I recently had an informal debate with someone who believes that obesity is caused simply by consuming more calories than you burn. In his mind, the obesity epidemic started because our modern processed food is too palatable, it overwhelms our hypothalamus and causes us to overeat. When I asked how that fact that dioxins – a common and ubiquitous family of environmental toxins that include PCBs in fish, beef and drinking water – cause obesity fit into his model he simply shrugged it off. His presumption is that you simply can’t equate obesity caused by dioxin consumption with “normal” obesity. This is in contrast to my thoughts that the root causes of obesity are probably universal.
A good model of obesity should be able to explain all of the different scenarios. I recently posted an article pointing out the fact that while the obesity epidemic was beginning in America, caloric consumption was much higher in Europe. The calories-in, calories out model of obesity can’t explain that. My guess is that someone in the calories-in, calories-out community would suggest that the source of my data – national agricultural economic agencies such as the American USDA – are untrustworthy, since they didn’t actually watch someone put the food into their mouth, they only tracked how much was sold. Still, it’s hard to handwave away a 500 calorie per day discrepancy between the food per person that was sold between the US and Switzerland in the decade of the 1960s, just as the obesity epidemic was accelerating in the US.
A good hypothesis of obesity should be able to answer these questions:
- Why did the obesity epidemic start in America despite the fact that more calories were consumed in European countries?
- Why did metabolic rates drop in the American South sometime before 1930? Why does everyone in the US now have metabolic rates equal to those in the American South in 1930?
- Why do starch eating cultures have such high metabolic rates?
- Why do hibernating animals consume polyunsaturated fat to help lower their metabolic rate?
- Why do obesogens such as dioxins1, tributyltin2, and BPA3 – found in plastic, the linings of canned beans and soup, etc – make us fat?
- Why is the body fat of obese humans particularly high in monounsaturated fat (MUFA)4?
- Why have the PUFA desaturases D5D and D6D been shown to have a causal role in the development of diabetes5?
- What causes the link between gut bacteria, inflammation and obesity?
- Why does leptin sensitivity fade in obesity?
In the coming series, I will look at the role of reductive stress as a unifying mechanism that can shed some light on all of these questions. In the first article, published today, I will explain what reductive stress is, what antioxidants and oxidative stress are and the relationship between them. I will look at the fundamental mechanism that controls metabolic rate and how vegetable oil undermines that, causing reductive stress in the first place. I will show that – at least in mouse models – if you eliminate reductive stress you eliminate obesity.
To my knowledge, no other model of obesity can explain such a wide ranging set of observations and facts associated with obesity. This is my attempt at a unified theory.
- 1.Chang JW, Chen HL, Su HJ, Lee CC. Abdominal Obesity and Insulin Resistance in People Exposed to Moderate-to-High Levels of Dioxin. Folli F, ed. PLoS ONE. Published online January 11, 2016:e0145818. doi:10.1371/journal.pone.0145818
- 2.Zuo Z, Chen S, Wu T, et al. Tributyltin causes obesity and hepatic steatosis in male mice. Environ Toxicol. Published online February 2011:79-85. doi:10.1002/tox.20531
- 3.Wang T, Li M, Chen B, et al. Urinary Bisphenol A (BPA) Concentration Associates with Obesity and Insulin Resistance. The Journal of Clinical Endocrinology & Metabolism. Published online February 1, 2012:E223-E227. doi:10.1210/jc.2011-1989
- 4.Scazzocchio B, Varì R, Silenzi A, et al. Dietary habits affect fatty acid composition of visceral adipose tissue in subjects with colorectal cancer or obesity. Eur J Nutr. Published online May 22, 2019:1463-1472. doi:10.1007/s00394-019-02003-7
- 5.Jäger S, Cuadrat R, Hoffmann P, Wittenbecher C, Schulze MB. Desaturase Activity and the Risk of Type 2 Diabetes and Coronary Artery Disease: A Mendelian Randomization Study. Nutrients. Published online July 28, 2020:2261. doi:10.3390/nu12082261