Reduced Sun Exposure Research Articles

Vitamin D levels in people with multiple sclerosis and community controls in Tasmania, Australia

Adequate 25(OH)D levels are required to prevent adverse effects on bone health. Population-based data on factors associated with 25(OH)D levels of people with MS have been lacking. To examine the prevalence and determinants of vitamin D insufficiency in a population-based sample of MS cases and controls, and to compare 25(OH)D status between MS cases and controls, taking into account case disability. We conducted a population based case-control study in Tasmania, Australia (latitude 41-43 degrees S) on 136 prevalent cases with MS confirmed by magnetic resonance imaging and 272 community controls, matched on sex and year of birth. Measurements included serum 25(OH)D, sun exposure, skin type, dietary vitamin D intake and disability including EDSS. A high prevalence of vitamin D insufficiency was found in MS cases and controls. Among MS cases, increasing disability was strongly associated with lower levels of 25(OH)D and with reduced sun exposure. Cases with higher disability (EDSS > 3) were more likely to have vitamin D insufficiency than controls (OR = 3.07 (1.37, 6.90) for 25(OH)D </= 40 nmol/l), but cases with low disability were not (OR = 0.87 (0.41, 1.86)). The strong associations between disability, sun exposure and vitamin D status indicate that reduced exposure to the sun, related to higher disability, may contribute to the high prevalence of vitamin D insufficiency found in this population-based MS case sample. Active detection of vitamin D insufficiency among people with MS and intervention to restore vitamin D status to adequate levels should be considered as part of the clinical management of MS.

Inaccuracies in self-reported histories of non-melanoma skin cancer

Non-melanoma skin cancer (NMSC) is a major cause of morbidity and health expenditure in Australia.1 Primary prevention of NMSC through reduced sun exposure has been widely promoted and seems to be reducing this burden.2 Secondary prevention aimed at reducing the increased risk (up to 15-fold) of subsequent lesions3,4 in patients following a first incident NMSC is an additional approach with the potential to reduce cost and morbidity. This letter reports on the findings of a pilot study undertaken to test the feasibility of recruiting patients with a first incident NMSC using the Tasmanian Cancer Registry (TCR). Accurate identification of subjects with a first NMSC is essential for studies investigating potentially modifiable risk factors for subsequent lesions. The TCR is the only Australian registry to record NMSC notifications. Individuals were selected

Poster 126: Rickets in a 13-year-old with cerebral palsy.

Setting: A tertiary care hospital. Patient: A 13-year-old boy with cerebral palsy (CP). Case Description: The patient presented with a 2-week history of difficulty with standing-pivot-transfers and headache, nausea, and vomiting. His medical history was as follows: preterm birth, intraventricular hemorrhage requiring a ventriculoperitoneal shunt, seizure disorder, and multiple orthopedic procedures. Physical examination showed an obese youngster with triplegic CP. He had clonus and demonstrated unusual muscle stiffness in his minimally involved arm during phlebotomy (tetany?) and a transient hemifacial spasm (spontaneous Chvostek’s sign?). His computed tomography scan was unchanged. Serum calcium was 5.4mg/dL (normal, 9.0–11.5mg/dL); ionized calcium was .69mmol/L (normal, 1.10–1.30mmol/L); and serum phosphorus was 3.3mg/dL (normal, 3.6–5.9mg/dL). An endocrine consultation was obtained. Additional labs included an elevated alkaline phosphatase (774IU/L; normal, 60–400IU/L); amylase (210IU/L; normal, 25–125IU/L); 1–25 dihydroxyvitamin D (10; reference range, 15–75); and intact parathyroid hormone with calcium (524pg/mL; normal, 10–65pg/mL). His calcium normalized over 2 weeks of treatment with intravenous infusions of calcium and oral calcium and vitamin D supplements. Simultaneously he regained lower-extremity strength for assisted transfers. Rickets were attributed to poor dietary habits (minimal milk intake), minimal sun exposure, and use of carbamazepine. Assessment /Results: New onset symptoms of weakness in this patient were due to previously undetected rickets, which resolved with appropriate treatment. Discussion: The clinical manifestations of rickets may not be recognized in older children and adults because symptoms can be subtle. There may be muscular weakness, limb pain, irritability, and listlessness. Conclusion: Rickets can present with weakness due to severe hypocalcemia. Patients may not develop symptoms until laboratory values are quite abnormal. Youngsters with significant mobility limitations may have reduced sun exposure. Youngsters with lactose intolerance, peculiar eating habits, or dark complexions may be at special risk.

Reduced sun exposure and tanning in children after 2 years of a school-based intervention (Australia).

This paper presents the results of the evaluation of measured suntan and parent-reported sun exposure in participating children after 2 years of the Kidskin study, a 5-year school-based sun protection intervention undertaken in Perth, Western Australia (1995-1999). The study involves three groups: a control, a "moderate", and a "high" intervention group. Participants were 5 or 6 years of age at the beginning of the study. Control schools received the standard Health Education curriculum, while intervention schools received a multicomponent intervention including a specially designed curriculum. Children in the high intervention group also received program materials over the summer vacation and were offered sun-protective swimwear at low cost. At the end of the second summer, suntan was measured and parents completed a questionnaire about their child's sun-related behavior. Children in the intervention groups--especially the high group--were less tanned at the end of the summer; this effect was greater for the back than for the forearms. These children were also reported to have received less sun exposure and made greater use of sun protection measures. Intensive school-based interventions can reduce tanning and reported sun exposure in children.

Longitudinal changes in serum 25-hydroxyvitamin D in older people

Cross-sectional studies have suggested that serum 25-hydroxyvitamin D (25OHD) levels decline with aging. We have examined this putative decline in a longitudinal study using participants in the New Mexico Aging Process Study. 25OHD levels were measured in participants in whom serum samples were available between 1980 to 1982 and 1989 to 1994 (37 men and 99 women). The available data for these visits included age, gender, and the date the sample was obtained. Questionnaires assessing physical activity and vitamin D intake were administered at the visits. A seasonal variation ( r = .25, P < .05) in 25OHD was demonstrated in the whole group of subjects. In 25 subjects who were not receiving vitamin D supplementation at either time and had samples obtained in the same season, both serum 25OHD ( P < .05) and physical activity ( P < .05) decreased over a mean period of 11.4 years. In 23 subjects who had samples obtained in the same season but used vitamin D supplements at both times, there was no change in serum 25OHD. Mean summer 25OHD levels did not change with the duration of study. On the other hand, the mean serum 25OHD declined with the duration of study when measured from winter to winter or spring to spring. Multiple regression analysis demonstrated that the month, activity level, vitamin D supplementation, and gender ( P < .001) were independent determinants of serum 25OHD levels. This study confirms that aging is associated with a reduction in serum 25OHD, and suggests that this decrease is a reflection of reduced sun exposure rather than aging per se. The reduction in serum 25OHD was the result of decreasing winter and spring 25OHD serum concentrations. It is clear that vitamin D supplementation can prevent the age-related decline in 25OHD levels.

Metabolic bone disease in gastrointestinal, hepatobiliary, and pancreatic disorders and total parenteral nutrition.

Privational vitamin D deficiency is assumed to be uncommon in the developed countries because of the routine fortification of foods with vitamin D. Malabsorption of vitamin D and calcium (especially in an environment of reduced sun exposure) therefore accounts for the majority of cases of metabolic bone disease seen in patients with various gastrointestinal disorders in the United States. Yet recognition of this often asymptomatic bone disease is unsatisfactory and frequently delayed for months or even years. This results in severe irreversible bone loss, putting patients at increased fracture risk for the remainders of their lives. As evident from the small number of published reports, it is obvious that little attention is given to understanding the pathogenesis and prevention of bone disease in patients with various gastrointestinal disorders. This review will summarize recent advances in the pathogenesis, prevention, and treatment of metabolic bone disease in patients with these disorders. We propose methods for identifying bone loss in such patients so that appropriate preventive measures can be instituted to avoid significant morbidity.

Sun Protection in Newborns

We investigated the effect of education on the sun exposure of newborns. Mothers of healthy newborns (n = 275) were enrolled in the spring of 1989 and interviewed by telephone in the fall of 1989. The mothers were divided into a control group, a low-level intervention group, and a high-level intervention group. Both the low-level and high-level interventions succeeded in reducing the amount of time the newborns were allowed to spend in direct sunlight. Both types of intervention also resulted in reduced sun exposure time for the mothers. Although the number of mothers who used sunscreen was approximately the same in all three groups, when sunscreen use was controlled for, the intervention groups spent significantly less unprotected time in the sun than the control group. The mothers and newborns in both intervention groups simply spent less time outdoors.

Vitamin D and bone health in the elderly

The state of vitamin D nutrition depends on synthesis in the skin under the influence of sunlight as well as on dietary intake. In European countries that do not fortify milk with vitamin D, reduced sun exposure is the major factor leading to a fall in body stores of vitamin D with age and to a high frequency of hypovitaminosis D in the elderly sick. In the US, because vitamin D is added to milk and the use of vitamin D supplements is more common, the dietary intake of vitamin D is relatively more important than in Europe, and the total vitamin D intake and body stores of vitamin D are generally higher. Nevertheless, body stores of vitamin D probably fall with age in the US as they do in Europe, and it is likely that some sick elderly persons in the US, especially among those confined to institutions, become vitamin D deficient. For several reasons, the vitamin D requirement increases with age, and a total supply of 15 to 20 micrograms/day (600 to 800 IU) from all sources is recommended. Special attention should be paid to persons most likely to need supplementation, such as the housebound, persons with malabsorption, and persons with interruption of the enterohepatic circulation. Osteomalacia, the bone disease produced by severe vitamin D deficiency, is less common in the US than in Europe, but subclinical vitamin D deficiency may contribute to the pathogenesis of hip fractures, both through increased liability to fall and through PTH-mediated bone loss. The extent to which vitamin D deficiency contributes to hip fractures in the US is unknown, and is an important area for future research. Excess intake of vitamin D or of its metabolites may result in hypercalcemia and extra-osseous calcification, particularly in arterial walls and in the kidney, leading to chronic renal failure. The dose of vitamin D that causes significant hypercalcemia is highly variable between individuals but is rarely less than 1000 micrograms/day. Smaller doses can cause hypercalciuria and nephrolithiasis and possibly impaired renal function. Vitamin D administration may raise plasma cholesterol but there is no convincing evidence that the risk of myocardial infarction is increased. The recommended total supply for the elderly of 20 micrograms/day is most unlikely to be harmful, except in patients with sarcoidosis or renal calculi.