Clearing up cholesterol and saturated fat myths

Tides and paradigms are shifting, as people slowly begin to realize that perhaps saturated fat and cholesterol are not the demons we've made them out to be and don't need to be avoided like the plague. Over the years there here have been numerous well critiqued and validated studies showing that saturated fats and cholesterol have been wrongly vilified as the harbinger of heart disease. How did we get set on this witch hunt to begin with? Why is it so ingrained in so many people that saturated fat=bad?

This is the first of a large two part article covering many of the misconceptions that most people have regarding the complex mechanism of heart disease. Heart disease has been the number one killer in this country for a century, nearly 1 in 3 Americans will die from some form of cardiovascular disease, the majority from coronary artery disease(CAD). Doctors often prescribe a low fat diet and statin medications to lower cholesterol in an effort to reduce the risk of atherosclerosis. But is this proper practice? And what evidence is it based on? And why is there such a large (and growing) group of dissenters in the medical field who feel we are misguided in the way we attempt to treat CAD? The goal of this article is to address the diet heart hypothesis and answer the following questions:

  1. What is heart disease and how prevalent is it? 
  2. What are saturated fats and cholesterol and why are they important?
  3. How did we come to our current views regarding saturated fats, cholesterol, and their relationship to CAD?
  4. Does consuming saturated fat or dietary cholesterol lead to higher levels of cholesterol in blood?
  5. Do higher levels of this serum cholesterol lead to plaque buildup and CAD?

Breaking Down the Diet-Heart and Lipid Hypothesis

Most of the American public and a majority of health professionals take the lipid hypothesis as gospel. The diet heart hypothesis was put forth as an answer to why America was experiencing a rise in deaths from CAD and states that consuming saturated fats or dietary cholesterol leads to an accumulation of blood lipids, which causes atherosclerosis.  

Fats- Whats the deal?

First lets talk about what fat itself really is. Most people know it is the most dense macronutrient yielding 9 calories a gram. A fat molecule is made up of a molecule of glycerol and three molecules of fatty acids which can be either saturated, monounsaturated, polyunsaturated, or trans fat. Some functions of fats include:

  1. Providing energy and in my opinion should be the primary source of fuel for your body. Carbs are important for the athlete or weightlifter but I always say that I would prefer if my body almost exclusively ran on fat, except for my intense workouts which I feel better when fueled with carbohydrates.
  2. Regulating hormones, fat is also a major component of prostaglandins which regulate many functions
  3. Enabling the absorption of the fat soluble vitamins A,D,E, and K.
  4. Helping to form the phospholipid component of cell membranes 
  5. They are the structural component to myelin in our body, which is the sheath that transports nerve impulses.

The fatty acids that make up fat are always a mix of saturated and unsaturated. The USDA recommends less than 10% of total calories come from saturated fat and the general consensus of the American public is that saturated fats are bad. To uncover if this is truly the case lets go over the components of saturated fat, and how it differs from unsaturated.

What makes a fat saturated? This is referring to the number of double bonds in the fatty acid.

Saturated fats are considered "fully saturated" with hydrogen atoms, as a result they contain no double bonds. They are found mostly in animal fats and coconut oil.

Monounsaturated fats contain one double bond and found in olive oil, almonds, pecans, cashews, peanuts and avocados.

Polyunsaturated have two or more double bonds and are found in sunflower, corn, soybean, and flaxseed oils, and also in foods such as walnuts and fish.

Saturated fats are less vulnerable to oxidation because it contains no double bonds which are prone to instability when under heat. When an oil oxidizes, it reacts with oxygen and forms various harmful compounds which have been shown to be carcinogenic and inflammatory. The more double bonds the more unstable a fat is when reacting with heat. This is also why fats or oils that are primarily composed of saturated fatty acids tend to be solid at room temperature and have a higher smoke point. Its important to avoid cooking in a highly polyunsaturated oil, saturated fats like coconut oil are best, and monounsaturated oils like olive oil are ok as well if cooked at lower temperatures.

Breaking saturated fat down even further we see three sub categories: short chain, medium chain, and long chain.

Short chain- consists of butyric and caproic acids, which are found in grass-fed dairy products. Plays an important role in gut health and inflammation levels. Also promotes growth of healthy colonic epithelium, and protects against colon cancer(1)

Medium chain-  caprylic, capric and lauric acids make up medium chain fatty acids. These are found in coconut and palm oil. I supplement with 2 tablespoons of mct oil daily due to it thermogenic effect as well as for it's muscle sparing and cognitive benefits. MCT's has been shown to aid in fat loss in multiple studies. (2,3)

Long chain-myristic acid, palmitic acid, and stearic acid. Mystric acid has been shown to raise LDL cholesterol levels (4) while palmitic is more neutral it too can contribute to an increase in LDL-c. These are the only two fatty acids that have been specifially linked with an increase in LDL. Stearic is shown to actually lower LDL-c (5). The main contributors of long chain fatty acids that should be avoided are industrial meats and heavily processed food. Grass-fed meat is found to have a more favorable balance of stearic acid to the LDL raising myristic and palmitic.(6)

Cholesterol simplified

We should also cover a very general definition of what cholesterol is as well.  Cholesterol is an organic compound that helps form every cell in our body. Its a structural component of every single cell in our body along with fats and vital to life. It helps us synthesize vitamin D, forms bile in our stomachs, and is a precursor needed for different hormones. Our bodies produce about 75% of the cholesterol in our body(800-1200mg daily), the other 25% comes from diet (300-500). Of the cholesterol our bodies produce 20% is made from the liver and the other 80% comes from our cells(7). Interestingly the brain, which accounts for about 2% of our weight, stores 25% of the cholesterol in our body largely to ensure vital connections between nerve endings in the brain. Cholesterol is essential for optimal brain function and low cholesterol has been associated with alzheimers.(8)

Our bodies internally regulate the amount of cholesterol we have by producing more endogenous cholesterol when less is consumed and producing less when dietary cholesterol intake increases.  Cholesterol, like fat, is not soluble in water and cannot be transported freely in our blood. Therefore they are transported by a water soluble protein molecule. This leads to the misconception that there is actually different type of cholesterol. This is not true, all cholesterol is the same identical chemical formula, there is no "good" or "bad" kind. When people refer to this what they are referring to is the kind of lipoprotein, typically HDL and LDL,  that is carrying the cholesterol in the blood.

Heart disease- what is it?

Heart disease facts (9)

  • Approximately 81 million American adults are living with cardiovascular disease
  • More than 17 million of those with CVD have atherosclerosis , a buildup of plaque
  • 1 in 3 deaths in America are due to heart disease, 1 in 6 specifically due to  atherosclerosis
  • Almost 800,000 people die from heart disease annually in the US. This equates to a death every 40 seconds
  • The total direct and indirect costs of cardiovascular disease in the US is over $315 billion

Heart disease has been the main cause of death in this country since 1921(10), yet atherosclerosis is still a very misunderstood disease. Much of the general public has a complete misconception of what this disease is. Many times when I ask a client or someone their definition of atherosclerosis, or coronary artery disease, they respond with something along these lines: consuming high fat foods (usually animal products) and dietary cholesterol causes saturated fat and cholesterol to enter the bloodstream and stick to the arterial walls and forms plaque. This narrowing of the arteries slows down blood flow to the heart, which could result in a blood clot and heart attack.

I'm not sure how this misconception has stayed alive but I know ridiculous commercials like this contributed====>

The conventional view of atherosclerosis is called the lipid hypothesis: "(as) the cholesterol level in the blood increases, it penetrates the arterial wall and gets stuck; white blood cells circulating in the blood then enter the arterial wall and gobble up the cholesterol; the accumulation of lipid-loaded white blood cells causes local injury, leading to cell death, calcification, and the development of a collagen-laden fibrous cap over the atherosclerotic lesion. When the cap ruptures, the blood clots, blocking the artery and causing a heart attack."

Now there's alot more to this including oxidation levels, particle size and density but this is widely considered the basic mechanism of atherosclerosis. 

Most people believe the diet-heart hypothesis to be a main causal factor in heart disease and think a lower fat and higher grain intake is "heart healthy". The diet-heart hypothesis states that the more saturated fat one consumes, the higher ones serum cholesterol levels rise leading to the development of atherosclerosis. The main goal of this article is to uncover whether saturated fat and dietary cholesterol indeed raise serum cholesterol and if higher levels of serum cholesterol are a causal factor of CAD.  

An history and review of the studies

The early days- New understandings of cholesterol 

In order to dissect the diet-heart hypothesis and understand how we have come to our current views it is important to understand our history. The theory that cholesterol is the cause of atherosclerosis goes back over 125 years. As far as I could find the first person to suggest that cholesterol led to the development of plaque was the German pathologist Rudolph Virchow after studying the arteries of cadavers in the late 19th century. In 1913 Russian pathologist Nikolay Anichkov followed up on work from a few years earlier done by a fellow student of the Military Medical Academy of St. Petersburg. His colleague was exploring a theory that dietary protein causes aging to accelerate and induced atherosclerosis in rabbits that were fed a diet of dairy and meat. Anichkov was looking for the specific component of the diet that led to the artery disease in the rabbits. He was able to induce atherosclerosis by feeding rabbits pure cholesterol from eggs in sunflower oil and concluded that excess blood cholesterol was the causal factor in the disease. Some people interpret this to mean that consuming diets high in cholesterol lead to accumulation of serum cholesterol levels even though Aniakchak himself said he did not think dietary cholesterol was a primary factor for humans since we are omnivores and can metabolize and regulate cholesterol unlike the rabbit herbivores. Later studies on dogs failed to produce similar effects since they are omnivores and can internally regulate excess cholesterol by turning it to bile or excreting it. Atherosclerosis can be induced in dogs when thyroid function is inhibited.

Things were quiet on the research forefront for almost 40 years after the rabbit fed study. In 1950 Dr. John Gorman and his research team published their studies trying to further the research from 40 years earlier. They replicated the experiments and then used new centrifuge technology to isolate the specific components that transport cholesterol. They discovered that lipid proteins were the carriers of cholesterol in the blood, and categorized them as either high density lipidproteins or low density lipidproteins. By looking at blood samples of heart healthy people and those with atherosclerosis, he was able to correlate high levels of LDL and triglycerides with higher rates of heart disease and high levels of HDL as lowering the risk. Since LDL was associated with higher risk and HDL with lower, "good" and "bad" cholesterol was born. Dr. Gorman's efforts caused an increased effort to fully understand the mechanisms of heart disease and how it related to diet. Studies soon followed from Edward Ahren that showed replacing saturated fat with polyunsaturated fats lowered LDL levels while carbohydrates increased triglycerides and lowered HDL.


Introducing the diet heart hypothesis

In 1955 during a World Health Organization conference Ancel Keys put forth the diet-heart hypothesis suggesting dietary fat intake should be low to maintain low blood cholesterol levels. He presented the following graph as the basis for his argument that high fat intake has a causal relationship with mortality rates from heart disease.

His ideas were not very well received at the time and most of his colleagues present voiced disagreement saying that correlation is not causation and that there was no real evidence fat intake would increase the likelihood of death from heart disease. In 1957 two of Key's colleagues who were present, Jacob Yerushalmy and Herman Hilleboe, published a critical paper of Key's conclusions. First and foremost they note that although data was available for 22 countries only 7 were used. Oh and those are the ones that just so that happened to correlate to his theory.. convenient. I believe a scientist is someone who seeks to prove their hypothesis incorrect, not someone seeking to prove it as true. This is what the graph would have actually looked like had all available countries been included:

Now we don't have nearly as clear a relationship with all 22 countries presented. For example: the United States has the #1 rate of mortality and the #1 amount of fat as a % of daily calories. The next highest mortality rate? Finland comes in at #2 despite being #14 when it comes to % of calories from fat. It is possible to draw an inverse relationship if the right countries were "cherry-picked" the same way Keys did. They also made sure to point out that a correlation does not imply causation and made note of more developed countries having more accurate accounting of coronary related death and also having more fat and protein available for consumption. Then they delved into the same stats Key's used much deeper to compare the correlation of fat and deaths with other aspects of diet. They found that high consumption of animal fat and protein leads to higher rates of death from heart disease while consuming more plant foods instead of animals leads to a higher rate of mortality from all other causes of death. This could also be because the more industrialized and advanced countries will have better medical infrastructure and lower rate of mortality in general than the less developed ones. These same developed countries have more access to animal meat than the poorer countries.

There was one more huge flaw in Keys theory. His statistics were actually based on food production and import/exports. So he found not the quantity of food people of that country actually ate, but the quantity that was available for consumption. It's likely much more fat is available and also wasted in an industrial country than in a developing one. In response to criticism Keys started the formal "Seven Countries Study" in 1958.

The early framework for what would become modern policy and perception

Despite having no human based studies to back up the theory that increased saturated fat and cholesterol intake led to heart disease there were multiple instances of The American Heart Association urging the American public to limit consumption of both between 1956-1960. However around the same time there were also statements saying more studies were needed before a claim could be made. In my opinion that sounds like there was some disagreement among those heavily involved in the AHA. It is known that some board members were replaced during this time. One of the new members of the board was none other than Ancel Keys.

I'm going to assume he was a driving force of the new guidelines the AHA put forth around 1960 recommending to reduce saturated fat and cholesterol intake from foods such as butter, fatty meat, egg yolks and full-fat milk and replace them with low fat equivalents and seed oils. Keys appeared on the cover of Time Magazine in 1961 in a feature story inditing saturated fat and blood cholesterol as the culprits of heart disease. Again all of this was before any major study was published showing any correlation between high serum cholesterol levels with heart disease. There was also no proof to support that eating saturated fat increased cholesterol or risk of heart disease. 

Within the next year the Framingham Massachusetts study released a landmark paper detailing its 10 year findings after starting a investigation into risk factors for heart disease in 1949. This study involved over 5000 members of the town recording their dietary and lifestyle habits and published the following conclusions(11): smoking, being overweight, and lack of exercise are risk factors for developing heart disease. It also found that men under the age of 50 with elevated serum cholesterol had a high risk of heart disease. This was widely publicized as proof that high blood cholesterol was a causal factor in heart disease. Oh yeah men over 50? No link between high cholesterol and any heart related issues. Women? No relationship either. Yet this one subsection of the study was proclaimed as the evidence needed to support massive changes in public policy. On average the men under 50 also happened to drink and smoke more, not workout and be more overweight. There was another fact not highly publicized: higher intakes of saturated fats and dietary cholesterol did not lead to either higher serum cholesterol levels or higher risk of heart disease, they in fact had an inverse relationship. 

The Studies

During the 1960's and early 70's there was still a large amount of disagreement on the diet-heart hypothesis. Many did not believe that recommending low fat and higher carbs was the solution since low LDL and high triglicerides had also been identified as risk factors and this diet had been shown to do exactly that. But governmental agencies were feeling pressure to ease the publics mind about the heart disease epidemic by providing it with a targeted solution, even if they were acting prematurely. There were a number of studies done to further explore the theory. Here are some of the more notable studies and events that have lead us to where we are today with our diet and drug recommendations. Currently most people and doctors advocate a low fat diet and believe blood cholesterol to be the cause of atherosclerosis.

I've included all the major supporting dietary studies for both sides that I could find to try come up with an answer to these two questions:

  1. Does consuming dietary cholesterol or saturated fat cause an increase in blood cholesterol or risk of heart diease?
  2. Do high levels of blood cholesterol or LDL-c cause coronary heart disease?


  • 1963- Diet and Plasma Cholesterol in 99 Bank Men(12): The interesting thing about this study is the fact that food intake was measured at home, and so its much more accurate than most other observational studies. There was no link found between animal fat and serum cholesterol levels. Almost everyone in the study ate a high amount of saturated fat and there was a large array of blood cholesterol levels that had no correlation to saturated fat intake.


  • 1963- A Longitudinal Study of Coronary Heart Disease(13): Sponsored by the American Heart Association, this was a large four year study using almost 2,000 men and showed no correlation between saturated fat intake and heart disease. The risk factors it did identify were early age of death of father, history of "noncardiac" chest discomfort, history of chronic cough, history of shortness of breath, history of peptic ulcer, presence of increased skinfold thickness, elevated blood pressure, elevated blood cholesterol, abnormalities in the electrocardiogram, and use of cigarettes and coffee. 


  • 1964- American Heart association extends low fat diet recommendations to general public


  • 1964-Cardiovascular Disease in the Masai(14): Dr. George Mann was a vocal critic of the diet heart hypothesis and published a paper about the Masai Tribe of East Africa. The young males of this tribe ate a diet that gave them over 50% of their daily caloric in take from fat, most of it saturated from milk, blood, and meat. Yet the average cholesterol level was 115mg/dl while the average American man's at the same time was 198mg/dl. Keys and other supporters of the diet heart hypothesis attributed it to some protective genetic variant the tribe must have.


  • 1965- The American Medical Association made similar diet recommendations to the public as the AHA


  • 1967-Epidemiological studies related to coronary heart disease. Characteristics of men aged 40‑59 in Seven Countries(15): This was Key's first big publication of his Seven Countries study. He showed a link between total saturated fat intake and serum cholesterol. This is cited by him and many other supporters as proof that saturated fat should be avoided. There were many who pointed our major problems with this study at the time. A critical review from the American Journal of Clinical Nutrition published in 1973 can be found here.


  • 1968- The effect of plasma-cholesterol-lowering diet in male survivors of myocardial infarction. A controlled clinical trial(16): Over 400 men involved who had recently experienced a myocardial infarction were studied over 5 years. One group was consuing low animal fat and dietary cholesterol, high amounts of vegetable oil and the other did not change their diet. For men under 60 there was a statistically significant decrease in rates of recurrent heart episodes when consuming low animal fat and high vegetable oil. No significance was found for those over 60. Serum cholesterol was higher in all who had re-infarction regardless of the diet group they were in.


  • 1969- Los Angeles Veterans Trial(17): An 8 year double blind study with over 800 participants. One group was given a diet of about 40% fat from animals, the experimental group had the animal fats replaced with vegetable oils. The cholesterol levels were 14% lower for the vegetable group but there was no significant difference in heart attacks or overall mortality. Incidents of cancer were higher in the experimental group despite having fewer smokers.


  • 1971- The Masai of East Africa: some unique biological characteristics(18): This was an expansion of Mann's earlier work on the tribe. Two groups of young Masai men were fed the same low cholesterol low fat diet but one was given 2000mg of cholesterol a day. They had no difference cholesterol levels from each other, with both around 175mg/dl, however they started with an average of 125mg/dl. Similar studies would be done with other tribes who had up to 50% of their calories come from saturated fat, their LDL and total cholesterol went up when eating more modernized diets low in fat.


  • 1972- Effect of cholesterol-lowering diet on mortality from coronary heart disease and other causes(19): this was a 12 year clinical trial that showed no effect on women but did show that a cholesterol lowering diet led to fewer cases of coronary heart disease in men. The experimental diet involved replacing milk fat with soybean oil, replacing butter with soft polyunsaturated margarine, less meat and eggs, and more root vegetables. The control diet remained the same. This study was not randomized or blinded and is one of the main ones cited in favor of the diet heart hypothesis. It is a cross over design which means they spent 6 years on one diet and then switched it to the other diet for another six years. This can cause all kinds of fluctuations and variations that I don't believe can all be attributed to fat intake.


  • 1972- Pure White and Deadly is released by John Yudkin. Yudkin was a loud opponent of the diet heart hypothesis and believed sugar to be much more to blame. This book was very well received and re-released over a decade later. In the end of the book he goes into detail how the firms with commercial interests in supporting the diet heart hypothesis tried to impede his publishing process. These are the same groups supporting the low fat movement and using marketing techniques dependent on our views of saturated fat as bad.


  • 1977- Diet and Heart: a Postscript(20): From the British Medical Journal this was a 20 year study with over 300 male participants. There was no link found between saturated fat intake and CHD and fiber was concluded to be protective.


  • 1977- The McGovern committee report is released which in senator McGovern's words was "the first comprehensive statement by any branch of Federal Government on risk factors in the American Diet." This report would form the foundation for our current dietary guidelines and was based on the diet heart hypothesis. The United States Department of Agriculture soon adopted the same guidelines and joined with the department of Health and Human services to release the first official low fat dietary guidelines 3 years later. There was a a recent article in the American Journal of Public Health that reviews the issuing of the guidelines, claiming they were made in the face of conflicting science.(19)


  • 1978- Dietary Intake and the Risk of Coronary Heart Disease in Japanese Men Living in Hawaii(20): Studied the diets of nearly 8000 men of japanese decent to determine links to CHD. Alcohol, and to a lesser extent carbohydrate intake were linked with higher incidence of CHD. Saturated fat had a negative correlation with CHD.


  • 1980- First official dietary guidelines published. It provided the following recommendations: 1- Increase carbohydrate intake to 55 to 60 percent of calories, 2- decrease dietary fat intake to no more than 30 percent of calories and recommended approximately equivalent distributions among saturated, polyunsaturated, and monounsaturated fats to meet the 30 percent target, 3- decrease cholesterol intake to 300 mg per day, 4- decrease sugar intake to 15 percent of calories, 5- decrease salt intake to 3 g per day. This was a much more modest recommendation than they initially intended to put out but they were met with major opposition from the dairy and meat industries who were quick to point out the flawed and conflicting research.


  • 1981-Diet, Serum Cholesterol, and Death From Coronary Heart Disease: The Western Electric Study(21): 20 year study of 1900 middle aged men in Chicago found a small correlation between saturated fat intake and blood cholesterol levels but there was no increase in heart disease related or total mortality. 


  • 1981- Enhanced macrophage degradation of low density lipoprotein(22): Researchers discovered that culturing endothelial cells with LDL caused dramatic changes to the LDL and gave it a dramatic ability to accumulate in white blood cells called macrophages. Macrophages are the precursors to the "foam cells" that populate atherosclerotic plaques. The researchers called this LDL "endothelial cell-modified LDL." Soon after, they discovered that the LDL was being "oxidatively modified."  This was the first study to open up eyes to the role of oxidized LDL in atherosclerosis 


  • 1982- Multiple Risk Factor Intervention Trial(23): a randomized primary prevention trial to test the effect of a multifactor intervention program on mortality from coronary heart disease in 12,866 high-risk men aged 35 to 57 years. The patients who ate low fat low cholesterol had slightly fewer cases of CHD. Though this was not statistically significant it was widely publicized. There was no significant decrease in serum cholesterol levels, mortality from heart disease or overall mortality. In fact all cause mortality was higher in those consuming the low fat and low cholesterol diet, most notably there was an increase in death from cancer.


Time Magazine has been quite influential throughout the years

Time Magazine has been quite influential throughout the years

  • 1984- The Lipid Research Clinics Coronary Primary Prevention Trial(24): The National Institute of Health funded a large $150 million study using 3800 men diagnosed with hypercholestermia following a low fat diet and using a cholesterol lowering non-statin drug called cholestyramine. Though widely publicized as proof that cholesterol lowering medications are a valuable tool due to drops in relative risk of coronary related events, there was not a significant decrease in death from heart disease or overall mortality. Still this study prompted Time Magazine to make this famous March 1984 cover. Despite the fact the the study was not done to determine dietary protocol at all, everyone followed the same diet. Time magazine extrapolated the diet heart hypothesis from the study and was a large reason for our current misconceptions.


  • 1984- Ten-year incidence of coronary heart disease in the Honolulu Heart Program(25): Nutrient intake was examined in over 8000 japanese men. Men who had coronoary heart disease also consumed a higher % of calories from protein and fat. The difference in saturate fat intake between those who had heart attacks was small but statistically significant. Those consuming higher fat also consumed less vegetables- which have been shown as possibly protective against heart disease.


  • 1988- Low-Density Lipoprotein Subclass Patterns(26): Further work is done on the variants of LDL and it is found that small dense LDL leads to higher risk than other more "fluffy" subclasses of LDL. To recap first there was only total cholesterol, then in the 1950's we discovered the different lipoproteins that transport cholesterol (LDL, VLDL, HDL). In the early 80's oxidized LDL was uncovered, and now its found that there are actually even more subclasses of lipoproteins that may be better indicators of risk. 


  • 1989- The Minnesota Coronary Survey(27): large double blind study where one group consumed most of its fat content in the form of polyunsaturated an the other mostly consumed saturated fats. Though cholesterol was significantly lower in the polyunsaturated group there was no change in cardiac events or total mortality.


  • 1989- Diet and 20-y mortality in two rural population groups of midle-aged men in Italy(28): Men who consumed less saturated fat suffered more deaths from CHD than those who consumed higher amounts. Its worth noting this is in a rural area in Italy where dairy is largely unprocessed and natural. It quite likely that the negative associations with saturated fats is often a result of the poor source they are coming from. 


  • 1993- Comparison of C-Reactive Protein and Low-Density Lipoprotein Cholesterol Levels(29) Inflammation has been associated with heart disease yet our main target is and has always been cholesterol. This study only involved women and concluded that inflammatory markers were more closely correlated with CHD than cholesterol. 


  • 2005- The Baltimore Longitudinal Study of Aging(30): There were 4 different types of diets examined. One with low saturated fat, one with high amounts of fruits and vegetables, one with higher amounts of saturated fat, and one that was low fat and high intake of fruit and vegetable. A diet low in saturated fat and high in fruits in vegetables is shown to have lower risk of heart disease and all cause mortality. No change in all cause mortality among the other diets but there were fewer deaths from CHD in the high fruit and vegetable group. 


  • 2006- The Woman's Health Initiative(31) One of the largest randomized dietary clinical trials ever lasting over 8 years and involving almost 50,000 women. There was no benefit found from a fat reducing diet despite the fact that LDL levels were lowered through the low fat diet. Women with the lowest levels of LDL had the highest risk of death.


  • 2007- LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study(32): researchers compared using LDL-c against LDL-p and found LDL-p to correlate more strongly with CHD. LDL-p is number of LDL particles, LDL-c is the typical test given and is the concentration of cholesterol in the particles. So yet another component of the ever evolving concept of cholesterol is uncovered.


  • 2010- Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease(33): A review of 21 combined studies totaling almost 350,000 participants found 0 link between saturated fat intake and risk of death from CHD or any other cause. This is the largest meta analysis of saturated fat's relationship with CHD.


  • 2011- Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid?(34): Over 52000 adults from 20-70 were evaluated and it was concluded that in women that cholesterol had an inverse relationship with all cause mortality and also mortality from heart disease.


  • 2014- Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary RiskA Systematic Review and Meta-analysis(35): This was a massive meta analysis of almo€st 80 studies and more than half a million people. There was no relationship between saturated fat intake and heart disease, and there was also no benefit found to substituting saturated fats for unsaturated vegetable oils.


  • 2014 Time Magazine Finally gets it right!- In response to the above study


Whew! That's an exhausting list of studies! Lets see if we can use them to come to some conclusions to the questions I posed earlier.

#1- Does consuming saturated fat or cholesterol in the diet lead to higher levels of blood cholesterol and risk of CHD?

We can find very solid evidence that consuming dietary cholesterol has very little affect on our blood cholesterol levels thanks to our internal mechanisms of regulation. This has been shown extensively in the Framingham Heart Study. Due to the fact that the main reason people believe dietary cholesterol to be harmful is to marketing tactics and media propaganda I wont go into depth covering this. There are no studies showing this in the general population. Even Ancel Keys has commented how dietary cholesterol has very little affect on humans serum cholesterol levels. There is a small portion of people who are classified as hyper responders and consuming large amounts of dietary cholesterol does raise both thier LDL-c and HDL-c but does not change the ratio or increase the risk of heart disease.

Earlier in this article I mentioned that its important to look at the best studies, not the most favorable or most recent ect.. The two best controlled and well designed studies, in fact the only two long double blind, single factor, randomized studies from above are the LA Veteran's Trial, and the Minnesota Coronary Survey. Both of these have demonstrated that replacing saturated fat with polyunsaturated vegetable oils lowers cholesterol, confirming findings from earlier similar studies.

In the LA Veterans study the only thing changed was the way the food was prepared. The control group's food was cooked in saturated animal fats while the experimental group's food was prepared in vegetable oils. The low saturated fat cooking process resulted in a 13% lower serum cholesterol concentration that was sustained over the course of the 8 years of the study. This drop in cholesterol did not translate to a statistically significant decrease in death from heart disease or heart attacks. Breaking down the numbers a little further you see that actually the low fat group had 9 fewer deaths from heart disease but had 14 more deaths total by the end of the study. Cancer occurred more frequently in experimental group. This is the only one of the studies that, although not significant, vegetable oil trended towards being protective against heart disease when used in place of animal fats. However it should be noted that the control group had much more heavy and moderate smokers than the experimental group. This would increase rates of heart disease and cancer, yet the increase in heart disease incidents was not significant and there was a lower rate of cancer.

The Minnesota Coronary Survey compared  the effects of a 39% fat control diet (18% saturated fat, 5% polyunsaturated fat, 16% monounsaturated fat, 446 mg dietary cholesterol per day) with a 38% fat treatment diet (9% saturated fat, 15% polyunsaturated fat, 14% monounsaturated fat, 166 mg dietary cholesterol per day) on serum cholesterol levels and cardiac events. Mean cholesterol for both groups was 209mg/dl at the beginning of the study. At the end the conrol group was 203mg/ml and the experiment was 175mg/dl. Though not statistically significant there was a trend towards higher rates of heart disease in the experimental group.

These two well controlled studies show that saturated fat raises serum cholesterol relative to unsaturated fats but this does not affect the chances of mortality from heart disease. A couple things to note. Lets temporarily take a stance that saturated fats do raise blood cholesterol. Lets look at the possibility that over the long term the high serum cholesterol levels associated with higher saturated fat intakes lower to a normal "healthy" range. The Maasai consumed much more saturated fat than the average American but had much lower cholesterol levels and rates of heart disease. In fact it was shown that when consuming a highly processed diet lower in fat their cholesterol levels sky rocketed. The Framingham study showed no link between higher levels of blood cholesterol and saturated fat intake. It has only been seen in a few very controlled studies when saturated fats where substituted for with vegetable oils, and their have been others showing the opposite. Most notably when fat is coming from natural sources and processed foods are limited. Another tribe that was studied was the Kitavans.(36) They are virtually free of any kind of cardiovascular disease or elevated serum cholesterol levels yet consume almost twice as much saturated fat than recommended in America and consume no grains or processed sugar.

So lets try to answer the first part of this question again: do saturated fats increase blood cholesterol? In the short term they will definitely raise cholesterol levels relative to polyunsaturated. However its not clear if this would sustain over the long term and there is evidence against it being related to blood cholesterol in a natural setting where processed foods are limited and fat sources are natural. So I will answer with a confident most likely- in a very controlled setting higher intakes of saturated fat relative to unsaturated fats will lead to sustained higher levels of blood cholesterol. However it has been shown that replacing saturated fats with carbs does not lead to the same drop in serum cholesterol as when replacing them with polyunsaturated fats.(37) When the type of fat and the environment is considered its likely that if consuming healthy natural foods blood cholesterol levels will not be correlated to saturated fat intake.

Looking at the rest of the studies we see that the majority of them all show saturated fat intake has very little effect on serum cholesterol levels, although a few are conflicting. Middle aged men in particular seem to be more affected, as do those in more urban populations. This is likely due to the damaging nature of highly processed fats. There is conflicting information in the studies which implies a causal relationship is not possible.

So we sorta have an answer to the first part of the question, but does it even matter if saturated fat intake does raise blood cholesterol? It has been well established that HDL-c is beneficial and protective against heart disease(38) and saturated fat raises HDL(39). Even though saturated fat can raise LDL-c in some people it also changes the particles from the small dense particles to the larger fluffy LDL-c.(40) Small LDL particles have been shown to be more prone to oxidation and are more damaging to the arterial wall(41). Large LDL particles have been shown to have no correlation to heart disease(42).This can help explain the answer to the second part of this question--- Does consuming saturated fat lead to heart disease?

So we know that saturated fat raises HDL which is protective against heart disease, and that it changes LDL particles from small and dense to fluffy and harmelss. But does saturated fat lead to heart disease? Are these positive things outweighed by the possible increase in LDL or some other mechanism? Again lets look at the best evidence available.

I've already provided the link to a detailed article critiquing Key's Seven Countries Study which is considered flawed today even by researchers who support the diet-heart hypothesis. I think a better designed study that could be used in support of saturated fat leading to heart problems is the study from 1968 listed above. This was one of the ones that replaces saturated fats with polyunsaturated and it found that in men under 60 who had recently experienced a cardiac infarction this low saturated fat diet led to less likely chance of re-infarction. There was no association with men over 60. There did not seem to be any confounders besides a slightly higher amount of those with high blood pressure in the control group. Also we have no information about rates of diabetes, cancer or all cause mortality to see if there was a shift in cause of death occurring. The LA Veterans trial did not support the hypothesis, and mortality and cancer was higher in the low saturated fat group despite having less smokers.

There are studies like the 1978 one of Japanese men that show saturated fat has a negative correlation with heart disease. The Framingham study and the Tecumseh study(43) among others provide strong evidence that saturated fat intake is not a causal factor in heart disease, in fact it's not even correlated. The 1982 MrFit study was very large and publicized as proof that saturated fat is a "bad fat" because the control group that consumed higher amounts had more cases of CHD. They also had less overall mortalities including from cancer, and no significant difference in serum cholesterol levels, or deaths from CHD. The Womans Health Initiative from 2006 showed very conclusively in women that low fat diet was not optimal for heart or overall health despite lowering LDL levels. I already referenced the largest metanalysis available and there are a few other large ones showing no correlation between saturated fat(44,45) and risk of heart disease.

Looking at all the studies I would say that saturated fat intake has no causal link to heart disease at all. The only population that could possibly have any heart disease related benefit from the low fat diet would be men under 60 who had recently had a myocardial infarction. There have been no solid studies relating higher intake of saturated fat with heart disease in the general population, and in fact it appears to be protective against cancer and other causes of mortality. 

Question: Does consuming saturated fat or cholesterol in the diet lead to higher levels of blood cholesterol and/or rates of heart disease?

Answer: Its been shown time and time again that dietary intake of cholesterol has very little if any effect on serum cholesterol levels. Saturated fat raises blood cholesterol relative to polyunsaturated fats, and do not appear to linked to heart disease and in fact appear to be protective against heart disease in woman and protective against cancer in both genders. Theres conflicting information on whether saturated fats will raise LDL in relation to other nutrients other than unsaturated fats. Even if LDL levels are raised, typically HDL is raised more. Total cholesterol:HDL-c has been shown to be much better marker of risk than LDL-c levels.(46)

#2- Do high levels of blood cholesterol cause heart disease and plaque?

Ok so maybe healthy and natural forms of saturated fat dont raise blood cholesterol levels over the long term, but do elevated blood cholesterol levels, regardless of how acquired, cause heart disease and for plaque? Omitting the studies on statins for the moment lets look at the rest. The American Heart Association identified a correlation of elevated serum cholesterol levels with heart disease. The 1968 study of a population of people who recently had heart attacks showed everyone who suffered a cardiac event had higher levels of serum cholesterol. The high saturated fat consuming Maasai tribe was shown to have much lower levels of blood cholesterol than the average American who experience a much greater prevalence of heart disease. As our understanding of the details and subtypes of lipoproteins expanded this association would be weakened and focus would shift more towards LDL-c.

We see many conflicting studies listed above showing either no relationship or at times an inverese relationship between blood cholesterol and CHD. The elderly and women in particular seem to have a very weak if not inverse relationship between heart disease an cholesterol. In 2012 a Norwegian study of more than 52,000 people it was found that women who had low cholesterol levels had higher mortality from all causes, including heart disease(47). A paper from the American Journal of Medicine in 2003 found that people over the age of 70 with total cholesterol levels below 160mg/dl had twice the risk of death than those with levels betweem 160-200mg/dl(48). Looking at the two best designed studies, The Minnesota Coronary Survey and the LA Veterans Trial we see no correlation between blood cholesterol and either rates of heart disease or overall mortality. They both dropped LDL but there was not a significant change in CHD mortality. The Minnesota Coronary Survey was trending higher rate of CHD mortality with lower LDL, while the LA Veterans Trial was trending the other slightly.

Traditionally we are told that LDL is the bad cholesterol mainly due to statin drug trials that reduce LDL-c and have been linked to decreases in heart disease. I will discuss it much more in depth in the next article but there is one important thing to note about the use of statin drugs. Its widely accepted that some of the benefits of statins go beyond the cholesterol lowering mechanisms. Statins lower inflammation and are thought to have other beneficial affects such as improved endothelial function. It's not neccessarily the lowering of LDL-c thats producing the small benefits received from statins.  This 1981 Framingham follow up shows that there can be a correlation between LDL-c and CHD in middle-aged men but as mentioned previously there have been stronger associations found with atherosclerosis such as: LDL-P, C-Reactive Protein, TC:HDL-c, and Triglycerides: HDL-c(49). So we have a couple things that show a correlation at times but we most definitely don't have a case to state any kind of causal factor. Our (mis)understanding of cholesterol and our guidelines for it have changed continuously and dramatically over the years so it's important to understand how complex the mechanisms of heart disease really are. Lets go in a little deeper into what atherosclerosis really is and how it relates to cholesterol.

Cholesterol is the main repair substance in the body and thus when there is damage to the arterial wall it will go to try and start the immune response to repair the endothelium. So it has been found in clots and plaque but is it because it caused the problem to begin with, or was it trying to help out? Does it cause the damage or is it a response to damage caused by something else? At the end of the day the whole catalyst for this all happening is oxidized cholesterol carrying lipoproteins becoming lodged in the endiothelial wall. There is debate over whether or not the cholesterol is oxidized prior to penetrating the arterial wall or if it occurs as a result once it is stuck. I do not wish to go in depth on this subject but keep in mind that unsaturated fats oxidize much more easily and if they are forming the majority of the phosopholipids transporting cholesterol they may contribute to more rapid oxidation and degeneration of the cholesterol.

So although we do not know for sure the order of the oxidation process we know that cholesterol penetrates the wall being transported by a lipoprotein. It either helps repair the damage and initiates a healthy immune response, or continues to accumulate and triggers pathological immune responses that can cause build up of plaque. There are different possibilities as to how this lipoprotein carrying mostly LDL gets into the wall to begin with. Lets go back to the traditional lipid-hypothesis once more. "as the cholesterol level in the blood increases, it penetrates the arterial wall and gets stuck; white blood cells circulating in the blood then enter the arterial wall and gobble up the cholesterol; the accumulation of lipid-loaded white blood cells causes local injury, leading to cell death, calcification, and the development of a collagen-laden fibrous cap over the atherosclerotic lesion. When the cap ruptures, the blood clots, blocking the artery and causing a heart attack."

Lets assume for time being that the lipid hypothesis is correct and analyze the very first statement. As the cholesterol level in the blood increases, it penetrates the arterial all. This is referring to blood cholesterol levels, LDL-c in particular. But remember there are different types of LDL. We are only worried about the small and dense LDL particles since they seem to penetrate the wall and oxidize easier and cause the most damage. We also know that serum cholesterol is not nearly as correlated with athersclerosis as the number of LDL particles. A low number of LDL-P doesnt neccessarily mean low levels of LDL-c, but it means most likely they are larger and less damaging carrying more cholesterol per molecule. The graph below was published in the 1981 Framingham followup

Notice how LDL-p usually correlates with LDL-c, hence why we have probably been using it as a marker for years, but doesnt always. Low LDL-p and High LDL-c is almost just as low risk as low-low. In fact for a couple years it was lower risk. An easy analogy to think of blood cholesterol is like a highway. LDL-c could be considered the amount of people on the highway. This is not neccassarily what we are concerned about. If there are a bunch of Surburbans and Expeditions on the highway there may be quite a few people traveling but no congestion or traffic. LDL-p can be thought of as the number of cars on the highway. So if theres an equal amount of people on the highway the one with more cars on the road is more likely to have an "accident." In this case that would be colliding with and damaging the endothelial wall. Low carb diets have been found to reduce LDL-p(50) while diets high in fructose have been shown to increase LDL-p(51).

The actual mechanisms of plaque and clots are very complicated. Basically an artery is damaged and scabs just like any other cut would on your body. When you have a scab on your knee it will eventually just fall off. That can't happen inside your veins or this will cause a clot. Our bodies try to over come this by sucking the scab back into the endothelial wall. Now if whatever is causing the damage is not stopped the body's healing mechanisms will not be able to keep up and a clot will form Now heres where a little disagreement comes in. There are some that disagree and claim that cholesterol is merely responding to damage occurring to the arteries caused by stress, elevated blood sugar and a process called glycation(52). If the underlying cause is not addressed LDL will continue to accumulate leading to the plaque forming process. It's worth noting that the highest risk individuals, ones with low LDL-c and high LDL-p, typically have metabolic syndrome and elevated blood sugar levels. In my opinion it seems that there are a confluence of forces at play and its likely a combination of things. It seems if artery walls are strong they will be less likely to suffer damage from the potentially dangerous LDL-p. Many people on statins have very low LDL but still have heart disease. Perhaps their walls are not as sturdy or they are more prone to a negative inflammatory immune response/ oxidation. This could mean that it takes less LDL-c to cause damage. Conversely maybe having high amounts of LDL-p could cause more potential damaging interactions with the arterial wall.

Question:  Do high levels of blood cholesterol cause heart disease and plaque?

Answer: High levels of blood cholesterol are not the cause of heart disease or plaque even though there is a correlation at times. There are many examples of high rates of heart disease with low LDL and vice versa. The cause of atherosclerosis is a sterol carrying lipoprotein oxidizing withing the endtholilial wall and triggering an immune response that can lead to plaque build up and potential of a clot. There is debate on how it gets there but looking through all the information it doesn't seem plausible to come to the conclusion that cholesterol has a causal effect to heart disease. The correlations with cholesterol are likely to be confounded by a variety of factors that simultaneously increase cholesterol levels and contribute to heart disease, like stress and inflammation. If cholesterol were indeed causal it would be for all populations and genders which it has shown not to be. Only middle aged men have a strong correlation between LDL and death from heart disease. Men over 70, who are the most likely to die out of everyone from CHD, have been shown to have no link between LDL and CHD mortality. It appears most likely that cholesterol is simply a cog in a very complicated and multifaceted process that is atherosclerosis. It is not causal, yet we have made this the target of cholesterol lowering drugs called statins, which we will explore in depth in the next article.


Recommended further reading

If saturated fat does not clog up arteries, what does?- Article from Clare Harding exploring some of the theoretical mechanisms of plaque and atherosclerosis.

What if bad fat isn't so bad?- Great article on menshealth via NBC news that analyzes the history of our diet recommendations and some of the studies that led us here.

The straight dope on cholesterol: 10 things you need to know-(part 1) (part 2)  Very detailed breakdown of what exactly cholesterol is and how it initiates the process of atherosclerosis

High Cholesterol And Heart Disease — Myth or Truth? : Very thorough article from Chris Masterjohn exploring cholesterol and  blood lipids role in heart disease