High Na intake and chronically elevated cortisol levels are independently associated with the development of chronic diseases. In adults, high Na intake is associated with high levels of urinary cortisol. We aimed to determine the association between urinary Na and K and urinary cortisol in a cross-sectional sample of Australian schoolchildren and their mothers. Participants were a sample of Australian children (n 120) and their mothers (n 100) recruited through primary schools. We assessed Na, K, free cortisol and cortisol metabolites in one 24 h urine collection. Associations between 24 h urinary electrolytes and 24 h urinary cortisol were assessed using multilevel mixed-effects linear regression models. In children, urinary Na was positively associated with urinary free cortisol (β=0·31, 95 % CI 0·19, 0·44) and urinary cortisol metabolites (β=0·006, 95 % CI 0·002, 0·010). Positive associations were also observed between urinary K and urinary free cortisol (β=0·65, 95 % CI 0·23, 1·07) and urinary cortisol metabolites (β=0·02, 95 % CI 0·03, 0·031). In mothers, urinary Na was positively associated with urinary free cortisol (β=0·23, 95 % CI 0·01, 0·50) and urinary cortisol metabolites (β=0·008, 95 % CI 0·0007, 0·016). Our findings show that daily Na and K intake were positively associated with cortisol production in children and their mothers. Investigation of the mechanisms involved and the potential impact of Na reduction on cortisol levels in these populations is warranted.

Pomegranate juice (PJ; also known as pomegreat pure juice) provides a rich and varied source of polyphenolic compounds that may offer cardioprotective, anti-atherogenic and antihypertensive effects. The aim of this study was to investigate the effect of PJ consumption on glucocorticoids levels, blood pressure (BP) and insulin resistance in volunteers at high CVD risk. Subjects (twelve males and sixteen females) participated in a randomised, placebo-controlled cross-over study (BMI: 26·77 (sd 3·36) kg/m2; mean age: 50·4 (sd 6·1) years). Volunteers were assessed at baseline, and at weeks 2 and 4 for anthropometry, BP and pulse wave velocity. Cortisol and cortisone levels in urine and saliva were determined by specific ELISA methods, and the cortisol/cortisone ratio was calculated. Fasting blood samples were obtained to assess plasma lipids, glucose, insulin and insulin resistance (homeostasis model assessment of insulin resistance). Volunteers consumed 500 ml of PJ or 500 ml of a placebo drink containing a similar amount of energy. Cortisol urinary output was reduced but not significant. However, cortisol/cortisone ratios in urine (P = 0·009) and saliva (P = 0·024) were significantly decreased. Systolic BP decreased from 136·4 (sd 6·3) to 128·9 (sd 5·1) mmHg (P = 0·034), and diastolic BP from 80·3 (sd 4·29) to 75·5 (sd 5·17) mmHg (P = 0·031) after 4 weeks of fruit juice consumption. Pulse wave velocity decreased from 7·5 (sd 0·86) to 7·44 (sd 0·94) m/s (P = 0·035). There was also a significant reduction in fasting plasma insulin from 9·36 (sd 5·8) to 7·53 (sd 4·12) mIU/l (P = 0·025) and of homeostasis model assessment of insulin resistance (from 2·216 (sd 1·43) to 1·82 (sd 1·12), P = 0·028). No significant changes were seen in the placebo arm of the study. These results suggest that PJ consumption can alleviate key cardiovascular risk factors in overweight and obese subjects that might be due to a reduction in both systolic and diastolic BP, possibly through the inhibition of 11β-hydroxysteroid dehydrogenase type 1 enzyme activity as evidenced by the reduction in the cortisol/cortisone ratio. The reduction in insulin resistance might have therapeutic benefits for patients with non-insulin-dependent diabetes, obesity and the metabolic syndrome.

The major glucocorticoid in man, cortisol, plays important roles in regulating fuel metabolism, energy partitioning and body fat distribution. In addition to the control of cortisol levels in blood by the hypothalamic–pituitary–adrenal axis, intracellular cortisol levels within target tissues can be controlled by local enzymes. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyses the regeneration of active cortisol from inert cortisone, thereby amplifying cortisol levels and glucocorticoid receptor activation in adipose tissue, liver and other tissues. 11β-HSD1 is under complex tissue-specific regulation and there is evidence that it adjusts local cortisol concentrations independently of the plasma cortisol concentrations, e.g. in response to changes in diet. In obesity 11β-HSD1 mRNA and activity in adipose tissue are increased. The mechanism of this up-regulation remains uncertain; polymorphisms in the HSD11B1 gene have been associated with metabolic complications of obesity, including hypertension and type 2 diabetes, but not with obesity per se. Extensive data have been obtained in mice with transgenic over-expression of 11β-HSD1 in liver and adipocytes, targeted deletion of 11β-HSD1, and using novel selective 11β-HSD1 inhibitors; these data support the use of 11β-HSD1 inhibitors to lower intracellular glucocorticoid levels and treat both obesity and its metabolic complications. Moreover, in human subjects the non-selective ‘prototype’ inhibitor carbenoxolone enhances insulin sensitivity. Results of clinical studies with novel potent selective 11β-HSD1 inhibitors are therefore eagerly awaited. The present article focuses on the physiological role of glucocorticoids in regulating energy partitioning, and the evidence that this process is modulated by 11β-HSD1 in human subjects.