Mild Anemia and Risk for All-Cause, Cardiovascular and Cancer Deaths in Apparently Healthy Elderly Koreans / 가정의학회지

BACKGROUND: Being common, mild anemia is sometimes considered a mere consequence of aging; however, aging alone is unlikely to lead to anemia. Therefore, this study aimed to investigate the association between mild anemia and total mortality and cause-specific mortality in apparently healthy elderly subjects. METHODS: A retrospective cohort study was conducted on 10,114 apparently healthy elderly individuals who underwent cancer screening and routine medical check-ups at one Health Promotion Center between May 1995 and December 2007. We defined mild anemia as a hemoglobin concentration between 10.0 g/dL and 11.9 g/dL in women and between 10.0 g/dL and 12.9 g/dL in men. We assessed the relationship between the overall, cardiovascular (CV), and cancer mortality and mild anemia using Cox proportional hazard models. RESULTS: Mild anemia was present in 143 men (3.1%) and 246 women (6.1%). During an average follow-up of 7.6 years, 495 deaths occurred, including 121 CV and 225 cancer deaths. After adjustments, mild anemia was associated with a 128% increase in the risk of all-cause mortality (hazard ratio [HR], 2.28; 95% confidence interval [CI], 1.54–3.37) in men and cancer-related mortality (HR, 2.25; 95% CI, 1.22–4.13), particularly lung cancer (HR, 2.70; 95% CI, 1.03–7.08) in men, but not in women. In the subgroup analyses based on smoking status, obesity, and age, the associations were more prominent in never or former smoker groups and the older group. CONCLUSION: The present study shows that overall and cancer-related mortality was associated with mild anemia in elderly men. Future prospective studies are needed to consolidate our findings.

No Association of Functional Polymorphisms in Methlylenetetrahydrofolate Reductase and the Risk and Minor Physical Anomalies of Schizophrenia in Korean Population

Methylenetetrahydrofolate reductase (MTHFR), a critical enzyme in folate metabolism, plays an important role in DNA methylation. It has been suggested that abnormal DNA methylation contributes to the pathogenesis of schizophrenia and congenital anomalies. The previous findings regarding the genetic relationship between MTHFR and schizophrenia are controversial. This study investigated the association of the two functional polymorphisms of MTHFR, C677T and A1298C, with the risk for schizophrenia. Furthermore, we conducted an updated meta-analysis on the two polymorphisms. In addition, we investigated the relationship between the polymorphisms and minor physical anomaly (MPA), which may represent neurodevelopmental aberrations in 201 schizophrenia patients and 350 normal control subjects. There was no significant association between either of the two polymorphisms and the risk of schizophrenia (chi-square = 0.001, df = 1, P = 0.971 for C677T; chi-square = 1.319, df = 1, P = 0.251 for A1298C). However, in meta-analysis, the C677T polymorphism showed a significant association in the combined and Asian populations (OR = 1.13, P = 0.005; OR = 1.21, P = 0.011, respectively) but not in the Korean and Caucasian populations alone. Neither polymorphism was associated with MPAs measured by the Waldrop scale (chi-square = 2.513, df = 2, P = 0.285). In conclusion, the present findings suggest that in the Korean population, the MTHFR polymorphisms are unlikely to be associated with the risk for schizophrenia and neurodevelopmental abnormalities related to schizophrenia.

Association between EGF A61G Polymorphism and Bipolar Disorder in Korean Population / 신경정신의학

OBJECTIVES: Epidermal growth factor (EGF) is a neurotrophic factor which regulates the intracellular signaling molecules. These molecules are also affected by mood stabilizers such as lithium and valproate. In addition, epidermal growth factor enhances neuronal survival, maturation and differentiation especially in midbrain dopaminergic neurons of which dysfunction may play a role in pathophysiology of bipolar disorders. Bipolar disorder has some genetic commonalities with schizophrenia, and several association studies of EGF have been done with schizophrenia. In this study, we tried to investigate the genetic association between EGF A61G polymorphism and bipolar disorder. METHODS: Total of 189 patients and 347 normal control were included. All patients satisfied the diagnostic criteria of DSM-IV for bipolar disorder type I (BPDI, N=146) and bipolar disorder type II (BPDII, N=43). Genomic DNA was extracted from the peripheral blood, and genotyping was performed by TaqManTM method. Genotype and allele frequency of EGF A61G polymorphism between the patients and the control were compared by contingency chi-square test or the Fisher's exact test. RESULTS: No association was found between EGF A61G polymorphism and susceptibility of BPDI, BPDII and bipolar disorder (all patients). Female patients with BPDII showed overexpression of AG genotype compared to that of control group (p=0.03). However, this association was not significant after correction of multiple testing. CONCLUSION: In conclusion, EGF A61G polymorphism has no association with susceptibility of bipolar disorder. However, the disease modifying role of EGF gene polymorphism for bipolar disorder remains to be elucidated in respect to factors such as gender difference or diagnostic subtype.