Browsing by MeSH term "Weight Gain"
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Publication Brain JNK and metabolic disease.(Springer, 2021-02) Nogueiras, Rubén; Sabio, Guadalupe; Fundación BBVA; Ministerio de Ciencia, Innovación y Universidades (España); Atresmedia; Comunidad de Madrid (España); Xunta de Galicia (España); Instituto de Salud Carlos III; Centro de Investigación Biomédica en Red - CIBEROBN (Fisiopatología de la Obesidad y Nutrición)Obesity, which has long since reached epidemic proportions worldwide, is associated with long-term stress to a variety of organs and results in diseases including type 2 diabetes. In the brain, overnutrition induces hypothalamic stress associated with the activation of several signalling pathways, together with central insulin and leptin resistance. This central action of nutrient overload appears very rapidly, suggesting that nutrition-induced hypothalamic stress is a major upstream initiator of obesity and associated diseases. The cellular response to nutrient overload includes the activation of the stress-activated c-Jun N-terminal kinases (JNKs) JNK1, JNK2 and JNK3, which are widely expressed in the brain. Here, we review recent findings on the regulation and effects of these kinases, with particular focus on the hypothalamus, a key brain region in the control of energy and glucose homeostasis. JNK1 blocks the hypothalamic-pituitary-thyroid axis, reducing energy expenditure and promoting obesity. Recently, opposing roles have been identified for JNK1 and JNK3 in hypothalamic agouti gene-related protein (AgRP) neurons: while JNK1 activation in AgRP neurons induces feeding and weight gain and impairs insulin and leptin signalling, JNK3 (also known as MAPK10) deletion in the same neuronal population produces very similar effects. The opposing roles of these kinases, and the unknown role of hypothalamic JNK2, reflect the complexity of JNK biology. Future studies should address the specific function of each kinase, not only in different neuronal subsets, but also in non-neuronal cells in the central nervous system. Decoding the puzzle of brain stress kinases will help to define the central stimuli and mechanisms implicated in the control of energy balance. Graphical abstract.Publication Endocannabinoid regulation of acute and protracted nicotine withdrawal: effect of FAAH inhibition(Public Library of Science (PLOS), 2011-11-30) Cippitelli, Andrea; Astarita, Giuseppe; Duranti, Andrea; Caprioli, Giovanni; Ubaldi, Massimo; Stopponi, Serena; Kallupi, Marsida; Sagratini, Gianni; Rodríguez de Fonseca, Fernando; Piomelli, Daniele; Ciccocioppo, Roberto; [Cippitelli,A; Ubaldi,M; Stopponi,S; Kallupi,M; Ciccocioppo,R] School of Pharmacy,Pharmacology Unit,University of Camerino,Camerino,Italy. [Astarita,G; Piomelli,D] Department of Pharmacology, University of California Irvine, Irvine, California, United States of America. [Duranti,A] Department of Biomolecular Sciences, Medicinal Chemistry and Technology Unit, University of Urbino Carlo Bo, Urbino, Italy. [Caprioli,G; Sagratini,G] School of Pharmacy, Medicinal Chemistry Unit, University of Camerino, Camerino,Italy. [Rodríguez de Fonseca,F] Fundación IMABIS, Hospital Carlos Haya de Málaga, Málaga, Spain. [Piomelli,D] Drug Discovery and Development, Italian Institute of Technology, Genova, Italy.Evidence shows that the endocannabinoid system modulates the addictive properties of nicotine. In the present study, we hypothesized that spontaneous withdrawal resulting from removal of chronically implanted transdermal nicotine patches is regulated by the endocannabinoid system. A 7-day nicotine dependence procedure (5.2 mg/rat/day) elicited occurrence of reliable nicotine abstinence symptoms in Wistar rats. Somatic and affective withdrawal signs were observed at 16 and 34 hours following removal of nicotine patches, respectively. Further behavioral manifestations including decrease in locomotor activity and increased weight gain also occurred during withdrawal. Expression of spontaneous nicotine withdrawal was accompanied by fluctuation in levels of the endocannabinoid anandamide (AEA) in several brain structures including the amygdala, the hippocampus, the hypothalamus and the prefrontal cortex. Conversely, levels of 2-arachidonoyl-sn-glycerol were not significantly altered. Pharmacological inhibition of fatty acid amide hydrolase (FAAH), the enzyme responsible for the intracellular degradation of AEA, by URB597 (0.1 and 0.3 mg/kg, i.p.), reduced withdrawal-induced anxiety as assessed by the elevated plus maze test and the shock-probe defensive burying paradigm, but did not prevent the occurrence of somatic signs. Together, the results indicate that pharmacological strategies aimed at enhancing endocannabinoid signaling may offer therapeutic advantages to treat the negative affective state produced by nicotine withdrawal, which is critical for the maintenance of tobacco use.Publication Endocannabinoid regulation of acute and protracted nicotine withdrawal: effect of FAAH inhibition.(Public Library of Science (PLOS), 2011-11-30) Cippitelli, Andrea; Astarita, Giuseppe; Duranti, Andrea; Caprioli, Giovanni; Ubaldi, Massimo; Stopponi, Serena; Kallupi, Marsida; Sagratini, Gianni; Rodríguez de Fonseca, Fernando; Piomelli, Daniele; Ciccocioppo, Roberto; [Cippitelli,A; Ubaldi,M; Stopponi,S; Kallupi,M; Ciccocioppo,R] School of Pharmacy,Pharmacology Unit,University of Camerino,Camerino,Italy. [Astarita,G; Piomelli,D] Department of Pharmacology, University of California Irvine, Irvine, California, United States of America. [Duranti,A] Department of Biomolecular Sciences, Medicinal Chemistry and Technology Unit, University of Urbino ‘‘Carlo Bo’’, Urbino, Italy. [Caprioli,G; Sagratini,G] School of Pharmacy, Medicinal Chemistry Unit, University of Camerino, Camerino,Italy. [Rodríguez de Fonseca,F] Fundación IMABIS, Hospital Carlos Haya de Málaga, Málaga, Spain. [Piomelli,D] Drug Discovery and Development, Italian Institute of Technology, Genova, Italy.Evidence shows that the endocannabinoid system modulates the addictive properties of nicotine. In the present study, we hypothesized that spontaneous withdrawal resulting from removal of chronically implanted transdermal nicotine patches is regulated by the endocannabinoid system. A 7-day nicotine dependence procedure (5.2 mg/rat/day) elicited occurrence of reliable nicotine abstinence symptoms in Wistar rats. Somatic and affective withdrawal signs were observed at 16 and 34 hours following removal of nicotine patches, respectively. Further behavioral manifestations including decrease in locomotor activity and increased weight gain also occurred during withdrawal. Expression of spontaneous nicotine withdrawal was accompanied by fluctuation in levels of the endocannabinoid anandamide (AEA) in several brain structures including the amygdala, the hippocampus, the hypothalamus and the prefrontal cortex. Conversely, levels of 2-arachidonoyl-sn-glycerol were not significantly altered. Pharmacological inhibition of fatty acid amide hydrolase (FAAH), the enzyme responsible for the intracellular degradation of AEA, by URB597 (0.1 and 0.3 mg/kg, i.p.), reduced withdrawal-induced anxiety as assessed by the elevated plus maze test and the shock-probe defensive burying paradigm, but did not prevent the occurrence of somatic signs. Together, the results indicate that pharmacological strategies aimed at enhancing endocannabinoid signaling may offer therapeutic advantages to treat the negative affective state produced by nicotine withdrawal, which is critical for the maintenance of tobacco use.Publication Evaluation of a protocol to detect malnutrition and provide nutritional care for cancer patients undergoing chemotherapy.(2020-12-03) Álvaro Sanz, Elena; Abilés, Jimena; Garrido Siles, Marga; Rivas Ruíz, Francisco; Tortajada Goitia, Begoña; Domínguez, Antonio RuedaPatients with cancer frequently experience malnutrition, which is associated with higher rates of morbidity and mortality. Therefore, the implementation of strategies for its early detection and for intervention should improve the evolution of these patients. Our study aim is to design and implement a protocol for outpatients starting chemotherapy, by means of which any malnutrition can be identified and treated at an early stage. Before starting chemotherapy for patients with cancer, a complete assessment was made of their nutritional status, using the Nutriscore screening tool. When nutritional risk was detected, an interventional protocol was applied. Of 234 patients included in the study group, 84 (36%) required an individualised nutritional approach: 27 (32.1%) presented high nutritional risk, 12 had a Nutriscore result ≥ 5 and 45 experienced weight loss during chemotherapy. Among this population, the mean weight loss (with respect to normal weight) on inclusion in the study was - 3.6% ± 8.2. By the end of the chemotherapy, the mean weight gain was 0% ± 7.3 (pPublication Hypothalamic JNK1-hepatic fatty acid synthase axis mediates a metabolic rewiring that prevents hepatic steatosis in male mice treated with olanzapine via intraperitoneal: Additional effects of PTP1B inhibition.(Elsevier, 2023-07) Ferreira, Vitor; Folgueira, Cintia; García-Altares, María; Guillén, Maria; Ruíz-Rosario, Mónica; DiNunzio, Giada; Garcia-Martinez, Irma; Alen, Rosa; Bookmeyer, Christoph; Jones, John G; Cigudosa, Juan C; López-Larrubia, Pilar; Correig-Blanchar, Xavier; Davis, Roger J; Sabio, Guadalupe; Rada, Patricia; Valverde, Ángela M; Marie Curie; Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF); Comunidad de Madrid (España); Unión Europea. Comisión Europea. H2020; Fundación Ramón Areces; Centro de Investigación Biomédica en Red - CIBERDEM (Diabetes y Enfermedades Metabólicas asociadas); Instituto de Salud Carlos III; Fundação para a Ciência e Tecnologia (Portugal)Olanzapine (OLA), a widely used second-generation antipsychotic (SGA), causes weight gain and metabolic alterations when administered orally to patients. Recently, we demonstrated that, contrarily to the oral treatment which induces weight gain, OLA administered via intraperitoneal (i.p.) in male mice resulted in body weight loss. This protection was due to an increase in energy expenditure (EE) through a mechanism involving the modulation of hypothalamic AMPK activation by higher OLA levels reaching this brain region compared to those of the oral treatment. Since clinical studies have shown hepatic steatosis upon chronic treatment with OLA, herein we further investigated the role of the hypothalamus-liver interactome upon OLA administration in wild-type (WT) and protein tyrosine phosphatase 1B knockout (PTP1B-KO) mice, a preclinical model protected against metabolic syndrome. WT and PTP1B-KO male mice were fed an OLA-supplemented diet or treated via i.p. Mechanistically, we found that OLA i.p. treatment induces mild oxidative stress and inflammation in the hypothalamus in a JNK1-independent and dependent manner, respectively, without features of cell dead. Hypothalamic JNK activation up-regulated lipogenic gene expression in the liver though the vagus nerve. This effect concurred with an unexpected metabolic rewiring in the liver in which ATP depletion resulted in increased AMPK/ACC phosphorylation. This starvation-like signature prevented steatosis. By contrast, intrahepatic lipid accumulation was observed in WT mice treated orally with OLA; this effect being absent in PTP1B-KO mice. We also demonstrated an additional benefit of PTP1B inhibition against hypothalamic JNK activation, oxidative stress and inflammation induced by chronic OLA i.p. treatment, thereby preventing hepatic lipogenesis. The protection conferred by PTP1B deficiency against hepatic steatosis in the oral OLA treatment or against oxidative stress and neuroinflammation in the i.p. treatment strongly suggests that targeting PTP1B might be also a therapeutic strategy to prevent metabolic comorbidities in patients under OLA treatment in a personalized manner.Publication Leading Factors for Weight Gain during COVID-19 Lockdown in a Spanish Population: A Cross-Sectional Study.(2021-03-10) Sánchez, Enric; Lecube, Albert; Bellido, Diego; Monereo, Susana; Malagón, María M; Tinahones, Francisco J; On Behalf Of The Spanish Society For The Study Of Obesity,The increase in sedentary behaviors during the COVID-19-induced lockdown may have led to a significant weight gain. To investigate this hypothesis, a representative sample of the Spanish adult population comprising 1000 subjects was enrolled in a cross-sectional study between 26 May and 10 June 2020. Computer-assisted telephone interviews were conducted consisting of 29 questions on the topic of lifestyle habits during the lockdown. The cohort comprised 51.5% women and 51% overweight or obese subjects and had a mean age of 50 ± 18 years. Of the respondents, 44.5% self-reported weight gain during the lockdown; of these, 58.0% were women, 69.9% had previous excess weight, 44.7% lived with a relative who also gained weight, and 73.5 experienced increased appetite. Further, an increased consumption of energy-dense products was found relative to respondents who did not gain weight (p ≤ 0.016 for all). Additionally, respondents were unaware that obesity is a poor prognostic factor for COVID-19 infection, lived in smaller flats, and had a lower level of education and lower monthly income. The factors independently associated with weight gain were female gender, previous overweight or obesity, lack of food care, increased appetite, and increased consumption of sugar-sweetened beverages, alcoholic beverages, and snacks (p ≤ 0.023 for all). Should another lockdown be mandated, extra caution is warranted to prevent weight gain.Publication Metabolic Effects of Oral Phenelzine Treatment on High-Sucrose-Drinking Mice(Multidisciplinary Digital Publishing Institute (MDPI), 2018-10) Carpene, Christian; Gomez-Zorita, Saioa; Chaplin, Alice; Mercader, JosepPhenelzine has been suggested to have an antiobesity effect by inhibiting de novo lipogenesis, which led us to investigate the metabolic effects of oral chronic phenelzine treatment in high-sucrose-drinking mice. Sucrose-drinking mice presented higher body weight gain and adiposity versus controls. Phenelzine addition did not decrease such parameters, even though fat pad lipid content and weights were not different from controls. In visceral adipocytes, phenelzine did not impair insulin-stimulated de novo lipogenesis and had no effect on lipolysis. However, phenelzine reduced the mRNA levels of glucose transporters 1 and 4 and phosphoenolpyruvate carboxykinase in inguinal white adipose tissue (iWAT), and altered circulating levels of free fatty acids (FFA) and glycerol. Interestingly, glycemia was restored in phenelzine-treated mice, which also had higher insulinaemia. Phenelzine-treated mice presented higher rectal temperature, which was associated to reduced mRNA levels of uncoupling protein 1 in brown adipose tissue. Furthermore, unlike sucrose-drinking mice, hepatic malondialdehyde levels were not altered. In conclusion, although de novo lipogenesis was not inhibited by phenelzine, the data suggest that the ability to re-esterify FFA is impaired in iWAT. Moreover, the effects on glucose homeostasis and oxidative stress suggest that phenelzine could alleviate obesity-related alterations and deserves further investigation in obesity models.Publication Modulation of hypothalamic AMPK phosphorylation by olanzapine controls energy balance and body weight.(Elsevier, 2022-12) Ferreira, Vitor; Folgueira, Cintia; Guillén, Maria; Zubiaur, Pablo; Navares, Marcos; Sarsenbayeva, Assel; López-Larrubia, Pilar; Eriksson, Jan W; Pereira, Maria J; Abad-Santos, Francisco; Sabio, Guadalupe; Rada, Patricia; Valverde, Ángela M; Ministerio de Ciencia e Innovación (España); Agencia Estatal de Investigación (España); Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF); Unión Europea. Comisión Europea. H2020; Marie Curie; Comunidad de Madrid (España); Fundación Ramón Areces; Centro de Investigación Biomédica en Red - CIBERDEM (Diabetes y Enfermedades Metabólicas asociadas); Instituto de Salud Carlos IIISecond-generation antipsychotics (SGAs) are a mainstay therapy for schizophrenia. SGA-treated patients present higher risk for weight gain, dyslipidemia and hyperglycemia. Herein, we evaluated the effects of olanzapine (OLA), widely prescribed SGA, in mice focusing on changes in body weight and energy balance. We further explored OLA effects in protein tyrosine phosphatase-1B deficient (PTP1B-KO) mice, a preclinical model of leptin hypersensitivity protected against obesity. Wild-type (WT) and PTP1B-KO mice were fed an OLA-supplemented diet (5 mg/kg/day, 7 months) or treated with OLA via intraperitoneal (i.p.) injection or by oral gavage (10 mg/kg/day, 8 weeks). Readouts of the crosstalk between hypothalamus and brown or subcutaneous white adipose tissue (BAT and iWAT, respectively) were assessed. The effects of intrahypothalamic administration of OLA with adenoviruses expressing constitutive active AMPKα1 in mice were also analyzed. Both WT and PTP1B-KO mice receiving OLA-supplemented diet presented hyperphagia, but weight gain was enhanced only in WT mice. Unexpectedly, all mice receiving OLA via i.p. lost weight without changes in food intake, but with increased energy expenditure (EE). In these mice, reduced hypothalamic AMPK phosphorylation concurred with elevations in UCP-1 and temperature in BAT. These effects were also found by intrahypothalamic OLA injection and were abolished by constitutive activation of AMPK in the hypothalamus. Additionally, OLA i.p. treatment was associated with enhanced Tyrosine Hydroxylase (TH)-positive innervation and less sympathetic neuron-associated macrophages in iWAT. Both central and i.p. OLA injections increased UCP-1 and TH in iWAT, an effect also prevented by hypothalamic AMPK activation. By contrast, in mice fed an OLA-supplemented diet, BAT thermogenesis was only enhanced in those lacking PTP1B. Our results shed light for the first time that a threshold of OLA levels reaching the hypothalamus is required to activate the hypothalamus BAT/iWAT axis and, therefore, avoid weight gain. Our results have unraveled an unexpected metabolic rewiring controlled by hypothalamic AMPK that avoids weight gain in male mice treated i.p. with OLA by activating BAT thermogenesis and iWAT browning and a potential benefit of PTP1B inhibition against OLA-induced weight gain upon oral treatment.Publication Population-wide weight loss and regain in relation to diabetes burden and cardiovascular mortality in Cuba 1980-2010: repeated cross sectional surveys and ecological comparison of secular trends(2013-04-09) Franco, Manuel; Bilal, Usama; Orduñez, Pedro; Benet, Mikhail; Morejón, Alain; Caballero, Benjamín; Kennelly, Joan F; Cooper, Richard SOBJECTIVE: To evaluate the associations between population-wide loss and gain in weight with diabetes prevalence, incidence, and mortality, as well as cardiovascular and cancer mortality trends, in Cuba over a 30 year interval. DESIGN: Repeated cross sectional surveys and ecological comparison of secular trends. SETTING: Cuba and the province of Cienfuegos, from 1980 to 2010. PARTICIPANTS: Measurements in Cienfuegos included a representative sample of 1657, 1351, 1667, and 1492 adults in 1991, 1995, 2001, and 2010, respectively. National surveys included a representative sample of 14 304, 22 851, and 8031 participants in 1995, 2001, and 2010, respectively. MAIN OUTCOME MEASURES: Changes in smoking, daily energy intake, physical activity, and body weight were tracked from 1980 to 2010 using national and regional surveys. Data for diabetes prevalence and incidence were obtained from national population based registries. Mortality trends were modelled using national vital statistics. RESULTS: Rapid declines in diabetes and heart disease accompanied an average population-wide loss of 5.5 kg in weight, driven by an economic crisis in the mid-1990s. A rebound in population weight followed in 1995 (33.5% prevalence of overweight and obesity) and exceeded pre-crisis levels by 2010 (52.9% prevalence). The population-wide increase in weight was immediately followed by a 116% increase in diabetes prevalence and 140% increase in diabetes incidence. Six years into the weight rebound phase, diabetes mortality increased by 49% (from 9.3 deaths per 10 000 people in 2002 to 13.9 deaths per 10 000 people in 2010). A deceleration in the rate of decline in mortality from coronary heart disease was also observed. CONCLUSIONS: In relation to the Cuban experience in 1980-2010, there is an association at the population level between weight reduction and death from diabetes and cardiovascular disease; the opposite effect on the diabetes and cardiovascular burden was seen on population-wide weight gain.Publication Prenatal Phthalate Exposure and Childhood Growth and Blood Pressure: Evidence from the Spanish INMA-Sabadell Birth Cohort Study(Us Dept Health Human Sciences Public Health Science, 2015-10) Valvi, Damaskini; Casas, Maribel; Romaguera, Dora; Monfort, Nuria; Ventura, Rosa; Martinez, David; Sunyer, Jordi; Vrijheid, MartineBACKGROUND: Human evidence on the effects of early life phthalate exposure on obesity and cardiovascular disease risks, reported by experimental studies, is limited to a few cross-sectional studies. OBJECTIVES: We evaluated the associations between prenatal phthalate exposure and childhood growth and blood pressure in a Spanish birth cohort study. METHODS: We assessed exposure using the average of two phthalate metabolite spot-urine concentrations collected from the mothers in the first and third pregnancy trimesters (creatinine-adjusted, n = 391). Study outcomes were the difference in age-and sex-specific z-scores for weight between birth and 6 months of age; and repeated age-and sex-specific z-scores for body mass index (BMI) at 1, 4, and 7 years; waist-to-height ratio at 4 and 7 years; and age-and height-specific z-scores for systolic and diastolic blood pressure at 4 and 7 years. RESULTS: The sum of five high-molecular-weight phthalate metabolites (Sigma HMWPm) was associated with lower weight z-score difference between birth and 6 months (beta per doubling of exposure = -0.41; 95% CI: -0.75, -0.06) and BMI z-scores at later ages in boys (beta = -0.28; 95% CI: -0.60, 0.03) and with higher weight z-score difference (beta = 0.24; 95% CI: -0.16, 0.65) and BMI z-scores in girls (beta = 0.30; 95% CI: -0.04, 0.64) (p for sex interaction = 0.01 and 0.05, respectively). The sum of three low-molecular-weight phthalates (Sigma LMWPm) was not significantly associated with any of the growth outcomes. Sigma HMWPm and Sigma LMWPm were associated with lower systolic blood pressure z-scores in girls but not in boys. CONCLUSIONS: This study suggests that prenatal phthalate exposure may be associated with postnatal growth and blood pressure in a sex-specific manner. Inconsistencies with previous cross-sectional findings highlight the necessity for evaluating phthalate health effects in prospective studies.Publication Preterm birth, infant weight gain, and childhood asthma risk: A meta-analysis of 147,000 European children(Elsevier, 2014-05) Voort, Agnes M. M. Sonnenschein-van der; Arends, Lidia R.; de Jongste, Johan C.; Annesi-Maesano, Isabella; Arshad, S. Hasan; Barros, Henrique; Basterrechea, Mikel; Bisgaard, Hans; Chatzi, Leda; Corpeleijn, Eva; Correia, Sofia; Craig, Leone C.; Devereux, Graham; Dogaru, Cristian; Dostal, Miroslav; Duchen, Karel; Eggesbo, Merete; van der Ent, C. Kors; Fantini, Maria Pia; Forastiere, Francesco; Frey, Urs; Gehring, Ulrike; Gori, Davide; van der Gugten, Anne C; Hanke, Wojciech; Henderson, Alexander J; Heude, Barbara; Iniguez, Carmen; Inskip, Hazel M; Keil, Thomas; Kelleher, Cecily C; Kogevinas, Manolis; Kreiner-Moller, Eskil; Kuehni, Claudia E; Kuepers, Leanne K.; Lancz, Kinga; Larsen, Pernille S; Lau, Susanne; Ludvigsson, Johnny; Mommers, Monique; Andersen, Anne-Marie Nybo; Palkovicova, Lubica; Pike, Katharine C; Pizzi, Costanza; Polanska, Kinga; Porta, Daniela; Richiardi, Lorenzo; Roberts, Graham; Schmidt, Anne; Sram, Radim J.; Sunyer, Jordi; Thijs, Carel; Torrent Quetglas, Maties; Viljoen, Karien; Wijga, Alet H; Vrijheid, Martine; Jaddoe, Vincent W. V.; Duijts, LiesbethBackground: Preterm birth, low birth weight, and infant catch-up growth seem associated with an increased risk of respiratory diseases in later life, but individual studies showed conflicting results. Objectives: We performed an individual participant data meta-analysis for 147,252 children of 31 birth cohort studies to determine the associations of birth and infant growth characteristics with the risks of preschool wheezing (1-4 years) and school-age asthma (5-10 years). Methods: First, we performed an adjusted 1-stage random-effect meta-analysis to assess the combined associations of gestational age, birth weight, and infant weight gain with childhood asthma. Second, we performed an adjusted 2-stage random-effect meta-analysis to assess the associations of preterm birth (gestational age < 37 weeks) and low birth weight (< 2500 g) with childhood asthma outcomes. Results: Younger gestational age at birth and higher infant weight gain were independently associated with higher risks of preschool wheezing and school-age asthma (P <. 05). The inverse associations of birth weight with childhood asthma were explained by gestational age at birth. Compared with term-born children with normal infant weight gain, we observed the highest risks of school-age asthma in children born preterm with high infant weight gain (odds ratio [OR], 4.47; 95% CI, 2.58-7.76). Preterm birth was positively associated with an increased risk of preschool wheezing (pooled odds ratio [pOR], 1.34; 95% CI, 1.25-1.43) and school-age asthma (pOR, 1.40; 95% CI, 1.18-1.67) independent of birth weight. Weaker effect estimates were observed for the associations of low birth weight adjusted for gestational age at birth with preschool wheezing (pOR, 1.10; 95% CI, 1.00-1.21) and school-age asthma (pOR, 1.13; 95% CI, 1.01-1.27). Conclusion: Younger gestational age at birth and higher infant weight gain were associated with childhood asthma outcomes. The associations of lower birth weight with childhood asthma were largely explained by gestational age at birth.Publication The prevalence of excessive weight in Balearic Islands' young and middle-aged women and its association with social and socioeconomic factors: a ten-year trend (2000-2010)(BioMed Central (BMC), 2015-09-02) Coll, Josep Ll; Bibiloni Esteva, Maria Del Mar; Salas, Rogelio; Pons, Antoni; Tur, Josep ABackground: Knowledge about trends in the socioeconomic patterning of overweight and obesity in women provides insights into the nature of the obesity epidemic. Therefore the aim was to assess a ten-year trend (2000-2010) in the prevalence of excessive weight in Balearic Islands' women and its association with socioeconomic factors. Method: Young (18-35 year-old) and middle-aged (36-55 year-old) women were selected from two population-based cross-sectional nutritional surveys carried out in the Balearic Islands, Spain. The participation rate was 80 % during 1999-2000 and 92.5 % during 2009-2010. Measured weight and height was obtained, and body mass index (kg/m(2)) was classified as follows: overweight (25.0 < 30), obese (>= 30) and excessive weight (>= 25). In both surveys, a general questionnaire including questions relating to socioeconomic status factors was used. Logistic regression was used to examine the association of excessive weight with socioeconomic variables and to test the interaction between the survey period and the socioeconomic factors. Results: Overall, while the prevalence of obesity mainly remained stable over the study period, the prevalence of overweight increased from 21.0 to 24.8 %. Young women showed an increased prevalence of overweight and excessive weight, from 14.1 to 20.9 % and from 20.9 to 28.6 %, respectively. Significant differences were not found in middle-aged women. Over the whole period, the incidence of excessive weight was higher among middle-aged and foreign women, but lower in women with a high educational profile and in employment. The prevalence of excessive weight in young women was also around 2.5 times higher in women who were living with at least one child at home. The tendency towards excessive weight in employed women decreased significantly between 2000 and 2010 in the younger age group (OR: 0.42; 95 % CI: 0.22-0.82). Conclusions: No significant increase in the prevalence of overweight/obesity was observed in middle-aged women, with a low level of education being the single socioeconomic variable associated with excessive weight in this target group. Overweight/obesity increased in young women with unemployment being the distinguishing socioeconomic factor associated with this increase.Publication Quality of Dietary Fat Intake and Body Weight and Obesity in a Mediterranean Population: Secondary Analyses within the PREDIMED Trial(Multidisciplinary Digital Publishing Institute (MDPI), 2018-12) Beulen, Yvette; Martinez-Gonzalez, Miguel A; van de Rest, Ondine; Salas-Salvado, Jordi; Sorli, Jose V; Gomez-Gracia, Enrique; Fiol Sala, Miquel; Estruch, Ramon; Santos-Lozano, Jose M; Schroeder, Helmut; Alonso-Gomez, Angel; Serra-Majem, Luis; Pinto, Xavier; Ros, Emilio; Becerra-Tomas, Nerea; Gonzalez, Jose I; Fito, Montserrat; Alfredo Martinez, J; Gea, AlfredoA moderately high-fat Mediterranean diet does not promote weight gain. This study aimed to investigate the association between dietary intake of specific types of fat and obesity and body weight. A prospective cohort study was performed using data of 6942 participants in the PREDIMED trial, with yearly repeated validated food-frequency questionnaires, and anthropometric outcomes (median follow-up: 4.8 years). The effects of replacing dietary fat subtypes for one another, proteins or carbohydrates were estimated using generalized estimating equations substitution models. Replacement of 5% energy from saturated fatty acids (SFA) with monounsaturated fatty acids (MUFA) or polyunsaturated fatty acids (PUFA) resulted in weight changes of -0.38 kg (95% Confidece Iinterval (CI): -0.69, -0.07), and -0.51 kg (95% CI: -0.81, -0.20), respectively. Replacing proteins with MUFA or PUFA decreased the odds of becoming obese. Estimates for the daily substitution of one portion of red meat with white meat, oily fish or white fish showed weight changes up to -0.87 kg. Increasing the intake of unsaturated fatty acids at the expense of SFA, proteins, and carbohydrates showed beneficial effects on body weight and obesity. It may therefore be desirable to encourage high-quality fat diets like the Mediterranean diet instead of restricting total fat intake.