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Background Little is known about the long-term mental health consequences of the pandemic in children and young people (CYP), despite extremely high levels of exposure to the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) virus and the disruption to schooling and leisure activities due to the resultant restrictions. There are mixed findings from systematic reviews of how the pandemic affected CYP's mental health, which may be due to heterogeneous methods and poor quality studies. Most, but not all, suggest deterioration in mental health but population level studies may obscure the differing experiences of subgroups. The study questions are: (i) are there subgroups of CYP with distinct mental health profiles over the course of the second year of the Coronavirus Disease 2019 (COVID-19) pandemic (between April 2021 and May 2022); and (ii) do vulnerability factors influence CYP's mental health trajectories. Methods and findings A matched longitudinal cohort study of non-hospitalised test-positive and test-negative 11- to 17-year-old CYP in England were recruited from the UK Health Security Agency having undergone PCR testing for COVID-19. They completed the Strengths and Difficulties Questionnaire (SDQ) at least twice over a 12-month follow-up period. Overall, 8,518 of 17,918 (47.5%) CYP who returned their first SDQ at 3 or 6 months post-testing were included in the analytical sample. Associations between age, sex, ethnicity, socioeconomic status (SES), and an educational health and care plan (EHCP, indicating special educational needs) on SDQ score trajectories were examined separately, after adjusting for PCR test result. Findings from multilevel mixed-effects linear regression model showed that on average mental health symptoms as measured by the total SDQ score increased over time (B = 0.11 (per month), 95% CI = 0.09 to 0.12, p < 0.001) although this increase was small and not clinically significant. However, associations with time varied by age, such that older participants reported greater deterioration in mental health over time (B = 0.12 (per month), 95% CI = 0.10 to 0.14 for 15 to 17y; 0.08 (95% CI = 0.06 to 0.10) for 11 to 14y; p.sub.interaction = 0.002) and by sex, with greater deterioration in girls. Children with an EHCP experienced less deterioration in their mental health compared to those without an EHCP. There was no evidence of differences in rate of change in total SDQ by ethnicity, SES, or physical health. Those with worse prior mental health did not appear to be disproportionately negatively affected over time. There are several limitations of the methodology including relatively low response rates in CLoCk and potential for recall bias. Conclusions Overall, there was a statistically but not clinically significant decline in mental health during the pandemic. Sex, age, and EHCP status were important vulnerability factors that were associated with the rate of mental health decline, whereas ethnicity, SES, and prior poor physical health were not. The research highlights individual factors that could identify groups of CYP vulnerable to worsening mental health., Author(s): Laura Panagi 1,*, Simon R. White 1, Snehal M. Pinto Pereira 2, Manjula D. Nugawela 3, Isobel Heyman 3, Kishan Sharma 4, Terence Stephenson 3, Trudie Chalder 5, Natalia [...]

Objectives: To explore the impact of various measurements of long‐term health conditions (LTCs) on the resulting prevalence estimates using data from a nationally representative dataset. Methods: Children and young people in the Millennium Cohort Study were followed at ages 3, 5, 7, 11, and 14 years (N = 15,631). We estimated the weighted prevalence of LTCs at each time point and examined the degree to which estimates agreed with alternate health indicators (special educational needs and disability [SEND], specific chronic conditions, and common chronicity criteria) using descriptive analyses, Cohen's kappa statistic, and percentage agreement. Results: The estimated weighted prevalence of LTCs peaked at 5 years old (20%). Despite high percentage agreement, we observed at best moderate chance‐corrected agreement between the type of LTC and reasons for SEND (kappas from 0.02 to 0.56, percentage agreement from 97% to 99%) or specified chronic conditions (kappas from 0.002 to 0.02, percentage agreement from 73% to 97%). Applying chronicity criteria decreased the estimated weighted prevalence of LTCs (3%). Conclusion: How long‐term conditions are defined drastically alters the estimated weighted prevalence of LTCs. Improved clarity and consistency in the definition and measurement of LTCs is urgently needed to underpin policy and commissioning of services. [ABSTRACT FROM AUTHOR]

Background: Children and young people (CYP) with long‐term physical conditions (LTCs) are more likely to have poorer mental health and more school absenteeism compared with CYP with no LTCs. However, there is limited longitudinal research, and the extent to which these difficulties persist in CYP with LTCs is unknown. Furthermore, little is known about the relative impact of different types of LTC on mental health and absenteeism. Methods: We investigated cross‐sectional and longitudinal associations of different LTCs with mental health and school absenteeism in a large (N = 7977) nationally representative survey of CYP in Great Britain and its 3‐year follow‐up. Psychopathology was assessed using the parent‐reported Strengths and Difficulties Questionnaire (SDQ), and diagnosis of any psychiatric disorder using the Development and Wellbeing Assessment (DAWBA). Days absent and persistent absence (missing 10% or more of school days) were reported by parents. Results: Compared with those with no LTCs, CYP with any LTC had higher SDQ total difficulties scores at baseline (adjusted mean difference 1.4, 1.1–1.6) and follow‐up (1.1, 0.8–1.4) and were more likely to have a psychiatric disorder at baseline (adjusted odds ratio [aOR] 1.59, 1.34–1.89) and follow‐up (1.75, 1.44–2.12). Children with any LTC also missed more days of school at baseline (adjusted incidence rate ratio 1.47, 1.31–1.64) and follow‐up (1.17, 1.00–1.36) and were more likely to be persistently absent (aOR baseline 1.78, 1.48–2.14; follow‐up 1.27, 1.00–1.61). Neurodevelopmental disorders, migraines and atopic conditions were particularly strongly associated with both mental health and absenteeism. Conclusions: Children with LTCs had poorer mental health and more school absence than those with no LTCs. Clinicians should routinely enquire about mental health and school attendance in CYP with LTCs and should collaborate with families and schools to ensure these children are provided with sufficient mental health and educational support. [ABSTRACT FROM AUTHOR]

Background: Previous research has shown an association between subjective wellbeing and incident diabetes. Less is known about the role of wellbeing for subclinical disease trajectories as captured via glycated hemoglobin (HbA1c). We aimed to explore the association between subjective wellbeing and future HbA1c levels, and the role of sociodemographic, behavioral and clinical factors in this association. Methods: We used data from the English Longitudinal Study of Ageing for this study (N = 2161). Subjective wellbeing (CASP-19) was measured at wave 2 and HbA1c was measured 8 years later at wave 6. Participants were free from diabetes at baseline. We conducted a series of analyses to examine the extent to which the association was accounted for by a range of sociodemographic, behavioral and clinical factors in linear regression models. Results: Models showed that subjective wellbeing (CASP-19 total score) was inversely associated with HbA1c 8 years later after controlling for depressive symptoms, age, sex, and baseline HbA1c (B = −0.035, 95% CI −0.060 to –0.011, p = 0.005). Inclusion of sociodemographic variables and behavioral factors in models accounted for a large proportion (17.0% and 24.5%, respectively) of the relationship between wellbeing and later HbA1c; clinical risk factors explained a smaller proportion of the relationship (3.4%). Conclusions: Poorer subjective wellbeing is associated with greater HbA1c over 8 years of follow-up and this relationship can in part be explained by sociodemographic, behavioral and clinical factors among older adults. [ABSTRACT FROM AUTHOR]

Background: Positive psychological characteristics in people with type 2 diabetes (T2D) are associated with better health and longevity, and one plausible physiological mechanism involves lower markers of inflammation. Positive affect is related to lower basal inflammatory markers and smaller inflammatory responses to acute stress, but this association in people with T2D remains to be examined.Purpose: To examine the relationship between happiness and inflammatory markers at baseline and in response to acute stress in people with T2D.Methods: One hundred forty people with T2D took part in laboratory-based stress testing. We aggregated daily happiness ratings over 7 days before stress testing. During the laboratory session, participants underwent two mental stress tasks-the mirror tracing and the Stroop task. Blood was sampled at baseline and post-stress (up to 75 min post-stress) to detect plasma interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1Ra), and monocyte chemoattractant protein-1 (MCP-1). Associations between happiness and inflammatory markers and responses were analyzed using multivariable linear regressions.Results: Greater daily happiness significantly predicted lower baseline and post-stress IL-6 concentrations, and lower baseline MCP-1, after adjusting for covariates. The association between happiness and reduced basal IL-6 maintained after further controlling for daily sadness. We did not find significant associations between daily happiness and inflammatory responses to acute stress. No associations were detected for IL-1Ra.Conclusions: Happier individuals with T2D have lower inflammatory markers before and after acute stress, albeit independent of stress responsivity. Findings could provide a protective physiological pathway linking daily happiness with better health in people with T2D. [ABSTRACT FROM AUTHOR]

Loneliness is linked with all‐cause mortality and coronary heart disease. Altered neuroendocrine and inflammatory responses to stress constitute potential pathways linking loneliness and ill‐health. Stress responsivity is modified in people with Type 2 diabetes, but it is unclear whether loneliness influences biological stress responses in this population. We assessed interleukin‐6 (IL‐6), interleukin‐1 receptor antagonist (IL‐1RA), monocyte chemoattractant protein‐1 (MCP‐1), and cortisol responses to acute stress in 135 people with Type 2 diabetes. Loneliness was measured used the Revised UCLA Loneliness Scale. Loneliness was inversely associated with cortisol output poststress (B = −4.429, p = 0.019) independent of age, sex, education, marital status, body mass index, and smoking. Lonelier individuals had raised MCP‐1 concentrations 75 min poststress independent of covariates (B = 0.713, p = 0.022). No associations between loneliness and IL‐6 or IL‐1RA concentrations were detected. These results suggest that loneliness is associated with disturbances in stress responsivity in people with diabetes, and the impact of loneliness on health in people with diabetes may be mediated in part through dysregulation of inflammatory and neuroendocrine systems. Future research is required to understand if such changes increase the risk of poorer outcomes in this population. Loneliness is a predictor of poorer physical health outcomes. In healthy samples, loneliness is associated with altered biological responses to laboratory stress. Here, we demonstrate for the first time the link between loneliness and stress responses in people with diabetes. Our findings suggest that loneliness is linked with stress‐related biological disturbance in this population. Specifically, we detected blunted cortisol stress responses and raised basal monocyte chemoattractant protein‐1 levels poststress in lonelier individuals with diabetes. These results offer the possibility that the influence of loneliness on health in people with diabetes may be partially mediated through neuroendocrine and inflammatory dysregulation. [ABSTRACT FROM AUTHOR]