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...