The video above, “The Fat Emperor: Insulin Versus Cholesterol,” features Ivor Cummins, a biochemical engineer with a background in medical device engineering and leading teams in complex problem solving.
In 2013, Cummins 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 three different doctors, he realized none of them really understood the root cause of these problems, or how to address them.
As a result, he delved into the medical literature, found the problem and reversed his abnormal test results. He also dropped 35 pounds in the process.
Eventually, he got more involved in health and began giving lectures such as this one, which was presented at the Low Carb USA Keto Getaway1 in Florida this past January. He also has a website, thefatemperor.com,2 where he notes:
“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 Cholesterol Conundrum
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, and not nearly the damaging culprit it’s 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 your triglycerides are high, it means you’re 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 two days, where it gets broken up and recycled. This is a beautiful system; alas, it is one that can be disrupted if you’re eating 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.
Beyond Cholesterol — What Really Causes Heart Disease?
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 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 (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.
How a High-Sugar Diet Causes Insulin Resistance and Type 2 Diabetes
But what makes one person insulin sensitive and another insulin resistant? This is where your diet comes into play. What you eat tends to be a primary deal-maker or deal-breaker. Other factors that promote systemic insulin resistance include:
|Lack of exercise||Stress||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 (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.
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 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. As noted by 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.
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 Master Measure
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.
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.”
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.