by John M. Poothullil
If you are a reader of this journal, you probably expect progress in every aspect of life. In science, progress comes from challenges to established beliefs and practices. For example, for centuries people believed that life, including that of humans, came into being as whole organisms, complete with organs inside pre-formed by the work of the “vital force.” This view changed after scientists saw empty spaces resembling cells in a thin slice of cork under a microscope. Of course, it is now accepted that the body is made up of individual living cells.
Scientific progress happens because we are willing to alter thinking in accord with new ideas. There is the potential for this to happen today around Type 2 diabetes, a condition with life-threatening and life-ending complications.
The current view is that “insulin resistance” causes Type 2 diabetes. In the 1930s, scientists noticed that some people developed high blood sugar, yet they had insulin in their bloodstream. Insulin is a hormone produced in the pancreas that tells cells to let glucose in so that cells can burn it for their fuel. The conundrum was that diabetic people had both plenty of insulin and high blood sugar. What could explain this? They came up with the theory of insulin resistance—that billions of cells in the liver, fat tissue, and muscle tissue are resistant to the message of insulin.
To validate a theory in science, one has to know the mechanism by which it works, and for objective validation the ability to measure it. The theory of insulin resistance fails in both of these criteria.
Even 80 years after the acceptance of the theory, there is no test to determine the mechanism of resistance in any of the above-mentioned sites. In addition, there is no test to establish the degree of insulin resistance in an individual. Results of these tests can help to decide more targeted treatment for each patient.
Yet, medical practitioners are instructed by specialists in hormonal diseases to treat Type 2 diabetes with insulin injections, or medications that make the pancreas pump out more insulin “to overcome the perceived resistance.” This is illogical because what is the value of treating insulin resistance by increasing insulin? If a patient has an infection with a strain of bacteria found to be resistant to an antibiotic, the doctor is not likely to increase the dosage of the same antibiotic.
The current management of Type 2 diabetes often leads to complacency among patients who think that keeping their blood sugar level within an acceptable range is all that is needed to “control” their high blood sugar. I have seen evidence of this in diabetic patients who inject extra units of insulin either before or after consuming a large meal, believing they are in charge because they can self-determine their dose of insulin.
What is important to know is that glucose in the blood does not disappear after an injection of insulin; it is most likely transferred to fat cells, to be stored as fat. Weight gain by those who take insulin injection attests to this. And when there is no space is available for more storage, the newly created fat stays in the blood with the potential to stick to the walls of blood vessels, creating complications from the blockage of blood flow to many areas in the body.
The irony of the current medical management of Type 2 diabetes is that even those who diligently maintain their three-month blood sugar level (the A1c test) within normal limits with insulin injections develop complications, such as nerve damage, heart attack, stroke, the need to amputate limbs, blindness, kidney failure, and impotence in men.
Preventing and Reversing Diabetes – Two Theories
The only way we can stop the march of Type 2 diabetes is through prevention. Endocrinologists, diabetes researchers, and medical policy makers all tell us that food intake and lack of exercise among people around the world leads to weight gain, which creates this “insulin resistance.” However, it is clear that the medical profession is failing to stop the march of diabetes, as it is spreading like a pandemic around the world, even though it is not a communicable disease.
In the US, 1 in 4 adults over 65 is fully diabetic and1 in 3 over age 20 has high blood sugar (called prediabetic). Diabetes is spreading at growing rates throughout India, Europe, Australia, China, and South America. Children are now being diagnosed with Type 2 diabetes. One in 10 pregnant women in the US develops “gestational diabetes.” It is obvious that if urgent action is not taken soon, the health care systems in many countries including the US may not have the financial and personal resources to take care of the tens of millions of people with Type 2 diabetes and its complications.
My position is that it is not logical to believe that only some humans are evolving into being insulin resistant. More importantly, the theory of insulin resistance has many inconsistencies. Why are only three types of cells, as stated above, resistant to insulin? How can cells decide to resist a natural body hormone while not resisting others? Why do pregnant women develop it within weeks, and why does it disappear within days after giving birth? If diabetic adults are not able to burn glucose because they are insulin resistant, how do they manage to walk, run, dance, jump and swim?
I have been researching the issues of hunger, satiation, and the cause of diabetes for nearly 30 years. In my view, no one has bothered to look at the problem of high blood sugar in another way: is it possible that high blood sugar happens because cells do not need glucose, even in the presence of insulin?
Framing the issue this way led me to investigate why cells might not need the glucose entering the bloodstream from foods we eat. Let me give the following explanation, and you will see that there is a very sound explanation for high blood sugar that has nothing to do with insulin resistance.
The complex carbohydrates we eat—including grains, legumes, fruits and vegetables—break down in the process of digestion into molecules of simple sugars, mostly glucose. The liver sends glucose out into the bloodstream for cells to burn, and it stores 120 grams of glucose for use when the body has used up its inventory of glucose.
After a meal, any glucose in excess of what the liver can store is converted to fat and sent out to be stored in your fat cells. But if you overconsume carbohydrates at every meal and between meals, it is very likely that you are absorbing excess glucose that gets stored in your fat cells. So eating bread, pizza, rice, corn, cakes, pastries, rolls, and many products made with grain flours is very likely to overload your liver with glucose that must be converted to fat.
Your cells are like hybrid engines that can burn either glucose or fatty acids to fuel their energy needs. Generally, glucose is utilized first, but when fatty acids are readily available, they can also be used for energy. The question is, what triggers your cells to switch to burning fatty acids rather than glucose, and isn’t this the clue to explaining high blood sugar?
How the Switch to Burning Fatty Acids Explains High Blood Sugar
I suggest that what is actually happening is that when your fat cells become full, due to the overconsumption of grains, they cannot accommodate any more of the fatty acid molecules. Instead, these are swept into the bloodstream. It is this abundance of fatty acids in your blood that triggers muscle cells to begin burning fatty acids rather than glucose
As your blood sugar level keeps climbing because of the lack of storage capacity for fatty acids, the control centers in the brain must decide whether to continue releasing more and more insulin to reduce the blood glucose level, or to tolerate a higher circulating level of glucose in the presence of excess fatty acids.
The brain decides that the first choice, releasing more insulin, can damage the functionality of the pancreas over the long-term, and so it is better to allow the excess glucose. This decision makes sense because the body can deal with excess glucose by getting rid of it through the kidney and urination once the level reaches above 180mg/dl.
Meanwhile, to reduce the high level of circulating fat and fatty acids in the blood, the control centers in the brain release growth hormone to instruct muscles to change their fuel preference from glucose to fatty acids. Growth hormone stimulates muscle to burn fatty acids at a very high rate for fuel instead of glucose. This is the only way to eliminate fat and fatty acids because they cannot be removed from the blood as it passes through the kidneys because fatty acids are not water soluble.
Furthermore, the liver also facilitates the switch to burning fatty acids. When fatty acid levels in the blood are high, the liver degrades large amounts of them into smaller molecules called acetyl coenzyme A. These molecules do not need a hormone like insulin outside cell walls to facilitate their entry inside, to be burned to produce energy. Muscles thus need less glucose for energy production and accept less of it from the blood, leaving glucose in the bloodstream.
The fatty acid burn switch is a normal metabolic response in the body when there is a high level of glucose. The problem is, if this “fatty acid burn switch” happens over a long period of time, an individual ends up with constant high blood sugar, and this leads to diabetes and the complications it causes.
The implications of this theory are far more conclusive about how to prevent diabetes than the insulin resistance theory. Rather than treating patients with medications to force the pancreas to pump out more insulin, or having patients inject insulin for the rest of their lives, we need to teach people to alter their diets to avoid grains that fill their fat cells and trigger the fatty acid burn switch. Grains and grain flour products are the biggest culprit in diabetes, as they produce the largest amount of glucose in the body that cannot be utilized immediately. This leads to fat storage, weight gain, and an excess of fatty acids in the bloodstream that the brain decides to burn rather than glucose.
If you have diabetes, have been gaining weight, or are finding yourself unable to control your eating, I hope you will change your thinking and choose to alter your eating habits regarding grain and grain flour products. My theory about Type 2 diabetes, fully explained in my book Eat Chew Live, can save millions of lives, perhaps yours and your loved ones.
About the author:
John M. Poothullil, MD, FRCP, is the author of Eat, Chew, Live: 4 Revolutionary Ideas to Prevent Diabetes, Lose Weight and Enjoy Food, which presents a radical new approach to diabetes and offers insights and guidance to help you prevent or reverse Type 2 diabetes.