Hair cortisol reduction and social integration enhancement after a mindfulness-based intervention in children.

BACKGROUND: Over recent decades, chronic stress at an early age has become a worrying health problem in children. We seek to evaluate an intervention involving mindfulness-based practices and prosocial activities in 7- to 8-year-old children. METHODS: Stress levels were determined using hair cortisol concentration (HCC), and social integration was measured by means of a sociogram. The program had previously proven to be effective in decreasing salivary cortisol levels and in favouring social integration in children. A total of 35 children participated in the study: 18 constituted the intervention group and 17 the wait-list group. In both groups, HCC and social integration were evaluated before and after the intervention conducted throughout an entire school year. RESULTS: The experimental group showed a significant reduction in HCC, as well as significant enhancement of social integration levels, whereas no changes were observed in the wait-list group. CONCLUSIONS: This is the first research to show that HCC, a reliable neuroendocrine indicator, decreased as a result of a mindfulness-based program. This successful outcome adds new evidence to previous findings regarding the reduction of chronic stress in children following participation in this program.

HIV-TB coinfection impairs CD8(+) T-cell differentiation and function while dehydroepiandrosterone improves cytotoxic antitubercular immune responses.

Tuberculosis (TB) is the leading cause of death among HIV-positive patients. The decreasing frequencies of terminal effector (TTE ) CD8(+) T cells may increase reactivation risk in persons latently infected with Mycobacterium tuberculosis (Mtb). We have previously shown that dehydroepiandrosterone (DHEA) increases the protective antitubercular immune responses in HIV-TB patients. Here, we aimed to study Mtb-specific cytotoxicity, IFN-γ secretion, memory status of CD8(+) T cells, and their modulation by DHEA during HIV-TB coinfection. CD8(+) T cells from HIV-TB patients showed a more differentiated phenotype with diminished naïve and higher effector memory and TTE T-cell frequencies compared to healthy donors both in total and Mtb-specific CD8(+) T cells. Notably, CD8(+) T cells from HIV-TB patients displayed higher Terminal Effector (TTE ) CD45RA(dim) proportions with lower CD45RA expression levels, suggesting a not fully differentiated phenotype. Also, PD-1 expression levels on CD8(+) T cells from HIV-TB patients increased although restricted to the CD27(+) population. Interestingly, DHEA plasma levels positively correlated with TTE in CD8(+) T cells and in vitro DHEA treatment enhanced Mtb-specific cytotoxic responses and terminal differentiation in CD8(+) T cells from HIV-TB patients. Our data suggest that HIV-TB coinfection promotes a deficient CD8(+) T-cell differentiation, whereas DHEA may contribute to improving antitubercular immunity by enhancing CD8(+) T-cell functions during HIV-TB coinfection.

Complex relationship between sex hormones, insulin resistance and leptin in men with and without prostatic disease.

OBJECTIVES: To assess sex hormones, leptin and insulin-resistance in men with prostate cancer (PCa) and benign prostatic hyperplasia (BPH) and to study associations between androgens and histologic score of prostate tissue in PCa. SUBJECTS AND METHODS: Two hundred ten men older than 45 years selected from 2906 participants of a population screening for PCa were studied: 70 with PCa, 70 with BPH and 70 controls (CG), matched by body mass index and age. Insulin, IGF-1, PSA, leptin, total, free (fT) and bioavailable testosterone (bT) and estradiol were measured. Each group was subdivided into two subgroups considering the presence of metabolic syndrome (MS); androgens and leptin levels were analyzed in the subgroups. RESULTS: Prostate cancer and BPH patients presented higher total, fT and bT levels than CG. IGF-1, insulin and HOMA index were higher in BPH than in the other two groups. PCa presented higher leptin [median (range) 6.5 (1.3-28.0) versus 4.8 (1.1-12.3) ng/ml; p < 0.01] and estradiol [median (range) 37.0 (20-90) versus 29.0 (20-118) pg/ml; p = 0.025] levels than CG. After dividing men considering the presence of MS, leptin was higher and total testosterone was lower in MS patients in all the groups. CONCLUSIONS: It was observed a coexistence of an altered hormone profile with increased sex hormones and leptin in PCa patients, in accordance with the new perspective of PCa pathogenesis.

[Vitamin D deficit in hospitalized patients]. / Déficit de vitamina D en pacientes hospitalizados.

We prospectively studied 60 consecutive patients in order to evaluate the prevalence of vitamin D deficiency. All of them were inpatients, and were evaluated from October 2013 through May 2014. Levels of 25 OH vitamin D were classified as sufficient (> 30 ng/ml), mild to moderate deficiency (15 to 30 ng/ml) and severe deficiency (< 15 ng/ml). The mean age was 72.1 ± 19.5 years; 43 were females and 17 males. Five percent of the patients had normal values of vitamin D, 31.6% had mild to moderate deficit and 63.3% had severe deficit of the vitamin. Severe deficit was associated with hypoalbuminemia, compared with mild to moderate deficit and with sufficient values (2.98 g/dl vs. 3.52 g/dl and vs. 4.39 g/dl, respectively, p: 0.012) and low levels of serum calcium (8.35 mg/dl vs. 8.61 mg/dl and 9.8 mg/dl, respectively, p: 0.003). Although there was a trend of low vitamin D levels with increasing age, female sex, immobilization, higher levels of glucose and glycated haemoglobin, more duration of hospitalization, we didn't find any statistically significance difference between groups. Vitamin D deficiency is common in hospitalized patients. It correlates with low levels of serum albumin and calcium. Improving diagnosis and recognition of this condition may enable us to improve the management of this deficit.

Life events are positively associated with luteinizing hormone in middle age adult men: role of cortisol as a third variable.

Previous studies have tested the relationship between chronic stress and sex hormones, but inconsistent results have been found. One possibility is that this association may depend on other biological factors. This study examined the relationship between stressful life events (LE) and sex hormones in men, and whether cortisol is involved in this relationship. From a total number of 2906 men who completed a screening for the early detection of prostate cancer, 139 healthy men (mean ± SD age, 57.8 ± 5.7 years) were included in this study. Participants were assessed with the Holmes and Rahe questionnaire in relation to their experience of LE during the previous 1-5 years. Salivary and serum cortisol was measured at 08:00-09:00 h, as well as luteinizing hormone (LH), total testosterone, epinephrine (E) and norepinephrine (NE). LE weight sum and LE number positively correlated with LH (r = 0.293, p = 0.004; r = 0.220, p = 0.031, respectively). In a multiple regression analysis, LE-sum explained an additional and significant 10.4% of the variance in LH levels, after statistically controlling for the effects of age, waist circumference (WC) and BMI (F(1,90) = 6.61, p < 0.05). Importantly, cortisol interacted with LE in relation to total testosterone. In men with high cortisol values (≥15.4 µg/dl), there was a statistically significant positive relationship between LE number and total testosterone levels (p = 0.05), while LE were unrelated to total testosterone in men with low cortisol. LE correlated with sex hormones, predicting LH values, and in men with high cortisol levels shows a possible moderator effect of cortisol on the relationship between LE and total testosterone.

Association between testosterone levels and the metabolic syndrome in adult men.

OBJECTIVE: To evaluate the relationship between testosterone levels and the metabolic syndrome (MS) in men older than 45 years. METHODS: Six hundred and sixty men (45-70 years) selected from 2906 participants of a population screening for prostate cancer were included in this study. Testosterone and the components of MS were assessed in all men. MS was diagnosed according to NCEP-ATP III criteria. Triglycerides (TG)/HDL-cholesterol (chol) index was calculated. RESULTS: The presence of MS was inversely associated with testosterone (χ2, p < 0.001), independently of age (OR 0.802, CI 95%: 0.724-0.887, p < 0.0001). Hypertension was the most frequent abnormality observed followed by elevated TG and waist circumference (WC). Testosterone correlated positively with HDL-chol (r: 0.14, p < 0.0001) and negatively with body mass index (BMI)(r: -0.29, p < 0.0001), WC (r: -0.26, p < 0.0001), TG (r: -0.20, p < 0.0001), TG/HDL-chol (r: -0.20, p < 0.0001), glucose (r: -0.11, p = 0.005) and MS score (r: -0.23, p < 0.0001). CONCLUSIONS: Our results show that in men older than 45 years, as long as testosterone levels decline, the prevalence of MS increases, independently of age. The correlations found between testosterone and four of the five components of MS, as well as with BMI and TG/HDL-chol ratio, a surrogate marker of insulin resistance, suggest considering male hypogonadism as a determinant of developmental abnormalities typical of MS.

Relationship between cortisol, life events and metabolic syndrome in men.

Psychological factors and stressful life events (LE) are considered to play a role in the onset of the metabolic syndrome (MS). We tested the association between LE and cortisol, a marker of chronic stress, with the risk of developing MS and their interaction. From a total number of 2906 men who completed a screening for the early detection of prostate cancer, 149 healthy men (mean ± SD age, 58.6 ± 7.7 years) were included in this study. Participants were assessed by the Holmes and Rahe questionnaire about their experience of LE during the previous 1-5 years. MS was diagnosed according to National Cholesterol Education Program-Adult Treatment Panel III (ATP-III) and International Diabetes Federation (IDF) criteria. Serum cortisol was measured at 08:00-09:00 h. Participants with MS (IDF criteria) reported significantly more past LE (p = 0.009) and greater summed weight of LE (p = 0.049) than those without MS. Furthermore, LE interacted with cortisol in relation to MS: in men with increased serum cortisol levels ( ≥ 13.7 µg/dl), number of LE significantly predicted MS-status (relative risk (RR) = 1.16, p = 0.03), whereas in men with low cortisol, LE were unrelated to MS (p = 0.52). We conclude that LE were significantly more prevalent in men with the MS than without the MS, according to IDF criteria, independent of the effects of age and body mass index, especially in men with increased serum cortisol levels.

Prenatal stress perturbs fetal iron homeostasis in a sex specific manner.

The adverse effects of maternal prenatal stress (PS) on child's neurodevelopment warrant the establishment of biomarkers that enable early interventional therapeutic strategies. We performed a prospective matched double cohort study screening 2000 pregnant women in third trimester with Cohen Perceived Stress Scale-10 (PSS-10) questionnaire; 164 participants were recruited and classified as stressed and control group (SG, CG). Fetal cord blood iron parameters of 107 patients were measured at birth. Transabdominal electrocardiograms-based Fetal Stress Index (FSI) was derived. We investigated sex contribution to group differences and conducted causal inference analyses to assess the total effect of PS exposure on iron homeostasis using a directed acyclic graph (DAG) approach. Differences are reported for p < 0.05 unless noted otherwise. Transferrin saturation was lower in male stressed neonates. The minimum adjustment set of the DAG to estimate the total effect of PS exposure on fetal ferritin iron biomarkers consisted of maternal age and socioeconomic status: SG revealed a 15% decrease in fetal ferritin compared with CG. Mean FSI was higher among SG than among CG. FSI-based timely detection of fetuses affected by PS can support early individualized iron supplementation and neurodevelopmental follow-up to prevent long-term sequelae due to PS-exacerbated impairment of the iron homeostasis.