Skipping breakfast is associated with adiposity markers especially when sleep time is adequate in adolescents

Adolescence is a critical stage of development and has an important influence on energy balancerelated behaviours (EBRBs). When adolescents are associated with obesity it can lead to increased cardiometabolic risk. Here we assess if EBRBs adopted by adolescents included in a subsample are associated with markers of total and abdominal adiposity in a multicentre European study, Healthy Lifestyle in Europe by Nutrition in Adolescence (HELENA-CSS) and a Brazilian study, Brazilian Cardiovascular Adolescent Health (BRACAH study), and whether sleep duration influence the association between skipping breakfast, physical activity and sedentary behaviours, with total and abdominal obesity (AO). Multilevel linear regression models using fixed and random intercepts were used to analyse the association between markers of obesity and EBRBs. Skipping breakfast was the prevalent behaviour in association with obesity among European and Brazilian boys besides European girls, even after stratification by sleep time. Moreover, European boys who slept properly and skipped breakfast had an increased waist circumference (WC), while body mass index (BMI) increased in Brazilian boys. Among Brazilian boys less sleep was protective for total obesity (β = −0.93 kg/m2; 95% CI: −1.80; −0.07). European girls when they were more sedentary, showed an increase in WC, especially for those who reported they slept adequately. Skipping breakfast was associated with total and AO in adolescents independent of sleep duration.The HELENA-CSS took place with the financial support of the European Community Sixth RTD Framework Program (contract FOOD-CT-2005-007034). This study was also supported by a grant from the Spanish Ministry of Health: Maternal, Child Health and Development Network (numberRD08/0072) and grants from the Spanish Ministry of Education (EX-2008-0641) and the Swedish Heart-Lung Foundation (20090635). And supported by grants from the Spanish Ministry of Science and Innovation (JCI-2010-07055 and RYC-2010-05957). The authors thanked for the contribution of the HELENA Study Group. We are grateful for the financial support to the authors: Dr. Elsie C. O. Forkert was given a post-doctoral schoolarship from the Sao Paulo Research Foundation FAPESP (proc.2018/02887-6). Dr. Augusto César F. De Moraes was given a post-doctoral scholarship from the National Council for Scientific and Technological Development (CNPq: proc. 313772/2014-2) and the São Paulo Research Foundation FAPESP (proc. 2014/13367-2 and 2015/14319-4). Full Prof. Luis A. Moreno was given a scholarship of a visiting professor from São Paulo Research Foundation FAPESP (proc. 2015/11406-3). Dr Prof Heráclito B Carvalho is in receipt of an advanced scientist scholarship from the National Council for Scientific and Technological Development (CNPq: proc. 300951/2015-9)

Dectin-1 Activation Exacerbates Obesity and Insulin Resistance in the Absence of MyD88

This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP, grant numbers 11/15682-4, 12/02270-2, 15/18121-4), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq, Regenera INCT Process Grant 465656/2014-5). JL is funded by the NIH/NIDDK R01DK106210. GDB is funded by the Wellcome Trust and the MRC Centre for Medical Mycology. Open access journalPeer reviewedPublisher PD

Unsaturated Fatty Acids Revert Diet-Induced Hypothalamic Inflammation in Obesity

Background: In experimental models, hypothalamic inflammation is an early and determining factor in the installation and progression of obesity. Pharmacological and gene-based approaches have proven efficient in restraining inflammation and correcting the obese phenotypes. However, the role of nutrients in the modulation of hypothalamic inflammation is unknown. Methodology/Principal Findings: Here we show that, in a mouse model of diet-induced obesity, partial substitution of the fatty acid component of the diet by flax seed oil (rich in C18:3) or olive oil (rich in C18:1) corrects hypothalamic inflammation, hypothalamic and whole body insulin resistance, and body adiposity. In addition, upon icv injection in obese rats, both v3 and v9 pure fatty acids reduce spontaneous food intake and body mass gain. These effects are accompanied by the reversal of functional and molecular hypothalamic resistance to leptin/insulin and increased POMC and CART expressions. In addition, both, v3 and v9 fatty acids inhibit the AMPK/ACC pathway and increase CPT1 and SCD1 expression in the hypothalamus. Finally, acute hypothalamic injection of v3 and v9 fatty acids activate signal transduction through the recently identified GPR120 unsaturated fatty acid receptor. Conclusions/Significance: Unsaturated fatty acids can act either as nutrients or directly in the hypothalamus, reverting dietinduced inflammation and reducing body adiposity. These data show that, in addition to pharmacological and geneti

Vitamins and iron blood biomarkers are associated with blood pressure levels in European adolescents. The HELENA study

[Objectives]: Previous research showed that low concentration of biomarkers in the blood during adolescence (i.e., iron status; retinol; and vitamins B6, B12, C, and D) may be involved in the early stages of development of many chronic diseases, such as hypertension. The aim was to evaluate if iron biomarkers and vitamins in the blood are associated with blood pressure in European adolescents.[Methods]: Participants from the Healthy Lifestyle in Europe by Nutrition in Adolescence cross-sectional study (N = 1089; 12.5–17.5 y; 580 girls) were selected by complex sampling. Multilevel linear regression models examined the associations between iron biomarkers and vitamins in the blood and blood pressure; the analyses were stratified by sex and adjusted for contextual and individual potential confounders.[Results]: A positive association was found in girls between RBC folate concentration and systolic blood pressure (SBP) (β = 3.19; 95% confidence interval [CI], 0.61–5.77), although no association between the vitamin serum biomarkers concentrations and diastolic blood pressure (DBP) was found. In boys, retinol was positively associated with DBP (β = 3.84; 95% CI, 0.51–7.17) and vitamin B6 was positively associated with SBP (β = 3.82; 95% CI, 1.46–6.18). In contrast, holotranscobalamin was inversely associated with SBP (β = −3.74; 95% CI, −7.28 to −0.21).[Conclusions]: Levels of RBC folate and vitamin B6 in blood may affect BP in adolescents. In this context, programs aimed at avoiding high BP levels should promote healthy eating behavior by focusing on the promotion of vegetable proteins and foods rich in vitamin B12 (i.e., white meat and eggs), which may help to achieve BP blood control in adolescents.The HELENA Study was financially support by the European Community SixthRTD Framework Programme (contract FOOD-CT-2005-007034). The writing group takes sole responsibility for the content of this article. This study was also supported by a grant from the Spanish Ministry of Health: Maternal, Child Health and Development Network (number RD08/0072), grant from the Spanish Ministry of Education (EX-2008-0641; AP-2008-03806) and the Swedish Heart-Lung Foundation (20090635). ACdeM received scholarship from S~ao PauloResearch FoundationdFAPESP (proc. 2011/11137-1 and 2011/20662-2). LAM received scholarship of visiting professor from the Brazilian government by Science without Borders Program by CNPq (National Counsel of Technological and Scientific Development) and CAPES (Coordination of Improvement of Higher Education Personnel) (proc. 007/2012). The GENUD Research Group cofinancedby the European Regional Development Fund (MICINN-FEDER)Peer reviewe

Rastreamento de câncer de colo uterino em funcionárias assintomáticas de uma fábrica do Rio Grande do Sul

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Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.