-IBIS-1.7.0-
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nervous system
Alzheimer's disease
Nutrition

dietary guidelines

therapeutic foods:

• increase foods that calm the Shen (Spirit), tonify the Heart, harmonize the Stomach and Spleen

• increase foods rich in Calcium, Phosphorus, Manganese, Sulfur, Iodine, tryptophan (Jensen, p. 63)

• egg yolk, kale, celery, fish, raw goat's milk, veal joint broth, cod roe, rice polishings, brewer's yeast, nutritional yeast (Jensen, p. 63)

fresh juices:

• celery, carrot, prune (Jensen, p. 63)

• prune and rice polishing (Jensen, p. 63)

• raw goat's milk and 1 tsp. sesame, sunflower, or almond butter, 1 tsp. honey and sliver of avocado (Jensen, p. 63)

• black cherry and egg yolk (Jensen, p. 63)

avoid:

• meat, alcohol, hot sauces, spicy foods, fried foods, fatty foods, rich foods, salty foods, coffee, caffeine, sweet foods and sugar

supplements

Vitamin B12

Folic acid

Melatonin: In vitro, melatonin has been found to protect neurons against ß-amyloid toxicity, inhibit amyloid formation, and has shown antioxidative properties. In a case report, Brusco et al describe the results of treating a pair of elderly, male twins with Alzheimer's disease. The one brother who was prescribed 6 mg of melatonin each evening. After three years assessment of both twins indicated that the one taking melatonin was at a higher functional level than his brother, with substantially less impairment of memory and speech. Further, the brother using melatonin daily melatonin showed significantly less progression of the cognitive and behavioral signs typical of Alzheimer's disease progression. In contrast, the twin who had not taken the melatonin showed marked deterioration.

(Brusco LI, et al. J Pineal Res 1998 Dec;25(4):260-263.)

footnotes

Brusco LI, Marquez M, Cardinali DP. Monozygotic twins with Alzheimer's disease treated with melatonin: Case report. J Pineal Res 1998 Dec;25(4):260-263.

Abstract: Monozygotic twins with Alzheimer's disease of 8 years duration were studied. The onset of the disease differed by about 6 months between twins and was characterized by a primary impairment of memory function. Clinical evaluation at the time of diagnosis indicated a similar cognitive and neuroimaging alteration in both patients, as well as a similar neuropsychologic impairment. A possible genetic origin of the disease was suggested by a similar disease suffered by the mother. Patients were initially treated with vitamin E (800 IU/day). Starting at approximately the same time (about 3 years ago), they received 50 mg/day thioridazine because of the behavioral and sleep disorder. One of the patients was treated with melatonin (6 mg orally) at bed time daily for 36 months. Evolution of the disease in the melatonin-treated patient indicated a milder impairment of memory function, with substantial improvement of sleep quality and reduction of sundowning. This led to discontinuance (after 3 months) of thioridazine treatment. Present clinical evaluation indicated a difference in functional stage of the disease between the twins (Functional Assessment Tool For Alzheimer's Disease, FAST), with a score of 5 in the twin who received melatonin and of 7b in the twin who did not receive it. Since experimental data on melatonin in animals indicated its antioxidant, antiapoptotic, and beta-amyloid-decreasing activity, the hypothesis that melatonin has a beneficial effect in Alzheimer's disease patients should be considered.