Parkinson's disease
Co-Q10
Parkinson's disease is a degenerative neurological disorder characterized by tremors, muscular rigidity, and slow movements. It is estimated to affect approximately 1% of Americans over the age of 65. Although the causes of Parkinson's disease are not all known, decreased activity of complex I of the mitochondrial electron transport chain and increased oxidative stress in a part of the brain called the substantia nigra are thought to play a role. Coenzyme Q10 is the electron acceptor for complex I as well as an antioxidant, and decreased ratios of reduced to oxidized coenzyme Q10 have been found in platelets of individuals with Parkinson's disease (55, 56). A 16-month randomized placebo-controlled trial evaluated the safety and efficacy of 300, 600, or 1200 mg/d of coenzyme Q10 in 80 people with early Parkinson's disease (57). Coenzyme Q10 supplementation was well tolerated at all doses and was associated with slower deterioration of function in Parkinson's disease patients compared to placebo. However, the difference was statistically significant only in the group taking 1200 mg/d. More recently, a small placebo-controlled trial showed that oral administraton of 360 mg/d of coenzyme Q10 for four weeks moderately benefited Parkinson's disease patients (58). Although these preliminary findings are promising, they need to be confirmed in larger clinical trials before recommending the use of coenzyme Q10 in early Parkinson's disease.


organic coffee
Parkinson’s Disease

Several large prospective cohort studies have found higher coffee and caffeine intakes to be associated with significant reductions in Parkinson’s disease risk in men (18-20). In a prospective study of 47,000 men, those who regularly consumed at least one cup of coffee daily had a risk of developing Parkinson’s disease over the next 10 years that was 40% lower than men who did not drink coffee (19). Caffeine consumption from other sources was also inversely associated with Parkinson’s disease risk in a dose-dependent manner. Studies in animal models of Parkinson’s disease suggest that caffeine may protect dopaminergic neurons by acting as an adenosine A2A-receptor antagonist in the brain (21). In contrast to the results of prospective studies in men, inverse associations between coffee or caffeine consumption and Parkinson’s disease risk were not observed in women (18, 19). The failure of prospective studies to find inverse associations between coffee or caffeine consumption and Parkinson’s disease in women may be due to the modifying effect of estrogen replacement therapy. Further analysis of a prospective study of more than 77,000 female nurses revealed that coffee consumption was inversely associated with Parkinson’s disease risk in women who had never used postmenopausal estrogen, but a significant increase in Parkinson’s disease risk was observed in postmenopausal estrogen users who drank at least 6 cups of coffee daily (22). In a prospective cohort study that included more than 238,000 women, a significant inverse association between coffee consumption and Parkinson’s disease mortality was also observed in women who had never used postmenopausal estrogen, but not in those who had used postmenopausal estrogen (18). It is not known how estrogen modifies the effect of caffeine on Parkinson’s disease risk (23). Although the results of epidemiological and animal studies suggest that caffeine may reduce the risk of developing Parkinson’s disease, it is premature to recommend increasing caffeine consumption to prevent Parkinson’s disease, particularly in women taking estrogen.

flavinoids
Neurodegenerative Disease

Inflammation, oxidative stress and transition metal accumulation appear to play a role in the pathology of several neurodegenerative diseases, including Parkinson's disease and Alzheimer’s disease. Because flavonoids have anti-inflammatory, antioxidant and metal chelating properties, scientists are interested in the neuroprotective potential of flavonoid-rich diets or individual flavonoids. At present, the extent to which various dietary flavonoids and flavonoid metabolites cross the blood brain barrier in humans is not known (84). Although flavonoid-rich diets and flavonoid administration have been found to prevent cognitive impairment associated with aging and inflammation in some animal studies (85-88), prospective cohort studies have not found consistent inverse associations between flavonoid intake and the risk of dementia or neurodegenerative disease in humans (89-93). In a cohort of Japanese-American men followed for 25-30 years, flavonoid intake from tea during midlife was not associated with the risk of Alzheimer’s or other types of dementia in late life (89). Surprisingly, higher intakes of isoflavone-rich tofu during midlife were associated with cognitive impairment and brain atrophy in late life (see Soy Isoflavones) (90). A prospective study of Dutch adults found that total dietary flavonoid intake was not associated with the risk of developing Parkinson disease (91) or Alzheimer’s disease (92), except in current smokers whose risk of Alzheimer’s disease decreased by 50% for every 12 mg increase in daily flavonoid intake. In contrast, a study of elderly French men and women found that those with the lowest flavonoid intakes had a risk of developing dementia over the next 5 years that was 50% higher than those with the highest intakes (93). Although scientists are interested in the potential of flavonoids to protect the aging brain, it is not yet clear how flavonoid consumption affects neurodegenerative disease risk in humans.

Sources

Food Sources

Dietary sources of flavonoids include tea, red wine, fruits, vegetables and legumes. Individual flavonoid intakes may vary considerably depending on whether tea, red wine, soy products or fruits and vegetables are commonly consumed [reviewed in (3)]. Although individual flavonoid intakes may vary, total flavonoid intakes in Western populations appear to average about 150-200 mg/day (3, 94). Information on the flavonoid content of some flavonoid-rich foods is presented in table 2 and table 3. These values should be considered approximate since a number of factors may affect the flavonoid content of foods, including agricultural practices, environmental factors, ripening, processing, storing and cooking. For more information about the flavonoid content of foods, see the USDA databases for the flavonoid and proanthocyanidin content of selected foods. For information on the isoflavone content of soy foods, see the separate article on Soy Isoflavones or the USDA database for the isoflavone content of selected foods.

Table 2. Anthocyanin, Flavanol and Proanthocyanidin Content of Selected Foods

Table 3. Flavone, Flavonol and Flavanone Content of Selected Foods

Supplements

Anthocyanins

Bilberry, elderberry, black currant, blueberry, red grape and mixed berry extracts that are rich in anthocyanins are available as dietary supplements without a prescription in the U.S. The anthocyanin content of these products may vary considerably. Standardized extracts that list the amount of anthocyanins per dose are available.

Flavanols

Numerous tea extracts are available in the U.S. as dietary supplements, and may be labeled as tea catechins or tea polyphenols. Green tea extracts are the most commonly marketed, but black and oolong tea extracts are also available. Green tea extracts generally have higher levels of catechins (flavanol monomers), while black tea extracts are richer in theaflavins and thearubigins (flavanol polymers found in tea). Oolong tea extracts fall somewhere in between green and black tea extracts with respect to their flavanol content. Some tea extracts contain caffeine, while others are decaffeinated. Flavanol and caffeine content vary considerably among different products, so it is important to check the label or consult the manufacturer to determine the amounts of flavanols and caffeine that would be consumed daily with each supplement. (For more information on tea flavanols, see the article on Tea.)

Flavanones

Citrus bioflavonoid supplements may contain glycosides of hesperetin (hesperidin), naringenin (naringin) and eriodictyol (eriocitrin). Hesperidin is also available in hesperidin-complex supplements (95).

Flavones

The peels of citrus fruits are rich in the polymethoxylated flavones, tangeretin, nobiletin and sinensetin (3). Although dietary intakes of these naturally occurring flavones are generally low, they are often present in citrus bioflavonoid supplements.


Neurodegenerative Disease

Although it is not yet clear whether a diet rich in fruits and vegetables will decrease the risk of neurodegenerative diseases like Alzheimer’s disease and Parkinson’s disease in humans, recent studies in animal models of these diseases suggest that diets high in fruits like blueberries (49) or tomatoes may be protective (50).


Neurodegenerative disease

Iron is required for normal brain and nerve function through its involvement in cellular metabolism, as well as the synthesis of neurotransmitters and myelin. However, accumulation of excess iron can result in increased oxidative stress, and the brain is particularly susceptible to oxidative damage. Iron accumulation and oxidative injury are presently under consideration as potential contributors to a number of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease (36). The abnormal accumulation of iron in the brain does not appear to be a result of increased dietary iron, but rather, a disruption in the complex process of cellular iron regulation. Although the mechanisms for this disruption in iron regulation are not yet known, it is presently an active area of biomedical research (37).

Drug Interactions

Medications that decrease stomach acidity, such as antacids, histamine (H2) receptor antagonists (e.g., cimetidine, ranitidine), and proton pump inhibitors (e.g., omeprazole, lansoprazole), may impair iron absorption. Taking iron supplements at the same time as the following medications may result in decreased absorption and efficacy of the medication: levodopa, levothyroxine, methyldopa, penicillamine, quinolones, tetracyclines, and bisphosphonates. Therefore, it is best to take these medications two hours apart from iron supplements. Cholestyramine resin, used to lower blood cholesterol levels, should also be taken two hours apart from iron supplements because it interferes with iron absorption. Allopurinol, a medication used to treat gout, may increase iron storage in the liver and should not be used in combination with iron supplements (23, 38).

Linus Pauling Institute Recommendation

Following the most recent RDA for iron should provide sufficient iron to prevent deficiency without causing adverse effects in most individuals. Although sufficient iron can be obtained through a varied diet, a considerable number of people do not consume adequate iron to prevent deficiency. A multivitamin/multimineral supplement containing 100% of the daily value (DV) for iron provides 18 mg of elemental iron. While this amount of iron may be beneficial for premenopausal women, it is well above the RDA for men and most postmenopausal women.

Adult men and postmenopausal women

Since hereditary hemochromatosis is relatively common and the effects of long-term dietary iron excess on chronic disease risk are not yet clear, men and postmenopausal women who are not at risk of iron deficiency should take a multivitamin/mineral supplement without iron. A number of multivitamins formulated specifically for men or those over 50 years of age do not contain iron.

Adults over the age of 65

A recent study in an elderly population found that high iron stores were much more common than iron deficiency (39). Thus, older adults should not generally take nutritional supplements containing iron unless they have been diagnosed with iron deficiency. Moreover, it is extremely important to determine the underlying cause of the iron deficiency, rather than simply treating it with iron supplements.

References


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Written by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University