Common pathway for all disease

Common pathway for all disease

The porphyrin pathway: the final common pathway?
Downey DC
Med Hypotheses. 2002 Dec ; 59(6): 615-21

When I was learning pathology a wise and knowledgeable mentor described
a final common pathway that allows many diseases to overlap in their
presentation. This pathway was never identified for it was unknown.
Recent books by physicians have suggested that maintaining body balance
and/or treatment by a substance could halt or repair damage caused by a
wide array of diseases, once again suggesting a common thread amongst
diseases. Again no mention was made regarding what was this common
denominator. I have been interested in people who have more than one
disease, feeling that there must be a link. My interest in the
porphyrin pathway has strengthened that impression. Since finding
Doss's list of diseases having porphyrin abnormalities unrelated to a
porphyria, I have worked on models that would allow me to show a way
where porphyrin abnormalities may be a part of the final common pathway
for all disease. I have finally decided that a spider's web is that
model. The following discussion will attempt to demonstrate that this
hypothesis could be true.
---------------------------------------------------------------------------=
--------------------

<<snip>>
ascorbate suppresses hepatic URO accumulation at low, but not high
hepatic iron levels
<<snip>>

Effect of iron and ascorbate on uroporphyria in ascorbate-requiring
mice as a model for porphyria cutanea tarda.
Gorman N, Zaharia A, Trask HS, Szakacs JG, Jacobs NJ, Jacobs JM,
Balestra D, Sinclair JF, Sinclair PR
Hepatology. 2006 Dec 22; 45(1): 187-194


Excess hepatic iron is known to enhance both porphyria cutanea tarda
(PCT) and experimental uroporphyria. Since previous studies have
suggested a role for ascorbate (AA) in suppressing uroporphyria in
AA-requiring rats (in the absence of excess iron), the present study
investigated whether AA could suppress uroporphyria produced by excess
hepatic iron. Hepatic URO accumulation was produced in AA-requiring
Gulo(-/-) mice by treatment with 3,3',4,4',5-pentachlorbiphenyl, an
inducer of CYP1A2, and 5-aminolevulinic acid. Mice were administered
either sufficient AA (1000 ppm) in the drinking water to maintain near
normal hepatic AA levels or a lower intake (75 ppm) that resulted in 70

% lower hepatic AA levels. The higher AA intake suppressed hepatic URO
accumulation in the absence of administered iron, but not when iron
dextran (300-500 mg Fe/kg) was administered. This effect of iron was
not due to hepatic AA depletion since hepatic AA content was not
decreased. The effect of iron to prevent AA suppression of hepatic URO
accumulation was not observed until a high hepatic iron threshold was
exceeded. At both low and high AA intakes, hepatic malondialdehyde
(MDA), an indicator of oxidative stress, was increased three-fold by
high doses of iron dextran. MDA was considerably increased even at low
iron dextran doses, but without any increase in URO accumulation. The
level of hepatic CYP1A2 was unaffected by either AA intake. Conclusion:

In this mouse model of PCT, AA suppresses hepatic URO accumulation at
low, but not high hepatic iron levels. These results may have
implications for the management of PCT. (HEPATOLOGY 2007;45:187-194.).


Abstract · PubMed FullText · SFX · GS Clip Export InterDB ·
Terms Related · Graph Tag · Scopus · Cites 10.1002/hep.21474


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Tom


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Re: Common pathway for all disease


ironjustice@aol . com wrote:
> The porphyrin pathway: the final common pathway?
> Downey DC
> Med Hypotheses. 2002 Dec ; 59(6): 615-21
>
> When I was learning pathology a wise and knowledgeable mentor described
> a final common pathway that allows many diseases to overlap in their
> presentation. This pathway was never identified for it was unknown.

If, sickness got something to do with spirituality........how is it
going to be known?...LOL...


> Recent books by physicians have suggested that maintaining body balance
> and/or treatment by a substance could halt or repair damage caused by a
> wide array of diseases, once again suggesting a common thread amongst
> diseases. Again no mention was made regarding what was this common
> denominator. I have been interested in people who have more than one
> disease, feeling that there must be a link. My interest in the
> porphyrin pathway has strengthened that impression. Since finding
> Doss's list of diseases having porphyrin abnormalities unrelated to a
> porphyria, I have worked on models that would allow me to show a way
> where porphyrin abnormalities may be a part of the final common pathway
> for all disease. I have finally decided that a spider's web is that
> model. The following discussion will attempt to demonstrate that this
> hypothesis could be true.
> -------------------------------------------------------------------------=
----------------------
>
> <<snip>>
> ascorbate suppresses hepatic URO accumulation at low, but not high
> hepatic iron levels
> <<snip>>
>
> Effect of iron and ascorbate on uroporphyria in ascorbate-requiring
> mice as a model for porphyria cutanea tarda.
> Gorman N, Zaharia A, Trask HS, Szakacs JG, Jacobs NJ, Jacobs JM,
> Balestra D, Sinclair JF, Sinclair PR
> Hepatology. 2006 Dec 22; 45(1): 187-194
>
>
> Excess hepatic iron is known to enhance both porphyria cutanea tarda
> (PCT) and experimental uroporphyria. Since previous studies have
> suggested a role for ascorbate (AA) in suppressing uroporphyria in
> AA-requiring rats (in the absence of excess iron), the present study
> investigated whether AA could suppress uroporphyria produced by excess
> hepatic iron. Hepatic URO accumulation was produced in AA-requiring
> Gulo(-/-) mice by treatment with 3,3',4,4',5-pentachlorbiphenyl, an
> inducer of CYP1A2, and 5-aminolevulinic acid. Mice were administered
> either sufficient AA (1000 ppm) in the drinking water to maintain near
> normal hepatic AA levels or a lower intake (75 ppm) that resulted in 70
>
> % lower hepatic AA levels. The higher AA intake suppressed hepatic URO
> accumulation in the absence of administered iron, but not when iron
> dextran (300-500 mg Fe/kg) was administered. This effect of iron was
> not due to hepatic AA depletion since hepatic AA content was not
> decreased. The effect of iron to prevent AA suppression of hepatic URO
> accumulation was not observed until a high hepatic iron threshold was
> exceeded. At both low and high AA intakes, hepatic malondialdehyde
> (MDA), an indicator of oxidative stress, was increased three-fold by
> high doses of iron dextran. MDA was considerably increased even at low
> iron dextran doses, but without any increase in URO accumulation. The
> level of hepatic CYP1A2 was unaffected by either AA intake. Conclusion:
>
> In this mouse model of PCT, AA suppresses hepatic URO accumulation at
> low, but not high hepatic iron levels. These results may have
> implications for the management of PCT. (HEPATOLOGY 2007;45:187-194.).
>
>
> Abstract · PubMed FullText · SFX · GS Clip Export InterDB ·
> Terms Related · Graph Tag · Scopus · Cites 10.1002/hep.21474
>
>
> Who loves ya.
> Tom
>
>
> Jesus Was A Vegetarian!
> * jesuswasavegetarian.7h . com
>
>
> Man Is A Herbivore!
> * tinyurl . com /a3cc3
> 
> 
> DEAD PEOPLE WALKING 
> * tinyurl . com /zk9fk