Is Vitamin D Supplementation Even Neccessary

[Mossy]

Can one take D3, K2, and A together ? I know E is taken separately from k

Well, Haidut’s Estroban, does have the E included with those three—so, if the dose is not too large, he feels it’s ok to take them together:

Estroban:
Vitamin A - 5,000 IU
Vitamin D - 2,000 IU
Vitamin E - 65mg (100 IU)
Vitamin K2 (MK-4) - 2mg

 

[Mossy]

Nice app indeed.

You don’t feel any better because you need to expose it all! I’m half kidding, check the references in this article

The Promising Evidence of Red and Near Infrared Light Therapy for Increasing Testosterone in Men

Haha—took me a second to get that.

Yeah, there is discussion on this forum about using red light in the nether regions, but there are some against it—or at least cautious about that area.

 

[Mossy]

So are we saying that supplemental D3 helps no one ? My level was 19, and since supplementing, my depression lifted considerably

I think I could objectively say that my D levels going up may have contributed a bit to my mental and cognitive functioning, but my crippling digestive and immune issues it didn’t effect.

 

[Broken man]

Nice info @Obi-wan, what about vitamin K?

 

[Obi-wan]

I had issues with Vit E and started the thread at Is Supplementing Vit E Actually Bad For You? being encapsulated in PUFA oil also with Vit D encapsulated in PUFA oil and also what sources they come from and amount used. I use IdeaLabs Vit K product anywhere from 10-20 drops per day. My hips get sore from the androgen depravation therapy that I am on and apply there which helps a lot. As @haidut once said your body will take as much Vit K as you give it. I think it blows VitD out of the water in terms of strengthening bones. One of my top supplements! Cheaper than CoQ10.

 

[Obi-wan]

LOL! He must have got the cannabis oil QUALIHEMP™ brand.

Travis, you are a funny guy!

 

[Dave Clark]

I just ordered the Calcirol product from IdeaLabs. When looking at the other topical vitamin D products on-line, I noticed they recommended applying it to the fattiest part of the body, as opposed to where the skin is thin, they claim it absorbs into the fat layers better, etc. Usually, topicals are better absorbed on the thin skin, I always apply to wrists, inner forearms, etc. Does anyone know if the topical vitamin D can/should be applied to wrists, thin skin areas, etc., or to the fattiest areas that I previously mentioned?

 

[Obi-wan]

@Travis said "you wouldn't necessarily want to take vitamin D at night since this could interfere with the mineralization and crystallization cycling of bone)." is a powerful statement! He also takes it transdermal every couple of days. Since he is a Guru (@Amazoniac agree's ) I take his recommendations seriously. Where is Amazoniac's girlfriend dear @Sheila in this conversation. Always love to hear from her! I will stick with natural sun bathing for now. All of you are invited to a pool party...@bzmazu is bringing pineapples

 

[Obi-wan]

Just wanted everyone to know @slovak_peat let me know his fathers PSA went from 79 down to 9.7 in 2 months. He is on Lupron but has also followed all the recommendations that @Travis has given!Travis now has super Guru status! He is a supreme lord!

 

[Braveheart]

@Travis said "you wouldn't necessarily want to take vitamin D at night since this could interfere with the mineralization and crystallization cycling of bone)." is a powerful statement! He also takes it transdermal every couple of days. Since he is a Guru (@Amazoniac agree's ) I take his recommendations seriously. Where is Amazoniac's girlfriend dear @Sheila in this conversation. Always love to hear from her! I will stick with natural sun bathing for now. All of you are invited to a pool party...@bzmazu is bringing pineapples

I'll drill a hole in one of the pineapples and fill it with rum...just for those who still enjoy a little "drink"... I'll supply the straws too!

 

[Blossom]

I'll drill a hole in one of the pineapples and fill it with rum...just for those who still enjoy a little "drink"... I'll supply the straws too!

Our first RPF pool party! Count me in!

 

[Amazoniac]

[3] Low Vitamin D Status despite Abundant Sun Exposure | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic

"On average, the 93 subjects reported being outside for 22.4 h/wk (1.6) with no sunscreen, and 28.9 h/wk (1.5) with and without sunscreen (Fig. 1). Of subjects, 40% (37 of 93) reported never using sunscreen. The resultant mean sun exposure index score, indicating hours per week of total body skin exposure with no sunscreen used, was 11.1 ± 0.7 (range 1.0–38.4). Only two subjects reported use of tanning booths; as such, the skin darkening noted previously reflects natural sunlight exposure."

"51% (47 of 93) of these subjects had low vitamin D status (Fig. 2)."

In this cohort of young adults, substantial variability in serum 25(OH)D concentration exists despite abundant sun exposure. Surprisingly, a 25(OH)D concentration that many would argue to be too low (10), is common in this highly sun-exposed population. Furthermore, regardless of the amount of sun exposure, the serum 25(OH)D concentration does not increase to more than approximately 60 ng/ml.

Although the presence of “low” 25(OH)D concentration in this population seems counterintuitive, this might be anticipated from an evolutionary standpoint because the high calcium intake of early humans (27) may have allowed maintenance of calcium homeostasis despite low vitamin D status."

"[..]in 18 Puerto Rican farmers with self-reported sun exposure from 32–70 h/wk, two individuals had a 25(OH)D level less than 30 ng/ml (31). Similarly, low 25(OH)D values were reported in some subjects who used a tanning bed at least once a week for 6 wk (32) and among outdoor workers with a sun index of 11.5 (22). Thus, even substantial sunlight or UV exposure does not ensure maintenance of vitamin D adequacy [based on circulating 25(OH)D] for all individuals, according to currently accepted standards."

"Holick et al. (33) documented that human skin has the intrinsic ability to limit vitamin D production. Moreover, a reduction in cutaneous concentration of 7-dehydrocholesterol and a concomitant declining capacity of the skin to make vitamin D occur with advancing age (34, 35). However, in our study the population was predominantly young, which should have obviated such reduced capability for vitamin D synthesis. Importantly, lizards with behaviorally high sun exposure have a lower capacity to produce vitamin D than closely related species with habitually less sun exposure (36). Thus, it appears likely that factors exist, which are not yet well understood, that can restrict skin production of vitamin D in response to UV radiation. In any case, it is crucial that we do not wantonly accept the concept that vitamin D deficiency is due exclusively to inadequate UV exposure. Rather, it seems self-evident from this study that low vitamin D status, as it is currently defined, may occur despite “more than adequate” sun exposure."​

[4] 25-Hydroxylation of vitamin D 3 : relation to circulating vitamin D 3 under various input conditions | The American Journal of Clinical Nutrition | Oxford Academic

"[..]at typical inputs of vitamin D3 (whether cutaneous or oral), there is rapid and near-quantitative conversion of vitamin D3 to 25(OH)D, which then serves not only as the functional status indicator of the nutrient but, more important, as its principal storage form in the body. Second, above typical serum vitamin D3 concentrations (ie, above ≈15 nmol/L), which are probably equivalent to a daily input of 2000 IU, the hepatic 25-hydroxylases become saturated and the reaction switches from first order to zero order. Third, the constant (maximal) production of 25(OH)D, irrespective of precursor concentration of vitamin D3, must be in excess of metabolic consumption, which is the reason that serum 25(OH)D continues to rise as vitamin D3 concentrations rise.

If correct, this explanation may help to clarify many of the uncertainties surrounding vitamin D physiology, one of which is the determination of the approximate concentration of serum 25(OH)D that may be considered optimal for health. Our data offer a different approach to estimating this value. One could plausibly postulate that the point at which hepatic 25(OH)D production becomes zero-order constitutes the definition of the low end of normal status. This value, as suggested from the equation in Figure 3, is at a serum 25(OH)D concentration of ≈88 nmol/L (35.2 ng/mL) (the y-axis intercept of the linear portion of the equation in Figure 3). It is interesting that this estimate is very close to that produced by previous attempts to define the lower end of the normal range from the relations of serum 25(OH)D to calcium absorption (29) and to serum parathyroid hormone concentration (ie, ≈75–85 nmol/L, or 30–34 ng/mL) (30).

In study A, with a supraphysiologic input, slow release from storage depots is indicated by the slow fall in 25(OH)D3 from its Cmax. The half-time of 25(OH)D is typically on the order of 20–30 d, whereas the approximate half-time in study A for the increment above baseline was >50 d. Fat is the most likely storage depot, although muscle storage cannot be ruled out. Fat storage of vitamin D3 is certainly the case in the rat (as well as in humans) when serum vitamin D3 concentrations are high. Analysis of body distribution in rachitic animals given 14C-labeled vitamin D3 every day for 2 wk showed that the largest amount, ≈10%, appeared in body fat and was slowly released into the circulation over the next several months along with a more polar metabolite—probably 25(OH)D, which had not been identified at that time (31). In obese human subjects, serum 25(OH)D is lower, serum vitamin D may be very low, and rises in serum vitamin D and 25(OH)D after either UV-B irradiation or oral administration of vitamin D2 are significantly lower in obese than in nonobese persons (32, 33).

Deposition in body fat almost certainly occurs in cases of vitamin D intoxication, and persistence of hypercalcemia for months has been attributed to sustained release of vitamin D from such body stores. Fat storage is also the best explanation for the seeming disappearance of vitamin D3 from the serum in the acute dosing experiment (study A). We cannot rule out some excretion of the large dose of vitamin D3, either directly or by various catabolic reactions; however, the fact that the AUC for the increment in serum 25(OH)D was not lower than that for the increment in serum vitamin D3 suggests little or no wastage of the ingested 100000 IU.

Taken together, these results show that, as is typical for enzyme systems, there is a practical limit to the first-order 25-hydroxylation of vitamin D3 and that, when vitamin D3 input exceeds that limit, vitamin D3 itself accumulates within the body, both in serum and probably in body fat. From the data presented in Figure 4, it would seem that that threshold occurs at a serum vitamin D3 concentration of ≈15 nmol/L. In turn, such a concentration, from the data of Figure 3, is reached on average at a vitamin D3 input of 2000 IU/d. We suggest that, below this input (whether cutaneous or oral), near-quantitative conversion of vitamin D3 to 25(OH)D3 occurs. Thus, at typical inputs, 25(OH)D3 would constitute the principal storage form of the vitamin."​

The impression that we had on the previous pages is right: when 25(OH)D is around 35 ng/mL, the liver's production is saturated, but there's a steep increase until 40 or a bit more.

[4]
"The relation between steady state concentrations of vitamin D3 and 25(OH)D3 is shown in Figure 4 and Figure 5. Figure 4 plots the data of studies B, C, E, and F, and Figure 5 is based on the data of study D. Both graphs show the replicability of the pattern of the relation. In both, the mean concentration of 25(OH)D rises very steeply from values close to zero to values of ≈100 nmol/L (40 ng/mL) and even higher. As is suggested visually, the relation is biphasic, with serum 25(OH)D rising very rapidly at low serum vitamin D3 concentrations and then more slowly, but with no apparent tapering off at progressively higher serum vitamin D3 concentrations."​

So the body is trying to conserve levels in the betweens, yet it's possible to keep pushing everything higher. It will try to put this sur and plus into storage. If you take too much, you might have to deal with it after discontinuing supplementation as it's released from fat.

Baseds on what was shared in the here, I wouldn't exceed the current upper limit without testing. I would consider more or less 2000 IU depending on sun and diet, and obtain the rest through an UVb lambI mean, lamp if needed because the skin might be able protect the body from the excess with a greater of the margins than supplements.

When in doubt, open heliology book , all there

 

[Braveheart]

The impression that we had on the previous pages is right: when 25(OH)D is around 35 ng/mL, the liver's production is saturated, but there's a steep increase until 40 or a bit more.

[4]
"The relation between steady state concentrations of vitamin D3 and 25(OH)D3 is shown in Figure 4 and Figure 5. Figure 4 plots the data of studies B, C, E, and F, and Figure 5 is based on the data of study D. Both graphs show the replicability of the pattern of the relation. In both, the mean concentration of 25(OH)D rises very steeply from values close to zero to values of ≈100 nmol/L (40 ng/mL) and even higher. As is suggested visually, the relation is biphasic, with serum 25(OH)D rising very rapidly at low serum vitamin D3 concentrations and then more slowly, but with no apparent tapering off at progressively higher serum vitamin D3 concentrations."​

So the body is trying to conserve levels in the betweens, yet it's possible to keep pushing everything higher. It will try to put this sur and plus into storage. If you take too much, you might have to deal with it after discontinuing supplementation as it's released from fat.

Baseds on what was shared in the here, I wouldn't exceed the current upper limit without testing. I would consider more or less 2000 IU depending on sun and diet, and obtain the rest through an UVb lambI mean, lamp if needed because the skin might be able protect the body from the excess with a greater of the margins than supplements.

When in doubt, open heliology book , all there

Amazoniac...Excellent...this is usable info, and momentarily makes sense....instead of the usual general inconclusive blather...this will help me, thanks

 

[Obi-wan]

Adequate amounts of vitamin D can be produced with moderate sun exposure to the face, arms and legs, averaging 5–30 minutes twice per week, or approximately 25% of the time for minimal sunburn. The darker the skin, and the weaker the sunlight, the more minutes of exposure are needed. Vitamin D overdose is impossible from UV exposure; the skin reaches an equilibrium where the vitamin degrades as fast as it is created.[24][152][153] -Wikipedia

Sunscreen absorbs or reflects ultraviolet light and prevents much of it from reaching the skin.[154] Sunscreen with a sun protection factor (SPF) of 8 based on the UVB spectrum decreases vitamin D synthetic capacity by 95%, and SPF 15 decreases it by 98%. - This is the problem, many use SPF25 or above

 

[Obi-wan]

Winter transdermal non PUFA application of 1000- 2000 IU's works

 

[Obi-wan]

Vitamin D toxicity is rare.[24] It is caused by supplementing with high doses of vitamin D rather than sunlight. The threshold for vitamin D toxicity has not been established; however, according to some research, the tolerable upper intake level (UL) is 4,000 IU/day for ages 9–71[137] (100 µg/day), while other research concludes that, in healthy adults, sustained intake of more than 1250 μg/day (50,000 IU) can produce overt toxicity after several months and can increase serum 25-hydroxyvitamin D levels to 150 ng/ml and greater.

Vitamin D overdose causes hypercalcemia, which is a strong indication of vitamin D toxicity – this can be noted with an increase in urination and thirst. If hypercalcemia is not treated, it results in excess deposits of calcium in soft tissues and organs such as the kidneys, liver, and heart, resulting in pain and organ damage.[24][27][4 -Wikipedia

 

[Mossy]

Just wanted everyone to know @slovak_peat let me know his fathers PSA went from 79 down to 9.7 in 2 months. He is on Lupron but has also followed all the recommendations that @Travis has given!Travis now has super Guru status! He is a supreme lord!

Incredible. I’ll search this out further, to see what the other reccomendations were.

 

[charlie]

Just wanted everyone to know @slovak_peat let me know his fathers PSA went from 79 down to 9.7 in 2 months. He is on Lupron but has also followed all the recommendations that @Travis has given!Travis now has super Guru status! He is a supreme lord!

I think a summary of these findings would be a blessing to many people.

 

[Braveheart]

OK, more good info...So, Help me w this... I get sub tropical 20-30 minutes sun on my naked bod, almost every day...min 4 days a week. That 30 mins should give me approx 10,000 iu... but maybe not, because I am tanned and 74 and my skin no longer converts sun as well...so I wonder?. Meanwhile I average about 4000 iu daily from food and supps. minimum...I see the sun as bonus. The body/skin regulates the amt it needs, right?...so I can't get too much from sun, right? But you can supplement too much. I better stop here...thoughts? Oh, and I make sure to get plenty of A (5/1 ratio) minimum....averaging around 25000 A... comments?...

 

[charlie]

Oh, and I make sure to get plenty of A (5/1 ratio) minimum....averaging around 25000 A...

And magnesium.