Our paper is out- a critical essay (🇩🇪 language): What is the Role of "the Psyche"? Long COVID and ME/CFS as Test Cases for Evidence-Based and Patient-Centered Psychiatry and Psychotherapy. @geschom Mirja Lisa Nicolas, Fabian Fritz, Ronja Büchner thieme-connect.de/products/e…

open.substack.com/pub/theint… Some thoughts on the DGNB's position paper regarding diagnostic methods for Post-COVID and ME/CFS. Formally, it is weak. An expert opinion without a search strategy. 1/4

open.substack.com/pub/theint… Gedanken zur Stellungnahme der DGNB bzgl. Diagnosemethoden bei Post-COVID und ME/CFS. Formal ist sie schwach. Eine Expertenmeinung ohne Suchstrategie. 1/4

1) Watched this presentation by Dr. Steve Gardner from PrecisionLife. Their genetic analysis suggests that ME/CFS is highly polygenic and heterogeneous. They are using their data to make drug repurposing trials more effective, for example on GLP-1 receptor agonists.

4/5 Now the question The Lancet doesn't want to answer. Where is the petition against the medical associations of Iran? Syria? North Korea? China? Russia? I was born in Iran. The regime has executed physicians. Imprisoned doctors for treating protesters. Denied healthcare to political prisoners as policy. No petition. No Lancet article. No campaign. 117 nations belong to the WMA. When the standard is applied to one country and one country only — the world's single Jewish state — the word for that is not "medical ethics." I grew up inside a regime that weaponized medicine. I know exactly what the politicization of the profession looks like. This is it.

3/5 What the boycott would actually destroy: PillCam — revolutionized GI diagnosis. Developed in Israel. ReWalk — robotic exoskeletons for paralyzed patients. Developed in Israel. Breakthrough AI diagnostics for cardiac imaging and cancer detection used in hospitals on every continent. Israel has among the highest per-capita rates of medical innovation on earth. These technologies save lives in London, Johannesburg, São Paulo, and New York. Suspending the IMA doesn't punish a government. It severs research collaborations and training partnerships. The patients who lose aren't Israeli. They're everyone.

🔴I agree with the general idea that elevated IgG titers to latent or persistent pathogens should not simply be dismissed as meaningless. But I would add a few mechanistic clarifications. First, not all herpesviruses establish latency in B lymphocytes as their main reservoir. EBV is the classic herpesvirus with a major B-cell reservoir. But CMV, HHV-6, VZV and other herpesviruses have different latency biology and different cellular or tissue reservoirs. So it is important not to generalize EBV biology to all herpesviruses. Second, latency is not simply a state in which infected cells become completely invisible or biologically inactive. This is especially clear with EBV. EBV has different latency programs. Latency 0 is the most immunologically silent state, but latency I, II and III still express viral antigens to different degrees, and these infected cells can be controlled by EBV-specific CD4 and CD8 T cells. For example, latency I, classically seen in Burkitt lymphoma, expresses EBNA1, and EBNA1-specific CD4 T-cell responses are part of the immune control of EBV-infected cells. But the same general principle applies more broadly: many latent or persistent pathogens are not simply “doing nothing.” Latently infected or persistently infected cells can express viral non-coding RNAs, microRNAs, latency-associated transcripts or other regulatory RNA species that can modulate immune sensing, inflammation, cell survival, antiviral responses and immune evasion. In herpesviruses, viral microRNAs and non-coding RNAs can help maintain latency, suppress lytic genes, reduce immune recognition, alter host-cell survival and shape the local inflammatory environment. Even latently infected EBV cells can express non-coding viral RNAs such as EBERs and EBV microRNAs. These can modulate inflammation, interfere with antiviral sensing, shape B-cell survival and contribute to immune evasion. EBV also has immunomodulatory strategies, including viral IL-10-like activity mainly associated with lytic or reactivation contexts, which can help dampen antiviral immune responses and reduce immune recognition. So “latent” does not necessarily mean silent, harmless or irrelevant. It often means that the virus is being actively contained by immune surveillance. In healthy people, the key point is not that latent viruses become totally invisible. The key point is that CD4 and CD8 T-cell surveillance, NK-cell function and other antiviral mechanisms keep these reservoirs highly contained. This is why most healthy carriers do not have constant clinically relevant reactivation. The pathogen is usually controlled, restricted to limited reservoirs, and only reactivates more meaningfully during periods of immune stress, acute infection, immunosuppression or loss of immune control. Where things become more interesting is in genetically susceptible individuals. Immunogenetic and evolutionary studies suggest that some ancestral HLA-II haplotypes, especially DR2-DQ6, DR3-DQ2 and DR4-DQ8, have broader or more promiscuous peptide-binding repertoires than many other HLA-II backgrounds. This broader antigen-presentation capacity may have been advantageous during acute infections, because it allowed stronger and more diverse CD4 T-cell responses against pathogens. But if the pathogen persists, reactivates, or uses latency/evasion mechanisms, the immune system can remain chronically stimulated. That chronic stimulation can induce sustained IFN-γ, tissue inflammation, ectopic HLA-II expression in tissues that do not normally present antigen at high levels, and continuous presentation of both pathogen-derived and self-derived peptides. In that environment, the probability of activating autoreactive T and B cells increases. This is where HLA background matters. 1/3 Continued in the next post.👇🏻

still studying showing brain hypomethabolism in long covid. journals.sagepub.com/doi/ful… years ago we demonstrated the same in adolescents pubmed.ncbi.nlm.nih.gov/3730… pubmed.ncbi.nlm.nih.gov/3583… and already two years ago I wrote in my book how #longcovid will revolutionize the way we see at neuropsychiatric conditions amazon.it/Long-Covid-No-Filt…

Researchers Find Long Covid More Common Than Willingness To Say Long Covid

response to herpesviruses: TNF-alpha promotor genes, IL-6 and IL-10 promoter genes, IRF5, STAT4, KIR, C4A and probably more. TLDR: An abnormally elevated set of herpesvirus titers in a chronically ill person should be the START of a detailed investigation, not the end. 🙏 /end

This includes our fan favorite, the MTHFR gene: poor methylation impairs T-cell regulation AND impairs natural killer cell function. Both of which stand as defenses against herpesvirus reactivation. Having variants of the HLA, especially HLA-DQ and HLA-DR can make you much 23/

"well some people just have higher herpesvirus titers than others". What's interesting about this in the context of complex chronic illness is that many gene mutations that are linked to #longCOVID and #MECFS are also linked to dysregulated herpesvirus IgG responses. This 22/

Afghanische Frauen leiden nicht wegen „toxischer Männlichkeit“. Sie leiden, weil eine islamistische Ideologie ihre Unterdrückung religiös begründet und Scharia-Gesetze Frauen und Mädchen aus dem öffentlichen Leben auslöschen. #Islam #Sharia #Taliban #Feminismus

Inhaltshinweis: Assistiertes Sterben Ihr Lieben, diesen Beitrag teilen wir für Kim 💜 So wie sie es sich gewünscht und selbst gestaltet hat. Kim war Teil unseres Herzteams. Sie hat mit ihrem brillanten Verstand unendlich viel beigetragen.

When you have a bad day at work but you don't smoke.

IN TWO DAYS, on MON 15th, you can have your voice heard directly by those attending the RCPsych Congress. Congress is well attended, with a strong online presence. By including #RCPsychIC we can connect directly & continue the conversation. Template to C P below 👇️

This „work reveals an unrecognized mechanism by which SARS-CoV-2 ORF3a reprograms lysosomal lipid metabolism, advancing our understanding of how viral infection rewires host cholesterol homeostasis.“

Another study shows cerebral hypometabolism in #LongCovid patients with PEM. Cerebral hypometabolism is a decrease in the brain's ability to turn glucose into energy, leading to a severe cellular energy deficit. journals.sagepub.com/doi/ful…

New paper in @TheLancet ft. PLRC member Dr. Megan Fitzgerald: "In this paper, a group of bioethicists, clinician-scientists and people.. with #LongCovid argue that it is ethically imperative to conduct trials of disease-modifying treatments for LC now." 🧵thelancet.com/journals/eclin…

Antidepressant effects of GLP-1 analogs mediated by microbes Liraglutide reduces depression via GLP-1R-independent, microbiota-dependent mechanism. Liraglutide enriches L. delbrueckii, ⬆️endocannabinoid 2-AG to normalize activity in emotional brain regions cell.com/cell-host-microbe/f…

Berlin ist ein Hotspot für das West-Nil-Virus. Eine Charité-Studie legt jetzt nahe, dass mehr Mücken das Virus in sich tragen als gedacht. Wie groß ist das Risiko? trib.al/mFXodGK