“Oooh! A new and exciting area of science – does it have big, important-sounding words? EXCELLENT – could it in anyway concievably be applied to homeopathy? F**k it! That’ll do!”
One of the many claims that Homeopathy makes is that of the “Similia Principle” or “like cures like”. It is this principle by which a homepath selects a remedy: Patient presents with symptom X. Compound Y causes symptom X. Give patient an ultramolecular dilution of compound Y to treat symptom X.
In the recent edition of Homeopathy “Special Issue: Biological models of homeopathy Part 2” a paper entitled “The similia principle: Results obtained in a cellular model system” concludes that
“results support the similia principle at the cellular level and add to understanding of how low dose stress conditions influence the regulatory processes underlying self-recovery”
They then document some experiments in which cells that are exposed to a high dose of “stress” (heat shock, or toxic compounds such as Arsenic or Cadmium) cope better with and react more intensly to a subsequent low dose of stress. Why this is surprising, I do not know. Adaptive responses and/or preconditioning of cells (both prokaryotic and eukaryotic) is well researched. A pubmed search for adaptive response generates over 17000 hits, for preconditioning over 8000. (correct as of Jan 29th 2010).
On a cellular/molecular level, this can be explained by more rapid production/activation of certain stress response proteins, such as heat shock proteins and protein folding chaperones – proteins which attempt to either prevent or reverse that damage caused by whatever stress factor is currently blighting the cell’s ability to proliferate and survive. The more rapid response to the second exposure to stress might be as a result of residual levels of certain transcription factors or activators within the cells. This is not explored in the paper. Another possibility is that the cells that survived the initial high dose of stress are intrinsically better able to adapt to the stress, either as a result of mutation or cellular niche or various other arm-wavey possibilities. The first assult with the stress causing compound has naturally selected for those cells with a better chance of survival – this is the basis of something called “Evolution.” Google it. I’m told It’s quite popular.
At the level of an organism, this is basically describes an immune system. An organism is confronted with a “stress”. The organism develops a response (e.g antibodies) to the stress. Next time the stress is encountered, response molecules are quickly produced in massive quantities to prevent damage from stress. Surely everyone saw this graph in GCSE/’A’-level biology?
It’s the basis by which all vaccines work, and how multicellular life responds to any sort of antigen. Very basic stuff. Hence It was taught at GCSE level (at least when I sat GCSE Biology in the early 90s).
This paper, however, does things differently – high dose first, then low dose – and seems to find some extra significance in this. Why? The relative sizes of the doses are immaterial, as long as cells/organism survive, it is now primed to respond to a second insult. IMHO, a more interesting study ( at least on a cellular/molecular level) would be how long does this “priming of the system” last? Does that time correlate in any way with known half lives for mRNA, transcription factors, phosphorylation of various proteins? Is this persistence of this effect related to the size of the initial insult? This is not commented on.
Figure 1 is a nice little diagram of their experimental design.
Fig 1 from here – used without permission, but fair use claimed.
There are two incredibly obvious ommissions in this experimental design…
Low dose, high dose, evaluate.
Low dose, no treatment, evalute.
I imagine that this has been done before – and if I was feeling mean I might suggest that the results maybe very similar to the “high dose/low dose” regimen, and have been ommited – but irrespsective of this – one needs to replicate this in your experimental design as a control. Ooops.
But that’s really nitpicking – important nitpicking, IMHO, but nitpicking nevertheless.
They then go on to use these observations to support the basic tenets of homeopathy.
- All these experiments are done with actual measurable amounts of compounds present (10uM, 0.3uM – handy, easy to understand concentrations like that). Unlike homeopathic remedies.
- When treating someone with a homeopathic remedy, the patient will persumably be taking the *cough* low dose1 *cough* at the same time as he/she is suffering with the effects of the high dose (note – Homeopathy treats symptoms, not causes – so it is easy to see how they might overlook this). So even if the concept of hormesis is real and valid in this context (and there is some controversy about that) what is the biological mechanism by which this occurs? After all a very big number plus a very small number is still a very big number – how does the body determine which compound is for what purpose?