Mental health conditions ‘run in families’, a common phrase that we often hear, but how much of this is true? How much is due to genetics and how much is due to the shared environments, or broader psychosocial factors?
Research shows that having a family history of a mental disorder increases the risk of developing that specific disorder. Mental health condition heritability is often assessed using relative risk measures (Kendler, 2013). For example, depression risk can be two to three times higher for individuals if they have an affected first-degree relative (Sullivan et al., 2012). This “doubling or tripling of risk” is alarming, but it is also a bit misleading.
What if a person’s baseline risk is low? Then that very-high-sounding risk might still be interpreted as a very modest overall likelihood. To clarify this crucial difference, Pedersen and colleagues (Pedersen et al., 2025) conducted a prospective cohort study to map out entire family trees and assess how having an affected relative influences one’s own risk.
Family history of a mental health condition is a risk factor, not a diagnosis. New research looks at how having an affected relative influences one’s own risk.
Methods
The researchers used Danish Multi-Generation registers to follow over 3 million people born between 1955–2006 to Danish-born parents. Follow-up started at age 15, and continued until first treatment of a mental health disorder, death, emigration, or Dec 31, 2021 (Due et al., 2024). Family relationships were mapped across first-, second- and third-degree relatives and linked to psychiatric diagnoses from national registers. A range of mental health conditions were examined, including depression, schizophrenia, substance use, and personality disorders.
The authors applied multi-state competing risk models (estimate chance of first diagnosis based on family history), incidence rate ratios (compare rates of how much risk comes from shared genetics and environment), to calculate:
- Lifetime risk up to age 60 – probability of diagnosis by age 60
- Age-specific absolute risks – the likelihood of diagnosis at different ages
- Risks by relative type – differences in risk by parental, sibling, or extended family history
- Proportion of non-familial cases – diagnoses with no affected close relatives
- Heritability – genetic contribution to risk only.
Results
The risk is universal, but varies by the types of relationship
Pedersen and colleagues (2025) analysed data of more than 3 million individuals, with 48.8% females to answer the question. They confirmed that any mental health condition in any family member (first-, second- or third-degree relatives) increases one’s lifetime and relative risk of developing the disorder. This relative risk varied significantly across disorders, ranging from a 2.35-times increased risk for depression up to a nearly 8-times increased risk for cannabis use disorder, when compared to those without an affected first-degree relative. The risk is highest for twins and gradually decreased as the relationship became more distant. A first-degree relative (parent or sibling) carries more relative risk than a second-degree relative (aunt, uncle, or grandparent).
What about absolute risk?
As well as relative risk, the authors explained the absolute risk of the observed associations. Let’s have a look at depression to explain the differences in these relationships:
- Having a first-degree relative with depression is linked to 2.35-times increased risk. This is the number that often sounds a bit alarming.
- The 2.35-times increase actually results in a lifetime risk of 15%. While this is double the general population’s risk, it means that even with an affected parent, you still have a high chance of not developing depression yourself.
The authors also explain how depression risk varies across family-trees:
- People with an affected first-degree relative are at 15.5% increased risk.
- People with an affected second-degree relative are at 13.5% increased risk.
- The general population’s risk is 7.8%.
- Those without affected relatives are at 4.7% increased risk.
Importantly, 60% of all depression cases occur in individuals with no affected first- or second-degree relatives. A similar pattern was observed for other disorders as well, from schizophrenia to substance use disorders.
Age-specific risk curves revealed how risks accumulate over time. This means that, for depression, a 30-year-old with an affected first-degree relative has a residual risk of 9% for developing depression by age 60, compared to 4% for someone without an affected relative. Similar trends were seen for substance use, schizophrenia, and personality disorders.
In short, while family history matters, having an affected relative is not a diagnosis and vice versa. This points the fingers at the complex interplay of genetics, environment, and life experiences.
Family history shapes mental health risk, but most diagnoses still occur in people without affected close relatives.
Conclusions
This study provides the most comprehensive understanding to date of how mental health conditions vary and cluster within families, and how absolute risk can quantify individual risk levels.
The findings make one thing clear: family history of a mental disorder does matter, particularly for individuals with close relatives or same-sex twins affected by mental disorders, but it is only part of the story.
Recognising both familial and non-familial risks is essential for developing balanced, personalised strategies for prevention, early support, and treatment of mental disorders.
Understanding both familial and non-familial influences is key to personalising prevention and early support for mental disorders.
Strengths and limitations
This study has several strengths. It is the first study to use national, population-based data and multi-generational family trees to provide absolute risk estimates across a wide range of adult mental disorders. The large sample size and long follow-up across different life stages allowed precise risk estimates and strong comparisons across disorders, sexes, and degrees of kinship. Using clinically recorded diagnoses from national registers also reduced recall bias, which is inherent in self-report. The study therefore offers detailed risk profiles that can inform both clinical risk assessment and population-level planning.
Several limitations also need to be considered.
- First, registry-based data only captures diagnosed and treated cases recorded in hospital and specialist outpatient departments; many individuals with mental health concerns (mild, subclinical, or untreated) may be missed. This probably underestimates absolute prevalence and could bias age-specific or familial risk estimates towards more severe cases.
- Second, although the family-tree reconstruction includes first- to third-degree relatives, completeness and depth of the diagnosis may decline with degree of kinship; more distant relatives are less likely to be comprehensively recorded or linked.
- Third, comorbidity is common in psychiatry, but registers may not fully capture overlapping diagnoses or symptom trajectories, complicating interpretation of disorder-specific risks.
- Fourth, diagnostic practices, health-seeking behaviours, and service availability likely changed between 1970 and 2021, which could influence results. These shifts may affect the results, because the risk estimates could partly reflect changes in the healthcare system rather than true differences in disorder patterns.
- Finally, the study population is Danish and European, so findings may not generalise to other settings. Future work should replicate findings in more diverse populations and integrate primary-care data, community surveys, and measures of psychosocial, environmental, and genetic factors.
This study provides precise, multi-generational risk estimates for mental disorders, but registry data may miss mild or untreated cases, and findings may not fully generalise beyond Denmark.
Implications for practice
This study has several important implications for clinical practice and public mental health. The results highlight the value of recording a detailed family psychiatric history, especially for first-degree relatives such as parents and siblings. This paper quantifies how risk varies across different relationship types and across the lifespan at a scale never done before. These estimates show that family history can supplement risk assessments and help guide early interventions. Age-specific risk estimates show when individuals may be most vulnerable and when preventive support might have greatest impact. This could help clinicians, easing decision-making and intervening more effectively. For example, through closer monitoring or early support during developmental stages where risk is highest.
However, a substantial proportion of individuals who develop a mental disorder come from families with no known psychiatric diagnosis. Heredity alone does not determine risk, and this finding challenges the common assumption that absence of family history implies low risk. In reality, environmental stressors, social adversity, trauma, biological vulnerabilities, and random genetic variation all play major roles and can trigger disorder onset even in families without diagnosed cases. This insight is crucial: while family history is a useful indicator, it cannot fully explain a diagnosis. Clinicians should focus more on symptoms, experiences, and context rather than assuming low risk based solely on background.
For public mental health and policy, together, these findings highlight the need for an integrated approach. Those with strong familial risk may benefit from targeted screening, early psychological support, and closer monitoring. Yet because many cases arise without family history, universal strategies remain essential. Investment in accessible mental health services, school-based programmes, anti-stigma initiatives, and early intervention remains crucial. Overall, family history is an important piece of the puzzle, but not the whole picture. Effective prevention and early support need to be broad, integrated, and available to all.
Family history can guide early support, but many people develop mental disorders without a known familial risk, highlighting the need for universal and targeted prevention.
Statement of interests
I have no conflicts of interest to declare. I was not involved in the study or related projects. AI tools were used at a minor level for copy editing.
Editor
Edited by Éimear Foley. AI tools assisted with language refinement and formatting during the editorial phase.
Links
Primary paper
Pedersen, C. B., Pedersen, M. G., Antonsen, S., Pedersen, E. M., Horsdal, H. T., Debost, J.-C., Mortensen, P. B., Petersen, L. V., Vilhjálmsson, B. J., Nielsen, J. F., Due, J. K., Søgaard, A., Igel, C., Thompson, W. K., Fan, C. C., Wray, N. R., McGrath, J. J., & Agerbo, E. (2025). Absolute and relative risks of mental disorders in families: a Danish register-based study. The Lancet Psychiatry, 12(8), 590-599. DOI: 10.1016/S2215-0366(25)00196-8
Other references
Due, J. K., Pedersen, M. G., Antonsen, S., Rommedahl, J., Agerbo, E., Mortensen, P. B., Sørensen, H. T., Lotz, J. F., Piqueras, L. C., & Fierro, C. (2024). Towards more comprehensive nationwide familial aggregation studies in Denmark: the Danish Civil Registration System versus the lite Danish Multi-Generation Register. Scandinavian Journal of Public Health, 52(4), 528-538.
Kendler, K. S. (2013). What psychiatric genetics has taught us about the nature of psychiatric illness and what is left to learn. Molecular psychiatry, 18(10), 1058-1066.
Sullivan, P. F., Daly, M. J., & O’Donovan, M. (2012). Genetic architectures of psychiatric disorders: the emerging picture and its implications. Nature Reviews Genetics, 13(8), 537-551.
