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.
Leptin and gherlin affect several cell groups in the hypothalamus, and in conjunction with the release of neuropeptides, appear to have the ability to drive brain plasticity. As Kolata relates with mice models, they can drive “rewiring” of the brain, changing the way neurons are connected to one another. Leptin, for example, can affect both gene transcription and depolarization of certain neurons, while also stimulating or inhibiting the release of neuropeptides.
Given the release of hormones from bodily tissues, the integrated brain/body systems, and the direct impacts on brain function, Cummings and Overduin argue (pdf) that we can have the “gastrointestinal regulation of food intake.”
Many conceptualizations of weight regulation present it as a homeostatic system, with a preset range that people occupy. I think a better way to think about weight regulation is through allostasis, as argued by McEwen & Wingfield (2003) (pdf). Allostasis is “achieving stability through change,” a process that “supports homeostasis” while dealing with ongoing individual and environmental challenges. Allostasis posits that “set points” can change over time, often pushed by regulatory systems such as those outlined in this blog entry.
The reason that allostasis might be a better conceptual tool is because weight regulation involves energy storage, energy expenditure, and energy ingestion—a dynamic problem that has to deal with both predictable (day/night cycles) and unpredictable (a sudden drought) elements. Our body is more than a furnace in a house—we are an interactive organism.
Yet allostasis also places stress on the need to maintain homeostatic stability and on the role of regulatory systems built into the body to both deal with change in the environment and ongoing behavioral demands as well as with maintaining energy balance. Pushed in certain directions or faced with an “overload,” normally adaptive responses can play out in ways that have little genetic connection with the past.
Animal studies and the problems of weight loss followed by weight gain highlight appetite, satiation, and cravings as a crucial part of maintaining a positive energy balance, hence leading to weight gain. Leptin and gherlin stimulate feeding; the hypothalamus, which these hormones affect, is linked into mid-brain systems that can regulate eating behavior. As Morton et al. (2006) (pdf) write, “in response to reduced body fat stores, adaptive changes occur in neuronal systems governing both food-seeking behaviour (important for meal initiation) and satiety perception (important for meal termination).”
To push the concept of allostasis, Morton et al. write “The integration of long-acting homeostatic and short-acting satiety signals may therefore involve direct actions of leptin on NTS (nucleus tractus solitarius) neurons that process input from vagal afferent fibres, in addition to its effects on neurons in the hypothalamus.” Furthermore, the lateral hypothalamic areas appears to work as “an integrative node for homeostatic, satiety and reward-related inputs that collectively govern motor programs that activate feeing behaviour.” Similarly, work on the arcuate nucleus (part of the hypothalamus) point to “nonlinearity in the relationship between the regulation of ARC neurons and their effects on food intake.”
Morton et al. (2006) argue for distinguishing between weight loss and weight gain, rather than treating these as one homeostatic system. They write, “During caloric restriction, there is little question that reduced neuronal input from adiposity-related hormones activates responses (increased food intake, decreased metabolic rate) that favour recovery of lost weight.” However, the reverse position—that “increased neuronal input from these hormones protects against weight gain”—remains an open and very much debated question. And this question is central to understanding why there is “obesity pathogenesis,” large weight gain by many individuals.
As they note, “if adiposity negative-feedback signals do not normally protect against weight gain, neuronal resistance to insulin and leptin cannot cause obesity. According to this view, the growing obesity epidemic can be attributed to an inherent lack of protection against obesity-promoting environmental factors, rather than to an underlying homeostatic disorder.”
What is clear is that “maintaining reduced body weight over the long term has proven to be exceedingly difficult for most people (Dokken & Tsao 2007),” something that Kolata’s book Rethinking Thin ably demonstrates. Dokken discuss research that shows variation in how quickly people put on weight and that these same people also “defend” against losing weight by becoming more metabolically efficient and experiencing increased hunger.
I’ll wrap up with a post from Capital Health WW-MD’s Notes entitled, Is Obesity a Question of Choice? Here WW-MD summarizes much of his blog’s arguments:
1) Weight is tightly controlled and cognition-driven changes in energy intake or output are immediately countered by the body’s natural ability to restore energy stores making long-term weight-loss maintenance a life-long struggle
2) For obesity treatments to work (irrespective of whether they are behavioral, pharmacological and/or surgical) they have to be continued indefinitely to avoid relapse
3) Lack of adequate access to obesity treatments within the health care system is largely a reflection of the continuing bias that obesity is a self-inflicted condition that can be controlled by will-power alone
4) Because obesity is a remarkably heterogeneous condition, no single treatment fits all
5) The vast majority of health professionals are not trained to deal with this condition (which is why for example the University of Guelph and Humber College in Ontario have now decided to offer a course specifically for fitness professionals wishing to work in this area).
3 thoughts on “Obesity and Some Behavioral Biology”
The biological arguments concerning obesity always make me question the state of the morbidly obese. Although morbid obesity (or “clinically severe obesity”) is an arbitrary distinction, I wonder if a person of such poundage would have the same difficulties losing weight as would an obese person. It seems that in today’s society the “set points” are on a unidirectional scale, with the lone path going up the fat mountain. Leptin and gherlin are obviously powerful hormones, able to rewire the brain, with some of the problems probably arising from an increase in hormonal receptors with weight gain, resulting in a decrease in sensitivity for small amounts of the hormones. Perhaps that supposition is my single-class-of-physiology knowledge (or lack thereof) poking through, but it would help to explain part of the problems with morbid obesity…of course it’s much more complex. I was disappointed that Kolata did not address the problem of extreme obesity. Is it just a case of our biology being maladaptive to a culture of abundance? I think she says one thing about people being overweight and it merely being biology, but I am going to scratch a chalkboard next to Kolata’s ears by saying that some degree of personal accountability must persist, even in the inheritable, biological view of obesity. Maybe I am misreading the biology, but the state of allostasis seems like weight can be set at certain points of life, indicating at least some control. That control may mean fifty pounds “overweight,” but it does not have to mean three hundred pounds.