Age-associated cognitive changes in community dwelling adults

最近的研究表明，咖啡因的摄入可以降低患抑郁症和认知能力下降的风险。然而，没有研究将非裔美国人与社会经济多样化的白人代表性城市样本进行比较。研究人员利用来自“生命多样性社区健康老龄化”（HANDLS）研究的数据，对1724名参与者的样本进行研究，以确定咖啡因摄入与抑郁症状和认知的关系。经过培训的采访者使用美国农业部的自动多次通过方法收集了两次24小时的面对面饮食召回。抑郁症状和整体认知分别使用两种有效的测量方法进行评估：流行病学研究中心抑郁量表（CES-D）和迷你精神状态检查（MMSE）。通常的咖啡因摄入量是基于两种回忆。数据分析采用t检验、卡方检验、相关分析和有序逻辑回归。结果：非洲裔美国人摄入的咖啡因明显少于白人（分别为890 -3.2毫克和244.0-8.7毫克）。咖啡因摄入与抑郁症状或整体认知无关。年龄、低于五年级的文化水平和低于高中教育程度与抑郁症状和认知功能显著相关。吸烟者患抑郁症的风险高出43%，但患认知障碍的风险仅高出3%。在HANDLS研究参与者中，低水平的饮食咖啡因摄入加上吸烟可能影响了与抑郁症状或整体认知缺乏联系。在这个样本中，低文化水平和受教育程度与抑郁症状和认知功能的关系似乎比咖啡因摄入更密切。

Recent research has linked caffeine consumption with a lower risk for depression and cognitive decline. However, no studies have examined the relationship in an African American compared to a white, socioeconomically diverse representative urban sample. Data from the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) study were used to determine the associations of caffeine use with depressive symptomatology and cognition in a sample of 1,724 participants. The United States Department of Agriculture's Automated Multiple Pass Method was used by trained interviewers to collect two, in-person 24-hour dietary recalls. Depressive symptoms and global cognition were assessed using two well-validated measures: the Center for Epidemiologic Studies Depressive Scale (CES-D) and Mini Mental State Examination (MMSE), respectively. Usual caffeine intake was based on both recalls. Data were analyzed with t- and chi-square tests, correlation analysis, and ordinal logistic regression. Results: African Americans consumed significantly less caffeine than did whites (89.0-3.2 and 244.0-8.7 mg respectively). Caffeine consumption was not associated with depressive symptomatology or global cognition. Age, less than 5th grade literacy, and less than high school education were significantly associated with both depressive symptoms and cognitive function. Smokers had a 43% greater risk for depression but only a 3% higher risk for cognitive impairment. The low level of dietary caffeine intake in combination with smoking among HANDLS study participants may have influenced the lack of association with depressive symptomatology or global cognition. For this sample, low literacy and education appear more highly associated with depressive symptoms and cognitive function than caffeine intake. In a second study, we examined whether race and poverty (income <125% of the federal poverty limit), modifies associations between diabetes and cognition in a biracial, urban-dwelling sample.: Using cross-sectional data for 2066 participants (mean age = 47.6 years, 56.8% women, 56.2% African American, 38.6% below poverty) from the first wave of the Healthy Aging in Neighborhoods of Diversity across the Life Span study, interactions among diabetes, race, and poverty status with eleven tests measured cognitive function were assessed in multiple regression analyses. Significant interactions among diabetes, race, and poverty status were observed. Among African Americans below poverty, diabetic individuals performed lower than non-diabetic individuals on California Verbal Learning Test Free Recall Short Delay (z = -0.444 0.123 versus z = -0.137 0.045) and Long Delay (z = -0.299 0.123 versus z = -0.130 0.045), Digit Span Backward (z = -0.347 0.109 versus z = -0.072 0.041), and the Brief Test of Attention (z = -0.452 -0.099 versus z = -0.099 0.047), and higher on Category Fluency (z = 0.114 0.117 versus z = -0.118 0.044). No consistent differences between diabetic and non-diabetic individuals were found for African American and white participants above poverty. Diabetes was associated with poorer verbal memory, working memory, and attention among African Americans living in poverty. Diabetic African Americans below poverty may have increased risk of cognitive deficit at a younger age. Improving health literacy, doctor-patient communication, and multidisciplinary medical care for impoverished individuals may reduce differences. Additional research is needed to clarify mechanisms underlying these associations. In a third study, we examined whether dietary antioxidants can inhibit reactions accompanying neurodegeneration and thus prevent cognitive impairment. We describe associations of dietary antioxidants with cognitive function in a large biracial population, while testing moderation by sex, race, and age and mediation by depressive symptoms. This was a cross-sectional analysis of 1274 adults (541 men and 733 women) aged 30 to 64 years at baseline (mean standard deviation = 47.5 9.3) in the Healthy Aging in Neighborhoods of Diversity Across the Lifespan Study, Baltimore city, MD. Cognitive performance in the domains of memory, language/verbal, attention, spatial, psychomotor speed, executive function, and global mental status were assessed. The 20-item Center for Epidemiologic Studies Depression Scale was used to measure depressive symptoms. Dietary intake was assessed with two 24-hour recalls, estimating daily consumption of total carotenoids and vitamins A, C, and E per 1000 kcal. Among key findings, 1 standard deviation ( approximately 2.02 mg/1000 kcal) higher vitamin E was associated with a higher score on verbal memory, immediate recall (beta = +0.64 0.19, p = .001), and better language/verbal fluency performance (beta = +0.53 0.16, p = .001), particularly among the younger age group. Women with higher vitamin E intake (beta = +0.68 0.21, p = .001) had better performance on a psychomotor speed test. The vitamin E-verbal memory association was partially mediated by depressive symptoms (proportion mediated = 13%-16%). In sum, future cohort studies and dietary interventions should focus on associations of dietary vitamin E with cognitive decline, specifically for domains of verbal memory, verbal fluency, and psychomotor speed.