On account of Covid-19: Depressogenic events, “vulnerability” and pharmaceutical treatment

A large amount of research on test animal subjects and observation research, has a great deal to tell us about the association between adverse / stress-triggering events and the onset of psychopathology (Holmes & Wellman, 2009). An unfortunate result of the Covid-19 era and the dramatic changes it has brought to our lives lies is the fact that many people are experiencing a period of anxiety and sadness unlike any other experienced during their lifetime. This short article intends to provide an informed and research-based comment on the so-called “vulnerability for psychopathology” and we hope that it will be of help to those who are currently dealing with symptoms of anxiety or depression.

According to research, and independently of Covid-19 and the situation at present, adverse  life events that are likely to greatly increase the possibility of psychopathology symptoms, are such as the death of a child or other loved one, miscarriages or other life-threatening events, including a person’s inability to receive the proper or adequate treatment for a life-threatening illness, being physically attacked or having fallen victim to a disaster (e.g. losing one’s home and/or having one’s life put at risk due to flooding, fire, etc.) or even being laid off from work or subjected to pay cuts (Kendler, Karkowski& Prescott, 1999; Phillips, Carroll & Der, 2015).

On the other hand, it has been suggested that not all people develop a psychopathology on account of one or more adverse events and that this vulnerability may be pre-existing, or even genetic (Zubin & Spring, 1977). However, the research on this subject aims at the better understanding of a psychopathological illness for purposes of finding better medicine. In other words, the goal of this type of research is not to separate people into “genetically vulnerable” and “non- or less-genetically vulnerable”.

Furthermore, besides the above mentioned frequent misunderstanding regarding the goal of genetic research, this type of research is essentially epigenetic due to the fact the human DNA is in constant interaction with the environment (Shadrina, Bondarenko&Slominsky, 2018). In addition, it has been discovered that alterations found in the cerebral architecture of people with a psychiatric diagnosis – what is often referred to as “reduced brain cells” – are also a common finding in persons with no psychiatric diagnosis who follow a sedentary lifestyle and/or experience periods of chronic stress and/or they are smokers and/or consume alcohol (Zipursky, Reilly, Murray, 2012). Strictly speaking, any of the above factors separately constitutes a risk factor for the onset of reduced brain cells. Similar results have been also reported in research on test subjects (Bowirrat et al., 2010; Czeh&Lucassen, 2007).

In any case, however, what this short article intends to emphasize is that the famous so-called “stress vulnerability” (Zubin & Spring, 1977), which postulates that when a person manifests psychopathology, this is elicited by stress-triggering events that bring to the surface a pre-existing vulnerability to stress, is actually a research hypothesis and not a finding in itself. The bottom line is that research examines the extent to which this hypothesis is true and currently, this particular question-hypothesis has not been answered at a genetic level. Methodologically speaking, research is currently incapable of providing such answer and, as mentioned before, the goal of such research is to better understand psychiatric illnesses or symptoms in order to produce better medicines, and not target and put labels on people.

Should I or shouldn’t I take medicine?

Regardless of the fact that you mustn’t bother yourselves whether your current need to take medicine against stress, depression or psychotic symptoms is genetically-motivated or not, do not let your body suffer. If your stress or mood affects your everyday life, sleep and nutrition, and by extension, your communication and decisions, do not hesitate to ask for help and receive pharmaceutical treatment. Observe your body’s reactions and inform your physician, in order to jointly regulate your treatment regime in a way that will be effective.

> If you notice the development of persisting anxiety, depression or stress, reduced physical energy, intense physical fatigue, insomnia or hypersomnia, or neglect of personal activities or personal hygiene, do not feel embarrassed and try to ask for help from a psychiatrist as soon as possible.

 > When taking medicine, do not hesitate to report to your physician your remarks and observations about the pharmaceutical treatment, in order to readjust your pharmaceutical treatment in a way that won’t cause you side effects.

Why recommend medicinal treatment? Medicinal treatment is recommended because when someone suffers intense dysphoria due to symptoms of anxiety and sadness, it is almost certain that this will affect the quality of that person’s sleep and diet. At the same time, sleep and diet disorders are directly associated with the onset and persistence of anxiety and sadness symptoms, thus establishing a vicious cycle. For more information on the correlation between sleep and diet with stress and depression click here. Apostolia Alizioti, B.Sc. (Psychol), M.Sc. (Health Psychol), M.B.A., GBC member of the British Psychological Society.

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References

Bowirrat, A., Chen, T. J., Blum, K., Madigan, M., Bailey, J., Chen, A. L., … Gold, M. (2010). Neuro-psychopharmacogenetics and neurological antecedents of posttraumatic stress disorder: unlocking the mysteries of resilience and vulnerability. Current Neuropharmacology, 8(4), 335-358. doi: 10.2174/157015910793358123

Czeh, B., & Lucassen, P. J. (2007). What causes the hippocampal volume decrease in depression? Are neurogenesis, glial changes and apoptosis implicated? European Archives of Psychiatry and Clinical Neuroscience, 257(5), 250-260. doi: 10.1007/s00406-007-0728-0s

Holmes, A. & Wellman, C. L. (1977). Stress-induced prefrontal reorganization and executive dysfunction in rodents. Neuroscience and Biobehavioral Reviews, 33, 773 -783. doi:10.1016/j.neubiorev.2008.11.005

Kendler, K. S., Karkowski, L. M., & Prescott, C. A. (1999). Causal relationship between stressful life events and the Onset of Major Depression. Am J Psychiatry, 156, 837–841. doi: 10.1176/ajp.156.6.837

Zipursky, R. B., Reilly, T., & Murray, R. M. (2012). The myth of schizophrenia as a progressive brain disease. Schizophrenia Bulletin, 39(6), 1363-1372. doi: 10.1093/schbul/sbs135

Zubin, J. & Spring B. (1977). Vulnerability – A new model of schizophrenia.  Journal of Abnormal Psychology, 88 (2), 103-126. Retrieved from: https://www.ncbi.nlm.nih.gov

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