Instead of the Sun
How Vitamin D became the Cure for Everything.
On May 3, 1951, the firstborn was born in an ordinary British family. Parents did everything to ensure that the baby grew up healthy and received all the necessary nutrients and trace elements, including vitamins. Therefore, every day the mother added a few drops of vitamin D to the mixture of cow's and goat's milk, which she fed her son — the pediatrician told her that this would increase the level of calcium in the blood and protect the boy from rickets.
But in the third month of life, the child began to refuse to eat, vomiting and constipation began. He began to grow worse, and at six months old, his parents turned to doctors. Not finding the cause of the problem, the doctors decided that it was a urinary tract infection — young children often suffer from it. Treatment did not help: when the child was already eight months old, he was admitted to another hospital with signs of dehydration, which does not look like an infection at all. There he was found to have an elevated level of calcium in his blood and nephrocalcinosis — the deposition of calcium salts in the tissues and vessels of the kidneys.
The new doctor removed excess calcium from the body and advised the mother to give the child less dairy products — and he quickly went on the mend. Only after 70 years, scientists found out that it was not the milk, but vitamin D — it was he who prevented the little Briton from growing. Despite this, pediatricians still recommend the vitamin to all children without exception. And millions of adults prescribe a miracle pill themselves.
But in the third month of life, the child began to refuse to eat, vomiting and constipation began. He began to grow worse, and at six months old, his parents turned to doctors. Not finding the cause of the problem, the doctors decided that it was a urinary tract infection — young children often suffer from it. Treatment did not help: when the child was already eight months old, he was admitted to another hospital with signs of dehydration, which does not look like an infection at all. There he was found to have an elevated level of calcium in his blood and nephrocalcinosis — the deposition of calcium salts in the tissues and vessels of the kidneys.
The new doctor removed excess calcium from the body and advised the mother to give the child less dairy products — and he quickly went on the mend. Only after 70 years, scientists found out that it was not the milk, but vitamin D — it was he who prevented the little Briton from growing. Despite this, pediatricians still recommend the vitamin to all children without exception. And millions of adults prescribe a miracle pill themselves.
Oatmeal, fish oil and ultraviolet
At the beginning of the XX century, there was no prevention of rickets for British boys yet. And they were sick — so often that rickets even began to be called "English disease".
No one knew how to treat rickets. They tried to feed the patients with calcium to strengthen the bones, but it didn't help much. And in the 1910s, biochemists one after another described three vitamins at once - A, B1 and C — and confirmed that they save from diseases, each from its own: xerophthalmia (dryness of the eye membranes), beriberi and scurvy, respectively. And then the British doctor Edward Mellanby thought that some vitamin, or rather its deficiency, could also be to blame for the development of rickets.
He noticed that the Scots had rickets more often than other Britons. And he conducted an experiment: he began to keep dogs on a typical Scottish diet, mainly consisting of oatmeal. The dogs quickly fell ill with rickets. Then Mellanby started adding fish oil to the diet — because his colleague Elmer McCollum found out that fish oil is rich in vitamin A. Symptoms in dogs quickly disappeared, and Mellanby concluded that vitamin A deficiency also causes rickets, and not just xerophthalmia.
However, McCollum himself, who also followed the success of his colleague, doubted this assumption. McCollum passed oxygen through fish oil to destroy vitamin A, and began giving it to rats. The conjunctiva and cornea of the animals dried up quickly due to xerophthalmia, but rickets did not begin in them. Both doctors came to the conclusion that fish oil, in addition to vitamin A, contains another antirachitic vitamin — and called it vitamin D.
At the same time when British scientists were feeding dogs oatmeal with fish oil, American Harry Steenbock studied rickets in a different way: he observed the concentration of calcium — which is associated with bone strength — in the blood of domestic goats. He noticed that in summer, when the goats grazed outdoors, there was more calcium in their blood than in winter, when they were kept in a pen without sunlight. And I suspected that it was ultraviolet light — just at that time, they were actively studying how much it gets on the skin with sunlight.
Steenbock began to irradiate rats with ultraviolet light and feed them at the same time a "Scottish" menu of oatmeal. And I didn't notice any rickets in them. The rats did not get sick, even when only their food was irradiated with ultraviolet radiation, and not themselves. From which the scientist deduced that both the feed and the skin contain a precursor substance, which under the action of ultraviolet light is activated and becomes an antirachitic vitamin.
The picture has developed. In order for there to be a lot of calcium in the blood — and therefore in the bones — a person needs vitamin D: either real, from food, or from a precursor in his own skin — but then sunlight will be needed. Otherwise, rickets occurs. It became clear why the disease became English — urbanization was to blame: in cities, houses were built close to each other, and sunlight barely got into the premises. In addition, the growing industries enveloped the cities in smog, which is why not all ultraviolet light reached the ground. And no one guessed to eat fish oil in time.
At the beginning of the XX century, there was no prevention of rickets for British boys yet. And they were sick — so often that rickets even began to be called "English disease".
No one knew how to treat rickets. They tried to feed the patients with calcium to strengthen the bones, but it didn't help much. And in the 1910s, biochemists one after another described three vitamins at once - A, B1 and C — and confirmed that they save from diseases, each from its own: xerophthalmia (dryness of the eye membranes), beriberi and scurvy, respectively. And then the British doctor Edward Mellanby thought that some vitamin, or rather its deficiency, could also be to blame for the development of rickets.
He noticed that the Scots had rickets more often than other Britons. And he conducted an experiment: he began to keep dogs on a typical Scottish diet, mainly consisting of oatmeal. The dogs quickly fell ill with rickets. Then Mellanby started adding fish oil to the diet — because his colleague Elmer McCollum found out that fish oil is rich in vitamin A. Symptoms in dogs quickly disappeared, and Mellanby concluded that vitamin A deficiency also causes rickets, and not just xerophthalmia.
However, McCollum himself, who also followed the success of his colleague, doubted this assumption. McCollum passed oxygen through fish oil to destroy vitamin A, and began giving it to rats. The conjunctiva and cornea of the animals dried up quickly due to xerophthalmia, but rickets did not begin in them. Both doctors came to the conclusion that fish oil, in addition to vitamin A, contains another antirachitic vitamin — and called it vitamin D.
At the same time when British scientists were feeding dogs oatmeal with fish oil, American Harry Steenbock studied rickets in a different way: he observed the concentration of calcium — which is associated with bone strength — in the blood of domestic goats. He noticed that in summer, when the goats grazed outdoors, there was more calcium in their blood than in winter, when they were kept in a pen without sunlight. And I suspected that it was ultraviolet light — just at that time, they were actively studying how much it gets on the skin with sunlight.
Steenbock began to irradiate rats with ultraviolet light and feed them at the same time a "Scottish" menu of oatmeal. And I didn't notice any rickets in them. The rats did not get sick, even when only their food was irradiated with ultraviolet radiation, and not themselves. From which the scientist deduced that both the feed and the skin contain a precursor substance, which under the action of ultraviolet light is activated and becomes an antirachitic vitamin.
The picture has developed. In order for there to be a lot of calcium in the blood — and therefore in the bones — a person needs vitamin D: either real, from food, or from a precursor in his own skin — but then sunlight will be needed. Otherwise, rickets occurs. It became clear why the disease became English — urbanization was to blame: in cities, houses were built close to each other, and sunlight barely got into the premises. In addition, the growing industries enveloped the cities in smog, which is why not all ultraviolet light reached the ground. And no one guessed to eat fish oil in time.
List of literature
- Familial Atypical Multiple Mole Melanoma Syndrome(ncbi.nlm.nih.gov)
- Familial Atypical Multiple Mole Melanoma Syndrome(sciencedirect.com)
- Familial atypical multiple mole melanoma syndrome(orpha.net)