Obesity and cognitive dementia are among the most serious threats to human health and well-being. Both disorders have received an enormous amount of research attention, yet their root causes remain to be elucidated. Furthermore, short of artificially imposing severe restrictions on food intake by surgically remodeling the gastrointestinal tract, there appear to be no proven effective therapies that produce sustained weight loss in people. Similarly, effectiveinterventions that prevent, reduce, or reverse the debilitating effects of AD-like dementias and other severe forms of cognitive decline are not yet available. The goal of research in the LBNH is to address these gaps in knowledge. Our work is based on a novel theoretical conceptualization which suggests that both obesity and cognitive dementia may arise from common dietary origins and brain pathologies. These pathologies result in a progressive deterioration of the ability to engage cognitive processes that contribute to the inhibitory control of intake. Interference with these processes, which appear to involve the hippocampus and its connections to other brain regions, can promote overeating of the same type of dietary factors that produced the pathologies. Our theoretical model describes how this can lead to a "vicious cycle" of excess intake, obesity, and progressive cognitive decline, which could begin early in life nd which could extend to failures in other forms of cognitive and memory functioning. By increasing understanding of how energy dysregulation and cognitive dysfunction may be interrelated in human and nonhuman animals, our research promises to yield new interventions that may more effectively treat or prevent both disorders.
Research with our collaborators at American University and at other universities is also beginning to examine the implications of our empirical findings and theoretical framework in two important domains. One goal is to identify and describe the relationships among diet, obesity, and cognitive functioning in school-age children. Similar to the population at large, the incidence of obesity has doubled in children ages 6-11 and has tripled in adolescents ages 12-19 since 1980. Although the most obvious and debilitating symptoms of cognitive dementias are manifested in old-age, there is evidence that brain pathologies underlying these disorders can begin at least 50 years earlier. Consistent with these reports are recent findings which link obesity to cognitive deficits that are revealed in childhood and that can continue to develop across the lifespan. Thus, while obesity is becoming widely recognized as a serious threat to the current and future physical health of our children, the threat posed by obesity to our children’s cognitive health will also receive our research attention.
In addition, we are also beginning to extend our conceptual framework to the problem of drug abuse and addiction. There are many behavioral and physiological parallels between excessive drug and food intake. It appears that the set of brain pathologies and cognitive/memory deficits that we have shown to be associated with overeating are also involved with drug abuse. We aim to explore these apparent interrelationships with the goals of advancing knowledge about the mechanisms that cause addictive behaviors (i.e., both drug and food “addictions”) and to identify important new targets for therapeutic interventions.