Is Vitamin D Supplementation Even Neccessary

[jb116]

Read Travis's post's above

That might be looking at metabolism in a vacuum. An analogy is coconut oil inhibiting DHT, but its overall effects as a food outweigh that.
I wouldn't call CO "anti-metabolic." At the same token, considering total effect, certain substances in their "slowing" effect might also be a check and balance
to things that "speed" up the system. Perhaps the more beneficial hormonal effects in taking a short break from caffeine for example. You can't have one without the other.
The whole aspect of sleep induction maybe is part of its benefit actually, especially for exhausted organisms running on stress.

Edit: @HDD posted some good, relevant quotes and info to my post

 

[Terma]

I would caution about ascribing effects of sunlight purely to Vit D (deepest apologies for the source, but you could find a dumber summary): New research reveals sun benefits that AREN'T linked to vitamin D | Daily Mail Online

 

[kayumochi]

I thibk that’s why RP recommends taking it with k2, as a prophylactic measure against vascular calcification and hypercalcemia...
I’d love to know also. From my experience when my serum vitamin D level was 27 I kept getting infections and since supplementing I feel more energetic and resilient to stress

Respiratory infections were a way of life for me before Vitamin D3 supplementation.

 

[dbh25]

Respiratory infections were a way of life for me before Vitamin D3 supplementation.

What dose were you taking?

 

[kayumochi]

What dose were you taking?

I have been taking 5000 - 10,000iu most days for several years now and the respiratory problems are history.

 

[sladerunner69]

tanning beds have been for me quite helpful supplement did nothing for me and others so.

Blue shorts creating blue light tisk tisk tisk. You need to find yourself some red shorts and how.

 

[TripleOG]

I'm curious why a UVB light like Sperti isn't used/talked about more.

Don't think I've come across a testimonial online that says it hasn't raised their blood levels or helped with skin issues. Using a halogen simultaneously should mimic the sun close enough(drastically less to no UVA) for a balanced spectrum. Or just use an incandescent or red light device to offset the UVB excitation.

Is it the price of entry that keeps people away?

 

[Blossom]

I would caution about ascribing effects of sunlight purely to Vit D (deepest apologies for the source, but you could find a dumber summary): New research reveals sun benefits that AREN'T linked to vitamin D | Daily Mail Online

From the article:
"Scientists now believe, for example, that exposure to sun prompts our bodies to produce nitric oxide, a chemical that helps protect our cardiovascular system — and the feelgood brain-chemical serotonin."
I'm sure that doesn't help anyone here feel better. Seriously though I still love getting sunshine. Maybe it just help us balance those things?

 

[Dolomite]

I wonder about too much vitamin D in the summer. I hated going back to school in the fall and always thought it was depressing but now I wonder if I felt like that because my metabolism was depressed after so much time outside in the sun. Also, I managed to gain weight by August. But once I was back inside and temperatures cooled off I lost it.

I have taken vitamin D for several years now. I think I will quit for the summer and assess in the fall.

 

[tara]

I would caution about ascribing effects of sunlight purely to Vit D

Peat and plenty of others here have had a bit to say about the theory and practice of red light (roughly orange through near infrared) supporting healthy metabolism via restoring the cytochrome oxidase enzyme. Also about the benefits of simple warming.

 

[Obi-wan]

I personally feel great when it's sunny and I am outside. We have had a lot of clouds and rain here in Northeast Pennsylvania so I look forward to the next 4 days in the sun. Plus will be going to the shore in New Jersey this weekend. I'll be getting plenty of natural Vit D with the sun so no need to supplement. I think supplementation is unnecessary for most people especially if you see where it is sourced and what it is packaged in. In retrospect I am liking transdermal Magnoil every day. It's interesting that we cannot over do it with the sun but with supplements we can

 

[hotte]

In my opinion high amounts e.g. 20000iu daily are safe if you take enough K2 and Magnesium

 

[Obi-wan]

From @haidut in 2014 "There is a study on PubMed showing vitamin E was associated with lower testosterone in middle aged men but the effect was not large. It also lowered estrogen as expected, and keep in mind that it also lowers prolactin. So the net effect is likely to be very positive for libido since that depends mostly on prolactin/dopamine and estrogen. Also, since dopamine and serotonin tend to be inversely correlated, vitamin E in lower doses should result in lower serotonin, which Ray has said should increase testosterone levels (he said pCPA has that effects by lowering serotonin). So, if you don't overdo the vitamin E (i.e. more than 400 IU per day for years, which is what the study looked at) then your testosterone should stay the same or maybe even increase so it's a win-win situation.
If you search the forum for my post on vitamin E being aromatase inhibitor, the study directly says that vitamin E acts like progesterone. So, that should clear/answer any questions about vitamin E effects. Btw, progesterone is also both an aromatase inhibitor and estrogen "receptor" antagonist. Together, progesterone and vitamin E are the only two substances that I know of that can do both. Vitamin K2 (MK-4) has studies showing it to be aromatase inhibitor and that it also stimulates testosterone synthesis in the testis. Combine that with the strong anti-estrogenic activity of vitamin A, and the mild anti-estrogenic activity of vitamin D, and you can see why some people using EstroBan have been reporting both stronger libido and better muscle building. I think the key is not to overdo vitamin E to avoid supressing testosterone in some people (i.e. prolactin can be lowered with as little as 400mg), vitamin D (studies show doses of more then 3,000 IU can be mildly estrogenic in some people) and make sure that when you take vitamin E and vitamin K at the same time, vitamin E is kept at less than 400 IU per dose. I think vitamin K2 probably has no upper physiological limit in terms of side effects and benefits. Studies with rats showed no adverse effects at doses of hundreds of milligrams, and the study showing increased testosterone synthesis in rats used a dose equivalent to a human dose of 100mg+ daily. But at those doses it will dwarf the cost of even the most expensive steroids used by bodybuilders, so hopefully you can find a cheap supplier of MK-4 if you decide that testosterone increase is what you want.

 

[Koveras]

Vitamin D is involved in thermoregualtion, and it's actually the molecule most suitable for the role. In addition to telling us how much sun we are exposed to, vitamin D₃ also tells-us how much heat we are exposed to: After the photolysis of the 9–10 carbon bond of 7-dehydrocholesterol, only the inactive cis-vitamin D₃ is formed lacking the precise stereochemistry needed to activate the vitamin D receptor. The conversion of cis-vitamin D₃ to active trans-vitamin D₃ is strictly a thermal process and can be accomplished by heating previtamin D₃ at 125° celsius, in octane, for one hour.⁽¹⁾

I'm telling you that thermally-induced cis-trans isomerization of vitamin D₃ and retinoic acid are our biochemical 'heat sensors.' Although cis-trans isomerization is an established way of transducing thermal energy into molecular transformation, its application to biochemical heat sensing—coupled with stereospecific receptors—has gone entirely unmentioned.. .

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]​

 

[Terma]

From the article:
"Scientists now believe, for example, that exposure to sun prompts our bodies to produce nitric oxide, a chemical that helps protect our cardiovascular system — and the feelgood brain-chemical serotonin."
I'm sure that doesn't help anyone here feel better. Seriously though I still love getting sunshine. Maybe it just help us balance those things?

Peat and plenty of others here have had a bit to say about the theory and practice of red light (roughly orange through near infrared) supporting healthy metabolism via restoring the cytochrome oxidase enzyme. Also about the benefits of simple warming.

In my n=1 and judging from other people's reports, both NO and red light give stronger and more immediate bodily effects than Vit D.

The problem is UVB triggers iNOS release. I haven't seen a report that gives any kind of proportion of the contribution between iNOS/(eNos/nNOS) from sunlight, but I imagine it more or less mirrors the excess UVB problem, as well as overexertion in heat. (e.g. "UVB exposure stimulates production of the pro-inflammatory cytokines such as interferon (IFN)- gamma, IL-6, and TNF-α, and prostaglandins which are implicated in progress of carcinogenesis [22]. These cytokines, as well as oxidative stress, stimulate gene expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 via NF-kB activation resulting in NO synthesis and inflammation.)

[Part of Vit D's role is upregulation of the FoxO3 nuclear factor to handle the oxidative stress from UVB]

 

[Mito]

Androgens (DHT, T) Treat Prostate Cancer, Especially When Combined With Vitamin D

 

[Obi-wan]

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."

 

[Mito]

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."

Maybe the estrogen to androgen ratio also has to be high enough for that androgen-linoleic acid mechanism to develop into prostate cancer? Proviron Is Curing My PFS Symptoms But Need Some Help

 

[Amazoniac]

I have been taking 5000 - 10,000iu most days for several years now and the respiratory problems are history.

Who killed the electrical car, though? Was the same person who decided to sanitize our wasser with chlorine?
A dose that improves respiratory problems doesn't mean it's the ideal one. You can improve one aspect while harming other part of the body.

Bad body odor from vit D supplements is a concerning sign. If such thing starts to happen, it's time to consider upping the intake of vitamin A (with E), vit C, magnesium and taurine. B vitamins are useful as well.

 

[Travis]

That whole post is fantastic and deserves its own thread.

I tried to look into the Retinoic acid -> UCP (and also PPARdelta, probably important) question a few times, but ultimately this stood in the way and made some of what I read invalid:
Retinoic acid has different effects on UCP1 expression in mouse and human adipocytes

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?'