by Dr. Bill Rawls
Posted 12/17/20

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Before the COVID-19 pandemic, Katherine S., 21, was like most young adults her age: Active, busy, engaged in life. A sophomore in college, she had recently transferred schools and moved back home to her parents’ beach house in Florida, where she was juggling studying with working at a popular local restaurant and bar. She was also training with her dad to do a 250-mile bike ride in France down the Normandy coast.

“They were training pretty hard, and then COVID hit,” says Peggy, Katherine’s mom. “By April it became pretty apparent that we were not going to France for this ride.” Still, Katherine and her dad kept training for a while, until an early Friday in June when she started to experience some early signs of COVID-19.

At first I felt like I had a cold: My nose was stuffy, I was really tired and chilled — I was just out of it,” says Katherine, who says she contracted the virus at the restaurant where she worked along with several other employees there. By happenstance, she had just been tested for COVID-19, as their county had requested that everyone do a drive-through test.

“On Monday, they called to tell her she was positive; by Wednesday, she was in bed and couldn’t move,” says Peggy. What followed wasn’t one of the typical experiences you hear about with COVID-19. Katherine didn’t breeze through the infection with mild or no symptoms like many young people do. Nor did she become so severely ill that she was admitted to the hospital and put on a ventilator, like we sometimes hear about with elderly patients or those who were already ill.

Katherine riding bicycle through field, sunset background

Instead, Katherine’s symptoms were miserable and debilitating enough to keep her mostly bedbound, and they stayed — and stayed. Early on, like many people who have come down with COVID, she lost her sense of taste and smell, and her appetite right along with them, leading her to eat next to nothing for the next month and a half.

She began experiencing severe headaches and extreme fatigue and total-body pain, in part from her respiratory symptoms and coughing fits. “I felt like my lungs were constantly on fire, and sometimes like there was an elephant sitting on my chest,” she says.

Katherine’s blood oxygen levels also repeatedly dropped precariously low (Peggy was monitoring them with a pulse oximeter), which landed her in the emergency room on three separate occasions. Next came the tachycardia (a heart rate over 100 beats per minute) and irregular heartbeats.

“I would be sitting at the table with my family doing absolutely nothing, and suddenly I’d get really hot and dizzy and my heart rate would shoot up — I passed out because of it,” says Katherine. “Other times, I felt like someone punched me really, really hard from the inside of my chest.” She recently saw a cardiologist at the Mayo Clinic, who captured her tachycardia using a holter heart monitor and advised her to make lifestyle changes like wearing compression socks and eating small salty snacks to counter dizziness.

(Content Notice: Please be aware that this article contains content about suicide. If you’re contemplating suicide, please call the National Suicide Prevention Lifeline at 1-800-273-8255 or dial 911. These services provide free, confidential support 24 hours/day, and can assist you with finding the resources you need to get help.)

Perhaps worst of all is what COVID-19 has done to Katherine’s brain. “My mental health state went down a lot,” she says. “For a few weeks, I was so depressed my psychologist had me on suicide watch. I was just ready to die; I didn’t want to feel the pain anymore.” Katherine is now taking medication for anxiety and depression, which has helped.

“I also have bad COVID brain — I’m brain foggy, I can’t think straight, my short-term memory and memory in general are bad. Sometimes I can’t find words. It’s horrible,” she explains. In fact, Katherine asked her mom to sit with her throughout our conversation to help answer questions and fill in blanks on the several occasions she couldn’t put her thoughts into words.

That conversation was just a few days ago — more than six months since Katherine first fell ill — and while some of her symptoms have lessened, others haven’t, and she’s still a long way off from the days of training for a 250-mile bike ride. And as it turns out, Katherine’s not alone in her long, hard journey back from COVID-19.

A Brief History of COVID-19

It’s hard to believe it’s been a year since doctors at the hospital in Wuhan, China began admitting patients with severe pneumonia of unknown origin. From the very beginning, the novel coronavirus that caused it — dubbed SARS-CoV-2 — frustrated healthcare officials. Though it could cause severe life-threatening pneumonia, more than half of people who contracted the virus were asymptomatic or had only mild symptoms.

zoomed out view of airplane flying through clear sky, leaving steam trail

With limited testing and no way of knowing who was contagious, the virus quickly spread throughout China and beyond, eventually becoming a global pandemic. A year later, with a vaccine here but still months away from being distributed to most of us, we still haven’t seen the peak of cases or deaths.

Though many people have died from COVID-19, many others who survived gradually returned to pre-COVID health. Those with mild illness, not surprisingly, recovered fairly quickly. As the pandemic wore on, however, a subset of patients emerged who remained chronically ill for months on end. Some still haven’t gotten better.

Self-dubbed as having “long COVID” or being “COVID long-haulers,” somewhere between 1 in 20 to as high as 1 in 5 people who come down with COVID-19 struggle with chronic debilitating symptoms for months on end. Reported symptoms are varied and have included fatigue, cough, shortness of breath, loss of taste and smell, muscle weakness, muscle and joint pain, headache, confusion, conjunctivitis, chest pain, irregular heart beat, and a range of neurological symptoms. Of all the symptoms, the neurological ones — brain fog, impaired memory, cognitive dysfunction — are possibly the most debilitating of all.

Interestingly, development of chronic symptoms hasn’t necessarily correlated with severity of the initial illness. It’s not uncommon for people who only have mild to moderate symptoms initially go on to develop chronic debilitating symptoms. To understand why it goes one way or the other, it helps to understand how the virus makes us sick in the first place.

How SARS-CoV-2 Causes Acute Illness

Like all viruses, SARS-CoV-2 requires interaction with living cells of a host organism to survive. The virus inserts itself into a living cell, takes over the machinery of the cell, and then cannibalizes the carbohydrates, fats, and proteins the cell is made of to make more viruses. Once the cell is full of newly minted viruses, it bursts, releasing a wave of viruses to infect other host cells.

sars, covid-19 virus cell

What we know as an infection is simply a foreign microbe (virus, bacteria, protozoa, or yeast) trying to gain access to abundant resources that cells of the body have to offer. To get at the resources, however, a microbe must first break through the body’s protective barriers.

For instance, our skin repels microbes from the outer environment, and the intestinal lining keeps microbes contained inside our gut. The lungs are also a barrier, but a more vulnerable one: The tissue layer between the incoming air and bloodstream is very thin to allow exchange of oxygen, and so lots of microbes specialize in using the nasal passageways and lungs as an entry point.

Though we think of SARS-CoV-2 as a respiratory virus, it’s only because that’s where it invades the body. It specializes in spread by air droplets and entry into the respiratory tract, and therefore that’s where we experience the greatest initial symptoms. Make no mistake, however: the respiratory tract is just the entry point; what the microbes want is access to cells deep in tissues throughout the body.

Because the body’s barriers aren’t nearly as secure as one might hope, the immune system places armed sentries made up of various types of white blood cells (WBCs) at the borders of every possible entry point — throughout the skin, along the intestinal tract, the pelvic organs, the mouth and nasal passages, and tissues of the lungs.

As soon as a virus like SARS-CoV-2 enters nasal passages and lungs, the immune system’s first responder WBCs (innate immune system) mount an immediate counteroffensive to repel the invaders. In the resulting skirmish, the intensity of symptoms that someone might experience at the initial infection depends on the following factors:

  1. The size of inoculation. Healthcare workers are up to 8 times more likely to get sick because they’re often exposed to higher concentrations of viruses thanks to close proximity to sick patients.
  2. The health of the host’s lung cells. Weak or stressed cells are more vulnerable to invasion. A person who smokes or lives in an area of poor air quality is at higher risk for increased severity of respiratory infections. History of cardiopulmonary illness or diabetes also increases risk of severe illness.
  3. The strength of the host’s immune system. An elderly person’s aging immune cells are less up to the task. Also, poor health habits weaken the immune system.
  4. How familiar the immune system is with the microbe. The human immune system is extraordinarily sophisticated. It evolved over millions of years from repetitive exposure to an enormous number of different microbes. For every trick that microbes have devised to get past immune system barriers, the immune system developed countermeasures to match it — layer upon layer of different levels of protection, all hardwired into your genes. The more familiar a microbe is to your immune system, the better it can manage it.

One example of viruses that we’re well prepared to contend with are those that cause the common cold. Among the list of the numerous viruses that cause common cold symptoms are four different types of coronaviruses that have been circulating within human populations for eons. They adapt and change with every encounter, so they can infect us over and over again, but our immune system retains enough familiarity to stop them quickly, and so cold symptoms are generally mild and transient.

Black man and woman sitting on couch, holding runny noses with tissues

SARS-CoV-2 is more threatening than the more common cold-causing coronaviruses because it skipped over from an animal host (likely bats), therefore the human immune system has less familiarity with it. However, the fact that half of people exposed to SARS-CoV-2 don’t become severely ill suggests that they have cross immunity, possibly from ancestral exposure to different coronaviruses that moved from animals to humans in the past.

The more foreign a microbe is to the immune system, the greater the intensity of the skirmish. If first-responder WBCs begin to fold under pressure, they and damaged lung cells release chemical messengers called cytokines to call in reinforcement WBCs. Intensification of illness is directly proportional to the amount of cytokines released — severe acute illness is associated with a “cytokine storm.”

Indeed, respiratory symptoms result as much from the reaction of the immune system to the virus as from the virus invading cells. White blood cells secrete strong acid and potent free radicals to kill viruses and destroy cells that have already been infected. If the virus is not quickly subdued, the acid and free radicals damage and weaken healthy lung cells.

In addition, debris and mucus created by dead and ailing cells block the flow of nutrients and oxygen to healthy cells, leaving them weak and more vulnerable to invasion by viruses. The resulting vicious cycle is the equivalent of a small-scale war going on in tissues of the lungs — the medical term for it is inflammation.

Irritation of nasal passageways, along with congestion from mucus, causes symptoms of coughing and sneezing — which works in the virus’s favor because it provides a perfect opportunity to spread to other unsuspecting hosts. As the war intensifies, capillaries (tiny blood vessels) in lung tissue become “leaky” to allow increasingly more WBCs to migrate into the area. Unfortunately, this also allows fluid to leak from the capillaries. Add to that the accumulating mucus, and congestion constricts air flow — air hunger is the inevitable symptom.

If fluid collection becomes consolidated into one area of the lungs, pneumonia sets in. Breathing then becomes difficult, if not impossible. The victim feels like they’re drowning. If the infection isn’t somehow brought under control, then death is the inevitable outcome — which is what makes SARS-CoV-2 so threatening.

How COVID-19 Causes Systemic Symptoms

Believe it or not, causing severe respiratory illness is not the intended goal of the SARS-CoV-2 virus. All it wants to do is get past the immune system’s defenses so that any and all cells in the body — aka food and resources — are fair game.

Of course, there are different strategies for making it across the goal line that require both strength and deception. One takes it directly into the brain: Studies have shown that SARS-CoV-2 can travel down the olfactory nerve into brain tissue, thus the telltale loss of smell and taste that Katherine experienced, and that has become characteristic of COVID-19 (Payus). Once inside the brain, it invades nerve cells and spreads.

Close-up woman wearing a face surgical mask holding her head and having headache on gray background. Selective focus. Flu, illness, pandemic concept

And because the immune system doesn’t place the same level of armed sentries inside brain tissue that it does at the outer barriers of the body, the viruses have a longer window of opportunity before the cells of the immune system become aware of its presence. This explains the so-called COVID brain fog and cognitive symptoms that Katherine and so many others struggle with, including memory loss, confusion, difficulty focusing, dizziness, and word loss.

Unfortunately, the virus and correlated symptoms don’t stop there. COVID long-haulers typically experience systemic symptoms beyond the brain. Inflammatory damage to heart muscle, skeletal muscle, liver tissue, kidneys, and other organs has been well documented in COVID-19. In addition, viral RNA and viral particles of SARS-CoV-2 have been found in autopsy specimens in cardiac tissue (Lindner), kidney, liver, brain, and blood (Puelles).

These findings imply that the viruses travel through the blood, but they need a vehicle to carry them. Though the exact mechanisms of how SARS-CoV-2 might spread through the blood have not been defined, I believe that a look at other microbes that use “stealth” strategies — including Borrelia burgdorferi (the primary Lyme disease bacteria), and many other microbes with similar characteristics, such as mycoplasma, chlamydia, and Epstein-Barr virus — might provide a clue. Other experts also suspect that SARS-CoV-2 uses these stealth strategies.

Many microbes (bacteria, viruses, protozoa, fungi) have mastered the ability to use the defenses of the immune system to their advantage. When they breach barriers at the initial infection — whether by inhalation, insect bite, or some other route — the microbes are gobbled up by WBCs attempting to get rid of them. The microbes, however, have developed the ability to remain alive inside the WBCs1.

The unsuspecting WBC becomes a vehicle of transport. Once safe and secure inside a WBC, microbes can hitch a ride to tissues throughout the body — even across the blood-brain barrier and into brain tissue. What’s more, there’s evidence that microbes can steer WBCs toward more desirable tissues. Once there, the microbes surface and infect other cells throughout tissues in the body.

Your tissues become peppered with cells infected with microbes — imagine a few infected cells randomly sandwiched between clusters of healthy cells in all your tissues — brain, heart, liver, joints, everywhere else. Once that happens, the immune system has a real dilemma on its hands. If it mounts a full-scale attack, the damage to adjacent healthy cells could be lethal.

So, instead, the immune system calls in specialized forces: The adaptive immune system. It uses antibodies to selectively target microbes and cells that have been infected with microbes. Sometimes, however, there’s collateral damage to normal cells — in the process of targeting infected cells, sometimes normal cells are mistakenly targeted. When normal cells are targeted by the immune system, it’s called autoimmunity. Multiple studies have indicated that SARS-CoV-2 may be a trigger for autoimmunity, especially if immune functions have been compromised.

Ultimately, this more targeted, scaled-back approach to eradicating infected cells that are peppered throughout the body can be a long and protracted process. Sometimes, the immune system is forced to allow some cells infected with microbes to persist. And that’s all the microbes want anyway — a mere presence. If they can persist, they can wait out opportunities for a resurgence and to spread to new hosts.

How COVID-19 Becomes a Chronic Illness

Whether chronic symptoms occur during the microbes’ struggle to hide safely away as well as the degree of those symptoms depends on two key things: the strength of the host’s immune system, and the health of their cells. If cells are healthy and immune system functions are strong, then viral activity may be kept low enough that symptoms may not occur at all.

In my research and experience with chronic Lyme and other chronic illnesses like fibromyalgia and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) however, I’ve learned that it doesn’t take much to tip the balance toward chronic symptomatic illness. Anything that adds additional stress to the immune system or weakens cells of the body allows microbes to flourish and infect more cells. The factors I’ve found to be most influential in weakening cells and leaving us vulnerable include:

  • Poor diet: Habitually eating a diet high in processed food and refined carbohydrates can deprive your body of the vital nutrients it needs to power up each day. Plus, a high-carb diet can lead to prolonged periods of elevated insulin levels, insulin resistance, a suppressed immune system, and altered hormone function.
  • Chronic stress: Pushing the stress button way too often and not allowing time for adequate sleep puts the body in a constant state of alert, causing all of its systems, and especially immune system functions, to become overly taxed.
  • Unrecognized exposure to toxic substances: Mold, pesticides, and byproducts from the creation of plastics and using petroleum and coal damage cells, compromise their function, and suppress immune system functions.
  • Not getting enough exercise: Prolonged inactivity actually stresses the body. It’s associated with decreased blood flow, retention of toxins, immune dysfunction, decreased endorphins, and low energy.

Any one or a combination of these factors add up to an overstressed immune system that underperforms when you need it most. If viral activity is great enough, symptoms become noticeable.

It’s possible, too, that the microbes alone may tip the balance toward chronic illness. As the SARS-CoV-2 virus has circulated around the world, mutations have created different strains with varying characteristics, some more aggressive than others and some more apt to cause chronic systemic symptoms than others.

What’s more, SARS-CoV-2 might not be acting alone: Coinfections with other microbes might be at play. Other viruses, bacteria, and fungi that infect the respiratory tract often travel together, especially during cold and flu season. Coinfections with multiple microbes simultaneously may be more common than we think — one study of 116 SARS-CoV-2 patients found that 20% of them were also infected with another microbe (a variety of bacteria, viruses, and fungi were tested) (Kim).

Side view close-up shot of doctor wearing protective uniform taking senior woman's nasal swab for coronavirus test using stick, copy space

Because most people with COVID-19 aren’t tested for other microbes and because there are so many microbe possibilities, the extent of coinfections and the role they play in both the severity of acute respiratory illness and the development of chronic illness has not been defined. I suspect it could be quite significant.

Beyond coinfections, you also have to consider the microbes that were already present in the body before SARS-CoV-2 came along. A growing body of evidence suggests that we all harbor very low concentrations of various types of microbes — bacteria, viruses, protozoa, and fungi — in our tissues whether we’re healthy or not.

Case in point: Two independent studies in 2016 and 2017 that were looking for bacteria in the brains of people with Alzheimers’s disease and multiple sclerosis, They not only found bacteria in every diseased brain, but also in every person who didn’t have neurological illness — hundreds of species of bacteria. These findings imply that having low concentrations of bacteria in the brain is a normal state!

Other independent studies have verified the presence of bacteria in the heart, vascular system, lungs, kidneys, bladder, joints, muscles, and even the human placenta — in healthy people. Where you find bacteria, expect to find the full range of microbes, including viruses, protozoa, and fungi. They get there using the same stealthy mechanisms that SARS-CoV-2 uses to get past the immune system and into tissues of the body.

They’re lots of them — too many to name them all. But just a few examples include:

  • Epstein-Barr virus, which 95% of the world’s population harbor in their tissues
  • A herpes simplex virus that causes fever blisters in 1 out of 5 people (and has also been linked to Alzheimer’s disease)
  • Mycoplasma pneumoniae, a bacteria that most of us pick up as a mild respiratory illness as children (and has been linked to rheumatoid arthritis)
  • Chlamydia pneumoniae, another bacterial childhood respiratory illness (linked to MS)
  • Toxoplasmosis, a protozoa that 60% of the world’s population harbors after picking it up from undercooked meat (also linked to depression, psychosis, and lymphoma)

The list goes on and on. We all have some of them, but each of us harbors a different assortment of microbes. Most notably, they typically don’t cause chronic illness unless immune system functions are disrupted. But if enough factors come together to disrupt immune system functions — possibly including infection with SARS-CoV-2 — microbes in tissues flourish and chronic symptomatic infection becomes established. And once that pot starts boiling over, it’s hard to stop.

The type of chronic symptoms that you might expect are a function of where in the body the tug-of-war between the microbes and the immune system is taking place and the inflammation it creates. For instance, increased microbes and resulting inflammation in the brain would cause symptoms like brain fog and cognitive dysfunction. Inflammation in the heart could cause irregular heartbeats. Low-grade inflammation throughout the body would result in chronic fatigue.

When you start considering the full range of symptoms possible with long COVID, not surprisingly, they resemble those of other chronic conditions that have been associated with post-infections. In other words, “long haul” syndromes are nothing new. Cases of prolonged post-influenza convalescence associated with symptoms including brain fog and chronic fatigue have been documented for more than a century.

Symptoms of long COVID overlap almost exactly with chronic fatigue syndrome and closely resemble fibromyalgia, suggesting that these chronic conditions may have common or similar origins. Indeed, chronic fatigue syndrome has been linked to Epstein-Barr virus and other microbes. Chronic Lyme disease, which is also now recognized as being associated with a variety of coinfections, shares many symptoms with long COVID. The common denominator for all of these chronic conditions: chronic immune dysfunction with increased microbial activity and disruption of cellular functions throughout the body.

There’s also concern that SARS-CoV-2 could predispose us to other chronic illnesses. In a study published in the medical journal The Lancet, researchers detailed three cases of Parkinson’s disease that occurred immediately after COVID. The researchers noted that loss of sense of taste and smell, a symptom that occurs in 65% of COVID sufferers, is a common early symptom of Parkinson’s disease. Add this to the growing list of chronic illnesses that have possible associations to microbes.

How to Help Prevent and Overcome Long COVID, Naturally

When I spoke to Katherine, her most pressing question was the one we would all have if in her shoes: How can I put this misery behind me?

And for the rest of us who have so far evaded COVID-19, the question is how can we prevent chronic suffering if we do contract the virus?

Right now, conventional therapy options are limited. How much benefit vaccines or antiviral therapies provide is still unknown. Even though the mutation rate of SARS-CoV-2 is lower than influenza, we don’t know whether the vaccine will eradicate the virus completely, or if the virus will mutate and come back to haunt us again and again. Already there are case reports, albeit rare, of people coming down with COVID-19 more than once.

While there are no absolute answers for what helps, if you’re struggling with long-COVID, there are some things you can do that certainly won’t hurt.

One of the most important steps is protecting the health of your immune cells and all the cells in your body. Healthy cells are less vulnerable to invasion by microbes, and they’re less likely to die and leave behind debris for the immune system to clean up. In other words, keeping your cells healthy takes stress off the immune system and allows it to do its primary job of protecting cells from microbes and keeping microbes in the body in check.

When seeking practical ways to protect your cells, I recommend you start with plants.

1. Start with Herbal Therapy.

Plants are multicellular organisms, just like we are. As such, plants must protect their cells from a wide range of stress factors: damaging free radicals, physical stress from harsh weather, toxic substances, harmful radiation, insects, invasive fungi, parasites, and, last but not least, every variety of microbe.

Close-up low angle view of a scientist analyzing a leaf at the laboratory

Plants do this with their own natural chemistry. In fact, plants are the most sophisticated chemists on the planet. The chemical substances that plants use to solve problems and protect cells are called phytochemicals. (Mushrooms, which are technically fungi, also have to deal with similar stress factors as plants; as such, they too produce a wide range of protective substances that mirror the protective properties of phytochemicals found in plants.)

Plant phytochemicals aren’t one thing, but rather a diverse assortment of hundreds of different chemical compounds that serve a variety of needs via different mechanisms. Some are antioxidants that protect cells from different types of free radicals, toxic substances, and harmful radiation.

Others promote balance of communication systems within the plant. Interestingly, plants use many of the same chemical messengers that our cells use to communicate including hormones and neurotransmitters. When cells are working together in harmony, the organism, whether plant or animal, is healthy.

One of the most important functions of phytochemicals is protecting cells from microbial invasion. By necessity, antimicrobial phytochemicals are selective: They inhibit potential pathogens (disease-causing microbes), but spare bacteria called normal flora because they produce substances that help suppress pathogens.

Because viruses are so ubiquitous in nature, all plants produce phytochemicals with antiviral properties. Unlike synthetic antiviral drugs, however, it isn’t just one chemical substance. Plants produce a wide spectrum of antiviral phytochemicals that inhibit different viruses by different mechanisms.

The antiviral properties of plant phytochemicals in general are well documented by scientific research. Here are some of their key, demonstrated properties:

  • Inhibit viral replication
  • Reduce viral RNA
  • Inhibit viral fusion with and entry into cells
  • Reduce expression of viral genes
  • Affect various viral enzymes
  • Kill viruses directly
  • Inhibit spike proteins (the SARS-CoV-2 is covered with spike proteins, which bind to cells and enable infection)
  • Inhibit ATPase activity (this inhibits entry of SARS-CoV-2 into cells)
  • Inhibit angiotensin converting enzyme (ACE) (used by SARS-CoV-2 to bind to the host cell membrane)
  • Block inflammatory cytokines and pathways of inflammation

While the research on effective therapies specifically for the SARS-CoV-2 virus is minimal — as is all research on the virus at this stage — there is a small but growing number of studies suggesting that herbs may have benefit for SARS-CoV-2-like viruses and thus for COVID-19 as well. For instance, research published in Frontiers in Pharmacology this September looked at a select list of herbs — predominantly based on species lists from the World Health Organization (WHO) and European Medicines Agency (EMA) — that are traditionally used for respiratory diseases.

After evaluating the existing data, it identified 17 herbs as either “positive” or “promising” as a symptomatic therapy for COVID-19. On the list: Althaea officinalis (marshmallow plant), Commiphora molmol (myrrh), Glycyrrhiza glabra (licorice), Hedera helix (English ivy), Sambucus nigra (elderberry), Andrographis paniculata (andrographis), and Allium sativum (garlic).

Leaves of plants with sunlight in nature.

Several studies have also looked at herbs commonly used in Traditional Chinese Medicine (TCM), which was widely applied in China where COVID-19 originated, and found promising results. One, published in the International Journal of Medical Sciences, analyzed 210 commonly administered herbs and found several of the most common ones had “direct anti-SARS-CoV-2 potential.” The mechanisms of action identified included activating immunoregulation, suppressing the inflammatory response, enhancing antioxidant activity, and modulating apoptosis (cell death).

Still other studies are starting to look more closely at individual herbs already known for desirable qualities like reducing inflammation and oxidative stress — factors consistently linked with COVID-19 illness. Curcumin, an active compound in turmeric with powerful anti-inflammatory action, is one of them. Others include bromelain for its anti-inflammatory and anti-coagulatory properties, as well as Malaysian Ganoderma lucidum aqueous extract and Egyptian Chlorella vulgaris ethanolic extract for their antioxidant and anti-inflammatory properties.

These studies just scratch the surface of the protective benefits that are transferred to us when we consume plant phytochemicals from food plants or herbs. In essence, our immune system gets a boost from the plant’s natural defenses. The three primary things that phytochemicals do for us:

  1. Antimicrobial phytochemicals directly inhibit SARS-CoV-2, but also suppress other microbes, including bacteria, protozoa, viruses, and fungi. This allows the immune system to regain its footing and get the microbes under control.
  2. By protecting our cells from harmful stress factors such as free radicals and toxic substances, cell turnover is reduced, along with the destructive inflammation that comes with it. This lessens the immune system’s workload so it can better do its job.
  3. Phytochemicals help normalize disrupted hormones and other chemical messengers in the body. Because all cells must be in constant communication for the body to function as a unit, wellness is only possible when cellular functions are coordinated. This includes toning down inflammatory cytokines that push the immune system into overdrive.

There are a few different ways to gain the benefits of protective plant phytochemicals. One: Eat your vegetables. Veggies offer greater health benefits than any other food source, but thanks to conventional farming practices, plant foods no longer contain the robust levels of protective phytochemicals found in wild plants. To gain full benefit, you must consume plants that are closer to their natural, wild state.

Adding culinary herbs like basil, oregano, and cinnamon to your food or drinking herbal teas can carry you a little closer, but it’s difficult to consume the quantities necessary to provide substantial benefit. The best way to gain the level of phytochemical protection you need to help your immune system win the internal battle against invasive microbes is to take herbal supplements — specifically, standardized botanical extracts.

Natural herbal medicine sets on old wooden table

Standardized botanical extracts take herbal supplements to the next level. They’re made with wild plants or plants that have been cultivated to enhance their phytochemical content and are grown in an environment that doesn’t introduce unwanted chemical toxins. The extraction process also yields the greatest concentration and the widest spectrum of phytochemicals in the plant. And the final product is standardized to a concentration of one or several key phytochemicals in the plant, so you know what you’re getting.

As I’ve noted, all plants produce antiviral phytochemicals, but some plants are stronger antivirals than others. It all has to do with where a particular plant evolved and what types of viruses it was exposed to. Those that were constantly exposed to viruses and other microbes produce more robust concentrations of antimicrobial phytochemicals.

Knowing this, and based on all my research on antimicrobial and immunomodulating herbs over the past dozen-plus years — to include the latest science on COVID-19 — the herbs that top my list (and most widely available) for anyone dealing with long COVID include:

  • Andrographis (Andrographis paniculata)
  • Garlic (Allium sativum)
  • Ginger (Zingiber officinale)
  • Chinese skullcap (Scutellaria baicalensis)
  • Houttuynia (Houttuynia cordata)
  • Isatis (Isatis tinctoria)
  • Kudzu (Pueraria montana)
  • Japanese knotweed (Polygonum cuspidatum)
  • Reishi mushroom (Ganoderma lucidum)
  • Bupleurum (Bupleuri radix)
  • Chlorella (Chlorella vulgaris)
  • Turmeric (Curcuma longa)
  • Bromelain (anti-inflammatory enzyme found in pineapples)

Note that you don’t have to take all of these herbs at once to gain benefit, but taking multiple herbs does provide a broader range of benefits and coverage for other microbes that may be present. As for how much of each to take, proper dosing depends on the product, so the best advice is to follow the directions on the bottle. Quality matters — take the time to research supplement companies that insist on top quality ingredients and are transparent about providing information about manufacturing practices.

2. Use the Right Micronutrient Support.

Your cells use up a lot of essential nutrients that are necessary for optimal function when you’re stressed or sick, so you can imagine that’s especially true when contending with COVID-19. For that reason, I recommend complementing herbs with the right combination of supportive micronutrients, particularly those on the list below, which are all supported by scientific research for COVID-19.


A deficiency in glutathione — a natural antioxidant produced in our cells but also found in food sources like spinach, avocado, asparagus, and okra — has been linked with a higher rate of serious illness and death from COVID-19. The essential antioxidant plays a key role in protecting mitochondria (the powerhouses of cells) from free-radical damage, as well as enhancing detoxification processes and fortifying immune functions. To avoid a glutathione deficiency, supplement with 500-1000 mg reduced powdered glutathione twice daily (doses are dependent on preparations used.

N-acetyl cysteine (NAC)

A precursor to glutathione with antioxidant and anti-inflammatory properties, NAC has been shown to help reduce the risk for influenza and influenza-like illnesses. This leads researchers to believe it might also attenuate the risk of developing COVID-19 and possibly ease severe symptoms as well. To optimize NAC levels, supplement with 500 mg twice daily. (Note that doses are dependent on preparations used.)

Zinc, Selenium, and Vitamin D

Getting enough of these three essential nutrients is key to supporting healthy immune function and helping your body resist viral infection and keep inflammation in check. In one research review, the authors suggest that supplementing with these nutrients at the early stage of COVID-19 infection might help prevent the illness from escalating to potentially life-threatening levels. Work with your healthcare provider to determine the appropriate supplement levels for you.

Vitamin C

Another key player in healthy immune function, vitamin C has known antiviral, anti-inflammatory, antioxidant, and immunomodulating properties. For that reason, our stores tend to get depleted quickly during acute infections, and COVID-19 is no exception. In promising news, supplementing with a high dose of intravenous C was shown to help reduce risk of cytokine storms in late-stage COVID-19 infection, and to ease inflammation and symptoms when paired with other therapies like curcumin and TCM. Since the body needs extra vitamin C when under stress, aim for 500-1000 mg of buffered vitamin C daily.

3. Do Your Part to Maintain Healthy Cells

Beyond herbs and micronutrients, another key to preventing the chronic immune dysfunction that leaves us vulnerable to long COVID (and all types of chronic illness) is doing everything you can in your everyday life to strengthen and support the cells in your body. And that means minimizing the lifestyle factors that weaken cells in the first place. I call these factors “system disruptors;” here are some simple yet vital ways to get around them.

element of wellness: nourish

Nourish Your Body.

Providing your cells with proper nourishment is essential for maintaining healthy cells:

  • Strive to eat more vegetables than anything else. Vegetables are packed with a greater concentration of the nutrients your cells need to function properly than any other food source. Vegetables are also loaded with beneficial fiber that promotes normal digestion and balance of microbes in the gut.
  • Eliminate processed food products. This automatically cuts out a load of unnecessary carbohydrates, refined oils, and calories your cells don’t need. It also cuts out gluten, a protein in wheat that many people are sensitive to.
  • Eat fresh, whole foods. The fresher your food is and the closer to its natural origins, the higher its potential to nourish your cells. In other words, it’s much better to enjoy an apple or a handful of fresh pecans for a snack than a processed “health” food bar.

element of wellness: purify

Purify Your Environment.

Though the earth’s atmosphere is more polluted with toxic substances than ever before, most of the pollution is concentrated around industry and high population density. If you’re smart, you can protect yourself.
Toxic chemicals can only enter the body by consuming food and liquids, breathing air containing toxic chemicals, and exposure of skin to toxic chemicals. Toxic substances can also include unnatural electromagnetic radiation sources.

  • Drink filtered water. Ensuring clean water is a simple matter of installing a top-grade water filter. For recommendations, check out the Environmental Working Group’s water filter guide.
  • Switch to organic foods where it matters. Staying away from processed foods automatically eliminates a lot of chemical food additives, but making the choice for organic takes “healthy” one step further.
  • Keep indoor air clean. Natural cleaning products, indoor plants, and regularly changing air filters go a long way toward keeping the air inside a house or workplace pure.

element of wellness: calm

Minimize Your Stress Levels.

Though it’s impossible to eliminate stress completely in life, you can learn to live around it.

  • Zero out stress hormones a couple of times a day. Stress tends to build up through the day like a tempest. All it takes is learning basic breathing techniques, taking a walk, or even a short midday nap to defuse it.
  • Make your world small. If stress is an issue, it’s important to tune out things that don’t directly impact your health and wellbeing. Focus on the things that you can control, and let everything else go.
  • Get 7-8 hours of sleep every night. This should be a top priority for overcoming any kind of chronic condition; you can’t get well without it. Sleep is when cells have down time to perform internal self repair. It’s especially important to restore normal brain function.

element of wellness: activate

Stay Physically Active.

The benefits are too long to tally, but the main thing physical activity does is stimulate blood flow, which increases flow of water, nutrients, and oxygen to cells. It also helps flush away debris, which is what detoxification is all about.

  • Stay consistent. Moving every day prevents accumulation of debris in the spaces between cells that inhibits good flow and prevents cells from recuperating.
  • Stay within your limits. In the early stages of recovery from any chronic illness, physical activity may be limited to non-strenuous activities, such as walking, qigong, and yoga. Do what you can until you can do more. Be careful not to exceed limits to prevent over-stressing the body. Regular training is important to move from one level to a higher level of performance.
  • Hit the (infrared) sauna. If your body is so inflamed that any kind of movement is challenging, infrared sauna is an option. Heating your body in a sauna stimulates blood flow and flushes built up debris from around cells.

Sometimes it’s hard to see the top of the hill when you’re sitting right at the bottom, but if you’re struggling with long COVID, keep reminding yourself that the crest is there — you can get your health back. But be patient with yourself, too: It does take time for your cells (especially nerve cells) to kick off the burden of the viruses and return to normal, but your immune system is always doing everything it can to make it happen.

When you make the effort to properly nourish your cells, remove any stress factors that are getting in the way of optimal immune function, and enhance the process by taking phytochemicals from botanical extracts, you can make it happen a lot faster.

Dr. Rawls is a physician who overcame Lyme disease through natural herbal therapy. You can learn more about Lyme disease in Dr. Rawls’ new best selling book, Unlocking Lyme.
You can also learn about Dr. Rawls’ personal journey in overcoming Lyme disease and fibromyalgia in his popular blog post, My Chronic Lyme Journey.

1. Mutambudzi M, Niedwiedz C, Macdonald EB, Leyland A, Mair F, Anderson J, Celis-Morales C, Cleland J, Forbes J, Gill J, Hastie C, Ho F, Jani B, Mackay DF, Nicholl B, O’Donnell C, Sattar N, Welsh P, Pell JP, Katikireddi SV, Demou E. Occupation and risk of severe COVID-19: prospective cohort study of 120 075 UK Biobank participants. Occup Environ Med. 2020 Dec 9:oemed-2020-106731. doi: 10.1136/oemed-2020-106731. Epub ahead of print. PMID: 33298533.
2. Harrison AG, Lin T, Wang P. Mechanisms of SARS-CoV-2 Transmission and Pathogenesis. Trends Immunol. 2020;41(12):1100-1115. doi:10.1016/
3. Khan S, Siddique R, Shereen MA, et al. Emergence of a Novel Coronavirus, Severe Acute Respiratory Syndrome Coronavirus 2: Biology and Therapeutic Options [published correction appears in J Clin Microbiol. 2020 Jul 23;58(8):]. J Clin Microbiol. 2020;58(5):e00187-20. Published 2020 Apr 23. doi:10.1128/JCM.00187-20
4. Belouzard S, Millet JK, Licitra BN, Whittaker GR. Mechanisms of coronavirus cell entry mediated by the viral spike protein. Viruses. 2012;4(6):1011-1033. doi:10.3390/v4061011
5. He J, Tao H, Yan Y, Huang SY, Xiao Y. Molecular Mechanism of Evolution and Human Infection with SARS-CoV-2. Viruses. 2020;12(4):428. Published 2020 Apr 10. doi:10.3390/v12040428
6. Li JY, You Z, Wang Q, et al. The epidemic of 2019-novel-coronavirus (2019-nCoV) pneumonia and insights for emerging infectious diseases in the future. Microbes Infect. 2020;22(2):80-85. doi:10.1016/j.micinf.2020.02.002
7. Menachery VD, Graham RL, Baric RS. Jumping species-a mechanism for coronavirus persistence and survival. Curr Opin Virol. 2017;23:1-7. doi:10.1016/j.coviro.2017.01.002
8. Boscolo-Rizzo P, Borsetto D, Fabbris C, Spinato G, Frezza D, Menegaldo A, Mularoni F, Gaudioso P, Cazzador D, Marciani S, Frasconi S, Ferraro M, Berro C, Varago C, Nicolai P, Tirelli G, Da Mosto MC, Obholzer R, Rigoli R, Polesel J, Hopkins C. Evolution of Altered Sense of Smell or Taste in Patients With Mildly Symptomatic COVID-19. JAMA Otolaryngol Head Neck Surg. 2020 Jul 2;146(8):729–32. doi: 10.1001/jamaoto.2020.1379. Epub ahead of print. PMID: 32614442; PMCID: PMC7333173.
9. Levy JM. Treatment Recommendations for Persistent Smell and Taste Dysfunction Following COVID-19-The Coming Deluge. JAMA Otolaryngol Head Neck Surg. 2020 Jul 2. doi: 10.1001/jamaoto.2020.1378. Epub ahead of print. PMID: 32614399.
10. Buja LM, Wolf DA, Zhao B, et al. The emerging spectrum of cardiopulmonary pathology of the coronavirus disease 2019 (COVID-19): Report of 3 autopsies from Houston, Texas, and review of autopsy findings from other United States cities. Cardiovasc Pathol. 2020;48:107233. doi:10.1016/j.carpath.2020.107233
11. Vardavas CI, Nikitara K. COVID-19 and smoking: A systematic review of the evidence. Tob Induc Dis. 2020;18:20. Published 2020 Mar 20. doi:10.18332/tid/119324
12. Zheng Z, Peng F, Xu B, et al. Risk factors of critical & mortal COVID-19 cases: A systematic literature review and meta-analysis. J Infect. 2020;81(2):e16-e25. doi:10.1016/j.jinf.2020.04.021
13. Branton, W., Lu, J., Surette, M. et al. Brain microbiota disruption within inflammatory demyelinating lesions in multiple sclerosis. Sci Rep 6, 37344 (2016).
14. Emery DC, Shoemark DK, Batstone TE, et al. 16S rRNA Next Generation Sequencing Analysis Shows Bacteria in Alzheimer’s Post-Mortem Brain. Frontiers in Aging Neuroscience. 2017 June 20; 9:195. doi: 10.3389/fnagi.2017.00195
15. Merello M, Bhatia KP, Obeso JA. SARS-CoV-2 and the risk of Parkinson’s disease: facts and fantasy. Lancet Neurol. 2020 Nov 27:S1474-4422(20)30442-7. doi: 10.1016/S1474-4422(20)30442-7. Epub ahead of print. PMID: 33253627.
16. Honigsbaum M, Krishnan L. Taking pandemic sequelae seriously: from the Russian influenza to COVID-19 long-haulers. Lancet. 2020;396(10260):1389-1391. doi:10.1016/S0140-6736(20)32134-6
17. Kemp HI, Corner E, Colvin LA. Chronic pain after COVID-19: implications for rehabilitation. Br J Anaesth. 2020;125(4):436-440. doi:10.1016/j.bja.2020.05.021
18. Davido B, Seang S, Tubiana R, de Truchis P. Post-COVID-19 chronic symptoms: a postinfectious entity?. Clin Microbiol Infect. 2020;26(11):1448-1449. doi:10.1016/j.cmi.2020.07.028
19. Callard F, Perego E. How and why patients made Long Covid [published online ahead of print, 2020 Oct 7]. Soc Sci Med. 2020;113426. doi:10.1016/j.socscimed.2020.113426
20. Wood E, Hall KH, Tate W. Role of mitochondria, oxidative stress and the response to antioxidants in myalgic encephalomyelitis/chronic fatigue syndrome: a possible approach to SARS-CoV-2 ‘long-haulers’? [published online ahead of print, 2020 Nov 21]. Chronic Dis Transl Med. 2020;10.1016/j.cdtm.2020.11.002. doi:10.1016/j.cdtm.2020.11.002
21. Morley JE. Editorial: COVID-19 – The Long Road to Recovery. J Nutr Health Aging. 2020;24(9):917-919. doi:10.1007/s12603-020-1473-6
22. Ehrenfeld M, Tincani A, Andreoli L, et al. Covid-19 and autoimmunity. Autoimmun Rev. 2020;19(8):102597. doi:10.1016/j.autrev.2020.102597
23. Icenogle T. COVID-19: Infection or Autoimmunity. Front Immunol. 2020;11:2055. Published 2020 Sep 11. doi:10.3389/fimmu.2020.02055
24. Picchianti Diamanti A, Rosado MM, Pioli C, Sesti G, Laganà B. Cytokine Release Syndrome in COVID-19 Patients, A New Scenario for an Old Concern: The Fragile Balance between Infections and Autoimmunity. Int J Mol Sci. 2020;21(9):3330. Published 2020 May 8. doi:10.3390/ijms21093330
25. Fredi M, Cavazzana I, Moschetti L, Andreoli L, Franceschini F; Brescia Rheumatology COVID-19 Study Group. COVID-19 in patients with rheumatic diseases in northern Italy: a single-centre observational and case-control study. Lancet Rheumatol. 2020;2(9):e549-e556. doi:10.1016/S2665-9913(20)30169-7
26. Lindner D, Fitzek A, Bräuninger H, Aleshcheva G, Edler C, Meissner K, Scherschel K, Kirchhof P, Escher F, Schultheiss HP, Blankenberg S, Püschel K, Westermann D. Association of Cardiac Infection With SARS-CoV-2 in Confirmed COVID-19 Autopsy Cases. JAMA Cardiol. 2020 Nov 1;5(11):1281-1285. doi: 10.1001/jamacardio.2020.3551. PMID: 32730555; PMCID: PMC7385672.
27. Dolhnikoff M, Ferreira Ferranti J, de Almeida Monteiro RA, et al. SARS-CoV-2 in cardiac tissue of a child with COVID-19-related multisystem inflammatory syndrome [published correction appears in Lancet Child Adolesc Health. 2020 Oct;4(10):e39]. Lancet Child Adolesc Health. 2020;4(10):790-794. doi:10.1016/S2352-4642(20)30257-1
28. Puelles VG, Lütgehetmann M, Lindenmeyer MT, et al. Multiorgan and Renal Tropism of SARS-CoV-2. N Engl J Med. 2020;383(6):590-592. doi:10.1056/NEJMc2011400
29. Payus AO, Liew Sat Lin C, Mohd Noh M, Jeffree MS, Ali RA. SARS-CoV-2 infection of the nervous system: A review of the literature on neurological involvement in novel coronavirus disease-(COVID-19). Bosn J Basic Med Sci. 2020;20(3):283-292. Published 2020 Aug 3. doi:10.17305/bjbms.2020.4860
30. Pezzini, A., Padovani, A. Lifting the mask on neurological manifestations of COVID-19. Nat Rev Neurol 16, 636–644 (2020).
31. Bridwell R, Long B, Gottlieb M. Neurologic complications of COVID-19. Am J Emerg Med. 2020;38(7):1549.e3-1549.e7. doi:10.1016/j.ajem.2020.05.024
32. Davis GK, Adlan A, Majewski J, Ibrahim B. SARS-CoV-2 pandemic and the cardiovascular system: What the non-cardiologist needs to know [published online ahead of print, 2020 Apr 30]. Clin Med (Lond). 2020;20(3):262-265. doi:10.7861/clinmed.2020-0158
33. South AM, Diz DI, Chappell MC. COVID-19, ACE2, and the cardiovascular consequences. Am J Physiol Heart Circ Physiol. 2020 May 1;318(5):H1084-H1090. doi: 10.1152/ajpheart.00217.2020. Epub 2020 Mar 31. PMID: 32228252; PMCID: PMC7191628.
34. Long B, Brady WJ, Koyfman A, Gottlieb M. Cardiovascular complications in COVID-19. Am J Emerg Med. 2020;38(7):1504-1507. doi:10.1016/j.ajem.2020.04.048
35. Xu L, Liu J, Lu M, Yang D, Zheng X. Liver injury during highly pathogenic human coronavirus infections. Liver Int. 2020;40(5):998-1004. doi:10.1111/liv.14435
36. Mohabbat AB, Mohabbat NML, Wight EC. Fibromyalgia and Chronic Fatigue Syndrome in the Age of COVID-19 [published online ahead of print, 2020 Nov 13]. Mayo Clin Proc Innov Qual Outcomes. 2020;10.1016/j.mayocpiqo.2020.08.002. doi:10.1016/j.mayocpiqo.2020.08.002
37. Desforges M, Le Coupanec A, Dubeau P, et al. Human Coronaviruses and Other Respiratory Viruses: Underestimated Opportunistic Pathogens of the Central Nervous System?. Viruses. 2019;12(1):14. Published 2019 Dec 20. doi:10.3390/v12010014 (Trojan Horse in general for viruses)
38. Desforges M, Le Coupanec A, Stodola JK, Meessen-Pinard M, Talbot PJ. Human coronaviruses: viral and cellular factors involved in neuroinvasiveness and neuropathogenesis. Virus Res. 2014;194:145-158. doi:10.1016/j.virusres.2014.09.011
39. Yachou Y, El Idrissi A, Belapasov V, Ait Benali S. Neuroinvasion, neurotropic, and neuroinflammatory events of SARS-CoV-2: understanding the neurological manifestations in COVID-19 patients. Neurol Sci. 2020;41(10):2657-2669. doi:10.1007/s10072-020-04575-3
40. Thakur A, Mikkelsen H, Jungersen G. Intracellular Pathogens: Host Immunity and Microbial Persistence Strategies. J Immunol Res. 2019;2019:1356540. Published 2019 Apr 14. doi:10.1155/2019/1356540
41. Santiago-Tirado FH, Doering TL. False friends: Phagocytes as Trojan horses in microbial brain infections. PLoS Pathog. 2017;13(12):e1006680. Published 2017 Dec 14. doi:10.1371/journal.ppat.1006680
42. Branton, W., Lu, J., Surette, M. et al. Brain microbiota disruption within inflammatory demyelinating lesions in multiple sclerosis. Sci Rep 6, 37344 (2016).
43. Emery DC, Shoemark DK, Batstone TE, et al. 16S rRNA Next Generation Sequencing Analysis Shows Bacteria in Alzheimer’s Post-Mortem Brain. Frontiers in Aging Neuroscience. 2017 June 20; 9:195. doi: 10.3389/fnagi.2017.00195
44. Zhu X, Ge Y, Wu T, et al. Co-infection with respiratory pathogens among COVID-2019 cases. Virus Res. 2020;285:198005. doi:10.1016/j.virusres.2020.198005
45. Massey BW, Jayathilake K, Meltzer HY. Respiratory Microbial Co-infection With SARS-CoV-2. Front Microbiol. 2020;11:2079. Published 2020 Aug 25. doi:10.3389/fmicb.2020.02079
46. Kim D, Quinn J, Pinsky B, Shah NH, Brown I. Rates of Co-infection Between SARS-CoV-2 and Other Respiratory Pathogens. JAMA. 2020;323(20):2085-2086. doi:10.1001/jama.2020.6266
A study of 116 SARS-CoV-2 + subjects found that 20% were co-infected with other pathogens
47. Azekawa S, Namkoong H, Mitamura K, Kawaoka Y, Saito F. Co-infection with SARS-CoV-2 and influenza A virus. IDCases. 2020;20:e00775. Published 2020 Apr 21. doi:10.1016/j.idcr.2020.e00775
48. Wu X, Cai Y, Huang X, et al. Co-infection with SARS-CoV-2 and Influenza A Virus in Patient with Pneumonia, China. Emerg Infect Dis. 2020;26(6):1324-1326. doi:10.3201/eid2606.200299
49. Cuadrado-Payán E, Montagud-Marrahi E, Torres-Elorza M, et al. SARS-CoV-2 and influenza virus co-infection. Lancet. 2020;395(10236):e84. doi:10.1016/S0140-6736(20)31052-7
50. Brufsky A. Distinct viral clades of SARS-CoV-2: Implications for modeling of viral spread. J Med Virol. 2020;92(9):1386-1390. doi:10.1002/jmv.25902
51. Polonikov A. Endogenous Deficiency of Glutathione as the Most Likely Cause of Serious Manifestations and Death in COVID-19 Patients. ACS Infect Dis. 2020;6(7):1558-1562. doi:10.1021/acsinfecdis.0c00288
52. Silvagno F, Vernone A, Pescarmona GP. The Role of Glutathione in Protecting against the Severe Inflammatory Response Triggered by COVID-19. Antioxidants (Basel). 2020;9(7):624. Published 2020 Jul 16. doi:10.3390/antiox9070624
53. Horowitz RI, Freeman PR, Bruzzese J. Efficacy of glutathione therapy in relieving dyspnea associated with COVID-19 pneumonia: A report of 2 cases. Respir Med Case Rep. 2020;30:101063. Published 2020 Apr 21. doi:10.1016/j.rmcr.2020.101063
54. Guloyan V, Oganesian B, Baghdasaryan N, et al. Glutathione Supplementation as an Adjunctive Therapy in COVID-19. Antioxidants (Basel). 2020;9(10):914. Published 2020 Sep 25. doi:10.3390/antiox9100914
55. De Flora S, Balansky R, La Maestra S. Rationale for the use of N-acetylcysteine in both prevention and adjuvant therapy of COVID-19. FASEB J. 2020;34(10):13185-13193. doi:10.1096/fj.202001807
56. Horowitz RI, Freeman PR. Three novel prevention, diagnostic, and treatment options for COVID-19 urgently necessitating controlled randomized trials. Med Hypotheses. 2020;143:109851. doi:10.1016/j.mehy.2020.109851
57. Moghaddam A, Heller RA, Sun Q, et al. Selenium Deficiency Is Associated with Mortality Risk from COVID-19. Nutrients. 2020;12(7):2098. Published 2020 Jul 16. doi:10.3390/nu12072098
58. Ali N. Role of vitamin D in preventing of COVID-19 infection, progression and severity. J Infect Public Health. 2020;13(10):1373-1380. doi:10.1016/j.jiph.2020.06.021
59. Grant WB, Lahore H, McDonnell SL, et al. Evidence that Vitamin D Supplementation Could Reduce Risk of Influenza and COVID-19 Infections and Deaths. Nutrients. 2020;12(4):988. Published 2020 Apr 2. doi:10.3390/nu12040988
60. Zemb P, Bergman P, Camargo CA Jr, et al. Vitamin D deficiency and the COVID-19 pandemic. J Glob Antimicrob Resist. 2020;22:133-134. doi:10.1016/j.jgar.2020.05.006
61. Abobaker A, Alzwi A, Alraied AHA. Overview of the possible role of vitamin C in management of COVID-19. Pharmacol Rep. 2020;72(6):1517-1528. doi:10.1007/s43440-020-00176-1
62. Wessels I, Rolles B, Rink L. The Potential Impact of Zinc Supplementation on COVID-19 Pathogenesis. Front Immunol. 2020;11:1712. Published 2020 Jul 10. doi:10.3389/fimmu.2020.01712
63. Pal A, Squitti R, Picozza M, et al. Zinc and COVID-19: Basis of Current Clinical Trials [published online ahead of print, 2020 Oct 22]. Biol Trace Elem Res. 2020;1-11. doi:10.1007/s12011-020-02437-9
64. Alexander J, Tinkov A, Strand TA, Alehagen U, Skalny A, Aaseth J. Early Nutritional Interventions with Zinc, Selenium and Vitamin D for Raising Anti-Viral Resistance Against Progressive COVID-19. Nutrients. 2020;12(8):2358. Published 2020 Aug 7. doi:10.3390/nu12082358
65. Skalny AV, Rink L, Ajsuvakova OP, et al. Zinc and respiratory tract infections: Perspectives for COVID‑19 (Review). Int J Mol Med. 2020;46(1):17-26. doi:10.3892/ijmm.2020.4575
66. Kieliszek M, Lipinski B. Selenium supplementation in the prevention of coronavirus infections (COVID-19). Med Hypotheses. 2020;143:109878. doi:10.1016/j.mehy.2020.109878
67. Bae M, Kim H. Mini-Review on the Roles of Vitamin C, Vitamin D, and Selenium in the Immune System against COVID-19. Molecules. 2020;25(22):5346. Published 2020 Nov 16. doi:10.3390/molecules25225346
68. Yang Y, Islam MS, Wang J, Li Y, Chen X. Traditional Chinese Medicine in the Treatment of Patients Infected with 2019-New Coronavirus (SARS-CoV-2): A Review and Perspective. Int J Biol Sci. 2020;16(10):1708-1717. Published 2020 Mar 15. doi:10.7150/ijbs.45538
69. Silveira D, Prieto-Garcia JM, Boylan F, et al. COVID-19: Is There Evidence for the Use of Herbal Medicines as Adjuvant Symptomatic Therapy?. Front Pharmacol. 2020;11:581840. Published 2020 Sep 23. doi:10.3389/fphar.2020.581840
70. Alschuler L, Weil A, Horwitz R, et al. Integrative considerations during the COVID-19 pandemic. Explore (NY). 2020;16(6):354-356. doi:10.1016/j.explore.2020.03.007
71. Zhang DH, Zhang X, Peng B, et al. Network pharmacology suggests biochemical rationale for treating COVID-19 symptoms with a Traditional Chinese Medicine. Commun Biol. 2020;3(1):466. Published 2020 Aug 18. doi:10.1038/s42003-020-01190-y
72. Ang L, Lee HW, Kim A, Lee JA, Zhang J, Lee MS. Herbal medicine for treatment of children diagnosed with COVID-19: A review of guidelines. Complement Ther Clin Pract. 2020;39:101174. doi:10.1016/j.ctcp.2020.101174
73. Huang YF, Bai C, He F, Xie Y, Zhou H. Review on the potential action mechanisms of Chinese medicines in treating Coronavirus Disease 2019 (COVID-19). Pharmacol Res. 2020;158:104939. doi:10.1016/j.phrs.2020.104939
74. Ahmad A, Rehman MU, Alkharfy KM. An alternative approach to minimize the risk of coronavirus (Covid-19) and similar infections. Eur Rev Med Pharmacol Sci. 2020 Apr;24(7):4030-4034. doi: 10.26355/eurrev_202004_20873. PMID: 32329879.
75. Hensel A, Bauer R, Heinrich M, et al. Challenges at the Time of COVID-19: Opportunities and Innovations in Antivirals from Nature. Planta Med. 2020;86(10):659-664. doi:10.1055/a-1177-4396
76. Levy E, Delvin E, Marcil V, Spahis S. Can phytotherapy with polyphenols serve as a powerful approach for the prevention and therapy tool of novel coronavirus disease 2019 (COVID-19)?. Am J Physiol Endocrinol Metab. 2020;319(4):E689-E708. doi:10.1152/ajpendo.00298.2020
77. Ngwa W, Kumar R, Thompson D, et al. Potential of Flavonoid-Inspired Phytomedicines against COVID-19. Molecules. 2020;25(11):2707. Published 2020 Jun 11. doi:10.3390/molecules25112707
78. Shahzad F, Anderson D, Najafzadeh M. The Antiviral, Anti-Inflammatory Effects of Natural Medicinal Herbs and Mushrooms and SARS-CoV-2 Infection. Nutrients. 2020;12(9):2573. Published 2020 Aug 25. doi:10.3390/nu12092573
79. Owoyele BV, Bakare AO, Ologe MO. Bromelain: A Review on its Potential as a Therapy for the Management of Covid-19. Niger J Physiol Sci. 2020 Jun 30;35(1):10-19. PMID: 33084621.
80. Zahedipour F, Hosseini SA, Sathyapalan T, et al. Potential effects of curcumin in the treatment of COVID-19 infection. Phytother Res. 2020;34(11):2911-2920. doi:10.1002/ptr.6738
81. Zhang HT, Huang MX, Liu X, Zheng XC, Li XH, Chen GQ, Xia JY, Hong ZS. Evaluation of the Adjuvant Efficacy of Natural Herbal Medicine on COVID-19: A Retrospective Matched Case-Control Study. Am J Chin Med. 2020;48(4):779-792. doi: 10.1142/S0192415X20500391. Epub 2020 May 15. PMID: 32420751.
82. Zhang Y, Li Y, Wang X, et al. Herbal plants coordinate COVID-19 in multiple dimensions – An insight analysis for clinically applied remedies. Int J Med Sci. 2020;17(18):3125-3145. Published 2020 Oct 22. doi:10.7150/ijms.50260
83. Portella CFS, Ghelman R, Abdala CVM, Schveitzer MC. Evidence map on the contributions of traditional, complementary and integrative medicines for health care in times of COVID-19. Integr Med Res. 2020;9(3):100473. doi:10.1016/j.imr.2020.100473
84. Ng JY. Global research trends at the intersection of coronavirus disease 2019 (COVID-19) and traditional, integrative, and complementary and alternative medicine: a bibliometric analysis. BMC Complement Med Ther. 2020;20(1):353. Published 2020 Nov 23. doi:10.1186/s12906-020-03151-8
85. Dabaghian F, Khanavi M, Zarshenas MM. Bioactive compounds with possible inhibitory activity of Angiotensin-Converting Enzyme-II; a gate to manage and prevent COVID-19. Med Hypotheses. 2020;143:109841. doi:10.1016/j.mehy.2020.109841
86. Lee DYW, Li QY, Liu J, Efferth T. Traditional Chinese herbal medicine at the forefront battle against COVID-19: Clinical experience and scientific basis. Phytomedicine. 2021;80:153337. doi:10.1016/j.phymed.2020.153337
87. Soni VK, Mehta A, Ratre YK, Tiwari AK, Amit A, Singh RP, Sonkar SC, Chaturvedi N, Shukla D, Vishvakarma NK. Curcumin, a traditional spice component, can hold the promise against COVID-19? Eur J Pharmacol. 2020 Nov 5;886:173551. doi: 10.1016/j.ejphar.2020.173551. Epub 2020 Sep 12. PMID: 32931783.
88. Anti-Inflammatory and Neuroprotective Role of Natural Product Securinine in Activated Glial Cells: Implications for Parkinson’s Disease
89. Yang F, Dong X, Yin X, Wang W, You L, Ni J. Radix Bupleuri: A Review of Traditional Uses, Botany, Phytochemistry, Pharmacology, and Toxicology. Biomed Res Int. 2017;2017:7597596. doi:10.1155/2017/7597596