COVID-19 is a serotonin-dependent disease

[lvysaur]

I can't find the source, but I read that COVID disrupts endogenous antibiotic mechanisms in the body, causing bacterial overgrowth. So that once the COVID is all gone (within a month or so) the body still has an elevated baseline amount of bacteria, causing chronic illness.

This was the case for me, and my long-COVID cleared up 80% after taking antibiotics.

I also had extreme diarrhea during the acute phase of COVID, and the worst thing that triggered it was meat. Hard to say if this is serotonin/tryptophan related, or just related to bacterial overgrowth putrefying meat in my GI tract (which is very bad hence the body wants to "spit it out" asap)

 

[tankasnowgod]

I can't find the source, but I read that COVID disrupts endogenous antibiotic mechanisms in the body, causing bacterial overgrowth. So that once the COVID is all gone (within a month or so) the body still has an elevated baseline amount of bacteria, causing chronic illness.

This was the case for me, and my long-COVID cleared up 80% after taking antibiotics.

I also had extreme diarrhea during the acute phase of COVID, and the worst thing that triggered it was meat. Hard to say if this is serotonin/tryptophan related, or just related to bacterial overgrowth putrefying meat in my GI tract (which is very bad hence the body wants to "spit it out" asap)

You realize, if this is the case, you admit that the so called "Long Covid" isn't "Long Covid" at all. It's a lingering or "long" bacterial infection.

Of course, why would an alleged "virus" cause this? This has never been mentioned for other common cold viruses, including all the boring old, non-novel corona viruses.

But, you know what is confirmed to increase bacterial loads in the body, especially the nasal and GI tract? Excessive mask wearing. Something that has dramatically increased in the past 2.5 years, even before places were "mandating" them.

 

[Fred]

I disagree. A positive PCR test coupled with a set of common symptoms of Covid is good enough indication that you’re actually infected.

and I don’t see anything wrong with it since treatment of either Covid or other common cold pathogens (like the other beta-Coronaviridae or gastrointestinal cold viruses) is virtually identical.

The common symptoms for covid are the same as the common symptoms for flu (and many other things), which is why the flu disappeared immediately when "covid" was rolled out.

 

[I'm.No.One]

This is probably why aspirin & cypro basically knocked out my entire families symptoms when we came down with it.

We basically had a rough cold for about 3 days, but the first day before I was like "take this" to my household sucked close to a flu level.

 

[Perry Staltic]

Way back when before I forgot that covid even exists, Dr Farid Jalali thought covid was serotonin syndrome caused by the release of serotonin from platelets that became activated by the virus thingie. I think it's more likely that the virus thingie had nothing to do with it and the serotonin poisoning was due to freaked out people ODing on SSRIs and cough syrup and the many serotonergic drugs used in hospitals to treat covid patients.

 

[LeeLemonoil]

Way back when before I forgot that covid even exists, Dr Farid Jalali thought covid was serotonin syndrome caused by the release of serotonin from platelets that became activated by the virus thingie. I think it's more likely that the virus thingie had nothing to do with it and the serotonin poisoning was due to freaked out people ODing on SSRIs and cough syrup and the many serotonergic drugs used in hospitals to treat covid patients.

I think Jalalis thesis is a good one. That’s part of a immune response, and especially part of deranged immune responses.

Given that SSRIs and Serotonergic drugs in various way disturbe the fine balance of when, how and how much the transmitter serotonine influences inflammation and immune responses it’s highly probable that most of the time this „Modulation“ is not to the benefit of the affected individual

 

[aliml]

Characterization of serotonin as a candidate biomarker of severity and prognosis of COVID-19 using LC/MS analysis

The coronavirus disease 2019 (COVID-19) pandemic has been associated with high mortality worldwide. Owing to its complicated pathophysiology, diagnost…

sciencedirect.com

A clear decrease in serum serotonin concentrations was observed in patients with COVID-19 as disease severity worsened. This observation is in agreement with that of a previous study, which demonstrated lower serum serotonin concentration in patients with severe COVID-19 than in patients with mild/moderate COVID-19; the previous study determined the serum concentration of serotonin using ELISA.22 Important physiological roles of serotonin have been reported in the immune, vascular, and digestive systems, as well as in the central nervous system.20,21 Therefore, the decreased serum concentrations of serotonin may be associated with the immune status of patients with COVID-19. Although the underlying mechanism is unclear, several metabolomic studies have revealed increased kynurenine and decreased tryptophan levels, along with a decrease in serotonin levels in patients with COVID-19.8, 9, 10, 11, 12, 13,15, 16, 17 In agreement with these findings, increased kynurenine and decreased tryptophan levels were also observed in the present study. Some of these previous studies proposed that the upregulation of the IDO enzyme in patients with COVID-19 may play a role in increased tryptophan conversion into kynurenine during the immune response to COVID-19. Regarding serotonin homeostasis, it has been proposed that IDO activation leads to significant consumption of tryptophan and limits its availability for serotonin production.20 As IDO is also involved in the conversion of serotonin to formyl-5-hydroxykynurenamine,20 its upregulation may also decrease the serum serotonin concentration by enhancing serotonin metabolism. Taken together, the decrease in serotonin levels as disease severity progressed can be attributed to the upregulation of IDO caused by SARS-CoV-2 infection.

In the present study, a decrease in serotonin concentrations was observed even between healthy subjects and patients with mild COVID-19, whereas alterations in tryptophan and kynurenine concentrations were not significant (Fig. 1). Furthermore, the prognostic ability of serotonin (but not of kynurenine and tryptophan) for further progression to more severe stages was confirmed in patients with moderate-stage COVID-19 (Fig. 2, Fig. 3). Therefore, there may be another mechanism other than the upregulation of IDO underlying the decrease in serotonin concentrations. To date, there is no established mechanism associated with COVID-19; however, recent reports have suggested several possibilities regarding the decreased serum serotonin levels. Serotonin is metabolized by IDO but also by monoamine oxidases (MAOs) and is synthesized from 5-hydroxy-l-tryptophan by l-dopa decarboxylase (DDC).20 In 2021, Cuperlovic-Culf et al.26 suggested an increase in MAO activity in patients with COVID-19 evidenced by alterations in several metabolite ratios upon reanalysis of previously published metabolomics data.9 Alternatively, in vitro experiments on epithelial cell lines (VeroE6 and A549) infected with SARS-CoV-2 revealed a strong negative correlation between viral RNA and DDC mRNA levels,27,28 which implied that patients with COVID-19 may have decreased DDC levels in their epithelial cells. Thus, IDO-independent alterations in serotonin homeostasis in patients with COVID-19 may also contribute to the decreased serum serotonin levels.

The present data further demonstrated the potential prognostic ability of serum serotonin for assessing the risk of developing severe and/or critical COVID-19 from moderate COVID-19. To date, the role of serotonin in COVID-19 prognosis has been unknown. However, serotonin treatment was reported to suppress the release of interleukin (IL)-6 and tumor necrosis factor (TNF)-α in cultured macrophages and lymphocytes,29 and of INF-γ in cultured whole blood.30 Nau et al. reported that the activation of the serotonin 2A receptor inhibits the intestinal production of IL-6 and the increase in circulating IL-6 levels caused by TNF-α in mice.31 Taken together, these results indicate that serotonin may suppress the release of pro-inflammatory cytokines, such as IL-6, which may explain why patients with COVID-19 with low serum serotonin concentrations had a higher risk of developing severe and/or critical disease from moderate COVID-19. Contrary to its anti-inflammatory effect, serotonin is known as accelerate blood coagulation,32 which may cause further increase the severity of COVID-19. However, as shown in Fig. 1, the serum serotonin concentrations in all patients with moderate-stage COVID-19 were mostly lower than those in healthy subjects. Therefore, at least among the patients with moderate-stage COVID-19 whom we recruited, excessive blood coagulation by serotonin may not have played a role in the progression of disease.

As serotonin plays important physiological roles in the immune, vascular, digestive, and central nervous systems,20,21 the decreased serotonin concentration with COVID-19 progression may also contribute to some of the symptoms of COVID-19. In particular, studies have demonstrated an association between COVID-19 and depression.33, 34, 35 It has also been reported that the serum serotonin levels inversely correlated with the degree of anxiety and depression36; thus, decreased serotonin levels with disease progression may be one of the causes of depressive syndrome of COVID-19, although the cause and effect remain unclear. On the contrary, the role of serotonin in the gastrointestinal symptoms has also been proposed. Ha et al. demonstrated increased plasma serotonin levels with COVID-19 severity and its strong correlation with the incidence of diarrhea.37 However, the plasma concentration of serotonin, which reflects pre-clotting state of the blood, could not be simply compared with serum serotonin concentration, which reflects post-clotting state of the blood. Thus, the association between serum serotonin levels and diarrhea remains unclear, warranting further research. In addition, an inverse correlation of plasma and serum serotonin levels against COVID-19 severity could not simplify the role of serotonin in COVID-19, but simultaneous analysis of plasma and serum serotonin levels may be capable of addressing the pathophysiological implication of serotonin on COVID-19.

 

[Perry Staltic]

.

 

[lvysaur]

But, you know what is confirmed to increase bacterial loads in the body, especially the nasal and GI tract? Excessive mask wearing.

Cope harder. Happened back when Fauci was anti-mask.

 

[tankasnowgod]

Cope harder. Happened back when Fauci was anti-mask.

No "cope" on my part.

And so what? Fauci doesn't run the country. He's an unelected bureaucrat, a public trustee. If you remember, the whole reason they were saying "DON'T WEAR MASKS!" at that time is because people were buying them up in bulk, and there was very limited supply for Healthcare workers. The Surgeon General even said as much-

Fact check: Trump surgeon general initially dismissed mask-wearing, but then endorsed

A deleted tweet from the now-former U.S. surgeon general that dismissed mask-wearing is being taken out of context.

www.usatoday.com

"Seriously people- STOP BUYING MASKS!" Adams purportedly tweeted on Feb. 29, 2020.

"They are NOT effective in preventing general public from catching #Coronavirus, but if healthcare providers can't get them to care for sick patients, it puts them and our communities at risk!

I mean, you can continue to believe in the existence of "viruses" if you want to, despite the fact that not a single one has ever been isolated or detected straight from any human bodily fluid (something no virologist will deny), there is no logical way to prove that ANY virus causes ANY symptom, and no one has ever seen a "live" virus, since electron microscopy will only allow you to see dead samples.

I really think the only reason you still believe in the "Novel Corona Virus" is that you have no idea how virology works. People criticize homeopathy for using treatments that have no detectable levels of substance in them, although they seem to be fine with virology, which also says virus levels, even in the sickest patients, are also at undetectable levels.

And regardless of any of that, no one denies that bacteria existed back then. So, you could have developed a long bacterial infection for any number of reasons at pretty much any time in your life.

 

[Brian Douglas]

I'd say yes, since people with depression (i.e. people with elevated serotonin and/or presumably already taking SSRI drugs) were found in several studies to be at higher risk for both infection and severe disease.

Didn't know where to stick this but something I thought you, Haidut, should see:

IS DEFIBROTIDE AN IMPORTANT TREATMENT FOR SPED, COVID AND LONG COVID?

Early treatment may provide endothelial protection and it may treat Long COVID.

wmcresearch.substack.com

 

[aliml]

Elevated Serotonin in COVID-19 Stimulates Anoctamin-1 Mediated Chloride Secretion in Lung and Intestinal Epithelial Cells​

Earlier studies demonstrated that blood 5-hydroxytryptamine (5-HT) is elevated in patients with COVID-19-associated diarrhea with higher severity of symptoms. We hypothesize that disruption of vectorial Cl transport by 5-HT may be critical in determining the alveolar flooding and abnormalities in intestinal Cl secretion through stimulation of anoctamin 1(ANO1) Cl channel. Using western blot, immunostaining, and electrophysiology, we characterized the localization of human ANO1 and its stimulation by 5-HT on Cl secretion in lung and intestinal epithelium. Because calcium-activated chloride current in human intestinal epithelia remains controversial, we examined the localization of ANO1 in the human terminal ileum and colonic tissue using confocal microscopy. Our results indicated that ANO1 was localized predominantly at the brush-border membrane and co-localized with the brush-border membrane marker villin. ANO1 is not present in goblet cells. The anti-ANO1 antibody recognized a protein of appropriate size in human colonic tissue. The specificity of the ANO1 antibody was tested by immunoblot analysis of lysates from human colorectal cancer tissues, where it displayed amplified ANO1 protein expression. We next confirmed ANO1-currents activated by 5-HT in the Caco-2 cells by patch-clamp measurements of whole-cell current. The application of 100 nM 5-HT produced a typical outward rectification. CaCCinh-A01, a specific ANO1 blocker, inhibited the currents. The half-maximal effective concentration value for the effects of 5-HT was estimated at 21.8 ± 13.7 nM with a Hill coefficient of 0.89 ± 0.16. These results indicated that 5-HT evoked calcium-activated Cl currents through ANO1 channels. ANO1 is expressed in Calu 3 cells. We next confirmed the presence of ANO1 currents activated by 5-HT in Calu-3 cells by the Ussing chamber experiments. Serosal addition of 5-HT produced an immediate and significant increase in Isc in Calu-3 cells that was inhibited by the ANO1 selective inhibitor T16Ainh-A01. Finally, we demonstrate that SARS-CoV2 infection led to enterochromaffin cell hyperplasia in the intestinal epithelium of Syrian Hamster with a possible elevation of 5-HT, which could explain the severity of symptoms in COVID-19 associated diarrheal patients.

https://doi.org/10.1096/fasebj.2022.36.S1.0R556

Ivermectin is a novel Anoctamin-1 inhibitor.

Inhibition of TMEM16A Ca2+-activated Cl− channels by avermectins is essential for their anticancer effects

Transmembrane member 16A (TMEM16A) encoded Ca2+-activated Cl− channels were found to be involved in tumorigenesis. Previous studies suggest the effect…

sciencedirect.com

 

[Runenight201]

I can't find the source, but I read that COVID disrupts endogenous antibiotic mechanisms in the body, causing bacterial overgrowth. So that once the COVID is all gone (within a month or so) the body still has an elevated baseline amount of bacteria, causing chronic illness.

This was the case for me, and my long-COVID cleared up 80% after taking antibiotics.

I also had extreme diarrhea during the acute phase of COVID, and the worst thing that triggered it was meat. Hard to say if this is serotonin/tryptophan related, or just related to bacterial overgrowth putrefying meat in my GI tract (which is very bad hence the body wants to "spit it out" asap)

What antibiotic did you use? Considering if I should run a course cuz my gut feels all messed up.

 

[lvysaur]

What antibiotic did you use?

Amoxicillin