The figures are high: for example, studies indicate that someone with obsessive compulsive disorder (OCD) is as many as four times more likely to have another family member with OCD than someone who does not.
The authors argue that the over-activity of the brain circuits involved in the anxiety response is inherited from parents and that this over-activity may then render a person vulnerable to developing anxiety later on. They found that three areas of the brain situated in the cerebellum or brain stem were implicated in hereditary mental ill-health. They found that the amygdala, the limbic system and the prefrontal cortex were all involved.
Specific nerve cell pathways dysfunction can also be inherited and this has been linked to the development of anxiety: if the pathways that connect particular brain regions do not function efficiently then problems related to mood or anxiety may result. This may manifest itself by affecting how people regulate their emotional reactions to potentially threatening stimuli.
Twin studies have illustrated the heredity of anxiety quite well. One study, for example, investigated identical (monozygotic) and non-identical (dizygotic) twins. The frequency of anxiety disorders was twice as high in identical twins as in non-identical twins. Anxiety disorders with co-morbid panic attacks were in excess of five times more frequent in identical twins as in non-identical twins.
So we can see that there is good evidence in support of the notion that there are genetic vulnerabilities for anxiety-proneness that are passed on biologically from one generation to the next. What is inherited though, is not the necessarily the propensity to develop the anxiety disorder per se but more the likelihood to inherit the temperament or personality traits that predispose the condition. There are a number of personality traits associated with increased likelihood of anxiety: overthinking; perfectionism; resistance to change/being open to experience; being highly empathic; a tendency to irritability and neuroticism; vivid imagination; and an avoidant temperament. In addition, studies exploring personality types have found that the Type D “distressed” personality (the tendency to experience both negative affect and social inhibition, leading to a high level of emotional distress that is consciously suppressed) is strongly associated with increased incidence of anxiety.
“Neuroticism” is one such trait proposed by personality theorists to render people more likely to develop an anxiety disorder. Neuroticism is a term used to describe someone's emotional stability and their tendency to be more perturbed emotionally by things that don't affect other people. In anxiety disorders, it is thought that a highly-neurotic person panics, and then learns to avoid anything which leads to panic again. In a sense, they become attuned to avoiding feeling fearful and therefore restrict their engagement in everyday life accordingly.
Neuroticism has been purported to be heritable. Twin studies suggest that 40 percent of the trait variance for neuroticism is heritable A recent study, which was the largest genetic study of a personality trait so far undertaken, found that neuroticism could be linked to nine new distinct gene-associations so argue there is a clear neuro-biological basis for a personality trait that seems to have a considerable impact upon people's health and well-being.
Heredity and genetics are slightly different, however. The key difference is that a hereditary disease can be passed through generations; whereas a genetic disease, may or may not be hereditary, but it is as a result of a change in an organism's genome. For example, epigenes are inheritable and are receptive to environmental influences, This is has been shown in studies of identical twins who despite having the same genes develop epigenetic variations. Studies show that stress can be transmitted trans-generationally through epigenetic changes. For example, glucocorticoid receptors (GCR) are involved in stress hormone regulation and research has found that peri-natal depression results in methylated GRC genes (methylation is an epigenetic change where genes are silenced). In infants, increases in methylation have been seen to cause an excessive release of stress hormones at stressful times. These changes occurred in response to maternal stress and persisted into adolescence.
So whilst there is strong evidence that the brain function that underpins anxiety may be inherited, there is still considerable scope for experience and environment to reduce the risk of developing a disorder. Individuals may inherit the predisposition to respond in a particular way to life events, as has been argued with neuroticism.
How are parenting traits and childhood experience connected to the development of anxiety?
However, acquisition of an anxiety disorder is often due to family dynamics or “scripts” that become learned behavior; this might include the failure to learn effective coping strategies; the prevalence of associated personality traits in parents or overprotective parental behaviors, for example. Parenting traits such as being overly controlling, emotionally cold or rejecting, and overprotection are known to be associated with anxiety; and parental practices involving these traits alongside neglect, lack of affection, anxious parenting, lack of sensitivity, being restrictive, isolating children socially, being critical, employing shame tactics, being overly rigid and preoccupied with the opinions of others are all implicated in the development of later anxiety disorders. All of this creates a climate that increases the likelihood of a child growing up and becoming anxious. For example, one study found that contrary to accepted notions of stress in pregnancy leading to anxiety in children, prenatal stress and offspring anxiety was more strongly associated with current maternal anxiety/depression rather than prenatal stress. All of this influences the attachment style, which is a strong family factor associated with anxiety. Attachment patterns can also be seen across families, so in a sense, this can also be “inherited”.
Interestingly, childhood is a time where early signs present themselves and where, it is argued, we need to be the most proactive. Specific phobias often tend to present in childhood or can at least be traced back to that time and often persist into adulthood. Early life trauma is a key risk factor for a number of mental health issues, including anxiety; and adolescents who self-harm are at a higher risk for an anxiety diagnosis by young adulthood.
Environments that are more conducive to a child being anxious and thus becoming an anxious adult are an important factor. Previous studies have found that physical, emotional and sexual abuse alongside other childhood adverse experiences are strongly associated with the development of both post-traumatic stress disorder and social anxiety disorder.
Other large-scale meta-analyses have found that early emotional trauma is a risk factor for panic, generalized anxiety, and social anxiety disorders in later life. Children who experience trauma appear to be more likely to have high levels of trait anxiety (the tendency to experience, focus upon, and report negative emotions such as fears, worries, and anxiety across many situations, especially those in which most people do not experience such responses) and anxiety sensitivity (fears of anxiety-related symptoms).
Trauma also has an impact upon the neural pathways associated with fear which creates a framework conductive to anxiety in later life. Neural imaging has shown differences in various parts of the brain when exposed to trauma: such as lasting changes in the volume of certain areas as well as increased and/or decreased functions in others. Studies show altered circuitry in many areas, but the amygdala, hippocampus, and prefrontal cortex seem to be particularly involved in the stress response; as do neuro-chemicals such as cortisol and norepinephrine.