Home > Winter 2011-2012 Newsletter |
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Alzheimer’s Mythbusting:
Genes, Berries, and Fish Oil
Is Alzheimer’s disease
genetic?
When it comes to evaluating risk for
developing a disease, there are factors
that we can control and others with
which we are simply born. When
a family member is diagnosed with
Alzheimer’s, many people become
worried they will also inevitably
fall victim to the disease because of
their genes. Fortunately, our genes
have a much smaller role to play in
this disease than is widely assumed.
Genetic factors only play a strong
role in less than 5% of all Alzheimer’s
cases where the inheritance among
family members is extremely high.
These families suffer from “Familial”
Alzheimer’s disease and you likely
already know if you are in one of
these families because there are only
a few hundred in the world.
For the rest of us, we are at risk for
what’s called late-onset or “sporadic”
Alzheimer’s disease, where the
greatest risk factor is increasing age.
Now this does not mean that genes
and family history have absolutely
no role in sporadic Alzheimer’s, it’s
just that their contribution is much
smaller. The most commonly studied
risk gene associated with Alzheimer’s
disease is called apolipoprotein
E-e4 (APOE-e4). Individuals who
inherit a copy of APOE-e4 — you
can have zero, one, or two copies
of any gene – are at an increased
risk for developing Alzheimer’s, but
this does not necessarily mean they
will develop it. An individual can
inherit two copies of APOE-e4 and
never develop Alzheimer’s because
the gene is not deterministic; it is
only a risk factor. In the U.S., the estimated lifetime risk of developing
Alzheimer’s for a 65-year-old man
is about 9%, while it is about 17%
for a woman of that same age (the
risk is higher because women live
longer). For individuals with an
affected first-degree relative (sibling
or parent), the risk for developing
the disease is slightly higher and
it’s also slightly increased for those
with an affected second-degree
relative (e.g., grandparents). Beyond
those relationships there is not a
significantly increased risk. Thus,
as is the case with many other
late-onset disorders, an individual’s
specific lifetime risk for Alzheimer’s
is determined by a combination of
genetic and environmental factors,
not a single determinant or gene.
What this means is that even a
woman whose father has Alzheimer’s
has a greater than 80% chance of
never developing the disease. While
those odds may not sound great
to many, they are very far from a
predestined fate of Alzheimer’s.
I read blueberries will prevent
me from getting Alzheimer’s
disease, is that true?
A popular misconception about
Alzheimer’s has to do with a part
of our lives we can control — our
diets. You might have heard that
eating certain berries or fish oils will
prevent someone from developing
the disease. While it’s true many
types of berries contain antioxidants,
which are generally beneficial to
your health, they have not been
shown to prevent Alzheimer’s.
Similarly, fish contain a fatty acid
called docosahexaenoic acid (DHA)
that has been shown in some studies to improve memory and protect
against age-related ailments. This has
spurred people to start taking fish oil
pills and other related supplements
in an effort to ward off Alzheimer’s.
However, other studies and clinical
trials have been unable to confirm
the beneficial effects of fish oils,
showing no appreciable effect in
large samples of people followed
over 18 months. Importantly, eating
more berries or taking fish oil
supplements in moderation has also
not been shown to be harmful to
anyone, so the only effect that these
dietary changes may have are on
your wallet.
Whether it’s a friend giving you
advice or a story you read in the
newspaper, it is important to factcheck
information about Alzheimer’s
disease. Myths such as, “genes are
the most important factor” or
“eating berries will protect you,” are
easily dismantled with a little bit of
research.
Eric Chang, Ph.D. received his doctorate
in Neural Science from
New York University
where he studied the
neurophysiological
mechanisms of Alzheimer’s
disease. He is currently an Assistant
Investigator at the Feinstein Institute for
Medical Research, the biomedical research
branch of the North Shore-LIJ Health
System. Eric has also been an active
member of the NYC Chapter Speaker’s
Bureau since 2005. He can be reached
at: echang1@nshs.edu.
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