This article outline a previously undescribed mechanism for understanding the molecular relationships between the hypothalamus and high-fat diets. Do they also hint at the creation of a fat pill?
John J. Medina, PhD
The neuroanatomical linkage that emerges from a normal part of business experience—the reaction to success and also to failure (especially if that failure happens to someone else)—is the focus of this column.
When I was a grad student—back in the Jurassic Era of molecular manipulations—my lab mates and I were all transfixed by the notion of a new technology: knockout animals (KOAs). This was because of its promise to solve a vexing problem.
I can almost hear Albert Ellis saying “Amen” to the data I am about to share. To explain his reaction, I have to talk about war.
Overly sensitive, aversive reactions to stress seem to run in families. The literature abounds with reports of relatives in these populations predisposed to depression, anxiety, and even suicide. Some family members present with glucocorticoid levels notched abnormally high, and in curiously deregulated concentrations. Behaviorally, they seem to exist at a permanent state of high alert.
I think I am going to talk about the neurobiology of happiness in my next column. The reason has to do with the nature of our 2-month journey into the biology of eating disorders—a subject that, considering the dearth of explanatory data, is tough to write about. It’s also a bit depressing, considering how difficult it can be to treat. This is the second installment in a 2-part series that focuses on the neurobiology of restricting-type anorexia nervosa (AN).
Appetite regulation is made up of complex interlocking, incentive-driven motivational hormonal and neuronal circuitries . . . that can be pulled in many directions, especially where food is cheap and readily available.