How much magnesium would you suggest?
My sister takes 4-5 capsules of Butyrex by Neesby with artesunate.
http://www.needs.com/product/TE_Neesby_Butyrex_250/b_TE_Neesby
This provides 400mg calsium and 200mg Magnesium and 3 gr. of butiric acid. Is this amount of magnesium enough? BTW, she has never complained about PN so far.

You can have that measured in a blood test. It is part of a standard CBC. That way you will know if she is getting enough.

Take care,
Sandra

Vickie

I know how overwhelming it all can be. Is there anyway you could provide some more information about your father's case? Like what other treatments he's had? Surgery? Is he resistant to hormone treatment now? If hormone resistant, has he tried ketoconazole? Does he have an oncologist now?

I think it would be wise to hit this with more than just artemisinin if at all possible...

Take care,
Sandra

I have looked into Artemisinin for my mother-in-law but she hasn't tried it yet since her Dr did not give her the OK (don't know why).
It can be purchased from
http://www.dogcancer.net.au/fight-cancer-products.php
and I have asked if it is for human comsumption.
Please contact them for further information

Cass

You can get artemisinin here:

http://www.iherb.com/Super-Artemisinin-60-Veggie-Caps/3484?at=0

If you want, my account number will get you a discount: ILE549

Here is an information wiki a friend and I've been working on:
http://artemisinin.pbworks.com/FrontPage

Hope this helps,
Sandra

Cass

Each tumor has different active markers that give us a hint if treatment works or not. Oncologists usually check markers every 3 weeks and expect to see a continues drop. We need at least 3 measurments in order to get an idea.

Why do you check DHEAs? I didn't know it is also a marker. Is this so for ER+ tumors?

Have you checked LDH and RBC sedimentation rate? These are also consindered markers. Especially LDH puzzles me a lot. When our Ca125 drops, LDH raises and nobody could give us a good explanation about it. What I have read is that while a patient goes into remission LDH has to return into normal values.

I wish you good results in the rest of your test !!

I use the same brand - only I use the pill form, not the liquid.

CEA doesn't seem to be active in my case either. My previous reading was 0.7 and this time was 0.6 ug/L With no oncologist, I've had to figure out what tests to get on my own.

>Each tumor has different active markers that give us a hint
>if treatment works or not. Oncologists usually check markers
>every 3 weeks and expect to see a continues drop. We need at
>least 3 measurments in order to get an idea.
>
>Why do you check DHEAs? I didn't know it is also a marker.
>Is this so for ER+ tumors?

It is a precursor to estrogen, and part of a complete hormone panel blood test. Here's an interesting study of the link to ER+ cancer:
http://cebp.aacrjournals.org/cgi/content/full/15/5/967

>Have you checked LDH and RBC sedimentation rate? These are
>also consindered markers. Especially LDH puzzles me a lot.
>When our Ca125 drops, LDH raises and nobody could give us a
>good explanation about it. What I have read is that while a
>patient goes into remission LDH has to return into normal
>values.

I have to research how to order those. They aren't on a standard lab requisition form.
Wonder if the elevated LDH is indicative of an inflammatory response to the body ridding itself of cancer? Just a guess.

>I wish you good results in the rest of your test !!

Thanks!

Regarding LDH, the best explanation has to do with tumor cell distruction. If this is correct, I would expect to see LDH droping after some time.

Another strange thing in my sister's case is that she has very high total cholesterol (279) and LDL (170). She checked those for first time, and it was really a big surprise, since my sister eats no animal fat and exercises regularly. Her HDL was really good (79) and this reduces possible risk. But anyway, this 279 is too much. I google around and found a relation of low LDL and cancer risk. High LDL is bad for heart, but it might protect cells against cancer. In other words, the opposite would be expected. So, I did this wild guess: could it be a physical reaction of her body in order to protect healthy cells against cancer?
Has anyone experienced anything similar?

Here is an overview of Dad's condition - sorry about the length of it but thought i would give you all the details.

Dad is a non-smoker, non drinker, no other health conditions or allergies.

Sept 2001
Diagnosed prostate cancer-PSA 100,gleason 9, Zoladex 10.9mg implanted,no other treatment prescribed (chemo, radiation etc) - drs said cancer had already spread although not indicated in bone scans -given 2 years to live. After Zoladex implanted PSA dropped to 6.4 and remained low.

April 2004
PSA rose to 886 - Zoladex no longer working

June 2004
Started Dr Donsbach's PROSTASOL - PSA 4.9 (Protocol below)
Prostasol (USA) - 9 caps
Ambrotose AO 2 caps
Vitamin C 10 grams
Selenium drops 6 drops
Fish Oil 3 caps
Zinc 1 tab
Curcuminiod 1 tab
Vitamin E 1000mg
Folic Acid 1 tab
Asprin ¼ tab
Multi vitamin 1 cap
Magnesium 2 tabs
Vitamin D 1 cap
Melatonin 1 cap

PSA remained low until....
November 2006
PSA 54.4 - Difficulty urinating - underwent a Endoscopic Laser Prostatectomy - Drs do not recognise Prostasol - implanted Zoladex 10.8mg, discontinued Prostasol - PSA 36 - continued supplements.

March 2007 - PSA 36
June 2007 - PSA 120

September 2007
PSA 170- did not renew Zoladex implant. Resumed Prostasol(USA)2daily & tried new product called Prosta Balance (Australian)2 daily

December 2007
PSA 110- stopped Prostasol(USA), kept taking Prosta Balance (Aus)

March 2008 - PSA 460

June 2008
PSA 55 - resumed Prostasol(USA)6 per day
"Whole Body Bone Scan: widespread osseous metastases almost to the level of superscan involving the trunk, particularly the sacral wings and iliac bones, the proximal femora, proximal humeri, the scapulae and the left parietooccipital region. Conclusion: Widespread osseous metastases. Marked urinary retention"

Nov 2008 - PSA 135

8 Dec 2008
PSA 150 - Fell and broke left femur. Operation to insert pin. Zoladex implanted. Discontinued Prostasol(USA).Oxycontin 20mg. Dad diagnosed as hormone refractory and cancer spread to bones and bone marrow suppressed. Oncologist said no more can be done.

25 Dec 09 - PSA 484
31 Dec 09 - PSA 801
5 Jan 09 - PSA 1129
3 Mar 09 - PSA 1813 - another Zoladex implanted

17 March - Contacted naturopath and started protocol below:
Infusions:
• Glutathione 500mg
• 15g Vitamin C
• Vitamin BForte injection (B1, B2, B3, B5, B6 and B12)
Supplements:
• Legalon (Floridis) 2 caps
• Sublingual B12 (Nutrition Care) 1 tab
• Folate 1 tab
• Activated B Complex (DVPI) 1 cap
• Polybac 8 (Nutrition Care)
• BioBran 3 satches daily
• Melatonin
Juices x1 daily:
• 1 beetroot (stalk, bulb, leaves)
• 1 iceberg lettuce
• 1 punnet strawberries
Protein Drink x 2 daily: (120-150g protein per day)
• Spirulina Powder
• Protein Powder
• Almond milk
• Coconut milk
• LSA powder
• Silken Tofu
• Cinnamon
• Vanilla Extract

20 April 09 - PSA 1700
contacted oncology professor in Switzerland. He suggested using Artemisinin and MDV3100, an androgen receptor antagonist

MDV3100 has two modes of activity, 1.prevents the androgen receptor from entering the cell's nucleus and triggering further growth of the tumor and, 2.continues to inhibit the grouth of the cancer even when the androgen receptor is overexpressed.

Data presented in October 2008 at the 20th EORTC-NCI-AACR Symposium from the ongoing open-label, dose-escalation , Phase1-2 clinical trial, showed encouraging and durable antitumor activity in the three expanded dose groups tested thus far, as measured by(PSA) declines, radiographic findings, circulating tumor cell changes and time on treatment.

28 April 09 - just found out that i will have difficulty bringing Artemisinin into Australia. Currently Dad is extremely anaemic and he is having injections to increase his haemoglobin. He is also in pain.

Has anyone heard about MV3100 and if it is effective? Looking back over Dad's PSA history, the USA Prostasol seemed to keep the readings at bay. i have also heard about Medpro Prostasol from Netherlands - has anyone tried it?
thanks
Vickie

Thanks so much for your informative post. I want to strongly suggest that you consider adding DCA to your treatment list. My MD has a PC patient who was in ICU (nearly in a coma he was on so much pain-killers). The man started DCA and was discharged from hospital and walking around in a week and a half! There are never any guarantees that DCA will work, but when it does - it is miraculous! Given your father's condition - it is certainly worth a shot.

I would also recommend that you email Jackie about expedited shipping. (I've sent her email address by Personal Message to you.)

Very best wishes,
Sandra

I believe the Swiss oncologist gave you good advice regarding the MDV3100.

There is another new drug that works well for patients with hormone resistant prostate cancer, HDK (high-dose ketoconazole). I believe HDK is given in combination with an 5-alpha-reductase inhibitor like Avodart or MDV3100, plus an LHRH agonist like Zoladex, plus an anti-androgen like Casodex or Flutamide, four different drugs total to overcome resistance. Since your dad is resistant to Zoladex his oncologist may wish to throw a different molecule at the cancer, like Eligard or Viadur. Your dad would presumably use MDV3100 in place of an older AR5 inhibitor like Avodart but you will need the advice of an excellent oncologist; both are new drugs.

You will need a physician's guidance regarding the treatments above, but it appears to me that your dad's doctors have by no means exhausted the conventional remedies at your disposal. The HDK in particular should be examined.

The Prostasol seems to have been more effective than the Zoladex and I'm surprised your dad was put back on Zoladex when he was clearly hormone refractory. The Prostasol may have contained more than the herbs listed, some formulations are reported to contain thalidomide, which is effective at knocking down advanced cancers. My dad was prescribed thalidomide for advanced PC and it was helpful for a time.

The treatments described above are the most powerful at your disposal, provided your dad's oncologist is prepared to employ them. But I would do more:

DCA can have miraculous results in cases like your dad's; also I am presently having good luck with Artemisinin. So my suggestion to you, and please remember I am not a physician and this is only my personal opinion, is to combine advanced hormonal treatments as described above, with DCA and Artemisinin.

The recommended Artemisinin protocol is outlined in post #1. You can add DCA at a dose of 10-15 mg/kg/day.

Best to you and your dad,

Parachute.

Just wanted to give you a quick update and thank you so much for your encouragement and assistance in moving forward with Dad's treatment.

Yesterday I met with Dad's oncologist, who in his previous consultation had said there was nothing more that could be done. After he saw the information about DCA and the trial in Alberta, he was more than happy to prescribe it and help monitor Dad's condition, along with our local MD. I was going to get the prescription filled at our local compounding chemist, however the cost is exorbitant - 10grams is $450 - something to do with taxes - so I have ordered from buydca.com and requested an urgent delivery. I haven't heard back from Jackie yet and I can't find a phone number for the company so that i can talk to someone about the cost of freight and arranging an urgent delivery etc....so needless to say i am anxious. I may have to buy a couple of grams from the chemist until we receive the order from buydca.

I have also ordered Prostasol from the UK and will use it instead of the hormonal blocker Zoladex.

I asked the oncologist about MDV3100. He said it is a fantastic product if i can get it however because it is owned by a pharaceutical company there is no way I would. Thanks Parachute for all the information about other drugs. I went through each one of them with the oncologist and he said none would be helpful for Dad and that the DCA would be better.

I also ordered Miracle Minerals just in case Dad has side effects

Today I am going to go through dad's protocal and delete what's not important. Just one question - what do you use to measure the DCA powder? is there a special machine i should get or are the kitchen scales okay? I've got an electronic set.

I've got to rush off now but will be back with more questions and updates.

Thank you again for your help, i couldn't have done it without you.

Vickie

I emailed their toll free number to you.

Best,
Sandra

Here is the page on dosage:
http://www.thedcasite.com/dca_dosage.html

You can probably have the pharmacist encapsulate the correct dosage (I'd suggest 15mg/kg/day) split into 2 doses.

If you don't have a scale, use a baking measuring spoon. An eighth of a teaspoon is 500 mg.

Best,
Sandra

I have hit a brick wall. I ordered DCa from buydca.com on Wednesday and they have just informed me that they have run out and will not be able to send any until next Monday (which is Tuesday Australian time), so I will have to to wait another week! Yesterday I was going to order a small amount from my local compounding chemist but they said they would have to order it in as well and they would receive it Monday. When I originally placed the order with BuyDCA, they said they would have it to me by Tuesday, so I didn't worry about getting a small amount locally.

Dad is deteriorating and we only have a small window of opportunity to do this....I am so frustrated..

If anyone can help I would be very grateful.

Vickie

Today I received the Artemisinin!! And the local compounding chemist just rang to let me know that they have the DCA this afternoon!!! and I should receive the Miracle Minerals today as well.

So I’m ready to start!

Hopefully sometime during the week the Medpro Prostasol will arrive. I have been studying the ingredients and can’t see any that will have a negative effect. It has a lot of Quercetin and I don’t think this will inhibit DCA.

Calcium Hydrogen Phosphate 110.0mg
Regrestrol (phytosterol complex containing beta-sitosterol, campesterol, stigmasterol and brassicasterol) 162.5mg
Microcrystalline Cellulose 339.5mg
Serenoa Repens (Saw Palmetto) 37.5mg
Quercetin 95% 39.5mg
Pygeum 37.5mg
Triglycerides 30.0mg
Magnesium stearate 29.0mg
Silicon dioxide (colloidal) 27.0mg
Panax pseudo-ginseng 25.6mg
Resveravine (8% resveratrol extract) 22.5mg
Sodium Starch Glycolate 20.0mg
Ganoderma lucidum 19.4mg
Hypromellose 9.0mg
Propyleenglycol 1.0mg

Before I begin the DCA and the Artemisinin with Dad I want to make sure that I have the supplements correct. Hope you help me figure them out.

I have read that you can take Artemisinin with DCA or alternate them – which is best?

SUPPLEMENT PROTOCOL
1. Black tea – 6 to12 cups a day of double tea bags
2. Fish oil (EPA/DHA) –300 mg/kg. Start at 50 to 100 mg/kg and use dose escalation
3. B1 (Benfotiamine) – Medicor suggests 80mg twice/day
4. Artemisinin – 2 caps a day
5. Silymarin – 1 cap/day
6. R+lipoic Acid – 600mg a day (Medicor prescribes 450mg/day)
7. MMS – twice a day – 3 drips mixed with 15 drips of citric acid
8. Melatonin – 1 cap/day
9. Baking Soda - from one teaspoon two to three times/day (equiv to about 8-12 grams day total) to 20 grams/day
10. Butyrate – don’t really know what it is – I’ll ask compounding chemist about it.
11. Selenium – not sure how much to take
12. Magnesium – not sure how much to take
13. Folate – 1 cap/day
14. COQ10- 1000mg/day

I have read so many postings and I have gathered all the suggested supplements and dosages. I’ve listed them below and not sure if any are really important.

Tetrathiomolybdate, or TM,– I’m going to ask my compounding chemist about it

PH Levels – I found this post about PH levels, so I think I’ll do this:
“My sister takes 1 teaspoon of baking soda 3 times per day (every 8 hours) and she could improve her PH from 5.5 to 7.4 !! Eating alcalic food is a better way, and also drinking high PH water. But baking sode makes the trick and it is OK.”

VITAMIN C – I’ve decided against the Vitamin C orally or infusions because I read a posting that Vitamin C is an anti-oxidant and works against DCA

Extra supplements:
1. Laetrile – 3 x 500mg tablets/day (apricot kernels)
2. Lymphasol – 3 caps/day
3. Germanium-132 – 1 cap /day
4. distilled Omega 3 (EPA/DHA) – 3 grams
5. shark liver oil – 1 cap/day - preferably c-statin (bindweed extract)instead
6. Vitamin D3 – 1 gram/day
7. Artemix – 1/day
8. L-carnitine
9. Vitamin/B6/B12 – 1 cap/day
10. Hepatapro – 1 cap/day
11. Patothenic Acid (B5) – one gram/day
12. Acetyl-L-Carnitine Argenate – 2 caps/day
13. Carnatine -4 caps/day

Thank you in advance for your help.

Vickie

http://cancerres.aacrjournals.org/cgi/content/abstract/66/9/4816

Bone metastasis is very common in advanced prostate cancer. Docetaxel has been shown to improve survival in patients with metastatic prostate cancer. However, treatment with docetaxel is associated with a certain degree of toxicity. Genistein, derived from soybeans, has been found to inhibit cancer cell growth without toxicity. We have recently reported that genistein could potentiate the antitumor activity of chemotherapeutic agents both in vitro and in vivo. However, the molecular mechanism of this novel effect of genistein has not been fully elucidated. In this study, we found that genistein significantly potentiated the antitumor, anti-invasive, and antimetastatic activities of docetaxel both in culture and in severe combined immunodeficient (SCID)-human model of experimental prostate cancer bone metastasis. We further conducted microarray analysis, real-time reverse transcription-PCR, Western blot analysis, small interfering RNA and cDNA transfection, matrix metalloproteinase-9 (MMP-9) activity assay, and invasion assay. We found that the expression of osteoprotegerin (OPG) was induced by genistein and inhibited by docetaxel, whereas genistein significantly down-regulated the expression and secretion of receptor activator of nuclear factor-B (RANK) ligand (RANKL) and inhibited osteoclast formation. Moreover, genistein down-regulated the expression and activity of MMP-9, which was induced by docetaxel treatment, and inhibited invasion of PC-3 cells. These results suggest that the observed potentiation of antitumor activity of docetaxel by genistein in the SCID-human model of experimental bone metastasis could be mediated by regulation of OPG/RANK/RANKL/MMP-9 signaling, resulting in the inhibition of osteoclastic bone resorption and prostate cancer bone metastasis. From these results, we conclude that genistein could be a promising nontoxic agent to improve the treatment outcome of metastatic prostate cancer with docetaxel. (Cancer Res 2006; 66(9): 4816-25)

Another drug that increases OPG is Zoledronic acid (Zometa, Zomera, Aclasta and Reclast) rapidly increases circulating OPG in patients with tumour indiced bone disease. It's primarily in trial for osteoarthris but there is increasing evidence that RANKL is involved in the spread of cancer and perhaps opposing it by the upregulation of Osteoprotegerin (OPG) the natural decoy protein that binds to RANKL may help.

A different approach is to inhibit RANKL directly but I think it has more side effects than upregulating OPG. The drug in trials for arthritis and cancer on that score is something called Denosumab.

I don't have a link for the following just the text:

"GH exposure was able to stimulate OPG secretion in a concentration-dependent manner. In addition, the OPG mRNA levels were increased, indicating that the hormone has a stimulatory effect on gene expression. The stimulatory effect on OPG expression and production was prevented by exposing the cells to tyrphostin AG490 (10 muM), an inhibitor of Janus kinase 2, which is one of the kinases involved in the intracellular pathway activated by the binding of GH to its receptor. Similar results were obtained when the cells were exposed to a receptor antagonist of GH, pegvisomant at 50 nM. GH exposure neither induced an increase in IGF-I expression nor secretion in hOB. These results suggest that the stimulation of OPG production induced by GH in hOB is specific and receptor mediated and further support the view that GH is able to modulate bone remodeling by directly influencing osteoblast-osteoclast crosstalk."

One thing I found interesting was that OPG is inhibited by administration of glucocorticoids which are often used to reduce pain and swelling caused by cancer and prevent nausea and vomiting induced by chemotherapy. They can also cause resistance to apoptosis and reduce immune response. However there may be no alternative to using them where the patients are dealing with extreme swelling and pain.

http://ndt.oxfordjournals.org/cgi/content/abstract/16/3/479

Conclusion. These findings indicate that short-term administration of glucocorticoids significantly suppresses serum OPG and osteocalcin. It might participate in the development of glucocorticoid-induced osteoporosis via an enhancement of bone resorption and suppression of bone formation.

And this:

"Osteoprotegerin (OPG)/osteoclastogenesis inhibitory factor regulates bone mass by inhibiting osteoclastic bone resorption. mTOR, which is the mammalian target of rapamycin, is a kinase and central regulator of cell growth, proliferation and survival. By using Rapamycin we studied whether mTOR pathway is associated with OPG protein production in the mouse bone marrow-derived stromal cell line ST2. Rapamycin markedly increased the level of soluble OPG in ST2 cells. This antibiotic treatment resulted in the suppression of phosphorylation of mTOR. Rapamycin had no effects on the proliferation, differentiation or apoptosis of the cells. Treatment with bone morphogenetic protein-4, which can induce OPG protein in ST2 cells, also resulted in a decrease in the density of the phospho-mTOR-band, suggesting that the suppression of the phospho-mTOR pathway is necessary for OPG production in ST2 cells. Thus, suitable suppression of mTOR phosphorylation is a necessary requirement for OPG production in bone marrow stromal cells."

I also think you are right to take Resveratrol:

http://mct.aacrjournals.org/content/5/3/621.abstract

Resveratrol is a naturally occurring phytoalexin with antioxidant and antiinflammatory properties. Recent studies suggest that resveratrol possesses anticancer effects, although its mechanism of action is not well understood. We now show that resveratrol inhibits Src tyrosine kinase activity and thereby blocks constitutive signal transducer and activator of transcription 3 (Stat3) protein activation in malignant cells. Analyses of resveratrol-treated malignant cells harboring constitutively-active Stat3 reveal irreversible cell cycle arrest of v-Src-transformed mouse fibroblasts (NIH3T3/v-Src), human breast (MDA-MB-231), pancreatic (Panc-1), and prostate carcinoma (DU145) cell lines at the G0-G1 phase or at the S phase of human breast cancer (MDA-MB-468) and pancreatic cancer (Colo-357) cells, and loss of viability due to apoptosis. By contrast, cells treated with resveratrol, but lacking aberrant Stat3 activity, show reversible growth arrest and minimal loss of viability. Moreover, in malignant cells harboring constitutively-active Stat3, including human prostate cancer DU145 cells and v-Src-transformed mouse fibroblasts (NIH3T3/v-Src), resveratrol treatment represses Stat3-regulated cyclin D1 as well as Bcl-xL and Mcl-1 genes, suggesting that the antitumor cell activity of resveratrol is in part due to the blockade of Stat3-mediated dysregulation of growth and survival pathways. Our study is among the first to identify Src-Stat3 signaling as a target of resveratrol, further defining the mechanism of antitumor cell activity of resveratrol and raising its potential application in tumors with an activated Stat3 profile.

Also silibinin:

http://clincancerres.aacrjournals.org/cgi/content/abstract/15/2/613

Results: Silibinin treatment reduced the lower urogenital weight (including tumor, prostate, and seminal vesicle) by 40% (P < 0.05) without any toxicity in mice. Silibinin decreased proliferating cell nuclear antigen expression and proliferating cells (P < 0.001) but increased cleaved caspase-3-positive cells (P < 0.01) and apoptotic cells (P < 0.001) and suppressed tumor microvessel density (P < 0.001) and vascular endothelial growth factor expression (P = 0.02). Decreased levels of cyclin-dependent kinases 2, 4, and 6, CDC2, and cyclins D1, D3, E, and A were observed, indicating an inhibitory effect of silibinin on cell cycle progression. Silibinin showed a tremendous increase in extracellular signal-regulated kinase 1/2 phosphorylation but decreased c-Jun NH2-terminal kinase 1/2 and p38 mitogen-activated protein kinase phosphorylation. A moderate decrease in phosphorylated and total levels of Akt was also noted. A marked inhibitory effect of silibinin on signal transducers and activators of transcription (STAT) 1 (Tyr701), STAT1 (Ser727), STAT3 (Tyr705), STAT3 (Ser727), and STAT5 (Tyr794) phosphorylation together with a decrease in their total levels was also observed.

Conclusions: These findings provide evidence for antitumor efficacy of silibinin against orthotopically growing prostate tumor in mice with multitargeted mechanistic insights and support its clinical investigation in prostate cancer.

My best to you and your family,

Mack

I was taking resveratrol, but I dropped it after reading this report. I think we need more information on dosage specific to cancer patients.

http://www.longevinex.com/resveratrol.asp?story=Resveratrol%20Sends%20Survival%20or%20Death%20Signals%20Depending%20Upon%20Dosage

Great post!

Take care,
Sandra

In the US most oncologists treating prostate cancer would have initiated Zoledronic acid early on, at the first suggestion of bone metastasis. Zoledronic acid provides significant pain relief as well as reducing the bone cycling that feeds the cancer. It can also help preserve bone integrity. I do not know whether Zoledronic acid would impair healing of the hip fracture.

I am told it is best to start with 1 mg to avoid Acute Phase Response, then increase to to 4 mg monthly, or if insurance will not cover monthly then every three to four months while monitoring b-CTX (C-Terminal Telopeptide, b-Crosslaps) with goal to lower Ctx to 75-100.

See:

http://www.prostate-cancer.org/resource/prostate_cancer_news.php4?id=35327

http://www.ncbi.nlm.nih.gov/pubmed/18604999

Best to you and your dad,

Parachute

I'm not sure how many pills your father can tolerate. The infusions from your naturopath may be easier on him. The B vitamins (1, 6, 12 and folic acid) are important to combat his anemia. If he does not get these in an infusion, suggest you add them in capsules. LEF's Complete B Complex is a good blend. Also add Benfotiamine - it is a better form of vitamin B-1. These can be taken anytime throughout the day.

Shark liver oil (not shark cartilage) is actually not for angiogenesis, but rather used to boost immune function. Dr. Yamamoto has used it with his patients. You can add the C-statin if you wish for angiogenesis.

Baking soda is alkalinizing yes, but it contains a lot of sodium. The lemon juice may accomplish this without the added sodium. You can use pH strips to monitor alkalinity of urine and saliva. Do this at least morning and evening.

TM is very tricky to monitor. It requires a very strict dosing schedule and frequent blood work. At this time, we also do not know how it will play with either artemisinin or DCA.

Very best wishes,
Parachute and Sandra

Here's a revised protocol using Artemisinin and Artemisinin derivatives with DCA:

First thing in the morning (empty stomach) take 7.5 mg/kg of DCA in 8 ounces of water (with a tablespoon or so of natural lemon juice). Next take 3 capsules of Lymphasol (contains lipoic acid - links to suppliers are below), Germanium 132 (150-300mg), 3 grams EACH of distilled Omega 3 (EPA/DHA), and 1 capsule of shark liver oil. Lymphasol aids absorption of fatty acids (omega 3 fish oils) and fish oils will aid absorption of Super Artemisinin.

Follow with 2 capsules of Nutricology Super Artemisinin in cottage cheese, plain yogurt or natural ice cream. You may add 1-2 capsules of artesunate (brand name 'Hepsunate' from Hepalin, link below). Take butyrate (do not open capsule) in the middle of this. Butyrate appears to act synergistically with artemisinin. I also take 250 mg each of magnesium and potassium. Both are alkalinizing minerals that cancer patients are often deficient in. Vitamin D3 (5,000 I.U.)

Have breakfast a half hour later.

Take the following supplements with lunch:
Floradix (right before lunch) Dr. Hoang recommends Minecel instead, which is an algae/phytoplankton blend.
Vitamin C 1 gram
Silymarin
Prostasol (I'm putting this here because of the antioxidants in it, which should be taken away from artemisinin).
Selenium 200-400 mcg

3 -4 hours after the evening meal, on an empty stomach: 7.5 mg/kg of DCA in water with lemon juice, 3 Lymphasol, 3 grams of Omega 3, 1 capsule shark liver oil, Germanium 132 (150-300mg). Two Super Artemisinin in cottage cheese, yogurt or natural ice cream. May add 1-2 capsules of Hepsunate - same as morning. Take butyrate in the middle of cottage cheese/yogurt/ice cream. Be sure to order Butyrate in capsules not as a liquid. 250 mg each of magnesium and potassium.

Melatonin (start with 5mg and work up to between 20-40mg taken ONLY at night), and Vitamin D3 (5,000 I.U) at bedtime. Please get a Vitamin D in an oil emulsion - much better absorption this way.

Maintain total D3 intake of 10,000 iu per day. Probably a good idea to test D3 levels... Quest Diagnostics provides a good (25-OH)-D3 assay here in the USA.

Suggest you ask your dad's doctor to monitor CBC and hepatic function.

Sources for supplements:
http://www.iherb.com/Allergy-Research-Group-Nutricology-Super-Artemisinin-60-Veggie-Caps/3484
http://www.iherb.com/Allergy-Research-Group-Nutricology-Organic-Germanium-50-Veggie-Caps/3442?at=0
http://www.goutwell.com/Lymphasol.html
http://www.goutwell.com/Minecel.html
http://www.goutwell.com/L-carnitineEX.html
http://www.hepalin.com/hepasunate50.htm
Butyrate capsules: http://www.illnessisoptional.com/ace/product.asp?ProdID=10724&CtgID
http://www.lef.org supplies most other supplements.

http://www.lef.org/Vitamins-Supplements/Item00702/Mega-Silymarin-with-Isosilybin-B.html

http://www.ncbi.nlm.nih.gov/pubmed/16309236

Synergistic cytotoxicity of artemisinin and sodium butyrate on human cancer cells.Singh NP, Lai HC.
Department of Bioengineering, Box 357962, University of Washington, Seattle, WA 98195-7962, USA. Narendra@u.washington.edu

BACKGROUND: Butyric acid is a short chain fatty acid produced by large bowel bacterial flora. It serves as an antiinflammatory agent and nutrient for normal colon cells. Butyric acid has also been shown to induce apoptosis in colon and many other cancer cells. Artemisinin is a compound extracted from the wormwood Artemisia annua L. It has been shown to selectively kill cancer cells in vitro and to be effective in treating animal and human cancer. We and others have found that the artemisinin analog, dihydroartemisinin (DHA), kills cancer cells by apoptosis. In the present study, the efficacy of a combined treatment of DHA and butyric acid at low doses in killing cancer cells was investigated. MATERIALS AND METHODS: Molt-4 cells (a human lymphoblastoid leukemia cell line) and freshly isolated human lymphocytes, cultured in complete RPMI-1640 medium, were first incubated with 12 microM of human holotransferrin at 37 degrees C in a humid atmosphere of 5% CO2 for one hour to enhance the iron concentration in the cells. Cells from each cell type were then divided into 20 flasks. These flasks were grouped into four sets of five cultures each. Zero, 5, 10 or 20 microM of DHA was added, respectively, to these sets and the cells were incubated at 37 degrees C for one hour. Zero, 1, 5, 10, or 20 mM of sodium butyrate was then added to the five cultures of each set, respectively. Thus, the treatments involved a combination of 4 doses of DHA and 5 doses of sodium butyrate. The cells were counted immediately before the addition of DHA, and at 24 and 48 hours after the addition of sodium butyrate. RESULTS: DHA alone at the 24-hour time-point and 20 microM concentration significantly reduced the number of Molt-4 cells in the culture by approximately 40% (p < 0.001, compared to non-treated control), whereas it did not significantly affect the number of normal human lymphocytes. Similarly, 1 mM sodium butyrate alone at 24 hours reduced the number of Molt-4 cells by approximately 32% (p < 0.001, compared to non-treated control), without significantly affecting normal human lymphocytes. The combination of 20 microM DHA and 1 mM sodium butyrate killed all Molt-4 cells at the 24-hour time-point and did not significantly affect lymphocytes. CONCLUSION: DHA in combination with butyric acid acts synergistically at low doses. The combination may provide a less toxic, inexpensive and effective cancer chemotherapy.

Another very recent study (last 2 days) deals with the importance of M-CSF as a target to inhibit:

http://www.sciencedaily.com/releases/2009/04/090428092820.htm

Many cancer treatments work by disrupting the formation of new blood vessels that feed growing tumors. Agents that block a vessel-promoting factor called VEGF have shown promise in human clinical trials. But recent studies in mice show that when treatment stops, tumor growth rapidly resumes. Now, Yoshiaki Kubota and colleagues find that blocking a different molecule, called M-CSF, suppressed tumor growth even after treatment was stopped.

Kubota and his team compared the efficacy of inhibitors against M-CSF and VEGF in mice with a certain kind of bone tumor. Three weeks of anti-VEGF treatment suppressed tumor growth but, similar to other recent reports, the tumors bounced back when the drug treatment was curtailed. Tumor growth in mice on a similar regiment of an M-CSF inhibitor remained suppressed in the absence of drug.

Another distinction between the two inhibitors was the type of vessel growth that was blocked. Blocking VEGF prevented dangerous vessels from growing such as those that feed tumors. But it also stopped beneficial vessels from growing, such as those that help injured tissues heal. Blocking M-CSF, on the other hand, only impeded bad vessel growth.

Most likely, the anti–M-CSF treatment had a lasting effect because it resulted in damage to the scaffolding that surrounds cancerous vessels, robbing the tumors of the structural support they need to grow. Meanwhile, the scaffold of mice treated with anti-VEGF remained intact.

M-CSF levels soar in patients with osteosarcoma (a malignant bone cancer), breast cancer and prostate cancer, making these cancers potentially the most responsive to M-CSF-blocking drugs Whether or not other types of cancer rely more on M-CSF than on VEGF for their blood supply remains unknown."

Mack: Also interesting as part of my notes is that sodium butyrate may increase OPG (which inhibits RANKL, another growth and spread factor overexpressed in cancer) but does not reduce M-CSF. I will try and find an accessible and direct M-CSF inhibitor when I have more time.

http://www.ncbi.nlm.nih.gov/pubmed/18406397?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

OBJECTIVE: Butyric acid (sodium butyrate; BA) is a major metabolic by-product of main periodontopathic bacteria present in subgingival plaque. In the present study, we examined the effects of BA on cell proliferation, alkaline phosphatase (ALPase) activity, mineralized nodule formation, extracellular matrix protein expression, macrophage colony-stimulating factor (M-CSF), and osteoprotegerin (OPG) in normal human osteoblasts. METHODS: The cells were cultured with 0, 10(-8), 10(-6) or 10(-4)M BA for up to 12 days. Mineralized nodule formation was detected by alizarin red staining, and the calcium content in mineralized nodules was determined using a calcium assay kit. The gene and protein expression levels for type I collagen, bone sialoprotein (BSP), osteopontin (OPN), M-CSF, and OPG were examined using real-time PCR and ELISA, respectively. RESULTS: Mineralized nodule formation and the calcium content of mineralized nodules were increased by BA in a dose-dependent manner. Cell proliferation and ALPase activity were not affected by the addition of BA. Following the addition of 10(-4)M BA, the expression levels of BSP, OPN, and OPG increased, whereas the expression levels of type I collagen and M-CSF were not markedly affected. CONCLUSION: These results suggest that BA stimulates bone formation by increasing the production of BSP and OPN, whereas it suppresses osteoclast differentiation by increasing the production of OPG by human osteoblasts."

Mack: And here is a reference that a peptide that mimics the 3rd TNF-like cysteine rich domain of mouse OPG was shown to inhibit RANKL/M-CSF (just the title)

http://sciencelinks.jp/j-east/article/200201/000020020101A0816668.php

Other notes:
Heparin inhibits OPG

Mack

kind regards
Vickie