https://www.nytimes.com/2018/09/05/well/move/the-best-sport-for-a-longer-life-try-tennis.html
https://time.com/4585396/sports-live-longer-exercise/
https://bjsm.bmj.com/content/51/10/812
https://time.com/5384491/best-exercise-for-longevity/
https://www.mayoclinicproceedings.org/article/S0025-6196(18)30538-X/fulltext

https://twitter.com/robinhanson/status/981291048965087232
https://archive.is/dUTD5
Would you endorse choosing policy to max the expected duration of civilization, at least as a good first approximation?
Can anyone suggest a different first approximation that would get more votes?

https://twitter.com/robinhanson/status/981335898502545408
https://archive.is/RpygO
How useful would it be to agree on a relatively-simple first-approximation observable-after-the-fact metric for what we want from the future universe, such as total life years experienced, or civilization duration?

We're Underestimating the Risk of Human Extinction: https://www.theatlantic.com/technology/archive/2012/03/were-underestimating-the-risk-of-human-extinction/253821/
An Oxford philosopher argues that we are not adequately accounting for technology's risks—but his solution to the problem is not for Luddites.

Anderson: You have argued that we underrate existential risks because of a particular kind of bias called observation selection effect. Can you explain a bit more about that?

Bostrom: The idea of an observation selection effect is maybe best explained by first considering the simpler concept of a selection effect. Let's say you're trying to estimate how large the largest fish in a given pond is, and you use a net to catch a hundred fish and the biggest fish you find is three inches long. You might be tempted to infer that the biggest fish in this pond is not much bigger than three inches, because you've caught a hundred of them and none of them are bigger than three inches. But if it turns out that your net could only catch fish up to a certain length, then the measuring instrument that you used would introduce a selection effect: it would only select from a subset of the domain you were trying to sample.

Now that's a kind of standard fact of statistics, and there are methods for trying to correct for it and you obviously have to take that into account when considering the fish distribution in your pond. An observation selection effect is a selection effect introduced not by limitations in our measurement instrument, but rather by the fact that all observations require the existence of an observer. This becomes important, for instance, in evolutionary biology. For instance, we know that intelligent life evolved on Earth. Naively, one might think that this piece of evidence suggests that life is likely to evolve on most Earth-like planets. But that would be to overlook an observation selection effect. For no matter how small the proportion of all Earth-like planets that evolve intelligent life, we will find ourselves on a planet that did. Our data point-that intelligent life arose on our planet-is predicted equally well by the hypothesis that intelligent life is very improbable even on Earth-like planets as by the hypothesis that intelligent life is highly probable on Earth-like planets. When it comes to human extinction and existential risk, there are certain controversial ways that observation selection effects might be relevant.

Summary : There are too many baroque explanations for the increased prevalence of obesity. I suggest a simple mechanism : falling food prices, rising incomes.

For a few years the herpetologists were concerned yet happy. Concerned, because many frog populations were crashing and some were going extinct. Happy, because confused puppies in Washington were giving them money, something that hardly ever happens to frogmen. The theory was that amphibians were ‘canaries in a coal mine’, uniquely sensitive to environmental degradation.

...

It took some time for herpetologists to admit that this chytrid fungus is the main culprit – some are still resisting. First, it was a lot like how doctors resisted Semmelweiss’ discoveries about the cause of puerperal fever – since doctors were the main method of transmission. How did this fungus get to the cloud forests of Costa Rica? On the boots of herpetologists, of course.

The second problem is Occam’s butterknife: even though this chytrid fungus is the main culprit, it’s just got to be more complicated than that. Even if it isn’t. People in the life sciences – biology and medicine – routinely reject simple hypotheses that do a good job of explaining the data for more complex hypotheses that don’t. College taught them to think – unwisely.

The prevalence of obesity has doubled over the last 25 years. We estimate the effects of multiple socio-environmental factors (e.g., physical demands at work, restaurants, food prices, cigarette smoking, food stamps, and urban sprawl) on obesity using NLSY data. Then we use the Oaxaca–Blinder decomposition technique to approximate the contribution of each socio-environmental factor to the increase during this time. Many socio-environmental factors significantly affect weight, but none are able to explain a large portion of the obesity increase. Decreases in cigarette smoking consistently explains about 2–4 % of the increase in obesity and BMI. Food stamp receipt also consistently affects the measures of weight, but the small decrease in food stamp program participation during the period we examine actually dampened the increases in obesity and BMI. Collectively, the socio-environmental factors we examine never explain more than about 6.5 % of the weight increases.

Someone asked me to go over a chapter he wrote, about the impact of certain customs on human health. One of them was the health advantages of quick burial: the problem is, usually there aren’t any.   People seem to think that the organisms causing decomposition are pathogenic, but they’re not.  People killed by trauma (earthquakes,  floods, bullets) are dead enough, but not a threat.  Sometimes, the body of someone that died of an infectious disease is contagious – smallpox scabs have been known to remain infectious for a long, long time – but most causative agents are unable to survive for long after the host’s death. Now if you’re dissecting someone,  especially if they’re fresh, you probably don’t want to nick yourself with the scalpel – but if you just walk past the corpse and refrain from playing with it, you’re usually OK.

The Dawn of Darwinian Medicine: https://sci-hub.tw/https://www.jstor.org/stable/2830330
TABLE 1 Examples of the use of the theory of natural selection to predict the existence of phenomena otherwise unsuspected
TABLE 2 A classification of phenomena associated with infectious disease

A new paper in Science , by Michael Mina et al,  strongly suggests that measles messes up your immunological defenses for two or three years. This is the likely explanation for the fact that measles inoculation causes much greater decreases in child morbidity and mortality than you’d expect from preventing the deaths directly due to measles infection. The thought is that measles whacks the cells that carry immunological memory, leaving the kid ripe for reinfections.  I think there can be a similar effect with anti-cancer chemotherapy.

If correct, this means that measles is much nastier than previously thought. It must have played a significant role in the demographic collapse of long-isolated peoples (such as the Amerindians). Its advent may have played a role in the population decrease associated with the decline of the Classical world.  Even though it is relatively new (having split off from rinderpest a couple of thousand years ago) strong selection for resistance may have  favored some fairly expensive genetic defenses (something like sickle-cell) in Eurasian populations.

We already know of quite a few complex side effects of infectious disease, such the different kind of immunosuppression we see with AIDs, Burkitt’s lymphoma hitting kids with severe Epstein-Barr infections followed by malaria, acute dengue fever that requires a previous infection by a different strain of dengue, etc: there may well be other important interactions and side effects, news of which has not yet come to Harvard.

The Computational Entomology Lab at UCR has produced simple graphics to allow people to visually understand the importance and utility of avoiding the outdoors at dawn and dusk. Using sensors to detect insect flight, we have monitored several species West Nile vector mosquitoes for their entire lifespan, in order to produce daily activity plots. As shown below, these plots strongly confirm the CDC advice (this figure helps you understand how to interpret the plots). For example, assuming you get up after dawn, and you need to spend most of your day outdoors: if you can manage to go indoors an hour before sunset, and stay indoors until an hour after sunset, your chances of being bitten by a mosquito is about two hundred times less than if you had spend those two indoor hours taking a noontime siesta, but stayed outdoors to watch the sunset.

Pokémon Go and Exposure to Mosquito-Borne Diseases: How Not to Catch ‘Em All: http://currents.plos.org/outbreaks/article/pokemon-go-and-exposure-to-mosquito-borne-diseases-how-not-to-catch-em-all/
Vector-borne diseases - Dengue outbreak in Madeira Island: https://www.slideshare.net/bonniefernley/session-5-rstmh/6

Background. Traditional models of psychiatric epidemiology often assume that the relationship between individuals and their environment is unidirectional, from environment to person. Accumulating evidence from developmental and genetic studies has made this perspective increasingly untenable.

Results. We identified 55 independent studies organized into seven categories: general and specific stressful life events (SLEs), parenting as reported by child, parenting reported by parent, family environment, social support, peer interactions, and marital quality. Thirty-five environmental measures in these categories were examined by at least two studies and produced weighted heritability estimates ranging from 7% to 39%, with most falling between 15% and 35%. The weighted heritability for all environmental measures in all studies was 27%. The weighted heritability for environmental measures by rating method was: self-report 29%, informant report 26%, and direct rater or videotape observation (typically examining 10 min of behavior) 14%.

The broader construct of antisocial behavior – which includes criminal offending, as well as aggression – also shows substantial genetic influence. In a meta-analysis combining effect sizes in 51 twin and adoption studies, Rhee and Waldman (2002) reported a heritability estimate of 41 per cent, with the remaining 59 per cent of variance being due to environmental factors. Interestingly, when comparing results for various definitions of antisocial behavior, only criminal offending appeared to be influenced by both additive genetic effects and non-additive genetic effects – possibly due to genetic dominance and epistatic interactions between genes – based on a pattern of results whereby, on average, identical (monozygotic) twin correlations are more than twice the value of fraternal (dizygotic) twin correlations, and also that biological parent–offspring correlations are less than fraternal twin correlations. Such non-additive genetic effects could arise if one or more high risk alleles act in a recessive fashion, or if certain alleles at one locus affect gene expression at other loci (epistasis).

One intriguing aspect of the literature on genetics and crime is that the strong and consistent genetic influence seen for property offending does not hold true for violent criminal convictions. None of the major adoption studies in Scandinavia or the United States found any elevated risk for violent convictions as a function of either biological or adoptive parent criminal offending, although one early twin study did find greater identical (monozygotic) than fraternal (dizygotic) concordance for violent convictions (see Cloninger and Gottesman, 1987). This pattern of twin, but not parent-offspring, similarity for violent criminal behavior suggests the possibility of non-additive genetic effects due to dominance or epistasis, which would result in increased resemblance for siblings (and twins), but not for parents and offspring. Thus, there may be genetic risk for violent crimes such as murder and rape, which may stem from rare recessive genes, or specific combinations of alleles that do not appear in studies of vertical transmission across generations.

A Swedish national twin study of criminal behavior and its violent, white-collar and property subtypes: https://www.cambridge.org/core/journals/psychological-medicine/article/a-swedish-national-twin-study-of-criminal-behavior-and-its-violent-white-collar-and-property-subtypes/0D9A88185ED0FD5525A5EBD5D2EBA117
For all criminal convictions, heritability was estimated at around 45% in both sexes, with the shared environment accounting for 18% of the variance in liability in females and 27% in males. The correlation of these risk factors across sexes was estimated at +0.63. In men, the magnitudes of genetic and environmental influence were similar in the three criminal conviction subtypes. However, for violent and white-collar convictions, nearly half and one-third of the genetic effects were respectively unique to that criminal subtype. About half of the familial environmental effects were unique to property convictions.

Heritability, Assortative Mating and Gender Differences in Violent Crime: Results from a Total Population Sample Using Twin, Adoption, and Sibling Models: https://link.springer.com/article/10.1007/s10519-011-9483-0
Using 36k twins, violent crime was moderately heritable (~ 55%) w/ 13% shared environment influence. Using 1.5 mil siblings, heritability was higher for males, & family environment higher for females. Moderate assortative mating for violent crime (r = .4).

The impact of neighbourhood deprivation on adolescent violent criminality and substance misuse: A longitudinal, quasi-experimental study of the total Swedish population: https://academic.oup.com/ije/article/42/4/1057/656274/The-impact-of-neighbourhood-deprivation-on
In the crude model, an increase of 1 SD in neighbourhood deprivation was associated with a 57% increase in the odds of being convicted of a violent crime (95% CI 52%–63%). The effect was greatly attenuated when adjustment was made for a number of observed confounders (OR 1.09, 95% CI 1.06–1.11). When we additionally adjusted for unobserved familial confounders, the effect was no longer present (OR 0.96, 95% CI 0.84–1.10). Similar results were observed for substance misuse. The results were not due to poor variability either between neighbourhoods or within families.

Childhood family income, adolescent violent criminality and substance misuse: quasi-experimental total population study: http://bjp.rcpsych.org/content/early/2014/08/14/bjp.bp.113.136200
https://www.economist.com/news/science-and-technology/21613303-disturbing-study-link-between-incomes-and-criminal-behaviour-have-and
What did surprise him was that when he looked at families which had started poor and got richer, the younger children—those born into relative affluence—were just as likely to misbehave when they were teenagers as their elder siblings had been. Family income was not, per se, the determining factor.

Indicators of domestic/intimate partner violence are structured by genetic and nonshared environmental influences: https://www.researchgate.net/publication/233737219_Indicators_of_domesticintimate_partner_violence_are_structured_by_genetic_and_nonshared_environmental_influences
Three indicators of IPV were measured and genetic factors accounted for 24% of the variance in hitting one's partner, 54% of the variance in injuring one's partner, and 51% of the variance in forcing sexual activity on one's partner. The shared environment explained none of the variance across all three indicators and the nonshared environment explained the remainder of the variance.

It’s not always easy figuring out how a pathogen causes disease. There is an example in mice for which the solution was very difficult, so difficult that we would probably have failed to discover the cause of a similarly obscure infectious disease in humans.

Mycoplasma pulmonis causes a chronic obstructive lung disease in mice, but it wasn’t easy to show this. The disease was first described in 1915, and by 1940, people began to suspect Mycoplasma pulmonis might be the cause. But then again, maybe not. It was often found in mice that seemed healthy. Pure cultures of this organism did not consistently produce lung disease – which means that it didn’t satisfy Koch’s postulates, in particular postulate 1 (The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms.) and postulate 3 (The cultured microorganism should cause disease when introduced into a healthy organism.).

Well, those postulates are not logic itself, but rather a useful heuristic. Koch knew that, even if lots of other people don’t.

This respiratory disease of mice is long-lasting, but slow to begin. It can take half a lifetime – a mouse lifetime, that is – and that made finding the cause harder. It required patience, which means I certainly couldn’t have done it.

Here’s how they solved it. You can raise germ-free mice. In the early 1970s, researchers injected various candidate pathogens into different groups of germ-free mice and waited to see which, if any, developed this chronic lung disease. It was Mycoplasma pulmonis , all right, but it had taken 60 years to find out.

It turned out that susceptibility differed between different mouse strains – genetic susceptibility was important. Co-infection with other pathogens affected the course of the disease. Microenvironmental details mattered – mainly ammonia in cages where the bedding wasn’t changed often enough. But it didn’t happen without that mycoplasma, which was a key causal link, something every engineer understands but many MDs don’t.

If there was a similarly obscure infectious disease of humans, say one that involved a fairly common bug found in both the just and the unjust, one that took decades for symptoms to manifest – would we have solved it? Probably not.

Cooties are everywhere.

gay germ search: https://westhunt.wordpress.com/2013/07/21/of-mice-and-men/#comment-15905
It’s hard to say, depends on how complicated the path of causation is. Assuming that I’m even right, of course. Some good autopsy studies might be fruitful – you’d look for microanatomical brain differences, as with nartcolepsy. Differences in gene expression, maybe. You could look for a pathogen – using the digital version of RDA (representational difference analysis), say on discordant twins. Do some old-fashioned epidemiology. Look for marker antibodies, signs of some sort of immunological event.

Do all of the above on gay rams – lots easier to get started, much less whining from those being vivisected.

Patrick Moore found the virus causing Kaposi’s sarcoma without any funding at all. I’m sure Peter Thiel could afford a serious try.

A journey into the brain: insight into how bacterial pathogens cross blood–brain barriers: http://sci-hub.tw/10.1038/nrmicro.2016.178
How do extracellular pathogens cross the blood-brain barrier?: https://www.ncbi.nlm.nih.gov/pubmed/11973156
Defense at the border: the blood–brain barrier versus bacterial foreigners: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3589978/

The idea that venesection was a good thing, or at least not so bad, on the grounds that one in a few hundred people have hemochromatosis (in Northern Europe) reminds me of the people who don’t wear a seatbelt, since it would keep them from being thrown out of their convertible into a waiting haystack, complete with nubile farmer’s daughter. Daughters. It could happen. But it’s not the way to bet.

Back in the good old days, Charles II, age 53, had a fit one Sunday evening, while fondling two of his mistresses.

Monday they bled him (cupping and scarifying) of eight ounces of blood. Followed by an antimony emetic, vitriol in peony water, purgative pills, and a clyster. Followed by another clyster after two hours. Then syrup of blackthorn, more antimony, and rock salt. Next, more laxatives, white hellebore root up the nostrils. Powdered cowslip flowers. More purgatives. Then Spanish Fly. They shaved his head and stuck blistering plasters all over it, plastered the soles of his feet with tar and pigeon-dung, then said good-night.

...

Friday. The king was worse. He tells them not to let poor Nelly starve. They try the Oriental Bezoar Stone, and more bleeding. Dies at noon.

Most people didn’t suffer this kind of problem with doctors, since they never saw one. Charles had six. Now Bach and Handel saw the same eye surgeon, John Taylor – who blinded both of them. Not everyone can put that on his resume!

You may wonder how medicine continued to exist, if it had a negative effect, on the whole. There’s always the placebo effect – at least there would be, if it existed. Any real placebo effect is very small: I’d guess exactly zero. But there is regression to the mean. You see the doctor when you’re feeling worse than average – and afterwards, if he doesn’t kill you outright, you’re likely to feel better. Which would have happened whether you’d seen him or not, but they didn’t often do RCTs back in the day – I think James Lind was the first (1747).

Back in the late 19th century, Christian Scientists did better than others when sick, because they didn’t believe in medicine. For reasons I think mistaken, because Mary Baker Eddy rejected the reality of the entire material world, but hey, it worked. Parenthetically, what triggered all that New Age nonsense in 19th century New England? Hash?

This did not change until fairly recently. Sometime in the early 20th medicine, clinical medicine, what doctors do, hit break-even. Now we can’t do without it. I wonder if there are, or will be, other examples of such a pile of crap turning (mostly) into a real science.

good tweet: https://twitter.com/bowmanthebard/status/897146294191390720
The brilliant GP I've had for 35+ years has retired. How can I find another one who meets my requirements?

1 is overweight
2 drinks more than officially recommended amounts
3 has an amused, tolerant atitude to human failings
4 is well aware that we're all going to die anyway, & there are better or worse ways to die
5 has a healthy skeptical attitude to mainstream medical science
6 is wholly dismissive of "a|ternative” medicine
7 believes in evolution
8 thinks most diseases get better without intervention, & knows the dangers of false positives
9 understands the base rate fallacy

EconPapers: Was Civil War Surgery Effective?: http://econpapers.repec.org/paper/htrhcecon/444.htm
contra Greg Cochran:
To shed light on the subject, I analyze a data set created by Dr. Edmund Andrews, a Civil war surgeon with the 1st Illinois Light Artillery. Dr. Andrews’s data can be rendered into an observational data set on surgical intervention and recovery, with controls for wound location and severity. The data also admits instruments for the surgical decision. My analysis suggests that Civil War surgery was effective, and increased the probability of survival of the typical wounded soldier, with average treatment effect of 0.25-0.28.

Medical Prehistory: https://westhunt.wordpress.com/2016/03/14/medical-prehistory/
What ancient medical treatments worked?

https://westhunt.wordpress.com/2016/03/14/medical-prehistory/#comment-76878
In some very, very limited conditions, bleeding?
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Bad for you 99% of the time.

https://westhunt.wordpress.com/2016/03/14/medical-prehistory/#comment-76947
Colchicine – used to treat gout – discovered by the Ancient Greeks.

https://westhunt.wordpress.com/2016/03/14/medical-prehistory/#comment-76973
Dracunculiasis (Guinea worm)
Wrap the emerging end of the worm around a stick and slowly pull it out.
(3,500 years later, this remains the standard treatment.)
https://en.wikipedia.org/wiki/Ebers_Papyrus

https://westhunt.wordpress.com/2016/03/14/medical-prehistory/#comment-76971
Some of the progress is from formal medicine, most is from civil engineering, better nutrition ( ag science and physical chemistry), less crowded housing.

Nurses vs doctors: https://westhunt.wordpress.com/2014/10/01/nurses-vs-doctors/
Medicine, the things that doctors do, was an ineffective pseudoscience until fairly recently. Until 1800 or so, they were wrong about almost everything. Bleeding, cupping, purging, the four humors – useless. In the 1800s, some began to realize that they were wrong, and became medical nihilists that improved outcomes by doing less. Some patients themselves came to this realization, as when Civil War casualties hid from the surgeons and had better outcomes. Sometime in the early 20th century, MDs reached break-even, and became an increasingly positive influence on human health. As Lewis Thomas said, medicine is the youngest science.

Nursing, on the other hand, has always been useful. Just making sure that a patient is warm and nourished when too sick to take care of himself has helped many survive. In fact, some of the truly crushing epidemics have been greatly exacerbated when there were too few healthy people to take care of the sick.

Nursing must be old, but it can’t have existed forever. Whenever it came into existence, it must have changed the selective forces acting on the human immune system. Before nursing, being sufficiently incapacitated would have been uniformly fatal – afterwards, immune responses that involved a period of incapacitation (with eventual recovery) could have been selectively favored.

when MDs broke even: https://westhunt.wordpress.com/2014/10/01/nurses-vs-doctors/#comment-58981
I’d guess the 1930s. Lewis Thomas thought that he was living through big changes. They had a working serum therapy for lobar pneumonia ( antibody-based). They had many new vaccines ( diphtheria in 1923, whopping cough in 1926, BCG and tetanus in 1927, yellow fever in 1935, typhus in 1937.) Vitamins had been mostly worked out. Insulin was discovered in 1929. Blood transfusions. The sulfa drugs, first broad-spectrum antibiotics, showed up in 1935.

DALYs per doctor: https://westhunt.wordpress.com/2018/01/22/dalys-per-doctor/
The disability-adjusted life year (DALY) is a measure of overall disease burden – the number of years lost. I’m wondering just much harm premodern medicine did, per doctor. How many healthy years of life did a typical doctor destroy (net) in past times?

...

It looks as if the average doctor (in Western medicine) killed a bunch of people over his career ( when contrasted with doing nothing). In the Charles Manson class.

Eventually the market saw through this illusion. Only took a couple of thousand years.

https://westhunt.wordpress.com/2018/01/22/dalys-per-doctor/#comment-100741
That a very large part of healthcare spending is done for non-health reasons. He has a chapter on this in his new book, also check out his paper “Showing That You Care: The Evolution of Health Altruism” http://mason.gmu.edu/~rhanson/showcare.pdf
--
I ran into too much stupidity to finish the article. Hanson’s a loon. For example when he talks about the paradox of blacks being more sentenced on drug offenses than whites although they use drugs at similar rate. No paradox: guys go to the big house for dealing, not for using. Where does he live – Mars?

I had the same reaction when Hanson parroted some dipshit anthropologist arguing that the stupid things people do while drunk are due to social expectations, not really the alcohol.
Horseshit.

I don’t think that being totally unable to understand everybody around you necessarily leads to deep insights.

https://westhunt.wordpress.com/2018/01/22/dalys-per-doctor/#comment-100744
What I’ve wondered is if there was anything that doctors did that actually was helpful and if perhaps that little bit of success helped them fool people into thinking the rest of it helped.
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Setting bones. extracting arrows: spoon of Diocles. Colchicine for gout. Extracting the Guinea worm. Sometimes they got away with removing the stone. There must be others.
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Quinine is relatively recent: post-1500. Obstetrical forceps also. Caesarean deliveries were almost always fatal to the mother until fairly recently.

Opium has been around for a long while : it works.

https://westhunt.wordpress.com/2018/01/22/dalys-per-doctor/#comment-100839
If pre-modern medicine was indeed worse than useless – how do you explain no one noticing that patients who get expensive treatments are worse off than those who didn’t?
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were worse off. People are kinda dumb – you’ve noticed?
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My impression is that while people may be “kinda dumb”, ancient customs typically aren’t.
Even if we assume that all people who lived prior to the 19th century were too dumb to make the rational observation, wouldn’t you expect this ancient practice to be subject to selective pressure?
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Your impression is wrong. Do you think that there some slick reason for Carthaginians incinerating their first-born?

Theodoric of York, bloodletting: https://www.youtube.com/watch?v=yvff3TViXmY

details on blood-letting and hemochromatosis: https://westhunt.wordpress.com/2018/01/22/dalys-per-doctor/#comment-100746

Starting Over: https://westhunt.wordpress.com/2018/01/23/starting-over/
Looking back on it, human health would have … [more]

Warne and Astle looked at 29 best-selling undergraduate textbooks, which is where psychology students learn about intelligence, because less than 10% of graduate courses offer an intelligence option.

3.3% of textbook space is dedicated to intelligence. Given its influence, this is not very much.

The most common topics start well, with IQ and Spearman’s g, but do not go on to the best validated, evidence-led Cattell-Horn-Carol meta-analytic summary, but a side-stream, speculative triarchic theory from Sternberg; and a highly speculative and non-specific sketch of an idea about multiple intelligences Gardner. The last is a particular puzzle, since it really is a whimsical notion that motor skill is no different from analytical problem solving. All must have prizes.
Commonly, environmental influences are discussed, genetic ones rarely.

What Do Undergraduates Learn About Human Intelligence? An Analysis of Introductory Psychology Textbooks: https://drive.google.com/file/d/0B3c4TxciNeJZOTl3clpiX0JKckk/view

Education or Indoctrination? The Accuracy of Introductory Psychology Textbooks in Covering Controversial Topics and Urban Legends About Psychology: http://sci-hub.tw/https://link.springer.com/article/10.1007/s12144-016-9539-7

Twenty-four leading introductory psychology textbooks were surveyed for their coverage of a number of controversial topics (e.g., media violence, narcissism epidemic, multiple intelligences) and scientific urban legends (e.g., Kitty Genovese, Mozart Effect) for their factual accuracy. Results indicated numerous errors of factual reporting across textbooks, particularly related to failing to inform students of the controversial nature of some research fields and repeating some scientific urban legends as if true. Recommendations are made for improving the accuracy of introductory textbooks.

this is completely unrelated AFAICT:

Mapping the scale of the narcissism epidemic: Increases in narcissism 2002–2007 within ethnic groups: https://www.sciencedirect.com/science/article/pii/S0092656608000949

The increasing numbers of Asian-Americans at the UCs over time may have masked changes in narcissism, as Asian-Americans score lower on the NPI. When examined within ethnic groups, Trzesniewski et al.’s data show that NPI scores increased significantly between 2002 and 2007 at twice the rate of the yearly change found over 24 years in Twenge et al. (2008a). The overall means also show a significant increase 2002–2007. Thus the available evidence suggests that college students are endorsing progressively more narcissistic personality traits over the generations.

Birth Cohort Increases in Narcissistic Personality Traits Among American College Students, 1982–2009: http://journals.sagepub.com/doi/abs/10.1177/1948550609355719

Both studies demonstrate significant increases in narcissism over time (Study 1 d = .37, 1982–2008, when campus is controlled; Study 2 d = .37, 1994–2009). These results support a generational differences model of individual personality traits reflecting changes in culture.

could this just be a selection effect (more people attending)?

The Vigor study was submitted in February 2001. The New England Journal of Medicine, a few months later, found that the authors had failed to mention some strokes and heart attacks near the end of the trial. The authors used a cutoff for cardiovascular effects (bad news) that was earlier than the cutoff for gastrointestinal effects (good news). why? Because they were weasels, of course. There was a lot of money riding on this drug’s success.

Other people began to notice the increased heart risks – looking at data from HMOs and such. Merck fought back. There was an MD at Stanford that was concerned about Vioxx: Merck called up the dean of Stanford Medical School at home and warned him about possible loss of financial support: he told them to go fuck themselves.

...

Now it is true that there were studies that showed greater efficacy: 21 such were reported by Scott S. Reuben, former chief of acute pain at Baystate medical Center in Springfield Mass. But as it turns out, he made them all up. There’s is no evidence that Merck knew about this, but it does perhaps say something about the general climate in big pharma.

Merck knew the gist of this for four years before they pulled the plug on the drug. They had their their drug reps lie about cardio risks, threatened researchers and sued journals that talked about the emerging cardio risks. Few physicians were aware of these risks, even though a close reading of the journals would have suggested it – because hardly any physicians read the journals.

Epidemiologists think that Vioxx caused something like 40,000 deaths.

...

In the 70s corporations were the bad guys, whether they were or not. Today, billionaires are your friend.

more inequality, more development, lazier women

Some disease syndromes almost have to be caused by pathogens – for example, any with a fitness impact (prevalence x fitness reduction) > 2% or so, too big to be caused by mutational pressure. I don’t think that this is the case for AD: it hits so late in life that the fitness impact is minimal. However, that hardly means that it can’t be caused by a pathogen or pathogens – a big fraction of all disease syndromes are, including many that strike in old age. That possibility is always worth checking out, not least because infectious diseases are generally easier to prevent and/or treat.

There is new work that strongly suggests that pathogens are the root cause. It appears that the amyloid is an antimicrobial peptide. amyloid-beta binds to invading microbes and then surrounds and entraps them. ‘When researchers injected Salmonella into mice’s hippocampi, a brain area damaged in Alzheimer’s, A-beta quickly sprang into action. It swarmed the bugs and formed aggregates called fibrils and plaques. “Overnight you see the plaques throughout the hippocampus where the bugs were, and then in each single plaque is a single bacterium,” Tanzi says. ‘

obesity and pathogens: https://westhunt.wordpress.com/2016/05/29/alzheimers/#comment-79757
not sure about this guy, but interesting: https://westhunt.wordpress.com/2016/05/29/alzheimers/#comment-79748
http://perfecthealthdiet.com/2010/06/is-alzheimer%E2%80%99s-caused-by-a-bacterial-infection-of-the-brain/

https://westhunt.wordpress.com/2016/12/13/the-twelfth-battle-of-the-isonzo/
All too often we see large, long-lasting research efforts that never produce, never achieve their goal.

For example, the amyloid hypothesis [accumulation of amyloid-beta oligomers is the cause of Alzheimers] has been dominant for more than 20 years, and has driven development of something like 15 drugs. None of them have worked. At the same time the well-known increased risk from APOe4 has been almost entirely ignored, even though it ought to be a clue to the cause.

In general, when a research effort has been spinning its wheels for a generation or more, shouldn’t we try something different? We could at least try putting a fraction of those research dollars into alternative approaches that have not yet failed repeatedly.

Mostly this applies to research efforts that at least wish they were science. ‘educational research’ is in a special class, and I hardly know what to recommend. Most of the remedial actions that occur to me violate one or more of the Geneva conventions.

APOe4 related to lymphatic system: https://en.wikipedia.org/wiki/Apolipoprotein_E

https://westhunt.wordpress.com/2012/03/06/spontaneous-generation/#comment-2236
Look,if I could find out the sort of places that I usually misplace my keys – if I did, which I don’t – I could find the keys more easily the next time I lose them. If you find out that practitioners of a given field are not very competent, it marks that field as a likely place to look for relatively easy discovery. Thus medicine is a promising field, because on the whole doctors are not terribly good investigators. For example, none of the drugs developed for Alzheimers have worked at all, which suggests that our ideas on the causation of Alzheimers are likely wrong. Which suggests that it may (repeat may) be possible to make good progress on Alzheimers, either by an entirely empirical approach, which is way underrated nowadays, or by dumping the current explanation, finding a better one, and applying it.

You could start by looking at basic notions of field X and asking yourself: How do we really know that? Is there serious statistical evidence? Does that notion even accord with basic theory? This sort of checking is entirely possible. In most of the social sciences, we don’t, there isn’t, and it doesn’t.

Hygiene and the world distribution of Alzheimer’s disease: Epidemiological evidence for a relationship between microbial environment and age-adjusted disease burden: https://academic.oup.com/emph/article/2013/1/173/1861845/Hygiene-and-the-world-distribution-of-Alzheimer-s

Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer’s disease: http://stm.sciencemag.org/content/8/340/340ra72

Fungus, the bogeyman: http://www.economist.com/news/science-and-technology/21676754-curious-result-hints-possibility-dementia-caused-fungal
Fungus and dementia
paper: http://www.nature.com/articles/srep15015

Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors: https://advances.sciencemag.org/content/5/1/eaau3333

These results imply that the drop in smoking in recent decades explains 14% of the concurrent rise in obesity.

On a broad scale, hereditary disease risks are similar for ancient hominins and modern-day humans, and the GRS percentiles of ancient individuals span the full range of what is observed in present day individuals. In addition, there is evidence that ancient pastoralists may have had healthier genomes than hunter-gatherers and agriculturalists. We also observed a temporal trend whereby genomes from the recent past are more likely to be healthier than genomes from the deep past.

Gwern has interesting take (abstract is misleading): https://twitter.com/gwern/status/871061144152178688

here it is in conclusion (and cf Figure 3A):
The genomic health of ancient individuals appears to have improved over time (Figure 3B). This calls into question the idea that genetic load has been increasing in human populations (Lynch 2016). However, there exists a perplexing pattern: ancient individuals who lived within the last few thousand years have healthier genomes, on average, than present day humans.

http://www.pnas.org/content/early/2017/08/08/1703856114
After controlling for age, BMI, and other variables, knee OA prevalence was 2.1-fold higher (95% confidence interval, 1.5–3.1) in the postindustrial sample than in the early industrial sample. Our results indicate that increases in longevity and BMI are insufficient to explain the approximate doubling of knee OA prevalence that has occurred in the United States since the mid-20th century. Knee OA is thus more preventable than is commonly assumed, but prevention will require research on additional independent risk factors that either arose or have become amplified in the postindustrial era.

https://academic.oup.com/oep/article-abstract/66/2/349/2362600/How-have-Europeans-grown-so-tall
The evidence suggests that the most important proximate source of increasing height was the improving disease environment as reflected by the fall in infant mortality. Rising income and education and falling family size had more modest effects. Improvements in health care are hard to identify, and the effects of welfare state spending seem to have been small.

GROWING TALL BUT UNEQUAL: NEW FINDINGS AND NEW BACKGROUND EVIDENCE ON ANTHROPOMETRIC WELFARE IN 156 COUNTRIES, 1810
1989: https://pseudoerasmus.files.wordpress.com/2017/03/baten-blum-2012.pdf
This is the first initiative to collate the entire body of anthropometric evidence during the 19th and 20th centuries, on a global scale. By providing a comprehensive dataset on global height developments we are able to emphasise an alternative view of the history of human well-being and a basis for understanding characteristics of well-being in 156 countries, 1810
-1989.

Bones of Contention: The Political Economy of Height Inequality: http://piketty.pse.ens.fr/files/BoixRosenbluth2014.pdf
- Carles Boix, et al.

Height in the Dark Ages: https://pseudoerasmus.com/2014/06/12/aside-angus-maddison/

It causes characteristic changes in the bones.  Key point:  it is vanishingly rare in Old World skeletons before the 17th century.  Those changes, however, been seen in some pre-Columbian Amerindian skeletons [work by Bruce Rothschild].

The obvious explanation is that RA is caused by some pathogen that originated in the Americas and later spread to the rest of the world.  Like the French disease.

https://westhunt.wordpress.com/2012/05/09/montezumas-revenge/
Everybody knows that the Amerindians were devastated by new infectious diseases after Columbus discovered America and made it stick. Smallpox, falciparum malaria, yellow fever, bubonic plague, cholera, measles, whooping cough, etc : by some estimates, the Amerindian population dropped by about 90%, worse than the Black Plague, which only killed off half of Europe. Naturally, you wonder what ailments the Americas exported to the rest of the world.

We know of two for sure. First, syphilis: the first known epidemic was in 1495, in Naples, during a French invasion. By 1520 it had reached Africa and China.

From the timing of the first epidemic, and the apparent newness of the disease, many have suspected that it was an import from the New World. Some, like Bartolome de las Casas, had direct knowledge: Las Casas was in Seville in 1493, his father and uncle sailed with Columbus on the second voyage, and he himself traveled to the New World in 1502, where he spent most of the rest of his life working with the Amerindians. Ruiz Diaz de Isla, a Spanish physician, reported treating some of Columbus’s crew for syphilis, and that he had observed its rapid spread in Barcelona.

I have seen someone object to this scenario, on the grounds that the two years after Columbus’s return surely couldn’t have been long enough to generate a major outbreak. I think maybe that guy doesn’t get out much. It has always looked plausible, considering paleopathological evidence (bone changes) and the timing of the first epidemic. Recent analysis shows that some American strains of pinta (a treponemal skin disease) are genetically closest to the venereal strains. I’d say the Colombian theory is pretty well established, at this point.

Interestingly, before the genetic evidence, this was one of the longest-running disputes among historians. As far as I can tell, part of the problem was (and is) that many in the social sciences routinely apply Ockham’s razor in reverse. Simple explanations are bad, even when they fit all the facts. You see this in medicine, too.

...

There are two other diseases that are suspected of originating in the Americas. The first is typhus, gaol fever, caused by a Rickettsial organism and usually spread by lice. Sometimes it recurs after many years, in a mild form called Brill’s disease, rather like chickenpox and shingles. This means that typhus is always waiting in the wings: if the world gets sufficiently messed up, it will reappear.

Typhus shows up most often in war, usually in cool countries. There is a claim that there was a clear epidemic in Granada in 1489, which would definitely predate Columbus, but descriptions of disease symptoms by premodern physicians are amazingly unreliable. The first really reliable description seems to have been by Fracastoro, in 1546 (according to Hans Zinsser in Rats, Lice, and History). The key hint is the existence of a very closely related organism in American flying squirrels.

Thinking about it, I have the impression that the legions of the Roman Republic didn’t have high casualties due to infectious disease, while that was the dominant cause of death in more recent European armies, up until the 20tth century. If smallpox, measles, syphilis, bubonic plague, perhaps typhus, simply hadn’t arrived yet, this makes sense. Falciparum malaria wasn’t much of a factor in northern Italy until Imperial times…

The second possibly American disease is rheumatoid arthritis. We don’t even know that it has an infectious cause – but we do know that it causes characteristic skeletal changes, and that no clear-cut pre-Columbian rheumatoid skeletons are known from the Old World, while a number have been found in the lower South. To me, this makes some infectious cause seem likely: it would very much be worth following this up with the latest molecular genetic methods.

American crops like maize and potatoes more than canceled the demographic impact of syphilis and typhus. But although the Old World produced more dangerous pathogens than the Americas, due to size, longer time depth of agriculture, and more domesticated animals, luck played a role, too. Something as virulent as smallpox or falciparum malaria could have existed in the Americas, and if it had, Europe would have been devastated.

https://westhunt.wordpress.com/2012/05/09/montezumas-revenge/#comment-2910
Malaria came from Africa, probably. There are old primate versions. Smallpox, dunno: I have heard people suggest viral infections of cows and monkeys as ancestral. Measles is derived from rinderpest, probably less than two thousand years ago.

Falciparum malaria has been around for a while, but wasn’t found near Rome during the Republic. It seems to have gradually moved north in Italy during classical times, maybe because the range of the key mosquito species was increasing. By early medieval times it was a big problem around Rome.

Smallpox probably did not exist in classical Greece: there is no clear description in the literature of the time. It may have arrived in the Greco-Roman world in 165 AD, as the Antonine plague.

The Pathogenesis of Rheumatoid Arthritis: http://sci-hub.tw/http://www.nejm.org/doi/full/10.1056/NEJMra1004965

https://westhunt.wordpress.com/2017/08/27/age-of-discovery-pandora/
In the Age of Discovery, Europeans were playing with fire. Every voyage of exploration risked bring back some new plague. From the New World, syphilis, probably typhus and rheumatoid arthritis. From India, cholera. HIV, recently, from Africa. Comparably important new pests attacking important crops and domesticated animals also arrived, such as grape phylloxera (which wiped out most of the vineyards of Europe) and potato blight ( an oomycete or ‘water mold’, from central Mexico).

If one of those plagues had been as potent as smallpox or falciparum malaria, you probably wouldn’t be reading this.

The germ theory was proposed by Girolamo Fracastoro in 1546, and expanded upon by Marcus von Plenciz in 1762. Such views were held in disdain, however, and Galen's miasma theory remained dominant among scientists and doctors. The nature of this doctrine prevented them from understanding how diseases actually progressed, with predictable consequences. By the early nineteenth century, smallpox vaccination was commonplace in Europe, though doctors were unaware of how it worked or how to extend the principle to other diseases. Similar treatments had been prevalent in India from just before 1000 A.D.[2] [N 1] A transitional period began in the late 1850s as the work of Louis Pasteur and Robert Koch provided convincing evidence; by 1880, miasma theory was struggling to compete with the germ theory of disease. Eventually, a "golden era" of bacteriology ensued, in which the theory quickly led to the identification of the actual organisms that cause many diseases.[3][4] Viruses were discovered in the 1890s.

Here’s what seems to be happening: you have cells in the testes that reproduce, producing one daughter cell like the parent and one that develops into a sperm cell. That’s the way it’s supposed to be. But carrying certain very specific mutations of FGFR2 or FGFR3 seem to cause occasional divisions that result in two daughter cells – so the pre-sperm cells that carry such mutations gradually become more and more common in the testes and produce a growing fraction of sperm with those mutations. It’s rather like cancer. You get clumps of cells producing the bad sperm.

Same things is happening with MEN2B (RET gene), which is also more common than it should be, although not as much so as achondroplasia.

Without this unusual mutational mechanism, there would be a shortage of dwarfs.

Two main factors interfered with an effective policy response to cholera (not counting ever-present human stupidity and obstinacy): bad science and 19th century liberalism.

Scientists at the time had convinced themselves that the germ theory of disease was just wrong. Yellow fever’s decimation of the French force in Haiti made it important, and when yellow fever hit Barcelona in 1822, French scientists were all over it. They concluded that there was no possibility of contact between yellow fever victims in Barcelona, and ruled out contagion. Mosquito transmission didn’t occur to them.

Worse yet, they generalized their error: they concluded that contagion was never the answer, and accepted miasmas as the cause, a theory which is too stupid to be interesting. Sheesh, they taught the kids in medical school that measles wasn’t catching – while ordinary people knew perfectly well that it was. You know, esoteric, non-intuitive truths have a certain appeal – once initiated, you’re no longer one of the rubes. Of course, the simplest and most common way of producing an esoteric truth is to just make it up.

On the other hand, 19th century liberals (somewhat like modern libertarians, but way less crazy) knew that trade and individual freedom were always good things, by definition, so they also opposed quarantines – worse than wrong, old-fashioned ! And more common in southern, Catholic, Europe: enough said! So, between wrong science and classical liberalism, medical reformers spent many years trying to eliminate the reactionary quarantine rules that still existed in Mediterranean ports.

some history: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3559034/
In some countries, the suspension of personal liberty provided the opportunity—using special laws—to stop political opposition. However, the cultural and social context differed from that in previous centuries. For example, the increasing use of quarantine and isolation conflicted with the affirmation of citizens’ rights and growing sentiments of personal freedom fostered by the French Revolution of 1789. In England, liberal reformers contested both quarantine and compulsory vaccination against smallpox. Social and political tensions created an explosive mixture, culminating in popular rebellions and uprisings, a phenomenon that affected numerous European countries (29). In the Italian states, in which revolutionary groups had taken the cause of unification and republicanism (27), cholera epidemics provided a justification (i.e., the enforcement of sanitary measures) for increasing police power.

...

Anticontagionists, who disbelieved the communicability of cholera, contested quarantine and alleged that the practice was a relic of the past, useless, and damaging to commerce. They complained that the free movement of travelers was hindered by sanitary cordons and by controls at border crossings, which included fumigation and disinfection of clothes (Figures 1,​,22,​,3).3). In addition, quarantine inspired a false sense of security, which was dangerous to public health because it diverted persons from taking the correct precautions. International cooperation and coordination was stymied by the lack of agreement regarding the use of quarantine. The discussion among scientists, health administrators, diplomatic bureaucracies, and governments dragged on for decades, as demonstrated in the debates in the International Sanitary Conferences (31), particularly after the opening, in 1869, of the Suez Canal, which was perceived as a gate for the diseases of the Orient (32). Despite pervasive doubts regarding the effectiveness of quarantine, local authorities were reluctant to abandon the protection of the traditional strategies that provided an antidote to population panic, which, during a serious epidemic, could produce chaos and disrupt public order (33).

I get the distinct impression that someone (probably someone other than Varro) came up with an approximation of germ theory 1500 years before Girolamo Fracastoro. But his work was lost.

Everybody knows, or should know, that the vast majority of Classical literature has not been preserved. Those lost works contained facts and ideas that might have value today – certainly there are topics that we understand much better because of insights from Classical literature. For example, Reich and Patterson find that some of the Indian castes have existed for something like three thousand years: this is easier to believe when you consider that Megasthenes wrote about the caste system as early as 300 BC.

We don’t put much effort into recovering lost Classical literature. But there are ways in which we could push harder – by increased funding for work on the Herculaneum scrolls, or the Oxyrhynchus papyri collection, for example. Some old-fashioned motivated archaeology might get lucky and find another set of Amarna cuneiform letters, or a new Antikythera mechanism.

https://westhunt.wordpress.com/2012/03/06/spontaneous-generation/
Here we have yet another case in which a discovery was possible for a long time before it was actually accepted. Aristotle is the villain here: he clearly endorses spontaneous generation of many plants and animals. On the other hand, I don’t remember him saying that people should accept all of his conclusions uncritically and without further experimentation for the next couple of thousand years, which is what happened. So maybe we’re all guilty.

...

Part of the funny here (not even counting practical experience) is that almost every educated man over these two millennia had read, and indeed studied deeply, a work with a fairly clear statement of the actual fly->egg->maggot->fly process. As I as I can tell, only one person (Redi) seems to have picked up on this.

“But the more Achilles gazed, the greater rose his desire for vengeance, and his eyes flashed terribly, like coals beneath his lids, as he lifted the god’s marvellous gifts and exulted. When he had looked his fill on their splendour, he spoke to Thetis winged words; ‘Mother, the god grants me a gift fit for the immortals, such as no mortal smith could fashion. Now I shall arm myself for war. Yet I fear lest flies infest the wounds the bronze blades made, and maggots breed in the corpse of brave Patroclus, and now his life is fled, rot the flesh, and disfigure all his body.’ ”

You’d think a blind man would have noticed this.

Anyhow, the lesson is clear. Low hanging fruit can persist for a long time if the conventional wisdom is wrong – and sometimes it is.

http://www.bede.org.uk/literature.htm

Transmission of the Greek Classics: https://en.wikipedia.org/wiki/Transmission_of_the_Greek_Classics
https://www.quora.com/How-much-writing-from-ancient-Greece-is-preserved-Is-it-a-finite-amount-that-someone-could-potentially-read

By way of comparison, the complete Loeb Classical Library (which includes all the important classical texts) has 337 volumes for Ancient Greek --- and those aren't 100,000 word-long door-stoppers.
https://www.loebclassics.com/
$65/year for individuals (I wonder if public libraries have subscriptions?)

http://www.roger-pearse.com/weblog/2009/10/26/reference-for-the-claim-that-only-1-of-ancient-literature-survives/
http://www.patheos.com/blogs/geneveith/2015/01/finding-the-lost-texts-of-classical-antiquity/
http://www.historyofinformation.com/narrative/loss-of-information.php
http://www.bede.org.uk/literature.htm

https://twitter.com/futurepundit/status/927344648154112000
https://archive.is/w86uL
1/ Thinking about what Steven Greenblatt described in The Swerve as a mass extinction of ancient books (we have little of what they wrote)
2/ If I could go back in time to, say, 100 AD or 200 AD I would go with simple tech for making books last for a thousand years. Possible?

https://www.gnxp.com/WordPress/2018/01/28/the-rapid-fading-of-information/
I’ve put a lot of content out there over the years. Probably on the order of 5 million words across my blogs. Some publications here and there. Lots of tweets. But very little of it will persist into future generations. Digital is evanescent.

But so is paper. I believe that even good hardcover books probably won’t last more than a few hundred years.

Perhaps we should go back to some form of cuneiform? Stone and metal will last thousands of years.

How long does a paperback book last?: https://www.quora.com/How-long-does-a-paperback-book-last

A 500 years vault for books?: https://worldbuilding.stackexchange.com/questions/137583/a-500-years-vault-for-books
There are about four solutions that have actually worked in history

1. The desert method
2. Give them to an institution which will preserve them
3. The opposite of secrecy: duplicate them extensively

4. Transcribe them to durable materials

It is hard to keep books for a really long time because paper, parchment and papyrus are easily destroyed. However books have been produced on much more durable materials. Nowadays a holographic copy can be laser etched into stainless steel. In Sumer, 5300 years ago they pressed them into clay tablets. If the document was important, they fired the clay; otherwise they just let it dry. The fired versions are close to indestructible.

1/4 WWC report having been depressed, rates still a bit higher for whites among upper classes
Prevalence of Depression by Race/Ethnicity: Findings From the National Health and Nutrition Examination Survey III: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1449298/
A Cross-Ethnic Comparison of Lifetime Prevalence Rates of Anxiety Disorders: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931265/

Racial-Ethnic Differences in Psychiatric Diagnoses and Treatment Across 11 Health Care Systems in the Mental Health Research Network: https://ps.psychiatryonline.org/doi/full/10.1176/appi.ps.201500217

https://westhunt.wordpress.com/2012/12/03/reversal-of-fortune-2/#comment-5940
“particularly in the fetus”. You’d think so, but people have looked at Dutch draftees who were in the womb during the famine of 1944. They found no effects of famine exposure on Ravens scores at age 19. Schizophrenia doubled, though. Schiz also doubled in the Chinese cohort exposed to the Great Leap Forward famine.

Cohort Profile: The Dutch Hunger Winter Families Study: https://academic.oup.com/ije/article/36/6/1196/814573
Nutrition and Mental Performance: https://sci-hub.tw/10.1126/science.178.4062.708
Schizophrenia after prenatal exposure to the Dutch Hunger Winter of 1944-1945: https://sci-hub.tw/10.1001/archpsyc.1992.01820120071010
Prenatal famine exposure and cognition at age 59 years: https://sci-hub.tw/10.1093/ije/dyq261

https://westhunt.wordpress.com/2012/12/03/reversal-of-fortune-2/#comment-5960
You might be right. There is reason to suspect that prenatal exposure to alcohol is far riskier in some populations than others – in particular populations that have limited historical exposure to alcohol. Fetal Alcohol Syndrome (FAS) is very rare in France, for example – yet they drink, I’m told.

https://westhunt.wordpress.com/2012/12/03/reversal-of-fortune-2/#comment-5961
The kind of conservatism that shows up politically doesn’t have any predictive value. In other words, liars and morons. They’re why God made baseball bats. Once upon a time, I said this: “The American right doesn’t have room for anyone who knows jack shit about anything, or whose predictions have ever come true.” I’ll stick with that.

full quote here: http://www.rpgcodex.net/forums/index.php?threads/planescape-torment-problems.9208/
The American right doesn't have room for anyone who knows jack shit about anything, or whose predictions have ever come true. Of course they're all liars. In the words of one of their semi-prominent members, himself plenty despicable: "Science, logic, rational inquiry, thoughtful reflection, mean nothing to them. It's all posturing and moral status games and sucking up to halfwits like GWB and clinging to crackpot religion, and of course amoral careerism. " I think my correspondent forgot to mention their propensity for eating shit and rolling around in their own vomit, but nobody's perfect.

lol:
https://westhunt.wordpress.com/2012/12/03/reversal-of-fortune-2/#comment-6045
I’ve mused that it’s generally believed that iodine benefits females more than males, and the timing of iodization in the US matches up reasonably well with the rise of feminism…

Japan: 1.1% -> 3.3%
China: 0.5% -> 8%
- wonder what's going on there
- Anglos fat af in general
- Latin America's pretty fat too

Horizontal transmission of T. gondii may involve three life-cycle stages, i.e. ingesting infectious oocysts from the environment or ingesting tissue cysts or tachyzoites which are contained in meat or primary offal (viscera) of many different animals. Transmission may also occur via tachyzoites contained in blood products, tissue transplants, or unpasteurised milk. However, it is not known which of these routes is more important epidemiologically. In the past, the consumption of raw or undercooked meat, in particular of pigs and sheep, has been regarded as a major route of transmission to humans. However, recent studies showed that the prevalence of T. gondii in meat-producing animals decreased considerably over the past 20 years in areas with intensive farm management.

A Population-Level Decline in Serum Testosterone Levels in American Men: http://sci-hub.tw/10.1210/jc.2006-1375
Secular trends in sex hormones and fractures in men and women: http://www.eje-online.org/content/166/5/887.full.pdf
https://twitter.com/toad_spotted/status/984543033285898246
https://archive.is/dcruu
Small n and older sample, but interesting that while testosterone decreases have been large for men they’ve been even larger (in % terms) for women; wonder if this contributes to declining pregnancy and sexual frequency, rising depression.

https://www.labcorp.com/assets/11476
http://www.theamericanconservative.com/articles/sperm-killers-and-rising-male-infertility/
https://www.theguardian.com/lifeandstyle/2017/jul/25/sperm-counts-among-western-men-have-halved-in-last-40-years-study
https://www.weforum.org/agenda/2017/08/most-men-in-the-us-and-europe-could-be-infertile-by-2060
Strangelove: https://youtu.be/N1KvgtEnABY?t=67

https://www.scientificamerican.com/article/sperm-count-dropping-in-western-world/
https://news.ycombinator.com/item?id=14855796
https://news.ycombinator.com/item?id=14857588
People offering human-centric explanations like cell phones: Note also that the sperm quality of dogs has decreased 30% since 1988.

https://www.cbc.ca/radio/quirks/august-3-2019-science-of-awe-blue-whales-and-sonar-chromosomes-and-sleep-and-more-1.5047142/man-and-man-s-best-friend-have-both-been-experiencing-declines-in-sperm-quality-1.5047150
https://news.ycombinator.com/item?id=20636757

mendelian rand.:
https://www.ncbi.nlm.nih.gov/pubmed/28448539
1 SD genetically instrumented increase in BMI was associated with a 0.25 SD decrease in serum testosterone
https://twitter.com/SilverVVulpes/status/857902555489341441

Ibuprofen linked to male infertility: study: https://nypost.com/2018/01/08/ibuprofen-linked-to-male-infertility-study/
http://www.pnas.org/content/115/4/E715.full

Tucker Carlson: "Men Seem To Be Becoming Less Male": https://www.realclearpolitics.com/video/2018/03/08/tucker_carlson_men_seem_to_be_becoming_less_male.html
Carlson interviewed Dr. Jordan Peterson who blamed the "insidious" movement being driven by the "radical left" that teaches there a problem of "toxic masculinity." He said ideological policies focus on "de-emphasizing masculinity may be part of the problem."

...

Those are the numbers. They paint a very clear picture: American men are failing, in body, mind and spirit. This is a crisis. Yet our leaders pretend it’s not happening. They tell us the opposite is true: Women are victims, men are oppressors. To question that assumption is to risk punishment. Even as women far outpace men in higher education, virtually every college campus supports a women’s studies department, whose core goal is to attack male power. Our politicians and business leaders internalize and amplify that message. Men are privileged. Women are oppressed. Hire and promote and reward accordingly.

https://pinboard.in/u:nhaliday/b:bd7b0a50d741
But it also hints at an almost opposite take: average testosterone levels have been falling for decades, so at this point these businessmen would be the only “normal” (by 1950s standards) men out there, and everyone else would be unprecedently risk-averse and boring.

In a simple model, a given mutant has an equilibrium frequency μ/s, when μ is the mutation rate from good to bad alleles and s is the size of the selective disadvantage. To estimate the total impact of mutation at that locus, you multiply the frequency by the expected harm, s: which means that the fitness decrease (from effects at that locus) is just μ, the mutation rate. If we assume that these fitness effects are multiplicative, the total fitness decrease (also called ‘mutational load’) is approximately 1 – exp(-U), when U is where U=Σ2μ, the total number of new harmful mutations per diploid individual.

https://westhunt.wordpress.com/2012/10/17/more-to-go-wrong/

https://westhunt.wordpress.com/2012/07/13/sanctuary/
interesting, suggestive comment on Africa:
https://westhunt.wordpress.com/2012/07/13/sanctuary/#comment-3671
https://westhunt.wordpress.com/2012/07/14/too-darn-hot/
http://infoproc.blogspot.com/2012/07/rare-variants-and-human-genetic.html
https://westhunt.wordpress.com/2012/07/18/changes-in-attitudes/
https://westhunt.wordpress.com/2012/08/24/men-and-macaques/
I have reason to believe that few people understand genetic load very well, probably for self-referential reasons, but better explanations are possible.

One key point is that the amount of neutral variation is determined by the long-term mutational rate and population history, while the amount of deleterious variation [genetic load] is set by the selective pressures and the prevailing mutation rate over a much shorter time scale. For example, if you consider the class of mutations that reduce fitness by 1%, what matters is the past few thousand years, not the past few tens or hundreds of of thousands of years.

...

So, assuming that African populations have more neutral variation than non-African populations (which is well-established), what do we expect to see when we compare the levels of probably-damaging mutations in those two populations? If the Africans and non-Africans had experienced essentially similar mutation rates and selective pressures over the past few thousand years, we would expect to see the same levels of probably-damaging mutations. Bottlenecks that happened at the last glacial maximum or in the expansion out of Africa are irrelevant – too long ago to matter.

But we don’t. The amount of rare synonymous stuff is about 22% higher in Africans. The amount of rare nonsynonymous stuff (usually at least slightly deleterious) is 20.6% higher. The number of rare variants predicted to be more deleterious is ~21.6% higher. The amount of stuff predicted to be even more deleterious is ~27% higher. The number of harmful looking loss-of-function mutations (yet more deleterious) is 25% higher.

It looks as if the excess grows as the severity of the mutations increases. There is a scenario in which this is possible: the mutation rate in Africa has increased recently. Not yesterday, but, say, over the past few thousand years.

...

What is the most likely cause of such variations in the mutation rate? Right now, I’d say differences in average paternal age. We know that modest differences (~5 years) in average paternal age can easily generate ~20% differences in the mutation rate. Such between-population differences in mutation rates seem quite plausible, particularly since the Neolithic.
https://westhunt.wordpress.com/2016/04/10/bugs-versus-drift/
more recent: https://westhunt.wordpress.com/2017/06/06/happy-families-are-all-alike-every-unhappy-family-is-unhappy-in-its-own-way/#comment-92491
Probably not, but the question is complex: depends on the shape of the deleterious mutational spectrum [which we don’t know], ancient and recent demography, paternal age, and the extent of truncation selection in the population.

Why It Was Easier to Be Skinny in the 1980s: https://www.theatlantic.com/health/archive/2015/09/why-it-was-easier-to-be-skinny-in-the-1980s/407974/
https://www.outsideonline.com/2030071/it-was-easier-be-skinny-1980s-thats-not-why-youre-overweight

The research of James Levine, an endocrinologist who works with the Mayo Clinic and Arizona State University, explains this puzzling phenomenon. In a carefully controlled overfeeding study, his team showed that the primary reason some people readily burn off excess calories is that they ramp up a form of calorie-burning called “non-exercise activity thermogenesis” (NEAT). NEAT is basically a fancy term for fidgeting. When certain people overeat, their brains boost calorie expenditure by making them fidget, change posture frequently, and make other small movements throughout the day. It’s an involuntary process, and Levine’s data show that it can incinerate nearly 700 calories per day. The “most gifted” of Levine’s subjects gained less than a pound of body fat from eating 1,000 extra calories per day for eight weeks. Yet the strength of the response was highly variable, and the “least gifted” of Levine’s subjects didn’t increase NEAT at all, shunting all the excess calories into fat tissue and gaining over nine pounds of body fat…

It strikes me that in many ways, life was gradually getting harder in the Old World, especially in the cradles of civilization.

slavery and Rome/early US: https://westhunt.wordpress.com/2016/06/17/in-a-handbasket/#comment-80503
Rome and innovation: https://westhunt.wordpress.com/2016/06/17/in-a-handbasket/#comment-80505
"Culture’s have flavors and the Roman flavor was unfavorable to being clever. The Greeks were clever but not interested in utility. While the central American civilizations liked to cut people’s hearts out and stick cactus spines through their penis in public. Let us all act according to national customs."
https://twitter.com/Evolving_Moloch/status/881652804900671489
https://en.wikipedia.org/wiki/Bloodletting_in_Mesoamerica

https://westhunt.wordpress.com/2014/07/05/let-no-new-thing-arise/
It helps to think about critical community size (CCS). Consider a disease like measles, one that doesn’t last long and confers lifelong immunity. The virus needs fresh, never-infected hosts (we call them children) all the time, else it will go extinct. The critical community size for measles is probably more than half a million – which means that before agriculture, measles as we know it today couldn’t and didn’t exist. In fact, it looks as if split off from rinderpest within the last two thousand years. Mumps was around in Classical times (Hippocrates gives a good description), but it too has a large CCS and must be relatively new. Rubella can’t be ancient. Whooping cough has a smaller CCS, maybe only 100,000, but it too must postdate agriculture.

"let no new thing arise":
http://www.theseeker.org/cgi-bin/bulletin/show.pl?Todd%20Collier/Que%20no%20hayan%20novedades.
http://itre.cis.upenn.edu/~myl/languagelog/archives/003347.html
http://www.bradwarthen.com/2010/02/que-no-haya-novedad-may-no-new-thing-arise/

https://westhunt.wordpress.com/2013/07/03/legionnaires-disease/
Before 1900, armies usually lost more men from infectious disease than combat, particularly in extended campaigns.  At least that seems to have been the case in modern Western history.

There are indications that infectious disease was qualitatively different – less important –  in  the Roman legions.  For one thing, camps were placed near good supplies of fresh water. The legions had good camp sanitation, at least by the time of the Principate. They used latrines flushed with running water in permanent camps  and deep slit trenches with wooden covers and removable buckets in the field.  Using those latrines would have protected soldiers from diseases like typhoid and dysentery, major killers in recent armies.  Romans armies were mobile, often shifting their camps.  They seldom quartered their soldiers in urban areas –  they feared that city luxuries would corrupt their men, but this habit helped them avoid infectious agents, regardless of their reasons.

They managed to avoid a lot of serious illnesses because the causative organisms  simply weren’t there yet. Smallpox, and maybe measles, didn’t show up until the middle Empire. Falciparum malaria was around, but hadn’t reached Rome itself, during the Republic. It definitely had by the time of the Empire. Bubonic plague doesn’t seem to have caused trouble before Justinian.  Syphilis for sure, and typhus probably,  originated in the Americas, while cholera didn’t arrive until after 1800.

the paper: http://www.pnas.org/content/112/49/15078

https://www.theatlantic.com/business/archive/2017/03/angus-deaton-qa/518880/
The Nobel laureate Angus Deaton discusses extreme poverty, opioid addiction, Trump voters, robots, and rent-seeking.

co-authored the "dead white people paper" w/ wife

http://andrewgelman.com/2017/03/23/mortality-rate-trends-age-ethnicity-sex-state/
point about expansion of education seems important
https://spottedtoad.wordpress.com/2016/01/17/correlates-of-middle-aged-white-mortality/

https://www.washingtonpost.com/news/wonk/wp/2017/03/24/the-disease-killing-white-americans-goes-way-deeper-than-opioids/
https://www.wsj.com/articles/death-rates-rise-for-wide-swath-of-white-adults-1490240740
http://www.newyorker.com/news/benjamin-wallace-wells/the-despair-of-learning-that-experience-no-longer-matters
https://www.nytimes.com/interactive/2017/09/02/upshot/fentanyl-drug-overdose-deaths.html

Diverging Life Expectancies and Voting Patterns in the 2016 US Presidential Election.: https://www.ncbi.nlm.nih.gov/pubmed/28817322
Changes in county life expectancy from 1980 to 2014 were strongly negatively associated with Trump's vote share, with less support for Trump in counties experiencing greater survival gains. Counties in which life expectancy stagnated or declined saw a 10-percentage-point increase in the Republican vote share between 2008 and 2016.

DESPAIR AND DECADES-LONG DEINDUSTRIALIZATION: https://spottedtoad.wordpress.com/2018/01/10/despair-and-decades-long-deindustrialization/

WE’VE BEEN HERE BEFORE: https://spottedtoad.wordpress.com/2018/01/12/weve-been-here-before/
A concept that seems to me to be missing from the Ruhm vs. Case/Deaton debate on “deaths of despair” is that of social crisis.

This seems to me to be the case for American Indians, who began experiencing what looks like a similar social crisis to non-college educated whites about a decade beforehand: rapidly escalating rates of suicide, drug overdoses, exit from the workforce, and even alcohol-related deaths (which were already very high for American Indians well before 2000, of course):

...

The common thread here would seem to be replacement of workforce participation with transfer payments, particularly cash transfers (since, my own reservations about Medicaid aside, increases in in-kind payments and SNAP since the 80s haven’t seemed to exert the same disruptive effect.) As I’ve said before, it seems very likely to me that technology will push an ever larger segment of society out of the economy, sooner or later, but how to prevent this from tearing apart our social fabric I don’t know.

Once It Was Overdue Books. Now Librarians Fight Overdoses.: https://www.nytimes.com/2018/02/28/nyregion/librarians-opioid-heroin-overdoses.html

somewhat related: https://www.theamericanconservative.com/dreher/male-loneliness-in-suburbia/

Washington didn’t micro-manage American Samoa, not being all that interested. A policy of benign neglect was interpreted by Poyer as an opportunity to act on his best judgment, in the finest traditions of the US Navy. He imposed quarantine. That was harder that it sounds, because of the frequent family visits between West Samoa and American Samoa – but Poyer also had the support of the local chiefs, who understood how serious imported epidemics could be. The people of American Samoa self-blockaded, on top of official quarantine: they sent out canoes to stop any and all visitors. They never had a single case.

Of course there was a disaster. Some people will think that it occurred in West Samoa. Others will think that the real disaster was in American Samoa.

https://westhunt.wordpress.com/2016/08/10/interview/

- IQ enhancement (somewhat apprehensive, wonder why?)
- ~20 years to CRISPR enhancement (very ballpark)
- cloning as an alternative strategy
- environmental effects on IQ, what matters (iodine, getting hit in the head), what doesn't (schools, etc.), and toss-ups (childhood/embryonic near-starvation, disease besides direct CNS-affecting ones [!])
- malnutrition did cause more schizophrenia in Netherlands (WW2) and China (Great Leap Forward) though
- story about New Mexico schools and his children (mostly grad students in physics now)
- clever sillies, weird geniuses, and clueless elites
- life-extension and accidents, half-life ~ a few hundred years for a typical American
- Pinker on Harvard faculty adoptions (always Chinese girls)
- parabiosis, organ harvesting
- Chicago economics talk
- Catholic Church, cousin marriage, and the rise of the West
- Gregory Clark and Farewell to Alms
- retinoblastoma cancer, mutational load, and how to deal w/ it ("something will turn up")
- Tularemia and Stalingrad (ex-Soviet scientist literally mentioned his father doing it)
- germ warfare, nuclear weapons, and testing each
- poison gas, Haber, nerve gas, terrorists, Japan, Syria, and Turkey
- nukes at https://en.wikipedia.org/wiki/Incirlik_Air_Base
- IQ of ancient Greeks
- history of China and the Mongols, cloning Genghis Khan
- Alexander the Great vs. Napoleon, Russian army being late for meetup w/ Austrians
- the reason why to go into Iraq: to find and clone Genghis Khan!
- efficacy of torture
- monogamy, polygamy, and infidelity, the Aboriginal system (reverse aging wives)
- education and twin studies
- errors: passing white, female infanticide, interdisciplinary social science/economic imperialism, the slavery and salt story
- Jewish optimism about environmental interventions, Rabbi didn't want people to know, Israelis don't want people to know about group differences between Ashkenazim and other groups in Israel
- NASA spewing crap on extraterrestrial life (eg, thermodynamic gradient too weak for life in oceans of ice moons)

https://spectrumnews.org/news/school-survey-india-reveals-low-autism-prevalence/
This Is How Much of Autism Is Genetic: http://time.com/4956316/how-much-of-autism-is-genetic/
Indeed, when Sandin tracked autism diagnoses over time among the sibling pairs, he found that genetics likely accounts for around 83% of the disorder. That compares to nearly 90% reported in previous studies of twins only. Using the new model, environmental factors probably contribute around 17% to the risk of developing autism.

Everyone is talking about how many households have insurance and acting as if the main challenge is to get healthy people to buy insurance. If Cutler is right, then health care policy boils down to:

1. Finding a fair way to share financial the burden of chronic illnesses. (Obviously, “fair” involves value judgments.)

2. Putting resources into public health measures and efforts to induce people to comply with behavioral advice that would help to prevent chronic illness.

Seroprevalence increased from 20% (95%-CI:17–23%) in the 18–29 age group to 77% (95%-CI:73–81%) in the 70–79 age group. Male gender, keeping cats and BMI ≥30 were independent risk factors for seropositivity, while being vegetarian and high socio-economic status were negatively associated. Based on these data, we estimate 1.1% of adults and 1.3% of women aged 18–49 to seroconvert each year. This implies 6,393 seroconversions annually during pregnancies. We conclude that T. gondii infection in Germany is highly prevalent and that eating habits (consuming raw meat) appear to be of high epidemiological relevance. High numbers of seroconversions during pregnancies pose substantial risks for unborn children. Efforts to raise awareness of toxoplasmosis in public health programs targeting to T. gondii transmission control are therefore strongly advocated.

lol:
A significant interaction was noted between age and sex (p-value = 0.023), since higher seroprevalences were observed among younger males and older females.

hmm...:
If toxo naturally can make people like cat piss, it’s already preadapted to become (with suitable genetic engineering) the model system for many kinds of infectious behavior modifiers.

De novo mutations in hundreds of different genes collectively cause 25-42% of severe developmental disorders (DD). The cause in the remaining cases is largely unknown. The role of de novo mutations in regulatory elements affecting known DD-associated genes or other genes is essentially unexplored. We identified de novo mutations in three classes of putative regulatory elements in almost 8,000 DD patients. Here we show that de novo mutations in highly conserved fetal-brain active elements are significantly and specifically enriched in neurodevelopmental disorders. We identified a significant two-fold enrichment of recurrently mutated elements. We estimate that, genome-wide, de novo mutations in fetal-brain active elements are likely to be causal for 1-3% of patients without a diagnostic coding variant and that only a small fraction (<2%) of de novo mutations in these elements are pathogenic. Our findings represent a robust estimate of the contribution of de novo mutations in regulatory elements to this genetically heterogeneous set of disorders, and emphasise the importance of combining functional and evolutionary evidence to delineate regulatory causes of genetic disorders.

Despite successes in identifying causes, it is often claimed that there are missing additional causes for even reasonably well-understood conditions such as lung cancer and coronary heart disease. Several lines of evidence suggest that largely chance events, from the biographical down to the sub-cellular, contribute an important stochastic element to disease risk that is not epidemiologically tractable at the individual level. Epigenetic influences provide a fashionable contemporary explanation for such seemingly random processes. Chance events—such as a particular lifelong smoker living unharmed to 100 years—are averaged out at the group level. As a consequence population-level differences (for example, secular trends or differences between administrative areas) can be entirely explicable by causal factors that appear to account for only a small proportion of individual-level risk. In public health terms, a modifiable cause of the large majority of cases of a disease may have been identified, with a wild goose chase continuing in an attempt to discipline the random nature of the world with respect to which particular individuals will succumb.

choice quote:
"With the perception (in my view exaggerated) that genome-wide association studies (GWASs) have failed to deliver on initial expectations,5 the next phase of enhanced risk prediction will certainly shift to ‘epigenetics’6,7—the currently fashionable response to any question to which you do not know the answer."

Two meta-analyses found that young Americans increasingly believe their lives are controlled by outside forces rather than their own efforts. Locus of control scores became substantially more external (about .80 standard deviations) in college student and child samples between 1960 and 2002. The average college student in 2002 had a more external locus of control than 80% of college students in the early 1960s. Birth cohort/time period explains 14% of the variance in locus of control scores. The data included 97 samples of college students (n = 18,310) and 41 samples of children ages 9 to 14 (n = 6,554) gathered from dissertation research. The results are consistent with an alienation model positing increases in cynicism, individualism, and the self-serving bias. The implications are almost uniformly negative, as externality is correlated with poor school achievement, helplessness, ineffective stress management, decreased self-control, and depression.

cultural or biological?

- Michael A. Woodley

We argue that in social species, interorganismal gene-gene interactions, which in previous literatures have been termed social epistasis, allow genomes carrying deleterious mutations to reduce via group-level pleiotropy the fitness of others, including noncarriers. This fitness reduction occurs by way of degradation of group-level processes that optimize the reproductive ecology of a population for intergroup competition through, among other mechanisms, suppression of free-riding.

--

Fitness indicators theory (Houle 2000; Miller 2000) predicts that the behavioral and physiological condition of prospective partners strongly influences female mate choice in particular, as these constitute honest indicators of underlying genetic quality. Furthermore, as deleterious mutations are pleiotropic (i.e., they can influence the development of multiple traits simultaneously), they are a source of genetic correlation among diverse behavioral and physiological domains, yielding a latent general fitness factor( f ). This optimizes the efficiency of sexual selection, as selection for quality with respect to one domain will increase the probability of selection for quality “across the board” (Houle 2000; Miller 2000). If purifying selection is primarily cryptic—working by virtue of those lower in f simply being less successful in competition for mates and therefore producing fewer offspring relative to those higher in the factor—then considerably less reproductive failure is needed to solve the mutation load paradox (19% instead of 88% based on simulations in Leseque et al. 2012).

...

Theoretical work involving humans suggests a loss of intrinsic fitness of around 1% per generation in the populations of modernized countries (Lynch 2016; Muller 1950). Thus, these might yet be undergoing mutational meltdown, albeit very gradually (i.e., over the course of centuries)

...

An interesting observation is that the fitness of the populations of modernized nations does appear to be rapidly decreasing—although not in a manner consonant with the direct action of deleterious mutations on the fitness of individuals (as per the mutation load paradox).

...

Increased education has furthermore encouraged individuals to trade fertility against opportunities to enhance their social status and earning power, with the largest fitness losses occurring among those with high status who potentially carry fewer deleterious mutations (i.e., by virtue of possessing higher levels of traits that exhibit some sensitivity to mutation load, such as general intelligence; Spain et al. 2015; Woodley of Menie et al. 2016a). Hitherto not considered is the possibility that the demographic transition represents a potential change in the fitness characteristics of the group-level extended phenotype of modernized populations, indicating that there might exist pathways through which deleterious mutations that accumulate due to ecological mildness could pathologically alter fertility tradeoffs in ways that might account for the maladaptive aspects of the fertility transition (e.g., subreplacement fertility; Basten, Lutz and Scherbov, 2013).

...

Cooperation, though offering significant fitness benefits to individual organisms and groups, involves some costs for cooperators in order to realize mutual gains for all parties. Free riders are individuals that benefit from cooperation without suffering any of the costs needed to sustain it. Hence, free riders enjoy a fitness advantage relative to cooperators via the former’s parasitism on the latter.

...

The balance of selection can alternate between the different levels depending on the sorts of selective challenges that a population encounters. For example, group selection may operate on human populations during times of intergroup conflict (i.e., warfare), whereas during times of peace, selection may tend to favor the fitness of individuals instead (Woodley and Figueredo 2013; Wilson 2002). A major factor that seems to permit group-level selection to be viable under certain ecological regimes is the existence of free-rider controls, i.e., features of the group’s social ecology that curb the reproductive fitness of the carriers of “selfish” genetic variants (MacDonald 1994; Wilson 2002).

...

High-status individuals participate in the generation and vertical cultural transmission of free-rider controls—these take the form of religious and ideological systems which make a virtue out of behaviors that overtly benefit the group, and a vice out of those that only favor individual-level fitness, via the promotion of ethnocentrism, martyrdom, and displays of commitment (MacDonald 1994, 2009, 2010; Wilson 2002). Humans are furthermore equipped with specialized mental adaptations for coordinating as part of a group, such as effortful control—the ability to override implicit behavioral drives via the use of explicit processing systems, which allow them to regulate their behavior based on what is optimal for the group (MacDonald 2008). The interaction between individuals of different degrees of status, i.e., those that generate and maintain cultural norms and those who are merely subject to them, therefore constitutes a form of social epistasis, as the complex patterns of interactions among genomes that characterize human culture have the effect of regulating both individual- and group-level (via the curbing of free-riding) fitness (MacDonald 2009, 2010).

Mutations that push the behavior of high-status individuals away from the promotion of group-selected norms may promote a breakdown of or otherwise alter these social epistatic interactions, causing dysregulation of the group’s reproductive ecology. Behavioral changes are furthermore a highly likely consequence of mutation accumulation, as “behavior” (construed broadly) is a large potential target for new mutations (Miller 2000; Lynch 2016) 1 owing to the fact that approximately 84% of all genes in the human genome are involved in some aspect of brain development and/or maintenance (Hawrylycz et al. 2012).

Consistent with the theorized role of group-level (cultural) regulatory processes in the maintenance of fitness optima, positive correlations exist between religiosity (a major freerider control; MacDonald 1994; Wilson 2002) and fertility, both at the individual differences and cross-cultural levels (Meisenberg 2011). Religiosity has declined in modernized nations—a process that has gone hand-in-hand with the rise of a values system called postmaterialism (Inglehart 1977), which is characterized by the proliferation of individualistic, secular, and antihierarchical values (Welzel 2013). The holding of these values is negatively associated with fertility, both at the individual level (when measured as political liberalism; Goldstone et al. 2011) and across time and cultures (Inglehart and Appel 1989). The rise of postmaterialist values is also associated with increasingly delayed onset of reproduction (Klien 1990) which directly increases the (population) mutation load.

Pathological Altruism

Some of the values embodied in postmaterialism have been linked to the pathological altruism phenomenon, i.e., forms of altruism that damage the intended recipients or givers of largesse (Oakley et al. 2012; Oakley 2013). Virtues associated with altruism such as kindness, fidelity, magnanimity, and heroism, along with quasi-moral traits associated with personality and mental health, may be under sexual selection and might therefore be sensitive, through the f factor, to the deleterious effects of accumulating mutations (Miller 2007).

...

Another form of pathologically altruistic behavior that Oakley (2013) documents is self-righteousness, which may be increasing, consistent with secular trend data indicating elevated levels of self-regarding behavior among Western populations (sometimes called the narcissism epidemic; Twenge and Campbell 2009). This sort of behavior constitutes a key component of the clever silly phenomenon in which the embrace of counterfactual beliefs is used to leverage social status via virtue signaling (e.g., the conflation of moral equality among individuals, sexes, and populations with biological equality) (Dutton and van der Linden 2015; Charlton 2009; Woodley 2010). There may be a greater number of influential persons inclined to disseminate such beliefs, in that the prevalence of phenotypes disposed toward egoistic behaviors may have increased in Western populations (per Twenge and coworkers’ research), and because egoists, specifically Machiavellians and narcissists, appear advantaged in the acquisition of elite societal stations (Spurk et al. 2015).

[Do Bad Guys Get Ahead or Fall Behind? Relationships of the Dark Triad of Personality With Objective and Subjective Career Success: http://sci-hub.tw/http://journals.sagepub.com/doi/abs/10.1177/1948550615609735

After controlling for other relevant variables (i.e., gender, age, job tenure, organization size, education, and work hours), narcissism was positively related to salary, Machiavellianism was positively related to leadership position and career satisfaction, and psychopathy was negatively related to all analyzed outcomes.]

...

By altering cultural norms, elite egoists may encourage the efflorescence of selfish behaviors against which some older and once highly influential cultural systems acted. For example, Christianity in various forms strongly promoted personal sacrifice for the good of groups and proscribed egoistic behaviors (Rubin 2015), but has declined significantly in terms of cultural power following modernization (Inglehart 1977). Thus, it is possible that a feedback loop exists wherein deleterious mutation accumulation raises population levels of egoism, either directly or indirectly, via the breakdown of developmental constraints on personality canalization; the resultantly greater number of egoists are then able to exploit relevant personality traits to attain positions of sociocultural influence; and through these … [more]

We find that as the county unemployment rate increases by 1 percentage point, the opioid death rate (per 100,000) rises by 0.19 (3.6%) and the ED visit rate for opioid overdoses (per 100,000) increases by 0.95 (7.0%). We also uncover statistically significant increases in the overall drug death rate that are driven in most specifications by increases in opioid deaths. These results hold when performing a state, rather than county, level analysis. The results are primarily driven by adverse events among whites, although there is some sensitivity to choice of models in the results for nonwhites. Additionally, the findings are relatively stable across time periods; they do not pertain only to recession years, but instead represent a more generalizable and previously unexplored connection between economic development and the severe adverse consequences of substance abuse.

We estimate that 42% of our cohort carry pathogenic DNMs in coding sequences; approximately half of these DNMs disrupt gene function and the remainder result in altered protein function. We estimate that developmental disorders caused by DNMs have an average prevalence of 1 in 213 to 1 in 448 births, depending on parental age. Given current global demographics, this equates to almost 400,000 children born per year.

A New Germ Theory: https://www.theatlantic.com/magazine/archive/1999/02/a-new-germ-theory/377430/
The dictates of evolution virtually demand that the causes of some of humanity's chronic and most baffling "noninfectious" illnesses will turn out to be pathogens -- that is the radical view of a prominent evolutionary biologist

A LATE-SEPTEMBER heat wave enveloped Amherst College, and young people milled about in shorts or sleeveless summer frocks, or read books on the grass. Inside the red-brick buildings framing the leafy quadrangle students listened to lectures on Ellison and Emerson, on Paul Verlaine and the Holy Roman Empire. Few suspected that strains of the organism that causes cholera were growing nearby, in the Life Sciences Building. If they had known, they would probably not have grasped the implications. But these particular strains of cholera make Paul Ewald smile; they are strong evidence that he is on the right track. Knowing the rules of evolutionary biology, he believes, can change the course of infectious disease.

https://www.theatlantic.com/past/docs/issues/99feb/germ2.htm
I HAVE a motto," Gregory Cochran told me recently. "'Big old diseases are infectious.' If it's common, higher than one in a thousand, I get suspicious. And if it's old, if it has been around for a while, I get suspicious."

https://www.theatlantic.com/past/docs/issues/99feb/germ3.htm

Paul W. Ewald: https://en.wikipedia.org/wiki/Paul_W._Ewald

Our initial meta-analysis supported the association of the DRD4 C-521T polymorphism, but not the VNTR polymorphism, with approach-related traits. This conclusion was qualified by evidence of significant publication bias and the failure to detect association in a replication sample comprising individuals at the extremes of the trait distribution. The association of the C-521T polymorphism observed in our initial meta-analysis was robust to the inclusion of these new data, but our revised meta-analysis indicated that the association was present for measures of novelty seeking and impulsivity but not for measures of extraversion.

Meta-analysis of the heterogeneity in association of DRD4 7-repeat allele and AD/HD: stronger association with AD/HD combined type: https://www.ncbi.nlm.nih.gov/pubmed/20468072

Molecular Psychiatry - High prevalence of rare dopamine receptor D4 alleles in children diagnosed with attention-deficit hyperactivity disorder: http://www.nature.com/mp/journal/v8/n5/full/4001350a.html

- "paternal age effect" just a selection effect (men w/ issues end up having kids later due to difficulty finding a mate)
- one other suggested inconsistent explanation: spermatogenic selfish-gene effect
- interesting discussion of sperm freezing

The D4 dopamine receptor (DRD4) locus may be a model system for understanding the relationship between genetic variation and human cultural diversity. It has been the subject of intense interest in psychiatry, because bearers of one variant are at increased risk for attention deficit hyperactivity disorder (ADHD) (1). A survey of world frequencies of DRD4 alleles has shown striking differences among populations (2), with population differences greater than those of most neutral markers. In this issue of PNAS Ding et al. (3) provide a detailed molecular portrait of world diversity at the DRD4 locus. They show that the allele associated with ADHD has increased a lot in frequency within the last few thousands to tens of thousands of years, although it has probably been present in our ancestors for hundreds of thousands or even millions of years.

...

Because the prominent phenotypic effects of 7R are in males, we need to ask what is the niche in human societies for males who are energetic, impulsive (i.e., unpredictable), and noncompliant? Whereas tests of hypotheses ought to be careful and conservative, generation of hypotheses ought to be speculative and free-ranging. There is a tradition of caution approaching self-censorship in discussions of human biological diversity, but we will break that tradition in what follows.

https://twitter.com/whyvert/status/827182543594086400
http://ipsr.berkeley.edu/uploads/department_events/1455839539-b80d181fb169f70b4/Dopamine-system%20genes%20and%20cultural%20acquisition.pdf

I’m recommending this review more strongly than usual because I’ve previously praised Taubes. He did a good job explaining how the pop wisdom of the ’90s – that fat was uniquely bad – wasn’t true. He did a good job showing the ways in which the old “just diet and exercise, nothing can go wrong” idea was simplistic and needed to be replaced with a good understanding of obesity set points. I learned some useful things from his books and I had positive feelings about him.

But from the first time I talked about him almost five years ago, I’ve stressed that his views about sugar are really, really wrong. I was previously willing to excuse this on the grounds that he wrote about a lot of other useful things and everybody’s allowed a bit of crazy speculation once in a while before a field is completely settled. But at this point things seem pretty settled and I no longer think his behavior is excusable. The ’90s are over, the pop wisdom that Taubes set out to debunk is sufficiently debunked, and he’s doubling down on his sugar theory despite an increasing pile of evidence against it.

I apologize if my past praise for Taubes’ writing have helped create a climate where people listen to his theories. His good qualities aren’t enough to justify the increasing amount of misinformation he’s putting out, and I don’t recommend him on any level as a source of nutritional advice.

https://slatestarcodex.com/2017/01/30/link-taubes-contra-guyenet-on-sugar/
https://twitter.com/whsource/status/824673839749623808