Why You Are Hungry After Losing Weight

Everyone knows it's difficult to lose weight; but it's possible. What's really difficult is keeping that weight off after you've lost it. Most people regain the weight they've lost, and then some.

Now researchers have a clue to why this is true.

A small Norwegian study of people with "severe obesity" (average 275  pounds, BMI 42.5 plus or minus 5) showed that everyone in their study was hungrier than they had been before the weight loss, which averaged 24 pounds.

The reason seemed to be that their hunger hormones were increased.

One hormone that was affected by the weight loss was ghrelin, which is produced by the stomach when it's empty and tells you it's time to eat again. After you've eaten, the levels of ghrelin decrease. One might expect that after a long time at a lower weight, the body would adapt and ghrelin levels would be reduced to normal. But this didn't happen, at least for two years.

What this means is that if you've lost weight, you can't expect things to go back to what they were like before you gained the weight. You'll always be hungrier than other people.

It's good to know this, because forewarned means forearmed. If you know ahead of time that increased hunger will be a problem, you will have time to figure out how to deal with it. If your health care people know that increased hunger will continue, they can try to help you figure out how to deal with it.

I think most overweight people think that if they could just lose weight, they'd be thin people, and they could eat like thin people. I certainly thought so when I was young and went on a diet because I weighed 105 pounds. Well, in college I had weighed 100.

I was going on a vacation in Puerto Rico and wanted to be able to eat whatever I wanted, so I lost those 5 pounds on a Weight Watchers diet, which in those days was a low-carb diet. Once in Puerto Rico, I cleaned my plate at restaurants and ate desserts and promptly regained all the weight I'd lost. Clearly I hadn't been transformed into a thin person who could eat everything in sight without gaining weight.

Again, being forewarned that your hunger will increase as you lose weight should help. If your health care people understand how difficult it is to maintain weight lost through dieting, they should be more empathetic about what you're going through and better able to help you to cope.

Many people, including me, find that low-carb diets reduce hunger, and the diet used for the weight loss was 50% carbohydrate. So this study provides no evidence about ghrelin levels if the dieters had restricted carbohydrates. Let's hope so. For me, at least, a lifetime without cookies would be better than a lifetime with hunger.

Can Viruses Produce Insulin?

Scientists at the Joslin Diabetes Center have found four viruses they say produce insulin-like proteins (viral insulin-like peptides, or VILPs)

The VILPs bound to human insulin receptors and stimulated all the signaling pathways that are stimulated by insulin.

The VILPs also bound to receptors for insulin-like growth factor 1, an insulin-like hormone that affects growth.

Mice injected with the peptides (peptides, like proteins, are chains of amino acids, but they're shorter) had lower blood glucose (BG) levels, indicating that the VILPs can have some of the actions of insulin.

So would these viruses affect BG levels under ordinary circumstances? It's known that they can infect fish and amphibians. And analyses showed that humans are exposed to these viruses in the intestine, possibly as a result of eating fish.

But do the viruses get into human cells? No one knows yet. The mice with lower BG levels were injected with the VILPs rather than getting the viruses from eating infected food.

Because this is such a new finding there's not yet much information about viral hormones that could affect humans, but because scientists think there are more than 300,000 viruses that can infect or be carried in mammals, there are certainly a lot of possibilities.

This finding has no practical application yet, but it opens up a whole new way of looking at hormones, and new approaches often lead to major breakthroughs.

Stay tuned.

Do Our Bones Control Our Weight?

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.