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Deprivation is a major risk to population health, in particular when experienced during childhood. Poor health in the early years accumulates and is expressed in adult health inequalities. Policy makers may aim to mitigate against the ill effects of deprivation by trying to increase social mobility and facilitating moves towards better earnings and living conditions or by protecting against the effects of downward moves and the experience of deprivation. This paper uses address change and property value data at the individual and family level to examine whether poor health outcomes occur more frequently among people who move between addresses and particularly those who move to properties with lower property values. We use the Northern Ireland Longitudinal Study, linking health and demographic data from 2001 and 2011 Censuses to house valuations for a representative 28% of the population aged 10–64 years (N = 342,681). Young persons (aged 10–15 years) living in a house valued at over £160,000 were half as likely to be reported as having mental ill health as those living in a house valued under £75,000 (OR = 0.49, CI: 0.31–0.78). There was no strong evidence that upward or downward mobility affected mental health or physical health for young people, but ill health of working aged persons showed a strong association with moving to houses of lower value. Results are discussed in terms of their implications for understanding the dynamics of social mobility and health and in terms of how various policies towards poverty may influence population health.

Altered oligodendrocyte structure and function is implicated in major psychiatric illnesses, including low cell number and reduced oligodendrocyte-specific gene expression in major depressive disorder (MDD). These features are also observed in the unpredictable chronic mild stress (UCMS) rodent model of the illness, suggesting that they are consequential to environmental precipitants; however, whether oligodendrocyte changes contribute causally to low emotionality is unknown. Focusing on 2'-3'-cyclic nucleotide 3'-phosphodiesterase (Cnp1), a crucial component of axoglial communication dysregulated in the amygdala of MDD subjects and UCMS-exposed mice, we show that altered oligodendrocyte integrity can have an unexpected functional role in affect regulation. Mice lacking Cnp1 (knockout, KO) displayed decreased anxiety- and depressive-like symptoms (i.e., low emotionality) compared with wild-type animals, a phenotypic difference that increased with age (3-9 months). This phenotype was accompanied by increased motor activity, but was evident before neurodegenerative-associated motor coordination deficits (≤ 9-12 months). Notably, Cnp1(KO) mice were less vulnerable to developing a depressive-like syndrome after either UCMS or chronic corticosterone exposure. Cnp1(KO) mice also displayed reduced fear expression during extinction, despite normal amygdala c-Fos induction after acute stress, together implicating dysfunction of an amygdala-related neural network, and consistent with proposed mechanisms for stress resiliency. However, the Cnp1(KO) behavioral phenotype was also accompanied by massive upregulation of oligodendrocyte- and immune-related genes in the basolateral amygdala, suggesting an attempt at functional compensation. Together, we demonstrate that the lack of oligodendrocyte-specific Cnp1 leads to resilient emotionality. However, combined with substantial molecular changes and late-onset neurodegeneration, these results suggest the low Cnp1 seen in MDD may cause unsustainable and maladaptive molecular compensations contributing to the disease pathophysiology.