Could what you learned about obesity be outdated? Two competing models shed new light on how obesity develops. The traditional energy-balance model focuses on excess calorie consumption, whereas the carbohydrate-insulin model suggests that modern diets shift the body’s metabolism, promoting fat storage. Although both theories have supporting evidence, scientists think that understanding these processes is crucial for preventing obesity. New research aims to clarify these mechanisms to achieve more effective ways to prevent obesity and treat the people who have it.
What you learned about obesity in high school health class may be wrong – another theory can explain how obesity gets its start.
Leading nutritional scientists, epidemiologists and metabolism researchers gathered in Copenhagen in 2023 to define two schools of thought as to how obesity begins. One model is likely familiar from your school days, but the other could explain why reducing food intake does not have the expected effects for some people with obesity.
Understanding how the vicious cycle of obesity starts is essential as the number of people with obesity climbs around the world, says Faidon Magkos, a University of Copenhagen professor who researches how metabolism changes in obesity.
Faidon Magkos and co-authors have presented the workshop’s findings in Nature Metabolism.
“Of course, knowing how obesity is caused does not necessarily mean that you can treat the people who have it – but you can definitely prevent it among people who do not have it,” Faidon Magkos says.
The energy-balance model
Proponents of both models acknowledge that obesity is extremely complex, involving genetic and epigenetic risk factors, social patterns, psychology and access to healthy food.
“Millions of factors may contribute to obesity in modern society, but all of these factors must eventually affect either how much you eat or what your body does with the food you eat,” Faidon Magkos says.
Most people are taught that obesity originates when a person starts eating more food than they need to support their physical activity and their basal metabolic function: the energy used to keep organs running while the body is at rest.
That is called the energy-balance model. “If you pick up a textbook on nutrition, you see this idea,” Faidon Magkos says.
Fundamentally, the energy-balance model suggests that obesity results from a breakdown in communication between the brain and the body. Organs and tissues send chemical signals to the brain to report on how much energy they are using, how much energy is available, and whether they need more, which the brain translates into hunger cues. The energy-balance model posits that, in obesity, something goes wrong with either the signals sent to the brain or how the brain interprets these signals.
“Many ultraprocessed foods could circumvent the brain’s ability to integrate signals on how much energy we need and how much energy we eat,” Faidon Magkos explains. “Once this happens, you have this sort of passive overfeeding – you start eating a little bit more than what you need.”
According to the energy-balance model, whether these extra calories are “from carbohydrate, fat or protein, it does not matter which macronutrient you get it from – if you do not have anything else to do with them, you will store them, mostly as fat,” he explains.
“And as we become bigger and bigger, the amount of energy we need to sustain that greater weight also increases. So energy expenditure also increases, and then this continues on in a vicious cycle,” Faidon Magkos says.
However, some researchers are not satisfied with this predominant model of obesity.
The carbohydrate-insulin model
The second model of obesity the researchers discussed does not start with excessive eating.
Instead, the carbohydrate-insulin model posits that something about the modern diet changes how our bodies partition incoming energy – how much of the food we eat is burned as fuel and how much is stored as fat.
As an excessive percentage of energy is routed to fat storage, the brain perceives that there is insufficient circulating energy to power the body. As a result, the brain might boost hunger cues to get more energy in the system or reduce energy expenditure – both of which can worsen the imbalance between the energy burned and the energy consumed.
Instead of communication between the brain and body’s energy stores breaking down or being overwhelmed (according to the energy-balance model), the carbohydrate-insulin model posits that the body handles incoming nutrients in a way that “tricks” the brain into believing that not enough energy is available. This model points to the nutritional composition of the food we eat as instigating these metabolic changes – particularly processed carbohydrates, simple sugars or foods that spike blood glucose and insulin – could encourage tissues in the body to store rather than burn incoming nutrients.
As such, “the treatment focus under the carbohydrate-insulin model would be to avoid carbohydrate or carbohydrate with a high glycaemic index and then allow your body to kind of reset itself,” Faidon Magkos says. “This would eventually make you eat less overall.”
Which model is right?
But which of the models do scientists favour? The energy-balance model is certainly more established and can be traced back to the 1900s, Faidon Magkos says. The carbohydrate-insulin model is a relative newcomer, only formalised about 20 years ago, although foundational ideas appear in studies as early as the 1940s.
In the scientific literature, “you can find evidence supporting either model,” he adds. During the conference, researchers agreed that both models could coexist – the energy-balance model could account for some cases of obesity and the carbohydrate-insulin model could be behind others, or both could operate during different stages of obesity development for the same person.
One reason that there is no clear answer is that capturing the earliest stages of obesity to identify the instigating factor is incredibly difficult and so is measuring the very small changes in energy balance or energy deposition that occur with every meal or every day, which can lead to weight gain and obesity in the long term. Faidon Magkos says that “you can argue that eating more makes us fatter, but being fatter by definition means that we need to eat more, so this argument cannot help us to understand the cause of obesity.”
“If you take a person who has obesity right now, determining what initiated that obesity is impossible” – where that chicken-and-egg cycle began, he says.
Learning how these processes work will require high-quality, long-term dietary studies, Faidon Magkos says – and those come with a considerable price tag. “Dietary studies suffer from a lack of funding compared with studies on the pharmacological treatment of obesity,” he adds. “There’s a staggering difference between the funding provided for drug studies versus lifestyle treatments.”
Understanding how obesity starts is more about effective prevention than developing treatments for established obesity, Faidon Magkos says.
It is similar to removing the cause of cancer and not curing it, he explains. “We know that smoking causes lung cancer, but quitting cigarettes will not treat the person who has lung cancer,” Faidon Magkos says.
