Role In Weight Gain Research Articles

Modulation of the Gut Microbiota by Olive Oil Phenolic Compounds: Implications for Lipid Metabolism, Immune System, and Obesity.

There is extensive information of the beneficial effects of virgin olive oil (VOO), especially on cardiovascular diseases. Some VOO healthy properties have been attributed to their phenolic-compounds (PCs). The aim of this review is to present updated data on the effects of olive oil (OO) PCs on the gut microbiota, lipid metabolism, immune system, and obesity, as well as on the crosstalk among them. We summarize experiments and clinical trials which assessed the specific effects of the olive oil phenolic-compounds (OOPCs) without the synergy with OO-fats. Several studies have demonstrated that OOPC consumption increases Bacteroidetes and/or reduces the Firmicutes/Bacteroidetes ratio, which have both been related to atheroprotection. OOPCs also increase certain beneficial bacteria and gut-bacteria diversity which can be therapeutic for lipid-immune disorders and obesity. Furthermore, some of the mechanisms implicated in the crosstalk between OOPCs and these disorders include antimicrobial-activity, cholesterol microbial metabolism, and metabolites produced by bacteria. Specifically, OOPCs modulate short-chain fatty-acids produced by gut-microbiota, which can affect cholesterol metabolism and the immune system, and may play a role in weight gain through promoting satiety. Since data in humans are scarce, there is a necessity for more clinical trials designed to assess the specific role of the OOPCs in this crosstalk.

12q14 microduplication: a new clinical entity reciprocal to the microdeletion syndrome?

Background12q14 microdeletion syndrome is characterized by low birth weight and failure to thrive, proportionate short stature and developmental delay. The opposite syndrome (microduplication) has not yet been characterized. Our main objective is the recognition of a new clinical entity - 12q14 microduplication syndrome. - as well as confirming the role of HMGA2 gene in growth regulation.Case presentationArray Comparative Genomic Hybridization (CGH), Karyotype, Fluorescence in situ Hybridization, Quantitative-PCR analysis and Whole exome sequencing (WES) were performed in a girl presenting overgrowth and obesity. Array CGH identified a 1.5 Mb 12q14.3 microduplication involving HMGA2, GRIP1, IRAK3, MSRB3 and TMBIM4 genes. Karyotype and FISH showed that duplication was a de novo insertion of 12q14.3 region on chromosome 9p resulting in an interstitial microduplication. Q-PCR confirmed the duplication only in the proband. WES revealed no pathogenic variants.ConclusionsPhenotypic comparison with patients with 12q14 microdeletion syndrome showed a reciprocal presentation, suggesting a phenotypically recognizable 12q14 microduplication syndrome as well as confirming the role of HMGA2 gene in growth regulation. It is also indicative that other genes, such as IRAK3 and MSRB3 might have of role in weight gain and obesity.

Role of inflammation markers in the prediction of weight gain and development of obesity in adults – A prospective study

Background and aimsThere is a growing body of literature confirming the association between inflammation and obesity. Recent research suggests that inflammation may play a role in weight gain. The aim of the study was to analyse whether serum inflammatory markers predict weight gain or development of obesity in a prospective study design. Methods and resultsThe baseline study (DILGOM 2007) consists of a population-based sample of 5024 Finnish men and women aged 25–75 years, of whom 3735 participated in the follow-up study in 2014. Baseline data collection included a questionnaire on health behaviour, physical examinations and blood samples including serum high-sensitivity C-Reactive Protein (hs-CRP), Interleukin-1 receptor antagonist (IL-1Ra), Interleukin-6 (IL-6), Tumor Necrosis Factor Alpha (TNF-alpha) and high molecular weight adiponectin (HMW adiponectin). Indicators of obesity were weight, body mass index (BMI), waist circumference and body fat percentage (% body fat). At baseline hs-CRP, IL-1Ra, IL-6, TNF-alpha and HMW adiponectin associated strongly (p < 0.0001) with obesity indicators. After adjustment for several potential predictors of obesity, hs-CRP and IL-1Ra associated inversely with changes in obesity indicators during the 7-year follow-up. These associations disappeared, however, after further adjustment for baseline BMI. Only HMW adiponectin retained a modest positive association with the change in weight (p = 0.008), in BMI (p = 0.007) and in waist circumference (p = 0.002). ConclusionThese findings suggest that the inflammatory markers, although highly associated with obesity, do not predict weight gain in an adult population. This could translate into inflammation being a result of obesity rather than a contributing factor to it.

Human Milk Short-Chain Fatty Acid Composition is Associated with Adiposity Outcomes in Infants

Presumed benefits of human milk (HM) in avoiding rapid infancy weight gain and later obesity could relate to its nutrient composition. However, data on breast milk composition and its relation with growth are sparse. We investigated whether short-chain fatty acids (SCFAs), known to be present in HM and linked to energy metabolism, are associated with infancy anthropometrics. In a prospective birth cohort, HM hindmilk samples were collected from 619 lactating mothers at 4-8 wk postnatally [median (IQR) age: 33.9 (31.3-36.5) y, body mass index (BMI) (kg/m2): 22.8 (20.9-25.2)]. Their offspring, born at 40.1 (39.1-41.0) wk gestation with weight 3.56 (3.22-3.87) kg and 51% male, were assessed with measurement of weight, length, and skinfold thickness at ages 3, 12, and 24 mo, and transformed to age- and sex-adjusted z scores. HM SCFAs were measured by 1H-nuclear magnetic resonance spectroscopy (NMR) and GC-MS. Multivariable linear regression models were conducted to analyze the relations between NMR HM SCFAs and infancy growth parameters with adjustment for potential confounders. NMR peaks for HM butyrate, acetate, and formic acid, but not propionate, were detected. Butyrate peaks were 17.8% higher in HM from exclusively breastfeeding mothers than mixed-feeding mothers (P=0.003). HM butyrate peak values were negatively associated with changes in infant weight (standardized B =-0.10, P=0.019) and BMI (B=-0.10, P=0.018) between 3 and 12 mo, and negatively associated with BMI (B=-0.10, P=0.018) and mean skinfold thickness (B=-0.10, P=0.049) at age 12 mo. HM formic acid peak values showed a consistent negative association with infant BMI at all time points (B<=-0.10, P<=0.014), whereas HM acetate was negatively associated with skinfold thickness at 3 mo (B=-0.10, P=0.028) and 24 mo (B=-0.10, P=0.036). These results suggest that HM SCFAs play a beneficial role in weight gain and adiposity during infancy. Further knowledge of HM SCFA function may inform future strategies to support healthy growth.

Weight Gain and Liver Steatosis in Patients with Inflammatory Bowel Diseases.

Background and Aim: Most studies focused on the benefits of weight loss on hepatic steatosis and no studies have been specifically designed to assess the role of weight gain on the development of liver steatosis in patients affected by inflammatory bowel diseases. The aim of this study was to analyse the relation between weight change over time and liver steatosis in patients with inflammatory bowel diseases. Methods: We retrospectively evaluated a population of 89 ambulatory patients in clinical remission or affected by mild disease, as determined from disease activity indices, with at least one follow-up visit. Transient elastography was used to quantify liver steatosis. Results: A total of 49 individuals (55%) were overweight/obese at baseline. A significant difference in weight change was found between participants that improved, were stable and worsened, over a mean follow-up of four years. (−1.0 kg ± 4; 2.5 kg ± 6; and 5.4 kg ± 5; respectively, p = 0.009). We found a greater probability of worsening in the hepatic fat content in individuals who gained more than 6% of body weight than in those gaining less than this value (log–rank (Mantel–Cox) χ2 test = 9.85; df = 1; p = 0.002). Conclusions: A body weight gain of 6% increases the probability of deterioration in liver steatosis over a period of four years in patients with inflammatory bowel diseases. Weight gain prevention with lifestyle interventions may be the cornerstone treatment of these patients.

The role of weight gain in explaining the effects of antipsychotic drugs on positive and negative symptoms: An analysis of the CATIE schizophrenia trial

Second-generation antipsychotics are associated with moderate benefits in terms of improved schizophrenia symptoms, but also with higher rates of side-effects such as excessive weight gain (WG); a consensus on their efficacy has not been reached. To date, no study has evaluated the interplay of treatments and side-effects in a single framework, which is a critical step to clarify the role of side-effects in explaining the efficacy of these antipsychotics. We used recent methods for mediation and interaction to clarify the role of WG in explaining the effects of second-generation drugs on schizophrenia symptoms. We used data from 1460 participants in the CATIE trial, assigned to either perphenazine (first-generation comparison drug), olanzapine, quetiapine, risperidone, or ziprasidone. The primary outcome was an individual's score on the Positive and Negative Syndrome Scale (PANSS) for symptoms of schizophrenia after 9 months, separately evaluated as positive (PANSS+), negative (PANSS−), and total PANSS score. WG after 6 months was investigated as a potential mediator and effect modifier. Results showed that, by limiting WG, patients would benefit of a considerably better improvement in terms of PANSS symptoms. In the scenario of weight change being controlled between −2% and 1% for all participants, patients assigned to olanzapine would experience the highest significant improvements in both PANSS+ (−2.66 points; 95% CI: −4.98, −0.35), PANSS− (−1.59; 95% CI: −4.31, 1.14), and total PANSS (−6.11; 95% CI: −13.13, 0.92). In conclusion, occurrence of excessive WG hampers the potentially beneficial effects of second-generation antipsychotics, thus suggesting future directions for treatment and interventions.

Obese Peers' Influence on Students' BMI: Heterogeneity in Race and Sex.

In this study, we investigate peer influence on obesity, with a focus on race and sex. We conducted econometric analysis of longitudinal health data of 277,566 public school students, ages 5-13 years. A percentage point increase in the proportion of obese students within the same grade increased a student's BMI z-scores by about 4 one-thousandths of a standard deviation. On racial peers, the standard deviation increase in BMI z-score is 3.9 one-thousandths for Hispanics or Caucasians and 4.9 one-thousandths for African Americans. Influence of obese peers is nearly identical for boys and girls. Such a small magnitude of obese peers' estimate suggests that classroom peers do not play a substantial role in weight gain or loss in elementary schools.

Cross-sectional association between soda consumption and body mass index in a community-based sample of twins

BackgroundConsumption of sugar-sweetened beverages, such as soda, have been shown to play an important role in weight gain. Although soda consumption has been associated with body mass index (BMI) in many studies, it has been difficult to ascertain a true causal relationship between soda consumption and BMI for two reasons. First, findings have been based largely on observational and cross-sectional studies, with much less evidence from randomized controlled trials. Second, the reported relationships may be confounded by genetic and shared environmental factors that affect both soda consumption and BMI. In the present study, we used the twin design to better understand the relationship between soda consumption and BMI by accounting for measured and unmeasured confounds in non-experimental data. Associations from genetically informed tests in twins are considered “quasi-causal,” suggesting that our confidence in the causal underpinning of the association between soda consumption and BMI has been strengthened. We hypothesized that the association between soda consumption and BMI would be significant both between and within twins.MethodsThis was a cross sectional study of 5787 same sex adult twin pairs (18–97 years, 66% female) from the community based Washington State Twin Registry. Structural equation modeling (SEM) was employed to investigate associations between soda consumption and BMI in the population (the phenotypic association between exposure and outcome among all twins treated as individuals) and within pairs of identical and fraternal twins (the quasi-causal association controlling for between pair genetic and environmental confounds).ResultsAmong all twins, there was a significant phenotypic association between soda consumption and BMI that held when controlling for age, sex, race, annual household income, and education level (P < 0.05). In the quasi-causal model, however, the effect of soda consumption on BMI was greatly reduced and no longer significant, with a large genetic confound in both men and women (P < 0.05).ConclusionAmong a large group of adult twin pairs, increased soda consumption was associated with increased BMI; however, the observed association was mediated by a genetic background common to both.

Polymorphisms in Lep and Lepr Genes in Infants: Correlation with Serum Leptin Values in the First 6 Months of Life

ABSTRACTObjective: Because several studies indicate that polymorphisms in leptin (Lep) and leptin receptor (Lepr) genes play a central role in determining obesity, we analyzed 2 single nucleotide polymorphisms (SNPs) in the Lep gene (Lep G2548A and A19G) and one in the Lepr gene (Lepr A668G) to verify the effect of the 3 SNPs on leptin concentrations in infancy.Methods: We enrolled 80 healthy Caucasian infants under 6 months of age, who were genotyped for the 3 SNPs with amplification refractory mutation system–mismatch amplification mutation assay (ARMS-MAMA) real-time polymerase chain reaction (PCR). Serum leptin values were measured with a radioimmunoassay method. Statistical significance was set at p < 0.05.Results: There were no significant differences between individually analyzed leptin polymorphisms Lep G2548A and A19G and serum leptin levels (p > 0.05). Because we found that Lep G2548A and A19G are in linkage disequilibrium on chromosome 7, we performed the haplotype analysis for Lep G2548A and Lep A19G. We obtained higher serum leptin levels in infants with the GG/GG haplotype (p < 0.05). Regarding receptor, we found higher leptin levels in GG-genotype infants for Lepr A668G (p < 0.001). Considering the 3 SNPs together, we found higher serum leptin values in GG/GG-GG infants (LepG2548A/A19G-Lepr A668G; p < 0.001).Conclusion: We obtained higher serum leptin levels in infants with the GG genotype for Lepr A668G, with haplotype GG/GG for Lep G2548A/A19G, and with GG/GG-GG (LepG2548A/A19G-Lepr A668G); thus, it seems that the genotype GG could be a protector against obesity development in infancy and adulthood. Moreover, these data confirm that not variations in the Lep gene as well as in the Lepr gene could play a role in weight gain. Further studies are needed to evaluate the role of genetics and the environment in a predisposition toward obesity later in life.

A Genome-Wide Association Study Using a Custom Genotyping Array Identifies Variants in GPR158 Associated With Reduced Energy Expenditure in American Indians.

Pima Indians living in Arizona have a high prevalence of obesity, and we have previously shown that a relatively lower energy expenditure (EE) predicts weight and fat mass gain in this population. EE is a familial trait (heritability = 0.52); therefore, in the current study, we aimed to identify genetic variants that affect EE and thereby influence BMI and body fatness in Pima Indians. Genotypic data from 491,265 variants were analyzed for association with resting metabolic rate (RMR) and 24-h EE assessed in a whole-room calorimeter in 507 and 419 Pima Indians, respectively. Variants associated with both measures of EE were analyzed for association with maximum BMI and percent body fat (PFAT) in 5,870 and 912 Pima Indians, respectively. rs11014566 nominally associated with both measures of EE and both measures of adiposity in Pima Indians, where the G allele (frequency: Pima Indians = 0.60, Europeans <0.01) associated with lower 24-h EE (β = −33 kcal/day per copy), lower RMR (β = −31 kcal/day), higher BMI (β = +0.6 kg/m2), and higher PFAT (β = +0.9%). However, the association of rs11014566 with BMI did not directionally replicate when assessed in other ethnic groups. rs11014566 tags rs144895904, which affected promoter function in an in vitro luciferase assay. These variants map to GPR158, which is highly expressed in the brain and interacts with two other genes (RGS7 and CACNA1B) known to affect obesity in knockout mice. Our results suggest that common ethnic-specific variation in GPR158 may influence EE; however, its role in weight gain remains controversial, as it either had no association with BMI or associated with BMI but in the opposite direction in other ethnic groups.

Psychological care before and after bariatric surgery

The management of an obese patient involves a multidisciplinary team. The psychological dimension often plays an important role in weight gain and must be taken into account early on in the care pathway. The support given to the patient must notably involve work on body image and how this changes as a result of bariatric surgery.

INSIG2 polymorphism and weight gain, dyslipidemia and serum adiponectin in Finnish patients with schizophrenia treated with clozapine.

To investigate INSIG2's association with obesity, weight change and serum lipid profile during clozapine treatment. Subjects with schizophrenia (n = 190) were genotyped, identifying seven SNPs. Genetic risk scores (GRSs) were calculated to adiponectin, high-density lipoprotein cholesterol, triglycerides and weight gain. In the model for weight gain, SNPs rs12151787, rs17047733 and rs10490626 were selected. Explanatory variables were BMI (p = 5.05 × 10-5), age (p = 0.003) and GRS (p = 2.81 × 10-5, p = 0.0002 after permutation). No GRS resulted for adiponectin or high-density lipoprotein cholesterol. Rs2161829 and rs10490620 were selected for triglycerides; this GRS was insignificant after permutation. INSIG2 plays a role in weight gain and obesity during clozapine treatment.

True, true, unrelated? A review of recent evidence for a causal influence of breakfast on obesity.

It has long been known that breakfast skipping is associated with obesity; however, well controlled clinical trials have only recently been conducted to determine a causative relationship. Skipping breakfast is likely to be detrimental for insulin sensitivity; however, randomized trials suggest that it does not play a large role in weight gain or weight loss. Specific breakfast strategies such as certain types of breakfast, and consuming more calories in the morning relative to the evening, however, may produce greater weight loss. The act of eating breakfast, compared to skipping it, does not appear to have a large impact on body weight. More specific strategies regarding the size and type of breakfast may be required for a substantial effect on weight loss, and improving glycemic regulation may be an important reason to consume breakfast rather than skipping it.

Relationship among obesity, depression, and emotional eating in young adults

Depressive symptoms are often associated with obesity, and emotional eating may play a considerable role in weight gain. This study aimed to examine the association among depression symptoms, emotional eating, and body mass index (BMI) in Mexican college students; and to assess emotional eating as mediator between depressive symptoms and BMI. A total of 1453 students at a public university in Mexico City completed the scale Self-Efficacy in Emotion- and Stress- Related Eating of the Eating and Appraisal Due to Emotions and Stress Questionnaire (EADES) to assess emotional eating, and the scale created by the Center for Epidemiologic Studies (CES-D) to identify depressive symptoms. Weight and height were measured to calculate BMI. Structural equation models (SEM) were used to assess emotional eating as mediator between depressive symptoms and BMI by sex. Depressive symptoms were associated with emotional eating in both men (Beta = −0.33, p < 0.001) and women (Beta = −0.46, p < 0.001). Emotional eating, in turn, was associated with BMI in men (Beta = −0.08, p < 0.001) as well as in women (Beta = −0.09, p < 0.001). Emotional eating was a mediator between depression and BMI, adjusted for age in both sexes. This finding suggests that emotion management should be taken into consideration in obesity prevention and treatment strategies applied to young adults.

A5230 - Influence and effects of the diet and bariatric surgery on the biological clock of peripheral tissues

One area of considerable interest is the degree to which eating patterns influence energy regulation and the risk of obesity. Animal studies have indicated that the timing of food intake may be linked to energy regulation. The vast majority of research on eating patterns among humans has focused on breakfast skipping versus consumption, particularly in children. Although the data are not completely consistent, most studies have concluded that, among children, skipping breakfast is associated with a higher risk of obesity, as well as lower overall diet quality and poorer cognitive performance. Dysregulation of nutrient availability can have an impact on survival during a fast or lead to obesity and related pathologies, such as type 2 diabetes, in response to overnutrition. The meal times (and number of meals consumed) differ greatly from culture to culture and through time. Indeed, timing of food intake is a modifiable behavior that may influence energy regulation and consequently the risk of obesity. A number of recent studies in animals have linked energy regulation and the circadian clock at the molecular, physiological and behavioral levels, findings that raise the possibility that the timing of food intake itself may play a significant role in weight gain. The aim of this study was to test the hypothesis that significant and sustained weight loss, induced by bariatric surgery and diet could modify the expression of clock genes, metabolism and physiology ones on human stomach Stomach explants from morbilidly patients with obesity disease obtained during bariatric surgery, were taken and placed into 24-well plates with DMEM and kept in an incubator at 37ºC for 1h to stabilize the tissues. After that, the explants were incubated with DMEM or oleic acid 100 µM during 6h and change every 6h for a full day. The samples considered control, remained overnight with DMEM.The samples with oleic acid remained the 6h but not continously, each test samples were kept treatment according to the time show:Time 0= initial timeTime 21h or 9pmTime 3h or 3amTime 9h or 9amTime 15h or 3pm Several epidemiological studies have suggested that the perturbation of circadian rhythm has adverse metabolic consequences (e.g., dyslipidemia) in humans. At the molecular level, circadian rhythms are encoded by an autoregulatory loop composed of a set of transcription activators (BMAL1 Brain and Muscle Arnt Like 1/CLOCK (Circadian Locomotor Output Cycles Kaput) that induce expression of repressors (PER (period) /CRY (cryptocromo).The mammalian molecular clock is not only expressed within the master suprachiasmatic nucleus pacemaker neurons, but also within nearly all cells. We have identify clock genes presence on stomach. The clock genes on the stomach tissue are regulated by oleic acid and by bariatric surgery. Not only the amount or type of food we ingest, but also the timing of food consumption seems to play a crucial role in the development of obesity and associated metabolic disorders. Circadian clocks are widely accepted to act as the timekeeping system of nearly every living organism, ensuring that physiological processes are carried out at the right time of day or night.However, the concept that the stomach is home to one of the food-entrainable oscillators that predicts the availability of food, especially when food becomes restricted, is the first time that is reported to be a peripheral clock.

Polycystic ovary syndrome: insight into pathogenesis and a common association with insulin resistance

Polycystic ovary syndrome (PCOS) is a common condition that typically develops in reproductive-age women. The cardinal clinical and biochemical characteristics of PCOS include reproductive dysfunction and hyperandrogenic features. PCOS is also strongly associated with obesity based on data from epidemiological and genetic studies. Accordingly, PCOS often becomes manifest in those women who carry a genetic predisposition to its development, and who also gain weight. The role of weight gain and obesity in the development of PCOS is mediated at least in part, through worsening of insulin resistance. Compensatory hyperinsulinaemia that develops in this context disrupts ovarian function, with enhanced androgen production and arrest of ovarian follicular development. Insulin resistance also contributes to the strong association of PCOS with adverse metabolic risk, including dysglycaemia, dyslipidaemia and fatty liver. Conversely, modest weight loss of just 5% body weight with improvement in insulin sensitivity, frequently results in clinically meaningful improvements in hyperandrogenic, reproductive and metabolic features. Future developments of novel therapies for obese women with PCOS should focus on promotion of weight loss and improvement in insulin sensitivity. In this context, therapies that complement lifestyle changes such as dietary modification and exercise, particularly during the maintenance phase of weight loss are important. Putative novel targets for therapy in PCOS include human brown adipose tissue.

Weight gain in Turner Syndrome: association to puberty induction? - longitudinal analysis of KIGS data.

Girls with Turner Syndrome (TS) treated or not treated with growth hormone (GH) are prone to overweight. Therefore, we hypothesize that puberty induction in TS is associated with weight gain. We analyzed weight changes (BMI-SDS) between onset of GH treatment and near adult height (NAH) in 887 girls with TS enrolled in KIGS (Pfizer International Growth Database). Puberty was induced with estrogens in 646 (72·8%) girls with TS. Weight status did not change significantly between GH treatment start and 1 year later (mean difference -0·02 BMI-SDS), but increased significantly (P < 0·001) until NAH (+0·40 BMI-SDS). The BMI-SDS increased +0·21 until start of puberty (P < 0·001). Girls with spontaneous and induced puberty showed similar BMI-SDS changes. Puberty induction at ≥12 years was associated with a significant (P < 0·001) less increase of BMI-SDS (+0·7 BMI-SDS) between baseline and NAH compared to puberty induction at <12 year (+1·0 BMI-SDS). In multiple linear regression analyses changes of BMI-SDS between baseline and NAH were negatively associated with baseline BMI-SDS (P < 0·001), GH doses (P = 0·015), and age at puberty induction (P < 0·001), positively with years on GH treatment (P = 0·004), while duration and dose of estrogens, its route of administration (transdermal/oral), changes of height-SDS, thyroxin and oxandrolone treatment, and karyotype did not correlate significantly to changes of BMI-SDS in this time period. Puberty does not seem to play a major role in weight gain in girls with TS since the majority of the increases in BMI-SDS occurred before puberty. However, late puberty induction seems to decrease the risk of weight gain.

Beverage intake and obesity in early childhood: evidence form primary health care clients in Northwest Argentina.

Sugar sweetened beverages (SSB) are thought to play an important role in weight gain. We examined the relationship between the intake of caloric and noncaloric beverages (SSB and water) and the nutritional status of children. In 2014, we randomly selected 16 public health clinics in four cities of Northwest Argentina and conducted a survey among mothers of children 0-6 years of age. Children's beverage intake was ascertained by 24-h dietary recall provided by the mothers. Children's weight and height measures were obtained from clinic's registries. We calculated the body mass index using the International Obesity Task Force standards. The analysis included 562 children 25 months to 6 years of age with normal or above normal nutritional status. Children's beverage consumption was as follows, water 81.8%, carbonated soft drinks (CSD) 49.7%, coffee/tea/cocoa 44.0%, artificial fruit drinks 35.6%, flavored water 17.9%, natural fruit juice 14.5%. In multivariate logistic regression models the likelihood of being obese v. being overweight or having normal weight doubled with an intake of one to five glasses of CSD (OR=2.2) and increased by more than three-fold with an intake of more than five glasses (OR=3.5). Drinking more than five glasses of water decreased the likelihood of being obese by less than half (OR=0.3). The percentage of children drinking more than five glasses of other beverages was low (3.3-0.9%) and regression models did not yield significant results. The study contributed evidence for reducing children's CSD intake and for promoting water consumption, together with the implementation of comprehensive regulatory public health policies.

Polycystic ovary syndrome: insight into pathogenesis and a common association with insulin resistance

Polycystic ovary syndrome (PCOS) is a common condition that typically develops in reproductive-age women. The cardinal clinical and biochemical characteristics of PCOS include reproductive dysfunction and hyperandrogenic features. PCOS is also strongly associated with obesity based on data from epidemiological and genetic studies. Accordingly, PCOS often becomes manifest in those women who carry a genetic predisposition to its development, and who also gain weight. The role of weight gain and obesity in the development of PCOS is mediated at least in part, through worsening of insulin resistance. Compensatory hyperinsulinaemia that develops in this context disrupts ovarian function, with enhanced androgen production and arrest of ovarian follicular development. Insulin resistance also contributes to the strong association of PCOS with adverse metabolic risk, including dysglycaemia, dyslipidaemia and fatty liver. Conversely, modest weight loss of just 5% body weight with improvement in insulin sensitivity, frequently results in clinically meaningful improvements in hyperandrogenic, reproductive and metabolic features. Future developments of novel therapies for obese women with PCOS should focus on promotion of weight loss and improvement in insulin sensitivity. In this context, therapies that complement lifestyle changes such as dietary modification and exercise, particularly during the maintenance phase of weight loss are important. Putative novel targets for therapy in PCOS include human brown adipose tissue.

Commentary: Antidepressants and diabetes risk: why are there discrepant findings from cohort studies based on patient records and those based on serial phenotyping?

Commentary: Antidepressants and diabetes risk: why are there discrepant findings from cohort studies based on patient records and those based on serial phenotyping?