Quote of the Day

In truth, German character—so admired and feared in some 500 years of European literature and history—led to the present Germanization of Europe. These days we recoil at terms like “national character” that seem tainted by the nightmares of the past. But no other politically correct exegesis offers better reasons why a booming Detroit of 1945 today looks like it was bombed, and a bombed-out Berlin of 1945 now is booming.

                          —Victor Davis Hanson, writing at Townhall.com

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Prevent or Delay Neuropathy in Type 1 Diabetes with Aggressive Control of Blood Sugar

I couldn’t find a picture of “neuropathy,” so enjoy this

Aggressive efforts to control blood sugar either delays or prevents clinical neuropathy in patients with type 1 diabetes, according to the Cochrane Collaboraton as reported in MedPage Today.  Type 2 diabetics showed a strong trend in the same direction, but did not quite reach statistical significance (p=0.06).  Tight control of diabetes is often at the cost of more frequent episodes of hypoglycemia.

Intensive blood sugar control is also a treatment for established neuropathy.

One in ten diabetics has neuropathy at the time of diagnosis.  After 10 years, four or five of every 10 have it.  The pain of neuropathy is worse than the numbness.

The medical community is still debating how aggressively blood sugars should be managed.

     Steve Parker, M.D.

PS: I don’t know what the Cochrane reviewers consider “tight control” because the article is behind a paywall, and the MedPage Today article didn’t address that either.

Reference: Callaghan BC, et al “Enhanced glucose control for preventing and treating diabetic neuropathy” Cochrane Database Syst Rev 2012; DOI:10.1002/14651858.CD007543.pub2.

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Darrin Carlson’s Minimalist Exercise

Not Darrin Carlson

Darrin Carlson on March 23 this year shared his ideas on the minimal amount of exercise and equipment needed to achieve reasonable fitness benefits.

I’m self-experimenting with just six exercises now.

Public health authorities for years have recommended physical activity in the range of 150 minutes a week. That ain’t gonna happen for most folks. Darrin says, “Two hours a week will work for most people….”

Jonathan Bailor, Chris Highcock, and others suggest 30-60 minutes a week may be enough. Even Darrin admits as much, for the super-dedicated.

     -Steve

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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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Quote of the Day

And you will know the truth, and the truth will make you free.

—John 8:32

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Trouble Seeing? Might Be Your Diabetes Drug

Macular edema is two to five times more common in type 2 diabetics taking pioglitazone or rosiglitazone, according to an article published June 11, 2012, by MedPage Today.  The original research was reported in Archives of Internal Medicine.

The macula is the dark area in the middle of the right half of this retina photo

The macula is the most sensitive part of the retina at the back of your eyeball.  Edema, or watery swelling, of the macula can impair vision.

Very few patients in the U.S. use rosiglitazone any longer because of concerns about heart toxicity.  Pioglitazone has recently been implicated as a cause of bladder cancer.

You can avoid some diabetes drug complications by controlling blood sugars with diet and exercise.

Steve Parker, M.D. 

Reference:
Idris I, et al “Association between thiazolidinedione treatment and risk of macular edema among patients with type 2 diabetes” Arch Intern Med 2012; DOI:10.1001/archinternmed.2012.1938.

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Adolescent Type 1 Diabetes on the Rise in U.S.

The prevalence of type 1 diabetes in U.S. adolescents rose by 23% between 2001 and 2009, according to University of Colorado researchers.

The journal Pediatrics just recently published an article stating that the incidence of diabetes and prediabetes in U.S. adolescents increased from 9% in 1999 to 23% in 2008. From that report, however, I couldn’t tell how much of the increase was type 1 versus type 2.

No one knows why type 1 diabetes in youths is increasing.  The rise in type 2 diabetes is likely related to higher obesity rates.

     Steve Parker, M.D.

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Evidence in Favor of HIIT

Tabata’s team used stationary bicycles

I ran across this recent scientific review article on HIIT (high-intensity interval training) and thought you might be interested. Looks like it’s slated for publication in The Journal of Physiology.

I’m interested in HIIT as a means to achieve fitness in much less time than the 150 minutes a week of exercise recommended by various public health authorities.  I don’t like to exercise, so I’m searching for a program with substantial benefits at only 60-90 minutes a week!  Can I get a “Amen!”?

Why didn’t the authors at least mention the oft-cited and apparently pioneering work of Izumi Tabata et al from 1996?

Steve Parker, M.D.

References:

Gibala et al. Adaptations to low-volume, high-intensity interval training (preliminary draft). Journal of Physiology, doi: 10.1113/jphysiol.2011.224725

Tabata, I., et al. Effects of moderate-intensity endurance and high-intensity intermittent training on anaerobic capacity and VO2max. Medicine and Science in Sports and Medicine, 1996 Oct;28(10):1327-30.

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Denise Minger on the Purported Cherry-Picker Ancel Keys

Keys lived his last years in Pioppi, Italy, not near the Tower of Pisa

Here’s her take on Ancel Keys, the father of cardiovascular epidemiology and the what we now consider the healthy Mediterranean diet. She is funny. Warning: Her post is only for serious nutrition science geeks.

Too bad he’s not alive to defend himself. He died young, almost reaching 101.  Check out his New York Times obituary.

Steve Parker, M.D.

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What Everybody Ought to Know About Exercise’ Effect on Weight

  • Your genetics largely determines your response to an exercise program
  • Physical activity isn’t a great way to lose weight
  • School-based or other programs to increase childhood physical activity probably won’t reverse childhood obesity statistics
  • Disregarding weight loss, exercise has other worthwhile metabolic advantages
  • Highly advanced societies shouldn’t blame our overweight problem on decreased levels of physical activity

Skyler Tanner slaughters some sacred cows in his blog post June 4, 2012. I pulled these bullet points from his post. Click on his embedded links for details.

Steve Parker, M.D.

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