I suppose since they are now telling us to eat our 'green leafies' ..
WITH .. our .. meat .. BECAUSE of the oxidation which is presented TO
... us .. BY .. the meat ..
The antioxidants in the plant food would / should offset the oxidation
by the meat ..
Then this article below which states IBS is CAUSED .. by .. oxidation
... would give one an .. idea .. meat .. may .. be .. a .. bad .. thing
...
Logic ..?
Eh ..
<<snip>>
It is concluded that peritoneal sclerosis derives mostly from sustained
oxidative injury to the peritoneal membrane.
<<snip>>
Int J Artif Organs. 2005 Feb;28(2):97-104. Related Articles, Links
A short review of experimental peritoneal sclerosis: From mice to men.
Gotloib L, Wajsbrot V, Shostak A.
Department of Nephrology, Hypertension and the Research Center for
Experimental Nephrology, 'Ha'Emek' Medical Center, Afula - Israel.
Peritoneal sclerosis has been induced in rodents in vivo by exposing
the membrane to a variety of experimental interventions: asbestos, 0.1%
chlorexidine, iron dextran, glucose degradation products, AGE deposits
derived from uremia per se, sodium hypochlorite, lypopolysaccharide,
low pH, pure water, silica or zymosan. With a few exceptions (pure
water, chlorhexidine and low pH), the other substances mentioned
operate setting out different degrees of oxidative stress. This short
review describes several experimental interventions in rodents, aimed
at acute exfoliation or long-term, sustained injury of the mesothelial
monolayer performed by means of intraperitoneal injections of different
oxidant agents. Acute exfoliation induced by deoxycholate resulted in a
depopulated monolayer coincident with immediate alteration of the
peritoneal permeability, evidenced by increased urea D/P ratio, higher
glucose absorption rate, elevated albumin losses in the effluent and
significant reduction of the ultrafiltration rate. In the long term (30
days), these manifestations of membrane failure persisted and coincided
with substantial peritoneal sclerosis. Peritoneal sclerosis was also
induced by IP injections of 0.125% trypsin and 6.6 mM/L solution of
formaldehyde. Using the doughnut rat model of mesothelial regeneration,
exposure to 4.25% glucose or 7.5% icodextrin solutions severely
hampered repopulation of the monolayer, which was replaced by a thick
sheet of fibrous tissue. It is concluded that peritoneal sclerosis
derives mostly from sustained oxidative injury to the peritoneal
membrane. Loss of the mesothelial monolayer is the first step in the
chain of events leading to this complication.
PMID: 15770597 [PubMed - in process]
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Who loves ya.
Tom