There has been “floated around” opinion that “calcium channels are the main, possibly the sole target for EMFs”. This opinion is somewhat uncritically praised and accepted as sort of proven “dogma” by non-scientist-activists.
I think it is premature to consider calcium channels as the sole targets of all types of EMF and a sole mechanism behind the observed EMF effects. This generalization is reaching too far, without sufficient scientific basis.
As Einstein said, “who can be so sure about nature?”.
I asked Henry Lai of his opinion in this matter. Henry is, in general, supportive of the “calcium hypothesis” but has several cautionary comments about the science.
So, not everything in “calcium hypothesis” is as clear as some present it…
Cautionary comments on “calcium hypothesis” from Henry Lai
I agree with Marty Pall that “calcium channels” is an important topic of investigation on the mechanisms of EMF bio-effects. But, I am not sure that “calcium channels” is the “sole” answer to the mechanism of EMF interaction with living materials. The idea that EMF (particularly ELF EMF) affects calcium channels is not new. But, there are some concerns on how big a role it plays.
- It is quite difficult to envision how alternating EMF affects calcium channels. The channels are activated when membrane potential depolarizes. That means the change that triggers the effect is spatially directional, i.e., the outer part of the cell membrane becomes “less positive” and a cell in question has to be aligned in a certain orientation with the detection of the EMF. This may be true in in vitro experiment, but not in in vivo experiments and “human exposure situations” when an animal (human) moves in the field.
- Temporally, it is difficult to understand how oscillating EMF affects calcium channels. The time period of change when exposed to an AC-field in the environment is probably too fast for the channels to detect, for ELF field and particularly for RF field. One has to consider that RFR may exert its effect by its low-frequency modulation-component and not the carrier frequency (see the study by Ross Adey on calcium efflux). If this was true, one would expect that modulated-RFR should be more potent that continuous-wave RFR of the same frequency and SAR. The literature does not support this.
- In 1992, Liburdy published a study (which I consider to be an ingenious experimental design and concept) showing that ELF-EMF affected calcium channels by “induced current” (or electric field, and not magnetic field). What it means is that to show effect on calcium channels, one has to use very low-frequency fields (< 10 Hz) and/or high intensity. In most of the recent studies on calcium channels, relatively high fields were used (1-10 mT). How could the results from “calcium channels” explain the epidemiological effects of increased cancer risk at 0.4 uT?
- How can “power window” and “frequency window” effects be explained by the assumption that EMF affects calcium channels?
- It is quite puzzling that most of the effects reported have been on the L-form of calcium channels. However, there are reports showing that ELF EMF inhibited the T-form. And, ELF had no significant effect on the N-form, but RFR activated it. If change in membrane polarization by EMF is the cause, should one expect similar effects on all forms of calcium channel? Do they use the same positively-charged polypeptide domain to open the channel?
- How does “cyclotron resonance” fit into this? There are many reports on calcium cyclotron resonance and EMF (probably as many as the “calcium antagonist” studies.) Much lower field intensity is needed for the cyclotron resonance effect (and 7 Hz).