Advanced Mediterranean Diet

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

I blogged about a study by Gu et al on April 30, 2010, that found significantly lower incidence of Alzheimer dementia in people in Manhattan who followed this dietary pattern:

• relatively high consumption of salad dressing, nuts, fish, tomatoes, fruits, dark green leafy vegetables, and cruciferous  vegetables
• relatively low consumption of poultry, red meat, butter, and high-fat dairy

About the same time, a National Institutes of Health expert panel pooh-poohed the possibility that diet had any effect one way or the other on Alzheimer’s. 

Why does this matter?  Five million U.S. adults have Alzheimer dementia already, and it’s going to get much worse over the coming decades.

A June, 2010, issue of Journal of the American Medical Association has a commentary by two doctors (Martha Morris, Sc.D., and Christine Tangney, Ph.D.), experts in the field of nutrition.  Here’s their explanation of the NIH panel’s negative findings:

Many of the inconsistencies among studies of dietary factors can be attributed to the complexity of nutrition science and the omission of nutrition expertise in the design and analysis of both epidemiological and randomized controlled trials.

Morris and Tangney think the findings of Gu et al are valid, confirming prior studies showing benefit to diets high in vitamin E (from food) and low in saturated fat from animals.  They point out that the animal foods may simply be displacing beneficial nutrients in other foods, rather than directly causing harm.

Until we have further data, anyone at risk for Alzhiemer’s may be better off following the dietary pattern above, or the Mediterranean diet.  The two are similar.

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 physican before making any dietary or exercise changes. 

Reference: Morris, M., & Tangney, C. (2010). Diet and Prevention of Alzheimer Disease JAMA: The Journal of the American Medical Association, 303 (24), 2519-2520 DOI: 10.1001/jama.2010.844

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.

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 January 14, 2010):

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

Researchers at Harvard and the University of Athens (Greece) report that the following specific components of the Mediterranean diet are associated with lower rates of death:

• moderate ethanol (alcohol) consumption
• low meat and meat product intake
• high vegetable consumption
• high fruit and nut consumption
• high ratio of monounsaturated fat to saturated fat
• high legume intake

Minimal, if any, contribution to mortality was noted with high cereal, low dairy, or high fish and seafood consumption. 

The researchers examined diet and mortality data from over 23,000 adult participants in the Greek portion of the European Prospective Investigation into Cancer and nutrition.  You’ll be hearing more about the EPIC study for many years.  Over an average follow-up of 8.5 years, 1,075 of participants died.  652 of these deaths were of participants in the lower half of Mediterranean diet adherence; 423 were in the upper half.

Alcohol intake in Greece is usually in the form of wine at mealtimes. 

The beneficial “high ratio of monounsaturated fat to saturated fat” stems from high consumption of olive oil and low intake of meat. 

It’s not clear if these findings apply to other nationalities or ethnic groups.  Other research papers have documented the health benefits of the Mediterranean diet in at least eight other countries over three continents. 

The researchers don’t reveal in this report the specific causes of death.  I expect those data, along with numbers on diabetes, stroke, and dementia, to be published in future articles, if not published already.  Prior Mediterranean diet studies indicate lower death rates from cardiovascular disease and cancer.   

Steve Parker, M.D.

Reference:  Trichopoulou, Antonia, et al.  Anatomy of health effects of the Mediterranean diet: Greek EPIC prospective cohort study.  British Medical Journal, 338 (2009): b2337.  DOI: 10.1136/bmj.b2337.

Additional Information:  Childs, Dan.  Take it or leave it?  The truth about 8 mediterranean diet staples.  ABC News online, June 24, 2009.  Accessed June 25, 2009.

Update June 26, 2009:

Here’s a direct quote from the study at hand:

Among the presumed beneficial components of the Mediterranean diet score, high consumption of all but fish and seafood was inversely associated with mortality, although none of these associations was statistically significant.

“. . . none of these associations was statistically significant.”  So I can understand some skepticism about this journal article. The researchers had to use some very sophisticated statistical manipulation to come up with the “healthy components” list. I’m not saying that’s wrong. I will admit that the statistical analysis is beyond my comprehension, so I’m trusting the authors and peer-review process to be honest and effective. My college statistics course was too many years ago.

The take-home point for me is that the health benefits of the Mediterranean diet probably stem from an overall combination of multiple foods rather than any single component.

Steve Parker, M.D.

And remember to exercise regularly, maintain a healthy weight (BMI 18.5-25), keep your blood pressure under 140/90, and don’t smoke.

-Steve