It is now well established that a severe infection caused by covid-19 is a result of excess ‘cytokines’ produced by our immune system[1]. If the quantity of cytokines exceeds a certain threshold it can even turn deadly. Cytokines are a category of ‘messenger proteins’ which our immune system produce to fight off the infection. There are different types of cytokines which are produced, but if they are produced in access, they cause painful symptoms. Beyond a certain limit they can even turn against our us, leading to organ failure, clog our veins, and even deplete oxygen levels and nutrients in the blood. Jo Marchant writes in one of her books:
“Scientists used to assume that any damage done when we have an infection was caused by the infecting organism. Slowly they realized, however, that many of the symptoms we suffer when we’re ill — fever, weight loss, tissue damage, even fatigue and depression — are triggered not by pathogens but by our own immune systems, mediated by messenger proteins called cytokines … too-high levels of TNF [a type of cytokine] essentially activate every white blood cell in the body. These clog up blood vessels, blocking blood flow and starving cells downstream of oxygen and nutrients.”[2]
While reading Jo Marchant’s book ‘Cure’ (published in 2017), I learned that the knowledge about cytokines causing these terrible symptoms is known to scientists since a few decades now. A disease known as sepsis also have symptoms very similar to covid-19[3]. The Jo-Merchant’s book goes further to explain the treatments which have been developed to suppress the over reaction of the immune system. The one which raised my eyebrows attempts to suppress the immune reaction or cytokine production by stimulating the vagus nerve. This stimulation can also be done noninvasively.
This stimulation of vagus nerve leads to what is known as the ‘autonomic balance’. The autonomic balance is a balance between the two halves of our nervous system. One half is called the sympathetic part, which is responsible for generating a fight/flight response to a threat; while the other half known as the parasympathetic part is activated when we are calm.
The causal link between autonomic disbalance due to high degree of stress (the cause) and an over-reacting immune system is not a recent discovery, rather it is known to concerned scientists since over 80 years now. Hans Seyle[4] who coined the term ‘stress’ some 80 years ago has explained this relationship, and since then it has been extensively studied.
I learned about Hans Seyle’s work when I read Dr. Gabor Mate’s book ‘When the Body Says No’[5]. Like Jo Marchant, Mate’ has also explained in detail how high long term stress can cause our immune system to turn against our selves causing a variety of the autoimmune diseases. Autoimmune disease is a range of disease where the immune system turn against itself. The domain of psychoneuroimmunology has also been studying the link between autoimmune and the stress for a long time.
What really caught my attention was that if the balance between the two halves has been lost then we also become more susceptible to illness of sorts or other words our immune system goes an extra mile to knock us down; and restoring the balance between the two halves of the nervous system can also restore the balance of the immune response. The domain of psychoneuroimmunology has been studying this connection between the nervous system and immune system since more than half a century now[6].
While exploring more literature like the work of Gabor Mate’s and Robert Sapolsky, I learned that and It is well established in the domain of psychoneuroimmunology that if the nervous system has been disbalanced for too long, it also pushes the immune system to go haywire[7]. This disbalance between the sympathetic and parasympathetic parts of the nervous system is typically caused due to high long-term stress. So, if we are under high degree of stress for a long time (for months and years), the nervous system gets stuck in a disbalanced state, which in turn causes the immune system to overreact when we catch an infection. The immune system perhaps do not get the signal when to stop producing the cytokines so it keeps on producing them. The excess cytokines thus knocks us down[8].
A measure of this autonomic balance and disbalance is known as heart rate variability or HRV. There have been studies on covid-19 patients, showing that those who suffered a critical and even fatal infection of covid-19 had an autonomic disbalance just before getting infected with the noval coronavirus[9]. There also has been pilot studies which shows that noninvasively stimulating the vagus nerve (major part of the parasympathetic side) to bring the balance between the two halves of the nervous system suppresses the production of excess cytokines in severe covid-19 cases [10].
Now experts are acknowledging that the effects of covid-19 infection on the body can also be seen as an autoimmune disease[11], more so in patients if symptoms do not go away even after months[12]. However, it appears that the contemporary medical establishment is perhaps missing the link between the autonomic disbalance caused by long term stress as the potential culprit behind the dysregulated immune response against coronavirus which even turns deadly in some cases.
Luckily some scientists have studied the link between stress and covid-19 infection, and are suggesting that high-long term stress could be a possible culprit behind the lethal over reaction of the immune system[13]. The studies which have established the link between autonomic disbalance and severity of covid-19 in patients, and stimulation of the vagus nerve to suppress the immune response, may also imply that perhaps it’s the long term stress which is the primary culprit here. Dexamethasone which is now effectively been used to treat covid-19 patients also affect the production of cortisol, the infamous stress hormone in the system.
After reading Gabor Mate’, Jo Marchant, also Robert Spolskey and Jenna Macciochi, to understand the relationship between stress and disease including autoimmune, also looking at the work of experts which have now shown that the link between autonomic disbalance and dysregulated immune response, one may infer that it may be very likely that chronic stress is a key culprit here.
In this context one may critically evaluate the impact of lockdowns to prevent covid-19 as ironically the lockdown have added stress in the lives of so many people, or restricted the possibility of them getting out of stressful situations [14]. A study conducted by a team of researchers from University of Nottingham suggests that:
“the constellation of psychological risk factors identified in young people in this cohort (i.e. poorer mental health and increased loneliness) have been shown time and again to dysregulate the immune system and increase the risk of viral infections, including coronavirus infections. Thus, the psychological repercussions of lockdown may also have directly affected their immunological competence and ability to resist COVID-19 infection”[15]
The virus can attack everyone, but the people who are chronically stressed and thus have a disbalanced nervous system, are perhaps less likely to successfully defend themselves against the virus, while those who are able to successfully regulate their stress or maintain an autonomic balance are perhaps more successful in defending themselves not just from covid-19 but a wide range of deadly disease including autoimmune and cancer (not everyone agrees here) in the long run.
More studies are needed to clearly establish if there is a link between long term stress and a dysregulated response against the novel coronavirus; however, looking at the past research on the impact of stress on our immune system, it is perhaps plausible to infer that the presence of long term stress in our system rather helps coronavirus to do more damage to our bodies.
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References
[1] Hojyo, S., Uchida, M., Tanaka, K. et al. How COVID-19 induces cytokine storm with high mortality. Inflamm Regener 40, 37 (2020). https://doi.org/10.1186/s41232-020-00146-3
[2] Marchant, J. (2016). Cure: A Journey into the Science of Mind over Body. New York: Crown Publishers
[3] Baqi S, Naz A, Sayeed MA, Khan S, Ismail H, Kumar V, Somjimal H, Aneela J, Imtiaz S, Aftab S. Clinical Characteristics and Outcome of Patients With Severe COVID-19 Pneumonia at a Public Sector Hospital in Karachi, Pakistan. Cureus. 2021 Feb 3;13(2):e13107. doi: 10.7759/cureus.13107. PMID: 33728127; PMCID: PMC7935076.
[4] Selye, H. (1956). The stress of life. New York: McGraw-Hill.
[5] Maté, G. (2003). When the body says no: The cost of hidden stress. Toronto: A.A. Knopf Canada.
[6] Maté G. (2005). The science of psychoneuroimmunology. Canadian Family Physician, 51(4), 489.
Pert CB, Ruff MR, Weber RJ, Herkenham M. Neuropeptides and their receptors: a psychosomatic network. J Immunol. 1985 Aug;135(2 Suppl):820s-826s. PMID: 2989371.
[7] Sapolsky, R. M. (2004). Why zebras don’t get ulcers. New York: Times Books. Chicago
[8] Marchant, J. (2016). Cure: A Journey into the Science of Mind over Body. New York: Crown Publishers
[9] Leitzke, M., Stefanovic, D., Meyer, JJ. et al. Autonomic balance determines the severity of COVID-19 courses. Bioelectron Med 6, 22 (2020). https://doi.org/10.1186/s42234-020-00058-0
[10] Nemechek P (2020) Transcutaneous auricular vagus nerve stimulation holds potential to suppress COVID-19 cytokine storm. Int Clin Med 4: DOI: 10.15761/ICM.1000179.
Fudim, M., Qadri, Y.J., Ghadimi, K. et al. Implications for Neuromodulation Therapy to Control Inflammation and Related Organ Dysfunction in COVID-19. J. of Cardiovasc. Trans. Res. 13, 894–899 (2020). https://doi.org/10.1007/s12265-020-10031-6
Staats, P., Giannakopoulos, G., Blake, J., Liebler, E. and Levy, R.M. (2020), The Use of Non-invasive Vagus Nerve Stimulation to Treat Respiratory Symptoms Associated With COVID-19: A Theoretical Hypothesis and Early Clinical Experience. Neuromodulation: Technology at the Neural Interface, 23: 784–788. https://doi.org/10.1111/ner.13172
[11] iu, Y., Sawalha, A. H., & Lu, Q. (2021). COVID-19 and autoimmune diseases. Current Opinion in Rheumatology, 33(2).
[12] Galeotti, C., & Bayry, J. (2020). Autoimmune and inflammatory diseases following COVID-19. Nature reviews. Rheumatology, 16(8), 413–414. https://doi.org/10.1038/s41584-020-0448-7
[13] Parshley, Lois. (Sep 3, 2020), Could stress be another preexisting condition that makes Covid-19 infections worse? Website: https://www.vox.com/2020/9/3/21419902/covid-19-risk-factors-chronic-stress-racism-immune-system, Last accessed on 9th June 2021
[14] Bourdillon N, Yazdani S, Schmitt L, Millet GP (2020) Effects of COVID-19 lockdown on heart rate variability. PLoS ONE 15(11): e0242303. https://doi.org/10.1371/journal.pone.0242303
[15] Jia, R., Ayling, K., Chalder, T., Massey, A., Broadbent, E., Morling, J. R., Coupland, C., & Vedhara, K. (2020). Young people, mental health and COVID-19 infection: the canaries we put in the coal mine. Public health, 189, 158–161. https://doi.org/10.1016/j.puhe.2020.10.018
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