COVID-19 ‘s Impact on Environmental Drivers on the Genetics of Depression and Mental Illness
By Wendy Finkelstein PA-C, Owner of Nephesh Enlightened Health and Functional Medicine
Mental Health is becoming a hot topic due to the COVID-19 pandemic. Society at large is experiencing the effects of isolation, self-quarantine, increase use in electronics, fear, and a sense of uncertainty. Prior to this pandemic, we already had over 300 million cases of documented depression related illnesses. This pandemic has raised this number dramatically in just over a few months. While depression may be genetic, could this pandemic be altering the environmental milieu of our biochemistry enough to exponentially increase the expressions of once dormant depression genetics?
All human beings have a primal response when survival is threatened. In many third world countries, since survival is a daily threat, this primal state and its resultant brain chemistry has been somewhat muted. Bombs can go off in the middle east and the very next day, markets are open, and business operates as usual. American’s on the other hand, have been for the most part protected by the real fears around survival. We are surrounded by convenience and privilege. Those that identify with survival often take selfies at the eye of the hurricane or after they waited 4 hours on a food line. They brag about how many rolls of toilet paper they scored and wear trendy masks while bike riding in the woods. They simply crave a sense of accomplishment, power and resilience.
Primal suffering takes on a whole different dynamic in modern societies. It looks more like suffering around “loss of control” “lack of belonging” “loss of stability” “weight gain” “not enough” and you can fill in the blanks. Our brains often are habituated to suffering around something and luckily it has not really been about true SURVIVAL, until now. This Pandemic has created an awareness of how hard wired we are for suffering and how what most of us thought was suffering was really a self-inflicted brain habit. Once the fear of true survival awakens your primal gears, we can begin to deeply comprehend what powerfully living really means.
How does all this tie into mental illness and depression? Well how we choose to experience this pandemic directly influences how are genetics express. We can focus on the news and death and isolate and allow all the rabbit holes of “what if” occupy our mind space, or we can stay grounded in the present moment. We can be grateful for another day of sunshine and we can safely socially distance. We can let go of attachments of having an opinion and surrender to the unknown and allow life to be as it is. We can honor the experience our physical bodies are having and take health and prevention measures to improve its vitality.
Fortunately, the study of epigenetics has laid a solid foundation and platform for preventing and treating depression related illness. Epigenetics is basically the study of how environment, age and lifestyle can change the expression of a gene. In other words, your DNA is the same but how your cells receive the DNA can change, and contribute to disease genesis.(10) This is how an individual with a genetic predisposition to diabetes can prevent it by choosing a healthy lifestyle.
Epigenetics, in my opinion, gives credibility to our innate ability to self-heal. We can better direct our cells functions simply by what we think. This forced isolation of this pandemic combined with the news, radical opinions, mask, and glove wearing, has drastically changed our environment and its influences on our thoughts. All ages are being affected and we are just now beginning to realize the negative impact this will have on the evolving psyche of our children.
Mental illness and depression have well known and proven genetic contributions that already include the role of polymorphisms on gene expression. These include associations with serotonin, noradrenalin, and dopamine neurotransmission. (5) Unfortunately, most genetic studies on depression have been unsuccessful. There are more than a million or more variants across the genome making the complexity to study large scale patterns very difficult. To observe trends, the study populations, need to be huge. And lastly there is just too much subjectivity in reporting and diagnostic criteria for depression. (3) Basically, depression is a unique experience and their likely are as many genetic variants as there are sufferers. The intention of the genome wide association studies (GWAS), to improve diagnosis, prevention, and treatment through a nuanced understanding of the genetics was definitely a good start, however it left out the most important and probably the most difficult to measure consideration,
How can we begin to understand the impact COVID-19 will have on mental health? Focusing on well-defined measures of the environment, where there has already been robust and consistent evidence to support a relationship between the exposure and depression is one way to start. In the same way that common experiences around socially established constructs like workplace inequality, violence, neighborhood demographics, social media, school and college stressors can contribute to common health trends , so can the experiences we are now having as a result of COVID-19.
Although the path for early detection of genetic risk for depression remains layered in obstacles, what is certain is that a deeper understanding of the diverse environmental root causes of depression is needed. Old, antiquated biological studies will continue to promote ineffective treatments. Thankfully, there are laboratories who are beginning to unravel the epigenetic expressions in real time. This means that as soon as new data comes out, software can assimilate in ways that will eventually lead to a large enough database to measure environmental trends on depression and mental health. One such lab is, Diagnostic Solutions Laboratory. They have at test called Genomic Insight.” Unlike any other DNA test on the market, Genomic Insight ® uses the most advanced artificial intelligence to allow clinicians unique insight into patient genomics. Using the Opus23® informatics platform, clinicians can now customize reports using an interactive dashboard that curates a patient’s genomic data in “real-time” by using the latest medical-literature databases and meta-data sets.”(11)
While this blog, was not intended to involve medical complexity of all the single nucleotide polymorphisms (SNP) that are susceptible to environmental influences on the genome, there are a few that I would like to mention, as they are very common in Depression.
An enzyme that facilitates the breakdown of dopamine and norepinephrine.
Variants in COMT will cause higher levels of dopamine due to slower breakdown, which can contribute to anxiety and insomnia.
Individuals can be more susceptible to dopamine fluctuations, which increase risk of mood swings.
People without COMT mutations are generally more even tempered.
Monoamine Oxidase (MAOA)
Also involved int the breakdown of neurotransmitters including serotonin, dopamine, norepinephrine
Variants in MAOA can lead to low/high levels of these neurotransmitters causing mood swings, OCD, anxiety, aggression, insomnia, and depression.
Symptoms are described as “wired and tired” feeling depleted but have a feeling of being overstimulated.
This gene has also been associated with a variety of other psychiatric disorders, including antisocial behavior.
This enzyme requires B2 (riboflavin) in sufficient levels to function normally.
Individuals tend to have lower tolerance to methylated supplements like folate which is due to its ability to raise neurotransmitters and slow down their breakdown.
Oxytocin Receptor (OXTR)
Protein which functions as receptor for the hormone and neurotransmitter oxytocin.
Oxytocin is commonly known as the snuggle hormone and is responsible for maternal bonding
Oxytocin receptors are also present in the central nervous system and regulate a range of behaviors, including stress and anxiety, social memory and recognition, sexual and aggressive behaviors
Solute carrier family 6 (neurotransmitter transporter, serotonin), member 4 (SLC6A4)
This gene has been shown to affect the rate of serotonin uptake and may play a role in aggressive behavior in Alzheimer disease patients, and depression-susceptibility in people experiencing emotional trauma.
It has been found that it can partly account for anxiety-related personality traits.
Tryptophan hydroxylase 2 (TPH2)
The TPH2 gene affect the rate of production of serotonin.
Drugs that alter serotonin levels are used in treating depression, generalized anxiety disorder and social phobia.
Depletion of serotonin is common between disorders such as obsessive-compulsive disorder, depression, and anxiety.
In summary, to prevent the expression of depression epigenetics we must first challenge how we are allowing our experience of COVD-19 shape our thoughts. It really comes down to perspective. Wanting this pandemic to be over versus choosing to experience this pandemic differently is a 2mm distinction that defines if you will suffer or live powerfully. Wanting something is very different than choosing it. Wanting something is not putting yourself in the driver seat, instead it is an unconscious way of allowing things to remain the same. For example, if it is raining, some will have an experience around thoughts like, its dark, I can’t go outside or my workout is ruined while another person will choose to use it as an opportunity to wear cool rain boots, listen to the beautiful sound the rain makes, or do a calming indoor yoga routine. We have the power to choose and therefore are the creators of our own experiences.
I am volunteering an hour a week to be available for anyone in need during this time please feel free to schedule yourself for a free 15-minute call. Remember you are not alone in this time and sometimes all you need is a voice in your ear reminding you of what you already know. You are loved and deserving of joy and belonging.
Power RA, Cohen-Woods S, Ng MY, et al. Genome-wide association analysis accounting for environmental factors through propensity-score matching: application to stressful live events in major depressive disorder. Am J Med Genet B Neuropsychiatr Genet. 2013;162B:521–9. [PubMed] [Google Scholar]
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