Deconstructing the Fear Response: Genetic and Environmental Factors

 

That fear is one of our most innate reactions is hardly a point of dissention. Thought to be rooted in the brain’s amygdala, fear responses are nearly ubiquitous amongst animal species, and are often associated with elevated heart rate, anxious behavior, freezing and avoidance responses, and the release of stress hormones. Allowing an organism to flee from predators, avoid unwanted confrontation, and cope with stressful situations, the role of fear in the survival of humans, and arguably nearly all species, has been evolutionarily crucial.

In his novel, The Agile Gene, Matt Ridley comes to a discussion of this inherent fear response, and the apparent predispositions that accompany it. In line with Seligman’s 1960s concept of “prepared learning,” fear responses elicited by monkeys in a laboratory were demonstrated to be induced more easily when the animals were presented with a snake, as opposed to a flower. When shown videotapes of other monkeys reacting with fear to a snake, the laboratory monkeys began to elicit the same response. In contrast, watching videos of monkeys reacting fearfully to a flower failed to garner similar behavior. The conclusion of the study, repeated many times over, using different subjects and fear-inducing variables, was that in learning, there is a substantial role for instinct.

At first glance, this concept appears almost intuitive. Prehistorically, the instinctive avoidance to things such as snakes and predators would undoubtedly be an evolutionary advantage, and those individuals exhibiting a fear response to such threats would more likely go on to propagate the species, compared to animals who did not fear or attempt to avoid dangerous stimuli. The argument here then, is for a sort of “fear gene” in which aversion to specific stimuli is transferred.

It is generally agreed upon that psychological disorders involving panic attacks and other major anxiety disorders are heritable to some extent (Morris-Rosendahl, 2002) as well, furthering the case for a genetically based (at least in part) fear response. As discussed by Morris-Rosendahl (2002),

Extensive genetic studies of the serotonin (5-hydroxytryptamine, 5-HT) transporter (5-HTT) gene have revealed how variation in gene expression can be correlated with anxiety phenotypes. Complete genome-wide linkage scans for panic disorder (PD) susceptibility genes have suggested a locus on chromosome arm 7p, and association studies have highlighted many candidate genes. A highly significant association between phobias, panic disorder, and a duplication at chromosomal region 15q24-26 is one of the most exciting findings to date.

While fear appears to have been an instinctive, evolutionarily advantageous response, the unwarranted and abnormal elicitation of the response in fear disorders is more perplexing.

In assuming that genetics play distinct role in the elicitation of fear – both normal and abnormal – we come a roadblock: cognitive resolution of abnormal fear responses. To expand this concept, consider the example of an individual suffering from intense panic disorder, in which debilitating panic attacks are experienced several times per day, for no identifiable reason. Medications have proven unsuccessful, as has psychotherapy. The only solution, in fact, is that the individual carries in his pocket a container of beta-blockers. Never needing to consume the drug, the individual’s symptoms are managed simply by the presence of the bottle.

How does the changing of a single environmental factor lead to the resolution of what we believe to be an instinctive response? Even more broadly, we know that for many individuals suffering from anxiety disorders, psychotherapy does have a substantial benefit. How do we reconcile the apparent genetic basis for fear and avoidance responses, with the simultaneous resolution of these responses, simply through altering the ways in which we think?

Ridley’s book is largely concerned with the argument that nature and nurture are not independent influences on the individual, but rather, act in concert to direct genetic expression. Timing and regulation of genes, he argues, results from environmental influence, and so nature acts via nurture. It appears safe to believe that even in acknowledging a genetic role for fear, there is a substantial opening left for the influence of environment. In the context of anxiety disorders, this possibility has been explored, with some findings suggesting interactions between genes and family dynamics, and even an interaction between caffeine-induced anxiety and gene polymorphism associated with anxiety (Hae-Ran, 2011).

Is it possible then, that treatments involving psychotherapy act to alter gene expression in ways we have yet to consider, as if therapy itself acts as a separate environmental factor by which genes are manipulated? For years, psychotherapists have worked to help individuals suffering from anxiety disorders to effectively manage their symptoms, with varying success. If greater resolution of symptoms could be tied to genetic manipulation and regulation, could a more effective treatment be on the horizon?

Psychotherapy has been shown to produce changes in genetic expression in diseases with more strongly linked to gene dysregulation. In a lifetime intervention study of men with prostate cancer who had declined immediate surgery, hormonal therapy, or radiation, therapy including stress-reduction techniques produced changes in expression of 501 genes, compared to pre-intervention expression (Ornish et al., 2008). While less is known about the genetic basis for anxiety and fear, could psychotherapy be working similarly? That the instinctive fear response is based is evolutionary biology is difficult to deny, and a mounting body of evidence points to genetic factors underlying the abnormal elicitation of anxiety. As we continue to discover more about the expression of genes implicated in anxiety disorders, might more targeted psychotherapeutic and genetic interventions be on the horizon?

 

References

 

Na HR , Kang EH , Lee JH , Yu BH . The genetic basis of panic disorder. J Korean Med Sci 2011;26: 701–710.

Ornish, D., Magbanua, M. J. M., Weidner, G., Weinberg, V., Kemp, C., Green, C., &Carroll, P. R. (2008). Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proceedings of the National Academy of Sciences, USA105, 8369–8374.

Schaffhausen, J. (2005) Fear Conditioning: How the Brain Learns about Danger. Joanna Schaffhausen, Motivation & Emotion, Brain Connection.

Ridley, M. (2003). The Agile Gene. New York, NY: Harper Collins Publishers Inc.

Morris-Rosendahl, D. J. (2002). Are there anxious genes? . Dialogues in Clinical Neuroscience4(3), 251–260.

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