Life needs stimulation. However, overstimulation can cause exhaustion and illness. During specific sensitive periods early in life, stress can even affect later mental health. Accumulating evidence points towards an important role of epigenetic mechanisms in the mediation of these long-term effects. But researcher struggle to find a clear connection between early life experiences and later mental health disparities.
Vanessa Lux, research fellow at the Department of Genetic Psychology, Ruhr Universität Bochum (RUB), now proposes that the observed epigenetic programming effects are not the result of an overstimulated stress system alone. "Most researchers looked at the stress system. Our dual-activation hypothesis proposes that in addition to the stress system the sensory systems also contribute to epigenetic changes. According to our model, glucocorticoids prime the epigenetic machinery for change while neural activation coordinates the programming mechanisms," says Lux. But this neural activation is not only present in stress related networks. Lux argues that when a stressor is perceived, the sensory networks are also activated and may also be involved in epigenetic modifications.
Dr. Lux summarized the existing evidence for her model in a thematic review that was recently published online in Current Genomics (Volume 19, 2018). The review shows that early life stress modifies epigenetic regulation of stress related genes through two pathways - neural activity and glucocorticoid exposure - and that the stress also impacts how the sensory systems develop. "This is not really a surprise. Stress is perceived through the senses. The more difficult question is, what epigenetic modifications are established in the sensory networks by the stressors and how this impacts mental health later in life", Dr. Lux says.
Currently, researchers have not paid much attention to the epigenetic modifications in the sensory networks. And this despite the fact, that the period early in life, which researchers think is the most vulnerable for the impact of stress on later mental health, is also a sensitive period of sensory development. Dr. Lux wants to change this: "We just started a series of experiments at the RUB to investigate the related epigenetic mechanisms. With our dual-activation hypothesis, we assume that the interplay between epigenetic programming effects in stress-related and in sensory networks contributes to the diverse symptomatology we see in mental health patients who experienced early life stress. The effects on the sensory networks should therefore be included in bottom-up characterizations of clinical diagnoses."
The research might also inspire new treatments for stress induced sensory dysfunctions such as tinnitus, hearing loss, visual impairment, or loss of sight. But other mental health patients will also profit. As Lux points out in her paper, people with severe mental illness often experience sensory dysfunctions. Knowing that there is a molecular link between the sensory systems and the stress system would encourage healthcare practitioners to take these sensory dysfunctions more seriously in their clients and consider appropriate therapeutic measures. At the end, a deeper insight into how our senses connect with the stress system would teach us all to better distinguish between healthy stimulation and where the stress begins, and address the resulting health problems more effectively.