Why vitamin D should not be called a vitamin
Vitamin D is a hormonal steroid (https://en.wikipedia.org/wiki/Vitamin_D).
It is derived from sterols called calciferols, namely
- cholecalciferol ('vitamin D3'), and
- ergocalciferol ('vitamin D2').
Intermediates include calcitriol (https://medical-dictionary.thefreedictionary.com/calcitriol).
The conventional view is that 'vitamin D' qualifies as a vitamin for Homo sapiens.
This is on the basis that it
- is required in small amounts,
- is supplied partly by the diet, and
- produces clear symptoms in deficiency.
Furthermore, deficiency can be remedied by supplementing the vitamin, without any other changes to the diet.
The solving of widespread rickets in the 1930’s by feeding suitably enriched milk to children (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6116165/) is conventionally regarded as a classic example of the effectiveness of supplementation of vitamins.
So, why would I doubt that ‘vitamin D’ is really a vitamin?
The short answer is that the human body can make this substance for itself.
This applies at every step of a complicated process. We can make
- the form of cholesterol initially needed,
- calciferol (photosynthetically in the skin),
- calcidiol (in the liver), and
- calcitriol (in the kidney).
Calcitriol, the active form of ‘vitamin D’, has since 1970 been generally acknowledged to be a steroid hormone, not a vitamin (https://pubmed.ncbi.nlm.nih.gov/24739090/#:~:text=The%20endogenous%20serum%20metabolite%20of,may%20exert%20several%20immunomodulatory%20activities and https://en.wikipedia.org/wiki/Calcitriol).
This shifts the real question to: if we can make these substances, why does our body sometimes fail to do so sufficiently? (see below)
If further answers are required for why this is not a real vitamin:
Even if ‘vitamin D’ were impossible for the human body to make, there is no plausible scenario in which our ancestors would have been able to rely on it in food, such that the physiological ability to make it was lost.
Humans arose in mild climates where oily, cold-water fish could not possibly have been an essential part of the diet. This leaves the only half-plausible dietary requirement as liver (where cholecalciferol tends to be stored in the vertebrate body).
Liver was prized by hunting humans, partly because it is a good source of other vitamins, particularly vitamin B12.
However, liver is specialised and scarce, as a food. This undermines any rationale based on the reliability of this as a source of ‘vitamin D’ for our human ancestors.
Furthermore, the active form of ‘vitamin D’, namely calcitriol, is in the first place a steroid hormone, rather than a vitamin. A it is virtually unavailable in any food eaten by humans.
Now, moving on to the question:
How does deficiency in ‘vitamin D’ arise?
There are two resources that might potentially be in limited supply in the chain of production that leads to the active form of ‘vitamin D'. These are the sterols that are converted into –ferols, and the ultraviolet radiation required to perform this conversion.
First, the sterols.
‘Vitamin D’ is a steroid, and is synthesised from a sterol. Therefore, it is possible that, for some reason, the human body fails to synthesise enough of the right sterol (7-dehydrocholesterol).
This might be because of an imbalance in the various lipids in the modern human diet, owing to
- too little saturated fat, including the ‘fatty acid’ butyric acid,
- too much polyunsaturated oil (particularly the oil of seeds of annual dicotyledonous crops), and
- antagonism between these two categories of lipids, at both the level of the fatty acids and the level of the triglycerides.
The human species today consumes much ‘vegetable oil’, even as we abstain from animal fats (https://www.healthline.com/nutrition/are-vegetable-and-seed-oils-bad#oxidation).
This hypothetically leads to imbalance in the lipids in our diets and our bodies – to the degree that it limits our innate ability to make the right cholesterol for the production chain of ‘vitamin D’.
Secondly, the electromagnetic radiation of the required wavelength:
Winter can provide little sunshine, and human races vary greatly in the permeability of the skin to the required ultraviolet light. Although insufficiency of UV light may seem more plausible than deficiency of suitable sterols, please bear in mind that the human body has a great capacity to store cholecalciferol in the liver.
This means that
- exposure to sun in summer may be sufficient for the whole year, even at high latitudes, and
- humans in dim climates can have fairly dark skins.
Please consider that
- even northern Europeans can tan, and
- Inuit, Tierra del Fuegans, and Tasmanian aboriginals had skin that, even in winter, was relatively dark.
So, here is a new appraisal.
Vitamins by definition are acquired mainly from food.
‘Vitamin D' does not qualify as a vitamin for humans for five main reasons:
- the main source of ‘vitamin D’ in humans is not the environment but auto-synthesis within human cells,
- a dependence on sunlight for the photosynthesis of calciferol in skin cells is not equivalent to a dependence on dietary sources,
- too few foods naturally contain significant concentrations of ‘vitamin D’ for a dietary dependence to have evolved in humans (because the only food capable of serving as a supplement for ‘vitamin D’ at a wide range of latitudes would have been liver),
- the role of liver, as the only plausible dietary source of ‘vitamin D’ for human ancestors, is correlative rather than causal (because of its value for several other vitamins, including vitamin B12), and
- whether auto-synthesised or absorbed from food, ‘vitamin D’ is largely inactive in all human cells until converted to a hormone.
For these reasons, there is no likely scenario, in terms of ancestral natural selection, for the evolution of a dietary dependence on ‘vitamin D’ in humans:
- liver could hardly have been such a reliable food in the Palaeolithic that such dependence on it could plausibly have evolved;
- the form absorbed from the gut is a precursor, rather than being active in the human body; and
- the active hormonal form is synthesised solely in the kidney and not acquired from any diet.
The treatment of rickets hardly vindicates ‘vitamin D’. This is because milk contains negligible calciferol without pharmaceutical interventions. Furthermore, the ‘milk’ administered was a fortified formula in which artificial calciferol acted as a prodrug.
My conclusion:
Beyond mere semantic reasons, the steroid hormone called ‘vitamin D’ – which is administered like a drug – should be removed from the list of vitamins for humans.
FOOTNOTES
The only possible environmental deficiency proven for calciferol is in a narrow range of wavelengths within the ultraviolet. However, this does not qualify calciferol as a vitamin, because by definition vitamins have their main sources in food (https://en.wikipedia.org/wiki/Vitamin), not electromagnetic radiation.
Most dietary sources of ‘vitamin D’ for humans have been created artificially, by adding (?irradiating) industrially manufactured calciferol, directly or indirectly, to milk, egg-yolks, and beef. Medication of ruminant livestock may also have inadvertently enriched the livers of these animals for human consumption, relative to the livers of wild ruminants eaten by Palaeolithic humans. Certain fishes naturally contain calciferol, and this is the basis of supplementation of ‘vitamin D’ via cod liver oil. However, most of these species of fishes live in cold seas, and would have been unavailable to ancestral humans.
Vitamin B12 is the only vitamin containing a metallic catalyst, namely cobalt. Because organic compounds can be synthesised in cells but metallic elements cannot, vitamin B12 is a more likely candidate than ‘vitamin D’ for controlling human physiology.
The kidney contains endocrine cells, although the main functions of the kidney are not endocrine.
Bovine milk naturally contains negligible concentrations of calciferol, and even butter is not intrinsically a significant dietary source of ‘vitamin D’ for humans. Furthermore, there is little evidence that dairy products solve osteomalacia or osteoporosis in adults, which like rickets are maladies of inadequate mineralisation of bone.
Calciferol, when administered as a prodrug by mouth or by injection, is spontaneously converted to calcitriol in the kidney. In certain circumstances, this results in a potentially lethal hormonal imbalance. Although calciferol is widely accepted as a human medicine, it is also successful as a poison in baiting programs for brush-tailed possum (Trichosurus vulpecula) in New Zealand, and domestic rats (Rattus spp.) more widely. The physiological mechanism appears similar in all cases, raising the question of over-prescription in humans.
Comments
Add a Comment