Claus Jensen to the Perth Group on Umber
I was wondering if you have seen the latest from Umber.
Some very specific claims are made, which I have underlined.
Jean Umber 19 May, 2010
I think it is an easy way to explain the
lack of death in
Another study (Kalinowski, 2004), show that the amount of peroxynitrite is normally greater in the umbilical vein endothelial cells isolated from blacks than in the same from whites.
Thus the amount of P24 is normally greater in black and the cut’off of the HIV test should be increased for the blacks.
There are some leaps of logic here but perhaps the gaps can be successfully filled in?
First, by perusing Umber’s references I can see that p24 ELISA was used among other things to “assess viral production” in vitro:
Virus production was assessed by p24 ELISA, western blot, and electron microscopy.
But I don’t know which HIV tests measure the amount of p24, and only that. If anything, I would have thought that the presence/amount of antibodies that react with p24 is what a test can tell us. But can a high concentration of p24-reactive antibodies be directly translated into high amounts of p24 (= viral activity) or vice versa, even on the Orthodoxy’s view?
Second, assuming that Umber is right in her interesting observation that the amount of p24 is dependent on peroxynitrite, how can we conclude that because the amount of peroxynitrite in certain cells in black people is high, the amount of p24 is high as well? An analogy: Fish are dependent on water, but just because there is water in my kitchen sink it doesn’t mean there are fish in there as well.
And how can we conclude that blacks naturally have higher levels of peroxynitrite than whites because some test subjects did?
Finally, Umber seems to think that elevated levels of p24 alone is a marker for AIDS. Is that because
1. p24 is detrimental to health in and of itself?
2. p24 is a reliable marker for elevated levels of peroxynitrite, which is detrimental to health?
3. p24 is a reliable marker for elevated levels of peroxynitrite, which in turn is a marker for other conditions (general oxidation), which is detrimental to health?
This still presupposes that blacks are naturally more oxidised than whites - with or without it being detrimental to their health?
Judging from the reference Umber considers it proven that p24 is a marker of oxidative stress (my third suggestion above), and that (American) blacks are supposed to be naturally more highly oxidised than whites.
Claus Jensen to Anthony Brink on Umber
1. Umber says that the HIV tests cut-off levels for Africans should be higher than for Caucasians, since they are more highly oxidised. If not, the tests lose predictive value by catching too many perfectly healthy people.
2. Umber’s reference for this says that the higher level of oxidation predisposes black Africans for certain conditions:
Conclusions – Compared with whites, the steady-state NO/O2/ONOO balance in endothelial cells from blacks is kept closer to the redox states characteristic for the endothelium-impaired function disorders. This may explain the differences in racial predisposition to the endothelium dysfunction during ongoing vascular disturbances with the hallmark of enhanced NO inactivation within the endothelium by oxidative stress. (Circulation 2004;109:2511-2517)
3. If higher oxidation of endothelial cells predisposes the African race(s) to endothelial dysfunction, is it not logical to assume that the higher oxidation predisposes for various other things – like “AIDS”?
4. If yes, the HIV tests at their present cut-off level do retain their overall predictive value in mixed study populations, since the higher level of oxidation predisposes blacks to croak easier than whites.