Opinion: our digestive system seems to be way more sophisticated than we tend to give it credit for
Our love affair with food could be just a gut feeling after all. Novel research shows that our digestive system influences our food preferences, shining a new light on the causes of obesity.
Our digestive system is more sophisticated than we give it credit for, interacting with the brain to let us know when we need food and when we are full.
It is easy to see that the amount of food we eat can condition our appetite: sensors in the stomach that detect expansion due to fullness can signal our brain to stop eating.
The type of food we eat is also important, so a meal high in calories will spend a longer time inside the stomach and the small intestine, prolonging the feeling of fullness and stopping us from eating more.
So there are ways in which food can control our brains and our digestion – and this is quite obvious in obesity, where mechanisms to stop us from eating more than we need to appear to not work properly, or to be overridden by the effects of food.
Stomach surgery – known as bariatric surgery – is currently the most effective treatment for extreme obesity.
In one type of bariatric surgery known as a gastric bypass, the size of the stomach is made smaller by reducing it to a small pouch that is then directly connected to the small bowel.
Patients that have received bariatric surgery have changed their preferences from high to low fat diets
The smaller stomach means that a small amount of food is enough to feel full, thus appeasing hunger and increasing the feeling of fullness. These were believed to be the main causes of weight loss following the surgery.
But that's not the case anymore.
In recent experiments, researchers performed a gastric bypass in rats and then let them choose between high and low fat diets.
You would think that since animals would be forced to eat a smaller amount of food, they would choose the high fat diet to obtain more calories, getting more bang for their buck.
As it turned out, the rats did exactly the opposite, consistently preferring low fat diets in spite of temptation. Animals that had not undergone surgery, however, went for the high fat diet every time.
This is not a uniquely ratty effect: patients that have received bariatric surgery have also changed their preferences from high to low fat diets, and also show reduced cravings for junk food.
This shows that the message does indeed originate in the gut
So why does this happen? Enter the humble gut.
As previously mentioned, the gut can send chemical messages to the brain, such as through a compound called oleoylethanolamide (OEA), which is produced in the gut when we eat fat and which signals the brain that we should probably stop eating soon.
The message of OEA is transmitted through the vagus nerve that travels between our digestive system and the brain, and there it increases the amount of another chemical called dopamine in a certain brain region. This gives us the feeling of fullness.
Interestingly, eating a high fat diet reduces the levels of OEA, so that the fullness signal is diminished or lost.
Analysis of the rats that had undergone gastric bypass surgery showed that the amount of OEA in their gut was increased even though the rats were eating a low fat diet.
Their brains also had increased levels of dopamine in the right regions, suggesting that the rats got plenty of fullness messages.
This means that surgery alone can cause the gut to increase the transmission of "stop eating" messages and thus get the feeling of fullness without the need for consuming highly fatty food.
The effects were lost when the vagus nerve was severed, showing that the message indeed originates in the gut.
In light of these and other results, an OEA supplement has been developed, and preliminary results in obese patients show that it can help them to lose weight while showing no apparent side effects.
It’s not just our tastes and moods – the gut itself plays an important role in these decisions
This is encouraging, but larger studies are needed to show whether treatment with OEA should become standard for obesity.
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Other studies have shown that OEA could also be used in other situations: research in animals has shown that treatment with OEA reduced symptoms associated with cocaine addiction.
It may seem strange that the same compound could affect such different processes as eating and being addicted to a drug, but food can activate reward mechanisms in our brain just as well as many drugs.
Luckily, it seems like chemicals produced in our gut can help with addictive behaviour.
It appears then that it’s not just our tastes and moods that decide what and how much we put into our bodies: the gut itself plays an important role in these decisions.
Learning more about how these gut–brain signals work could pave the way for the development of new treatments for obesity and addiction.
The views expressed here are those of the author and do not represent or reflect the views of RTÉ.
