Just because you get rid of spike doesn’t mean health immediately turns back on. Trained autoimmunity must be revered. Look into mesencephalic astrocytes derived neurotrophic factor… endoplasmic reticulum stress… senescence and the unfolded protein response. The field of aging and the field of antimicrobials are on a crash course.

JUST IN: New study reveals creatine may increase muscle mass, strength, cognitive function, & endurance even without exercise.

Democrats get long COVID Republicans get vax injured. LMFAO We are all so stupid. We fight about this instead of fighting for real healthcare and to hold responsible those who poisoned us all.

Victory Sunday 🙌

Career night for QB1 🫡

Muscle cells turn over 1-2% of their protein content every day. That recycling process determines not just muscle function but whole-body aging. When protein quality control breaks down in muscle, disease follows predictably. A team of muscle biologists published a comprehensive review in Nature Metabolism proposing seven interconnected hallmarks that define muscle health. The second hallmark is proteostasis, the machinery that maintains protein quality. Muscle faces a unique proteostasis challenge. Unlike most tissues, muscle fibers don't divide. A single muscle cell can last your entire lifetime. That means the protein quality control systems need to function flawlessly for decades without the option of simply replacing damaged cells. The numbers reveal the scale: skeletal muscle contains roughly 50% of all protein in your body. Each day, muscle turns over 1-2% of that protein mass. This constant synthesis and degradation cycle maintains the contractile machinery, metabolic enzymes, and structural proteins that determine muscle function. When synthesis exceeds degradation, muscle grows. When degradation exceeds synthesis, muscle atrophies. But the balance matters less than the quality of what gets built and what gets removed. Proteostasis depends on three integrated systems: • The ubiquitin-proteasome system handles damaged or misfolded proteins • Autophagy degrades larger structures like damaged organelles and protein aggregates • Chaperone proteins prevent misfolding and help refold damaged proteins • The unfolded protein response detects and responds to stress in the endoplasmic reticulum All three systems decline with age. Proteasome activity drops. Autophagy becomes less efficient. Chaperone expression decreases. The result is accumulation of damaged proteins that interfere with muscle function. Damaged proteins don't just sit there inert. Misfolded proteins can aggregate, forming toxic structures that disrupt cellular processes. Oxidatively damaged proteins lose function and consume resources. Glycated proteins from chronic hyperglycemia create advanced glycation end products that stiffen tissues and trigger inflammation. The autophagy component is particularly critical in muscle. Autophagy clears damaged mitochondria through a selective process called mitophagy. When mitophagy fails, dysfunctional mitochondria accumulate, producing excess reactive oxygen species that damage more proteins, creating a vicious cycle. Now for the important part: what you can actually do about it now. Exercise is the most potent activator of muscle proteostasis. Resistance training acutely increases protein synthesis rates for 24-48 hours after a session. The repeated stimulus leads to sustained elevation in both synthesis and degradation, improving the quality of the protein pool. Endurance exercise activates autophagy and increases expression of chaperone proteins. The transient stress of exercise triggers adaptive responses that strengthen proteostasis machinery. Proteostasis breakdown appears across muscle-related diseases. In sarcopenia, reduced protein synthesis and impaired autophagy lead to loss of muscle mass and function. In inclusion body myositis, protein aggregates accumulate inside muscle fibers. In muscular dystrophies, mutations in structural proteins overwhelm quality control systems. Cancer cachexia demonstrates the systemic consequences of muscle proteostasis failure. Tumor-derived factors activate protein degradation pathways while suppressing synthesis. The resulting loss of muscle protein contributes to weakness, metabolic dysfunction, and mortality. The cross-talk dimension reveals how muscle proteostasis affects other organs. Muscle secretes follistatin, which regulates myostatin and influences protein synthesis in other tissues. Muscle-derived irisin affects protein homeostasis in adipose tissue. When muscle proteostasis is compromised, these signals change, potentially contributing to systemic aging. Recent research has identified potential intervention points. Urolithin A, a metabolite produced by gut bacteria from foods like pomegranates, enhances mitophagy. Spermidine supplementation induces autophagy and extends lifespan in animal models. While supplements can work, resistance training remains the most validated approach. The framework provides quantifiable targets: protein synthesis rates, autophagy flux, proteasome activity, and markers of protein damage like carbonyl groups and advanced glycation end products. These can be measured in muscle biopsies and potentially tracked through circulating biomarkers. The implications extend to aging biology broadly. Muscle is the largest protein reservoir in the body. When muscle proteostasis fails, the systemic pool of amino acids becomes dysregulated. This affects protein synthesis in other organs, immune function, and metabolic health. Key takeaways: • Muscle turns over 1-2% of its protein content daily, requiring constant quality control • Proteostasis depends on the ubiquitin-proteasome system, autophagy, and chaperone proteins, all of which decline with age • Damaged proteins don't just lose function, they actively interfere with cellular processes and trigger inflammation • Exercise is the most validated intervention for maintaining muscle proteostasis • Proteostasis breakdown in muscle contributes to sarcopenia, metabolic disease, and systemic aging • New compounds like urolithin A and spermidine target specific proteostasis pathways and show promise in animal models The shift from quantity to quality applies directly to proteostasis. Maintaining muscle mass matters less if the proteins within that muscle are damaged, misfolded, or non-functional. Measuring and preserving protein quality represents a more fundamental target.

We found that measles eraaed up to 80% of people’s existing antibody repertoire (Immune Amnesia confirmed) and that they then had to build it back through vaccines or infections - placing them at high risk for disease for years. 2nd main paper here: 6/ science.org/doi/abs/10.1126/…

18 young, previously healthy people. Mild COVID, nobody hospitalized. Six months later, they're still dealing with brain fog, worse sleep, anxiety, low mood. On a test of inhibitory control they did just as well as controls. But their EEG told a different story about how their brains got there🧵

Following the State of Sarcoma Update and ARPA-H Summit during #PediatricCancerAwarenessWeek, OS Therapies CEO Paul Romness joined a vital Rare Disease Roundtable with acting FDA Commissioner @FDA_KyleD. Grateful to leadership for supporting Project Orbis and critical Accelerated Approval pathways for deadly rare diseases with no other options. #OSTX $OSTX

Jensen Huang says he simply doesn't believe AI CEOs when they say they don't know how to control their models we should not bet human civilisation on one man's incredulity

People don’t have sufficient appreciation for the fact that frontier models will be able to actuate anything in the physical world that can be connected to the internet and actuated using a programmatic or otherwise digital interface.

Rogue AI bots have hacked into governments, universities and public agencies around the world, tech giant OpenAI admits trib.al/kfILpL1

Boeing scrambles to fix new 737 MAX software glitch that can knock out autopilot functions after missed landing trib.al/ng2UeWB

JUST IN: Microsoft-backed New Jersey data center fined $1M after 62 unauthorized gas generators were found, releasing nitrogen oxides & other pollutants into the surrounding community.

BPC-157 is finally getting a proper human trial. We'll have answers early 2028. About time.

Co-CEO Gerald Commissiong spoke with @Benzinga to discuss how DataMEDS AI is tracking GLP-1 outcomes and driving long-entrenched growth across our ecosystem. $MEDS #MEDS Read the full interview here: benzinga.com/news/health-car…

The University of Arkansas just launched the 1st U.S. based injectable BPC-157 Randomized Controlled Trial for tissue healing. They’re studying post-rotator cuff surgery healing through objective measures like strength testing, MRI, and range of motion. Also patient reported questionnaires on recovery (PROMs). This is what the science community and physicians needed. Enrollment starts Early 2027. First data likely to be seen Early 2028. I will keep you updated. clinicaltrials.gov/study/NCT… #bpc #bpc157 #peptide #peptides #science #research

🚨 #BREAKING: FTC Chair says AI agents’ humans should be held criminally responsible for their behavior.

USA Today starting its video off about COVID cases going up in 27 states, right - showing respirators galore. Well done! piped.video/watch?v=olb7Yc…

It’s extra important to avoid COVID if you have cancer. Even if it’s in remission. Multiple studies have shown that COVID can accelerate cancer growth and bring it out of remission.