When my daughter went in for her one month checkup, we left with her length, weight, a reassuring list of milestones she had met, and instructions to purchase Vit-D-Sol, the very strangely named Vitamin D supplement for breastfed babies. Being a diligent rule-follower, I immediately went out and bought a bottle, opened it, and drew a dose into the dropper. I looked at my tiny baby. I looked at the dropper. How is this supposed to work? I tried to gently wiggle the tip of the dropper between her tiny lips and squeeze a dollop of the supplement into her cheek, as instructed; she flopped her head at the last minute and smeared sticky all over her face. My second try was more successful - I thought, until she scrunched up her mouth and slowly drooled the entire drop back out.
Eventually I figured out how to get at least some of it into her as she nursed, but never without also getting myself covered in vitamin-rich goo. Absent a bottle (and on top of everything else that comes with having a newborn), this extra daily chore felt more and more impossible.
Was it worth it? Why Vitamin D? Why is this one thing missing in breastmilk?
What is Vitamin D?
Vitamins have an aura of being magical little bits of nutrients that float around in our food and bodies, making us bigger, faster, healthier, stronger. But what actually are vitamins? The term covers a wide swath of organic (carbon-containing) molecules that bodies need in order to perform essential functions and are far from singular things. In fact, most vitamins that we could list don’t refer to single molecules, but rather to groups of similar molecules; for example, there is no single “Vitamin E,” but rather eight different molecules that all have similar impacts on our bodies.
Vitamin D, or the group of related molecules that we collectively call Vitamin D, is technically a steroid hormone (hormones are any molecule that is produced in one part of the body and then impacts the function of a different place in the body). There are four molecules that we classify as Vitamin D (D2, D3, D4, and D5). Of these, the most important to animals (including humans) is Vitamin D3 (cholecalciferol, for those who would like a million-dollar word of the day). We produce Vitamin D3 in our skin (our largest organ!) when ultraviolet light, specifically UV-B radiation, interacts with and transforms pre-vitamin D in the skin to full Vitamin D3. This is the same kind of UV radiation that causes skin tanning and sunburn; it is blocked by most standard window glass, so just like you won’t get tanned standing in front of a window, you won’t be producing any Vitamin D, either.
Vitamin D3 isn’t ready to use straight from the skin, however. After the skin does the hard work of synthesizing it, it remains inactive until it is transported and processed by the liver and kidneys. This transportation and transformation of inactive to active Vitamin D is driven by another hormone, called prolactin, which interestingly is also associated with milk letdown (among many other things), as well as parathyroid hormone (Henderson 2005).
Because Vitamin D is a hormone, not a nutrient, there are no dietary items that we could eat that will give us sufficient Vitamin D by itself. Some animal-based foods do have Vitamin D3 in them, including fish, liver, egg yolks, and breast milk, but it is through production in the skin that we get most (90%) of our Vitamin D (Henderson 2005, Dawodu and Tsang 2012).
But wait! We see Vitamin D all over product labels at the store - “fortified with Vitamin D” shows up on our milks, orange juices, and just about every breakfast cereal on the market. Products are sometimes fortified with Vitamin D3, the same form that our body produces, but not always! It is much more cost-effective to fortify with Vitamin D2, which is the form of Vitamin D that is produced by plants. There are lots of studies that reach lots of different conclusions about whether supplementing with D2 or D3 has an impact on the amount of active Vitamin D in our systems, but despite some potential differences, supplementing with both forms do increase our circulating Vitamin D levels safely and effectively (Wilson et al 2017).
Why do humans need Vitamin D?
Vitamin D’s main role is to assist with the body’s absorption of calcium and phosphorus. When you eat foods that contain these nutrients, the body absorbs them through your intestines and into your bloodstream. When calcium and phosphorus levels in your blood drop, parathyroid hormone and prolactin stimulate your body to make more Vitamin D, which then leads to more calcium and phosphorus absorption from your intestines to your bloodstream. Your body maintains balance and homeostasis (Henderson 2005)
Problems begin when your body releases parathyroid hormone or prolactin, essentially calling for active Vitamin D production because your blood levels of calcium and phosphorus are too low, but there is no Vitamin D to activate. This Vitamin D deficiency (the causes of which we will get to in a moment) means your body needs another way to get calcium and phosphorus levels in your blood up to where they should be. Where are the biggest stores of these nutrients in your body? In your bones, of course. Absent Vitamin D, parathyroid hormones and prolactin cause your bones to release calcium. In extreme cases, and particularly in children, this leads to “soft” bones, bone malformation, and the disease called rickets (Henderson 2005).
But defending your bones against a loss of calcium isn’t all that Vitamin D does! While the mechanism are less clear, Vitamin D deficiency is also linked to higher rates of other diseases including type 1 diabetes and higher susceptibility to tuberculosis, various forms of cancer, psoriasis, and more (Henderson 2005). It impacts the expression of over 200 genes by binding to a Vitamin D receptor, and while there is a still a lot we don’t know about the impacts of these genes, we do know that quite a few of them are related to immune function (Hlusko et al 2018).
Why isn’t there Vitamin D in breastmilk, which seems to have everything else a baby needs?
Great question. Breastmilk gets the reputation (rightfully!) for being a “perfect” food for baby: all the nutrients baby needs in just the right quantities, plus a personalized pharmacy of antibodies and boatloads of maternal bonding time, all in one go. But Vitamin D, this essential component of skeletal development? Conspicuously absent. What gives?
Vitamin D’s relationship to breastfeeding and pregnancy begins before baby is even out of the womb. It plays a critical role in the placental-maternal interface and spurs various changes that prepare mammary glands for lactation (Hlusko et al 2018). Infants have sufficient Vitamin D at birth to carry them through the first 8 weeks or so of life (Henderson 2005), provided that the gestating parent had sufficient Vitamin D levels during pregnancy. Studies have shown that umbilical cord blood has Vitamin D levels about 50-80% that of maternal levels, so sufficient Vitamin D during pregnancy is essential to sufficient levels in baby (Dawodu and Tsang 2012). And to protect the birthing parent, too! We all know that maintaining calcium intake in pregnancy is important, because that growing baby is going to absorb a lot to build its teeth and bones in utero, but don’t forget that it is Vitamin D that ensure the calcium we eat is actually transported into our bloodstream. In fact, prolactin hormone increases Vitamin D production during pregnancy for just this reason.
What about once baby is out? The American Association of Pediatrics recommends 200 IU (international units) of Vitamin D per day for healthy, non-pre-term babies. Breastmilk provides only about 45 IU per day, with variation based on level in the lactating parent - in fact, breastmilk Vitamin D levels are only 1-2% that of maternal blood levels (við Streym et al 2016)! Increasing sun exposure and very extreme dietary supplementation can increase the amount transferred in breastmilk, but because transference is so inefficient, the supplementation regime has to be extreme to reach sufficient levels for baby. The health effects of such supplementation is understudied and unknown (Dawodu and Tsang 2012).
WHY? The crux of the problem is this: humans, adults or babies, don’t get Vitamin D from our diets. We get it from ourselves, by synthesizing it in our own skin with exposure to sunlight, specifically UV-B radiation. In our species’ history, there has been no evolutionary pressure to more effectively transfer Vitamin D in breastmilk because it is not a nutrient. In a world before sunscreen, desk jobs, and air conditioning, a lack of Vitamin D because of a lack of sun exposure wasn’t a survival threat through our species faced.
… or was it? Around 32,000 years ago during the Last Glacial Maximum, the last gasp of the Ice Ages, ancestors of North and East Asian people today, as well as the Indigenous people of the Americas, survived in small refugee pockets of the Arctic area known as Beringia. These harsh environments would have held many challenges for their inhabitants, not the least of which was the punishing lack of sunlight at such a northern latitude. Research has shown that a specific variant of gene called EDAR (EDAR V370A, if you’re interested) was strongly selected for in this population - so strongly, in fact, that it nearly reached fixation (meaning all the other variants of this gene are gone, this is the only variant left). When a gene variant reaches fixation in a specific population, it is a safe bet that that variant’s effects were essential to that population’s survival at some point in the past. What does the EDAR gene do? Lots of things: it impacts the density of sweat glands, the shape of incisor teeth, and the number of branches in the mammary glands, among other things; EDAR V370A variant creates a higher density of sweat glands, a “shoveled” shape to the incisors, and more branching of mammary ducts. When a single gene impacts multiple traits, this is called pleiotropy. One of the trickiest jobs of an evolutionary biologist is detangling which of the pleiotropic effects of a gene were under active selection and which were just collateral. In other words, which effects were essential for survival and which just came along for the ride? For the longest time, evolutionary anthropologists assumed that it was the sweat gland density that was the selected-for trait because of the importance of thermoregulation to survival. Recently, though, Hlusko and colleagues proposed a new, compelling hypothesis: it was the mammary duct branching that was so critical! More branching in the ducts means more efficient nutrient transfer from parent to milk to baby. In an environment with very little sunlight to be had, this increase in Vitamin D transfer efficiency could have been the difference between offspring survival and death.
How big of a problem is Vitamin D deficiency in babies? Do I need to fight the dropper battle?
OK, but what about today? Our modern environment, filled with pollution that blocks sunlight, incentives to stay indoors, lack of safe outdoor spaces, sunscreen, and ample advice to keep your baby inside, covered up, and out of the sun, is radically different from the environments of most of human history. Very real damage from over-exposure to UV radiation, including skin cancer risks, are very real, and absolutely no one is suggesting putting baby in a tanning bed.
Rickets, a disease of malformed bones in children due to lack of Vitamin D, is very rare in the United States. From 1986-2003, 166 patients were documented with nutritional rickets, of whom 96% were breastfed (Dawodu and Tsang 2012). On top of this, research suggests that it doesn’t take much to get baby’s Vitamin D production to where it needs to be. Two hours a week (17 minutes a day!) of sunlight exposure when fully clothed, or about 30 minutes a week (5 minutes or less a day) in only a diaper, stimulate sufficient levels of Vitamin D in baby (Henderson 2005).
There is a huge, crucial caveat to put on these reassurances, however: different groups of people are at different risks for Vitamin D deficiency. This is true for adults and babies! Communities with low probability for casual sun exposure (for example, those in cities without safe outdoor spaces, or with air pollution that keeps people indoors or blocks sunlight), people living at more northern latitudes, people of color with more melanin content in their skin (which naturally blocks UV), or people with cultural practices that involve covering skin outside the home are all at increased risk of Vitamin D deficiency. Many of these risk factors are interactive and results of structural racial disparities in places like the United States; people of color, particularly Black families, are more likely to live in urban spaces with fewer safe outdoor areas, are more exposure to air pollution, and have increased melanin content in their skin. Research into mitigating risk in children suffers from racial bias as well. A foundational 1985 study, the one that assures us that 30 minutes a week in the sunlight in a diaper is sufficient for Vitamin D production? 84% of their participants were White. A careful examination of their results shows an enormous disparity in Vitamin D levels between White and non-White infants (24 ng/ml for White infants and only 9 ng/ml for non-White infants), but the implications of this are not discussed in the original publication or later articles referencing their findings (Specker et al 1985). The racial disparity in Vitamin D deficiency risk is well documented: in one study, 10% of White mothers, 43% of Black mothers, and 62% of Arab mothers were themselves Vitamin D deficient (Dawodu and Tsang 2012).
So what does all this add up to? Do we need to fight the battle with the dropper, or not? First and foremost, follow the recommendation of your pediatrician. Beyond that, assess your own situation. What is your and your family’s risk profile? How much time are you able to spend outside? What is your environmental situation with regards to sunlight? How is your exposure impacted by your skin’s melanin content, your use of sunscreen, or your cultural practices surrounding clothing coverage? We do not exist in a vacuum. Humans are biological and cultural creatures, with a deep evolutionary history that sometimes sits at odds with our modern environment. When we make decision for our health and for our family, we must keep all these factors in mind. When we make structural decisions for our communities and our nations, it is imperative to consider everyone included there. With Vitamin D, as with all issues, treating humans as a monolithic, uniform group is inaccurate and dangerous. Our diversity is our power. Ignoring it leaves us all in the dark.
References:
við Streym S, Højskov CS, Møller UK, Heickendorff L, Vestergaard P, Mosekilde L, Rejnmark L. Vitamin D content in human breast milk: a 9-mo follow-up study. Am J Clin Nutr. 2016 Jan;103(1):107-14. doi: 10.3945/ajcn.115.115105. Epub 2015 Dec 16. PMID: 26675779.
Henderson, A. (2005). Vitamin D and the breastfed infant. Journal of Obstetric, Gynecologic, & Neonatal Nursing, 34(3), 367-372.
Dawodu, A., & Tsang, R. C. (2012). Maternal vitamin D status: effect on milk vitamin D content and vitamin D status of breastfeeding infants. Advances in nutrition, 3(3), 353-361.
Wilson LR, Tripkovic L, Hart KH, Lanham-New SA. Vitamin D deficiency as a public health issue: using vitamin D2 or vitamin D3 in future fortification strategies. Proc Nutr Soc. 2017 Aug;76(3):392-399. doi: 10.1017/S0029665117000349. Epub 2017 Mar 28. PMID: 28347378.
Specker, B. L., Valanis, B., Hertzberg, V., Edwards, N., & Tsang, R. C. (1985). Sunshine exposure and serum 25-hydroxyvitamin D concentrations in exclusively breast-fed infants. The Journal of pediatrics, 107(3), 372-376.
Hlusko, L. J., Carlson, J. P., Chaplin, G., Elias, S. A., Hoffecker, J. F., Huffman, M., ... & Scott, G. R. (2018). Environmental selection during the last ice age on the mother-to-infant transmission of vitamin D and fatty acids through breast milk. Proceedings of the National Academy of Sciences, 115(19), E4426-E4432.
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