E— Health Effects on Cognitive Aging

Shari R. Waldstein

Intact cognitive function is a critical dimension of quality of life. Cognitive difficulties can be disruptive to individuals' sense of well-being and to their everyday functioning. Age-related decrements in cognition are well documented (Salthouse, 1991; Wilson et al., 1997), but they are not thought to be entirely due to primary biological aging processes. In this regard, it has been suggested that age-related cognitive changes are attributable, at least in part, to systemic medical diseases (here defined as nonneurological diseases that affect one or more physiological systems) that are common in older adults (Fozard et al., 1990). Indeed, approximately four out of five Americans over the age of 65 have at least one or more chronic medical conditions (La Rue, 1992).

In recent years, the relation of systemic disease to cognition has received increasingly intensive investigation. Results of numerous available studies indicate that diseases of virtually any physiological system can have deleterious effects on cognitive function (Elias et al., 1989; Siegler and Costa, 1985; Tarter et al., in press, 1988). Although these influences may be particularly pertinent to older adults, who experience an increased incidence and prevalence of disease, systemic diseases have been shown to affect cognitive performance in persons of all ages in both cross-sectional and longitudinal investigations. Therefore disease-cognition relations should viewed from a life-span perspective. In this regard, degree of lifetime exposure to systemic illness(es) may be of critical importance in determining cognitive outcomes in older age.

The purpose of this paper is, first, to provide a brief overview of the types of systemic diseases and several associated lifestyle and biological factors that are known to affect the normal range of cognitive functioning (in the absence



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The Aging Mind: Opportunities in Cognitive Research E— Health Effects on Cognitive Aging Shari R. Waldstein Intact cognitive function is a critical dimension of quality of life. Cognitive difficulties can be disruptive to individuals' sense of well-being and to their everyday functioning. Age-related decrements in cognition are well documented (Salthouse, 1991; Wilson et al., 1997), but they are not thought to be entirely due to primary biological aging processes. In this regard, it has been suggested that age-related cognitive changes are attributable, at least in part, to systemic medical diseases (here defined as nonneurological diseases that affect one or more physiological systems) that are common in older adults (Fozard et al., 1990). Indeed, approximately four out of five Americans over the age of 65 have at least one or more chronic medical conditions (La Rue, 1992). In recent years, the relation of systemic disease to cognition has received increasingly intensive investigation. Results of numerous available studies indicate that diseases of virtually any physiological system can have deleterious effects on cognitive function (Elias et al., 1989; Siegler and Costa, 1985; Tarter et al., in press, 1988). Although these influences may be particularly pertinent to older adults, who experience an increased incidence and prevalence of disease, systemic diseases have been shown to affect cognitive performance in persons of all ages in both cross-sectional and longitudinal investigations. Therefore disease-cognition relations should viewed from a life-span perspective. In this regard, degree of lifetime exposure to systemic illness(es) may be of critical importance in determining cognitive outcomes in older age. The purpose of this paper is, first, to provide a brief overview of the types of systemic diseases and several associated lifestyle and biological factors that are known to affect the normal range of cognitive functioning (in the absence

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The Aging Mind: Opportunities in Cognitive Research of dementia). Next, a more detailed description of the relation of hypertension and other cardiovascular diseases to cognition is provided. Methodological and conceptual challenges to this field of research are discussed, and future research directions are enumerated. In general, the investigations described in this paper utilized clinical neuropsychological tests to measure cognitive functioning. These tests can be grouped according to the major domain of cognitive functioning assessed and include measures of attention, learning and memory, executive functions, visuospatial and visuoconstructional skills, psychomotor abilities, perceptual skills, and language functions. Screening tests such as mental status examinations and composite measures such as intelligence tests were also used. The interested reader is referred to Lezak (1995) for a detailed discussion of this particular taxonomy of tests. In addition, an appendix at the end of this paper lists brief descriptions of the major domains of cognitive functions and several representative tests that are commonly used in the literature described below. HEALTH AND COGNITION Numerous health-related factors have been demonstrated to influence cognition (with effect sizes ranging from small to large). Examples include lifestyle, endocrine, and genetic factors, systemic diseases, neurotoxic exposures, and medical and surgical treatments for disease. Each of these general areas is considered briefly below, with positive findings emphasized for illustrative purposes. Lifestyle A variety of lifestyle factors are known to affect cognitive function. Such factors may impact cognition by exerting direct biological influence on the brain or by promoting various systemic diseases (e.g., cardiovascular, pulmonary) that indirectly affect the brain. Less healthful lifestyles also tend to aggregate among individuals with lower levels of education and may, in part, explain previously noted associations between low education and/or socioeconomic status and poorer cognitive function (Kilander et al., 1997). Examples of such lifestyle factors include smoking, excessive alcohol consumption, illicit drug use, dietary factors, and physical inactivity. With respect to health-compromising behaviors, several studies have revealed poorer cognitive performance among individuals who smoke tobacco products (M.F. Elias et al., in press; Galanis et al., 1997; Hill, 1989; Launer et al., 1996). Heavy alcohol consumption also has known deleterious effects on cognition (Rourke and Løberg, 1996; Tarter and Van Thiel, 1985). However, across a range of habitual drinking, several investigations have noted an in-

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The Aging Mind: Opportunities in Cognitive Research verted U-or J-shaped relation between alcohol consumption and cognitive function (Dufouil et al., 1997; M.F. Elias et al., in press; P.K. Elias et al., in press; Launer et al., 1996). Drugs of abuse (e.g., opiates, cocaine) have been associated with poorer cognitive performance (Carlin and O'Malley, 1996; Strickland and Stein, 1995). In addition, several dietary insufficiencies, such as vitamin B6, vitamin B12, thiamine, folate, and zinc, have been related to cognitive difficulties (Lester and Fishbein, 1988; Riggs et al., 1996; Whitehouse et al., 1993). Greater caloric consumption in middle age has been shown to predict poorer mental status in old age (Fraser et al., 1996), and a proportionally greater intake of dietary refined carbohydrates has predicted lower IQ scores in children (Lester et al., 1982). Health-enhancing behaviors have been associated with better cognitive functioning. For example, greater intake of vitamin C, an antioxidant, has been related to enhanced cognitive test performance and/or a lower prevalence of cognitive impairment (Gale et al., 1996; Jama et al., 1996; Paleologos et al., 1998). Greater levels of physical fitness (or physical activity) have also been associated with higher levels of cognitive functioning (Dustman et al., 1994). In addition, several investigations have revealed improvements in cognitive performance with aerobic exercise training (Emery and Blumenthal, 1991; Kramer et al., 1998). Endocrine and Genetic Factors Various hormonal factors have been associated with cognitive functioning. Again, direct biological effects on the brain are likely, in addition to indirect effects via promotion of systemic diseases. Relevant examples include poorer cognitive function in individuals with low levels of estrogen (Gordon et al., 1988; Erlanger et al., 1999), both high and low levels of various thyroid and pituitary hormones (Beckwith and Tucker, 1988; Gordon et al., 1988; Whitehouse et al., 1993; Erlanger et al., 1999), and either high basal levels of cortisol or greater stress-induced cortisol responses (Kirschbaum et al., 1996; Lupien and McEwen, 1997; McEwen and Sapolsky, 1995; Seeman et al., 1997; Erlanger et al., 1999). Beneficial effects of estrogen replacement therapy have also been noted (Haskell et al., 1997; Erlanger et al., 1999). Genetic factors may predispose individuals to systemic diseases and influence numerous biological variables that can affect cognitive performance. One such factor that has received much recent attention is apolipoprotein E (APOE) polymorphism. Although most commonly examined in relation to dementias, the presence of one or two APOE-ε4 alleles has also been associated with poorer cognitive function, particularly on tests of learning, memory, and psychomotor speed, among nondemented individuals across a wide range of ages (Bondi et al., 1995; Carmelli et al., 1998; Flory et al., 1999; Yaffe et al., 1997). Genetic influences may also modify the impact of disease on cogni-

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The Aging Mind: Opportunities in Cognitive Research tion. In this regard, Haan et al. (1999) found that individuals with carotid atherosclerosis, peripheral vascular disease, or diabetes mellitus, in addition to an APOE-ε4 allele, experienced a significantly greater rate of cognitive decline than individuals without an APOE-ε4 allele and or cardiovascular disease. Neurotoxicity Environmental or occupational exposure to chemicals, such as solvents and lead, exerts direct neurotoxic effects on the brain and is associated with diminished cognitive functioning (Hartmann, 1995; Morrow et al., in press). Both peak exposures and chronic low-level exposures are of concern. Individuals of lower socioeconomic status may be more likely to experience neurotoxic exposures. Systemic Diseases Numerous systemic diseases have been associated with poorer cognitive functioning. Examples include cardiovascular diseases, such as hypertension and myocardial infarction (Waldstein and Elias, in press; Waldstein et al., in press); pulmonary diseases, such as chronic obstructive pulmonary disease and asthma (Fitzpatrick et al., 1991; Hopkins and Bigler, in press; Grant et al., 1987; Prigatano et al., 1983); pancreatic diseases, such as diabetes mellitus (Reaven et al., 1990; Ryan, in press; Ryan et al., 1993); hepatic diseases, such as cirrhosis (Moss et al., 1995; Tarter and Van Thiel, in press); renal diseases (Hart et al., 1983; Pliskin et al., in press); autoimmune diseases, such as systemic lupus erythematosus (Beers, in press; Glanz et al., 1997); various cancers (Berg, 1988); sleep disorders, such as obstructive sleep apnea syndrome (Bédard et al., 1993; Kelly and Coppel, in press); and the human immunodeficiency virus and AIDS (Heaton et al., 1995; Kelly et al., 1996). Disparities in health status among racial and ethnic minority groups and individuals of lower socioeconomic status or educational attainment are well documented (Haan and Kaplan, 1985; Haan et al., 1989; Kaplan and Keil, 1993). It is therefore possible that comorbidities may, in part, explain prior relations of race/ethnicity (e.g., for black Americans), lower education, and low socioeconomic status to poorer performance on cognitive tests. Health status should therefore be controlled in such investigations (Whitfield et al., 2000). Medical and Surgical Treatments A variety of medical and surgical treatments for disease have been shown to impact cognitive performance. Improvements, decrements, and absence

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The Aging Mind: Opportunities in Cognitive Research of change have been noted in association with various medications, such as antihypertensive agents (Muldoon et al., 1991, 1995) and corticosteroid or theophylline treatment for asthma (Hopkins and Bigler, in press; Stein et al., 1996). Mixed findings are also apparent in association with surgical interventions, such as coronary artery bypass surgery (Newman et al., in press). Some improvements in cognitive performance have been associated with oxygen-related treatments for chronic obstructive pulmonary disease and obstructive sleep apnea syndrome (Hopkins and Bigler, in press) and chronic hemodialysis (Pliskin et al., in press). Summary Numerous lifestyle, biological, disease-related, and iatrogenic factors have been shown to influence cognitive function in persons of all ages. Research associated with each particular factor poses several common and unique sets of methodological and conceptual challenges, discussion of which is beyond the scope of this paper. Findings in each area are often mixed and may, in part, reflect these challenges. As mentioned above, positive results have generally been highlighted here to illustrate the striking range of potential health effects on cognition. In the following section, a more detailed description of the relation of hypertension and other cardiovascular diseases to cognitive function is presented as an example of research on health and cognition and its associated challenges. CARDIOVASCULAR DISEASE AND COGNITION Cardiovascular disease is the leading cause of death in the United States, affecting one in every five individuals (American Heart Association, 1998) and conferring substantially elevated risk for stroke and vascular dementia. However, prior to the development of cerebrovascular complications, even early manifestations of cardiovascular disease, such as hypertension, are associated with diminished cognitive function (Waldstein and Elias, in press; Waldstein et al., in press). A deleterious impact of cardiovascular disease on the brain is not surprising when one considers the purpose of normal cardiovascular function. The cardiovascular system (i.e., the heart and vasculature) is responsible for supplying blood that transports oxygen, glucose, and other essential nutrients to all cells of the body. Because the brain is relatively unable to store nutrients, it is dependent on the cardiovascular system for a constant supply of blood and is highly vulnerable to interruptions of blood flow. Approximately one-fifth of the cardiac output is provided to the brain each minute, and even very brief cessation of this blood supply can damage the brain. Subtle reductions in cerebral blood flow that occur in association with cardiovascular disease

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The Aging Mind: Opportunities in Cognitive Research (in addition to other mechanisms discussed below) can therefore have negative short-and long-term consequences for the brain. When available studies to date are considered in aggregate, the relation of cardiovascular diseases to cognitive function has been one of the more extensively investigated of the research areas discussed above (Waldstein and Elias, in press; Waldstein et al., in press). Because hypertension is often one of the earliest manifestations of cardiovascular disease and can occur without substantial occult comorbidities, there is an opportunity to conduct tightly controlled investigations of hypertension and cognition. Perhaps for this reason, hypertension has been studied fairly intensively and thus is examined here as a pertinent illustration of health-cognition relations. Hypertension Hypertension—defined as a sustained systolic and diastolic blood pressure greater than or equal to 140 millimeters of mercury (mm Hg) and/or 90 mm Hg, respectively, as measured on at least two separate occasions (Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, 1997)—affects one in four adults in the United States, or 50 million individuals (American Heart Association, 1998). Approximately 90 to 95 percent of all cases involve essential hypertension, a term that refers to a sustained blood pressure elevation of unknown cause. However, the etiology of essential hypertension actually involves a complex interplay of genetic and environmental factors (Kaplan, 1998). Elevated blood pressure that is attributable to a known medical disorder is called secondary hypertension. Risk factors for hypertension include a positive family history, older age, male gender (until age 55, after which prevalence rates are greater among women), black race, and numerous lifestyle and behavioral factors such as excess body weight, physical inactivity, dietary factors including high sodium and low potassium or calcium intake, excessive alcohol consumption, oral contraceptive use, various psychosocial factors, and stress-related cardiovascular reactivity (American Heart Association, 1998; Joint National Committee, 1997; Kaplan, 1998). Hypertension is a major risk factor for atherosclerosis, coronary heart disease, and stroke (Stamler, 1992). Hypertension and Cognitive Function The relation of hypertension to cognitive function has been studied for over 50 years (for reviews see M.F. Elias et al., in press; Elias and Robbins, 1991; Waldstein, 1995; Waldstein and Katzel, in press; Waldstein et al., 1991a). Results of numerous case-control and cross-sectional, population-based stud-

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The Aging Mind: Opportunities in Cognitive Research ies indicate that hypertensives generally perform more poorly than normotensives across multiple domains of cognitive function, including learning and memory, attention, abstract reasoning and other executive functions, visuospatial, visuoconstructional, perceptual, and psychormotor abilities (e.g., Boller et al., 1977; Blumenthal et al., 1993; Elias et al., 1987, 1990b; Robbins et al., 1994; Shapiro et al., 1982; Waldstein et al., 1991b, 1996; Wallace et al., 1985). To date, hypertension typically has not predicted poorer performance on tests of general verbal intelligence or language abilities, although further investigation is necessary (e.g., Blumenthal et al., 1993; Boller et al., 1977; Waldstein et al., 1991b, 1996). Dose-response relations have been observed between progressive increments in blood pressure level and reduced cognitive performance (e.g., Elias et al., 1990b, Robbins et al., 1994). In addition, low levels of blood pressure have been associated with poorer cognitive function (Costa et al., 1998; Guo et al., 1997), and curvilinear (inverted U-shaped) relations of blood pressure to cognitive performance have also been noted (Glynn et al., 1999). Although it is generally presumed that alterations in cognition occur as a result of pathological consequences of hypertension, lower levels of cognitive test performance have also been found to precede blood pressure elevation in individuals who are at risk for hypertension. More specifically, normotensive young adults who have a parental history of hypertension show lower levels of performance on tests of visuoperceptual, visuospatial, and visuoconstructional skill and speed of short-term memory search in comparison to the young adult offspring of normotensive parents (Pierce and Elias, 1993; Waldstein et al., 1994). These associations may thus reflect genetic and or environmental factors that predispose individuals to the development of hypertension. Longitudinal or follow-up studies generally note the persistence of hypertensive-normotensive differences in cognitive performance over time, often with additional cognitive decline among hypertensives (e.g., Haan et al., 1999; Miller et al., 1984; Elias et al., 1986, 1996, 1998; Wilkie and Eisdorfer, 1971). Chronicity of hypertension has been identified as a critical variable in such investigations. Indeed, life-time exposure to elevated blood pressure may be a more potent predictor of poor cognitive outcome in older adults than cross-sectionally measured blood pressure (Elias et al., 1993; Swan et al., 1998). Chronicity of hypertension was emphasized in several recent epidemiological studies in which persistent blood pressure elevation, measured across numerous examinations, predicted poorer cognitive functioning and/or greater rate of cognitive decline (Elias et al., 1993, 1998; Swan et al., 1998). Similarly, higher blood pressure during middle age has been shown to predict poorer cognitive outcomes in older age (Elias et al., 1993; Swan et al., 1996; Launer et al., 1995; Kilander et al., 1998).

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The Aging Mind: Opportunities in Cognitive Research Moderator Variables Although many studies have revealed lower average levels of cognitive function in hypertensive groups, there is also pronounced interindividual variability within these groups with respect to performance (Waldstein, 1995). This variability may be explained, in part, by relevant moderators. In this regard, hypertension has been shown to interact with both age and education in studies of cognitive function. Age as Moderator Several investigations have found interactions of age and hypertension such that young (less than 40 to 50 years of age) hypertensives performed more poorly than young normotensives on tests of attention, memory, executive functions, and psychomotor abilities, whereas middle-aged (upper limits ranging from 56 to 72 years) hypertensive and normotensive groups performed comparably (Elias et al., 1990b; Schultz et al., 1979; Waldstein et al., 1996). Madden and Blumenthal (1998) also noted that both young (ages 18 to 40) and middle-aged (ages 41 to 59) hypertensives displayed a slightly greater error rate on a test of visual selective attention than young or middle-aged normotensives, whereas older (ages 60 to 78) hypertensives and normotensives did not differ in performance. In contrast, such interactions were not noted among three age cohorts (55–64, 65–74, and 75–88 years) in a sample of 1,695 participants in the Framingham Heart Study on tests of memory, visual organization, attention, verbal comprehension, and concept formation (Elias et al., 1995). In sum, when interactive effects of age and hypertension (or blood pressure) are noted, poorer performance tends to aggregate among the younger individuals in any particular investigation. Waldstein (1995) suggests that such trends may reflect survival effects and selective attrition from studies (see Feinleib and Pinsky, 1992), as individuals with early-onset hypertension develop cardiovascular and cerebrovascular complications and are thus excluded from investigations. Furthermore, it is possible that early-onset hypertension confers greater risk for cognitive impairment than late-onset hypertension. In general, interactions of age and hypertension may best be examined in longitudinal studies in order to address some of these methodological difficulties. Other Moderators In one study, hypertensives having lower levels of educational attainment performed more poorly than comparably educated normotensives, whereas more highly educated hypertensives and normotensives did not differ in their performance (Elias et al., 1987). Relative preservation of cognitive function among more highly educated persons has also been noted in other contexts and may suggest protective effects associated with higher

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The Aging Mind: Opportunities in Cognitive Research socioeconomic status and or an enhanced ''cognitive reserve" (Katzman, 1993). Another source of variability in cognitive performance among hypertensives relates to the heterogeneity of this disorder (Kaplan, 1998; Streeten et al., 1992). In this regard, it is possible that certain subgroups of hypertensives are more likely than others to experience diminished cognitive performance. For example, hyperinsulinemic hypertensives perform more poorly than either normoinsulinemic hypertensives or normotensives (Kuusisto et al., 1993). In addition, high levels of sympathetic nervous system arousal (as indicated by increased plasma renin activity) have been associated with diminished psychomotor performance among hypertensives (Light, 1975, 1978). Mediation of Age-Related Variance Continuous blood pressure levels have been found to partially mediate age-related variance in cognitive performance. In one investigation, systolic and diastolic blood pressure attenuated by almost 58 percent the age-related variance in performance of an attention-shift reaction time task (Madden and Blumenthal, 1998). Similarly, Elias et al. (1998) found that longitudinally assessed systolic blood pressure was associated with a 50 percent reduction in the relation between age and performance of Wechsler Adult Intelligence Scale (WAIS) subtests reflecting visualization-performance ability. These findings suggest that blood pressure is an important mediator of cognitive aging. Methodological Issues The study of hypertension and cognition faces a number of methodological challenges (Waldstein et al., 1998). For example, the accurate measurement of blood pressure is critical to any investigation of hypertension and cognition. Interpretation of a number of studies, particularly several population-based investigations, has been limited by the measurement of blood pressure on a single occasion. This methodology greatly limits measurement reliability (Llabre et al., 1988) and precludes hypertension classification (Joint National Committee, 1997). Other studies have relied on self-reported hypertensive status (Zelinski et al., 1998; Desmond et al., 1993). A sole reliance on self-reported health status should be avoided, if possible, due to limits in reliability and validity and likely underestimation of health-cognition relations. Measurement of cognitive function, again particularly in certain population-based investigations, has been limited by use of brief screening measures

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The Aging Mind: Opportunities in Cognitive Research (such as a mental status exam) or very few cognitive tests. Sampling of a broad range of cognitive functions is critical to understanding hypertension-cognition relations. Investigations of hypertension and cognition typically control for numerous confounding variables by statistical adjustment (covariance), matching procedures, and/or study exclusions. Control variables often include age, education, alcohol consumption, anxiety, and depression, and they sometimes include smoking status, occupational status, race/ethnicity, socioeconomic status, and (if relevant) antihypertensive medications. Particularly in case-control studies, hypertensives are commonly either unmedicated or are removed from antihypertensive medication prior to the study. Individuals with medical, neurological, or psychiatric comorbidities are generally excluded from case-control studies. However, because of the resultant exclusion of hypertensives with major end-organ damage, the impact of hypertension on cognition may be underestimated, particularly among older adults. Longitudinal studies of hypertension and cognition do not always control for comorbidities such as diabetes mellitus and coronary heart disease. This is an important consideration, because hypertension is highly prevalent among individuals having certain medical or psychiatric comorbidities (e.g, depression, diabetes mellitus). Furthermore, hypertension may bear relatively stronger or weaker relations to cognition in the presence of more severe cardiovascular or metabolic diseases. For example, Elias et al. (1997) have found synergistic effects of hypertension and noninsulin-dependent diabetes mellitus with respect to diminished cognitive function. However, Phillips and Mate-Kole (1997) did not find hypertension to be a predictor of cognitive performance in patients with peripheral vascular disease. In this group of patients, more potent manifestations of cardiovascular disease may have overshadowed any effects of hypertension. Longitudinal investigations also have to contend with problems related to study attrition. It is often the least healthy or least motivated individuals who drop out of ongoing studies. Several available statistical methods for analyzing longitudinal datasets, such as two-stage growth curve analysis and survival analysis, will take such attrition into consideration (Collins and Horn, 1991; Dwyer and Feinleib, 1992; McCardle et al., 1991) Clinical Significance Although hypertensives generally should not be characterized as clinically impaired on cognitive tests (Elias et al., 1987), the impact of hypertension on cognition can be considered clinically significant at an individual level and significant at the population level. In this regard, although a full range of effect sizes is apparent (from d < 0.1 to d > 1.0), numerous case-control studies have found that hypertensive-normotensive differences in cognitive

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The Aging Mind: Opportunities in Cognitive Research test scores are characterized by large effect sizes (Waldstein et al., 1991a). Indeed, several studies have found that the performance of hypertensives falls below that of normotensives by up to one standard deviation (Waldstein et al., 1991a, 1991b). At the individual level, this magnitude of difference could, for example, translate into a below-average versus average (or average versus above-average) test score. Among individuals, even subtle alterations in cognitive functioning can have negative consequences. Such changes can be distressing and may thus impact quality of life. Lowering of cognitive performance associated with hypertension is also considered significant at the population level (M.F. Elias et al., in press). In this regard, a significantly increased risk for poor cognitive performance, both cross-sectionally and longitudinally, is associated with hypertension or progressive increments in blood pressure (M.F. Elias et al., in press). Data from the Framingham Heart Study indicate that chronic hypertensives displayed an increased risk of performing in the lowest quartile of the distribution of scores on several learning and memory tests, with odds ratios ranging from 1.29 to 1.62 (Elias et al., 1995). Underlying Mechanisms Numerous neurobiological mechanisms have been proposed to underlie the relation between hypertension and diminished cognitive function (see Elias and Robbins, 1991; Waldstein, 1995; Waldstein et al., 1991a; Waldstein and Katzel, in press). In this regard, studies have demonstrated that hypertensives exhibit reduced cerebral blood flow and/or metabolism, particularly in frontal, temporal, "watershed," and subcortical (e.g., basal ganglia) regions, autoregulatory disturbance, endothelial dysfunction, increased atherosclerosis in carotid and large cerebral arteries, increased cerebral white matter disease, silent infarction, cerebral atrophy, and cellular and neuro-chemical dysfunction (for a review, see Waldstein and Katzel, in press). However, it is rare that such mechanistic factors are considered in conjunction with cognitive performance. In this regard, both van Swieten et al. (1991) and Schmidt et al. (1993) found that hypertensives having significant white matter disease performed more poorly than either normotensives or hypertensives without notable white matter disease. However, because white matter lesions are generally not seen in young or middle-aged persons, it has been hypothesized that alterations in neurophysiology are more likely to account for the cognitive difficulties noted among hypertensives in these age groups (Waldstein, 1995). Waldstein and Katzel (in press) have suggested that numerous factors may promote the neuropathological changes that can influence cognitive performance in hypertensives. These include the direct effects of elevated blood pressure, in addition to other factors that tend to co-occur with hypertension,

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