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Vitamin D And The Prevention Of Rickets Health Essay

In recent years, Vitamin D has become an extensively researched and documented vitamin. Recent growing evidence suggests that vitamin D deficiency may be a risk factor for the development of many chronic diseases, including autoimmune conditions, cardiovascular diseases and cancer (McGrath, 2001). However, evidence for the use of Vitamin D in the prevention of rickets is irrefutable. This essay aims to address the role of vitamin D in the prevention of rickets and to assess the adequacy of vitamin D status in the prevention of rickets in Northern European countries. In particular, the problems associated with acheiveing an adequate maternal and infant vitamin D status in such countries will be discussed.

Association between Vitamin D and the Prevention of Rickets

The main role of Vitamin D is to aid in the control of calcium and phosphate levels in the blood. When vitamin D deficiency occurs, only 10-15% of dietary calcium and 50-60% of dietary phosphorus are absorbed (Bouillon et al, 2001). The subsequent decrease in serum-ionized calcium levels is immediately recognised by the calcium sensor in the parathyroid glands, that respond through the increased production and secretion of parathyroid hormone (PTH). To achieve calcium and phosphate homeostasis in the blood, the PTH causes calcium and phosphate, the main minerals in bone, to be released from the bones into the blood stream (Holick, 2006).

Rickets is a preventable childhood bone disorder, whereby defective mineralisation at the epiphyseal growth plate occurs, affecting bone development (Kumar et al,2012). The epiphyseal cartilage continues to grow but is not replaced by bone matrix and mineral, causing the bones to become painful, soft, weak and malformed, which can lead to bone deformities (NHS, 2012). Many factors can result in defective mineralisation of the osteoid, the organic matrix of bone. For normal mineralisation, adequate levels of vitamin D, calcium and phosphate, adequate activity of alkaline phosphatase, a normal pH at the osteoid surfaces and normal osteoid composition are all necessary (Kumar et al,2012). The most common cause of rickets is vitamin D deficiency (NHS, 2012). Vitamin D has been used to treat and prevent rickets long before it was identified and isolated in 1937. Cod-liver oil is recorded to have been prescribed for the treatment of rickets as early as in 1824 (Wolf, 2004).

As rickets represents the extreme end of the spectrum of vitamin D deficiency, a state of deficiency occurs months before rickets is obvious on physical examination (FSAI, 2007). Early signs of deficiency include growth failure, lethargy and irritability (Mølgaard et al, 2003). The standard blood test to measure vitamin D status is a measure of serum 25hydroxyVitaminD. Circulating levels of 25(OH)D3 are the product of dietary intake and

exposure to sunlight. The optimal vitamin D level is defined as a level of vitamin D intake or synthesis of 1α,25(OH)2D3 that is high enough to maintain calcium levels (Need, 2006). Values of 25(OH)D >50 nmol/L may be considered acceptable, 25-50 as vitamin D insufficient, 12.5-25 as deficiency and <12.5 as serious deficiency (Pedersen, 2008). Plasma 25(OH)D concentration in rickets ranges from undetectable to approximately 20nmol/l (SACN, 2007).

The Sun as a Source of Vitamin D for Infants in Northern Europe

The skin has a high capacity to synthesize vitamin D. Without fortification, only certain foods such as fatty fish contain more than low amounts of vitamin D. Therefore, many children will depend entirely on sun exposure to obtain sufficient vitamin D to prevent rickets. However, if sun exposure is low, the production of the vitamin in the skin can be insufficient to provide adequate stores in the body (Mølgaard et al, 2003). Rickets was a major, devastating health consequence of the Industrial Revolution which resulted from the increased smog over urban areas, preventing sun exposure. Early in the 20th century more than 90 percent of children in Northern Europe showed evidence of this bone deforming condition. The encouragement of sensible sun exposure and the fortification of milk with vitamin D resulted in almost complete eradication of the disease (Holick, 2010)

Despite the skin’s ability to synthesise vitamin D using the sun’s UV radiation, depending on this source of vitamin D alone is not appropriate for infants, especially those living in areas of high latitudes, such as in Northern Europe. Infants’ skin is extremely sensitive to the sun and particularly vulnerable to the harmful effects of UV radiation. Excessive sun exposure in children is likely to contribute to skin cancer in later life (WHO, 2009). It is hence recommended that infants should not be exposed to direct sunlight (HSE, 2012).

At latitudes above 35˚, very little vitamin D3 is synthesised by the skin between the months of November and March (Hollis, 2005), as the path length for the UVB photons to travel is increased, due to the angle of the sun (Holick, 2006). At the 61° latitude in Norway, sunlight does not promote vitamin D synthesis during the 6 winter months, with mean serum levels of 25(OH)D3 around 57nmol/l (Brustad et al, 2004).

Maternal Vitamin D Status

Although it is recommended that infants should avoid exposure to sunlight, the decrease in possible exposure to the UVB photons in nothern latitudes still has an impact on infants’ vitamin D status and the incidence of rickets. Infants vitamin D stores at birth are solely dependant on maternal vitamin D status, of which they only obtain 50-60% of. In northern Europe, maternal status is frequently inadequate to meet the infant’s requirements (Wagner et al, 2008). Vitamin D insufficiency is common in women of childbearing age, with often very low reported intakes. In Ireland, women of childbearing age have an intake of 3.5ug/day (Slan, 2007). One survey found that only 1% of women surveyed reported taking a vitamin D supplement during pregnancy (Tarrant et al, 2011). Not only does this affect the infant’s stores at birth, if exclusively breastfed without supplementation, the infant is at a very high risk of vitamin D deficiency and the development of rickets, as breast milk is commonly low in vitamin D, containing approximately 25IU/litre (Dawadu et al, 2012). This occurs at a time when rapid growth and development is occuring during the first 12 months of life, a time crucial for the healthy development of the skeletal system as ossification of the bones is occuring (HSE, 2010).

Approach to Preventing Vitamin D Deficiency in Northern Europe

The question remains as to whether Northern European countries have the ability to satisfactorily meet the vitamin D status required to prevent rickets. Serum 25hydroxyVitaminD is an excellent marker of body stores that would ensure that all marginal maternal and infant vitamin D stauses would be noted and supplements recommended. The cost of this blood test is approximately £20 - £50 in the UK. Therefore it would be neither practical nor cost-effective to screen all mothers and infants for vitamin D deficiency, resulting in a population health approach being the best option to erradicate the problem, including fortification and supplementation. However, those with risk factors eg. infants who are exclusively breastfed, have dark skin, are premature or those taking anti-seizure medications, and symptoms of hypocalcaemia and D deficiency should receive this blood test. (NHS, 2011)

In Ireland, the HSE formulated a policy in 2010 whereby all infants between 0-12 months should receive a supplement containing 5 μg of vitamin D per day. This amount is considered adequate to maintain serum 25 OH D concentrations of greater than 27.5 nmol/L, which prevents rickets in the majority of children (Misra et al, 2008). Whether combined with breastmilk or infant formula fortified with vitamin D, 5 μg per day is considered to be a safe intake, as it is just one-fifth of the Tolerable Upper Intake Level with no risk of toxicity. (HSE, 2010)

In Norway, cod liver oil is recommended as a supplement for infants and toddlers between the ages of 0 and 2 years for it’s contribution to vitamin D status during the winter months. The recommended daily intake is according to the Nordic Nutrition Recommendations 2012, which is 10 μg/d for the age groups 6-24 months and 7.5ug for children aged two and older (Huotari et al,2008). This can be achieved through an increased intake of oily fish or through supplementation with cod liver oil. Studies were carried out to compare the average vitamin D intake from 2 year olds taking supplements versus those who weren’t. It was found that those taking supplements (38% of the population) had an average vitamin D intake of 6.1ug versus 2.8ug in those who were not taking supplements (Almadfa, 2009).

Mandatory fortification of fluid milks and margarines with vitamin D was introduced in Finland in 2003-2004. In Finnish 4-year olds, this was shown to increase serum concentrations of 25(OH)D from 54.7 before the introduction of fortification to 64.9 nmol/l (Piirainen, 2007). Another study carried out in 2008 showed the average intake of vitamin D in 1 year olds to be sufficient at 12.2ug/day plus or minus a standard deviation of 4.6ug (Kyttälä et al, 2008).

In the UK, the Department of Health recommend supplementation of 7-8.5ug per day to all children aged 6 months to 5 years, breastfed infants from one month if their mother has not taken vitamin D supplements throughout pregnancy and to formula fed infants when receiving less than 500ml of infant formula a day. 10ug per day is recommended for pregnant and lactating mothers (Davies et al, 2012). The National Diet and Nutrition Survey found the mean plasma 25(OH)D concentration for children 1.5-4.5 years was 68.1nmol/l. Plasma 25(OH)D concentration was below 25nmol/l in 1% of children, but a further 18% had marginal levels of 25-49 nmol/l (Gregory et al, 1995).

A resurgence of rickets has been recorded in recent years among ethnic minority groups in some Northern European countries, notably in the United Kingdom, the Netherlands, and Denmark. This tends to mainly be due to their dress and religion (Ashraf et al, 2002). In recent times, there are increasing numbers of dark skinned people living in Ireland also, who require greater amounts of ultraviolet light to produce vitamin D (FSAI, 2007).

Conclusion

It appears that although the pathophysiology of nutritional rickets and preventive measures are well recognised, the disease is not eradicated in industrialised countries (Thacher et al, 2006). It would seem reasonable to assume that not all cases of rickets may be documented and therefore the problem may be greatly underestimated. In Northern Europe, a number of factors contribute to the existance of nutritional rickets despite this knowledge. Although supplementation is greatly recommended for both breastfed and supplementary fed infants, compliance with these recommendations appears to be inadequate (Tarrant et al, 2011). The high latitude results in several months during the year where no vitamin D is being synthesised by the skin. The increase in dark skinned people living in Northern Europe has also been accountable for the increase in rickets, as the requirement for ultraviolet light to synthesise vitamin D is greater. Intake of vitamin D among women of child-bearing age is low across Northern Europe. Currently, vitamin D supplementation is not recommended by the WHO to pregnant and lactating women. As hypovitaminosis D in pregnancy greatly impacts on the sufficiency of infant vitamin D status, recommendations on vitamin D supplementation during pregnancy should be addressed (Tarrant et al, 2011).


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