By Greg Arnold, DC, CSCS, September 25, 2009, abstracted from “Dietary supplementation with a combination of α-lipoic acid, acetyl-l-carnitine, glycerophosphocoline, docosahexaenoic acid, and phosphatidylserine reduces oxidative damage to murine brain and improves cognitive performance” in the January 2009 issue of Nutrition Research

Alzheimer Disease has doubled among Americans since 1980, currently affecting more than 4.5 million Americans, and expected to hit 16 million by 2050 (1).  The condition costs $100 billion each year to treat (2).  Fortunately, there are a number of ways to help protect yourself against Alzheimer Disease (AD), including increasing your intake of apples (3), vitamin E (4), grape seed extract (5), green tea (6), and fish oil (7); increasing your HDL cholesterol (8), and exercising (9).

Now a new study in mice (10) has found that a group of antioxidants given together may help with mental health.  Previous research in mice has shown that nutrient deficiency hampers mental performance (11) and dietary supplementation helps slow down and even reverse the declines due to dietary deficiencies (12, 13). Building on this research, researchers divided nine mice into three groups with three mice in each group.  The groups were fed the following diets for four weeks

Group 1: “Deficient Diet”, lacking folate and vitamin E. The “deficient diet” was also supplemented with iron (50 grams/500 grams of food) to increase free radical production and simulate aging (14).
Group 2: “Complete Diet”, supplemented with folic acid (4 mg/kg of food) and vitamin E (50 IU/kg of food
Group 3: This group received the above “complete” or “deficient” diets supplemented with the following antioxidants per kilogram of food: 200 mg alpha lipoic acid, 500 mg acetyl-l-carnitine, 6 grams DHA (a fat found in fish oil), 100 mg glycerophosphocholine (GPC) (15), and 50 mg phosphatidylserine.  

Before and after the study, the mice completed a standard Y maze (16) for 5-minutes at a time and the researchers collected tissue samples to measure free radical levels.

Regarding oxidative stress in the mice from the diets (measured as TBARS, an oxidation measuring system (17)), while the “deficient” diet (without folic acid and vitamin E) “only slightly increased oxidative stress” compared to the “complete diet” (folic acid and vitamin E included; 1.75 vs. 1.40 Molar/mg protein), mice supplemented with the extra antioxidants had “significantly reduced levels of oxidative species in brain tissue.”  Specifically, antioxidant supplementation of the “complete” and “deficient” diets produced TBARS levels of 0.5 (64% decrease) and 0.6 (66% decrease) Molar/mg protein, respectively.

For the Y-maze, mice on the “deficient” diets had a 15% decrease in efficiency compared to mice on the “complete diet”.  When mice on the “deficient” diet were given the antioxidant supplements, the decrease seen in the original “deficient” group was prevented, with only a 0.5% decrease in efficiency.

The researchers admit that “we have not examined the complete mechanism(s) by which these supplements provided the degree of [nerve protection]” but suggest that it may have to do with helping protect the mitochondria, the structure in each cell that makes energy (17).  They went on to conclude that “These findings add to the growing body of research indicating that key dietary supplementation may delay the progression of age-related cognitive decline.”

Greg Arnold is a Chiropractic Physician practicing in Danville, CA.  You can contact Dr. Arnold directly by emailing him at mailto:PitchingDoc@msn.com or visiting his web site at  www.CompleteChiropracticHealthcare.com

Reference:

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15. “What is Glycerophosphocholine?” posted on http://greenmedica.com/product-info/what-is-glycerophosphocholine-gpc.html
16. “Ymaze” posted on www.mcg.edu/Core/Labs/sabc/Ymaze.htm
17. G. Aliev, J. Liu, J.C. Shenk, K. Fischbach, G.J. Pacheco and S.G. Chen et al., Neuronal mitochondrial amelioration by feeding acetyl-l-carnitine and lipoic acid to aged rats, J Cell Mol Med (2008) [electronic publication ahead of print].