11
Mar
2011
11
Mar
2011
We’re constantly warned of the damaging and ageing effect of the sun’s rays on our skin, but in avoiding sun exposure, could we be doing ourselves more harm than good?
Exposure to UVB radiation provides the mechanism for more than 90% of the vitamin D production in most individuals (Norval M, 2009) but wearing a sunscreen with an SPF as low as eight reduces the skin's production of vitamin D by an incredible 95% (Reichrath J, 2008).
Why Is Vitamin D So Essential?
Despite its name, vitamin D is actually a prohormone and is essential for numerous functions throughout the body. It plays a key role in calcium metabolism making it integral to bone health. (DeLuca HF, 2004). It’s also essential for healthy neuromuscular, cardiovascular and immune function, respiratory system function and cognitive function (Christakos S, 2013). Vitamin D is also vitally important to skin health as it is directly involved the proliferation and differentiation of keratinocytes. If adequate amounts of vitamin D are not available, epidermal cells cannot differentiate optimally. (Matsumoto K, 1991)
Deficiency – It’s More Common Than We Think
Vitamin D deficiency is more common than previously believed. The Centers for Disease Control and Prevention reported that the percentage of American adults with sufficient vitamin D levels (defined by 25(OH) D of at least 75 nmol/L) declined significantly between 1994 – 2001. Between 1988-1994, 60% of Caucasian Americans has sufficient vitamin D levels, this dropped to approximately 30% in 2001-2004 and from approximately 10% to 5% in African Americans during this same time (Kennel KA, 2010). This means that from 2001-2004, an astounding 70% of Caucasian Americans and 90-95% of African Americans were estimated to have insufficient vitamin D levels.
Vitamin D and Skin Type
An interesting point to note is that the darker a person’s skin type, the lower their ability to synthesise Vitamin D. Vitamin D3 is produced in skin through ultraviolet irradiation of 7-dehydrocholesterol. It is biologically inert and must be metabolized to 25-hydroxyvitamin D3 in the liver and then to 1alpha,25-dihydroxyvitamin D3 in the kidney before function (DeLuca HF, 2004).
An extract from the journal Science in 1967 states: In northern latitudes, there is a selection for white skins that allow maximum photoactivation of 7-dehydrocholesterol into vitamin D at low intensities of ultraviolet radiation. In southern latitudes, there is a selection for black skins able to prevent up to 95% of the incident ultraviolet from reaching the deeper layers of the skin where vitamin D is synthesized. (Loomis WF, 1967)
In a modern world where migration is common, people whose skin type has adapted to prevent excess vitamin D synthesis in their native, sunny environment are particularly prone to a deficiency when living in a sun-deprived country such as the UK. My client list comprises a diverse ethnic background. Muslim women who cover themselves for religious reasons are often found to be Vitamin D deficient. My Asian clients with Fitzpatrick IV-V skin type are also commonly deficient. That said, I have also seen plenty of Fitzpatrick Type I clients with low, or borderline vitamin D levels. Most of us spend a significant proportion of our time indoors meaning that regardless of skin type, anyone can be affected.
How Do We Assess Vitamin D Levels?
Vitamin D levels can be easily assessed using a simple blood test. Ingested and cutaneously produced vitamin D is quickly converted to 25(OH)D, but in serum, only a small fraction of 25(OH)D is converted to 1,25(OH)2D, its active metabolite. Therefore measuring the total 25(OH)D level is the best test to assess levels of vitamin D (Kurt A. Kennel).
I routinely test my client’s 25(OH)D levels through The Doctor’s Laboratory (TDL) but a number of laboratories offer this service. It can be done independently or as part of a more comprehensive vitamin and mineral screen. When possible I prefer to run a comprehensive micronutrient panel and then retest the specific deficient nutrients at two to three months post supplementation.
Deficiency is defined as a serum 25(OH)D level of less than 50 nmol per L. Insufficiency is defined as a serum 25(OH)D level of 50 to 75 nmol per L (Bordelon P, 2009). Of the last 20 clients that I have tested, six were deficient, six had suboptimal levels and just eight had optimal levels. Those with optimal levels were usually either supplementing or spent a significant amount of time abroad. Two of those who tested deficient had levels below 10nmol per L.
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