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What Precision Prevention Misses: A Migration-Informed Approach to Risk

By Chul Hyun, MD, PhD, MPH

This article was originally published in Health Affairs Forefront on February 12, 2026. 10.1377/forefront.20260209.506668

Dr. Chul S. Hyun is the Director of the Gastric Cancer Prevention and Screening Program at Yale School of Medicine. A graduate of the University of Miami School of Medicine, he completed his residency at Georgetown University and a fellowship in Gastroenterology and Liver Diseases at Yale. He has been instrumental in community-based health initiatives through the Center for Viral Hepatitis (CVH) and the Stomach Cancer Task Force (SCTF), focusing on reducing health disparities through culturally tailored education, screening, and preventive care.

Over the past decade, health policy and clinical practice have increasingly embraced precision medicine. Advances in genomics, molecular diagnostics, and biomarker-driven care have transformed how disease is classified, diagnosed, and treated, reshaping expectations for individualized care and driving innovation across health systems. In parallel, the concept of precision prevention has emerged, emphasizing targeted preventive strategies based on differential risk. Much of this progress has focused on incorporating genomic, biomarker, and individualized risk information into prevention frameworks, extending the logic of precision medicine upstream. Yet, these advances have remained more aspirational than operational in most health systems, and they have not fundamentally reshaped how prevention is organized at the population level. Despite longstanding recognition that disease risk is unevenly distributed, prevention and screening continue to rely on age-based thresholds and static risk categories that implicitly assume homogeneous baseline risk. As a result, prevention often lags behind treatment in its ability to account for meaningful differences in how— and when—risk is acquired.

One important dimension of risk remains underdeveloped in contemporary prevention thinking: population mobility and early-life geographic exposure, particularly for conditions with long latency periods or early-life acquisition. Clinicians routinely ask about country of birth, childhood residence, prior health systems, and past exposures when assessing risk, and public health practice similarly recognizes that risk does not reset when individuals cross borders or relocate. Yet, this recognition remains largely informal. Decisions about screening eligibility and preventive interventions are rarely guided by systematic assessment of life-course exposure histories, even when such information is readily available. Instead, migration-related risk is often handled through informal clinical judgment rather than explicit prevention logic, relying on disease-specific exceptions or narrow carve-outs rather than generalizable policy frameworks. This gap does not reflect a lack of evidence or awareness, but a broader disconnect between how risk is understood in practice and how prevention is operationalized in policy. By leaving migration and life-course exposure implicit, health systems miss an opportunity to align prevention strategies with what is already known about the origins of disease risk.

Migration As Life-Course Exposure

In health discourse, “migration” is often narrowly interpreted as synonymous with immigration status. This framing obscures a broader and more policy-relevant reality: Population mobility is a defining feature of modern societies. Migration includes international movement, but also internal relocation across regions with differing environmental and infectious exposures; transitions between rural and urban settings; and movement across health systems with distinct prevention infrastructures, screening norms, and patterns of care. Crucially, migration is not a demographic label or a proxy for social identity. It is an exposure history that can leave durable biological and structural imprints on disease susceptibility. Where individuals live during formative periods—and the health systems through which early prevention and care occur—can shape risk trajectories in ways that persist long after relocation. These exposures do not dissipate simply because an individual later resides in a different geographic or health system context.

Epidemiologic evidence consistently shows that risk for many chronic and infection-associated diseases is shaped early in life, often decades before clinical manifestation. For conditions with long latency periods, the temporal distance between exposure and disease onset can obscure the relevance of early-life geography in contemporary risk assessment. As populations become increasingly mobile, reliance on current residence as a proxy for cumulative exposure becomes increasingly tenuous. Risk travels with people, even when prevention policies remain place- bound. Importantly, recognizing the role of migration does not require granular exposure measurement or complex modeling. Broad indicators—such as place of birth, childhood residence, or prior health system context—are already captured—or could be readily captured—in clinical and administrative data. The challenge lies not in data availability, but in whether these signals are systematically incorporated into prevention decision making.

When Prevention Fails To Track Risk

The consequences of leaving migration and life-course exposure implicit are practical and predictable. Prevention systems misalign resources with how risk is actually acquired, generating missed opportunities and inefficiencies. Individuals whose risk was established early in life may enter the health system classified as average risk under conventional criteria, only to present later with advanced disease despite long-standing, identifiable exposure histories. At the same time, prevention policies may direct screening toward individuals whose baseline risk is comparatively low simply because they meet age-based thresholds. The result is a prevention paradigm that is simultaneously undertargeted and overinclusive.

A clear example is gastric cancer, in which risk is largely determined by Helicobacter pylori infection—designated a Group 1 carcinogen by the World Health Organization— typically acquired in childhood. Epidemiologic studies consistently show that individuals migrating from high- incidence regions retain elevated gastric cancer risk decades after relocation. Yet, US prevention remains anchored in age-based thresholds and symptom-driven evaluation rather than exposure history, leading many individuals with long-standing, identifiable risk to be classified as average- risk until late-stage diagnosis. A parallel pattern is seen in chronic hepatitis B infection, in which early-life acquisition drives lifelong risk of cirrhosis and hepatocellular carcinoma. Although screening and surveillance guidelines exist, implementation often depends on clinician awareness rather than systematic identification based on birthplace or early- life exposure, resulting in wide variation in prevention uptake despite well-established epidemiologic evidence.

These failures are not random. They reflect structural weaknesses across the prevention pipeline. Life-course exposure is often captured inconsistently at intake and relegated to unstructured clinical history that cannot be used systematically. Prevention guidelines rely heavily on age and current residence, offering little guidance on when early-life exposure or prior health system context should modify action. And because migration-informed risk remains implicit, health systems lack clear metrics to assess whether prevention strategies align with cumulative exposure rather than administrative convenience. While downstream treatment decisions grow increasingly individualized, upstream prevention continues to operate on coarse population assumptions, undermining the internal logic of precision medicine itself.

Toward Explicit, Migration-Informed Prevention

A migration-informed approach offers a pragmatic extension of precision medicine by shifting attention upstream from treatment optimization to prevention targeting. Rather than competing with genetic or molecular tools, it complements them by incorporating a dimension of risk that is often decisive and comparatively inexpensive to assess. What this approach requires is not disease-specific reinvention or rigid thresholds, but a clearer prevention logic. First, prevention frameworks must explicitly recognize early-life geography and prior health system context as legitimate, actionable components of risk assessment, rather than treating them as informal background information. Disease-specific guidelines can then operationalize this principle in ways that reflect differences in latency, exposure mechanisms, and preventive effectiveness.

Second, making migration-informed risk explicit improves accountability and evaluability of prevention strategies. When exposure histories remain implicit, prevention performance cannot be meaningfully assessed. Explicit incorporation allows health systems to evaluate whether prevention strategies align with epidemiologic risk shaped by life-course exposure, enabling systematic learning and refinement over time. Finally, for health systems, this approach offers a practical opportunity to improve targeting without expanding cost or complexity. Much of the relevant information already exists within clinical and administrative infrastructure. What is missing is intentional integration into prevention logic and policy—treating exposure history not as background context, but as prevention-relevant data.

Emerging analytic tools, including machine-learning–based risk stratification, could facilitate the operationalization of migration-informed prevention without introducing new clinical burdens. For example, routinely collected data elements—such as country of birth, age at migration, language preference, and prior health system contact—could be integrated into automated risk indices to flag individuals whose cumulative exposure history suggests elevated risk despite meeting conventional “average-risk” criteria. In this context, artificial intelligence does not redefine risk; it helps health systems consistently identify it at scale, transforming already documented but rarely actionable exposure histories into prevention-relevant signals.

Conclusion

Precision medicine has transformed diagnosis and treatment, yet prevention often remains anchored in assumptions that no longer reflect how risk is acquired across the life-course. Population mobility and early-life exposure shape disease susceptibility in durable ways, yet these realities remain largely implicit in prevention policy—with tangible consequences in conditions such as gastric cancer and chronic hepatitis B, in which failure to operationalize migration-informed prevention has contributed to delayed diagnosis and preventable morbidity despite decades of epidemiologic evidence. A migration- informed approach does not introduce new technologies or argue for narrow exceptions; rather, it makes explicit a dimension of risk that many clinicians already recognize but that health systems rarely operationalize. As medicine continues to invest in increasingly sophisticated downstream precision, comparable intentionality is needed upstream. Making life-course exposure visible within prevention policy is a necessary step toward ensuring that precision medicine fulfills its promise—not only in treatment, but also in prevention.

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