We have saved millions of lives
June 21, 2020 9:20 PM   Subscribe

In a recent episode of SciShow (YouTube), Hank Green and his writers share two pieces of good news about the COVID-19 pandemic. First is that for those who get the sickest from the disease, there is finally a drug with solid evidence that it saves lives: the commonly-available generic corticosteroid dexamethasone (Mayo Clinic). Second is that research is now becoming available to quantify exactly how effective quarantining, social distancing, and other policies and recommendations have been at reducing the spread of the virus, and it's pretty dramatic.

A study of the pandemic in Europe (Flaxman et al., Nature) estimates that as of May 4th when the data set was compiled, "across 11 countries, since the beginning of the epidemic, 3,100,000 [2,800,000 - 3,500,000] deaths have been averted due to interventions" like quarantining, closing schools, requiring masks, and so on. Other researchers using a different method to estimate the impact of such policies in six countries (Hsiang et al., Nature) found that they "may have reduced the severity of the outbreak by a total of 55–66 million confirmed cases" across China, South Korea, Italy, Iran, France, and the United States during the early phase of exponential spread in each of these countries. Both studies note a number of potential limitations with the way they compute their estimates, but when multiple independent approaches yield similar results, scientists tend to grow confident that the results are real.

It's been a long quarantine and for many of us a return to real normalcy looks like it is still months away. But the evidence that's becoming available about how the spread of the virus has changed in response to anti-contagion policies worldwide makes it clear that our collective sacrifice has worked and continues to work: thanks to our scientific understanding of infectious disease, our ability to identify and rapidly disseminate information about the new virus, and our collective willingness to accept personal sacrifice for the greater good, we have saved literally millions of lives.
posted by biogeo (29 comments total) 59 users marked this as a favorite
 
Good.
posted by ®@ at 9:51 PM on June 21


Obviously, a lot more to be said, and I'm concerned about how early we're opening in parts of the US... and that we don't seem to have a clearly communicated plan.

But good.
posted by ®@ at 9:52 PM on June 21 [4 favorites]


Hey there, I would like to share my direct first person experiences of this in China - I have a couple YT videos on this topic here and here. I am just some random guy, not very well connected or informed, but to sum up my experience seeing this play out in a 3rd tier city in China:
  • People followed instructions, and there was a very strict quarantine early on
  • Tracking systems (on people's phones) have allowed health authorities to quite precisely locate and target their testing and quarantining efforts, to minimise disruption
  • Good testing and tracking allows people to "get over it" more quickly - as in my example, once we were confirmed there were no new cases in our province, people trusted that news and have been out living normal lives with minimal restrictions again, and (relatively) safely
posted by Meatbomb at 9:59 PM on June 21 [25 favorites]


Oh and one more thing: inter-provincial and even inter-city travel is tracked and controlled. Always has been the case, but it is a benefit in this health situation. For sure there are privacy and freedom issues at play here, but at least in this case it has been a good thing.
posted by Meatbomb at 10:01 PM on June 21 [5 favorites]


As part of getting on a massive Mt Everest kick I got to learn that "Dex" is what they use to treat people who get pulmonary edema -- "HAPE" -- up on the mountain. So I guess it makes sense it's applicable to losing lung function due to COVID.
posted by Heywood Mogroot III at 10:35 PM on June 21 [2 favorites]


A bit more excerpted from the Hsiang et al. paper:
Our central estimates suggest that there would be roughly 37 million more cumulative confirmed cases (corresponding to 285 million more total infections, including the confirmed cases) in China, 11.5 million more confirmed cases in South Korea (38 million total infections), 2.1 million more confirmed cases in Italy (49 million total infections), 5 million more confirmed cases in Iran (54 million total infections), 1.4 million more confirmed cases in France (45 million total infections), and 4.8 million more confirmed cases (60 million total infections) in the US had these countries never enacted any anti-contagion policies since the start of the pandemic.
This supports the idea that the policies and their implementation (including individuals' compliance with those policies) in China have been particularly effective at reducing the spread of infection. Though adjusted for population it's not huge, something like 10% more effective than the United States, but that's still a whole lot of extra lives saved.
posted by biogeo at 10:48 PM on June 21


makes it clear that our collective sacrifice has worked and continues to work: thanks to our scientific understanding of infectious disease, our ability to identify and rapidly disseminate information about the new virus, and our collective willingness to accept personal sacrifice for the greater good, we have saved literally millions of lives.

Until a lot of people decided to freaking stop recently, anyway, once "everything reopened!"
posted by jenfullmoon at 10:52 PM on June 21 [8 favorites]


Also Meatbomb, sorry you missed out on that peach!
posted by biogeo at 10:55 PM on June 21 [1 favorite]


I have been prescribed dexamethasone in the past. Even neurologists seem reluctant to prescribe it any more because of the numerous side effects. These range from tragic levels of acne to fiery heartburn to sleeplessness to irritability you “menstrual irregularities” (not an issue for me personally, so I am not sure on details) to congestive heart failure to psychotic reaction.

Better than a funeral, but it’s not a fun time.
posted by ricochet biscuit at 11:00 PM on June 21 [9 favorites]


It's also an immunosuppressant, which is not something you want people taking casually when the body is already weakened by infection. People on ventilators already have very low survival odds, so this is something administered basically as a last ditch method to save the patient's life.
posted by They sucked his brains out! at 11:18 PM on June 21 [8 favorites]


But also the body's immune response, the "cytokine storm", is one of the serious effects COVID-19 inflicts on the patient. So suppressing that immune response appears to not be a bad thing.
posted by Windopaene at 11:31 PM on June 21 [6 favorites]


So suppressing that immune response appears to not be a bad thing.

No, it's a bad thing. It's just that sometimes it is a reasonable gamble - if the alternative is death.

This is not something you can take as an outpatient. This is just another (probably, hopefully) helpful option for when your lung function degrades to the point that you're being intubated.
posted by Anoplura at 11:42 PM on June 21 [7 favorites]


It's an odd middle ground. Low immune response is bad. High immune response is bad (and suppressing helps). Middle immune response is the bunch of non-symptomatic or mild "barely knew you had it" cases. In the High immune response case your body ends up doing more damage while fighting the virus than the virus would do by itself. It's a sort of thing that is only once you're in the hospital and under supervision so they can keep an eye on you and hopefully take care of any reduced immune response complications.

This makes a bit of sense to me at least... the two times I've been on prednisone (another corticosteroid) was in response to finding out that I was allergic to penicillin and then sulfa antibiotics. Supervised cranking down that immune system response turns out to be a good strategy.
posted by zengargoyle at 11:49 PM on June 21 [3 favorites]


At the beginning of the semester, when I am teaching the general subject of drug toxicities, I tell my students that many drugs have a small number of side effects that you have to worry about. I use the glucocorticoids (which includes dexamethasone) as an example of a drug class with about a dozen significant side effects that need to be memorized. These hormones turn on something like 15% of all genes that can be turned on.

The good news is that this will be short term use.
posted by dances_with_sneetches at 1:33 AM on June 22 [9 favorites]


I saw an article from the BBC about this last week. It hasn't really been secret.

After the hydroxychloroquine debacle I don't think this is something the government would want to announce. First, it's not a cure-all. It's specifically to combat the cytokine storm that some patients suffer under Covid. Second, it's really not something you want a bunch of people running out and taking as a preventative because of the side-effects. From what I read this is a "keep the people off the ventilators" kind of last-ditch effort drug. Though I'm not a doctor.
posted by schroedinger at 4:18 AM on June 22 [3 favorites]




When I did a bit of climbing I've heard dexamethasone is also used for acute mountain sickness, in an emergency, or prophylactically. Although it seems no one knows how it really works, and it doesn't improve your oximetry or any other objective measures. So much of medicine is scarily "no idea how it works, but take it and you may feel better".
posted by xdvesper at 5:08 AM on June 22 [1 favorite]


Also on the good news front there is a vaccine candidate starting wider scale phase 3 clinical trial with several others about to follow.
posted by interogative mood at 5:38 AM on June 22 [2 favorites]


Derek Lowe's post about dexamethasone at his blog In the Pipeline covers a lot of the specific details of the study and their implications.
posted by Spathe Cadet at 6:36 AM on June 22 [5 favorites]


I heard about that dexamethasone study on the This Week in Virology podcast, which I've really been enjoying. They linked to this article about it. It's so great to have some positive news.
posted by beandip at 6:47 AM on June 22 [1 favorite]


But also the body's immune response, the "cytokine storm", is one of the serious effects COVID-19 inflicts on the patient. So suppressing that immune response appears to not be a bad thing.

The body's inflammatory system and clotting systems are heavily intertwined. If you activate an inflammatory pathway you're also probably activating a clotting pathway as well. It's suspected that this happened evolutionarily because typically the cause of incoming pathogens will usually be a wound of some kind.

When your body has cytokines messaging at max it's also cranking out enzymes called plasmins to break down clots away from the site of the "wound". These will break down fibrin into shorter molecular chains and will see a rise in D-dimers, the final product of this pathway. One of the problems that can happen is that the body can't keep up with the amount of plasmin required to stop clots from forming when the immune system is ramping up to max. Clot forms, clot travels to lungs, patient gets a good old PE, patient clutches chest and dies. Happens in regular infections in older people not just COVID-19.

Researchers have been finding a way to mediate this response since the start. Trials of Tocilizumab, an IL-6 antagonist, sadly stalled out and I was really disappointed to hear it but dexamethasone coming out as a drug we can use to fight this thing is really good news.
posted by Your Childhood Pet Rock at 6:58 AM on June 22 [12 favorites]


shall i use this thread for an update of non-political non-trump covid-19 updates (as the last one is archived)? Just a quick Malaysia update (previously I've mentioned that we've been using dexamethasone for critical patients with good results): we officially stopped using hydroxychroloquine, as we've found no discernable positive effects.
posted by cendawanita at 7:49 AM on June 22 [12 favorites]


But. But but but. The models for the effectiveness of various measures in reducing disease spread were produced by specialists in economics, electrical engineering, public policy, etc. Not an epidemiologist among them. Diseases don't behave in a way that is amenable to "reduced-form econometric methods, commonly used to measure the effect of policies on economic growth". If so, we would all be dead of SARS and MERS by now.
posted by sonofsnark at 9:36 AM on June 22 [3 favorites]


Dexamethasone is being used to treat Covid-19 (or more specifically, its side effects), not to inhibit its spread.
posted by schroedinger at 11:08 AM on June 22 [1 favorite]


The researchers who published the econometrics-based model (Hsiang et al.) for six countries worldwide are indeed approaching it from a policy-analysis, rather than epidemiological, perspective, but the researchers who published the model for eleven European countries (Flaxman et al.) are mostly coming from public health and statistics, using a partially mechanistic model rooted in epidemiological methods (though it seems extended with a Bayesian approach to estimating true infection rates from reported deaths). I would argue that these are complementary approaches, and that they are producing qualitatively similar results should bolster our confidence in both of them.

Hsiang et al. appear aware of the potential the criticism that their econometrics-based model may be limited by not directly modeling any epidemiological mechanism, but note that there is prior evidence supporting its applicability:
We employ well-established “reduced-form” econometric techniques[5,14] commonly used to measure the effects of events[6,15] on economic growth rates. Similar to early COVID-19 infections, economic output generally increases exponentially with a variable rate that can be affected by policies and other conditions. Here, this technique aims to measure the total magnitude of the effect of changes in policy, without requiring explicit prior information about fundamental epidemiological parameters or mechanisms, many of which remain uncertain in the current pandemic. Rather, the collective influence of these factors is empirically recovered from the data without modeling their individual effects explicitly (see Methods). Prior work on influenza[16], for example, has shown that such statistical approaches can provide important complementary information to process-based models.
That reference to prior work on influenza is this paper (Kandula et al., Royal Society Interface), which is available open-access.
posted by biogeo at 2:13 PM on June 22 [4 favorites]


The long road to a Covid-19 vaccine 
Long read Financial Times no paywall.
posted by adamvasco at 6:43 PM on June 22 [2 favorites]


"The body's inflammatory system and clotting systems are heavily intertwined. If you activate an inflammatory pathway you're also probably activating a clotting pathway as well."

Thrombosis plays a significant role in the mortality of COVID-19 — I recall the early clinical report of a surgeon witnessing numerous clots rapidly forming in brain tissue while he operated, something he'd never before seen.

The coagulopathy associated with COVID-19 is distinctive enough that in many places it's being referred to as COVID-19–associated coagulopathy (CAC), to differentiate it from sepsis-induced coagulopathy (SIC) and disseminated intravascular coagulopathy (DIC).

Here's a brief recent editorial summary from The Lancet, "COVID-19 coagulopathy: an evolving story".

And here's a pretty comprehensive review in a paper published a couple of weeks ago, "COVID-19 and its implications for thrombosis and anticoagulation".

This paragraph from the latter paper is interesting, given my prior comment about SARS-CoV-2 and ACE2:
Endotheliopathy and COVID-19

Consistent with vascular endothelial dysfunction with SIC, an endotheliopathy appears to contribute to the pathophysiology of microcirculatory changes in SARS-CoV-2 infections. The receptor for viral adhesion is an ACE2 receptor on endothelial cells, with viral replication causing inflammatory cell infiltration, endothelial cell apoptosis, and microvascular prothrombotic effects. Recent reports demonstrate viral inclusions within endothelial cells and sequestered mononuclear and polymorphonuclear cellular infiltration, with evidence of endothelial apoptosis in the postmortem of SARS-CoV-2 infection. As a result, microcirculatory dysfunction contributes to the clinical sequelae in patients with COVID-19. From a clinical perspective, in addition to the systemic hypercoagulability and potential for thromboembolic complications, the described microvascular endothelial injury with microcirculatory clot formation noted in postmortem evaluation is consistent with a thrombotic microangiopathy that may occur in patients. The endotheliopathy may also explain reports of cerebrovascular complications in younger patients, myocardial ischemia, and increasing reports of both micro- and macrocirculatory thromboembolic complications.
posted by Ivan Fyodorovich at 2:18 AM on June 23 [3 favorites]


Belgium’s Federal Agency for Medicines and Health Products (FAMHP) has already authorised 18 clinical trials involving treatments and vaccines against Covid-19, as of 18 June.
posted by adamvasco at 4:21 PM on June 23 [1 favorite]


How will the world's poorest people get a coronavirus vaccine?
Rich countries’ governments are putting all their trust in a marriage of markets and philanthropy called Gavi.
posted by adamvasco at 4:12 PM on June 25


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