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Vitamin K supplements failed to improve BMD in postmenopausal osteopenia
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Women with osteopenia after menopause demonstrating low vitamin K1 concentrations did not improve bone mineral density with long-term vitamin K1 supplements for the deficiency, according to research presented at the American Society for Bone and Mineral Research 2014 Annual Meeting.
“Overall, vitamin K1 supplementation does not reduce bone loss in postmenopausal women with low bone mass, even among those who have low levels of serum vitamin K1,” Maryam S. Hamidi, PhD, of the University Health Network in Toronto, told Endocrine Today.
Hamidi, along with Angela M. Cheung, MD, PhD, also of the University Health Network, and colleagues analyzed data from 159 women in their postmenopausal years with baseline fasting serum vitamin K1 concentrations ≤1 nmol/L; patients were from the ECKO trial.
The mean age of the patients (94% white, 19% apolipoprotein E4 carriers) was 59 ± 7 years and mean BMI was 25.6 ± 4.2 kg/m2. At baseline, median serum vitamin K1 concentration was 0.6 nmol/L (interquartile range, 0-0.8), and 31% of women had concentrations of zero.
The women received either 5 mg vitamin K1 (n=80) or placebo (n=79) once daily. The researchers advised the women to maintain a total daily intake of 1,500 mg calcium and 800 IU vitamin D throughout the trial.
BMD changes were evaluated at 2 years in four sites: lumbar spine, femoral neck, total hip and ultradistal radius. Changes in bone turnover were assessed based on 2-year change in osteocalcin, C-terminal telopeptide and percentage of undercarboxylated osteocalcin. Two-sample t tests were used to determine all outcomes.
At 24 months, median serum vitamin K1 with treatment was 17.4 nmol/L (interquartile range, 9-27.9) vs. 1 nmol/L (interquartile range, 0.5-1.8) with placebo. A significant decrease was seen in serum levels of total osteocalcin and percentage of undercarboxylated osteocalcin with treatment vs. placebo.
“This is exactly what we would expect with vitamin K supplementation,” Hamidi said.
No significant differences were seen between groups for any of the BMD outcomes or for C-terminal telopeptide.
“We do not recommend the use of vitamin K1 supplementation for prevention of bone loss in postmenopausal women who have low bone mass,” Hamidi said. “However, healthy diets that include green plant foods, which are good sources of vitamin K1, may be beneficial for bone health.” — by Allegra Tiver
For more information:
Hamidi M. Abstract #1078. Presented at: ASBMR 2014 Annual Meeting; Sept. 12-15, 2014; Houston.
Disclosure: Hamidi reports no relevant financial disclosures.
Perspective
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Nelson Watts, MD, FACP, MACE, CC
The first challenge of any study where we’re talking about a nutrient is to define what is enough, what is not enough and how we can see who is deficient. With vitamin K, I’m not sure anybody really has a good idea about that.
The standard way we define “normal” doesn’t work when it comes to nutrients and vitamins. If you look back to laboratory reports from 15 years ago, you see the “normal” range for cholesterol listed as 200 to 300; we know now the desirable range is less than 200. So, I don’t know what a desirable range is for vitamin K.
The second challenge, if you could define a level that is too low, is to define the consequences of being too low in order to design a study to see whether or not correcting the deficiency would have beneficial effects.
There are certainly hypothetical reasons to think that vitamin K would be important in bone health. Most of protein in the bone matrix is collagen, but of the 10% or so that is not collagen, osteocalcin is the most plentiful. Vitamin K seems to be essential for modification of osteocalcin and, at least in part, related to the size and orientation of the crystals of mineral within the bone surface.
For a study design, we would need to recruit only people who are deficient and give them a sufficient amount of vitamin K to correct the problem. Since we don’t know what a deficient level and we don’t know what an adequate level is, I can’t really judge whether or not this study tells us anything useful.
A bigger question goes back to vitamin D; if you polled people at meetings, everybody would agree it is an important substance for bone health, but there is still disagreement among experts as to what an adequate level is from a public health point of view. A recent Institute of Medicine Report suggests a blood level of 20 ng/mL would be sufficient, whereas the bone community believes a level of 30 ng/mL would be a minimum desirable level.
Then there’s a problem with the laboratory measurements of vitamin D because almost everything we do in medicine is not going to work out like balancing a checkbook, where you get exactly the same number that someone else had. The variability among vitamin D measurements, particularly from one lab to another, can be extreme. That complicates the issue further, and it’s the same situation with vitamin K.
All the placebo-controlled trials with vitamin D have enrolled many subjects who were already adequate and therefore could not benefit from supplementation. A null result doesn’t tell you that vitamin D isn’t helpful in people who are deficient; it simply tells you that if you go out in unselected population, you can’t see a measurable benefit.
On the vitamin K issue, the question is still open. But before looking for another intervention trial, research is needed to try to better define what would be an optimal level of vitamin K, how we would define vitamin K deficiency and what the potential consequences of vitamin K deficiency might be. Then, a replacement trial can be done in subjects who are deficient in vitamin K to look for the proof that fixing it corrects the deficiency.
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