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Plague of Frogs | West Hunter
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.
west-hunter  scitariat  reflection  stories  troll  lol  science  low-hanging  occam  parsimony  bio  medicine  meta:medicine  ability-competence  explanans  disease  parasites-microbiome  spreading  world  nature  environment  climate-change  hypochondria  academia  questions  epidemiology  incentives  interests 
february 2018 by nhaliday
All models are wrong - Wikipedia
Box repeated the aphorism in a paper that was published in the proceedings of a 1978 statistics workshop.[2] The paper contains a section entitled "All models are wrong but some are useful". The section is copied below.

Now it would be very remarkable if any system existing in the real world could be exactly represented by any simple model. However, cunningly chosen parsimonious models often do provide remarkably useful approximations. For example, the law PV = RT relating pressure P, volume V and temperature T of an "ideal" gas via a constant R is not exactly true for any real gas, but it frequently provides a useful approximation and furthermore its structure is informative since it springs from a physical view of the behavior of gas molecules.

For such a model there is no need to ask the question "Is the model true?". If "truth" is to be the "whole truth" the answer must be "No". The only question of interest is "Is the model illuminating and useful?".
thinking  metabuch  metameta  map-territory  models  accuracy  wire-guided  truth  philosophy  stats  data-science  methodology  lens  wiki  reference  complex-systems  occam  parsimony  science  nibble  hi-order-bits  info-dynamics  the-trenches  meta:science  physics  fluid  thermo  stat-mech  applicability-prereqs  theory-practice 
august 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.

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.

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

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.
west-hunter  scitariat  discussion  ideas  speculation  critique  disease  parasites-microbiome  usa  age-of-discovery  europe  embodied  history  early-modern  multi  spreading  random  counterfactual  🌞  occam  parsimony  archaeology  cost-benefit  india  asia  africa  agriculture  uncertainty  outcome-risk  red-queen  epidemiology  thick-thin  pdf  piracy  study  article  survey  iron-age  the-classics  mediterranean  novelty  poast 
may 2017 by nhaliday
10 Occam’s Workouts done – Occam’s Protocol Results | Four Hour Body Couple
"To say that I’m happy with the results so far would be an understatement. To reiterate – this is 5 hours in the gym, total."
Tim  Ferriss  Occam  Protocol  review  results 
march 2017 by dandv
The language of geometry: Fast comprehension of geometrical primitives and rules in human adults and preschoolers
The child’s acquisition of language has been suggested to rely on the ability to build hierarchically structured representations from sequential inputs. Does a similar mechanism also underlie the acquisition of geometrical rules? Here, we introduce a learning situation in which human participants had to grasp simple spatial sequences and try to predict the next location. Sequences were generated according to a “geometrical language” endowed with simple primitives of symmetries and rotations, and combinatorial rules. Analyses of error rates of various populations—a group of French educated adults, two groups of 5 years-old French children, and a rare group of teenagers and adults from an Amazonian population, the Mundurukus, who have limited access to formal schooling and a reduced geometrical lexicon—revealed that subjects’ learning indeed rests on internal language-like representations. A theoretical model, based on minimum description length, proved to fit well participants’ behavior, suggesting that human subjects “compress” spatial sequences into a minimal internal rule or program.
study  psychology  cog-psych  visuo  spatial  structure  neurons  occam  computation  models  eden  intelligence  neuro  learning  language  psych-architecture  🌞  retrofit 
february 2017 by nhaliday
Information Processing: Epistasis vs additivity
On epistasis: why it is unimportant in polygenic directional selection: http://rstb.royalsocietypublishing.org/content/365/1544/1241.short
- James F. Crow

The Evolution of Multilocus Systems Under Weak Selection: http://www.genetics.org/content/genetics/134/2/627.full.pdf
- Thomas Nagylaki

Data and Theory Point to Mainly Additive Genetic Variance for Complex Traits: http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1000008
The relative proportion of additive and non-additive variation for complex traits is important in evolutionary biology, medicine, and agriculture. We address a long-standing controversy and paradox about the contribution of non-additive genetic variation, namely that knowledge about biological pathways and gene networks imply that epistasis is important. Yet empirical data across a range of traits and species imply that most genetic variance is additive. We evaluate the evidence from empirical studies of genetic variance components and find that additive variance typically accounts for over half, and often close to 100%, of the total genetic variance. We present new theoretical results, based upon the distribution of allele frequencies under neutral and other population genetic models, that show why this is the case even if there are non-additive effects at the level of gene action. We conclude that interactions at the level of genes are not likely to generate much interaction at the level of variance.
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february 2017 by nhaliday

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