Mykola Iabluchanskyi

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...