Page 38 - Summer2014
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NUTRITIONAL THERAPIES FOR ALZHEIMER'S DISEASE


              The damage observed in AD brains is complex and multifactorial. Any intervention intended to delay or possibly
           reverse this damage should therefore be a multipronged strategy designed to address as many of the contributing factors
           as possible. The majority of these potentially helpful practices are nutritional, but two can be considered lifestyle modifi-
           cations. Obviously, the foundation of what might be considered an “anti-Alzheimer’s strategy” is a reduced carbohydrate
           diet. Beyond that, there are numerous nutritional supplements that could be effective based on their biochemical func-
           tions:

           •   Chromium picolinate: Chromium is required for proper function of the insulin receptor, and has been proven to aid
              in glucoregulation and insulin sensitivity. 58,59
           •   Zinc: Insulin degrading enzyme requires zinc as a cofactor.
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           •   High-quality cod liver oil: To balance the n-6/n-3 ratio and decrease inflammation. Generally, oils rich in n-6 fatty
              acids induce inflammation in the body, while n-3-rich oils stimulate anti-inflammatory pathways. The ratio of n-6 to
              n-3 in the modern American diet is estimated to be as high as 30:1, while our evolutionary dietary patterns suggest
              we are physiologically suited to a ratio closer to 3:1. 36,60  Additionally, dietary imbalances of these fatty acids cause
              imbalances in their incorporation into cellular and organelle membranes, resulting in altered permeability and in-
              creased vulnerability to lipid peroxidation.

           •   Medium-chain triglycerides (MCTs): These saturated fatty acids (found mostly in coconut and palm kernel oils) are
              metabolized differently from others and can serve as a source of ketones even in the absence of carbohydrate re-
              striction. 61

           •   L-Carnitine: This amino acid is required by carnitine palmitoyltransferase-1, the enzyme responsible for shuttling
              fatty acids into the mitochondria, as well as other enzymes in the breakdown of fats.  A patient on a reduced car-
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              bohydrate diet with the specific intention of ramping up fatty acid oxidation and ketogenesis could likely benefit
              from supplemental carnitine.

           •   Coenzyme Q : CoQ  is a vital member of the mitochondrial electron transport system (and therefore generation
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              of ATP) and also a potent antioxidant. CoQ  administration has been shown to reduce production of ROS by mito-
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              chondria exposed to Aβ in animal models of diabetes.  With the AD brain struggling to produce energy and under
              great oxidative stress, CoQ  could be a powerful adjunct.
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           •   Antioxidants: In addition to increasing antioxidant-rich foods in the diet, supplemental N-acetyl-cysteine for glutathi-
              one regeneration might be helpful. (It’s noteworthy that the fruits highest in antioxidants are also lower in glycemic
              index and load; namely, berries.) Supplemental superoxide dismutase might also be beneficial.
           •   Physical activity: Physical activity induces recruitment of GLUT4s and ultimately helps maintain insulin sensitivity.
              Resistance training or weightlifting might prove particularly beneficial, as it would serve to increase muscle mass and
              potentially increase insulin sensitivity. This might be especially protective if started early in life so as to minimize the
              impact of sarcopenia (loss of muscle mass) as one ages.

           •   Stress reduction: Cortisol, the primary glucocorticoid “stress hormone,” releases glucose in response to acute
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              stressors.  In our hyper-stressful modern environment, our bodies almost always perceive dire threats all around
              us. Chronically high cortisol levels could induce hyperglycemia even in the context of a reduced carbohydrate diet.

           •   B : While B  is not necessarily required for a therapeutic diet for AD, it is important to note that memory loss and
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              cognitive decline are insidious signs of long-term B  deficiency. Sufficient stomach acid is required for B  absorption,
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              and stomach acid production naturally declines with age. Combine this with the possibility that older people are
              less likely to consume B -rich foods (which can take more effort to prepare than convenient, ready-to-eat refined
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              carbohydrates), and B  deficiency becomes fairly common in the elderly. B  deficiency can even be mistaken for
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              AD, so it’s worthwhile to have B  levels tested if AD is suspected.
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