By Dr. Mercola
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:
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.
How to Avoid Heart Disease
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'll want it below 3. As for preventing or reversing
hyperinsulinemia or insulin resistance, the following general guidelines
will set you on the right track:
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. My optimized nutritional plan can guide you through this process.
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 eight 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.
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