The Epidemiology of Vitamin D

22 January 2012

Interview with

Elina Hypponen, University College London

Chris -   Up first this week is University College London Reader in Epidemiology and Public Health, Elina Hypponen; so how deficient are we?

Elina -  I think we are pretty deficient especially at this time of year.  Everything of course depends on which thresholds we use to define vitamin D deficiency.  If we consider what many scientists nowadays call the optimum concentrations, up to 90% of us have serum levels that are lower than that.

Chris -   So where does the majority of the vitamin D that's washing around in my 90% deficient body currently come from?

Elina -   Well currently, it only comes from oily fish that you might be eating because that's the main dietary source in the UK diet.  We currently don't have any meaningful food fortification strategies which leaves the UK diet fairly deficient in vitamin D.  During other times of year, most notably in the summer, we get most of the vitamin D through sunlight induced synthesis in the skin, but at the moment, there is no sunlight induced synthesis because the suns rays don't reach the Earth at the right angle to induce any synthesis in the skin.

the sunChris -   So how does that process actually take place?  What is the sunlight doing in the skin to make the vitamin D?

Elina -   It converts the vitamin D precursor that is present in the skin to provitamin D which then can be metabolised further to vitamin D and active metabolites.

Chris -   Is it any aspect of light or is it specifically one colour of light that does that best?

Elina -   It's a certain wavelength of UVB radiation.

Chris -   You actually need to see UVB in order to do it?

Elina -   That's right.

Chris -   What times of year do we get to the point where actually the sunlight has not got enough UVB in it to make the vitamin D we need?

Elina -   When we look at the population studies, we see a very clear, beautiful pattern in serum 25(OH)D concentrations which are the marker for vitamin D nutritional or vitamin D status in general.  If you look at those, the concentrations typically are at their highest around September time which is reflecting the synthesis during the whole of the summer.  But from October onwards, there starts to be a very steady decline in concentration and they go down until March.  After which, the concentration starts slightly to rise again and that's a very, very strong pattern that we can see in the UK.  

Chris -   I saw an advert in Australia when I was there and it said, "If you are shorter than your shadow then you're probably not making enough vitamin D."

Elina -   Yeah, I think that's a nice rule of thumb.

Chris -   In other words, when we've got short days in winter, we just haven't got enough light input.  So what sorts of complications and consequences are there of the population, having this vitamin D deficiency?

Elina -   Sometimes, even for a researcher who is working in the field, it can be quite overwhelming the amount of health outcomes that are associated with vitamin D.  It starts from bone health but then extends to more or less any possible chronic disease as well as infectious diseases.  For me, it's always been quite comforting, to think about the vitamin D receptors which are required for the mediation of the hormonal actions of vitamin D.  They are present all over the body, so they are in major organs such as the brain, heart, pancreas, skin, also in pregnancy-specific tissues such as the placenta and the uterine lining.  If there is a receptor for a hormone, then most likely that hormone has, or at least has had, some sort of influence on the function or metabolism in that body.

Chris -   You said that the vast majority of the population are going to be getting quite vitamin D deficient as the winter progresses.  So come March, what are the consequences for the average person in the population?  What diseases tend to rear their ugly heads or become more common as a consequence of this?

Elina -   In population studies, we see associations with diabetes markers, we see increases in blood pressure, lung function is improved after certain points.  Various types of consequences are potential.  The problem is that the causality underlying many of these associations hasn't been proven.  The randomised trials have given very good evidence for outcomes such as osteoporosis and others which are related to bone health and more recently, there was the Cochrane Review which is a meta-analysis of all randomised controlled trials which showed that vitamin D supplementation was associated with an overall 6% of reduction in mortality risk.  So there are various types of potential outcomes but there is much for us to learn.

Chris -   What about the disease that the guy we're going to be speaking with next - George Ebers,  he works on multiple sclerosis - What about the association with that?

Elina -   Well I haven't personally worked that much with multiple sclerosis but I have worked more with type 1 diabetes and that's really what initially sets me to become interested in vitamin D.  We did a study using a birth cohort from Northern Finland which was initiated in the 1960s when they used to have this policy of giving very high doses of vitamin D supplementation to infants.  They gave 2,000 international units which is 5 times more than currently recommended to all infants, or at least that was the recommendation.  When we looked at the association between the vitamin D supplementation in infants and their subsequent risk of type 1 diabetes, there was really a strikingly strong reduction.  So the risk was 80% lower for those infants who had received vitamin D supplementation compared to those who hadn't.  There was also independent evidence for a dose dependent effect, so that when we only looked at those children who all had received vitamin D supplementation, the association was stronger the higher the dose had been.  That was a very striking indication from an observational study.  Type 1 diabetes is very closely related to multiple sclerosis because they are both autoimmune conditions and many of the etiological pathways would apply equally to both of them.

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