Is obstructive sleep apnea associated with cortisol levels? A systematic review of the research evidence

a San Diego State University & University of California, San Diego, Joint Doctoral Program in Clinical Psychology, San Diego, UCSD Mail Code 0804, La Jolla, CA, United Statesb Department of Psychiatry, University of California, San Diego, CA, United StatesReceived 8 March 2011. Revised 21 May 2011. Accepted 23 May 2011. Available online 30 July 2011.View full text The pathophysiology of obstructive sleep apnea (OSA) has been associated with dysregulation of the hypothalamic pituitary adrenal (HPA) axis; however a relationship between OSA and altered cortisol levels has not been conclusively established. We conducted a systematic review using the PRISMA Guidelines based on comprehensive database searches for 1) studies of OSA patients compared to controls in whom cortisol was measured and 2) studies of OSA patients treated with continuous positive airway pressure (CPAP) in whom cortisol was measured pre and post treatment. Five electronic databases were searched along with the reference lists of retrieved studies. The primary outcomes were 1) differences in cortisol between OSA and control subjects and 2) differences in cortisol pre-post CPAP treatment. Sampling methodology, sample timing and exclusion criteria were evaluated. Fifteen studies met the inclusion criteria. Heterogeneity of studies precluded statistical pooling. One study identified differences in cortisol between OSA patients and controls. Two studies showed statistically significant differences in cortisol levels pre-post CPAP. The majority of studies were limited by assessment of cortisol at a single time point. The available studies do not provide clear evidence that OSA is associated with alterations in cortisol levels or that treatment with CPAP changes cortisol levels. Methodological concerns such as infrequent sampling, failure to match comparison groups on demographic factors known to impact cortisol levels (age, body mass index; BMI), and inconsistent control of variables known to influence HPA function may have limited the results.

prs.rt("abs_end");Obstructive sleep apnea; Cortisol; Continuous positive airway pressure; Systematic review

Figures and tables from this article:

Fig. 1. PRISMA trial flow used to identify studies for detailed analysis of cortisol in 1) patients with obstructive sleep apnea and healthy controls and 2) patients with obstructive sleep apnea before and after treatment with continuous positive airway pressure. AHI = Apnea hypopnea index; CPAP = Continuous positive airway pressure.

View Within ArticleTable 1. The 7 included studies of cortisol in patients with OSA versus controls.

Na = No information; OSA = Obstructive sleep apnea; BMI = Body mass index; AHI = Apnea hypopnea index; EDS = Excessive daytime sleepiness; w = with; wo = without.

View Within ArticleTable 2. The 8 included studies of cortisol in patients with OSA treated with CPAP.

Na = No information; OSA = Obstructive sleep apnea; BMI = Body mass index; AHI = Apnea hypopnea index; EDS = Excessive daytime sleepiness; SE = Standard error of the mean; w = with; wo = without.

View Within ArticleCopyright © 2011 Elsevier Ltd. All rights reserved.

prs.rt('data_end');

View the original article here

Is obstructive sleep apnea associated with cortisol levels? A systematic review of the research evidence

a San Diego State University & University of California, San Diego, Joint Doctoral Program in Clinical Psychology, San Diego, UCSD Mail Code 0804, La Jolla, CA, United Statesb Department of Psychiatry, University of California, San Diego, CA, United StatesReceived 8 March 2011. Revised 21 May 2011. Accepted 23 May 2011. Available online 30 July 2011.View full text The pathophysiology of obstructive sleep apnea (OSA) has been associated with dysregulation of the hypothalamic pituitary adrenal (HPA) axis; however a relationship between OSA and altered cortisol levels has not been conclusively established. We conducted a systematic review using the PRISMA Guidelines based on comprehensive database searches for 1) studies of OSA patients compared to controls in whom cortisol was measured and 2) studies of OSA patients treated with continuous positive airway pressure (CPAP) in whom cortisol was measured pre and post treatment. Five electronic databases were searched along with the reference lists of retrieved studies. The primary outcomes were 1) differences in cortisol between OSA and control subjects and 2) differences in cortisol pre-post CPAP treatment. Sampling methodology, sample timing and exclusion criteria were evaluated. Fifteen studies met the inclusion criteria. Heterogeneity of studies precluded statistical pooling. One study identified differences in cortisol between OSA patients and controls. Two studies showed statistically significant differences in cortisol levels pre-post CPAP. The majority of studies were limited by assessment of cortisol at a single time point. The available studies do not provide clear evidence that OSA is associated with alterations in cortisol levels or that treatment with CPAP changes cortisol levels. Methodological concerns such as infrequent sampling, failure to match comparison groups on demographic factors known to impact cortisol levels (age, body mass index; BMI), and inconsistent control of variables known to influence HPA function may have limited the results.

prs.rt("abs_end");Obstructive sleep apnea; Cortisol; Continuous positive airway pressure; Systematic review

Figures and tables from this article:

Fig. 1. PRISMA trial flow used to identify studies for detailed analysis of cortisol in 1) patients with obstructive sleep apnea and healthy controls and 2) patients with obstructive sleep apnea before and after treatment with continuous positive airway pressure. AHI = Apnea hypopnea index; CPAP = Continuous positive airway pressure.

View Within ArticleTable 1. The 7 included studies of cortisol in patients with OSA versus controls.

Na = No information; OSA = Obstructive sleep apnea; BMI = Body mass index; AHI = Apnea hypopnea index; EDS = Excessive daytime sleepiness; w = with; wo = without.

View Within ArticleTable 2. The 8 included studies of cortisol in patients with OSA treated with CPAP.

Na = No information; OSA = Obstructive sleep apnea; BMI = Body mass index; AHI = Apnea hypopnea index; EDS = Excessive daytime sleepiness; SE = Standard error of the mean; w = with; wo = without.

View Within ArticleCopyright © 2011 Elsevier Ltd. All rights reserved.

prs.rt('data_end');

View the original article here

Prenatal Factors influence Kwashiorkor: Evidence for the Predictive Adaptation Model

AppId is over the quota AppId is over the quota

Severe acute malnutrition in childhood manifests as oedematous (kwashiorkor, marasmic kwashiorkor) and non-oedematous (marasmus) syndromes with very different prognoses. Kwashiorkor differs from marasmus in the patterns of protein, amino acid and lipid metabolism when patients are acutely ill as well as after rehabilitation to ideal weight for height. Metabolic patterns among marasmic patients define them as metabolically thrifty, while kwashiorkor patients function as metabolically profligate. Such differences might underlie syndromic presentation and prognosis. However, no fundamental explanation exists for these differences in metabolism, nor clinical pictures, given similar exposures to undernutrition. We hypothesized that different developmental trajectories underlie these clinical-metabolic phenotypes: if so this would be strong evidence in support of predictive adaptation model of developmental plasticity.

We reviewed the records of all children admitted with severe acute malnutrition to the Tropical Metabolism Research Unit Ward of the University Hospital of the West Indies, Kingston, Jamaica during 1962–1992. We used Wellcome criteria to establish the diagnoses of kwashiorkor (n = 391), marasmus (n = 383), and marasmic-kwashiorkor (n = 375). We recorded participants’ birth weights, as determined from maternal recall at the time of admission. Those who developed kwashiorkor had 333 g (95% confidence interval 217 to 449, p<0.001) higher mean birthweight than those who developed marasmus.

These data are consistent with a model suggesting that plastic mechanisms operative in utero induce potential marasmics to develop with a metabolic physiology more able to adapt to postnatal undernutrition than those of higher birthweight. Given the different mortality risks of these different syndromes, this observation is supportive of the predictive adaptive response hypothesis and is the first empirical demonstration of the advantageous effects of such a response in humans. The study has implications for understanding pathways to obesity and its cardio-metabolic co-morbidities in poor countries and for famine intervention programs.

Posted in evolutionary medicine