This is a tale of two drugs, whose individual fortunes have taken very different turns just this week. (And it’s only Wednesday!) The first is a drug that I’ve written quite a lot about going back to March, while the second one came out of nowhere in a press release announcing clinical trial findings just yesterday. Those of you who follow the news can no doubt immediately identify the two drugs. The first drug is hydroxychloroquine, while the second drug is a steroid called dexamethasone. From an evidence-based perspective, the first has, other than a blip, nearly completed its cycle of a meteoric rise followed by a punishing fall.
Hydroxychloroquine
If someone had told me that I’d have spent so much digital ink writing about an antimalarial drug like hydroxychloroquine being touted as a cure for a deadly infectious disease based on its promotion by a French “brave maverick scientist” and the President of the United States, I’d have told you that, even during the Trump era, something like that is just too bizarre to happen. Welcome to 2020, though. In this hellscape of a year, based on the observation of 80 patients full of confirmation bias, Chinese doctors in Wuhan noted that no patients with lupus erythematosis became ill with COVID-19 and hypothesized that the chloroquine or hydroxychloroquine that they were taking might be the reason. (These drugs are also mildly immunosuppressive, hence their use to treat autoimmune diseases.) Of course, during a pandemic, it is people who are immunosuppressed are the very people who most rigorously obey orders to practice social distancing and self-quarantine and thereby protect themselves from infection. Be that as it may, the Chinese doctors started using the antimalarial drugs, and anecdotal evidence of success was reported, leading to randomized clinical trials that were announced by the Chinese government to have been “promising.” None of this stopped China from incorporating these drugs into its recommended regimen. The World Health Organization followed suit, as did several countries, and thus was born a new de facto standard of care for COVID-19 based on, in essence, no evidence other than some in vitro evidence that the drugs inhibit replication of SARS-CoV-2, the virus that causes COVID-19, anecdotes, and incredibly weak clinical trial evidence.
Even the U.S. FDA caved, likely influenced by Donald Trump, who had become a relentless booster of the drug (along with the aforementioned French brave maverick doctor Didier Raoult, Dr. Mehmet Oz, and various quacks), and issued an emergency use authorization (EUA) for chloroquine and hydroxychloroquine, permitting their use outside of clinical trials. In the US, as in much of the rest of the world, hydroxychloroquine became the de facto standard of care in those dark days of March and April, as the pandemic hit parts of the US, like New York, Boston, and my own part of the country, Detroit, with a vengeance. As I said at the time, April 1 (which seems like ancient history, the FDA EUA was dangerous politics, not science.
So guess what? On Monday, the FDA revoked its EUA for hydroxychloroquine:
The Food and Drug Administration said Monday it is ending its emergency use authorization for chloroquine and hydroxychloroquine, the anti-malaria drugs backed by President Donald Trump to combat Covid-19.
The agency determined the drugs were “unlikely to be effective in treating COVID-19 for the authorized uses in the EUA.”
“Additionally, in light of ongoing serious cardiac adverse events and other serious side effects, the known and potential benefits of CQ and HCQ no longer outweigh the known and potential risks for the authorized use,” the FDA wrote in its notice Monday.
The FDA issued the emergency use authorization for the drugs in March. The EUA meant that doctors would be allowed to use the drugs on patients hospitalized with Covid-19 even though they had not been formally approved by the agency.
Here’s the FDA’s letter revoking the EUA:
FDA has determined that the criteria under section 564(c) of the Act for issuance of the EUA referenced above are no longer met. Under section 564(c)(2) of the Act, an EUA may be issued only if FDA concludes “that, based on the totality of scientific evidence available to the Secretary, including data from adequate and well-controlled clinical trials, if available, it is reasonable to believe that: (A) the product may be effective in diagnosing, treating, or preventing—(i) such disease or condition [….]; and (B) the known and potential benefits of the product, when used to diagnose, prevent, or treat such disease or condition, outweigh the known and potential risks of the product […].” As explained in the attached memorandum, based on a review of new information and a reevaluation of information available at the time the EUA was issued, FDA now concludes that these criteria are no longer met. The bases for this decision include the following:FDA has concluded that, based on this new information and other information discussed in the attached memorandum, it is no longer reasonable to believe that oral formulations of HCQ and CQ may be effective in treating COVID-19, nor is it reasonable to believe that the known and potential benefits of these products outweigh their known and potential risks. Accordingly, FDA revokes the EUA for emergency use of HCQ and CQ to treat COVID-19, pursuant to section 564(g)(2) of the Act. As of the date of this letter, the oral formulations of HCQ and CQ are no longer authorized by FDA to treat COVID-19.
- We now believe that the suggested dosing regimens for CQ and HCQ as detailed in the Fact Sheets are unlikely to produce an antiviral effect.
- Earlier observations of decreased viral shedding with HCQ or CQ treatment have not been consistently replicated and recent data from a randomized controlled trial assessing probability of negative conversion showed no difference between HCQ and standard of care alone.
- Current U.S. treatment guidelines do not recommend the use of CQ or HCQ in hospitalized patients with COVID-19 outside of a clinical trial, and the NIH guidelines now recommend against such use outside of a clinical trial.
- Recent data from a large randomized controlled trial showed no evidence of benefit for mortality or other outcomes such as hospital length of stay or need for mechanical ventilation of HCQ treatment in hospitalized patients with COVID- 19.
And it’s true, as well. Even as long ago as a month and a half ago, there was a drip-drip-drip of negative studies. True, they weren’t randomized, double-blind clinical trials, but rather observational studies. Still, they were enough to lead me to conclude that it was unlikely that hydroxychloroquine would be found in randomized trials to have significant activity against COVID-19. This is starting to be confirmed with, for instance, the publication of a a randomized controlled clinical trial of the drug as post-exposure prophylaxis that was entirely negative. This was followed by two more, first, a Spanish post-exposure prophylaxis trial that was also negative. Then there was the Recovery Trial from the UK, which failed to find a benefit from hydroxychloroquine in hospitalized patients treated with the drug.
Steroids: They never go out of style
Speaking of the Recovery Trial, the one thing about its finding that hydroxychloroquine has no activity against COVID-19 in patients hospitalized with COVID-19 that bothered me two weeks ago, when it was first announced, is that there was no manuscript, no peer-reviewed paper. It was science by press release. There was also a difference. While the supposed finding that hydroxychloroquine showed no benefit in hospitalized patients with COVID-19 was reported almost as an afterthought, the press release from the Recovery Trial reported yesterday was breathlessly reported as “new hope” for COVID-19 by basically every news outlet I recall seeing, with hardly a word of skepticism or caution, with the BBC news being all in, complete with the headline Coronavirus: Dexamethasone proves first life-saving drug, spun thusly:
A cheap and widely available drug can help save the lives of patients seriously ill with coronavirus.
The low-dose steroid treatment dexamethasone is a major breakthrough in the fight against the deadly virus, UK experts say.
The drug is part of the world’s biggest trial testing existing treatments to see if they also work for coronavirus.
It cut the risk of death by a third for patients on ventilators. For those on oxygen, it cut deaths by a fifth.
Had the drug had been used to treat patients in the UK from the start of the pandemic, up to 5,000 lives could have been saved, researchers say.
And it could be of huge benefit in poorer countries with high numbers of Covid-19 patients.
The UK government has 200,000 courses of the drug in its stockpile and says the NHS will make dexamethasone available to patients.
Prime Minister Boris Johnson said there was a genuine case to celebrate “a remarkable British scientific achievement”, adding: “We have taken steps to ensure we have enough supplies, even in the event of a second peak.
Notice that last paragraph? This finding is being presented in nationalistic terms, as a great triumph of British science, a gift from Britain to the world. All of this, before there’s even a peer-reviewed scientific paper describing what was actually found. Instead, all we have is science by press release.
Personally, I like the way that Science News presented the press release:
A low-cost steroid may save the lives of some people who are on ventilators or supplemental oxygen because of COVID-19, preliminary data from a large clinical trial suggest.
Dexamethasone, a steroid in use for decades, reduced deaths of COVID-19 patients on ventilators by about a third compared with standard care, researchers reported in a news release June 16. Deaths of COVID-19 patients on supplemental oxygen were reduced by about 20 percent. Researchers found no benefit for hospitalized patients who didn’t need extra oxygen.
If the results hold up to scrutiny once scientists have a chance to review the full data, the drug would be the first to reduce the risk of death from the disease.
And:
“It’s not a fix. It’s not a cure. It’s not a miracle, but it is really, really useful,” Landray says. He expects doctors around the world will embrace the therapy. He says that the United Kingdom’s National Health Service may soon declare dexamethasone the standard treatment for people on ventilators because of COVID-19.
Still not great, but much better than the BBC’s British boosterism.
But what do we know? Here’s the press release. It’s labeled as a statement from the Chief Investigators of the Randomised Evaluation of COVID-19 Therapy (RECOVERY) Trial on dexamethasone, but, make no mistake, it’s a press release:
In March 2020, the RECOVERY (Randomised Evaluation of COVid-19 thERapY) trial was established as a randomised clinical trial to test a range of potential treatments for COVID-19, including low-dose dexamethasone (a steroid treatment). Over 11,500 patients have been enrolled from over 175 NHS hospitals in the UK.
On 8 June, recruitment to the dexamethasone arm was halted since, in the view of the trial Steering Committee, sufficient patients had been enrolled to establish whether or not the drug had a meaningful benefit.
A total of 2104 patients were randomised to receive dexamethasone 6 mg once per day (either by mouth or by intravenous injection) for ten days and were compared with 4321 patients randomised to usual care alone. Among the patients who received usual care alone, 28-day mortality was highest in those who required ventilation (41%), intermediate in those patients who required oxygen only (25%), and lowest among those who did not require any respiratory intervention (13%).
Dexamethasone reduced deaths by one-third in ventilated patients (rate ratio 0.65 [95% confidence interval 0.48 to 0.88]; p=0.0003) and by one fifth in other patients receiving oxygen only (0.80 [0.67 to 0.96]; p=0.0021). There was no benefit among those patients who did not require respiratory support (1.22 [0.86 to 1.75]; p=0.14).
Based on these results, 1 death would be prevented by treatment of around 8 ventilated patients or around 25 patients requiring oxygen alone.
Given the public health importance of these results, we are now working to publish the full details as soon as possible.
That’s nice. Presumably you could have had a manuscript ready before the press release. You might even have published it on a preprint server while it was undergoing peer review. Because I’m dedicated to science-based medicine, I say the same thing about the press release from a couple of weeks ago describing a result that I’m inclined to agree with, namely that hydroxychloroquine doesn’t benefit hospitalized patients with COVID-19. I’m tired of all this science by press release.
The first thing to note here is that, if the results are as the Recovery Trial team say they are, dexamethasone only benefits sick patients, those who, at least, require oxygen. Unlike some of the nonsense I’ve seen on social media, taking dexamethasone to prevent COVID-19 is not advisable based on this study. Accepting the results at face value, it only benefited patients who were either requiring supplemental oxygen or who required mechanical ventilation. It did not benefit those with mild disease. In fact, knowing the mechanism of steroids, we should not be surprised. Steroids are immunosuppressants. In patients without disease, they would very likely increase susceptibility to infection and COVID-19, rather than protect against infection.
That being said, one has to compare the mechanistic probability that hydroxychloroquine would have activity against COVID-19 to the mechanistic probability that a steroid like dexamethasone would have a therapeutic effect. Hydroxychloroquine is notorious for demonstrating anti-viral activity in cell culture that failed to translate into humans (or even animals). So it’s not surprising that its activity in cell culture against SARS-CoV-2, the virus that causes COVID-19, appears not to have translated into activity against the coronavirus in humans. On the other hand, steroids are powerful immunosuppressants. If the inflammatory reaction causing lung injury, the adult respiratory distress syndrome (ARDS), due to SARS-CoV-2 is the reason people are dying, then blunting the overactive immune reaction with the use of a steroid like dexamethasone could well decrease mortality.
I can’t help but quote this particularly apt Tweet:
Personally, I can’t help but note that the question of whether steroids like dexamethasone improve survival in ARDS (regardless of the cause, including COVID-19), regardless of the cause, is not a new question. ICU docs were debating the question in the late 1980s, when I started by surgery internship, continued debating it the entire time that I was doing my surgery residency in the early 1990s, and are still debating it today. Indeed, in my own current department there was recently a talk discussing the management of ARDS that mentioned when and how to introduce steroids. You’d think that after decades of controversy, with literally dozens of randomized trials of steroids in severe ARDS, we’d have an answer, but we really don’t. Personally, I like this observation:
Steroid reduces mortality in some studies, but not others. This is a topic of perpetual, internecine struggle which will probably never be resolved.
And this one:
At this point, there is a fair body of evidence that patients with severe pneumonia or septic shock may benefit from steroid (in the absence of contraindications). Whether mortality benefit occurs is contentious, but it does seem that steroid accelerates ventilator weaning and ICU discharge (which are meaningful, patient-centered outcomes). So steroid makes sense for patients with {pneumonia+ARDS} or {sepsis+ARDS}. That isn’t a change in my practice.
The real question is whether patients with ARDS who don’t have pneumonia or sepsis should be treated with steroid. This remains murky. Patients may need to be judged on a case-by-case basis (depending on whether the suspected cause of ARDS is thought to be a steroid-responsive process). In the absence of any clear-cut answer, one possible approach is to use CRP as a signal for patients with systemic inflammation who might benefit from steroid. There is some precedent for this in the literature, as one RCT of pneumonia used CRP as a cutoff to adjudicate whether steroid would be used.11
In other words, in severe inflammatory diseases of the lungs, it was unclear whether dexamethasone or other steroids are of benefit. That’s why I really, really, really want to see the actual data. That’s why I agree with Atul Gawande:
Maybe, just maybe, dexamethasone is as effective a treatment as it’s being sold as. Maybe. Even if it is, it is still not the way out of the COVID-19 pandemic. It might decrease mortality of COVID-19 patients requiring oxygen or ventilator support, but otherwise it’s a whole lot of nothing, and that’s even if you accept the Recovery Trial press release at face value, which, at this time, I do not.
50 replies on “Dexamethasone and hydrochloroquine: A tale of two drugs for COVID-19”
I know the world is waiting for a cure for CVID-19, but this continual science by press release is not helping. It put pressure on front line doctors to change their practice in the absence of evidence that the change will help.
^^that.
It is not a tale of two drugs; it is a tale of two disease phases. The first phase is a viral like infection, somewhat akin to the flu. Around Day 7 to Day 9 some patients begin to transition to the second phase of the disease. The second phase of the disease is increasingly severe immunological function that takes on all the features of immunological dysfunction, beginning with shortness of breath, problems with oxygenation and coagulopathy, to acute respiratory distress syndrome resulting in some in ventilator assistance and finally to the immunological derangement known as the cytokine storm.
One etiological agent SARS2/COVD=-19; two disease phases. Each phase requiring its own therapy. Fairly standard in medicine.
Science based medicine requires that any study initiated test the hypothesis . The hypothesis is that HCQ will reduce viral infection and progression to phase 2. This could have been easily tested by comparing the rate of hospitalization of a treated group to a non-treated group. All the studies quoted against HCQ never tested this hypothesis
This hypothesis is based on the known mechanism of how HCQ should work. The mechanism for HCQ is that it impairs viral entry into the cells. The first is that it binds sialic residues; the residues necessary for the virus to latch onto the cell; and alters the TMPRSS2 fusion protein necessary for entry of the virus into the cell. Once the virus is in the cell HCQ is less effective, although it may have some interference with viral replication by altering pH.
Once the virus is in the cell and replicating away HCQ will become increasingly less effective.
As the virus replicates the disease changes. The mechanism for this, at least in a large cohort, are fairly well elucidated. It is an increasing immunological dysfunction with all the halllmakrs of an super autoimmune response. At this phase, potent immuno-suppression is required; of which steroids are still the mainstay. It should not be a surprise that patients who have progressed to ventilator assistance respond to immuno-suppression.
Other disease models:
Drug reaction: varying degrees, from a mild rash to a life threatening Stevens-Johnson syndrome; treatment: corticosteroids.
Rheumatological diseases: anti-inflammatants of various degrees of strength; often accompanied by (wait for it) corticosteroids.
Inflammatory bowel disease: biological suppressors of inflammation targeting various pathways; and often accopanied by (wait ofr it) corticosteroids.
Asthma: various types of inflammatory suppression with a major core component of (wait or it) corticosteroids.
If we are to have science based medicine then we should have science based medicine. This is more than passively accepting the results of studies of the experts. We need to understand the question being asked and ensure that the study being quoted is structured to ask the right question. A core aspect of modern medicine is to elucidate the mechanism and then design a medication to interrupt the pathway. Why are we accepting anything less when it comes to COVID-19?.
Often the language becomes our enemy if the question is asked in such a way that it allows one to overlook the mechanism. If the question is asked “is it a cure for COVID-19?’ and the answer is that corticosteroids reduce death, the only conclusion can be drawn from this information is that corticosteroids reduces death in late stage COVID-19. It does not address the issue as to whether it is a cure for COVID-19. If we ask the question are HCQ regimens useful in preventing or impairing progress of the disease and then only test whether the regimens are effective after the disease has progressed to the severe immunological dysfunction, we have answered nothing.
One adheres to science and its required structure of observation, hypothesis, test of hypothesis, refine hypothesis and retest hypothesis. It is brutal in that it demands the professor prove the claim. One can adhere to nonsense put in scientific format. That is scientism. These are two competing views of the world. We should not claim to follow science when we follow scientism. I think this is what Mark Twain was referencing when he said cauliflower is nothing but cabbage with a college education.
Citation needed.
Is there a different phase of the disease for each cycle of viral replication?
I’d like to see an article from any reputable medical source that supports your ideas.
Also, you might read the first post on the SBM website.
Somehow, Pathcoin has a better and more complete understanding of how COVID works than any doctor who has actually studied or treated it. It’s a miracle.
@ PF
Not worth going into detail; but, I have been following the current pandemic since early January, have read around 200 medical journal articles, reports from CDC, WHO, Swedish Health Agency (I’m fluent at Swedish), and excellent papers by Atlantic Monthly, and Center for Infectious Disease Research and Policy, plus probably skimmed several hundred more. I assure you that the vast majority of doctors and public health officials understand COVID far better than Pathcoin and he is wrong about his black and white seeing either science or scientism. I’ve already, in several exchanges, refuted previous comments by him, to which he didn’t even try to respond, so it would be a waste of time to try again.
However, whoever you are, thinking he knows more than “any doctor who has actually studied or treated it” just adds you to the ranks of morons that sometimes post on this website.
I will briefly just counter his idea of science. It is NOT important that one first observe, then form a hypothesis. What is important with any research is to include a detailed description of the sampling approach, detailed description of the subjects, detailed description of the treatment, include all subjects who you began with, if they left study, try to do follow-up, make ALL date available (not claiming proprietary information) and finally NOT REPORTING RESULTS IN PRESS BEFORE PEER-REVIEWED. I repeat, doesn’t matter the reasoning for doing the study; however, when in emergency situations, OK to try different treatments, based on minimal to non-existent criteria, as long as subjects completely informed and, as already stated, all data made available and not released to press.
And, again, your nuts if you think that doctors and public health people don’t understand COVID-19; but, we are all learning more and more daily.
@ Joel
“However, whoever you are, thinking he knows more than “any doctor who has actually studied or treated it” just adds you to the ranks of morons that sometimes post on this website.”
PF wrote It’s a miracle”… There was some clear amount of irony that you missed there.
@Joel: I think you missed the sarcasm in PF’s comment.
Reminder to all, tone doesn’t come through well in text, so remember to use the /s tag for sarcastic comments.
@ Pathcoin
The hypothesis that Hydroxychloroquine blocks entry into the cell was based on one in vitro study.
I won’t waste my time going point by point with your comment as I’ve already refuted your previous comments and you have failed to respond, to find one fault with what I wrote.
So nice that you can parrot what science is all about. Too bad you really don’t understand what you are writing.
Joel A. Harrison, PhD, MPH writes,
“I’ve already refuted your previous comments and you have failed to respond, to find one fault with what I wrote.”
MJD says,
Orac is to blame. Specifically, it states, “Want to respond to Orac? Here’s your chance. Leave a reply! ”
@ Joel,
It could be written, ” Want to respond to Orac, and others? Here’s your chance. Leave a reply!”
@ Narad,
Good to see that you’re using the “Cancel reply” option more often.
If you actually read the post it addresses several studies that asked whether HCQ works as post exposure prophylaxis, corresponding to your first stage, and found it didn’t.
The post is exactly following the science.
Exactly this. I don’t know how better to describe testing HCQ in Pathcoin’s “first phase” than “post exposure prophylaxis”.
Can we please stop beating this dead horse and move on to other studies?
@Pathcoin
Could you elaborate? And is there something about bats and sialic acid that mutes the pathogenicity of these same viruses in bats?
[…] ● NEWS ● #respectfulinsolence #Science ☞ #Dexamethasone and #hydrochloroquine : A tale of two drugs for COVID-19 https://www.respectfulinsolence.com/2020/06/17/dexamethasone-and-hydrochloroquine-a-tale-of-two-drugs-fo… […]
Hydroxychloroquine redux? Let’s hope not. No BBC and Boris repeat performances of Fox News and Trump. No understudy for Didier Rault this time though. The biggest difference is the initial studies. Dexamethasone appears to have been a large scale RCT of thousands. The story suggests that the evidence was simply too great to enrol more control patients. The advantage that UK doctors had was the NHS.
It’s also being made clear that the treatment only helps the very, very sick patients. Could be that the NHS has saved Boris’s bacon – twice.
The very old-school chief of the academic department I worked in for many years was fond of saying, “Nobody should die of an untreatable disease without the benefit of a trial of steroids.”
There’s also a saying that applies both to cardiology and dermatology (and possibly to nephrology as well):
If it’s wet, dry it. If it’s dry, wet it. And when all else fails, use steroids.
Anyone remember that episode of House where they couldn’t determine which of two or three ‘mystery diseases’ the patient had? Hmmm that’s nearly every episode… Anyway, House says it doesnt matter because the treatment is the same….steroids.
Even if dexamethosone did nothing to reduce mortality, I would think it would still be considered valuable if it helped to keep patients from progressing from simply needing supplementary oxygen to requiring mechanical ventilation or if clipped a bit of time off of hospital stay or time required on a ventilator. None of these things are of huge significance, but dex is cheap, seemingly pretty safe and (I think) reasonably easy to manage at least for short term use.
Yes, despite my opening comment in this thread, I am finding less concern with the rush to dexamethosone than that to hydroxychloroquine. It is only going to be used for the most severe patients, has a relatively good safety profile, is cheap and so there is not much to lose.
I am still annoyed by the science by press release though. If they had made the data available at least it could be looked at to see how well the claims stacked up.
I sort of see the “science by press release” thing as the product of too many graduates of marketing communications programs and too much “branding.”
As Orac discussed in his post about the WHO and asymptomatic spread, there is a need for great care and real aptitude in science communication to the general public. In this case the public is excited and scientists are annoyed. If things don’t pan out, scientists will be disgusted and the general public will be less inclined to trust science.
@ Michael J. Dochniak (MJD)
You write:
“I’ve already refuted your previous comments and you have failed to respond, to find one fault with what I wrote.”
MJD says,
Orac is to blame. Specifically, it states, “Want to respond to Orac? Here’s your chance. Leave a reply! ”
Maybe you are so dense; but seems the vast majority who post comments understand they can comment on what others write.
I haven’t found Orac to censor any of my posts questioning some of the positions here.
@ Sheila
Finally, you write something that is valid. Yep, Orac doesn’t censor as opposed to websites like Age of Autism that are really an echo chamber where a group of unscientific illogicals reinforce each other, regardless of how absurd some of the articles and comments are.
@ F68.10
I think you are right that I missed the irony, so, my apologies to PF. And just one more example of Pathcoin’s being out of his depth.
By the way, I came across an article discussing the Swiss political system in comparison to American. You might find it of interest:
Matthew Stevenson (2020 Jun 17). Get Rid of the Presidency. Counterpunch. Available at: https://www.counterpunch.org/2020/06/17/get-rid-of-the-presidency/print/
@ Joel
“By the way, I came across an article discussing the Swiss political system in comparison to American. You might find it of interest.”
I tend to make the same kind of points (not with the same language) in the case of France (though we don’t have Trump…). But just mention the mere idea of having a committee of seven persons in charge of the executive branch in France, and everyone goes completely bonkers… They Want Their King. Makes them feel safe somehow. Beats me…
Though, one valid point to be made against a committee system is that it makes decision making on matters of foreign policy much more complicated. I think that’s one of the reasons the french would not want a committee and would rather have a King: the feeling that it dilutes the efficiency of decision making with respect to foreign policy and specifically military force. The topic of the inefficiency of parliamentarian decision making during the French Vietnam War always comes back on table…
But otherwise, yes, I do think the idea of concentrating executive power in The Most Exhuberant Moron available on the mediatic market of ideas to be one of the starkest betrayal of enlightenment values. All the more if it reduces politics to a reality show that obliterates important matters from the eyes of the public.
I noticed that trough our history, we keep looking of That Providential Man to direct us. The two latest examples being Macron and the Druid.
So I can’t refute this criticism.
You may be onto something about foreign policy. We French supposedly stopped being a colonial power in 1965-68, but we actually still have plenty of… common concerns with former colonies. Up to “military advisors”.
In theory, our parliament and senate should act as committees, or providers of specialized committees. And also in theory, our prime minister should have more sway than the President. But in the past decades, I feel there has been a strong move to consolidate the powers into the President’s hands.
@ F68.10
There is another major problem with French “democracy.” The two who get the highest votes go to the second round; but if there are 3 or 4 candidates to the left, they divide the votes and two candidates, perhaps, one moderate and one to the right could end up, even if getting only, perhaps, 30% and 25%, go to the second round.
@ Joel
“There is another major problem with French “democracy.””
Almost everyone around here seems to see it as a strength. But it’s even worse than that: the system also applies to legislative elections: two turns. Only two best candidates are kept (occassionally, depending on scores) for second turn. And this is performed for each “circonscription”. In the end, this gives huge huge scores for the more mainstream parties compared with what would happen if things were more “proportional”. Specifically designed to guarantee that Parliament has a majority that is numerically strong even if popular mandate is weak. Designed this way specifically to avoid the kind of parliamentarian crisis that brought down the 4th republic amidst the decolonisation wars. The system gives neat parliamentarian majority but also allows the far right to atomise the opposition if ever they get to power.
In the swiss system, the far right or assimilable is very much present in the system. But they are constrained by all other political forces who won’t let them claim the “I have 30% vote! I won the election!” gambit. This did happen in 2007. Reaction by other political forces has been swift: “you’re included in the system; if you play your drama queen, it won’t go down well.” Far right denounced it as a coup by moderates in 2007. Roughly the closest you can get to civil war in modern Switzerland.
A documentary by the swiss media called The Downfall of Christoph Blocher (english subtitles available) relates how that system handles the far right. SVP fanatics still think of this episode (a vote that took liberties with tradition but not with the law, with some unusual shenanigans by swiss standards) as a Conspiracy by the Deep State…
Right and far right are very much present in the system and the country is overall very much conservative. And semi-direct democracy kind of crystallizes that status quo. Which makes it a big no-no seen from the french left. But it also guarantees that you cannot govern without the left, and therefore that the far right cannot have much leeway. Even if the far right “wins” the elections with 30% votes. If they do not “cooperate”, they are insistently reminded that the complement of 30% is 70%, and that 70% > 30%. Comparatively, the french system allows you to seize power with 30% votes… It was designed for that: “Stability” of the executive branch in the face of “Parliamentarian instability”.
My comment regarding Pathcoin was 100% sarcasm. But he probably didn’t understand that either, eh?
@ PF
Are you Canadian? I earned my first masters degree at Carleton U, 1970. And, typical Canadian end of sentence was “eh.”?
Dr Harrison is a wizard (a la Tolkin), Pathcoin’s a monomaniac. Sadly that position is taken ’round these parts, but I guess we’ll keep him for now.
“Maybe, just maybe, dexamethasone is as effective a treatment as it’s being sold as. Maybe. Even if it is, it is still not the way out of the COVID-19 pandemic.”
As is argued, very persuasively and in detail, in an article published yesterday by Prof Devi Sridhar, chair of global public health at the University of Edinburgh, and one of the most thoughtful and best-informed commentators on the pandemic:
https://www.theguardian.com/world/commentisfree/2020/jun/17/dexamethasone-may-be-part-of-the-covid-19-puzzle-but-its-no-magic-bullet?CMP=twt_gu&utm_source=Twitter&utm_medium#Echobox=1592404495
Liking that link. Thanks.
@ Athaic
Yep, to some extent you are right about seeking a providential man, a messiah. I find, for instance, American nomination conventions appalling, people cheering, people in tears. Then when the President fails, many refuse to acknowledge, as we see with Trump supporters. Some still praising how well he has handled the pandemic. What planet are they from?
No-one with a shred of self respect should worship somebody that much.
The healthiest view of politicians should be ‘none of them are particularly reliable but this one is the least worst choice’.
What ever happened to Politicalguineapig (PgP)?
I wanted to tell her that she was right and, as it turns out, Trump did “wreck everything.”
https://www.businessinsider.com/trump-americans-wearing-masks-show-disapproval-not-as-preventive-measure-2020-6
Now, even his stupid supporters that do wear them will be shamed into not doing so.
from reddit:
@ Tim
Trump is the first President in my lifetime who makes it quite clear that everything is about him, a malignant narcissist. Makes one wonder about the intelligence or, actually, the lack of intelligence of the mass of his supporters. Of course, some of his supporters, e.g., industry, billionnaires, could care less as long as it benefits them; but most of his policies hurt the vast majority of his supporters.
If I didn’t possess aphantasia, I would Imagine the cover (and story) of this book to be the quintessential representation of trump and his followers (worshipers?).
https://www.theguardian.com/film/2020/jun/19/ian-holm-dies-alien-chariots-of-fire-bilbo-baggins
I’d like to add he was also Mr. Kurtzmann in Terrie Gilliam’ Brazil (1985):
Ohhh! It looks like the MAGAs are having a spot of trouble getting the masks off the libtards…
http://freerepublic.com/focus/f-chat/3857382/posts
smh
https://thehill.com/homenews/campaign/503781-tulsa-fire-department-says-trump-rally-attendance-was-about-6200
Hmm. I guess there will be thousands of cell phone videos of this purported ‘blocking’ by Dump supporters… Nope, it is all foreheads and MAGA hats. “Dammit, Dora! You used the front-facing camera again!
— Humans: A Brief History of How We F*cked It All Up,Tom Phillips, 2018
https://i.redd.it/lybvcx5qca651.jpg
Everybody Hurts… sometimes
https://twitter.com/KristerJohnson/status/1274772592746848256
Just as an FYI, the reason I haven’t paid much attention to the blog since Friday is a grant deadline, which was today. I should be back to more regular posting beginning tomorrow, after having a chance to recover and maybe have a dram or two of the old single malt tonight to celebrate.
People suffering from TDS need to read the latest study (it of course was done by those Trump loving, right wind extremist at the, Henry Ford Health System in Southeast Michigan) and reported on that Trump loving network CNN.
Orac didn’t learn anything from the very first study that showed Hydroxychloroquine was not effective and had to do a major mia culpa AKA; I screwed the pooch with my ‘conformational bias’
“Dr. Marcus Zervos, division head of infectious disease for Henry Ford Health System, said 26% of those not given hydroxychloroquine died, compared to 13% of those who got the drug.”
https://www.ijidonline.com/article/S1201-9712(20)30534-8/fulltext
I’m well aware of the study. It’s retrospective, not randomized, and has significant likelihood of bias given that a lot of hydroxychloroquine patients ALSO got dexamethasone and there appears to be indication bias. In other words, in light of the two existing randomized controlled trials that failed to find evidence of efficacy for this drug, this HFH study is unimpressive and not good evidence that hydroxychloroquine is effective.??♂️
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