It is well known that sitting for a long time is unhealthy and contributes to, among other things, the risk of obesity. But no one has explained how this happens.
An obvious explanation is that if you're sitting, you're not exercising, but studies have shown that this is not the answer. Sitting and the amount of exercise are independently associated with risk.
Now a group of researchers has come up with a new idea. They propose that our bones, specifically the osteocytes in the long bones, can sense our weight, and when the weight goes up they signal to the brain that we should eat less. They call this a gravitostat.
The researchers show that this weight control is independent of leptin, the hormone produced by fat cells that tells us to eat less when we get fat enough. People who are overweight often have what is called leptin resistance, meaning the leptin system isn't working well.
The researchers used mice and rats to demonstrate their theory, loading the animals with weights and following their effect on body weight. They found that as they added weights in capsules, the animals' body weight (obviously less the weight of the capsules) decreased steadily. And this weight loss was not due to increased energy expenditure, but to decreased food intake.
In addition to the weight loss, insulin resistance decreased.
Not long ago, scientists thought that fat was an inert substance used only for storing energy. Now they know that fat cells are actually endocrine organs that secrete hormones, for example, leptin, that affect other organs.
Then they thought bones were inert structures that mainly functioned to support our weight. Now they're finding that the bones too seem to be endocrine organs.
What's next? Fingernails?
Whatever, the concept of a gravitostat has a possible practical application, unlike so much of today's diabetes and obesity research, which is one reason I don't report on much of it. Most patients can't use information about some new transcription factor or biochemical pathway to affect their diabetes control.
But if weighting mice with capsules made them lose weight, would weighting humans with increased loads help them lose weight? Would it make your diet work better if instead of just walking, you walked while carrying a 10-or 25-pound load in a knapsack? The rodents were loaded with 15% of their initial body weight.
For a long time I've felt that when people lose a lot of weight, one reason they stall is that they're no longer moving such a big load as before. They start with muscles capable of carrying a large load, but as they lose the weight, those muscles aren't working as hard. So I thought it would make sense to add weights to the body as the weight was lost to avoid losing muscle along with the fat.
In fact, I had grandiose plans to develop weight-carrying vests to which you could add weights as you lost. If you lost significant weight, you would be amazed to find how heavy the vests had become. I planned to get rich on my scheme. Unfortunately, a little research discovered that such vests already exist, so I had to cancel my plans for a villa on the Riviera.
So using existing vests and weights, would they help humans, like the rodents, lose weight? Remember that rodent research doesn't always translate into human results.
But what's to lose other than a few bucks? Unlike experimental drugs, weights shouldn't have side effects, unless you dropped them on your toes.
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