Stick to the Med diet
COLUMBIA UNIVERSITY'S MAILMAN SCHOOL OF PUBLIC HEALTH
A healthier diet is associated with a reduced dementia risk and slower pace of aging, according to a new study at Columbia University Mailman School of Public Health and The Robert Butler Columbia Aging Center. The findings show that a diet-dementia association was at least partially facilitated by multi-system processes of aging.
While literature had suggested
that people who followed a healthy diet experienced a slowdown in the processes
of biological aging and were less likely to develop dementia, until now the
biological mechanism of this protection was not well understood. The results
are published in the Annals of Neurology(link is
external and opens in a new window).
“Much attention to nutrition in dementia research focuses on the way specific nutrients affect the brain” said Daniel Belsky, PhD, associate professor of Epidemiology at Columbia School of Public Health and the Columbia Aging Center, and a senior author of the study.
“We tested the hypothesis that healthy diet protects against dementia by
slowing down the body’s overall pace of biological aging.”
The researchers used data from the second generation of the Framingham Heart Study, the Offspring Cohort. Originating in 1971, participants in the latter were 60 years of age or older, were free of dementia, and also had available dietary, epigenetic, and follow-up data.
The
Offspring Cohort were followed-up at nine examinations, approximately every 4
to 7 years. At each follow-up visit, data collection included a physical
examination, lifestyle-related questionnaires, blood sampling, and, starting in
1991, neurocognitive testing.
Of 1,644 participants included in the analyses, 140 of
the participants developed dementia. To measure the pace of aging, the
researchers used an epigenetic clock called DunedinPACE developed by Belsky and
colleagues at Duke University and the University of Otago. The clock measures
how fast a person’s body is deteriorating as they grow older, “like a
speedometer for the biological processes of aging”, explained Belsky.
“We have some strong evidence that a healthy diet can
protect against dementia,” said Yian Gu, PhD, associate professor of
Neurological Sciences at Columbia University Irving Medical Center and
head of the Mailman School Neuroepidemiology Unit, and the other
senior author of the study, “But the mechanism of this protection is not well
understood.” Past research linked both diet and dementia risk to an accelerated
pace of biological aging.
“Testing the hypothesis that multi-system biological aging is a mechanism of underlying diet-dementia associations was the logical next step,” explained Belsky.
The research determined that higher adherence to
the Mediterranean-Dash Intervention for Neurodegenerative Delay diet (MIND)
slowed the pace of aging as measured by DunedinPACE and reduced risks for
dementia and mortality. Furthermore, slower DunedinPACE accounted for 27
percent of the diet-dementia association and 57 percent of the diet-mortality association.
“Our findings suggest that slower pace of aging mediates part of the relationship of healthy diet with reduced dementia risk, and therefore, monitoring pace of aging may inform dementia prevention,” said first author Aline Thomas, PhD, a postdoc at the Columbia Department of Neurology and Taub Institute for Research on Alzheimer's Disease and the Aging Brain(link is external and opens in a new window).
“However, a portion of the diet-dementia association remains unexplained,
therefore we believe that continued investigation of brain-specific mechanisms
in well-designed mediation studies is warranted.”
“We suggest that additional observational studies be
conducted to investigate direct associations of nutrients with brain aging, and
if our observations are also confirmed in more diverse populations, monitoring
biological aging, may indeed, inform dementia prevention,” noted Belsky.
Co-authors are Calen Ryan and Jiayi Zhou, Columbia Aging
Center; and Avshalom Caspi, Terrie Moffitt, and Karen Sugden, Duke University.
The study was supported by the National Institute on
Aging grants R01AG061378, R01AG073402, R01AG059013, R01AG061008, R01AG073207
and R01AG049789.
