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In my opinion, a very logical theory of weight regulation is George Bray's "Nutrient Balance Hypothesis" that he refers to as a "sympathetic model of homeostasis" (1). The essence of this theory is that peptides that regulate appetite also regulate sympathetic activity (thermogenesis). Specifically, peptides that decrease appetite tend to INCREASE thermogenesis. The reverse is also true: peptides that increase appetite tend to DECREASE thermogenesis. These peptides, however, are not all cut out of the same cloth. For example: neuropeptide Y increases carbohydrate intake, galanin increases fat intake, and growth hormone-releasing hormone increases protein intake. This is also an important part of Bray theory:
Interestingly, even the TIME of day that one gets hungry is regulated by peptides. We are biochemical puppets. I suspect that some peptides have more effect on thermogenesis than appetite. Thus, whether an obese person is hyperphagic (large eater) would depend on their mix of peptide imbalances. An excess of peptides that primarily reduce thermogenesis would explain why many obese people do not have large appetites. The greater ones obesity, the greater the biochemical (peptide, enzyme, etc.) imbalances. This is true whether one is hyperphagic or not. The sum of these biochemical imbalances determines how high your set point is. My approach is to lower my set point by normalizing as many of these imbalances as possible. The closer to normal that I am able to make my biochemistry, the lower my set point becomes. |
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1.) Bray GA "The nutrient balance hypothesis: peptides, sympathetic activity, and food intake." Ann N Y Acad Sci (1993 Mar) Vol 676, Pg 223-41, PMID: 0008489134. 2-NA.) Bray GA "Barriers to the treatment of obesity" Ann Intern Med 1991, Vol 115 (2), Pg 152-3. PMID: 0001760006. 3-NA.) Dulloo AG and Stock MJ "Ephedrine in the treatment of obesity" Int J Obes Relat Metab Disord 1993, Vol 17 Suppl 1 Pg S1-2. PMID: 0008384172. 4-NA.) Pasquali, R. and Casimirri, F. "Clinical aspects of ephedrine in the treatment of obesity." Int J Obes Relat Metab Disord. 1993 Feb; 17 Suppl 1:S65-8, PMID: 0008384185. |
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Do you really think that
thermogenesis is being neglected in biomedical research? Isn't the main problem related to
our general lack of knowledge about the cause(s) of obesity? For example, although there
is strong circumstantial evidence that the brain controls body weight, we do not have a
comprehensive theory of how body weight is maintained. We need more research and
cooperation -- new information is spreading at a glacial pace throughout the scientific
and medical communities.
I agree that
the brain controls body weight. In particular, the hypothalamus seems to be the
computer-like controller of body weight. It acts to maintain ones body weight
(homeostasis) whether ones set point is 150 pounds or 350 pounds. When we diet our
biochemistry is altered in ways that increase appetite and decrease thermogenesis.
Overfeeding causes biochemical alterations that decrease appetite and increase
thermogenesis. Either way, the set point is defended. Trying to lose weight is like
playing chess against an opponent that cheats by making several moves at once.