Vitamin K status, supplementation and vascular disease: a systematic review and meta-analysis

Lees, Jennifer S; Fa, Chapman; Witham, Miles D.; Jardine, Alan G.; Mark, Patrick B.

doi:10.1136/heartjnl-2018-313955

Cited by 56 publications

(72 citation statements)

References 50 publications

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“…The ratio of fully carboxylated to undercarboxylated osteocalcin in serum (OR) reflects the vitamin K status. 8 A low OR in healthy people indicates a subclinical vitamin K deficiency, which is common in Western societies. 9 Very low ORs have been associated with osteoporotic fractures.…”

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confidence: 99%

Increased serum osteocalcin levels and vitamin K status by daily cheese intake

Lundberg¹,

Holand

Holo

et al. 2020

Int J Clin Trials

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Background: Cheese is a major source of long-chained vitamin K2 variants. How intake of vitamin K2 rich cheese affects vitamin K and osteocalcin has not been studied. The aim was to establish a maximum efficacy dose (MED) after daily intake of vitamin K2-rich cheese (Jarlsberg®) based on increase in ratio between carboxylated and undercarboxylated osteocalcin during a five-week diet.Methods: 20 healthy healthy volunteers (HV) were recruited. The daily intake of Jarlsberg® cheese in the study varied from 20 to 152 g. Clinical investigation was performed initially and after three, four and five weeks with measurement of vital signs, hematological and biochemical variables, carboxylated and undercarboxylated osteocalcin and vitamin K. The ratio OR= carboxylated/undercarboxylated osteocalcin was the main variable.Results: The MED decreased with treatment duration and was estimated to 57 g/day (95% CI: 47-67) after five weeks diet, resulting in a mean OR increase of 30% (95% CI: 23.8-36.8). Both OR and serum osteocalcin followed a quadratic dose response curve. For osteocalcin, a maximal increase of 46% was estimated at 59 g/day for five weeks. The serum content of long-chained vitamin K2 increased significantly with increasing cheese dose. The increase were mainly obtained the first three weeks and kept unchanged the following two weeks. The cheese doses close to the MED caused nearly significant reductions in total cholesterol, LDL-cholesterol, the LDL/HDL ratio and significant reduction in the blood pressures after five weeks diet (p≤0.05).Conclusions: MED of Jarlsberg® cheese was estimated to 57 g/day. Daily intake of Jarlsberg® cheese increased the osteocalcin level, vitamin K2 and positively affected the lipid patterns and blood pressure.

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confidence: 99%

Increased serum osteocalcin levels and vitamin K status by daily cheese intake

Lundberg¹,

Holand

Holo

et al. 2020

Int J Clin Trials

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“…The biological rationale for a role of this vitamin lies in its ability to activate MGP, which is a potent inhibitor of ectopic calcification. Although the meta-analysis by Lees and coworkers illustrates that there is still a considerable gap in our knowledge [19], the results of controlled trials look promising. Whether high doses of phylloquinone or of one of the menaquinones or both will be best still needs to be explored.…”

Section: Discussionmentioning

confidence: 99%

“…Although MK-7 supplements may improve arterial stiffness [74], data from various trials are not consistent. Recently, Lees and coworkers performed a meta-analysis of clinical trials that assessed the effect of vitamin K (1 or 2) supplementation on vascular function and found that compared to control measures, vitamin K supplementation significantly reduced the progression of vascular calcification [19]. However, this conclusion was based on only three trials, two of which evaluated vitamin K1 and only one vitamin K2.…”

Section: Vitamin K Supplementationmentioning

confidence: 99%

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Pharmacological and Nutritional Modulation of Vascular Calcification

et al. 2019

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Vascular calcification is an independent predictor of cardiovascular disease, and therefore, inhibition or regression of this processes is of clinical importance. The standard care regarding prevention and treatment of cardiovascular disease at this moment mainly depends on drug therapy. In animal and preclinical studies, various forms of cardiovascular drug therapy seem to have a positive effect on vascular calcification. In particular, calcium channel blockers and inhibitors of the renin–angiotensin–aldosteron system slowed down arterial calcification in experimental animals. In humans, the results of trials with these drugs are far less pronounced and often contradictory. There is limited evidence that the development of new atherosclerotic lesions may be retarded in patients with coronary artery disease, but existing lesions can hardly be influenced. Although statin therapy has a proven role in the prevention and treatment of cardiovascular morbidity and mortality, it is associated with both regression and acceleration of the vascular calcification process. Recently, nutritional supplements have been recognized as a potential tool to reduce calcification. This is particularly true for vitamin K, which acts as an inhibitor of vascular calcification. In addition to vitamin K, other dietary supplements may also modulate vascular function. In this narrative review, we discuss the current state of knowledge regarding the pharmacological and nutritional possibilities to prevent the development and progression of vascular calcification.

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“…Moreover, in longitudinal studies, dp-ucMGP was found to be an independent predictor of CV morbidity and mortality. The authors suggested that larger, controlled trials should test the effect of vitamin K intake -through carboxylation of dp-ucMGP-on VC and CVD in uremic patients (69). The design and results of the intervention studies that assessed the effects of vitamin K supplementation on MGP forms and various endpoints are summarized in Table 1.…”

Section: Vitamin K: the Essential Co-factor Of Mgpmentioning

confidence: 99%

Vascular Calcification in Chronic Kidney Disease: The Role of Vitamin K- Dependent Matrix Gla Protein

et al. 2020

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Arterial calcification is highly prevalent in chronic kidney disease (CKD) patients and is associated with cardiovascular (CV) morbidity and mortality. Patients at early CKD stages are more likely to suffer a fatal CV event than to develop end-stage renal disease and require hemodialysis treatment. The heavy CV burden of these patients cannot be solely explained by traditional calcification risk factors. Moreover, the pathophysiologic mechanisms underlying this association are complex and yet not fully understood. Although vascular calcification was regarded as a passive degenerative process for over a century, this theory changed by recent evidence that pointed toward an active process, where calcification promoters and inhibitors were involved. Matrix Gla Protein (MGP) has been established as a strong inhibitor of calcification both in vitro and in vivo. Not only it prevents mineralization of the arterial wall, but it is the only factor that can actually reverse it. To become fully active, MGP must undergo carboxylation of specific protein bound glutamate residues, a process fully dependent on the availability of vitamin K. Low vitamin K status leads to inactive, uncarboxylated forms of MGP and has been repeatedly associated with accelerated vascular calcification. Aim of this review is to present the pathophysiologic mechanisms underlying the activation and function of MGP and review the existing, accumulating data regarding the association between vitamin K, MGP and vascular calcification/CV disease in CKD patients.

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Vitamin K status, supplementation and vascular disease: a systematic review and meta-analysis

Cited by 56 publications

References 50 publications

Increased serum osteocalcin levels and vitamin K status by daily cheese intake

Increased serum osteocalcin levels and vitamin K status by daily cheese intake

Pharmacological and Nutritional Modulation of Vascular Calcification

Vascular Calcification in Chronic Kidney Disease: The Role of Vitamin K- Dependent Matrix Gla Protein

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