BREAKING! COVID-19 Drugs: Columbia Researchers Find That Serotonin And SSRI Drugs Like Fluvoxamine Can Cause Heart Valve Disease!
: Researchers from Columbia University’s Department of Surgery in collaboration with the Pediatric Heart Valve Center at Children’s Hospital of Philadelphia (CHOP), the University of Pennsylvania, and the Valley Hospital Heart Institute have discovered that serotonin can impact the mitral valve of the heart and potentially accelerate a cardiac condition known as degenerative mitral regurgitation.
Selective serotonin reuptake inhibitors or SSRIs are a class of drugs that are typically used as antidepressants in the treatment of major depressive disorder, anxiety disorders, and other psychological conditions and include drugs like fluvoxamine (Faverin, Luvox), Fluoxetine (Prozac) and Sertraline (Zoloft) and they increase serotonin levels not only in the brain but also in the bloodstream!
Due to ‘half-baked’ studies, certain charlatan groups like the FLCCC, certain stupid Thai doctors (supported by young “rich spoilt brats” involved in money laundering and illegal crypto exchanges, and also forest monks) and also garbage American ‘experts’ including an American gastroenterologist on twitter were advocating Fluvoxamine or Fluoxetine as a prophylactic or therapeutic drug for COVID-19 as well as Long COVID!
Thailand Medical News in our various COVID-19 Drugs
coverages have been warning about the usage of Fluvoxamine for COVID-19 or Long COVID as it can cause heart issues which can sometimes be fatal.
Degenerative mitral valve (MV) regurgitation (MR) is a highly prevalent heart disease that requires surgery in severe cases.
The study team from Columbia shows that a decrease in the activity of the serotonin transporter (SERT) accelerates MV remodeling and progression to MR.
Using studies of a population of patients with MR, the researchers showed that selective serotonin reuptake inhibitor (SSRI) use and SERT promoter polymorphism 5-HTTLPR LL genotype were associated with MV surgery at younger age.
Functional characterization of 122 human MV sampl
es, in conjunction with in vivo studies in SERT−/− mice and wild-type mice treated with the SSRI fluoxetine, showed that diminished SERT activity in MV interstitial cells (MVICs) contributed to the pathophysiology of MR through enhanced serotonin receptor (HTR) signaling. SERT activity was decreased in LL MVICs partially because of diminished membrane localization of SERT.
Shockingly, it was found that in mice, fluoxetine treatment or SERT knockdown resulted in thickened MV leaflets. Similarly, silencing of SERT in normal human MVICs led to up-regulation of transforming growth factor β1 (TGFβ1) and collagen (COL1A1) in the presence of serotonin.
Furthermore, treatment of MVICs with fluoxetine not only directly inhibited SERT activity but also decreased SERT expression and increased HTR2B expression.
It was also found that fluoxetine treatment and LL genotype were also associated with increased COL1A1 expression in the presence of serotonin in MVICs, and these effects were attenuated by HTR2B inhibition.
The study findings suggest that assessment of both 5-HTTLPR genotype and SERT-inhibiting treatments may be useful tools to risk-stratify patients with MV disease to estimate the likelihood of rapid disease progression.
The study findings were published in the peer reviewed journal: Science Translational Medicine.
DMR or degenerative mitral regurgitation is one of the most common types of heart valve disease. The mitral valve is located between the left atrium and left ventricle of the heart. It closes tightly when the heart contracts to prevent blood from leaking back into the left atrium.
Typically, in DMR, the shape of the mitral valve becomes distorted, preventing the valve from closing completely. This allows blood to leak back toward the lungs (regurgitation), limiting the amount of oxygen-rich blood moving through the heart to the rest of the body.
Hence, DMR can bring about symptoms like fatigue and shortness of breath. Because of the reduced efficiency in circulation, the heart has to work harder, which over time causes permanent damage. This can lead to a number of serious and life-threatening cardiac issues, including fatal outcomes involving atrial fibrillation and heart failure.
Worse, there is currently no treatment for mitral valve degeneration.
Co-author,Dr Giovanni Ferrari, scientific director of the Cardiothoracic Research Program at Columbia University told Thailand Medical News, “Certain medications can ease the symptoms and prevent complications, but they do not treat the mitral valve. If the degeneration of the mitral valve becomes severe, surgery to repair or replace the valve is needed.”
The monoamine neurotransmitter, serotonin plays a part in a wide range of body functions, including emotional state, digestion, sleep, memory, and blood clotting. Serotonin’s role as a neurotransmitter helps your brain regulate mood; lower levels of serotonin are associated with anxiety and depression.
Typically, serotonin binds to specific receptors on the surface of a cell, sending a signal to the cell to act accordingly. A protein known as the serotonin transporter (SERT or 5-HTT) moves serotonin into the cell to be reabsorbed and recycled, a process known as serotonin reuptake.
Drugs called selective serotonin reuptake inhibitors (SSRIs) bind to the SERT to reduce serotonin reuptake, allowing serotonin to remain available for longer periods. This increased serotonin availability can help improve symptoms of mood disorders. SSRIs are some of the most widely prescribed types of antidepressants.
The research examined clinical data from more than 9,000 patients who had undergone valve repair or replacement surgery for DMR and evaluated 100 mitral valve biopsies.
Dr Ferrari added, “Studying the data of these patients, our study team found that taking SSRIs was associated with severe mitral regurgitation that needed to be treated with surgery at a younger age than for patients not taking SSRIs.”
The research team also studied in vivo mouse models using transgenic mice lacking the SERT gene and normal mice. They discovered that mice without a SERT gene developed thicker mitral valves and that normal mice treated with high doses of SSRIs also developed thickened mitral valves.
Utilizing genetic analysis, the study team identified genetic variants in the SERT gene region 5-HTTLPR that affect SERT activity. They found that a “long” variant of 5-HTTLPR makes SERT less active in the mitral valve cells, especially when there are two copies (one maternal and one paternal). DMR patients with the “long-long” variant needed mitral valve surgery more often than those with other variants.
Interestingly, mitral valve cells from DMR patients with the “long-long” variant were more prone to react to serotonin by producing more collagen, changing the shape of the mitral valve. Additionally, mitral valve cells with the “long-long” variant of 5-HTTLPR were more sensitive to fluoxetine and other SSRIs than those with other variants.
The research findings indicate that for DMR patients with the “long-long” variant, taking SSRIs lowers SERT activity in the mitral valve. The study team suggest testing DMR patients for potential low SERT activity by genotyping them for 5-HTTLPR, which can be determined easily from a DNA sample obtained from the blood or a mouth swab.
Dr Ferrari added, “Assessing patients with DMR for low SERT activity may help identify patients who may need mitral valve surgery earlier. Promptly fixing a mitral valve that is very leaky would protect the heart and could prevent congestive heart failure.”
Patients currently on SSRIs for conditions other than COVID-19, should talk to their physicians about switching to other alternatives while those who are taking it for COVID-19 or long COVID, should stop taking it immediately and go for a detailed heart screening. It should be noted that already SARS-CoV-2 infections directly and indirectly causes a variety of heart and cardiovascular issues and the last thing a person should take is a drug that can further aggravate the condition of the heart!
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