Is Vitamin D Supplementation Even Neccessary

Travis

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Ever go to the beach and observe how many people are sleeping in the late afternoon. Also ever feel tired after leaving the beach. I layed out by the pool yesterday and...fell asleep! So @Travis is correct in "Vitamin D is involved in thermoregulation" Just add a couple cans of beer and you will sleep like a baby. One way to wake up was to jump in the ocean. Another negative for supplemental Vit D. Buy a cheap brand in Soy oil and really start yawning...I wonder if @Travis will stop applying it trandermally?

Yes, yes, and I certainly have. I know believe that vitamin D is generally overrated as a vitamin and also that functionally-equivalent irradiated seco-steroids can be found in essentially any sun-grown leaf (i.e. spinach, kale). A little-known fact is that even vitamin D₃ proper has been isolated from leaves, and also that near-equivalent seco-steroids would be expected to be formed upon irradiation of their respective near-equivalent phytosterols:

2-Figure1-1.png


Of course these phytosterols must be first converted into their respective 7-dehydro forms before photolysis will occur, but just do a search to see how often these are found in leaves. Seven-dehydrositosterol has been isolated from Rauwolfia serpentina,⁽²⁾ 7-dehydrocampesterol is actually a fully-functional,⁽⁴⁾ and vitamin D₃ proper can be found even in the common tomato plant.⁽¹⁾

I believe that most correlations involving latitude and sunshine probably might have more to do with melatonin, a more powerful hormone on most accounts. Of course there is nothing wrong with getting vitamin D₃ naturally, only that experimental evidence plainly shows that it represses thermogenin.

[1] Prema, T. "Vitamin D₃ and its metabolites in the tomato plant." Phytochemistry (1996)
[2] Karmakar, T. "7-dehydrositosterol from Rauwolfia serpentina." Phytochemistry (1983)
[3] Prema, T. "Free vitamin D₃ metabolites in Cestrum diurnum leaves." Phytochemistry (1994)
[4] Ruigh, W. "7-Dehydrocampesterol, a New Provitamin D." Journal of the American Chemical Society (1942)
[5] Boland, R. "Isolation of vitamin D₃ metabolites from Solanum malacoxylon leaf extracts incubated with ruminal fluid." Planta medica (1987)
 
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Travis

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You might be interested in looking into how vitamin D influences the level and activity of transient receptor potential (TRP) channels. Many of them are involved in thermoregulation, I think TRPV1 being one of the better studied ones in that regard.

Vitamin D seems to increase the absorption of calcium through it's effect on TRPV6/TRPV5 channels.

There a couple papers showing Vitamin D to upregulate TRPM2 - and that seems to be one of the ones involved in thermoregulation.

Endocrinology. 1996 Feb;137(2):400-9.
Characterization of a vitamin D3-resistant MCF-7 cell line.
Narvaez CJ1, Vanweelden K, Byrne I, Welsh J.

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3], the active metabolite of vitamin D3, is a potent inhibitor of breast cancer cell growth both in vivo and in vitro. We have previously demonstrated that 1,25-(OH)2D3 induces morphology (pyknotic nuclei, chromatin and cytoplasmic condensation, and nuclear matrix protein reorganization) consistent with the activation of apoptosis in MCF-7 cells. These morphological changes in 1,25-(OH)2D3-treated cells are associated with up-regulation of TRPM-2/clusterin and cathepsin B (genes associated with mammary gland apoptosis) and down-regulation of bcl-2, an antiapoptotic gene. Thus, the inhibitory effects of 1,25-(OH)2D3 on MCF-7 cell growth involve activation of apoptosis. To investigate the mechanisms by which vitamin D3 activates apoptosis, we have selected a vitamin D3-resistant variant (MCF-7D3Res cells) by continuous culture of MCF-7 cells in 100 nM 1,25-(OH)2D3. The MCF-7D3Res cells represent a stably selected phenotype that grows equally well with or without 100 nM 1,25-(OH)2D3. In contrast to the MCF-7 cells from which they were derived (MCF-7WT cells), MCF-7D3Res cells do not exhibit apoptotic morphology, DNA fragmentation, or up-regulation of apoptosis-related proteins after treatment with 1,25-(OH)2D3. MCF-7D3Res cells exhibit cross-resistance to several vitamin D3 analogs that are potent growth regulators of MCF-7WT cells. MCF-7WT and MCF-7D3Res cells exhibit comparable sensitivity to induction of apoptosis and up-regulation of clusterin in response to the antiestrogen 4-hydroxytamoxifen. MCF-7D3Res cells express comparable levels of the vitamin D receptor (VDR), as assessed by Western blotting or ligand binding, as MCF-7WT cells. In both sensitive and resistant cell lines, 1,25-(OH)2D3 up-regulates whereas 4-hydroxytamoxifen down-regulates VDR protein expression, indicating appropriate homologous and heterologous VDR regulation in MCF-7D3Ras cells. Gel shift analyses indicate that nuclear extracts from MCF-7WT and MCF-7D3Res cells bind equally well to the DR3 consensus vitamin D3 response element. These data suggest that MCF-7D3Res cells have a functional VDR that is uncoupled from a functional apoptotic pathway. MCF-7D3Res cells offer a unique model system for identification of the mechanisms by which vitamin D3 regulates the cell death pathway in breast cancer cells.​

J Steroid Biochem Mol Biol. 1996 Jul;58(4):367-76.
1,25-Dihydroxyvitamin D3 induces morphological and biochemical markers of apoptosis in MCF-7 breast cancer cells.
Simboli-Campbell M1, Narvaez CJ, Tenniswood M, Welsh J.

1,25-Dihydroxyvitamin D3 [1,25(OH)2(D)3], the active metabolite of vitamin D, is a potent inhibitor of breast cancer cell growth both in vivo and in vitro. To complement data which documents the anti-proliferative effects of 1,25(OH)2(D)3, we assessed the role of apoptosis in vitamin D-mediated growth arrest of MCF-7 cells. Time course studies indicated that 100 nM 1,25(OH)2(D)3 significantly reduces MCF-7 cell numbers within 48 h of treatment. Morphological assessment demonstrated that MCF-7 cells treated with 1,25(OH)2(D)3 for 48 h exhibit characteristic apoptotic features, including cytoplasmic condensation, pyknotic nuclei, condensed chromatin and nuclear matrix re-organization. In situ end labelling with terminal transferase indicated that cells exhibiting apoptotic morphology in 1,25(OH)2(D)3-treated cultures were positive for DNA strand breaks. These morphological features of apoptosis were accompanied by an increase in the cell death rate assessed as soluble DNA-histone complexes indicative of DNA fragmentation. To complement the morphological data, we assessed the temporal expression of two proteins which have been associated with apoptosis in mammary cells and tumors. The steady state mRNA levels for TRPM-2/clusterin and cathepsin B mRNA were significantly up-regulated in MCF-7 cells treated with 1,25(OH)2(D)3 compared to control cells. Time-dependent increases in the expression of TRPM-2/clusterin and cathepsin B proteins were detected by Western blotting in 1,25(OH)2(D)3-treated cells. These findings indicate that, in addition to its anti-proliferative effects, 1,25(OH)2(D)3 activates the apoptotic cell death pathway in MCF-7 breast cancer cells.​


Science. 2016 Sep 23;353(6306):1393-1398. Epub 2016 Aug 25.
The TRPM2 channel is a hypothalamic heat sensor that limits fever and can drive hypothermia.
Song K1, Wang H1, Kamm GB1, Pohle J1, Reis FC2, Heppenstall P3, Wende H1, Siemens J4.

Body temperature homeostasis is critical for survival and requires precise regulation by the nervous system. The hypothalamus serves as the principal thermostat that detects and regulates internal temperature. We demonstrate that the ion channel TRPM2 [of the transient receptor potential (TRP) channel family] is a temperature sensor in a subpopulation of hypothalamic neurons. TRPM2 limits the fever response and may detect increased temperatures to prevent overheating. Furthermore, chemogenetic activation and inhibition of hypothalamic TRPM2-expressing neurons in vivo decreased and increased body temperature, respectively. Such manipulation may allow analysis of the beneficial effects of altered body temperature on diverse disease states. Identification of a functional role for TRP channels in monitoring internal body temperature should promote further analysis of molecular mechanisms governing thermoregulation and foster the genetic dissection of hypothalamic circuits involved with temperature homeostasis.​

Temperature (Austin). 2016 Nov 10;4(1):21-23. doi: 10.1080/23328940.2016.1258445. eCollection 2017.
The TRPM2 channel in temperature detection and thermoregulation.
Kamm GB1, Siemens J1.

Comment on
The TRPM2 channel is a hypothalamic heat sensor that limits fever and can drive hypothermia. [Science. 2016]​

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The nuclear receptors RORα and RORγ regulate 'clock genes' having a sinusoidal cycle, some of which are transcription factors which will maintain the same rhythm after weeks of darkness. The retinoid orphan receptors (RORα, RORβ, and RORγ) are melatonin receptors yet vitamin D also binds with two of the three—retinoic acid binds the third. This is another instance of 'light hormones' antagonizing melatonin, the 'darkness hormone.' The response element of B cathepsin is compatible with RORβ but this one is not known to be influenced at all by vitamin D. These are the only three vitamin D receptors that I know of, yet two of them are capable of regulating 'clock genes.'

'There is some evidence that the normal levels of circadian rhythm gene expression in the skin can be suppressed by UVB radiation, as demonstrated for Per1, Clock and Bmal1 in human keratinocytes (65).' ―Desotelle

There is also cryptochrome, a fluorescent tryptophan-rich transcription factor that can be found in the cell nucleus. This and RORβ also periodically fluctuate, yet RORβ usually loses expression upon differentiation (but perhaps it's expressed in cancer cells, which Robert Becker describes generally as being 'undifferentiated'). In plants, cryptopchrome induces dNA transcritption upon stimulation with light.

vitamin D.png

[These genes normally oscillate periodically in near-perfect sine waves. This disruption by UV light can perhaps be thought to occur via cryptochrome or through the formation of vitamin D, known to repress both RORα and -γ.]

Judging by how uncoupling protein works, I'd expect any receptor producing heat to effect cATP in some way. The obvious candidates for a cell membrane receptor would be G-protein coupled phosphodiesterase or adenylate cyclase, the latter increasing cyclic AMP and hence metabolism—producing heat. But of course the heat sensation isn't the heat itself, and can in fact can occur completely independent of it: Capsaicin activates a membrane receptor giving the impression of heat when there's none, and molecules such as menthol can do the exact opposite. Since the perception of heat must travel from its source all the way to the brain, this information must necessarily be transmitted inside of the microtubule lumen (these are found at the very center of every functional nerve, surrounded by myelin). Since the 'tryptophan channel' appears devoted to consciousness and pain, then perhaps the 'phenylalanine channel' carries the heat signal. The microtubule scientists exclusively concentrate on tryptophan, and for good reason, but the lumen of microtubules is lined with other fluorescent rings besides: the phenol rings of tyrosine, the phenyl rings of phenylalanine, and even imidazole rings of histidine are all expressed in repeating patterns inside. The Förster resonance energy transfer scientists also focus on tryptophan, and also for good reason, but I don't see any reason why the others couldn't also transfer information.

I could be worth noting that the UV spectra of capsaicin and eucolyptol have a peak at the 280·nm wavelength, perhaps implying that tyrosines could carry the heat signal inside the nerves. The phenol side-chain of tyrosine overlaps this frequency.

Terzaghi, W. "Light-regulated transcription." Annual review of plant biology (1995)
Moens, P. "Detection of tryptophan to tryptophan energy transfer in proteins." The protein journal (2004)
Desotelle, J. "The circadian control of skin and cutaneous photodamage." Photochemistry and photobiology (2012)
Craddock, T. "The feasibility of coherent energy transfer in microtubules." Journal of the Royal Society Interface (2014)
Kawara, S. "Low-dose ultraviolet B rays alter the mRNA expression of the circadian clock genes in cultured human keratinocytes." Journal of investigative dermatology (2002)
Ghisaidoobe, A. "Intrinsic tryptophan fluorescence in the detection and analysis of proteins: a focus on Förster resonance energy transfer techniques." International journal of molecular sciences (2014)
 

benaoao

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BUT according to @Travis, " And of course I think everyone -in my opinion- should avoid linoleic acid. I found a straightforward mechanism for the link between linoleic acid and prostate cancer. First, an eicosanoid derived from arachidonic acid by the name of leukotriene B4 acts on its receptor; this event upregulates transcription for the androgen receptor in the prostate (and elsewhere). One of the effects of androgens is to increase ornithine decarboxylase and it needs the androgen receptor for this to occur. Ornithine decarboxylase is the main enzyme responsible for producing polyamines. This should come as no surprise as androgens are always anabolic, and there has to be some way to explain how they can induce growth. This links the three main molecular agents together-eicosanoids, androgens, and polyamines-known to be involved in the etiology of prostate cancer in a relatively straightforward , transcriptional manner."

But linoleic acid barely converts to AA, so unless you’re eating lots of vegetable oils with no anti oxidants LA is a non issue
 

Travis

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BUT according to @Travis, " And of course I think everyone -in my opinion- should avoid linoleic acid. I found a straightforward mechanism for the link between linoleic acid and prostate cancer. First, an eicosanoid derived from arachidonic acid by the name of leukotriene B4 acts on its receptor; this event upregulates transcription for the androgen receptor in the prostate (and elsewhere). One of the effects of androgens is to increase ornithine decarboxylase and it needs the androgen receptor for this to occur. Ornithine decarboxylase is the main enzyme responsible for producing polyamines. This should come as no surprise as androgens are always anabolic, and there has to be some way to explain how they can induce growth. This links the three main molecular agents together-eicosanoids, androgens, and polyamines-known to be involved in the etiology of prostate cancer in a relatively straightforward , transcriptional manner."

But we now have the clock genes to consider, which could have significance. Polyamines do reliably induce growth, best demonstrated in those classic methionine rat studies, and likely by inducing the transcription of housekeeping genes involved in general metabolism. Other genes can also be transcribed more specifically through transcription factors, some of which oscillate periodically.


There are review articles on this topic, and there's obviously been quite a bit of work in this area. Although polyamines induce cell transcription and replication reliably enough to be renamed 'prolifamines' without much objection, the things which regulate clock genes are: melatonin, vitamin D₃, retinoic acid, light, and perhaps corticosteroids. Interferons are unique cytokines which can disrupt the clock cycle, and the class I interferons are thought to specialize in intercepting virus infected cells. Interferons have unique membrane-to-nucleus signalling mechanisms, and I don't know of any other cytokine capable of disrupting the internal cell clock.

'Up to 10% of the genome of cells is expressed, at the RNA level, in a circadian-coordinated manner, with each tissue displaying unique tissue-specific expression profiles.' ―Wood

'It is reported that in colorectal cancer, the incidence is significantly increased in women working at night >3 days a month for ≥15 years, and the survival time of patients with regular rhythms is 5-fold higher than patients with circadian rhythm disorders (64). Keith et al (65) have suggested that circadian rhythm was a more important carcinogenic factor than the family history of breast cancer.' ―Feng

According to Patricia Wood: disruptions in 'period 2' gene (Per2) cycling are most powerfully associated with cancer, among all clock gene distruptions: Jianguo Liu [sic] had discovered that the periodic nuclear transcription factor Per2 encodes for interferon-γ. The 'period' proteins don't seem to be regulated directly by melatonin, but are thought to dimerize with the cryptochromes where they rhythmically-suppress their own transcription. [?] Two separate studies prove that Per2 is induced by blue light, after which it could perhaps builds-up to the point of suppressing its own formation (assuming it really does this). The 'clock' and 'bmal1' genes, on the other hand, are regulated by the ROR(α,β,γ) melatonin receptors. The genes transcribed by the melatonin receptors should tend to increase at night and those activated by the light—perhaps by using retinoic acid—should tend to increase during the day (and should increase most strongly in the retina, pineal, suprachiasmic nucleus, and skin).

Relative-mRNA-temporal-profiles-of-clock-genes-along-the-light-dark-LD-cycle-were.png

[The blue trace is the control, or the apparently-normal group; the other traces are experimental groups.]

But clock disorders found in certain cells could be more the result of the local environment than a dysfunction in the cell. These oscillations do seem to decay in isolated cells after a few weeks of darkness, but the fact that it takes so long indicates that there's a redundant molecular feedback mechanism strengthening the natural cycle, providing entrainment.
 
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Travis

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But linoleic acid barely converts to AA, so unless you’re eating lots of vegetable oils with no anti oxidants LA is a non issue
Can you name just one thing besides linoleic acid which can convert into arachidonic acid?
 

Travis

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'Acknowledgements and funding

This research was associated with the USDA Multistate Regional Research Project NC1039, and funded in part by the Tennessee Agricultural Experiment Station (JW).'
 

Travis

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Im not saying it doesn’t convert, it does, but the rate at which it converts is .3 up to .6%. Which is barely anything
Is that a fact? If arachidonic acid is really so difficult to synthesize from linoleic acid, could you then explain this study. It appears that this conversion is actually so easy that babies can do it, and at much higher levels than you claim.

Demmelmair, H. "Estimation of arachidonic acid synthesis in full term neonates using natural variation of ¹³C content." Journal of pediatric gastroenterology and nutrition (1995)

linoleic acid.png

[The graph on left shows that even infants can make the conversion within hours; the chart on the right indicates that 23.3% of arachidonic acid, on average, comes from linoleic acid ingested during the previous four days.]

This one had used ¹³carbon-labeled linoleic acid to give the infants followed by gas chromatography–mass spectrometry to detect the arachidonic acid, a far less ambiguous approach than used in most studies—ones that cannot discriminate between arachidonic acid made yesterday and that made a month ago. This article had went entirely without mention by the author of that USDA-sponsored review article you'd linked. This makes me question his motives, but before I accuse him of 'cherry picking' perhaps we can find others.. .
 

Terma

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Nice find. This certainly makes sense because activated retinoic acid is a 'light hormone,' and as such should do the opposite for a nocturnal species. The light-activated cis-trans isomerization of retinoic acid is the most well-known photochemical effect in biochemistry, commonly used a heuristic device and serving as the canonical first step in the light transduction pathway of visual perception. [The Rube Goldberg-like molecular mechanics of the canonical pathway would actually be prohibitively slow, and the cis-trans isomerization of retinal could merely serve as a shade to exclude excessive light. The real mediator of vision, as far as I'm concerned, is the fluorescence/Förster resonance energy transfer between indoles.] The thermal isomerization of vitamin D, on the other hand, is a 'heat signal' and should have much less interspecial variation.

This is interesting that you bring this up, because after reading about a nuclear retinoic acid receptor I had the idea that Accutane™ (a.k.a isotretinoin, 13-cis-retinoic acid) could actually work after photo-isomerization on the skin. The reason is that 13-cis-retinoic acid is not known to bind to any receptor at all with appreciable affinity, leaving its mechanism of action historically unexplained. However, I had done a search and found that someone had thought of this before:

Tsukada, M. "13-cis retinoic acid exerts its specific activity on human sebocytes through selective intracellular isomerization to all-trans-retinoic acid and binding to retinoid acid receptors." Journal of investigative dermatology (2000)

Although little known, Accutane™ is merely a prodrug for endogenous all-trans-retinoic acid. Since this isomerization is light activated and occurs mainly on the skin, isotretinoin largely bypasses the strict feedback mechanisms normally keeping circulating retinoic acid in range. I think this perhaps could have been known by the drug's designers, yet never reported due to its embarrassing implications: 'If Accutane™ is merely just an overpriced and relatively dangerous way to get all-trans-retinoic acid on the skin, why not just put all-trans-retinoic acid on the skin?'

That makes a ton of sense, both the nocturnality of rodents and the skin photo effect on 13-cis isomerization. That gives me a lot to think about, wow, thank you for that.

I read quite a bit about the cell clockwork; however, I have a hard time figuring out which proteins/genes/hormones are inverted in nocturnal vs diurnal animals. For example as you alluded to, melatonin is the darkness hormone and that is constant for all organisms. However, for example the NAD (at least in liver) and cortisol levels are elevated at the beginning of the activity period, so different for nocturnals vs diurnals (firefox spellcheck says that's not a word, **** firefox).

In other words it would be amazing to compile a list of which proteins/genes/hormones are dependent on nocturnality (firefox spellcheck says that's not a word, **** firefox) and which are independent of it.

You wrote that "maybe" glucocorticoids are involved in circadian regulation; having read a lot I can tell definitely that they are a major regulator, though I don't feel like linking right now. In fact, that is probably the single most important and beneficial function of glucocorticoids. Otherwise cortisol is the worst hormone and all of its other effects are negative, dispensable or can be achieved with better substances (e.g. anti-inflammatory effects).
 

benaoao

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Cortisol isn’t a bad hormone, it’s constantly triggering it that is bad. Without Cortisol you’re dead... this forum needs to stop the witch hunt sometimes. Hormones, fatty acids, sugars and amino acids exist for a reason. It’s pretty much always a U shape where “not enough” is as bad or worse than “too much”. Ray Peat’s work is focused on the too much part, and rightfully so for most people living la vida in the West, it doesn’t mean getting as close to 0 as possible is optimal.

Although in the case of vitamin D, the “not enough” are definitely more prevalent. I like it transdermal... I’ll share a study showing how a patented vitamin D topical solution works so much better than all orals

Edit - actually it’s discussed here, nice chart. Transdermal vs Oral Vitamin D Absorption
 

Terma

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Cortisol isn’t a bad hormone, it’s constantly triggering it that is bad. Without Cortisol you’re dead...

That's technically true but it's also an exaggeration and misrepresentation of its role in daily life in today's world.

For the most part the immediate glucose regulation which is life-threatening is regulated by glucagon, and secondarily by norepinephrine [source]. Cortisol might become limiting if the liver is poor, but even that is speculative.

Cortisol is necessary for health by amplifying the circadian rhythm in other words allowing you to wake up properly in the morning. But that is a narrow window.

Most of the benefits ascribed to cortisol by some people are a misunderstanding and they actually come from growth hormone, which is beneficial if activated at the proper times, and it is specifically because it has several opposite effects to cortisol in tissue localization and from its compensatory increase of IGF-1.

Most rheumatologists for example now know that hydrocortisone is extremely damaging long-term and its use has become limited (replaced by popular anti-inflammatories, which can also do great damage, but that's another story).

If you compile all its effects I think you can objectively say Cortisol is the relatively worst hormone, and in effect, "bad", in the context of a society in which macronutrient scarcity has been eliminated.
 

benaoao

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I agree with what you’re saying, I’m nitpicking often I’ll admit it.

The last part is key, I think the society may have eliminated macro scarcity but micronutrients are the real problem. Unfortunately using cronometer is much more difficult than myfitnesspal or the almighty IDGAF/YOLO/FOMO life
 

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Amazoniac

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I'm sharing them already because I'm not sure if I'll read since the sun is not important, contrary to our microbiome.

- https://www.hindawi.com/journals/bmri/2016/1934518/

"It has been proved that blue light (415 nm), but not red light (630 nm), is able to induce pigmentation in type III and IV healthy subjects. Moreover, when compared to UVB irradiation, the blue light induces a significantly more pronounced hyperpigmentation that lasts up to 3 months [81]. This means that blue light is capable of affecting epidermal cells and, in particular, that melanocytes are very sensitive to this radiation. Again, it raises the question about blue light effects on skin immune cells."

[42] How much sunlight is enough? - Photochemical & Photobiological Sciences (RSC Publishing)

- Comparing the effects of sun exposure and vitamin D supplementation on vitamin D insufficiency, and immune and cardio-metabolic function: the Sun Exposure and Vitamin D Supplementation (SEDS) Study



- Skin, Sun, and Vitamin A: From Aging to Cancer
 
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Amazoniac

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Here's a Youtube channel of a brazilian doctor that treats his patients with high-dose vit D as a standardized protocol for various of the ailments. I can't tell if they're speaking spanish or portuguese because it's the same language, but the titles are comprehensible, there's before and after treatment, and subtitles in a few videos.
Note how some of the patients have a nice tan before starting the protocol: it's likely that is something else that's causing the problem, not a lack of sun exposure.
 
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benaoao

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I can't tell if they're speaking spanish or portuguese because it's the same language,

that's so unnecessary and flat out wrong lol. Geeze.

Anyway - wouldn't an excessive sun exposure yield the same problems? More isn't necessarily better as seen in Hawaiians who weren't high in spite of hours outside (can't find the article right now). At some point - newsflash - the sun is damaging, and inflammation raises cholesterol which would lower vitamin D. Since vitamin D is made from 7-D-cholesterol

Like almost anything humans try and recreate with reductionist models, I do think it’s the SUN that yields the most benefits, and like almost anything with humans who try and recreate with reductionist models, abusing what's good leads to issues further down the line.

I'll stick to what's close enough to the sun aka UVB. The effect of ultraviolet radiation from a novel portable fluorescent lamp on serum 25-hydroxyvitamin D3 levels in healthy adults with Fitzpatrick ... - PubMed - NCBI
 
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Remember where your supplemental D comes from... I just got back from the beach and feel better...
 

Amazoniac

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that's so unnecessary and flat out wrong lol. Geeze.

Anyway - wouldn't an excessive sun exposure yield the same problems? More isn't necessarily better as seen in Hawaiians who weren't high in spite of hours outside (can't find the article right now). At some point - newsflash - the sun is damaging, and inflammation raises cholesterol which would lower vitamin D. Since vitamin D is made from 7-D-cholesterol

Like almost anything humans try and recreate with reductionist models, I do think it’s the SUN that yields the most benefits, and like almost anything with humans who try and recreate with reductionist models, abusing what's good leads to issues further down the line.

I'll stick to what's close enough to the sun aka UVB. The effect of ultraviolet radiation from a novel portable fluorescent lamp on serum 25-hydroxyvitamin D3 levels in healthy adults with Fitzpatrick ... - PubMed - NCBI
Like it was mentioned before, it takes some commitment to get adverse effects from sun exposure. Since the same problems are appearing in people regardless of how tanned they are, it must be something else that's causing it.
 

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