochondrial level of NAD Dictate Cell Survival. (5)

It has been proposed that higher levels of NAD may allow the activation of Sirtuin genes, a family of genes that increase cell’s ability to resist stress and apoptosis, an extremely beneficial aspect for Parkinson’s and Alzheimer’s.

The mitochondrial NADH has shown a preference for R-Alpha Lipoic Acid (Lipoic Acid). In animal studies liver-cells mitochondria has shown to reduce exogenous (supplemental) Lipoic Acid.

The reduction of R-Alpha Lipoic Acid by NADH would result in an increase in the cellular levels of NAD, as well as, the formation of a potent mitochondrial anti-oxidant (di-hydro-lipoic acid: the reduced form of R-Alpha Lipoic).

Based on the above, there is a great need to further investigate the role of clinical diets, containing R-Alpha Lipoic, not only in Diabetic Retinopathy but also Parkinson’s and Alzheimer’s.

1. The Journal of Clinical Endocrinology & Metabolism. Feb. 2009, 94(2):410–415.

2. Experimental Diabetes Research Volume 2007, Article ID 21976.

3. Investigative Ophthalmology & Visual Science, April 2006, Vol. 47, No. 4.

4. Free Radical Biology & Medicine - Elsevier. Vol 22, Issue 3, 1997, Pp 535-542.

5. Cell, Vol. 130, Issue 6, 1095-1107, 21 Sept. 2007.

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