The research team, led by Abbie Evans and William S. Hart of the University of Warwick together with collaborators including Eunok Jung of Konkuk University and Robin N. Thompson of the University of Oxford, developed an age-structured mathematical model designed to capture two intertwined processes. The first is the demographic transition itself: the shifting distribution of ages within a population as fertility declines and longevity increases. The second is behavioural adaptation, the ways in which individuals and institutions respond to demographic change, most notably through extended workforce participation as societies age and older people remain economically active for longer. By coupling these processes within a single framework, the model moves beyond static snapshots of contact patterns and instead tracks how outbreak risk evolves across decades of structural change.

The central quantity the model estimates is the probability of a major outbreak, defined as the likelihood that a single pathogen introduction into a population leads to sustained transmission rather than rapid extinction. This probability is a cornerstone of outbreak risk assessment, yet it is often estimated using contact data from a single point in time. The new study argues that such snapshots can be misleading when the underlying population is changing. Contact patterns, which describe how often individuals of different ages interact, are strongly age-dependent: children mix intensively at school, working-age adults encounter large numbers of colleagues and commuters, and older adults typically have fewer daily contacts. Susceptibility and infectiousness, meanwhile, can also vary with age depending on the pathogen in question.

To ground the model in realistic data, the authors drew on demographic projections for the Republic of Korea, a country whose fertility rate has fallen among the lowest in the world and whose age structure is transforming faster than almost any other. Korea’s trajectory makes it a natural laboratory for studying the epidemiological consequences of population ageing, since the changes it will experience over the coming decades are ones that many other nations, including China, Italy and Japan, are likely to follow. The researchers combined these projections with age-specific contact matrices, which quantify the rates at which individuals in each age band interact with those in every other band, and with pathogen-specific assumptions about how susceptibility and infectiousness scale with age.

The headline finding is that population ageing may, in many scenarios, reduce the probability that an imported infection triggers a major outbreak. The mechanism is intuitive: as the share of older individuals in the population grows and the share of children and young adults shrinks, the average number of contacts per person declines, since older individuals tend to have fewer social interactions than younger age groups. Fewer contacts mean fewer opportunities for transmission, which lowers the effective reproduction number and makes sustained chains of spread less likely. For pathogens whose transmissibility does not increase sharply with age, an older population therefore acts as a partial buffer against epidemic take-off.

However, the study shows that this protective effect is far from universal, and the authors identify two main factors that can attenuate or even reverse it. The first is the pathogen’s own age profile. For infections whose susceptibility or infectiousness increases with age, the demographic advantage of an older population shrinks, because the growing fraction of older individuals is precisely the group most likely to acquire and transmit infection. In such cases, ageing does not simply reduce the number of transmission opportunities; it shifts those opportunities toward the individuals for whom each contact carries the greatest epidemiological weight. The model demonstrates that the direction and magnitude of the age gradient in susceptibility and infectiousness can therefore determine whether demographic change raises or lowers outbreak risk.

The second attenuating factor is behavioural. As societies age, labour force participation among older adults is expected to rise, whether through later retirement ages, pension reforms or the need to sustain shrinking workforces. When older individuals remain in employment, their daily contact rates increase, eroding the contact advantage that retirement confers. The study specifically models extended workforce participation as a behavioural response to demographic change and finds that it increases the number of contacts older individuals have, thereby offsetting the reduction in outbreak probability that ageing alone would produce. This coupling between demography and behaviour is the study’s key conceptual contribution: the two cannot be assessed in isolation, because demographic transitions induce behavioural responses that feed back into transmission dynamics.

The implications for public health planning are significant. Outbreak risk assessments are typically built on contact surveys and demographic data from the recent past, and models calibrated to current conditions may project inaccurate risks for future decades. If a country’s age structure is changing rapidly, the probability that a given pathogen, say a novel respiratory virus or a re-emerging vaccine-preventable infection, establishes sustained transmission may shift substantially over a planning horizon of twenty to thirty years. The study suggests that governments preparing pandemic preparedness strategies should incorporate demographic projections and anticipated behavioural changes, such as rising retirement ages, into their risk models rather than assuming a stationary population with fixed mixing patterns.

The work also highlights the value of computational approaches that integrate multiple drivers of epidemic risk. Age-structured models of this kind allow researchers to disentangle the separate contributions of contact rates, susceptibility, infectiousness and population composition, and to ask counterfactual questions: how would outbreak risk change if retirement ages rose by five years, or if a pathogen’s age gradient in severity were steeper? By varying these components systematically, the authors show that the net effect of demographic change on outbreak vulnerability is the product of competing forces, some of which reduce risk and others of which increase it. This decomposition provides a template for applying the same analysis to other countries and other pathogens.

More broadly, the study is a reminder that infectious disease risk is embedded in social structure. The probability that a pathogen introduction becomes an epidemic is not a fixed biological property of the pathogen alone; it emerges from the interaction between the pathogen’s characteristics and the age distribution, contact behaviour and economic organisation of the host population. As demographic transitions reshape societies worldwide, the authors argue that accounting for demographic and socio-behavioural context will be essential for accurately assessing future outbreak risks and for designing interventions, from vaccination targeting to workplace policies, that remain effective as populations age.

Subject of Research: Age-structured modelling of how demographic change and behavioural responses alter the probability of major infectious disease outbreaks

Article Title: Demographic changes and behavioural responses shape vulnerability to infectious disease outbreaks

Article References: Evans, A., Hart, W. S., Jung, E., Nah, K., Bonic-Babic, K., Jung, S.-M., & Thompson, R. N. (2026). Demographic changes and behavioural responses shape vulnerability to infectious disease outbreaks. PLOS Computational Biology, 22(10), e1014319. https://doi.org/10.1371/journal.pcbi.1014319

Image Credits: AI Generated

DOI: 10.1371/journal.pcbi.1014319

Keywords: population ageing, infectious disease outbreaks, mathematical modelling, age-structured model, contact patterns, South Korea, workforce participation, outbreak probability, epidemiology, PLOS Computational Biology, demographic transition, behavioural adaptation

The study, led by Huseyin Nezih Ozdemir, Iryna Klopotovska and Diego Kaski of the SENSE Research Unit in UCL’s Department of Clinical and Movement Neurosciences, was conducted at the National Hospital for Neurology and Neurosurgery in London between April 2025 and April 2026. Consecutive patients aged 18 and over arriving at the dizziness clinic underwent a structured ten-question interview before their clinical consultation. Crucially, the interviewer recorded answers about symptom timing, triggers, avoidance behaviours and behavioural responses before any diagnosis had been established. The final diagnoses were then made independently by a vestibular neurologist who was blinded to the interview responses, using established criteria from the Bárány Society and the International Classification of Headache Disorders. This design ensured that the behavioural data could not be contaminated by knowledge of the diagnosis.

The cohort of 109 patients had a mean age of 55.3 years, and 71.5 percent were female. Thirty-three patients were diagnosed with vestibular migraine, thirty-three with persistent postural-perceptual dizziness, fourteen with benign paroxysmal positional vertigo and fifteen with orthostatic dizziness. Smaller groups included patients with central structural disorders such as posterior circulation stroke and other peripheral vestibular conditions including bilateral vestibular loss. When the researchers applied logistic regression to the interview data, four clear behavioural profiles emerged, each mapping closely onto the known biology of the underlying disorder.

The strongest single predictor belonged to vestibular migraine. Patients who reported that reading while travelling as a passenger in a vehicle brought on their dizziness were more than twenty times more likely to have vestibular migraine than any other diagnosis, with an odds ratio of 20.99. This finding fits with the idea that vestibular migraine reflects a heightened vulnerability to sensory conflict, the discordance between visual motion signals and vestibular input that occurs when the eyes track a page while the inner ear registers the movement of a car. It also builds on earlier work from the same group showing that motion sickness while reading in a moving car is highly predictive of the condition. For patients with persistent postural-perceptual dizziness, visually stimulating environments such as crowded, busy or visually complex settings were the strongest precipitating factor, carrying an odds ratio of 12.45, consistent with the disorder’s characteristic over-reliance on visual cues for spatial orientation.

The two remaining diagnoses produced equally distinctive patterns. For benign paroxysmal positional vertigo, head movements and positional changes were the dominant trigger, with an odds ratio of 11.51, exactly what would be expected from the abnormal movement of displaced calcium carbonate crystals, or otoconia, within the semicircular canals. Patients with orthostatic dizziness, by contrast, pointed to standing up quickly as their principal trigger, reflecting the transient drop in cerebral blood flow that occurs during orthostatic stress. In each case, the reported precipitant was not an arbitrary preference but a direct behavioural echo of the underlying mechanism: sensory conflict in vestibular migraine, visual dependence in persistent postural-perceptual dizziness, otoconial displacement in positional vertigo and cerebral hypoperfusion in orthostatic dizziness.

Avoidance behaviours proved just as diagnostic as triggers. Patients with vestibular migraine disproportionately avoided bright or noisy environments and sought refuge by resting in dark, quiet rooms, mirroring the visual and auditory hypersensitivity that characterises migraine more broadly. Those with persistent postural-perceptual dizziness avoided visually busy places such as supermarkets, crowded streets or scrolling screens, and notably reported trying to maintain their activity despite the symptoms, an effort to push through the persistent, physically non-disabling dizziness that defines the condition. Patients with benign paroxysmal positional vertigo reported deliberately avoiding quick head movements and staying still during attacks, an understandable strategy to prevent the violent, brief episodes of rotational vertigo that position changes provoke. Orthostatic dizziness patients avoided sudden standing and tended to sit or lie down slowly, a sensible countermeasure against orthostatic intolerance, although this particular association did not reach statistical significance, likely because of the smaller size of that subgroup.

Temporal patterns added a further layer of discrimination. Episodic dizziness was significantly associated with vestibular migraine, while patients with persistent postural-perceptual dizziness were far more likely to report continuous dizziness lasting days or longer, in keeping with the chronic nature of that disorder. Patients with benign paroxysmal positional vertigo characteristically reported brief episodes lasting seconds to minutes, matching its paroxysmal presentation. Although patients with positional vertigo and orthostatic dizziness tended to describe dizziness that comes and goes, these associations did not reach statistical significance, a limitation the authors attribute to the relatively small numbers in those diagnostic groups.

The clinical implications of the work are considerable. Because neuroimaging has limited utility in most cases of dizziness and definitive tests are lacking for many vestibular syndromes, diagnosis rests heavily on history taking, and patients’ descriptions of symptom quality are notoriously imprecise. Structured questions about avoidance and coping could capture dimensions of the patient’s experience that conventional symptom questions miss. Asking simply whether a patient avoids supermarkets, refrains from turning their head quickly, or retreats to a dark room when dizzy may sharpen diagnostic accuracy, shorten the long delays many patients experience before correct treatment, and potentially prevent progression to chronic dizziness. Beyond diagnosis, recognising these behaviours may help clinicians understand how the disorders impair daily and occupational functioning, since triggers such as bright environments or awkward head positions have been shown to interfere with work tasks and contribute to reduced productivity and absenteeism.

Perhaps the most intriguing aspect of the findings is that patients developed these behavioural signatures without any formal knowledge of disease mechanisms. The researchers argue that such adaptations arise intuitively through repeated symptom experience, which is precisely what makes them informative: they represent the body’s own experiment on the disorder, conducted over months or years. The behaviours therefore function as natural biomarkers, reflecting pathophysiology rather than clinical teaching. The authors also caution that avoidance behaviours can themselves contribute to disability, and identifying them may open the door to rehabilitation strategies that prevent deconditioning and fear-driven withdrawal from activity.

The study is not without limitations. The structured interview was not a validated instrument, several diagnostic subgroups were small, limiting statistical power for some response categories, and the single-centre design in a specialised London clinic may constrain generalisability. Larger cohorts will be needed to confirm the diagnostic value of these behavioural markers and to quantify their impact on patients’ functioning. Even so, the message is clear and potentially transformative for routine practice: when a patient says they feel dizzy, the clinician should ask not only what it feels like and when it happens, but what the patient does about it. The answers, this research suggests, may point directly to the diagnosis hiding behind one of medicine’s most vague and common complaints.

Subject of Research: Behavioural signatures as diagnostic clues in common vestibular disorders causing dizziness

Article Title: What patients do when they feel dizzy: behavioural signatures reveal diagnostic clues in common vestibular disorders

Article References: Ozdemir, H. N., Klopotovska, I., & Kaski, D. (2026). What patients do when they feel dizzy: behavioural signatures reveal diagnostic clues in common vestibular disorders. Journal of Neurology, 273(10), Article 587. https://doi.org/10.1007/s00415-026-14133-0

Image Credits: AI Generated

DOI: 10.1007/s00415-026-14133-0

Keywords: dizziness, vestibular disorders, vestibular migraine, PPPD, BPPV, orthostatic dizziness, avoidance behaviour, coping strategies, behavioural adaptation, diagnosis, vertigo, neurology