Preformed “Vitamin D” – Can One Serving of Fish or Eggs be All You Need to Satisfy Your Daily Vitamin D Requirement?

 

“Salmon eggs benedict”, the ‘perfect’ combo for 25OHD3 (recipe)

 

“If, as has been suggested, 25(OH)D3 has five times greater bioactivity than vitamin D3, one cooked serve (100 g) of white fish, and one cooked serve of cage or free-range eggs (120 g) may provide 50% or 100%, respectively, of the current guidelines for the adequate intake of vitamin D (5 µg) for Australians aged 1–50 years,” Australian researchers conclude in a recent paper that measured the concentration of vitamin D3 and 25-hydroxyvitamin D3 (25(OH)D3) in four species of white fish (barramundi, basa, hoki and king dory), and chicken eggs (cage and free-range), purchased from Adelaide, Brisbane, Melbourne, Perth and Sydney.

 

Samples included local, imported and wild-caught fish, and eggs of varying size from producers with a range of hen stocking densities (see overview in Table 1). Raw and cooked samples were analysed using high performance liquid chromatography with photodiode array. Limits of reporting were 0.2 and 0.1 μg/100 g for vitamin D3 and 25(OH)D3, respectively.

 

Table 1: Retail sources + characteristics of white fish & eggs from Australia for analysis of vitamin D3 and + 25-hydroxy-vitamin D3 (Dunlop 2017)| SA: South A.; QLD: Queensland; VIC: Victoria; WA: Western A.; NSW: New South Wales.

 

As you can see in Figures 1+2, the vitamin D3 content of cooked white fish ranged from <0.1 to 2.3 μg/100 g. Likewise highly significant was the vitamin D3 content of cooked cage and free-range eggs that ranged from 0.4 to 0.8 μg/100 g and 0.3 to 2.2 μg/100 g, respectively.

 

Figure 1: New data for vitamin D3, 25-hydroxyvitamin D3 content in white fish (Dunlop 2017).

 

If the previously cited assumption that … holds true, however, it’s not so much the vitamin D3 content that should get you excited. It’s rather the amount of the physiologically active form of “vitamin D”, i.e. 25(OH)D3 or calcifediol, of which you will find approximately 0.3 to 0.7 μg/100 in fish and values ranging from 0.4 to 1.2 μg/100 g, and 0.5 to 0.8 μg/100 g in eggs from caged and free-range hens, respectively. That’s at least 4 times more than in beef and still 2.5-times more than in chicken meat (Strobel 2013), which are also overlooked sources of ready-made calcifediol, which will otherwise have to be synthesized in the liver by hydroxylation of vitamin D3 (note: dairy contains only relatively little 25(OH)D3, because the concentration in milk is only 1% of the concentration in serum – to increase the 25(OH)D3 content to values above the average 0.02 µg/100 g farmers would have to add calcifediol to their dairy cows’ feed | Ovesen 2003).

 

Figure 2: New data for vitamin D3 and 25-hydroxyvitamin D3 content in chicken eggs (Dunlop 2017).

 

The question we still have to answer, though, is this hypothesis indeed correct? In her 2007 paper, Jette Jakobsen writes about the bioavailability and bioactivity of 25-hydroxyvitamin D3 that…
“[t]hough no consensus has been established for the potency between vitamin D3 and 25-hydroxyvitamin D3, the proposed factor 5 is generally accepted” (Jakobsen 2007).
Unfortunately, her review also highlights that few studies investigated the bioavailability and bioactivity factor for vitamin D metabolites. What’s more: the one study that existed when the review was written reports a bioactivity factor of “only” 1.7.

 

There’s little doubt that 25(OH)D3 is the more potent form of vitamin D

 

More recently, Jetter et al. (2014) have reported that calcifediol at a dosage of 20 μg daily did, while vitamin D3, administered at the same dosage, did not bring up d-ficient individuals vitamin D levels to the normal range. Based on their observation the researchers from the University Hospital Zurich conclude that: “Calcifediol, given daily, weekly, or as a single bolus is about 2–3 times more potent than vitamin D3” (Jetter 2014). These encouraging results have been confirmed even more recently by Shieh et al. (2017) whose study in 35 vitamin D deficient adults showed that 25(OH)D3 increases total and free 25D levels more rapidly than D3, regardless of race/ethnicity (see Figure 3).

 

Figure 3: Changes in vitamin D metabolites with D3 vs 25D3. (a) Total 25D and (b) free 25D (Shieh 2017).

 

Very similar results have been reported by Vaes et al (2017) in their dose–response study in older adults, whose results provide additional evidence of the superiority of orally ingested 25(OH)D3 over vitamin D3, i.e. regular “vitamin D supplements”. While the former boosted the vitamin D serum levels of all subjects way into the green zone with only 10µg/d, it took twice the amount of vitamin D3 to achieve a decent (albeit sign. less pronounced) effect on the elderly subjects’ vitamin D levels.

 

25(OH)D3 not yet listed on food labels – you may be getting more than you though

Against that background, a reform of the nutrient labels may be required – and that not only in Australia, where 25(OH)D3 is not recognized in the Australia New Zealand Food Standards Code as contributing to the vitamin D content of foods (FSAN). For animals, on the other hand, 25(OH)D3 has long been used as a fortificant – including in layer poultry farming. As the scientists point out, …

“[…]failure to measure 25(OH)D3 in food may [thus] result in considerable underestimation of vitamin D intakes [and may] provide a possible explanation for the gap between the calculated total basal input of vitamin D (sun exposure plus traditional food sources of vitamin D) and measured serum 25(OH)D concentrations.” (Dunlop. 2017)

Ah,… and in case you’re asking yourselves why we still are D-ficient, the answer is simple: inflammation diminishes your vitamin D stores (re-read my article about vitamin D as an acute phase reactant | cf. Waldron 2013) and out lifestyles are just that: highly (pro-)inflammatory. The comparatively small intake from one serving of fish or eggs will thus only suffice, if you (a) get enough sun, and/or (b) lead a healthy lifestyle that limits the inflammatory assault on your vitamin D stores.

 

What should I know and (not) do? No, you don’t have to throw away your D3 supplements and replace them with 25(OH)D pills. In fact, you will be hard pressed to find those pills at the healthfood/-supplement outlets of your choice, anyway. Calcifediol is, as of now, available only as a food additive for animal feed and a medicinal product. As a naturally occurring vitamin D metabolite in foods, it should, however, be allowable in FDA-approved supplements… I just haven’t yet seen one.

 

Before corresponding supplements are unleashed on supplement-addicted customers, though, it would be nice to see more studies into its long-term/high-dose safety and dose-response curves being done (the available data shows no toxicity issues | McKiernan 2015; Barros 2016; Vaes 2017; Shieh 2017). Plus: Depending on what those studies tell us about the true dose-effect curves of dietary 25(OH)D3 you may not even need them if you eat enough fish and eggs. Before this data is available, we can yet only rely on math + speculation. If we assume that a healthy individual living in the Nothern hemisphere needs say 2,000 IU/day of D3 to maintain what we currently call “normal levels” (no one knows if that’s optimal or not), the optimal case scenario (i.e. calcifediol is 5x more potent than D3) would say that you’d need 400IU of calcifediol to achieve the same effect you’d see with 2,000IU of D3 – that however, would mean that you’d have to eat ~1kg of eggs and fish… not realistic, but as I said all just hypothetical, anyway | Comment!

 

References:

  • Barros, Xoana, et al. “Comparison of two different vitamin D supplementation regimens with oral calcifediol in kidney transplant patients.” Journal of nephrology 29.5 (2016): 703-709.
    Food Standards Australia and New Zealand. Food Standards Code. Available online: http://www.foodstandards.gov.au/code/Pages/default.aspx (accessed on 24 June 2017)
  • Jakobsen, Jette. “Bioavailability and bioactivity of vitamin D 3 active compounds–Which potency should be used for 25-hydroxyvitamin D 3?.” International Congress Series. Vol. 1297. Elsevier, 2007.
  • Jetter, Alexander, et al. “Pharmacokinetics of oral vitamin D 3 and calcifediol.” Bone 59 (2014): 14-19.
  • McKiernan, Fergus E., et al. “Modified-Release Calcifediol Controls Elevated iPTH, Corrects 25 (OH) D Levels and Reduces Bone Markers in CKD Patients.” Late-breaking Bone, Calciotropic Hormones & Vitamin D II. Endocrine Society, 2015. LBF-036.
  • Ovesen, Lars, Christine Brot, and Jette Jakobsen. “Food contents and biological activity of 25-hydroxyvitamin D: a vitamin D metabolite to be reckoned with?.” Annals of Nutrition and Metabolism 47.3-4 (2003): 107-113.
  • Shieh, Albert, et al. “Effects of Cholecalciferol vs Calcifediol on Total and Free 25-Hydroxyvitamin D and Parathyroid Hormone.” The Journal of Clinical Endocrinology & Metabolism 102.4 (2017): 1133-1140.
  • Strobel, Norbert, et al. “Vitamin D and 25-hydroxyvitamin D determination in meats by LC–IT-MS.” Food chemistry 138.2 (2013): 1042-1047.
  • Vaes, Anouk MM, et al. “Dose–response effects of supplementation with calcifediol on serum 25-hydroxyvitamin D status and its metabolites: A randomized controlled trial in older adults.” Clinical Nutrition (2017).
  • Waldron, Jenna Louise, et al. “Vitamin D: a negative acute phase reactant.” Journal of clinical pathology (2013): jclinpath-2012.

 

Source: http://suppversity.blogspot.com/2017/06/preformed-vitamin-d-one-serving-of-fish.html

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