Die Genetik beeinflusst die anhaltende Angst bei jungen Erwachsenen nachdrücklich, wie eine neue Twin -Studie. Die Ergebnisse zeigen, dass rund 60% der Angststabilität im Alter von 23 bis 26 Jahren durch die Genetik erklärt werden können. Umwelterlebnisse scheinen eine größere Rolle bei kurzfristigen Höhen und Tiefen der Angst im Laufe der Zeit zu spielen.
Genetics strongly influence persistent anxiety in young adults, new twin study suggests
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I’ve linked to the news release in the post above. In this comment, for those interested, here’s the link to the peer reviewed journal article:
https://www.cambridge.org/core/journals/psychological-medicine/article/heritability-of-generalized-anxiety-stability-a-longitudinal-twin-study-among-young-adults/45F5A148AEBCDF7989DCA36D1102AF3B
From the linked article:
**Genetics strongly influence persistent anxiety in young adults, new twin study suggests**
A large twin study suggests that while generalized anxiety symptoms often fluctuate from year to year during early adulthood, there is a stable core to these symptoms that is strongly shaped by genetic factors. **The findings, published in Psychological Medicine, indicate that around 60% of the stability in anxiety from ages 23 to 26 can be explained by genetic influences. Meanwhile, environmental experiences appeared to play a bigger role in the short-term ups and downs of anxiety over time.**
The research also provides evidence that anxiety in young adulthood tends to cluster into two distinct dimensions: physical distress and a pattern involving excessive worry and avoidance. Interestingly, the two symptom dimensions were found to share much of their genetic basis, even though they differed somewhat in how environmental influences shaped them.
Heritability is a measure used in genetics to estimate the proportion of variation in a trait—like anxiety—that can be attributed to inherited genetic differences between people. A heritability estimate of 60%, for example, does not mean that a person’s anxiety is 60% determined by their genes. Instead, it means that, across a population, 60% of the variation in a given trait can be linked to genetic differences.
Great, so genetics are responsible for baseline anxiety and things like trauma are really going to ramp things up.
This uses twins data, I’m wondering if they controlled for similar environments? I read that the dataset they used accounted for this by using monozygotic vs dizygotic twins, but if I recall literature has come out showing that monozygotic twins may also get treated similarly from the environment (how other people interact with them, how they are treated, etc) from how similar they look and are genetically. I could be wrong about this, and if so someone more knowledgeable in genetics can correct me, but skimming through this paper I didn’t find if they tried to control for the similar treatment dizygotic twins would get over monozygotic.
Did they do something like paying special attention to specific monozygotic or dizygotic twins that were separated at or near birth to account for how these results hold for people in very different environments? I couldn’t find anything like that in this paper, but it’s certainly possible.
Rachel Yehuda’s work shows that what looks like “genetic stability” in anxiety often reflects **heritable stress biology** rather than fixed DNA sequence.
Trauma exposure alters methylation on stress-related genes like **NR3C1** (glucocorticoid receptor) and **FKBP5**, both of which regulate cortisol output. These changes have been documented in Holocaust survivors, veterans, and even their children, meaning the biology of stress sensitivity itself can be passed down.
Cortisol drives a **glutamate cascade to neurons**, which raises baseline excitability. That cascade links directly to insomnia and REM sleep disorder, persistent muscle tone, tremor, and even cramping and spasticity. In other words, what twin studies call “genetic stability of anxiety” is often the inherited wiring of the stress–cortisol–glutamate pathway.