Cyproheptadine Prevents / Reverses Soft Tissue Calcification

haidut

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Human equivalent dose was about 12mg daily, duration was just 4 days. Cyproheptadine prevented AND reversed soft tissue calcification by acting as an anti-heparin agent, which is similar to what vitamin K2 does.

http://www.ncbi.nlm.nih.gov/pubmed/14324165

"...In the rat, cyproheptadine prevents the soft-tissue calcification elicited by various mast-cell depletors at their subcutaneous injection site. This action does not appear to result from the anti-histaminic anti-serotonin properties of cyproheptadine, which showed in addition an in vitro anti-heparin effect."
 

haidut

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lexis said:
post 103380 Is calcification the cause behind erectile dysfunction?

Nope, most cases are high serotonin, prolactin and estrogen and thus hypogonadism.
 
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NathanK

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Hypogonadism =/= erectile dysfunction. They are often bunched together incorrectly, imo.

My belief is that low androgen is a hormone conversion issue while ED is likely a neurotransmitter dysfunction. They're as related as anything in the body via the brain, but separate. One can have one without the other quite easily.

Otherwise, this study is quite cool!
 

Peata

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haidut said:
post 103376 Human equivalent dose was about 12mg daily, duration was just 4 days. Cyproheptadine prevented AND reversed soft tissue calcification by acting as an anti-heparin agent, which is similar to what vitamin K2 does.

http://www.ncbi.nlm.nih.gov/pubmed/14324165

"...In the rat, cyproheptadine prevents the soft-tissue calcification elicited by various mast-cell depletors at their subcutaneous injection site. This action does not appear to result from the anti-histaminic anti-serotonin properties of cyproheptadine, which showed in addition an in vitro anti-heparin effect."


So Cyp would be good to take along with aspirin, maybe. If you're not also taking vit. K?
 
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haidut

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NathanK said:
post 103493 Hypogonadism =/= erectile dysfunction. They are often bunched together incorrectly, imo.

My belief is that low androgen is a hormone conversion issue while ED is likely a neurotransmitter dysfunction. They're as related as anything in the body via the brain, but separate. One can have one without the other quite easily.

Otherwise, this study is quite cool!

The hormone conversion is controlled by the brain. If you have high prolactin / serotonin, you will have hypogonadism. For optimal sexual function, testosterone needs to be above 700 and prolactin below 5 (for males). Anybody with prolactin above 10 will likely have testosterone below 500, and of course low dopamine.


Peata said:
post 103526
haidut said:
post 103376 Human equivalent dose was about 12mg daily, duration was just 4 days. Cyproheptadine prevented AND reversed soft tissue calcification by acting as an anti-heparin agent, which is similar to what vitamin K2 does.

http://www.ncbi.nlm.nih.gov/pubmed/14324165

"...In the rat, cyproheptadine prevents the soft-tissue calcification elicited by various mast-cell depletors at their subcutaneous injection site. This action does not appear to result from the anti-histaminic anti-serotonin properties of cyproheptadine, which showed in addition an in vitro anti-heparin effect."


So Cyp would be good to take along with aspirin, maybe. If you're not also taking vit. K?

Cyproheptadine can also cause bleeding issues, so I would not use it together with aspirin. Anything that inhibits serotonin will reduce platelet aggregation.
 
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Peata

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haidut said:
post 103528
NathanK said:
post 103493 Hypogonadism =/= erectile dysfunction. They are often bunched together incorrectly, imo.

My belief is that low androgen is a hormone conversion issue while ED is likely a neurotransmitter dysfunction. They're as related as anything in the body via the brain, but separate. One can have one without the other quite easily.

Otherwise, this study is quite cool!

The hormone conversion is controlled by the brain. If you have high prolactin, you will have hypogonadism.
Peata said:
post 103526
haidut said:
post 103376 Human equivalent dose was about 12mg daily, duration was just 4 days. Cyproheptadine prevented AND reversed soft tissue calcification by acting as an anti-heparin agent, which is similar to what vitamin K2 does.

http://www.ncbi.nlm.nih.gov/pubmed/14324165

"...In the rat, cyproheptadine prevents the soft-tissue calcification elicited by various mast-cell depletors at their subcutaneous injection site. This action does not appear to result from the anti-histaminic anti-serotonin properties of cyproheptadine, which showed in addition an in vitro anti-heparin effect."


So Cyp would be good to take along with aspirin, maybe. If you're not also taking vit. K?

Cyproheptadine can also cause bleeding issues, so I would not use it together with aspirin. Anything that inhibits serotonin will reduce platelet aggregation.

Ah, I see now. I think I read that too soon after waking and thought it said it was the opposite effect. Thanks.
 
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Peata

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haidut said:
Cyproheptadine can also cause bleeding issues, so I would not use it together with aspirin. Anything that inhibits serotonin will reduce platelet aggregation.

A follow-up if you see this: Can you still take Cyproheptadine and aspirin in the same day - only take them a certain amount of hours apart? Or should you just not use aspirin at all while on Cyp?
 

haidut

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Peata said:
post 103533
haidut said:
Cyproheptadine can also cause bleeding issues, so I would not use it together with aspirin. Anything that inhibits serotonin will reduce platelet aggregation.

A follow-up if you see this: Can you still take Cyproheptadine and aspirin in the same day - only take them a certain amount of hours apart? Or should you just not use aspirin at all while on Cyp?

That I don't know. I would ask a pharmacist as they can check their extensive DB on whether you can take in the same day. Not sure why you want to take both given that aspirin has been shown to inhibit calcification.
http://www.ncbi.nlm.nih.gov/pubmed/10718766
 
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lexis

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haidut said:
post 103528 The hormone conversion is controlled by the brain. If you have high prolactin / serotonin, you will have hypogonadism. For optimal sexual function, testosterone needs to be above 700 and prolactin below 5 (for males). Anybody with prolactin above 10 will likely have testosterone below 500, and of course low dopamine.

How about increasing DHT with caffeine or topical DHT?
 
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haidut

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lexis said:
post 103569
haidut said:
post 103528 The hormone conversion is controlled by the brain. If you have high prolactin / serotonin, you will have hypogonadism. For optimal sexual function, testosterone needs to be above 700 and prolactin below 5 (for males). Anybody with prolactin above 10 will likely have testosterone below 500, and of course low dopamine.

How about increasing DHT with caffeine or topical DHT?

Sure, it can be done. I think smaller doses of DHEA taken regularly raise tissue DHT just as well as topical DHT but without the suppression of endogenous hormonal synthesis. And you don't need prescription for it.
 
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paymanz

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haidut said:
post 103543
Peata said:
post 103533
haidut said:
Cyproheptadine can also cause bleeding issues, so I would not use it together with aspirin. Anything that inhibits serotonin will reduce platelet aggregation.

A follow-up if you see this: Can you still take Cyproheptadine and aspirin in the same day - only take them a certain amount of hours apart? Or should you just not use aspirin at all while on Cyp?

That I don't know. I would ask a pharmacist as they can check their extensive DB on whether you can take in the same day. Not sure why you want to take both given that aspirin has been shown to inhibit calcification.
http://www.ncbi.nlm.nih.gov/pubmed/10718766
how they can synergy in inhibiting soft tissue calcification? i read everywhere that heparin causes soft tissue calcification.
sorry for second mistaken with warfarin
 
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NathanK

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haidut said:
post 103594
lexis said:
post 103569
haidut said:
post 103528 The hormone conversion is controlled by the brain. If you have high prolactin / serotonin, you will have hypogonadism. For optimal sexual function, testosterone needs to be above 700 and prolactin below 5 (for males). Anybody with prolactin above 10 will likely have testosterone below 500, and of course low dopamine.

How about increasing DHT with caffeine or topical DHT?

Sure, it can be done. I think smaller doses of DHEA taken regularly raise tissue DHT just as well as topical DHT but without the suppression of endogenous hormonal synthesis. And you don't need prescription for it.
From my understanding, the direct steroid pathway from DHEA to DHT is: DHEA->Androstenedione->Testosterone->DHT.

Therefore, wouldn't any increase in testosterone hypothetically increase DHT? We would just have to watch to ensure we arent converting our DHEA into too much estrogen, which could be monitored by labs or judging nipple sensitivity. A cheap PSA test would tell us if we are converting too much testosterone to DHT as well though likely nothing to worry about with small DHEA supplementation (more for DHT creams I suppose).
 
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NathanK

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haidut said:
post 103528
NathanK said:
post 103493 Hypogonadism =/= erectile dysfunction. They are often bunched together incorrectly, imo.

My belief is that low androgen is a hormone conversion issue while ED is likely a neurotransmitter dysfunction. They're as related as anything in the body via the brain, but separate. One can have one without the other quite easily.

The hormone conversion is controlled by the brain. If you have high prolactin / serotonin, you will have hypogonadism. For optimal sexual function, testosterone needs to be above 700 and prolactin below 5 (for males). Anybody with prolactin above 10 will likely have testosterone below 500, and of course low dopamine.
I think we are on the same page with the exception of any direct libido and testosterone connection. I don't believe there is one from many testimonials I have read and from personal experience. For example, I had sub-500 testosterone with PRL at 8, but I always had a pretty good libido. I've also read and heard many stories of guys on TRT that still have serious libido issues.

Granted, if someone has high prolactin/ serotonin/ estrogen it will inhibit many widespread processes, which needs to be fixed first and foremost. Many things will be resolved just by focusing on these/this area.

A little closer to specific pathways, like increasing testosterone, I would focus on optimizing steroid conversion from cholesterol in the liver, which would be directly related to increasing metabolism and liver function. I am not familiar with how the brain controls steroid conversions directly as you said with maybe the exception of hypothalamic GnRH inhibition via stress hormones such as estrogen. I suppose that does play a pretty big role.

Libido is more along the dopamine pathway, or at least there is a higher correlation, so I would focus on optimizing dopamine and inhibiting dopamine antagonists. Prolactin of course being the biggest one :). This is all just my understanding and extrapolation from complex matters of course...
 
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haidut

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NathanK said:
post 104228
haidut said:
post 103528
NathanK said:
post 103493 Hypogonadism =/= erectile dysfunction. They are often bunched together incorrectly, imo.

My belief is that low androgen is a hormone conversion issue while ED is likely a neurotransmitter dysfunction. They're as related as anything in the body via the brain, but separate. One can have one without the other quite easily.

The hormone conversion is controlled by the brain. If you have high prolactin / serotonin, you will have hypogonadism. For optimal sexual function, testosterone needs to be above 700 and prolactin below 5 (for males). Anybody with prolactin above 10 will likely have testosterone below 500, and of course low dopamine.
I think we are on the same page with the exception of any direct libido and testosterone connection. I don't believe there is one from many testimonials I have read and from personal experience. For example, I had sub-500 testosterone with PRL at 8, but I always had a pretty good libido. I've also read and heard many stories of guys on TRT that still have serious libido issues.

Granted, if someone has high prolactin/ serotonin/ estrogen it will inhibit many widespread processes, which needs to be fixed first and foremost. Many things will be resolved just by focusing on these/this area.

A little closer to specific pathways, like increasing testosterone, I would focus on optimizing steroid conversion from cholesterol in the liver, which would be directly related to increasing metabolism and liver function. I am not familiar with how the brain controls steroid conversions directly as you said with maybe the exception of hypothalamic GnRH inhibition via stress hormones such as estrogen. I suppose that does play a pretty big role.

Libido is more along the dopamine pathway, or at least there is a higher correlation, so I would focus on optimizing dopamine and inhibiting dopamine antagonists. Prolactin of course being the biggest one :). This is all just my understanding and extrapolation from complex matters of course...

Testosterone and DHT inhibit TPH and prolactin. Progesterone is a stronger inhibitor of both TPH and prolactin but testosterone is not far behind. Thus, the male hormones depend on and affect brain steroids. As such, I don't think we can separate brain function from steroidogenesis. Everything is systemic like Ray says.
 
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NathanK

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haidut said:
Testosterone and DHT inhibit TPH and prolactin. Progesterone is a stronger inhibitor of both TPH and prolactin but testosterone is not far behind. Thus, the male hormones depend on and affect brain steroids. As such, I don't think we can separate brain function from steroidogenesis. Everything is systemic like Ray says.
I wasn't separating those two; just the direct link of libido and testosterone. But, yes, everything is sytematic so it's hard to separate much.

On a relevant note, I asked Ray this question once after I'd heard more than a few guys say they felt better with higher estrogen labs and purposefully kept them higher for that reason. I'd felt that before too, but didn't understand how that was possible. I'd ask them their prolactin and they told me that it was normal. Mine had never been above 8 either. Anyway, I thought it was worth sharing.

Me: "Why is it that with higher serum estrogen, and normal prolactin levels, that some men have higher libido?"

Ray: It’s a brain excitant, and is produced locally in the brain from testosterone even when the serum estrogen isn’t high. I think the absence of higher prolactin means that something is protecting systemically against estrogen, which activates prolactin via serotonin and cortisol. Cortisol increases the formation of serotonin a direct stimulus to prolactin, and the androgens and progesterone oppose cortisol’s effects.

Cell. 2009 Oct 2;139(1):61-72.
Estrogen masculinizes neural pathways and sex-specific behaviors.
Wu MV1, Manoli DS, Fraser EJ, Coats JK, Tollkuhn J, Honda S, Harada N, Shah NM.
Sex hormones are essential for neural circuit development and sex-specific behaviors. Male behaviors require both testosterone and estrogen, but it is unclear how the two hormonal pathways intersect. Circulating testosterone activates the androgen receptor (AR) and is also converted into estrogen in the brain via aromatase. We demonstrate extensive sexual dimorphism in the number and projections of aromatase-expressing neurons. The masculinization of these cells is independent of AR but can be induced in females by either testosterone or estrogen, indicating a role for aromatase in sexual differentiation of these neurons. We provide evidence suggesting that aromatase is also important in activating male-specific aggression and urine marking because these behaviors can be elicited by testosterone in males mutant for AR and in females subjected to neonatal estrogen exposure. Our results suggest that aromatization of testosterone into estrogen is important for the development and activation of neural circuits that control male territorial behaviors.
Comment in
• Sex on the brain. [Cell. 2009]

Biol Psychiatry. 2006 Aug 1;60(3):288-95. Epub 2006 Feb 3.
Estrogen selectively increases tryptophan hydroxylase-2 mRNA expression in
distinct subregions of rat midbrain raphe nucleus: association between gene
expression and anxiety behavior in the open field.
Hiroi R, McDevitt RA, Neumaier JF.
Department of Psychology, University of Washington, Seattle, Washington 98195, USA.
BACKGROUND: Ovarian steroids modulate anxiety behavior, perhaps by regulating the serotonergic neurons in the midbrain raphe nucleus. The regulation of the brain-specific isoform of rat tryptophan hydroxylase (TPH2) by ovarian hormones has not yet been investigated. Therefore, we examined the effects of estrogen and progesterone on TPH2 mRNA in the rat dorsal and median raphe nuclei (DRN and MRN, respectively) and whether TPH2 mRNA levels correlated with anxiety behavior.
METHODS: Ovariectomized rats were treated for two weeks with placebo, estrogen or estrogen plus progesterone, exposed to the open field test, and TPH2 mRNA was quantified by in situ hybridization histochemistry.
RESULTS: Estrogen increased TPH2 mRNA in the mid-ventromedial and caudal subregions of the DRN and the caudal MRN. Combined estrogen and progesterone treatment did not change TPH2 mRNA relative to ovariectomized controls. TPH2 mRNA in caudal DRN was associated with lower anxiety-like behavior, whereas TPH2 mRNA in rostral dorsomedial DRN was associated with increased anxiety-like behavior.
CONCLUSIONS: These results suggest that estrogen may increase the capacity for serotonin synthesis in discrete subgroups of raphe neurons, and reinforce previous observations that different subregions of DRN contribute to distinct components of anxiety behavior.

Mol Cell Neurosci. 1994 Apr;5(2):176-81.
Intracranial dehydroepiandrosterone blocks the activation of tryptophan
hydroxylase in response to acute sound stress.
Singh VB, Kalimi M, Phan TH, Boadle-Biber MC.
Department of Physiology, Medical College of Virginia, Virginia Commonwealth
University, Richmond 23298-0551.
Bilateral infusion of dehydroepiandrosterone (DHEA) given
intracerebroventricularly blocked the sound stress-induced increase in tryptophan hydroxylase activity observed ex vivo in midbrain and cortex but had no effect on the level of tryptophan hydroxylase activity from sham-stressed rats. DHEA (20 micrograms total dose) given bilaterally into the region of the central nucleus of the amygdala, 30 min prior to 1 h sound stress, also blocked the increase in enzyme activity in a dose-dependent manner. The DHEA treatment did not alter the activation of the enzyme seen in vitro in the presence of phosphorylating conditions. The effect of DHEA was steroid specific in that other sex steroids, such as estrogen, androgens, or progesterone, were without any effect.
Coadministration, 20 micrograms each, of the potent glucocorticoid agonist, RU 28362, with DHEA 30 min prior to 1 h sound stress completely blocked the DHEA suppressive effect on sound stress-induced increases in tryptophan hydroxylase activity. The results obtained suggest that DHEA blocks this increase in tryptophan hydroxylase activity by antagonizing the effects of glucocorticoid.

Biol Psychiatry. 2000 Mar 15;47(6):562-76.
Steroid regulation of tryptophan hydroxylase protein in the dorsal raphe of
macaques.
Bethea CL, Mirkes SJ, Shively CA, Adams MR.
Division of Reproductive Sciences, Oregon Regional Primate Research Center, Beaverton, OR, USA.
BACKGROUND: Tryptophan hydroxylase (TPH) is the rate-limiting enzyme for the synthesis of serotonin, and serotonin is a pivotal neurotransmitter in the
regulation of mood, affective behavior, pituitary hormone secretion, and numerous autonomic functions. We previously demonstrated that estradiol (E) and progesterone (P) increase TPH mRNA levels in the dorsal raphe of macaques.
METHODS: This study employed western blotting and densitometric quantitation to determine whether the changes observed at the level of gene expression were manifested by changes in TPH protein expression and whether modified estrogens or progestins had actions similar to the native ligands. In addition, the effect ofthe antiestrogen tamoxifen was examined. Ovariectomized (ovx) rhesus and cynomolgus macaques were untreated or treated with E, P, E+P, equine estrogens (EE), medroxyprogesterone (MPA), EE+MPA, or tamoxifen. The dorsal raphe region was subjected to Western analysis.
RESULTS: E treatment for 28 days increased TPH protein mass four to six fold over ovariectomized controls. Addition of P to the E regimen or treatment with P for 28 days after E priming did not alter TPH from E treatment alone. Treatment of ovx macaques with a low dose of P caused a two-fold increase in TPH protein. Treatment of ovariectomized macaques for 30 months with EE alone or MPA alone significantly increased TPH protein; however, unlike P, the addition of MPA to the EE regimen blocked the stimulatory effect of EE. Tamoxifen treatment significantly reduced TPH protein compared to EE and ovariectomized control animals.
CONCLUSION: The stimulatory effect of E and P on TPH protein in the dorsal rapheof macaques correlates with the previously observed effect at the level of mRNA expression. P had no effect on the stimulatory action of E, whereas MPA blocked the stimulatory effect of EE. Tamoxifen acted as a potent antiestrogen on TPH protein expression. If TPH protein mass influences serotonin synthesis, then these steroids will impact many autonomic systems that are regulated by serotonin.

Brain Res. 1975 Jul 25;93(1):123-32.
Regulation of 5-hydroxytryptamine metabolism in mouse brain by adrenal
glucocorticoids.
Neckers L, Sze PY.
The effects of glucocorticoid hormone on the metabolism of brain
5-hydroxytryptamine (5-HT) were studied in mice. A single injection of
hydrocortisone acetate (HCA; 20 mg/kg, i.p.) accelerated the accumulation of 5-HT
in whole brain after inhibition of monoamine oxidase activity by paragyline. The
hormone did not appear to change brain tryptophan hydroxylase or
5-hydroxytryptophan decarboxylase activity. However, tryptophan levels in brain
were elevated by 50% within 1 h after treatment with HCA. The effect of HCA on
brain tryptophan levels was localized mainly in the nerve endings. In vitro
synaptosomal preparations, HCA at 10(-5)-10(-7)M or corticosterone at 10(-5) M
was found to stimulate the uptake of L-[3H]-tryptophan by the synaptosomes while
androgenic and progesterone-like steroids were ineffective. These results
demonstrate that glucocorticoids may directly act on nerve terminals in the
regulation of 5-HT synthesis through an action on the uptake of tryptophan.
 
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haidut said:
post 103376 Human equivalent dose was about 12mg daily, duration was just 4 days. Cyproheptadine prevented AND reversed soft tissue calcification by acting as an anti-heparin agent, which is similar to what vitamin K2 does.

http://www.ncbi.nlm.nih.gov/pubmed/14324165

"...In the rat, cyproheptadine prevents the soft-tissue calcification elicited by various mast-cell depletors at their subcutaneous injection site. This action does not appear to result from the anti-histaminic anti-serotonin properties of cyproheptadine, which showed in addition an in vitro anti-heparin effect."

Do you think Vit K2 stops the negative effects of Heparin on bone health?

I have been on Heparin about a year. My blood tests showed that my calcium levels are below the lab ranges.

Thank you.
 
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haidut

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Berk_Peat said:
post 105538
haidut said:
post 103376 Human equivalent dose was about 12mg daily, duration was just 4 days. Cyproheptadine prevented AND reversed soft tissue calcification by acting as an anti-heparin agent, which is similar to what vitamin K2 does.

http://www.ncbi.nlm.nih.gov/pubmed/14324165

"...In the rat, cyproheptadine prevents the soft-tissue calcification elicited by various mast-cell depletors at their subcutaneous injection site. This action does not appear to result from the anti-histaminic anti-serotonin properties of cyproheptadine, which showed in addition an in vitro anti-heparin effect."

Do you think Vit K2 stops the negative effects of Heparin on bone health?

I have been on Heparin about a year. My blood tests showed that my calcium levels are below the lab ranges.

Thank you.

Don't know about heparin effect on bones but K2 prevents glucocorticoid effect on bones. Heparin takes the circulating calcium and puts it into the soft tissue. Vitamin K2 prevents that and puts the calcium back in the bones. But I don't know that heparin has direct effect on bones that vitamin K2 somehow antagonizes.
 
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