The thing about taking probiotics is that if you have some defect either physical injury or genetic problem then the probiotics will just increase the amount of LPS in the system.
I started researching the permeability issue and one of the apoLipoproteins and dht. The hypothesis was that if dht in susceptible individuals would somehow screw with apolipoprotein E(making it "null" so to speak in dht susceptible individuals) then we would have a smoking gun
so to speak on how gut bacteria get an overload of LPS in our systems.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4485310/
Recent data demonstrate that intestinal microorganisms could influence lipid metabolism and act as environmental factors triggering development of metabolic and cardiovascular diseases (
Vrieze et al., 2010;
Goldsmith and Sartor, 2014).
The lack of gut microbiota in germ-free apolipoprotein E (ApoE)-null mice, an experimental model of human atherosclerosis, was found to induce the development of atherosclerotic plaques even when animals were fed a standard low-cholesterol diet.
Colonization with normal human microbiota prevented atherogenesis in germ-free ApoE-null mice fed a standard low-cholesterol diet but not a diet with high cholesterol content (
Stepankova et al., 2010). Indeed, these observations suggest on the atheroprotective effects of human colonic commensal bacteria.
Increased intestinal microbiota-derived lipopolysaccharide (LPS) load from the colon lumen was shown to be associated with various metabolic abnormalities including induction of adipose inflammation and insulin resistance (
Cani et al., 2007).
Bacterial LPS could be delivered from the gut to the circulation through chylomicron-associated transport and
via tight junctions in the epithelial lining (
Caesar et al., 2010).
LPS is absorbed by enterocytes and transferred to the Golgi apparatus where chylomicrons synthesized by enterocytes are stored before secretion (
Sabesin and Frase, 1977). Inhibition of chylomicron formation suppressed intestinal LPS absorption (
Ghoshal et al., 2009). High-fat meal intake increases circulating levels of LPS (
Amar et al., 2008).
Enhanced LPS load across the tight junctions of the gut epithelium was observed in animal models of human obesity and associated with the rearrangement of tight junction proteins, reduced epithelial barrier function, and increased gut permeability, endotoxemia, and inflammation (
Brun et al., 2007;
Cani et al., 2008).
Administration of antibiotics or prebiotic oligofructose was shown to improve the integrity of intestinal epithelium and decrease serum low density lipoproteins (LDLs) and liver inflammation (
Cani et al., 2009
{ I have read in some other newsgroups(non-hair) about certain types of antibiotics in which the people were reporting hair growth. The thing is when people who arent really looking at hair growth but just recovery from a disease and notice hair growth is a very important find.
Oligofructose? .....HMMM
