Cognitive function in a middle aged cohort is related to higher quality dietary pattern 5 and 25 years earlier: the CARDIA study.

BACKGROUND: Preserving cognitive function is an important public health issue. We investigated whether dietary pattern associates with cognitive function in middle-age. METHODS: We studied 2435 participants in the community-based Coronary Artery Risk Development in Young Adults (CARDIA) study of black and white men and women aged 18-30 in 1985-86 (year 0, Y0). We hypothesized that a higher A Priori Diet Quality Score, measured at Y0 and Y20, is associated with better cognitive function measured at Y25. The diet score incorporated 46 food groups (each in servings/day) as the sum of quintile ranks of food groups rated beneficial, 0 for food groups rated neutral, and reversed quintile ranks for food groups rated adverse; higher score indicated better diet quality. Y25 cognitive testing included verbal memory (Rey Auditory-Verbal Learning Test (RAVLT)), psychomotor speed (Digit Symbol Substitution Test (DSST)) and executive function (Stroop). RESULTS: Per 10-unit higher diet score at Y20, the RAVLT was 0.32 words recalled higher, the DSST was 1.76 digits higher, and the Stroop was 1.00 seconds+errors lower (better performance) after adjusting for race, sex, age, clinic, and energy intake. Further adjustment for physical activity, smoking, education, and body mass index attenuated the association slightly. Diet score at Y0 and increase in diet score over 20 years were also positively associated with each cognitive test. CONCLUSIONS: A higher quality dietary pattern was associated with better cognitive function 5 years and even 25 years later in apparently healthy middle-aged adults.

An update on type 2 diabetes, vascular dementia and Alzheimer's disease.

The risk of dementia is increased in people with type 2 diabetes mellitus (T2DM). This review gives an update on the relation between T2DM and specific dementia subtypes - i.e. Alzheimer's disease and vascular dementia - and underlying pathologies. We will show that while epidemiological studies link T2DM to Alzheimer's disease as well as vascular dementia, neuropathological studies attribute the increased dementia risk in T2DM patients primarily to vascular lesions in the brain. Risk factors for dementia among patients with T2DM are also addressed. Currently, there is evidence that microvascular complications, atherosclerosis and severe hypoglycemic events increase dementia risk. However, for a more complete understanding of risk factors for dementia in T2DM a life time perspective is needed. This should identify which individuals are at increased risk, what are vulnerable periods in life, and what are windows of opportunity for treatment. Currently, there are no DM specific treatments for dementia, but we will review observations from clinical trials that tried to prevent cognitive decline through intensified glycemic control and address other clinical implications of the association between T2DM and dementia.

Predicting risk of dementia in older adults: The late-life dementia risk index.

OBJECTIVE: To develop a late-life dementia risk index that can accurately stratify older adults into those with a low, moderate, or high risk of developing dementia within 6 years. METHODS: Subjects were 3,375 participants in the Cardiovascular Health Cognition Study without evidence of dementia at baseline. We used logistic regression to identify those factors most predictive of developing incident dementia within 6 years and developed a point system based on the logistic regression coefficients. RESULTS: Subjects had a mean age of 76 years at baseline; 59% were women and 15% were African American. Fourteen percent (n = 480) developed dementia within 6 years. The final late-life dementia risk index included older age (1-2 points), poor cognitive test performance (2-4 points), body mass index <18.5 (2 points), > or =1 apolipoprotein E epsilon4 alleles (1 point), cerebral MRI findings of white matter disease (1 point) or ventricular enlargement (1 point), internal carotid artery thickening on ultrasound (1 point), history of bypass surgery (1 point), slow physical performance (1 point), and lack of alcohol consumption (1 point) (c statistic, 0.81; 95% confidence interval, 0.79-0.83). Four percent of subjects with low scores developed dementia over 6 years compared with 23% of subjects with moderate scores and 56% of subjects with high scores. CONCLUSIONS: The late-life dementia risk index accurately stratified older adults into those with low, moderate, and high risk of developing dementia. This tool could be used in clinical or research settings to target prevention and intervention strategies toward high-risk individuals.

Central obesity and increased risk of dementia more than three decades later.

BACKGROUND: Numerous reports show that a centralized distribution of adiposity is a more dangerous risk factor for cardiovascular disease and diabetes than total body obesity. No studies have evaluated whether the same pattern exists with dementia. The objective was to evaluate the association between midlife central obesity and risk of dementia three decades later. METHODS: A longitudinal analysis was conducted of 6,583 members of Kaiser Permanente of Northern California who had their sagittal abdominal diameter (SAD) measured in 1964 to 1973. Diagnoses of dementia were from medical records an average of 36 years later, January 1, 1994, to June 16, 2006. Cox proportional hazard models adjusted for age, sex, race, education, marital status, diabetes, hypertension, hyperlipidemia, stroke, heart disease, and medical utilization were conducted. RESULTS: A total of 1,049 participants (15.9%) were diagnosed with dementia. Compared with those in the lowest quintile of SAD, those in the highest had nearly a threefold increased risk of dementia (hazard ratio, 2.72; 95% CI, 2.33-3.33), and this was only mildly attenuated after adding body mass index (BMI) to the model (hazard ratio, 1.92; 95% CI, 1.58-2.35). Those with high SAD (>25 cm) and normal BMI had an increased risk (hazard ratio, 1.89; 95% CI, 0.98-3.81) vs those with low SAD (<25 cm) and normal BMI (18.5-24.9 kg/m(2)), whereas those both obese (BMI >30 kg/m(2)) and with high SAD had the highest risk of dementia (HR, 3.60; 95% CI, 2.85-4.55). CONCLUSIONS: Central obesity in midlife increases risk of dementia independent of diabetes and cardiovascular comorbidities. Fifty percent of adults have central obesity; therefore, mechanisms linking central obesity to dementia need to be unveiled.

Glycosylated hemoglobin level and development of mild cognitive impairment or dementia in older women.

BACKGROUND: Biological mechanisms linking diabetes and cognition continue to grow, yet the association remains controversial in elders. Whether glycosylated hemoglobin (HbA1C) level, a marker of glucose control, is predictive of the development of cognitive impairment or dementia is unknown. We determined the association between HbA1C level and risk of developing cognitive impairment in older women, mostly without diabetes. METHODS: We studied 1983 postmenopausal women (mean age, 67.2 years) with osteoporosis who had HbA1C level measured at baseline. Development of mild cognitive impairment (MCI) or dementia over 4 years was determined as part of a dementia ancillary study. We analyzed risk of MCI or dementia for every 1% of HbA1C as well as risk associated with HbA1C >or= 7%. RESULTS: The mean level of HbA1C was 5.8% (range 3.0% to 12.1%) and 86 (4.3%) women developed MCI or dementia. For every 1% increase in HbA1C, women had a greater age-adjusted likelihood of developing MCI (OR= 1.50; 95% CI 1.14-1.97) and of developing MCI or dementia (OR=1.40; 95% CI 1.08 - 1.83). For those with HbA1C level >or= 7% (n=49), the age-adjusted risk for developing MCI was increased nearly 4-fold (OR= 3.70; 95% CI 1.51-9.09) and was increased nearly 3-fold for developing MCI or dementia (OR=2.86; 95% CI 1.17-6.98). When we excluded women with diagnosed diabetes (n=53), the association between HbA1C and MCI lessened somewhat but remained elevated (unadjusted OR=1.59; 95% CI 1.01-2.50; age-adjusted OR=1.42; 95% CI 0.89-2.28). Multivariate analyses adjusted for age, education, race, depression, alcohol use and treatment with raloxifene yielded similar results. INTERPRETATION: We found an association between HbA1C level and risk of developing MCI or dementia in postmenopausal osteoporotic women primarily without diabetes. Our findings support the hypothesis that glucose dysregulation is a predictor for cognitive impairment.

Midlife cardiovascular risk factors and risk of dementia in late life.

OBJECTIVE: To evaluate if midlife cardiovascular risk factors are associated with risk of late-life dementia in a large, diverse cohort. METHOD: The authors conducted a retrospective cohort study of 8,845 participants of a health maintenance organization who underwent health evaluations from 1964 to 1973 when they were between the ages of 40 and 44. Midlife cardiovascular risk factors included total cholesterol, diabetes, hypertension, and smoking. Diagnoses of dementia were ascertained by medical records from January 1994 to April 2003. RESULTS: The authors identified 721 participants (8.2%) with dementia. Smoking, hypertension, high cholesterol, and diabetes at midlife were each associated with a 20 to 40% increase in risk of dementia (fully adjusted Cox proportional hazards model: HR 1.24, 95% CI 1.04 to 1.48 for hypertension, HR 1.26, 95% CI 1.08 to 1.47 for smoking, HR 1.42, 95% CI 1.22 to 1.66 for high cholesterol, and HR 1.46, 95% CI 1.19 to 1.79 for diabetes). A composite cardiovascular risk score was created using all four risk factors and was associated with dementia in a dose-dependent fashion. Compared with participants having no risk factors, the risk for dementia increased from 1.27 for having one risk factor to 2.37 for having all four risk factors (fully adjusted model: HR 2.37, 95% CI 1.10 to 5.10). CONCLUSION: The presence of multiple cardiovascular risk factors at midlife substantially increases risk of late-life dementia in a dose dependent manner.

Evaluation of infantilizing speech in a rehabilitation setting: relation to age.

The purpose of the present study was to assess whether reactions to infantilizing speech and content are a function of age when levels of dependence within an institutional environment are controlled. Ten individuals below the age of sixty-five were compared with ten above age sixty-five. Respondents were given two sets of materials designed to produce comparative ratings of adult and infantilized speech content and intonation. The over sixty-five age group did not detect a difference between adult and infantilizing content. The under sixty-five age group reacted more negatively to infantilizing content than did the older group. Independence scores were not significantly correlated with either set of speech ratings, or to age. The difference between older and younger adults with the same level of functional impairment supports the empirical literature that infantilization is due in part to stereotyped expectations regarding the aged as more dependent and hence in need of childlike treatment.