Vitamin D and Pandemics: Reducing Coronavirus Risk
By Ian Wishart
The question of whether vitamin D plays a role in protecting us from influenza and other pandemic viruses was raised earlier in my Vitamin D book, but in 2020 the rubber hit the road.
SARS-CoV2, better known just as “coronavirus”, “the ‘rona” or “COVID-19” (after the disease it causes), swept through the world.
Officially, it emerged in Wuhan, China in December 2019. Unofficially, satellite photos revealed Wuhan hospital carparks were clogged as far back as August 2019, and retro-testing of wastewater samples shows it was present in Europe and South America in the final quarter of 2019.
For those of us paying attention in the west, news broke on 31 December 2019 of a small cluster of cases in Wuhan infected with an unknown virus. Drudgereport in the USA picked up the story, but in most other media it didn’t rate a mention as the world obsessed over the first impeachment of Donald Trump.
Companies importing products from China were among the first to realise there was a threat, because the factories making products for the world began going offline after mid January. By the time the rest of the planet woke up, however, it was far too late to stop.
So, what do we know about SARS-CoV2?
It’s actually the third epidemic strain of coronavirus we’ve faced in the 21st century. The previous two – SARS and MERS – originated in animals and made a species-jump to humans. They had a higher kill rate but were harder to catch, and both outbreaks fizzled out.
This latest coronavirus was different. Its transmission efficiency, known in medical science as its “r0” (R-zero, or reproductive rate) was similar to the r2-r3 of the common cold, putting it ahead of the r1.4 to r2.8 of the 1918 Spanish Flu pandemic. In simple terms, at r2 an infected covid patient would be expected to infect two other people, who would each go on to infect two more.
However, the mutant variants of the virus, like the UK and Brazilian strains, are estimated to be up to 70% more infectious, putting their r-zero at r4 or higher. That means, in the absence of social distancing measures or effective vaccines, a much faster spread of coronavirus in the community.
As noted, it’s not the first animal virus to jump to humans for the first time in the past 100 years, but its relationship to the virus that causes the common cold has created competing narratives between “doves” and “hawks” on how COVID-19 should be managed.
The doves argue that it’s a respiratory illness like a cold, and that humans will quickly develop natural immunity to its severe forms if we allow it to circulate unhindered. Countries that notably adopted this reasoning early in the pandemic included Sweden, the USA and UK, and Brazil. The UK abandoned the herd immunity approach – but not before allowing the Trojan Horse into the city for a few weeks. By the time of Britain’s u-turn it was actually too late. In the United States, the herd immunity strategy was less one of deliberate intent and more one of blundering confusion caused by 50 different states having 50 different agendas for controlling the outbreak, and a president desperate to re-open the economy to salvage his re-election chances. Brazil, with widely-differing municipal, state and federal approaches, and a covid-dove president in Jair Bolsonaro, shares similarities to the US strategy.
Then there are the covid hawks – countries like New Zealand, Taiwan, Australia, China and Vietnam – who have adopted an eradication strategy. Hawks believe the zoonotic origin of SARS-CoV2 makes it a dangerous virus to play “chicken” with until we know much more about its long term health impacts. “What if it is not going to evolve into a minor cold?,” they argue, “what if the virus causes long term damage that ends up crippling the health system and economy for decades?”
They point to human immunodeficiency virus (HIV) – the infection behind the AIDS epidemic. HIV originated in African monkeys in the early to mid 20th century and eventually came to medical attention in the early 1980s.
The eerie link between SARS-CoV2 and HIV, apart from evidence that both exhibit an ability to hide from the immune system, is that HIV’s initial infection manifests as a mild flu – just a few days of feeling under the weather followed by an apparent full recovery. Yet nobody infected with HIV realised there was more to it, and that within five to ten years they would be dead.
No health officials, no doctors, no one had a clue that an animal virus was spreading through our communities with the power to wipe out humanity. If HIV had been as easy to catch as COVID-19, imagine how many people would have unwittingly caught that “mild flu” initially, only to be hit by HIV’s true payload five years later, long after everyone on the planet had caught the “mild flu” in the interim. Would you even be here to read this, had history taken that turn in the 1980s, or would there now be tumbleweeds drifting across the decaying tarmac of deserted cities?
It wasn’t good medical science or planning that prevented a monkey virus from eradicating humans – it was sheer blind luck. HIV was a blood disease, transmissible not by sneezing or breathing but primarily by the kind of sexual activity more likely to cause skin abrasions that the virus could enter through. It was hard to catch. Covid isn’t, and the worrying aspect is we still have no idea what the long term payload might really be.
When COVID-19 first appeared, it manifested as a respiratory illness. Humans are familiar with those, and millions of us catch flu every year but only around 0.1% die.
What we didn’t know in early 2020, but we do now, is that covid is not really a respiratory illness – it’s a vascular one. Unlike flu, which is mostly confined to the heart-lung axis, and which most people fully recover from in a week or two, the coronavirus behind COVID-19 has a spike protein that specialises in binding the virus to a cell structure found in blood vessels and virtually every major organ of the human body, a structure known as the ACE2 receptor.
Covid hits the lungs because our lungs are lined with ACE2 receptors, but while it works its magic there it is also hitting the ACE2 receptors lining every blood vessel, causing literally thousands of potential stroke-initiating blood clots. And it can hit our livers, kidneys, pancreas, ovaries, testes, brain and other vital organs. Scientists are worried the virus could make humans sterile, as the British Medical Journal noted in February 2021:
“The increased social and economic burden caused by the novel COVID-19 outbreak is gradually becoming a worrisome issue for the health sector. The novel coronavirus invades the target cell by binding to ACE2, which is widely expressed in the ovaries, uterus, vagina and placenta. Significantly, the SARS-CoV-2 is said to interrupt female fertility through regulating ACE2. Thus, it is essential to investigate if the novel COVID-19 hampers female fertility, given that there is no systematic and comprehensive evidence on the association of COVID-19 with female fertility.”
In the early stages of the pandemic, the media, politicians and health bosses concentrated almost exclusively on death rates and admissions to ICU for acute covid cases. The prevailing assumption was that if you could beat respiratory covid you were home free and would quickly make a full recovery. The revelation that most of the dead were elderly boosted the feeling of youthful invincibility: this was a disease that caught the “low-hanging fruit”, people already waiting to die.
Now, we know far more.
Studies are beginning to show hidden organ damage, even in those with only mild or asymptomatic cases:
“In a young, low-risk population with ongoing symptoms, almost 70% of individuals have impairment in one or more organs four months after initial symptoms of SARS-CoV-2 infection. There are implications not only for burden of long COVID but also public health approaches which have assumed low risk in young people with no comorbidities.”
Why is this significant? Because it means SARS-CoV2 not only harvests those with existing co-morbidities – it creates a new crop of previously healthy people with new underlying conditions they don’t even know they have. Unwittingly, those virus-damaged mild cases may get hit hard the next time they are exposed to covid, and if 70% now have comorbidities instead 20% it’s not rocket science to figure out the future trajectory of COVID-19.
In January 2021, Texas trauma surgeon Dr. Brittany Bankhead-Kendall told US network CBS that 70% to 80% of her covid outpatients – including those who tested positive but were asymptomatic – display evidence of serious lung damage when x-rayed:
“Post-covid lungs look worse than any type of terrible smokers’ lung we’ve ever seen…Everyone’s just so worried about the mortality thing and that’s terrible and it’s awful. But man, and all the survivors and the people who have tested positive this is, it’s going to be a problem.
“There are still people who say ‘I’m fine I don’t have any issues’ and you pull up their chest X-ray and they absolutely have a bad chest X-ray,” Bankhead-Kendall told CBS.
The Brazilian city of Manaus may be the canary in the mineshaft here. In the first wave, Manaus was hit hard by COVID-19, so hard that a team of Brazilian research scientists doing antibody testing in the city mid 2020 estimated that 66% of the city had caught covid between March and August:
“In June, one month following the epidemic peak, 44% of the population was seropositive for SARS-CoV-2, equating to a cumulative incidence of 52%, after correcting for the false-negative rate of the antibody test. The seroprevalence fell in July and August due to antibody waning. After correcting for this, we estimate a final epidemic size of 66%. Although non-pharmaceutical interventions, plus a change in population behavior, may have helped to limit SARS-CoV-2 transmission in Manaus, the unusually high infection rate suggests that herd immunity played a significant role in determining the size of the epidemic.”
By October, antibody serology had hit 76%, well and truly past the 70% “herd immunity” threshold.
Under ordinary circumstances, researchers expected that natural immunity from community exposure would save Manaus from a further outbreak for at least six months to a year. It wasn’t to be.
By Christmas 2020, Manaus was again being plunged into a pandemic as a second wave of SARS-CoV2 surged in. People died as hospitals ran out of oxygen, their wards spilling over with Brazilians struggling to breathe.
Terrifyingly, covid’s lingering nature deep in the body had incubated a mutant strain, known as the P1 variant, which differed enough from the first wave strain that it made the population’s hard-won antibodies useless. A study by Imperial College, London and the University of Sao Paulo estimated P1 was born around 6 November and was evading up to 61% of the accumulated herd immunity and reinfecting those who had been exposed the first time.
Unfortunately, for those of us who knew how to read the signs, this was the writing that had always been on the wall. A year ago, in April 2020, I warned:
“What about herd immunity? Surely if we allow this coronavirus to sweep through and give the survivors immunity, then the problem is solved? That’s the logic of many keyboard commentators.
“If only it were that simple. Again I find myself repeating: there are coronaviruses that cause the common cold. Have you become immune to those yet? We don’t even know if Covid19 survivors have any immunity at all…or whether next season they will find themselves struck down again, fighting for their lives – again. We don’t know if every last one of us is going to have to run that gauntlet every flu season for years to come. We don’t know whether people who received a mild dose were simply lucky because the virus never reached their lungs, and that all bets are off next season – particularly if it hits you while you have an existing chest cold. We don’t know what long term lung and heart damage is being done to young people who get this.
“In short, time will tell but we currently don’t know what we don’t know, although now we know how the Neanderthals felt – every time they ventured out of the cave to forage for food they were at risk from bears, wolves and sabre-tooth cats. The Wuhan bat virus may be smaller, but it’s capable of killing more humans than sabre-tooths ever did. That feeling of being hunted and stalked by something as you touch a supermarket trolley is an eerily primal throwback.”
In June 2020, while Manaus and Brazil were still battling the first wave, I posted an analysis of what a second wave anywhere might look like if 70% of the population developed antibodies in the first wave:
“One of the big unanswered questions about coronavirus is how big the second wave – if any – will be. Now, a new study puts forward a possible answer: three times worse than you think.
“The interesting research comes out of France, where scientists believe the higher covid19 death rate in the over-60s is because they had survived exposure fifty years ago to the Hong Kong flu pandemic of 1968/69.
“Those who have been paying attention to my reports will recall there’s already been research showing coronavirus may be using our immune systems to attack us, a process known as ‘Antibody Dependent Enhancement’.
“The French team worked out that the last big flu pandemic ripped through the world in the late 1960s, and anyone born prior to 1968 may have developed antibodies to it.
“They believe covid19 may have used those 1968 antibody responses in people to cause the cytokine storms that killed so many covid19 patients over 60.
“They mapped the data and found the same generation of boomers and early Gen-Xers were hardest hit by the original SARS in 2003:
‘The comparison of the 2003 and 2020 data..shows a striking difference between a panel of several European countries (France, Spain, Italy) with respect to the Hong Kong results. All curves share a common shape: a constant null range followed by a marked (exponential) increase starting in the ”30-39” age group for the 2003 data and ”50-59” group for all countries in 2020. This 20 years shift at the onset of the exponential regime can be interpreted as resulting from the existence of a common cause (situated approximately30-40 years before 2003 and 50-59 years before 2020, that is, between 1960 and 1970) that affected all people living at that date and which could explain why there are, 30 (respectively 50) years later, affected by the coronavirus outbreaks in a more severe way. Since the cause occurred before 1970 people born after this date will have no fragility, which is precisely what is seen in the plot.’
“The interesting thing is this: People who were aged 50 back in 1968 would be 102 today, so clearly the current covid patients who developed antibodies to the HK flu in ’68 must for the most part have been young at the time. Like today’s asymptomatic coronavirus carriers, they may not even have realised they were exposed to the Hong Kong flu. Yet five decades later, another virus used those old antibodies to kill them. We’ll return to that five decade pattern shortly.
“You will recall I have been warning that contrary to popular opinion, you don’t actually want to be exposed to covid19 even in a mild or asymptomatic form, because it means you will develop antibodies that the virus could use to bite you later..which is exactly what the French team is now warning:
‘We interpret this as an evidence that previous infection history can negatively impact the individual outcome of a future infection. Note that historically the 1960-70 decade is rich in epidemic / virus related events: the Hong Kong flu of 1968-1969 (that killed an estimated 1 million people worldwide) but also the start of the identification of the four endemic human coronaviruses (mid-1960s). Note that such a conclusion is consistent with recent investigations, see  that showed that individuals are prone to repeated infection with coronaviruses, with the unfortunate consequence that not only the immunity may vanish (sometimes within a year) but that the re-infection can be more severe. Data displayed in the figure 2 substantiates the same conclusion.’
“Just how severe? The new study estimates a genuine second wave (re-exposing people who’ve already had it) of covid19 globally, once 70% of the population have antibodies…could be up to three times deadlier than the lives lost in reaching the 70% spread (currently only 5-10% of the populations worst hit so far have been exposed, so there’s plenty more potential burn – multiply the current global death toll by seven to crudely guesstimate that 70% initial coverage).
“In other words, the initial infection is only the first course…under this scenario the virus will serve up its main course down the track, triggering immune storms in people previously exposed or given vaccines. The study warns vaccine researchers to take the threat seriously.
‘If a sensitizing process in the immune response triggered by SARS-CoV-2 exists, the pandemic nature of the 2019/20 COVID-19 outbreak will likely have noticeable effects on the overall population health state. In particular, this implies that additional care has to be observed when validating vaccines against the COVID-19.
‘The deterioration of the immune function can be evident on two occasions: either when a second epidemic occurs or when submitted to a challenge. The challenge can be very diverse, not necessarily in the form of a fully-fledged epidemic but also a small infection with an endemic coronavirus. This may manifest in the form of multi-organ inflammation.’
“That’s pretty sobering. They suspect the antibodies created in the Hong Kong flu were a timebomb lying dormant in the over 50s that covid19 was able to exploit. And they suspect the global nature of this current pandemic, creating antibodies in children and everyone else it touches, could be this generation’s viral timebomb moving forward, with the added zing that a person carrying covid antibodies might even be triggered by something as insignificant as the common cold in the future.
“Given that modern science has not had much direct real-time experience with coronavirus or big influenza pandemics, it may be that we are watching a longitudinal study play out before our eyes. It may be that this is the way viral contagions actually work.
“Remember the five decade pattern I mentioned? HK flu in ’68 created antibodies in young people in the swinging sixties, most of whom brushed it off at the time. Their older parents and grandparents bore the brunt of the 68 flu, perhaps because their immune systems had in turn been pre-primed by exposure to the 1918 Spanish flu.
“When you dig through the records you find these pandemics travel in waves. Before 1918, which was a new strain of flu virus, the previous big ‘flu’ epidemic had been 1889/1890, three decades earlier. That pandemic is now also believed to have been a novel coronavirus, not influenza. Before 1889, there had been a similar flu pandemic across the world in 1848/1849, infecting up to 50% of the population.
“Each generation it seems, gets a major viral infection and develops antibodies. Those who survive recover and move on, but the viruses are playing a long game, and the antibodies they create become doorkeys opening our bodies up to the next big invader later in our lives.
“In an NIH briefing on the 1918 pandemic, it notes that for reasons that doctors of that time couldn’t explain, the second season of a pandemic was always worse than the first:
‘The experience with the 1889–1890 pandemic taught medical authorities that pandemic influenza was a disease of very high morbidity and low case fatality, although it seemed that in the outbreaks immediately following a pandemic, morbidity rates could be expected to decline and case fatality rates to rise.’
“In New Zealand newspapers of 1918, the first wave of the Spanish flu was seen as a rather mild, ‘five day flu’ which, in rare cases extended into a second week and possibly death from pneumonia. The victims, as with most flu’s, were the elderly or unwell. But the 1919 reports were different. Young people were reported as getting first symptoms at 10am and being dead in their beds by 3pm. This wasn’t a ‘five day flu’. There were reports of supposedly healthy people dropping dead on the pavement. Autopsies revealed cytokine storms in the lungs, blood clots and ‘cerebral-spinal meningitis’ – massive inflammation of the central nervous system.
“All of these things sound like covid19 at work in the elderly. They are also classic examples of antibody dependent enhancement (ADE), where the victim dies because their immune system antibodies betray them.
“Will there be a second wave of covid19? New Zealand might dodge the bullet if its borders stay tight and tracing is gold standard, because so few kiwis were infected the first time around. As for the continents, the virus has spread too far. Let’s hope this latest research is wrong.
“History, however, suggests it might be right.”
That was written back on 1 June 2020.
So, what do we now know after a year of dancing with the ‘rona? We know that:
- It is killing between one and two percent of all those who get symptoms
- It is causing hidden organ damage to the millions who don’t die, including up to 70% of the asymptomatic who don’t even know they have had it
- It preys on underlying conditions
- It has managed to create new underlying conditions in previously healthy young people, making them vulnerable to the next wave
- Contrary to early scientific expectations, SARS-CoV2 has managed to mutate in much more dangerous forms all over the world, some of them immuno- and vaccine-evasive
- That the emergence of new mutations means vaccines may always be six months behind the surges in effectiveness
- In addition to organ damage, the virus appears to vastly increase the risk that survivors may later develop early onset Parkinson’s and other neurodegenerative disorders
- The virus may lead to a big rise in male and female infertility
- The virus causes ‘long covid’ in up to 30% of all those infected, even the asymptomatic, and significant numbers have had to quit their jobs as a result of chronic ill health, which is a massive threat to future economic productivity
Now that we know there are good reasons to avoid exposure to COVID-19, what are the options to help us avoid it? As the second wave bites, Brazilians, like many others worldwide, have flocked to alternative therapeutics to try and ward off COVID-19, with sales of Ivermectin up nearly 600%:
“Embora não haja evidências científicas de que essa seja uma verdade, levantamento feito pelo Conselho Federal de Farmácia (CFF) mostra que as vendas da hidroxicloroquina, por exemplo, mais que dobraram, passando de 963 mil em 2019 para 2 milhões de unidades em 2020. O aumento foi ainda maior no caso da Ivermectina, atingindo 557,26%.”
All that self-medication can lead to unintended consequences, such as young people suffering ivermectin-related liver failure.
One of the few bright lights in the pandemic darkness is vitamin D. While you will see grumpy health officials continuing to downplay the importance of vitamin D, nonetheless the evidential trend of favourable research is building like a tsunami. Early on in the pandemic, scientists began to notice a link between how much vitamin D a patient had and their likely outcome.
“Vitamin D deficiency is associated with compromised inflammatory responses and higher pulmonary involvement in COVID-19 affected patients. Vitamin D assessment, during COVID-19 infection, could be a useful analysis for possible therapeutic interventions,” reported an Italian team.
A Turkish study on the Lancet site lays out the reasons we think vitamin D works:
“The effects of vitamin D on the treatment and complications of COVID-19 and its potential contribution to the reduction of the incidence of the pandemic are among the most frequently researched topics. Vitamin D has antiviral activity and inhibitor effect of virus replication by stimulating the release of cathelicidin and defensin proteins in monocytes and macrophages.
“Vitamin D has an important role in the prevention of respiratory system infections due to its effects such as stimulating the chemotaxis of T-lymphocytes and clearing respiratory pathogens by inducing apoptosis and autophagy in the infected epithelium. It has been reported that the low T-lymphocyte level was found in some groups of COVID-19 patients with severe symptoms. Considering that vitamin D supplement increases the level of T-lymphocytes, this supports hypotheses that it could be useful in the treatment of COVID-19.
“The severe progress of COVID-19 in some cases is one of the most important problems of the pandemic. The studies have indicated that thrombotic events and cytokine storm increase in severe COVID-19 patients. These are held responsible for leading to death during COVID-19 infection. It is well known that vitamin D sufficiency reduces the risk of cytokine storm and regulates thrombotic pathways. It has been reported that the vitamin D sufficiency may reduce increased inflammatory markers and cytokine storm during the COVID-19 disease, the vitamin D deficiency may relate to severity and mortality of COVID-19. Consequently, the effect of vitamin D deficiency on the COVID-19 infection/outcomes is an attractive topic.”
The Turks number-crunched the data from 23 studies over the past year and worked out that vitamin D levels below 20ng/mL give you a 1.64 times higher risk of catching covid and 2.58 times higher risk of a severe dose, but they couldn’t establish a significant reduction in mortality. They concluded:
“Vitamin D deficiency increases the risk of COVID-19 infection and the potential for the severity of the disease. Therefore, vitamin D supplements should be added to prevention and treatment protocols for COVID-19 disease. There are insufficient data to prove its effect on mortality.”
Researchers at Boston University obtained the blood test vitamin D levels of 287 covid patients from their routine medical check-ups in the year before the pandemic, then investigated how they had coped with the disease. In patients aged over 65, historic vitamin D levels higher than 30ng/mL were associated with a 67% reduction in risk of death, a 78% drop in the risk of acute respiratory distress syndrome (ARDS, or the cytokine storm in the lungs), and a 74% risk reduction for sepsis.
Such associations of high vitamin D levels with reduced risk of infection and serious illness may go some way to explaining how the UK variant can cause thousands of deaths a day during a dark British winter, but a returning New Zealand traveller infected with the same variant at the height of the sunny southern hemisphere summer can go on a week-long road trip all over NZ and no one else tests positive – not even her husband who’d been travelling with her.
On the other side of the debate, there are studies that have found high dose vitamin D is useless.
A Brazilian study of 240 patients in the largest randomized double blind controlled trial so far, gave one group of patients a single dose of vitamin D at 5000µg (200000 IU), and the other group a placebo dose. It didn’t work:
“The primary end point, hospital length of stay, was not significantly different between the vitamin D3 group and the placebo group (median [interquartile range] of 7.0[4.0-10.0] days vs 7.0 [5.0-13.0] days; log-rank P = .59; unadjusted hazard ratio for hospital discharge, 1.07 [95% CI, 0.82-1.39]; P = .62).
“There were no significant differences in the secondary outcomes between the vitamin D3 group and the placebo group, including in-hospital mortality (7.6%vs 5.1%; difference, 2.5% [95% CI, −4.1% to 9.2%]; P = .43), admission to the intensive care unit, or need for mechanical ventilation. Administration of a high dose of vitaminD3 also did not appear to improve outcomes in the subgroup of 115 patients with vitamin D deficiency (25[OH]D <20 ng/mL) at randomization.”
On the face of it, the Brazilian study doesn’t look good for vitamin D. However, as an accompanying editorial in the JAMA medical journal noted, there were problems with the Brazil trial. Perhaps the biggest of these was that seriously ill patients were excluded:
“Accordingly, most of the patient population would be considered moderately ill and the results cannot be generalized to critically ill patients, who were excluded. This is important because the benefit of other anti-inflammatory therapies among patients with COVID-19 (eg, dexamethasone, tocilizumab) is highly dependent on severity of illness, with moderately ill patients receiving little or no benefit and severely ill patients receiving a substantial benefit.”
Additionally, warned JAMA, the study didn’t address whether vitamin D was useful as a preventative, nor did it show whether smaller regular doses of vitamin D were more effective than one massive single dose.
Another 2021 study sheds crucial light on this, after discovering that single high dose vitamin D just doesn’t work, which may be why there are conflicting studies on vitamin D:
“The value of vitamin D supplementation in the treatment or prevention of various conditions is often viewed with scepticism as a result of contradictory results of randomised trials. It is now becoming apparent that there is a pattern to these inconsistencies. A recent large trial has shown that high-dose intermittent bolus vitamin D therapy is ineffective at preventing rickets – the condition that is most unequivocally caused by vitamin D deficiency.
“There is a plausible biological explanation since high-dose bolus replacement induces long-term expression of the catabolic enzyme 24-hydroxylase and fibroblast growth factor 23, both of which have vitamin D inactivating effects.
“Meta-analyses of vitamin D supplementation in prevention of acute respiratory infection and trials in tuberculosis and other conditions also support efficacy of low dose daily maintenance rather than intermittent bolus dosing. This is particularly relevant during the current COVID-19 pandemic given the well-documented associations between COVID-19 risk and vitamin D deficiency. We would urge that clinicians take note of these findings and give strong support to widespread use of daily vitamin D supplementation.”
And there is more tantalising evidence that Vitamin D plays a key role as a preventative. A Croatian case study reports on a 66 year old obese male with Type 2 diabetes, arterial hypertension, psoriasis and severe arthritis taking immunosuppressant drugs – this guy was a walking poster-boy for serious covid complications. However, part of his psoriasis treatment had included several months of sunbed use for UVB phototherapy just before he was diagnosed with covid, raising his vitamin D blood levels to 93 nmol/L (37 ng/mL).
Instead of getting worse, his mild symptoms disappeared after three days and he was never hospitalised.
“We would like to emphasize the sufficient plasma 25-OH-vitamin D3 (calcifediol, precursor of an active form of the vitamin D3) level in the presented patient, which could have had, at least in part, positive impact on the disease course and outcome. Namely, since time when the possible favorable effects of vitamin D3 in COVID-19 patients have been proposed, several well-designed and convincing studies have clearly shown association between vitamin D deficiency and more severe COVID-19 clinical manifestations.
“As a recent meta-analysis shows, the need for hospitalization and mortality due to COVID-19 is significantly higher in people with insufficient levels of vitamin D. Study by Jain and colleagues found that prevalence of vitamin D deficiency among patients with severe COVID-19 manifestations treated in intensive care units was as high as 96.82%, in contrast to 32.96% in completely asymptomatic patients.”
COVID-19 causes massive inflammation in victims, but doctors are trialling new methods of delivering vitamin D therapy to combat that. In one study, covid patients were given “pulses” of high doses vitamin D – 60000 IU a day for eight to ten days – to boost blood levels and reduce covid inflammation markers. Another group were not given vitamin D. It worked:
“Eighty seven out of one hundred and thirty subjects have completed the study (VD:44, NVD:43). Vitamin D level has increased from 15.65 ± 5.54 ng/ml to 88.96 ± 31.55 ng/ml after Pulse D therapy in VD group and highly significant (p<0.01) reduction of all the measured inflammatory markers was noted. Reduction of markers in NVD group was insignificant (p>0.05) . The difference in the reduction of markers between the groups (NVD vs VD) was highly significant (p<0.01).
“Conclusions: Therapeutic improvement in vitamin D to 80-100 ng/ml has significantly reduced the inflammatory markers associated with COVID-19 without any side effects. Hence, adjunctive Pulse D therapy can be added safely to the existing treatment protocols of COVID-19 for improved outcomes.”
Next time you read a news article warning you not to take more than 400 IU a day because “it may be dangerous”, you have permission to laugh out loud. This trial delivered 150 times that amount per day for ten days.
Pulse dosing of 60000 IU daily also quickly eliminated covid in mild and asymptomatic patients in India:
“The key question is the effect of short‑term vitamin D supplementation in improving outcomes. Rastogi et al. randomized asymptomatic or mildly symptomatic SARS‑CoV‑2 RNA‑positive vitamin D‑deficient (25[OH]D <20 ng/mL) Indian individuals to receive high dose (60,000 IU) of cholecalciferol for 7 days or placebo. Greater proportion of those who received cholecalciferol turned SARS‑CoV‑2 RNA negative with a significant decrease in fibrinogen.”
Researchers at the Mayo Clinic have reached the same conclusion – daily doses work, one-off massive bolus doses do not:
“In a meta-analysis of randomized controlled trials of vitamin D supplementation, daily or weekly, but not bolus doses of vitamin D, were associated with a reduced risk of respiratory infection, particularly among those with 25(OH)D values <10 ng/mL.2 This contextual framework underpins the rationale for studying the therapeutic benefit of vitamin D in COVID-19.”
Mayo studied 144 covid patients hospitalised in New York and Boston, and found clear links between vitamin D levels and risk of death:
“Patients with lower serum 25(OH)D values within 6 months before or during hospital admission for COVID-19 had increased mortality and need for invasive mechanical ventilation.
“Particular strengths of this study include the racial diversity represented and the consistency of the relationship of 25(OH)D concentrations with mortality and invasive mechanical ventilation across different multivariable models, adjusting for a variety of covariates that could affect illness severity or vitamin D status.
“The median 25(OH)D concentration was 28 ng/mL, and mortality in those with 25(OH)D values <30 ng/ml was 25%, compared with 9% in those with values ≥30 ng/mL. Similar results were obtained using a 25(OH)D threshold of 20 ng/mL in a sensitivity analysis. Approximately half of the patients had 25(OH)D measurements prior to infection and hospitalization for COVID-19.”
With Latin America one of the global hotbeds of the pandemic, there’s enormous interest in whether vitamin D supplements can head off the COVID-19 stampede at the pass, and whether a daily ounce of prevention is better than a cure:
“Long‑term regular vitamin D supplementation may protect against infections such as SARS‑CoV‑2 more effectively compared with oral bolus administered after COVID‑19 diagnosis.”
So, how much vitamin D should you take to optimise your immune defence against covid? A Mexican research team recently asked the same question:
“Due to the need to establish accessible strategies for the prevention of complications from COVID‑19, the authors of the present review agree with the current proposal of Grant et al, who suggested that individuals with low levels of 25(OH)D should be supplemented for a month with 10,000 IU/day (250 μg) of vitamin D3 for the rapid restoration of the desired concentrations between 40 and 60 ng/ml (100 and 150 nmol/l).
“For maintenance, this should be followed by daily supplementation of 5,000 IU (125 μg). Notably, that baseline monitoring of 25(OH)D concentrations should be considered. In addition, avoiding high doses of calcium and assessing the consumption of magnesium and vitamin K2 should be considered for the prevention of long‑term adverse effects of high doses of vitamin D.”
One of the most intriguing studies on vitamin D and covid, however, comes from the Spanish city of Cordoba. There, 76 hospitalised covid patients were separated into two groups in a randomised controlled trial on a 2:1 ratio. Fifty patients were given 21280 IU of vitamin D in its calcifediol form on the day of admission, and top-up doses of 10640 IU on days three and seven, then weekly until either discharge or admission to intensive care – whichever came first.
“All hospitalized patients received as best available therapy the same standard care (per hospital protocol) including a combination of hydroxychloroquine and azithromycin. Outcomes of effectiveness included the rate of ICU admission and deaths. Only 1 of 50 patients treated with calcifediol (2%), but 13 of 26 untreated patients (50%), required ICU admission.”
It was a glittering result for vitamin D, reducing ICU admissions from 50% to 2%, but at the same time a damning result for hydroxychloroquine.
The Spanish study ran into some flak soon after publication over whether its blinding was done properly:
“However, a comprehensive mathematical reanalysis by an independent group concluded that the randomization, large effect size, and high statistical significance address many of these concerns. In particular, it showed that random assignment of patients to treatment and control groups was highly unlikely to distribute comorbidities or other prognostic indicators sufficiently unevenly to account for the large effect size, and that imperfect blinding would need to have had an implausibly large effect to account for the reported results.”
In other words, the magnitude of the difference – 2% vs 50% needing ICU, and the larger pool of patients taking vitamin D which should have increased the numbers who might need ICU – is so big that the results stand regardless.
So, where does that leave us?
To summarise, COVID-19 is not “just the flu”, and treating it with that kind of contempt is like swimming in shark-infested waters with a gash on your leg. As a novel animal virus, we are still learning what it can do to us and how it differs from other viruses we have become accustomed to.
In any crisis, the agenda is normally determined by the greatest need. In the early days, when it looked like this was just a bad chest infection that most people recovered from, the agenda was set by TV images of overcrowded hospital wards and refrigerated trucks acting as temporary morgues. “Death” was the metric that we measured covid danger with. If you didn’t die you were good, move on and make room for the next patient please.
But the media, politicians and health officials got it wrong. The metric we really needed to be using was “life”: what was the danger to survivors, what was the danger to the vast majority of people who were either asymptomatic or who just felt unwell for a couple of days at home?
It is one thing for an 86 year old to die of covid. It is an entirely different story when people in their teens, 20s and 30s are sustaining hidden damage to their organs and fertility: they still have decades to live, in theory. Yet covid could take decades off their lifespan and hundreds of thousands or even millions off their earning potential. Spanish Flu in 1918 created a generation of broken people, and misery and desperation that created the conditions for the Second World War.
Will vaccines save us this time around? Maybe, maybe not. Key questions remain, like when will the vaccine wear off? Will we find out too late? Will mutants like the P1 arise that can evade the vaccines and again spread around the world before pharmaceutical companies can catch up? Given the time lag involved in vaccine design and rollout to the public, are we forever going to be always six months to 18 months behind the 8-ball, playing whack-a-mole with an ever changing virus?
The good news is there is something we can all do: we can chug down vitamin D in the hope of reducing our risk of a covid infection in the first place, and increasing our survival chances in the second.
But it won’t eliminate the risk entirely. If vitamin D could eradicate all viruses we would not still have HIV, herpes and others capable of living inside us forever. Vitamin D powers our immune systems, but by definition a virus that evades immune systems makes even vitamin D’s job much harder.
Compared to ivermectin and hydroxychloroquine, however, using vitamin D as the fence at the top of the cliff, instead of an ambulance at the bottom, is a no-brainer.
The evidence on vitamin D shows it may truly be as close to a miracle as we are going to get in this pandemic.
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