The typical body weight that an individual maintains without conscious effort is their set point weight. Set point weights are prime examples of how the body maintains homeostatic equilibrium (i.e. maintains it’s weight despite changes in food intake and exercise). Set point weights are the reason people don’t actually weigh 4000 pounds. If we had to consciously monitor all the calories entering our bodies via food and all the calories leaving our bodies via exercise to maintain weight, then it would be perfectly conceivable, in theory, for someone to weigh up to 4000 pounds by overfeeding each day. Of course, this doesn’t happen because there are bodily systems in place that act to maintain our body weights at set point, even in obese individuals. In fact, scientists calculated that if we ate just one soda cracker too many each day, then we would gain 2 pounds per year (4 times what most individuals gain yearly) if our bodies didn’t have mechanisms for maintaining a fixed body weight, a set point weight. Naturally, the question becomes “how do we change our set point?”.

 

In one fascinating study, the authors created two groups of rats – one with lesions to the hypothalamus, effectively reducing their set point weight, and the other, with no lesions. The lesioned rats lost weight rapidly, then their weight started stabilizing around a seemingly new, lower set point. After several weeks of ad libitum feeding (i.e. ‘eat as much as you want’), some subset of both groups of rats were restricted of food for a couple weeks. This created 4 groups in total: lesion-unrestricted, lesion-restricted, non-lesion-unrestricted, non-lesion-restricted. During the food restriction period, the restricted rats lost weight compared to their unrestricted counterparts, as expected. Interestingly, the lesion-restricted rats lost the same amount of weight as the non-lesion-restricted rats. The only difference is that these two groups started at seemingly different set points before losing the weight. Furthermore, as soon as the restriction period was over, the restricted rats gained all the weight back so that they had the same weight as their unrestricted counterparts. In other words, after food restriction, the weights of the restricted rats went back to their set point. All together, the researchers were able to change the rats’ set points directly, then observe the maintenance of these set points despite changes in food intake. Although we clearly cannot go around slicing through brains to ‘cure’ obesity, this study provides some valuable insight into how and where set points are determined in brain.

So, how do we realistically change our set points? There are several potential contributing factors; the most common of which include stress management, and food and exercise quality. Notice that these are all things that that affect the body’s hormonal state. By putting the emphasis on quality, we are putting the emphasis on changing the body’s hormones in lasting ways that may contribute to ultimately changing our body’s set point weight.

The beautiful thing about the set point model, in my eyes, is twofold: it encourages a more empathetic discussion about the obese, and it makes it more probable that we actually get closer to solving the problem of obesity itself because it is a more realistic lense through which to look at the weight than simply talking about eating less and exercising more.

References

Bailor, J. (2012a). Lower your Set-Point, Kant, & Smarter Exercise. Retrieved from http://thesmarterscienceofslim.com/ep-4-how-to-lower-your-set-point-weight-pragmitism-smarter-exercise-introduction/

Bailor, J. (2012b). Your Set-Point Weight. Retrieved May 4, 2015, from http://thesmarterscienceofslim.com/your-set-point-weight/

Keesey, R. E., & Hirvonen, M. D. (1997). Body weight set-points: determination and adjustment. The Journal of Nutrition, 127, 1875S–1883S.

Weigle, D. (1990). Human Obesity Exploding the Myths. The Western Journal of Medicine, 153(4).