Vitamin D

Vitamin D

There are only a few natural dietary sources of vitamin D: oily fish (salmon, mackerel), fish liver oils, eggs and liver. Plant foods are poor sources of vitamin D.  Some foods are fortified with vitamin D, including certain breakfast cereals, margarines, milks, infant formulas and orange juices. 

Vitamin D can be synthesised in the skin from exposure to UVB rays in sunshine.  However, the ability to synthesise vitamin D is dependent on a variety of different factors, such as the season, latitude, skin pigmentation and clothing.   Northern Europe lies at a latitude between 40-60ºN, with Cork at a latitude of 51ºN.  In these regions, from October to March, the sun is not strong enough to ensure cutaneous synthesis of vitamin D ( Webb et al, 1988 ).  For this reason, people in northern European countries, such as Ireland, achieve their highest levels of vitamin D towards the end of the summer and have their lowest vitamin D concentrations towards the end of winter and beginning of spring ( Hill et al, 2008 ).

The colour of a person’s skin can influence the amount of vitamin D produced from sunshine.  Melanin is the pigment that gives skin a darker colour; it is a natural sun-block, so people with darker skin produce less vitamin D with the same sunlight exposure. Clothing and sunscreen lotions also block UVB rays from reaching the skin, decreasing cutaneous synthesis of vitamin D.

Vitamin D recommendations in Ireland, UK, EU, America and Australia/New Zealand (µg/day).

 

 

 

Age Category

 

 

 

Ireland RDA1

 

 

 

UK RNI2

 

 

 

EU PRI3

 

 

 

America AI4

 

 

 

Australia/New Zealand

 

NRV5

 

 

 

 

 

0-6 mths

 

 

 

8.5*

 

 

 

 

 

 

 

 

 

5

 

 

 

5

 

 

 

7-12 mths

 

 

 

7*

 

 

 

 

 

 

10-25

 

 

 

5

 

 

 

5

 

 

 

1-3 y

 

 

 

10

 

 

 

 

 

 

10

 

 

 

5

 

 

 

5

 

 

 

4-6 y

 

 

 

0-10

 

 

 

 

 

 

0-10

 

 

 

5

 

 

 

5

 

 

 

7-10 y

 

 

 

0-10

 

 

 

 

 

 

0-10

 

 

 

5

 

 

 

5

 

 

 

11-14 y

 

 

 

0-15

 

 

 

 

 

 

0-15

 

 

 

5

 

 

 

5

 

 

 

15-17 y

 

 

 

0-15

 

 

 

 

 

 

0-15

 

 

 

5

 

 

 

5

 

 

 

18-50 y

 

 

 

0-10

 

 

 

 

 

 

0-10

 

 

 

5

 

 

 

5

 

 

 

51-64 y

 

 

 

0-10

 

 

 

 

 

 

0-10

 

 

 

10

 

 

 

10

 

 

 

65-70 y

 

 

 

10

 

 

 

 

 

 

10

 

 

 

10

 

 

 

10

 

 

 

>70 y

 

 

 

10

 

 

 

 

 

 

10

 

 

 

15

 

 

 

15

 

 

 

Pregnancy

 

 

 

10

 

 

 

10

 

 

 

10

 

 

 

5

 

 

 

5

 

 

 

Lactation

 

 

 

10

 

 

 

 

 

 

10

 

 

 

5

 

 

 

5

 

 

 

1 Food Safety Authority of Ireland, 1999; 2UK Department of Health, 1998; 3Scientific Committee of Food, 1993; 4Institute of medicine, 1997;5National Health and Medical Research Council, 2005; *Department of Health, 1991

 

 

 

 

 

 

Functions of vitamin D

A primary function of vitamin D is maintaining calcium concentrations within an optimal narrow range.  If circulating calcium concentrations are low, parathyroid hormone (PTH) is secreted and converts 25(OH)D to the active 1,25(OH)2D.  Increases in 1,25(OH)2D normalise serum calcium at three sites:

  • by enhancing dietary calcium absorption in the intestine

  • by increasing urinary calcium re-absorption in the kidney

  • by mobilising calcium from bone

Vitamin D has many other important functions not related to calcium, including:

  • cell differentiation and proliferation

  • glucose metabolism

  • immune regulation

Absorption and Metabolism of vitamin D

Vitamin D is a fat-soluble vitamin and is passively absorbed into the body with dietary fats, such as long chain fatty acids (LCFA's). Vitamin D absorption mainly occurs in the small intestine and is influenced by the content of the intestine, for example the presence of bile salts. Approximately 60-90% of vitamin D is absorbed.  In times of depletion, vitamin D is reabsorbed in the large intestine to prevent any unnecessary loss from the bile, as bile is the primary method for vitamin D excretion. After absorption in the small intestine, vitamin D is transported to all sites in the body.

Both cutaneous and dietary-derived vitamin D are transported to the liver where vitamin D is hydroxylated to 25-hydroxyvitamin D [25(OH)D]. This is an intermediate form of vitamin D and is used as a marker for measuring vitamin D status. The second hydroxylation step occurs in the kidney, where 25(OH)D is converted to 1,25-dihydroxyvitamin D [1,25(OH)2D; calcitriol].  This is the active form of vitamin D and is vital for numerous functions in the body. Non-hydroxylated 25(OH)D is stored in adipose tissue or further metabolised and excreted in bile.

Vitamin D deficiency is a global health issue, potentially resulting in  rickets in children and  osteomalacia or  osteoporosis  in adults. Concentrations of serum 25(OH) D below 100nmol/L have been linked to an increased risk of chronic diseases such as  CVD  certain cancers , certain inflammatory related diseases  and  diabetes  Serum 25(OH)D concentration is the generally accepted biomarker of vitamin D status, which is the major form of circulating vitamin D in the body. In general, vitamin D deficiency has been defined as 25(OH)D concentrations less than 10-25nmol/L.  Although concentrations ranging from >25-100nmol/l have been classified as being sufficient, concentrations of >50nmol/l or >80nmol/l are the most commonly used values for sufficiency ( Lips et al, 2004  Heaney, 2005 ).  Studies are ongoing to determine what thresholds of 25(OH)D are most appropriate to denote sufficiency in population groups.


Vitamin D toxicity is extremely rare.  Excessive sunlight exposure cannot cause vitamin D toxicity, as there is a limited ability by the skin to produce vitamin D ( Holick, 2004 ). The toxic threshold for vitamin D consumption is unknown but a daily dietary intake of up to 50ug is considered safe. Extreme intakes of vitamin, in the range of >250ug/d, has been found to cause adverse effects such as nausea, vomiting, poor appetite, constipation, weakness and weight loss.  The main symptom of vitamin D toxicity is hypercalcemia, primarily resulting from intestinal calcium hyperabsorption and to a lesser degree from calcium release from the bone ( Zittermann, 2003 ). Vitamin D toxicity can cause other serious adverse outcomes such as elevated serum calcium, which can result in severely high blood pressure and calcification of soft tissue such as the kidneys, heart, lungs and blood vessel walls. Such high circulating levels are generally reached only by excessive dietary intake and supplement use. However, such cases are extremely rare and there is no link between vitamin toxicity and commonly consumed foods.



There are many methods used to measure 25(OH)D concentrations.  At UCC, 25(OH)D is measured in serum using an enzyme linked immunosorbent assay ().  The quality and accuracy of the serum 25(OH)D analysis in UCC is assured on an ongoing basis by participation in the vitamin D external quality assessment scheme (DEQAS).

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