AlphaBetaDelta
333 posts


@SabinehazanMD @Kevin_McKernan Love to watch your work, have you published anywhere how to best manage the restoration of the biffido?
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@Kevin_McKernan Hard for people that are missing microbes.
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The Spotify version is less likely to be taken down.
Dr. Alexis Jazmyn@dralexisjazmyn
Live on Spotify! @Kevin_McKernan
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@KristinaRevay Hi,are you talking about the CD3, CD4, CD8, CD19 type panels or something else? What do you usually see as off in the results? Or the IncellDx Panel?
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@MtShastaWriter @SillyPutty78 Ive been ordering lymphocyte & monocyte subset panels for 4 yrs, since Jan 2020 infx. Normal CBC’s but Severe, persistent monocyte dysregulation, so YES it does make U immunocompromised. Even 1 infectn.
MDs dont do these panels & wrongly conclude U R fine based on a normal CBC
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@Nick_Wellings @Kat_in_the_Hat3 I use daily and have used for years. It is also part of RB protocol. As far as I know there were no issues with it.
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Probiotics help reduce gut pathogens, sure - but which ones? In this meta-analysis, Lactobacillus-based probiotics and Saccharomyces boulardii decolonized 71% and 77% of pathogens effectively.
"The use of probiotics and prebiotics in decolonizing pathogenic bacteria from the gut; a systematic review and meta-analysis of clinical outcomes"

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@Ivi81 Can you explain what those two tests are please? And it's the top one you relate to your symptoms?
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@1goodtern I have followed your brave work for quite a while now. Please have a closer look into the vaccines, even some of the CDCs own slides showed it has a negative efficacy after some time and that's not including all the vaccine damaged like myself.
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@CiaraGlenville Keep sharing your insights :-) Can you please advise which test panel is this?
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Vitamin B6 levels &a connection to acetylcholine? #LongCovid
I acknowledge my gross privilege in getting these tests but maybe it’ll help some others with similar patterns. May be relevant for B6 deficiency OR toxicity.
Seeing my doc Tuesday, happy for suggestions/ what to ask!
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AlphaBetaDelta 리트윗함

@spoonless_me Very glad to hear! How much of the Choline and Benfothiamine are you taking?
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@devj3ns @fiordilatte12 There is an app called FlutterShark
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@fiordilatte12 You could check the licence page. First, if it uses the default flutter one and secondly if it uses packages from pub.dev.
This is the most effective method I'm aware of. I'm eager to discover if there are any quicker, reliable alternatives.
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Soon, scrolling with two fingers in #flutter won't scroll twice as faster anymore.
Yesterday a PR for multi-touch drag strategies was merged.
What do you think about that?
github.com/flutter/flutte…
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@joshuamcclure @ShaneyWright What do you find it helps with?
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@ShaneyWright Kanna helps me. A lot. Recent discovery for me.
ncbi.nlm.nih.gov/pmc/articles/P…
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Whatever the root driver of #LongCovid, patients need something – anything – to quell the chronic inflammation happening in their bodies ASAP. This cannot wait. It's beyond urgent. We've been waiting since 2020 & its almost 2024 already. 4 years. 4 years. Pathetic. A disgrace.
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@manruipa @LongCovidAdvoc @LongCOVIDPhysio @covid_madrid @longcovidspain @long_covid @remissionbiome @MECFSNews @PlzSolveCFS @benh_mecfs @exceedhergrasp1 Is Tryptophan supplementation a good idea in your opinion?
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🧵𝐂𝐚𝐮𝐭𝐢𝐨𝐧 𝐟𝐨𝐫 𝐩𝐚𝐭𝐢𝐞𝐧𝐭𝐬 𝐰𝐢𝐭𝐡 𝐌𝐄/𝐂𝐅𝐒 𝐚𝐧𝐝 𝐋𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃 𝐚𝐟𝐭𝐞𝐫 𝐫𝐞𝐬𝐮𝐥𝐭𝐬 𝐨𝐟 𝐚 𝐧𝐞𝐰 𝐬𝐭𝐮𝐝𝐲 🚨 (1/2)
The following is a comparative analysis of two models that explain serotonergic alterations.
𝐂𝐨𝐦𝐩𝐚𝐫𝐚𝐭𝐢𝐯𝐞 𝐀𝐧𝐚𝐥𝐲𝐬𝐢𝐬: Intestinal Serotonin Models in the Context of Viral Infections 📊
Serotonin (5-HT), known for its functions in the central nervous system, also plays a critical role in gut function. Different models attempt to explain the implications of serotonin in the context of viral infections. I analyze here two models: the model presented by Wong AC, et al and our model.
𝐖𝐨𝐧𝐠 𝐀𝐂, 𝐞𝐭 𝐚𝐥. 𝐦𝐨𝐝𝐞𝐥 (cell.com/cell/fulltext/… ):
1️⃣ 𝐏𝐫𝐨𝐩𝐨𝐬𝐢𝐭𝐢𝐨𝐧: It suggests that viral infection inhibits the uptake of tryptophan, the precursor of serotonin. This would lead to a decrease in serotonin production at the intestinal level.
2️⃣ 𝐈𝐦𝐩𝐥𝐢𝐜𝐚𝐭𝐢𝐨𝐧𝐬:
- With less serotonin, 5-HT3 receptors in the vagus nerve would not be activated, being responsible for the decrease in serotonin at the central nervous system level.
- This model does not adequately address how an increase in intestinal motility would be generated if there is a decrease in serotonin, given that elevated serotonin stimulates motility generating diarrhea and gastrointestinal symptoms that occur in many patients with ME/CFS and Long COVID.
- It is also not explained how the vagus nerve could be overactivated, causing symptoms of dysautonomia.
- This model suggests platelet hyperactivation primarily due to viral inflammation and interferon production. While it recognizes a procoagulant state, it does not detail the specific role of serotonin or intracellular mechanisms in platelets in relation to hypercoagulability
𝐎𝐮𝐫 𝐦𝐨𝐝𝐞𝐥 (…nslational-medicine.biomedcentral.com/articles/10.11… ) :
1️⃣ 𝐏𝐫𝐨𝐩𝐨𝐬𝐢𝐭𝐢𝐨𝐧: Activation of TLR3 by EBER (or TLR2 by EBV dUTPases) or other viral RNA would inhibit and reduce SERT (serotonin transporter) expression, leading to serotonin accumulation at the extracellular level in inflamed tissues such as the intestinal mucosa.
2️⃣ 𝐈𝐦𝐩𝐥𝐢𝐜𝐚𝐭𝐢𝐨𝐧𝐬:
- Elevated intestinal serotonin would activate 5-HT3 receptors, increasing intestinal motility and causing symptoms such as diarrhea.
- Increased serotonin could also overactivate the vagus nerve, explaining symptoms of dysautonomia.
- The decrease of serotonin in the central nervous system would be produced by the passage of viral RNAs that activate TLR3 receptors of microglia, causing the release of proinflammatory cytokines IL-1β and TNF-α, which increase the expression and activity of the serotonin transporter SERT in astrocytes, causing an increase in serotonin (5-HT) reuptake and a decrease in its extracellular levels.
- Both the increase in proinflammatory cytokines and the increase in oxidative and nitrosative stress (ROS/RNS) by activation of microglia through TLR3 could lead to increased IDO activity in microglia, resulting in reduced tryptophan (TRP) levels, increased quinurenine catabolites and decreased 5-HT synthesis.
- In our model, TLR3 activation, in addition to its effect on serotonin transporters (SERT) in the intestine, would also influence platelets. Inhibition of SERT in platelets by the action of TLR3 would reduce the ability of platelets to reuptake serotonin at the intestinal level. This leads to additional accumulation of serotonin in the intestinal tissue, further aggravating symptoms. Extracellular serotonin also activates 5-HT receptors on platelets. This activation, together with viral RNAs acting on platelet TLR3, leads to platelet hyperactivation. This state of platelet hyperactivation would contribute to hypercoagulability.
𝐂𝐨𝐢𝐧𝐜𝐢𝐝𝐞𝐧𝐜𝐞𝐬 𝐛𝐞𝐭𝐰𝐞𝐞𝐧 𝐛𝐨𝐭𝐡 𝐦𝐨𝐝𝐞𝐥𝐬:
1️⃣ 𝐒𝐞𝐫𝐨𝐭𝐨𝐧𝐢𝐧 𝐜𝐞𝐧𝐭𝐫𝐚𝐥𝐢𝐳𝐚𝐭𝐢𝐨𝐧: Both models agree that, at the central nervous system level, there is a decrease in serotonin. This central reduction could contribute to neurological and psychological symptoms, such as fatigue, anhedonia and other symptoms.
2️⃣ 𝐐𝐮𝐢𝐧𝐮𝐫𝐞𝐧𝐢𝐧𝐞 𝐥𝐞𝐯𝐞𝐥𝐬: Both models recognize an increase in the quinurenine pathway during viral infections. However, they differ in their implications. In our model it is suggested that increased proinflammatory cytokines and oxidative/nitrosative stress leads to increased IDO activity, which reduces tryptophan levels and increases quinurenine catabolites in the central nervous system. This results in a decrease in serotonin synthesis in the CNS.The model of Wong AC, et al. while acknowledging the increase in quinurenine levels, suggests that this increase is not the main reason behind serotonin depletion during viral inflammation, but rather decreased tryptophan uptake. But it is not specifically commented that it would occur at the CNS level.
3️⃣ 𝐈𝐧𝐟𝐥𝐮𝐞𝐧𝐜𝐞 𝐨𝐟 𝐓𝐋𝐑𝟑: In both models, the role of TLR3 in the context of viral infection is recognized, although its influence on serotonin varies between models.
4️⃣ 𝐒𝐲𝐬𝐭𝐞𝐦𝐢𝐜 𝐈𝐦𝐩𝐥𝐢𝐜𝐚𝐭𝐢𝐨𝐧𝐬: In both the model in the article and the one proposed by the user, alterations in serotonin levels, either by depletion or accumulation, have implications beyond the gastrointestinal tract, affecting systems such as the vagus nerve and, potentially, the autonomic system in general.
5️⃣ 𝐏𝐥𝐚𝐭𝐞𝐥𝐞𝐭 𝐚𝐜𝐭𝐢𝐯𝐚𝐭𝐢𝐨𝐧: While the model of Wong AC, et al. focuses on general inflammation and interferon production as drivers of hypercoagulability, our model provides a specific mechanism involving both viral RNAs and serotonin and their interaction with platelets. In this respect, both models may be complementary in describing different disease processes.
6️⃣ 𝐈𝐧𝐭𝐞𝐫𝐚𝐜𝐭𝐢𝐨𝐧 𝐰𝐢𝐭𝐡 𝐒𝐒𝐑𝐈 𝐃𝐫𝐮𝐠𝐬: Both models recognize that administration of selective serotonin reuptake inhibitors (SSRIs) in the context of these disorders may have unpredictable effects and potentially exacerbate or moderate symptoms, depending on the individual patient's situation and which model is considered more accurate.
𝐂𝐨𝐧𝐬𝐢𝐝𝐞𝐫𝐚𝐭𝐢𝐨𝐧𝐬 𝐟𝐨𝐫 𝐏𝐚𝐭𝐢𝐞𝐧𝐭𝐬 𝐨𝐧 𝐒𝐒𝐑𝐈 𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭:
Because SSRIs inhibit serotonin reuptake, they may have complex effects in this setting:
1️⃣ According to the model of Wong AC, et al SSRIs could compensate for the decrease in serotonin by increasing its availability.
2️⃣ In our model, SSRIs could improve the availability of 5-HT in the central nervous system. However, it could exacerbate gut symptoms and inflammation due to an increase in 5-HT availability at the gut level, possibly exacerbating symptoms.
𝐂𝐨𝐧𝐜𝐥𝐮𝐬𝐢𝐨𝐧:
1️⃣ Serotonin homeostasis in the context of viral infections is an area that requires further investigation.
2️⃣ Given that many patients with ME/CFS have had worsening symptoms with SSRIs and the possible consequence of serotonin accumulation at the gut level in one of the two models, it would be prudent not to recommend these treatments in both diseases until both processes are verified.
3️⃣ It is also possible that both models describe different stages of the same disease, for example, in acute or chronic phases or in flare processes.
🔄 Share it with other patients so they can understand their disease - 𝐤𝐧𝐨𝐰𝐥𝐞𝐝𝐠𝐞 𝐢𝐬 𝐩𝐨𝐰𝐞𝐫! 📚
#EBV #LongCOVID #MECFS #MyalgicEncephalomyelitis #Health #Research #News #microE2324 #Medicine #Microbiology #VIRUS #ChronicDiseases #SARSCOV2 #COVID #LongHaulers #MCAS #ME #MyE #CFS
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@MarcosSnchezMu1 @thechronicchloe Which H1 do you find helpful?
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@thechronicchloe That's a problem, we don't know hoy homogenous is this ME/LC group. However, you don't need to have hives or ithing. I get a lot better with anti H1, but only those that cross the blood brain barrier, which makes me think fatigue is mostly a brain symptom. Personally I think it
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@DKlemitz @BeetaBaran @SabinehazanMD Right, so far sounds like the S1 CD16 monocyte test by IncellDx is the best we have so far?
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@BeetaBaran @SabinehazanMD 1/I can't find a blood test that directly measures the free spike protein in the blood. Instead the following measures so-called anti-bodies as a proxy. citymd.com/services/lab-t….
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A pet scan will not show you microbiome dysbiosis or loss of Bifidobacteria. Long covid is from spike protein which is from the Vax. Vax kills your bifidobacteria, which predisposes you, in my opinion, and from the research I have done, to decreasing your immunity which can lead to cancer. Follow the Bifidobacteria… contact @Progenabiome we figured it out, but we will not be publishing the treatment or discussing it. Trolls and suits are paying attention to developing a business, but Medicine is an art. #letdrsbedrs #savethebif All my best and remember immunity is in your gut..




Walter M Chesnut@Parsifaler
🚨 Clinicians; I recommend performing full-body PET scans of Long COVID patients. I believe the evidence now shows, as I previously hypothesized, that the Spike Protein induces the cellular environment of Cancer. The SP transforms the body into a systemic Warburg Effect metabolism. This is why those with Long COVID present with the symptoms of metastatic cancer. Myriad, perhaps millions, of microtumors are induced. Cancer seeds. The SP is most likely the most oncogenic protein ever observed (created). Post to follow. sciencedirect.com/science/articl…
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@tinkerbell_ish Did you notice a change in your neuropathy?
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#TheNicotineTest I could feel PEM kicking in yesterday so I put on a 3.5mg patch
Within a couple of hours I no longer felt poisoned & flu-like
On the left is an average night's sleep for me, on the right is a nicotine patch sleep 🤯
I'm going to do another round! 5.2mg today


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@LAVistaNY @holmanm Are there adverse problems for someone taking Serrapeptase for someone on Plavix and recent heart attack and stenting
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@angryhacademic Thanks for your paper! Is there a reason you favour those two anticoagulatants instead of Apixaban used in the 'triple therapy'?
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Latest paper from Dr Robin Kerr & me:
#LongCovid is primarily a Spike protein Induced Thrombotic Vasculitis
researchsquare.com/article/rs-293…
Here we proposed that long covid is primarily a spike protein-induced thrombotic vasculitis, & we use Robin as a supporting case study 🧵
#TeamClots

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@RealJasonNelson Everyone with a loved one fighting cancer should buy this immediately and get it in them!! Stage 4 BC in November and in 4 months had no evidence of disease. I take it three weeks a month and one week a month I take ivermectin!

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@richterj85 What was the flush like on that amount of Niacin?
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Just out of curiosity -
#LongCovid/#MECFS/#POTS folks, have you found at least one thing that you're **reasonably sure** moved the dial for you?
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