Tag Archives: atherosclerosis

Paleolithic Diet Improved Metabolic Syndrome in Just Two Weeks

Wish I were here

Wish I were here

A Paleolithic-type diet over two weeks improves several heart disease risk factors in folks with metabolic syndrome, according to Netherlands-based researchers.

The investigators wondered if the paleo diet, independent of weight loss, would alter characteristics of the metabolic syndrome. They seem to be the first scientists to do a study like this.

“Metabolic syndrome” may be a new term for you. It’s a collection of clinical features that are associated with increased future risk of type 2 diabetes and atherosclerotic complications such as heart attack and stroke. One in six Americans has metabolic syndrome, including almost one in four of adults. The most common definition of metabolic syndrome (and there are others) is the presence of at least three of the following characteristics:

  • high blood pressure (130/85 or higher, or using a high blood pressure medication)
  • low HDL cholesterol: under 40 mg/dl (1.03 mmol/l) in a man, under 50 mg/dl (1.28 mmol/l) in a women (or either sex taking a cholesterol-lowering drug)
  • triglycerides over 150 mg/dl (1.70 mmol/l) (or taking a triglyceride-lowering drug)
  • abdominal fat: waist circumference 40 inches (102 cm) or greater in a man, 35 inches (88 cm) or greater in a woman
  • fasting blood glucose over 100 mg/dl (5.55 mmol/l)

These five criteria were identical to the ones used in the study at hand. But the study participants were required to have only two of the five, not three, for unclear reasons. I found no consensus definition elsewhere that would define metabolic syndrome as only two of the five conditions. Study participants ate either a paleo-style diet or a reference/control diet. Those eating the reference diet didn’t quite have the metabolic syndrome since they had a mean (“average”) of 2.7 metabolic syndrome characteristics. The paleo group had 3.7 characteristics.

How Was the Study Done?

Average age of the 34 study participants was 53 and they were generally healthy. None had diabetes, cardiovascular disease, or systolic pressure over 180 mmHg. Smokers were excluded. Mean body mass index was 32 (obese). Only 9 of the 34 subjects were men. Subjects were randomized to either a Paleolithic-type diet (n=18) or a “healthy reference diet based on the guidelines of the Dutch Health Council” (n=14). Efforts were made to keep body weight stable during the two-week study. Participants were nearly all caucasian.

All meals were home-delivered free of charge by a catering service.

The Paleolithic-type diet “…was based on lean meat, fish, fruit, leafy and cruciferous vegetables, root vegetables, eggs and nuts. Dairy products, cereal grains, legumes, refined fats, extra salt and sugar were not part of it.” [I like their version of the paleo diet.] Protein supplied 24% of calories while carbohydrate was 32% and fat 41%.

You can consult the full text of the published article for details of the Dutch Health Council diet. Calories were 17% from protein, 50% from carbohydrate, and 29% from fat. Alcohol isn’t mentioned at all.

Despite randomization, the paleo diet group had more metabolic syndrome characteristics than the reference diet group. For instance, 78% of the paleo group had elevated fasting glucose compared to 44% of the reference group. And 67% of the paleo group had low HDL cholesterol compared to just 13% of the reference group. These glucose and HDL differences were statistically significant. 39% of the paleo had high triglycerides compared to 19% of the others. Furthermore, the paleos’ average body weight was 98 kg (216 lb) compared to 86 kg (189 lb) in the others. The paleo group had 3.7 characteristics of the metabolic syndrome versus 2.7 in the other cohort.

Go John trail at Cave Creek Regional Park in Scottsdale, Arizona

Go John trail at Cave Creek Regional Park in Scottsdale, Arizona

Results

Compared to the reference diet, the paleo-style diet:

  • lowered systolic pressure by 9 points and diastolic by 5
  • total cholesterol fell by 0.52 mmol/l (20 mg/dl)
  • triglycerides fell by 0.89 mmol/l (79 mg/dl)
  • HDL cholesterol (good) rose by 0.15 mmol/l (6 mg/dl)
  • body weight fell by 1.32 kg (3 lb)
  • one metabolic syndrome characteristic resolved

No significant changes were seen in intestinal permeability ( by differential sugar absorption test on urine), salivary cortisol, and inflammation (hsCRP, TNFα).

Fasting plasma insulin and HOMA-IR fell in the paleo group but not the other.[Good news for folks with diabetes or prediabetes.] Yet the authors write, “Regarding glucose intolerance we did not find significant changes in our study.”

Fasting blood glucose for the group as a whole at baseline was about 1o8 mg/dl (6.0 mmol/l). Fasting glucose fell in both groups: 16 mg/dl (0.9 mmol/l) in the paleo group, 6 mg/dl (0.35 mmol/l) in the other. This was not a statistically significant difference between the groups. These numbers are from the text of the report; looking at the tables, I calculate different and less impressive reductions. The falls in fasting glucose from baseline were statistically significant for both diets.

Nearly all the statistical analysis focused on comparing the paleo diet group to the reference diet group.

My Comments

Overall, I’m not very pleased with this study. My biggest problems are 1) the unfortunate randomization that created dissimilar experimental groups,  2) the use of two diet protocols, 3) some of the study participants didn’t even have metabolic syndrome, and 4) as is typical for paleo diet studies, not many experimental subjects were involved.

The randomization led to significant differences in the metabolic syndrome patients in the two diet groups. I’m puzzled why the authors don’t comment on this. It’s a problem with clinical studies involving low numbers of participants. Ideally, you want to apply the two different diets to groups of people that are as similar as possible. These groups weren’t that similar.

The investigators’ main goal was to study whether a paleo-style diet, independent of weight loss, alters characteristics of the metabolic syndrome. Then why introduce another variable, the Dutch Health Council diet? Is it the gold standard for treating metabolic syndrome? Has it even been used to treat metabolic syndrome? The authors don’t tell us. And why not restrict participation to subjects who meet the common international definition of metabolic syndrome (at least three of the five characteristics)? Why not just take all your subjects and switch them from their standard Netherlands diet to the paleo diet? That would increase your statistical power, and would have avoided the randomization mis-match in which some in the reference diet group didn’t even have metabolic syndrome.

Here we’ve got two different experimental groups, and we’re applying a different diet to each group. The results are going to be messy and difficult to interpret. It’s always better if you can alter just one variable.

Since the paleo and reference diet cohorts were so different at baseline, why not make it easy to simply compare the paleo diet group’s “before and after numbers”? Maybe the analysis is there and I’m just not smart enough to see it.

There weren’t enough men in the study to tell us anything about the paleo diet in men with metabolic syndrome.

The statistical analysis was difficult for me to read and understand. There’s a good chance I’ve missed or misinterpreted something.

This paleo diet reduced fasting blood sugar significantly, making me think it may help in management of diabetes and prediabetes.

I estimate that as much as a quarter of the experimental subjects didn’t even have metabolic syndrome, so the study title is a bit of a misnomer.

This paleo diet did result in resolution of one metabolic syndrome characteristic, which is a good thing. So you could say the diet improves metabolic syndrome, even resolves it in some folks if it drops their metabolic syndrome characteristics from three to two. It predominantly helps lower blood pressure and triglycerides, and reduces excess weight modestly. In white women. Compared to the healthy Dutch Health Council diet.

If I had metabolic syndrome, I’d do something about it in hopes of lowering my future risk of diabetes and atherosclerotic complications. Standard physician advice is to lose excess weight and exercise regularly. There’s no consensus on diet yet. I think carbohydrate restriction is important. If the study at hand is reproducible in a larger study population, the paleo diet is a reasonable approach. Dietitian Franziska Spritzler has a great review of nutritional management of metabolic syndrome at her blog. The Mediterranean diet supplemented with nuts helps improve metabolic syndrome. The Spanish Ketogenic Mediterranean Diet may cure metabolic syndrome.

Steve Parker, M.D.

Update: I took a fresh look at this study as if it were simply a paleo diet trial involving 18 subjects who had metabolic syndrome. If I’m interpreting Table 5 correctly, and I think I am, these are the statistically significant changes after two weeks:

  • abdominal circumference decreased by 3.1 cm
  • systolic and diastolic blood pressures dropped by 8.5 and 8, respectively
  • fasting glucose dropped by 0.4 mmol/l (7 mg/dl)
  • fasting insulin fell
  • HOMA-IR decreased (less insulin resistance)
  • total cholesterol decreased from 220 to 193 mg/dl (5.7 to 5.0 mmol/l)
  • LDL-cholesterol decreased from 135 to 124 mg/dl (3.5 to 3.2 mmol/l)
  • triglycerides decreased from 168 to 89 mg/dl (1.9 to 1.0 mmol/l)

HDL cholesterol was unchanged.

The fall in AUC (area under the curve) for insulin approached but didn’t reach statistical significance (p=0.08)

Body weight fell from 98 kg (216 lb) to 95.3 kg (210 lb) but I found no p value. HDL-cholesterol was unchanged (the higher HDL I mentioned above is only in comparison to the reference diet, in which HDL fell)

All of these changes (except the lack of change in HDL-chol) would tend to promote health in someone with metabolic syndrome, prediabetes, or overweight type 2 diabetes.

Reference: Boers, Inga, et al. Favorable effects of  consuming a Palaeolithic-type diet on characteristics of the metabolic syndrome: a randomized controlled pilot-studyLipids in Health and Disease. 2014 Oct 11;13:160. doi: 10.1186/1476-511X-13-160.

Do Intestinal Parasites Help Prevent Atherosclerosis?

A trio of Indian researchers suggest a new hypothesis to explain the modern pandemic of atherosclerosis (hardening of the arteries). They repeat the notion that atherosclerosis is uncommon in modern hunter-gatherers. But why?

Reviewing evolution-linked risk factors suggests that there are four aspects to the etiology of atherosclerosis namely, decreased intestinal parasitism, oversensitivity of evolutionarily redundant mast cells, chronic underactivation of AMPK (cellular energy sensor) and a deficiency of vitamin D. A combination of these four causes appear to have precipitated the atherosclerosis pandemic in modern times.

Click for the abstract. Pretty far out stuff. I haven’t read the full article. The authors are in the Departments of Pharmacology and Pharmacy Practice.

Mouth Bacteria May Be an Important Cause of Heart Disease

…according to an article at University Herald.

paleo diet, Steve Parker MD,calcium, osteoporosis

That milk mustache is a tell-tale sign she’s not eating pure paleo

The idea is that nasty bacteria around your gums somehow cause arterial inflammation in your heart arteries, which could lead to heart attacks. I’ve written about this before.

A quote from the article:

The researchers followed 420 adults as part of the Oral Infections and Vascular Disease Epidemiology Study (INVEST), a randomly sampled prospective cohort of Northern Manhattan residents. Participants were examined for periodontal infection. Overall, 5,008 plaque samples were taken from several teeth, beneath the gum, and analyzed for 11 bacterial strains linked to periodontal disease and seven control bacteria. Fluid around the gums was sampled to assess levels of Interleukin-1β, a marker of inflammation. Atherosclerosis in both carotid arteries was measured using high-resolution ultrasound.

Over a median follow-up period of three years, the researchers found that improvement in periodontal health-health of the gums-and a reduction in the proportion of specific bacteria linked to periodontal disease correlated to a slower intima-medial thickness (IMT) progression, and worsening periodontal infections paralleled the progression of IMT. Results were adjusted for potential confounders such as body mass index, cholesterol levels, diabetes, and smoking status.

Thickening of the arterial lining is linked to higher rates of heart attack and stroke.

It remains to be seen whether alteration of gum bacteria and periodontal disease via oral self-care and dental care will reduce cardiovascular risk going forward. Stay tuned.

Read more at http://www.universityherald.com/articles/5322/20131101/brushing-your-teeth-could-prevent-heart-disease.htm#rvx294vC7VKJ6Qu3.99

High Carbohydrate Diet May Cause Atherosclerosis

…and that condition underlies most heart attacks, strokes, and poor circulation to limbs. Here’s the conclusion from an abstract:

High-carbohydrate diets, particularly in the form of high-glycemic index carbohydrate, have the ability to directly induce atherosclerosis. Based on anthropologic facts, the reason for these dietary-induced, insulin-mediated, atherogenic metabolic perturbations are suggested to be an insufficient adaptation to starch and sugars during human evolution. Restriction of insulinogenic food (starch and sugars) may help to prevent the development of atherosclerosis, one of the most common and costliest human diseases.

medical clearance, treadmill stress test

This treadmill stress test is looking for atherosclerotic heart disease, aka coronary artery disease and coronary heart disease

The article was published in 2006. In 2007, Harvard’s Dr. Frank Hu  was singing the same tune about carbohydrates. Jenny Brand-Miller and associates implicate high-glycemic-index carbohydrates as a cause of atherosclerotic heart disease in women, but I don’t recall any similar evidence in men. Yet.

I know many diabetics hate to cut dietary carbohydrates. If this new theory of atherosclerosis pans out, maybe carb restriction will be easier to stomach.

 

h/t Mangan

Heart Attacks Hinge on LDL Cholesterol Particle Number (LDL-P)

medical clearance, treadmill stress test

This treadmill stress test is looking for hidden heart disease

…according to Drs. Thomas Dayspring and James Underberg. I don’t know if these guys are right or not. I bet it’s more complicated than LDL particle number. I’m always skeptical of grand unification theories.

People with diabetes tend to have shorter life spans than average. One reason is a predisposition to heart disease, specifically coronary artery disease that leads to heart attacks.

Most heart attacks (aka myocardial infarctions) do indeed seem to be caused by acute rupture of an atherosclerotic plaque that’s been present for years. Two key questions are:

  1. What causes the plaque?
  2. Why causes it to rupture?

Underberg and Dayspring write:

The only absolute requirement for plaque development is the presence of cholesterol in the artery: although there are additional heart risk factors like smoking, hypertension, obesity, family history, diabetes, kidney disease, etc., none of those need to be present. Unfortunately, measuring cholesterol in the blood, where it cannot cause plaque, until recently has been the standard of risk-testing. That belief was erroneous and we now have much better biomarkers to use for CV risk-assessment. The graveyard and coronary care units are filled with individuals whose pre-death cholesterol levels were perfect. We now understand that the major way cholesterol gets into the arteries is as a passenger, in protein-enwrapped particles, called lipoproteins.

Particle entry into the artery wall is driven by the amount of particles (particle number) not by how much cholesterol they contain. Coronary heart disease is very often found in those with normal total or LDL-cholesterol (LDL-C) levels in the presence of a high LDL particle number (LDL-P). By far, the most common underlying condition that increases LDL particle concentration is insulin resistance, or prediabetes, a state where the body actually resists the action of the sugar controlling hormone insulin. This is the most common scenario where patients have significant heart attack risk with perfectly normal cholesterol levels. The good news is that we can easily fix this, sometimes without medication. The key to understanding how comes with the knowledge that the driving forces are dietary carbohydrates, especially fructose and high-fructose corn syrup. In the past, we’ve often been told that elimination of saturated fats from the diet would help solve the problem. That was bad advice. The fact is that until those predisposed to insulin resistance drastically reduce their carbohydrate intake, sudden deaths from coronary heart disease and the exploding diabetes epidemic will continue to prematurely kill those so afflicted.

***

 And for goodness’ sake, if you want to live longer, start reducing the amount of dietary carbohydrates, including bread, potatoes, rice, soda and sweetened beverages (including fruit juices), cereal, candy – the list is large).

Read the whole enchilada.

Offhand, I don’t recall any clinical study looking at LDL cholesterol particle number in folks who switched to a paleo diet. Given the prominence of coronary heart disease, I’m sure Dayspring and Underberg would favor a low-carb version of the paleo diet for anyone going the paleo route. Here’s my version of low-carb paleo.

Underberg and Dayspring don’t mention LDL particle size, such as small/dense and large/fluffy; the former are thought by many to be much more highly atherogenic, while the latter may not be at all. Is this idea outdated?

Whoever figures out the immediate cause of plaque rupture and how to reliably prevent it will win a Nobel Prize in Medicine.

Steve Parker, M.D.

About Dayspring and Underberg:

Thomas Dayspring MD, FACP, FNLA   Director of Cardiovascular Education, The Foundation for Health Improvement and Technology, Richmond, VA. Clinical Assistant Professor of Medicine, University of Medicine and Dentistry of New Jersey, New Jersey Medical School.

James Underberg MD, FACP, FNLA   Clinical Assistant Professor of Medicine in the Division of General Internal Medicine at NYU Medical School and the NYU Center for Cardiovascular Disease Prevention . Director of the Bellevue Hospital Primary Care Lipid Management Clinic.

h/t Dr. Axel Sigurdsson

Paleo Diet Advocates Fear Modernity

…according to David Gorski at Science-Based Medicine.

Gee, I hadn’t noticed that fear.  Maybe it’s subconscious.

Dr. Gorski makes some good points along with others I disagree with.  I expect the commentators at SBM will address many of the controversial points.  They’re a smart readership.

One uncommon observation of his is that the “complementary and alternative medicine” believers tend to embrace the paleo diet and lifestyle.  I’ve noticed that also.  To the extent that the CAM folks are often unscientific or anti-scientific, those of us examining the paleo diet from a scientific viewpoint have to be wary of “guilt by association.”

A major point that Dr. Gorski didn’t address is that living hunter-gatherers studied over the last century or two don’t have nearly as much cardiovascular disease and death as modern Western societies.  That’s a common meme in the paleosphere, started by the prominent paleo book authors.  (I’ve not reviewed the original sources.)  I’m talking about lower rates of heart attacks, strokes, hypertension, peripheral arterial disease, and premature death.  Note that the mere presence of atherosclerosis may not correlate with these hard clinical endpoints.

Are Saturated Fats Really All That Bad?

This is an epic post of mine from the old Advanced Mediterranean Diet blog, originally dated July 6, 2009. That was a watershed year for me in terms of accepting nutritional dogma, because of the ideas in this article.  This was also before I ever gave serious consideration to the paleo diet.

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

No saturated fat in grapes

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 (aka hardening of the arteries).

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.

You needed a break

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 level, 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’ll 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 uttering 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 19, 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.

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.