Experts have been telling us from the very beginning of the coronavirus outbreak that older people with serious, underlying, chronic conditions—such as high blood pressure, heart disease, and Type II diabetes—have a harder time fighting off this novel respiratory infection. And that they’re more likely to die from it.
Of course, people with those conditions have a higher overall risk of dying compared to the rest of the population. But these chronic conditions are typically well-managed, and patients are not typically at extreme risk of more serious complications from respiratory infections, like flu or pneumonia.
But now, a professor at Louisiana State University has just published a new, unsettling theory about why people with these underlying conditions may be more susceptible to COVID-19 and have a harder time getting over it. And his theory involves a type of drug commonly prescribed to patients with these conditions…
Scientists learn how the lungs affect your whole body
Back in the 1970s, scientists began studying a then-obscure enzyme produced by the lungs called angiotensin converting enzyme (ACE). We eventually learned this lung enzyme has an important role in regulating blood pressure. In fact, it can ultimately cause angiotensin to make blood vessels constrict, thereby raising blood pressure. And it can promote sodium retention directly and indirectly (by increasing levels of the hormone aldosterone, which enhances sodium and water retention by the kidney).
Before that point, researchers and doctors mainly thought about the lungs in terms of respiration. So, the idea that the lungs somehow affect the body’s overall biochemistry and physiology—and even your blood pressure—was new.
And it was something I had experience with early in my career…
In fact, during the summer of 1975, I was fortunate to be awarded an undergraduate research fellowship at the City of Hope National Medical Research Center in Duarte, CA. I chose to work in the Pulmonary Biochemistry Lab—under the direction of Dr. Jack Lieberman.
That summer, we studied ACE as well as alpha-one antitrypsin (A1-AT), which determines your genetic susceptibility to smoke-related lung diseases. I even ended up writing my undergraduate college thesis on the important role the lungs play in the body’s overall biochemistry and physiology (not just respiration).
I then went on to medical school at the University of Pennsylvania, where I had a physiology and medicine class with Dr. Alfred P. Fishman. He had just published a monograph (a major technical report) entitled, “The non-respiratory biochemistry of the lung.”
Well, it wasn’t too long before big pharma capitalized on this important, new understanding about ACE to create two new classes of drugs to treat high blood pressure. They called the new drugs ACE inhibitors and angiotensin receptor blockers (ARBs).
The drugs work, as their names suggest, by inhibiting or blocking ACE production in the lungs. And from the beginning, the drugs had one well-known, common—but ultimately “acceptable”—side effect…
A terrible, annoying cough.
As the years went by, researchers found that people who take these drugs also have a significantly higher risk of developing serious, chronic, and potentially deadly lung diseases, even lung cancer, as I reported last year.
So, even before this new coronavirus theory, we knew all along that these drugs clearly disrupt respiratory function…and can cause serious harm in the lungs.
Which brings us back to the new theory…
Do ACE inhibitors and ARBs make patients more susceptible to the coronavirus?
As we all know, the coronavirus’ main target is your respiratory system. And we now also know that the microbe binds, specifically, to ACE2 receptors to gain entry into the lungs. As a result, susceptible people can develop pneumonia and fatal respiratory failure in 10 to 14 days after contracting the virus.
Now, here’s the rub…
Because ACE is a normal part of lung function, when drugs block this enzyme, the lung responds by making more receptors for it.
So, people with underlying conditions, such as high blood pressure and Type II diabetes, who take ACE inhibitors and ARBs actually have increased levels of ACE2 receptors, which theoretically puts out a “welcome mat” for the coronavirus to take hold in the lungs.
Plus, an early analysis of 1,099 patients with confirmed COVID-19 infections found that patients with underlying, chronic conditions had more severe reactions to the virus. And these patients typically met the criteria for treating their conditions with ACE inhibitors and ARBSs, which, as we’re learning, could potentially worsen their reaction to COVID-19.
As I mentioned at the beginning of this Dispatch, experts have known from the get-go that people with underlying, chronic conditions are, “for some reason,” much more likely to develop severe respiratory infections, pneumonia, and fatal respiratory arrest as a result of COVID-19. Meanwhile, children seem to experience mostly mild, non-fatal infections.
Well, as this research suggests, a reason for this discrepancy could be that older people with these chronic conditions are prescribed ACE inhibitors and ARBs, whereas young children are not.
So, here’s what I recommend: If you take one of these drugs, it’s imperative that you discuss all the current findings with your doctor as soon as possible. In addition, start taking some practical steps RIGHT NOW to boost your immunity and lung health, including supplementing with 10,000 IU of vitamin D daily.
For more recommendations, check out my Pandemic Protection Playbook: How to become “immune ready” in every season. (To learn more about this essential guide, click here now!)
And lastly—there are other drugs that work well for high blood pressure, heart disease, and Type II diabetes (and they don’t impair lung function). For guidance about how to support your heart and lung health without resorting to the harmful drugs, refer to my two online learning protocols: my Heart Attack Prevention and Repair Protocol and Breathe Better Lung Health Protocol.
“Hypothesis: angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may increase the risk of severe COVID-19.” Journal of Travel Medicine, 2020; pii: taaa041. doi.org/10.1093/jtm/taaa041
“ACE inhibitors and angiotensin receptor blockers may increase the risk of severe COVID-19, paper suggests.” Science Daily, 3/23/20. (sciencedaily.com/releases/2020/03/200323101354.htm)
“People Who Are at Higher Risk for Severe Illness.” Centers for Disease Control, 4/2/20. (cdc.gov/coronavirus/2019-ncov/need-extra-precautions/people-at-higher-risk.html)
“Are patients with hypertension and diabetes mellitus at increased risk for COVID-19 infection?” The Lancet, 3/11/2020; 8(40): PE21. doi.org/10.1016/ S2213-2600(20)30116-8