Is fluvoxamine effective against covid-19?

effective drug against covid

Fluvoxamine is an anti-depressant drug that belongs to the class of drugs known as SSRI’s (selective serotonin reuptake inhibitors). It’s normally used to treat depression and anxiety. Lately, there’s been a lot of discussion over whether fluvoxamine might be effective as a treatment for covid-19.

Wait, what?!

Yes, that was my initial reaction. Why would an anti-depressant have any role in treating covid-19?

Well, apart from its effects on serotonin signalling in the nervous system, fluvoxamine has an activating effect on a receptor called S1R, which is involved in regulating the immune system. Since the most frequent reason for bad outcomes in patients suffering from covid-19 is that the immune system goes berserk, the thinking is that fluvoxamine might help to prevent such bad things from happening. And since fluvoxamine is a cheap, generic drug that’s been around for decades, that would be great if it turned out to be true. Unlike the new anti-covid drugs coming out from Pfizer and Merck, it wouldn’t destroy countries’ health budgets if used widely. Roughly 10-15% of most western countries’ populations are already on an SSRI.

Back in November 2020, a trial showing promising results was published in the Journal of the American Medical Association (JAMA). 152 people diagnosed with covid, with mild symptoms not requiring hospitalization at the point of inclusion in the study, who had experienced symptoms for less than a week, were randomized to receive either fluvoxamine daily for two weeks or a matching placebo. Four patients ended up being hospitalized in the placebo group, while not a single patient was hospitalized in the fluvoxamine group.

This was a small study, so the results were suggestive of benefit, but they hardly constituted proof of anything. Which is probably why the study ended up being ignored. Until now, that is.

Another study investigating fluvoxamine as a treatment for covid-19 recently published its results in Lancet Global Health. Like the earlier study, it was a double-blind randomized controlled trial. But it was bigger, much bigger. 1,497 patients were randomized to receive either fluvoxamine or placebo. For a randomized trial that is a big number.

The trial was carried out in Brazil. It recruited adults with symptoms suggestive of covid-19 and a positive covid antigen test, who had started to develop symptoms less than a week earlier. As in the previous trial, participants could not be sick enough that they required hospitalization on inclusion in the study, since the whole point of the trial was to see whether the drug decreases risk of hospitalization. The average time after symptom onset at which participants were included was four days.

In order to be included in the study, participants also had to have some underlying health condition that would predispose them to more severe disease – this is a sensible decision, because very few people with covid-19 actually end up requiring hospitalization, so even with 1,500 people it’s questionable whether you would find a statistically significant difference in hospitalizations, even if a drug works, if you didn’t restrict yourself to high risk individuals.

Participants in the intervention group received 100 mg of fluvoxamine twice per day for ten days, while those in the placebo received an identical placebo. So, how did things turn out?

10.3% of participants in the fluvoxamine group ended up being hospitalized, compared with 13.1% of participants in the placebo group. If the effect is real, that would mean that for every 35 people with covid that you treated with fluvoxamine, you could prevent one hospitalization. Which doesn’t sound extremely impressive, but it’s not nothing. The relative risk reduction is 22%, which would mean that roughly one in five hospitalization could be prevented – for a stretched health care system in the middle of a big covid wave, that could be a meaningful differnce.

But is the effect real?

Well, that’s hard to say. The result isn’t statistically significant (p-value 0.09), which could mean that the study was simply too small to find a difference, or it could mean that the difference found in the study was due to chance and there is in fact no real world difference.

It’s worth noting that the authors themselves claim that there is a statistically significant difference, and that 11% in the fluvoxamine group suffered a “primary event”, compared with 16% in the control group. However, this is based on some statistical shenanigans, where the researchers have combined hospitalizations with emergency room stays longer than six hours. From my perspective, spending an extra hour or two in an emergency room is a completely different thing from being hospitalized, and the two shouldn’t be conflated. They certainly shouldn’t be combined in to a composite end point.

Additionally, the primary endpoint was changed to its final form (hospitalizations + emergency room visits longer than six hours) in March, when the authors had already started gathering data, which is very suspicious, and suggests that they chose the primary end point after they’d looked at the data and seen what would generate a “statistically significant” result. This is a big no-no – you’re supposed to choose the primary end point before you start gathering data, and then stick with it.

Otherwise it’s too easy to cheat and mine the data until you get a result that seems important, and then claim that what you discover is what you were looking for all along. So, as usual, the best thing to do is to ignore what the authors claim about their results, and instead look directly at the data. And what those data show is, as mentioned, a 10% vs 13% difference in hospitalizations that isn’t statistically significant.

What about deaths?

2.2% of participants in the fluvoxamine group died, compared with 3.3% in the placebo group. If real, that would mean that you could prevent one death for every 99 high-risk adults with early stage covid that you treat with fluvoxamine. That might not sound extremely impressive, but it would also mean that 31% of covid deaths could be prevented simply by giving people fluvoxamine at an early stage in the disease course. As before, however, the difference doesn’t reach statistical significance (p-value 0.24). Whether that means the result is due to chance, or that the study was simply too small to detect a difference, even though one exists, is impossible to say.

So, what can we conclude?

This study has generated a lot of buzz, but that buzz is based on a composite outcome of questionable validity. The results are certainly trending towards a benefit, but more data is needed before a firm conclusion can be drawn as to whether fluvoxamine has any role in treating covid-19 or not.

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26 thoughts on “Is fluvoxamine effective against covid-19?”

  1. “Since the most frequent reason for bad outcomes in patients suffering from covid-19 is that the immune system goes berserk”

    Is that in vaccinated or unvaccinated cases?

  2. A little mistake here in this sentence, you used fluoxetine, not fluvoxamine: “…and that 11% in the fluoxetine group suffered a “primary event”…”

  3. What about timing?
    I would like to see a study where hundreds of thousands of people had some pills prior to getting ill. Directly after symptom onset they start taking them. Preferrably doubble blind RCT but I would also regard an observational study (big enough) having high value if the signal is strong enough. (This whole Fluvoxanine thing stared at a mental hospital where patient were on this drug before the virus reach them. Noone (?) became ill if i remember it correctly)
    The same goes for IVM.
    But of course, nobody really cares about saving lives, it just a matter of making profit.

  4. I recall hearning an interview with some doctor last year which started the whole fluvox train. In it he claimed that individuals in some kind of institution (prison, hospital??) who were on fluoxetine (ie Prozac) had a much lower mortality/morbidity from Covid than those who were not. Cannot find the link.

    A possibly significant difference between the two studies you discuss is the dose used: earlier study used 100mg/day; the second 200mg, a full average therapeutic dose for depression. This echos the study that “proved” hydoxychloraquine was not just ineffective, but damaging – they used a very high dose in very sick patients as I recall.

  5. Very sensible assessment. Also the mechanism of simply calming people down (especially those who know they are at heightened risk) could be protective, which is fair enough, but not really what is being proposed.

    Given how many people are already on SSRIs you would have thought that some observational data could be found relating to differential outcomes in that group if there are any. If it only works when you are put on fluvoxamine but not when you are already on it, that would argue for my hypothesis.

  6. Hi, I’m CEV and thoroughly depressed in main part due to horrid side effects from 1st AZ jab. I’m currently taking fluvoxamine. I asked my doc for it specifically because of the studies. If it helps me stay out of ICU and the sanatorium I’ll be happy with the outcome. 🙂

  7. “The results are certainly trending towards a benefit, but more data is needed before a firm conclusion can be drawn as to whether fluvoxamine has any role in treating covid-19 or not.”

    Ridiculous. No, you do not need more data. No, you do not need a firm conclusion.

    The data very obviously says it works – whether or not their conclusions are correct. That both studies could be wrong is completely irrelevant because both certainly trend towards positive efficacy in the same direction as most of the other studies. The key point I’m making is – fluvoxamine is safe to use, so even if it doesn’t work, that’s okay.

    By the way, the first small study used 100 mg doses three times a day for 15 days. The second much larger study used 100 mg doses once a day for 10 days. These two studies are in no way comparable -except they both said fluvoxamine works. Or more correctly, they both did not say that fluvoxamine does not work.

    If it’s safe to use and might work, what do you have to lose? That should be the one and only conclusion of all these studies. The statistics, which are always wrong in more ways than anyone can
    ever know, can be ignored. That’s why so-called Medical Science and evidence-based medicine are bunk and that’s why biomedical studies cannot be replicated, even by the same researcher.

    The correct covid treatment protocol is to stack as many possibly effective safe interventions as possible.

    Additionally, parsing studies on vitamin D3 and Ivermectin is also a ridiculous waste of time – they too are safe and cheap and likely effective.

    1. I disagree. Fluvoxamine, like all SSRI’s causes a lot of pretty nasty side effects, especially during the first few weeks of use. So I don’t think it should be used unless it’s been clearly shown to work. Vitamin D and ivermectin have much better side effect profiles, so I’m more inclined to agree with you when it comes to them, that there is little to lose.

      1. Fluvoxamine, being an SSRI, should not be used indefinitely – that’s right.

        But it for 15 days, three times a day, No Problemo. It’s benign safety profile is better than other SSRIs and it can be used just as well for kids and oldsters. Even if you overdose (10 grams), no real problem. Has there ever been a death? I don’t think so and there are no known problems associated with long term use. One might take some care if the individual has renal impairment, but that’s easily monitored.

        Side effects such as mild headache or mood swings or transitory tingles are not particularly nasty and they should resolve in a week, if not, you adjust the dose. The objective is to end a real-life covid crisis which can get out of hand and kill you dead (if over 70 with 2.6 comorbidities) and that’s where the primary focus and concern should be, not on temporary discomfort. Same with D3 and Ivermectin.

        The reason for the pandemic is mostly due to academic medicine insisting on expensive long-term studies of drugs that are proven safe and vouched for by front-line doctors. And the reason for that is pharma profit, not patient safety. It’s the precautionary principal stood on it’s head.

  8. Yet another way then to traet this “novel” disease that apparently had no cure!

    This young, British lawyer has filed a complaint with the International Criminal Court ‘on behalf of the peoples of the UK, alleging crimes committed by UK government officials and international world leaders of various violations of the Nuremberg Code’.

    In it, she mentions several remedies that seem to have been deliberately over looked including Hydroxychloroquine, Ivermectin and Favipiravir.

    1. The question is where are all the other lawsuits? This is yet another anomaly alongside no animal safety studies, unblinding of the initial cohort, no autopsies, no medical need for the injection, media silence, Fauci still in charge, pandemic definition changed to not require massive deaths, vaccine definition changed to not require , quarantining healthy people, so-called vaccines that do not work, ignoring disparaging and censoring effective inexpensive safe drugs protocols, medical journals publishing obviously flawed studies, threatening MDs who treat early with loss of license, ignoring the preponderance of the evidence regarding lab creation, ignoring bioweapon engineered viral sequences, ignoring the oldsters who are by far most at risk, FDA ignoring the Ivermectin systematic review, no natural immunity anymore, science being censored, more vaccines because the first ones did not work, no media coverage at all of the vaccine deaths, saying the pandemic is caused by the unvaxxed, vaxx deaths greater than viral deaths (6:1 if age 20, 2:1 if age 80), no stop condition, calling Nobel prize winners conspiracy theorists, labeling science not aligned with the false narrative a conspiracy theory, calling anyone who questions the fake narrative a dangerous conspirator, ignoring vaccine pressure as the cause of variants, not empaneling the usual safety boards overseeing the rollout, vaccinating into a pandemic, scrubbing vaccine deaths off VAERS, telling everyone the vaccines are safe, the lack of informed consent, mandates on lockdowns and masks that have no policy-level (scientific) evidence, no consideration of total harms, shutting down small business but not the big box stores, injecting little kids with no medical necessity, and lies, lies everywhere – for an illness that has killed just .012% of the global population and has a IFR of 0.14% compared to 0.1% for the influenza.

      So where are all the lawsuits against the media lies, the national governments, Pharma, the politicians, state and local governments and businesses illegally mandating masks, vaccine passports, and injections, the captured regulatory agencies, the MDs who inject despite the evidence, Fauci, hospitals the vent you even when you do not test positive?

      That’s a lot of money left lying on the ground – all with prima facie evidence. Where are the lawyers when we need them?

      1. There are only about 2,500 lawsuits at the moment – there should be Millions. Literally, everyone in the world should be suing their governments and Pharma and everyone involved perpetrating this crime against humanity. The United Nations has been taken over by the World Economic Forum so they’re no help. And what about the billions of compliant citizens who just do what they’re told without question? Sue them too. Since it’s the global Elites and the CCP and Global Finance that seem to be behind this perfidious campaign, there’s plenty of money to be had.


  9. Hi Sebastian, I have some thoughts about the recent WHO and ECDC report estimating that almost half a million human lives (60+ years) in Europe have been saved. What are your thoughts on that and is there any official statistics which shows that the vaccine has caused more deaths than saved lives?
    There has been more than 85 000 side effect cases. How many have actually been identified and what percentage are by definition serious of these?
    I’d be very thankful for your answers.

      1. The point is not that RCTs are bad or that they can be corrupted, as anything can, but that RCTs can only focus on one thing and can be confounded in some situations, whereas retrospective studies can get many different kinds of data. In fact, without anecdotal data, we would know precious little as regards medicine.

        In the context of covid, let’s consider how much of our data is anecdotal/retrospective…

        1) nursing homes are hotbeds of covid
        2) covid is spread by aerosols
        3) PCR is pretty useless in diagnosing mild covid by itself
        4) data about covid cases is useless, whereas data about covid deaths has some utility
        5) covid vaccines wane quickly compared with polio vaccines
        6) covid is a coagulopathic disease (that data comes from autopsies, which are anecdotal)
        7) Mask mandates have no effect on spread of covid
        8) Social distancing has no effect on spread of covid
        9) older people have more risk from covid
        10) about 40% of the population has inherent immunity to covid

        …for a few examples

        Let me quote some from Healy, as he makes some great observations about RCTs…

        “This is true in every clinical situation where drugs and conditions cause superficially similar effects – diabetes and glitazones both cause heart failure, osteoporosis and bisphosphonates both cause fractures – and this makes it impossible for an algorithmic exercise as most RCTs are to establish what is happening.”

        translation…cause and effect goes out the window when there are similarities between conditions and treatment effects

        “In a depression trial, investigators focus intensely on one thing – does Prozac have an effect on mood. Pretty well everything else is ignored. The statistics we use don’t work unless there is an intense effort to collect everything we can about this one outcome.

        And so, depression trials miss something that happens to almost everyone who takes an SSRI within 30 minutes of the first pill – your genitals go numb. You can search the RCTs on these drugs and all you will find is that perhaps 5% of people have sexual issues on these drugs.

        Emotional numbing is another extremely common effect almost completely missed. This is how these drugs help. This is how these drugs might help someone diagnosed as depressed but the key point is that it is much more common than depression recovery.

        Similarly in the vaccine trials, the common thing is a multiplicity of Spike protein effects – doing this we hope might help but if we are hypnotized by what is hoped for we will miss and have missed what these Spike proteins are actually doing.

        ***If we just depend on RCTs, we end up knowing almost nothing about a drug.***”

        When it comes to medical questions and research, questions of confounders and hypotheses are up in the air. So we must choose the best tool for the job, which depends on what is the mountain and what is the mole hill. Sometimes bias is a mountain, but not always nor even often. And RCTs are typically expensive to run, which limits who can use them as a tool. Which is not clinicians. And we have a whole lotta clinicians out there and it would be a shame to not use their knowledge, observations, and expertise.

        RCTs should be considered just one tool in the toolbox. Not the “gold standard,” by any means. That is just pharma’s propaganda, intended to allow them to capture research.

  10. I got Covid for Christmas, does anyone know of a good list of readily available supplements that can help the immune system?

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