Contemporary contestations over working time: time for health to weigh in

Non-communicable disease (NCD) incidence and prevalence is of central concern to most nations, along with international agencies such as the UN, OECD, IMF and World Bank. As a result, the search has begun for ‘causes of the cause’ behind health risks and behaviours responsible for the major NCDs. As part of this effort, researchers are turning their attention to charting the temporal nature of societal changes that might be associated with the rapid rise in NCDs. From this, the experience of time and its allocation are increasingly understood to be key individual and societal resources for health (7–9). The interdisciplinary study outlined in this paper will produce a systematic analysis of the behavioural health dimensions, or ‘health time economies’ (quantity and quality of time necessary for the practice of health behaviours), that have accompanied labour market transitions of the last 30 years - the period in which so many NCDs have risen sharply

Assessing causal relationships in genomics: From Bradford-Hill criteria to complex gene-environment interactions and directed acyclic graphs

Observational studies of human health and disease (basic, clinical and epidemiological) are vulnerable to methodological problems -such as selection bias and confounding- that make causal inferences problematic. Gene-disease associations are no exception, as they are commonly investigated using observational designs. A rich body of knowledge exists in medicine and epidemiology on the assessment of causal relationships involving personal and environmental causes of disease; it includes seminal causal criteria developed by Austin Bradford Hill and more recently applied directed acyclic graphs (DAGs). However, such knowledge has seldom been applied to assess causal relationships in clinical genetics and genomics, even in studies aimed at making inferences relevant for human health. Conversely, incorporating genetic causal knowledge into clinical and epidemiological causal reasoning is still a largely unexplored area

Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis

A comprehensive literature search was performed to collate evidence of mitochondrial dysfunction in autism spectrum disorders (ASDs) with two primary objectives. First, features of mitochondrial dysfunction in the general population of children with ASD were identified. Second, characteristics of mitochondrial dysfunction in children with ASD and concomitant mitochondrial disease (MD) were compared with published literature of two general populations: ASD children without MD, and non-ASD children with MD. The prevalence of MD in the general population of ASD was 5.0% (95% confidence interval 3.2, 6.9%), much higher than found in the general population (∼0.01%). The prevalence of abnormal biomarker values of mitochondrial dysfunction was high in ASD, much higher than the prevalence of MD. Variances and mean values of many mitochondrial biomarkers (lactate, pyruvate, carnitine and ubiquinone) were significantly different between ASD and controls. Some markers correlated with ASD severity. Neuroimaging, in vitro and post-mortem brain studies were consistent with an elevated prevalence of mitochondrial dysfunction in ASD. Taken together, these findings suggest children with ASD have a spectrum of mitochondrial dysfunction of differing severity. Eighteen publications representing a total of 112 children with ASD and MD (ASD/MD) were identified. The prevalence of developmental regression (52%), seizures (41%), motor delay (51%), gastrointestinal abnormalities (74%), female gender (39%), and elevated lactate (78%) and pyruvate (45%) was significantly higher in ASD/MD compared with the general ASD population. The prevalence of many of these abnormalities was similar to the general population of children with MD, suggesting that ASD/MD represents a distinct subgroup of children with MD. Most ASD/MD cases (79%) were not associated with genetic abnormalities, raising the possibility of secondary mitochondrial dysfunction. Treatment studies for ASD/MD were limited, although improvements were noted in some studies with carnitine, co-enzyme Q10 and B-vitamins. Many studies suffered from limitations, including small sample sizes, referral or publication biases, and variability in protocols for selecting children for MD workup, collecting mitochondrial biomarkers and defining MD. Overall, this evidence supports the notion that mitochondrial dysfunction is associated with ASD. Additional studies are needed to further define the role of mitochondrial dysfunction in ASD

Characteristics of work-related fatal and hospitalised injuries not captured in workers’ compensation data

OBJECTIVES: (1) To identify work-related fatal and non-fatal hospitalised injuries using multiple data sources, (2) to compare case-ascertainment from external data sources with accepted workers’ compensation claims and (3) to investigate the characteristics of work-related fatal and hospitalised injuries not captured by workers’ compensation. METHODS: Work-related fatal injuries were ascertained from vital statistics, coroners and hospital discharge databases using payment and diagnosis codes and injury and work descriptions; and work-related (non-fatal) injuries were ascertained from the hospital discharge database using admission, diagnosis and payment codes. Injuries for British Columbia residents aged 15–64 years from 1991 to 2009 ascertained from the above external data sources were compared to accepted workers’ compensation claims using per cent captured, validity analyses and logistic regression. RESULTS: The majority of work-related fatal injuries identified in the coroners data (83%) and the majority of work-related hospitalised injuries (95%) were captured as an accepted workers’ compensation claim. A work-related coroner report was a positive predictor (88%), and the responsibility of payment field in the hospital discharge record a sensitive indicator (94%), for a workers’ compensation claim. Injuries not captured by workers’ compensation were associated with female gender, type of work (natural resources and other unspecified work) and injury diagnosis (eg, airway-related, dislocations and undetermined/unknown injury). CONCLUSIONS: Some work-related injuries captured by external data sources were not found in workers’ compensation data in British Columbia. This may be the result of capturing injuries or workers that are ineligible for workers’ compensation, or the result of injuries that go unreported to the compensation system. Hospital discharge records and coroner reports may provide opportunities to identify workers (or family members) with an unreported work-related injury and to provide them with information for submitting a workers’ compensation claim