Anonymous ID: 88dab6 Aug. 2, 2021, 12:48 p.m. No.14252753   🗄️.is 🔗kun   >>2804 >>3009 >>3109

>>14252395

>>14247640 RE: SUNLIGHT, VITAMIN D

 

I agree overall with this post, but…

 

anon wrote: "Vitamin D is made from LDL cholesterol when it is activated by 312 nm UVB light."

 

hmmm, that's a new one for me that I'll have to dig up and confirm. First of all, Low density lipoprotein (LDL) wasn't known in 1920 when vitamin D was discovered, so I find it hard to phantom that LDL plays any critical role in Vitamin D3's activity.

 

My understanding is that vitamin D3, like all other sterol hormones, begins with cholesterol sulfate in the skin. Sunlight, prolly at 312nm UVB, converts it to 7-OH cholesterol sulfate and then it travels to other parts of the body where its eventually its converted to its most active form as Vitamin D3. However, when produced by the body, VitD3 is always sulfated until the very last step. The sulfated salt binds to protein in red blood cells which act as a storage site for a variety of sulfated sterols, including DHEA sulfate. Then, when needed by specific cells, the sulfate is cleaved off by enzymes and the hormone is activated intracellularly. This is why naturally produced vitamin D3 sulfate is always preferable to oral supplements of Vitamin d3 because without the sulfate, much of it is simply stored in our fat with no way to get to where it needs to go without the sulfate attached or it has to rely on LDL or HDL.

 

BTW, all major sex steroids start as cholesterol sulfate as well as Q10, which takes 16 steps. Some research suggests that some statin drugs can deplete Q10 muscle stores up to 50% after the first month of statin therapy. But, what about statins effects on testosterone and estrogen levels if cholesterol synthesis is shut down in the liver? Statins do have some therapeutic benefits (anti-inflammatory?) independent of its reduced cholesterol synthesis, which prolly explains some if its short term weak reduction in heart attack risk (1 in 100 people treated). For example, one interesting effect of statins is that they increase circulating vitamin D3 levels. How? No one really knows but prolly by freeing up orally received vitamin D3 trapped in fat. After all, the body, the brain especially needs cholesterol, to function properly. Thus, if the liver isn't making it because of statins, the body goes looking for cholesterol in our fat stores.

 

As always, do your own research because what I just wrote was from memory based on my review of the literature 10 years ago. However, here is a recent review paper, which covers 25OHD3-3-sulfate and 25OHD3-3-glucuronide in the enterohepatic circulation. The 3-glucuronide conjugate in the mammalian system is new to me, but it shouldn't be because I recall that some weeds actually synthesize 25OHD3-3-glucuronide. We discovered these forms when cows grazing too much on certain weeds developed hypercalciumea (sp?).

 

Transport Disposition of Vitamin D3 Conjugates in the Enterohepatic Circulation

October 2018

https://doi.org/10.1096/fasebj.31.1_supplement.1062.2

 

also check out this site which has a wealth of info on cholesterol sulfate and other good stuff

https://people.csail.mit.edu/seneff/