Please see my answer on Quora for the most up-to-date version of this article.
I’m the Executive Director for the COVID-19 Early Treatment Fund (CETF), an organization that funds researchers from all over the world pursuing promising drugs against COVID. We’ve evaluated more than 60 grant proposals and funded 14. This gives me a bird’s eye view of many of the most promising treatments.
The advice you get from the CDC and Dr. Fauci is very conservative based on the most proven science. They will not recommend a drug unless it passes Phase 1, 2, and 3 trials because doing so would violate the public trust; they must only recommend treatments that pass the bar that the medical community has set. This is why you won’t hear Dr. Fauci talking about most of the treatments listed below. It’s not because he’s a bad guy; it’s because his position simply doesn’t allow him to do that.
The net result of the current CDC advice is that in America about 100,000 people die from COVID each month. And even if you recover, a lot of people will be left with long-term to permanent impairments in neurological or lung function. A third of recovered patients from COVID will return to the hospital within 5 months and 1 in 8 die. It couldn’t be more obvious that the current advice isn’t working out very well.
But if our goal is simply to minimize the number of deaths per unit time, and we are OK about being wrong once in a while because saving lives is more important than our reputation, then we can look at drugs that are just shy of the Phase 3 bar and ask the question: is it more likely that this drug will save lives? Cause even more deaths? Or could it go either way and we need to wait for more data?
When we change the problem we are trying to solve, we find that we have evidence-based treatments today that have a high probability to significantly reduce the hospitalization and death rates and reduce the chance of any long term impacts with virtually no incremental risk. It thus wrong, and an unnecessary loss of life, to “wait for more data” (such as a phase 3 trial).
A key opinion leader (KOL) panel, people from NIH, CDC, and top academic institutions, met on Jan 22 to review the fluvoxamine evidence. They voted afterward to support “shared decision making” TODAY (between doctor and patient) on fluvoxamine by more than a 2:1 margin (note only 20 of the 30 cast votes). So they were voting in their PERSONAL capacity, and NOT in their OFFICIAL capacity. So even though the guidelines panel will wait for a phase 3 trial because of the “public trust” issue in their recommendations, the doctors overwhelming agreed that the weight of the evidence merited a discussion today between doctors and patients (and NOT waiting for more data).
What this means is if you are interested in maximizing your life expectancy, you must look outside the CDC guidelines.
The confidence level in some of these drugs is quite high.
For example, for fluvoxamine, with the two studies, it is 99.99% certain that the drug works, and there is a 95% chance that it will reduce hospitalization/death rates by 75% or more. NOBODY has been able to come up with a comparable case (where there are multiple independent observational trials with large effect sizes and high statistical significance, a clear mechanism of action, an RCT and RWE with p<.0001) where the phase 3 failed! Therefore, the chance of failure of Phase 3 should be considered negligible. A simple mathematical expectation calculation based on the 95% effect size (75%) and the probability of failing in Phase 3 (less than 1%), makes it obvious that taking the drug is better than not taking the drug.
So you don’t have to trust me or the experts; you can trust your own math calculations. No matter what your assumptions are, it’s hard to conclude anything but it’s better to take the drug.
Therefore, waiting for “more data” (such as a phase 3 trial) before making a decision is simply dumb because there are no good solutions today. If you were drowning and someone threw you a life preserver, would you avoid using it until the phase 3 trial completed? I wouldn’t! I’d use it and if it didn’t work, you’d request that they throw you the life preserver with the next highest effect size.
Similarly, using HCQ as the excuse to raise the evidence bar is dumb. If the first 3 life preservers broke and someone threw you a fourth life preserver would you say, “Hah, I’m not falling for it this time! Let me see the phase 3 data first!” ?
Nearly all the drugs listed below are the most effective when used as soon as you know you are infected. Because tests can take a while to come back, if it were me, and I thought I was exposed to COVID and had one or more of the telltale symptoms, I would rush to get a fluvoxamine prescription ASAP.
These drugs can still be used at later stage, in the disease but:
- you may have to use the drug longer than 14 days (one hospitalized patient took 9 weeks to fully recover on a fairly low dose of FLV)
- you may have to increase the dose to that you can tolerate without side-effects (never exceed the FDA limits)
- you may be too late to reverse permanent damage caused by the virus.
Fluvoxamine and Ivermectin have emerged as the two most promising drugs on my list. Both can be prescribed today by any doctor off-label, are widely available, extremely effective, low cost, supported by strong evidence, and have a low side effect profile. Both drugs may be given at any stage.
If everyone in the world just did one thing differently, talking to their doctor about whether they should start fluvoxamine or ivermectin immediately after they learned they were COVID positive, our hospitals and ICUs would be nearly empty today and there would be very few “long haulers.”
The problem is that the level of evidence for these novel treatments doesn’t yet rise to the level now required to change treatment guidelines which require large Phase 3 RCTs and/or an EUA. This is a huge problem because this is a pandemic and FDA approved drugs should be held to a lower standard of proof than novel drugs since they have a known safety profile.
For example, the p value of the Fluvoxamine evidence after just 2 studies (both with 100% effectiveness) is just .0001, i.e., 99.99% certainty that the outcome didn’t happen because we randomly got a lucky mix of patients. There is a 95% chance the effect size is 75% or better.
But people don’t trust the math because only 60% of Phase 2 studies are confirmed in Phase 3. Put it another way, if you are about to be shot by a gunman and someone hands you a bulletproof vest that had a 100% success rate in protecting the last 157 people, do you say, “I need more data”? Or do you take the vest? That’s the decision we are talking about here. The NIH would want more data before advising you to put on the vest.
But the evidence for both drugs doesn’t rely on just multiple randomized trials. It relies on many independent data points, evidence of all different types. The chance that there is no protective effect for these two drugs is close to zero. So there is an almost certain benefit and the downsides for fluvoxamine, for example, are about the same as taking tylenol for 2 weeks according to doctors who are most familiar with the drug.
There is an excellent op-ed in the WashPost by Dr. Jeffrey Klausner about using drugs like fluvoxamine off-label immediately using a process known as “shared decision making.”
You should always consult with your doctor before following taking any supplement or drug. There are a variety of options available below. You and you doctor may be more comfortable with some than others, so I’ve listed a range of options. If your doctor won’t prescribe the drug, certain online telehealth providers such as CityHealth Urgent Care are able to assist with getting a prescription. For hospitalized patients, court orders may be necessary.
The biggest mistake people make is underestimating this disease. I can’t tell you how many people will read this article and ignore the advice perhaps reasoning, “well if this is true, I’d be reading about it in the press.” That’s a good argument, but it is wrong. As I explained earlier, this is the next level of evidence down and the press will only report on the top tier evidence because they don’t want to tarnish their reputation or raise “false hopes.” The problem of course is that the CDC guidelines are inadequate: everyone now knows that with hospital capacity now at an all time high as this is being written. So, I would argue, we should look at the treatments with the “next best” level of evidence. That’s why I wrote this article.
The side effects of this disease (including organ damage, permanent blindness, and death) can happen relatively quickly and be devastating and irreversible. If I got infected, I would, without hesitation, treat it as early as possible using the options below. I would not wait for first symptoms as your first symptoms could be irreversible. Would you play Russian roulette with your brain and body? I wouldn’t. If you lose the results can be devastating.
A lot of physicians will consider these drugs only for patients who are most at risk of hospitalization. I think this is a huge mistake because it’s your life and nobody can tell you for certain how the virus will affect you. If there is no downside to the drug and it can reduce your chance of hospitalization by 90%, why wouldn’t you want the drug? For fluvoxamine and ivermectin, for example, the dosage is so low that any side effects are rare, minor, and go away when you stop the drug. A lot of this is simply fear of the unknown: their inexperience in prescribing the drug and trying anything new. Doctors who prescribe the drug on regular basis (psychiatrists) have no such fear.
Here’s a list of the options I would consider to treat the virus. This is not to say that these are your only good choices; these are simply the ones I believe are the most effective with the best scientific evidence. Whether or not to combine these options is something you should discuss with your doctor.
For me personally, I’m not on any drug for prevention. If I get COVID, I’ll take camostat, lactoferrin, metformin, and fluvoxamine. In the unlikely event I had worsening symptoms, I’d add in ivermectin, doxazosin, and fenofibrate.
Case 1: Drugs for prevention
Note that none of these options actually prevents you from getting COVID. If you are exposed with enough virus, you will get it. What these drugs will do is fight the virus super early when it is easiest to defeat.
- COVID vaccination: I will try to get vaccinated as soon as possible. After you are fully vaccinated (2 weeks after your second dose is the safest margin), you can generally ignore the rest of this article. In the US, the differences between the vaccines are minimal; I would get the first one offered to me. You can still get the virus even if you are vaccinated. If your symptoms are noticeable, then the drugs below can help.
- MMR-II vaccination: If you have a measles-mumps-rubella vaccine, there is correlation that if you get COVID it will be less severe. This may explain why kids don’t get much COVID. The speculation was confirmed in an RCT in Brazil in January 2021: Volunteers vaccinated with the triple viral had a 54% reduction in the possibility of having Covid-19 symptoms, while the risk of being hospitalized dropped to 74%. The paper is not yet out though so for now this is too early to recommend.
- Ivermectin (IVM): All drugs have risks. But if I felt I was a high risk of getting COVID (e.g., a family member was diagnosed or I was more socially active), my first choice would be prophylaxis by taking .1mg/kg of Ivermectin every week, i.e., taking two 3mg tablets every Monday. In developing that dosing, I consulted with Dr. Pierre Kory, founder of the FLCCC. As if January 1, 2021, there is a great deal of evidence supporting this choice, more so than any other option listed below (including 59 RCTs now in progress on Ivermectin for the treatment of COVID, 3 of which are in the US). There is a wide body of evidence suggesting that ivermectin is effective against a wide range of both DNA and positive-sense single-stranded RNA viruses such as SARS-CoV-2. The Carvallo study is incredibly impressive (0 of 788 people got sick vs. 58% in the matched group). A more recent study in Bangladesh found similar results (note that dosing there was once a month which was not sufficient to protect everyone). Dr. Kory, who arguably knows more about IVM for COVID than just about anyone, is walking the talk by using IVM as a preventative rather than being vaccinated. Merck can put out a Company Statement saying that ivermectin is useless against COVID, but that doesn’t make it true. People will have different opinions and that’s there opinion. The IDSA also came out with a recommendation that Ivermectin only be used in the context of a clinical trial because they didn’t like the quality of the studies.
- Lactoferrin: Jonathan Sexton and colleagues at University of Michigan have demonstrated anti-viral effect of lactoferrin in vitro. The suggested dosing for treating the virus is 1g twice a day (i.e., a total of 2g/day). No prescription needed. Available on Amazon. Adding lactoferrin can’t hurt and may give you some additional protection.
Case 2: Drugs for treatment once you are infected
Every virologist would tell you that the best way to fight a virus is to treat it early with antiviral. For that reason, I have worn an Oura ring every night since the pandemic started because a night time temperature rise is often an early sign of infection (not a daytime temperature rise). If I see my temperature rise beyond my normal range, I’m going to pay extra get a same-day COVID test to verify. The virus doubles in size in vivo around every 10-12 hours (we think), so every hour is valuable for getting the best possible outcome.
- Approved monoclonals: Because I meet the eligibility criteria, I would try to get one of the two monoclonal antibody treatments approved by the FDA. Bamlanivimab is made by Lilly, casirivimab and imdevimab are made by Regeneron. They require a infusion (a 30 minute process or longer) which is done either in your home or the hospital. It is not yet known whether the monoclonals will be effective against virus mutations. Basically, it gives me an extra edge in fighting the virus. The FDA I think made an error in setting the dosage well below what was proven effective so this option gives you an “edge” rather than being 100% one and done.
- Fluvoxamine (FLV): As soon as I found out I was COVID positive, I would immediately start taking 50mg twice a day since this was shown to be the minimum effective dose for a 100% effect size. However the numbers in the Seftel study at that dose were small (N=77 in the treatment group), so it is possible that a higher dose may provide even better protection (e.g., for elderly), but the side effect profile is higher. You can ramp up to 100mg twice a day safely and the psychotropic effects are minimal for a 14 day duration even at the higher dose. On average, at 50mg BID, it takes about 3 days to reverse COVID symptoms and return to normal. Even lower doses appear to work as well, e.g., 50mg once a day. I would avoid caffeine while on drug (FLV jacks up the intensity and duration). It is even safe to take the drug at this dose and duration if you are pregnant (that should tell you how safe it is!). I’ve not yet heard of a single case of someone taking the drug and not recovering. The retrospective data shows that some people on the drug still get hospitalized, but it isn’t yet clear if they got hospitalized because of the COVID or for some other reason. There are several reasons I prefer FLV to ivermectin: 1) I personally know and can vouch for the quality and integrity of researchers and the trial methodologies, 2) the trial was published in JAMA showing a 100% success rate and despite 120,000 views, nobody found any confounders, 3) it continued to be 100% successful as a monotherapy in a real-world study with a very challenging patient ethnicity mix, 4) in the opinion of mainstream docs at this point, FLV is the hands-down choice between the two because of the quality and consistency of the evidence and the clear mechanisms of action, 5) It’s really hard to argue with the 100% success record (compared to inconsistent readouts with IVM) 6) its effective at low dosing and has no side effects at that dose, 7) we know that it is safe long term for anyone who takes it, 8) it gets out of your system fast as soon as you stop taking it, 9) In the Seftel trial at Golden Gate fields, there were 0% hospitalization and 0% long haulers vs. 12.5% hospitalization and 60% long haulers in the no treatment group, 10) in general, doctors have less of a problem prescribing FLV than IVM, and 11) costs less than $10 for the entire treatment even if you don’t have insurance. The immediate release FLV (generic) is cheaper and more available and is actually preferable to the controlled release version (since it gets to work faster for you).
Another option is to enroll in the fluvoxamine clinical trial.
- Fluvoxamine is the perfect option for people who don’t have a doctor, don’t have health insurance, or can’t afford to pay a doctor. The trial is free and is open to anyone in the US in all states. You can enroll from the comfort of your home; no clinic visits are required. You don’t even need a computer to enroll. The extra benefit is you’ll help contribute to scientific research. I personally don’t know of any doctor that has seriously looked at all the data with an open mind that wouldn’t take this drug if they got COVID.
- Ivermectin: Ivermectin comes in second for the drug I would take if I got COVID (for the five reasons cited in the previous paragraph). The dosing for IVM once you are sick with COVID is not the same as the dose for prevention. At this stage you are looking at much higher dosing than was used for prevention: 0.2mg/kg per day for up to 5 days (vs. the 0.1mg/kg once a week for prevention). IVM is a potent antiviral and anti-inflammatory. See the FAQ on Ivermectin for more info. IVM will give you an 83% reduction in your chance of death if you get COVID. See also Should I take ivermectin or fluvoxamine or both?
- Colchicine: This drug is 25% effective in reducing hospitalization. See Efficacy of Colchicine in Non-Hospitalized Patients with COVID-19. So this is an option if you can’t get any of the other drugs above. The mechanism is probably synergistic with ivermectin and fluvoxamine, so adding colchicine likely can’t hurt.
- Mirtazapine: This drug was remarkably effective on its own in Hoertel’s retrospective antidepressant study (effect size comparable to fluvoxamine). This paper Inverse Association between Serotonin 2A Receptor Antagonist Medication Use and Mortality in Severe COVID-19 Infection - PubMed provides independent confirmation of the massive effect size. When used with a 14-day course of Fluvoxamine 50mg BID in early treatment of COVID-19, one would simply add mirtazapine 15 mg once daily, administered in a single dose, preferably in the evening just prior to sleep. Mirtazapine is similar to cyproheptadine in its mechanism of action, as a direct antagonist of 5-HT2 receptors (A and C primarily, but also B). Mirtazapine has some sedative activity similar to cyproheptadine via its H1 inverse agonist activity, but it is well tolerated when taken at night.
There are a number of experts who believe that the combination of fluvoxamine and mirtazapine may prove to be a highly effective early treatment in COVID-19 (i.e., will emerge as the standard of care) for several reasons:
- 96% effect size: Each drug is around 80% effective on its own (in multiple studies), so the math suggests that the combo should be around 96% risk reduction (because the receptors each covers are complementary (serotonin transporter in fluvoxamine, 5-HT2 receptors in mirtazapine) as is the mechanism of action: fluvoxamine depletes serotonin in the platelets, and mirtazapine is a direct antagonist of 5-HT2 receptor, so any excess serotonin released from activated platelets in severe COVID-19 has a lower risk to inflict serotonin-mediated lung and systemic injury.
- Lower side effects: The combination is safe, commonly prescribed in treatment of depression, easy to do, and better tolerated than either drug alone (i.e., mirtazapine counteracts the insomnia and the nausea one may get with fluvoxamine used, particularly at higher initiation doses). Mirtazapine on its own, or in combination with other SSRIs, does not cause “serotonin syndrome,” since its mechanism of action excludes this possibility (mirtazapine is a serotonin antagonist).
- Win-win: The combo is a “have your cake and eat it too” match made it heaven: higher efficacy, lower side effect profile.
- Familiar: A large number of people are already on the combination of mirtazapine and an SSRI today (for depression treatment), and therefore physicians are comfortable prescribing the combination without fear of harm. Mirtazapine is cheap and widely available. Mirtazapine alone is very commonly prescribed. One physician wrote: “Remeron is my favorite anti-depressant. I use Remeron as my primary anti-depressant because it is the best at promoting sleep and reducing anxiety levels”
- Expert recommendation: If Farid Jalali MD or his family got COVID-19, this is what he’d personally consider for his loved ones (he had his parents on early SSRI and mirtazapine during their COVID-19 illness) as a safe and very promising early therapy with a highly plausible mechanism of action to prevent severe illness. Farid is an expert on the increasingly recognized role of platelets and platelet serotonin in COVID-19. Watch Farid’s 1.5 hour lecture and you will be convinced:
Harder to get drugs:
- SNG001: Only available in clinical trials, this inhaled interferon can reduce chance of getting serious COVID by 79% (see Synairgen's inhaled interferon for COVID-19 enhances short, harmless version of virus entry point: study).
- Bromhexine and nitazoxanide: Bromhexine is available over the counter outside the US and nitazoxanide is FDA approved. The combination may prove to be more more effective than bromhexine and HCQ because nitazoxanide is effective on its own. Note that a large effect (5x) was confirmed in an open label randomized trial of bromhexine and HCQ.
- AZD7442: There is another promising monoclonal, AZD7442, that is long-lasting, but only available in clinical trials. See COVID-19 long-acting antibodies discovered by Vanderbilt University Medical Center move to phase 3 clinical trials.¶
- Camostat: The antiviral with the next best track record so far is camostat. This is the drug that is the first choice for many of the world’s top coronavirus experts because it inhibits TMPRSS2, a key enzyme needed for the virus to replicate. Camostat is readily available via enrolling in a clinical trial out of Yale University. If you are in the New Haven area, please enroll in the Yale clinical trial. It will soon be open at more sites such as the University Hospital network in Ohio. Do not exceed 2.4g per day! Typical dosing is 200mg every 8 hours (i.e., 600mg per day), but if you can tolerate double that, you’ll likely give the virus a more difficult time (at the expense of some nausea).
- Interferon lambda: This drug is only available in a clinical trial in certain locations. The virus basically turns off your immune system when it gets into your body, so by injecting exogenous interferon, it basically compensates for this and returns your immune system to normal. This drug is extremely safe with a very low side effect profile (so low it is unmeasurable). One study showed it is far more effective than any of the approved monoclonals. It’s also much easier to administer than a monoclonal; it is a single shot in the arm, ideally within 3 days of first symptoms (the earlier the better). But there were conflicting studies on this drug published just 9 days apart (Stanford vs. Toronto), so there will be a Phase 3 trial to resolve the conflict. If it validates the Toronto study, this drug could rise to be the most important single drug to get as soon as you know you are infected since it will likely work for all mutations of the virus (and can be useful for future pandemics as well).
- GS-441524: This drug is a precursor drug in the manufacture of remdesivir. It has been shown to be safe in humans, cheap and easy to manufacture, and can be put in pill form. It is remarkably effective against all RNA viruses (including the coronavirus). This drug may be the most important discoveries in the fight against COVID and future viruses.
- EXO-CD24: This drug just completed phase 1 trials where 29 of 30 patients with moderate to severe COVID recovered in 3–5 days.
Case 3: Drugs for use post-infection (anti-inflammatories)
Once I learned I was infected, I would ALSO immediately also start on an anti-inflammatory drug. The reason is simple: to reduce the chance of permanent brain damage that could disable me for the rest of my life.
I’ve listed the drugs in order of effect size. I wouldn’t have any qualms about taking any of these drugs/supplements.
- Fluvoxamine: (see above)
- Ivermectin (see above)
- Doxazosin: Doxazosin has a clear mechanism of action for lowering inflammation. Dosage is 2 mg taken once a day. I’ve got hypertension already (that isn’t fully controlled with the meds I take now), so there is no risk to me that it would lower my blood pressure too low. The researcher who discovered this is Bert Vogelstein, who is the most cited scientist of all time in any field. I know many top people at John Hopkins have stockpiled this drug after Bert discovered it. That pretty much tells you what you need to know. The effect size is around 50% in observational data (often the effect will be larger in an RCT) and there are no randomized trials or real world evidence prospective trials like with fluvoxamine, so that’s why this ranks a distant second to fluvoxamine. It should definitely be tested ASAP.
- Fenofibrate: Like with Metformin, I would not hesitate to get a prescription for fenofibrate. This drug is cheap, widely available, and widely used. It has a very low side-effect profile and has been shown in human studies to be very protective against inflammation in the lungs. Used alone, gives you approximately a 6x better chance of escaping an ICU admission. Dosage is 145 mg/d, the same as in the clinical trial.
- Budesonide: The findings from 146 people – of whom half took 800 micrograms of the medication twice a day and half were on usual care – suggests that inhaled budesonide reduced the relative risk of requiring urgent care or hospitalization by 90% in the 28-day study period. Participants allocated the budesonide inhaler also had a quicker resolution of fever, symptoms and fewer persistent symptoms after 28 days. See Common asthma treatment reduces need for hospitalisation in COVID-19 patients, study suggests. However, Pre-print fails to distinguish between the reduction in urgent care, ER, and hospitalizations. It’s a composite endpoint (which is fair), but what’s the breakdown? example(s): A 90% reduction in hospitalizations = game changer. A 90% reduction in urgent care visits = underwhelming in an open-label, non-blinded trial What is it? (Unknown). So we really don’t know what to make of this drug!
- Metformin: If I wasn’t already on metformin, I’d get a prescription for it. Metformin has a very low side effect profile, it’s very safe (it’s safer than drinking orange juice, for example) and I was very impressed with the data showing it provides an extra margin of protection by reducing the chance of hospitalization by 40% according to observational data. So it’s a no-brainer addition to the mix even though fluvoxamine is already at 100%. According to Carolyn Bramante, who is running the metformin clinical trial at the University of Minnesota, the best dose is 500mg in AM and 1,000mg in PM.
- Hydroxychloroquine: This is hugely controversial. There are respected physicians who swear by it and point to this meta-analysis which is not peer reviewed and has numerous flaws. That doesn’t mean it doesn’t work. It just means that the scientific evidence of its benefit is less clear cut. For example, the Marik Sepsis Protocol works, but it hasn’t been replicated in RCTs. That doesn’t mean it doesn’t work. Clearly some physicians are using HCQ and claiming to have excellent results while other physicians remain quite skeptical. Around 95% of people get better on their own so unless you rigorously have controls, doctors who try HCQ can easily be fooled into thinking it is effective. However, there is a new paper out suggesting that combining HCQ with a TMPRSS2 inhibitor like bromhexine might be extremely effective. The paper states that “suppression of TMPRSS2 restores the antiviral efficiency of hydroxychloroquine.” The speculation of a large effect (5x) was confirmed in an open label randomized trial. There is also a HCQ and bromhexine clinical trial.
Case 4: Drugs for use if you get hospitalized
All of the drugs mentioned above are likely to still work once someone has been hospitalized, with the caveat that the more serious the case, the less likely the above drugs are likely to work. Once you are hospitalized, the options are much more limited and the effect sizes are smaller.
- Fluvoxamine: This hasn’t been formally studied in a hospitalized setting but every single anecdote we’ve heard (over 10) has shown that patients turn around quite quickly, even if they are hospitalized and are on high flow oxygen, in the ICU, or on a vent. A patient who was intubated took 300mg FLV per day. His CRP (a measure of inflammation) had been exponentially rising prior to the FLV. Immediately his CRP started declining and in only 14 days hit normal levels. Then, when the medication was removed, the CRP climbed be to higher than before in just 2 days and then he died. The FLV was keeping him alive. He would likely have fully recovered if they weren’t forced to remove the drug. They key point here is that it can take more than a week for people to see improvement if they start on FLV at a late stage. Tracking inflammation biomarkers such as CRP is a good way to verify that the drug is, in fact, working. One hospitalized patient treated by Alex Natividad MD took over 9 weeks on a dosage of 50mg BID to recover to normal. So be patient if you are taking it late stage.
- Cyproheptadine: This is an anti-serotonin drug. There's a big difference between COVID ARDS and non-COVID etiologies of ARDS, the degree of serotonin liberation which is basically highly toxic to multiple organs including lungs. One physician reports “we have 24-year olds with respiratory rates of 55 per minutes and impending doom completely resolve their tachypnea to normal respiratory rate within one day and get discharged within 48 hours with simple blockage of liberated serotonin.” Dosing is 12mg TID. Physicians having been using this for 6 months because it works. We are not sure whether it is for all ICU patients, or just for those showing signs that are suspicious for serotonin syndrome. Typically you don’t stop the SSRI: typically serotonin syndrome is due to platelets releasing serotonin, so it may be better to keep the SSRI in order to inhibit further release of serotonin from platelets. Cyproheptadine is a centrally acting antihistamine and anticholinergic: older adults will get delirious.
- Ivermectin: Same story as before. It still works at this stage, just not as well. Lots of data showing a beneficial effect at this stage in the disease.
- Cyclosporine: Use this at the late stage to combat inflammation. It will kill any immune response which is why you only want to use it late stage.
- Fluoxetine: There is convincing observational data that this drug works to increase your chances if you get hospitalized. I heard of an intubated patient who was given everything with no effect and the doctors were sure the person would die and gave the patient fluoxetine orally. Within 48 hours, the patients inflammatory biomarkers had dropped by an order of magnitude. SSRIs tend to be more useful at earlier stages and Cyproheptadine is going to be more effective at the late stage.
- Leronlimab: Now in Phase 3 trials. A promising drug for mitigating the cytokine storm for very sick patients.
- Zinc: Zinc has been shown in a clinical trial to reduce mortality by ~24%.
- RLF-100: This experimental drug can improve your chances of getting out of the ICU by a factor of 2.66 over the current standard of care.
Case 5: Long haul COVID
We don’t know yet for sure what will work best if you’ve had your COVID symptoms for over a month. Of course the best way is to have avoided the problem in the first place (e.g., by early treatment with fluvoxamine to prevent the damage).
Ivermectin is reportedly effective against long-haul COVID.
Fluvoxamine does work for all the long-haul patients who have tried it so far that we are aware of (6 of 6 patients). Sometimes it may take 7 days to see an effect.
If fluvoxamine makes things worse, Dr. Jalali advises patients to try a tricyclic antidepressant such as amitriptyline. This is counter-intuitive. See Serotonin and Platelets.
Why we cannot educate the doctors and must instead educate the public
We have done videos on the Doctor’s Channel where the docs educate the docs, but the viewership is too small. We’ve been shut out of all larger forums (Medcram, UCSF, etc) and told to “come back when you have phase 3 data and maybe we’ll let you speak.”
IDSA has not reviewed fluvoxamine but we are still trying.
The FDA will take months to review our EUA. And that’s considered “fast.”
No major academic hospital will hold a meeting to consider the fluvoxamine data, no matter how compelling it is. If you don’t have Phase 3 data, you will not be able to get on the agenda. It doesn’t matter how many lives you can save (not a criteria for getting on agenda). The reason is to protect the reputation of the institution.
No public health official in the US has allowed the docs doing the research to educate the docs in their county on life-saving evidence. It’s all about respecting the CDC guidelines. So those forums are off the table.
Jeff Klausner did convene a KOL meeting, but that was just 30 people. They overwhelmingly recommended shared decision making.
Shared decision making requires the patient to broach the subject because it is considered “improper” for a doctor to suggest treatments not proven in a phase 3 trial since this would be considered as “pushing” unproven treatments on a patient. So even if docs agree to do it, since there isn’t a good way to educate patients to ask, it doesn’t get done.
So patient education (like this answer) is important, as are sites that collect info such as the articles on Steve Kirsch Home page. Without patient education, there is no reason for the docs to act now. They will just wait for the Phase 3 trial and/or an EUA and not take any reputational risks in the interim reasoning if the science is good, the NIH would add to the guidelines.
Why you can’t educate the public directly
Without mainstream support by doctors, the press (with rare exceptions by smaller publications) will not write any stories about you or run your op-eds, even if lives may be saved.
You can try to advertise in newspapers, e.g., mention the expert panel recommendation to talk to your doctor and have that signed by 50 top docs. That would get people’s attention. The problem is that 1) the newspaper may refuse to run the ad since it would be promoting false cures that go against CDC guidelines and 2) it costs money and nobody is donating money to support such an effort.
You can’t speak to large group because they say “why don’t you educate our local doctors?” CATCH-22!
Why the NIH committee isn’t including fluvoxamine
We don’t know why, we are not allowed to find out why, and they are not allowed to tell us even if they wanted to.
NIH COVID guidelines committee consists of unpaid, volunteer committee of busy clinicians with no full time administrative staff.
Multiple NIH committee members participated in the Jan 22 KOL meeting. We have been told fluvoxamine is on their radar for consideration.
The timeline and deliberations are confidential.
Why other methods won’t work
You can’t go to a member of Congress. The HSGAC committee under Senator Johnson asked the NIH Guidelines committee how they made their decisions and was told that they continuously evaluate the data.
Shining a light in these processes is now harder because Biden signed an order to shut down transparency.
Celebrities won’t tweet about unproven treatments not on the CDC guidelines because they don’t want to tarnish their reputation. They are happy to do so after it is on the guidelines. Louis Gossett Jr. recorded a video on how he used ivermectin to save his life, but fewer than 10,000 people have viewed it.
Elon Musk won’t tweet about it.
President Biden will defer to his task force. The Biden task force then defers to the NIH.
You can post an article on Quora, but just 40,000 people who have read this article… rounding error in the grand scheme of things.
So now you know just how totally broken the system is.
This is why the virus kills so many people: we have the treatments, but our systems prevent us from using effective treatments.
Age range for fluvoxamine
Is there an age range where taking the drugs is riskier than the risk of hospitalization/death/long-haul COVID from the virus? Here are the risk numbers for hospitalization and death by age from the CDC and if you compare these numbers to the risk of death from 14 days of fluvoxamine at 50mg BID, you will find that the risk of death from the virus always is greater than the risk of death from the SSRI (provided it is properly prescribed). Kids recover from COVID but a very small subset do not and we have no way to figure out yet who that subset is. One difference is the cd147 activation of platelets increases as people age, we think so there may be far less platelet activation in kids due to this virus, presumably and that may be one of the reasons why kids have an easier time with the virus. Some doctors will say for kids under 10, it’s unneeded, for kids 10–14, debatable, and for kids > 14, for sure. But when you consider how little is known about MIS-C, and how dangerous it is (it is fatal for some kids), the advice not to give fluvoxamine to your kids could be a fatal mistake. What parent is willing to gamble on that? Fluvoxamine is only FDA approved for kids 8 and older. And kids may not be able to ramp the drug dosing as fast as adults (e.g., 50mg BID may be way to aggressive for kids).
Don’t underestimate the virus. I would treat it as soon as I knew I was infected, no matter what my age or risk factors were in order to minimize the risk of long-term/permanent organ damage.
As of Feb 13, 2021, my belief is that strongest combination will prove to be fluvoxamine and mirtazapine (50mg BID of fluvoxamine + 15mg QHS for mirtazapine for 14 days) due to the fact both are strong protectors standout drugs on their own and both operate using complementary mechanisms. If I were diagnosed today, this is the combo I would take without a doubt. Surprisingly, the side effects of the combo are actually lower than either drug on its own! So you can have your cake and eat it too: better protection, lower side effects!
If everyone in the world chose from the drugs in this article after learning they were infected, I believe that our hospitals and ICUs would be nearly empty today.
Would I take both drugs? See Should I take ivermectin or fluvoxamine or both?
In general if I’m not getting better day by day, I wouldn’t hesitate at all to add drugs like mirtazapine, lactoferrin, metformin, doxazosin, fenofibrate, bromhexine, and nitazoxanide, etc. to the mix, but it’s really impossible to know in which order so that may be gated by your doctor and availability of the drugs more than anything else.
I have collected the evidence supporting the use of fluvoxamine to make it easier for doctors to learn about the drug. Here is the data for ivermectin.
The available evidence today is so compelling that on December 22, 2020, Vikas Sukhatme, MD, ScD, Dean of Emory University School of Medicine, speaking on his own behalf, called for physicians to consider the off-label use of fluvoxamine in treating COVID. At a minimum, all physicians should be recommending their COVID patients enroll in the fluvoxamine clinical trial.
Why aren’t more physicians following the lead of Dr. Sukhatme? Dr. Joseph Ladapo answered that question very eloquently in his superb Wall St. Journal op-ed, “Too much caution is killing patients.” I wish every physician would read that op-ed. Most don’t have time to do the research, so they just follow the CDC guidance which basically says do nothing (unless you qualify for a monoclonal).
The bottom line is when there is a pandemic that is killing 90,000 Americans a month and we have an FDA approved drug with 100% effect size in two randomized clinical trials and confirmatory evidence of efficacy in 4 independent observational studies, physicians should be encouraged to offer those drugs to their patients for consideration.
But sadly, as of Jan 24, this isn’t happening. Doctors and politicians are ignoring the evidence in plain sight because they are too busy to do the research. This isn’t just in the US, but in other countries as well such as the UK and Canada. Watch this video at 7:00 and 11:50. It’s eye opening.
On Jan 31, 2021, I wrote a (very long) op-ed on why the FDA should issue an EUA for fluvoxamine immediately but the core argument is it would save far more lives than it would possibly risk. A Stanford infectious disease professor told me he thought it was criminal that docs are saying “we will wait for the phase 3 study on fluvoxamine” when the evidence on the table is so compelling.
Finally, If you’d like to make a donation to fund scientific research, please check out the CETF donation page.
There are four ways to get fluvoxamine:
- Tell your doctor if you have COVID and get a prescription. Some docs will give you a prescription in advance, to be used ONLY if you have COVID, so you have the drugs on hand if you get sick.
- Tell your doctor you are depressed. This usually avoids long arguments.
- CityHealth Urgent Care will prescribe fluvoxamine if you are COVID positive and don’t have any drug interactions, etc. that would disqualify you. This is done via telemedicine over the Internet so available to anyone in the US.
- Docs that prescribe ivermectin are also an option. This is international list. Generally, if you are cool with IVM, then point them at this article if they have any questions (or my website www.skirsch.io)
As of Feb 13, only 40,000 people have seen this article and that isn’t enough to make a difference. Please help spread the word by upvoting this article and sharing it both to your followers on Quora (using the recycle icon below), but also on Twitter, Facebook, and LinkedIn by using the “right arrow” below that is just to the left of the three dots.