"The Immune System and COVID-19 Treatment"
Though there are more than 400 clinical treatment trials underway,
currently, there is no specific proven therapy for COVID-19.
And we should not expect a vaccine or effective antiviral drug
to be available anytime soon.
Although, we are developing COVID-19 vaccines at pandemic speed.
Just for reference, the average vaccine takes more than a decade to develop,
with an average failure rate of 94%.
Many have asked me for advice on what they can eat to help
bolster their immune system.
“How Not to Die from Infections” is, after all, the title of chapter 5
of my book How Not to Die, and I do have more than a hundred
free videos online at NutritionFacts.org that reference immune function.
And there are amazing studies, like randomized double-blind trials showing,
for example, that eating broccoli sprouts can reduce
viral loads for influenza, decrease virus-induced inflammation,
and boost our antiviral natural killer cell activity.
Just from eating some broccoli sprouts!
But this isn’t the flu.
I certainly support general, commonsense advice to stay healthy
during the crisis, put forth by trusted authorities
such as American College of Lifestyle Medicine.
This includes getting sufficient sleep – seven to nine hours,
keeping active, reducing stress, staying connected—albeit remotely—
to friends and family, and eating healthfully
a diet centered around whole plant foods.
The World Health Organization agrees: fruits, vegetables, legumes
like beans, split peas, chickpeas, and lentils, nuts, whole grains,
cutting down on sugars, cutting down on meat, dairy, and junk,
and cutting down on salt.
"Optimal Nutritional Status for a Well-Functioning Immune System
Is an Important Factor to Protect against Viral Infections."
However, one must resist the urge to jump on the snake-oily spamwagon
of foods to boost your immune system given our near-total ignorance
of the immunological aspects of this new disease,
because enhancing specific arms of the immune system could hypothetically
even make things worse.
Let me explain.
Take the example of this married couple, both same age,
admitted to the hospital on the same day for the same COVID-19 infection,
fever, shortness of breath.
Tragically the wife was immunocompromised,
because she was on chemo for breast cancer at the time.
Yikes!
Whereas her husband had an intact immune system.
The wife did fine, though, out of the hospital in under a week,
whereas the husband ended up in intensive care.
Wait, the immunocompromised patient did better?
How is that possible?
Because unlike other common viruses, coronaviruses have not shown
to cause a more severe disease in immunosuppressed patients.
Why?
Because your own immune response appears to be the main driver
of lung tissue damage during infection.
Starting around the second week of symptoms, the virus can trigger
what’s called a cytokine storm.
It’s like an autoimmune reaction
where your body over-reacts and in attacking coronavirus
your lungs get caught in the crossfire.
In the first week of the illness it’s the virus itself that’s triggering
most of your symptoms, but then in severe cases,
it’s our own inflammatory response that takes over
in causing most of the damage.
It’s striking that many of our innate immune signaling pathways,
these cytokine chemical messengers our immune cells release,
is aimed at killing off our own cells.
But that makes total sense.
The virus turns our own cells against us into little virus factories,
so it’s part of our own antiviral defense to kill off
our own cells to dead end viral replication.
Viruses can’t replicate in dead cells so cell suicide
is like a way to create firebreaks,
but in burning down the village in order to save it,
we may not survive the process.
This has led some to consider immunosuppression as a treatment
for severe COVID-19, but of course immunosuppression
for hyperinflammation in COVID-19 might be a double-edged sword.
So when you see like broccoli sprouts can whip up natural killer cell activity
within two days is that a good thing or
a bad thing for something like COVID-19?
It was good for seasonal flu, but who knows with this new coronavirus.
Young children have relatively immature immune systems and normally suffer
disproportionally from viral infections such as the flu,
but not, apparently, from COVID-19, or SARS, or MERS for that matter—
the other two deadly coronaviruses.
It’s interesting, one theory as to why children seem protected
suggests that greater pre-existing exposure to common cold coronaviruses
offers kids some cross- protection against the new virus.
But ironically, a competing theory suggests it’s their lack of exposure
to similar viruses that’s safeguarding them.
There’s a phenomenon known as ADE, antibody dependent enhancement,
a phenomenon first described more than 50 years ago.
In most cases, the antibodies our bodies make to target pathogens
neutralize them or, at the very least, tag the invaders for removal.
Sometimes, though, antibodies can actually facilitate viral infection
and exacerbate disease.
This may be the case with SARS, where antibodies generated against
the viral spike proteins were sometimes found to promote infection.
In monkeys, an experimental SARS vaccine
resulted in aggravated lung damage.
Now vaccine developers are well aware of this phenomenon
and would work to ensure any commercial vaccine would be free
from this failing, but it has been used to venture a guess to account
for the unusual age distribution of severe COVID-19 cases.
Perhaps similar coronaviruses circulated silently decades ago,
and those old enough to have been exposed to them
are now experiencing exaggerated responses to COVID-19.
But young people never saw them so they don’t get the over-reaction.
I’m not suggesting this speculation is true.
I just use it to illustrate the complexity of our immune interactions.
Viruses attack, we counterattack, and then viruses sometimes evolve
to use our own counterattack— in their favor.
Just a word of caution before trying to specifically boost
some element of our immune system before understanding
the full scope of the new threat.
Given the uncertainties, the best strategy is…
to not get infected in the first place, especially not until
effective treatments and a functioning healthcare system are available.