Journal of the American College of Nutrition 19(2): 242-255 2000
Abstract:
Objective: To examine associations of midlife tofu consumption
with brain function and structural changes in late life.
Methods: The design utilized surviving participants of a longitudinal
study established in 1965 for research on heart disease, stroke, and
cancer. Information on consumption of selected foods was available
from standardized interviews conducted 1965-1967 and 1971-1974.
A 4-level composite intake index defined "low-low" consumption as
fewer than two servings of tofu per week in 1965 and no tofu in the prior
week in 1971. Men who reported two or more servings per week at both
interviews were defined as "high-high" consumers. Intermediate or less
consistent "low" and "high" consumption levels were also defined.
Cognitive functioning was tested at the 1991-1993 examination, when
participants were aged 71 to 93 years (n=3734). Brain atropy was
assessed using neuroimage (n=574) and autopsy (n=290) information.
Cognitive function data were also analyzed for wives of a sample of
study partcipants (n=502) who had been living with the participants at
the time of their dietary interviews.
Results: Poor cognitive test performance, enlargement of ventricles
and low brain weight were each significantly and independently
associated with higher tofu consumption. A similar association of midlife
tofu intake with poor late life cognitive test scores was also observed
among wives of cohort members, using the husbands answers to food
frequency questions as proxy for the wife's consumption. Statistically
significant associations were consistently demonstrated in linear
multivariate regression models. Odds ratios comparing endpoints
among "high-high" with "low-low" consumers were mostly in the range
of 1.6 to 2.0.
Conclusions: In this population, higher midlife tofu consumption was
independently associated with indicators of cognitive impairment and
brain atrophy in late life.
Additional note by poster:
" Tofu genistein may induce brain atropy by inhibiting adult neurogenesis,
as follows."
see Neurosci Lett 272(2): 123-6 Sep 10,1999
and Exp Neurol 159(1): 164-76 Sep 1999
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