Are Anxiety Disorders Genetic? Heritability, Polygenic Risk, and Environment
Author: Ukrainian Psychological Hub · Published: October 1, 2026 · Editorial Policy
Yes. Anxiety disorders have a meaningful genetic component, but they are not inherited like a single-gene condition. Current evidence supports a complex, polygenic model in which many genetic variants each contribute tiny amounts to susceptibility, while development, learning, stress, family context, and other environmental factors also shape whether anxiety symptoms become persistent, impairing, and clinically diagnosable. NIMH describes common anxiety and depression as arising from a combination of life experiences, environment, and genetic variation.
That distinction matters because the everyday question “Is anxiety genetic?” actually contains several different scientific questions. Does anxiety run in families? How heritable are particular anxiety disorders? Which DNA variants are associated with risk? Can a polygenic score predict who will develop an anxiety disorder? How much of family transmission is genetic versus environmental? Modern genetic research can answer parts of these questions, but it does not support genetic determinism, a single “anxiety gene,” or a DNA test that can diagnose an anxiety disorder.
The short answer: anxiety disorders are heritable, polygenic, and environmentally shaped
The best-supported summary is that genetic differences contribute to variation in liability to anxiety, while environmental and developmental influences contribute substantially as well. Reviews of twin and molecular-genetic research consistently describe anxiety as a complex trait rather than a Mendelian disorder. A major review of anxiety genetics emphasizes evidence from twin studies, molecular genetics, and genome-wide association studies while also pointing toward gene–environment processes and shared genetic architecture across related traits. Ask and colleagues reviewed this evidence in Psychological Medicine.
The term “genetic” therefore means increased susceptibility associated with inherited variation across many parts of the genome. It does not mean that a person is born with an inevitable clinical disorder. A genetic predisposition changes probability, not destiny. MedlinePlus defines genetic predisposition as an increased likelihood of disease rather than a direct cause.
The umbrella term anxiety disorders also requires care. Anxiety Disorders contains several distinct diagnoses with different symptom patterns and clinical boundaries. Genetic studies may pool diagnoses, use one disorder, use self-reported lifetime anxiety, or measure anxiety symptoms continuously. Their estimates are therefore not interchangeable.
What does heritability actually mean?
Heritability is a population statistic. It estimates how much of the variation in a trait, in a particular population under particular environmental conditions, is statistically associated with genetic differences among people. MedlinePlus explains that heritability is specific to a population and environment and can change as circumstances change.
A heritability estimate of 0.40 does not mean that 40% of one person’s anxiety was caused by genes and 60% by environment. It means that, under the assumptions of the study, about 40% of variation in liability or the measured trait across that studied population was attributable to genetic variation. This is one of the most important corrections to popular explanations of psychiatric genetics.
Heritability also does not measure immutability. A highly heritable trait can still be influenced by experience or intervention. Conversely, a low or moderate heritability estimate does not imply that biology is unimportant. MedlinePlus explicitly separates heritability from both individual causation and changeability.
Heritable is not the same as familial
A condition can cluster in families because relatives share genes, environments, behaviors, stressors, resources, cultural patterns, and ways of responding to threat. “Runs in families” is therefore broader than “is inherited genetically.” MedlinePlus makes this distinction directly: familial traits can be shared for reasons other than genetics. See the MedlinePlus explanation of heritability.
Heritability is not one fixed number for anxiety
There is no single scientifically correct percentage for “the heritability of anxiety.” Estimates depend on what is measured, how cases are defined, age, sex, ancestry, study design, ascertainment, statistical model, and whether researchers are studying a diagnosis, a symptom scale, or a broader internalizing phenotype. A number from one study should not be pasted onto every anxiety disorder.
What did classic family and twin studies find?
Family and twin research established the basic conclusion that anxiety liability has a genetic component well before large genome-wide studies became possible. In a 2001 meta-analysis, first-degree relatives of affected people showed substantially higher odds of related anxiety conditions than relatives of unaffected comparison participants. Twin analyses in that review estimated heritability around 0.43 for panic disorder and 0.32 for generalized anxiety disorder. Hettema, Neale, and Kendler reported these findings in the American Journal of Psychiatry.
Those numbers are historically important, but they should not be treated as universal constants. The 2001 review used the diagnostic groupings and evidence available at that time; it also included obsessive-compulsive disorder in its review set. In current DSM-5-TR and ICD-11 organization, OCD is not classified as an anxiety disorder. The older literature is useful for genetic epidemiology, but current clinical classification still matters.
The same classic twin literature also highlighted environmental influence. For panic disorder, the remaining liability in the meta-analysis was attributed primarily to nonshared environmental effects under the twin model. “Nonshared environment” does not mean a single identifiable life event; it is a statistical component that includes experiences that differ between relatives and can also absorb measurement error and model limitations.
Why twin-study heritability and DNA-based heritability are different
Twin studies infer genetic influence from patterns of resemblance among relatives with known expected genetic similarity. Genome-wide methods estimate how much variation is tagged by measured DNA variants, usually common single-nucleotide polymorphisms. These methods ask related but different questions, so their estimates should not be expected to match.
A large UK Biobank analysis of lifetime anxiety disorder and current anxiety symptoms found SNP-based heritability estimates of about 26% and 31%, respectively, and described anxiety disorders as having twin-study heritabilities commonly in the 30–60% range. Purves and colleagues reported these results in Molecular Psychiatry. The gap between family-based and SNP-based estimates can reflect unmeasured genetic variation, imperfect tagging, phenotype differences, model assumptions, and statistical power.
The safest interpretation is therefore qualitative before it is quantitative: genetic variation matters, it is distributed across the genome, and the exact fraction captured depends on the phenotype and method.
Anxiety disorders are polygenic
Polygenic means that many genetic variants contribute to risk, with each common variant usually having a very small effect. There is no single variant that functions as an “anxiety gene” for the major common anxiety disorders. This pattern resembles many other complex human traits and psychiatric conditions.
NIMH explains that most variants associated with mental disorders do not directly cause them and that most known variants change risk only by tiny amounts. Its public genetics guidance also states that current genetic tests cannot accurately predict who will develop a mental disorder.
Polygenicity also explains why a person can carry many risk-associated variants without developing a disorder, while another person can develop an anxiety disorder without carrying an unusually high burden on any currently available polygenic score. Genetic risk is probabilistic and distributed, not a binary switch.
What genome-wide association studies have changed
Genome-wide association studies, or GWAS, scan large numbers of genetic variants across many participants and test whether particular variants are statistically associated with a phenotype. Modern anxiety GWAS have moved the field beyond small candidate-gene studies and have begun to identify reproducible loci and biological pathways. They still explain only part of individual variation and do not turn association into personal prediction.
The 2024 multi-ancestry anxiety GWAS
A 2024 Nature Genetics study analyzed data from more than 1.2 million participants, including 97,383 anxiety cases across five continental ancestry groups. The researchers identified 51 anxiety-associated loci, 39 described as novel, and highlighted 115 genes through transcriptomic and proteomic analyses. Friligkou and colleagues reported the study in Nature Genetics.
This study was especially important because psychiatric genomics has historically been dominated by European-ancestry samples. The cross-ancestry design improved discovery and showed that European-derived polygenic scores had statistically detectable associations with anxiety in several other ancestry groups. Statistical association across groups, however, is not the same as accurate or equitable clinical prediction.
The 2026 GWAS of major anxiety disorders
A 2026 Nature Genetics meta-analysis examined 122,341 European-ancestry cases and 729,881 controls and identified 58 genome-wide significant loci in major anxiety disorders. The study focused on major anxiety phenotypes including generalized anxiety disorder, panic disorder, and phobias, and highlighted GABAergic signaling among the biological findings. Strom and colleagues reported the results in Nature Genetics.
A pathway signal is a clue about biology, not a direct treatment prescription. Finding enrichment in GABA-related biology does not establish that every person with an anxiety disorder has a specific GABA abnormality, nor does it show that one medication class is genetically indicated for an individual. GWAS identifies statistical architecture at the population level.
The 2026 GWAS of generalized anxiety symptoms
A separate 2026 Nature Human Behaviour study analyzed quantitatively measured generalized anxiety symptom severity in 693,869 people of European ancestry across 14 cohorts. It identified 80 independent genome-wide significant variants across 74 loci and estimated SNP-based heritability at 5.9%. Skelton and colleagues published these findings in Nature Human Behaviour.
That 5.9% estimate should not be compared mechanically with the older twin estimates for diagnosed panic disorder or GAD. The phenotype was generalized anxiety symptom severity across large population cohorts, and the method estimated the portion captured by common measured variants. Different phenotype, different method, different number.
The same study found that polygenic scores explained only a modest fraction of variation in validation samples—roughly 1.2% to 2.9% depending on the sample and ancestry context. That is useful for research, but it is far from a deterministic individual prediction.
What is a polygenic risk score?
A polygenic risk score, often abbreviated PRS or PGS, combines information from many variants into a single statistical index. Each variant is weighted according to its association in a discovery GWAS, and the weights are summed for an individual. The resulting score estimates relative genetic liability within the context of the reference data used to build and validate it.
A PRS is not a diagnosis. It does not measure current fear, worry, avoidance, impairment, or whether diagnostic criteria are met. It also does not tell a clinician which anxiety disorder a person has. The International Society of Psychiatric Genetics states that psychiatric PRS are currently research analyses and are not recommended for identifying high-risk individuals or diagnosing psychiatric patients.
Why ancestry matters for polygenic scores
Polygenic scores usually perform best in populations genetically similar to the data used to train them. Differences in linkage disequilibrium, allele frequencies, environmental contexts, and study composition can reduce transferability across ancestry groups. This is one reason multi-ancestry recruitment is scientifically and ethically important.
The 2024 multi-ancestry anxiety study is a meaningful step toward broader representation, but it does not eliminate the longstanding imbalance in genomic datasets. Clinical use requires not merely statistical significance but reliable calibration, replication, added predictive value, and evidence that performance is acceptable across populations.
Does anxiety run in families?
Yes, anxiety disorders and anxiety-related traits can cluster in families. Family history is therefore clinically relevant background information. Yet family history is a composite signal: relatives share genes, but they may also share stressful circumstances, threat models, socioeconomic conditions, coping patterns, access to care, and learned responses to uncertainty.
Large family high-risk research across mental disorders shows that children of affected parents have elevated risks for psychiatric outcomes, including continuity within disorder families. A 2023 World Psychiatry meta-analysis by Uher and colleagues synthesized more than 200 family high-risk and registry studies. Such studies quantify familial risk; they do not isolate the genetic fraction of that risk.
If a parent has an anxiety disorder, will the child inherit it?
A child can inherit genetic variants that influence susceptibility, but a parent’s diagnosis does not create a fixed probability that the child will develop the same disorder. The child receives a unique combination of parental variants, and development occurs in a distinct environment. Family history raises concern at the population level without determining an individual outcome.
It is also possible for parent–child resemblance to be environmentally transmitted. In a children-of-twins study, researchers found evidence consistent with direct environmental transmission of parental anxiety and neuroticism to adolescent offspring rather than a purely genetic explanation for the intergenerational association. Eley and colleagues reported the study in the American Journal of Psychiatry. This design has assumptions and does not prove one universal family mechanism, but it demonstrates why “familial” cannot be translated automatically into “genetic.”
Genes and environment work together rather than taking turns
The familiar nature-versus-nurture question is too simple for anxiety disorders. Genetic liability develops within environments, and environments are encountered by people with different inherited propensities. NIMH explicitly describes anxiety research as examining both genetic and environmental contributors. See NIMH’s Anxiety Disorders research overview.
Environmental influences can include adverse experiences, chronic stress, acute life events, health events, family interactions, social context, learning histories, and protective experiences. None is required for every person, and none should be treated as a universal explanation for all anxiety disorders.
Gene–environment interaction
Gene–environment interaction means that the effect of an environmental exposure may differ according to genetic background, or that the effect of genetic liability may differ across environments. It is conceptually different from simply adding a genetic effect and an environmental effect together. Reviews of stress- and anxiety-related disorders describe this framework as important, while also emphasizing the need for large, well-powered and replicable studies. Sharma and colleagues reviewed gene-by-environment research in the Annual Review of Psychology.
Specific candidate-gene interaction claims deserve particular caution. Earlier psychiatric research often tested one or a few genes against one exposure, producing findings that were difficult to replicate reliably. Contemporary research increasingly favors genome-wide and polygenic approaches rather than treating a single candidate variant as a clinically meaningful vulnerability marker.
Gene–environment correlation
Genetic and environmental pathways can also correlate. People partly shape, select, or evoke environments in ways related to heritable traits. A temperament associated with behavioral inhibition, for example, can influence which situations a person enters and how others respond to them. This makes simple partitions such as “genes versus environment” even less realistic.
The environment is not simply one minus heritability
If a study estimates heritability at 40%, it is tempting to call the remaining 60% “environment.” That arithmetic is too crude. Depending on the design, the residual can include nonshared environmental variance, shared environmental variance, measurement error, unmeasured genetic effects, gene–environment interplay, and departures from model assumptions. Heritability is a model-based estimate, not a complete causal accounting system.
Do different anxiety disorders share genetic risk?
Yes, genetic studies indicate substantial shared liability across anxiety-related phenotypes and with broader internalizing traits. The 2026 major-anxiety GWAS reported genetic relationships across anxiety phenotypes and with traits such as depression and neuroticism. The 2021 genetics review similarly describes shared genetic architecture as an important feature of the field. See the review by Ask and colleagues and the 2026 Nature Genetics study.
Shared genetic liability does not erase diagnostic boundaries. Generalized Anxiety Disorder, Panic Disorder, Social Anxiety Disorder, Specific Phobia, and Separation Anxiety Disorder remain distinct clinical diagnoses even when they share some genetic risk.
The same principle applies to neighboring conditions. Genetic correlation with depression, neuroticism, OCD, PTSD, or other phenotypes does not turn those conditions into subtypes of anxiety disorders. Genetic overlap is evidence about shared liability, not a replacement for clinical classification.
Are some anxiety disorders more heritable than others?
Historical twin estimates differ across disorders, but the precision and evidence base are uneven. Panic disorder and GAD had enough large twin studies for quantitative synthesis in the classic 2001 meta-analysis; other diagnoses often had smaller evidence bases. Modern GWAS frequently pool several anxiety disorders to obtain enough statistical power.
Because the studies use different samples and phenotypes, a ranking of disorders by a single heritability percentage would overstate what the evidence can support. A diagnosis-specific estimate should be interpreted within the exact study design, not used as a universal biological score.
What about anxiety symptoms without an anxiety disorder?
Anxiety symptoms exist on continua in the population, and quantitative traits can be genetically informative. The 2026 generalized-anxiety-symptom GWAS is a good example: it measured symptom severity rather than requiring everyone in the analysis to have a formal diagnosis. The study explicitly analyzed quantitatively measured generalized anxiety symptoms.
A genetic association with anxiety symptoms does not mean that normal anxiety is a disorder. Fear, worry, and physiological arousal can be adaptive responses. Clinical diagnosis depends on a disorder-specific pattern involving factors such as persistence, excessiveness or disproportion, avoidance, distress, impairment, and differential diagnosis.
Can DNA tell which anxiety disorder someone has?
No current genetic test can determine whether a person has GAD, panic disorder, social anxiety disorder, agoraphobia, specific phobia, separation anxiety disorder, or selective mutism. Diagnosis is clinical. It relies on history, the pattern and duration of symptoms, functional impact, context, and exclusion or assessment of relevant medical, substance-related, and psychiatric alternatives.
This is why a family history or high polygenic score cannot substitute for clinical assessment. Genetic data describe susceptibility; diagnosis describes the person’s current or historical clinical syndrome.
Can genetic testing predict who will develop anxiety?
Not with clinically reliable accuracy at present. NIMH states that current genetic tests cannot accurately predict a person’s risk of developing a mental disorder and that it is too early to use such tests to diagnose or treat mental disorders. NIMH’s genetics guidance addresses this directly.
The International Society of Psychiatric Genetics likewise describes polygenic risk scores for major psychiatric disorders as research analyses rather than tools recommended for clinical diagnosis or identifying high-risk individuals. See the ISPG Genetic Testing Statement.
What about direct-to-consumer DNA reports?
A consumer report may present a relative genetic tendency based on a subset of variants, but that should not be interpreted as a diagnosis or a reliable personal forecast. Performance depends on the variants included, the discovery sample, ancestry, phenotype definition, statistical model, and validation. A number that looks precise can still have limited clinical predictive value.
A report also cannot measure the environmental and developmental information needed to understand a person’s actual clinical risk. Family history, current symptoms, life context, medical conditions, medications, substance use, and functional impairment remain separate sources of information.
Does finding risk genes mean researchers know the biological cause?
Not automatically. A genome-wide significant locus identifies a region statistically associated with a phenotype. Mapping that association to a causal variant, causal gene, cell type, developmental period, biological pathway, and clinical mechanism requires additional evidence. Functional genomics can narrow hypotheses, but association alone is not a complete causal chain.
The 2024 and 2026 studies provide far richer biological clues than earlier anxiety GWAS, yet their discoveries remain population-level research findings. The 2024 multi-ancestry study and the 2026 major-anxiety GWAS should be read as advances in genetic architecture and mechanism discovery, not as personalized causal explanations.
What does genetic overlap with depression or neuroticism mean?
Genetic correlation means that some variants influencing one phenotype also statistically influence another. Anxiety, depression, neuroticism, sleep phenotypes, and broader internalizing tendencies can share parts of their genetic architecture. That may help explain why symptoms and diagnoses often co-occur.
Genetic correlation does not mean the phenotypes are identical, and it does not tell which condition is present in an individual. It is a population-level relationship across genetic effects. Clinical distinctions remain necessary because symptom content, course, triggers, impairment, and treatment evidence can differ.
Can trauma or stress cause anxiety despite genetic risk?
Stressful experiences can contribute to anxiety outcomes, but the relationship is probabilistic. Trauma is neither necessary nor sufficient for an anxiety disorder, and many people exposed to severe stress do not develop one. Likewise, people can develop anxiety disorders without identifying a single dramatic precipitating event.
Genetic liability can coexist with environmental triggers and maintaining processes. A person may have elevated susceptibility and then encounter stress, illness, social adversity, or learning experiences that alter the trajectory. Another person with similar inherited liability may never cross a clinical threshold.
Does a genetic component make anxiety harder to treat?
No such conclusion follows from heritability. Heritability says nothing by itself about whether a condition is treatable or whether symptoms can change. MedlinePlus explicitly notes that heritability does not indicate how easy or difficult a trait is to change.
Genetic research may eventually help identify biological subgroups or treatment-response patterns, but routine anxiety treatment is not selected from an anxiety PRS. Evidence-based psychotherapy and medication decisions are based on the specific disorder, severity, comorbidity, medical context, treatment history, patient preferences, adverse-effect considerations, and clinical guidance.
Why estimates differ across studies
Differences in heritability and GWAS results are expected because anxiety is measured in many ways. One study may use structured diagnostic interviews; another may use electronic health records, self-reported lifetime diagnosis, questionnaire scores, broad phobia groupings, or a cross-disorder phenotype. Each design trades precision, sample size, representativeness, and measurement consistency differently.
Age matters because genetic and environmental influences can change across development. Sex composition matters because prevalence and symptom patterns differ. Ancestry matters because genetic architecture is studied through population-specific patterns of variation and linkage. Ascertainment matters because a clinical sample is not equivalent to a general-population cohort.
Consequently, a careful article about anxiety genetics should report what a number actually describes instead of compressing all studies into one headline percentage.
What is established, what is promising, and what remains uncertain?
Established evidence
Anxiety-related phenotypes show meaningful heritability; major anxiety disorders are genetically complex and polygenic; family history is associated with increased risk; common variants collectively contribute to liability; environmental and developmental factors also matter; and current genetic information does not determine an individual diagnosis.
Strong and rapidly developing evidence
Large GWAS now identify dozens of reproducible anxiety-associated loci and increasingly informative biological pathways. Multi-ancestry studies are improving representation, and cross-trait analyses are clarifying shared genetic architecture. The 2024 and 2026 studies substantially expand the molecular evidence base compared with only a few years earlier.
Promising but not clinically mature
Polygenic scores can stratify statistical liability in research samples, and genetic findings may eventually contribute to prevention, mechanism-based therapeutics, or treatment-response prediction. Their current predictive performance and portability are insufficient for routine individual anxiety diagnosis or risk forecasting.
Claims that require caution
Single-gene explanations, deterministic interpretations of family history, consumer PRS presented as diagnosis, one-size-fits-all heritability percentages, and specific candidate-gene-by-stress stories should be treated cautiously. Epigenetic findings are scientifically interesting, but no routine epigenetic test currently diagnoses an anxiety disorder or determines an individual treatment plan.
What should someone do with a family history of anxiety?
Family history can be useful context because it may indicate elevated vulnerability and can help clinicians understand patterns across relatives. It can also motivate earlier attention to persistent avoidance, distress, impairment, or escalating symptoms. It should not be used to label an asymptomatic person as having a disorder.
For a person currently experiencing anxiety, the practical question is not whether the symptoms are “genetic enough.” The relevant questions are what symptoms are present, how persistent and impairing they are, what situations or thoughts organize the fear or worry, whether another medical or psychiatric condition needs consideration, and what evidence-based interventions fit the actual presentation.
Clinical boundaries: genetics does not collapse distinct diagnoses into one disorder
Genetic overlap is compatible with clinical differentiation. Broad worry in GAD, recurrent unexpected panic attacks in panic disorder, fear of negative evaluation in social anxiety disorder, circumscribed fear in specific phobia, and separation-focused fear in separation anxiety disorder are not interchangeable simply because their genetic liabilities overlap.
This is also why OCD, PTSD and trauma-related disorders, illness anxiety, attachment anxiety, neuroticism, and historical anxiety neurosis should not be reclassified as anxiety-disorder subtypes on the basis of shared genetic correlations or symptom overlap. Genetic research studies dimensions that cross diagnostic borders; clinical classification still assigns different canonical territories.
Frequently asked questions
Are anxiety disorders genetic or environmental?
Both genetic and environmental factors contribute. The most accurate model is multifactorial: many small genetic effects interact with development, learning, stress, family and social context, and other environmental influences.
Is anxiety hereditary?
Anxiety-related liability can be inherited, and anxiety disorders can cluster in families. But inheritance is polygenic and probabilistic, not a simple parent-to-child transmission pattern.
What percentage of anxiety is genetic?
There is no single percentage for all anxiety. Twin estimates for particular disorders have often been moderate, while SNP-based estimates vary by phenotype and method. A percentage describes variation in a studied population, not how much of one person’s anxiety came from genes.
Is there an anxiety gene?
No single gene explains the common anxiety disorders. Large GWAS identify many associated loci, each generally contributing a small amount to risk within a highly polygenic architecture.
Can anxiety skip a generation?
Because common anxiety liability is polygenic and influenced by environment, it does not follow the simple inheritance patterns implied by “skipping a generation.” Relatives can differ substantially in both genetic combinations and life experience.
If both parents have anxiety disorders, will their child develop anxiety?
Risk may be higher in families with more affected relatives, but there is no deterministic outcome. A child’s risk reflects a unique genetic combination plus developmental and environmental factors, and a family history is not a diagnosis.
Can a genetic test diagnose anxiety?
No. Current genetic tests and polygenic scores cannot diagnose anxiety disorders. Diagnosis requires clinical assessment of symptoms, duration, impairment, context, and relevant differential diagnoses.
Can a polygenic score predict my future anxiety?
Current anxiety polygenic scores can show statistical associations in research samples but explain only a limited proportion of individual variation. Professional psychiatric-genetics guidance does not recommend them for routine diagnosis or individual risk identification.
Does family history mean my anxiety is genetic?
Not by itself. Family clustering can reflect genes, shared and nonshared environments, modeling and learning, correlated stressors, and interactions among these factors.
Can someone have an anxiety disorder with no family history?
Yes. The absence of a known family history does not rule out genetic susceptibility or an anxiety disorder, and the presence of family history does not establish one.
Does being genetically vulnerable mean anxiety is permanent?
No. Heritability does not determine course or treatability. Symptoms and functioning can change substantially over time, including with effective psychological or pharmacological treatment when clinically appropriate.
Related Articles
References
Ask, H., Cheesman, R., Jami, E. S., et al. (2021). Genetic contributions to anxiety disorders: where we are and where we are heading. Psychological Medicine, 51(13), 2231–2246. PubMed
Eley, T. C., McAdams, T. A., Rijsdijk, F. V., et al. (2015). The intergenerational transmission of anxiety: a children-of-twins study. American Journal of Psychiatry, 172(7), 630–637. PubMed
Friligkou, E., Løkhammer, S., Cabrera-Mendoza, B., et al. (2024). Gene discovery and biological insights into anxiety disorders from a large-scale multi-ancestry genome-wide association study. Nature Genetics, 56, 2036–2045. doi:10.1038/s41588-024-01908-2
Hettema, J. M., Neale, M. C., & Kendler, K. S. (2001). A review and meta-analysis of the genetic epidemiology of anxiety disorders. American Journal of Psychiatry, 158(10), 1568–1578. PubMed
International Society of Psychiatric Genetics. Genetic Testing Statement. Official statement
MedlinePlus Genetics. What does it mean to have a genetic predisposition to a disease? MedlinePlus
MedlinePlus Genetics. What is heritability? MedlinePlus
National Institute of Mental Health. Anxiety Disorders. NIMH
National Institute of Mental Health. Looking at My Genes: What Can They Tell Me About My Mental Health? NIMH
Purves, K. L., Coleman, J. R. I., Meier, S. M., et al. (2020). A major role for common genetic variation in anxiety disorders. Molecular Psychiatry, 25(12), 3292–3303. PubMed
Sharma, S., Powers, A., Bradley, B., & Ressler, K. J. (2016). Gene × Environment determinants of stress- and anxiety-related disorders. Annual Review of Psychology, 67, 239–261. PubMed
Skelton, M., et al. (2026). Genome-wide meta-analysis of quantitatively measured generalized anxiety symptoms in individuals of European ancestry. Nature Human Behaviour, 10, 1594–1608. doi:10.1038/s41562-026-02476-7
Strom, N. I., Verhulst, B., Bacanu, S. A., et al. (2026). Genome-wide association study of major anxiety disorders in 122,341 European-ancestry cases identifies 58 loci and highlights GABAergic signaling. Nature Genetics, 58, 275–288. doi:10.1038/s41588-025-02485-8
Uher, R., Pavlova, B., Radua, J., et al. (2023). Transdiagnostic risk of mental disorders in offspring of affected parents: a meta-analysis of family high-risk and registry studies. World Psychiatry, 22(3), 433–448. PubMed