Mykola Iabluchanskyi

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 ...