3 results
Adolescent depression and subsequent earnings across early to middle adulthood: a 25-year longitudinal cohort study
- Anna Philipson, Iman Alaie, Richard Ssegonja, Henrik Imberg, William Copeland, Margareta Möller, Lars Hagberg, Ulf Jonsson
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- Journal:
- Epidemiology and Psychiatric Sciences / Volume 29 / 2020
- Published online by Cambridge University Press:
- 29 April 2020, e123
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- Article
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- Open access
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Aims
The few available studies on early-onset depression and future earnings offer ambiguous findings, and potential sources of heterogeneity are poorly understood. We examined the differences in adult earnings of males and females with and without a history of depressive disorder in adolescence, with specific focuses on (1) future earnings in clinical subtypes of adolescent depression; (2) the growth and distribution of earnings over time within these subgroups and (3) the mediating role of subsequent depressive episodes occurring in early adulthood.
MethodsData were drawn from the Uppsala Longitudinal Adolescent Depression Study, a community-based cohort study initiated in Uppsala, Sweden, in the early 1990s. Comprehensive diagnostic assessments were conducted at age 16–17 and in follow-up interviews 15 years later, while consecutive data on earnings for the years 1996 to 2016 (ages 20–40) were drawn from population-based registries. The current study included participants with a history of persistent depressive disorder (PDD) (n = 175), episodic major depressive disorder (MDD) (n = 82), subthreshold depression (n = 64) or no depression (n = 218) in adolescence. The association of adolescent depression with earnings in adulthood was analysed using generalised estimating equations. Estimates were adjusted for major child and adolescent psychiatric comorbidities and parental socioeconomic status. The indirect (mediated) effect of depression in early adulthood (ages 19–30) on earnings in mid-adulthood (31–40) was estimated in mediation analysis. The study followed the ‘STrengthening the Reporting of OBservational studies in Epidemiology’ (STROBE) guidelines.
ResultsEarnings across early to middle adulthood were lower for participants with a history of a PDD in adolescence than for their non-depressed peers, with an adjusted ratio of mean earnings of 0.85 (0.77–0.95) for females and 0.76 (0.60–0.95) for males. The differences were consistent over time, and more pronounced in the lower percentiles of the earnings distributions. The association was partially mediated by recurrent depression in early adulthood (48% in total; 61% for females, 29% for males). No reduction in earnings was observed among participants with episodic MDD in adolescence, while results for subthreshold depression were inconclusive.
ConclusionsOur findings suggest that future earnings of adolescents with depressive disorders are contingent on the duration and natural long-term course of early-onset depression, emphasising the need for timely and effective interventions to avoid loss of human capital.
2 - Molecular mechanisms of neonatal brain injury and neural rescue
- from Section 1 - Scientific background
- Edited by A. David Edwards, Denis V. Azzopardi, Alistair J. Gunn
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- Book:
- Neonatal Neural Rescue
- Published online:
- 05 March 2013
- Print publication:
- 04 April 2013, pp 16-32
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Summary
Introduction
Perinatal brain injury is a common cause of life-long neurological deficits and there is an urgent need to better understand its pathophysiology and to find strategies for prevention and treatment. The etiology is complex and multifactorial but hypoxia–ischaemia (HI), infection/inflammation and excitotoxicity (see below) are considered important causes or precipitating insults of preventable/treatable forms of perinatal brain injury. In this review, we will focus on mechanisms of brain injury in response to acute sterile insults in the developing brain that occur in term (e.g., neonatal encephalopathy) or preterm infants.
Genetic background, developmental age, sex and brain maturity affect vulnerability and the mechanisms of brain injury [1,2]. Furthermore, antecedents such as infection/inflammation, intrauterine growth restriction or pre-exposures to hypoxia can modulate brain vulnerability in response to acute insults [3–5]. Brain injury evolves over time and different mechanisms are critical during the primary, secondary and tertiary phases (Figure 2.1). Indeed, recent experimental data suggest that interventions can be effective if administered hours, days or even weeks after the primary insult [6,7].
17 - Hypoxic–ischemic encephalopathy
- from Section 4 - Clinical aspects
- Edited by Hugo Lagercrantz, Karolinska Institutet, Stockholm, M. A. Hanson, Laura R. Ment, Yale University, Connecticut, Donald M. Peebles, University College London
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- Book:
- The Newborn Brain
- Published online:
- 01 March 2011
- Print publication:
- 07 January 2010, pp 261-280
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Summary
The role of hypoxia–ischemia in perinatal brain injury
Injury to the brain depends on not only the type and severity of insult, but also the maturity of the tissue. Hypoxic–ischemic encephalopathy is generally considered to be characteristic of the term infant who has experienced a severe perinatal deficit in cerebral oxygen delivery leading to disruption of cerebral energy metabolism (Volpe, 1994). This is frequently followed by a global hypoxic–ischemic injury, with a widespread although not uniform distribution of apoptotic and necrotic cell death. Nevertheless, focal cerebral infarction is also seen in term infants, and may be underdiagnosed unless sophisticated techniques such as diffusion-weighted magnetic resonance imaging (MRI) are used (Cowan et al., 1994). Hypoxic–ischemic changes are also seen in many stillbirths although in these infants apoptotic death may be particularly prominent (Edwards et al., 1997).
Uncertainty about the role of intrauterine hypoxemia or cerebral ischemia is exacerbated by the imprecise measures of fetal oxygenation or cerebral blood flow available to clinicians. Observations of clinical variables such as cardiotocography or meconium staining of the liquor may mislead if interpreted as precise measures of fetal cerebral hypoxia and ischemia (Nelson et al., 1998). However, more accurate techniques such as magnetic resonance spectroscopy (MRS) have defined at least a subgroup of infants with characteristic hypoxic–ischemic injury, and it is clear that cerebral hypoxia and/or ischemia is involved in a significant proportion of neonatal encephalopathy (Azzopardi et al., 1989).