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A variety of studies have investigated endocrinological aspects of ecology, cooperation and immune system activation in Taï chimpanzees, making use of the ever-growing number of validated biomarkers used on non-invasive samples by the endocrinology laboratory at the MPI EVAN. In particular, the measurement of urinary oxytocin allows for insights into benefits of food-sharing, bonds and the potential physiological mechanism behind cooperation. Measures of urinary cortisol in combination with creatinine and C-peptide allow for the investigation of causes of seasonal variation in stress levels while patterns of immune system activation are monitored by the measurement of urinary neopterin. Future studies will profit from combined analysis of endocrine and immune parameters in relation to behaviour and reproductive success to investigate life-history trade-offs. Across-site comparisons of behaviour and endocrine patterns will help us to understand how variation in ecological and physiological parameters form the social setting of a population which leads to relatively low intergroup hostility, low leverage of males over females and relatively high levels of female sociality at Taï.
The experiments described in this research communication compared cortisol concentrations in plasma and saliva samples collected from dairy cattle before and after an adrenocorticotropic hormone (ACTH) application. For that purpose, blood and saliva samples were collected from five dairy cows at determined time intervals before (490 min and down to 0 min) and after (10 min and up to 500 min) an ACTH application. Mean baseline cortisol concentrations were greater in plasma compared to saliva. The relative increases and decreases in plasma and salivary cortisol concentrations following ACTH were similar. After ACTH, we observed an increase in cortisol concentrations in plasma after 10 min and in saliva after 20 min. The time of peak concentrations after ACTH were reached at 70 and 80 min for plasma and saliva, respectively. After peak concentrations, values steadily declined and returned to baseline values at 169 ± 15 min in plasma and 170 ± 14 min in saliva. Ratios between salivary and plasma cortisol concentrations were on average 0.09 and did not change substantially during the ACTH challenge. There was a strong positive relationship between salivary and plasma cortisol concentrations. These results indicate that salivary cortisol concentrations can be a good indicator of ACTH-induced plasma cortisol concentrations in dairy cattle.
Previous studies have shown that healthy older adults may be less sensitive to the effects of acute cortisol levels on memory performance than young adults. Importantly, being overweight has recently been associated with an increase in both cortisol concentration and cortisol receptors in central tissues, suggesting that Body Mass Index (BMI) may contribute to differences in the relationship between memory and acute cortisol. This study investigates the role of BMI in the relationship between memory performance and acute cortisol levels in older people (M = 64.70 years; SD = 4.24). We measured cortisol levels and memory performance (working memory and declarative memory) in 33 participants with normal BMI (normal BMI = 18.50–24.99) and 36 participants with overweight BMI (overweight BMI = 25–29.99). Overweight BMI participants showed worse performance on word-list learning (p = .036, 95% CI [0.08, 2.18], η2p = 0.07). Higher cortisol levels were related to higher proactive interference (β = .364, p = .016, 95% CI [0.07, 0.66]), and BMI did not moderate any of the relationships investigated. In accordance with previous studies, our results show worse memory performance in individuals with overweight BMI. However, our results do not support the idea that memory performance in older people with higher BMI may be more sensitive to differences in acute cortisol levels than in older people with normal BMI. More research is needed to test this hypothesis with obese individuals (BMI > 30 Kg/cm2).
Recent studies have highlighted the dysregulation of hypothalamic-pituitary-adrenal (HPA) axis activity and its end products, cortisol and dehydroepiandrosterone (DHEA), in women with a history of intimate partner violence (IPV) victimization. These studies analyzed several coping styles, but they neglected to examine the use of violent strategies to confront IPV and the way these strategies affect HPA functioning. This latter proposal would be based on the gender symmetry model of IPV, which sustains that IPV is generally symmetrical, but that women’s violence tends to be a reaction to male violence. Hence, the main objective of the present study was to examine whether women’s violent reactions to IPV would significantly predict salivary cortisol and DHEA levels, as well as the cortisol/DHEA ratio (assessed through two saliva samples per day on four consecutive work days), controlling for the women’s prior IPV abuse, psychopathology, and demographic variables. Our data demonstrated that, specifically, psychological confrontation strategies predicted vespertine cortisol levels (adj R2 = .18, β = .447, p < .01) and the cortisol/DHEA ratio (adj R2 = .08, β = .322, p < .05), even after controlling several confounding variables, whereas physical and total confrontation in response to IPV did not predict these hormonal parameters.
The aim of this piece of research was to study the existence of clusters based on anger, empathy and cortisol and testosterone measures associated with aggressive behavior in school-aged children. The sample group comprised 139 eight-year-old children (80 boys and 59 girls). Aggressive behavior was measured using the Direct and Indirect Aggression Scale. Both psychological and biological variables were used to determine psychobiological profiles. The psychological variables considered were trait anger, measured using the State-Trait Anger Expression Inventory for Children and Adolescents, and empathy, measured using the Empathy Quotient-Child Version. Testosterone and cortisol concentrations were measured through saliva samples and analyzed using an ELISA (Enzyme-linked immunosorbent assay). A Cluster Analysis revealed three clusters which were clearly different as regards their psychological and biological characteristics. The analysis of variance (ANOVA) revealed that the cluster characterized by having higher anger levels, lower empathy levels and higher testosterone and cortisol levels was more aggressive than the other two (p < .0001, η2 = .19). The results indicate that studying psychological and biological variables together may help establish differentiated aggression patterns among children.
Sleep disturbance is a symptom of and a well-known risk factor for depression. Further, atypical functioning of the HPA axis has been linked to the pathogenesis of depression. The purpose of this study was to examine the role of adolescent HPA axis functioning in the link between adolescent sleep problems and later depressive symptoms. Methods: A sample of 157 17–18 year old adolescents (61.8% female) completed the Pittsburgh Sleep Quality Inventory (PSQI) and provided salivary cortisol samples throughout the day for three consecutive days. Two years later, adolescents reported their depressive symptoms via the Center for Epidemiological Studies Depression Scale (CES-D). Results: Individuals (age 17–18) with greater sleep disturbance reported greater depressive symptoms two years later (age 19–20). This association occurred through the indirect effect of sleep disturbance on the cortisol awakening response (CAR) (indirect effect = 0.14, 95%CI [.02 -.39]). Conclusions: One pathway through which sleep problems may lead to depressive symptoms is by up-regulating components of the body’s physiological stress response system that can be measured through the cortisol awakening response. Behavioral interventions that target sleep disturbance in adolescents may mitigate this neurobiological pathway to depression during this high-risk developmental phase.
We review studies of whether cortisol levels following psychosocial stress exposure differ between patients with psychosis and healthy control subjects.
Original research published between 1993 and February 2019 was included in the literature search. Studies that used experimentally induced psychosocial stress and reported stress response measures of plasma or saliva cortisol levels in patients at any stage of illness (i.e. high risk, first episode and chronic phase) were included.
A total of 17 studies were included. Although there was evidence of inconsistencies in measures, we observed moderate evidence of an association with stress-induced cortisol blunting response across studies.
This review highlights recent evidence of blunting of cortisol response following experimentally induced psychosocial stress. While there was some evidence of this blunted response across illness types and stages, the strongest evidence was observed for those with chronic schizophrenia. Due to the low number of studies, in particular in bipolar disorder, much work is still needed to accurately characterise the biological effects of stress in psychosis.
Psychosocial stress, uncontrolled eating and obesity are three interrelated epidemiological phenomena already present during youth. This broad narrative conceptual review summarises main biological underpinnings of the stress–diet–obesity pathway and how new techniques can further knowledge. Cortisol seems the main biological factor from stress towards central adiposity; and diet, physical activity and sleep are the main behavioural pathways. Within stress–diet, the concepts of comfort food and emotional eating are highlighted, as cortisol affects reward pathways and appetite brain centres with a role for insulin, leptin, neuropeptide Y (NPY), endocannabinoids, orexin and gastrointestinal hormones. More recently researched biological underpinnings are microbiota, epigenetic modifications and metabolites. First, the gut microbiota reaches the stress-regulating and appetite-regulating brain centres via the gut–brain axis. Second, epigenetic analyses are recommended as diet, obesity, stress and gut microbiota can change gene expression which then affects appetite, energy homeostasis and stress reactivity. Finally, metabolomics would be a good technique to disentangle stress–diet–obesity interactions as multiple biological pathways are involved. Saliva might be an ideal biological matrix as it allows metagenomic (oral microbiota), epigenomic and metabolomic analyses. In conclusion, stress and diet/obesity research should be combined in interdisciplinary collaborations with implementation of several -omics analyses.
Early life stress (ELS) is a risk factor for the development of depression in adolescence; the mediating neurobiological mechanisms, however, are unknown. In this study, we examined in early pubertal youth the associations among ELS, cortisol stress responsivity, and white matter microstructure of the uncinate fasciculus and the fornix, two key frontolimbic tracts; we also tested whether and how these variables predicted depressive symptoms in later puberty. A total of 208 participants (117 females; M age = 11.37 years; M Tanner stage = 2.03) provided data across two or more assessment modalities: ELS; salivary cortisol levels during a psychosocial stress task; diffusion magnetic resonance imaging; and depressive symptoms. In early puberty there were significant associations between higher ELS and decreased cortisol production, and between decreased cortisol production and increased fractional anisotropy in the uncinate fasciculus. Further, increased fractional anisotropy in the uncinate fasciculus predicted higher depressive symptoms in later puberty, above and beyond earlier symptoms. In post hoc analyses, we found that sex moderated several additional associations. We discuss these findings within a broader conceptual model linking ELS, emotion dysregulation, and depression across the transition through puberty, and contend that brain circuits implicated in the control of hypothalamic–pituitary–adrenal axis function should be a focus of continued research.
Adverse caregiving, for example, previous institutionalization (PI), is often associated with emotion dysregulation that increases anxiety risk. However, the concept of developmental multifinality predicts heterogeneity in anxiety outcomes. Despite this well-known heterogeneity, more work is needed to identify sources of this heterogeneity and how these sources interact with environmental risk to influence mental health. Here, working memory (WM) was examined during late childhood/adolescence as an intra-individual factor to mitigate the risk for separation anxiety, which is particularly susceptible to caregiving adversities. A modified “object-in-place” task was administered to 110 youths (10–17 years old), with or without a history of PI. The PI youths had elevated separation anxiety scores, which were anticorrelated with morning cortisol levels, yet there were no group differences in WM. PI youths showed significant heterogeneity in separation anxiety symptoms and morning cortisol levels, and WM moderated the link between caregiving and separation anxiety and mediated the association between separation anxiety and morning cortisol in PI youth. Findings suggest that (a) institutional care exerts divergent developmental consequences on separation anxiety versus WM, (b) WM interacts with adversity-related emotion dysregulation, and (c) WM may be a therapeutic target for separation anxiety following early caregiving adversity.
This study examined the interplay between a polygenic composite and cortisol activity as moderators of the mediational pathway among family adversity, youth negative emotional reactivity to family conflict, and their psychological problems. The longitudinal design contained three annual measurement occasions with 279 adolescents (Mean age = 13.0 years) and their parents. Latent difference score analyses indicated that observational ratings of adversity in interparental and parent–child interactions at Wave 1 predicted increases in a multimethod, multi-informant assessment of youth negative emotional reactivity to family conflict from Waves 1 to 2. Changes in youth negative emotional reactivity, in turn, predicted increases in a multi-informant (i.e., parents, adolescent, and teacher) assessment of psychological problems from Waves 1 to 3. Consistent with differential susceptibility theory, the association between family adversity and negative emotional reactivity was stronger for adolescents who carried more sensitivity alleles in a polygenic composite consisting of 5-HTTLPR, DRD4 VNTR, and BDNF polymorphisms. Analyses of adolescent cortisol in the period surrounding a family disagreement task at Wave 1 revealed that overall cortisol output, rather than cortisol reactivity, served as an endophenotype of the polygenic composite. Overall cortisol output was specifically associated with polygenic plasticity and moderated the association between family adversity and youth negative emotional reactivity in the same for better or for worse manner as the genetic composite. Finally, moderator-mediated-moderation analyses indicated that the moderating role of the polygenic plasticity composite was mediated by the moderating role of adolescent cortisol output in the association between family adversity and their emotional reactivity.
Childhood adversity is associated with poor mental and physical health outcomes across the life span. Alterations in the hypothalamic–pituitary–adrenal axis are considered a key mechanism underlying these associations, although findings have been mixed. These inconsistencies suggest that other aspects of stress processing may underlie variations in this these associations, and that differences in adversity type, sex, and age may be relevant. The current study investigated the relationship between childhood adversity, stress perception, and morning cortisol, and examined whether differences in adversity type (generalized vs. threat and deprivation), sex, and age had distinct effects on these associations. Salivary cortisol samples, daily hassle stress ratings, and retrospective measures of childhood adversity were collected from a large sample of youth at risk for serious mental illness including psychoses (n = 605, mean age = 19.3). Results indicated that childhood adversity was associated with increased stress perception, which subsequently predicted higher morning cortisol levels; however, these associations were specific to threat exposures in females. These findings highlight the role of stress perception in stress vulnerability following childhood adversity and highlight potential sex differences in the impact of threat exposures.
Resilience is the ability of an animal to return soon to its initial productivity after facing diverse environmental challenges. This trait is directly related to animal welfare and it plays a key role in fluctuations of livestock productivity. A divergent selection experiment for environmental variance of litter size has been performed successfully in rabbits over ten generations. The objective of this study was to analyse resilience indicators of stress and disease in the divergent lines of this experiment. The high line showed a lower survival rate at birth than the low line (−4.1%). After correcting by litter size, the difference was −3.2%. Involuntary culling rate was higher in the high than in the low line (+12.4%). Before vaccination against viral haemorrhagic disease or myxomatosis, concentration of lymphocytes, C-reactive protein (CRP), complement C3, serum bilirubin, triglycerides and cholesterol were higher in the high line than in the low line (difference between lines +4.5%, +5.6 µg/ml, +4.6 mg/ml, +7.9 mmol/l, +0.3 mmol/l and +0.4 mmol/l). Immunological and biochemical responses to the two vaccines were similar. After vaccination, the percentage of lymphocytes and CRP concentration were higher in the low line than in the high one (difference between lines +4.0% and +13.1 µg/ml). The low line also showed a higher increment in bilirubin and triglycerides than the high line (+14.2 v. +8.7 mmol/l for bilirubin and +0.11 v. +0.01 mmol/l for triglycerides); these results would agree with the protective role of bilirubin and triglycerides against the larger inflammatory response found in this line. In relation to stress, the high line had higher basal concentration of cortisol than the low line (+0.2ng/ml); the difference between lines increased more than threefold after the injection of ACTH 1 to 24, the increase being greater in the high line (+0.9 ng/ml) than in the low line (+0.4 ng/ml). Selection for divergent environmental variability of litter size leads to dams with different culling rate for reproductive causes and different kits’ neonatal survival. These associations suggest that the observed fitness differences are related to differences in the inflammatory response and the corticotrope response to stress, which are two important components of physiological adaptation to environmental aggressions.
The increasing availability of automated milk dispensers on dairy farms facilitates ad libitum milk supply but weaning calves from high milk allowances is challenging. This study evaluated effects of gradual weaning methods on starter intake, growth, selected blood parameters and weaning distress in ad libitum fed dairy calves during weaning and early post-weaning periods. Thirty-six male Holstein (n = 30) or crossbred (n = 6) calves were individually housed from days 2 to 14 of age and had ad libitum access to milk replacer (MR) from teat buckets. From days 15 to 84 of age, calves were grouped and had ad libitum access to MR, starter, straw and water from automated feeders. At day 35, calves were blocked (age and breed), and randomly assigned to a weaning method: (1) linear fixed (LIN), MR supply was stepped down to 6 l/day on day 36, and linearly reduced between days 36 to 63 from 6 to 2 l/day. (2) Step-down (STEP), MR supply was stepped down to 6 l/day from days 36 to 48, 4 l/day from days 49 to 56 and 2 l/day from days 57 to 63. (3) Dynamic (DYN), at day 36, MR supply was reduced for each individual calf to 75% of the average voluntary consumption between day 29 and 35, then maintained for 9 days, reduced to 50% for 10 days, and to 25% for 9 days. The DYN calves received more MR during weaning than LIN calves, whereas STEP calves had intermediate MR intake. Starter intake was not affected by weaning method. The DYN calves (1.33±0.08 kg/day) grew faster and were heavier than STEP calves (1.10±0.08 kg/day) during post-weaning period, whereas no difference was observed between LIN calves (1.23±0.08 kg/day) and others. At days 70 and 84, concentrations of β-hydroxybutyric acid were higher in LIN calves compared to STEP and DYN calves. Hair cortisol concentrations were not affected by weaning method. During the gradual weaning process CP intake seemed to recovered earlier than metabolizable energy (ME) intake in all treatments, suggesting that ME rather than CP could be the first limiting factor for growth during weaning. These results highlight the post-weaning benefits of DYN and LIN weaning methods when compared with more abrupt step-down strategies.
The link between circulating glucocorticoids and leptin in beef calves has not been explored but has been noted in several studies. The aim of this study is to determine the effects of exogenous glucocorticoids given at birth and 1 day of age on serum leptin concentrations in beef calves. Ruminant animals secrete leptin, which is thought to be important for the programming of the hypothalamic appetite centers. Angus crossbred cows (n = 31) bred via natural service were utilized for this experiment. At parturition (day 0), calf BW was recorded and each calf was infused intravenously with either a hydrocortisol sodium succinate solution (HC, 8 males and 8 females) at a dosage of 3.5 μg/kg of BW or a similar volume of saline solution (CONT, 7 males and 8 females). Each calf was given a second infusion of its respective treatment 24 h postpartum at 1.5 μg/kg of BW for HC treatment. Calf treatment was blocked by sex, dam body condition score (BCS), and dam age. Blood samples were taken via jugular venipuncture before infusion, daily from days 0 to 5, then every other day up to day 17. Serum leptin and cortisol concentrations were analyzed via radioimmunoassay. Dam age, dam BCS, calf BW, and serum leptin and cortisol concentrations were analyzed using MIXED procedure of SAS. Dam age was not different (P = 0.81) among HC and CONT calves (4.9±0.5 and 4.7±0.5, respectively). Dam BCS was not different between treatments (5.7±0.2 and 5.6±0.2 HC and CONT, respectively; P = 0.66). There was no difference in calf birth BW between treatments (P = 0.87) and averaged 38.3±1.4 kg. Cortisol concentrations were not different between both treatments (P = 0.23) from birth to day 4 of age. Calves that received the HC treatment showed significantly reduced (P = 0.03) leptin concentrations on days 1 to 13. Calf BW from 60 to 150 days of age was not different between CONT and HC treated calves (P = 0.65). These data indicate that exogenous glucocorticoids can be used to suppress neonatal leptin levels in calves. This could lead to changes in voluntary feed intake of treated calves.
This study explores the conceptualization of mother–infant cortisol attunement both theoretically and empirically, and its association with mother–infant attachment disorganization. In a community sample (N = 256), disorganization and cortisol were assessed during the Strange Situation Procedure (SSP) at infant age 17 months. Salivary cortisol was collected at baseline, and 20 and 40 min after the SSP. We utilized three statistical approaches: correlated growth modeling (probing a simultaneous conceptualization of attunement), cross-lagged modeling (probing a lagged, reciprocal conceptualization of attunement), and a multilevel model difference score analysis (to examine the pattern of discrepancies in mother–infant cortisol values). Correlated growth modeling revealed that disorganized, relative to organized, dyads had significant magnitude of change over time, such that, among disorganized dyads, as mothers had greater declines in cortisol, infants had greater increases. The difference score analysis revealed that disorganized, relative to organized, dyads had a greater divergence between maternal and infant cortisol values, such that maternal values were lower than infant values. Disorganized attachment status was not significantly associated with attunement when conceptualized as reciprocal and lagged in the cross-lagged model. Findings suggest that mother–infant dyads in disorganized attachment relationships, who are by definition behaviorally misattuned, are also misattuned in their adrenocortical responses.
In pig husbandry, pregnant females are often exposed to stressful conditions, and their outcomes on maternal and offspring health have not been well evaluated. The present study aimed at testing whether improving the welfare of gestating sows could be associated with a better maternal health during gestation, changes in the composition of lacteal secretions and improvement in piglet survival. Two contrasted group-housing systems for gestating sows were used, that is, a French conventional system on slatted floor (C, 49 sows) and an enriched system using larger pens on deep straw (E, 57 sows). On the 105th days of gestation (DG105), sows were transferred into identical farrowing crates on slatted floor. Saliva was collected from all sows on DG35, DG105 and DG107. Blood samples were collected on DG105 from all sows and on the 1st day of lactation (DL1) from a subset of them (C, n=18; E, n=19). Colostrum and milk samples were collected from this subset of sows at farrowing (DL0) and DL4. Saliva concentration of cortisol was greater in C than in E sows at DG35 and DG105, and dropped to concentrations comparable to E sows after transfer into farrowing crates (DG107). On DG105, plasma concentrations of haptoglobin, immunoglobulins G (IgG) and A (IgA), blood lymphocyte counts and plasma antioxidant potential did not differ between groups (P > 0.10), whereas blood granulocyte count, and plasma hydroperoxide concentration were lower in E than in C sows (P < 0.05). Concentrations of IgG and IgA in colostrum and milk did not differ between the two groups. The number of cells did not differ in colostrum but was greater in milk from E than C sows (P < 0.05). Pre-weaning mortality rates were lower in E than C piglets (16.7% v. 25.8%, P < 0.001), and especially between 12 and 72 h postpartum (P < 0.001). Plasma concentration of IgG was similar in E and C piglets on DL4. In conclusion, differences in salivary cortisol, blood granulocyte count and oxidative stress markers between groups suggested improved welfare and reduced immune solicitation during late gestation in sows of the E compared with the C system. However, the better survival observed for neonates in the E environment could not be explained by variations in colostrum composition.
The hypothalamic–pituitary–adrenal axis (HPAA) plays a critical role in the functioning of all other biological systems. Thus, studying how the environment may influence its ontogeny is paramount to understanding developmental origins of health and disease. The early post-conceptional (EPC) period could be particularly important for the HPAA as the effects of exposures on organisms’ first cells can be transmitted through all cell lineages. We evaluate putative relationships between EPC maternal cortisol levels, a marker of physiologic stress, and their children’s pre-pubertal HPAA activity (n=22 dyads). Maternal first-morning urinary (FMU) cortisol, collected every-other-day during the first 8 weeks post-conception, was associated with children’s FMU cortisol collected daily around the start of the school year, a non-experimental challenge, as well as salivary cortisol responses to an experimental challenge (all Ps<0.05), with some sex-related differences. We investigated whether epigenetic mechanisms statistically mediated these links and, therefore, could provide cues as to possible biological pathways involved. EPC cortisol was associated with >5% change in children’s buccal epithelial cells’ DNA methylation for 867 sites, while children’s HPAA activity was associated with five CpG sites. Yet, no CpG sites were related to both, EPC cortisol and children’s HPAA activity. Thus, these epigenetic modifications did not statistically mediate the observed physiological links. Larger, prospective peri-conceptional cohort studies including frequent bio-specimen collection from mothers and children will be required to replicate our analyses and, if our results are confirmed, identify biological mechanisms mediating the statistical links observed between maternal EPC cortisol and children’s HPAA activity.
The impact of maltreatment spreads across many developmental domains and extends across the entire life span. Identifying unidirectional or bidirectional drivers of developmental cascades of the effects of maltreatment experiences is critical to efficiently employing interventions to promote resilient development in maltreated children. This 1-year longitudinal study utilized a multiple-levels approach, investigating “bottom-up” and “top-down” cascades using structural equation modeling between cortisol regulation, externalizing behavior, and peer aggression. Neither a bottom-up model driven by cortisol regulation nor a top-down model driven by peer aggression fit the data well. Instead, lower rates of externalizing behavior at Year 1 most strongly predicted improvements at all levels of analysis (reduced cortisol, externalizing behavior, and peer aggression) at Year 2. These results provide initial indication of a mechanism through which interventions for maltreated children may be most effective and result in the most substantial positive changes across developmental domains.
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.