Tag Archives: coronary heart disease

Sulfonylurea Drugs Linked to Heart Disease in Women

…according to this article at Diabetes Care. The study population was the Nurses Health Study. The longer the sulfonylurea was used, the stronger the association with Coronary Heart Disease. CHD is by far the most common cause of heart attacks. On the bright side, the drugs were not linked to stroke risk. Remember, correlation is not causation, blah, blah, blah…

This report is another reason to do all you can to control blood sugars with diet and exercise, minimizing the risks—known and unknown—of long-term drugs.

I rarely start my patients on sulfonylureas these days.

Steve Parker, M.D.

High Carbohydrate Diet May Cause Atherosclerosis

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

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

medical clearance, treadmill stress test

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

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

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

 

h/t Mangan

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

medical clearance, treadmill stress test

This treadmill stress test is looking for hidden heart disease

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

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

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

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

Underberg and Dayspring write:

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

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

***

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

Read the whole enchilada.

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

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

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

Steve Parker, M.D.

About Dayspring and Underberg:

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

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

h/t Dr. Axel Sigurdsson

The Carbohydrate and Chronic Disease Connection

Simple dinner roll, or a future HEART ATTACK?

Adherents of the paleo diet and low-carb diets will love this post; it supports their choices.

Dentists are considering a return to an old theory that dietary carbohydrates first cause dental diseases, then certain systemic chronic diseases, according to a review in the June 1, 2009, Journal of Dental Research.  It’s written by Dr. Philippe P. Hujoel, who has been active in dental research for decades and is affiliated with the University of Washington (Seattle). He is no bomb-throwing, crazed, radical.

We’ve known for years that some dental and systemic diseases are associated with each other, both for individuals and populations. For example, gingivitis and periodontal disease are associated with type 2 diabetes and coronary heart disease. The exact nature of that association is not clear. In the 1990s it seemed that infections – chlamydia, for example – might be the unifying link, but this has not been supported by subsequent research.

The “old theory” to which I referred earlier is the Cleave-Yudkin idea from the 1960s and ’70s that excessive intake of digestible carbohydrates, in the absence of good dental care, leads both to certain dental diseases – caries (cavities), periodontal disease, certain oral cancers, and leukoplakia – and to some common systemic chronic non-communicable diseases such as coronary heart disease, type 2 diabetes, some cancers, and dementia. In other words, dietary carbohydrates cause both dental and systemic diseases – not all cases of those diseases, of course, but some.

In the context of excessive carbohydrate intake, the article frequently mentions sugar, refined carbs, and high-glycemic-index carbs. Dental effects of excessive carb intake can appear within weeks or months, whereas the sysemtic effects may take decades.

Hujoel compares and contrasts Ancel Keys’ Diet-Heart/Lipid Hypothesis with the Cleave-Yudkin Carbohydrate Theory. In Dr. Hujoel’s view, the latest research data favor the Carbohydrate Theory as an explanation of many cases of the aforementioned dental and systemic chronic diseases. If correct, the theory has important implications for prevention of dental and systemic diseases: namely, dietary carbohydrate restriction.

I agree with Dr. Hujoel that we need a long-term prospective trial of serious low-carb eating versus the standard American high-carb diet. Take 20,000 people, randomize them to one of the two diets, follow their dental and systemic health over 15-30 years, then compare the two groups. Problem is, I’m not sure it can be done. It’s hard enough for most people to follow a low-carb diet for four months. And I’m asking for 30 years?!

Dr. Hujoel writes:

Possibly, when it comes to fermentable carbohydrates, teeth would then become to the medical and dental professionals what they have always been for paleoanthropologists: “extremely informative about age, sex, diet, health.”

Dr. Hujoel mentioned a review of six studies that showed a 30% reduction in gingivitis score by following a diet moderately reduced in carbs. He mentions the aphorism: “no carbohydrates, no caries.” Anyone prone to dental caries or ongoing periodontal disease should do further research to see if switching to low-carb eating might improve the situation.

Don’t be surprised if your dentist isn’t very familiar with the concept.

Steve Parker, M.D.

Reference: Hujoel, P. Dietary carbohydrates and dental-systemic diseasesJournal of Dental Research, 88 (2009): 490-502.

Mendosa, David. Our dental alarm bell. MyDiabetesCentral.com, July 12, 2009.

Jimmy Moore’s 2012 interview with Dr. Hujoel.

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.

Heart Disease Declining In U.S.

The U.S. Centers for Disease Control and Prevention reported this year that the prevalence of self-reported coronary heart disease in the U.S. declined from 6.7% of the population in 2006, to 6% in 2010.  Figures were obtained by telephone survey.  Coronary heart disease, the main cause of heart attacks, remains the No.1 cause of death in the U.S.

Self-reports of heart disease may not be terribly reliable.  However, I remember an autopsy study from Olmstead County, Minnesota, from a few years ago that confirmed a lower prevalence of coronary heart disease.  I wrote about that at my old NutritionData.com Heart Health Blog, but those posts are hard to find.

The CDC report mentioned also that mortality rates from coronary heart disease have been steadily declining for the last 50 years. 

Improved heart disease morbidity and mortality figures probably reflect better control of risk factors (e.g., smoking, high blood pressure), as well as improved treatments.  I’ve never seen an estimate of the effect of reduced trans fat consumption. 

Obesity and diabetes always mentioned as risk factors for heart disease, yet obesity and diabetes rates have skyrocketed over the last 40 years.  You’d guess heart disease prevalance to have risen, but you’d have guessed wrong.  In view of high obesity rates, some pundits have even suggested that the current generation of Americans wil be the first to see a decrease in average life span. 

The American Diabetes Association offers a free heart disease risk calculator, if you’re curious about your own odds.  My recollection is that the calculator works whether or not you have diabetes.

Steve Parker, M.D.

Paleo Diet Is More Satiating Than Mediterranean-Style in Small Study

Swedish researchers reported in 2010 that a Paleolithic diet was more satiating than a Mediterranean-style diet, when compared on a calorie-for-calorie basis in heart patients.  Both groups of study subjects reported equal degrees of satiety, but the paleo dieters ended up eating 24% fewer calories over the 12-week study.

The main differences in the diets were that the paleo dieters had much lower consumption of cereals (grains) and dairy products, and more fruit and nuts.  The paleos derived 40% of total calories from carbohydrate compared to 52% among the Mediterraneans.

Even though it wasn’t a weight-loss study, both groups lost weight.  The paleo dieters lost a bit more than the Mediterraneans: 5 kg vs 3.8 kg (11 lb vs 8.4 lb).  That’s fantastic weight loss for people not even trying.  Average starting weight of these 29 ischemic heart patients was 93 kg (205 lb).  Each intervention group had only 13 or 14 patients (I’ll let you figure out what happened to to the other two patients).

I blogged about this study population before.  Participants supposedly had diabetes or prediabetes, although certainly very mild cases (average hemoglobin A1c of 4.7% and none were taking diabetic drugs)

As I slogged through the research report, I had to keep reminding myself that this is a very small, pilot study.  So I’ll not bore you with all the details.

Bottom Line

This study suggests that the paleo diet may be particularly helpful for weight loss in heart patients.  No one knows how results would compare a year or two after starting the diet.  The typical weight-loss pattern is to start gaining the weight back at six months, with return to baseline at one or two years out.

Greek investigators found a link between the Mediterranean diet and better clinical outcomes in known ischemic heart disease patients.  On the other hand, researchers at the Heart Institute of Spokane found the Mediterranean diet equivalent to a low-fat diet in heart patients, again in terms of clinical outcomes.  U.S. investigators in 2007 found a positive link between the Mediterranean diet and lower rates of death from cardiovascular disease and cancer

We don’t yet have these kinds of studies looking at the potential benefits of the paleo diet.  I’m talking about hard clinical endpoints such as heart attacks, heart failure, cardiac deaths, and overall deaths.  The paleo diet definitely shows some promise.

I also note the Swedish investigators didn’t point out that weight loss in overweight heart patients may be detrimental.  This is the “obesity paradox,” called “reverse epidemiology” at Wikipedia.  That’s a whole ‘nother can o’ worms.

Keep your eye on the paleo diet.

Steve Parker, M.D.

Reference: Jonsson, Tommy, et al.  A paleolithic diet is more satiating per calorie than a mediterranean-like diet in individuals with ischemic heart diseaseNutrition and Metabolism, 2010, 7:85.