Obesity and Some Behavioral Biology

All right, weight regulation is really damn complex.  I am going to admit that upfront.  It involves many of the things we’ve talked about on this website in reference to brains—the body, multiple brain systems, complex interactions, and so forth.  Sure, most of the research does not include much context or culture or even environmental interaction, but then again, the research is aimed at getting at some basic biology, at understanding the mechanisms and processes involved in weight regulation.

So, what do we have?  In no particular order other than my impressions from reviewing the literature, (1) the importance of body-based systems in appetite and weight regulation, (2) the usefulness of allostasis in understanding weight, energy, eating and activity regulation; (3) satiation and appetite as more important in obesity than energy balance, which generally plays a modifying role; (4) the need to consider weight gain and weight loss separately; (5) the role of physical activity might play in driving weight regulation; and (6) the considerable limitations of “will power” to affect any of the above points, due to how our brains and bodies are set up and the considerable mismatch between our western ideology of self and how we actually work.

In this post I’ll cover stuff on the first four.  See Greg’s comment on Genetics and Obesity for more on #5-Activity, and for now, I hope that the ability of cognitive control over hormone release and lower brain systems should at least be fairly obvious.  (As for getting all this done by yesterday, I had a senior colleague spring a surprise guest lecture on me—so that meant dropping lots of on-going stuff to get that ready… Excuses, excuses.) 

So, body-based systems.  Two hormones, leptin and ghrelin, play a powerful role in shaping energy regulation, eating and weight.  The trick is that leptin is released by white adipose tissue (fat) and gherlin by the stomach and intestine.  Both have direct effects in our brains, overturning our general view of the brain as a master organ.  Leptin and gherlin act in concerted fashion, like many regulatory systems in the body (e.g., sympathetic and parasympathetic peripheral nervous systems).  For example, Zigman and Elmquist (2003) (pdf) liken them to the Yin and Yang of body weight control.  They characterize leptin as “a molecular signal of energy abundance” and gherlin as “an important indicator of energy insufficiency.”  In mice, increasing circulating leptin can decrease food intake, while gherlin stimulates feeding.  However, neither has proven broadly effective as dietary drugs, because weight and energy regulation are not driven by one sole hormone except in rare genetic deficiency cases.

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