We attempted to investigate whether vitamin K2 (menatetrenone)
treatment effectively prevents the incidence of new fractures in
osteoporosis. A total of 241 osteoporotic patients were enrolled in a
24-month randomized open label study. The control group (without
treatment; n = 121) and the vitamin K2-treated group (n = 120), which
received 45 mg/day orally vitamin K2, were followed for lumbar bone
mineral density (LBMD; measured by dual-energy X-ray absorptiometry
[DXA]) and occurrence of new clinical fractures. Serum level of
Glu-osteocalcin (Glu-OC) and menaquinone-4 levels were measured at the
end of the follow-up period. Serum level of OC and urinary excretion of
deoxypyridinoline (DPD) were measured before and after the treatment.
The background data of these two groups were identical. The incidence
of clinical fractures during the 2 years of treatment in the control
was higher than the vitamin K2-treated group (chi2 = 10.935; p =
0.0273). The percentages of change from the initial value of LBMD at 6,
12, and 24 months after the initiation of the study were -1.8 +/- 0.6%,
-2.4 +/- 0.7%, and -3.3 +/- 0.8% for the control group, and 1.4 +/-
0.7%, -0.1 +/- 0.6%, and -0.5 +/- 1.0% for the vitamin K2-treated
group, respectively. The changes in LBMD at each time point were
significantly different between the control and the treated group (p =
0.0010 for 6 months, p = 0.0153 for 12 months, and p = 0.0339 for 24
months). The serum levels of Glu-OC at the end of the observation
period in the control and the treated group were 3.0 +/- 0.3 ng/ml and
1.6 +/- 0.1 ng/ml, respectively (p < 0.0001), while the serum level
of OC measured by the conventional radioimmunoassay (RIA) showed a
significant rise (42.4 +/-6.9% from the basal value) in the treated
group at 24 months (18.2 +/- 6.1% for the controls;p = 0.0081). There
was no significant change in urinary DPD excretion in the treated
group. These findings suggest that vitamin K2 treatment effectively
prevents the occurrence of new fractures, although the vitamin
K2-treated group failed to increase in LBMD. Furthermore, vitamin K2
treatment enhances gamma-carboxylation of the OC molecule.
Effect of menatetrenone on bone mineral density and
incidence of vertebral fractures in postmenopausal women with
osteoporosis: a comparison with the effect of etidronate.
J Orthop Sci 2001; 6(6): 487-92.
Iwamoto J, Takeda T, Ichimura S.
The purpose of the present study was to compare the effects of
etidronate and menatetrenone on bone mineral density (BMD) and the
incidence of vertebral fractures in postmenopausal women with
osteoporosis. Seventy-two osteoporotic women, more than 5 years after
menopause, 53-78 years of age, were randomly divided into three
administration groups: E group; intermittent cyclical etidronate (200
mg/day, 14 days per 3 months; n = 25); M group; menatetrenone (45
mg/day, daily; n = 23); and C group (control); calcium lactate (2
g/day, daily; n = 24). Forearm BMD was measured by dual-energy X-ray
absorptiometry at 0, 6, 12, 18, and 24 months after the treatment
started. There were no significant differences in age, body mass index,
years since menopause, and initial BMD among the three groups. One-way
analysis of variance (ANOVA) with repeated measurements showed a
significant decrease in BMD in the C group (P < 0.0001). Two-way
ANOVA with repeated measurements showed a significant increase in BMD
in the M group compared with that in the C group (P < 0.0001), and a
significant increase in BMD in the E group compared with that in the C
and M groups (P < 0.0001 and P < 0.01, respectively). The indices
of new vertebral fractures/1000 patient-years in the E and M groups
were significantly higher than that in the C group (chi(2) = 47.7; P
< 0.0001 and chi(2) = 42.4; P < 0.0001, respectively), and did
not differ significantly between the E and M groups. The present
preliminary study provides evidence to suggest that, despite the lower
increase in BMD produced by menatetrenone, this agent, as well as
etidronate, may have the potential to reduce osteoporotic vertebral
fractures in postmenopausal women with osteoporosis.
SUPPLEMENT FACTS:
Serving Size: 1 Capsule
%DRI
Menatetrenone (MK-4) 15mg (12500%)
*Dietary Reference Intake not established.
Other ingredients: microcrystalline cellulose. Capsule: hypromellose, sorbitol, silicon dioxide, water.
AOR guarantees that no ingredients not listed on
the label have been added to the product. Contains no wheat, gluten,
corn, nuts, dairy, soy, eggs, fish or shellfish.
Suggested Use
Take one to three capsules daily with fat-containing meals, or as directed by a qualified health consultant.
Main Applications
As reported by literature:
• Bone health
• Brain health
• Cardiovascular function
Source
Solanesol (from Nicotiana tabacum).
Pregnancy / Nursing
Do not use.
Cautions
• Clinical trials have documented that
menatetrenone does not induce hemostatic activation. However, it will
interfere with the activity warfarin (Coumadin®) and possibly other
anticoagulant ("blood thinning") medications. Patients prescribed
anticoagulants must not take this supplement.
• STORE IN A COOL DARK PLACE. HARMLESS CLUMPING MAY OCCUR AT TEMPERATURES EXCEEDING 35C
*These statements have not been evaluated by the FDA. If in doubt consult with a licensed naturopathic physician before use. Physician’s at Genesis Health Systems can be reached at 480.284.8155 and we are happy to consult with you about this product and helping you achieve optimal health.
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