Health factors measured included anxiety and depression (Hospital and Anxiety Depression Scale), cognitive complaint (Sickness Impact Profile) and sleep.
Cytokine-induced CNS inflammation has been theorized to contribute to cognitive dysfunction in sickness and neurodegenerative disease.
Different measures of cognitive function, long-term sickness absence and depression used across the cohorts.
Thus, the association between lower cognitive status and long-term sickness absence is in part explained by a pathway via educational attainment and adult social class.
The unadjusted association between childhood cognitive ability and long-term sickness absence was estimated and shown as ORs, with 95% CIs, for each of the four quartiles of childhood cognition compared with the reference and for the overall trend.
We predicted that the central communication of peripheral inflammation is associated with pro-inflammatory cytokine release and achieved through direct modulation of interoceptive pathways engendering core cognitive and motivational components of sickness behavior, including subjective fatigue and lethargy.
The associations between childhood cognitive ability and long-term sickness absence, adjusted for the covariables, are shown in table 2. This shows that for each cohort, there is a strong impact of cognitive ability measured in childhood on the outcome several decades later.
This inflammatory model has been shown previously to stimulate a low-grade peripheral inflammatory response with associated cognitive, behavioral, and emotional components of sickness (24,25).
Outcome indicators included SS symptom severity and cognitive function, evaluated with the Simulator Sickness Questionnaire (SSQ) and d2 test of attention, respectively.
The impact of cognitive ability on later long-term sickness absence attained conventional statistical significance in all three cohorts though most strongly for the 1958 cohort.
