Do You Get Enough Vitamin A to Stop Colds and Flus?
Vitamin A is critical for your immune system. You need vitamin A for strong antibody actions, for B and T-helper cells, and for the regeneration of mucosal epithelial cells as a barrier against infection. Chronic vitamin A deficiencies early in life can affect the very structure of the lungs, and make someone predisposed to respiratory illnesses.
If you’re deficient in vitamin A, it weakens both your innate and adaptive immune responses; without enough of it, your defenses will be weaker in general, and your reaction to new viruses may be more severe than they would be with appropriate levels of the vitamin.
Vitamin A is also involved with the way that cells communicate with one another. The researchers in this study have stated that a breakdown in that process due to vitamin A depletion from fighting against the virus, is one factor behind Covid-19 severity, including the intensive inflammation that makes the disease so dangerous.
This is all the more reason to make sure that you’re getting consistent levels of vitamin A. That means selecting a supplement that provides the nutrient in a retinol form, rather than as beta-carotene which must be converted by the body into vitamin A.
Abstract:
Sarohan AR, Kızıl M, İnkaya AÇ, Mahmud S, Akram M, Cen O. A novel hypothesis for COVID-19 pathogenesis: Retinol depletion and retinoid signaling disorder. Cell Signal. 2021 Nov;87:110121.
The SARS-CoV-2 virus has caused a worldwide COVID-19 pandemic. In less than a year and a half, more than 200 million people have been infected and more than four million have died. Despite some improvement in the treatment strategies, no definitive treatment protocol has been developed. The pathogenesis of the disease has not been clearly elucidated yet. A clear understanding of its pathogenesis will help develop effective vaccines and drugs. The immunopathogenesis of COVID-19 is characteristic with acute respiratory distress syndrome and multiorgan involvement with impaired Type I interferon response and hyperinflammation. The destructive systemic effects of COVID-19 cannot be explained simply by the viral tropism through the ACE2 and TMPRSS2 receptors. In addition, the recently identified mutations cannot fully explain the defect in all cases of Type I interferon synthesis. We hypothesize that retinol depletion and resulting impaired retinoid signaling play a central role in the COVID-19 pathogenesis that is characteristic for dysregulated immune system, defect in Type I interferon synthesis, severe inflammatory process, and destructive systemic multiorgan involvement. Viral RNA recognition mechanism through RIG-I receptors can quickly consume a large amount of the body’s retinoid reserve, which causes the retinol levels to fall below the normal serum levels. This causes retinoid insufficiency and impaired retinoid signaling, which leads to interruption in Type I interferon synthesis and an excessive inflammation. Therefore, reconstitution of the retinoid signaling may prove to be a valid strategy for management of COVID-19 as well for some other chronic, degenerative, inflammatory, and autoimmune diseases.
