Can anyone comment on doing the DAV therapy (Doxycycline Azithromycin Vitamin C) and Rapamycin at the same time. Is it a good idea or not? Thanks for any input.
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I am sorry for your problems. You are certainly a good and kind son-in-law.
I have done the DAV therapy twice. Once I stopped taking rapamycin the second time I was on my regular 1/week schedule. I had zero side effects or any subjective effects which I assume is because I don’t have any known cancer.
If I were to advise anyone, and I wouldn’t want to, who had a cancer problem that wasn’t being helped by conventional methods, I would take Dr. Blagosklonny’s advocacy and take the highest tolerable dose of rapamycin. His opinion papers indicate that he believes it is a cancer treatment.
As for the DAV treatment, I would follow the regimen advocated by Joseph.
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It seems that Sirolimus (Rapamycin) can be effective at weakening cancer on its own. However, when a traditional chemotherapy is added, the effects are even greater. I wish we hadused Rapamycin in addition to chemo in the first place!
After consulting with the hospital, we are considering the last chemotherapy that they have available, TS-1 combined with Sirolimus. TS-1 converts to 5-Fluorouracil in the body. Unfortunately, the cancer may already be resistant to it as it was used in another treatment already. Still, we hope that the addition of Sirolimus will make the drug effective again. If so, then this could open up the door to trying other chemo drugs already used paired with Sirolimus to extend lifespan.
In the early-treatment experiment, the tumor growth rate was inhibited by 48% in the group treated by rapamycin alone, by 34% in the 5-fluorouracil-treated group, and by 60% in the group treated with rapamycin plus 5-fluorouracil compared to the control mice
There are already precedents set for Gemcitabine resistant cancers, such as adding Sirolimus, where the resistant cancers are affected by Gemcitabine more than non-resistant cancers due to the Sirolimus.
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Perhaps consider
Our clinical trials looking into Fast-Mimicking Diet (FMD) and cancer prevention and treatment are ongoing. But if early results are any indication, it could be a powerful new weapon in the arsenal we have to fight, and one day defeat, cancer.
Papers etc here Cancer - Valter Longo can also check the latest clinical trials
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Update: Father in law took his fast acting insulin and then forgot to eat, so it’s probably not the Rapamycins fault for the hypoglycemia.
Found this other comment by John Hemming citing research that sodium citrate (+ other citrates) can potentiate both chemotherapy and Rapamycin in the treatment of cancer : A concern about senolytics not supported by mouse studies - #7 by John_Hemming
This may be related to the alternate medicine Alkaline Approach mentioned by Viktor above. Sodium citrate (balanced with other citrates, like potassium and magnesium citrates and taken in several doses over the day to avoid electrolyte imbalances) does indeed Alkalinize many tissues including cancer tissues. John Hemming has reported that his Urine has a PH of 9 or 10! The oral dosage in mice that was effective for cancer is 500mg/kg/day, not clear how that scales to humans.
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This is the mass vs square meters of skin question. Obviously for a 80kg human if that scales it would be 40g. I tend to measure the mass of citrate which is perhaps 2/3 of the citrate salt (it varies depending on the cation). There is an additional complication that the different salts have a tendency to have a bit of water with them as well.
There is an interesting question as to whether the alkanisation of the tissues is itself positive separate to the provision of citrate.
Blood transfusions tend to come with a large dose of sodium citrate as well.
As an alternative scaling
https://www.publish.csiro.au/bi/pdf/bi9670687#:~:text=From%20Figure%201%20the%20surface,2-90·4%20cm2%20.
From Figure 1 the surface area of a mouse weighing 25·7 g is estimated to be 78·6 cm2 , with a range (95% confidence limits) of 68·2-90·4 cm2 .
So lets say the mouse is 25g which means a dose of 500mg*0.025= 12.5mg
Using the figure of 1.6square metres for humans and 80square centimetres (80/10000 square meters) the ratio would be 200 which gives a dose of 2.5g.
I think 2.5g is very low.
Alternatively mice eat about 5g a day and humans perhaps 1.2kg which is a ratio of 240.
That fits closer to the skin ratio. The mass ratio is 3,200.
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correction: you mean obviously 12.5mg
You are right about this. I will fix the post.
Another peptide worth looking into regarding cancer is PNC 27. And specially for pancreatic cancer:
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Good call. It’s called safeguard for good reason, not much downside. My daughter has been on high dose for a long time and she just got scanned a couple days ago, no evidence of disease.
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Since we are talking about last-ditch efforts, I might add this paper reviewing different peptides which may fight cancers. I have no firsthand knowledge of these but the paper came up in something else I was reading (PNC-27 out of pure interest as someone who had cancer and is intrigued by peptides and their possibilities). Maybe there are some possibilities for your family they may be synergistic (or not obstructive) to what you are already trying.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5359827/
In the paper they mention specifically for pancreatic cancers:
| PNC-2 and PNC-7 | in vitro | Pancreatic cancer (MIA-PaCa) cells | [109] |
|---|
|Cardiac natriuretic peptides|In vitro & in vivo|Pancreatic cancer (HPAC), renal carcinoma (SW156), breast adenocarcinoma (HCCI428), ovarian adenocarcinoma (NIHOVCAR-3), modularly thyroid carcinoma (TT), glioblastoma (LNZTA3WT4) and lung carcinoma (NCI-H1963) cells|
p16 In vitro Pancreatic cancer (AsPC-1 and BxPC-3) cells [166]
PNC-27 In vitro Cervical carcinoma (HeLa), colon cancer (SW1417 and H11299), breast cancer (MDA-MB-453 and MCF-7), osteosarcoma (SAOS2), leukaemia (K562), pancreatic cancer (MIA-PaCa-2) and melanoma (A-2058) cells. Rat k-ras-transformed pancreatic cancer (TUC-3) and transformed endothelial (E49) cells [214, 216, 217]
PNC-21 In vitro Cervical carcinoma (HeLa), colon cancer (SW1417 and H1299), breast cancer (MDA-MB-453), and osteosarcoma (SAOS2) cells. Rat k-ras-transformed pancreatic cancer (TUC-3) and transformed endothelial (E49) cells [214]
PNC-28 In vitro & in vivo Breast cancer (MDA-MB-453), colon cancer (H1299 and SW1417), osteosarcoma (SAOS2), cervical carcinoma (HeLa) and pancreatic cancer (MiaPaCa-2) cells. Rat k-ras-transformed pancreatic cancer (TUC-3) and transformed endothelial (E49) cells [214, 219,
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You have my sympathy.
IMO: I would certainly not pursue alternative medicine or other unproven therapies at the beginning of discovering cancer. But, once it reaches stage four and the doctor’s therapy is not stopping or curing the cancer, all bets are off.
What have you got to lose by trying any alternative solutions?
My wife died from the complications of breast cancer. I am so sorry I did not intervene with the doctors’ therapies when it continued to progress.
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Nanoparticle delivery of innate immune agonists combined with senescence-inducing agents promotes T cell control of pancreatic cancer
New combination therapy approach for pancreatic cancer.
https://www.science.org/doi/10.1126/scitranslmed.adj9366
Unlike other tumor types, existing immunotherapies have not proven very successful for pancreatic ductal adenocarcinoma (PDAC), necessitating the development of additional approaches. Here, Chibaya et al. developed a combination therapy approach that included nanoparticle delivery of STING and TLR4 agonists, which stimulate the immune response, in combination with the MEK inhibitor trametinib and CDK4/6 inhibitor palbociclib, which promote senescence of tumor cells. The combination therapy induced robust antitumor immune responses that controlled tumor burden in implanted and autochthonous PDAC mouse models. These data support further development of this potent combination therapy for PDAC.
Pancreatic ductal adenocarcinoma (PDAC) has quickly risen to become the third leading cause of cancer-related death in the United States. This is in part because of its fibrotic tumor microenvironment (TME) that contributes to poor vascularization and immune infiltration and subsequent chemo- and immunotherapy failure. Here, we investigated an immunotherapy approach combining delivery of stimulator of interferon genes (STING) and Toll-like receptor 4 (TLR4) innate immune agonists by lipid-based nanoparticle (NP) coencapsulation with senescence-inducing RAS-targeted therapies, which can remodel the immune suppressive PDAC TME through the senescence-associated secretory phenotype.This two-pronged approach produced potent T cell–driven and type I interferon–mediated tumor regression and long-term survival in preclinical PDAC models dependent on both tumor and host STING activation.
Collectively, our results suggest that engineering approaches to target multiple cell types and immune suppressive barriers through induction of type I IFN signaling in the PDAC TME could pave the way for coordinated innate and adaptive immune responses to achieve immunotherapy successes that have thus far been elusive for patients with PDAC.
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The antiparasitic drugs fenbendazole and mebendazole can also be considered as a last ditch effort in case of cancer in general;
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Two weeks ago, we celebrated my father-in-law’s 80th birthday at a restaurant. He could walk and manage on his own although he had bouts of pain. It has been 3 years and 3 months since the initial diagnosis.
My father-in-law is now in the hospital. He is too weak to walk or even sit up. He can no longer talk or eat. He survives on an IV drip. He is in constant horrible pain such that he is continually moaning and crying. Only the morphine provides release.
When he is discharged from the hospital, he will be moved to hospice where he will stay until death. This is not how you want to die.
The only shining light is that my wife and her sisters are constantly at his side, holding his hand and talking with him. He is lucky in this sense as no one else in his ward has visitors that are constantly at their side. Too many elderly die alone.
The best treatment for cancer is prevention. That’s a big reason why many of us are taking Rapamycin. Cancer is a horrible way to die.
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He took 1 mg of Rapamycin daily (off and on) since June. It appears that dose had no effect. A higher dose may have worked better, but he didn’t want to try that.
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Increasingly, researchers are adopting the view that it makes sense to regard and treat cancer as a metabolic disease primarily. Yes, it may be instigated by a mutation of other insult to the cell, but the best way to stop it is to make its environment inhospitable to growth. Witness the research focusing on the TME tumor microenvironment. This is approach is also central to Jason Fong’s view in The Cancer Code, and aligns with the emerging view that most disease has an underlying metabolic component. For a practical and comprehensive approach, Jane Mclelland “How to Starve Cancer without Starving Yourself.” She provides specific strategies including some of the things discussed above: doxicycline and other antibiotics, metformin, melatonin, helminths (dewormers) such as fenbendazole. Why does a dewormer work so well against cancer?
If you read Fong you learn that a cancer cell is a cell that has gone into survival mode and has jettisoned its higher level programming and its role as a cooperative member of a complex eukaryotic multi-cell organism. A cancer cell is in heavy growth, every man for himself mode. Having been “injured,” has dropped back to a level of function that makes it behave like a simple single cell organism, abandoning its specialized higher level functioning and it role in the larger society/organism. So a drug like fenbendazole that attacks a simple organism is effective in attacking a cancer cell.
Mclelland together with Fong are by far the most insightful and also practical books I have read on cancer genesis, behavior, and treatment. Cannot recommend highly enough.
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I tend to agree with the view that it is a failure of OxPhos leading in the main to aberrant splicing.
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For general interest purposes:
A specific variant of pancreatic cancer:
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