Menatetrenone effectively maintains health in bones and the vascular system.

PRODUCT = Peak K2 from AOR:  90 Vegi-caps               

Each Capsule Contains

Vitamin K2 (as Menatetrenone)      15 mg     

Other Ingredients

Microcrystalline cellulose  Capsule: Vegetarian

Product does not contain any peanuts, tree nuts, soy, corn, dairy, shellfish, eggs, yeast, gluten, or artificial sweeteners.

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

Biofermentation

Pregnancy / Nursing

Do not use.

Cautions

�Persons taking anticoagulant (�blood thinning�) medications such as warfarin (Coumadin^®) must not take this supplement.

�STORE IN A COOL DARK PLACE. HARMLESS CLUMPING MAY OCCUR AT TEMPERATURES EXCEEDING 35^OC.

Menatetrenone

Vitamin K is an essential nutrient, best known for its role in blood clotting. Plants make one form of vitamin K (phylloquinone, or vitamin K1) for their use. But your body doesn�t use all of the K1 in your diet �as is.� Instead, the body converts some of this plant form of the vitamin into a different vitamin K molecule: Menatetrenone, or MK-4, a form of vitamin K2. Tissues vary in their vitamin K needs, and it�s become clear that some tissues have a specific need for Menatetrenone, which is not met by phylloquinone. For some purposes (like blood clotting), phylloquinone works fine; but extensive evidence shows that Menatetrenone has unique effects on bone health not shared by phylloquinone.

�Fracture victims� levels of Menatetrenone are more depressed than are their levels of phylloquinone.

�Areas where more K2 is consumed in the diet have lower fracture rates.

�Menatetrenone inhibits the resorption (teardown) of bone caused by the local cellular messenger  prostaglandin E2 (PGE2). The same concentration of phylloquinone has no effect. Menatetrenone also cuts down on the bone cells� formation of PGE2 in the first place.

�Menatetrenone is able to reduce the creation of osteoclasts (cells involved in the teardown of bone tissue) out of early cell types � but again, phylloquinone has no such power.

�Menatetrenone, but not phylloquinone, actually increases the programmed cell death (�apoptosis�) of existing osteoclasts.

�Menatetrenone strengthens the bone-building legions of the osteoblasts (cells involved in the manufacture of new bone), mildly increasing both their numbers and their activity.

Over the course of the last decade, at least sixteen clinical trials have been performed using Menatetrenone, and every single one has found that K2 supplements protect bone health. Menatetrenone not only slows, halts, or even reverses loss of bone mass: it dramatically reduces your risk of suffering a fracture.

�In one trial, women who took an ultra-high dose Menatetrenone supplement for 24 weeks increased their bone mineral density by an impressive 2.2%, even as the women taking a placebo (dummy pill) lost 7.31% of their bone density.

�In another trial, Menatetrenone was put to the test in a direct comparison against the bisphosphonate drug etidronate (Didrocal^®). Menatetrenone preserved bone mass, and also slashed fracture risk by roughly two thirds over the course of two years.

� In a third trial, osteoporotic women taking Menatetrenone supplements sustained nearly no bone loss over two years, while cutting fracture risk by 64% as compared with non-supplementing women.

The ability of bones to withstand fractures is not just determined by the quantity of bone (as measured by Bone Mineral Density (BMD)), but also by the quality of bone � bone �microarchitecture,� including especially �trabecular connectivity.� Evidence suggests that Menatetrenone�s most important effects are on bone quality, not bone quantity.

�Clinical trials have found that Menatetrenone provides as much protection against fracture as drugs that have much more powerful effects on BMD. Clearly, Menatetrenone�s bone-protective effects extend to aspects of bone health beyond the BMD numbers.

�Menatetrenone provides powerful protection against the loss of trabecular connectivity in laboratory animal models of menopausal osteoporosis.

�Menatetrenone supplements increase bone quality in young, healthy animals.

To get the amount of Menatetrenone used to produce these effects in clinical trials and experimental studies requires a specific Menatetrenone supplement.

�Existing science shows that phylloquinone does not provide the same benefits as Menatetrenone. No clinical trials using phylloquinone supplements have been performed to show reduced fracture risk.

�The body�s ability to convert phylloquinone into Menatetrenone is limited, flattening out at levels far below what�s used in clinical trials. This ability is further reduced with aging.

�Very little vitamin K2 exists in the diet, even in the richest food sources.

�While the body�s friendly bacteria produce some K2, little or none of this K2 is absorbed.

Menatetrenone�s health benefits extend well beyond the skeletal system. Emerging science is now documenting the role of vitamin K � and specifically of Menatetrenone � in protecting our cardiovascular health, and the health of that all-important organ, the brain.

vi. Vermeer C. �Prevention of arterial calcification by vitamin K2.� In Miki T (ed). �Vitamin K: A Conference Record. Renewing Bone Metabolism.� 2000; Tokyo: Intermedd Inc, 2-21.

Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis.

J Bone Miner Res 2000 Mar; 15(3): 515-21.

Shiraki M, Shiraki Y, Aoki C, Miura M.

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.

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.

Inverse association of dietary vitamin K-2 intake with cardiac events and aortic atherosclerosis: the Rotterdam Study.

Thromb Haem 2001 Jul; 85(Suppl): AbsP473.
Geleijnse JM, Vermeer C, Jurgers LJ, Grobbee DE, Pols HA, Witteman JC.

Vitamin K-dependent proteins have been identified in vascular tissue but our knowledge concerning their function in the vessel wall is far from complete. An exception in this respect is matrix Gla-protein, which was demonstrated to be a potent inhibitor of arterial calcification. We examined the relation of dietary vitamin K-1 and K-2 intake with aortic atherosclerosis and cardiac events in the general, older cohort of the population-based Rotterdam Study. Diet was assessed by a trained dietician at baseline (1990-1993) in 5435 subjects, 5420 of which were followed for cardiac events until 31 March 1996. The analysis included 4794 subjects without a history of myocardial infarction. For 4462 subjects, baseline radiographic data on calcification of the abdominal aorta were available. Relative risks (RRs) for myocardial infarction and cardiac death, and odds ratios (ORs) for aortic atherosclerosis were obtained in tertiles of energy-adjusted vitamin K-1 and K-2 intake. Findings were adjusted for age, sex, body mass index, smoking, diabetes, education, and dietary factors. In subjects with a high intake of vitamin K-2 (>33 µg/day), reduced risks were observed for incident myocardial infarction (116 events; RR = 0.43 [95% CI 0.24-0.74]),compared to subjects with a low intake (<22 µg/day). Similar findings were obtained for cardiac death (74 events; RR = 0.37 [0.17-0.87]). For severe aortic atherosclerosis (240 cases), odds ratios were reduced in the mid and upper tertiles of vitamin K-2 intake (OR = 0.67 [0.48-0.94] and 0.45 [0.31-0.67], respectively) compared to the lower tertile. The dietary intake of vitamin K-1 showed no consistent relation with cardiac events or aortic atherosclerosis. These findings suggest a protective effect of vitamin K-2 against coronary heart disease, which could be mediated by the degree of carboxylation of vascular Gla-proteins.

The possible role of vitamin K deficiency in the pathogenesis of Alzheimer's disease and in augmenting brain damage
associated with cardiovascular disease.

Med Hypotheses. 2001 Aug; 57(2): 151-5.
Allison AC.

The incidence of Alzheimer's disease (AD) increases with age and in carriers of the apolipoprotein E4 genotype. A relative deficiency of vitamin K, affecting the extrahepatic functions of the vitamin, is common in ageing men and women. The concentration of vitamin K is lower in the circulating blood of APOE4 carriers than in that of persons with other APOE genotypes. Evidence is accumulating that vitamin K has important functions in the brain, including the regulation of sulfotransferase activity and the activity of a growth factor/tyrosine kinase receptor (Gas 6/Axl). The hypothesis is now proposed that vitamin K deficiency contributes to the pathogenesis of AD and that vitamin K supplementation may have a beneficial effect in preventing or treating the disease. Vitamin K may also reduce neuronal damage associated with cardiovascular disease.

Menetetrenone (2-methyl 1,3 tetraprenyl-1, 4-naphtoquinone; vitamin K2 ) is a vitamin K homolog. To evaluate its efficacy on cortical bone mineral density and its safety, a 24-week double-blind placebo-controlled study was conducted by enrolling 80 osteoporotic patients. Patients were either given 90mg/day of vitamin K2  (n = 39) or a placebo (n = 41). Bone density was assessed on the X-ray film of the right second metacarpal bone using the microdensitometric method. In the vitamin K2  group bone density increased by 2.20 % ± 2.48% from the baseline; in the placebo group, it decreased by �7.31% ± 3.65% (P = .037. K2  vs placebo). Urinary excretion of y-carboxyglutamic acid (Gla) significantly increased from 72.61 ± 4.08nmole/mg creatinine before treatment to 88.36 ± 5.35 in the 24^th week after completion of the vitamin K2  treatment (P = .008). In the placebo group, there were no significant changes in urinary Gla excretion. In the 24^th week of the treatment, the urinary calcium/creatinine ratio in the vitamin K2  group decreased from 0.137 ± 0.018 to 0.118 ± 0.016; in the placebo group, it increased from 0.153 ± 0.018 to 0.189 ± 0.029. As a result, the 24-week levels in the vitamin K2 and placebo groups became significantly different (P = .028). There were a few adverse effects attributable to vitamin K2. Our findings suggest that vitamin K2 at a dosage of 90mg/day is effective in maintaining peripheral cortical bone density and is safe in treatment for osteoperosis.