Medical Science is Sometimes Wrong – And Diabetes is a Clear Case
Every medical practitioner hopes for the best outcome in those they treat. However, sometimes, unexpectedly severe side effects or, worse, resistance to the prescribed medication, complicates the treatment of a disease or condition.
For example, when penicillin was discovered, it saved a lot of limbs and lives by killing bacteria that entered wounds in unsanitary conditions such as in a war zone. At that time, it was believed that all bacterial infections could be controlled in this fashion. Unfortunately, it was discovered that while some bacteria did respond to penicillin, others became resistant to it. These bacteria develop resistance by modifying the insulin-binding protein on their surface, thus denying penicillin’s ability to attach to the bacterial wall. Doctors were thus forced to use a different antibiotic rather than administer more penicillin.
Similarly, when it was found that leukemia cells can become resistant to a chemotherapeutic agent by changing the configuration of the receptor the agent was supposed to be attached to, oncologists found out that increasing the dose of the agent only caused more side effects and was not much help to the patient.
Given the above, I believe that it is legitimate to ask a related question about resistance. Why are we treating patients diagnosed with Type 2 diabetes with drugs that force the pancreas to produce more insulin, or inject insulin into the body if the purported cause of the diabetes is insulin resistance?
After insulin was discovered, it did not take long to establish the benefit of injecting it into children who had elevated blood sugar; it normalized the blood sugar and prevented the consequences of Type 1 diabetes. The quality of their life improved along with the length of their lifespan. Type 1 diabetes was thus accepted by everyone as a hormonal disease and endocrinologists assumed the role of being the physicians responsible for treating the condition.
When adults showed elevated blood sugar, it was therefore natural to consider this, too, as a hormonal disease, similar to Type 1 diabetes. However, when it was detected that at the time of diagnosis, adults with high blood sugar also had normally functioning insulin in their blood, the diagnosis did not make sense. Rather, doctors needed a mechanism to explain the cause of what was then called “adult-onset” diabetes.
Roughly 80 years ago, they developed the hypothesis of insulin resistance—specifically that liver cells, muscle cells, and fat cells—only three out of about 200 types of body cells—somehow become insulin resistant. The theory became an immediate hit with endocrinologists, who became forceful proponents of the idea, so much so, that nobody dared to ask for validation of the concept. No one could identify the mechanism by which only these three types of cells in the body developed this defect to respond to insulin. Once the concept was incorporated into medical textbooks, despite the lack of proof, it became unquestionable.
Why the Insulin Resistance Theory is Actually Questionable
I started looking at the theory of insulin resistance after coming in contact with Type 2 diabetic patients who suffered leg amputation, heart attack, kidney damage, and vision difficulties—even after being treated with insulin injections. The more I investigated this, the more I disagreed with the logic of insulin resistance as a causative factor of Type 2 diabetes. If they were being treated with insulin, why did they suffer from all the side effects and consequences of diabetes? I present my reasoning below and you can judge for yourself.
1. No loss of the body’s ability to regulate heat
If the millions of cells in the body are resistant to insulin, particularly in our muscle tissue, we would expect the body to have great difficulty regulating its consistent internal temperature, 98.6 degrees Fahrenheit. The heat released from each cell during metabolic activity contributes to maintaining your body’s core temperature, with skeletal muscles contributing a significant share.
2. No loss of muscle strength
If insulin resistance prevented muscles from using their normal amount of glucose, we would expect to see evidence of a weakening of muscle function. However, diabetes does not prevent people from running, jumping, lifting heavy boxes, dancing, skiing, or walking.
3. No loss of triglyceride production in the liver
If the liver becomes resistant to insulin, we would expect that triglyceride formation in the liver should be correspondingly reduced. Yet the level of circulating triglycerides is higher than normal when a Type 2 diabetic person exhibits an elevated glucose level in the blood.
4. No finding of any agents that block insulin
With many diseases, an agent such as an antibody is sometimes found to block the utilization of molecules in cells. Yet no one has discovered or demonstrated an agent that blocks the binding of insulin with the insulin receptor on cells at the time Type 2 diabetes is diagnosed.
5. No proof that changes in cells cause a failure to recognize the presence of insulin
Some might suggest that resistance to insulin could occur because the cells that should respond to the presence of insulin outside them do not do so. However, here again there is no evidence of fluctuations in the number of insulin receptors or a lower level of function in the insulin-resistant organs corresponding to the fluctuating levels of insulin.
6. No other cells of the body appear to develop insulin resistance
It is known that every type of body cell needs glucose to function and that some cells vary in the type of specialized glucose “transport modules” within them that carry glucose from outside the cell to its interior. One could say that insulin resistance is due to the differences in the glucose transporters among muscle, fat, and liver cells and their sensitivity to insulin. However, this has never been shown and is frankly quite illogical.
In short, it is time to admit that medical science is wrong about insulin resistance to explain Type 2 diabetes. We need a different logic if we are to prevent Type 2 diabetes from expanding in populations around the world, and help millions of current diabetics reverse their high blood sugar.
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