Social health (SH) markers, including marital status, contact frequency, network size, and social support, have been linked with increased cognitive capability. However, the underlying mechanisms remain poorly understood. We aim to investigate whether depression symptoms and inflammatory biomarkers mediate associations between SH and cognitive outcomes.

We used data from waves 1-9 of the English Longitudinal Study of Ageing, involving 7,136 participants aged 50 or older at baseline. First, we examined associations between SH (wave 1) and depression and inflammatory biomarkers (C-reactive protein (CRP) and fibrinogen) (wave 2) using linear regression models. Second, we tested associations between a) SH and b) depression and inflammation with subsequent standardised verbal fluency and memory in wave 3 and change between waves 3-9, indexed using slopes derived from multilevel models. We adjusted for age, sex, socio-economic position, cardiovascular disease, basic and instrumental activities of daily living, health behaviours, and baseline depression symptoms and cognition. We will also conduct causal mediation analysis.

All SH markers, except contact frequency, were associated with lower subsequent depression, but not inflammatory biomarkers. Greater contact frequency (e.g. once-twice a week vs <once per year: β=0.18 [0.01, 0.36]) and less negative support (β=0.02 [0.00, 0.03]) were associated with higher verbal fluency. Larger network size (>6 people vs none: β=0.007SD/year [0.001, 0.012]), less negative (β=0.001SD/year [0.001, 0.002]) and more positive support (β=0.001SD/year [0.000, 0.001]) were linked with slower memory decline, and more positive support predicted slower verbal fluency decline (β=0.001SD/year [0.000, 0.001]). Depression symptoms were associated with lower memory and verbal fluency, and faster memory decline (β=-0.001SD/year [-0.001, -0.000]) and verbal fluency (β=-0.001SD/year [-0.001, -0.000]). CRP was associated with lower verbal fluency (β=-0.02 [-0.04, 0.00]), whereas fibrinogen was linked with faster memory decline (β=-0.001SD/year [-0.003, -0.000]).

Depression symptoms and SH showed associations with subsequent cognitive capability and change. SH was linked with lower depression, but not inflammatory biomarkers. Findings highlight the potential for depression to underpin associations between SH and cognition, a pathway which we will test using causal mediation analysis. We will also examine whether findings replicate in the Swedish National Study of Aging and Care in Kungsholmen.

Although the COVID-19 pandemic has affected depression, evidence of the role of pre-pandemic history of depression remains limited.

We investigated how long-term trajectories of depressive symptomatology before the COVID-19 pandemic were related to depression during the pandemic, over and above the latest pre-pandemic depression status. Furthermore, we examined whether those experiencing depression closer to the pandemic were at higher risk during the pandemic.

Employing data from waves 4–9 of the English Longitudinal Study of Ageing (2008–2009 to 2018–2019), we used group-based trajectory modelling on 3925 English older adults aged 50+ years to identify distinctive trajectories of elevated depressive symptoms (EDS). Fully adjusted logistic models were then used to examine the associations between trajectories and depression during the COVID-19 pandemic (June–July and November–December 2020).

We identified four classes of pre-pandemic trajectories of EDS. About 5% were classed as ‘enduring EDS’, 8% as ‘increasing EDS’, 10% as ‘decreasing EDS’ and 77% as ‘absence of EDS’. Compared with respondents with absence of EDS, those with EDS history were more likely to have depression during the COVID-19 pandemic, particularly those with enduring or increasing EDS in the previous 10 years. Moreover, the frequency of EDS was more crucial in predicting the risks of depression during the pandemic than the timing of the latest episode.

Trajectories of depressive symptomatology are an important risk factor for older adults’ mental health, particularly in the context of crisis. Older people with enduring or increasing EDS should receive particular attention from policy makers when provisioning post-pandemic well-being support.

During the COVID-19 pandemic, older and clinically vulnerable people were instructed to shield or stay at home. Policies restricting social contact and human interaction pose a risk to mental health, but we know very little about the impact of shielding and stay-at-home orders on the mental health of older people.

To understand the extent to which shielding contributes to poorer mental health.

We used longitudinal data from wave 9 (2018/2019) and two COVID-19 sub-studies (June/July 2020; November/December 2020) of the English Longitudinal Study of Ageing, and constructed logistic and linear regression models to investigate associations between patterns of shielding during the pandemic and mental health, controlling for sociodemographic characteristics, pre-pandemic physical and mental health, and social isolation measures.

By December 2020, 70% of older people were still shielding or staying at home, with 5% shielding throughout the first 9 months of the pandemic. Respondents who shielded experienced worse mental health. Although prior characteristics and lack of social interactions explain some of this association, even controlling for all covariates, those shielding throughout had higher odds of reporting elevated depressive symptoms (odds ratio 1.87, 95% CI 1.22–2.87) and lower quality of life (β = −1.28, 95% CI −2.04 to −0.52) than those who neither shielded nor stayed at home. Shielding was also associated with increased anxiety.

Shielding seems associated with worse mental health among older people, highlighting the need for policy makers to address the mental health needs of those who shielded, both in the current pandemic and for the future.

The COVID-19 pandemic has disrupted lives and livelihoods, and people already experiencing mental ill health may have been especially vulnerable.

Quantify mental health inequalities in disruptions to healthcare, economic activity and housing.

We examined data from 59 482 participants in 12 UK longitudinal studies with data collected before and during the COVID-19 pandemic. Within each study, we estimated the association between psychological distress assessed pre-pandemic and disruptions since the start of the pandemic to healthcare (medication access, procedures or appointments), economic activity (employment, income or working hours) and housing (change of address or household composition). Estimates were pooled across studies.

Across the analysed data-sets, 28% to 77% of participants experienced at least one disruption, with 2.3–33.2% experiencing disruptions in two or more domains. We found 1 s.d. higher pre-pandemic psychological distress was associated with (a) increased odds of any healthcare disruptions (odds ratio (OR) 1.30, 95% CI 1.20–1.40), with fully adjusted odds ratios ranging from 1.24 (95% CI 1.09–1.41) for disruption to procedures to 1.33 (95% CI 1.20–1.49) for disruptions to prescriptions or medication access; (b) loss of employment (odds ratio 1.13, 95% CI 1.06–1.21) and income (OR 1.12, 95% CI 1.06 –1.19), and reductions in working hours/furlough (odds ratio 1.05, 95% CI 1.00–1.09) and (c) increased likelihood of experiencing a disruption in at least two domains (OR 1.25, 95% CI 1.18–1.32) or in one domain (OR 1.11, 95% CI 1.07–1.16), relative to no disruption. There were no associations with housing disruptions (OR 1.00, 95% CI 0.97–1.03).

People experiencing psychological distress pre-pandemic were more likely to experience healthcare and economic disruptions, and clusters of disruptions across multiple domains during the pandemic. Failing to address these disruptions risks further widening mental health inequalities.