Graham Wilfred Ewing*
Mimex Montague Healthcare, UK
*Corresponding author: Graham Wilfred Ewing, Mimex Montague Healthcare, UK
Submission: June 26, 2020Published: April 7, 2021
ISSN: 2577-2007Volume7 Issue2
The science being used to justify lockdowns in countries throughout the world exhibits many shortcomings. How someone becomes infected or how the SARS-COV-2 virus transmits between patients remains very poorly understood [1]. This article reviews the effect which SARS-COV-2 has on the body, the various factors which make people less vulnerable to infection than others, why some therapies work and others do not, and ultimately how patients can best be treated.
It is clear that locking-down a population by minimising the transmission of the virus to a country from another country, or between infected people within a country, will slow the transmission of the virus and reduce the numbers of people who are infected but it has now been recognised that only 0.075-0.08% of the UK population become infected, develop severe complications, and die. Other countries appear to have significantly lower rates of infection and death [2] allegedly because they activated their plans to combat such events much earlier than the UK authorities. Some countries have comparable rates of infections and deaths but did not implement a severe lockdown and some countries which did not implement a lockdown appear to have had much worse outcomes.
In the case of a severe outbreak of influenza there have been up to 20-30,000 deaths in the UK yet a severe lockdown was not considered to be necessary so why on this occasion did the authorities adopt a different model and lock down almost the whole population? Their decision-making was heavily influenced by experts in disease modelling who forecast 250-500,000 deaths, perhaps more, yet their models were clearly based upon a set of erroneous assumptions in which they assumed the homogeneity of the population, and failed to take into account age, the significance of pre-existing morbidities, etc.
The prevailing model for a severe influenza outbreak is not to test everyone but instead to test and/or treat those who had the most severe symptoms however with SARS-COV-2 it was decided to effectively reverse the prevailing model and test as many people as possible. ‘Test, test, test’ became the mantra - the same philosophy used to manage the Ebola outbreak in Central Africa - yet identifying someone who was infected often had little effect on the overall course of the outbreak because the infection was not seriously inconveniencing the vast majority of the population.
Any testing regime should
A. Look to identify those who have been infected,
B. Those who are currently infected, and
C. Those who could be infected in future. The problem for the authorities is that scientific opinion initially assumed that everyone who was infected would be at risk of hospitalisation and/or death yet it is now recognized that, at least in the UK, only ca 0.06-0.07% of the (ca 42,500 of the UK’s 65M) population has died. There is also a further issue:
D. How many have died from the medical interventions and not the consequences of the infection? Perhaps this will never be known.
Nevertheless, the recent findings that dexamethasone reduces
the number of deaths in those who have been placed on a ventilator
illustrates that some died as a result of being treated by ventilators.
Recent studies show that SARS-COV-2 has been circulating
earlier than previously thought; perhaps in Wuhan since mid-late
Q3 2019 [3]; and hence that the numbers of people who have been
infected may be much greater, perhaps up to 40 times greater
[4], than was previously thought. This appears to indicate that ca
5-15% of the population, perhaps more, of the population have
been infected with this virus.
It is not yet known whether some people e.g., the younger
element of the population, develop antibodies. There is a vibrant
debate around this issue. Do some people become infected and yet
do not develop antibodies? Up to 45% of those infected are believed
to be asymptomatic [5]. If so, can anything be done to prevent the
virus spreading? Moreover, does it really matter whether it spreads
widely in the population? If we can protect the ‘at-risk’ groups then
surely it does not really matter if the virus circulates? Do some
people become infected yet are asymptomatic? Do some people
become ‘superspreaders’? Does the disease only become significant
in those who have a specific level of vulnerability? If so, has it
already reached the level commonly known as ‘herd immunity’ in
the at-risk group [6]?
It is now recognised that most normally healthy people are
unaffected by the virus so it really does not matter whether they are
in contact with others who have been infected with the virus. For
them exposure to the virus leads to an infection which is at worst
comparable to infection by the influenza virus. In general most
children experience a mild set of symptoms, conceivably because
children have far greater levels of T cells, which conceivably
intervenes more effectively at the point of infection, and hence have
a more robust immune response than adults [7,8]. This raises the
intriguing possibility that much greater numbers of people in the
‘at-risk’ category have been vulnerable to the virus than those in
the wider population.
Those that are worst affected are those who have pre-existing
medical conditions, in particular impaired breathing due to an
inflammatory response in the lungs which influences the prevailing
capacity of the lungs to deliver O2, the diabetic and obese [9], those
with kidney and/or liver insufficiency, those who are immune
suppressed, the frail/elderly, and those who are severely stressed
[10]. It affects people who live a sedentary lifestyle, who are
physically inactive, perhaps who spend a lot of time working on
computers, are immunosuppressed e.g., who have had cancer or
are being treated for cancer, etc. In general, the ‘fit elderly’ are not
predisposed to this virus.
Although the most vulnerable group is the >65 years a significant
number, less than 50%, are in the workforce. An estimated 100-200
nurses and doctors in the UK have died in the course of their duties.
Working in the health and social care frontline makes them 6 times
more likely to be infected [11] which illustrates that SARS-COV-2 is
a problem for healthcare and less so for the wider population. These
numbers can reasonably be expected to vary between countries -
some countries have greater levels of obesity, more people over the
age of 65 years, and other risk factors - and hence would expect
to have greater or lesser levels of SARS-COV-2 hospitalisations and
deaths however not all of those who are predisposed to this virus
are in the >65 years age group. In Germany the average of age of
those infected, and/or dying, is much lower than in other countries
because the German authorities have been well prepared for the
pandemic, implemented lockdown at a much earlier stage, and
prevented transmission to care homes.
The transmissibility of the virus appears to be within several
days. It occurs earlier than it can be detected using diagnostic
tests. This presents a dilemma for those who seek to track the
transmission of the virus. Can it ever be tracked down and choked
at or before the point of transmission? It appears not because the
virus moves faster than the tracers. If not why is the incidence of
infection reducing - in the late spring/early summer months?
Accordingly if only 5-15% of the population have had the
infection the transmission of the virus will slow down but can
be expected to persist in the population unless there are other
factors at play which have not been taken into account e.g. if SARSCOV-
2 behaves in the same way as all previous coronaviruses
it can reasonably be expected to die and/or decline in the wider
population during the spring and summer months, at least in those
who lead an outdoor lifestyle. Under strong sunlight SARS-COV-2
has a half-life of just 2 minutes [12,13] so as the countries in the
northern hemisphere enter the spring period i.e., after 21st March,
the length of exposure to the summer sunlight will increase, the
intensity of the sunlight will increase, and the effect of UV light can
reasonably be expected to have a virucidal effect upon this virus.
Indeed, if this is the case the usefulness of quarantining
everyone indoors must now be questioned. If the most vulnerable
groups are kept isolated and free from sunlight they will not develop
the vitamin D levels which help them to optimize their immune
response and fight against bacterial and viral infections with the
result that the virus will circulate for longer in the community. It
highlights the fundamentally unsafe practice of containing the most
frail elderly patients in care homes (or sheltering from sunlight)
where they are often kept isolated and out of natural sunlight i.e.
in an environment which is conceivably a breeding ground for the
transmission of such viruses.
The utility of testing has been questioned. It is certainly useful
to know how many in a population are infected or have been
infected but the usefulness of quarantine/lock-down is uncertain
for the reasons outlined. It may also be useful to know the health
profiles of the 0.06-0.07% of the at-risk population and quarantine
those who are in this ‘at-risk’ category. This could be done by
checking their health profiles (assuming that their health records
were sufficiently detailed) however the actual profile of the most
vulnerable groups has not yet been clearly established although
there is now general acceptance of the medical profiles of the most
at-risk groups. Accordingly, it is likely that the regular range of
tests currently used to screen the health of such patients may be
inadequate for this purpose. A more advanced screening test may be required to screen these patients during the latter stages of this
pandemic and/or in preparedness for future pandemics.
At the time of writing the Ro factor is ca 0.7-0.9 in the major
industrialized nations in the northern hemisphere despite their
best efforts to track and trace people who have been infected with
the virus despite quarantining the vast bulk of the population. The
number of deaths in care homes is now in decline and the numbers
in the wider population is now declining steadily and has reached
manageable proportions (typically less than 100 deaths per day).
Sweden which has a less strict lock-down has had fewer people
infected and until recently had fewer deaths in their population
but, importantly, has kept their economy running. This serves to
cast doubt on the benefits and/or effectiveness of the lock-down
applied in the UK i.e., it has been an invaluable mechanism to slow
or prevent the spread of the virus in the community, but it has never
eradicated the virus. There are more factors at play than person to
person transmission but of course it was intended to ‘flatten the
curve’ and was not intended to eradicate the virus.
It is worth cautioning the use of ‘number of death’ statistics
because many of these patients did not die at the time that they
were infected. They were infected many weeks previously.
In addition [14] the BAME populace appear to be suffering a
disproportionately high number of deaths due to the virus e.g.,
Pakistani origin patients were 3.29 times more likely to die of the
virus. This conceivably illustrates that exposure to sunlight is a
significant factor in the etiology of SARS-COV-2 infection. Patients
with non-Caucasian skin-types require different levels of sunlight
to stimulate the production of vitamin D which plays a role in their
immune response to viral infection.
Sunlight is commonly associated with the production of
vitamin D which plays a role in the immune response however
over 100 medical conditions respond to the effect of sunlight
which indicates that the beneficial effect of sunlight may not be
solely due to the effect of vitamin D but also to the effect of sunlight
upon other metabolic processes i.e., that sunlight functions as
a photomodulator/photoactivator of a wide range of metabolic
processes [15]. Accordingly if people shelter in their homes, and/
or use other means to prevent their exposure to sunlight, they
predispose themselves to adversely low levels of vitamin D and
greater predisposition to infection [16-18]; Werring D et al. report
the occurrence of blood clots and ischaemic stroke in 6 SARS-COV-2
patients in the age range 53-85 years [19]; and Prietl & colleagues
[20] illustrated that low levels of vitamin D are associated with
the occurrence of upper respiratory tract infections (URTI)
including influenza, COPD and asthma. Perhaps therefore vitamin
D supplementation could be of value in preventing the onset of
SARS-COV-2 type infections and/or as a way of stimulating immune
function in those who are more severely affected.
This leads to the issues discussed by Ewing in his recent paper
[21] which is now extended in this paper. When patients are
infected with CoVid-19 this brings to bear a number of issues:
I. Why does the supply of cytokines and other related
immune function proteins fail to act upon the virus?
In cases of SARS-COV-2 infection the lungs are infected and
inflamed which steadily reduces oxygen saturation and leads to
acidosis and hypoxia. As the infection worsens the body responds
by expressing cytokines and other immune proteins however those
that are severely affected by the virus are those with pre-existing
medical conditions which are accompanied by elevated levels
of acidity in the blood and consequently lower levels of essential
minerals, in particular magnesium and zinc. This is significant
because cytokines require magnesium to function [22]. As cytokines
are inactive in a magnesium deficient context the body responds by
supplying more cytokines and/or the prevailing levels of cytokines
accumulates - the so-called ‘cytokine storm’.
Seeking an explanation for this we look for precedents and note
that in the treatment of pre-eclampsia [23] in vivo MgSO4 treatment
substantially reduced maternal TNF-α and IL-6 production i.e.,
the immunomodulatory effects of concern were mediated by
magnesium. Moreover, there are many studies and/or medical
papers which recognise that magnesium plays a significant role in
the immune response [24,25]. In addition, Mannon et al. [26] have
used sodium bicarbonate to stimulate anti-inflammatory pathways
and the immune response i.e., the immune response can be altered
by adjusting intercellular pH therefore the combination of sodium
bicarbonate (oral or iv) and Magnesium Sulphate can reasonably be
expected to combat the cytokine storm.
This is supported by noting that the first line treatment of SARSCOV-
2 patients is the use of electrolytes and/or fluids [27] and also
that the use of magnesium [28] with vitamins B12 and D have been
shown to have a positive effect upon older SARS-COV-2 patients.
II. Do they have sufficient lung capacity to deliver O2?
In the most affected categories patients have reduced lung
capacities by virtue of their obesity which reduces their ability to
inhale and supply O2. Accordingly, an infection such as SARS-COV-2
will reduce their effective lung capacity still further.
III. What happens if the inflammation caused by the infection
reduces the supply of O2 to a critical level?
In such cases the prevailing medical dogma and standard
operating procedures is that the patient should be give support
by CPAP or, in the most severe cases be treated using ventilators.
The evidence illustrates that CPAP has been a valuable intervention
in some patients although there is no way of knowing whether
the patient would have recovered without CPAP i.e., there was no
placebo group against which the results and/or outcomes could be
compared. The evidence in favour of ventilators is much less clear.
Ca 40-60% of patients placed on ventilators have succumbed to the
infection and died which suggests that ventilators are not having
the expected levels of success treating SARS-COV-2 [29].
Now it has been recognised that the administration of
dexamethasone can reduce the inflammatory response in the lungs and thereby reduce the number of deaths in those who are
ventilated [30]. If so, is the inflammatory response due to the viral
infection, the onset of acidosis, or is it due to the potentially allergic
effect of the ventilator?
IV. Can they absorb the O2 being delivered i.e., do they have
sufficient haemoglobin and/or is the haemoglobin able to
absorb O2?
The use of ventilators is based upon the assumption that
the problem lies with the physical capacity and/or capability
of the lungs to supply of O2 to the alveoli where it is absorbed by
haemoglobin however many of the those in the ‘at-risk’ category
have low levels of haemoglobin [31]. Moreover the absorption
of oxygen by haemoglobin declines under increasingly acidic
conditions which is the case in those in the ‘at-risk’ category. The
successful use of ECMO [32] indicates that both issues - of lung
capacity and the ability of the blood to absorb O2 - must be taken
into account. Moreover what is the long-term effect on the patient’s
mental and physical health of being treated by ventilator i.e. if they
survive?
V. Is the heart able to circulate O2 through the lungs?
The diabetic and obese patient encounters a range of diabetic
comorbidities which often involve cardiac testing. Excess strain
on the heart as it pumps blood with elevated viscosity (thickness)
leads to strain on the cardiac musculature; a range of pathological
indications; elevated blood pressure; etc. Moreover the function
of cardiac musculature is dependent upon the supply of O2 in
order to function. The heart has the greatest oxygen consumption
by comparison with all other human organs. If it does not get
sufficient oxygen a condition known as ischaemia (ischaemic heart
disease) develops. Pathologies which contribute to this condition
include coronary heart disease and atherosclerosis. This is
significant because if the heart is not supplied with oxygen it will be
increasingly less able to pump blood around the blood vessels and
through the lungs. In effect slowing the rate at which oxygen can be
absorbed by haemoglobin.
I. Can the accumulation of CO2 be removed?
Consequently, impaired heart function leads to the accumulation
of CO2 in the blood and inter and extra-cellular mediums. The main
mechanism for removal of CO2 is via the lungs so reduced lung
function leads to acidosis.
VI. Can the accumulation of CO2 be removed?
Consequently, impaired heart function leads to the accumulation
of CO2 in the blood and inter and extra-cellular mediums. The main
mechanism for removal of CO2 is via the lungs so reduced lung
function leads to acidosis.
VII. Does the accumulation of CO2 hinder the absorption of O2?
The autonomic nervous system works most effectively at a
neutral pH (pH 7.35). At this level there is a balance/equilibrium
between the levels of essential minerals and transition metals. In
order to neutralise excess acidity in the body the body
a. Exudes a bicarbonate-rich bile from the pancreas and
b. Converts CO2 into HCO3. Failure to maintain the pH in the
range 7.0-7.35 leads to acidosis which adversely influences
the prevailing levels of Mg and Zn and reduces the immune
response.
CO2 is one of the main contributors to acidosis. Others include
the consumption of acidified beverages, red meat, stress, and the
accumulation of excess body fat. The enzyme carbonic anhydrase
metabolises CO2 into HCO3 which is alkaline. Carbonic anhydrase
requires Zn in order to function so increased levels of acidity in the
blood severely impacts upon the removal of CO2 via the lungs.
Whilst the use of iv saline solution and/or electrolytes will
likely have some beneficial effect, the author suggests that the
use of iv HCO2 would reduce levels of CO2 and be more effective,
more rapidly. Moreover, in the ICU context, there is likely to be an
immediate need to introduce Mg and Zn, in order to stimulate the
patient’s immune response, and thereby stimulate the activity of
Carbonic Anhydrase to eliminate CO2.
VIII. How does this explain the occurrence of blood clots?
Elevated levels of obesity elevates the levels of blood lipids
and fats, and the levels of blood acidity which accompanies and/
or leads to the onset of clotting in atherosclerosis [33]. The
successful use of saline and electrolytes in most patients illustrates
that the fundamental problem - that of acidosis - leads to hypoxia,
pneumococcal inflammation and/or infection, and death.
IX. SARS-COV-2 increases predisposition to diabetes.
It is recognised that [34,35] people with chronic type 2 diabetes
and obesity are most at risk. This occurs because their greater
body mass, in particular around the abdominal areas, influences
the function of their diaphragm and hence their ability to inhale.
Consequently they have lower effective lung capacity, their supply
of oxygen to the blood is inhibited, they have lower levels of
haemoglobin and hence cannot absorb oxygen, and they become
vulnerable when exposed to infections which further reduce their
effective lung capacity. It creates acidosis and hypoxia.
This will inevitably influence those with type 1 diabetes, in
particular those who are not otherwise physically fit, and it will
make those who are otherwise healthy have a greater risk of
becoming diabetic, because acidosis reduces the rate at which
pre-pro-insulin is genetically expressed, the storage of the zinchexamer
in the pancreas, the metabolism of insulin with its reactive
substrate the insulin receptor protein, and the prevailing levels of
chromium in the smooth muscles.
If zinc levels get too low the conversion of CO2 to HCO3 -
performed by Carbonic Anhydrase - is no longer able to proceed.
The seriousness of this situation in which the body’s existence is
challenged requires that it absorbs Zn stores from the pancreas
in order to reduce CO2 levels and thereby regulate the body’s
intercellular pH however the consequence of this is that the
pancreas becomes less able to store insulin and as a result the
patient shows signs of diabetes [36,37].
Finally, this virus is now circulating widely around the world
therefore it is now almost inevitable that further rounds of infection
will occur. What are the implications for medicine in 2020/21?
Can it ever be possible to return to the pre-SARS-COV-2 models
of healthcare in which the patients routinely attend primary or
secondary care consultations? If you wish to have a consultation with
your doctor you will need to wear a face mask but this is a relatively
minor inconvenience. Of greater concern is whether people will
wish to work in the healthcare professions if this predisposes
them, and their families, to greater risk of infection. How many
doctors will retire from the medical profession earlier than normal
retirement dates? How will this influence medical protocols? For
example how will be patients be screened in scanning equipment?
Will they need to be cleaned after every patient? This will drive up
costs yet again! Will social distancing become the norm in clinics
and hospitals and erode work efficiency?
There is a clearly now, more than ever before, a need for accurate
Remote Online Technology Platforms which enable the patient
to consult their doctor or to be tested and/or treated remotely.
There is now, more than ever, the need for radical and disruptive
technologies which allow healthcare to be provided remotely.
Graham Ewing is Chief Executive of Mimex Montague Healthcare
Limited - a company devoted to the commercialization of the first
comprehensive way of screening and treating the patient using a
precise and sophisticated mathematical model of the relationship
between sense perception, brain function, the autonomic nervous
system and physiological systems, and cellular and molecular
biology (known by the brand name ‘Strannik’).
© 2021 Graham Wilfred Ewing. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and build upon your work non-commercially.