Det tok heldigvis ikke lang tid før mer kyndige kommentatorer så på magnetstudiet jeg nevnte i går. Det er Science-Based Medicine som går gjennom noen sider ved artikkelen.
I likhet med meg (og alle andre skeptikere jeg har sett kommentere det), finner de det interessant, men synes det er et par hakk oversolgt. Og ikke overraskende finnes det noen mulige problemer i studiet og forfatternes tolkning:
First, there is not a consistent dose response effect, as the strongest field (400mT) showed no effect. The authors make the post-hoc analysis that there is an upper therapeutic threshold, but this was not predicted by the original hypothesis and there is no known mechanism for such a threshold. The more standard interpretation of such a result is a lack of consistent dose-response. Also, the effect was only seen in the histamine induced inflammation and not CA induced inflammation – again, not predicted by the working hypothesis of the study. If SMF works through vasoconstriction of dilated arteries, as the authors hypothesize, why would the mechanism of inflammation matter? Therefore, these results do not show a consistent or predicted pattern, and could easily be interpreted, if taken together, as a null effect.
The authors also looked at the effects of pharmacologically blocking L-type Ca(2+) channels or nitric oxide (NO) to see if either blocked the effects of the SMF. This is a clever and established way to infer mechanism of action, and they found that the former, but not the latter, did block the effect of decreased inflammation by a SMF. Therefore the authors hypothesize that the SMF may work its effect through calcium channels. But again, random effects cannot adequately be ruled out, given the large number of outcomes that were measured in total.
Ellers er det ikke minst problemer med å overføre fra denne mulige effekten hos rotter til noe faktisk effekt hos mennesker…
As the authors recognize, SMF strength decreases significantly with distance. Rat paws are very small, and it is therefore practical to apply a strong SMF at tissue depth. A human joint or limb, however, is significantly larger requiring a much stronger SMF in order to maintain adequate strength at tissue depth. If these results represent a real physiological effect, they may not apply at all to humans or may simply be impractical.
Forfatteren av innlegget, Steve Novella, utvider diskusjonen av temaetpre-kliniske vs. kliniske studier på sin egen blogg.
Og så kunne vi ønske oss at både den ene og den andre tok dette inn over seg, heller enn å løpe avgårde med misvisende mirakelberetninger i begeistringens (eller avskrivingens) rus.