Tag Archives: coronary heart disease

Bix Reports: Tea And Apples Are Good For The Heart 

Green tea

Green tea

The healthful component of tea and apples seems to be epicatechins. Bix, the Fanatic Cook, writes:

“Other good sources of epicatechins, besides apples and tea, include blackberries, broad beans, cherries, black grapes, pears, raspberries, and chocolate. Red wine also contains epicatechins….”

Source: New Study: Tea And Apples Are Good For The Heart | Fanatic Cook

Bix worries about the alcohol in wine causing cancer. Keep your consumption low to moderate and cancer shouldn’t be a problem.

TeaGuardian.com says green and white teas have the most catechins (same as epicatechins, I assume for now).

The study at hand involved Dutch men, so we don’t know if results apply to women. It’s an observational study. The men with the highest epicatechin consumption had a 38% lower risk of death from coronary heart disease compared to the lowest consumers. Perhaps because it was a relatively small study involving only Dutch men, the researcher write that “More studies are needed before conclusions can be drawn.

Steve Parker, M.D.

PS: Have you heard that the Mediterranean diet is also good for your heart?

Should You Avoid Saturated Fats If You Already Have Heart Disease?

kkk

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

If you already have coronary artery disease, Dr. Axel Sigurdsson says that ongoing saturated fat intake probably doesn’t matter, in terms of future cardiac events (like heart attacks) or risk of death from any cause.

Dr. Sigurdsson is a cardiologist in Iceland.

Some quotes from his blog:

For decades, cardiologists have advised patients with heart disease to restrict the intake of saturated fats and dietary cholesterol. Many patients still believe this to be the cornerstone of their lifestyle modification.

The main reason for avoiding saturated fats is the assumption that they adversely affect the lipid profile of our patients.

*   *   *

Recent studies suggest that the recommendation to avoid saturated fats may have been premature and not based on solid scientific evidence.

Now, a recently published Norwegian study shows that dietary intake of saturated fatty acids was not associated with risk of future events or death among patients with established coronary artery disease.

It is important to keep in mind that most of the patients were receiving secondary prevention drug therapy including aspirin, beta blockers and statins.

Anyhow, the results of the study certainly suggest that high intake of saturated fats is not a risk factor among patients with coronary heart disease receiving modern-day treatment.

These recent scientific data don’t imply hat we should urge our patients to consume high amounts of saturated fats. They only tell us that there is no association and accordingly, restriction won’t help.

So, it’s certainly a lifeline for those who believe red meat, whole-fat milk, cheese, cream, butter and eggs can be a part of a healthy diet.

On the other hand we must realise that scientific studies often provide contradictory results. A US study published last year suggested that greater adherence to a low carbohydrate diet high in animal sources of fat and protein was associated with higher all-cause and cardiovascular mortality following acute heart attack.

It appears the jury is still out…

RTWT.

Frequent Nuts Consumption Linked to 50% Lower Risk of Fatal Heart Attack

JAMA Internal Medicine has the details. Frequent consumption would be at least four times a week. 

High Adiponectin May Not Protect Against Stroke and Heart Disease After All

I’ve written in the past about adiponectin, a hormone-like protein that may help protect against disease.  Obese folks have less of it.  However, a new study published in Obesity Reviews found no protection against stroke and coronary heart disease (like heart attacks) in people with higher levels of adiponectin.

Read the abstract.

Nuts: What’s Not to Love?

MPj04031620000[1]Nut consumption is strongly linked to reduced coronary heart disease, with less rigorous evidence for several other health benefits, according to the American Journal of Clinical Nutrition.

This is why I’ve included nuts as integral components of the Ketogenic Mediterranean Diet and the Advanced Mediterranean Diet.

Regular nut consumption is associated with health benefits in observational studies of various populations, within which are people eating few nuts and others eating nuts frequently. Health outcomes of the two groups are compared over time. Frequent and long-term nut consumption is linked to:

  • reduced coronary heart disease (heart attacks, for example)
  • reduced risk of diabetes in women (in men, who knows?)
  • less gallstone disease in both sexes
  • lower body weight and lower risk of obesity and weight gain

The heart-protective dose of nuts is three to five 1-ounce servings a week.

Steve Parker, M.D.

Reference: Sabaté, Joan and Ang, Yen. Nuts and health outcomes: New epidemiologic evidence. American Journal of Clinical Nutrition, 89 (2009): 1,643S-1,648S.

Overweight Youth Point To Increase In Heart Disease

No doubt you have noticed the expanding girths of  U.S. yoots.  What are the health implications?  Research published in the New England Journal of Medicine suggests a disturbing answer.

Heavy youths tend to stay heavy as they age.  Researchers looked at the incidence of overweight adolescents in the year 2000 and then estimated the prevalence of obesity in the year 2020.  Thirty to 44% of 35-year-olds in 2020 are expected to be obese.

Using computer simulation, investigators estimated that by 2035 the prevalence of coronary heart disease will increase by 5 to 16% because of the increased obesity.  In other words, the increasing obesity in these young and middle-aged adults will result in over 100,000 excess cases of coronary heart disease.

That is, if current trends continue.  But I see nothing on the horizon likely to alter that societal trend in the near future.  I’m doing my part.  How about you?

Steve Parker, M.D.

References:  Bibbins-Domingo, K, et al.  Adolescent Overweight and Future Adult Coronary Heart Disease.  New England Journal of Medicine, 357 (2007): 2,371-2,379.

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.

Why Is the Mediterranean Diet So Healthy?

I’ve found that nearly everbody’s eyes glaze over if I try to explain how, physiologically, the Mediterranean diet promotes health and longevity. Below are some of the boring details, for posterity’s sake, from my 2007 book, The Advanced Mediterranean Diet: Lose Weight, Feel Better, Live Longer.

Many of the nutrient-disease associations I mention below are just that: associations, linkages, not hard proof of a benefit. Available studies are often contradictory. For instance, there may be 10 observational studies linking whole grain consumption with reduced deaths from heart disease, while three other studies find no association, or even suggest higher death rates. (I’m making these numbers up.) If you want hard proof, you’ll have to wait. A long time. Such is nutrition science. Take it all with a grain of salt.

Also note that the studies supporting my claims below are nearly all done in non-diabetic populations.

Coronary Heart Disease

Coronary heart disease, also known as coronary artery disease, is the No.1 cause of death in the world. It’s responsible for 40% of deaths in the United States and other industrialized Western countries. The Mediterranean diet is particularly suited to mitigating the ravages of coronary heart disease. Mediterranean diet cardiac benefits may be related to its high content of monounsaturated fat (in olive oil), folate, and antioxidants.

The predominant source of fat in the traditional Mediterranean diet is olive oil, which is rich in monounsaturated fatty acids. High intake of olive oil reduces blood levels of triglycerides, total cholesterol, and LDL (“bad”) cholesterol. HDL or “good” cho-lesterol is unaffected. Olive oil tends to lower blood pressure in hypertensive people. Monounsaturated fatty acids reduce cardiovascular risk substantially, particularly when they replace simple sugars and easily digestible starches. Monounsaturated fatty acids and olive oil may also reduce breast cancer risk. The cardioprotective (good for the heart) and cancer-reducing effects of olive oil may be partially explained by the oil’s polyphenolic compounds.

Nuts are another good source of monounsaturated fatty acids and polyunsaturated fatty acids, including some omega-3 polyunsaturated fatty acids. Nuts have been proven to be cardioprotective. They lower LDL and total cholesterol levels, while providing substantial fiber and numerous micronutrients, such as vitamin E, potassium, magnesium, and folic acid. Compared with those who never or rarely eat nuts, people who eat nuts five or more times per week have 30 to 50% less risk of a fatal heart attack. Lesser amounts of nuts are also cardioprotective, perhaps by reducing lethal heart rhythm dis-turbances.

Another key component of the Mediterranean diet is fish. Fish are excellent sources of protein and are low in cholesterol. Fatty, cold-water fish are particularly good for us because of their omega-3 polyunsaturated fatty acids: eicosapentaenoic acid (EPA) and docosahexanaenoic acid (DHA). The other important omega-3 polyunsaturated fatty acid is alpha-linolenic acid (ALA), available in certain plants. Our bodies can convert ALA into EPA and DHA, but not very efficiently. Fish oil supplements, which are rich in EPA, lead to lower total cholesterol and triglyce-ride levels. Fish oil supplements have several properties that fight atherosclerosis (hardening of the arteries). In people who have already had a heart attack, the omega-3 polyunsaturated fatty acids have proven to dramatically reduce cardiac deaths, especially sudden death, and nonfatal heart attacks. So omega-3 polyunsaturated fatty acids are “cardioprotective.”

The first sign of underlying coronary heart disease in many people is simply sudden death from a heart attack (myocardial infarction) or heart rhythm disturbance. These unfortunate souls had hearts that were ticking time bombs. I have little doubt that a significant number of such deaths can be prevented by adequate intake of cold-water fatty fish. As a substitute for fish, fish oil supplements might be just at beneficial. The American Heart Association also recommends fish twice weekly for the general population, or fish oil supplements if whole fish isn’t feasible. Compared with fish oil capsules, whole fish are loaded with vitamins, minerals, and protein. The richest fish sources of omega-3 polyunsaturated fatty acids are albacore (white) tuna, salmon, sar-dines, trout, sea bass, sword-fish, herring, mackerel, anchovy, halibut, and pompano.

Cardioprotective omega-3 polyunsaturated fatty acids (mainly ALA) are also provided by plants, such as nuts and seeds, legumes, and vegetables. Rich sources of ALA include walnuts, butternuts, soy-beans, flaxseed, almonds, leeks, purslane, pinto beans, and wheat germ. Purslane is also one of the few plant sources of EPA. Several oils are also very high in ALA: flaxseed, canola, and soybean. Look for them in salad dressings, or try cooking with them.

Macular Degeneration

Omega-3 fatty acid and fish consumption may also be “eye-protective.” Eating fish one to three times per week apparently helps prevent age-related macular degeneration (AMD), the leading cause of blindness in people over 50 in the United States. While AMD has a significant hereditary component, onset and progression of AMD are affected by diet and lifestyle choices. For instance, smoking cigarettes definitely increases your risk of developing AMD. Other foods associated with lower risk of AMD are dark green leafy vegetables, orange and yellow vegetables and fruits: spinach, kale, collard greens, yellow corn, broccoli, sweet potatoes, squash, orange bell peppers, oranges, mangoes, apricots, peaches, honeydew melon, and papaya. Two unifying phytochemicals in this food list are lutein and zeaxanthin, which are also found in red grapes, kiwi fruit, lima beans, green beans, and green bell peppers. Increasing your intake of these foods as part of the Advanced Mediterranean Diet may well help preserve your vision as you age.

Alzheimer’s Dementia

Another exciting potential benefit of fish consumption is prevention or delay of Alzheimer’s dementia. Several recent epidemiologic studies have suggested that intake of fish once or twice per week significantly reduces the risk of Alzheimer’s. Types of fish eaten were not specified. No one knows if fish oil capsules are equivalent. For now, I’m sticking with fatty cold-water fish, which I call my “brain food.”

Vitamin E supplements may slow the progression of established Alzheimer’s disease; clinical studies show either modest slowing of progression or no benefit. As a way to prevent Alzheimer’s, however, vitamin E supplements have been disappointing. On the other hand, high dietary vitamin E is associated with reduced risk of developing Alzheimer’s. Good sources of vitamin E include vegetable oils (especially sunflower and soybean), sunflower seeds, nuts, shrimp, fruits, and certain vegetables: sweet potatoes, asparagus, beans, broccoli, Brussels sprouts, carrots, okra, green peas, sweet peppers, spinach, and tomatoes. All of these are on your new diet.

Wine

For centuries, the healthier populations in the Mediterranean region have enjoyed wine in light to moderate amounts, usually with meals. Epidemiologic studies there and in other parts of the world have associated reasonable alcohol consumption with prolonged lifespan, reduced coronary artery disease, diminished Alzheimer’s and other dementias, and possibly fewer strokes. Alcohol tends to increase HDL cholesterol, have an antiplatelet effect, and may reduce C-reactive protein, a marker of arterial inflammation. These effects would tend to reduce cardiovascular disease. Wine taken with meals provides antioxidant phytochemicals (polyphenols, procyanidins) which may protect against atherosclerosis and some cancers.

What’s a “reasonable” amount of alcohol? An old medical school joke is that a “heavy drinker” is anyone who drinks more than the doctor does. Light to moderate alcohol consumption is generally consi-dered to be one or fewer drinks per day for a woman, two or fewer drinks per day for a man. One drink is 5 ounces of wine, 12 ounces of beer, or 1.5 ounces of 80 proof distilled spirits (e.g., vodka, whiskey, gin). The optimal health-promoting type of alcohol is unclear. I tend to favor wine, a time-honored component of the Mediterranean diet. Red wine in particular is a rich source of resveratrol, which is thought to be a major contributor to the cardioprotective benefits associated with light to moderate alcohol consumption. Grape juice may be just as good—it’s too soon to tell.

I have no intention of overselling the benefits of alcohol. If you are considering habitual alcohol as a food, be aware that the health benefits are still somewhat debatable. Consumption of three or more alcoholic drinks per day is clearly associated with a higher risk of breast cancer in women. Even one or two drinks daily may slightly increase the risk. Folic acid supplementation might mitigate the risk. If you are a woman and breast cancer runs in your family, strongly consider abstinence. Be cautious if there are alcoholics in your family; you may have inherited the predisposition. If you take any medications or have chronic medical conditions, check with your personal physician first. For those drinking above light to mod-erate levels, alcohol is clearly perilous. Higher dosages can cause hypertension, liver disease, heart failure, certain cancers, and other medical problems. And psychosocial problems. And legal problems. And death. Heavy drinkers have higher rates of violent and accidental death. Alcoholism is often fatal. You should not drink alcohol if you:

■ have a history of alcohol abuseor alcoholism
■ have liver or pancreas disease
■ are pregnant or trying to become pregnant
■ may have the need to operatedangerous equipment or machinery, such as an automobile, while under the influence of alcohol
■ have a demonstrated inability tolimit yourself to acceptable intake levels
■ have personal prohibitions due to religious, ethical, or other reasons.

Cancer

Do you ever worry about cancer? You should. It’s the second leading cause of death. Over 500,000 people die from cancer each year in the United States. One third of people in the United States will develop cancer. Twenty percent of us will die from cancer. About half the deaths are from cancer of the lung, breast, and colon/rectum. Are you worried yet?

According to the American Cancer Society, one third of all cancer deaths can be attributed to diet and inadequate physical activity. So we have some control over our risk of developing cancer. High consumption of fruits and vegetables seems to protect against cancer of the lung, stomach, colon, rectum, oral cavity, and esophagus, although other studies dispute the protective linkage. Data on other cancers is limited or inconsistent. If you typically eat little or no fruits and vegetables, you can start today to cut your cancer risk by up to one half. Five servings of fresh fruits and vegetables a day seems to be the protective dose against cancer. Make it a life-long habit. The benefits accrue over time. Fruits and vegetables contain numerous phytochemicals thought to improve or maintain health, such as carotenoids (e.g., lycopene), lignans, phytosterols, sulfides, isothyocyanates, phenolic compounds (including flavonoids, resveratrol, phytoestrogens, antho-cyanins, and tannins), protease inhibitors, capsaicin, vitamins, and minerals.

In addition to cancer prevention properties, fruits and vegetables provide fiber, which is the part of plants resistant to digestion by our enzymes. The other source of fiber is grain products, especially whole grains. Liberal intake of fiber helps prevent constipation, diverticular disease, hemorrhoids, irritable bowel syndrome, and perhaps colon polyps. Soluble fiber helps control blood sugar levels in diabetics. It also reduces LDL cholesterol levels, thereby reducing risks of coronary heart disease. Whether or not related to fiber, high fruit and vegetable intake may reduce the risks of coronary heart disease and stroke. Legume consumption in particular has been associated with a 10 to 20% lower risk of coronary heart disease, with the effective dose being around four servings per week.

Fiber and Whole Grains

Processed, refined grain products have much less fiber than do whole grains. For instance, white all-purpose enriched flour has only about one fourth the fiber of whole wheat flour. The milling process removes the bran, germ, and husk (chaff), leaving only the endosperm as the refined product, flour. Endosperm is mostly starch and 10–15% protein. Many nutrients are lost during processing. The germ is particularly rich in vitamins (especially B vitamins), polyunsaturated fatty acids, antioxidants, trace minerals, and phytochemicals. Phytochemicals protect us against certain chronic diseases. Bran is high in fiber and nutrients: B vitamins, iron, magnesium, copper, and zinc, to name a few. Enriched grain products are refined grains that have had some, but certainly not all, nutrients added back, typically iron, thiamin, niacin, riboflavin, and folate. Why not just eat the whole grain? Whole grain products retain nearly all the nutrients found in the original grain. Hence, they are more nutritious than refined and enriched grain products.

Liberal intake of high-fiber whole grain foods, as contrasted with refined grains, is linked to lower risk of death and lower incidence of coronary heart disease and type 2 diabetes mellitus. For existing diabetics, whole grain consumption can help im-prove blood sugar levels. Three servings of whole grains per day cut the risk of coronary heart disease by about 25 percent compared with those who rarely eat whole grains. Regular consumption of whole grains may also substantially reduce the risk of sev-eral forms of cancer.

Average adult fiber intake in the United States is 12 to 15 grams daily. Expert nutrition panels and the American Heart Association recommend 25 to 30 grams daily from whole grains, fruits, and vegetables.

The health benefits of the Mediterranean diet likely spring from synergy among multiple Mediteranean diet components, rather than from a single food group or one or a few food items.

Steve Parker, M.D.