PubMed · 15035142
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Hideaki Kishimoto. 2004. [CM-100].. https://pubmed.ncbi.nlm.nih.gov/15035142/
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BACKGROUND: In a great many of observational studies, whether there is a relevance of resistin levels on bone mineral density (BMD) and fracture occurrence has been inconsistently reported, and the causality is unclear. METHODS: We aim to assess the resistin levels on BMD and fracture occurrence within a Mendelian randomization (MR) analysis. Exposure and outcome data were derived from the Integrative Epidemiology Unit (IEU) Open genome wide association studies (GWAS) database. Screening of instrumental variables (IVs) was performed subject to conditions of relevance, exclusivity, and independence. Inverse variance weighting (IVW) was our primary method for MR analysis based on harmonized data. Weighted median and MR-Egger were chosen to evaluate the robustness of the results of IVW. Simultaneously, heterogeneity and horizontal pleiotropy were also assessed and the direction of potential causality was detected by MR Steiger. Multivariable MR (MVMR) analysis was used to identify whether confounding factors affected the reliability of the results. RESULTS: After Bonferroni correction, the results showed a suggestively positive causality between resistin levels and total body BMD (TB-BMD) in European populations over the age of 60 [β(95%CI): 0.093(0.021, 0.165), P = 0.011]. The weighted median [β(95%CI): 0.111(0.067, 0.213), P = 0.035] and MR-Egger [β(95%CI): 0.162(0.025, 0.2983), P = 0.040] results demonstrate the robustness of the IVW results. No presence of pleiotropy or heterogeneity was detected between them. MR Steiger supports the causal inference result and MVMR suggests its direct effect. CONCLUSIONS: In European population older than 60 years, genetically predicted higher levels of resistin were associated with higher TB-BMD. A significant causality between resistin levels on BMD at different sites, fracture in certain parts of the body, and BMD in four different age groups between 0-60 years of age was not found in our study.
1,1,1-Trichloro-2,2'bis(p-chlorophenyl) ethane (DDT) was the first widely used synthetic pesticide and is extremely persistent in both the environment and the human body. The introduction of DDT revolutionised agricultural production and has been credited with the elimination of malaria from the United States and Europe. However, DDT is also known to have had major environmental consequences and has been associated with dramatic declines in many animal populations. Although DDT use has generally been restricted since the early 1970s, exposure to the pesticide remains widespread. In developed countries, slow elimination from the body means a large proportion of the population still have detectable levels of DDT, or its metabolite DDE, in their serum or adipose tissue. In developing countries, the pesticide continues to be used for vector control and a significant proportion of breast-fed babies has daily intakes above recommended levels. This review considers the epidemiological evidence for possible adverse effects of human exposure to DDT. Much of this research is weakened by methodological flaws. However, recent methods in breast cancer research using nested studies in cohorts with stored biological samples have allowed a more rigorous assessment of a putative role for DDT in disease aetiology. While DDT does not appear to play a causative role in breast cancer development, there is suggestive evidence for a role in the aetiology of other conditions such as pancreatic cancer, neuropsychological dysfunction, and reproductive outcomes. Research into these and other conditions would benefit from the same rigorous approaches used in breast cancer research. Until further high quality evidence is available, it is still too early, even 60 years after the introduction of this once ubiquitous chemical, to pass judgement on the role of DDT in a number of common diseases.
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