INSULIN RESISTANCE PART 5 – OBESITY

We are continuing on in our series related to insulin resistance. This week we want to discuss how insulin resistance relates to metabolic syndrome and obesity. Once again, borrowing from Dr. Ben Bikman’s work, an expert on insulin resistance, obesity (or excess fat on the body) is the metabolic consequence of insulin resistance and hyperinsulinemia.

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Hyperinsulinemia (too much insulin production) is a result of insulin resistance. If your cells cannot use insulin effectively, your blood sugar goes up. This signals your pancreas to make even more insulin to process that extra sugar. This is hyperinsulinemia.

Insulin promotes the growth of fat cells, and weight gain is a side effect. Not only does insulin promote fat cell growth, but it also blocks fat cells from sharing their fat to be used by the body. That’s a double whammy!

Giving more insulin to dysfunctional cells does not fix the problem. Rather, it makes it worse. And because insulin resistance and obesity go hand in hand, the more insulin you throw into a hyperinsulinemic person’s body, the greater fat storage you will promote.

Weight loss happens because of improved insulin sensitivity. Insulin resistance didn’t just get better because someone lost weight by eating too low-calorie. You have to target a lifestyle diet that will not increase blood sugar and insulin production if you want to improve insulin resistance and lose weight, because all calories are not created equal.

We are trying to simplify this information to make it easier to understand. There can be other reasons for weight gain and obesity, and there is a lot of debate on this topic.

Hormones are behind much of the debate, whether it is the hormone insulin or a low-functioning thyroid, etc. The bottom line is that hormones determine how your body uses the food you eat for many functions; however, no single hormone promotes fat cell growth as much as insulin.

So now that we’ve discussed how insulin and insulin resistance can cause obesity, it’s important to note that it can work both ways. Obesity is a consequence of insulin resistance, but it can also be the cause of insulin resistance. We know… It’s complicated.

For the most part, fat accumulation/fat storage happens in a couple of ways. Where it is stored on the body makes a difference. One pattern of fat storage is right beneath the skin. It is called subcutaneous fat. We primarily see this on the hips and thighs.

We store both subcutaneous and visceral fat, which is the fat inside the trunk of your body that surrounds your organs (like your heart liver, kidney and intestines). And while there are always exceptions to the rules, visceral fat promotes insulin resistance much more than subcutaneous fat.

Visceral fat leads to insulin resistance and disease. Visceral fat increases inflammation, and it causes oxidative stress.

Oxidative stress is an imbalance between free radicals and antioxidants, meaning you have too many free radicals, and not enough antioxidants. Free radicals harm your body cells and tissues, including the fats and proteins that allow them to work normally, while antioxidants protect your body from damage.

When it comes to fat accumulation, you have to look at the size of your fat cells. As fat cells increase, they become very full, so that excess fat spills over into the blood and can end up getting stored in other tissues.

Insulin then sends a very strong signal to store that fat, whether it means pulling that fat directly from the bloodstream or making new fat from glucose – meaning from a high-glycemic meal or snack.

At the same time, insulin also prevents or blocks fat from leaving the fat cell. Our fat cells can grow in two ways. We can either increase the number of them, which leaves the individual fat cells smaller, or the number of fat cells can remain the same and just grow bigger.

When a fat cell reaches its maximum size, it tries to limit its growth by becoming resistant to the demands of insulin to store more fat. However, if your fat cells remain small and just increase in number, they never get to that limit and stay insulin sensitive, allowing us to add on more weight.

If you are increasing the number of fat cells you have, this results in you able gaining more weight and having a hard time losing weight. Therefore, the size or number of your fat cells can determine how easy or difficult your weight loss becomes.

Then you add in leptin resistance, which is the hormone that tells your body to burn fat, and you have an added problem. Most obese people have a lot of leptin, because it is produced in fat cells – so excess fat should mean lots of fat burning leptin.

However, leptin is no longer effective in obesity at regulating appetite. Leptin is supposed to prevent insulin secretion and keep us thin. But just like insulin, too much leptin for too long results in your body becomes resistant. Now insulin is free to store fat without anything getting in its way – no inhibition.

It’s a vicious cycle, because the thing that increases leptin in the first place is insulin! Insulin is what stimulates leptin production in your fat tissues to start with – so once again… too much insulin (hyperinsulinemia) means too much leptin, and now you have insulin and leptin resistance, which produces weight gain.

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