Dietary sugar/starches intake and Barrett’s esophagus: a pooled analysis

Barrett’s esophagus (BE) is the key precursor lesion of esophageal adenocarcinoma, a lethal cancer that has increased rapidly in westernized countries over the past four decades. Dietary sugar intake has also been increasing over time, and may be associated with these tumors by promoting hyperinsulinemia. The study goal was to examine multiple measures of sugar/starches intake in association with BE. This pooled analysis included 472 BE cases and 492 controls from two similarly conducted case–control studies in the United States. Dietary intake data, collected by study-specific food frequency questionnaires, were harmonized across studies by linking with the University of Minnesota Nutrient Database, and pooled based on study-specific quartiles. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for age, sex, race, total energy intake, study indicator, body mass index, frequency of gastro-esophageal reflux, and fruit/vegetable intake. In both studies, intake of sucrose (cases vs. controls, g/day: 36.07 vs. 33.51; 36.80 vs. 35.06, respectively) and added sugar (46.15 vs. 41.01; 44.18 vs. 40.68, respectively) were higher in cases than controls. BE risk was increased 79% and 71%, respectively, for associations comparing the fourth to the first quartile of intake of sucrose (ORQ4vs.Q1 = 1.79, 95% CI = 1.07–3.02, Ptrend = 0.01) and added sugar (ORQ4vs.Q1 = 1.71, 95% CI = 1.05–2.80, Ptrend = 0.15). Intake of sweetened desserts/beverages was associated with 71% increase in BE risk (ORQ4vs.Q1 = 1.71, 95% CI = 1.07–2.73, Ptrend = 0.04). Limiting dietary intake of foods and beverages that are high in added sugar, especially refined table sugar, may reduce the risk of developing BE

A pooled analysis of dietary sugar/carbohydrate intake and esophageal and gastric cardia adenocarcinoma incidence and survival in the USA

Background: During the past 40 years, esophageal/gastric cardia adenocarcinoma (EA/ GCA) incidence increased in Westernized countries, but survival remained low. A parallel increase in sugar intake, which may facilitate carcinogenesis by promoting hyperglycaemia, led us to examine sugar/carbohydrate intake in association with EA/GCA incidence and survival. Methods: We pooled 500 EA cases, 529 GCA cases and 2027 controls from two US population-based case-control studies with cases followed for vital status. Dietary intake, assessed by study-specific food frequency questionnaires, was harmonized and pooled to estimate 12 measures of sugar/carbohydrate intake. Multivariable-adjusted odds ratios (ORs) and hazard ratios [95% confidence intervals (CIs)] were calculated using multinomial logistic regression and Cox proportional hazards regression, respectively. Results: EA incidence was increased by 51-58% in association with sucrose (ORQ5vs.Q1=1.51, 95% CI=1.01-2.27), sweetened desserts/beverages (ORQ5vs.Q1=1.55, 95% CI=1.06-2.27) and the dietary glycaemic index (ORQ5vs.Q1=1.58, 95% CI=1.13-2.21). Bodymass index (BMI) and gastro-esophageal reflux disease (GERD) modified these associations (Pmultiplicative-interaction ≤ 0.05). For associations with sucrose and sweetened desserts/beverages, respectively, the OR was elevated for BMI < 25 (ORQ4-5vs.Q1-3=1.79, 95% CI=1.26-2.56 and ORQ4-5vs.Q1-3=1.45, 95% CI=1.03-2.06), but not BMI≥25 (ORQ4-5vs.Q1-3=1.05, 95% CI=0.76-1.44 and ORQ4-5vs.Q1-3=0.85, 95% CI=0.62-1.16). The EA-glycaemic index association was elevated for BMI≥25 (ORQ4-5vs.Q1-3=1.38, 95% CI=1.03-1.85), but not BMI < 25 (ORQ4-5vs.Q1-3=0.88, 95% CI=0.62-1.24). The sucrose-EA association OR for GERD < weekly was 1.58 (95% CI=1.16-2.14), but for GERD≥weekly was 1.01 (95% CI=0.70-1.47). Sugar/carbohydrate measures were not associated with GCA incidence or EA/GCA survival. Conclusions: If confirmed, limiting intake of sucrose (e.g. table sugar), sweetened desserts/ beverages, and foods that contribute to a high glycaemic index, may be plausible EA risk reduction strategies

A latent class approach to identify multi-risk profiles associated with phylogenetic clustering of recent hepatitis C virus infection in Australia and New Zealand from 2004 to 2015

INTRODUCTION:Over the last two decades, the incidence of hepatitis C virus (HCV) co-infection among men who have sex with men (MSM) living with HIV began increasing in post-industrialized countries. Little is known about transmission of acute or recent HCV, in particular among MSM living with HIV co-infection, which creates uncertainty about potential for reinfection after HCV treatment. Using phylogenetic methods, clinical, epidemiological and molecular data can be combined to better understand transmission patterns. These insights may help identify strategies to reduce reinfection risk, enhancing effectiveness of HCV treatment as prevention strategies. The aim of this study was to identify multi-risk profiles and factors associated with phylogenetic pairs and clusters among people with recent HCV infection. METHODS:Data and specimens from five studies of recent HCV in Australia and New Zealand (2004 to 2015) were used. HCV Core-E2 sequences were used to infer maximum likelihood trees. Clusters were identified using 90% bootstrap and 5% genetic distance threshold. Multivariate logistic regression and latent class analyses were performed. RESULTS:Among 237 participants with Core-E2 sequences, 47% were in a pair/cluster. Among HIV/HCV co-infected participants, 60% (74/123) were in a pair/cluster, compared to 30% (34/114) with HCV mono-infection (p < 0.001). HIV/HCV co-infection (vs. HCV mono-infection; adjusted odds ratio (AOR), 2.37, 95% confidence interval (CI), 1.45, 5.15) was independently associated with phylogenetic clustering. Latent class analysis identified three distinct risk profiles: (1) people who inject drugs, (2) HIV-positive gay and bisexual men (GBM) with low probability of injecting drug use (IDU) and (3) GBM with IDU & sexual risk behaviour. Class 2 (vs. Class 1, AOR 3.40; 95% CI, 1.52, 7.60), was independently associated with phylogenetic clustering. Many clusters displayed homogeneous characteristics, such as containing individuals exclusively from one city, individuals all with HIV/HCV co-infection or individuals sharing the same route of acquisition of HCV. CONCLUSIONS:Clusters containing individuals with specific characteristics suggest that HCV transmission occurs through discrete networks, particularly among HIV/HCV co-infected individuals. The greater proportion of clustering found among HIV/HCV co-infected participants highlights the need to provide broad direct-acting antiviral access encouraging rapid uptake in this population and ongoing monitoring of the phylogeny.Sofia R Bartlett, Tanya L Applegate, Brendan P Jacka, Marianne Martinello, Francois MJ Lamoury .. David Shaw ... et al