135 replies to this topic

[zawy]

I haven't been provided a link, or study so I am continuing with this product.

I provided the link to the abstract in this thread, right below the quote. I had to pay to get the full text. I'm not sure it completely proves curcumin causes cancer or has the other dangers, but humans have never been exposed to it in vivo due to it's lack of bio-availability. So effectively delivering it in a lipo form deserves caution, including knowledge of the published dangers. We have evolved to cope with compounds that can be made from low temp, low pressure, DNA-based "cells" and curcumin is an example of this class. But we have not specifically been exposed to it internally in the past, so it's not completely clear it should be treated as something safer than pharmaceuticals. If smaller mammals do not have the bio-availability problem, then maybe we still have some of the general genetic design that confers some protection to being exposed to it directly in the blood stream. This is the case with resveratrol, which does not have the dangers reported above for curcumin, and resveratrol is still not being delivered as effectively as the new curcumin forms are attempting. So that's two "orders of magnitude" that pure curcumin in the blood could be more dangerous than glucuronated and sulfonated forms of resveratrol in the blood.

Even large doses of resveratrol have to be considered carefully because they are way outside the range of evolutionary adaptation. Comparable examples are high dose selenium and I.V. vit C. The second most reliable result of taking resveratrol (as reported and tabulated in the resv forum) is fairly serious tendon and/or ligament injuries in those taking more than 1 g/day. No one knows the dangers of doing it long term. Again, just a brief look indicates that if someone takes a "deliverable" form of high-dose curcumin, they should expect much worse until research says otherwise. My comments do not apply if someone has a life-threatening disease that has a trial going on, like colon cancer, prancreatic cancer, or Alzheimer's. Then by all means, take resv and curcumin to the max.

Here is more from the 2005 "anti-curcumin" work:

Here, we report that
curcumin induces p53 degradation and, thus, inhibits p53-
induced apoptosis. Curcumin induced degradation of p53 under
conditions of defective ubiquitination, like several NQO1 inhibitors
including dicoumarol (14, 15, 20, 21, 23). Curcumin was also
shown to induce degradation of different proteins, including
cyclin D1 (39), p185ErbB2 (40, 41), c-Jun (42), CEBP, and
CEBP (43). It will be interesting to determine whether these
proteins are degraded by curcumin also by an ubiquitin independent
mechanism.
NQO1 is a flavoenzyme that catalyzes two electron reduction
of quinones and some other electrophiles by using NAD(P)H as
an electron donor. We found that curcumin inhibits NQO1
activity. Like dicoumarol that competes with NAD(P)H for
binding to NQO1, curcumin also disrupted WT p53-NQO1
complexes and induced p53 degradation. Curcumin inhibits the
activity of thioredoxin reductase (29), another flavoprotein that
uses NADPH as an electron donor (44). These findings suggest
that curcumin may displace NAD(P)H from NQO1 and possibly
also from other NAD(P)H using enzymes and, thus, inhibit their
activity.
Our studies have shown that curcumin and dicoumarol destabilize
WT p53 by inhibiting NQO1 activity and promoting the
dissociation of p53–NQO1 complexes. Curcumin and dicoumarol
might also affect p53–NQO1 interaction by causing
changes in the p53 molecule itself. Many of the cellular functions
of p53 are regulated by various redox regulating p53-interacting
proteins including thioredoxin (reviewed in ref. 15). Curcumin
inhibits the activity of thioredoxin reductase, resulting in reduced
binding of p53 to DNA, possibly due to changes in p53
folding (29). In addition to inhibiting NQO1 activity, curcumin
might, therefore, also change the folding of p53 in a manner that
disrupts NQO1–p53 complex formation. It was recently reported
that NAD and NADH bind to p53 tetramers and change their
conformation (45). NADH also induces a conformational
change in NQO1 (46) and increases p53–NQO1 interaction (22).
Thus, NAD(P)H could affect both p53 and NQO1 to promote
their interaction and p53 stabilization. We have shown that
NQO1 is physically associated with the 20S proteasomes and this
association prevents the degradation of p53 that is bound to
NQO1 (22). Thus, by displacing NAD(P)H and dissociating NQO1–p53 complexes, curcumin and dicoumarol promote the
ubiquitin-independent 20S proteasome-mediated degradation of
p53. We have previously shown that binding of NQO1 to the
human cancer hot-spot p53 R273H mutant was 3-fold higher
compared to its binding to WT p53 (23). The failure of dicoumarol
and curcumin to effectively dissociate NQO1–p53 R273H
complexes can explain the resistance of the p53 R273H mutant
to degradation by both of these compounds. However, R273H
can still be degraded by the ubiquitin-dependent pathway by
overexpression of Mdm2 (23) or by the ubiquitin-independent
pathway by knocking down NQO1 by siRNA.

22. Asher, G., Tsvetkov, P., Kahana, C. & Shaul, Y. (2005) Genes Dev. 19, 316–
321.
23. Asher, G., Lotem, J., Tsvetkov, P., Reiss, V., Sachs, L. & Shaul, Y. (2003) Proc.
Natl. Acad. Sci. USA 100, 15065–15070.
29. Moos, P. J., Edes, K., Mullally, J. E. & Fitzpatrick, F. A. (2004) Carcinogenesis
25, 1611–1617.
39. Mukhopadhyay, A., Banerjee, S., Stafford, L. J., Xia, C., Liu, M. & Aggarwal,
B. B. (2002) Oncogene 21, 8852–8861.
40. Hong, R. L., Spohn, W. H. & Hung, M. C. (1999) Clin. Cancer Res. 5, 1884–1891.
41. Tikhomirov, O. & Carpenter, G. (2003) Cancer Res. 63, 39–43.
42. Uhle, S., Medalia, O., Waldron, R., Dumdey, R., Henklein, P., Bech-Otschir,
D., Huang, X., Berse, M., Sperling, J., Schade, R. & Dubiel, W. (2003) EMBO
J. 22, 1302–1312.
43. Balasubramanian, S. & Eckert, R. L. (2004) J. Biol. Chem. 279, 24007–24014.
44. Mustacich, D. & Powis, G. (2000) Biochem. J. 346, 1–8.
45. McLure, K. G., Takagi, M. & Kastan, M. B. (2004) Mol. Cell. Biol. 24, 9958–9967.

Edited by zawy, 18 September 2009 - 01:48 PM.

[zawy]

The following 2008 review has a good section on the "cautionary tale" of curcumin. I saved it to my hard drive because it may not be available on that NZ website for long.

http://www.curcumin....cial-Trials.pdf

Eventhough not bio-available, it appears to still be active away from the G.I. which is why so many trials are in progress. So I think 1 to 2 g/d would be good for good health, but I would be cautious at this level if it is somehow delivered "as curcumin" to the blood. I might stick with simple curcumin at 1 g/d with peperine. This would achieve about the 0.2% in diet used in some of the rodent work.

Edited by zawy, 18 September 2009 - 02:35 PM.

[tham]

Tocopherol succinate and the analog, alpha-TEA.


http://www.ebmonline.../full/229/9/954

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....pubmed/15377836

http://repositories....andle/2152/2729

[ppp]

Tocopherol succinate and the analog, alpha-TEA.


http://www.ebmonline.../full/229/9/954

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....pubmed/15377836

http://repositories....andle/2152/2729

Isn't the problem with this that when taken orally it gets rapidly metabolised to other forms of vitamin E that don't have the same apoptosis causing effect?

Edited by ppp, 18 September 2009 - 06:48 PM.

[Lufega]

how about IP 6?

The Overlooked Cancer Cure From Japan

[tham]

The second study showed that "dry" vitamin E succinate
does have some benefit in lung cancer.

Maybe Zawy could give some insight as to an oral conversion
of the IC50 of 18 mcg/ml mentioned in the study.

http://www.ncbi.nlm....l=pubmed_docsum


Thus Abram Hoffer's inclusion of tocopherol succinate :

http://www.imminst.o...o...=0&p=295417

[tham]

Monoclonal antibodies in cancer.

http://jco.ascopubs....full/26/11/1774

http://www.sciencece...ancer-treatment

[ppp]

The second study showed that "dry" vitamin E succinate
does have some benefit in lung cancer.

Maybe Zawy could give some insight as to an oral conversion
of the IC50 of 18 mcg/ml mentioned in the study.

http://www.ncbi.nlm....l=pubmed_docsum


Thus Abram Hoffer's inclusion of tocopherol succinate :

http://www.imminst.o...o...=0&p=295417

I swapped emails with a researcher who had looked at the anti-cancer efficacy of vitamin E succinate. She pointed out that the in vivo studies generally used intraperitoneal or intravenous delivery, and that oral delivery was useless for achieving the required doses. I'd love to be proved wrong on this, so if anyone has evidence to the contrary please go ahead.

[zawy]

Maybe Zawy could give some insight as to an oral conversion
of the IC50 of 18 mcg/ml mentioned in the study.

http://www.ncbi.nlm....l=pubmed_docsum

I swapped emails with a researcher who had looked at the anti-cancer efficacy of vitamin E succinate. She pointed out that the in vivo studies generally used intraperitoneal or intravenous delivery, and that oral delivery was useless for achieving the required doses.

18 ug/mL or 18 mg/L was in vitro. So you would have to inject 5*18mg = 90 mg to temporarily get 18 mg/L in 5 L of blood. As I said before, I don't know how well these in vitro studies are comparable to blood volume like this, but I've seen others here do it. But absorption, metabolization, and retention are the far greater determiner of outcome than error in this comparison. There are also more "wholistic" effects from not being in vivo.

Getting back to selenite, the following study in rats shows very high toxicity of the selenite and selenate forms at 6 ppm in diet, most of them dying in only 3 weeks. 6 ppm in diet for humans is 3,000 mcg/day to 6,000 mcg/day depending if they are talking wet or dry weight, probably wet (6,000 mcg/day). This is the calorie conversion method is most accurate for many compounds (more accurate than body surface area used by EPA and FDA which provides a larger margin of safety for toxic compounds). However, for some things like some vitamins, straight body weight conversion can be more accurate. This might mean 30,000 is the equivalent dose to kill most humans in 3 weeks, if the comparison to rats and humans is valid.

http://jn.nutrition....print/104/3/306

In support of the body-weight conversion method, 7 ppm selenite in chicken diet for at least 8 weeks was not deadly but had large negative effects in reproduction. This is still anout 6,000 mcg/d on the calorie method. The hens weigh about 2 kg and ate about 130 g/day.

http://jn.nutrition....ract/108/7/1114


The less effective, safer selenium form given to people at 15,000 mcg/day in the phase 1 trial was very safe for one week, and 7,500 mcg/day was safe long term. The different forms of selenium seem to be similarly toxic in rats, and hopefully that same situation in humans would exist.

http://www3.intersci...557480/abstract

Rats getting 40 ug/kg/d selenite for 15 days showed negative liver effects. This would be 40*70 = 2,800 ug/d in 70 kg people using straight body weight conversion.

http://www3.intersci...557480/abstract

This is probably the best (and oldest) study on toxicity in mice and rats due to using selenite and selenate in drinking water (i like the comparison better). 0.2% in water seemed to be pretty toxic. This may be different than a prior post. That would be 4,000 mcg/day in 2 L/day people. Generally there did not seem to be a big difference in selenite and selenate in their review of past work.
http://jn.nutrition....eprint/92/3/334


from a web site on th enegative effects of selenite:
"larger doses of inorganic selenium has an oxidative effect that increases undesirable lipofuscin production. [36] The selenium in inorganic selenite is in the plus four valance state which is very oxidative. The selenium of selenomethionine is in the minus two valance state. The lipofuscin accumulation in the liver can be accounted for by the fact that in order for selenium to go from the inorganic plus four valance state to the plus minus valance state, six electrons must be obtained from liver cells. The safety of inorganic selenium is about one-third that of selenomethionine. [37]

Inorganic sources of selenium do not find their way to muscle protein to an appreciable extent. If laboratory animals are fed selenomethionine, selenium soon increases in all organs, muscles, GPX and hemoglobin. When inorganic selenium is fed to animals, it accumulates in the liver, kidneys and GPX.

Inorganic selenium reacts spontaneously with sulphydryl groups to form selenotrisulfides. This can severely disrupt the structure of proteins. Inorganic selenium reacts with the sulfhydryl groups of glutathione to form selenopersulfide and free selenide. Inorganic selenium, due to its free-radical promoting oxidative nature, is mutagenic and has caused cataracts at high doses in mice. [44] In contrast, selenium-containing amino acids are stable, less toxic, and do not have mutagenic or oxidizing activity."

http://www.healthy.n...icle.asp?Id=577

Based on this very limited toxicity info, even as a cancer patient, I would be very careful taking 3,750 mcg/day of selenite as indicated by the previous cancer patient in tham's post. Tham's previous reference to a researcher saying 1,700 mcg (?) is a upper safe limit may be about right (same author as the above quote). This is less wiggle room for cancer patients than I previously thought and posted here. So for myself with serious cancer, I would start out at 5,000 mcg for no more than a week and then drop to 2,500 mcg if I weighed 150 pounds, and try to check liver function. I have taken 5,000 mcg in a single dose on three occasions in the past two days and seem to feel not quite up to par, more so after the 3rd dose this morning before reading and typing all the above, on an empty stomach. I also had some inflammation in the finger joints and lips this morning which occurs if I eat too much of certain foods like "sulphited" alcohol or during chronic weeks of spicy tomato paste. It's been months since the last instance.

Edited by zawy, 20 September 2009 - 03:25 PM.

[zawy]

More on selente toxicity and availability:

"the lowest reported daily dose that produced early pathological changes in the nails characteristic of selenosis was circa 900 /tg of Se (as Na2SeO3) [selenite] consumed over 2 yr"

http://jn.nutrition....print/116/1/170

The above was citing the 1983 article below:

"In our institute, a male worker, 62 yr old, believing that selenium would benefit his health, took one tablet of 2 mg sodium selenite per day for more than 2 yr, until he was warned that he had been intoxicated. He did not have any symptoms of indisposition but presented with thickened, fragile nails, and garlic odor in dermat excretions. After he stopped his oral sodium selenite, the surface of new nail growth became smooth and gradually recovered. Evidently, an intake of 1 mg Se daily from sodium selenite for a long time is definitely chronically toxic to humans. His blood and hair selenium concentrations were 0.179 ppm [that's 1 uM ... that's less than expected and 5 times less than ideal] and 0.828 ppm on the day he stopped his selenium intake. Therefore, determination of tissue selenium level alone is not adequate for the diagnosis of selenosis without differentiation of the forms of selenium ingested. These observations and those of others suggest that the behavior of organic selenium is different from inorganic. In our endemic selenosis area deformation of the nail may appear, and it is reasonable to assume that the daily dietary selenium [non-selenite] intake of 4.99 mg is chronically toxic. This is five times the critical level of which selenite produced familiar types on the case reported above. "
http://www.ajcn.org/...nt/37/5/872.pdf

Keeping in mind the last quote above is from China in 1983.

OK, so we have sources that say selenite is 3, 5, and 6 times more toxic than organic forms, eventhough it accumulates less. The 3 and 6 times more toxic comments seem to come from re-calculations of the comments above.

[ppp]

More on selente toxicity and availability:

"the lowest reported daily dose that produced early pathological changes in the nails characteristic of selenosis was circa 900 /tg of Se (as Na2SeO3) [selenite] consumed over 2 yr"

http://jn.nutrition....print/116/1/170

The above was citing the 1983 article below:

"In our institute, a male worker, 62 yr old, believing that selenium would benefit his health, took one tablet of 2 mg sodium selenite per day for more than 2 yr, until he was warned that he had been intoxicated. He did not have any symptoms of indisposition but presented with thickened, fragile nails, and garlic odor in dermat excretions. After he stopped his oral sodium selenite, the surface of new nail growth became smooth and gradually recovered. Evidently, an intake of 1 mg Se daily from sodium selenite for a long time is definitely chronically toxic to humans. His blood and hair selenium concentrations were 0.179 ppm [that's 1 uM ... that's less than expected and 5 times less than ideal] and 0.828 ppm on the day he stopped his selenium intake. Therefore, determination of tissue selenium level alone is not adequate for the diagnosis of selenosis without differentiation of the forms of selenium ingested. These observations and those of others suggest that the behavior of organic selenium is different from inorganic. In our endemic selenosis area deformation of the nail may appear, and it is reasonable to assume that the daily dietary selenium [non-selenite] intake of 4.99 mg is chronically toxic. This is five times the critical level of which selenite produced familiar types on the case reported above. "
http://www.ajcn.org/...nt/37/5/872.pdf

Keeping in mind the last quote above is from China in 1983.

OK, so we have sources that say selenite is 3, 5, and 6 times more toxic than organic forms, eventhough it accumulates less. The 3 and 6 times more toxic comments seem to come from re-calculations of the comments above.

Doesn't all this suggest that it's better to stick to 1000mcg of selenite and add in some methyselenocysteine if you want to go higher?

[DeadMeat]

how about IP 6?

The Overlooked Cancer Cure From Japan

IP6 is very interesting. Perhaps also see these abstracts about a supplement/diet/herbal mix or whatever it is, called selected vegetables(SV). Inositol hexaphosphate(IP6) is apparently one of the main active ingredients, although you can't really neglect the other compounds of course. But at least as a whole it seems to work quite well for something non toxic and it even works in humans. Although I assume that for real results, much higher dosages of the active compounds would be necessary.
http://www.ncbi.nlm.nih.gov/pubmed/10453443

This phase I/II study evaluates the influence of selected vegetables (SV) that contain known antitumor components on the survival of stage III-IV non-small cell lung cancer (NSCLC) patients. All patients were treated with conventional therapies. SV was added to the daily diet of 5 stage I patients in the toxicity study group (TG) and 6 stage III and IV patients in the treatment group (SVG), but not to the diet of 13 stage III and IV patients in the control group (CG). Age, Karnofsky performance status (KPS), and body mass index of SVG and CG patients were comparable at entry. KPS declined in the CG patients (79 +/- 8 to 55 +/- 11) but improved in the SVG patients (75 +/- 8 to 80 +/- 13) one to three months after entry. Weight change in the CG, SVG, and TG patients was -12 +/- 5%, -2 +/- 2%, and +4 +/- 4%, respectively. The median survival time and mean survival of the CG patients were 4 and 4.8 months, but in the SVG patients they were 15.5 and 15 months (p < 0.01). No clinical signs of toxicity were found in the TG patients in the 24-month study period. Adding SV to the daily diet of NSCLC patients was found to be nontoxic and associated with improved weight maintenance, KPS, and survival of stage III and IV NSCLC patients.

http://www.ncbi.nlm.nih.gov/pubmed/11588907

Previously, a specific dietary supplement, selected vegetables (SV), was found to be associated with prolonged survival of stage III and IV non-small cell lung cancer (NSCLC) patients. In this study, several anticancer components in SV were measured; the anticancer activity of SV was assessed using a lung tumor model, line 1 in BALB/c mice. SV was also used in conjunction with conventional therapies by stage IIIB and IV NSCLC patients whose survival and clinical responses were evaluated. A daily portion (283 g) of SV was found to contain 63 mg of inositol hexaphosphate, 4.4 mg of daidzein, 2.6 mg of genistein, and 16 mg of coumestrol. Mouse food containing 5% SV (wt/wt) was associated with a 53-74% inhibition of tumor growth rate. Fourteen of the 18 patients who ingested SV daily for 2-46 months were included in the analyses; none showed evidence of toxicity. The first lead case remained tumor free for > 133 months; the second case showed complete regression of multiple brain lesions after using SV and radiotherapy. The median survival time of the remaining 12 patients was 33.5 months, and one-year survival was > 70%. The median survival time of the 16 "intent-to-treat" patients (including ineligible patients) was 20 months, and one-year survival was 55%. The Karnofsky performance status of eligible patients was 55 +/- 13 at entry but improved to 92 +/- 9 after use of SV for five months or longer (p < 0.01). Five patients had stable lesions for 30, 30, 20, 12, and 2 months; two of them, whose primary tumor was resected, used SV alone and demonstrated an objective response of their metastatic tumors. In addition to the two lead cases, eight patients had no new metastases after using SV. Three patients had complete regression of brain metastases after using radiotherapy and SV. In this study, daily ingestion of SV was associated with objective responses, prolonged survival, and attenuation of the normal pattern of progression of stage IIIB and IV NSCLC. A large randomized phase III clinical trial is needed to confirm the results observed in this pilot study.

[Gerald W. Gaston]

IP6 is very interesting. Perhaps also see these abstracts about a supplement/diet/herbal mix or whatever it is, called selected vegetables(SV).

I had never heard of Selected Vegetables/Sun’s Soup until now. Thanks for bringing it up. Here is a link to it on NCI:

http://www.cancer.go...fessional/page4

[niner]

Interesting stuff. After a little digging, I found a place that sells Sun's Soup: http://sunfarmcorp.com/index.htm
It's freeze dried. They won't tell you the price unless you call or write to them. It must be scary high...

[Gerald W. Gaston]

Interesting stuff. After a little digging, I found a place that sells Sun's Soup: http://sunfarmcorp.com/index.htm
It's freeze dried. They won't tell you the price unless you call or write to them. It must be scary high...

Probably so... I'll fill out the form and see what they send me.

From their FAQ:

Why are your products priced the way they are?

Doing clinical research in an attempt to validate claims of efficacy is very expensive. We are attempting to provide our products direct to consumers now at the lowest possible cost. In doing so, we have been able to provide our products as a dietary supplement that is less expensive than almost all dietary supplements in our category on the market today, on a cents per gram per day basis. Since we sell in bulk quantities only, the cost at first might seem high to the consumer, but in the end the consumer will realize the lowest cost on a cents per gram per day basis than other dietary supplement options. Please note that disclosure of our research activities does not constitute an endorsement of any disease modifying claim by our products as we do not make any claims for any product we sell.

[ppp]

@ppp

I don`t know how the situation in UK is regarding mebendazole, in Germany there is a 500mg version, Vermox Forte. Have you tried to get some from an EU drugstore?
There are always several ways to get medicines. In my opinion mebendazole is really worth a try. How is the therapy of your son going on?

In the UK mebendazole is only available OTC as 100mg tablets in packets of 1, 4 or 8. I can find no source of the 500mg tablets you mention. Also cimetidine (tagamet) is a prescription drug. I guess you're right, if I decide to go down this route then an EU or other online pharmacy will be the best option.

Things have not been going well recently. My son's disease has progressed and he now has four tumours in three different sites. We're waiting now to kick off on third line chemo (gemcitibane and docetaxel).

[kismet]

It's nice that you mention IP6, guys, but you're quite mistaken about the dose. The SV extract has nothing to do with IP6 whatsoever, nothing. 63mg is a homeopathic dose and we're not into vodoo, are we? If it did work, then not because of IP6. The best and only human studies used 8-10 grams and all the extensive animal studies use approx. the same metabolic-rate adjusted dose. I think I mentioned this in one of the cancer threads anyway.

Edited by kismet, 21 September 2009 - 04:36 PM.

[tham]

Frankly, I wonder why your friend is not trying the Chinese herbs,
Oldenlandia diffusa and Scutellaria barbata/baicalensis,
particularly when the studies I have linked show activity against
drug resistant SCLC and NSCLC lines ?

Bill too, never showed any interest, for whatever reason.

They are very safe, apart from diarrhea if too much is taken,
and contraindication with warfarin or similar drugs due to
mild anticoagulant effects.

If you find boiling raw herbs tedious and inconvenient, some
Chinest herbal stores also have them as capsules.

Many Chinese in Malaysia are familiar with them, and these
two herbs would be the first they would reach for in cancer.

Scutellaria baicalensis is one of the 50 fundamental herbs
in traditional Chinese medicine. It is also one of the herbs
in this sachet of detoxifying herbal formula granules which
I keep in my office, and take every now and then.

This guy in one of my branch offices, who has the relatively
rare bone and soft tissue cancer, malignant fibrous
histiocytoma (MFH) in his right thigh for nearly a decade,
has been taking OIdenandia capsules and is still doing well.
MFH has a high affinity for lung metastases.


http://www.ehow.com/...-treatment.html


SPC-A1 is an NSCLC line.

http://www.ncbi.nlm....l=pubmed_docsum


B16-F10 is a melanoma lung metastasis model.

http://www.ncbi.nlm....l=pubmed_docsum


H69VP, multidrug-resistant SCLC line.

http://www.ncbi.nlm....l=pubmed_docsum


A549, NSCLC. Wogonin is one of the principal anticancer
flavonoid in both S.baicalensis and barbata.

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum


SPC-A1, NSCLC.

http://www.ncbi.nlm....l=pubmed_docsum


Lewis lung, NSCLC. Luteolin is one of the anticancer flavonoids
in S. barbata.

http://www.ncbi.nlm....l=pubmed_docsum


H460, NSCLC.

http://www.ncbi.nlm....l=pubmed_docsum


H441, NSCLC.

http://www.ncbi.nlm....l=pubmed_docsum



http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

[DeadMeat]

It's nice that you mention IP6, guys, but you're quite mistaken about the dose. The SV extract has nothing to do with IP6 whatsoever, nothing. 63mg is a homeopathic dose and we're not into vodoo, are we? If it did work, then not because of IP6. The best and only human studies used 8-10 grams and all the extensive animal studies use approx. the same metabolic-rate adjusted dose. I think I mentioned this in one of the cancer threads anyway.

Considering the amounts of IP-6 in normal food, 63mg isn't much yea.
http://www.mdanderson.org/education-and-research/departments-programs-and-labs/departments-and-divisions/clinical-nutrition/complementary-therapies/clinical-nutrition-ip-6.html
The shiitake mushroom stuff mentioned in the NCI report is probably more important, or something else of course.

we're not into vodoo, are we?

No, not me at least. Not that there is anything wrong with it. A far as I know they don't use homeopathy, but just normal concentrations of herbal/animal medicine/poison stuff. You really don't want to drink a voodoo zombie potion thinking its homeopathy.

http://www.ncbi.nlm.nih.gov/pubmed/3077265

Voodoo is a folk religion that emerged from the interaction of West African ethnotheologies with European Christian rituals. Haitian Voodoo priests control two major practices which might be of interest to toxicologists: healing and poisoning. Intoxications arising from therapeutic activities pertaining to this cult are of the same kind as those encountered in the practice of Modern Medicine. Remedies used in Voodoo originate generally from plants, as do most prescription drugs; however, the poisons are extracted from both plant and animal tissues, then administered to intended victims as a means of punishment established by a clandestine justice system. The present paper reviews recent attempts at analyzing some of the most lethal Voodoo poisons which appear to induce catalepsy. Although tetrodotoxin was singled out as the probable active ingredient, chromatographic analyses of such poisons as well as the presence of yet unidentified neurotoxicants in Caribbean fish and amphibians familiar to Voodoo practitioners suggest otherwise. To gain more insight into this problem, it is proposed that chemical analyses and toxicological studies be carried out on each ingredient individually, then on combinations of ingredients contained in these Voodoo potions. Such a strategy could help discriminate between active and inactive components and focus on the real toxic elements.

[zawy]

Frankly, I wonder why your friend is not trying the Chinese herbs,
Oldenlandia diffusa and Scutellaria barbata/baicalensis,
particularly when the studies I have linked show activity against
drug resistant SCLC and NSCLC lines ?

He is trying skullcap (Scutellaria), but i have not looked into it yet. He's only trying what I've recommended. I've have been concentrating on selenite so much that I haven't had time to study the herbs, except to find out that maybe shiitake active ingredient may not reach needed concentrations unless its I.V. . If i had not been studying the selenite, I would not have known to greatly reduce the vit C and that the selenite he is taking is risky (5,000 mcg/d selenite + 2,000 mcg/d as SeCys, 200 lb - tall and thin). I also found out not to take the 5 g/day of green tea before surgery due to it reducing clotting. I'm advising that tomorrow morning before the ct scan be the last selenite for now, giving him 5 or so days before surgery to hopefully repair the generalized selenite damage with vit C before surgery. Still can't do vit E due to blood thinning.

I briefly looked into IP6 years ago and was not impressed. I have not had time to look into it now to reconsider that opinion, and he's reached a pill limit. 5 more grams of something is beyond the limit, but i could have taken something out.

I would like to see this forum hash out a strong evidence-based tolerable protocol for every type of cancer. It's certainly not a task that the medical community or wikipedia seem up to. But if we did get enough references and efficient wording then it could be translated to wikipedia for the cancer and the compound. Wikipedia seems strong when it comes to cancer in the curcumin and resveratrol articles, but weak on the mushroom and selenium articles. All cancer articles are not going to accept any positive comments about a supplement unless the references are strong.

Thanks for all the links, I'll get back to them when I can.

[tham]

Lentinan had been used in Japan for decades as an anticancer
drug, but only by injection and is not active orally.

AHCC is active orally, but not so established compared to PSK.

http://en.wikipedia....elated_Compound

http://www.cancergui...t_lentinan.html

http://www.luye.cn/product.php?id=29

http://www.springerl...0lk8115vr07383/


Maitake also does not have much evidence backing it for
its anticancer properties. Over a decade ago, this librarian
whom I knew at the local National Library had breast cancer.
I suggested to her husband to give her Maitake D--fraction,
but it was useless.

The only mushroom with an established cancer fighting record
is Coriolus versicolour (turkey tail), given in Japan as a drug,
PSK, for decades.

I first heard of PSK over a decade ago, whille looking a a
chemotherapy reference manual in that same library, where
there were several pages dedicated to it.

http://www.ncbi.nlm....pubmed/10696116

[ppp]

Lentinan had been used in Japan for decades as an anticancer
drug, but only by injection and is not active orally.

AHCC is active orally, but not so established compared to PSK.

http://en.wikipedia....elated_Compound

http://www.cancergui...t_lentinan.html

http://www.luye.cn/product.php?id=29

http://www.springerl...0lk8115vr07383/


Maitake also does not have much evidence backing it for
its anticancer properties. Over a decade ago, this librarian
whom I knew at the local National Library had breast cancer.
I suggested to her husband to give her Maitake D--fraction,
but it was useless.

The only mushroom with an established cancer fighting record
is Coriolus versicolour (turkey tail), given in Japan as a drug,
PSK, for decades.

I first heard of PSK over a decade ago, whille looking a a
chemotherapy reference manual in that same library, where
there were several pages dedicated to it.

http://www.ncbi.nlm....pubmed/10696116

PSK looks interesting. Anyone here take it?

[zawy]

3 of the mushrooms you've mentioned look well-researched. What's the dose as food and as extract? What are some links to in vivo data? A summary list of 3 things for each nutrient would be good: 1) nutrient name, 2) dose, and 3) links to the best in vivo data. Bioavailability connects the in vivo to recommended dose, but may result in too many links Here's another mushroom with a lot of cancer research: Reishi aka Língzhī aka Ganoderma lucidum.

The article is good for those trying to to look at oral selenite and blood plasma in humans.

http://jn.nutrition..../full/129/4/865

[tham]

On PSK and PCP.

There was a longer thread on it, but I can't find it.

http://www.imminst.o...o...st&p=123010

[DeadMeat]

The best and only human studies used 8-10 grams and all the extensive animal studies use approx. the same metabolic-rate adjusted dose. I think I mentioned this in one of the cancer threads anyway.

In the pilot clinical trials they seem to have used IP₆ together with its precursor Inositol to increase the effects(or the other way around). I can't seem to find the source studies for the human trials online(not even the abstracts of them). But at least the results are mentioned in some overview articles.
http://jn.nutrition.org/cgi/content/full/133/11/3778S

Inositol hexaphosphate (IP₆) is a naturally occurring polyphosphorylated carbohydrate that is present in substantial amounts in almost all plant and mammalian cells. It was recently recognized to possess multiple biological functions. A striking anticancer effect of IP₆ was demonstrated in different experimental models. Inositol is also a natural constituent possessing moderate anticancer activity. The most consistent and best anticancer results were obtained from the combination of IP₆ plus inositol. In addition to reducing cell proliferation, IP₆ increases differentiation of malignant cells, often resulting in a reversion to normal phenotype. Exogenously administered IP₆ is rapidly taken into the cells and dephosphorylated to lower-phosphate inositol phosphates, which further interfere with signal transduction pathways and cell cycle arrest. Enhanced immunity and antioxidant properties can also contribute to tumor cell destruction. However, the molecular mechanisms underlying this anticancer action are not fully understood. Because it is abundantly present in regular diet, efficiently absorbed from the gastrointestinal tract, and safe, IP₆ holds great promise in our strategies for the prevention and treatment of cancer. IP₆ plus inositol enhances the anticancer effect of conventional chemotherapy, controls cancer metastases, and improves the quality of life, as shown in a pilot clinical trial. The data strongly argue for the use of IP₆ plus inositol in our strategies for cancer prevention and treatment. However, the effectiveness and safety of IP₆ plus inositol at therapeutic doses needs to be determined in phase I and phase II clinical trials in humans.

http://www.inocell.com/pdf/cancer_prevention.pdf

An enhanced antitumor activity without compromising the patient's quality of life was demonstrated in a pilot clinical trial involving 6 patients with advanced colorectal cancer (Dukes C and D) with multiple liver and lung metastasis [78]. Inositol + IP₆ was given as an adjuvant to chemotherapy according to Mayo protocol. One patient with liver metastasis refused chemotherapy after the first treatment, and she was treated only with Inositol + IP₆; her control ultrasound and abdominal computed topography scan after 14 months after surgery showed a significant reduced growth rate. Overall a reduced growth rate was noticed and in some cases even tumor regression was noted. Additionally When Inositol + IP₆ was given in combination with chemotherapy, side-effects of chemo-therapy (drop in leukocyte and platelet counts, nausea, vomiting, and alopecia) were diminished and patients were able to perform their daily activities [78]. The same group of clinicians have been following up to 22 patients with colorectal carcinoma (Dukes B2, C and D) surgically operated and submitted to adjuvant polychemotherapy, Mayo protocol and radiotherapy, in addition to Inositol + IP₆, and found that these patients manifested diminished side-effects of chemotherapy with improved quality of life [79]. Beneficial effect of Inositol + IP₆ was further observed in the treatment of ductal invasive invasive breast carcinoma [80,81]. Not only that chemotherapy was never interrupted, but combination of Inositol + IP₆ contributed to diminished chemotherapy–related side-effects, improved quality of life, and prolonged survival of patients with metastatic recurrence of breast cancer [80,81]. A long-term survival of a patient with advanced non-small cell lung cancer treated with Inositol + IP₆ combined with chemo-radiotherapy was also recently recently reported [82]. However, further prospective and controlled randomised clinical trials are necessary to confirm these observations.

Quite interestingly and conveniently, prophylactic dosage of Inositol + IP₆ is low (1.5 – 2.0 g/day) and the cancer therapeutic dosage may be as high as 8-12 g/day. In the absence of a dose-determination study in humans, these values were extrapolated from animal data. And orally, it has been found to be safe at a dosage several fold higher than the maximum therapeutic dose. Thus inclusion of this safe and effective combination of Inositol + IP₆ in our strategies for prevention and therapy of cancer as well as other chronic diseases is warranted.

Edited by DeadMeat, 23 September 2009 - 07:04 PM.

[tham]

Here's the other post on PSK.

http://www.imminst.o...o...st&p=128336

[zawy]

I got my friend's scans and compared before and after. In 5 weeks it grew 5% in diameter plus or minus maybe 2%. My comparison image is below.

Comments for those really concerned about the accuracy of my measurements: You may notice some errors in the measurement points and math, but the 5%+/-2% is as accurate as anyone can get. The top view revealed somewhere between 0 and 5% increase, but the 3D view made it more clear there was an increase. The 3D looks like it is about 10% bigger, but there are 5 pixels of fuzz per edge compared to the older image, and the older image as shown is 1.5% smaller. The space between the tumor and vein was the give away, but after correcting for the fuzz, the difference is not as big as it seems. The images are carefully aligned to be at the same angle and it is the location where distance between the tumor and vein are the greatest. Fuzz was determined by the 26 and 36 mark points. Another point indicated it could be as high as 7. The reference points are between two out-shoots of a vein.

So, there's no evidence that 2 weeks of 5 mg/d selenite plus 2 mg/day other forms had any effect. It is important to note that the first week included high dose vit C, about 10 g/d, which is known to decrease selenite effectiveness.

Attached Files

•  COMPARE3.gif   72.37KB   14 downloads

Edited by zawy, 24 September 2009 - 08:23 PM.

[kismet]

It is important to note that the first week included high dose vit C, about 10 g/d, which is known to decrease selenite effectiveness.

But oral vitamin C is not known to produce any anti-cancer effects, why did you choose this therapy? While in your initial post you mentioned high dose i.v. vitamin C (the only regimen with some promise).

Edited by kismet, 24 September 2009 - 09:35 PM.

[zawy]

I don't have my vit c books with me, but I believe there are 4 studies showing impressive benefit in cancer patients who are not getting chemo. Off hand I know of Pauling/Cameron and japanese work (Fukumora or something like that). I am not aware of better studies in this area, but the Mayo Clinic did two studies that had negative findings. Their first trial was with patients on chemo and that is the source of the belief that vit c with chemo does not help. In their second trial, the vit c was applied for only 2 months, even abruptly stopped which is known to make the person susceptible to infections. They also did not adjust for the control patients taking vitamin c on their own. This should be expected from the mayo clinic which is rabidly anti-supplement. If you don't believe me, go to their web site and do a search on any supplement you think anyone should take. They will disagree with you, even emphasizing the dangers of whatever natural nutrition you thought was good for people...except of course if it is packaged in a box, mixed together, and called food. They really, really, really, do not want anyone taking a pill unless a prescription is required to get it.

I'm still looking at the images and wondering if the 3D rendering is adding too much fuzz or something that i am not accounting for correctly. I had said 0% to 5% from the top pictures from which the 3D images were derived, but the images by themselves don't show any increase in size. For example, if you take the too small pictures at the bottom of my post above, you can see the new tumor is 3% smaller, not 5% larger. But I have not yet been able to find something to calibrate the 2D image sizes like i was able to do for the 3D image.