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Vitamin K2 vs PC

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Prostate Cancer
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Posted 2/19/2020 5:02 AM (GMT 0)
Well, those mice luck out once again. Also, seems to me these doses are really high ( in mg per kg) compared to what we are likely to get from supplementation, much less from diet. And of course, this proves nothing as far as us humans go. And I am really hoping that this general info won't trigger anyone, it is just one study among many to keep in mind. And it is a bit old, from 2013, I'm surprised I am just finding it. Also, I do not suggest skipping whatever your treatment is or will be and just going with vitamin K2. Even in combo with vitamin D3, which it seems to pair nicely with. I do not recommend ignoring medical advice and trying to cure yourself with vitamins instead. Don't do it!

Still, it seems to me worthy of discussion, or just a quick read for general back ground info. It will probably be a long time before we see any actual human trials, if ever. Still, for me anyway, it seems worth being aware of, as we all pursue our conventional treatments. I am including some highlights here, and you can just skim for the bold areas, but if interested, I suggest reading the entire study:
https://www.ncbi.nlm.nih.gov/pmc/articles/pmc3767046/#__ffn_sectitle
"Vitamin K2, a Naturally Occurring Menaquinone, Exerts Therapeutic Effects on Both Hormone-Dependent and Hormone-Independent Prostate Cancer Cells

In recent years, several studies have shown that vitamin k2 (VK2) has anticancer activity in a variety of cancer cells. The antitumor effects of VK2 in prostate cancer are currently not known. In the present study, we sought to characterize the anticancer potential of VK2 in both androgen-dependent and -independent prostate cancer cells. Our investigations show that VK2 is able to suppress viability of androgen-dependent and androgen-independent prostate cancer cells via caspase-3 and -8 dependent apoptosis. We also show that VK2 treatment reduces androgen receptor expression and PSA secretion in androgen-dependent prostate cancer cells. Our results also implicate VK2 as a potential anti-inflammatory agent, as several inflammatory genes are downregulated in prostate cancer cells following treatment with VK2...........Finally, in a nude mice model, VK2 administration resulted in significant inhibition of both androgen-dependent and androgen-independent tumor growth. Overall, our results suggest that VK2 may be a potential therapeutic agent in the treatment of prostate cancer.................

Those undergoing hormonal therapy eventually develop aggressive hormone unresponsive disease. Hence, one of the major focuses in prostate cancer research is the discovery of better chemotherapeutic agents for the advanced hormone-resistant, metastatic form of this disease.

Vitamin k is a fat soluble vitamin that plays a major role in the clotting cascade by acting as a coenzyme for a vitamin k dependent carboxylase that catalyzes the carboxylation of glutamic acid residues to produce gamma-carboxyglutamic acid . Vitamin k also appears to work in regulation of bone metabolism through a similar mechanism via gamma carboxylation of bone matrix proteins . There are two naturally-occuring vitamin k compounds, vitamin k1 (phylloquinone) and vitamin k2 (menaquinone). Interestingly, vitamin k2 (VK2) intake seems to be associated with greater benefits of reduced coronary calcification when compared to vitamin k1 consumption . In recent years, various reports have shown that VK2 has antioncogenic effects in various cancer cell lines, including leukemia, lung cancer, ovarian cancer, and hepatocellular cancer [5–9]. Although the exact mechanisms by which VK2 exert its antitumor effect are still unclear, processes such as cell cycle arrest, apoptosis and induction of differentiation appear to contribute to the therapeutic effects of VK2 [5–9]. The antitumor effects of VK2 have been most extensively studied in hepatocellular cancer. Yamamoto and colleagues showed that downregulation of hepatoma-derived growth factor is partially responsible for the growth suppression properties of VK2 in hepatocellular cell lines [10]. In another study, Otsuka and colleagues showed that VK2 inhibits growth and invasion of hepatocellular cell lines via activation of protein kinase A [11]. Recent studies also suggest a role for VK2 in the prevention of cancer, as a randomized trial of 43 women with viral hepatitis treated with high dose VK2 showed an 80% decreased risk of developing hepatocellular carcinoma [12].

In view of VK2 potential to reduce osteoporosis [13] and atherosclerosis risk and given the fact that these two pathologies are frequently associated with prostate cancer patients undergoing hormonal therapy [14, 15], development of VK2 as a treatment strategy for prostate cancer would have far reaching impact on prostate cancer patients. Previously, Nimptsch et al. showed an inverse relationship between dietary intake of VK2 and risk of prostate cancer [16]. Interestingly, serum undercarboxylated osteocalcin (ucOC), a biomarker of vitamin k status, is inversely associated with VK2 intake and the development of advanced prostate cancer [17]. These studies thus suggest that the intake of VK2 may be beneficial in preventing the progression of prostate cancer. Moreover, VK2 is also shown to enhance the chemotherapeutic efficacy of conventional anticancer drug Sorafenib in hepatocellular carcinoma [18]. Unlike its synthetic counterpart, vitamin k3, there are no known side effects associated with ingestion of high doses of VK2 [19]. To date, however, no studies have been conducted to assess the therapeutic potential of VK2 in the treatment of prostate cancer. To our knowledge, this is the first comprehensive study which demonstrates the therapeutic potential of VK2 against both forms of prostate cancer (hormone dependent and hormone independent) using in vitro and in vivo models with mechanistic details of VK2 action. ...................................

Fluorescent microscopic analysis demonstrated that LNCaP, 22RV1, and DU-145 cells treated with VK2 were indeed undergoing apoptosis (Figure 3)............All three cell lines displayed a dramatic increase in apoptosis following treatment (P < 0.05), as shown by a high caspase activity after the treatment...........3.5.6. VK2 Inhibits Tumor Growth of Human Prostate Cancer Cell Xenografts Implanted in Immunodeficient Mice

We next sought to determine the antitumor effects of VK2 in vivo against androgen-dependent and androgen-independent prostate cancer cells. Nude mice were subcutaneously implanted with LNCaP, 22RV1, and DU145 cells. Nude mice in the treatment group were fed water containing VK2 (20 mg/kg/day) for 6 weeks. These results revealed treatment with VK2 significantly reduced LNCaP, 22RV1, and DU145 derived tumor growth in vivo (Figure 10). Based upon these results, treatment with VK2 appears to inhibit tumor growth of both androgen-dependent and androgen-independent cells in vivo.

4. Discussion

Previous epidemiological studies have linked low dietary intake of VK2 and the development of prostate cancer [16, 17]. Little is known, however, regarding the antitumor potential of VK2 in prostate cancer cell lines. In the present study, we therefore sought to characterize the antitumor potential of VK2 in both androgen-dependent and independent-prostate cancer cells. Apoptosis or programmed cell death is a key process regulating cancer development and progression. Dysregulation of apoptosis represents one of the major hallmarks of cancer [37]. Therapies that cause apoptotic elimination of cancer cells with limited side effects are therefore critical in the treatment of cancer. Our results of this study show that VK2 is able to suppress viability of androgen-dependent and androgen-independent prostate cancer cell lines in a dose dependent manner............ We also show here that the reduced proliferation induced by VK2 is the result of caspase-3 and -8 dependent apoptosis. Thus, our study reiterates the apoptotic potential of VK2 against prostate cancer cells as has been previously reported for other cancer types [5–7].

5. Conclusion

Collectively, the findings in the present study suggest that caspase-3 induction, downregulation of phosphorylated AKT, inhibition of NF-kB, and reduction of androgen receptor expression may represent the molecular mechanisms by which VK2 reduces cell proliferation, induces apoptosis, and reduces the angiogenic potential of prostate cancer cells as outlined in Figure 11. Based upon the previous epidemiological studies of vitamin k2 in prostate cancer [16, 17, 62] and the results presented here, further investigations are warranted to elucidate the therapeutic potential of VK2 against androgen-dependent and androgen-independent prostate cancer. ".
Posted 2/19/2020 12:43 PM (GMT 0)
Here's an article with some more recent references.

Djin
Posted 2/19/2020 3:30 PM (GMT 0)
Collectively, the findings in the present study suggest that caspase-3 induction, downregulation of phosphorylated AKT, inhibition of NF-kB, and reduction of androgen receptor expression may represent the molecular mechanisms by which VK2 reduces cell proliferation, induces apoptosis, and reduces the angiogenic potential of prostate cancer cells as outlined in Figure 11. Based upon the previous epidemiological studies of vitamin k2 in prostate cancer [16, 17, 62] and the results presented here, further investigations are warranted to elucidate the therapeutic potential of VK2 against androgen-dependent and androgen-independent prostate cancer. ".
==
... and in the background you can hear the sound of crickets chirping
Posted 2/19/2020 4:28 PM (GMT 0)

DjinTonic said...
Here's an article with some more recent references.

Djin

Thanks for the link! Interestinly, there is also this in that article:
"
Vitamin K is a group of naturally occurring fat-soluble chemicals characterized by a common naphthoquinone ring. This structural feature they share with some drugs used for cancer chemotherapy.
This partly explains why vitamin K has attracted interest in the prevention and treatment of cancer.

The anticancer effect of vitamin K was first reported about 60 years ago when the intravenous injection of the vitamin K3 (Menadione-synthetic form of vitamin K) extended the survival of inoperable bronchial carcinoma patients.

Vitamin K3 in combination with vitamin C enhances the suppression of cancer cell growth by activating oxidative stress. Oxidative stress refers to a disproportion between the production of reactive oxygen species in the cells and the ability of the organism to detoxify them or neutralize the resulting damage. Reactive oxygen species are intermediary products of many biological reactions. They contain oxygen and readily react with proteins, lipids, and DNA, often causing their damage. Examples of reactive oxygen species include peroxides, superoxide, hydroxyl radical and oxygen.".

Why is that interesting(to me at least)? Back when I got my high risk diagnosis, my PSA had been rising pretty rapidly. It even went up a good bit ( from 9 something to just shy of 11) during the 3 weeks I was waiting to see a urologist, during which time I had a round of Cipro, hoping to bring it down if it was prostatitis. At that time there was an FDA "orphan" drug being investigated called Apatone. It had a couple of very interesting placebo controlled trials, then it just disappeared, never to be heard of again far as I can tell. Maybe they dropped it because of the difficulty getting a patent(it was nothing more than a certain ratio of vitamin K3(synthetic K1) and vitamin C. Or maybe it was dropped for some other reason maybe, just no good, who knows? I linked these studies here back about the time I joined.

So, as it was just a certain ratio of those 2 vitamins, I decided to take it at a dose = to about 10 gms of Vit C per day, along with however much Vitamin k3 that would be (there was a product called Prosstay back then that contained those ratios). I did this for the about 2 months after my G9 diagnosis as I tried to decide on RT vs surgery, ended up with surgery. Anyway, coincidentally I'm sure, for the first time in all the years I had been checking my PSA(a bit over a decade), after those 2 months- and following my biopsy(which can raise PSA for a while) and diagnosis- my PSA dropped about 25%. This reference in your article about K3 combined with C is the first I have read about that in many several years.
Posted 2/19/2020 9:10 PM (GMT 0)
I had added vit K with D, still sounds like a good thing,..
especially for mice!
Posted 2/20/2020 1:23 PM (GMT 0)
The mice are doing great.
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