5 - Innovative Approaches to Memory Training for Older Adults

Editors: Backman, Lars; Hill, Robert D.; Neely, Anna Stigsdotter

Title: Cognitive Rehabilitation in Old Age, 1st Edition

Copyright 2000 Oxford University Press

> Table of Contents > Part III - The Influence of Health and Health Behaviors on the Rehabilitation of Cognitive Processes in Late Life > 8 - Smoking and Cognitive Function: Issues in Cognitive Rehabilitation

8

Smoking and Cognitive Function: Issues in Cognitive Rehabilitation

Robert D. Hill

Karen Rothballer Seelert

Cigarette smoking is a pervasive high-risk behavior that has been linked to the early emergence and rapid progression of chronic disease in middle and late life. The mechanisms through which smoking impairs healthy functioning and predisposes older adults to chronic illness has been well documented (Fielding, 1985; LaCroix et al., 1991). The vast majority of this research points to the deleterious effects of chronic smoking on both physiological capacity and efficiency as it relates to specific organ systems (Jenkins, Rosenman, & Zyzanski, 1968; Lange et al., 1989; Shinton & Beevers, 1989). What is less well understood about cigarette smoking is its potential to interact with cognitive processes in both normal and diseased aging.

The current chapter explores the mechanisms through which smoking may influence cognitive function across the adult life span as well as examines the impact that smoking behavior may have on rehabilitation efforts in those individuals who smoke into old age and are at risk for cognitive impairment. One goal of this chapter is to develop a conceptual model that outlines specific pathways through which smoking influences cognitive function. Through this model, several important issues are explored: (a) Cigarette smoking exerts both a direct and indirect effect on cognitive performance direct in that cigarettes themselves contain psychoactive substances that are delivered to the brain via smoke inhalation, and indirect in that chronic use of cigarettes can produce stable changes in systemic efficiency that, in turn, influence brain function; (b) even though smoking has been shown to be hazardous to overall physical health, some aspects of tobacco consumption (e.g., nicotine delivery) may have facilitative effects on cognition. For example, some evidence links cigarette smoking to lowered incidence rates in Alzheimer's disease (AD; Lee, 1994). On the other hand, the role of smoking as an exacerbating agent in vascular and pulmonary

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disease may magnify the deleterious impact that these exert on cognitive processes (Launer et al., 1996).

This chapter also examines how the connection between cognitive function and chronic smoking may impact cognitive rehabilitation efforts in older adults. Specific sections throughout the chapter highlight these issues and address such questions as: (a) What role might cognitive variables play in smoking cessation and relapse prevention planning? (b) Can efforts to improve cognitive function through compensatory techniques such as physical exercise or memory training benefit older smokers? (c) How does the relationship between cognition and cigarette smoking enhance our understanding of strategies for remediating cognitive loss in diseases of aging such as AD?

An Explanatory Model

Figure 8.1 is an overview of the pathways through which cigarette smoking may mediate cognitive abilities. This figure highlights both (a) the acute and long-term action and (b) the direct and indirect effects of cigarette smoking on cognitive function. By necessity, any model that attempts to capture a phenomenon that involves such a wide array of potential relationships as can be found in cigarette smoking and cognitive function is limiting. However, it can be used as a starting point to organize different bodies of research that have connected cigarette smoking to cognitive performance variables. This model can also facilitate discussion on the possible role that cigarette smoking may play as a mediating variable in late-life cognitive change.

Three pathways are depicted through which cigarette smoking may exert an influence on cognitive function, through (a) nicotine delivery, (b) chronic disease, and

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psychological factors. The nicotine delivery pathway highlights the acute effects of smoking on cognitive function and is based on the notion that cigarette smoke inhalation is an efficient delivery method of nicotine to the brain. The bold arrows characterizing the smoking-nicotine pathway denote the direct effect of cigarette-delivered nicotine on cognitive function. The latter two pathways that show a bold arrow from cigarette smoking to chronic disease and psychological factors denote the direct effect of smoking on these processes. The lighter arrows pointing to cognitive function denote the mediating role that smoking plays on cognitive processes.

Figure 8.1. Smoking and cognition: An explanatory model.

It is noteworthy that in most of this research, cognitive function is defined specifically through measures of attention, memory, and psychomotor skills. Measures of attention have included, but are not limited to, alertness and sustained attention (as assessed through vigilance tasks), selectivity (measures of attentional switching and selective attention), and processing capacity (measures of processing speed). With regard to memory, investigations have utilized measures of long- and short-term memory, working memory, and even incidental memory. The measurement of psychomotor skills has included simple and choice reaction time tasks as well as pure psychomotor speed (e.g., tapping). Finally, measures of cognitive impairment have been employed to determine the extent to which smoking can predict the early emergence of organic brain syndromes such as Alzheimer's disease (AD).

Cigarette Smoking, Nicotine, and Short-Term Cognitive Function

There is substantial disagreement as to whether cigarette smoking exerts a short-term deleterious or facilitative effect on cognitive function, particularly with regard to its role as a nicotine delivery mechanism. Of the studies that have investigated acute effects of cigarette smoking, most presume that the active agent is nicotine. Given this assumption, the sections that follow examine (a) the extent to which nicotine itself can influence cognitive performance and (b) the acute effects of cigarette-delivered nicotine on cognitive function.

Nicotine as a Cognitive Enhancer

Nicotine has been described as a tertiary amine that binds with nicotinic cholinergic receptors in the brain (Benowitz, 1996) and, even in relatively low doses, produces a number of predictable physiological and behavioral responses in animals and in humans (Baron, 1996). In humans, nicotine as a central nervous system (CNS) stimulant has been shown to produce a sympathetic nervous system response that is characterized by increased heart and respiratory rate, increased blood pressure, and blood vessel vasoconstriction, as well as changes in body temperature. Nicotine also increases metabolic activity (Perkins et al., 1994), and some research has even suggested that it influences the endocrine system, primarily by stimulating the release of beta endorphins. In this regard, nicotine has been linked to increased levels of ACTH and Cortisol (Benowitz, 1996; Newhouse et al., 1990). It has also been documented that nicotine tolerance develops rapidly in humans; that is, increased dosages are needed to maintain stable levels of drug efficacy over time (Perkins et al., 1994).

Nicotine has been linked to a number of behavioral phenomena in animals, including

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increased locomotor activity and rate of conditioning, and this research has generally supported the hypothesis that nicotine is a cognitive enhancer. The strength of this assertion, however, varies with the concentration of nicotine delivered, the delivery interval, the type of experimental animal used, and the kind of performance tasks employed (Stolerman, Mirza, & Shoaib, 1995).

In humans, studies have examined the relative impact of small amounts of nicotine delivered to nonsmokers (via subcutaneous injection, tablets, nasal sprays, gum, and transdermal patches) on cognitive function. Although research supports its enhancing effects on psychomotor performance (see West & Jarvis; 1986; Perkins et al., 1990), findings are somewhat mixed with regard to nicotine's influence on more complex cognitive tasks, with some studies supporting nicotine as a cognitive enhancer (Provost & Woodward, 1991; Wesnes & Warburton, 1984; Wesnes, Warburton, & Matz, 1983), while others have been unable to reliably establish such an effect (Dunne, MacDonald, & Hartley, 1986; Heishman, Snyder, & Henningfield, 1991). Several generalizable findings have emerged from this research with regard to the impact of nicotine on nonsmokers. First, nicotine administered in sufficient quantities accelerates motor function. Second, nicotine appears to have a short-term enhancing effect on selected indices of cognitive function, given that the dose is optimal and the tasks contain attentional and/or psychomotor properties (e.g., reaction time, vigilance, sustained attention tasks). Whether nicotine enhances memory function or complex cognitive abilities in any reliable way remains an open question.

Based on data that nicotine can have a short-term effect on cognition, its role as an active ingredient in cigarette smoke is examined next. What is critical in this literature is the proposition that if change in smoking behavior can alter cognitive function in the short run in relatively young, nonaddicted smokers, cognitive rehabilitation efforts in older long-term smokers will be influenced by both the length of time that the individual has smoked and the frequency of cigarettes smoked within a given time interval.

Cigarette Smoking and Short-Term Cognitive Function

Although the particulates in cigarette smoke contain potentially several thousand different identifiable compounds, including carbon monoxide (CO), acetaldehyde, and many nonnicotine alkaloids (Dube & Green, 1982), evidence suggests that nicotine is the substance in cigarettes that exerts the greatest psychopharmacological effect on human performance (Stolerman et al., 1995). It is an established fact that cigarettes contain nicotine, although the dosage level varies widely across brands, ranging from less than 0.5 mg to more than 4.0 mg per cigarette. Further, nicotine is rapidly absorbed into the blood from inhaled cigarette smoke and requires less than 20 seconds to pass the blood-brain barrier, so that cigarette smoking can be construed as a highly efficient nicotine delivery mechanism (Benowitz, 1996).

Given the cognitive enhancing properties of nicotine, it should be expected that studies would generally confirm the cognitive enhancing effects of cigarette smoke. Interestingly, this has not been the case. Findings from this literature have varied, with some research demonstrating cognitive advantages associated with cigarette intake (see Wesnes & Warburton, 1984), while others have found no cognitive benefits and even detrimental effects on cognitive performance (Andersson, 1975; Andersson & Hockey, 1977; Gonzales & Harris, 1980; Hill, 1989; Spilich, June, & Renner, 1992).

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These studies have employed a variety of methodological strategies, including contrasting regular smokers with never-smokers, regular smokers with occasional smokers, nondeprived versus deprived smokers (who vary with regard to the deprivation interval), and even smokers who vary with regard to the time they smoke their first cigarette (early morning versus afternoon). Given this variability in the literature, several reviews have highlighted experimental control problems that make it difficult to interpret these data (see Levin, 1992; Spilich, 1994; Stolerman et al., 1995), including (a) difficulty in accurately assessing smoking history in current and former smokers, (b) individual differences in tissue concentrations of nicotine at the time of testing (which is particularly problematic in long-term smokers), and (c) sampling biases. Further, this research has not made a systematic attempt to disentangle the specific effects of nicotine from those of other substances in cigarette smoke that may offset its nicotine's influence, such as carbon monoxide (CO).

Several theories have been proposed to explain how cognitive performance may be affected by cigarette consumption. The first suggests that cigarette-delivered nicotine should objectively enhance cognition. Thus, those who smoke cigarettes at the time of testing should outperform comparable nonsmokers on selected cognitive tasks that are sensitive to the CNS-arousing properties of nicotine. In support of this contention, West and Hack (1991) examined the effect of cigarette smoking on a memory search task in regular and occasional smokers. Subjects were tested before and after a 24-hour period of abstinence, at which point they smoked cigarettes that either contained nicotine or were nicotine-free. Smoking the nicotine-containing cigarettes resulted in increased search speed in both groups of smokers, and it was concluded that nicotine was responsible for this increase. Several methodological problems are noteworthy, however. First, there was not a nonsmoking control group, and second, although search speed increased when the nicotine-containing cigarette was smoked, search efficiency was not assessed. These issues underscore the difficulty of disentangling the specific effects of nicotine from the overall impact of cigarette smoking on cognitive performance.

The second, and perhaps more compelling, theory postulates that acute cognitive deficits may occur in smokers during nonsmoking intervals between cigarettes. This withdrawal effect hypothesis (Levin, 1992; Parrot, 1994) suggests that the resumption of smoking may compensate for this transitory decrement by reinstating nicotine and creating a perception (on the part of the smoker) of cognitive benefits due to smoking. This theory coincides with the known addictive potential of nicotine and is also supported by research that has found that the short-term cognitive enhancing effect of nicotine varies depending on the length of cigarette deprivation (length of time between cigarettes) and baseline levels of cigarette intake (heavy versus light smokers). In support of this theory, studies indicate that tobacco use is associated with improved mood and perceptions of well-being in smokers, but that withdrawal can lead to depressed mood as well as increased anxiety and decrements in perceived cognitive function (e.g., difficulty concentrating, inability to focus attention; Gilbert, 1979; Hughes, Hatsukami, Mitchell, & Dahlgren, 1986; Wesnes & Warburton, 1983). Data are not available, however, that gauge the extent to which such deficits are magnified in long-term smokers or whether a reinstatement of cigarette smoking can reduce such deficits.

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Issues in Cognitive Rehabilitation

With few exceptions, research on the short-term effects of cigarette smoking on cognitive performance has been confined to individuals who were relatively young with brief smoking histories (less than 10 years). Thus, it is difficult to generalize these findings to older adults who are chronic smokers (20 or more years) and who may be cognitively impaired or at risk for cognitive impairment. Further, most of the research in this domain has focused on laboratory studies that have examined the extent to which nicotine (delivered with or without cigarettes) impacts performance on experimental tasks, and how such tasks may or may not be relevant in day-to-day functioning.

Two studies specifically address the short-term impact of cigarette smoking on (a) older adults and (b) applied tasks relevant to cognitive rehabilitation program planning. A cross-sectional study conducted by Hill (1989) documented performance decrements in a sample of older self-reported smokers (mean age = 72 years) across cognitive tasks that were dichotomized with regard to the presence or absence of processing speed. Smokers were disadvantaged on tasks that placed heavy demands on speeded processing. The second study involved a series of experiments conducted by Spilich et al. (1992), who examined college students, grouped as smokers or non-smokers, who performed graded cognitive tasks that increased in complexity with regard to time and performance demands. Smokers were further divided into a deprived and nondeprived subgroup. The nondeprived smokers were given cigarettes containing 1.2 mg of nicotine, and deprived smokers were given nicotine-free cigarettes. Tasks ranged from a simple visual search paradigms to a complex driving-simulation procedure. No differences between groups were found in visual search; however, differences favoring the nonsmokers were found on the simulated driving procedure.

These two studies suggest that chronic smokers may show the greatest deficits in cognitive performance on those tasks that push the limits of information processing resources. Older smokers may be at particularly high risk for these deficits due to the fact that aging itself is associated with diminished cognitive function (see Salthouse, 1991). Further, older smokers, as a group, are at higher risk for chronic disease which, in turn, has been shown to be associated with poorer cognitive performance. Although Hill (1989) reported screening older smokers for disease, he postulated that even in this case subclinical disease processes may have exerted a subtle influence on those cognitive tasks that placed the heaviest demands on processing resources (e.g., speeded verses non-speeded tasks).

In support of this contention, some research has alluded to poorer driving performance in smokers versus nonsmokers (DiFranza, Winters, Goldberg, Cirillo, & Biliouris, 1986; Heimstra, Bancroft, & DeKoch, 1967), although in these studies age and years of smoking were specifically examined as mediating variables. Assessing the frequency of driving-related problems (e.g., traffic violations, minor and major accidents, automobile-related deaths) between older smokers and nonsmokers seems warranted. Should research support this contention in older drivers who smoke cigarettes, changing smoking habits may be an important component in optimizing performance skills, particularly in older drivers who are showing early signs of age-related cognitive impairment. In addition, smoking status may be an important factor in predicting

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how long older adults in cognitively demanding occupations (airline pilot, air traffic controller, corporate executive, computer programmer) can maintain optimal on-the-job performance. Quitting smoking may be advised to preserve cognitive flexibility that may be critical in such occupations (Strayer & Kramer, 1994).

Cigarette Smoking, Chronic Disease, and Cognitive Function

Population-based longitudinal and cross-sectional research has examined cigarette smoking as one of many lifestyle predictors of cognitive stability and/or change in middle to late adulthood. Methods of assessing cognitive function in this context have included brief mental status exams and an array of cognitive tasks selected to track the normal aging process and predict early cognitive impairment. These studies make few claims as to why cigarette smoking predicts cognitive function and/or change across the life course; however, the link between cigarette smoking, the emergence of chronic disease in middle and late life, and cognitive functioning is apparent.

Smoking as a Predictor of Cognitive Function in Healthy Aging

Cross-sectional and longitudinal data in community-dwelling middle-aged and late-life adults have produced somewhat mixed results regarding the role that cigarette smoking plays in indices of cognitive performance. In cross-sectional data, Farmer et al. (1987) documented that self-reported smokers performed more poorly than non-smokers in two out of eight of their cognitive tasks, namely, immediate recall and similarities. Hultsch, Hammer, and Small (1993), in a sample of 484 subjects who were all over 55 years of age, found minimal if any relationship between tobacco use and cognitive performance. A unique aspect of this study was the wide array of measures employed, including verbal processing time, working memory, vocabulary, verbal fluency, world knowledge and word and text recall. Emery, Huppert, and Schein (1997), in a population-based study of 4,399 subjects who ranged in age from 19 to 94 years, found that smoking behavior was not related to performance on any of their cognitive tasks, and in several (e.g., choice reaction time and immediate memory), smokers outperformed nonsmokers. Smoking was defined as a categorical variable, namely, never-smoker, past smoker (quit at least 1 year ago), and current smoker. What is interesting in this study is that pulmonary function, as assessed by objective spirometry (forced expiratory velocity in 1 second; FEV1), was related to diminished cognitive function even after controlling for demographics and smoking status. This finding is surprising in light of strong evidence that smoking diminishes pulmonary efficiency and capacity in old age (Lange et al., 1989). The lack of pulmonary deficits in these smokers was indicative of their overall good health and may have represented a sampling bias favoring the inclusion of disease-free smokers. This study does, however, represent an ambitious attempt to test the hypothesis that pulmonary function is a mechanism through which cigarette smoking may interact with cognitive processes. A more definitive test of this assumption would be to examine whether an interaction between smoking and cognitive performance would emerge in subjects with pulmonary disease.

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Several longitudinal studies have also included cigarette smoking as a factor in cognitive decline in older adults. Herbert et al. (1993) examined the relationship between smoking and cognitive function in a sample of 1,201 adults aged 65 years and older from East Boston, Massachusetts. Using a composite variable of tobacco consumption that included self-reported smoking status (never-smoker, former smoker, and current smoker) and pack-years of smoking, the authors noted a decline in performance from baseline in those former smokers who had a relatively long pack-year history. Launer, Feskens, Kalmijn, and Kromhout (1996) reported data from the Zutphen Elderly Study, a large community-based longitudinal sample in the Netherlands consisting of 1,266 men. Subjects were initially categorized as current smokers, never-smokers, and former smokers. Former and never-smokers were further dichotomized by length of time they had engaged in smoking (more or less than 10 years). Cognitive function was assessed by means of the Mini-Mental State Examination (MMSE). Smokers showed MMSE performance declines, which were most marked in those who also had disease symptoms. From these data, the authors argued that smoking may interact with disease processes to accelerate late-life cognitive decline.

Galanis et al. (1997), reporting data from 3,429 middle-aged Japanese-American men who were part of the Honolulu Heart Program, found that age-related cognitive decrements were magnified in those who were continuous smokers. Although this was a subgroup of individuals who were healthier than the overall study sample as demonstrated by their positively skewed test scores, smoking continued to be associated with increased cognitive decline, particularly in those diagnosed with vascular disease. Interestingly, cognitive performance in those who were long-term quitters (more than 5 years) was indistinguishable from that of never-smokers.

In a final study, Prince, Lewis, Bird, Blizard, and Mann (1996) analyzed data from 2,567 hypertensive adults (65 74 years of age) from the Medical Research Council's (MRC) Trial of the Treatment of Moderate Hypertension in Older Subjects. They selected a paired associate learning task that was administered to all participants at entry, followed by 1-, 9-, 21-, and 54-month retest intervals. Smoking status was dichotomized (smoker or nonsmoker) and included as part of a collection of risk factor variables for cardiovascular disease. Smoking was not a significant predictor of change in cognitive function in the overall sample; however, it did predict change in a subgroup of postmenopausal women who had lower socioeconomic status (SES) and less education and were of lower intelligence. It should be noted that as a group, smokers in this sample were more likely to die at an earlier age, creating a potential bias in favor of healthier smokers, who may have been less likely to experience chronic disease.

From these studies, it could be argued that in community-dwelling adults, cigarette smoking may be most influential as a predictor of performance change over time, rather than of cognitive function at any specific point in time. The effects of long-term smoking on cognitive function, therefore, are likely to become more apparent when multiple assessments are made over increasing time intervals, particularly when indicators of disease are also present. In the section that follows, we examine how cigarette smoking is likely to interact with chronic disease. In this regard, two assumptions are made: (a) that cigarette smoking is a risk factor for many disease states, including cardiovascular and pulmonary disease, and (b) that continued smoking into late life increases the risk of premature disease and disease-related mortality. Both of

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these assumptions highlight potential sources of bias in research that includes smoking status as an explanatory variable in cognitive decline in diseased aging.

Cigarette Smoking and Cognitive Function in Chronic Disease

Highlighted in this section are cardiovascular disease, pulmonary disease, and Alzheimer's disease (AD). Cardiovascular and pulmonary disease were selected because (1) they have been linked to declines in cognitive performance without respect to smoking per se, and (2) cigarette smoking is a prominent risk factor in the emergence and progression of these disease states. Alzheimer's disease represents a twist in terms of a proposed association between cigarette smoking and decreased incidence rates in AD.

Vascular Disease

Cigarette smoking is a well-known risk factor for cardiovascular disease (CVD), and this risk has been consistently documented in numerous epidemiological studies (Aronow, 1990; Jajich, Ostfeld, & Freeman, 1986). There are several mechanisms through which cigarette smoking may contribute to the early emergence and more rapid progression of CVD. The first, as described earlier in this chapter, is due primarily to the effect of nicotine on sympathetic nervous system activation. The second is the long-term systemic impact of smoking on overall cardiovascular capacity and efficiency, including (a) repeated episodes of systemic and coronary vasoconstriction; (b) increased concentrations of free fatty acids low density lipoprotein (LDL) cholesterol, and fibrinogen; (c) reduced High Density Lipoprotein (HDL) cholesterol; and (d) increased platelet reactivity (Winniford, 1990). Combined with other particulates in cigarette smoke such as carbon monoxide (CO), these effects gradually compromise cardiac capacity and efficiency. These chronic effects also appear to be dose-related, heavier smoking over longer time intervals further damaging functioning.

The link between CVD and cognitive function has received considerable attention in the research literature, although the findings have been somewhat mixed. Several studies have documented a relationship between CVD and diminished cognitive function (Elias, D'Agostino, Elias, & Wolf, 1995; Elias & Robbins, 1991), while others have found no such relationship (Farmer et al., 1987). A study that attempted to make a causal link between cigarette smoking, CVD, and cognitive function was reported by Frasure-Smith and Rolicz-Woloszyk (1982), who self-reported memory problems in 157 middle-aged males recovering from ischemic heart disease. At the time of the interview, which was approximately 1 year following initial hospitalization for an incident of ischemic heart disease, 39% of their subjects reported experiencing memory difficulties, and cigarette smoking was reported to be a contributing factor. Most intriguing was that those who had quit smoking since the initial hospitalization were twice as likely to complain about memory problems as those who continued to smoke. The authors proposed two seemingly contrasting effects of cigarette smoking on memory complaints, namely, an acute enhancing effect likely due to the action of nicotine and a chronic deleterious effect caused primarily by the role of cigarette smoking in speeding the progression of CVD.

It is important to note the potential role that cigarette smoking may play in magnifying the deleterious effects of cerebrovascular disease. For the purpose of this chapter,

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cerebrovascular disease is defined as a variant of CVD that influences only those aspects of the vascular system responsible for blood-oxygen transfer to the central nervous system. Although the literature that examines the role of cigarette smoking in cognitive decline through cerebrovascular disease is small in comparison to the literature on CVD, cerebrovascular disease may provide the most powerful test of this relationship. For example, hypertension (which is highly influenced by cigarette smoking) has been linked to reduced cerebral blood flow and brain atrophy in middle- and late-life adults (Hatazawa et al., 1984). Cerebrovascular disease is a well-known risk factor in dementia, and it has been consistently documented that chronic smokers have reduced regional cerebral blood flow when compared to nonsmokers (Kubota, Yamaguchi, Fujiwara, & Matsuzawa, 1987). Further, long-term continuous smoking has even been associated with increased brain atrophy due in part to its effects on cerebrovascular disease (Kubota, Matsuzawa, Fujiwara, Yamaguchi, Wantanabe, & Ono, 1987). From this literature, it is possible to specifically implicate cigarette smoking as an exacerbating agent in cerebrovascular disease, which in turn results in documentable changes in brain capacity and function and accelerated cognitive decline. Although this represents a strong argument for predicting that smokers will suffer larger cognitive deficits in the presence of cerebrovascular disease, research has yet to document this logic. For example, Desmond, Tatemichi, Paik, and Stern (1993) were unable to find a significant effect of smoking behavior as a predictor of cognitive decline in their sample of older adults with cerebrovascular disease. This may have been due to their constrained definition of cigarette smoking, as well as to the relative health of their diseased smokers. Nonetheless, more research is needed to more fully explore this assumption.

Pulmonary Disease

Extensive literature exists linking (a) cigarette smoking to chronic pulmonary disease and (b) chronic pulmonary disease to impairment in cognitive function. Evidence indicates that cigarette smoking is a major risk factor for chronic lung disease in middle-aged and older adults. The pattern of lung injury due to cigarette smoke involves sustained declines in forced vital capacity (FVC), abnormal increases in mucous production, the excessive accumulation of neutrophils, increased airway obstruction, and declines in the optimal exchange of oxygen and carbon dioxide (Coultas & Samet, 1989). The Framingham Study documented a more rapid decline in FVC and FEV over a 10-year period in smokers versus nonsmokers, with highly accelerated declines in those who continued to smoke into the fifth and sixth decade of life (Ashley, Kannel, Sorlie, & Mason, 1975). Chronic obstructive pulmonary disease (COPD) is an impressive example of the cumulative impact that long-term smoking can have on lung functioning. Within COPD, cigarette smoking magnifies disease processes by blocking small airway passages, reducing gas exchange, and creating hypoxemic effects (Weiss, 1984), and these connections are so well established that the first-line treatment for COPD is mandatory smoking cessation.

The link between pulmonary disease and cognitive functioning has also been well established. In a study examining age-related pulmonary efficiency and cognitive function in 3,812 community-dwelling adults 65 years and older, Cook et al. (1989) found that objective declines in peak expiratory flow were associated with deficit performance in simple measures of immediate memory, attention, and orientation. Two related studies that contrasted pulmonary disease patients with nondiseased subjects

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on a battery of cognitive tasks found a significant relationship between the degree of hypoxemia in the presence of disease and neuropsychological impairment (Grant et al., 1987; Prigatano, Parsons, Wright, Levin, & Hawryluk, 1983). Grant, Heaton, McSweeney, Adams, and Timms (1980) examined 121 individuals (average age 65.1 years) with hypoxemic COPD on a battery of neuropsychological tests that included measures of attention, language, abstract reasoning, and perceptual motor skills. A positive correlation was reported between measures of lung function and performance across each of these neuropsychological tasks. It is noteworthy that although the smoking status of patients in this study was not assessed, the authors implicated chronic hypoxemia (a common feature of COPD in the presence of cigarette smoking) as the most likely explanation for the poorer cognitive performance in those patients with more severe manifestations of COPD.

In sum, data indicate that cigarette smoking alters pulmonary function through predictable declines in lung efficiency and overall capacity. Decline in pulmonary health is a precursor to pulmonary disease, of which smokers are at very high risk. Smoking in the presence of pulmonary disease places the individual at high risk for acute pulmonary deficits and speeds the overall disease. The role of smoking as an exacerbating agent is likely to be important in gauging the extent to which COPD diminishes cognitive function in old age and may be an important factor to consider in cognitive rehabilitation programming in older adults who have cognitive deficits associated with COPD.

Alzheimer's Disease

What has been of primary interest with regard to Alzheimer's disease, cognition, and cigarette smoking is the long-term impact of nicotine on brain neuroanatomy. Briefly, some epidemiological evidence has indicated that cigarette smokers have a lower incidence of Alzheimer's disease, and this has led to the belief that smoking into advanced age may be protective of AD (Graves et al., 1991; Lee, 1994). It should be noted, however, that these findings have not consistently been endorsed by the scientific community (Graves & Mortimer, 1994; Shalat, Seltzer, Pidcock, & Baker, 1987). In either case, such research has important implications in identifying potential pathways that may underlie the linkage between cigarette smoking, AD, and cognitive decline in AD.

The most compelling pathway is underscored by the finding that nicotinic cholinergic receptors in the brain may play a significant role in cognition, and that in AD, such receptors are in very short supply (Stolerman et al., 1995). Given the connection between nicotine, nicotinic receptors, and cognitive functioning in AD, interventions have attempted to capitalize on this relationship by administering nicotine at various dosage levels to early AD patients in the hope of offsetting cognitive losses associated with the disease (see Levin, 1992; Stolerman et al., 1995). The short-term effectiveness of this approach is highlighted by a double-blind placebo-controlled study with six AD patients that involved continuous delivery of nicotine (via a transdermal patch) over a 7-day period (Wilson et al.,1995). Those receiving nicotine showed improved learning in the short run; however, no long-term follow-up was conducted. Thus, whether such a strategy could produce substantial and consistent improvement in cognitive functioning in AD remains an open question. It should be noted that none of the aforementioned interventions employed cigarette smoking as the nicotine delivery mechanism. In fact, subjects in such studies have generally been nonsmoking volunteers.

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Thus, such data may provide evidence only for the efficacy of nicotine and do not address the role of cigarette smoking (and its modification) in the progression of cognitive deterioration in AD.

Another explanation of the epidemiological data demonstrating fewer smokers with AD is that cigarette smoking may be a marker variable of other, more salient confounding factors. For example, cigarette smokers have a higher morbidity rate than comparable nonsmokers, and if sampling targets older individuals, a bias may exist in favor of younger smokers who are somewhat healthier at baseline than nonsmokers. In other instances, cigarette smokers may be misrepresented in specific disease categories (or in other subgroups) that are screened when healthy volunteers are selected in studies tracing the course of AD. Letenneur, Dartigues, Commenges, Pacale, Tessier, and Orgogozo (1994) found smoking status to be initially highly predictive of AD; however, after controlling for the effects of occupational category and educational level, its predictive power disappeared. Thus, great care should be emphasized in suggesting the beneficial effects of cigarette-delivered nicotine on brain function, particularly as related to the onset of AD. What appears to be absent in this literature is an appreciation of the complex (and predictable) impact that cigarette smoking could exert on AD through reductions in cerebral blood flow, diminished oxygen transfer, and impaired pulmonary and vascular functioning. Disentangling any beneficial effects of cigarette-delivered nicotine from the role that cigarette smoking plays in exacerbating disease processes is warranted in future research.

Issues in Cognitive Rehabilitation

It is not surprising that continued smoking in the presence of chronic disease will have adverse consequences on cognitive function; thus, smoking cessation is a recommended strategy to minimize continued cognitive decline. However, what is less obvious and may have important implications in smoking cessation efforts in older diseased adults is the complex interrelationship between smoking, cognitive processes, and disease, as well as how these may influence the potential success of relapse prevention efforts. This potential interrelationship was proposed by Frazure-Smith and Rolicz-Woloszyk (1982), who suggested that continued smoking in the presence of CVD may mask its effects on cognitive function. Thus, quitting smoking may be perceived as causing more cognitive problems than it alleviates. Given that older adults are likely to make global attributions about even short-term cognitive deficits (Bolla, Lingren, Bonaccorsy, & Bleecker, 1991), addressing these as a part of relapse prevention programming may be critical in helping older quitters maintain abstinence. One way to address such issues is through focused memory-training interventions that could help older quitters learn to compensate for such short-term deficits. Although memory training has, to date, focused primarily on nondiseased, high-functioning older adults, a few strategies namely, spaced retrieval and simplified mnemonic procedures (see Camp & McKitrick, 1992) have been used to remediate cognitive loss in impaired groups. It may be useful to incorporate such strategy training in the maintenance of smoking cessation.

From the COPD literature, it is possible to identify impaired oxygen transfer as the specific disease mechanism causing cognitive loss in the late-life smoker. A definitive test of this assumption would be to examine cognitive function in subjects who vary

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with regard to smoking status and the presence or absence of COPD. Should this relationship be established, not only would it provide evidence for the importance of quitting to preserve cognitive function in COPD, but mechanisms to upregulate oxygen transfer to the brain might also be recommended. One such mechanism may be a regular program of physical exercise, since some research has suggested that exercise training can enhance cognitive function in old age through increased oxygenation to the brain (see Dustman et al., 1984). Thus, the effect of exercise on cognitive variables following smoking cessation in the presence of disease may be a particularly promising cognitive rehabilitation strategy.

Cigarette Smoking, Psychological Variables and Cognitive Function

As noted in Figure 8.1, psychological variables are another pathway through which cigarette smoking may exert an indirect influence on cognitive function. In this regard we highlight two processes: (a) personality style and (b) depression. Although the connection between cigarette smoking and cognitive processes has been investigated in this context, the rationale underlying this research, to date, has been to examine the propensity of individuals with psychological vulnerabilities to utilize cigarette smoking as a compensatory mechanism for suboptimal affective and/or cognitive function.

A few early studies have suggested that cigarette smoking may be used to mediate deficits in information processing as a result of personality style. The central element of this proposal is the stimulating and/or tranquilizing effect of nicotine. Eysenck (1965) first proposed this line of reasoning based on the notion that both introverts and extroverts mediate arousal levels in order to optimize information processing; that is, extroverts attempt to increase a characteristically low baseline level of arousal, whereas introverts work to decrease high baseline arousal levels. The proposition that cigarette smoking could be used to optimize cognitive function in this way is intriguing, and a few studies have examined this hypothesis with mixed results regarding the potential action of cigarette smoking (Revell, Warburton, & Wesnes, 1985; Warburton, Wesnes, & Revell, 1983). Thus, this issue remains open to future research.

Research indicates that depressive symptoms may influence cognitive function, and this finding is highlighted by the observation that in some instances, cognitive decrements inherent in depressive symptomatology have been mistaken for organic brain syndrome (Newhouse & Hughes, 1991). In a series of studies, Forsell, Jorm, and Winblad (1994) examined a large sample of depressed older adults who were participating in a population-based study in Sweden. Among these individuals, depressive symptomatology was found to cluster into two distinct categories reflecting (a) mood (dysphoria, appetite disturbance, feelings of guilt, suicidal ideation) and (b) motivation (lack of interest, psychomotor change, loss of energy, and concentration difficulties). Following this research, B ckman, Hill, and Forsell (1996) found motivational symptoms were most predictive of deficits in cognitive function. Given that related research suggests that cigarette smoking may be used by some depressed individuals to self-medicate for depressive symptoms (Hughes et al. 1986), it could be argued that depressed older adults may utilize cigarette smoking in a similar way to compensate for cognitive deficits associated with depression. Such a link could provide a possible explanation as to why it is difficult for depressed older adults, who may be at risk for

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cognitive impairment, to stop smoking and avoid relapse (Hall, Mu oz, & Reus, 1994). Although it is difficult to draw generalizable conclusions on the role that cigarette smoking may play as a mediator of cognitive loss in depression in old age, this may represent an important avenue for future research.

Issues in Cognitive Rehabilitation

The major postulate of this section is that cigarette consumption may be used by smokers to optimize cognitive processes within a particular personality style, or to compensate for cognitive deficiencies associated with an affective state, namely, depression. If cigarette smoking as a form of self-medication does play a role in mediating cognitive loss in this way, two important questions arise: (a) How does it operate? (b) What are its implications in strategy training to remediate cognitive deficits related to psychological factors?

With regard to the first question, nicotine once again appears to be a likely candidate, given its previously described psychopharmacological action. In this case, it may be that nicotine simply acts to relieve cognitive symptoms associated with depression, or it may be that cigarette smoking exerts a more general antidepressant effect, enhancing cognitive function by acting on the disease process itself. What is needed is research that can disentangle the specific effect of nicotine from other components of cigarette smoke that may be influencing depression. With regard to the implications for cognitive rehabilitation, if cigarette smoking is complicating a physical disease (e.g., CVD or COPD) yet is also being used by the individual as a way to mediate cognitive problems associated with depression or personality style, efforts to address and/or replace this role should be made prior to attempting smoking cessation. As more research emerges, it may be that nicotine-like compounds (e.g., nicotine agonists) will become increasingly important in the development of more efficacious pharmacological treatments for psychiatric illnesses such as depression.

Summary and Implications

This chapter has examined the potential short- and long-term roles that cigarette smoking may play in cognitive functioning in late life. An explanatory model was created to provide a framework to organize the empirical literature related to this issue. It is without question that habituation to cigarette smoking occurs even in short-term smokers, and that quitting smoking is a difficult undertaking. It may be that cognitive factors play a mediating role in enhancing the addictive potential of cigarettes by creating a false perception that smoking is critical for optimal cognitive function. Further, the direct impact that cigarette smoking has on cognitive function has been explored in terms of the short- and long-term effects of nicotine on the CNS. Although considerable evidence suggests that nicotine can have cognitive enhancing effects, it remains unclear whether cigarette-delivered nicotine can produce objective (and reliable) short-term gains in cognitive function. In the presence of disease, cigarette smoking exacerbates disease processes as has been shown in CVD and COPD, both of which are linked to diminished cognitive function. Thus, cigarette smoking may play an indirect role in cognitive decline by accelerating disease progression. The

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cumulative effect of cigarette smoking on cerebral vascular disease provides a potential test of this logic by demonstrating significant functional and structural declines in the brains of older smokers in comparison to nonsmokers.

A major goal of this chapter has been to link research on cognitive processes in old age and cigarette smoking to issues in cognitive rehabilitation. To this end, we have highlighted the following:

  • Short-term losses in cognitive function from nicotine withdrawal as part of the quitting process could put older smokers into a vicious relapse cycle. Rehabilitation counselors could anticipate this issue by providing education and compensatory strategy training. We also examined how everyday activities, such as driving, may be affected by the interaction of cigarette smoking and cognitive functioning and have recommended further research on this issue.

  • Compensatory interventions such as physical exercise and memory training may be useful for older smokers who are experiencing cognitive deficits associated with a chronic disease state. These strategies may also be important components in comprehensive smoking cessation planning to offset cognitive losses associated with smoking cessation in the presence of disease. Such interventions may help the individual to refocus the experience of cognitive loss as a transitory process in improving health through smoking cessation.

  • Research examining nicotine as a cognitive enhancer in AD and, to a lesser extent, in depression introduces the potential use of nicotinic compounds in the treatment of these, as well as other, diseases of aging.

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Cognitive Rehabilitation in Old Age
Cognitive Rehabilitation in Old Age
ISBN: 0195119851
EAN: 2147483647
Year: 2000
Pages: 18

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