S-VV's desperation medicine

[S-VV]

As we can see, the micro biome is far from benign, and while it may be necessary to develop immune tolerance, it has some serious drawbacks. Since current technology does not permit permanent gut bacteria depletion, the next best thing is to have a micro biome that will kill you in 60 years with a heart attack, rather than one which will precipitate Lupus in a few months.

I believe that in the coming centuries, chronic targeted* microbiome depletion will be a popular life extension strategy.

*because some select species should offer more benefit than harm when their numbers are kept low to avoid inflammatory LPS production.

 

[S-VV]

Ok, one last study and I shall end my microbiome-phobic ramblings:

Decreased tumor necrosis factor-alpha and interleukin-1alpha production from intrahepatic mononuclear cells in chronic ethanol consumption and upregulation by endotoxin.
Batey R1, Cao Q, Madsen G, Pang G, Russell A, Clancy R.
Author information

Abstract
The relationship between the changes in liver pathology and the production of interleukin (IL)-1alpha, IL-6, and tumor necrosis factor-alpha (TNF-alpha) by intrahepatic mononuclear cells was studied in rats fed alcohol and subsequently exposed to lipopolysaccharide (LPS). Rats were fed 40% ethanol in drinking water, whereas control rats were provided with a chow diet with isocaloric or 2% sucrose drinking solutions for up to 20 weeks. Decreased IL-1alpha and TNF-alpha production in 24-hr culture supernatants of mononuclear cells isolated from liver perfusate was detected while IL-6 remained unchanged over 20 weeks. When animals were injected with LPS (1.0 microg/kg body weight), there was a 5-fold rise in ALT levels in the ethanol-fed group, but not in control groups. Increased IL-6 and TNF-alpha levels in the serum and supernatant of cultured intrahepatic mononuclear cells stimulated with or without LPS or concanavalin A was observed. There was a correlation between levels of ALT and TNF-alpha, but not IL-6. T cells and Kupffer cells were the major source of TNF-alpha in culture supernatants of hepatic perfusate mononuclear cells from ethanol-consuming rats injected LPS. In addition, pathological liver injury was evident, which suggests a pathogenic role for TNF-alpha in alcohol-induced liver disease

Summary: Ethanol fed rats had reduced inflammatory cytokines, whereas ethanol + LPS infused rats had lived damage. Its not the alcohol that kills you, its the microbiota ('s LPS)

 

[S-VV]

Targeting the gut barrier for the treatment of alcoholic liver disease