Religious Coping Strategies in Healthy Elderly and in Those at Risk for Dementia

Evidence suggests that participation in religious activity among the elderly is associated with slower progression of Alzheimer’ s disease (Kaufman et al. 2007), lower morbidity and mortality (Holt and Dellmann-Jenkins 1992; Levin and Schiller 1987; McCullough et al. 2000), reduced cognitive aging (Corsentino et al. 2009), lower levels of depression and psycholog­ical stress (Ironson et al. 2002' Koenig et al. 1992), and enhanced qual­ity of life and well-being (Ellison and Levin 1998' Koenig 1994' Koenig 2000; Koenig, Hays, et al. 1999; Koenig, Idler, et al. 1999; Larson et al. 1992; Levin 1994). Religiosity, however, can also sometimes have a deleterious impact on some measures of mental health in some elderly individuals (Krause 2004' Krause et al. 1998). For better or worse, religious practices become increasingly important to many people as they age (Dillon and Wink 2007), yet very little is known about religious cognition in the aging brain/mind.

To our knowledge, no neurocognitive model of religious cognition in aging has yet been developed or rigorously tested—this despite the well-attested impact of religiosity on mind, brain, and overall health and well-being in the elderly. There is, therefore, an urgent need to develop explicit models of religious cognition that can focus research efforts on identification of potential mechanisms that mediate the impact of religious cognitions and practices on cognitive aging and on both posi­tive and negative health outcomes. The model I have proposed and will describe here is known as the “decoupling” model (described below and in McNamara 2009). It is focused on the impact of religious cognition on self-control and self-regulation, processes known to be crucial for health and well-being (Baumeister and Vohs 2004). It is, therefore, an ideal model to assess potential mediating cognitive pathways of religion’s effects on self-regulation, cognitive aging, and health outcomes.

Adults over age 65 are at increased risk for mood disorder, mild cogni­tive impairment, and higher rates of chronic disease (Anstey et al. 2009; Centers for Disease Control and Prevention 2008; Conwell and Duberstein 2001; Hybels and Blazer 2003; Lebowitz et al. 1997; Zihl et al. 2010). Those elderly who engage in regular religious practices are protected to some sig­nificant extent against these adverse outcomes (Krause 2004; Krause et al. 1998; Koenig et al. 1992; Corsentino et al. 2009). Elderly people more often rely on religious coping practices than do younger controls (Koenig et al. 1990; Van Ness and Larson 2002; McFarland 2010) and more often engage in religious cognition (Koenig et al. 1990; Van Ness and Larson 2002; McFar­land 2010) for problem solving. Negative forms of religious coping, delete­rious to health and well being (e.g., obsessing about punitive supernatural agents, etc.), are also all too common among the elderly.

Measures of religiosity such as frequent prayer or meditation, frequent attendance at religious services, and “intrinsic” forms of religiosity appear to have beneficial effects on some aspects of physical and mental health in the elderly (Koenig, Hays, et al. 1999; Koenig, Idler, et al. 1999; Musick et al. 2000; Koenig, McCullough, and Larson 2001; Powell, Shahabi, and Thoresen 2003). Other forms of religiosity can negatively impact mental health (Magyar-Russell and Pargament 2006). There have been forceful criticisms of many religion and health studies (see Lawrence 2002; Sloan and Bagiella 2002; Sloan, Bagiella, and Powell 1999; Sloan et al. 2000; Sloan and Ramakrishnan 2006). And there have also been more positive over­all assessments (see Koenig 2000; Koenig 2001, “Religion and Medicine II”; Koenig 2001, “Religion and Medicine III”; Koenig 2001, “Religion and Medicine IV”; Koenig, The healing 2001; Miller and Thoresen 2003; Thore­sen and Harris 2002; Williams and Sternthal 2007). Yet, while many early studies failed to account for key confounding variables and other covari- ates, more recent research efforts are less vulnerable to such criticisms. Recent meta-analytic reviews of well-controlled studies and randomized clinical trials of religious practices and health outcomes (Townsend et al. 2002; Powell, Shahabi, and Thoresen 2003; Coruh et al. 2005) all concluded that religious practices of various kinds such as private meditation and prayer and frequent attendance at religious services enhance a variety of health outcomes. Despite the apparent protective effects of religiosity on health outcomes in the aged, there are still no neurocognitive models that can address how religious cognition might influence health in aging.

We (McNamara 2001, 2002, 2006, 2009; McNamara, Andresen, and Gellard 2003; McNamara, Durso, and Brown 2006; McNamara, Durso, Brown, and Harris 2006; McNamara, Durso, and Harris 2006; Butler, McNamara, and Durso 2009) have been developing a research program that addresses the need for a neurocognitive model of religiosity that can help to account for religion’s effects on the aging brain/mind. We suggest that a distinguishing mark of religious cognition in aging is that religious cognitions involve privileged access to the self and can help promote development of generative aspects of the self in aging. Religious cognition can therefore become a powerful tool in processes of self-regulation and elderly people avail themselves of this tool. This impact of religiousness on self-regulation can also help to explain negative effects of religiosity when they occur. Since we are interested in understanding religion’s effects on cognition and health, we have built upon previous models of various aspects of the religious mind (reviews in Andresen 2001) as well as more general models of self-regulation (Baumeister and Vohs 2004).

Consistent with the work of many other investigators (see reviews in McCullough and Willoughby 2009 and McNamara 2009) in these and related fields, we argue that one major pathway by which religion influences health out­comes (particularly in the elderly) is via its effects on self-regulation. At the cognitive level, we argue that religious cognition (e.g., triggered in prayer, meditation, or ritual contexts, etc.) is characterized by a transient “decou­pling” of the present self-concept from control over attentional resources of the individual and then a linking up or integration of the current self with some version of an ideal future self or god-concept. When operating normally, this linking of present with ideal selves and/or with supernatu­ral agents promotes positive self-development and enhances control over attentional resources and behavior of the individual. Strengthening self­control, in turn, promotes improved self-regulation and improved health outcomes in the long run (McNamara 2009; McCullough and Willoughby 2009)   . The transient decoupling of self and attentional mechanisms, how­ever, can also lead to liminal states of consciousness that open the individ­ual to negative outcomes if integration of old self into an ideal generative self is not accomplished. The generative self builds on Erickson’s idea of generativity versus despair as an emotional and spiritual challenge in old age. The generative self delivers wisdom and the blessings and gifts of experience to others.

We situate our theory of religion’s effect on self-regulation within the tradition of work on so-called possible selves. According to Markus and Nurius (1986), possible selves are images of what people hope to become, expect to become, or fear becoming in the future. Possible selves appear to be elaborated out of imaginary narratives involving the self both in childhood and in adulthood (e.g., Erikson 2001; Markus and Ruvolo 1989; Whitty 2002). Possible selves consist of a description of a set of behavioral actions aimed at some goal designed to overcome some conflict, along with causes and consequences of those imaginary actions, with an end state that is described as an event. According to narrative theorists (Bruner 1995; Ricoeur 1984; Oatley 2007), narratives about future selves provide interpretations about what we see as possible. As stories they help to inte­grate material about conflict involving the present self into a resolution of that conflict—a resolution involving a higher, more complete, and more complex self.

Empirical work has supported this narrative-related integrative func­tion of possible selves. We evaluate our current and past selves with refer­ence to possible selves. Possible selves become relevant for self-regulation when they are recruited into the subset of self-knowledge that is active in working memory (Markus and Kunda 1986; Markus and Nurius 1986). Obviously when a possible self is periodically or chronically activated it becomes particularly important for evaluation of current representa­tions of the self as well as discrepancy reduction behaviors or engage­ment of approach and/or avoidance behaviors (Norman and Aron 2003). For example, frequent attendance at religious services or performance of religious rituals will periodically activate a number of possible selves, including an ideal self. The chronically activated ideal self is then in a position to contribute to self-regulation by providing a standard by which to evaluate progress toward a goal and resolution of internal and social conflicts (Oyserman et al. 2004). People use possible selves as behavioral standards to guide conflict resolution and self-regulation more generally (e.g., Hoyle and Sowards 1993; Hoyle and Sherrill 2006; Kerpelman and Lamke 1997; Oyserman et al. 2004). Hoyle and Sherrill (2006) have pointed out that possible selves map particularly well into hierarchically orga­nized control-process models of self-regulation (e.g., Carver and Scheier 1981; Hoyle and Sowards 1993). Behavioral reference points or standards are organized in these models of self-regulation in a hierarchical fashion from abstract and general to concrete and specific. A particular behavioral standard derives from the level above it. The highest levels of standards are global ideals. In the context of religious ritual, these global standards are the ideal selves that the current self is urged to become or desires to become. The highest global standard is the god-concept toward which the entire religious service is oriented.

In our decoupling model of religious cognition, religious practices are thought to create a subtle and brief decentering (of the self) effect that leads ultimately to greater self-control. We postulate four basic cognitive processes that occur in religious cognition (situated within the cognitive architecture proposed by Nichols and Stich [2000] to account for pretend play): (1) A transient and subtle reduction in agency such that the self relaxes control over attentional and behavioral responses. (2) The self-concept is then placed into a suppositional or liminal state (a pos­sible worlds box); that liminal state is filled with potentially positive and negative consequences. On the positive side, decoupling of the self from cognitive control mechanisms puts the individual into a receptive and integrative mode, thereby allowing the individual to perform a lot of off­line maintenance and integrative information-processing tasks. On the negative side, the decoupling process can, if prolonged and depending on context, lead to dangerous disintegrative psychic states including fanati­cism and psychotic and delusionary states, particularly if step 4 fails or is delayed. (3) A search is activated in semantic memory for an ideal self that can link up with and integrate the old self. (4) Integration of old and ideal self is accomplished with the help of normal inferential machinery and an “updater” that deletes nonuseful material and adds as much of the ideal self (in the form of new beliefs, and so on) as possible to the old self construct. The updater also establishes control of the new Self (via belief-desire systems) over behavioral output systems.

Dietary strategies to prevent the development of heart disease

For several decades, the prevention of CHD (including the prevention of ischaemic recurrence after a prior AMI) has focused on the reduction of the traditional risk factors: smoking, HBP, hypercholesterolaemia. Priority was given to the prevention (or reversion) of vascular atherosclerotic stenosis. As discussed above, it has become clear in secondary prevention that clinical efficiency needs to primarily prevent the fatal complications of CHD such as SCD. This does not mean, however, that we should not try slowing down the atherosclerotic process, and in particular plaque inflammation and rupture. Indeed, it is critical to prevent the occurrence of new episodes of myocardial ischaemia whose repetition in a recently injured heart can precipitate SCD or CHF. Myocardial ischaemia is usually the consequence of coronary occlusion caused by plaque rupture and subsequent thrombotic obstruction of the artery.

Recent progress in the understanding of the cellular and biochemical pathogenesis of atherosclerosis suggests that, in addition of the traditional risk factors of CHD, there are other very important targets of therapy to prevent plaque inflammation and rupture. In this regard, the most important question is: how and why does plaque rupture occur?

Most investigators agree that atherosclerosis is a chronic low-grade inflam­mation disease. Pro-inflammatory factors (free radicals produced by cigarette smoking, hyperhomocysteinaemia, diabetes, peroxidised lipids, hypertension, elevated and modified blood lipids) contribute to injure the vascular endothelium, which results in alterations of its antiatherosclerotic and antithrombotic properties. This is thought to be a major step in the initiation and formation of arterial fibrostenotic lesions. From a clinical point of view, however, an essential distinction should be made between unstable, lipid-rich and leucocyte-rich lesions and stable, acellular fibrotic lesions poor in lipids, as the propensity of these two types of lesion to rupture into the lumen of the artery, whatever the degree of stenosis and lumen obstruction, is totally different.

In 1987, we proposed that inflammation and leucocytes play a role in the onset of acute CHD events. This has recently been confirmed. It is now accepted that one of the main mechanisms underlying the sudden onset of acute CHD syndromes, including unstable angina, myocardial infarction and SCD, is the erosion or rupture of an atherosclerotic lesion, which triggers thrombotic complications and considerably enhances the risk of malignant ventricular arrhythmias. Leucocytes have been also implicated in the occurrence of ventricular arrhythmias in clinical and experimental settings, and they contribute to myocardial damage during both ischaemia and reperfusion. Clinical and pathological studies showed the importance of inflammatory cells and immune mediators in the occurrence of acute CHD events, and prospective epidemiological studies showed a strong and consistent association between acute CHD and systemic inflammation markers. A major question is to know why there are macrophages and activated lymphocytes in atherosclerotic lesions and how they get there. Issues such as local inflammation, plaque rupture and attendant acute CHD complications follow.

 

Steinberg et al. proposed in 1989 that oxidation of lipoproteins causes accelerated atherogenesis. Elevated plasma levels of low-density lipoproteins (LDL) are a major factor of CHD, and reduction of blood LDL levels (for instance by drugs) results in less CHD. However, the mechanism(s) behind the effect of high LDL levels is not fully understood. The concept that LDL oxidation is a key characteristic of unstable lesions is supported by many reports. Two processes have been proposed. First, when LDL particles become trapped in the artery wall, they undergo progressive oxidation and are internalised by macrophages, leading to the formation of typical atherosclerotic foam cells. Oxidised LDL is chemotactic for other immune and inflammatory cells and up-regulates the expression of monocyte and endothelial cell genes involved in the inflammatory reaction.

The inflammatory response itself can have a profound effect on LDL, creating a vicious circle of LDL oxidation, inflammation and further LDL oxidation. Second, oxidised LDL circulates in the plasma for a period sufficiently long to enter and accumulate in the arterial intima, suggesting that the entry of oxidised lipoproteins within the intima may be another mechanism of lesion inflammation, in particular in patients without hyperlipidaemia. Elevated plasma levels of oxidised LDL are associated with CHD, and the plasma level of malondialdehyde-modified LDL is higher in patients with unstable CHD syndromes (usually associated with plaque rupture) than in patients with clinically stable CHD. In the accelerated form of CHD typical of post-transplantation patients, higher levels of lipid peroxidation and of oxidised LDL were found as compared to the stable form of CHD in non-transplanted patients. Reactive oxygen metabolites and oxidants influence thrombus formation, and platelet reactivity is significantly higher in transplanted patients than in non-transplanted CHD patients

The oxidised LDL theory is not inconsistent with the well-established lipid-lowering treatment of CHD, as there is a positive correlation between plasma levels of LDL and markers of lipid peroxidation and a low absolute LDL level results in reduced amounts of LDL available for oxidative modification. LDL levels can be lowered by drugs or by reducing saturated fats in the diet. Reduction of the oxidative susceptibility of LDL was reported when replacing dietary fat with carbohydrates. Pharmacological/quantitative (lowering of cholesterol) and nutritional/qualitative (high antioxidant intake) approaches of the prevention of CHD are not mutually exclusive but additive and complementary. An alternative way to reduce LDL concentrations is to replace saturated fats with polyunsaturated fats in the diet. However, diets high in polyunsaturated fatty acids increase the polyunsaturated fatty acid content of LDL particles and render them more susceptible to oxidation which would argue against use of such diets (see above the section on SCD and n-6 PUFA).

In the secondary prevention of CHD, such diets failed to improve the prognosis of the patients (for a review see de Lorgeril et al.). In that context, the traditional Mediterranean diet, with low saturated fat and polyunsaturated fat intakes, appears to be the best option. Diets rich in oleic acid increase the resistance of LDL to oxidation independent of the content in antioxidants and results in leucocyte inhibition. Thus, oleic acid-rich diets decrease the pro-inflammatory properties of oxidised LDL. Constituents of olive oil other than oleic acid may also inhibit LDL oxidation. Various components of the Mediterranean diet may also affect LDL oxidation. For instance, alpha­tocopherol or vitamin C, or a diet combining reduced fat, low-fat dairy products and a high intake of fruits and vegetables, was shown to favourably affect either LDL oxidation itself or/and the cellular consequences of LDL oxidation.

Finally, significant correlation was found between certain dietary fatty acids and the fatty acid composition of human atherosclerotic plaques, which suggests that dietary fatty acids are rapidly incorporated into the plaques. This implies a direct influence of dietary fatty acids on plaque formation and the process of plaque rupture. It is conceivable that fatty acids that stimulate oxidation of LDL (n-6 fatty acids) induce plaque rupture, whereas those that inhibit LDL oxidation (oleic acid), inhibit leucocyte function (n-3 fatty acids) or prevent `endothelial activation’ and the expression of pro-inflammatory proteins (oleic acid and n-3 fatty acids) contribute to pacify and stabilise the dangerous lesions. In that regard, it is noteworthy that moderate alcohol consumption, a well-known cardioprotective factor, was recently shown to be associated with low blood levels of systemic markers of inflammation, suggesting a new protective mechanism to explain the inverse relationship between alcohol and CHD rate. In the same line, the potential of dietary n-3 fatty acids to reduce the production of inflammatory cytokines by leucocytes (as discussed in section 3.2 on dietary fatty acids and CHF) should be underlined. As both dietary n-3 fatty acids and moderate alcohol consumption are major characteristics of the Mediterranean diet, it is not surprising to observe that this diet was associated with lower rate of new episodes of CHF in the Lyon Diet Heart Study.

Thus, any dietary pattern combining a high intake of natural antioxidants, a low intake of saturated fatty acids, a high intake of oleic acid, a low intake of omega-6 fatty acids and a high intake of omega-3 fatty acids would logically produce a highly cardioprotective effect. This is consistent with what we know about the Mediterranean diet pattern and with the results of the Lyon Diet Heart Study, and was recently confirmed by epidermiological studies.

Best ten strategies to get the most out of your Brain

Your brain is wonderfully malleable, a treasure to be molded and nurtured throughout life, from birth to old age, as affirmed by the exciting new research reported on this website. There is every reason to believe your brain can give you a lifetime of happiness, intellectual vigor, and sat­isfying achievements based on the new concept of the brain as a growing, changing organ sculpted by environmental influences, most profoundly by the nutrients, vitamins, and supplements that nourish it every day.

Unfortunately, the typical American diet is not con­ducive to creating and supporting superior brains. On the other hand, a look at what we eat suggests that we are doing virtually everything to ruin our brains.

We eat the wrong type fats guaranteed to cause disruption in the functioning of our brain cells, perhaps ending in neuronal death. We overeat sugar, dumping excessive glucose—over and above that needed to feed and energize brain cells—into the brain where it reacts with free radicals to literally burn brain cells to death.

We eat so many calories and get so little exercise that half of all adult Americans are now categorized as obese. Such calorie overloads create more free radical activity in the brain, condemning brain cells to dysfunc­tion and death. We have turned our brains into a waste­land of free radical activity. We shun exercise that energizes the brain. We skimp on fruits and vegetables, full of antiox­idants, that might save our brain cells from malfunction and destruction. With our deficient diets, we cheat our­selves of precious nutrients, such as B vitamins and vita­min E, essential for good mental functioning.

We induce subtle and serious damage to our brains because of avoid­able clogged blood vessels, high blood pressure, insulin resistance, and high homocysteine. We cheat our infants and children of brain-building foods. We fail to stimulate our brains or those of our children with mental activity that prods the growth of brain cells and their interconnections.

The frontier research that makes up this website dictates that it is imperative to consider the severe jeopardy in which we put ourselves and society by ignoring the health of our brains. Of course, not all the scientific information is in, but more than enough is known to point to the right foods and supplements that can make a dramatic difference in pre­serving the magnificence of our most precious human asset. The evidence, I think, compels all of us to look on our own brain with new respect and optimism, knowing that its power and destiny are truly up to each of us.

Based on the extensive research, here are ten crucial actions you can take now to preserve and enrich your brain’s functioning and health:

The evidence is utterly compelling that taking modest doses of a variety of vitamins and minerals is excellent brain insurance: They can preserve and improve intellec­tual functioning and emotional well-being, most likely at all ages. Pregnant women should take multivitamins with their doctors’ advice to help guarantee healthy babies. As many as one-half of ordinary schoolchildren might improve IQ scores by taking multivitamins, according to Dr. David Benton, leading British researcher.

Many adolescents and adults eat diets lacking basic vitamins and minerals essen­tial for proper brain function, such as folic acid and sele­nium; a multivitamin can fill in deficiencies. Remember: Suboptimal brain functioning from such deficiencies is usually subtle and unnoticed, often taken for granted; nor are the deficiencies always apparent on blood tests. A com­bination of vitamins and minerals, found in multivitamin formulas, can help restore optimal intellectual function and lift mood at the same time.

A multivitamin is absolutely essential for older people who tend to need more nutrient help to support an aging brain. Studies show that older people who take a range of vitamins and minerals, especially for a number of years, have better cognitive function and feel better as they age. B vitamins, especially, are critical in preserving aging brains and preventing dementia and depression in old age. Again, subtle deficiencies, easily corrected by a multivita­min, can rob older people of optimal brain functioning and even help bring on brain disease, including dementia.

Usually taking only a multivitamin-mineral pill is not enough. Most do not contain sufficiently high amounts of powerful brain-protecting vitamin E and vitamin C, for example, let alone important alpha lipoic acid and coen­zyme Q10. In some studies, people who took only multivi­tamins showed a decline in cognitive function with age whereas those who took high doses of individual antioxi­dants, such as vitamin E, did not. In one recent study, not a single elderly person taking individual tablets of vitamin E or vitamin C developed Alzheimer’s disease.

Four antioxidant supplements are absolutely essential: vitamin E, vitamin C, alpha lipoic acid, and coenzyme Q10, says antioxidant authority Dr. Lester Packer at the Univer­sity of California, Berkeley. He also recommends gingko biloba and PycnogenolTM as powerful brain protectors. It’s far smarter to take several antioxidants instead of just one, he says, because they do not work in isolation; their brain-protecting powers are much stronger when they work together.

Should children take antioxidants in addition to a multi­vitamin? Yes, says Dr. Packer. He recommends half the usual adult dose of antioxidants for children. After all, the earlier the brain gets antioxidants, the less the expected free-radical damage through the years which may be reflected in old age as memory loss, dementia, and even Alzheimer’s disease. Antioxidants can also help stave off chronic diseases such as diabetes, clogged arteries, and high blood pressure, which also over time can harm the brain.

This means fruits and vegetables, loaded with various antioxidants, some probably not yet even identified. Thrilling new animal experiments at Tufts give a glimpse of the power of antioxidant-packed foods on the brain. Feeding animals common high-antioxidant fruits and veg­etables, such as blueberries, spinach, and strawberries, has slowed down brain deterioration, revved up mental facul­ties and even reversed memory and learning losses in old animals. Its mind-boggling to think such fruits and veg­etables can rejuvenate the brain!

Virtually all fruits and vegetables contain antioxidants. Its not dif­ficult to take in high doses of antioxidants in modest amounts of fruits and vegetables. Just three prunes, one cup of mixed blueberries and strawberries, plus 1/2 cup of cooked spinach would put you far over the top for the very highest antioxidant daily intake recommended by author­ities.

Generally, highest in antioxidants are brightly colored fruits and berries and green leafy vegetables. Snacking on berries, cherries, grapes, apples, prunes, raisins—instead of or even in addition to the usual chips—could make all the difference in intellectual power and emotional well­being.

Its hard to say enough about the fantastic powers of such a common beverage as plain tea in protecting cells, including brain cells, from damage. As Dr. John Weisburger, renowned scientific researcher, now at the American Health Foundation, has said often: “Tea should be the national health beverage.” Its one of the easiest, quickest ways to infuse the body and brain with antioxidants. Put one tea bag in a cup of boiling water. Let it brew for five minutes and drink it. In an instant you have taken in about 1200 ORAC units of antioxidants—about one-third to one-fourth the total daily recommended amounts, according to Tufts University researchers.

Iced tea counts, too. You can simply pour the cup of tea over ice. However—and this is important—you do not get any significant amounts of antioxidants in herbal teas, commercial bottled teas, or powdered tea mixes, accord­ing to Tufts analyses. The tea must be made from “real” tea leaves, loose or in bags. Further, you can use either plain black tea (yes, the stuff you see on supermarket shelves, such as Lipton’s, Twinings, Bigelow) or more exotic Asian green tea. Although green tea has received much hype for its anticancer chemicals, black tea actually has more total antioxidant activity than green tea, Tufts researchers found. So you don’t have to go to green tea to get the benefits.

Suggestion: Try substituting at least one cup of tea a day for your regular coffee. Drink iced tea instead of soft drinks. Order iced tea at restaurants, after asking if it is freshly made from real tea.

You can take the perfectly good brain you were born with and screw up its communication circuits by feeding it the wrong type of fat—at any age, from birth, through childhood and adolescence, middle age and old age. Your brain cannot function optimally on a diet of the wrong fats. Few people realize how critical fatty acids are at the mol­ecular level of brain cells in fostering clear and rapid mes­sage transmission and energy production that keeps cells alive and vital. Probably the most dangerous to brain cells is saturated animal fat—so pervasive in fast foods, such as hamburgers and shakes.

Unquestionably, animals fed diets high in saturated ani­mal fat are dumber, with impaired memories and learning ability. Animal fat, other research shows, distorts the nor­mal configuration of nerve cell membranes, stifles the growth of synapses (communication junctions), and dis­turbs the biochemistry of neurotransmitters, the message carriers. Such fat also tends to promote “insulin resistance” later in life, even in youngsters, which leads to abnormal metabolism of insulin and blood sugar, which the brain depends on as its sole source of energy.

Also detrimental to cells: too much polyunsaturated veg­etable oil, such as corn oil (so-called omega-6s), that can set up chronic inflammatory responses in brain tissue, thought to eventually lead to subtle brain damage, strokes, and Alzheimer’s disease. Eating trans fatty acids, in processed foods such as most margarines, donuts, and fast-food french fries, also can foster blood vessel damage that is detrimen­tal to blood circulation in the brain.

The fat your brain most needs is so-called omega-3 found in fish oil. It’s the evolutionary stuff that formed your brain, and without it, brain cells cannot possibly function at optimal levels. Developing brains—in the womb, infancy and childhood—especially require omega-3 type fish oil to construct the best neuronal architecture and biochemical wiring. Failure to get enough omega-3 in the early devel­opmental periods can result in lower IQs later in life. Nor can adult brains achieve top cognitive potential without adequate supplies of omega-3 fatty acids. Such fat is needed to spur growth of dendrites and synapses, the neu­ron’s mechanisms for processing messages throughout the brain. One fraction of fish oil, called DHA, has been shown to enhance brain power, memory, and learning and may even prevent and possibly treat Alzheimer’s disease.

Omega-3 fat also tells your brain to feel good. It is a mood elevator, preventing and even relieving major depres­sion. It can also help prevent brain damage from alcoolism, and may even be a preventive and treatment for some cases of schizophrenia. Kids and adults with atten­tion deficit disorder and dyslexia may suffer from omega-3 deficiencies, which when corrected, lead to better brain functioning.

Eating fatty fish a couple of times a week—or an ounce or two a day—is enough to keep brain cells happy. The alternative: Take fish oil supplements, especially DHA type supplements.

As you age, your brain may need a boost to counteract subtle declines in memory, possibly from a drop in neuro­transmitter activity or damage to neurons from disease or routine attacks by free radical chemicals. Some over-the-counter supplements can help rejuvenate brain cell activ­ity. A favorite is ginkgo biloba, taken by many prominent brain researchers to try to ward off age-related memory loss. Another supplement is phosphatidylserine or PS, reputed to stimulate production of the “memory” neuro­transmitter acetylcholine, which may decline as you get older.

These are worth a try as a way of preventing or over­coming short-term memory problems, which are a part of normal aging, according to brain researchers. They may or may not work, depending on the nature of the problem and biochemical individuality. Their great upside: Unlike potent pharmaceutical drugs which have severe side effects, over-the-counter brain-boosters have no or only minor side effects. Still, if you are under treatment for disease or are taking medications, you should consult your doctor before taking such supplements, especially to rule out potentially hazardous interactions.

8.         Watch sugar, including blood sugar.

Eating too much sugar, and certain other carbohydrates, is not a good idea for brains of any age. Sugar overloads can inspire “insulin resistance,” throwing blood sugar (glu­cose) levels out of whack, as well as causing permanent damage to brain cells, leading to malfunction and death. However, since the brain runs on energy derived mostly from carbohydrates, it’s essential to have the right amount of blood sugar available to the brain at every instant to promote memory, learning, other cognitive functions. Best carbohydrates for an optimally functioning brain: those that are digested slowly.

9.         Restrict calories—lose weight.

Being overweight is not good for your brain. It can fos­ter insulin resistance, high blood pressure, and possibly diabetes—leading to impaired memory, accelerated aging, and subtle damage to brain cells. The one sure-fire way to slow down the aging process, rescuing the brain as well as other organs from increased free radical damage, is to cut back on calories.

10.     Take good care of yourself.

A more gentle approach to life can reduce chronic men­tal stress, which floods your brain inappropriately with adrenaline and other stress-activated chemicals that can actually inflict damage on neurons. Physical exercise, new research proves, improves blood flow to the brain and even perks up mental activity in specific parts of the brain. Keeping your blood vessels free of clogging and damage is essential to preserving brain function. That means con­trolling blood pressure, bad-type cholesterol, and the blood toxin homocysteine, all of which promote strokes and Alzheimer’s disease. Stimulate your brain by learning and doing new things; such mental gymnastics actually encourage growth of new brain cell connections, enlarg­ing memory and learning capacity.

The most important thing to remember is that your brain is growing and changing every instant. It thrives on stimulation, exercise, education, and the right diet and sup­plements. It is never too early or too late to decide to shape your own brain’s destiny.