Friday Hope: GABA as a Potentially Powerful Therapeutic and its Relation to SPED/Sympathetic Overdrive: Hope for Long COVID

GABA Reduced Severity of Illness and Death in Murine-Cornavirus Infected Mice

FIGURE 1

In my continuing series to present, when relevant, hopeful news in our battle with SARS-CoV-2 and its Spike Protein, I believe that GABA supplementation may prove to be a very powerful therapeutic against COVID-19 and SPED/Spike Protein damage. In particular, against the induced Sympathetic Overdrive, which, I also believe, is a major contributing factor to COVID/Spike morbidity and mortality.

When administered to mice infected with the Murine Coronavirus, GABA had a profound effect.

In terms of illness, MHV-1-infected control mice began to display signs of illness two days post-infection and rapidly became severely ill thereafter, with their illness peaking around day 7 post-infection (Figure 1B and Supplemental Figure S2). In contrast, the mice receiving GABA immediately after MHV-1 inoculation developed only mild illness. Illness scores in the mice given GABA at 3 days post-infection was also significantly reduced compared to that in the control group (Figure 1B and Supplemental Figure S2). Thus, GABA treatment immediately after MHV-1 infection, or 3 days later when the clinical signs of the disease were apparent, reduced the severity of the disease.

GABA treatment led to significantly reduced death rates in MHV-1-infected mice. Six days after inoculation, the mice in the control group began to succumb to their illness and only 3/9 mice survived on day 14 post-infection (Figure 1C). In contrast, all of the mice (n = 10) given GABA starting immediately after MHV-1 inoculation survived (Figure 1C). Of the mice that began GABA treatment at 3 days post-infection, 9/10 mice survived.

The conclusion of the paper poses a question which, I believe, I can partially answer.

Much remains to be learned about the mechanisms by which GABAA-R agonists protected MHV-1-infected mice from severe pneumonitis and whether these observations extend to SARS-CoV-2 infection in humans. Given that GABA and homotaurine can affect many biological processes and that viral infection is a very dynamic process, it is clear that GABAA-R agonist dosing needs to be carefully studied and optimized for different stages of coronavirus infection. Our observations provide a springboard for further investigations into whether targeting GABAA-Rs can provide new avenues to limit severe illness due to infection with SARS-CoV-2 and other novel coronaviruses.

GABAA-Receptor Agonists Limit Pneumonitis and Death in Murine Coronavirus-Infected Mice
https://www.mdpi.com/1999-4915/13/6/966/htm

In my previous posts I have described the mechanism by which I believe the Spike Protein is inducing Sympathetic Overdrive and how I believe this is a satisfactory explanation for Long COVID.

Interestingly, GABA is very effective at quelling a Sympathetic Overdrive response.

Interaction between glutamate and GABA systems in the integration of sympathetic outflow by the paraventricular nucleus of the hypothalamus
https://pubmed.ncbi.nlm.nih.gov/16877560/

I believe GABA should not only be immediately trialed in those suffering from COVID, but also in those suffering from Long COVID. I believe it may prove to be a very powerful therapeutic.

Happy Friday to all. As always, thank you for the continued support and may God bless us all.