Re: The science of obesity: what do we really know about what makes us fat? An essay by Gary Taubes
Gary Taubes views on obesity and obesity research are well known1, and he is not alone in being concerned with the quality of much of the nutritional research on noncommunicable diseases2. However, this historical essay also contains some statements that are factually incorrect. In addition, his complex theories on the causation of obesity seem to ignore much of the evidence accumulated in recent years.
The only data with which to assess the claim that “increases in calories worldwide are largely carbohydrates and those carbohydrates are largely sugars - sucrose and high fructose corn syrup” come from the Food and Agriculture Organization (these has been summarized graphically3). Food energy supply per person has indeed increased but the supply of sugars has remained stable for the last 40 years (FAO supply data substantially overestimate actual dietary intake). These data undermine one of the pillars of his hypothesis, namely that the worldwide epidemic of obesity can be attributed to increased consumption of sugars, rather than overconsumption generally.
In addition, long term controlled intervention studies, in which increased consumption of sugar-containing food or drink has been encouraged, have not shown any increase in body weight that cannot be attributed to the concomitant increase in food energy intake4.
The “energy balance” hypothesis of obesity is dismissed solely on the grounds that it has failed to lead to a universally effective treatment, disregarding the fact that no treatment can be effective unless the subject co-operates. Long term adherence to any calorie controlled diet is difficult. At the same time he supports the, now discarded, “hormonal regulatory disorder” hypothesis of obesity, offering only anecdotal evidence that it has led to any more effective treatment.
That overconsumption of food energy of any macronutrient composition leads to fat storage is well established experimentally. This observation is to be expected, since body fat is the only available repository of any size for excess food energy intake. The body has no ability to store excess energy intake as alcohol or protein, and only limited ability to store carbohydrate. If food energy intake exceeds immediate requirement, alcohol, carbohydrate and protein energy is used preferentially and fat is stored5.
Taubes hypothesis rests on two assertions and one assumption. The first assertion is that consumption of carbohydrates leads to chronically raised insulin levels. It is well established that in normal individuals this is not the case6. The second is that there is appreciable redirection of food energy from carbohydrates towards fat synthesis and consequent storage. The evidence does not support this idea. Conversion of carbohydrate to fat in the human is a minor pathway, even under conditions of substantial overfeeding of sugar to already obese subjects 7,8. Finally, the assumption is that this hypothetical redirection of carbohydrate energy into fat storage arises from overconsumption of carbohydrates while paradoxically leading to unsatisfied hunger, causing the subject to overeat. Thus he is able to argue that overconsumption is a consequence of disordered hormonal regulation rather than its cause. This is a circular argument.
What is also missing from this explanation of obesity is any indication as to why such disordered hormonal regulation should afflict some people and not others.
1. Taubes G “Why We Get Fat: And What to Do about It” Anchor Books, 2012, “The Diet Delusion” Vermillion, 2009 and “Good Calories Bad Calories. Fats, Carbs, and the Controversial Science of Diet and Health” Knopf Publishing Group, 2007.
2. Bohan Brown MM, Brown AW and Allsion DB (2012) Nutritional epidemiology in practice: learning from data or promulgating beliefs? American Journal of Clinical Nutrition. Epub ahead of print. DOI:103945/ajcn.112.052472.
4. Te Morenga L, Mallard S, Mann J. Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies. BMJ 2013; 346:e7492.
5. Shetty PS et al. (1994) Alterations in fuel selection and voluntary food intake in response to iso-energetic manipulation of glycogen stores in man. American Journal of Clinical Nutrition 60: 534-543.
6. Tabak AG et al. (2009) Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study. Lancet 373:2215-2221.
7. Hellerstein MK (2001) No common energy currency: de novo lipogenesis as the road less travelled. American Journal of Clinical Nutrition. 74: 707-708.
8. McDevitt RM et al. (2001) De Novo lipogenesis during controlled overfeeding in lean and obese women. 74: 737-746.
Competing interests: R C Cottrell is an employee of the World Sugar Research Organisation, a not for profit scientific research organisation funded by the sugar industry.