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RationaleExperimental studies suggest that exposures may impact respiratory health across generations via epigenetic changes transmitted specifically through male germ cells. Studies in humans are however limited. We aim to identify epigenetic marks in offspring associated with father’s preconception smoking.MethodsWe conducted epigenome-wide association studies (EWAS) in the RHINESSA cohort on father’s any preconception smoking (N=875 offspring) and father’s pubertal onset smoking ResultsFather’s smoking commencing preconception was associated with methylation of blood DNA in offspring at two Cytosine-phosphate-Guanine sites (CpGs) (False Discovery Rate (FDR) PRR5andCENPP. Father’s pubertal onset smoking was associated with 19 CpGs (FDR TLR9, DNTT, FAM53B, NCAPG2, PSTPIP2, MBIP, C2orf39, NTRK2, DNAJC14, CDO1, PRAP1, TPCN1, IRS1andCSF1R). These differentially methylated sites were hypermethylated and associated with promoter regions capable of gene silencing. Some of these sites were associated with offspring outcomes in this cohort including ever-asthma (NTRK2), ever-wheezing (DNAJC14, TPCN1), weight (FAM53B, NTRK2) and BMI (FAM53B, NTRK2) (P< 0.05). Pathway analysis showed enrichment for gene ontology pathways including regulation of gene expression, inflammation and innate immune responses.ConclusionFather’s preconception smoking, particularly in puberty, is associated with offspring DNA methylation, providing evidence that epigenetic mechanisms may underly epidemiological observations that pubertal paternal smoking increases risk of offspring asthma, low lung function and obesity.

Background: Research in non-genetic inheritance indicates that grandparents’ smoking habits and their childhood experiences of trauma can influence the physical and psychological attributes of their grandchildren. This was particularly apparent for outcomes such as autism and obesity where the population prevalence changed over time. Other factors which have changed temporally include religious and spiritual beliefs (RSBs) which have been declining in Western populations.Methods: We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC) to explore whether grandparental exposures were associated with the religious and/or spiritual beliefs of their grandchildren as measured with a positive response to the question “Do you believe in God or some divine power?” . In line with other inter/trans-generational human studies we hypothesised that: (H1) grandparents’ childhood exposures to cigarette smoking (whether in utero or by active smoking) and/or exposure to traumatic events during childhood will be associated with their grandchild’s RSB; (H2) associations will differ between maternal and paternal lines of inheritance; (H3) relationships will vary with age at grandparental exposure, and (H4) associations will differ between grandsons and granddaughters.Results: We found significant associations between the grandchild’s RSB and both the grandparents’ smoking and their childhood trauma histories (H1 supported). These associations were mainly found down the maternal line (H2 possibly supported) and results varied with age of exposure of the grandparents; being strongest for in utero exposure of cigarette smoke and for pre-puberty exposure of traumatic events (H3 supported), and that granddaughters were more affected than grandsons (H4 supported).Conclusions: We hope that these results will motivate collection of similar data to further evaluate these questions in other populations, including a possible role for biological mechanisms.

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BackgroundDNA methylation (DNAm) is an epigenetic mark that can be used to understand interindividual variability in genomic regulation, and it is influenced by many genetic and environmental factors. Co-methylation between DNAm sites is a known phenomenon but the full architecture of relationships between the approximately 450,000 (450k) sites most commonly measured in epidemiological studies has not been described. We investigate whether the cis and trans interindividual co-methylation structure amongst the 450k sites changes across the lifecourse, whether it differs between UK-born White and Pakistani individuals, and how it may be related to genome regulation.ResultsWe find stability across the life course (birth to adolescence), across cohorts, and between two ethnic groups. Highly correlated DNAm sites in close proximity are highly heritable, influenced by nearby genetic variants (cis mQTLs), and are enriched for transcription factor (TF) binding sites related to regulation of short RNAs essential for cellular function transcribed by RNA polymerase III. Highly correlated sites that are either distant, or on different chromosomes, are driven by both common and unique environmental factors, and methylation at these sites is less likely to be driven by genotype. They are enriched for a multitude of TF binding sites and for inter-chromosomal chromatin contact sites, suggesting that DNA co-methylation of distant sites may be related to long-range cooperative TF interactions.ConclusionsWe conclude that DNA co-methylation, especially in cis, has a stable structure from birth to adolescence and between white British and Pakistani individuals. We hypothesise that co-methylation may have roles in genome regulation in humans, including 3D chromatin architecture. The stable structure we have identified might have implications for the future design and interpretation of epigenetic studies.

The idea that information can be transmitted to subsequent generation(s) by epigenetic means has been studied for decades but remains controversial in humans. Epidemiological studies have established that grandparental exposures are associated with health outcomes in their grandchildren, often with sex-specific effects; however the mechanism of transmission is still unclear. We conducted Epigenome Wide Association Studies (EWAS) to test whether grandmaternal smoking during pregnancy is associated with altered DNA methylation (DNAm) in their adolescent grandchildren. We used data from a birth cohort, with discovery and replication datasets of 1225 and 708 individuals (respectively), aged 15-17 years, and tested replication in the same individuals at birth and 7 years. We show for the first time that DNAm at a small number of loci is associated with grandmaternal smoking in humans, and their locations in the genome suggest hypotheses of transmission. We observe and replicate sex-specific associations at two sites on the X chromosome, one located in an imprinting control region and both within transcription factor binding sites (TFBSs). In fact, we observe enrichment for TFBSs among the CpG sites with the strongest associations, suggesting that TFBSs may be a mechanism by which grandmaternal exposures influence offspring DNA methylation. There is limited evidence that these associations appear at earlier timepoints, so effects are not static throughout development. The implication of this work is that effects of smoking during pregnancy may induce DNAm changes in later generations and that these changes are often sex-specific, in line with observational associations.

Epigenome-wide association studies (EWAS) seek to quantify associations between traits/exposures and DNA methylation measured at thousands or millions of CpG sites across the genome. In recent years, the increase in availability of DNA methylation measures in population-based cohorts and case-control studies has resulted in a dramatic expansion of the number of EWAS being performed and published. To make this rich source of results more accessible, we have manually curated a database of CpG-trait associations (with p-4) from published EWAS, each assaying over 100,000 CpGs in at least 100 individuals. From January 7, 2022, The EWAS Catalog contained 1,737,746 associations from 2,686 EWAS. This includes 1,345,398 associations from 342 peer-reviewed publications. In addition, it also contains summary statistics for 392,348 associations from 427 EWAS, performed on data from the Avon Longitudinal Study of Parents and Children (ALSPAC) and the Gene Expression Omnibus (GEO). The database is accompanied by a web-based tool and R package, giving researchers the opportunity to query EWAS associations quickly and easily, and gain insight into the molecular underpinnings of disease as well as the impact of traits and exposures on the DNA methylome. The EWAS Catalog data extraction team continue to update the database monthly and we encourage any EWAS authors to upload their summary statistics to our website. Details of how to upload data can be found here: http://www.ewascatalog.org/upload. The EWAS Catalog is available at http://www.ewascatalog.org.

The adverse effects on the child of maternal smoking in pregnancy is well-recognized, but little research has been carried out on the possible non-genetic effects of ancestral smoking prior to the pregnancy including parental initiation of cigarette smoking in their own childhoods or a grandmother smoking during pregnancy. Here, we summarize the studies that have been published mainly using data from the Avon Longitudinal Study of Parents and Children. We demonstrate evidence that ancestral smoking prior to or during pregnancy can often be beneficial for offspring health and both ancestor- and sex-specific. More specifically, we report evidence of (i) adverse effects of the father starting to smoke pre-puberty on his son’s development; (ii) beneficial effects on the grandson if his maternal grandmother had smoked in pregnancy; and (iii) mainly adverse effects on the granddaughter when the paternal grandmother had smoked in pregnancy. The ancestor- and sex-specificity of these results are consistent with earlier studies reporting associations of health and mortality with ancestral food supply in their parents’ and grandparents’ pre-pubertal childhoods., Review of published ALSPAC studies demonstrate ancestral smoking prior to pregnancy can be beneficial or detrimental for offspring health and development and often both ancestor- and sex-specific.

Background Engagement in multiple risk behaviours can have adverse consequences for health during childhood, during adolescence, and later in life, yet little is known about the impact of different types of interventions that target multiple risk behaviours in children and young people, or the differential impact of universal versus targeted approaches. Findings from systematic reviews have been mixed, and effects of these interventions have not been quantitatively estimated. Objectives To examine the effects of interventions implemented up to 18 years of age for the primary or secondary prevention of multiple risk behaviours among young people. Search methods We searched 11 databases (Australian Education Index; British Education Index; Campbell Library; Cumulative Index to Nursing and Allied Health Literature (CINAHL); Cochrane Central Register of Controlled Trials (CENTRAL), in the Cochrane Library; Embase; Education Resource Information Center (ERIC); International Bibliography of the Social Sciences; MEDLINE; PsycINFO; and Sociological Abstracts) on three occasions (2012, 2015, and 14 November 2016)). We conducted handsearches of reference lists, contacted experts in the field, conducted citation searches, and searched websites of relevant organisations. Selection criteria We included randomised controlled trials (RCTs), including cluster RCTs, which aimed to address at least two risk behaviours. Participants were children and young people up to 18 years of age and/or parents, guardians, or carers, as long as the intervention aimed to address involvement in multiple risk behaviours among children and young people up to 18 years of age. However, studies could include outcome data on children > 18 years of age at the time of follow-up. Specifically,we included studies with outcomes collected from those eight to 25 years of age. Further, we included only studies with a combined intervention and follow-up period of six months or longer. We excluded interventions aimed at individuals with clinically diagnosed disorders along with clinical interventions. We categorised interventions according to whether they were conducted at the individual level; the family level; or the school level. Data collection and analysis We identified a total of 34,680 titles, screened 27,691 articles and assessed 424 full-text articles for eligibility. Two or more review authors independently assessed studies for inclusion in the review, extracted data, and assessed risk of bias.We pooled data in meta-analyses using a random-effects (DerSimonian and Laird) model in RevMan 5.3. For each outcome, we included subgroups related to study type (individual, family, or school level, and universal or targeted approach) and examined effectiveness at up to 12 months' follow-up and over the longer term (> 12 months). We assessed the quality and certainty of evidence using the Grades of Recommendation, Assessment, Development and Evaluation (GRADE) approach. Main results We included in the review a total of 70 eligible studies, of which a substantial proportion were universal school-based studies (n = 28; 40%). Most studies were conducted in the USA (n = 55; 79%). On average, studies aimed to prevent four of the primary behaviours. Behaviours that were most frequently addressed included alcohol use (n = 55), drug use (n = 53), and/or antisocial behaviour (n = 53), followed by tobacco use (n = 42). No studies aimed to prevent self-harm or gambling alongside other behaviours.Evidence suggests that for multiple risk behaviours, universal school-based interventions were beneficial in relation to tobacco use (odds ratio (OR) 0.77, 95% confidence interval (CI) 0.60 to 0.97; n = 9 studies; 15,354 participants) and alcohol use (OR 0.72, 95% CI 0.56 to 0.92; n = 8 studies; 8751 participants; both moderate-quality evidence) compared to a comparator, and that such interventions may be effective in preventing illicit drug use (OR 0.74, 95% CI 0.55 to 1.00; n = 5 studies; 11,058 participants; low-quality evidence) and engagement in any antisocial behaviour (OR 0.81, 95% CI 0.66 to 0.98; n = 13 studies; 20,756 participants; very low-quality evidence) at up to 12 months' follow-up, although there was evidence of moderate to substantial heterogeneity (I² = 49% to 69%). Moderate-quality evidence also showed that multiple risk behaviour universal school-based interventions improved the odds of physical activity (OR 1.32, 95% CI 1.16 to 1.50; I² = 0%; n = 4 studies; 6441 participants). We considered observed effects to be of public health importance when applied at the population level. Evidence was less certain for the effects of such multiple risk behaviour interventions for cannabis use (OR 0.79, 95% CI 0.62 to 1.01; P = 0.06; n = 5 studies; 4140 participants; I² = 0%; moderate-quality evidence), sexual risk behaviours (OR 0.83, 95% CI 0.61 to 1.12; P = 0.22; n = 6 studies; 12,633 participants; I² = 77%; low-quality evidence), and unhealthy diet (OR 0.82, 95% CI 0.64 to 1.06; P = 0.13; n = 3 studies; 6441 participants; I² = 49%; moderate-quality evidence). It is important to note that some evidence supported the positive effects of universal school-level interventions on three or more risk behaviours.For most outcomes of individual- and family-level targeted and universal interventions, moderate- or low-quality evidence suggests little or no effect, although caution is warranted in interpretation because few of these studies were available for comparison (n ≤ 4 studies for each outcome).Seven studies reported adverse effects, which involved evidence suggestive of increased involvement in a risk behaviour among participants receiving the intervention compared to participants given control interventions.We judged the quality of evidence to be moderate or low for most outcomes, primarily owing to concerns around selection, performance, and detection bias and heterogeneity between studies. Authors' conclusions Available evidence is strongest for universal school-based interventions that target multiple- risk behaviours, demonstrating that they may be effective in preventing engagement in tobacco use, alcohol use, illicit drug use, and antisocial behaviour, and in improving physical activity among young people, but not in preventing other risk behaviours. Results of this review do not provide strong evidence of benefit for family- or individual-level interventions across the risk behaviours studied. However, poor reporting and concerns around the quality of evidence highlight the need for high-quality multiple- risk behaviour intervention studies to further strengthen the evidence base in this field.

Background We aimed to undertake a Cochrane systematic review to quantify the effect of multiple risk behaviour interventions on prevention of substance use, antisocial behaviour, sexual risk, vehicle risk, self-harm, gambling, physical inactivity and unhealthy diet among individuals aged 8–25 years as little is known about their effectiveness (CD009927). Methods Eleven databases were searched to 14 November 2016. Randomised controlled trials were included that addressed two or more risk behaviours in individuals aged 0–18 years. Data were pooled in a random-effects meta-analysis in Revman 5.3. For each outcome, we included subgroups relating to study type (individual, family or school-level and universal or targeted in approach). The quality of evidence was assessed using the GRADE approach. Results We identified 34 680 titles, screened 27 691 articles and included seventy studies. We found moderate quality evidence indicating that universal school-level interventions were beneficial in relation to tobacco use (odds ratio [OR] 0.77, 95% confidence interval [CI] 0.60–0.97, n=15 354, I2 57%), alcohol use (OR 0.72, 95% CI 0.56 to 0.92, n=8,751, I2 58%), and physical activity (OR 1.32, 95% CI 1.16 to 1.50, n=6 441, I2 0%) compared to a comparator. Lower quality evidence indicated possible benefit for drug use (OR 0.74, 95% CI 0.55 to 1.00, n=11 058, I2 69%) and antisocial behaviour (OR 0.81, 95% CI 0.66 to 0.98, n=20 756, I2 66%), while findings were less certain for sexual risk behaviour (OR 0.80, 95% CI 0.60 to 1.08, n=13 351, I2 80%; low quality evidence) and unhealthy diet (OR 0.82, 95% CI 0.64 to 1.06, n=6441, I2 49%, moderate quality evidence). Analyses indicated that family- and individual-level interventions probably have little or no effect on these outcomes, although fewer such studies were identified. The quality of studies was judged to be of moderate or low quality for most outcomes, primarily owing to concerns around selection, performance and detection bias, and heterogeneity between studies. Conclusion Available evidence is strongest for universal school-level interventions that target multiple risk behaviours demonstrating that they may be effective in preventing certain risk behaviours. However, concerns around poor reporting and study quality highlight the need to strengthen the evidence base in this field. This abstract is based on preliminary findings from a Cochrane review currently underway. Upon completion and approval, the final version is expected to be published in the Cochrane Database of Systematic Reviews.

ObjectivePsoriasis and eczema are common inflammatory skin diseases that have been reported to be associated with obesity. However, causality has not yet been established. We aimed to investigate the possible causal relationship between body mass index (BMI) and psoriasis or eczema.MethodsFollowing a review of published epidemiological evidence of the association between obesity and either psoriasis or eczema, Mendelian Randomization (MR) was used to test for a causal relationship between BMI and these inflammatory skin conditions. We used a genetic instrument comprising 97 single nucleotide polymorphisms (SNPs) associated with BMI. One-sample MR was conducted using individual-level data (401,508 individuals) from the UK Biobank and the Nord-Trøndelag Health Study (HUNT), Norway. Two-sample MR was performed with summary-level data (731,021 individuals) from published BMI, psoriasis and eczema GWAS. The one-sample and two-sample MR estimates were meta-analysed using a fixed effect model. To explore the reverse causal direction, MR analysis with genetic instruments comprising variants from recent genome-wide analyses for psoriasis and eczema were used to test if inflammatory skin disease has a causal effect on BMI.ResultsPublished observational data show an association of greater BMI with both psoriasis and eczema case status. The observational associations were confirmed in UK Biobank and HUNT datasets. MR analyses provide evidence that higher BMI causally increases the odds of psoriasis (by 53% per 5 units higher BMI; OR= 1.09 (1.06 to 1.12) per 1 kg/m2; P=4.67×10-9) and eczema (by 8% per 5 units higher BMI; OR=1.02 (1.00 to 1.03) per 1 kg/m2; P=0.09). When investigating causality in the opposite direction, MR estimates provide little evidence for an effect of either psoriasis or eczema influencing BMI.ConclusionOur study, using genetic variants as instrumental variables for BMI, shows that higher BMI leads to a higher risk of inflammatory skin disease. The causal relationship was stronger for psoriasis than eczema. Therapies and life-style interventions aimed at controlling BMI or targeting the mechanisms linking obesity with skin inflammation may offer an opportunity for the prevention or treatment of these common skin diseases.

Background Psychotic Symptoms (PS) are often distressing and can be predictive of schizophrenia, other psychiatric disorders and suicide attempts in adulthood, particularly if they persist during adolescence. Previous research in diagnosis-discordant monozygotic twin-pairs and patient-control samples has demonstrated that changes in epigenetic processes could be potential biomarkers of the emergence and persistence of PS. Investigation in large, pre-clinical population-based samples is urgently required. The aim of this study is to explore the association between DNA methylation and the emergence, persistence, and remission of PS in childhood and adolescence. Methods DNA methylation data (Illumina 450k) were obtained from the ARIES subsample of the ALSPAC birth cohort at birth, age 7, and age 15/17 (N=901). PS were assessed in private interviews with the participants at ages 12 and 18. EWAS were conducted to determine the association between DNA methylation at each time-point and reports of PS at ages 12 and 18, controlling for pregnancy and birth-related covariates and cell-type composition. Gene Ontology (GO) term enrichment analyses of the top probes were performed to identify important pathways. The top probes from each EWAS were used to investigate the role of DNA methylation in the persistence and remission of PS by comparing individuals with no history of PS, those whose symptoms persisted, and those whose symptoms remitted. Multilevel models were then constructed to test the association between the longitudinal methylomic trajectory of the top CpG sites and the trajectory of psychotic symptoms. Results from a replication of the top findings in an independent cohort will also be presented. Results A number of probes were differentially methylated (p Discussion Findings from this large, population-based study suggest that epigenetic processes at multiple stages of development may be associated with the emergence, remission, and persistence of PS in late childhood and adolescence. Research uncovering biomarkers associated with pre-clinical PS is important as it has the potential to facilitate early identification of individuals at increased risk and target preventive interventions.

ObjectiveTo assess the reliability of treatment recommendations based on network meta-analysis (NMA).Study Design and SettingWe consider evidence in an NMA to be potentially biased. Taking each pairwise contrast in turn, we use a structured series of threshold analyses to ask: (1) “How large would the bias in this evidence base have to be before it changed our decision?” and (2) “If the decision changed, what is the new recommendation?” We illustrate the method via two NMAs in which a Grading of Recommendations Assessment, Development and Evaluation (GRADE) assessment for NMAs has been implemented: weight loss and osteoporosis.ResultsFour of the weight-loss NMA estimates were assessed as “low” and six as “moderate” quality by GRADE; for osteoporosis, six were “low,” nine were “moderate,” and 1 was “high.” The threshold analysis suggests plausible bias in 3 of 10 estimates in the weight-loss network could have changed the treatment recommendation. For osteoporosis, plausible bias in 6 of 16 estimates could change the recommendation. There was no relation between plausible bias changing a treatment recommendation and the original GRADE assessments.ConclusionsReliability judgments on individual NMA contrasts do not help decision makers understand whether a treatment recommendation is reliable. Threshold analysis reveals whether the final recommendation is robust against plausible degrees of bias in the data.

Background Psoriasis is a common inflammatory skin disease that has been reported to be associated with obesity. We aimed to investigate a possible causal relationship between body mass index (BMI) and psoriasis. Methods and findings Following a review of published epidemiological evidence of the association between obesity and psoriasis, mendelian randomization (MR) was used to test for a causal relationship with BMI. We used a genetic instrument comprising 97 single-nucleotide polymorphisms (SNPs) associated with BMI as a proxy for BMI (expected to be much less confounded than measured BMI). One-sample MR was conducted using individual-level data (396,495 individuals) from the UK Biobank and the Nord-Trøndelag Health Study (HUNT), Norway. Two-sample MR was performed with summary-level data (356,926 individuals) from published BMI and psoriasis genome-wide association studies (GWASs). The one-sample and two-sample MR estimates were meta-analysed using a fixed-effect model. To test for a potential reverse causal effect, MR analysis with genetic instruments comprising variants from recent genome-wide analyses for psoriasis were used to test whether genetic risk for this skin disease has a causal effect on BMI. Published observational data showed an association of higher BMI with psoriasis. A mean difference in BMI of 1.26 kg/m2 (95% CI 1.02–1.51) between psoriasis cases and controls was observed in adults, while a 1.55 kg/m2 mean difference (95% CI 1.13–1.98) was observed in children. The observational association was confirmed in UK Biobank and HUNT data sets. Overall, a 1 kg/m2 increase in BMI was associated with 4% higher odds of psoriasis (meta-analysis odds ratio [OR] = 1.04; 95% CI 1.03–1.04; P = 1.73 × 10−60). MR analyses provided evidence that higher BMI causally increases the odds of psoriasis (by 9% per 1 unit increase in BMI; OR = 1.09 (1.06–1.12) per 1 kg/m2; P = 4.67 × 10−9). In contrast, MR estimates gave little support to a possible causal effect of psoriasis genetic risk on BMI (0.004 kg/m2 change in BMI per doubling odds of psoriasis (−0.003 to 0.011). Limitations of our study include possible misreporting of psoriasis by patients, as well as potential misdiagnosis by clinicians. In addition, there is also limited ethnic variation in the cohorts studied. Conclusions Our study, using genetic variants as instrumental variables for BMI, provides evidence that higher BMI leads to a higher risk of psoriasis. This supports the prioritization of therapies and lifestyle interventions aimed at controlling weight for the prevention or treatment of this common skin disease. Mechanistic studies are required to improve understanding of this relationship., In a mendelian randomization study, Ashley Budu-Aggrey and co-workers study the influence of body mass index on psoriasis., Author summary Why was this study done? Psoriasis is a common inflammatory skin disease that has been reported to be associated with obesity. However, the direction of causality has not been established. Understanding the causal relationship could inform the management or prevention of disease. What did the researchers do and find? A mendelian randomization (MR) approach was used to investigate the causal relationship between higher body mass index (BMI) and psoriasis. Our analysis included data for a total of 753,421 individuals from two of the largest population-based studies available as well as published genome-wide association studies (GWASs). We found evidence that higher BMI causally increases the risk of psoriasis, supporting observational reports in previous literature. Conversely, there was no evidence to support a causal effect of psoriasis genetic risk upon BMI. What do these findings mean? Our findings suggest that obesity contributes to the pathogenesis of psoriasis, and highlight possible mechanistic relationships. If our findings regarding genetically influenced BMI can be extended to elevated BMI that is amenable to modification by diet or behavior, then they could carry health implications. Further work will be required to determine the effect of a short-term intervention aimed at reducing BMI upon psoriasis patients after disease onset, ideally within a clinical trial setting.

Background: Epilepsy is a long-term condition that requires self-management, but currently, there is no well evaluated epilepsy self-education or self-management intervention in the United Kingdom (UK).Aim: The aim of this study was to examine the views and experiences of the first participants of the Self-Management in epILEpsy UK (SMILE UK) program to assist the development of a full trial.Method: In-depth semistructured interviews and group discussions were conducted with 10 people with poorly controlled epilepsy to explore their views and experiences of the self-management program. Interviews wereaudio-recorded, transcribed, and analyzed thematically.Results:All participants viewed the program positively. Three themes emerged: i) peer support was experienced through knowledge sharing, disclosure of experiences, and exchange of contact details; ii) participants felt betterequipped to enter discussions with doctors and other health-care professionals about their condition; and iii) participants reported an improvement in their personal life through increased confidence to live with epilepsy and acceptance of their diagnosis.Conclusion: A brief group self-management intervention increased knowledge and confidence in managing epilepsy.