SARS-CoV-2, the virus that causes COVID-19, attacks the body in a number of ways. One of the most insidious is the way it causes blood clots in the arteries, veins and microscopic blood vessels. This can set off a stroke or heart attack, and in the case of COVID-19, microscopic clots could reduce blood flow to the lungs, restricting the exchange of oxygen.
It hasn’t been clear exactly why the virus causes these blood clots, so scientists have been studying the phenomenon. Here’s one possible answer they’ve uncovered…
The trouble with certain antibodies
A recent University of Michigan study has revealed that SARS-CoV-2 can trigger the production of autoimmune antibodies circulating in the blood. These antibodies then attack the blood cells, which form clots in the blood vessels.
Autoantibodies are associated with autoimmune diseases, but outside of SARS-CoV-2 infection, doctors have previously only seen these clot-causing antibodies in patients with the autoimmune disease antiphospholipid syndrome. Finding them in COVID-19 patients was surprising, to say the least.
“In patients with COVID-19, we continue to see a relentless, self-amplifying cycle of inflammation and clotting in the body,” says co-corresponding study author Dr. Yogen Kanthi, an assistant professor at the Michigan Medicine Frankel Cardiovascular Center and a Lasker Investigator at the National Institutes of Health’s National Heart, Lung, and Blood Institute. “Now we’re learning that autoantibodies could be a culprit in this loop of clotting and inflammation that makes people who were already struggling even sicker.”
“We know people with the highest levels of autoantibodies did worse in terms of respiratory function, and the antibodies caused inflammation even in healthy cells,” says Dr. Yu (Ray) Zuo, an assistant professor of internal medicine and a rheumatologist at Michigan Medicine and first author of the study.
The researchers discovered that about half of the patients they studied who were very sick with COVID-19 showed a combination of high levels of both the dangerous antibodies and hyperactive neutrophils (also linked to gum health and heart disease), normally helpful white blood cells that have become dangerous to healthy cells as well as unwelcome viral invaders.
In April, the research team was the first to report that patients hospitalized for severe COVID-19 had higher levels of neutrophil extracellular traps (NETs) in their blood. These NETs are fibers formed outside the neutrophils that capture and kill bacteria, but as is the case with neutrophils, super-activated NETs can start attacking the healthy cells surrounding them.
To learn more, in this most recent study the researchers studied the explosive neutrophils and the COVID-19 antibodies together in mouse models to see if this could be if this sinister pairing was responsible for the clots.
“Antibodies from patients with active COVID-19 infection created a striking amount of clotting in animals — some of the worst clotting we’ve ever seen,” Dr. Kanthi says.
More study needed
The researchers warn these findings aren’t yet ready for clinical adoption. The team’s next step is to find out whether severely ill COVID-19 patients with high levels of these antibodies have better outcomes if the antibodies are blocked or removed. If so, it could warrant aggressive treatment like plasmapheresis, where the blood is drained through an IV, filtered, and replaced with fresh plasma without the troublesome antibodies.
The team also plans additional research to identify the triggers and targets of the antibodies, as well as determine how long these antibodies remain in circulation after recovery from SARS-CoV-2. The latter point could answer questions surrounding the use of convalescent plasma in COVID-19 treatment.
The researchers are also running DICER, a randomized clinical trial testing a well-known, inexpensive anticlotting agent, dipyridamole, in patients with COVID-19 to determine whether it’s more effective than placebo in reducing excessive blood clots. They believe dipyridamole has the potential to block the specific type of inflammation occurring in COVID patients.
Reducing blood clot risk
The best way to lower your risk of COVID-19-related blood clots is not to get the virus in the first place. Wear your mask, wash your hands, and keep your distance from people outside your own household. These steps are especially important as cases spike in the colder months.
If you do test positive for SARS-CoV-2, don’t despair. Many COVID-19 cases end up being mild, and for the most part, people are able to recover at home. But, as Virginia Tims-Lawson notes in this May article, promoting healthy blood flow may be worth considering.
Make sure you’re getting exercise and eating a whole-food diet rich in fruits and vegetables, and if you smoke, stop. Also, if you’re not taking blood thinners (or just want to run these by your doctor), try adding to your diet the following supplements:
- Nattokinase, which produces an agent that helps keep the blood from clotting excessively;
- CoQ10, which fuels your heart cells with much-needed energy; and
- Vitamin K2, which reroutes calcium from the blood, where it can cause abnormal thickening in the arteries, to the bones where it’s needed most.
Editor’s note: There are numerous safe and natural ways to decrease your risk of blood clots including the 25 cent vitamin, the nutrient that acts as a natural blood thinner and the powerful herb that helps clear plaque. To find out about these and more, click here to read our free report!
New Cause of COVID-19 Blood Clots Identified — University of Michigan Health Lab
Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19 — Science Translational Medicine
Higher Levels of NETs in Blood Associated with More Severe COVID-19 — University of Michigan Health Lab
Neutrophils — British Society for Immunology
3 Reasons the Stroke Risk from COVID-19 is So Dangerous — Easy Health Options