Penny le Couteur & Jay Burreson (40 page)

Another group of alkaloids of quite different structure was probably, although indirectly, responsible for thousands of witch burnings in Europe. But these compounds were not used in hallucinogenic ointments. The effects of some of the alkaloid molecules from this group can be so devastating that whole communities, afflicted with horrendous suffering, assumed that the catastrophe was the result of an evil spell cast by local witches. This group of alkaloids is found in the ergot fungus,
Claviceps purpurea,
that infects many cereal grains but especially rye. Ergotism or ergot poisoning was until fairly recently the next-largest microbial killer after bacteria and viruses. One of these alkaloids, ergotamine, causes blood vessels to constrict; another, ergonovine, induces spontaneous abortions in humans and livestock; while others cause neurological disturbances. Symptoms of ergotism vary depending on the amount of the different ergot alkaloids present but can include convulsions, seizures, diarrhea, lethargy, manic behavior, hallucinations, distortion of the limbs, vomiting, twitching, a crawling sensation on the skin, numbness in the hands and feet, and a burning sensation becoming excruciatingly painful as gangrene from decreased circulation eventually sets in. In medieval times this disease was known by various names: holy fire, Saint Anthony's fire, occult fire, and Saint Vitus' dance. The reference to fire relates to the terrible searing pain and blackened extremities caused by the progression of gangrene. Often there was loss of hands, feet, or genitals. Saint Anthony was considered to have special powers against fire, infection, and epilepsy, making him the saint to appeal to for relief from ergotism. The “dance” of Saint Vitus' dance refers to twitching and convulsive contortions due to the neurological effects of some of the ergot alkaloids.

It is not hard to envisage a situation where a large number of villagers or townsfolk were struck by ergotism. A particularly rainy period just before harvest would encourage fungus growth on rye; poor storage of the cereal in damp conditions would promote further growth. Only a small percent of ergot in flour is needed to cause ergot poisoning. As more and more of a town's inhabitants displayed the dreaded symptoms, people might start to wonder why their community had been singled out for disaster, especially as adjacent towns had no sign of the disease. It could have seemed quite plausible that their village had been bewitched. As in many natural disasters, the blame was often placed on the innocent head of an elderly woman, someone who was no longer useful for childbearing and who may have had no family support. Such women often lived on the outskirts of the community, perhaps surviving on their skills as herbalists and unable to afford even the modest sum required to purchase flour from the miller in town. This level of poverty would have saved a woman from ergotism but ironically, as maybe the only person untouched by the ergot poisons, she became even more vulnerable to the accusation of witchcraft.

Ergotism has been known for a long time. Its cause was hinted at in reports from as early as 600 B.C., when the Assyrians noted “a noxious pustule in the ear of grain.” That ergot alkaloids from “noxious grasses” could cause miscarriages in cattle was recorded in Persia around 400 B.C. In Europe the knowledge that fungus or mold on grains was the cause of the problem seems to have been lost—if it was ever known— during the Middle Ages. With damp winters and improper storage, mold and fungus flourished. In the face of famine, infected grain would have been used rather than discarded.

The first recorded occurrence of ergotism in Europe, in A.D. 857, is from Germany's Rhine valley. Documented reports of forty thousand deaths in France in the year 994 are now attributed to ergotism, as are another twelve thousand in 1129. Periodic outbreaks occurred throughout the centuries and continued into the twentieth century. In 1926-1927 more than eleven thousand people were afflicted with ergotism in an area of Russia near the Ural Mountains. Two hundred cases were reported in England in 1927. In Provence, France, in 1951, four died and hundreds more became ill from ergotism after ergot-infected rye was milled and the flour sold to a baker, although the farmer, miller, and baker were supposedly all aware of the problem.

There are at least four occasions when ergot alkaloids are claimed to have played a role in history. During a campaign in Gaul, in the first century B.C., an epidemic of ergotism among Julius Caesar's legions caused great suffering, reduced the effectiveness of his army, and possibly curtailed Caesar's ambitions to enlarge the Roman Empire. In the summer of 1722 Peter the Great's Cossacks camped at Astrakhan, at the mouth of the Volga River on the Caspian Sea. Both the soldiers and their horses ate contaminated rye. The resulting ergotism supposedly killed twenty thousand troops and so crippled the tsar's army that his planned campaign against the Turks was aborted. Thus Russia's goal of a southern port on the Black Sea was stopped by ergot alkaloids.

In France, in July 1789, thousands of peasants rioted against wealthy landowners. There is evidence that this episode, termed
La Grande Peur
(the Great Fear), was more than just civil unrest associated with the French Revolution. Records attribute the destructive spree to a bout of insanity in the peasant population and cite “bad flour” as a possible cause. The spring and summer of 1789 in northern France had been abnormally wet and warm—perfect conditions for the growth of the ergot fungus. Was ergotism, much more prevalent among the poor, who ate moldy bread out of necessity, a key factor in the French Revolution? Ergotism was also reported to be rife in Napoleon's army during its journey across the Russian plains in the fall of 1812. So maybe the ergot alkaloids, along with the tin in uniform buttons, share some responsibility for the Grande Armée's collapse on the retreat from Moscow.

A number of experts have concluded that ergot poisoning was ultimately responsible for the accusations of witchcraft against some 250 people (mainly women) during 1692 in Salem, Massachusetts. The evidence does indicate an involvement of the ergot alkaloids. Rye was grown in the area in the late seventeenth century; records show warm, rainy weather during the spring and summer of 1691; and the village of Salem was located close to swampy meadows. All of these facts point to the possibility of fungal infestation of the grain used for the community's flour. The symptoms displayed by the victims were consistent with ergotism, particularly convulsive ergotism: diarrhea, vomiting, convulsions, hallucinations, seizures, babbling, bizarre distortions of the limbs, tingling sensations, and acute sensory disturbances.

It seems probable that, at least initially, ergotism may have been the cause of the Salem witch-hunts; almost all the thirty victims who claimed to be bewitched were girls or young women, and young people are known to be more susceptible to the effects of the ergot alkaloids. Later events, however, including the trials of the alleged witches and an increasing number of accusations, often of people outside the community, point more to hysteria or just plain malice.

Symptoms of ergot poisoning cannot be turned off and on. The common phenomenon in the trials—victims throwing a convulsive fit when confronted by the accused witch—is not consistent with ergotism. No doubt relishing the attention and realizing the power they wielded, the so-called victims would denounce neighbors they knew and townsfolk they had scarcely heard of. The suffering of the real victims of the Salem witch-hunts—the nineteen hanged (and one pressed to death by a pile of rocks), those tortured and imprisoned, the families destroyed—may be traced to ergot molecules, but human frailty must bear ultimate responsibility.

Like cocaine, ergot alkaloids, although toxic and dangerous, have had a long history of therapeutic use, and ergot derivatives still play a role in medicine. For centuries herbalists, midwives, and doctors used extracts of ergot to hasten childbirth or produce abortions. Today ergot alkaloids or chemical modifications of these compounds are used as vasoconstrictors for migraine headaches, to treat postpartum bleeding, and as stimulants for uterine contractions in childbirth.

The alkaloids of ergot all have the same common chemical feature; they are derivatives of a molecule known as lysergic acid. The OH group (indicated with an arrow, below) of lysergic acid is replaced by a larger side group, as shown in the ergotamine molecule (used to treat severe migraine headaches) and the ergovine molecule (used to treat postpartum hemorrhages). In these two molecules the lysergic acid portion is circled.

In 1938, having already prepared a number of synthetic derivatives of lysergic acid of which some had proved useful, Albert Hofmann, a chemist working in the research laboratories of the Swiss pharmaceutical company Sandoz, in Basel, prepared another derivative. It was the twenty-fifth derivative he had made, so he called lysergic acid diethylamide LSD-25, now known, of course, as just LSD. Nothing exceptional was noted about the properties of LSD.

It was not until 1943, when Hofmann again made this derivative, that he inadvertently experienced the first of what was to become known in the 1960s as an acid trip. LSD is not absorbed through the skin, so Hofmann probably transferred LSD from his fingers to his mouth. Even a slight trace would have produced what he described as an experience of “an uninterrupted stream of fantastic pictures, extraordinary shapes with intense kaleidoscope play of colors.”

Hofmann decided to deliberately take LSD to test his assumption that this was the compound producing the hallucinations. The medical dosage for lysergic acid derivatives such as ergotamine was at least a few milligrams. Thinking, no doubt, that he was being cautious, he swallowed only a quarter of a milligram, an amount at least five times that needed to produce the now well-known hallucinogenic effects. LSD is ten thousand times more potent as a hallucinogen than naturally occurring mescaline, found in the peyote cactus of Texas and northern Mexico and used for centuries by native Americans in their religious ceremonies.

Rapidly growing dizzy, Hofmann asked his assistant to accompany him as he rode his bicycle home through the streets of Basel. For the next few hours he went through the full range of experiences that later users came to know as a bad trip. As well as having visual hallucinations, he became paranoid, alternated between feelings of intense restlessness and paralysis, babbled incoherently, feared choking, felt he had left his body, and perceived sounds visually. At some point Hofmann even considered the possibility that he might have suffered permanent brain damage. His symptoms gradually subsided, though his visual disturbances persisted for some time. Hofmann awoke the morning after this experience feeling totally normal, with a complete memory of what had happened but seemingly with no side effects.

In 1947 the Sandoz company began to market LSD as a tool in psychotherapy and in particular for the treatment of alcoholic schizophrenia. In the 1960s LSD became a popular drug for young people around the world. It was promoted by Timothy Leary, a psychologist and one-time member of the Harvard University Center for Research in Personality, as the religion of the twenty-first century and the way to spiritual and creative fulfillment. Thousands followed his advice to “turn on, tune in, drop out.” Was this alkaloid-induced escape from everyday life in the twentieth century so different from that experienced by women accused of witchcraft a few hundred years before? Though centuries apart, the psychedelic experiences were not always positive. For the flower children of the 1960s, taking the alkaloid-derivative LSD could lead to flashbacks, permanent psychoses, and in extreme cases suicide; for the witches of Europe, absorbing the alkaloids atropine and scopolamine from their flying salves could lead to the stake.

 

 

The atropine and ergot alkaloids did not cause witchcraft. Their effects, however, were interpreted as evidence against large numbers of innocent women, usually the poorest and most vulnerable in society. Accusers would make a chemical case against the witch: “She must be a witch, she says she can fly” or “she must be guilty, the whole village is bewitched.” The attitudes that had allowed four centuries of persecution of women as witches did not change immediately once the burnings were stopped. Did these alkaloid molecules contribute to a perceived heritage of prejudice against women—a view that may still linger in our society?