It occurred, after listening to various (UK and International) politicians trying to explain behaviour that the rest of the country (and most of the world) understands is bereft of justification, that the energy spent in defending the indefensible, could instead be applied to promoting vitamin D3.
Early in the 2019 Sars-Cov-2 discovery period, vitamin D3 was highlighted by many researchers as having the capacity to improve and enhance immunity, especially regarding anti-viral activities. Over the following months numerous follow up studies continued to tease out associations and correlations and slowly but surely the evidence of a vitamin D immune related benefit began to become clear.
Vitamin D Vs Partygate
To those of us already primed to support the interaction of a secosteroid in mucosal immune function this seemed clear, and the risk to benefit ratio of consumption was one that made common sense. 1,25(OH)2D3 is the most extensively characterised active, naturally occurring D3 metabolite that, not only systematically regulates calcium homeostasis and bone metabolism, but also possesses immunomodulatory properties. Clinically, a normal D3 level is associated with better outcomes in patients with a variety of autoimmune and infectious diseases[1]. Yet the political support for this cheap, safe and easy to use supplement was at best weak and in most cases absent. Perhaps if it had been pitched as a ‘working party’, it may have received the attention it deserves in relation to health generation and sustainability?
A paper published in PLOS ONE on the 3rd Feb 2022 delivers a comprehensive retrospective analysis of pre-Covid infection Vit D3 status and the respective outcomes[2]. The authors succinctly state: Among hospitalized COVID-19 patients, pre-infection deficiency of vitamin D was associated with increased disease severity and mortality. Further determining causality as opposed to correlation. Vitamin C, another simple, safe and cheap nutrient has also shown benefits to human health, well beyond prevention of scurvy, and is finally undergoing some meaningful UK based trials.
Vitamin C is not found in birthday cake!
Vitamin C is best known for its antioxidant properties, being able to scavenge damaging reactive oxygen species, thus protecting the body’s cells and tissues from oxidative damage and dysfunction. However, the vitamin also has numerous other important functions within the body, many of which are known to support healthy immune function. During infection, vitamin C levels can become depleted and a person’s requirement for vitamin C increases with the severity of the infection. Vitamin C exerts its antiviral properties by supporting lymphocyte activity, increasing interferon-α production, modulating cytokines, reducing inflammation, improving endothelial dysfunction, and restoring mitochondrial function[3].
Quercetin enhances Vitamin C effects
Utilising the bioflavonoid quercetin alongside vitamin C provides a synergistic benefit[4]. Studies suggest that quercetin supplementation may promote antioxidant, anti-inflammatory, antiviral, and immunoprotective effects[5], [6],[7]. Can further enhance immunocompetence.
Quercetin has been studied in various types and models of viral infection due to its promising antiviral effects in inhibiting polymerases, proteases, reverse transcriptase, suppressing DNA gyrase, and binding viral capsid protein[8],[9],[10].
Why nutrients should be delivered in suitcases to the nation!
Why should everyone look to ensure optimal vitamin D and vitamin C status, after all the Sars-Cov-2 infection and hospitalisation rate is dropping and endemicity is predicted? This must surely mean that we can return to our previous ambivalence around nutrient optimisation, metabolic quality and immune and environment interactions?
Endemicity, is of course a catchy concept, surely it means we can just ‘live’ with the virus, or indeed any future derivation of the virus, and a combination of experience, immune resilience and relevant critical care will make it no more problematic than the flu – a premise proposed previously, that has been at best overplayed.
Flu is one of many examples that show why endemic can’t be thought of as the inverse of pandemic; the two terms are not opposite ends of a spectrum. Endemic doesn’t mean the virus is suddenly not going to be highly problematic.
It is an unfortunate coincidence that the word endemic begins with end. The arrival of endemicity is the beginning of a long and complicated relationship between a pathogen and its host population. ‘En demos’. In the people.
The immunity we have raised against infections of both viruses has proved to be far fickler than hoped for, and needs to be somewhat frequently topped off, regardless of whether non-vaccinated or vaccinated and, or, recovered from prior infection. The immune system benefits from ongoing support, it contains the widest range of gene variation of all human cells and carries a vast range of natural immune capacity. Not only for Covid, but also for all of the other common infectious diseases such as respiratory syncytial virus, rhinovirus, other coronaviruses, and a glut of different bacteria, just to name a few.
To confidently say that the Sars-Cov-2 pandemic will give way to endemicity is to suggest a single end point; saying that it will become endemic suggests that what comes next is up to the pathogen alone. But the post-pandemic phase will be shaped by the choices and actions we make. If our future with it is a truce we strike with the virus, it’s one that we will renegotiate, over and over again by realising that the immune system is a constantly changing variable – to imagine it requires no support or development will be to fly in the face of contemporary immunology and the extensive epidemiolocal experiences to date.
Concluding quote
“There is and can be no ultimate solution for us to discover, but instead a permanent need for balancing contradictory claims, for careful trade-offs between conflicting values, toleration of difference, consideration of the specific factors at play when a choice is needed, not reliance on an abstract blueprint claimed to be applicable everywhere, always, to all people.” Isiah Berlin: Against Dogma
Consider this when helping family and friends to understand the relevance of lifestyle choices and the utilisation of supplementation.
References
[1] Postlethwaite AE, Tuckey RC, Kim TK, et al. 20S-Hydroxyvitamin D3, a Secosteroid Produced in Humans, Is Anti-Inflammatory and Inhibits Murine Autoimmune Arthritis. Front Immunol. 2021;12:678487. Published 2021 Jun 30.
[2] Dror AA, Morozov N, Daoud A, Namir Y, Yakir O, et al. (2022) Pre-infection 25-hydroxyvitamin D3 levels and association with severity of COVID-19 illness. PLOS ONE 17(2)
[3] Carr, Anitra C, and Silvia Maggini. “Vitamin C and Immune Function.” Nutrients vol. 9,11 1211. 3 Nov. 2017,
[4] Colunga Biancatelli RML, Berrill M, Catravas JD and Marik PE (2020) Quercetin and Vitamin C: An Experimental, Synergistic Therapy for the Prevention and Treatment of SARS-CoV-2 Related Disease (COVID-19). Front. Immunol. 11:1451
[5] Robaszkiewicz A, Balcerczyk A, Bartosz G. Antioxidative and prooxidative effects of quercetin on A549 cells. Cell Biol Int. (2007) 31:1245–50.
[6] Uchide N, Toyoda H. Antioxidant therapy as a potential approach to severe influenza-associated complications. Molecules. (2011) 16:2032–52.
[7] Nair MP, Kandaswami C, Mahajan S, Chadha KC, Chawda R, NairandSchwartz SAH. The flavonoid, quercetin, differentially regulates Th-1 (IFNgamma) and Th-2 (IL4) cytokine gene expression by normal peripheral blood mononuclear cells. Biochim Biophys Acta. (2002) 1593:29–36
[8] Shinozuka K, Kikuchi Y, Nishino C, Mori A, Tawata S. Inhibitory effect of flavonoids on DNA-dependent DNA and RNA polymerases. Experientia. (1988) 44:882–5.
[9] Bachmetov L, Gal-Tanamy M, Shapira A, Vorobeychik M, Giterman-Galam T, Sathiyamoorthy P, et al. Suppression of hepatitis C virus by the flavonoid quercetin is mediated by inhibition of NS3 protease activity. J Viral Hepat. (2012) 19:e81–8.
[10] Spedding G, Ratty A, Middleton E Jr. Inhibition of reverse transcriptases by flavonoids. Antiviral Res. (1989) 12:99–110.
