I have not created a Inosine/DMAE thread, but I might start one. Ten years ago, there was a blog article by an ME/CFS patient which analyzed the Imunovir (isoprinosine) patent. He realized from the patent that inosine plus DMAE would be just as effective as Imunovir. That blog no longer exists, but I copied all the details, so I may post those details in a new thread.
Inosine + DMAE is about 10 times cheaper than Imunovir: if you were to take 2 grams of the drug Imunovir daily, this would cost you about $5 a day; whereas a daily dose of inosine 2 grams + DMAE 700 mg will cost about $0.50.
Thanks very much Pauline91. I've updated my above post to say "this method will not always detect jawbone infection". I've also inserted the same statement into the jawbone cavitation section of my roadmap (perhaps you might like to give that section a quick glance, and check everything stated is accurate).
A cone beam is a new one for me. Is that a new method of detecting jawbone cavitations? Should I include it in the roadmap?
A Cone beam computed tomography (or CBCT) is a 3D scan, used widely by implantologists in conventional dentistry, but never by regular dentists. Bio dentists use it to determine whether there is a cavitation in the jawbone or a tooth infection. It seems to be pretty acccurate (yes, I would add it in the roadmap)
I gave the cavitation section a glance, yes everything seems accurate. Something that might be worth adding, though: cavitations are very often resulting from wisdom teeth removal. Cavitations in the site of extraction of wisdom teeth often seem to be causing adrenal fatigue (and CFS). I remember this from the movie "Root Cause" by Justin Lyons, but I dont have any scientific study about it though. Also, the meridian tooth chart states that lower wisdom teeth are directly connected to energy metabolism: https://toothbody.com/interactive-meridian-tooth-chart/
Also, here are 2 other testimonies of people whose CFS disappeared after removing root canals and/or cavitations: Dukey's testimony and .
There are also some recovery stories on the Facebook support group about cavitations ("NICO, jawbone infection, root canals, implants, cavitations")
I think you would need to substitute it with another amino alcohol. DMAE is an amino alcohol, and this is what is required to make Imunovir.
According to the 2009 deleted blog post analysing the Imunovir patents, Imunovir is a combination of inosine, acetamidobenzoic acid, and di-methyl-amino-isopropanol (DMAIP).
DMAIP is classed as amino alcohol. But the patents state that other amino alcohols can be used, and the patents state specifically that the amino alcohol di-methyl-amino-ethanol (DMAE) is fine to use.
In the patents, they mix inosine and DMAIP together in aqueous solution to create a molecular complex, where these two molecules loosely bond together. So presumably inosine and DMAE will also bond together in your stomach if you take these supplements at the same time. The patents claim inosine and amino alcohol can be given separately "as long as they have a chance to get together in the body of the animal."
The patents say that in antiviral tests against herpesvirus, inosine on its own is ineffective, but once bonded to DMAIP, it then has antiviral effects.
When I have had a chance to read the patents more thoroughly, I will post a new thread.
Note that the acid found in Imunovir (acetamidobenzoic acid) is not very important, it's just there as a buffer, to neutralize the alkalinity of DMAIP. Other acids like HCl can be used as a substitute.
As a natural antioxidant, UA provides up to 60% of the antioxidant capacity in human blood . UA preserves the peroxidase activity of both cytosolic Superoxide Dismutase 1 (SOD and extracellular SOD3, which defend against the formation of superoxide (O2−) and peroxynitrite . UA can also effectively prevent cytoskeleton from the insults caused by peroxynitrite-induced inactivation of cellular enzymes . In addition, UA is capable of binding iron and inhibits iron-dependent ascorbate oxidation, thus preventing against oxidative stress-induced injuries. As such, a reduced UA concentration may adversely lead to increased oxidative stress and damage to neural cells. However, recent studies indicate that UA’s antioxidant property couldn’t explain all of its beneficial effects in the CNS. One study found that astroglia are required for UA to exert its protective effects on the spinal cord against injury . UA stimulates expression of a glutamate transporter in astroglia, by which it protects neurons from glutamate-induced toxicity. Besides its capability of scavenging reactive oxygen species, UA can also indirectly confer neuronal protection via activation of astroglia. On the other hand, lower UA levels may be generated during CNS inflammation due to overconsumption of UA in scavenging excessive oxidative stress . Notably, administration of UA to an experimental autoimmune/allergic encephalomyelitis mouse model, given either before or after the appearance of symptoms, promoted the survival rate of these mice . Administration of UA effectively decreased oxidative stress and neuronal deaths in animal models of PD . Interestingly, treatment of patients with a UA precursor, inosine, prevented progression of MS in all 11 patients tested and even improved the symptoms of some patients . Thus, it is highly likely that a reduced serum UA level is a predictor rather than a consequence of neurodegeneration. Therefore, it is plausible to speculate that the neurodegenerative processes in patients with the neurological disorders may be exacerbated by the compromised neuroprotective effects due to the decreased UA levels.