Homœopathic Links 2014; 27(2): 63
DOI: 10.1055/s-0034-1368430
EDITORIAL
Sonntag Verlag in MVS Medizinverlage Stuttgart GmbH & Co. KG Stuttgart · New York

EDITORIAL

Harry van der Zee
Further Information

Publication History

Publication Date:
05 June 2014 (online)

 

    In a recent publication “Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma” (Nature 2014)[1], the authors concluded that their “findings provide a rationale for why some BRAF or MEK inhibitor-resistant melanoma patients may regain sensitivity to these drugs after a ‘drug holiday’ and identify patients with EGFR-positive melanoma as a group that may benefit from re-treatment after a drug holiday.”

    It had been observed earlier that melanoma that become resistant to specific chemotherapy (BRAF or MEK inhibitors) started to decrease in size once the therapy was stopped instead of growing more rapidly. The reason for this is that the tumour has become dependent on the drug to survive. The tumours gain resistance by changing the chemistry of the inside of a cell. However, the researchers showed this process left the cancer cells dependent on the drug – like an addict. After a “drug holiday” of several weeks, this changed chemistry inside the cell reverses and as a result the drug resistance resolves and the patient can be put back on the same drug. Experts expect that this principle may be true for many more drugs and several studies are on their way to investigate this.

    Why do I share this with you? What struck me is that the mechanism is very similar to what homeopaths observe when using Q-potencies. The remedy is stopped and started depending on the response of the patient. An occurring aggravation while on the remedy is reason to stop it, while a relapse while off of the medication is reason to resume taking it. Homeopaths have been using the principal of “drug holidays” ever since Hahnemann.

    Another fascinating development in cancer therapy is the individualisation of each and every case. Instead of a standard treatment for a certain type of cancer, researchers have found that to drastically improve results therapy must be tailor-made to the patient based on individual genetic differences. This development not only involves cancer and may spread to a wide range of diseases.

    To minimise side effects and to maximise results there are several developments researchers are working on that will make it possible for a drug to only become active or released once the target organ has been reached.

    The term “hormesis” was coined and used for the first time by Southam and Ehrlich in 1943 to replace what was earlier know as the “Arndt-Schulz rule”, which says: for every substance, small doses stimulate, moderate doses inhibit, large doses kill. Low exposures to toxins and other stressors generate a favourable biological response. A toxin showing hormesis thus has the opposite effect in small doses as in large doses. It is conjectured that low doses of toxins might activate the repair mechanisms of the body. The repair process fixes not only the damage caused by the toxin, but also other low-level damage that might have accumulated before without triggering the repair mechanism.

    What we can observe in general medicine is a development that includes individualisation of treatment, lower doses of medicine and drug holidays. This will not change allopathic treatment into homeopathy but it seems to me that recent developments in medicine may – be it step-by-step – help bridge the current gap between allopathy and homeopathy. I only have to look at my own history to realise the great benefits that both school medicine and homeopathy have brought to my health and well-being. Iʼm grateful to all searchers of truth as they are the ones that help build future medicine – a form of health care that integrates and values different systems of healing, and to the benefit of the patient distils for each and every case the best possible treatment. A wonderful dream indeed. Itʼs up to all of us to make it real.

    Harry van der Zee, MD, Editor


    #
    Zoom Image

    1 Bernards R et al. Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma. DOI: 10.1038/nature13121




    Zoom Image