Worrying is a feeling that all of us experience time to time, especially, when we face stressful events. However, some people are born to worry. You may ask: “How does it come?” The answer to this question has been received by the late 1990, when a group of scientists at the Canadian Institute for Advanced Research had found a robust relationship between early adversity and lifelong anxiety and perceived stress. This finding inspired Dr. Meaney, a professor at McGill University, to explain how stress can change the very way our genes function. He had been studying the phenomenon called stress dysregulation (SDR) among rodents. SDR appeared when rodents were overactive to stressors and stayed in a stressed-out state even after the stressor was removed. Investigating this issue, he found that rodents who had been deprived of maternal nurturing demonstrated not only physiological differences but also modified behavioural patterns.
The biological explanations of these findings were found in the growing field of epigenetics. Up to our days, the scientists who are working in this area are studying an epigenetic change to genes that control the stress system in terms of normal fetal development. Epigenetic specialists argue that normal fetal development plays a major role in response to physical input life span through controlling how and when genes work. Taking into consideration this idea, Dr. Meaney wandered whether it was possible to explain early nurturing as a sort of social experience could have a similar effect in understanding stress dysregulation.
If you remember, I have already talked about the stress response system. Just recall, that when you face a threat, your stress response system arouses or extinguishes in proportion to threats. If you face a fearful situation, the system releases more cortisol making your body to prepare for a “fight-or-flight” response. When the fearful situation disappears, the level of cortisol reaches the baseline. The same biological process should have been happening among new born rats in Dr. Meaney’s study. However, when those rodents started experiencing stress at a high level due to poor maternal nurturance or lack of it, something prevented to normalize the level of cortisol. A similar process is known as “stress methylation”, when an external factor like extreme childhood stress without comfort might cause an epigenetic change.
Methylation is a group of specific chemical molecules that is attached to a so-called “switch on-off” button that exists in every gene. Thus, in Dr. Meaney’s study, “stress methylation” the gene, whose job is to tell hypothalamic–pituitary–adrenal axis (HPA axis) – a system involved in controlling the body’s stress response in regulating the levels of cortisol – stays silent. High levels of stress exposed in early life can switch off the key gene that controls this stress system. When it happens, the live organism is functioning as it is constantly facing a threatening situation. In other words, the body stays in a worrying state.
Combining the ideas from epigenetics and findings from investigations of the SDR, Daniel P. Keating concluded that stress can change the very way our genes function. Applying his inferences to investigating low socioeconomic status as a marker of early life adversity, he discovered that this epigenetic change, which does not affect the DNA at all, can be passed down to the next generation. “This remarkable finding means that the social experience of early adversity can make a change that becomes part of our biology—and part of our biological inheritance: nurture becoming nature” (Keating, 2017, p. 36).
The information is based on Keating’s (2017) book Born Anxious: The Lifelong Impact of Early Life Adversity—and How to Break the Cycle.
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