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We are the Clare Inclusive Research Group (CIRG) a group of advocates with a learning disability, funded by the Irish support agency the Brothers of Charity (B.O.C.), Clare Services. As a long-established inclusive research group we were approached to reflect on our journey as advocates and researchers. In this article we talk about our work, challenging and helping repeal discriminating Irish law regarding intimate relationships. We then talk about our understanding of advocacy and inclusive research and make recommendations to make this work more effective. Method: As a group of members of CIRG, with the coordinator of the group, we developed this article using online Zoom discussion calls to identify themes, circulating online explanations of drafts followed by Zoom reflections and finally responding to academic reviews. The direct comments made by us as advocate researchers have been retained as they were expressed. Conclusions, Limitations and recommendations: One of our team remarked “advocacy and inclusive research are twins”. We concluded that they are very close but not identical. Our work together on this article led us to create a discussion paper, Manifesto for Inclusive Research. This was adopted as a touchstone for presentations at the first webinar roundtable of the newly formed Inclusive Research IASSID Special Interest Research Group in March 2022. In it we set out guidelines for creating inclusive research which require accessible information and valuing our input in terms that match our status as experts by experience in inclusive research. We challenge academic inclusive researchers who explore the world of intellectual disability to stand shoulder to shoulder with advocate inclusive researchers. Through our work together, we aim to create more fulfilling lives for us all.

Background/purpose: There is a need to comprehensively investigate the relationship between tooth eruption and obesity. The study aimed to investigate the relationship between erupted permanent tooth number and obesity among 12-year-old children in a population-based study. Materials and methods: A random sample of 806 12-year-old schoolchildren in Hong Kong was recruited. Oral examinations were conducted and the eruption status of the permanent teeth was assessed. Body height, body weight, waist circumference (WC), hip circumference, and triceps skinfold thickness (TRSKF) were measured to assess the adiposity statuses [weight-height ratio (W/H) and body mass index (BMI) for general obesity; WC and waist-hip ratio (WHR) for central obesity; and TRSKF for peripheral obesity]. The relationships between erupted permanent tooth number and adiposity statuses were examined in bivariate analysis and analysis of covariance. Results: The response rate was 82.9% (n = 668/806). Three hundred and forty-six (50.9%) children had 28 teeth erupted. Second molars had the highest rate of noneruption (17.5–35.8%). The mean number and standard deviation (SD) of erupted permanent tooth were 26.4 (2.4). The mean value and SD were 31.1 (6.3) for W/H, 19.8 (3.7) for BMI, 70.4 (9.4) for WC, 0.82 (0.06) for WHR, and 11.8 (4.5) for TRSKF, respectively. After accounting for sociodemographic factors, analysis of covariance identified that W/H, BMI, WC, and WHR were positively associated with the number of erupted permanent teeth (P

Abstract Background Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders which are more common in males. The ‘prenatal sex steroid’ hypothesis links excessive sex-steroid exposure during foetal life with the behavioural differences observed in ASD. However, the reason why sex steroid exposure may be excessive remains unclear. Epidemiological studies have identified several environmental risk factors associated with ASD, including developmental vitamin D (DVD) deficiency. We have demonstrated in an animal model that DVD-deficiency is associated with a hyper-inflammatory response in placentas from male but not female foetuses. Vitamin D also regulates the expression of several steroidogenic enzymes in vitro. Therefore using this animal model, we have examined whether DVD-deficiency leads to increased sex-steroid levels in both the maternal and foetal compartments. Methods Female rats are fed a vitamin D deficient diet from 6 weeks before mating until tissue collection at embryonic day 18. We examined the levels of testosterone, androstenedione and corticosterone in maternal plasma, foetal brains and amniotic fluid. We further examined gene expressions of steroidogenic enzymes and DNA methylation of aromatase promoters in foetal brains as a potential molecular mechanism regulating testosterone expression. Results We show that DVD-deficiency increases testosterone levels in maternal blood. We also show elevated levels of testosterone and androstenedione in the amniotic fluid of female but not male DVD-deficient foetuses. Testosterone levels were also elevated in DVD-deficient male brains. Vitamin D, like other steroid-related hormones, regulates gene expression via methylation. Therefore we examined whether the significant elevation in testosterone in male brains was due to such a potential gene-silencing mechanism. We show that the promoter of aromatase was hyper-methylated compared to male controls. Limitations A reduction in aromatase, in addition to causing excessive testosterone, could also lead to a reduction in estradiol which was not examined here. Conclusions This study is the first to show how an epidemiologically established environmental risk factor for ASD may selectively elevate testosterone in male embryonic brains. These findings provide further mechanistic support for the prenatal sex steroid theory of ASD.