Sunlight and Vitamin D Are Not the Same Thing

An Essay on Hector DeLuca’s 2013 Testimony to the Endocrine Society

One Line Late in the Interview

In June 2013, at the Endocrine Society’s annual meeting in San Francisco, historian Mike Chappelle recorded an oral history with Hector DeLuca. Toward the end of the interview, he asked about autoimmunity.¹

DeLuca’s group at Wisconsin had for years studied the standard mouse model of MS, known technically as EAE. They found a specific waveband of ultraviolet light that suppresses the disease in mice. That waveband does not produce vitamin D.

“The correlation between sunlight, vitamin D, and multiple sclerosis is only a correlation,” DeLuca says. “It’s not cause and effect.”¹

The man saying this identified 25-hydroxy-vitamin D3 in 1968 and isolated 1,25-dihydroxy-vitamin D3 in 1971. He and his group cloned the vitamin D receptor in 1987. Most of the vitamin D analogs on the pharmaceutical market came from his laboratory. On the record for the Endocrine Society’s own archive, he told the historian that the sunlight-MS-vitamin D link, one of the most heavily promoted claims for vitamin D beyond its role in bone health, is not causally mediated by vitamin D.

The rest of the interview, read as testimony rather than tribute, is comparably illuminating.

Interview with Mike Chappelle

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A Compound Named From a Process

To understand what “vitamin D” refers to, follow the sequence DeLuca lays out.

At the turn of the twentieth century, German nutrition chemists led by Justus von Liebig held that adequate diet was defined by adequate amounts of protein, carbohydrate, fat, and salts. Stephen Babcock at Wisconsin observed that shoe leather had the same proximate analysis as the German-defined adequate diet but could not sustain life. Something was missing from the analysis, and the analysis could not detect what.

E.B. Hart’s single-grain experiment confirmed the inference. Cattle fed adequate protein, carbohydrate, and fat from wheat died. Cattle fed the same proximate analysis from corn survived. Elmer McCollum was assigned the problem. He smuggled rats into the College of Agriculture basement. Rats were classified as enemies of the farm and formally banned from the college. He repeated the experiment with purified diets varying only in fat source. Lard-fed rats died. Butterfat and cod-liver-oil rats lived. He named the water-soluble missing factor “B” and the fat-soluble missing factor “A.”² Casimir Funk had already coined “vital amines” in 1911.³ The E was dropped. Vitamins had been named as unidentified categories in feed experiments before anyone had extracted a molecule.

McCollum then performed the experiment that split vitamin D from vitamin A. He bubbled oxygen through cod liver oil, destroying the more oxidation-sensitive component. The oxidized oil no longer cured vitamin A deficiency but still cured rickets in dogs.⁴ A second fat-soluble factor was inferred. It was named vitamin D by position in the alphabetical sequence.

Harry Steenbock, who had been working with goats since 1916, had observed that summer sunlight kept his animals in positive calcium balance while winter indoor confinement drove them into negative balance.⁵ Reading Kurt Huldschinsky’s Vienna work curing rachitic children with UV lamps,⁶ Steenbock began radiating rats with an ultraviolet lamp. He radiated the air the rats breathed. Nothing. He radiated their cages. Nothing. He radiated their food. That worked. He isolated the non-saponifiable lipid fraction of the irradiated food and found it retained the anti-rachitic activity.⁵

This was the discovery. An industrial UV irradiation process applied to a lipid fraction of food produces something that cures rickets. The process worked before anyone had a molecular structure. Milk was irradiated. Oats were irradiated. Rickets, a disease of urban and industrial poverty, declined worldwide.

Only afterward was a chemical isolated. A British team at the National Institute for Medical Research, working from an earlier observation by Rosenheim and Webster, irradiated ergosterol from yeast and isolated the active material from the mixture.⁷ They named it vitamin D2. Vitamin D2 is a substance created by bombarding a plant sterol with ultraviolet light. Adolf Windaus later identified vitamin D3 by an analogous process applied to 7-dehydrocholesterol.⁸ Both compounds are, in their commercial forms, industrial synthetics from their origin.

DeLuca lays out this entire sequence in about three minutes of the interview. He shows no sign of considering it unusual. It was, and remains, the field’s own account of how the substance was discovered.

Steenbock’s Beer Cars and the WARF Machine

Steenbock filed a patent on the food-irradiation process in 1924.⁹ DeLuca describes the motivation directly. A beer company had started irradiating beer. “According to Steenbock the story told me, they had cars of beer on rails ready to ship that had been radiated by his process.”¹ Steenbock wanted licensing control to prevent the process from being applied to products that could not usefully produce vitamin D and would, in his phrase as DeLuca recalls it, “delude the people.”¹

The University of Wisconsin refused the patent. Commercial involvement was, in the phrasing of the era, “dirty commercial money.”¹ By that point, Quaker Oats had already deposited one million dollars in 1925 (roughly eighteen million in 2026 terms) to license the irradiation process.¹⁰ Steenbock used the money to create the Wisconsin Alumni Research Foundation with graduate dean Charles Slichter. WARF took the position that inventions belonged to their inventors and would fund basic research at Wisconsin from licensing income.

WARF became the template. Other universities adopted variants. The Bayh-Dole Act of 1980 universalized what Wisconsin had done since the 1920s.¹¹ DeLuca describes the effect matter-of-factly. After Bayh-Dole, “all over the country every school had their intellectual property managers, and they began to do what Wisconsin had been doing for many years.”¹

DeLuca’s career was built inside this apparatus. In 1968, when his group isolated 25-hydroxy-vitamin D3, he took the compound to WARF’s patent counsel the same year and filed. Decades later he formed his own company to develop 2MD, a bone-selective analog. He advised Tetrionics, which synthesized compounds for licensing testing and was later absorbed by Sigma-Aldrich Fine Chemicals. He worked with Bone Care International, which licensed one of his analogs for osteoporosis treatment.¹

The research infrastructure and the commercial infrastructure are a single system. From inside, they are not distinct, which is why DeLuca describes them together without any felt need to separate them. The vitamin D research program at Wisconsin began as a food-fortification licensing operation. Every subsequent development, from the metabolite identifications through the receptor cloning to the analog patents, sits on the same foundation. This is not an accusation. It is what the interview says.

The Precursor Sold as a Nutrient

DeLuca’s own research program began with a simple question. He had trained in organic chemistry. Radioactive labeling had become practical. He wanted to know what vitamin D3 actually does in the body. So he labeled vitamin D3 and gave it to animals at physiologic doses, not the huge pharmacological doses that had rendered earlier tracer studies uninterpretable, and tracked where the label went.

The label did not stay on vitamin D3. Vitamin D3 disappeared. The radioactivity turned up in something else. In 1968, from pig serum, DeLuca’s group identified 25-hydroxy-vitamin D3.¹²

He then labeled 25-hydroxy-vitamin D3 and repeated the experiment. That compound also disappeared. The radioactivity turned up in something else again. His group sacrificed sixteen hundred experimentally depleted chickens to isolate enough of the target compound from their intestinal tissue. In late 1970 they identified 1,25-dihydroxy-vitamin D3, and confirmed the structure by synthesis in 1973.¹³

Here is the pathway DeLuca described in his mid-1970s reviews. In skin, a molecule called 7-dehydrocholesterol absorbs ultraviolet light between 282 and 300 nanometers and converts to previtamin D3, which becomes vitamin D3. Vitamin D3 travels on a carrier protein to the liver, where an enzyme now designated CYP2R1 attaches a chemical group at position 25, producing 25-hydroxy-vitamin D3. This form travels to the kidney, where a second enzyme (CYP27B1) attaches another chemical group at position 1, under the control of parathyroid hormone. Only after both conversions is the compound biologically active.¹⁴ It then acts on intestine, bone, and kidney to raise serum calcium and phosphorus.

DeLuca uses the word “hormone” throughout the interview. The receptor his group cloned in 1987 sits in the steroid receptor superfamily.¹⁵ What is sold in bottles as vitamin D3 is a precursor of a steroid hormone. Two enzymatic conversions are required to make it active. Both conversions are regulated. The kidney conversion occurs only when serum calcium is low, triggered by parathyroid hormone. The body does not produce the active form if serum calcium is adequate.

The body also eliminates it. DeLuca’s group identified a 24-hydroxylation pathway that inactivates both the precursor and the active hormone, converting them to calcitroic acid for excretion by the kidneys. They proved this pathway was inactivation, not activation, by synthesizing a form of 25-hydroxy-vitamin D that was chemically blocked from being 24-hydroxylated, and feeding it to animals across two generations. No pathology developed.¹ The 24-hydroxylation pathway is degradation. The compound induces the enzyme that degrades it. The 24-hydroxylase does not appear in vitamin-D-depleted animals until 1,25-dihydroxy-vitamin D is supplied. The body treats this substance as something to be actively broken down.

DeLuca’s group identified thirty-three metabolites of vitamin D over the years. Most sit on degradation pathways.

A prior essay in this series raised a deeper question about whether the compounds sold as vitamins exist as discrete entities in living tissue at all, or whether they are products of the isolation methodology itself.²² That question applies to the metabolites DeLuca identified. His pathway was established by adding reagents, extracting sample material, and chromatographing it through many steps. Whether 25-hydroxy-vitamin D3 and 1,25-dihydroxy-vitamin D3 exist in living cells in the forms he isolated, or are produced downstream of the extraction, cannot be determined from within his methodology. Nothing in what follows depends on settling that question. Even on his own terms, DeLuca describes a compound whose action does not fit the category of nutrient.

Vitamin D’s First Love

Near the end of the interview, discussing the analog program, DeLuca delivers as a technical challenge what would in a different setting be a startling admission.

“Vitamin D, its first love, so to speak, is to raise serum calcium and phosphorus to mineralize bone. So the problem we’ve got is to breed that hypercalcemic action out of the molecule.”¹

This is a statement about what vitamin D does. It raises serum calcium and phosphorus. Bone mineralization is one downstream consequence: calcium and phosphorus driven into bone matrix by supersaturated serum. Vitamin D toxicity is another: the same calcium and phosphorus driven into arteries, kidneys, heart valves, and cornea. The therapeutic action and the toxic action are the same action expressed in different tissues.

Cholecalciferol at 0.075 percent is the active ingredient in several EPA-registered commercial rodenticides.¹⁶ It kills rats by inducing hypercalcemia and metastatic calcification. This is the mechanism DeLuca describes as vitamin D’s “first love.” The description is not interpretation. It is what the safety data sheets say and what the mechanism-of-death literature reports. A prior essay in this series traced that identity in detail.¹⁷ What the DeLuca interview adds is confirmation from inside the field. The architect describes the therapeutic mechanism and the killing mechanism as one mechanism. He describes his life’s work on analogs as an effort to preserve downstream effects while removing the calcium-raising action that carries the whole compound.

His best candidate, 2MD, showed selectivity for bone and parathyroid without hypercalcemia in preclinical work. It was not developed for osteoporosis because a fracture trial would cost approximately a billion dollars. “Whether it will ever be done, I don’t know,” DeLuca tells Chappelle.¹ After five decades of analog synthesis at Wisconsin, the field cannot separate the desired action from the calcium-raising action well enough to justify the pivotal trial.

The Receptors Elsewhere

Discussing the vitamin D receptor, DeLuca notes almost in passing that when his group used radio-labeled 1,25-dihydroxy-vitamin D, they observed specific nuclear localization of the hormone in tissues unrelated to calcium metabolism. Pancreatic islet cells. Keratinocytes. Lymphocytes. Parathyroid glands. Osteoblasts.

“What does that have to do with calcium homeostasis?” he asks. He does not answer the question. What he says instead is that the field began to realize vitamin D “has functions beyond just healing rickets and healing osteomalacia. We haven’t found many of those yet, but that’s all in progress.”¹

The inference, that a receptor observed in a tissue implies a physiological role of the ligand in that tissue, has produced the current inventory of claims: vitamin D for cancer, cardiovascular disease, diabetes, chronic inflammatory conditions, general wellness. In the same interview, DeLuca states that receptors are present in many tissues and that most of the presumed extra-skeletal functions have not been demonstrated. His work on multiple sclerosis, which he describes at length, concluded that the sunlight-MS correlation is not mediated by vitamin D at all.

The Mendelian Randomization Reply

Mendelian randomization is the epidemiological instrument most often invoked to defend the vitamin-D-MS link. It uses inherited variants as natural experiments. If people who inherit patterns of variants that raise blood vitamin D also have lower MS rates, and if the variants act on MS only through vitamin D, the causal link is inferred without a controlled trial. Mokry and colleagues published such an analysis in 2015 and reported a substantial effect.¹⁸ The finding has been widely cited.

The method rests on one central assumption. The inherited variants must affect MS risk through no other pathway. DeLuca’s own finding, a UV waveband that suppresses the MS mouse model without producing vitamin D, is precisely the finding that makes this assumption untenable. If sunlight has protective effects on MS through pathways that do not require vitamin D, then inherited variants in the vitamin D metabolic pipeline may be affecting those other pathways too. This concern has been raised in the MR literature for the DHCR7 variant in particular, since that enzyme sits upstream of both vitamin D and cholesterol synthesis and cannot cleanly be attributed to one pathway or the other.

The Mendelian randomization literature cannot substitute for the direct experimental test the architect’s own laboratory performed. His work showed that sunlight and vitamin D can be dissociated. Any statistical inference that assumes they cannot is arguing past his finding.

The One Confirmed Extra-Skeletal Function

One confirmed extra-skeletal action stands. In the parathyroid gland, the vitamin D receptor suppresses parathyroid hormone secretion.¹⁹ This is the mechanism exploited in dialysis patients, the primary commercial market for DeLuca’s analogs. Dialysis patients have lost the kidney enzyme CYP27B1 and cannot produce 1,25-dihydroxy-vitamin D. Without it, their parathyroid glands secrete uncontrolled parathyroid hormone in an effort to raise serum calcium. Exogenous 1,25-dihydroxy-vitamin D or its analogs suppress the parathyroid gland by directly raising calcium and by acting on the vitamin D receptor in the gland itself.

The confirmed extra-skeletal function of vitamin D, then, is to suppress the endocrine response that would otherwise mobilize calcium from bone once serum calcium has been raised by other means. This is what the analogs do. It is why they are prescribed to dialysis patients. It is also why vascular calcification and cardiovascular death dominate the mortality profile in that population.²⁰

What the Transcript Establishes

None of the material in the DeLuca oral history is hidden. Nothing in the interview is coy. What is remarkable is that public discourse about vitamin D, and much of the medical literature that shapes it, bears so little resemblance to what he says.

The substance called vitamin D was defined by an industrial UV irradiation process before any chemical structure was known. The first isolated molecule (vitamin D2) came from bombarding yeast-derived ergosterol with ultraviolet light. Vitamin D3 was isolated from an analogous process applied to a cholesterol derivative. The commercial product has been an industrial synthetic from its origin.

The molecule sold as vitamin D is a precursor. It is not biologically active. Two enzymatic conversions, one in the liver and one in the kidney, are required to produce 1,25-dihydroxy-vitamin D, which DeLuca calls a hormone throughout. Both conversions are regulated. The body operates a dedicated enzymatic pathway that eliminates both the precursor and the active hormone. The active hormone induces the enzyme that degrades it.

The therapeutic action of the compound is the raising of serum calcium and phosphorus. Every claimed benefit and every mechanism of toxicity flows from this action. The mechanism DeLuca describes, induced hypercalcemia driving metastatic calcification, is the mechanism by which cholecalciferol-based rodenticides kill rats.

The research program was funded from its origins by the Wisconsin Alumni Research Foundation, itself created from Steenbock’s food-irradiation patent revenues. WARF’s licensing model became the Bayh-Dole framework universalized in 1980. DeLuca’s own companies license his analogs to the dialysis market.

Mike Chappelle posted the interview publicly on his Substack in July 2026, prompted by Jamie Andrews’s essay The Vitamin D Hoax.²¹ The primary source has been available and unremarked upon for thirteen years.

No traditional culture ever needed sheep’s wool dissolved in chloroform and irradiated to be healthy. The DeLuca interview does not put it that way. What it describes is an industrial synthetic whose therapeutic action is the mechanism cholecalciferol-based rodenticides use to kill rats, and whose flagship extra-skeletal claim, the sunlight-MS pathway, has been ruled out by the architect’s own laboratory.

The rest of the story, thirteen years after DeLuca sat down with Chappelle, is still being told without reference to what he said.

How to Explain This to a Six-Year-Old

Imagine you go outside on a sunny day. The sun feels good on your skin. Grown-ups have been telling you for a long time that the sun makes something called “vitamin D” inside your body, and that vitamin D is what makes you healthy.

Now imagine a very important scientist. He spent his whole life studying vitamin D. He made most of the vitamin D medicines that doctors give people. He knows more about vitamin D than almost anyone in the world.

One day someone recorded him talking. And here is what he said.

He said his own science experiments showed that the part of sunlight that helps sick people get better is not the part that makes vitamin D. It is a different part. So when grown-ups say “sunlight is good for you because it makes vitamin D,” that turns out not to be quite right. The sunlight might be helping in a totally different way, and vitamin D might not have much to do with it.

He also said something else. The little pills people take that say “vitamin D” on the bottle are made in a factory. They are not the same as sunlight. The stuff in the pills is very close to what people use to kill rats. The rats eat it and their bodies fill up with too much calcium, and that is how they die. When people take the pills, the same thing happens in a smaller way.

And he said one more thing. Your body works very hard to break the pill medicine down and get rid of it, the same way your body works to get rid of things it does not want inside. If your body wanted the medicine, it would keep it. It does not keep it. It breaks it down and sends it out.

The scientist said all of this a long time ago. He was not hiding. Nobody was listening.

Sunlight is good. Real food is good. But the little pills in the bottle are not sunlight, and they are not food, and the scientist who spent his whole life making them said so.

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References

1. Chappelle, Mike. “Interview with Hector F. DeLuca, PhD.” Mike Chappelle Substack, July 4, 2026. Original interview conducted June 15, 2013, at the Endocrine Society annual meeting, Moscone Center, San Francisco. All direct DeLuca quotations in this essay are from this transcript.

2. McCollum, E.V., and Davis, M. “The necessity of certain lipins in the diet during growth.” Journal of Biological Chemistry 15 (1913): 167–175.

3. Funk, C. “On the chemical nature of the substance which cures polyneuritis in birds induced by a diet of polished rice.” Journal of Physiology 43 (1911): 395–400.

4. McCollum, E.V., Simmonds, N., Becker, J.E., and Shipley, P.G. “Studies on experimental rickets. XXI. An experimental demonstration of the existence of a vitamin which promotes calcium deposition.” Journal of Biological Chemistry 53 (1922): 293–312.

5. Steenbock, H., and Black, A. “Fat-soluble vitamins. XVII. The induction of growth-promoting and calcifying properties in a ration by exposure to ultraviolet light.” Journal of Biological Chemistry 61 (1924): 405–422.

6. Huldschinsky, K. “Heilung von Rachitis durch künstliche Höhensonne.” Deutsche Medizinische Wochenschrift 45 (1919): 712–713.

7. Askew, F.A., Bourdillon, R.B., Bruce, H.M., Jenkins, R.G.C., and Webster, T.A. “The distillation of vitamin D.” Proceedings of the Royal Society B 107 (1931): 76–90. Rosenheim, O., and Webster, T.A. “The parent substance of vitamin D.” Biochemical Journal 21 (1927): 389–397, provided the earlier framework identifying ergosterol as the D-precursor.

8. Windaus, A., Schenck, F., and von Werder, F. “Über das antirachitisch wirksame Bestrahlungsprodukt aus 7-Dehydrocholesterin.” Hoppe-Seyler’s Zeitschrift für Physiologische Chemie 241 (1936): 100–103.

9. US Patent 1,680,818 (Steenbock, filed 1924, granted 1928). “Antirachitically active product and process of making same.”

10. Apple, Rima D. “Patenting University Research: Harry Steenbock and the Wisconsin Alumni Research Foundation.” Isis 80, no. 3 (1989): 375–394.

11. Bayh-Dole Act, Public Law 96-517, December 12, 1980. Formally the Patent and Trademark Law Amendments Act.

12. Blunt, J.W., DeLuca, H.F., and Schnoes, H.K. “25-Hydroxycholecalciferol. A biologically active metabolite of vitamin D3.” Biochemistry 7, no. 10 (1968): 3317–3322.

13. Holick, M.F., Schnoes, H.K., DeLuca, H.F., Suda, T., and Cousins, R.J. “Isolation and identification of 1,25-dihydroxycholecalciferol. A metabolite of vitamin D active in intestine.” Biochemistry 10, no. 14 (1971): 2799–2804. Semmler, E.J., Holick, M.F., Schnoes, H.K., and DeLuca, H.F. “The synthesis of 1α,25-dihydroxycholecalciferol, a metabolically active form of vitamin D3.” Tetrahedron Letters 40 (1972): 4147–4150 (structural confirmation by total synthesis).

14. DeLuca, H.F. “Recent advances in our understanding of the vitamin D endocrine system.” Journal of Laboratory and Clinical Medicine 87 (1976): 7–26. DeLuca also presented an earlier synthesis in Federation Proceedings 33 (1974).

15. Burmester, J.K., Maeda, N., and DeLuca, H.F. “Isolation and expression of rat 1,25-dihydroxyvitamin D3 receptor cDNA.” Proceedings of the National Academy of Sciences 85 (1988): 1005–1009. Baker, A.R., McDonnell, D.P., Hughes, M., et al. “Cloning and expression of full-length cDNA encoding human vitamin D receptor.” Proceedings of the National Academy of Sciences 85, no. 10 (1988): 3294–3298 (Haussler-O’Malley collaboration). Both groups published receptor cloning work in 1987–1988.

16. EPA-registered rodenticides with cholecalciferol as the active ingredient at 0.075 percent: Rampage, Terad3, Agrid3, Quintox. Manufacturer product labels and safety data sheets. Cholecalciferol CAS Number: 67-97-0.

17. Unbekoming. “The Vitamin D Paradox: What They Don’t Tell You About Cholecalciferol.” Lies are Unbekoming Substack, August 17, 2025.

18. Mokry, L.E., Ross, S., Ahmad, O.S., Forgetta, V., Smith, G.D., Leong, A., Greenwood, C.M.T., Thanassoulis, G., and Richards, J.B. “Vitamin D and Risk of Multiple Sclerosis: A Mendelian Randomization Study.” PLoS Medicine 12, no. 8 (2015): e1001866. The DHCR7 pleiotropy concern has been raised in subsequent methodological reviews of the vitamin D MR literature; DHCR7 (7-dehydrocholesterol reductase) sits at the fork between vitamin D precursor availability and cholesterol synthesis.

19. Silver, J., Naveh-Many, T., Mayer, H., Schmelzer, H.J., and Popovtzer, M.M. “Regulation by vitamin D metabolites of parathyroid hormone gene transcription in vivo in the rat.” Journal of Clinical Investigation 78, no. 5 (1986): 1296–1301. Subsequent literature has established the vitamin D receptor’s role in suppressing PTH gene expression in the parathyroid gland.

20. Sigrist, M.K., Taal, M.W., Bungay, P., and McIntyre, C.W. “Progressive vascular calcification over 2 years is associated with arterial stiffening and increased mortality in patients with stages 4 and 5 chronic kidney disease.” Clinical Journal of the American Society of Nephrology 2, no. 6 (2007): 1241–1248. Cardiovascular disease accounts for approximately half of all deaths in dialysis populations; vascular calcification is a major driver.

21. Andrews, Jamie. “The Vitamin D Hoax.” The Virology Controls Studies Project Substack, June 2026.

22. Unbekoming. “Do Vitamins Exist?” Lies are Unbekoming Substack, January 11, 2026.

Truth Be Told: I’ve Accepted an Invitation to Speak on The Unvaccinated

On September 17th, I’ll be giving a one-hour presentation titled The Unvaccinated as part of a six-hour livestream called Truth Be Told. This is the first time I have accepted an invitation to an event, and I have been honoured with the opening act. The livestream begins at 12pm EST.

Vaccination is the subject closest to my heart, and this is another opportunity to spread the word. The format will preserve the pen name.

Jamie Andrews (Decentralized Science Projects) and Agent131711 (Dinosaurs) will also be presenting. Jamie’s Virology Control Studies work led to an interview here last year. Agent’s research shaped my essays on vitamin D and dinosaurs. Tickets are here. The code UNBEKOMING is $5 off and applies automatically at that link. Replay available afterwards. Hope you can make it.