stuck in some osteoporosis/K info since we have been occasionally asked
about breastfeeding/osteoporosis and options for treatment besides
weaning and fosamax.
20: Acta Paediatr. 1998 Sep;87(9):960-2.  Related Articles, Links


Vitamin K in preterm breastmilk with maternal supplementation.

Bolisetty S, Gupta JM, Graham GG, Salonikas C, Naidoo D.

Department of Neonatology, Royal Hospital for Women, Sydney, Australia.

Six healthy lactating mothers who gave birth to preterm infants at a
median
post conceptional age of 29.5 (range 26-30) weeks were given 2.5 mg
phylloquinone (vitamin K1) orally daily for 2 weeks beginning at a median
postconceptional age of 31.5 (range 28-32) weeks. Phylloquinone was
measured
in the breastmilk daily for 14 d. Trough plasma phylloquinone
concentrations
were also determined on four occasions. Phylloquinone levels in the
breastmilk increased from a baseline of 3 +/- 2.3 ng ml(-1) to 22.6 +/-
16.3
ng ml(-1) (mean +/- SD) after the first dose (p < 0.05); a gradual
increase
was noted until phylloquinone levels reached a plateau of 64.2 +/- 31.4
ng
ml(-1) after the sixth daily dose.

10: Calcif Tissue Int.  2003 Jul;73(1):21-6.

Vitamin K1 supplementation retards bone loss in postmenopausal women
between
50 and 60 years of age.

Braam LA, Knapen MH, Geusens P, Brouns F, Hamulyak K, Gerichhausen MJ,
Vermeer C.

Department of Biochemistry, University of Maastricht, The Netherlands.

Although several observational studies have demonstrated an association
between vitamin K status and bone mineral density (BMD) in postmenopausal
women, no placebo-controlled intervention trials of the effect of
vitamin K1
supplementation on bone loss have been reported thus far. In the trial
presented here we have investigated the potential complementary effect of
vitamin K1 (1 mg/day) and a mineral + vitamin D supplement (8
microg/day) on
postmenopausal bone loss. The design of our study was a randomized,
double-blind, placebo-controlled intervention study; 181 healthy
postmenopausal women between 50 and 60 years old were recruited, 155 of
whom
completed the study. During the 3-year treatment period, participants
received a daily supplement containing either placebo, or calcium,
magnesium, zinc, and vitamin D (MD group), or the same formulation with
additional vitamin K1 (MDK group). The main outcome was the change in
BMD of
the femoral neck and lumbar spine after 3 years, as measured by DXA. The
group receiving the supplement containing additional vitamin K1 showed
reduced bone loss of the femoral neck: after 3 years the difference
between
the MDK and the placebo group was 1.7% (95% Cl: 0.35-3.44) and that
between
the MDK and MD group was 1.3% (95% Cl: 0.10-3.41). No significant
differences were observed among the three groups with respect to change
of
BMD at the site of the lumbar spine. If co-administered with minerals and
vitamin D, vitamin K1 may substantially contribute to reducing
postmenopausal bone loss at the site of the femoral neck.

Publication Types: Clinical Trial Randomized Controlled Trial

PMID: 14506950 [PubMed - indexed for MEDLINE]
```````````````````````````````````````````````````````````````````

there's another study out there that indicates that 5mg K per day
improves bone density faster than fosamax.....



11: J Biol Chem.  2003 Nov 7;278(45):43919-27. Epub 2003 Aug 14.

Vitamin K2 regulation of bone homeostasis is mediated by the steroid and
xenobiotic receptor SXR.

Tabb MM, Sun A, Zhou C, Grun F, Errandi J, Romero K, Pham H, Inoue S,
Mallick S, Lin M, Forman BM, Blumberg B.

Department of Developmental and Cell Biology, University of California,
Irvine, California 92697-2300, USA.

Vitamin K2 is a critical nutrient required for blood clotting that also
plays an important role in bone formation. Vitamin K2 supplementation
up-regulates the expression of bone markers, increases bone density in
vivo,
and is used clinically in the management of osteoporosis. The mechanism
of
vitamin K2 action in bone formation was thought to involve its normal
role
as an essential cofactor for gamma-carboxylation of bone matrix proteins.
However, there is evidence that suggests vitamin K2 also has a
transcriptional regulatory function. Vitamin K2 bound to and activated
the
orphan nuclear receptor SXR and induced expression of the SXR target
gene,
CYP3A4, identifying it as a bona fide SXR ligand. Vitamin K2 treatment of
osteosarcoma cells increased mRNA levels for the osteoblast markers bone
alkaline phosphatase, osteoprotegerin, osteopontin, and matrix Gla
protein.
The known SXR activators rifampicin and hyperforin induced this panel of
bone markers to an extent similar to vitamin K2. Vitamin K2 was able to
induce bone markers in primary osteocytes isolated from wild-type murine
calvaria but not in cells isolated from mice deficient in the SXR
ortholog
PXR. We infer that vitamin K2 is a transcriptional regulator of
bone-specific genes that acts through SXR to favor the expression of
osteoblastic markers. Thus, SXR has a novel role as a mediator of bone
homeostasis in addition to its role as a xenobiotic sensor. An important
implication of this work is that a subset of SXR activators may function
as
effective therapeutic agents for the management of osteoporosis.

PMID: 12920130 [PubMed - indexed for MEDLINE]

Krispy Note: Before you read this next one, the mistake is milligrams. It
should read mcg. and how interesting that men get more, again... The
German's think the minimum is 900 mcg. We are not even close. Why we need
more research given what already exists is quite beyond me.

12: Zhongguo Yi Xue Ke Xue Yuan Xue Bao.  2003 Jun;25(3):346-9.

[Vitamin K and osteoporosis]

[Article in Chinese]

Luo LZ, Xu L.

Department of Scientific Research, PUMC Hospital, CAMS, PUMC, Beijing
100730, China.

There is a closely relationship between vitamin K and osteoporosis. As a
cofactor for carboxylase activity, vitamin K can facilitate the
conversion
of glutamyl to gamma-carboxyglutamyl residues and influence the synthesis
and excretion of gamma-carboxylation of osteocalcin to increase the
formation of bone. Vitamin K can also effectively inhibit the absorption
of
bone mass. Besides, there are increasing evidences that vitamin K can
effect
the synthesis and excretion of nephrocalcin and interlukin-1,6 that can
regulate calcium balance and bone metabolism. Meanwhile, there is a
consistent line of evidence in human epidemiologic and intervention
studies
that clearly demonstrate that vitamin K can not only increase bone
mineral
density in osteoporotic people, but also reduce fracture rates to improve
bony health. However more researches are required before vitamin K is
widely
applied in prevention and treatment of osteoporosis. The American Medical
Association recently has increased the dietary reference intakes of
vitamin
K to 90 mg/d for females and 120 mg/d for males.

Publication Types: Review Review, Tutorial

PMID: 12905754 [PubMed - indexed for MEDLINE]

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