One molecule, two remedies
The claim at the centre of this history is that rickets, the soft and bowed bones once endemic among children in industrial cities, is caused by the lack of a single fat-soluble factor, distinct from vitamin A, that the body can either take in through diet or manufacture for itself when skin is exposed to sunlight. Once that factor was isolated and understood, the argument went, rickets should be almost entirely preventable, either by dietary supplementation such as cod liver oil or by deliberate exposure to sunlight or ultraviolet light. This was not obvious in advance. Early researchers initially attributed the protective effect of cod liver oil to vitamin A, the fat-soluble factor already known at the time, and only careful experiments distinguishing the two established that a separate substance, eventually named vitamin D, was doing the actual work of preventing the disease.
Separating vitamin D from vitamin A
Edward Mellanby’s experiments on dogs between roughly 1918 and 1920 first tied diet directly to the development of rickets, though he read his own results through the lens of vitamin A. It was Elmer McCollum, working in the early 1920s, who separated the two factors by heating and aerating cod liver oil until its vitamin A content was destroyed, and finding that the oil still prevented rickets regardless, evidence that a distinct substance was responsible; he named it vitamin D. A parallel line of treatment came from direct light exposure: Kurt Huldschinsky showed over the winter of 1918 to 1919 that ultraviolet lamps could treat rachitic children, and Harry Steenbock demonstrated in 1923 that irradiating food itself with ultraviolet light raised its vitamin D content. Adolf Windaus’s team then closed the chemical loop in 1925, showing that ultraviolet light converts a cholesterol-related compound in skin, 7-dehydrocholesterol, directly into vitamin D3, work recognised with the 1928 Nobel Prize in Chemistry.
What the fortification programmes proved
The causal chain established by this work has held up completely and still underlies clinical practice: vitamin D deficiency, whether from insufficient sunlight, insufficient diet, or both, is recognised as the principal cause of nutritional rickets in infants, and the biochemistry behind it, sunlight converting a skin compound into the vitamin’s precursor form, which the liver and kidneys then convert into its active hormone, has been traced in full detail. The public health consequence has held up just as well: once milk fortification programmes began in the early 1930s, alongside routine supplementation for infants, rickets fell so sharply in wealthier countries that by the middle of the twentieth century it was described as having been virtually eliminated, a direct and measurable result of applying a specific biochemical finding at national scale.
Where the certainty runs out
What has not held up as neatly is any claim that more vitamin D is straightforwardly better once its role in bone health is well covered. Expert bodies in different countries disagree by a considerable margin on what blood level should count as sufficient, and once its supposed benefits are extended beyond bone, into claims about heart disease, cancer risk or infection, the evidence becomes far thinner and often does not hold up under closer review, with major assessments explicitly declining to credit the vitamin with most of those wider effects. Rickets itself has also proved less permanently solved than the mid-century optimism suggested: cases in some wealthy countries have risen noticeably since the early 2000s, a resurgence driven not by any change in the underlying biology but by shifts in clothing, diet and how much time children spend outdoors.
A disparity built into the biology
The biology also explains a real and persisting disparity rather than a purely historical one. Because skin pigmentation reduces how efficiently ultraviolet light converts into the vitamin, populations whose ancestry lies near the equator synthesise it less readily at higher latitudes, particularly if diet or clothing further limits sun exposure, which is reflected in deficiency statistics that run noticeably higher for some ethnic groups living at temperate latitudes today. Countries have responded to the same underlying finding in different ways: some mandate fortification of staple foods such as milk, while others leave it voluntary, an administrative choice built directly on a hundred-year-old piece of biochemistry rather than any new scientific disagreement about the vitamin’s role in bone health itself.
Is it worth your time
This is worth understanding because the discovery sequence is genuinely satisfying: two separate treatments, cod liver oil and sunlight, that looked unrelated turned out to work through exactly the same molecule, and untangling that took careful, deliberate experiments rather than a single flash of insight. Anyone wanting a clean example of nutritional science solving a visible, disfiguring childhood disease at national scale will find it here, along with the concrete public health machinery, fortification and supplementation, that followed from it. It is less useful as a guide to the newer, broader claims made for vitamin D, where the evidence is considerably weaker, and the return of rickets in wealthy countries in recent decades is a reminder that a solved problem can become unsolved again.