This matters profoundly, notes Clarisse Geraci, Global Health Marketing Manager at Gnosis by Lesaffre.
Researchers using the Rotterdam Study cohort found that more than 82% of older adults had detectable CAC.
A CAC score of 0 signifies healthy vascular ageing, whereas a score of 1000-plus indicates an unhealthy coronary ageing phenotype with a markedly elevated cardiovascular, non-cardiovascular and all-cause mortality risk.¹
Directing it to bones and away from arteries, vitamin K2 as menaquinone-7 activates proteins that regulate calcium.
Previous preclinical and clinical studies have demonstrated that the inhibition of the vitamin K cycle by vitamin K antagonists accelerates the formation of uncarboxylated MGP (ucMGP), leading to extensive arterial calcification.
Based on the collective results of this research, the new trial aimed to determine whether long-term supplementation with vitamin K2 can slow the rate of CAC progression.
Research recognised by JAMA Cardiology
Published in JAMA Cardiology, the “VitaK-CAC” trial has garnered significant attention; 30 days after publication, the study has been viewed more than 20,000 times.
This 2-year, randomised, placebo-controlled trial involved 180 symptomatic patients with CAC scores ranging from 50 to 400 Agatston units (AU).
Participants received either 360 µg of vitamin K2 (as MenaQ7®) or a placebo daily.
To quantify vitamin K2’s effect on the calcification process, CT scans were used to measure changes in calcium score and mass at 12 and 24 months and the incidence of new calcifications, while blood tests assessed vitamin K status.
Distinctive outcomes
In the placebo group, the median CAC score increased from 145 AU at baseline to 173 AU after 1 year and to 214 AU after 24 months.
In the vitamin K2 group, values were 135, 150 and 184 AU, respectively. The evolution of the CAC score with time was significantly slower in the active treatment group than in the placebo cohort.
The total AU differential was 49 for the vitamin K2 group and 69 for the placebo group.
Calcium mass score analysis showed comparable results. In the placebo group, calcium mass increased from a median baseline of 26 to 33 mg after the first year and to 38 mg after the second year.
The vitamin K2 group measurements were 25, 28 and 32 mg, respectively. The total difference was 12 mg for the placebo after 2 years and 7 mg for the vitamin K2 group — approximately 42% less progression in calcium mass versus placebo.
The authors stated they were “confident that [vitamin K2] can slow coronary calcification” based on the Agatston and the calcium mass scores.
Further, after 2 years, increases in CAC score correlated with the number of non-calcified plaques that partially calcified, suggesting that vitamin K2 slows calcification in developing plaques but does not affect already calcified plaques.
Although the new data support the hypothesis that long-term supplementation with vitamin K2 (in this case, 2 years) slows down the process of CAC in symptomatic CAD, this effect is deemed modest.
Notably, plasma levels of vitamin K1 remained unchanged throughout the study.
The VitaK-CAC trial is another indelible step following previous breakthrough research, such as the 3-year trial when healthy postmenopausal women supplementing with 180 µg of vitamin K2 (as MenaQ7) daily experienced improved arterial stiffness (dp-ucMGP was reduced by 50% compared with a placebo).²
More trials are planned to confirm the results of vitamin K2 supplementation in CAC.
