LONGECITY

A friend of mine was recently told she had some calcification in her breast tissue; I was wondering if Vitamin K2 could help remove it or are there any other supplements she can try? The only studies I have seen with Vitamin K2 and calcification pertained to arteries, but I have yet to see research that claims it can also remove calcification in other tissues of the body. Anyone here have any information or knowledge in regards to supplements that can remove calcification from other parts of the body?

Intravenous EDTA would be her best option.

Magnesium, K2, chanca piedra.

Intravenous EDTA would be her best option.

Is IV EDTA safe ?
I've heard that it can drive serum calcium low quickly enough to be dangerous.
This would likely have a long term effect on calcification, though.

Magnesium, K2, chanca piedra.

I see, but is there data showing Vitamin K2 or magnesium being effective or is it merely an assumption based on data that shows it (Vit. K2) can remove calcification from arteries? Anyway, I thank you all for the recommendations; I'm not to sure about the EDTA though.

Vitamin C lowers calcium and copper. High calcium may be about high copper.

Larry Wilson says high copper causes biounavailable calcium. Its not really high calcium its not bioavailable. And that's why it shows up as calcifications.

Its a nutritional imbalance that can be corrected with the right approach. But it isn't just about calcium. Its about balancing other things, everything really.

Any form of EDTA will basically even things out (hopefully) but then the next step would be a regimen that avoids another inbalance and restores depleted minerals.

Really high calcium (and high copper) can cause anxiety, possibly fears, an over active sympathetic nervous system (a heightened fight or flight response) besides some other symptoms.

Magnesium, K2, chanca piedra.

I see, but is there data showing Vitamin K2 or magnesium being effective or is it merely an assumption based on data that shows it (Vit. K2) can remove calcification from arteries?

K2, yes, there are RCTs showing it to be effective. Data on magnesium is weaker, but promising (although, it's not in the same league as K2+D3).

Anyway, I thank you all for the recommendations; I'm not to sure about the EDTA though.

Definitely not EDTA. I don't have time to go into detail, but you can look up one of my recent posts on EDTA vs K2 for some background.
Edited by kismet, 12 June 2009 - 11:25 AM.

Can you find out what else is in the tissue besides just calcium? Eg are we looking at a plaque. Is there a high count of dead macrophages?
Edited by caston, 12 June 2009 - 11:45 AM.

Can you find out what else is in the tissue besides just calcium? Eg are we looking at a plaque. Is there a high count of dead macrophages?

What would you recommend if it did have a high count of dead macrophages ?
Is there a way to hasten the clean-up ?
I'm looking for comprehensive ways to attack plaque.

Subscribe to Dr Davis' TYP and write a review, I'd love read one. Yeah, it does cost money.

Can you find out what else is in the tissue besides just calcium? Eg are we looking at a plaque. Is there a high count of dead macrophages?

No, there's no dead macrophages; the report mentions her breast tissue is extremely dense which affects sensitivity of the mammography and that benign calcification were found on both breasts.

Magnesium, K2, chanca piedra.

I see, but is there data showing Vitamin K2 or magnesium being effective or is it merely an assumption based on data that shows it (Vit. K2) can remove calcification from arteries?

K2, yes, there are RCTs showing it to be effective. Data on magnesium is weaker, but promising (although, it's not in the same league as K2+D3).

Anyway, I thank you all for the recommendations; I'm not to sure about the EDTA though.

Definitely not EDTA. I don't have time to go into detail, but you can look up one of my recent posts on EDTA vs K2 for some background.

Can you point me to those studies, I told my friend about Vitamin K2 and she replied that has nothing to do with it, "K2 cleans your arteries". So, I think I'm going to have to show her the research before she agrees to use K2 for her breast calcification.

Is the calcification associated with arteries or soft tissues? It won't necessarily help with BAC; I guess you should use either 1000mcg K1, ~200mcg MK-7 or about 45mg MK-4 (maybe less will do, but I don't know any data in humans, though) for any therapeutic effects.
There's much else that you could do, but no time to mention it all...

The two landmark papers are:
Thromb Haemost. 2004 Feb;91(2):373-80.Beneficial effects of vitamins D and K on the elastic properties of the vessel wall in postmenopausal women: a follow-up study.
Braam LA, Hoeks AP, Brouns F, Hamulyák K, Gerichhausen MJ, Vermeer C.

Am J Clin Nutr. 2009 Jun;89(6):1799-807. Epub 2009 Apr 22.
Vitamin K supplementation and progression of coronary artery calcium in older men and women.
Shea MK, O'Donnell CJ, Hoffmann U, Dallal GE, Dawson-Hughes B, Ordovas JM, Price PA, Williamson MK, Booth SL.
....the result is not particulary impressive, but it's probably real.
Edited by kismet, 12 June 2009 - 10:33 PM.

Is the calcification associated with arteries or soft tissues? It won't necessarily help with BAC; I guess you should use either 1000mcg K1, ~200mcg MK-7 or about 45mg MK-4 (maybe less will do, but I don't know any data in humans, though) for any therapeutic effects.
There's much else that you could do, but no time to mention it all...

The two landmark papers are:
Thromb Haemost. 2004 Feb;91(2):373-80.Beneficial effects of vitamins D and K on the elastic properties of the vessel wall in postmenopausal women: a follow-up study.
Braam LA, Hoeks AP, Brouns F, Hamulyák K, Gerichhausen MJ, Vermeer C.

Am J Clin Nutr. 2009 Jun;89(6):1799-807. Epub 2009 Apr 22.
Vitamin K supplementation and progression of coronary artery calcium in older men and women.
Shea MK, O'Donnell CJ, Hoffmann U, Dallal GE, Dawson-Hughes B, Ordovas JM, Price PA, Williamson MK, Booth SL.
....the result is not particulary impressive, but it's probably real.

I mentioned in the first post that it dealt with soft tissue not arteries, which is why I asked if anyone had information about tissue calcification and K2. I have plenty of K2 studies that speak of calcification of the arteries yet I have none that deal with soft tissue and from the tittle of the two articles you gave it appears the studies are about arteries not soft tissue.

Edit: I googled breast calcification and from the descripstions it appears that she has macrocalcification which can be associated with aging breast arteries (she is 46), so perhaps K2 might help though you did mention K2 not helping with breast arteries (Assuming BAC is some sort of abbreviation of breast arteries?). The Mayo clinic also mentions that a lot of women have benign calcification after a certain age so it's not something to be too worried about getting yearly check-ups are recommended.
Edited by Dmitri, 13 June 2009 - 04:22 AM.

Edit: I googled breast calcification and from the descripstions it appears that she has macrocalcification which can be associated with aging breast arteries (she is 46), so perhaps K2 might help though you did mention K2 not helping with breast arteries (Assuming BAC is some sort of abbreviation of breast arteries?). The Mayo clinic also mentions that a lot of women have benign calcification after a certain age so it's not something to be too worried about getting yearly check-ups are recommended.

Oh, it seems I misread your post. You're right there's no data in humans, but there's no reason it shouldn't help; similar pathogenesis of the two. One epidemiologic study showed that dietary K2 was only weakly (not-significantly) linked to BAC (breast artery calcification), contrary to the CVD/CAC link.
One of the few proven treatments for soft tissue calcification is (cyclical) etidronate, but it's probably overkill in her case.
Edited by kismet, 13 June 2009 - 03:47 PM.

Edit: I googled breast calcification and from the descripstions it appears that she has macrocalcification which can be associated with aging breast arteries (she is 46), so perhaps K2 might help though you did mention K2 not helping with breast arteries (Assuming BAC is some sort of abbreviation of breast arteries?). The Mayo clinic also mentions that a lot of women have benign calcification after a certain age so it's not something to be too worried about getting yearly check-ups are recommended.

Oh, it seems I misread your post. You're right there's no data in humans, but there's no reason it shouldn't help; similar pathogenesis of the two. One epidemiologic study showed that dietary K2 was only weakly (not-significantly) linked to BAC (breast artery calcification), contrary to the CVD/CAC link.
One of the few proven treatments for soft tissue calcification is (cyclical) etidronate, but it's probably overkill in her case.

So, K2 does not protect against the possible side effects of too much D3? The issue of D3 increasing the risk of soft tissue calcification has been discussed on other threads and someone mentioned K2 could protect against that. In fact one of the reasons I was taking K2 was because I thought it protected against soft tissue calcification. However, I only take 2,000 IU of D3 which scientists believe is a safe dosage so I don't think I should be worried about it, but what about those who take 5,000-10,000 IU; would Vitamin A protect against the side affects of D3? Also, my firend no longer wants to take her Calcium supplement. She believes the calcium supplements had something to do with her breast calcifications. I highly doubt it though since the search I performed says it can be caused by inflammation, past injuries or aging arteries.
Edited by Dmitri, 13 June 2009 - 08:02 PM.

This suggests that too much or too little vitamin D activity leads to inappropriate calcification, reinforcing the need for supplementation guided by blood tests:

1: J Steroid Biochem Mol Biol. 2009 Mar;114(1-2):78-84.Links
Vitamin D and aging.
Tuohimaa P. Medical School, 33014 University of Tampere, Finland. pentti.tuohimaa@uta.fi

Recent studies using genetically modified mice, such as FGF23-/- and Klotho-/- mice that exhibit altered mineral homeostasis due to a high vitamin D activity showed features of premature aging that include retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism and short lifespan. The phenotype reversed by normalizing vitamin D and/or mineral homeostasis. Thus, hypervitaminosis D due to an increased 1alpha-hydroxylase activity seems to be a cause of the premature aging. In several studies, we have described that a complete or partial lack of vitamin D action (VDR-/- mice and CYP27B1-/-) show almost similar phenotype as FGF23-/- or Klotho-/- mice. VDR mutant mice have growth retardation, osteoporosis, kyphosis, skin thickening and wrinkling, alopecia, ectopic calcification, progressive loss of hearing and balance as well as short lifespan. CYP27B1-/- mice do not show alopecia nor balance deficit, which might be apoVDR-dependent or calcidiol-dependent. The features are typical to premature aging. The phenotype is resistant to a normalization of the mineral homeostasis by a rescue diet containing high calcium and phosphate. Taken together, aging shows a U-shaped dependency on hormonal forms of vitamin D suggesting that there is an optimal concentration of vitamin D in delaying aging phenomena. Our recent study shows that calcidiol is an active hormone. Since serum calcidiol but not calcitriol is fluctuating in physiological situations, calcidiol might determine the biological output of vitamin D action. Due to its high serum concentration and better uptake of calcidiol-DBP by the target cells through the cubilin-megalin system, calcidiol seems to be an important circulating hormone. Therefore, serum calcidiol might be associated with an increased risk of aging-related chronic diseases more directly than calcitriol. Aging and cancer seem to be tightly associated phenomena. Accumulation of damage on DNA and telomeres cause both aging and cancer, moreover the signalling pathways seem to converge on tumour suppressor protein, p53, which seems to be regulated by vitamin D. Also, the insulin-like growth factor signalling pathway (IGF-1, IGFBPs, IGFR) and fibroblast growth factor-23 (FGF-23) regulate growth, aging and cancer. Vitamin D can regulate these signalling pathways, too. Also NF-kappaB and telomerase reverse transcriptase (TERT) might be molecular mechanisms mediating vitamin D action in aging and cancer. Calcidiol serum concentrations show a U-shaped risk of prostate cancer suggesting an optimal serum concentration of 40-60 nmol/L for the lowest cancer risk. Therefore, it is necessary to study several common aging-associated diseases such as osteoporosis, hypertension and diabetes known to be vitamin D-dependent before any recommendations of an optimal serum concentration of calcidiol are given.

PMID: 19444937 [PubMed - indexed for MEDLINE

So, K2 does not protect against the possible side effects of too much D3? The issue of D3 increasing the risk of soft tissue calcification has been discussed on other threads and someone mentioned K2 could protect against that.

Most probably it does, although, I don't think that vitamin D promotes calcification or CVD at levels of ~50ng/ml. I just pointed out that, interestingly, an epidemiologic study showed no association with BAC after adjusting for confounders, while many studies confirmed an association with regular CVD and other types of arterial calcification...

Also, my firend no longer wants to take her Calcium supplement. She believes the calcium supplements had something to do with her breast calcifications. I highly doubt it though since the search I performed says it can be caused by inflammation, past injuries or aging arteries.

The science on calcium is indeed conflicting (won't hurt to drop it if she doesn't desperately need it and replaces it with vitamin K/D). Aging is most likely the culprit...
Edited by kismet, 13 June 2009 - 09:05 PM.

This suggests that too much or too little vitamin D activity leads to inappropriate calcification, reinforcing the need for supplementation guided by blood tests:

1: J Steroid Biochem Mol Biol. 2009 Mar;114(1-2):78-84.Links
Vitamin D and aging.
Tuohimaa P. Medical School, 33014 University of Tampere, Finland. pentti.tuohimaa@uta.fi

Recent studies using genetically modified mice, such as FGF23-/- and Klotho-/- mice that exhibit altered mineral homeostasis due to a high vitamin D activity showed features of premature aging that include retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism and short lifespan. The phenotype reversed by normalizing vitamin D and/or mineral homeostasis. Thus, hypervitaminosis D due to an increased 1alpha-hydroxylase activity seems to be a cause of the premature aging. In several studies, we have described that a complete or partial lack of vitamin D action (VDR-/- mice and CYP27B1-/-) show almost similar phenotype as FGF23-/- or Klotho-/- mice. VDR mutant mice have growth retardation, osteoporosis, kyphosis, skin thickening and wrinkling, alopecia, ectopic calcification, progressive loss of hearing and balance as well as short lifespan. CYP27B1-/- mice do not show alopecia nor balance deficit, which might be apoVDR-dependent or calcidiol-dependent. The features are typical to premature aging. The phenotype is resistant to a normalization of the mineral homeostasis by a rescue diet containing high calcium and phosphate. Taken together, aging shows a U-shaped dependency on hormonal forms of vitamin D suggesting that there is an optimal concentration of vitamin D in delaying aging phenomena. Our recent study shows that calcidiol is an active hormone. Since serum calcidiol but not calcitriol is fluctuating in physiological situations, calcidiol might determine the biological output of vitamin D action. Due to its high serum concentration and better uptake of calcidiol-DBP by the target cells through the cubilin-megalin system, calcidiol seems to be an important circulating hormone. Therefore, serum calcidiol might be associated with an increased risk of aging-related chronic diseases more directly than calcitriol. Aging and cancer seem to be tightly associated phenomena. Accumulation of damage on DNA and telomeres cause both aging and cancer, moreover the signalling pathways seem to converge on tumour suppressor protein, p53, which seems to be regulated by vitamin D. Also, the insulin-like growth factor signalling pathway (IGF-1, IGFBPs, IGFR) and fibroblast growth factor-23 (FGF-23) regulate growth, aging and cancer. Vitamin D can regulate these signalling pathways, too. Also NF-kappaB and telomerase reverse transcriptase (TERT) might be molecular mechanisms mediating vitamin D action in aging and cancer. Calcidiol serum concentrations show a U-shaped risk of prostate cancer suggesting an optimal serum concentration of 40-60 nmol/L for the lowest cancer risk. Therefore, it is necessary to study several common aging-associated diseases such as osteoporosis, hypertension and diabetes known to be vitamin D-dependent before any recommendations of an optimal serum concentration of calcidiol are given.

PMID: 19444937 [PubMed - indexed for MEDLINE

Thank You for posting that information. Do you know what people who take 10,000 IU think of the study? If I recall Duke takes 10,000 IU and his blood levels were 79ng; I asked him why he was taking such a high dose when Kismet had previously posted that levels above 50 ng could be harmful, yet he ignored me. However, he replied to someone else about a cardiologist recommending serum levels between 60-70 ng.

Here's the thread: http://www.imminst.o...o...30&start=30
Edited by Dmitri, 14 June 2009 - 04:05 AM.

Krillin seems to think the levels should be in the mid-50's, and has some interesting posts about the issue.

Also, I was at 19ng/mL when I got my vitamin D levels first checked (after a vacation in Miami, no less!) but supplementing at 5000IU/day (with one tablet of LEF's Super K) made my levels shoot up to the high 60's in a couple of months. Individual metabolism varies considerably.

This is a topic I have been interested in for a while. Specifically the decalcification of the pineal gland. Have you looked at Serrapeptase? I haven't tried it but have seen anecdotal reports of its ability to chelate and remove bad stuff for lack of a better word.

Pineal gland calcification? Has this been a radiographic finding? If so, does it entail a sleep pathology?

So, K2 does not protect against the possible side effects of too much D3?

Read this blog and another posting the following month. The first link comments on vitamin A's role in protecting against vitamin D toxicity by "curbing excess production of vitamin K-dependent proteins".

My thinking is that conclusions about the relationship between vitamins D and K when vitamin A is not controlled for in the experiment are suspect.

This state of affairs sucks when you think about it. With much of the world at non-optimal levels of vitamin D, it throws the baseline way off for any number of experiments.

StrangeAeons,
I believe that the pineal starts to calcify in most around puberty. I am not sure if there is
a beneficial reason for this change of condition but its gets more calcified through out life and
hinders melatonin output. I don't know that there is any way to reverse this but it has been a curiousity for me for quite some time now. Just imagine having the pineal of a 12 year old. Or the thymus. I have read that arginine may play some role in the reversal of the thymus shrinkage.

This is a topic I have been interested in for a while. Specifically the decalcification of the pineal gland.

H.P. Lovecraft had a cure for that, but the side effects were horrendous...

But seriously, never heard of calcifying pineal glands before. Guess maybe supplementing with melatonin as you age would overcome the calcification issue?
Edited by nameless, 29 June 2009 - 09:33 PM.

I just recalled that I recently read that sun gazing may strenthen the pineal. Not sure if it decalcifies it but that is worth looking into.

This is a topic I have been interested in for a while. Specifically the decalcification of the pineal gland.

H.P. Lovecraft had a cure for that, but the side effects were horrendous...

But seriously, never heard of calcifying pineal glands before. Guess maybe supplementing with melatonin as you age would overcome the calcification issue?

Here's some strange stuff : http://www.projectav...php/t-1539.html
I've heard legends about Frankincense and pineal decalcification before.

There is a recognised medical condition for extreme calcification of the vascular system known as calciphylaxis.

I have found this article:

Nanobacteria-Caused Mitral Valve Calciphylaxis in a Man With Diabetic Renal Failure

http://www.medscape....rticle/469588_1

"The electron microscopy of the thrombotic vegetation demonstrated nanobacterium as a nidus for carbonate apatite formation. Investigation for the presence of nanobacteria in the multiple organs involved in systemic calciphylaxis may be of help in elucidating the pathogenesis of this frequently fatal disorder."

Could much of the formation of the "carbonate apatite" and calcification of tissues actually be pathological calcification?

http://www.heartfixe...lcification.htm

From the above article:

"N. sanguineum can be cultured from kidney stones, calcified arteries, and polycystic kidney tissue (which involves pathological calcification), and its antigen has been detected in dental pulp stones and calcified pineal tissue. "
Edited by caston, 30 June 2009 - 02:54 PM.

This stuff is really interesting..

Someone even listed on the stock exchange with a company dedicated to this concept:

http://www.nanobaclabs.com/

What do you all think?

This stuff is really interesting..

Someone even listed on the stock exchange with a company dedicated to this concept:

http://www.nanobaclabs.com/

What do you all think?

Nanobacteria are mineralo fetuin complexes.
Raoult D, Drancourt M, Azza S, Nappez C, Guieu R, Rolain JM, Fourquet P, Campagna B, La Scola B, Mege JL, Mansuelle P, Lechevalier E, Berland Y, Gorvel JP, Renesto P. Unité des Rickettsies, Centre National de la Recherche Scientifique UMR 6020, IFR 48, Faculté de Médecine, Marseille, France. Didier.Raoult@medecine.univ-mrs.fr

"Nanobacteria" are nanometer-scale spherical and ovoid particles which have spurred one of the biggest controversies in modern microbiology. Their biological nature has been severely challenged by both geologists and microbiologists, with opinions ranging from considering them crystal structures to new life forms. Although the nature of these autonomously replicating particles is still under debate, their role in several calcification-related diseases has been reported. In order to gain better insights on this calciferous agent, we performed a large-scale project, including the analysis of "nanobacteria" susceptibility to physical and chemical compounds as well as the comprehensive nucleotide, biochemical, proteomic, and antigenic analysis of these particles. Our results definitively ruled out the existence of "nanobacteria" as living organisms and pointed out the paradoxical role of fetuin (an anti-mineralization protein) in the formation of these self-propagating mineral complexes which we propose to call "nanons." The presence of fetuin within renal calculi was also evidenced, suggesting its role as a hydroxyapatite nucleating factor.

PMID:18282102