Category Archives: Diet-Heart Hypothesis

Low-Carb High-Fat Diet OK for Heart

Posted on January 25, 2022 | Comments Off on Low-Carb High-Fat Diet OK for Heart
Photo by Malidate Van on Pexels.com

Mainstream physicians are still hesitant to recommend low-carb diets because they are usually high in fat, potentially with heart-toxic levels of saturated fats. A recent scientific article supported low-carb eating for heart health.

Link to article

ABSTRACT

Background

Carbohydrate restriction shows promise for diabetes, but concerns regarding high saturated fat content of low-carbohydrate diets limit widespread adoption.Objectives

This preplanned ancillary study aimed to determine how diets varying widely in carbohydrate and saturated fat affect cardiovascular disease (CVD) risk factors during weight-loss maintenance.

Methods

After 10–14% weight loss on a run-in diet, 164 participants (70% female; BMI = 32.4 ± 4.8 kg/m2) were randomly assigned to 3 weight-loss maintenance diets for 20 wk. The prepared diets contained 20% protein and differed 3-fold in carbohydrate (Carb) and saturated fat as a proportion of energy (Low-Carb: 20% carbohydrate, 21% saturated fat; Moderate-Carb: 40%, 14%; High-Carb: 60%, 7%). Fasting plasma samples were collected prerandomization and at 20 wk. Lipoprotein insulin resistance (LPIR) score was calculated from triglyceride-rich, high-density, and low-density lipoprotein particle (TRL-P, HDL-P, LDL-P) sizes and subfraction concentrations (large/very large TRL-P, large HDL-P, small LDL-P). Other outcomes included lipoprotein(a), triglycerides, HDL cholesterol, LDL cholesterol, adiponectin, and inflammatory markers. Repeated measures ANOVA was used for intention-to-treat analysis.

Results

Retention was 90%. Mean change in LPIR (scale 0–100) differed by diet in a dose-dependent fashion: Low-Carb (–5.3; 95% CI: –9.2, –1.5), Moderate-Carb (–0.02; 95% CI: –4.1, 4.1), High-Carb (3.6; 95% CI: –0.6, 7.7), P = 0.009. Low-Carb also favorably affected lipoprotein(a) [–14.7% (95% CI: –19.5, –9.5), –2.1 (95% CI: –8.2, 4.3), and 0.2 (95% CI: –6.0, 6.8), respectively; P = 0.0005], triglycerides, HDL cholesterol, large/very large TRL-P, large HDL-P, and adiponectin. LDL cholesterol, LDL-P, and inflammatory markers did not differ by diet.

Conclusions

A low-carbohydrate diet, high in saturated fat, improved insulin-resistant dyslipoproteinemia and lipoprotein(a), without adverse effect on LDL cholesterol. Carbohydrate restriction might lower CVD risk independently of body weight, a possibility that warrants study in major multicentered trials powered on hard outcomes.

Parker here. These findings are no surprise to me.

Steve Parker, M.D.

PS: The Advanced Mediterranean Diet (2nd Ed.) includes a low-carb option.

Steve Parker MD, Advanced Mediterranean Diet
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PPS: Ketogenic diets are all low-carb.

front cover of KMD: ketogenic mediterranean diet
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Posted in Diet-Heart Hypothesis, Heart Disease, Ketogenic Mediterranean Diet, Low-Carb Eating, Low-Carb Mediterranean Diet

If You’re Looking for Reasons to Avoid Processed Meats, Unprocessed Red Meat, and Poultry, Here You Go…

Posted on October 28, 2020 | Comments Off on If You’re Looking for Reasons to Avoid Processed Meats, Unprocessed Red Meat, and Poultry, Here You Go…
Steak vs vegetarian

Public health authorities in the West have been trying for years to scare us away from eating meat. Here’s an abstract of one of the weak studies that support that contention. Herein, heavier consumers of processed meats, unprocessed red meat, and poultry were a increased risk of cardiovascular disease. Fish and poultry were not linked to increased risk of death, while processed meat and unprocessed red meat were. And fish was not linked to cardiovascular disease. The authors admit that the differences in outcome were small.

Importance 

Although the associations between processed meat intake and cardiovascular disease (CVD) and all-cause mortality have been established, the associations of unprocessed red meat, poultry, or fish consumption with CVD and all-cause mortality are still uncertain.

Objective 

To identify the associations of processed meat, unprocessed red meat, poultry, or fish intake with incident CVD and all-cause mortality.

Design, Setting, and Participants 

This cohort study analyzed individual-level data of adult participants in 6 prospective cohort studies in the United States. Baseline diet data from 1985 to 2002 were collected. Participants were followed up until August 31, 2016. Data analyses were performed from March 25, 2019, to November 17, 2019.

Exposures 

Processed meat, unprocessed red meat, poultry, or fish intake as continuous variables.

Main Outcomes and Measures 

Hazard ratio (HR) and 30-year absolute risk difference (ARD) for incident CVD (composite end point of coronary heart disease, stroke, heart failure, and CVD deaths) and all-cause mortality, based on each additional intake of 2 servings per week for monotonic associations or 2 vs 0 servings per week for nonmonotonic associations.

Results 

Among the 29 682 participants (mean [SD] age at baseline, 53.7 [15.7] years; 13 168 [44.4%] men; and 9101 [30.7%] self-identified as non-white), 6963 incident CVD events and 8875 all-cause deaths were adjudicated during a median (interquartile range) follow-up of 19.0 (14.1-23.7) years. The associations of processed meat, unprocessed red meat, poultry, or fish intake with incident CVD and all-cause mortality were monotonic (P for nonlinearity ≥ .25), except for the nonmonotonic association between processed meat intake and incident CVD (P for nonlinearity = .006). Intake of processed meat (adjusted HR, 1.07 [95% CI, 1.04-1.11]; adjusted ARD, 1.74% [95% CI, 0.85%-2.63%]), unprocessed red meat (adjusted HR, 1.03 [95% CI, 1.01-1.06]; adjusted ARD, 0.62% [95% CI, 0.07%-1.16%]), or poultry (adjusted HR, 1.04 [95% CI, 1.01-1.06]; adjusted ARD, 1.03% [95% CI, 0.36%-1.70%]) was significantly associated with incident CVD. Fish intake was not significantly associated with incident CVD (adjusted HR, 1.00 [95% CI, 0.98-1.02]; adjusted ARD, 0.12% [95% CI, −0.40% to 0.65%]). Intake of processed meat (adjusted HR, 1.03 [95% CI, 1.02-1.05]; adjusted ARD, 0.90% [95% CI, 0.43%-1.38%]) or unprocessed red meat (adjusted HR, 1.03 [95% CI, 1.01-1.05]; adjusted ARD, 0.76% [95% CI, 0.19%-1.33%]) was significantly associated with all-cause mortality. Intake of poultry (adjusted HR, 0.99 [95% CI, 0.97-1.02]; adjusted ARD, −0.28% [95% CI, −1.00% to 0.44%]) or fish (adjusted HR, 0.99 [95% CI, 0.97-1.01]; adjusted ARD, −0.34% [95% CI, −0.88% to 0.20%]) was not significantly associated with all-cause mortality.

Conclusions and Relevance 

These findings suggest that, among US adults, higher intake of processed meat, unprocessed red meat, or poultry, but not fish, was significantly associated with a small increased risk of incident CVD, whereas higher intake of processed meat or unprocessed red meat, but not poultry or fish, was significantly associated with a small increased risk of all-cause mortality. These findings have important public health implications and should warrant further investigations.

Source: Associations of Processed Meat, Unprocessed Red Meat, Poultry, or Fish Intake With Incident Cardiovascular Disease and All-Cause Mortality | Cardiology | JAMA Internal Medicine | JAMA Network

Steve Parker, M.D.

PS: The traditional Mediterranean diet is low in meat and prominently features fish.

Steve Parker MD, Advanced Mediterranean Diet

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Posted in Diet-Heart Hypothesis, Heart Disease, Longevity, Stroke

From Larry Husten: Saturated Fats Linked To Heart Disease Once Again

Posted on November 28, 2016 | Comments Off on From Larry Husten: Saturated Fats Linked To Heart Disease Once Again

“A prominent group of nutrition researchers have once again linked saturated fats to increased coronary heart disease.

The new paper, published in BMJ, is the third paper in the past year to decry saturated fats. Along with the previous two papers, published in JACC and JAMA Internal Medicine, the BMJ paper uses data from two large observational studies to support the widely held view that high intake of saturated fat should be replaced with unsaturated fats, complex carbohydrates, or plant-based proteins. The senior author of all three papers is Frank Hu, the Harvard University nutrition researcher who has been a leading figure in the prosecution of saturated fats.

But some critics, including a BMJ editorialist, continue to raise concerns that observational data like this is not capable of demonstrating the negative effect of saturated fats. The new paper also raises additional concerns about the role of co-authors who work in the food industry.’

Source: Saturated Fats Linked To Heart Disease Once Again

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Posted in Coronary Heart Disease, Diet-Heart Hypothesis

Still Taking Fish Oil Supplements? Think Again

Posted on October 30, 2014 | 2 comments

Salmon is one the the cold-water fatty fish loaded with omega-3 fatty acids

Salmon is one the the cold-water fatty fish loaded with omega-3 fatty acids

I’ve been sitting on this research report a few years, waiting until I had time to dig into it. That time never came. The full report is free online (thanks, British Medical Journal!). I scanned the full paper to learn that nearly all the studies in this meta-analysis used fish oil supplements, not the cold-water fatty fish the I recommend my patients eat twice a week. If you’re taking fish oil supplements on your doctor’s advice, don’t stop without consulting her.

Here’s the abstract:

Objective: To review systematically the evidence for an effect of long chain and shorter chain omega 3 fatty acids on total mortality, cardiovascular events, and cancer.

Data sources: Electronic databases searched to February 2002; authors contacted and bibliographies of randomised controlled trials (RCTs) checked to locate studies.

Review methods Review of RCTs of omega 3 intake for 3 6 months in adults (with or without risk factors for cardiovascular disease) with data on a relevant outcome. Cohort studies that estimated omega 3 intake and related this to clinical outcome during at least 6 months were also included. Application of inclusion criteria, data extraction, and quality assessments were performed independently in duplicate.

Results: Of 15 159 titles and abstracts assessed, 48 RCTs (36 913 participants) and 41 cohort studies were analysed. The trial results were inconsistent. The pooled estimate showed no strong evidence of reduced risk of total mortality (relative risk 0.87, 95% confidence interval 0.73 to 1.03) or combined cardiovascular events (0.95, 0.82 to 1.12) in participants taking additional omega 3 fats. The few studies at low risk of bias were more consistent, but they showed no effect of omega 3 on total mortality (0.98, 0.70 to 1.36) or cardiovascular events (1.09, 0.87 to 1.37). When data from the subgroup of studies of long chain omega 3 fats were analysed separately, total mortality (0.86, 0.70 to 1.04; 138 events) and cardiovascular events (0.93, 0.79 to 1.11) were not clearly reduced. Neither RCTs nor cohort studies suggested increased risk of cancer with a higher intake of omega 3 (trials: 1.07, 0.88 to 1.30; cohort studies: 1.02, 0.87 to 1.19), but clinically important harm could not be excluded.

Conclusion: Long chain and shorter chain omega 3 fats do not have a clear effect on total mortality, combined cardiovascular events, or cancer.

Steve Parker, M.D.

Reference: Hooper, Lee et al. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review. BMJ  2006;332:752-760 (1 April), doi:10.1136/bmj.38755.366331.2F (published 24 March 2006).

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Posted in Diet-Heart Hypothesis, Heart Disease, Supplements

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Heart Attacks: It All Boils Down to LDL-P

Posted on October 7, 2013 | 2 comments

…according to Drs. Thomas Dayspring and JamesUnderberg. By LDL-P, they mean LDL cholesterol particle number. I don’t know if these guys are right or not. I bet it’s more complicated than LDL particle number.

Most heart attacks (aka myocardial infarctions) 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 them 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).

Underberg and Dayspring don’t mention 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. Is that outdated?

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

Read the whole enchilada.

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.

Steve Parker, M.D.

h/t Dr. Axel Sigurdsson

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Posted in Coronary Heart Disease, Diet-Heart Hypothesis, Heart Disease

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Heart-Healthy Lifestyle Also Cuts Cancer Risk By Half

Posted on March 19, 2013 | 1 comment

…according to a report in MedPageToday.

I'm still not convinced that severe sodium restriction is necessary or even possible for most people

I’m still not convinced that severe sodium restriction is necessary or even possible for most people

The American Heart Association has published guidelines aiming to reduce premature death and illness caused by cardiovascular diseases such as heart attacks, high blood pressure, and strokes.

The guidelines focus on seven factors critical to cardiovascular health:

  • smoking
  • blood sugar
  • blood pressure
  • physical activity
  • total cholesterol
  • body mass index (BMI)
  • ideal diet

Using data from the Atherosclerosis Risk In Communities study (almost two decades’ follow-up), researchers found that those who maintained goals for six or seven of the American Heart Association critical factors had a 51% lower risk of cancer compared with those meeting no goals.

For detailed information about the specific goals, click here.

As you might expect, I was curious about what the American Heart Association considered a heart-healthy diet.  I quote the AHA summary:

The recommendation for the definition of the dietary goals and metric, therefore, is as follows: “In the context of a diet that is appropriate in energy balance, pursuing an overall dietary pattern that is consistent with a DASH [Dietary Approaches to Stop Hypertension]-type eating plan, including but not limited to:

  • Fruits and vegetables: ≥ 4.5 cups per day
  • Fish: ≥ two 3.5-oz servings per week (preferably oily fish)
  • Fiber-rich whole grains (≥ 1.1 g of fiber per 10 g of carbohydrate): ≥ three 1-oz-equivalent servings per day
  • Sodium: < 1500 mg per day
  • Sugar-sweetened beverages: ≤ 450 kcal (36 oz) per week

Intake goals are expressed for a 2000-kcal diet and should be scaled accordingly for other levels of caloric intake. For example, ≤ 450 calories per week represents only up to one quarter of discretionary calories (as recommended) coming from any types of sugar intake for a 2000-kcal diet.

Diet recommendations are more complicated than that; read the full report for details.  Only 5% of study participants ate the “ideal diet.”  The Mediterranean diet easily meets four out of five of those diet goals; you’d have to be extremely careful to reach the sodium goal on most any diet.

Cardiovascular diseases and cancer are among the top causes of death in Western societies.  Adhering to the guidelines above may kill two birds with one stone.

Steve Parker, M.D.

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Posted in Cancer, Coronary Heart Disease, Diet-Heart Hypothesis, Exercise, Heart Disease, High Blood Pressure

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Time to Abandon the Diet-Heart Hypothesis?

Posted on May 25, 2012 | Comments Off on 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.

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Are Saturated Fats Really All That Bad?

Posted on February 22, 2012 | 4 comments

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-analysis. Annals 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.

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