Social support of romantic partners moderates cortisol response to stress

It is important to clearly define stress and social support in order to better understand how the body regulates when under stressful conditions because stress has implications for treatment and coping interventions. The widely known stress hormone cortisol is frequently used as an index of the body’s abilty to regulate itself during stress because cortisol has a profound impact on health and development. Consistently, strong evidence from research has found that social support from affiliated others serve as a buffer of stress, and certain types of social support may enhance stress regulation more than others. Self-report subjective measurements of stress can provide valuable information on saliency of the stressor, however the chance of response biases is possible due to a number of contributing factors that entails answering questionnaires. The same can be found for subjective social support self-report measurements. In addition to external factors of social support, recent research has found that oxytocin, known as the social bonding hormone, can also buffer the negative impact of stress and attenuate cortisol activity. Typically, when social support is provided, endogenous levels of oxytocin is increased in stressful moments. In this thesis study, I presented a theoretical model to examine moderating effects of different social support measures on the association between stress and cortisol levels in romanticly dating couples. The findings showed that perceived social support moderately buffered cortisol stress reactivity, while nonverbal behavioral support significantly buffered cortisol stress reactivity. Oxytocin reactivity and level of exposure only showed a trend effect on cortisol stress reactivity. Consummate love between the couples significantly buffered cortisol stress reactivity. The findings of this study gave empirical support for specific measures of social support in predicting cortisol reactivity to psychosocial stress in each of its own way

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Puberty as a moderator on risk for psychopathology symptoms and autistic stereotypy exacerbation in adolescents with and without ASD

Mental health problems among adolescents remain a public health concern in the U.S. despite growing efforts to support mental wellbeing of youth. A part of the problem is a dearth of knowledge on evidence-based mechanisms on declining mental health in a particular subset of adolescents, and that subset is males and males on the autism spectrum. While studies on gender preponderance of mental health disorders contribute to the knowledge base on treating categorical psychopathology disorders sensitive to gendered issues, limitations include overlooking heterotypic comorbidities and understanding its underlying processes leading up to the development of mental health problems. Pubertal maturation is a process at which all adolescents transition through and for some adolescents, internalizing and externalizing symptoms may arise and can be overlooked. This is partly due to puberty viewed as a normative process for all adolescents going through “raging hormones,” a misconception of the role of hormones and behavior during development. Along with the social and physical changes that come with adolescent development, neurobiological activities are taking place implicating brain development and behaviors. Hormones play a role in adolescent development; however, their mechanistic impact, particularly in males, is less understood. This dissertation had three specific aims. The first aim was to investigate the effect of pubertal maturation on internalizing and externalizing (I-E) symptoms in children and adolescent males across development. The second aim was to examine the role of puberty and autistic stereotypy on I-E symptoms in typically developing and autistic youths. The third aim was to test the effect of pubertal hormone testosterone, physical changes, and autistic stereotypy on depressive symptoms in typically developing and autistic adolescent males. Findings from this dissertation contribute to a small literature knowledge base on male adolescent development and psychopathology comorbidities

Symptom Trajectories in Boys: The Role of Puberty and Hormones in Longitudinal Patterns of Internalizing, Externalizing, and ADHD Symptoms

Little research is centered on male-specific developmental factors for elevated psychopathology. We address this critical gap in the literature by investigating the complex interplay of pubertal development, hormonal influence, and internalizing, externalizing, and ADHD symptom trajectories in boys assigned male at birth. We employed an accelerated longitudinal design across three timepoints of data collection, allowing us to capture both between-individual and within-individual developmental trajectories. Using growth curve models, we explored the influences of age, puberty, and hormonal levels on internalizing, externalizing, and ADHD symptoms. Pubertal stage and hormones were significantly associated with variations in psychopathology. Specifically, morning DHEA levels predicted lower initial levels of internalizing symptoms, while higher morning testosterone levels were associated with higher initial levels of internalizing symptoms. Our investigation into pubertal effects highlighted the nuanced relationship between pubertal stage and internalizing symptoms, moderated by age. Boys who were more mature in pubertal stage exhibited lower internalizing and ADHD symptom levels, reinforcing the significance of the timing of pubertal development. By partially unraveling the complex interactions that shape psychological well-being during adolescence, these insights hold potential implications for targeted interventions and the development of refined developmental models of psychopathology

Childhood Inhibition Predicts Adolescent Social Anxiety: Findings from a Longitudinal Twin Study

An enduring issue in the study of mental health is identifying developmental processes that explain how childhood characteristics progress to maladaptive forms. We examine the role that behavioral inhibition (BI) has on social anxiety (SA) during adolescence in 868 families of twins assessed at ages 8, 13, and 15 years. Multimodal assessments of BI and SA were completed at each phase, with additional measures (e.g., parenting stress) for parents and twins. Analyses were conducted in several steps: first, we used a cross-lagged panel model to demonstrate bidirectional paths between BI and SA; second a biometric Cholesky decomposition showed that both genetic and environmental influences on childhood BI also affect adolescent SA; next, multilevel phenotypic models tested moderation effects between BI and SA. We tested 7 potential moderators of the BI to SA prediction in individual models and included only those that emerged as significant in a final conditional model examining predictors of SA. Though several main effects emerged as significant, only parenting stress had a significant interaction with BI to predict SA, highlighting the importance of environmental moderators in models examining temperamental effects on later psychological symptoms. This comprehensive assessment continues to build the prototype for such developmental psychopathology models

Pubertal Effects on Executive Functioning Among Autistic and Non-Autistic Youth: A Cross Sectional Study

Investigating the role of puberty on executive function (EF) development is important for understanding how maturation and its related changes can impact neural systems underlying EF in autistic (AT) adolescents. Studies document chronological age-related differences in EF among AT youth, but the impact of puberty is understudied. We examined the role of cross-sectional pubertal status (Pubertal Development Scale adrenal and gonadal indices), autism status, and assigned sex at birth on parent-reported EF (Behavior Rating Inventory of Executive Function: inhibition, shift, working memory) in AT and non-autistic (NA) youth. We hypothesized AT youth, particularly females, would show more EF problems in late puberty relative to NA youth. AT males and females and NA females in late puberty had fewer shift problems relative to pre-pubertal youth, whereas NA males in late puberty had more shift problems relative to pre-pubertal NA males. There were no significant assigned sex or puberty differences in working memory for adrenal development and in any EF domain for gonadal development. Findings suggest adrenal puberty contributes to flexibility and may promote certain EF domains in AT youth. Longitudinal research using diverse measures of puberty and EF is needed to clarify findings

Opening up understanding of neurodiversity: a call for applying participatory and Open Scholarship practices

Recent movements towards a more open, intersectional, and inclusive academia(Birhane & Guest,  2020)  focus  on  the  need  to  address  traditional  power  imbalances  detrimentally affecting  under-represented  individuals  (e.g.,  women:  Pownall  &  Rogers,  2021;  people  of colour:  Berhe  et  al.,  2022;  non-WEIRD  [Western,  Educated,  Industrialised,  Rich,  and Democratic]  societies:  Puithllam  et  al.,  2022).  Hitherto,  neurodivergent  perspectives —i.e. non-pathological  variations  in  human  brains  (Walker,  2021)—are  often  overlooked  and misunderstood  within  behavioural  and  cognitive  sciences.  It  is  common  to  encounter assumptions that anything outside of neurotypicality is at best dismissed as outlier data, or at worst, considered disadvantageous and in need of ‘fixing’ (e.g., Gernsbacher & Pripas-Kapit, 2012). Such viewpoints hinder a broader understanding of human behaviour and cognition. Here,  we    call  for  more open and Participatory  Research on  neurodiversity  through addressing the issue of power imbalance.</p

Bridging neurodiversity and open scholarship:how shared values can guide best practices for research integrity, social justice, and principled education

Not all people conform to what is socially construed as the norm and divergences should be expected. Neurodiversity is fundamental to the understanding of human behaviour and cognition. However, neurodivergent individuals are often stigmatised, devalued, and objectified. This position statement presents the perspectives of neurodivergent authors, the majority of whom have personal lived experiences of neurodivergence(s), and discusses how research and academia can and should be improved in terms of research integrity, inclusivity and diversity. The authors describe future directions that relate to lived experience and systematic barriers, disclosure, directions on prevalence, stigma, intersection of neurodiversity and open scholarship, and provide recommendations that can lead to personal and systematic changes to improve acceptance of neurodivergent individuals’ lived experiences within academia

Global impact of the COVID-19 pandemic on subarachnoid haemorrhage hospitalisations, aneurysm treatment and in-hospital mortality: 1-year follow-up

Background: Prior studies indicated a decrease in the incidences of aneurysmal subarachnoid haemorrhage (aSAH) during the early stages of the COVID-19 pandemic. We evaluated differences in the incidence, severity of aSAH presentation, and ruptured aneurysm treatment modality during the first year of the COVID-19 pandemic compared with the preceding year. Methods: We conducted a cross-sectional study including 49 countries and 187 centres. We recorded volumes for COVID-19 hospitalisations, aSAH hospitalisations, Hunt-Hess grade, coiling, clipping and aSAH in-hospital mortality. Diagnoses were identified by International Classification of Diseases, 10th Revision, codes or stroke databases from January 2019 to May 2021. Results: Over the study period, there were 16 247 aSAH admissions, 344 491 COVID-19 admissions, 8300 ruptured aneurysm coiling and 4240 ruptured aneurysm clipping procedures. Declines were observed in aSAH admissions (-6.4% (95% CI -7.0% to -5.8%), p=0.0001) during the first year of the pandemic compared with the prior year, most pronounced in high-volume SAH and high-volume COVID-19 hospitals. There was a trend towards a decline in mild and moderate presentations of subarachnoid haemorrhage (SAH) (mild: -5% (95% CI -5.9% to -4.3%), p=0.06; moderate: -8.3% (95% CI -10.2% to -6.7%), p=0.06) but no difference in higher SAH severity. The ruptured aneurysm clipping rate remained unchanged (30.7% vs 31.2%, p=0.58), whereas ruptured aneurysm coiling increased (53.97% vs 56.5%, p=0.009). There was no difference in aSAH in-hospital mortality rate (19.1% vs 20.1%, p=0.12). Conclusion: During the first year of the pandemic, there was a decrease in aSAH admissions volume, driven by a decrease in mild to moderate presentation of aSAH. There was an increase in the ruptured aneurysm coiling rate but neither change in the ruptured aneurysm clipping rate nor change in aSAH in-hospital mortality