Is Vitamin D Supplementation Even Neccessary

[Obi-wan]

Anyone get low blood pressure from magnesium ?

Vit D is supposed to lower blood pressure. I have been laying out in the sun lately and noticed I get very tired and lazy and like to have a cup of coffee afterwards...

 

[Amazoniac]

The vitamin D hype is nothing but marketing to sell vitamin d supplements.

West, I just read your post on the other thread. Can you explain what you find wrong with supplementation?

 

[dreamcatcher]

"Since all-disease (autoimmune diseases, metabolic syndrome, type 2 diabetes, cancer) mortality risk is reduced to 1.0 with serum vitamin D levels ≥100 nmol/L [10], we call all responsible public health authorities to consider designating as the recommended dietary allowance (i.e., the average daily level of intake sufficient to meet the nutrient requirements of nearly all healthy people, presuming minimal sun exposure) intake levels corresponding to those proposed by the Endocrine Society Expert Committee (2011) as safe upper tolerable daily intake doses for patients at risk for vitamin D deficiency (<50 nmol/L): 2000 IU for those <1 year of age, 4000 IU for those aged 1-18 years, and 10 000 IU for those aged >18 years."

That's because nothing can afflict marble statues with the exception of lichen, but they can be washed off from the surfaces. Zeus has many of them around the world and he's always annoyed when they're not polished and shining. He claims it's the porous surfaces that allow colonization, just like our teeth. He sends a storm to careless cities as punishment.

The one above leads us to these two:

1. Letter to Veugelers, P.J. and Ekwaru, J.P., A Statistical Error in the Estimation of the Recommended Dietary Allowance for Vitamin D. Nutrients 2014, 6, 4472–4475; doi:10.3390/nu6104472
2. Quantifying the vitamin D economy | Nutrition Reviews | Oxford Academic

They discuss how without supplementation people already obtain from sun and diet more than usually estimated. And this is relevant because the amount of supplementation required to normalize 25(OH)D will depend on those. If the person avoids the sun and doesn't eat foods that can provide some vit D, then more supplement is needed. In foods, the forms are varied, and some animal products contain 25(OH)D that is being considered here more potent than others, leading to the under of the estimations of dietary supply.

Just the assumption that gurus who have marked seasonal variations in terms of sun of the intensities need a fixed amount of supplement throughout the year is suspicious. But to provide a generalized recommendation, they use supplemental amounts that can normalize the level for almost everyone, however this also means that others will be getting the too muchies. Toxicity is not in the questions. The problem is that it's all over the place: some have normal levels without any supplementation, others need insane amounts (normalizing at what cost?).

1.

"The best-fit regression line through the data, as can be seen in the figure, intersects the Y-axis at a value of 34 ng/mL (85 nmol/L), reflecting an intake from food and sun amounting to somewhat more than 3000 IU per day (5)."​

These 3000 IU sun/diet + their 3875 IU supplements = 7000 IU total. This is their proposed RDA, which serves to prevent a deficiency and guarantees that nearly everyone has their blood 25(O and H)D of at least 20 ng/mL. But for normalizing to 35 ng/mL they're proposing 9200 IU total (3000 IU sun/diet + 6200 IU supplements). This is concerning because at the same time that it guarantees that almost everyone reaches those 35 ng/mL there will be people with their levels above 80 ng/mL. This is why it's best to the err on the cautions of the sides and supplement 2000 IU (or more depending on how much of those 3000 IU you're getting) if you're not going to be monitoring through the bloodies of the tests.

Zeus has suggested to spread the supplementation throughout the day to avoid the peaks mentioned below:

2.

"It has been well established for roughly 30 years that in fair-skinned individuals, a single exposure to UV-B at one whole-body minimum erythema dose can produce a rise in serum 25D that is equivalent to an oral dose of D3 in the range of 10,000 to 25,000 IU.7 One minimum erythema dose can be produced by as little as 10–15min of whole-body exposure at mid-day in mid-summer in a pale-skinned individual."

"Studies by Armas et al.,8 using controlled doses of UV-B and careful measurement of skin pigmentation, have begun to quantify the relationship between UV-B irradiance and 25D response. Figure 3 depicts the rise in serum 25D after 4 weeks of three UV-B sessions per week, each delivering 30 mJ UV-B. As Figure 3 shows, and as has long been known in a general way, increase in serum 25D is an inverse function of skin pigmentation. In this instance, pale-skinned individuals of northern European ancestry exhibited a rise in serum 25D of 9 ng/mL (23 nmol/L) at the end of 4 weeks of exposure. By contrast, in extremely dark-skinned individuals, the rise was 4.5 ng/mL (11.2 nmol/L), or just slightly less than half as great as in pale-skinned individuals."

"However[,] serum D3 levels are not the most appropriate measure of an individual’s ability to respond to UV-B radiation."

"[..]solar synthesis does not account for very much of the total daily input in contemporary urban populations."

"[..]the simple D3 content of an animal food product would not be representative of the total vitamin D activity contained therein, as it would fail to capture the portion of the activity due to 25D present in the various tissues concerned. Recent publications have shown that meat can contain substantial quantities of 25D[20–25] and that consumers of meat exhibit higher human 25D status than nonconsumers.[26,27]"

"Despite the still fragmentary character of the data, the analyses published to date indicate that input gaps left after estimating solar inputs (on the order of 1,300–1,600 IU/day, as noted above) could well be filled by hitherto unrecognized food sources. For example, Taylor et al.21 report a combined (D3 plus 25D) content of 112 IU vitamin D equivalents for 200 g of beef tenderloin and 230 IU equivalents for one large egg. The latter figure is confirmed in data developed by McDonnell et al.26 from the Grassroots Health database. In their cross-sectional analysis, one egg consumed daily was associated with 2 ng/mL greater level of serum 25D (implying an egg-related intake of ~200 IU/egg).
In their estimates, Taylor et al.21 used a potency factor of 5x for 25D, based on the observation28–30 that oral 25D elevates serum 25D concentration to a substantially greater extent than does an equimolar oral dose of D3. This potency factor has implications that go well beyond food content and is discussed further below (see especially, Partitions and Masses)."

"Intestinal absorption of D3 is mainly from the jejunum and ileum. Absorbed vitamin D can be found in both the portal venous blood and the lymph that drains the small intestine. The lymphatic ducts are the typical route for fats, and in the presence of fat in the intestinal lumen, probably much of the absorbed vitamin D is transported that way, along with cholesterol and other lipids. The lymph drains into the systemic venous circulation, as does vitamin D absorbed from the epidermis. The lymphatic pathway may have particular physiological significance for orally acquired vitamin D, since it avoids a first pass of the absorbed vitamin D through the liver. This suggests that the quantitative relationship between vitamin D and 25D will be the same regardless of whether vitamin D enters from the skin or the gut."

"Skin input occurs via passive diffusion of vitamin D into the blood from the plasma membrane of epidermal skin cells (where the photoconversion of 7- dehydrocholesterol occurs). This diffusion from the skin into the blood is slow, with a half-time of about 3 days.7 This half-time means that when regular sun exposure is the principal source of D3, serum D3 concentration will be essentially constant."

"Dosing frequency for oral vitamin D supplementation regimens will affect serum concentration of D3 in predictable and often very striking ways. This fact has been largely overlooked to date, as the serum concentration of D3 has been generally considered to be of no particular interest in its own right. The rationale for infrequent (or bolus) dosing is that it leads to better adherence and that an excess amount ingested today will be stored in fat for use tomorrow. However, this assumption overlooks the effect of infrequent dosing regimens on D3 blood concentrations."

"Serum D3 has a half-time variously estimated to be in the range of 0.5–3.5 days, with most investigators favoring a value of about 1.0 days. In contrast, D3 produced in skin moves into the blood with a half-time of about 3 days. This means that when skin synthesis is the principal source of D3, serum D3 concentration will be essentially constant around the clock, as D3 input to the blood from the skin (though produced mainly at mid-day) is effectively constant. With oral ingestion, intestinal absorptive input of D3 occurs mainly during a 4-h period following ingestion. (In one study, a TMAX of as much as 12 h was reported.65 As this is well beyond the usual mouth-to-cecum transit time, the 12-h figure, if confirmed, would suggest appreciable colonic absorption, or small bowel mucosal retention, or a delay pool in the intestinal lymphatics.) In any case, assuming a 1.0-day half-time, serum D3 concentration will inevitably follow a sawtooth pattern, particularly if oral ingestion is the principal input." "Under input conditions in excess of daily use, unused D3 will accumulate in fat, and its concentration there would be predicted to damp the oscillations of D3 concentration in serum to some extent."

"Aside from the possible importance of D3 concentration as the substrate for autocrine activity of vitamin D, there is general agreement that serum 25D concentration is currently the principal indicator of vitamin D status.70 This is because extrarenal conversion of 25D to 1,25D operates at concentrations below the kM for the tissue 1 -a-hydroxylases; hence, serum 25D concentration limits the amount of 1,25D a tissue can synthesize when its cells are stimulated to produce a vitamin D-dependent response. While there is no consensus as to the optimal serum 25D concentration, there is also no disagreement about the importance of the substrate, regardless of which concentration may be deemed optimal."​

Of course I found this on my newsfeed today:

Vitamin D supplements don't help bone health, major study concludes

 

[Arrade]

Of course I found this on my newsfeed today:

Vitamin D supplements don't help bone health, major study concludes

That’s probably because dumb shits don’t use Vit K at the same time

 

[Collden]

Never realized how much vit D is in fatty fish, wild salmon has almost 1000IU per 3oz serving, trout is 700IU/100g. Used to think that people living in the north just evolved a need for less Vit D since its almost impossible to get much from the sun above lat 55-60, but now I'm thinking they just got it all from fatty fish. It doesnt seem unreasonable that a traditional northern diet could've provided several thousand IUs per day considering how much fish they ate.

 

[dreamcatcher]

That’s probably because dumb shits don’t use Vit K at the same time

Haha lol..goes to the kitchen and swallows a bottle of K2

 

[Arrade]

Haha lol..goes to the kitchen and swallows a bottle of K2

HAHA

 

[Amazoniac]

Oral calcidiol is a good form of vitamin D supplementation

"Among other precursors of vitamin D employed in clinical practice, calcidiol is the most recently introduced for treatment of hypovitaminosis D (8). Pharmacokinetic studies demonstrated the hydrophilic properties of calcidiol, as well as a shorter half-life (10–13 days) in comparison with cholecalciferol (9). These data suggest the possible advantage of calcidiol, compared to cholecalciferol, in the management of deficient states in patients with liver disease, obese patients (where there is a lower trapping of calcidiol vs cholecalciferol in the adipose tissue), as well as to avoid any possible toxic effect when high doses are used (10). Also, conditions associated with intestinal malabsorption can represent an indication for calcidiol use, as it is better absorbed than cholecalciferol. The use of calcidiol in the setting of secondary hyperparathyroidism associated with chronic kidney disease has also been advocated, as high PTH levels can inhibit the liver cytochrome and eventually reduce the synthesis of calcidiol (11). Finally, data on the immunological effect of calcidiol vs cholecalciferol suggest a possible use in patients at high risk of infections (12)."​

@haidut

 

[haidut]

Oral calcidiol is a good form of vitamin D supplementation

"Among other precursors of vitamin D employed in clinical practice, calcidiol is the most recently introduced for treatment of hypovitaminosis D (8). Pharmacokinetic studies demonstrated the hydrophilic properties of calcidiol, as well as a shorter half-life (10–13 days) in comparison with cholecalciferol (9). These data suggest the possible advantage of calcidiol, compared to cholecalciferol, in the management of deficient states in patients with liver disease, obese patients (where there is a lower trapping of calcidiol vs cholecalciferol in the adipose tissue), as well as to avoid any possible toxic effect when high doses are used (10). Also, conditions associated with intestinal malabsorption can represent an indication for calcidiol use, as it is better absorbed than cholecalciferol. The use of calcidiol in the setting of secondary hyperparathyroidism associated with chronic kidney disease has also been advocated, as high PTH levels can inhibit the liver cytochrome and eventually reduce the synthesis of calcidiol (11). Finally, data on the immunological effect of calcidiol vs cholecalciferol suggest a possible use in patients at high risk of infections (12)."​

@haidut

Thanks.
If anybody has issues with oral cholecalciferol those can usually be resolved with topical application. Also, I think calcidiol is a prescription drug in USA so can't release it for human use.

 

[Amazoniac]

This article was posted on Zeus' Calcirol thread. It's worth reading everything.

Inflammation and vitamin D: the infection connection

"In a healthy individual, the complex interplay between innate and adaptive immunity cooperates to mount an appropriate response to infection through regulation of the vitamin D endocrine system [140]. The immune system detects and responds to the presence of intracellular bacteria by producing more 1,25(OH)2D to activate the VDR and express the crucial endogenous AMPs which enable the innate immune system to target intracellular pathogens [141]. Renal production of 1,25(OH)2D is tightly self-regulated, with the end product down-regulating its own further production. In contrast, extra-renal tissues (e.g., uterine decidua and placenta, colon, breast, prostate, spleen, bone, keratinocytes, melanoma and synovial cells, pulmonary monocytes and macrophages, etc.) which produce 1,25(OH)2D are regulated by cytokines (e.g., interferon-gamma), lipopolysaccharide, nitric oxide and intracellular VDBP, which activate the enzyme CYP27B1 to stimulate conversion of 25(OH)D to 1,25(OH)2D [142]. This extra-renal production of 1,25(OH)2D in tissues infected with intracellular bacteria can result in an excess in production of 1,25(OH)2D which may contribute to depletion and low levels of 25(OH)D [143] (Fig. 4)."

"Because extra-renal production of 1,25(OH)2D is primarily dependent on the availability of 25(OH)D [144], supplementation with vitamin D to increase 25(OH)D may promote the production of 1,25(OH)2D in non-renal tissues that are sites of intracellular infection and result in hypervitaminosis-D. Sunlight appears to play a part in this process and many patients with autoimmune disease report sun sensitivity."

"We hypothesize that when nucleated cells are parasitized by intracellular bacteria, extra-renal production of 1,25(OH)2D increases, the kidneys lose control of 1,25(OH)2D production, and pro-hormone 25(OH)D decreases due to rapid conversion to 1,25(OH)2D. The following mechanisms are thought to be responsible (Fig. 5):

- Inflammatory cytokines [but not Diokines] activate CYP27B1, an enzyme that causes more 25(OH)D to be converted to 1,25(OH)2D [146].
- The microbial-repressed VDR cannot transcribe CYP24A1 (formerly 24-hydroxylase), an enzyme that breaks down excess 1,25(OH)2D [147].
- Excess 1,25(OH)2D binds the PXR (pregnane X receptor), to inhibit conversion of vitamin D3 to 25(OH)D so 25(OH)D is down-regulated [148].
- 1,25(OH)2D inhibits the hepatic synthesis of 25(OH)D [149]."​

"Thus, low 25(OH)D may be a consequence of the inflammatory process. More studies are concluding that suboptimal circulating levels of vitamin D appear to be caused by the disease process. Waldronn et al. [150] found serum 25(OH)D was decreased following an acute inflammatory insult (i.e., orthopedic surgery) and concluded that hypovitaminosis-D may be the consequence rather than cause of chronic inflammatory diseases. Ferder et al. [151] state, “…there may be a relationship between inflammatory processes induced by chronic overstimulation of the renin angiotensin system (RAS) and the worldwide vitamin D deficiency. In fact, the pandemic of vitamin D deficiency could be the other face of increased RAS activity, which could potentially cause a lower activity or lower levels of Vitamin D.”"

"Measuring both 25(OH)D and 1,25(OH)2D (and PTH, calcium, phosphate when indicated) as clinical markers in chronic disease is more likely to provide a true picture of vitamin D status, than measuring 25(OH)D alone [155, 156] (Table 1). Measuring 1,25(OH)2D should be considered in patients with low 25(OH)D, abnormal laboratory results (especially inflammatory markers), a diagnosis of autoimmune disease or other chronic inflammatory illness, or signs of chronic systemic inflammation. For example, elevated 1,25(OH)2D may serve as a marker of Crohn’s disease [52]. The 1,25(OH)2D test is a delicate assay which is only done in specialized laboratories. False low results have been observed due to apparent sample mishandling; freezing for transport is advised to prevent sample degradation due to agitation. A high result is always accurate."

 

[rei]

It is criminal to continue to call this a vitamin, when the actual, factual, description of what we are talking about is a HORMONE that is manufactured in the skin in response to sunlight.

What is needed is some actual research into the different compounds of the vit D family and how they actually interact. D3 has been proven effective, but what is it's role in comparison to the other compounds, especially around sunlight on skin? D3 is not the ultimate cause of effect.

 

[Sourdoughbanana]

"Thus, low 25(OH)D may be a consequence of the inflammatory process. More studies are concluding that suboptimal circulating levels of vitamin D appear to be caused by the disease process. Waldronn et al. [150] found serum 25(OH)D was decreased following an acute inflammatory insult (i.e., orthopedic surgery) and concluded that hypovitaminosis-D may be the consequence rather than cause of chronic inflammatory diseases. Ferder et al. [151] state, “…there may be a relationship between inflammatory processes induced by chronic overstimulation of the renin angiotensin system (RAS) and the worldwide vitamin D deficiency. In fact, the pandemic of vitamin D deficiency could be the other face of increased RAS activity, which could potentially cause a lower activity or lower levels of Vitamin D.”"

is the opposite true re: 25OHD status and inflammation? I just got pre-winter bloods back: 93 ng/mL. Needless to say I'm very happy about them. They were at 59 ng/mL in March (In Canada - I didn't supplement much at the time, but was tanning bi monthly ish). Low inflammation?

 

[dreamcatcher]

This article was posted on Zeus' Calcirol thread. It's worth reading everything.

Inflammation and vitamin D: the infection connection

"In a healthy individual, the complex interplay between innate and adaptive immunity cooperates to mount an appropriate response to infection through regulation of the vitamin D endocrine system [140]. The immune system detects and responds to the presence of intracellular bacteria by producing more 1,25(OH)2D to activate the VDR and express the crucial endogenous AMPs which enable the innate immune system to target intracellular pathogens [141]. Renal production of 1,25(OH)2D is tightly self-regulated, with the end product down-regulating its own further production. In contrast, extra-renal tissues (e.g., uterine decidua and placenta, colon, breast, prostate, spleen, bone, keratinocytes, melanoma and synovial cells, pulmonary monocytes and macrophages, etc.) which produce 1,25(OH)2D are regulated by cytokines (e.g., interferon-gamma), lipopolysaccharide, nitric oxide and intracellular VDBP, which activate the enzyme CYP27B1 to stimulate conversion of 25(OH)D to 1,25(OH)2D [142]. This extra-renal production of 1,25(OH)2D in tissues infected with intracellular bacteria can result in an excess in production of 1,25(OH)2D which may contribute to depletion and low levels of 25(OH)D [143] (Fig. 4)."

"Because extra-renal production of 1,25(OH)2D is primarily dependent on the availability of 25(OH)D [144], supplementation with vitamin D to increase 25(OH)D may promote the production of 1,25(OH)2D in non-renal tissues that are sites of intracellular infection and result in hypervitaminosis-D. Sunlight appears to play a part in this process and many patients with autoimmune disease report sun sensitivity."

"We hypothesize that when nucleated cells are parasitized by intracellular bacteria, extra-renal production of 1,25(OH)2D increases, the kidneys lose control of 1,25(OH)2D production, and pro-hormone 25(OH)D decreases due to rapid conversion to 1,25(OH)2D. The following mechanisms are thought to be responsible (Fig. 5):

- Inflammatory cytokines [but not Diokines] activate CYP27B1, an enzyme that causes more 25(OH)D to be converted to 1,25(OH)2D [146].
- The microbial-repressed VDR cannot transcribe CYP24A1 (formerly 24-hydroxylase), an enzyme that breaks down excess 1,25(OH)2D [147].
- Excess 1,25(OH)2D binds the PXR (pregnane X receptor), to inhibit conversion of vitamin D3 to 25(OH)D so 25(OH)D is down-regulated [148].
- 1,25(OH)2D inhibits the hepatic synthesis of 25(OH)D [149]."​

"Thus, low 25(OH)D may be a consequence of the inflammatory process. More studies are concluding that suboptimal circulating levels of vitamin D appear to be caused by the disease process. Waldronn et al. [150] found serum 25(OH)D was decreased following an acute inflammatory insult (i.e., orthopedic surgery) and concluded that hypovitaminosis-D may be the consequence rather than cause of chronic inflammatory diseases. Ferder et al. [151] state, “…there may be a relationship between inflammatory processes induced by chronic overstimulation of the renin angiotensin system (RAS) and the worldwide vitamin D deficiency. In fact, the pandemic of vitamin D deficiency could be the other face of increased RAS activity, which could potentially cause a lower activity or lower levels of Vitamin D.”"

"Measuring both 25(OH)D and 1,25(OH)2D (and PTH, calcium, phosphate when indicated) as clinical markers in chronic disease is more likely to provide a true picture of vitamin D status, than measuring 25(OH)D alone [155, 156] (Table 1). Measuring 1,25(OH)2D should be considered in patients with low 25(OH)D, abnormal laboratory results (especially inflammatory markers), a diagnosis of autoimmune disease or other chronic inflammatory illness, or signs of chronic systemic inflammation. For example, elevated 1,25(OH)2D may serve as a marker of Crohn’s disease [52]. The 1,25(OH)2D test is a delicate assay which is only done in specialized laboratories. False low results have been observed due to apparent sample mishandling; freezing for transport is advised to prevent sample degradation due to agitation. A high result is always accurate."

How do you get rid of the bacteria?

 

[Cirion]

It is criminal to continue to call this a vitamin, when the actual, factual, description of what we are talking about is a HORMONE that is manufactured in the skin in response to sunlight.

What is needed is some actual research into the different compounds of the vit D family and how they actually interact. D3 has been proven effective, but what is it's role in comparison to the other compounds, especially around sunlight on skin? D3 is not the ultimate cause of effect.

This is a good point. Nothing can ever replace real sunlight. Taking a vitamin D supplement, in my opinion, at best can stave off severe deficiency symptoms like low vitamin D induced depression. It can not replace sunlight for optimal health. In my experience at least.

I'd love to learn more about what actually happens in the body when you get sunlight VS. when you take a supplement.

 

[somuch4food]

It is criminal to continue to call this a vitamin, when the actual, factual, description of what we are talking about is a HORMONE that is manufactured in the skin in response to sunlight.

I agree. Vitamin D is often touted as a magic pill with high dosage therapies. Just the fact that it gets so much publicity in mainstream media makes me wary of it.

 

[Amazoniac]

is the opposite true re: 25OHD status and inflammation? I just got pre-winter bloods back: 93 ng/mL. Needless to say I'm very happy about them. They were at 59 ng/mL in March (In Canada).

If you need to bring the levels this high to feel better, you might not be addressing the cause of the issue. It can be a Netherlands deficiency. What about the other tests related to vitamin D?

How do you get rid of the bacteria?

Inflammation and vitamin D: the infection connection

It is criminal to continue to call this a vitamin, when the actual, factual, description of what we are talking about is a HORMONE that is manufactured in the skin in response to sunlight.

Guru, search for images on '7-dehydrocholesterol and cholecalciferol' (D3), you'll notice the resemblance. Example.

 

[somuch4food]

Never realized how much vit D is in fatty fish, wild salmon has almost 1000IU per 3oz serving, trout is 700IU/100g. Used to think that people living in the north just evolved a need for less Vit D since its almost impossible to get much from the sun above lat 55-60, but now I'm thinking they just got it all from fatty fish. It doesnt seem unreasonable that a traditional northern diet could've provided several thousand IUs per day considering how much fish they ate.

I am from Canada. I have no recollection whatsoever of my grandma preparing fish. She's still active at 82. I think there is enough vitamin D in fattier meat cuts and dairy to sustain us.

 

[Amazoniac]

I am from Canada. I have no recollection whatsoever of my grandma preparing fish. She's still active at 82. I think there is enough vitamin D in fattier meat cuts and dairy to sustain us.

Have you readed this section?
Inflammation and vitamin D: the infection connection

 

[somuch4food]

Have you readed this section?
Inflammation and vitamin D: the infection connection

I did not click the link because from your quotes because I thought it was well over my head, but after opening it, I see that I can understand some points.

Thanks @Amazoniac. I was still on the fence about vitamin D. That study reinforces my position that vitamin D is not a vitamin at all.

What I keep seeing is that it plays a significant role in calcium metabolism and that it can be a marker for chronic inflammation. I see also that cholesterol is mentioned as a precursor to skin production of 25(OH)D:

"Bogh et al. [22] measured the baseline serum 25(OH)D and total cholesterol levels of 182 fair-skinned and dark-skinned subjects; and studied the effect of UV radiation on their serum 25(OH)D levels. They found the amount of serum 25(OH)D produced was determined by the amount of cholesterol in the skin, not on skin pigmentation."

Since cholesterol has had such a bad rap, it's not surprising that people would now be deficient in 25(OH)D.

 

[dreamcatcher]

This is a good point. Nothing can ever replace real sunlight. Taking a vitamin D supplement, in my opinion, at best can stave off severe deficiency symptoms like low vitamin D induced depression. It can not replace sunlight for optimal health. In my experience at least.

I'd love to learn more about what actually happens in the body when you get sunlight VS. when you take a supplement.

It's not what Ray Peat thinks though. His email to me:
"A deficiency of vitamin D can greatly increase the susceptibility to colds and other infections; have you been using a supplement of it? Because of the lack of sunshine in Oregon from fall to spring, I’m using about 20,000 IU of vitamin D per day on my skin."