- Developing obesity results in changes to the brain involving its system for telling a person when they have had enough to eat, a new study finds.
- The study also suggests that such changes may be permanent, perhaps explaining why it is difficult for so many people to keep weight off.
- The study adds new insights to investigating a complicated topic that requires much more research to understand fully.
A new study suggests that obesity causes permanent changes in the brain that prevent it from telling a person when to stop consuming fats and, to a lesser degree, sugar. It may provide an explanation for why weight loss is so difficult to maintain.
In people with obesity, the striatum, the brain region associated with food acquisition, continues to seek food even after the consumption of lipids or fats. The brain also fails to promote a sense of satisfaction by releasing the hormone dopamine.
In lean participants, the delivery of lipids or fats to the digestive system quietened activity in the striatum as dopamine release provided a sense of reward that conveyed satisfaction.
As a follow-up, study participants with obesity were made to lose weight over a period of three months for subsequent testing of the effect on brain response to food intake.
Keeping weight off, even after losing a substantial amount, is notoriously difficult. A 2018 study found that people who lost a significant amount of weight gained about half of it back after two years. By five years, they had regained about 80% of it.
It is possible to keep weight off, but this requires fundamental lifestyle changes, and the new study suggests the brain’s satiety system may not be an ally in this endeavor.
The study is published in
Previous research in animals has found that a high intake of fats disrupts the brain’s nutrient sensing, and the new study sought to test this in humans.
The researchers worked with lean people and people with obesity to observe differences in the brain’s response to lipids, fats, and glucose delivered directly to participants’ stomachs to eliminate the potential influence of flavor and appearance in the brain’s response.
During the 30 minutes following delivery of the nutrients, functional magnetic resonance imaging (fMRI) scans revealed activity in the nucleus accumbens, caudate nucleus, and putamen subregions of the participants’ striatum.
“We were specifically interested in this region as it has been proposed to function as a post-ingestive caloric sensor and to play an important role in the adaptation of feeding behavior to changes in the caloric value of energy intake,” write the authors.
To measure dopamine release, the researchers used single-photon emission computed tomography during the same time post-nutrient period.
In lean participants, neuronal activity in the striatum reduced after delivery of the nutrients, and dopamine levels increased, indicating a sense of reward. However, the striatum remained active in people with obesity, and for
“We concluded that our findings were compatible with a miscommunication between the gastrointestinal tract and the brain.”
– Dr. Mireille Serlie, corresponding author of the study
The same striatum response was observed with glucose, although the brain did increase dopamine levels with sugar. This aligns with previous research by the authors.
“We earlier showed that two years after bariatric surgery, there is a change in the dopamine system in humans,” said Dr. Serlie.
Dr. Stephanie Borgland, who was not involved in the study, expressed concern that the phrase “severely impaired” in the study’s title – “Brain responses to nutrients are severely impaired and not reversed by weight loss in humans with obesity: a randomized crossover study” — may overstate its findings.
While Dr. Borgland found the study “interestingly designed,” she expressed a desire for more extensive statistical comparisons between lean participants, people with obesity, and those who had lost weight during the follow-up period.
Dr. Borgland thus agreed with one of the study’s stated limitations: “The authors acknowledge that the study is underpowered (not a large enough sample of people) to compare differences between groups.”
The study also does not address differences between lean participants and those who lost weight after three months, raising a few questions. To begin with, the 10% weight loss meant that the latter still qualified as obese.
“It is possible that there were still metabolic differences between lean and post-diet obese subjects contributing to the neural activity effects,” pointed out Dr. Borgland.
“Alternatively, the rapid weight loss may have had its own effects [on] neural circuit function that may have offset changes in the mesolimbic system,” she added.
One tentative assumption the study makes is that the changes to the brain’s satiety system occur as a result of obesity, rather than being a cause of it.
“At this moment, we do not know what the underlying cause of our findings is,” said Dr. Serlie. “Based on other studies, we hypothesize that this is acquired during the course of weight gain or unhealthy eating behavior.” She explained that animal research suggests this scenario.
“But exactly when and how is an important unanswered question,” added Dr. Serlie.
According to Dr. Borgland, “It is quite possible that there are innate differences in reward system function that changes eating behavior leading to obesity. There are also noted changes in brain function due to dietary type and metabolic disorder that could also influence neural activity.”
The authors of the study warn that their findings should be treated with caution. “Obesity is a complex disease and many factors play a role in weight gain, weight loss, and weight maintenance,” said Dr. Serlie.
“Our findings contribute to the understanding of [the] regulation of food intake and the role of the brain in obesity, but many more studies are needed to really understand the biology of eating behavior and where it goes wrong in obesity,”
– Dr. Serlie
Along these lines, Dr. Borgland pointed out:
“Overeating is the primary driver of obesity. However, there are several genetic associations with obesity that would predispose one to obesity even though they don’t eat that much more than a ‘lean’ person would,” she added.
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