nhaliday + red-queen   32

Why Sex? And why only in Pairs? - Marginal REVOLUTION
The core conclusion is that mutations continue to rise with the number of sex-participating partners, but in simple Red Queen models the limiting features of the genotypes is the same whether there are two, three, or more partners.

Men Are Animals: http://www.overcomingbias.com/2018/06/men-are-animals.html
I agree with all the comments citing motility/sessility.
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january 2018 by nhaliday
Bouncing Off the Bottom | West Hunter
Actually going extinct would seem to be a bad thing, but a close call can, in principle, be a good thing.

Pathogens can be a heavy burden on a species, worse than a 50-lb sack of cement. Lifting that burden can have a big effect: we know that many species flourish madly once they escape their typical parasites. That’s often the case with invasive species. It’s also a major strategy in agriculture: crops often do best in a country far away from their place of origin – where the climate is familiar, but most parasites have been left behind. For example, rubber trees originated in South America, but they’re a lot easier to grow in Liberia or Malaysia.

Consider a situation with a really burdensome pathogen – one that specializes in and depends on a single host species. That pathogen has to find new host individuals every so often in order to survive, and in order for that to happen, the host population has to exceed a certain number, usually called the critical community size. That size depends on the parasite’s persistence and mode of propagation: it can vary over a huge range. CCS is something like a quarter of a million for measles, ~300 for chickenpox, surely smaller than that for Epstein-Barr.

A brush with extinction- say from an asteroid strike – might well take a species below the CCS for a number of its pathogens. If those pathogens were limited to that species, they’d go extinct: no more burden. That alone might be enough to generate a rapid recovery from the population bottleneck. Or a single, highly virulent pathogen might cause a population crash that resulted in the extinction of several of that species’s major pathogens – quite possibly including the virulent pathogen itself. It’s a bottleneck in time, rather than one in space as you often see in colonization.

Such positive effects could last a long time – things need not go back to the old normal. The flea-unbitten species might be able to survive and prosper in ecological niches that it couldn’t before. You might see a range expansion. New evolutionary paths could open up. That brush with extinction could be the making of them.

When you add it all up, you begin to wonder if a population crash isn’t just what the doctor ordered. Sure, it wouldn’t be fun to be one of the billions of casualties, but just think how much better off the billions living after the bottleneck will be. Don’t be selfish.
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november 2017 by nhaliday
Darwinian medicine - Randolph Nesse
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
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november 2017 by nhaliday
Of Mice and Men | West Hunter
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.
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september 2017 by nhaliday
Mechanisms of microbial traversal of the blood–brain barrier
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/
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september 2017 by nhaliday
Alzheimers | West Hunter
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
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july 2017 by nhaliday
Defection – quas lacrimas peperere minoribus nostris!
https://quaslacrimas.wordpress.com/2017/06/28/discussion-of-defection/

Kindness Against The Grain: https://srconstantin.wordpress.com/2017/06/08/kindness-against-the-grain/
I’ve heard from a number of secular-ish sources (Carse, Girard, Arendt) that the essential contribution of Christianity to human thought is the concept of forgiveness. (Ribbonfarm also has a recent post on the topic of forgiveness.)

I have never been a Christian and haven’t even read all of the New Testament, so I’ll leave it to commenters to recommend Christian sources on the topic.

What I want to explore is the notion of kindness without a smooth incentive gradient.

The Social Module: https://bloodyshovel.wordpress.com/2015/10/09/the-social-module/
Now one could propose that the basic principle of human behavior is to raise the SP number. Sure there’s survival and reproduction. Most people would forget all their socialization if left hungry and thirsty for days in the jungle. But more often than not, survival and reproduction depend on being high status; having a good name among your peers is the best way to get food, housing and hot mates.

The way to raise one’s SP number depends on thousands of different factors. We could grab most of them and call them “culture”. In China having 20 teenage mistresses as an old man raises your SP; in Western polite society it is social death. In the West making a fuss about disobeying one’s parents raises your SP, everywhere else it lowers it a great deal. People know that; which is why bureaucrats in China go to great lengths to acquire a stash of young women (who they seldom have time to actually enjoy), while teenagers in the West go to great lengths to be annoying to their parents for no good reason.

...

It thus shouldn’t surprise us that something as completely absurd as Progressivism is the law of the land in most of the world today, even though it denies obvious reality. It is not the case that most people know that progressive points are all bogus, but obey because of fear or cowardice. No, an average human brain has much more neurons being used to scan the social climate and see how SP are allotted, than neurons being used to analyze patterns in reality to ascertain the truth. Surely your brain does care a great deal about truth in some very narrow areas of concern to you. Remember Conquest’s first law: Everybody is Conservative about what he knows best. You have to know the truth about what you do, if you are to do it effectively.

But you don’t really care about truth anywhere else. And why would you? It takes time and effort you can’t really spare, and it’s not really necessary. As long as you have some area of specialization where you can make a living, all the rest you must do to achieve survival and reproduction is to raise your SP so you don’t get killed and your guts sacrificed to the mountain spirits.

SP theory (I accept suggestions for a better name) can also explains the behavior of leftists. Many conservatives of a medium level of enlightenment point out the paradox that leftists historically have held completely different ideas. Leftism used to be about the livelihood of industrial workers, now they agitate about the environment, or feminism, or foreigners. Some people would say that’s just historical change, or pull a No True Scotsman about this or that group not being really leftists. But that’s transparent bullshit; very often we see a single person shifting from agitating about Communism and worker rights, to agitate about global warming or rape culture.

...

The leftist strategy could be defined as “psychopathic SP maximization”. Leftists attempt to destroy social equilibrium so that they can raise their SP number. If humans are, in a sense, programmed to constantly raise their status, well high status people by definition can’t raise it anymore (though they can squabble against each other for marginal gains), their best strategy is to freeze society in place so that they can enjoy their superiority. High status people by definition have power, and thus social hierarchy during human history tends to be quite stable.

This goes against the interests of many. First of all the lower status people, who, well, want to raise their status, but can’t manage to do so. And it also goes against the interests of the particularly annoying members of the upper class who want to raise their status on the margin. Conservative people can be defined as those who, no matter the absolute level, are in general happy with it. This doesn’t mean they don’t want higher status (by definition all humans do), but the output of other brain modules may conclude that attempts to raise SP might threaten one’s survival and reproduction; or just that the chances of raising one’s individual SP is hopeless, so one might as well stay put.

...

You can’t blame people for being logically inconsistent; because they can’t possibly know anything about all these issues. Few have any experience or knowledge about evolution and human races, or about the history of black people to make an informed judgment on HBD. Few have time to learn about sex differences, and stuff like the climate is as close to unknowable as there is. Opinions about anything but a very narrow area of expertise are always output of your SP module, not any judgment of fact. People don’t know the facts. And even when they know; I mean most people have enough experience with sex differences and black dysfunction to be quite confident that progressive ideas are false. But you can never be sure. As Hume said, the laws of physics are a judgment of habit; who is to say that a genie isn’t going to change all you know the next morning? At any rate, you’re always better off toeing the line, following the conventional wisdom, and keeping your dear SP. Perhaps you can even raise them a bit. And that is very nice. It is niceness itself.

Leftism is just an easy excuse: https://bloodyshovel.wordpress.com/2015/03/01/leftism-is-just-an-easy-excuse/
Unless you’re not the only defector. You need a way to signal your intention to defect, so that other disloyal fucks such as yourself (and they’re bound to be others) can join up, thus reducing the likely costs of defection. The way to signal your intention to defect is to come up with a good excuse. A good excuse to be disloyal becomes a rallying point through which other defectors can coordinate and cover their asses so that the ruling coalition doesn’t punish them. What is a good excuse?

Leftism is a great excuse. Claiming that the ruling coalition isn’t leftist enough, isn’t holy enough, not inclusive enough of women, of blacks, of gays, or gorillas, of pedophiles, of murderous Salafists, is the perfect way of signalling your disloyalty towards the existing power coalition. By using the existing ideology and pushing its logic just a little bit, you ensure that the powerful can’t punish you. At least not openly. And if you’re lucky, the mass of disloyal fucks in the ruling coalition might join your banner, and use your exact leftist point to jump ship and outflank the powerful.

...

The same dynamic fuels the flattery inflation one sees in monarchical or dictatorial systems. In Mao China, if you want to defect, you claim to love Mao more than your boss. In Nazi Germany, you proclaim your love for Hitler and the great insight of his plan to take Stalingrad. In the Roman Empire, you claimed that Caesar is a God, son of Hercules, and those who deny it are treacherous bastards. In Ancient Persia you loudly proclaimed your faith in the Shah being the brother of the Sun and the Moon and King of all Kings on Earth. In Reformation Europe you proclaimed that you have discovered something new in the Bible and everybody else is damned to hell. Predestined by God!

...

And again: the precise content of the ideological point doesn’t matter. Your human brain doesn’t care about ideology. Humans didn’t evolve to care about Marxist theory of class struggle, or about LGBTQWERTY theories of social identity. You just don’t know what it means. It’s all abstract points you’ve been told in a classroom. It doesn’t actually compute. Nothing that anybody ever said in a political debate ever made any actual, concrete sense to a human being.

So why do we care so much about politics? What’s the point of ideology? Ideology is just the water you swim in. It is a structured database of excuses, to be used to signal your allegiance or defection to the existing ruling coalition. Ideology is just the feed of the rationalization Hamster that runs incessantly in that corner of your brain. But it is immaterial, and in most cases actually inaccessible to the logical modules in your brain.

Nobody ever acts on their overt ideological claims if they can get away with it. Liberals proclaim their faith in the potential of black children while clustering in all white suburbs. Communist party members loudly talk about the proletariat while being hedonistic spenders. Al Gore talks about Global Warming while living in a lavish mansion. Cognitive dissonance, you say? No; those cognitive systems are not connected in the first place.

...

And so, every little step in the way, power-seekers moved the consensus to the left. And open societies, democratic systems are by their decentralized nature, and by the size of their constituencies, much more vulnerable to this sort of signalling attacks. It is but impossible to appraise and enforce the loyalty of every single individual involved in a modern state. There’s too many of them. A Medieval King had a better chance of it; hence the slow movement of ideological innovation in those days. But the bigger the organization, the harder it is to gather accurate information of the loyalty of the whole coalition; and hence the ideological movement accelerates. And there is no stopping it.

Like the Ancients, We Have Gods. They’ll Get Greater: http://www.overcomingbias.com/2018/04/like-the-ancients-we-have-gods-they-may-get… [more]
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june 2017 by nhaliday
Rheumatoid Arthritis | West Hunter
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.cc/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.
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may 2017 by nhaliday
In a handbasket | West Hunter
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.
west-hunter  scitariat  history  iron-age  medieval  early-modern  discussion  europe  civilization  technology  innovation  agriculture  energy-resources  disease  parasites-microbiome  recent-selection  lived-experience  multi  mediterranean  the-classics  economics  usa  age-of-discovery  poast  aphorism  latin-america  farmers-and-foragers  cultural-dynamics  social-norms  culture  wealth-of-nations  twitter  social  commentary  quotes  anthropology  nihil  martial  nietzschean  embodied  ritual  wiki  reference  ethnography  flux-stasis  language  jargon  foreign-lang  population  density  speculation  ideas  war  meta:war  military  red-queen  strategy  epidemiology  public-health  trends  zeitgeist  archaeology  novelty  spreading  cost-benefit  conquest-empire  malthus  pre-ww2  the-south  applicability-prereqs 
april 2017 by nhaliday
Evolution of Virulence | West Hunter
Once upon a time, I thought a lot about evolution and pathogens. I still do, on occasion.

It used to be the case [and still is] that many biologists thought that natural selection would inevitably tend towards a situation in which pathogens did infinitesimal harm to their host. This despite the epidemics all around them. I remember reading a book on parasitology in which the gormless author mentioned a certain species of parasitic copepod that routinely blinded the fish they attached to. He said that many a naive grad student would think that that these parasitic copepods were bad for the fish, but sophisticated evolutionists like himself knew (and would explain to the newbies) that of course the fish didn’t suffer any reduction in fitness by going blind – theory said so ! Clearly, that man had a Ph.D.

If a pathogen can gain increased reproduction by tapping host resources, or by doing any damn thing that helps itself and hurts the host, that tactic may pay, and be selected for. It depends on the balance between the advantages and costs – almost entirely those to the pathogen, since the pathogen evolves much more rapidly than the host. In some cases, as much as a million times faster – because of generations that may be 20 minutes long rather than 20 years, because pathogens often have very large populations, which favors Fisherian acceleration, and in many cases, a relatively high mutation rate. Pathogen evolution is, at least some cases, so rapid that you see significant evolutionary change within a single host. Along the same lines, we have seen very significant evolutionary changes in antibiotic resistance among pathogenic bacteria over the past few decades, but I’m pretty sure that there hasn’t been much evolutionary change in mankind since I was a kid.

So when analyzing virulence, people mostly consider evolutionary pressures on the pathogens, rather than the host. Something like the Born-Oppenheimer approximation.
west-hunter  bio  disease  parasites-microbiome  red-queen  thinking  incentives  evolution  🌞  deep-materialism  discussion  mutation  selection  time  immune  scitariat  maxim-gun  cooperate-defect  ideas  anthropic  is-ought  gender  gender-diff  scale  magnitude  stylized-facts  approximation  analogy  comparison  pro-rata 
april 2017 by nhaliday
INFECTIOUS CAUSATION OF DISEASE: AN EVOLUTIONARY PERSPECTIVE
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
pdf  study  speculation  bio  evolution  sapiens  parasites-microbiome  red-queen  disease  west-hunter  🌞  unit  nibble  len:long  biodet  EGT  wild-ideas  big-picture  epidemiology  deep-materialism  🔬  spearhead  scitariat  maxim-gun  ideas  lens  heterodox  darwinian  equilibrium  medicine  heuristic  spreading  article  psychiatry  QTL  distribution  behavioral-gen  genetics  population-genetics  missing-heritability  gender  sex  sexuality  cardio  track-record  aging  popsci  natural-experiment  japan  asia  meta:medicine  profile  ability-competence  empirical  theory-practice  data  magnitude  scale  cost-benefit  is-ought  occam  parsimony  stress  GWAS  roots  explanans  embodied  obesity  geography  canada  britain  anglo  trivia  cocktail  shift  aphorism  stylized-facts  evidence  inference 
february 2017 by nhaliday
Evolution of Resistance Against CRISPR/Cas9 Gene Drive | Genetics
CRISPR/Cas9 gene drive (CGD) promises to be a highly adaptable approach for spreading genetically engineered alleles throughout a species, even if those alleles impair reproductive success. CGD has been shown to be effective in laboratory crosses of insects, yet it remains unclear to what extent potential resistance mechanisms will affect the dynamics of this process in large natural populations. Here we develop a comprehensive population genetic framework for modeling CGD dynamics, which incorporates potential resistance mechanisms as well as random genetic drift. Using this framework, we calculate the probability that resistance against CGD evolves from standing genetic variation, de novo mutation of wild-type alleles, or cleavage repair by nonhomologous end joining (NHEJ)—a likely by-product of CGD itself. We show that resistance to standard CGD approaches should evolve almost inevitably in most natural populations, unless repair of CGD-induced cleavage via NHEJ can be effectively suppressed, or resistance costs are on par with those of the driver. The key factor determining the probability that resistance evolves is the overall rate at which resistance alleles arise at the population level by mutation or NHEJ. By contrast, the conversion efficiency of the driver, its fitness cost, and its introduction frequency have only minor impact. Our results shed light on strategies that could facilitate the engineering of drivers with lower resistance potential, and motivate the possibility to embrace resistance as a possible mechanism for controlling a CGD approach. This study highlights the need for careful modeling of the population dynamics of CGD prior to the actual release of a driver construct into the wild.
study  org:nat  bio  genetics  evolution  population-genetics  models  CRISPR  unintended-consequences  geoengineering  mutation  risk  parasites-microbiome  threat-modeling  selfish-gene  cooperate-defect  red-queen 
february 2017 by nhaliday
The Evolutionary Genetics of Personality Revisited
While mutations clearly affect the very low end of the intelligence continuum, individual differences in the normal intelligence range seem to be surprisingly robust against mutations, suggesting that they might have been canalized to withstand such perturbations. Most personality traits, by contrast, seem to be neither neutral to selection nor under consistent directional or stabilizing selection. Instead evidence is in line with balancing selection acting on personality traits, likely supported by human tendencies to seek out, construct and adapt to fitting environments.

shorter copy: http://www.larspenke.eu/pdfs/Penke_&_Jokela_2016_-_Evolutionary_Genetics_of_Personality_Revisited.pdf

The Evolutionary Genetics of Personality: http://www.larspenke.eu/pdfs/Penke_et_al_2007_-_Evolutionary_genetics_of_personality_target.pdf
Based on evolutionary genetic theory and empirical results from behaviour genetics and personality psychology, we conclude that selective neutrality is largely irrelevant, that mutation-selection balance seems best at explaining genetic variance in intelligence, and that balancing selection by environmental heterogeneity seems best at explaining genetic variance in personality traits. We propose a general model of heritable personality differences that conceptualises intelligence as fitness components and personality traits as individual reaction norms of genotypes across environments, with different fitness consequences in different environmental niches. We also discuss the place of mental health in the model.
study  spearhead  models  genetics  iq  personality  🌞  evopsych  evolution  sapiens  eden  pdf  explanation  survey  population-genetics  red-queen  metabuch  multi  EEA  essay  equilibrium  robust  big-picture  biodet  unit  QTL  len:long  sensitivity  perturbation  roots  EGT  deep-materialism  s:*  behavioral-gen  chart  intelligence  article  speculation  psychology  cog-psych  state-of-art 
december 2016 by nhaliday
The Membrane – spottedtoad
All of which is to say that the Internet, which shares many qualities in common with an assemblage of living things except for those clear boundaries and defenses, might well not trend toward increased usability or easier exchange of information over the longer term, even if that is what we have experienced heretofore. The history of evolution is every bit as much a history of parasitism and counterparasitism as it is any kind of story of upward movement toward greater complexity or order. There is no reason to think that we (and still less national or political entities) will necessarily experience technology as a means of enablement and Cool Stuff We Can Do rather than a perpetual set of defenses against scammers of our money and attention. There’s the respect that makes Fake News the news that matters forever more.

THE MADCOM FUTURE: http://www.atlanticcouncil.org/images/publications/The_MADCOM_Future_RW_0926.pdf
HOW ARTIFICIAL INTELLIGENCE WILL ENHANCE COMPUTATIONAL PROPAGANDA, REPROGRAM HUMAN CULTURE, AND THREATEN DEMOCRACY... AND WHAT CAN BE DONE ABOUT IT.

https://twitter.com/toad_spotted/status/984065056437653505
https://archive.is/fZLyb
ai robocalls/phonetrees/Indian Ocean call centers~biologicalization of corporations thru automation&global com tech

fly-by-night scams double mitotically,covered by outer membrane slime&peptidoglycan

trillion $ corps w/nonspecific skin/neutrophils/specific B/T cells against YOU
ratty  unaffiliated  contrarianism  walls  internet  hacker  risk  futurism  speculation  wonkish  chart  red-queen  parasites-microbiome  analogy  prediction  unintended-consequences  security  open-closed  multi  pdf  white-paper  propaganda  ai  offense-defense  ecology  cybernetics  pessimism  twitter  social  discussion  backup  bio  automation  cooperate-defect  coordination  attention  crypto  money  corporation  accelerationism  threat-modeling  alignment 
december 2016 by nhaliday
The Life-Span of Empires
empires die but don't age

The author examined the distribution of imperial lifetimes using a data set that spans more than three millennia and found that it conforms to a memoryless exponential distribution in which the rate of collapse of an empire is independent of its age.

same is true for species apparently
but it's a power law for larger taxa
pdf  study  history  anthropology  civilization  risk  aphorism  regularizer  objektbuch  distribution  stylized-facts  economics  cliometrics  cycles  red-queen  competition  iron-age  mediterranean  new-religion  the-classics  gibbon  leviathan  nihil  cultural-dynamics  great-powers  time  longevity  conquest-empire  multiplicative  power-law  hari-seldon 
december 2016 by nhaliday
Diamond on domestication | West Hunter
Jared Diamond, in discussing animal domestication, claims that the local availability of species with the right qualities for domestication was key, rather than anything special about the biology or culture of the humans living there. In some cases that may be true: there aren’t many large mammals left in Australia, and they’re all marsupials anyway. Stupid marsupials. He claims that since Africans and Amerindians were happy to adopt Eurasian domesticated animals when they became available, it must be that that suitable local animals just didn’t exist. But that’s a non sequitur: making use of an already-domesticated species is not at all the same thing as the original act of domestication. That’s like equating using a cell phone with inventing one. He also says that people have had only mixed success in recent domestication attempts – but the big problem there is that a newly domesticated species doesn’t just have to be good, it has to be better than already-existing domestic animals.

...

In fact, in my mind the real question is not why various peoples didn’t domesticate animals that we know were domesticable, but rather how anyone ever managed to domesticate the aurochs. At least twice. Imagine a longhorn on roids: they were big and aggressive, favorites in the Roman arena.

Let me throw out an idea originated by an old friend, Ivy Smith. Consider mice, cats, and toxoplasma. Toxoplasma is a protozoan with a two stage life cycle: one in an intermediate host (mice and rats, among others) and a definitive host (some feline). Toxoplasma only reproduces sexually in the definitive host, and it ‘wants’ to end up there. It manipulates the behavior of the intermediate host in ways that increase the probability of transmission to the definitive host. For one thing, it makes mice like the smell of cat urine, which elicits fear in uninfected mice. In fact, it seems that toxoplasma-infected mice are sexually excited by cat urine. How weird – a parasite rechanneling sexual interest…

The idea is that at least some individual aurochs were not as hostile and fearful of humans as they ought to have been, because they were being manipulated by some parasite. The parasite might have caused a general reduction of fear or aggression without infecting or aiming at humans – or, maybe, humans really were the definitive host, and the parasite knew exactly what it was doing. The beef tape worm – which we originally acquired from lions or hyenas back in Africa a couple of million years ago – might have gained from making infected bovines quiet, passive, maybe even overly friendly in the presence of humans. This would have made domestication a hell of a lot easier.

Parenthetically, such host manipulation may play a really important ecological role. For all we know, if canids and felids had to rely purely on their own abilities, they’d starve.

The beef tape worm may not have made it through Beringia. More generally, there were probably no parasites in the Americas that had some large mammal as intermediate host and Amerindians as the traditional definite host. Amerindians simply hadn’t been there very long. Domesticating bison may have too hard for unaided humans, back in the day.

https://westhunt.wordpress.com/2017/08/02/i-will-reread-and-review-jared-diamonds-book-guns-germs-and-steel/
https://westhunt.wordpress.com/category/ggs/
https://westhunt.wordpress.com/2017/08/03/why-the-aurochs-could-not-be-domesticated/
https://westhunt.wordpress.com/2017/08/04/buffalo-gourds-and-josephson-junctions/
Every technique is in competition with rival techniques. This inhibits the development of new techniques, even if they have high potential in the long run. To succeed, they have to beat out existing techniques in the short run.

For example, there are potential advantages for superconducting electronics for computing, but CMOS keeps improving. It’s a moving target: it’s not enough to be good, or interesting, you have to be better. Soon, not in 50 years. This is particularly difficult considering the enormous amount of resources currently invested in improving semiconductor computing technology.

In the same way, one successful domestication tends to inhibit other domestications. Several crops were domesticated in the eastern United States, but with the advent of maize and beans, most were abandoned. Maybe if those Amerindians had continued to selectively breed sumpweed for a few thousand years, it would have been competitive: but nobody is that crazy. Pretty crazy, but not that crazy.

https://westhunt.wordpress.com/2013/08/26/the-masters-of-the-future/
In Guns, Germs, and Steel, Jared Diamond argues that all human groups have equal mental capabilities – except for the inhabitants of New Guinea, who are clearly smarter than the human norm.

If this is the case, there’s money to be made. Good performance in a lot of high-paying jobs requires intelligence above some fairly high threshold. Such people are scarce [outside of New Guinea], and that means that their labor is expensive. The fraction of individuals above a high threshold increases dramatically with a higher mean, and since people in PNG don’t have high incomes, there is a fantastic arbitrage opportunity here. You could locate some of the many geniuses that must exist in PNG, rapidly and inexpensively teach them high-tech skills (which they would learn easily, since they’re geniuses, natch), apply for H1B visas, and them resell them to the highest Silicon Valley bidder. This wouldn’t last, of course – these guys would not stay peons forever. They’d be generating their own start-ups in a few years, founding hedge funds, dominating the Vegas poker tournaments, etc. Some, less materialistic, would become grandmasters, win Fields medals, or write seminal books about the attractions of cannibalism. Still, you could make a lot of money in the short run, and if you were careful to build good relationships with your employees, they might let you in on the ground floor of an IPO later.

Poul Anderson, always a visionary, foresaw this. A character in one his books put it thusly:” I am a racist – a dedicated, fanatical racist – who maintains, and can scientifically prove, that his own race is inferior. The only true humans on earth, my friends, the main line of evolution, the masters of the future, are the lordly Melanesians. ”

Of course that character was feigning insanity, but still.

https://westhunt.wordpress.com/2014/12/04/world-without-stars/#comment-63613
https://westhunt.wordpress.com/2017/08/08/png-data/
PNG = Papua New Guinea
https://westhunt.wordpress.com/2017/08/14/png-uber-alles/
https://westhunt.wordpress.com/2017/08/16/persistence/
https://westhunt.wordpress.com/2017/08/18/something-changed/
https://westhunt.wordpress.com/2017/08/21/psychometrics/
https://westhunt.wordpress.com/2017/08/22/regional-change/
https://westhunt.wordpress.com/2017/08/26/domesticated-animals-and-human-disease/
https://westhunt.wordpress.com/2017/08/29/not-without-honor/

final review:
Guns, Germs, and Steel revisited: https://westhunt.wordpress.com/2017/09/04/guns-germs-and-steel-revisited/

https://westhunt.wordpress.com/2017/09/04/guns-germs-and-steel-revisited/#comment-95596
He never says he was willing to wave the point, so how do you know that?

Next, europeans and Chinese ( northeast Asians) test smarter than anyone else. Noticeably so. And they act it, more or less. kinda sorta. More complicated mistakes.

https://westhunt.wordpress.com/2017/09/04/guns-germs-and-steel-revisited/#comment-95761
lower genetic diversity in Amerindians+possibility that fast mutating viruses might adapt to their host and hit relatives harder
west-hunter  technology  antiquity  sapiens  nature  speculation  parasites-microbiome  🌞  farmers-and-foragers  domestication  scitariat  ideas  questions  toxo-gondii  multi  books  review  critique  africa  agriculture  agri-mindset  long-short-run  incentives  info-dynamics  group-selection  gwern  india  asia  red-queen  pop-diff  poast  aphorism  developing-world  oceans  arbitrage  race  scifi-fantasy  psychometrics  psychology  cog-psych  iq  intelligence  psych-architecture  paying-rent  realness  disease  scale  civilization  population  density  prudence  marginal  novelty  earth  direction  geography  path-dependence  china  europe  immune  spreading  diversity  galor-like  genetics  genomics  alt-inst  competition  capitalism  cost-benefit  tradeoffs  big-peeps  sex  sexuality 
november 2016 by nhaliday
Genetic Ancestry and Natural Selection Drive Population Differences in Immune Responses to Pathogens: Cell
Skin Deep: https://westhunt.wordpress.com/2016/10/30/skin-deep/
There are a couple of new papers out in Cell about demonstrated immunological differences between Africans and Europeans. We already knew that the course of various infectious diseases can be quite different in people from those two different races, while autoimmune risks are also different (lupus for example is considerably more common in blacks). Researchers found that inflammatory responses were considerably stronger in Africans than Europeans. African macrophages zapped bacteria three times faster than European macrophages.

I wonder if this increased inflammatory tendency is behind the increased risk for sarcoidosis in blacks (12-fold higher death rate). If so, maybe you could help the clinical course by damping down inflammation.

The African pattern almost certainly worked better in Africa (chock-full o’ of pathogens, including many adapted to man or close relatives), while the European pattern worked better outside of Africa – on the whole cooler and less of a microbial playpen.

Henry and I, along with others, put out a paper on this subject a few years ago.

Some of the milder-inflammation alleles in Europeans originated in Neanderthals. Logical, since they too had adapted to the lower pathogen load in ice-age Europe and Central Asia. This probably meant that Neanderthals couldn’t have returned to Africa.

This is all impossible if race does not exist, or if Lewontin had had anything to valid to say on the subject. Of course race does exist, while Lewontin is a fountain of nonsense.
study  bio  disease  sapiens  comparison  org:nat  recent-selection  immune  red-queen  parasites-microbiome  pop-structure  pop-diff  multi  west-hunter  scitariat  race  africa  farmers-and-foragers  usa  europe  commentary  summary  conceptual-vocab  realness  definition  philosophy 
october 2016 by nhaliday
52 Concepts You Missed in School for your Cognitive Toolkit | Peter McIntyres
idk about the actual quality of these but the idea of cataloguing useful mental models/biases is nice

his description of Aumann's agreement theorem seems to be incorrect/miss the point
idk  rationality  thinking  psychology  metabuch  list  top-n  models  conceptual-vocab  skeleton  pareto  occam  mood-affiliation  fermi  red-queen  schelling  revealed-preference  GT-101  counterfactual  marginal  signaling  local-global  regression-to-mean  chart 
january 2016 by nhaliday

bundles : patterns

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