“Obesity in Remission” is a new lexeme in my vocabulary. I discovered it in this long and provocative (for me) comment in Lancet Diabetes and Endocrinology published online (login req’d). A link to the Lancet summary and to the full text of the comment was provided by this Medscape Medical News piece. Why it was provocative for me will be the subject of Part 2 of this series. This post is a long excerpt from the beginning of the comment to explain in context “Obesity in Remission.”
“Many clinicians are not adequately aware of the reasons that individuals with obesity struggle to achieve and maintain weight loss,1 and this poor awareness precludes the provision of effective intervention.2 Irrespective of starting weight, caloric restriction triggers several biological adaptations designed to prevent starvation.3 These adaptations might be potent enough to undermine the long-term effectiveness of lifestyle modification in most individuals with obesity, particularly in an environment that promotes energy overconsumption. However, they are not the only biological pressures that must be overcome for successful treatment. Additional biological adaptations occur with the development of obesity and these function to preserve, or even increase, an individual's highest sustained lifetime bodyweight. For example, preadipocyte proliferation occurs, increasing fat storage capacity. In addition, habituation to rewarding neural dopamine signaling develops with the chronic overconsumption of palatable foods, leading to a perceived reward deficit and compensatory increases in consumption.4 Importantly, these latter adaptations are not typically observed in individuals who are overweight, but occur only after obesity has been maintained for some time.3 Thus, improved lifestyle choices might be sufficient for lasting reductions in bodyweight prior to sustained obesity. Once obesity is established, however, bodyweight seems to become biologically stamped in and defended. Therefore, the mere recommendation to avoid calorically dense foods might be no more effective for the typical patient seeking weight reduction than would be a recommendation to avoid sharp objects for someone bleeding profusely.
“Evidence suggests that these biological adaptations often persist indefinitely, even when a person re-attains a healthy BMI via behaviourally induced weight loss.3 Further evidence indicates that biological pressure to restore bodyweight to the highest-sustained lifetime level gets stronger as weight loss increases.5 Thus, we suggest that few individuals ever truly recover from obesity; individuals who formerly had obesity but are able to re-attain a healthy bodyweight via diet and exercise still have ‘obesity in remission’ and are biologically very different from individuals of the same age, sex, and bodyweight who never had obesity.3, 5 For most individuals, these biological adaptations need to be addressed for weight loss to be sustained long-term. We believe these mechanisms largely explain the poor long-term success rates of lifestyle modification, and obligate clinicians to go beyond mere recommendations to eat less and move more.”
“Individuals who formerly had obesity but are able to re-attain a healthy bodyweight via diet and exercise still have ‘obesity in remission’ and are biologically very different from individuals of the same age, sex, and bodyweight who never had obesity.” Boy, who among us (overweight and obese) cannot relate to this statement? The authors of this “comment” in Lancet, who are all recognized, distinguished authorities in Obesity, have explained in understandable terms the dilemma that so many of us have experienced. I commend them for their efforts to share their understanding with other clinicians, urging that they should “go beyond mere recommendations to eat less and move more. For this: “Bravo,” as far as it goes.These distinguished experts in obesity have described how “these mechanisms,” specifically “these biological adaptations,” “need to be addressed for weight loss to be sustained long-term.” I love that it that they think it should “obligate clinicians” to go further, and I look for them to explain how. My hopes soar with phrases like “promotes energy overconsumption” and “increases fat storage capacity” that suggest they might know the mechanism, but then they associate “avoiding calorically dense food” with a means of “seeking weight reduction.” Alas, my hopes are dashed. See Part 2 next to see how they did it.
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