The COVID-19 pandemic has undoubtedly changed the course of countless lives. And for many of those who have contracted the disease, the effects can still be felt even if they’ve “officially” recovered.1
Commonly known as long COVID, this side effect of the SARS-CoV-2 infection affects millions worldwide, and many struggle with symptoms for more than a year.2 For a few years, researchers have been hitting dead ends as to what causes these long-term issues. Now, a new study has uncovered strong evidence that can answer their longstanding theories — microclots.3
New Research Deepens Understanding of Long COVID
In a study published in the Journal of Medical Virology, researchers set out to learn what makes long COVID so persistent. Trying a new angle, they focused on the blood itself, and found that those with long COVID carry abnormal microscopic structures. Specifically, fibrin microclots fused with immune cell debris.4
To perform the analysis, the team used advanced imaging to determine how the microclot structures form, what they contain, and how they differ from healthy blood. For the study population, they selected adults with long COVID who continued to struggle with problems such as exhaustion, shortness of breath, brain fog, dizziness, and chest tightness long after the initial infection had been resolved.
• There were stark differences in blood structure — According to the researchers, the test samples consistently showed larger, denser, and more complex microclot structures than those seen in healthy controls.
Digging deeper into the data, they discovered that the microclots were intertwined with neutrophil extracellular traps, or NETs. These are sticky webs of DNA and enzymes that neutrophils release when activated. NET-rich clots resist normal breakdown processes, which means your body winds up with lingering blockages at the microvascular level.
• The impact of NETs — The researchers reported major increases in several NETs markers — myeloperoxidase, neutrophil elastase, and circulating cell-free DNA — in the long COVID group. These are enzymes and DNA fragments that act like glue inside the clots. The more NET material the researchers found, the more microclots appeared, and the larger those clots became.
• Another noteworthy detail is the sheer density of the structures — Under fluorescence microscopy, the microclots in long COVID blood showed thick, tangled layers that looked compact and resistant to breakdown. Healthy controls also had microclots, but they were sparse and far less structured.
• How deeply embedded the NET components were within the clots — They were not lightly attached to the surface. Instead, DNA strands and neutrophil enzymes were woven through the interior of the fibrin structures. This is important because fibrin-based clots normally break down with the help of enzymes like plasmin.
When DNA and neutrophil proteins are interlaced throughout the clot, the breakdown process becomes inefficient and slow, which explains why long COVID lasts for months — or even years.
• Different markers also showed different strengths of association with microclot formation — For example, circulating DNA strongly paralleled microclot density, whereas some other markers rose but did not track as precisely with clot burden. It means future testing may rely on specific markers to help identify which biological processes are driving persistent symptoms. It also opens the door for individualized interventions.
• NETs act as scaffolding — When neutrophils eject their DNA and enzymes, they create long, sticky strands designed to trap pathogens. In long COVID, these strands latch onto fibrin — a protein involved in clotting — and build layered, tangled structures. Once formed, they float through the bloodstream, lodging in tiny vessels and creating micro-obstructions. The result is impaired microcirculation and reduced oxygen transfer.
• Another mechanism the researchers described involves the resistance of these clots to fibrinolysis — Because NET components stiffen and reinforce the fibrin structure, the body’s usual cleanup systems struggle to dissolve them. This leads to chronic retention of microclots, continued vascular stress, and prolonged symptoms.
• The amount of NET material increased directly alongside the amount of microclots — This means the immune and clotting systems are interacting in a loop, each one pushing the other. Over time, this loop drains your energy, stresses your cardiovascular system, and keeps inflammation alive long after the virus is gone.
You’re Already at Risk of Blood Clots Once You Get Infected
In an earlier study published in Hematology Reports, researchers reviewed evidence on how the SARS-CoV-2 virus can trigger dangerous clotting problems during the infection and long after someone tests negative. Their goal was to identify how the virus flips the body into a clot-forming state, why this risk lasts for months, and which biological events drive the damage.5
The researchers reviewed how both acute and long-term clotting problems interfere with blood flow, stress the cardiovascular system, and set the stage for health issues that perfectly match with the descriptions of long COVID.
• Rates of clotting complications — Deep-vein thrombosis and pulmonary embolism increased dramatically among hospitalized COVID patients, and the researchers reported that many cases appeared even while patients received anticoagulant therapy designed to prevent clots.
• What happened after people left the hospital — Extended clotting risk showed up in multiple studies, with patients showing clot formation weeks to months after the initial infection had passed.
• A comparison of clot complications across different groups — The authors noted that those with preexisting cardiovascular disease, diabetes, obesity, or advanced age were more likely to experience severe clotting events, but younger and previously healthy people were not exempt.
• SARS-CoV-2 creates imbalance between clot formation and clot breakdown — Under normal conditions, your body constantly forms tiny clots and dissolves them. But according to the researchers, COVID disrupts this balance by releasing clot-promoting chemicals, damaging vessel walls, and activating platelets at unusually high rates. Once this imbalance begins, your body forms clots faster than it dissolves them.
• Biological mechanisms that tie the processes together — The paper explains how the virus infects endothelial cells, which are the thin linings inside your blood vessels. When these cells are damaged, they release substances that encourage clotting, narrow the vessel opening, and attract platelets to the injury site.
The result is a chain reaction — damaged endothelium signals inflammation, inflammation triggers platelet activation, and activated platelets send more clotting signals.
• The immune system’s involvement — COVID-19 stimulates a wave of inflammatory cytokines, which are chemical messengers that tell the body to mount a defense. When these cytokines rise too high, your clotting system receives constant signals to activate. This is why some people feel as if their bodies never shut off even after the infection is gone. Their inflammatory and clotting pathways remain switched on, draining energy and straining the heart, lungs, and muscles.
• How platelet behavior changes during and after infection — Platelets are tiny cell fragments that help your blood clot when you’re injured. According to the researchers, the SARS-CoV-2 virus drives platelets into a highly activated state where they clump together more easily, interact abnormally with immune cells, and release clot-promoting substances.
That heightened reactivity does not always return to normal right away. If you have lingering symptoms, this platelet activation is part of the reason your blood flow feels impaired even when scans or standard tests look fine.
Strategies to Help Manage Long COVID Better
At its core, long COVID is a matter of mitochondrial dysfunction. If these energy factories inside your cells don’t function at an optimal rate, your energy levels will ultimately be affected. If you know someone who is suffering from this condition, these strategies can help:
1. Proteolytic enzymes — Whenever I encounter someone who is experiencing long COVID symptoms, one of the first things I tell them is to take proteolytic enzymes, which help clear residual spike protein from the body. Nattokinase, lumbrokinase, and serrapeptase are among the best-studied enzymes for this purpose. They help dismantle remaining spike fragments, ease inflammation and give the brain and tissues space to recover.
Lumbrokinase is significantly more potent — roughly 30 times stronger than nattokinase and about 300 times stronger than serrapeptase — so, it’s typically my preferred choice. These enzymes are best taken on an empty stomach, at least an hour before, or two hours after, consuming protein. If taken with food, they will be diverted into digesting your meal instead of clearing problematic proteins from the bloodstream.
2. Follow the I-RECOVER protocol — The Independent Medical Alliance (IMA), previously known as the FLCCC, offers a detailed plan called the I-RECOVER protocol. It’s one of the most thorough guides available for addressing post-vaccine and post-infection complications. It outlines strategies for detoxification, calming inflammation, and restoring mitochondrial function — all foundational steps for improving health after COVID-related injuries.
3. Reduce intake of linoleic acid (LA) — Your mitochondria rely on a unique lipid called cardiolipin,6 which is located within the inner membrane structures (cristae) where energy is produced. The quality and stability of cardiolipin are influenced by the fats in your diet. This is more important than most people realize, as the wrong dietary fats distort cristae structure and hinder energy production.
Cardiolipin also acts as an internal safety system, signaling damaged cells to initiate apoptosis by activating caspase-3. When cardiolipin becomes oxidized, especially from excess LA consumption, it loses this ability. Without proper signaling, dysfunctional cells persist and may eventually become cancerous.
LA is found in excess in vegetable oils (which are used heavily in ultraprocessed and restaurant foods), condiments, nuts and seeds, adulterated olive and avocado oils, and animal products from grain-fed livestock such as conventional chicken and pork. That said, I recommend you to download my Mercola Health Coach app once it’s available. It has a feature called the Seed Oil Sleuth, which monitors your LA intake to a tenth of a gram.
4. Methylene blue — This solution can be very effective for the exhaustion and neurological challenges that linger after COVID infection or getting the shot. It functions as an electron carrier, essentially acting like a rechargeable energy source. Unlike many compounds that perform a similar role, it does not promote harmful oxidative reactions.
When mitochondrial respiration or oxygen utilization is impaired, methylene blue can reroute electron flow, restoring energy production even when normal pathways are blocked. It can also compensate for reduced blood flow by improving mitochondrial efficiency when tissues aren’t receiving enough oxygenated hemoglobin.
Its benefits extend beyond the time it remains in the body — methylene blue induces biochemical changes that enhance oxygen-processing pathways and may even promote the formation of new mitochondria over time.
Dosing is hermetic. Low amounts provide benefits that high amounts can negate. Most experts recommend relatively high doses for longer-term treatments, such as 0.5 milligram (mg) to 1 mg per kilogram of body weight for cognitive support. For a person weighing 150 pounds, that would be a dose of 34 to 68 milligrams. I believe this is excessive and unnecessary.
Doses of more than 3 to 5 milligrams are likely never needed unless you are undergoing treatment for a life-threatening condition such as carbon monoxide or cyanide poisoning.
The average dose for most adults that reduces or eliminates reductive stress is only 5 mg, once a day, regardless of weight. It has a half-life of over twelve hours and will gradually build up if you take it every day, so higher doses are not needed. Only use pharmaceutical-grade methylene blue in capsule or tablet form, as industrial and chemical varieties frequently contain contaminants like heavy metals. Taking it with vitamin C can enhance absorption.
To learn more, read “The Surprising Health Benefits of Methylene Blue.” It features an interview with methylene blue expert Francisco Gonzalez-Lima, Ph.D., who has spent many years studying this drug.
5. Check your iron levels — Excess iron is another major disruptor of mitochondrial function, and many people — aside from menstruating women or individuals with significant blood loss — tend to accumulate too much. In contrast, copper deficiency is widespread.
Iron and copper need to be in balance because they depend on each other for proper metabolism. Low ferritin does not necessarily mean you are low in iron. More often, it reflects inadequate copper, which is required to recycle iron efficiently. Copper is also essential for mitochondrial energy production, detoxification, and overall metabolic health.7 You can learn more about this in “The Poorly-Understood Role of Copper in Anemia.”
You can increase copper by supplementing with 4 to 10 mg of copper bisglycinate daily or by consuming copper-rich foods like bee pollen, grass fed beef liver, and acerola cherry (which contains the copper-dense enzyme tyrosinase).
To reduce excess iron, routine blood donation is a simple and effective method. This usually involves donating two to four times annually, or removing smaller amounts monthly (shown below) if large donations aren’t well-tolerated. If you have severe chronic obstructive pulmonary disease (COPD) or congestive heart failure, consult a physician first. But most people can safely follow this recommendation to maintain healthier iron levels.
| Men | Postmenopausal women | Premenopausal women |
|---|---|---|
| 150 ml | 100 ml | 50 ml |
Frequently Asked Questions (FAQs) About Microclots in Long COVID Blood
Q: What is the main biological cause recently identified behind long COVID symptoms?
A: Research shows that long COVID is strongly linked to fibrin microclots mixed with immune cell debris, especially neutrophil extracellular traps (NETs). These dense, abnormal clots restrict microcirculation and reduce oxygen delivery, driving fatigue, breathlessness, brain fog, and other persistent symptoms.
Q: How do NETs make long COVID microclots harder for the body to clear?
A: NETs form sticky webs of DNA and enzymes that bind to fibrin, creating thick, compact clots that resist normal breakdown. Because the body struggles to dissolve them, these microclots accumulate, prolonging vascular stress and maintaining symptoms for months or years.
Q: Does COVID increase clotting risk even after mild illness or recovery?
A: Yes. Evidence shows that even mild cases trigger inflammation, endothelial injury, and hypercoagulation, causing clotting risks that persist long after testing negative. Many people continue developing clots weeks to months after infection, which explains post-recovery chest tightness, fatigue, and shortness of breath.
Q: Is long COVID rooted in mitochondrial dysfunction?
A: Long COVID disrupts mitochondria through microvascular blockages, inflammation, and oxidative stress. This energy deficit explains fatigue, post-exertional crashes, and slow recovery, and supports treatments focused on restoring mitochondrial function.
Q: What strategies can help improve long COVID?
A: Commonly recommended approaches include proteolytic enzymes to clear residual proteins, the I-RECOVER protocol, reducing linoleic acid intake to optimize mitochondrial health, using pharmaceutical-grade methylene blue, and balancing iron and copper levels through diet or blood donation.



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