Insulin Is the Real Reason for Heart Disease
In Y 2013 Ivor Cummins, a biochemical engineer with a background in medical device engineering and leading teams in complex problem solving, ran into health problems.
His serum ferritin was very high, which is a potent risk factor for heart disease, as were his liver enzymes. After consulting with 3 different medical doctors, he realized none of them understood the root cause of these problems, or how to address them.
As a result, Mr. Cummins delved into the medical literature, found the problem and reversed his abnormal test results. He also dropped 35lbs in the process.
Eventually, he got more involved in health and began giving lectures, and developed a website, thefatemperor.com.
There he notes the following:
“I refer primarily to the ‘diet-heart’ hypothesis, which proposed that dietary saturated fat elevated blood cholesterol, and the latter drove heart disease mortality like nothing else.
The evidence at the time was loose correlation, certainly not causation, and seems almost laughably naïve in retrospect.
However, the tenaciousness of this flawed hypothesis has turned out to be no laughing matter, condemning millions to the misery of obesity, type 2 diabetes and an extraordinary range of inflammatory diseases.
The factors that conspired to perpetuate the flawed hypotheses were many: academic and research community hubris, political forces, economic imperatives, profiteering from the food and pharmaceutical industries, and the groupthink psychology that underpins the worsening ‘diabesity epidemic.
After 25 years in technical/management positions with a personal specialty in complex problem solving, I have been inspired to … bring an engineering-style approach to the current situation.”
The vast majority (80%) of the cholesterol in your body is made by your liver. The remaining 20% comes from your diet. If we consume less, our body will compensate by making more, and vice versa.
Contrary to popular belief, cholesterol is a crucial molecule necessary for optimal health, and not nearly the damaging culprit it has been made out to be.
Since cholesterol is a fatty substance, it does not travel well through your water-based bloodstream.
Hence it is encapsulated in a lipoprotein. 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 our triglycerides are high, it means we are eating too many net carbohydrates, because it’s actually sugar that causes triglycerides to rise, not dietary fat.
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 colloquially 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 2 days, where it gets broken up and recycled. This system is one that can be disrupted if we eat too many unhealthy foods.
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.
According to Dr. Thomas Dayspring, a lipidologist, expert on cholesterol, most heart attacks are due to insulin resistance. He has also stated that LDL “is a near-worthless predictor for cardiovascular issues.”
In layman’s terms Mr. 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 (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, meaning fat that protects your health and fat that promotes disease. The Key difference is the presence or absence of insulin sensitivity.
The higher our insulin resistance, the worse markers such as fasting insulin, triglyceride-HDL ratio and HbA1c will be, suggesting an increased risk for diseases such as diabetes and heart disease.
Recent research has shown that 2 specific metrics: circulating adiponectin and macrophages, can with near 100% accuracy predict your obese phenotype, meaning whether one is obese insulin sensitive or obese insulin resistant.
The Big Q: What makes one person insulin sensitive and another insulin resistant?
The Big A: Diem what we eat tends to be a primary deal-maker or deal-breaker.
Other factors that promote systemic insulin resistance include, the following:
- Insufficient sleep
- Lack of exercise
- Omega-6-rich vegetable oils
- Low vitamin D/lack of sun exposure
- Sedentary behavior
- Low omega-3
More often than not, excessive amounts of glucose from net carbs, meaning total carbohydrates minus fiber are what set the disease process into motion by causing ones insulin level to spike. When repeated over time, the adipose fat tissue begins to lose its systemic signaling capabilities, precipitating insulin resistance.
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 is 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 the pancreas to diminish its production of insulin, and the hyperinsulinemia that prevented lipolysis of triglycerides in your fat cells will cease. Subsequently, the liver will begin to output glucose even when 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 is nothing to prevent the blood glucose from rising. As noted by Mr. Cummins, it can take many years for this process to play out before you end up with a diagnosis of type 2 diabetes. But you could have gotten a heads-up years, if not decades, earlier using a simple blood test.
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% of hyperinsulinemic patients passed the fasting glucose test, and 50% passed the glucose tolerance test. Only 20% of patients had the type 1 pattern signaling healthy post-prandial insulin sensitivity and low diabetes risk.
Cummins believes that using Kraft’s test, about 65 percent of Americans or more probably would have hyperinsulinemia or “diabetes in situ.” And, according to Kraft, “Those with cardiovascular disease not identified with diabetes … are simply undiagnosed.”
A Key take-home messages here is that insulin resistance and hyperinsulinemia are 2 sides of the 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.
Evidence suggests high total cholesterol and even high LDL are insignificant when trying to determine your heart disease risk. Your best predictor is your insulin sensitivity.
Considering how insulin resistance drives chronic disease in general, not just heart disease, I strongly recommend measuring your fasting insulin on a regular basis, and taking immediate action if you find yourself inching toward insulin resistance.
Your fasting insulin level can be determined by a simple, inexpensive blood test. A normal fasting blood insulin level is below 5, but ideally you will want it below that number.
- Dramatically reduce your net carbs and eliminate processed fructose, as this is what set this cascade of metabolic dysfunction into motion in the first place. Replace the lost calories with higher amounts of healthy fats, not protein.
- Normalize your omega-3-to-omega-6 ratio. Most get far too little omega-3, found in fatty fish such as wild Alaskan salmon, sardines, anchovies, fish oil and krill oil, and too much omega-6, as it is plentiful in processed vegetable oils and hence processed and fried foods.
- Optimize your Vitamin D level by getting regular, sensible sun exposure.
- Other nutrients of importance include magnesium and vitamins K2 and C.
- Get 8 hours of high quality sleep each night to normalize your hormonal system. Research has shown sleep deprivation can have a significant bearing on your insulin sensitivity.
- Get regular exercise, as it is a powerful way to help normalize your insulin sensitivity.
Eat healthy, Exercise regularly, Be healthy, Live lively
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