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Why do the Fluge/Mella trials seem to be more successful than off/trial reports?


Senior Member
Interesting, then how to explain Dr Hyde's findings that ME tends to appear in the Fall / early Winter?
Perhaps he's talking about endemic cases. Cases don't fall to zero in the winter they just drop off quite a bit.


Senior Member
Canary islands
@Manganus so perhaps autoimmunity is over represented in darker latitudes thus inflating the RTX response rate in Bergen

Yeah, perhaps. But if so, it's still relevant and interesting.
One point is that many people actually do live on these latitudes. They need a cure as much as anyone else, particularly if the prevalence is higher - which I believe.

Another point is that anything that improves the understanding of the mechanisms of our disease is badly needed.

And perhaps the higher prevalence is a secondary effect of the adaption to living so far away from Africa, from where our evolutionary forefathers may have emigrated some 60.000 years ago.
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I may have misunderstood this, esp as it was the first 'live' cfs event I attended, but when Fluge spoke at Norwich early this year I understood him to say that the Stage 2 rutuximab trials included some participants who they knew were responders from previous treatment / Stage 1 trials. Clearly this could make a sense in a Phase 2 trial where the primary questions are about type & length of response, not proportion of responders. If only a sub-set of pwcfs respond, which is the expectation, it would have been terrible to spend the money on a Phase 2 trial which happened not to include any participants who respond to the treatment! But if I'm right about this, it could have artificially inflated the Phase 2 trial response rates.

Once they had Phase 2 data, the recruitment and all other aspects of the much larger Phase 3 blinded trial will have been constructed to give a more accurate assessment of the proportion of participants who respond, which participants respond, etc. etc.

Could this explain lower responder rates among a general population of pwcfs, and maybe expectations of lower responder rates for the Phase 3 trial?


Senior Member
I had thoughts along these lines: there was a major outbreak of giardiasis (Giardia lamblia infection) in Bergen, Norway in 2004 (an estimated 2500 cases), so this lingering pathogen may now be common in the intestines of a subset of people in Bergen. Giardia lamblia is linked to ME/CFS, as well as autoimmune diseases. Fluge and Mella are based in Bergen, so it occurred to me that their cohort may contain lots of people who developed ME/CFS as a result of Giardia lamblia. More in this post.

I think they've adressed this. I think that zero or perhaps one of their patients got ME from the outbreak.


Senior Member
I think they've adressed this. I think that zero or perhaps one of their patients got ME from the outbreak.

OK, that's interesting. Is that mentioned in one of the Fluge and Mella studies?

I was wondering though whether as a result of the outbreak, there might be a higher percentage of people in Bergen who have Giardia lamblia in their intestines, due to person to person transmission. It says here that:
One of the highest risk groups are people living in the same household as a case of giardiasis because Giardia can be transmitted by the faecal-oral route from person-to-person. Between 35-70% of people infected with Giardia have no symptoms but are still infectious to others. Without treatment, infectivity can continue months resulting in potential infection or re-infection of others.

The general prevalence of Giardia lamblia (also called Giardia intestinalis) in industrialized countries is 2–7%. Ref: 1 People can be asymptomatically infected with Giardia lamblia, as well as the infection leading to giardiasis.

So although there may not be many patients in Fluge and Mella's cohort that can trace their ME/CFS directly back to the Giardia outbreak, perhaps it is possible that the cohort could still contain a higher than normal percentage of people with Giardia in their intestines?
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