Obesity is in the head, apparently - neurons, leptin or supplements? Or none of the above?

How to banish “leptin resistance”

According to research by Japan’s Nagoya University, hunger is indicated by messages triggered by specific neurons found in the brain: “It is often hard to lose weight and it becomes harder with age. While it seems simple enough to eat less, signals in the brain are telling people to eat more. Modern science is starting to understand that it is, in fact, all in the head but in a very particular way.”

If I understand this right, in our brains is lodged a protein called melanocortin-4 (MC4R) receptor that is “expressed in a subset of hypothalamic neurons and genetic deficiencies in the gene that codes for it result in overeating and obesity in rodents and humans.”

So far, so heavy.

Now, this precious MC4R apparently resides in tiny hair-like protrusions from neuronal bodies that are called primary cilia. And these things – the primary cilia and the MC4R -- transfer signals that increase energy expenditure.

Here’s the important thing. They shorten with age, at least they do with the old obese rats that were the subject of the research. That means there aren’t so many of these signals being sent.

Having got that far, the researchers then shortened the MC4R-positive primary cilia in young rats, sort of turning them into older ones. What they were trying to do was see if the young rats put on weight and fat, which they did.

Now we get to leptin, which is said to be a hormone produced mainly by fat cells. As the study notes, leptin is important in regulating energy balance, body weight and metabolism, all of which obviously have a lot to do with obesity. Apparently (and I’m taking their word for it), leptin communicates the body’s energy status to the brain. If leptin levels are high, it tells the brain we need to eat more.

Actually, the term they used was “promote satiety”.

The big point is that leptin levels in obese people can be stuck on high (hence the market for leptin supplements). This is known as leptin resistance. And in a roundabout way, the shortening of the cilia we mentioned above can contribute to leptin resistance.

That’s probably as much science as readers can take but, suffice to say, the researchers may be right or wrong about all this being a cause of obesity. But even if they’re right “there is a silver lining”, according to Lifespan. And that is that “dietary restriction robustly generates short MC4R cilia in aged rats.”

In short, the assumed predisposition to obesity as we age can be reversed through “lifestyle interventions”.  

Although the research is based on rats, the professor who headed the study hopes he’s found a treatment for obesity that would come in the shape of a pill. Meantime, he says, moderate eating habits could hold at bay the deterioration of the MC4R-positive cilia and preserve the brain’s anti-obesity system for as long as possible. And that is obviously good advice.

My problem though is that the research suggests in effect that obesity in older people is a result of factors outside our control. And yet most people who do a lot of exercise, whatever their age, is assuredly not obese. You don’t need a study to prove this; it’s a matter of observation. So where’s the leptin resistance?

I’d buy a pair of running shoes before swallowing a pill. It might make you feel better too.