Some recent headlines:
Before the idea of fats lurking in the dusty shadows of your floorboards (or belly button lint) goes any further, I wanted to provide a quick clarification of what is really going on. I also wanted to provide a comment from my friend and topic expert, Dr. Michael Roberts.
Most of these media headlines are in reference to a recent study that examined a number of semi-volatile chemical compounds and mixtures in indoor dust. Of particular interest, they were interested if these common chemical mixtures activated a specific receptor in the human body, the peroxisome proliferator-activated nuclear receptor or 'PPARgamma'. Why?
First, there is no doubt that such questions are important, as environmental toxins can negatively affect our health in many different ways. As a side note, I highly recommend visiting the Environmental Working Group's website to explore the potential environmental toxins in the everyday products you use, including the food you and your family eat.
More specifically here, PPARgamma2 is a receptor mostly present in adipose (fat) tissue. It regulates fat storage. In other words, when the receptor is stimulated and ‘turned on’, it triggers fat molecule (lipid) uptake out of the blood, and into fat cells to be stored. Subsequently, glucose becomes our main source of energy.
Thus, this receptor is not the issue when we eat a healthy diet and maintaining a physically active lifestyle. It is an issue when we eat a poor diet, resulting in a lot of fat molecules floating around in our blood that could be stored in fat cells – with the help of the PPARgamma2 receptor.
But still, perhaps those individuals who are classified as having excess body fat (obese) could be activating this receptor too much?
At this point, such a question is purely speculative.
What if we did not have a PPAgamma Receptor?
The speculation is heightened, knowing that humans can have a genetic polymorphism of the PPARgamma receptor (Pro12Ala). These individuals have about a 50% increased odds of being obese than those without the Pro12Ala polymorphism.3
Also, if you take a mouse, who has been specifically bred to not have the PPARgamma receptor, and overfeed it to induce obesity (hyperphagia), it does not gain as much weight as a normal mouse who is also overfed. In addition, it does not develop the same level of glucose intolerance or insulin resistance – precursors to diabetes.2
Thus, the speculation of the link between the PPARgamma2 and obesity is encouraging researchers to look into it further, and rightfully so.
Back to the Dust Study
So, what did the study find?
In short, they found that the chemical mixtures found in dust collected from different indoor areas (e.g. office, gymnastics studio, and home living areas) could activate the PPARgamma receptor during a lab experiment with purchased cell cultures1 The authors conclude, "Our results suggest that many semi-volatile compounds [present] in house dust, are possible PPARgamma agonists [i.e. initiates a chemical response]."
** NO humans or animals were used in this study, and there was NO direct test of the effect of dust on obesity.
To help clarify, I asked my long-time friend and topic expert, Dr. Michael Roberts from Auburn University, to leave us with his thoughts.
The data published by Stapleton and colleagues is indeed impressive, and it uses cutting-edge molecular biology techniques. It also goes to show that our exposure to household chemicals could be affecting various aspects of physiology.
However, I really think this study needs to be taken into context. Simply stated, it is highly unlikely that dust is not the driving force behind the obesity epidemic. Obesity is a multi-factorial disease, and there is clear-cut data showing that the main drivers are increased levels of sit-time and the over-consumption of highly processed foods.
That said, this and other studies, are beginning to emphasize that there are even more external factors (like dust, plastics and household chemicals) that are ‘mingling’ with our fat cells, and this may put many folks a little bit more behind the eight ball in their attempt to stay healthy.
- Fang, M., Webster, T. F., & Stapleton, H. M. (2015). Activation of Human Peroxisome Proliferator-Activated Nuclear Receptors (PPARγ1) by Semi-Volatile Compounds (SVOCs) and Chemical Mixtures in Indoor Dust. Environmental Science and Technology.
- Jones, J. R., Barrick, C., Kim, K. A., Lindner, J., Blondeau, B., Fujimoto, Y., ... & Magnuson, M. A. (2005). Deletion of PPARγ in adipose tissues of mice protects against high fat diet-induced obesity and insulin resistance. Proceedings of the National Academy of Sciences, 102(17), 6207-6212.
- Yao, Y. S., Li, J., Jin, Y. L., Chen, Y., & He, L. P. (2015). Association between PPAR-γ2 Pro12Ala polymorphism and obesity: a meta-analysis. Molecular biology reports, 42(6), 1029-1038.