Dietary Links to Alzheimer's Disease
Summary: Recent findings that elderly African-Americans
and Japanese living in the United States have much higher prevalence of
Alzheimer’s disease (6.24% and 4.1%, respectively) than those still living
in their ethnic homelands (<2%) suggested that environmental rather than
genetic factors are the primary agents causing Alzheimer’s disease. Recent
papers linking clinical expression of Alzheimer’s disease to oxidative
stress and cerebral infarct suggest that diet is a key factor in the development
of Alzheimer’s disease. To test this hypothesis, regression
analyses were performed on the prevalence of Alzheimer’s disease in the
65+ age population for 11 countries obtained from 18 community-wide studies
versus components of the national diets.
J Neurosci Res 2002 Nov 1;70(3):361-6
Cholesterol and pathological processes in Alzheimer's disease.
Yanagisawa K. Department of Dementia Research, National Institute for Longevity Sciences, Obu, Japan. firstname.lastname@example.org
Fundamental questions on the pathogenesis of Alzheimer's disease (AD) are how nontoxic, soluble amyloid beta-protein (A beta) is converted to its toxic, aggregated form and how functional tau is hyperphosphorylated to form neurofibrillary tangles. Growing evidence from recent biochemical and cell biological studies suggests that altered cholesterol metabolism in neurons may underlie such pathological processes. The possibility that cholesterol is a risk factor in the development of AD has also been supported by recent epidemiological studies. Based on this line of evidence, it is noteworthy to examine the potency of cholesterol-lowering medicine and/or diet in suppressing the development or the progression of AD.
Arch Neurol 2002 Aug;59(8):1258-63
Caloric intake and the risk of Alzheimer disease.
Luchsinger JA, Tang MX, Shea S, Mayeux R. Gertrude H. Sergievsky Center, Columbia University, PH-19, 630 W 168th St, New York, NY 10032. email@example.com
BACKGROUND: Diet may play a role
in Alzheimer disease (AD).
Med Hypotheses 2001 Sep;57(3):318-23
Does a vegan diet reduce risk for Parkinson's disease?
McCarty MF. Pantox Laboratories, San Diego, California 92109, USA.
Three recent case-control studies conclude that diets high in animal fat or cholesterol are associated with a substantial increase in risk for Parkinson's disease (PD); in contrast, fat of plant origin does not appear to increase risk. Whereas reported age-adjusted prevalence rates of PD tend to be relatively uniform throughout Europe and the Americas, sub-Saharan black Africans, rural Chinese, and Japanese, groups whose diets tend to be vegan or quasi-vegan, appear to enjoy substantially lower rates. Since current PD prevalence in African-Americans is little different from that in whites, environmental factors are likely to be responsible for the low PD risk in black Africans. In aggregate, these findings suggest that vegan diets may be notably protective with respect to PD. However, they offer no insight into whether saturated fat, compounds associated with animal fat, animal protein, or the integrated impact of the components of animal products mediates the risk associated with animal fat consumption. Caloric restriction has recently been shown to protect the central dopaminergic neurons of mice from neurotoxins, at least in part by induction of heat-shock proteins; conceivably, the protection afforded by vegan diets reflects a similar mechanism. The possibility that vegan diets could be therapeutically beneficial in PD, by slowing the loss of surviving dopaminergic neurons, thus retarding progression of the syndrome, may merit examination. Vegan diets could also be helpful to PD patients by promoting vascular health and aiding blood-brain barrier transport of L-dopa. Copyright 2001 Harcourt Publishers Ltd.
The incidence of dementia and intake of animal products: preliminary findings from the Adventist Health Study.
Giem P, Beeson WL, Fraser GE. Department of Preventive Medicine, School of Medicine, Loma Linda University, CA 92350.
We investigated the relationship between animal product consumption and evidence of dementia in two cohort substudies. The first enrolled 272 California residents matched for age, sex, and zip code (1 vegan, 1 lacto-ovo-vegetarian, and 2 'heavy' meat eaters in each of 68 quartets). This design ensured a wide range of dietary exposure. The second included 2,984 unmatched subjects who resided within the Loma Linda, California area. All subjects were enrolled in the Adventist Health Study. The matched subjects who ate meat (including poultry and fish) were more than twice as likely to become demented as their vegetarian counterparts (relative risk 2.18, p = 0.065) and the discrepancy was further widened (relative risk 2.99, p = 0.048) when past meat consumption was taken into account. There was no significant difference in the incidence of dementia in the vegetarian versus meat-eating unmatched subjects. There was no obvious explanation for the difference between the two substudies, although the power of the unmatched sub-study to detect an effect of 'heavy' meat consumption was unexpectedly limited. There was a trend towards delayed onset of dementia in vegetarians in both substudies.