Category Archives: Dietary Fat

Bix Sez: We’ve Known For Decades That Low-Fat Diets Can Reverse Diabetes

“So, we’ve known for at least 30 years, 60 years by the looks of that 1955 Lancet study, that low-fat diets could arrest the symptoms of diabetes or prevent the disease altogether.

Robbins’ “Diet For A New America” was a popular lay-person’s book (1st edition sold over a million copies), not a medical tome. It was in the social realm. Why isn’t its low-fat advice common knowledge? I’ll tell you … It’s for reasons that induce stores like Natural Grocers to ban Dr. Greger’s plant-based book. It’s because having people eat a low-fat, high-fiber diet would hurt sales of animal food: beef, pork, chicken, fish, eggs, and all manner of dairy food – cheese, yogurt, milk, butter, cream. That’s why. And you know how the meat and dairy industries keep a lid on the science that could really help people? They come out with their own studies, often meta-analyses which go back in time and cherry pick studies that defend their position.”

Source: We’ve Known For Decades That Low-Fat Diets Can Reverse Diabetes | Fanatic Cook

One of the references Robbins uses to support his contention is a 1979 article in American Journal of Clinical Nutrition. It’s a study of 20 men, all of whom were on insulin for what I assume is type 2 diabetes. What’s odd is that the men were all “lean.” In real life, at least 85% of type 2 diabetics are overweight or obese. Not lean. Nevertheless, many of the men were able to stop insulin on the low-fat/high fiber diet. But these weren’t typical T2 diabetics.

Dietary Saturated Fat Doesn’t Influence Future Course of Coronary 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.

Steve Parker, M.D.

Why Everybody Should Eat Nuts

Nuts with more omega-3 fatty acids (compared to omega-6) may be the healthiest

Nuts with the lowest omega-6/omega-3 fatty acid ratios may be the healthiest. In other words, increase your omega-3s and decrease omega-6s.

Conner Middelmann-Whitney explains in her recent post at Psychology Today. In a nutshell, they are linked to longer life and better health. For example:

In the largest study of its kind, Harvard scientists found that people who ate a handful of nuts every day were 20% less likely to die from any cause over a 30-year period than those who didn’t consume nuts. The study also found that regular nut-eaters were leaner than those who didn’t eat nuts, a finding that should calm any fears that eating nuts will make you gain weight.

The report also looked at the protective effect on specific causes of death. “The most obvious benefit was a reduction of 29% in deaths from heart disease—the major killer of people in America,” according to Charles S. Fuchs, director of the Gastrointestinal Cancer Treatment Center at Dana-Farber, the senior author of the report and a professor of medicine at Harvard Medical School. “But we also saw a significant reduction—11% —in the risk of dying from cancer,” added Fuchs.

Read the whole enchilada.

Nuts are integral to my Advanced Mediterranean Diet, Low-Carb Mediterranean Diet, Paleobetic Diet, and Ketogenic Mediterranean Diet.

Walnuts seem to have the lowest omega-6/omega-3 fatty acid ratio of all the common nuts. That may make them the healthiest nut. The jury is still out. Macadamia nuts have a good ratio, too. Paleo dieters focus on cutting out omega-6s and increasing omega-3s. Julianne Taylor has a great post on how to do that with a variety of foods, not just nuts.

Steve Parker, M.D.

A Default Position on the Omega-6/Omega-3 Debate

ASBMB Today has a well-written balanced article on the omega-6/omega-3 fatty acid ratio debate written by Rajendrani Mukhopadhyay.  A fair amount of it is understandable to non-science majors.  The main question is whether the high consumption of omega-6 fatty acids in Western societies is unhealthy.

It’s estimated that throughout most of human evolution, our dietary omega-6/omega-3 ration has been around 3:1 or 2:1.  Today, it’s about 15:1, thanks to a large increase in omega-6 consumption.  Are our bodies adapted for the lower ratio?  A hard-core paleo diet like Dr. Cordain’s aims for that lower ratio.

Both sides of the debate agree that we would probably be better off eating more omega-3 fatty acids, as found in cold-water fatty fish.

I’m an omega-6/omega-3 ratio agnostic at this point.  I’ve never studied it in depth, so I have no strong opinion either way.

Here are a couple excerpts from the article to pique your interest:

No one is disputing that we’re eating more omega-6 than our predecessors did. Over the past 100 years, consumption of linoleic acid [an omga-6] has increased dramatically in the U.S., mainly through the use of soybean oil. Soybean oil intake has gone up from being 1 percent of calories in the American diet to as much as 10 percent, according to Hibbeln. Lands, Salem and others contend that the rise, driven by the processed food and agriculture industries, has happened without anyone knowing its effects. “If I were now to try to get permission to change 10 percent of the calories in the U.S. diet, I would need a very large body of data unequivocally proving that it was safe,” says Hibbeln. “No such body of data exists for soybean oil. But it’s in our diet. We’re the experiment. It’s been a very large, uncontrolled intervention.”

Experts like Harris and Willett say this increase has been to our benefit. “We have seen a massive decline in cardiovascular disease mortality and huge increase in life expectancy,” says Willett. “Not all the benefit is due to the increase in linoleic acid, but almost certainly much of it is. It was not an absolute disaster.” But the lipid biochemists counter that it’s not just cardiovascular disease at stake. They say diabetes, obesity and even psychiatric disorders are some outcomes of a diet heavy on omega-6s.

I’ve never before heard anybody credit linoleic acid with a major role in our  “huge increase in life expectancy” over the last century.  I doubt that’s the case.  I vote more in favor of better sewage systems, cleaner water, better hygiene, antibiotics, or improvements in surgery and medical care.

Evolutionary biologist Theodosius Dobzhansky said, “Nothing in biology makes sense except in the light of evolution.”  If that’s true, the default position is that lower amounts of omega-6 fatty acid are better than our current high consumption.  It’s up to the high-consumption proponents to prove otherwise.

Steve Parker, M.D.

h/t David Despain

PS: Dobzhansky was a Christian, by the way.

PPS: A Twitter reader (@pronutritionist) suggested that the modern Western dietary omega-6/omega=3 ratio is 9.6, not 15:1, citing Amer J Clin Nutr.  My source for 15:1 is Journal of Nutrition and Metabolism, vol. 2012, article ID 539426, doi 10.1155/2912/539426, by E. Patterson et al. I admit it’s not a great reference. Cordain’s 2002 book, The Paleo Diet, says 10:1.  Maybe it is closer to 10:1.  I’m sure there’s lots of inter-person variability.

What Happened to Lard?

Lard? Wut choo talkin’ ’bout, Willis?

Lard may be making a come-back. An NPR article reviews its fall from grace, with mention of Crisco, Upton Sinclair, and Procter and Gamble.

Steve Parker, M.D.

h/t Laura Dolson

What’s Our Preferred Fuel?

Dr. Jay Wortman has been thinking about whether our bodies prefer to run on carbohydrates (as a source of glucose) or, instead, on fats. The standard American diet provides derives about half of its energy from carbs, 35% from fats, and 15% from proteins. So you might guess our bodies prefer carbohydrates as a fuel source. Dr. Wortman writes:

Now, consider the possibility that we weren’t meant to burn glucose at all as a primary fuel. Consider the possibility that fat was meant to be our primary fuel. In my current state of dietary practice, I am burning fat as my main source of energy. My liver is converting some of it to ketones which are needed to fuel the majority of my brain cells. A small fraction of the brain cells, around 15%, need glucose along with a few other tissues like the renal cortex, the lens of the eye, red blood cells and sperm. Their needs are met by glucose that my liver produces from proteins. The rest of my energy needs are met with fatty acids and these come from the fats I eat.

Dr. Wortman, who has type 2 diabetes, in the same long post also writes about oolichan grease (from fish), an ancestral food of Canandian west coast First Nations people.

Drs. Jeff Volek and Stephen Finney have done research on athletes using a low-carb, high-fat diet.

Steve Parker, M.D.

Right Diet Preserves Brain Function and Size

mp9004223691.jpgThe journal Neurology reports that the proper diet seems to help prevent age-related brain shrinkage and cognitive decline.

From the press release:

People with diets high in several vitamins or in omega 3 fatty acids are less likely to have the brain shrinkage associated with Alzheimer’s disease than people whose diets are not high in those nutrients, according to a new study published in the December 28, 2011, online issue of Neurology, the medical journal of the American Academy of Neurology.

Those with diets high in omega 3 fatty acids and in vitamins C, D, E and the B vitamins also had higher scores on mental thinking tests than people with diets low in those nutrients. These omega 3 fatty acids and vitamin D are primarily found in fish. The B vitamins and antioxidants C and E are primarily found in fruits and vegetables.

So the dietary pattern linked to preservation of brain size and function in this study is: high omega-3 fatty acids and vitamins B, C, D, and E. I don’t know if study participants were getting these nutrients from supplements or from food or a combination. (I haven’t read the full article.)

To find foods high in the aforementioned nutrients, you can use NutritionData’s Nutrient Search Tool.

Note that the time-honored Mediterranean diet is also associated with lower rates of dementia and slower rate of age-related mental decline.

I previously reported that a supplement cocktail of three B vitamins slowed the rate of brain shrinkage.

Steve Parker, M.D.

Reference: Bowman, G.L., et al. Nutrient biomarker patterns, cognitive function, and MRI measures of brain aging. Neurology. doi: 10.1212/WNL.0b013e3182436598

h/t to Randall Parker at FuturePundit

Sources of Calories in U.S. Diet Over Last Four Decades

Italian seaside totally unrelated to this post

Do you ever wonder how many of the total calories in the aveage U.S. diet come from added sugars? Grains? Dairy products? Added fats?

You’d have to do some detailed nutrient analysis to get your personal numbers, but if you’d like U.S. averages, see this cool infographic at Civil Eats.

The graph also shows how many calories are or were available for consumption per capita over time (without accounting for wastage in restaurants). It’s based on U.S. Department of Agriculture data.

A superficial glance suggests that U.S. per capita daily calorie consumption has increased by about 600 from the 1970s until now. But remember, these numbers don’t discount for restaurant wastage. Nor do I see an adjustment for children versus adults. I’ve seen other calculations of an extra daily 150 calories (women) to 300 calories (men). Even the lower numbers could explain our explosion of overweight and obesity.

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 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.