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Background: Previous findings imply a potential positive association between BMI and all-cause mortality in individuals with psoriasis, yet direct evidence remains absent. This study aimed to fill this gap. Methods: We utilized data from the National Health and Nutrition Examination Survey (NHANES) for the periods 2003-2006 and 2009-2014. Participants' BMI was categorized as lean (<25), overweight (25 ≤ BMI < 30), and obese (BMI ≥ 30). Psoriasis status was determined through self-reporting. The main outcome measured was all-cause mortality up to December 2019. We accounted for multiple covariates, such as sociodemographic factors and histories of smoking and alcohol consumption. Our statistical analyses mainly included Kaplan-Meier survival analysis, Restricted Cubic Spline (RCS) and Multivariate Cox Regression (MCR). We also applied propensity score matching (PSM) to verify the robustness of our findings. Results: Among 22,876 participants, 618 (2.70%) reported a history of psoriasis. An overall effect from the MCR analysis showed that, among individuals with psoriasis, a higher baseline BMI was independently associated with an increased risk of all-cause mortality, noting a 5.5% rise in mortality risk per BMI unit [hazard ratio (HR) = 1.055, 95% CI: 1.004-1.110, p = 0.035]. This significant relationship persisted after PSM. A statistically significant positive correlation was consistent among males, smokers, and individuals younger than 60. However, no such association was found in individuals without a history of psoriasis. Additionally, no significant difference in mortality risk was found between lean and overweight groups with psoriasis, according to the RCS regression and stratified analysis. Conclusion: Our findings indicated a trend that, higher BMIs significantly correlated with increased risks of all-cause mortality in people with psoriasis, particularly among obese ones. However, the impact of being overweight on this relationship remains underexplored. Moreover, the necessity to employ alternative metrics beyond BMI for body fat assessment to further investigate these associations is critical.
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Objective: This study explored the efficacy of acupuncture and metformin in enhancing insulin sensitivity among women with polycystic ovary syndrome (PCOS) and insulin resistance (IR), distinguishing between overweight/obese and lean groups. Methods: A post-hoc analysis of a randomized trial (NCT02491333) was undertaken. Participants were women aged 18-40 with PCOS and IR. They were randomized to receive true acupuncture with a placebo, metformin with sham acupuncture, or sham acupuncture with a placebo for 4 months, with follow-up visits over 3 months. Our study, involving 339 women, assessed the differential impact of acupuncture and metformin on insulin sensitivity in overweight/obese [body mass index (BMI) ≥ 24] versus lean women (BMI < 24). Primary outcomes measured changes in the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) at 4 and 7 months. Secondary outcomes assessed changes in glucose area under the curve (glucoseAUC) during the oral glucose tolerance test (OGTT) and BMI changes at 4 months. Results: Overweight/obese participants were generally older with higher measurements in various health metrics, but lower levels in specific hormonal metrics compared to lean women (p < 0.05). Among overweight/obese women, metformin outperformed acupuncture in reducing HOMA-IR levels (p = 0.004) and showed a significant drop from the baseline after 4 months (p < 0.05). In contrast, acupuncture's effect on HOMA-IR did not significantly differ from sham acupuncture at 4 and 7 months. For lean women, metformin and acupuncture showed comparable improvements in HOMA-IR, with notable declines at 4 and 7 months (p < 0.05). Acupuncture proved more beneficial for lean women than their overweight/obese counterparts after 4 months (p = 0.021). Conclusion: In overweight/obese women with PCOS and IR, acupuncture was less effective than metformin in enhancing insulin sensitivity. However, in lean women, acupuncture's efficacy was comparable to metformin. Further studies are required to validate these observations.
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Cancers are among the difficult-to-treat diseases despite advances in diagnosis and treatment. Although newer effective targets remain to be discovered, targeted therapy has emerged as a promising field. In the last decade, contactin 1 (CNTN1) has surfaced as an important cancer-related molecule. CNTN1 is a neuronal membrane glycoprotein, which, if overexpressed, is found in different cancer cell lines, cancer tissues, and transgenic mice. It is positively associated with lymphatic invasion, metastasis, late TNM stage, and a short overall survival time. However, the role of CNTN1 in cancer cell proliferation remains unclear. In addition, CNTN1 is involved in cancer cell invasion, migration, metastasis, and chemoresistance by promoting epithelial-mesenchymal transition and mediating several signal transduction pathways. Several studies suggest CNTN1 as a new therapeutic target for cancers. This review aims to summarize the research developments on CNTN1 in various cancers, to establish its role in epithelial-mesenchymal transition and signal transduction pathways, and to identify promising areas for further investigation.