Be Wary Of Vitamin D Supplementation

yerrag

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sweetpeat

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Just updating from my posts from above concerning topical vs. oral vitamin D. I made a gradual switch to oral by taking 2000iu for a week, then 3000 for a week and so on until I reached 10,000iu. I did this over the course of about 8 weeks then retested. Vitamin D levels went from 22 to 35. Calcium, phosphorus still good. PTH came down to 28 from 33. So oral worked better than topical for me at bringing vitamin D levels up.

However, my liver enzymes jumped up quite a bit and have gone above range:
AST from 26 to 43 (range is 0-40)
ALT from 33 to 63 (0-32)
GGT from 49 to 79 (0-60)

I think my jaw literally dropped when I saw this. Is vitamin D to blame for this? Or just a coincidence? Maybe there is another culprit but I made no other significant changes that I can think of. I have stopped supplementing D for now. It is spring here so I'm taking advantage of the sun. I will re-test in a couple months.
 

baccheion

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Just updating from my posts from above concerning topical vs. oral vitamin D. I made a gradual switch to oral by taking 2000iu for a week, then 3000 for a week and so on until I reached 10,000iu. I did this over the course of about 8 weeks then retested. Vitamin D levels went from 22 to 35. Calcium, phosphorus still good. PTH came down to 28 from 33. So oral worked better than topical for me at bringing vitamin D levels up.

However, my liver enzymes jumped up quite a bit and have gone above range:
AST from 26 to 43 (range is 0-40)
ALT from 33 to 63 (0-32)
GGT from 49 to 79 (0-60)

I think my jaw literally dropped when I saw this. Is vitamin D to blame for this? Or just a coincidence? Maybe there is another culprit but I made no other significant changes that I can think of. I have stopped supplementing D for now. It is spring here so I'm taking advantage of the sun. I will re-test in a couple months.
Any reason you're not taking D3 with magnesium and vitamin K(2 MK-4)?

50-100 IU/kg/day D3 tends to be a good range.
 

baccheion

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Yes, I had read that too. That's why I was shocked to see liver enzymes go up when increasing vitamin D.
10,000 IU/week isn't that much. Some speak of an initial shock when first taking vitamin D that makes the body hungry for even more. On the other hand, they report serum also goes down.
 

sweetpeat

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10,000 IU/week isn't that much. Some speak of an initial shock when first taking vitamin D that makes the body hungry for even more. On the other hand, they report serum also goes down.
I didn't explain it properly above: I was taking 2000/day for a week, then raising it by 1000/day each week until I reached 10,000/day.
 

baccheion

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I didn't explain it properly above: I was taking 2000/day for a week, then raising it by 1000/day each week until I reached 10,000/day.
Maybe something is wrong. 2,000 - 10,000 IU should've raised serum more than that. On the other hand, maybe it takes 6 months or so.
 

sunraiser

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High enzymes are associated with low vitamin D. Maybe you're not taking enough. Try taking 50-100 IU/kg daily for a few months.

Vitamin D status, liver enzymes, and incident liver disease and mortality: a general population study. - PubMed - NCBI

This does not mean taking vitamin D restores liver function, it just means healthy people have good vitamin D status (with the calcium metabolism to support it).

@sweetpeat I would say the vitamin D absolutely could've caused this by causing imbalance in liver detox cofactors. Did you get alkaline phosphatase tested? I would bet it's on the low end.

Going with your instincts and stopping, then retesting in a few months sounds like a good idea.
 

baccheion

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This does not mean taking vitamin D restores liver function, it just means healthy people have good vitamin D status (with the calcium metabolism to support it).

@sweetpeat I would say the vitamin D absolutely could've caused this by causing imbalance in liver detox cofactors. Did you get alkaline phosphatase tested? I would bet it's on the low end.

Going with your instincts and stopping, then retesting in a few months sounds like a good idea.
Yea, that higher enzymes imply weaker liver function and associated vitamin D synthesis. Vitamin D is mostly synthesized in the kidneys and skin, though I suppose the liver has to supply cholesterol.

To the OP: what other supplements are you taking?
 

sweetpeat

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@sweetpeat I would say the vitamin D absolutely could've caused this by causing imbalance in liver detox cofactors. Did you get alkaline phosphatase tested? I would bet it's on the low end.

Going with your instincts and stopping, then retesting in a few months sounds like a good idea.
Yes, I did test alkaline phosphatase. It was 123 in February (range is 39-117). It fell a little to 118 after supplementing vitamin D. Because it was elevated and vitamin D was low and it was the end of winter, I thought supplementing the D might be a good idea. Maybe it was too much too fast...
 

sunraiser

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Yes, I did test alkaline phosphatase. It was 123 in February (range is 39-117). It fell a little to 118 after supplementing vitamin D. Because it was elevated and vitamin D was low and it was the end of winter, I thought supplementing the D might be a good idea. Maybe it was too much too fast...

It was still 118 after supplementing 10k vitamin d per day? Do you crave and eat any calcium rich foods?
 

Amazoniac

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- Vitamin D: A D-lightful solution for health

"When an adult in a bathing suit (woman in a bikini type bathing suit) has their whole body exposed to a tanning bed that was equivalent to being exposed to sunlight that caused a light pinkness to their skin 24 hours later (defined as one minimal erythemal dose) raised their blood level of vitamin D similar to the adult taking approximately 15,000-20,000 IU of vitamin D as a single dose.(Fig 4) Vitamin D made in the skin has at least 2-3 times longer in the circulaton when compared to ingesting vitamin D.(Fig 4)(45)"​

That's for venom D2. A single dose might not make a difference and it could be alright to claim that the increase is similar for both, but it's something to keep in mind:

- Vitamin D2 vs. vitamin D3: They are not one and the same

"Although both forms of vitamin D have historically been considered as equal in their physiological effects, studies since the 1980s exploring their comparative efficacy in raising vitamin D status show conflicting results, either concluding that both forms are equally effective or that vitamin D3 is more effective than vitamin D2. No studies have reported or suggested that vitamin D2 is more effective than vitamin D3."

The recently published D2–D3 Study, alongside mounting data from several intervention trials and a metaanalysis, provides firm evidence that vitamin D3 is more effective than vitamin D2 at raising total 25(OH)D concentrations. This does not mean that vitamin D2 is ineffective at raising total 25(OH)D; indeed, the rise in total 25(OH)D following D2 intake over the 12-week intervention period was adequate for health (i.e. there were clinically relevant improvements in vitamin D status) yet vitamin D3 was more than twice as effective.

"The positive effect of vitamin D2 is reassuring, as this type of vitamin D is still widely consumed; it is the primary dietary source of vitamin D for vegans and other population groups who, for cultural or religious reasons, may wish to avoid animal products. Thus, it should not be ruled out as a means to securing an adequate vitamin D status."​

..

- A Dermatologist's Perspective on Vitamin D

"It has been shown that full body exposure of fair-skinned individuals to 10 to 15 minutes of midday summer sun is equivalent to one MED and resulted in the synthesis of approximately 15,000 IU/d of vitamin D3.[48] By this reasoning, exposure of 15% of the body surface area (eg, face, hands, and arms) to a level of one-third MED should result in cutaneous biosynthesis of 1000 IU/d of vitamin D3.[11,12,27,44,48-51] It is difficult and not prudent to extrapolate these results to the general populace because cutaneous biosynthesis of vitamin D depends on factors that alter solar UV-B intensity, such as latitude, altitude, cloud cover, smog levels, and season. Other factors associated with vitamin D biosynthesis include body surface area exposed and skin pigmentation.[1-9,11,12,48-50]"​

- Optimal vitamin D3 daily intake of 2000 IU inferred from modeled solar exposure of ancestral humans in Northern Tanzania

"After numerous sunlight exposures, a person adapts to the doses exceeding his own MED for unexposed skin because of the natural sun protective effects such as tanning and skin thickening. MED value for the natural black skin adapted to high solar intensity is approximately 5 times larger than the unexposed (prior photo-adaptation) MED value [31]. For lighter skin (II and III photo-type) such as the MED increase is smaller ~4 [32]."


"Holick's rule states that exposing 1/4 of the body to 1/4 MED of sunlight will produce VD3E[ffective] dose equivalent to 1000 IU taken orally, i.e., adequate daily amount to keep healthy status of vitamin D. Dowdy et al. noticed that the whole body exposure during Holick's experiment was due to fluorescent tubes not due to noon sunlight [33]."

"The rule of thumb for vitamin D3 production due to sunlight says that just a few minutes of out-door activities around noon in summer is enough to get an adequate vitamin D level. Our results show that it is difficult to reach the target level of the serum 25(OH)D concentration which the human ancestors had in Africa before starting the migration to other continents. We propose the rule for getting optimal vitamin D level, i.e. 1/3 MED of near noon solar exposure of 1/3 of our body during warm subperiods of the year. It means that ~1 MED exposure is necessary for those exposing only face and palms. This is rather health risk option as the MED barrier could be easily broken during outdoor activities. Thus exposing larger part of body and then avoiding doses close to MED is safe solution but not possible in midlatitudinal regions during cold part of the year. Our rule provides approximately twice higher minimum vitamin D3 effective dose to keep healthy level of vitamin D3 than those provided by standard Holick's rule. The proposed daily exposure is then equivalent to ~2000 IU vitamin D3 taken orally."

"Similarly, the oral equivalent was inferred from the model study with simulated (by fluorescent tubes) typical UK summer's exposures of 1/3 skin area [24]. The Endocrine Society recommends 1500–2000 IU/d vitamin D intake for all adults, even for the category 70+ yr, to raise the serum 25(OH)D concentration above 75 nmol/L [34]. Experimental studies revealed that the 2000 IU/d supplementation during winter months led to ~30–45 nmol/L increase of the serum 25(OH)D concentration and it reached ~100 nmol/L in the end of the supplementation [35,36]. Such intake level is also supported by our calculations based on life style of the human ancestors and the solar exposure over their dwelling environment. Our finding gives an additional argument to the recent recommendations of vitamin D oral supplementation. Thus 2000 IU/d of vitamin D3 supplementation throughout the whole year is necessary for many contemporary humans with limited out-door activity."

"The rule of 1/3 MED solar exposure on uncovered 1/3 part of body is rather for young healthy persons (~20 yr) as the efficiency of vitamin D3 synthesis decreases significantly with age, e.g. the senior adults must double their solar exposure to meet the effects of solar exposure by young adults [37]. Oral supplementation of at least 2000 IU vitamin D per day is then only a possible option for elder persons to keep optimal vitamin D level. The recommended daily supplementation of 2000 IU is much below tolerable upper intake level for vitamin D equal to 10,000 IU per day [34,38]."​
 

Hildy

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I asked them all for a shill fee, with no success.

Now, seriously, according to your graph, supplementing with 2000 IU or 8000 IU hardly raises the levels above the 100 bar. And 6000 UI actually raises more your blood levels than 8000 UI, lol.

In Hollick's book, a whole lot of good happens to those around this 100 value.
He states toxicity begins only at 150.

The auto-immune people use 40000 to 250000 IU /day, with just a restriction on lactate products and an obligation to drink 2 liters/day of water.

Out of 4500 treated patients, only 2 encountered toxicity, and that's because they were laxist in their diet. Both totally recovered after going back to the strict protocol.

Makes you wonder how really toxic is Vitamin D.

I reckon deficiency is way more toxic.
Wow!
So if you are drinking sufficient amounts of milk, how much magnesium and vit D and vit k does one need to take? Do you go by weight?
 

Hildy

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From an interview with Dr Coimbra:

"Patients with autoimmune disorders have a genetically inherited resistance against the effects of Vitamin D. This resistance affects the immunomodulatory actions of vitamin D, and is a partial, not a complete, resistance. Due to this resistance these people are predisposed to develop autoimmune disorders.

The exact mechanism of this resistance is not clear yet. There are various diseases linked to genetic mutations in the vitamin D receptor, making these people resistant to vitamin D.

The resistance may also be due to an alteration of the enzymes dealing with the conversion and activation of vitamin D, which are two hydroxylases. So there are many different possibilities: an alteration of the first hydroxylase, of the second hydroxylase, an alteration of the vitamin D receptor itself, and a genetic alteration of the protein that captures vitamin D and carries it along into the bloodstream.

All these genetic alterations may explain the individual resistance to vitamin D and an individual may even suffer from two or three of these issues contributing to his / her resistance to the effects of vitamin D.

This is not just a hypothesis: polymorphic changes in one of the two vitamin D hydroxylases (particularly 1-alpha-hydroxylase), or in vitamin D receptor, or in DBP (vitamin D Binding Protein) have been identified and reported in association with autoimmunity."
After all these MS patients got better with the high doses of vitamin D, what then was their maintenance dosages?
Btw, I appreciate that you posted these results. The evidence seems pretty compelling to me that Vitamin D therapy works for many diseases.
 
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Amazoniac

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- The Importance of Vitamin C for Hydroxylation of Vitamin D3 to 1,25(OH)2D3 in Man

"The study included 20 female subjects. All of them were normal and none had any disease which could interfere negatively with the calcium phosphorus metabolism nor were they taking drugs. They were on a controlled diet which provided 1,000 mg/die [not an adaptation to prolactinese, Trawis would suggest it's in oleamidese] of elementary calcium and 100 mg/die of ascorbic acid."


Intrajugular treatment results:

upload_2019-10-18_20-48-15.png

"[..]we have demonstrated that ascorbic acid increases 1,25(OH)2D3 levels in man at paraphysiologic dose (150 mg), while no significant variation in serum 25(0H)D3, serum Ca++ serum PTH and other parameters was observed. Surprisingly, at a pharmacologic dose (1.000 mg) ascorbic acid decreased serum 1,25(OH)2D3 levels and caused an increase in serum Ca++."

upload_2019-10-18_20-48-27.png

"The increase in serum 1,25(OH)2D3 observed after paraphysiologic dose of ascorbic acid due to a direct effect of vitamin C on renal 1-alpha-hydroxylase enzyme could be explained, while no role of Ca++ could be postulated. The decrease in serum 1,25(OH)2D3 caused by the pharmacologic dose of ascorbic acid could be due to the increase in serum Ca++ or by an inhibition of ascorbate on 1-alpha-hydroxylase enzyme."

"The increase in serum Ca++ observed after 1.000 mg of ascorbate (after either acute stimulus and chronic stimulus) could be explained by the reducing effect of the vitamin on the Ca-binding protein."

upload_2019-10-18_20-48-37.png

"Although serum Ca++ level is important in the regulation of circulating 1,25(0H)2D3, a direct inhibitory effect of ascorbic acid on renal 1-alpha-hydroxylase enzyme cannot be excluded."

"The decrease in serum 25(OH)D3 observed in the first study (although not significant) and the increase in serum 25(OH)D3 observed in the second study (although not significant) by a feed-back regulation of serum 1,25(OH)2D3 levels could be explained."​

HE PUT IT IN ALL CAPS, TOO

He was proud of that one
THERE'S A CHANCE THAT HE DID IT TO FORMAT THE TITLE IN ACCORDANCE TO THE d-LIGHTFUL UNCLE PUN. WE'LL NEVER KNOW IF IT'S MEANT TO BE READ SCREAMING BUT IT SEEMS TO BE CONTAGIOUS. YOUR FELINE FRIENDS ARE NOT INTERESTED IN KNOWING BECAUSE IT'S A RISK TO THEIR SENSITIVE HEARING. OPEN VETERAN BOOK , MEOW DERE
 
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Amazoniac

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- Vitamin D Deficiency and Its Importance - A Global Problem of Today, Realistic or Not?

"Vitamin D plays an essential role in the maintenance of calcium and phosphorus homeostasis, consequently affecting bone formation. Calcium and phosphorous absorption from nutritional sources is poor, only 10-15% of calcium and 60% of phosphorous are absorbed, while at optimal vitamin D concentrations, the absorption of calcium and phosphorous is 30-40% and 80%, respectively (19). During certain periods when there is an increased need for Ca2+, such as during development, pregnancy and lactation, 60-80% of Ca2+ in food can be absorbed if the vitamin D status is sufficient; the status is sufficient when there is an the increased concentration of circulating 1,25-dihydroxyvitamin D, which reflects the extent of mineral absorption (1)."

"Pharmacokinetic processes of vitamin D are well known because of a large number of studies with radiolabelled vitamin D3 in both humans and animals, which can considerably facilitate the clinical application of vitamin D according to the characteristics of an individual. The proximal part of the small intestine is the location where the majority of vitamin D absorption occurs. An essential factor for this process is the presence of normal bile acid secretion due to the lipophilic structure of vitamin D. Bile acid is an indispensable factor for the incorporation of nonpolar molecules of vitamin D into the micelles of bile salt, after which it can be absorbed into the liquid phase. Normal stomach and pancreas secretion and diffusion through the liquid layers are additional factors for this pharmacokinetic step. In compliance with the aforementioned factors, the cause of reduced absorption is clear in intestinal diseases such as biliary obstruction, chronic pancreatitis, Crohn’s disease, renal insufficiency, etc. (42, 43). The effect of malabsorption syndrome on vitamin D absorption was evaluated by Satia and co-workers, and their results indicate that vitamin D3 absorption was higher in healthy subjects than in patients with malabsorption disease (44)."

"The following pharmacokinetic step, distribution, begins after the absorption of exogenous vitamin D in the small intestine. Distribution occurs due to the transfer of absorbed vitamin D into the lymphatic system. Vitamin D is then transported to circulation and binds to the vitamin D binding protein after which the resulting complex continues to the liver. Because the vitamin D binding protein is a key substance for distribution, it should be noted that hepatic impairment, nephrotic syndrome and malnutrition negatively impact distribution while pregnancy and estrogen therapy have contradictory effects (45)."​

- Advanced Nutrition and Human Metabolism (978-1-133-10405-6)

"In contrast to vitamin D from the diet, vitamin D3 that is made in the skin slowly diffuses from the skin into the blood and is picked up for transport by the hepatically synthesized DBP. About 60% of plasma vitamin D is bound to DBP for transport. The vitamin D bound to DBP is delivered primarily to the liver but may be picked up by other tissues, especially muscle and adipose tissue, before hepatic uptake. Thus, the difference in the transport mechanisms for the vitamin formed in the skin (i.e., going directly from the skin into the blood bound to DBP) and that absorbed from the digestive tract (i.e., incorporating into chylomicrons, entering the lymphatic system, and then entering the blood) affects the distribution of the vitamin in the body."​

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

"One point of note is that adequate 25(OH)D3 is associated with improved absorption of essential elements including calcium, magnesium, iron, phosphate, zinc, and copper [12]. What has largely been forgotten, however, is that higher levels of 25(OH)D3 have been linked to enhanced absorption of toxic elements such as aluminum, cadmium, cobalt, and lead as well as radioactive isotopes including cesium and radioactive strontium [12]. It has also been observed in the chick that vitamin D increases zinc and cadmium absorption [42]. Vitamin D has no effect on mercury absorption in the chick intestine but increases cobalt and iron absorption in the presence of low calcium [43]. In children, elevated 25(OH)D3 levels in the summertime are associated with a seasonal increase in blood lead levels via increased intestinal absorption [44]. It is also well recognized that bioaccumulation of such toxic metals in turn appears to disrupt physiological functioning of vitamin D within the body. For example, accrual of lead or cadmium diminishes the activity of vitamin D, by blocking the normal renal synthesis of active 1,25-dihydroxyvitamin D [12]. There is also evidence discussed in the literature of myriad adverse effects that various toxic metals including cadmium, lead, mercury, and aluminum can have on normal biological processes including uptake, absorption, and assimilation of assorted essential minerals [16, 17]—which may consequently result in health problems. Toxic metals themselves can also accrue in various tissues and have been directly linked to various adverse health outcomes [45–47]. Table 1 provides an overview of the complex interaction between vitamin D and various inorganic elements—both required minerals and toxic metals."

upload_2019-10-22_9-43-16.png

"The question therefore arises as to whether the alleged rise in morbidity and mortality associated with elevation of 25(OH)D3 (>150nmol/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)D3 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]. Lead, for example, may be abundant in bone and brain where it tends to accumulate, with potentially little evidence of such accrual with blood or urine testing [50]."

"It is also evident that vitamin D does not act solely in isolation. Impaired vitamin D functioning and insufficient levels of essential minerals can have synergistic and cumulative adverse action on biological function with significant pathophysiological impact. For example, vitamin D metabolism is dependent on sufficient magnesium as a cofactor for vitamin D to bind to its transport protein and for this vitamin to convert into the active form via hydroxylation in renal and hepatic sites [51]. Furthermore magnesium deficiency may upregulate the 24(OH)ase enzyme in the kidney resulting in catabolism of active vitamin D [51]."

"Furthermore, any determinant such as accrued toxic metals that would exacerbate zinc deficiency also has a potential detrimental impact on physiological function. Along with iron, boron, manganese, and copper, the essential mineral zinc is important as a cofactor in bone health. Specifically, zinc facilitates bone formation by stimulating the osteoblast [58]. While the average daily intake of zinc is considered to be only 46–63% of the RDA, various toxic metals have a detrimental impact on zinc uptake into the body (Table 1). Additionally a study on mineral content of foods has found that more than 80% of Americans do not achieve the RDA or the estimated safe and adequate daily dietary intake of calcium, magnesium, copper, zinc, and iron. The result of such widespread deficiency may be increased risk of toxic element absorption [59]."

"The complex interaction between the essential element calcium, vitamin D, and toxic metals is also evident in various reports from the literature [Table 1]. While no more than 800mg of calcium a day may be required when vitamin D levels are adequate, the typical diet in North America may be inadequate to supply even this limited amount [60]. Furthermore, as is noted in Table 1, toxic metals may impair calcium uptake resulting in deficiency states. While much recent attention has been devoted to the finding that excess calcium intake may actually cause harm, increasing the risk of myocardial infarction by 31% and stroke by 20% [61], it is important to remember that sufficiency of calcium is required for normal physiological function, a clinical state that may be compromised by vitamin D insufficiency or toxic metal bioaccumulation."​

- Magnesium Supplementation in Vitamin D Deficiency (yes, your life is in loop mode)

"Several steps in the vitamin D metabolism depend on magnesium as a cofactor, such as vitamin D binding to vitamin D binding protein, 25(OH)D synthesis, 1,25 (OH)2D synthesis, 25-hydroxylase synthesis, and VDR expression for cellular effects (Figure 1). Mg deficiency can also decrease PTH synthesis and secretion and also the number of available VDRs in target cells.[18–21] Serum 1,25(OH)2D concentrations frequently remain low in patients with Mg deficiency despite vitamin D intake[22–24] Mg deficiency is also known to cause vitamin D–resistant hypocalcaemia, which can only be corrected after the proper replacement of Mg. Taking large doses of vitamin D without Mg replacement has been shown to induce atherosclerosis in swine coronary arteries.[25]"

upload_2019-10-22_9-43-55.png

??

- Assessment of vitamin D status – a changing landscape

Summary:
"In recent years it has been shown that vitamin D deficiency is associated with an increased incidence as well as the progression of a broad range of diseases including osteoporosis, rickets, cardiovascular disease, autoimmune disease, multiple sclerosis and cancer. Consequently, requests for the assessment of vitamin D status have increased dramatically. Despite significant progress in the analysis of vitamin D metabolites and an expansion of our pathophysiological knowledge of vitamin D, the assessment of vitamin D status remains a challenging and partially unresolved issue. Current guidelines from scientific bodies recommend the measurement of 25-hydroxy vitamin D (25-OHD) in blood as the preferred test. However, growing evidence indicates significant limitations of this test, including analytical aspects and interpretation of results. In addition, the relationships between 25-OHD and various clinical indices, such as bone mineral density and fracture risk, are rather weak and not consistent across races. Recent studies have systematically investigated new markers of vitamin D status including the vitamin D metabolite ratio (VMR) (ratio between 25-OHD and 24,25-dihydroxy vitamin D), bioavailable 25-OHD [25-OHD not bound to vitamin D binding protein (DBP)], and free 25-OHD [circulating 25-OHD bound to neither DBP nor albumin (ALB)]. These parameters may potentially change how we will assess vitamin D status in the future. Although these new biomarkers have expanded our knowledge about vitamin D metabolism, a range of unresolved issues regarding their measurement and the interpretation of results prevent their use in daily practice. It can be expected that some of these issues will be overcome in the near future so that they may be considered for routine use (at least in specialized centers). In addition, genetic studies have revealed several polymorphisms in key proteins of vitamin D metabolism that affect the circulating concentrations of vitamin D metabolites. The affected proteins include DBP, 7-dehydrocholesterol synthase and the vitamin D receptor (VDR)."

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- Natural Vitamin D Content in Animal Products

- Vitamin D: a critical and essential micronutrient for human health (is was posted)

"Since the discovery of vitamin D, vitamin D was associated with oily fish products. It was driven by the early observation that the amount of vitamin D in a teaspoon of cod liver oil was sufficient to prevent rickets in infants. It is still the fish liver oil that contains the highest amounts of vitamin D3. The highest reported concentration was found in skipjack liver oil 144,400 μg/100 g (Takeuchi et al., 1984). The fish liver oils besides other nutritional ingredients might contain high levels of vitamin A. The vitamin A to vitamin D ratio in the fish liver oils is species and fishing area dependent. The ratio range starts with a factor of 0.5 for skipjack liver oil and can even reach an extreme ratio of 119 (pollack liver oil) (Takeuchi et al., 1984). This wide vitamin A to vitamin D ratio range is the reason why fish liver oils often need further processing. In fresh fish products we observe a huge variation in the vitamin D3 content per 100 g wet weight (Egaas and Lambertsen, 1979; Takeuchi et al., 1984, 1986; Kobayashi et al., 1995; Mattila et al., 1995a, 1997; Ostermeyer and Schmidt, 2006; Lu et al., 2007; Byrdwell et al., 2013) (Table 1)."​

Wowever:

- Efficacy of fish intake on vitamin D status: a meta-analysis of randomized controlled trials

- Bioavailability and bioactivity of vitamin D3 active compounds – Which potency should be used for 25-hydroxyvitamin D3?
- Challenges to Quantify Total Vitamin Activity: How to Combine the Contribution of Diverse Vitamers?
- Vitamin D Vitamers Affect Vitamin D Status Differently in Young Healthy Males


- The History and Modern Controversies of Vitamin D Fortification and Supplementation (good overview)


- Cytochromes P450 are essential players in the vitamin D signaling system

- Case Report: Vitamin D-Mediated Hypercalcemia in Fungal Infections

- Vitamin D hormone regulates serotonin synthesis. Part 1: relevance for autism
- Vitamin D and the omega-3 fatty acids control serotonin synthesis and action, part 2: relevance for ADHD, bipolar disorder, schizophrenia, and impulsive behavior
 

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