kaffiend
Senior Member
- Messages
- 167
- Location
- California
I'm fairly certain that the follow-up study in 2010 tested immediately after exercise. The 2003 study showed c4a split products at 6 hours post-exercise. Timing is everything.
GcMAF, inflammation and individual response
- Thread starter serg1942
- Start date
I'm fairly certain that the follow-up study in 2010 tested immediately after exercise. The 2003 study showed c4a split products at 6 hours post-exercise. Timing is everything.
mojoey
Senior Member
- Messages
- 1,213
That was my impression as well.
Let's put it this way: if our hypothesis was that c4a was dropped by the gcmaf, and that the drop had a negative correlation with symptoms getting worse, then the fact that c4a might be elevated by a particularly active trip would absolutely put a wrench in that. However, what we're finding is that the baseline c4a's are fairly low across the board (which is the opposite of what you would expect based on the 2003 study) and that in fact, re-testing of c4a shows a 300% to 1000% increase from their baseline values in people that started out with low baselines and regressed from the gcmaf.
So if anything, the fact that the c4a exhibited a delayed increase after activity might support our theory because if it weren't for increased activity, the baseline c4a might be lower and the total percentage increase found at post-gcmaf re-testing higher!
If we're to apply any significant lessons from the 2003 study, we need to see 1) what percentage the c4a shifted by 2) what the absolute counts were and 3) how much exertion past anaerobic threshold an "active trip to belgium" is compared to 20 minutes biking at 70% of a healthy person's max load.
I do think this poses a confounding variable which makes this far less black and white than any of us had hoped, but then again, few biomarkers (if any) are affected by only a single variable. So although we can't make this retroactive analysis as controlled as we want, we can still our common sense and see if we can derive some fairly obvious trends.
Let's put it this way: if our hypothesis was that c4a was dropped by the gcmaf, and that the drop had a negative correlation with symptoms getting worse, then the fact that c4a might be elevated by a particularly active trip would absolutely put a wrench in that. However, what we're finding is that the baseline c4a's are fairly low across the board (which is the opposite of what you would expect based on the 2003 study) and that in fact, re-testing of c4a shows a 300% to 1000% increase from their baseline values in people that started out with low baselines and regressed from the gcmaf.
So if anything, the fact that the c4a exhibited a delayed increase after activity might support our theory because if it weren't for increased activity, the baseline c4a might be lower and the total percentage increase found at post-gcmaf re-testing higher!
If we're to apply any significant lessons from the 2003 study, we need to see 1) what percentage the c4a shifted by 2) what the absolute counts were and 3) how much exertion past anaerobic threshold an "active trip to belgium" is compared to 20 minutes biking at 70% of a healthy person's max load.
I do think this poses a confounding variable which makes this far less black and white than any of us had hoped, but then again, few biomarkers (if any) are affected by only a single variable. So although we can't make this retroactive analysis as controlled as we want, we can still our common sense and see if we can derive some fairly obvious trends.
slayadragon
Senior Member
- Messages
- 1,122
- Location
- twitpic.com/photos/SlayaDragon
Unfortunately, I've never had C4a measured correctly, so I can't contribute as much as I would like.
However, my understanding is that C4a is related specifically to mold reactivity. Having a high C4a means that people are "over tolerance" -- being exposed to more mold than their bodies can handle.
When i started taking Famvir, my mold reactivity went up for three days. Then it went down below baseline.
When I started taking Valcyte, my mold reactivity went up for several months. I compensated by moving to a particularly pristine environment. After about six months, it went down below baseline and then continued to decline.
Now, after 12 months on the drug and an additional five months off of it, my mold reactivity is close to resolved. I'm affected by blatantly moldy buildings (e.g. ones where, when I look up, there are big water marks on the ceiling and that would have knocked me out three years ago), but not appreciably at all to smaller exposures. (There's a particular type of outdoor toxin that continues to be problematic though.)
I thus would posit that the IRIS flare of Valcyte, ARV's and (it seems) GcMAF makes people more reactive for a while, increasing their C4a's when exposure remains unchanged.
In theory, extended time on the drugs has the potential of decreasing reactivity below baseline. But if the IRIS is too severe (signified by C4a levels being out of control high), that may never happen. And detox (which I've worked on intensively, more than anyone I've ever encountered) seems extremely important too.
Of course, this is just conjecture, based on my own experiences and other people's reports.
Best, Lisa
However, my understanding is that C4a is related specifically to mold reactivity. Having a high C4a means that people are "over tolerance" -- being exposed to more mold than their bodies can handle.
When i started taking Famvir, my mold reactivity went up for three days. Then it went down below baseline.
When I started taking Valcyte, my mold reactivity went up for several months. I compensated by moving to a particularly pristine environment. After about six months, it went down below baseline and then continued to decline.
Now, after 12 months on the drug and an additional five months off of it, my mold reactivity is close to resolved. I'm affected by blatantly moldy buildings (e.g. ones where, when I look up, there are big water marks on the ceiling and that would have knocked me out three years ago), but not appreciably at all to smaller exposures. (There's a particular type of outdoor toxin that continues to be problematic though.)
I thus would posit that the IRIS flare of Valcyte, ARV's and (it seems) GcMAF makes people more reactive for a while, increasing their C4a's when exposure remains unchanged.
In theory, extended time on the drugs has the potential of decreasing reactivity below baseline. But if the IRIS is too severe (signified by C4a levels being out of control high), that may never happen. And detox (which I've worked on intensively, more than anyone I've ever encountered) seems extremely important too.
Of course, this is just conjecture, based on my own experiences and other people's reports.
Best, Lisa
globalpilot
Senior Member
- Messages
- 626
- Location
- Ontario