Mental health and COVID-19: The impact of a virtual course for family caregivers of adults with intellectual and developmental disabilities.

BACKGROUND: The COVID-19 pandemic has significantly impacted family caregivers of adults with intellectual and developmental disabilities (IDD). This study evaluated a virtual course for family caregivers from across Canada, focused on supporting the mental health and well-being of adults with IDD and their families. The evaluation examined the feasibility and acceptability of the course, as well as the impact of the intervention on participants' overall health and well-being. METHODS: The 6-week virtual course, informed by a parallel Extension for Community Healthcare Outcomes (ECHO) course for service providers, combined didactic instruction with applied activities. A total of 126 family caregiver course participants consented to be part of the research evaluation delivered over three cycles between October 2020 and April 2021. Attendance was measured at each weekly session. Satisfaction was assessed weekly and post-program. Learning, self-efficacy, and well-being were assessed pre- and post-course, and again at follow-up (8 weeks post-course). Mixed-effects models assessed changes between and within individuals across time. RESULTS: Participants had consistent attendance, low-dropout rates, and reported high satisfaction, with 93% of participants reporting that their expectations for the course were met. Compared with pre-course, participants reported improved self-efficacy and well-being post-course, which were maintained at follow-up. CONCLUSIONS: An interactive and applied virtual education course delivered to a large group of family caregivers of adults with IDD was both feasible and acceptable. It positively impacted participants' well-being by offering much needed mental health support and creating a peer-led community of practice.

Disparities in diabetes prevalence and preventable hospitalizations in people with intellectual and developmental disability: a population-based study.

AIMS: To describe and compare population-level aspects of diabetes and diabetes primary care among people with and without intellectual and developmental disabilities. METHODS: Administrative health data accessed from the Institute for Clinical Evaluative Sciences was used to identify a cohort of Ontarians with and without intellectual and developmental disabilities between the ages of 30 and 69 years (n = 28 567). These people were compared with a random sample of people without intellectual and developmental disabilities (n = 2 261 919) according to diabetes prevalence, incidence, age, sex, rurality, neighbourhood income and morbidity. To measure diabetes primary care, we also studied hospitalizations for diabetes-related ambulatory care-sensitive conditions. RESULTS: Adults with intellectual and developmental disabilities had a consistently higher prevalence and incidence of diabetes than those without intellectual and developmental disabilities. Disparities in prevalence between those with and without intellectual and developmental disabilities were most notable among women, younger adults and those residing in rural or high income neighbourhoods. In terms of hospitalizations for diabetes-related ambulatory care-sensitive conditions, people with intellectual and developmental disabilities were 2.6 times more likely to be hospitalized. CONCLUSIONS: Adults with intellectual and developmental disabilities are at high risk of developing and being hospitalized for diabetes. The findings of the present study have a number of important implications related to the early detection, prevention and proper management of diabetes among adults with intellectual and developmental disabilities.

An integrative framework for stochastic, size-structured community assembly.

We present a theoretical framework to describe stochastic, size-structured community assembly, and use this framework to make community-level ecological predictions. Our model can be thought of as adding biological realism to Neutral Biodiversity Theory by incorporating size variation and growth dynamics, and allowing demographic rates to depend on the sizes of individuals. We find that the species abundance distribution (SAD) is insensitive to the details of the size structure in our model, demonstrating that the SAD is a poor indicator of size-dependent processes. We also derive the species biomass distribution (SBD) and find that the form of the SBD depends on the underlying size structure. This leads to a prescription for testing multiple, intertwined ecological predictions of the model, and provides evidence that alternatives to the traditional SAD are more closely tied to certain ecological processes. Finally, we describe how our framework may be extended to make predictions for more general types of community structure.

Back pain and obesity in the 1958 British birth cohort. cause or effect?

An association between obesity and back pain has been observed, but the underlying causal direction is uncertain. We examined the temporal sequence among back pain, BMI, and weight gain using data from the 1958 British birth cohort followed to age 33 (4395 men and 4468 women). Heights and weights were measured at ages 7 and 33, and self-reported at age 23. Back pain was classified as: chronic, incident, early onset but recovered, and never. Those with chronic pain gained more weight between ages 23 and 33 than those with no pain, significantly for women (7.39 kg vs. 6.29 kg). Women who were obese at age 23 years had an elevated risk of subsequent back pain onset (32-33 years) (adjusted OR = 1.78). No significant relationships were found for men. The risk of pain onset among women was evident in relation to BMI at baseline (age 23) and cannot therefore be explained by an effect of back pain on adiposity.

Body mass index and height from childhood to adulthood in the 1958 British born cohort.

The purpose of this study was to assess relations among height, weight, and body mass index (BMI) at different ages from childhood to adulthood, and to examine long-term relations among timing of puberty, height, and BMI. Longitudinal data from the 1958 British birth cohort (all children born between March 3rd and 9th, 1958) were used. Height and weight were measured at ages 7, 11, 16, 23 (self-reported), and 33 y; pubertal status was assessed at ages 11 and 16 y. Data for 5700 females and 5512 males were analyzed. Adult height was well predicted from childhood, with strong correlations (r = 0.7 for both sexes) between height at ages 7 and 33 y. Correlations for BMI were weaker, especially between childhood and early adulthood (r = 0.33 for males and 0.37 for females, ages 7 and 33 y), although they increased with increasing age. Although the fattest children had the highest risks of adult obesity, most obese adults had not been fat at earlier ages: only 17% and 18% of obese 33-y-old men and women, respectively, had been fat at age 7 y. A strong and evenly graded association was found between timing of puberty and BMI, with higher mean BMIs for the earlier maturers at ages 7-33 y. The moderate prediction of adult BMI in this large and unselected sample suggests that although the prevention of childhood fatness may be desirable, most obese adults could not be identified from their childhood BMI, and hence, preventive strategies need to be population-based.

Measurement and long-term health risks of child and adolescent fatness.

This paper reviews child and adolescent adiposity measures and associated long-term health risks. The first section argues that anthropometric measures are practical for large scale epidemiological studies, particularly the body mass index. Limitations of this and other measures are presented. The second section summarises the evidence on the relationship between child and adolescent and adult adiposity. This is based on a search for relevant literature in the following computerised databases: Medline (1985-96), BIDS (EMBASE and Science Citation Index 1985-96). The literature search revealed that the child to adult adiposity relationship is now well-documented, although methodological differences hinder comparisons. Nonetheless, consistently elevated risks of adult obesity are evident for fatter children, although the prediction of adult obesity from child and adolescent adiposity measures is only moderate. Fewer studies could be identified in relation to long-term health risks of child and adolescent adiposity. It is therefore difficult to specify categories of risk associated with childhood adiposity without more information from long-term studies. Further evidence is also required to confirm the suggestion from some studies that adult disease risks are associated with a change in adiposity from normal weight in childhood to obesity in adulthood. However, on the basis of the evidence available, it is argued that population-based approaches to the prevention of obesity are likely to be more effective than approaches targeted as fat children. Population-based approaches are desirable, first because of the poor prediction of adult obesity from child and adolescent measures, and second, because of risks of adult mortality and morbidity may be elevated for individuals who become overweight after adolescence.

Women's reproductive health: the role of body mass index in early and adult life.

BACKGROUND: Higher risks of menstrual problems and infertility have been found in underweight and overweight women but evidence is inconsistent especially in relation to the effect of age of onset of obesity. OBJECTIVE: To determine whether body mass index (BMI) in adulthood or childhood affects the reproductive health of women. METHODS: Heights, weights (at 7, 11, 16, 23 and 33y) and reproductive data were available for 5799 females in the 1958 British birth cohort study. Body mass index (BMI) was calculated as weight/height2. Age-specific cut-offs were used to define overweight and obesity. Reproductive outcomes reported at age 33 included: menstrual problems (also reported at 16y), hypertension in pregnancy and subfertility. RESULTS: Early menarcheal age was associated with higher risks of menstrual problems by 16y but this relationship did not persist to 33y. Obesity at 23y and obesity at 7y both independently increased the risk of menstrual problems by age 33 (OR = 1.75, OR = 1.59 respectively) after adjusting for other confounding factors. Obesity at 23y increased the risk of hypertension in pregnancy (OR = 2.37), after adjusting for confounders. Consistent with these findings, obese women at 23y were less likely to conceive within 12 months of unprotected intercourse after adjustment for confounders (RR = 0.69). CONCLUSIONS: Overweight and obesity in early adulthood appears to increase the risk of menstrual problems, hypertension in pregnancy and subfertility. Other than menstrual problems, childhood body mass index had little impact on the reproductive health of women.

Child to adult body mass index in the 1958 British birth cohort: associations with parental obesity.

OBJECTIVES: To assess relations between the adiposity of children and their parents and to establish whether tracking of adiposity from childhood to adulthood varies according to the parental body mass index (BMI). METHODS: Longitudinal data from the 1958 British birth cohort study were used (6540 men and 6207 women). The height and weight of the study subjects were measured at 7, 11, 16, 23 (self reported), and 33 years. Parental height and weight were self reported when their children were 11 years old. The children were classified into six parental BMI (weight/height2) groups. RESULTS: At each age of follow up the mean BMI of the children increased as the parental BMI increased. Higher risks of adult (33 year) obesity were evident among children with overweight or obese parents: the odds for sons and daughters with two obese parents (compared with those with both parents of normal BMI) were 8.4 and 6.8, respectively. The children of two obese parents also showed the strongest child to adult tracking of BMI as indicated by the correlation between ages 7 and 33 (r = 0.46, 0.54, sons and daughters, respectively). CONCLUSIONS: The children of obese and overweight parents have an increased risk of obesity. Subjects with two obese parents are fatter in childhood and also show a stronger pattern of tracking from childhood to adulthood. As the prevalence of parental obesity increases in the general population the extent of child to adult tracking of BMI is likely to strengthen.