Vitamin K (VK) acts as a cofactor for γ-glutamylcarboxylase, which catalyzes the posttranslational modification (γ-carboxylation of glutamate residues) of blood coagulation factors and bone proteins to create Gla-proteins. It is also involved in maintaining the blood coagulation system and bone metabolism, and suppressing vascular calcification. When the tissue distribution of VK was examined in animals, relatively large amounts of VK were found in the brain, pancreas, and gonads, in addition to the liver, bone, and blood vessels. However, this tissue distribution pattern of VK is not always consistent with that of Gla-proteins. This observation suggests that VK may exert unknown functions other than Gla-protein formation in tissues. Animal studies using various amounts of VK in experimental diets have shown that VK has an anti-inflammatory effect via the inhibition of NF-κB activation, increases testosterone production in the testis via activation of the cAMP‒protein kinase A axis, and modulates the expression of bile acid synthesis–related genes in the liver via activation of the nuclear receptor PXR. In addition, geranylgeraniol (GGOH), a side chain moiety of menaquinone-4 and a type of VK₂, has been shown to have similar effects in animal and cell culture studies. In this review, we describe the novel functions of VK and GGOH and discuss the potential contribution of these ingredients to health promotion.

View full abstract

Selenium deficiency is known to cause heart failure due to decreased mitochondrial function and increased oxidative stress. Keshan disease, an endemic disease in China, is believed to be a myocardial disorder primarily caused by selenium deficiency. The incidence of Keshan disease has decreased due to dietary improvements, and it is now considered a disease that has largely been overcome in modern society.
In contrast, a European study published in 2020 reported that 20% of heart failure patients had hyposelenemia, suggesting that selenium deficiency is not uncommon in contemporary heart failure cases.
We investigated the prevalence and clinical outcomes of hyposelenemia in heart failure patients in Japan. Using the Japanese standard cutoff value of 105 μg/L, we found that 51.6% of heart failure patients had selenium deficiency. Furthermore, heart failure patients with hyposelenemia experienced a high rate of re-admission due to heart failure.
Currently, it remains unclear whether selenium supplementation is beneficial for heart failure patients with hyposelenemia. Additional research is required to assess the efficacy of selenium supplementation in this patient population.

View full abstract