[ExI] The Dementia Plague

Rafal Smigrodzki rafal.smigrodzki at gmail.com
Wed Oct 10 17:17:01 UTC 2012


On Tue, Oct 9, 2012 at 5:33 PM, Anders Sandberg <anders at aleph.se> wrote:

>
> It is known that some saturated fatty acids reduce cognitive performance
> somewhat, likely through effects on brain metabolism. And the brain is a
> massive energy user in the body. So a link between disturbances in energy
> allocation and bad things happening in the brain is not too far fetched.
> These studies reinforce it. But I don't think they provide much evidence for
> us to change diet because we fear AD: rather, we should eat healthy because
> we should fear *all* the known killers. Adding an extra is almost redundant,
> unless we figure out some metabolic tweak that forces us to make tradeoffs.
>
### You are correct. The underlying metabolic derangement responsible
for insulin resistance, whether in the brain or, in the case of type
II diabetes, in skeletal muscle, is mitochondrial suppression which
directly leads to impaired glucose utilization and low metabolic
energy supply. I think there is convincing evidence that brain
mitochondrial dysfunction is responsible for AD, and the amyloid story
is just a distraction. I have no doubts that any effective treatment
of AD will have to address, directly or indirectly, the mitochondrial
issue. However, it is not entirely clear what specific dietary
modifications could have a major effect on AD incidence. There are
studies indicating that a lifelong history of caloric overfeeding
correlates with later development of AD, just as it correlates with
diabetes and the metabolic syndrome. It probably makes sense to stay
lean, avoid high-caloric density food, eat your veggies - but then,
this is what you already hear when talking about prevention of heart
disease, diabetes and cancer.

On the other hand, there is an FDA approved dietary supplement for
treatment (not prevention) of AD, Axona (http://www.about-axona.com/)
which acts by partially circumventing the mitochondrial suppression
using ketone bodies.

Thus the mitochondrial/metabolic theory of AD generates some
nutritional advice, although of a limited kind. More importantly, it
implies that the billions of dollars spent on amyloid approaches have
been completely wasted.

Rafal



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