Do Men and Women Have a Different Association between Fear-Avoidance and Pain Intensity in Chronic Pain? An Experience Sampling Method Cohort-Study.

BACKGROUND: Fear-avoidance is one of the factors associated with chronic pain. However, it remains unclear whether the association between fear-avoidance and pain depends on sex. The present study aimed to investigate whether the association between fear-avoidance and pain intensity differed between men and women in chronic pain patients. Additionally, the potential confounding effect of affective experiences on the association between fear-avoidance and pain intensity was analyzed. METHOD: This cohort study included hospital referred chronic pain patients (n = 45). Short momentary assessment questions according to the experience sampling method (ESM) were used to repeatedly assess patients' pain intensity, level of fear-avoidance and positive as well as negative affect during their daily life. Linear mixed-effects models were applied in the statistical analysis. Unadjusted and adjusted models were made, in which the latter corrected for statistically significant affective experiences and baseline variables, taking the Aikake Information Criterion into account to assess a better model of fit. RESULTS: The results demonstrated an association between fear-avoidance and pain intensity that differed for men and women. In men (n = 13), no association between these variables was found (-0.04 (95% CI: -0.14, 0.06) with a p-value of 0.48), whereas in women (n = 32), an increase in fear-avoidance was associated with a (slight) increase in pain intensity (0.18 (95% CI 0.06, 0.30) with a p-value of 0.003). Affect did not confound the above-mentioned findings. CONCLUSION: Our data supports previous research highlighting the importance of sex differences in pain experience. These findings may be relevant for clinicians to consider more personalized (i.e., gender specific) pain management in chronic pain patients.

Sphingolipids in Alzheimer's disease, how can we target them?

Altered levels of sphingolipids and their metabolites in the brain, and the related downstream effects on neuronal homeostasis and the immune system, provide a framework for understanding mechanisms in neurodegenerative disorders and for developing new intervention strategies. In this review we will discuss: the metabolites of sphingolipids that function as second messengers; and functional aberrations of the pathway resulting in Alzheimer's disease (AD) pathophysiology. Focusing on the central product of the sphingolipid pathway ceramide, we describ approaches to pharmacologically decrease ceramide levels in the brain and we argue on how the sphingolipid pathway may represent a new framework for developing novel intervention strategies in AD. We also highlight the possible use of clinical and non-clinical drugs to modulate the sphingolipid pathway and sphingolipid-related biological cascades.