Chronic pain is a prevalent and debilitating condition with significant impacts on individuals and society. While the role of diet in chronic pain is well-known, the relationship between special dietary choices and chronic pain remains unclear. This study investigates the causal associations between 20 dietary habits and chronic pain using a Mendelian randomization (MR) approach. Publicly available genome-wide association study data from the UK Biobank dataset were utilized for secondary analysis, and genetic instrumental variables strongly correlated with 20 different dietary habits were selected. Multisite chronic pain (MCP) scores were used as the primary outcome, with site-specific chronic pain (SSCP) including back pain, headache, knee pain, neck pain, and hip pain as secondary outcomes. The inverse-variance-weighted (IVW) method was the primary method used in the MR. The weighted median (WM) and Mendelian randomization pleiotropy residual sum and outlier test (MR-PRESSO) methods were used as sensitivity analyses. This study identified causal associations between specific dietary habits and chronic pain. A high intake of cheese, cereal, dried fruits, and fresh fruits was associated with lower MCP scores. Conversely, high alcohol, salt, pork, and poultry intakes were associated with higher MCP scores. Similar associations between special dietary habits and some types of SSCP, such as back and neck pain, were also observed. The findings were consistent across different statistical methods, and sensitivity analyses confirmed the reliability of the results. In conclusion, our study provides evidence of a causal relationship between various dietary habits and different types of chronic pain based on secondary analysis of the UK Biobank dataset. Adhering to an anti-inflammatory diet, including increased consumption of fruits and cereal while reducing salt and pork intake, may potentially alleviate chronic pain symptoms.

Exposure to many kinds of bisphenols (BPs) is common, and the effects of BP mixtures may differ from those of individual BPs. Therefore, evaluating combined exposure effects is necessary. Our study evaluated the individual and combined exposure effects of bisphenol A (BPA), bisphenol S (BPS) and bisphenol AF (BPAF) on embryonic development using an embryonic stem cell test (EST) and a concentration additive (CA) model at relatively high doses to uncover the interaction model of the three BPs. Environmentally relevant concentrations were then used to evaluate the possible effects of the individual and combined BPs at actual human exposure levels. Exposure to relatively high-dose BPA, BPS and BPAF inhibited embryonic stem cell differentiation into cardiomyocytes and exhibited weak embryo toxicity. Individually, BPA, BPS and BPAF inhibited endoderm, mesoderm and ectoderm marker expression but enhanced pluripotency marker expression. Combined exposure to BPs had an additive effect on cardiomyocyte differentiation and embryonic stem cell proliferation based on the CA model. Environmentally relevant individual or combined BP doses (10 ng/ml individual BPA, BPS and BPAF doses or 1 ng/ml and 10 ng/ml BP mixture doses) failed to cause oxidative stress, DNA damage or apoptosis changes in stem cell differentiation. The cardiomyocyte differentiation ratio also did not change significantly. Individual and combined exposure to environmentally relevant BP doses led to a significant increase in collagen expression. BPAF and the combination of BPs increased the type 1 collagen level, while the combination also increased the type 3 collagen level, which may be related to p38 pathway activation. The p38 pathway inhibitor SB203580 inhibited the increase in collagen during cardiomyocyte differentiation caused by low-dose BPs. These results suggest that relatively high-dose BPs in combination have an additive effect on cardiomyocyte differentiation. Low-dose BPs individually and in combination may affect cardiomyocyte collagen through the p38 pathway.

Surgical smoke is widespread in operating rooms, and fine particles are the main toxic components. However, the effect of fine particles in surgical smoke on embryonic development has not yet been studied. This study evaluated the effect of fine particles in surgical smoke on embryonic development and compared it with that of atmospheric fine particles. Afterwards, differentiated cardiomyocytes were purified, and the effect of exposure to fine particles in surgical smoke on cardiomyocyte differentiation was evaluated. Fine particles in surgical smoke exhibited weak embryotoxicity toward an embryonic stem cell test model, and their inhibitory effect on cardiomyocyte differentiation was slightly stronger than that of atmospheric fine particles. Fine particles in surgical smoke specifically inhibited the differentiation of the mesoderm lineage and promoted the differentiation of the ectoderm lineage. Furthermore, fine particles in surgical smoke reduced the beating rate of purified cardiomyocytes, promoted mitophagy, reduced ATP production and increased the reactive oxygen species (ROS) content. Antioxidants attenuated the inhibition of cardiomyocyte differentiation and the reduction in the cardiomyocyte beating rate caused by fine particles in surgical smoke and simultaneously restored mitophagy and other processes to the control levels. However, mitophagy inhibitors treatment blocked only the inhibition of cardiomyocyte differentiation caused by fine particles in surgical smoke; it had little effect on other changes caused by fine particles. Based on the results described above, we propose that fine particles in surgical smoke and atmospheric fine particles exhibit similar levels of toxicity toward embryonic development. Fine particles in surgical smoke potentially affect the beating of cardiomyocytes by damaging mitochondria and increasing oxidative stress.