Bay Leaf: An Infusion of Antioxidants – Taming the Sugar Disease

Who would have guessed that so much healing could come from one small dried leaf! But that’s bay leaf—infusing your body with antioxidant protection as easily as it infuses flavor into poached fish.

While cooking, the aroma of bay leaf intensifies as it releases its volatile oils—its scent-giving plant compounds that are also among the most powerful antioxidants in existence.

In fact, when researchers in Korea tested 120 spices, herbs, and vegetables for their antioxidant power—their power to reduce oxidation, the internal rust that can erode every cell of your body (and the precious DNA within cells)—they found bay leaf was at the top of the list. It was stronger than vitamin C, an A-1 antioxidant. It was stronger than BHA and BHT, synthetic antioxidants so powerful they’re routinely used to preserve food. And it was equal to several antioxidant superstars, such as the resveratrol in red wine and the EGCG in green tea.

There are more than 80 active compounds in bay leaf, but the specific antioxidants that it uses to help keep disease at bay are the volatile oil cineole (also found in eucalyptus) and a class of compounds called sesquiterpenes. And they may be particularly effective against an epidemic blighting the health of more than 20 million Americans: type 2 diabetes, the disease of excess of blood sugar (glucose).

Taming the Sugar Disease

A team of researchers (led by Richard Anderson, PhD, a scientist at the Beltsville Human Nutrition Research Laboratory of the US Department of Agriculture, who is an expert in natural treatments for type 2 diabetes) studied 40 people with the disease, dividing them into four groups.

Three of the groups took bay leaf supplements—either one, two, or three grams a day. Another group took a placebo.

After one month, the bay leaf groups had big drops in blood sugar levels—up to 26 percent. But that’s not all. They also had a 32 to 40 percent drop in “bad” artery-clogging LDL cholesterol, a 20 to 24 percent drop in total cholesterol, a 20 to 29 percent rise in “good” artery-cleaning HDL cholesterol, and a 25 to 34 percent drop in triglycerides, another heart-harming blood fat. Meanwhile, the placebo group had no changes in any of those parameters.

How did this spice produce such a powerful effect? Writing in the Journal of Clinical Biochemistry and Nutrition, the researchers speculate that the “bioactive compounds” in bay leaf might improve: insulin sensitivity (the ability of the hormone insulin to usher glucose out of the bloodstream and into cells), glucose uptake (the ability of the cells to deal with insulin once it arrives), antioxidant status (less oxidation translates into better control of glucose), inflammatory response (ditto for less chronic inflammation), and glucose emptying (the speed at which glucose is absorbed—with slower being better for balanced blood sugar).

Given the fact that type 2 diabetes increases the risk of heart disease six-fold, with 75 percent of people with diabetes dying from cardiovascular disease—those results are, well, heartening.

Healing by the Bay

But bay leaf doesn’t stop at type 2 diabetes.

Cellular and animal studies—the first scientific steps in proving the power of the spice to improve health in us humans—show that it might be natural medicine for:

Cancer. Several studies on cancer cells show that parthenolide—a compound in bay leaf—works several ways to foil cancer. And in a Russian study, an injection of bay leaf extract slowed the appearance and growth of breast tumors in mice with experimentally induced breast cancer. Other studies show that bay leaf inhibits leukemia and cervical cancer.

Arthritis. Bay leaf is a traditional remedy for the symptoms of arthritis. And in animal experiments, doctors in the Middle East found its volatile oils could alleviate the pain and swelling of the disease. Bay leaf possesses anti-inflammatory properties “comparable to those of analgesics [painkillers] and non-steroidal anti-inflammatory drugs [such as ibuprofen and naproxen],” they concluded in Phytotherapy Research.

Ulcers and poor digestion. Another traditional use of bay leaf: treating stomach problems. Recently, researchers in Turkey found bay leaf oil prevented stomach ulcers in rats. Other studies show it can aid digestion by stimulating the healthy secretion of stomach acids that break down food.

Bacterial infection. Bay leaf fights bacteria. Researchers in Morocco infected animals with 16 different strains of an infectious organism—but bay leaf helped keep the germs in check, showing a “strong inhibitory effect” on E. coli, Salmonella, and Listeria (all of which can cause food poisoning). In Pakistan, researchers found bay leaf was effective at controlling 176 different strains of bacteria.

SASARS (severe acute respiratory syndrome). Bay leaf can beat back viruses, too. Research from laboratories around the world shows bay leaf oil can slow or kill the SARS virus—the cause of the highly contagious respiratory illness that, in 2003, infected 8,000 people and killed 800 before it was contained.

Wound healing. Researchers found that volatile oils in bay leaf helped speed wound healing in laboratory animals.

Mosquito bites. Essential oil from bay leaves is a traditional mosquito repellant, and a study in the Journal of Ethnopharmacology found it could repel mosquitoes for up to two hours.

Getting to Know Bay Leaf

The bay leaf is picked and dried from the bay laurel tree, a densely leafed evergreen that grows profusely along the Mediterranean Sea (although it’s cultivated in many countries). And people have been picking it for thousands of years.

When physicians in ancient Greece completed their studies they were crowned with laurel branches—baca (branches) lauris (laurel), the origin of the word baccalaureate. Likewise, for the ancient Romans, bay laurel was a symbol of victory and courage—with winners of chariot races crowned with leafy branches of bay laurel.

THE ANCIENT ROMANS CROWNED THE WINNER OF A CHARIOT RACE WITH A WREATH OF BAY LAUREL.

While people no longer wear it, we certainly cook with it. Bay leaf is one of the most popular and well-used spices in North American cooking. It’s a rare kitchen that doesn’t contain a jar of bay leaves—unless they’ve been used up! Bay leaf adds aroma to soups, stews, soups, beans, marinades, and fish boils. It’s a key ingredient in San Francisco’s famed cioppino, a fisherman’s stew simmered in a rich tomato sauce. It’s frequently used in pickling spices. And it’s one of the spices used to cure corned beef—not an American original, but definitely an American favorite.

Bay leaf is generally used in savory dishes in both the US and Europe—though the British (ever the culinary oddballs!) like to add it to custards and puddings, too.

Bay leaf and French cooking are bons amis. It’s the key spice in the bouquet garni that is enclosed in cheesecloth and added to long-simmering soups, stews, and stocks. It’s also key to the simmering poaching liquid called court boullion. It’s added to food made en papillote, a technique in which fish is wrapped in parchment to steam in its own juices. And it’s used to aromatize the French fish stewsbouillabaisse and bourride.

In fact, bay leaf is indispensable to all the cuisines in the Mediterranean basin—it’s one of the ingredients that make the Mediterranean diet among the healthiest in the world. On the Greek island of Corfu, for example, fresh bay leaves are wrapped around sikopsoma, a flat cake made of dried, spiced figs.

How to Buy Bay Leaf

The only true bay leaf—and the one used in most scientific studies—comes from the bay laurel tree. But around the world, the term bay leaf is used to describe a variety of different leaves, none of which are bay laurel. If you encounter California bay, Mexican bay, Indian bay, Indonesian bay, or West Indian bay, be aware that they’re not true bay leaf. In fact, they’re an entirely different species. Indian bay, for example, is the dried leaf of the same tree that produces cinnamon, and West Indian bay comes from the bay rum tree. Most of these bay leaves have a stronger flavor than bay laurel.

Bay leaf comes fromthe bay laurel tree.

Bay leaf is rarely sold fresh for culinary use, as its perfume is more pronounced and less bitter when dried. Dried leaves also infuse more flavor into food.

The majority of bay leaves produced and sold for export are from Turkey and Greece, with most bay leaf sold in the US from Turkey. It comes in two grades, but only one (usually referred to as “hand selected”) is considered suitable—because it’s not shipped with extraneous debris.

Look for leaves that are whole, uniform in size and color, and free of stems and bits of bark. The leaves should be clean and green. The darker the color and the larger the leaves, the better. Yellowing is a sign that they have been exposed to light for too long.

In the Kitchen with Bay Leaf

The woodsy, pungent aroma and flavor of bay leaf, with its slight hint of eucalyptus, is infused when it comes in contact with simmering liquid. The scent and flavor intensifies the longer it cooks, though if you leave bay leaf in the pot too long (more than a few hours) it starts to lose its aroma.

Bay leaf may help prevent and/or treat:

Arthritis (osteo- and rheumatoid)

Cancer

Diabetes, type 2

Food poisoning

Indigestion

Mosquito bites

Severe acute respiratory syndrome (SARS)

Ulcer

Wounds

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Bay leaf pairs well with these spices:

Amchur

Black cumin seed

Black pepper

Basil

Cinnamon

Cumin

Garlic

Onion

Oregano

Parsley

Rosemary

Sage

Thyme

and complements recipes featuring:

Pot roast

Sauces

Soups

Seafood boil

Steamed food

Stews

Tomato sauces

Caution: Bay leaves should always be removed and discarded before serving. Swallowing bay leaf can obstruct or even puncture the intestine.

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Other recipes containing bay leaf:

Alsatian Pork and Sauerkraut

Boeuf Bourguignon

Bouquet Garni

Chesapeake Bay Seafood Seasoning

Penne and Sausage with Fennel Tomato Sauce

Spice de Provence

By-the-Bay Fisherman’s Chowder

There are as many recipes for fisherman’s stew as there are fishermen. This hearty meal-in-one is based on San Francisco’s famed cioppino, which is characterized by a tomato-based broth and, of course, by bay leaf. This recipe makes good use of other healing spices, such as cumin and cinnamon. Substitute any fish or seafood of your liking.

2 tablespoons olive oil

2 cups chopped white onion

1 cup chopped celery

3 cloves garlic, minced

2 cups canned crushed tomatoes with puree

1 twenty-eight-ounce can diced tomatoes with juices

1 cup clam juice

2 cups fish or vegetable stock

1½ cups white wine

¼ tablespoon red wine vinegar

2 tablespoons Asian chili sauce

½ teaspoon dried oregano

1 teaspoon ground fennel

1 teaspoon celery seed

½ teaspoon chili powder

½ teaspoon black cumin seeds

½ teaspoon ground cumin

½ teaspoon ground cinnamon

½ teaspoon dried thyme

2 bay leaves

Salt and freshly ground black pepper to taste

½ pound sea scallops, cut in half

½ pound shrimp, peeled, deveined, and coarsely chopped

2 pounds firm white fish, such as sea bass

1 cup fresh parsley

1. Heat the oil in a large heavy pot over medium-high heat. Add the onions and celery and sauté until soft but not brown, about six minutes. Add garlic and cook one minute more. Lower the heat and add the crushed and diced tomatoes and their juices and simmer 10 minutes.

2. Add the clam juice, stock, wine, red wine vinegar, and Asian chili sauce. Combine the oregano, fennel, celery seeds, chili powder, black cumin, cumin, cinnamon, and thyme. Add the combined spices and bay leaves. Simmer, partially covered, for 30 minutes. Add the salt and pepper to taste.

3. Add the scallops, shrimp, and fish to the broth, cover and simmer until cooked through, about 10 minutes. Adjust seasoning and turn off the heat. Let the soup sit for about an hour. Reheat and serve, sprinkled with parsley.

Makes 6 servings.

Bay leaf goes with virtually any food simmered in liquid, especially roasting meat and boiled seafood. Steaming brings out even more of its natural flavor.

One or two medium-sized bay leaves are all that you need to flavor a dish for a family-size meal. Add it at the beginning of cooking.

Generally, bay leaf is used in savory dishes, but it will enhance sweets based in milk or cream sauces.

Bay leaves are used for flavoring only, as their infused oils permeate the ingredients in which they’re cooked. Make sure you discard the leaves when cooking is complete. (The medical literature doesn’t only contain research about bay leaf’s many virtues—it’s also filled with scary stories of digestive damage after a spiky bay leaf was mistakenly consumed.)

Here are ideas for getting more bay leaf in your life and your diet:

• Add a leaf or two to the water when boiling carrots, potatoes, or noodles.

• Add bay leaf to simmering tomato sauces, even when you are heating up commercial pasta sauce.

• Steam shrimp in beer infused with bay leaf.

• Add more fragrance to rice by putting a bay leaf or two into your dried rice canister.

• Add a bay leaf to meat or to fish baked or grilled in foil.

• Make a French court bouillon for poaching fish, by combining two parts water to one part white wine, along with chopped carrots, onions, a pinch of thyme, and a bay leaf. Cover and simmer one hour before adding fish. Use enough liquid to immerse the fish completely.

Antioxidants in foods and their effects on cardiovascular disease

An antioxidant (AO) can be defined as any substance that, when present at a concentration lower than that of an oxidizable substrate, significantly slows down or inhibits the oxidation of the substrate itself (Halliwell and Gutteridge, 1999). It is clear that the definition is exclusively functional, and that this class of compounds includes substances with highly diverse structures. In addition, while a classical distinction between AO considers only water-soluble and lipid-soluble compounds, a wide range of compounds with potent AO properties in various systems, but also with additional effects on various cellular functions (e.g. interactions with enzymes), is characterized by amphiphilic features. This type of characteristic is not generally considered in describing AO compounds.

Actions of antioxidants

Removal of oxygenRemoval of ions with catalytic activitiesRemoval of key intermediates in the oxidation processTrapping of initiating radicalsChain-breakers

The main actions of antioxidants are listed above. The contexts in which antioxidants operate may differ as follows.

The past decades have brought about major changes, both in quantitative and qualitative terms, in our way of eating. Before the Second World War, food, mainly as unprocessed natural food items, was purchased in relatively small quantities, to be consumed quickly, stored for short times, in the presence of unsophisticated refrigeration systems, and cooked by few experienced persons in a family. In recent times, instead, foods are purchased and stored in bulk, as LSV (oils or solid fats, artefacts introduced by humans), which tend to oxidize at the surface, or, frequently, as fast foods, preprocessed mechanically or by heat or freezing. The antioxidant actions in LSV systems are based mainly on the presence and activities of a few natural antioxidants, such as tocopherols, carotenoids and, in special conditions, glutathion and ascorbic acid. Some antioxidant compound from natural sources, however, have been shown to be antioxidant in bulk lipids, but do not function as antioxidant in tissues.

The main natural antioxidants acting in LSV systems are hydrophilic phenols, such as the tocopherols. They are true membrane, organelle and adipocyte, or oil droplet antioxidants, since this is the way lipids are displayed in natural tissues. Supporting the tocopherols is the reductive glutathione±ascorbic acid cascade. The tocopherols show some paradoxical behaviour: a-tocopherol is almost ineffective in vegetable oils, modestly effective by itself in animal fats, but more effective, even, than the synthetic antioxidants buthyl hydrox anisole (BHA) and buthyl hydroxy tyrosol (BHT), in HSV situations (Porter, 1993). In bulk oils the effectiveness of tocopherols in the descending order is S, -y, a and a, the opposite of the order predicted from common indexes (e.g. reduction potential).

A general feature of antioxidants in natural foods, especially from plant sources, is that most of them (e.g. phenolics) are produced as protective compounds against several stressful conditions (oxidative and other), and are present as complex mixtures, with somewhat diversified functional features (redundance) and in given quantitative proportions. Some of the latter properties are transferred to animals through the food chain.

The generation of oxygen-derived radicals in biological systems, through cell-independent and cell-mediated processes, results in the production of a variety of oxidation products, generated from lipids, proteins, nucleic acids and sugars. Owing to the complexity of the processes leading to substrate oxidation, it is relevant that the antioxidant defence strategies in biological systems are generally highly evolved. In fact, although several complex biological molecules (e.g. lipoproteins) are quite susceptible to oxidation in vitro, i.e. after isolation from biological systems, they are instead rather resistant to oxidative stress in the physiological medium (plasma).

Also, cells in vivo appear to behave rather differently, with respect to susceptibility to ROS, from cultured cells, frequently used for several types of studies. Cells in culture are often exposed to unphysiological states of oxidative stress, while being depleted of AO (Visioli et al., 2000), and the consequence is that effects are produced that are largely artefactual owing to an abnormal generation of ROS. Several studies on the effects of antioxidants may therefore have been affected by these artefacts (Halliwell, 2003).

Dietary antioxidants and the prevention of CHD: epidemiological evidence

A large number of epidemiological studies have evaluated potential relationships between dietary intake of antioxidants and coronary heart disease (CHD). Among these, the Nurses’ Health study, included over 87 000 female nurses 34 to 59 years of age, who completed dietary questionnaires that assessed their consumption of a wide range of nutrients, including vitamin E. During follow-up of up to 8 years 552 cases of major coronary disease were documented. As compared with women in the lowest fifth of the cohort with respect to vitamin E intake, those in the top fifth had a relative risk of major coronary disease of 0.66 after adjustment for age and smoking. Further adjustment for a variety of other coronary risk factors and nutrients, including other antioxidants, had little effect on the results. Similarly, the Health Professionals’ Follow-up study, among almost 40 000 males of 40±75 years, followed up for four years, showed a lower risk of coronary disease among men with higher intakes of vitamin E.

Kushi et al. studied over 34 000 postmenopausal women with no cardio­vascular disease who in early 1986 completed a questionnaire that assessed, among other factors, their intake of vitamins A, E and C from food sources and supplements. After 7 years of follow-up, results suggested that in post­menopausal women the intake of vitamin E from food was inversely associated with the risk of death from coronary heart disease. This association was particularly striking in the subgroup of 21 809 women who did not consume vitamin supplements (relative risks from lowest to highest quintile of vitamin E intake, 1.0, 0.68, 0.71, 0.42 and 0.42; P for trend = 0.008). After adjustment for possible confounding variables, this inverse association remained (relative risks from lowest to highest quintile, 1.0, 0.70, 0.76, 0.32 and 0.38; P for trend = 0.004). By contrast, the intake of vitamins A and C was not associated with lower risks of dying from coronary disease.

On the other hand, a negative result came from the Rotterdam Study in which 4802 participants aged 55±95 years, who were free of myocardial infarction (MI) at baseline and for whom dietary data assessed by a semiquantitative food frequency questionnaire were available, were followed up for 4 years: an association between vitamin C or vitamin E and MI was not observed.

Other studies have evaluated plasma levels of different antioxidants, such as vitamins E, C and ,3-carotene in populations affected or not by CHD. The WHO/ Monica project has been one of the largest studies that have analysed the intake of these vitamins in populations with different incidence of CHD mortality. In populations with similar values of serum cholesterol and blood pressure, an inverse correlation between CHD mortality and vitamin E plasma levels was observed; conversely, no relation existed between CHD mortality, and other vitamins. In areas with low and medium coronary mortality, plasma levels of vitamin E were 26±28 pM, while at sites with most frequent CHD mortality plasma levels were 20±21.5 µM.

 

The authors also estimated that the threshold risk for cardiovascular disease would be <25 µM, which, in this particular population, corresponds to < 4.3 µmol vitamin E/mmol cholesterol. This finding is consistent with other studies showing an inverse correlation between vitamin E plasma levels and cardiovascular mortality. It was noticed, in particular, that in persons with high risk for cardiovascular mortality the vitamin E/cholesterol ratio was 3.5, while in persons with low risk the ratio was almost 5. The inverse correlation between vitamin E levels and CHD was also noted in another observational study in which 110 people with angina were compared with 394 controls. The study demonstrated that patients with a history of angina had a lower vitamin E/cholesterol ratio than controls (3.66 vs. 3.86 µmol/mol, P < 0.01) with a significant adjusted odds ratio for angina between patients in the lowest and highest quartile.

In a cross-sectional survey within a random sample of a single urban setting in India, the relation between risk of cardiovascular disease (CVD) and plasma levels of vitamin E was examined in 595 elderly subjects. Plasma levels of vitamin E appeared significantly inversely related to CVD. The adjusted odds ratios for CVD between the lowest and the highest quintiles of vitamin E levels were 2.53, after adjustment for confounding variables.

Another study, designed to assess the degree of association between vitamin E and CHD in a sample of the Tunisian population, included 62 angio­graphically confirmed coronary atherosclerotic patients and 65 age- and sex-matched controls. A trend toward a meaningful decrease of plasma tocopherol was observed in affected patients compared with controls (P = 0.06). Vitamin E concentrations standardised for cholesterol and lipid concentrations were significantly lower (P < 0.02) in coronary patients than in controls (4.35 Ô 1.03 vs. 4.82 Ô 1.23 mmol/mol) for cholesterol-adjusted vitamin E. This association between vitamin E and CHD remained unchanged independent of age, sex, smoking habit, hypertension and diabetes.

These findings have been further corroborated by another study in which 102 apparently healthy subjects were followed up for 47.4 months. A higher risk of cardiovascular events in subjects in the lowest quartile of vitamin E plasma levels compared with those in the highest was found.

In a recent study the association between preclinical carotid atherosclerosis and both the intake and plasma concentrations of antioxidant vitamins was evaluated. Among 5062 participants in Progetto Atena, a population-based study on the aetiology of cardiovascular disease and cancer in women, 310 women were examined by B-mode ultrasound to detect early signs of carotid atherosclerosis. The participants answered a food-frequency questionnaire, and their plasma concentrations of vitamin E, vitamin A and carotenoids were measured. The occurrence of atherosclerotic plaques at the carotid bifurcation was inversely associated with tertiles of vitamin E intake. Similarly, the ratio of plasma vitamin E to plasma cholesterol was inversely related to the presence of plaques at the carotid bifurcation. No association was found between the intake of other antioxidant vitamins (vitamins A and C and carotenoids) or their plasma concentrations and the presence of carotid plaques. The results of a few similar previous studies were instead unclear.

Taken together, these data suggest that vitamin E is an important predictor of CHD and may represent an independent risk factor for atherosclerosis and its complication. Owing to the lack of standardization and a somewhat large dispersion of vitamin E/cholesterol ratio values, accurate analysis of vitamin E levels in patients and healthy subjects is crucial in developing clinical practice and interventional trials. Very recently, for instance, healthy subjects were shown to have values of vitamin E of 3.6 µmol/mmol cholesterol, which is much less than that reported in control population. This finding also raises serious concerns on the methodology used for measuring vitamin and strongly suggests the need for standardization of the assay.

Dietary prevention of sudden cardiac death (SCD): the role of dietary fatty acids, alcohol and antioxidants

SCD is usually defined as death from a cardiac cause occurring within one hour from the onset of symptoms.’ In many studies, however, investigators used quite different definitions, with a time frame of 3 or even 24 hours in the old World Health Organization definition. The magnitude of the problem is considerable since SCD is a very common, and often the first, manifestation of CHD, and it accounts for about 50 per cent of cardiovascular mortality in developed countries.’ In most cases, SCD occurs without prodromal symptoms and out of hospital. As a matter of fact, this mode of death is a major public health issue. Since up to 80 per cent of SCD patients had CHD, the epidemiology and potential preventive approaches of SCD should, in theory, parallel those of CHD. In other words, any treatment aimed at reducing CHD should reduce the incidence of SCD.

We now examine whether diet (and more precisely, certain dietary factors) may prevent (or help prevent) SCD in patients with established CHD. We focus our analyses on the effects of the different families of fatty acids, antioxidants and alcohol.

The hypothesis that eating fish may protect against SCD is derived from the results of a secondary prevention trial, the Diet And Reinfarction Trial (DART), which showed a significant reduction in total and cardiovascular mortality (both by about 30 per cent) in patients who had at least two servings of fatty fish per week. The authors suggested that the protective effect of fish might be explained by a preventive action on ventricular fibrillation (VF), since no benefit was observed on the incidence of nonfatal acute myocardial infarction (AMI). This hypothesis was consistent with experimental evidence suggesting that n-3 polyunsaturated fatty acids (PUFA), the dominant fatty acids in fish oil and fatty fish, have an important effect on the occurrence of VF in the setting of myocardial ischaemia and reperfusion in various animal models, both in vivo and in vitro. In the same studies, it was also apparent that saturated fatty acids are proarrhythmic compared with unsaturated fatty acids. Using an elegant in vivo model of SCD in dogs, Billman and colleagues recently demonstrated a striking reduction of VF after intravenous administration of pure n-3 PUFA, including both the long-chain fatty acids present in fish oil and alpha-linolenic acid, their parent n-3 PUFA occurring in some vegetable oils. These authors found that the mechanism of this protection results from the electrophysiological effects of free n-3 PUFA when these are simply partitioned into the phospholipids of the sarcolemma without covalently bonding to any constituents of the cell membrane. After dietary intake, these fatty acids are preferentially incorporated into membrane phospholipids.

Nair and colleagues have also shown that a very important pool of free (non­esterified) fatty acids exists in the normal myocardium and that the amount of n­3 PUFA in this pool is increased by supplementing the diet in n-3 PUFA. This illustrates the potential of diet to modify the structure and biochemical composition of cardiac cells. In the case of ischaemia, phospholipases and lipases quickly release new fatty acids from phospholipids, including n-3 fatty acids in higher amounts than the other fatty acids, thus further increasing the pool of free n-3 fatty acids that can exert an antiarrhythmic effect.

It is important to remember that the lipoprotein lipase is particularly active following the consumption of n-3 PUFA. One hypothesis is that the presence of the free form of n-3 PUFA in the membrane of cardiac muscle cells renders the myocardium more resistant to arrhythmias, probably by modulating the conduction of several membrane ion channels. So far, it seems that the very potent inhibitory effects of n-3 PUFA on the fast sodium current, INa, and the L-type calcium current, ICaL, are the major contributors to the anti-arrhythmic actions of these fatty acids in ischaemia. Briefly, n-3 PUFA act by shifting the steady-state inactivation potential to more negative values, as was also observed in other excitable tissues such as neurons.

Another important aspect of the implication of n-3 PUFA in SCD is their role in the metabolisation of eicosanoids. In competition with n-6 PUFA, they are the precursors to a broad array of structurally diverse and potent bioactive lipids (including eicosanoids, prostaglandins and thromboxanes), which are thought to play a role in the occurrence of VF during myocardial ischaemia and reperfusion.

Other clinical data show suppression (by more than 70 per cent) of ventricular premature complexes in middle-aged patients with frequent ventricular extrasystoles randomly assigned to take either fish oil or placebo. Also, survivors of AMI and healthy men receiving fish oil were shown to improve their measurements of heart rate variability, suggesting other mechanisms by which n-3 PUFA may be antiarrhythmic.

Support for the hypothesis of a clinically significant antiarrhythmic effect of n-3 PUFA in the secondary prevention of CHD, as put forward in DART, came from two randomised trials testing the effect of ethnic dietary patterns (instead of that of a single food or nutrient), i.e. a Mediterranean type of diet and an Asian vegetarian diet, in the secondary prevention of CHD. The two experimental diets included a high intake of essential alpha-linolenic acid, the main vegetable n-3 PUFA. Whereas the incidence of SCD was markedly reduced in both trials, the number of cases was very small and the antiarrhythmic effect cannot be entirely attributed to alpha-linolenic acid as these experimental diets were also high in other nutrients with potential antiarrhythmic properties, including various antioxidants. These findings were extended by the population-based case-control study conducted by Siscovick and colleagues on the intake of n-3 PUFA among patients with primary cardiac arrest, compared with that of age- and sex-matched controls. Their data indicated that the intake of about 5±6 grams of n-3 PUFA per month (an amount provided by consuming fatty fish once or twice a week) was associated with a 50 per cent reduction in the risk of cardiac arrest. In that study, the use of a biomarker, the red blood cell membrane level of n-3 PUFA, considerably enhanced the validity of the findings, which also were consistent with the results of many (but not all) cohort studies suggesting that consumption of one to two servings of fish per week is associated with a marked reduction in CHD mortality compared with no fish intake. In most studies, however, the SCD endpoint is not reported.

In a large prospective study (more than 20 000 participants with a follow-up of 11 years), Albert et al. examined the specific point that fish has antiarrhythmic properties and may prevent SCD. They found that the risk of SCD was 50 per cent lower for men who consumed fish at least once a week than for those who had fish less than once a month. Interestingly, the consumption of fish was not related to non-sudden cardiac death suggesting that the main protective effect of fish (or n-3 PUFA) is related to an effect on arrhythmia. These results are consistent with those of DART but differ from those of the Chicago Western Electric Study, in which there was a significant inverse association between fish consumption and non-sudden cardiac death, but not with SCD. Several methodological factors may explain the discrepancy between the two studies, especially the way of classifying deaths in the Western Electric Study. This again illustrates the limitations of observational studies and the obvious fact that only randomised trials can definitely provide a clear demonstration of causal relationships.

The GISSI-Prevenzione trial was aimed at helping in addressing the question of the health benefits of foods rich in n-3 PUFA (and also in vitamin E) and their pharmacological substitutes. Patients (n = 11324) surviving a recent AMI (<3 months) and having received the prior advice to come back to a Mediterranean type of diet were randomly assigned supplements of n-3 PUFA (0.8 g daily), vitamin E (300 mg daily), both or none (control) for 3.5 years. The primary efficacy endpoint was the combination of death and nonfatal AMI and stroke. Secondary analyses included overall mortality, cardiovascular (CV) mortality and SCD. The exact definition of SCD was not given in the paper. However, the clinical events were validated by an ad hoc committee of expert cardiologists,25 who presumably used the current definition of SCD. Treatment with n-3 PUFA significantly lowered the risk of the primary endpoint (the relative risk decreased by 15 per cent). Secondary analyses provided a clearer profile of the clinical effects of n-3 PUFA (Table below). Overall mortality was reduced by 20 per cent and CV mortality by 30 per cent. However, it was the effect on SCD (45 per cent lower) that accounted for most of the benefits seen in the primary combined endpoint and both overall and CV mortality. There was no difference across the treatment groups for nonfatal CV events, a result comparable to that of DART.3 Thus, the results obtained in this randomised trial are consistent with previous controlled trials, large-scale observational studies and experimental studies,4-7 which together strongly support an effect of n-3 PUFA in relation with SCD.

Clinical efficacy of (n-3) PUFA in the GISSI-Prevenzione Trial.

Relative risk (95% confidence interval)

Death, nonfatal AMI and strokeNonfatal cardiovascular events

Source: modified from GISSI-Prevenzione investigators.

An important point is that the protective effect of n-3 PUFA on SCD was greater in the groups of patients who complied more strictly with the Mediterranean diet. This suggests a positive interaction between n-3 PUFA and some components of the Mediterranean diet which is, by definition, not high in n-6 PUFA and low in saturated fats, but rich in oleic acid, various antioxidants and fibre, and associated with a moderate consumption of alcohol (see below for further comments).

Regarding the other dietary fatty acids, animal experiments have clearly indicated that a diet rich in saturated fatty acids is associated with a high incidence of ischaemia- and reperfusion-induced ventricular arrhythmia, whereas PUFA of either the n-6 or n-3 family reduce that risk. Many (but not all) epidemiological studies have shown consistent associations between the intake of saturated fatty acids and CHD mortality. However, the SCD endpoint is usually not analysed in these studies. In addition, a clear demonstration of a causal relationship between dietary saturated fatty acids and SCD would require the organisation of a randomised trial, which is not ethically acceptable. Thus, besides the effect of saturated fatty acids on blood cholesterol levels, the exact mechanism(s) by which saturated fats increase CHD mortality remain unclear. If animal data, demonstrating a proarrhythmic effect of saturated fatty acids, are confirmed in humans, the first thing to do in order to prevent SCD in humans would be to drastically reduce the intake of saturated fats. In fact, this has been done in randomised dietary trials and, as expected, the rate of SCD decreased in the experimental groups. However, as written above about the same trials, the beneficial effect cannot be entirely attributed to the reduction of saturated fats, because other potentially antiarrhythmic dietary factors, including n-3 PUFA, were also modified in these trials.

In contrast to n-3 PUFA, few data have been published so far regarding the effect of n-6 PUFA on the risk of SCD. Roberts et al. have reported that the percentage content of linoleic acid (the dominant n-6 PUFA in the diet) in adipose tissue (an indicator of long-term dietary intake) was inversely related to the risk of SCD, which was defined in that study as instantaneous death or death within 24 hours of the onset of symptoms. This is in line with most animal data and may suggest that people at risk of SCD may benefit from increasing their dietary intake of n-6 PUFA, in particular linoleic acid, in the same way as for n­3 PUFA. However, n-3 PUFA were more effective on SCD than n-6 PUFA in most animal experiments.

In addition, diets high in n-6 PUFA increase the linoleic acid acid content of lipoproteins and render them more susceptible to oxidation, which would be an argument against such diets because lipoprotein oxidation is a major step in the inflammatory process that renders atherosclerotic lesions unstable and prone to rupture.

Erosion and rupture of atherosclerotic lesions were shown to trigger CHD complications (see below the section on plaque inflammation and rupture) and myocardial ischaemia and to considerably enhance the risk of SCD. As a matter of fact, in the secondary prevention of CHD, diets high in n-6 PUFA failed to improve the overall prognosis of the patients. Also, in the Dayton study, a mixed primary and secondary prevention trial, in which the chief characteristic of the experimental diet was the substitution of n-6 PUFA for saturated fat, the number of SCD was apparently lower in the experimental group than in the control group (18 vs. 27) but the number of deaths from other causes, in particular cancers, was higher in the experimental group (85 vs. 71), thus offsetting the potential protective effect of n-6 PUFA on SCD and having no effect at all on mortality. Such negative effects were not reported with n-3 PUFA. Thus, despite the beneficial effect of n-6 PUFA on lipoprotein levels, which could, in theory, reduce SCD in the long term by reducing the development of atherosclerosis, it seems preferable not to increase the consumption of n-6 PUFA beyond the amounts required to prevent deficiencies in the essential n-6 fatty acid, linoleic acid (approximately 4±6 per cent of the total energy intake), which are found in the current average Western diet. As a substitute for saturated fat, the best choice is obviously to increase the intake of vegetable monounsaturated fat (oleic acid) in accordance with the Mediterranean diet pattern. If oleic acid has apparently no effect on the risk of SCD (at least by comparison with n-3 and n-6 PUFA), its effects on blood lipoprotein levels are similar to those of n-6 PUFA and it has the great advantage of protecting lipoproteins against oxidation.

Thus, the best fatty acid combination to prevent SCD (and other complications of CHD) and, in other words, the cumulative antiarrhythmic, antioxidant and hypolipidaemic effects, would result from the adoption of a diet close to the Mediterranean diet pattern.

Finally, Roberts et al. reported no significant relationship between trans isomers of oleic and linoleic acids in adipose tissue and the risk of SCD whereas Lemaitre et al. found that cell membrane trans isomers of linoleic acid (but not of oleic acid) are associated with a large increase in the risk of primary cardiac arrest. As for the role of trans fatty acids on ventricular arrhythmias, it has not been investigated in experimental models.

Thus, although specific human data on the effect of saturated fatty acids on SCD are lacking, results of several trials suggest that it is important to reduce their intake in the secondary prevention of CHD. Despite a possible beneficial effect on the risk of SCD, increasing consumption of n-6 PUFA should not be recommended in clinical practice for patients with established CHD. Diets including low intakes of saturated fatty acid (as well as trans isomers of linoleic acid) and n-6 PUFA (but enough to provide the essential linoleic acid) and high intakes of n-3 PUFA and oleic acid (Mediterranean diet pattern) appear to be the best option to prevent both SCD and nonfatal AMI recurrence.

The question of the effect of alcohol on heart and vessel diseases has been the subject of intense controversy in recent years. The consensus is now that moderate alcohol drinking is associated with reduced cardiovascular mortality, although the exact mechanism(s) by which alcohol is protective are still unclear. In contrast, chronic heavy drinking has been incriminated in the occurrence of atrial as well as ventricular arrhythmias in humans, an effect called `the holiday heart’ because it is often associated with binge drinking by healthy people, specifically during the weekend. Studies in animals have shown varying and apparently contradictory effects of alcohol on cardiac rhythm and conduction, depending on the animal species, the experimental model and the dose of alcohol. If given acutely to non-alcoholic animals, ethanol may even have antiarrhythmic properties.

In humans, few studies have specifically investigated the effect of alcohol on SCD. The hyperadrenergic state resulting from binge drinking, as well as from withdrawal in alcoholics, seems to be the main mechanism by which alcohol induces arrhythmias in humans. In the British Regional Heart Study, the relative risk of SCD in heavy drinkers (more than six drinks per day) was twice as high as in occasional or light drinkers. However, the effect of binge drinking on SCD was more evident in men with no pre-existing CHD than in those with established CHD. In contrast, in the Honolulu Heart Program, the risk of SCD among healthy middle-aged men was positively related to blood pressure, serum cholesterol, smoking and left ventricular hypertrophy but inversely related to alcohol intake. In fact, the effect of moderate `social’ drinking on the risk of SCD in non-alcoholic subjects has been addressed so far in only one study.

Investigators of the Physicians’ Health Study assessed whether light-to­moderate alcohol drinkers apparently free of CHD at baseline have a decreased risk of SCD. After controlling for multiple confounders, men who consumed two to four drinks per week or five to six drinks per week at baseline had a significantly reduced risk of SCD (by 60±80 per cent) as compared with those who rarely or never consumed alcohol. Analyses were repeated after excluding deaths occurring during the first 4 years of follow-up (in order to exclude the possibility that some men who refrained from drinking at baseline did so because of early symptoms of heart diseases), and also using the updated measure of alcohol intake ascertained at year 7 to address potential misclassification in the baseline evaluation of alcohol drinking. These secondary analyses basically provided the same results and confirmed the potential protective effect of moderate drinking on the risk of SCD. Despite limitations (the selected nature of the cohort, an exclusively male study group, no information on beverage type and drinking pattern), this study suggests that a significant part of the cardioprotective effect of moderate drinking is related to the prevention of SCD. Further research should be directed at understanding the mechanism(s) by which moderate alcohol drinking may prevent ventricular arrhythmias and SCD.

In practice, the current state of our knowledge suggests that in CHD patients at risk of SCD, there is no reason not to allow moderate alcoholic drinking. From a practical point of view, we advise drinking no more than one or two drinks per day, preferably wine, preferably during the evening meal, and never before driving a car or undertaking dangerous work.

The issue about the effect of dietary antioxidants on the risk of CHD in general and on SCD in particular is more controversial. Regarding vitamin E, for instance, the most widely studied dietary antioxidant, discrepant findings between the expected benefits based on epidemiological observations and the results of clinical trials were published. In a recent controlled trial, a significant decrease in nonfatal AMI and a non-significant increase in cardiovascular mortality (in particular in the rate of SCD) were reported with a daily regimen of 400±800 mg of vitamin E in patients with established CHD. Because of certain methodological shortcomings (which we will not discuss here), this trial was said to confuse rather than clarify the question of the usefulness of vitamin E supplementation in CHD, and provided no indication about possible links between vitamin E and the prevention of SCD.

The GISSI-Prevenzione trial brings new information in this regard. Unlike those of n-3 PUFA, the results of vitamin E supplementation do not support a significant effect on the primary endpoint, namely a combination of death and nonfatal AMI and stroke. However, the secondary analysis provides a clearer view of the clinical effect of vitamin E in CHD patients, which cannot be easily dismissed. In fact, among the 193 and 155 cardiac deaths that occurred in the control and vitamin E group, respectively, during the trial (a difference of 38, P <0.05), there were 99 and 65 SCDs (a difference of 34, P< 0.05), which indicated that the significant decrease in cardiovascular mortality (by 20 per cent) in the vitamin E group was almost entirely due to a decrease in the incidence of SCD (by 35 per cent). In contrast, nonfatal cardiac events and non-sudden cardiac deaths were not influenced. These data suggest that vitamin E may be useful for the primary prevention of SCD in patients with established CHD.

The vitamin E data of the GISSI trial do not stand in isolation. In an in vivo dog model of myocardial ischaemia, we also reported a protective effect of vitamin E on the incidence of VF (the main mechanism of SCD) with a 16 per cent rate in the vitamin E group and 44 per cent in the placebo group (P< 0.05). Also in line with the GISSI results, infarct size, which is the main determinant of acute heart failure and non-sudden cardiac death, was larger in the supplemented group (58.5 per cent of the ischaemic area) than in the placebo group (41.9 per cent, P <0.05). Such ambivalent effects of vitamin E may at least partly explain why its effects were neutral or non-significant in many studies, with the negative effects hiding the beneficial ones. Nevertheless, the GISSI trial showed that cardiovascular mortality and SCD were significantly reduced by vitamin E, and the effect on overall mortality showed a favourable trend (P = 0.07). Finally, the recently published HOPE trial, testing the effect of 400 IU of vitamin E daily in patients at high risk of CHD (therefore in primary prevention) and reporting an apparent lack of effect of vitamin E, does not help us to solve the issue of whether or not vitamin E is protective against SCD.51 In that trial, it is not clear whether the patients actually took the capsules during meals (a prerequisite for intestinal absorption of vitamin E), whether the patients were more or less deficient in vitamin E (no blood measurement), whether some of them were taking vitamin supplements (a common practice nowadays among certain populations), and SCD was apparently not among the predefined endpoints. In addition, patients with left ventricular dysfunction, a major determinant of the risk of SCD, were not eligible.

Clinical efficacy of vitamin E in the GISSI-Prevenzione Trial. See text for comments

Relative risk (95% confidence interval)

Death, nonfatal AMI and strokeNonfatal cardiovascular events

Source: modified from GISSI-Prevenzione investigators.25

Vitamin E and other antioxidants in the prevention of cardiovascular disease

Oxidative stress is believed to play a crucial role in the initiation and progression of atherosclerosis disease. Steinberg and colleagues were among the first to postulate that modified low-density lipoprotein (LDL) could account for the accumulation of lipid within macrophages, a critical early step in the formation of the atherosclerotic plaque. In the early phases, native LDL may amass in the subendothelial arterial space and may be minimally oxidized by resident vascular cells through the activity of such enzymes as 12/15-lipoxygenase. In turn, this minimally modified LDL leads to the production of chemotactic factors and granulocyte and macrophage colony-stimulating factors, which enhance recruitment of circulating monocytes and their differentiation to macrophages in the vessel wall.

Plaque stability is believed to be influenced by levels of inflammatory mediators locally, which may stimulate expression of a number of proteolytic enzymes that lead to plaque fragility and rupture. These inflammatory actions encourage further oxidization of LDL, leading to both structural and functional changes in the vessel. Macrophages avidly accumulate LDL particles modified by oxidation or acetylation through a number of scavenger receptors, including CD36 and scavenger receptors A-I/II, leading to the formation of foam cells and development of the atherosclerotic plaque. At the same time, oxidized LDL species are directly toxic to vascular cells, and lead to endothelial injury and dysfunction, disabling, among other things, the intrinsic antiplatelet effects of this protective barrier, as well as the generation of nitric oxide, with deleterious effects on vascular tone and reactivity.

The importance of oxidized LDL in atherogenesis has been further confirmed by the use of specific antibodies to oxidized LDL, which have been shown to be local to atherosclerotic lesions in the vessel wall. Oxidative stress may con­tribute to atherogenesis by mechanisms that are not necessarily linked to LDL oxidation. For example, free radical oxygen species such as superoxide anion can rapidly react with and inactivate nitric oxide, enhancing proatherogenic mechanisms (e.g. leucocyte adherence to endothelium, impaired vasorelaxation, platelet aggregation).

Although enzymatic and nonenzymatic oxidation of LDL seems to be involved, its relevance in the evolution of human atherosclerosis is still unclear. An important matter of discussion is the evident discrepancy between experi­mental and clinical trials with antioxidants, that, in fact, provided divergent results. Most trials with antioxidants in experimental models of atherosclerosis demonstrated that this treatment is able to retard the progression of athero­sclerosis while the results of clinical trials are conflicting, in that positive as well as negative effects has been reported. The investigation of antioxidants for prevention of atherosclerosis stems from observational trials that demonstrated the existence of an inverse relationship between the consumption of antioxidant vitamins and the risk of cardiovascular events. However, meta-analysis of the observational studies indicated that among antioxidant vitamins, vitamin E was the only one that exerted a beneficial effect against atherosclerotic complications.

On the basis of these data almost all the trials have been based on the assumption that supplementation with vitamin E would represent a useful approach for preventing cardiovascular disease. However, candidates for anti­oxidant treatment were not accurately defined: any patient at risk of cardiovascular events has been indiscriminately enrolled in those trials. We argue that antioxidant status represents an important marker of oxidative stress, its determination may be useful for better identifying candidates for antioxidant treatment. In order to substantiate this hypothesis, data inherent to oxidative stress and antioxidant status in patients at risk for cardiovascular disease and in patients included in observational and interventional trials have been reviewed. As antioxidant vitamin E has been the subject of the most important research in this field, our analysis is essentially concentrated on the clinical relevance of this vitamin in patients with cardiovascular disease.

How Antioxidants Work – Preventing Free Radical Damage and Oxidation

Vitamins C, E, and beta-carotene aren’t the only antioxi­dants. Many phytochemicals also have antioxidant proper­ties, from which we derive great benefit. Antioxidant, once again, is a term referring to any substance that helps to nul­lify the deleterious, albeit natural, side effects of oxygen consumption within cells. Oxygen may seem like a harmless substance. We breathe it in all day long. All cells require oxygen to function. Oxygen is necessary for human life. However, oxygen consumption releases by-products that are potentially damaging to cells.

In our bodies, when cells use oxygen for energy, they pro­duce by-products or waste products called free radicals. Free radicals are oxygen by-products missing an electron, which they have given up during the oxidation process.

Free radi­cals “roam” through the body searching for electrons to cor­rect the imbalance. The nearest molecule with an available electron is “robbed” by the free radical, and every cell robbed of an electron is slightly damaged. This is a natural process. Our cell membranes contain vitamin E to help neu­tralize free radical activity before cell damage can occur.

However, our bodies weren’t designed to handle the on­slaught of free radicals produced by environmental pollu­tants common to everyday life today: car exhaust, cigarette smoke, certain chemical additives in foods, and so on. With­out sufficient antioxidant protection, over time, free radical damage can become an insurmountable obstacle to good health. Many scientists believe that cumulative free radical damage contributes to chronic diseases like cancer, heart disease, arthritis, and macular degeneration.

The name antioxidant suggests that these compounds nul­lify the negative effects of oxidation on cells, and that is ex­actly what they do. If you dipped a cut piece of apple in lemon juice, it wouldn’t turn brown as quickly because lemon juice contains ascorbic acid (a common form of vita­min C), an antioxidant. Another form of oxidation occurs when fat turns rancid. Tocopherols, a common form of vita­min E, are often used to preserve foods with fat because the vitamin E retards the oxidation, or spoilage, process. Ex­actly how antioxidants work is still largely unknown, but they appear to work in several ways in the body.

Antioxi­dants seem to prevent free radical damage in the first place. They also may shuttle carcinogenic compounds generated by free radical damage out of the body before they can do any damage. And, as we’ve mentioned before, while the ver­dict is not yet in on whether antioxidant vitamin supple­ments do any good at all in the prevention of chronic disease, antioxidant consumption from fresh vegetables does seem to offer a significant measure of protection against free radical damage.

MEDITERRANEAN WAYS TO ADD VEGETABLES

How did the people eating the traditional Mediterranean diet pack so many vegetables into their daily meals? Easily and deliciously. In the Mediterranean, vegetable consump­tion is not just a matter of eating any vegetable at any time, in whatever state is most convenient. Vegetable selection is a matter of pride, vegetable preparation an art, and vegetable consumption a pure pleasure. Most essentially, in the Mediterranean, vegetables are chosen according to what is in season.

Outdoor produce markets throughout the Mediterranean offer the season’s best, freshest, most vibrant vegetables. Your local grocer, farmer’s market, or produce stand is also likely to feature the freshest locally grown produce. Even if the vegetables in season in your area aren’t those in season in the Mediterranean, eating the freshest seasonal produce is still eating in the Mediterranean way. Seek out the best sources for vegetables in your area, and you may discover that vegetables taste much better than you think. Here are a few more Mediterranean-inspired tips for adding vegetables to your day. You’ll wonder how you ever ate without them!

Looking for a fast-food lunch? A wedge of hearty wheat bread, a small chunk of feta or other cheese, a few slices of ripe tomato, a handful of leafy greens drizzled with olive oil and a squeeze of fresh lemon juice, and a ripe peach or other seasonal fruit for dessert take less time to prepare than going through the drive-through. Bring your Mediterranean lunch to work with you and everyone will wonder what upscale deli supplied your meal.The next time you make spaghetti, stir a shredded carrot and a finely chopped green or red pepper, a few mushrooms, or a handful of chopped spinach into the sauce. Vegetable additions add color, flavor, and nutritional power to your pasta dinner.Instead of grilling burgers, grill vegetables, Mediterranean style. Slice onions, peppers, zucchini, portabella mushroom caps, eggplant, and tomatoes into thick slices, drizzle with olive oil, and grill. If you want to add a Middle Eastern flair, skewer the vegetables into shish kebabs. A chunk or two of chicken or lamb among the vegetables would be authentic and would add an extra dash of protein. Serve with lemon wedges.Drizzle those plain vegetables with a little olive oil and a sprinkling of fresh grated cheese, or garnish with a splash of tomato sauce or a few sun-dried tomatoes. Tomato sauce also adds culinary interest to broiled fish.If you can relate to former U.S. President George H. W. Bush when it comes to broccoli (his aversion to this beautiful vegetable was well known), maybe you just haven’t had it cooked really well. Try steaming broccoli just until it is very bright green and tender. Toss with a little olive oil, sea salt, minced garlic, and a few flakes of red pepper. Serve and eat immediately. Perfectly cooked broccoli is a joy. Overcooked or old broccoli is enough to make anyone dislike the stuff.Leafy green salads are an important part of many Mediterranean meals. Get in the habit of including a bowl of leafy greens with olive oil and a little lemon juice or vinegar with at least one meal every day. A few extra chopped vegetables and a little grated cheese will make your greens even more interesting and nutrient-rich. (Just remember to forgo the creamy dressing in favor of a dressing with an olive oil base.) Do you think you don’t have enough time to chop up a salad? Take advantage of food industry technology and splurge on ready-to-eat bagged veggies and greens. Selections are plentiful, many types are organic, and they come pre washed. What could be quicker?Eat pizza in the Mediterranean style. Unlike American pizzas, Mediterranean pizzas are typically thin, light concoctions with just a few toppings. Fresh tomato sauce and one or two featured vegetables (mushrooms, garlic slices, onion, zucchini, broccoli, peppers) and a very light sprinkling of mozzarella or Parmesan cheese on a fresh-baked (or store-bought, if you are pressed for time) whole-grain crust makes a perfect light dinner. Many Mediterranean pizzas don’t even include cheese. In the mood for some-thing more substantial? The more veggies, the better! Add roasted eggplant, mushrooms, red peppers (better than green if you want that lycopene punch)—you name it! See how much your pizza can hold. Load up and enjoy!Are you or your kids getting bored with peanut butter sandwiches? Add chopped or shredded carrots for a surprising, refreshing, flavorful crunch.Pumpkin is an American vegetable, but its nutritional value is Mediterranean in spirit! Stir canned pumpkin into hot oatmeal for breakfast with a little cinnamon and brown sugar. Add a generous spoonful to applesauce for a light dessert, or stir some into vanilla yogurt for an added zing.Microwave a sweet potato or yam until soft for a quick, carotenoid- and fiber-rich snack, or try baked sweet potato fries or yam chips, brushed lightly with olive oil and baked at 400 degrees until lightly browned and fork-tender, about twenty minutes, or longer if you’ve got a large pan full.

The one thing you can do to make your diet more “Mediterranean” is to begin eating more fresh vegetables to-day. Whether or not they were traditionally grown and consumed in the Mediterranean, the very concept of eating the vegetables grown on the land around you captures the essence of the traditional Mediterranean diet. Vegetables add beauty to your plate, excitement to your palate, and a host of vital substances to your body.

Antioxidants and Minerals in The Mediterranean Diet

Antioxidants are substances that combat the negative ef­fects of oxygen in cells. When the body uses oxygen for en­ergy, it produces by-products called free radicals that have a potentially damaging effect on cells. Antioxidants neutralize this effect, essentially shuttling free radicals and even car­cinogenic substances out of the body before they can do damage.

Three of the most potent antioxidants are the vitamins C, E, and the substance beta-carotene, which the body converts to vitamin A.

These vitamins have been a long-time research focus in disease prevention, and have been repeatedly linked to decreased risk of many chronic conditions, including heart disease, cancer, cataracts, and more. Research with the AIDS virus suggests that vitamin E and beta-carotene may slow the progression of HIV to AIDS. Vitamin E may pro­tect from heart disease in a number of ways, by slowing or preventing oxidation of “bad” (LDL) cholesterol, and possi­bly by reducing the tendency of blood to clot.

The protective antioxidant power of vitamin E has also been shown to increase dramatically when vitamin C and beta-carotene are consumed. Shown to work in concert to modify the risk of many chronic diseases and age-related degenerative conditions, a balance of these three antioxi­dants seems to be most effective in the body, and the ab­sence of one seems to negatively impact the effectiveness of the others. For example, vitamin C flushes out free radicals in the body’s fluids, while beta-carotene and vitamin E neu­tralize free radicals in fat tissue.

Beta-carotene was once a star in the world of cancer pre­vention, and supplementation with this nutrient became popular. It seemed to make sense, given its antioxidant capa­bilities. However, research using beta-carotene supplements brought about some surprising results. In one famous study, beta-carotene supplementation was linked with an increase (not a decrease) in lung cancer among smokers. (This is an example of the possible dangers of supplementation.) Study subjects who did not smoke, however, were not negatively affected by the supplementation. Smokers typically have de­pleted stores of vitamins C as well as E.

Significantly, no such toxicity has been shown to exist when beta-carotene is consumed via vegetables. On the con­trary, studies suggest that vitamins from food sources have a positive effect on a number of chronic conditions. One study linked increased vitamin C and beta-carotene consumption primarily from food (as opposed to supplements) to better old-age memory in a long-term Swiss study begun in 1971 and published in 1997.

However, the results of studies seek­ing to determine the value of vitamin supplements are, in general, hazy. Some research seems to suggest supplements can have a positive effect on health (especially with vitamin E). Other studies suggest supplements have no effect. Still others indicate that vitamin supplements, especially in mega-doses, can actually be injurious to health. However, vitamins in their natural form—potently supplied in vegetables— appear to be beneficial to health in countless, complex ways, as yet only minimally understood.

Just about every vegetable is packed with vitamins, and the traditional Mediterranean diet supplies vitamin-rich veg­etables in abundance, and in far higher proportion than is typical in the American diet. Eating more vegetables, and a wider variety of vegetables, is an excellent first step toward eating in a Mediterranean-inspired fashion. It is also the safest and probably most effective way to reap the benefits of the many vitamins—antioxidants and others—your body requires.

Minerals work with vitamins in many bodily processes, and regulate a few essential functions, such as muscle con­tractions and nerve impulses. They are also part of our bod­ies: bones, teeth, and nails all contain minerals. The major minerals, including calcium, magnesium, and potassium, can all be found in certain vegetables. Many vegetables con­tain trace minerals as well, such as iron, selenium, and zinc.

Selenium has been the subject of much research. Another antioxidant, selenium appears to boost the action of certain anticancer enzymes in the body, and may even prevent pre­mature aging. Plants incorporate selenium from the soil in which they are grown. Garlic is a good source of selenium.

Calcium is essential for bone strength and to slow the rate of bone loss associated with aging. Calcium also assists muscle contractions, including the heart muscle; facilitates proper nerve functioning; and helps the blood to clot. Calcium deficiencies can result in osteoporosis and may con-tribute to high blood pressure and possibly colon cancer. While most people think of dairy products as the best sources of calcium (they are indeed good sources), many vegetables supply calcium as well. In fact, the calcium in some vegetables (such as kale) is even more available to the body than the calcium in dairy products. Other calcium-rich vegetables include dark leafy greens such as mustard greens, turnip greens, and broccoli.

Magnesium is another mineral essential to bone strength and growth, as well as to nerve and muscle cells. It warrants a mention here because magnesium and calcium work together in the body to perform many important functions, and a magnesium deficiency also hinders the body’s ability to use calcium (as well as potassium and sodium). Rich sources include dark green vegetables like spinach, as well as other foods common to the Mediterranean diet such as whole grains, nuts, and legumes.

The relation between antioxidants and memory performance

Carotenoids on the Brain

There’s plenty of evidence that what Tufts researchers found in animals happens in humans. Among 1400 older men and women, those with the highest blood levels of fruit and vegetable antioxidants called carotenoids (beta-and alpha-carotene, lutein, zeaxanthin, cryptoxanthin, and lycopene) were smarter, according to tests at the French government’s medical research institute (INSERM). Indi­viduals with the highest blood carotenoids, indicating they ate the most fruits and vegetables, scored 35 to 40 percent higher on tests of logical reasoning and visual attention than those with the lowest blood levels of carotenoids. Pre­sumably, the high carotenoids produced stronger brain power by shielding brain cells from free radical damage due to aging.

Similarly, Swiss researchers recently found that high blood levels of antioxidant vitamin C and beta-carotene actually predicted a superior memory in old age. In a large ongoing study of aging, Walter J. Perrig, Ph.D., and colleagues at the University of Berne recently tested the memory per­formance of 442 healthy men and women ages sixty-five to ninety-four. Dr. Perrig compared their memory scores with blood samples, taken recently and twenty-two years previ­ously. Strikingly, those with the most blood vitamin C and beta-carotene, at both time periods, scored highest on tests of memory involving recall, recognition, and vocabulary. Thus, high blood antioxidants were an accurate forecast of memory strength two decades later. Researchers concluded that these antioxidants “play an important role in brain aging and . . . the prevention of progressive cognitive impairments.” In short, if you want to preserve your mem­ory as you get old, be sure to take in lots of antioxidants, vitamin C and beta-carotene in particular.

Tomatoes and the Nun Experiments

It’s almost incredible that the amount of tomatoes you eat over a lifetime could help determine how vital your brain is in old age. But striking research by David Snowdon, M.D., at the Sanders-Brown Center on Aging at the University of Kentucky, says it’s true. Dr. Snowdon is director of an ongoing study of aged nuns, many over a hundred years old. He has found that the more lycopene—a potent antioxidant—in their blood, the sharper their mental acu­ity in old age. Lycopene gets into the blood virtually only one way: from eating tomatoes.

In Dr. Snowdon’s study of eighty eight women ages sev­enty-seven to ninety-eight, those with low blood lycopene were least able to take care of themselves in old age—least able to walk, bathe, dress, and feed themselves. Such women with a “lycopene deficiency” in fact were nearly four times more apt to require assistance than those with above average lycopene. Dr. Snowdon theorizes that antiox­idant lycopene in tomatoes helps neutralize free radical chemicals throughout the body, including the brain, keep­ing it intact and functioning better and longer. Indeed low cognitive function, presumably related to free radical dam­age in the brain, strongly predicted a progressive loss of independence in activities of daily living.

Although watermelon and pink grapefruit contain smidgens of lycopene, by far the major source is the tomato, notably processed tomato products, such as tomato paste, tomato sauce, and canned tomatoes. A recent Italian study showed that eating tomato puree with 16.5 milligrams of lycopene daily for twenty-one days boosted the blood’s antioxidant capacity dramatically. Free radical damage to cells’ DNA (genetic material) dropped an astonishing 33 per­cent.

WHERE TO FIND BRAIN-SAVING LYCOPENE

1 ounce

Tomato paste                               16 mg

Tomato ketchup                            5 mg

Spaghetti sauce                              5 mg

Tomato sauce                                5 mg

Tomatoes, canned                         3 mg

Tomato soup                                 3 mg

Tomato juice                                 3 mg

Vegetable juice                              3 mg

Watermelon                                   1 mg

Pink grapefruit                              1 mg

Fresh tomatoes                less than 1 mg