“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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