Letter from the Publisher

OHM Conference

Just before the Academy Awards, Orthomolecular Health Medicine (OHM) held its annual meeting in San Francisco. OHM is a small group of physicians who have focused on orthomolecular and integrative medicine for the past three decades. Richard Kunnion, MD, who founded the group, continues to lead the organization with enthusiasm, ignoring the rigors of recent major surgery. Robert Rowen, MD, editor of Second Opinion newsletter, updated us on oxidative therapies focusing on benefits of ultraviolet blood irradiation and ozone therapies. Frank Shallenberger, MD, who offers advanced training for physicians in ozone therapy, expanded on Rowen’s discussion. Both Rowen and Shallenberger have shared the difficulties of most medical pioneers – harassment and ostracism by medical authorities. It is gratifying that we could enjoy their teaching at OHM; both have been increasingly accepted by doctors and patients.

Also sharing the limelight at OHM was Ron Hunninghake, MD, who carries on the work of Linus Pauling, PhD. Hunninghake specializes in administering intravenous vitamin C for cancer, infectious disease, and inflammatory disorders. Hunninghake’s research clearly demonstrates that although vitamin C is considered an antioxidant, intravenous vitamin C acts as a prooxidant or oxidizing agent, reducing neoplastic and inflammatory activity in part by its intracellular production of hydrogen peroxide. The OHM conference highlighted the powerful role that glutathione, vitamin C, and ozone offer as prooxidant agents. It remains disgracefully negligent that conventional medicine ignores these therapies despite the fact that not only are they tremendously effective in many debilitating chronic disorders but their safety record shames the iatrogenic record of pharmaceuticals prescribed daily. Why is there such a disdain for remedies that are safer and so much less expensive?

Professor Duesberg and Aneuploidy

Also presenting at OHM was Peter Duesberg, PhD. Duesberg is an professor of molecular and cell biology at the University of California at Berkeley. He is renowned for his genetic work isolating the first oncogene in his studies of retroviruses. His gene research has been widely published, leading to election to the National Academy of Sciences and extensive grants from the National Institutes of Health. In the 1990s, Duesberg’s ongoing research led to evidence that argued against the generally held hypothesis that HIV causes AIDS. Duesberg’s work observed that carrying the HIV virus did not prove causation; instead, AIDS required destruction of the immune system from long-term consumption of recreational drugs and treatment with AZT, a putative antiviral HIV treatment. Duesberg’s hypothesis was published widely in the 1990s and had the support of 1993 chemistry Nobel Prize winner Kary Mullis. However, the AIDS medical establishment and AIDS community have widely condemned Duesberg’s unpopular hypothesis and Duesberg has been ostracized. He has been systematically refused grants based on his anti-HIV position.

Duesberg continued to do medical research at Berkeley despite a lack of confidence from academic colleagues. For the last decade, his research has focused on cancer. As one of the first scientists to discover an oncogene, he has been very familiar with the genetic hypotheses for causation of cancer. Duesberg’s work in the 2000s began to question genetic causation. His thinking was that although there was some increased risk for cancer based on having an oncogene, a large majority of individuals having an oncogene do not develop cancer. Mutagens demonstrated a much more rapid development of cancer in “normal tissue” compared with tissue with an oncogene. Why would mutagens lead to rapid neoplastic change?

Chromosome studies of cancer tissue demonstrate starkly different karyotypes (chromosome count and structure) compared with normal tissues. Human karyotypes normally have 23 paired chromosomes for total of 46. Down syndrome is characterized by a karyotype of 47 chromosomes based on three separate but identical number 21 chromosome. Chromosome probes of well-studied HeLa cancer tissue demonstrate a karyotype of multiple chromosomes. Instead of 46 chromosomes, there are over 70 chromosomes. Some chromosomes are triplicate as in Down syndrome, some are groups of four, a few are only a single chromosome, and some are only parts or pieces of a chromosome. Further, a few chromosomes are bindings of one chromosome with a second chromosome. These irregular duplications and chromosome bindings are known as chromosome aneuploidy. Duesberg hypothesizes that aneuploidy is the cause of cancer.

Unlike a normal karyotype, an aneuploid set of chromosomes is unstable. Most aneuploid cells rapidly die. Rarely aneuploid cells reproduce and survive – those that do reproduce and are essentially immortal. Being aneuploid conveys the ability to be flexible. Harsh environmental conditions do not spell death for the aneuploid cell; instead the aneuploidy allows for unlimited adaptability, enabling resistance to chemotherapy, radiation, and other agents. Also aneuploid cells are highly individualized. No two tumors share identical aneuploidy.

I thought Duesberg’s work was mind-blowing; I still cannot stop thinking about it. It explains why our war on cancer is off track – why examination for oncogenes is of minimal value, why sensitivity test for chemotherapy agents is even more questionable, and why cancer work must now start from scratch looking at the chromosome and aneuploidy. I thank Dr. Duesberg for being able not only think to outside of the box but to withstand the snarling denigration that he had experienced from colleagues and friends.

Look forward to reading more about Duesberg’s work in future issues.

Jonathan Collin

Reference

Duesberg P et al. Is carcinogenesis a form of speciation? Cell Cycle. July 1, 2011;10(13):2100–2114.