soon after a high-carbohydrate meal. This happens because
the pancreas, the organ that secretes insulin, isn’t an
instrument of precision; it’s more like a blunt tool, meant to
help us store fat during times of plenty (when summer fruit
has ripened on trees, for example) to ensure that we survive
periods of food scarcity (during winters or droughts). It can
be particularly sloppy when tasked with carving the
“carbage” from our circulation, often dropping blood sugar
to the floor and triggering hunger, fatigue, and brain fog. At
this point in the day, we often reach for more carbs and
sugary snacks, which treat our withdrawal, tricking us into
thinking that these foods are our friends.
The problems associated with chronically elevated
insulin, however, extend far past lunchtime.
Hyperinsulinemia is now being thought of as a “unifying
theory” of chronic disease by some researchers, and its
impact on the brain is particularly worrisome.^12 This is
perhaps best illustrated by the effects of insulin on a
mysterious protein that we produce in our brains called
amyloid beta.
If this sticky protein sounds familiar, it’s because for
many decades it was thought to cause Alzheimer’s disease.
When the brains of Alzheimer’s patients were examined
upon autopsy, they were found to be riddled with plaques
composed of clumps of “misfolded” amyloid protein. The
idea that removing the plaques could cure Alzheimer’s
disease formed the basis of the so-called amyloid
hypothesis, but so far, experimental drugs that have reduced
the plaque haven’t been successful at stopping disease
progression or improving cognition. With growing suspicion