Changes in health in England, with analysis by English regions and areas of deprivation, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013.

BACKGROUND: In the Global Burden of Disease Study 2013 (GBD 2013), knowledge about health and its determinants has been integrated into a comparable framework to inform health policy. Outputs of this analysis are relevant to current policy questions in England and elsewhere, particularly on health inequalities. We use GBD 2013 data on mortality and causes of death, and disease and injury incidence and prevalence to analyse the burden of disease and injury in England as a whole, in English regions, and within each English region by deprivation quintile. We also assess disease and injury burden in England attributable to potentially preventable risk factors. England and the English regions are compared with the remaining constituent countries of the UK and with comparable countries in the European Union (EU) and beyond. METHODS: We extracted data from the GBD 2013 to compare mortality, causes of death, years of life lost (YLLs), years lived with a disability (YLDs), and disability-adjusted life-years (DALYs) in England, the UK, and 18 other countries (the first 15 EU members [apart from the UK] and Australia, Canada, Norway, and the USA [EU15+]). We extended elements of the analysis to English regions, and subregional areas defined by deprivation quintile (deprivation areas). We used data split by the nine English regions (corresponding to the European boundaries of the Nomenclature for Territorial Statistics level 1 [NUTS 1] regions), and by quintile groups within each English region according to deprivation, thereby making 45 regional deprivation areas. Deprivation quintiles were defined by area of residence ranked at national level by Index of Multiple Deprivation score, 2010. Burden due to various risk factors is described for England using new GBD methodology to estimate independent and overlapping attributable risk for five tiers of behavioural, metabolic, and environmental risk factors. We present results for 306 causes and 2337 sequelae, and 79 risks or risk clusters. FINDINGS: Between 1990 and 2013, life expectancy from birth in England increased by 5·4 years (95% uncertainty interval 5·0-5·8) from 75·9 years (75·9-76·0) to 81·3 years (80·9-81·7); gains were greater for men than for women. Rates of age-standardised YLLs reduced by 41·1% (38·3-43·6), whereas DALYs were reduced by 23·8% (20·9-27·1), and YLDs by 1·4% (0·1-2·8). For these measures, England ranked better than the UK and the EU15+ means. Between 1990 and 2013, the range in life expectancy among 45 regional deprivation areas remained 8·2 years for men and decreased from 7·2 years in 1990 to 6·9 years in 2013 for women. In 2013, the leading cause of YLLs was ischaemic heart disease, and the leading cause of DALYs was low back and neck pain. Known risk factors accounted for 39·6% (37·7-41·7) of DALYs; leading behavioural risk factors were suboptimal diet (10·8% [9·1-12·7]) and tobacco (10·7% [9·4-12·0]). INTERPRETATION: Health in England is improving although substantial opportunities exist for further reductions in the burden of preventable disease. The gap in mortality rates between men and women has reduced, but marked health inequalities between the least deprived and most deprived areas remain. Declines in mortality have not been matched by similar declines in morbidity, resulting in people living longer with diseases. Health policies must therefore address the causes of ill health as well as those of premature mortality. Systematic action locally and nationally is needed to reduce risk exposures, support healthy behaviours, alleviate the severity of chronic disabling disorders, and mitigate the effects of socioeconomic deprivation. FUNDING: Bill & Melinda Gates Foundation and Public Health England.

What explains between-school differences in rates of smoking?

BACKGROUND: Schools have the potential to influence their pupils' behaviour through the school's social organisation and culture (non-formal school characteristics), as well as through the formal curriculum. This paper examines whether these school characteristics (which include a measure of quality of social relationships) can account for school differences in smoking rates. METHODS: This study uses a longitudinal survey involving 5,092 pupils in 24 Scottish schools. Pupils' smoking (at age 15/16), cognitive measures, attitude to school and pupils' rating of teacher pupil relationships (at age 13/14) were linked to school level data comprising teacher assessed quality of pupil-staff relationships, school level deprivation, staying on rates and attendance. Analysis involved multi-level modelling. RESULTS: Overall, 25% of males and 39% of females reported smoking, with rates by school ranging from 8% to 33% for males and from 28% to 49% for females. When individual socio-economic and socio-cultural factors were controlled for there was still a large school effect for males and a smaller (but correlated) school effect for females at 15/16 years. For girls their school effect was explained by their rating of teacher-pupil relationships and attitude to school. These variables were also significant in predicting smoking among boys. However, the school effect for boys was most radically attenuated and became insignificant when the interaction between poor quality of teacher - pupil relationships and school level affluence was fitted, explaining 82% of the variance between schools. In addition, researchers' rating of the schools' focus on caring and inclusiveness was also significantly associated with both male and female smoking rates. CONCLUSION: School-level characteristics have an impact on male and female pupils' rates of smoking up to 15/16 years of age. The size of the school effect is greater for males at this age. The social environment of schools, in particular the quality of teacher-pupil relationships, pupils' attitude to school and the school's focus on caring and inclusiveness, can influence both boys' and girls' smoking. This provides support for the school-wide or "Health Promoting School" approach to smoking prevention.

Is the relation of social class to change in hearing threshold levels from childhood to middle age explained by noise, smoking, and drinking behaviour?

Recent work shows that variation in adult hearing function is related both to social class of origin and current social class. This study examines how much of this relationship after adjustment for childhood hearing impairment is explicable by occupational noise, current smoking, and alcohol consumption. A cohort of 9023 persons born in the UK during one week in 1958 was followed periodically, and hearing threshold levels (HTLs) were measured at 1 kHz and 4 kHz at age 45 years. Most (71% and 68%, at 1 kHz and 4 kHz respectively) of the relation to social class of origin of adult HTLs remains after adjustment for these other factors. For the relation to current social class, corresponding values are 64% and 44% (though varying by gender). The magnitude of social class effect is comparable to that of occupational noise. Susceptibility to hearing impairment is likely to be appreciably determined in early childhood.

Cessation of hormone replacement therapy after reports of adverse findings from randomized controlled trials: evidence from a British Birth Cohort.

OBJECTIVES: We examined the cessation of hormone replacement therapy (HRT) among British women, by educational level, social class, and cardiovascular risk factors, at the time of publicity about 2 clinical trials of HRT that were halted after adverse findings. METHODS: A total of 1387 women aged 57 years reported their monthly HRT use between January 2002 and February 2003. A succession of regression-based time-series models were fitted to detect changes in the proportion of HRT users stratified by education level, social class, hypertension, and obesity. RESULTS: The overall percentage of HRT users declined from 31% in January 2002 to less than 26% by February 2003. Changes in trends of HRT use were first detected in June 2002 (for women with advanced secondary educational qualification or higher) and in July 2002 (for all other groups). The rate of decline was greatest for women with no formal educational qualifications, from the manual social class, or who were hypertensive or obese. CONCLUSIONS: These decreases coincided with the announced cessation of a large US clinical trial of HRT. This publicity may have had a differential influence on the immediate decline in HRT use by various groups of British women.

Estrogen-related receptor gamma and hearing function: evidence of a role in humans and mice.

Since estrogen is thought to protect pre-menopausal women from age-related hearing loss, we investigated whether variation in estrogen-signalling genes is linked to hearing status in the 1958 British Birth Cohort. This analysis implicated the estrogen-related receptor gamma (ESRRG) gene in determining adult hearing function and was investigated further in a total of 6134 individuals in 3 independent cohorts: (i) the 1958 British Birth Cohort; (ii) a London ARHL case-control cohort; and (iii) a cohort from isolated populations of Italy and Silk Road countries. Evidence of an association between the minor allele of single nucleotide polymorphism (SNP) rs2818964 and hearing status was found in females, but not in males in 2 of these cohorts: p = 0.0058 (London ARHL) and p = 0.0065 (Carlantino, Italy). Furthermore, assessment of hearing in Esrrg knock-out mice revealed a mild 25-dB hearing loss at 5 weeks of age. At 12 weeks, average hearing thresholds in female mice((-/-)) were 15 dB worse than in males((-/-)). Together these data indicate ESRRG plays a role in maintenance of hearing in both humans and mice.

Hearing in 44-45 year olds with m.1555A>G, a genetic mutation predisposing to aminoglycoside-induced deafness: a population based cohort study.

Background The mitochondrial DNA mutation m.1555A>G predisposes to permanent idiosyncratic aminoglycoside-induced deafness that is independent of dose. Research suggests that in some families, m.1555A>G may cause non-syndromic deafness, without aminoglycoside exposure, as well as reduced hearing thresholds with age (age-related hearing loss). Objectives To determine whether adults with m.1555A>G have impaired hearing, a factor that would inform the cost-benefit argument for genetic testing prior to aminoglycoside administration. Design Population-based cohort study. Setting UK. Participants Individuals from the British 1958 birth cohort. Measurements Hearing thresholds at 1 and 4 kHz at age 44-45 years; m.1555A>G genotyping. Results 19 of 7350 individuals successfully genotyped had the m.1555A>G mutation, giving a prevalence of 0.26% (95% CI 0.14% to 0.38%) or 1 in 385 (95% CI 1 in 714 to 1 in 263). There was no significant difference in hearing thresholds between those with and without the mutation. Single-nucleotide polymorphism analysis indicated that the mutation has arisen on a number of different mitochondrial haplogroups. Limitations No data were collected on aminoglycoside exposure. For three subjects, hearing thresholds could not be predicted because information required for modelling was missing. Conclusions In this cohort, hearing in those with m.1555A>G is not significantly different from the general population and appears to be preserved at least until 44-45 years of age. Unbiased ascertainment of mutation carriers provides no evidence that this mutation alone causes non-syndromic hearing impairment in the UK. The findings lend weight to arguments for genetic testing for this mutation prior to aminoglycoside administration, as hearing in susceptible individuals is expected to be preserved well into adult life. Since global use of aminoglycosides is likely to increase, development of a rapid test is a priority.

An investigation into causal links between victimization and offending in adolescents.

There is a considerable body of evidence from earlier research to show that offending is associated with an increased risk of victimization, and being a victim with an increased risk of offending. There have been few earlier studies of the link. These have generally set out to test specific explanations, for example, the idea that the same lifestyles or routine activities may be associated with both victimization and offending. In a current study of a cohort of 4,300 adolescents in Edinburgh we have found a correlation of 0.421 between crime victimization and self-reported offending at the age of 15 when offending peaks. Variables chosen to test three broad types of theory - life-style and routine activities, weak social bonds, aspects of personality - are shown to be related both to victimization and to offending in adolescence. The present analysis uses latent class growth mixture models to track the dynamic relationships over time between adolescent victimization and offending both before and after controlling for these explanatory variables. In the short term, offending is strongly related to a later rise in victimization, but in the longer term to a fall that tends to cancel out the earlier rise. These findings remain the same after controlling for the ten explanatory variables. Victimization is associated with a later rise in offending in the longer term. The theoretical perspectives suggested by earlier researchers are fairly successful in explaining this linkage running from victimization to offending. Future research should focus on the role of peer influence in linking victimization and offending, and should push forward the analysis into the adult years. The implications for criminal justice policy could be far-reaching.

Bedsharing, roomsharing, and sudden infant death syndrome in Scotland: a case-control study.

OBJECTIVE: To examine the hypothesis that bedsharing with an infant is associated with an increased risk of sudden infant death syndrome (SIDS). STUDY DESIGN: A 1:2, case:control study in Scotland UK, population 5.1 million, including 123 infants who died of SIDS between January 1, 1996 and May 31, 2000, and 263 controls. The main outcome measure was sharing a sleep surface during last sleep. RESULTS: Sharing a sleep surface was associated with SIDS (multivariate OR 2.89, 95% CI 1.40, 5.97). The largest risk was associated with couch sharing (OR 66.9, 95% CI 2.8, 1597). Of 46 SIDS infants who bedshared during their last sleep, 40 (87%) were found in the parents' bed. Sharing a bed when <11 weeks (OR 10.20, 95% CI 2.99, 34.8) was associated with a greater risk, P = .010, compared with sharing when older (OR 1.07, 95% CI 0.32, 3.56). The association remained if mother did not smoke (OR 8.01, 95% CI 1.20, 53.3) or the infant was breastfed (OR 13.10, 95% CI 1.29, 133). CONCLUSIONS: Bedsharing is associated with an increased risk of SIDS for infants <11 weeks of age. Sharing a couch for sleep should be strongly discouraged at any age.

Used infant mattresses and sudden infant death syndrome in Scotland: case-control study.

OBJECTIVE: To examine the proposition that a used infant mattress is associated with an increased risk of sudden infant death syndrome. DESIGN: Case-control study. SETTING: Scotland (population 5.1 million, with about 53 000 births a year). PARTICIPANTS: 131 infants who died of sudden infant death syndrome between 1 January 1996 and 31 May 2000 and 278 age, season, and obstetric unit matched control infants. MAIN OUTCOME MEASURES: Routine use of an infant mattress previously used by another child and place of last sleep. RESULTS: Routine use of an infant mattress previously used by another child was significantly associated with an increased risk of sudden infant death syndrome (multivariate odds ratio 3.07, 95% confidence interval 1.51 to 6.22). Use of a used infant mattress for last sleep was also associated with increased risk (6.10, 2.31 to 16.12). The association was significantly stronger if the mattress was from another home (4.78, 2.08 to 11.0) than if it was from the same home (1.64, 0.64 to 4.2). CONCLUSION: A valid significant association exists between use of a used infant mattress and an increased risk of sudden infant death syndrome, particularly if the mattress is from another home. Insufficient evidence is available to judge whether this relation is cause and effect.