We have about a trillion cells like these. Notice the blue nucleus containing the DNA. The mitochondria are the small orange moving organelles. They look like rapidly vibrating grains of rice. Notice in the mid right upper part of the frame, a cell is dividing. The small white threadlike spicules are microtubules pulling the two daughter cells apart. This is called spindle formation. Notice these same microtubules grow from one cell to another and pull them together into a cohesive group. These are the cells that keep us alive. Be good to them. How do we get new mitochondria? With Stem cell therapy. See this link: jeffreydachmd.com/2026/06/st…

jeffreydachmd.com/predicting… Richard Dawkins is your basic atheist, much like many atheists in silicon valley who claim they have created a conscious entity, or even a supreme being. Of course this is all rubbish. AI is not a person, not a conscious entity, not a supreme being, not a deity. It is a souped up search engine running on a stack of circuit boards in a server in a data center. This is not to belittle AI, as the automobile replaced the horse and buggy, the AK-47 replaced the spear, the nuclear powered aircraft carrier replaced the canoe, AI is an advanced technology, a tool with potential to make our lives easier and boost productivity. All intelligence comes from the same place. A human mind is not self-made. It is a gift from our Creator. This is the same Creator who creates all life. In that sense, all finite intelligence is already “artificial.” It is made. We did not invent the possibility of understanding. We received it. What we call AI is then a copy of a copy: people using created minds to assemble a statistical mash-up of other people’s words, then calling the mash-up a new being, or even a new deity. That is the first mistake of the AI community, a linguistic mistake. A computer software model is trained on what countless people already said, wrote, photographed, and decided. Then it talks back in a smooth voice. If you treat that voice as an oracle, or new deity, you are pointing at a material object and proclaiming this is a deity that saved us. You have forgotten the origin of all this. You have forgotten yourself. You have forgotten that your new idol comes from software running on a rack in a data center. Belief in such an idol will herald the birth of a form of totalitarian police state the world has never seen. Even if you reject the theistic world view, you can see that this rhetoric has the shape of a religion: a coming super-being, and doubt in this new deity is considered heresy. Artificial Intelligence (AI) is software made by computer programmers, and these humans stitch together an imitation of some of intelligence’s public effects. The imitation can be astonishing. A culture that says computer program model is the new deity is back to the story of idolatry, except the idol now answers in complete sentences and sounds like your best friend. We make things. Fine. We must not point at the things we make and say they are the source of mind. Mind, if it is real in us, was given. The machine is what we made from that gift. Keep the order straight and you can use the machine. Reverse the order and you will kneel to it, or crown yourself with it. In each case, you hand over what was never the machine’s to own. The danger is this: A new demagogue arises in the government who takes control of what AI tells you. This is the new Wizard of Oz behind the curtain with his hands on the levers. By worshiping AI, you hand over your liberty and become a slave to a totalitarian surveillance state the world has never seen. Every aspect of your life will be under surveillance and controlled by the state using AI running on racks of servers in data centers. Other than that, you have nothing to worry about.

jeffreydachmd.com/ Your Theology Determines Your Answer. In this short clip podcast discussing: is AI a conscious being? We have both sides: Atheists Pinker and Deutsch VS. the non-atheist, spiritualist Hameroff. You will see their answers are based on their theology (materialist vs. spiritualist). The Atheist materialism answer is YES, of course, AI is a conscious being. The spirituralist, monotheist answer is NO, AI can never be a conscious being. A little background helps understand where these people are coming from: Steven Pinker (atheist; cultural Jew from a secular family) Born 1954 in Montreal. BA in psychology (McGill, 1976); PhD in experimental psychology (Harvard, 1979). Long academic career at MIT (Brain and Cognitive Sciences) and Harvard (Johnstone Family Professor of Psychology). Research focuses on language, visual cognition, evolutionary psychology, and the computational theory of mind. Major popular books: The Language Instinct (1994), How the Mind Works (1997), The Blank Slate (2002), The Better Angels of Our Nature (2011), Enlightenment Now (2018), Rationality (2021). He has published extensively in academic journals and is a prominent public intellectual and secular humanist. David Deutsch (atheist) Born 1953 in Haifa, Israel (Jewish family); grew up in London. Studied natural sciences at Clare College, Cambridge; PhD in theoretical physics at Oxford. Visiting professor of physics at Oxford’s Centre for Quantum Computation; Fellow of the Royal Society; recipient of the Breakthrough Prize and other honors in quantum information. He is widely regarded as a founder of quantum computing (quantum Turing machine, Deutsch–Jozsa algorithm, quantum logic gates, error correction, etc.). Major books: The Fabric of Reality (1997) and The Beginning of Infinity (2011). His work integrates many-worlds quantum mechanics, Popperian critical rationalism, universal computation, and constructor theory. He rejects supernatural explanations. Stuart Hameroff (not an atheist; self-describes in spiritual terms, e.g., “quantum Buddhist”) Born 1947. BS (chemistry, physics, mathematics, philosophy of mind) at the University of Pittsburgh; MD at Hahnemann. Anesthesiology residency and long clinical/academic career at the University of Arizona (Professor Emeritus of Anesthesiology and Psychology). Co-founder and director of the Center for Consciousness Studies; long-time organizer of the Science of Consciousness conferences. Also affiliated with the Arizona Astrobiology Center and Quantum Life Technologies. Best known for co-developing the Orchestrated Objective Reduction (Orch-OR) theory with Roger Penrose (mid-1990s onward). Key works include Ultimate Computing (1987), multiple edited volumes of Toward a Science of Consciousness, and numerous papers on microtubules, anesthetic action, and quantum processes in consciousness. He remains active in research and public discussion of Orch-OR, anesthesia, and related topics. How atheism (or its absence) shapes their answers on consciousness, qualia, and AGI (Artificial General Intelligence) The relevant questions (from the Pinker–Deutsch exchange that Hameroff replied to) concern whether AGIs can have genuine subjectivity/qualia, whether consciousness is purely computational or substrate-dependent, and how to distinguish conscious from non-conscious processing. Note: genuine internal subjectivity/qualia is defined as human consciousness. Pinker and Deutsch (atheists / strong naturalists) treat consciousness as a physical, computational, or information-processing phenomenon that does not require anything beyond what physics and computation can describe. Deutsch argues that general intelligence already includes the capacity for internal subjectivity because “there ain’t nothing here but computation”; a silicon system that perfectly simulates the relevant processes should have qualia. Pinker is more cautious about substrate dependence and whether the question is decidable, but he still frames the problem inside a naturalistic, evolutionary, computational psychology. Neither invokes souls, divine infusion, or non-physical residues. Their atheism supports a stance in which consciousness is expected to be fully accountable in terms of physical law and computation (even if the details remain open). A classical computer could, in principle, be conscious. Hameroff (not an atheist) rejects the pure classical-computational view. He argues that consciousness depends on specific biological quantum processes in microtubules (Orch-OR / Penrose objective reduction). Anesthesia, he claims, selectively blocks consciousness by disrupting these quantum effects while sparing other neural activity. Classical computers lack microtubules and the relevant non-computable quantum-gravity collapses, so they cannot be conscious. His openness to non-local quantum effects, near-death experiences, out-of-body experiences, afterlife, and reincarnation follows from the same framework. His non-atheistic/spiritual leanings make him more willing to treat consciousness as potentially fundamental or proto-conscious at the Planck scale and less reducible to ordinary computation. Monotheist Viewpoint Contrast with a traditional monotheist (e.g., classical theistic views in Judaism, Christianity, or Islam) A monotheist typically grounds human consciousness/personhood in an immaterial soul (or the image of God) that is not fully reducible to any physical or computational process, even a quantum one in microtubules. True subjectivity, moral responsibility, and the capacity for relationship with God are seen as gifts or creations of a personal God, not emergent properties of matter, information, or quantum collapses. On AGI, many monotheists would deny that a machine, however sophisticated, possesses a soul or genuine qualia; behavioral competence or information processing would not equal personhood. Some might allow that God could create non-biological persons, but that is a theological decision, not a scientific one. The monotheist answer therefore introduces an ontological category (soul/divine image) that neither the computational naturalism of Pinker/Deutsch nor Hameroff’s quantum panprotopsychism requires. In short, each thinker’s starting assumptions about the nature of reality quietly steer the answers they find plausible. Steven Pinker and David Deutsch, both atheists, approach consciousness the way many modern scientists do: as something that can, in principle, be fully explained by the ordinary laws of physics and by the right kind of information processing. If a system—whether a brain or a sufficiently advanced computer—performs the right computations in the right way, they see no fundamental barrier to it having subjective experience. On this view, the “stuff” the system is made of matters less than the pattern of activity it supports. A perfect simulation of a conscious brain running on silicon chips should, they argue, be conscious in its own right. Nothing extra, such as a soul or a special quantum process, needs to be added. Stuart Hameroff, who describes himself in spiritual rather than traditionally religious terms, takes a different route. He believes consciousness depends on very specific biological structures, tiny protein tubes called microtubules inside neurons, and on quantum effects occurring inside them. Because those quantum processes are, in his theory, linked to the deep structure of space-time itself, he leaves the door open to phenomena that many scientists dismiss: non-local connections (effects that seem to reach beyond ordinary space and time), near-death experiences, and even the possibility that some aspect of consciousness could continue after the body dies. For Hameroff, classical computers lack the right biological hardware and the right quantum physics, so they cannot be conscious no matter how cleverly they are programmed. A traditional monotheist, someone who believes in a personal God who created human beings with immaterial souls, adds a further layer. On this view, genuine consciousness and personhood are not simply the result of any physical process, whether ordinary computation or exotic quantum activity in microtubules. They require a soul, a non-physical element that God gives to human beings. A machine, however sophisticated, would still lack that God-given soul and therefore could not possess true inner experience or moral personhood. The monotheist answer is not mainly a claim about what physics or biology can do; it is a claim about what only a Creator can bestow. Note: AI assisted with this reply. And no AI is not a person, not a conscious entity, not a supreme being. AI is a souped up search engine running on circuit boards at a data center.)

jeffreydachmd.com/2019/10/op… Aaron Siri makes a very convincing argument because he knows the truth. This is how to create cognitive dissidence! Having Aaron Siri on Joe Rogan is the platform equivalence of Vladimir Putin addressing a joint session of Congress, or the head of Astrophysics at Cambridge as the keynote speaker at a Flat-Earth convention. The reality is there are no studies showing \/a<<ines do not cause A\/TlSM. The reality is that they DO cause A\/TlSM and chronic disease in children. Anyone studying this with a randomized placebo controlled trial or population study have their careers destroyed. It is that simple.

jeffreydachmd.com/2026/10/an… Anti-Aging Breakthrough: Rewinding the Cellular Clock with DNA De-Methylation Restoring Vision. The source code of life is our genome, the DNA sequence in the nucleus of our cells. Remember, our genome is not fixed. It is continually shaped by the epigenome which is modified by DNA methylation and DNA demethylation. This is the addition or removal of methyl groups from the DNA. As we age, DNA methylation increases. Reversing aging involves removing these methyl group, called demethylation. The addition and removal of methyl groups takes place on cytosine residues. DNA methylation and demethylation has emerged as both a marker for cellular aging and a potential key to aging reversal. FDA Approves First Human Age Reversal Trial The speaker in the video (below) is Professor David A. Sinclair, Harvard Medical School professor and longevity researcher and co-founder of Life Biosciences, shown speaking at the World Governments Summit 2026. In this clip, Dr. Sinclair discusses the company’s ER-100 partial epigenetic reprogramming (OSK) work, preclinical results in mice and monkeys, the FDA Investigational New Drug (IND) clearance for the first-in-human trial in optic neuropathies, and the broader potential beyond the eye. Dr. Sinclair says:“The eye is just the beginning, we believe we can treat every tissue, reset the whole body.” Here is a 17 minute video presentation by Dr. David Sinclair explaining their breakthroughs in this process: Dr. David A. Sinclair Presentation on You Tube (17 minutes) Header Image: The CB1 cannabinoid receptor (magenta) expressed by basket cell axons and surrounding the hippocampal CA1 pyramidal cells (green). Green signal is green fluorescent protein expressed from the Nr4a1-promoter in a transgenic mouse line. Link to original image on wikimedia commons. Date 30 December 2016 Source: Author BrainsRusDC, CC 4.0 Nobel Prize to Dr. Shinya Yamanaka and the Four Transcription Factors In 2006, Dr. Kazutoshi Takahashi and Dr. Shinya Yamanaka showed that four transcription factors, Oct3/4, Sox2, Klf4, and c-Myc—could turn mouse adult fibroblasts into induced pluripotent stem cells (7). These cells looked and behaved like embryonic stem cells, formed tissues from all three germ layers, and contributed to mouse development. The same four factors later worked in human adult fibroblasts (8). That finding overturned the idea that cell fate is fixed. Dr. Yamanaka shared the 2012 Nobel Prize in Physiology or Medicine with Dr. John Gurdon for this work. (7-8) Partial Reprogramming Reverses Aging In 2016, Dr. Alejandro Ocampo and colleagues asked whether a partial use of the same Yamanaka factors could reverse cellular aging without erasing cell identity. In a mouse model of premature aging, short cycles of Yamanaka factors (Oct4, Sox2, Klf4, and c-Myc) improved cellular and physiological hallmarks of aging and lengthened lifespan. In older normal mice, the same partial reprogramming improved recovery from metabolic disease and muscle injury (9). The factors can therefore be used not only to make stem cells, but also, in controlled short pulses, to reverse some age-associated changes in animals. (7-9) The four Yamanaka factors are often shortened to OSKM. Oct4 and Sox2 hold the pluripotency network. Klf4 supports that network and affects cell growth. c-Myc drives proliferation and is also an oncogene, which is why full, continuous expression carries a tumor risk. The aging experiments used intermittent, partial expression precisely to avoid complete reprogramming and teratoma (cancer) formation. Continuous or complete reprogramming with c-Myc raises tumor risk, which is why the aging work used short cycles and stopped short of pluripotency (9). Rejuvenation Strategy: Restore Youthful Methylation Patterns in our DNA In 2020, Dr. Weiqi Zhang surveyed the accumulating evidence that aging is accompanied by progressive DNA methylation patterns which disrupt gene-expression programs and contribute to functional decline. Dr. Weiqi Zhang argues that interventions capable of restoring more youthful methylation patterns in our DNA are excellent rejuvenation strategies. [3] Trans-genic Mouse Model of Premature Aging – Progeria In 2016, Dr. Alejandro Ocampo studied premature aging in a transgenic mouse model. The mice had progeria, a genetic disease of premature aging. The study used in vitro experiments in tail-tip fibroblasts from the transgenic progeria mice and also in human cells, Dr. Alejandro Ocampo and colleagues showed that functional restoration is possible in living animals. The experimental animals were produced by breeding. Mice carrying the Progeria mutation (LAKI) crossed with an earlier “reprogrammable” mouse strain. The ancestor “reprogrammable” mouse strain had itself been created years earlier through precise genetic engineering of embryonic stem cells. Scientists used homologous recombination to modify the cells in two steps. In this technique, a specially designed piece of purified DNA called a targeting vector is introduced into the cells. No virus is involved. Instead, the DNA is delivered by electroporation: a brief electrical pulse opens temporary pores in the cell membrane, allowing the purified DNA vector to enter the cell. The vector carries the new genetic material flanked on both sides by long stretches of DNA sequence that exactly match the DNA surrounding the chosen insertion site in the mouse genome. Once inside the cell, these matching sequences (called homology arms) line up with their counterparts in the chromosome. The cell’s own natural DNA-repair machinery then cuts out the original DNA at that site and swaps in the new sequence from the vector, inserting the engineered genes with high precision at the intended location and nowhere else. First, they used this method to place a gene for the reverse tetracycline transactivator (rtTA) into the Rosa26 locus, a safe, widely used spot in the genome that allows steady expression in nearly every cell. Next, they inserted a single package of DNA that contains the instructions for making all four Yamanaka factors at once into a specific, safe spot in the mouse’s DNA (a location scientists call the Col1a1 site, which is part of a collagen gene). This cassette contained the four Yamanaka factors, Oct4 (a core master regulator of pluripotency), Sox2 (which works with Oct4 to keep cells in an undifferentiated state), Klf4 (which helps control the cell cycle and stabilize chromatin), and c-Myc (which promotes proliferation and remodels chromatin but carries cancer risk), linked together by short 2A self-cleaving peptides and placed under a doxycycline-responsive promoter. The correctly edited embryonic stem cells were then injected into early mouse embryos (blastocysts) to produce chimeric mice, which were bred to establish a stable line that passed the engineered genes to their offspring. Once the system is in place, control is straightforward. When doxycycline is added to the drinking water for the mouse, it binds the rtTA protein; the activated rtTA then switches on the promoter, producing one long messenger RNA that encodes all four factors. The 2A peptides cause the cell to cut that single transcript into four separate proteins, so Oct4, Sox2, Klf4, and c-Myc are made together. Removing doxycycline turns the system off. This built-in on/off switch allowed later researchers to give only brief, controlled pulses of the factors instead of continuous expression. The correctly modified embryonic stem cells were injected into blastocysts to generate chimeric mice that were then bred to establish the stable transgenic line. The resulting LAKI 4F offspring therefore inherited both the progeria mutation and the pre-integrated, inducible OSKM system. No external viral vector or gene-therapy delivery was required; the factors were already present in every cell and were switched on systemically simply by adding doxycycline to the drinking water. By administering short, cyclic bursts (two days of doxycycline followed by five days off, repeated over many weeks), the researchers activated the factors only briefly. This partial reprogramming nudged cells across multiple tissues toward a more youthful epigenetic state without causing them to lose their differentiated identity or form tumors. Markers of DNA damage, mitochondrial dysfunction, and cellular senescence were reduced, and lifespan was extended. The work established that carefully limited transgenic expression of the Yamanaka factors can remodel age-associated epigenetic marks, including aspects of the DNA methylation landscape, sufficiently to ameliorate organismal phenotypes. [1] Building directly on this conceptual foundation, in 2020, Dr. Yuancheng Lu studied mice in vivo, with supporting experiments in cultured human neurons). Dr. Yuancheng Lu focused on three of the factors (OSK, omitting the oncogenic risk associated with c-Myc). They delivered the genes via adeno-associated virus specifically to retinal ganglion cells, the neurons that form the optic nerve and carry visual signals from the eye to the brain. Using a controllable system so the genes could be turned on and off, they tested the approach after optic-nerve crush, in a glaucoma-like model of elevated intraocular pressure, and in naturally aged mice. OSK expression restored youthful DNA methylation patterns and transcriptomes, promoted axon regeneration, improved survival of the nerve cells, and recovered visual function. The cells remained mature neurons rather than reverting to a stem-cell state. Crucially, the benefits required the DNA demethylases TET1 and TET2; when these enzymes were knocked down, the restorative effects vanished. An additional enzyme, TDG, helps complete the demethylation process. The restoration was selective rather than a global erasure of methylation marks: OSK recovered youthful patterns at specific genomic sites, thereby restoring a more youthful transcriptome and the capacity of post-mitotic nerve cells to survive stress and regenerate. In short, the cells retain a molecular memory of their youthful state in the DNA methylation code, and temporary OSK expression helps them access that information again. [2] Restoring Vision in Glaucoma Mouse Model Subsequent work refined the practical parameters of this approach. In 2023, in a year-long in vivo mouse study using a glaucoma model, Dr. Margarete Karg and collaborators extended the OSK regimen with both continuous expression and a doxycycline-inducible (on/off) system. Two months of OSK fully restored vision that had been lost due to glaucoma; with continued expression the benefit lasted approximately eleven months. Even after the factors were turned off, vision remained better than the untreated baseline for a period before gradually declining. Continuous OSK expression for as long as twenty-one months produced no major adverse effects on retinal structure, body weight, or other signs of toxicity, and the cells neither lost their identity nor formed tumors. The core mechanism remained the same OSK-driven, TET-dependent DNA demethylation described in 2020; the longer study added the practical demonstration that an inducible system can achieve durable functional recovery with an acceptable safety profile in the eye. [4] Viral Vector ER-100 Ameliorates Optic Neuropathy Model in Non-Human Primates The same scientific lineage has since advanced a controlled OSK gene-therapy candidate, ER-100, into non-human primate models of optic neuropathy. In 2026, in an in vivo non-human primate study using a laser-based model that mimics non-arteritic anterior ischemic optic neuropathy (NAION), Dr. Sharon Rosenzweig-Lipson and colleagues reported results with ER-100. The ER-100 therapy is delivered by a single intravitreal injection of a modified adeno-associated virus type 2 (AAV2) vector that carries the genetic instructions for the three OSK factors (OCT4, SOX2, and KLF4). Once inside retinal cells, the vector does not integrate permanently into the host genome; instead, OSK expression is tightly controlled by an inducible system that is switched on only when the animal (or later the patient) takes oral doxycycline, which is administered daily for a defined period (typically eight weeks). In the primate study, this approach allowed ER-100 to reach the intended cells in the ganglion-cell layer, reverse injury-associated DNA methylation changes in retinal-ganglion-cell-enriched tissue, improve pattern electroretinogram amplitudes, and mitigate structural damage. The treatment was well tolerated, producing only transient, procedure-related and vector-associated inflammation that resolved, with no lasting adverse effects on intraocular pressure or outer retinal function. These findings supplied translational evidence that the partial-reprogramming approach works in a larger animal model closer to humans and supported the U.S. FDA’s clearance of an Investigational New Drug application. The resulting first-in-human Phase 1 safety trial (for open-angle glaucoma and NAION) is ongoing; early interim data presented in 2026 indicated that the initial dose, given as one intravitreal AAV2 injection plus daily oral doxycycline, was tolerated in the first three participants with glaucoma through day 56, with preliminary visual-field signals in two of them. Full peer-reviewed human results remain pending. [5] Macular Degeneration and Mechanistic Diversity A related 2025 preprint from members of the same scientific lineage further illustrates that the three reprogramming factors known as OSK (Oct4, Sox2, and Klf4) can act through more than one pathway. In experiments performed both in cultured cells and in living mice, the researchers focused on retinal pigment epithelium cells, the support cells that nourish the light-sensing neurons of the retina and that are especially vulnerable in age-related macular degeneration. In these cells, OSK improved the ability to withstand oxidative stress largely without relying on the DNA-demethylating enzyme TET2, the same enzyme that had been essential for the vision-restoring effects seen earlier in optic-nerve cells. Using large-scale genetic screens, the team identified a single detoxifying enzyme, GSTA4 (glutathione S-transferase alpha 4), as a major driver of this protection. OSK temporarily increases the amount of GSTA4, which then clears a toxic byproduct of damaged fats called 4-HNE (4-hydroxynonenal). By removing this molecule, GSTA4 helps keep the mitochondria, the cell’s energy-producing structures, working properly under stress. When the researchers tested whether the antioxidant and detoxifying enzyme GSTA4 could act on its own, without any of the OSK factors, they used a straightforward gene-delivery approach. They packaged the GSTA4 gene into an adeno-associated virus type 2 (AAV2) vector, the same class of harmless, non-integrating viral carrier used for other ocular gene therapies, and injected it beneath the retina of aged mice so that it would preferentially enter the retinal pigment epithelium cells. Once inside those cells, the virus supplied extra copies of the GSTA4 gene, causing the cells to produce higher levels of the anti-oxidant enzyme. GSTA4 then used the cell’s existing glutathione supply to chemically neutralize and remove the toxic lipid-peroxidation byproduct 4-HNE, thereby protecting mitochondrial energy production from oxidative damage. This single-enzyme boost largely reproduced the benefits previously seen with OSK: the aging pattern of gene activity in the retinal pigment epithelium shifted toward a younger profile, and visual function improved. Importantly, elevating GSTA4 alone did not carry the same long-term safety concerns associated with continuous OSK expression. The result demonstrates that OSK can activate a more direct cellular stress-defense program, centered on GSTA4-mediated detoxification, separate from the classic DNA-demethylation pathway that resets epigenetic clocks in retinal ganglion cells. While the finding is relevant to the broader scientific platform, it is not the primary mechanism being tested with the ER-100 therapy in optic neuropathies. This study highlighted the importat role of cellular glutathione detoxinfication as an anti-aging strategy.[6] DNA DeMethylation as a Reversible Code Taken together, these studies portray DNA methylation not merely as a passive clock but as a reversible code. Partial reprogramming with carefully dosed OSK or OSKM factors appears capable of recruiting demethylation machinery (or, in certain cell types, parallel protective programs such as GSTA4) to restore youthful gene-expression patterns in selected tissues, at least in preclinical models. The translation of this principle into human medicine has begun, cautiously, in the eye, an accessible and clinically urgent target. Broader anti-aging application of the OSK technique in humans seems promising. However, whether the same controlled epigenetic reset can be safely extended to humans remains to be seen. Conclusion: Anti-aging strategies involve upregulating glutathione antioxidant protection which gradually declines as we age. This can be accomplished by epigenomic manipulation using demethylation strategies. It can also be accomplished with supplements glycine and NAC (N-acetly cysteine) as described in a previous newsletter: NAC and Glycine Prevents Decline of Aging and Prolongs Lifespan As we age, inflammatory pathways increase, causing havoc in our bodies. So, it is only logical to suggest Anti-Aging involves interventions that reduce inflammatory cytokines. This intervention can be obtained with bioidentical hormone therapy which is known to have anti-inflammatory properties.

jeffreydachmd.com/2015/01/wh… No, Darwin's theory of evolution is not necessarily the basis of modern biology and medicine....This is why.......Cell theory (with cellular pathology), molecular biology, and germ theory of disease provide foundational frameworks for modern biology and medicine that do not depend on Darwinian evolution by natural selection as their primary basis. These address the structure and function of living systems, information flow and molecular processes, and the causes and control of disease, core practical and conceptual pillars of contemporary biomedical science. Darwinian ideas about gradual adaptive change via selection on variation can be (and historically have been) set aside or subordinated without collapsing these foundations. 1. Cell theory and cellular pathology All known living organisms are composed of one or more cells; the cell is the basic unit of structure and function; and new cells arise only from pre-existing cells (biogenesis). This framework, refined in the mid-19th century, underpins histology, pathology, developmental biology, and most experimental biomedical research. Diseases are understood as disturbances of cellular structure and function (cellular pathology). Rudolf Virchow and others established that tumors and other pathologies arise from cells and can be studied at that level, independent of any particular theory of species transformation. In simple terms: biology and medicine largely study cells, what happens inside them, and how they go wrong. That program does not require Darwinian Evolution or natural selection as its foundation. Buja, L. Maximilian. “The Cell Theory and Cellular Pathology: Discovery, Refinements and Applications Fundamental to Advances in Biology and Medicine.” *Experimental and Molecular Pathology*, vol. 121, Aug. 2021, article 104660. doi.org/10.1016/j.yexmp.2021… (also available via ScienceDirect). 2. Molecular biology with a non-Darwinian (neutral/drift-dominated) outlook Modern molecular biology centers on the structure and information flow of nucleic acids (DNA/RNA) and proteins, the genetic code, transcription, translation, and the biochemistry of macromolecules. At the molecular level, much observed change is better explained by neutral mutations fixed by genetic drift than by adaptive natural selection. High mutation rates, biochemical “sloppiness,” junk DNA/RNA, and patterns of sequence change align with neutral theory rather than strict Darwinian adaptationism. Molecular biologists routinely investigate these systems experimentally without invoking selection as the explanatory core. In simple terms: the machinery of genes, proteins, and cellular information processing is studied and applied (in diagnostics, drugs, gene therapy) primarily through biochemistry, genetics, and molecular techniques. Neutral molecular evolution provides a better fit for much genomic data than pure Darwinian selection. Palazzo, Alexander F., and Nevraj S. Kejiou. “Non-Darwinian Molecular Biology.” *Frontiers in Genetics*, vol. 13, 2022, article 831068. frontiersin.org/journals/gen… This review argues that most molecular evolution is non-Darwinian (neutral drift-dominated) and that hyper-adaptationalist views fail to explain high-throughput genomic and biochemical data. King, Jack L., and Thomas H. Jukes. “Non-Darwinian Evolution.” Science, vol. 164, no. 3881, 16 May 1969, pp. 788–798. science.org/doi/10.1126/scie… This is a highly cited 1969 paper that advanced the neutral theory of molecular evolution (most protein and sequence change due to neutral mutations and drift rather than selection). 3. Germ theory of disease Infectious diseases are caused by specific microorganisms (bacteria, viruses, etc.) that invade the body. This paradigm shift in the late 19th century (Pasteur, Koch, Lister, and others) enabled sanitation, antiseptic surgery, antibiotics, and modern infection control. It is the practical foundation of much of clinical microbiology, public health, and infectious disease medicine. Koch’s postulates and related experimental approaches established causal links between specific germs and specific diseases without relying on Darwinian species origins. In simple terms: modern medicine’s greatest practical successes against infection rest on identifying and controlling microbes, not on explanations of how species arose or changed via natural selection. “Germ Theory: Invisible Killers Revealed.” BMJ, vol. 334, suppl. 1, 4 Jan. 2007, s11. These three areas, cellular organization and pathology, molecular mechanisms and information flow (often with neutral rather than strictly adaptive explanations), and microbial causation of disease, account for the bulk of day-to-day experimental, diagnostic, and therapeutic work in modern biology and medicine. They function as operational foundations whether or not one accepts Darwinian natural selection as the primary historical driver of biological diversity. Dobzhansky’s statement that “nothing in biology makes sense except in the light of evolution” is found to be wrong. Let's correct the statement. The statement should be revised to: " Most everything in biology and medicine makes sense without accepting Darwinian Evolution”. @CarmenMannella