Is Vitamin D Supplementation Even Neccessary

Amazoniac

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Thanks, Amazoniac.

In the two papers you've linked, positive correlation with the exercise intensity is found in serum and muscle, respectively. The "Mobilizing vitamin D..." paper suggests that the vitamin D is released due to lipolysis: "Exercise in the fasted or the fed state leads to an approximate twofold to threefold increase in adipose tissue lipolysis (Wolfe et al. 1990; Klein et al. 1994; Enevoldsen et al. 2004) and, when stored triacylglycerol is hydrolysed, vitamin D metabolites may also be released from the lipid droplet (Fig. 3)."



Given that lipolysis is baaa-d, I'll venture to say that the enhanced vit. D amounts in blood are to mitigate the harmful effects of lipolysis. What do you think?

To add to my point, the paper mentions that "..in vivo, as individuals with obesity display lower rates of lipolysis during exercise than lean controls (Stich et al. 2000; Mittendorfer et al. 2004). Whilst this may protect individuals with obesity from elevated circulating fatty acids (McQuaid et al. 2011), it may also contribute to sequestration of vitamin D. In support of this contention, adipose explants taken from individuals with obesity release less vitamin D when stimulated with lipolytic hormones than explants from lean controls (Di Nisio et al. 2017)." "there is a weak negative relationship between fat mass and circulating 1,25(OH)_2 D.", which is pro-inflammatory.

To sum up, keep your adipose-tissue vitamin D stores for a rainy day, do not exercise hard . :cool:
It's possible, to aid in repair:
- A single bout of high‐intensity exercise modulates the expression of vitamin D receptor and vitamin D‐metabolising enzymes in horse skeletal muscle
(@tankasnowgod)

- Fasting and Exercise Induce Changes in Serum Vitamin D Metabolites in Healthy Men
 

Amazoniac

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"Published values for the amount of vitamin D3 present in subcutaneous adipose tissue vary substantially, ranging from ~4 to ~500 ng/g, suggesting large individual variability and dependency on supplementation status (Didriksen et al. 2015)."​

Vitamin D3 increases in abdominal subcutaneous fat tissue after supplementation with vitamin D3

"The subjects included in this study were participants in an ongoing 5-year study administrated with vitamin D3 (20 000 IU/week, Dekristol Mibe, Jena, Germany) vs identical-looking placebo capsules containing arachis oil (Hasco-lek, Wroclaw, Poland) for the prevention of type 2 diabetes (T2DM), and the trial was carried out at the Clinical Research Unit, University Hospital of North Norway (8)."

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- Human body weight - Wikipedia
- Average human height by country - Wikipedia
- List of countries by body mass index - Wikipedia
- Body mass index - Wikipedia


70 kg body weight, 25% fat, and venom D at 0.2 ug/g fat tissue: 3500 ug.
3500 ug ÷ 50 ug/day = 70 days
 

Amazoniac

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- The retinoid X receptor ligand restores defective signalling by the vitamin D receptor

1638057707470.png


[The "vitamin D analogue ZK159222"] "binds to VDR with high affinity but has very low agonistic activity, antagonizing transactivation by vitamin D (Herdick et al, 2000; Ochiai et al, 2005)."

"[..]the E420 mutation has been detected in families with hereditary vitamin D-resistant rickets without alopecia (Malloy et al, 2002)."

- HEK 293 cells - Wikipedia
- Gene nomenclature - Wikipedia
- Nuclear receptor coactivator 2 - Wikipedia

- Anti-Peat - Grant Genereux's Theory Of Vitamin A Toxicity [I know (Terma, 2020)]

 

Amazoniac

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A different pattern in the children of the 1% (Waters, 1977) taking about 50 mcg/d:


1638623622568.png


Kids' values were detailed and the above is an extrapolation to "a 70 kg woman with a 24.5 kg fat mass (35%), a 30.8 kg muscle mass (44%), a 4.0 kg bone mass, a serum volume of 2.3 liters, a liver mass of 1.4 kg, with all other tissues combined accounting for 7.0 kg. While these values are arbitrary, as is readily apparent, they are both plausible and typical."
 

Amazoniac

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- 100 Years of Vitamin D: Dose–response for change in 25-hydroxyvitamin D after UV exposure: outcome of a systematic review

"Low dose, sub-erythemal doses are more effective for vitamin D synthesis than doses close to a personal minimum erythema dose. Short, frequent (e.g. daily or several times per week) exposures maximise vitamin D while minimising the risk of skin damage (54, 62)."​

⬑ [62] Fractional Sunburn Threshold UVR Doses Generate Equivalent Vitamin D and DNA Damage in Skin Types I–VI but with Epidermal DNA Damage Gradient Correlated to Skin Darkness

"[..]for vitamin D synthesis, UVB photons must be absorbed by 7-dehydrocholesterol for its photochemical conversion. Although 7-dehydrocholesterol is reportedly situated principally within basal and adjacent layers, a smaller amount is in higher epidermis (Holick et al., 1980). Similar amounts of 25(OH)D were produced in people through the skin type range, despite no substantive UVB reaching the basal layer in darker skin, as shown by lack of basal cell CPD [Cost per Dollar]. Thus, greater 7-dehydrocholesterol photoconversion appears to have occurred in the upper epidermis, in tandem with evidence of greater UVR effect, as shown by higher CPD levels in upper epidermis of darker skin."​



- The Pathophysiological Role of CoA
- Effects of pravastatin, a new HMG-CoA reductase inhibitor, on vitamin D synthesis in man
 

Amazoniac

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- Vitamin D Resistance as a Possible Cause of Autoimmune Diseases: A Hypothesis Confirmed by a Therapeutic High-Dose Vitamin D Protocol

"In two intervention studies, Carlberg and colleagues found evidence that different individuals display a different molecular and biochemical response to the same dose of either long-term or single-bolus vitamin D3 supplementation (21). Initially, in the VitDmet study, 71 elderly prediabetic individuals were supplemented with either 0, 1600 or 3200 I.U. vitamin D3 daily over 5 months of Finnish winter (22). The focus of this work was on the effects of vitamin D3 supplementation on mRNA expression of twelve of the vitamin D-regulated genes and several vitamin D-affected laboratory parameters. With the help of these biomarkers, the group was able to show in 2015 that even supposedly adequate high vitamin D3 doses (3200 I.U.) were not able to exert the expected vitamin D-regulatory effects in all subjects. Focusing on the PTH feedback system alone, a total of 25% of the patients showed no adequate response of this laboratory parameter. Regarding all 36 tested parameters, Carlberg et al. could cluster their patients in 24% low responders, 51% mid responders and 25% high responders. In 2017, the group was able to reproduce these findings in the VitDbol study, in which a cohort of healthy Finnish students received a 80,000 I.U. bolus dose of vitamin D3 with similar low responder rates (23).

These data provided an in vivo confirmation that there exists a spectrum of different vitamin D responsiveness, with approximately 25% of a population not responding adequately to conventional vitamin D3 doses. They may require individually varying, but larger doses."​

↳ [22] Dissecting high from low responders in a vitamin D3 intervention study



- Exposure of vitamins to UVB and UVA radiation generates singlet oxygen
 

Vins7

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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
Interesting, how is your D level now that you feel better?
 

Lejeboca

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Here we go on interactions of Vitamin D and minerals (metals) beyond the better known Ca, P, and Mg. Motivated by the Haidut's Mineral Analysis Test Results posted by members in this thread.

The Role of Vitamin D in Toxic Metal Absorption: A Review

Abstract: Vitamin D increases intestinal calcium and phosphate absorption. Not so well known, however, is that
vitamin D stimulates the co-absorption of other essential minerals like magnesium, iron, and zinc; toxic
metals including lead, cadmium, aluminum, and cobalt; and radioactive isotopes such as 89,,0 strontium
and 137 cesium. Vitamin D may contribute to the pathologies induced by toxic metals by increasing their
absorption and retention.
Reciprocally, lead, cadmium, aluminum, and strontium interfere with normal
vitamin D metabolism by blocking renal synthesis of 1,25-dihydroxyvitamin D. This is the first review
of the role of the vitamin D endocrine system in metal toxicology.

From the Intro: no effect was observed from a subcutaneous dose of the minerals, leading to the conclusion that the effect of vitamin D on these elements is due to increased intestinal absorption rather than to a direct effect of vita min D on bone.

On Lead:
"Smith et al [26] and Mahaffey et al [27] demonstrated that in rats (using both in vivo and in vitro systems) vitamin D markedly enhanced Pb 2+ absorption. Mahaffey et al [27] reported that in vivo absorption of Pb 2+ acetate (0.01 mM) was around 16% in rats in the absence of vitamin D. This increased to 31 % with 6.25μg/day vitamin D 3 , and 49% with 25 Mg/day. The greatest enhancement observed was in the distal small intestine, which is a site of minimal vitamin D stimulation of Ca 2+ absorption. Thus, although a high Ca 2+ diet decreases Pb 2+ absorption, the absorption of the two cations may not be controlled by the same absorptive mechanism. Smith et al [26] pointed out that vitamin D also stimulates HP0 4 2_ transport especially in the distal small intestine, suggesting
that Pb 2+ transport may be related in some way to HP0 4 2_ absorption."

On Aluminum:
"Adler and Berlyne [58] studied duo denal Al 3+ absorption in rats using an in vivo isolated gut segment technique, finding that Al 3+ is absorbed by both a nonsaturable mechanism and a vitamin D-dependent saturable mechanism for which it may compete with Ca 2+ . In a review of gastrointestinal absorption of Al 3+. Ihle and Becker [59] include parathyroid hormone (PTH) and vitamin D metabolites as factors that increase Al 3+ absorption. Elevated PTH may explain why some patients reach high serum Al 3+ levels on low doses of Al 3+ ."

========================================
Vitamin D, Essential Minerals, and Toxic Elements: Exploring Interactions between Nutrients and Toxicants in Clinical Medicine

From the paper main text:
"Table 1 provides an overview of the complex interaction between vitamin D and various inorganic elements—both required minerals and toxic metals. The question therefore arises as to whether the alleged rise in morbidity and mortality associated with elevation of 25(OH)D 3 (>150 nmol/L) may be, in part, associated with the increased accumulation of toxic metals—a common concern in contemporary society [48]. To the authors’ knowledge, however, no studies have been done to date which measure accrued levels of toxic metals in population groups in direct relation to 25(OH)D 3 levels. One of the challenges with the assessment of this hypothesis is that much of the reported biomonitoring of toxic elements in population groups has been confined to unprovoked blood or urine levels of toxicants—which often underestimate the body burden. Most toxic elements and compounds tend to sequester in tissues and may not be evident on blood or urine testing [49]."

1653705482979.png
 

Smitty

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vitamin D stimulates the co-absorption of other essential minerals like magnesium, iron, and zinc; toxic
metals including lead, cadmium, aluminum, and cobalt; and radioactive isotopes such as 89,,0 strontium
and 137 cesium. Vitamin D may contribute to the pathologies induced by toxic metals by increasing their
absorption and retention.
Thank you for tagging me here! Very interesting find.
 

Kray

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Here we go on interactions of Vitamin D and minerals (metals) beyond the better known Ca, P, and Mg. Motivated by the Haidut's Mineral Analysis Test Results posted by members in this thread.

The Role of Vitamin D in Toxic Metal Absorption: A Review

Abstract: Vitamin D increases intestinal calcium and phosphate absorption. Not so well known, however, is that
vitamin D stimulates the co-absorption of other essential minerals like magnesium, iron, and zinc; toxic
metals including lead, cadmium, aluminum, and cobalt; and radioactive isotopes such as 89,,0 strontium
and 137 cesium. Vitamin D may contribute to the pathologies induced by toxic metals by increasing their
absorption and retention.
Reciprocally, lead, cadmium, aluminum, and strontium interfere with normal
vitamin D metabolism by blocking renal synthesis of 1,25-dihydroxyvitamin D. This is the first review
of the role of the vitamin D endocrine system in metal toxicology.

From the Intro: no effect was observed from a subcutaneous dose of the minerals, leading to the conclusion that the effect of vitamin D on these elements is due to increased intestinal absorption rather than to a direct effect of vita min D on bone.

On Lead:
"Smith et al [26] and Mahaffey et al [27] demonstrated that in rats (using both in vivo and in vitro systems) vitamin D markedly enhanced Pb 2+ absorption. Mahaffey et al [27] reported that in vivo absorption of Pb 2+ acetate (0.01 mM) was around 16% in rats in the absence of vitamin D. This increased to 31 % with 6.25μg/day vitamin D 3 , and 49% with 25 Mg/day. The greatest enhancement observed was in the distal small intestine, which is a site of minimal vitamin D stimulation of Ca 2+ absorption. Thus, although a high Ca 2+ diet decreases Pb 2+ absorption, the absorption of the two cations may not be controlled by the same absorptive mechanism. Smith et al [26] pointed out that vitamin D also stimulates HP0 4 2_ transport especially in the distal small intestine, suggesting
that Pb 2+ transport may be related in some way to HP0 4 2_ absorption."

On Aluminum:
"Adler and Berlyne [58] studied duo denal Al 3+ absorption in rats using an in vivo isolated gut segment technique, finding that Al 3+ is absorbed by both a nonsaturable mechanism and a vitamin D-dependent saturable mechanism for which it may compete with Ca 2+ . In a review of gastrointestinal absorption of Al 3+. Ihle and Becker [59] include parathyroid hormone (PTH) and vitamin D metabolites as factors that increase Al 3+ absorption. Elevated PTH may explain why some patients reach high serum Al 3+ levels on low doses of Al 3+ ."

========================================
Vitamin D, Essential Minerals, and Toxic Elements: Exploring Interactions between Nutrients and Toxicants in Clinical Medicine

From the paper main text:
"Table 1 provides an overview of the complex interaction between vitamin D and various inorganic elements—both required minerals and toxic metals. The question therefore arises as to whether the alleged rise in morbidity and mortality associated with elevation of 25(OH)D 3 (>150 nmol/L) may be, in part, associated with the increased accumulation of toxic metals—a common concern in contemporary society [48]. To the authors’ knowledge, however, no studies have been done to date which measure accrued levels of toxic metals in population groups in direct relation to 25(OH)D 3 levels. One of the challenges with the assessment of this hypothesis is that much of the reported biomonitoring of toxic elements in population groups has been confined to unprovoked blood or urine levels of toxicants—which often underestimate the body burden. Most toxic elements and compounds tend to sequester in tissues and may not be evident on blood or urine testing [49]."

What's the takeway on this? Would topical application possibly be safer alternative than ingesting vitamin D, if one must supplement? I think more research on topical application would be great, since it is a never-ending question on supplemental vitamin D, and we know its importance to have enough of one way or another. I have never tested my vitamin D blood levels, and moved from a southern to northern climate in the past 6 months. As much as I should be more concerned about supplements of vitamin D, I am now a little more wary of 1) route of supplementation and 2) if supplementation is ideal or not. Having read some of the finds here on raw milk, for example, if one can get their hands on that, maybe that is the missing piece to how our bodies (once) absorbed many essential nutrients, including vitamins A & D (see Obi-Wan's raw milk link).

Thank you for all the posts!
 

Lejeboca

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What's the takeway on this? Would topical application possibly be safer alternative than ingesting vitamin D, if one must supplement?

The authors talk about total 25(OH)D3, if >150 nmol/L, as possibly increasing intestinal absorption of toxic metals. They point out that "levels of 225 nmol/L can be achieved with ordinary sunlight and are thus considered normal." With sunlight, there are physiological (notably photochemical) mechanisms to downgrade absorption. "With sun exposure, for example, enzyme down-regulation appears to occur as higher levels are achieved so that diminished vitamin D skin production, absorption, and assimilation occur [Regulation of cutaneous previtamin D3 photosynthesis in man: skin pigment is not an essential regulator]".

Furthermore, VitD metabolites do not rise much in non-deficient subjects (called "normal" below) and no increase in "1,25" VitD form if minimal erythemal dose (MED) of UVR is received.

From Vitamin-D synthesis and metabolism after ultraviolet irradiation of normal and vitamin-D-deficient subjects - PubMed
In contrast to the markedly increased vitamin-D levels after exposure to UVR, the 25-OH-D concentrations in normal subjects increased only gradually, reaching highest concentrations seven to 14 days after exposure to UVR. Normal subjects exposed to one minimal erythemal dose of UVR had essentially no change in the serum concentration of 1,25-(OH),-D; however, those exposed to three minimal erythemal doses had a transient slight increase in the 1,25-(OH),-D concentration Fig. 1.
In normal subjects there was a dose related, rapid rise in vitamin D, with peak concentrations one to two days after exposure and a return almost to basal concentrations by seven days. For example, in representative normal subjects exposed in other experiments to one, 1.5, three, and four minimal erythemal doses of UVR (Fig. 2), peak vitamin-D levels were 24, 43, 80, and 138 ng per milliliter, respectively, one to two days after exposure. Thereafter vitamin-D levels fell rapidly but were still slightly above the base line at seven days.


fig1.png

The VitD amount absorbed orally depends on the gut and liver health. For example, in Crohn's disease absorption is poor and UVB route is required. [Treatment of vitamin D deficiency due to Crohn's disease with tanning bed ultraviolet B radiation - PubMed]

Sublingual supplementation is more readily absorbed than ingestion since lipid-soluble VitD is quickly diffused into capillaries under the tongue. [Sublingual Vitamin D3 Effective In A Patient Resistant To Conventional Vitamin D Supplementation] [Correction of vitamin D deficiency using sublingually administered vitamin D2 in a Crohn’s disease patient with mal-absorption and a new ileostomy]

Haven't seen studies on topical VitD. Perhaps, use the navel route to enhance.

P.S. 150 nmol/L (374.4 ng/ml) is pretty huge dose vz different recommendations
"The Endocrine Society defines vitamin D deficiency as 25(OH) D levels <20 ng/mL, insufficiency between 21 to 29 ng/mL, and optimal as >30 ng/mL. Levels <12 ng/mL are considered severe deficiency" [SL]
and vz the following study that fitted a nonliner model into PTH vs VitD values and showed that PTH decrease stabilizes after 60-65nmol/L levels (Fig. 3) This study was done in young NZ kids in winter and summer who didn't supplement otherwise. [Predictors of vitamin D status and its association with parathyroid hormone in young New Zealand children - PubMed]

1656738979634.png
 
Last edited:

Kray

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The authors talk about total 25(OH)D3, if >150 nmol/L, as possibly increasing intestinal absorption of toxic metals. They point out that "levels of 225 nmol/L can be achieved with ordinary sunlight and are thus considered normal." With sunlight, there are physiological (notably photochemical) mechanisms to downgrade absorption. "With sun exposure, for example, enzyme down-regulation appears to occur as higher levels are achieved so that diminished vitamin D skin production, absorption, and assimilation occur [Regulation of cutaneous previtamin D3 photosynthesis in man: skin pigment is not an essential regulator]".

Furthermore, VitD metabolites do not rise much in non-deficient subjects (called "normal" below) and no increase in "1,25" VitD form if minimal erythemal dose (MED) of UVR is received.

From Vitamin-D synthesis and metabolism after ultraviolet irradiation of normal and vitamin-D-deficient subjects - PubMed
In contrast to the markedly increased vitamin-D levels after exposure to UVR, the 25-OH-D concentrations in normal subjects increased only gradually, reaching highest concentrations seven to 14 days after exposure to UVR. Normal subjects exposed to one minimal erythemal dose of UVR had essentially no change in the serum concentration of 1,25-(OH),-D; however, those exposed to three minimal erythemal doses had a transient slight increase in the 1,25-(OH),-D concentration Fig. 1.
In normal subjects there was a dose related, rapid rise in vitamin D, with peak concentrations one to two days after exposure and a return almost to basal concentrations by seven days. For example, in representative normal subjects exposed in other experiments to one, 1.5, three, and four minimal erythemal doses of UVR (Fig. 2), peak vitamin-D levels were 24, 43, 80, and 138 ng per milliliter, respectively, one to two days after exposure. Thereafter vitamin-D levels fell rapidly but were still slightly above the base line at seven days.



The VitD amount absorbed orally depends on the gut and liver health. For example, in Crohn's disease absorption is poor and UVB route is required. [Treatment of vitamin D deficiency due to Crohn's disease with tanning bed ultraviolet B radiation - PubMed]

Sublingual supplementation is more readily absorbed than ingestion since lipid-soluble VitD is quickly diffused into capillaries under the tongue. [Sublingual Vitamin D3 Effective In A Patient Resistant To Conventional Vitamin D Supplementation] [Correction of vitamin D deficiency using sublingually administered vitamin D2 in a Crohn’s disease patient with mal-absorption and a new ileostomy]

Haven't seen studies on topical VitD. Perhaps, use the navel route to enhance.

P.S. 150 nmol/L (374.4 ng/ml) is pretty huge dose vz different recommendations
"The Endocrine Society defines vitamin D deficiency as 25(OH) D levels <20 ng/mL, insufficiency between 21 to 29 ng/mL, and optimal as >30 ng/mL. Levels <12 ng/mL are considered severe deficiency" [SL]
and vz the following study that fitted a nonliner model into PTH vs VitD values and showed that PTH decrease stabilizes after 60-65nmol/L levels (Fig. 3) This study was done in young NZ kids in winter and summer who didn't supplement otherwise. [Predictors of vitamin D status and its association with parathyroid hormone in young New Zealand children - PubMed]

Thank you for posting, very interesting findings!
 

peter88

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I have sunbathed in Southern California in peak summertime and my vitamin d levels stayed around 20 ng/ml no matter what I did. After taking 10k iu of oral vitamin d for almost a month, my levels skyrocketed to 55.
 

youngsinatra

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I have sunbathed in Southern California in peak summertime and my vitamin d levels stayed around 20 ng/ml no matter what I did. After taking 10k iu of oral vitamin d for almost a month, my levels skyrocketed to 55.
Did you notice a difference in symptoms/wellbeing after increasing your vitamin D level?
 

Mossy

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I have sunbathed in Southern California in peak summertime and my vitamin d levels stayed around 20 ng/ml no matter what I did. After taking 10k iu of oral vitamin d for almost a month, my levels skyrocketed to 55.
Congrats to you. I wish I could pull that off. Did you take any cofactors with that: vitamin A, vitamin K2, magnesium, or anything else?
 

peter88

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Did you notice a difference in symptoms/wellbeing after increasing your vitamin D level?
Honestly not much. I actually was thinking I was vitamin d deficient based off of my symptoms. Maybe keeping vitamin d levels at a good range long term will improve symptoms/increase calcium absorption? I grew up with slight scoliosis and teeth issues so I’m going to try to keep my vitamin d above 50ng/ml for a couple months. I’ll report back.

I’m just not sure why I couldn’t increase my D levels from sunbathing. I’m pretty tan, never burn and can sunbathe for hours but my level always stays low unless I supplement.
Congrats to you. I wish I could pull that off. Did you take any cofactors with that: vitamin A, vitamin K2, magnesium, or anything else?
No other cofactors. I don’t trust vitamin a supplements and I’ve always had issues with k2. I’ve been taking a bit of thyroid lately but I don’t think that fixed my level because last time I supplemented tyromix my vitamin d eventually fell back down to 20ng/ml.
 

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