The authors’ central argument is that prolonged crises should not be viewed merely as social or psychological events. They are also biological conditions capable of reshaping stress-related and ageing-related molecular pathways. In the short term, the human stress response is adaptive: the hypothalamic-pituitary-adrenal axis releases cortisol, mobilising energy and sharpening attention to survive immediate threats. But when stress persists for months or years, as it has for millions of Ukrainians since the 2022 invasion, these responses can become maladaptive. Chronic activation of the HPA axis, altered glucocorticoid signalling and disrupted sleep initiate a cascade of physiological dysregulation that compounds the vulnerabilities that already come with advanced age.

The Perspective maps this cascade with considerable technical detail. Sustained cortisol elevation promotes abdominal and visceral fat accumulation, and adipose tissue itself becomes inflamed, secreting inflammatory cytokines that drive insulin resistance. This intersects with inflammaging, the low-grade chronic inflammation characteristic of old age, which is now recognised as a shared driver of diabetes, cardiovascular disease, frailty and neurodegeneration. Cellular senescence adds another layer: stressed, damaged cells stop dividing but remain metabolically active, releasing the senescence-associated secretory phenotype, a cocktail of pro-inflammatory signals that further amplifies tissue dysfunction. The authors also highlight mitochondrial dysfunction, noting that psychological stress has been repeatedly linked to impaired mitochondrial energetics, and that declining skeletal muscle mitochondrial function is closely associated with reduced walking speed and aerobic capacity in older adults.

Skeletal muscle occupies a particularly central place in this framework. Ageing muscle already suffers from anabolic resistance, a blunted response to protein intake and physical activity that makes maintaining muscle mass progressively harder. During crises, irregular nutrition, food insecurity and reduced physical activity intensify this problem, accelerating sarcopenia. When muscle loss combines with expanding fat mass, the result can be sarcopenic obesity, a condition associated with worse clinical outcomes than either sarcopenia or obesity alone. Ukrainian research has begun to quantify this threat, with studies establishing epidemiological cut-off values for sarcopenic obesity in the Ukrainian population, and analyses of older Ukrainian war refugees documenting a heavy burden of chronic disease carried across borders.

The crisis-related exposures themselves are well documented. Studies from conflict zones, including a mixed-design study from the Gaza Strip, show that wartime food insecurity drives both weight loss and nutritional deterioration. Nationwide cross-sectional research in Ukraine after the first year of the Russian invasion found high prevalence of stress, anxiety and post-traumatic stress disorder symptoms, and a related preprint reported that older Ukrainians showed somewhat decreased sensitivity to stress and severity of anxiety, depression and PTSD, a finding consistent with other evidence that older age can sometimes buffer psychological distress even while physiological vulnerability remains high. Work on Ukrainian youth has also linked war exposure to dietary changes and PTSD, underscoring that the nutritional and psychological dimensions of crisis are inseparable.

What makes this Perspective distinctive is its systems-level framing. The authors argue that mental health, metabolic health, nutrition, muscle function and rehabilitation are currently addressed in isolation, when in reality they are biologically intertwined. A distressing event elevates cortisol, which alters appetite hormones and food cravings, promotes central fat deposition, disturbs sleep, and worsens insulin sensitivity. Poor sleep independently disrupts glucose metabolism. Inflammation connects adipose tissue, muscle and the immune system in a self-reinforcing loop. Immunometabolic dysregulation, in which immune cells shift their metabolism and adopt inflammatory programs, links psychological trauma to the metabolic syndrome. Breaking any single link in this chain is unlikely to succeed if the others remain under siege.

The authors propose that functional ability, the capacity to perform the activities of daily living, should serve as the key integrative indicator for older adults during and after prolonged crises. Functional ability reflects the combined effects of psychological stress, metabolic ageing, muscle loss, multimorbidity and changes in the living environment, such as displacement into unfamiliar housing without social support. Measuring it, rather than tracking individual biomarkers in isolation, would give health systems a single, meaningful signal of how well older populations are withstanding crisis conditions, and could guide where rehabilitation and nutritional interventions deliver the greatest benefit.

Ukraine’s circumstances give the framework real-world urgency. The country faces a rapidly ageing population, a high burden of non-communicable diseases, mass displacement, growing mental health needs and disrupted health care access, all at once. Notably, Ukraine has launched a national Health Screening 40+ program intended to make preventive screening more accessible, an initiative the authors cite as a timely entry point for biologically informed assessment. Screening initiatives, they argue, should incorporate mental health assessment, metabolic screening including waist circumference as a clinical vital sign for visceral obesity, nutritional assessment, muscle function testing and rehabilitation rather than treating these as separate silos.

The framework also draws on the concept of hormesis, the principle that mild, intermittent stressors such as exercise or intermittent fasting can strengthen stress-response systems, whereas severe or prolonged stress overwhelms them. Recent work from the same research group has explored intermittent fasting as a hormetic signal for adaptation, suggesting that nutritional timing might partly counteract the maladaptive biology of chronic crisis stress where food supply permits. Whether such interventions are feasible in active conflict zones remains an open question, but the underlying message is clear: the biology of ageing is not fixed, and crisis conditions can push it in either direction.

Ultimately, the article is a call to widen the lens of both gerontology and humanitarian response. If prolonged crises accelerate metabolic ageing through measurable molecular pathways, then the health consequences of war will continue to accrue long after the fighting stops, surfacing as diabetes, frailty, dementia and lost independence among today’s older adults. Recognising stress biology as a bridge between humanitarian emergency and chronic disease offers policymakers a way to intervene earlier, and offers researchers a rigorous agenda for understanding how societies age under pressure. Ukraine, the authors suggest, is not merely a case study but a warning for every ageing society that may one face prolonged crisis.

Subject of Research: Stress biology and metabolic ageing in older adults during prolonged crises, using Ukraine as a case study

Article Title: Stress biology and metabolic ageing in older adults during prolonged crises: Ukraine as an example

Article References: Lushchak, O., Strilbytska, O., Petakh, P., & Kamyshnyi, O. (2026). Stress biology and metabolic ageing in older adults during prolonged crises: Ukraine as an example. Biogerontology, 27(5), Article 158. https://doi.org/10.1007/s10522-026-10502-4

Image Credits: AI Generated

DOI: 10.1007/s10522-026-10502-4

Keywords: stress biology, metabolic ageing, older adults, Ukraine, HPA axis, inflammaging, sarcopenic obesity, cellular senescence, insulin resistance, mitochondrial dysfunction, frailty, functional ability