Advanced Mediterranean Diet

Women double their risk of developing coronary heart disease if they have high consumption of carbohydrates, according to research recently published in the Archives of Internal Medicine. 

Men’s hearts, however, didn’t seem to be affected by carb consumption. I mention this crucial sex difference because many experts believe that replacing saturated fat with carbohydrates is a major cause of heart disease.  If true, it seems to apply only to women.

[Another nutrition science trend to keep an eye on is the thought that excessive consumption of omega-6 fats contributes to hardening of the arteries, including coronary heart disease.  I’m talking about soy oil, safflower oil, corn oil, among others.  No doubt, we’re eating a lot more omega-6 now than at the start of the 20th century.]

We’ve known for a while that high-glycemic-index eating was linked to heart disease in women but not men.  Glycemic index is a measure of how much effect a carbohydrate-containing food has on blood glucose levels.  High-glycemic-index foods raise blood sugar higher and for longer duration in the bloodstream.

High-glycemic-index foods include potatoes and white bread, for example.

The study at hand included over 47,000 Italians who were interrogated via questionnaire as to their food intake, then onset of coronary heart disease—the cause of heart attacks—was measured over the next eight years. 

Among the 32,500 women, 158 new cases of coronary heart disease were found.

Researchers doing this sort of study typically compare the people eating the least carbs with those eating the most. The highest quartile of carb consumers and glycemic load had twice the rate of heart disease compared to the lowest     quartile. 

The Cleave-Yudkin theory of the mid-20th century proposed that excessive amounts of refined carbohydrates cause heart disease and certain other chronic systemic diseases.  Gary Taubes has also written extensively about this.  The research results at hand support that theory in women, but not in men. 

Practical Applications

Do these research results apply to non-Italian women and men?  Probably to some, but not all.  More research is needed.

Women with a family history coronary heart disease—or other CHD risk factors—might be well-advised to put a limit on total carbs, high-glycemic-index foods, and glycemic load.  I’d stay out of that “highest quartile.”  Don’t forget: heart disease is the No. 1 killer of women.

See NutritionData’s Glycemic Index page for information you can apply today.

FYI, the Low-Carb Mediterranean Diet  and Ketogenic Mediterranean Diet are also low in glycemic index.

Steve Parker, M.D.

Disclaimer:  All matters regarding your health require supervision by a personal physician or other appropriate health professional familiar with your current health status.  Always consult your personal physician before making any dietary or exercise changes.

 Update May 28, 2011: Alert reader Nadia Hassan brought to my attention that I had originally written that pasta has a high glycemic index.  Citing appropriate references, Nadia convinced me that pasta has a low-to-moderate glycemic index, from around 30 to 60.  Its GI also is higher if over-cooked.  Today I corrected my original post. 

References: 

Sieri, Sabina, et al. Dietary glycemic load and index and risk of coronary heart disease in a large Italian cohort.  The EPICOR study.  Archives of Internal Medicine, 170 (2010): 640-647.

Barclay, Alan, et al.  Glycemic index, glycemic load, and chronic disease risk - a meta-analysis of observational studies [of mostly women].  American Journal of Clinical Nutrition, 87 (2008): 627-637.

The higher the consumption of saturated fat, the lower the risk of death from stroke, according to Japanese researchers in a recent American Journal of Clinical Nutrition. 

Most physicians in the West would have predicted the opposite: saturated fats increase your risk of stroke.  Western physicians tend to think most strokes and heart attacks are caused by the same process, atherosclerosis, and would be aggravated by saturated fat consumption.  We’re learning that ain’t necessarily so.

Most strokes in the Western world are thought to be linked to atherosclerosis (hardening of the arteries) of relatively large arteries. In Japan, most strokes not caused by bleeding in the head are actually lacunar infarctions involving small arteries in the brain, not necessarily involving atherosclerosis. 

Another major difference between East and West is that saturated fat consumption in Japan is far lower than in the West.

Are you confused yet?

It seems to me that comparing strokes in Japan versus the West is comparing apples to oranges.  The take-away point to me is that we have to be quite wary of generalizing the research results applicable to one culture or ethnic group, to others.

Steve Parker, M.D.

Reference: Yamagishi, K., Iso, H., Yatsuya, H., Tanabe, N., Date, C., Kikuchi, S., Yamamoto, A., Inaba, Y., Tamakoshi, A., & , . (2010). Dietary intake of saturated fatty acids and mortality from cardiovascular disease in Japanese: the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC) Study American Journal of Clinical Nutrition, 92 (4), 759-765 DOI: 10.3945/ajcn.2009.29146

To reduce coronary heart disease, we need to focus on reducing consumption of refined carbohydrates rather than fat and cholesterol, according to Dr. Frank Hu.

Dr. Hu is not a wild-eyed, bomb-throwing radical. He’s a Harvard professor of nutrition and epidemiology with both M.D. and Ph.D. degrees.  High-glycemic-index carbs in particular are the bad boys, he writes in an editorial published in the American Journal of Clinical Nutrition earlier this year.

Additional details are at my April 26, 2010, post at the Self/NutritionData Heart Health Blog.

Steve Parker, M.D.

The current issue of the American Journal of Clinical Nutrition includes a meta-analysis of 21 published studies that address whether saturated fat in our diets causes heart attacks and strokes. 

Bottom line?  The accusations against saturated fat are false.

Here’s the authors’ summary:

A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of coronary heart diseases or cardiovascular disease. 

I’m not aware of any new studies examining this issue, so the authors likely have re-hashed old studies as others have done.

What’s newsworthy is that this watershed science is published in one of the premier nutrition journals. 

Next thing you know, AJCN may review Gary Taubes’ 2007 magnum opus, Good Calories, Bad Calories.

Steve Parker, M.D.

Reference:  Siri-Tarino, Patty, et al.  Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.  American Journal of Clinical Nutrition, January 13, 2010. doi:10.3945/ajcn.2009.27725

Here’s my  review of good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease, by Gary Taubes, 2007.  I give it five stars on Amazon.com’s five-star system (”I love it”).

♦   ♦   ♦

This brilliant book deserves much wider currency among physicians, dietitians, nutritionists, and obesity researchers.  The epidemic of overweight and obesity over the last 30 years should make us question the reigning theories of obesity treatment and prevention.  Taubes questioned those theories and pursued answers wherever the evidence led.  He shares in GCBC his eye-opening, even radical, well-reasoned findings. 

Ultimately, this tome is an indictment of the reigning scientific community and public nutrition policy-makers of the last four decades.  That explains why, two years after publication, this serious, scholarly work has not been reviewed by the New England Journal of Medicine, the Journal of the American Medical Association, the American Journal of Clinical Nutrition , and the Journal of the American Dietetic Association (as of August, 2009).

In Part 1, Taubes examines the scientific evidence for what he calls the fat-cholesterol hypothesis.  More commonly known as the diet-heart hypothesis, it’s the idea that dietary fat (especially saturated fat) and cholesterol clog heart arteries, causing heart attacks.  Taubes finds the evidence unconvincing.  He’s probably right.

Part 2, The Carbohydrate Hypothesis, revives and older theory from the mid-twentieth cenury that is elsewhere called the Cleave-Yudkin carbohydrate theory of dental and chronic systemic disease.  In the carbohydrate theory,  high intake of sugary foods, starches, and refined carbohyrates leads first to dental disease (cavities, gum inflammation, periodontal disease) then, later, to obesity and type 2 diabetes, coronary heart disease, perhaps even cancer and Alzheimer’s Disease.  These are, collectively, the “diseases of civilization.”

Part 3 tackles obesity and weight regulation.  Taubes writes that “…fattening and obesity are caused by an imbalance—a dysequilibirium—in the hormonal regulation of adipose [fat] tissue and fat metabolism.”  Think of the transformation of a skinny 10-year-old girl into a voluptuous young woman.  It’s not over-eating that leads to curvaceous fat deposits, growth of mammary tissue, and increase in height; it’s hormonal changes beyond her control. 

The primary hormonal regulator of fat storage is insulin, per Taubes.  Elevated insulin levels lead to storage of food energy as fat.  Carbohydrates stimulate insulin secretion and make us fat. 

Although it’s a brilliant book, by no means do I agree with all Taubes’ conclusions.  For instance, if carbohydrates cause heart disease, why is glycemic index only very weakly associated with coronary heart disease in men?  It’s way too early to blame cancer and Alzheimers on carbohydrates.  Primitive cultures may not exhibit many of the diseases of civilization because their members die too young.  Taubes is clearly an advocate of low-carb eating.  Why didn’t he directly address the evidence that fruits, vegetables, and whole grains in the right amounts are healthy?

I have to give Taubes credit for thinking “outside the box.”  His search for answers included reviews of esoteric literature and interviews with scientists in the fields of genetics, athropology, public policy, physiologic psychology, and paleontology, to name a few.

Towards the end of the book, Taubes describes a Mediterranean-style or “prudent” diet that is popular these days.  After five years of research for his book, he says that whether a very low-carb meat diet is healthier than a prudent diet “… is still anybody’s guess.”  It’s hard for me to put aside numerous observational studies associating health benefits with legumes, fruits, vegetables, and whole grains.  So my “guess” is that the Mediterranean-style diet is healthier.  Perhaps the answer is different for each individual.  Heck, maybe the answer is low-carb Mediterranean.  Both Taubes and I are prepared to accept either result when we have proof-positive data.    

Taubes doesn’t base his opinions on late-breaking scientific results.  Instead, his research findings mostly span from 1930 to 1980, especially 1940 to 1960.  Once the fat-cholesterol (diet-heart) hypothesis took root around 1960 and blossomed in the 1970s, these data were ignored by the entrenched academics and policy-makers of the day. 

To be fair, I’ve got to mention this is not light reading.  A majority of people never read another book after they graduate high school.  Of those who do, many (like me) will have to look up the definition of “tautology,” “solecism,” etc. 

I was taught in medical school years ago that “a calorie is a calorie is a calorie.”  Meaning: if you want to lose excess weight, it doesn’t matter if you cut calories from fat, protein, or carbohydrates.  I really wonder about that now.

Steve Parker, M.D 

Additional Reading

Bray, George A.  Viewpoint: Good Calories, Bad Calories by Gary Taubes.  Obesity Reviews, 9 (2008): 251-263.

Taubes, Gary.  Letter to Editor: Response to Dr. George Bray’s review of Good Calories, Bad Calories.  Obesity Reviews, 10 (2008): 96-98.

Despite popular belief, dietary fat - whether saturated or not - is not associated with higher risk of death or illnesss from coronary heart disease, according to a study just published in Annals of Nutrition and Metabolism.  The exception is trans fatty acids.

This is yet another challenge to the Diet-Heart Hypothesis.

New Zealand researchers re-examined all the high-quality science regarding the effect of dietary fats on coronary artery disease, the leading cause of death in the developed world.  Atherosclerosis in the heart arteries causes chest pain (angina), heart failure, heart attacks, and death.

Note the major findings of this meta-analysis:

• total fat intake is not associated with coronary artery disease (at fat intake ranges between 27 and 47% of total energy)
• higher trans fatty acid intake is linked to higher cardiac events and deaths
• saturated fatty acid consumption is not associated with heart deaths or events (within the range of 9-20% of total energy from saturated fat)
• data on polyunsaturated fatty acids and heart disease are “inconsistent and unreliable”
• monunsaturated fatty acid intake was not associated with heart disease (in the range of 13-20% of total energy from MUFA)
• higher omega-3 fatty acid intake (from fish, or fish oil supplements) is linked to lower risk of heart disease, although the data are not as strong as the authors would like  

With the exception of omega-3 fats and trans fats, the researchers report, “The available evidence from cohort and randomized controlled trials is unsatisfactory and unreliable to make judgment about and substantiate the effects of dietary fat on risk of CHD [coronary heart disease].”

But they have made a judgement: Saturated and total fats are not related to heart disease.

In an interesting post-script, the authors mention “Expert Consultation,” which sounds like an oversight panel.  This committee apparently insisted on modification of the article to the effect that “replacing saturated fat with polyunsaturated fat reduces CHD [coronary heart diseases] risk.”  Reading between the lines, I suspect that was a hard pill for the authors to swallow.

Steve Parker, M.D.

Reference:  Skeaff, C. Murray and Miller, Jody.  Dietary fat and coronary heart disease: Summary of evidence from prospective cohort and randomised controlled trials.  Annals of Nutrition and Metabolism, 55 (2009): 173-201. Available free online September 15, 2009.

A low-carb, high-protein diet is associated with worse atherosclerosis,  at least in lab mice genetically predisposed to atherosclerosis.  It’s entirely unclear whether these findings apply to humans.

Researchers used a strain of lab mice that can develop atherosclerosis within months rather than the 20-30 years necessary for development in humans.  If the mouse model of atherosclerosis were identical to the human model, research with applicability to humans would be so much easier.  Investigators compared mice fed either a “Western” type diet or a low-carb, high-protein diet.  Both diets had about 43% of calories derived from fat.

One persistent criticism of Atkins-style diets is that they may contribute to human atherosclerosis via the saturated fats in animal sources of protein.  We don’t have a definite answer to that issue.  Even if the Diet-Heart Hypothesis is wrong, an Atkins-style diet could still cause or prevent atherosclerosis - or other illnesses for that matter - through mechanisms as yet unknown. 

After seriously questioning the Diet-Heart Hypothesis, I’m seeing very low-carb eating in a much more favorable light, at least for overweight people. 

HeartWire has a balanced article on the recent research, with quotes from Drs. Eric Westman and Jeff Volick, low-carb advocates.

Steve Parker, M.D.

Reference:  Busko, Marlene.  Atherosclerosis heightened in mice fed low-carb, high-protein diet.  HeartWire, August 26, 2009.

Dentists are considering a return to an old theory that dietary carbohydrates first cause dental diseases, then certain systemic chronic diseases, according to a review in the June 1, 2009, Journal of Dental Research. 

We’ve known for years that some dental and systemic diseases are associated with each other, both for individuals and populations.  For example, gingivitis and periodontal disease are associated with type 2 diabetes and coronary heart disease.  The exact nature of that association is not clear.  In the 1990s it seemed that infections - chlamydia, for example - might be the unifying link, but this has not been supported by subsequent research.     

The article is written by Dr. Philippe P. Hujoel, who has been active in dental research for decades and is affiliated with the University of Washington (Seattle).  He is no bomb-throwing, crazed, radical. 

The “old theory” to which I referred is the Cleave-Yudkin idea from the 1960s and ’70s that excessive intake of fermentable carbohydrates, in the absence of good dental care, leads both to certain dental diseases - caries (cavities), periodontal disease, certain oral cancers, and leukoplakia - and to some common systemic chronic non-communicable diseases such as coronary heart disease, type 2 diabetes, some cancers, and dementia.  In other words, dietary carbohydrates cause both dental and systemic diseases - not all cases of those diseases, of course, but some.   

Dr. Hujoel does not define “fermentable” carbohydrates in the article.  My American Heritage Dictionary defines fermentation as:

1. the anaerobic conversion of sugar to carbon dioxide and alcohol by yeast
2. any of a group of chemical reactions induced by living or nonliving ferments that split complex organic compunds into relatively simple substances

As reported in David Mendosa’s blog at MyDiabetesCentral.com, Dr. Hujoel said, “Non-fermentable carbohydrates are fibers.”  Dr. Hujoel also shared some personal tidbits there. 

In the context of excessive carbohydrate intake, the article frequently mentions sugar, refined carbs, and high-glycemic-index carbs.  Dental effects of excessive carb intake can appear within weeks or months, whereas the sysemtic effects may take decades. 

Hujoel compares and contrasts Ancel Keys’ Diet-Heart/Lipid Hypothesis with the Cleave-Yudkin Carbohydrate Theory.  In Dr. Hujoel’s view, the latest research data favor the Carbohydrate Theory as an explanation of many cases of the aforementioned dental and systemic chronic diseases.  If correct, the theory has important implications for prevention of dental and systemic diseases: namely, dietary carbohydrate restriction.

Adherents of the paleo diet and low-carb diets will love this article; it supports their choices.

I agree with Dr. Hujoel that we need a long-term prospective trial of serious low-carb eating versus the standard American high-carb diet.  Take 20,000 people, randomize them to one of the two diets, follow their dental and systemic health over 15-30 years, then compare the two groups.  Problem is, I’m not sure it can be done.  It’s hard enough for most people to follow a low-carb diet for four months.  And I’m asking for 30 years?!   

Dr. Hujoel writes:

Possibly, when it comes to fermentable carbohydrates, teeth would then become to the medical and dental professionals what they have always been for paleoanthropologists: “extremely informative about age, sex, diet, health.”

Dr. Hujoel mentioned a review of six studies that showed a 30% reduction in gingivitis score by following a diet moderately reduced in carbs.  He mentions the aphorism: “no carbohydrates, no caries.”  Anyone prone to dental caries or ongoing periodontal disease should do further research to see if switching to low-carb eating might improve the situation. 

Don’t be surprised if your dentist isn’t very familiar with the concept.  Has he ever mentioned it to you?

Steve Parker, M.D.,

author of The Advanced Mediterranean Diet and the Diabetic Mediterranean Diet blog

Reference:  Hujoel, P.  Dietary carbohydrates and dental-systemic diseases.  Journal of Dental Research, 88 (2009): 490-502.

Mendosa, David.  Our dental alarm bell.  MyDiabetesCentral.com, July 12, 2009.

I’ve been thinking a lot lately about saturated fats.  Weird, huh?

The American Heart Association recommends that Americans limit the amount of saturated fats they eat to less than 7 percent of total daily calories.  If you eat 2,000 calories a day, no more than 140 of them should come from saturated fats.  That’s about 16 grams of saturated fats.

In over two decades of clinical practice, I’ve never run across a patient willing to do that calculation.  Not many physicians could tell you the “seven percent rule.”

One of the two major themes of Gary Taubes’ book, Good Calories, Bad Calories, is that dietary saturated fats are not particularly harmful to our health, if at all.  From what I’ve been taught, this is sacrilegious.  “Saturated fats are a major cause of heart disease and strokes,” I’ve heard and read over and over.  In brief, this is the Diet-Heart Hypothesis or the “lipid hypothesis”: Dietary saturated fat, total fat, and cholesterol are directly related to coronary heart disease and other forms of atherosclerosis.

In his review of Taubes’ book, Dr. George Bray didn’t even address Taubes’ point about saturated fats, writing instead, “read and decide for yourself.”

That started me thinking either that the Diet-Heart Hypothesis is indefensible or that Dr. Bray is lazy.  I don’t think he’s lazy.  Dr. Bray is a Grand High Pooh-Bah in the fields of obesity and nutrition.

The American Heart Association in 1957 recommended that polyunsaturated fats replace saturated fats. 

U.S. public health recommendations in 1977 were to reduce fat intake to 30% of total calories to lower the risk of coronary heart disease.  Slowly, some fats were replaced mostly with carbohydrates, highly refined ones at that.  This shift tends to raise triglycerides and lower HDL cholesterol levels, which may themselves contribute to atherosclerosis.  Current recommendations are, essentially, to keep saturated fatty acids as low as possible.

One concern about substituting carbohydrates for fats is that blood sugar levels rise, leading to insulin release from the pancreas, in turn promoting growth of fat tissue and potentially leading to weight gain.  Some believe that the public health recommendation to reduce total fat (which led to higher carbohydrate intake) is the reason for the dramatic rise in overweight and diabetes we’ve seen over the last 30 years.

Note that if intake of saturated fats is inadequate, our bodies can make the saturated fats it needs from carbohydrates.  These are generally the same saturated fats that are present in dietary fats of animal origin.  The only exceptions are the two essential fatty acids:  alpha-linolenic acid and linoleic acid.

Why would saturated fats be harmful?  Apparently because they raise blood levels of cholesterol (including LDL cholesterol - “bad cholesterol”), which is thought to be a cause of atherosclerosis, which increases the risk of coronary heart disease and stroke.  I don’t recall seeing any mention of a direct toxic effect of saturated fats (or fatty acids) on arterial walls, where the rubber meets the road.  [Saturated fats are broken down in the small intestine to glycerol and fatty acids.]

Dietary saturated fats also raise HDL cholesterol - “good cholesterol” - although not to the degree they raise LDL.

Let’s not forget many other factors that cause, contribute to, or predict coronary heart disease and atherosclerosis: smoking, family history, high blood pressure, obesity, diabetes, oxidative stress, homocysteine, systemic inflammation, high-glycemic index diets, C-reactive protein, lack of exercise, and others.  I discussed dietary factors in my April 14, 2009, blog post.

Often overlooked in discussion of dietary fat effects is the great variability of response to fats among individuals.  Response can depend on genetics, sex, fitness level, overweight or not, types of carbohydrates eaten, amount of total dietary fat, etc.  And not all saturated fats affect cholesterol levels.

Many of the journal articles listed as references below support the idea that the link between dietary saturated fats and coronary heart disease is not strong, and may be nonexistent.  Read them and you will find that:

• Some studies show no association between dietary saturated fats and coronary heart disease.
• Some studies associate lower rates of coronary heart disease with higher saturated fat intake.
• Higher saturated fat intake was associated with less progression of coronary atherosclerosis in women.
• Lowering saturated fat intake did not reduce total or coronary heart disease mortality.

“Read and decide for yourself,” indeed.  I think you’ll begin to question the reigning dogma.

For example, here’s a conclusion from the Hooper article (from 2001):

In this review we have tried to separate out whether changes in individual fatty acid fractions are responsible for any benefits to health (using the technique of meta-regression). The answers are not definitive, the data being too sparse to be convincing. We are left with a suggestion that less total fat or less of any individual fatty acid fraction in the diet is beneficial.

And a conclusion of the J.B. German article:

At this time [2004], research on how specific saturated fatty acids contribute to coronary artery disease and on the role each specific saturated fatty acid play in other health outcomes is not sufficient to make global recommendations for all persons to remove saturated fats from their diet.  No randomized clinical trials of low-fat diets or low-saturated fat diets of sufficient duration have been carried out; thus, there is a lack of knowledge of how low saturated fat intake can be without the risk of potentially deleterious health outcomes.

Zarraga and Schwartz (2006) conclude:

Numerous studies have been conducted to help provide dietary recommendations for optimal cardiovascular health.  The most compelling data appear to come from trials that tested diets rich in fruits, vegetables, MUFAs [monounsaturated fatty acids], and PUFAs [polyunsaturated fatty acids], particularly the n-3 PUFAs.  In addition, some degree of balance among various food groups appears to be a more sustainable behavioral practice than extreme restriction of a particular food group.

Here’s another of my favorite quotes on this topic, from the J.B. German article:

If saturated fatty acids were of no value or were harmful to humans, evolution would probably not have established within the mammary gland the means to produce saturated fatty acids . . . that provide a source of nourishment to ensure the growth , development, and survival of mammalian offspring.

Take-Home Points

The connection between dietary saturated fat and coronary heart disease is weak. 

[I may be excommunicated from the medical community for this.  You won’t hear it from most physicians or dietitians.  They don’t have time to spend 80 hours on this topic, so they stick with the party line.  And maybe I’m wrong anyway.]

The scientific community is slowly moving away from the original Diet-Heart/Lipid Hypothesis.  It is being replaced with stronger anti-atherosclerosis theories that promote:

• fruit and vegetable intake
• whole grain intake
• low-glycemic index eating
• increased consumption of plant oils and fish
• moderate intake of nuts
• ? moderate intake of low-fat diary (e.g., DASH diet) [less consensus on this point]

So, saturated fats and dietary cholesterol are being crowded out of the picture, or ignored.  In many cases, saturated fats have literally been replaced by poly- and monounsaturated fats (plant oils).  Several clinical studies indicate that’s a healthy change, but it may be related more to the healthfulness of the plant oils than to detrimental effects of saturated fats.

The original Diet-Heart Hypothesis won’t die until the American Heart Association and U.S. public health agencies put a gun to its head and pull the trigger.  That will take another 10 years or more.

If you want to hedge your bets, go ahead and limit your saturated fat intake.  It probably won’t hurt you.  It might help a wee bit.  By the same token, I’m not going on an all-meat and cheese, ultra-high-saturated fat diet; I don’t want to miss out on the healthy effects of fruits, vegetables, whole grains, fish, nuts, and low-glycemic index carbohydrates.  Some would throw red wine into the mix.  This “prudent diet” reflects what I hereby christen The 21st Century Diet-Heart Hypothesis. 

If you’re worried about coronary heart disease and atherosclerosis, spend less time counting saturated fat grams, and more time on other risk-reducing factors: diet modification as above, get regular exercise, control your blood pressure, achieve a healthy weight, and don’t smoke.  More bang for the buck.

What do you think?

Steve Parker, M.D.

Disclaimer:  All matters regarding your health require supervision by a personal physician or other appropriate health professional familiar with your current health status.  Always consult your personal physician before making any dietary or exercise changes.

Selected References Contradicting or Questioning the Diet-Heart Hypothesis (updated February 17, 2012):

Astrup, A., et al (including Ronald Krause, Frank Hu, and Walter Willett).  The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010.  American Journal of Clinical Nutrition, 93 (2011): 684-688.

[The authors believe that replacing saturated fats with polyunsaturated fats (but not carbohydrates) can reduce the risk of coronary heart disease (CHD).  For the last four decades, low-fat diets replaced fat with carbohydates. So they believe saturated fatty acids cause CHD or polyunsaturated fatty acids prevent it.  I see no mention of total fat intake in this article written by major names in nutritional epidemiology and lipid metabolism. “In countries following a Western diet, replacing 1% of energy intake from saturated fatty acids with polyunsaturated fatty acids has been associated with a 2–3% reduction in the incidence of CHD.” “Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total saturated fatty acids because individual saturated fatty acids may have different cardiovascular effects and major saturated fatty acid food sources contain other constituents that could influence coronary heart disease risk.”]

A Feb. 19, 2012,  press release from the Harvard School of Public Health covered much of the same ground.  It’s titled “Time to Stop Talking About Low-Fat, say HSPH Nutrition Experts.”

Siri-Tarino, Patty, et al.  Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.  American Journal of Clinical Nutrition, January 13, 2010. doi:10.3945/ajcn.2009.27725

Skeaff, C. Murray and Miller, Jody.  Dietary fat and coronary heart disease: Summary of evidence from prospective cohort and randomised controlled trials.  Annals of Nutrition and Metabolism, 55 (2009): 173-201.

Halton, Thomas, et al.  Low-carbohydrate-diet score and the risk of coronary heart disease in women.  New England Journal of Medicine, 355 (2006): 1,991-2,002.

German, J. Bruce, and Dillard, Cora J.  Saturated fats: What dietary intake?  American Journal of Clinical Nutrition, 80 (2004): 550-559.

Ravnskov, U.  The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease.  Journal of Clinical Epidemiology, 51 (1998): 443-460.

Ravsnskov, U.  Hypothesis out-of-date.  The diet-heart idea.  Journal of Clinical Epidemiology, 55 (2002): 1,057-1,063.

Ravnskov, U, et al.  Studies of dietary fat and heart disease.  Science, 295 (2002): 1,464-1,465.

Taubes, G.  The soft science of dietary fat.  Science, 291 (2001): 2535-2541.

Zarraga, Ignatius, and Schwartz, Ernst.  Impact of dietary patterns and interventions on cardiovascular health.  Circulation, 114 (2006): 961-973.

Mente, Andrew, et al.  A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease.  Archives of Internal Medicine, 169 (2009): 659-669.

Parikh, Parin, et al.  Diets and cardiovascular disease: an evidence-based assessment.  Journal of the American College of Cardiology, 45 (2005): 1,379-1,387.

Bray, G.A.  Review of Good Calories, Bad Calories.  Obesity Reviews, 9 (2008): 251-263.  Reproduced at the Protein Power website of Drs. Michael and Mary Dan Eades. [Perhaps this doesn’t belong here.]

Hooper, L., et al.  Dietary fat intake and prevention of cardiovascular disease: systematic review.  British Medical Journal, 322 (2001): 757-763.

Weinberg, W.C.  The Diet-Heart Hypothesis: a critique.  Journal of the American College of Cardiology, 43 (2004): 731-733.

Mozaffarian, Darius, et al.  Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women.  American Journal of Clinical Nutrition, 80 (2004): 1,175-1,184.

Related editorial:  Knopp, Robert and Retzlaff, Barbara.  Saturated fat prevents coronary artery disease?  An American paradox.  American Journal of Clinical Nutrition, 80 (2004): 1.102-1.103.

Yusuf, S., et al.  Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study.  Lancet, 364 (2004): 937-952.  [ApoB/ApoA1 ratio was a risk factor for heart attack, so dietary saturated fat may play a role if it affects this ratio.]

Hu, Frank.  Diet and cardiovascular disease prevention: The need for a paradigm shift.  Journal of the American College of Cardiology, 50 (2007): 22-24.

[Dr. Hu de-emphasizes the original diet-heart hypothesis, noting instead that “. . . reducing dietary GL [glycemic load] should be made a top public health priority.”]

Oh, K., et al.  Dietary fat intake and risk of coronary heart disease in women: 20 years of follow-up of the Nurses’ Health Study.  American Journal of Epidemiology, 161 (2005): 672-679.

Parker, Steve.  Time to abandon the diet-heart hypothesis?  Advanced Mediterranean Diet Blog, May 1, 2009.

Parker, Steve.  New study confirms the heart-healthy Mediterranean diet.  Advanced Mediterranean Diet Blog, April 14, 2009.  [Examination of the Mente study listed above.]

Selected References Supporting the Diet-Heart Hypothesis (by no means exhaustive)

Ascherio, A.  Epidemiologic studies on dietary fats and coronary heart disease.  American Journal of Medicine, 113 (supplement) (2002): 9S-12S. 

Griel, Amy and Kris-Etherton, Penny.  Beyond saturated fat: The importance of the dietary fatty acid profile on cardiovascular disease.  Nutrition Reviews, 64 (2006): 257-262.

[Primarily a response to the Mozaffarian article above.]

Erkkila, Arja, et al.  Dietary fatty acids and cardiovascular disease: An epidemiological approach.  Progress in Lipid Research, 47 (2008): 172-187.

In January, 2009, The American Journal of Medicine published a 62-page supplement (vol. 122, number 1A) entitled “Management of Atherosclerosis: A Practical Guide in 2008.”

I scanned it with attention to the Diet-Heart Hypothesis: the idea that dietary factors - such as saturated fat, total fat, cholesterol - cause or aggravate atherosclerosis.  Atherosclerosis is colloquially referred to as “hardening of the arteries,” and is a major cause of heart attacks, strokes, and peripheral arterial disease.

One section, “The Pathology of Atherosclerosis: Plaque Development and Plaque Responses to Medical Treatment” is written by William Insull, M.D., who is with the Lipid Research Clinic at Baylor College of Medicine.  Here are selected quotes, and my comments in brackets:

Several risk factors may intensify or provoke atherosclerosis through their effects on low-density lipoprotein (LDL) particles and inflammation.  These risk factors most frequently include hypertension, tobacco smoking, diabetes mellitus, obesity, and genetic predispositon; the molecular details of how they work are  not yet known.

[No mention of diet.]

Early fatty streak development [thought to be a precursor to atherosclerosis] begins in childhood and adolescence. . . .   The initial step occurs when LDL particles leave the blood and enter the arterial intima, where, if LDL levels are increased, they accumulate.

[Not entirely clear whether he’s referring to increase LDL in the bloodstream or inside the intima cells - I suspect inside the cells.]

All of these changes may be significantly influenced by risk factors, notably the stress of local hemodynamics and blood flow patterns, hypertension, tobacco smoking, and diabetes, as well as genetically determined arterial susceptibility or resistance to atherosclerosis.  The mechanism of these risk factors in influencing atherosclerosis are the target of intensive investigation by molecular pathology, along with proteomics and genomics, conducted to determine the exact molecular biological prosesses involved in their development.

[Again, no mention of diet.]

Dr. Insull does include a table on page S11 that mentions therapeutic reduction of  atherogenic plasma lipoproteins by diet, exercise, statins, and other lipid-lowering therapies, but there is no further mention of diet in his article.

Another section, “”Sick Fat,” metabolic Disease, and Atherosclerosis,” is by Harold E. Bays, M.D., of the Louisville (KY) Metabolic and Atherosclerosis Research Center.  Selected quotes:

Most major CHD [coronary heart disease] risk factors are modifiable; these include metabolic disorders such as type 2 diabetes mellitus, hypertension, and dyslipidemia.

[No mention of diet.]

His Table 2, “Major risk factors for future atherosclerotic coronary heart disease events” includes history of atherosclerosis, type 2 diabetes, high blood pressure, dyslipidemia, cigarette smoking, adiposopathy, age 45 or older (men), age 55 or older (women), and family history of CHD.

[No mention of diet.]

Among hunter-gatherer populations who follow their indigenous lifestyles, CHD is a rarity.  This is in large measure due to a striking reduction in major CHD risk factors, such as markedly reduced [blood] cholesterol levels, in these populations.

[No mention of dietary cholesterol and saturated fats in this context.]

High blood pressure increases CHD risk.  Large-scale observational data show a doubling of mortality from ischemic heart disease and stroke for every 20 mm Hg increase in systolic blood pressure or 10 mm Hg increase in diastolic blood pressure.

[Off topic, but a “fun fact,” at least to a doctor.]

As most primary care clinicians are acutely aware, one of the most basic interventions for treating and/or preventing the most common diseases found in medical practice, including CHD, is encouraging patients to adopt favorable nutritional and lifestyle habits.

[No additional text clarifies his “favorable nutritional . . .  habits.”]

A later section, “Prevention and Treatment of Atherosclrosis: A Practitioner’s Guide for 2008,” is by Sandra J. Lewis, M.D., with the Oregon Health and Science University in Portland.

Dr. Lewis reiterates the aforementioned major risk factors for atherosclerosis, adding physical inactivity, and not mentioning diet as a major risk factor.  She recommends inquiring about eating habits, and encourages “healthy eating.”  A quote:

Therapeutic lifestlye changes constitute first-line therapy for reducing LDL cholesterol levels in persons at risk for atherosclerotic CV [cardiovascular] events.  All persons, regardless of their short- or long-term risks, should be counseled to adopt positive changes, including a low-cholesterol diet, increased physical activity, and cessation of smoking.  Diets should include limits for saturated fats, polyunsaturated fats, monounsatrauted fats, total fat, carbohydrates, and protein.  Total cholesterol ineake should be kept to under 200 mg/day.

These recommendations seem to emanate from the 2001 report of the National Cholesterol Education Program, Adult Treatment Panel III.  Note: they refer to treatment of people with higher-than-optimal LDL cholesterol levels, not to the general population.

My Comments

I was glad to see this in the mail, because I’ve been questioning the validity of the Diet-Heart Hypothesis.  This monograph seemed like the perfect place for a review of it.

The overall tone of the monograph is very much in favor of statin drugs for reducing the morbidity and mortality of atherosclerosis, particularly in the coronary arteries.  Statins are powerful LDL cholesterol-lowering agents.  But that proves nothing one way or the other about the Diet-Heart Hypothesis.

Little in this 62-page monograph supports the diet-heart hypothesis and the idea that everyone needs to limit intake of saturated fat, total fats, or cholesterol.

I’m not prepared today to abandon the Diet-Heart Hypothesis.  But I’ll continue consideration of that option.

Steve Parker, M.D.