By Raphael Nyarkotey Obu
Root Causes of Insulin Resistance, Pre-Diabetes, Metabolic Syndrome, and Type 2 Diabetes
Type 2 diabetes involves loss of insulin and leptin sensitivity. This makes it easily preventable and nearly 100 percent reversible without drugs. One of the driving forces behind type 2 diabetes is excessive dietary fructose, which has adverse effects on all of metabolic hormones—including two key players: insulin and leptin.
There is no question in my mind that regularly consuming more than 25 grams of fructose per day will dramatically increase your risk of insulin/leptin resistance, metabolic syndrome, and chronic diseases, including obesity, type 2 diabetes, cancer, heart disease, arthritis, and Alzheimer’s. It’s important to realize that even though fructose is relatively “low glycemic” on the front end, it actually reduces the receptor’s affinity for insulin, leading to chronic insulin resistance and elevated blood sugar on the back end. So, while you may not notice a steep increase in blood sugar immediately following fructose consumption, it is likely changing your entire endocrine system’s ability to function properly behind the scenes…
Another major cause of type 2 diabetes is the consumption of the vast amount of glucose derived from the high carbohydrate diet that has been recommended for the last half century by conventional medical and media recommendations. All carbohydrates that are not fiber will be quickly metabolized into sugar, and it makes little sense to eat large amounts of sugar to keep your blood sugar lower.
The misconception of the cause of diabetes may be the biggest problem. Conventional medicine describes diabetes as a disease characterized by elevated blood sugar. This “dysregulation of blood sugar control” is typically explained as “an inability of your body to produce enough insulin.” To control diabetes with that view, it would be rational to prescribe insulin or drugs that raise insulin to counteract the elevated blood sugar. The reality however is that type 2 diabetes is NOT the result of insufficient insulin production. It’s actually the result of too much insulin being produced on a chronic basis primarily from eating the high carbohydrate, low fat diet recommended by the ADA and AHA to prevent and treat this.
This overwhelms and “deafens” your insulin receptors, hence the term “insulin resistance.” It’s the chronically elevated insulin levels that make your body “resistant” to understanding the signals sent by the insulin. This also occurs with leptin. It’s really important to realize that T2 diabetes is not caused by elevated blood sugar or “insulin deficiency” per se. The root cause is insulin and leptin resistance which is why prescribing insulin is one of the WORST things you can do for type 2 diabetes, as it will actually worsen your insulin and leptin resistance over time. You do not need more insulin. You need to restore the sensitivity of your insulin and leptin receptors by keeping their levels low!
If you’re still having trouble understanding why taking insulin is a terrible choice in type 2 diabetes consider this; when your blood sugar becomes elevated, insulin is released to direct the extra energy (sugar) into storage. A small amount is stored as a starch called glycogen, but the majority is stored as fat. Therefore, insulin’s primary role is not to lower your blood sugar, but rather to store this extra energy as fat for future needs when food may not be available. The fact that insulin lowers your blood sugar is merely a “side effect” of this energy storage process. Taking more insulin just makes you fatter!
Your body’s cells become desensitized to insulin, leptin, and other hormones, by being overexposed to these hormones—be it by eating food that causes excessive secretion, or by injection. Diabetes treatments that concentrate merely on lowering blood sugar by adding insulin therefore tend to worsen rather than remedy the actual problem of metabolic miscommunication.
As Dr. Rosedale has previously stated: “Type 2 diabetes is brought on by constantly having too much insulin and leptin circulating secondary to the same diet that has been recommended to treat diabetes and heart disease, a high carbohydrate, low-fat diet. Then giving these diabetics more insulin is adding gasoline to the fire. Doctors couldn’t be doing more harm if they tried.”
Leptin—An Oft-Ignored KEY Player in Type 2 Diabetes Development
While much conventional advice centers around insulin, leptin is another hormone that plays an integral role in the development of type 2 diabetes. Leptin is produced in your fat and other cells, and one of its primary roles is regulating your appetite and body weight. Leptin tells your brain when to eat, how much to eat, and most importantly, when to stop eating. Leptin also instructs your brain as to what to do with the available energy.
Now remember, when your blood sugar becomes elevated, insulin is released to direct the extra energy into storage—the majority of which is stored as fat, and leptin is produced in these fat cells. The more fat you have, the more leptin is produced. Furthermore, as the sugar gets metabolized in your fat cells, the fat releases further surges in leptin. This is why I typically talk about insulin and leptin resistance, as they work in tandem. Moreover, leptin is largely responsible for the accuracy of insulin signaling and whether or not you become insulin-resistant. If you’re insulin resistant, you’re more than likely leptin resistant as well, especially if you’re overweight or obese.
Because when you develop leptin resistance, your brain can no longer hear leptin’s signals, resulting in chronic hunger, overeating, inability to properly burn fat and, typically, obesity. Insulin resistance, and ultimately type 2 diabetes, follow suit. Just as with insulin, the only known way to reestablish proper leptin signaling is through proper diet. High consumption of carbohydrates, especially fructose, are again the prime culprit and the root cause of leptin resistance. Lack of exercise and abnormal gut flora also contribute and/or exacerbate insulin and leptin resistance. Leptin’s importance in blood glucose control and diabetes is powerfully illustrated by recent studies that show its ability, even in low doses, to lower blood glucose in both type 1 and 2 diabetics, and this is an exciting new potential treatment.
New Warning: Insulin Can Rapidly Produce Type 1 Diabetes in Type 2 Diabetics
Please understand that medications and supplements are not the answer for type 2 diabetes. Diabetes drugs fail to address the underlying problem, and many, like Avandia, can have dangerous side effects. Avandia is linked to 43 percent increased risk of heart attack and 64 percent higher risk of cardiovascular death, compared with other treatments. Instead, type 2 diabetes is best controlled by restoring your insulin and leptin sensitivities. This is done by eliminating grains and sugars—especially fructose—from your diet, getting plenty of healthy fats, exercising, and sleeping well. Further details on this will be provided below, in the treatment section.
As noted earlier, recent research published in the Journal of Clinical Endocrinology & Metabolism16 confirms what Dr. Ron Rosedale has stated for the last two decades, which is that insulin treatment can provoke otherwise reversible type 2 diabetes to progress into type 1 insulin deficient and therefore insulin-dependent diabetes. The study found that giving genetically engineered recombinant insulin to type 2 diabetics with certain genetic susceptibility can trigger their bodies to produce antibodies that destroy their insulin producing cells (pancreatic islet cells). You may not realize that all human insulin, the type typically used, is GMO or genetically modified which might be responsible for this autoimmune reaction.
Basically, it triggers an autoimmune disease response, producing a condition in which you have both type 1 and type 2 diabetes simultaneously. The average time of type 1 diabetes onset was 7.7 months. One study participant developed type 1 diabetes in just over one month! According to the authors, acute deterioration of blood glucose control after administering insulin is a warning sign of this problematic side effect. According to this study, the genes predisposing you to this autoimmune-type response to insulin are:
Type 1 diabetes high risk HLA class II (IDDM1), thought to play a role in about half of all type 1 diabetes cases
VNTR genotype (IDDM2), which is believed to predispose you to type 2 diabetes
This is yet another way conventional diabetic treatment pushes diabetics into premature death… Research17 published last year revealed that treating type 2 diabetes with insulin more than doubled patients’ risk of all-cause mortality. It also leads to:
|Twice as many myocardial infarctions||1.4 time more strokes||2.1 time more neuropathy||1.4 times more cancer|
|1.7 time more major adverse cardiac events||3.5 times more renal complications||1.2 times more eye complications||2.2 times more deaths|
Adapted from Mercola. Com
Another study published in Diabetologia18, 19 in May of this year, found that diabetic cancer patients also have a significantly elevated risk of death. Diabetic patients using insulin at the time of their cancer diagnosis had a four times higher mortality rate one year after cancer diagnosis, compared to non-diabetic patients, or those who did not use insulin to control their diabetes. While this was an observational study, which means it cannot establish causality, it is worth noting nonetheless.
Dr. Rosedale has also said; “All of these increased rates of chronic diseases caused by taking insulin may be because it is doing exactly the opposite of what has been shown in many studies to reduce cancer, total mortality, and extend lifespan; reducing insulin. In fact, T2 diabetes is often considered to be a model of accelerated aging because of the high insulin. In other words, treating diabetics by overly raising insulin, either with drugs or insulin itself, is only further accelerating their aging, associated chronic diseases, and death, and should be considered malpractice.”
Future Diabetic Vaccines?
As noted by GreenMedInfo.com,20 these findings also raise serious warnings against diabetic vaccines:
“[T]here are a number of trials underway to produce vaccines containing insulin intended to induce a ‘tolerogenic immune response’ and therefore ameliorate autoimmune type 1 diabetes. Clearly, however, their findings run contrary to this expectation, revealing that it is possible that introducing exogenous forms of insulin may stimulate the opposite reaction and induced autoimmunity against the hormone, or the cells in the pancreas responsible for producing it.”
It also raises questions about the safety and effectiveness of synthetic insulin. Virtually all of the insulin sold in the US is synthetic, synthesized from recombinant DNA technology, which differs considerably from natural animal-derived insulin. Interestingly, it could be that it’s the “inactive” ingredients or additives, such as polysorbate 20, that produce an exaggerated immune response in susceptible individuals—similar to that encountered with vaccines. Sayer Ji also notes that:
“Furthermore, synthetic insulin does not have the same conformational state – i.e. it does not assume the same complex folded form – of natural human insulin, or more closely related pig insulin. This presents a ‘recognition’ problem from the perspective of the immune system which may identify the foreign protein as ‘other’ generating acute or sustained autoimmune reactions to it as a result…
Research22 dating back to the early 1980s compared synthetic E. Coli derived insulin with porcine (pig) derived insulin in diabetic children and found that porcine insulin was more effective at lowering HbA1 values (a marker of damage associated with elevated blood sugar), superior at reducing fasting glucose concentrations, and less antibody reactive to insulin than synthetic insulin. While pig derived insulin has its limitations, especially considering there are limits to how much can be produced, clearly it is more appropriate than synthetic versions if it is true that the latter is incapable of reproducing the same therapeutic outcome for diabetics.”