disease is riddled with these aging toxins, containing three
times the amount of AGEs as in a normal brain.^10 (Dutch
neurobiologist D. F. Swaab, in his book We Are Our Brains,
actually described the disease as a premature, accelerated,
and severe form of brain aging.) Glycation clearly plays a
role in this process, and this explains partly why elevated
blood sugar increases the risk of dementia, even among
nondiabetics.^11 But you don’t need to have dementia to
suffer the effects of AGEs on your cognition. Non-demented
adults free of type 2 diabetes with higher levels of AGEs
appeared to show an accelerated loss of cognitive function
over time, impaired learning and memory, and reduced
expression of genes that promote neuroplasticity and
longevity.^12
To get a sense of the rate at which AGEs are being
formed in your body, doctors can use a test typically used to
manage diabetes called the hemoglobin A1C, which looks at
the amount of sugar stuck to red blood cells. Blood cells are
in circulation for an average of four months, facing constant
exposure to the varying levels of sugar in your blood before
getting sent off to retirement in your spleen. The A1C
therefore paints a picture of your average blood sugar over
the last three months or so, and may be a powerful marker
of risk for cognitive decline or even diminished cognitive
performance.
In late 2015, I had the opportunity to visit Charité
Hospital in Berlin, one of Germany’s most research-
intensive medical institutions and home of a study that
examined the relationship between blood sugar and memory