Novel Theory Unravels Peculiar COVID-19 Symptoms and Highlights the Importance of Vitamin D
Written by Susan Parker | Updated on May 28, 2025
Reviewed by Susan Parker
Key Takeaways
COVID-19 affects the body through ACE2 receptors in various organs.
Bradykinin storm may be the main cause of COVID-19 symptoms.
Vitamin D can help prevent a bradykinin storm and reduce severity of illness.
Frequently Asked Questions
Key Takeaways
COVID-19 affects the body through ACE2 receptors in various organs.
Bradykinin storm may be the main cause of COVID-19 symptoms.
Vitamin D can help prevent a bradykinin storm and reduce severity of illness.
Frequently Asked Questions
We understand that the coronavirus primarily impacts the lungs. It is intriguing, however, that around half of hospitalized patients experience neurological symptoms such as dizziness, delirium, seizures, and strokes.
Moreover, why do one in every five hospitalized patients exhibit signs of heart damage despite not having previous cardiac problems?
Common symptoms like dry cough and fatigue, along with uncommon ones such as swollen and bruised toes, can all be clarified by the bradykinin hypothesis. This theory, in which vitamin D plays a vital role, sheds light on the various presentations of the virus.
In the summer, medical researchers tapped into the strength of the world’s second-fastest computer, Summit, at Oak Ridge National Laboratory, University of Tennessee.
Their objective was to harness Summit's capabilities to improve their comprehension of how COVID-19 impacts the human body. By scrutinizing data from 40,000 genes across 17,000 genetic samples of the virus, Summit provided valuable insights after analyzing 2.5 billion genetic combinations over a week.
For the lead researcher, Dr. Daniel Jacobson, the analysis by Summit was groundbreaking, unveiling a novel disease model that could demystify many aspects of the virus.
Summit's discoveries suggest that the virus typically commences its infection by entering the nose and binding to ACE2 receptors, which are abundant in that region. This initial interaction enables the virus to spread to other ACE2-rich areas in the body, like the intestines, kidneys, and heart, resulting in associated symptoms.
While some of this was previously understood, the supercomputer highlighted that the virus manipulates the body to boost ACE2 expression in areas where it is usually low, like the lungs, facilitating rapid viral replication.
As a consequence of this process, the coronavirus disrupts the body's ability to regulate bradykinin, a peptide critical in various bodily functions, including blood vessel dilation and blood pressure control.
The uncontrolled production of bradykinin leads to a "bradykinin storm," believed to be the primary driver of symptoms, contrary to the commonly cited "cytokine storm" involving an exaggerated immune response.
The implications of a bradykinin storm are worrisome, as it induces blood vessels, including those in the brain, to become permeable. This occurrence may compromise the blood-brain barrier, allowing harmful substances to enter and potentially cause brain damage.
Permeable blood vessels can also account for milder manifestations like swollen and bruised "COVID toes."
In addition to affecting the heart through ACE2 receptors, the bradykinin storm can result in decreased blood pressure and irregular heartbeats.
Strikingly, the cardiac symptoms of COVID-19 resemble those induced by ACE inhibitor medications for hypertension, which also raise bradykinin levels. Dry cough and fatigue, common side effects of ACE inhibitors, align with classic COVID-19 symptoms.
The most concerning consequences are observed in the lungs, where permeable blood vessels cause fluid accumulation. This leakage can incite lung inflammation as immune cells leak into surrounding tissues.
Moreover, the body's response increases lung hyaluronic acid production, forming a gel-like substance when combined with lung fluid. This process contributes to the sensation described by Dr. Jacobson as "breathing through Jell-O" and explains the limited efficacy of ventilators in severe cases.
The bradykinin hypothesis may elucidate why men have a higher mortality rate than women, as women possess double the protective protein that aids in regulating bradykinin levels.
Dr. Jacobson and his team propose nine medications that could mitigate bradykinin production or signaling, reduce hyaluronic acid levels, or enhance blood clotting. These options include hormone and steroid medications, as well as drugs influencing blood flow and those directly disrupting bradykinin development.
Notably, the researchers advocate for vitamin D as a non-pharmacological intervention.
Vitamin D is significant due to its impact on the renin-angiotensin system, a hormonal regulator crucial for kidney and cardiovascular functions.
Disruption of this system by COVID-19 triggers bradykinin release. Vitamin D can alleviate renin production, preventing the onset of a bradykinin storm.
These findings add to the mounting evidence highlighting vitamin D's role in modulating inflammatory responses during infections.
The researchers emphasized, "Patients deficient in Vitamin D face increased risk of ARDS [acute respiratory distress syndrome] in general, and such deficiencies correlate with the severity of COVID-19 illness."
With reduced sunlight exposure post-summer, vitamin D supplementation becomes even more crucial. This new research underscores the protective advantages of vitamin D against severe COVID-19 infections and flu during the upcoming winter season.
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