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Association of Morbid Obesity With FTO and INSIG2 Allelic Variants—Invited Critique
Edward H. Livingston, MD
Arch Surg. 2008;143(3):241.
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Obesity incidence has been rising rapidly, much too quickly to say it is caused by genetic changes. Clearly, the population's overall increased body weight from past years relates to overeating and diminished physical activity. However, a genetic overlay is likely, since not all who overeat become obese and relatively few people become morbidly obese. Morbidly obese patients undergoing bariatric surgery lose substantial amounts of weight, but despite severe restriction of food ingestion or the creation of significant nutrient malabsorption, they remain obese at their stabilized postoperative weight, their BMIs generally not falling below 35.
There is strong genetic pressure to maintain body weight. For that reason, there are very efficient systems that convert ingested nutrients into stored fat. Similarly, there are complex, redundant systems to ensure that we seek and ingest food. Unlimited food availability is a recent phenomenon, representing only a small fraction of the . . . [Full Text of this Article]
RELATED ARTICLE
Association of Morbid Obesity With FTO and INSIG2 Allelic Variants
Xin Chu, Robert Erdman, Meghan Susek, Heather Gerst, Kimberly Derr, Mouna Al-Agha, G. Craig Wood, Christina Hartman, Stephanie Yeager, Mary Ann Blosky, Wanda Krum, Walter F. Stewart, David Carey, Peter Benotti, Christopher D. Still, and Glenn S. Gerhard
Arch Surg. 2008;143(3):235-240.
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