Circadian clock desynchronisation and metabolic syndrome.

There is emerging evidence in the literature to suggest that disruption of the normal circadian rhythm (sleep-wake cycle signalling) is a potential risk factor to explain the increased incidence of metabolic syndrome. Over the last century, obesity, diabetes and other components of metabolic syndrome have been on the rise. On the other hand, the amount of sleep has decreased from an average of 6-8 h per night. Furthermore, the quality of sleep has declined with more individuals voluntarily decreasing their amount of sleep to work or enjoy leisure activities. Over the last decade, researchers have examined the relationship between disruption in human circadian system and the emergence of symptoms related to metabolic syndrome. Indeed, epidemiological studies suggest a relation between sleep duration and diabetes and obesity. Moreover, experimental animal and human studies suggest such a relation. These studies propose optimum sleep duration of 7-8 h per night to avoid circadian rhythm disruption and suggest that sleep disturbance, whether iatrogenic or disease-related, should be considered as a risk factor for metabolic syndrome, and be addressed. This field is in its infancy and further understanding of specific pathophysiological pathways of circadian desynchronisation will help in developing novel preventive and therapeutic strategies.

Primary hyperparathyroidism and vitamin D in African Americans.

OBJECTIVES: Vitamin D deficiency is more common in African Americans than in the general population or other ethnicities. Vitamin D deficiency also occurs more frequently in patients with primary hyperparathyroidism (PHPT) than in the general population. Currently, the limited data on vitamin D deficiency in African Americans with primary hyperparathyroidism (PHPT) is inconsistent as to whether the vitamin D deficiency observed in PHPT is yet even more pronounced in Africans with PHPT relative to non-African Americans with PHPT. METHODS: On the basis of biochemical, radiological, and surgical (adenoma weight) parameters, African Americans have been reported to have a more severe form of PHPT than non-African Americans. However, comparative clinical manifestations of PHPT in African Americans have not been well described. RESULTS: Current guidelines recommend vitamin D repletion in mild, asymptomatic PHPT when levels of 25-hydroxyvitamin D are less than 20 ng/mL. Studies that reported vitamin D repletion with ergocalciferol or cholecalciferol in PHPT have not stratified data according to ethnicity. Discrepancies therefore exist between repleting vitamin D in African Americans who may potentially have a more severe PHPT profile, but simultaneously a more pronounced vitamin D deficiency. CONCLUSION: Effectively designed clinical trials are necessary to evaluate the indications, efficacy, and safety of vitamin D in African Americans with PHPT.