Why Thin People Can Become Diabetic—and it’s Not Insulin Resistance
There is a blatantly illogical explanation in medicine about Type 2 diabetes being caused by insulin resistance. On one hand, it is claimed that weight gain in the form of excess fat causes insulin resistance, and other hand, it is also claimed thin people, who by definition, do not seem to have to extra fat, can develop insulin resistance, too. In my view, this is contradictory and points to yet another reason that insulin resistance as the cause of Type 2 diabetes does not make sense.
Let me give you four reasons why it makes no sense biologically that insulin resistance occurs in both obese people and thin (lean) people and causes Type 2 diabetes:
1. In obese people, the current medical teaching is that the accumulation of excess fat causes insulin resistance as well as impairs insulin-producing cells in the pancreas. Meanwhile, to explain why thin people get diabetes, it is believed that these people suffer from a rare genetic “defect” characterized by a lack of fatty tissue. In other words, on one hand, excess fat causes insulin resistance while on the other hand insufficient fat can also cause it.
2. The amount of fat tissue a person has is actually a function of the number of fat cells and the capacity of each cell to store fat (also called triglyceride). The number of fat cells increases from childhood ending with about 50 billion in an average adult. Obese adults do not have more fat cells than they had before, but they have larger fat cells, up to 4 times the normal size, when filled to capacity with fat. When a person loses weight, the number of fat cells remain the same, but each cell loses fat. We know that obese people who lose weight can lower their blood sugar and even reverse diabetes. But this presents another paradox: Why don’t obese diabetics who supposedly had insulin resistance from too much fat become lean diabetics who supposedly have too little fat when they lose weight?
3. Fat production is strongly stimulated by insulin. Therefore, if a person has insulin resistance, we should expect them to be lean because of reduced production and storage of fat in their fat cells. Yet, the vast majority of people with type 2 diabetes, considered resistant to insulin, continue to gain weight by adding fat. Diabetes experts explain this paradox as an “adaptive” mechanism. But, what is the reason for this adaptation? At what percentage of fullness will fat cells abandon the adaptation and become fully resistant to insulin? What is the ratio of cells resistant to insulin to those not resistant, when a person experiences elevated blood sugar?
4. Although lean people have the same genes from the day they are born, the tendency to develop diabetes does not usually start until later in life. When it does happen, the sites of insulin resistance are exactly the same as in a heavy or obese person who develops type 2 diabetes. So, my question is, why is the activity of the lean person’s genes related to the development of type 2 diabetes delayed? What prompts the gene(s) to express the resistance to insulin later in life? In a lean person, how do cells in the target organs know what hormone they should become resistant to and when exactly to start and, even more importantly, change the internal programming of millions of cells from sensitivity of insulin to resistance? At present, even after eighty years of research, I might add, there is no scientific explanation for these questions.
All in all, I suggest that these contradictions, paradoxes and illogical explanations support my analysis, based on 20 years of study, that weight gain does not cause insulin resistance nor do lean people develop Type 2 diabetes because they have a genetic defect in which their lack of fat tissue also causes insulin resistance.
Rather, my theory to explain Type 2 diabetes makes far more sense. As I have explained in many prior blogs, and in my book Eat Chew Live, every person has only so much capacity for fat storage, whether you are lean, average, pregnant, or heavy. When you consume carbohydrates of any kind, and your body cannot immediately use the glucose that food produces, it gets stored in your fat cells in the form of triglycerides.
Eventually, if you continue to fill your fat cells, at some point, they can no longer store more fat. Any ongoing overconsumption of carbohydrates, especially grains and grain-based flour products, will then fill your bloodstream with fatty acids released from the triglycerides that could not be stored. Because muscle cells can burn either glucose or fatty acids, what happens at this point of overconsumption is what I call the “fatty acid burn switch.” Your muscles begin burning the fatty acids as they enter muscle cells more easily than glucose. This leaves the excess glucose in your bloodstream, hence high blood sugar and eventually Type 2 diabetes.
This same process applies to people of any build or weight, and explains why thin people can develop Type 2 diabetes as much as heavy or obese people. So, if you are thin, pay attention to your consumption of grains and grain-based products. You are not immune from developing high blood sugar or Type 2 diabetes!!!
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