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Shading the sunshine vitamin

Just a few weeks ago, the nutrition community in Ireland gathered in the small town of Limavady in Northern Ireland to lay to rest one of ours, the late Dr Julie Wallace, an outstanding academic at the University of Ulster. Julie was young and in the prime of her scientific career which centered around vitamin D, the topic of this week’s blog and I will draw on a very recent paper of Julie’s in outlining what vitamin D does and doesn’t do. The main function of vitamin D is to facilitate the absorption of calcium from the gut, and then to facilitate its transport from blood into bone cells where it is used in bone growth. The earliest indication of vitamin D deficiency is rickets in children where their normal bone growth is impaired due to inadequate calcium levels, directly arising from poor vitamin D status. When expert committees sit down every so often to pour over the scientific literature to come up with dietary recommendations that ultimately find their way to your packet of Cornflakes, they usually leave vitamin D to the last. That’s because vitamin D is the “sunshine” vitamin. Every cell in the human body makes cholesterol for its own needs and one of the building blocks of cholesterol is acted on by UV light in skin cells leading ultimately to blood vitamin D. In effect, the impact of sunshine on the body’s vitamin D status was generally held by these committees to far outweigh dietary sources, thus downgrading its nutritional importance.

Then, out of nowhere, vitamin D began to climb up the popularity ratings in human nutrition. Firstly, the bizarre finding of inadequate blood levels of vitamin D in sun drenched Australia, began to raise concerns among nutritionists that over-zealous protection from sunrays to reduce the risk of skin cancer might in fact have an unexpected adverse effect. The Aussies developed a major communications programme around “Slip, Slop, Slap” (slip on long sleeved clothing, slop on sunscreen and slap on a hat). Australia has the highest level of skin cancer in the world and their cancer authorities recommend that fair skinned people can get enough vitamin D in summer from a few minutes of sunlight on their face, arms and hands before 10 am or after 3 pm on most days of the week.

This downgrading of vitamin D by the cancer specialists, began to conflict with new findings of a potential role of vitamin D in heart disease.  A significant body of data had begun to emerge ten or more years ago, linking low vitamin D status to the adverse effects of obesity, specifically the “metabolic syndrome” (insulin resistance, impaired glucose function, high blood lipid level and high blood pressure). The vast majority of these studies were “observational” meaning that in an available cohort, people with the metabolic syndrome had generally speaking lower levels of blood vitamin D. Of course, this cannot prove cause and effect. For example, people with the metabolic syndrome are overweight or obese and it could be that obesity was causing the low vitamin D levels and not the other way round. Indeed, that is exactly what a very recent paper from the late Julie Wallace shows and of course it makes intuitive sense
. Vitamin D is a fat-soluble so it prefers a fatty environment than a watery one. Thus the more fat we lay down, the more vitamin D wants to move from blood, which is a watery tissue to fatty tissue. In effect, fat people dilute their blood vitamin D levels raising the question as to whether the overweight and obese need higher than average vitamin D recommendations.

Thus the putative link between vitamin D and the metabolic syndrome and obesity is not looking so good. The only real test comes from an intervention study and myself and my colleagues here in UCD led such a study along with our collaborators in UCC. We gave 160 subjects either a reasonable dose of vitamin D (shown in previous studies to raise blood vitamin D levels within 4 weeks) or a placebo over a 4 week period and we completed this study in two phases: in the sprong just after te darkest part of the year and in Autumn, just after the sunniest part. Vitamin D levels rose in the group given vitamin D but there was no effect on any one of the 14 blood markers of the metabolic syndrome that we measured.  We then decided to rank the subjects into those with very low and very high initial levels of blood vitamin D to see if we could find an effect at the extremes. We didn’t. We then moved into new territory for this type of research using a statistical technique known a cluster analysis. Effectively, you say to the computer (You know that I know that you don’t actually speak to computers so get metaphoric please) to sort the subjects out into groups according to our 14 blood markers of the metabolic syndrome such that subjects within a cluster share a common profile and the different clusters are quite different from one another. We then asked if any one of these clusters responded to vitamin D therapy and one did. It was characterised by low levels of vitamin D in blood AND high levels of two special hormones released into blood from adipose tissue (resistin and adiponectin).
So our data would suggest that there is a subset of the population who do show quite a dramatic reduction in the adverse effects of obesity in response to vitamin D.

This is an issue that will remain on the agenda for some time to come given the intense and opposing views on this topic. What the data does show is (a) that one well designed intervention study is worth a thousand observational studies and (b) future intervention studies will have to classify people into groups which balance not just age, weight, sex and so forth but their genetic and metabolic sensitivity to the intervention. The future just got personal.


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