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Insulin Is the True Cause of Heart Disease, NOT cholesterol

Ivor Cummins, a biochemical engineer with a background in medical device engineering and leading teams in complex problem solving.

“The Fat Emperor: Insulin Versus Cholesterol,” features Ivor Cummins in the video :

It is a well known fat that hyperinsulinism is the cause of heart disease, in fat one of major factor or true cause for heart disease. Insulin causes chronic inflammation and inflammation is the most predictive parameter for coronary heart disease. Insulin, and the hyperinsulinemia that prevented lipolysis of triglycerides in your fat cells will cease.

The Cholesterol is not the cause for heart disease

The vast majority — about 80 percent — of the cholesterol in your body is made by your liver. The remaining 20 percent comes from your diet. If you consume less, your body will compensate by making more, and vice versa.

Contrary to popular belief, cholesterol is a crucial molecule necessary for optimal health, material for more than 120 hormones produce by adrenal glands, testis and ovary and not nearly the damaging culprit it’s been made out to be.

Cummins likens the very low-density lipoprotein (VLDL) your liver makes to a boat that shuttles not only cholesterol but also triglycerides through your bloodstream to your tissues.

The VLDL will dock onto receptors in your muscle tissue, where it releases triglycerides to be used for energy. Cummins accurately notes that eating fat is not the cause of high triglycerides.

If your triglycerides are high, it means you’re eating too much net carbohydrates, because it’s actually sugar that causes triglycerides to rise, not dietary fat.

Burning of sugar produce a lot of free radicals and require efficient anti-oxidant. Anti-oxidants require are Superoxide dismutase, Gluthathione peroxidase and catalase.

Once the VLDL has dropped off the triglycerides to be burnt for energy (or stored as fat if you’re not using the energy due to inactivity), the VLDL becomes a low-density lipoprotein (LDL), which in conventional thinking is a “bad” kind of cholesterol.

High-density lipoprotein (HDL) is known as “good” cholesterol, and the HDL is indeed beneficial in that it acts as a master manager, helping protect the LDL against oxidation and transport triglycerides and cholesterol in and out of the VLDL.

In a healthy person, the LDL will be reabsorbed by the liver after about two days, where it gets broken up and recycled. As a general rule, a high-sugar diet will cause damaged LDLs to rise, beneficial HDLs to drop, triglycerides and, often, total cholesterol to rise. All of these are conventional indicators of atherosclerosis or inflammation in your arteries that can precipitate a heart attack. One of analysis by a team from Harvard University shows, ratio of Triglyceride to HDL cholesterol is better predictor of risk of coronary artery disease. They classified into four group, the ratio that is highest one quarter has sixteen fold higher heart attack rate that the lowest one quarter. And high Triglyceride and low HDL is a known fat cause by high sugar intake or/and high carbohydrate intake, not due to fat intake.

What Really Causes Heart Disease?

Most heart attacks are due to insulin resistance. Dr. Thomas Dayspring, an expert on cholesterol, stated that LDL “is a near-worthless predictor for cardiovascular issues.”

In simple layman’s terms Cummins goes on to demonstrate 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 person who has good insulin sensitivity has a low risk level for cardiovascular disease (CVD)
  • A metabolically obese yet normal weight individual who is insulin resistant has a high risk
  • A metabolically unhealthy obese individual who is insulin resistant also has a high risk
  • But a metabolically healthy obese 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 are obese insulin sensitive or obese insulin resistant.

How a High-Sugar Diet Causes Insulin Resistance and Type 2 Diabetes

More often than not, excessive amounts of glucose from total carbohydrates minus fiber are what set the disease process into motion by causing your insulin level to spike in order to maintain glucose that supposes to be in very tight range. When repeated over time, your adipose fat tissue begins to lose its systemic signaling capabilities, precipitating insulin resistance. When you are insulin resistance, you need higher amount of insulin molecules in order to maintain good level of glucose.

Diet comes into play in developing insulin resistant or maintain sensitive to insulin. Other factors that promote systemic insulin resistance include:

  • Obesity of high visceral fat
  • Smoking
  • Genetics
  • Insufficient sleep
  • Physical inactivity
  • Stress (leads to chronic elevated cortisol, cortisol bring up glucose, high glucose require more insulin)
  • Omega-6-rich vegetable oils
  • Low vitamin D/lack of sun exposure
  • Sedentary behavior

While glucose can be used by most cells in your body, fructose, on the other hand, must be processed by your liver before it can be used. It’s actually metabolized in a way similar to alcohol — a similarity evident in non-alcoholic fatty liver disease (NAFLD). Small amounts of fructose will not cause a problem, but very large amounts will over time trigger systemic 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 release glucose even when you’re not eating, and this is when your blood glucose finally begins to increase and seen in diabetic type 2 seen in metabolic syndrome.

Measuring Metabolic Syndrome

Metabolic syndrome is a constellation of factors including:

  • Low HDL cholesterol
  • High triglycerides
  • Large waist circumference
  • High blood pressure
  • High blood sugar

Having three or more of these factors over a certain level is considered evidence of metabolic dysfunction that sets the stage for chronic disease, including not only atherosclerosis and CVD but also gout, cancer, stroke, diabetes, Alzheimer’s, NAFLD, arthritis and more.

As noted by Cummins, metabolic syndrome is actually more aptly named insulin resistance syndrome. Moreover, since insulin secretion is the “master measurement” for insulin resistance, measuring your insulin level — particularly after a meal (post-prandial) — will give you the information you really need without having to evaluate those other five measurements.

The epidemic of insulin resistance

Dr. Joseph Kraft, former chairman of the department of clinical pathology and nuclear medicine at St. Joseph’s Hospital, wrote the book “Diabetes Epidemic and You: Should Everyone Be Tested?” Based on data from some 14,000 patients, he developed a test that is a powerful predictor of diabetes. 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.

Interestingly, he noticed five distinctive patterns suggesting that a vast majority of people were already diabetic, even though their fasting glucose was normal. In fact, 90 percent of hyperinsulinemic patients passed the fasting glucose test, and 50 percent passed the glucose tolerance test. Only 20 percent of patients had the type 1 pattern signaling healthy post-prandial insulin sensitivity and low diabetes risk.

One of the take-home messages here is that insulin resistance and hyperinsulinemia 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 full-blown diabetes lest you change your dietary course.

How Hyperinsulinemia/Insulin Resistance Causes Heart Disease

In summary, insulin resistance and/or hyperinsulinemia promote fatty liver — a combination that in turn drives high blood insulin and associated mechanistic pathways that shuttle lipids (fats) into your vascular walls, which is a hallmark of atherosclerosis. It also leads to high blood glucose, particularly post-prandial blood glucose, and this too has mechanistic pathways that 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, 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 asindicative of inflammatory issues, and not as the LDL itself being the problem!

In its entirety, all of these factors are what flag the development of heart disease. Other factors that can influence your CVD risk include smoking and other environmental pollutants, especially heavy metals, so addressing and eliminating these kinds of toxic exposures would also be prudent.

References
– thefatemperor.com