Breakdown of the claims
There are a couple of claims contained together in this question.
- Vitamin D is formed on the skin (as well as in).
- Relatively large amounts remain on the skin or are secreted immediately from sun-sexposure onto the skin.
- In both cases the vitamins need an up to 48h waiting period to be (re-)absorbed by the body/skin.
- That washing away those vitamins is a major diminishing factor of sunlight vitamin D production and blood levels.
In accordance with the original claim I will mostly not differentiate between the different forms of vitamin D, like cholecalciferol (D3) as formed in the skin or the "active form" calcitriole (D1).
Analysis of claims
This "Vitamin D is formed in your sebum" (" the vitamin D3 that is formed is on the surface of your skin") is certainly not true in any meaningful amount.
But this doesn't stop 'experts on the net' from repeating this claim. Sometimes with reasoning, but without experiments to confirm that. But with ample additional reason, namely the conflict of interest that is called: reasons to sell supplements in the latter:
The only other possibility I can think of is an obscure paper from
1937, a paper that continues to be ignored. The authors obtained
surface oils from young men, sebum. In the first experiment, they
irradiated the oils and in a second experiment irradiated the young
men. They collected the sebum and showed that irradiated sebum cured
rickets in rats (showing effective treatment of rachitic rats was the
only way of measuring vitamin D activity in 1937). The authors
concluded, “The evidence presented in the two groups of experiments
indicates that washing the human skin by the usual methods removes
vitamin D and its precursors from the outer layer of the skin.”
Helmer AC, Jensen CH: Vitamin D precursors removed from the skin by
washing. Studies Inst Divi Thomae 1937, 1:207-216.
Even more upsetting, they concluded, “There is definitive evidence
that the secretions from the skin contains precursors of vitamin D,
which after irradiation are to be reabsorbed by the body, and the
removal of which tends to produce a dearth of the vitamin unless it be
supplied in some other form.” I could not see evidence that they
supported this statement with their research. What they showed was
Humans make some vitamin D on the surface of their skin, which water
washes off. How much humans make on the surface and how much inside
the skin, no one knows. However, the vitamin D levels of the African
tribesmen support (but do not prove) the proposition that humans
living in a natural state make a significant proportion of vitamin D
on the surface of their skin for later absorption. Assuming the
African hunter-gatherers do not take showers twice a day that so many
cosmetically brainwashed Americans do, then simple water, especially
soapy water, routinely washes off oils containing vitamin D in modern
humans. This means we must add soap and frequent showering to the list
of things that explain why modern vitamin D levels continue to
decline, decade after decade.
That life guards apparently in Hawaii do not shower compared to surfers according to this argument seems like a bit of a stretch.
The original research article that seems to be used there appears to be
"Low Vitamin D Status despite Abundant Sun Exposure"
N. Binkley; R. Novotny; D. Krueger; T. Kawahara; Y. G. Daida ...
The Journal of Clinical Endocrinology & Metabolism, Volume 92, Issue 6, 1 June 2007, Pages 2130–2135, https://doi.org/10.1210/jc.2006-2250
In there neither showering nor washing are mentioned. What is mentioned:
A probable explanation for the “low” 25(OH)D status of some
individuals is found in their failure to obtain high circulating D3
concentrations. Possible explanations for this include inadequate
cutaneous production of D3, enhanced cutaneous destruction of
previtamin D3 or vitamin D3, down-regulation of cutaneous synthesis by
sun-induced melanin production, or abnormalities of transport from the
skin to the circulation.
This was a very small sample and a study with multiple more shortcomings.
Just correlating self-reported exposure time with blood levels?
What if the life guards are egg munching carnivores and the surfers all underweight vegans? Vitamin D needs precursors, not just sunlight. (The surfer-study at least claimed to have controlled for dietary vitamin D intake. 'How' was left unrevealed.)
Reasons for doubt
First line of reason would be: people with darker skin living in higher latitudes have lower levels of D3 in their blood because melanin competes with the vitamin building molecules in capturing UVB. What colour has the sebum of people with darker skin? Melanin is in the skin, not on it.
Second, what is sebum?
Sebum, secreted by the sebaceous gland in humans, is primarily composed of triglycerides (~41%), wax esters (~26%), squalene (~12%), and free fatty acids (~16%). Vitamin D is not built from "fat" or fatty acids but cholesterol like molecules together with some proteins, both usually absent in sebum but present in the skin.
Third, how is vitamin D formed with sunlight exposure?
During exposure to sunlight, the solar ultraviolet B photons (290-315 nm) penetrate into the skin where they cause the photolysis of 7-dehydrocholesterol to precholecalciferol. Once formed, precholecalciferol undergoes a thermally induced rearrangement of its double bonds to form cholecalciferol. An increase in skin pigmentation, aging, and the topical application of a sunscreen diminishes the cutaneous production of cholecalciferol. Latitude, season, and time of day as well as ozone pollution in the atmosphere influence the number of solar ultraviolet B photons that reach the earth's surface, and thereby, alter the cutaneous production of cholecalciferol.
Frontiers in sebaceous gland biology and pathology:
(notice the barrier and the direction of arrows)
Synthesis and metabolism of vitamin D metabolites in human skin. Note
that sebocytes and various other cell types present in epidermal or
dermal compartments possess the enzymatic machinery [cytochrome P450
(CYP)27B1] to synthesize the biologically active vitamin D metabolite
1,25-dihydroxyvitamin D3. 7-DHC, 7-dehydrocholesterol; preD3,
previtamin D3; 25OHD3, 25-hydroxyvitamin D3; 1,25(OH)2D3,
1,25-dihydroxyvitamin D3; 24,25(OH)2D3, 24,25-dihydroxyvitamin D3;
1,24,25(OH)3D3, 1,24,25-trihydroxyvitamin D3; CYP27A1, vitamin
D-25-hydroxylase, 25OHase; CYP27B1, 25-hydroxyvitamin
D-1α-hydroxylase, 1αOHase; CYP24A1, 1,25-dihydroxyvitamin
D-24-hydroxylase, 24OHase; Δ7-R, 7-DHC-Δ7-reductase.
Synthesising vitamin D needs more than just sunlight. Irradiating cholesterol does not yield what you want. You need those enzymes that are not present on your skin. Any vitamin D present on skin comes from within.
From Wolfgang Herrmann and Rima Obeid (Eds): "Vitamins in the prevention of human diseases", 2011, Walter de Gruyter, Berlin/New York:
Cutaneously synthesized or orally ingested vitamin D is transported in the circulation bound to vitamin D binding protein (DBP). In the blood, only a small fraction is present as free, unbound vitamin D metabolites. The 25-hydroxylation of both vitamin D2 or vitamin D3, is the initial step in vitamin D activation. This takes place primarily in the liver. […] Nevertheless, extra-hepatic sources of 25-hydroxylation have been described in humans as well. They include macrophages, fibroblasts, keratinocytes and arterial endothelial cells (Gascon-Barre, 2005).
Meaning two things: The main producer sites for the vitamin do not secrete out of the skin and only a small fraction would be present to do so.
There are no reports of vitamin D intoxication in healthy adults after intensive sunlight exposure. Vitamin D in the skin reaches a plateau after only 15–30 min of UVB exposure. Then, vitamin D-inactive substances such as lumisterol and tachysterol are produced, which do not reach the systemic circulation.
That means that only a small amount is available:
Its precursor 7-dehydrocholesterol in the plasma mem- branes of both epidermal basal and suprabasal keratinocytes and dermal fibroblasts is converted to previtamin D3. Cutane- ously synthesized vitamin D3 is released from the plasma membrane and enters the systemic circulation bound to vitamin D-binding protein (DBP) […]
Factors influencing vitamin D levels
Nutrient deficiencies are usually the result of dietary inade- quacy, impaired absorption and use, increased requirement, or increased excretion. Vitamin D deficiency can occur when usual intake is lower than recommended levels over time, exposure to sunlight is limited, the kidneys cannot convert 25(OH)D to its active form, or absorption of vitamin D from the digestive tract is inadequate. Vitamin D-deficient diets are associated with milk allergy, lactose intolerance, ovo-vegetarianism, and veganism .
Regarding the amount of vitamin D production in human skin, it depends on several variables including environmental factors such as geographic latitude, season, time of day, weather conditions (cloudiness), amount of air pollution and surface reflection which can all interfere with the amount of UVB radiation reaching the skin […]
The skin is unique in being not only the source of vitamin D for the body but also in being capable of responding to the active metabolite of vitamin D, 1,25(OH)2D. Both 1,25(OH)2D and its receptor (VDR) play essential roles in the skin.
From: Vitamin D and the skin: Focus on a complex relationship: A review
Note the role of vitamin D that has to go from the skin through liver and kidney back to the skin to have these effects.
And finally fourth: how much evidence does this guru cite for his version of "be careful with soap"?
"New evidence suggests" that one has to be able to read it to gauge its accuracy and validity.
Guru's link number iv, entitled "iv Acta Biochimica Polonica. 2012 Mar 17. [Epub ahead of print]" is indeed the same link as the third link again (UVB-Primer.pdf from Colorado State University).
Answering this fourth question has to go like "zero evidence". In fact it is such a crazy idea in itself, that I had to go through web-archive to even get to the part cited in the OP question, since it has apparently been silently retracted since then. Only in the older comments do people talk quite lively about "showering" despite the article no longer mentioning it now.
Seems sad to not have an excuse for avoiding the shower? But if you need one, "vitamin D reduction" is most certainly not very suitable.
Vitamin D is present on the human skin, and transported there with sebum, but only in small amounts compared to what is transported away inwards. Whether from sunlight or nutrition, excretion of that substance is low. Synthesised with sunlight vitamins are mostly transported away from the skin into the rest of the system, not outwards.
Once present on the skin the vitamin can be absorbed through the skin, regardless of origin. But again, compared to internally absorbed amounts or currently illegal ointments containing vitamin D the amount is very, very small – not meaningful.
As a fat soluble substance on the surface of skin it then can be washed away from there. But the impact of the small fraction present on the skin is not a justifiable excuse to avoid washing for 48 hours after sun exposure.
20 minutes of sun exposure have been experimentally shown to be enough time in regular individuals at not too extreme latitudes to produce adequate amounts of vitamin D (while totally disregarding washing behaviour).
If washing would be a concern for vitamin D (re-)absorption than washing would not be the only problem there: the skin microbiome eats away at it, your own sweat washes it away, abrasion diminishes it and then we have this impractical invention of clothing where a lot of the sebum from your skin ends up in if you look at white collars after wearing them for a while.
In Summary: a very small grain of truth seems to be in the original claims. The proportions and conclusions drawn from that are widely off. As phrased in the title, the claim is true in theory – but very largely irrelevant in application.