Why COVID-19 is probably not a respiratory disease — and what’s really going on

Let me preface by saying I am not a doctor — but I do a lot of data analysis in my job. Like most Americans, I’ve been following the news about the coronavirus closely.

I’ve noticed a theme emerging in reports from frontline medical workers that suggests COVID-19 is more of a blood-based illness than it is respiratory. And when we look at it through that lens, everything seems to add up. Consider the following:

Male vs. female mortality rates

Across the world, health officials have noted that men both contract and succumb to COVID-19 at higher rates than women. The mortality rate of men compared to women is almost double — and from a data standpoint, there’s something to that.

Studies have shown that men, generally speaking, have higher blood pressure than women, possibly linked to testosterone levels. Because of this gender disparity, doctors are even experimenting with giving COVID-19 patients estrogen treatments.

But that doesn’t explain why men contract the disease at a higher rate. Considering our testing capacity has been limited, doctors have had to reserve testing for patients exhibiting known, more serious COVID-19 symptoms. For that reason, it makes sense that women are being diagnosed less often.

If this blood hypothesis is true, it would hold that once mass testing is in place, we’d see that men and women probably contract the disease at similar rates overall, but that women are more likely to be mild or asymptomatic and therefore not meet the criteria for rationed testing.

In South Korea, where mass testing was implemented, women accounted for just shy of 60% of cases — but less than 48% of fatalities as of the time of this writing.

Young people

Everyday, we see reports of young, healthy people with no underlying conditions succumbing to the disease. Meanwhile, others find out they already had COVID-19 and didn’t even know it. Why?

Whatever is causing seemingly low-risk, healthy people to die is critical — they are tragic but important pieces of the puzzle. Their cases are the ones where we might find isolated variables and insight about how the disease operates.

What we do know is that those hard-to-explain victims are often dying of strokes and pulmonary embolisms: blood clots. My lack of medical knowledge comes up here, but I’m going to hazard a guess. Blood types.

We know that some blood types are more prone to clotting than others (e.g., AB blood types have a higher risk of clotting than O types). That would explain the at-first-glance, arbitrary and catastrophic outcomes on seemingly low-risk patients.

Next steps: Johns Hopkins University has been tracking diagnosis and deaths from hospitals across the country. Hospitals should separately track and analyze deaths of younger patients with no co-morbidities (like diabetes, obesity, or hypertension) for further analysis. I suspect we would see a higher frequency of a specific blood type in those patients.

Pre-existing conditions

The pre-existing conditions that increase the odds that a person will have a more severe or fatal COVID-19 infection are blood based (or impact blood): diabetes, obesity, and hypertension.

Were it truly a respiratory illness, we’d probably be hearing more about conditions such as asthma being tightly correlated with less desirable outcomes.

Smokers

In the early weeks of the pandemic, we often heard smoking was a risk factor for more severe COVID-19 symptoms. We hear less about that now.

It follows that smokers probably overall have more lung damage than non-smokers and therefore should be at higher risk when it comes to a commutable and deadly respiratory illness. We’d expect the mortality rate of smokers with COVID-19 to be a lot higher than non smoker patients — I’d say many times over. However, it seems that the correlation between smoking and succumbing to COVID-19 aren’t that statistically significant.

Sure, smokers are more likely to die from the disease. But smokers are, in general, more likely to die from most illnesses. They also tend to be lower income, have less access to health care, and are more likely to engage in other health-compromising lifestyle choices.

The somewhat higher COVID-19 mortality rate among smokers isn’t convincing enough to be tied to smoking itself. Without a stronger correlation between this should-be deadly duo, we have to reconsider the initial assumption that the respiratory system is the main vessel of the virus’s death march.

Mortality rates of people on ventilators

Given that the symptoms of a severe COVID-19 infection include shortness of breath, it made sense that we looked to the respiratory system for answers (as well as smoking as a risk factor).

But we’re struggling to find them.

One of the final stages of succumbing to the disease is pneumonia — a condition where the lungs fill up with fluid. Current medical protocol calls for assisted breathing on ventilators.

Though reports on statistics have varied, it’s becoming increasingly clear that the majority of COVID-19 patients put on ventilators do not make it. Many studies estimate that less than 20% of people who are put on ventilators survive. And believe it or not — that’s the conservative estimate. Other reports estimate figures closer to 10%. That’s statistically significant.

But if we think about the virus as ‘thickening’ blood to the point that the lungs cannot maintain the blood-oxygen levels needed to survive, it makes sense that assisted breathing doesn’t help. And that’s what the numbers reflect. Not-so-coincidently, low blood-oxygen levels are often a precursor to pneumonia.

This is unfortunate considering the amount of resources (and equally importantly, response time) we have put into providing hospitals with expensive ventilators (with the best intentions, of course).

Additionally, if this blood hypothesis has truth, ventilators’ ineffectiveness only increases the likelihood of hospitals being overwhelmed. Patients occupy beds for weeks on end while the virus basically runs its course unobstructed as we try to treat the lungs…and blood continues to ‘thicken.’


The road ahead

Ablood-thickening, highly commutable virus sounds pretty grim, and, well, it is. Despite sounding like a plot line from a dystopian horror film, this could be good news.

The image above shook the world. It is Princess Diana shaking hands with an HIV patient. When it was released in 1987, there was an uproar response and backlash. You see, at the time, HIV’s mode of transmission was unknown. Contact — such as handshaking — couldn’t be ruled out.

We now know that HIV/AIDS is a sexually transmitted disease and that Diana wouldn’t contract it this way. But that’s only with the benefit of hindsight and a deeper understanding of how HIV works.

The scariest part about COVID-19 are the unknowns. The more we know about it — particularly major milestones like the mode of transmission and replication mechanisms — the closer we’ll be to moving past this.

I want to add here that even if there’s some truth behind this hypothesis, it only speaks to how the virus works in the body. It does not speak to the mode of transmission — and until we know that, we have to take every precaution (such as wearing face masks) to avoid spreading it further.

If the virus does primarily impact blood viscosity, we could change the course of treatment. Perhaps when COVID-19 confirmed patients are admitted to hospitals, they can be put on a blood thinner regimen right away.

Blood thinners are fairly widely available and because they have been in use for some time, doctors understand how they operate and when a patient might need closer monitoring.

We know that, for the most part, the human immune system can fight off this virus — but it needs time. Unfortunately, for those more prone to blood clotting for one reason or another (gender, pre-existing conditions, blood types), time is of the essence. Blood thinners could potentially buy the patient’s immune system the runway it needs to learn how to suppress the virus.

If that were true, we’d be in much better shape. It’s no substitute for a vaccine, but could increase survival rates, free-up precious hospital bandwidth, and solve for some of those ‘unknowns’ that add so much fear to the equation (like the responses to Princess Diana’s photo).

“I think at this point, so much is still unknown…what was initially deemed a respiratory disease has now proven to be much more complex,” says Michelle Wallace, a scientist of immuno-oncology at Allogene Therapeutics, Inc., a biotech company in San Francisco. “The first case in California, Feb. 6th, had been completely over looked because the patient had passed of a cardiac event. As we gather more data the complexity isn’t shrinking. It will take time to unravel this puzzle, but the only thing we can be absolutely sure of right at this moment is how little we truly know.”

It’s precisely those unknowns that call for strict lockdowns and the disruption of everyday life as we know it. Let’s look at COVID-19 through a different lens — as a blood, not respiratory, illness and see where that takes us.

Since Johns Hopkins has emerged as the central reporting point for hospitals across the U.S., let’s start including the blood types, pressure readings, and perhaps even a sample for every diagnosed patient and fatality. I’m confident that when we do, we will find patterns, correlations, and insights that can help us understand — and fight — this mysterious and deadly virus.

Every x we solve in this coronavirus equation is one step closer to reclaiming our lives.

Jack Tazman is a Baltimore, Maryland native. He attended Washington University where he studied political science.

Since then, he worked as a writer for various national news organizations specializing in politics and policy.

He now resides in New York City as a freelance writer and political consultant.

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