A paper published recently in Nature Metabolism presents two competing hypotheses of obesity, highlights their similarities and differences, and proposes a way forward for future research. The co-authors are sixteen researchers and clinicians well known in the field of weight loss research and who often find themselves on opposing sides of the debate about the true causes of obesity. They acknowledged in the paper that it was necessary to set aside previous biases and that moving the field forward in a way that ultimately leads to effective obesity treatments requires “keeping an open mind,” and “stepping out of one’s comfort zone.”
The competing hypotheses are the energy balance model (EBM) and the carbohydrate-insulin model (CIM). As stated in the paper, “The EBM allows for calorie-independent, macronutrient-specific effects on peripheral hormones, metabolism and substrate oxidation but posits that excess energy intake results in similar net fat deposition in adipose tissue regardless of the macronutrient composition of the diet.” In other words, people with obesity have accumulated excess fat mass because they have taken in excess energy, and the same amount of excess energy would have resulted in an equivalent increase in fat mass regardless of whether those calories came from broccoli or potato chips.
On the other hand, “According to the CIM, the primary cause of increased obesity prevalence is an alteration in fuel partitioning that favors channeling of ingested energy-yielding substrates away from pathways of oxidation toward storage in adipose and perhaps other tissues.” The CIM posits that the hormonal and metabolic effects of different macronutrients have a powerful effect on fuel partitioning such that energy is preferentially stored rather than “burned.” The biggest “culprits” in this context are refined carbohydrates, which induce a rise in insulin (and a higher-than-normal rise in those with insulin resistance), which signals fat storage rather than fat oxidation. If an individual consumes more energy than their body requires, the CIM considers this to be a secondary effect of the energy being sequestered by the hormonal milieu influenced more by the composition of the food consumed rather than the total amount.
Both models acknowledge the difficulties people face when trying to make long-lasting dietary changes in the face of hyperpalatable, inexpensive, and seemingly ubiquitous ultra-processed foods, as well as the influence of sleep patterns, physical activity, environmental factors (such as endocrine-disrupting chemicals), and psychosocial factors (e.g., education level, socioeconomic status). But the CIM posits that rather than being counseled to reduce energy intake overall, people would be better served being advised to specifically limit consumption of the high-carbohydrate foods that, via frequent and sustained rises in insulin, are leading the body to partition energy more toward storage rather than liberation and oxidation.
A fundamental difference between the models is, “according to the EBM, the ability of the brain to control food intake is overwhelmed or disrupted by the food environment, resulting in increased energy intake despite internal signals of energy sufficiency. By contrast, according to the CIM, the ability of the brain to control food intake remains intact, which is why food consumption increases and/or energy expenditure decreases in response to internal cues signaling less available energy resulting from altered fuel partitioning in the periphery.”
By the EBM, the brain’s ability to sense hunger and fullness is disrupted by the modern food environment (there’s a reason you “can’t eat just one!”), whereas the CIM suggests that the brain’s sensing mechanisms remain intact, and the reason individuals are driven to consume more energy is that, owing to fuel being partitioned toward storage, an “internal starvation” occurs under which the brain senses that there is not enough energy available, which would naturally lead someone to eat more. And this shunting of energy toward storage is not the result of excessive food intake; it results from the intake of foods that induce this shift, namely, refined carbohydrates.
As noted in the paper, the differences between these two models of obesity are more than merely semantic. They posit different causes for the accumulation of excess fat, which has implications for the most effective ways to reverse or prevent this, which in turn has implications for public policy, the food industry, and clinical practice.
To learn more about the differences between these competing models of obesity, this earlier paper is also recommended: Competing paradigms of obesity pathogenesis: energy balance versus carbohydrate-insulin models.