I recently got to try my co-working space’s laptop screen extender, a Xebec Tri-Screen
It was amazing and also obviously both too big and too small. The screens are 10.1, enough to take notes but not really read them, yet too heavy for my laptop hinge to support, so I could use it on a table but not my lap, and it drew power faster than the laptop could resupply.
I went looking for competitors, but space is thin. A lot of the listings on Amazon seem sketchy, with serious grammar and vocabulary errors, even when the company itself has a solid proofread website. Some of them require permanent adhesives on your laptop, which isn’t ideal for the shared device at the office. I assembled everything in a spreadsheet here, but they all require major compromises.
If you have informed opinions on any of these, or see one I missed, please let me know. I realize my magic larger and higher resolution but somehow lighter and less power-hungry screen doesn’t exist yet, but surely there must be something somewhere else on the pareto frontier.
Back when I was at Google we had a phrase, “I don’t know how to count that low”. It was used to dismiss normal-company-sized problems as beneath our dignity to engage with: if you didn’t need 100 database shards scattered around the globe, were you even doing real work?
It was used as a sign of superiority within Google, but it also pointed at a real problem: I once failed a job interview at a start-up when I wondered out loud if the DB was small enough to be held in memory, when it was several orders of magnitude lower than when I should even have begun worrying about that. I didn’t know the limit because it had been many years since I’d had a problem that could be solved with a DB small enough to be held in its entirety in memory. And they were right to fail me for that: the fact that I was good at solving strictly more difficult problems didn’t matter because I didn’t know how to solve the easier ones they actually had. I could run but not walk, and some problems require walking.
It’s a problem, but it can be a pleasant kind of problem to have, compared to others. Another example: my dad is a Ph.D. statistician who spent most of his life working in SAS, a powerful statistical programming language, and using “spreadsheet statistics” as a slur. When I asked permission to share this anecdote he sent me a list of ways Excel was terrible.
Then he started consulting for me, who was cruelly unwilling to pay the $9000 license fee for SAS when Google Sheets was totally adequate for the problem (WHO HAS FOOD AT HOME NOW DAD?!?).*
My dad had to go through a horrible phase of being bad at the worse tool, and found a lot of encouragement when I reframed “I could have done this with one line in SAS and am instead losing to this error-riddled child’s toy” to “I didn’t know how to count that low, but now that it matters I am learning”. And then he tried hard and believed in himself and produced that analysis of that informal covid study that was wonderful statistically and super disappointing materially. And I retrained on smaller numbers and got that job at that start-up.
These are the starkest examples of how I’ve found “I don’t know how to count that low” useful. It reframes particularly undignified problems as signs of your capacity rather than incapacity, without letting you off the hook for solving them. Given how useful it’s been to me and how little I’ve seen of it in the wild, I’d like to offer this frame to others, to see if it’s useful for you as well.
*If any of you are going to bring up R: yes, it’s free, and yes, he has some experience with it, but not enough to be self-sufficient, I knew Sheets better, and I knew it was totally adequate for what we were doing or were likely to do in the future.
Appendix: I know you’re going to ask, so here is his abbreviated of grievances with Excel. Note that this was Excel in particular; I have no idea if it applies to Google Sheets. I also would allow that this must have been years ago and Excel could have gotten better, except AFAIK they never fixed the problem with reading genes as dates so they get no benefit of a doubt from me.
I attended a talk by a statistician at Microsoft. He said that Microsoft had decided that there was no competitive advantage in making Excel statistics better because no statistician used it for serious problems except for data entry, so:
1. he was the only statistician at Microsoft 2. he knew of seven serious statistical problems in Excel, but they wouldn’t give him the money to fix them. 3. Excel’s problems fell into two categories: 3a. terrible numerical analysis: it was widely verified if you took a number of single-digit numbers and calculated their standard deviation, and then took the same numbers and added a million to them, the standard deviation was often different, when it should be exactly the same. 3b.
statistical errors – like not understanding what you’re copying out of a textbook and getting it wrong.
Thanks to Ray Arnold and Duncan Sabien for beta-reading, and my dad for agreeing have his example shared.
A client came to me to investigate the effect of high altitude on child development and has given me permission to share the results. This post bears the usual marks of preliminary client work: I focused on the aspects of the question they cared about the most, not necessarily my favorite or the most important in general. The investigation stops when the client no longer wants to pay for more, not when I’ve achieved a particular level of certainty I’m satisfied with. Etc. In this particular case they were satisfied with the answer after only a few hours, and I did not pursue beyond that.
That out of the way: I investigated the impact of altitude on childhood outcomes, focusing on cognition. I ultimately focused mostly on effects visible at birth, because birth weight is such a hard to manipulate piece of data. What I found in < 3 hours of research is that altitude has an effect on birth weight that is very noticeable statistically, although the material impact is likely to be very small unless you are living in the Andes.
Children gestated at higher altitudes have lower birth weights
This seems to be generallysupported by studies which are unusuallyrigorous for the field of fetal development. Even better, it’s supported in both South America (where higher altitudes correlate with lower income and lower density, and I suspect very different child-rearing practices) and Colorado (where the income relationship reverses and while I’m sure childhoods still differ somewhat, I suspect less so). The relationship also holds in Austria, which I know less about culturally but did produce the nicest graph.
This is a big deal because until you reach truly ridiculous numbers, higher birth weight is correlated with every good thing, although there’s reason to believe a loss due to high altitude is less bad than a loss caused by most other causes, which I’ll discuss later.
[Also for any of you wondering if this is caused by a decrease in gestation time: good question, the answer appears to be no.]
Children raised at higher altitudes do worse on developmental tests
There is a fairamount of data supporting this, and some even attempt to control for things like familiar wealth, prematurity, etc. I’m not convinced. The effects are modest, I expect families living at very high altitudes (typically rural) to be different in many ways from lower altitudes (typically urban) in ways that cause their children to score differently on tests without it making a meaningful impact on their life (and unlike birth weight, I didn’t find studies based in CO, where some trends reverse). Additionally, none of the studies looked specifically at children who were born at a lower altitude and moved, so some of the effects may be left over from the gestational effects discussed earlier.
Hypoxia may not be your only problem
I went into this primed to believe reduced oxygen consumption was the problem. However, there’s additional evidence that UV radiation, which rises with altitude, may also be a concern. UV radiation is higher in some areas for other reasons, which indeed seems to correlate with reductions in cognition.
How much does this matter? (not much)
Based on a very cursory look at graphs on GIS (to be clear: I didn’t even check the papers, and their axes were shoddily labeled), 100 grams of birth weight corresponds to 0.2 IQ points for full term babies.
The studies consistently showed ~0.09 to 0.1 grams lower birth weight per meter of altitude. Studies showed this to be surprisingly linear; I’m skeptical and expect the reality to be more exponential or S shaped, but let’s use that rule of thumb for now. 0.1g/m means gestating in Denver rather than at sea level would shrink your baby by 170 grams (where 2500g-4500g is considered normal and healthy). If this was identical to other forms of fetal weight loss, which I don’t think it is, it would very roughly correspond to 0.35 IQ points lost.
However, there’s reason to believe high-altitude fetal weight loss is less concerning than other forms. High altitude babies tend to have a higher brain mass percentage and are tall for their weight, suggesting they’ve prioritized growth amidst scarce resources rather than being straight out poisoned. So that small effect is even smaller than it first appears.
There was also evidence out of Austria that higher altitude increased risk of SIDS, but that disappeared when babies slept on their backs, which is standard practice now.
So gestating in Denver is definitely bad then? (No)
There are a billion things influencing gestation and childhood outcomes, and this is looking at exactly one of them, for not very long. If you are making a decision please look at all the relevant factors, and then factor in the streetlight effect that there may be harder to measure things pointing in the other direction. Do not overweight the last thing I happened to read.
In particular, Slime Mold Time Mold has some interesting data (which I haven’t verified but am hoping to at least ESC the series) that suggests higher altitudes within the US have fewer environmental contaminants, which you would expect to have all sorts of good effects.
Yesterday* I talked about a potential treatment for Long Covid, and referenced an informal study I’d analyzed that tried to test it, which had seemed promising but was ultimately a let down. That analysis was too long for its own post, so it’s going here instead.
Gez Medinger ran an excellent-for-its-type study of interventions for long covid, with a focus on niacin, the center of the stack I took. I want to emphasize both how very good for its type this study was, and how limited the type is. Surveys of people in support groups who chose their own interventions is not a great way to determine anything. But really rigorous information will take a long time and some of us have to make decisions now, so I thought this was worth looking into.
Medinger does a great analysis in this youtube video. He very proactively owns all the limitations of the study (all of which should be predictable to regular readers of mine) and does what he can to make up for them in the analysis, while owning where that’s not possible. But he delivers the analysis in a video rather than a text post ugh why would you do that (answer: he was a professional filmmaker before he got long covid). I found this deeply hard to follow, so I wanted to play with the data directly. Medinger generously shared the data, at which point this snowballed into a full-blown analysis.
I think Medinger attributes his statistics to a medical doctor, but I couldn’t find it on relisten and I’m not watching that damn video again. My statistical analysis was done by my dad/Ph.D. statistician R. Craig Van Nostrand. His primary work is in industrial statistics but the math all transfers, and the biology-related judgment calls were made by me (for those of you just tuning in, I have a BA in biology and no other relevant credentials or accreditations).
As best I can determine, Medinger sent a survey to a variety of long covid support groups, asking what interventions people had tried in the last month, when they’d tried them, and how they felt relative to a month ago. Obviously this has a lot of limitations – it will exclude people who got better or worse enough they didn’t engage with support groups, it was in no way blinded, people chose their own interventions, it relied entirely on self-assement, etc.
Differences in Analysis
You can see Medinger’s analysis here. He compared the rate of improvement and decline among groups based on treatments. I instead transformed the improvement bucket to a number and did a multivariate analysis.
Much better (near or at pre-covid)
A little better
A little worse
You may notice that the numerical values of the statements are not symmetric- being “a little worse” is twice as bad as “a little better” is good. This was deliberate, based on my belief that people with chronic illness on average overestimate their improvement over short periods of time. We initially planned on doing a sensitivity analysis to see how this changed the results; in practice the treatment groups had very few people who got worse so this would only affect the no-treatment control, and it was obvious that fiddling with the numbers would not change the overall conclusion.
Also, no one checked “significantly worse”, and when asked Medinger couldn’t remember if it was an option at all. This suggests to me that “Much worse” should have a less bad value and “a little worse” a more bad value. However, we judged this wouldn’t affect the outcome enough to be worth the effort, and ignored it.
We tossed all the data where people had made less than two weeks ago (this was slightly more than half of it), except for the no-change control group (140 people). Most things take time to have an effect and even more things take time to have an effect you can be sure isn’t random fluctuation. The original analysis attempted to fix this by looking at who had a sudden improvement or worsening, but I don’t necessarily expect a sudden improvement with these treatments.
We combined prescription and non-prescription antihistamines because the study was focused on the UK which classifies several antihistamines differently than the US.
On row 410, a user used slightly nonstandard answers, which we corrected to being equivalent to “much improved’, since they said they were basically back to normal.
Medinger uses both “no change” and “new supplements but not niacin” as control groups, in order to compensate for selection and placebo effects from trying new things. I think that was extremely reasonable but felt I’d covered it by limiting myself to subjects with >2 weeks on a treatment and devaluing mild improvement.
I put my poor statistician through many rounds on this before settling on exactly which interventions we should focus on. In the end we picked five: niacin, anti-histamines, and low-histamine diet, which the original analysis evaluated, and vitamin D (because it’s generally popular), and selenium (because it had the strongest evidence of the substances prescribed the larger protocol, which we’ll discuss soon).
Unfortunately, people chose their vitamins themselves, and there was a lot of correlation between the treatments. Below is the average result for people with no focal treatments, everyone with a given focal treatment, and everyone who did that and none of the other focal treatments for two weeks (but may have done other interventions). I also threw in a few other analyses we did along the way. These sample sizes get really pitifully small, and so should be taken as preliminary at best.
Niacin, > 2 weeks
Selenium, > 2 week
Vitamin D, > 2 week
Antihistamines, > 2 weeks
Low-histamine diet, > 2 weeks
Change (1 = complete recovery)
95% Confidence Interval
Niacin, > 2 weeks
Selenium, > 2 weeks
Vitamin D, > 2 week
Antihistamines, >2 weeks
Low histamine diet
Niacin, > 2 weeks, no other focal treatments
Selenium, > 2 weeks, no other focal treatments
Vitamin D, > 2 week, no other focal treatments
Antihistamines, >2 weeks, no other focal treatments
Low histamine diet, > 2 weeks, no other focal treatments
All focal treatments
Niacin + Antihistamines, >2 weeks
Niacin + Low Histamine Diet, > 2 weeks
Selenium + Niacin, no histamine interventions
Niacin, > 2 weeks, no other focal treatments, ignore D
Selenium, > 2 weeks, no other focal treatments, ignore D
1 = treatment used
0 = treatment definitely not used
– = treatment not excluded
Confidence interval calculation assumes a normal distribution, which is a stretch for data this lump and sparse but there’s nothing better available.
[I wanted to share the raw data with you but Medinger asked me not to. He was very fast to share with me though, so maybe if you ask nicely he’ll share with you too]
You may also be wondering how the improvements were distributed. The raw count isn’t high enough for really clean curves, but the results were clumped rather than bifurcated, suggesting it helps many people some rather than a few people lots. Here’s a sample graph from Niacin (>2 weeks, no exclusions)
Reasons this analysis could be wrong
All the normal reasons this kind of study or analysis can be wrong.
Any of the choices I made that I outlined in “Differences…”
There were a lot of potential treatments with moderate correlations with each other, which makes it impossible to truly track the cause of improvements.
Niacin comes in several forms, and the protocol I analyze later requires a specific form of niacin (I still don’t understand why). The study didn’t ask people what form of niacin they took. I had to actively work to get the correct form in the US (where 15% of respondents live); it’s more popular but not overwhelmingly so in the UK (75% of respondents), and who knows what other people took. If the theory is correct and if a significant number of people took the wrong form of niacin, it could severely underestimate the improvement.
This study only looked at people who’d changed things in the last month. People could get better or worse after that.
There was no attempt to look at dosage.
For a small sample of self-chosen interventions and opt-in participation, this study shows modest improvements from niacin and low histamine diets, which include overlap with the confidence interval of the no-treatment group if you exclude people using other focal interventions. The overall results suggest that either something in the stack is helping, or that trying lots of things is downstream of feeling better, which I would easily believe.
Thank you to Gez Medinger for running the study and sharing his data with me, R. Craig Van Nostrand for statistical analysis, and Miranda Dixon-Luinenburg for copyediting.
* I swear I scheduled this to publish the day after the big post but here we are three days later without it unpublished, so…
This article contains an interview with a doctor who believes NAD+ is the secret to covid’s heavy morbidity and mortality toll. The description was unusually well done for internet crackpottery. This is hard to convey rigorously, but it had a mechanistic-ness and the right level of complexity about it, and it made the right level of promises for a treatment. None of this is to say it’s definitely correct, but it had a bunch better chance of being correct than your average alt-covid-cure scribbled out in crayon. So I did some checks on it.
[Didn’t you say the risk of long covid was small? NO I SAID IT WAS TOO SMALL TO MEASURE AGAINST THE DELUGE OF CRAP THAT HAPPENS TO US EVERYDAY THAT IS NOT THE SAME]
This post is organized as follows:
Description of theory.
Long section defining terms. These are all useful for understanding the claims I check later on, but depending on who you are they may not be helpful, and you may find the contextless infodump kind of a drag. Feel free to skip if it’s not useful to you personally, and know that it’s there if you need it.
Deep dive onto particular claims the article makes.
Does it work?
Is it safe?
My personal experience with the protocol
This is your reminder that my only credential is a BA in biology and I didn’t specialize in anything relevant. It is a sign of civilizational inadequacy that this post exists at all, and you should think really hard and do your own research before putting too much weight on it.
For those of you would like to skip to the take home message: science is very hard, I’m glad they’re running larger studies to follow up on all of these because that’s a reasonable thing for a rich society to do, but I’m not super hopeful about this protocol.
As described by Dr. Ade Wentze:
There is an extremely widely used coenzyme in your body, NAD. The more active form of this compound, NAD+, is depleted by covid (converted to NADH). In people with a preexisting deficiency or difficulty rebounding after depletion, covid infection results in a persistent NAD+ deficit. This is bad in and of itself, but causes additional problems when your body tries to make up for it by requisitioning all your tryptophan to make more. Tryptophan is also a precursor for serotonin, so this leads to either low serotonin or activation of mast cells to release their serotonin stores, accompanied by histamines (which cause allergies and other issues).
There is a lot of vocabulary in that theory and in the supporting claims, which I go over here. If you’re reading for conclusions rather than deep understanding I would skip this.
Nicotinamide adenine dinucleotide is a coenzyme that plays an essential role in hundreds of chemical reactions in your cells, including many relating to processing energy and genetic transcription. This is a mixed blessing as a foundation for crackpot theories go: something involved in hundreds of processes across every kind of tissue in your body can cause almost any symptom, which is great because long covid has a lot of symptoms to cover. On the other hand, it can cause almost any symptom, which means it’s hard to disprove, and you should distrust things in proportion to the difficulty to disprove them. Alas, sometimes core processes are impaired and they do express that impairment in a range of unpredictable ways that vary across people, but it’s also an easy home for crackpots.
NAD+ has two major components, one made from either tryptophan or aspartic acid (both amino acids), or by altering niacin.
Like many vitamins, niacin aka vitamin B3 refers to a few different closely related compounds (most commonly nicotinic acid, nicotinamide, nicotinamide riboside, and inositol nicotinate, but there are others) that are almost but not quite interchangeable.
Niacin is commonly prescribed for treating high cholesterol, although a metareview found it did not reduce overall mortality and may contribute to the development of type-2 diabetes.
Severe niacin deficiency is called pellagra, and can be caused by either insufficient consumption or problems processing the vitamin. Pellagra is mostly defined as niacin deficiency but can also be caused by tryptophan deficiency, which you may remember is another path to manufacturing NAD+. Pellagra can cause diarrhea, dermatitis, dementia, and death, which are not a great match for acute or long covid. Niacin supplementation treats pellagra, often within a few days.
Sirtuin 1, also known as NAD-dependent deacetylase sirtuin-1, is a protein that regulates the expression of some genes in ways that haven’t yet been made clear to me but seem to be associated with aging (more SIRT1 is associated with better outcomes, although we haven’t broken down cause and effect). As indicated by its name, it’s dependent on NAD+ to operate, which means NAD+ is involved in the regulation of expression of some genes via some mechanism, which means niacin is involved in the regulation of expression of some genes via some mechanism.
SIRT1 is downregulated in cells that have high insulin resistance and inducing its expression increases insulin sensitivity, suggesting the molecule is associated with improving insulin sensitivity.
Another many-purposed enzyme whose activities include DNA repair, killing cells that are beyond repair. PARP requires NAD+ as a coenzyme.
Groups with low NAD+ suffer more from covid
NAD+ declines with age
NAD+ does definitely decline with age but so does literally everything bad in your body, so I don’t find this very compelling.
Correlation between NAD+ levels and Age in (A) Males (B) Females (source)
Obese people have lower NAD+ levels, leading to worse outcomes
Yes, although obese people tend to do worse on a lot of metrics. However, that paper highlights that SIRT1 seems to be involved in this correlation somehow.
Diabetics have worse NAD+ levels
Yes, although diabetics also have more immune problems generally (definitely Type 2, some pop sites said the same for Type 1 and that’s believable but I didn’t quickly find a paper I liked that backed the claim).
Low selenium is associated with bad outcomes in covid
The post cites Zhang et al, which took advantage of high variations in selenium consumption in China to do a natural experiment. Variations in the population selenium levels do seem insanely correlated with the overall cure rate (defined as not dying). The study took place in February 2020 so neither data collection nor treatment was very good, but damn that is interesting.
Moreover, this study, which came out several months after the blog post was published, took advantage of the same variation and came to the same conclusion, with a much larger sample size and much more reasonable case fatality rate (1.17% in areas with no deficiency to 3.16% in severely deficient areas, P = 0.002). (Note: several authors on that paper are also named Zhang, but I assume that’s because it’s a common name in China).
Some pharma company thinks selenium is promising enough to launch a trial for it, although recruitment hasn’t started yet.
The pre-print servers are littered with natural experiments highlighting correlations that failed as interventions, but this is very strong for a correlation.
Niacin just generally seems to help lung damage
That is indeed what their citation says, however that paper’s only source looked at the effect of niacin on lung damage in hamsters deliberately induced with a chemotherapy drug, and it’s not obvious to me that that translates to damage from infection or immune reaction. There are some other scattered studies in rodents, combining niacin with other substances, none of which looked at damage from infectious disease.
The treatment for NAD+ deficiency is niacin
Their citation backs this up: niacin supplementation led patients (n=5) and controls (healthy people given the same supplementation, n=8) to increased NAD+ levels, and arguably increased strength, although with that much variation and such a small sample size I’m not convinced. Martens et al supports this with modest benefits seen in n=24 subjects.
A few minutes investigation found some other studies:
Dietary niacin deficiency led to NAD+ deficiency in baby rats. This paper works damn hard to hide its sample size but I think it was 10-15 per treatment group.
The same author exposed some rats (n=6 per treatment group) to excess oxygen and found that those with a niacin deficient diet had less NAD+ in the lungs and responded less to the damage caused by excess oxygen, but had the same wet/dry ratio as their well-fed friends (wet/dry ratio is a measure of lung health).
Ng et al found that in catfish liver NAD increased linearly with dietary niacin supplementation, but health returns like size and mortality dropped off between 6 and 9 mg/kg. They further found that tryptophan supplementation could not make up for a niacin deficiency (in catfish).
Plus niacin is so well established as a treatment for pellagra that no one bothers to cite anything for it, and that does seem to mediate through NAD+.
Nicotinic acid may act as a one of a kind bioenergetic “pump” of inflammatory molecules out of cells
They link to a preprint which has since been taken down, and I could not find it on my own.
NAD+ problems have been indicated in chronic fatigue syndrome
Everything has been indicated in chronic fatigue syndrome; I’m not looking this up.
Mast cells indeed produce serotonin, in mice. Note that that paper highlights fluoxetine as a way to reverse serotonin deficiency in mast-cell-deficient mice, and since the article was published fluoxetine has shown promise as a covid treatment. However this study says that while serotonin-producing mast cells are common, humans in particular don’t have them while healthy (although it still shows serotonin affecting mast cell movements). This appears to be an area of some controversy.
Some Guy did an informal study based on this theory and it worked
Some guy (Birth name: Gez Mendinger) did indeed report this, and I have to say, for an uncredentialed dude on youtube recommending OTC supplements to treat a nebulously defined disease, this guy looks really credible, and his reasonably good analysis was quite promising. He shared his results with me, and it continued to look promising when I first dug into it with assistance from a statistician, but the deeper we drilled the less promising it looked (details). By the end, the most I could say is “yeah, worth a harder look”, but the history of things that look promising in small, poorly organized studies that wilt under large, well-organized ones is just too dismal to ignore.
Mouse study shows low NAD+ hurts you via SIRT1
The interview also cites this mouse study featuring a direct NAD+ drip and a slightly different coronavirus. They show improved symptoms but not viral load. They don’t list the sample size anywhere I can find, judging from the low-resolution graph it looks like 7 mice in the control group and maybe 12 in the treatment group? Except for the embolism test which had many more mice.
(apologies for poor image quality, the PDF was crap)
(note: that article was up when I started this post but disappeared before I verified the SIRT1-specific part of the claim)
Quercetin increases NAD+ levels
Yes, in rats and mice. Specifically, it speeds up the transition from NADH to NAD+
Male pattern balding and low vitamin D are both associated with poor covid outcomes and low NAD+.
The balding citation does indeed say that, but it only looked at hospitalized patients so it’s useless. Moreover, balding is associated with a testosterone derivative, and testosterone weakens the immune system. But when I went to find some cites for those, I found that within hospitalized patients, low testosterone was associated with worse outcomes. However these patients were already hospitalized, so the causality could easily go the other way.
Meanwhile I found severalfolk-wisdomlevel comments indicating a link between NAD+ and male pattern balding, but nothing rigorous.
Low vitamin D does seem to be associated with poor covid outcomes, maybe, but treatment doesn’t seem to help (at least not if you wait until patients are hospitalized).
Chang and Kim assert that Vitamin D activates the NAD-SIRT1 pathway in fat cells in vitro, which if it held up elsewhere would be even stronger evidence for the overall theory than this claim attempts. Byers et al found that vitamin D did not protect guinea pigs against the NAD+ depleting effects of mustard gas. This is not a slam dunk.
Covid depletes NAD+ by activating PARP
Curtin et al lay out a theoretical case for using PARP-inhibitors to treat covid-caused ARDS.
Heer et al “we show that SARS-CoV-2 infection strikingly upregulates MARylating PARPs and induces the expression of genes encoding enzymes for salvage NAD synthesis from nicotinamide (NAM) and nicotinamide riboside (NR), while downregulating other NAD biosynthetic pathways” (notably, the forms not used in the protocol), “overexpression of PARP10 is sufficient to depress cellular NAD and that the activities of the transcriptionally induced enzymes PARP7, PARP10, PARP12 and PARP14 are limited by cellular NAD and can be enhanced by pharmacological activation of NAD synthesis”, “MHV induces a severe attack on host cell NAD+ and NADP+.” (MHV being used as a model)
Long covid and Pellagra share a lot of symptoms, including hyponosmia
Scatteredclaims pellagra causes hyponosmia but you have to look really hard, it doesn’t show up on any of the common descriptions. I checked in Spanish and didn’t find anything either.
Sen (published only last month) suggests that serotonin deficiency causes anosmia and other neuro symptoms in covid. They propose a different method for the depletion (ACE2 is a mechanism for moving serotonin into the cell), but it’s not mutually exclusive with Wentzel’s theory (that NAD+ depletion causes the body to use up tryptophan trying to produce more NAD+).
Your body hijacks tryptophan to make NAD+ at the expense of serotonin
Tryptophan can indeed be used to make NAD (albeit niacin is better) and serotonin. How your body prioritizes under a given set of circumstances is anyone’s guess.
NAD+ and the immune system
Probably at least some of long covid stems from autoimmune issues, as witnessed by the fact that it’s much more common in women and sometimes helped by steroids. The post and paper don’t make any claims on this beyond the effect of NAD+ on mast cells, which are implicated in autoimmune disorders, but out of curiosity I did some quick googling and found that NAD+ downregulate inflammation via CD4 cells (in mice) and activating SIRT1, the pathway mentioned previously (still in mice).
Not that good. Feels associational rather than mechanistic. However Bordoni et al (published after the cited paper) found covid-19 was associated with diminished SIRT1- but Pinto et al found covid-19 upregulated SIRT1 and cite another study claiming that under conditions of energetic stress (which would imply low NAD+), SIRT1 substitutes for ACE2 (the receptor covid uses to enter the cell. Smith suggests that downregulating SIRT1 is good for fighting covid. So SIRT1, NAD+, and covid are probably related, but the first two items are very common so this isn’t damning.
Notably, this paper doesn’t explain why covid would deplete NAD+ more than other infectious diseases, which is an enormous hole.
Does it work?
The mechanism and empirical data are definitely enough to merit more rigorous follow-up studies (which are in progress) and definitely not slam dunks. But you may need to make a decision before that’s in, so the real question is “should I take this stack if I get sick? Should my parents?”
My tentative answer is: the prescribed stack probably won’t physically hurt you (but see the next section), and it’s fairly cheap, so the limiting factor is probably “what do you have the energy to try”. This is a better thing to try than the interventions whose proof was actively made up or have been investigated and discarded, but there undoubtedly are or will be equally probable things floating around, and choosing between them will be a matter of taste..
If you do end up giving this a shot, for covid long or acute, I invite you to preregister your complaints and intention with me (a comment here or email firstname.lastname@example.org), so I can create my own little study. If you don’t feel like doing that I still encourage you to announce the intention somewhere, as a general good practice (I did so here).
So you’re saying it’s safe then?
Anything that does anything is dangerous to you in sufficient dosages. If you’re considering an unverified supplement stack, you should carefully investigate the potential side effects of each substance and consider it in light of what you know of your own health (especially other medications you’re taking). Consider talking to a doctor, if you have a good one.
If any of you are thinking “oh niacin’s a water-soluble vitamin it must be fine”: that’s a pretty good heuristic but it doesn’t hold for niacin in particular.
As mentioned previously, I acquired lingering progressive chest congestion/inflammation from (probably) my covid vaccine. It’s always possible there was another reason but the timing and symptoms really do not match anything else.
Since I never had covid (probably), my reaction can’t come from the infection itself, only my immune response to it. Since the theory doesn’t specify a mechanism that’s not disqualifying, but they do make it sound like it starts as a covid problem not an immune problem.
I started this supplement stack before doing any deep verification. The original blog post pattern matched to the kind of thing that was worth trying, everything on the list I either knew was generally safe or confirmed with a quick check (my doctor later confirmed my opinion on safety without endorsing the stack for any particular use), and I had a lot of client work to do. Shoemaker’s children go barefoot, and all that. So by the time I was writing this I had been on the recommended supplement stack (and some other things besides) for 3 weeks, and was beginning to wean down.
Overall: my chest pain got better but the timing fits better with attribution to a different intervention. The rash I got on matches very well with the supplement stack. I nonetheless was craving it after I weaned off, so probably there’s at least one thing in it I need, which hopefully isn’t the same as the thing causing the rash.
[Alert twitter readers may have questions, since I previously was more positive on the stack. I had a major regression when I got a non-covid cold, and had to go back on the other treatment]
Interestingly, my tolerance for niacin increased and then plummeted. Originally I could take 250mg (the smallest size I could find in the right form) with only very mild flush, and that got better over time, to the point I tried 500 mg once (a mistake). But around week 3 my flush was getting worse. Lowering the dose helped, but it’s getting worse again, so I’m continuing to titrate down. This is extremely consistent with filling up NAD+ reserves over time, although very far from conclusive.
I was originally much more positive on this treatment/theory. I gave it more credit on Twitter, but that’s nothing compared to the excited messages I sent a few friends after an initial lit review. I wrote several much more positive versions of this post (and the forthcoming study analysis), but there kept being one more thing to check, until I talked my way down to what you see here. Some of my downgrade stemmed from asking better statistical questions, but some of it was just the emotional process of talking myself down from something that initially looked so promising, but ultimately had a similar amount of holes to many other things that looked equally promising and failed to pay off. This represents dozens of hours of work from me and my statistician, for the very disappointing result of “fringe treatment probably doesn’t do very much but can’t rule it out”. Reality is infinitely disappointing.
Thanks to Alex Ray and my Patreon Patrons for partially funding this investigation, and Miranda Dixon-Luinenburg for copyediting.
Sometimes people imply that epistemic spot checks are a waste of time, that it’s too easy to create false beliefs with statements that are literally true but fundamentally misleading. And sometimes they’re right.
On the other hand, sometimes you spend 4 hours and discover a tenet of modern parenting is based on absolutely nothing.
Sorry, did I say 4 hours? It was more like 90 minutes, but I spent another 2.5 hours checking my work just in case. It was unnecessary.
You are probably familiar with the notion that eating dirt is good for children’s immune systems, and you probably call that Hygiene Hypothesis, although that’s technically incorrect.
Hygiene Hypothesis can refer to a few different things:
A broader hypothesis that exposure to nominally harmful germs provides the immune system training and challenge that ultimately reduces allergies.
One particular form of this involves exposure to macroparasites, but that seems to have fallen out of favor.
The hypothesis that exposure to things usually considered dirty helps populate a helpful microbiome (most often gut, but plausibly also skin, and occasionally eyeball), and that reduces allergies. This is more properly known as the Old Friends hypothesis, but everyone I know combines them.
Pushback on the idea that everything children touch should be super sanitized
The idea that eatingdirt in particular is beneficial for children for vague allergy-related reasons.
I went into this research project very sold on the Hygiene Hypothesis (broad sense), and figured this would be a quick due diligence to demonstrate it and get some numbers. And it’s true, the backing for Hygiene and Old Friends Hypothesis seems reasonably good, although I didn’t dig into it because even if they’re true, the whole eating dirt thing doesn’t follow automatically. When I dug into that, what I found was spurious at best, and what gains there were had better explanations than dirt consumption.
This post is not exhaustive. Proving a negative is very tiring, and I felt like I did my due diligence checking the major books and articles making the claim, none of which had a leg to stand on. Counterevidence is welcome.
Being born via c-section instead of vaginally impoverishes a newborn’s microbiome, and applying vaginal fluid post-birth mitigates that
This has reasonable pilot studies supporting it, to the point I mentioned it to a pregnant friend.
There are reports that a mother’s previous c-sections lower a newborn’s risks even further, but I suspect that’s caused by the fact below
Having older siblings reduces allergies
Study. The explanation given is a more germ-rich environment, although that’s not proven.
Daycare reduces later allergies, with a stronger effect the earlier you enter, unless you have older siblings in which case it doesn’t matter
Study. Again, there are other explanations, but contagious diseases sure look promising.
Living with animals when very young reduces allergies
This one is a little more contentious and I didn’t focus on it. When the animal appears seems to matter a lot.
One very popular study used to bolster Dirt Eating is a comparison of Amish and Hutterite children. Amish children get ~⅙ of the allergies Hutterite children do, which pop articles are quick to attribute to dirt “because Amish children work on farms and Hutterite children don’t.” But there are a lot of differences between the populations: dust in Amish homes have 6x the bacterial toxins of Hutterite homes, the children have much more exposure to animals, and drink unpasteurized milk.
Limitations of Farm Studies
Even if Amish children did eat more dirt and that was why they were healthier, there’s no transfer from that to urban parks treated with pesticides and highwayexhaust. They might be net positive, the contaminants might not matter that much, your park in particular might be fine, no one has proven this dirt is harmful, etc. But you should not rest your decision on the belief that that dirt has been proven beneficial, because no one has looked.
There are several very small mouse studies showing mice had fewer allergies when exposed to Amish dirt, but:
They are very small.
They are in mice.
The studies I found never involve feeding the mice dirt. Instead, they place it in bedding, or directly their nasal passages, or gently waft it into the cage with a fan.
So eating dirt is bad then?
I don’t know! It could easily be fine or even beneficial, depending on the dirt (but I suspect the source of dirt matters a lot). It could be good on the margin for some children and bad for others. Also, avoiding a constant battle to keep your toddler from doing something they extraordinarily want to do is its own reward. What I am asserting is merely that anyone who confidently tells you eating arbitrary dirt is definitely good is wrong, because we haven’t done the experiments to check.
I think any of [communicable diseases, animals, unpasteurized milk] have more support as anti-allergy interventions than dirt, but I hesitate to recommend them given that a high childhood disease load is already known to have significant downsides and the other two are not without risks either.
The frightening thing about this for me is how this became common knowledge even, perhaps especially, among my highly intelligent, relatively authority-skeptical friends, despite falling apart the moment anyone applied any scrutiny. I already thought the state of medical knowledge and the popular translation of that knowledge was poor, but somehow it still found a way to disappoint me.
This post was commissioned by Sid Sijbrandij. It was preregistered on Twitter. I am releasing it under the Creative Commons Attribution 4.0 license. Our initial agreement was that I would be paid before starting work to avoid the appearance of influence; in practice I had the time free and the paperwork was taking forever so I did the research right away and sat on the results for a week.
Thanks to Miranda Dixon-Luinenburg for copyediting.
Zinc lozenges are pretty well established to prevent or shorten the duration of colds. People are more likely to get colds while travelling, especially if doing so by plane and/or to a destination full of other people who also travelled by plane. I have a vague sense you shouldn’t take zinc 100% of the time, but given the risks it might make sense to take zinc prophylactically while travelling.
How much does zinc help? A meta-analysis I didn’t drill into further says it shortens colds by 33%, and that’s implied to be for people who waited until they were symptomatic to take it: taken preemptively I’m going to ballpark it at 50% shorter (including some colds never coming into existence at all). This is about 4 days, depending on which study you ask.
[Note: only a few forms of Zinc work for this. You want acetate if possible, gluconate if not, and it needs to be a lozenge, not something you swallow. Zinc works by physically coating your throat to prevent infection, it’s not a nutrient in this case. You need much more than you think to achieve the effect, the brand I use barely fits in my tiny mouth.]
Some risk factors for illness in general are “being around a lot of people”, “poor sleep” and “poor diet”. These factors compound: being around people who have been around a lot of people, or who have poor sleep or diet, is worse than being around a lot of well-rested, well-fed hermits. Travel often involves all of these things, especially by air and especially for large gatherings like conferences and weddings (people driving to camp in the wilderness: you are off the hook).
I struggled to find hard numbers for risk of infection during travel. It’s going to vary a lot by season, and of course covid has confused everything. Hocking and Foster gives a 20% chance of catching a cold after a flight during flu season, which seems high to me, but multiple friends reported a 50% chance of illness after travel, so fill in your own number here. Mine is probably 10%.
If my overall risk of a cold is 10%, and I lower the duration by 50%/4 days, I’ve in expectation saved myself 0.4 days of a cold, plus whatever damage I would have done spreading the cold to others, plus the remaining days are milder. Carrying around the lozenges, remembering to take them, and working eating and drinking around them is kind of inconvenient, so this isn’t a slam dunk for me but is worth best-effort (while writing this I ordered a second bottle of zinc to sit in my travel toiletry bag). It’s probably worth a lot for my friends with a 50% risk of illness, have unusually long colds, or live with small children who get cranky when sick. You know better than me where you fall.
Things that would change this cost-benefit estimate:
Personal reaction to zinc, or beliefs about its long term effects
Covid (all the numbers I used were pre-covid)
Different estimates for risk of illness during travel
Different estimates for the benefit of zinc
Personal susceptibility to illness
Caveats: anything that does anything real can cause damage. The side effects we know about for zinc lozenges are typically low, but pay attention to your own reaction in case you are unlucky. I remain an internet person with no medical credentials or accreditation. I attempt to follow my own advice and I’ve advised my parents to do this as well, but sometimes I’m rushed and forget.
ETA: I originally wrote this aimed at friends who already believed zinc was useful but hadn’t considered prophylactic use, and as such didn’t work very hard on it. I mistook some rando meta-analysis for a Cochrane review, and didn’t look further. There’s a pre-registered study that has come out since showing no effect from zinc. There could be other studies showing the opposite, I haven’t looked very closely. Plausibly that makes publishing this irresponsible- you definitely should judge me for mistaking a review that mentioned Cochrane for an actual Cochrane review. OTOH, writing too defensively inhibits learning, and I want to think my readers in particular are well calibrated on how much to trust off the cuff writing (but I hindered that by mislabeling the review as from Cochrane).
The date is November 10th, 2019. Covid has plausibly started, but I don’t know it yet. I am a huge fan of Dan Carlin’s Hardcore History podcast, and have been conducting my own lit review on civilizational collapse. I have been eagerly anticipating Carlin’s upcoming book, The End is Always Near, for months (affiliate link). I am in a coffee shop with a friend, very excited to have a dedicated time to read and Epistemic Spot Check it.
I do not remember what I read. I remember that I lost all interest in Carlin’s podcast afterward, and was so sure I’d remember the problem that I didn’t write it down, which led to 2 years of awkwardly saying “yeah his book was so terrible I lost interest, no don’t remember why, yes I see how that’s less useful for you.” I never checked any claims it made; I’d have records of that, which means that whatever the problem was, it wasn’t just a factual error
I sat down today to read enough of the book to remind myself of why I so vehemently disliked it, and in the course doing so discovered that I had written down the problems in Goodreads, but had forgotten that along with everything else. (I also got the date wrong: I remember starting it in January, but that doesn’t fit because I know I was reading one of its sources in December). My review, in its entirety:
I went in wanting a meaty history book with many claims I could follow up on. In the first few chapters I could only extract a few claims, always what other historians thought (but without countervailing arguments), and it never coheres into models or cruxes.
Mystery solved, I guess. It’s not actually clear to me I should have given up on the podcast based on this, since I don’t remember it having the same problem. But since I already went through all this trouble, let me read a chapter or two and see if I agree with my pre-covid assessment.
Claim: “In many earlier eras of history writing, a large part of the historian’s or author’s goal was to impart or teach some sort of moral lesson, usually by historical example.” (footnote on page 1)
Ah yes, the before times, when people manipulated nominally factual data to their own ends. So glad we grew out of that in … *checks watch* … hmmm, must be broken.
Claim: Sparta super kicked ass (page 7)
Bret Devereaux spent a long time debunking this and I spent a somewhat shorter time checking his work (it passed). Carlin also repeatedly says “Spartan” when he means “Spartan ruling class”, which is a common mistake but I think a revealing one.
Okay, I have finished chapter 1, which is seven pages long. It is titled “Do Tough Times Make for Tougher People?”, a reference to this meme:
I do not know if Carlin thinks tough times create tougher people. If you put a gun to my head I would say “Probably, except for if literally anything else is involved, perhaps?” I do not know how he defines toughness. This is dumb. Toughness is easy to define, he shouldn’t have to spell it out, and yet I’m rereading the pages trying to figure out a coherent definition that makes sense and is meaningful all the way through. I feel fuzzy and slippery and then angry that I feel that way.
Contrast that with Devereaux’s 6 part series, The Fremen Mirage, which addresses the same question. Devereaux takes a strong stance (“no they fucking don’t”) and spends only two paragraphs before defining exactly the argument he is making. Then he spends a while complaining about people who cite “…weak men create times…” without strict definitions.
Devereaux’s Fremen Mirage is full of claims that are both load-bearing (as in, if they were wrong, the argument would collapse) and capable of being resolved one way or the other. It’s tractable to check his work and come to a conclusion. Meanwhile, I did write down some claims from chapter one of The End… but… none of them matter? Of the things that could be called cruxes, they’re all vague and would at best take a lot of work to develop an informed opinion on. But I think that’s optimistic, and most of them are not actually provable or disprovable in a meaningful way.
So there you go. The End is Always Near was not even tractable enough to be worth checking.
Thanks to Miranda Dixon-Luinenburg, Justis Mills, and Daniel Filan for copyediting. Patreon patrons you’re off the hook for this one since it was so short.
Sometimes I consume media that makes factual claims. Sometimes I look up some of these claims to see how much trust I should place in said media, in a series I call epistemic spot checks. Over the years, I’ve gone back and forth on how useful this is. Focusing on evaluating particular works instead of developing a holistic opinion on an entire subject does feel perverse to me. OTOH, sometimes non-fiction is recreational, and I don’t think having some of my attention directed by people I find insightful and trustworthy is a bad thing, as long as I don’t swallow their views unquestioningly. Additionally, there’s a pleasant orderliness to doing ESCs, like the intellectual equivalent of cleaning my house. It’s not enough in and of itself, but it can free up RAM such that there’s room for deeper work.
I started listening to Darryl Cooper’s Martyr Made last year as part of a deep dive on cults, but kept going because I found him incredibly insightful. After listening to the 30+ hours of the God’s Socialist sequence, I Googled around and found a few accusations of racism against Cooper. I didn’t believe the accusations then, and I still don’t. People can go through the motions of saying what other people tell them to, but they can’t fake what Cooper does, which is to approach every human being as someone worthy of respect and compassion, whose actions are probably reasonable given their incentives. I value that a lot more than proper signaling.
Some time later I found an archive of Cooper’s deleted Twitter logs, and, uh, I get where people are coming from on the racism thing. I still absolutely believe in his respect and compassion for everyone except members of the USSR leadership (and even then, he’ll say very nice things about the intentions of early communists). However, the thing about doing that genuinely instead of choosing a side and signaling allegiance is that it doesn’t compress well to 140 characters, and he said a bunch of things that were extremely easy to round to terrible beliefs. I might also have mistaken him for racist, if all I had was his Twitter. But given the podcasts, I am very sure that he respects-and-has-compassion-for every human being.
[Between when I started listening and when I published this Cooper returned to Twitter, which I have mixed feelings about. Namely “I think this is bad for him intellectually and emotionally” vs. “He’s talking to me! Hurray!”]
I’m not a big fan of emotion in my history podcasts. Martyr Made is an exception. Cooper goes hours out of his way to make sure you understand how something felt, without ever coming across as dishonest or manipulative. Some of that is that he often uses himself as an example and is very upfront about his flaws. Some of that is the aforementioned respect and compassion seeping into everything he does. Some is good writing.
For example, God’s Socialist is nominally about Jim Jones and the Jonestown massacre, but Cooper doesn’t believe Jonestown makes any sense unless you understand the 60s, hippies, the Civil Rights movement, and the Black Power movement. The prologue consists of a description of various race riots/race wars, the contemporary and just-pre-Civil-Rights-movements, and easily 15 minutes on his interactions with some homeless people in his neighborhood. For the last of these, he observes that though he’s occasionally kind, he mostly just ignores the individuals in question, and that sometimes he thinks that on Judgement Day the only thing that’s going to matter is how he failed to really help those men- whatever he did, it was for the wrong motives and much too little. I wrote a bunch of angry notes about how virtue ethics was bullshit while listening to this part, but by the end it became clear that he wasn’t making a call to any particular action, it was just an honest accounting of suffering in the world. He was walking me through it because he felt it was necessary to understand Jim Jones, whose first acts as an adult were taking care of people most of society was stepping over.
All of this is to say: Martyr Made is one of my favorite pieces of nonfiction in the world. I’ve learned so much from it both factually and emotionally, but I felt vulnerable talking about that until I was absolutely rock solid on the author’s epistemics. I finally had time to do an epistemic spot check on the start of God’s Socialist (still my favorite sequence in the series), and I’m extremely relieved to announce that he nailed it, although just like my ESC of Acoup, it is not so amazingly perfect that the follow up wasn’t worth doing (and I assume Cooper would agree with that, just like Bret Devereaux did).
A word on ESCs: there’s a range of things it can mean to check someone’s epistemics. Sometimes it means checking their simple concrete facts. You would be amazed how many problems this catches. Another is to check leaps of logic: they can have their facts right but draw wildly incorrect inferences from them. Finding these requires more cognition, but is also fairly easy. Cooper did great on both of these, which was not surprising. My concern was always that his facts were literally true but unrepresentative. Accurate-in-spirit representation is one of the hardest things to judge, especially about really contentious issues like racial violence where second opinions are just another thing to fact check. What I can say is that everything I checked I was either able to concretely verify, or was extremely consistent with what I was able to find but was open to other interpretations, because it’s a contentious area with motivated record keeping.
The God’s Socialist sequence of Martyr Made is 30 hours long. I have ESCed the prologue, which is 90 minutes long, and some especially load-bearing claims I remembered from later in the podcast. I also happen to have already read one of Cooper’s most quoted sources, The Warmth of Other Suns (affiliate link), back in 2014. 2014 is a long time ago and I didn’t ESC Warmth at the time, but what Cooper quoted was generally in accordance with my memory of it, on both a factual and model level.
Without further adieu…
Claim: A 2007 report from the Southern Poverty Law Center on Latino-on-Black violence in Los Angeles (1:02)
He reads this report very nearly word for word. All the differences I caught were very minor wording issues that didn’t change the meaning. I also checked some of SPLC’s claims
SPLC: “Since 1990, the African-American population of Los Angeles has dropped by half as blacks relocated to suburbs”, “Now, about 75% of Highland Park residents are Latinos. Only 2% are black. The rest are white and Asian.” (8:17)
This was shockingly annoying to verify because I could find stats by year for LA county but not LA the city, and the county includes the suburbs. I did verify that:
In 2000 (seven years before the SPLC report came out), Highland Park was 72.4% Latino and 2.4% black (source).
Note that if you read the Wikipedia article it says 8.4% black, but it cites my source above. This is plausibly an issue of how to assign mixed-race people (since Wikipedia’s percentages add up to >100%), or the ongoing confusion about how Latino is an ethnicity, not a race.
However, that particular neighborhood was already 2.2% black in 1990, although it was a little whiter and less Latino (source).
An LA time article also describes South LA shifting from an approximately 1:1 ratio of Latino and Black residents to 2:1 (Highland Park is in northeast LA).
Claim: A number of specific incidents of Latino-on-Black violence in Los Angeles, and some nebulous statistics
I Googled several of these as they came up and they always checked out, although LA’s a big city and Cooper is looking over a long time period, so it would be easy to cherry pick.
Cooper also gave some statistics on hate crime. However, these were always either for a particular neighborhood (too small, data liable to be noisy), or not quite as damning as his tone suggested they were. I found some statistics that came out the same year this episode did that support the general concept that Latino-on-Black violence happens, but I don’t trust the LAPD’s truthseeking on hate crimes.
Which is to say, Cooper’s claims are well sourced and completely consistent with the available data, but the data is poor and his opinions are more controversial than he acknowledges. I’m sure someone with different motivations could use the same data to make the opposite case, or a different one entirely. Here’s an article published the same year as the SPLC report, calling the claims ridiculous. My tentative take on this is that racial tensions were high and spilling over into violence, but the claims that “all black people in LA were greenlit” (meaning, gang members had the okay from leaders to shoot them) and “all black people in Latino neighborhoods in LA were greenlit” are clearly insane; the murder rate would be much higher if that were true.
Claim: Quote from Warmth of Other Suns: “In 1950, city aldermen and housing officials proposed restricting 13,000 new public housing units to people who had lived in Chicago for two years. The rule would presumably affect colored migrants and foreign immigrants alike. But it was the colored people who were having the most trouble finding housing and most likely to seek out such an alternative.” (23:00)
This quote is accurate, but my memory of it wasn’t: I had in my notes that this proposal was enacted, and only rechecked the recording when I couldn’t find any such record and wanted to see if he cited a source. His source, Warmth of Other Suns, cites a 1950 newspaper article that I couldn’t find online (it probably exists in ProQuest’s Historical Newspaper archive, but I lack access despite trying ProQuest via multiple libraries).
Claim: Description of the Cicero Riots of 1951 (31:00)
Everything he says is in accordance with the Wikipedia article: it was a horrific multi-day riot and lynching episode triggered by a black family moving into a white neighborhood.
Cooper doesn’t mention this, but fun fact: according to Wikipedia, the landlord allowed the family to move in not for any noble anti-racism or even free-market motivations, but to punish the neighborhood for fining her for something else.
Claim: Southern white people did not want black people to leave during the Great Migration, because they needed them as labor (35:00)
Warmth of Other Suns says the same, although that’s not independent confirmation because it’s at least one of Cooper’s sources as well. Wikipedia agrees.
Claim: Northern union leaders were resistant to black migrants because they reduced labor’s power (43:00)
I could not find a smoking gun on this, which makes sense because labor is not going to want to admit it. However I found a number of articles, modern and contemporary, on companiesbringing in black workers from the south as strikebreakers, and it would be extremely weird if that didn’t upset union leaders.
Claim: Jim Jones began as a dynamic and promising civil rights movement leader, branched out into communism (1:05:20)
Note that this was not true of the leadership of Jonestown, which was overwhelmingly white. Cooper gets into this later in the sequence.
Claim: Jim Jones led successful efforts to integrate businesses in Indianapolis (memory)
This claim came later in the sequence. It and the similar claim below were very significant to me and a number of changes in my own models rest on them, so I expanded the scope of the project to include them.
There are many sources repeating this claim, including Wikipedia, some book, and r/HistoryAnecdotes, and none denying it. I am a little suspicious because everyone seems to agree on exactly how many restaurants he integrated, but no one names them. They do name a hospital, but it seems like maybe “integrated” means “he accidentally got assigned to a black ward (because his doctor was black) and refused to leave”. But it’s not surprising that restaurants he integrated either no longer exist or don’t want to be remembered as “the place that excluded minorities until forced to change by the guy who later led America’s largest simultaneous suicide”.
Claim: Jim Jones helped members of his racially-integrated church tremendously (memory)
I found many secondary or tertiary sources saying this and no arguments against, but the only primary sources I could find joined the church in California. I couldn’t find any reports from people who joined while the church was in Indiana. That doesn’t seem damning to me; it’s kinda hard to tell people your lights got turned back on by Jim Jones before he was famous. This interview with a woman who joined in California and narrowly escaped the mass suicide confirms everything it can: she was a true believer in a bunch of good things but also kind of a joiner who ping-ponged between organizations until she found peace with People’s Temple. Another CA joiner talks about joining because her sister needed a rehab program and was recommended to People’s Temple’s program.
Claim: Jim Jones adopted multiple children of color (memory)
True. The Jones family adopted three Korean children, one part-Native American child, and one black child, who they named James Jones Jr (they also had one biological child and adopted a white child from a People’s Temple member. There are also some People’s Temple kids of unclear paternity).
I recognize that transracial adoption is contentious and actions that were considered progressive and inclusive 60 years ago are now viewed as bad for the children they were supposed to benefit. I also get that lots of adoptive white parents were unprepared to deal with the realities of racism, or harbor it themselves, and that harmed their kids. The whole mass suicide thing casts some doubt on Jim Jones as a parent too. Nonetheless, a white man naming his black son after himself in 1961 was an extraordinarily big deal for which he undoubtedly paid a very high price, and from all this I have to conclude that fighting racism was extremely important to early Jim Jones.
Overall all of the claims were at least extremely defensible. I wish Cooper acknowledged more of the controversy around his interpretations, but I also appreciate that he comes to actual conclusions with models instead of spewing a bunch of isolated facts. I also wish he provided show notes with citations, because he’s inconsistent about providing sources in the audio.
Doing this check reinforced my belief that having one source for any of your beliefs is malpractice and processing multiple sources is a requirement, however I will very happily continue to have Cooper as a significant source of information, and if I’m totally honest I’m not even going to check all his work this extensively.
When I did the original math I felt a little pang that I didn’t check the source of the 1o minutes of exercise = 1 microlife value, but the result was so overwhelming it didn’t matter. When I added in the time to travel and actually exercise it became a much closer thing, so the error bars on that estimate began to matter. Thanks to reader Steve B. I was able to access the appendix of the microlife article that provided sources for the value of exercise, which turns out to be these two papers.
Both papers are strictly correlational (average exercise per week vs. lifespan), making no attempt to correct for the fact that healthier people will find it easier to exercise and are more likely to do other life-extending things. Exercise was determined by self report, and it looks like those microlifes come from a reduced chance of dying during the study, rather than being tacked on to the end of your life.
There’s a lot of evidence that exercise reduces various markers and effects change associated with a longer life, so I’m pretty sure it’s still good, but I no longer have any faith in this particular number.