The Cause of Coronary Artery Disease


The conventional theory of the cause of coronary artery disease has been driven by the so called “Diet Heart Hypothesis.” This was the idea that diets that were high in saturated fats raised blood cholesterol which caused atherosclerotic blockage of arteries. This was started by several flawed studies. The first was done by Nikolai Anichkov in 1913. He found that when he fed rabbits diets that were high in cholesterol, that they developed coronary atherosclerosis. This was and still is considered a groundbreaking study proving the role of cholesterol in heart disease. The problem was that rabbits are herbivores, not accustomed to eating cholesterol as there is no cholesterol in plant foods. Hence their bodies were not adapted to consuming dietary cholesterol. When the same experiments were done using dogs which are carnivores, no such coronary lesions developed.  Furthermore, when it was eventually agreed that dietary cholesterol played no role in atherosclerosis in humans, the American Heart Association and USDA eventually dropped the 30 year old recommendation that all Americans should restrict dietary cholesterol. So why didn’t they drop the recommendations to limit saturated fat? Well, the other early study that was influential and that was also flawed was the Seven Countries Study by a physiologist named Ancel Keyes where he looked at dietary saturated fat intake in various countries and compared it with the incidence of heart disease in those countries. The problem with his study was that he hand picked the seven countries that fit his hypothesis and ignored those that didn’t, namely France and Switzerland which have among the highest saturated fat intake and the lowest incidence of heart disease. None the less, he was able to convince the scientific community that his hypothesis was correct and subsequently convinced the US government to formulate guidelines telling people to limit saturated fat intake. What happened in studies that tested the hypothesis that reduction in saturated fats reduced CAD?  Several have been done. Two of the most notable studies where polyunsaturated fats were substituted for saturated fats were the Minnesota Coronary Experiment and the Sydney Diet Heart Study. The Minnesota Coronary Experiment was done by Ancel Keys’ own staff at the University of Minnesota. Here, long term residents in psychiatric hospitals were put on regular vs diets where saturated fats were replaced by polyunsaturated vegetable fats. The results were the opposite of what was expected. The experimental group had more deaths due to heart disease as well as total deaths. The authors waited 15 years to publish these results. When author of Good Calories Bad Calories, Gary Taubes asked the principle investigator why he waited to long, the response was that they were disappointed with the results. See related recent editorial about this (1).  The Sydney Diet Heart Study showed similar results ie higher coronary and all cause mortality in the group that ate the diet where polyunsaturated fats were substituted for saturated fats.  For every 30 point reduction in total cholesterol, there was a 20% increase in deaths. The results of this study also laid dormant in storage until they were recently discovered and published (2).

The problem with the diet heart hypothesis is that not only does intake of saturated fat, which can raise total cholesterol, but also raises HDL or good cholesterol, not correlate with heart disease, but that blood cholesterol itself doesn’t correlate with heart disease either. A landmark ongoing study of diet, cholesterol and heart disease that has been going on since 1948 is the Framingham Heart Study. There 5,200 residents of the town of Framingham in Massachusetts have been followed since 1948. The initial much heralded finding was that serum cholesterol correlated with heart disease. However as the study went on it later turned out that total cholesterol had weak correlation with heart disease in men only below the age of 50 and no correlation with heart disease after 50. In women there was no correlation with heart disease before 50 and a reverse correlation after 50. That is after the age of 50, the higher a woman’s cholesterol, the longer she lived.  See Gary Taubes’ NYT article describing this (3). Several other studies have shown the same thing, ie basically, the higher your cholesterol, the longer you live.  See Verner Wheelock’s excellent blog on this (4).

Another damning study is the “UCLA Study” where 137,000 patients who were admitted for heart disease from 541 hospitals were studied for 5 years (5).  They found that over 75% had LDL cholesterol levels below 130, considered to be a good level, and 50% had levels below 100, a level considered to be ideal and well below normal. A meta analysis published in BMJ in 2016 looked at 19 studies involving 68,0000 patients, found an inverse relationship between LDL levels and mortality in patients over 60, similar to Framingham findings above (6).

So if there is no data that high total or in particular LDL cholesterol correlates with heart, disease why is there still belief of it’s role in causing heart disease?  Enter statins and the medical industrial complex. When belief was high that blood cholesterol correlated with heart disease, the search was on to find classes of drugs that would lower blood cholesterol. The most powerful class discovered was the statin class. Statins inhibit production of cholesterol which causes and increase in liver LDL which increases removal of cholesterol particles. Several studies were done by the manufacturers that showed reduction in cardiac events, however reduction in total mortality was weak. And when analyses were done of long term benefits it was found that they might prolong live by only 3-4 days for every 5 years of use.  However there is conflicting data on the benefit of statins as well.   A recent study of 100,000 Medicare patients who had suffered a myocardial infarction showed that those that were intolerant of statins, ie could not and did not take them, had slightly higher incidences of heart events but lower overall mortality (7).  There is also data that the benefit that has been shown with statins has more to do with anti inflammatory effects than cholesterol lowering.  Numerous studies have shown no correlation with the degree of LDL lowering and degree of benefit in statin trials.

So when it became apparent that LDL itself had basically no correlation with heart disease, investigators started to look at subgroups of lipid particles such as small dense LDL and apoB which is a marker of total LDL particles. It turns out that increased levels of small dense LDL and apoB particles do correlate with incidence of CAD.  So it was then believed that if a person has a high number of small dense LDL particles ie high apoB count, and since these particles do correlate with heart disease, that these particles must cause atherosclerosis by getting into the walls of arteries and triggering atherosclerosis.  Ok, so, finally, a study of one of the new potent LDL lowering drugs, PCSK9 inhibitors, evolocumab, was recently published, the FOURIER TRIAL (8).  This drug lowered LDL significantly to very low levels. It also raised HDL and lowered triglycerides. Basically, all the lipid parameters and particle numbers were “fixed” to all be in what would be considered ideal ranges. LDL cholesterol was reduced to 30. Apo B was reduced by 49%. Other lipid parameters were fixed as well. Lp(a) was reduced by 27%. HDL was increased by 8.4%. Apo A1 was increased by 6.5%. Triglycerides were reduced by 16%. Basically all the numbers were in as good a range as could be hoped for. They were basically “perfect.”  So how did the patients do?  In the patients on the drug, the incidence of events over the two year period was 9.8% compared to 11.3% in the control group. This is hardly earth shattering.  So, in these patients who had as “good” a total lipid profile as could possibly be imagined, the incidence of events was 10% over two years, which is still considered extremely high as far as percent risk scores go. According to the Framingham risk calculator, a 20% ten year risk of coronary events is the highest category for cardiac risk.  These patients had a 10% incidence of cardiac events in only two years.  That is, these patients still suffered cardiac events at what is considered an extremely high rate.  Cardiac events were not reduced anywhere close to what would be considered a low cardiac risk category. What’s more, you guessed it, the subjects on this powerful LDL lowering drug had higher total mortality. So, again, you can basically fix all the lipid particle numbers of at risk patients to what would be considered perfect lipid profiles, yet they still had a high incidence of cardiac events.

So when it became apparent that LDL was not such a good indicator of cardiac risk along came Ronald Kraus who showed us that there were two main types of LDL particles ie small dense or so called dangerous LDL particles that did have a correlation with heart disease and large “fluffy” LDL particles that supposedly did not.  The small dense type was associated with diabetes and metabolic syndrome (more on that below) and was called pattern B.  The large fluffy type was called pattern A.   In that pattern B is found most often in patients with metabolic syndrome and diabetes, which does correlate with significantly higher risk of heart disease, this distinction made sense.  This is also the basis for the now much touted Apo B to Apo A ratio which basically accounts for total number of LDL particles vs HDL particles which takes into effect the number of LDL particles ie the smaller LDL particles having the higher number.  However, this relationship also does not hold up completely either.  In a recent study (9), it was found that in patients who had suffered an MI, those with pattern B actually had a LOWER  follow up mortality than those with pattern A!  What the..?

Maybe lipid moieties or particles, ie LDL, apo B, apo A ratios, HDL have no causative role in coronary artery disease whatsoever, rather they are merely markers of a condition that is the real cause of coronary artery disease, ie insulin resistance and what is probably the real cause of atherosclerosis, high circulating insulin levels.

In 1988, at the Banting lecture series, Gerald Reavens presented his discovery of insulin resistance and metabolic syndrome which he called “syndrome X.”  This syndrome consists of resistance of tissues, to effects of insulin, causing the pancreas to secrete more and more insulin to overcome this resistance in order to maintain glucose homeostasis ie normal glucose levels.  It is characterized by high resting and food stimulated insulin levels.  The insulin resistant condition or metabolic syndrome has other characteristic features, namely central obesity, hypertension, elevated blood sugar, lipid abnormalities, mainly elevated triglycerides and lowered HDL cholesterol and finally vascular disease.  Insulin resistance is most likely caused by the consumption of large amounts of sugar over long periods of time.  This sugar consumption has an affect on the liver whereby the liver can’t handle the large amounts of the fructose part of sugar and the liver converts it to fat which accumulates in the liver.  This leads to initially insulin resistance within the liver.  This role of sugar in causing insulin resistance which starts in the liver and the subsequent development of metabolic syndrome and the diseases associated with it is eloquently laid out by Gary Taubes in his outstanding book, The Case Against Sugar.  As the pancreas secretes more and more insulin to overcome this liver resistance, other organs such as muscle and fat or adipocytes then become resistant as well, probably as a result of more and more exposure to higher and higher insulin levels.  The pancreas compensates by secreting more and more insulin as the insulin resistance becomes worse and worse until eventually it can’t secrete enough insulin to keep glucose levels controlled and the blood glucose rises and a person is then identified as diabetic.  The whole time insulin levels are rising due to this sugar induced insulin resistance, but while blood glucose levels are still normal, the individual has what is called prediabetic.  As Gary Taubes describes in The Case Against sugar, consumption in the US and throughout the world has gone up over 20 fold since the beginning of the 19th century and diabetes has paralleled this going up incidence over 8 fold over the past 100 years.  It is estimated that 50% of the US population has diabetes or prediabetes.  25% of Americans have fatty liver.  Not only is insulin resistance associated with obesity, diabetes, and vascular disease, it is the cause of the vast majority of those conditions.  It is felt that over 80% of hypertensive patients and 80% of cardiac patients are either diabetic or pre diabetic and if one uses the insulin tolerance test developed by Robert Kraft, one could identify nearly all patients with coronary artery disease as diabetic or pre diabetic.  Recent studies have identified fatty liver as a stronger predictor of vascular disease than any other cardiac risk factor including total cholesterol, LDL, HDL levels (10, 11).

So what about lipids?  Numerous studies have identified HDL and triglycerides as the strongest predictors of heart disease as far as lipid markers go.  As stated above small dense LDL and high apoB to apoA ratios also correlate with heart disease.  However, what all these so called atherogenic lipid marker patterns have in common is that all are characteristic of the metabolic syndrome.  In fact the most “atherogenic” patterns of lipids ie high triglycerides, low HDL, high apoB, small dense LDL are all only seen in metabolic syndrome, strongly implicating metabolic syndrome in the cause of atherosclerosis.  So is it these lipid particles that all the researchers and drug companies have focused on for so long that are the atherogenic trigger of vascular disease caused by metabolic syndrome?  Or is it something else?  As the FOURIER trial described above showed, when all these particles were normalized by drugs, there was still an extremely high level of cardiac events.  You have all these lipid particles brought to ideal levels yet there was still a high level of cardiac events.  So if it is not the lipid particles that are characteristic of cit metabolic syndrome that causes vascular disease, what is it?  I would propose that there is a strong case that insulin itself and high insulin levels of the metabolic syndrome are the primary drivers of vascular atherosclerotic disease and that all the lipid particles and particle patterns associated with the metabolic syndrome are nothing more than markers of the syndrome ie high insulin levels, and have no causal roll in the promotion of atherosclerosis whatsoever.  The true feature of metabolic syndrome that damages the lining of arteries leading to atherosclerosis is not the so called atherogenic lipid particles, but rather the effects of a high insulin level itself on the walls of arteries that causes them to develop atherosclerosis.  Taubes discusses this possibility in Good Calories Bad Calories. On page 189, he cites Harvard researchers who in 2005 felt vascular disease was possibly due to direct action of insulin on vessel walls.  Rabbits fed high cholesterol diets “developed plaques throughout their arteries.”  But diabetic rabbits (type 1) did not until they were infused insulin along with the high cholesterol diets wherein “plaques and lesions will promptly blossom everywhere.” “This phenomenon was first reported in 1949 in rabbits, and then, a few years later, in chickens, and later in dogs, too.” “In the late 1960’s , Robert Stout of Queen’s University on Belfast published a series of studies reporting that insulin enhances the transport of cholesterol and fats into the cells of the arterial wall and stimulates the synthesis of cholesterol and fat in the arterial lining.”  A paper published in 2016 did a genetic analysis and concluded,  “These results support the causal role of insulin in the pathogenesis of CHD.  Efficient treatment and prevention of insulin resistance is essential to prevent future CHD events ” (12).  The following study among others showed that “although several old studies provided conflicting results, the majority of large observational studies show strong dose-dependent associations for injected insulin with increased CV risk and worsened mortality.”  (13,14.)

So what is the cause of coronary artery disease? As I detailed above I don’t believe it has anything to do with so called “atherogenic” lipids.  I believe the prime cause of the development of atherosclerotic vascular lesions is the effect of high insulin levels which are the prime characteristic of metabolic syndrome, insulin resistance and type 2 diabetes.  The insulin causes the initial injury to the vessel wall, then the cascade of events ie macrophages ingesting LDL particles, foam cells etc are secondary reactions.  Many, including myself, believe that the development of atherosclerotic plaques are part of the body’s reaction and attempted repair mechanism to the initial wall injury.  Ie blaming the cholesterol deposits and plaque development is like blaming the fire department and fire trucks for the damage of the fire. I feel that in most cases the majority of the initial artery wall damage is done my insulin but other factors, mainly hypertension alone can cause the initial injury as well in some individuals.  Most cases of hypertension are associated with metabolic syndrome, again the result of too much sugar consumption for too long a period of time.  However not all hypertensives have metabolic syndrome and high insulin levels.  Coarctation of the aorta is a congenital condition where the aorta has a narrowing in the arch.  This causes elevated blood pressure in the head, arms and heart arteries, but not the lower extremities.  These individuals obviously do not have metabolic syndrome.  They develop severe atherosclerosis in the arteries of their heart and brain and usually die in their 30’s and 40’s of myocardial infarctions and strokes.  So something has to cause the initial arterial wall injury be it high insulin levels or the effect of hypertension, and the atherosclerotic process is nothing more than the body’s reparative response to the initial injury and lipid particles and the plaque forming process are nothing more than the firemen and fire trucks trying to put out the fires.



To be continued…..


Low Carb High Fat Diet to Treat Diabetes

Low Carbohydrate, High Fat, Atkins type diet should be the first step in treatment of all diabetics, both type one and two. Numerous studies and practice experience testimonies have confirmed this. See Eric Westman’s second video below. The most comprehensive review of the data supporting using LCHF to treat diabetes was cited in the tremendous article by R D Feinman PhD per this link:

RD Feinman PhD: Low Carbohydrate Restriction as First Approach in Diabetes Management

The LCHF diet consistently lowers glucose and A1C. Dr. Westman cites numerous cases where his patients were able to get off all medication including insulin within weeks and in one case in days, see his second video below.  The number emerging is that over half of all diabetics who go on the diet come off most if not all their diabetic medications. Although the diet is high in fat including saturated fat, the diet consistently lowers triglycerides and raises HDL, the two most important lipid markers correlating with risk for heart disease. Also contrary to what one would think it is diets that are low in fat and high in carbohydrate such as the American Heart Association Low Fat “Heart Healthy” diet that increase blood saturated fat levels, thus increasing cardiac  disease risk.  Low carb, high fat diets to the opposite ie lower blood saturated fat levels.  Phinney and Volek showed this.  See their videos and books cited below.   In addition, low fat diets lower HDL, “good cholesterol,” raise triglycerides, and even though they lower LDL, “bad cholesterol,” they convert most of that LDL cholesterol to the small dense or truly dangerous form of LDL cholesterol.  Low carbohydrate diets, on the other hand, which in some cases will raise total and LDL cholesterol, convert the LDL to the large, buoyant, harmless form of LDL cholesterol, thereby lowering risk of heart disease far greater than low fat diets will.  Dietary saturated fat consumption which will increase in most low carb diets also has never been shown to increase risk of heart disease in numerous studies.  All this is covered and referenced in detail in the above linked article, as well as in Nina Teicholz’ tremendous book, “Big Fat Surprise, Why Butter, Meat, and Cheese belong in an Healthy Diet,” as referenced below as well as linked to a video of hers below.



There is a great online resource for diabetics interested in using a low carb diet to treat and reverse diabetes.  It is called Virta Health.  They provide online guidance in using low carb diet to treat your diabetes.  You can access it by this link:


Low Carb High Fat Diet For Weight Loss and Diabetes Control–Getting Started

Quick start LCHF guide:

Why carbohydrate restriction rather than total calories or fats?

In a nutshell: It’s about insulin.  Insulin has two main functions.  1. It enables glucose to enter cells so they can utilize it for energy. 2. It promotes the deposition of fat into the bodies fat stores. The higher the insulin level, the more fat is deposited into and locked into fat stores.  Carbohydrates are the primary food type that stimulates insulin release. Eating foods very high in sugar and refined carbohydrates causes significant spikes in insulin levels which not only cause more storage of the food you just ate into fat, but also adversely affects your liver and muscle tissues over time causing these organs to become resistant to insulin.  This insulin resistance then requires the pancreas to secrete more and more insulin to overcome this resistance which leads to higher and higher insulin levels which leads to more and more deposition of fat into fat cells resulting in obesity as well as metabolic syndrome which entails diabetes, hypertension, and vascular disease, ie heart disease and strokes.  See Gary Taubes “Why We Get Fat” video below. Eventually the pancreas is no longer able to keep up with ever increasing insulin resistance in the liver and muscle and sugar levels start to rise causing diabetes.  The only way to reverse this and get insulin levels reduced to the point where they no longer keep fat locked into the fat cells is to lower the primary food type that causes insulin to rise, carbohydrates.  If carbohydrates are removed from the diet or drastically lowered, the insulin levels begin to fall, eventually falling to the point where fat is no longer trapped in fat cells and is released into the blood to be available to be used by the body for fuel.  Your brain can’t tell if this fat in the blood came from something you just ate or fat stores.  This is why you aren’t hungry on a low carb diet.  Weight loss results.  In diabetics this weight loss improves insulin sensitivity resulting in improvement and often reversal of diabetes.  See Eric Westman, MD and Sarah Hallberg, MD videos below. Basically, with a carbohydrate restricted diet, you are reversing the basic causes of obesity and diabetes namely sugar and carbohydrates raising insulin which causes fat deposition and storage.  Years of eating foods high in carbohydrate especially sugar and refined carbohydrates, with resultant high spikes in insulin, over time causes the development of insulin resistance which leads to chronically elevated insulin levels and resultant metabolic syndrome and diabetes. Cutting carbohydrates reverses all this.


Limit all sugar: sweets, desserts, sodas, sweet tea, and juice, all juice!  Liquid sugar ie sugar sodas and juice are absolutely the worst offenders in causing obesity and diabetes.  Fructose, half of the molecule sucrose in table sugar is a main cause of fatty liver.

Limit starches and starchy vegetables: bread, potatoes, rice, noodles, corn, grains, flour, beans (baked, butter), peas, butter beans, field peas, corn bread, grits, cereal, fruit (yes fruit), and milk.

What you can eat: meat (any kind: beef, pork, poultry, fish, lamb), eggs, cheese, nuts (1 to 2 oz per day), and “green vegetables” ie broccoli, cauliflower, collards, okra, cabbage, squash, lettuce, tomatoes, string beans, onions, mushrooms, olives, pickles, etc.

It’s called low carb, high fat for a reason.  You replace carbohydrate calories with fat calories (not protein).  This diet keeps you in ketosis for enhanced weight loss and performance, as well as cancer fighting properties.  See books and video references below.  Add butter to vegetables and dry meats instead of gravy, which has flour.  Cook collards and turnip greens with ham hocks, fat back, pig tails, and bacon grease like your grandmother did.  Eat regular not lean meat and regular ground beef, not lean hamburger.

It’s ok to fry food in healthy fats like lard, butter (grass fed if you can afford it–not margarine), beef tallow, (again like your grandmother did), or coconut oil rather than artificially processed vegetable oils like corn, safflower, soy, canola.   The vegetable oils, except olive, avocado, and coconut, are too high in omga 6 fats and are harmful, cause cancer.  That’s right, the opposite of what the government has been telling you for the past 40 years, namely to substitute saturated animal fats with polyunsaturated vegetable oils. Well it was the wrong advice.  See Nina Teicholz video below.  Just don’t batter the food first.  Remember nothing with flour.

Grass fed beef and dairy, ie butter, is best.  Higher in omega 3 oils, vitamin K2, more natural.

Milk has carbohydrate namely lactose so it needs to be limited.  Watch the carbs 11 to 12 gm per 8 oz portion.  If you do drink some milk make it whole, not reduced fat.  Fat free milk causes far more weight gain than whole milk.

Yogurt is made from milk and the label will list the carbohydrate content of the milk it was made from, again 11 to 12 gm per 8 oz serving.  But yogurt is made with active bacterial cultures which ferment the lactose to lactic acid hence the bitter taste and, as a result, the carbohydrate content is not the same as the original milk.  That is, it has been reduced by the bacterial fermentation.

What about alcohol?– beer: way too much carbohydrate; wine: better but limit; hard liquor: ok, very little carbohydrate in hard liquor.

What about diet drinks? — Best to limit these too.  The brain senses sweet and sends a message to the pancreas to release insulin and the insulin then drives ALL the calories you just ate, carbs, fats, and proteins into your fat stores. It’s best just to drink water.

Try to keep total carbs or at least net carbs (total carb grams minus fiber grams) under 20 grams per day.

Test urine daily with urine keto sticks to be sure you are in ketosis which usually correlates with weight loss.


Key books to read:

1. Any version Atkins diet books, esp “New Atkins for New You” By Eric Westman, Steve Phinney, and Jeff  Volek.

2. “Why We Get Fat” by Gary Taubes

3. “Good Calories, Bad Calories” by Gary Tubes

4.  “The Case Against Sugar” by Gary Taubes

5.  “The Salt Fix” by James DiNicolantonio

6. “The Art and Science of Low Carb Living” by Phinney and Volek.

7. “Big Fat Surprise Why Butter Meat and Cheese Belong in a Healthy Diet” by Nina Teicholz.

7. “The Great Cholesterol Con”  by Malcolm Kendrick.

8. “Cholesterol Clarity” by Jimmy Moore.

9. “Keto Clarity” by Jimmy Moore.

10.  “How Statin Drugs Really Lower Cholesterol and Kill You One Cell at a Time” by Hannah and James Yoseph.


Key Articles:

Copy and paste the web addresses to your address bar

1. Dietary Carbohydrate Restriction as the First Approach in Treatment of Diabetes

2.Gary Taubes New York Times:  “What if It’s All Been a Big Fat Lie?”:

3. Low Carb Diet Recommended for Diabetics by Bob Shepard.

4.  Carbohydrate restriction should be the basis of treatment of diabetes.

Oped: diet the key to diabetes epidemic


5.  Article by Osma Hamdy, medical director obesity program, Joslin Clinic Harvard Medical School. “The era of recommending low fat, high carbohydrate diets to treat diabetics should come to an end.”  The Harvard Joslin Clinic has been the premier diabetes research center in the world for over 80 years.

Key On Line Videos –all searchable on Youtube:

Eric Westman’s video on how to do a low carb diet.


Eric Westman, MD, professor of lifestyle medicine ,Duke University Medical School.  Excellent video on the science of low carb diets to treat diabetes.


Eric Westman: the science behind low carb high fat diets to treat diabetes:


Sarah Hallberg: Reversing diabetes with low carbohydrate high fat diet.

Steve Phinney physiology and clinical aspects of low carb diets.  Recent developments part 1

Steve Phinney Recent developments part 2


Gary Taubes Youtube “Why We Get Fat”


Still believe fats and cholesterol cause heart disease?  Watch this video.



Phinney and Volek Jumpstart full interview:


Jeff Volek: The Many Facets of Keto Adaptation:

Steve Phinney: The Art and Science of Low Carb Living and Performance

Steve Phinney: The Aboriginal Argument:

Jeff Volek: How your blood panels respond to a ketogenic diet:

Tom Naughton: Diet, Health and the Wisdom of Crowds

Dr. Dominic D’Agostino ketogenic diet for cancer


Robert Lustig, MD “The Bitter Truth