Despite being referred to as a vitamin, vitamin D is actually a steroid hormone (also called calcitriol). Vitamin D, which our bodies synthesize in response to UV radiation from the sun, controls the expression of more than 200 genes and the proteins that those genes regulate. It is essential for mineral metabolism (it regulates the absorption and transport of calcium, phosphorous, and magnesium) and for bone mineralization and growth. Specifically, it helps to maintain appropriate calcium balance in the blood. It achieves this by working with the parathyroid gland to determine how much calcium will be deposited or excreted from bones as well as by modifying the amount of calcium that is excreted by the kidneys and how much is absorbed in the gut during digestion. This function operates in parallel to phosphorous metabolism, which is also regulated in part by vitamin D.
It is also crucial for regulating several key components of the immune system, including the formation of important antioxidants. Very importantly, vitamin D has recently been shown to decrease inflammation and may be critical in preventing and/or treating autoimmune and inflammatory diseases. Very importantly, Vitamin D has recently been shown to modulate inflammation and may be critical in autoimmune and inflammatory diseases!! Conversely, inadequate vitamin D levels have been repeatedly associated with inappropriate immune responses, demonstrating this vitamin’s essential value in maintaining healthy immunity.
Vitamin D is also involved in the biosynthesis of neurotrophic factors, regulating release of such important hormones as serotonin (required not only for mental health but also for healthy digestion!) and insulin. Vitamin D helps control cell growth, so it is essential for wound healing. In addition, it activates areas of the brain responsible for biorhythms. Scientists continue to discover new ways in which vitamin D is essential for human health; for example, it may help prevent cancer. See also See also Fructose and Vitamin D Deficiency: The Perfect Storm?, Why Sun Exposure Is So Important, and Regulating Circadian Rhythm (and why that’s important).
Research has shown that vitamin D helps regulate gastrointestinal inflammation and enhances gut barrier function (see What Is A Leaky Gut? (And How Can It Cause So Many Health Issues?)). Vitamin D also activates proteins important for detoxifying lithocholic acid (a secondary bile acid that’s toxic for intestinal cells). One way vitamin D helps maintain the integrity of the gut mucosal barrier is by enhancing the intercellular junctions that control gut permeability, as well as reducing inflammatory cytokines like interleukin-8. And, people with higher levels of vitamin D have been shown to have lower levels of the very inflammatory bacterial protein endotoxin in the blood, possibly due to vitamin D’s ability to improve gut barrier integrity. Observational studies have shown that people with higher levels of vitamin D are less likely to develop IBD, especially Crohn’s disease.
The composition of our gut microbiome is also sensitive to our vitamin D status (see What Is the Gut Microbiome? And Why Should We Care About It?). One study found that vitamin D supplementation (at a dose of 980 IU per kg bodyweight per week for four weeks, followed by another four weeks of taking 490 IU per kg of bodyweight) significantly reduced levels of Gammaproteobacteria, including the most common opportunistic pathogens, while also increasing the bacterial richness of the gut microbiome (one of the signature features of a healthy microbiome!). In addition, the supplementation protocol increased the number of CD8+ T immune cells in the upper gastrointestinal tract, pointing to a benefit for immunity. In a pilot study using 16 healthy volunteers, high-dose vitamin D supplementation (980 IU/kg bodyweight weekly for four weeks, followed by 980 IU/kg bodyweight weekly for another four weeks) altered the composition of the microbiota in the upper GI tract: the relative abundance of Gammaproteobacteria decreased (including Pseudomonas and Escherichia/Shigella), and the bacterial richness increased. In another human study, 20 adults with low vitamin D levels (below 30 ng/ml) were given 600, 4,000, or 10,000 IUs per day of vitamin D. The intervention led to a dose-dependent increase in the relative abundance of Bacteroiodes and Parabacteroides, while Faecalibacterium, Clostridia, and Ruminococcaceae significantly decreased. Yet another human trial, this one on 26 adults with vitamin D levels below 50 nmol/L who were also overweight or obese, found that high dose vitamin D supplementation (100,000 IU loading dose followed by 4,000 IU daily for 16 weeks) led to higher abundance of Lachnospira, lower abundance of Blautia, and—when vitamin D levels surpassed 75 nmol/L—a lower abundance of Ruminococcus and greater abundance of Coprococcus.
Observational studies have shown that people with higher levels of vitamin D are less likely to develop IBD, especially Crohn’s disease. Meanwhile, vitamin D deficiency is linked with gut dysbiosis and severe colitis. Additional research shows vitamin D deficiency may contribute to metabolic syndrome by aggravating diet-induced imbalances in the microbiota, including by decreasing the production of defensins (anti-microbial molecules needed for maintaining healthy gut flora); the subsequent imbalance leads to fatty liver disease, elevated blood sugar, and other hallmarks of metabolic syndrome. In rodents, vitamin D supplementation appears to improve metabolic syndrome via effects on the gut. And, people with higher levels of vitamin D have been shown to have lower levels of harmful endotoxin in the blood, possibly due to vitamin D’s ability to improve gut barrier integrity.
With vitamin D, as with all nutrients, it’s possible to get too much of a good thing. In a mouse model of colitis, animals were supplemented with high-dose vitamin D (10,000 IU/kg), moderate vitamin D (2,280 IU/kg), or no vitamin D. The mice receiving the highest dose developed the most severe colitis, and the high-dose control group (receiving vitamin D but not exposed to dextran sodium sulphate to induce colitis) ended up with microbiota compositions that were similar to those of the DSS-treated group, including a rise in Sutterella—suggesting that the high vitamin D dosing caused a shift to a pro-inflammatory microbiome. Additionally, the high-dose vitamin D mice saw a significant drop in serum vitamin D levels in conjunction with developing colitis, likely due to vitamin D metabolites dropping in response to intestinal inflammation that was caused by excessive vitamin D intake.
Getting Enough Vitamin D
Unlike some other vitamins and all minerals, we are able to make our own vitamin D. Specialized skin cells are activated when we expose our skin to UVB waves (by going outside and enjoying some sunlight on bare skin). After it’s synthesized in the skin, the inactive form of vitamin D must travel to the liver, where it’s further modified, and then is activated by the kidneys (so people with liver or kidney disease often have low vitamin D). Vitamin D can also can be obtained from foods, including oily fish (such as salmon, tuna, and mackerel), mushrooms, fish roe, liver, and eggs. The RDA for adults is 600 IU/day, though it’s important to note that we can store vitamin D in the liver (during the winter months, for example). The foods highest in vitamin D are pink salmon (465IU/serving), mackerel (211IU/serving), sardines (164IU/serving), and egg yolks (37IU/serving).
About 75% of Westerners are deficient in vitamin D. Severe vitamin D deficiency is called rickets, in which the bones of infants and children fail to mineralize. While vitamin D deficiency increases the risk for a variety of chronic health problems, it can also manifest in adults as:
- fatigue,
- osteomalacia (bone pain),
- muscle weakness, aches or cramps, and/or
- mood changes like depression.
It’s important to ask your healthcare provider to test your levels or choose at at-home vitamin D test to monitor your own levels. Optimal serum vitamin D levels are between 50 and 70 ng/mL.
If you’re deficient, it can be tough to get enough vitamin D3 from sun exposure and foods, so consider supplementing with vitamin D (5,000 IU daily is a standard dose to address deficiency but ask your healthcare provider for a recommendation based on your personal health history) and recheck every three months to make sure you don’t overshoot the mark. Vitamin D levels in excess of 100 ng/mL can also cause health problems, and the cusp for a negative impact on the gut microbiome is 75 ng/mL.
Vitamin D-enhanced mushrooms are a uniquely great source for supplemental vitamin D, containing 400IU to upwards of 2,400IU per 100 grams fresh weight. Mushrooms make vitamin D (mainly D2 form, but also D3 and D4) in response to UV radiation, and simply exposing mushrooms to UV light can enrich their vitamin D content dramatically (this is why wild mushrooms can have 100X more vitamin D than store-bought). Studies have shown that mushroom D2 is just as effective as vitamin D3 supplements at raising and maintaining blood levels of 25-hydroxyvitamin D, a marker for a person’s vitamin D status. Mushroom D2 is much more stable than vitamin D2 supplements too. You can DIY by slicing mushrooms and placing them in direct sun for 20 to 60 minutes before preparing and eating them daily, see also Elevating Mushrooms to Food Group Status. A fantastic, organic, clean and convenient option is Real Mushrooms Mushroom D2, which simply contains shiitake and agaricus (button) mushroom extracts and are standardized to 1,000IU per capsule. (Another option is Real Mushrooms Mushroom D2Z, which contains agaricus, chaga and reishi extracts in addition to zinc bisglycinate.)
Real Mushrooms make (IMO) the highest possible quality medicinal mushroom extracts, see also The Power of Medicinal Mushrooms: An Overview. The mushrooms are wild-harvested, organic and sustainably-sourced and you’ll always find a measurement of beta-glucans and triterpenoids (where applicable) on their labels. Plus, all of the products are free of starch, grain and fillers (surprisingly common in mushroom extracts). They make powders that are easy to add to coffee or a smoothie, capsules that make getting your daily serving of mushroom super easy, and even dairy-free dark chocolate made with extracts from five different mushrooms!
Citations
Bashir, M., B. Prietl, M. Tauschmann, et al. 2016. “Effects of high doses of vitamin D3 on mucosa-associated gut microbiome vary between regions of the human gastrointestinal tract.” European Journal of Nutrition. 55(4):1479–1489. doi:10.1007/s00394-015-0966-2.
Bikle DD. Vitamin D metabolism, mechanism of action, and clinical applications. Chem Biol. 2014;21(3):319-329.
Cardwell G, Bornman JF, James AP, Black LJ. A Review of Mushrooms as a Potential Source of Dietary Vitamin D. Nutrients. 2018;10(10):1498. Published 2018 Oct 13. doi:10.3390/nu10101498
Charoenngam, N., A. Dhirvani, T.A. Kalajian, A. Song, and M.F. Holick. 2020. “The Effect of Various Doses of Oral Vitamin D3 Supplementation on Gut Microbiota in Healthy Adults: A Randomized, Double-blinded, Dose-response Study.” Anticancer Research. 40(1):551-556. doi: 10.21873/anticanres.13984.
Ghaly, S., N.O Kaakoush, F. Lloyd, et al. 218. “High Dose Vitamin D supplementation alters faecal microbiome and predisposes mice to more severe colitis.” Scientific Reports. 8(11511). doi:10.1038/s41598-018-29759-y.
Grober U, Spitz J, Reichrath J, Kisters K, Holick MF. Vitamin D: Update 2013: From rickets prophylaxis to general preventive healthcare. Dermatoendocrinol. 2013;5(3):331-347.
Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2011;96(7):1911-1930
Naderpoor, N., A. Mousa, L.F. Gomez Arango, H.L Barrett, M. Dekker Nitert, and B. de Courten. 2019. “Effect of Vitamin D Supplementation on Faecal Microbiota: A Randomised Clinical Trial.” Nutrients. 11(12):2888. doi:10.3390/nu11122888.
Sutton AL, MacDonald PN. Vitamin D: more than a “bone-a-fide” hormone. Mol Endocrinol. 2003;17(5):777-791.