Reaction time and incident cancer: 25 years of follow-up of study members in the UK Health and Lifestyle Survey

<b>Objectives</b><p></p> To investigate the association of reaction time with cancer incidence.<p></p> <b>Methods</b><p></p> 6900 individuals aged 18 to 94 years who participated in the UK Health and Lifestyle Survey in 1984/1985 and were followed for a cancer registration for 25 years.<p></p> <b>Results</b><p></p> Disease surveillance gave rise to 1015 cancer events from all sites. In general, there was essentially no clear pattern of association for either simple or choice reaction time with cancer of all sites combined, nor specific malignancies. However, selected associations were found for lung cancer, colorectal cancer and skin cancer.<p></p> <b>Conclusions</b><p></p> In the present study, reaction time and its components were not generally related to cancer risk

Reaction Time and Mortality from the Major Causes of Death:The NHANES-III Study

Studies examining the relation of information processing speed, as measured by reaction time, with mortality are scarce. We explored these associations in a representative sample of the US population

Pre-pandemic cognitive function and COVID-19 mortality:Prospective cohort study

Poorer performance on standard tests of pre-morbid cognitive function is related to an elevated risk of death from lower respiratory tract infections but the link with coronavirus (COVID‑19) mortality is untested. Participants in UK Biobank, aged 40 to 69 years at study induction (2006–10), were administered a reaction time test, an indicator of information processing speed, and also had their verbal-numeric reasoning assessed. Between April 1st and September 23rd 2020 there were 388 registry-confirmed deaths (138 women) ascribed to COVID-19 in 494,932 individuals (269,602 women) with a reaction time test result, and 125 such deaths (38 women) in the subgroup of 180,198 people (97,794 women) with data on verbal-numeric reasoning. In analyses adjusted for age, sex, and ethnicity, a one standard deviation slower reaction time was related to a higher rate of death from COVID-19 (hazard ratio; 95% confidence interval: 1.18; 1.09, 1.28), as was a one standard deviation disadvantage on the verbal-numeric reasoning test (1.32; 1.09, 1.59). While there was some attenuation in these relationships after adjustment for additional covariates which included socio-economic status and lifestyle factors, the two pre-pandemic indicators of cognitive function continued to be related to COVID-19 mortality

Depressive symptoms and obesity: instrumental variable analysis using mother–offspring pairs in the 1970 British Cohort Study

Background: The extent to which depression and obesity are causally related remains to be determined. We used intergenerational data on mother–offspring pairs in an instrumental variable analysis to examine the longitudinal association between adolescent depressive symptoms and body mass index (BMI) in adulthood. Methods: A total of 4733 mother–offspring pairs were identified from the 1970 British Cohort Study. Mothers completed the Malaise Inventory to assess depressive symptoms on three occasions across their offsprings' childhood/adolescence (aged 5, 10 and 16 years). Height and weight were recorded in mother and offspring (aged 16 years). Measures of height, weight and the Malaise Inventory were repeated in the participant at the age of 42 years. Results: Maternal malaise score was associated with offspring malaise score, thus confirming the validity of the chosen instrumental variable. A higher mother’s malaise score was associated with higher offspring BMI at follow-up (B=0.043; 95% confidence interval (CI): 0.013, 0.072). There was a higher risk of adulthood offspring obesity in mothers with two or three episodes of depression compared with one or none (odds ratio, 1.42; 95% CI: 1.14, 1.76). The maternal malaise–offspring BMI association remained (P=0.003) after adjustment for offspring malaise score, suggesting that maternal mental health influences offspring obesity through mechanisms other than depression. Results from standard and instrumental variable analyses did not support a causal pathway in a direction from BMI to depression. Conclusions: Our data support a causal pathway linking adolescent depressive symptoms to adiposity in adulthood over 26 years follow-up. The reverse direction, that is, adiposity to depression, was not supported