Tag Archives: saturated fat

How a single high-fat “meal” (palm oil) affects liver metabolism 

I thought we were through demonizing saturated fats.

I put my headline’s “meal” in quotes because the only item in the meal was palm oil. That doesn’t look like one of my meals.

From MNT:

“Individuals who consume higher levels of saturated fats are more likely to feel the effects of a range of health conditions, including non-alcoholic fatty liver disease. Although this link is well-known, exactly how and why it develops is not yet clear.

Recent research investigates the effects of a single high-fat meal on the liver.Non-alcoholic fatty liver disease (NAFLD), as the name suggests, is a condition in which excess fat is stored in the liver of an individual who drinks little or no alcohol.

Marked by liver inflammation, NAFLD most commonly affects people in their 40s and 50s, and especially those who are obese. It can cause scarring of the liver and permanent damage. At its worst, it can lead to liver failure.NAFLD is primarily characterized by an increased buildup of fat in the liver, and this buildup is often accompanied by insulin resistance, thereby increasing the risk of type 2 diabetes and cardiovascular disease.”

Source: How a single high-fat meal affects liver metabolism – Medical News Today

German researchers fed a single palm oil meal to 14 healthy men, and some mice.

The article writer doesn’t make it clear whether results apply to the men, the mice, or all combined. Anyway, they found

  • Elevated blood triglycerides
  • Increased glucagon (a pancreas hormone that raises blood sugar)
  • Whole body insulin sensitivity decreased 25 percent
  • Hepatic insulin sensitivity decreased 15 percent
  • Adipose (fat) tissue insulin sensitivity decreased 34 percent
  • Triglycerides in the liver – the main constituent of body fat in humans  – also rose by 35 percent

All of these changes would tend to promote not only NAFLD but also type 2 diabetes.

Whether these adverse changes would be see with other saturated fats or polyunsaturated fats is left unstated in the report.

From UpToDate.com: “The pathogenesis of nonalcoholic fatty liver disease has not been fully elucidated. The most widely supported theory implicates insulin resistance as the key mechanism leading to hepatic steatosis, and perhaps also to steatohepatitis. Others have proposed that a “second hit,” or additional oxidative injury, is required to manifest the necroinflammatory component of steatohepatitis. Hepatic iron, leptin, antioxidant deficiencies, and intestinal bacteria have all been suggested as potential oxidative stressors.”

I’ve been hearing for years that NAFLD is going to be a big deal. At least every other shift I work in the hospital, I see someone with evidence for fatty liver on ultrasound or CT scan.

The mainstay of therapy for NAFLD is weight loss for those who are obese or overweight. It’s probably a good idea to avoid all alcohol consumption, too.

If you need to lose weight, check out my books.

Steve Parker, M.D.

Steve Parker MD, Advanced Mediterranean Diet

Two diet books in one

 

Should You Avoid Saturated Fats If You Already Have Heart Disease?

kkk

Most heart attacks occur in folks with pre-existing coronary artery disease that’s been present for years

If you already have coronary artery disease, Dr. Axel Sigurdsson says that ongoing saturated fat intake probably doesn’t matter, in terms of future cardiac events (like heart attacks) or risk of death from any cause.

Dr. Sigurdsson is a cardiologist in Iceland.

Some quotes from his blog:

For decades, cardiologists have advised patients with heart disease to restrict the intake of saturated fats and dietary cholesterol. Many patients still believe this to be the cornerstone of their lifestyle modification.

The main reason for avoiding saturated fats is the assumption that they adversely affect the lipid profile of our patients.

*   *   *

Recent studies suggest that the recommendation to avoid saturated fats may have been premature and not based on solid scientific evidence.

Now, a recently published Norwegian study shows that dietary intake of saturated fatty acids was not associated with risk of future events or death among patients with established coronary artery disease.

It is important to keep in mind that most of the patients were receiving secondary prevention drug therapy including aspirin, beta blockers and statins.

Anyhow, the results of the study certainly suggest that high intake of saturated fats is not a risk factor among patients with coronary heart disease receiving modern-day treatment.

These recent scientific data don’t imply hat we should urge our patients to consume high amounts of saturated fats. They only tell us that there is no association and accordingly, restriction won’t help.

So, it’s certainly a lifeline for those who believe red meat, whole-fat milk, cheese, cream, butter and eggs can be a part of a healthy diet.

On the other hand we must realise that scientific studies often provide contradictory results. A US study published last year suggested that greater adherence to a low carbohydrate diet high in animal sources of fat and protein was associated with higher all-cause and cardiovascular mortality following acute heart attack.

It appears the jury is still out…

RTWT.

Endocrine Groups Agree on Healthy Lifestyle and Diet Choices

MedPageToday has the poop.

Patients may need help managing metabolic and endocrine disorders with healthy eating and lifestyle choices, and now there’s a comprehensive set of clinical guidelines, issued jointly by the American Association of Clinical Endocrinologists, the American College of Endocrinology, and the Obesity Society, to assist them.

I lost interest when they recommended avoiding saturated fats. There’s no call for that.

All patients, in addition to receiving an education in nutrition and meal preparation, should engage in 150 minutes or more of physical activity weekly, and learn ways to avoid a sedentary lifestyle, receive adequate sleep, and budget time to relax and reduce stress. Patients should also generally consume a mix of animal and plant proteins and carbohydrates. They should reduce the fat consumed with dairy and animal products, and avoid saturated fats.

***

Two key recommendations he noted were that healthy eating with a focus on fresh foods — such as fruits and vegetables — was central to a healthy meal plan, and that there was no evidence to support consumption of vitamin supplements except in deficient populations.

Read the rest.

A Half-Century of Misguided Dietary Recommendations

Philip Calder writes in the British Medical Journal about a re-analysis of an old study. Middle-aged men with heart disease were placed either on 1) a diet high in linoleic acid, a predominant omega-6 fatty acid, or 2) their habitual diet.  The men on the high-omega-6 diet had a higher subsequent overall and cardiac death rate.

“These findings argue against the “saturated fat bad, omega 6 PUFA good” dogma and suggest that the American Heart Association advisory that includes the statement “higher [than 10% of energy] intakes [of omega-6 PUFAs] appear to be safe and may be even more beneficial” may be misguided. The more cautious UK dietary recommendations on fat and fatty acids, which include the statement, “There is reason to be cautious about high intakes of omega 6 PUFAs, ”seem fully justified in the light of the current study’s findings.”

Time to Abandon the Diet-Heart Hypothesis?

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 began questioning the validity of the Diet-Heart Hypothesis in 2009. 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.

Steve Parker, M.D.

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 because of the ideas in this article.

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 factorsin 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 October 4, 2016):

Grasgruber, Pavel, et al. FOOD CONSUMPTION AND THE ACTUAL STATISTICS OF CARDIOVASCULAR DISEASES: AN EPIDEMIOLOGICAL COMPARISON OF 42 EUROPEAN COUNTRIES. Food & Nutrition Research 2016, 60: 31694 – http://dx.doi.org/10.3402/fnr.v60.31694 “Our results do not support the association between cardiovascular diseases and saturated fat, which is still contained in official dietary guidelines. Instead, they agree with data accumulated from recent studies that link cardiovascular disease risk with the high glycaemic index/load of carbohydrate-based diets. In the absence of any scientific evidence connecting saturated fat with cardiovascular diseases, these findings show that current dietary recommendations regarding cardiovascular diseases should be seriously reconsidered.”

Puaschitz, Nathalie, et al. Dietary Intake of Saturated Fat Is Not Associated With Risk of Coronary Events Or Mortality In Patients With Established Coronary Artery Disease. Journal of Nutrition, Feb. 1, 2015. First published online Dec. 10, 2014. doi: 10.3945/jn.114203505. The title of the article says it all. A strong majority (81%) of the 2412 study participants were men, so I’m not sure the results apply to women.

Chowdhury, Rajiv, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysisAnnals of Internal Medicine 2014;160(6):398-406-406. doi:10.7326/M13-1788  The conclusion of this meta-analysis: “Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

Ramsden, Christopher, et al.  Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis.  British Medical Journal 2013; 346 doi: http://dx.doi.org/10.1136/bmj.e8707 (Published 5 February 2013). Cite this as: BMJ 2013;346:e8707  (Almost 500 middle-aged men with a recent coronary event were followed over time.  Those who substituted saturated fat with omega-6 fatty acid (polyunsaturated fatty acid, mostly linoleic acid) had higher death rates (cardiac and overall deaths) than those who continued their habitual diet.)  Also see editorial by Philip Calder in the same issue.

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.