Auxotrophy is the inability of an organism to synthesize a particular organic compound required for its growth.
Pathogens that are NAD+ auxotrophs would drain you of your precious intra and extracellular NAD+ causing lower levels of SIRT and PARP (fixes DNA) etc.
"...Some pathogens, such as the yeast Candida glabrata and the bacterium Haemophilus influenzae are NAD+ auxotrophs – they cannot synthesize NAD+ – but possess salvage pathways and thus are dependent on external sources of NAD+ or its precursors.
Even more surprising is the intracellular pathogen Chlamydia trachomatis, which lacks recognizable candidates for any genes involved in the biosynthesis or salvage of both NAD+ and NADP+, and must acquire these coenzymes from its host..."
http://en.wikipedia....ne_dinucleotide
http://en.wikipedia....andida_glabrata
http://en.wikipedia....ilus_influenzae
http://en.wikipedia....dia_trachomatis
I do not know how common infections with these bacteria are, or if they stay at subclinical levels causing many of the effects of aging?
Here are the studys that prompted me to post.
Leishmania Donovani infection, spread by sandflies, (who hasn't been bitten) is likely to be common.
Not only are they NAD+ Auxotrophs, they downregulate a number of macrophage defense mechanisms and cause epigenetic changes to PKC, JAK/STAT, MAPK, NF-kB, etc. in our defence systems!
Leishmania donovani Infection Causes Distinct Epigenetic DNA Methylation Changes in Host Macrophages
"...Leishmania protozoan parasites are NAD+ auxotrophs. Consequently, these parasites require assimilating NAD+ precursors (nicotinamide, nicotinic acid, nicotinamide riboside) from their host environment to synthesize NAD+..
...These include genes coding for proteins involved in signaling pathways such as the JAK/STAT signaling, calcium signaling, MAPK signaling, Notch signaling, and mTOR signaling, as well as cell adhesion involving integrin beta 1, and changes in host oxidative phosphorylation. We thus propose that L. donovani infection induces epigenetic changes in host DNA methylation to enable L. donovani survival differentiation and replication within the infected macrophage.
Similarly, it was recently reported that Toxoplasma gondii induces chromatin remodeling leading to unresponsiveness of its host cells to IFN-γ. In addition, intracellular bacteria and viruses may trigger epigenetic changes in their host cells, an elegant mechanism to alter gene transcription favoring the pathogens infection, replication and survival..."
http://www.ncbi.nlm....les/PMC4192605/
So; it looks like bacteria and parasites can suck the life out of us and epigenetically change many of the genes associated with aging.
Virii 'skip all that messing about' and simply insert their own DNA into our cells.
This is a subject that has been discussed before, but threads seem to die as few are willing to venture down this 'rabbit hole'.
http://www.longecity...ause-of-aging/
I hope this more targeted info stimulates lots of research into NAD+ Auxotrophs and pathogens that cause epigenetic changes similar to those seen in aging.
Most important is finding supps and meds to prevent and eradicate these pathogens and thus the aging phenotype!
There seem to be promising new anti-virals to go with the old stalwarts but not much in the way of antibacterials?
- Teixobactin kills all gram+ bacteria 100%
- http://www.longecity...m-bacteria-100/
- Neem?
- http://www.longecity...c-maleria-etc/
- New anti-virus drug that targets MOST viruses
- http://www.longecity...s-most-viruses/
- DRACO kills all virus infected cells?
- http://www.longecity...infected-cells/
- Bavituximab
- http://www.longecity...available-soon/
- BHT
- http://www.longecity...opic/42592-bht/
- http://www.longecity...-of-taking-bht/
- A "new" look at coconut oil
- http://www.longecity...ut-oil-article/
Mods:
I posted here as its the sub forum with the most interest in NAD+ and supps and meds to upregulate the genes discussed here, as well as supps and meds to eradicate these pathogens.
If you feel another sub forum is more appropriate; plz feel free to move it.