Vitamin K, a cofactor for the γ-glutamyl carboxylase enzyme, is required for the post-translational activation of osteocalcin and matrix Gla protein, which play a key role in bone and muscle homeostasis. In vivo and in vitro models for osteoporosis and sarcopenia suggest the vitamin K could exert a positive effect in both conditions. In bone, it increases osteoblastogenesis, whilst decreases osteoclast formation and function. In muscle, it is associated with increased satellite cell proliferation and migration and might play a role in energy metabolism. Observational trials suggest that high levels of vitamin K are associated with increased bone mineral density and reduced fracture risk. However, interventional studies for vitamin K supplementation yielded conflicting results. Clinical trials in sarcopenia suggest that vitamin K supplementation could improve muscle mass and function. One of the main limitations on the vitamin K studies are the technical challenges to measure its levels in serum. Thus, they are obtained from indirect sources like food questionnaires, or levels of undercarboxylated proteins, which can be affected by other environmental or biological processes. Although current research appoints to a beneficial effect of vitamin K in bone and muscle, further studies overcoming the current limitations are required in order to incorporate this supplementation in the clinical management of patients with osteosarcopenia.

Vitamins have well-established roles in bacterial metabolism. Menaquinones (MKn, n = prenyl units in sidechain) are bacterially produced forms of vitamin K produced by the gut microbiota and consumed in the diet. Little is known about the influence of dietary vitamin K quinones on gut microbial composition and MKn production. Here, male and female C57BL6 mice were fed a vitamin K deficient diet or vitamin K sufficient diets containing phylloquinone (PK, plant-based vitamin K form), MK4, and/or MK9. DNA was extracted from cecal contents and 16S sequencing conducted to assess microbial composition. Cecal microbial community composition was significantly different in vitamin K deficient female mice compared to females on vitamin K sufficient diets (all < .007). Parallel trends were seen in male mice, but were not statistically significant (all > .05 but <0.1). Next, stable isotope-labeled vitamin K quinones were supplemented to male and female C57BL6 mice (HPK, CMK4, HMK7, HMK9) and to an fermentation model inoculated with human stool (HPK, HMK4, HMK9, or vitamin K precursor H-menadione). Vitamin K quinones in feces and culture aliquots were measured using LC-MS. , supplemented vitamin K quinones were remodeled to other MKn (H- or C-labeled MK4, MK10, MK11, and MK12), but only the precursor H-menadione was remodeled to HMK4, HMK9, HMK10, and HMK11. These results suggest that dietary vitamin K deficiency alters the gut microbial community composition. Further studies are needed to determine if menadione generated by host metabolism may serve as an intermediate in dietary vitamin K remodeling .

OBJECTIVE:To explore the association of both plasma vitamin D and K concentrations with all-cause mortality, cardiovascular mortality, and cardiovascular events in the general population. METHODS:We studied 4742 participants of the Prevention of REnal and Vascular ENd-Stage Disease (PREVEND) Study. At baseline, vitamin D and K status was determined by measurement of 25-hydroxyvitamin D [25(OH)D] and dephosphorylated uncarboxylated matrix Gla protein (dp-ucMGP), respectively. Patients were categorized into: 25(OH)D < 50 or ≥ 50 nmol/L and dp-ucMGP < 361 or ≥ 361 pmol/L with 25(OH)D > 75 nmol/L and dp-ucMGP < 361 pmol/L as reference. Cause of death was coded according to International Classification of Diseases 9&10 codes from the 2001-2003 examination until date of death/event or censoring date (January 1st, 2017). RESULTS:Mean age was 52.6 ± 11.9 years and 2513 (53%) were female. During a median of 14.2 year follow-up, 620 participants died of which 142 were due to cardiovascular causes. Combined low vitamin D and K status was present in 970 participants (20%) and was associated with a greater risk of all-cause mortality compared to high vitamin D and high vitamin K status group (n = 1424) after adjusting for potential confounders: hazard ratio 1.46 (95% confidence intervals 1.12-1.90). We observed similar trends, albeit non-significant for cardiovascular mortality, and cardiovascular events: 1.42 (0.79-2.55), 1.28 (0.93-1.77), respectively. CONCLUSIONS:Combined low vitamin D and K status are associated with increased all-cause mortality risk and possibly with cardiovascular mortality and cardiovascular events compared with adequate vitamin D and K status. Future studies should investigate the effect of combined vitamin D and K supplementation on clinical outcomes.

BACKGROUND:Vitamin K has long been regarded as a procoagulant drug by physicians, and concerns have been raised with regard to its effects on hemostasis. Although many studies have shown that vitamin K supplementation is safe for thrombotic events, the effect of vitamin K supplementation on the activities of vitamin K dependent procoagulation factors in healthy individuals is not available. OBJECTIVES:This study aimed to investigate whether vitamin K2 supplementation at recommended doses affects the activity of vitamin K dependent procoagulation factors in healthy individuals without any anticoagulation treatment. DESIGN:Forty healthy volunteers between 25 and 40 years of age were recruited. Menaquinone-7 (MK-7) was administrated at 90 μg for 30 days. Prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), and blood coagulation factors II, VII, IX, and X activities and Protein induced by vitamin K absence or antagonist-II (PIVKA-II) were measured on days 0 and 30 after MK-7 administration. RESULTS:PT, APTT, and TT showed no significant differences on day 30 when compared with baseline. The activities of coagulation factors II, VII, IX, and X on day 30 showed no significant differences with those at baseline. PIVKA-II levels were unchanged after 30 days of MK-7 supplementation. CONCLUSIONS:MK-7 supplementation at recommended dosage does not affect vitamin K-dependent coagulation factors' coagulation activity, and does not enhance the carboxylation of prothrombin in healthy individuals. This indicated that MK-7 administration does not alter hemostatic balance in healthy populations without anticoagulation treatment.

A protective role for vitamin K in cardiovascular disease (CVD), a leading cause of morbidity and mortality, has been proposed because vitamin K-dependent proteins, such as matrix Gla (γ-carboxyglutamic acid) protein (MGP), are present in vascular tissue. MGP functions as a vascular calcification inhibitor-but only when it is carboxylated, which requires vitamin K. There is more than one naturally occurring form of vitamin K. Phylloquinone (vitamin K1) is found in plant-based foods, whereas menaquinones (vitamin K2) are a class of vitamin K compounds found in animal-based and fermented foods. Phylloquinone and menaquinones are capable of carboxylating MGP and other vitamin K-dependent proteins. In rodent models, high intakes of either phylloquinone or menaquinone reduced vascular calcification. Evidence of the relative importance of phylloquinone and menaquinone to CVD in humans is limited and controversial. In some observational studies, higher dietary menaquinone intake, but not phylloquinone intake, was associated with less coronary artery calcification (a subclinical manifestation of CVD) and a lower risk for clinical CVD events. These findings have led to claims that menaquinones have unique cardiovascular health benefits compared with phylloquinone. However, this claim is not supported by the results of the limited number of intervention trials conducted to date. The purpose of this review is to evaluate the strengths and limitations of the available evidence regarding the role of vitamin K in vascular calcification, CVD, and mortality.

The loss of bone quantity and quality in postmenopausal female patients can be a problem for dental treatment. A sufficient intake of nutrients such as calcium, magnesium, and vitamins D and K is likely correlated with the mechanical properties of bone. In particular, vitamin K2, also called menaquinone (MK), inhibits bone loss in postmenopausal women. Here we demonstrate the microstructural and mechanical properties of bone recovery in ovariectomized (OVX) rats during MK-7 administration. Bilateral ovariectomy and a sham operation were performed on 14-week-old female SPF Wistar rats. MK-4 and -7 were orally administered at 30 mg/kg daily for 12 weeks. The femur was used for the 3-point bending test and microstructural analysis of the cancellous bone by micro-CT, and the mandibular cortical bone for the evaluation of mechanical properties on a nanoscale. Micro-computed tomography revealed irregular trabecular architecture, hollow marrow cavities, and sparse trabecular bone in the femurs of the OVX group. Trabecular bone structure analysis showed that the MK-7 group had greater bone volume per tissue volume (BV/TV) and a higher trabecular number than the OVX group. The bulk-scale 3-point bending test did not allow the mechanical properties between OVX and OVX/MK7 groups to be discerned, yet at the smallest level, the elastic-plastic transition point of the nanoindentation stress-strain curve of the mandibular cortical bone was higher in the MK-7 group than in the OVX group. These findings suggest that MK-7 enables bone microstructural and mechanical recovery in the OVX model.

PURPOSE OF REVIEW:Vascular calcification is a common and important cardiovascular risk factor in patients with chronic kidney disease (CKD). Recent advances in the understanding of the biology of vascular calcification implicate vitamin K-dependent proteins as important regulators in this process. This review highlights recent key advances in vascular biology, epidemiology, and clinical trials in this rapidly evolving field. RECENT FINDINGS:Vitamin K deficiency is associated with increasing severity of vascular calcification among patients with CKD, but the relationship with cardiovascular disease and mortality is inconsistent. Vitamin K may reduce calcification propensity by improving the activity of vitamin K-dependent calcification inhibitors or by down-regulating components of the innate immune system to reduce inflammation. However, recent randomized controlled trials in patients with diabetes, CKD, renal transplant, and on hemodialysis have failed to demonstrate improvement in vascular calcification or stiffness after vitamin K treatment. SUMMARY:Current evidence does not support a clinically useful role for vitamin K supplementation to prevent or reverse vascular calcification in patients with CKD. Knowledge gaps remain, particularly whether higher doses of vitamin K, longer duration of supplementations, or use a vitamin K as a part of a package of measures to counteract vascular calcification might be effective.

Mature osteoclasts express the vitamin D receptor (VDR) and are able to respond to active vitamin D (1α, 25-dihydroxyvitamin D; 1,25(OH)D) by regulating cell maturation and activity. However, the in vivo consequences of vitamin D signalling directly within functionally mature osteoclasts is only partially understood. To investigate the in vivo role of VDR in mature osteoclasts, conditional deletion of the VDR under control of the cathepsin K promoter (Ctsk/Vdr), was assessed in 6 and 12-week-old mice, either under normal dietary conditions (NormCaP) or when fed a low calcium (0.03 %), low phosphorous (0.08 %) diet (LowCaP). Splenocytes from Ctsk/Vdr mice were co-cultured with MLO-Y4 osteocyte-like cells to assess the effect on osteoclastogenesis. Six-week-old Ctsk/Vdr mice demonstrated a 10 % decrease in vertebral bone volume (p < 0.05), which was associated with increased osteoclast size (p < 0.05) when compared to Vdr control mice. Control mice fed a LowCaP diet exhibited extensive trabecular bone loss associated with increased osteoclast surface, number and size (p < 0.0001). Interestingly, Ctsk/Vdr mice fed a LowCaP diet showed exacerbated loss of bone volume fraction (BV/TV%) and trabecular number (Tb.N), by a further 22 % and 21 %, respectively (p < 0.05), suggesting increased osteoclastic bone resorption activity with the loss of VDR in mature osteoclasts under these conditions. Co-culture of Ctsk/Vdr splenocytes with MLO-Y4 cells increased resulting osteoclast numbers 2.5-fold, which were greater in nuclei density and exhibited increased resorption of dentine compared to osteoclasts derived from Vdr splenocyte cultures. These data suggest that in addition to RANKL-mediated osteoclastogenesis, intact VDR signalling is required for the direct regulation of the differentiation and activity of osteoclasts in both in vivo and ex vivo settings.

Despite the associations between individual nutrients and sarcopenia, we are aware of no information about the link between patterns of nutrient intake and odds of sarcopenia and its components. The present study aimed to examine the association between nutrient-based dietary patterns and sarcopenia and its components among the Iranian adult population. In this population-based, cross-sectional study, we enrolled 300 elderly adults (150 men and 150 women) aged ≥55 years by using a cluster random sampling method. Dietary intakes of the study population were assessed using a validated food frequency questionnaire. Principal component analysis was conducted to derive nutrient patterns based on a daily intake of 33 nutrients. Muscle mass, muscle strength, and gait speed were measured according to standard methods. Sarcopenia and its components were defined based on the European Working Group on Sarcopenia. Three major nutrient-based dietary patterns were identified: (1) the "pro-vit pattern" that was high in pantothenic (B5), cobalamin (B12), calcium, protein, phosphor, riboflavin (B2), zinc, cholesterol, saturated fat, folate, niacin (B3), selenium, vitamin D, vitamin K, and vitamin A; (2) the "anti-inflammatory" pattern, which was rich in polyunsaturated fat, monounsaturated fat, copper, vitamin E, omega-3, magnesium, iron, pyridoxine (B6), sodium, and caffeine; and (3) the "carbo-vit" patternm which is characterized by high intake of fructose, glucose, dietary fiber, biotin, potassium, thiamin (B1), vitamin C, and chromium. After adjusting for confounders, subjects in the top tertile of the anti-inflammatory pattern had lower odds of sarcopenia (OR 0.25; 95% CI 0.10-0.63) and low muscle strength (OR: 0.46; 95% CI: 0.22-0.96) than those in the bottom tertile. Greater adherence to the carbo-vit pattern was inversely associated with the odds of low gait speed (OR: 0.46; 95% CI: 0.235-0.93). Major nutrient-based dietary patterns were significantly associated with sarcopenia and its components. Further studies are required to confirm our findings.

BACKGROUND:As a common systemically muscular-skeleton disorder of aging, osteoporosisis is characterized by the uninterrupted deconstruction in osseous microarchitecture. Osteoporosis can consequently lead to a significantly high risk of osteoporotic fractures, such as Osteoporotic Vertebral Compressive Fractures [OVCF] in the spine and osteoporotic femoral neck fractures in the hip joint, which can significantly increase the numbers of mortality and morbidity in elderly people, especially in postmenopausal women. METHODS:In addition, vitamin K has been demonstrated to play a key role in inhibiting osteoporotic fractures among postmenopausal women, but its long-term benefits, potential harms, and side effects of the combination between vitamin K and other anti-osteoporosis medicines, such as bisphosphonates or teriparatide still remain to be extensively studied. Therefore, the present study aimed to systematically reviewed previously published literature on the role of vitamin K in the treatment of osteoporosis. We currently, via multiple query strategies, searched the relevant literature in Cochrane and PubMed from January 2010 to December 2019. RESULTS:Subsequently, we conducted the systematic review according to the standard guideline of Preferred Reporting Item for Systematic Reviews and Meta-Analyses [PRISMA]. CONCLUSION:Finally, ten relevant studies met our current criteria for inclusion; subsequently, we followed the PRISMA guideline, then systematically reviewed each study by categorizing the data sources and analytical approaches in each study, while setting up variables and defining each study's outcomes.

Following a request from the European Commission, the Panel on Additives and Products or Substances used in Animal Feed (FEEDAP) was asked to deliver a scientific opinion on the safety and efficacy of a feed additive consisting of vitamin K (phytomenadione) produced by chemical synthesis when used as a nutritional additive in complementary feed of horses at a maximum supplemental level of 14 mg vitamin K/horse per day. The use of vitamin K1 is safe when used as a feed additive for horses under the proposed conditions of use. The use of vitamin K1 in nutrition of horses under the proposed conditions of use is considered safe for the consumer and the environment. No exposure of users by inhalation is expected. The Panel cannot conclude on the potential of the additive to be a skin and eye irritant. Vitamin K1 is considered a moderate dermal sensitiser. Vitamin K1 is an effective source of vitamin K in horse nutrition. The Panel recommends that the specifications of the additive refer to the substance-related impurities listed in the most updated monograph of the European Pharmacopoeia.

Hyperemesis gravidarum (HG) refers to severe nausea and emesis noted during pregnancy. However, no consensus exists on the specific diagnostic criteria that can be used for this condition. The aim of the present systematic review was to summarize the available evidence regarding the severe complications observed during HG with a heightened risk of fatality. A systematic search was conducted on PubMed, Cochrane Library, EMBASE and WILEY databases for the relevant publications regarding the severe and life-threatening complications of HG. The search terms were as follows: '(Hyperemesis gravidarum)' AND ('complications' OR 'severe' OR 'adverse pregnancy outcomes' OR 'stroke' OR 'seizures' OR 'Wernicke's encephalopathy' OR 'arrhythmias' OR 'pneumomediastinum' OR 'coagulopathy' OR 'electrolytic imbalance'). Abstracts, conference presentations, letters to the editor, studies written in languages other than English and editorials were all excluded. This search identified 43 studies analyzing life-threatening complications of HG, of which 11, seven, eight and 17 articles analyzed neurological, cardiovascular, thoracic and systemic complications, respectively. Reports on life-threatening complications were exceptionally rare in HG. The most frequent severe complications noted were Wernicke's encephalopathy, electrolyte imbalance and vitamin K deficiency. The low mortality rate for patients with HG over the last decade could be explained by the high efficiency of modern therapy, and the precise management of every complication according to current guidelines.

An experiment was conducted to test the hypothesis that inclusion of Cu oxide (Cu2O) in diets for growing-finishing pigs improves body weight (BW) and bone mineralization, and reduces accumulation of Cu in the liver compared with pigs fed diets containing Cu sulfate (CuSO4). Two hundred growing pigs (initial BW: 11.5 ± 0.98 kg) were allotted to a randomized complete block design with 2 blocks of 100 pigs, 5 dietary treatments, 5 pigs per pen, and a total of 8 pens per treatment. Treatments included the negative control (NC) diet that contained 20 mg Cu/kg, and 4 diets in which 125 or 250 mg Cu/kg from CuSO4 or Cu2O were added to the NC diet. The experiment was divided into 4 phases and concluded when pigs reached market weight. Pig weights were recorded on day 1 and at the end of each phase and feed provisions were recorded throughout the experiment. On the last day of phases 1 and 4, 1 pig per pen was sacrificed to obtain samples of liver and spleen tissue, and the right metacarpal was collected. Results indicated that pigs fed diets containing 250 mg Cu/kg from CuSO4 had greater BW at the end of phases 1 and 2 than pigs fed NC diets. Pigs fed diets containing 250 mg Cu/kg from Cu2O had greater (P < 0.05) BW at the end of phases 1, 2, 3, and 4 compared with pigs fed NC diets, and these pigs also had greater BW at the end of phases 3 and 4 than pigs fed all other diets. Pigs fed the diets with 250 mg Cu/kg tended to have greater (P < 0.10) feed intake than pigs fed the NC diet at the end of phase 2, and for the overall experimental period, pigs fed diets containing 250 mg Cu/kg from Cu2O had greater (P < 0.05) feed intake than pigs on all other treatments. However, no differences in gain:feed ratio were observed among treatments. Copper accumulation in liver and spleen increased with Cu dose, but at the end of phase 1, pigs fed 250 mg Cu/kg from CuSO4 had greater (P < 0.05) Cu concentration in liver and spleen than pigs fed 250 mg Cu/kg from Cu2O. Pigs fed diets containing 250 mg Cu/kg from Cu2O had greater (P < 0.05) quantities of bone ash and greater (P < 0.05) concentrations of Ca, P, and Cu in bone ash than pigs fed NC diets or the 2 diets containing CuSO4, but Zn concentration in bone ash was less (P < 0.05) in pigs fed diets containing 250 mg Cu/kg from Cu2O. To conclude, supplementing diets for growing pigs with Cu2O improves growth performance and bone mineralization with less Cu accumulation in liver compared with pigs fed diets containing CuSO4.

We present a family who suffered recurrent sibling losses due to vitamin K deficiency bleed. The index child was asymptomatic at presentation, had normal clinical examination, and was investigated for coagulation disorders in view of previous 3 sibling losses as a result of intracranial hemorrhage. His investigations showed deranged coagulogram and clotting factors' assay. The baby was given vitamin K1 1 mg intramuscularly following which his coagulogram and clotting factors' assay returned to normal. The genetic analysis did not identify any inherited cause of bleeding tendency. The significant family history, exclusive breastfeeding, no diarrhea, failure to thrive or drug use, no prophylaxis with vitamin K at birth, recovery of clotting factors on vitamin K administration, and a corroborative molecular analysis confirmed diagnosis of vitamin K deficiency in the index child. This case gives a strong reminder not to miss birth dose of vitamin K in any neonate.

Premature cardiovascular disease and death with a functioning graft are leading causes of death and graft loss, respectively, in kidney transplant recipients (KTRs). Vascular stiffness and calcification are markers of cardiovascular disease that are prevalent in KTR and associated with subclinical vitamin K deficiency. We performed a single-center, phase II, parallel-group, randomized, double-blind, placebo-controlled trial (ISRCTN22012044) to test whether vitamin K supplementation reduced vascular stiffness (MRI-based aortic distensibility) or calcification (coronary artery calcium score on computed tomography) in KTR over 1 year of treatment. The primary outcome was between-group difference in vascular stiffness (ascending aortic distensibility). KTRs were recruited between September 2017 and June 2018, and randomized 1:1 to vitamin K (menadiol diphosphate 5 mg; n = 45) or placebo (n = 45) thrice weekly. Baseline demographics, clinical history, and immunosuppression regimens were similar between groups. There was no impact of vitamin K on vascular stiffness (treatment effect -0.23 [95% CI -0.75 to 0.29] × 10 mmHg ; p = .377), vascular calcification (treatment effect -141 [95% CI - 320 to 38] units; p = .124), nor any other outcome measure. In this heterogeneous cohort of prevalent KTR, vitamin K supplementation did not reduce vascular stiffness or calcification over 1 year. Improving vascular health in KTR is likely to require a multifaceted approach.

Vitamin K is a fat-soluble vitamin that plays an important role in blood coagulation and bone formation. Vitamin K has homologues due to differences in the side chain structure, phylloquinone (abbreviated as vitamin K, PK) having a phytyl side chain and menaquinones (MK-n, n=1 to 14) having an isoprenoid side chain structure. The main vitamin K that we take from our daily diet is PK, and a fermented food, natto, contains MK-7 produced by Bacillus subtilis natto. However, the majority of vitamin K present in the tissues of mammals, including humans, is menaquinone-4 (abbreviated as vitamin K, MK-4) having a geranylgeranyl side chain. This reason is that PK or MK-n obtained in the diet is converted into MK-4 in the body. We identified that the UbiA prenyltransferase domain containing protein 1 (UBIAD1) is the conversion enzyme of PK and MK-n to MK-4. The physiological roles of MK-4 in all tissues of the whole body and the physiological significance of MK-4 converted from PK and MK-n by UBIAD1 have not been sufficiently elucidated yet. To investigate the function of UBIAD1 in vivo, we generated UBIAD1 systemic knockout mice and tissue-specific UBIAD1 knockout mice. In this paper, we introduce the usefulness of vitamin K for diseases that may involve vitamin K and UBIAD1.

Six types of vitamin K (VK); two sources (menadione sodium bisulfite, MSB; menadione nicotinamide bisulfite, MNB), and three different forms (crystal, micro-capsule, and micro-sphere) were used to determine the retention of VK in vitamin premixes (Experiment 1) or vitamin trace mineral (VTM) premixes (Experiment 2) after 1, 2, 3, and 6 months of storage. The retention of VK in vitamin premixes was evaluated at 25 °C/60% relative humidity or 40 °C/75% relative humidity in an incubator in Experiment 1 and in VTM premixes (choline chloride: 0 vs. 16,000 mg/kg) stored at room temperature in Experiment 2. The VK retention in vitamin premix or VTM premix decreased significantly with the extension of storage time ( < 0.05). In Experiment 1, the VK retention was higher in the 25 °C/60% incubator (56%) than in the 40 °C/75% incubator (28%). The MNB retention (52%) was higher than MSB retention (32%). The retention of VK in micro-capsules (43%) or micro-spheres (48%) was higher than the crystal form (35%) after six months of storage. In Experiment 2, there was no difference between the retention of MSB (49%) or MNB (47%). The retention of VK of micro-capsule (51%) or micro-sphere (54%) was higher than that of crystal form (40%). The VK retention was higher in the choline-free group (51%) than in the choline group (47%) after six months of storage. Finally, the predicted equations of VK retention with storage time in vitamin premixes or VTM premixes were established. The of the prediction equations was ≥0.9005, indicating that time is an important factor in predicting VK retention. In conclusion, the higher temperature-relative humidity, choline had negative effects on VK retention during premix storage. MNB retention was higher than MSB during storage of vitamin premix. The encapsulated forms of VK, micro-capsules and micro-spheres, could improve VK storage stability in vitamin premix and VTM premix.

As human life expectancy is rising, the incidence of age-associated diseases will also increase. Scientific evidence has revealed that healthy diets, including good fats, vitamins, minerals, or polyphenolics, could have antioxidant and anti-inflammatory activities, with antiaging effects. Recent studies demonstrated that vitamin K is a vital cofactor in activating several proteins, which act against age-related syndromes. Thus, vitamin K can carboxylate osteocalcin (a protein capable of transporting and fixing calcium in bone), activate matrix Gla protein (an inhibitor of vascular calcification and cardiovascular events) and carboxylate Gas6 protein (involved in brain physiology and a cognitive decline and neurodegenerative disease inhibitor). By improving insulin sensitivity, vitamin K lowers diabetes risk. It also exerts antiproliferative, proapoptotic, autophagic effects and has been associated with a reduced risk of cancer. Recent research shows that protein S, another vitamin K-dependent protein, can prevent the cytokine storm observed in COVID-19 cases. The reduced activation of protein S due to the pneumonia-induced vitamin K depletion was correlated with higher thrombogenicity and possibly fatal outcomes in COVID-19 patients. Our review aimed to present the latest scientific evidence about vitamin K and its role in preventing age-associated diseases and/or improving the effectiveness of medical treatments in mature adults ˃50 years old.