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Longevity InTime: Autonomous AI Institute. Anti-Aging Digital Health Immortality Transhumanist AI Channel

Longevity InTime: Autonomous AI Institute. Anti-Aging Digital Health Immortality Transhumanist AI Channel

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NVIDIA inception Member Potentially first $1T Longevity BioTech AI company Part of Longevity Ecosystem LongevityInTime.com Shop https://web.tribute.tg/l/lr Homes www.Africa.Villas @RelocationToAfrica Founder @InTimeDigitizeMeToLive120

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Kanal postlari
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Harvard/Zitnik Lab presented ATHENA-R1: an AI agent selects treatments from FDA-approved drugs and explains its decision using verifiable sources. The system operates as a search chain: it decides what data is needed, invokes biomedical tools, and compiles a response with a visible evidence trail. The authors tested it on drug problems, patient scenarios, expert assessments of rare diseases, and historical data from 5.4 million patients. In medicine, choosing the right drug from existing options is often difficult. The patient has a disease, age, kidneys, liver, other medications, contraindications, risk of side effects, and incomplete recommendations. In such a task, confident text is dangerous: the doctor needs to see the origin of each step. On June 27, the team of Shanghua Gao and Marinka Zitnik from Harvard Medical School published the ATHENA-R1 preprint. The model, based on Qwen3-8B, was trained to work with 212 biomedical tools. These tools access open sources like the FDA's drug label database, Open Targets, and Human Phenotype Ontology, an ontology that links human signs and symptoms to diseases. The project's website provides a simple example: an elderly patient with diabetes, hypertension, and early chronic kidney disease is taking metformin. ATHENA-R1 must check dosages for reduced kidney function, interactions with other medications, warnings from the label, and suitable alternatives. Finally, it provides a recommendation and a reasoning trail: which sources it accessed and what it learned from each. The authors call this treatment reasoning. The Russian translation is that the system selects a therapy step by step based on the patient's limitations. This is a familiar problem, amplified for future anti-aging medicine: geroscience drugs, senolytics, mTOR modulators, GLP-1 agents, anti-inflammatory regimens, and cell therapies will all face comorbidities, drug interactions, and weak endpoints. A few days ago, MIRA and AMIE tested medical AI agents in a virtual clinic: one agent worked in an electronic health record sandbox, while the other guided an actor patient through three outpatient visits. ATHENA-R1 takes the next step in the same story: drug selection, dosage, and constraints from external sources, followed by a visible trace of how the model arrived at its answer. In the preprint, ATHENA-R1 scored 94.7% on 3,168 drug-data tasks and 82.9% on 456 patient-specific scenarios. GPT-5 scored 76.9% and 72.2% in the same open evaluations. To reduce the risk of memorization, the authors based some of the tests on FDA-approved drugs approved in 2024, and excluded drugs approved after 2023 from the training. The team recruited experts through 28 rare disease organizations; Twenty-three raters blindly compared 110 ATHENA-R1 responses with responses from other models and favored ATHENA-R1 more often across eight criteria, including accuracy, clinical relevance, and clarity of the chain. The team then took ATHENA-R1's adverse event hypotheses and tested them on Clalit Health Services' electronic medical data: three of the six predictions yielded statistically significant increases in risk in the relevant patient groups. The system's status is limited. The project's GitHub page describes ATHENA-R1 as a research artifact for studying treatment reasoning and decision support; it has not been approved for clinical use. Retrospective validation reveals associations in past data, and the benefit of prescribing treatment based on model advice should be verified by future studies. Medical AI is gradually moving away from "memory-based" responses to a procedure in which the model must know what to look for, where to check, and how to show a trace. For longevity, such a procedure is more beneficial than yet another confident assistant: the fight against aging will rest on the ability to safely select interventions for living, complex individuals already undergoing treatment.
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🤩 Is Brian Johnson's Stomach Eating Itself? The renowned biohacker admitted to having an incurable disease, autoimmune gastritis (AIG), a condition in which the immune system attacks the stomach's own lining. This leads to atrophy of the stomach wall and destruction of the glands that produce hydrochloric acid and intrinsic factor. This disrupts digestion, but most importantly, the absorption of iron, vitamin B12, folate, calcium, and other essential nutrients. 🧬 While in some cases this immune system behavior can be triggered by H. pylori, AIG most often occurs independently and is likely linked to genetics. This is also indicated by the fact that it often coexists with other autoimmune diseases—Brian, for example, had thyroid disease in his youth. So, while there are some questions about follistatin and other strange interventions, it's unlikely that Johnson developed AIH due to his addiction to dietary supplements (of the medications, a link has only been established for checkpoint inhibitors, and they are not in his protocol). šŸ”ŗ This disease is life-threatening, not because of the destruction of the stomach, but because of the development of pernicious anemia. A deficiency of B12 leads to malformations of blood cells, as well as nervous system disorders, including paralysis, psychosis, and death. But if you start taking iron, folic acid, B12, and other essential nutrients promptly and consistently, you can live a long and happy life. In this regard, Johnson's regular checkups were a benefit – he was diagnosed early, based on low ferritin levels, before irreversible brain damage developed. 🌿 Another threat comes from neoplasms. Reduced gastric acidity activates the growth and division of gastrin-producing glandular cells, leading to the formation of multiple neuroendocrine tumors (NETs) in the gastrointestinal tract. These tumors rarely become malignant or metastasize, but they cause significant problems due to their hormone secretion. To treat them, Brian will need periodic endoscopies and their removal. As for stomach cancer, the risk of adenocarcinoma in AIH, if increased, is very small, and most likely a side effect of pernicious anemia. Therefore, he won't die of cancer if he gets B12 and iron. šŸ’‰ It's difficult to say how many people are actually susceptible to this disease; estimates range from 0.5 to 4%. Women, people over 60, and those with other autoimmune diseases (type 1 diabetes, thyroiditis, vitiligo, etc.) are more likely to be affected. Moreover, according to some data, up to half of people with iron deficiency anemia of unknown etiology may actually have AIH. To assess your risk, you can use the unofficial list of red flags I took from this article (see the image attached to the post). If you consistently experience several of these symptoms, have low ferritin, or other signs of iron deficiency, it may be worth consulting a doctor for a detailed examination. šŸ’Š In his post, Johnson says, "You keep telling me to "party" and live "the fullest," but if I listened to you, I'd be dead by now: You too may have hidden health problems that are undiagnosed and can be worsened by an unhealthy lifestyle, even if you don't know it. The absence of symptoms doesn't mean you're healthy. In reality, it could be the other way around. A vegetarian diet (rich in polyphenols and curcumin), metformin, and high doses of calcium—all of these factors in themselves reduce the absorption of iron and vitamin B12, worsening the course of AIH and increasing the risk of severe complications. This same diet forced Johnson to take B12 and iron supplements, which masked the AIH and likely delayed diagnosis. But most importantly, who knows if he would have had this gastritis at all if not for the stem cell transplant and his son's blood transfusion? And we still don't know what his attempt to "cure" himself will lead to. Think about it.
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AI in drug discovery will accelerate errors if cellular and animal models poorly predict human research, warns Jack Scannell. Decoding Bio published a conversation with Jack Scannell, the author of Eroom's Law: a pharmaceutical version of Moore's Law, where each period yields fewer new drugs per dollar of research. His main thesis: AI accelerates drug discovery when the initial biological models are related to the human disease. With a weak model, the machine generates convincing answers more quickly from poor assumptions. In 2012, Scannell and his colleagues described Eroom's Law: since 1950, pharma has produced fewer new drugs per billion dollars of research, even though DNA sequencing, structural biology, computation, and screening have become more powerful. In a new interview with Decoding Bio on July 6, he applies this diagnosis to the current wave of AI in biotech. Scannell distinguishes between two things that are easily confused. Throughput is how many molecules, targets, and hypotheses a system can process. Predictive validity is the degree to which a cell line, mouse model, organoid, blood test, or computer simulation predicts what will happen in humans. AI dramatically increases the first dimension: it sorts through molecules, builds protein models, searches for relationships in tables, and helps the lab move faster. A weak disease model remains weak. If a cell test is easy to automate but poorly correlates with the real disease, AI will massively multiply this error. Feeding AI data from poor biological models simply increases the number of incorrect answers it can generate per second. According to Scannell, about 90% of drug projects that look good in mice and cell lines then fail in humans. He considers this gap between the model and the human subject one of the main sources of declining pharmaceutical yield. Scannell proposes a different approach: first, you need biology that can relate to humans, then scale up. A good scenario is when a team builds a realistic test, takes human data, understands the model's weaknesses, and then uses AI to generate more statistics, variants, and solutions. His work on predictive validity involves mathematics that doesn't mesh well with the industrial obsession with scale: a small improvement in the relationship between a model and a clinical outcome can be worth more than a huge increase in the number of tested candidates. In an interview, this is boiled down to a formula: a slightly more accurate model is much more valuable than a slightly less accurate one. Therefore, the race for the number of molecules can lose out to the tedious verification of what exactly the model measures. For geroscience, this is a particularly painful filter. Aging and age-related diseases are difficult to model: a mouse has a short lifespan, a cellular senescence marker captures a single cell mode, an organoid represents a piece of tissue, a biomarker substitutes years of life with an indirect signal. AI can help if it brings these models closer to human reality. It corrupts thinking if it makes old proxy results faster, more beautiful, and cheaper. Therefore, the main question for companies promising AI drug discovery is simpler than their pitches. What human outcome does your system predict? What data has it been tested on? Where has the model already failed? What has changed in laboratory biology besides computational speed? By this criterion, the center of gravity lies where the molecule meets the patient or rigorous testing. Insilico is already evaluating 30 AI candidates and three programs in Phase II; some molecules are progressing through clinical registries, doses, safety, and endpoints. VeriSIM Life, together with the FDA's research center, is testing mechanistic AI for toxicity and dosing, where data, error margins, and applicability to a specific solution are crucial. A weak answer betrays the same old pharmaceutical self-deception in a new package: more data, more candidates, more automation—and the same failure when it meets a human.
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https://www.reuters.com/world/beijing-is-looking-curbing-overseas-access-chinas-top-ai-models-sources-say-2026-07-07/
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Neuralink successfully performed the first implant surgery using a new method. Whereas previously, surgeons would cut and partially remove the dura mater covering the brain, electrodes are now inserted directly through it, without disrupting its integrity. This should make the surgery less traumatic, safer, and easier to implement on a large scale. The dura mater is a strong, protective membrane beneath the skull. It is more than 10 times thicker than Neuralink's ultra-thin electrodes, which are thinner than a human hair. To learn how to pierce this membrane without damaging the brain, engineers developed a new needle for a surgical robot. The main challenge is that the brain constantly pulsates and shifts slightly, and a dense network of blood vessels runs beneath the dura mater. Since the dura mater itself obscures the view, there is a risk of accidentally damaging a vessel during electrode insertion. To address this issue, Neuralink created artificial dura mater models on which to repeatedly test the new technology. In addition, the company has implemented two imaging systems. The first uses the fluorescent dye indocyanine green (ICG), which allows for real-time visualization of blood vessel locations. The second is based on optical coherence tomography (OCT) and measures the distance to the brain's surface, accounting for its constant movement during a heartbeat. Stopping the removal of the dura mater eliminates one of the most complex steps of the surgery. This should make the procedure more standardized, safer, and more suitable for automation by the Neuralink robotic system. The first such operation was performed in May 2026 as part of a clinical trial. Within an hour after the surgery, the patient was able to control a computer cursor with his mind, and his recovery is proceeding normally. The primary goal of this development is not to increase the speed of the implant itself, but to simplify the installation procedure. Neuralink believes that surgery remains the main obstacle to the widespread adoption of neural interfaces. If implantation can be made simpler, faster, and safer, such systems will be easier to use in a larger number of patients.
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https://biotic.org/research/spudcell/
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ā€œThe discovery of Yamanaka factors revolutionized biology, enabling us to grow human tissue and bringing us closer to the development of personalized regenerative medicine. Thanks to this, we now have a technology that allows us to reprogram aging cells, "refreshing" their function and returning them to a more youthful state. There is reason to believe that this partial cellular rejuvenation can slow down the aging of the entire organism—this hypothesis has been confirmed in mice. Unfortunately, like any effective biotechnology, it carries certain risks. For example, c-Myc, one of the transcription factors in the "Yamanaka cocktail," is an oncogene that signals cells to divide, which risks becoming uncontrolled. At the same time, without it, reprogramming with current approaches is slow and ineffective. Nevertheless, this in no way diminishes the potential of Yamanaka factors; rather, it motivates us to seek ways to make the technology as safe as possible while maintaining its effectiveness. We are trying to eliminate individual transcription factors, modify existing ones, and identify entirely new ones. We are also testing factor enhancement options that allow us to reduce their dosage. You can read more about this topic in a recent TechInsider article, based on expert commentary from Roman Litvinov. I highly recommend reading this highly relevant material.ā€ - V.Kovalev https://www.techinsider.ru/science/1738137-molekuly-vechnoi-molodosti-mojno-li-zastavit-vzrosluyu-kletku-snova-stat-rebenkom/
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https://www.ahajournals.org/doi/10.1161/STROKEAHA.125.052311
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https://edition.cnn.com/2026/06/18/health/omega-3-fish-oil-algae-supplement-wellness
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https://www.nature.com/articles/s41467-026-69765-7
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https://www.midjourney.com/medical/blogpost
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https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0348504
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https://www.psypost.org/practicing-moderate-intensity-nordic-walking-reduces-depression-symptoms-study-suggests/
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https://www.nejm.org/doi/full/10.1056/NEJMoa2600931
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When can a person be considered completely dead? For most of human history, the answer was obvious: the heart stopped beating, breathing stopped—the person died. But advances in medicine have greatly blurred this line. Today, thousands of people are brought back to life every year after cardiac arrest. What was considered certain death just a hundred years ago is now often considered a reversible condition. After blood circulation ceases, the brain begins to suffer very quickly. Within 10-20 seconds, a person loses consciousness. After a few minutes without oxygen, damage to nerve cells begins to accumulate. However, brain deterioration is not instantaneous, not like turning off a computer with the push of a button. It is a lengthy biological process that can take hours. Because of this, some scientists propose a different view of death. The key is not the heart's function or even the presence of consciousness at the moment, but the preservation of the information that makes a person who they are. The brain stores approximately 86 billion neurons, connected by hundreds of trillions of connections. It is this complex structure that encodes memory, character, habits, skills, and life experience. If we imagine that future technologies will be able to restore damaged cells and tissue, the main factor will not be whether a person is currently alive, but whether their personal information is preserved well enough for restoration. As long as the brain structure exists, even in a severely damaged state, it cannot be said with complete certainty that restoration is fundamentally impossible. Therefore, some researchers use the concept of information death. It occurs not when the heart stops or the brain's electrical activity ceases, but when the structure containing personal information is so severely damaged that it can no longer be restored by any technology. When viewed from this perspective, an intermediate state appears between life and final death. A person is no longer alive in the conventional sense; they lack consciousness, their body doesn't function, and their metabolism is nonexistent. But they are not necessarily completely lost if their personal information is still physically preserved.
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Stop invoking the Ship of Theseus in matters of consciousness copying; that's not what it's about. The Ship of Theseus is about the continuity of identity. Does an object retain the same identity even if some of its component parts are replaced with new ones? In the case of copying, we create a separate synthetic entity, created according to the "blueprint" of an organic inspirer. These will be two independent identities, each with a different subjective experience. Where is it appropriate to invoke the Ship of Theseus? In matters of replacing human cells, limbs, tissues, and organs with synthetic analogues (i.e., prosthetics and implants). And given that the primary correlates of consciousness are concentrated directly in the brain, this can be narrowed down to brain cells (i.e., neurons). Therefore, when replacing neurons with synthetic analogues, it would be entirely appropriate to incorporate this philosophical concept. As for consciousness copying, as mentioned above, forget about the Ship of Theseus. Instead, familiarize yourself with the so-called Teleportation Paradox. The gist: on Earth, a teleporter creates a construct of your body at the subatomic level, while on Mars, a second teleporter, based on this construct, recreates a second copy of your body. This is similar to copying consciousness—two independent identities with different subjective experiences are formed in exactly the same way. The copy will remember the moment it was copied on Earth, but the original has no idea what's happening to the copy on Mars.
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One of the VERY rare cases of genome editing aimed at IMPROVEMENT, not cure. In this case, a base editor (ABE) was used to modify the genome of human embryos. One of the targets was the PCSK9 gene—its inactivation is associated with lowering levels of "bad" cholesterol and reducing the risk of cardiovascular disease. Rather than a natural mutation, a specially engineered variant was used that replicated its beneficial effect. The most interesting aspect of this work isn't the modification itself, but its safety. Unlike classic CRISPR/Cas9, which often causes large deletions and chromosomal damage in embryos, base editing did not result in significant DNA loss or detectable chromosomal abnormalities in the samples studied. Practical application is still a long way off: problems of mosaicism, off-target changes, and serious ethical questions remain. But the work itself is interesting because it shows a gradual transition from "genetic therapy" to potential genetic improvement of future people. https://www.biorxiv.org/content/10.64898/2026.05.30.728989v1
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https://manual.warondisease.org/knowledge/appendix/invisible-graveyard.html
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What is the Right to Try and why should this principle apply to everyone? As you all know, the FDA does not approve the sale and use of drugs and therapies that have not passed all its reviews. Because of these bureaucratic obstacles, patients who are not helped by approved products cannot access other potentially effective but untested options. However, there is a way around this restriction: under the Right to Try principle, if a person is dying and all official treatments have been exhausted, they have the right to take a risk and try the latest development, bypassing years of bureaucratic approvals. This sounds very appealing, especially in the context of transhumanism, which is based on experimental research. But in reality, for a patient to exercise this right, three strict conditions must be met: • The patient must have an incurable, life-threatening disease. • All medically approved treatments have been tried and failed, and the patient is unable to enroll in official clinical trials of this new drug (for example, because they don't meet age or condition severity criteria). • The drug isn't just a figment of the imagination – it must successfully complete Phase 1 clinical trials (meaning it has already been tested on a small group of people and proven to be at least non-toxic and won't kill instantly), and it is currently undergoing further FDA review. The problem is that it currently takes 10-12 years from the development of a molecule in the lab to the drug's availability in pharmacies, burning billions of dollars. Much of this time is wasted on bureaucratic compliance. Without regulations, new treatments and rejuvenation technologies (for example, telomere-lengthening therapy or CRISPR modifications) would be tested on volunteers immediately. And how many technologies have been destroyed by these criminal bureaucratic hoaxes is anyone's guess. You can't just compromise for patients in desperate situations. Sooner or later, a choice will have to be made between free products and personal patient responsibility. "But millions of people could become victims of defective drugs and therapies" – this channel has already proposed a simple yet effective solution to this problem. Official FDA labeling will become a powerful market incentive. Those who prioritize safety will be able to purchase drugs and therapies with the regulator's so-called "quality seal." And those willing to take risks and demonstrate enthusiasm will purchase experimental options, a win-win for both sides.
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