Tuesday, February 21, 2006

Birdflu Update -6CCR5 , Sulpher and the 1918 Flu

Birdflu Survival Update -6

Dated 22/02/2006

CCR5 , Sulpher and the 1918 Flu

The 1918 flu attacked sulpher-deprived individuals through the receptor site CCR5 (see previous writings).

The 1918 flu was a direct mutation from birds to humans (ie no intermediate animal or human reactor was involved) . Hence there was no vector of the disease remaining after the human pandemic burned out . No reinfection from a animal source was possible , since there was no animal source and the burn-out happened quickly enough that the virus could not get a foothold in an animal species . So the epidemic vanished quickly .

If the same happens today , we can expect a quick , sharp pandemic involving nations that have been cutting down on sulpher emissions : USA and Europe .

A low-sulpher community (like SA) would be inclined to favour an endemic version of human bird-flu , since the African genetic diversity would be combined with bird-flu in a high-probability scenario of lower mortality ,but endemic reservoirs .

This might have already happened with HIV , since HIV uses CCR5 as well .

A testable prediction then would be that the recent (1 Jan 2006) introduction of low-sulpher diesel in SA would lead to a marked increase in the HIV/AIDS rates .

A worst case scenario would then be a sharp pandemic (50% death rate) in genetically uniform populations , with it then vanishing . However , genetically various populations (ie Africa) will have a lower initial mortality , but will then form a pool of endemic vectors .

Intriguing is the correlation between West Nile Fever and CCR5 . The mutation on CCR5 that gives a degree of immunity to 1918-flu , bubonic plague and HIV leads to a greater susceptibility to West Nile Fever .

Clearly , there is a very old correlation here . Attention is drawn to the high-sulpher content of the environment of the surviving hominins after the Toba event .

Historically , smallpox decreased bubonic plague below pandemic levels by blocking access to CCR5 . Suspicion exists that other diseases using CCR5 (like HIV) is now increasing because this blocker has been removed .

One wonders if the disruption in smallpox vaccination during WWI and the low-sulpher environment led to a random mutation of the bird-flu gaining sufficient foothold to become an epidemic .

Why should viruses be so sensitive to the sulpher concentration ? Because cells are so sensitive to sulpher concentrations . Attention is drawn to the cascade of epigenetic switches caused by a 80 ppm concentration of H2S , switching off the genes of even advanced mammals in a very precise sequence . (Suspended animation : see Scientific American) (Total anoxia does the same) . This is a partial apoptosis , since the total breakdown of the cell does not take place , but harmful oxidizing elements are apoptised .

What is even more intriguing , is that restoring oxygen leads to revivication without major support mechanisms . Ie , it is programmed in , and the program of partial apoptosis and anapoptosis is still fully operative (ie still used in routine cell operations) .

The suspicion arises that the first multi-cellular organisms evolved to be able to survive in both oxygen-rich and oxygen-poor , sulpher-rich environments . Initially , the ur-cell could do both , but not very well . Putting a cell-wall in between increased efficiency drastically . Parasites evolved for each mode , but would tend to specialize on aerobic or anaerobic after the schism got established by Darwinnian selection of more efficient phenotype preferred by a particular gene structure .

The joker here is the immune system . It places a bias on the organism , favouring the survival of positive changes , either aerobic or anaerobic .

So , breathing in succession 80 ppm H2S and pure Oxygen , while taking antibiotics should see off any cellular competitors in quick fashion .

The increase in asthma can be more accurately correlated to the lack of “mephitic vapours” . Ie the smells from the toilet . Note that the whipsaw effect above is a cascade , and that the process can be interrupted by the lack of a single element in the cascade . The lack of sufficient H2S concentration in developmental stages can lead to severe immune system imbalances . Note that small boys like bad smells . Why?

This leads to the irresistible conclusion that continuous washing is bad for human males , since it impairs their immune system . I always knew that !

Smell seems to have been neglected . If 80 ppm H2S triggers the organism into stasis (an experimental fact ) , smells ( or more exactly , chemical signals ) can cause huge effects . It is not the smell exactly . The chemical throws a switch in the genetic machinery of the cells . The result can be out of proportion to the concentration (will have to be , as concentrations are diluted by the volume of space .)

Epigenetic programming is obvious . Post-natal epigenetic programming using whipsawing H2S techniques might persuade some cells into becoming stem cells . Note that regenerators like crocs , tadpoles , etc seek anaerobic environments

Note that the techniques are simple and reasonably risk-free .

You can do this at home , especially as last resort .

Can it make you younger?
Whipsawing is a form of post-natal epigenetic programming . It definitely slows ageing , but regeneration might take a bit more work . Crocs and sharks keep on growing , until they cannot be supported by their ecosystem . I see no reason why humans should be different.

The only way old humans could survive is by emigrating to the outer spaces . Imagine a universe populated by concentric rings of bores . Yuck.


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