COVID19: Over It, But Not Over It
COVID19. You’ve heard about it… you’re sick of hearing about it. I know I know, we were SO ready for all those sunny summer picnics and cocktails with friends and live music and hugs and in-person aromatherapy workshops and cracking open your latest loaf of sourdough with someone other than your loaf of a cat. But we’re in deep enough now to realize it’s not just magically going away. Uuuuuugh.
So let’s talk about COVID19. What it is, how we can prevent its spread, nutritional interventions, and what role complementary medicine, including essential oils, might play in this whole crappy global pandemic scenario.
Coronavirus: What It Is
COVID19 refers to the present coronavirus disease we know and loathe, first discovered in 2019. It is an infectious disease caused by the crown-shaped (hence “corona”) virus SARS-CoV-2.
Coronaviruses are a large family of viruses that typically cause mild-to-moderate upper-respiratory tract illnesses (think: the common cold). Hundreds of coronaviruses are known to thrive among pigs, primates, camels, bats, and cats, and these viruses can jump from animal populations to humans in what’s known as zoonotic transfer, or a spillover event. Three novel coronaviruses have sloshed over to humans from animal reservoirs in the past two decades, causing widespread sickness and death (NIH, 2020).
Almost 20 years ago, 2002 (what is up with years composed of 0s and 2s?) hit us with an outbreak of SARS-CoV, the virus that causes severe acute respiratory syndrome (SARS). SARS-CoV likely originated in horseshoe bats. As wildlife habitats were disturbed and wild animals brought to markets, the virus jumped to humans. Over 8,000 people were afflicted with SARS in 26 countries; 774 died.
Fortunately, the reign of SARS-CoV was short-lived. The majority of human-to-human infections occurred in health care settings with weak infection control practices, and once the leaks in protocol were plugged up the outbreak ended. Intensive contact tracing and case isolation measures put a stop to the spread, and the virus vanished by 2004.
SARS was heralded as the first pandemic of the 21st century. Turns out it was the harbinger of worse to come.
A decade after the first SARS outbreak, Middle East respiratory syndrome (MERS) appeared, an affliction caused by the camel-derived MERS-CoV coronavirus. MERS-CoV continues to set off sporadic and localized outbreaks.
The third novel coronavirus to emerge in this century is the one that’s currently kicking our butts: SARS-CoV-2. First detected in China in December 2019, the virus rapidly spread. By the following March the World Health Organization declared COVID19 a global pandemic.
Like the OG SARS-CoV, SARS-CoV-2 likely jumped to humans from bats. The unnerving quality of these two coronaviruses, along with MERS-CoV, is the capacity of the virus to infect animals, evolve, and then re-infect humans as a novel virus (Dutton, 2020).
As of June 29th, 2020 10 million cases of COVID19 and nearly 500,000 deaths have been reported globally. Several countries recently documented their highest number of new cases in a 24-hour period (WHO, 2020).
Despite record numbers of new cases, some countries are re-opening their societies and economies. Everyone is eager to get back to “normal.” We may be “over it,” but this is far from over.
Signs, Symptoms, and Disease Progression
The disease presentation of COVID-19 ranges in severity from asymptomatic infection to severe pneumonia and death. According to a report based on 55,924 laboratory-confirmed cases, typical signs and symptoms of COVID19 include:
- Fever (87.9%)
- Dry cough (67.7%)
- Fatigue (38.1%)
- Sputum production (33.4%)
- Shortness of breath (18.6%)
- Sore throat (13.9%)
- Headache (13.6%)
- Myalgia (muscle aches) or arthralgia (joint pain) (14.8%)
- Chills (11.4%)
- Nausea or vomiting (5.0%)
- Nasal congestion (4.8%)
- Diarrhea (3.7%)
- Hemoptysis (coughing up blood) (0.9%)
- Conjunctival congestion (0.8%)
Signs and symptoms, including mild respiratory symptoms and fever, typically appear an average of 5-6 days post-infection (with a range of 1-14 days) (WHO-China Joint Mission, 2020).
Of those patients who are hospitalized, up to one third require mechanical ventilation in an intensive care unit. Fatality rates are disproportionately distributed by demographic. Higher risk is associated with old age and comorbidities including:
- Chronic kidney disease
- Chronic obstructive pulmonary disease (COPD)
- Immunocompromised state from solid organ transplant
- Serious heart conditions (heart failure, coronary artery disease, cardiomyopathies)
- Sickle cell disease
- Type 2 diabetes mellitus (CDC, 2020)
SARS-CoV-2 is transmitted when an infected person expels virus-laden droplets and someone else inhales them, or touches an infected surface and then their own eyes, mouth, or nose. The lining of the nose is studded with a cell-surface receptor known as angiotensin-converting enzyme 2 (ACE2), which the virus uses to enter cells. ACE2 is localized throughout the body and normally functions to regulate blood pressure. In this case, it renders tissues vulnerable to infection. Once SARS-CoV-2 enters a cell it commandeers the cellular machinery in order to replicate itself and stage the conquest of new cells.
As the virus amplifies itself inside the body, an infected person may begin to shed it into the environment. Viral shedding is particularly prevalent during the first week following infection, and may occur in the absence of discernible symptoms. Then again, an infected person may develop a fever, dry cough, sore throat, loss of smell and taste, and head and body aches.
In the event that the immune system fails to subdue SARS-CoV-2 during this initial phase, the virus migrates to the lungs, where it skews pernicious, and as we well know, deadly.
The branches of the lungs’ respiratory tree terminate in tiny air sacs called alveoli, which are lined by a single layer of cells ample in ACE2 receptors. Under normal conditions, the alveoli deliver oxygen to the circulatory system via tiny adjacent blood vessels known as capillary beds. In COVID19, however, the battle between the immune system and the virus stymies this process, and impedes oxygen absorption from the lungs into the bloodstream.
White blood cells flood to the site, releasing inflammatory mediators that muster more immune cells to target and destroy virus-infected cells. Fluid and dead cells accumulate, creating a sludge of pus that forms the underlying pathology of pneumonia. Symptoms include coughing, fever, and rapid, shallow respiration.
Some patients recover from this, but others deteriorate, often abruptly, and develop a condition known as acute respiratory distress syndrome (ARDS). Blood oxygen levels drop and patients struggle to breathe. These patients end up on ventilators, and many die. Autopsies reveal alveoli clogged with fluid, white blood cells, mucus, and the wreckage of lung cells.
Respiratory failure from ARDS is the leading cause of mortality in COVID19. Keep in mind that the lungs may be ground zero, but other organs — the heart and blood vessels, kidneys, gut, and brain — can also suffer collateral damage (Wadman et al., 2020).
The signature catastrophic immunopathology associated with COVID19 is the dysregulated immune reaction known as a cytokine storm. Cytokine storm syndrome (CSS), also known as hypercytokinemia, is characterized by a severe immune reaction in which the body rapidly releases a surfeit of cytokines into the blood.
The concept of a cytokine storm, already somewhat fanciful in name, has clearly captured the imagination and spawned a whole suite of sobriquets: “overly exuberant inflammation” (Jamilloux et al., 2020), “immune reaction gone wild” (Dance, 2020), and “disastrous overreaction of the immune system” (Wadman et al., 2020).
The term “cytokine storm” was coined in 1993 to specify the hypercytokinemia observed in graft-versus-host disease, a condition wherein donor bone marrow or stem cells attack the recipient. CSS has since been associated with viral infections including influenza and SARS, autoimmune diseases, hematologic conditions, and certain medications.
An overabundance of cytokines may lead to the spread of immune cells throughout the body, where they attack healthy tissues, destroy red and white blood cells, and damage the liver. Blood vessels leak, filling the lungs with fluid and causing blood pressure to drop. Blood clots form and restrict blood flow throughout the body. Organs starved for blood can lead to shock, permanent organ damage, and death.
What is the normal function of cytokines, and where do they go wrong?
Cytokines are a complex group of small proteins involved in intercellular signaling and communication. These molecules control cell proliferation and differentiation, regulation of angiogenesis (the development of new blood vessels), and immune and inflammatory responses. They are involved in both short distance (autocrine, paracrine), and long-distance (endocrine) signaling.
There are many types of cytokines which share overlapping and synergistic functions. The network of cytokine responses can be imagined as an intricate web with sundry redundancies and alternate pathways. For our purposes, we’ll look at their role in inflammation.
Acute inflammation is typically adaptive. When localized in skin or other tissue, inflammation serves to increase blood flow, allows immune cells and plasma proteins to reach sites of injury, increases local temperatures, which promotes host defense against infectious agents, and generates pain, which alerts the host to the healing process at hand.
The hallmarks of acute inflammation include:
- Rubor (redness)
- Tumor (swelling or edema)
- Calor (heat)
- Dolor (pain)
- “Functio laesa” (loss of function)
Inflammatory responses, though part of the healing process, often occur at the expense of the function of neighboring organs. Organs may suffer from tissue edema increasing local pressure, or from a reduction in tissue perfusion (delivery of blood to the capillary beds). Fortunately the body has evolved ways to manage the damage the immune system can inflict on the host; indeed, it’s kept on a tight leash.
Soon after inflammation is initiated, compensatory repair processes step in. These repair processes, in many cases, are able to restore tissues and organs to full function. Inflammation is a protective behavior on the part of an organism that functions to remove injurious stimuli and initiate the healing process. There are cases, however, where the failsafes fail, and “hyperinflammation” ensues.
When inflammation is severe and tissue structures are significantly damaged, healing involves fibrosis, also known as fibrotic scarring. Fibrosis is a pathological form of wound healing in which connective tissue excessively replaces normal parenchymal tissue (the functional tissue of an organ). This leads to marked tissue remodeling and the formation of permanent scar tissue, which can result in persistent organ dysfunction.
In cytokine storm syndrome, dysregulation and perpetuated activation of immune cells such as lymphocytes and macrophages results in the overproduction of cytokines. This leads to overwhelming systemic inflammation and multi-organ failure with high mortality (England et al., 2020).
Diagnosing CSS is still a work in progress. Patients typically present with fever, and about half will experience nervous system symptoms including headache, seizures or, coma. Elevated blood levels of ferritin and increased concentrations of C-reactive protein act as measures of acute inflammation (Dance, 2020).
The challenge in cytokine storm syndrome is to control the immune response and prevent it from wreaking havoc on the body, while simultaneously taking down the virus that triggered the immune response in the first place. Scientists are uncertain whether patients will benefit from suppression or enhancement of immune responses, and pose the key question: “How can antiviral immunity be reinforced and hyperinflammatory damages be avoided?” (Jamilloux et al., 2020).
The answer may lie with the promotion of inflammation resolution. The body does this naturally, with endogenous anti-inflammatory cytokines and lipid mediators known as resolvins. Most COVID19 clinical trials thus far have focused on antiviral and antiinflammatory strategies, but stimulation of inflammation resolution presents “a novel host-centric therapeutic avenue.”
Some mediators of inflammation resolution, which promote debris clearance and inflammatory cytokine suppression, are currently in clinical trials for other inflammatory diseases. These may be rapidly extrapolated for the management of COVID19 (Panigrahy et al., 2020).
Prevent the Spread of COVID19
According to the CDC, the best way to reduce your risk of getting COVID19 is to limit interactions with other people. It’s as simple as that. If you do choose to make contact, take precautions.
When venturing outside of your household:
- Ask yourself, are these activities worth the risk?
- Wear a face covering. Avoid people without face coverings; ask the maskless among you to don face coverings.
- Keep six feet between your and others.
- Spend time outdoors.
- Wash your hands frequently, for at least 20 seconds (here’s plenty of songs to get your suds on to).
- If soap and water are not available, use a hand sanitizer that contains at least 60% alcohol.
Prioritize your overall health during the pandemic
- Physical activity
- Mental health
- Socially distanced human connection
- Contact your healthcare provider for preventative services, or to treat underlying medical conditions. Don’t delay care — emergency departments have contingency infection prevention plans to protect you from getting COVID19 if you need care (CDC, 2020).
SARS-CoV-2 is totally new to humans, which means that, in terms of herbs, vitamins, and essential oils, we don’t know what, if anything, works to combat COVID19. Social distancing is the one practice we know works for sure. If you’re going to use complementary approaches, use them in addition to, not as a substitute for, social distancing and proper hygiene practices.
See the American Herbalists Guild COVID19 Resource page for up-to-date information on herbal approaches.
Check out this medically-reviewed article for an overview of the efficacy of vitamins and supplements in supporting immune function.
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