Search

Background: Youth expeditions are regarded as beneficial and even “life-changing” experiences for young people, however the evidence on their perceived long-term impact is limited. Purpose: The purpose of this research was to examine the perceived long-term influence of expeditions in participants’ lives 29 and more years after going on a 3–6 week land-based self-sufficient wilderness expedition. Methodology/Approach: This study used a retrospective two-phase sequential research design. The first phase involved a web-based survey followed by individual semi-structured interviews in the second phase. Findings/Conclusions: For the majority of the 144 web-based survey respondents (93.8%), their first BES expedition experience was “enjoyable and meaningful”. Twenty-six interviews were conducted with people who had gone on their first BES expedition 29 to 66 years ago. Interviewed participants perceived seven long-lasting influences of expeditions: (1) ‘Connecting with others’, (2) ‘Fulfilling potential’ such as gaining confidence and resilience, (3) ‘Development of leisure activities and outdoor knowledge/skills’, (4) ‘Knowing thyself’, (5) ‘Sharing the experience’ to others, (6) ‘Impact on academic and professional life’, and (7) ‘Connecting with nature and the world’. Implications: This study provides evidence that the influence of wilderness expedition experiences can be long-lasting and significant on participants’ lives 29 and more years later.

Background: The sustainability of health benefits in response to lifestyle-based interventions remains unclear in children with overweight and obesity, and cardiometabolic disease (CMD). We determi...

Background and ObjectivesSerum antioxidant vitamins and carotenoids may protect against neurodegeneration with age. We examined associations of these nutritional biomarkers with incident all-cause and Alzheimer disease (AD) dementia among US middle-aged and older adults.MethodsUsing data from the third National Health and Nutrition Examination Surveys (1988–1994), linked with Centers for Medicare & Medicaid follow-up data, we tested associations and interactions of serum vitamins A, C, and E and total and individual serum carotenoids and interactions with incident AD and all-cause dementia. Cox proportional hazards regression models were conducted.ResultsAfter ≤26 years follow-up (mean 16–17 years, 7,283 participants aged 45–90 years at baseline), serum lutein+zeaxanthin was associated with reduced risk of all-cause dementia (65+ age group), even in the lifestyle-adjusted model (per SD: hazard ratio [HR] 0.93, 95% CI 0.87–0.99;p= 0.037), but attenuated in comparison with a socioeconomic status (SES)–adjusted model (HR 0.92, 95% CI 0.86–0.93;p= 0.013). An inverse relationship was detected between serum β-cryptoxanthin (per SD increase) and all-cause dementia (45+ and 65+) for age- and sex-adjusted models (HR 0.86, 95% CI 0.80–0.93;p< 0.001 for 45+; HR 0.86, 95% CI 0.80–0.93;p= 0.001 for 65+), a relationship remaining strong in SES-adjusted models (HR 0.89, 95% CI 0.82–0.96;p= 0.006 for 45+; HR 0.88, 95% CI 0.81–0.96;p= 0.007 for 65+), but attenuated in subsequent models. Antagonistic interactions indicate putative protective effects of 1 carotenoid may be observed at lower levels other carotenoids or antioxidant vitamin.DiscussionIncident all-cause dementia was inversely associated with serum lutein+zeaxanthin and β-cryptoxanthin levels. Further studies with time-dependent exposures and randomized trials are needed to test neuroprotective effects of supplementing the diet with select carotenoids.Classification of EvidenceThis study provides Class II evidence that incident all-cause dementia was inversely associated with serum lutein+zeaxanthin and β-cryptoxanthin levels.

International audience

High concentrations of carotenoids are protective against cardiometabolic risk traits (CMTs) in adults and children. We recently showed in non-diabetic Mexican American (MA) children that serum α-carotene and β-carotene are inversely correlated with obesity measures and triglycerides and positively with HDL cholesterol and that they were under strong genetic influences. Additionally, we previously described a Pediatric Metabolic Index (PMI) that helps in the identification of children who are at risk for cardiometabolic diseases. Here, we quantified serum lycopene and β-cryptoxanthin concentrations in approximately 580 children from MA families using an ultraperformance liquid chromatography-photodiode array and determined their heritabilities and correlations with CMTs. Using response surface methodology (RSM), we determined two-way interactions of carotenoids and PMI on Matsuda insulin sensitivity index (ISI). The concentrations of lycopene and β-cryptoxanthin were highly heritable [h2 = 0.98, P = 7 × 10–18 and h2 = 0.58, P = 1 × 10–7]. We found significant (P ≤ 0.05) negative phenotypic correlations between β-cryptoxanthin and five CMTs: body mass index (− 0.22), waist circumference (− 0.25), triglycerides (− 0.18), fat mass (− 0.23), fasting glucose (− 0.09), and positive correlations with HDL cholesterol (0.29). In contrast, lycopene only showed a significant negative correlation with fasting glucose (− 0.08) and a positive correlation with HDL cholesterol (0.18). Importantly, we found that common genetic influences significantly contributed to the observed phenotypic correlations. RSM showed that increased serum concentrations of α- and β-carotenoids rather than that of β-cryptoxanthin or lycopene had maximal effects on ISI. In summary, our findings suggest that the serum carotenoids are under strong additive genetic influences and may have differential effects on susceptibility to CMTs in children.

Dysmetabolic obesity during childhood and adolescence currently represents one of the greatest therapeutic challenge for healthcare systems worldwide. The global rates of obesity have more than doubled in the last 30 years. Recent meta-analysis from national surveys and food composition studies suggest an inverse association between lower carotenoid levels and the prevalence of Metabolic Syndrome in the general population, independent of serum retinol (vitamin A) levels. In children, two double-blind randomised placebo-controlled studies describing the effects of diet vs. mixed carotenoid supplementation on insulin resistance, adipokines and the rate of accrual of subcutaneous abdominal fat, implicate supplementation of these compounds to achieve targetable levels may be useful in the management of obesity accrual in this population. We will discuss the role of carotenoids and their conversion products (retinoids) in adipogenesis, lipolysis, insulin resistance and the pathophysiology of the metabolic syndrome and review the animal studies, which help support these findings.

Elevated blood homocysteine (Hcy) among middle-aged adults can increase age-related disease risk, possibly through other biochemical and hematological markers. We selected markers for hyperhomocysteinemia among middle-aged adults, studied time-dependent Hcy-marker associations and computed highly predictive indices of hyperhomocysteinemia, with cross-sectional and longitudinal validations. We used data from the National Health and Nutrition Examination Survey (NHANES III, phase 2, nmax = 4000), the NHANES 1999&ndash, 2006 (nmax = 10,151) and pooled NHANES (cross-sectional validation). Longitudinal validation consisted of mixed-effects linear regression models (Hcy predicting markers&rsquo, annual rates of change), applied to the Healthy Aging in Neighborhoods of Diversity Across the Life Span (HANDLS, n = 227&ndash, 244 participants, k = 2.4 repeats/participant, Agebase: 30&ndash, 65 years) data. Machine learning detected nine independent markers for Hcy &gt, 14 &micro, mol/L (NHANES III, phase 2): older age, lower folate and B-12 status, higher serum levels of creatinine, uric acid, alkaline phosphatase, and cotinine, mean cell hemoglobin and red cell distribution widths (RDW), results replicated in the 1999&ndash, 2006 NHANES [AUC = 0.60&ndash, 0.80]. Indices combining binary markers increased elevated Hcy odds by 6.9&ndash, 7.5-fold. In HANDLS, first-visit Hcy predicted annual increase in creatinine, RDW and alkaline phosphatase, with third-visit index (2013&ndash, 2018) directly predicting Hcy (2004&ndash, 2009). We provide evidence of the internal and external validity of indices composed of several biomarkers that are strongly associated with elevated Hcy.

Serum uric acid (SUA), a causative agent for gout, is linked to dietary factors, perhaps differentially by race. Cross-sectional (SUAbase, i.e. baseline SUA) and longitudinal (SUArate; i.e. annual rate of change in SUA) associations of SUA with diet were evaluated across race and sex–race groups, in a large prospective cohort study of urban adults. Of 3720 African American (AA) and White urban adults participating in the Healthy Aging in Neighborhoods of Diversity across the Life Span study, longitudinal data (2004–2013,k=1·7 repeats, follow-up, 4·64 (sd0·93) years) onn2138 participants were used. The main outcome consisted of up to two repeated measures on SUA. Exposures included the dietary factors such as ‘added sugar’, ‘alcoholic beverages’, ‘red meat’, ‘total fish’, ‘legumes’, ‘total dairy product’, ‘caffeine’, ‘vitamin C’ and a composite measure termed ‘dietary urate index’. Mixed-effects linear regression models were conducted, stratifying by race and by race×sex. A positive association between legume intake and SUAratewas restricted to AA, whereas alcohol intake was positively associated with SUAbaseoverall without racial differences. Added sugars were directly related to SUAbaseamong White men (Prateamong AA women, unlike among White women. Nevertheless, dairy product intake was associated with a lower SUAbaseamong Whites. Finally, the dietary urate index was positively associated with both SUAbaseand SUArate, particularly among AA. In sum, race and sex interactions with dietary intakes of added sugars, dairy products and legumes were detected in determining SUA. Similar studies are needed to replicate these findings.

The role of dairy foods and related nutrients in cardiometabolic health aetiology is poorly understood. We investigated longitudinal associations between the metabolic syndrome (MetS) and its components with key dairy product exposures. We used prospective data from a bi-racial cohort of urban adults (30–64 years at baseline (n 1371)), the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS), in Baltimore City, MD (2004–2013). The average of two 24-h dietary recalls measured 4–10 d apart was computed at baseline (V1) and follow-up (V2) waves. Annual rates of change (Δ) in dairy foods and key nutrients were estimated. Incident obesity, central obesity and the MetS were determined. Among key findings, in the overall urban adult population, both cheese and yogurt (V1 and Δ) were associated with an increased risk of central obesity (hazard ratio (HR) 1·13; 95 % CI 1·05, 1·23 per oz equivalent of cheese (V1); HR 1·21; 95 % CI 1·01, 1·44 per fl oz equivalent of yogurt (V1)]. Baseline fluid milk intake (V1 in cup equivalents) was inversely related to the MetS (HR 0·86; 95 % CI 0·78, 0·94), specifically to dyslipidaemia–TAG (HR 0·89; 95 % CI 0·81, 0·99), although it was directly associated with dyslipidaemia–HDL-cholesterol (HR 1·10; 95 % CI 1·01, 1·21). Furthermore, ΔCa and ΔP were inversely related to dyslipidaemia–HDL and MetS incidence, respectively, whereas Δdairy product fat was positively associated with incident TAG–dyslipidaemia and HDL-cholesterol–dyslipidaemia and the MetS. A few of those associations were sex and race specific. In sum, various dairy product exposures had differential associations with metabolic disturbances. Future intervention studies should uncover how changes in dairy product components over time may affect metabolic disorders.

Context Serum 25-hydroxyvitamin D [25(OH)D], and dietary and supplemental vitamin D may influence cognitive outcomes. Objectives Sex-, age-, and race-specific associations of vitamin D status and intake with longitudinal change in various cognitive domains were examined in a large sample of ethnically and socioeconomically diverse US urban adults. Design Two prospective waves of data from the Healthy Aging in Neighborhoods of Diversity across the Life Span study were used. Participants Adults in Baltimore, Maryland, aged 30 to 64 years at baseline (n = 1231 to 1803), were followed for a mean (± standard deviation) of 4.64 ± 0.93 years. Visit 1 occurred between 2004 and 2009; visit 2, between 2009 and 2013; there were 1.5 to 2.0 visits per participant. Main outcome and exposure measures Cognitive performance was assessed using 11 test scores covering domains of global cognition, attention, learning/memory, executive function, visuospatial/visuoconstruction ability, psychomotor speed, and language/verbal. Serum 25(OH)D, vitamin D intake, and use of supplements containing vitamin D were the key exposures. Results A consistent relationship was found between vitamin D status (overall) and supplemental intake (older women and black adults), with a slower rate of decline in the domain of verbal fluency. Higher dietary intake of vitamin D was linked to slower rate of decline in verbal memory among younger women, and a slower rate of decline in visual memory/visuoconstructive abilities among white adults. All other associations were inconsistent. Conclusions Vitamin D status and intakes were inversely related to domain-specific cognitive decline in US urban adults.

Background: The link between longitudinal cognitive change and polymorphisms in the vitamin D receptor (VDR) and MEGALIN [or LDL receptor-related protein 2 (LRP2)] genes remains unclear, particularly among African-American (AA) adults.Objectives: We aimed to evaluate associations of single nucleotide polymorphisms (SNPs) for VDR [rs11568820 (Cdx-2:T/C), rs1544410 (BsmI:G/A), rs7975232 (ApaI:A/C), rs731236 (TaqI:G/A)] and LRP2 [rs3755166:G/A,rs2075252:C/T, rs2228171:C/T] genes with longitudinal cognitive performance change in various domains of cognition.Methods: Data from 1024 AA urban adult participants in the Healthy Aging in Neighborhoods of Diversity Across the Life Span (Baltimore, Maryland) with complete genetic data were used, of whom 660-797 had complete data on 9 cognitive test scores at baseline and/or the first follow-up examination and complete covariate data (∼52% female; mean age: ∼52 y; mean years of education: 12.6 y). Time between examination visits 1 (2004-2009) and 2 (2009-2013) ranged from

Systemic inflammation may influence trajectories of depressive symptoms over time, perhaps differentially by sex and race. Inflammatory markers and the Center for Epidemiologic Studies-Depression scale [total score: CES-Dtotal and four distinctive domains: somatic complaints, depressed affect, positive affect and interpersonal problems] were examined among African-American (AA) and White urban adults participating in the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) study [2004–2013, Agebase:30–64 y, mean ± SD follow-up time: 4.64 ± 0.93 y, N = 150 (with cytokine data) to N = 1,767 (with other inflammatory markers)]. Findings suggest that serum concentrations of high-sensitivity C-reactive protein (hsCRP), z-inflammation composite score [ICS, combining elevated hsCRP and ESR with low serum albumin and iron], and serum interleukin (IL) 1β were positively associated with ΔCES-Dtotal (Δ: annual rate of increase) among Whites only. IL-12 was directly related to ΔCES-Dtotal among men and AA. The race-specific associations of hsCRP, ICS, IL-1β and the sex-specific association of IL-12 with ΔCES-Dtotal were replicated for the “depressed affect” domain. Similarly, among men, lower serum albumin and higher ICS were linked with higher baseline “somatic complaints”. IL-10 among AA and IL-12 among men were inversely related to Δ“positive affect”, while “interpersonal problems” were cross-sectionally associated with IL-6 among AA and IL-10 among Whites. Finally, baseline ICS was positively associated with incident “elevated depressive symptoms” (EDS: CES-Dtotal ≥ 16) among AA (HR = 1.28, 95% CI: 1.04–1.56, P = 0.017). Overall, systemic inflammation was directly linked to increased depressive symptoms over time and at baseline, differentially across sex and race groups. More longitudinal research is needed to replicate our findings.

Background Studies uncovering factors beyond socio-economic status (SES) that would explain racial and ethnic disparities in mortality are scarce. Methods Using prospective cohort data from the Third National Health and Nutrition Examination Survey (NHANES III), we examined all-cause and cause-specific mortality disparities by race, mediation through key factors and moderation by age (20–49 vs. 50+), sex and poverty status. Cox proportional hazards, discrete-time hazards and competing risk regression models were conducted (N = 16,573 participants, n = 4207 deaths, Median time = 170 months (1–217 months)). Results Age, sex and poverty income ratio-adjusted hazard rates were higher among Non-Hispanic Blacks (NHBs) vs. Non-Hispanic Whites (NHW). Within the above-poverty young men stratum where this association was the strongest, the socio-demographic-adjusted HR = 2.59, p

Uric acid, a waste metabolite among humans, was linked to various cognitive outcomes. We describe sex and age-group specific associations of baseline serum uric acid (SUAbase) and significant change in SUA (ΔSUA: 1 versus 0 = decrease versus no change; 2 versus 0 = increase versus no change) with longitudinal annual rate of cognitive change among a large sample of urban adults. Data from the Healthy Aging in Neighborhoods of Diversity across the Life Span study, 2004-2009 (visit 1) and 2009-2013 (visit 2) were used. Of 3,720 adults selected at baseline (age range: 30-64 y), complete data were available for N = 1,487-1,602 with a mean repeat of 1.5-1.7 visits/participant. Cognitive test domains spanned attention, processing speed, learning/memory, executive function, visuo-spatial/visuo-construction ability, language/verbal, and global cognitive function. SUA was measured at both visits. Multiple mixed-effects regression analyses were conducted. In the total population, a higher SUAbase was associated with a faster annual rate of decline on a measure of visual memory/visuo-construction ability (the Benton Visual Retention Test) by γ= 0.07 with a standard error of 0.02, p

Carotenoids may strengthen the association of antioxidant vitamins A, C, and E with favorable cognitive outcomes over time, though a few prospective studies have examined this hypothesis. We evaluated the longitudinal data from 1251 participants in the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) study (Age at visit 1 in 2004&ndash, 2009 (v1): 30&ndash, 65 years). Vitamins A, C, and E dietary intakes and total and individual dietary carotenoids were computed using two 24-h recalls at v1. Cognitive tests, covering global mental status and domains of memory/learning, attention, psychomotor speed, visuo-spatial, language/verbal, and executive function were conducted at v1 and/or v2 (2009&ndash, 2013), mean &plusmn, SD follow-up: 4.66 &plusmn, 0.93 years. Mixed-effects linear regression models detected an interaction between vitamin E and total (and individual) carotenoids for three of 11 cognitive tests at v1, with only one meeting the statistical significance upon multiple testing correction whereby vitamin E was linked with greater verbal memory performance in the uppermost total carotenoid tertile (&gamma, 0a = +0.26 &plusmn, 0.08, p = 0.002), a synergism largely driven by carotenoid lycopene. Vitamins A and C showed no consistent interactions with carotenoids. In conclusion, we provide partial evidence for synergism between vitamin E and carotenoids in relation to better baseline cognitive performance, pending further studies with time-dependent exposures and randomized trials directly examining this synergism.

Context Modifiable factors that reduce the burden of the metabolic syndrome (MetS), particularly plant-derived biomarkers, have been a recent focus of rising interest. Objective This systematic review and meta-analysis, which follows PRISMA guidelines, evaluates evidence from a period of 20 years that links vitamin A and carotenoids with the occurrence of MetS and following the PRISMA guidelines. Data sources PubMed and Cochrane databases (January 1997 through March 2017) were systematically assessed for studies, including case-control, cross-sectional, and cohort studies, that evaluated the associations of MetS with carotenoids and retinyl esters and retinol (vitamin A). Data extraction Key measures of associations were harmonized into odds ratios (ORs) and 95% confidence intervals (95%CI) of MetS per 1 standard deviation (SD) of exposure using forest plots and random effects models that pooled data points from 11 cross-sectional studies. Begg's funnel and harvest plots were constructed. Results An inverse association between total carotenoids and MetS was found [ORpooled, 0.66; 95%CI, 0.56-0.78; 1 SD ∼ 0.82 µmol/L; n = 5 studies]. This association was the strongest for β-carotene, followed by α-carotene and β-crypotoxanthin. No association was detected between retinol and MetS (ORpooled, 1.00; 95%CI, 0.88-1.13; 1 SD ∼ 2.14 µmol/L; n = 6 studies). Publication bias was absent, and harvest plots indicated consistency upon replication for β-carotene and total carotenoid exposures. Conclusions This review and meta-analysis suggests that, unlike retinol, total and individual carotenoids were inversely related to MetS.

Objectives/Background: Systemic inflammation can affect cognitive performance over time. The current study examined associations between systemic inflammation and cognitive performance among African Americans and Whites urban adults, stratifying by sex, and age group and by race.Patients/Methods: Among 1,555–1,719 White and African-American urban adults [Agebase: 30–64y, 2004-2013, mean±SD follow-up time(y): 4.64 ± 0.93y], conducted linear mixed-effects regression models were conducted to test associations of inflammatory markers [C-reactive protein, Erythrocyte Sedimentation Rate (ESR), albumin, iron, and an inflammation composite score (ICS)] with longitudinal cognitive performance.Results: Among key findings, CRP was linked to poorer baseline mental status among younger women (≤50y, γ01 = –0.03 ± 0.01, p = 0.002) and poorer attention in older women (>50y, γ01 = −0.024 ± 0.007, p < 0.004) and African-Americans (γ01 = −0.029 ± 0.008, p < 0.001). ESR was related to faster decline on verbal memory among older men (>50y, γ11 = −0.008 ± 0.003, P = 0.009); with poorer performance on attention tests overall (γ01 = −0.010 ± 0.003, P = 0.003) and among African-Americans (γ01 = −0.013 ± 0.004, P = 0.002); on verbal fluency among older women (>50y,γ01 = −0.037 ± 0.013, P = 0.004) and on executive function: overall (γ01 = +0.62 ± 0.21, P = 0.004), older men (>50y, γ01 = +1.69 ± 0.53, P = 0.001) and African-Americans (γ01 = +0.84 ± 0.28, P = 0.002). Albumin was linked to slower attention decline among older men (>50y, γ11 = +0.329 ± 0.103, P = 0.009), over-time improvement in executive function overall (γ11 = −6.00 ± 2.26, P = 0.008), and better baseline psychomotor speed among African-Americans (γ01 = +0.56 ± 0.19, P = 0.003). Finally, ICS predicted faster decline on visual memory/visuo-constructive abilities among older men (>50y, γ11 = +0.17 ± 0.06, p = 0.003).Conclusion: In sum, strong associations between systemic inflammation and longitudinal cognitive performance were detected, largely among older individuals (>50y) and African-Americans. Randomized trials targeting inflammation are warranted.

Epidemiological studies have confirmed associations of the vitamin D receptor (VDR) and vitamin D-related gene polymorphisms with adiposity and other metabolic disturbances. Those associations may be sex-specific. We evaluated the cross-sectional and longitudinal relationships between metabolic disturbances and haplotypes constructed from single nucleotide polymorphisms of VDR (BsmI:G/A: rs1544410; ApaI:A/C: rs7975232; and TaqI:G/A: rs731236) and MEGALIN (rs3755166:G/A; rs2075252:C/T and rs2228171:C/T) genes, in a sample of African-American adults. From 1,024 African Americans participating in the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS, 2004–2013, Baltimore, MD), our analyses included 539 participants with complete genetic, baseline covariate and metabolic outcome data (at baseline and follow-up). Mean ± SD period of follow-up was 4.64 ± 0.93 y. Multivariable-adjusted Cox proportional hazards and logistic regression models were conducted. Among key findings, in men, incident hypertension was inversely related to MEGALIN1 (GCC), [HR = 0.45, 95% CI: 0.23–0.90, p = 0.024]. Overall, there was a direct, linear dose-response association between VDR2 (AAG: BAt) and MetS at baseline [OR = 1.60, 95% CI: 1.11–2.31, p = 0.012], while among men, VDR3 (GAA: bAT) was inversely related to baseline MetS [OR = 0.40, 95% CI: 0.19–0.81, p = 0.011]. In conclusion, VDR and MEGALIN gene variations can affect prevalent MetS and the incidence rate of hypertension, respectively, among African-American urban adults.

The relationship among inadequate vitamin D status, obesity, and cardiometabolic risk and the potential impact of physical activity-based interventions on vitamin D status are poorly characterized in children. This study aimed to address these issues.We studied a total of 21 adolescents (15 obese and 6 normal weight; age: 14-18 years; Tanner stageIV). Adolescents with obesity (n = 15) underwent a randomized controlled (8 in the intervention group and 7 in the control group) 3-month physical activity-based lifestyle intervention. 25-Hydroxy vitamin D [25(OH)D] by mass spectrometry, adiponectin, leptin, high-sensitivity C-reactive protein (CRP), insulin, and glucose were measured and body composition was assessed by dual-energy x-ray absorptiometry (DXA). Analysis of covariance and mixed-effects model were used to compare mean change in 25(OH)D between intervention and nonintervention groups. Bootstrap method was used to validate the estimates and principle component analysis reduced the variables in the data for adjustment.25(OH)D was lower (P 0.001) in the obese versus lean adolescents. Homeostasis model assessment-insulin resistance, CRP, fat mass (FM), and body mass index z-score were negatively correlated with baseline 25(OH)D, while adiponectin showed a positive correlation. After adjustment for baseline biomarkers of cardiometabolic risk, the concentration of 25(OH)D increased in the obese intervention group (P = 0.06), but not in the nonintervention group. Fat-free mass increased and FM decreased (P 0.05 for both) in the intervention group. The magnitudes of increase in 25(OH)D and decrease in FM directly correlated (P 0.05).The increase in circulating 25(OH)D concentration by physical activity-based lifestyle-only intervention in adolescents with obesity, who did not receive vitamin D supplementation, suggests a putative independent role of physical activity-based interventions in the regulation of vitamin D status and potentially in the mitigation of risk factors of cardiovascular disease.

Serum uric acid (SUA), a causative agent for gout among others, is affected by both genetic and dietary factors, perhaps differentially by sex. We evaluated cross-sectional (SUAbase) and longitudinal (SUArate) associations of SUA with a genetic risk score (GRS), diet and sex. We then tested the interactive effect of GRS, diet and sex on SUA. Longitudinal data on 766 African-American urban adults participating in the Healthy Aging in Neighborhood of Diversity across the Lifespan study were used. In all, three GRS for SUA were created from known SUA-associated SNP (GRSbase (n 12 SNP), GRSrate (n 3 SNP) and GRStotal (n 15 SNP)). Dietary factors included added sugar, total alcohol, red meat, total fish, legumes, dairy products, caffeine and vitamin C. Mixed-effects linear regression models were conducted. SUAbase was higher among men compared with that among women, and increased with GRStotal tertiles. SUArate was positively associated with legume intake in women (γ=+0·14; 95 % CI +0·06, +0·22, P=0·001) and inversely related to dairy product intake in both sexes combined (γ=−0·042; 95 % CI −0·075, −0·009), P=0·010). SUAbase was directly linked to alcohol consumption among women (γ=+0·154; 95 % CI +0·046, +0·262, P=0·005). GRSrate was linearly related to SUArate only among men. Legume consumption was also positively associated with SUArate within the GRStotal’s lowest tertile. Among women, a synergistic interaction was observed between GRSrate and red meat intake in association with SUArate. Among men, a synergistic interaction between low vitamin C and genetic risk was found. In sum, sex–diet, sex–gene and gene–diet interactions were detected in determining SUA. Further similar studies are needed to replicate our findings.

Objectives To determine whether children with type 1 diabetes mellitus (T1DM) have evidence of increased aortic stiffness or early atherosclerosis as measured by magnetic resonance imaging (MRI). Background T1DM increases risk for cardiovascular disease in adults but whether this process starts in childhood is unknown. Subjects A total of 54 T1DM patients (15.4 ± 2.6 yr) and 30 age-matched controls (14.8 ± 2.7 yr) participated. Methods MRI was performed to assess aortic arch pulse wave velocity (PWV), strain, and distensibility of the ascending and descending thoracic aorta and measures of atherosclerosis. Results Groups were well-matched for age, pulse pressure, and gender. Low-density lipoprotein-cholesterol (LDL-C) was higher in T1DM (119.3 ± 50 vs. 76.1 ± 13.5 mg/dL, p < 0.0001). There was a trend toward decreased strain and distensibility in T1DM vs. controls in the ascending (distensibility: T1DM 62.2 ± 19.9 kPa−1 × 10−3, control 71.6 ± 26.4 kPa−1 × 10−3, p = 0.08) and descending aorta (strain: T1DM 25.8 ± 6.2% vs. control 28.3 ± 6.8%, p = 0.09). There was no difference in arch PWV. Advancing age and male gender was negatively associated with aortic stiffness. Hemoglobin A1c (HbA1c) was inversely related to descending aorta strain and distensibility (p < 0.05). Children with diabetes in the lowest two tertiles of insulin sensitivity demonstrated thoracic descending aortas with significantly lower strain (p = 0.027) and distensibility (p = 0.039) and increased measures of wall irregularity (p = 0.005). There were no differences in measurements of atherosclerosis between the two groups. Conclusions Adolescents with T1DM, especially those with lower insulin sensitivity, demonstrated a trend toward stiffer, less compliant thoracic aortas, which was inversely associated with diabetes control. These data suggest large vessel aortopathy starts early in T1DM.

Background Children with type 1 diabetes (T1D) and elevated LDL-C have an increased risk for cardiovascular disease, a process that can begin in childhood. Objective To assess the safety and efficacy of atorvastatin improving lipid profiles in children with T1D and elevated LDL-C. Subjects Sixty children (31M/29F) with T1D, mean age: 15 ± 0.3 yr, mean diabetes duration: 6.8 ± 0.5 yr, HbA1c: 8.8 ± 0.2%, with mean LDL-C 124 ± 4.0mg/dl were recruited. Methods After a 3-month run-in period, subjects were randomized double-blindly to atorvastatin or placebo for 6 months. Lipoprotein subfractions were measured by ion mobility and glucose control by HbA1C; continuous glucose monitors were worn quarterly. Results After a run-in period, 42 subjects were randomized. There were decreases in total cholesterol (−21%), LDL-C (−32%), non-HDL-C (−31%) and apoB (−26%) in the atorvastatin group versus placebo (p < 0.001). Lipoprotein subparticles (LDL-large 1 and 2A, IDL-large and small, VLDL- medium and small) decreased with statins (p < 0.03 all). Insulin sensitivity scores remained constant in both groups and correlated inversely with apoB (r = −0.312 p = 0.039) and small LDL 3A (r = −0.404 p = 0.007). One subject had asymptomatic elevation of creatinine kinase which normalized after atorvastatin discontinuation. Conclusions Atorvastatin lowered LDL-C, apoB, and atherogenic lipoprotein subparticles in children with T1D and elevated LDL-C without worsening insulin resistance. The drug was well tolerated and safe. Long-term studies would provide better insight on the impact of these interventions in the development of cardiovascular disease in children with diabetes.

Cell, animal and human studies dealing with carotenoids and carotenoid derivatives as nutritional regulators of adipose tissue biology with implications for the etiology and management of obesity and obesity-related metabolic diseases are reviewed. Most studied carotenoids in this context are β-carotene, cryptoxanthin, astaxanthin and fucoxanthin, together with β-carotene-derived retinoids and some other apocarotenoids. Studies indicate an impact of these compounds on essential aspects of adipose tissue biology including the control of adipocyte differentiation (adipogenesis), adipocyte metabolism, oxidative stress and the production of adipose tissue-derived regulatory signals and inflammatory mediators. Specific carotenoids and carotenoid derivatives restrain adipogenesis and adipocyte hypertrophy while enhancing fat oxidation and energy dissipation in brown and white adipocytes, and counteract obesity in animal models. Intake, blood levels and adipocyte content of carotenoids are reduced in human obesity. Specifically designed human intervention studies in the field, though still sparse, indicate a beneficial effect of carotenoid supplementation in the accrual of abdominal adiposity. In summary, studies support a role of specific carotenoids and carotenoid derivatives in the prevention of excess adiposity, and suggest that carotenoid requirements may be dependent on body composition.

Total white blood cell count (TWBCC) and percentage (%) composition of lymphocytes (PL) or neutrophils (PN) are linked to mid- and late-life depression, though sex-specific temporal relationships between those inflammatory markers and depressive symptoms remain unclear. The association between inflammation and depressive symptoms in longitudinal data on ethnically and socioeconomically diverse urban adults was examined with two hypotheses. In hypothesis 1, we examined the relationship between TWBCC, PL and PN with change in level of depressive symptoms from baseline to follow-up, stratifying by sex. In hypothesis 2, we examined reverse causality, by testing the relationship of depressive symptoms with change in TWBCC, PL and PN. Multiple linear mixed-effects regression models were performed to examine both the hypotheses. The sample sizes of participants (n) and repeated observations (n’) were: Hypothesis 1 (n=2009; n’=3501); Hypothesis 2 (n=2081; n’=3560). Among key findings (Hypothesis 1), in women, higher TWBCC was linked to a faster increase in depressive symptom total score (γ1112±s.e.: +0.81±0.28, P=0.003), with a slower increase over time in the positive affect subdomain coupled with faster increases in depressed affect and somatic complaints. Among women, baseline score on somatic complaints was positively associated with low PN (γ01a=+1.61±0.48, P01a=+1.16±0.45, P=0.011), whereas baseline score on positive affect was inversely related to higher PL (γ01a=−0.69±0.28, P=0.017). Results among men indicated that there was a positive cross-sectional relationship between low TWBCC and depressive symptoms, depressed affect and an inverse cross-sectional relationship with positive affect. However, over time, a low TWBCC in men was linked to a higher score on positive affect. There was no evidence of a bi-directional relationship between WBC parameters and depressive symptoms (Hypothesis 2). In sum, TWBCC and related markers were linked to depressive symptoms, mostly among women. Further longitudinal studies are needed to replicate this sex-specific association.

Cell, animal and human studies dealing with carotenoids and carotenoid derivatives as nutritional regulators of adipose tissue biology with implications for the etiology and management of obesity and obesity-related metabolic diseases are reviewed. Most studied carotenoids in this context are β-carotene, cryptoxanthin, astaxanthin and fucoxanthin, together with β-carotene-derived retinoids and some other apocarotenoids. Studies indicate an impact of these compounds on essential aspects of adipose tissue biology including the control of adipocyte differentiation (adipogenesis), adipocyte metabolism, oxidative stress and the production of adipose tissue-derived regulatory signals and inflammatory mediators. Specific carotenoids and carotenoid derivatives restrain adipogenesis and adipocyte hypertrophy while enhancing fat oxidation and energy dissipation in brown and white adipocytes, and counteract obesity in animal models. Intake, blood levels and adipocyte content of carotenoids are reduced in human obesity. Specifically designed human intervention studies in the field, though still sparse, indicate a beneficial effect of carotenoid supplementation in the accrual of abdominal adiposity. In summary, studies support a role of specific carotenoids and carotenoid derivatives in the prevention of excess adiposity, and suggest that carotenoid requirements may be dependent on body composition.

OBJECTIVES: On 11 March 2004, 10 simultaneous explosions at four different locations of the rail network in Madrid caused 198 deaths and 2312 persons were injured. The aim of this manuscript is to describe the prehospital health-related activities from the Emergency Medical Service of Madrid and to analyze the responses, the major conclusions, and the lessons learned. METHODS: Three meetings were held with professionals from the Emergency Medical Service of Madrid who were involved in the catastrophe. Two experts in quality management chaired the meetings. Detailed data were gathered on what occurred at the sites following the explosions. Additional data were gathered from professionals from the Coordination Service of Urgencies and from those who assisted relatives and friends of victims in the days following the bombings. All of the data were collected and were included in the final report. RESULTS: We describe the activities carried out by the Coordination Service of Urgencies at each site immediately after the explosions and during the 11 days following the catastrophe. The successful performances and those that need to be improved at the four sites and elsewhere are detailed. CONCLUSIONS: The main reasons for the 'positive responses' are the number of resources that acted, the professional abilities, and the flexibility of the services. The 'areas to be improved' are communications, the establishment of the top of the command at each site, and the organization of supplies for catastrophic assistance. From the analysis, we describe the main lessons learned and we present proposals for improvement, should a future catastrophe occur. Language: en

Background Despite recent advances in improved glycemic control, the magnitude of lifetime risk from premature cardiovascular disease in individuals with type 1 diabetes remains at least 10 fold higher than in the general population. The availability of lipoprotein fractionation has allowed the spotlight for this increased risk to shift from dysglycemia to diabetes-induced dyslipidemia associated with insulin resistance. Interventions designed to simultaneously improve both factors can have distinct and additive effects on slowing the initiation and progression of atherosclerotic lesions. As fullblown cardiovascular disease is not evident during childhood, there is a critical need to identify the most predictable surrogate markers that could assign elevated risk, as well as the design of safe and targeted interventions that could improve outcomes in this population. Conclusion This review will examine the evidence supporting the notion that cardiovascular disease in type 1 diabetes is associated with significant insulin resistance and it begins in childhood, making it necessary to design rational clinical trials that will significantly reduce risk in this population.

Elevated fatty acid binding proteins (FABP) may play a role in obesity and co-morbidities. The role of nutritional interventions in modulating these levels remains unclear. The aim of thispost hocstudy was to determine the effect of overweight (OW) on FABP4 and FABP5 in boys in relation to indices of adiposity, insulin resistance and inflammation, and to investigate the effects of a 6-month supplementation with an encapsulated fruit and vegetable juice concentrate (FVJC) plus nutritional counselling (NC) on FABP levels. Apost hocanalysis of a double-blind, randomised, placebo-controlled study of children recruited from the general paediatric population was performed. A total of thirty age-matched prepubertal boys (nine lean and twenty-one OW; aged 6–10 years) were studied. Patients received NC by a registered dietitian and were randomised to FVJC or placebo capsules for 6 months. FABP4, FABP5, glucose, insulin, homeostasis model assessment-insulin resistance (HOMA-IR), glucose-induced acute insulin response (AIR), lipid-corrected β-carotene (LCβC), adiponectin, leptin, high-sensitivity C-reactive protein (hs-CRP), IL-6 and body composition by dual-energy X-ray absorptiometry were determined before and after the intervention. FABP were higher (P v.lean boys and correlated directly with HOMA-IR, abdominal fat mass (AFM), hs-CRP, IL-6, and LCβC (P P P < 0·05 for all) but not FABP5. OW boys showed elevated FABP4 and FABP5, but only FABP4 was lowered by the FVJC supplement.

Objectives We tested a model in which Helicobacter pylori seropositivity (Hps) predicted iron status, which in turn acted as a predictor for markers of 1-C metabolism that were then allowed to predict antioxidant status. Methods National Health and Nutrition Examination Surveys (NHANES 1999–2000) cross-sectional data among adults aged 20–85 y were analyzed (n = 3,055). Markers of Hps, iron status (serum ferritin and transferrin saturation (TS)); 1-C metabolism (serum folate (FOLserum), B-12, total homocysteine (tHcy), methylmalonic acid (MMA)) and antioxidant status (vitamins A and E) were entered into a structural equations model (SEM). Results Predictors of Hps included older age, lower education and income, racial/ethnic groups (lowest among Non-Hispanic Whites), and lifetime cigarette smoking. SEM modeling indicated that Hps had a direct inverse relationship with iron status (combining serum ferritin and TS) which in turn was positively related to 1-C metabolites (higher serum folate, B-12 or lower tHcy/MMA) that were positively associated with antioxidant status (combining serum vitamins A and E). Another pathway that was found bypassed 1-C metabolites (Hps → Iron_st → Antiox). The sum of all indirect effects from Hps combining both pathways and the other indirect pathways in the model (Hps → Iron_st → OneCarbon; Hps →OneCarbon →Antiox) was estimated at β = -0.006±0.003, p

Children with type 1 diabetes (T1D) and elevated LDL-C have an increased risk for cardiovascular disease, a process that can begin in childhood.To assess the safety and efficacy of atorvastatin improving lipid profiles in children with T1D and elevated LDL-C.Sixty children (31M/29F) with T1D, mean age: 15 ± 0.3 yr, mean diabetes duration: 6.8 ± 0.5 yr, HbA(1c) : 8.8 ± 0.2%, with mean LDL-C 124 ± 4.0mg/dl were recruited.After a 3-month run-in period, subjects were randomized double-blindly to atorvastatin or placebo for 6 months. Lipoprotein subfractions were measured by ion mobility and glucose control by HbA1C; continuous glucose monitors were worn quarterly.After a run-in period, 42 subjects were randomized. There were decreases in total cholesterol (-21%), LDL-C (-32%), non-HDL-C (-31%) and apoB (-26%) in the atorvastatin group versus placebo (p0.001). Lipoprotein subparticles (LDL-large 1 and 2A, IDL-large and small, VLDL- medium and small) decreased with statins (p0.03 all). Insulin sensitivity scores remained constant in both groups and correlated inversely with apoB (r = -0.312 p = 0.039) and small LDL 3A (r = -0.404 p = 0.007). One subject had asymptomatic elevation of creatinine kinase which normalized after atorvastatin discontinuation.Atorvastatin lowered LDL-C, apoB, and atherogenic lipoprotein subparticles in children with T1D and elevated LDL-C without worsening insulin resistance. The drug was well tolerated and safe. Long-term studies would provide better insight on the impact of these interventions in the development of cardiovascular disease in children with diabetes.

Background and Objectives: Abdominal subcutaneous and visceral adipose tissues (SAT and VAT) contribute to the established association between obesity and metabolic risk, likely through signaling m...

Purpose of review The magnitude of lifetime risk of cardiovascular disease (CVD) has radically increased along with the high prevalence of obesity in children. The spotlight is now on dysfunctional adiposity as a precursor for the development of premature CVD. As full-blown CVD is not present in childhood, there is a critical need for surrogate markers to best assess, predict, and treat the children who are vulnerable to developing CVD. Recent findings Accumulation of excess fat mass can be conceived as a derangement in the balance between energy intake and expenditure. This appears to provoke various structural and metabolic alterations leading to adipocyte dysfunction, with important cardiovascular health consequences. Subclinical inflammation, insulin resistance, oxidative stress, and endothelial dysfunction appear to play important roles early in the clinical course of obesity. Summary Associations between biomarkers and noninvasive measures of early atherosclerosis in children continue to emerge and several biomarkers appear to be promising. At present, there are no explicit data to recommend any of these biomarkers as a routine clinical marker of CVD in children. More work is needed to validate these biomarkers and to improve understanding of their role in CVD risk prediction in the pediatric population.

The performance of English and Spanish subjects was examined in two experiments using a lexical decision task in which the effects of semantic priming and stimulus degradation were systematically varied. The Orthographic Depth Hypothesis predicts that priming and degradation will interact in the orthographically “deep” language (English) but not in the “shallow” one (Spanish). In the first experiment, the two factors were found to interact in a similar way in both English and Spanish groups. In the second experiment, in which only Spanish subjects participated, the interaction was again present but only in those subjects who showed an overall facilitation effect on primed words. The results are consistent with the use of the so-called “direct” route in Spanish and are at variance with other previous findings which have suggested that reading in shallow orthographies occurs via the “indirect” phonological route. There was also evidence that nonword rejection times were slower in Spanish subjects a...

ObjectiveTo determine the effects of placebo vs an encapsulated supplement of fruit and vegetable juice concentrate (FVJC) on serum β-carotene levels, insulin resistance, adiposity, and subclinical inflammation in boys.Study designThirty age-matched prepubertal boys (9 lean and 21 overweight (OW); age range, 6-10 years) were studied. All participants received nutrition counseling and were randomized to receive FVJC or placebo capsules for 6 months. Total cholesterol, triglycerides, lipid corrected β-carotene, serum retinol, glucose, insulin, retinol binding protein-4, leptin, adiponectin, leptin-to-adiponectin ratio, high-sensitivity C-reactive protein, and interleukin-6 were measured before and after the 6-month intervention. Homeostasis model assessment-insulin resistance (HOMA-IR), acute insulin response to intravenous glucose, along with abdominal fat mass (dual-energy x-ray absorptiometry) were also determined.ResultsBaseline β-carotene concentrations correlated inversely with HOMA-IR, leptin-to-adiponectin ratio, and abdominal fat mass (P≤.01). FVJC intake increased β-carotene concentrations (P≤.001) but did not influence retinol or retinol binding protein-4. Retinol insufficiency

Background The associations between nutritional biomarkers and measures of sleep quantity and quality remain unclear. Methods Cross-sectional data from the National Health and Nutrition Examination Surveys (NHANES) 2005–2006 were used. We selected 2,459 adults aged 20–85, with complete data on key variables. Five sleep measures were constructed as primary outcomes: (A) Sleep duration; (B) Sleep disorder; (C) Three factors obtained from factor analysis of 15 items and labeled as “Poor sleep-related daytime dysfunction” (Factor 1), “Sleepiness” (Factor 2) and “Sleep disturbance” (Factor 3). Main exposures were serum concentrations of key nutrients, namely retinol, retinyl esters, carotenoids (α-carotene, β-carotene, β-cryptoxanthin, lutein+zeaxanthin, lycopene), folate, vitamin B-12, total homocysteine (tHcy), vitamin C, 25-hydroxyvitamin D (25(OH)D) and vitamin E. Main analyses consisted of multiple linear, logistic and multinomial logit models. Results Among key findings, independent inverse associations were found between serum vitamin B-12 and sleep duration, 25(OH)D and sleepiness (as well as insomnia), and between folate and sleep disturbance. Serum total carotenoids concentration was linked to higher odds of short sleep duration (i.e. 5–6 h per night) compared to normal sleep duration (7–8 h per night). Conclusions A few of the selected serum nutritional biomarkers were associated with sleep quantity and quality. Longitudinal studies are needed to ascertain temporality and assess putative causal relationships.

The regionalization method has been applied to the attenuation coefficients of the vertical components of Rayleigh waves for the Southern Atlantic-Indian Ocean to obtain the attenuation across the ridge region. The obtained ridge attenuation coefficients are similar to those for the North Atlantic ridge and much lower than the values for the East Pacific Rise. Inversion theory, in its stochastic form, shows that the low-Q zone under the ridge sems to be located between 50 km and 200 km depth, with the maximum Q-1 value (≅15×10-3) at a depth of about 140 km. Comparison of the ridge model in this study with models for the North Atlantic ridge and East Pacific Rise, obtained by others, indicates that the attenuation coefficients for the study region are similar to those for the North Atlantic ridge, and much weaker than those for the East Pacific Rise. Since the spreading rate in the southern part of the Atlantic-Indian Ocean is similar to that in the North Atlantic, and lower than the corresponding rate in the Pacific, it seems that there is a close relation between spreading rates and low-Q regions under the ridges, with the Q values being higher in the region where the spreading rates are lower.The above results suggest that the creep rate under the ridge of the Southern Atlantic-Indian Ocean may be similar to that for the Atlantic, and much lower than for the Pacific Ocean for regions of comparable ages.

Summary. Fundamental-mode Rayleigh walies generated by several earthquakes situated on great circle paths traversing pairs of seismograph stations in American and European coastal regions and on Atlantic islands have been analysed to obtain anelastic attenuation coefficients, group and phase velocities, and specific quality factors at periods between 15 and 100s. Inversions of the dispersion and attenuation data have yielded shear velocity and shear wave internal friction (Qj') models of the upper mantle for regions of varying age in the Atlantic Ocean. The attenuation coefficients and internal friction values can be related to the age of the Atlantic Ocean floor, older regions being characterized by lower internal friction (or higher Q) values. A lowQ zone is prominent in the upper mantle of all regions less than 65 Myr in age, but is poorly developed in older regions. In contrast to the attenuation results, no systematic variations of Rayleigh or shear velocities with age can be resolved using the dispersion data of this study. A comparison of internal friction models beneath the Atlantic with those beneath the Pacific indicates that for regions of similar age internal friction is smaller (or Q larger) beneath the Atlantic than beneath the Pacific, especially in the younger regions immediately contiguous with the ridges. In particular, the upper mantle low-velocity, low-Q zone is less prominent beneath the Atlantic. The fact that spreading rates of the lithospheric plates are also smaller in the Atlantic suggests that internal friction and the rate of long-term creep in the mantle are closely related.