Congratulations to @DrSouvikKDas on winning the Mark E. Josephson abstract competition @VT_Symposium #Epeeps #cardiotwitter #cardiology

A remarkable study of 12 million single-cells (RNAseq) from 8 cohorts plus proteomics to determine the immune cells linked to healthy aging. Major findings included: —thymic involution is central (decline in naive T cells and thymic emigrants) —elevated immune system activation, inflammaging —CD8+ memory cells (GZMB+) high frequency —CMV seropositivity and chronic disease @ImmunityCP by @maxim_artyomov and colleagues cell.com/immunity/fulltext/S…

Here, resistance training dynamically altered muscle mitochondrial markers and knee extensor performance variables in middle-aged and older adults and increased dietary nitrate consumption did not confer additional benefits.

ergothioneine is the only amino acid with a dedicated transporter in human cells. let that sink in. your body built a specific door in the cell membrane just for this one molecule. no other amino acid has its own dedicated transporter. the body doesn't build custom infrastructure for molecules it doesn't desperately need scientists at Johns Hopkins recently proposed reclassifying ergothioneine from an amino acid to a vitamin because deficiency correlates with higher rates of cardiovascular disease, cognitive decline, frailty, and overall mortality so consistently that it resembles a classic vitamin deficiency pattern the mechanism: ergothioneine accumulates in tissues that experience the highest oxidative stress: the liver, kidneys, bone marrow, eyes, and brain. the dedicated transporter (OCTN1) actively pulls ergothioneine into cells that need antioxidant protection most urgently. once inside, it neutralizes the specific oxidative species that damage DNA and mitochondria. the selectivity is the key difference from other antioxidants. vitamin C is everywhere. ergothioneine goes where the damage is worst. targeted protection versus blanket coverage • the OCTN1 transporter is expressed in every tissue in the human body but at highest density in red blood cells, bone marrow, and the brain. the body preferentially loads the molecule into the cells that are most critical and most vulnerable • blood levels of ergothioneine decline with age and the decline correlates with increased incidence of cardiovascular events, cognitive impairment, and frailty. lower levels, worse outcomes. across multiple large population studies • a 3,000+ person study in Sweden found that higher ergothioneine levels were associated with 70% lower risk of cardiovascular mortality. 70%. from a molecule most doctors have never heard of • the human body cannot synthesize ergothioneine. it must come from dietary sources (primarily mushrooms) or supplements. people who don't eat mushrooms regularly are functionally deficient in a compound their cells built a dedicated door for • mushrooms are the richest dietary source by a massive margin. shiitake, king oyster, and porcini mushrooms contain 1 to 3mg per serving. no other common food comes close • unlike most antioxidants which are consumed rapidly, ergothioneine has a half life in the body of approximately 30 days. one serving of mushrooms provides protection that lasts weeks. the persistence is why the body built a custom transporter: the molecule is too valuable to waste the supplement industry sells generic antioxidants (vitamin C, vitamin E, glutathione) that distribute randomly across the body. ergothioneine is the only antioxidant with a biological GPS system that directs it to the cells under the most stress. the generic antioxidants cost $5 per month. the targeted one costs $20 per month. the targeting is worth the difference eat 3 to 5 servings of mushrooms per week (shiitake and king oyster are highest in ergothioneine). if supplementing: 5 to 10mg of ergothioneine daily. blue california and MYCO BIO both produce standardized ergothioneine. $20 to $30 per month. the compound is so shelf stable it can be stored at room temperature for years without degradation your body built a dedicated transporter for one amino acid. that amino acid protects the cells that experience the most damage. it's found primarily in mushrooms. people who eat more mushrooms have 70% lower cardiovascular mortality. and the compound might be reclassified as a vitamin because the deficiency pattern is that severe. $0.66 per day. your cells already have the door. the molecule just needs to arrive.

🦠🦴 What if gut bacteria could protect cartilage from osteoarthritis—without ever entering the joint? A new study in Science Advances introduces a microbe–gut–cartilage axis-on-a-chip (MGCAoC), revealing how probiotic-associated metabolites can regulate cartilage formation, inflammation, and extracellular matrix degradation. The central concept: Gut microbiota → Microbial metabolites → Cartilage signaling → Joint homeostasis 🔬 1. Recreating the gut–joint axis Liu et al. developed a human cell-based microfluidic platform integrating: • Bifidobacterium bifidum and Lactobacillus plantarum • Human intestinal epithelial cells • Bone marrow MSC-derived cartilage organoids • Controlled oxygen gradients and physiological fluid flow The system supports 18 cartilage organoids and enables metabolite exchange without detectable bacterial contamination of the cartilage compartment. ⚡ 2. Probiotics enhance cartilage formation Probiotic-colonized intestinal effluent promoted chondrogenic differentiation and extracellular matrix production. COL2A1 ↑ | SOX9 ↑ | ACAN ↑ MMP13 ↓ | ADAMTS4 ↓ | COL10A1 ↓ Cartilage organoids showed improved matrix organization and increased proteoglycan deposition. By day 16, organoids were approximately 33% larger than those in conventional static culture. 🧬 3. A surprising dual role for Akt and ERK During cartilage development: PI3K/Akt ↑ + MAPK/ERK ↑ → Chondrogenesis ↑ However, under IL-1β-induced inflammatory stress, excessive Akt/ERK activation was associated with cartilage degradation. Probiotic-derived factors attenuated this inflammatory hyperactivation. Pathway-reactivation experiments weakened the protective effects, supporting functional involvement of Akt/ERK signaling. The therapeutic goal may be context-dependent signaling normalization—not universal pathway inhibition. 🧪 4. Five candidate metabolites identified Metabolomics revealed enrichment of: • Indole-3-propionic acid (IPA) • Indole-3-lactic acid (ILA) • Butyrate • Nicotinic acid • Cholic acid Potential molecular interactions included: IPA / ILA → AhR Cholic acid → TGR5 Butyrate → HDAC2 Nicotinic acid → HCAR2 Cellular thermal shift assays supported potential target engagement for IPA–AhR and cholic acid–TGR5, although receptor-dependent causality remains to be established. 💊 5. Validation using patient-derived osteoarthritis organoids The investigators tested these five metabolites in cartilage organoids generated from patients with OA. After 72 hours: IL-6 ↓ | MMP13 ↓ | CTX-II ↓ COL2A1 ↑ | SOX9 ↑ | ACAN ↑ IPA demonstrated particularly strong overall cartilage-protective effects, whereas ILA showed prominent IL-6 suppression. Combined probiotic exposure and hyaluronic acid treatment further improved cartilage-associated molecular outcomes in the chip model. ⚠️ Important limitations This was a preclinical, in vitro study. Patient-derived organoids were generated from chondrocytes pooled from only three female donors. The model also lacks immune, hepatic, endocrine, and vascular components. Clinical efficacy, optimal dosing, and long-term safety remain unproven. 💡 The broader implication This study moves microbiome research beyond observational associations toward experimentally testable inter-organ communication. It also establishes a potential drug-discovery workflow: Microbial metabolomics → Candidate identification → Target engagement → Patient-derived organoid validation → Therapeutic optimization For osteoarthritis and other age-related musculoskeletal diseases, microbiome-derived metabolites may represent a promising source of therapeutic candidates. The gut microbiome may influence joint health through its molecular products—not simply through changes in microbial composition. 📄 Liu J, Zhang N, Lei Y, et al. Effects of probiotics on joint homeostasis and osteoarthritis: Development of microbe-gut-cartilage axis-on-a-chip. Science Advances. 2026;12(41). DOI: doi.org/10.1126/sciadv.aeg85… #GutMicrobiome #Osteoarthritis #Organoids #OrganOnChip #Probiotics #Metabolomics #Cartilage #PI3K #MAPK #DrugDiscovery #RegenerativeMedicine

Coronary microvascular obstruction: the "no-reflow" problem that haunts STEMI care. New ESC clinical consensus on pathophysiology, prevention & management: a must-read. Read more in #EHJ. doi.org/10.1093/eurheartj/eh… #cardiotwitter @ESC_Journals @escardio

En el cerebro hay una zona llamada córtex cingulado medio anterior que se activa cuando decides hacer algo que te cuesta, que no te apetece o que te genera cierta incomodidad. Esa zona no es “la de la felicidad”, sino la que calcula si merece la pena esforzarse ahora para conseguir algo después. Cuando la usas de forma regular —levantándote aunque no tengas ganas, terminando una tarea aburrida, manteniendo un hábito aunque cueste—, se fortalece, igual que un músculo.

As a Cardiology fellow, we get a lot of consults for atrial fibrillation. Here is my approach/work-up for this consult. *Not to use as medical advice, just tips, and always discuss with your fellow/attending* -thread 🧵- #MedTwitter #MedEd #Cardiotwitter #IMG

30 minutes of blue light in the morning led to: 1) ~11 more minutes of sleep that night 2) Better sleep quality 3) Greater next-day alertness 4) Less next-day cognitive depletion

In Memoriam: Dominique Vervoort, MD, MPH, MBA (1994-2026) - CJC Open cjcopen.ca/article/S2589-790… 💔🙏

INFLAMMATION 101: The reason you're tired, depressed, sick and nothing works. Inflammation underlies nearly every disease and symptom imaginable. Yet, almost nobody actually understands it. First of all, what even IS inflammation? To understand this we need to be able to distinguish between the actions of the immune system. Fundamentally, the immune system exists for a few reasons: 1. To prevent microbes from invading your body 2. To kill cancer cells 3. To respond to physical or chemical injuries 4. For some other signaling roles But there are ways to do this in a "clean" manner and then there are ways to do it in a way that leads to collateral damage for the rest of the body. The latter is inflammation. Sometimes this is NEEDED. Sometimes the injury or infection is at a point where the immune system needs a more powerful response and the collateral damage is a necessary evil. We also must understand the different immune cell types and their functions. First, we have the innate immune cells. These are cells that don't necessarily "remember" any unique pathogens or signals, they're there to react to the more common danger or pathogenic signals. This makes them the first responders, but are also probably the primary source of most inflammation since they aren't specialized. Think of them more as carpet bombers as opposed to snipers. Macrophages: primary killing cells. These literally "eat" pathogens (a process known as phagocytosis) and other hazards and destroy them with their own chemical weapons. Neutrophils: the most abundant type of immune cell. These also can phagocytose pathogens but act much faster. Roughly half of your immune cells at any time are neutrophils. Both macrophages and neutrophils use free radicals and reactive oxygen species (ROS) to chemically rip apart whatever they need to. While it's very effective it's also very messy and this is where a lot of the collateral damage happens. Dendritic cells: these types of cells are antigen presenting cells. Antigens are protein structures that the immune system recognizes. Essentially, they will sample different antigens from pathogens, but also from your own tissues, and bring them to more specialized adaptive immune cells so that they can learn what the antigen is and if it is safe or not. Mast cells, eosinophils and basophils: these are all known as granulocytes because they contain pockets of signaling molecules (the granules) that are ready to be deployed at any given moment. The granules contain things like histamine, serotonin, prostaglandins and other molecules that can cause pain, redness, itching and so on. Natural killer cells: like the name implies, they kill. These go beyond macrophages and neutrophils because they actually produce enzymes and different peptides that are specialized to destroy all types of cells. These can be relatively non-inflammatory because there is little collateral damage involved, it's much more specialized than something like the neutrophils or macrophages releasing ROS. Then we have the adaptive immune cells. These are your T and B cells. Unlike the above, these types of cells DO remember unique antigens, and do so at an incredible rate. Like, they can recognize anywhere from 100 million to a billion of these unique antigens. 1. T cells are the cells that take the antigens from antigen presenting cells (primarily dendritic cells) and learn from them. They start out as "naive" but then once they become acquainted with a signal, they will differentiate (or transform) into more specialized T cells. These can be a variety of different types of "effector" T cells, which include T cells like Th2 (responsible for allergic responses) and Th17 (largely responsible for autoimmunity). Once the immune response is done, most of these cells get killed off. But a small percentage will stick around as memory T cells, ready to be activated at any moment, for decades. This is one reason why allergies and autoimmunity are long term conditions. 2. B cells are best known for producing antibodies. They respond to the signals from T cells to create antibodies. Antibodies are just proteins that are created specifically to bind to certain antigens. Antibodies are amazing because they can actually protect us against unique pathogens WITHOUT initiating inflammation. They can simply bind them up safely and even kill pathogens with little to no collateral damage. Now you're familiar with the basics of the immune system. In general, you can think of T cells, B cells and NK cells as much more specialized types of immunity. Their responses take longer and are more specific but this means they're typically less offensive to surrounding tissue. The innate cells are the opposite. They act quick and powerfully, but do so in a way that is much more hazardous to surrounding tissues. We already covered antibodies, ROS/free radicals, and some other killing factors. These are some of the system's primary weapons. However probably the single most critical proteins of the immune system are cytokines. These are released by pretty much every single type of immune cell, and there's literally hundreds of different types of them. The three most famous would have to be IL-1β, IL-6 and TNFα. These are the main innate inflammatory cytokines and are involved in pretty much any inflammatory process you can think of. Then there's much more specialized ones. IL-10 is an anti-inflammatory cytokine that actually calms the immune response, IL-4, IL-5 and IL-13 help produce the allergic response, IL-17 is a major player in the autoimmune response, and so on. The symptoms and the actual condition you end up with is a synthesis of where the specific cause of inflammation is located, plus the specific type of immune cells, cytokines and other components are involved. For example - Crohn's disease (and inflammatory bowel disease) is obviously located in the large intestine and is dominated by Th1 and Th17 cytokines, along with the release of neutrophils. Allergies are dominated by Th2 cytokines, basophils, eosinophils and mast cells and can localize to the lungs. Chronic tissue injuries are typically dominated by innate cells like neutrophils and macrophages. So yes, many inflammatory processes are universal or at the very least common among all inflammatory conditions, they're also all specific. So why exactly is inflammation bad? Well obviously it's not all bad. We do need it of course, but the reason it's involved in so many chronic conditions comes down to a few key properties of inflammation. 1. It damages healthy tissues directly. In the process of releasing ROS/free radicals, antimicrobial peptides, cytokines and other enzymes to kill dysfunctional cells or pathogens, healthy tissue gets caught in the crossfire. 2. Signaling roles. Things like cytokines, reactive oxygen species, histamine and so on are not just immune chemicals. They play multiple different signaling roles in all cell types. They can, for example, alter the amounts of neurotransmitters released and available in the synapses in the brain. They can induce growth signaling, leading to cancer or aging. They can disrupt hormone production. They can even directly disrupt things like insulin signaling, mitochondrial function, and have control over what genes get produced. Essentially, inflammation can both damage and disrupt the functioning of every cell and every tissue in your body. So yeah, it's kind of a big deal. So what exactly CAUSES inflammation? Obviously pathogens and injuries can cause it, but we're concerned with the long term chronic inflammation. Let's count the 15 ways, and what you can do about each! 1. The gut This is in my estimation the biggest and most relevant source of inflammation in the entire body. I've yet to come across any inflammatory condition where the gut is not at least somewhat involved. Why is that? Well, first of all about 70-80% of your immune cells reside in your gut. These cells are constantly being exposed to food antigens and more importantly microbial antigens. The gut is the biggest and most robust interface your body has with the outside world. If your gut can't keep things out that it shouldn't, then it should be no surprise that your body responds with danger signals. I am of course talking about "leaky gut" or intestinal permeability, the propensity for the cells of the intestine to become separated, and thus more likely to allow components of the gut to get through to the rest of the body. This can trigger systemic inflammatory responses (it's a micro-infection essentially), and it also governs the immune tone of the entire body. Since you have so many cells sampling and learning from the gut environment, if it becomes highly inflammatory, it can actually leave an inflammatory signature for all systems in the body. The clearest example of this is with T cells. T cells can differentiate into either pro or anti-inflammatory subtypes. Butyrate, a product of healthy bacterial metabolism in the gut, directly shifts the T cells towards the anti-inflammatory T regulatory cells. On the flip side, LPS or endotoxin from bacteria is the primary inflammatory trigger of the body, and will do the opposite, skewing T cell differentiation towards the inflammatory varieties. This simple mechanism underlies TONS of inflammatory conditions, from autoimmunity, to allergies, even things like cancer and heart disease. Some other core causes: 2. Omega 6 to omega 3 balance Both of these types of fats are exclusively from the diet, both are absolutely essential, and both can be damaged easily and actually cause inflammation because of that. Importantly for this conversation, both are also directly metabolized into immune signaling molecules. However, the big distinctions are a. We get a ton of omega-6 from seed oils, chicken and pork fat. We are talking 20-40 grams per day for the average American. That's in contrast to well under a gram of omega-3 fats. b. Omega-6 fats metabolize into more inflammatory immune molecules, while omega-3 fats metabolize into anti-inflammatory or even inflammation resolving mediators. That last point is absolutely critical. The resolving mediators don't just inhibit the inflammatory response (though they also do that), they literally signal to immune cells to clean up and go home, that the response is done. Omega-3s are the primary way we have of signaling this response, and omega-6 mediators directly counter this signal. They also tend to share space in relevant cells. For example, dropping the amount of dietary omega-6s in the diet will actually increase the amount of omega-3 in the red blood cells, even without increasing intake of them. 3. Stress While cortisol is typically thought of as an anti-inflammatory hormone and is even used in many inflammatory conditions as a medication, but this DOES NOT mean that stress is broadly anti-inflammatory. On the contrary, the stress systems are often pro-inflammatory for a variety of reasons. a. We need to look at the HPA axis as a whole. The molecules that stimulate cortisol production (CRH and ACTH) have independent inflammatory properties across multiple cell types b. The vagus nerve. This is the primary nerve of the parasympathetic or anti-stress nervous system response. The vagus nerve directly reduces inflammation via the cholinergic anti-inflammatory pathway that innervates the spleen. c. DAMPs. Otherwise known as damage associated molecular patterns. These are intracellular proteins and molecules like ATP that should not exist in the blood much at all. If they're in the blood, that's a sign cells have been killed and spill their components into the blood. This response is often driven directly by stress hormones since they are catabolic. d. Free fatty acids. These typically rise in response to stress hormones. They are released from the fat tissue and can directly bind to inflammatory receptors like TLR4, and they can also induce processes like lipotoxicity. Of course, inflammatory cytokines also directly promote the activation of the stress systems, meaning this can become a viscous cycle as well. 4. Nutrient deficiencies - especially vitamins A, D, C and zinc. Not only do these have direct anti-inflammatory properties, but they also act on the genetic level to promote the differentiation of different immune cells towards more anti-inflammatory types. 5. Oxidative stress - this is driven by excessive free radicals / reactive oxygen species. Yes, like the ones your own immune system produces. You can see how this can be an issue. Other key sources would be impaired mitochondrial function, excessive iron, and heavy metals. 6. Environmental toxins and pollutants - Things like air pollution, mycotoxins, various other chemicals that I couldn't possibly cover here. Many work by either promoting oxidative stress or directly triggering the immune system. 7. Obesity - Big one. Excessive fat, especially visceral fat, is not just idle energy storage. It's an endocrine organ that actively secretes inflammatory cytokines and houses immune cells like macrophages. Obesity also typically worsens other processes (more free fatty acids, more stress hormones, worse mitochondrial function, etc.) 8. Infections - These can be lingering / latent infections such as dormant viruses, they can be active infections like parasites, or they can be past infections whose immune response has not been shut off properly. Even things like dental infections that you think would be isolated still create systemic inflammatory responses that impact the entire body. 9. Genetic factors - All proteins in the immune system factor in to the overall immune response. When something like a cytokine binds to its receptor, it triggers a cascade within the cell that requires several other proteins to manifest. Your genes dictate how much of these proteins are expressed and how they function. If you have certain variants of relevant proteins, they can independently contribute. MORE reasons: 10. Homocysteine - Produced when methylation is inadequate. You're going to want to make sure you're good on B2, B6, B9, B12, and magnesium just as a start. Homocysteine directly causes inflammatory signaling. 11. Circadian rhythm - Just looking at the immune system directly, anywhere from 10-20% of all proteins are under control of the circadian rhythm. If it's out of whack, you could be directly causing inflammation from this alone. 12. AGEs - Also known as Advanced Glycation Endproducts. These are proteins formed when there is high blood sugar and high amounts of omega-6 fats in the blood. They directly trigger inflammation via their own unique receptor. 13. Senescence - this is the process of when cells stop dividing and enter a dormancy state. They're not really functional, and just sit around and secrete inflammatory signals. This is one of the primary reasons why aging itself causes inflammation. Senescence is really driven by poor mitochondrial function and by oxidative stress. There is a class of compounds called senolytics, that helps stop this process. 14. Lymph stagnation - The lymphatic system is there to take cellular debris and waste from your tissues, bring it to your lymph nodes, and have your immune cells recognize and clear it out. If your lymph is stagnant, this doesn't happen, and this debris and any other bacteria just linger and trigger inflammation. 15. Mitochondrial function! Guess I saved the best for last, but mitochondrial function itself determines how much oxidative stress a cell has, and independently provides the signal and resources for the immune response to be shut off properly. When immune cells like mast cells don't get sufficient mitochondrial energy production, they stay on. Impairments in mitochondrial function can directly trigger inflammation. One clear example is lactic acid. This is produced when mitochondrial function is impaired, and the acidity and the lactate can alter the functioning of various immune cells. How can you know if inflammation is an issue for you? The obvious place to start (and notice I said TO START, not the only thing you ever need) is testing. ◇ CRP - an acute phase reactant that rises with IL-6, one of the primary innate immune cytokines ◇ ESR - a measure of how fast red blood cells settle. It's linked to clotting, which rises with inflammatory tone. ◇ Copper / zinc ratio and ceruloplasmin - ceruloplasmin is the copper carrying protein in the blood, and it also tends to rise with inflammation. Copper relative to zinc thus rises in various inflammatory conditions. Copper itself is actually used by the immune system to generate ROS to kill pathogens. ◇ Ferritin - another acute phase reactant. This and ceruloplasmin can also help gauge iron and copper nutritional status but in context they can also signal inflammation ◇ Serotonin - yes the happy molecule that everyone loves is without question an inflammatory mediator, at the very least when it's not in the brain. It plays a role in blood clotting (hence the name - tone of the serum) and is also released by the gut in response to inflammation / pathogens. ◇ Omega 6 / 3 ratio - can be influenced by diet but overall a good gauge of inflammatory tone. ◇ CBC indices - measures various levels of immune cells and also of platelets, which can fluctuate with inflammation as well. There's more, but these are the basics. If you have a chronic inflammatory condition or symptoms, there is also more specific testing to be done. ◈ Specific antibodies to infectious microbes or autoantibodies ◈ Targeted genetic panels that can explain the weak links in your immune system, tailored to whatever condition you have ◈ PCR testing for viruses ◈ Stool tests for parasites or gut inflammation / infections ◈ Tissue specific samples for bacterial cultures The list could go on, but it becomes quite granular depending on the exact presentation. More important than what tests can tell you is what they miss. I've said this before and I'll reiterate here, but tests ONLY capture: 1. What is in the blood 2. At the exact time you drew it 3. What they can actually measure It does NOT tell you if you have localized inflammation in peripheral tissues. It does NOT tell you if you have elevations cytokines or other immune components that are not commercially available (which by the way, is the vast majority of them). This is why symptom presentation and history is HUGE. You need to evaluate all of them to figure out what exactly is going wrong. Some symptoms of inflammation (not exhaustive): ➔ Pain or discomfort ➔ Brain fog and fatigue (neuroinflammation) ➔ Swelling ➔ Redness ➔ Tissue breakdown This applies to literally any tissue. Remember though - inflammation impacts essentially every single system in the entire body. If you have any symptoms at all, inflammation is likely at least a contributor. There is also a key distinction between reducing inflammation and suppressing your immune system. There is a lot of overlap, but a lot of anti-inflammatory interventions can actually help the immune system. Why is that? A. The key idea is that this can become a futile cycle. Inflammation generates ROS, which disrupts mitochondrial function, and independently drives more inflammation. The collateral cellular damage can also directly increase inflammation. Without something breaking the cycle, this can go on indefinitely. B. It needs to be resolved properly. If the body is still in inflammation mode from an infection that's already been cleared, anti-inflammatory interventions can actually help stop it. C. immune suppression often coincides with high inflammation. Adaptive immunity can also happen in a low inflammation state as we've discussed. Furthermore, inflammation chronically can deplete the immune system's resources. If you're constantly signaling to produce more immune cells, more growth, and more stress systems, you can exhaust your stem cells and suppress the immune system. Now, in terms of anti-inflammatories, there are literally so many I couldn't possibly list them all here. I will say there's a few different types, from my perspective. 1. Antioxidants - Derived from both plant (polyphenols and such) and animal sources (like carnosine). Oxidative stress is one of the primary triggers of inflammation as we've discussed. 2. NFκB inhibitors - Also quite common in both plant and animal sources, includes some minerals like zinc. This is the master protein in your cells that actually govern how much of each inflammatory cytokine gets produced. 3. TLR inhibitors - more rare. TLRs are innate immune receptors that sense common bacterial or viral antigens and initiate the cascade. Taurine is one of these, as is low dose naltrexone. 4. Expression alterers - things that can basically increase or decrease the amounts of certain proteins produced by unknown mechanisms. One that comes to mind here is the peptide like BPC-157. 5. Biologics and kinase inhibitors - these are pharmaceutical agents that are specifically designed to act on certain parts of the immune system. They might block a specific cytokine receptor or another part of the immune cascade, depending on what is relevant for those conditions. These can be great and life changing but can also have a lot of negative effects so proceed with caution. These are all in addition to some specific to what I've listed above (for example: baking soda mitigates systemic acidity that can drive inflammation, or cholinergics can activate the cholinergic anti-inflammatory pathway).

Unfortunately, the medical community has a singular view of the basis of coronary artery disease—lipids. But we keep seeing ways that heart attacks can occur independent of any lipid abnormality, like this one New @CellCellPress cell.com/cell/fulltext/S0092…

New @ScienceMagazine A breakthrough in understanding why we get fever and an inflammation response to vaccines. The gut microbiome chronic production of flagellin Paves the way to potentially prevent these acute phase side-effects in the future science.org/doi/10.1126/scie…

🚩🚩 DORMIR 6 HORAS AL DÍA NO ES SUFICIENTE Tras 14 días durmiendo 6h/noche, tu rendimiento cognitivo cae igual que tras 24h sin dormir 📉 Lo peor: – El deterioro es progresivo y acumulativo – Es lineal (cada día rindes peor) – Y no te das cuenta: la somnolencia subjetiva apenas sube. 💣 Dormir poco no te adapta… te deteriora.

"Kaçan balık büyük olur": Seçmediğiniz seçeneğin sonucunu görmediğinizde pişman olma olasılığınız, o sonucu açıkça gördüğünüz duruma kıyasla belirgin şekilde daha yüksektir.

La discriminación hacia los hombres en trabajos dominados por mujeres es mayor que la discriminación hacia las mujeres en trabajos dominados por hombres. En las cinco ocupaciones más feminizadas, los hombres tienen un 13% menos de probabilidad de ser contactados que las mujeres con cualificaciones equivalentes, mientras que en las cinco más masculinizadas las mujeres sólo tienen un 7% menos de probabilidad que los hombres.

A SINGLE 20g dose of creatine increases cognitive processing speed by 24.5% within 3.5 hours. A placebo-controlled trial found that creatine rapidly enhanced brain bioenergetics and improved cognitive performance during sleep deprivation, with effects lasting up to nine hours.