Immune-neuroendocrine patterning and response to stress. A latent profile analysis in the English longitudinal study of ageing.

Psychosocial stress exposure can disturb communication signals between the immune, nervous, and endocrine systems that are intended to maintain homeostasis. This dysregulation can provoke a negative feedback loop between each system that has high pathological risk. Here, we explore patterns of immune-neuroendocrine activity and the role of stress. Using data from the English Longitudinal Study of Ageing (ELSA), we first identified the latent structure of immune-neuroendocrine activity (indexed by high sensitivity C-reactive protein [CRP], fibrinogen [Fb], hair cortisol [cortisol], and insulin growth-factor-1 [IGF-1]), within a population-based cohort using latent profile analysis (LPA). Then, we determined whether life stress was associated with membership of different immune-neuroendocrine profiles. We followed 4,934 male and female participants, with a median age of 65 years, over a four-year period (2008-2012). A three-class LPA solution offered the most parsimonious fit to the underlying immune-neuroendocrine structure in the data, with 36 %, 40 %, and 24 % of the population belonging to profiles 1 (low-risk), 2 (moderate-risk), and 3 (high-risk), respectively. After adjustment for genetic predisposition, sociodemographics, lifestyle, and health, higher exposure to stress was associated with a 61 % greater risk of belonging to the high-risk profile (RRR: 1.61; 95 %CI = 1.23-2.12, p = 0.001), but not the moderate-risk profile (RRR = 1.10, 95 %CI = 0.89-1.35, p = 0.401), as compared with the low-risk profile four years later. Our findings extend existing knowledge on psychoneuroimmunological processes, by revealing how inflammation and neuroendocrine activity cluster in a representative sample of older adults, and how stress exposure was associated with immune-neuroendocrine responses over time.

Polygenic predisposition, sleep duration, and depression: evidence from a prospective population-based cohort.

Suboptimal sleep durations and depression frequently cooccur. Short-sleep and long-sleep are commonly thought of as symptoms of depression, but a growing literature suggests that they may be prodromal. While each represents a process of mutual influence, the directionality between them remains unclear. Using polygenic scores (PGS), we investigate the prospective direction involved in suboptimal sleep durations and depression. Male and female participants, aged ≥50, were recruited from the English Longitudinal Study of Ageing (ELSA). PGS for sleep duration, short-sleep, and long-sleep were calculated using summary statistics data from the UK Biobank cohort. Sleep duration, categorised into short-sleep ("≤5 h"), optimal-sleep (">5 to <9 h"), and long-sleep ("≥9 h"), was measured at baseline and across an average 8-year follow-up. Subclinical depression (Centre for Epidemiological Studies Depression Scale [≥4 of 7]) was also ascertained at baseline and across an average 8-year follow-up. One standard deviation increase in PGS for short-sleep was associated with 14% higher odds of depression onset (95% CI = 1.03-1.25, p = 0.008). However, PGS for sleep duration (OR = 0.92, 95% CI = 0.84-1.00, p = 0.053) and long-sleep (OR = 0.97, 95% CI = 0.89-1.06, p = 0.544) were not associated with depression onset during follow-up. During the same period, PGS for depression was not associated with overall sleep duration, short-sleep, or long-sleep. Polygenic predisposition to short-sleep was associated with depression onset over an average 8-year period. However, polygenic predisposition to depression was not associated with overall sleep duration, short-sleep or long-sleep, suggesting different mechanisms underlie the relationship between depression and the subsequent onset of suboptimal sleep durations in older adults.

Immune-Neuroendocrine Patterning and Response to Stress. A latent profile analysis in the English Longitudinal Study of Ageing.

Psychosocial stress exposure can disturb communication signals between the immune, nervous, and endocrine systems that are intended to maintain homeostasis. This dysregulation can provoke a negative feedback loop between each system that has high pathological risk. Here, we explore patterns of immune-neuroendocrine activity and the role of stress. Using data from the English Longitudinal Study of Ageing (ELSA), we first identified the latent structure of immune-neuroendocrine activity (indexed by high sensitivity C-reactive protein [CRP], fibrinogen [Fb], hair cortisol [cortisol], and insulin growth-factor-1 [IGF-1]), within a population-based cohort using latent profile analysis (LPA). Then, we determined whether life stress was associated with membership of different immune-neuroendocrine profiles. We followed 4,934 male and female participants with a median age of 65 years over a four-year period (2008-2012). A three-class LPA solution offered the most parsimonious fit to the underlying immune-neuroendocrine structure in the data, with 36%, 40%, and 24% of the population belonging to profiles 1 (low-risk), 2 (moderate-risk), and 3 (high-risk), respectively. After adjustment for genetic predisposition, sociodemographics, lifestyle, and health, higher exposure to stress was associated with a 61% greater risk of belonging to the high-risk profile (RRR: 1.61; 95%CI=1.23-2.12, p=0.001), but not the moderate-risk profile (RRR=1.10, 95%CI=0.89-1.35, p=0.401), as compared with the low-risk profile four years later. Our findings extend existing knowledge on psychoneuroimmunological processes, by revealing how inflammation and neuroendocrine activity cluster in a representative sample of older adults, and how stress exposure was associated with immune-neuroendocrine responses over time.

Socioeconomic determinants of inflammation and neuroendocrine activity: A longitudinal analysis of compositional and contextual effects.

Socioeconomic determinants are well-established modulators of inflammation and neuroendocrine activity. Less clear is whether neighbourhood-contextual or individual-compositional factors are more closely associated with gradients in these biomarkers. Here, we examine how immune and neuroendocrine activity are cross-sectionally and longitudinally nested in meso-level socioeconomic characteristics. Participants, male and female, aged ≥50, were recruited from the English Longitudinal Study of Ageing (ELSA). Neighbourhood (Index of Multiple Deprivation [IMD]) and individual (Wealth/Education/Occupational Social Class [Occupation]) factors were drawn from wave 4 (baseline; 2008). Immune and neuroendocrine biomarkers (indexed by C-reactive protein [CRP; n = 3,968]; fibrinogen [n = 3,932]; white blood cell counts [WBCC; n = 4,022]; insulin-like growth factor-1 [IGF-1; n = 4,056]) were measured at baseline and 4-years later (wave 6; 2012). Covariates at baseline included demographic, clinical, and lifestyle variables. Lower socioeconomic status was associated with heighted inflammation and lower neuroendocrine activity unadjusted both cross-sectionally and longitudinally. With few exceptions, cross-sectional associations remained significant after full adjustment. Prospectively, low IMD remained associated with higher CRP and WBCC; wealth with WBCC; and education and occupation with fibrinogen and WBCC. IMD-biomarker associations were reduced when wealth was simultaneously taken into account. Lifestyle accounted for the greatest variance in associations between socioeconomic indicators and inflammation (≤42.11%), but demographics were more salient to neuroendocrine activity (≤88.46%). Neighbourhood-contextual factors were stronger indicators of aberrant biomarker activity than individual-compositional factors in cross-sectional analyses but were largely explained by wealth differences prospectively. Therefore, immune and neuroendocrine changes depended on the composition of the population living in an area, rather than the area itself.

Ability or luck: A systematic review of interpersonal attributions of success.

The role of luck in success has a relatively minor, albeit consistent history in academic discourse, with a striking lack of literature engaging with notions of luck within occupational environments. Elucidating why people attribute their own success to luck over ability has predominated in the literature, with interpersonal attributions receiving less attention. Here, we center on systematically summarizing the evidence on interpersonal attributions of success as a function of ability or luck, with a particular focus on whether these differs by gender and race. The perception of the success of others from different sociodemographic groups, and how it is attributed, is a crucial leverage point for inclusion and diversity. Particularly as women and ethnic groups continue to be systematically disadvantaged in the workforce. Ignoring the role of luck conceals and augments privilege, even if not deliberately or consciously invoked. Using the Prisma protocol, this review offers evidence from experiments, published between 1970 and 2020, derived from five electronic bibliographic databases; Business Source Complete; PsychINFO; Scopus; Web of Science; and Google Scholar. There were a limited number of studies on gender that found an effect, but with few exceptions, the papers that pertain to race converged on the understanding that interpersonal attributions of success were predicated on this immutable factor. Such that black individuals were more often viewed as lucky in their success and less able, which translates to lesser opportunity and reward. Decades of research have pointed to individuals making systematic attribution errors in success by gender and race; this review only partially substantiates this consensus and provides narrow support for the view that those believed to be the most talented in society may merely be the luckiest. We add to evidence that context matters.

Systemic inflammation and emotional responses during the COVID-19 pandemic.

The impact of the COVID-19 pandemic on population mental health is of global concern. Inflammatory processes are thought to contribute to mental ill-health, but their role in experiences of psychological distress during the pandemic has not been investigated. We tested the hypothesis that elevated inflammatory biomarkers (high-sensitivity plasma C-reactive protein [CRP] and plasma fibrinogen) measured pre-pandemic would be positively predictive of increased depressive symptoms experienced during the pandemic. Data were analysed from the English Longitudinal Study of Ageing (ELSA), with 3574 individuals aged >50 for CRP and 3314 for fibrinogen measured in waves 8 (2016/17) or 9 (2018/19). Depressive symptoms were measured with a short version of the Centre for Epidemiological Studies Depression Scale (CES-D) pre-pandemic (2016-2019) and during the pandemic (June/July 2020). Participants with higher baseline CRP concentrations had 40% higher odds of developing depressive symptoms during the pandemic (ORadjusted = 1.40, 95% CI 1.12-1.73, p = 0.003) after full adjustment. Fibrinogen concentrations were also associated with depressive symptoms during the pandemic (ORadjusted = 1.23, 95% CI 1.04-1.46, p = 0.019), but this association was no longer significant after controlling for lifestyle factors (smoking status, alcohol consumption and physical activity). In this large population study, systemic inflammation measured 1-3 years pre-pandemic was associated with greater depressed mood during the early months of the pandemic. This finding is consistent with the hypothesis that higher levels of inflammation increase the vulnerability of older people to impaired mental health in the presence of the widespread stress of the COVID-19 pandemic.