In June, international diabetes organizations endorsed provocative new guidelines suggesting physicians should consider gastric bypass surgery for a greatly expanded number of diabetics—those with a body mass index of 30 and above as opposed to just those with a BMI of 40 or more. Research has shown that the surgery helps people lose more weight, maintain the loss longer and achieve better blood glucose levels than those who slim down by changing diet and exercise habits. Now a study in mice suggests the effectiveness of bariatric surgery may stem in part from changes it causes in the brain.
According to the study, published in the International Journal of Obesity, gastric bypass surgery causes the hyperactivation of a neural pathway that leads from stomach-sensing neurons in the brain stem to the lateral parabrachial nucleus, an area in the midbrain that receives sensory information from the body, and then to the amygdala, the brain's emotion- and fear-processing center.
The obese mice underwent so-called Roux-en-Y bypass surgery, in which surgeons detach most of the stomach, leaving only a tiny pouch connected to the small intestine. Shortly after the surgery, the mice begin to show increased activation in this neural pathway, along with reduced meal size and a preference for less fatty food. They also begin to secrete higher levels of satiety hormones. Similar behavioral and hormonal patterns are found in humans after bypass surgery, suggesting that the brain changes may also be similar—but the authors say looking at this particular circuit in humans with brain imaging is difficult because the resolution is not up to the task.
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According to senior author Hans-Rudolf Berthoud of L.S.U.'s Pennington Biomedical Research Center, the change in brain activity is probably caused by the sudden novel contact of undigested food hitting the small intestine rather than the predigested mix that usually comes from the stomach. “These patients basically have to relearn how to eat. They were used to large portions and wolfed the food down. It was pleasurable for them. But if they do that after surgery, that hurts them,” Berthoud says. The brain areas made hyperactive by the surgery probably reflect this new negative feedback, which is a powerful learning tool.
In a few weeks the pathway was no longer hyperactive in the mice, perhaps indicating that the brain recruited other processes to support reduced eating, Berthoud says. He adds that this pathway is probably only a small piece of the puzzle. Past studies suggest that bariatric surgery also affects the brain's reward system, making fatty foods less pleasurable. One question that remains is why bypass surgery does not lead to the frustratingly slow metabolism seen in people who lose large amounts of weight by drastic lifestyle changes. In a much publicized study earlier this year, researchers found that contestants on the television show The Biggest Loser still had a sluggish metabolism six years after their giant weight loss. Bariatric patients, according to similar studies, achieve a stable, normalized metabolism within a year.
Gastric bypass surgery is not without risks or side effects, of course. Yet as the studies pile up showing that weight loss from dieting is nearly impossible to maintain long term, Berthoud and other researchers hope to keep elucidating bariatric surgery's pros and cons. “This is a very complex story,” he says.
