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I have been conducting research on Alzheimer’s disease for over forty years; this is a devastating disease for which there is no cure and no treatment that can alter its progression. Yet its impact, its importance to society, and the likelihood of ever finding a cure will certainly become moot during the next 20 years. Why? Obesity and its consequences for the health of the world’s population will ultimately dwarf all other public health concerns, including Alzheimer’s disease.
By the year 2030, it is estimated that almost 60% of the world’s population will be overweight or severely obese. Since 1991 the obesity epidemic has been responsible for a 77% increase in death rates. Childhood obesity will double over the next 20 years. Thus, the probability of large numbers of people living long enough to develop Alzheimer’s disease will become very low. The accumulation of excess body fat will accelerate aging, and the subsequent increase in obesity-related disorders, in an ever-increasing proportion of the world’s population, particularly the children.
The effects of obesity on the brain and general health of adults has been well characterized; in contrast, the impact of obesity on brain health in childhood remains largely unknown. The problem is that the human brain develops quite rapidly during the first few years of life; in particular, the hippocampus and frontal lobes that are responsible for learning and memory and higher cognitive functions continue to grow and develop during this critical period of time. The diet and metabolic status during this time period could impact cognitive function for the remainder of the child’s life.
Many factors contribute to childhood obesity, including: genetic (and epigenetic) predisposition, a social trend towards higher caloric intake, reduced energy expenditure, and parental obesity. During intrauterine development fetal overnutrition as a consequence of maternal obesity and gestational diabetes lead to significantly higher fat mass in infants. Long term obesity leads inevitably to a constellation of metabolic disorders including glucose intolerance, dyslipidemia, high blood pressure, and elevated levels of inflammatory proteins throughout the body and brain. It’s this last factor, inflammation, which produces such negative consequences on brain function throughout life.
A few years ago it became clear that fat cells produce inflammation by releasing specialized proteins called cytokines. The more fat cells you have the more cytokines get released into your blood. I study the effects of cytokines in the brain. A few years ago I discovered that these proteins are capable of inducing shrinkage of brain regions (primarily gray matter- where the neurons live) that are used in the process of learning new things and recalling old memories. The longer the inflammation was present, the more brain shrinkage occurred.
A recent MRI study among 83 teenage females showed that weight gain was related to low gray matter volume in regions critical for the control of behavioral inhibition. This greatly increased their risk for future weight gain. Thus, the condition is self-perpetuating. The consequences of the fat deposition lead to insulin resistance and impaired cognitive ability in pre-pubertal children. During adolescence, extreme obesity underlies impairments in attention, mental flexibility, and control of punished behaviors. One recent study examined the relationships between academic performance, cognitive functioning, and BMI among 2,519 young children. BMI was inversely correlated with general mental ability even after controlling for demographics, lifestyle factors, and lipid profiles. However, BMI was not related to academic achievement.
Overall, obesity is implicated in lower performance on cognitive control tasks. As students became more obese they tended to score higher on teacher-reported externalizing behavior problems, and lower on teacher ratings of self-control. The good news is that the consequences of inflammation due to body fat are likely to develop slowly and require many years to be fully expressed. However, the sooner one loses the fat the sooner the brain can begin to recover. This risk factor is preventable!
© Gary L. Wenk, Ph.D. Author of Your Brain on Food, 2nd Edition, 2015 (Oxford University Press)
