Extremely interesting Robyn! My take away from this is as follows:
being fair skinned, self employed and living in a beach side suburb of Sydney, I'm lucky and have the opportunity to get adequate sun exposure. (I'd hate to be dark skinned and living somewhere like northern Europe as it seems a real health hazard) I wonder if this partly explains the generally poorer health of black Americans given many live in a climate not suited to dark skin and have no hope of ever getting sufficient sun exposure and probably being chronically deficient in Vitamin D.
Given that the situation seems to be that Vit D supplementation is very unlikely to be as good as sunlight, potentially carries risks and that food sources can't supply it, I'll prioritise sensible sun exposure, cover sun damaged skin such as forearms, avoid sunscreens, not shower or swim for at least 3 hrs after sun exposure.
If my labs show levels under say 65 nmol/L I'll review and consider supplements.
My concern with supplements though, is (apart from not trusting their contents are what they are supposed to be) they may cause the body to shutdown endogenous production of Vit D if it perceives levels are adequate and then I'd be reliant on the inferior supplemental form ongoing. (sure, a great business model for industry)
How does one deal with periods of extended wet and cloudy weather as Sydney has experienced in the last 4 years or so?
"I wonder if this partly explains the generally poorer health of black Americans given many live in a climate not suited to dark skin and have no hope of ever getting sufficient sun exposure and probably being chronically deficient in Vitamin D." - Yep, I'm sure that's a big part of it.
I originally had a section on safe sun exposure in this part of the series, but decided to leave it to the end of the series, when I'll wrap up with evidence-based recommendations for obtaining vitamin D. Spoiler alert though: if you have even sporadic sun exposure at Sydney's latitude, especially to the less-tanned parts of your body, you'll be OK even when there's weeks of wet/very cloudy weather.
Another fantastic article Robyn, well worth the paid subscription!
I’m interested in what level of benefit comes from us being exposed to the full spectrum of light when we get sunlight and whether we fully understands this process yet, as opposed to the analysis of the individual spectrums?
You're asking exactly the right question re light. I strongly recommend reading John Ott's book Health and Light (hard to get in print these days but you can read it for free at https://archive.org/details/healthlighteffec00ottj). It was published way back in 1976 but is well worth reading because it describes Ott's extensive experiments on the effect of light of various spectral compositions, on animal and human health and behaviour.
We are no longer getting nearly as much exposure to infrared light as our ancestors; infrared saunas offer comparable benefits to 'old fashioned' saunas, but whether they help to compensate for our lack of exposure to IR light, I do not know.
P.S. just wanted to make it 100% clear that infrared light has no benefits for vitamin D productions; only UVB stimulates this. But IR light - and near-infrared - does stimulate nitric oxide production which increases blood flow and speeds up wound healing.
Thanks for another great article. Non-vitamin D is something I’ve been keenly aware of for a long time so I didn’t learn a lot other than the mechanism for self regulation of production via sun exposure. The issue of supplementation is a bit different with vitamin D as you can’t just say eat your veggies. Where I live sun angle in winter is about 24° so not going to get sufficient sun exposure unless I were to stand outside all day naked where the air temperature would be below freezing. So, I do supplement with D3/K2.
I’m sure you will cover this in upcoming posts, but regarding vitamin D toxicity, specifically cholecalciferol as rat poison. There is a writer here on Substack (agent131711) that says that cholecalciferol is not like rat poison, or is used in rat poison, but IS rat poison. Yes , some rat poison uses cholecalciferol as its active ingredient because it is toxic to animals. But, a dose that would be toxic to a human would be 1000 times more than even a high dose of vitamin D.
I’m not worried about overdosing. Look forward to more.
I'm familiar with the 'cholecalciferol is rat poison' argument and agree that it's not really relevant to standard vitamin D supplement dosing protocols.
I'll get to your first question in a subsequent part of this miniseries. As for the 2nd and 3rd questions, the answer to both is yes. You can obtain calcitriol on prescription if you fulfil the diagnostic indicators at https://www.austrahealth.com.au/calcitriol-drug-information.html.
(2 of 3) Most people without proper vitamin D3 supplementation or recent extensive UV-B exposure (which is not very effective for those with brown or black skin) have 25-hydroxyvitamin D levels in the 10 to 25 nanogram per millilitre range. Doctors regard this as normal, and most of them aim for at least 20 ng/mL, which is sufficient to enable the kidneys to play their role in regulating calcium-phosphate-bone metabolism.
In the UK, Australia, New Zealand and some other countries, the level of 25-hydroxyvitamin D is reported in nanomols per litre. Multiply the ng/mL figure by 2.5 to get the nmol/L value.
This research shows that the *pre*-operative levels of 25-hydroxyvitamin D affected the risk of post-operative infections, both surgical site and hospital-acquired infections. For 50 ng/mL or more circulating 25-hydroxyvitamin D, the risk of each kind of infection was about 2.5%. The further below this level the 25-hydroxyvitamin D level was, the higher the risk of both types of infection. At 20 ng/mL, which is a typical level for people who do not supplement vitamin D3 properly, or at all, and who have not had a lot of UV-B skin exposure in the last month or two, the risk of each kind of infection was 25%. Some people have levels as low as 10 or even 5 ng/mL - especially brown or black skinned people living far from the equator. At 10 ng/mL, the risk of each kind of infection rose to 40%.
While severe illness may somewhat depress the 25-hydroxyvitamin D, due to the immune system using more of it, lack of supplements, liver dysfunction and/or lack of UV-B skin exposure, this research shows very clearly that the association of low 25-hydroxyvitamin D with illness is primarily causative with the low level weakening the immune system (since many types of immune cell can no longer respond to their changing circumstances when their intracrine and paracrine signaling systems are not supplied with enough 25-hydroxyvitamin D),so causing worse disease.
Most doctors and immunologists are not aware of this research. So if a patient's 25-hydroxyvitamin D level is, for instance, 50 ng/mL, which is just enough to supply their immune system properly, the doctor may consider them at risk of toxicity and so may advise them to cease or reduce vitamin D3 supplementation. Toxicity only becomes a potential problem (hypocalcemia and so calcification of the arteries and weakening of bones) above 150 ng/mL - a level which can only be attained by ingesting lots of vitamin D3 a day, for months - such as 1.25 mg 50,000 IU a day. (Yet some people do this, under medical supervision, to suppress auto-immune disorders including MS, rheumatoid arthritis, psoriasis, cluster headaches, migraine etc. See the Coimbra and related protocols: https://vitamindstopscovid.info/06-adv/, https://www.coimbraprotocol.com/the-protocol-1 and Finamor et al. 2013: https://www.tandfonline.com/doi/full/10.4161/derm.24808.)
https://vitamindstopscovid.info/00-evi/#00-how-much has recommendations from New Jersey based Professor of Medicine, Sunil Wimalawansa, based on his 2021 article in Nutrients: https://www.mdpi.com/2072-6643/14/14/2997, on how much vitamin D3 to supplement (according to body weight and obesity status) on order to safely attain at least the 50 ng/mL level of circulating 25-hydroxyvitamin D the immune system needs to function properly, without the need for blood tests or medical monitoring.
For average weight adults, this is about 0.125 milligrams = 5000 IU a day on average. This is a gram every 22 years. Pharma-grade vitamin D3 costs about USD$2.50 a gram ex-factory.
This takes several months to raise the 25-hydroxyvitamin D level safely over 50 ng/mL. So it is best to take more for a few weeks to accelerate the process when pregnant.
For clinical emergencies, such as Kawasaki disease, MIS-C, sepsis, COVID-19 etc. a bolus dose of vitamin D3, such as 10 mg 400,000 IU for a 70 kg 154 lb adult, can raise the level of 25-hydroxyvitamin D in a few days. A single oral dose of 1 milligram of calcifediol (again for 70 kg BW), which *is* 25-hydroxyvitamin D, can attain this in 4 hours. See Prof. Wimalawansa's article and: https://vitamindstopscovid.info/00-evi/#4.7.
I will just add one small comment to the excellent notes by Robin; that despite Robyn’s emphasis on the likelihood of superior impact of solar obtained vitamin D; those who are most vulnerable to illness— the chronically ill, the frail elderly are usually never exposed to large enough doses of UVB rays to obtain sufficient vitamin D.
Therefore public health policies and professional societies ought to have shifted their guidance (per the bench science which Robin has so carefully elucidated and has been available for well over a decade) to inform health care practitioners to monitor vitamin D levels and ensure that the vulnerable have levels sufficient to allow for the interactive and paracrine signaling.
Paracrine signaling from vitamin D is crucial to prevent a person from having uncontrolled cytokine activation through balancing T helper 1 (Th1) and T helper 2 cells.
RCTs will never demonstrate the biological impact of vitD in the same way we show the outcome of a drug because pharmaceutical products typically have singular receptors that they target; therefore you study a dose: response relationship. Vitamin D is a pleiotropic substance with so many impacts within different cell types ; it does not behave like a drug. If you review the RCTs, you find that until the last four years— most studies used ‘homeopathic ‘ doses of vitamin D which were designed by their low doses to never be able to detect a response. The IOM’s RDA allowances for vitD were challenged (in peer reviewed journals) by two epidemiological teams pointing out the research design flaws which resulted in doses too low by a factor of ten. They never even gave a scientific response, let alone revisited the RDA.
(And to respond to another earlier commenter…) On the south side of Chicago, many black residents believe the State has always been an adversary. Looking at the NHANES data on the disproportionately low vitD levels and understanding the suppression of information by public health actors— would you disagree?
Regarding the frail elderly receiving insufficient sunlight exposure to meet their vitamin D needs, this was exactly the point I made in the article. Did you read it?
I will be addressing all your other claims in subsequent parts of this miniseries.
(1 of 3) For most practical purposes, vitamin D3 cholecalciferol is a vitamin, since few people who live far from the equator can get enough UV-B skin exposure to generate enough vitamin D3 to raise circulating 25-hydroxyvitamin D to the 50 ng/mL 125 nmol/L (1 part in 20,000,000 by mass) level which the immune system needs to function properly. Such UV-B is only available in sufficient quantities from high elevation sunlight on clear summer days, without clothing, glass or sunscreen attenuating it. The same UV-B wavelengths damage DNA and so raise the risk of skin cancer. This is not to say that there are no physical and mental benefits from sunlight and/or being outdoors in general. Just that to rely on natural sunlight is insufficient for good health, and buying a special UV-B lamp is more expensive and risky (skin cancer) than taking vitamin D3 supplements.
In most or all countries, most people have only a fraction of the 25-hydroxyvitamin D their immune system needs to function properly. The problems begin before birth: https://vitamindstopscovid.info/00-evi/#3.2, with preeclampsia, pre-term birth and the later development of autism, ADHD, intellectual disability and schizophrenia.
Infectious diseases, cancer and auto-immune diseases are more prevalent, harmful and deadly than they would be if everyone had at least 50 ng/mL 25-hydroxyvitamin D. https://vitamindstopscovid.info/00-evi/#3.3 cites and discusses research concerning low 25-hydroxyvitamin D levels, which are common, greatly increasing the risk of neurodegeneration - Alzheimer's disease, Parkinson's disease, dementia with Lewy bodies etc.
25-hydroxyvitamin D is produced, primarily in the liver, from vitamin D3 which is ingested or produced in the (ideally white) skin by ultraviolet-B irradiation, which breaks a carbon ring in 7-dehydrocholesterol. There is very little vitamin D3 in food, fortified or not.
A hormone is a blood-borne long-distance signaling molecule - a substance produced somewhere in the body, which goes into circulation in the bloodstream and cerebrospinal fluid, where its concentration (level) alters the behavior of one or more types of cell. Hormonal AKA endocrine signalling is a means by which an organ, such as the kidneys, can control or influence other parts of the body.
Neither vitamin D3 nor 25-hydroxyvitamin D function as hormones. They are not signaling molecules. 25-hydroxyvitamin D circulating in the bloodstream takes months to build up with healthy intakes of supplemental vitamin D3. "Vitamin D" blood tests measure the level (concentration) of 25-hydroxyvitamin D, which is not a vitamin.
Vitamin D3's primary or sole role is to be converted (hydroxylated, by adding an oxygen-hydrogen hydroxyl group to the 25th carbon), primarily in the liver, to circulating 25-hydroxyvitamin D, which has a half-life there measured in months, or weeks at higher, healthy, levels.
The best known role for 25-hydroxyvitamin D is to supply the kidneys, which convert some of it to a very low level (ca. 0.05 ng/mL) of circulating 1,25-dihydroxyvitamin D (calcitriol), by hydroxylating it on the number 1 carbon. 25-hydroxyvitamin D is also known as calcifediol and "calcidiol", which I think is best avoided since it looks and sounds much like "calcitriol".
This kidney-produced calcitriol functions as a hormone, since it affects the behaviour of multiple cell types around the body which are involved in calcium, phosphate and bone metabolism. The kidney's rate of calcitriol production is controlled by the level of parathyroid hormone (the parathyroid gland senses calcium ion levels) and by the level of fibroblast growth factor 23 (FSF23) which is secreted by osteocytes, the primary cell-type of bone: https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2020.00592/full .
This is the one hormonal function of the three compounds which are, commonly but incorrectly, all referred to as "vitamin D". Vitamin D3 is a vitamin. 25-hydroxyvitamin D and calcitriol are not vitamins. Calcitriol can function as a hormone, as just described. However, all the other cell types which convert 25-hydroxyvitamin D to calcitriol do so in ways which have nothing to do with hormonal signaling.
Many types of immune cell respond to a particular (different for each cell type) condition by hydroxylating 25-hydroxyvitamin D to calcitriol, inside the cell, with the calcitriol binding to so-called "vitamin D receptor" molecules (a better term would be "calcitriol receptor", since it binds only very weakly to vitamin D3 and 25-hydroxyvitamin D). The bound complex finding its way to the nucleus. There it binds to the "retinol X" molecule and the triple-bound complex alters gene transcription to RNA (and so alters the cell's protein synthesis and so behaviour) in complex and powerful ways. The transcription of dozens of genes is up-regulated and the transcription of dozens of other genes is down-regulated. The exact details of these gene expression changes differs from one cell type to the next.
This is intracrine signaling - the cell producing a compound, here calcitriol, which functions as an intracrine agent which is sensed within the same cell and so alters its behaviour. This is unrelated to hormonal signaling. A variation is paracrine signaling, in which some of the calcitriol diffuses out of the cell, raising the intracellular calcitriol level in that area (millimetres, I guess) well above the very low hormonal background level. This raised level is detected by other cell types an changes their behavior.
Most doctors and immunologists have never heard of 25-hydroxyvitamin D to calcitriol intracrine and paracrine signaling. There being no peer-reviewed journal tutorial on these, I wrote one in 2020: https://vitamindstopscovid.info/02-intracrine/. Intracrine signaling is sometimes incorrectly referred to as "autocrine" signaling. I made this mistake initially. Autocrine signaling involves the compound leaving the cell but altering its behavior by being detected by receptors on the outside of the cell membrane.
(3 of 3) Thanks for citing Tintut et al. 2021 "Potential Impact of the Steroid Hormone, Vitamin D, on the Vasculature" https://sci-hub.se/10.1016/j.ahj.2021.05.012. They suggest that vitamin D3, carried in the bloodstream by cylomicrons (tiny fat globules) after being ingested (but not from UV-B produced vitamin D3) is somehow a problem for the endothelial cells which line blood vessels.
The most important site of hydroxylation to produce circulating 25-hydroxyvitamin D is the liver. They suggest on page 6 that this vitamin D3 may be hydroxylated more rapidly in the liver in this form than the vitamin D3 which comes from the skin and is transported in the blood primarily bound to the "vitamin D binding protein" (which also binds to 25-hydroxyvitamin D and calcitriol), and less strongly to albumin proteins. Maybe so - I had not read this. If so, why would this be a problem for the vasculature?
On page 7 they correctly note that (very) high levels of circulating 25-hydroxyvitamin D or calcitriol can lead to calcification of the arteries. Vitamin D3 has a half-life of days in the bloodstream, and calcitriol hours. Very high levels (150 ng/mL or more) of 25-hydroxyvitamin D can cause hypocalcemia, calcification of the arteries and bone loss due to two mechanisms at least. Firstly, since it binds weakly to the "vitamin D" receptor molecules which some cells used to sense the very low level of hormonal calcitriol, those receptors are activated excessively even in the absence of being activated much by hormonal calcitriol. The second mechanism is that with high 25-hydroxyvitamin D levels, the kidneys tend to produce more calcitriol, resulting in a raised level of calcitriol. See Fig 1b in Tang et al. 2019: https://www.nature.com/articles/s41598-019-43462-6.
On page 8 they state that 25-hydroxyvitamin D levels "greater than 36 ng/mL (75 nmol/L)" are "considered unsafe". This is a common but completely ill-informed belief. The authors do not challenge it an so presumably accept it as true. They should read the research I cite and discuss at: https://vitamindstopscovid.info/00-evi/.
On pages 8 and 9 the authors speculate about 25-hydroxyvitamin D being hydroxylated to calcitriol (which they refer to as the 25-hydroxyvitamin D being "activated") in endothelial cells, implying that harm would result from too high a level of circulating 25-hydroxyvitamin D. Perhaps so, but this is just a suggestion and they present no evidence that it is pathological at some level of 25-hydroxyvitamin D they do not specify.
Their references 65 and 66 are cited in "Aortic endothelial cells produce and respond to the active hormone in an autocrine manner, including inhibition of growth and of angiogenic activities such as sprouting and formation of networks." However, they are not sure (page 11) whether the ill effects of excessive 25-hydroxyvitamin D and/or calcitriol, in forming vascular calcification, are local (due to VDR activation in endothelial cells) or systemic (such as resulting from a calcium ion level which exceeds what it is supposed to be, which is a nearly saturated level with a very narrow healthy range). On line 191 they mention evidence for systemic, and against local, mechanisms.
On page 12 they mention obese mice being at greater risk of "vitamin D hormone" (they count all three compounds as this, not just calcitriol, which is not, itself, vitamin D) toxicity. They are surely are unaware of the Quraishi research (see previous comments) which show that 50 ng/mL or more circulating 25-hydroxyvitamin D is needed for proper immune system function in the generally morbidly obese subjects in that Massachusetts General Hospital post-operative research.
They correctly note that 25-hydroxyvitamin D levels are generally lowered by obesity. See https://5nn.info/temp/250hd-obesity/ for links to research on the two proposed mechanisms.
On page 13 they mention ""vitamin D-hormone" inhibition of osteoclasts also occurs in the artery wall". But osteoclasts are in bone, not artery walls. A Google search led me to Jaing et al. 2021 https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2021.639740/full which mentions: "osteoclast-like cells have also been detected in calcified arterial walls wherein they possibly inhibit vascular calcification, similar to the catabolic process of bone mineral resorption." This would mean that osteoclast-like cells would reduce vascular calcification.
This is a speculative article by authors who have no idea about the immune system's need for at least 50 ng/mL circulating 25-hydroxyvitamin D. I don't think provides observations or persuasive arguments which support "concern that diet-derived vitamin D, carried into arterial walls on LDL particles, may promote the calcification of atherosclerotic plaque."
There probably is some locally significant hydroxylation of skin-produced vitamin D3 in the skin, to 25-hydroxyvitamin D, which would then diffuse into all the cells there and so enable them to work better (with better intracrine and paracrine signaling, for those cell types which do this with 25-hydroxyvitamin D >> calcitriol) even if the circulating level of 25-hydroxyvitamin D is very low. This would be one mechanism by which UV-B exposure of skin affected by psoriasis is effective.
See: https://vitamindstopscovid.info/06-adv/ for inflammatory auto-immune disorders being caused or worsened by both low 25-hydroxyvitamin D and lack of helminths, and suppressed both by high (e.g. 100ng/mL or more) 25-hydroxyvitamin D levels and/or deliberately introduced helminth infections: https://helminthictherapywiki.org.
Gibson et al. 2015 Dietary Vitamin D and Its Metabolites Non-Genomically Stabilize the Endothelium" https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0140370 report that ingested vitamin D3 promotes health by directly assisting endothelial cells, using some unknown mechanism, without the need for hydroxylation to 25-hydroxyvitamin D and then again to calcitriol. I have not looked at this in detail, so I don't know how significant it is, or what other research supports it or not. This is interesting and potentially significant research, including regarding sepsis and ARDS.
Thankyou so much Robin have stopped both Vit D supplementation and cholesterol reduction with statins after reading the story about Ansel Keys Cholesterol Con exposed by Prof Tim Noakes.
Still experiencing tinnitus (potential statin side effect) but have put that down to damage of the ear Military exposure- Gun Shots close range.
There really has been a pile-on to Ansel Keys, ever since Gary Taubes made up some nonsense about him and a whole lot of other authors copied-and-pasted without ever having read Keys' many papers for themselves. I highly recommend that you do exactly that.
It's very clear that Noakes has not in fact read Keys' work, because even in part 1 of this series he rehashes the same false claims that Taubes made, and Teichholz plagiarised without acknowledging Taubes. Heck, Noakes even admits that he read ABOUT Keys's work rather than reading it for himself, with this statement: "Only when I read and re-read the game-changing books by the path-finders for truth in this matter - Russell L. Smith and Edward R. Pinckney (74), Thomas J. Moore ((75), Gary Taubes (1) and Nina Teichholz (3) - did I begin to understand the truth."
He then repeats in Part 2, "The ideas and arguments I present are not original in that I am not their original source. Rather they have been covered in compelling detail in the four iconic books (i.e. those by Smith, Taubes etc), and in a number of others that confine themselves to what has become known as the Cholesterol Scam or the Cholesterol Con."
In other words, Noakes is rehashing other people's arguments, which in turn are rehashings of other people's arguments. This is intellectual laziness, which I utterly despise.
I try not to offer opinions, but instead to base my assessments on the facts, as best I can ascertain them. The process of ascertaining facts can be challenging, and it's never possible to be absolutely certain of just about anything! But when I see people making statements that are clearly factually incorrect - and stating them with total conviction - it gets my goat.
Lots of logically connected theories can lay the foundations for a compelling story, but may miss the bullseye of truth by quite some margin. For example, this paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3897598/ has a prehistoric perspective that is pure made up drivel. What causes rickets, do we see this condition occuring these days in people who don't get any direct sunlight? There are other points but I don't want to do a Robin Whittle about it:-)
I don’t think you need me to point out drivel in that paper, all you need do is read each statement in the ‘prehistoric perspective’. The first statement reads, ‘Life forms began to evolve in the oceans over 1 billion years ago’. The next statement reads, ‘They took advantage of sunlight and used it as an energy source to generate carbohydrates’. Both statements are unprovable nonsense made up in somebody’s imagination. There are infinite likely scenarios for how life began, to even suggest it began ‘a billion years ago’ is preposterous, yet alone to write it as a statement of fact. The ‘prehistoric perspective’ really sets the tone for the entire paper.
I get that there is a condition called Rickets, but what causes it? While it may be correlated with inadequate sunlight exposure, that may not be the cause. Are people with Rickets tested for nutritional deficiencies and toxins? Conditions within industrialising European cities were horrific, especially for child workers (slaves) and it is likely many were suffering from novel toxic exposure and lack of nutrition. Lack of sunlight would make a convenient cover story for profit-hungry industrialists with little regard for human life.
Are you disputing that life forms utilise sunlight to generate carbohydrates?
And did you read the link above re rickets occurring presently in Australia, and the particular demographic/cultural groups in which it occurs? It's pretty bloody clear that inadequate sunshine exposure causes rickets.
'If it's pretty bloody clear' that inadequate sunshine exposure causes rickets, then please reference the papers that prove it, there must be many robust papers showing factual data supporting that bold statement. The papers would ensure that other potential causative factors have been analysed and discounted.
It is yet to be proven that all aquatic life 'breathe' oxygen or utilise sunlight.
Did you find the supporting data for the two statements listed in my previous reply?
Extremely interesting Robyn! My take away from this is as follows:
being fair skinned, self employed and living in a beach side suburb of Sydney, I'm lucky and have the opportunity to get adequate sun exposure. (I'd hate to be dark skinned and living somewhere like northern Europe as it seems a real health hazard) I wonder if this partly explains the generally poorer health of black Americans given many live in a climate not suited to dark skin and have no hope of ever getting sufficient sun exposure and probably being chronically deficient in Vitamin D.
Given that the situation seems to be that Vit D supplementation is very unlikely to be as good as sunlight, potentially carries risks and that food sources can't supply it, I'll prioritise sensible sun exposure, cover sun damaged skin such as forearms, avoid sunscreens, not shower or swim for at least 3 hrs after sun exposure.
If my labs show levels under say 65 nmol/L I'll review and consider supplements.
My concern with supplements though, is (apart from not trusting their contents are what they are supposed to be) they may cause the body to shutdown endogenous production of Vit D if it perceives levels are adequate and then I'd be reliant on the inferior supplemental form ongoing. (sure, a great business model for industry)
How does one deal with periods of extended wet and cloudy weather as Sydney has experienced in the last 4 years or so?
"I wonder if this partly explains the generally poorer health of black Americans given many live in a climate not suited to dark skin and have no hope of ever getting sufficient sun exposure and probably being chronically deficient in Vitamin D." - Yep, I'm sure that's a big part of it.
I originally had a section on safe sun exposure in this part of the series, but decided to leave it to the end of the series, when I'll wrap up with evidence-based recommendations for obtaining vitamin D. Spoiler alert though: if you have even sporadic sun exposure at Sydney's latitude, especially to the less-tanned parts of your body, you'll be OK even when there's weeks of wet/very cloudy weather.
Another fantastic article Robyn, well worth the paid subscription!
I’m interested in what level of benefit comes from us being exposed to the full spectrum of light when we get sunlight and whether we fully understands this process yet, as opposed to the analysis of the individual spectrums?
And, do IR saunas provide similar benefits?
Thanks again
You're asking exactly the right question re light. I strongly recommend reading John Ott's book Health and Light (hard to get in print these days but you can read it for free at https://archive.org/details/healthlighteffec00ottj). It was published way back in 1976 but is well worth reading because it describes Ott's extensive experiments on the effect of light of various spectral compositions, on animal and human health and behaviour.
We are no longer getting nearly as much exposure to infrared light as our ancestors; infrared saunas offer comparable benefits to 'old fashioned' saunas, but whether they help to compensate for our lack of exposure to IR light, I do not know.
P.S. just wanted to make it 100% clear that infrared light has no benefits for vitamin D productions; only UVB stimulates this. But IR light - and near-infrared - does stimulate nitric oxide production which increases blood flow and speeds up wound healing.
Another intriguing article Robyn. 'Vitamin'D supplementation formed part of advised Covid 19 protocol. Has its inclusion been revised?
Not by the authors of the protocols... but stay tuned for subsequent parts of this miniseries!
Thanks for another great article. Non-vitamin D is something I’ve been keenly aware of for a long time so I didn’t learn a lot other than the mechanism for self regulation of production via sun exposure. The issue of supplementation is a bit different with vitamin D as you can’t just say eat your veggies. Where I live sun angle in winter is about 24° so not going to get sufficient sun exposure unless I were to stand outside all day naked where the air temperature would be below freezing. So, I do supplement with D3/K2.
I’m sure you will cover this in upcoming posts, but regarding vitamin D toxicity, specifically cholecalciferol as rat poison. There is a writer here on Substack (agent131711) that says that cholecalciferol is not like rat poison, or is used in rat poison, but IS rat poison. Yes , some rat poison uses cholecalciferol as its active ingredient because it is toxic to animals. But, a dose that would be toxic to a human would be 1000 times more than even a high dose of vitamin D.
I’m not worried about overdosing. Look forward to more.
I'm familiar with the 'cholecalciferol is rat poison' argument and agree that it's not really relevant to standard vitamin D supplement dosing protocols.
Hi Robyn, Trevor Osborne here. I have 3 questions:
1. Can taking high doses of D3 (20,000 or higher) cause kidney damage?
2. My kidney function is around 33%. Is this level going to reduce my kidney's ability to do its job in converting to active form?
3. Is it possible for me to take the active form so my kidney's don't have to convert?
I'll get to your first question in a subsequent part of this miniseries. As for the 2nd and 3rd questions, the answer to both is yes. You can obtain calcitriol on prescription if you fulfil the diagnostic indicators at https://www.austrahealth.com.au/calcitriol-drug-information.html.
(2 of 3) Most people without proper vitamin D3 supplementation or recent extensive UV-B exposure (which is not very effective for those with brown or black skin) have 25-hydroxyvitamin D levels in the 10 to 25 nanogram per millilitre range. Doctors regard this as normal, and most of them aim for at least 20 ng/mL, which is sufficient to enable the kidneys to play their role in regulating calcium-phosphate-bone metabolism.
In the UK, Australia, New Zealand and some other countries, the level of 25-hydroxyvitamin D is reported in nanomols per litre. Multiply the ng/mL figure by 2.5 to get the nmol/L value.
Typical reference ranges supplied with the results of 25-hydroxyvitamin D blood tests are 20 to 40 ng/mL (50 to 100 nmol/L). Yet research shows clearly that the immune system needs at least 50 ng/mL (125 nmol/L = 1 part in 20,000,000 by mass) to function properly: Quraishi et al. 2014 https://jamanetwork.com/journals/jamasurgery/fullarticle/1782085 - and their graphs combined: https://vitamindstopscovid.info/00-evi/#00-50ngmL.
This research shows that the *pre*-operative levels of 25-hydroxyvitamin D affected the risk of post-operative infections, both surgical site and hospital-acquired infections. For 50 ng/mL or more circulating 25-hydroxyvitamin D, the risk of each kind of infection was about 2.5%. The further below this level the 25-hydroxyvitamin D level was, the higher the risk of both types of infection. At 20 ng/mL, which is a typical level for people who do not supplement vitamin D3 properly, or at all, and who have not had a lot of UV-B skin exposure in the last month or two, the risk of each kind of infection was 25%. Some people have levels as low as 10 or even 5 ng/mL - especially brown or black skinned people living far from the equator. At 10 ng/mL, the risk of each kind of infection rose to 40%.
While severe illness may somewhat depress the 25-hydroxyvitamin D, due to the immune system using more of it, lack of supplements, liver dysfunction and/or lack of UV-B skin exposure, this research shows very clearly that the association of low 25-hydroxyvitamin D with illness is primarily causative with the low level weakening the immune system (since many types of immune cell can no longer respond to their changing circumstances when their intracrine and paracrine signaling systems are not supplied with enough 25-hydroxyvitamin D),so causing worse disease.
Most doctors and immunologists are not aware of this research. So if a patient's 25-hydroxyvitamin D level is, for instance, 50 ng/mL, which is just enough to supply their immune system properly, the doctor may consider them at risk of toxicity and so may advise them to cease or reduce vitamin D3 supplementation. Toxicity only becomes a potential problem (hypocalcemia and so calcification of the arteries and weakening of bones) above 150 ng/mL - a level which can only be attained by ingesting lots of vitamin D3 a day, for months - such as 1.25 mg 50,000 IU a day. (Yet some people do this, under medical supervision, to suppress auto-immune disorders including MS, rheumatoid arthritis, psoriasis, cluster headaches, migraine etc. See the Coimbra and related protocols: https://vitamindstopscovid.info/06-adv/, https://www.coimbraprotocol.com/the-protocol-1 and Finamor et al. 2013: https://www.tandfonline.com/doi/full/10.4161/derm.24808.)
https://vitamindstopscovid.info/00-evi/#00-how-much has recommendations from New Jersey based Professor of Medicine, Sunil Wimalawansa, based on his 2021 article in Nutrients: https://www.mdpi.com/2072-6643/14/14/2997, on how much vitamin D3 to supplement (according to body weight and obesity status) on order to safely attain at least the 50 ng/mL level of circulating 25-hydroxyvitamin D the immune system needs to function properly, without the need for blood tests or medical monitoring.
For average weight adults, this is about 0.125 milligrams = 5000 IU a day on average. This is a gram every 22 years. Pharma-grade vitamin D3 costs about USD$2.50 a gram ex-factory.
This takes several months to raise the 25-hydroxyvitamin D level safely over 50 ng/mL. So it is best to take more for a few weeks to accelerate the process when pregnant.
For clinical emergencies, such as Kawasaki disease, MIS-C, sepsis, COVID-19 etc. a bolus dose of vitamin D3, such as 10 mg 400,000 IU for a 70 kg 154 lb adult, can raise the level of 25-hydroxyvitamin D in a few days. A single oral dose of 1 milligram of calcifediol (again for 70 kg BW), which *is* 25-hydroxyvitamin D, can attain this in 4 hours. See Prof. Wimalawansa's article and: https://vitamindstopscovid.info/00-evi/#4.7.
I will be addressing all these claims in subsequent parts of this miniseries.
I will just add one small comment to the excellent notes by Robin; that despite Robyn’s emphasis on the likelihood of superior impact of solar obtained vitamin D; those who are most vulnerable to illness— the chronically ill, the frail elderly are usually never exposed to large enough doses of UVB rays to obtain sufficient vitamin D.
Therefore public health policies and professional societies ought to have shifted their guidance (per the bench science which Robin has so carefully elucidated and has been available for well over a decade) to inform health care practitioners to monitor vitamin D levels and ensure that the vulnerable have levels sufficient to allow for the interactive and paracrine signaling.
Paracrine signaling from vitamin D is crucial to prevent a person from having uncontrolled cytokine activation through balancing T helper 1 (Th1) and T helper 2 cells.
RCTs will never demonstrate the biological impact of vitD in the same way we show the outcome of a drug because pharmaceutical products typically have singular receptors that they target; therefore you study a dose: response relationship. Vitamin D is a pleiotropic substance with so many impacts within different cell types ; it does not behave like a drug. If you review the RCTs, you find that until the last four years— most studies used ‘homeopathic ‘ doses of vitamin D which were designed by their low doses to never be able to detect a response. The IOM’s RDA allowances for vitD were challenged (in peer reviewed journals) by two epidemiological teams pointing out the research design flaws which resulted in doses too low by a factor of ten. They never even gave a scientific response, let alone revisited the RDA.
(And to respond to another earlier commenter…) On the south side of Chicago, many black residents believe the State has always been an adversary. Looking at the NHANES data on the disproportionately low vitD levels and understanding the suppression of information by public health actors— would you disagree?
Regarding the frail elderly receiving insufficient sunlight exposure to meet their vitamin D needs, this was exactly the point I made in the article. Did you read it?
I will be addressing all your other claims in subsequent parts of this miniseries.
(1 of 3) For most practical purposes, vitamin D3 cholecalciferol is a vitamin, since few people who live far from the equator can get enough UV-B skin exposure to generate enough vitamin D3 to raise circulating 25-hydroxyvitamin D to the 50 ng/mL 125 nmol/L (1 part in 20,000,000 by mass) level which the immune system needs to function properly. Such UV-B is only available in sufficient quantities from high elevation sunlight on clear summer days, without clothing, glass or sunscreen attenuating it. The same UV-B wavelengths damage DNA and so raise the risk of skin cancer. This is not to say that there are no physical and mental benefits from sunlight and/or being outdoors in general. Just that to rely on natural sunlight is insufficient for good health, and buying a special UV-B lamp is more expensive and risky (skin cancer) than taking vitamin D3 supplements.
Please read the research articles cited and discussed at: https://vitamindstopscovid.info/00-evi/ .
In most or all countries, most people have only a fraction of the 25-hydroxyvitamin D their immune system needs to function properly. The problems begin before birth: https://vitamindstopscovid.info/00-evi/#3.2, with preeclampsia, pre-term birth and the later development of autism, ADHD, intellectual disability and schizophrenia.
Infectious diseases, cancer and auto-immune diseases are more prevalent, harmful and deadly than they would be if everyone had at least 50 ng/mL 25-hydroxyvitamin D. https://vitamindstopscovid.info/00-evi/#3.3 cites and discusses research concerning low 25-hydroxyvitamin D levels, which are common, greatly increasing the risk of neurodegeneration - Alzheimer's disease, Parkinson's disease, dementia with Lewy bodies etc.
25-hydroxyvitamin D is produced, primarily in the liver, from vitamin D3 which is ingested or produced in the (ideally white) skin by ultraviolet-B irradiation, which breaks a carbon ring in 7-dehydrocholesterol. There is very little vitamin D3 in food, fortified or not.
A hormone is a blood-borne long-distance signaling molecule - a substance produced somewhere in the body, which goes into circulation in the bloodstream and cerebrospinal fluid, where its concentration (level) alters the behavior of one or more types of cell. Hormonal AKA endocrine signalling is a means by which an organ, such as the kidneys, can control or influence other parts of the body.
Neither vitamin D3 nor 25-hydroxyvitamin D function as hormones. They are not signaling molecules. 25-hydroxyvitamin D circulating in the bloodstream takes months to build up with healthy intakes of supplemental vitamin D3. "Vitamin D" blood tests measure the level (concentration) of 25-hydroxyvitamin D, which is not a vitamin.
Vitamin D3's primary or sole role is to be converted (hydroxylated, by adding an oxygen-hydrogen hydroxyl group to the 25th carbon), primarily in the liver, to circulating 25-hydroxyvitamin D, which has a half-life there measured in months, or weeks at higher, healthy, levels.
The best known role for 25-hydroxyvitamin D is to supply the kidneys, which convert some of it to a very low level (ca. 0.05 ng/mL) of circulating 1,25-dihydroxyvitamin D (calcitriol), by hydroxylating it on the number 1 carbon. 25-hydroxyvitamin D is also known as calcifediol and "calcidiol", which I think is best avoided since it looks and sounds much like "calcitriol".
This kidney-produced calcitriol functions as a hormone, since it affects the behaviour of multiple cell types around the body which are involved in calcium, phosphate and bone metabolism. The kidney's rate of calcitriol production is controlled by the level of parathyroid hormone (the parathyroid gland senses calcium ion levels) and by the level of fibroblast growth factor 23 (FSF23) which is secreted by osteocytes, the primary cell-type of bone: https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2020.00592/full .
This is the one hormonal function of the three compounds which are, commonly but incorrectly, all referred to as "vitamin D". Vitamin D3 is a vitamin. 25-hydroxyvitamin D and calcitriol are not vitamins. Calcitriol can function as a hormone, as just described. However, all the other cell types which convert 25-hydroxyvitamin D to calcitriol do so in ways which have nothing to do with hormonal signaling.
Many types of immune cell respond to a particular (different for each cell type) condition by hydroxylating 25-hydroxyvitamin D to calcitriol, inside the cell, with the calcitriol binding to so-called "vitamin D receptor" molecules (a better term would be "calcitriol receptor", since it binds only very weakly to vitamin D3 and 25-hydroxyvitamin D). The bound complex finding its way to the nucleus. There it binds to the "retinol X" molecule and the triple-bound complex alters gene transcription to RNA (and so alters the cell's protein synthesis and so behaviour) in complex and powerful ways. The transcription of dozens of genes is up-regulated and the transcription of dozens of other genes is down-regulated. The exact details of these gene expression changes differs from one cell type to the next.
This is intracrine signaling - the cell producing a compound, here calcitriol, which functions as an intracrine agent which is sensed within the same cell and so alters its behaviour. This is unrelated to hormonal signaling. A variation is paracrine signaling, in which some of the calcitriol diffuses out of the cell, raising the intracellular calcitriol level in that area (millimetres, I guess) well above the very low hormonal background level. This raised level is detected by other cell types an changes their behavior.
Most doctors and immunologists have never heard of 25-hydroxyvitamin D to calcitriol intracrine and paracrine signaling. There being no peer-reviewed journal tutorial on these, I wrote one in 2020: https://vitamindstopscovid.info/02-intracrine/. Intracrine signaling is sometimes incorrectly referred to as "autocrine" signaling. I made this mistake initially. Autocrine signaling involves the compound leaving the cell but altering its behavior by being detected by receptors on the outside of the cell membrane.
I will be addressing all these claims in subsequent parts of this miniseries.
(3 of 3) Thanks for citing Tintut et al. 2021 "Potential Impact of the Steroid Hormone, Vitamin D, on the Vasculature" https://sci-hub.se/10.1016/j.ahj.2021.05.012. They suggest that vitamin D3, carried in the bloodstream by cylomicrons (tiny fat globules) after being ingested (but not from UV-B produced vitamin D3) is somehow a problem for the endothelial cells which line blood vessels.
The most important site of hydroxylation to produce circulating 25-hydroxyvitamin D is the liver. They suggest on page 6 that this vitamin D3 may be hydroxylated more rapidly in the liver in this form than the vitamin D3 which comes from the skin and is transported in the blood primarily bound to the "vitamin D binding protein" (which also binds to 25-hydroxyvitamin D and calcitriol), and less strongly to albumin proteins. Maybe so - I had not read this. If so, why would this be a problem for the vasculature?
On page 7 they correctly note that (very) high levels of circulating 25-hydroxyvitamin D or calcitriol can lead to calcification of the arteries. Vitamin D3 has a half-life of days in the bloodstream, and calcitriol hours. Very high levels (150 ng/mL or more) of 25-hydroxyvitamin D can cause hypocalcemia, calcification of the arteries and bone loss due to two mechanisms at least. Firstly, since it binds weakly to the "vitamin D" receptor molecules which some cells used to sense the very low level of hormonal calcitriol, those receptors are activated excessively even in the absence of being activated much by hormonal calcitriol. The second mechanism is that with high 25-hydroxyvitamin D levels, the kidneys tend to produce more calcitriol, resulting in a raised level of calcitriol. See Fig 1b in Tang et al. 2019: https://www.nature.com/articles/s41598-019-43462-6.
On page 8 they state that 25-hydroxyvitamin D levels "greater than 36 ng/mL (75 nmol/L)" are "considered unsafe". This is a common but completely ill-informed belief. The authors do not challenge it an so presumably accept it as true. They should read the research I cite and discuss at: https://vitamindstopscovid.info/00-evi/.
On pages 8 and 9 the authors speculate about 25-hydroxyvitamin D being hydroxylated to calcitriol (which they refer to as the 25-hydroxyvitamin D being "activated") in endothelial cells, implying that harm would result from too high a level of circulating 25-hydroxyvitamin D. Perhaps so, but this is just a suggestion and they present no evidence that it is pathological at some level of 25-hydroxyvitamin D they do not specify.
Their references 65 and 66 are cited in "Aortic endothelial cells produce and respond to the active hormone in an autocrine manner, including inhibition of growth and of angiogenic activities such as sprouting and formation of networks." However, they are not sure (page 11) whether the ill effects of excessive 25-hydroxyvitamin D and/or calcitriol, in forming vascular calcification, are local (due to VDR activation in endothelial cells) or systemic (such as resulting from a calcium ion level which exceeds what it is supposed to be, which is a nearly saturated level with a very narrow healthy range). On line 191 they mention evidence for systemic, and against local, mechanisms.
On page 12 they mention obese mice being at greater risk of "vitamin D hormone" (they count all three compounds as this, not just calcitriol, which is not, itself, vitamin D) toxicity. They are surely are unaware of the Quraishi research (see previous comments) which show that 50 ng/mL or more circulating 25-hydroxyvitamin D is needed for proper immune system function in the generally morbidly obese subjects in that Massachusetts General Hospital post-operative research.
They correctly note that 25-hydroxyvitamin D levels are generally lowered by obesity. See https://5nn.info/temp/250hd-obesity/ for links to research on the two proposed mechanisms.
On page 13 they mention ""vitamin D-hormone" inhibition of osteoclasts also occurs in the artery wall". But osteoclasts are in bone, not artery walls. A Google search led me to Jaing et al. 2021 https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2021.639740/full which mentions: "osteoclast-like cells have also been detected in calcified arterial walls wherein they possibly inhibit vascular calcification, similar to the catabolic process of bone mineral resorption." This would mean that osteoclast-like cells would reduce vascular calcification.
This is a speculative article by authors who have no idea about the immune system's need for at least 50 ng/mL circulating 25-hydroxyvitamin D. I don't think provides observations or persuasive arguments which support "concern that diet-derived vitamin D, carried into arterial walls on LDL particles, may promote the calcification of atherosclerotic plaque."
There probably is some locally significant hydroxylation of skin-produced vitamin D3 in the skin, to 25-hydroxyvitamin D, which would then diffuse into all the cells there and so enable them to work better (with better intracrine and paracrine signaling, for those cell types which do this with 25-hydroxyvitamin D >> calcitriol) even if the circulating level of 25-hydroxyvitamin D is very low. This would be one mechanism by which UV-B exposure of skin affected by psoriasis is effective.
See: https://vitamindstopscovid.info/06-adv/ for inflammatory auto-immune disorders being caused or worsened by both low 25-hydroxyvitamin D and lack of helminths, and suppressed both by high (e.g. 100ng/mL or more) 25-hydroxyvitamin D levels and/or deliberately introduced helminth infections: https://helminthictherapywiki.org.
Gibson et al. 2015 Dietary Vitamin D and Its Metabolites Non-Genomically Stabilize the Endothelium" https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0140370 report that ingested vitamin D3 promotes health by directly assisting endothelial cells, using some unknown mechanism, without the need for hydroxylation to 25-hydroxyvitamin D and then again to calcitriol. I have not looked at this in detail, so I don't know how significant it is, or what other research supports it or not. This is interesting and potentially significant research, including regarding sepsis and ARDS.
Thankyou so much Robin have stopped both Vit D supplementation and cholesterol reduction with statins after reading the story about Ansel Keys Cholesterol Con exposed by Prof Tim Noakes.
Still experiencing tinnitus (potential statin side effect) but have put that down to damage of the ear Military exposure- Gun Shots close range.
There really has been a pile-on to Ansel Keys, ever since Gary Taubes made up some nonsense about him and a whole lot of other authors copied-and-pasted without ever having read Keys' many papers for themselves. I highly recommend that you do exactly that.
Thanks, Prof Tim Noakes went into the Ansel Keys claims very deeply. Here is the link if you're interested. It is in 14 parts.
https://thenoakesfoundation.org/ancel-keys-cholesterol-con-part-1-how-an-insecure-and-unproven-hypothesis-became-a-global-unchallenged-dogma-by-prof-tim-noakes/
https://thenoakesfoundation.org/ancel-keys-cholesterol-con-part-2-by-prof-tim-noakes/
It's very clear that Noakes has not in fact read Keys' work, because even in part 1 of this series he rehashes the same false claims that Taubes made, and Teichholz plagiarised without acknowledging Taubes. Heck, Noakes even admits that he read ABOUT Keys's work rather than reading it for himself, with this statement: "Only when I read and re-read the game-changing books by the path-finders for truth in this matter - Russell L. Smith and Edward R. Pinckney (74), Thomas J. Moore ((75), Gary Taubes (1) and Nina Teichholz (3) - did I begin to understand the truth."
He then repeats in Part 2, "The ideas and arguments I present are not original in that I am not their original source. Rather they have been covered in compelling detail in the four iconic books (i.e. those by Smith, Taubes etc), and in a number of others that confine themselves to what has become known as the Cholesterol Scam or the Cholesterol Con."
In other words, Noakes is rehashing other people's arguments, which in turn are rehashings of other people's arguments. This is intellectual laziness, which I utterly despise.
First rule of understanding a topic is to read the original source material, not the interpretations of it. I wrote about this, specifically in relation to the (intentional???) misstatements about Keys, in https://robynchuter.substack.com/p/never-trust-always-verify-even-your.
Thanks very much for your opinion. I respect it and you of course.
I try not to offer opinions, but instead to base my assessments on the facts, as best I can ascertain them. The process of ascertaining facts can be challenging, and it's never possible to be absolutely certain of just about anything! But when I see people making statements that are clearly factually incorrect - and stating them with total conviction - it gets my goat.
Interesting article, many good points and a few very dubious ones:-)
what parts were dubious?
Lots of logically connected theories can lay the foundations for a compelling story, but may miss the bullseye of truth by quite some margin. For example, this paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3897598/ has a prehistoric perspective that is pure made up drivel. What causes rickets, do we see this condition occuring these days in people who don't get any direct sunlight? There are other points but I don't want to do a Robin Whittle about it:-)
I'm interested in what you found to be "pure made up drivel" in that paper.
Rickets still does occur to this day in people with inadequate sunlight exposure - e.g. in Saudi Arabia due to full-body clothing (see https://jcimcr.org/pdfs/JCIMCR-v2-1311.pdf). Rickets rarely occurs in Australia, but the handful of cases reported occurred overwhelming in dark-skinned immigrants (primarily from Africa) and in girls who were partially or fully veiled (see https://www.mja.com.au/journal/2012/196/7/incidence-vitamin-d-deficiency-rickets-among-australian-children-australian).
I don’t think you need me to point out drivel in that paper, all you need do is read each statement in the ‘prehistoric perspective’. The first statement reads, ‘Life forms began to evolve in the oceans over 1 billion years ago’. The next statement reads, ‘They took advantage of sunlight and used it as an energy source to generate carbohydrates’. Both statements are unprovable nonsense made up in somebody’s imagination. There are infinite likely scenarios for how life began, to even suggest it began ‘a billion years ago’ is preposterous, yet alone to write it as a statement of fact. The ‘prehistoric perspective’ really sets the tone for the entire paper.
I get that there is a condition called Rickets, but what causes it? While it may be correlated with inadequate sunlight exposure, that may not be the cause. Are people with Rickets tested for nutritional deficiencies and toxins? Conditions within industrialising European cities were horrific, especially for child workers (slaves) and it is likely many were suffering from novel toxic exposure and lack of nutrition. Lack of sunlight would make a convenient cover story for profit-hungry industrialists with little regard for human life.
Are you disputing that life forms utilise sunlight to generate carbohydrates?
And did you read the link above re rickets occurring presently in Australia, and the particular demographic/cultural groups in which it occurs? It's pretty bloody clear that inadequate sunshine exposure causes rickets.
'If it's pretty bloody clear' that inadequate sunshine exposure causes rickets, then please reference the papers that prove it, there must be many robust papers showing factual data supporting that bold statement. The papers would ensure that other potential causative factors have been analysed and discounted.
It is yet to be proven that all aquatic life 'breathe' oxygen or utilise sunlight.
Did you find the supporting data for the two statements listed in my previous reply?