Brand-name antidepressants may survive some patients.
While France reports its first wave of Covid-19 in February 2020, Nicolas Hoertel is all about its patients.
Hoertel is an associate professor of psychiatry at the University of Paris and a psychiatrist at Corentin Celton Hospital, specializing in elderly psychiatry. Information from China has made it clear that the threat of serious illness or death from Covid-19 increases particularly beyond the age of 65. At least a portion of all patients at the 90-bed facility where Hoertel is a psychiatrist were in great threat.
However, when the wave peaked, he noticed that patients at his center almost never had symptoms severe enough to warrant hospitalization. In fact, between February 2020 and March 2021, 4 of its patients had to be hospitalized for covid-19.
More than 90% of the 88,933 deaths in France in the last year occurred in others over the age of 65. And yet, in the psychiatric hospital filled with patients taking antidepressants, many of whom belonged to this high-risk age group, only one died. A really striking contrast when you compare it with other services for seniors.
Antidepressants, according to evidence, helped these patients survive.
Intrigued by this revelation, from January to April 2020, Hoertel worked with a total of 39 hospitals (23 acute, 20 adult, 3 pediatric) in and around Paris to expand a multicenter observational retrospective study analyzing outcomes for COVID-19 patients. And his team discovered something remarkable: While some antidepressants seemed to have no effect on the results, several did so to an astonishing degree.
They found that Covid-19 cases leading to intubation or death can be reduced by up to 72%. The most promising antidepressants? These are surnames among those with treatment-resistant depression: venlafaxine, mirtazapine, escitalopram, paroxetine, and fluoxetine.
While Hoertel was applying in France, Angela Reiersen, a psychiatrist at Washington University School of Medicine in St. Louis, Louis, noted studies indicating that fluvoxamine might be helpful in treating sepsis, a disease that releases cytokines into the bloodstream and is fatal.
Knowing that “cytokine storms” are linked to severe cases of covid-19, Reiersen contacted his colleague Eric Lenze to do a study together. The couple conducted a double-blind, placebo-controlled study to determine whether early use of the antidepressant fluvoxamine via covid-19 patients can simply decrease serious outcomes. The researchers found that clinical deterioration occurred in 0 of 80 patients in the fluvoxamine group and in 6 of 72 in the placebo group.
Now, studies in at least 3 countries (France, USA)The U. S. Food and Drug Administration (USA) support the idea that some antidepressants may be an effective early remedy for covid-19.
Not only does it appear to be effective, but it is also quite safe and reasonable: millions of people are already taking the drugs. And compared to the only other true early remedy for covid-19, monoclonal antibodies, an antidepressant remedy is incredibly affordable.
Perhaps at most, if more studies verify those initial findings, Inverse experts said antidepressants are very likely to be as effective at combating the serious consequences of variant viruses as they were in the study.
The exact mechanism through which those antidepressants mitigate the severe effects of Covid-19 is still unclear, there are 3 convincing hypotheses:
There is irrefutable evidence of all of the above. And it can be a mixture of all three.
When Hoertel began formulating hypotheses, he thought, like Lenze and Reiersen, that anti-inflammatory speculation is probably the ultimate reaction due to something called the Sigma 1 receptor (S1R). Activation of S1R is not unusual with antidepressants and this activation would possibly produce anti-inflammatory effects. But as the study progressed, the French psychiatrist thought it was less likely.
“Some of the antidepressants that target Sigma 1 that had very clever effects and others that target the same receptor, not so much,” Hoertel told Inverse. “So, for us, this explanation doesn’t work. “
He says it’s imaginable that this anti-inflammatory has a positive effect, but that’s not the answer his team was looking for. “It’s not satisfying,” he says. It’s not about explaining all of our findings. “
The explanation he found most convincing was the third: the enzyme hypothesis. It was proposed by a German physician and researcher, Erich Gulbins. Instead of focusing on the virus’s spike protein that allows it to penetrate and reflect into a human cell, Gulbins tried to figure out what was going on in the host cell.
Based on his studies on waxy lipid molecules called ceramides, as well as paintings by scholars like Hoertel, Gulbins hypothesizes that when the novel coronavirus enters the cell, it activates an enzyme called acid sphingomyelase (ASM). When this enzyme is activated, ceramides are produced.
Ceramides serve as the open door for the virus to enter the cell, where it can reproduce. What these antidepressants do is inhibit those enzymes. Fewer enzymes means fewer ceramides and fewer open doors for the virus to enter a human cell.
When a virus particle enters your body, the virus begins to look for cells where it can reproduce. But if the “ceramide gate” theory is correct, the cells of other people taking ASM inhibitors are small strengths and the virus cannot locate an entrance.
What’s exciting about this option, all of this is being tested and replicated, is not just that it would offer an inexpensive, easy-to-obtain and effective remedy for Covid-19, but what that could mean for variants.
Vaccines teach the body what to look for and what to oppose. The coronavirus enters cells thanks to its spike protein. The vaccine then gives your body a picture of the spike protein and says to “create antibodies that attack and kill what’s attached. “that peak. “
While some vaccines are very effective compared to some variants, other variants can pose more problems. The explanation for why some vaccines would possibly be less effective compared to some of the variants is due to mutations in the spike proteins. When a virus mutates and mutations what its antibodies have been trained to look for, they may miss it; It is based on the difference between the mutation and what the antibodies have been trained to fight.
If the virus just walks out the doors to get through, it can’t locate a mobile phone and replicate itself, no matter what mutation guise it may be wearing. He might just be disguised as a female explorer promoting Thin Mints and the door wouldn’t yet. open.
Lenze cautions against getting too bogged down on which of the three mechanisms works, and emphasizes that whatever mechanism makes antidepressants help, “they work regardless of variants,” he tells Inverse.
What is important, he emphasizes, is that those are effective, reasonable medications and, if taken early, can spare you the serious consequences of Covid-19. Eventually it will be determined what mechanism is in the paintings (and probably not too far away). the future) through more clinical trials and double-blind studies, such as the at-home study it is running called Stop Covid 2.
While more studies and clinical trials are needed to verify what the initial data shows, Hoertel is hopeful. But he wants to be clear: The likelihood that some of those antidepressants will provide some coverage rather than serious illness shouldn’t stop you from getting vaccinated or being too confident at your point of coverage — there’s still too much that wants to be replicated and verified.
Instead, he says, we stick to his example: “Be positive but careful. “