The Other Causes of Obesity

The most commonly cited causes of the obesity epidemic over the last 30 years are decreases in physical activity and increased consumption of unhealthy foods: the Big Two. For these as causes, we have what can only be described as an overwhelming quantity of evidence.

However, many other causes of increased obesity have been suggested such as environmental endocrine disruptors or chronic sleep deprivation. In an editorial in the International Journal of Obesity, Keith et al. argue that for some of them the evidence is quite solid -- meriting further study and possibly public health intervention.

Their logic goes like this:

For most Additional Explanations, we offer the conclusion that a factor (e.g., X) that has contributed to the epidemic will logically follow acceptance of two propositions: (1) X has a causal influence on human adiposity and (2) during the past several decades, the frequency distribution of X has changed such that the relative frequency of values of X leading to higher adiposity levels has increased. In the absence of countervailing forces, if both propositions are true, obesity levels will increase.

Criterion (1) and (2) are the same criterion that we use to conclude that the Big Two were not only correlated with obesity but were causative of obesity. Recognizing that there is a mechanistic reason that factor X increases obesity is fundamental for distinguishing factors that are simply correlated from factors that are causative.

Their argument is that he Big Two are not the only causes for which these two criterion are satisfied, and we are giving those other factors unfair treatment.

What are the other possible factors? They review ten (although there are many more):

• Sleep debt
• Environmental endocrine disruptors
• Reduction in the variability in ambient temperature
• Decreased smoking
• Increased use of drugs that increase weight
• Changes in average age and distribution of ethnicities throughout the population
• Increased age of first childbirth
• Effects of maternal diet on the obesity of the resulting child -- Epigenetic effects
• High BMI associated with greater reproductive fitness
• Assortative mating

For all of the factors listed above, there is evidence that (1) that they are associated with increased obesity and (2) that they have increased over the last 30 years. (I am not going to go into the evidence for each; the paper is free online so you can read it if you like.)

Here is a swanky chart that they have outlining some of these factors (Click to enlarge):

(Antidepressants are one type of drug that is associated with obesity. AC = Air conditioning. PBDE is a known endocrine disruptor.)

What to make of these other factors? Here is there conclusions:

Having laid out several of these possible contributing factors, it is interesting to consider what their relative importance may be and whether there are interconnections among these putative causal variables. With respect to their relative importance, importance can be judged in multiple ways. For example, one could judge importance in terms of the amount of variance in BMI explained, the magnitude of the mean increase in BMI, a population attributable fraction or some other measure of effect. Unfortunately, we do not believe we are currently at the point where we can confidently say what the effect size metrics are for each of these putatively causal variables and therefore cannot confidently evaluate their relative importance on these metrics. Another way to consider the importance of variables is their potential modifiability. It is unlikely that anyone would suggest that we should have more people take up smoking as a way of controlling body weight. Therefore, further consideration of the effects of smoking cessation on population increases on BMI may be less important than consideration of other factors that we might be more willing or able to modify. In this regard, factors such as sleep reduction and increased use of heating and air-conditioning might be things that are easily modifiable and for which modifications in the direction that would hypothetically reduce obesity levels would also have added benefits (e.g., a more healthy and alert population and less use of fossil fuels). Thus, these types of putative contributing factors may be more important in terms of meriting more attention.

...

If the Additional Explanations we have offered are probable contributors to the epidemic as we believe, then additional research is warranted to evaluate how much they actually contribute, their mechanisms of action, their interaction effects and how they may be countermanded. Although we are not suggesting in this paper that one discount the potential effects of the Big Two, if Additional Explanations are veracious, the expectations for the likely public health impact of programs that only target the Big Two might be tempered. Public health practitioners and clinicians may need to address a broader range of influential factors to more adequately address the epidemic.

Skirting for the moment the issue of the individual veracity of any particular factor, I think this is a reasonable point of view. We want to limit obesity. We believe the Big Two play a role -- and they undoubtedly do. But if there are other things that are affecting obesity rates, we need to evaluate these effects individually and see what we can do to fix them too.

What I take away from this paper is the my one philosophical principle: The reality of a situation is always more complicated than you think.