According to Dr. Thomas Dayspring, a lipidologist (expert on cholesterol), most heart attacks are due to insulin resistance. In the video above, biochemical engineer Ivor Cummins explains the role insulin resistance plays in heart disease, and why cholesterol is not the problem.12

In simple layman’s terms Cummins demonstrates the connection between the metabolic functionality of adipose fat — which actually acts as a signaling organ — and insulin sensitivity, and how and why:

  • A metabolically healthy normal weight (MHNW) person who has good insulin sensitivity has a low risk level for cardiovascular disease (CVD)
  • A metabolically obese yet normal weight (MONW) individual who is insulin resistant has a high risk
  • A metabolically unhealthy obese (MUO) individual who is insulin resistant also has a high risk
  • But a metabolically healthy obese (MHO) individual who has good insulin sensitivity is at low risk for CVD

In other words, there’s healthy body fat and unhealthy body fat, or put another way, fat that protects your health and fat that promotes disease. The key difference is the presence or absence of insulin sensitivity. The higher your insulin resistance, the worse markers such as fasting insulin, triglyceride-HDL ratio and HbA1c will be, suggesting you’re at increased risk for diseases such as diabetes and heart disease.

Recent research has shown that two specific metrics — circulating adiponectin and macrophages — can with near 100 percent accuracy predict your obese phenotype, meaning whether you’re obese insulin sensitive or obese insulin resistant. But what makes one person insulin sensitive and another insulin resistant? This is where your diet comes into play.

More often than not, excessive amounts of glucose from net carbs (total carbohydrates minus fiber) are what set the disease process into motion by causing your insulin level to spike. When repeated over time, your adipose fat tissue begins to lose its systemic signaling capabilities, precipitating insulin resistance.

Eventually, the high sugar load will cause your pancreas to diminish its production of insulin, and the hyperinsulinemia that prevented lipolysis of triglycerides in your fat cells will cease. Subsequently, your liver will begin to output glucose even when you’re not eating, and this is when your blood glucose finally begins to skyrocket.

Prior to this, the elevated insulin actually kept the blood glucose in check. But as insulin production drops, there’s nothing to prevent the blood glucose from rising anymore.

Eighty Percent of Americans Are Insulin Resistant to Some Degree

The late Dr. Joseph Kraft, former chairman of the department of clinical pathology and nuclear medicine at St. Joseph’s Hospital in Chicago, wrote the book “Diabetes Epidemic and You: Should Everyone Be Tested?” In it, he presents data that suggests 80 percent of Americans are in fact insulin resistant, or have “diabetes in situ.”

Based on data from 14,000 patients,13 Kraft developed a powerful predictive test for diabetes.14 He would have the patient drink 75 grams of glucose, and then measure their insulin response over time, at half-hour intervals for up to five hours.

He noticed five distinctive patterns suggesting that a vast majority of people were already diabetic, even though their fasting glucose was normal. Only 20 percent of patients had healthy post-prandial insulin sensitivity and low diabetes risk. According to Kraft, “Those with cardiovascular disease not identified with diabetes … are simply undiagnosed.”

One of the take-home messages here is that insulin resistance and hyperinsulinemia (a condition marked by excess insulin in your blood relative to your level of glucose) are two sides of the same coin, as they drive and promote each other. In other words, if you have hyperinsulinemia, you are essentially insulin resistant and on your way toward developing Type 2 diabetes.

In summary, both insulin resistance and hyperinsulinemia promote fatty liver and high blood glucose, and both of those in turn promote atherosclerosis. High blood pressure is another side effect of insulin resistance that drives atherosclerosis by placing stress on your arteries. As noted by Cummins, most idiopathic hypertension (high blood pressure with no known cause) is now thought to be caused by hyperinsulinemia.

Hyperinsulinemia/insulin resistance promotes inflammation, causing your visceral fat to release inflammatory cytokines and systemic signaling molecules. Over time, your visceral fat becomes increasingly resistant as well, causing the systemic signaling to falter. Taken as a whole, this cascade of events drives atherogenic dyslipidemia, characterized by the now familiar culprits: high LDL cholesterol, oxidized LDL and triglycerides, and low HDL.

According to Cummins, while high LDL is a very erratic marker for heart disease risk, an elevated LDL “particle count” is actually a very good marker for insulin resistance. Thus, the LDL metrics should be more thought of as indicative of inflammatory issues, and not as the LDL itself being the problem. In their entirety, all of these factors are what flag the development of heart disease.

Article From: https://articles.mercola.com