Anxiety Can Run in Families — But Why Does It Change Over Time?

Stability and change are not the same question

A single anxiety score mixes together several things: a person’s longer-term tendency, what is happening at that moment, measurement noise and the specific symptom scale used. Repeated measurements allow researchers to ask which part is stable and which part changes.

Twin models can then estimate how much of the variation in those stable and changing components is statistically associated with genetic, shared-environmental and nonshared-environmental differences. Those estimates describe variation in a population — not the cause of one person’s anxiety.

Six waves in young adulthood: genes explained much of continuity, environment more of change

A 2025 study used 6,429 twin pairs from the Twins Early Development Study and measured generalized anxiety at six waves between ages 23 and 26.

Heritability at individual waves was estimated at about 39–46%, while the latent factor representing stable generalized anxiety across waves was about 60% heritable. Genetic factors largely accounted for continuity, whereas environmental factors contributed more to changes in symptom severity.

The important interpretation is not that “60% of anxiety is genetic”. The stable factor is a model-derived population construct built from repeated measurements. It is specifically designed to isolate continuity and reduce occasion-specific variation.

Even the symptom structure matters

The same 2025 study found evidence for two generalized-anxiety dimensions: worry-avoidance and somatic-distress symptoms. Their genetic correlations were higher than their environmental correlations.

That matters because two people can have similar total anxiety scores for different symptom reasons. Genetic and environmental estimates depend on exactly what researchers measure and how symptom dimensions are combined.

Broader distress shows a similar stability-versus-change pattern — with an important caveat

Another 2025 study followed 2,279 Australian twins up to six times from adolescence into adulthood. Its outcome was broader psychological distress rather than generalized anxiety alone.

The best-fitting model showed largely stable additive-genetic influences across ages 12–35, with smaller age-specific genetic effects and predominantly transient environmental influences. This supports the broader idea that continuity and short-term change can have different etiological patterns.

But broader psychological distress combined anxiety- and depression-related symptoms. It should not be presented as if it replicated a generalized-anxiety estimate.

The 2026 adult study complicates the simple story in a useful way

A 2026 Journal of Affective Disorders study analysed 4,854 twins from the Washington State Twin Registry who completed seven measurements of anxious symptoms during the COVID-19 pandemic.

The researchers separated trait-like and state-like anxiety and examined early, middle and late adulthood. Nonshared environmental variance in the state component accounted for the largest share in early and late adulthood, while genetic variance in the trait component was larger in middle adulthood.

Those percentages should not be exported as universal age rules. The data were collected during an unusual historical period, and the model describes that sample and measurement context. The main lesson is that the balance between stable and changing components can itself vary across adulthood.

Different anxiety phenotypes do not share one heritability number

A meta-analysis of 13 twin cohorts and 42,585 participants examined social anxiety disorder and social-anxiety symptoms. Genetic and nonshared environmental influences explained much of the variation, but the relative genetic contribution was lower in adults than in younger groups.

An older broad meta-analysis also found familial and genetic contributions across several anxiety disorders, including generalized anxiety and panic disorder, while nonshared environmental influence remained important. These sources are useful context, not permission to collapse panic, social anxiety, generalized anxiety and other phenotypes into one number.

Why change does not prove a purely environmental cause

When symptom severity changes after a life event, it is tempting to say the environment caused the change. Longitudinal twin models show that nonshared environmental variance often contributes to change, but they do not identify every specific causal exposure.

Measurement error is also part of nonshared environmental variance in classical twin models unless modeled separately. New genetic effects can emerge at particular ages as well. “Change” therefore should not be translated into “environment alone”.

Why genetic continuity does not mean treatment resistance

A stable genetic contribution tells us something about the statistical sources of persistent differences between people. It does not tell us that symptoms cannot improve or that treatment cannot work.

Heritability and treatment response answer different questions. A trait can be highly heritable and still respond to psychological, social or medical intervention. TwinPare Research should keep that distinction explicit rather than turning genetic influence into fatalism.

The TwinPare boundary

TwinPare Research can explain the difference between stable and changing symptom components, population heritability and individual experience. It can also explain why repeated measurements are more informative than one isolated score.

TwinPare Health & Fitness should not diagnose generalized anxiety disorder or another anxiety condition from HRV, sleep, activity, questionnaires or behavioral patterns, and it should not calculate a genetic anxiety percentage. Persistent or impairing anxiety, panic symptoms or safety concerns require appropriate professional assessment.