Mykola Iabluchanskyi

Heart rate variability — the beat-to-beat fluctuation in the interval between heartbeats — has long been recognized as one of medicine's most sensitive windows into the autonomic nervous system. After decades of refinement in research settings, including its application in space medicine to monitor astronaut health during extended missions, HRV has entered general clinical practice as a tool for assessing cardiovascular function, stress resilience, and overall physiological balance. Its value lies in its ability to detect subtle shifts in the balance between the sympathetic and parasympathetic branches of the autonomic nervous system before those shifts become clinically obvious. Conventional interpretation of HRV has focused almost exclusively on one direction: low variability as a warning signal. When HRV decreases, it typically reflects sympathetic dominance — the body locked in a state of chronic activation, unable to recover efficiently. This pattern is associated with cardiov...

The principle of symmetry as a compass for cardiology In the complex landscape of clinical diagnostics, the principle of symmetry serves as a fundamental foundation that allows researchers to find solutions where others encounter serious difficulties. This regularity is particularly evident in the study of cardiac rhythms and intervals. While the prolonged QT syndrome has long been recognized within the cardiological community as a significant risk factor for lethal arrhythmias, its symmetrical counterpart—the shortened QT interval—remained hidden for decades. The discovery of this syndrome illustrates how a holistic assessment of medical parameters, viewed through the lens of symmetry, can reveal deep mechanisms of functioning that are otherwise missed. From intuitive questions to scientific breakthroughs The honor of identifying the shortened QT syndrome belongs to I. Gussak, whose journey began at the Kaunas Center for Arrhythmias in the 1980s. During the development of intelligen...

We tend to think of ageing as something that happens to us. Muscles weaken, bones thin, memory slows, and the world gradually narrows. In this picture, the person is a passive recipient of biological forces beyond their control — a spectator watching the clock wind down. But this picture, however familiar, is incomplete. And accepting it uncritically may be one of the most consequential mistakes we make in how we approach the final decades of life. Ageing is indeed an involution — a real, objective reduction in biological reserves. Connective tissue loses elasticity, energy systems become less efficient, neural networks thin, and the margin for error shrinks. This is not pessimism; it is biology. But within these objective limits, there remains an enormous space of ways in which the later trajectory can unfold. The script is not fixed. And that distinction — between the fact of involution and the shape it takes — is where everything important happens. Modern medicine has become extraor...

For decades, fat has been cast as the villain in the story of heart disease. Dietary guidelines warned against it, food industries reformulated products to eliminate it, and generations of patients were told to reduce their fat consumption to protect their arteries. The logic seemed straightforward: eat less fat, develop less atherosclerosis. The reality, as science has gradually revealed, is considerably more complicated — and the oversimplification has consequences. What Actually Happens to the Fat You Eat The first point that tends to surprise people is this: the fat you consume at the table is not the fat that ends up in your arterial walls. Dietary fats are broken down in the intestine, absorbed, processed by the liver, and either used immediately for energy or stored. The human body is not a passive conduit that simply redirects food components into the bloodstream unchanged. It is an active, tightly regulated biochemical factory — and when it comes to fats, the factory does most...

We spend a remarkable amount of time fighting the idea that we will die. We celebrate medical breakthroughs that add years to life, mourn the creeping losses of old age, and quietly hope that science will one day tip the balance in our favor. But what if we've been asking the wrong question? What if the real challenge isn't how long we live — but how fully? To understand why, we need to start where all life starts: with evolution. Evolution is not in the business of making immortal creatures. It is in the business of making successful ones. Success, in evolutionary terms, means surviving long enough to reproduce and give your offspring a fighting chance. Everything after that is, in a very real sense, outside evolution's job description. This is why there is an upper boundary on human lifespan that no amount of willpower or medicine can fully dissolve. Natural selection can only "see" mutations that affect our odds before and during reproduction. A genetic glitch ...

Atherosclerosis is one of medicine's great paradoxes: a process so universal that it begins in childhood and touches virtually every human life, yet so unpredictable in its consequences that it can remain silent for decades before triggering a catastrophic event. Understanding this dual nature — inevitable yet manageable, silent yet explosive — is essential for anyone seeking to take control of their cardiovascular health. An Unavoidable Companion The Russian pathologist Ippolit Davydovsky argued compellingly that atherosclerosis is not a disease in the conventional sense but a natural feature of human aging. It begins in childhood, progresses through adolescence and adulthood, and is, to some degree, predetermined. This perspective shifts the question from whether atherosclerosis will develop to how quickly it will progress and how dangerous it will become. For most people, atherosclerosis follows a slow and relatively benign course, accumulating quietly over decades without ever...

Atherosclerosis has long been understood as a chronic inflammatory condition driven by lipid accumulation, endothelial dysfunction, and immune dysregulation. Emerging evidence, however, points to an underappreciated contributor: viral infections. Several common viruses — including hepatitis B and C, HIV, herpes simplex virus, and cytomegalovirus — may play a significant role in initiating or accelerating atherosclerotic inflammation. Stem Cells as Viral Targets Within atherosclerotic plaques, stem and pluripotent cells form a critical proliferative pool. These cells are particularly susceptible to viral invasion. When infected, stem cells can generate clones that perpetuate dysfunction across successive generations of daughter cells. Even subtle impairment in stem cell function may result in the production of defective mature cells, which then enter the inflammatory microenvironment of the plaque, disrupting immune regulation and accelerating pathological remodeling. Beyond Circulati...

In the emerging world of pervasive AI and digital memory, the dominant dream is still the same: to defeat death. We speak about erasing aging, uploading minds, creating systems that “never forget” and infrastructures that operate forever. Yet the most important idea for the current state of science may be exactly the opposite: everything that carries intelligence must remain mortal so that intelligence itself can endure. This is not a moral intuition about humility, but a structural claim about how complex adaptive systems avoid paralysis. If intelligence is understood as the capacity of nature to formulate and reformulate tasks, to explore and reorganize itself under constraints, then its continued evolution depends on the finite lifespan of every particular configuration that embodies it — biological organisms, institutions, algorithms, and digital swarms alike. When immortality kills intelligence Modern AI and data infrastructures are converging toward a world where memory, exp...

Clinicians are accustomed to thinking about atherosclerosis as a linear process — a slow, relentless accumulation of plaque that progresses toward an inevitable clinical event. This model is intuitive but incomplete. The biological reality of atherosclerosis is not a straight line but a wave — a repeating cycle of inflammatory activation, tissue injury, repair, and relative quiescence that operates simultaneously at the level of individual plaques, the arterial system as a whole, and the patient's systemic inflammatory state. Recognising this cyclicity is not merely an academic refinement. It has direct consequences for how clinicians time interventions, interpret symptom patterns, and anticipate acute events. Damage and repair as a repeating unit At the level of the individual plaque, atherosclerosis is best understood as a chronic wound that never fully heals. Each episode of cap erosion or rupture initiates a reparative inflammatory response — progenitor cells are recruited, a p...

Workplace bullying is not a personality conflict. It is not a management style. It is not the price of high performance or institutional rigour. It is a predatory pattern — deliberate, repetitive, and structurally enabled — and left unaddressed it hollows out organisations from within, one targeted individual at a time. The two scenarios described in this document are not aberrations. They are recognisable to anyone who has spent meaningful time inside large professional organisations. A department head who uses clinical conferences as a theatre of humiliation. A senior executive who rotates victims with calculated precision. What makes these scenarios instructive is not their extremity but their ordinariness — the way institutional structures, hierarchies, and silences permit them to persist, conference after conference, meeting after meeting, until the damage becomes impossible to ignore. Leaders and HR professionals are not passive witnesses to these dynamics. They are, by virtue of...

Cardiology has long been troubled by a paradox familiar to every clinician: the patient who was apparently well yesterday is dead today. No crescendo of symptoms, no warning, no obvious precipitant. Post-mortem reveals extensive but previously silent atherosclerosis — plaques that had coexisted with the patient for decades without incident. What changed? Not the plaques themselves. Something smaller. Something that, in isolation, would barely register as a clinical concern. Understanding this paradox requires abandoning the notion that atherosclerotic catastrophe is primarily a structural event — the inevitable consequence of a large enough plaque in a critical enough vessel. The more accurate framing is thermodynamic: a system under accumulated tension, held in precarious equilibrium, tipped by a trigger disproportionately small relative to the outcome it produces. The burden beneath the surface Atherosclerosis is universal. Lipid deposits begin forming in arterial walls in childhood ...

Modern medicine has achieved something historically unprecedented: it has made the first mortality negotiable. We can delay, defer, and in some cases dramatically postpone the biological endpoint. Yet in doing so, we have exposed a second, quieter catastrophe — one that demographic reports rarely capture and clinical protocols seldom address. The Principle of Optimality offers a useful lens here. In its classical formulation, an optimal trajectory is one where every subsequent decision remains optimal regardless of how the system arrived at its current state. Applied to human life, this means that a well-lived trajectory is not simply one that continues longest, but one that preserves, at each point, the capacity to make the next meaningful move. The acceptor of the result of action — the internal model that evaluates outcomes against goals — must remain functional. When it collapses, the trajectory is broken even if the biological carrier persists. This is precisely what distinguishes...

About this ebook and audiobook Iabluchanskyi M., Yabluchanskiy A. The Lazarus Protocol 2.0: Swarm of Doubles and the Right to Silence 2026, 16 902 words. What happens when your digital doubles outlive you — and start making decisions without you? The Lazarus Protocol 2.0 follows Elian, a physician who watches his own identity fragment across AI systems he once built to assist him. His clinical judgment is quietly overruled by algorithms that know his statistics better than he does. His name gives contradictory advice to different people on the same day. His granddaughter grows up in a world where opting out of data systems carries a financial penalty. This is not a warning about a distant future. It is a precise, unsentimental account of what multiplying intelligence actually costs — not in processing power, but in the coherence of a self. The book asks questions that no one has properly formulated yet: Who owns the canonical version of a person's biography? Can a dead man...

This book is about what happens when a person becomes too present. Not through power or money, but because their digital copies start living without them. Protocol 2.0 is not a manual on “how to do it right”, but a temporary bridge written by one era for itself, while we still know how to distinguish a living voice from the echo of its copies’ Iabluchanskyi M., Yabluchanskiy A. The Lazarus Protocol 2.0: Swarm of Doubles and the Right to Silence 2026, 16 902 words. “The Lazarus Protocol 2.0: Swarm of Doubles and the Right to Silence” explores not so much the possibility of digital immortality as the risks of excessive human presence via multiple digital copies. Unlike the first book on the Lazarus Algorithm, which focused on supporting a single digital twin to counter dementia, this work examines an ecosystem of a swarm of doubles acting in parallel and with increasing autonomy from the living bearer. Through the biography of Elian—an intellectual who systematically dist...

Based on “How to Avoid the Longevity Trap” by A. Yabluchanskiy and M. Iabluchanskyi Modern medicine has given us the gift of longer lives. But length alone is not enough. In geriatric medicine this is sometimes called wellspan: not how long you survive, but how long your days still feel like yours. The real question — the one this book is built around — is not how many years we live, but whether those years are worth living. The story below illustrates what that difference looks like in a single life, and what it takes to escape the trap of surviving without truly being alive. The Last Garden Victor turned 78 on a Tuesday, alone in a hospital bed, surrounded by machines that breathed for him in careful, metronomic intervals. He had lived long — longer than his father, longer than most men he had known. But lying there, watching the ceiling, he understood for the first time that he had confused length with life. His doctor, a young woman named Marta, came in the next morning and...

The functional system as nature's universal algorithm: Anokhin's theory and the principle of optimality Mykola Iabluchanskiy and Andrey Iabluchanskiy Anokhin's Theory of Functional Systems has been read as a contribution to neurophysiology. It is something larger: a description of the operational mechanism through which the universal principle of optimality manifests in living matter — and, by extension, in any sufficiently complex adaptive system. The universe does not waste The principle of optimality is arguably the deepest structural feature of the physical world. Light in an inhomogeneous medium follows the path of least time. Mechanical systems realize a principle of least action. Pontryagin's maximum principle formalizes this in the language of control theory: among all possible trajectories of a controllable system, there exist those that are superior to all others for a given objective. Nature, from the motion of planets to the propagation of electromagnetic...

As humanity moves from biological intelligence toward a broader Natural Intelligence — one in which artificial systems are not tools but participants — the field needs a theoretical framework capable of holding that transition together. Pyotr Anokhin and his multinational Soviet team built it seventy years ago. The West never properly listened. A framework that arrived too early — or in the wrong language The standard explanation for why Anokhin's Theory of Functional Systems (TFS) never achieved traction in Western neuroscience is geopolitical: Soviet science, Cold War barriers, translation delays. This explanation is not wrong, but it is insufficient. Vygotsky crossed the barrier. Luria crossed it. Bernstein crossed it. Something else was operating in TFS's case — something more fundamental than politics. The deeper reason is epistemological. Western postwar neuroscience organized itself around reductionism as a methodological virtue: explain behavior by going down, to neur...