Vitamin K Deficiency

Vitamin K acts as a coenzyme of carboxylase, catalyzing the carboxylation of several vitamin K dependent proteins. Beyond its well-known effects on blood coagulation, it also exerts relevant effects on bone and the vascular system. In this review, we point out the relevance of an adequate vitamin K intake to obtain sufficient levels of carboxylated (active form) vitamin K dependent proteins (such as Osteocalcin and matrix Gla protein) to prevent bone health. Another bone-related action of Vitamin K is being a ligand of the nuclear steroid and xenobiotic receptor (SXR). We also discuss the recommended intake, deficiency, and assessment of vitamin K. Furthermore, we review the few available studies that have as pre-specified outcome bone fractures, indicating that we need more clinical studies to confirm that vitamin K is a potential therapeutic agent for bone fractures.

Vitamin K is essential for the synthesis of few coagulation factors. Infants can easily develop vitamin K deficiency owing to poor placental transfer, low vitamin K content in breast milk, and poor intestinal absorption due to immature gut flora and malabsorption. Vitamin K deficiency bleeding (VKDB) in infancy is classified according to the time of presentation: early (within 24 h), classic (within 1 week after birth), and late (between 2 week and 6 months of age). VKDB in infancy, particularly late-onset VKDB, can be life-threatening. Therefore, all infants, including newborn infants, should receive vitamin K prophylaxis. Exclusive breastfeeding and cholestasis are closely associated with this deficiency and result in late-onset VKDB. Intramuscular prophylactic injections reduce the incidence of early-onset, classic, and late-onset VKDB. However, the prophylaxis strategy has recently been inclined toward oral administration because it is easier, safer, and cheaper to administer than intramuscular injection. Several epidemiological studies have shown that vitamin K oral administration is effective in the prevention of VKDB in infancy; however, the success of oral prophylaxis depends on the protocol regimen and parent compliance. Further national surveillance and studies are warranted to reveal the optimal prophylaxis regimen in term and preterm infants.

Intestinal diseases, such as inflammatory bowel diseases (IBDs) and colorectal cancer (CRC) generally characterized by clinical symptoms, including malabsorption, intestinal dysfunction, injury, and microbiome imbalance, as well as certain secondary intestinal disease complications, continue to be serious public health problems worldwide. The role of vitamin K (VK) on intestinal health has drawn growing interest in recent years. In addition to its role in blood coagulation and bone health, several investigations continue to explore the role of VK as an emerging novel biological compound with the potential function of improving intestinal health. This study aims to present a thorough review on the bacterial sources, intestinal absorption, uptake of VK, and VK deficiency in patients with intestinal diseases, with emphasis on the effect of VK supplementation on immunity, anti-inflammation, intestinal microbes and its metabolites, antioxidation, and coagulation, and promoting epithelial development. Besides, VK-dependent proteins (VKDPs) are another crucial mechanism for VK to exert a gastroprotection role for their functions of anti-inflammation, immunomodulation, and anti-tumorigenesis. In summary, published studies preliminarily show that VK presents a beneficial effect on intestinal health and may be used as a therapeutic drug to prevent/treat intestinal diseases, but the specific mechanism of VK in intestinal health has yet to be elucidated.

Background/Objectives: The benefits of vitamin K are well established in skeletal and cardiovascular health through activation of vitamin K-dependent proteins, including osteocalcin and matrix Gla protein. Emerging evidence also links vitamin K to pathways that influence body composition, including insulin sensitivity, adiponectin regulation, lipid oxidation, and inflammation. Vitamin K deficiency is linked to adverse health outcomes. We therefore evaluated whether menaquinone-7 (MK-7) supplementation alters body composition in adults with low vitamin K status. Methods: A total of 243 participants (166 women and 77 men) with low vitamin K status received 180 mcg of menaquinone-7 (MK-7), a form of Vitamin K, daily for one year. Changes in body mass index (BMI), body weight, fat mass, lean mass, and visceral adipose tissue (VAT) were assessed. Results: At baseline, higher dp-ucMGP, indicating lower vitamin K status, was positively associated with BMI (r = 0.223; p p p p = 0.041). Responders (≥183 pmol/L dp-ucMGP drop) showed improvements in fat mass (-1.93%, p = 0.039), waist-to-hip ratio (-1.43%, p = 0.012), BMI (-1.37% ± 3.21, p = 0.004), and weight (-1.25%, p = 0.008), while non-responders exhibited an increase in VAT (+7.28%, p = 0.002). Women, especially premenopausal ones, experienced greater reductions in BMI, fat mass, and weight. dp-ucMGP levels significantly decreased in 90.9% of women (p Conclusions: Lower vitamin K status was associated with higher BMI, fat mass, and visceral adipose tissue. After one year of MK-7 supplementation, a modest reduction in BMI was observed, with more pronounced improvements in body composition among women. While these sex related differences may suggest that men require higher doses to achieve comparable responses, the current evidence remains preliminary. Further studies with larger cohorts are needed to clarify these findings.