Category Archives: Coronary Heart Disease

Do Eggs Cause Heart Attacks and Premature Death?

At the beginning of my 30-year medical career, egg consumption was condemned as a cause of heart attacks.  Heart attacks can kill.  How did eggs kill?  It was thought to be related to the cholesterol content – 200 mg per egg – leading to higher serum cholesterol levels, which clogged arteries (atherosclerosis), leading to heart attacks.

Fifteen years ago the pendulum began to swing the other direction: Egg consumption didn’t seem to matter much, if at all.

The evidence is usually collected in observational, epidemiologic studies of large groups of people.  The groups are analyzed in terms of overall health, food intake (e.g., how many eggs per week), healthy lifestyle factors, etc.  Egg consumption of the group is broken down, for example, into those who never eat eggs, eat 1-4  eggs per week, eat 5-10 per week, or over 10 eggs weekly.  A group is followed and re-analyzed over 10-20 years and rates various diseases and causes of death are recorded.  Researchers don’t follow just 25 people like this over time.  You need thousands of participants to find statistically significant differences.

The debate about eggs was re-opened (although never really closed) by the publication in April, 2008, of an article in The American Journal of Clinical Nutrition.  Scientists of the Physicians’ Health Study suggest that consumption of seven or more eggs weekly is associated with significantly increased risk, over 20 years, of all-cause mortality.  Interestingly, this level of consumption did not cause heart attacks or strokes.  Study participants, by the way, were 21,327 Harvard-educated male physicians.  5,169 deaths occurred during 20 years of follow-up.  If you’re not a Harvard-educated male physician, the study results may not apply to you.

When physicians with diabetes  – type 2’s mostly, I assume –  were analyzed separately, consumption of even less than seven eggs per week was associated with higher all-cause mortality.

Several other observational studies looking at this same issue have found no association between egg consumption and cardiovascular disease, heart attacks, and all-cause mortality.

Bottom line?  If you worry about egg consumption, limit to 7 or less per week.  If you have type 2 diabetes, consider limiting to 4 or less per week.

I wouldn’t be surprised if a study were published next week saying “eat as many eggs as you want; they don’t have adverse health effects.”

Remember, all the cholesterol is in the yolk.  Try making an omelet using the whites only.  But in our lifetimes you’ll never see an observational study looking at egg white consumption and mortality rates.

I’m still not convinced egg consumption is worth losing sleep over.  “More studies are needed…”

Steve Parker, M.D.References:

Djousse, L. and Gaziano, J. M.  Egg consumption in relation to cardiovascular disease and mortality: the Physicians’ Health Study.  American Journal of Clinical Nutrition, 87 (2008): 964-969.

Dawber, T.R, et al.  Eggs, serum cholesterol, and coronary heart disease.  American Journal of Clinical Nutrition, 36 (1982): 617-625.

Nakamura, Y., et al.  Egg consumption, serum cholestrol, and cause-specific and all-cause mortality: the National Integrated Project for Prospective Observation of Non-communicable Disease and Its Trends in the Aged, 1980.  American Journal of Clinical Nutrition, 80 (2004): 58-63.

Evidence In Favor of Healthfulness of Whole Grains

I bought a sack of potatoes the other day.  The advertising on the sack proclaimed   these potatoes as “Gluten-Free!”.  As if other potatoes have gluten (they don’t).

In these days of gluten-free this and gluten-free that, the health benefits of grains—especially wheat—are being questioned.

A 2008 review article in a scientific journal confirmed the association between high whole grain intake and reduced incidence of cardiovascular disease.  Heart disease and strokes (subsets of cardiovascular disease) are the first and fourth leading causes of death, respectively, in the U.S.

The article authors, Philip Mellen, Thomas Walsh, and David Herrington, reviewed the scientific literature on the subject and found seven pertinent published observational studies.  Study participants were divided into those with high average whole grain intake (2.5 servings per day) and those with low average intake (0.2 servings a day, or 1 serving every 5 days).  Compared with low intake, participants with high intake had 21% lower risk of cardiovascular disease events, such as heart disease, stroke, and death from cardiovascular disease.

Refined grain intake, such as standard white bread, was not associated with cardiovascular disease one way or the other.

The authors conclude, “There is a consistent, inverse association between dietary whole grains and incident cardiovascular disease…and clinicians should redouble efforts to incorporate clear messages on the beneficial effects of whole grains into public health and clinical practice endeavors.”

I’ll be the first to admit that observational studies don’t prove that whole grains reduce the risk of cardiovascular disease.  They identify an association that should lead to additional testing of the hypothesis.  I don’t see any proof on the foreseeable horizon.

If heart attacks and strokes ran in my blood lines (genes), I’d try to incorporate two or three daily servings of whole grain into my diet, assuming I had no good reasons to avoid grains.

That being said, I’m also convinced that many can live long health lives without grains.

Steve Parker, M.D.

References and resources:

Mellen, Philip, et al.  Whole grain intake and cardiovascular disease: A meta-analysis.  Nutrition, Metabolism & Cardiovascular Diseases, 18, (2008): 283-290.

The Whole Grains Council.  Learn more about the benefits of various whole grains and how to find whole grain products.  Many recipes here, plus links to hundreds of recipes at other websites.

After Heart Attack, Which Is Better Diet: Low-Fat or Mediterranean?

For the last 12 years, the answer has been “Mediterranean.”  But a new study challenges that conclusion.

By the way, “diet” in this blog post refers to “a habitual way of eating” rather than a weight-loss program.

Researchers at The Heart Institute of Spokane (Washington) set out to compare the effects of a Mediterranean-style diet and a conventional “heart-healthy” low-fat diet in people who had suffered a heart attack within the last six months.  To test whether diet intervention per se had any effect, a “usual-care” group of patients (101 participants) was also studied.

Methodology

Dietary intervention participants were randomized to either:

  1. low-fat diet (American Heart Association Step II) (50 participants).  Main goals were to reduce cholesterol intake to under 200 mg/day and saturated fat to under 7% of total calories, or
  2. Mediterranean-style diet (51 participants) with the same cholesterol and saturated fat goals, plus an increased intake of omega-3 fatty acids (to over 0.75% of calories) and monounsaturated fats (to 20-25% of calories).  Emphasis was on consumption of cold-water fish 3-5 times per week, and on oils from olives, soybeans, and canola.

Both diets encouraged intake of fresh fruits and vegetables – at least 5 servings a day – and whole grains.  Loss of excess weight was not a goal.

Diet intervention participants were given two individual counseling sessions with a dietitian within the first month, with additional sessions at months 3, 6, 12, 18, and 24.  Participants also attended six group sessions.  Three-day food diaries were examined periodically to assess compliance with dietary recommendations.  Various lipids and omega-3 fatty acids were measured in plasma.  I assume that judicious wine consumption was at least mentioned as part of the Mediterranean diet, but actual intake was not reported.

The “usual-care” group, also known as controls, “received dietary advice from medical center dietitians.  American Heart Association Step II guidelines were presented as a nutrition class or video and written materials.”  Just one presentation, apparently.

All participants were followed on average for almost four years.  “The primary outcome [emphasis added] was a composite of end points including all-cause and cardiac deaths, myocardial infarction, hospital admission for heart failure, unstable angina, or stroke.”  Obviously,  you want to avoid these primary outcome end points.

Results

  • Avoidance of the primary outcome end points was the same in both the low-fat and Mediterranean diet groups.  Each intervention group had eight primary outcome end points.
  •  Forty of the 101 people in the usual care group suffered one or more of the primary outcome end points.  Only 16 of the 101 dietary intervention patients suffered one or more of the primary outcome end points.  Compared to the usual care group, the dietary intervention patients were only one-third as likely to suffer cardiac death, death from any cause, heart attack, hospital admission for heart failure, unstabe angina, or stroke.  This is a significant difference.
  • Goals for cholesterol, saturated fat, and omega-3 intake were achieved, or nearly so, in the dietary intervention groups.
  • Neither diet intervention group lost weight.
  • After two years, there were no differences between low-fat and Mediterranean groups in terms of HDL cholesterol, LDL cholesterol, triglycerides, and fasting glucose.
  • Among the diabetics (10 in each intervention group), there were no differences in fasting glucose.
  • The drop-out rate was low.

Take-Home Points

In the researchers’ words:

[This study] demonstrates that low-fat and Mediterranean-style diets can be similarly effective strategies for therapeutic lifestyle change, particularly when applied with equal intensity of intervention.

[This study] highlights the importance of heart-healthy diets in patients who have recently had [heart attacks].  The 2 intervention groups had relatively low intakes of cholesterol and saturated fat, but only Mediterranean-style diet partipants increased omega-3 fat consumption.  Because neither cardiovascular events nor risk factors differed between interventions , [this study] does not substantiate claims that increased omega-3 fat intake, predominantly from eating fish, adds benefit beyond a diet emphasizing reduced cholesterol and saturated fat.

The authors admit that the small number of participants is a weakness of their study.

They also cite another study, Medi-RIVAGE, that tends to support their findings.  Yet the Medi-RIVAGE “data predicted a 9% reduction in cardiovascular disease risk with the low-fat diet and a 15% reduction with this particular Mediterranean diet.”  According to the Medi-RIVAGE study abstract, “After a 3-mo intervention, both diets [low-fat and Mediterranean] significantly reduced cardiovascular disease risk factors to an overall comparable extent.”

The seeming equality of the low-fat and Mediterranean diets is a surprise to me.  I would have predicted superiority of the Mediterranean diet.  Alcohol and nut consumption have been associated with improved cardiovascular outcomes in several observational studies.  I wonder if these two intervention groups had the same or different consumption of alcohol and nuts.

But these researchers may be on to something here.  That is,  low-fat and Mediterranean diets – with intensive dietary instruction – are equally good diet interventions for preventing future cardiac events in people who have had a recent heart attack.  Dr. Dean Ornish’s vegetarian program might also stack up well against these two diets and “usual care.”

Before I abandon my preference for the Mediterranean diet in prevention of cardiac disease, I’d like to see the findings of this study confirmed by a larger one.  In addition to cardiovascular benefits, the Mediterranean diet is associated with:

No diet other than the Mediterranean can legitimately claim all these benefits.  And it tastes good.

Steve Parker, M.D.

References:

Tuttle, Katherine R., et al.  Comparison of Low-Fat Versus Mediterranean-Style Dietary Intervention After First Myocardial Infarction (from The Heart Institute of Spokane Diet Intervention and Evaluation Trial).  American Journal of Cardiology, 101 (2008): 1,532-1,531.

Vincent-Baudry, Stephanie, et al.  The Medi-RIVAGE study: reduction of cardiovascular disease risk factors after a 3-mo intervention with a Mediterranean-type diet or a low-fat diet.  American Journal of Clinical Nutrition, 82 (2005): 964-971.

Alcohol Habit (Especially Wine) Starting in Middle-Age Reduces Heart Attack and Stroke

Jesus turned water into wine at a wedding.  His mother asked him to do it.  Of all the miracles he performed and could have performed, I wonder why this is the first one recorded in the Holy Bible.

We have known for years that low or moderate alcohol consumption tends to lower the risk of cardiovascular disease such as heart attack and stroke, and prolongs life span.  Physicians have been hesitant to suggest that nondrinkers take up the habit.  We don’t want to be responsible for, or even accused of, turning someone into an alcoholic.  We don’t want to be held accountable for someone else’s drunken acts.  Every well-trained physician is quite aware of the ravages of alcohol use and abuse.  We see them up close and personal in our patients.

A scientific study from a few years ago, however, lends support to a middle-aged individual’s decision to start consuming moderate amounts of alcohol on a regular basis.  It even provides a positive defense if a doctor recommends it to carefully selected patients.

This research, by the way, was supported by a grant from the National Heart, Lung, and Blood Institute, not the wine/alcohol industry.

Methodology

Researchers at the Medical University of South Carolina examined data on 15,637 participants in the Atherosclerosis Risk in Communities (ARIC) study over a 10-year period.  These men and women were 45 to 64 years old at the time of enrollment, living in four communities across the U.S.  Of the participants, 27% were black, 73% nonblack, 28% were smokers, and 80% of them had high blood pressure, high cholesterol, or diabetes.

Out of 15,637 participants at the time of enrollment, 7,359 indicated that they didn’t drink alcohol.  At baseline, these 7,359 had no cardiovascular disease except for some with high blood pressure.    Subsequent interviews with them found that six percent of the nondrinkers – 442 people – decided independently to become moderate alcohol drinkers.  Or at least they identified themselves as such.

“Moderate” intake was defined as 1-14 drinks per week for men, and 1-7 drinks a week for women.  Incidentally, 0.4% of the initial non-drinking cohort – 21 people – became self-identified heavy drinkers.

93.6% of the 7,359 non-drinkers said that they continued to be non-drinkers.  These 6,917 people are the “persistent nondrinkers.”

Type of alcohol consumed was also surveyed and broken down into 1) wine-only drinkers, or 2) mixed drinkers: beer, liquor, wine.

Researchers then monitored health outcomes for an average of 4 years, comparing the “new moderate drinkers” with the “persistent nondrinkers.”

Results

  •  Over 4 years, 6.9% of the new moderate drinkers suffered a cardiovascular event, defined as a heart attack, stroke, a coronary heart disease procedure (e.g, angioplasty), or death from cardiovascular disease.
  • Over 4 years, 10% of the persistent nondrinkers suffered a cardiovascular event.
  • The new moderate drinkers were 38% less likely than persistent nondrinkers to suffer a new cardiovascular event (P = 0.008, which is a very strong association).  The difference persisted even after adjustment for demographic and cardiovascular risk factors.
  • There was no difference in all-cause mortality (death rate) between the new moderate drinkers and the persistent nondrinkers.
  • New  drinkers had modest but statistically significant improvements in HDL and LDL cholesterol and mean blood pressure compared with persistent nondrinkers.
  • 133 new moderate drinkers consumed only wine
  • 234 new moderate drinkers consumed mixed types of alcohol
  • Wine-only drinkers were 68% less likely than nondrinkers to suffer a cardiovascular event.
  • “Consumers of moderate amounts of beer/liquor/mixed (which includes some wine) tended to also be less likely to have had a subsequent cardiovascular event than nondrinkers…but the difference was not significant.”

A Few Study Limitations

  • Four years is a relatively brief follow-up, especially for cancer outcomes.  Alcohol consumption is associated with certain types of cancer.
  • If moderate alcohol consumption indeed lowers death rates as suggested by several other studies, this study may not have lasted long enough to see it.
  • The alcohol data depended on self-reports.

Take-Home Points

The study authors cite four other studies that support a slight advantage to wine over other alcohol types.  It’s a mystery to me why they fail to stress the apparent superiority of wine in the current study.  Several other studies that found improved longevity or cardiovascular outcomes in low-to-moderate drinkers suggest that the type of alcohol does not matter.  Perhaps “the jury is still out.”  In the study at hand, however, it is clear that the reduced cardiovascular disease rate in new moderate drinkers is associated with wine.

In all fairness, other studies show no beneficial health or longevity benefit to alcohol consumption.  But at this point, the majority of published studies support a beneficial effect.

Wine is a component of the traditional healthy Mediterranean diet.  The Mediterranean diet is associated with prolonged life span and reduced cardiovascular disease.  This study strongly suggests that wine is one of the causative healthy components of the Mediterranean diet.

Starting a judicious wine habit in middle age is relatively safe for selected people and may, in fact, improve cardiovascular health, if not longevity.

Now the question is, red or white.  Or grape juice?

Steve Parker, M.D.

Reference:  King, Dana E., et al.  Adopting Moderate Alchohol Consumption in Middle Age: Subsequent Cardiovascular Events.  American Journal of Medicine, 121 (2008): 201-206.

Huge Study Confirms Health and Longevity Benefits of Mediterranean Diet

Italian researchers reported in the September 11, 2008, online issue of the British Medical Journal what is already known:

“Greater adherence to a Mediterranean diet is associated with a significant improvement in health status, as seen by a significant reduction in overall mortality (9%), mortality from cardiovascular diseases (9%), incidence of or mortality from cancer (6%), and incidence of Parkinsons’s disease and Alzheimer’s disease (13%).  These results seem to be clinically relevant for public health, in particular for encouraging a Mediterranean-like dietary pattern for primary prevention of major chronic diseases.”

Methodology

Researchers, mostly at the University of Florence, performed a meta-analysis of 12 other published studies that looked at the effects of a Mediterranean-style eating pattern on health and longevity.  [Meta-analyses are popular, in part, because they are cheap.  This study required no specific funding.]

Most, if not all, of these 12 studies were observational, and involved 1,574,299 participants.  Six of the 12 studies were in Mediterranean countries, the others were in the U.S., northern Europe, and Australia.  Study participants were followed between 3.7 and 18 years.

The researchers devised their very own Mediterranean diet scale based on study participants’ intake of various foods.  Participants were given a point if they had higher than average intake of vegetables, fruits, legumes, cereals, fish, and red wine during meals.  They were given a point if they had lower than average intake of red meat, processed meats, and dairy products.  Due to differences among the 12 studies, “the total adherence scores…varied from a minimum of 0 points indicating low adherence to a maximum of 7-9 points reflecting high adherence to a Mediterranean diet.”

(This version of a Mediterranean diet score is problematic.  Curiously, olive oil – the predominant source of fat in the traditional Mediterranean – is not in the score.  Olive oil is a key characteristic of the Mediterranean diet.  Furthermore, the study authors also state that dairy products are “presumed not to form part of a Mediterranean diet.”  Most experts would argue that cheese and yogurt are a significant part of the Mediterranean diet, if only in low amounts.  I also doubt that participants in the 12 original studies  were surveyed whether they drank red wine – as contrasted with white – and whether it was with meals or not.  I admit I did not read each of the 12 component studies.  The underlying cause of this idiosyncratic definition of the Mediterranean diet is that the 12 original studies themselves used different definitions of the Mediterranean diet.  The meta-analysts had to pigeonhole the data.  There are a handful of respected Mediterranean diet scores in existence, but the authors of this study couldn’t apply them across the board due to database inconsistency or inadequacy.)

Results

“The cumulative analysis of 12 cohort studies shows that a two point increase [emphasis added] in the score for adherence to a Mediterranean diet determines a 9% reduction, in overall mortality, a 9% reduction in mortality from cardiovascular diseases, a 6% reduction in incidence of or mortality from neoplasm [cancer], and 13% reduction in incidence of Parkinson’s disease and Alzheimer’s disease.”

The only one of the 12 original studies focused on Alzheimer’s disease, and it showed a 17% reduction in participants with high adherence to the Mediterranean diet.  The two studies that focused on Parkinson’s disease revealed a 7% reduction in men, and 15% reduction in women.  These reduced incidence figures, again, apply to a two-point increase in Mediterranean diet adherence score.

Discussion

The authors indicate that their report is the first ever meta-analysis of the data associating the Mediterranean diet with reduced mortality and chronic disease in the general population.  Congratulations, guys!

The authors’ idiosyncratic Mediterranean diet score is unusual and won’t be widely adopted.  However, the 12 studies comprising the meta-analysis did have reasonable Mediterranean diet characteristics.

Combining Alzheimer’s data with Parkinson’s data doesn’t make sense to me, nor did the authors try to explain it.   You could lump them into the category of “neurodegenerative diseases,” but they aren’t the only ones by any means.  The single Alzheimer’s study, by the way, was quite small compared to the two Parkinson’s studies.

Nearly all the popular media stories reported the findings as I did in my first paragraph above, which may be  misleading.  The specific improvements in mortality and various disease rates is per two-point increase in Mediterranean diet score.  For example, consider the 9% reduction in overall mortality.  If a population increased its Mediterranean score by four points, would overall mortality be reduced by 18%?  I’ve read this study four times and cannot answer my own question.  But I suspect that the answer is “yes.”  So the news here may better than it seems at first blush.

In other words: If a population’s score goes from 5 to 7, the death rate is reduced by 9%.  If that same population then moved its score from 7 to 9, would mortality improve another 9%?  I think so, but this study as written does not make it clear.

I’m starting to see why the popular media simplified the study findings.  The reporting on this study is amazingly uniform.  They must have all gotten the same news release.

Of course, “populations” don’t die or get cancer, heart attacks, strokes, Alzheimer’s, or Parkinson’s disease.  Individuals do that.  If I as an individual had a low Mediterranean diet score, I’d try to improve my score by at least two points.  A good place to start would be a review of the Mediterranean diet.

Steve Parker, M.D.

Reference:  Sofi, Francesco, et al.  Adherence to Mediterranean diet and health status: Meta-analysis.  British Medical Journal, 337; a1344.  Published online September 11, 2008.  doi:10.1136/bmj.a1344

Feeling Tired and Easily Fatigued? It May Be Your Medication

“Dr. Parker tells me to exercise but I’m always exhausted!”

Especially if you’re a woman taking a statin drug.

-Steve

Omega-3 Fatty Acids Supplements May Offer No Benefit to Heart Patients

Supplementing with omega-3 fatty acids doesn’t do anything to reduce the future risk of heart-related events or overall death rates in previously diagnosed heart patients, according to a May 14, 2012, article in Archives of Internal Medicine.

This use of supplements is called secondary prevention.  Taking supplements before onset of disease is primary prevention.

This study didn’t address whether overall consumption of omega-3 fatty acids, as in real food, is heart-protective.

If you’re a heart patient spending hard-earned money on omega-3 supplements, ask you doctor if you can spend your money on something else.

Steve Parker, M.D.

2009 Study Confirms the Heart-Healthy Mediterranean Diet

Canadian researchers sought to systematically evaluate the strength of the evidence supporting links between dietary factors and coronary heart disease. Coronary heart disease (CHD) is the number one cause of death in Western societies.

It’s important to understand the two types of studies meta-analyzed by the Canadians.

Prospective cohort studies can be used to identify a dietary factor that may be associated with a disease or outcome. For example, researchers could study the health of 20,000 people over the course of 10 years, giving them questionnaires to find out what foods they typically ate. They might find after 10 years that the people who ate the most saturated fat tended to die earlier and had more heart attacks and strokes compared to the people who ate the least saturated fat. This would establish an association between dietary saturated fat and premature death, heart attacks, and strokes. It does not prove that saturated fats cause those outcomes, it’s just an association.

Randomized trials, often called randomized controlled trials (RCTs), typically take two groups of people and apply an intervention to one group but not the other. The groups are followed over time to see if there is a difference in outcome. For example, take another group of 20,000 people. Randomly assign 10,000 of them to eat more-than-usual saturated fat. The other 10,000 similar people serve as the control group, eating their usual amount of saturated fat. Follow these 20,000 people over 10 years, then compare their health outcomes: death, heart attacks, strokes. If the high-saturated-fat group has worse outcomes, you are much closer to proving that dietary saturated fat causes premature death, heart attacks, and strokes.

Methodology

The scientists located and analyzed every English-language prospective cohort study (146 studies) or randomized trial (43) investigating food intake and coronary heart disease (CHD), from 1950 through June, 2007. They wrote:

We used the Bradford Hill guidelines to derive a causation score based on four criteria (strength, consistency, temporality, and coherence) for each dietary exposure in cohort studies and examined for consistency with the findings of randomized trials.

The different dietary patterns evaluated in studies were noted. The “Mediterranean” dietary pattern emphasizes a higher intake of vegetables, legumes, fruits, nuts, whole grains, cheese or yogurt, fish, and monounsaturated relative to saturated fatty acids. The “prudent” dietary pattern is characterized by a high intake of vegetables, fruit, legumes whole grains, and fish and other seafood. The “western” pattern is characterized by a high intake of processed meat, red meat, butter, high-fat dairy products, eggs, and refined grains.

Results

Strong evidence (four Bradford Hill criteria satisfied) supported protection against CHD with consumption of:

  • vegetables
  • nuts
  • monounsaturated fatty acids [prominent in olive oil, for example]
  • Mediterranean diet
  • prudent diet

Modertately strong evidence (three criteria satisfied) supported protection against CHD with consumption of:

  • fish
  • marine omega-3 fatty acids
  • folate
  • whole grains
  • dietary vitamins E and C (as opposed to vitamin supplements)
  • beta carotene
  • alcohol
  • fruit
  • fiber

Strong evidence supported the following as harmful dietary factors, in terms of CHD:

Researchers found insufficient evidence (two or less criteria) to support an association between CHD and:

  • total fat
  • saturated and polyunsaturated fatty acids
  • eggs
  • meat
  • milk
  • vitamin supplements E and C
  • alpha-linolenic acid

Selected Comments of the Researchers [my comments in brackets]

Cohort studies provide abundant evidence of an association with total mortality for many dietary exposures. Randomized controlled trials corroborate these associations for the consumption of omega-3 fatty acids and a Mediterraneandiet because most of the other dietyary factors have not been evaluated to date.

Among the dietary exposures with strong evidence of causation from cohort studies, only a Mediterranean dietary pattern is related to CHD in randomized trials. [The association is inverse: Higher adherence to the Mediterranean diet leads to lower rates of CHD.]

A wealth of epidemiologic studies have evaluated associations between dietary exposures and CHD. The general consensus from the evidence currently available is that a reduced consumption of saturated and trans-fatty acids and a higher intake of fruits and vegetables, polyunsaturated fatty acids including omega-3 fatty acids, and whole grains are likely beneficial. This is reflected in the revised Dietary Guidelines for Americans 2005 from the US Departments of Health and Human Services and Agriculture. However, little direct evidence from RCTs supports these recommendations. [Emphasis added.] In some cases, RCTs have not been conducted, and RCTs that have been conducted have generally not been adequately powered or have evaluated surrogate end points rather than clinical outcomes.

Single-nutrient RCTs have yet to evaluate whether reducing saturated fatty acid intake lowers the risk of CHD events.

More recently, the lack of benefit of diets of reduced total fat has been established [in women only? (reference below)], and the evidence supporting the adverse effect of trans-fatty acids on cholesterol levels and CHD has increased, which is reflected in our findings. [This is the only mention of cholesterol in the report.]

My Comments

I wonder about vegetarian/vegan diets. Have they been tested for efficacy against CHD? What about Dr. Dean Ornish’s program?

Although not mentioned in the text of the article, Table 3 on page 664 shows that the positive association between CHD and high-glycemic index/load is much stonger in women than in men. Relative risk for women on a high-glycemic index/load diet was 1.5 (95% confidence interval = 1.29-1.71), and for men the relative risk was 1.06 (95% confidence interval = 0.91-1.20). I question whether the association for men is statistically significant.

Why wasn’t there discussion of dietary cholesterol? The public and physicians have been told for years that dietary cholesterol causes or aggravates coronary heart disease. Is there no evidence?

Note that the researchers found no clear association between CHD and saturated and total fat intake. In traditional medical circles, these findings are considered sacrilegious!

Medical schools and cardiologists have been teaching for thirty or more years that they are related positively. “Positively” means the more saturated and total fat in your diet, the more likely you are to develop atherosclerosis, which in the heart is coronary heart disease. Dietary cholesterol is often thrown into the equation. The is the dogmatic Diet-Heart Hypothesis.  It doesn’t hold much water these days, if any.

Steve Parker, M.D.

References:

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.

van Dam, R.M., et al. Dietary glycemic index in relation to metabolic risk factors and incidence of coronary heart disease: the Zutphen Elderly Study. European Journal of Clinical Nutrition, 54 (2000): 726-731.

Howard, B.V., et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association, 295 (2006): 655-666.

Glycemic Index and Chronic Disease Risk (Mostly in Women)

I’ve written about glycemic index (GI), glycemic load (GL), and glycemic diets in preparation for today’s post.

The concept of glycemic index was introduced by Jenkins et al in 1981 at the University of Toronto.

Studies investigating the association between disease risk and GI/GL have been inconsistent. By “inconsistent,” I mean some studies have made an association in one direction or the other, and other studies have not. Diseases possibly associated with high-glycemic diets have included diabetes, cardiovascular disease, cancer, gallbladder disease, and eye disease.

“Diet” in this post refers to a habitual way of eating, not a weight loss program.

Researchers with the University of Sydney (Sydney, Australia) identified the best-designed published research reports investigating the relationship between certain chronic diseases and glycemic index and load. The studied diseases were type 2 diabetes, coronary heart disease, stroke, breast cancer, colorectal cancer, pancreatic cancer, endometrial cancer, ovarian cancer, gallbladder disease, and eye disease.

Methodology

Literature databases were searched for articles published between 1981 and March, 2007. The researchers found 37 studies that enrolled 1,950,198 participants ranging in age from 24 to 76, with BMI’s averaging 23.5 to 29. These were human prospective cohort studies with a final outcome being occurrence of a chronic disease (not its risk factors). Twenty-five of the studies were conducted in the U.S., five in Canada, five Europe, and two in Australia. Ninety percent of participants were women [for reasons not discussed]. Food frequency questionnaires were used in nearly all the studies. Individual studies generated between 4 to 20 years of follow-up, and 40,129 new cases of target diseases were identified.

Associations between GI, GL, and risk of developing a chronic disease were measured as rate ratios comparing the highest with the lowest quantiles. For example, GI and GL were measured in the study population. The population was then divided into four groups (quartiles), reflecting lowest GI/GL to medium to highest GI/GL diets. The lowest GI/GL quartile was compared with the highest quartile to see if disease occurrence was different between the groups. Some studies broke the populations into tertiles, quintiles, deciles, etc.

Findings

Comparing the highest with the lowest quantiles, studies with a high GI or GL independently

  • increased the risk of type 2 diabetes by 27 (GL) or 40% (GI)
  • increased the risk of coronary heart disease by 25% (GI)
  • increased the risk of gallbladder disease by 26% (GI) or 41% (GL) (gallstones and biliary colic, I assume, but the authors don’t specify)
  • increased the risk of breast cancer by 8% (GI)
  • increased risk of all studied diseases (11) combined by 14% (GI) or 9% (GL)

Overall, high GI was more strongly associated with chronic disease than was high GL

So low-GI diets may offer greater protection against disease than low-GL diets.

Comments from the Researchers

They speculate that low-GI diets may be more protective than low-GL because the latter can include low-carb foods such as cheese and meat, and low-GI, high-carb foods. Both eating styles will reduce glucose levels after meals while having very different effects in other areas such as pancreas beta cell function, free fatty acid levels, triglyceride levels, and effects on satiety.

High GI and high GL diets, independently of known confounders, modestly increase the risk of chronic lifestyle-related diseases, with more pronounced effects for type 2 diabetes, coronary heart disease, and gallbladder disease.

Direct quotes:

. . . 90% of participants were female; therefore, the findings may not be generalizable to men.

There are plausible mechanism linking the development of certain chronic diseases with high-GI diets. Specifically, 2 major pathways have been proposed to explain the association with type 2 diabetes risk. First the same amount of carbohydrate from high-GI food produces higher blood glucose concentrations and a greater demand for insulin. The chronically increased insulin demand may eventually result in pancreatic beta cell failure, and, as a consequence, impaired glucose tolerance. Second, there is evidence that high-GI diets may directly increase insulin resistance through their effect on glycemia, free fatty acids, and counter-regulatory hormone secretion. High glucose and insulin concentrations are associated with increased risk profiles for cardiovascular disease, including decreased concentrations of HDL cholesterol, increased glycosylated protein, oxidative status, hemostatic variables, and poor endothelial function

Low-GI and/or low-GL diets are independently associated with a reduced risk of certain chronic diseases. In diabetes and heart disease, the protection is comparable with that seen for whole grain and high fiber intakes. The findings support the hypothesis that higher postprandial glycemia is a universal mechanism for disease progression.

My Comments

Studies like this tend to accentuate the differences in eating styles since they compare the highest with the lowest post-prandial (after meal) glucose levels. Most people are closer to the middle of the pack, so a person there has potentially less to gain by moving to a low-GI diet. But still some to gain, on average, particularly in regards to avoiding type 2 diabetes and coronary heart disease.

(To be fair, many population-based studies use this same quantile technique. It increases the odds of finding a statistically significant difference.)

Only two of the 37 studies examined coronary heart disease, the cause of heart attacks. One study was the massive Nurses’ Health Study database with 75,521 women. The other was the Zutphen (Netherlands) Elderly Study which examined men 64 and older. Here’s the primary conclusion of the Zutphen authors verbatim:

Our findings do not support the hypothesis that a high-glycemic index diet unfavorably affects metabolic risk factors or increases risk for CHD [coronary heart disease] in elderly men without a history of diabetes or CHD.

So there’s nothing in the meta-analysis at hand to suggest that high-GI/GL diets promote heart disease in males in the general population.

However, the recent Canadian study in Archives of Internal Medicine found strong evidence linking CHD with high-glycemic index diets. Although not mentioned in the text of that article, Table 3 on page 664 shows that the association is much stonger in women than in men. Relative risk for women on a high-glycemic index/load diet was 1.5 (95% confidence interval = 1.29-1.71), and for men the relative risk was 1.06 (95% confidence interval = 0.91-1.20). See reference below.

Nine of the 37 studies examined the occurrence of type 2 diabetes. Only one of these studied men only – 42,759 men: the abstract is not available online and the Sydney group does not mention if high-GI or high-GL was positively associated with onset of diabetes in this cohort. Two of the diabetes studies included both men and women, but the abstracts don’t break down the findings by sex. (I’m trying to deduce if the major overall findings of this meta-analysis apply to men or not.)

I don’t know anybody willing to change their diet just to avoid the risk of gallstones. It’s only after they develop symptomatic gallstones that they ask me what they can do about them. The usual answer is surgery.

The report is well-done and seems free of commercial bias, even though several of the researchers are authors or co-authors of popular books on low-GI eating.

Steve Parker, M.D.

References:

Barclay, Alan W.; Petocz, Peter; McMillan-Price, Joanna; Flood, Victoria M.; Prvan, Tania; Mitchell, Paul; and Brand-Miller, Jennie C. Glycemic index, glycemic load, and chronic disease risk – a meta-analysis of observational studies [of mostly women]. American Journal of Clinical Nutrition, 87 (2008): 627-637.

Brand-Miller, Jennie, et al. “The New Glucose Revolution: The Authoritative Guide to the Glycemic Index – The Dietary Solution for Lifelong Health.” Da Capo Press, 2006.

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.

Dental Problems and Chronic Systemic Disease: A Carbohydrate Connection?

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.

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 article is 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.

The “old theory” to which I referred is the Cleave-Yudkin idea from the 1960s and ’70s that excessive intake of fermentable 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.

Dr. Hujoel does not define “fermentable” carbohydrates in the article. My American Heritage Dictionary defines fermentation as:

  1. the anaerobic conversion of sugar to carbon dioxide and alcohol by yeast
  2. any of a group of chemical reactions induced by living or nonliving ferments that split complex organic compunds into relatively simple substances

As reported in David Mendosa’s blog at MyDiabetesCentral.com, Dr. Hujoel said, “Non-fermentable carbohydrates are fibers.” Dr. Hujoel also shared some personal tidbits there.

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.

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

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. Has he ever mentioned it to you?

Steve Parker, M.D.

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

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