The elderly are especially at risk for malnutrition. Disease, depression, polypharmacy, poverty, inadequate care, malabsorption and social isolation are contributing factors. The 1993 Nutrition Screening Initiative found that 1/4 of all elderly patients and 1/2 of all hospitalized elderly may suffer from malnutrition. The study results prompted a spokesperson for the American Dietetic Association to state: "Our health care system is a little malnourished itself." In long term care settings, where it is estimated that from 10 to 85% of older adults may be malnourished, the nutrition provider "must carefully consider many complex physical, medical and psychosocial factors to deliver individualized nutritional care."
A European initiative (the "Health Promotion Program") has been undertaken to prevent weight loss in patients with Alzheimer's disease. Weight loss in Alzheimer's patients was first observed by Alois Alzheimer in 1901. A number of studies have consistently observed weight loss in patients with dementia, and in particular, Alzheimer's disease. This weight loss increases the risk of infections, skin ulcers, and consequently decreases quality of life in Alzheimer's patients. The cause is certainly related in part to reduced functional capacity in Alzheimer's patients, but other hypotheses hold that neuro-endocrine or metabolic factors are implicated. One study has even correlated the burden the disease places on the caregiver with the degree of weight loss in the Alzheimer's patient. This implies that supportive measures aimed at relieving caregivers' stress may indirectly impact patient's nutritional status.
The progression of neurological disease may also be slowed by application of antioxidant support. In the treatment of Parkinson's Disease, Kedar N. Prasad of the University of Colorado Health Sciences Center proposes an antioxidant-laden cocktail of natural beta-carotene (30mg/day); d-alpha tocopheryl succinate (600 IU/day) vitamin C(4g/day) coenzyme Q10 (200mg/day), NADH (10mg/day)l N-acetyl-cysteine (500 mg/day) zinc (30 mg/day) and selenium (200 mcg/day).
Inflammation may contribute to the progression of neurodegenerative diseases. Attenuation of inflammation can be achieved via the aforementioned antioxidant support; it can also be accomplished via nutritional modulation of protaglandin metabolism. Administration of essential fatty acids like EPA and GLA and supplementation with nutrient co-factors like zinc and vitamin C that favor endogenous production of anti-inflammatory eicosanoids can positively impact many disorders.
Defects in methylation results from aberrant homocysteine metabolism . Homocysteine may play a role in the etiology of cardiovascular disease, stroke, venous thrombosis, arthritis, Alzheimer's Disease and vascular dementia. The key nutrients for reversal of homocysteinemia are vitamin B6; vitamin B12 and folic acid. Screening for vitamin B12 deficiency in the elderly can yield a high number of abnormal results even in the absence of anemia. Vitamin B12 deficiency may result from malabsorption or lack of hydrochloric acid common in the elderly. Measurements of serum methylmalonic acid and homocysteine are more sensitive methods for confirmation of B12 deficiency than radioisotope assays or serum B12 levels. In one study of 86 B12 deficient patients who responded to cobalamin therapy, neuropsyciatric abnormalities were noted in 28%, many times in the absence of anemia.
Once relegated to the status of a rare genetic disorder, the concept of mitochondrial dysfunction is taking on new importance in a more nuanced approach to understanding of degenerative processes. Ensuing nutritional deficiencies attendant to aging or debilitation might further compromise efficiency of ATP production. The results could be failure of energy production in the cells of the brain. Nutrients that support mitochondrial function include coenzyme Q10, vitamin E, riboflavin, niacin, l- carnitine, and magnesium. Recently, a new "stabilized" form of NADH for oral administration ("Enada") has been proposed for treatment of dementia, Parkinson's Disease, Chronic Fatigue Syndrome and other debilitating ailments.
Even hidden food intolerances may contribute to the development of Alzheimer's Disease, for example, atypical presentation of coeliac disease in the absence of classic intestinal manifestations. Recent research has demonstrated a high prevalence of antigliadin antibodies (IgG, IgA or both) in patients with neurological dysfunction of obscure etiology (57 percent versus 5 percent in neurological controls and 12 percent in normal controls). There was a nearly tenfold increase in neurological dysfunction or dementia in gluten-sensitive individuals compared to those not gluten-sensitive. Detection was made more elusive by the fact that only 35 percent of patients who developed neurological problems had histological evidence of celiac disease. Two-thirds had no clinical signs of celiac disease.
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