Beware of those who cite Otto Warburg in their opening sentence. Oops!
Warburg (1883-1970) was awarded a Nobel Prize in 1931. He believed that cancer was caused by "the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar." [Wiki]
This is paraphrased across cancer sites as "cancer hates oxygen" &/or "cancer loves sugar".
Here is the the opening to the description of the Oxy DHQ product [1]:
"An underlying cause of unwanted cellular replication is low cellular oxygenation levels. In newly formed cells, low levels of oxygen damage respiration enzymes so that they cells cannot produce energy using oxygen. These cells can then turn bad.
In 1931 Dr. Warburg won his first Nobel Prize for proving cancer is caused by a lack of oxygen respiration in cells. He stated in an article titled The Prime Cause and Prevention of Cancer that "the cause ... is no longer a mystery, we know it occurs whenever any cell is denied 60% of its oxygen requirements.""
Warburg put the cart before the horse. Cancer develops under normoxic conditions. Tumor growth is not hampered by a normal blood supply, where red blood cell hemoglobin is loaded up with oxygen. But tumors eventually outgrow their blood supply. Inadequate oxygen in afflicted cancer cells (hypoxia) results in HIF-1alpha [Hypoxia-Inducible Factor 1-alpha] as a survival response. An important HIF action is the generation of VEGF [Vascular Endothelial Growth Factor], which stimulates the generation of new blood vessels (angiogenesis). Turns out that tumors like oxygen after all.
So Oxy DHQ exists because of a false premise.
How might we get more oxygen to cancer cells anyway? With normal lung function, blood becomes almost fully oxygenated. ADT tends to cause border-line anemia. (With restoration of testosterone, the red blood cell count returns to normal.) So the task of getting oxygen to PCa is harder when on ADT.
It would be dangerous to have free oxygen in circulation. The oxygen would have to be in a form where oxidation could not occur. The form would have to be taken up by the cancer cells & the oxygen released. I don't follow how Oxy DHQ does that.
On the face of it, tumors should do less well when, because of size, they become hypoxic. But, in fact, the survival mechanisms induced by HIF make the cells extraordinarily difficult to kill. Hypoxia would be a good thing if HIF could be inhibited. It's not a new concept - from 20015 [2]:
"Hypoxia is a prominent micro-environmental feature in many types of solid tumors due to inadequate vascularization. It accounts for developing both radiotherapy and chemotherapy resistance. Tumor cells respond to changes in oxygen via delegating the transcriptional factor HIF-1α for orchestrating vast number of its essential cellular functions. Considering the profound impacts of HIF-1α on cancer progression via gene expression and the unsatisfactory efficacy of chemotherapy, there has been enormous growing interest in the biology of HIF-1α pathway and the development of direct or indirect HIF-1 inhibitors. The identification of novel HIF-1 inhibitors involves panels of cell-based or cell-free screens and assays, but the complexity involved in the regulation of the HIF-1αpathway has made the process of rational design of HIF-1α inhibitors very challenging. To date, no selective HIF-1α inhibitor has been clinically approved, partially due to the requirements of targeting protein-protein interactions without affecting other pathways. Nevertheless, there have been several approved drugs that indirectly affect the HIF-1αpathway and could serve as adjuvant therapy for certain types of cancers along with the existing treatments. Future directions would be directed towards developing drugs that are more specific for HIF-1 inhibition by better understanding of the molecular structure of domains that mediate critical functions of HIF-1. With the rapid advancement of molecular biology and emerging strategies in efficiently disrupting protein-protein interactions, it is very promising that selective HIF-1 inhibitors can be developed in the future."
In the absence of HIF inhibitors, & in the interest of avoiding HIF-mediated treatment resistance, the logical conclusion is that we should, indeed, be trying to get more oxygen to the cancer. Not because the cancer cells will die when oxygen is restored (far from it), but because HIF induction is to be avoided if current therapies are to have a sporting chance. &, in any case, PCa is much more aggressive when HIF has been induced.
There is already a treatment that can do that: the nitroglycerine patch - a vasodilator.
In 2009, Siemens conducted a study [3] on "men with an increasing prostate-specific antigen (PSA) level after surgery or radiotherapy" using "a low-dose, slow-release transdermal GTN {glyceryl trinitrate} patch".
"The calculated PSADT {PSA doubling time} of the treatment group before initiating GTN was 13.3 months, not significantly different from that of the matched control group at 12.8 months. In an intention-to-treat analysis, the end-of-study PSADT for the treatment group was significantly different at 31.8 months".
"The prolongation of the PSADT and the safety of the drug, coupled with the corresponding preclinical in vitro and in vivo data documenting the ability of nitric oxide to attenuate hypoxia-induced progression of prostate cancer, warrant further testing".
-Patrick
[1] gethealthyagain.com/oxydhq....
1st meeting with RO tomorrow morning what questions should I ask?
What (might) keeps you from asking for help?
Joe Tillotson is in Heaven 
Can I ask what to expect during the initial hormone therapy + five to eight weeks of radiation?
PSA rising during triplet therapy. What to ask the oncologist?
