Rye has the unique potential to be infected with a parasitic fungus, Claviceps purpurea, that produces a human toxin called ergotamine. When ingested via, say, a loaf of rye bread, it exerts a range of hallucinogenic effects on humans, partly because it is converted to lysergic acid diethylamide, commonly known as LSD.
History is filled with fascinating and terrifying stories of humans exposed to rye and ergotamine. Because some victims afflicted with contaminated rye experienced an intense dermatitis (skin inflammation), the condition became known as St. Anthony’s Fire, named after the early 11th-century sanctuary operated by monks to treat victims of ergot poisoning. During the Middle Ages, writers described hysterical outbursts afflicting previously normal people, including thrashing and writhing while shouting, “I’m burning!” The afflicted would eventually collapse, after which their bodies would blacken. And at least one observer has ascribed the madness of the Salem witch trials to ergotamine poisoning after determining that many of the 19 young women accused of being witches lived near a rye field. A “witch cake” made of rye flour was fed to a dog to confirm a “bewitching” effect. The rye itself was, of course, entirely innocent, since it was the common parasitic infestation of the grass that was to blame. But, as with so many other matters surrounding the relationship between the seeds of grasses and the hapless humans who try to consume them, it should come as no surprise that it is a relationship fraught with danger.
The history of rye consumption dates back to the early days of wheat consumption, when humans first experimented with consuming einkorn (the ancient predecessor of modern wheat). Rye, was another grass that grew as a weed in fields of wheat. This is a prefect example of Vavilovian mimicry, or the ability of a weed to mimic a cultivated plant. This weed came to be recognized by humans as yet another seed of a grass that could be consumed, and farmers often harvested both wheat and rye with the same sickle or thresher without bothering to separate them. Rye has gained some blessings in nutritional circles because compared to wheat, it has less potential to trigger insulin, despite identical potential for raising blood sugar.
Rye and wheat share a high content of gliadin protein, with all its potentially toxic effects. Rye gliadin is called secalin, although the structures are nearly identical. The secalin protein has similar potential to do bad things as its gliadin counterpart. Likewise, the lectin of rye is nearly identical to wheat’s destructive lectin, wheat germ agglutinin, and therefore shares its potential for causing intestinal toxicity, clumping red blood cells, provoking abnormal growth of immune system lymphocytes, and mimicking insulin. Rye shares with wheat a peculiar and only recently recognized phenomenon: the formation of acrylamide, a compound believed to be a carcinogen and neurotoxin. Rye and wheat contain a high content of the amino acid asparagine, which, when heated at high temperatures during baking or deep-frying, reacts with the plentiful carbohydrates present to form acrylamide. (It also forms in French fries.) Modern reliance on nitrogen-rich synthetic fertilizers also boosts the asparagine content of rye and wheat, increasing acrylamide formation further. For all practical purposes, given the crossbreeding that has occurred via natural Vavilovian means as well as the breeding efforts of humans, the differences are minor, meaning that they are virtually one and the same. Being wheat-free should also mean being rye-free.
