Hi everybody:
I am in receipt of the latest EMF RAPID "Breakout Group Reports for Epidemiological Research Findings," a final report of the symposium which was held in San Antonio, Texas, January 12-14, 1998.
Actually, in this message I am forwarding only a portion of the results of the San Antonio meeting: 'quoted segments' of a paper prepared by Dr. Robert Liburdy, PhD, of the Lawrence Berkeley National Laboratory. Liburdy's paper is attached as "Appendix One" to the final report of the meeting. (It is actually an addendum to the discussion report of "Role of Mechanistic Data in Strengthening the Epidemiology Findings." This was one of the breakout groups at the meeting.)
Knowing of the high level of interest within this group concerning the Melatonin Thesis, and because I consider that what follows from Liburdy's paper is "state of the art" on the subject, I quote at length below from that paper. It reflects much of what was discussed in the breakout group at the meeting, where I also was present and can attest to the fact that this information was presented and discussed (generally) as reported here by Dr. Liburdy.
Liburdy's paper is too long for me to include all of it below. In selecting the quotations I have (below), I am trying to give you as much of the 'flavor' as possible -- because there is important new information here about the Melatonin Thesis!
I do not have good fax capabilities. Those of you who may want the complete document should e-mail Mary Wolfe at NIEHS, <wolfe@niehs.nih.gov>.
What follows is quoted directly from Liburdy's paper. I am omitting quotation marks and the numerous references he cites within his text. I will comment briefly at the end....
Cheerio.......
Submitted by Robert Liburdy, Ph.D.
The melatonin hypothesis was discussed in detail during the breakout group discussions. Since the breakout group section reporting on the _in vitro_ studies relating to the melatonin hypothesis did not capture all the details of the discussion that took place, additional comments are provided here. For example, the breakout group discussed the action of EMF on other drugs and chemicals that regulate cell growth, such as tamoxifen; refer to the figure developed during the discussions. Since there is no presentation of this research in the report, this material is provided in this appendix. Literature references for these studies are listed at the end of the Appendix.
A. _In Vitro evidence for melatonin effects_
A series of studies has shown that EMF exposure as low as 12 mG (1.2 uT) inhibits melatonin oncostatic activity on MCF-7 breast cancer cells. [refs skipped.] This work has been independently replicated in two different laboratories. Thus, three laboratories have independently reported this bioeffect at 12 mG, and a summary of the results across these three laboratories with a discussion of the biological and EMF exposure protocols was presented at the 2nd World Congress for Electricity and Magnetism in Biology & Medicine; and a manuscript for publication in the proceedings is in peer-review.
The role that these _in vitro_ findings play in the melatonin hypothesis was discussed by the breakout group. Demonstration of a direct EMF effect on the activity or biological activity of the hormone melatonin is a new finding which modifies the original melatonin hypothesis. The original hypothesis states that EMF reduces the circulating levels of melatonin, and this will result in elevated levels of estrogen and prolactin which increases the risk of breast cancer.
The melatonin hypothesis invokes a general mechanism that has relevance to all hormone dependent tissue responsive to estrogen and/or prolactin, such as human mammary epithelial tissue, ovarian tissue, and prostate tissue. The _in vitro_ findings that EMF can block melatonin's oncostatic action at the cellular level modifies the melatonin hypothesis and broadens it to address EMF's effects on melatonin's oncostatic action of target cells. This has several important consequences.
First, a concomitant reduction in melatonin's oncostatic activity complements an _in vivo_ reduction in circulating levels of melatonin.
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Second, it is important to consider the consequences of blocking melatonin's oncostatic action and how this may act in combination with a reduction of circulating levels of melatonin. For example, a biological system's "full response" to EMF could involve both effects to reduce melatonin's biological activity. In this case, the "target cell" effect and the "circulation" effect would occur in conjunction to elevate risk of cancer. However, a reduction in circulating levels of melatonin does not have to take place for the "target cell" effect to occur. Importantly, in this case, an EMF effect on reducing melatonin's oncostatic action would occur in the absence of a reduction in circulating levels of melatonin.
As a result, the melatonin hypothesis is not strictly dependent on a reduction of circulating melatonin, but is operative when EMF blocks melatonin's oncostatic activity either a) by an EMF interaction at the target cell level, b) by an EMF effect on circulating levels of melatonin, or c) by both interactions.
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A comment was made by Dr. Liburdy regarding the magnitude of the melatonin effect on cell proliferation. The experiments conducted by Liburdy, Blackman, and Luben assessed the effect of melatonin on MCF-7 cells over one (1) cell division cycle _in vitro_ over approximately seven days of culture. This is a standard approach for _in vitro_ cell growth studies. In contradistinction, however, these cells would continue to divide exponentially _in vivo_ as a tumor mass over many subsequent cell division cycles. Thus, a change in proliferation of 15-25% for exponentially growing cells would translate rapidly into a large change in cell numbers over multiple cell division cycles. In this light, a change in cell proliferation of 15-25% for exponentially growing cells should be interpreted as significant within this biological context.
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A.1. _In vitro evidence extending the melatonin effect to other growth regulating drugs and cell types_
Dr. Liburdy commented that tamoxifen is known to inhibit human breast cancer cell growth, _in vitro_ and _in vivo_, and this action is shown by the dashed line in the Figure. EMF studies from his laboratory have recently been reported for the anti-estrogen tamoxifen (Harland & Liburdy, 1997), and these were summarized. In the Figure the tamoxifen pathway which blocks estrogen growth promotion (dashed line), is inhibited by magnetic fields ("X" in the Figure). In the tamoxifen experiments MCF-7 cell growth was reduced in a dose-dependent manner by pharmacologically relevant levels of tamoxifen, and this action was inhibited by 12 mG magnetic fields. Thus, a second growth regulating compound (tamoxifen) was inhibited by environmental level EMF. Since tamoxifen is known to act through the estrogen receptor, these studies suggest that the estrogen receptor may be involved in this EMF interaction.
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In summary, the _in vitro_ studies discussed above indicate that environmental
level magnetic fields can block or inhibit the action of several growth
regulating compounds that act through the estrogen receptor, as well as
the hormone melatonin. These effects have been observed in two human
breast cancer cell lines (ER+): MCF-7 and T47D cells. Further studies
are required to identify specific, underlying biological mechanisms of
action, and to extend these findings to
additional cell types.
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A brief commentary from guru.......
The two-pronged attack of EMF exposure upon human cell activity reported by Dr. Liburdy (above) constitutes the strongest evidence so far that the melatonin hypothesis provides _at least one_ STRONG "mechanism" explanation for what is being found in the epidemiology studies.....
I do not believe that melatonin will prove to be the "only" one. And I do not claim that it is "the most basic mechanism." We are not likely to ever see that: the action of the electrons in either "resonating with" or "disrupting" other electrons thereby resulting in chemical activity. What we are beginning to see is the chemical activity.....
The "science community" studying this issue (except for a few more daring souls) is still not willing to credit this ***three times replicated*** evidence as "definitive" of an EMF health hazard..... That is evident to me by the "waffling" verbiage appearing in the reports that are coming out of this EMF RAPID review effort.
Question: Who was it that ever started public policy down the road of requiring a "definitive" standard of "proof" before government and others (like the medical community) can begin to institute protective policies on behalf of the public??? ... And, equally important, tell the truth to the public about what WE DO KNOW!!!.....
Many of us on this list believe we know the answer. It was the vested interests...... They are not the ones to define the way public policy should be made on these matters. Not in the case of lead or tobacco or EMF. And it is well nigh time that a new standard -- more protective of public health considerations -- be thrust into the public policy decision-making machinery.
This requires that the public be given the truth...... Then the public will DEMAND action in their interest rather then in the industry's interest.
Frankly, it is my observation (after nearly five years exposure to the EMF "science community") that science, by and large, has a great facility for describing "what we do NOT know" -- but very little acility when it comes to describing or reporting (to the public and to the government) WHAT WE DO KNOW........
(I wonder, is that a result of the constant need to justify more research funding?)
I am informed that we still do not have a "definitive" explanation of the tobacco hazard _in a scientific sense_. Yes, it has evidently been formulated (finally) -- and we see it being acted upon -- in a public health sense. But science still does not know all the "mechanisms" that explain tobacco's harmful biological action.....
This "hang-up" that we are experiencing in arriving at the so-called "proof" or "definitive findings" of the EMF hazard ... does not do credit to the substantial gains in our knowledge that have come about over the past five years.
We now KNOW, for example, that biological activity can occur as a consequence of EMF exposure levels which are present in our environment. We have replicated evidence that at least one of the responsible mechanisms has been identified -- melatonin and the estrogen receptors.....
We owe some special thanks to the likes of Liburdy, Blackman, Luben... for the work they have done on the melatonin thesis over the past five years. We are also greatly indebted to Richard Stevens of Battelle Laboratory for "seeing through the fog" of this EMF mystery as early as 1985 and putting forth the "melatonin hypothesis." These men have required nearly as much courage as wisdom and perseverance to bring us to the point where we are today......
Are their more of you "out there" of equal courage, wisdom and perseverance???? You are needed now ... as this matter reaches a critical junction in the 1998 Report to the Congress......
P.S. Some time ago, one of this group asked me where I got the idea that EMF could be a factor in the prostate cancer surge now being seen in industrial countries???? It's there ... in the text of Dr. Liburdy's paper......
Cheerio......
Roy Beavers(EMFguru)
rbeavers@llion.org