There’s a time and a place for fear in human evolution. Namely, it’s a survival trait that allows us to detect and flee from life-threatening situations. Experiencing fear is healthy, as it trains us to make safer decisions. However, it can become unhealthy when fear rises continuously and unnecessarily in non-life-threatening situations, as is the case for many people suffering from anxiety, PTSD, and similar disorders.
Any thought or behavior that repeats strengthens our neural pathways, and the repeated rise in fear is no different. It triggers our fight or flight response repeatedly until it becomes neurologically ingrained, creating a vicious cycle in which harmless stimuli can elicit panic.
While some people are more prone to fear than others, new research from Sweden has illuminated the underlying mechanism (a protein and enzyme) in the brain, which might explain why. This new study gives greater insight into various anxiety-related disorders, fear, and alcohol dependency.
Scientists already know that during fear responses in the brain, the amygdala in the brain is connected to the frontal lobes through a pathway of nerve cells. This pathway is disrupted in individuals with various anxiety disorders. Now, scientists are trying to uncover the exact molecular mechanisms that take place during fear responses.
This study examined PRDM2, a protein, and epigenetic enzyme. Epigenetic, meaning it responds to the environment. PRDM2 can change or suppress the way many genes are expressed. Scientists have seen that PRDM2 levels are lower in people who experience alcohol dependence, which can cause more heightened reactions to stress. Research suggests that similar mechanisms are involved in people with anxiety as well.
How does fear get stuck? The brain “remembers” fear.
Memories are created and remembered through “consolidation,” a process that allows new memories to be saved and stored long-term. It can affect this process when PRDM2 levels are lowered, as is the case with anxiety, alcohol dependency or PTSD.
“We have identified a mechanism in which increased activity in the network between the frontal lobes and the amygdala increases learned fear reactions. We show that down-regulation of PRDM2 increases the consolidation of fear-related memories.”- Estelle Barbier, assistant professor in the Center for Social and Affective Neuroscience (CSAN), and the Department of Biomedical and Clinical Sciences (BKV) at Linköping University.
Because reduced PRDM2 plays a role in anxiety and alcohol dependency, it may explain why some individuals are more prone to these conditions (which are often seen together). Currently, there are no tools or mechanisms for increasing PRDM2; therefore, Estelle Barbier, who led the study, says individuals with anxiety disorders may see great results from therapies that “weaken or erase fear memories,” such as EMDR or hypnotherapy.