Dear Dr. Jaeger,
I would like to share some thoughts with you with the request for further medical clarification.
For transport and treatment I take to avoid a crash (PEM):
1500mg Pregabalin
45 mg Tavor
-> This helps me a lot with the energy. My overall condition improves by a few hours. Both drugs act on the GABA receptors.
The exact effect on the metabolic pathomechanism is unknown.
However, it is conceivable that:
a) it has an effect on aerobic metabolism (e.g. the oxidative carboxylation, and the production of acetyl-CoA or electron release by the reduction of FAD+ to FAD and so that it positively affects the respiratory chain. The consequence would be an increased provision of ATP- Molecules (32 per glucose molecule) and thus a more efficient cell function;
b) an effect on the erythrocytes and the associated better supply of oxygen molecules have;
c) it has a direct effect on fibrinogen production. Perhaps these molecules have the property of temporarily dissolving fibrinogen
Of course, these are only amateur points of attack for possible further research. The fact is that
many ME/CFS patients are tavor-dependent, as this active ingredient leads to an improvement in
Overall performance, which, in my opinion, can only be explained by the cellular level of metabolism
shall.
Prof. Ron Davis put human T cells under cell stress by injecting the salt into the cell. He sat one cell culture is good, the other is not. By means of his famous nano-needle experiment, in which he the cell stress by measuring the impedance of the cell membrane when pumping out the cell of the salt by measuring the cell, he was able to clearly measure that the cell cultures with Tavor molecules much more efficiently and quickly recovered from cellular stress. The mechanism remains unknown.
In addition, there is the outstanding success of Abilify, which I myself experienced for 4 1/2 months.
My request to you is: please do not ignore these facts. You could contribute to the puzzle solution.
Regarding my stay last year: My theory is in the logical consequence of the above hypotheses that my O2 saturation was normal and there was no significant amount of fibrinogen, as I was under the influence of pregabalin and Tavor stood to survive my journey.
In the meantime, I have also learned that the health problems also affect many LC patients some time after the apheresis they came back again. If you want to remove weeds, it must be on grab the root. What I mean by this: In accordance with the research of Amy Proal, VanElzakker, Chia and many more. I assume an enterovirus reservoir that is suitable for both the reactivation of EBV as well as all other symptoms is responsible. This reservoir sits presumably in the intestinal mucosa in the epithelial cells. This also speaks for my greatly increased AK- Values in relation to Coxsackie B4 (1:640 - the enterovirus Foundation takes a persistent infection from a value of more than 1:160). This virus must be destroyed.
Another disturbing study concerns me: the lipids could be a possibility of the virus, to multiply and lead to damage to the epithelial cells:
"Viroplasms interact with and possibly trigger the formation of LDs, inducing and recruiting them during the replication cycle (Cheung et al., 2010; Saxena et al., 2015).
Rotaviruses have joined the growing list of viruses and microbes that interact with LDs during their replication and depend on cellular lipid homoeostasis, including hepatitis C virus (Miyanari et al., 2007; Boulant et al., 2007; Shavinskaya et al., 2007; Salloum et al., 2013; Paul et al., 2014; Liefhebber et al., 2014; Shahidi et al., 2014; Filipe et al., 2015), dengue virus (Samsa et al., 2009; Jain et al., 2014; Soto-Acosta et al., 2014), GB virus B (Hope et al., 2002), bunyavirus (Wu et al., 2014) and the intracellular parasites Chlamydia (Kumar et al., 2006), Mycobacterium tuberculosis (Daniel et al., 2011) and Mycobacterium leprae (Mattos et al., 2011). On a wider scale, FA biosynthesis has been recently recognized as being essential for the replication of a large number of viruses such as enteroviruses, West Nile virus, human cytomegalovirus, Kaposi sarcoma associated herpes virus and Epstein Barr virus (Chukkapalli et al., 2012)."
And:
"Viruses from the Flaviviridae family, namely dengue virus (DENV), hepatitis C virus (HCV), West Nile virus (WNV), and Zika virus (ZIKV), interact with LDS to usurp the host lipid metabolism for their own viral replication and pathogenesis. In general, during Flaviviridae infections it is observed an increasing the number of host intracellular LDs. Several viral proteins interact with LDs during different steps of the viral life cycle."
So far, so good. Were it not for this contradiction:
"Following infection of cells with either RNA viruses (Zika, Dengue, Influenza A) or a DNA (Herpes Simplex Virus-1) virus, LDs were rapidly upregulated, and this response was also replicated following stimulation with viral mimic agonists. This upregulation of LDs following infection was the results of the study were based on the results of a study of the effects of the LD upregulation, and the results of a study of the effects of the LD upregulation on the LD upregulation of the LD upregulation on the LD upregulation of the LD upregulation on the LD upregulation of the LD upregulation on the LD upregulation of the LD upregulation. The cell the ability to mount an effective immune response was greatly reduced when inhibiting EGFR, thus inhibiting LD upregulation during infection, also
leading to an increase in viral replication."
So there seems to be a risk that the removal of the LD by apheresis will damage my immune system
weaken.
"The accumulation of LDs has become a hallmark of infection, and is often thought to be virally driven; however, recent evidence is pointing to a role for the upregulation of LDs in the production of a successful immune response to viral infection. The fatty acids housed in LDs are also gaining interest due to the role that these lipid species play during viral infection, and their link to the synthesis of bioactive lipid mediators that have been found to have a very complex role in viral infection. This review explores the role of LDs and their subsequent lipid mediators during viral infections and poses a paradigm shift in thinking in the field, whereas LDs may play pivotal roles in protecting the host against viral infection."
All in all, I would suggest combining apheresis with another antiviral combination therapy to support. Currently, I am being adjusted to Valtrex, that in high doses it has antiviral properties against EBV has.
I would like to try to treat the enteroviruses with IFN-Lambda. This only works in the epithelial cells of the mucosa, so that it does not have the side effect profile of other IFN treatments gaps.
Your thoughts on this would be of great interest to me.
Best regards,
[REDACTED]
