Treating cancer with amplitude-modulated electromagnetic fields: a potential paradigm shift, again?

Abstract

!! ! ! ! ! ! ! The Zimmermanet al(2012) study published here, coupled with the group’s two preceding papers (Barbaultet al, 2009; Costaet al, 2011), identify a potential modality for treating tumours at a dramatic reduction in trauma and cost. This set of clinical and explanatory laboratory results should be understood in the context of the history of research into the biological effects of electromagnetic fields (EMFs). The most successful clinical application is the use of EMF to initiate fusion in fractured long bones that would not otherwise heal. Pulsed fields were designed to simulate the natural piezoelectric signals generated from bones under varying stress while walking (e.g., Bassett, 1985). There are also other reports that EMF can reduce pain and stimulate wound healing after surgery. The group’s two previous clinical reports were critical to the design of this new Zimmermanet alstudy. Barbaultet al(2009) described how they obtained the specific frequencies for different tumour diagnoses, which are then used in the amplitudemodulated (AM)-EMF treatment of those patients to stabilise the disease beyond normal expectations. Costaet al(2011) reported surprising clinical benefits from using the specific AM-EMF signals to treat advanced hepatocellular carcinoma, stabilising the disease and even producing partial responses up to 58 months in a subset of the patients. Now Zimmermanet alhave examined the growth rate of human tumour cell lines from liver and breast cancers along with normal cells from those tissues exposed to AM-EMF. Reduced growth rate was observed for tumour cells exposed to tissuespecific AM-EMF, but no change in growth rate in normal cells derived from the same tissue type, or in tumour or normal cells from the other tissue type. The growth rate inhibitory response was field-strength (SAR) and exposure-time dependent. In ancillary tests, they observed reduction in gene expression and increases in mitotic spindle dysfunction only for the AM-EMF exposure that reduced the cell growth rate. The work of Zimmermanet al, Costaet aland Barbaultet alwas not done in a vacuum. More than 30 years ago, Suzanne Bawin working in Ross Adey’s lab (Bawinet al, 1975), with independent replication by my group (Blackmanet al, 1979), demonstrated that biological effects could be caused by certain AM frequencies on a carrier wave but not other frequencies, similar to the current work. Subsequent reports in the 1980s by several groups continued to support and extend the initial findings (Adey, 1992; Blackman, 1992). This growing collection of reports demonstrating AM-EMFinduced biological effects led to recognition by national and international authorities that this modality needed to be considered in hazard evaluation, in addition to field-induced heating as a cause for health concern. The National Council on Radiation Protection and Measurements (1986) recommended a reduction in the allowable exposure intensity limits for AM radiation above a certain level, and the World Health Organization (1993) explicitly acknowledged AM as a future issue to be examined in setting exposure guidelines. Unexpectedly, research funding for this area dried up around 1990 and scientific advances dramatically slowed. A promising area of research fell by the wayside. The Zimmermanet alpaper, providing essential laboratory data to support the two previous clinical treatment papers, has resurrected the promising AM-EMF paradigm. It should lead to a major reevaluation of this novel and potentially effective treatment for cancer and possibly other conditions. This study demonstrates the fundamental requirement for a biological ‘information content’ code (i.e., the AM spectral profile, much like different AM radio stations with different content ‐ e.g., all news, or music) that can affect tumour cells from the tissue of origin, while apparently being ignored by normal cells from various tissues and tumour cells from different tissues of origin. The correspondence between AM-EMF-induced effects on cell proliferation, gene expression, and mitotic spindle dysfunction provide some clues to a possible biological mechanism of action.