Tag Archives: coronary artery disease

June 11, 2016 · 9:30 PM

Should You Reduce Saturated Fat Consumption If You Have Heart Disease?

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

For the bulk of my medical career, physicians thought that saturated fat caused heart disease, specifically coronary artery disease and heart attacks. Most doctors still think that. In 2009, I spent 80 hours reviewing the scientific literature supporting the saturated fat/heart disease connection. The evidence was very weak, if not nonexistent.

But what if you are already a heart disease patient? Would continuing saturated fat consumption have any effect on your longevity and risk of future heart attacks? 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 that 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.

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August 16, 2015 · 3:41 AM

Book Review: The South Asian Health Solution

Indian woman cooking chapati

Indian woman cooking chapati

Here’s my review of The South Asian Health Solution: A culturally tailored guide to lose fat, increase energy, avoid disease by Ronesh Sinha, published in 2014.

♦   ♦   ♦

Dr. Sinha practices internal medicine in northern California (Silicon Valley) and has a large dose of South Asians in his clinic. “South Asia” usually encompasses India, Pakistan, Nepal, Bangladesh, Bhutan, Sri Lanka and Maldives. It is home to one fifth of the world’s population. This book pertains mostly to Indians, which is Dr. Sinha’s ethnicity. I live in the Pheonix, AZ, area and we have a fair number of Indian engineers and physicians.

WHY DO SOUTH ASIANS NEED THEIR OWN SPECIAL HEALTH GUIDE?

Because Dr. Sinha says they have unique genetic and cultural issues that predispose them to type 2 diabetes, abdominal obesity, coronary artery disease, high blood pressure, and adverse cholesterol numbers. For example, compared to natives who stay in their home countries, South Asian immigrants to the West have 3–4 times higher prevalence of diabetes, he says. Dr Sinha has a program that he’s convinced will prevent or forestall these medical problems in South Asians.

Dr. Sinha says South Asians eat too many carbohydrates and are too sedentary. Especially those who have moved to the West (e.g., US, UK, Europe, Canada). He notes that the core of the typical South Asian diet is flat breads, lentils, rice, fried crispy snacks (with heart-poisoning trans fats), culminating in 150–200 daily grams of carbohydrate more than he sees in other ethnics in California. Western fast foods, sodas, and sweets compound the problem.

He says “most South Asians are skinny-fat,” meaning skinny legs and arms but with a fat belly from visceral fat. This is also called sarcopenic obesity. The usual “healthy” body mass index (BMI) numbers don’t apply to Asians. The World Health Organisation classifies Asians as underweight if BMI is 18.4 or less, healthy at BMI of 18.5 to 13, overweight at BMI 23.1 to 25, and obese if BMi is over 25. These numbers are lower than those used for non-Asian populations.

Another issue in his South Asian patient population is vitamin D deficiency related to their dark skin (hence, less vitamin D production) and too much time indoors. He says vitamin D deficiency promotes inflammation and insulin resistance. More on this below.

Some South Asians have a K121Q gene mutation that causes insulin resistance, which in turn can cause disease. And whether it’s genetic or not (but I think it is), he says South Asians tend to have higher Lp(a) [aka lipoprotein(a)], which causes early and aggressive coronary artery disease. They also tend to have small dense LDL, leading to a lower-than-expected total cholesterol level which may be deceptively low.

Sinha notes a strong vegetarian preference in Indians but spends almost no time discussing it. From the book, I can’t tell if Indian vegetarians are lacto-ovo-vegetarians, pescetarians, or vegans. The author is not a vegetarian.

Gadi Sagar temple on Gadisar Lake, Jaisalmer, Rajasthan, India

Gadi Sagar temple on Gadisar Lake, Jaisalmer, Rajasthan, India

 

SINHA’S GRAND UNIFICATION THEORY OF DISEASE CAUSATION

So, South Asians, at least in the West, have a high-carb diet, are too sedentary, and have genetic tendencies to heart disease and diabetes. How do these factors cause disease? It’s all tied together with insulin resistance. Insulin is the main hormone that keeps our blood sugar from rising too high after we digest a meal. Insulin drives blood sugar into our body cells to be used as energy or stored as fat or glycogen. If our tissues have insulin resistance, blood sugar levels rise. As a compensatory effort, our pancreas excretes more insulin in to the blood stream than would normally be the case. Whether or not that eventually lowers blood sugar levels, the higher insulin levels themselves can cause toxicity. For example, higher insulin levels raise blood pressure, which damages the cells lining the insides of our arteries, leading to chronic inflammation and atherosclerosis (hardening of the arteries). Some of the arterial damage is mediated through small dense LDL cholesterols (aka type B LDL), which is promoted by high insulin levels (hyperinsulinemia). Insulin resistance also results in a defective and overactive immune system, which further promotes chronic inflammation. This inflammation is “…the root cause of almost every imaginable chronic disease…from heart attacks and strokes to Alzheimers Disease.”

Anyway, this is Dr. Sinha’s hypothesis, and there is some scientific evidence to support it. Sinha says that the concept of insulin resistance “weaves together virtually every chronic ailment currently afflicting South Asians.” That may be a bit hyperbolic: He carves out no exceptions for arthritis, asthma, eczema, migraines, glaucoma, macular degeneration, hearing loss, erectile dysfunction, hepatitis C, prostate enlargement, toenail fungus, or male-pattern baldness.

Dr. Sinha’s Grand Unification Theory of Disease Causation has some support among physicians and scientists, but is by no means universally accepted among them. As for myself, I think he’s over-simplifying (for his readership’s sake?) and getting a bit ahead of the science.

Most clinicians aren’t testing directly for insulin resistance. What are the indirect clues? Belly fat, low HDL cholesterol, high trigylcerides, high blood pressure, prediabetes, and type 2 diabetes. These are components of the metabolic syndrome. Not everybody with one or more of these factors has insulin resistance but many do.

WHAT’S HIS PROGRAM?

If Sinha is correct, the South Asian Health Solution is a “low-insulin lifestyle” achieved through carbohydrate-reduced eating, exercise, and avoidance or resolution of belly fat. These help improve all components of the aforementioned metabolic syndrome. The backbone of the plan is carbohydrate restriction. For low-carb eating, avoid wheat bread and Indian flat breads (e.g., chapatis, naans, parathas, puris, phulkas), aloo (primarily potatoes and starchy vegetables), rice and other grains, beans, and sugar. Keep track of your net carbohydrates (he likes FitnessPal.com, which includes South Asian foods).

If you need to burn off body fat, limit carbs to 50–100 grams/day (digestible or net carbs, I assume). Aim for 100–150 grams/day to maintain health and weight loss.

You might be able to add “safe starches” later: white rice, potatoes. To replace your Indian flat breads, learn how to make them with substitutes for wheat flour: coconut flour or almond flour (no skins) or almond meal (skin included). Recipe on page 347. Rice alternatives are cauliflower “rice,” shredded cabbage, broccoli slaw, chopped broccoli, and chopped carrots.

He likes ghee, extra virgin olive oil, coconut oil, and butter. Avoid high omega-6 fatty acid consumption, as in vegetable oils. Of course, avoid trans fats. Good fats are saturated, monousaturated, and omega-3s.

He provides a few low-carb recipes, surprisingly without specific carb counts: chapatis, microwave bread, cauliflower pizza, coconut cauliflower rice, shredded cabbage sabji, gajar halwa (carrot pudding), and coconut ladoo.

Dr. Sinha doesn’t provide a comprehensive meal plan. He trusts his California South Asians to figure out how and what to eat. They’re smarter than average (he never says that, but that’s been my experience with South Asians in my world).

Dr. Sinha is also a huge proponent of exercise. He’ll tell you about squats, lunges, planks, burpees, yoga, and Tabata intervals. He agrees with me and Franziska Spritzler that “physical activity is the most effective fountain of youth available.”

Steve Parker, M.D., Conquer Diabetes and Prediabetes

Taking a rest from the fountain of youth

 

I skipped some of the chapters due to lack of time and interest: women’s issues (e.g., pregnancy, polycystic ovary syndrome, post-partum depression, osteoporosis), childhood, fatigue and stress management, and anti-aging.

MISCELLANEOUS TIDBITS

  • He likes high-sensitivity CRP testing.
  • His metabolic goals for South Asians are: 1) keep waist circumference under 35 inches (90 cm) in men, under 31 inches (80 cm) in women, 2) keep triglycerides under 100 mg/dl (1.13 mmol/l), 3) keep HDL cholesterol over 40 mg/dl (1.03 mmol/l) for men, and above 50 mg/dl (1.29 mmol/l) for women, 4) keep systolic blood pressure 120 or less, and diastolic pressure 80 or less, 5) keep fasting blood sugar under 100 mg/dl (5.6 mmol/l) and hemoglobin A1c under 5.7%, and 6) keep hs-CRP under 1.0 mg/dl.
  • He says HDL cholesterol helps reduce insulin resistance via apoprotein A-1 (apo A-1), which increases glucose uptake by cells.
  • He likes to follow the triglyceride/HDL ratio. If under 3, it means low risk of insulin resistance being present.
  • He likes to follow total cholesterol/HDL cholesterol ratio: ideal is under 3.5.
  • Statins are way over-used.
  • Ignore total cholesterol level by itself.
  • Stress control and sleep are important.
  • The author had some metabolic syndrome components: high triglycerides, low HDL cholesterol, and type B LDL (small, dense particles).
  • He dislikes the usual-recommended low-fat, low-cholesterol diet.
  • 4 tbsp (60 ml) of extra virgin olive oil daily seems to lower blood pressure.
  • Magnesium supplementation may lower blood pressure.
  • The liver stores about 100 grams of glycogen and muscles store 300–500 grams.
  • Vanaspati is a “cheap ghee substitute” made from vegetable oil and widely used in Indian restaurants and many Indian processed foods. Avoid it since it’s a source of trans fats.
  • Aloo sabji is a potato dish.
  • Traditional Indian herbs/spices include turmeric, cardamon, ginger, and cilantro.
  • Find an Indian medication guide at http://www.medguideindia.com/show_brand.php.
  • Coconut milk is a traditional fat in India.
  • Curry, curry, curry.
  • http://www.pamforg/southasian.
  • http://southasiahealthsolutions.org.
  • Non-alcoholic steatohepatitis (NASH) is quite common in South Asians, seemingly linked to visceral (abdominal) obesity and insulin resistance related to carbohydrates.
  • The book has no specific focus on diabetes.

THUMBS UP OR DOWN?

Overall, I like many of Dr. Sinha’s ideas. They seem to be supported by his experience with his own patients. I trust him. I bet many South Asians and non-Asians eating the Standard American Diet would see improved health by following his low-carb, physically active program.

Steve Parker, M.D.

 

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April 20, 2015 · 2:47 AM

Major U.S. Diet Changes over the Last 100 Years

Medical student Kris Gunnars has an article at Business Insider, of all places, that shows graphically many of the major U.S. dietary changes of the last hundred years. In this case, transmogrification may be a better term than mere “changes.” Much of the Western world has evolved in similar fashion.

You need to read the article and ponder the graphs if you question why we have so much obesity, type 2 diabetes, heart disease, hypertension, and perhaps cancer. You’ll see dramatic increases in consumption of added sugars, industrial seed oils (esp. soybean), soda pop and fruit juice (added sugar!), total calories, and fast food. You’ll see how much we’ve increased dining away from home. Butter consumption is down drastically, but doesn’t seem to have done us much good, if any.

Sugar cane

Sugar cane

 

There’s fairly good evidence that coronary artery disease (CAD) the cause of most heart attacks) was very prominent between 1960 to 2000 or so, but it’s been tapering off in recent years and didn’t seem to be very common 100 years ago. Understand that you can have it for 20 years or more before you ever have symptoms (angina) or a heart attack from it. In fact, the disease probably starts in childhood. I’ve always wondered about the cause of the CAD prevalence trends, and wondered specifically how much of the long-term trend was related to trans-fat consumption. But I’ve never been able to find good data on trans-fat consumption. Kris came up with a chart of margarine consumption, which may be a good proxy for trans-fats. Another of his charts includes shortening, a rich source of trans-fats and probably also a good proxy. I remember growing up in the 1960s that we always had a 1/2 gallon tin can of Crisco hydrogenated fat in the cupboard. Shortening consumption increased dramatically from 1955 until dropping like a rock around 2000.

The timeline curves for trans-fat consumption (by proxy) and prevalence of coronary heart disease seem to match up fairly well, considering a 20 year lag. In the early 1990s, we started cutting back on trans-fats, and here we are now with lower mortality and morbidity from coronary artery disease. (CAD is very complex; lower rates of smoking surely explain some of the recent trend.)

Read the whole enchilada. Very impressive. Highly recommended.

Steve Parker, M.D.

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June 14, 2012 · 2:00 AM

Are Dietary Saturated Fats Dangerous?

This is an epic post from my old Advanced Mediterranean Diet blog, originally dated July 6, 2009. That was a watershed year for me because of the ideas in this article.  If you or your doctor think low-carb eating is dangerous because it may be higher in saturated fat, this post should convince you otherwise.

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 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.

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July 18, 2011 · 2:17 AM

Waist-Hip Ratio: How to Determine, and What It Means

High WHR

A comment left under my recent post on healthy weight ranges reminded me about the waist-hip ratio.

The risk of heart and vascular disease is more closely linked to distribution of excess fat than with degree of obesity as measured by overall weight or body mass index. Waist-hip ratio (WHR) is a measure of abdominal or central obesity, the type of fat distribution associated with coronary artery disease. A high ratio indicates the android body habitus.  The Journal of the American College of Cardiology two months ago reported that heart patients (coronary artery disease) with “central obesity” had a greater risk of death.  A high WHR is one measure of central obesity.

To determine your waist-hip ratio:

1.   While standing, relax your stomach—don’t
      pull it in. Measure around your waist mid-
      way between the bottom of the rib cage and
      the top of your pelvis bone. Usually this is at
      the level of your belly button, or an inch
      higher. Don’t go above the rib cage. Keep the
      measuring tape horizontal to the ground and
      don’t compress your skin.
2.   Then measure around your hips at the
      widest part of your buttocks. Keep the tape
      horizontal to the ground and don’t compress
      your skin.
3.   Divide the waist by the hip measurement.
      The result is your waist-hip ratio.

For example, if your waist is 44 inches (112 cm) and hips are 48 inches (122 cm): 44 divided by 48 is 0.92, which is your waist-hip ratio.

Scientists haven’t yet determined the ideal WHR, but it is probably around 0.85 or less for women, and 0.95 or less for men. Ratios above 1.0 are clearly associated with risk of cardiovascular disease such as heart attacks. The higher the ratio, the higher the risk. Compared with body mass index, WHR is a much stronger predictor of coronary artery disease. Several of the other obesity-related illnesses are also correlated with WHR, but the relationship between WHR and cardiovascular disease is particularly strong.

Steve Parker, M.D.

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December 14, 2010 · 11:07 AM

Book Review: Why We Get Fat

Gary Taubes’s new book, Why We Get Fat: And What To Do About It, comes on the market later this month.  I give it five stars per Amazon.com’s ranking system (I love it).

♦   ♦   ♦

At the start of my medical career over two decades ago, many of my overweight patients were convinced they had a hormone problem causing it.  I carefully explained that’s rarely the case.  As it turns out, I may have been wrong.  And the hormone is insulin.

Mr. Taubes wrote this long-awaited book for two reasons: 1) to make the ideas in his 2007 masterpiece (Good Calories, Bad Calories) more accessible to the public, and 2) to speed up the process of changing conventional wisdom on overweight.  GCBC was the equivalent of a college-level course on nutrition, genetics, history, politics, science, physiology, and biochemistry. Many nutrition science geeks loved it while recognizing it was too difficult for the average person to digest.

Paradigm Shift

The author hopes to convince us that “We don’t get fat because we overeat; we overeat because we’re getting fat.”  We need to think of obesity as a disorder of excess fat accumulation, then ask why the fat tissue isn’t regulated properly.  A limited number of hormones and enzymes regulate fat storage; what’s the problem with them?

Mr. Taubes makes a great effort convince you the old “energy balance equation” doesn’t apply to fat storage.  You remember the equation: eat too many calories and you get fat, or fail to burn up enough calories with metabolism and exercise, and you get fat.  To lose fat, eat less and exercise more.  He prefers to call it the “calories-in/calories-out” theory.  He admits it has at least a little validity.  Problem is, the theory seems to have an awfully high failure rate when applied to weight management over the long run.  We’ve operated under that theory for the last half century, but keep getting fatter and fatter.  So the theory must be wrong on the face of it, right?  Is there a better one?

So, Why DO We Get Fat?

Here is Taubes’s explanation.  The hormone in charge of fat strorage is insulin; it works to make us fatter, building fat tissue.  If you’ve got too much fat, you must have too much insulin action.  And what drives insulin secretion from your pancreas?  Dietary carbohydrates, especially refined carbs such as sugars, flour, cereal grains, starchy vegetables (e.g., corn, beans, rice, potatoes), liquid carbs.  These are the “fattening carbs.”  Dozens of enzymes and hormones are at play either depositing fat into tissue, or mobilizing the fat to be used as energy.  It’s an active process going on continously.  Any regulatory derangement that favors fat accumulation will CAUSE gluttony (overeating) or sloth (inactivity).  So it’s not your fault. 

What To Do About It

Cut back on carb consumption to lower your fat-producing insulin levels, and you turn fat accumulation into fat mobilization.

Before you write off Taubes as a fly-by-night crackpot, be aware that he’s received three Science-in-Society Journalism Awards from the National Association of Science Writers.  He’s a respected, professional science writer.  Having read two of his books, it’s clear to me he’s very intelligent.  If he’s got a hidden agenda, it’s well hidden.

One example  illustrates how hormones control growth of tissues, including fat tissue.  Consider the transformation of a skinny 11-year-old girl into a voluptuous woman of 18. Various hormones make her grow and accumulate fat in the places we now see curves.  The hormones make her eat more, and they control the final product.  The girl has no choice.  Same with our adult fat tissue, but with different hormones. If some derangement is making us grow fatter, it’s going to make us more sedentary (so more energy can be diverted to fat tissue) or make us overeat, or both.  We can’t fight it.  At not least very well, as you can readily appreciate if look at the people around you at any American shopping mall.

This’N’That

Taubes’s writing is clear and persuasive.  He doesn’t beat you over the head with his conclusions. He lays out a logical series of facts and potential connections and explanations, helping you eventually see things his way.  If insulin controls fat storage by building and maintaining fat tissue, and if carboydrates drive insulin secretion, then the way to reduce overweight and obesity is carbohydrate-restricted eating, especially avoiding the fattening carbohydrates.  I’m sure that’s true for many folks, perhaps even a majority.

If you’re overweight and skeptical about this approach, you could try out a very-low-carb diet for a couple weeks or a month at little expense and risk (but not zero risk).  If Mr. Taubes and I are right, there’s a good chance you’ll lose weight.  At the back of the book is a university-affiliated low-carb eating plan.

If cutting carb consumption is so critical for long-term weight control, why is it that so many different diets—with no focus on carb restriction—seem to work, if only for the short run?  Taubes suggests it’s because nearly all diets reduce carb consumption to some degree, including the fattening carbs.  If you reduce your total daily calories by 500, for example, many of those calories will be from carbs.  Simply deciding to “eat healthy” works for some people: stopping soda pop, candy bars, cookies, desserts, beer, etc.  That cuts a lot of fattening carbs right there.

Losing excess weight or controlling weight by avoiding carbohydrates was the conventional wisdom prior to 1960, as documented by Mr. Taubes.  Low-carb diets for obesity date back almost 200 years.  The author attributes many of his ideas to German internist Gustav von Bergmann (1908).   

Taubes discusses the Paleolithic diet, mentioning that the average paleo diet derived about a third of total calories from carbohdyrates (compared to the standard American diet’s 55% of calories from carb).  My prior literature review  found 40-45% of paleo diet calories from carbohydrate.  I’m not sure who’s right.

Minor Bone of Contention RE: Coronary Heart Disease

Mr. Taubes provides numerous scientific references to back his assertions.  I checked out one in particular because it didn’t sound right.  Some background first. 

Reducing our total fat and saturated fat consumption over the last 40 years was supposed to lower our LDL cholesterol, thereby reducing the burden of coronary heart disease, which causes heart attacks.  Instead, we’ve experienced the obesity epidemic as those fats were replaced by carbohydrates.  Taubes mentions a 2009 medical journal article by Kuklina et al, in which Taubes says Kuklina points out the number of heart attacks has not decreased as we’ve made these diet changes.  Kuklina et al don’t say that.  In fact, age-standardized heart attack rates have decreased in the U.S. during the last decade. 

Furthermore, autopsy data document a reduced prevalence of anatomic coronary heart disease in people aged 20-59 from 1979 to 1994, but no change in prevalence for those over 60. The incidence of coronary heart disease decreased in the U.S. from 1971 to 1998 (the latest reliable data).  Death rates from heart disease and stroke have been decreasing steadily over the last 40 years in the U.S.; coronary heart disease death rates are down by 50%.  I do agree with Taubes that we shouldn’t credit those improvements to reduced total and saturated fat consumption.  [Reduced trans fat consumption may play a role, but that’s off-topic.] 

I think Mr. Taubes would like to believe that coronary artery disease is either more severe or unchanged in the last few decades because of low-fat, high-carb eating.  That would fit nicely with some of his theories, but it’s not the case.  Coronary artery disease is better now thanks to a variety of factors, but probably not diet (setting aside the trans-fat issue).

Going Forward

Low-carb dieting was vilified over the last half century partly out of concern that the accompanying high fat consumption would cause premature heart attacks, strokes, and death.  We know now that total dietary fat and saturated fat have little to do with coronary heart disease and atherosclerosis (hardening of the arteries), which sets the stage for a resurgence of low-carb eating.  

I advocate Mediterranean-style eating as the healthiest, in general.  It’s linked with prolonged life and lower risk of heart disease, stroke, dementia, diabetes, and cancer.  On the other hand, obesity is a strong risk factor for premature death and development of heart disease, stroke, diabetes, and cancer.  If consistent low-carb eating cures the obesity, is it healthier than the Mediterranean diet?  Maybe so.  Would a combination of low-carb and Mediterranean be better?  Maybe so.  I’m certain Mr. Taubes would welcome a decades-long interventional study comparing low-carb with the Mediterranean diet.  But that’s probably not going to happen in our lifetimes. 

Gary Taubes rejects the calories-in/calories-out theory of overweight that hasn’t done a very good job for us over the last 40 years.  Taubes’s alternative ideas deserve serious consideration.

Steve Parker, M.D.

Update December 18, 2010: I found Mr. Taubes’s reference for stating that Paleolithic diets provide about a third of calories from carbohydrate (22-40%), based on modern hunter-gatherer societies).  See References below.   

References:
Coronary heart disease autopsy data:  American Journal of Medicine, 110 (2001): 267-273.
Reduced heart attacks:  Circulation, 12 (2010): 1,322-1,328.
Reduced incidence of coronary heart disease:  www.UpToDate.com, topic: “Epidemiology of Coronary Heart Disease,” accessed December 11, 2010.
Death rates for coronary heart disease:  Journal of the American Medical Association, 294 (2005): 1,255-1,259.

Cordain, L., et al.  Plant-animal subsistance ratios and macronutrient energy estimations in worldwide hunter-gatherer diets.  American Journal of Clinical Nutrition, 71 (2000): 682-692.

Disclosure:  I don’t know Gary Taubes.  I requested from the publisher and received a free advance review copy of the book.  Otherwise I received nothing of value for this review.

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.

Update April 22, 2013: 

As mentioned above, WWGF was based on Taubes’ 2007 book, Good Calories, Bad Calories. You may be interested in a highly critical review of GCBC by Seth at The Science of Nutrition.

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January 16, 2010 · 2:00 AM

Eat the Right Carbs to Alleviate Diabetes and Heart Disease

Harvard’s Dr. Frank Hu in 2007 called for a paradigm shift in dietary prevention of heart disease, de-emphasizing the original diet-heart hypothesis and noting instead that “. . . reducing dietary GL [glycemic load] should be made a top public health priority.”  Jim Mann at the University of Otago (Dunedin, New Zealand) authored a 2007 review of carbohydrates and effects on heart disease and diabetes.  Here are highlights from the article summary in the European Journal of Clinical Nutrition:

The nature of carbohydrate is of considerable importance when recommending diets intended to reduce the risk of type II diabetes and cardiovascular disease and in the treatment of patients who already have established diseases. Intact fruits, vegetables, legumes and whole grains are the most appropriate sources of carbohydrate. Most are rich in [fiber] and other potentially cardioprotective components.  Many of these foods, especially those that are high in dietary fibre, will reduce total and low-density lipoprotein cholesterol and help to improve glycaemic control in those with diabetes.

Frequent consumption of low glycaemic index foods has been reported to confer similar benefits, but it is not clear whether such benefits are independent of the dietary fibre content of these foods or the fact that low glycaemic index foods tend to have intact plant cell walls.

A wide range of carbohydrate intake is acceptable, provided the nature of carbohydrate is appropriate. Failure to emphasize the need for carbohydrate to be derived principally from whole grain cereals, fruits, vegetables and legumes may result in increased lipoprotein-mediated risk of cardiovascular disease, especially in overweight and obese individuals who are insulin resistant.

Why does this matter to me and readers of this blog?  Dietary carbohydrates are a major determinant of blood sugar levels, tending to elevate them.  Chronically high blood sugar levels are associated with increased complication rates from diabetes.  People with diabetes are prone to develop heart disease, namely coronary artery disease, which causes heart attacks, weakness of the heart muscle, and premature death. 

Steve Parker, M.D.

References: 

Mann, J.  Dietary carbohydrate: relationship to cardiovascular disease and disorders of carbohydrate metabolism.  European Journal of Clinical Nutrition, 61 (2007): Supplement 1: S100-11.

Hu, Frank.  Diet and cardiovascular disease prevention: The need for a paradigm shift.  Journal of the American College of Cardiology, 50 (2007): 22-24.

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Filed under Carbohydrate, coronary heart disease, Fiber, Fruits, Glycemic Index and Load, Grains, legumes, Vegetables

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