Thread by @crimkadid

Jonathan Hutchinson was a Victorian era surgeon who had what some called an obsession with the idea that eating rancid fish was the true cause of leprosy. His 1906 book on the subject is now just a mocked Victorian curio, but I will show you how close he was to the truth.

By 1600 leprosy was extinct in most of Europe. In some places though the disease lingered on, above all in Norway, whose last leper died only in 1946. Medical historians debated for decades “What is it that makes Norwegians so uniquely disgusting?”, which I thought was funny.

“Why Norway?” is a tough question to answer until you see Jonathan Hutchinson’s map from “Leprosy and Fish Eating”, which shows firstly that only West Norwegians suffered from the disease and second that there was a huge concentration of lepers at the famous fishery of Lofoten.

You need to understand: having such a concentration of lepers at Lofoten is like seeing a malaria map where the most dangerous area is marked “Mosquito City”. Hutchinson’s Norwegian correspondent pointed out to him that “leprosy is essentially a disease of the seacoast.”

Hutchinson’s map is too perfect: is it rigged? All indicators are no; the Norwegian discoverer of the leprosy bacterium, Gerhard Hansen, worked as head doctor of the Lofoten fishing fleet, then at the world’s largest leper house in Bergen, then and now Norway's fishing capital.

Interestingly Iceland, colonized by west Norwegians, also continued to suffer from the disease in the early 20th century. According to the Danish Dr. Ehlers, who thought Hutchinson was crazy, it was concentrated "among the fisher folk" of the southwest:

From 1844 to 1937 leprosy experienced a resurgence in two New Brunswick counties. The center of the outbreak was Tracadie, a French Canadian _fishing village_. It's amazing that Hutchinson wasn't carted off to a mental institution like Semmelweis.

Leprosy died hard in all the populations of the Atlantic Norwegian diaspora: the Shetlands were “the last stronghold of indigenous leprosy in Britain”. You might conclude that the disease was genetic (medieval people did) but Norwegians in Minnesota were almost immune to it.

There were four chief strongholds of leprosy in Europe when Hutchinson wrote his book in 1906: West Norway, Iceland, Iberia, and Crete. This map shows seafood consumption in Europe today.

Where was leprosy concentrated in Iberia? The bacterium was comfortable along the ocean for some odd reason, which was the pattern seen most everywhere else on Earth in Hutchinson’s day.

In China

South America (note that things have changed: today leprosy in Brazil is concentrated in the Amazon):

All of Earth c. 1891:

Presently leprosy only thrives in areas backward enough that its symptoms are not quickly treated. Even so, Hutchinson’s observations still seem valid: the highest leprosy detection rates today are in Kiribati and Micronesia, places that also suffer from Ciguatera fish poisoning

Hutchinson was clearly right to connect fish eating and leprosy, but his opponents were able to easily prove that many lepers had never consumed fish. He made two distinct assertions and because the second was proven incorrect, the first was also unjustly rejected.

By attempting to explain the pattern instead of just observing it I risk making the same mistake as Hutchinson but I can’t help myself. My guess, as strange as it sounds, is that fish eating indirectly leads to leprosy because it is _healthy_.

Historians feel the basic question of leprosy’s disappearance has been solved: both tuberculosis and leprosy are caused by a Myobacterium, they provide cross immunity to each other and tuberculosis, being the more contagious disease. tends to win out. From Plagues and Peoples:

Does that mean that if leprosy was common in 19th century Norway that tuberculosis was also rare? Yes and this is true too of Iceland, where TB was rare before 1880. Now instead of asking “Why was leprosy common in Norway?” we can ask “Why was tuberculosis uncommon?”

The argument in "Leprosy and Fish Eating" can be salvaged and its significance greatly increased if the real reason fish consumption seemed to cause leprosy was that it actually protected against competing tuberculosis, a much deadlier disease.

Hutchinson should have at least considered this possibility, because fish oil was an extremely popular 19th century treatment for tuberculosis. This idea was very old, but became broadly known in the Anglosphere after an 1849 study of London consumptives.

The problem with the oil, as its promoters acknowledged, was that it was only effective in the earliest stages of the disease and did not affect established tubercles. When Koch discovered the underlying bacillus in 1882 interest in fish oil as treatment declined.

The important question: do omega-3 fatty acids, protective against inflammation, depression, and schizophrenia, also protect against TB? At bare minimum they do boost serum Vitamin D, which is closely linked to disease risk.

Putting aside the important question of cause, it is incomprehensible to me that almost no one has noticed this association in the last 116 years. Imagine a parallel Earth where scientists were smart enough to cure malaria but not to figure out that it was spread by mosquitoes.