Analysis by Dr. Joseph Mercola Fact Checked
October 04, 2021
STORY AT-A-GLANCE
· A Spanish study found
giving supplemental vitamin D3 (calcifediol) to hospitalized patients with
PCR-confirmed COVID-19 — in addition to standard care — reduced ICU admissions
by 82% and mortality by 64%
· People who already had
higher vitamin D at baseline were 60% less likely to die
· Many are now calling for
official vitamin D recommendations to be issued by their governments
· Other recent research found
vitamin D is a contributing factor to COVID-19 outbreaks and infection
severity. Surges in daily positive tests during the fall of 2020 in 18 European
countries linearly correlate with latitude, and, hence, sun exposure and
vitamin D levels
· One of the reasons vitamin
D is so important against COVID-19 has to do with its influence on T cell
responses. Vitamin D receptor signals regulate T cell responses and therefore play
an important role in your body’s defense against viral and bacterial infections
This article was previously published February 22,
2021, and has been updated with new information.
Vitamin D plays
an important role in most diseases, including infectious disease, which is why
from the very beginning of the COVID-19 pandemic, I suspected that optimizing
vitamin D levels among the general population would significantly lower
COVID-19 incidence and death.
Since then,
mounting evidence reveals this is indeed the case, as researchers have
repeatedly demonstrated that higher vitamin D levels reduce rates of positive
tests, hospitalizations and mortality related to this infection.
Vitamin D3 Reduces COVID
Infection and Mortality
A
now-retracted, preprint Spanish study1,2 found that giving
supplemental vitamin D3 (calcifediol) to hospitalized patients with
PCR-confirmed COVID-19 reduced ICU admissions by 82% and mortality by 64%.3 People who already
had higher vitamin D at baseline were 60% less likely to die.
Another study
was published in June 2021.4 In this study, researchers concluded that
“vitamin D deficiency is associated with an increased risk of COVID-19
infection and mortality across a wide range of countries.”
Other studies
have shown that “vitamin D deficiency to address COVID-19 warrants aggressive
pursuit and study.”5 Retrospective data demonstrated that a
deficiency was also associated with an increased risk of COVID1-19 infection.6
Renewed Calls for Vitamin D
Recommendations
In response to
the now-retracted study, British MP David Davis tweeted that hospitals should
consider giving vitamin D3 to every COVID patient in every hospital in the
temperate latitudes. Since other, peer-reviewed, studies like the ones I
mentioned above support higher vitamin D levels being connected to a better
chance of survival from COVID, it seems reasonable that Davis’ suggestion is
not out of line, regardless of the one retracted article.
Many others are
also calling for official vitamin D recommendations to be issued by their
governments. Among them is Emer Higgins,7 a member of the Irish
political party Fine Gael, who called on the Irish health minister, Stephen
Donnelly, to include vitamin D supplementation in its “Living with COVID-19”
strategy, slated for launch at the end of February 2021.
Higgins leaned
on evidence from the Irish Covit-D Consortium,8 which shows vitamin D
helps optimize your immune response. "There is negligible risk in this
strategy and potentially a massive gain," she said. According to the
Covit-D Consortium, the nutrient can lower the risk of death from COVID-19 in
the elderly by as much as 700%.9
Low Vitamin D Linked to
COVID-19 Outbreaks and Severity
Another study10 published in the
journal Scientific Reports confirmed vitamin D is a contributing factor to
COVID-19 outbreaks and infection severity. According to the authors, the surges
in daily positive test results during the fall of 2020 in 18 European countries
linearly correlate with latitude, and hence sun exposure and vitamin D levels.
They point out that:
"The country surge date corresponds to the
time when its sun UV daily dose drops below ≈ 34% of that of 0° latitude.
Introducing reported seasonal blood 25-hydroxyvitamin D (25(OH)D) concentration
variation into the reported link between acute respiratory tract infection risk
and 25(OH)D concentration quantitatively explains the surge dynamics ...
The date of the surge is an intrapopulation
observation and has the benefit of being triggered only by a parameter globally
affecting the population, i.e. decreases in the sun UV daily dose.
The results indicate that a low 25(OH)D
concentration is a contributing factor to COVID-19 severity, which, combined
with previous studies, provides a convincing set of evidence."
While it's
well-recognized that most elderly individuals are deficient in vitamin D, the
problem is widespread in all age categories, including children.
As noted in a
February 2021 study11 comparing vitamin D levels in breast milk
collected in 1989 and 2016/2017, vitamin D concentrations are consistently
higher during the summer but, overall, vitamin D levels have declined since
1989. As a result, pregnant and lactating mothers and their infants may require
vitamin D supplementation for optimal health.
Vitamin D Is Crucial for
Optimal T Cell Responses
One of the
reasons why vitamin D is so important against COVID-19 has to do with its
influence on T cell responses. Animal research12 published in 2014
explained how vitamin D receptor signals regulate T cell responses and
therefore play an important role in your body's defense against viral and
bacterial infections.
As noted in
that study, when vitamin D signaling is impaired, it significantly impacts the
quantity, quality, breadth and location of CD8 T cell immunity, resulting in
more severe viral and bacterial infections.
Strong antibody response correlates with more severe clinical disease while T-cell response is correlated with less severe disease.
What's more,
according to a December 11, 2020, paper13 in the journal
Vaccine: X, high-quality T cell response actually appears to be far more
important than antibodies when it comes to providing protective immunity
against SARS-CoV-2 specifically:14
"The first SARS-CoV-2 vaccine(s) will likely
be licensed based on neutralizing antibodies in Phase 2 trials, but there are
significant concerns about using antibody response in coronavirus infections as
a sole metric of protective immunity.
Antibody response is often a poor marker of prior
coronavirus infection, particularly in mild infections, and is shorter-lived
than virus-reactive T-cells …
Strong antibody response correlates with more
severe clinical disease while T-cell response is correlated with less severe
disease; and antibody-dependent enhancement of pathology and clinical severity
has been described.
Indeed, it is unclear whether antibody production
is protective or pathogenic in coronavirus infections. Early data with
SARS-CoV-2 support these findings. Data from coronavirus infections in animals
and humans emphasize the generation of a high-quality T cell response in
protective immunity."
The authors go
on to state that epitopes associated with SARS-CoV2 have been identified on CD4
and CD8 T-cells in the blood from patients who have successfully recovered from
COVID-19, and that these epitopes "are much less dominated by spike
protein than in previous coronavirus infections."15
As a refresher,
aside from SARS-CoV-2, there are six other coronaviruses known to cause
respiratory disease in humans:16
·
Types 229E, NL63, OC43 and
KHU1 are quite
common and cause mild to moderate respiratory infections such as the common
cold.
·
SARS-CoV (Severe Acute
Respiratory Syndrome coronavirus), associated with severe respiratory illness.17,18
·
MERS-CoV (Middle East
Respiratory Syndrome coronavirus) which, like SARS, causes more severe
respiratory infections than the four common coronaviruses.19
Understanding the Role of
Epitopes
What do they
mean by "epitopes associated with SARS-CoV2 have been identified on CD4
and CD8 T-cells"? Epitopes20 are sites on the virus that allow antibodies
or cell receptors in your immune system to recognize it. This is why epitopes
are also referred to as "antigenic determinants," as they are the
part that is recognized by an antibody, B-cell receptor or T-cell receptor.
Most antigens —
substances that bind specifically to an antibody or a T-cell receptor — have
several different epitopes, which allow it to be recognized by several
different antibodies. Importantly, some epitopes can cause autoimmunological
pathogenic priming if you've been previously infected with SARS-CoV-2 or
exposed via a COVID-19 vaccine.21
In other words,
if you've had the infection once, and get reinfected (either by SARS-CoV-2 or a
sufficiently similar coronavirus), the second bout has the potential to be more
severe than the first. Similarly, if you get vaccinated and are then infected with
SARS-CoV-2, your infection may be more severe than had you not been vaccinated.
For this
reason, "these epitopes should be excluded from vaccines under development
to minimize autoimmunity due to risk of pathogenic priming," a recent
paper22 in the Journal of
Translational Autoimmunity warns.
One of the
reasons why mRNA gene therapy "vaccines" are causing so many problems
may in fact be because they have failed to "screen out unsafe epitopes to
reduce autoimmunity due to homology between parts of the viral protein and the
human proteome," according to that Journal of Translational Autoimmunity
paper.23
Natural SARS-CoV-2
Infection Induces Broad Epitope Coverage
The authors of
the Vaccine: X paper point out that while most COVID-19 gene therapy
"vaccines" focus on the SARS-CoV-2 spike protein as a natural
antigen, "natural infection by SARS-CoV-2 induces broad epitope coverage,
cross-reactive with other betacoronaviruses."
Indeed, this
has been demonstrated in a number of studies, including a Singaporean study24,25,26 that found common
colds caused by the betacoronaviruses OC43 and HKU1 might make you more
resistant to SARS-CoV-2 infection, and that the resulting immunity might last
as long as 17 years.
In other words,
if you've beat a common cold caused by a OC43 or HKU1 betacoronavirus in the
past, you may have a 50/50 chance of having defensive T-cells that can
recognize and help defend against SARS-CoV-2. What the Vaccine: X authors are
basically warning about is that the so-called vaccines are unlikely to provide
the same level of immunity as natural infection does, and may even cause
pathogenic priming.
Vitamin D Speeds Viral
Clearance
Other research,27 published in November
2020 in the Postgraduate Medical Journal, shows oral vitamin D supplementation
also helps speed up SARS-CoV-2 viral clearance. This study included only
asymptomatic or mildly symptomatic SARS-CoV-2-positive individuals who also had
vitamin D deficiency (a vitamin D blood level below 20 ng/mL).
Participants
were randomly assigned to receive either 60,000 IUs of oral cholecalciferol
(nano-liquid droplets) or a placebo for seven days. The target blood level was
50 ng/mL. Anyone who had not achieved a blood level of 50 ng/mL after the first
seven days continued to receive the supplement until they reached the target
level.
Periodically,
all participants were tested for SARS-CoV-2 as well as fibrinogen, D-dimer,
procalcitonin and CRP, all of which are inflammatory markers. The primary
outcome measure of the study was the proportion of patients testing negative
for COVID-19 before Day 21 of the study, as well as changes in inflammatory
markers. As reported by the authors:28
"Forty SARS-CoV-2 RNA positive individuals
were randomized to intervention (n=16) or control (n=24) group. Baseline serum
25(OH)D was 8.6 and 9.54 ng/mL, in the intervention and control group,
respectively.
10 out of 16 patients could achieve 25(OH)D>50
ng/ml by day-7 and another two by day-14 … 10 (62.5%) participants in the
intervention group and 5 (20.8%) participants in the control arm became
SARS-CoV-2 RNA negative. Fibrinogen levels significantly decreased with
cholecalciferol supplementation unlike other inflammatory biomarkers.
[A] greater proportion of vitamin D-deficient
individuals with SARS-CoV-2 infection turned SARS-CoV-2 RNA negative with a
significant decrease in fibrinogen on high-dose cholecalciferol
supplementation."
More Evidence Vitamin D
Impacts COVID-19
If you haven't
already gone to the free website I created to educate the world about vitamin
D, please do now. It's www.stopcovidcold.com. You can download the free
condensed version of the paper I had published last year that is easier to read
and full of graphics to illustrate the information.
October 31, 2020,
my own vitamin D review,29 co-written with William Grant, Ph.D., and Dr.
Carol Wagner, both of whom are part of the GrassrootsHealth expert vitamin D
panel, was published in the peer-reviewed journal Nutrients. You can read
the paper for free on the journal's website.
As noted in
that paper, dark skin color, increased age, preexisting chronic conditions and
vitamin D deficiency are all features of severe COVID disease and, of these,
vitamin D deficiency is the only factor that is readily and easily modifiable.
You may be able
to reverse chronic disease, but that typically takes time. Optimizing your
vitamin D, on the other hand, can be achieved in just a few weeks, thereby
significantly lowering your risk of severe COVID-19.
In our paper,
we review several of the mechanisms by which vitamin D can reduce your risk of
COVID-19 and other respiratory infections, including but not limited to the
following:30
·
Reducing the survival and replication of viruses31
·
Reducing inflammatory cytokine
production
·
Maintaining endothelial integrity — Endothelial
dysfunction contributes to vascular inflammation and impaired blood clotting,
two hallmarks of severe COVID-19
·
Increasing angiotensin-converting enzyme 2 (ACE2)
concentrations, which prevents the virus from entering cells via the ACE2
receptor — ACE2 is downregulated by SARS-CoV-2 infection, and by increasing
ACE2, you also avoid excessive accumulation of angiotensin II, a peptide
hormone known to increase the severity of COVID-19
Vitamin D is
also an important component of COVID-19 prevention and treatment for the fact
that it:
·
Boosts your overall immune function by modulating
your innate and adaptive immune responses
·
Reduces respiratory distress32
·
Improves overall lung function
·
Helps produce surfactants in your lungs that aid in
fluid clearance33
·
Lowers your risk of comorbidities associated with
poor COVID-19 prognosis, including obesity,34 Type 2 diabetes,35 high blood pressure36 and heart disease37
Data from 14 observational
studies — summarized in Table 1 of our paper38 — suggest that
vitamin D blood levels are inversely correlated with the incidence and/or
severity of COVID-19, and the evidence currently available generally satisfies
Hill's criteria for causality in a biological system.39 Our paper40 also details several
features of COVID-19 that suggest vitamin D deficiency is at play in this
illness.
- 1 Preprints in The Lancet January 22, 2021
- 2 Preprints in The Lancet January 22, 2021 (PDF)
- 3 Preprints in The Lancet January 22, 2021, PDF page 3 (Added value of this study)
- 4 Health Security, June 7, 2021;19(3)
- 5 medRxiv, May 13, 2020; doi.org/10.1101/2020.05.08.20095893
- 6 JAMA Infectious Diseases, 2020;3(9)
- 7 Irish Times February 15, 2021
- 8 Irish Journal of Medical Science November 21, 2020
- 9 Herald December 30, 2020
- 10 Scientific Reports January 21, 2021; 11 Article number 1981
- 11 Nutrients 2021; 13(2): 573
- 12 The Journal of Nutrition October 15, 2014; 144(12): 2073-2082
- 13, 14, 15 Vaccine: X December 11, 2020; 6: 1000076
- 16 Signal Transduct Target Ther. June 10, 2020; 5(1): 89
- 17 Mayoclinic.org, SARS
- 18, 19 NBC News March 5, 2020
- 20 Creative Diagnostics Immunology
- 21, 22, 23 Journal of Translational Autoimmunity 2020; 3: 1000051
- 24 Biorxiv preprint DOI: 10.1101/2020.05.26.115832 (PDF)
- 25 Daily Mail June 12, 2020
- 26 Science Times June 12, 2020
- 27 Postgraduate Medical Journal November 12, 2020 DOI: 10.1136/postgradmedj-2020-139065
- 28 Postgraduate Medical Journal November 12, 2020 DOI: 10.1136/postgradmedj-2020-139065, Results
- 29, 30, 40 Nutrients October 31, 2020;12, 3361; doi:10.3390/nu12113361
- 31 Nutrients, 2020;12:988
- 32 Advances in Pharmacological Sciences 2018; 2018: 8494816
- 33 ATS Journals October 5, 2010; 183(10)
- 34 Medicina 2019 Sep; 55(9): 541
- 35 Diabetes.co.uk January 15, 2019
- 36 The Lancet Diabetes & Endocrinology September 1, 2014; 2(9): 682-684
- 37 Current Treatment Options in Cardiovascular Medicine 2012 Aug; 14(4): 414–424
- 38 Nutrients October 31, 2020;12, 3361; doi:10.3390/nu12113361, Table 1
- 39 Nutrients October 31, 2020;12, 3361; doi:10.3390/nu12113361, Table 3