The impact of paternal alcohol, tobacco, caffeine use and physical activity on offspring mental health: a systematic review and meta-analysis

Plain language summary More research has focused on the impact mothers’ behaviours (such as smoking or alcohol use) during and around pregnancy may have on their children’s health, with less research investigating the role paternal health behaviours may play. This review captured what research was currently available that investigated the impact of paternal alcohol, tobacco, caffeine use, and physical activity during pregnancy on children’s mental health. We showed that this area is currently under researched, finding only eight studies. However, of the research that was already published we found evidence of paternal health behaviours having an impact on children’s mental health. The strongest evidence was shown for paternal smoking during pregnancy having a negative impact on children’s hyperactivity/ADHD. No studies measured paternal caffeine use or physical activity around pregnancy. This review highlights the lack of research that has investigated the association between paternal modifiable health behaviours around pregnancy and offspring mental health. Despite including four different types of paternal health behaviours and a broad definition of offspring mental health across any age, only eight studies were shown. This review suggests further research within this area is needed which may influence health warnings to potential fathers to be both before conception and during pregnancy

The relationships between women’s reproductive factors:a Mendelian randomisation analysis

BACKGROUND: Women’s reproductive factors include their age at menarche and menopause, the age at which they start and stop having children and the number of children they have. Studies that have linked these factors with disease risk have largely investigated individual reproductive factors and have not considered the genetic correlation and total interplay that may occur between them. This study aimed to investigate the nature of the relationships between eight female reproductive factors. METHODS: We used data from the UK Biobank and genetic consortia with data available for the following reproductive factors: age at menarche, age at menopause, age at first birth, age at last birth, number of births, being parous, age first had sexual intercourse and lifetime number of sexual partners. Linkage disequilibrium score regression (LDSC) was performed to investigate the genetic correlation between reproductive factors. We then applied Mendelian randomisation (MR) methods to estimate the causal relationships between these factors. Sensitivity analyses were used to investigate directionality of the effects, test for evidence of pleiotropy and account for sample overlap. RESULTS: LDSC indicated that most reproductive factors are genetically correlated (r(g) range: |0.06–0.94|), though there was little evidence for genetic correlations between lifetime number of sexual partners and age at last birth, number of births and ever being parous (r(g) < 0.01). MR revealed potential causal relationships between many reproductive factors, including later age at menarche (1 SD increase) leading to a later age at first sexual intercourse (beta (B) = 0.09 SD, 95% confidence intervals (CI) = 0.06,0.11), age at first birth (B = 0.07 SD, CI = 0.04,0.10), age at last birth (B = 0.06 SD, CI = 0.04,0.09) and age at menopause (B = 0.06 SD, CI = 0.03,0.10). Later age at first birth was found to lead to a later age at menopause (B = 0.21 SD, CI = 0.13,0.29), age at last birth (B = 0.72 SD, CI = 0.67, 0.77) and a lower number of births (B = −0.38 SD, CI = −0.44, −0.32). CONCLUSION: This study presents evidence that women’s reproductive factors are genetically correlated and causally related. Future studies examining the health sequelae of reproductive factors should consider a woman’s entire reproductive history, including the causal interplay between reproductive factors. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12916-022-02293-5

The COVID-19 pandemic and the menstrual cycle: research gaps and opportunities

International audienceSince the beginning of the COVID-19 pandemic, discussions on social media and blogs have indicated that women have experienced menstrual changes, including altered menstrual duration, frequency, regularity, and volume (heavier bleeding and clotting), increased dysmenorrhea, and worsened premenstrual syndrome. There have been a small number of scientific studies of variable quality reporting on menstrual cycle features during the pandemic, but it is still unclear whether apparent changes are due to COVID-19 infection/illness itself, or other pandemic-related factors like increased psychological stress and changes in health behaviours. It is also unclear to what degree current findings are explained by reporting bias, recall bias, selection bias and confounding factors. Further research is urgently needed. We provide a list of outstanding research questions and potential approaches to address them. Findings can inform policies to mitigate against gender inequalities in health and society, allowing us to build back better post-COVID

Prenatal alcohol exposure and facial morphology in a UK cohort

AbstractHigh levels of prenatal alcohol exposure are known to cause an array of adverse outcomes including foetal alcohol syndrome (FAS); however, the effects of low to moderate exposure are less-well characterised. Previous findings suggest that differences in normal-range facial morphology may be a marker for alcohol exposure and related adverse effects. Therefore, in the Avon Longitudinal Study of Parents and Children, we tested for an association between maternal alcohol consumption and six FAS-related facial phenotypes in their offspring, using both self-report questionnaires and the maternal genotype at rs1229984 inADH1Bas measures of maternal alcohol consumption. In both self-reported alcohol consumption (N=4,233) and rs1229984 genotype (N=3,139) analyses, we found no strong statistical evidence for an association between maternal alcohol consumption and facial phenotypes tested. The directions of effect estimates were compatible with the known effects of heavy alcohol exposure, but confidence intervals were largely centred around zero. We conclude that, in a sample representative of the general population, there is no strong evidence for an effect of prenatal alcohol exposure on normal-range variation in facial morphology.</jats:p

The long-term impact of folic acid in pregnancy on offspring DNA methylation : follow-up of the Aberdeen folic acid supplementation trial (AFAST)

Funding This work was supported by the NIHR Bristol Biomedical Research Centre at the University Hospitals Bristol NHS Foundation Trust and the University of Bristol. The views expressed in this publication are those of the authors and not necessarily those of the NHS, the National Institute for Health Research or the Department of Health. R.C.R., G.C.S., N.K., T.G., G.D.S. and C.L.R. work in a unit that receives funds from the University of Bristol and the UK Medical Research Council (MC_UU_12013/1, MC_UU_12013/2 and MC_UU_12013/8). This work was also supported by CRUK (grant number C18281/A19169) and the ESRC (grant number ES/N000498/1). C.M.T. is supported by a Wellcome Trust Career Re-entry Fellowship (grant number 104077/Z/14/Z).Peer reviewedPublisher PD

Examining Health Outcomes in Juvenile Idiopathic Arthritis:A Genetic Epidemiology Study

OBJECTIVE: Juvenile idiopathic arthritis (JIA) is the most common pediatric rheumatic disease; however, little is known about its wider health impacts. This study explores health outcomes associated with JIA genetic liability. METHODS: We used publicly available genetic data sets to interrogate the genetic correlation between JIA and 832 other health‐related traits using linkage disequilibrium score regression. Two‐sample Mendelian randomization (2SMR) was used to examine four genetic correlates for evidence of causality. RESULTS: We found robust evidence (adjusted P [P (adj)] < 0.05) of genetic correlation between JIA and rheumatoid arthritis (genetic correlation [r (g)] = 0.63, P (adj) = 0.029), hypothyroidism/myxedema (r (g) = 0.61, P (adj) = 0.041), celiac disease (CD) (r (g) = 0.58, P (adj) = 0.032), systemic lupus erythematosus (r (g) = 0.40, P (adj) = 0.032), coronary artery disease (CAD) (r (g) = 0.42, P (adj) = 0.006), number of noncancer illnesses (r (g) = 0.42, P (adj) = 0.016), paternal health (r (g) = 0.57, P (adj) = 0.032), and strenuous sports (r (g) = −0.52, P (adj) = 0.032). 2SMR analyses found robust evidence that genetic liability to JIA was causally associated with the number of noncancer illnesses reported by UK Biobank (UKBB) participants (increase of 0.03 noncancer illnesses per doubling odds of JIA, 95% confidence interval 0.01‐0.05). CONCLUSION: This study illustrates genetic sharing between JIA and a diversity of health outcomes. The causal association between genetic liability to JIA and noncancer illnesses suggests a need for broader health assessments of patients with JIA to reduce their potential comorbid burden. The strength of genetic correlation with hypothyroidism and CD implies that patients with JIA may benefit from CD and thyroid function screening. Strong positive genetic correlation between JIA and CAD supports the need for cardiovascular risk assessment and risk factor modification