Title : Obesity has a protective effect?
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Obesity has a protective effect?
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Obesity is not widely regarded as a protection mechanism. Quite the opposite. Usually it is regarded as one of the causal factors of metabolic syndrome and insulin resistance. I think obesity is a disease marker, but ultimately serves to protect the body against the effects of hyperinsulinemia. I explain.
Gina Kolata, a reporter from the New York Times wrote a very interesting recent article, called ' skinny and 119 pounds, but health characteristics of obesity '. In this article, Claire Johnson, a patient with a rare case of lipodystrophy, a genetic disorder characterized by the lack of fat is described. She was thin, but always hungry and could never get fat, because fat cells lacked.
In college, Claire discovered he had a huge, fatty liver, polycystic ovaries and severely elevated triglycerides - all hallmarks of obesity. However, she was super thin. finally she was diagnosed in 1996 with lipodystrophy by Dr. Simeon Taylor, who was chief of diabetes at the National Institute of Diabetes, Digestive and Kidney Diseases. I had several other patients all with the same rare genetic syndrome. These patients had the most severe insulin resistance who had never seen, but nothing that I could see fat (subcutaneous variety). Patients also developed over time high blood pressure and type 2 diabetes, diseases usually associated with obesity.
In rodent models of lipodystrophy, researchers transplanted some fat back into fat mice. Metabolic syndrome disappeared! The fat was protective against insulin resistance, noncausal! What's going on here?
We have to understand new paradigm of resistanc insulin and to understand how insulin resistance, obesity, fatty, fatty liver and pancreas are actually all different forms of protecting our body uses. But what is the underlying disease? Hyperinsulinemia.
Dr. Roger Unger had eludicated the basic concepts of syndrome a few years ago in this article . We will take one step at a time. As I described in my book "The Code of obesity ', the basic problem is hyper-insulinemia. There are many possible causes of too-much-insulin, but one of the most important is excessive dietary intake of refined carbohydrates and especially sugar. However, this is not the only cause. 
insulin has several functions. One is to allow glucose into cells. Another it is to stop the production of glucose and burning fat in the liver (gluconeogenesis). After this stop, then glycogen in the liver and becomes excess carbohydrates and proteins in the fat through the de novo lipogenesis. insulin is a hormone, basically, the body signal to store part of the energy input food either as glycogen or fat.
When insulin falls during the fasting, the opposite occurs. the body releases some of this energy stored food to nourish the body. That's why they do not die during sleep. If food and fasting are relatively balanced, then everything works as planned.
However, if insulin becomes excessive, then the body is always trying to store glycogen and fat. Since there is much room for glycogen, which produces fat. (Note -. This is normal This process is reversed during fasting) Exports of liver this fat as triglycerides, along with very low-density lipoprotein (VLDL) to other organs, but especially fat cells called adipocytes
. Now, the adipocytes are specialized cells to store fat. Having more fat cells is not particularly dangerous. That's what he does. Besides taking up space that does not really matter. The fat cell is designed to keep the fat, so do not get sick of it. Obesity itself is not the cause of the problem. The fundamental problem occurs when fat where it is not supposed to get. 
is usually first noticed in the liver. It is not assumed that the fat stored in the liver. However, under conditions of hyperinsulinemia and excess carbohydrates, you can develop. Glucose eventually become fat and too much of it ends up in the liver instead of fat cells. Fat cells (adipocytes) are trying to protect the body by holding the fat in a safe place. Fat in fat cells is well. Fat in the liver is not.
Fat cells actually have a secondary protection mechanism. The expansion of fat cells stimulate the release of leptin, which will make us stop eating. However, over time the chronic excessive leptin release will create leptin resistance, which is what we find in common obesity.
So the liver is very, very difficult that there is nothing more authentic than fat. However, insulin is pushing very, very hard to push more fat in the liver. In the case of Claire Johnson, no adipocytes to maintain this excess fat so it must remain in the liver and other organs.So, which is a liver that can be done? Develop insulin resistance of course! The liver is screaming 'Get glucose out of here! It is killing me'. So the piles outside glucose in the blood. Insulin resistance is not a bad thing, is a protection mechanism . How is protecting us from? The name suggests. Insulin resistance develops to resist insulin. The problem is an excess of insulin.
Meanwhile, the liver is busy trying to pump as much fat as it can. It is pumping out triglycerides like his life depended on it, which it does. Therefore triglyceride levels in blood rise (a classic sign of metabolic syndrome). It is trying to relieve congested liver fat by exporting out. Muscles and fat, muscle and fat is obtained. 
The pancreas also get some fat and get fatty pancreas . As the pancreas is distended with fat, it produces less insulin. Why? Because it comes to protecting the body from the effects of too much insulin! The body knows very well the problem is too-much-insulin. Therefore the development of fatty pancreas protects us from the closure of production.
Both fatty liver create insulin resistance and fatty pancreas, creating reducing insulin levels results in the same thing. Increase blood glucose, but organ protection against this excessive insulin. This high blood glucose causes the symptoms of diabetes - excessive thirst, excessive urination and weight loss. Blood glucose exceeds the renal threshold for glucose.
The kidneys normally reabsorbed all glucose passing through. However, when the glucose level is above about 10 mmol / L, the kidney can not reabsorb all. Glucose is excreted in the urine out with plenty of water. The weight is lost in the form of large amounts of glucose urinated outside the body. Is this bad? Not good!
The problem is accurate too much glucose and too much insulin . The body has been protected by removing all excess glucose. The lower blood glucose reduces insulin, also creates and weight loss. These are all mechanisms of protection taken by the body to protect against too much insulin.
With this new understanding, we can see that obesity, insulin resistance, high triglycerides and dysfunction of beta cells are all protection mechanisms against the same problem -. HYPERINSULINEMIA 
So what happens when presented with your doctor? Ignoring hyperinsulinemia (s) decides that the problem is instead hyperglycemia so .... prescribed insulin! This destroys carefully so carefully protection mechanisms implemented by the body. Requires glucose back into the body and crams more fat in the congested, fatty liver and nausea, fatty pancreas. No more glucose is excreted out of the urine, so that instead of all stays inside the body to wreak havoc. Beautiful. Nice.
This is, incidentally, the exact protective mechanism, the class of inhibitors of SGLT-2 drugs provides. These drugs reduce the renal threshold of glucose so that you urinate outside glucose - exactly what happens during uncontrolled type 2 diabetes. What if you do not block the protective effect, but enhance it?
The study EMPA-REG it was launched last year. Using one of these new drugs reduces the risk of death by 38% and the risk of cardiovascular death by 32%. Such benefits were exactly what we were looking for. Because this drug actually gets to the root of the problem. Too much glucose and excess insulin. This lowers glucose and insulin reduces. Of course, if we do not treat type 2 diabetes at all, they probably would have had the same benefit.
There are two main problems with metabolic syndrome. Glucotoxicity and toxicity of insulin. Not good for trade increased toxicity of insulin to reduce glucose toxicity. That's what we do when we treat people with insulin or sulphonyureas. Instead, it only makes sense to reduce both glucose toxicity and toxicity of insulin. Medications such as SGLT2 inhibitors do this, but the diet is obviously the best way. Diets low in carbohydrates. Intermittent fasting.
Finally, obesity, fatty liver, and type 2 diabetes and all manifestations of metabolic syndrome are caused by the same underlying problem. NO insulin resistance. The problem is hyperinsulinemia. It is insulin, stupid!
The power to frame the problem this way is that it discloses the solution immediately. The problem is excess insulin and excess glucose? The solution is to reduce insulin and glucose bottom. How? Nothing simpler. Low-carbohydrate, high-fat diets. intermittent fasting.
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