The scientific journals are full of articles discussing the use of NSAIDs, COX2 Inhibitors, and Aspirin to kill cancer cells in the lab. There are also many articles talking about the use of these agents for cancer chemoprevention and for people who already have cancer. In fact, several are already cleared by the FDA as treatment options for cancer chemoprevention and for use with traditional treatment regimens.
However, the general consensus of all the journal articles is that these agents aren’t actually useful as cancer treatment and/or suppression agents because you can’t safely get their concentrations high enough in the blood.
I do not believe this is true. In fact, although I am uncertain of the reliability of being able to safely impact tumors that reside on the brain side of the blood-brain barrier, I strongly believe that you can achieve sufficient plasma concentrations.
Although a knowledgeable physician/pharmacist team is needed – it is probable that most patients can safely achieve blood concentrations that should be adequate to impact the growth of several different cancer types.
I explain this belief in the excerpt pasted below. It’s from the protocol you can find at this link: http://thatcrazypharmacist.com/?p=452
NF-Kappa B is one of the pathways that this protocol targets. Many NSAIDs are capable of impacting this pathway, and of inhibiting cancer cell growth and/or inducing apoptosis. But, translation of this property to humans is challenging because it is difficult to safely achieve free plasma concentrations that are sufficient to elicit the desired effect because of drug metabolism, associated toxicities, and plasma protein binding.
Salicylate based NSAIDs (aspirin and salsalate) are pharmacokinetically unique in that their metabolism and plasma protein binding is saturable – thus enabling the generation of significant free plasma levels. It is known that the levels that are safely achievable are sufficient to impact NF-Kappa B as the result of studies into their ability to shut down cellular crosstalk from the NF-Kappa B pathway to insulin receptors.1-7, 63-64
The selective-COX2-inhibitor celecoxib also appears to be capable of impacting NF-Kappa B, but it shares the metabolism and protein binding limitations the NSAIDs have. However, it is capable of impacting this pathway at much lower concentrations than the NSAIDs do. It appears probable that this is the basis for its ability to impact colorectal adenomas and adenomatous polyps at twice daily 400 mG doses.13, 15, 21 Despite an impressive body of evidence supporting its ability to impact cancer growth and propagation it was not chosen as the primary agent for NF- Kappa B impact because of its questionable status relative to cardiovascular events and physicians’ reluctance to use it because of those questions.
Remember – you must ALWAYS have a physician’s support to try these ideas. I’m just a pharmacist – not a physician, and I’m providing information for you to review and discuss with your physician.