Today is the winter solstice (in the Northern Hemisphere; it’s the summer solstice below the equator), which means that today is the “shortest” day of the year, with the least amount of sunlight. Much of the average person’s vitamin D is synthesized through the skin, from ultraviolet light in sunlight. Which means that the less sun exposure, the less they can manufacture vitamin D, and the more necessary it is to get adequate vitamin D through food or artificial sources.
Here’s a neat calculator to determine how long a person of various skin colorings would need to be out in the sun, to get a set amount of vitamin D. It calculates the “Recommended UV exposure of face, hands and arms at least every other day to obtain sufficient vitamin D, equivalent of 25 micrograms vitamin D, if no dietary vitamin D is available.” You can go with some preset cities (like London), or put in your own latitude and longitude (that calculator here), your skin color (Pale Caucasian, Blond Caucasian, Darker Caucasian, Mediterranean, Middle Eastern, Black), the day and month, whether it’s clear or overcast, and even whether you’re on sand, snow, lawn, etc. Pretty interesting. The good news, is you can do this; the bad news is… it might be difficult to get this much vitamin D. I put in a “Pale Caucasian” (because the darker the skin, the longer you need to be exposed to the sun), in London on today, a cloudless sky, around midday, on the lawn… and it would take 24 hours to get that much vitamin D. Actually, it might be more, because it had the same value for all skin types, so I guess it maxes out at 24 hours. Changing the time of the year to July 21, and standing on sand (which is reflective), reduces the exposure time to 4 minutes for pale caucasian and 21 minutes for black. You can, of course expose more skin to the sun to reduce your time, but I don’t know many people who would be comfortable standing naked on sand in London in the middle of December. Chicago’s a bit better — a pale caucasian would only have to stand with arms, face, and hands exposed for 49 minutes (on concrete) every other day to get the quota; but a “Middle Eastern” would have to stand outside nearly 3 hours; and a “Black” would again max out at 24 hours.
So what? So this — rickets is the disease most strongly associated with vitamin D deficiency. We don’t have rickets any more [well, it’s not common, anyway], because we discovered the link between it and vitamin D deficiency decades ago, and have supplemented with vitamin D ever since. But that doesn’t mean that the minimum amount of vitamin D that is sufficient enough to ward off rickets is sufficient enough for optimum health. I did a Google Scholar search for “vitamin D” and “pregnancy,” just to see what it came up with. I’m not going to try to find the full studies of these things; I’m not going to research to see if I can find holes in the research; I’m not looking at different types of vitamin D, or the quality of supplements, or anything like that; I’m going to assume that all the research is valid, non-biased, accurate, etc. This is a skim-job on vitamin D, but I bet it’ll turn up some interesting things.
A study of Asian mothers in the UK found, “Five of these infants developed symptomatic hypocalcaemia. Almost twice as many infants in the control group were small for gestational age (29% v 15%), but there were no significant differences between the two groups of infants in antropometric measurements. Infants in the control group, however, had larger fontanelles, suggesting impaired ossification of the skull.”
This Australian study looked at pregnant women who were darker-skinned and/or veiled themselves outside, and found that “80% were at high risk of vitamin D deficiency.”
A Finnish study looked at the link between Type 1 Diabetes in children who did and did not take vitamin D supplementation in the first year of life, and found, “Vitamin D supplementation was associated with a decreased frequency of type 1 diabetes.” This Norwegian study found that cod liver oil and/or vitamin D supplements taken either by the mother during pregnancy, or by the child in the first year of life, also reduced type 1 diabetes.
This 2005 study called for new dietary guidelines for vitamin D supplementation, saying, “Recent studies reveal that current dietary recommendations for adults are not sufficient to maintain circulating 25(OH)D levels at or above this level, especially in pregnancy and lactation.”
Another study looked at vitamin D levels in black and white pregnant women residing in the Northern United States; the abstract follows:
In utero or early-life vitamin D deficiency is associated with skeletal problems, type 1 diabetes, and schizophrenia, but the prevalence of vitamin D deficiency in U.S. pregnant women is unexplored. We sought to assess vitamin D status of pregnant women and their neonates residing in Pittsburgh by race and season. Serum 25-hydroxyvitamin D (25(OH)D) was measured at 4–21 wk gestation and predelivery in 200 white and 200 black pregnant women and in cord blood of their neonates. Over 90% of women used prenatal vitamins. Women and neonates were classified as vitamin D deficient [25(OH)D <37.5 nmol/L], insufficient [25(OH)D 37.5–80 nmol/L], or sufficient [25(OH)D > 80 nmol/L]. At delivery, vitamin D deficiency and insufficiency occurred in 29.2% and 54.1% of black women and 45.6% and 46.8% black neonates, respectively. Five percent and 42.1% of white women and 9.7% and 56.4% of white neonates were vitamin D deficient and insufficient, respectively. Results were similar at <22 wk gestation. After adjustment for prepregnancy BMI and periconceptional multivitamin use, black women had a smaller mean increase in maternal 25(OH)D compared with white women from winter to summer (16.0 ± 3.3 nmol/L vs. 23.2 ± 3.7 nmol/L) and from spring to summer (13.2 ± 3.0 nmol/L vs. 27.6 ± 4.7 nmol/L) (P < 0.01). These results suggest that black and white pregnant women and neonates residing in the northern US are at high risk of vitamin D insufficiency, even when mothers are compliant with prenatal vitamins. Higher-dose supplementation is needed to improve maternal and neonatal vitamin D nutriture.
A Saudi study said, “We conclude that BMD in healthy Saudi females is significantly lower than in their USA counterparts. This may be due in part to increased number of pregnancies and longer duration of lactation together with prevalent vitamin D deficiency.” Or, perhaps it’s because they’re covered head to toe, in obedience to Sharia law, so even though they live in a very sunny area, they still don’t get enough vitamin D. I mean, the religious police shut 15 girls in to burn to death in their school, because they didn’t have their burqas on, having left them in the foyer when they entered the building! How much sunlight does the average Saudi woman get? Perhaps if she uncovers herself in an enclosed courtyard (as was mentioned in the above Australian study), she would get enough; but what if she doesn’t have that? What if the only time she unveils herself is when she’s indoors with the windows shut?
A study published in 1995 said that, “These findings suggest that subclinical vitamin D deficiency is still a cause for concern in Asian women. More active measures need to be taken to implement current recommendations to improve their vitamin D intake in pregnancy.”
This BMJ article has for the abstract, “Vitamin D has steroid hormonal effects which can produce clinical symptoms and signs unrelated to calcium homoeostasis. Its deficiency has been implicated as a risk factor for diabetes, ischaemic heart disease, and tuberculosis in Asians. In this review, the incidence, aetiology, prevention, and treatment of symptomatic vitamin D deficiency in childhood are considered. A renewed public health campaign is required in the UK to address the continuing problem of vitamin D deficiency in Asian families.” I’m including it mostly because it has a ton of links and studies that may yield more information.
This 2007 article concluded, “Increasing maternal vitamin D intakes during pregnancy may decrease the risk of wheeze symptoms in early childhood.”
A 1994 article titled, “Do North American women need supplemental vitamin D during pregnancy or lactation?” said this:
Studies in European and other countries have shown that vitamin D deficiency during pregnancy may adversely affect fetal growth, bone ossification, tooth enamel formation, and neonatal calcium homeostasis. Whether effects of vitamin D deficiency on pregnant or lactating mothers differ from effects observed in nonpregnant or nonlactating women is not clear. Poor maternal vitamin D status during lactation results in low breast-milk vitamin D. However, human milk usually contains small vitamin D amounts and, under normal circumstances, the sunshine exposure of human-milk–fed infants is the major factor affecting their vitamin D status. Mothers at risk of vitamin D deficiency are those who avoid dairy products, which are routinely vitamin D fortified, and live in more northern latitudes. Dark-skinned women also are theoretically at risk of vitamin D deficiency. Sunshine exposure is a major vitamin D source, and given adequate exposure, supplemental vitamin D is not necessary. However, defining adequate sunshine exposure is difficult.
A study of Pakistani women living in Norway concluded, “This study has shown that Pakistani women living in Oslo are at great risk of developing vitamin D deficiency during pregnancy. The main reasons for this are avoidance of sun exposure, a low dietary intake of vitamin D, and no or little use of supplementation.”
Another BMJ study said, “These results suggest that vitamin D supplementation during pregnancy would be beneficial for mothers, whose intake from diet and skin synthesis is appreciably less than 500 IU of vitamin D daily.”
A study of Asian Indians noted that they tend to have vitamin D deficiency when emigrating to northern Europe, and also to the southern United States, and “are at risk for developing vitamin D deficiency, rickets, and osteomalacia.”
This 1997 abstract was interesting:
Environmental factors are important in the aetiology of glucose intolerance, type II diabetes and IHD. The lack of vitamin D, which is necessary for adequate insulin secretion, relates demographically to increased risk of myocardial infarction. These disorders are connected, degenerative vascular disease increasing with glucose intolerance and diabetes and, with its risk factors, comprising syndrome ‘X’. Evidence is presented suggesting that vitamin D deficiency may be an avoidable risk factor for syndrome ‘X’, adding another preventative measure to current recommendations which are aimed at reducing the worldwide epidemic of these disorders. Experimentally, vitamin D deficiency progressively reduces insulin secretion; glucose intolerance follows and becomes irreversible. Relationships between vitamin D status, glucose tolerance and 30 min insulin secretion during oral glucose tolerance tests are reported in British Asians; insulin secretion, but not glycaemia, improving with short-term supplementation. Studies showing reduction in blood pressure and in risk of heart attack and diabetes with exercise (usually outdoor), rarely consider the role of vitamin D status. Glycaemia and insulin secretion in elderly European men, however, relate to vitamin D status, independent of season or physical activity. Prolonged supplementation can improve glycaemia. Hypertension improves with vitamin D treatment with or without initial deficiency. Vitamin D status and climate are reviewed as risk factors for myocardial infarction; the risk reducing with altitude despite increasing cold. Glycaemia and fibrinogenaemia improve and insulin secretion increases in summer. Variation in vitamin D requirements could arise from genetic differences in vitamin D processing since bone density can vary with vitamin D-receptor genotype. Vitamin D receptors are present in islet β cells and we report insulin secretion in healthy Asians differing profoundly with the Apa I genotype, being independent of vitamin D status. Those at risk of vitamin D deficiency include the elderly, those living indoors or having a covered-up style of dress, especially dark-skinned immigrants, and pregnant women, and these are groups recognized as being at increased risk of diabetes.
This study looked at a recurrence of vitamin D deficiency and the recurrence of rickets, vitamin D toxicity, and limiting sun exposure in an attempt to avoid skin cancer:
itamin D deficiency in utero and during the first year of life has devastating consequences and may imprint on the child’s life chronic diseases that will shorten his/her life span (24, 57). In utero, vitamin D deficiency results in reduced intrauterine long bone growth and slightly shorter gestation (121). This has been linked to increased risk of osteoporosis and fractures later in life (24, 60, 61, 82, 122). Children born and raised at latitudes below 35° for the first 10 years have a 50% reduced risk of developing multiple sclerosis later in life (103, 104). Neonates who are vitamin D deficient during the first year of life are 2.4-fold more likely to develop type 1 diabetes compared with children who received 2,000 IU of vitamin D3/day (105). It has been suggested that the increased risk of developing schizophrenia may be initiated in utero and during childhood due to vitamin D deficiency (102). Muscle function, innate immunity, cellular growth and maturation, immunomodulation, insulin secretion, as well as regulation of calcium, phosphorus, and bone metabolism are all affected or controlled by vitamin D. Thus, ensuring that women during pregnancy are vitamin D sufficient and that newborns either be immediately evaluated for their vitamin D status by measuring 25(OH)D levels in cord blood or given vitamin D prophylactically should be a high priority. Vitamin D deficiency should be immediately treated with at least 1,000 IU of vitamin D2 or vitamin D3/day for the first week of life. Alternatively, a single dose of 200,000 IU of vitamin D should suffice for the first few months of life.There has been a great fear about causing vitamin D intoxication in neonates. This resulted from the poorly described outbreak of neonatal hypercalcemia in the 1950s in Great Britain (123), which led to the enactment of laws in Europe forbidding the fortification of dairy products as well as all other products with vitamin D. In 1997 the Institute of Medicine recommended that the AI for infants and children of all ages be 200 IU/d. The same recommendation was made for pregnant and lactating women. The safe upper limit for infants ages 0–12 months was 1,000 IU/d and for children older than 1 year of age, 2,000 IU/d. However, it is now obvious based on the historical literature (14–16) as well as the recent literature (23, 24, 30, 36, 81, 86, 87) that these recommendations are inadequate without sensible sun exposure. It is well documented that neonates and children can tolerate a single dose of 200,000 IU of vitamin D2 or vitamin D3 or doses of vitamin D up to 3,000 IU/d without any untoward side effects. Indeed 400–1,000 IU/d to maintain serum 25(OH)D levels between 30–50 ng/ml should be the goal, just as it is in adults. Infants and children have routinely received 400–2,000 IU vitamin D2 or vitamin D3/day for the first years of life without any reports of toxicity (23, 80, 105, 107). Typically, doses of more than 50,000 IU/d of vitamin D2 were found to cause toxicity (12–14).
In Canada, it is recommended that all infants receive 400 IU/d from birth. This recommendation has been successfully implemented and has not resulted in any reported cases of vitamin D intoxication or hypercalcemia. I believe that the 200 IU of vitamin D that is recommended by the American Academy of Pediatrics is suboptimal (124). This dose may prevent overt rickets but will not prevent vitamin D deficiency.
Hopefully, history will not repeat itself. The widespread concern about any direct sun exposure increasing the risk of the relatively benign and nonlethal squamous and basal cell cancers needs to be put into perspective. It is chronic excessive exposure to sunlight and sunburning experiences during childhood that increases risk of nonmelanoma skin cancer (125). Melanoma, one of the most feared cancers because of its ability to rapidly metastasize before it is obvious to either the patient or physician, has been branded as a sun-induced skin cancer. However, most melanomas occur on the least sun-exposed areas, and it has been reported that occupational exposure to sunlight decreases risk of melanoma (125).
The 30-year campaign to recommend abstinence from sun exposure has not stemmed the increase in skin cancer incidence (125). It is curious that in the 1930s and 1940s, when children were encouraged to be exposed to sunlight and artificial UV radiation to treat rickets, the incidence of skin cancer did not increase. Thus, there needs to be a reevaluation of the beneficial effect of sensible exposure to sunlight as noted by the Australian College of Dermatologists and the Cancer Council Australia, which recommend a balance between avoiding an increase risk of skin cancer and achieving enough UV radiation to maintain adequate vitamin D levels.
And p. 8 of this 343-page pdf says, “Vitamin D intake above current dietary reference intakes was not reported to be associated with an increased risk of adverse events. However, most trials of higher doses of vitamin D were not adequately designed to assess long-term harms.” This 2007 Review Article suggested, “the absence of toxicity in trials conducted in healthy adults that used vitamin D dose 250 µg/d (10 000 IU vitamin D3) supports the confident selection of this value as the UL.”
Dr. Mercola had an article on premature birth, saying that it is or can be linked to insufficient Vitamin D (with multiple links).
The Vitamin D Council website has readable articles about vitamin D, toxicity, minimum requirements, skin cancer due to sun exposure, etc.
So, I’m going to supplement with vitamin D, in addition to my prenatal vitamins, especially if I can’t get exposure to the sun due to the cold, cloudiness, etc. And I’ll try to consume more foods that naturally contain vitamin D. Ideally, I’d get vitamin D the natural way if possible; but I don’t have anything against pills when necessary.
Some of these studies were intriguing in one way that perhaps most people wouldn’t have thought of — and there are probably more diseases that are affected by deficient vitamin D than we’re even aware of — but the talk about rickets and type 1 diabetes in children made me think of the different skin colors that people have all across this world of ours. Whether you believe in evolution or creation, just about everyone believes that all of us humans came originally from the same source — either several thousand years ago, or a few hundred thousand years ago. Vitamin D deficiency would explain in large measure the divergence of skin colors — in parts of the world that didn’t get as much sun exposure, darker children and adults would be more likely to die earlier due to diabetes, or be deformed due to rickets, or possibly have other diseases that would shorten their lives, or make them less fertile, or less able to find a mate and pass on genetics. However, if the environment provided enough vitamin D through food (such as in fish like salmon), darker-skinned people like the Inuits could survive. Maybe not in Norway, but in Alaska. And darker-skinned people could survive in the Mediterranean; and even darker-skinned people could survive in the equator and below. Lighter-skinned people might have succumbed to too much sun exposure, died of skin cancer, or perhaps died of other diseases related to too much sun in Africa, India, Asia, etc. Natural selection, driven largely by vitamin D sufficiency or deficiency, when combined with geographic dispersion, could account for the so-called races we see. And, vitamin D could possibly account for some of the maternal and neonatal disparities we see that are marked as racial differences. What if women could improve their own health, and that of their children, by making sure that they increase their intake of vitamin D, whether through food, vitamins, or sunshine?
Even with all the studies I’ve listed above, I’d like to see other, larger studies, which explore more aspects of health (particularly pregnancy, birth and postpartum), which really put vitamin D under the microscope. Are there seasonal trends to diseases, and poor outcomes (high blood pressure, pre-eclampsia, C-sections, inductions, etc.) that might be related to vitamin D and sunshine? We see racial trends in America, which obviously could be related to vitamin D — someone of my skin tone needs much less sunshine exposure than darker women, but more exposure than lighter women. Are there geographic trends, with certain diseases occurring more frequently, or worse, in the northern areas of the country, that tend to get less sunshine? And they’re colder, so people are more likely to be bundled up even if the sun is shining in winter. What if it’s something as simple as getting more vitamin D to women who don’t get enough? Maybe there’s quite a bit of truth to the ditty, “Open up your heart and let the sunshine in.” Food (salmon, tuna, milk) for thought…