Dysbiosis of Medicine in the 21st century: Coronavirus and Acute Respiratory Syndromes

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Written in conjunction with: Dr S.H. Vilane

Coronaviruses were first described in poultry in the 1930’s, causing respiratory, gut, liver and neurological diseases in animals. 7 Coronaviruses are known to cause disease in humans: 4 most frequently cause symptoms of the common cold, with the remaining 3 causing severe and sometimes fatal respiratory failure in humans. These have caused major outbreaks of deadly pneumonia in the 21st century:

  1. SARS-CoV-2 is the cause of the COVID-19 disease which began in Wuhan, China in late 2019.
  2. MERS-CoV is a betacoronavirus that caused for the 2012 MERS outbreak. It was first identified in a patient from Saudi Arabia.
  3. SARS-CoV caused the 2002 SARS outbreak which began in Guangdong, China.

COVID-19, MERS and SARS started in areas where people, pigs, wild game and birds intermingled. Once any of these organisms has contracted a virus, they can infect each other (across species), providing ample opportunity for the genetic recombination of viral material (a process in which there is a change in several viral genes that code for various viral proteins). This leads to the emergence of new viral strains, some of which can be highly pathogenic.

Various vectors- especially migrating birds/bats with their faecal droplets- and traveling humans then spread this to different populations. In the 21st century, it is particularly modern modes of travel and high numbers of business and leisure tourists that have facilitated the recent and current spread of these devastating respiratory syndromes.

Viruses causing respiratory syndromes, such as corona and influenza viruses, then gain entry via the upper respiratory tract (the nose and mouth), commonly as aeresolised sprays or droplets from an infected individual. They also gain entry when someone who has touched a contaminated surface then touches their nose or mouth. From here, they then spread into the lungs.

In the lungs, the resultant viral pneumonia has the potential to severely damage lung tissues, making them susceptible to bacterial infection, such as pneumonia. When this occurs, a deadly combination arises.

To understand how these processes have contributed to the current COVID-19 pandemic, it is important to cast an eye back in time to examine what history has taught us from previous pandemics.

The Spanish Flu of 1918

The Spanish Flu pandemic of 1918 is estimated to have decimated an estimated 17 to 50 million people (possibly even 100 million people) worldwide. Retrospective studies have since shown that it is the H1N1 strain that was responsible for this fatal outbreak. What made the H1N1 devastating in addition to its virulence is thought to include the following thoughts and facts:

  1. The H1N1 strain is not remarkably different from the seasonal flu of today, except in one crucial regard: it had devastating effects on the immune system. It killed the ‘healthier’ people in the prime of their lives, leaving in it’s wake young orphans to be raised by grandparents. This ‘mortality pattern’ significantly differs from the current COVID-19 trend, which decimates the elderly, and those with co-morbidities such as cancer, diabetes, obesity, and immuno-compromising conditions such as HIV. Graphically put:
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It is thought that the robust immune systems in the 15–40yr age group went into overdrive, and quickly depleted and overwhelmed their immune systems, eventually succumbing to the influenza and opportunistic bacterial infections.

2. Other theories postulate that the mortality was highest in the younger adults but blames the lethality of the influenza pandemic on the impoverished state of the victims, as the Spanish flu was Post World War 1. During this period of poor socioeconomic state the 15–40 yr age group was the largest sector of the population as people did not live long then. Most of them had also been conscripted into the war. Thus, the war and the resultant malnutrition, disease, stress and influx of individuals from different geographic locations (where the opportunity to develop immunity had not presented itself) contributed to The H1N1 spread. This was worsened by the fact that they were traveling and so took the illness with them, exposing others.

Simply put, with poor nutrition, stress of war and a naive immune system, they stood no chance and became easy fodder for the virus.

3. Another explanation for the lethality of the Spanish flu was the use of aspirin in large doses (at the time) for viral infections where it is now contraindicated because of the resultant brain damage (encephalitis) from the interaction of the virus, blood vessel damage and aspirin. This condition is known as Reyes Syndrome, and explains why the World Health Organisation (WHO) has advised not to use brufen, ibruprufen and other non-steroidal anti-inflammatories (NSAIDs) when managing COVID-19 patients.

Central to COVID-19, SARS, MERS and H1N1 is the development of a vigorous immune response that fills the lungs with fluid in all fatal cases, hastening their death.Simply put: the host’s immune system brings a nuclear bomb to a fist fight. The result: fluid filled lungs which decrease the amount of oxygen diffusing into the rest of the body. This is known as ARDS- Acute Respiratory Distress Syndrome.

However in H1N1, MERS and SARS, the period from infection to developing disease (incubation period) is too short, and those who developed the disease succumbed quickly without spreading the infection. With COVID-19, however, many (as much as 80%) are asymptomatic, with 10% developing mild infection, and 5–10% of them developing severe disease and dying.

It is the asymptomatic and mild groups that pose the greatest danger as they can spread viral infection without any warning.

With improvement in living, socioeconomic factors and scientific marvels, the life expectancy has also improved: many more are living past 60, 70 and even 80 years of age. It is this group and those with underlying comorbidities that COVID-19 has savagely maimed.

In 1918, there were no antibiotics or ventilators to treat those with severe manifestation of the Spanish Flu.

In the 21st century, we have potent antibiotics, ‘rapid’ accurate testing and ventilators. But, the mortality has been astronomical. Health systems, hospitals, equipment, and medical personnel have buckled. Our 21st century prowess has been left impotent without a shotgun pill or injection to terminate the COVID-19 infection.

Science had to resort to basic infectious and public health protocols: wash and sanitize your hands, wear face masks, self-isolate, as well as government enforced lockdowns and quarantines. The theme is to flatten the curve, i.e. limit the spread of infection so that health facilities can cope. Mega-hospitals the size of stadiums have been erected overnight, hospital passages have been converted to intensive care units and doctors have had to play God in deciding who goes to intensive care units and who gets ventilated. Refrigerated trucks no longer transport ice cream or frozen fish, but dead bodies.

It is the goal of modern science to unravel how this pandemic happened, and guide governments in how to quickly put the fires out. From the Spanish Flu, SARS, MERS and SARS-CoV, medical science has failed to predict pandemics, including the current COVID-19 pandemic. Lessons from the recent past have simply failed to predict this outbreak. Even when the alarm was sounded, governments were too slow to react and there were no concerted efforts.

The missing puzzle

Is the Spanish Flu, MERS, SARS and COVID-19 a biochemical multi-nutritional deficiency disorder? With a viral trigger?

Nutrition and COVID-19

As we unravel the virus and the immunological response to it, many theories will abound. Maybe a shotgun injection or pill will be found in the immediate term. In the medium-long term, a vaccine is the final hope in eradicating COVID-19.

It seems COVID-19 is not likely to follow the usual pattern of most virulent diseases burning themselves out by killing their hosts before their hosts can interact with other people. In that way the disease never comes back. But COVID-19 is a salient contagion, with a longer incubation period and viral shedding that goes on for extensive amounts of time as it decimates those susceptible to severe disease.

We contest that the common denominator with these Coronaviruses is poor host nutritional status, biochemically and immunologically.

Hotspots around the world have subclinical and clinical critical vitamin, mineral and trace element deficiency.

Several trace elements, minerals and vitamins are essential micronutrients and are required for various bodily functions and well being of our immune systems. Several trace elements such as selenium, zinc and chromium have immune modulating functions and thus influence the susceptibility to the course and outcome to various viral and bacterial infections.

Several trace elements exhibit antiviral activity and inhibit virus replication in the host cells, thus decreasing viral activity. Many act as anti-oxidants or help such function that not only regulate immune responses of the host, but also may alter the genetic code of the virus. The grave consequence of this may be emergence of a new infection.

The trace elements, viruses and immune system interactions highlight the importance of trace elements. Nutrition of the host does not only optimize the immune responses to infections, but also prevents viral mutation which could increase viral pathogenicity.

Cytokines storms, COVID-19, mineral and trace elements deficiency(zinc and selenium):

Increase in oxidative stress is well recognized in certain populations and especially in critically ill patients. The resultant systemic inflammatory response leads to an increase in toxic metabolic products, known as Reactive Oxygen Species, and depletion of endogenous protective anti-oxidant micro-nutrients leading to initiation, continuation and fatality of the critical illness.

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Table taken from: U.C. Chaturvedi: Viral Infections and trace elements: a complex interaction.


This is a critical trace element which we obtain through diet. It carries out it’s functions through complex enzymes known as Seleno-proteins.

Plant foods are the major dietary sources of selenium, but so are various meats and seafood. The amount of selenium in the soil determines it’s amount in the plant foods that are grown in that soil, as well as the selenium levels in animals that then feed on these plants.

China, the original epicenter of the coronavirus outbreak, is a good case study: estimates for China’ selenium deficiency range from 51% to 72% of the entire population (according to a WHO estimate).

Through the selenocysteine protienaise enzyme, selenium is involved in most aspects of cell biochemistry and function and influences the immune system. It protects the host immune cells (neutrophils) from Reactive Oxygen Species that are produced to kill the ingested organism. Selenium is associated with reduced damage of lung cells in animal models. It also enhances resistance to infection through cytokines production and the subsequent immune response.

Selenium is thus a key micronutrient in counteracting the development of virulence and inhibition of progression of severe forms of COVID-19.

This is further evidenced by data from critically ill patients: blood selenium levels are lower in critically ill patients as compared to healthy individuals, especially in patients with severe sepsis or shock admitted to intensive care units.

Zinc Deficiency

Zinc deficiency can change immune functions and adversely affect the course of several diseases. Zinc is the structural component of a wide variety of proteins, neuropeptides, hormone receptors and polynucleopeptides. The best known zinc dependent enzyme and hormone is copper-zinc-superoxide dismutase, essential for formation of lymphocytes that kill viruses. Zinc metal proteins are thus useful in preventing the transmission of viral diseases.

COVID-19 and chronic diseases

Obesity, type 2 diabetes and insulin resistance are chronic diseases. They are associated with development of comorbidities such as atherosclerosis, hypertension, heart and renal failure, and strokes. They are regulated by multiple genetic and environmental factors (diet, exercise and stress) leading to inflammation/inflammatory responses in immune cells.

The increase in Reactive Oxygen Species and ongoing low grade chronic inflammation are hallmarks of these chronic diseases.

It is not only the excessive consumption of food, but the macro and micro nutrient composition of these diets that influences the initiation and progression of these diseases.

On these grounds, diet is a major environmental insult contributing to an increased incidence and severity of these chronic diseases.


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Our contention is that the person who is going to have severe COVID-19 can be identifiable by:

  1. Poor nutrition/diet
  2. Chronic disease
  3. Poor immune system
  4. A positive COVID-19 test

Poor nutrition, chronic disease and poor immune have all got:

  1. Clinical symptoms and signs
  2. Biochemical objective tests

Our second contention is thus that nutrition and dietary interventions are necessary in the critical COVID-19 patient, and that the population at large are not recieving appropriate responses.

Since ancient times plants, nuts, oils and seafoods have been the most important source of nutrients and medicine, and have immune modulating activity. Consumption of whole foods should be encouraged as a long term strategy.

Specific supplementation on a large scale on basic nutritional staple foods must be considered especially in high risk groups such as the elderly, the immunosuppresed and those with a high burden of disease. Perhaps time has arrived that primary health care has to be utilized in ways similar to the immunization and pregnancy clinics for infants and pregnant women respectively: adults should have a nutritional card that requires annual verification.

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Diagram taken from: M. Beck: Trace Elements, Immune Function, and Viral Evolution.

In addition, low carbohydrate diets are increasingly used to help patients with obesity and type 2 diabetes. Notwithstanding any controversy, international guidelines now recognise the validity and endorse these diets as therapeutic nutritional approach, in appropriate patients.

Between sanitizing your hands, practicing social distancing, placing countries under lockdown, and ventilation in ICU for those with severe disease, nutrition must be improved. This is necessary as we do not have a curative pill or injection, and prospects of a vaccine are years away.

Between the race for the cure, and the vaccine, the human condition (NUTRITION) has been neglected and forgotten: the dysbiosis of Medicine?


  1. J. Taubenberger. 2012. Reconstruction of the 1918 Influenza Virus: Unexpected Rewards from the past. NIH National Library of Medicine.
  2. J. Taubenberger. 2006. 1918 Influenza: the Mother of All Pandemics. NIH National Library of Medicine.
  3. Y.H. Lee. 2016. Serum Selenium Levels in Patients with Respiratory Diseases. Journal of Thoracic Disease.
  4. Liver Doctor. Nd. Viral Infections More Dangerous in Selenium Deficient People. https://www.liverdoctor.com/viral-infections-more-dangerous-in-selenium-deficient-people/
  5. G. Nicholson. Mitochondrial Dysfunction and Chronic Disease: Treatment with Natural Supplements. Intergrative Medicine: A Clinician’s Journal.
  6. T. Kelly. 2020. Low Carbohydrate Diets in the Management of Obesity and Type 2 Diabetes: A Review From Clinicans Using the Approach in Practice. NIH National Library of Medicine.

Your neighbourhood physician-politician. 2nd year medicine. Instagram: @asandevilane

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