25 January 2019 In Pregnant Women

AIM: This paper systematically reviews the literature on the effects of prenatal alcohol exposure on early child development from birth to 5 years with the aim to synthesize the developmental outcomes associated with prenatal alcohol exposure, and inform further research to improve our knowledge of the manifestations of prenatal alcohol exposure.

METHODS: Electronic databases (MEDLINE, Psych INFO, and Psych ARTICLES) were searched to find papers on the developmental outcomes of prenatal alcohol exposure in neonates, infants and toddlers and pre-school aged children. Studies were selected based on participants self-reporting alcohol consumption during pregnancy (either prospectively or retrospectively) and/or children being diagnosed with FASD based on a standardized assessment that includes a dysmorphology examination. The search was limited to peer-reviewed, English language studies involving human subjects, up to 5.5 years old.

RESULTS: Out of the 1,684 titles screened, a total of 71 papers were identified as relevant and included in this review. The majority of studies were prospective longitudinal studies. A range of assessment modalities (or tools) was used to determine neurodevelopmental outcomes of prenatal exposure to alcohol in the age group under review, the most frequently described being the Bayley Scales of Infant and Toddler Development (BSID) (n = 19). Studies varied in terms of the dose, frequency, and timing of alcohol consumption during pregnancy and methodology used to assess alcohol consumption. Findings demonstrate extensive evidence for poor global developmental outcomes in children prenatally exposed to alcohol, particularly with moderate to severe levels of prenatal alcohol exposure.

CONCLUSION: The outcomes related to lower levels of prenatal alcohol exposure as well as outcomes in specific developmental domains, are poorly understood. Further research should aim to clarify the more subtle or less easily measurable manifestations of prenatal alcohol exposure on early development when the potential for greatest impact of interventions is highest.

25 January 2019 In Pregnant Women

OBJECTIVES: Fetal alcohol spectrum disorders (FASD) is a worldwide problem. Maternal alcohol consumption is an important risk factor for FASD. It remains unknown which alcohol consumption patterns most strongly predict FASD. The objective of this study was to identify these.

DESIGN: Systematic literature review.

METHODS: We searched in PubMed, PsychINFO, PsycARTICLES, ERIC, CINAHL, Embase and MEDLINE up to August 2018. The query consisted of keywords and their synonyms related to FASD, pregnancy and behaviour. Studies were excluded when not published in English, were reviews or involved non-human subjects. Substantial heterogeneity precluded aggregation or meta-analysis of the data. Instead, data were qualitatively inspected.

RESULTS: In total, 21 studies were eligible for further data analysis. All studies that measured both maternal alcohol drinking behaviours and FASD reported retrospective data on maternal drinking patterns, employing both continuous and categorical measures and exhibiting substantial heterogeneity in measures of alcohol consumption (eg, timing of exposure, quantification of alcohol measure and definition of a standard drink). Study quality improved over time and appeared higher for studies based on active case ascertainment, especially when conducted in schools and when behaviour was assessed through interviews.

CONCLUSIONS: We aimed to identify specific maternal drinking behaviour(s) related to FASD. The state of the literature precludes such conclusions. Evidence-based preventive measures necessitate identifying which prenatal alcohol drinking behaviour(s) are most in need of intervention. Therefore, we formulate three recommendations for future research. First, future studies can optimise the value of the collected dataset through specifying measurements and reporting of maternal drinking behaviours and avoiding categorised measures (nominal or ordinal) whenever possible. Second, samples should not be selected based on FASD status, but instead, FASD status as well as maternal alcohol consumption should both be measured in a general population sample. Finally, we provide 10 reporting guidelines for FASD research.

05 December 2018 In Cancer

Alcohol has consistently been shown to increase breast cancer (BC) risk. This association may be modified by single nucleotide polymorphisms in alcohol dehydrogenase isoenzymes ADH1B and ADH1C. The Netherlands Cohort Study comprises 62 573 women, aged 55-69 years at baseline (1986). Follow-up for postmenopausal BC for 20.3 years was available. Genotyping of 6 tag SNPs in ADH1B and ADH1C, respectively, was performed on DNA from toenails. A case-cohort approach was used for analysis (complete data available for: nsubcohort= 1301; ncases= 1630). Cox regression models for postmenopausal BC were applied to determine marginal effects of alcohol intake and SNPs using a dominant genetic model, as well as multiplicative interaction of the two. Results were also obtained for subtypes by estrogen (ER) and progesterone receptor (PR) status. Multiple testing was adjusted for by applying the false discovery rate (FDR). Alcohol intake (categorical) increased the risk of postmenopausal BC (ptrend=0.031). Trends for ER and PR subgroups followed a similar pattern. Continuous modelling of alcohol resulted in a hazard rate ratio (HR) for overall postmenopausal BC of 1.09 (95% CI: 1.01 - 1.19) per 10g/d of alcohol. SNPs were not associated with BC risk. No effect modification of the alcohol-BC association by SNP genotype was seen after FDR-correction in overall BC and ER/PR subgroups. In conclusion, alcohol was shown to increase the risk of postmenopausal BC. This association was not significantly modified by common ADH1B and ADH1C SNPs, neither in overall BC nor in hormone receptor defined subtypes.

05 December 2018 In Liver Disease

BACKGROUND: Alcohol is a known cause of cirrhosis, but it is unclear if the associated risk varies by whether alcohol is drunk with meals, or by the frequency or type of alcohol consumed. Here we aim to investigate the associations between alcohol consumption with meals, daily frequency of consumption, and liver cirrhosis.

METHODS: The Million Women Study is a prospective study that includes one in every four UK women born between 1935 and 1950, recruited between 1996 and 2001. In 2001 (IQR 2000-03), the participants reported their alcohol intake, whether consumption was usually with meals, and number of days per week it was consumed. Cox regression analysis yielded adjusted relative risks (RRs) for incident cirrhosis, identified by follow-up through electronic linkage to routinely collected national hospital admission, and death databases.

FINDINGS: During a mean of 15 years (SD 3) of follow-up of 401 806 women with a mean age of 60 years (SD 5), without previous cirrhosis or hepatitis, and who reported drinking at least one alcoholic drink per week, 1560 had a hospital admission with cirrhosis (n=1518) or died from the disease (n=42). Cirrhosis incidence increased with amount of alcohol consumed (>/=15 drinks [mean 220 g of alcohol] vs one to two drinks [mean 30 g of alcohol] per week; RR 3.43, 95% CI 2.87-4.10; p<0.0001). About half of the participants (203 564 of 401 806) reported usually drinking with meals and, after adjusting for amount consumed, cirrhosis incidence was lower for usually drinking with meals than not (RR 0.69, 0.62-0.77; p<0.0001; wine-only drinkers RR 0.69, 0.56-0.85; all other drinkers RR 0.72, 0.63-0.82). Among 175 618 women who consumed seven or more drinks per week, cirrhosis incidence was greater for daily consumption than non-daily consumption (adjusted RR 1.61, 1.40-1.85; p<0.0001). Daily consumption, together with not drinking with meals, was associated with more than a doubling of cirrhosis incidence (adjusted RR 2.47, 1.96-3.11; p<0.0001).

INTERPRETATION: In middle-aged women, cirrhosis incidence increases with total alcohol intake, even at moderate levels of consumption. For a given weekly intake of alcohol, this excess incidence of cirrhosis is higher if consumption is usually without meals, or with daily drinking. FUNDING: UK Medical Research Council and Cancer Research UK.

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