What Does a Low-Glycemic Index Diet Look Like?

Posted on May 28, 2012 | Comments Off on What Does a Low-Glycemic Index Diet Look Like?

Any diet that contains carbohydrates can be ranked as being either low-, medium-, or high-glycemic, referring to the glycemic index or load. This ranking system would apply to both weight-loss diets and habitual ways of eating.

Specific foods with significant amounts of carbohydrate have been tested for their ability to rapidly raise blood sugar levels as compared to eating pure glucose, a type of sugar. The number generated by the test is the glycemic index (GI) and ranges between 0 and 100.

Here are some GI values from Wikipedia’s entry on glycemic index:

Low GI (55 or less)

  • most fruit and vegetables (except potatoes, watermelon), grainy breads [made of or resembling grain?], pasta, legumes/pulses, milk, products extremely low in carbohydrates (fish, eggs, meat, nuts, oils), brown rice

Medium GI (56 – 69)

  • whole wheat products, basmati rice, orange, sweet potato, table sugar, most white rices (eg, jasmine),

High GI (70 and above)

  • corn flakes, baked potato, watermelon, croissant, white bread, extruded cereals (eg, Rice Krispies), straight glucose (100)

Low-GI diets encourage the low-GI foods. High-GI diets favor the high-GI foods.  Well, duh!

The Human Nutrition Unit at the University of Sydney (Australia) maintains a free online database of glycemic index values of various foods. For example, the GI of Doritos is 42 (corn chips, plain, salted, 1998).

Steve Parker, M.D.

Additional Resources

GI News: The Official Glycemic Index Newsletter

“The Official Website of the Glycemic Index and GI Database”

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2009 Study Confirms the Heart-Healthy Mediterranean Diet

Posted on May 27, 2012 | Comments Off on 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.

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Yet Another Epidemic: Fatty Liver In Teens

Posted on May 26, 2012 | Comments Off on Yet Another Epidemic: Fatty Liver In Teens

MedPage Today on May 25, 2012 has an article documenting the rise of fatty liver disease in U.S. teenagers.  Prevalence is now up to one in 10 teens.

An expert quoted in the article says it’s tied in with the rise of childhood obesity.

Youth obesity in the U.S. tripled from the early 1980s to 2000, ending with a 17% obesity rate. Overweight and obesity together describe 32% of U.S. children. Some experts believe this generation of kids will be the first in U.S. history to suffer a decline in life expectancy, related to obesity.

I wrote about a small research study that found a very-low-carb diet more effective against fatty liver, compared to a low-calorie diet.  But that involved adults.

University of Colorado researchers indicate that for weight loss, a low-carb, high-protein diet is safe and effective in adolescents.

Diet researchers found in 2008 that a modified low-carbohydrate Mediterranean diet had significant potential to reduce fatty liver.  My Low-Carb Mediterranean Diet (minus the wine option) would probably help overweight teens with fatty liver disease, but it’s never been tested in such a clinical trial.

Steve Parker, M.D.

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Glycemic Index and Chronic Disease Risk (Mostly in Women)

Posted on May 26, 2012 | 3 comments

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.

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Time to Abandon the Diet-Heart Hypothesis?

Posted on May 25, 2012 | Comments Off on Time to Abandon the Diet-Heart Hypothesis?

In January, 2009, The American Journal of Medicine published a 62-page supplement (vol. 122, number 1A) entitled “Management of Atherosclerosis: A Practical Guide in 2008.”

I scanned it with attention to the Diet-Heart Hypothesis: the idea that dietary factors – such as saturated fat, total fat, cholesterol – cause or aggravate atherosclerosis. Atherosclerosis is colloquially referred to as “hardening of the arteries,” and is a major cause of heart attacks, strokes, and peripheral arterial disease.

One section, “The Pathology of Atherosclerosis: Plaque Development and Plaque Responses to Medical Treatment” is written by William Insull, M.D., who is with the Lipid Research Clinic at Baylor College of Medicine. Here are selected quotes, and my comments in brackets:

Several risk factors may intensify or provoke atherosclerosis through their effects on low-density lipoprotein (LDL) particles and inflammation. These risk factors most frequently include hypertension, tobacco smoking, diabetes mellitus, obesity, and genetic predispositon; the molecular details of how they work are not yet known.

[No mention of diet.]

Early fatty streak development [thought to be a precursor to atherosclerosis] begins in childhood and adolescence. . . . The initial step occurs when LDL particles leave the blood and enter the arterial intima, where, if LDL levels are increased, they accumulate.

[Not entirely clear whether he’s referring to increase LDL in the bloodstream or inside the intima cells – I suspect inside the cells.]

All of these changes may be significantly influenced by risk factors, notably the stress of local hemodynamics and blood flow patterns, hypertension, tobacco smoking, and diabetes, as well as genetically determined arterial susceptibility or resistance to atherosclerosis. The mechanism of these risk factors in influencing atherosclerosis are the target of intensive investigation by molecular pathology, along with proteomics and genomics, conducted to determine the exact molecular biological prosesses involved in their development.

[Again, no mention of diet.]

Dr. Insull does include a table on page S11 that mentions therapeutic reduction of atherogenic plasma lipoproteins by diet, exercise, statins, and other lipid-lowering therapies, but there is no further mention of diet in his article.

Another section, “”Sick Fat,” metabolic Disease, and Atherosclerosis,” is by Harold E. Bays, M.D., of the Louisville (KY) Metabolic and Atherosclerosis Research Center. Selected quotes:

Most major CHD [coronary heart disease] risk factors are modifiable; these include metabolic disorders such as type 2 diabetes mellitus, hypertension, and dyslipidemia.

[No mention of diet.]

His Table 2, “Major risk factors for future atherosclerotic coronary heart disease events” includes history of atherosclerosis, type 2 diabetes, high blood pressure, dyslipidemia, cigarette smoking, adiposopathy, age 45 or older (men), age 55 or older (women), and family history of CHD.

[No mention of diet.]

Among hunter-gatherer populations who follow their indigenous lifestyles, CHD is a rarity. This is in large measure due to a striking reduction in major CHD risk factors, such as markedly reduced [blood] cholesterol levels, in these populations.

[No mention of dietary cholesterol and saturated fats in this context.]

High blood pressure increases CHD risk. Large-scale observational data show a doubling of mortality from ischemic heart disease and stroke for every 20 mm Hg increase in systolic blood pressure or 10 mm Hg increase in diastolic blood pressure.

[Off topic, but a “fun fact,” at least to a doctor.]

As most primary care clinicians are acutely aware, one of the most basic interventions for treating and/or preventing the most common diseases found in medical practice, including CHD, is encouraging patients to adopt favorable nutritional and lifestyle habits.

[No additional text clarifies his “favorable nutritional . . . habits.”]

A later section, “Prevention and Treatment of Atherosclrosis: A Practitioner’s Guide for 2008,” is by Sandra J. Lewis, M.D., with the Oregon Health and Science University in Portland.

Dr. Lewis reiterates the aforementioned major risk factors for atherosclerosis, adding physical inactivity, and not mentioning diet as a major risk factor. She recommends inquiring about eating habits, and encourages “healthy eating.” A quote:

Therapeutic lifestlye changes constitute first-line therapy for reducing LDL cholesterol levels in persons at risk for atherosclerotic CV [cardiovascular] events. All persons, regardless of their short- or long-term risks, should be counseled to adopt positive changes, including a low-cholesterol diet, increased physical activity, and cessation of smoking. Diets should include limits for saturated fats, polyunsaturated fats, monounsatrauted fats, total fat, carbohydrates, and protein. Total cholesterol ineake should be kept to under 200 mg/day.

These recommendations seem to emanate from the 2001 report of the National Cholesterol Education Program, Adult Treatment Panel III. Note: they refer to treatment of people with higher-than-optimal LDL cholesterol levels, not to the general population.

My Comments

I began questioning the validity of the Diet-Heart Hypothesis in 2009. This monograph seemed like the perfect place for a review of it.

The overall tone of the monograph is very much in favor of statin drugs for reducing the morbidity and mortality of atherosclerosis, particularly in the coronary arteries. Statins are powerful LDL cholesterol-lowering agents. But that proves nothing one way or the other about the Diet-Heart Hypothesis.

Little in this 62-page monograph supports the diet-heart hypothesis and the idea that everyone needs to limit intake of saturated fat, total fats, or cholesterol.

Steve Parker, M.D.

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Why Are Kidney Stones Increasingly Common?

Posted on May 25, 2012 | Comments Off on Why Are Kidney Stones Increasingly Common?

MedPage Today on May 24, 2012, reported a substantial increase (70%) in the prevalence of kidney stones in the U.S. over the last two decades. Stone prevalence rose from 5.2% to 8.8% of the population.  Prevalence was based on the periodic National Health and Nutrition Examination Survey, which asked participants, “Have you ever had kidney stones?”

Stone prevalence began rising even earlier.  Again according to the third NHANES, prevalence increased from 3.8 percent in the period 1976 to 1980 to 5.2 percent in the years 1988 to 1994.

Older studies estimated that one in 10 men and one of every 20 women will have at least one painful stone by the age of 70.

What are kidney stones make of?  

Three out of four patients with kidney stones form calcium stones, most of which are composed primarily of calcium oxalate or, less often, calcium phosphate.  Pure uric acid stones are less than 10 percent of all stones.

Why the increased stone prevalence?  Does diet count?

Unfortunately, the article doesn’t offer any reasons or even speculation as to why kidney stones are more prevalent.  Kidney stones have a genetic component, but our genes have changed very little over just two decades.  I have to wonder if diet plays a role.

UpToDate.com reviewed diet as a risk factor for kidney stones.  Some quotes:

There are several dietary factors that may play an important role in many patients: fluid, calcium, oxalate, potassium, sodium, animal protein, phytate, sucrose, fructose, and vitamin C intake. Lower intake of fluid, calcium, potassium, and phytate and higher intake of sodium, animal protein, sucrose, fructose, and vitamin C are associated with an increased risk for calcium stone formation. The type of beverage may also influence the risk. The effect of calcium intake is paradoxical, with a decreased risk with increased dietary calcium and an increased or no change in risk with calcium supplements.

The combination of dietary factors may also have a significant impact upon stone risk. As an example, the Dietary Approaches to Stop Hypertension (DASH) diet is high in fruits and vegetables, moderate in low-fat dairy products, and low in animal protein. Based upon an analysis of three large cohorts, adherence to a DASH-style diet lowered the risk for kidney stones among men, older women, younger women, high body mass index (BMI) individuals, and low BMI individuals. Thus, the DASH diet is a reasonable option in the attempt to reduce the risk of stone recurrence.

Higher sucrose [table sugar] intake is associated with an increased risk of stone formation in younger and older women.
Standard advice to prevent initial and recurrent kidney stones is to avoid low urine output.  Do that by drinking plenty of fluid.
Although I pay about $400 a year for access to UpToDate, they offer free public access to some of the website.  Here’s the UpToDate poop sheet on kidney stones.
Extra credit:  Medical conditions that predispose to kidney stones include primary hyperparathyroidism, obesity, gout, diabetes, and medullary sponge kidney.

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Mediterranean Diet Cuts Stroke Risk In Women

Posted on May 24, 2012 | Comments Off on Mediterranean Diet Cuts Stroke Risk In Women

The journal Circulation in 2009 reported that the Mediterranean diet reduces risk of stroke in women by 13%. This supplements our prior knowledge that the healthy diet is associated with lower risk of coronary heart disease in both men and women.

Researchers in Boston analyzed the records of 74,886 middle-aged women in the Nurses’ Health Study to deteremine how closely they followed a Mediterranean diet pattern. They followed participants’ health status for 20 years, noting how many women developed stroke, coronary heart disease, and “cardiovascular death” (fatalities from strokes and coronary heart disease combined).

Compared with the women who adhered minimally to the Mediterranean diet pattern, the women with highest compliance had 13% fewer strokes. Consistent with earlier studies, the Mediterranean dieters had 39% lower risk of cardiovascular death and 29% lower risk for coronary heart disease (again, comparing the women with highest and lowest compliance).

Take-Home Points

To gain the health benefits of the Mediterranean diet, consider making changes to the way you eat.

Here are the characteristics of the traditional Mediterranean diet:

  • It maximizes natural whole foods and minimizes highly processed ones
  • Small amounts of red meat
  • Less than four eggs per week
  • Low to moderate amounts of poultry and fish
  • Daily fresh fruit
  • Seasonal locally grown foods with minimal processing
  • Concentrated sugars only a few times per week
  • Wine in low to moderate amounts, and usually taken at mealtimes
  • Milk products (mainly cheese and yogurt) in low to moderate amounts
  • Olive oil as the predominant fat
  • Abundance of foods from plants: vegetables, fruits, beans, potatoes, nuts, seeds, breads and other whole grain products

Steve Parker, M.D.

Reference: Fung, Teresa, et al. Mediterranean diet and incidence of and mortality from coronary heart disease and stroke in women. Circulation, 119 (2009): 1,093-1,100.

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Calcium Supplementation Linked to Heart Attacks

Posted on May 24, 2012 | Comments Off on Calcium Supplementation Linked to Heart Attacks

A new European study suggests that calcium supplements almost double the risk of having a heart attack, at least in Germans.  You can read the full report in the current issue of Heart.

The medical literature on this issue is a confusing mess.  In other words, lots of conflicting results.

Huge numbers of women in the U.S. are taking calcium supplements either to treat or prevent osteoporosis and the associated broken bones (e.g., hips, wrists, spine).

What I’d like to know, and what nobody knows, is what is the effect of calcium supplementation on average longevity and quality of life.  Maybe I’d accept a higher risk of heart attack if calcium supplementation prolonged lifespan by two years.

In the interest of brevity, I’ll just say that the best way to get your calcium is probably through food rather than supplements.

Shereen Jegtvig has an article at About.com listing foods rich in calcium.

Exercise can also help keep your bones strong and break-resistant.

Steve Parker, M.D.

PS: If your doctor has you on a calcium supplement, you’d best get his blessing before you stop it.

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Yo-Yo Dieting In Women Has No Effect On Death Rates

Posted on May 23, 2012 | Comments Off on Yo-Yo Dieting In Women Has No Effect On Death Rates

Yo-yo dieting isn’t so bad after all.

Fifteen years ago there was lots of hand-wringing in the medical community about the potential dire physical consequences of “weight cycling” – also known as yo-yo dieting. You know, lose a bunch of weight, gain it back, lose it again, gain it back, etc.

After a while, yo-yo dieting as a medical issue dropped off the radar screen. 

A 2009 study in the Archives of Internal Medicine reported on the cardiovascular and mortality effects of yo-yo dieting in women in the massive Nurses’ Health Study. One in four of these women could be classified as weight cyclers. The worst ones were defined as those who lost at least 9.1 kg ( 20 pounds) at least three times.

It turns out the weight cyclers had the same rates of death from cardiovascular disease or any cause as the women who didn’t cycle. They did eventually gain more overall weight as they aged, compared to the non-cyclers.

Note that this study investigated death rates only. So there may have been effects on rates of high blood pressure, diabetes, gout, stroke, etc, that we wouldn’t know about.

Steve Parker, M.D.

Field, Alison, et al. Weight cycling and mortality among middle-aged or older women. Archives of Internal Medicine, 169 (2009): 881-886.

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Which Components of the Mediterranean Diet Prolong Life?

Posted on May 22, 2012 | 1 comment

Researchers at Harvard and the University of Athens (Greece) report that the following specific components of the Mediterranean diet are associated with lower rates of death:

  • moderate ethanol (alcohol) consumption
  • low meat and meat product intake
  • high vegetable consumption
  • high fruit and nut consumption
  • high ratio of monounsaturated fat to saturated fat
  • high legume intake

Minimal, if any, contribution to mortality was noted with high cereal, low dairy, or high fish and seafood consumption.

The researchers examined diet and mortality data from over 23,000 adult participants in the Greek portion of the European Prospective Investigation into Cancer and nutrition. You’ll be hearing more about the EPIC study for many years. Over an average follow-up of 8.5 years, 1,075 of participants died. 652 of these deaths were of participants in the lower half of Mediterranean diet adherence; 423 were in the upper half.

Alcohol intake in Greece is usually in the form of wine at mealtimes.

The beneficial “high ratio of monounsaturated fat to saturated fat” stems from high consumption of olive oil and low intake of meat.

It’s not clear if these findings apply to other nationalities or ethnic groups. Other research papers have documented the health benefits of the Mediterranean diet in at least eight other countries over three continents.

The researchers don’t reveal in this report the specific causes of death. I expect those data, along with numbers on diabetes, stroke, and dementia, to be published in future articles, if not published already. Prior Mediterranean diet studies indicate lower death rates from cardiovascular disease and cancer.

Steve Parker, M.D.

Reference: Trichopoulou, Antonia, et al. Anatomy of health effects of the Mediterranean diet: Greek EPIC prospective cohort study. British Medical Journal, 338 (2009): b2337. DOI: 10.1136/bmj.b2337.

Additional Information: Childs, Dan. Take it or leave it? The truth about 8 mediterranean diet staples. ABC News online, June 24, 2009. Accessed June 25, 2009.

Addendum:

Here’s a direct quote from the study at hand:

Among the presumed beneficial components of the Mediterranean diet score, high consumption of all but fish and seafood was inversely associated with mortality, although none of these associations was statistically significant.

“. . . none of these associations was statistically significant.” So I can understand some skepticism about this journal article. The researchers had to use some very sophisticated statistical manipulation to come up with the “healthy components” list. I’m not saying that’s wrong. I will admit that the statistical analysis is beyond my comprehension, so I’m trusting the authors and peer-review process to be honest and effective. My college statistics course was too many years ago.

The take-home point for me is that the health benefits of the Mediterranean diet probably stem from an overall combination of multiple foods rather than any single component.

And remember to exercise regularly, maintain a healthy weight (BMI 18.5-25), keep your blood pressure under 140/90, and don’t smoke.

-Steve

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