Today's gold standard is the Roux-en-Y gastric bypass. Pioneered in 1977, the procedure creates a small pouch at the top of the stomach and reroutes the small intestine to connect to it. The bypassed section gets reconnected to the intestine, forming a 'Y' shape, so that it can still drain fluids and bacteria, reducing the risk of festering growth.
Even in the early days of gastric bypass, surgeons noticed that the operation had swift effects on metabolism: patients' blood-sugar levels normalized within a week or so. “We were surprised by the rapidity of the improvement,” read a 1987 study reporting on 397 procedures3, “even though the patients were still clearly morbidly obese.”
Patients said that they were not as hungry as before the surgery, and that they ate fewer meals and snacked less. Over time, their food preferences seemed to change, too; anecdotal reports suggested that they often chose salads over desserts and fatty foods. These shifts could not be explained by reduced stomach size alone, Cummings notes — if the reason was mechanical, patients would simply eat lots of small meals. “That got the field wondering, what's going on with hunger, here?”
In 2002, Cummings and his colleagues identified one of the first biochemical markers associated with the bypass. They had tracked blood levels of ghrelin, the 'hunger hormone' produced by cells in the gastrointestinal tract, in more than two dozen people. Normally, ghrelin levels rise sharply when the stomach is empty and then drop after a meal. Surgery suppressed these fluctuations, Cummings found4. The normal peaks and valleys of ghrelin production went pancake flat. “It's pretty dramatic,” he says.
But getting a better handle on the mechanisms required an animal model. Lee Kaplan, director of the Massachusetts General Hospital Weight Center in Boston, looked to rats — a daunting task given their tiny innards. He recruited a young surgeon from Greece, Nicholas Stylopoulos, and the duo, along with a few other research groups, began to publish papers on what happened to the animals after surgery. The research has shown that just like in people, bypass surgery stabilizes glucose levels5, boosts metabolism6 and steers the animals to choose low-fat over high-fat meals7.
Today's gold standard is the Roux-en-Y gastric bypass. Pioneered in 1977, the procedure creates a small pouch at the top of the stomach and reroutes the small intestine to connect to it. The bypassed section gets reconnected to the intestine, forming a 'Y' shape, so that it can still drain fluids and bacteria, reducing the risk of festering growth.
Even in the early days of gastric bypass, surgeons noticed that the operation had swift effects on metabolism: patients' blood-sugar levels normalized within a week or so. “We were surprised by the rapidity of the improvement,” read a 1987 study reporting on 397 procedures3, “even though the patients were still clearly morbidly obese.”
Patients said that they were not as hungry as before the surgery, and that they ate fewer meals and snacked less. Over time, their food preferences seemed to change, too; anecdotal reports suggested that they often chose salads over desserts and fatty foods. These shifts could not be explained by reduced stomach size alone, Cummings notes — if the reason was mechanical, patients would simply eat lots of small meals. “That got the field wondering, what's going on with hunger, here?”
In 2002, Cummings and his colleagues identified one of the first biochemical markers associated with the bypass. They had tracked blood levels of ghrelin, the 'hunger hormone' produced by cells in the gastrointestinal tract, in more than two dozen people. Normally, ghrelin levels rise sharply when the stomach is empty and then drop after a meal. Surgery suppressed these fluctuations, Cummings found4. The normal peaks and valleys of ghrelin production went pancake flat. “It's pretty dramatic,” he says.
But getting a better handle on the mechanisms required an animal model. Lee Kaplan, director of the Massachusetts General Hospital Weight Center in Boston, looked to rats — a daunting task given their tiny innards. He recruited a young surgeon from Greece, Nicholas Stylopoulos, and the duo, along with a few other research groups, began to publish papers on what happened to the animals after surgery. The research has shown that just like in people, bypass surgery stabilizes glucose levels5, boosts metabolism6 and steers the animals to choose low-fat over high-fat meals7.
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