BorisVSchmid

I can imagine that a dominant hypothesis could play a role in the predictions of future trajectories of climate on earth, but not so much for things like measuring past temperature / sea level rise.

To twist the analogy back to Alzheimer - all these scientists still agreed on the patient-level diagnosis of Alzheimer.

Depending on the complexity of the model it would take me at least a month for a single paper. What makes it fully unbelievable to me is the claim of detecting p-value hacking in many of these 130 papers while doing 3 papers every 2 days.

To make that claim for a single paper I would 1. have to be able to reproduce their p-value, and 2. spend enough time with the model to understand how/what assumptions were unfairly tweaked to get to that p-value.

Just running your own implementation of a model on your own dataset and getting an insignificant or different p-value is not enough. You might just have implemented the model wrongly.

Depends on how you mean the question. ancient DNA analysis has settled that the first two plague pandemics were Yersinia pestis, so if your question was on what kind of bacterium caused the Black Death - that is Yersinia pestis.

If it is about the manifestation of the disease (the clinical symptoms), those we only know from historical descriptions and that is not something a model can change :-). So yeah, many infected people would still have had buboes. Buboes are also the expected result from plague acquired from fleas (whether they were human fleas or rat fleas).

What might be less known is that there is a pretty high chance (10-20%) that a person suffering from bubonic plague progresses to pneumonic plague. That basically is a death warrant for that person, but it also means that he/she might spread the disease further through air-droplets. If the conditions are right, you might get a pneumonic plague epidemic intermingled with a bubonic plague epidemic. Model-wise, that is one scenario we haven't looked into, but we have seen something like that play out in Madagascar last year.

Potentially, but I am a bit sceptical. Plague reached a lot of new territory during the third pandemic (for example, australia and the americas), while still having a low mortality. One could check whether native populations to those continents were especially hard hit compared to people from European descent. I haven't heard anything like that.

There were indeed hundreds of outbreaks during those centuries. The outbreaks we selected were the ones for which we could find daily or weekly mortality records, as that gives you an epidemic curve that you can fit mathematical model to.

We didn't use all of the cities for which we had outbreaks, but selected nine that covered a large part of the time period, and a large geographic region. Here is the list:

Givry, France, 1348. Florence, Italy, 1400. Barcelona, Spain, 1490. London, England, 1563-1564. Eyam, England, 1666. Gdansk, Poland, 1709. Stockholm, Sweden, 1710-1711. Moscow, Russia, 1771. Malta, Malta, 1813.

Not a bad first impulse :-). It often pays in science to wait a few years/follow-up studies before fully accepting something. What is thought to be true in plague is especially fluid now with ancient DNA studies on human remains coming out regularly, each with its own narrative on how to explain the phylogenetic tree.

That said, there are some long-standing questions in plague research, one of which is why the first and second plague pandemic were that much more lethal than the third plague pandemic. Prior to the aDNA work, people speculated that medieval plague was a different pathogen altogether, but that hypothesis has been put to rest now. An alternative theory has been that plague could spread through human ectoparasites, and we found a novel way to test that theory. That resulted in this paper.

The 2017 madagascar one might actually have been a combination of rats and pneumonic plague. But yeah, it is good to pay attention to all possible routes of transmission and see where you can intervene.