Beliefs about benefits and harms of medications and supplements for brain health.

The role of medications and supplements for brain health is a fast-changing and growing field, making it difficult for patients to receive updated and accurate information. The objective of this study was to assess patients' beliefs about the helpfulness or harmfulness of various medications and supplements on brain health. A convenience sample of adults from an integrated healthcare system completed a web-based survey. Descriptive statistics were used for this hypothesis-generating study. A total of 1661 respondents completed the survey. The majority of respondents were female (77%), between the ages of 51-70 (64%), and white (89%). Across the selected medications and supplements purported to improve a person's brain health (vitamin E, ginkgo biloba, hormones such as estrogen or testosterone, fish oil, and statins), 46-64% of respondents reported not knowing or skipped the item regarding their helpfulness to improve brain health. One out of four respondents reported benefits of vitamin E and nearly half reported benefits of fish oil on brain health; neither benefit is supported by current evidence. For the two medication classes evaluated for increasing dementia risk (proton pump inhibitors and anticholinergics used as sleep aids), 63-77% of respondents reported not knowing or skipped the item regarding their harmfulness to brain health. Survey respondents largely reported not knowing the potential benefits and harms of different medications and supplements for brain health. Improved health communication on pharmaceutical effects on dementia risk is greatly needed, and its development and dissemination should involve healthcare providers, patients, and media outlets.

Patterns of antihypertensive and statin adherence prior to dementia: findings from the adult changes in thought study.

BACKGROUND: Detecting patients with undiagnosed dementia is an important clinical challenge. Changes in medication adherence might represent an early sign of cognitive impairment. We sought to examine antihypertensive and statin adherence trajectories in community-dwelling older adults, comparing people who went on to develop dementia to those who did not. METHODS: We analyzed data from Adult Changes in Thought (ACT), a population-based cohort study embedded within an integrated healthcare delivery system. Analyses included 4368 participants aged ≥65 years who had at least one follow-up visit. Research-quality dementia diagnoses were used to identify cases. We selected non-dementia control visits matched on age, sex, and study cohort that occurred at similar ACT follow-up time as the case's dementia onset; we treated this as the index date. Participants were included if they were prevalent users of either a statin or antihypertensive medication on the first day of follow up - 3 years prior to the index date. Using prescription fill dates and days supply, we calculated daily binary medication availability measures for each participant ('days covered') over 3 years leading up to the index date. We used group-based trajectory models to identify patterns of antihypertensive and statin adherence, and used conditional logistic regression to examine associations between adherence trajectories and dementia. RESULTS: Four trajectories were identified for antihypertensive users (292 cases, 3890 control visits), including near perfect (n = 1877, 36.6% cases, 45.5% controls), high (n = 1840, 43.2% cases, 44.1% controls), moderate (n = 365, 18.5% cases, 8.0% controls) and early poor adherence (n = 100, 1.7% cases, 2.4% controls). Odds of dementia was 3 times greater for those with moderate antihypertensive adherence compared to those with near perfect adherence (adjusted OR 3.0, 95% CI 2.0, 4.3). Four trajectories were identified for statin users (148 cases, 1131 control visits), including high (n = 1004, 75.0% cases, 79.0% controls), moderate (n = 192, 19.6% cases, 14.4% controls), early poor (n = 43, 2.0% cases, 3.5% controls), and delayed poor adherence (n = 40, 3.4% cases, 3.1% controls). No association was detected between statin adherence trajectories and dementia. CONCLUSIONS: Patterns of medication adherence may be useful to identify a subset of people at higher likelihood of developing dementia.

Brain Health and Dementia Prevention: A Mixed-method Analysis.

Objective: In this study, we assessed patient knowledge, beliefs, and attitudes about brain health and strategies for Alzheimer's disease and related dementias (ADRD) prevention. Methods: We administered a Web-based survey consisting of 17 questions about brain health and strategies for ADRD prevention in a convenience sample of 1661 patients in an integrated healthcare delivery system in Washington state between February and March 2018. We calculated frequency distributions of the quantitative data and conducted inductive content analysis of qualitative data. Results: Most respondents were female (77%), 51-70 years of age (64%), and white (89%). Although most agreed it is possible to improve brain health and reduce personal ADRD risk, one- third lacked confidence that they could take action to reduce personal ADRD risk. Participants' responses to open-ended questions revealed 10 themes grouped into 3 organizing categories regarding their perceptions about how to prevent ADRD onset: (1) understand ADRD; (2) stay engaged; and (3) manage one's own health and healthcare. Conclusions: Survey respondents were engaged and aware of dementia prevention, but they lacked access to personally action- able evidence..

Patterns of Dementia Treatment and Frank Prescribing Errors in Older Adults With Parkinson Disease.

Importance: Dementia is common in Parkinson disease, but few data exist on dementia treatment patterns or the concurrent use of acetylcholinesterase inhibitors (ACHEIs) and anticholinergic medications, a frank prescribing error. Objectives: To describe dementia treatment patterns, and to determine the extent to which the concurrent use of ACHEIs and drugs with strong anticholinergic activity occurs among individuals with Parkinson disease in the United States. Design, Setting, and Participants: This cross-sectional analysis included adult Medicare beneficiaries (aged 65 years or older) with Parkinson disease diagnosis with 12 consecutive months of inpatient, outpatient, and prescription drug coverage from January 1, 2014, through December 31, 2014. Beneficiaries with other parkinsonian syndromes were excluded. Demographic, geographic, prescription claims, and other data were extracted from the 2014 Carrier, Beneficiary Summary, and Prescription Drug Event research identifiable files of the Centers for Medicare & Medicaid Services. Data analysis was conducted from August 1, 2017, to November 30, 2017. Main Outcomes and Measures: Primary outcomes were use of dementia drug, specific dementia medication, and concurrent exposure to a high-potency anticholinergic drug and an ACHEI. Descriptive analyses and multivariable logistic regression models determined the extent to which patient characteristics and comorbid conditions were associated with dementia treatment or with a high-potency anticholinergic and ACHEI never event. Results: Of 268 407 Medicare beneficiaries with Parkinson disease (mean [SD] age, 78.9 [7.5]; 134 575 male [50.1%]), most were identified in the files as white (232 831 [86.7%]), followed by black (14 629 [5.5%]), Hispanic (7176 [2.7%]), Asian (7115 [2.7%]), and Native American (874 [0.3%]). Among these beneficiaries, 73 093 (27.2%) were given a prescription for at least 1 antidementia medication. The most commonly prescribed medication was donepezil hydrochloride (46 027 [63.0%] users), followed by memantine hydrochloride (30 578 [41.8%] users) and rivastigmine tartrate (19 278 [26.4%] users). Dementia drugs were more likely to be prescribed to black (adjusted odds ratio [AOR], 1.33; 95% CI, 1.28-1.38) and Hispanic (AOR, 1.28; 95% CI, 1.22-1.35) beneficiaries and less likely for Native American beneficiaries (AOR, 0.62; 95% CI, 0.51-0.74). Women were less likely than men to be given a prescription for dementia medication (AOR, 0.85; 95% CI, 0.84-0.87). Of the 64 017 beneficiaries receiving an ACHEI, 28 495 (44.5%) experienced at least 1 high-potency anticholinergic-ACHEI event. Hispanic (AOR, 1.11; 95% CI, 1.00-1.23) and women (AOR, 1.30; 95% CI, 1.25-1.35) beneficiaries had greater odds of experiencing this never event. Statistically significant clusters of the prevalence of this prescribing error were observed across the United States (Moran I = 0.24; P < .001), with clusters of high prevalence in the southern and midwestern states. Conclusions and Relevance: Dementia medication use by persons with Parkinson disease varies by race/ethnicity and sex; potentially inappropriate prescribing is common among those being treated for cognitive impairment and varies by race/ethnicity, sex, and geography. These findings may serve as national and local targets for improving care quality and outcomes for persons with Parkinson disease.

Cumulative Antidepressant Use and Risk of Dementia in a Prospective Cohort Study.

OBJECTIVES: To determine whether antidepressant use is associated with dementia risk. DESIGN: Prospective cohort study. SETTING: Kaiser Permanente Washington (KPWA), an integrated healthcare delivery system. PARTICIPANTS: Community-dwelling individuals aged 65 and older without dementia and with 10 years or more of KPWA enrollment at baseline (N=3,059). MEASUREMENTS: Primary exposures were selective serotonin reuptake inhibitors (paroxetine vs other), tricyclic antidepressants, and serotonin antagonist and reuptake inhibitors. Using health plan pharmacy data, we calculated cumulative medication exposure, defined as total standardized daily doses (TSDDs), over rolling 10-year windows. Exposure in the most recent year was excluded to avoid use related to prodromal symptoms. The Cognitive Abilities Screening Instrument was administered every 2 years; low scores triggered clinical evaluation and consensus diagnosis procedures. Dementia risk was estimated according to medication use using Cox proportional hazards models. RESULTS: During a mean follow-up of 7.7 years, 775 participants (25%) developed dementia; 659 (22%) developed possible or probable Alzheimer's disease. Individual antidepressant classes were not associated with differences in dementia risk, although paroxetine use was associated with higher risk of dementia for all TSDD categories than no use (0-90 TSDDs: hazard ratio (HR)=1.69, 95% confidence interval (CI)=1.18-2.42; 91-365 TSDDs: HR=1.40, 95% CI=0.88-2.23; 366-1095 TSDDs: HR=2.13, 95% CI=1.32-3.43; ≥1095 TSDDs: HR=1.42, 95% CI=0.82-2.46). CONCLUSION: Most commonly prescribed nonanticholinergic depression medications used in late life do not appear to be associated with dementia risk. Paroxetine and other anticholinergic antidepressants may be exceptions in older individuals. Future studies are warranted to improve scientific understanding of potential associations in other settings and populations.

Proton Pump Inhibitor Use and Dementia Risk: Prospective Population-Based Study.

OBJECTIVES: To determine whether higher cumulative proton pump inhibitor (PPI) exposure is associated with greater dementia risk. DESIGN: Prospective population-based cohort study. SETTING: Kaiser Permanente Washington, an integrated healthcare delivery system in Seattle, Washington. PARTICIPANTS: Individuals aged 65 and older without dementia at study entry (N = 3,484). MEASUREMENTS: Participants were screened for dementia every 2 years, and those who screened positive underwent extensive evaluation. Dementia outcomes were determined using standard diagnostic criteria. Time-varying PPI exposure was determined from computerized pharmacy data and consisted of total standardized daily doses (TSDDs) dispensed to an individual in the prior 10 years. We also assessed duration of use. Multivariable Cox regression was used to estimate the association between PPI exposure and time to dementia or Alzheimer's disease (AD). RESULTS: Over a mean follow-up of 7.5 years, 827 participants (23.7%) developed dementia (670 with possible or probable AD). PPI exposure was not associated with risk of dementia (P = .66) or AD (P = .77). For dementia, the risk for specific levels of cumulative exposure compared to no use was: 365 TSDDs (HR 0.87, 95% CI 0.65-1.18), 1,095 TSDDs (HR 0.99, CI 0.75-1.30) and 1,825 TSDDs (HR 1.13, CI 0.82-1.56). These TSDD levels represent approximately 1, 3 and 5 years of daily use respectively. Duration of PPI use was not associated with dementia outcomes either. CONCLUSION: Proton pump inhibitor use was not associated with dementia risk, even for people with high cumulative exposure. Although there are other safety concerns with long-term PPI use, results from our study do not support that these medications should be avoided out of concern about dementia risk.

Anesthesia Exposure and Risk of Dementia and Alzheimer's Disease: A Prospective Study.

OBJECTIVES: To evaluate the associations between anesthesia and dementia or Alzheimer's disease (AD) risk using prospectively collected data. DESIGN: Cohort study. PARTICIPANTS: Community-dwelling members of the Adult Changes in Thought cohort aged 65 and older and free of dementia at baseline (N = 3,988). MEASUREMENTS: Participants self-reported all prior surgical procedures with general or neuraxial (spinal or epidural) anesthesia at baseline and reported new procedures every 2 years. People undergoing high-risk surgery with general anesthesia, other surgery with general anesthesia, and other surgery with neuraxial anesthesia exposures were compared with those with no surgery and no anesthesia. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for dementia and AD associated with time-varying lifetime and recent (past 5 years) anesthesia exposures. RESULTS: At baseline, 254 (6%) people reported never having anesthesia; 248 (6%) had had one or more high-risk surgeries with general anesthesia, 3,363 (84%) had had one or more other surgeries with general anesthesia, and 123 (3%) had had one or more surgeries with neuraxial anesthesia. High-risk surgery with general anesthesia was not associated with greater risk of dementia (HR = 0.86, 95% CI = 0.58-1.28) or AD (HR = 0.95, 95% CI = 0.61-1.49) than no history of anesthesia. People with any history of other surgery with general anesthesia had a lower risk of dementia (HR = 0.63, 95% CI = 0.46-0.85) and AD (HR = 0.65, 95% CI = 0.46-0.93) than people with no history of anesthesia. There was no association between recent anesthesia exposure and dementia or AD. CONCLUSION: Anesthesia exposure was not associated with of dementia or AD in older adults.

Benzodiazepine use and risk of incident dementia or cognitive decline: prospective population based study.

OBJECTIVE: To determine whether higher cumulative use of benzodiazepines is associated with a higher risk of dementia or more rapid cognitive decline. DESIGN: Prospective population based cohort. SETTING: Integrated healthcare delivery system, Seattle, Washington. PARTICIPANTS: 3434 participants aged ≥ 65 without dementia at study entry. There were two rounds of recruitment (1994-96 and 2000-03) followed by continuous enrollment beginning in 2004. MAIN OUTCOMES MEASURES: The cognitive abilities screening instrument (CASI) was administered every two years to screen for dementia and was used to examine cognitive trajectory. Incident dementia and Alzheimer's disease were determined with standard diagnostic criteria. Benzodiazepine exposure was defined from computerized pharmacy data and consisted of the total standardized daily doses (TSDDs) dispensed over a 10 year period (a rolling window that moved forward in time during follow-up). The most recent year was excluded because of possible use for prodromal symptoms. Multivariable Cox proportional hazard models were used to examine time varying use of benzodiazepine and dementia risk. Analyses of cognitive trajectory used linear regression models with generalized estimating equations. RESULTS: Over a mean follow-up of 7.3 years, 797 participants (23.2%) developed dementia, of whom 637 developed Alzheimer's disease. For dementia, the adjusted hazard ratios associated with cumulative benzodiazepine use compared with non-use were 1.25 (95% confidence interval 1.03 to 1.51) for 1-30 TSDDs; 1.31 (1.00 to 1.71) for 31-120 TSDDs; and 1.07 (0.82 to 1.39) for ≥ 121 TSDDs. Results were similar for Alzheimer's disease. Higher benzodiazepine use was not associated with more rapid cognitive decline. CONCLUSION: The risk of dementia is slightly higher in people with minimal exposure to benzodiazepines but not with the highest level of exposure. These results do not support a causal association between benzodiazepine use and dementia.

Prescription Opioids and Risk of Dementia or Cognitive Decline: A Prospective Cohort Study.

OBJECTIVES: To determine whether prescription opioid use is associated with higher dementia risk or greater cognitive decline. DESIGN: Prospective cohort study. SETTING: Group Health, an integrated healthcare delivery system. PARTICIPANTS: Community-dwelling individuals aged 65 and older without dementia with at least 10 years of Group Health enrollment at baseline (N = 3,434; median age 74). MEASUREMENTS: The Cognitive Abilities Screening Instrument (CASI) was administered every 2 years. Low scores triggered detailed evaluation, and a multidisciplinary committee assigned dementia diagnoses. From computerized pharmacy data, cumulative opioid exposure was defined as total standardized doses (TSDs) dispensed over 10 years (excluding the most recent year because of possible prodromal symptoms). For comparison, use of nonsteroidal anti-inflammatory drugs (NSAIDs), characterized similarly, was examined. Dementia risk was analyzed using Cox proportional hazards models and CASI trajectory using linear regression models and generalized estimating equations. RESULTS: Seven hundred ninety-seven participants (23%) developed dementia over a mean follow-up of 7.3 years; 637 (19%) had possible or probable Alzheimer's disease. For cumulative opioid use, the hazard ratios (HRs) for dementia were 1.06 (95% confidence interval (CI) = 0.88-1.26) for 11 to 30 TSDs, 0.88 (95% CI = 0.70-1.09) for 31 to 90 TSDs, and 1.29 (95% CI = 1.02-1.62) for 91 or more TSDs, versus 0 to 10 TSDs. A similar pattern was seen for NSAID use. Heavier opioid use was not associated with more-rapid cognitive decline. CONCLUSION: People with the heaviest opioid or NSAID use had slightly higher dementia risk than people with little or no use. These results may reflect an effect of chronic pain on cognition or residual confounding. Although opioids have other risks, little evidence of long-term cognitive harm specific to opioids was found.

Cumulative use of strong anticholinergics and incident dementia: a prospective cohort study.

IMPORTANCE: Many medications have anticholinergic effects. In general, anticholinergic-induced cognitive impairment is considered reversible on discontinuation of anticholinergic therapy. However, a few studies suggest that anticholinergics may be associated with an increased risk for dementia. OBJECTIVE: To examine whether cumulative anticholinergic use is associated with a higher risk for incident dementia. DESIGN, SETTING, AND PARTICIPANTS: Prospective population-based cohort study using data from the Adult Changes in Thought study in Group Health, an integrated health care delivery system in Seattle, Washington. We included 3434 participants 65 years or older with no dementia at study entry. Initial recruitment occurred from 1994 through 1996 and from 2000 through 2003. Beginning in 2004, continuous replacement for deaths occurred. All participants were followed up every 2 years. Data through September 30, 2012, were included in these analyses. EXPOSURES: Computerized pharmacy dispensing data were used to ascertain cumulative anticholinergic exposure, which was defined as the total standardized daily doses (TSDDs) dispensed in the past 10 years. The most recent 12 months of use was excluded to avoid use related to prodromal symptoms. Cumulative exposure was updated as participants were followed up over time. MAIN OUTCOMES AND MEASURES: Incident dementia and Alzheimer disease using standard diagnostic criteria. Statistical analysis used Cox proportional hazards regression models adjusted for demographic characteristics, health behaviors, and health status, including comorbidities. RESULTS: The most common anticholinergic classes used were tricyclic antidepressants, first-generation antihistamines, and bladder antimuscarinics. During a mean follow-up of 7.3 years, 797 participants (23.2%) developed dementia (637 of these [79.9%] developed Alzheimer disease). A 10-year cumulative dose-response relationship was observed for dementia and Alzheimer disease (test for trend, P < .001). For dementia, adjusted hazard ratios for cumulative anticholinergic use compared with nonuse were 0.92 (95% CI, 0.74-1.16) for TSDDs of 1 to 90; 1.19 (95% CI, 0.94-1.51) for TSDDs of 91 to 365; 1.23 (95% CI, 0.94-1.62) for TSDDs of 366 to 1095; and 1.54 (95% CI, 1.21-1.96) for TSDDs greater than 1095. A similar pattern of results was noted for Alzheimer disease. Results were robust in secondary, sensitivity, and post hoc analyses. CONCLUSIONS AND RELEVANCE: Higher cumulative anticholinergic use is associated with an increased risk for dementia. Efforts to increase awareness among health care professionals and older adults about this potential medication-related risk are important to minimize anticholinergic use over time.

Frailty and incident dementia.

BACKGROUND: We sought to examine whether frailty is associated with dementia, Alzheimer's disease (AD), and non-AD dementia risk. METHODS: This is a prospective population-based cohort derived from an integrated health maintenance organization. The sample consisted of 2,619 participants aged 65 and older without dementia at baseline followed from 1994 to 2010. Frailty was defined as having at least 3 of the following criteria: weakness (grip strength), slowness (walking speed), weight loss, low physical activity, and self-reported exhaustion. Follow-up occurred every 2 years to identify incident dementia, possible or probable AD, and non-AD dementia using standard research criteria. Covariates came from self-report and study measures. We used adjusted Cox proportional hazards models to examine the association between frailty and each outcome. RESULTS: Over a mean follow-up of 6.5 years, 521 participants developed dementia (of which 448 developed AD). In the model adjusted for age, sex, education, and race, the hazard ratio for frailty was 1.78 (95% confidence interval [CI] 1.32-2.40). In the fully adjusted models, the hazard ratio for frailty was 1.20 for all-cause dementia (95% CI 0.85-1.69), 1.08 for AD (95% CI 0.74-1.57), and 2.57 for non-AD dementia (95% CI 1.08-6.11). For all-cause dementia, we found an interaction between baseline cognitive score and frailty (p = .02); hazard ratio for frailty was 1.78 for those with higher global cognition (95% CI 1.14-2.78) and 0.79 for those with lower global cognition (95% CI 0.50-1.26). CONCLUSION: Frailty was associated with dementia when adjusting only for demographic variables but not in the fully adjusted model. Frailty was associated with higher risk of developing non-AD dementia but not AD. Although frailty was not associated with all-cause dementia in the entire sample, an association did exist in participants with higher cognitive scores. Mechanisms underlying these associations remain to be elucidated.

Histamine-2 receptor antagonist use and incident dementia in an older cohort.

OBJECTIVES: To examine whether histamine-2 receptor antagonist medications (H2RAs) are associated with a lower incidence of all-cause dementia or Alzheimer's disease (AD), as some studies have suggested. DESIGN: Prospective population-based cohort SETTING: Group Health, an integrated health maintenance organization, Seattle, Washington. PARTICIPANTS: Two thousand nine hundred twenty-three participants aged 65 and older without dementia at baseline, with initial recruitment between 1994 and 1996. MEASUREMENTS: Follow-up occurred every 2 years to identify incident dementia and AD using standard criteria. Exposure to H2RAs was determined based on automated pharmacy data. Three aspects of exposure (time-varying) were examined based on standard daily dose (SDD): cumulative use, intensity of use (highest SDD in any prior 2-year window), and cumulative use stratified according to recency (1-3 years vs >3 years before). RESULTS: Over a mean follow-up of 6.7 years, 585 subjects developed dementia (453 developed AD). Total cumulative exposure was not associated with dementia (P=.35; omnibus test) or AD (P=.23). The adjusted hazard ratios for the highest exposure category (>1,080 SDDs) compared with light or no use were 1.28 (95% confidence interval (CI)=0.95-1.72) for dementia and 1.41 (95% CI=1.00-1.97) for AD. Intensity of use was not associated with dementia (P=.39) or AD (P=.63). Examining exposure according to recent and distant cumulative use also showed no association with dementia (P=.11) or AD (P=.30). CONCLUSION: No association was found between H2RA use and risk of all-cause dementia or AD using more-detailed and -extensive information about past H2RA use than any prior study.

Antioxidant vitamin supplement use and risk of dementia or Alzheimer's disease in older adults.

OBJECTIVES: To examine whether use of vitamins C or E alone or in combination was associated with lower incidence of dementia or Alzheimer's disease (AD). DESIGN: Prospective cohort study. SETTING: Group Health Cooperative, Seattle, Washington. PARTICIPANTS: Two thousand nine hundred sixty-nine participants aged 65 and older without cognitive impairment at baseline in the Adult Changes in Thought study. MEASUREMENTS: Participants were followed biennially to identify incident dementia and AD diagnosed according to standard criteria. Participants were considered to be users of vitamins C or E if they self-reported use for at least 1 week during the month before baseline. RESULTS: Over a mean follow-up+/-standard deviation of 5.5+/-2.7 years, 405 subjects developed dementia (289 developed AD). The use of vitamin E was not associated with dementia (adjusted hazard ratio (HR)=0.98, 95% confidence interval (CI)=0.77-1.25) or with AD (HR=1.04; 95% CI=0.78-1.39). No association was found between vitamin C alone (dementia: HR=0.90, 95% CI=0.71-1.13; AD: HR=0.95, 95% CI=0.72-1.25) or concurrent use of vitamin C and E (dementia: HR=0.93, 95% CI=0.72-1.20; AD: HR=1.00, 95% CI=0.73-1.35) and either outcome. CONCLUSION: In this study, the use of supplemental vitamin E and C, alone or in combination, did not reduce risk of AD or overall dementia over 5.5 years of follow-up.

Dementia and Alzheimer's disease in community-dwelling elders taking vitamin C and/or vitamin E.

BACKGROUND: Since increased oxidative stress may impair cognition and be a risk factor for dementia, there has been interest in determining whether use of antioxidants could protect against such events. OBJECTIVE: To determine whether supplement use of vitamins C and/or E in a community-based sample of older African American and white individuals delayed incident dementia or Alzheimer's disease (AD). METHODS: We selected a subgroup from the Duke Established Populations for Epidemiologic Studies of the Elderly, a longitudinal study of community-representative persons aged 65-105 years living in 5 adjacent counties in North Carolina, and followed them for dementia (1986-1987 through June 2000). Information gathered during in-home interviews included sociodemographic characteristics, health status, health service use, and vitamin use. Diagnosis of dementia and AD was based on evaluations using the clinical and neuropsychological batteries of the Consortium to Establish a Registry for Alzheimer's Disease, with final determination by consensus agreement of specialists using Diagnostic and Statistical Manual of Mental Disorders, third revision, and National Institute for Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders criteria. RESULTS: Of 616 persons initially dementia-free (mean age 73 y; 62% female; 62% African American), 141 developed dementia, of whom 93 developed AD. Increased age and mobility problems were risk factors for dementia (only age for AD), while an increased number of outpatient visits reduced the likelihood of developing dementia. Neither use of any vitamins C and/or E (used by 8% of subjects at baseline) nor high-dose use reduced the time to dementia or AD. CONCLUSIONS: In this community in the southeastern US where vitamin supplement use is low, use of vitamins C and/or E did not delay the incidence of dementia or AD.

Risks for frequent antimicrobial-treated infections in postmenopausal women.

BACKGROUND AND AIMS: Infections are a major cause of morbidity and mortality in older adults. Little is known about factors that alter the susceptibility to infection in the older population. This study in postmenopausal women examines health-related conditions and behavioral factors that may increase the risk of frequent infections, defined as having, on average, one or more infections per year. METHODS: A prospective cohort study with 5 years of follow-up was conducted in 1320 women aged 55 to 80 years. The subjects were Group Health Cooperative of Puget Sound (GHC) enrollees screened for a large fracture prevention trial who also participated in a survey of dietary and supplemental vitamin use. The main outcome, total number of infection events per subject, was derived from a new method of identifying outpatient infections based on the antimicrobial prescription fills recorded in GHC automated pharmacy records. RESULTS: Prevalent lung disease (OR = 6.1, 95% CI 2.8-13.4), receiving a prescription for vitamin C (OR = 2.1, 95% CI 1.4-3.4), and the second and third tertiles of the Chronic Disease Score (OR = 1.7, 95% CI 1.1-2.7 and OR = 2.4, 95% CI 1.5-3.9, respectively) were associated with 5 or more antimicrobial-treated infections during follow-up. A body mass index (BMI) of less than 22 kg/m2 (OR = 0.6, 95% CI 0.3-1.0) was suggestive of an association. CONCLUSIONS: The study provides new information on risk factors for outpatient infections and raises new questions regarding the susceptibility to frequent infections in older women. In addition, the automated pharmacy record method used in this study offers a low-cost alternative for use in future epidemiologic research.

Is antioxidant use protective of cognitive function in the community-dwelling elderly?

BACKGROUND: The role of oxidative stress in the pathogenesis of diseases such as macular degeneration, certain types of cancer, and Alzheimer's disease has received much attention. Thus, there is considerable interest in the potential contribution of antioxidants to the prevention of these diseases. OBJECTIVE: The objective of this study was to determine whether use of supplemental antioxidants (vitamins A, C, or E, plus selenium or zinc) was associated with a reduced risk of development of cognitive impairment or cognitive decline in a representative sample of the community-dwelling elderly. METHODS: The sample consisted of 2082 nonproxy subjects from the Duke Established Populations for Epidemiologic Studies of the Elderly who were not cognitively impaired at the 1989-1990 interview (baseline for the present analysis). Medication use was determined during in-home interviews. Cognitive function was assessed 3 and 7 years from baseline in terms of incident cognitive impairment, as measured on the Short Portable Mental Status Questionnaire (SPMSQ) using specific cut points (number of errors) based on race and education, and cognitive decline, defined as an increase of > or = 2 errors on the SPMSQ. Multivariate analyses were performed using weighted data adjusted for sampling design and controlled for sociodemographic characteristics, health-related behaviors, and health status. RESULTS: At baseline, 224 (10.8%) subjects were currently taking a supplement containing an antioxidant. During the follow-up period, 24.0% of subjects developed cognitive impairment and 34.5% experienced cognitive decline. Current antioxidant users had a 34.0% lower risk of developing cognitive impairment compared with non-antioxidant users (adjusted relative risk [RR], 0.66; 95% CI, 0.44-1.00) and a 29.0% lower risk of experiencing cognitive decline (adjusted RR, 0.71; 95% CI, 0.49-1.01). CONCLUSION: The results of this analysis suggest a possible beneficial effect of antioxidant use in terms of reducing cognitive decline among the community-dwelling elderly.