Association of serum calcium concentrations with fibrinogen and homocysteine in nondiabetic Korean subjects

Abstract

Considerable evidence shows that increased serum calcium levels are associated with metabolic disorders, cardiovascular disease, and increased mortality. This study investigated whether serum calcium, within a normal range, is significantly associated with serum fibrinogen and homocysteine, markers of increased cardiovascular disease risk in nondiabetic Korean subjects.A cross-sectional analysis was performed on 1096 subjects (mean age, 55.1 ± 11.1 years; 36.1% women) undergoing a general health checkup. Serum biochemistry was analyzed including serum albumin-corrected calcium (Cac), insulin resistance (IR, using homeostasis model assessment [HOMA]), fibrinogen, and homocysteine.Compared with patients within the lowest Cac quartile, those with higher Cac levels had increased fibrinogen and homocysteine levels as well as an increased proportion of smoking, dyslipidemia, and HOMA-IR. Correlation analyses revealed linear relationships for Cac with fibrinogen and homocysteine in both genders. After adjustment for confounding factors, serum Cac was significantly associated with high fibrinogen (odds ratio [OR] for the highest vs the lowest quartile = 1.76, 95% confidence interval [CI] = 1.09–2.83, P = 0.02) and homocysteine (OR = 1.83, 95% CI = 1.07–3.11, P = 0.027). Multivariate regression models showed that Cac was linearly associated with fibrinogen (standardized β = 0.14, P < 0.001) and homocysteine (standardized β = 0.07, P = 0.009).High normal calcium concentrations were independently associated with increased levels of fibrinogen and homocysteine. Further investigation is needed to validate whether slightly increased calcium levels within the normal range indicate a higher risk of cardiovascular disease.

Relationships between minerals’ intake and blood homocysteine levels based on three machine learning methods: a large cross-sectional study

“…Increasing calcium intake may promote Hcy metabolism through this pathway. It has also been found that blood calcium levels are positively correlated with Hcy [ 46 ], which is contrary to our conclusions and may be due to the fact that the correlation between blood calcium levels and dietary calcium intake may not be direct. The results of an 8-week zinc intervention trial in postmenopausal women implied that zinc supplementation may improve blood folate levels and reduce blood Hcy levels after zinc supplementation, and correlation analyses found a negative correlation between folate levels and blood Hcy levels after zinc supplementation [ 43 ].…”

Point-of-care platelet function tests: relevance to arterial thrombosis and opportunities for improvement

“…[27] Sustained hyperor hypocalcaemic disorders have significant physiological effects that can contribute to onset and progression of cardiovascular disorders or bleeding, respectively. Considerable evidence shows that hypercalcaemia is associated with an increased risk of developing cardiovascular disease, arterial thrombosis and death [28][29][30]. As extracellular iCa concentration determines the rate of platelet reactivity to various agonists [31], variation in plasma iCa concentration results in highly variable aggregation response to agonists, especially if the agonist is applied in submaximal concentration [32].…”

Consumption of very low-mineral water may threaten cardiovascular health by increasing homocysteine in children

“…In our previous study, consuming VLW increased serum Ca in children ( 18 ). Increased serum Ca can increase serum homocysteine by mediating atherothrombosis ( 19 ). But the serum homocysteine was not associated with the serum Ca in this study.…”

“…Dyslipidemia and lipid oxidation are risk factors for cardiovascular diseases (37)(38)(39)(40). Both homocysteine metabolism and Ca homeostasis disorders can disturb lipid metabolism and induce oxidative stress (19,20,41). The serum Apo B, Apo B/Apo A1, and oxLDL was higher in children drinking very low-mineral DDW.…”

“…Calcium is an essential hemostatic cofactor and second messenger involved in intracellular signalings, such as the vascular system. Disturbed Ca homeostasis directly leads to increased levels of homocysteine and dyslipidemia ( 19 ). In addition, Ca may disturb mitochondrial b-oxidation and increase oxidative stress, facilitating lipid oxidation ( 20 ).…”