Category Archives: Heart Health

Olive Oil Shown To Promote Atherosclerosis

Olive OilThe following studies provide evidence for the atherosclerosis-promoting effect of olive oil, in monkeys, mice, and humans:

1. Hepatic Origin of Cholesteryl Oleate in Coronary Artery Atherosclerosis In African Green Monkeys, Enrichment By Dietary Monounsaturated Fat, Journal of Clinical Investigation, 1997

“[We observed in monkeys] that the amount of coronary artery atherosclerosis was similar in the monounsaturated and saturated fat groups, in spite of the significantly improved LDL cholesterol concentration and LDL/HDL cholesterol ratio in the former.”

2. Dietary Monounsaturated Fatty Acids Promote Aortic Atherosclerosis In LDL Receptor–Null, Human ApoB100–Overexpressing Transgenic Mice, Arteriosclerosis, Thrombosis, and Vascular Biology, 1998

Mice were fed one of 6 diets with different fatty acid content: saturated, monounsaturated (cis and trans), polyunsaturated (n-3 and n-6), and a control diet.

“The reduction in aortic atherosclerosis was not found when either cis or trans monounsaturated fatty acids were fed. Rather, just as much atherosclerosis was seen when cis monounsaturated fat diets were fed as when saturated fat was fed, and significantly more atherosclerosis was seen when the trans monounsaturated fatty acids were fed.”

This is an important outcome when one considers that monounsaturated fats, often in the form of olive oil, are widely promoted as being healthful and effective for protection against heart disease.

3. Effect Of Fat And Carbohydrate Consumption On Endothelial Function, Lancet, December, 1999

“Consumption of a meal high in monounsaturated fat was associated with acute impairment of endothelial function when compared with a [low-fat] carbohydrate-rich meal.”

4. The Postprandial Effect Of Components Of The Mediterranean Diet On Endothelial Function, Journal of the American College of Cardiology, November 2000

“Contrary to part of our hypothesis, our study found that omega-9 (oleic acid)-rich olive oil impairs endothelial function postprandially.

The mechanism appears to be oxidative stress because the decrease in FMD was reduced (71%) by the concomitant administration of vitamins C and E. Balsamic vinegar (red wine product) and salad reduced the postprandial impairment in endothelial function to a similar extent (65%).

In a clinical study, olive oil was shown to activate coagulation factor VII to the same extent as does butter (44). Thus, olive oil does not have a clearly beneficial effect on vascular function.”

The major unsaturated fatty acids in olive oil are oleic acid (18:1n-9) and linoleic acid (18:2n-6) (42). A high-oleic and linoleic acid meal has recently been shown to impair FMD in comparison with a low-fat meal (28). (That’s the study above by Ong et al.)

In terms of their effects on postprandial endothelial function, the beneficial components of the Mediterranean and Lyon Diet Heart Study diets appear to be the antioxidant-rich foods—vegetables, fruits … not olive oil. Dietary fruits, vegetables, and their products appear to provide some protection against the direct impairment in endothelial function produced by high-fat foods, including olive oil.”

Clearly, olive oil is not the heart-healthy food it’s made out to be. It truly is a feat of marketing that a food which has been shown over and over to impair artery function exists in peoples’ minds as an elixir. The Mediterranean diet, with its generous portions of fruits, vegetables, and whole grains, improves health not because of olive oil, but in spite of it.

Time Magazine: “Eat Butter”

TimeMagEatButterThe cover of Time Magazine’s next issue is going to say “Eat Butter.” The associated cover story by Bryan Walsh is entitled “Ending The War On Fat.” I haven’t read the article, so I don’t know what he bases his claims on. But I have read thousands of studies in my lifetime, and “eat butter” is not my conclusion. My cover story would read “Don’t Eat Butter.”

Here’s the video that accompanied Time’s story. It’s emceed by Walsh. It’s going to tell you that everything you’ve been led to believe about fat is wrong.  It’s wrong.

Dr. McDougall addressed Time’s upcoming story here. Marion Nestle addressed it here. (Nestle says saturated fat consumption is down, and so are deaths from heart disease.)

There is an abundance of research that implicates consumption of saturated fat in the development of heart disease. I am curious how Walsh will present this. McDougall says that one particular study, paid for by the National Dairy Council, is often cited to justify the “eat butter” proclamation:

Meta-Analysis Of Prospective Cohort Studies Evaluating The Association Of Saturated Fat With Cardiovascular Disease, American Journal of Clinical Nutrition, March 2010

However, that study was taken to task, not least of which by the renowned Dr. Stamler, in the very same issue where the study was published:

Diet-Heart: A Problematic Revisit, Jeremiah Stamler, American Journal of Clinical Nutrition, March 2010

Stamler infers that the authors’ intent was not to clarify the association between fat and heart disease, but to inject doubt.

“… the authors seem to be dissociating themselves from prevailing national and international dietary recommendations to the general population for primordial, primary, and secondary prevention of CHD/CVD and the established major metabolic risk factors. But they are not explicit. Is that their intent?

What are those prevailing recommendations?

“Specifically, do they disagree with the merits of heart-healthy fare on the basis of DASH-, OmniHeart-, Mediterranean-, East Asian–type eating patterns, which emphasize vegetables, fruit, whole grains, legumes/seeds/nuts, fat-free/low-fat dairy products, fish/shellfish, lean poultry, egg whites, seed oils in moderation, alcohol (if desired) in moderation, and portion size/calorie controlled and deemphasize red and processed meats, cheeses, ice cream, egg yolks, cookies/pastries/pies/cakes/other sweets/sweetened beverages, snacks, and salt/commercial foods with added salt. Estimated nutrient composition of this fare is as follows: total fat ≈20–25% of kcal, SFA 6–7%, MUFA 7–9%, PUFA 7–9%, cholesterol <100 mg/1000 kcal, total protein 18–25%, vegetable protein 9–12%, carbohydrate 55–60% (mostly complex), fiber 30–35 g/d, 50–65 mmol Na/d (2900–3770 mg NaCl/d), mineral/vitamin intake high (6). A vast array of concordant multidisciplinary research evidence is the sound foundation for these recommendations.”

Nothing has changed. Don’t eat butter.

Eggs, Dietary Cholesterol, And Heart Disease

Dr. Greger is taking on eggs today (again):

So, do eggs and other sources of dietary cholesterol raise the risk for heart disease? Dr. Greger argues they do.

EggsScrambled2As I’ve come to understand, you have to look at the whole diet. For instance, for a given amount of saturated fat eaten, a given amount of dietary cholesterol (eggs) eaten at the same time will raise serum LDL cholesterol higher than if that dietary cholesterol was paired with a polyunsaturated fat, such as corn oil.1

Also, is any of that dietary cholesterol oxidized? Because if it is (and unless you eat it raw and very close in time to the demise of its source, some of it will be) it will contribute to the development of atherosclerosis and heart disease (and to the growth of cancer, as I just wrote). So says Fred Kummerow, a 98-year-old emeritus professor of comparative biosciences at the University of Illinois:

“Oxidized lipids contribute to heart disease both by increasing deposition of calcium on the arterial wall, a major hallmark of atherosclerosis, and by interrupting blood flow, a major contributor to heart attack and sudden death.”

And Professor Kummerow is of a mind that cholesterol is actually good for your heart! (Fortunately, our bodies manufacture all we need.)

Also, fruits and vegetables contain compounds that act as anti-oxidants, slowing further oxidation of consumed fats. You have to look at the whole diet.

You can’t judge well the effect of a single nutrient outside the context of the whole diet. It’s also risky to generalize the effects you may see of a nutrient in a small and perhaps homogeneous group. Nutrients, like dietary cholesterol, act differently in men vs. women, in old vs, young, in healthy vs. diseased (e.g. diabetes).

What is helpful, in my opinion, is to reflect upon the body of evidence. In this case, it looks like their exists a credible body of evidence to support limiting egg (and other dietary cholesterol) consumption.

1 Hypercholesterolemic Effect Of Dietary Cholesterol In Diets Enriched In Polyunsaturated And Saturated Fat, Atherosclerosis, Thrombosis, and Vascular Biology, 1994

Eskimos’ Fat-Rich Diet Turns Out To Be Really Unhealthy

EskimoDiet2This new review that analyzed the diets and health of Eskimos and Inuits found that all their oily fish, far from being “heart-healthy” was, to use the lead author’s word, “dangerous”:

“Fishing” For The Origins Of The “Eskimos And Heart Disease” Story. Facts Or Wishful Thinking?, Canadian Journal of Cardiology, 14 April 2014

“During the 1970s, two Danish investigators, Bang and Dyerberg, upon being informed that the Greenland Eskimos had a low prevalence of coronary artery disease (CAD) set out to study the diet of this population. Bang and Dyerberg described the “Eskimo diet” as consisting of large amounts of seal and whale blubber (i.e. fats of animal origin) and suggested that this diet was a key factor in the alleged low incidence of CAD. This was the beginning of a proliferation of studies that focused on the cardioprotective effects of the “Eskimo diet”.

In view of data, which accumulated on this topic during the past 40 years, we conducted a review of published literature to examine whether mortality and morbidity due to CAD are indeed lower in Eskimo/Inuit populations compared to their Caucasian counterparts. Most studies found that the Greenland Eskimos as well as the Canadian and Alaskan Inuit have CAD as often as the non-Eskimo populations. Notably, Bang and Dyerberg’s studies from the 1970s did not investigate the prevalence of CAD in this population; however, their reports are still routinely cited as evidence for the cardioprotective effect of the “Eskimo diet”. We discuss the possible motives leading to the misinterpretation of these seminal studies.”

One thing you can say for sure … their diet is not protecting them from heart disease.

The press release:
Investigators Find Something Fishy With Classical Evidence For Dietary Fish Recommendation

Lead investigator George Fodor said:

“Bang and Dyerberg’s seminal studies from the 1970s are routinely invoked as ‘proof’ of low prevalence of CAD in Greenland Eskimos ignoring the fact that these two Danish investigators did not study the prevalence of CAD. Instead, their research focused on the dietary habits of Eskimos and offered only speculation that the high intake of marine fats exerted a protective effect on coronary arteries.”

Not only do Eskimos develop CAD at the same rate as non-Eskimos, but

“[Eskimos] have very high rates of mortality due to cerebrovascular events (strokes). Overall, their life expectancy is approximately 10 years less than the typical Danish population and their overall mortality is twice as high as that of non-Eskimo populations.”

Fodor et al. said the reason CAD prevalence was thought to be less 40 years ago was because Eskimos’ rural lifestyle and inaccessible geography prevented access to medical care which led to inaccurate and incomplete death records.

Dr. Fodor:

“Considering the dismal health status of Eskimos, it is remarkable that instead of labeling their diet as dangerous to health, a hypothesis has been construed that dietary intake of marine fats prevents CAD and reduces atherosclerotic burden.”

Salmon is not a health food.

Study: Marathon Runners Have More Plaque


Jim Fixx in 1980. He died about 4 years after this photo was taken, of a heart attack during his daily run. He was 52. His autopsy revealed considerable plaque build-up.

Shaun sent this study:

Increased Coronary Artery Plaque Volume Among Male Marathon Runners, Missouri Medicine, March/April 2014

Background: This hypothesis, that long-term marathon running is protective against coronary atherosclerosis, was tested by quantitatively assessing coronary artery plaque using high resolution coronary computed tomographic angiography (CCTA) in veteran marathon runners compared to sedentary control subjects.

Methods: Men in the study completed at least one marathon yearly for 25 consecutive years. All study subjects underwent CCTA, 12-lead electrocardiogram, measurement of blood pressure, heart rate, and lipid panel. A sedentary matched group was derived from a contemporaneous CCTA database of asymptomatic healthy individuals.

Results: Male marathon runners (n = 50) as compared with sedentary male controls (n = 23) had increased total plaque volume (200 vs. 126 mm3, p < 0.01), calcified plaque volume (84 vs. 44 mm3, p < 0.0001), and non-calcified plaque volume (116 vs. 82 mm3, p = 0.04).

Conclusion: Long-term male marathon runners may have paradoxically increased coronary artery plaque volume.

How could this be?

“… an emerging body of scientific data suggests that chronic, excessive, high-intensity exercise may induce oxidative stress and myocardial fibrosis, accelerate atherosclerosis, increase vascular wall thickness, and increase cardiac chamber stiffness.”

So, what constitutes excessive? They cited the Copenhagen City Heart Study which followed 1,878 runners and 10,158 non-runners for up to 35 years. It uncovered a U-shaped curve … those who exercised too little and also too much had increased risk for mortality compared to moderate exercisers.

“… the benefits of running were most significant for those who jogged between 1 to 2.5 hours per week, at a slow to moderate pace, with a frequency of about three times per week. In those runners who were performing higher volume, higher intensity running, the long-term mortality rates were not significantly different from non-runners. In other words, excessive running may have abolished the remarkable improvements in longevity conferred by lower doses of running.”

One hour a week is less than 10 minutes a day. At a slow to moderate pace. That was the best for health and longevity.  Wow.

It looks like running itself may damage blood vessels. But what about diet? You’ll note that both the marathoners and sedentary men had elevated LDL cholesterol (sedentary: 108 mg/dl, marathoners: 112), and, some would say, elevated total cholesterol (sedentary: 183 mg/dl, marathoners 186).  All that running may have been whittling away their weight, but it wasn’t whittling away their cholesterol.

As Dr. Esselstyn famously showed,1 cholesterol is strongly impacted by diet:

“After 5 years on Dr. Esselstyn’s plant-based diet, the average total cholesterol levels of his research group dropped from 246 milligrams per deciliter to 137 mg/dL This is the most profound drop in cholesterol ever documented in the medical literature in a study of this type.”

The Wall Street Journal covered this study and similar ones in Why Runners Can’t Eat Whatever They Want, Studies Show There Are Heart Risks to Devil-May-Care Diets—No Matter How Much You Run, and included this quote from the editor of Runner’s World:

“Ambrose Burfoot, winner of the 1968 Boston Marathon and editor-at-large of Runner’s World magazine, is 67 years old, 6 feet tall and only 147 pounds. A lifelong vegetarian, he subsists mostly on fruits, vegetables and nuts, though he also eats “cookies and all dairy products—cheeses, ice creams etc.,” he wrote in an email.

“Last March I learned that I have a very high coronary calcium,” he said.”

I know several vegetarians with high cholesterol, over 200 mg/dl. A good chunk of their calories come from animal foods – eggs, butter, cheese, yogurt, and other dairy products. “I have to get my protein,” they tell me. Dr. Esselstyn found that when his patients dropped the dairy, their cholesterol dropped along with it.

It may very well be, as Shaun says, that you can’t run from your diet.

By the way, the technology used to measure plaque, coronary computed tomographic angiography (CCTA), was referred to as “noninvasive.” Not true. All radiation is invasive. This report by the National Academies Press says that all ionizing radiation damages cells. There is no level of exposure below which damage to a cell does not occur.

1Prevent and Reverse Heart Disease, January 2008

Today’s Study On The Risks Of Consuming Saturated Fat

Butter and knifeComparison Of Predictive Performance Of Various Fatty Acids For The Risk Of Cardiovascular Disease Events And All-cause Deaths In A Community-based Cohort, Atherosclerosis, September, 2013

This was a prospective study from Taiwan, 1833 men and women (average age 60) were followed for about 10 years. The relative risk (RR) of death in the highest quartile compared with the lowest quartile (of fatty acids in their blood) was:

1.33 for saturated fats (95% confidence interval [CI], 1.01–1.75, test for trend, P = 0.015)
1.71 for trans fats (95% CI, 1.27–2.31, test for trend, P = 0.0003)
0.77 for EPA (95% CI, 0.59–1.00, test for trend, P = 0.048)
0.89 for DHA (95% CI, 0.68–1.18, test for trend, P = 0.354)

Note that there was a higher risk of death for only saturated fats and trans fats (the RR was above 1.00). Note also that even though the RR was below 1.00, that is, appeared to show protection for the omega-3 fatty acids EPA and DHA, it did not rise to a level of significance, especially for DHA.

“CONCLUSIONS: Our data provides strong evidence to support that plasma saturated fats and trans fats can predict all-cause death and CVD [cardiovascular disease] more effectively than other fatty acid markers.”

That Saturated Fat Study: Harvard Responds


Walter Willett, MD, Dr. PH

Harvard posted Dr. Willett and colleagues’ response to the dietary fat study I’ve been posting about (here and here). Dr. Willett is chair of the Department of Nutrition at Harvard School of Public Health.

Dietary Fat And Heart Disease Study Is Seriously Misleading, Harvard School of Public Health, 19 March 2014

The journal Annals of Internal Medicine recently published a paper suggesting there is no evidence supporting the longstanding recommendation to limit saturated fat consumption. Media reporting on the paper included headlines such as “No link found between saturated fat and heart disease” and articles saying “Saturated fat shouldn’t be demonized” springing up on social media.

Dr. Willett emphasized that because this meta-analysis contains multiple serious errors and omissions, the study conclusions are misleading and should be disregarded.

Here’s Harvard’s official response as it appears on the Annals of Internal Medicine website:

The meta-analysis of dietary fatty acids and risk of coronary heart disease by Chowdhury et al. (1) contains multiple errors and omissions, and the conclusions are seriously misleading, particularly the lack of association with N-6 polyunsaturated fat. For example, two of the six studies included in the analysis of N-6 polyunsaturated fat were wrong. The relative risks for Nurses’ Health Study (NHS) (2) and Kuopio Ischemic Heart Disease Study (KIHD) (3) were retrieved incorrectly and said to be above 1.0. However, in the 20-year follow-up of the NHS the relative risk for highest vs lowest quintile was 0.77 (95 percent CI: 0.62, 0.95); ptrend = 0.01 (the authors seem to have used the RR for N-3 alpha-linolenic acid from a paper on sudden cardiac death), and in the KIHD the relative risk was 0.39; 95% confidence interval [CI], 0.21-0.71) (the origin of the number used in the meta-analysis is unclear). Also, relevant data from other studies were not included (4 and 5).

Further, the authors did not mention a pooled analysis (6) of the primary data from prospective studies, in which a significant inverse association between intake of polyunsaturated fat (the large majority being the N-6 linoleic acid) and risk of CHD was found. Also, in this analysis, substitution of polyunsaturated fat for saturated fat was associated with lower risk of CHD. Chowdhury et al. also failed to point out that most of the monounsaturated fat consumed in their studies was from red meat and dairy sources, and the findings do not necessarily apply to consumption in the form of nuts, olive oil, and other plant sources. Thus, the conclusions of Chowdhury et al. regarding the type of fat being unimportant are seriously misleading and should be disregarded.


Walter Willett
Frank Sacks
Meir Stampfer

Harvard University

1. Chowdhury R, Warnakula S, Kunutsor S, et al. Association of dietary, circulating, and supplement fatty acids with coronary risk. Ann Intern Med 2014; 160(6):398-406.
2. Oh K, Hu FB, Manson JE, Stampfer MJ, Willett WC. Dietary fat intake and risk of coronary heart disease in women: 20 years of follow-up of the Nurses’ Health Study. Am J Epidemiol 2005;161:672-9.
3. Laaksonen DE, Nyyssonen K, Niskanen L, Rissanen TH, Salonen JT. Prediction of cardiovascular mortality in middle aged men by dietary and serum linoleic and polyunsaturated fatty acids. Arch Intern Med 2005;165:193-199.
4. de Goede J, Geleijnse JM, Boer JM, Kromhout D, Verschuren WM. Linoleic acid intake, plasma cholesterol and 10-year incidence of CHD in 20,000 middle-aged men and women in the Netherlands. Br J Nutr 2012;107:1070-6.
5. Dolecek TA. Epidemiological evidence of relationships between dietary polyunsaturated fatty acids and mortality in the multiple risk factor intervention trial. Proc Soc Exp Biol Med 1992;200:177-82.
6. Jakobsen MU, O’Reilly EJ, Heitmann BL, Pereira MA, Bälter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman D, Stevens J, Virtamo J, Willett WC, Ascherio A. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr 2009:1425-32.

After reading this, I am curious how this study in the Annals withstood peer review.

When people think “carbohydrates,” do they think … carrots and apples? Do they think beans and lentils? Or do they think highly processed, white-flour-white-sugar breads, boxed breakfast cereals, bagels, pretzels, crackers, cookies, cakes, muffins? If you are cutting back on fat, especially saturated fat, you will, by default, be eating more carbohydrates. It is the former (carrots, apples, beans, lentils, corn, peas, oats, yams, squash) where carbs should ideally be coming from, not the latter. The former is the essence of a whole food, plant-based diet.

That Saturated Fat Study

One more comment about the fatty acid study I posted about a few days ago, the one that found no difference in cardiovascular disease (CVD) risk between those who ate the most vs. those who ate the least saturated fat:

Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis, Annals of Internal Medicine, 18 March 2014

One way you can arrive at all your groups showing similar risk, which this study found, is when there isn’t much difference in consumption among your comparison groups. Or when most of your participants are consuming saturated fat above a threshold where risk for CVD increases.

About this meta-analysis, Jeff Novick writes:

“One major problem with this study is they did not look at any studies where the saturated fat intake was less than 7%, which is the level recommended by the [American Heart Association]. … Most of the diets had saturated fat intakes in the range of 10-15% (or more).”

7% is a lot of saturated fat. If someone was eating 2000 calories a day, 7% is about 16 grams of saturated fat. For relativity’s sake, there are 2 grams of saturated fat in a 3 ounce serving of beef chuck. One chicken thigh, just 2 ounces, has 3 grams of saturated fat.

Does reducing saturated fat below 7%, what you would find in a whole food, plant-based (WFPB) diet, reduce CVD risk? This study couldn’t say.

Here’s a study that found replacing saturated fat with polyunsaturated fat reduced risk for heart attack.  (Saturated fat comes primarily from animals – meat and dairy. Polyunsaturated fat comes primarily from plants.)

Effects On Coronary Heart Disease Of Increasing Polyunsaturated Fat In Place Of Saturated Fat: A Systematic Review And Meta-analysis Of Randomized Controlled Trials, PLOS Medicine, March 2010

“Conclusions: These findings provide evidence that consuming PUFA in place of SFA reduces CHD events in RCTs.”*

Here’s the press release: Replacing Those Saturated Fats, Harvard, March 2010

“But a new study by researchers at Harvard School of Public Health (HSPH) provides the first conclusive evidence from randomized clinical trials that people who replace saturated fat in their diet with polyunsaturated fat reduce their risk of coronary heart disease by 19 percent, compared with control groups of people who do not.”

For every 5 percent increase (measured as total energy) in polyunsaturated fat consumption, coronary heart disease risk was reduced by 10 percent.

Remember this? “Give that chicken fat back to the chicken!”

* PUFA: Polyunsaturated Fatty Acids
SFA: Saturated Fatty Acids
CHD: Coronary Heart Disease
RCT: Randomized Controlled Trials