A common link in the modifiable risk factors for severe COVID-19

Submitted by Michael Schaier

Tags: coronavirus COVID-19

A common link in the modifiable risk factors for severe COVID-19

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Since the beginning of the COVID pandemic, much has been learned about the pathophysiology of this virus and the risk factors that predispose some to worse outcomes. As expected, the elderly and immunocompromised have been shown to have increased morbidity and mortality due to the body's weakened ability to fight off infection. Certain comorbidities, namely hypertension, diabetes, and obesity, are also linked with a stronger acute-phase of the infection, often requiring hospitalization. Drucker (2021) notes that these latter diagnoses often correlate with higher risk for infection and coagulopathies in addition to endothelial dysfunction. With regards to hypertension, this is further evidenced by data that correlates endothelial cell dysfunction with excess sodium (Robinson, Edwards, & Farquhar, 2019). This is significant as damage to the endothelium, specifically the endothelial glycocalyx, is a known precursor for coagulopathies (Schött, Solomon, Fries, & Bentzer, 2016).

These data help to validate the observed findings of increased risk of severe COVID with the above listed comorbidities. However, in many cases, there is a modifiable “risk factor” that precedes these named risk factors, namely the dietary choices that lead to these comorbidities. Poor dietary habits generally include a diet that is high in salt, sugar, fat, and cholesterol; these lead to the medical conditions of hypertension, diabetes, obesity, and coronary artery disease (Krauss, Eckel, Howard, Appel, Daniels., Deckelbaum,... & Bazzarre, 2000). Furthermore, it is also plausible to suggest that many who are not mindful of proper dietary choices will also consume fewer essential nutrients, particularly immune boosting nutrients such as zinc and vitamin-C. As stated, due to these poor dietary habits, many people place themselves at a greater risk for a more severe infection should they be exposed to COVID.

Often these diagnoses are not identified immediately as the person is asymptomatic and the body compensates for any deficits (Šestan, Marinović, Kavazović, Cekinović, Wueest., Wensveen, ... & Polić, 2018; Taddei, Bruno, Masi, & Solini, 2018). Arguably, they are at a higher risk, but would not be aware of it as they do not yet have the official diagnosis. However, once they are infected with COVID, the virus overwhelms their bodies to the point where their bodies can no longer compensate. COVID is a virus notorious for triggering an exaggerated immune response, leading to both inflammation of the lungs as well as blood clots that circulate the body (Smadja, Mentzer, Fontenay, Laffan, Ackermann, Helms,... & Griffioen, 2021). The shortness of breath stresses the body with less oxygen, requiring greater effort to maintain adequate oxygenation. This then challenges the body to keep with its basic needs, let alone maintaining any compensatory mechanisms. Additionally, the body is further impacted by circulating blood clots, which have already been shown to negatively impact several internal organs, such as the lungs, kidneys, heart, and brain (Silva Andrade, Siqueira, de Assis Soares, de Souza Rangel, Santos, dos Santos Freitas,... & Barh, 2021). Recent reports have shown that even non-hospitalized people previously infected with COVID were found to develop kidney issues 6 months post-COVID (Bowe, Xie, Xu, & Al-Aly, (2021); this latter finding could perhaps be due to undetected microclots that were not significant enough to cause immediate health issues. The consideration of these underlying pathologies of the virus helps to clarify why not only those who are identified as at-risk, but also those whose bodies rely on compensatory mechanisms are also at a greater risk of hospitalization.

The pattern has been noted that certain comorbidities are diagnosed during the acute-phase of COVID, however, the consideration that the disease disrupted the body’s compensatory measures as a direct cause could add new perspective to the science. This consideration should further highlight the importance of health maintenance across all populations with respect to proper nutrition. COVID has taught us many things. From new knowledge in science and medicine to remembering and reinforcing already known evidence-based health measures, there is a lot to take away from this pandemic. There is still much to be learned about COVID, but the more puzzle pieces that are identified, the better the mystery can be solved.


  1. Bowe, B., Xie, Y., Xu, E., & Al-Aly, Z. (2021). Kidney outcomes in long covid. Journal of the American Society of Nephrology.

  2. Drucker, D. J. (2021). Diabetes, obesity, metabolism and SARS-CoV-2 infection: The end of the beginning. Cell metabolism.

  3. Krauss, R. M., Eckel, R. H., Howard, B., Appel, L. J., Daniels, S. R., Deckelbaum, R. J., ... & Bazzarre, T. L. (2000). AHA Dietary Guidelines: revision 2000: A statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation, 102(18), 2284-2299.

  4. Robinson, A. T., Edwards, D. G., & Farquhar, W. B. (2019). The influence of dietary salt beyond blood pressure. Current hypertension reports, 21(6), 1-11.

  5. Schött, U., Solomon, C., Fries, D., & Bentzer, P. (2016). The endothelial glycocalyx and its disruption, protection and regeneration: a narrative review. Scandinavian journal of trauma, resuscitation and emergency medicine, 24(1), 1-8.

  6. Šestan, M., Marinović, S., Kavazović, I., Cekinović, Đ., Wueest, S., Wensveen, T. T., ... & Polić, B. (2018). Virus-induced interferon-γ causes insulin resistance in skeletal muscle and derails glycemic control in obesity. Immunity, 49(1), 164-177.

  7. Silva Andrade, B., Siqueira, S., de Assis Soares, W. R., de Souza Rangel, F., Santos, N. O., dos Santos Freitas, A., ... & Barh, D. (2021). Long-COVID and Post-COVID Health Complications: An Up-to-Date Review on Clinical Conditions and Their Possible Molecular Mechanisms. Viruses, 13(4), 700.

  8. Smadja, D. M., Mentzer, S. J., Fontenay, M., Laffan, M. A., Ackermann, M., Helms, J., ... & Griffioen, A. W. (2021). COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects. Angiogenesis, 1-34.

  9. Taddei, S., Bruno, R. M., Masi, S., & Solini, A. (2018). Epidemiology and pathophysiology of hypertension. ESC CardioMed, 2377-2388.