T-helper cells, free thiols, glutathione peroxidase-3 (GPx3), nicotinamide adenine dinucleotide phosphate (NADPH). Those are all important terms for scientists and clinical researchers working hard to fight diseases by elucidating humoral and cellular immunity in animals and humans.
Now more than ever, international studies are going down all avenues to find answers. They are not grasping at straws, but pursuing all potential prospects that might lead us out of this crisis. Every study, no matter how small continues to bring new facts to light. The old adage “further research is needed” may sound hackneyed, but it’s those little nuggets of facts revealed that bring us just one step closer.
The small study on 33 patients led by Professor Arash Moghaddam of the Aschaffenburg Trauma and Orthopedic Research Group (ATORG) produced more evidence about how selenium deficiency can impact clinical courses and outcomes in severely ill COVID-19 patients. The results of this observational study were published in Nutrients in summer 2020 – just as most countries were coming out of the pandemic induced lock-down. This peer-reviewed, open-access journal is committed to rapid publication, boasting a 4-year impact factor of 5.329. In other words, get new and reliable results out in the public domain so that other scientists can expand upon them.
It’s not news that infections with the severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), the underlying cause of the coronavirus disease (COVID-19) are associated with high mortality, especially in the elderly and individuals with pre-existing conditions such as chronic obstructive pulmonary disease, hypertension, diabetes, or cancer. A new item on this list of conditions potentially attributing to poorer outcomes now includes selenium deficiency. Selenium is an immensely important trace element for our health and a well-balanced immune response. It is well established that the risk of dying from sepsis or polytrauma is inversely related to selenium status. In this recent and first study worldwide, Professor Moghaddam’s team explored the hypothetical question as to whether this inverse relation also applies to COVID-19. They asked: Is severe selenium deficiency prevalent among COVID-19 patients and is it associated with slower recovery and poor survival? The findings were that indeed a statistical correlation exists between a severe course of COVID-19 and low selenium levels. The scientists measured the three biomarkers of total serum selenium, selenoprotein concentration and GPx3 activity. Their conclusion: Evaluation of selenium status not only may provide diagnostic information on the clinical course and outcome of a SARS-CoV-2 infection. The adjuvant use of selenium in severely ill and selenium-deficient patients may be beneficial. Referred to as fascinating by the local newspaper, the study’s findings also support the idea of a favorable effect of selenium overall on the course of the disease. All other recently published studies investigating the role of selenium in the treatment of COVID-19 also suggest that it may be of relevance to SARS-CoV-2 infections, their clinical course and patient’s recovery.
Certain micronutrients have long been established as supportive treatment of and protection against viral diseases given that an individual’s nutritional status is an essential factor in their immunity. Alongside essential trace elements like selenium, zinc, iron, magnesium and copper, other important micronutrients include vitamins A, B6, B12, C, D and E. Among these micronutrients, selenium is certainly key to a balanced immune system and plays a special role in fighting viral infections.
Selenium deficiency appears to promote mutations in the genetic material of influenza viruses. These mutations can then make the virus more aggressive or virulent and contribute to a rapid evolution of pathogenic viral species. Oxidative stress appears to play an important role in this process. Many viral infections lead to an increased production of free radicals. These, in turn, can promote the multiplication of viruses. Selenium is a component of important endogenous antioxidative enzymes and can help render free radicals harmless and counteract this harmful process. A selenium deficiency can also impair the activity of type 1 (TH1) T-helper cells that are an important part of the cellular immunity. During an infection, TH1 cells release messenger substances that attract certain macrophages. These macrophages absorb the affected cells and render the pathogens harmless.
In COVID-19 patients, selenium levels are found to be low. Potentially low selenium levels may decline further with growing inflammation as has been observed with sepsis and polytrauma. Selenium requirements may increase during stays on the intensive care unit under inflammatory and hypoxic conditions. A declining selenium level may even constitute a surrogate marker for disease severity.
According to Professor Moghaddam, it appears meaningful, timely, and promising to initiate population-wide measures aimed at identifying subjects with pre-existing selenium deficits, not just as a preventive measure for viral infections, spread, and virulence development, but also to reduce the individual risk for cardiovascular mortality, cancer and death from severe disease. Time will tell how COVID-19 patients receiving adjuvant selenium might better cope with their infection and which factors hang in the balance.
To find out more about the impact of selenium on viral infections and COVID-19, download biosyn’s newly released folder: