Page 33 - Summer2014

Significant epidemiological and clinical (people with one allele) have a five-fold increased Not only is
evidence has emerged that suggests AD belongs risk of developing AD, and homozygotes (two
among the “diseases of civilization,” primarily alleles) are estimated to have a staggering life- the brain as
caused by modern Western diets and lifestyles time risk between 50-90 percent. Despite this susceptible to
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at odds with human physiology. High intakes of seemingly damning genetic heritage, the ApoE4 metabolic and
refined carbohydrates and omega-6-rich poly- allele is neither required nor sufficient for devel-
unsaturated oils, low antioxidant intake, lack of opment of AD, as 50 percent of people with AD environmental
physical activity, and misguided avoidance of are not carriers, and some E4 homozygotes never insults as the
cholesterol and saturated fats combine to create a develop the disease. On the other hand, the other rest of the
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perfect storm for glycation and oxidative stress in known risk factor—hyperinsulinism—elevates
the brain, ultimately resulting in severe cognitive risk by 43 percent independently of ApoE status. body, it is
decline that renders nearly impossible the tasks As hyperinsulinemia occurs in approximately especially

involved in everyday living. 40 percent of people over age sixty, it’s not sur- vulnerable to
Our evolutionarily discordant dietary prising that it correlates with a condition that
environment has been linked to conditions as preferentially strikes the aging. 14 the detrimental
diverse as heart disease, diabetes, rheumatoid Some researchers believe the connection effects of
arthritis, polycystic ovarian syndrome (PCOS), between impaired glucose metabolism, insulin modern
and schizophrenia. Often, the brain is seen as a signaling and AD is so strong that they refer to
2,3
space unto itself, as though the blood-brain bar- AD as “type 3 diabetes.” In fact, type 2 diabe- Western diets.
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rier were an impenetrable border that spares the tes (T2D)—a condition stemming from broken
brain the deleterious effects the rest of the body glucose metabolism and insulin signaling—has
suffers as a result of a physiologically incongru- been identified as an additional risk factor for
ous diet. However, research on AD confirms that developing AD. 16,17 Moreover, the pathological
not only is the brain as susceptible to metabolic changes that occur in AD in the brain physi-
and environmental insults as the rest of the body, cally resemble those seen in the pancreas and
but due to its high energy demands, dispropor- vasculature in T2D. Type 2 diabetics who
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tionate oxygen consumption, high concentration carry ApoE4 alleles are at the greatest risk for
of oxidation-prone long-chain polyunsaturated AD, with an even more severe risk reserved for
fatty acids (PUFAs), and decreased capacity for those treated with exogenous insulin. This sug-
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regeneration, the brain is especially vulnerable gests that either T2D or related features of the
to the detrimental effects of modern Western metabolic syndrome bring about AD, or that they
diets. 2-10 are separate consequences of the same underly-
Research into AD pathology, like that of ing cause—and moreover, that insulin is a key
many of its chronic, degenerative illness coun- factor.
terparts, is riddled with uncertainty regarding That not all type 2 diabetics develop AD and
which factors are causative and which are merely not all AD patients are diabetic should disabuse
correlative. Nevertheless, up-to-date literature us of the notion that diabetes causes AD. What
points to genetic and environmental factors is more likely—and what the research seems to
that greatly increase the risk for developing this support—is that they are physiological cousins.
condition. The risk profile has a strong basis in That is, they result from the same underlying
epigenetics—the influence of diet and lifestyle metabolic imbalances, but manifest differently
on how particular genotypes are expressed. The depending on which parts of the body are af-
two most striking risk factors appear to be hy- fected.
perinsulinism and possession of one or two E4 Clinically, AD patients have decreased cog-
alleles for the apolipoprotein E gene (ApoE4), nitive function and lapses in memory that decline
which is involved in lipid processing. (See sidebar progressively and ultimately affect performance
on page 34.) of tasks involved in everyday living. Physiologi-
Possession of an E4 allele is so strongly cally, AD is characterized by several physical
correlated with AD that one study author calls it hallmarks that can be measured or observed via
the “susceptibility gene.” ApoE4 heterozygotes biopsy, positron emission tomography (PET)
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