Brazil

Article

Brazil is a recurring place in the Astral Codex Ten archive, appearing 40 times across 40 issues between February 16, 2021 and April 01, 2026. The archive places it in contexts such as “one in Brazil”; “second place was Brazil with 195K”; “Some will merely decline, as they have some capacity to address challenges (Brazil, India, Canada)“. It most often appears alongside India, China, Scott.

Metadata

Category: Places
Mention count: 40
Issue count: 40
First seen: February 16, 2021
Last seen: April 01, 2026

Appears In

- India (21 shared issues)
- China (19 shared issues)
- Scott (19 shared issues)
- Germany (18 shared issues)
- Israel (18 shared issues)
- United States (17 shared issues)
- US (16 shared issues)
- Australia (15 shared issues)
- Canada (15 shared issues)
- France (15 shared issues)
- Europe (14 shared issues)
- Japan (13 shared issues)

External Links

Source Context

Recovered passages from the original issue text. When the raw archive preserved outbound links inside the source passage, they are listed directly under the quote.

Coronavirus: Links, Discussion, Open Thread

February 16, 2021 · Original source

We should also be concerned about a fifth wave (possibly overlapping with the fourth wave; they may not have obviously separate peaks). Virologists have identified two new strains, one in South Africa, one in Brazil, which probably have "immune escape" - the ability to infect people who have already gotten, recovered from, and developed antibodies to the original strain (or been vaccinated against it). Both strains already have a few cases in the US. It will take them a few months to spread to the point where they're relevant, but they should eventually be the majority of new cases.

Inline links: already have, a few cases in the US

Prediction: 66% chance that sometime this year, the South African and Brazilian strains - or other new strains with similar dynamics - will be a majority of coronavirus cases in the US.Some sources describe these strains as "vaccine resistant". This is a matter of degree. The UK strain is probably very slightly vaccine-resistant (most sources are describing it as not vaccine resistant, but if you look closely this is another "well we can't prove it is" situation, and the best point estimates suggest some tiny amount of extra resistance which probably doesn't make a big difference.). The South African strain is significantly vaccine resistant. The Brazilian strain is too new to know much about, but seems to be very similar to the South African strain and I would be surprised if its numbers differed very much.

Some sources describe these strains as "vaccine resistant". This is a matter of degree. The UK strain is probably very slightly vaccine-resistant (most sources are describing it as not vaccine resistant, but if you look closely this is another "well we can't prove it is" situation, and the best point estimates suggest some tiny amount of extra resistance which probably doesn't make a big difference.). The South African strain is significantly vaccine resistant. The Brazilian strain is too new to know much about, but seems to be very similar to the South African strain and I would be surprised if its numbers differed very much.

Mantic Monday: Judging April COVID Predictions

February 23, 2021 · Original source

True. US was at 353,000, second place was Brazil with 195K.

Your Book Review: The Accidental Superpower

May 21, 2021 · Original source

We didn’t just get tremendous economic growth though – we got “magical” results, but they were based on a one-time confluence of factors that “overwhelmed the normal rule that lots of twenty-and thirty-somethings make for an expensive-capital environment.” What were these one-time accelerants? He identifies the peace dividend – cuts in military spending that allowed capital to be put to more productive uses – as one such change, along with the emergent dominance of the US dollar, particularly boosted by Russian demand thanks to the collapse of their currency, and a later boost in demand thanks to the East Asian financial crisis. With the Europeans’ decision to eliminate national currencies (agreed upon in a 1992 treaty, with the Euro to be introduced in 1999), they became relatively unattractive, and the Euro itself (an “unprecedented experiment in pan-government planning”) was too risky. Many holders of European currencies switched to the US dollar, such that between 1994 and 2002 (“when the euro finally got some traction and the surge dialed back”) there was a $2 trillion increase in the money supply. Zeihan also points to a collapse in commodities prices influenced by the elimination of Russian demand, but continued Russian production of oil and other commodities, followed by a collapse in demand thanks to the East Asian financial crisis. This story of capital coming to the West (“allowing consumption-driven growth not simply to soar, but to explode”) is one of chance world events. However, the story of capital coming from the Boomer cohort is one of demographics. By the 2000s, they’re the mature workers of Zeihan’s four stages described above – and as the bulge in the demographic pyramid, they started flooding the world with capital. Accordingly, “The cost of credit plummeted to levels never before experienced.” Zeihan suggests that developed-world demographics are the cause of booms in places that haven’t been well-developed, from Southern Europe to Brazil, Russia, and India. But he says it’s quickly coming to an end; Boomer savings into stocks and bonds will be moving to low-risk instruments and then turning into withdrawals rather than savings, and the cohort behind them is too small to replace all of that capital. And it’s a worldwide phenomenon: In every single developed country there is currently an American-style population inversion between the about-to-retire and the about-to-be-mature-workers age groups. Japan’s Boomers bulge is a decade older than the American equivalent, while Spain’s is roughly fifteen years younger. Everyone else falls somewhere in between. It dictates a period of chronically low growth and high credit costs, just not on precisely the same time frame. The undeveloped world is that way because it can’t self-fund, so without foreign capital, their growth will come to an end. In sum, the 1990-2005 period of high growth and easy capital was a historical anomaly; “the post-Cold War financial flight was a once-in-a-generation event” and the demographic bulge that coincided with it won’t come around again for decades, if ever. 4 2: America’s incredible advantages As noted above, Zeihan really likes America’s position in the world. He likes its demographics (relative to other developed countries) and loves its geography. Taking the population question first, in America, “the demographic inversion is only a temporary development.” America is younger than the rest of the developed world, as it urbanized later and its enormous size made having kids easier despite that urbanization (i.e., the suburbs exist). This makes the demographic crunch a single-generation issue, as the Millennials are a huge cohort. And even if they weren’t, America assimilates immigrants more easily than other places – Zeihan attributes this to it being a “settler society” – which can help with demographic problems. The rest of the developed world doesn’t have similar cohorts following their massive Boomer and Gen-X analogues. Accordingly: While the American financial world will be past its period of maximum stress by 2030, for the rest of the world 2030 will simply be another year of an ever-deepening imbalance between retirees and taxpayers, with smaller and smaller generations coming up the ranks generating less and less growth. For the developed world beyond the United States—and even large portions of the developing world—chronic capital poverty and permanent recession will be the new normal from which there is no return. Together with America’s Millennial-led growth and abundant energy (there’s a chapter explaining how shale is a done deal that, as of the mid-2014 writing, already made America the world’s largest energy producer 5), by 2030 Zeihan sees it as practically the only country with an economy worth noting. Anyone who is familiar with American geography should see the argument that’s coming about that aspect of Zeihan’s model. Isn’t the Mississippi River a pretty big deal? And those oceans on the east and west coasts seem like nice borders. Indeed, while he gives us many reasons why there was always going to be an American superpower, geography is central to his story. He has lots to say about America’s internal river systems, farmland, and other geographic features. What mountain barriers exist are apparently better than in other countries in terms of allowing internal transport; the Rockies have major passes, several of which have large cities within them, and the easiest pass in the Appalachians featured America’s first National Road, 130 miles of buried logs that linked two rivers, and thus the east coast with the best farmland in the world. As we saw with his exposition on the Nile, Zeihan puts a lot of emphasis on the value of river systems. He argues that America’s waterway network alone should be sufficient for “global dominance.” The numbers he provides in support of this point are impressive. For example, “the Mississippi is only one of twelve major navigable American rivers. Collectively, all of America’s temperate-zone rivers are 14,650 miles long. China and Germany each have about 2,000 miles, France about 1,000. The entirety of the Arab world has but 120.” He praises US barrier islands that mitigate oceanic destruction and effectively create another river system, as well as the fact that the river system is an actual network. All of this gives America more internal waterways than the rest of the world combined. Thus, we get cheap transportation for “Nebraska corn or Tennessee whiskey or Texas oil or New Jersey steel or Georgia peaches or Michigan cars,” enabling savings that “can be used for whatever Americans (or their government) want, from iPhones to aircraft carrier battle groups.” America doesn’t have to spend on artificial infrastructure, like German roads and rails, but when it does, the competition from the rivers keeps transport costs low. Cheap internal transportation has other benefits. “It’s a recipe for small government and high levels of entrepreneurship,” as small government keeps taxes low, leaving people with plenty of capital. Some people may think of the American consumer with disdain, but it isn’t a new phenomenon. Zeihan points out that America has been the world’s largest consumer market “since shortly after the Civil War.” His observation about a robust food supply forming the base of any civilization bodes well for America, which apparently has the largest connected stretch of quality farmland in the world (the Midwest), the value of which is exponentially increased by the fact that it overlaps with so many of these amazing river systems. It isn’t just the Midwest that he gushes over. California’s Central Valley and the Sacramento River, and Washington and Oregon’s farmland with the Columbia and Snake Rivers get praise. The only major farmland more than 150 miles from a navigable waterway is some of the Great Plains near the Rockies. ***** Zeihan provides a reminder that national security is actually a thing, and that at its most basic level, it’s about protection against invasions. It was something of a shock reading about America’s land borders in that context. “As Santa Anna discovered during the Texas Independence War, there is no good staging location in (contemporary) Mexican territory that could strike at American lands.” And, “Canada’s border with the United States is much longer, more varied, and even more successful at keeping the two countries separated,” thanks to mountains and thick forests over much of it. The mid-continent lands are much more connected, but Zeihan frames these Canadian areas as basically American; they’re physically separated from Canada’s core eastern provinces, so trade with them is weaker than with the closer American states. Then there are the oceans. As much as Zeihan loves deserts for protection, he loves oceans more (particularly in a post-World War II world; more on that below). We get a story about the War of 1812 nearly splitting America into three when the British attacked Baltimore. America learned about “strategic vulnerability and sea approaches,” as the attack “on Baltimore—indeed, the entire war effort—would have been impossible without launching grounds in Canada and the Caribbean.” American foreign policy since then can be understood with respect to this lesson. Zeihan cites it as inspiration for America’s steps to make its ocean borders truly impenetrable, such as working to sever Canada from Britain, and the imperial-era acquisitions of Alaska, Hawaii, Midway, Puerto Rico, and de facto control of Cuba (preventing enemies from cutting off Mississippi River-based trade from the rest of the world). There’s more to Zeihan’s being awestruck by America than his analysis of its balance of transport advantages. He argues that America has been the world leader for agriculture, technology, finance, and industry since the Civil War, and runs through a litany of reasons for its preeminence: America is like a continent-sized island (because of its effective land borders), which is always going to be a more natural naval power than a more landlocked country.

Inline links: 4, 5

The second half of The Accidental Superpower is filled with Zeihan’s predictions about what happens if the big thesis is right. Some states will fail, as they don’t have what’s needed to survive (Syria, Greece, Libya). Some will decentralize, as they’re in the same boat, just not as hard up (Russia, China). Some will merely decline, as they have some capacity to address challenges (Brazil, India, Canada). Some will cope (UK, France, Peru, Philippines). A few will join the US as “masters of the chaos,” as they have favorable geographies and other advantages (Australia, Argentina, Angola, Turkey, Indonesia, Uzbekistan).

Your Book Review: Humankind

May 28, 2021 · Original source

It turns out something like this has actually been tried. In 2004 in Torres, Venezula, an outside candidate, Julio Chavez was elected mayor on a platform of turning power over to the people. And he did. Hundreds of gatherings of residents took place which decided 100% of how the budget would be spent. The result was a huge success, with less corruption, more infrastructure, fewer glory projects, and a much more engaged electorate. Julio has retired, but the process is still going on under his successor. Last year 15,000 people participated in setting the budget. This isn't a one off, Porto Alegre, Brazil, started allocating a quarter of its budget this way in 1989, today more than 1,500 cities from New York to Hamburg are doing something in this space. "[This is] one of the biggest movements of the twenty-first century," writes Bregman, "but the chances are you've never heard of it." I certainly hadn't. Apparently, citizens engaging in calm, constructive, detailed dialogue is lousy box office, and none of them have hired promoters or bought ad time. Lousy box office it might be, but trusting our populations might just be the recipe for revitalising our democracies.

Instead Of Pledging To Change The World, Pledge To Change Prediction Markets

June 07, 2021 · Original source

This is nice, but I can't help but remember eg Australia's 2009 Copenhagen summit pledge to decrease emissions 5% by 2020 (in fact, they increased 17%). Or Brazil's pledge at the same summit to cut emissions 38% by 2020 (in fact, they increased 45%). Or Canada's pledge for -20% (they got +1%). I'm not cherry-picking bad actors here, I'm just going through the alphabet (pledges source, outcomes source) . For that matter, what about George W. Bush's pledge to return Americans to the moon by 2020?

Inline links: pledges source, outcomes source, pledge to return Americans to the moon

Book Review: How Asia Works

June 28, 2021 · Original source

Klaus Deininger, one of the world’s leading authorities on land policy and development, has spent decades assembling data that show how the nature of land distribution in poor countries predicts future economic performance. Using global land surveys done by the United Nations’ Food and Agriculture Organisation (FAO), he has worked out that only one significant developing country has managed a long-term growth rate of over 2.5 per cent with a very unequal distribution of land. That country is Brazil, the false prophet of fast growth which collapsed in a debt crisis in the 1980s in large part because of its failure to increase agricultural output. Deininger’s two big conclusions are that land inequality leads to low long-term growth and that low growth reduces income for the poor but not for the rich. In short, if poor countries are to become rich, then the equitable division of land at the outset of development is a huge help. Japan, Korea and Taiwan put this in place.

Lockdown Effectiveness: Much More Than You Wanted To Know

July 07, 2021 · Original source

Still, most places that were worse than Sweden had good reasons to do worse than Sweden. Italy was hit very early and has the highest percent of elderly people in Europe. The US and Brazil were very large diverse countries with bungled federal responses and borderline-COVID-denialist leaders. Belgium counted its coronavirus deaths in an unusual way that inflated the numbers relative to other countries. In the end, Sweden still ended out with a death rate about double the European average. Seems pretty bad.

Inline links: counted its coronavirus deaths in an unusual way

August 02, 2021 · Original source

Mark Lutter of CCI is kind of bummed about this. He has to meet with government officials and advocate for charter cities, and he would love to be able to say something like “Amazon is planning a charter city in Brazil”, and since everyone recognizes Amazon is an important dignified corporation and Brazil is an important dignified country, they’ll agree that this all seems like the sort of thing important dignified people do and they’re on board with it. Instead, all the important dignified people involved demand secrecy, and your choices are the husband-and-wife team interested in “ecstatic birthing” or those Black Hammer guys from the last links roundup. It’s individually rational, but bad for the charter city movement in general.

Inline links: the last links roundup

Meetups Everywhere 2021: Times And Places

August 23, 2021 · Original source

SÃO PAULO, BRAZIL (RSVP) Contact: Fernando, fdesmello[at]gmail[dot]com Time: 2:00 PM, Saturday, September 11 Location: Ibirapuera Park, in front of the entrance to the Planetarium. I will be carrying a sign with 'ACX MEETUP' on it. Coordinates: https://w3w.co/refrain.hacking.workforce

Inline links: RSVP, https://w3w.co/refrain.hacking.workforce

Ivermectin: Much More Than You Wanted To Know

November 17, 2021 · Original source

Okay, fine, they misspelled “recovery” once. But they spelled it right the other time! That puts it in the top 50% for ivermectin papers! The fraud-hunters have examined this paper closely and are unable to find any signs of fraud. @PubPeer on the Mahmud trial of ivermectin in covid patients.\n\nI have now reviewed the individual patient data master sheet.\n\nI did not find any irregularities and the summary data matches the published data.\n\n","username":"K_Sheldrick","name":"Kyle Sheldrick","profile_image_url":"","date":"Sat Jul 17 11:06:25 +0000 2021","photos":[],"quoted_tweet":{},"reply_count":0,"retweet_count":2,"like_count":12,"impression_count":0,"expanded_url":{"url":"https://pubpeer.com/publications/E1D65711EF28D14517731BEACB89C8#2","title":"PubPeer - Ivermectin in combination with doxycycline for treating COVI...","description":"There are comments on PubPeer for publication: Ivermectin in combination with doxycycline for treating COVID-19 symptoms: a randomized trial (2021)","domain":"pubpeer.com"},"video_url":null,"belowTheFold":true}" data-component-name="Twitter2ToDOM"> I think this paper is legitimate and that its findings need to be seriously considered. Serious consideration doesn’t always meant they’re true - sometimes if we have strong evidence otherwise we can dismiss things without understanding why. And there’s always the chance it was a fluke, right? Can something have a p-value less than 0.001 and still be a fluke? Szenta Fonseca et al: This is a chart review from Brazil. Researchers looked at various people who had been treated for COVID in an insurance company database, saw whether they got ivermectin or not, and saw whether the people who got it did better or worse. About a hundred people got it, and a few hundred others didn’t. The people who got it did not do any better than anyone else, and you’ll notice this is one of the rare red boxes on the table above. But we shouldn’t take this study seriously. Nobody took any effort to avoid selection bias, so it’s very possible that sicker people were given more medication (including ivermectin), which unfairly handicaps the ivermectin group. Also, it’s hard to tell from the paper who was on how much of what, and the discussion of ivermectin seems like kind of an afterthought after discussing lots of other meds in much more depth. This is another one I feel comfortable ignoring. Cadegiani et al: A crazy person decided to put his patients on every weird medication he could think of, and 585 subjects ended up on a combination of ivermectin, hydroxychloroquine, azithromycin, and nitazoxanide, with dutasteride and spironolactone "optionally offered" and vitamin D, vitamin C, zinc, apixaban, rivaraxoban, enoxaparin, and glucocorticoids "added according to clinical judgment". There was no control group, but the author helpfully designated some random patients in his area as a sort-of-control, and then synthetically generated a second control group based on “a precise estimative based on a thorough and structured review of articles indexed in PubMed and MEDLINE and statements by official government agencies and specific medical societies”. Patients in the experimental group were twice as likely to recover (p < 0.0001), had negative PCR after 14 vs. 21 days, and had 0 vs. 27 hospitalizations. Speaking of low p-values, some people did fraud-detection tests on another of Cadegiani’s COVID-19 studies and got values like p < 8.24E-11 in favor of it being fraudulent. And, uh, he’s also studied whether ultra-high-dose antiandrogens treated COVID, and found that they did, cutting mortality by 92% . But the trial is under suspicion, with a BMJ article calling it “[the worst] violations of medical ethics and human rights in Brazil’s history” and “an ethical cesspit of violations”. [update 2022: this section originally contained more accusations against Cadegiani. Alexandros Marinos does a deeper dive with information not available at the time I wrote this, and finds some of them were overstated or false by implication] Anyway, let’s not base anything important on the results of this study, mmkay? A defiant Flavio Cadegiani. Imagine a guy who looks like this telling you to take ultra-high-dose antiandrogens. Ahmed et al: And we’re back in Bangladesh. 72 hospital patients were randomized to one of three arms: ivermectin only, ivermectin + doxycycline, and placebo. Primary endpoint was time to negative PCR, which was 9.7 days for ivermectin only and 12.7 days for placebo (p = 0.03). Other endpoints including duration of hospitalization (9.6 days ivermectin vs. 9.7 days placebo, not significant). This looks pretty good for ivermectin and does not have any signs of fraud or methodological problems. If I wanted to pick at it anyway, I would point out that the ivermectin + doxycycline group didn’t really differ from placebo, and that if you average out both ivermectin groups (with and without doxycycline) it looks like the difference would not be significant. I had previously committed to considering only ivermectin alone in trials that had multiple ivermectin groups, so I’m not going to do this. I can’t find any evidence this trial was preregistered so I don’t know whether they waited to see what would come out positive and then made that their primary endpoint, but virological clearance is a pretty normal primary endpoint and this isn’t that suspicious. It’s impossible to find any useful commentary on this study because Elgazzar (the guy who ran the most famous fraudulent ivermectin study) had the first name Ahmed, everyone is talking about Elgazzar all the time, and this overwhelms Google whenever I try to search for Ahmed et al. For now I’ll just keep this as a mildly positive and mildly plausible virological clearance result, in the context of no effect on hospitalization length or most symptoms. Chaccour et al: 24 patients in Spain were randomized to receive either medium-dose ivermectin or placebo. The primary outcome was percent of patients with negative PCR at day 7; secondary outcomes were viral load and symptoms. The primary endpoint ended up being kind of a wash - everyone still PCR positive by day 7 so it was impossible to compare groups. Ivermectin trended toward lower viral load but never reached significance. Weirdly, ivermectin did seem to help symptoms, but only anosmia and cough towards the end (p = 0.03), which you would usually think of as lingering post-COVID problems. The paper says: Given these findings, consideration could be given to alternative mechanisms of action different from a direct antiviral effect. One alternative explanation might be a positive allosteric modulation of the nicotinic acetylcholine receptor caused by ivermectin and leading to a downregulation of the ACE-2 receptor and viral entry into the cells of the respiratory epithelium and olfactory bulb. Another mechanism through which ivermectin might influence the reversal of anosmia is by inhibiting the activation of pro-inflammatory pathways in the olfactory epithelium. Inflammation of the olfactory mucosa is thought to play a key role in the development of anosmia in SARS-CoV-2 infection This seems kind of hedge-y. If you’re wondering where things went from there, Dr. Chaccour is now a passionate anti-ivermectin activist: @Finneganporter in @BusinessInsider \n\nThe roots of #ivermectin mania: How South America incubated a fake-medicine craze that took the US by storm\n\n","username":"carlos_chaccour","name":"Dr. Carlos Chaccour ??????","profile_image_url":"","date":"Sun Nov 07 18:40:28 +0000 2021","photos":[],"quoted_tweet":{},"reply_count":0,"retweet_count":2,"like_count":9,"impression_count":0,"expanded_url":{"url":"https://www.businessinsider.in/international/news/the-roots-of-ivermectin-mania-how-south-america-incubated-a-fake-medicine-craze-that-took-the-us-by-storm/articleshow/87554081.cms","image":"https://bucketeer-e05bbc84-baa3-437e-9518-adb32be77984.s3.amazonaws.com/public/images/88d08e70-c9e2-46d4-a5df-96807b6c3a13_2000x1000.jpeg","title":"The roots of ivermectin mania: How South America incubated a fake-medicine craze that took the US by storm","description":"The popularity of unproven anti-parasitic drug ivermectin as a COVID-19 treatment is surging. Its use has roots in South America, where it was hyped by populist","domain":"businessinsider.in"},"video_url":null,"belowTheFold":true}" data-component-name="Twitter2ToDOM"> So I guess he must think of this trial as basically negative, although realistically it’s 24 people and we shouldn’t put too much weight on it either way. Ghauri et al: Pakistan, 95 patients. Nonrandom; the study compared patients who happened to be given ivermectin (along with hydroxychloroquine and azithromycin) vs. patients who were just given the latter two drugs. There’s some evidence this produced systematic differences between the two groups - for example, patients in the control group were 3x more likely to have had diarrhea (this makes sense; diarrhea is a potential ivermectin side effect, so you probably wouldn’t give it to people already struggling with this problem). Also, the control group was twice as likely to be getting corticosteroids, maybe a marker for illness severity. Primary outcome was what percent of both groups had a fever: on day 7 it was 21% of ivermectin patients vs. 65% of controls, p < 0.001. No other outcomes were reported. I don’t hate this study, but I think the nonrandom assignment (and observed systematic differences) is a pretty fatal flaw. I can’t find anyone else talking about this one. At least no one seems to be saying anything bad. Babaloba et al: Be warned: if I have to refer to this one in real-life conversation, I will expand out the “et al” and call it “Babalola & Alakoloko”, because that’s really fun to say. This was a Nigerian RCT comparing 21 patients on low-dose ivermectin, 21 patients on high-dose ivermectin, and 20 patients on a combination of lopinavir and ritonavir, a combination antiviral which later studies found not to work for COVID and which might as well be considered a placebo. Primary outcome, as usual, was days until a negative PCR test. High dose ivermectin was 4.65 days, low dose was 6 days, control was 9.15, p = 0.035. Figure 2 is apparently a photograph of the computer screen where they did this calculation. Gideon Meyerowitz-Katz, part of the team that detects fraud in ivermectin papers, is not a fan of this one: He doesn’t say there what means, but elsewhere he tweets this figure: It’s always a bad sign when your study features in an image with “NUMEROUS IMPOSSIBLE NUMBERS” in red at the top. I think his point is that if you have 21 people, it’s impossible to have 50% of them have headache, because that would be 10.5. If 10 people have a headache, it would be 47.6%; if 11, 52%. So something is clearly wrong here. Seems like a relatively minor mistake, and Meyerowitz-Katz stops short of calling fraud, but it’s not a good look. I’m going to be slightly uncomfortable with this study without rejecting it entirely, and move on. Ravakirti et al: Here we’re in Eastern India - not exactly Bangladesh again, but a stone’s throw away from it. In this RCT patients were randomized into an ivermectin group (57) and a placebo group (58). Primary outcome was negative PCR on day 6, because doing it on day 7 like everyone else would be too easy. As with several other groups, this was a bad move; too few people had it to make a good comparison; it was 13% of intervention vs. 18% of placebo, p = 0.3. Secondary outcomes were also pretty boring, except for the most important: 4 people in the placebo group died, compared to 0 in ivermectin (p = 0.045). On the one hand, this is one outcome of many, reaching the barest significance threshold. Another fluke? Still, there are no real problems with this study, and nobody has anything to say against it. Let’s add this one to the scale as another very small and noisy piece of real evidence in ivermectin’s favor. Bukhari et al: Now we’re in Pakistan. 50 patients were randomized to low-dose ivermectin, another 50 got standard of care including vitamin D. There was no placebo, but primary outcome was number of days to reach negative PCR, which it seems hard for placebo to affect much, so I don’t care. 5 controls and 9 ivermectin patients left the hospital against medical advice and could not be followed up, which is bad but not necessarily study-ruining. They never measured their supposed primary outcome of “days to reach negative PCR” directly, but they did measure how many people had negative PCR on various days, and ivermectin had a clear advantage - for example, on day 7, it was 37/50 for IVR and only 20/50 for control. Even if we assume all the lost-to-followup patients had maximally bad-for-the-hypothesis results, that’s still a positive finding. Nobody else has much to say about this one, certainly no accusations that they’ve found anything suspicious. Keep. Mohan et al: India. RCT. 40 patients got low-dose ivermectin, 40 high-dose ivermectin, and 45 placebo. Primary outcomes were time to negative PCR, and viral load on day 5. In the results, they seem to have reinterpreted “time to negative PCR” as the subtly different “percent with negative PCR on some specific day”. High-dose ivermectin did best (47.5% negative on day 5) and placebo worst (31% negative), but it was insignificant (p = 0.3). There was no difference in viral load. All groups took about the same amount of time for symptoms to resolve. More placebo patients had failed to recover by the end of the study (6) than ivermectin patients (2), but this didn’t reach statistical significance (p = 0.4). Overall a well-done, boring, negative study, although ivermectin proponents will correctly point out that, like basically every other study we have looked at, the trend was in favor of ivermectin and this could potentially end up looking impressive in a meta-analysis. Biber et al: This is an RCT from Israel. 47 patients got ivermectin and 42 placebo. Primary endpoint was viral load on day 6. I am having trouble finding out what happened with this; as far as I can tell it was a negative result and they buried it in favor of more interesting things. In a "multivariable logistic regression model, the adjusted odds ratio of negative SARS-CoV-2 RT-PCR negative test" favored ivermectin over placebo (p = 0.03 for day 6, p = 0.01 for day 8), but this seems like the kind of thing you do when your primary outcome is boring and you’re angry. Gideon Meyerowitz-Katz is not a fan: He notes that the study excluded people with high viral load, but the preregistration didn’t say they would do that. Looking more closely, he finds they did that because, if you included these people, the study got no positive results. So probably they did the study, found no positive results, re-ran it with various subsets of patients until they did get a positive result, and then claimed to have “excluded” patients who weren’t in the subset that worked. I’m going to toss this one. Elalfy et al: What even is this? Where am I? As best I can tell, this is some kind of Egyptian trial. It might or might not be an RCT; it says stuff like “Patients were self-allocated to the treatment groups; the first 3 days of the week for the intervention arm while the other 3 days for symptomatic treatment”. Were they self-allocated in the sense that they got to choose? Doesn’t that mean it’s not random? Aren’t there seven days in a week? These are among the many questions that Elalfy et al do not answer for us. The control group (which they seem to think can also be called “the white group”) took zinc, paracetamol, and maybe azithromycin. The intervention group took zinc, nitazoxanide, ribavirin, and ivermectin. There were very large demographic differences between the groups of the sort which make the study unusable, which they mention and then ignore. From there, they follow this normal and totally comprehensible flowchart: There is no primary outcome assigned, but viral clearance rates on day seven were 58% in the yellow group compared to 0% in the white group, which I guess is a strong positive result. This table… …looks very impressive, in terms of the experimental group doing better than the control, except that they don’t specify whether it was before the trial or after it, and at least one online commentator thinks it might have been before, in which case it’s only impressive how thoroughly they failed to randomize their groups. Overall I don’t feel bad throwing this study out. I hope it one day succeeds in returning to its home planet. Lopez-Medina et al: Colombian RCT. 200 patients took ivermectin, another 200 took placebo. They originally worried the placebo might taste different than real ivermectin, then solved this by replacing it with a different placebo, which is a pretty high level of conscientiousness. Primary outcome was originally percent of patients whose symptoms worsened by two points, as rated on a complicated symptom scale when a researcher asked them over the phone. Halfway through the study, they realized nobody was worsening that much, so they changed the primary outcome to time until symptoms got better, as measured by the scale. In the ivermectin group, symptoms improved that much after 10 days; in the placebo group, after 12, p = 0.53. By the end of the study, symptoms had improved in 82% of ivermectin users and 79% of controls, also insignificant. 4 patients in the ivermectin group needed to be hospitalized compared to 6 in the placebo group, again insignificant. This study is bigger than most of the other RCTs, and more polished in terms of how many spelling errors, photographs of computer screens, etc, it contains. It was published in JAMA, one of the most prestigious US medical journals, as opposed to the crappy nth-tier journals most of the others have been in. When people say things like “sure, a lot of small studies show good results for ivermectin, but the bigger and more professional trials don’t”, this is one of the two big professional trials they’re talking about. Ivermectin proponents make some good arguments against it. In order to get as big as it did, Lopez-Medina had to compromise on rigor. Its outcome is how people self-score their symptoms on a hokey scale in a phone interview, instead of viral load or PCR results or anything like that. Still, this is basically what we want, right? In the end, we want people to feel better and less sick, not to get good scores on PCR tests. Also, it changed its primary outcome halfway through; isn’t that bad? I think maybe not; the reason we want a preregistered primary outcome is so that you don’t change halfway through to whatever outcome shows the results you want. The researchers in this study did a good job explaining why they changed their outcome, the change makes sense, and their original outcome would also have shown ivermectin not working (albeit less accurately and effectively). I don’t know of any evidence that they knew (or suspected) final results when switching to this new outcome, and it seems like the most reasonable new outcome to switch to. Finally, their original placebo tasted different from ivermectin (though they switched halfway through). This is one of the few studies where I actually care about placebo, because people are self-rating their symptoms. But realistically most of these people don’t know what ivermectin is supposed to taste like. Also, they did a re-analysis and found there was no difference between the people who got the old placebo and the new one. I’m making a big deal of this because ivmmeta.com - the really impressive meta-analysis site I’ve been going off of - puts a special warning letter underneath their discussion of this study, urging us not to trust it. They don’t do this for any of the other ones we’ve addressed so far - not the one by the guy whose other studies were all frauds, not the one where 50% of 21 people had headaches, not the unrandomized one where the groups were completely different before the experiment started, not even the one by the guy accused of crimes against humanity. Only this one. This makes me a lot less charitable to ivmmeta than I would otherwise be; I think it’s hard to choose this particular warning letter strategy out of well-intentioned commitment to truth. They just really don’t like this big study that shows ivermectin doesn’t work. Also, the warning itself irritates me, and includes paragraphs like: RCTs have a fundamental bias against finding an effect for interventions that are widely available — patients that believe they need treatment are more likely to decline participation and take the intervention [Yeh], i.e., RCTs are more likely to enroll low-risk participants that do not need treatment to recover (this does not apply to the typical pharmaceutical trial of a new drug that is otherwise unavailable). This trial was run in a community where ivermectin was available OTC and very widely known and used. Nobody else worries about this, and there are a million biases that non-randomized studies have that would be super-relevant when discussing those, but somehow when they’re pro-ivermectin the site forgets to be this thorough. I think a better pro-ivermectin response to this study is to point out that all the trends support ivermectin. Symptoms took 10 days to resolve in the ivermectin group vs. 12 in placebo; 4 ivermectin patients were hospitalized vs. 6 placebo patients, etc. Just say that this was an unusually noisy trial because of the self-report methodology, and you’re confident that these small differences will add up to significance when you put them into a meta-analysis. Roy et al: We’re back in East India, and back to non-randomized trials. 56 patients were retrospectively examined; some had been given ivermectin + doxycycline, others hydroxychloroquine, other azithromycin, and others symptomatic treatment only. We don’t get any meaningful information about how this worked, but we are told that they did not differ in “clinical well-being reporting onset timing”. Whatever. Chahla et al: The first of many Argentine trials. 110 patients received medium-dose ivermectin; 144 were kept as a control (no placebo). This was “cluster randomized”, which means they randomize different health centers to either give the experimental drug or not. This is worse than regular randomization, because there could be differences between these health centers (eg one might have better doctors who otherwise give better treatment, one might be in the poor part of town and have sicker patients, etc). They checked to see if there were any differences between the groups, and it sure looks like there were (the experimental group had twice as many obese people as the controls), but as per them, these differences were not statistically significant. Note that if this did make a difference, it would presumably make ivermectin look worse, not better. The primary outcome was given as “increase discharge from outpatient care with COVID-19 mild disease”. This favored the treatment; only 2/110 patients in the ivermectin group failed to be discharged, compared to 20 patients in the control group. But, uh, these were at different medical centers. Can’t different medical centers just have different discharge policies? One discharges you as soon as you seem to be getting better, the other waits to really make sure? This is an utterly crap endpoint to do a cluster randomized controlled trial on. If you’re going to do cRCT, which is never a great idea, you should be using some extremely objective endpoint that doctors and clinic administrators can’t possibly affect, like viral load according to some third-party laboratory, using the same third-party laboratory for both clinics. This is such a bad idea that I can’t help worrying I’m missing or misunderstanding something. If not, this is dumb and bad and should be ignored. Mourya et al: We’re back in India. This is a nonrandomized study comparing 50 patients given ivermectin to 50 patients given hydroxychloroquine. No primary outcome was named, but they focus on PCR negativity. Only 6% of patients in the hydroxychloroquine group were negative, compared to 90% of patients in the ivermectin group! On what day did they do the test? Uh, kind of random, and they admit that “in [the hydroxychloroquine group], mean time difference from the date of initiation of treatment and second test was significantly longer (7.24±2.75 days) as compared to 5.22±1.21 days in [the ivermectin group] (p=0.021).” Since they assessed these groups at different times, we shouldn’t draw any conclusions from them getting different results. Except that as far as I can tell this should handicap ivermectin, making it especially impressive that it did better. But also, the ivermectin group was made mostly of people who had been asymptomatic at the beginning (70%), and the hydroxychloroquine group had almost no asymptomatic cases (8%) . They were giving the ivermectin to healthy people and the hydroxychloroquine to sick people! They admit deep in the discussion that this “may be a confounding factor”. So basically they got totally different groups of people, tested them at totally different times, and the two sets of test results differed. So what? So this is why normal people do RCTs instead of whatever the heck this is, that’s what. Loue et al: …this one isn’t going to be an RCT either. Loue tells a story about a cluster of COVID cases at the French nursing home where he works. He asked people if they wanted to try ivermectin; 10 did and 15 didn’t. 1 ivermectin patient died, compared to 5 non-ivermectin patients. The non-ivermectin group looked a bit sicker than the ivermectin group in the inevitable Table 1, though it’s hard to tell. One interesting possible confounder (not mentioned, but I’m imagining it) is that demented patients probably couldn’t consent to ivermectin and ended up in the control group. This is another case of “I’m not going to trust anything that isn’t an RCT”. Merino et al: Another (sigh) non-RCT. Mexico City tried a public health program where if you called a hotline and said you had COVID, they sent you an emergency kit with various useful supplies. One of those supplies was ivermectin tablets. 18,074 people got the kit (and presumably some appreciable fraction took the ivermectin, though there’s no way to prove that). Their control group is people from before they started giving out the kits, people from after they stopped giving out the kits, and people who didn’t want the kits. There are differences in who got COVID early in the epidemic vs. later, and in people who did opt for medical kits vs. didn’t. To correct these, the researchers tried to adjust for confounders, something which - as I keep trying to hammer home again and again - never works. They found that using the kit led to a 75% or so reduction in hospitalization, though they were unable to separate out the ivermectin from the other things in the kit (paracetamol and aspirin), or from the placebo effect of having a kit and feeling like you had already gotten some treatment (if I understand right, the decision to go to the hospital was left entirely to the patient). I think this study is a moderate point in favor of giving people kits in order to prevent hospital overcrowding, but I’m not willing to accept that it tells us much about ivermectin in particular. Faisal et al: This one was published in The Professional Medical Journal (mispelled as “Profesional Medical Journal” in its URL), so you know it’s going to be good! It describes itself as “a cross-sectional study”, but later says it “randomized patients into two groups”, which would make it an RCT - I think they might just be using the term “cross-sectional” different from the standard American usage. A hospital in Pakistan got 50 patients on ivermectin + azithromycin, and another 50 on azithromycin alone. Primary outcome was not mentioned, and the data were presented confusingly, but a typical result is that only 4% of the ivermectin group had symptoms lasting more than 10 days, whereas 16% of the control group did, p < 0.01. They do a really weird thing where they compare how long it took symptoms to resolve between IVM and control groups within each bin. That is, if I’m understanding correctly, they ask “of the people who took between 3-5 days for symptoms to resolve, did they resolve faster for IVM or control?”. This is an utterly bizarre analysis to perform, although it doesn’t affect the fact that their other results still seem to favor ivermectin. Maybe I’m confused about what’s going on here. I’ve mostly been letting people off easy on no placebo, but I as far as I can tell (not very far) this paper seems to be going off whether patients reported continuing to have symptoms to the hospital doing the study, and I think that is potentially susceptible to placebo effects. Additionally, there’s no preregistration, and even though they talk a lot about doing PCR tests they don’t present the results. This is by no means the worst study here but I still think it’s pretty low quality and I don’t trust it. Aref et al: This one is published in the International Journal Of Nanomedicine, even though I’m pretty sure that isn’t a real thing. In this case the “nanomedicine” is a new nasal spray version of ivermectin which is so confusing I cannot for the life of me figure out what dose they are giving these patients. This Egyptian study gives 57 patients intranasal ivermectin plus hydroxychloroquine, azithromycin, oseltamavir, and some vitamins; another 57 patients get all that stuff except the ivermectin. Primary outcome is not stated, but they look at various symptoms, all of which look better in the ivermectin group: 95% of ivermectin patients got negative PCRs at some time point, compared to 75% of controls, p = 0.004. I am pretty suspicious of this study, not least because it comes from Egypt which has an awful reputation for fake studies, and it returns extreme results that I wouldn’t expect even if ivermectin was actually a wonder drug. But I cannot find any particular thing wrong with it, nor did anyone else I looked at, so I will grudgingly let it stand. Krolewiecki et al: Another Argentine study. This one is a real RCT. 30 patients received ivermectin, 15 were the control group (no placebo, again). Primary outcome was difference in viral load on day 5. The trend favored ivermectin but it was not statistically significant, although they were able to make it statistically significant if they looked at a subset of higher-IVM-plasma-concentration patients. They did not find any difference in clinical outcomes. A pro-ivermectin person could point out that in the subgroup with the highest ivermectin concentrations, the drug seemed to work. A skeptic could point out that this is exactly the kind of subgroup slicing that you are not supposed to do without pre-registering it, which I don’t think this team did. I agree with the skeptic. Vallejos et al: Another Argentine study. It’s big (250 people in each arm). It’s an RCT. It tries to define a primary outcome (“Primary outcome: the trial ended when the last patient who was included achieved the end of study visit”), but that’s not what “primary outcome” means, and they don’t offer an alternative. Other outcomes: no difference in PCR on days 3 or 12. Hospitalization is nonsignificantly better in the ivermectin group (14 vs. 21, p = 0.2), but death is nonsigificantly better in the placebo group (3 vs. 4, p = 0.7). This isn’t even the kind of nonsignificant that might contribute to an exciting meta-analysis later. This is just a pure null result. I cannot find any problem with this study, and neither can anyone else I checked. This is the biggest RCT we’ve seen so far, so we should take it seriously. TOGETHER Trial: Speaking of big RCTs… This one hasn’t been published yet. There’s a video of a talk about it, but I am not going to watch it, because it is a video, so I am getting information secondhand from eg here. Apparently, it compares 677 people (!) randomized to ivermectin to 678 people randomized to placebo. 86 ivermectin patients ended up in the hospital compared to 95 placebo patients, p-value not significant. This was a really big professional trial done by bigshot researchers from a major Canadian university, and the medical establishment is taking it much more seriously than any of these others. When it comes out, it will probably get published in a top journal. When discussing Lopez-Medina, I wrote: When people say things like “sure, a lot of small studies show good results for ivermectin, but the bigger and more professional trials don’t”, this is one of the two big professional trials they’re talking about. This is the other one. Not coincidentally, it’s also the other trial that ivmmeta.com has a warning letter underneath telling you to disregard. Their main concern is that instead of truly randomizing patients to ivermectin vs. placebo, they did a time-dependent randomization that meant during some weeks more patients were getting one or the other. This is a problem because the trial takes place in Brazil, where different variants were more common at different times. Here’s their image: On the one hand, I have immense contempt for ivmmeta for letting all those other awful studies pass and then pulling out all the stops to try to nitpick this one. I have no idea if their proposed randomization failure really happened. And no doubt the reason they’re even able to investigate this is that this study is really careful and transparent - most of them don’t tell you anything about their randomization method. I would be shocked if other studies don’t have all these problems and worse. On the other hand, the point isn’t to be fair, it’s to be right. And this is a potential confounder. Not a huge one. But a potential one. I guess all we can do is try to bound the damage. Even if the confounding is 100% real and bad, there’s no way to make this study consistent with the crazy super-pro-ivermectin results of studies like Espitia-Hernandez and Aref. And even if we deny any confounding, we see the same slight pro-ivermectin trend - 86 hospitalizations vs. 95 - that we’ve seen in so many other studies. Nothing is going to make me believe that this isn’t in the top 33% of studies we’ve been looking at, so let’s add it as grist for the meta-analysis (though maybe not quite as much grist as its vast size indicates) and move on, angrily. Buonfrate et al: An Italian RCT. Patients were randomized into low-dose ivermectin (32), placebo (29), or high-dose ivermectin (32). Primary outcome was viral load on day 7. There was no significant difference (average of 2 in ivermectin groups, 2.2 in placebo group). They admit that they failed to reach the planned sample size, but did a calculation to show that even if they had, the trial could not have returned a positive result. Clinically, an average of 2 patients were hospitalized in each of the ivermectin arms, compared to 0 in the placebo arm - which bucks our previously-very-constant pro-ivermectin trend. Mayer et al: Not an RCT. Patients in an Argentine province were offered the opportunity to try ivermectin; 3266 said yes and become the experimental group, 17966 said no and became the control group. There were many obvious differences between the groups, but they all seemed to handicap ivermectin. There was a nonsignificant trend toward less hospitalization and significantly less mortality (1.5% vs. 2.1%, p = 0.03). While looking into this study, I learned the term “immortal time bias”. This means a period in between selection for the study and the beginning of study recording where patient outcomes are not counted. I think the problem here is that if you signed up for the system on Day X, and if you got sick before they could give you ivermectin, you were in the control group. See this Twitter thread, I have not confirmed everything he says. This only hardens my resolve to stay away from non-RCTs. Borody et al: Our last paper! …is it a paper? I can’t find it published anywhere. It mostly seems to be on news sites. Doesn’t look peer-reviewed. And it starts with “Note that views expressed in this opinion article are the writer’s personal views”. Whatever. 600 Australians were treated with ivermectin, doxycycline, and zinc. The article compares this to an “equivalent control group” made of “contemporary infected subjects in Australia obtained from published Covid Tracking Data”; this is not how you control group, @#!% you. Then it gets excited about the fact that most patients had better symptoms at the end of the ten-day study period than the beginning (untreated COVID resolves in about ten days). Why are these people wasting my time with this? Let’s move on. The Analysis If we remove all fraudulent and methodologically unsound studies from the table above, we end up with this: Gideon Meyerowitz-Katz, who investigated many of the studies above for fraud, tried a similar exercise. I learned about his halfway through, couldn’t help seeing it briefly, but tried to avoid remembering it or using it when generating mine (also, I did take the result of his fraud investigations into account), so they should be considered not quite independent efforts. His looks like this: He nixed Chowdhury, Babaloba, Ghauri, Faisal, and Aref, but kept Szenta Fonseca, Biber (?), and Mayer. There was correlation of 0.45, which I guess is okay. I asked him about his decision-making, and he listed a combination of serious statistical errors and small red flags adding up. I was pretty uncomfortable with most of these studies myself, so I will err on the side of severity, and remove all studies that either I or Meyerowitz-Katz disliked. We end up with the following short list: We’ve gone from 29 studies to 11, getting rid of 18 along the way. For the record, we eliminated 2/19 for fraud, 1/19 for severe preregistration violations, 10 for methodological problems, and 6 because Meyerowitz-Katz was suspicious of them. …but honestly this table still looks pretty good for ivermectin, doesn’t it? Still lots of big green boxes. Meyerowitz-Katz accuses ivmmeta of cherry-picking what statistic to use for their forest plot. That is, if a study measures ten outcomes, they sometimes take the most pro-ivermectin outcome. Ivmmeta.com counters that they used a consistent and reasonable (if complicated) process for choosing their outcome of focus, that being: If studies report multiple kinds of effects then the most serious outcome is used in calculations for that study. For example, if effects for mortality and cases are both reported, the effect for mortality is used, this may be different to the effect that a study focused on. If symptomatic results are reported at multiple times, we used the latest time, for example if mortality results are provided at 14 days and 28 days, the results at 28 days are used. Mortality alone is preferred over combined outcomes. Outcomes with zero events in both arms were not used (the next most serious outcome is used — no studies were excluded). For example, in low-risk populations with no mortality, a reduction in mortality with treatment is not possible, however a reduction in hospitalization, for example, is still valuable. Clinical outcome is considered more important than PCR testing status. When basically all patients recover in both treatment and control groups, preference for viral clearance and recovery is given to results mid-recovery where available (after most or all patients have recovered there is no room for an effective treatment to do better). If only individual symptom data is available, the most serious symptom has priority, for example difficulty breathing or low SpO2 is more important than cough. I’m having trouble judging this, partly because Meyerowitz-Katz says ivmmeta has corrected some earlier mistakes, and partly because there really is some reasonable debate over how to judge studies with lots of complicated endpoints. By this point I had completely forgotten what ivmmeta did, so I independently coded all 11 remaining studies following something in between my best understanding of their procedure and what I considered common sense. The only exception was that when the most severe outcome was measured in something other than patients (ie average number of virus copies per patient), I defaulted to one that was measured in patients instead, to keep everything with the same denominator. My results mostly matched ivmmeta’s, with one or two exceptions that I think are within the scope of argument or related to my minor deviations from their protocol. Placebo vs. ivermectin groups sometimes differed in size, which I’ve adjusted for and rounded off. Probably I’m forgetting some reason I can’t just do simple summary statistics to this, but whatever. It is p = 0.15, not significant. This is maybe unfair, because there aren’t a lot of deaths in the sample, so by focusing on death rather than more common outcomes we’re pointlessly throwing away sample size. What happens if I unprincipledly pick whatever I think the most reasonable outcome to use from each study is? I’ve chosen “most reasonable” as a balance between “is the most severe” and “has a lot of data points”: Now it’s p = 0.04, seemingly significant, but I had to make some unprincipled decisions to get there. I don’t think I specifically replaced negative findings with positive ones, but I can’t prove that even to myself, let alone to you. [UPDATE 5/31/22: A reader writes in to tell me that the t-test I used above is overly simplistic. A Dersimonian-Laird test is more appropriate for meta-analysis, and would have given 0.03 and 0.005 on the first and second analysis, where I got 0.15 and 0.04. This significantly strengthens the apparent benefit of ivermectin from ‘debatable’ to ‘clear’. I discuss some reasons below why I am not convinced by this apparent benefit.] (how come I’m finding a bunch of things on the edge of significance, but the original ivmmeta site found a lot of extremely significant things? Because they combined ratios, such that “one death in placebo, zero in ivermectin” looked like a nigh-infinite benefit for ivermectin, whereas I’m combining raw numbers. Possibly my way is statistically illegitimate for some reason, but I’m just trying to get a rough estimate of how convinced to be) So we are stuck somewhere between “nonsignificant trend in favor” and “maybe-significant trend in favor, after throwing out some best practices”. This is normally where I would compare my results to those of other meta-analyses made by real professionals. But when I look at them, they all include studies later found to be fake, like Elgazzar, and unsurprisingly come up with wildly positive conclusions. There are about six in this category. One of them later revised their results to exclude Elgazzar and still found strong efficacy for ivermectin, but they still included Niaee and some other dubious studies. The only meta-analysis that doesn’t make these mistakes is Popp (a Cochrane review), which is from before Elgazzar was found to be fraudulent, but coincidentally excludes it for other reasons. It also excludes a lot of good studies like Mahmud and Ravakirti because they give patients other things like HCQ and azithromycin - I chose to include them, because I don’t think they either work or have especially bad side effects, so they’re basically placebo - but Cochrane is always harsh like this. They end up with a point estimate where ivermectin cuts mortality by 40% - but say the confidence intervals are too wide to draw any conclusion. I think this basically agrees with my analyses above - the trends really are in ivermectin’s favor, but once you eliminate all the questionable studies there are too few studies left to have enough statistical power to reach significance. Except that everyone is still focusing on deaths and hospitalizations just because they’re flashy. Mahmud et al, which everyone agrees is a great study, found that ivermectin decreased days until clinical recovery, p = 0.003? So what do you do? This is one of the toughest questions in medicine. It comes up again and again. You have some drug. You read some studies. Again and again, more people are surviving (or avoiding complications) when they get the drug. It’s a pattern strong enough to common-sensically notice. But there isn’t an undeniable, unbreachable fortress of evidence. The drug is really safe and doesn’t have a lot of side effects. So do you give it to your patients? Do you take it yourself? Here this question is especially tough, because, uh, if you say anything in favor of ivermectin you will be cast out of civilization and thrown into the circle of social hell reserved for Klan members and 1/6 insurrectionists. All the health officials in the world will shout “horse dewormer!” at you and compare you to Josef Mengele. But good doctors aren’t supposed to care about such things. Your only goal is to save your patient. Nothing else matters. I am telling you that Mahmud et al is a good study and it got p = 0.003 in favor of ivermectin. You can take the blue pill, and stay a decent respectable member of society. Or you can take the horse dewormer pill, and see where you end up. In a second, I’ll tell you my answer. But you won’t always have me to answer questions like this, and it might be morally edifying to observe your thought process in situations like this. So take a second, and meet me on the other side of the next section heading. … … … … … The Synthesis Hopefully you learned something interesting about yourself there. But my answer is: worms! As several doctors and researchers have pointed out (h/t especially Avi Bitterman and David Boulware), the most impressive studies come from places that are teeming with worms. Mahmud from Bangladesh, Ravakirti from East India, Lopez-Medina from Colombia, etc. Here’s the prevalence of roundworm infections by country (source). But alongside roundworms, there are threadworms, hookworms, blood flukes, liver flukes, nematodes, trematodes, all sorts of worms. Add them all up and somewhere between half and a quarter of people in the developing world have at least one parasitic worm in their body. Being full of worms may impact your ability to fight coronavirus. Gluchowska et al write: Helminth [ie worm] infections are among the most common infectious diseases. Bradbury et al. highlight the possible negative interactions between helminth infection and COVID-19 severity in helminth-endemic regions and note that alterations in the gut microbiome associated with helminth infection appear to have systemic immunomodulatory effects. It has also been proposed that helminth co-infection may increase the morbidity and mortality of COVID-19, because the immune system cannot efficiently respond to the virus; in addition, vaccines will be less effective for these patients, but treatment and prevention of helminth infections might reduce the negative effect of COVID-19. During millennia of parasite-host coevolution helminths evolved mechanisms suppressing the host immune responses, which may mitigate vaccine efficacy and increase severity of other infectious diseases. Treatment of worm infections might reduce the negative effect of COVID-19! And ivermectin is a deworming drug! You can see where this is going… The most relevant species of worm here is the roundworm Strongyloides stercoralis. Among the commonest treatments for COVID-19 is corticosteroids, a type of immunosuppresant drug. The types of immune responses it suppresses do more harm than good in coronavirus, so turning them off limits collateral damage and makes patients better on net. But these are also the types of immune responses that control Strongyloides. If you turn them off even very briefly, the worms multiply out of control, you get what’s called “Strongyloides hyperinfection”, and pretty often you die. According to the WHO: The current COVID-19 pandemic serves to highlight the risk of using systemic corticosteroids and, to a lesser extent, other immunosuppressive therapy, in populations with significant risk of underlying strongyloidiasis. Cases of strongyloidiasis hyperinfection in the setting of corticosteroid use as COVID-19 therapy have been described and draw attention to the necessity of addressing the risk of iatrogenic strongyloidiasis hyperinfection syndrome in infected individuals prior to corticosteroid administration. Although this has gained importance in the midst of a pandemic where corticosteroids are one of few therapies shown to improve mortality, its relevance is much broader given that corticosteroids and other immunosuppressive therapies have become increasingly common in treatment of chronic diseases (e.g. asthma or certain rheumatologic conditions). So you need to “address the risk” of strongyloides infection during COVID treatment in roundworm-endemic areas. And how might you address this, WHO? Treatment of chronic strongyloidiasis with ivermectin 200 µg/kg per day orally x 1-2 days is considered safe with potential contraindications including possible Loa loa infection (endemic in West and Central Africa), pregnancy, and weight <15kg. Given ivermectin’s safety profile, the United States has utilized presumptive treatment with ivermectin for strongyloidiasis in refugees resettling from endemic areas, and both Canada and the European Centre for Disease Prevention and Control have issued guidance on presumptive treatment to avoid hyperinfection in at risk populations. Screening and treatment, or where not available, addition of ivermectin to mass drug administration programs should be studied and considered. This is serious and common enough that, if you’re not going to screen for it, it might be worth “add[ing] ivermectin to mass drug administration programs” in affected areas! Dr. Avi Bitterman carries the hypothesis to the finish line: First two images are with all relevant studies; second two are a sensitivity analysis that removes some of the most dubious. The good ivermectin trials in areas with low Strongyloides prevalence, like Vallejos in Argentina, are mostly negative. The good ivermectin trials in areas with high Strongyloides prevalence, like Mahmud in Bangladesh, are mostly positive. Worms can’t explain the viral positivity outcomes (ie PCR), but Dr. Bitterman suggests that once you remove low quality trials and worm-related results, the rest looks like simple publication bias: This is still just a possibility. Maybe I’m over-focusing too hard on a couple positive results and this will all turn out to be nothing. Or who knows, maybe ivermectin does work against COVID a little - although it would have to be very little, fading to not at all in temperate worm-free countries. But this theory feels right to me. It feels right to me because it’s the most troll-ish possible solution. Everybody was wrong! The people who called it a miracle drug against COVID were wrong. The people who dismissed all the studies because they F@#king Love Science were wrong. Ivmmeta.com was wrong. Gideon Meyerowitz-Katz was…well, he was right, actually, I got the worm-related meta-analysis graphic above from his Twitter timeline. Still, an excellent troll. Also, the best part is that I ignorantly asked, in my description of Mahmud et al above: And it was! It was a fluke! A literal, physical, fluke! For my whole life, God has been placing terrible puns in my path to irritate me, and this would be the worst one ever! So it has to be true! The Scientific Takeaway About ten years ago, when the replication crisis started, we learned a certain set of tools for examining studies. Check for selection bias. Distrust “adjusting for confounders”. Check for p-hacking and forking paths. Make teams preregister their analyses. Do forest plots to find publication bias. Stop accepting p-values of 0.049. Wait for replications. Trust reviews and meta-analyses, instead of individual small studies. These were good tools. Having them was infinitely better than not having them. But even in 2014, I was writing about how many bad studies seemed to slip through the cracks even when we pushed this toolbox to its limits. We needed new tools. I think the methods that Meyerowitz-Katz, Sheldrake, Heathers, Brown, Lawrence and others brought to the limelight this year are some of the new tools we were waiting for. Part of this new toolset is to check for fraud. About 10 - 15% of the seemingly-good studies on ivermectin ended up extremely suspicious for fraud. Elgazzar, Carvallo, Niaee, Cadegiani, Samaha. There are ways to check for this even when you don’t have the raw data. Like: The Carlisle-Stouffer-Fisher method: Check some large group of comparisons, usually the Table 1 of an RCT where they compare the demographic characteristics of the control and experimental groups, for reasonable p-values. Real data will have p-values all over the map; one in every ten comparisons will have a p-value of 0.1 or less. Fakers seem bad at this and usually give everything a nice safe p-value like 0.8 or 0.9.

95% of ivermectin patients got negative PCRs at some time point, compared to 75% of controls, p = 0.004. I am pretty suspicious of this study, not least because it comes from Egypt which has an awful reputation for fake studies, and it returns extreme results that I wouldn’t expect even if ivermectin was actually a wonder drug. But I cannot find any particular thing wrong with it, nor did anyone else I looked at, so I will grudgingly let it stand. Krolewiecki et al: Another Argentine study. This one is a real RCT. 30 patients received ivermectin, 15 were the control group (no placebo, again). Primary outcome was difference in viral load on day 5. The trend favored ivermectin but it was not statistically significant, although they were able to make it statistically significant if they looked at a subset of higher-IVM-plasma-concentration patients. They did not find any difference in clinical outcomes. A pro-ivermectin person could point out that in the subgroup with the highest ivermectin concentrations, the drug seemed to work. A skeptic could point out that this is exactly the kind of subgroup slicing that you are not supposed to do without pre-registering it, which I don’t think this team did. I agree with the skeptic. Vallejos et al: Another Argentine study. It’s big (250 people in each arm). It’s an RCT. It tries to define a primary outcome (“Primary outcome: the trial ended when the last patient who was included achieved the end of study visit”), but that’s not what “primary outcome” means, and they don’t offer an alternative. Other outcomes: no difference in PCR on days 3 or 12. Hospitalization is nonsignificantly better in the ivermectin group (14 vs. 21, p = 0.2), but death is nonsigificantly better in the placebo group (3 vs. 4, p = 0.7). This isn’t even the kind of nonsignificant that might contribute to an exciting meta-analysis later. This is just a pure null result. I cannot find any problem with this study, and neither can anyone else I checked. This is the biggest RCT we’ve seen so far, so we should take it seriously. TOGETHER Trial: Speaking of big RCTs… This one hasn’t been published yet. There’s a video of a talk about it, but I am not going to watch it, because it is a video, so I am getting information secondhand from eg here. Apparently, it compares 677 people (!) randomized to ivermectin to 678 people randomized to placebo. 86 ivermectin patients ended up in the hospital compared to 95 placebo patients, p-value not significant. This was a really big professional trial done by bigshot researchers from a major Canadian university, and the medical establishment is taking it much more seriously than any of these others. When it comes out, it will probably get published in a top journal. When discussing Lopez-Medina, I wrote: When people say things like “sure, a lot of small studies show good results for ivermectin, but the bigger and more professional trials don’t”, this is one of the two big professional trials they’re talking about. This is the other one. Not coincidentally, it’s also the other trial that ivmmeta.com has a warning letter underneath telling you to disregard. Their main concern is that instead of truly randomizing patients to ivermectin vs. placebo, they did a time-dependent randomization that meant during some weeks more patients were getting one or the other. This is a problem because the trial takes place in Brazil, where different variants were more common at different times. Here’s their image: On the one hand, I have immense contempt for ivmmeta for letting all those other awful studies pass and then pulling out all the stops to try to nitpick this one. I have no idea if their proposed randomization failure really happened. And no doubt the reason they’re even able to investigate this is that this study is really careful and transparent - most of them don’t tell you anything about their randomization method. I would be shocked if other studies don’t have all these problems and worse. On the other hand, the point isn’t to be fair, it’s to be right. And this is a potential confounder. Not a huge one. But a potential one. I guess all we can do is try to bound the damage. Even if the confounding is 100% real and bad, there’s no way to make this study consistent with the crazy super-pro-ivermectin results of studies like Espitia-Hernandez and Aref. And even if we deny any confounding, we see the same slight pro-ivermectin trend - 86 hospitalizations vs. 95 - that we’ve seen in so many other studies. Nothing is going to make me believe that this isn’t in the top 33% of studies we’ve been looking at, so let’s add it as grist for the meta-analysis (though maybe not quite as much grist as its vast size indicates) and move on, angrily. Buonfrate et al: An Italian RCT. Patients were randomized into low-dose ivermectin (32), placebo (29), or high-dose ivermectin (32). Primary outcome was viral load on day 7. There was no significant difference (average of 2 in ivermectin groups, 2.2 in placebo group). They admit that they failed to reach the planned sample size, but did a calculation to show that even if they had, the trial could not have returned a positive result. Clinically, an average of 2 patients were hospitalized in each of the ivermectin arms, compared to 0 in the placebo arm - which bucks our previously-very-constant pro-ivermectin trend. Mayer et al: Not an RCT. Patients in an Argentine province were offered the opportunity to try ivermectin; 3266 said yes and become the experimental group, 17966 said no and became the control group. There were many obvious differences between the groups, but they all seemed to handicap ivermectin. There was a nonsignificant trend toward less hospitalization and significantly less mortality (1.5% vs. 2.1%, p = 0.03). While looking into this study, I learned the term “immortal time bias”. This means a period in between selection for the study and the beginning of study recording where patient outcomes are not counted. I think the problem here is that if you signed up for the system on Day X, and if you got sick before they could give you ivermectin, you were in the control group. See this Twitter thread, I have not confirmed everything he says. This only hardens my resolve to stay away from non-RCTs. Borody et al: Our last paper! …is it a paper? I can’t find it published anywhere. It mostly seems to be on news sites. Doesn’t look peer-reviewed. And it starts with “Note that views expressed in this opinion article are the writer’s personal views”. Whatever. 600 Australians were treated with ivermectin, doxycycline, and zinc. The article compares this to an “equivalent control group” made of “contemporary infected subjects in Australia obtained from published Covid Tracking Data”; this is not how you control group, @#!% you. Then it gets excited about the fact that most patients had better symptoms at the end of the ten-day study period than the beginning (untreated COVID resolves in about ten days). Why are these people wasting my time with this? Let’s move on. The Analysis If we remove all fraudulent and methodologically unsound studies from the table above, we end up with this: Gideon Meyerowitz-Katz, who investigated many of the studies above for fraud, tried a similar exercise. I learned about his halfway through, couldn’t help seeing it briefly, but tried to avoid remembering it or using it when generating mine (also, I did take the result of his fraud investigations into account), so they should be considered not quite independent efforts. His looks like this: He nixed Chowdhury, Babaloba, Ghauri, Faisal, and Aref, but kept Szenta Fonseca, Biber (?), and Mayer. There was correlation of 0.45, which I guess is okay. I asked him about his decision-making, and he listed a combination of serious statistical errors and small red flags adding up. I was pretty uncomfortable with most of these studies myself, so I will err on the side of severity, and remove all studies that either I or Meyerowitz-Katz disliked. We end up with the following short list: We’ve gone from 29 studies to 11, getting rid of 18 along the way. For the record, we eliminated 2/19 for fraud, 1/19 for severe preregistration violations, 10 for methodological problems, and 6 because Meyerowitz-Katz was suspicious of them. …but honestly this table still looks pretty good for ivermectin, doesn’t it? Still lots of big green boxes. Meyerowitz-Katz accuses ivmmeta of cherry-picking what statistic to use for their forest plot. That is, if a study measures ten outcomes, they sometimes take the most pro-ivermectin outcome. Ivmmeta.com counters that they used a consistent and reasonable (if complicated) process for choosing their outcome of focus, that being: If studies report multiple kinds of effects then the most serious outcome is used in calculations for that study. For example, if effects for mortality and cases are both reported, the effect for mortality is used, this may be different to the effect that a study focused on. If symptomatic results are reported at multiple times, we used the latest time, for example if mortality results are provided at 14 days and 28 days, the results at 28 days are used. Mortality alone is preferred over combined outcomes. Outcomes with zero events in both arms were not used (the next most serious outcome is used — no studies were excluded). For example, in low-risk populations with no mortality, a reduction in mortality with treatment is not possible, however a reduction in hospitalization, for example, is still valuable. Clinical outcome is considered more important than PCR testing status. When basically all patients recover in both treatment and control groups, preference for viral clearance and recovery is given to results mid-recovery where available (after most or all patients have recovered there is no room for an effective treatment to do better). If only individual symptom data is available, the most serious symptom has priority, for example difficulty breathing or low SpO2 is more important than cough. I’m having trouble judging this, partly because Meyerowitz-Katz says ivmmeta has corrected some earlier mistakes, and partly because there really is some reasonable debate over how to judge studies with lots of complicated endpoints. By this point I had completely forgotten what ivmmeta did, so I independently coded all 11 remaining studies following something in between my best understanding of their procedure and what I considered common sense. The only exception was that when the most severe outcome was measured in something other than patients (ie average number of virus copies per patient), I defaulted to one that was measured in patients instead, to keep everything with the same denominator. My results mostly matched ivmmeta’s, with one or two exceptions that I think are within the scope of argument or related to my minor deviations from their protocol. Placebo vs. ivermectin groups sometimes differed in size, which I’ve adjusted for and rounded off. Probably I’m forgetting some reason I can’t just do simple summary statistics to this, but whatever. It is p = 0.15, not significant. This is maybe unfair, because there aren’t a lot of deaths in the sample, so by focusing on death rather than more common outcomes we’re pointlessly throwing away sample size. What happens if I unprincipledly pick whatever I think the most reasonable outcome to use from each study is? I’ve chosen “most reasonable” as a balance between “is the most severe” and “has a lot of data points”: Now it’s p = 0.04, seemingly significant, but I had to make some unprincipled decisions to get there. I don’t think I specifically replaced negative findings with positive ones, but I can’t prove that even to myself, let alone to you. [UPDATE 5/31/22: A reader writes in to tell me that the t-test I used above is overly simplistic. A Dersimonian-Laird test is more appropriate for meta-analysis, and would have given 0.03 and 0.005 on the first and second analysis, where I got 0.15 and 0.04. This significantly strengthens the apparent benefit of ivermectin from ‘debatable’ to ‘clear’. I discuss some reasons below why I am not convinced by this apparent benefit.] (how come I’m finding a bunch of things on the edge of significance, but the original ivmmeta site found a lot of extremely significant things? Because they combined ratios, such that “one death in placebo, zero in ivermectin” looked like a nigh-infinite benefit for ivermectin, whereas I’m combining raw numbers. Possibly my way is statistically illegitimate for some reason, but I’m just trying to get a rough estimate of how convinced to be) So we are stuck somewhere between “nonsignificant trend in favor” and “maybe-significant trend in favor, after throwing out some best practices”. This is normally where I would compare my results to those of other meta-analyses made by real professionals. But when I look at them, they all include studies later found to be fake, like Elgazzar, and unsurprisingly come up with wildly positive conclusions. There are about six in this category. One of them later revised their results to exclude Elgazzar and still found strong efficacy for ivermectin, but they still included Niaee and some other dubious studies. The only meta-analysis that doesn’t make these mistakes is Popp (a Cochrane review), which is from before Elgazzar was found to be fraudulent, but coincidentally excludes it for other reasons. It also excludes a lot of good studies like Mahmud and Ravakirti because they give patients other things like HCQ and azithromycin - I chose to include them, because I don’t think they either work or have especially bad side effects, so they’re basically placebo - but Cochrane is always harsh like this. They end up with a point estimate where ivermectin cuts mortality by 40% - but say the confidence intervals are too wide to draw any conclusion. I think this basically agrees with my analyses above - the trends really are in ivermectin’s favor, but once you eliminate all the questionable studies there are too few studies left to have enough statistical power to reach significance. Except that everyone is still focusing on deaths and hospitalizations just because they’re flashy. Mahmud et al, which everyone agrees is a great study, found that ivermectin decreased days until clinical recovery, p = 0.003? So what do you do? This is one of the toughest questions in medicine. It comes up again and again. You have some drug. You read some studies. Again and again, more people are surviving (or avoiding complications) when they get the drug. It’s a pattern strong enough to common-sensically notice. But there isn’t an undeniable, unbreachable fortress of evidence. The drug is really safe and doesn’t have a lot of side effects. So do you give it to your patients? Do you take it yourself? Here this question is especially tough, because, uh, if you say anything in favor of ivermectin you will be cast out of civilization and thrown into the circle of social hell reserved for Klan members and 1/6 insurrectionists. All the health officials in the world will shout “horse dewormer!” at you and compare you to Josef Mengele. But good doctors aren’t supposed to care about such things. Your only goal is to save your patient. Nothing else matters. I am telling you that Mahmud et al is a good study and it got p = 0.003 in favor of ivermectin. You can take the blue pill, and stay a decent respectable member of society. Or you can take the horse dewormer pill, and see where you end up. In a second, I’ll tell you my answer. But you won’t always have me to answer questions like this, and it might be morally edifying to observe your thought process in situations like this. So take a second, and meet me on the other side of the next section heading. … … … … … The Synthesis Hopefully you learned something interesting about yourself there. But my answer is: worms! As several doctors and researchers have pointed out (h/t especially Avi Bitterman and David Boulware), the most impressive studies come from places that are teeming with worms. Mahmud from Bangladesh, Ravakirti from East India, Lopez-Medina from Colombia, etc. Here’s the prevalence of roundworm infections by country (source). But alongside roundworms, there are threadworms, hookworms, blood flukes, liver flukes, nematodes, trematodes, all sorts of worms. Add them all up and somewhere between half and a quarter of people in the developing world have at least one parasitic worm in their body. Being full of worms may impact your ability to fight coronavirus. Gluchowska et al write: Helminth [ie worm] infections are among the most common infectious diseases. Bradbury et al. highlight the possible negative interactions between helminth infection and COVID-19 severity in helminth-endemic regions and note that alterations in the gut microbiome associated with helminth infection appear to have systemic immunomodulatory effects. It has also been proposed that helminth co-infection may increase the morbidity and mortality of COVID-19, because the immune system cannot efficiently respond to the virus; in addition, vaccines will be less effective for these patients, but treatment and prevention of helminth infections might reduce the negative effect of COVID-19. During millennia of parasite-host coevolution helminths evolved mechanisms suppressing the host immune responses, which may mitigate vaccine efficacy and increase severity of other infectious diseases. Treatment of worm infections might reduce the negative effect of COVID-19! And ivermectin is a deworming drug! You can see where this is going… The most relevant species of worm here is the roundworm Strongyloides stercoralis. Among the commonest treatments for COVID-19 is corticosteroids, a type of immunosuppresant drug. The types of immune responses it suppresses do more harm than good in coronavirus, so turning them off limits collateral damage and makes patients better on net. But these are also the types of immune responses that control Strongyloides. If you turn them off even very briefly, the worms multiply out of control, you get what’s called “Strongyloides hyperinfection”, and pretty often you die. According to the WHO: The current COVID-19 pandemic serves to highlight the risk of using systemic corticosteroids and, to a lesser extent, other immunosuppressive therapy, in populations with significant risk of underlying strongyloidiasis. Cases of strongyloidiasis hyperinfection in the setting of corticosteroid use as COVID-19 therapy have been described and draw attention to the necessity of addressing the risk of iatrogenic strongyloidiasis hyperinfection syndrome in infected individuals prior to corticosteroid administration. Although this has gained importance in the midst of a pandemic where corticosteroids are one of few therapies shown to improve mortality, its relevance is much broader given that corticosteroids and other immunosuppressive therapies have become increasingly common in treatment of chronic diseases (e.g. asthma or certain rheumatologic conditions). So you need to “address the risk” of strongyloides infection during COVID treatment in roundworm-endemic areas. And how might you address this, WHO? Treatment of chronic strongyloidiasis with ivermectin 200 µg/kg per day orally x 1-2 days is considered safe with potential contraindications including possible Loa loa infection (endemic in West and Central Africa), pregnancy, and weight <15kg. Given ivermectin’s safety profile, the United States has utilized presumptive treatment with ivermectin for strongyloidiasis in refugees resettling from endemic areas, and both Canada and the European Centre for Disease Prevention and Control have issued guidance on presumptive treatment to avoid hyperinfection in at risk populations. Screening and treatment, or where not available, addition of ivermectin to mass drug administration programs should be studied and considered. This is serious and common enough that, if you’re not going to screen for it, it might be worth “add[ing] ivermectin to mass drug administration programs” in affected areas! Dr. Avi Bitterman carries the hypothesis to the finish line: First two images are with all relevant studies; second two are a sensitivity analysis that removes some of the most dubious. The good ivermectin trials in areas with low Strongyloides prevalence, like Vallejos in Argentina, are mostly negative. The good ivermectin trials in areas with high Strongyloides prevalence, like Mahmud in Bangladesh, are mostly positive. Worms can’t explain the viral positivity outcomes (ie PCR), but Dr. Bitterman suggests that once you remove low quality trials and worm-related results, the rest looks like simple publication bias: This is still just a possibility. Maybe I’m over-focusing too hard on a couple positive results and this will all turn out to be nothing. Or who knows, maybe ivermectin does work against COVID a little - although it would have to be very little, fading to not at all in temperate worm-free countries. But this theory feels right to me. It feels right to me because it’s the most troll-ish possible solution. Everybody was wrong! The people who called it a miracle drug against COVID were wrong. The people who dismissed all the studies because they F@#king Love Science were wrong. Ivmmeta.com was wrong. Gideon Meyerowitz-Katz was…well, he was right, actually, I got the worm-related meta-analysis graphic above from his Twitter timeline. Still, an excellent troll. Also, the best part is that I ignorantly asked, in my description of Mahmud et al above: And it was! It was a fluke! A literal, physical, fluke! For my whole life, God has been placing terrible puns in my path to irritate me, and this would be the worst one ever! So it has to be true! The Scientific Takeaway About ten years ago, when the replication crisis started, we learned a certain set of tools for examining studies. Check for selection bias. Distrust “adjusting for confounders”. Check for p-hacking and forking paths. Make teams preregister their analyses. Do forest plots to find publication bias. Stop accepting p-values of 0.049. Wait for replications. Trust reviews and meta-analyses, instead of individual small studies. These were good tools. Having them was infinitely better than not having them. But even in 2014, I was writing about how many bad studies seemed to slip through the cracks even when we pushed this toolbox to its limits. We needed new tools. I think the methods that Meyerowitz-Katz, Sheldrake, Heathers, Brown, Lawrence and others brought to the limelight this year are some of the new tools we were waiting for. Part of this new toolset is to check for fraud. About 10 - 15% of the seemingly-good studies on ivermectin ended up extremely suspicious for fraud. Elgazzar, Carvallo, Niaee, Cadegiani, Samaha. There are ways to check for this even when you don’t have the raw data. Like: The Carlisle-Stouffer-Fisher method: Check some large group of comparisons, usually the Table 1 of an RCT where they compare the demographic characteristics of the control and experimental groups, for reasonable p-values. Real data will have p-values all over the map; one in every ten comparisons will have a p-value of 0.1 or less. Fakers seem bad at this and usually give everything a nice safe p-value like 0.8 or 0.9.

Links For December

December 30, 2021 · Original source

2: Claim via NPR: When Brazil had high inflation in the 1990s, some economists developed a plan: price everything in inflation-adjusted units, so that people felt like things were “stable”, then declare that the Inflation Adjusted Unit was the new currency. How Fake Money Saved Brazil. Also interesting: they tried it because the new finance minister knew no economics, recognized his ignorance, and was willing to call up random economists and listen to their hare-brained plans.

Inline links: How Fake Money Saved Brazil

Highlights From The Comments On Health Care Systems

January 27, 2022 · Original source

I'm very far from being an expert in health care systems, but I'd like to offer a bit of insight into the Brazilian system since Scott demanded to know what developing countries do and Brazil is my home country. Brazil is in a very curious position regarding health care, since the current Constitution established in 1988 provides that we will have universal health care provided by the State (Sistema Único de Saúde, or SUS to keep with the three letters) but at the same there is an abundant proliferation of private medicine practice - hospitals, clinics, insurance companies, doctors can work outside the universal public system in for profit systems and not get paid by the state. This basically means we have at the same time a system with a lot of state-run hospitals and clinics, as well as state-employed doctors, other facilities run by private operators but funded by the State (considered part of the universal system) and also 100% private enterprises. This creates a situation in which a very large portion of the middle, upper-middle and upper class all have private insurance - provided by their employers or paid by the user - and the poor have universal coverage under the public system. However, the universal public system ranges enormously in quality: for example, we have simultaneously one of the best vaccination systems in the world for free but months of waiting time to get a simple doctor's appointment or years of waiting to get a surgery. Some types of surgical procedures provided by the state are good and others are not, same with exams, and the state-run hospitals also vary enormously on quality. The users of most private insurance companies also have a lot of low quality services, albeit with shorter waiting times and more options. A few of the really expensive ones provide quality services for the richer individuals. Also it's worth noting that a lot of the best doctors don't accept insurance payment at all and charge a fee for each appointment.

Brazil also has a very commended drug price system involving patent breaking but I don't really know much about it, only that it really makes most drug prices really low.

The political side of things is also very complicated especially because the left-wing blocks any productive discussion on reform since it considers the public system untouchable and refuses to acknowledge its shortcomings most of the time - or blame them on underfunding and "neoliberal policies". A lot of upper class left-wing people haven't used the public system once in their life but still consider it perfect. Brazilian things.

Predictions For 2022

February 01, 2022 · Original source

VOX PREDICTIONS 1. Democrats will lose their majorities in the House and Senate (95%): SELL TO 90% 2. Inflation in the US will average under three percent (80%): HOLD 3. Unemployment in the US will fall below four percent by November (80%): SELL to 60% if they mean in November, otherwise hold 4. Supreme Court will overturn Roe v. Wade (65%): SELL to 60% 5. Stephen Breyer will retire from the Supreme Court (55%): N/A 6. Emmanuel Macron will be reelected president of France (65%): HOLD 7. Jair Bolsonaro will be reelected president of Brazil (55%): SELL to 50% 8. Bongbong Marcos will be elected president of the Philippines (55%): BUY to 60% 9. Rebels will not capture Addis Ababa (55%): N/A 10. China will not reopen its borders in the first half of 2022 (80%): BUY to 90% 11. Chinese GDP will continue to grow for the first 3/4 of the year (95%): SELL to 90% 12. 20% of US kids between 0.5 and 5 years old will get at least one COVID vaccine by year's end (65%): HOLD 13. WHO will designate another Variant Of Concern by year's end (75%): HOLD 14. 12 billion COVID shots will be given out globally by 11/2022 (80%): HOLD 15. At least one country will have less than 10% of people vaccinated with two shots by 11/2022 (70%): BUY to 95% 16. A psychedelic drug will be decriminalized/legalized in at least one more US state (75%): HOLD 17. AI will discover a new drug promising enough for clinical trials (85%): HOLD 18. US govt will not renew the ban on funding gain-of-function research (60%): HOLD 19. The Biden administration will set the social cost of carbon at $100/ton or more (70%): HOLD 20. 2022 will be warmer than 2021 (80%): HOLD 21. Kenneth Branagh's Belfast will win Best Picture (55%): SELL to 30% 22. Norway will win the most medals at the 2022 Winter Olympics (60%): HOLD

YGLESIAS PREDICTIONS 1. Democrats lose both houses of Congress (90%) HOLD 2. Democrats lose at least two Senate seats (80%) HOLD 3. Democrats lose fewer than six Senate seats (80%) HOLD 4. Nancy Pelosi announces retirement plans (70%) HOLD 5. Stephen Breyer does not retire (60%) N/A 6. Some version of Build Back Better passes (60%) HOLD 7. Joe Biden is still president (90%) HOLD 8. At least one Biden cabinet-rank official resigns (70%) HOLD 9. No military conflict between the PRC and Taiwan (a worryingly low 90%) HOLD 10. New U.S. sanctions on Russia (70%) HOLD 11. Saudi Arabia and Israel establish diplomatic relations (60%) SELL to 50% 12. Fewer U.S. Covid deaths in 2022 than in 2021 (80%) BUY to 90% 13. Emmanuel Macron re-elected (60%) HOLD 14. Traffic light coalition exploits loopholes to get around the constitutional debt brake (70%) HOLD 15. No recession in 2021 (90%) SELL to 80% 16. Liz Cheney loses primary (80%) HOLD 17. Some version of USICA passes Congress (70%) HOLD 18. Lula elected president of Brazil (60%) SELL to 50% 19. China officially abandons Covid Zero (70%) HOLD 20. Fewer U.S. Covid-19 deaths in 2022 than in 2020 (80%) BUY to 90% 21. Additional booster shots of mRNA vaccines authorized for seniors (80%) HOLD 22. November 2022 year-on-year CPI growth is below 6% (70%) BUY to 80% 23. November 2022 year-on-year CPI growth is above 4% (70%) SELL to 50% 24. The Fed ends up doing more than its currently forecast three interest rate hikes (60%) HOLD 25. Russia does not invade Ukraine (60%) HOLD 26. Viktor Orbán loses power in Hungary (60%) HOLD 27. Sinn Fein becomes the largest party in the Northern Ireland assembly (60%) HOLD 28. The U.S. and Canada reach an agreement on softwood lumber (70%) HOLD 29. Democrats go down at least one governor on net (60%) HOLD 30. The unemployment rate stays between 4 and 5% (70%) SELL to 60% if you mean 12/22, to 40% if you mean it never gets outside that range at all

ACX Grants ++: The First Half

February 03, 2022 · Original source

#38: Promote Citizens’ Assemblies And Lotteries The newDemocracy Foundation is an organisation in Australia that develops, demonstrates, and promotes innovations in democracy. Its focus is on deliberative democracy and random selection. We have worked with the UN and the OECD to develop international standards of best practice and founded the Democracy R&D network. We’re designed and operated ground-breaking projects in Melbourne, Geelong, and Canberra, and have collaborated with international partners in Brazil, Spain, North Macedonia, and Malawi. We require funding to take advantage of an opportunity in Australian politics. Citizens’ assemblies and democratic lottery are gaining traction but the ecosystem for their implementation still requires support and training that is best provided by an independent organisation like ours. Additional funding could allow us to expand our project capacity, conduct needed research or improve our advocacy and reach to politicians. I’m happy to answer any questions or provide a brief organisation overview, you can reach me at kyle.redman@newdemocracy.com.au You can view our website here: www.newdemocracy.com.au.

Who Gets Self-Determination?

March 30, 2022 · Original source

Somebody’s going to ask “but what about the Confederacy?” The position that most tempts me is “The Confederacy had every right to secede, because every region that wants to secede has that right - but immediately upon granting them independence, the Union should have invaded in order to stop the atrocity of slavery”. I say it tempts rather convinces because it suggests a moral duty to conquer any country doing sufficiently bad things (should the Union have invaded Brazil too, for the same reason?) I’m still not sure how I feel about this. Assuming we’re against invading foreign countries on principle, a utilitarian might refuse to let the Confederacy leave in the hope of preventing the establishment of a permanent slave power. But I would still think of that as one of those rights violation which utilitarians occasionally allow for the greater good.

Highlights From The Comments On Xi Jinping

April 28, 2022 · Original source

[But] if you’re at an intersection in the US as a driver and it’s 2am and there same situation the vast majority of Americans will just wait for a green light. In Brazil or Thailand they will just blow past it like a jaywalking American.

Your Book Review: The Righteous Mind

July 15, 2022 · Original source

There’s one point in the book where he mentions contact with Marxism, and that’s when he was travelling to Brazil to get some data on the moral intuitions of people outside the US. He mentions that he went to a conference but people were all Marxist so he left and went somewhere else. This was in the sense of their approach to psychology, and to be honest I’ve heard what I think is the kind of “theory” he’s gesturing at hearing there and I’d leave as well, but it’s a real weakness that this is the only time that any sort of Marxism or socialism really turns up in a book that’s supposed to help liberals understand challenges to their ideology and empathise with other points of view, and supposed to provide a sort of “theory of everything” for political differences.

Slightly Against Underpopulation Worries

August 04, 2022 · Original source

Brazil, Japan, and Germany Brazil will go from 210 million today to 190 million in 2100.

Brazil will go from 210 million today to 190 million in 2100.

Book Review: What We Owe The Future

August 23, 2022 · Original source

His biggest concern here is reindustrialization. The first Industrial Revolution relied on coal. But we have already exhausted most easy-to-mine surface coal deposits. Could we industrialize again without this resource? As any Minecraft player knows, charcoal is a passable substitute for coal (apparently Brazil’s steel industry runs on it!) But:

Race-based slavery ended in the US in 1865 and in Brazil in 1888. Saudi Arabia ended its own form of slavery in 1962. Since then there has been some involuntary labor in prisons and gulags, but nothing like the system of forced labor that covered most of the world in the early 1800s. And although we may compare some modern institutions to slavery, it seems almost inconceivable that slavery as open and widespread as the 19th century norm could recur without a total change of everything in society.

Meetups Everywhere 2022: Times & Places

August 26, 2022 · Original source

SÃO PAULO, BRAZIL Contact: [Update on 2025-02-03: Removed at organizers’s request] Time: Saturday, September 10, 2:00 PM Location: Ibirapuera Park in Praca do Porquinho. I will be wearing a white t-shirt, be very tall and have a sign. Coordinates: 588MC85Q+6X Event link(s): LessWrong BOGOTÁ, COLOMBIA Contact: Dan P, shorty[dot]george[dot]productions[at]gmail[dot]com Time: Sunday, September 18, 4:00 PM Location: Illy Cafe, Kr 15 with Park Virrey. Sign will say ACX Coordinates: 67P7MWFW+3F7 Event link(s): LessWrong MEDELLÍN, COLOMBIA Contact: HP, hp-med-acx[at]proton[dot]me Time: Sunday, September 18, 5:00 PM Location: Hija Mia Nomada Coordinates: 67R66C7G+8V Event link(s): LessWrong MÉRIDA, MEXICO Contact: Mati Roy, mathieu[dot]roy[dot]37[at]gmail[dot]com, Facebook Time: Sunday, August 28, 5:00 PM Location: Parque Gardenia, C. 65-A, Residencial Floresta, 97309 Mérida, Yuc. Coordinates: 76HG2C7X+8F Event link(s): LessWrong, Facebook event Group info: Facebook group Notes: Please let me know if you'll be coming. MEXICO CITY, MEXICO Contact: Calcifer, fagarrido[at]gmail[dot]com, Discord: Francisco (Mexico City)#0227 Time: Saturday, September 10, 4:00 PM Location: Comedor de los Milagros. I'll be wearing a green shirt and will carry a 'ACX/CDMX Meetup' sign. Coordinates: 76F2CR6P+37 Event link(s): LessWrong Group info: We are a rather new group. We've been meeting sporadically since April, and we recently settled on a formal twice-per-month frequency. We have a WhatsApp group which we use mostly for coordination purposes. Send me an email if you want in. Notes: If possible, RSVP on Less Wrong to get a sense of how many people to expect. Feel free to come if you haven't RSVP'd, though! PUNTA DEL ESTE, URUGUAY Contact: Manuel, acx[at]maraoz[dot]com Time: Saturday, September 24, 5:00 PM Location: Borneo Coffee, patio del fondo. Ruta 10, 20001 La Barra, Departamento de Maldonado, Uruguay Coordinates: 48Q734PQ+58 Event link(s): LessWrong

Inline links: 588MC85Q+6X, LessWrong, 67P7MWFW+3F7, LessWrong, 67R66C7G+8V, LessWrong, Facebook, 76HG2C7X+8F, LessWrong, Facebook event, Facebook group, 76F2CR6P+37, LessWrong, 48Q734PQ+58, LessWrong

Links For October

October 12, 2022 · Original source

15: Related: Lula’s opponent, incumbent Jair Bolsonaro, is under fire after a video surfaced of him saying that he would eat human flesh, and that in fact he tried to do this once but his friends talked him out of it. Is Brazil okay?

Inline links: after a video surfaced of him saying that he would eat human flesh

Response To Alexandros Contra Me On Ivermectin

February 01, 2023 · Original source

I mention Cadegiani’s “involvement” in a scandal where the Brailizan government created a COVID recommendation app that recommended ivermectin to everyone. Marinos points out that it did alter its recommendations based on the patient (eg what other drugs it recommended, what dose of ivermectin to use), and although it had some problems it was overall an okay app whose only “crime” was operating on the assumption that ivermectin was a great COVID drug.

Gideon (correctly) phrased this as a non-sinister albeit potentially weird misstep by the study authors, but in trying to summarize Gideon, I (incorrectly) phrased it as a sinister attempt to inflate results. After looking into it, I think Alexandros is completely right and I was completely wrong. Although I sometimes get details wrong, this one was especially disappointing because I incorrectly tarnished the reputation of Biber et al and implicitly accused them of bad scientific practices, which they were not doing. I believed I was relaying an accusation by Gideon (who I trust), but I was wrong and he was not accusing them of that. I apologize to Biber et al, my readers, and everyone else involved in this. My only reservation is that I don’t want to say too strongly that Gideon’s critique is wrong: I haven’t looked through the study documents enough to say with certainty that Alexandros’ reanalysis of the protocol issues is correct (though the superficial check I’ve done looks that way). But my mistakes are completely separate from anything Gideon did and definitely real and egregious. Cadegiani et al (Alexandros 50% right) Flavio Cadegiani did several studies on ivermectin in Brazil; I edited this section in response to criticism by Marinos and others, but the earliest version I can find on archive.is (I can’t guarantee it was the first I wrote) said: A crazy person decided to put his patients on every weird medication he could think of, and 585 subjects ended up on a combination of ivermectin, hydroxychloroquine, azithromycin, and nitazoxanide, with dutasteride and spironolactone "optionally offered" and vitamin D, vitamin C, zinc, apixaban, rivaraxoban, enoxaparin, and glucocorticoids "added according to clinical judgment". There was no control group, but the author helpfully designated some random patients in his area as a sort-of-control, and then synthetically generated a second control group based on “a precise estimative based on a thorough and structured review of articles indexed in PubMed and MEDLINE and statements by official government agencies and specific medical societies”. Patients in the experimental group were twice as likely to recover (p < 0.0001), had negative PCR after 14 vs. 21 days, and had 0 vs. 27 hospitalizations. Speaking of low p-values, some people did fraud-detection tests on another of Cadegiani’s COVID-19 studies and got values like p < 8.24E-11 in favor of it being fraudulent. Also in Cadegiani news: he apparently has the record for completing one of the fastest PhDs in Brazilian history (7 months), he was involved in a weird scandal where the Brazilian government tried to create a COVID recommendation app but it just recommended ivermectin to everybody regardless of what input it got, and he describes himself as: …the only author of the sole book in Overtraining Syndrome, the prevailing sport-related disease among amateur and professional athletes. He is also responsible for approximately 70% of the articles published in the field in the world in the last 05 years, and reviewer for more than 90% of the manuscripts in the field. And, uh, he’s also studied whether ultra-high-dose antiandrogens treated COVID, and found that they did, cutting mortality by 92% . Which sounds great, except that it looks like most of this is that the control group had a shockingly high mortality rate, much higher than makes sense even in the context of severe COVID. I think the charitable explanation here is that he made this data up too. But the Brazilian Parliament seems to be going with an uncharitable explanation, seeing as they have recommended that Cadegiani be charged with crimes against humanity. Anyway, let’s not base anything important on the results of this study. You can find Alexandros’ full critique here, but again I’ll try to summarize it as best I can. Alexandros is unhappy with my portrayal of Cadegiani’s background. I cite details that make him look strange and maybe fake, but there are other details that make him seem more impressive, like that he won gold medals at a Brazilian Scientific Olympiad.

Inline links: the earliest version I can find on archive.is, involved in a weird scandal, describes himself as, recommended that Cadegiani be charged with crimes against humanity, here

Alexandros is unhappy with my portrayal of Cadegiani’s background. I cite details that make him look strange and maybe fake, but there are other details that make him seem more impressive, like that he won gold medals at a Brazilian Scientific Olympiad.

Your Book Review: The Educated Mind

July 14, 2023 · Original source

But this isn’t unique to the Potawatomi, or to Native Americans — you can find these “cognitive strengths” showing up in the Maori of New Zealand, the !Kung San of Botswana, the Yanomami of Brazil… in fact, anthropologists have found these “cognitive strengths” in every society they’ve researched: all but one of them show up in Donald Brown’s list of human universals. Like clothing and fire, these ways of encoding information were part of humanity’s original toolkit, equipping each person with the collected knowledge of their tribe so they could survive in environments that found them tasty.

Inline links: Donald Brown’s list of human universals

Meetups Everywhere 2023: Times & Places

August 25, 2023 · Original source

BUENOS AIRES, ARGENTINA Contact: David Contact Info: david[dot]f[dot]rivadeneira[at]gmail[dot]com Time: Saturday, September 9th, 11:30 AM Location: Café Cortázar, José A. Cabrera 3797. En la entrada. Coordinates: https://plus.codes/48Q3CH3J+F3 Notable Guests: Luca de Leo Brazil RIO DE JANEIRO, RJ, BRAZIL Contact: Tiago Macedo Contact Info: tiago[dot]s[dot]m[dot]macedo[at]gmail[dot]com Time: Saturday, September 16th, 4:00 PM Location: Praça Nelson Mandela, right at the Botafogo subway station. It is possible that, once everyone is there, we'll go to a nearby Starbucks, just one street-crossing from the initial location. Coordinates: https://plus.codes/589R2RX8+H7 Group Link: gist.github.com/tiago-macedo/40c1cdfd3bde6d2bcadde463ac8b3cf2 Notes: I'll bring a chessboard. If at most 5 people show up (other than me), I'll either order pizza or coffee for everyone.

Inline links: https://plus.codes/48Q3CH3J+F3, https://plus.codes/589R2RX8+H7

RIO DE JANEIRO, RJ, BRAZIL Contact: Tiago Macedo Contact Info: tiago[dot]s[dot]m[dot]macedo[at]gmail[dot]com Time: Saturday, September 16th, 4:00 PM Location: Praça Nelson Mandela, right at the Botafogo subway station. It is possible that, once everyone is there, we'll go to a nearby Starbucks, just one street-crossing from the initial location. Coordinates: https://plus.codes/589R2RX8+H7 Group Link: gist.github.com/tiago-macedo/40c1cdfd3bde6d2bcadde463ac8b3cf2 Notes: I'll bring a chessboard. If at most 5 people show up (other than me), I'll either order pizza or coffee for everyone.

Inline links: https://plus.codes/589R2RX8+H7

CURITIBA, PARANA, BRAZIL Contact: Demian Contact Info: demianet[at]gmail[dot]com Time: Saturday, September 23rd, 4:00 PM Location: Hostel Social - Coffee Bar, R. Brigadeiro Franco, 2691 - Rebouças, Curitiba - PR, 80220-100 Coordinates: https://plus.codes/586GHP4F+FWF Notes: All welcome. If possible, RSVP by e-mail

Inline links: https://plus.codes/586GHP4F+FWF

Your Book Review: Why Nations Fail

August 25, 2023 · Original source

We probably shouldn't judge this book too much on hindsight, given it's about the long run and AR were prudent with their predictions: "the fact that the extractive regime of President Mubarak was overturned by popular protest in February 2011 does not guarantee that Egypt will move onto a path to more inclusive institutions." Even so, the clear implication was that the Arab Spring was on the right track and Brazil was setting itself up for the long run better than China.

THE RISE OF BRAZIL since the 1970s was not engineered by economists of international institutions instructing Brazilian policymakers on how to design better policies or avoid market failures. It was not achieved with injections of foreign aid. It was not the natural outcome of modernization. Rather, it was the consequence of diverse groups of people courageously building inclusive institutions. Eventually these led to more inclusive economic institutions.

I think it's fair to say this hasn't aged particularly well.

Inline links: aged, well

Dictator Book Club: Chavez

November 02, 2023 · Original source

A sublimely gifted politician with empathy for the poor, the power of Croesus, the result, fiasco. While he thundered about bringing equilibrium to the universe and polarised his country, foaming passions into hate, neighbours built more sustainable economies and tackled long-term poverty. Allies like Bolivia, Nicaragua, and Ecuador saluted the comandante but did not emulate his economic model, for that way lay ruin. Brazil seized regional leadership. Venezuela atrophied. Nothing worked, but there was money and spectacle. An empty revolution, then. No paradise, no hell, just limbo, a bleak misty in-between where ambition and delusion played out its ancient story. The farces and follies did not add up to despotic horror but they bore the melancholy echo of opportunity squandered, of what might have been, and there was the tragedy.

Highlights From The Comments On Kidney Donation

November 07, 2023 · Original source

Although historically some countries have observed impressive increases after introduction of presumed consent, such as Belgium, others have fared badly with either no difference or an actual drop in organ donation rates, including Singapore, Brazil, Chile, Sweden, and more recently Wales.

Son Of Bride Of Bay Area House Party

December 12, 2023 · Original source

His eyes light up. “So. The Boring Company. Exciting idea! Dig tunnels, end traffic. But Elon’s grown old. Gotten distracted. It’s been five years and he’s dug a grand total of two miles. The machines just don’t drill fast enough. It’s sad to see a great founder lose his touch like that. Not that I had a better idea. Until last month! That was when I read about paleoburrows. These are long tunnels they find in Brazil. Farmers would be plowing their field and fall into one. Nobody knew where they came from. Until they brought in a paleontologist. He figured it out right away. They’re the burrows of giant ground sloths. People describe them as ‘a hamster the size of an elephant’. Some of the tunnels go half a mile. Let’s say it took a year for the sloth to dig that. So give three sloths two years, and you’ve beaten Musk!

Inline links: paleoburrows

Spring Meetups Everywhere 2024

March 30, 2024 · Original source

BUENOS AIRES Contact: David Rivadeneira Contact Info: david[dot]f[dot]rivadeneira[at]gmail[dot]com Time: Thursday, April 11th, 7:00 PM Location: Gorriti 5996, C1414 BKL, Buenos Aires Coordinates: https://plus.codes/48Q3CH95+5C Group Link: https://chat.whatsapp.com/LhvhRq8wyLILlyMoL1IJ4J Brazil FLORIANÓPOLIS, BRAZIL Contact: Adiel Contact Info: adiel[at]airpost[dot]net Time: Saturday, April 13th, 4:00 PM Location: Angeloni Beira Mar, at the food court. I'll be wearing a yellow hat. Coordinates: https://plus.codes/584HCFGF+326 Notes: Everyone is welcome! Email me and I'll add you to the WhatsApp group.

Inline links: https://plus.codes/48Q3CH95+5C, https://chat.whatsapp.com/LhvhRq8wyLILlyMoL1IJ4J, https://plus.codes/584HCFGF+326

FLORIANÓPOLIS, BRAZIL Contact: Adiel Contact Info: adiel[at]airpost[dot]net Time: Saturday, April 13th, 4:00 PM Location: Angeloni Beira Mar, at the food court. I'll be wearing a yellow hat. Coordinates: https://plus.codes/584HCFGF+326 Notes: Everyone is welcome! Email me and I'll add you to the WhatsApp group.

Inline links: https://plus.codes/584HCFGF+326

RIO DE JANEIRO, BRAZIL Contact: Tiago Macedo Contact Info: tiago[dot]s[dot]m[dot]macedo[at]gmail[dot]com Time: Sunday, April 28th, 3:00 PM Location: Praça Nelson Mandela, Botafogo, Rio de Janeiro. We will sit at a large circular bench in the middle of the square, right in front of a subway exit. I will have a piece of paper with a big "ACX" written on it. IMPORTANT: After some time, if a large group has joined, we might decide to go elsewhere nearby! Please contact the organizer. Coordinates: https://plus.codes/589R2RX8+P64 Group Link: Gist Notes: If you show up and don't see anyone, don't despair. The group might have decided to go somewhere close, either to eat or avoid the sun. Information on where we are will be posted to the meetup page, but feel free to contact me by email.

Inline links: https://plus.codes/589R2RX8+P64, Gist

Highlights From The Comments On The Lab Leak Debate

April 09, 2024 · Original source

1: Comments Arguing Against Zoonosis — 1.1: Is COVID different from other zoonoses? — 1.2: Were the raccoon-dogs wild-caught? — 1.3: 92 early cases — 1.4: COVID in Brazilian wastewater — 1.5 Biorealism’s 16 arguments — 1.6: DrJayChou’s 7 arguments — 1.7: How much should coverup worry us? — 1.8: Have Worobey and Pekar been debunked? — 1.9: Was there ascertainment bias in early cases — 1.10: Connor Reed / Gwern on cats — 1.11: Rootclaim’s response to my post

This alone isn’t fatal to lab leak. It’s perfectly possible for the lab to leak (let’s say) November 5th, the virus spreads a bit, and then a month later someone goes to the wet market, coughs on a vendor, and starts the officially recognized pandemic. But if that were true, you’d expect (let’s say) 30 cases by early December. Let’s say the wet market vendor was exactly Case # 30. She infected the other wet market vendors, starting a pandemic with an obvious center at the wet market and lots of infected wet market vendors and patrons. What about Case # 29? If they were (let’s say) a barista, how come they didn’t infect people at their coffee shop? How come there wasn’t a second obvious cluster radiating out from a coffee shop, lots of coffee-shop-linked cases, etc? How come there weren’t 30 equally-sized clusters? In order to avoid this, you either need to claim that the wet market was a perfect superspreader location, or that the pattern with lots of cases in the wet market and few-to-none anywhere else was a result of ascertainment bias. Saar made both those arguments during the debate, but I thought Peter rebutted them effectively. 1.4: COVID in Brazilian wastewater Nicholas Halden (blog) writes: What should we make of this study, which found the presence of covid in Brazilian wastewater in late 2019? Consider the doubling times. The study says that scientists working in late 2020 found COVID in samples of Brazilian wastewater from November 27, 2019. This was long before the first detected case of transmission in Brazil on March 13, 2020. Between November 27, 2019 and March 13, 2020 is about 16 weeks, so 32 COVID doubling times. 32 doubling times with no lockdown is enough time for COVID to infect every single person in Brazil. If COVID had infected everyone in Brazil before the first recognized case, we would have noticed. (again, COVID doubling time isn’t exactly invariably 3.5 days, but here we’re talking about numbers big enough that the exact details don’t matter very much) So if COVID was in Brazil on November 27, it must have fizzled out instead of going pandemic. How likely is that? If one person had COVID, it’s not too unlikely - not all COVID cases transmit it forward. If (let’s say) twenty people had COVID, it’s very unlikely - at that point, the law of large numbers takes over; in a freak coincidence, every single patient would have to fail to infect anyone else. So almost certainly fewer than 20 people in Brazil had COVID in November 27. So which is more likely - that somehow 20 people had COVID long before the virus was officially detected, and on a totally different continent, yet somehow a scientist looking through wastewater found the water from exactly those people and managed to detect the virus? Or that there was a sampling error, which happens all the time in these kinds of things? Peter wrote a blog post on some of these issues. He found that there were positive tests from wastewater samples as early as March 2019, which doesn’t fit anyone’s timeline, including lab leakers’. And most of these positives (including the Brazilian sample) contained later strains of the virus with mutations it picked up late in 2020. So these were almost certainly false positives from contamination. 1.5: Biorealism’s 16 arguments Biorealism has a list of sixteen arguments, which he liked so much that he posted it three times in the ACX comments, twice on Less Wrong, twice on Manifold, and about a dozen times on Twitter under multiple account names. Some posts were slightly different from others, but a typical version is: Importantly, Miller incorrectly claimed the N501Y mutation would result from passage in hACE2 mice (mixed them up with BALB/c mice). The major papers Miller relied on have been seriously challenged since the debate. See Stoyan and Chiu (2024), Weissman (2024), Bloom (2023) and Lv et al (2024). Overall the circumstantial evidence makes lab v plausible: Peter admitted getting this wrong during the debate. I think this very minor point about mice mutations was approximately his only mistake in 15 hours of debating, and he admitted it as soon as he noticed. Biorealism somehow heard about this (obviously not through watching the debate, as we’ll see in a moment), then left about 20-30 comments starting with it, under various accounts, on various platforms, as if it somehow discredited Peter. This is making me somewhat less charitable to him and his 16 arguments than I would be otherwise. 1. Chinese researchers Botao & Lei Xiao observed lab origin was likely given the nearest known relatives to SARS-CoV-2 were far from Wuhan. Wuhan Institute of Virology (WIV) sampled SARS-related bat coronaviruses where the nearest relatives are found in Yunnan, Laos and Vietnam ~1500km away. They refuse to share their records. The ancestral viruses of SARS were found equally far from where SARS spilled over into humans, so we know it’s possible (and likely) for viruses to travel that far. 2. Patrick Berche, DG at Institut Pasteur in Lille 2014-18, notes you would expect secondary outbreaks if it arose via the live animal trade. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10234839/ There are constant outbreaks of weird coronaviruses in animal handlers. See eg this paper, which estimates about 60,000 of these per year. None of these ever go anywhere, because the farmers are in rural areas that aren’t dense enough to sustain a high R0, and the epidemic fizzles out after a single digit number of cases. Any early outbreaks of COVID would have vanished into this long and mostly unnoticed list. 3. Molecular data: Only sarbecovirus with a furin cleavage site. Well adapted to human ACE2 cells. Low genetic diversity indicating a lack of prior circulation (Berche 2023). Restriction site SARS-CoV-2 BsaI/BsmBI restriction map falls neatly within the ideal range for a reverse genetics system and used previously at WIV and UNC. Ngram analysis of the codon usage per Professor Louis Nemzer https://twitter.com/BiophysicsFL/status/1667232580255490053?t=IJgitS5cw364ioclzVWxaA&s=19 The SARS2 backbone is very low in CG and CpG. While the 12-nt insert that gives it the FCS is extremely high in both. Almost as if it was some kind of chimera of a consensus sequence and a codon-optimized polybasic cleavage site? https://twitter.com/BiophysicsFL/status/1752800486837678377?t=EpIRgyybJVaPgeMP5xdstA&s=19 https://www.biorxiv.org/content/10.1101/2022.10.18.512756v1 https://link.springer.com/article/10.1007/s10311-021-01211-0?fbclid=IwAR1HMUMtLIAFOFppVasQDeoIAYrVhP8j4YoPO4wnaTOUiKLsllZl_oKryOw Most of this was discussed extensively in the second session of the debate, which I recommend. The CGG-CGG arginine codon usage is particularly unusual but used in synthetic biology. I asked a synthetic biologist about this. He said: » “Nope. I would literally never do this if I was designing a small insert (maybe I wouldn't notice if it happened by chance with ~1 in 25 odds in a naive codon optimization algorithm as part of a larger sequence). High GC% is bad. Tandem repeat is worse. Several other perfectly fine arginine codons. And I wouldn't engineer a viral genome using human codon usage. An engineer would not do it.” 4. DEFUSE full proposal: virus 20% different from SARS1, consensus seq assembled with 6 segments, without disrupting coding seq, BsmBI order, FCS. SARS2: 20% different than SARS1, 6 evenly spaced fragments w BsmBI and BsaI restriction sites, FCS. Jesse Bloom, Jack Nunberg, Robert Townley, Alexandre Hassanin have observed this workflow could have lead to SARS-CoV-2. Work often begins before funding sought or goes ahead anyway. Re: 4 - Also scattered across second section of debate, also not going to retread 5. Market cases were all lineage B. Lv et al (2024) indicates there was a single point of emergence and A came before B. So market cases not the primary cases. See also Bloom (2021), Kumar et al (2022). Peter Ben Embarek said there were likely already thousands of cases in Wuhan in December 2019.https://t.co/50kFV9zSb6 https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/34398234/ https://academic.oup.com/bioinformatics/article/38/10/2719/6553661 There was a Lineage A sample in the market, lab leak proponents just try to ignore/dismiss/conspiracize it away. The first two known Lineage A cases were very close to the market. Lv (is this even a real name? It sounds like Roman numeral? But I guess that’s what you expect in a country ruled by someone named Xi) found some weird COVID variants in Shanghai that might or might not mean anything; you can see some discussion of the implications here, but I don’t think they’re strong evidence either way. If A was first, it means some really weird stuff coincidences have to happen to give us the spread rates and genetic clock data we get, but they’re not necessarily weirder in the zoonosis hypothesis than the lab leak one. The claim that there were “thousands of cases in Wuhan in December 2019” is very easy to disprove by doubling rate arguments like the one above, by the blood bank study mentioned above, by the WHO’s failed case search, and by many other lines of argument. 6. Evidence for lineage A in the market is based on a low quality sample according to Liu et. al. (2023). I really think lab leakers need to decide whether they think China is a sinister actor trying to cover up the truth, or whether they should trust every offhand comment by Chinese government officials as gospel. Dr. Liu doesn’t explain in what sense he thinks the Lineage A sample is “low-quality”, and the Western scientists who I asked about this said they didn’t understand this complaint and that the sample was fine. A Western team re-analyzing the same sample describes it as “conclusively contain[ing] Lineage A.” I think most lab leakers have switched from trying to deny the genetics to claiming that this was “contamination”, which also doesn’t make sense (the sample is genetically very early). Note that aside from this sample, the first two Lineage A cases discovered were both very close to the wet market. 7. Bloom (2023) shows market samples do not support market origin. There is also no evidence of transmission in the claimed susceptible animals elsewhere. https://academic.oup.com/ve/advance-article/doi/10.1093/ve/vead089/7504441 Discussed extensively in my article as well as the first section of the debate. 8. Lineage A and B only two mutations apart. François Ballox, Bloom and Virginie Courtier-Orgogozo note this is unlikely to reflect two separate animal spillovers as opposed to incomplete case ascertainment of human to human transmission (Bloom 2021). Discussed extensively in my article as well as the first section of the debate. 9. Sampling bias. George Gao, Chinese CDC head at the time, acknowledged to the BBC stating they may have focused too much on and around the market and missed cases on the other side of the city. David Bahry outlines the documented bias. Michael Weissman has shown this mathematically. https://journals.asm.org/doi/10.1128/mbio.00313-23 https://academic.oup.com/jrsssa/advance-article-abstract/doi/10.1093/jrsssa/qnae021/7632556 Re: Dr. Gao, see above comment about Chinese officials. See the section Ascertainment Bias below for why I disagree with this specific claim, which also addresses the Michael Weissman argument. 10. Spatial statistics experts show the Worobey claim the market was the early epicentre was flawed. https://academic.oup.com/jrsssa/advance-article-abstract/doi/10.1093/jrsssa/qnad139/7557954 Re: 10 - See Confirmation Of The Centrality Of The Huanan Market Among Early COVID-19 Cases, a response to the paper you cite: The centrality of Wuhan's Huanan market in maps of December 2019 COVID-19 case residential locations, established by Worobey et al. (2022a), has recently been challenged by Stoyan and Chiu (2024, SC2024). SC2024 proposed a statistical test based on the premise that the measure of central tendency (hereafter, "centre") of a sample of case locations must coincide with the exact point from which local transmission began. Here we show that this premise is erroneous. SC2024 put forward two alternative centres (centroid and mode) to the centre-point which was used by Worobey et al. for some analyses, and proposed a bootstrapping method, based on their premise, to test whether a particular location is consistent with it being the point source of transmission. We show that SC2024's concerns about the use of centre-points are inconsequential, and that use of centroids for these data is inadvisable. The mode is an appropriate, even optimal, choice as centre; however, contrary to SC2024's results, we demonstrate that with proper implementation of their methods, the mode falls at the entrance of a parking lot at the market itself, and the 95% confidence region around the mode includes the market. Thus, the market cannot be rejected as central even by SC2024's overly stringent statistical test. I think this response is pretty strong. In one analysis, they show that even though the other paper’s methodology is worse than theirs, if you apply it correctly (instead of inappropriately excluding various cases like the paper’s authors did), the center of all early cases in Hubei province lands on the wet market parking lot. In another analysis, they show that the other paper’s recommended tests wouldn’t have correctly pointed to the offending water pump in the famous John Snow cholera outbreak, but theirs would have. Still, I think it’s useful to supplement fancy statistics with normal common sense, so I recommend just looking at the map of early cases: …and deciding whether you think the assumptions behind a specific statistical test are likely to debunk the idea that cases are centered around the wet market. 11. Wuhan used as a control for a 2015 serological study on SARS-related bat coronaviruses due to its urban location. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6178078/ I don’t know why this point is supposed to matter. If you mean that Wuhan isn’t directly exposed to bats, nobody ever said it was. The zoonotic theory is that wildlife carted in from other areas of China started the pandemic in the wet market. 12. Superspreader events also seen at wet markets in Beijing and Singapore (Xinfadi and Jurong). This was discussed very extensively in the debates, both in section 1 and section 3. Wet markets weren’t “superspreader locations” - in fact, the disease spread no more quickly there than anywhere else. They were the first place in those cities that the pandemic started, due to contaminated animal products. If anything, this supports zoonosis. See also my discussion with Saar on this point below. 13. WIV refuse to share their records with NIH who terminated subaward in 2022. Wider suspension over biosafety concerns. https://www.bloomberg.com/news/articles/2023-07-18/us-suspends-wuhan-institute-funds-over-covid-stonewalling Although WIV has not been especially forthcoming, some of their databases were leaked in various ways and showed that they did not have any viruses capable of transforming into COVID. 14. PLA involvement at WIV and MERS research prior to SARS-COV-2. MERS features several similarities with SARS-CoV-2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7022351/ I can’t even tell what conspiracy theory you’re trying to propose with this one; if you spell it out I can try to explain why it might be false. 15. SARS1 leaked several times and SARS-COV-2 has leaked from a BSL-3 lab in Taiwan. Agreed that SARS leaked several times. It also spilled over from animals several times. During the debate, a lab leak rate of once per lab per 500 years was proposed (everyone agreed to steelman this by 10x for WIV numbers); I would be interested to know whether anything about the study of SARS challenges that number. 16. Unpublished infectious clone identified from Wuhan contradicting arguments such reverse genetics systems would be published. https://www.biorxiv.org/content/10.1101/2023.02.12.528210v1.full I asked some scientists about this paper and here’s what they told me. Wuhan University sequenced some rice. In the middle of the sequence, there’s an unexpected sequence from a common coronavirus, HKU4. The most likely explanation is that someone else in Wuhan was working on the coronavirus and there was cross-contamination. Plausibly this is Wuhan Institute of Virology, who is known to work with coronaviruses. This is cool detective work, but it’s not clear what it’s supposed to prove. I think some lab leakers are using it to prove that WIV can do reverse genetics, but they admitted this already in a published paper so that’s not too helpful. I think others are using it to prove WIV had “secret viruses” in their catalogue, but the rice virus wasn’t secret, it was HKU4, which is common and which WIV has already published papers about. 1.6: DrJayChou’s 7 Arguments Once again, I cannot stress enough how much better a take you might have on this debate if you watch it. “The first known case predates the market outbreak by a month” - this is not the consensus position. I cannot say for sure what Dr. Chou means by this, but I suspect he’s referring to one of the many claims to this effect that Peter effectively debunked during the debate (Connor Reed, Mr. Chen, the 92 cases, Brazil, etc).

Inline links: blog, writes, this study, wrote a blog post on some of these issues, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10234839/, this paper, https://twitter.com/BiophysicsFL/status/1667232580255490053?t=IJgitS5cw364ioclzVWxaA&s=19, https://twitter.com/BiophysicsFL/status/1752800486837678377?t=EpIRgyybJVaPgeMP5xdstA&s=19, https://www.biorxiv.org/content/10.1101/2022.10.18.512756v1, https://link.springer.com/article/10.1007/s10311-021-01211-0?fbclid=IwAR1HMUMtLIAFOFppVasQDeoIAYrVhP8j4YoPO4wnaTOUiKLsllZl_oKryOw, https://t.co/50kFV9zSb6, https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/34398234/, https://academic.oup.com/bioinformatics/article/38/10/2719/6553661, here, describes it as, https://academic.oup.com/ve/advance-article/doi/10.1093/ve/vead089/7504441, https://journals.asm.org/doi/10.1128/mbio.00313-23, https://academic.oup.com/jrsssa/advance-article-abstract/doi/10.1093/jrsssa/qnae021/7632556, https://academic.oup.com/jrsssa/advance-article-abstract/doi/10.1093/jrsssa/qnad139/7557954, Confirmation Of The Centrality Of The Huanan Market Among Early COVID-19 Cases, https://substackcdn.com/image/fetch/$s_!BNAm!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2Fffd4cddb-6e3e-41f5-8ef6-ec0b27bec600_626x426.webp, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6178078/, https://www.bloomberg.com/news/articles/2023-07-18/us-suspends-wuhan-institute-funds-over-covid-stonewalling, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7022351/, https://www.biorxiv.org/content/10.1101/2023.02.12.528210v1.full, a published paper, has already published papers about, https://substackcdn.com/image/fetch/$s_!yA9U!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2F467dd304-190a-4437-8920-d498c433dffb_1600x960.jpeg

“The first known case predates the market outbreak by a month” - this is not the consensus position. I cannot say for sure what Dr. Chou means by this, but I suspect he’s referring to one of the many claims to this effect that Peter effectively debunked during the debate (Connor Reed, Mr. Chen, the 92 cases, Brazil, etc).

Highlights From The Comments On "The Origin Of Woke"

May 07, 2024 · Original source

Matheus from Brazil writes:

Inline links: writes

Here in Brazil we do have 50% black population (not black in the same sense as Americans). We didn't fight a civil war to end slavery and we didn't have segregation after ending slavery. We are cordial men (see: https://translate.google.com/translate?sl=pt&tl=en&hl=pt-BR&u=https://pt.wikipedia.org/wiki/Homem_cordial&client=webapp ). We had our first black president in 1909, but neither he nor the people made much of it.

Inline links: https://translate.google.com/translate?sl=pt&tl=en&hl=pt-BR&u=https://pt.wikipedia.org/wiki/Homem_cordial&client=webapp

I am saying this because Brazil offers a nice comparison. We do have quotas. Quotas for public universities and quotas for public service. The federal law for public service quotas is 20% (much lower than the general population). There was some pushback when Congress approved these laws, but people mostly accepted it. Not even Bolsonaro pushes back on them. And I think quotas for university aren't the worst idea (you're educating people instead of putting them as traffic controllers) and the 20% number for public service isn't doing the same harm that the African National Congress quotas did on their country. Corporate life isn't harmed beyond that.

Your Book Review: How Language Began

July 19, 2024 · Original source

This is what he looks like. According to Wikipedia, the context for this picture is: “Noam Chomsky speaks about humanity's prospects for survival” Since around 1957, Chomsky has dominated linguistics. And this matters because he is kind of a contrarian with weird ideas. Is language for communicating? No, it’s mainly for thinking: (What Kind of Creatures Are We? Ch. 1, pg. 15-16) It is, indeed, virtual dogma that the function of language is communication. ... there is by now quite significant evidence that it is simply false. Doubtless language is sometimes used for communication, as is style of dress, facial expression and stance, and much else. But fundamental properties of language design indicate that a rich tradition is correct in regarding language as essentially an instrument of thought, even if we do not go as far as Humboldt in identifying the two. Should linguists care about the interaction between culture and language? No, that’s essentially stamp-collecting: (Language and Responsibility, Ch. 2, pg. 56-57) Again, a discipline is defined in terms of its object and its results. Sociology is the study of society. As to its results, it seems that there are few things one can say about that, at least at a fairly general level. One finds observations, intuitions, impressions, some valid generalizations perhaps. All very valuable, no doubt, but not at the level of explanatory principles. … Sociolinguistics is, I suppose, a discipline that seeks to apply principles of sociology to the study of language; but I suspect that it can draw little from sociology, and I wonder whether it is likely to contribute much to it. … You can also collect butterflies and make many observations. If you like butterflies, that’s fine; but such work must not be confounded with research, which is concerned to discover explanatory principles of some depth and fails if it has not done so. Did the human capacity for language evolve gradually? No, it suddenly appeared around 50,000 years ago after a freak gene mutation: (Language and Mind, third edition, pg, 183-184) An elementary fact about the language faculty is that it is a system of discrete infinity, rare in the organic world. Any such system is based on a primitive operation that takes objects already constructed, and constructs from them a new object: in the simplest case, the set containing them. Call that operation Merge. Either Merge or some equivalent is a minimal requirement. With Merge available, we instantly have an unbounded system of hierarchically structured expressions. The simplest account of the “Great Leap Forward” in the evolution of humans would be that the brain was rewired, perhaps by some slight mutation, to provide the operation Merge … There are speculations about the evolution of language that postulate a far more complex process … A more parsimonious speculation is that they did not, and that the Great Leap was effectively instantaneous, in a single individual, who was instantly endowed with intellectual capacities far superior to those of others, transmitted to offspring and coming to predominate. At best a reasonable guess, as are all speculations about such matters, but about the simplest one imaginable, and not inconsistent with anything known or plausibly surmised. It is hard to see what account of human evolution would not assume at least this much, in one or another form. I think all of these positions are kind of insane for reasons that we will discuss later. (Side note: Chomsky’s proposal is essentially the hard takeoff theory of human intelligence.) Most consequential of all, perhaps, are the ways Chomsky has influenced (i) what linguists mainly study, and (ii) how they go about studying it. Naively, since language involves many different components—including sound production and comprehension, intonation, gestures, and context, among many others—linguists might want to study all of these. While they do study all of these, Chomsky and his followers view grammar as by far the most important component of humans’ ability to understand and produce language, and accordingly make it their central focus. Roughly speaking, grammar refers to the set of language-specific rules that determine whether a sentence is well-formed. It goes beyond specifying word order (or ‘surface structure’, in Chomskyan terminology) since one needs to know more than just where words are placed in order to modify or extend a given sentence. Consider a pair of sentences Chomsky uses to illustrate this point in Aspects of the Theory of Syntax (pg. 22), his most cited work: (1a) I expected John to be examined by a specialist. (2a) I persuaded John to be examined by a specialist. The words “expected” and “persuaded” appear in the same location in each sentence, but imply different ‘latent’ grammatical structures, or ‘deep structures’. One way to show this is to observe that a particular way of rearranging the words produces a sentence with the same meaning in the first case (1a = 1b), and a different meaning in the second (2a != 2b): (1b) I expected a specialist to examine John. (2b) I persuaded a specialist to examine John. In particular, the target of persuasion is “John” in the case of (2a), and “the specialist” in the case of (2b). A full Chomskyan treatment of sentences like this would involve hierarchical tree diagrams, which permit a precise description of deep structure. You may have encountered the famous sentence: “Colorless green ideas sleep furiously.” It first appeared in Chomsky’s 1957 book Syntactic Structures, and the point is that even nonsense sentences can be grammatically well-formed, and that speakers can quickly assess the grammatical correctness of even nonsense sentences that they’ve never seen before. To Chomsky, this is one of the most important facts to be explained about language. A naive response to Chomsky’s preoccupation with grammar is: doesn’t real language involve a lot of non-grammatical stuff, like stuttering and slips of the tongue and midstream changes of mind? Of course it does, and Chomsky acknowledges this. To address this point, Chomsky has to move the goalposts in two important ways. First, he famously distinguishes competence from performance, and identifies the former as the subject of any serious theory of language: (Aspects of the Theory of Syntax, Ch. 1, pg. 4) The problem for the linguist, as well as for the child learning the language, is to determine from the data of performance the underlying system of rules that has been mastered by the speaker-hearer and that he puts to use in actual performance. Hence, in the technical sense, linguistic theory is mentalistic, since it is concerned with discovering a mental reality underlying actual behavior. Observed use of language or hypothesized dispositions to respond, habits, and so on, may provide evidence as to the nature of this mental reality, but surely cannot constitute the actual subject matter of linguistics, if this is to be a serious discipline. Moreover, he claims that grammar captures most of what we should mean when we talk about speakers’ linguistic competence: (Aspects of the Theory of Syntax, Ch. 1, pg. 24) A grammar can be regarded as a theory of a language; it is descriptively adequate to the extent that it correctly describes the intrinsic competence of the idealized native speaker. Another way Chomsky moves the goalposts is by distinguishing E-languages, like English and Spanish and Japanese, from I-languages, which only exist inside human minds. He claims that serious linguistics should be primarily interested in the latter. In a semi-technical book summarizing Chomsky’s theory of language, Cook and Newson write: (Chomsky’s Universal Grammar: An Introduction, pg. 13) E-language linguistics … aims to collect samples of language and then describe their properties. … I-language linguistics, however, is concerned with what a speaker knows about language and where this knowledge comes from; it treats language as an internal property of the human mind rather than something external … Not only should linguistics primarily be interested in studying I-languages, but to try and study E-languages at all may be a fool’s errand: (Chomsky’s Universal Grammar: An Introduction, pg. 13) Chomsky claims that the history of generative linguistics shows a shift from an E-language to an I-language approach; ‘the shift of focus from the dubious concept of E-language to the significant notion of I-language was a crucial step in early generative grammar’ (Chomsky, 1991b, pg. 10). … Indeed Chomsky is extremely dismissive of E-language approaches: ‘E-language, if it exists at all, is derivative, remote from mechanisms and of no particular empirical significance, perhaps none at all’ (Chomsky, 1991b, pg. 10).1 I Am Not A Linguist (IANAL), but this redefinition of the primary concern of linguistics seems crazy to me. Is studying a language like English as it is actually used really of no particular empirical significance? And this doesn’t seem to be a one-time hyperbole, but a representative claim. Cook and Newson continue: (Chomsky’s Universal Grammar: An Introduction, pg. 14) The opposition between these two approaches in linguistics has been long and acrimonious, neither side conceding the other’s reality. … The E-linguist despises the I-linguist for not looking at the ‘real’ facts; the I-linguist derides the E-linguist for looking at trivia. The I-language versus E-language distinction is as much a difference of research methods and of admissible evidence as it is of long-term goals. So much for what linguists ought to study. How should they study it? The previous quote gives us a clue. Especially in the era before Chomsky (BC), linguists were more interested in description. Linguists were, at least in one view, people who could be dropped anywhere in the world, and emerge with a tentative grammar of the local language six months later. (A notion like this is mentioned early in this video.) Linguists catalog the myriad of strange details about human languages, like the fact that some languages don’t appear to have words for relative directions, or “thank you”, or “yes” and “no”. After Chomsky's domination of the field (AD), there were a lot more theorists. While you could study language by going out into the field and collecting data, this was viewed as not the only, and maybe not even the most important, way to work. Diagrams of sentences proliferated. Chomsky, arguably the most influential linguist of the past hundred years, has never done fieldwork. In summary, to Chomsky and many of the linguists working in his tradition, the scientifically interesting component of language is grammar competence, and real linguistic data only indirectly reflects it. All of this matters because the dominance of Chomskyan linguistics has had downstream effects in adjacent fields like artificial intelligence (AI), evolutionary biology, and neuroscience. Chomsky has long been an opponent of the statistical learning tradition of language modeling, essentially claiming that it does not provide insight about what humans know about languages, and that engineering success probably can’t be achieved without explicitly incorporating important mathematical facts about the underlying structure of language. Chomsky’s ideas have motivated researchers to look for a “language gene” and “language areas” of the brain. Arguably, no one has yet found either—but more on that later. How Chomsky attained this stranglehold on linguistics is an interesting sociological question, but not our main concern in the present work2. The intent here is not to pooh-pooh Chomsky, either; brilliant and hard-working people are often wrong on important questions. Consider that his academic career began in the early 1950s—over 70 years ago!—when our understanding of language, anthropology, biology, neuroscience, and artificial intelligence, among many other things, was substantially more rudimentary. Where are we going with this? All of this is context for understanding the ideas of a certain bomb-throwing terrorist blight on the face of linguistics: Daniel Everett. How Language Began is a book he wrote about, well, what language is and how it began. Everett is the anti-Chomsky. II. THE MISSIONARY We all love classic boy-meets-girl stories. Here’s one: boy meets girl at a rock concert, they fall in love, the boy converts to Christianity for the girl, then the boy and girl move to the Amazon jungle to dedicate the rest of their lives to saving the souls of an isolated hunter-gatherer tribe. Daniel Everett is the boy in this story. The woman he married, Keren Graham, is the daughter of Christian missionaries and had formative experiences living in the Amazon jungle among the Sateré-Mawé people. At seventeen, Everett became a born-again Christian; at eighteen, he and Keren married; and over the next few years, they started a family and prepared to become full-fledged missionaries like Keren’s parents. First, Everett studied “Bible and Foreign Missions” at the Moody Bible Institute in Chicago. After finishing his degree in 1975, the natural next step was to train more specifically to follow in the footsteps of Keren’s parents. In 1976, he and his wife enrolled in the Summer Institute of Linguistics (SIL) to learn translation techniques and more viscerally prepare for life in the jungle: They were sent to Chiapas, Mexico, where Keren stayed in a hut in the jungle with the couple’s children—by this time, there were three—while Everett underwent grueling field training. He endured fifty-mile hikes and survived for several days deep in the jungle with only matches, water, a rope, a machete, and a flashlight. Everett apparently had a gift for language-learning. This led SIL to invite Everett and his wife to work with the Pirahã people (pronounced pee-da-HAN), whose unusual language had thwarted all previous attempts to learn it. In 1977, Everett’s family moved to Brazil, and in December they met the Pirahã for the first time. As an SIL-affiliated missionary, Everett’s explicit goals were to (i) translate the Bible into Pirahã, and (ii) convert as many Pirahã as possible to Christianity. But Everett’s first encounter with the Pirahã was cut short for political reasons: (Don’t Sleep There Are Snakes, Ch. 1, pg. 13-14) In December of 1977 the Brazilian government ordered all missionaries to leave Indian reservations. … Leaving the village under these forced circumstances made me wonder whether I’d ever be able to return. The Summer Institute of Linguistics was concerned too and wanted to find a way around the government’s prohibition against missionaries. So SIL asked me to apply to the graduate linguistics program at the State University of Campinas (UNICAMP), in the state of São Paulo, Brazil. It was hoped that UNICAMP would be able to secure government authorization for me to visit the Pirahãs for a prolonged period, in spite of the general ban against missionaries. … My work at UNICAMP paid off as SIL hoped it would. Everett became a linguist proper sort of by accident, mostly as an excuse to continue his missionary work. But he ended up developing a passion for it. In 1980, he completed Aspects of the Phonology of Pirahã, his master’s thesis. He continued on to get a PhD in linguistics, also from UNICAMP, and in 1983 finished The Pirahã Language and Theory of Syntax, his dissertation. He continued studying the Pirahã and working as an academic linguist after that. In all, Everett spent around ten years of his life living with the Pirahã, spread out over some thirty-odd years. As he notes in Don’t Sleep, There Are Snakes: (Prologue, pg. xvii-xviii) I went to the Pirahãs when I was twenty-six years old. Now I am old enough to receive senior discounts. I gave them my youth. I have contracted malaria many times. I remember several occasions on which the Pirahãs or others threatened my life. I have carried more heavy boxes, bags, and barrels on my back through the jungle than I care to remember. But my grandchildren all know the Pirahãs. My children are who they are in part because of the Pirahãs. And I can look at some of those old men (old like me) who once threatened to kill me and recognize some of the dearest friends I have ever had—men who would now risk their lives for me. Everett interviewing some Pirahã people. (source) Everett did eventually learn their language, and it’s worth taking a step back to appreciate just how hard that task was. No Pirahã spoke Portuguese, apart from some isolated phrases they used for bartering. They didn’t speak any other language at all—just Pirahã. How do you learn another group’s language when you have no languages in common? The technical term is monolingual fieldwork. But this is just a fancy label for some combination of pointing at things, listening, crude imitation, and obsessively transcribing whatever you hear. For years. It doesn’t help that the Pirahã language seems genuinely hard to learn in a few different senses. First, it is probably conventionally difficult for Westerners to learn since it is a tonal language (two tones: high and low) with a small number of phonemes (building block sounds) and a few unusual sounds3. Second, there is no written language. Third, the language has a variety of ‘channels of discourse’, or ways of talking specialized for one or another cultural context. One of these is ‘whistle speech’; Pirahãs can communicate purely in whistles. This feature appears to be extremely useful during hunting trips: (Don’t Sleep, There Are Snakes, Ch. 11, pg. 187-188) My first intense contact with whistle speech came one day when the Pirahãs had given me permission to go hunting with them. After we’d been walking for about an hour, they decided that they weren’t seeing any game because I, with my clunking canteens and machete and congenital clumsiness, was making too much noise. “You stay here and we will be back for you later.” Xaikáibaí said gently but firmly. … As I tried to make the best of my solitary confinement, I heard the men whistling to one another. They were saying, “I’ll go over there; you go that way,” and other such hunting talk. But clearly they were communicating. It was fascinating because it sounded so different from anything I had heard before. The whistle carried long and clear in the jungle. I could immediately see the importance and usefulness of this channel, which I guessed would also be much less likely to scare away game than the lower frequencies of the men’s normal voices. Fourth, important aspects of the language reflect core tenets of Pirahã culture in ways that one might not a priori expect. Everett writes extensively about the ‘immediacy of experience principle’ of Pirahã culture, which he summarizes as the idea that: (Don’t Sleep, There Are Snakes, Ch. 7, pg. 132) Declarative Pirahã utterances contain only assertions related directly to the moment of speech, either experienced by the speaker or witnessed by someone alive during the lifetime of the speaker. One way the language reflects this is that the speaker must specify how they know something by affixing an appropriate suffix to verbs: (Don’t Sleep, There Are Snakes, Ch. 12, pg. 196) Perhaps the most interesting suffixes, however (though these are not unique to Pirahã), are what linguists call evidentials, elements that represent the speaker’s evaluation of his or her knowledge of what he or she is saying. There are three of these in Pirahã: hearsay, observation, and deduction. To see what these do, let’s use an English example. If I ask you, “Did Joe go fishing?” you could answer, “Yes, at least I heard that he did,” or “Yes, I know because I saw him leave,” or “Yes, at least I suppose he did because his boat is gone.” The difference between English and Pirahã is that what English does with a sentence, Pirahã does with a verbal suffix. Everett also convincingly links this cultural principle to the lack of Pirahã number words and creation myths. On the latter topic, Everett recalls the following exchange: (Don’t Sleep, There Are Snakes, Ch. 7, pg. 134) I sat with Kóhoi once and he asked me, after hearing about my god, “What else does your god do?” And I answered, “Well, he made the stars, and he made the earth.” Then I asked, “What do the Pirahãs say?” He answered, “Well, the Pirahãs say that these things were not made.” And all of this is to say nothing of the manifold perils of the jungle: malaria, typhoid fever, dysentery, dangerous snakes, insects, morally gray river traders, and periodic downpours. If Indiana Jones braved these conditions for years, we would consider his stories rousing adventures. Everett did this while also learning one of the most unusual languages in the world. People on the bank of the Maici river. (source) By the way, he did eventually sort of achieve his goal of translating the Bible. Armed with a solid knowledge of Pirahã, he was able to translate the New Testament’s Gospel of Mark. Since the Pirahã have no written language, he provided them with a recorded version, but did not get the reaction he expected: (Don’t Sleep, There Are Snakes, Ch. 17, pg. 267-268) When we returned to the village, I recorded Mark’s gospel in my own voice for the Pirahãs to listen to. I then brought in a wind-up tape recorder to play the recording, and I taught the Pirahãs how to use it, which, surprisingly enough, some of the children did. Keren and I left the village and returned a few weeks later. The people were still listening to the gospel, with children cranking the recorder. I was initially quite excited about this, until it became clear that the only part of the book that they paid attention to was the beheading of John the Baptist. “Wow, they cut off his head. Play that again!” One reaction to hearing the gospel caught Everett even more off-guard: (Don’t Sleep, There Are Snakes, Ch. 17, pg. 269) "The women are afraid of Jesus. We do not want him." "Why not?" I asked, wondering what had triggered this declaration. "Because last night he came to our village and tried to have sex with our women. He chased them around the village, trying to stick his large penis into them." Kaaxaóoi proceeded to show me with his two hands held far apart how long Jesus's penis was—a good three feet. But the Pirahã had an even more serious objection to Jesus: (Don’t Sleep, There Are Snakes, Ch. 17, pg. 265-266) Part of the difficulty of my task began to become clear to me. I communicated more or less correctly to the Pirahãs about my Christian beliefs. The men listening to me understood that there was a man named Hisó, Jesus, and that he wanted others to do what he told them. "The Pirahã men then asked, "Hey Dan, what does Jesus look like? Is he dark like us or light like you?" I said, "Well, I have never actually seen him. He lived a long time ago. But I do have his words." "Well, Dan, how do you have his words if you have never heard him or seen him?" They then made it clear that if I had not actually seen this guy (and not in any metaphorical sense, but literally), they weren't interested in any stories I had to tell about him. Period. This is because, as I now knew, the Pirahãs believe only what they see. Sometimes they also believe in things that someone else has told them, so long as that person has personally witnessed what he or she is reporting. In the end, Everett never converted a single Pirahã. But he did even worse than converting zero people—he lost his own faith after coming to believe that the Pirahã had a good point. After keeping this to himself for many years, he revealed his loss of faith to his family, which led to a divorce and his children breaking contact with him for a number of years afterward. But Everett losing his faith in the God of Abraham was only the beginning. Most importantly for us, he also lost his faith in the God of Linguistics—Noam Chomsky. III. THE WAR In 2005, Everett’s paper “Cultural constraints on grammar and cognition in Pirahã: Another look at the design features of human language” was published in the journal Cultural Anthropology. An outsider might expect an article like this, which made a technical observation about the apparent lack of a property called ‘recursion’ in the Pirahã language, to receive an ‘oh, neat’ sort of response. Languages can be pretty different from one another, after all. Mandarin lacks plurals. Spanish sentences can omit an explicit subject. This is one of those kinds of things. But the article ignited a firestorm of controversy that follows Everett to this day. Praise for Everett and his work on recursion in Pirahã: He became a pure charlatan, although he used to be a good descriptive linguist. That is why, as far as I know, all the serious linguists who work on Brazilian languages ignore him. Noam Chomsky, MIT professor and linguist

Inline links: Wikipedia, hard takeoff, grammar, 1, this video, don’t appear to have words for relative directions, “thank you”, “yes” and “no”, long been an opponent, 2, Daniel Everett, Sateré-Mawé people, prepared, Bible and Foreign Missions, 1975, SIL, viscerally prepare, Pirahã people, https://substackcdn.com/image/fetch/$s_!42Ji!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2F5c899185-e1a2-4358-ae6a-e9298f6c7cdb_1600x1002.jpeg, source, 3, number words, https://substackcdn.com/image/fetch/$s_!yx-R!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2F77975f2c-ef0f-47d7-9ed9-f22bbe04f78b_1024x768.jpeg, source, Cultural constraints on grammar and cognition in Pirahã: Another look at the design features of human language

People on the bank of the Maici river. (source) By the way, he did eventually sort of achieve his goal of translating the Bible. Armed with a solid knowledge of Pirahã, he was able to translate the New Testament’s Gospel of Mark. Since the Pirahã have no written language, he provided them with a recorded version, but did not get the reaction he expected: (Don’t Sleep, There Are Snakes, Ch. 17, pg. 267-268) When we returned to the village, I recorded Mark’s gospel in my own voice for the Pirahãs to listen to. I then brought in a wind-up tape recorder to play the recording, and I taught the Pirahãs how to use it, which, surprisingly enough, some of the children did. Keren and I left the village and returned a few weeks later. The people were still listening to the gospel, with children cranking the recorder. I was initially quite excited about this, until it became clear that the only part of the book that they paid attention to was the beheading of John the Baptist. “Wow, they cut off his head. Play that again!” One reaction to hearing the gospel caught Everett even more off-guard: (Don’t Sleep, There Are Snakes, Ch. 17, pg. 269) "The women are afraid of Jesus. We do not want him." "Why not?" I asked, wondering what had triggered this declaration. "Because last night he came to our village and tried to have sex with our women. He chased them around the village, trying to stick his large penis into them." Kaaxaóoi proceeded to show me with his two hands held far apart how long Jesus's penis was—a good three feet. But the Pirahã had an even more serious objection to Jesus: (Don’t Sleep, There Are Snakes, Ch. 17, pg. 265-266) Part of the difficulty of my task began to become clear to me. I communicated more or less correctly to the Pirahãs about my Christian beliefs. The men listening to me understood that there was a man named Hisó, Jesus, and that he wanted others to do what he told them. "The Pirahã men then asked, "Hey Dan, what does Jesus look like? Is he dark like us or light like you?" I said, "Well, I have never actually seen him. He lived a long time ago. But I do have his words." "Well, Dan, how do you have his words if you have never heard him or seen him?" They then made it clear that if I had not actually seen this guy (and not in any metaphorical sense, but literally), they weren't interested in any stories I had to tell about him. Period. This is because, as I now knew, the Pirahãs believe only what they see. Sometimes they also believe in things that someone else has told them, so long as that person has personally witnessed what he or she is reporting. In the end, Everett never converted a single Pirahã. But he did even worse than converting zero people—he lost his own faith after coming to believe that the Pirahã had a good point. After keeping this to himself for many years, he revealed his loss of faith to his family, which led to a divorce and his children breaking contact with him for a number of years afterward. But Everett losing his faith in the God of Abraham was only the beginning. Most importantly for us, he also lost his faith in the God of Linguistics—Noam Chomsky. III. THE WAR In 2005, Everett’s paper “Cultural constraints on grammar and cognition in Pirahã: Another look at the design features of human language” was published in the journal Cultural Anthropology. An outsider might expect an article like this, which made a technical observation about the apparent lack of a property called ‘recursion’ in the Pirahã language, to receive an ‘oh, neat’ sort of response. Languages can be pretty different from one another, after all. Mandarin lacks plurals. Spanish sentences can omit an explicit subject. This is one of those kinds of things. But the article ignited a firestorm of controversy that follows Everett to this day. Praise for Everett and his work on recursion in Pirahã: He became a pure charlatan, although he used to be a good descriptive linguist. That is why, as far as I know, all the serious linguists who work on Brazilian languages ignore him. Noam Chomsky, MIT professor and linguist

Inline links: source, Cultural constraints on grammar and cognition in Pirahã: Another look at the design features of human language

Meetups Everywhere 2024: Times & Places

August 29, 2024 · Original source

Contact: Matt Contact Info: mw[dot]coop[d ot]r[a t]gmail[d ot]com Time: Saturday, September 14th, 03:00 PM Location: Meet at Facultad de Derecho, right outside of the Ache Grill and Starbucks. We will have some kind of sign that says ACX Meetup Coordinates: https://plus.codes/48Q3CJ85+QPH Brazil FLORIANÓPOLIS, BRAZIL Contact: Adiel Contact Info: adiel[at]airpost[dot]net Time: Saturday, October 19th, 04:00 PM Location: Angeloni Beira Mar, at the food court. I’ll be wearing a yellow hat. Coordinates: https://plus.codes/584HCFGF+326 Group Link: https://chat.whatsapp.com/C2WFfuFX07 [ignore this part] W0UBMnTeooN6 Notes: Everyone is welcome! There will be cookies.

Inline links: https://plus.codes/48Q3CJ85+QPH, https://plus.codes/584HCFGF+326

Contact: Adiel Contact Info: adiel[at]airpost[dot]net Time: Saturday, October 19th, 04:00 PM Location: Angeloni Beira Mar, at the food court. I’ll be wearing a yellow hat. Coordinates: https://plus.codes/584HCFGF+326 Group Link: https://chat.whatsapp.com/C2WFfuFX07 [ignore this part] W0UBMnTeooN6 Notes: Everyone is welcome! There will be cookies. SÃO PAULO, BRAZIL Contact: Bruno Vieira Contact Info: vbruno2002[at]gmail[dot]com Time: Friday, September 20th, 06:00 PM Location: INOVA USP - 20/09/2024 - 18:00. Av. Prof. Lúcio Martins Rodrigues, 370 - Butantã, São Paulo - SP, 05508-020 Coordinates: https://plus.codes/588MC7VF+25 Group Link: https://chat.whatsapp.com/GZSMt9x [ignore this part] MXUpFjJai4u0hlB Notes: Don't bring kids or dogs, please. I'm still working out dinner, join the group chat so we can properly represent you with our decisions. RSVPs required at https://www.sympla.com.br/evento/acx-meetup-sao-paulo/2607686

Inline links: https://plus.codes/584HCFGF+326, https://plus.codes/588MC7VF+25, https://www.sympla.com.br/evento/acx-meetup-sao-paulo/2607686

ACX Endorses Harris, Oliver, Or Stein

October 30, 2024 · Original source

A long time ago, I wrote about the difference between ingroup, outgroup, and fargroup. Ingroup and outgroup you know. But how come people have stronger emotions about Ibram X. Kendi (or Chris Rufo) than about Kim Jong-un or whoever's committing the latest genocide in Sudan? It's not because you're American and naturally care about American affairs - how about that Brazilian judge who banned Elon Musk's X? It's because all those guys are part of your psychodrama and some Sudanese psychopath isn't. Well, Kamala Harris' price controls are my outgroup; Donald Trump setting tariffs is my fargroup.

Inline links: the difference between ingroup, outgroup, and fargroup

Meetups Everywhere Spring 2025: Times & Places

March 25, 2025 · Original source

Contact: Eitan Sprejer Contact Info: eitusprejer[a t]gmail[period]com Time: Sunday, April 27th, 05:00 PM Location: Green Eat Billinghurst: https://maps.app.goo.gl/E4YH12kLxri7jBXLA Coordinates: https://plus.codes/48Q3CH6R+48 Group Link: https://chat.whatsapp.com/BfD [remove this bit] p6v3bMwGEfwNGKnhJwV Brazil BELO HORIZONTE Contact: David Reis Contact Info: davidreis[a t]gmail[period]com Time: Saturday, April 12th, 04:00 PM Location: Diamond Mall 1rst Floor Food Court, in front of McDonalds. Address Av. Olegário Maciel, 1600 Coordinates: https://plus.codes/58GR33C3+R4J Group Link: https://chat.whatsapp.com/C0S [remove this bit] Ze8fdU8O1WgLd4GsST6

Inline links: https://plus.codes/48Q3CH6R+48, https://plus.codes/58GR33C3+R4J

ACX Grants 1-3 Year Updates

June 18, 2025 · Original source

Since 2022, Alice has undertaken qualitative research in nine world regions: Mexico, Costa Rica, Brazil, Morocco, Italy, Spain, Britain, US, Poland, Turkey, India, Uzbekistan, South Korea and Hong Kong. Through this globally comparative analysis, she analyses the drivers and obstacles to gender equality. Gender interventions will be more impactful if they target locally binding constraints - in the Middle East, North Africa and South Asia, this is "the honour-income trade-off" (whereby male honour depends on female seclusion, and women tend to remain at home. Meanwhile, Latin America and the Caribbean face a different obstacle: pervasive violence elevates femicides. Over the past few years, she's held visiting appointments at Stanford, Chicago, and Yale, while providing policy advice to the World Bank, and sharing insights with a public audience via Substack (www.ggd.world). In April 2025, she gave a TedTalk on romantic love as an under-rated driver of gender equality.

Your Review: Alpha School

June 27, 2025 · Original source

“Powered by AI (not teachers).” If all of this makes your inner Bayesian flinch, you’re in good company. After twenty‑odd years of watching shiny education fixes wobble and crash—KIPP, AltSchool, Summit Learning, One-laptop-per-child, No child left behind, MOOCs, Khan‑for‑Everything—you should be skeptical. Either Alpha is (a) another program for the affluent propped up by selection effects, or (b) a clever way to turn children into joyless speed‑reading calculators. Those were, more or less, the two critical camps that emerged when Alpha’s parent company was approved to launch the tuition‑free Arizona charter school this past January. Unfortunately, the public evidence base on whether this is “real” is thin in both directions. Alpha’s own material is glossy and elliptical; mainstream coverage either repeats Alpha’s talking points, or attacks the premise that kids should even be allowed to learn faster than their peers. Until Raj Chetty installs himself in the hallway with a clipboard counting MAP percentiles it is hard to get real information on what exactly Alpha is doing, whether it is actually working beyond selection effects, and if there is anyway it could scale in a way that all the other education initiatives seemed to fail to do. I first heard about Alpha in May 2024, and in the absence of randomized‑controlled clarity, I did what any moderately obsessive parent with three elementary-aged kids and an itch for data would do: I moved the family across the country to Austin for a year and ran the experiment myself (unfortunately, despite trying my best we never managed to have identical twins, so I stopped short of running a proper control group. My wife was less disappointed than I was). Since last autumn I’ve collected the sort of on‑the‑ground detail that doesn’t surface in press releases, or is available anywhere online: long chats with founders, curriculum leads, “guides” (not teachers), Brazilian Zoom coaches, sceptical parents, ecstatic parents, and the kids who live inside the Alpha dashboard – including my own. I hope this seven-part review can help share what the program actually is and that this review is more open minded than the critics, but is something that would never get past an Alpha public relations gatekeeper: Starting Point: My Assumptions: how my views on elite private schools, tutoring and acceleration shaped the experiment (and this essay). WHAT is the existing education environment.

Writing (Mostly on AlphaWrite) If a student gets all their lessons done in the allotted time they can choose which subjects to work ahead on – they can try and balance subjects, work on the ones they are struggling on the most, or just push ahead in the ones they are already excelling in (They do get coaching on this from guides on a regular basis, but the kids make their own choices). A typical lesson involves watching a curated YouTube video followed by specifically selected problem sets within the third party tools. After every question the student is given feedback – either “Great Job!” (with the option to click and learn more) or “Incorrect” followed by explanations on why the question was wrong and a mini-remedial lesson to fill in the knowledge gap. If a pattern of stumbles appears the system will automatically task the student to book a “coaching call” with a remote teacher (most of these teachers seem to be based in Brazil). Kids can also choose to self-book calls with the “coaches” at any time (my daughter told me today that she was having trouble with a math problem set and she booked a coaching call. I asked her how long it took between when she booked it and when she had the call and she said it depends on how busy the coaches are. Today she booked it at 11:10 and had the call at 11:15, but she said once it took her two days to get the meeting. I asked her how often she has a call and she said less than once a day, but more than once a week). The kids also automatically do a coaching call before they can schedule a “mastery test” which covers all the grade level material in a subject (like a final exam). At the end of the day the students get a report on their achievements that day, as well as overall feedback (this is potentially where the “AI” comes in. The computers track both clicks and eye tracking. It can tell both what the student clicked, but also if they were paying attention or distracted, or how much effort they put into reading the feedback when they got questions wrong). All of this is shared with the parents on our own dashboard. Here is what that dashboard looks like for a couple of recent classes for one of my kids: In this example, on this particular day, my daughter spent 13-minutes on Language Arts during her 2-hour learning time. She got 100% of the problems correct (when you scroll over the blue circle it reads 16/16) and completed “one mastery” (meaning she got credit for the lesson because she got more than 80% correct on the mastery test). She also spent 19-minutes on Math (not during the standard 2-hour learning block, hence “non-2h session”), getting 60% of the questions correct (6/10), so she did not earn a math “mastery” that day. For both subjects there is a “Coaching button” (not every subject on every day has coaching). Here is what the Language Arts feedback looks like (where she killed it that day): Clicking on the example “here” hyperlinks takes you to a live stream of the moment the system believes backs up the feedback it provided. You can see her face on video and watch what she is doing on the screen. Here is the feedback for math that day (that did not go as well): The constructive feedback to save eye strain: Not spending enough time on the subject

Inline links: https://substackcdn.com/image/fetch/$s_!1AbF!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2F9f81f4e2-0b80-40a3-926e-a486ac11d666_473x356.png, https://substackcdn.com/image/fetch/$s_!2bzu!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2Fd91f1a06-93ad-4b36-b903-c09c91478df7_747x293.png, https://substackcdn.com/image/fetch/$s_!faJ9!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2F13b6b02c-db96-49c1-80c5-4dec89fab5d9_744x249.png

Meetups Everywhere 2025: Times and Places

August 29, 2025 · Original source

Contact: Leo Contact Info: jaquablouisbertrand[a t]gmail[period]com Time: Sunday, September 14th, 4:00 PM Location: Memorial Union Terrace around the brat stand. Coordinates: https://plus.codes/86MG3HGX+QX4 Group Link: https://groups.google.com/g/madison-wi-acx Notes: Email directly for details. Will make a group message if there's sufficient interest. South America Brazil BELO HORIZONTE Contact: David Reis Contact Info: davidreis[a t]gmail[period]com Time: Saturday, October 4th, 4:00 PM Location: Patio Savassi in front of Fany Bonbons Coordinates: https://plus.codes/58GR3358+MC Group Link: https://chat.whatsapp.com/C0S [remove this bit] Ze8fdU8O1WgLd4GsST6

Inline links: https://plus.codes/86MG3HGX+QX4, https://groups.google.com/g/madison-wi-acx, https://plus.codes/58GR3358+MC

Highlights From The Comments On Fatima

October 24, 2025 · Original source

I didn’t mention it in my post because it seemed to be an extraneous detail, but this reader seems to have independently noticed something similar. 3: As a child, I was on many boring car rides with no one to talk to. I would stare out the window often, and occasionally, just at the sun. I would do this -specifically- because of this phenomenon- I had always assumed everyone knew/understood this was something that happened. It was surreal reading it described as a mystery. The way it would appear to me is that if I stared at the sun long enough (through a glass car window), there would appear a very strong blue after image (light blue- as a child, I thought it similar to the color of Neptune/Uranus as shown in books). This after image would be the same size as and almost- but not quite- line up with the sun. It would then proceed to circle the actual sun. The image was very crisp, but the movement was not- moving in a sort of ‘pulse’ (imagine very slow animation, the image not smoothly moving but jumping from one position to the next to give the illusion of movement). This movement was centered roughly around the sun, but since the image was offset it gave an appearance of ‘corkscrewing’ or spinning, not a perfect circle (that is, the image overlapped the center of rotation, rather than rotating around it). The circling would continue some time (as a child I remember thinking it went for a long time, as an adult I would guess in reality it was only some seconds, certainly less than a minute), and would end when I either looked away or the sun became too bright and I was forced to shut my eyes … What made me realize this is definitely, in my mind, the same as being described is because as a child I was convinced the image was falling- I did not, as a child- think it was the sun itself, but thought that it might be the planet Neptune (because it was blue and a large orb (appearing as a disc to the eye) somewhere, presumably, in space). But as said, I was at the time concerned it was falling, and would occasionally badger my parents about it- whether it was possible the blue orb I saw in front of the sun was Neptune, and if so whether it was going to hit the earth because it looked like it was coming towards us. I understood it wasn’t something you would see if you just looked at the sun- rather in my child mind, I assumed it was in some way that staring at the sun let me see more clearly things around it, though as I grew older I increasingly understood the image to likely be caused by staring, rather than revealed. I remember as a child sort of knowing it was an afterimage but also that it was much sharper and more clear than most afterimages. 4: I was in a room at the boarding school I used to attend, looking out through the window. I recall it being low in the sky but circumstancially it would have been midday (so I presume winter months, since I don’t recall thinking that was unusual). The sky was fairly clear. I stared at it for what felt like three minutes at the time but was probably in hindsight 45 seconds. I was a bored child (probably about eight or nine) left alone in a room and it seemed like a fun idea to stare at the sun. The sun seemed to become covered by lots of large irregularly shaped black-brown spots, with the light itself shining from cracks between them. It looked kind of like a simplistic video game lava texture. 5: I was looking at the sun because I was young and stupid. It stopped shining but remained white, except for a few sunspots that could be seen by the naked eye and which indicated the sun was rapidly spinning. There were no other unusual experiences. 6: On several occasions outside I have seen my entire visual field become tinted various colors. Ever since I heard about eye fatigue and after-image based illusions I explained this to myself as it being very bright out and the color tint being from my green being worn out (making everything pinkish) or my blue being worn out (making everything greenish yellow). Unlike typical afterimages which had particular areas in my field of view, these were almost always across my entire visual field, with occasional hot spot areas where deeper afterimages existed. On each of these occasions it has been bright out and once noticing it, unless I have gone inside, it progresses between colors, though I can’t remember any specific order, only that pink is what I remember most frequently. Lasts until I go somewhere darker or the sun is covered by clouds for a while. Including as an aside, since its beyond the event, but relevant to optical experiences, I have a history of staring out into space without realizing it, failure to blink to the point of eye redness and wateriness, falling asleep with my eyes open, and distractedly looking at bright things for long enough without noticing that I develop a disruptive after image for a while after that makes it hard to read. These things make my baseline for having stared at the sun or not squinted enough on a bright day higher, and, to me, seem to explain why these things happen to me on bright days without clouds or rain, since the cloud protection wouldn’t be a necessary factor in my brightness exposure. i wanted to share since this seems like a difference in some part from the sungazers (who saw auras specifically around the sun) but which matches some of the accounts of the Fatima incident. 7: As a kid, I would stare at the sun sometimes (I eventually abandoned this after I got a headache from doing it; I don’t know whether this has caused any of my minor eye problems later in life), and it would usually resolve to a discolored disk “swirling” slowly around the bright outline of the sun. I assume this is what people mean when they say the sun was “spinning”, although I’m not completely sure. I do not believe I was primed to see something interesting, since I grew up in a nonreligious household and nobody talked to me about sungazing; I only did it because people told me not to stare at the sun for very long. 8: There was an upcoming eclipse when I was a kid and all the talk about “don’t look at the sun” was a temptation I could not resist. I stared at the sun at least a couple of times, but somebody caught me doing it (I think my mother but I do not remember in detail) and made me stop. It was very much like the Fatima miracle people describe—in fact I was a bit confused when I started reading your post because it was immediately clear to me that this is just what it looks like when you stare at the sun (or I guess, under some circumstances?). I did not realize until now that this was a rare or special experience. From what I recall, the rim of the sun remained sharp and bright, but within the circle, the color changed the longer I looked. It had a silvery, almost liquid appearance. I remember the spinning vividly, but it felt to me like it was an illusion happening because of small eye movements, and by shifting my eyes a little bit I could exaggerate or lessen the movement. I could see bright color changes too, around the edge and as afterimages or “tracers” after moving my focus. The “falling to earth” description seems pretty similar to how I remember the tracers appeared when I looked away. I do not remember exactly how long I looked, but I would guess perhaps 1-3 minutes at a time. 9: My mother and sister went sun viewing in ~2009. It was a six-to-nine months long fad in southern Minas Gerais (São João del Rei diocese), Brazil. People reported seeing Jesus and Mary in the sun, and that it spun. No reports of it changing color, though. I dont know the logistical details, who organized these outings (I was indeed just a child, my mom also didn’t care enough at the time to ask things like that). It was a series of monthly weekend mystical appearances that occurred in a bunch of different small cities, attracting, in a rough guess, 500 to a thousand pilgrims each. Always in a rural location, sometimes near small chapels. They did not charge money for the viewing, I believe only the transportation people made a profit. My sister remembers being very hungry, as they didn’t serve (or sell) food at the place, and it went from morning to sundown. My father was a complete skeptical; my mother, extremely Catholic, did not question its veracity: it was just something religious to do, and religion is good. The practice died that same year, because the local Bishop was hard against it, forbidding it. My sister didn’t see anything. My mother also saw nothing, but left feeling spiritually in peace, a very positive sentiment. 10: I used to be very confused about why the sun was portrayed as yellow, because I had looked directly at the sun (I don’t recall how many times; perhaps only once, and I was pretty young), and the sun was clearly bright pink. My default mental image of the sun is still that of a bright pink disk. It did not change colors or move or do any of the other exotic things mentioned in your post. 11: As a kid (maybe 10-13?), I would stare into the sun repeatedly for the weird experience of overexposed eyes. I’d never heard of the Fatima miracle prior to your article, but parts of it seem completely normal to my experience. The center of the sun soon stops looking intolerably bright, and instead seems like a disc of metal of an uncertain color. Its apparent color irregularly shifts between purple, silver, blue and green. My interpretation at the time was that my eyes were probably unable to strongly identify the color, because if I told myself that I expected it to be silver, it would normally be seen as silver. I have to emphasize how non-radiant the center of the sun appears at this point; it looks more like an object illuminated by the sun than like a light source But the outer rim of the sun remains bright. I assume this is because those parts of the retina have not been completely overexposed, and so can still give accurate signals that they’re receiving a ton of light. And the exact amount of ‘bright outside’ and its exact location on the sun varies a lot based on small eye movements; the central disc can appear to shift around and grow/shrink slightly in the sun. In short, the descriptions of the sun as a silver or pulsating multi-colored disc with fireworks on the outside seem entirely normal for “sungazing” for me. I did not see: 1) Rotation 2) The sun falling to earth and looking like it’s going to crush me 3) Any apparitions of people 12: Outside my home, I would frequently stare at the sun for long periods, between the ages of (young, my memory goes back to 4-ish) and 7. I would stare at various times of day — noon, sunset, etc. I wasn’t looking for anything in particular, just curious. I had a habit of staring for long periods at everything around me. The sun appeared various colors on first looking at it, most commonly orange or yellow. On closer inspection, this turned to white. Then shimmery blue patches would appear in the white, always touching the edge, which would appear to spin and reverse quickly. This impression of a blue-white rapidly spinning sun was observed reliably whenever the sun was far enough above the horizon on a clear day. It would continue as long as I looked at the sun. I think I would look for several minutes at a time; less than an hour. (Among my family and friends I was well known for ‘blanking out’ and staring at things for long periods.) As far as I was aware, it was not an ‘optical effect’, just the sun’s normal appearance. I had no impression of the sun falling to earth. I was a very imaginative child with many imaginary friends, ufo sightings, and mysterious experiences. I don’t remember anything imaginative, visionary, creative, etc. associated with looking at the sun. It just seemed like a straightforward observation, like many I made. In later years, I have often observed, as you have, conditions of mist, cloud, rain or (most memorably) snow or ice, which allow the sun to be seen easily as a silvery round disc like the moon. Outside of these conditions, sunrises, and sunsets, I don’t look at the sun anymore, and have never had any vision damage i know of. 13: I’m less stupid than I used to be, but when younger would sometimes look at the sun out of curiosity. I also spent much too much time lighting things on fire with a magnifying glass. So this is not so much “I saw a miracle” as “here are my general notes from looking at the sun”. The silvery sun thing is something I can attest to. At first the sun is too bright to look at, but after a couple of seconds it goes silvery and is more bearable. A slightly twirling of the sun is also something I’ve seen. It’s more like a rotation of its black border? Something like if you’d make a drawing of the sun with a black pen and then coloured it in with yellow (or whatever), the border (i.e. the black ink of the pen) rotates? This doesn’t make sense when I describe it like that, but my brain sees it twirling. I don’t recall colour changes other than everything looking washed out. 14: The first [time I saw it],(before I knew about Fatima) was in summer (I think August). The sun was setting (about an hour before sunset), and I saw the sun change color (alternating blue and pink with an apparent rotational motion around its center, like a Catherine wheel). I don’t remember if it was obscured by clouds. I don’t remember how long the event lasted. After discovering the Fatima event, I decided to personally verify the hypothesis that it was a natural phenomenon due to temporary vision changes. During September 2022, on a couple of occasions, in the early afternoon, while the sun was obscured by translucent clouds, I saw color changes (alternating blue and pink), a rotational motion (like a Catherine wheel), and the sun oscillating (as if vibrating or moving rapidly in a zigzag pattern). On both occasions, the event lasted about a minute, as I then had to look away due to discomfort. On only one occasion, after a heavy rain, and much later (around 5:00 PM), I managed to gaze at the cloudless sun, and only for a few seconds. I saw the same phenomena as when it was covered by clouds, but following this occasion, an afterimage appeared in the center of my field of vision that remained for a couple of days (the afterimage was not severe enough to prevent me from carrying out my activities, including reading and writing, and once it disappeared, I did not suffer any permanent damage to my vision). I must admit that, with the exception of the first case, I had to force myself to look at the sun, as a slight discomfort was present from the first few seconds. In the above cases the edge of the solar disk was not blurred. These were the best of 45 answers. Most of the rest saw normal afterimages, or wanted to say that they, too, had seen the sun look like a pale full moon behind clouds, or saw weird things in the sky that didn’t seem Fatima-related. Interview With A Medjugorje Witness One person filled out the form to say they had seen the miracle at Medjugorje, and kindly agreed to anonymously answer followup questions: SA: Tell me what happened. MW: I was in Medjugorje, I don’t remember the exact year but late 90s or early 2000s. This was not at the same time as one of the apparitions. We were outside, I think in the evening in summer (6pm maybe) Some people pointed out the sun, which was low in the sky, maybe just above eye level from our vantage point, nowhere near setting. Me and my mum looked at it, and it was spinning and pulsing, almost throbbing. I always compared it to a Catherine Wheel before even knowing it was a common comparison, it matched the way it was almost violently moving at risk of leaping off its axis. It changed colours, like it was having a filter passing over it. Not a smooth gradient change but as if a coloured lens was moved over it. There were points it had two or more colours over different sections. I don’t remember the exact colours but it included deep sunset reds, when the sky was high over the horizon. There wasn’t any pain or discomfort from looking at it. Eventually it stopped. The reaction from the people I was with was more quiet awe. Oddly subdued for such a strange moment! We didn’t discuss with others there, as we didn’t speak the same language. I don’t remember any other visions or apparitions. I was a believer at the time, so I was quite sensitive to what I felt were spiritual experiences, but I didn’t encounter any others on this trip. My mum has had other spiritual experiences there, including what she says was a vision of Mary in the 80s which was seen by herself and several others. I’m an atheist these days, and obviously don’t put much stock in the Marian appararitions in Medjugorje now. For instance, it seems the fire and brimstone idea of hell was a Renaissance invention, and the looming end times dynamic has been a constant across many religions. But the sun miracle remains a completely unexplainable experience! SA: What led you to go to Medjugorje? When you set off, did you know about sun miracles? Was there an expectation of seeing one? MW: My mum took me. She’s been on quite a few occasions over the years and took me there on 2/3 occasions. I didn’t know about sun miracles happening there and had no expectation of seeing any. I was aware of the Fatima sun miracle. And my mum often watched quite dramatic, apocalyptic VHSs with meteors falling from the sky etc, so I had a finely developed sense of imminent supernatural events! SA: How long did you spend in Medjugorje before seeing the miracle? How long did you stay afterwards? Did you make multiple attempts to see the miracle before it happened? Did you try to see it again afterwards? MW: I think the trip was 7-10 days. It happened in the second half of the trip, 2-3 days from the end maybe. I definitely kept an eye on the sun when it approached a similar time of day. Now I look into it, the daily apparations were at 6.40pm, I don’t remember if that was the exact time of the sun miracle but it would have been close to that time. I came back to Medjugorje with my mum as a teenager and brother, nothing happened that time! SA: Did you get any chance to talk to other people in Medjugorje, either pilgrims or locals, and gauge what percent of them had seen the miracle, or how many times they had seen it? MW: I didn’t get to discuss with anyone. A short “wow did you see that” with my mum, but it’s not even the weirdest thing she’s seen there given she thinks she saw Mary appear. SA: When people gestured to you to look at the sun, did you see the miracle immediately, or did it take you a while of concentrating and straining? If the latter, how long? MW: I remember it being fairly immediate. Obviously I had to look at the sun, as it’s not like the surroundings were going disco coloured, it didn’t affect the actual light the sun gave off on my surroundings. But I don’t remember staring at a normal looking sun for any period before the effect started. It was wobbling and spinning right away, although the colour changes may have come after the violent spinning. SA: Having [now] read about the theories that it’s just afterimages, or illusions, or something like that - does that accord with your experience? Does it feel like you just saw minor perturbations that could have been illusions? Or did it seem perfectly clear, totally beyond the ability to be an illusion? MW: It felt completely beyond any possibility of it being an illusion. It was too instantaneous, and the effects too strong. No clouds or signs of interference over the sun. And someone else drew my attention to it! For afterimages specifically, they still have that very strong searing quality, which wasn’t a factor here in the same way. SA: Did it look like it looks in the videos linked in the post? MW: No, it didn’t bear much resemblance to the videos. The pulsing wasn’t present with what I saw. Violent spinning and colour changes only, and an effect kind of similar to an eclipse initially that changed to colours changing, but not in the same fashion as an afterimage. SA: Can you tell me more about being an atheist? How does this mesh with you having seen a hard-to-explain miracle? MW: I just gradually became disillusioned with Catholicism. My mum is very devout and pushed it very hard on me, so there’s a strong aspect of teenage rebellion. Fundamentally, I couldn’t reconcile the existence of the kind, loving, individually interested God I’d been taught about with the world as I came to see it (partly the problem of evil, partly seeing the gap between OT and NT as signs of scripture being a historical construct). So either God didn’t exist, did in a form that I had no respect or interest in. The sun miracle was a major reason I called myself agnostic for a very long time. To this day, I can’t explain what happened. I just accept that certain, supernatural appearing, phenomena can occur which we can’t explain. Now I’ve stopped believing such things are possible, they’ve stopped happening. Which I’ve taken as evidence that there’s some degree of self induced receptiveness, like shamanist practices, at play. Although I know the counterargument would be I’ve merely closed myself off from God. SA: Thank you. Ethan: It Wasn’t The Sun Ethan Muse, who wrote the original pro-miracle post that started this discussion, responded to me here: It Wasn’t The Sun. His main goal remains supporting Dalleur’s assertion that Fatima was an objective miracle, implemented through a fiery object which was not the real sun (and therefore cannot be explained by the sun giving people afterimage-related hallucinations), and which was seen by many distant witnesses (and therefore cannot be explained by suggestibility). I won’t answer every one of his objections, both in the interests of time and because I don’t have good answers to every one of his objections, but some highlights: 1.1.1: Cloud Dimming In my original post, I was unimpressed by the “miracle” of people seeing the sun very clearly (including the sharp outline of the solar disc) without being blinded, because I had seen this myself regularly, when the sun was partly dimmed by clouds. Some of the Fatima witnesses had said it couldn’t be clouds, because the disc was visible very clearly rather than the foggy appearance you would get from - well - fog, but I insisted this didn’t update me, because I myself had seen the disc clearly through cloud cover. Ethan says I must be mis-remembering, because my claimed experience is physically impossible: The luminance of the solar disc at its zenith is on the order of 10⁹ cd/m².1 The maximum luminance that an on-axis, compact source can have without causing observers to experience discomfort glare is on the order of 10³ cd/m². Bringing the Sun’s luminance down from 10⁹ cd/m² to 10³ cd/m² requires an attenuation factor of 10⁶. By Beer’s law, that presupposes clouds with an optical depth of roughly 14. When obscured by clouds that thick, the solar beam is essentially extinguished. All that reaches observers is light that has undergone multiple scattering within clouds, emerging from many directions rather than straight paths from the solar disc. The solar disc is reduced to a bright patch or vanishes entirely. Why does Scott have the impression that he has stared at the Sun while it was veiled by thin clouds without experiencing discomfort? It is possible that he is remembering episodes where he briefly glanced at the Sun when it was low on the horizon. Even then, however, luminance should have exceeded the comfort ceiling. Another possibility is that he is accurately recalling that the Sun appeared to be pale, but is forgetting that he squinted, experienced discomfort glare, and/or diverted his gaze. Against this, I posted a Discord poll in which 13/16 respondents agreed they had seen the same thing. After my post, people in the ACX Discord channel independently replicated the poll, with the following results: The Discord comments were pretty interesting, because some people said they could imagine this happening during a forest fire or something - and other people said no, what were they talking about, this happened all the time with totally normal clouds. It really does seem like there’s a pretty sharp distinction between people who recognize and don’t recognize the description. Some people chimed in on the comments of the main post, or the form I set up for people who wanted to send reports, saying the same. From Measure: I have seen the [thin clouds make the sun easy to look at with a crisp edge] phenomenon many times (midwest US, usually early in the morning, but occasionally nearer midday). From a respondent to my survey: I have not seen the sort of behavior described, but I just wanted to say that when there’s just the right amount of cloud cover I can *definitely* look at the sun without my eyes hurting, and it looks like a dull silvery-grey disc. I happen to catch the sun like this every few months (I live in New England), peer at it for a few seconds to see if I can make out sunspots with the naked eye, then think better of my eye health and look away. It’s really weird to me that some people you asked had never experienced this. I thought it was a mundane, normal thing everyone knows! How do we square this with Ethan’s claim that this is impossible? I have no expertise in optical physics and cannot begin to comment on this. GPT-5, after I attempt to give it a neutral prompt that doesn’t reveal which side of the issue I’m on, says that the disc-like sun is possible, and Ethan is wrong because “Cloud droplets are large (Mie regime) and have a strongly forward-peaked phase function. Even when they dim the Sun a lot, they don’t behave like a perfect diffuser”. I don’t know what this means or whether it’s actually a good response. I welcome input from human physicists in the comments. In a private conversation, Ethan continued to assert that I was misremembering, and that all the Discord users and commenters who agreed with me had been contaminated by my testimony and become victims of suggestibility. I think this is a pretty crazy point to suddenly convert to the doctrine of eyewitness fallibility, contamination, and suggestibility - but I leave further discussion to people who understand optical physics. Despite believing I’m right on this factual point, I’m no longer sure it matters - some of the Medjugorje pilgrims say they saw the miracle in a completely clear sky, and that while it was happening it didn’t hurt to stare at the sun. 1.1.2: Eyewitness Testimony Ethan takes issue with my citing Fatima expert Stanley Jaki’s claim that “the great majority of eyewitness accounts, and certainly the most important ones, contain emphatic references to the continued presence of clouds.” He says that: Scott neglects the fact that those ‘emphatic references’ both explicitly and implicitly contradict his proposal . . . Sampling from Scott’s collection of testimonies from 60 eyewitnesses, I found 15 statements that unambiguously describe the behavior of clouds during the event. All of them confirm that, although clouds were present and sometimes passed in front of the ‘Sun,’ cloud coverage was partial, nonuniform, and intermittent. I agree with Doug Summers Stay’s proposal that: I don’t see any mention here of different layers of clouds. It is possible to have both cumulus clouds and cirrus clouds at the same time, so what we think of as “clouds” part and behind them is another layer of clouds blocking the sun. It seems to me, especially from watching the videos and videos in the comments, that there is some rare kind of clouds, perhaps caused by high ice crystals, that can produce a variety of optical effects: motion, changing color, and changing size. That this should happen at a time when a lot of people are looking at the sun expecting something to happen is a big coincidence, but in the end only a coincidence. On this model, there was a thick layer, obvious as clouds to the observers, which had been producing the rainstorm, and which cleared just before the miracle. There was also a thinner layer, which dimmed the sun but didn’t hide it, and which was sometimes - but not consistently - reported as clouds by witnesses. Many witness testimonies say that, although the main layer of clouds had cleared, there was some kind of veil over the sun. O Seculo: The sun had a kind of veil like transparent gauze so that eyes could gaze at it. Almeida describes the sun as …a disc of smoky silver. Compare to our photo of the sun filtered through clouds: From Domingos Pinto Coelho: The sun, until then concealed, showed itself among the clouds that moved fairly fast. Because their density was variable, the veil which they threw over the king of stars was diaphanous. Like the multitude, we then looked toward the sun with rapt attention, and through the clouds, we saw it under new aspects. From Nascimento e Sousa: The sun, which was surrounded by clouds, trembled hesitatingly…I saw there a very pronounced yellow color, and it seemed to me that I saw a silver color beneath the solar disc, but I don’t guarantee that. From Maria de Campos: We started to see the disk of the sun, and see it clearly against the dark gray layer which covered the entire sky…we saw something like a silver-lined veil, with a round shape, as if it were a full moon. Again, I’m not sure this matters, since some of the later miracles were in a clear sky. 1.1.3 - Inconsistency Ethan points out that if the sun were partially veiled by clouds, to the point where it was not too bright to stare at, then it presumably also would not bright enough to produce weird entoptic phenomena and hallucinations. When we discussed this, I had no better solution than to say that maybe there was a level of brightness which was dim enough to look at, but still bright enough to produce phenomena/hallucinations. But again, I’m no longer sure this matters. Many people in the comments to the original post report staring at the completely-non-veiled sun without feeling pain or having negative effects, many Medjugorje pilgrims say they saw the miracle in a completely clear sky without pain, and fire kasina practitioners can get imagery/phenomena from looking at dim or medium-brightness lights. I agree with Ethan that the sun at midday is so bright that it’s painful for me to look at for even a fraction of a second, and I don’t understand how so many people are saying they stare at the sun for minutes at a time at any time of day just because they’re bored. 2: Distant Witnesses Ethan was able to find more medium-distant witnesses than I could: The two witnesses at Alburitel, who I thought were in the same group, were actually in two different groups (is it surprising that our only witnesses from each of these two groups are each other’s brother?)

Inline links: It Wasn’t The Sun, https://substackcdn.com/image/fetch/$s_!iQhN!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2F7a99a023-dcb0-4cb2-98ef-e0800fc7b5a3_1107x174.png, https://substackcdn.com/image/fetch/$s_!x0Vw!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2Fc6946e4b-8bb6-4169-8954-a33875f9d053_1059x265.png, Measure, says that the disc-like sun is possible, and Ethan is wrong because, https://substackcdn.com/image/fetch/$s_!N1Km!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2F1ad98a6a-898d-44ec-9b8b-a759d4303cca_151x132.png

Meetups Everywhere Spring 2026: Times & Places

April 01, 2026 · Original source

Contact: Ben Contact Info: benjamin.boerigter@gmail.com Time: Saturday, April 4, 2:00 PM Location: Memorial Union Coordinates: https://plus.codes/86MG3JG2+G26 Additional Notes: Feel free to bring kids! Forecast for the day looks iffy so we can meet inside the Rathskeller, near one of the fireplaces. I will be wearing a shirt with the image of an iguana on it, with a small sign labeled "ACX Meetup." South America Brazil BELO HORIZONTE Contact: David Reis Contact Info: davidreis[at]gmail[dot]com Time: Thursday, April 23, 03:00 PM Location: Copa Cozinha Savassi - Rua Paraíba, 858, Belo Horizonte - MG, 30130-145 Coordinates: https://plus.codes/58GR3388+CP Group Link: https://chat.whatsapp.com/C0SZ [remove this bit] e8fdU8O1WgLd4GsST6

Inline links: benjamin.boerigter@gmail.com, https://plus.codes/86MG3JG2+G26, https://plus.codes/58GR3388+CP

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Astral Codex Ten

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Brazil

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