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Background De novo lipogenesis (DNL) is the primary metabolic pathway synthesizing fatty acids from carbohydrates, protein, or alcohol. Our aim was to examine associations of in vivo levels of selected fatty acids (16:0, 16:1n7, 18:0, 18:1n9) in DNL with incidence of type 2 diabetes (T2D). Methods and findings Seventeen cohorts from 12 countries (7 from Europe, 7 from the United States, 1 from Australia, 1 from Taiwan; baseline years = 1970-1973 to 2006-2010) conducted harmonized individual-level analyses of associations of DNL-related fatty acids with incident T2D. In total, we evaluated 65,225 participants (mean ages = 52.3-75.5 years; % women = 20.4%-62.3% in 12 cohorts recruiting both sexes) and 15,383 incident cases of T2D over the 9-year follow-up on average. Cohort-specific association of each of 16:0, 16:1n7, 18:0, and 18:1n9 with incident T2D was estimated, adjusted for demographic factors, socioeconomic characteristics, alcohol, smoking, physical activity, dyslipidemia, hypertension, menopausal status, and adiposity. Cohort-specific associations were meta-analyzed with an inverse-variance-weighted approach. Each of the 4 fatty acids positively related to incident T2D. Relative risks (RRs) per cohort-specific range between midpoints of the top and bottom quintiles of fatty acid concentrations were 1.53 (1.41-1.66; p < 0.001) for 16:0, 1.40 (1.33-1.48; p < 0.001) for 16:1n-7, 1.14 (1.05-1.22; p = 0.001) for 18:0, and 1.16 (1.07-1.25; p < 0.001) for 18:1n9. Heterogeneity was seen across cohorts (I2 = 51.1%-73.1% for each fatty acid) but not explained by lipid fractions and global geographical regions. Further adjusted for triglycerides (and 16:0 when appropriate) to evaluate associations independent of overall DNL, the associations remained significant for 16:0, 16:1n7, and 18:0 but were attenuated for 18:1n9 (RR = 1.03, 95% confidence interval (CI) = 0.94-1.13). These findings had limitations in potential reverse causation and residual confounding by impreci

Background De novo lipogenesis (DNL) is the primary metabolic pathway synthesizing fatty acids from carbohydrates, protein, or alcohol. Our aim was to examine associations of in vivo levels of selected fatty acids (16:0, 16:1n7, 18:0, 18:1n9) in DNL with incidence of type 2 diabetes (T2D). Methods and findings Seventeen cohorts from 12 countries (7 from Europe, 7 from the United States, 1 from Australia, 1 from Taiwan; baseline years = 1970-1973 to 2006-2010) conducted harmonized individual-level analyses of associations of DNL-related fatty acids with incident T2D. In total, we evaluated 65,225 participants (mean ages = 52.3-75.5 years; % women = 20.4%-62.3% in 12 cohorts recruiting both sexes) and 15,383 incident cases of T2D over the 9-year follow-up on average. Cohort-specific association of each of 16:0, 16:1n7, 18:0, and 18:1n9 with incident T2D was estimated, adjusted for demographic factors, socioeconomic characteristics, alcohol, smoking, physical activity, dyslipidemia, hypertension, menopausal status, and adiposity. Cohort-specific associations were meta-analyzed with an inverse-variance-weighted approach. Each of the 4 fatty acids positively related to incident T2D. Relative risks (RRs) per cohort-specific range between midpoints of the top and bottom quintiles of fatty acid concentrations were 1.53 (1.41-1.66; p < 0.001) for 16:0, 1.40 (1.33-1.48; p < 0.001) for 16:1n-7, 1.14 (1.05-1.22; p = 0.001) for 18:0, and 1.16 (1.07-1.25; p < 0.001) for 18:1n9. Heterogeneity was seen across cohorts (I2 = 51.1%-73.1% for each fatty acid) but not explained by lipid fractions and global geographical regions. Further adjusted for triglycerides (and 16:0 when appropriate) to evaluate associations independent of overall DNL, the associations remained significant for 16:0, 16:1n7, and 18:0 but were attenuated for 18:1n9 (RR = 1.03, 95% confidence interval (CI) = 0.94-1.13). These findings had limitations in potential reverse causation and residual confounding by impreci

BACKGROUND: De novo lipogenesis (DNL) is the primary metabolic pathway synthesizing fatty acids from carbohydrates, protein, or alcohol. Our aim was to examine associations of in vivo levels of selected fatty acids (16:0, 16:1n7, 18:0, 18:1n9) in DNL with incidence of type 2 diabetes (T2D). METHODS AND FINDINGS: Seventeen cohorts from 12 countries (7 from Europe, 7 from the United States, 1 from Australia, 1 from Taiwan; baseline years = 1970-1973 to 2006-2010) conducted harmonized individual-level analyses of associations of DNL-related fatty acids with incident T2D. In total, we evaluated 65,225 participants (mean ages = 52.3-75.5 years; % women = 20.4%-62.3% in 12 cohorts recruiting both sexes) and 15,383 incident cases of T2D over the 9-year follow-up on average. Cohort-specific association of each of 16:0, 16:1n7, 18:0, and 18:1n9 with incident T2D was estimated, adjusted for demographic factors, socioeconomic characteristics, alcohol, smoking, physical activity, dyslipidemia, hypertension, menopausal status, and adiposity. Cohort-specific associations were meta-analyzed with an inverse-variance-weighted approach. Each of the 4 fatty acids positively related to incident T2D. Relative risks (RRs) per cohort-specific range between midpoints of the top and bottom quintiles of fatty acid concentrations were 1.53 (1.41-1.66; p < 0.001) for 16:0, 1.40 (1.33-1.48; p < 0.001) for 16:1n-7, 1.14 (1.05-1.22; p = 0.001) for 18:0, and 1.16 (1.07-1.25; p < 0.001) for 18:1n9. Heterogeneity was seen across cohorts (I2 = 51.1%-73.1% for each fatty acid) but not explained by lipid fractions and global geographical regions. Further adjusted for triglycerides (and 16:0 when appropriate) to evaluate associations independent of overall DNL, the associations remained significant for 16:0, 16:1n7, and 18:0 but were attenuated for 18:1n9 (RR = 1.03, 95% confidence interval (CI) = 0.94-1.13). These findings had limitations in potential reverse causation and residual confounding by impre

Vanwege tekorten op de woningmarkt enerzijds en de moeizame exploitatie van recreatieparken anderzijds, is permanente bewoning op recreatieparken een structureel maatschappelijk verschijnsel geworden. Permanente bewoning is wettelijk niet toegestaan en kan samengaan met diverse vormen van sociale problematiek. De sociale crisis die ontstond op camping Fort Oranje is voor de GGD WestBrabant aanleiding geweest preventieve werkwijzen voor recreatieparken te ontwikkelen. Dit artikel beschrijft twee pilots die in dit verband werden opgezet. De ambitie was bewoners van recreatieparken in beeld te krijgen en waar nodig te ondersteunen, en om een stem te geven aan hun verhaal.

Background: Global dietary recommendations for and cardiovascular effects of linoleic acid, the major dietary omega-6 fatty acid, and its major metabolite, arachidonic acid, remain controversial. To address this uncertainty and inform international recommendations, we evaluated how in vivo circulating and tissue levels of linoleic acid (LA) and arachidonic acid (AA) relate to incident cardiovascular disease (CVD) across multiple international studies. Methods: We performed harmonized, de novo, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries. Multivariable-adjusted associations of circulating and adipose tissue LA and AA biomarkers with incident total CVD and subtypes (coronary heart disease, ischemic stroke, cardiovascular mortality) were investigated according to a prespecified analytic plan. Levels of LA and AA, measured as the percentage of total fatty acids, were evaluated linearly according to their interquintile range (ie, the range between the midpoint of the first and fifth quintiles), and categorically by quintiles. Study-specific results were pooled using inverse-variance-weighted meta-analysis. Heterogeneity was explored by age, sex, race, diabetes mellitus, statin use, aspirin use, omega-3 levels, and fatty acid desaturase 1 genotype (when available). Results: In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15 198 incident cardiovascular events occurred among 68 659 participants. Higher levels of LA were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke, with hazard ratios per interquintile range of 0.93 (95% CI, 0.88-0.99), 0.78 (0.70-0.85), and 0.88 (0.79-0.98), respectively, and nonsignificantly with lower coronary heart disease risk (0.94; 0.88-1.00). Relationships were similar for LA evaluated across quintiles. AA levels were not associated with higher risk of cardiovascular outcomes; in a comparison of extrem

Background and aims: Population-based studies often use plasma fatty acids (FAs) as objective indicators of FA intake, especially for n-3 FA and linoleic acid (LA). The relation between dietary and circulating FA in cardiometabolic patients is largely unknown. We examined whether dietary n-3 FA and LA were reflected in plasma lipid pools in post-myocardial infarction (MI) patients. Methods and results: Patients in Alpha Omega Cohort filled out a 203-item food-frequency questionnaire from which eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), alpha-linolenic acid (ALA), and LA intake were calculated. Circulating individual FA (% total FA) were assessed in cholesteryl esters (CE; n = 4066), phospholipids (PL; n = 838), and additionally in total plasma for DHA and LA (n = 739). Spearman correlation coefficients (rs) were calculated for dietary vs. circulating FA. Circulating FA were also compared across dietary FA quintiles, overall and in subgroups by sex, obesity, diabetes, statin use, and high alcohol intake. Patients were on average 69 years old and 79% was male. Moderate correlations between dietary and circulating levels were observed for EPA (rs ∼0.4 in CE and PL) and DHA (rs ∼0.5 in CE and PL, ∼0.4 in total plasma), but not for ALA (rs ∼0.0). Weak correlations were observed for LA (rs 0.1 to 0.2). Plasma LA was significantly lower in statin users and in patients with a high alcohol intake. Conclusions: In post-MI patients, dietary EPA and DHA were well reflected in circulating levels. This was not the case for LA, which may partly be influenced by alcohol use and statins.

BACKGROUND: We aimed to investigate prospective associations of circulating or adipose tissue odd-chain fatty acids 15:0 and 17:0 and trans-palmitoleic acid, t16:1n-7, as potential biomarkers of dairy fat intake, with incident type 2 diabetes (T2D). METHODS AND FINDINGS: Sixteen prospective cohorts from 12 countries (7 from the United States, 7 from Europe, 1 from Australia, 1 from Taiwan) performed new harmonised individual-level analysis for the prospective associations according to a standardised plan. In total, 63,682 participants with a broad range of baseline ages and BMIs and 15,180 incident cases of T2D over the average of 9 years of follow-up were evaluated. Study-specific results were pooled using inverse-variance-weighted meta-analysis. Prespecified interactions by age, sex, BMI, and race/ethnicity were explored in each cohort and were meta-analysed. Potential heterogeneity by cohort-specific characteristics (regions, lipid compartments used for fatty acid assays) was assessed with metaregression. After adjustment for potential confounders, including measures of adiposity (BMI, waist circumference) and lipogenesis (levels of palmitate, triglycerides), higher levels of 15:0, 17:0, and t16:1n-7 were associated with lower incidence of T2D. In the most adjusted model, the hazard ratio (95% CI) for incident T2D per cohort-specific 10th to 90th percentile range of 15:0 was 0.80 (0.73-0.87); of 17:0, 0.65 (0.59-0.72); of t16:1n7, 0.82 (0.70-0.96); and of their sum, 0.71 (0.63-0.79). In exploratory analyses, similar associations for 15:0, 17:0, and the sum of all three fatty acids were present in both genders but stronger in women than in men (pinteraction < 0.001). Whereas studying associations with biomarkers has several advantages, as limitations, the biomarkers do not distinguish between different food sources of dairy fat (e.g., cheese, yogurt, milk), and residual confounding by unmeasured or imprecisely measured confounders may exist. CONCLUSIONS: In a larg

There has been an increasing interest in urban forests and the levels of biodiversity they contain. Currently there are no spatially explicit maps of tree species richness in urban areas. This research tests and identifies GIS and remote sensing metrics (climate, area, productivity, three-dimensional structure) hypothesized to be associated with species richness in native forests and identifies methods that can be applied to predict and map tree species richness in cities. We quantified tree species richness, floristic composition, and structure in 28 1-ha plots in the city of Los Angeles. Climate and remote sensing metrics from high-resolution aerial imagery (10 cm), QuickBird (60 cm), Landsat (30 m), MODIS (250 m), and airborne lidar (2 m) were collected for each plot. There were 1208 individual stems and 108 trees identified to species. Species richness ranged from 2 to 31 species per ha and averaged 17 species per ha. Tree canopy cover from QuickBird explained the highest portion of variance (54%) in tree species richness followed by NDVI from Landsat (42%). Tree species richness can be higher in residential urban forests than native forests in the United States. Spatially explicit species richness maps at 1 ha can be created and tested for cities in order to identify both hotspots and coldspots of tree species richness and changes in species richness over time.

The original version of this article unfortunately contained a mistake. One of the authors name was incorrectly listed as “Darrell E. Jenerette” and should be corrected as “G. Darrel Jenerette”. The original article was corrected.

This study used tree data from field plots in urban areas to describe forest structure in urban areas throughout California. The plot data were used with numerical models to calculate several ecosystem services produced by trees. A series of transfer functions were calculated to scale-up results from the plots to the landscape using urban tree canopy (UTC) mapped at 1-m resolution for each combination of 6 land use classes and climate zones. California's UTC covered 15% of the urban area and contained 173.2 million trees, five per city resident. UTC per capita was lowest among U.S. states (90.8 m2), indicating ample opportunity for tree planting. Oaks were the most abundant taxon (22%) and overall plantings were youthful. The annual value of ecosystem services was estimated at $8.3 billion and the urban forests asset value was $181 billion. Assuming an average annual per tree management cost of $19 and benefit of $47.83, $2.52 in benefit was returned for every dollar spent. The threat posed by Invasive Shot Hole Borer (Euwallacea sp.) illustrates that urban forests are a relatively fragile resource whose contributions to human health and well-being can be suddenly jeopardized. One scenario projected that should Southern California cities lose 50% (11.6 million) of all susceptible trees, the value of ecoservices foregone over 10 years was $616.6 million. The approximate cost of removing and replacing the trees was $15.9 billion. Strategies to reduce the risk of catastrophic loss by increasing the resilience of California's urban forests are discussed.

Excessive amounts of moisture in product coal can influence the efficiency of downstream utilization processes due to a decreased calorific value and handling problems. Stockpiles can be used to decrease the moisture content of coal by means of gravity drainage and evaporation. This paper is focused on the evaporation of moisture from a coal stockpile surface with the aim of investigating the effect of particle size on the rate of evaporation as well as the depth to which evaporation extends. It was observed that moisture initially evaporates at a higher rate from a stockpile consisting of fine particles (-6.7 mm) than from coarser particles (-13.2 mm +6.7 mm). This high rate of evaporation is restricted to the outer shell of the fine coal stockpile. However, for coarse coal, the porous nature increases the depth at which evaporation occurs. Evaporation of moisture was observed up to the fourth day of each experimental run, after which steady state was obtained. It was shown the water can evaporate from the surface into the body of the stockpile, depending on the coal particle size and void spacing. An experimental reclaim depth of 0.4 m was achieved after 4 days

BACKGROUND: A growing number of cohort studies suggest a potential role of dairy consumption in type 2 diabetes (T2D) prevention. The strength of this association and the amount of dairy needed is not clear. OBJECTIVE: We performed a meta-analysis to quantify the associations of incident T2D with dairy foods at different levels of intake. DESIGN: A systematic literature search of the PubMed, Scopus, and Embase databases (from inception to 14 April 2015) was supplemented by hand searches of reference lists and correspondence with authors of prior studies. Included were prospective cohort studies that examined the association between dairy and incident T2D in healthy adults. Data were extracted with the use of a predefined protocol, with double data-entry and study quality assessments. Random-effects meta-analyses with summarized dose-response data were performed for total, low-fat, and high-fat dairy, (types of) milk, (types of) fermented dairy, cream, ice cream, and sherbet. Nonlinear associations were investigated, with data modeled with the use of spline knots and visualized via spaghetti plots. RESULTS: The analysis included 22 cohort studies comprised of 579,832 individuals and 43,118 T2D cases. Total dairy was inversely associated with T2D risk (RR: 0.97 per 200-g/d increment; 95% CI: 0.95, 1.00; P = 0.04; I2 = 66%), with a suggestive but similar linear inverse association noted for low-fat dairy (RR: 0.96 per 200 g/d; 95% CI: 0.92, 1.00; P = 0.072; I2 = 68%). Nonlinear inverse associations were found for yogurt intake (at 80 g/d, RR: 0.86 compared with 0 g/d; 95% CI: 0.83, 0.90; P < 0.001; I2 = 73%) and ice cream intake (at ∼10 g/d, RR: 0.81; 95% CI: 0.78, 0.85; P < 0.001; I2 = 86%), but no added incremental benefits were found at a higher intake. Other dairy types were not associated with T2D risk. CONCLUSION: This dose-response meta-analysis of observational studies suggests a possible role for dairy foods, particularly yogurt, in the prevention of T2D. Resu

BackgroundA higher milk consumption may be associated with a lower stroke risk. We conducted a comprehensive systematic review and dose–response meta‐analysis of milk and other dairy products in relation to stroke risk.Methods and ResultsThrough a systematic literature search, prospective cohort studies of dairy foods and incident stroke in stroke‐free adults were identified. Random‐effects meta‐analyses with summarized dose–response data were performed, taking into account sources of heterogeneity, and spline models were used to systematically investigate nonlinearity of the associations. We included 18 studies with 8 to 26 years of follow‐up that included 762 414 individuals and 29 943 stroke events. An increment of 200 g of daily milk intake was associated with a 7% lower risk of stroke (relative risk 0.93; 95% CI 0.88–0.98; P=0.004; I2=86%). Relative risks were 0.82 (95% CI 0.75–0.90) in East Asian and 0.98 (95% CI 0.95–1.01) in Western countries (median intakes 38 and 266 g/day, respectively) with less but still considerable heterogeneity within the continents. Cheese intake was marginally inversely associated with stroke risk (relative risk 0.97; 95% CI 0.94–1.01 per 40 g/day). Risk reductions were maximal around 125 g/day for milk and from 25 g/day onwards for cheese. Based on a limited number of studies, high‐fat milk was directly associated with stroke risk. No associations were found for yogurt, butter, or total dairy.ConclusionsMilk and cheese consumption were inversely associated with stroke risk. Results should be placed in the context of the observed heterogeneity. Future epidemiological studies should provide more details about dairy types, including fat content. In addition, the role of dairy in Asian populations deserves further attention.

Background: Dietary polyunsaturated fatty acids (PUFA) are inversely related to coronary heart disease (CHD) in epidemiological studies. We examined the associations of plasma n-6 and n-3 PUFA in cholesteryl esters with fatal CHD in a nested case-control study. Additionally, we performed a dose-response meta-analysis of similar prospective studies on cholesteryl ester PUFA. Methods: We used data from two population-based cohort studies in Dutch adults aged 20-65y. Blood and data collection took place from 1987-1997 and subjects were followed for 8-19y. We identified 279 incident cases of fatal CHD and randomly selected 279 controls, matched on age, gender, and enrollment date. Odds ratios (OR) were calculated per standard deviation (SD) increase of cholesteryl ester PUFA. Results: After adjustment for confounders, the OR (95% CI) for fatal CHD per SD increase in plasma linoleic acid was 0.89 (0.74-1.06). Additional adjustment for plasma total cholesterol and systolic blood pressure attenuated this association (OR:0.95; 95% CI: 0.78-1.15). Arachidonic acid was not associated with fatal CHD (OR per SD:1.11; 95% CI: 0.92-1.35). The ORs (95% CI) for fatal CHD for an SD increase in n-3 PUFA were 0.92 (0.74-1.15) for alpha-linolenic acid and 1.06 (0.88-1.27) for EPA-DHA. In the meta-analysis, a 5% higher linoleic acid level was associated with a 9% lower risk (relative risk: 0.91; 95% CI: 0.84-0.98) of CHD. The other fatty acids were not associated with CHD. Conclusion: In this Dutch population, n-6 and n-3 PUFA in cholesteryl esters were not significantly related to fatal CHD. Our data, together with findings from previous prospective studies, support that linoleic acid in plasma cholesteryl is inversely associated with CHD.

Background and aims - There are few prospective studies on fatty acid status in relation to incident stroke, with inconsistent results. We assessed the associations of plasma n-6 and n-3 PUFA in cholesteryl esters with the risk of total stroke and stroke subtypes in Dutch adults. Methods and results - We conducted a nested case–control study using data from a population-based cohort study in adults aged 20–65 years. Blood sampling and data collection took place during 1993–1997 and subjects were followed for 8–13 years. We identified 179 incident cases of stroke and 179 randomly selected controls, matched on age, gender, and enrollment date. Odds ratios (OR) with 95% confidence intervals (95%CI) were calculated per standard deviation (SD) increase of PUFA in cholesteryl esters using multivariable conditional logistic regression. Cases comprised 93 ischemic, 50 hemorrhagic, and 36 unspecified strokes. The n-6 PUFA linoleic acid and arachidonic acid contributed ~55% and ~6.5% respectively to total plasma fatty acids, whereas the n-3 PUFA alpha-linolenic acid contributed ~0.5% and eicosapentaenoic acid plus docosahexaenoic acid (EPA-DHA) ~1.3%. After adjustment for confounders, n-6 and n-3 PUFA were not associated with incident total stroke or stroke subtypes. The OR (95% CI) for total stroke was 0.95 (0.74–1.23) per SD increase in linoleic acid and 1.02 (0.80–1.30) per SD increase in arachidonic acid. ORs (95% CI) for total stroke were 0.94 (0.72–1.21) for alpha-linolenic acid and 1.16 (0.94–1.45) for EPA-DHA. Conclusion - In the present study, plasma n-6 or n-3 fatty acids were not related to incident stroke or stroke subtypes.