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.

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.

“The 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.” - V.Kovalev

https://www.techinsider.ru/science/1738137-molekuly-vechnoi-molodosti-mojno-li-zastavit-vzrosluyu-kletku-snova-stat-rebenkom/

https://biotic.org/research/spudcell/

A synthetic cell created virtually from scratch

SpudCell (as it's called) is capable of performing three key functions characteristic of living cells: absorbing nutrients, growing, and dividing. After each feeding, it can reproduce for approximately five generations in a row. One division takes about 12 hours at a temperature of 30°C. For comparison, the common bacterium Escherichia coli divides approximately every 30 minutes.

The structure of the artificial cell is significantly simpler than its natural counterparts. It consists of only 150-200 different molecules, while real cells contain millions or even billions of molecules. Its genome is also significantly smaller: approximately 90,000 base pairs versus approximately 4.6 million for E. coli.

Despite its superficial resemblance to bacteria, SpudCell functions differently from natural cells. For example, it lacks a cytoskeleton—an internal system of protein structures that helps cells maintain their shape and divide. Instead, division occurs through the accumulation of proteins near the cell membrane, which mechanically force it to split into two parts.

SpudCell is not yet capable of independently producing ribosomes—the molecular complexes responsible for protein synthesis. Therefore, with each feeding, it must be supplemented with ready-made ribosomes obtained from E. coli bacteria. Without these, the artificial cell will not be able to continue to exist and reproduce.

The researchers also demonstrated that the artificial cells can be subject to natural selection. When a change was introduced into the genome that increased the production of one of the growth proteins, these cells began to grow and divide faster than the rest. However, this is not yet considered full-fledged evolution, as the change was human-made and did not arise by chance.

According to the authors, the current version of SpudCell is practically useless from a practical standpoint. It does not produce useful substances, does not perform specialized functions, and cannot exist independently outside of a laboratory setting. However, the researchers view it as a basic platform that can be programmed in the future to solve various problems.

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.

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.

🤩 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).

🔺 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.

💉 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.

💊 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.

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.

A portion of the tech elite is starting to serve up a selection of embryos and future editing of heredity as a way to catch up with superintelligence. On April 16, Mother Jones published a large exposé on how former MIRI researcher Tsvi Benson-Tilsen, the Berkeley Genomics project, and a circle of related investors are linking the fear of AGI (Artificial General Intelligence) with the market for "enhanced children." Here, embryo selection, discussions of future heredity editing, and the money of people invested in both AI and genomics startups converge. AGI refers to an artificial general intelligence system that can solve a wide range of tasks at or beyond the level of human capabilities. In the AI-risk environment, the fear is formulated as follows: the next step for such a system may be to become superhuman, and humans will no longer understand its goals and lose control. Benson-Tilsen worked for seven years at the Machine Intelligence Research Institute, where they tried to solve this very problem. According to Mother Jones, he came to the conclusion that he himself was not capable of solving it, and that others had not succeeded either. His response now is biological. At the end of 2024, he launched the Berkeley Genomics Project. On the project's website, the mission is stated directly: to open the path to safe and accessible heritable genome engineering, i.e., to modify DNA in an embryo or reproductive cells so that these edits are inherited not only by the child but also by their descendants. Among the promised benefits listed are protection from diseases, protection from severe mental disorders, a longer life and more healthy years, and a "more capable mind." The political continuation is also stated: the USA should lead in this technology. It is essential to distinguish between two things. Today, the market primarily sells embryo selection: during IVF, several embryos are obtained, their DNA is checked, and parents are helped to choose one for transfer. For some severe hereditary diseases, such a check is understandable. For complex traits like intelligence, everything is much weaker. They depend on many genes, as well as the environment, nutrition, family, and school. A calculation in Cell in 2019 gave an average expected gain of about 2.5 IQ points when choosing from five embryos. This is little. The history of SAT scores has shown how quickly the conversation about "innate abilities" begins to confuse heredity with language, school, and environment. Until the full-fledged "construction of geniuses," the market has not yet reached. But the language of the field has already moved further than practice. Brian Armstrong described a future IVF clinic in his post on X as a "Gattaca screen": "The IVF clinic of the future will combine several technologies: the production of egg cells from skin or blood, the selection of an embryo that best fits the parents' request, ideally from thousands of options, editing the embryo for disease prevention or improvement, and artificial wombs." In this formula, an entire conveyor belt is assembled. First, egg cells are made from skin or blood cells. Then, many embryos are created. Then, they are compared according to genetic probabilities, one is chosen, additional edits are made, and the pregnancy is carried out in an artificial womb. Moreover, the artificial womb is already being assembled: there are models of embryos, artificial placentas, and a hermetically sealed environment for the development of the fetus outside the body. A set of controversial technologies is already being presented as a single product roadmap. The topic goes beyond the debate about fertility and disease prevention. The same tech elite networks are simultaneously fueling the AGI agenda, financing AI, and starting to justify heritable human upgrades as a response to the risk from these systems. Yesterday, the market was selling wealthy parents a slightly more advantageous choice between embryos — we already had a sepa…

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A major review: weight loss, heart protection, and long life in obesity medications differ. On July 8, BMJ published a review of 262 randomized trials - studies where participants are randomly assigned a medication or a comparator - with nearly 100,000 participants. The medications differ significantly in terms of weight, cardiac outcomes, side effects, and quality of life. Subcutaneous semaglutide was the only medication with a convincing reduction in overall mortality; these data came mainly from studies of people with already high cardiovascular risk. The market has become accustomed to comparing such medications by the number of kilograms lost. For someone who wants to live longer, this scale is too crude. Weight may decrease quickly, but the data on survival, heart function, and well-being remain different for each medication. The review authors compared 19 medications and found: in terms of weight loss, tirzepatide and the combination of cagrilintide with semaglutide led. Subcutaneous semaglutide reduced body mass by approximately 9.8% more strongly than a single lifestyle change. But among all medications, only it showed a convincing reduction in overall mortality: by 19% in 17 trials with 25,264 participants. The risk of myocardial infarction was 28% lower. The reduction in mortality in this review refers to subcutaneous semaglutide in people with existing cardiovascular diseases. For people without such diseases and for medications with similar effects, separate data are needed: absolute risks and outcomes may differ. Tirzepatide, for example, reduced the risk of heart failure, and the data on its effect on overall mortality have lower confidence. Weight loss and quality of life assessments differed. The authors considered a clinically significant difference to be 10 points on the well-being scale. All medications remained below this threshold; subcutaneous semaglutide had a score of 2.9 points. In the study of body composition with fat, tirzepatide also reduced lean mass - tissues that include muscles, water, and other components of the body. For each medication, one must ask which specific outcome it changes: weight, myocardial infarction, mortality, ability to move, or everyday well-being. Then - in whom exactly was this tested and how long was it observed. The scale on the weights answers its own question; prolonging life requires data on mortality and organ function. Source: BMJ Telegraph.

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Professor of Yale Samuel Moyn suggests giving the young more votes: the debate on aging has already become a debate on rights. In July interviews about the book "Gerontocracy in America", Moyn asserts that power, money, and voters in the US are too skewed towards older generations. Among his ideas are age limits for part of the positions and different political weight for people with different remaining life expectancy. On July 13, The New York Times made a separate video report on this debate. Yale law and history professor Samuel Moyn has just released the book "Gerontocracy in America", around which the discussion has unfolded. Gerontocracy, in his definition, is the concentration of power among older generations through money, property, and the setup of elections. In a July 9 interview with Yale University, Moyn cites such figures: the age of half of the members of the US Congress is over 60, half of the voters are 52 and older, and workers over 55 make up about a quarter of the workforce, compared to 10% in 1990. He links this picture to the fact that it is harder for young people to get housing, jobs, and political representation. Moyn does not limit himself to changing faces in Congress. He suggests discussing age limits for part of the positions, compulsory voting, and a different way of counting votes. In a debate with political scientist Yascha Mounk, he explains his logic as follows: a person who will live longer with the consequences of a law has a greater stake in it. Hence the idea of giving young people more political weight. Here, the debate on aging turns into a debate on the value of remaining life. Moyn wants to protect future generations from decisions that they will live with longer than everyone else. But age poorly separates power from powerlessness. He himself acknowledges that elderly people without means also suffer from the current system. Wealth and influence are concentrated among a minority, and age often coincides with this concentration. Radical life extension makes his argument more dangerous and clearer. If political weight depends on life expectancy, the state gets a reason to reduce a person's vote precisely because they will live longer. Health and survival become the basis for reducing political rights. The same problem has already arisen in the debate on space resources, which can determine human lifespan. There, the rich can buy more time to live. With Moyn, lifespan becomes the criterion by which the state gives different political weight. In both cases, access to rights depends on the length of life. Gerontocracy arises where power is not changing, wealth is accumulating, and access to decisions is closed. Young people need representation and protection of the future; older people need full rights and reliable social protection. The struggle against death requires a common right to a long life, rather than the distribution of civil rights by age.

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#digest for July 14 Full article • The Alzheimer’s Association will invest $100 million to investigate: does the medication add protection against dementia to the prevention program • At the ICML workshop, Bruno was presented - an AI assistant that is supposed to keep track of the work of a scientific group • Takeshi Kozai: a neurointerface in 20 years should preserve living tissue around the electrode • JAMA: in Americans of the same age, dementia over 40 years has become approximately two-thirds less common • A large review: weight loss, heart protection, and long life in obesity medications diverge • Some techno-elite are starting to offer embryo selection and future gene editing as a way to catch up with superintelligence • Professor Samuel Moyn of Yale proposes giving the young more votes: the debate about aging has already become a debate about rights Telegraph Digest @UkhvatNews - July 14 When talking about the "wave of dementia", people usually combine two different facts into one sentence. The first fact: there are more people living up to 80, 90, and 100 years. The second: the likelihood of losing memory, orientation, and independence increases with age. From this, it is easy…

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