COVID-19: New information to help you stay safe
July 22nd 2020. This report has been prepared by Colin Rose for Uni-Vite Healthcare to provide some answers to key questions and help in staying safe during the COVID-19 epidemic.
We will explain why age is by far the biggest risk factor for a serious reaction, what can help as protection, when a vaccine may be available, how long immunity may last, and what the long term health effects are of this unprecedented threat.
Why is age by far the biggest risk factor for COVID-19?
You’ll know that most people below the age of 50 – but not all – will have mild symptoms with the new coronavirus. Above the age of 65, the risk of severe symptoms rises by 23 times! To the point that 80% of all hospitalisations are in that age category. And the fatality rate for people over 80 is 18% – almost 1 in 5.
The reason is that older people generally, but not necessarily, have some or all of these increased risk factors:
- More chronic (long term) inflammation in cells, tissues and organs
- Compromised, less effective, immune systems
- Co-morbidities (other health conditions) like high blood pressure, cardiovascular disease, diabetes and COPD – Chronic Obstructive Pulmonary Disease. COPD is caused by a narrowing of the airways in the lungs.
- Extra body fat – to the point where a BMI (body mass index) of over 30 (obesity) increases the risk of a severe reaction by 7 times. Even being overweight (a BMI of 28) has a 5 times increased risk. The average UK BMI is 27.5.
A key article in the Journal Aging, published end May 2020, concludes that ALL these risk factors are strongly associated with accelerated ageing – where biological ageing is running faster than chronological ageing1.
So what helps delay ageing will also help reduce the impact of COVID-19. That will enable us to list what we believe are the most effective risk reduction actions at the end of this article.
How COVID-19 attacks
If you look at a picture of the virus, you’ll see protein spikes sticking out.
On these spikes are rounded ends. At these ends is a part that docks with the receptor in human tissue called the ACE-2 receptor. It is this receptor which allows the virus to gain entry into the heart, the lungs, the lining of blood vessels and other tissues.
Through this route, COVID-19 can trigger a unique constellation of symptoms, including excessive inflammation, respiratory distress, pneumonia, free radical damage, inflammatory responses leading to blood clotting, and what has been described as unusually ‘sticky blood’. Therefore, potentially to heart disease, stroke and neurological dysfunction.
It is because COVID-19 replicates in the upper airways, more than previous coronaviruses do, that makes it more transmissible.
The significance of the ACE-2 entry point is why researchers are making an improved immune response against the spike protein a vaccine strategy – see important updated news on vaccines later in this report.
How does it go catastrophically wrong? Stress on the immune system
In younger people with better immune systems, white blood immune cells called neutrophils and macrophages migrate to the sites of infection and clear infected cells and their debris.
In older people, this immune response is normally slower and less effective – a condition called immuno-senescence. The body produces fewer B and T white blood cells. Moreover, B-cells’ ability to produce antibodies declines, as does T-cells’ ability to respond to antigens. This means more and more cells can become infected, which increases the ‘viral load’ – and the sheer weight of the virus becomes overwhelming.
Reduced immune response can generate high levels of inflammation and lead to a cytokine storm, where the body attacks itself. Cytokines, which are signalling molecules, put out a call for an excess of immune cells.
During a cytokine storm these immune cells flood and attack the lungs they should be protecting – causing what intensive care doctor Chris Meadows calls “a raging fire in the lungs” and severe breathing difficulty. Hence the focus on oxygen for ICU (intensive care unit) patients.
Blood vessels begin to leak and the blood itself clots, becoming very sticky, potentially leading to a stroke or heart attack. Blood pressure drops dangerously, organs begin to fail, and fever starts. Effectively, the body now considers its own tissues as invaders and has instituted a catastrophically inappropriate response.
The flow of excess immune cells to sites of infection results in more widespread inflammation and compromises not only the lungs and heart, but the kidney, liver and brain. Even mild cases have reported tiredness, and problems with memory and staying focused.
In addition, coronaviruses are known to initiate epigenetic changes (changes in genes), where protective genes are switched off, potentially accelerating the rate that the immune system ages.
All of which makes COVID-19 a very dangerous virus indeed to high risk groups and much more than a flu-like respiratory disease.
What can help fight the disease?
Steroids can help dampen down the overactive immune system as evidenced by the success of the steroid dexamethasone in reducing death rates. But, of course, you need your immune system to be working, albeit at a lower intensity. So it’s clearly far better to protect yourself from infection and/or block the inflammatory sequence that can lead to a cytokine storm.
Foods and nutrients with a high anti-inflammatory effect can help – as will those that keep the immune system functioning well. We list these at the end of the report.
What are the symptoms of COVID-19?
The UK NHS currently recognises 3 main symptoms:
- Fever or chills
- Loss of taste or smell (new)
The American CDC (Centers for Disease Control and Prevention) adds 9 other symptoms:
- Shortness of breath or difficulty breathing
- Muscle or body aches
- Sore throat
- Congestion or runny nose
- Nausea or vomiting
The problem is that many other conditions can cause similar symptoms to these additional nine – flu, for example. The safest reaction, if you do exhibit any of these other symptoms, is to assume you might have COVID-19 and get tested. (And take the flu jab this autumn.)
There is a gradient of severity
A very recent analysis2 of almost 17,000 patients, (median age 72), has found that symptoms and outcomes can be put into ‘clusters’ of increasingly severe outcomes. Spotting what cluster a patient is in can help identify how they should be treated – to try to prevent progression to hospitalisation and improve the chance of recovery and survival.
The average time from identified infection to hospitalisation was 4 days, average duration of stay was 7 days and 17% were admitted to ICU. 60% of hospital admissions were men.
Although the analysis confirmed that 53% had comorbidities, (other underlying health issues), 47% did not. But mortality was much lower in this latter group. The median age of those who died in hospital from COVID-19 in the UK was 80 years, and only 12% of these patients had no documented comorbidity.
The six groups, in order of severity, were:
- Having a respiratory problem (cough, sore throat, ear pain, runny nose, chest pain. Outcome: 16% required a trip to hospital with 1.5% oxygen support.
- Respiratory problems but with added fever and lack of appetite. Outcome: 17.5% needed a hospital visit and 4.5% oxygen support.
- Gastrointestinal problems like vomiting and diarrhoea, but not many other symptoms. Outcome: 24% needed a hospital visit with 3.7% oxygen support.
- Severe fatigue, chest pains and cough: Outcome: 24% needed a hospital visit and 8.6% oxygen support.
- Severe fatigue, confusion and skipped meals: Outcome: 25% needed at least one hospital visit and 10% oxygen support.
- Acute respiratory issues, chest pains, fatigue and gastrointestinal problems. Outcome: 46% needed at least one hospital visit and 20% needed oxygen support.
How long does it take for infection to show?
Most people will show symptoms after 4-6 days. But it can be between 1 and 14 days. You can be infectious for 2 days before symptoms manifest and for 10 days after. Average infection duration is 10 days.
Average recovery time is 14 days, but it can take weeks, or in some cases months.
How do we become immune?
When pathogens enter your body, your immune system is activated:-
- Bacteria and viruses, like the one that causes COVID-19, have proteins called antigens on their surfaces. Each type of virus has its own unique antigen.
- White blood cells of your immune system make proteins called antibodies to fight the antigen. Antibodies attach to antigens like a key fits into a lock, to destroy the invading virus.
- Once you’ve been exposed to a virus, your body makes memory cells. If you’re exposed to that same virus again, these cells recognise it and instruct your immune system to make antibodies against it.
What about a vaccine?
We’re going to need a vaccine because this virus is so highly transmissible. And since so many people are infected but without many – or even any – symptoms, how can you trace all the contacts?
Historically, it’s taken years to show that a new vaccine is both safe and effective. The leading science journal Nature recently pointed out that 90% of all vaccines that start clinical trials never make it to the end, either because they’re not triggering an effective immune response or a safety concern arises.
The fastest vaccine ever developed was the mumps vaccine and that took four years.
However, the devastation to the health and economies of the world wreaked by COVID-19 means that billions are being poured into compressing the normal timeline. Pharmaceutical companies are using multiple approaches that include conventional inactivated viruses and new, but unproven, technologies like messenger RNA (mRNA) vaccines.
Out of over 170 vaccines under development, here are the frontrunners.
USA’s Moderna has a vaccine using a new technology – which went from a computer design in January to a human study in just three months.
Messenger RNA (mRNA) uses genetic instructions to build just the coronavirus’s spike protein rather than a weakened version of the virus itself. This then alerts the immune system to build antibodies. Although RNA-based vaccines are easy to develop, none has yet been licensed anywhere in the world or been manufactured and distributed at scale.
Moderna had 45 people on a successful Phase 1 trial that showed strong immune response, but with some mild/moderate side effects that included fatigue or muscle ache. It is planning a Phase 3 trial to start later in July involving 30,000 participants. Phase 3 trials are designed to confirm and expand the results of the small-scale Phase 1 and 2 trials.
Oxford University and AstraZeneca have what is called an adenoviral vector vaccine. The Oxford vaccine is made from a chimpanzee cold virus that has been genetically altered to produce the coronavirus’s characteristic ‘spike’ protein. This tricks the body into thinking it has been infected and so triggers the immune response.
The Oxford team now has 4,000 people in a UK Phase 3 trial and is enrolling 5,000 people in Brazil, also in a Phase 3 trial. The lack of safety problems in the study so far is a good sign – as is the fact that it has triggered both antibodies AND a T-cell response, as reported July 21st. This means it is prompting both an innate and an acquired immune system response. There is some indication that immunity with this type of vaccine may require two injections.
An insider has said: “Oxford is likely to have the first efficacy data in the world” for a COVID-19 vaccine, possibly as early as August 2020, meaning distribution of the vaccine “could begin in the fall”.
Other companies using the adenoviral vector vaccine approach include Johnson and Johnson and China’s CanSino Biologics.
Some scientists caution that while adenoviral vectors have been tested in far more people than mRNA vaccines, the technology is used in only one commercial vaccine today: a rabies vaccine used to immunise wild animals.
There is another potential problem. Just as human bodies develop immune responses to most real viral infections, our bodies can develop immunity to the adenoviral vectors themselves. That could make booster shots of adenoviral vector vaccines problematic. On sensing a second injection, our bodies might unleash an antibody attack on the vaccine itself.
Nevertheless, the Oxford concept is probably our best bet for an early vaccine.
Other front running vaccine developers are BioNTech and Pfizer, a German/American collaboration, which has launched clinical trials of four separate vaccines in Europe and the USA with money from the US ‘Warp Speed’ fund. It reported on July 1st 2020 that initial results showed a good immune response after two shots and claimed that if Phase 3 trials succeed and are approved by regulators, it could start manufacturing ‘up to 100 million doses’ by the year end 2020.
Imperial College London are also using an adenoviral vector vaccine, described as a ‘self-amplifying RNA’ vaccine. A Phase 3 trial in 6,000 people is due to start in October. Their advantage is manufacturing scale – one litre of the Imperial COVID-19 vaccine could be used to vaccinate two million people. To produce that many doses with a conventional vaccine, you could need ten thousand litres.
Earliest dates for a vaccine
Dr Anthony Fauci is the USA’s top infectious disease expert and has frequently clashed with Donald Trump over coronavirus ‘facts’. He says he’s “cautiously optimistic” scientists will be able to create at least one safe and effective vaccine by the end of the year, or early 2021.
Multiple different vaccines?
To ensure that a vaccine is safe in all recipients – young, elderly, healthy or those with risk factors for severe reactions to COVID-19 – each of these sub-populations needs to be represented in clinical trials.
That’s why Dr Peter Hotez from the UN Foundation predicts that there won’t be one vaccine – but several vaccines with different purposes. One vaccine may mostly target the people at highest risk of getting severely ill or dying. Another might be tailored to people with underlying chronic conditions like diabetes or heart disease.
There could even be a vaccine that provokes a particularly rapid immune response for healthcare workers – since so many healthcare workers get sick, because they inevitably experience such high ‘viral loads’.
In June 2020, the US FDA issued guidelines for the approval of a COVID-19 vaccine. In common with previous guidelines the threshold for effectiveness is 50% – patients who receive the vaccine should be at least HALF (50%) as likely to be infected. That may sound less than ideal on a personal level, but on a national scale it would save millions of infections and enable health services to cope with an expected second wave.
A note of caution. Douglas Reed, an aerobiologist at the University of Pittsburgh Center for Vaccine Research warns of a possibility that vaccinated people could still spread the virus. He says: “Ideally, you want a vaccine that would protect against disease and against transmission, so that we can kind of break the chain.”
How do we measure immunity? Antibody tests
Antibody tests, also called serology tests, measure antibodies to coronavirus in the blood. If you have antibodies, it means you have been exposed to the virus and your immune system has made antibodies against it.
Because COVID-19 is so new, there hasn’t been much time for scientists to check the accuracy of antibody tests. They might create many false-positive results.
Testing for antibodies too soon after an illness can also cause false results. It takes 5-10 days from when you get infected to develop antibodies against the COVID-19 virus. But in most virus cases, full antibody production takes about 14 days.
If you’ve had COVID-19, are you immune?
We don’t yet know for sure – or how long the immunity may last.
Most people who have recovered from COVID-19 do make antibodies against the virus. But so far, there is no clear evidence that this will protect them against the virus if they’re exposed to it again. Here’s what we do know.
Studies show that people are protected against the coronaviruses that cause the common cold for up to a year after an infection – and antibodies against the SARS coronavirus last for up to 4 years.
However, studies have found that most people who have recovered from COVID-19 without hospitalisation do not produce high levels of the antibodies which block the virus from infecting cells.
Worryingly, researchers at Kings College London found that antibody responses to the coronavirus can peak three weeks after onset of symptoms, but then begin to decline after as little as two months. So we may need several generations of vaccine to get to a truly effective one – which was what happened with the flu vaccines in the early years.
Whilst these early indications don’t necessarily translate to final vaccine results, it is a caution that a vaccine might not be the immediate ‘get out of jail’ solution that we all hope for.
Could herd immunity protect us?
Herd immunity happens when a large part of the population – the herd – is immune to a virus either because they got vaccinated or had already been infected. This makes it harder for a virus to spread.
The more contagious a virus is, the more people are needed for herd immunity to take effect. The COVID-19 virus is so contagious that it’s estimated about 70% of people in a community will need to be immune to have herd protection. The New Scientist published figures on 20th June estimating that the percentage of people who have been infected in the UK could be between 20% and 27%.
A peer-reviewed study published in the Lancet medical journal in early July 2020 claimed that COVID-19 antibodies in Spain’s population were as yet “insufficient to provide herd immunity.”
The ‘game changer’ drug? Interferon beta
On July 20th, a new drug called SNG001 from biotech company Synairgen was announced. It doesn’t necessarily stop you getting infected, but it cuts the risk of a severe reaction by a claimed 79%. The trial size was small – 50 people – and results have still to be published in a peer reviewed journal, but what we do know is that it uses a protein called interferon beta-1a (IFN-beta), which the body naturally produces when faced with a viral infection.
Meantime, several foods also naturally increase the body’s own production of interferon beta – including black and green tea (at the levels of 5 cups a day), and shiitake and maitake mushrooms. Vitamin D seems to enhance the effect of IFN-beta.
Protective measures against infection
Face masks and social distancing
Countries like the UK and USA, which are taking longer to achieve widespread mask usage, whether by policy or cultural attitude, have suffered more virus cases and fatalities.
The UK is now in line with many other countries to mandate wearing a facemask in shops. Analysts at the Lancet conclude this could cut the average risk of infection by up to 15%. The N95-style mask offers the most protection, compared with disposable masks. So, although they are stuffy and uncomfortable, the potential drop in transmission is significant.
The Lancet paper (based on 172 international studies) found that eye protection (face shields) offered a 12% reduced risk and that reduction to 1 metre distancing is a reasonable change. The increase in risk by reducing from 2 metres to 1 metre is just 2%.
Airborne transmission including aerosol (smaller) droplets
Until now, the WHO – and therefore most governments – have maintained that the virus is spread mainly by contaminated surfaces and by droplets generated by coughing, sneezing and talking. These droplets are relatively big and thought to travel moderately short distances – no more than 2 metres – and then drop quickly from the air.
On July 8th 2020, however, an international group of 237 clinicians, infectious-disease physicians, epidemiologists, engineers and aerosol scientists urged the medical community to acknowledge the potential for airborne transmission by far smaller aerosol (the word derives from ‘aero-solution’) droplets. These can travel further and possibly stay in the air for hours.
It is the potential for ‘aerosol’ transmission that makes indoor gatherings risky and supports the wearing of masks in shops.
Researchers concerned about airborne aerosol transmission point to the case of a choir rehearsal near Seattle, Washington, on 10th March. Sixty-one members of the chorale gathered for a 2½ hour practice. Despite the availability of hand sanitiser, and choir members refraining from close contact and handshakes, at least half – 33 choristers – contracted COVID-19 and two eventually died.
A key researcher quoted in the leading journal Nature states: “There is a substantial probability that normal speaking causes airborne virus transmission in confined environments”. Other researchers have shown that aerosols of COVID-19 remained infectious for at least 16 hours, and were more infectious than aerosols of the SARS or MERS coronaviruses.
As a result, the German Department of Health has stated that any room with several people in it should be well ventilated and is considering recommending against air re-circulation in buildings and/or filtering through UV light. I understand that the WHO is reconsidering its stance on aerosol transmission.
Public transport and taxis are recognised as bringing elevated risk, as are offices and lifts – but one barely mentioned route for aerosol transmission is the lavatory.
Here’s how. If someone recovers from COVID-19 they will stop shedding the virus from respiration after about 10 days. But the virus can still be in stools for as much as 17 days – and the act of flushing can ‘aerosolise’ faecal particles. So office workers should be warned to close loo lids and toilets should be regularly swabbed with disinfectant.
The virus lingers in faeces because the gastrointestinal tract has millions of cells that express the protein called ACE-2 (angiotensin-converting enzyme 2) which, as we have seen, is the receptor that helps the virus attach to the surface of the host cell.
Hand washing and sanitisation
The average person touches their face, nose or eyes 10 times an hour. And these are the three key entry points for the coronavirus. So using a sanitiser into or out of a shop is not being fussy – it is a sensible precaution for yourself and others. As is frequent hand washing with soap.
Extra vitamin D?
The UK’s National Institute for Clinical Excellence (NICE) points out that there are no studies on the use of vitamin D for the treatment of COVID-19. Although NICE acknowledges that there is a correlation between lower vitamin D status and the development of COVID-19, they say this might be confused by other factors, like a high BMI and underlying health conditions.
This might be overly cautious. A study published in the journal Aging Clinical and Experimental Research looked at coronavirus and vitamin D levels in 20 European countries. It commented:
“Vitamin D has been shown to protect against acute respiratory infections … and older adults, the group most deficient in vitamin D, are also the ones most seriously affected by COVID-19.”
The online journal medRxiv further analysed coronavirus data from 10 countries. They found that low vitamin D levels are associated with a dangerously overactive immune response, whereas vitamin D helps keep this danger and inflammation under control.
What can you do to help protect yourself and your family?
It’s very clear from the opening of this report that chronological age is only a crude risk factor for turning the coronavirus from an illness into a killer. The real dangers are the weakening of the immune system and accumulated high levels of inflammation – which we and others have called ‘inflamm-ageing’.
So, with the probability of us getting a vaccine around early 2021, but that it may not initially give long-lasting immunity, this is what we suggest in addition to the measures above. The aim is not necessarily to prevent infection but to help cut the risk of a severe outcome:
Increase foods known to support and enhance the immune system and reduce inflammation
These include dark polyphenol-rich red and blue berry fruits, citrus fruits (for vitamin C), green and black tea, garlic, leafy green vegetables (broccoli and kale are especially good), nuts and seeds and avocados (for vitamin E), shellfish (zinc) and mushrooms.
To these, add foods that support a healthy microbiome/gut – which is home to at least 70% of your immune system cells. Feature fermentable fibre foods – oats, whole grains, beans and legumes like chickpeas and soybeans – and fermented foods like sauerkraut, kefir and real yoghurts that are an important source of probiotics. Plus prebiotic foods that feed your probiotic bacteria, like garlic, onions, leeks, asparagus and flaxseeds.
Maintain activity levels
Ensure you are physically active for half an hour or more on at least 5 days a week – exercise boosts immune function.
Take a daily health supplement
A daily comprehensive supplement like NutriShield is formulated to boost the levels of anti-inflammatory, plant derived nutrients like polyphenols in your diet. It also contains many nutrients that underpin the working of the immune system, including zinc, folic acid, copper and vitamins A, B6, B12, D3, E, and Omega 3.
Consider an immune supplement
An immuno-modulator like ImmunoShield can help normalise the immune response. If an immune response is weak, an immuno-modulator strengthens it, but if the response is excessive, it brings it back towards normal. That’s why the evidence is that Wellmune 1-3, 1-6 beta glucans in ImmunoShield will not cause or contribute to a cytokine storm.
Look at a probiotic supplement
Some probiotic strains have been shown to support the natural production of antibodies and may increase the production of T-cells and Natural Killer cells. These strains include Lactobacillus rhamnosus, L. casei and the very robust Bacillus coagulans They are included in the multi-strain probiotic Microbiotic Plus.
Take extra vitamin D3
For most people, 800 IU of vitamin D3 should be enough in the summer. But once we get to October, we recommend supplementing at 2,000 IU a day (see Uni-Vite Vitamin D). And if you feel you want extra protection, this level is well below the upper safe limit even during the sunnier months (the UK upper safe limit for vitamin D supplementation being 5,000 IU).
I hope this report has been helpful.
- Why does COVID-19 disproportionately affect older people: Mueller et al, Aging (Albany NY). 2020 May 29;12(10):9959-9981. doi: 10.18632/aging.103344. Epub 2020 May 29.PMID: 32470948
- Features of 16,749 hospitalised UK patients with COVID-19 using the ISARIC WHO Clinical Characterisation Protocol: Annemarie Docherty et al, MedRxiv preprint
- Physical distancing, face masks, and eye protection to prevent person-to-person transmission of SARS-CoV-2 and COVID-19: a systematic review and meta-analysis: Derek. K. Chu et al; Lancet June 27 2020
- COVID-19: Gastrointestinal manifestations and potential fecal-oral transmission: Gu J, Han B, Wang J, Gastroenterology (2020), doi: https://www.gastrojournal.org/article/S0016-5085(20)30281-X/pdf
- Probability of aerosol transmission of SARS-CoV-2; Bonn D, Smith SH, Somsen A, van Rijn C, Kooij S, van der Hoek L, Bem RA 10.1101/2020.07.16.20155572 — Posted: 2020-07-18
- Probiotics and immune health. Fang Yan & D.B. Polk; Current Opinion in Gastroenterology: November 2011