There are several simple measures that can improve your resistance to picking up the coronavirus infection:
- Wash hands for 20 seconds with soap (or us a hand sanitiser with 60% alcohol).
- Eat a nutrient-dense, healthy diet.
- Minimise sugar, caffeine and alcohol consumption.
- Get at least 6 hours sleep.
- Exercise regularly.
- Minimise / release stress
- Spend time in nature and in the sunshine.
Maintain optimum levels of vitamins A, C and D3
- Vitamin A: 50001u daily
- Vitamin C: 3 – 5000mg daily
- Vitamin D3: 2 – 5000iu daily
- Zinc: 20 mg daily
- Probiotics (from fermented foods or supplements)
- Iodine: 25mg daily.
- Echinacea Purpura
- Vitamin A: 100 000iu daily for 4 days
- Vitamin C: 1000mg hourly up to bowel tolerance
- Vitamin D3: 50 000iu daily for 4 days
- Magnesium citrate / malate / chelate / chloride: 400mg daily
- Zinc: 20 – 40mg daily
- Vitamin B Complex
- L-lysine: 1 – 2gm daily
- Echinacea purpura
- Intravenous vitamin C: 12.5 – 25mg in sterile water, with added magnesium S04 and vitamin Bs
- H202 3% nebulisation for 30 minutes, 3 to 4 times a day
- Intravenous ozone
- Rife resonator frequency treatments
Recommendations supplied by SASIM Chairperson Dr. David Nye.
One of my student doctors asked my opinion on the management of coronavirus. Here follows my suggestions gleamed from the literature.
1. Vitamin C is still my favorite antiviral agent most certainly for the more serious forms of the infection especially the pneumonia (Acute respiratory distress syndrome-ARDS). It seems that this is due to an underlying ‘cytokine storm’ causing the high mortality. This ‘storm’ can also happen with the influenza virus.
Vitamin C is well placed to deal with this scenario. It is a powerful antioxidant protecting cells from oxidative stress. It has immune cell stimulating functions, increasing phagocytosis. It supports endothelial cell function and improves microcirculation. It supports wound healing and collagen synthesis. One of the doctors working at the epicentre of the virus outbreak has published the following information:
We call upon all those in the leadership, and those providing direct assistance patients, to bravely and rapidly apply large dose intravenous vitamin C (IVC) to help those patients and to stop this epidemic.
Coronaviruses and influenza are among the pandemic viruses that can cause lethal lung injuries and death from ARDS. Viral infections cause a “cytokine storm” that can activate lung capillary endothelial cells leading to neutrophil infiltration and increased oxidative stress (reactive oxygen and nitrogen species) that further damages lung barrier function. ARDS, which is characterized by severe hypoxemia, is usually accompanied by uncontrolled inflammation, oxidative injury, and the damage to the alveolar-capillary barrier. The increased oxidative stress is a major insult in pulmonary injury such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), two clinical manifestations of acute respiratory failure with substantially high morbidity and mortality.
Dr Mao is the chief of emergency medicine department in a major Shanghai hospital and already had lots of experience with the use of vitamin C in life threatening diseases. He co-authored the Shanghai Guidelines for the treatment of Covid-19 infection, an official document endorses by the Shanghai Medical Association and Shanghai city government. They treated 50 cases of moderate to severe cases of Covid-19 infection with high dose IV vitamin C. The dose was in the range of 10-20 grams a day for 7-10 days. All patients who received IV vitamin C improved and there was no mortality. Those receiving vitamin C has a shorter hospitalisation by 3-5 days. One very serious patient received 50 grams over 4 hours with a dramatic recovery. No side effects reported.
Expert consensus on comprehensive treatment of coronavirus disease in Shanghai 2019. Chinese journal of Infectious Diseases 2020,38. Wang D et al
The following is an article from the Orthomolecular Association, who have much experience in the use of high dose vitamin C:
How Vitamin C Reduces Severity and Deaths from Serious Viral Respiratory Diseases
by Andrew W. Saul, Editor
Orthomolecular Medicine News Service, Feb 10, 2020
Vitamin C and its application to the treatment of nCoV Coronavirus
Most deaths from coronavirus are caused by pneumonia. Vitamin C has been known, for over 80 years, to greatly benefit pneumonia patients.
In 1936 Gander and Niederberger found that vitamin C lowered fever and reduced pain in pneumonia patients. 
Also in 1936, Hochwald independently reported similar results. He gave 500 mg of vitamin C every ninety minutes. 
McCormick gave 1000 mg vitamin C intravenously, followed by 500 mg orally every hour. He repeated the injection at least once. On the fourth day, his patient felt so well that he voluntarily resumed work, with no adverse effects. 
In 1944 Slotkin and Fletcher reported on the prophylactic and therapeutic value of vitamin C in bronchopneumonia, lung abscess, and purulent bronchitis. “Vitamin C has greatly alleviated this condition and promptly restored normal pulmonary function.” 
Slotkin further reported that “Vitamin C has been used routinely by the general surgeons in the Millard Fillmore Hospital, Buffalo, as a prophylactic against pneumonia, with complete disappearance of this complication.” 
According to the US Centers for Disease Control, there are about 80,000 dead from annual influenzas, escalating to pneumonia, in the USA. Coronavirus is a very serious contagious disease. But contagion to a virus largely depends on the susceptibility of the host. It is well established that low vitamin C levels increase susceptibility to viruses. 
Vitamin C lowers mortality
It is one thing to be sick from a virus and another thing entirely to die from a viral-instigated disease. It must be emphasized that a mere 200 mg of vitamin C/day resulted in an 80% decrease in deaths among severely ill, hospitalized respiratory disease patients. 
A single, cheap, big-box discount store vitamin C tablet will provide more than twice the amount used in the study above.
And yes, with vitamin C, more is better.
Frederick R. Klenner and Robert F. Cathcart successfully treated influenza and pneumonia with very high doses of vitamin C. Klenner published on his results beginning in the 1940s;  Cathcart beginning in the 1970s.  They used both oral and intravenous administration.
“Vitamin C is effective in reducing duration of severe pneumonia in children less than five years of age. Oxygen saturation was improved in less than one day.” 
A recent placebo controlled study concluded that “vitamin C should be included in treatment protocol of children with pneumonia so that mortality and morbidity can be reduced.” In this study, the majority of the children were infants under one year of age. By body weight, the modest 200 mg dose given, to tiny babies, would actually be the equivalent of 2,000-3,000 mg/day for an adult. 
Although many will rightly maintain that the dose should be high, even a low supplemental amount of vitamin C saves lives. This is very important for those with low incomes and few treatment options.
We’re talking about twenty cents’ worth of vitamin C a day to save lives now.
1. Gander and Niederberger. Vitamin C in the handling of pneumonia.” Munch. Med. Wchnschr., 31: 2074, 1936.
2. Hochwald A. Beobachtungen uber Ascorbinsaurewirkung bei der krupposen Pneumonie.” Wien. Arch. f. inn. Med., 353, 1936.
3. McCormick WJ. Have we forgotten the lesson of scurvy? J Applied Nutrition, 1962, 15:1 & 2, 4-12.
4. Slotkin & Fletcher. Ascorbic acid in pulmonary complications following prostatic surgery. Jour. Urol., 52: Nov. 6, 1944.
5. Slotkin GE. Personal communication with WJ McCormick. December 2, 1946.
6. Saul AW. Nutritional treatment of coronavirus. Orthomolecular Medicine News Service, 16:6, Jan 30, 2020. (22 references and 50 recommended papers for further reading)
7. Hunt C et al. The clinical effects of Vitamin C supplementation in elderly hospitalised patients with acute respiratory infections. Int J Vitam Nutr Res 1994;64:212-19.
8. Klenner FR. Observations on the dose and administration of ascorbic acid when employed beyond the range of a vitamin in human pathology. J Applied Nutrition 1971, 23:3&4.
Klenner FR. (1948) Virus pneumonia and its treatment with vitamin C. J South Med Surg 110:36-8.
Klenner, FR. (1951) Massive doses of vitamin C and the virus diseases. J South Med and Surg, 113:101-107.
Klenner, FR. (1971) Observations on the dose and administration of ascorbic acid when employed beyond the range of a vitamin in human pathology. J. App. Nutr., 23:61-88.
All of Dr. Klenner’s papers are listed and summarized in: Clinical Guide to the Use of Vitamin C (ed. Lendon H. Smith, MD, Life Sciences Press, Tacoma, WA, 1988.
9. Cathcart RF. (1981) Vitamin C, titrating to bowel tolerance, anascorbemia, and acute induced scurvy. Med Hypotheses. 7:1359-76.
Cathcart RF. (1993) The third face of vitamin C. J Orthomolecular Med, 7:197-200.
Additional Dr. Cathcart papers are posted at http://www.doctoryourself.com/biblio_cathcart.html
10. Khan IM et al. (2014) Efficacy of vitamin C in reducing duration of severe pneumonia in children. J Rawalpindi Med Col (JRMC). 18(1):55-57.
Oral vs IV vitamin C
One of the most interesting articles I have read recently appeared in the Townsend Letter(march 2020) concerning the very rapid rise in blood ascorbate levels following oral consumption. In fact oral consumption of 4,000mg of ascorbic acid taken my mouth can produce the same rapid increase in plasma concentration as an intravenous infusion. That actually supports my own experience with Influenza, taking one gram vitamin C every hour. While liposomal vitamin C may still be the best approach when using oral vitamin C nevertheless this study suggests that the common cheap vitamin C actually does get well absorbed. Vitamin C does not last in the blood very long so that taking the oral form may even extent the usefulness of IV vitamin C or even replace it.
Dr Klingardt is a very well know Integrative doctor in the USA with lots of experience in treating serious virus infections. In a recent report he advised the following approach to the 2019-nCov virus.
1. Vitamin C IV 50-200mg/kg which works out to 4-15 gms/day for 3 days
2. A mixture of the following tinctures:
- Artemesia Annua
- 2 dropper full 2x/day as preventive or 4x/day if ill.
3. Vitamin D 6000-10,000IU/day
4. Hypochlorous acid spray as a disinfectant.
5. Chloroquine for vey serious cases. 500mg bd for 10 days
6. Switch off WiFi.
Clearly vitamin C is the gold standard right now. I suggest everyone be taking 3-5 grams per day orally and increase to hourly or even more frequently if any symptoms appear.If you can get IV vitamin C then go for it but it does appear that the oral form taken frequently may also do the trick. Vitamin D and some of the tinctures suggested by Dr Klingardt may be useful additions.
This is not a battle we are fighting, but a journey. The earth is calling us back home to pay attention to its needs and be less self centred but caring for the earth we walk on, the plants and animals that surround us and our own fellow participants in the world of human involvement.
By Dr Bernard Brom
The Functional Medicine Approach to COVID-19: Virus-Specific Nutraceutical and Botanical Agents
Health professionals and the public must be well informed about the COVID-19 virus, the disease it causes, and how it spreads. This information is readily available and not within the scope of this document. At this time, there are no specific vaccines or uniformly successful treatments for COVID-19. In this context of insufficient evidence, the scope of this document will be to assess the scientific plausibility of promising prevention approaches and therapeutic (nutraceutical and botanical) interventions and then to offer clinical recommendations.
With respect to interventions, the practice of Functional Medicine emphasizes the primacy of safety, validity, and effectiveness. In the novel context of COVID-19, validity in the form of published evidence is lacking. Therefore, “validity” relies upon inferences from the mechanisms of action of individual agents and/or published outcomes data supporting their mitigating effects on illness from other viral strains. Likewise, data for the “effectiveness” of interventions targeting the viral mechanisms of COVID-19 are nascent and rapidly emerging. In this context, the following recommendations represent the Functional Medicine approach to the COVID-19 crisis:
Adherence to all health recommendations from official sources to decrease viral transmission.
Optimizing modifiable lifestyle factors in order to improve overall immune function (an introductory document on ‘Boosting Immunity’ is available here):
- Reduces progression from colonization to illness.
Personalized consideration of therapeutic agents that may:
- Favorably modulate cellular defense and repair mechanisms.
- Favorably modulate viral-induced pathological cellular processes.
- Promote viral eradication or inactivation.
- Mitigate collateral damage from other therapeutic agents.
- Promote resolution of collateral damage and restoration of function.
Treatment of confirmed COVID-19 illness (as per conventional standards and practice):
- May reduce the severity and duration of acute symptoms and complications.
- May support recovery and reduce long-term morbidity and sequelae.
Additional references are being collated and will be made available in the future.
Clinical Recommendations and Mechanisms of Action
We encourage practitioners to learn about the mechanism of invasion, replication, and pathophysiology of the COVID-19 virus. Much of what we know has been extrapolated from basic science research on SARS-CoV-2. Excellent resources are available online, including the free YouTube lectures through Dr. Roger Seheult:
This document discusses the mechanisms of action of a number of different botanical and nutraceutical agents. These agents can be considered as immunoadjuvants, defined as substances that act to accelerate, prolong, or enhance antigen-specific immune responses by potentiating or modulating the immune response.
A coronavirus such as SARS-CoV-2 can be deadly because of its ability to stimulate a part of the innate immune response called the inflammasome, which can cause uncontrolled release of pro-inflammatory cytokines, leading to cytokine storm and severe, sometimes irreversible, damage to respiratory epithelium. The SARS-CoV-2 virus has been shown to activate the NLRP3 inflammasome.[3,4] A 2016 review article entitled “Natural compounds as regulators of NLRP3 inflammasome-mediated IL-beta production” notes that “resveratrol, curcumin, EGCG [epigallocatechin gallate], and quercetin are potent inhibitors of NLRP3 inflammasome-mediated IL-1beta production, typically acting at more than one element of the involved pathways. However, it should be noted that these polyphenols have an even much broader biological effect, as they influence a variety of pathways.” For example, these polyphenols modulate NF-kB upregulation, which is useful to counteract the COVID-19 ’hyper-inflammation.
A preprint released on March 23, 2020, identified the ability of plant bioactive compounds to inhibit the COVID-19 main protease (Mpro), which is necessary for viral replication. There is much excitement surrounding the recent identification of Mpro, and it is a current potential pharmaceutical drug target. Kaempferol, quercetin, luteolin-7-glucoside, demethoxycurcumin, naringenin, apigenin-7glucoside, oleuropein, curcumin, catechin, and epicatechin-gallate were the natural compounds that appeared to have the best potential to act as COVID-19 Mpro inhibitors. Though further research is necessary to prove their efficacy, this study provides the biologic plausibility and mechanistic support (COVID-19 protease inhibition) to justify their use.
For these reasons, we recommend the following compounds, at standard dosages, to prevent activation of the NLRP3 inflammasome, to decrease NF-kB activation, and to potentially inhibit COVID-19 replication. There is no literature to support a regimen of a single vs. multiple agents. Our recommendation is to use higher dosing and/or multiple agents when patient contextual factors (e.g., patient desire, pre-existing inflammation, multiple co-morbidities, higher risk, etc.) and/or therapeutic decision-making warrant such use.
In the recommendations below, the following criteria are used to identify strength of evidence and risk of harm.
Quercetin has been shown to have antiviral effects against both RNA (e.g., influenza and coronavirus) and DNA viruses (e.g., herpesvirus). Quercetin has a pleiotropic role as an antioxidant and anti-inflammatory, modulating signaling pathways that are associated with post-transcriptional modulators affecting post-viral healing.
Curcumin has been shown to modulate the NLRP3 inflammasome, and a preprint suggests that curcumin can target the COVID-19 main protease to reduce viral replication.
Green tea, in addition to modulating the NLRP3 inflammasome and, based on a preprint, potentially targeting the COVID-19 main protease (Mpro) to reduce viral replication, has also been shown to prevent influenza in healthcare workers.
N-acetylcysteine promotes glutathione production, which has been shown to be protective in rodents infected with influenza. In a little-noticed six-month controlled clinical study enrolling 262 primarily elderly subjects, those receiving 600 mg NAC twice daily, as opposed to those receiving placebo, experienced significantly fewer influenza-like episodes and days of bed confinement.
Resveratrol, a naturally occurring polyphenol, shows many beneficial health effects. It has been shown to modulate the NLRP3 inflammasome. In addition, resveratrol was shown to have in vitro activity against MERS-CoV.
Activated vitamin D,1,25(OH) D, a steroid hormone, is an immune system modulator that reduces the expression of inflammatory cytokines and increases macrophage function. Vitamin D also stimulates the expression of potent antimicrobial peptides (AMPs), which exist in neutrophils, monocytes, natural killer cells, and epithelial cells of the respiratory tract. Vitamin D increases anti-pathogen peptides through defensins and has a dual effect due to suppressing superinfection. Evidence suggests vitamin D supplementation may prevent upper respiratory infections.
However, there is some controversy as to whether it should be used and the laboratory value that should be achieved. Research suggests that concerns about vitamin D (increased IL-1beta in cell culture) are not seen clinically. The guidance we suggest is that a laboratory range of >50 and < 80ng/mL serum 25-hydroxy vitamin D may help to mitigate morbidity from COVID-19 infection.
Melatonin has been shown to have an inhibitory effect on the NLRP3 inflammasome. This has not gone unnoticed by the COVID-19 research community, with two recent published papers proposing the use of melatonin as a therapeutic agent in the treatment of patients with COVID-19.,
Vitamin A is a micronutrient that is crucial for maintaining vision, promoting growth and development, and protecting epithelium and mucus integrity in the body. Vitamin A is known as an anti-inflammation vitamin because of its critical role in enhancing immune function. Vitamin A is involved in the development of the immune system and plays regulatory roles in cellular immune responses and humoral immune processes through the modulation of T helper cells, sIgA, and cytokine production. Vitamin A has demonstrated a therapeutic effect in the treatment of various infectious diseases.
Elderberry (Sambucus nigra) is seen in many medicinal preparations and has widespread historical use as an anti-viral herb. Based on animal research, elderberry is likely most effective in the prevention of and early infection with respiratory viruses. One in-vitro study reported an increase in TNF-alpha levels related to a specific commercial preparation of elderberry leading some to caution that its use could initiate a “cytokine storm.” However, these data were not confirmed when the same group performed similar studies, which were published in 2002. Therefore, these data suggest it is highly implausible that consumption of properly prepared elderberry products (from berries or flowers) would contribute to an adverse outcome related to overproduction of cytokines or lead to an adverse response in someone infected with COVID-19.
PEA is a naturally occurring anti-inflammatory palmitic acid derivative that interfaces with the endocannabinoid system. There was a significantly favorable outcome in five of six double blind placebo-controlled trials looking at acute respiratory disease due to influenza. Dosing was generally 600 mg three times daily for up to three weeks. There are multiple mechanisms of action associated with PEA, from inhibition of TNF-alpha and NF-kB to mast cell stabilization. In influenza, it is thought that PEA works by attenuating the potentially fatal cytokine storm.
Vitamin C contributes to immune defense by supporting various cellular functions of both the innate and adaptive immune system. Vitamin C accumulates in phagocytic cells, such as neutrophils, and can enhance chemotaxis, phagocytosis, generation of reactive oxygen species, and ultimately microbial killing. Supplementation with vitamin C appears to be able to both prevent and treat respiratory and systemic infections. Vitamin C has been used in hospital ICUs to treat COVID-19 infection.
Zinc contributes to immune defense by supporting various cellular functions of both the innate and adaptive immune system. There is also evidence that it suppresses viral attachment and replication. Zinc deficiency is common, especially in those populations most at risk for severe COVID-19 infections, and it is challenging to accurately diagnosis with laboratory measures. Supplementation with zinc is supported by evidence that it both prevents viral infections and reduces their severity and duration. Moreover, it has been shown to reduce the risk of lower respiratory infection, which may be of particular significance in the context of COVID-19.
In the recommendations above, the following criteria are used to identify strength of evidence and risk of harm:
This resource is only intended to identify nutraceutical and botanical agents that may boost your immune system. It is not meant to recommend any treatments, nor have any of these been proven effective against COVID-19. None of these practices are intended to be used in lieu of other recommended treatments. Always consult your physician or healthcare provider prior to initiation. For up-to-date information on COVID-19, please consult the Centers for Disease Control and Prevention.
Source: Institute For Functional Medicine (follow link for full references)
Healing in the time of Corona
Thanks to a clever little virus, our collective hamster wheel has come to an abrupt halt, throwing many of us off and spinning in the other direction, towards ourselves.
My fear is that between the Vitamin C popping, baking and Zoom calls, we are avoiding the questions that lie beneath the conspiracy theories and that bring us face to face with our mortality. Questions that may not have an answer but that invite us explore what lies beyond our fear-based reactions and habitual patterns of stress to a more curious and open place within ourselves and between each other.
We have been given a great deal of time to confront some frightful and wonderful things about ourselves, our world, our purpose, our vocation and our relationships. To grieve the loss of what has been taken away and what we choose to let go of. Time to consider the meaning of health.
This pandemic is a healing crisis, a process that is happening whether we choose to co-operate with or not. And it is certainly not the last crisis we will face as humanity. Hiding behind a mask will only get us so far. This is an opportune time to create the new neural pathways for resilient, adaptable and robust systems within the body-mind, and within society.
Many of us are well into this process already, catalysed by our own personal crisis or life experience. But for the first time, we journey together to co-create the foundation for a new way of living and being.
Here are some principles of healing to consider and anchor to as we sense our way through this followed by some practical ways to apply them:
- Healing is a dynamic. Health is not a fixed or static state. It is a moment to moment process directed by the forces of nature to serve a state of balance. It is a cycle of release and restoration, birth and death, weeding and sowing, letting go and letting come. Illness itself is part of the healing process and part of the attempt to return to homeostasis. Understanding this gives us the opportunity to participate with it rather than avoiding, suppressing, or working against it. This can only happen when we are awake, aware and responsive.
- Healing is relational. Each part of a system is in communication with the other. Healing requires relationship, between heart and mind, doctor and patient, organism and nature. Relationship begins with the ability of one part to be in gentle communication with the other, so that a creative response can be generated, demanding the dissolving of the borders of siloed constructs within ourselves and between each other.
Build resilience: learn to relax
Our role in supporting the healing process is to create the conditions in which the healing process can be optimised.
The Corona pandemic has sparked a reactive need to ‘boost’ the immune system as a defence against the virus. Wellness experts are all dispensing a great deal of advice on the best supplements to take, diet to follow or breathing technique to practice. While these are all helpful, there is a risk of falling into the ‘quick fix trap’ when it comes to immune health and health in general. The immune system is a complex multidimensional system that is connected to our gut health, our endocrine system and is deeply linked to our physiological responses to stress. The body either senses danger or safety. A perception of danger activates a defensive response while a perception of safety activates a healing response.
In our current situation, the information that we are constantly being exposed to and nature of our thoughts is causing overfiring of danger signals, and all within the safety of our own homes. This confused state and the experience of anxiety and fear at this time are normal and appropriate. However, its prolonged nature means that for many there is no way to process, release or integrate it. The chronic activation of the fear response, causes dis-regulation of the immune system, increase in inflammatory markers and a compromised digestive system. A perfect storm ensues.
A key to building a resilient immune system is through awareness and relaxation training.
Relaxation training through various mindfulness and breathing practices helps us to notice our physiological responses to habitual stressful thoughts and is a means to override it. Training relaxation in the midst of crisis may not change the situation but it does create the environment in which our self-healing system can be optimised and helps to build our inner resources of immunity. It also gives us the best chance of coming up with a more creative solution to deal with it. The ability to do this is one of the greatest gifts of being human.
Just as our thoughts and emotions are reflected in the way we breathe, the way we breathe can send signals of safety to the brain via the Vagus nerve. Conscious breathing is a powerful and accessible tool that anyone can easily learn, practice and share. While there are thousands of breathing techniques that are available, coherent breathing is one of the most well researched techniques. It has been widely used in patients with PTSD, refugees and patients in hospitals. It balances the nervous system and builds resilience in the immune system.
Practice slowing down the respiratory rate to 3 to 6 breaths a minute:
- Breath through the nose for a slow count of 5 seconds (depending on your capacity) and breathe out for the same amount of time.
- It is recommended that you practice this for 20 minutes a day to get the full benefit.
No one can afford not to learn the basics of breath awareness and conscious breathing. Relaxation training is not an idea or lofty notion. It is a practical science that is the foundation of health.
Stay awake: cultivate inner sight
Inner-sight is the ability to compassionately respond to what we become aware of.
The Covid-19 experience is one of intense vulnerability. All previous constructs of safety are crumbling, whether it be with regards to our health or economic well-being. The collective crisis may also bring up previous trauma as historical grief layered with anticipatory grief as worst-case scenarios keep us up at night. While we will mount physiological states of stress in reaction to this, the survival response will also show up in defensive behavioural reactions.
It is important to note how reactive and defensive behaviours may be playing out. Bringing a deep awareness to these responses offers us a profound opportunity for growth and creative choice.
- Distraction and avoidance. Spending more time than normal on YouTube, Netflix, social media and overworking is a way of avoiding the discomfort of what we are feeling.
- Obsession. This stems from our need to be in control and make our world feel safe and ordered. This may play out in obsession with news, cleaning up, tidying.
- Suppression. Difficulty talking and expressing the way we feel is normal when we can’t make sense of it ourselves. A common reaction is an internalisation and suppression of feelings eventually leading to amygdala hijacks (aggressive outbursts) and passive aggressive behaviour.
- Dissociation. This is another protection strategy. We ‘bypass’ uncomfortable feelings that we experience physically and emotionally through over-intellectualising or spiritual practices. This can lead to being “dis-embodied”
- Projection. When we feel out of control, we look for someone or something to project onto. We tend to blame, judge ourselves and others, polarise and compare. Racism and class distinction become heightened.
- Numbing. When we feel physical and emotional pain, we tend to over consume substances like high calorie foods, alcohol, cigarettes and drugs that acts as a short-term soothing balm or numbing agent, but that will cause harmful effects over time.
- Hoarding. The survival response also manifests in primal hoarding behaviour that plays out as we saw in the stockpiling of food, toilet paper, and in some countries, even guns!
Bringing a non-judgmental awareness to these patterns offers us the opportunity to heal, grow and transform. Mindfulness, breath awareness, somatic practices and journaling are some of the tools that can build the architecture of deepened awareness.
Feeding the fire: facing fears
Healing is the relationship between breath and death.
If we follow the road of our fear to its source, we will probably meet the fear of our fate – Death.
Whether we believe that we can reconcile this fear intellectually or not, all life forms have a primal instinct of self-preservation. Humans have taken this primal fear to the point of arrogance.
We go to great lengths to preserve life at all costs even if the cost is quality of life or challenging natural laws. This is the delicate tightrope that we are walking right now with regards to this pandemic.
Consider for a moment the possibilities of confronting this fear head on? What choices would we make? What would we let go of? What would we embrace? Risk?
There is a Buddhist practice called feeding the fire, the practice of confronting one’s greatest fear.
On the other side of the acceptance of our mortality comes a great liberation.
The Covid-19 experience is bringing some kind of death experience to all of us in some way, whether it is the death of a loved one, the loss of a business, an identity, an ideology or a lifestyle, something has ended. It requires a mourning, a grieving, a ‘letting go’ to a ‘letting come’ as Otto Scharmer, founder of the Presencing Institute so poignantly describes.
The acceptance of death brings an awakening to life, a deepened commitment to what is most important to us. Grief strips us bare and carries us to a state of beautiful naked vulnerability that we can embrace with tender compassion for ourselves and others. The beauty of collective suffering is empathy, compassion, the deepest seeds of our humanity. This is the fertile ground in which to plants the seeds of our future.
Opening the heart: stay embodied
An open heart is the fertile ground to plant the seeds of our future.
Right now, our emotional reactions feel intense, heightened, gripping, overwhelming.
Fear lives beneath the waves of frustration, anxiety, grief, irritation, overwhelm, disbelief, loneliness, claustrophobia, boredom and disbelief.
Emotions are powerful energetic experiences that require a healthy expression. How do we navigate our emotional life in a way that is not overwhelming or paralysing? How do we ride the waves of the feelings as they come without defaulting to our reactive and defensive behaviours?
Deepening our relationship with our emotional and mental patterns and finding healthy channels of expression is key. Generative conversations, writing, creating, meditating, movement and breathing are all ways that support us to channel, release and integrate our emotions. Somatic and creative practices are particularly important. This gets us out of the cycle of mental processing which can stand in the way of the release, integration and healing.
Here is a short practice you can try when you are feeling fearful, anxious or overwhelmed:
- Get skilled at ‘locating’ the emotion.
- What is the most prominent sensation you are experiencing in your body right now?
- Deepen your awareness of sensation e.g. can you trace around it? Does it have an epicentre?
- Is it prickly, sharp, heavy or tight?
- Now become aware of your breathing, slow down the inhalation and ‘direct it’ towards the centre of the sensation or use the breath to ‘expand’ the space around the sensation.
- As you release the exhale imagine that you are softening the edges and melting the resistance.
- Do this for 2 to 3 minutes.
- Relax your breathing and notice what you are experiencing.
Although none of us have clear answers to any of this, we can create and maintain an open-hearted resilience. The alternative fear-based reactions are what got us here in the first place. Let us not succumb to them and let this moment slip from our hands. Let us create the environment for creative ideas to emerge through a curious mind, healthy body and open heart. The most sustainable and innovative solutions for our future will emerge through our deep respect of ancient wisdom, alignment with natural laws, humility and highest capacities for compassion, creativity and healing. This is our challenge, our calling and our responsibility.
By Dr. Ela Manga
MBBCh (Wits) DCH (SA) DipObst (SA) CBP
Dr. Manga is an integrative medical doctor, author, speaker and leading voice in the field of mind-body medicine and wellness. Her background in western medicine, study of wisdom traditions and deep curiosity has informed her unique approach to health and well-being. She is an expert in the field of energy management and burnout. Her first book Breathe: Strategising Energy in the Age of Burnout, is fast becoming the go to guide for managing energy and optimising physical and mental health.
EC Microbiology Special Issue – 2020:
Use of Echinaforce to Prevent Coronavirus Infections
By Dr. Andreas Schapowal
ENT Specialist, Hochwangstr, Switzerland
The current outbreak of zoonotic coronavirus SARS-CoV-2 epidemic has produced a lot of media attention and uncertainty on how to protect against the infection. The WHO recommends typical hygiene measures as published here. Intensive research is focusing on a specific vaccination against SARS-CoV-2 and on antiviral medications acting directly against this virus.
Individuals may wish to modulate their unspecific immune system towards better protection against respiratory tract infections.
The extract of Echinacea purpurea Echinforce® (EF) from A. Vogel AG, Switzerland is licensed in Switzerland and other countries for the prevention and treatment of respiratory tract infections. There is scientific evidence from several in-vitro and in-vivo studies including double-blind, randomized, controlled, clinical studies following GCP guidelines and published in peer-reviewed journals. This scientific evidence shows as follows.
In vitro effects on enveloped respiratory viruses:
- EF in vitro inactivates enveloped respiratory viruses at physiologically relevant concentrations [1,2]:
- Influenza A and B at concentrations of 0.58 – 50 μg/ml1
- Respiratory syncytial virus (RSV) at 2.5 μg/ml
- Herpes simplex virus (HSV) at 0.39 μg/ml
- EF inhibits virally induced expression of pro-inflammatory cytokines including interleukin (IL) 6 or IL 8 by epithelial cells.
Effects were seen with many kinds of viral stimuli including coronavirus .
- The multicomponent extract non-specifically and irreversibly interferes with viral docking receptors (e.g. influenza) to block infectivity of pathogens [2,3]. EF further reduces secretion of pro-inflammatory cytokines upon viral infection.
In vitro effects on coronaviruses:
- EF in vitro inactivates infectivity of α- and β-Coronaviruses (HCoV-229E, SARS-CoV and MERS-CoV) at concentrations < 10 μg/ml .
- Similar to other enveloped viruses direct contact of virus and EF is required for full inactivation.
- Intracellular effects (e.g. inhibition of viral replication) is only seen at very high concentrations, less likely to play a role in vivo.
- Replication in an organotypic cell culture system (MucilAir™) shows that prophylactic application of EF prevents coronavirus
infection also under more in vivo-like situations.
Results show that antiviral effects of EF apply to a broad range of enveloped respiratory viruses. Due to its non-specific action, coronaviruses and potentially the new occurring SARS-CoV-2 are susceptible to EF as well, though the latter virus has not been studied yet.
In vivo effects of EF on enveloped respiratory viruses:
Preventive application of EF over 4 months reduced enveloped virus infections (nasal samples from symptomatic patients positively tested for influenza, RSV, coronaviruses, parainfluenza or metapneumoviruses): 24 infections, of which 21 were coronaviruses (9: 229E;11: HKU1; 1: OC43) were detected with EF and 47 samples in the placebo group, of which 33 were positive for coronaviruses (15: 229E;17: HKU1; 1: OC43). Whereas the effect on enveloped viruses was statistically significant with p= 0.0114, the difference for coronaviruses was not (p = 0.154) possibly due to low sample size.
Another randomized, blinded, controlled study with n = 203 children (4 – 12 years) administered EF over 4 months and collected nasal secretions for pathogen analysis analogous to Jawad . Again, a total of 47 enveloped virus infections with control was reduced to 28 infections with EF (p = 0.0218). No difference was seen in this study including children for coronavirus infections in particular .
In a meta-analysis of six clinical studies with a total auf 2458 participants  the use of Echinacea extracts was associated with reduced risk of recurrent respiratory infections (RR 0.649, 95% CI 0.545 – 0.774, p < 0.0001). Ethanolic extracts from echinacea like EF appeared to provide superior effects over pressed juices and increasing dosing during acute episodes further enhanced these effects.
Three independent studies found that in individuals with higher susceptibility, stress or a state of immunological weakness, Echinacea halved the risk of recurrent respiratory infections. Complications including pneumonia, otitis media, pharyngitis and tonsillitis were also less frequent with echinacea treatment.
Despite the limited evidence, available in vitro data suggest that EF may provide protection against enveloped virus infections. As viral inhibition is non-specific, a broad range of membranous viruses may be covered, possibly including the newly occurring SARS-CoV-2.
Two randomized, blinded, controlled clinical studies support the preventive effects against enveloped viruses. A meta-analysis gives evidence for reducing the risk of recurrent respiratory tract infections and complications with echinacea treatment.
I recommend Echinaforce for the prevention and treatment of respiratory tract infections in children from 4 years on and adults, in the absence of clinically tested and specific therapeutic options also for the possible prevention of coronavirus infections. The available evidence suggests a preventive rather than therapeutic benefit, whereas suspected SARS-CoV-2 infections require consultation with a medical practitioner.
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PLoS Pathogens – November 2010:
Zn Inhibits Coronavirus and Arterivirus RNA Polymerase Activity In Vitro and Zinc Ionophores Block the Replication of These Viruses in Cell Culture
- Aartjan te Velthuis, University of Cambridge
- Sjoerd van den Worm, Oregon Health and Science University
- Ralph S Baric, University of North Carolina at Chapel Hill
- Martijn J van Hemert, Leiden University Medical Centre
Increasing the intracellular Zn2+ concentration with zinc-ionophores like pyrithione (PT) can efficiently impair the replication of a variety of RNA viruses, including poliovirus and influenza virus. For some viruses this effect has been attributed to interference with viral polyprotein processing. In this study we demonstrate that the combination of Zn2+ and PT at low concentrations (2 μm Zn2+ and 2 μm PT) inhibits the replication of SARS-coronavirus (SARS-CoV) and equine arteritis virus (EAV) in cell culture.
The RNA synthesis of these two distantly related nidoviruses is catalyzed by an RNA-dependent RNA polymerase (RdRp), which is the core enzyme of their multiprotein replication and transcription complex (RTC). Using an activity assay for RTCs isolated from cells infected with SARS-CoV or EAV—thus eliminating the need for PT to transport Zn2+ across the plasma membrane—we show that Zn2+ efficiently inhibits the RNA-synthesizing activity of the RTCs of both viruses. Enzymatic studies using recombinant RdRps (SARS-CoV nsp12 and EAV nsp9) purified from E. coli subsequently revealed that Zn2+ directly inhibited the in vitro activity of both nidovirus polymerases.
More specifically, Zn2+ was found to block the initiation step of EAV RNA synthesis, whereas in the case of the SARS-CoV RdRp elongation was inhibited and template binding reduced. By chelating Zn2+ with MgEDTA, the inhibitory effect of the divalent cation could be reversed, which provides a novel experimental tool for in vitro studies of the molecular details of nidovirus replication and transcription.
Zinc ions are involved in many different cellular processes and have proven crucial for the proper folding and activity of various cellular enzymes and transcription factors. Zn2+ is probably an important co-factor for numerous viral proteins as well. Nevertheless, the intracellular concentration of free Zn2+ is maintained at a relatively low level by metallothioneins, likely due to the fact that Zn2+ can serve as intracellular second messenger and may trigger apoptosis or a decrease in protein synthesis at elevated concentrations [1,2,3].
Interestingly, in cell culture studies, high Zn2+ concentrations and the addition of compounds that stimulate cellular import of Zn2+, such as hinokitol (HK), pyrrolidine dithiocarbamate (PDTC) and pyrithione (PT), were found to inhibit the replication of various RNA viruses, including influenza virus , respiratory syncytial virus  and several picornaviruses [6,7,8,9,10,11]. Although these previous studies provided limited mechanistic information, this suggests that intracellular Zn2+ levels affect a common step in the replicative cycle of these viruses.
In cell culture, PT stimulates Zn2+ uptake within minutes and inhibits RNA virus replication through a mechanism that has only been studied in reasonable detail for picornaviruses [11,12]. In vitro studies with purified rhinovirus and poliovirus 3C proteases revealed that protease activity was inhibited by Zn2+ [13,14], which is in line with the inhibition of polyprotein processing by zinc ions that was observed in cells infected with human rhinovirus and coxsackievirus B3 .
The replication of segmented negative-strand RNA viruses such as influenza virus, however, does not depend on polyprotein processing and the effect of PDTC-mediated Zn2+ import was therefore hypothesized to result from inhibition of the viral RNA-dependent RNA polymerase (RdRp) and cellular co-factors . Moreover, an inhibitory effect of Zn2+ on the activity of purified RdRps from rhinoviruses and hepatitis C virus was noted, but not investigated in any detail [15,16].
Details on the effect of zinc ions are currently largely unknown for nidoviruses. This large group of positive-strand RNA (+RNA) viruses includes major pathogens of humans and livestock, such as severe acute respiratory syndrome coronavirus (SARS-CoV), other human coronaviruses, the arteriviruses equine arteritis virus (EAV), and porcine reproductive and respiratory syndrome virus (PRRSV) [17,18]. The common ancestry of nidoviruses is reflected in their similar genome organization and expression strategy, and in the conservation of a number of key enzymatic functions in their large replicase polyproteins .
A hallmark of the corona- and arterivirus replicative cycle is the transcription of a 59- and 39- coterminal nested set of subgenomic (sg) mRNAs from which the viral structural and accessory protein genes are expressed [20,21].
Analogous to picornaviruses [13,22], zinc ions were demonstrated to inhibit certain proteolytic cleavages in the processing of the coronavirus replicase polyproteins in infected cells and cell-free systems [23,24]. In this study we report that the zinc-ionophore pyrithione (PT) in combination with Zn2+ is a potent inhibitor of the replication of SARS-coronavirus (SARS-CoV) and equine arteritis virus (EAV) in cell culture. To assess whether – besides a possible effect on proteolytic processing – nidovirus RTC subunits and RNA synthesis are directly affected by Zn2+, we employed in vitro systems for SARS-CoV and EAV RNA synthesis that are based on membrane-associated RTCs isolated from infected cells (from here on referred to as RTC assays) [25,26]. In addition, we used in vitro recombinant RdRp assays to directly study the effect of zinc ions on the RdRps of SARS-CoV and EAV [27,28].
Using these independent in vitro approaches, we were able to demonstrate that Zn2+ directly impairs nidovirus RNA synthesis, since it had a strong inhibitory effect in both RTC and RdRp assays. Interestingly, the Zn2+ -mediated inhibition could be reversed through the addition of a Zn2+ chelator (MgEDTA).
We therefore applied this compound to stop and restart the in vitro RNA-synthesizing activity at will. This convenient tool allowed us to study various mechanistic aspects of arteri- and coronavirus RNA synthesis in more detail. Additionally, the zinc-mediated inhibition of nidovirus RNA synthesis described here may provide an interesting basis to further explore the use of zinc-ionophores in antiviral therapy.
Zinc and pyrithione inhibit nidovirus replication in vivo Zinc ions are involved in many different cellular processes, but the concentration of free Zn2+ is maintained at a relatively low level by metallothioneins . Zn2+ and compounds that stimulate import of Zn2+ into cells, such as PT, were previously found to inhibit replication of several picornaviruses, including rhinoviruses, foot-and-mouth disease virus, coxsackievirus, and mengovirus in cell culture [6,7,8,9,10,11]. To determine whether Zn2+ has a similar effect on nidoviruses, we investigated the effect of PT and Zn2+ on the replication of EAV and SARS-CoV in Vero-E6 cells, using reporter viruses that express green fluorescent proteins (GFP), i.e., EAV-GFP  and SARS-CoV-GFP .
EAV-GFP encodes an N-terminal fusion of GFP to the viral nonstructural protein 2 (nsp2), one of the cleavage products of the replicase polyproteins, and thus provides a direct readout for translation of the replicase gene. In SARS-CoV-GFP, reporter expression occurs from sg mRNA 7, following the replacement of two accessory protein-coding genes (ORFs 7a and 7b) that are dispensable for replication in cell culture.
We first assessed the cytotoxicity of a range of PT concentrations (0–32 mM) in the presence of 0 to 8 mMZnOAc2. Treatment with PT of concentrations up to 32 μm in combination with <4 mM ZnOAc2 did not reduce the viability of mock-infected cells after 18 h (Fig. 1A), as measured by the colorimetricMTS (3-(4,5-dimethylthiazol-2-yl)-5- (3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) viability assay. As elevated Zn2+ concentrations are known to inhibit cellular translation, we also used metabolic labeling with 35S-methionine to assess the effect of PT and Zn2+ on cellular protein synthesis. Incubation of Vero-E6 cells for 18 h with the combinations of PT and Zn2+ mentioned above, followed by a 2-h metabolic labeling, revealed no change in overall cellular protein synthesis when the concentration of ZnOAc2 was ,4 mM (data not shown).
Using these non-cytotoxic conditions we subsequently tested the effect of PT and ZnOAc2 on EAV-GFP and SARS-CoV-GFP replication. To this end, Vero-E6 cells in 96-well plates were infected with a multiplicity of infection (m.o.i.) of 4. One hour post infection (h p.i.), between 0 and 32 mM of PT and 0, 1, or 2 mM ZnOAc2 were added to the culture medium. At 17 h p.i., a time point at which GFP expression in untreated infected cells reaches its maximum for both viruses, cells were fixed, and GFP fluorescence was quantified.
The reporter gene expression of both SARS-CoV-GFP and EAV-GFP was already significantly inhibited in a dose-dependent manner by the addition of PT alone (Fig. 1B and C). This effect was significantly enhanced when 2 mM of Zn2+ was added to the medium. We found that addition of ZnOAc2 alone also reduced virus replication, but only at levels that were close to the 50% cytotoxicity concentration (CC50) of ZnOAc2 in Vero-E6 cells (,70 mM, data not shown). This is likely due to the poor solubility of Zn2+ in phosphate-containing medium and the inefficient uptake of Zn2+ by cells in the absence of zinc-ionophores. The combination of 2 mM PT and 2 mM ZnOAc2 resulted in a 9861% and 8563% reduction of the GFP signal for EAV-GFP and SARS-CoV-GFP, respectively. No cytotoxicity was observed for this combination of PT and ZnOAc2 concentrations. From the dose-response curves in Fig. 1, a CC50 value of 82 mM was calculated for PT in the presence of 2 mM zinc. Half maximal inhibitory concentrations (IC50) of 1.4 mM and 0.5 mM and selectivity indices of 59 and 164 were calculated for SARS-CoV and EAV, respectively.
Zn2+ reversibly inhibits the RNA-synthesizing activity of isolated nidovirus RTCs We previously developed assays to study the in vitro RNAsynthesizing activity of RTCs isolated from cells infected with SARS-CoV or EAV [25,26]. In these RTC assays [a-32P]CMP is incorporated into both genomic (replication) and sg mRNA (transcription) (Fig. 2). This allowed us to monitor the synthesis of the same viral RNA molecules that can be detected by hybridization of RNA from nidovirus-infected cells. A benefit of these assays is that the activity does not depend on continued protein synthesis and that it allows us to study viral RNA synthesis independent of other aspects of the viral replicative cycle .
To investigate whether the inhibitory effect of PT and zinc ions on nidovirus replication in cell culture is reflected in a direct effect of Zn2+ on viral RNA synthesis, we tested the effect of Zn2+ addition on RTC activity. For both EAV (Fig. 2A) and SARS-CoV (Fig. 2B), a dose-dependent decrease in the amount of RNA synthesized was observed when ZnOAc2 was present. For both viruses, a more than 50% reduction of overall RNA-synthesis was observed at a Zn2+ concentration of 50 mM, while less than 5% activity remained at a Zn2+ concentration of 500 mM. Both genome synthesis and sg mRNA production were equally affected.
To test whether the inhibition of RTC activity by Zn2+ was reversible, RTC reactions were started in the presence or absence of 500 mM Zn2+. After 30 min, these reactions were split into two aliquots and magnesium-saturated EDTA (MgEDTA) was added to one of the tubes to a final concentration of 1 mM (Fig. 3A). We used MgEDTA as Zn2+ chelator in these in vitro assays, because it specifically chelates Zn2+ while releasing Mg2+, due to the higher stability constant of the ZnEDTA complex.
Uncomplexed EDTA inhibited RTC activity in all reactions (data not shown), most likely by chelating the Mg2+ that is crucial for RdRp activity [27,28], whereas MgEDTA had no effects on control reactions without Zn2+ (Fig. 3B, compare lane 1 and 2). As shown in Fig. 2, the EAV RTC activity that was inhibited by Zn2+ (Fig. 3B&C, lane 3) could be restored by the addition of MgEDTA (Fig. 3B, lane 4) to a level observed for control reactions without Zn2+ (Fig. 3B, lane 1). Compared to the untreated control, the EAV RTC assay produced approximately 30% less RNA, which was consistent with the 30% shorter reaction time after the addition of the MgEDTA (100 versus 70 min for lanes 1 and 4, respectively).
Surprisingly, SARS-CoV RTC assays that were consecutively supplemented with Zn2+ and MgEDTA incorporated slightly more [a-32P]CMP compared to untreated control reactions (Fig. 3C; compare lane 1 and 4). This effect was not due to chelation of the Zn2+ already present in the post-nuclear supernatant (PNS) of SARS-CoV-infected cells, as this increase was not observed when MgEDTA was added to a control reaction without additional Zn2+ (Fig. 3C, lane 2).
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