Is Vitamin D Supplementation Even Neccessary

[Dave Clark]

Why not just apply the vit D3 supplement to the skin as opposed to ingesting it, assuming adequate light exposure isnt available (I’m pretty sure the skin synthesizes cholecalciferol)? Perhaps applying enough to maintain serum levels and then get sunlight or light exposure as much as you can when you can would be a decent idea. Blood tests may also be a good idea.

I know there are a few products made with topical vitamin d in mind. Primal-D, AnuMed, BioMulsiun, Life Flow, etc. are the ones I havve seen. Wondering if IdeaLabs or Health Natura vitamin D would be effective topically?

 

[Obi-wan]

From @Amazoniac on the Calcirol thread Calcirol - Liquid Vitamin D3. Carolyn Dean has some important points regarding D3 and Magnesium By the way Calcirol is a transdermal D3 from Idea Labs.

@haidut mentioned the synergy of Vit D3 with Androgens since D3 is a hormone. Since I am on Androgen deprivation therapy I will take a pass. Got to keep that PSA down.

Calcitriol also has other effects, including some on cell growth -Wikipedia. Proliferation as well as differentiation

 

[Braveheart]

Why not just apply the vit D3 supplement to the skin as opposed to ingesting it, assuming adequate light exposure isnt available (I’m pretty sure the skin synthesizes cholecalciferol)? Perhaps applying enough to maintain serum levels and then get sunlight or light exposure as much as you can when you can would be a decent idea. Blood tests may also be a good idea.

Peat says oral not effective for many, especially if you are overweight?...can't find quote at this minute

 

[Cirion]

Does this magnesium deficiency induced by too much vitamin D also occur if you get lots of sunlight / go to the tanning bed a lot, but don't supplement any vitamin D?

I'm gonna guess - Yes, just from my own experiences - I have been getting symptoms of magnesium deficiency lately - even though I generally get at least 400-500 mg a day, makes me think I need upwards of 1000 mg a day of magnesium at least.

I should definitely test my levels to see where I'm at.

 

[InChristAlone]

But this is the problem:

Spoiler: Cloudiest cities in the US and A

Yeah I grew up in one of the cloudiest cities. And I became myopic pretty early on. I also stopped growing at 9 yrs old.

 

[Amazoniac]

Some words from Chris:

- https://www.westonaprice.org/an-anc...-naked-ape-hypothesis-of-optimal-serum-25ohd/

"we should emphasize serum 25(OH)D much less and emphasize the nutrient density and nutrient balance of the overall diet and lifestyle much more"

"The naked ape hypothesis essentially holds that the requirement for a certain 25(OH)D concentration circulating in serum was fixed into our genome during some critical prehistoric window wherein humans exposed themselves to maximal levels of sunshine, that this level can be estimated by examining humans with maximal sun exposure today, that we should presume this level to be safe and optimal, and that the burden of evidence lies on anyone suggesting otherwise."

"When we consider that scientists estimate both the loss of fur and the gain of dark skin pigmentation to date back to about 1.2 million years ago, moreover, but estimate that light skin didn’t even begin evolving in Northern Europeans and East Asians until some 30,000 years ago (7), long after evidence for widespread use of clothing, it becomes clear that we were never truly “naked apes” at all. Taken at face value, the available evidence instead suggests that approximately as long ago as we lost the protection from the sun afforded by fur we gained the protection afforded by dark skin, and that we began clothing ourselves in more innovative ways long before we began losing the protection of dark skin."

"In several [Pacific] islands regulatory measures had been adopted requiring the covering of the body. This regulation had greatly reduced the primitive practice of coating the surface of the body with coconut oil, which had the effect of absorbing the ultra-violet rays thus preventing injury from the tropical sun. This coating of oil enabled them to shed the rain which was frequently torrential though of short duration."

"Thus, our prehistoric ancestors were unlikely to ever have been “naked apes” because they seem to always have been clothed by at least dark skin, and to have used animal hides, clothing, colored pigments, and perhaps botanical sunscreens throughout huge portions of their history, some of these things being used, according to current estimates, long before light skin ever developed."

"Naked apes or not, humans certainly lived in prehistoric times. To what extent can modern lifeguards or any other group provide a proxy for the 25(OH)D levels of prehistoric humans?

If there is any such proxy, modern lifeguards certainly don’t fit the bill.

To begin with, lifeguards are paid to work throughout the day. Traditionally living humans, like other animals, seek shade from the hot sun in a way that lifeguards can’t, even if they have some sunscreen and an umbrella. One paper noted the universality of shade-seeking behavior among non-human primates such as gorillas, chimpanzees, and baboons, and suggested that humans dwelling in the African savannah would similarly have engaged in these behaviors throughout their evolution (12)"

"Maasai spend most of their days in the sun, wearing clothes that cover mainly their upper body and upper legs. It is important to note that, whenever possible, they avoid direct exposure to the sun and prefer a shady place, especially during midday...

Hadzabe spend most of their days in the sun. Similar to the Maasai tribe, they avoid direct exposure to the fierce sun whenever possible, and most of their activities are planned in the early morning and late afternoon, while spending the middle part of the day sleeping, eating or talking in a cooler place under a tree or rock."

"The lifeguards had 20-fold the risk of kidney stones compared to the general population in northern Israel. In southern Israel, the risk was only elevated 12-fold, but this is because the general population in southern Israel had twice the risk of kidney stones as the general population of northern Israel, consistent with observational studies cited in the paper showing that the closer you get to the equator, the more the risk of kidney stones increases, likely because calcification of the kidneys is the most sensitive sign of vitamin D toxicity (15)."

"These lifeguards did not have elevated levels of calcium in their blood, but they did have elevated levels of calcium in their urine, which the authors attributed to excess 25(OH)D; insufficient urinary output, which the authors attributed to dehydration; and elevated levels of uric acid in their blood, which the authors suggested resulted from “solar damage to the skin.” All three of these could be attributed to too much sun exposure, and the authors suggested that they “probably all contribute to the susceptibility of lifeguards to form kidney stones.”

These data seem to flatly contradict both the idea that vitamin D is only toxic at doses that cause hypercalcemia (contradicted also by animal experiments, including 15) and the idea that you can’t get too much vitamin D from the sun."

"vitamin D metabolism could differ between Caucasians and non-Caucasians, and it strongly suggests that if we used people without substantial European ancestry as our model for 25(OH)D status in sun-rich environments, we would generate much lower estimates"

"Indeed, a paper entitled “Low Vitamin D Status Despite Abundant Sun Exposure” (17) found that, among students and skateboarders with abundant exposure to the Hawaiian sun, whites had a mean 25(OH)D of 37 ng/mL while Asians had a mean value of only 25 ng/mL. Unfortunately the authors did not report sun exposure separately by race, but the average among all the subjects was over 22 hours per week exposing half the body to the sun without any sunscreen.

Consistent with the possibility that Asians have lower 25(OH)D than whites even when exposed to abundant tropical sun exposure, rural Indians who expose their face, chest, back, legs, arms, and forearms to the Indian sun for nine hours per day have even lower levels. One study reported a mean of 24 ng/mL in males and 19 ng/mL in females (18).

Of course if we really wanted to understand likely 25(OH)D values in our prehistoric African ancestors, we would do well to look at Africans rather than Asians. At first glance, the studies of the Maasai and Hadza from Fritz Muskiet’s lab (13) may seem to contradict the point I am making. After all, the means for these populations were between 40 and 50 ng/mL.

We can resolve these discrepancies, however, simply by adjusting the values to account for discrepancies in different methods of measuring 25(OH)D."

"I adjusted the values to correspond to those of the DiaSorin radioimmunoassay using the discrepancies found in references 17 and 19. While this does not necessarily make the values more accurate, it makes them easier to compare to one another, and since the DiaSorin assay is the one most commonly used in the literature, it makes it easier to situate these values in the context of the general body of scientific literature. What we see is that the variation in values among the different groups is significantly reduced after adjustment, and with the exception of rural Indians, the values lie between 30 and 40 ng/mL. This is considerably lower than the values presented in Dr. Vieth’s 1999 paper, which ranged from 42 to 65 ng/mL."

"Traditionally living non-whites in tropical regions have lower 25(OH)D, in the range of 30-40 ng/mL when adjusted to correspond to the most common assay used in the literature. These populations, however, are not good proxies for prehistoric 25(OH)D because the climate was different in the prehistoric past and vitamin D synthesis probably tended to be lower back then."

"The evidence suggests we were never truly naked apes, that modern lifeguards and other populations dominated by European ancestry are not good proxies for the 25(OH)D levels of our prehistoric ancestors inhabiting equatorial Africa, and that the 25(OH)D requirement was never indelibly fixed into our genome but has continued to evolve over time."

"What the evidence from modern lifeguards tells us is that it seems to be possible to get too much vitamin D even from the sun, and their 20-fold elevated risk of kidney stones could perhaps be a harbinger of worse things to come, like an increased risk of heart disease from arterial calcification."

"As always, of course, context is critical. Perhaps the levels of 25(OH)D found in Israeli lifeguards are harmless or even beneficial in the context of a nutrient-dense and balanced diet rich in all of vitamin D’s synergistic partners. But where does the burden of evidence lie? Drs. Heaney and Holick maintain that “the burden of proof must be placed on those who propose that lower intakes (and lower serum levels) are without risk of preventable dysfunction or disease.” Why shouldn’t the burden of “proof” lie on those who advocate high levels of 25(OH)D as safe and optimal when they are considerably higher than those found in numerous populations with abundant sun exposure and when they are known to be associated with large increases in the risk of soft tissue calcification?

Do we really need to prove a negative — that no problems exist at lower levels — when we have positive evidence of harm at higher levels?"​

- https://www.westonaprice.org/an-anc...a-deficiency-of-calcium-instead-of-vitamin-d/

"Although commonly used as one, 25(OH)D is not a specific marker of vitamin D status. 25(OH)D is a compound that we make from vitamin D in our liver. Vitamin D will indeed dose-dependently increase 25(OH)D, but many other factors affect the rate at which 25(OH)D is synthesized, used, or degraded. These include variations in the genetics of vitamin D metabolism, intakes of other nutrients, crisis states such as inflammation, and disease states such as cancer.

Some of the factors that cause low 25(OH)D are bad and some of them are good. While there is likely some critical threshold below which low 25(OH)D almost certainly indicates a major problem, this is not necessarily the case with moderately low 25(OH)D. In order to determine whether moderately low 25(OH)D is a good thing or a bad thing, and in order to understand what, if anything, to do about it, we need to understand why it’s low."

"In order to understand why a deficiency of calcium can cause low 25(OH)D, we need only consider the most well established and best understood role of vitamin D: to regulate the level of calcium in our blood.

If our blood level of calcium drops for any reason — for example, if we aren’t consuming or absorbing enough calcium from our food — our endocrine system quickly launches a systematic program to bring that level back to normal (1). Our parathyroid glands ramp up their production of parathyroid hormone, which sends a signal to our kidneys to ramp up their conversion of 25(OH)D to calcitriol, the most active form of vitamin D. Calcitriol then increases serum calcium in two ways: preventing loss of calcium in the urine and feces, and extracting calcium from bone.

Or one could splice it three ways: we absorb more calcium from our food, and we lose more from our bones into our blood, but we lose less from our blood into our urine.

Even a slight increase in calcitriol can lead to a big drop in 25(OH)D. This may seem counter-intuitive at first, but it makes more sense if we realize that when we look at the concentration of a compound in the blood, we are taking a static snapshot of a dynamic process. Molecules are always coming and going. As a result, maintaining a constant blood level of a given compound requires a continuous supply of that compound itself. Since calcitriol is made from 25(OH)D, maintaining a given concentration of calcitriol also requires a continuous supply of 25(OH)D.

Calcitriol disappears far more rapidly than 25(OH)D (2). The amount of 25(OH)D that would sustain a certain concentration of itself in the blood for a day would only maintain the same concentration of calcitriol for an hour. So if the body decides to maintain a slightly higher concentration of calcitriol, it would have to levy a much heavier tax on the supply of 25(OH)D.

We should expect, then, that a deficient intake of calcium will lead to increased production of calcitriol, and thereby to depletion of 25(OH)D.

Would an excess of calcium, conversely, cause higher than normal 25(OH)D? Maybe, but not necessarily. While excess calcium would be expected to suppress the production of parathyroid hormone and calcitriol, thereby sparing 25(OH)D, it also elicits additional responses to suppress serum calcium: in response to high levels of calcium, our thyroid glands produce calcitonin, which not only blocks the loss of calcium from bone (1), but appears to stimulate the production of an enzyme that degrades both 25(OH)D and calcitriol to other products generally thought to be inactive (3). Excess calcium could, therefore, have conflicting effects on 25(OH)D, preventing its conversion to calcitriol but increasing its degradation through an alternative pathway, perhaps leading to no net change in 25(OH)D at all.

Overall, then, we would expect that a deficiency in calcium would cause low 25(OH)D, and that correcting the deficiency would normalize the 25(OH)D, but that beyond a certain threshold, increasing calcium intake might not increase 25(OH)D any further."

"dietary calcium deficiency causes our parathyroid glands to make more parathyroid hormone, thus increasing the conversion of 25(OH)D to the more active calcitriol. As a result, 25(OH)D tanks."

"calcium deficiency stimulates the production of calcitriol regardless of vitamin D intake, while vitamin D deficiency has no effect on calcitriol levels"

"the predominant effect of calcium is to spare 25(OH)D."

"There is some observational evidence suggesting that one of the reasons rural Indians with abundant sun exposure have such low 25(OH)D is because of low intakes of bioavailable calcium (9). These particular Indians consume diets dominated by cereal grains, with relatively few animal products and vegetables providing only five percent of calories. Cereal grains provide very little calcium but large amounts of phytate, which inhibits the absorption of calcium. As calcium intake increases among these subjects and phytate intake declines, 25(OH)D status improves"

"one of the reasons that the Maasai and Hadza have considerably higher 25(OH)D status than rural Indians (as discussed in the previous post in this series) despite all three groups being exposed to abundant sunshine is because calcium deficiency is prevalent among neither the Maasai nor the Hadza. The Maasai herd cattle and consume large amounts of dairy products. In addition to animal products, the Hadza consume some 14 percent of their diet as baobab, which some investigators have said is one of the Hadza’s five food groups (10), and which is very rich in calcium (11)."

"Calcium is widely distributed in plant foods, but the amounts are often small and in some calcium-rich leafy greens like spinach, the availability is terrible. Calcium absorption from kale, however, is better than that from conventional, commercial milk (12). Numerous cruciferous vegetables provide anywhere from half as much to twice as much absorbable calcium, cup for cup, as commercial milk (13)."
I had to add this one because of Travisord.

"As a thumb of the rules, then, I would say that if someone has low 25(OH)D and she is eating two to three servings of dairy products or soft, edible bones, or two to three cups of cruciferous vegetables per day (which have their downsides), then calcium deficiency is unlikely to be the explanation. If one is not eating these foods, however, it could very easily be the explanation. In such a case, the person has little to lose and much to gain by including more calcium-rich foods."

"If poor calcium intake is depleting vitamin D stores and thereby causing low 25(OH)D, throwing extra vitamin D at the problem is not the optimal solution. It will not be the most effective way of normalizing the hormonal milieu or preventing bone loss. Only calcium can correct a calcium deficiency. Throwing a calcium supplement at the problem is not the ideal solution either. Both vitamin D and calcium supplements leave the diet lacking in a broad spectrum of other important nutrients found in dairy products, bones, and leafy greens."​

- https://chrismasterjohnphd.com/2017/05/16/tell-difference-vitamin-d-calcium-deficiencies/

"The higher your calcitriol is, all the way from low through the reference range to high, the more probable the deficiency is calcium rather than vitamin D. It’s not diagnostic, but helping us to understand the probability better makes it very useful. That’s the blood work. The second part of this is a diet and lifestyle analysis. Do you go outside regularly and get unprotected sun exposure? You don’t want to burn, that’s terrible for your skin. But you need to get some unprotected sun exposure during the day in order to get vitamin D from the sun.

If you don’t, that’s strike one against your vitamin D. The second question is do you eat fatty fish, pasture-raised egg yolks, or take cod liver oil? If you don’t, you’re not getting significant food sources of vitamin D and that’s strike two. The third question is do you take a supplement? If not that’s strike three.

If you’re not getting vitamin D from any of those places, vitamin D deficiency is very probable. For calcium, the most concentrated sources of bioavailable calcium are dairy products, edible bones, but not bone broth, and cruciferous vegetables like kale and broccoli. If you’re eating those foods in several servings per day there’s a good chance you’re getting enough calcium. If you’re not, there’s a good chance you’re deficient."

"If you’re getting significantly less than a gram, then you may be deficient. And if you’re getting 500 milligrams or less, then I think calcium deficiency is very probable. Now you could be deficient in both vitamin D and calcium. In that case calcitriol will be hard to interpret.

But PTH will still be high. And your diet and lifestyle analysis will indicate both problems. Looking for an agreement between the blood work and the dietary and lifestyle analysis is the best way to find the problem.

And thinking through the diet and lifestyle analysis also clues you into what the solutions to the problem are. For example, if you’re not eating calcium-rich foods, the solution is to eat calcium-rich foods. Correcting the diet and lifestyle is always the preferable first choice. But supplements can be important if that isn’t sufficient to fix the problem."​

- https://chrismasterjohnphd.com/2017/05/18/vitamin-d-normal-pth-high/

"if PTH is high then the body perceives a deficiency of some kind and either it’s perceiving that correctly or it’s perceiving that incorrectly. If the D has reached normal levels and the body still perceives a deficiency in the system, the first thing that I would look at is calcium"

"[Calcitriol:] the higher it is the greater the probability of calcium deficiency"

"If P and T and H goes down in response to more D or more calcium or more of both, then test which one of those factors or whether the combination is the best way to reduce it in that person."

"Alternatively, the PTH may be high for reasons that are not related to nutrition, and if that’s the case it’s very important to identify the cause. Non-nutritional elevations in PTH are called primary hyperparathyroidism and there are three major causes of primary hyperparathyroidism. The first one is a non-cancerous tumor in the parathyroid gland called an adenoma. That’s the most common cause. The second most common cause is an enlargement of normal cells in the parathyroid gland called parathyroid hyperplasia, and the least common cause is parathyroid cancer.
That’s less than 1% of all non-nutritional reasons for elevations of PTH."​

 

[Obi-wan]

Chris Masterjohn is a wealth of knowledge. +1 for raw milk consumption. My mother had parathyroid hyperplasia. She had a medical procedure where they put an incision in her neck and one by one took out a parathyroid (you have 4 on your thyroid) , cut it up and put it back in while keeping a monitor on her finger to monitor blood calcium. After the second one the calcium overload in her blood abruptly stopped. Just chopped it up and put it back in.

 

[InChristAlone]

Chris Masterjohn is a wealth of knowledge. +1 for raw milk consumption. My mother had parathyroid hyperplasia. She had a medical procedure where they put an incision in her neck and one by one took out a parathyroid (you have 4 on your thyroid) , cut it up and put it back in while keeping a monitor on her finger to monitor blood calcium. After the second one the calcium overload in her blood abruptly stopped. Just chopped it up and put it back in.

Yeah the major cause of blood calcium over 10 is parathyroid.

 

[Braveheart]

Chris Masterjohn is a wealth of knowledge. +1 for raw milk consumption. My mother had parathyroid hyperplasia. She had a medical procedure where they put an incision in her neck and one by one took out a parathyroid (you have 4 on your thyroid) , cut it up and put it back in while keeping a monitor on her finger to monitor blood calcium. After the second one the calcium overload in her blood abruptly stopped. Just chopped it up and put it back in.

I forgot how much raw milk you consume per day?

 

[Obi-wan]

I forgot how much raw milk you consume per day?

about 2 glass fulls a day usually at night with dark chocolate. Its the best. I tried store bought and it had no taste

 

[Braveheart]

about 2 glass fulls a day usually at night with dark chocolate. Its the best. I tried store bought and it had no taste

I have access to good raw from local grass fed dairy, but the fat content concerns me a bit...will probably go back on it, after reading the good Masterjohn article. I was doing the same...3 lattes, w the last having the local Mayan cacoa powder.

 

[HealthisWealth]

Thank you Mito...am 74, was aware of this...plus I am quite tanned which also hinders D conversion in skin...because of no testing avail to me I just kind of wing it, in hopes?...I get full body tropical sun 30 min per most days, plus average 4000 iu supp...keeping ratio of A TO D at 5 to 1...with all the sun I get I can handle/need a little extra A. Anyway, this drives me a little nuts because I'm just trying to put it all together for my age/situation and the info is often more confusing than not. Thanks for this note.

Hi

So how many iu of vitamin A do you supplemen everyday?

 

[Braveheart]

Hi

So how many iu of vitamin A do you supplemen everyday?

Hi, my average A for the week is around 30,000 iu...this from food and supplements...eat lots of A containing foods...Supp 15k oral once a week and IdeaLabs rest of week when needed... to keep approx 5 to 1 ratio A/D. I track everything but do not include sun as I can only estimate that...try to reach 4000 D daily...sun is bonus? With all the sun I get I go over a little on the A.

 

[charlie]

I track everything but do not include sun as I can only estimate that...try to reach 4000 D daily...sun is bonus?

They have an app for every thing.

https://play.google.com/store/apps/details?id=com.ontometrics.dminder

 

[Mito]

Some more words from Chris:

https://chrismasterjohnphd.com/2016/05/11/the-daily-lipid-podcast-9-balancing/

“So if we are to ignore the layer of complexity that phosphorus adds, we would say that parathyroid hormone levels are our body’s natural judgement about whether the vitamin D-calcium economy is adequate. I said that vitamin D would spare the need for parathyroid hormone, calcium would do the same thing – if more calcium’s coming in in the diet, you have more in the serum without the need for calcitriol stimulating it. Maintaining the serum calcium at a healthy level without the need for parathyroid hormone to get activated, that’s going to reduce the need for PTH, and in fact it’s even going to spare 25(OH)D from being converted into calcitriol, so if you make someone calcium-deficient, regardless of their vitamin D exposure from the sun, or their intake of vitamin D from foods, their 25(OH)D as a marker – a supposed marker – of vitamin D status, that will drop, because it’s being driven into making calcitriol.

And so when we look at serum calcium, we don’t really get anything useful in most circumstances, because it’s so tightly regulated. When we look at calcitriol, we don’t really see anything useful, because it’s so tightly regulated. When we look at 25(OH)D, well, that’s pretty useful, and we, routinely now, we screen 25(OH)D as a marker of vitamin D status. But it’s not so useful as we might think it is, because, well, is your 25(OH)D low because you’re not getting enough vitamin D, or is it because you’re not getting enough calcium, and you’re not sparing that vitamin D, you’re exhausting the supply of vitamin D. There are lots of other things that affect it – genetics play a role, inflammation plays a role, cancer plays a role, other nutrients like vitamin A play a role. So 25(OH)D is useful, but you don’t know whether it’s high or low because the input is high or low, or because you’re using it at a higher rate, and you don’t necessarily know whether you’re using it at a higher rate because your body is just really good at activating it, or if it’s because your parathyroid glands are saying, hey, there’s a deficiency in this system, we need to ramp up the production of parathyroid hormone, and ramp up the production of calcitriol and deplete the vitamin D supply in order to engage in that process.

So I’m a huge advocate of measuring PTH levels, because if the reference range of 25(OH)D is set at the level that we expect across the population to result in maximally suppressed PTH, why don’t we look at the individual, to see if that individual’s PTH is maximally suppressed. Why, why do we – if we can take that individual’s blood anyway, if we’re already doing that and measuring stuff in it, why wouldn’t we see whether that individual’s PTH is actually maximally suppressed? Because, you know, the more and more we understand about the complexities in this pathway, the more and more we understand that many things affect 25(OH)D. And if we’re measuring 25(OH)D once a year, why don’t we consult the parathyroid gland’s expertise, if it’s monitoring the vitamin D-calcium economy millions of times a day. So, in my opinion, we’re sort of over-using and over-interpreting 25(OH)D as a marker of vitamin D status; what we should be doing is looking at parathyroid hormone and seeing, from what I’ve seen in my working paradigm right now, is that in general if you’re in the lower half of the reference range – so I’m not talking about outside of it, outside of the upper end or the lower limit, I’m talking about within the reference range. If you’re in the reference range you don’t have a parathyroid disorder, great. But within the reference range, if you’re in the lower half, it’s my current thought based on the literature that I’ve seen, that probably that lower half is the sweet spot for being pretty confident that your vitamin D-calcium economy is adequate, as determined by the resident expert, your parathyroid gland.”

 

[Braveheart]

They have an app for every thing.

https://play.google.com/store/apps/details?id=com.ontometrics.dminder

Yes, am aware of this...thanks Charlie...I know pretty much what I am getting at high noon at this latitude...it's a lot...have to find my notes...my age and tan confounds the standard formulas though and sometimes wonder if I shouldn't back down on the supp a bit...spent much time over this in the past and looks like time to revisit what I am doing. Thanks again!

 

[Braveheart]

https://chrismasterjohnphd.com/2016/05/11/the-daily-lipid-podcast-9-balancing/

“So if we are to ignore the layer of complexity that phosphorus adds, we would say that parathyroid hormone levels are our body’s natural judgement about whether the vitamin D-calcium economy is adequate. I said that vitamin D would spare the need for parathyroid hormone, calcium would do the same thing – if more calcium’s coming in in the diet, you have more in the serum without the need for calcitriol stimulating it. Maintaining the serum calcium at a healthy level without the need for parathyroid hormone to get activated, that’s going to reduce the need for PTH, and in fact it’s even going to spare 25(OH)D from being converted into calcitriol, so if you make someone calcium-deficient, regardless of their vitamin D exposure from the sun, or their intake of vitamin D from foods, their 25(OH)D as a marker – a supposed marker – of vitamin D status, that will drop, because it’s being driven into making calcitriol.

And so when we look at serum calcium, we don’t really get anything useful in most circumstances, because it’s so tightly regulated. When we look at calcitriol, we don’t really see anything useful, because it’s so tightly regulated. When we look at 25(OH)D, well, that’s pretty useful, and we, routinely now, we screen 25(OH)D as a marker of vitamin D status. But it’s not so useful as we might think it is, because, well, is your 25(OH)D low because you’re not getting enough vitamin D, or is it because you’re not getting enough calcium, and you’re not sparing that vitamin D, you’re exhausting the supply of vitamin D. There are lots of other things that affect it – genetics play a role, inflammation plays a role, cancer plays a role, other nutrients like vitamin A play a role. So 25(OH)D is useful, but you don’t know whether it’s high or low because the input is high or low, or because you’re using it at a higher rate, and you don’t necessarily know whether you’re using it at a higher rate because your body is just really good at activating it, or if it’s because your parathyroid glands are saying, hey, there’s a deficiency in this system, we need to ramp up the production of parathyroid hormone, and ramp up the production of calcitriol and deplete the vitamin D supply in order to engage in that process.

So I’m a huge advocate of measuring PTH levels, because if the reference range of 25(OH)D is set at the level that we expect across the population to result in maximally suppressed PTH, why don’t we look at the individual, to see if that individual’s PTH is maximally suppressed. Why, why do we – if we can take that individual’s blood anyway, if we’re already doing that and measuring stuff in it, why wouldn’t we see whether that individual’s PTH is actually maximally suppressed? Because, you know, the more and more we understand about the complexities in this pathway, the more and more we understand that many things affect 25(OH)D. And if we’re measuring 25(OH)D once a year, why don’t we consult the parathyroid gland’s expertise, if it’s monitoring the vitamin D-calcium economy millions of times a day. So, in my opinion, we’re sort of over-using and over-interpreting 25(OH)D as a marker of vitamin D status; what we should be doing is looking at parathyroid hormone and seeing, from what I’ve seen in my working paradigm right now, is that in general if you’re in the lower half of the reference range – so I’m not talking about outside of it, outside of the upper end or the lower limit, I’m talking about within the reference range. If you’re in the reference range you don’t have a parathyroid disorder, great. But within the reference range, if you’re in the lower half, it’s my current thought based on the literature that I’ve seen, that probably that lower half is the sweet spot for being pretty confident that your vitamin D-calcium economy is adequate, as determined by the resident expert, your parathyroid gland.”

Great..I understand, makes sense...but this requires lab true? What about the majority of this world, including mine, without access to testing? ...and the billions before us who survived without...there must be a simpler way.

 

[Arrade]

Which is why I think tanning once a week should be sufficient. 6-9 minutes doubles vitamin D levels in Canadians who don’t take oral D.

Canadian Study Finds Tanning Salon Sunbeds Effective for Raising Vitamin D Levels - GrassrootsHealth

Looks like blood levels of 40-60 ng/ml is somewhat of a consensus. Whatever the Canadian government says about sun being the worst enemy.

Needed an excuse to use the beds

 

[Mito]

Great..I understand, makes sense...but this requires lab true? What about the majority of this world, including mine, without access to testing? ...and the billions before us who survived without...there must be a simpler way.

I wonder if Peat ever does lab testing (I would assume not)? Peat seems to have learned to guide his health very well without labs.

 

[Braveheart]

I wonder if Peat ever does lab testing (I would assume not)? Peat seems to have learned to guide his health very well without labs.

I think he keeps it pretty simple...doesn't take a lot or overdo anything and is in tune w his bod.