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1.
Milbank Q ; 102(1): 141-182, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38294094

RESUMO

Policy Points Income is thought to impact a broad range of health outcomes. However, whether income inequality (how unequal the distribution of income is in a population) has an additional impact on health is extensively debated. Studies that use multilevel data, which have recently increased in popularity, are necessary to separate the contextual effects of income inequality on health from the effects of individual income on health. Our systematic review found only small associations between income inequality and poor self-rated health and all-cause mortality. The available evidence does not suggest causality, although it remains methodologically flawed and limited, with very few studies using natural experimental approaches or examining income inequality at the national level. CONTEXT: Whether income inequality has a direct effect on health or is only associated because of the effect of individual income has long been debated. We aimed to understand the association between income inequality and self-rated health (SRH) and all-cause mortality (mortality) and assess if these relationships are likely to be causal. METHODS: We searched Medline, ISI Web of Science, Embase, and EconLit (PROSPERO: CRD42021252791) for studies considering income inequality and SRH or mortality using multilevel data and adjusting for individual-level socioeconomic position. We calculated pooled odds ratios (ORs) for poor SRH and relative risk ratios (RRs) for mortality from random-effects meta-analyses. We critically appraised included studies using the Risk of Bias in Nonrandomized Studies - of Interventions tool. We assessed certainty of evidence using the Grading of Recommendations Assessment, Development and Evaluation framework and causality using Bradford Hill (BH) viewpoints. FINDINGS: The primary meta-analyses included 2,916,576 participants in 38 cross-sectional studies assessing SRH and 10,727,470 participants in 14 cohort studies of mortality. Per 0.05-unit increase in the Gini coefficient, a measure of income inequality, the ORs and RRs (95% confidence intervals) for SRH and mortality were 1.06 (1.03-1.08) and 1.02 (1.00-1.04), respectively. A total of 63.2% of SRH and 50.0% of mortality studies were at serious risk of bias (RoB), resulting in very low and low certainty ratings, respectively. For SRH and mortality, we did not identify relevant evidence to assess the specificity or, for SRH only, the experiment BH viewpoints; evidence for strength of association and dose-response gradient was inconclusive because of the high RoB; we found evidence in support of temporality and plausibility. CONCLUSIONS: Increased income inequality is only marginally associated with SRH and mortality, but the current evidence base is too methodologically limited to support a causal relationship. To address the gaps we identified, future research should focus on income inequality measured at the national level and addressing confounding with natural experiment approaches.


Assuntos
Nível de Saúde , Renda , Humanos , Estudos Transversais
2.
Arch Dis Child ; 109(3): 233-239, 2024 02 19.
Artigo em Inglês | MEDLINE | ID: mdl-38262695

RESUMO

OBJECTIVE: To examine trends in socio-economic and ethnic inequalities in childhood overweight and obesity in the England between 1995 and 2019 in survey data and to compare these to administrative data. DESIGN: Observational repeated cross-sectional study using the Health Survey for England (HSE) and National Child Measurement Programme (NCMP). OUTCOME: Age and sex standardised overweight, obesity and overweight including obesity. ANALYSIS: Inequalities assessed by parental education, family structure, ethnicity (binary non-white vs white) and area-level Index of Multiple Deprivation. Estimates stratified by age and sex. Trends compared against NCMP data (age 4-5 and 10-11 years). RESULTS: Prevalence of childhood overweight including obesity increased from 26.0% in 1995 to 31.7% in 2019, with the highest and fastest growing levels in those aged 11-15 years, rising from 29.7% to 38.0%. Despite a plateau in overall childhood obesity since 2004, differences between groups demonstrated widening inequalities over time. Inequalities widened by area-level deprivation, household educational attainment, household structure and ethnicity driven primarily by increased prevalence among socioeconomically disadvantaged children. For example, the gap between children from households with no qualifications versus degree-level qualifications increased from -1.1% to 13.2%, and the gap between single-parent households and couple households increased from 0.5% to 5.3%. HSE trends in prevalence of childhood overweight and obesity by deprivation quintile were consistent with those in NCMP. CONCLUSION: Overall levels of child overweight and obesity increased between 1995 and 2004. Since then, increases in prevalence among less advantaged groups have driven widening of inequalities.


Assuntos
Obesidade Infantil , Criança , Humanos , Obesidade Infantil/epidemiologia , Estudos Transversais , Sobrepeso/epidemiologia , Fatores Socioeconômicos , Inglaterra/epidemiologia , Inquéritos Epidemiológicos , Prevalência , Índice de Massa Corporal
3.
Int J Soc Determinants Health Health Serv ; : 27551938241255041, 2024 May 20.
Artigo em Inglês | MEDLINE | ID: mdl-38767141

RESUMO

This article systematically reviews evidence evaluating whether macroeconomic austerity policies impact mortality, reviewing high-income country data compiled through systematic searches of nine databases and gray literature using pre-specified methods (PROSPERO registration: CRD42020226609). Eligible studies were quantitatively assessed to determine austerity's impact on mortality. Two reviewers independently assessed eligibility and risk of bias using ROBINS-I. Synthesis without meta-analysis was conducted due to heterogeneity. Certainty of evidence was assessed using the GRADE framework. Of 5,720 studies screened, seven were included, with harmful effects of austerity policies demonstrated in six, and no effect in one. Consistent harmful impacts of austerity were demonstrated for all-cause mortality, life expectancy, and cause-specific mortality across studies and different austerity measures. Excess mortality was higher in countries with greater exposure to austerity. Certainty of evidence was low. Risk of bias was moderate to critical. A typical austerity dose was associated with 74,090 [-40,632, 188,792] and 115,385 [26,324, 204,446] additional deaths per year. Austerity policies are consistently associated with adverse mortality outcomes, but the magnitude of this effect remains uncertain and may depend on how austerity is implemented (e.g., balance between public spending reductions or tax rises, and distributional consequences). Policymakers should be aware of potential harmful health effects of austerity policies.

4.
Lancet Reg Health Eur ; 27: 100585, 2023 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-37035237

RESUMO

The UK, and other high-income countries, are experiencing substantial increases in living costs. Several overlapping and intersecting economic crises threaten physical and mental health in the immediate and longer term. Policy responses may buffer against the worst effects (e.g. welfare support) or further undermine health (e.g. austerity). We explore fundamental causes underpinning the cost-of-living crisis, examine potential pathways by which the crisis could impact population health and use a case study to model potential impacts of one aspect of the crisis on a specific health outcome. Our modelling illustrates how policy approaches can substantially protect health and avoid exacerbating health inequalities. Targeting support at vulnerable households is likely to protect health most effectively. The current crisis is likely to be the first of many in era of political and climate uncertainty. More refined integrated economic and health modelling has the potential to inform policy integration, or 'health in all policies'.

5.
Lancet Child Adolesc Health ; 7(11): 786-796, 2023 11.
Artigo em Inglês | MEDLINE | ID: mdl-37774733

RESUMO

BACKGROUND: An increase in acute severe hepatitis of unknown aetiology in previously healthy children in the UK in March, 2022, triggered global case-finding. We aimed to describe UK epidemiological investigations of cases and their possible causes. METHODS: We actively surveilled unexplained paediatric acute hepatitis (transaminase >500 international units per litre) in children younger than 16 years presenting since Jan 1, 2022, through notifications from paediatricians, microbiologists, and paediatric liver units; we collected demographic, clinical, and exposure information. Then, we did a case-control study to investigate the association between adenoviraemia and other viruses and case-status using multivariable Firth penalised logistic regression. Cases aged 1-10 years and tested for adenovirus were included and compared with controls (ie, children admitted to hospital with an acute non-hepatitis illness who had residual blood samples collected between Jan 1 and May 28, 2022, and without known laboratory-confirmed diagnosis or previous adenovirus testing). Controls were frequency-matched on sex, age band, sample months, and nation or supra-region with randomised selection. We explored temporal associations between frequency of circulating viruses identified through routine laboratory pathogen surveillance and occurrence of cases by linear regression. SARS-CoV-2 seropositivity of cases was examined against residual serum from age-matched clinical comparison groups. FINDINGS: Between Jan 1 and July 4, 2022, 274 cases were identified (median age 3 years [IQR 2-5]). 131 (48%) participants were male, 142 (52%) were female, and one (<1%) participant had sex data unknown. Jaundice (195 [83%] of 235) and gastrointestinal symptoms (202 [91%] of 222) were common. 15 (5%) children required liver transplantation and none died. Adenovirus was detected in 172 (68%) of 252 participants tested, regardless of sample type; 137 (63%) of 218 samples were positive for adenovirus in the blood. For cases that were successfully genotyped, 58 (81%) of 72 had Ad41F, and 57 were identified as positive via blood samples (six of these were among participants who had undergone a transplant). In the case-control analysis, adenoviraemia was associated with hepatitis case-status (adjusted OR 37·4 [95% CI 15·5-90·3]). Increases in the detection of adenovirus from faecal samples, but not other infectious agents, in routine laboratory pathogen surveillance correlated with hepatitis cases 4 weeks later, which independently suggested an association (ß 0·06 [95% CI 0·02-0·11]). No association was identified for SARS-CoV-2 antibody seropositivity. INTERPRETATION: We observed an association between adenovirus 41F viraemia and paediatric acute hepatitis. These results can inform diagnostic testing recommendations, clinical management, and exploratory in vitro or clinical studies of paediatric acute hepatitis of unknown aetiology. The role of potential co-factors, including other viruses and host susceptibility, requires further investigation. FUNDING: None.


Assuntos
COVID-19 , Hepatite , Pré-Escolar , Feminino , Humanos , Masculino , Doença Aguda , Estudos de Casos e Controles , SARS-CoV-2 , Reino Unido/epidemiologia
6.
AIDS ; 16(11): 1545-50, 2002 Jul 26.
Artigo em Inglês | MEDLINE | ID: mdl-12131193

RESUMO

OBJECTIVE: To measure the effect of HIV on survival in rural Africa. DESIGN: A retrospective cohort study with more than 10 years follow-up. METHODS: Individuals with known HIV status in the 1980s were identified from previous population surveys in Karonga District, northern Malawi. Follow-up studies were conducted in 1998-2000 to trace 197 HIV-positive and 396 age-sex-matched HIV-negative individuals and their spouses. RESULTS: Information was obtained on all but 11 index individuals. Half (302) were found and the others were reported to have died (161) or to be alive outside the district (119). Ten year survival was 36% in the HIV-positive cohort and 90% in the initially HIV-negative cohort. The death rate was 93.3 per 1000 person-years in the HIV-positive individuals, and 11.3 in the initially HIV-negative individuals. Survival time since the initial test in HIV-positive individuals decreased with age, but relative survival, compared with HIV-negative individuals, was similar across age groups. The effect of HIV on survival was similar in men and women. Spouses of HIV-positive individuals had four times the mortality rate, and among survivors, four times the HIV prevalence, of spouses of initially HIV-negative individuals. CONCLUSION: HIV-infected individuals had very high mortality rates, but one-third were still alive at 10 years. This is consistent with median survival from seroconversion being similar to that found in developed countries before antiretroviral therapy. Mortality rates in HIV-positive individuals increased with age, but relative mortality changed little with age.


Assuntos
Síndrome da Imunodeficiência Adquirida/mortalidade , Soropositividade para HIV/mortalidade , Síndrome da Imunodeficiência Adquirida/epidemiologia , Adolescente , Adulto , Fatores Etários , Idoso , Feminino , Seguimentos , Soropositividade para HIV/epidemiologia , Humanos , Malaui/epidemiologia , Masculino , Análise por Pareamento , Pessoa de Meia-Idade , Vigilância da População , Modelos de Riscos Proporcionais , Fatores Sexuais , Cônjuges , Análise de Sobrevida , Taxa de Sobrevida
7.
J Virol ; 76(24): 12890-9, 2002 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-12438614

RESUMO

We have tracked the early years of the evolution of the human immunodeficiency virus type 1 (HIV-1) epidemic in a rural district of central east Africa from the first documented introductions of subtypes A, D, and C to the present predominance of subtype C. The earliest subtype C sequences ever reported are described. Blood samples were collected on filter papers from 1981 to 1984 and from 1987 to 1989 from more than 44,000 individuals living in two areas of Karonga District, Malawi. These samples included HIV-1-positive samples from 200 people. In 1982 to 1984, HIV-1 subtypes A, C, and D were all present, though in small numbers. By 1987 to 1989, 152 (90%) of a total of 168 sequences were subtype C and AC, AD, and DC recombinants had emerged. Four of the subtype C sequences from 1983 to 1984 were closely related and were found at the base of a large cluster of low diversity that by the late 1980s accounted for 40% of C sequences. The other two early C sequences fell into a separate and more diverse cluster. Three other clusters containing sequences from the late 1980s were identified. Each cluster contained at least one sample from a person who had recently arrived in the district. From 18 HIV-1-positive spouse pairs, 12 very closely related pairs of sequences were identified. We conclude that there were multiple introductions of HIV-1 with limited spread, followed by explosive growth of a subtype C cluster, probably arising from a single introduction in or before 1983.


Assuntos
HIV-1/classificação , Adulto , Sequência de Aminoácidos , Feminino , Genes env , Genes gag , Proteína gp120 do Envelope de HIV/química , HIV-1/genética , HIV-1/isolamento & purificação , Humanos , Malaui , Masculino , Dados de Sequência Molecular , Filogenia , Fatores de Tempo
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