29 October 2018 In Phenolic compounds

There is a growing body of evidence implicating the gut 'microbiome' role in overall human health. Bacterial species belonging to the genera Lactobacillus and Bifidobacterium are generally considered to be beneficial and are commonly used in probiotic applications, whereas increases in some genera including Clostridum, Eubacterium and Bacteroides are implicated in negative health outcomes. Dietary polyphenols are bioactive compounds that have been found to increase the numbers of beneficial bacteria and antimicrobial actions against pathogenic bacteria, however most studies have been conducted in animal models or in-vitro colonic models. The aim of this systematic review was to provide an overview of recent trials on the effect of dietary grape and red wine polyphenols on the gut microbiota in humans. Following PRISMA guidelines, a systematic review was conducted of electronic databases (PubMed, CINAHL, Cochrane Library, Wed of Science and Scopus) to identify human intervention trials examining the effect of grape or wine polyphenols on gut microbiota. Seven trials met the inclusion criteria. One study looked at changes in gut microbiota following the ingestion of de-alcoholised red wine or red wine, and six studies referred to gut microbiota as intermediates in formation of phenolic metabolites. All studies confirmed that ingested polyphenols from grape and red wine, were modulated by gut microbiota, increasing numbers of polyphenolic metabolites which were found in blood, urine, ileal fluid and faeces. Intake of polyphenols derived from grape and red wine can modulate gut microbiota and contribute to beneficial microbial ecology that can enhance human health benefits. Additionally, grape and red wine polyphenols were modulated by the gut microbiota and there is a potential for a two-way relationship between the gut microbiota and polyphenolic compounds. Nevertheless, additional research is required to fully understand the complex relationship between gut microbiota and dietary polyphenols before any health claims can be made in relation to human health.

06 September 2018 In Pregnant Women

BACKGROUND AND OBJECTIVES: Although prenatal alcohol and nicotine exposure are associated with reduced cognition in children, associations between consumption of alcohol during lactation and cognition have not been examined. We aimed to examine whether drinking or smoking while breastfeeding lowers children's cognitive scores. We hypothesized that increased drinking or smoking would be associated with dose-dependent cognitive reductions.

METHODS: Data were sourced from Growing Up in Australia: The Longitudinal Study of Australian Children. Participants were 5107 Australian infants recruited in 2004 and assessed every 2 years. Multivariable linear regression analyses assessed relationships between drinking and smoking habits of breastfeeding mothers and children's Matrix Reasoning, Peabody Picture Vocabulary Test-Third Edition and Who Am I? scores at later waves.

RESULTS: Increased or riskier wave 1 maternal alcohol consumption was associated with reductions in Matrix Reasoning scores at age 6 to 7 years in children who had been breastfed (B = -0.11; SE = 0.03; 95% confidence interval: -0.18 to -0.04; P = .01). This relationship was not evident in infants who had never breastfed (B = -0.02; SE = 0.10; 95% confidence interval = -0.20 to 0.17; P = .87). Smoking during lactation was not associated with any outcome variable.

CONCLUSIONS: Exposing infants to alcohol through breastmilk may cause dose-dependent reductions in their cognitive abilities. This reduction was observed at age 6 to 7 years but was not sustained at age 10 to 11 years. Although the relationship is small, it may be clinically significant when mothers consume alcohol regularly or binge drink. Further analyses will assess relationships between alcohol consumption or tobacco smoking during lactation and academic, developmental, physical, and behavioral outcomes in children.

27 July 2018 In General Health

OBJECTIVE: To examine the association between an overall maternal healthy lifestyle (characterized by a healthy body mass index, high quality diet, regular exercise, no smoking, and light to moderate alcohol intake) and the risk of developing obesity in offspring.

DESIGN: Prospective cohort studies of mother-child pairs.

SETTING: Nurses' Health Study II (NHSII) and Growing Up Today Study (GUTS) in the United States.

PARTICIPANTS: 24 289 GUTS participants aged 9-14 years at baseline who were free of obesity and born to 16 945 NHSII women.

MAIN OUTCOME MEASURE: Obesity in childhood and adolescence, defined by age and sex specific cutoff points from the International Obesity Task Force. Risk of offspring obesity was evaluated by multivariable log-binomial regression models with generalized estimating equations and an exchangeable correlation structure.

RESULTS: 1282 (5.3%) offspring became obese during a median of five years of follow-up. Risk of incident obesity was lower among offspring whose mothers maintained a healthy body mass index of 18.5-24.9 (relative risk 0.44, 95% confidence interval 0.39 to 0.50), engaged in at least 150 min/week of moderate/vigorous physical activities (0.79, 0.69 to 0.91), did not smoke (0.69, 0.56 to 0.86), and consumed alcohol in moderation (1.0-14.9 g/day; 0.88, 0.79 to 0.99), compared with the rest. Maternal high quality diet (top 40% of the Alternate Healthy Eating Index 2010 diet score) was not significantly associated with the risk of obesity in offspring (0.97, 0.83 to 1.12). When all healthy lifestyle factors were considered simultaneously, offspring of women who adhered to all five low risk lifestyle factors had a 75% lower risk of obesity than offspring of mothers who did not adhere to any low risk factor (0.25, 0.14 to 0.47). This association was similar across sex and age groups and persisted in subgroups of children with various risk profiles defined by factors such as pregnancy complications, birth weight, gestational age, and gestational weight gain. Children's lifestyle did not significantly account for the association between maternal lifestyle and offspring obesity risk, but when both mothers and offspring adhered to a healthy lifestyle, the risk of developing obesity fell further (0.18, 0.09 to 0.37).

CONCLUSION: Our study indicates that adherence to a healthy lifestyle in mothers during their offspring's childhood and adolescence is associated with a substantially reduced risk of obesity in the children. These findings highlight the potential benefits of implementing family or parental based multifactorial interventions to curb the risk of childhood obesity.

27 July 2018 In Cardiovascular System

OBJECTIVE: To investigate the association between alcohol consumption (at baseline and over lifetime) and non-fatal and fatal coronary heart disease (CHD) and stroke.

DESIGN: Multicentre case-cohort study.

SETTING: A study of cardiovascular disease (CVD) determinants within the European Prospective Investigation into Cancer and nutrition cohort (EPIC-CVD) from eight European countries.

PARTICIPANTS: 32 549 participants without baseline CVD, comprised of incident CVD cases and a subcohort for comparison.

MAIN OUTCOME MEASURES: Non-fatal and fatal CHD and stroke (including ischaemic and haemorrhagic stroke).

RESULTS: There were 9307 non-fatal CHD events, 1699 fatal CHD, 5855 non-fatal stroke, and 733 fatal stroke. Baseline alcohol intake was inversely associated with non-fatal CHD, with a hazard ratio of 0.94 (95% confidence interval 0.92 to 0.96) per 12 g/day higher intake. There was a J shaped association between baseline alcohol intake and risk of fatal CHD. The hazard ratios were 0.83 (0.70 to 0.98), 0.65 (0.53 to 0.81), and 0.82 (0.65 to 1.03) for categories 5.0-14.9 g/day, 15.0-29.9 g/day, and 30.0-59.9 g/day of total alcohol intake, respectively, compared with 0.1-4.9 g/day. In contrast, hazard ratios for non-fatal and fatal stroke risk were 1.04 (1.02 to 1.07), and 1.05 (0.98 to 1.13) per 12 g/day increase in baseline alcohol intake, respectively, including broadly similar findings for ischaemic and haemorrhagic stroke. Associations with cardiovascular outcomes were broadly similar with average lifetime alcohol consumption as for baseline alcohol intake, and across the eight countries studied. There was no strong evidence for interactions of alcohol consumption with smoking status on the risk of CVD events.

CONCLUSIONS: Alcohol intake was inversely associated with non-fatal CHD risk but positively associated with the risk of different stroke subtypes. This highlights the opposing associations of alcohol intake with different CVD types and strengthens the evidence for policies to reduce alcohol consumption.

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