In the US, the incidence of obesity (The World Health Organization defines ‘obesity’ as a body mass index (BMI) of greater than 30) has almost tripled in the last fifty years. In 1960, the percentage of the US population that was obese was 13%. By 2010, that figure was 36%. It is estimated that by 2015, there will be 700 million obese people worldwide (Drummond & Gibney, 2013; but note that the rate of increase in obesity rates is a matter of dispute—see Rokholm, Baker, & Sørensen, 2010). There is great concern over this rise in obesity rates because of the known deleterious effects of obesity on health and well being. For example, a general finding is that individuals who are obese are at a higher risk of mortality (even if their blood pressure and blood cholesterol are normal; see Kramer, Zinman, & Retnakaran, 2013).
As you read in Chapter 12 of Biopsychology, researchers have been pondering the reasons for the obesity epidemuc. The ‘big two’ used to be held up as the major reasons for the epidemic: (1) a decrease in physical activity, and (2) an increase in consumption of unhealthy foods. However there has been growing dissatisfaction with these two explanations, in large part because the evidence for their playing a significant role in the rise in obesity rates is weak (see McAllister et al., 2009). Accordingly, researchers have been looking elsewhere for explanations, and a long list has now developed of potential contributors to the epidemic. The purpose of the present post is to provide a short list of some of the more theoretically interesting alternate explanations for the obesity epidemic: non-obvious contributors to the obesity epidemic. When considering the following putative contributors, i t is important to emphasize that no single contributor is likely to account for the entirety of the obesity epidemic. Rather, it is more likely that there are many contributors that have collectively created the ‘perfect storm’ that is the obesity epidemic.
Decreases in Tobacco Smoking
The consumption of tobacco products has been in steady decline since the early 1980s (see Baum, 2009), and this decline closely aligns with the rise in obesity rates (Baum, 2009). That is, there seems to be a fairly strong inverse relationship between cigarette smoking rates and obesity rates. What remains to be seen is whether that alignment holds for different countries. That is, some countries have had declines in smoking rates much more recently: Does the rise in obesity in those countries follow a similar timeline?
Iatrogenesis means physician-induced illness. Pharmaceutical iatrogenesis, in the context of the obesity epidemic, means obesity that is caused by prescription medications. For many drugs, there has been a rise in the numbers of prescriptions since the late 1970s and early 1980s, and many of those drugs have weight gain as a common significant side effect. For example, beta blockers, which are commonly prescribed for the treatment of hypertension, have weight gain as a side effect. Some antidepressant medications (see Serretti & Mandelli, 2009), and many antipsychotic medications, also have weight gain as one of their significant side effects. What is of particular note with this theory is that the timeline for the rise of many weight-gain-inducing prescription medications closely follows the timeline for the rise in obesity rates (see McAllister et al, 2009).
Epigenetics and Transgenerational Epigenetic Effects
Cloned mice, although usually born with a normal body weight, often develop adult-onset obesity. This finding is relevant to the present discussion because the process of cloning results in epigenetic abnormalities (see McAllister et al., 2009), and thus highlights the fact that epigenetic mechanisms can have an impact on body weight.
Obesity research has actually been a major contributor to our knowledge base surrounding epigenetic mechanisms, and has been an especially rich source of information regarding transgenerational epigenetic effects (see Youngson & Morris, 2012).
Some of the data supporting the contribution of transgenerational epigenetic effects is epidemiological. For example, data from Sweden indicate that food availability in grandfathers is positively correlated with the risk of diabetes and cardiovascular disease as well as mortality in grandsons (see Karatsoreos et al., 2013).
A recent review by Karatsoreos et al. (2013) highlighted several manipulations that were associated with a transgenerational epigenetic obesity effect in rodents. For example, Karatsoreos et al. reported on the work of Jimenez-Chillaron et al. (2009), which showed that, in mice, maternal consumption of a high fat diet (from the time of preconception to the weaning period) leads to an increased body length and reduced insulin sensitivity in offspring and grand-offspring. Although this is not in itself evidence of the transmission of obesity to the grand offspring, it does highlight the fact that what an organism consumes during its lifespan can have a direct effect on the physiology of their children and grandchildren, and so on. It seems what we choose to eat has much grander implications than we once thought.
Increase in Marijuana Consumption
Now we have all heard of one side effect of marijuana consumption: the craving for high-calorie foods (the munchies). Cannabis sativa is known to increase appetite in animals (see Kirkham, 2009). Could increases in the consumption of marijuana account for the rise in obesity rates? Relating to the previous topics of epigenetics and transgenerational epigenetic effects, there is now preliminary evidence of a transgenerational epigenetic effect of THC consumption: Hurd and colleagues have provided preliminary data showing that the offspring of parents administered THC exposure (raised by drug-naive surrogate parents) were observed to have impaired motivation, increase anxiety/compulsive behaviours, and increased body weight. (see Karatsoreos et al., 2013).
Other Contributors and Some Potential Solutions
A number of other contributors have been noted besides the ones listed here. For a relatively comprehensive review, see the reviews by Zinn (2010) and McAllister et al. (2009).
For an excellent recent review article that discusses potential interventions for the obesity crisis, see the paper by Freedman (2011).
Baum, C. L. (2009). The effects of cigarette costs on BMI and obesity. Health Economics, 18, 3-19.
Drummond, E. M., & Gibney, E. R. (2013). Epigenetic regulation in obesity. Current Opinion in Clinical Nutrition and Metabolic Care, 16, 392-397.
Flegal, K. M. Kit, B. K., Orpana, H., & Graubard, B. L. (2013). Association of all-cause mortality with overweight and obesity using standard body mass index categories. JAMA, 309, 71-82.
Freedman, D. H. (2011). How to fix the obesity crisis. Scientific American, 304, 40-47.
Jimenez-Chillaron, J. C., …, Patti, M. E. (2009). Intergenerational transmission of glucose intolerance and obesity by in utero undernutrition in mice. Diabetes, 58, 460-468.
Karatsoreos, I. N., Thaler, J. P., Borgland, S. L., Champagne, F. A., Hurd, Y. L., & Hill, M. N. (2013). Food for thought: Hormonal, experiential, and neural influences on feeding and obesity. Journal of Neuroscience, 33, 17610-17616.
Kirkham, T. C. (2009). Cannabinoids and appetite: food craving and food pleasure. International Review of Psychiatry, 21, 163-171. doi: 10.1080/09540260902782810. full text
Kramer, C. K., Zinman, B., & Retnakaran, R. (2013). Are metabolically healthy overweight and obesity benign conditions? Annals of Internal Medicine, 159, 758-769. doi: 10.7326/0003-4819-159-11-201312030-00008. full text
McAllister, E. J., … Allison, D. B. (2009). Ten putative contributors to the obesity epidemic. Critical Reviews in Food and Nutrition, 49, 868-913.
Rokholm, B., Baker, J. L., & Sørensen, T. I. A. (2010). The levelling off of the obesity epidemic since the year 1999—a review of evidence and perspectives. Obesity Reviews, 11, 835-846.
Serretti, A., & Mandelli, L. (2010). Antidepressants and body weight: A comprehensive review and meta-analysis. Journal of Clinical Psychiatry, 71, 1259-1272.
Youngson, N. A., & Morris, M. J. (2012). What obesity research tells us about epigenetic mechanisms. Philosophical Transactions of the Royal Society B Biological Sciences, 20110337. http://dx.doi.org/10.1098/rstb.2011.0337
Zinn, A. R. (2010). Unconventional wisdom about the obesity epidemic. American Journal of the Medical Sciences, 340, 481-491.