Avastin: A Failed Drug – The Predictable- and the Predicted-Comes True
Avastin: A Failed Drug
The Predictable- and the Predicted-Comes True
In 2007, I predicted that Avastin (and other drugs in its class) will prove to be failed drugs. On December 16, 2010, that prediction was validated. The Food and Drug Administration (FDA) revoked approval of this drug for breast cancer, declaring it ineffective. Neither the journalists who wrote The New York Times’ first-page Avastin story nor any other journalist recognized the real story in FDA’s action: it was a shameful journalistic delinquency. Thousands of people were unjustifiably given an ineffective and toxic drug and no journalist warned them against it.
Rather than apologize to people poisoned by the drug, the head of FDA’s cancer drug division made this bizarre statement: “Please note that these findings are also disappointing for the FDA as well.” By then the yearly cost of the drug often reached $100,000 or more, and it had become one of the most popular cancer drugs in the world, with 2009 sales of about $3.5 billion, $2.3 billion of that in the United States.
I made a clear, unequivocal prediction that Avastin will prove to be a failed drug with the following words in my book entitled “The Crab, Oxygen, and Cancer Volume I: The Dysox Model of Cancer (2007):
A current dogma in the field of oncology states that cancer causes the production of new blood vessels-a process called tumor angiogenesis – to fulfill its growth requirements. From that dogma the field derives its second dogma: Cancer can be cured or controlled by inhibiting angiogenesis with drugs called angiogenesis inhibitors. In this chapter, I challenge both dogmas by presenting personal observations and reflections on the subject. Then I put forth the Dysox Model of Angiogenesis, according to which angiogenesis occurs as a consequence and not the cause of mechanisms by which cancer grows and spreads. From that statement, the clinical significance of this model should be self-evident: angiogenesis inhibitor drugs cannot be expected to provide long-term benefits in controlling cancer (page 264).
Avastin, of course, is one member of the family of angiogenesis inhibitor drugs. I have seen patients who took Avastin and discontinued it after they developed deep, foul-smelling, and bleeding ulcers on their faces, heads, and other parts of the body. Imagine my anguish in observing such poisoning by an ineffective drug. Never mind that the drug’s hapless victims would have paid $100,000 or more a year had they continued the treatment, as some others do.
Deceptions, Damned Deception, and Chemo Statistics
Mark Twain knew something about liars, lies, and statistics. He would have grinned broadly reading about the Avastin dollars and deceptions in a 2008 report. It revealed that the follow-up trials showed drug efficacy that was far lower than that reported in the initial trials. No surprise there since doctors are paid more for conducting initial trials than for follow-up trials. The following data shows the dramatic contrast between the two sets of trials and reflect the deep corruption in conducting and reporting trials:
Survival with Avastin after 18 months
Initial Trials Later Trials
Breast 1.7 months 0.8 months (24 days)
Lung 2 months 0.4 (12 days)
Colorectal 4.7 months 1.4 months
Notwithstanding the above dismal results with this toxic drug, 29,000 American women with breast cancer were receiving it in 2010. A similar number of women with colon and lung cancer in the country were on the drug. Genentech is expected to appeal the decision. No doubt that Wall Street analysts will continue to spin the truth and forecast fabulous riches for the drug’s manufacturer. And they might prove right. Such is the power of deceptions in chemo statistics!
Who Should Take Avastin?
I present the above facts to assist people in answering this question. The final decision rests with the individual. Would I take Avastin myself? My answer is such not because I do not think that an extension of life even for one more day is not highly significant. I offer my response in light of my answer to the following two questions:
x What would be the quality of my life during the 24-day extension of life with a toxic drug?
x What else could be bought with the $100,000 or so the drug will cost for one year?
The truth is that one-fifth of that amount ($20,000.00 per year) spent on healthy, well-prepared meals, nutrient supplements, training in meditation, and measures for effective bowel and liver detox will give me vastly superior clinical results.
All failed drugs trigger lobbying by some patients and doctors. And so it is the case with Avastin now. A 2010 report on Avastin withdrawal in The New York Times included the following quote “I’m really afraid it’s not going to be available to anyone…It has saved my life.” I wonder how many readers might doubt that most such “patients and doctors” lobbying is actually planned-often with chocolates and candy as incentives-offered by drug representatives of the company.
It reminded me of a patient with lung cancer who said, “My oncologist told me I’m the only patient in his practice who responded to Avastin. I haven’t told him anything about what I do in your program.” Several months later, she returned, with full relapse of all symptoms and told me that she had “fallen off the wagon.” We started the program and again she responded well to our program (described in The Crab, Oxygen, and Cancer). This cycle was repeated twice more to convince both of us that her clinical benefits were not drawn from Avastin but from a robust program of nutrition, detox, and meditation.
Of course, not all patients respond to a strong integrative program. My point: lobbying by patients and doctors rarely has any true merit when multiple large trials and extended clinical experience establishes a drug to be a failed drug.
For readers interested in the subject of new blood formation in tumors (angiogenesis) and those curious about how I arrived at my prediction that Avastin will prove to be a failed drug, I include below additional text from my book entitled “The Crab, Oxygen, and Cancer. Volume I: The Dysox Model of Cancer (2007)”
Close to finishing the manuscript of this book, I wondered if I needed to include a brief chapter on angiogenesis, a subject that is presently considered to be “red hot” in oncology. Later that day when I stepped out of the warm office into the cold street air, two questions arose that had never crossed my mind before: First, why would cancer trigger angiogenesis except to commit suicide? Second, why would cancer want to commit suicide? Those questions were followed by a third and chilling question: Why had I uncritically accepted the prevailing dogma that cancer causes angiogenesis to spread and that it can be cured and/or controlled with anti-angiogenesis drugs? Then came, in quick succession, the following five questions:
? If cancer really causes angiogenesis to spread itself, why wouldn’t extra oxygen brought into the tumor by those new blood vessels incapacitate and/or kill cancer cells?
? If angiogenesis was essential for tumor growth, why wouldn’t the removal of excess acids in and around cancer not weaken cancer cells?
? If angiogenesis were the mechanism for tumor expansion, why wouldn’t the drainage of free radicals in and around cancer not strengthen the immune cells in their fight against cancer cells?
? If I were to accept the prevailing dogma of angiogenesis, would it not cast serious doubt about the validity of my ideas of the biologic roles of the three cancer furies?
? Beyond that, if I were to accept the prevailing dogma of angiogenesis, would it not invalidate the Dysox Model of Cancer?
None of those questions disturbed me. Those questions answered themselves as soon as they arose. For over two decades, I had trained myself to look at the problems of medicine only through the prism of oxygen homeostasis. It only seemed right then that I should look at the phenomenon of tumor angiogenesis through that prism as well.
However, there were other troubling thoughts. My questions were pitting me against the entire oncology community. Specifically, if my ideas of the three cancer furies are right, then the prevailing notion of cancer causing angiogenesis to expand could not be entirely correct. If the universally accepted ideas about tumor angiogenesis were valid, I could not be right. Either way, it was an unsettling proposition. I say universally accepted because I did not recall if I had ever read or heard an opinion to the contrary. An ugly question arose: What is the possibility that everyone in the field of angiogenesis had climbed out on the wrong limb of the tree? If they have been on the right track, how could I have been on the wrong track? And for so long?
For continuing the above text, the readers are referred to The Crab, Oxygen, and Cancer. Volume I: The Dysox Model of Cancer (2007).