Objective: To examine the cross-sectional relationship between nutrient status and psychometric and imaging indices of brain health in dementia-free elders.Methods: Thirty plasma biomarkers of diet were assayed in the Oregon Brain Aging Study cohort (n ϭ 104). Principal component analysis constructed nutrient biomarker patterns (NBPs) and regression models assessed the relationship of these with cognitive and MRI outcomes.Results: Mean age was 87 Ϯ 10 years and 62% of subjects were female. Two NBPs associated with more favorable cognitive and MRI measures: one high in plasma vitamins B (B1, B2, B6, folate, and B12), C, D, and E, and another high in plasma marine -3 fatty acids. A third pattern characterized by high trans fat was associated with less favorable cognitive function and less total cerebral brain volume. Depression attenuated the relationship between the marine -3 pattern and white matter hyperintensity volume. Conclusion:Distinct nutrient biomarker patterns detected in plasma are interpretable and account for a significant degree of variance in both cognitive function and brain volume. Objective and multivariate approaches to the study of nutrition in brain health warrant further study. These findings should be confirmed in a separate population. Neurology The epidemiology of Alzheimer disease (AD) suggests a role for nutrition. [1][2][3][4][5][6][7] Despite studies in favor of a single or a few nutrients in the prevention of AD, the translation to formal clinical trials testing vitamin E, B vitamins, or docosahexaenoic acid have been disappointing. [8][9][10][11][12] Given the interactive nature of nutrient action and metabolism, it is not surprising that a single or few nutrient approaches for neurodegenerative disease are tenuous. [13][14][15] These results impart the rationale for novel methodologic approaches that appreciate the interactive features of nutrients and model their collective influence in the promotion of brain health.Food frequency questionnaires (FFQ) have traditionally been used to construct dietary patterns.16 FFQ is relatively inexpensive and fairly comprehensive, but this method is subject to faulty recall of dietary intake and does not account for variability in nutrient absorption, both of which are issues in the elderly. 17,18 We have recently reported a reliable blood test that assesses nutritional status in people at risk for dementia. 19 In the current study, we examine the relationship of nutrient biomarkers with cognitive function and MRI.To capture the effect of nutrients in combination, we construct nutrient biomarker patterns using principal component analysis (PCA). Cluster analysis, 20 index scores, 21 and reduced rankFrom the

Oxidative damage is a consistent finding in a number of central nervous system (CNS) disorders. Uric acid (UA) is a potent hydrophilic antioxidant that is modified by diet and drug. Several lines of evidence suggest that plasma UA may modulate outcomes in neurologic disease, but little attention has been paid to CNS levels of UA. Our objective was to test the hypothesis that cerebrospinal fluid (CSF) UA is determined by plasma UA, modified by blood-brain barrier (BBB) integrity and associated with rate of cognitive decline in Alzheimer's disease (AD). Also, since UA and ascorbic acid may act as antioxidants for one another, we also explored a potential interaction between them in the brain. Thirty-two patients with mild to moderate AD (Mini-Mental Status Exam 19 ± 5) participated in a longitudinal biomarker study for one year involving standardized clinical assessments. CSF and blood were collected at baseline for UA, ascorbic acid, and albumin. Cognitive measures were collected at baseline and again one year later. CSF UA was independent of age, gender, and AD severity. CSF and plasma UA were positively correlated (r = 0.669, p = 0.001) and BBB impairment was associated with higher CSF levels of UA (p = 0.028). Neither plasma nor CSF UA reached significant association with rates of cognitive decline over 1 year. CSF UA and CSF ascorbic acid were positively correlated (r = 0.388, p = 0.001). The hypothesis that CSF UA is determined by plasma UA and BBB integrity is supported, as is the hypothesis that UA and ascorbic acid are associated in CSF but not plasma. Adequately powered prospective studies would help assess any role for UA in primary and secondary prevention of AD.

Overall diet quality was inversely associated with prevalent and future frailty status in this cohort of older men.

Morbidity and mortality from colorectal cancer (CRC) can be attenuated through guideline concordant screening and intervention. This study used Medicaid and commercial claims data to examine individual and geographic factors associated with CRC testing rates in one state (Oregon). A total of 64,711 beneficiaries (4516 Medicaid; 60,195 Commercial) became newly age-eligible for CRC screening and met inclusion criteria (e.g., continuously enrolled, no prior history) during the study period (January 2010–December 2013). We estimated multilevel models to examine predictors for CRC testing, including individual (e.g., gender, insurance, rurality, access to care, distance to endoscopy facility) and geographic factors at the county level (e.g., poverty, uninsurance). Despite insurance coverage, only two out of five (42%) beneficiaries had evidence of CRC testing during the four year study window. CRC testing varied from 22.4% to 46.8% across Oregon's 36 counties; counties with higher levels of socioeconomic deprivation had lower levels of testing. After controlling for age, beneficiaries had greater odds of receiving CRC testing if they were female (OR 1.04, 95% CI 1.01–1.08), commercially insured, or urban residents (OR 1.14, 95% CI 1.07–1.21). Accessing primary care (OR 2.47, 95% CI 2.37–2.57), but not distance to endoscopy (OR 0.98, 95% CI 0.92–1.03) was associated with testing. CRC testing in newly age-eligible Medicaid and commercial members remains markedly low. Disparities exist by gender, geographic residence, insurance coverage, and access to primary care. Work remains to increase CRC testing to acceptable levels, and to select and implement interventions targeting the counties and populations in greatest need.

Regulatory regions of the human genome can be modified through epigenetic processes during prenatal life to make an individual more likely to suffer chronic diseases when they reach adulthood. The modification of chromatin and DNA contributes to a larger well-documented process known as “programming” whereby stressors in the womb give rise to adult onset diseases, including cancer. It is now well known that death from ischemic heart disease is related to birth weight; the lower the birth weight, the higher the risk of death from cardiovascular disease as well as type 2 diabetes and osteoporosis. Recent epidemiological data link rapid growth in the womb to metabolic disease and obesity and also to breast and lung cancers. There is increasing evidence that “marked” regions of DNA can become “unmarked” under the influence of dietary nutrients. This gives hope for reversing propensities for cancers and other diseases that were acquired in the womb. For several cancers, the size and shape of the placenta are associated with a person’s cardiovascular and cancer risks as are maternal body mass index and height. The features of placental growth and nutrient transport properties that lead to adult disease have been little studied. In conclusion, several cancers have their origins in the womb, including lung and breast cancer. More research is needed to determine the epigenetic processes that underlie the programming of these diseases.