COVID-19 is a coronavirus, which is potentially lethal, especially in the
elderly
Predisposing factors are age, high blood pressure, heart disease, and diabetes,
and in around 90% of deaths, there was at least one co-morbidity.
Resistance to COVID-19 morbidity appears to drop as production of melatonin decreases with
age
Factors affecting production of melatonin, such as vitamin B12 levels, and the
levels of supporting vitamins and minerals will therefore affect resistance to
COVID-19 sequelae Resistance to
COVID-19 in China has been found to be proportional to regional Selenium
concentrations Resistance to
COVID-19 has been found to be dependent on vitamin D levels, with a dramatic
rise in mortality as vitamin D goes from sufficient to deficient. Resistance to
respiratory infections, such as COVID-19 is higher in those who have normal
glutathione levels in respiratory secretions The COVID-19 virus enters cells via ACE-2
receptors on cells Expression of ACE-2 receptors is increased
with the use of ACE-2 receptor blockers (ARBs) Potentially the use of the ARBs could
increase the uptake of COVID-19 This may explain why people on
anti-hypertensive medication are more at risk of COVID-19 infections. Risk factors for COVID-19 related deaths
include increased signs of sepsis, high blood pressure, heart disease
CVD increase 10.6%,
lung disease 7.3%, diabetes 6.3%, being immuno-suppressed 5.6% and blood clotting issues,
however, the greatest risk is with increasing age. In some regards, the death rate is more
dependent upon the standard of health care than any thing else with death
rates of only 1-2% in countries such as Israel and Australia, but as
high as 11.8, 19 and 11.8% in Spain, France and Italy respectively (as of
26/03/20). This is going to be catastrophic in Africa, where death rates from
the flu are very high.
Many of the anti-hypertensive medicines, including Captopril and
enalapril, and also selenopril directly interact with ACE and inhibit their
action. Potentially, though, the reduce activity of ACE would lead to an
up-regulation of ACE by the cells, and hence provide more receptors for COVID-19
to bind to, thereby increasing the severity of the infection. Recently a new
inhibitor selenoneine has been identified as a potential ACE inhibitor (Seko
etal, 2019). Whilst this molecule, a selenium-containing imidazole, does contain
Selenium, its action is completely different to that of dietary or supplemental
Selenite, which is involved in production of Selenoproteins.
Melatonin, together with vitamin D, stimulates neuronal stem
cells to differentiate into oligodendrocytes, which are the cells in the brain
that are responsible for myelination of the nerves in the brain. Melatonin is
thus critically important in the young for neuronal development as the child
grows and matures. Production of melatonin gradually starts to
decline after puberty. To date there have been no fatalities due to COVID-19 in
children under the age of 9, and there is a gradual increase in fatality rate
with age, which is inversely proportional to the drop in melatonin
production with age (Gravid etal, 2007). One reason postulated for this is
melatonin's unique ability to inhibit the activation of the inflammatory
cascade. In this way destruction of mitochondrial energy production during the
inflammatory response can be inhibited. In the lung, the site of COVID-19
infection, melatonin can thereby inhibit the acute respiratory distress
syndrome, thereby reducing the damage to the lungs and thereby the need for
intubation and mechanical ventilation of the lungs, with the associated damage
(Wu etal, 2020). Recent studies comparing melatonin levels to viral isolation
revealed that "melatonin usage was associated
with a nearly 30 percent reduced likelihood of testing positive for SARS-CoV-2
(Consult QD 2020). Melatonin has also been shown to be protective against multiple
organ failure, circulatory failure, as well as preventing mitochondrial damage
in experimental sepsis, and able to reduce lipid peroxidation, one of the
indices of inflammation and mortality in human newborns with sepsis (Escames
etal, 2006; Lopez etal 2006; Escames etal, 2005; Carillo-Vico etal, 2005;
Srinivasan etal, 2010; Reiter etal, 2001; 2017; Biancatelli etal 2020) Melatonin
has also been shown to modulate the inflammatory response through its modulation
of Inflammasome activation (Favero etal, 2017)
Melatonin levels as we age
Grivas and Savvidou, 2007
COVID-19 fatality rate by age (China)
Production of melatonin is critically dependent upon maintaining sufficient
levels of the methylating agent, S-Adenosylmethionine, a product of the
methylation cycle, a cycle which is dependent on functional activity of methyl
vitamin B12. Functional activity of vitamin B12 is in turn dependent upon
functional vitamin B2, or more specifically FMN and FAD. Production of FMN and
FAD, in turn is dependent upon intake of vitamin B2, Iodine, Selenium and
Molybdenum. Deficiencies in any or all of these will lead to lower active
vitamin B2 being present, and from there lower active methyl B12, and hence
lower levels of melatonin. Potentially there is another reason for higher
lethality in those with low melatonin, and that is the potential accumulation of
the adrenalin pre-cursor- serotonin, leading to serotonin levels typically seen
in serotonin syndrome, a syndrome that has been associated with acute pulmonary
edema (Wu etal, 2015; Shah and Jain, 2016; Ferslew etal, 1998). Vitamin B12 has
long been known to have a role in damping down the inflammatory response via
several mechanisms Scavenging of
Nitric Oxide Inhibition of
NFkappaB, an important inflammatory mediator More recently
high dose intravenous Methyl B12 has been suggested as a safe and cost
effective treatment for the Acute Respiratory Distress Syndrome, that is one
of the major causes of death from COVID-19 (Wheatley, 2006; Manzanares and
Hardy, 2010). If this is found to be true, then
one would assume that daily topical administration of Methyl B12 in Transdermoil High dose sodium
selenite given to patients with severe systemic inflammatory response syndrome,
sepsis, and septic shock, was found to reduce mortality rate (Angstwurm etal,
2007). The virulence of several respiratory viruses was found to be increased in
Selenium deficient mice (Beck etal, 2003; 2001; 1994). Selenium supplementation with 200
ug/day selenium has been found to reduce the viral load in HIV (Hurwitz etal,
2007; Baum etal, 1997). Recent data analysis from China has shown that the areas with the highest
Selenium concentrations has lower death rates than those with low Selenium.
Selenium potentially has many roles in protection. It is required as a cofactor
by glutathione peroxidase, which is involved in inactivating inflammatory
hydrogen peroxide. It is critical in the activation of vitamin B2, and in
thereby in maintaining free glutathione inside the cells, and active B2 (as FMN
and FAD) are both required to maintain the activity of methylB12, and so is
involved in the production of melatonin. Levels of Selenium decline in the body
with age, and are generally lower in males, due to the targeting of Selenium to
the testes, hence potentially explaining the higher death rate in males than
females of the same age.
Zhang etal, 2020 Resistance to
COVID-19 in China has been reported to be correlated with regional Selenium
status (Zhang etal, 2020, Rayman etal, 2020;
Discussion paper). Part of the
inflammatory cascade involves the activation of oxygen by NADPH Oxidase to
generate the reactive oxygen species O2**, This in turn is further activated to
generate hydrogen peroxide (H2O2). Under normal
circumstances the H2O2 is then converted to hydroxide and
then water by the Selenoprotein Glutathione-Peroxidase (GSHPx(Se).
In Selenium
deficiency this reaction is reduced and so dangerous H2O2
would accumulate inside the cell and cause massive intracellular damage.
Further, the reduction of oxidized glutathione (GSSG) requires the FAD-dependent
enzyme glutathione reductase (GSH reductase). In Selenium deficiency activation
of vitamin B2 is incomplete and hence levels of FMN and FAD would be lower
inside the cell. This has the dual effect of reducing the activity of GSH-reductase,
but also, because of the requirement for FMN and FAD in the cycling of methyl
B12, lack of FMN and FAD would lead to lower methylation and reduced production
of GSH, through lower activity of the sulphation cycle in Methyl B12 deficiency.
Studies in which
glutathione production has been inhibited have shown to result in very high
levels of free radicals accumulating within cells (Kurniawan etal, 2020),
further supporting the hypothesis that reduced GSHPx and GSH reductase activity
can result in massively increased oxygen radical damage. Uncontrolled NADPH-oxidase
have been shown to play a critical role in Hyperoxia-induced acute lung injury (Carnesecchi
etal 2009). Hyperoxia has also been shown to increase ROS production by human
pulmonary artery endothelial cells (Parinandi etal, 2003). NADPH oxidase
activity in inflammasomes has also been shown to be responsible for the
production of pulmonary fibrosis, a feature of COVID-19 infections (Sun etal,
2015). Potentially hyperoxygenation of the lungs during Ventilator treatment
could potentiate the ROS damage, particularly in those that are Selenium, or B12
deficient (Carnesecchi
eta. This may explain the very high death rate (92%) in those over 65 who
are placed on ventilators. Despite these associations, no Health expert has yet
to suggest that populations supplement with Selenium. As of 13/05/2020, there
were 286,000 deaths from COVID-19. How many of these could have been prevented
just by adequate Selenium supplementation? Iron deficiency
has been associated with an increased susceptibility to respiratory infections (Jayaweera etal,
2019; Stepan etal, 2018; Tansarli etal 2013), and with a poorer outcome in
patients with other respiratory infections, such as influenza A (H1N1)(Bai
etal, 2010;. Iron deficiency has also
been associated with a poorer outcome for congestive heart failure, a potential
complication of Coronavirus infection (Nickol etal, 2015). Iron supplementation
has been shown to reduce morbidity due to upper respiratory infections (de Silva
etal, 2003; Hurrell 2007). Persons using PPIs for treatment of obesity are known
to have lower iron levels (Yu etal, 2017), and as such might be expected to have
higher incidence of URTI. Iron is also essential for energy production and for
carrying oxygen, hence a deficiency of iron could contribute to respiratory
failure seen in COVID patients. Elevation of serum ferritin is seen in COVID-19
infections. Along with iron,
zinc deficiency has been associated with an increased incidence of acute
respiratory infections (Bailey etal, 2015) Vitamin B12 has a
critical role in energy production through it's role in production of CoQ10,
creatine, and its role in the production of the Krebs cycle enzyme, aconitase.
Hence decreased levels of active B12 should be correlated with lower metabolic
energy in Krebs may be associated with reduced energy production and as such may
contribute to respiratory failure in COVID-19 patients. Studies have
reported a consistent association between low serum concentrations of
25-OH-Vitamin D and susceptibility to acute respiratory tract infections
(Martinez etal, 2017; Ginde etal, 2009; Joliffe etal, 2013: Kim etal, 2015;
Remmelts etal, 2012; Leow etal, 2011; Mathias etal 2015). Vitamin D supplementation has also been shown to reduce
mortality to respiratory tract infections, particularly in the elderly (Bjelakovic
etal, 2011). Current suggestions are supplementation with 1000-4000 IU of
vitamin D per day, with bolus supplementation (ie once per week) not recommended
(Sizar etal 2020). It has been suggested that the heavy mortality observed
following Coronavius infection may be associated with low vitamin D levels in
countries such as Italy, and Scandinavia. Low vitamin D is also prevalent in the
UK, with a rise in rickets being seen in children. Vitamin D has been shown to
decrease the production of pro-inflammatory molecules, and as such may reduce
the "cytokine storm" that is associated with the pathogenesis of COVID-19.
Vitamin D has also been shown to be essential for immune function, and low
vitamin D is associated with greater susceptibility to both bacterial and viral
infections. Vitamin D levels tend to decrease with age, as too vitamin D
deficiency associated conditions such as diabetes and obesity, all three of
which have been associated with mortality to COVID-19. In Ireland, 47% of people
over 85 are deficient in vitamin D, with 27% of those over 70. Vitamin D
deficiency is very common in the community with 42% of Americans deemed vitamin
D deficient. Deficiency increases in black people (82%) and Hispanics (70%). The
highest death rate in the US occurs in African-Americans. In nursing homes in
Australia, where a significant number of cases of deaths, 86% of women, and 68%
of men were found to have vitamin levels below 28 nmols/litre. Despite the known
protective effect of vitamin D, no health authority has yet to suggest that the
population increase their vitamin D. This alone could have lead to a dramatic
reduction in the death rate from COVID-19 and also reduce the deaths from other
respiratory viruses and from seasonal flu. Recent studies
have identified the protective effect of vitamin D levels against COVID in
Europe (Pugach and Pugach, 2020) Recent studies in
the UK have supported the above (see
SMH). Despite this, no government agency has come out and suggested that
people should supplement with vitamin D during the pandemic, not even the WHO.
This is despite the information above being freely available in the literature
to any health professional or advisor to governments. In some countries, they
have even closed down the beaches and so reduced the ability of the population
to gain effective levels of vitamin D. Some selected data from the UK studies
Studies have now
shown that despite the success of the smart sun campaigns, such as the slip,
slop, slap campaign, which is largely responsible for the lowering of the
population vitamin D levels, there has been little change in the incidence of
melanoma. Studies comparing
vitamin D deficiency rates with death rate show a linear correlation between the
number of deaths and the percentage death rate from COVID-19
Pugash and Pugash,
2020 Death rates from
COVID-19 vary greatly from country to country, with some recording death rates
from infection as low as 0.4%, but others with death rates as high as 12%.
Thus, whilst within a country
the predisposing factors are
high blood pressure, heart disease CVD ^ 10.6%, lung disease ^
7.3%, diabetes ^ 6.3%, being immunosuppressed ^ 5.6% and blood clotting issues,
and age, by far the biggest predisposing factor for the death is the
country in which you live, which depending upon country can vary from a death
rate of less than 0.6% to over 12%.
Currently it is unknown why the rates vary, however, if these reasons could be
identified it may go a long way to reducing the severity of the condition, which
will be an essential component of dealing with the virus, particularly during
the waiting period between now and the development of a vaccine. It is possible,
though that the variability in testing goes some way to explain the differences. This will be
more even more important if a successful vaccine is not developed. We have
dedicated a separate page to a discussion of possible causes of the varying
death rates.. Vitamin A.
Vitamin A was originally thought of as the anti-infective vitamin, and vitamin A
deficiency has been implicated in the severity of diarrhoea and measles.
Supplementation with vitamin A has reduced the morbidity and severity of a range
of infectious diseases including HIV, malaria, measles and measles-related
pneumonia (Semba 1999). The ability to generate an immune response to
inactivated bovine coronavirus vaccines is compromised in calves with low
vitamin A (Lee etal, 2013). Vitamin C.
Vitamin C has been shown to support immune function and to be able to protect
against coronavirus infections (Hemila 2003). Vitamin C is also essential for
the formation of hydroxyproline, an essential amino acid for the production of
high tensile collagen. Lack of vitamin C, could potentially lead to alveolar
collapse, due to "weak" collagen. Vitamin D.
Vitamin D has known immune functions including stimulation of maturation of
immune cells, but also in activation of several proteins in Krebs cycle.
Decreased vitamin D levels in calves has been reported to increase
susceptibility of calves to bovine Coranavirus (Nonnecke etal, 2014).
Potentially the greatly reduced vitamin D levels in the population due to the
adoption of high SPF cosmetics, could increase the morbidity and mortality to
coronavirus. Activation of vitamin D requires adequate amounts of iron,
activated vitamin B2 (FAD), vitamin B12 and folate. Interestingly, vitamin D
levels were very low in Italy, one of the countries with the highest death rate
from COVID-19 (Giustina etal, 2020; Garami 2020). Potentially doubling the
vitamin D levels in the population could have a much more beneficial effect than
any of the molecules currently under study to aid in reducing the inflammatory
storm. Selenium. Selenium
has an important role in the body, not only in anti-oxidant defense but also in
the activation of vitamin B2, and then the activation of vitamin B6, vitamin K
and also for vitamin A. High dose sodium selenite has been found to reduce viral
loads, and to reduce mortality in patients with severe systemic inflammatory
response syndrome, sepsis, and septic shock. Selenium is also a vital mineral
for the activation of vitamin B2. The Selenoprotein, glutathione peroxidase has
been shown to reduce damage caused by hydrogen peroxidase radicals and thereby
reduce the inflammatory response. In addition free selenite has been postulated
to oxidize the viral protein disulfide isomerase and thereby reduce its ability
to penetrate healthy cell membranes (Kieliszek and Lipinski 2020).
Vitamin B2.
Activation of vitamin B12, vitamin B6, vitamin A and vitamin K are all dependent
upon functional vitamin B2. Maintenance of reduced glutathione is also dependent
upon active B2.
Vitamin B12. High dose vitamin B12 has the potential to increase melatonin
levels, and to also have a beneficial effect as far as modulation of the immune
response. Vitamin B12 has also been demonstrated to inhibit the RNA-polymerase
activity of the nsp12-protein from COVID-19 (Narayanan and Nair 2020).
Vitamin B12 is also essential for production of glutathione via its role in the
sulphation cycle. Iron. Iron
deficiency has been associated with an increased susceptibility to respiratory
infections (Jayaweeraetal, 2019). High dose vitamin B12 has the potential to increase melatonin
levels, and to also have a beneficial effect as far as modulation of the immune
response. Melatonin.
There is the potential to give melatonin to increase the resistance to COVID-19.
Doses of 3, 6 and 10 mg, have been given to patients in ICU, were found to be
safe. Further doses of 1 g per day have been given for a month with no effect
(Zhang etal 2020).. General.
Some general information on nutrition and fight COVID-19 has been summarized by
Zhang and Liu (2020). Unfortunately, as long as the medical profession refuses
to accept the importance of minerals such as Selenium, and vitamins D, B12 and
B2 and iron in increasing the resistance to viral infections and in controlling
the severity of infections, they will never recommend supplements as a
preventative option against infection. Potentially simple supplementation with
vitamin D, to double the vitamin D levels in the population, supplementation with Selenite, to double
the levels of Selenium in the population, and topical or injected vitamin B12 could have reduced
the death rate from COVID-19 to one eighth of the current rate, potentially
saving over 1,600,000 lives (as of 12/01/2021). With current rates of doubling
by end of March, 2021, this would potentially mean saving 3,200,000 lives!! Video of the
mechanism behind severe systemic inflammatory response syndrome with COVID-19
https://www.youtube.com/watch?v=PWzbArPgo-o See
https://www.worldhealth.net/news/risk-factors-covid-19-related-death-identified/ Co-morbidities
raise the risk of death from Corona. Thus, in China the death rate in those with
no co-morbidities was 0.9%, but was much higher for those with Cardiovascular
disease (10.5%), diabetes (7.3%), Chronic respiratory diseases (such as COPD,
6.3%), Hypertension (6.0%) and cancer (5.6%). In many countries, including the
US, many people in the population have at least one underlying health condition
(US, 60%). The progression of
the disease can lead to a critical point in which a decision must be made as to
whether to admit the patient to critical care. See an explanation of the virus
and who it infects and kills from a summary of UK
Data In common with the
statistics from both China and UK, the greatest death rate was seen in persons
with more than one risk factor. Frequency of comorbidities was Hypertension
(57%), Obesity (41.7%), Diabetes (31.7%), Morbid Obesity (19%), Coronary Heart
Disease (10.4%), Asthma (8.4%). Each condition, can also be shown to be
associated with functional vitamin B2 deficiency, and as such could also be
associated with Selenium deficiency, however, neither functional B2 levels or
Selenium levels have been measured in the patients, nor those that succumbed to
the infection. It can be seen, that the hospitalization rate for people
One year into the Pandemic, it is interesting to compare the actual death rate
from COVID in the USA to that from other causes. As can be seen death from COVID
over most ages is less than 5% of total deaths in these age-groups. Further, if
the population had been advised to supplement with vitamin D, Selenium and
vitamin B12, the number of death due to COVID would potentially be reduced to
less than 10% of those observed making the outbreak of little consequence, when
compared to all cause mortality.
Many researchers are of the belief that there is every reason to believe that it should be possible to develop a
coronavirus vaccine for humans, as many individuals who have been infected with
the virus recover, and over 90% of those infected in China have now recovered.
Further, it is known that passive immunity gained from bovine colostrum will
protect calves against bovine coronavirus, if the titre is high enough (Bok etal,
2018). Recently
Moderna has generated an mRNA vaccine against COVID-19. Best estimates for a
vaccine to be on the market are still 18 months. Potential problems for the
vaccine would be lack of immunogenicity in all persons. Thus, even for well
established viral vaccines such as Hepatitis B, even after 3 injections there is
less than a 90% seroconversion rate. Similarly, vaccine effectiveness for the
common flu vaccine is only 19-60%, however, this is to a continually evolving
flu virus, with effectiveness higher, the higher the similarity of the vaccine to
the current flu virus. Whether COVID-19 will do that, is not known (https://www.cdc.gov/flu/vaccines-work/effectiveness-studies.htm
). Recently an analysis has been performed looking at the immunological response
to hepatitis B vaccine (Yang etal, 2016), where the data looked very similar to
that observed for the current COVID-19 outbreak. Thus, the vaccine was much more
effective in the young, with protection more effective in females than males,
and less effective in those with concomitant diseases, with a BMI >25 or those
who smoked. Epitope mapping has identified potential peptide sequences that
could be incorporated in a subunit vaccine, which if successful could be more
rapidly scaled up than a whole viral vaccine (Feng etal, 2020). Vaccine trials
have already been performed in monkeys, where it was found that severity of
infection was dependent upon viral titers, so even in these preliminary trials
they did not get 100% protective immunity (Barouch 2020). The utility of any
vaccine is also questionable. Thus, as of 1st July 2020, most of Europe and the
UK, and even the USA and Canada have already to come out of the pandemic, with
much of the population being immune, as such these countries are unlikely to
need to use a vaccine. Potentially, only the countries that have had severe
restrictions and hence have had very few cases, such as Australia and New
Zealand would benefit from a vaccine. In this instance, is the hundreds of
millions of dollars being spent on vaccine development and testing warranted? Several
alternative strategies are possible which would potentially ameliorate the
condition and reduce mortality Antivirals -
currently none seem to be working. Peptide mimetics.
Small peptides, that either mimic the binding site on ACE2, could potentially
neutralize the viral binding protein, and reduce infectivity. These can be
produced at large scale, however, it would not be possible to deliver these
orally so that would need to be administered by injection, or via technologies
such the TransdermOil™ technology. Anti-scabies
treatment. A group in Melbourne Australia has found that a single dose of the
drug Ivermectin could stops SARS-COV2 virus in culture (Caly etal, 2020) Repeat TB
vaccinate, potentially could reduce the severity of infection Vitamin D
supplementation possibly could reduce the death rate to one twentieth of
current levels (see above). Dexamethazone
treatment has shown promise in greatly reducing the inflammatory response and
reducing death rates by at least one half.
Given the possible association of decreasing melatonin with age, and raising
death rate with age, combined with the known anti-inflammatory effect of
melatonin and its ability to down-regulate the innate response and the excess
inflammatory response to viral infections (Reiter
etal, 2017), it has been postulated that high dose
melatonin may be an effective adjunct therapy in treatment of COVID-19 (Reiter
etal, 2020; Zhang etal, 2020; Anderson and Reiter, 2020).
It would seem useful to compare Coronavirus to the Flu. The annual burden of Flu
in the US since 2010 has been between 9,300,000 to 45,000,000. Of these there
were 140,000 to 810,000 hospitalizations with an annual death rate of 12,000 to
61,000 (CDC). Claims are that Coronavirus is different to flu in that the death
rates for flu are in both the young and old. Globally, however, death rates go
up for flu. <65 years - 0.1 to 6.5 per 100,000; 65-74 years 2.9-44.0 per 100,000
and for over 75, 17.9 to 223.5 per 100,000 (0.234%) (Iuliano etal, 2018). it is
not known if susceptibility to COVID-19 is related to blood type, however, it
has been shown in many studies that susceptibility to Influenza virus is, with
type B and AB being much less able to generate effective antibody responses to
Influenza A. Preliminary studies from China suggest that susceptibility to
COVID-19 may be slightly higher in type A blood types. These data support the
general concept that one's ability to fight the infection is affected by one's
genetics (see section above on Vaccine).
Potentially the increased mortality from Coronavirus could be simply due to the
increase in the incidence of the many comorbities for death from COVID-19 with
aging, and would suggest that people who have exercised often, and maintained
healthy life-style and hence have no co-morbidities are being rewarded for their
life-time of healthy living by having a low mortality rate from the virus. In
contrast those who have not taken care of their health have an increased
mortality rate, which increases rapidly with more and more comorbidities. It may
not be quite to straight forwards, because if that was the case, one would expect that in Europe, the countries with
the highest rates of Hypertension, Obesity, Diabetes, Morbid Obesity, and Coronary Heart
Disease should have the highest death rates. This does not appear to be the
case, however. Thus if you look at the incidence of Diabetes, it does increase
with age, however, death from diabetes in Europe, UK and Sweden have some of the
lowest death rates from diabetes, yet the highest death rate from COVID-19.
Currently the
majority of tests for Coronavirus test whether you have a detectable amount of
the virus. The results of the test are being widely misunderstood to mean that
the person does not have the virus, whereas this may not be true. All the test
means is that at the time of testing the person being tested had undetectable
amounts of the virus. It does not mean that if you tested the same person 4 or 5
hours later, they would still test negative for the virus. Other than
isolation of the virus, several markers of COVID-19 infection have been noted.
Generally these are similar to those for most viral infections and include
elevated TSH, with lower T4/T3, elevated ferritin, with lower Haemoglobin and
Haematocrit, elevated activated complement markers, amongst others. Post viral fatigue
is common in those recovering from COVID-19 infections, and presumably is a
result of the increased demand for active B2 - hence the elevation in TSH, which
then leads to functional B2 deficiency, thereby resulting in functional B12
deficiency, with resultant drop in production of CoQ10 and creatine, leading to
poor energy conversion, and prolonged fatigue. See
PostViralFatigue
Spike Proteins See
Link
Covid and ACE-2 receptors: https://www1.racgp.org.au/newsgp/clinical/ace-inhibitors-arbs-and-covid-19-what-gps-need-to?feed=RACGPnewsGPArticles
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Copyright © 2018 B12 Oils. All Rights Reserved.
Vitamin B12 Deficiency and COVID-19
COVID-19 Infection
Potential increase
in Infection with ACE inhibitors
Vitamin B12
and the Production of Melatonin
Vitamin B12
and the inflammatory Response
Selenium and the inflammatory Response
Iron and Resistance to Respiratory infections
Zinc and Resistance to Respiratory infections
Vitamin B12 Deficiency and Energy metabolism
Vitamin D Deficiency and Respiratory Infections
Death Rates from
COVID-19
Nutritional Support for Dealing with COVID-19
Mechanism of invasion of COVID-19
Review of Statistics on outbreak in China
Review of
Statistics on outbreak in Great Britain
Review of
Statistics on outbreak in New York
Coranavirus
Vaccine
Other Strategies
Treatment with Melatonin
Comparison to Flu
Diseases of Aging
Testing
Markers of infection
Post viral fatigue
Research
References
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