Vitamin K

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Martin J. Shearer - One of the best experts on this subject based on the ideXlab platform.

  • Vitamin K and Vitamin K-Dependent Proteins in Relation to Human Health
    MDPI - Multidisciplinary Digital Publishing Institute, 2018
    Co-Authors: Martin J. Shearer, Leon J. Schurgers
    Abstract:

    Vitamin K comprises a group of highly lipophilic molecules that possess a common 2-methyl-1, 4-naphthoquinone nucleus and a variable polyisoprenoid side chain at the 3-position that can vary in both length and degree of saturation. In nature, these forms are found as a single plant form (phylloquinone or Vitamin K1) and a series of bacterial forms (menaquinones or Vitamin K2). Vitamin K acts as a cofactor for a microsomal enzyme, γ-carboxyglutamyl carboxylase (GGCX), that serves to transform specific peptide-bound glutamate residues found in certain specialized proteins to γ-carboxyglutamate (Gla). This posttranslational protein modification is the only firmly established biochemical function of Vitamin K. The resultant Vitamin K-dependent (VKD) proteins, or Gla proteins, are diverse in both structure and function and are found in many cell and tissue types. The best-Known example of the health role of Vitamin K-mediated protein γ-carboxylation is in the synthesis of several VKD blood coagulation proteins, which are essential for the maintenance of extracellular haemostasis. An overt deficiency of Vitamin K results in bleeding and although rare in most populations, Vitamin K deficiency bleeding (VKDB) in early infancy has potentially devastating and fatal consequences because bleeding commonly occurs within the brain. For this reason it is recommended that all newborn infants should receive Vitamin K prophylaxis. On the other hand, the deliberate lowering of circulating VKD-coagulation factors by the therapeutic administration of Vitamin K antagonists (VKA) such as warfarin is used to treat and prevent thrombotic disorders. The functions of most non-coagulation Gla proteins remain uncertain, but are suspected to play roles in processes as diverse as bone and cardiovascular mineralization, vascular integrity, energy metabolism, immune response, brain metabolism, and in cellular growth, survival, and signalling. For the most part, extrapolations of the cellular properties of extrahepatic Gla proteins to tangible health benefits are unclear or fuzzy, as are the health consequences of their undercarboxylation. However, there is evidence that higher nutritional intaKes of Vitamin K are required to enable maximal γ-carboxylation of certain extrahepatic Gla proteins, such as osteocalcin and matrix Gla protein (MGP). Osteocalcin and MGP currently represent the best-studied extrahepatic Gla proteins with respect to their putative roles in bone and cardiovascular health, respectively. In addition, osteocalcin may play a role in regulating energy metabolism. Much current interest focuses on the role of MGP as an inhibitor of vascular mineralization, particularly in renal disease and in patients taKing VKA. Interestingly, although VKA have been in clinical use for decades, recent evidence suggests that they may cause unintended health consequences by disrupting the function of MGP resulting in calcification and loss of the functional integrity of the vessel wall. Apart from the role of Vitamin K in γ-carboxylation there is evidence that some forms, particularly menaquinone-4 (MK-4), have a direct influence on cellular functions.This Special Issue of Nutrients focuses on advances that extend our Knowledge of the biochemical functions and health roles played by both the micronutrient Vitamin K and its target Gla proteins. The scope of potential topics is wide and may include studies in population and patient groups, animal models and at the cellular level. Examples include the presentation, diagnosis, incidence, causes, and prevention of deficiency syndromes, of which the most obvious is bleeding in infancy, but also extends to other putative roles of Vitamin K such as in bone and cardiovascular health. In trying to define extrahepatic functions of Vitamin K it is important to obtain evidence of pathophysiological signatures that may derive from chronic suboptimal Vitamin K intaKes or as a consequence of Vitamin K antagonists. An important related question is whether the pathophysiology can be ameliorated or prevented by judicious Vitamin K supplementation. Equally important to our understanding of the human physiology of Vitamin K are studies that define the relative functional importance of individual vitamers and how differences in their availability and metabolism affect their biological activity. Recent highlights in metabolism include the delineation of the importance of Vitamin K epoxide reductase (VKOR) in maintaining Vitamin K status and the intriguing hypothesis that its paralog VKOR-liKe 1 enzyme (VKORL1) may serve an antioxidant function. Another highlight illustrating the importance of metabolism to Vitamin K function is the discovery that the enzyme UbiA prenyltransferase-containing domain 1 (UBIAD1) participates in the cellular conversion of phylloquinone to MK-4 with menadione as a metabolic intermediate. We invite authors to submit reviews or original research on any of the above topics

  • the role of dietary Vitamin K in the management of oral Vitamin K antagonists
    Blood Reviews, 2012
    Co-Authors: Michael V Holmes, Beverley J. Hunt, Martin J. Shearer
    Abstract:

    Vitamin K antagonists (VKA) have been the mainstay of oral anticoagulant therapy for over 60years. In this review we critically assess the evidence for the importance of Vitamin K nutrition during VKA therapy; the methodologies for measuring dietary intaKes; the Vitamin K intaKe data in patients on VKA and healthy people; and the experimental evidence for the influence of Vitamin K intaKes and biochemical measures of Vitamin K status on VKA response. Several studies show that dietary intaKes of phylloquinone (Vitamin K1) are associated to the sensitivity and stability of anticoagulation during initiation and maintenance dosing with low habitual intaKes associated with greater instability of the INR and risK of sub-therapeutic anticoagulation. Preliminary evidence suggests that the stability of anticoagulation therapy may be improved by daily Vitamin K supplementation, but further studies are needed to find out whether this, or other dietary interventions, can improve anticoagulant control in routine clinical practice.

  • Vitamin K in parenteral nutrition.
    Gastroenterology, 2009
    Co-Authors: Martin J. Shearer
    Abstract:

    Vitamin K (as phylloquinone and menaquinones) is an essential cofactor for the conversion of peptide-bound glutamate to γ-carboxy glutamic acid (Gla) residues in a number of specialized Gla-containing proteins. The only unequivocal deficiency outcome is a bleeding syndrome caused by an inability to synthesize active coagulation factors II, VII, IX, and X, although there is growing evidence for roles for Vitamin K in bone and vascular health. An adult daily intaKe of about 100 μg of phylloquinone is recommended for the maintenance of hemostasis. Traditional coagulation tests for assessing Vitamin K status are nonspecific and insensitive. Better tests include measurements of circulating Vitamin K and inactive proteins such as undercarboxylated forms of factor II and osteocalcin to assess tissue and functional status, respectively. Common risK factors for Vitamin K deficiency in the hospitalized patient include inadequate dietary intaKes, malabsorption syndromes (especially owing to cholestatic liver disease), antibiotic therapy, and renal insufficiency. Pregnant women and their newborns present a special risK category because of poor placental transport and low concentrations of Vitamin K in breast milK. Since 2000, the Food and Drug Administration has mandated that adult parenteral preparations should provide a supplemental amount of 150 μg phylloquinone per day in addition to that present naturally, in variable amounts, in the lipid emulsion. Although this supplemental daily amount is probably beneficial in preventing Vitamin K deficiency, it may be excessive for patients taKing Vitamin K antagonists, such as warfarin, and jeopardize their anticoagulant control. Natural forms of Vitamin K have no proven toxicity.

  • Vitamin K and Vitamin K-dependent proteins.
    British journal of haematology, 2008
    Co-Authors: Martin J. Shearer
    Abstract:

    The more recent introduction of techniques to assess Vitamin K status is also leading to a deeper understanding of the nutritional and clinical role of Vitamin K. Progress has been particularly rapid in the last decade and is the purpose of this annotation to review the advances in different areas

  • Vitamin K Metabolism
    Sub-cellular biochemistry, 1998
    Co-Authors: Paul Newman, Martin J. Shearer
    Abstract:

    The discovery of Vitamin K can be largely attributed to the Danish scientist HenriK Dam, whose worK on sterol metabolism in chicKs required the feeding of carefully controlled diets, some of which were depleted in lipids (Dam, 1929). This often caused internal hemorrhages and other symptoms similar to scurvy, but which Dam showed to be incurable by large doses of Vitamin C. The finding of the lacK of influence of cod liver oil concentrates (as a source of Vitamins A and D), but the protective effect of cereals and seeds, prompted Dam to suggest that the bleeding syndrome was caused by a lacK of an essential dietary component that was different from Vitamins A, D, and C (Dam and Schoenheyder, 1934; Dam, 1934). Further worK by Dam with experimental diets showed the factor was fat soluble, heat stable and occurred in various animal and plant tissues, hog liver fat being one of the best sources. In 1935, after ruling out Vitamin E (hog liver fat was many times as active as wheat-germ oil), Dam proposed that the antihemorrhagic factor was a new fat-soluble Vitamin that he called “Koagulations Vitamin” or Vitamin K (Dam, 1935a,b). Other rich sources of Vitamin K were found to be green leaves such as alfalfa. Another surprisingly rich souce was bran or fishmeal which had become putrifled by the action of bacteria (Almquist and StoKstad, 1935; Almquist et al., 1938), suggesting that microbial action as well as plant biosynthesis is capable of producing the factor. Improvements in the assay method based on the restoration of normal clotting time in hemorrhagic chicKs led to the proposal that a lacK of Vitamin K caused a deficiency in prothrombin activity and that Vitamin K might be some Kind of coenzyme or prosthetic group required for active prothrombin (Schoenheyder, 1936). However, subsequent worK showed that prothrombin precipitates were active after all lipids had been removed and that Vitamin K concentrates could not induce blood to clot (Dam et al., 1936).

Darrel W. Stafford - One of the best experts on this subject based on the ideXlab platform.

  • A hetero-dimer model for concerted action of Vitamin K carboxylase and Vitamin K reductase in Vitamin K cycle.
    Journal of theoretical biology, 2011
    Co-Authors: Shubin Liu, Darrel W. Stafford, Charles H. Davis, John Kulman, Lee G. Pedersen
    Abstract:

    a b s t r a c t Vitamin K carboxylase (VKC) is believed to convert Vitamin K, in the Vitamin K cycle, to an alKoxide- epoxide form which then reacts with CO2 and glutamate to generate g-carboxyglutamic acid (Gla). Subsequently, Vitamin K epoxide reductase (VKOR) is thought to convert the alKoxide-epoxide to a hydroquinone form. By recycling Vitamin K, the two integral-membrane proteins, VKC and VKOR, maintain Vitamin K levels and sustain the blood coagulation cascade. Unfortunately, NMR or X-ray crystal structures of the two proteins have not been characterized. Thus, our understanding of the Vitamin K cycle is only partial at the molecular level. In this study, based on prior biochemical experiments on VKC and VKOR, we propose a hetero-dimeric form of VKC and VKOR that may explain the efficient oxidation and reduction of Vitamin K during the Vitamin K cycle. & 2011 Published by Elsevier Ltd.

  • The conversion of Vitamin K epoxide to Vitamin K quinone and Vitamin K quinone to Vitamin K hydroquinone uses the same active site cysteines.
    Biochemistry, 2007
    Co-Authors: Da Yun Jin, Jian Ke Tie, Darrel W. Stafford
    Abstract:

    Vitamin K epoxide (or oxido) reductase (VKOR) is the target of warfarin and provides Vitamin K hydroquinone for the carboxylation of select glutamic acid residues of the Vitamin K-dependent proteins which are important for coagulation, signaling, and bone metabolism. It has been Known for at least 20 years that cysteines are required for VKOR function. To investigate their importance, we mutated each of the seven cysteines in VKOR. In addition, we made VKOR with both C43 and C51 mutated to alanine (C43A/C51A), as well as a VKOR with residues C43−C51 deleted. Each mutated enzyme was purified and characterized. We report here that C132 and C135 of the CXXC motif are essential for both the conversion of Vitamin K epoxide to Vitamin K and the conversion of Vitamin K to Vitamin K hydroquinone. Surprisingly, conserved cysteines, 43 and 51, appear not to be important for either reaction. For the in vitro reaction driven by dithiothreitol, the 43−51 deletion mutation retained 85% and C43A/C51A 112% of the wild-ty...

  • Purified Vitamin K epoxide reductase alone is sufficient for conversion of Vitamin K epoxide to Vitamin K and Vitamin K to Vitamin KH2.
    Proceedings of the National Academy of Sciences of the United States of America, 2006
    Co-Authors: Teng-yi Huang, Jason Williams, Darrel W. Stafford
    Abstract:

    More than 21 million prescriptions for warfarin are written yearly in the U.S. Despite its importance, warfarin's target, Vitamin K epoxide reductase (VKOR), has resisted purification since its identification in 1972. Here, we report its purification and reconstitution. HPC4, a calcium-specific antibody that recognizes a 12-aa tag, was used to purify and identify VKOR. Partial reconstitution is achieved on the column by washing with 0.4% dioleoylphosphatidylcholine/0.4% deoxycholate. Activity is completely recovered by dialysis against a buffer containing a reducing agent but lacKing dioleoylphosphatidylcholine/deoxycholate. Removal of detergent from the eluted proteins apparently facilitates liposome formation. Purified recombinant VKOR with tag is ≈21 KDa, as expected; fully active; and >93% pure. The concentration of warfarin for 50% inhibition is the same for purified protein and microsomes. It has been reported that VKOR is a multisubunit enzyme. Our results, however, suggest that a single peptide can accomplish both the conversion of Vitamin K epoxide to Vitamin K and Vitamin K to reduced Vitamin K. This purification will allow further characterization of VKOR in relation to other components of the Vitamin K cycle and should facilitate its structural determination.

  • Purification of a Single Peptide with Vitamin K Epoxide to Vitamin K and Vitamin K to Vitamin KH2 Activity.
    Blood, 2006
    Co-Authors: Pei Hsuan Chu, Teng-yi Huang, Jason Williams, Darrel W. Stafford
    Abstract:

    More than 21 million prescriptions for warfarin are written yearly in the US. Yet, in spite of its importance, Vitamin K epoxide reductase (VKOR), the target of warfarin, has resisted purification since its identification in 1972. We report the first successful purification and reconstitution of activity of a recombinant human Vitamin K epoxide reductase. A series of detergents were screened to determine that best for solubilization of VKOR from microsomes. Detergents tested that were effective in solubilization of VKOR also led to loss of measurable activity. This loss of activity supports our previous prediction that VKOR is embedded in and requires a membrane environment for enzymatic activity. The short-chain phospholipid, DHPC (1,2-Dihexanoyl-sn-Glycero-3-Phosphocholine) was the detergent of choice to efficiently extract VKOR from the microsomes, even though this reagent completely inhibited enzyme activity. Partial reconstitution was achieved on-column by washing with 0.4 % dioleoylphosphatidylcholine/0.4% deoxycholate. Complete recovery of activity was achieved by removing the deoxycholate through dialysis in the presence of the reducing reagent, THP (Tris(hydroxypropyl)phosphine). During dialysis, the solution became cloudy indicating the formation of membrane-liKe structure. Purified recombinant VKOR is ~21 KDa (~18.5 KDa + tag); fully active; and over 93% pure. The concentration of warfarin for 50% inhibition is the same for purified protein and microsomes. It has been reported and assumed that VKOR is a multi-subunit enzyme. Our results, however, suggest that a single peptide can accomplish the reaction. The trace amounts of contaminating proteins were identified by mass spectrometry; however, none are apparently relevant to the VKOR reaction. Moreover, the turn-over number of purified VKOR (0.25 sec-1 is approximately two-fold higher than microsomes and about 10 fold higher than the turnover number of gamma-glutamyl carboxylase for CO2 addition. In addition to the Vitamin K epoxide to Vitamin K reaction, our results also indicate that VKOR can efficiently convert Vitamin K to Vitamin K epoxide. Our results suggest that ancillary proteins (other than a thioredoxin-liKe enzyme) are not necessary for full VKOR activity. This purification will allow further characterization of VKOR in relation to other components of the Vitamin K cycle and should facilitate its structural determination.

  • The Vitamin K cycle
    Journal of thrombosis and haemostasis : JTH, 2005
    Co-Authors: Darrel W. Stafford
    Abstract:

    Summary.  Post-translational modification of glutamate to gamma carboxyl glutamate is required for the activity of Vitamin K-dependent proteins. Carboxylation is accomplished by the enzyme gamma glutamyl carboxylase (GGCX) which requires the propeptide-containing substrate and three co-substrates: reduced Vitamin K, CO2, and O2. Most propeptides bind tightly to GGCX and all of the Glu residues that will be modified are modified during one binding event. Complete carboxylation is thus dependent upon the rate of carboxylation and the dissociation rate constant of the substrate from the GGCX enzyme. If the propeptide is released before carboxylation is complete, partially carboxylated Vitamin K-dependent proteins are produced. The rate of carboxylation is mainly controlled by the level of reduced Vitamin K available for the reactions while the dissociation rate constant is dependent upon both the propeptide and the Gla domain of the substrate. In addition, there are allosteric effects that increase the rate of dissociation of the fully carboxylated substrates. Carboxylation requires the abstraction of a proton from the 4-carbon of glutamate by reduced Vitamin K and results in the conversion of Vitamin K to Vitamin K epoxide. The Vitamin K epoxide must be recycled to Vitamin K before it can be reused, a reaction catalyzed by the enzyme Vitamin K epoxide reductase (VKOR). The gene for VKOR has recently been identified but the enzyme itself has not been purified to homogeneity. It appears, however, that most of the variability observed in patients response to warfarin may be attributed to variability in the VKOR gene.

Heather J. Ipema - One of the best experts on this subject based on the ideXlab platform.

  • Use of Oral Vitamin K for Prevention of Late Vitamin K Deficiency Bleeding in Neonates When Injectable Vitamin K is Not Available
    The Annals of pharmacotherapy, 2012
    Co-Authors: Heather J. Ipema
    Abstract:

    OBJECTIVE:To evaluate the literature describing use of oral Vitamin K1 (phytonadione) to prevent late Vitamin K deficiency bleeding (VKDB) in neonates when injectable Vitamin K preparations are not available.DATA SOURCES:Articles were retrieved through MEDLINE (1946–February 2012) using the terms Vitamin K, Vitamin K deficiency bleeding, newborn, neonate, and prophylaxis. Reference citations from publications identified were reviewed.STUDY SELECTION AND DATA EXTRACTION:All articles published in English on the use of prophylactic oral Vitamin K in neonates were evaluated. The largest epidemiologic studies discussing the efficacy of continuous oral Vitamin K prophylaxis were reviewed. Individual, smaller clinical trials were not reviewed.DATA SYNTHESIS:For prevention of early, classic, and late VKDB, use of intramuscular Vitamin K 1 mg is preferred over oral administration because of superior efficacy. Single oral doses protect against early VKDB, but multiple oral doses are needed for late VKDB prophylaxis...

Sarah L. Booth - One of the best experts on this subject based on the ideXlab platform.

  • The Contribution of Lipids to the Interindividual Response of Vitamin K BiomarKers to Vitamin K Supplementation.
    Molecular nutrition & food research, 2019
    Co-Authors: Jennifer M. Kelly, Jose M. Ordovas, Gregory Matuszek, Caren E. Smith, Gordon S. Huggins, Hassan S. Dashti, Reiko Ichikawa, Sarah L. Booth
    Abstract:

    SCOPE: A better understanding of factors contributing to interindividual variability in biomarKers of Vitamin K can enhance the understanding of the equivocal role of Vitamin K in cardiovascular disease. Based on the Known biology of phylloquinone, the major form of Vitamin K, it is hypothesized that plasma lipids contribute to the variable response of biomarKers of Vitamin K metabolism to phylloquinone supplementation. METHODS AND RESULTS: The association of plasma lipids and 27 lipid‐related genetic variants with the response of biomarKers of Vitamin K metabolism is examined in a secondary analysis of data from a 3‐year phylloquinone supplementation trial in men (n = 66) and women (n = 85). Year 3 plasma triglycerides (TG), but not total cholesterol, LDL‐cholesterol, or HDL‐cholesterol, are associated with the plasma phylloquinone response (men: β = 1.01, p < 0.001, R² = 0.34; women: β = 0.61, p = 0.008, R² = 0.11; sex interaction p = 0.077). Four variants and the TG‐weighted genetic risK score are associated with the plasma phylloquinone response in men only. Plasma lipids are not associated with changes in biomarKers of Vitamin K function (undercarboxylated osteocalcin and matrix gla protein) in either sex. CONCLUSION: Plasma TG are an important determinant of the interindividual response of plasma phylloquinone to phylloquinone supplementation, but changes in biomarKers of Vitamin K carboxylation are not influenced by lipids.

  • age group and sex do not influence responses of Vitamin K biomarKers to changes in dietary Vitamin K
    Journal of Nutrition, 2012
    Co-Authors: Jennifer T Truong, Ala Al Rajabi, Xueyan Fu, Edward Saltzman, Gerard E Dallal, Caren M Gundberg, Sarah L. Booth
    Abstract:

    Inadequate Vitamin K intaKe has been associated with abnormal soft tissue calcification. Older adults may have insufficient intaKes of Vitamin K and respond less to Vitamin K supplementation compared with younger adults. However, little is Known about the determinants that influence the response to Vitamin K supplementation. Our primary objective was to assess dietary and nondietary determinants of Vitamin K status in healthy younger and older adults. In a nonrandomized, nonmasKed study, 21 younger (18–40 y) and 21 older (55–80 y) men and women consumed a baseline diet (200 μg phylloquinone/d) for 5 d, a phylloquinone-restricted diet (10 μg phylloquinone/d) for 28 d, and a phylloquinone-supplemented diet (500 μg phylloquinone/d) for 28 d. Changes in Vitamin K status marKers in response to Vitamin K depletion and repletion were studied and the influences of BMI, body fat, and circulating TG were assessed by including them as covariates in the model. Despite baseline differences in measures of Vitamin K status, plasma phylloquinone tended to increase (P = 0.07) and the percentage of uncarboxylated osteocalcin and uncarboxylated prothrombin both improved with phylloquinone supplementation (P < 0.007), regardless of age group or sex. Only the excretion of urinary menadione, a Vitamin K metabolite, was greater among younger adults in response to depletion than in older adults (P = 0.012), regardless of sex. Adiposity measures and circulating TG did not predict response of any measures. In conclusion, poor Vitamin K status can be similarly improved with Vitamin K supplementation, regardless of age group or sex.

  • Vitamin K intaKe and atherosclerosis
    Current opinion in lipidology, 2008
    Co-Authors: Arja T. Erkkilä, Sarah L. Booth
    Abstract:

    Purpose of reviewIt has been hypothesized that insufficient intaKe of Vitamin K may increase soft-tissue calcification owing to impaired γ-carboxylation of the Vitamin K-dependent protein matrix γ-carboxyglutamic acid. The evidence to support this putative role of Vitamin K intaKe in atherosclerosis

  • Determinants of Vitamin K status in humans.
    Vitamins and hormones, 2008
    Co-Authors: Sarah L. Booth, Ala Al Rajabi
    Abstract:

    To understand the role of Vitamin K in human health, it is important to identify determinants of Vitamin K status throughout the life cycle. Our current understanding of Vitamin K physiology and metabolism only partially explains why there is wide interindividual variation in Vitamin K status, as measured by various biochemical measures. Dietary intaKe of Vitamin K is one of the primary determinants of Vitamin K status, and intaKes vary widely among age groups and population subgroups. How dietary sources of Vitamin K are absorbed and transported varies with the form and food source of Vitamin K. LiKewise, the role of plasma lipids as a determinant of Vitamin K status varies with the form of Vitamin K ingested. There is also some evidence that other fat-soluble Vitamins antagonize Vitamin K under certain physiological conditions. Infants are at the greatest risK of Vitamin K deficiency because of a poor maternal-fetal transfer across the placenta and low Vitamin K concentrations in breast milK. During adulthood, there may be subtle age-related changes in Vitamin K status but these are inconsistent and may be primarily related to dietary intaKe and lifestyle differences among different age groups. However, there is some suggestion that absence of estrogen among postmenopausal women may be a determinant of Vitamin K, status. Genetics may explain some of the observed interindividual variability in Vitamin K, but to date, there are few studies that have systematically explored the associations between individual genetic polymorphisms and biochemical measures of Vitamin K status.

  • Vitamin K status in the elderly.
    Current opinion in clinical nutrition and metabolic care, 2007
    Co-Authors: Sarah L. Booth
    Abstract:

    Purpose of review Poor Vitamin K nutrition has recently been linKed to several chronic diseases associated with abnormal calcification, which affect many elderly. To understand the impact of Vitamin K nutrition on healthy aging it is necessary to assess both the determinants and the adequacy of Vitamin K nutritional status of the elderly. Recent findings Overall, elderly persons consume more Vitamin K than young adults. However, a subgroup of the elderly population does not meet the current recommended dietary intaKes for this nutrient. The first meta-analysis evaluating the data on the role of Vitamin K and bone health concluded that increased intaKes of Vitamin K are warranted to reduce bone loss and fracture risK among the elderly. Recent studies suggest that nondietary determinants of Vitamin K status need to be factored into any discussion on the adequacy of nutritional status of the elderly. One promising area of research is the interrelationship between estrogen and Vitamin K. Summary Evidence is emerging to support recommendations to increase intaKes of Vitamin K among the elderly to reduce bone loss and fracture risK. Much more research is required, however, to identify nondietary determinants of Vitamin K status, and their impact on the elderly.

Michael V Holmes - One of the best experts on this subject based on the ideXlab platform.

  • the role of dietary Vitamin K in the management of oral Vitamin K antagonists
    Blood Reviews, 2012
    Co-Authors: Michael V Holmes, Beverley J. Hunt, Martin J. Shearer
    Abstract:

    Vitamin K antagonists (VKA) have been the mainstay of oral anticoagulant therapy for over 60years. In this review we critically assess the evidence for the importance of Vitamin K nutrition during VKA therapy; the methodologies for measuring dietary intaKes; the Vitamin K intaKe data in patients on VKA and healthy people; and the experimental evidence for the influence of Vitamin K intaKes and biochemical measures of Vitamin K status on VKA response. Several studies show that dietary intaKes of phylloquinone (Vitamin K1) are associated to the sensitivity and stability of anticoagulation during initiation and maintenance dosing with low habitual intaKes associated with greater instability of the INR and risK of sub-therapeutic anticoagulation. Preliminary evidence suggests that the stability of anticoagulation therapy may be improved by daily Vitamin K supplementation, but further studies are needed to find out whether this, or other dietary interventions, can improve anticoagulant control in routine clinical practice.