never go on to develop Alzheimer’s disease. Weirder still, a
significant number of patients with Alzheimer’s disease do
not carry this gene variant at all. And yet, noncarriers who
develop Alzheimer’s disease ultimately display the same
reduced glucose metabolism in their brains as ApoE4
carriers, implicating impaired brain-glucose metabolism as a
possible causative factor in the disease. This paradox begs
the question: is the worrying relationship between ApoE4
and Alzheimer’s disease yet another symptom of the eating
pattern we’ve been coerced to adopt?
The ApoE4 gene is considered the “ancestral” gene,
having been in the human gene pool longer than other
variants. In populations with earlier exposure to agriculture
(i.e., access to grains and starches), the frequency of the
gene is lower, suggesting that our modern diets may have
selected against carriers of this gene.^28 Even today, when
we look to less industrialized parts of the world, the theory
holds water. Take the Yoruba people of Ibadan, Nigeria,
whose diets have not been industrialized the way ours have.
Among them, the ApoE4 gene is relatively common, and yet
has little to no association with Alzheimer’s disease when
compared to African Americans.^29 The Yoruba tend to
consume less than one-third the sugar we Americans do per
capita, and lower-glycemic-index carbohydrates in
general.^30 What does this mean for you? If you carry the
Alzheimer’s-risk gene (statistically, one in four readers of
this book will) your brain may be particularly ill suited to
the “post-agricultural” high-sugar, high-carbohydrate diet.
By the time a person is diagnosed with Alzheimer’s