Lack of asthma in rural Africa

Three decades before Pritchard contracted hookworm, a British explorer named Richard Godfrey was traveling in the Gambia, a small country located along the Gambia River in West Africa. Godfrey wanted to determine the prevalence of asthma in this region and compare this figure with the UK. Most likely, the conclusion that Godfrey came to seemed incredible and even impossible: he could not find a single asthmatic in a randomly selected group of 231 people, which included children and adults from rural areas [166]. Godfrey carefully examined medical records from rural hospitals and again did not find a single case of asthma among the 1,200 described asthma-like symptoms. It seemed that there was not a single person suffering from asthma in rural Africa.

However, in Banjul, the capital of the Gambia with a population of 44,000, the situation is very different. The city was rapidly becoming Westernized, with an average of eight asthma patients a day going to local hospitals, most of them regular patients. Interestingly, almost all of these patients belonged to the upper classes. In other words, in the Gambia, asthma affected the richest segment of the most urbanized population. What could explain this pattern? The level of IgE in rural Gambians was more than two and a half times higher than in their urban compatriots with asthma. In addition, they had much more parasites.

“The idea that allergic diseases may reflect the ongoing activity of the immune system that has been rendered unnecessary by a person’s cleanliness is quite appealing,” Godfrey wrote in 1975. And then, if I may say so, he predicted Pritchard’s experiments. “If this is indeed the case, then perhaps it is not so unrealistic to expect the emergence of a method for treating allergic diseases through a harmless drug from a parasitic antigen that can stimulate the production of IgE.”

Godfrey tested the idea directly. He took turns exposing lung fragments (extracted for other reasons during surgical operations) to the blood serum of Africans and Britons, and then to allergens, in this case pollen. If the tissue was washed first with African and then British serum, it did not react to pollen. Exposure to the African serum prevented immune cells from learning to respond to hay fever. However, when Godfrey first used a British serum and then an African one, the pollen caused an allergic reaction. The African serum, hardened in battles with parasites, had almost magical anti-allergic properties. On the other hand, the British serum showed the opposite trend, creating conditions for the development of allergies.

“One theoretical approach to preventing or treating allergic diseases is to intentionally induce high IgE reactivity — for example, through artificial parasite infestation,” the editors of the Lancet wrote in an article on Godfrey’s research [168]. The mere mention of this idea caused a storm of indignation and concern. Many scientists were convinced that precisely because helminths stimulate the production of IgE, such an experiment would cause the very allergic diseases that it is supposed to prevent.

“I was horrified to find that your editorial … ends with an illogical and, of course, extremely dangerous sentence,” one scholar wrote. Another was “startled” by the suggestion. A third researcher drew attention to the fact that many Malay children, almost half of whom are carriers of helminths, suffer from hay fever and asthma. But then came a breath-taking letter. Thirty-three-year-old British parasitologist John Turton infected himself with 250 hookworm larvae, ostensibly to study IgE levels [169]. First, he had a severe stomach ache, which eventually passed, and then an unexpected miracle happened: hay fever, which had plagued him since he was eight years old, disappeared.

“In the summers of 1975 and 1976, I had no symptoms,” Turton told readers of the Lancet. He acknowledged that this is an isolated example, but the results suggested that helminths do indeed suppress the allergic reaction and that they have therapeutic potential. His observation at least refuted the claim that helminths, by increasing the level of allergic antibodies, exacerbate allergic diseases. Turton said the following about this: “I definitely can’t accept… that a parasitic infection supposedly exacerbates an existing allergy.”Three decades before Pritchard contracted hookworm, a British explorer named Richard Godfrey was traveling in the Gambia, a small country located along the Gambia River in West Africa. Godfrey wanted to determine the prevalence of asthma in this region and compare this figure with the UK. Most likely, the conclusion that Godfrey came to seemed incredible and even impossible: he could not find a single asthmatic in a randomly selected group of 231 people, which included children and adults from rural areas [166]. Godfrey carefully examined medical records from rural hospitals and again did not find a single case of asthma among the 1,200 described asthma-like symptoms. It seemed that there was not a single person suffering from asthma in rural Africa.

However, in Banjul, the capital of the Gambia with a population of 44,000, the situation is very different. The city was rapidly becoming Westernized, with an average of eight asthma patients a day going to local hospitals, most of them regular patients. Interestingly, almost all of these patients belonged to the upper classes. In other words, in the Gambia, asthma affected the richest segment of the most urbanized population. What could explain this pattern? The level of IgE in rural Gambians was more than two and a half times higher than in their urban compatriots with asthma. In addition, they had much more parasites.

“The idea that allergic diseases may reflect the ongoing activity of the immune system that has been rendered unnecessary by a person’s cleanliness is quite appealing,” Godfrey wrote in 1975. And then, if I may say so, he predicted Pritchard’s experiments. “If this is indeed the case, then perhaps it is not so unrealistic to expect the emergence of a method for treating allergic diseases through a harmless drug from a parasitic antigen that can stimulate the production of IgE.”

Godfrey tested the idea directly. He took turns exposing lung fragments (extracted for other reasons during surgical operations) to the blood serum of Africans and Britons, and then to allergens, in this case pollen [167]. If the tissue was washed first with African and then British serum, it did not react to pollen. Exposure to the African serum prevented immune cells from learning to respond to hay fever. However, when Godfrey first used a British serum and then an African one, the pollen caused an allergic reaction. The African serum, hardened in battles with parasites, had almost magical anti-allergic properties. On the other hand, the British serum showed the opposite trend, creating conditions for the development of allergies.

“One theoretical approach to preventing or treating allergic diseases is to intentionally induce high IgE reactivity — for example, through artificial parasite infestation,” the editors of the Lancet wrote in an article on Godfrey’s research. The mere mention of this idea caused a storm of indignation and concern. Many scientists were convinced that precisely because helminths stimulate the production of IgE, such an experiment would cause the very allergic diseases that it is supposed to prevent.

“I was horrified to find that your editorial … ends with an illogical and, of course, extremely dangerous sentence,” one scholar wrote. Another was “startled” by the suggestion. A third researcher drew attention to the fact that many Malay children, almost half of whom are carriers of helminths, suffer from hay fever and asthma. But then came a breath-taking letter. Thirty-three-year-old British parasitologist John Turton infected himself with 250 hookworm larvae, ostensibly to study IgE levels. First, he had a severe stomach ache, which eventually passed, and then an unexpected miracle happened: hay fever, which had plagued him since he was eight years old, disappeared.

“In the summers of 1975 and 1976, I had no symptoms,” Turton told readers of the Lancet. He acknowledged that this is an isolated example, but the results suggested that helminths do indeed suppress the allergic reaction and that they have therapeutic potential. His observation at least refuted the claim that helminths, by increasing the level of allergic antibodies, exacerbate allergic diseases. Turton said the following about this: “I definitely can’t accept… that a parasitic infection supposedly exacerbates an existing allergy.”

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