Today’s post comes courtesy of my friend and frequent collaborator Dr Jean-Philippe Chaput. It is a Letter to the Editor that was written by Dr Chaput along with Angelo Tremblay and Eric Doucet in response to a recent paper in the Journal of the American Medical Association.
In the new paper, Katherine Flegal and colleagues perform a systematic review and meta analysis of the available evidence linking body mass index (BMI) with mortality. They included 97 studies, with a combined sample of 2.88 million people. Here is what they found (my emphasis):
Relative to normal weight, both obesity (all grades) and grades 2 and 3 obesity were associated with significantly higher all-cause mortality. Grade 1 obesity [BMI of 30-34.9] overall was not associated with higher mortality, and overweight was associated with significantly lower all-cause mortality. The use of predefined standard BMI groupings can facilitate between-study comparisons.
Not surprisingly, the paper has generated a lot of discussion, most notably from Harvard epidemiologist Walter Willett who claimed that “Stated politely, the paper is a pile of rubbish“. Drs Chaput and colleagues wrote a letter in response to this paper, which unfortunately was not accepted for publication by JAMA. But he has graciously allowed me to post it below, and given the amount of discussion on Peter’s previous post explaining why BMI is a poor measure of your health, I think it will be of interest to our readers. I have bolded some sections to emphasize the key arguments. Enjoy!
The results recently reported by Flegal and colleagues1 about reduced all-cause mortality in overweight individuals compared with normal weight individuals seem counterintuitive but are concordant with what would be predicted by normal human physiology. The research on adipose tissue over the last decades has indeed emphasized that the role of fat cells in biological regulation goes much beyond the storage of excess energy/lipid. A gain of 5 to 10 kg of body fat has numerous biological effects which seem to a priori promote what would appear to be a series of relatively positive outcomes rather than detrimental physiological and metabolic effects.
These effects become more apparent when overweight and class 1 obese individuals are subjected to weight-reducing programs to lead to a reduction of what could be initially perceived as excessive fat storage. As recently reviewed,2,3 fat loss promotes the following adverse effects: 1) an increase in the drive to eat, 2) a greater than predicted decrease in energy expenditure being at least partly related to a release from adipose tissue of persistent organic pollutants and to a decrease in plasma leptin levels, 3) an increase in the Beck Depression Inventory score associated to hypoglycemia and reduced plasma triiodothyronin levels, and 4) an increase in a posteriori weight gain (regain) related with reduced adipose tissue lipolysis.
In our opinion, we can draw from these observations that early body fat gains that characterize an overweight status likely exert a protective homeostatic role. In fact, increased energy storage in the form of body fat may help to manage an environment that is seemingly becoming more toxic, at least as far as energy balance is concerned. An increasing number of obesogenic factors related to our modern way of life, such as demanding mental work4 and an increase in atmospheric CO2 levels5, to name a few, are being identified and characterized.
Thus, the increase in body fat characterizing overweight people is more likely to represent a normal allostatic response than a pathological process. In this context, it is not surprising to note a reduced mortality in overweight individuals. However, as for many regulatory physiological processes, fat gain cannot entirely compensate for a chronic detrimental stimulation, which is again consistent with the Flegal et al. data indicating that mortality rates are increased in grades 2 and 3 obesity. A preventive approach that attempts to reduce the obesogenic nature of our society is probably the only long-term viable solution to improve our health, even if it does not easily fit within the priorities of an economically globalized world.
Angelo Tremblay, PhD
Éric Doucet, PhD
Jean-Philippe Chaput, PhD
- Flegal KM, Kit BK, Orpana H, Graubard BI. Association of all-cause mortality with overweight and obesity using standard body mass index categories: a systematic review and meta-analysis. JAMA. 2013;309(1):71-82.
- Chaput JP, Doucet E, Tremblay A. Obesity: a disease or a biological adaptation? An update. Obes Rev. 2012;13(8):681-691.
- Tremblay A, Chaput JP. Obesity: the allostatic load of weight-loss dieting. Physiol Behav. 2012;106(1):16-21.
- Chaput JP, Drapeau V, Poirier P, Teasdale N, Tremblay A. Glycemic instability and spontaneous energy intake: association with knowledge-based work. Psychosom Med. 2008;70(7):797-804.
- Hersoug LG, Sjödin A, Astrup A. A proposed potential role for increasing atmospheric CO2 as a promoter of weight gain and obesity. Nutr Diab. 2012;2:e31.
Flegal, K. (2013). Association of All-Cause Mortality With Overweight and Obesity Using Standard Body Mass Index CategoriesA Systematic Review and Meta-analysisAll-Cause Mortality Using BMI Categories JAMA, 309 (1) DOI: 10.1001/jama.2012.113905