It is thought that calcium (Ca) and magnesium (Mg) may be related to mental disorders such as depression; however, there have been few studies investigating the association between Ca and Mg nutrition status with depression in middle-aged female adults. Study subjects in this study included 105 women between the ages of 41 and 57 years. The subjects were divided into three groups according to the Zung Self-rating Depression Scale (SDS) score: Group I (SDS score < 33 percentile; n = 32), Group II (33 percentile ≤ SDS score < 67 percentile; n = 37), and Group III (67 percentile ≤ SDS score; n = 36). Anthropometric measurements, dietary intake survey using 3-day dietary records, SDS questionnaire and measurement of serum Ca and Mg were obtained and analyzed. No differences were observed in Ca, plant Ca, and Mg intake among the three groups. However, animal Ca intake by Group III was 141.3 mg, which was significantly lower than 207.6 mg by Group I and 198.3 mg by Group II (P = 0.0345). There were no significant differences in serum levels of Ca, and Mg among the three groups. Correlation analysis indicated that the SDS score had negative correlations with Ca intake (r = -0.2927, P < 0.01) and animal Ca (r = -0.3411, P < 0.001) after adjusting for age, menopause and energy intake. In conclusion, dietary Ca and animal Ca had negative associations with SDS score among middle-aged Korean female adults. Additional analysis of factors related to the association of calcium and magnesium nutritional status and depression is necessary.

The purpose of this study was to investigate the effect of silicon (Si) supplementation on bone mineral density (BMD) and bone metabolism parameters relative to calcium (Ca) intake levels in ovariectomized rats. A total of 72 female Wistar rats (6 weeks) were ovariectomized (OVX) and divided into six groups, and Si (500 mg of Si per kilogram of feed) was or was not administered with diets containing various levels of Ca (0.1%, 0.5%, and 1.5%) for 10 weeks. The groups were as follows: (1) Ca-deficient group (0.1% Ca), (2) Ca-deficient with Si supplementation group, (3) adequate Ca group (0.5% Ca), (4) adequate Ca with Si supplementation group, (5) high Ca group (1.5% Ca), and (6) high Ca with Si supplementation group. Si supplementation significantly increased the BMD of the femur and tibia in Ca-deficient OVX rats, while no change was observed with Si supplementation in the BMD of the spine, femur, and tibia in the adequate and high Ca groups. Serum alkaline phosphatase and osteocalcin levels were not affected by Si supplementation or Ca intake levels. C-telopeptide type I collagen levels were significantly decreased as a result of Si supplementation in Ca-deficient OVX rats. In summary, Si supplementation produced positive effects on bone mineral density in Ca-deficient OVX rats by reducing bone resorption. Therefore, Si supplementation may also prove to be helpful in preventing osteoporosis in postmenopausal women whose calcium intake is insufficient.

The effect of manganese (Mn) supplementation on bone mineral density (BMD) and bone metabolism parameters was determined in ovariectomized Sprague-Dawley rats. Rats were divided into four groups (OVX, OVX+Mn, sham, sham+Mn) and fed with different intake levels of manganese (adequate 0.001% Mn, supplementation 0.01% Mn) for 12 weeks. BMD of the lumbar vertebrae, femur, and tibia were significantly lowered in ovariectomized rats compared to the sham group. In addition, BMD of the lumbar vertebrae was significantly increased by Mn supplementation in the sham groups. Serum C-telopeptide cross-links of type I collagen (CTx), bone resorption biomarker, alkaline phosphatase (ALP), and bone formation biomarkers were not significantly different among the four groups. However, serum osteocalcin, a more sensitive bone formation biomarker, was significantly increased by Mn supplementation. To summarize, Mn supplementation resulted in increased BMD and bone formation. Based on our findings, more research is needed to better understand the effects of manganese supplementation on bone formation and resorption.

BackgroundRecent reports on Propionibacterium acnes (P. acnes) suggest that this bacterium is prevalent in the prostate, is associated with acute and chronic prostatic inflammation, and might have a role in prostate carcinogenesis.MethodsTo evaluate the pathogenic role of this indigenous bacterium, we screened for the bacterium in radical prostatectomy specimens using enzyme immunohistochemistry with a novel P. acnes-specific monoclonal antibody (PAL antibody), together with an anti-nuclear factor-kappa B (NF-κB) antibody. We examined formalin-fixed and paraffin-embedded tissue sections of radical prostatectomy specimens from 28 patients with prostate cancer and 18 age-matched control patients with bladder cancer, but without prostate cancer.ResultsImmunohistochemistry with the PAL antibody revealed small round bodies within some non-cancerous glandular epithelium and stromal macrophages in most prostate samples. Prostate cancer samples had higher frequencies of either cytoplasmic P. acnes or nuclear NF-κB expression of glandular epithelium and higher numbers of stromal macrophages with P. acnes than control samples. These parameters were also higher in the peripheral zone than in the transitional zone of the prostate, especially in prostate cancer samples. Nuclear NF-κB expression was more frequent in glands with P. acnes than in glands without P. acnes. The number of stromal macrophages with the bacterium correlated with the grade of chronic inflammation in both the PZ and TZ areas and with the grade of acute inflammation in the TZ area.ConclusionsImmunohistochemical analysis with a novel monoclonal antibody for detecting P. acnes in the prostate suggested that intraepithelial P. acnes infection in non-cancerous prostate glands and inflammation caused by the bacterium may contribute to the development of prostate cancer.

Iron may induce oxidative stress via production of reactive oxygen species, facilitating mammary carcinogenesis. This study investigated the role of iron in relation to oxidative stress as a potential risk factor in the development of breast cancer (BC). BC patients (n = 121) and healthy age-matched controls (n = 149) were entered into the study. Iron and antioxidant vitamins intakes were estimated using a quantitative food frequency questionnaire. Thirty one subjects from each group provided blood samples for measurement of serum iron, plasma malondialdehyde (MDA) and ferric reducing ability of plasma (FRAP). Total and non-heme iron intake of BC patients were lower than those of the controls. However, the serum iron level was significantly higher in BC patients. Plasma MDA levels were also significantly higher in BC patients whereas no significant difference in FRAP values were observed between the two groups. Log-transformed serum iron concentration showed no significant correlation with MDA or FRAP. These results suggest that serum iron overload may be a breast cancer risk factor possibly due to increased oxidative stress.