The dexamethasone suppression test DST was originally applied in the late s as a laboratory diagnostic tool for major depression in adults Carroll ; Carroll et al. In the decades since, the DST has become the most extensively studied biological parameter of depression in adult Casat et al. Although the diagnostic utility of the DST has been questioned more recently due to its lower specificity in inpatient samples e. Moreover, it has been argued that the lack of specificity of the DST does not negate its clinical relevance. Given that adult studies have consistently demonstrated that heightened cortisol response to the DST is associated with more severe depressive symptomatology, it may serve as an index of clinical severity e.
Livingston et al. Livingston and Martin-Cannici Targum and Capodanno Klee and Garfinkel Appelboom-Fondu and Kerkhofs A wide range of variability in DST results was found across individual studies, likely due to the large number of studies using small samples sizes. Indeed, approximately half of these published reports included only 15 or fewer depressed children or adolescents and a comparably small number of non-depressed control participants. Important trends are apparent, however, when considering these findings in aggregate. Most salient and consistent with the overall meta-analytic finding based on the smaller set of studies reported by Lopez-Duran et al.
This overall rate of cortisol non-suppression among juvenile depressed samples compiled of results from child, adolescent, as well as from inpatient and outpatient samples is comparable to that reported in samples of depressed adults APA Thus, these data suggest that abnormal HPA axis functioning as measured by cortisol non-suppression following the DST is associated with at least some forms of child and adolescent depression. Also consistent with a robust finding from the adult DST literature, the rates of cortisol non-suppression in inpatient depressed children and adolescents were approximately double those found in outpatient samples.
This pattern is unsurprising. Assuming that inpatients as a group tend to be individuals with more serious forms of psychopathology, dysfunction, and impairment than their outpatient counterparts, it is intuitive that greater HPA axis dysregulation might be present among more severely depressed young people. As noted above, parallel evidence for this contention can be found in the adult data; severe MDD patients showed greater post-DST non-suppression than did those with less symptomatology APA Unfortunately, this hypothesis cannot be directly examined within individual studies conducted with child and adolescent samples, much less between samples of inpatients and outpatients.
Most DST studies conducted with young people relied on assessment methods that assigned a simple categorical diagnosis of depression based on clinician-administered, semistructured interviews. Only Birmaher et al. However, these investigators reported unexpected results; adolescents who scored higher on the self-reported Hamilton Rating Scale for Depression HAM-D; Hamilton had a lower rate of non-suppression following the DST Birmaher et al.
Of more direct relevance to viewing the association between depression and HPA axis dysregulation through a developmental psychopathology perspective, the available DST data allow for a preliminary comparison of the rates of cortisol non-suppression among children versus adolescents. Ostensibly contrary to the expectations of theoretical models proposing progressive HPA axis dysfunction across development consequent to recurrent stress exposure e.
However, a potentially confounding methodological factor must be considered in the interpretation of these unexpected data. Critically, the dose of dexamethasone most frequently used in studies with children was 0. It is possible, as some have argued e. One possible result of an overly high dose of dexamethasone could be the uniform suppression of cortisol regardless of diagnostic status. Pfeffer et al. In conducting the DST with children at the threshold of adolescence, these investigators found that the 0. Accordingly, the pattern of slightly higher rates of non-suppression observed among child relative to adolescent samples may reflect a systematic difference in the dose of dexamethasone used between age groups, rather than any developmental differences in HPA axis functioning.
Future work comparing child and adolescent response to the DST would benefit from the consistent or, best, physically proportionate application of dexamethasone dose. Naylor et al. A final and considerable limitation of the extant literature examining the DST among pediatric samples pertains to the generally ambiguous diagnostic classification of participants. Many studies reportedly utilized rigorous diagnostic procedures such as repeated, multi-informant, semistructured clinical interviews to diagnose MDD based on DSM or RDC criteria e.
However, the majority of studies either made no explicit attempt to characterize let alone control for the possible comorbid status of depressed participants, or—when comorbidities were determined—simply defaulted to major depression as the primary diagnosis. Thus, as has been argued in the adult DST literature Zimmerman et al. As mentioned above, studies conducted with depressed adults have consistently demonstrated that a substantial proportion of these adults hypersecrete cortisol across various measured indices of basal HPA axis functioning.
For example, when compared with non-depressed controls, depressed adults tend to exhibit higher mean h plasma levels of cortisol, increased frequency of cortisol secretion episodes, greater magnitudes of cortisol released during each pulse, an earlier time of cortisol rise during sleep, and an overall loss of the usual circadian rhythm Christensen et al. Puig-Antich et al.
Mathew et al. Goodyer et al. Adam et al. MDD T10 showed elevated cortisol levels prior to sleep onset afternoon, evening, night. For these purposes, the 56 baseline MDD participants were excluded from that part of the study. Further complicating a systematic comparison of results between depressed and non-depressed children and adolescents across studies is the well-known and substantial inter- and intra-personal variability in daily cortisol production due to a number of variables.
For instance, not only are basal levels thought to represent individual differences in temperamental or trait dimensions e. Likewise, given that sleep disruption is a criterial symptom of the diagnosis of major depression, it is certainly possible that systematic group differences exist in the sleep-wake cycles of depressed versus non-depressed young people. Thus, to control for these group and individual differences and enable meaningful comparison of data between depressed and non-depressed samples, it is arguably necessary to analyze diurnal cortisol trajectories aligned by time of sleep onset rather than by objective clock times e.
Methodological and biological heterogeneity notwithstanding, several important patterns emerge from results found across studies of HPA basal functioning. First, the majority of published reports failed to detect statistically significant differences between depressed and control youths on any measure of basal cortisol secretion.
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More specifically, and contrary to reliable findings in the adult data, none of the studies conducted with children and adolescents found significant differences between groups of depressed and control youths on any of the following basal cortisol summary variables: h mean level, overall peak, daytime mean, pulse frequency, or pulse amplitude. It is interesting to note, however, that overall non-significant trends of cortisol hypersecretion were often found among samples of depressed young people. It is certainly plausible that the aforementioned small samples sizes typically utilized throughout this literature seriously limited the power of any individual study to detect more subtle deviations from normative diurnal pattern of cortisol production.
Indeed, significant basal elevations appeared to be more often reported by those studies with larger samples sizes i. This argument is further strengthened by the positive result of a recent meta-analysis that revealed a statistically significant tendency for depressed children and adolescents to have higher basal cortisol levels relative to non-depressed controls Lopez-Duran et al.
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Intriguingly, Lopez-Duran et al. This is somewhat surprising, given that the association between dysregulation of basal cortisol secretion and depression appears to be more robust in adults. It is worth noting, though, that one of the few studies to directly and carefully compare the HPA axis activity of depressed children and adolescents found that only depressed adolescents had elevated cortisol levels in the period preceding sleep onset Forbes et al. Thus, there may be a pattern in which pediatric depression becomes increasingly linked to basal HPA axis dysfunction with advancing age.
Interestingly, Casat et al. However, there are certain distinguishing characteristics of this study that may account for these divergent results. These investigators utilized a methodology distinct from the majority of other studies of basal cortisol levels and patterns, and they included the smallest number of depressed participants i.
Taken together, these limitations raise the possibility that these aberrant results are spurious. Perhaps most revealing, though, are the three longitudinal studies on the relations between HPA axis function and adolescent depression Adam et al. Although cortisol levels had not distinguished the youths with and without depression in concurrent analyses Dahl et al. Thus, a systemic dysregulation of diurnal HPA axis activity predicted subsequent suicidal behavior in young people with depression. Finally, Adam et al. Those young adults who had highly elevated CAR a year earlier were three times more likely to have developed MDD, compared to average.
Together, these three studies offer strong evidence that dysregulated basal HPA activity precedes and predicts the development of depression and associated behaviors in adolescence and early adulthood. As suggested in the meta-analysis by Lopez-Duran et al. Rather, exaggerated CAR, elevated morning and evening cortisol, and lower cortisol after sleep onset all appear to characterize youths who are at greater risk for developing depression.
The chain of physiological activation of the HPA axis begins far upstream in the hypothalamus with the release of CRH, ultimately leading to the release of cortisol and DHEA for review, see Sapolsky et al. Given the central role of CRH as the driver for this sequence of activation, some investigators have hypothesized that the cortisol-related abnormalities observed among depressed adults may be due to enhanced secretion of CRH Gold et al.
This research, which has almost exclusively relied on adult samples, has repeatedly demonstrated that depressed individuals tend to have elevated cortisol and blunted ACTH secretion in response to CRH infusion, relative to normal controls see Birmaher et al. Accordingly, a normal cortisol response to blunted ACTH secretion is evidence of HPA axis dysregulation in the form of a hyper-responsive adrenal cortex see Gold et al.
Surprisingly, only four studies have compared cortisol and ACTH responses between samples of depressed and non-depressed children and adolescents following CRH challenge Birmaher et al. In contrast to the adult data, none of these studies found significant differences in overall cortisol or ACTH secretion between depressed and non-depressed groups of children Birmaher et al.
With the exception of the study conducted by Ronsaville et al. Nonetheless, a closer examination of the scarce literature on CRH in the young suggests important directions for further investigation. If these replicated the albeit limited historical data, they would establish continuities with the adult data.
For example, Birmaher et al. Similar to the findings in adults, it is possible that some depressed young people may manifest HPA axis dysregulation through adrenal cortex hyper-responsivity. Such evidence, however preliminary, is also in accord with a salient pattern found in DST studies, namely the pronounced differences in HPA axis functioning between inpatients and outpatients.
Birmaher et al. First, their suggestion that the depressed inpatients in their sample may have been more severely depressed than the outpatient subgroup was not supported by secondary analyses that revealed no significant group differences between inpatients and outpatients on either the Hamilton Depression Rating Scale or the depression module from the K-SADS-P. Such hypotheses remain speculative and significant questions remain as to how to account for possible group differences in CRH studies between inpatient and outpatient samples of depressed young people.
Likewise, the study conducted by Kaufman et al. These investigators examined the results of CRH challenge among samples of depressed abused and depressed non-abused outpatient children, as well as age-matched normal controls. Although no differences in cortisol secretion were found post-CRH infusion between groups, one group of children differed significantly—and in the unexpected direction—with regard to their subsequent ACTH levels.
When compared with depressed children without a history of abuse and control children, depressed abused children had significantly higher peak, total, and net ACTH secretion post-CRH challenge. Exploratory analyses of this disparity revealed that increased ACTH secretion was only observed in depressed abused children who were experiencing ongoing chronic adversity e.
Taking a developmental psychopathology perspective, although Kaufman et al. This hypothesis of progressive HPA axis dysregulation in response to chronic stress exposure parallels the pattern reported in animal studies e. While hypothalamic CRH represents the physiological trigger for activation of the HPA system, psychological activation of this system begins upstream with affective information processed in the limbic system.
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The limbic system, in turn, stimulates CRH-releasing neurons in the hypothalamus e. Since the limbic system serves as the primary conduit between cognitively processed exogenous stressors and endogenous physiological signals, psychological stressors represent important probes of the higher-order functioning of the HPA axis. Surprisingly, there has been little research in this area. As discussed previously in the introductory sections, although both depression and the transition to adolescence are associated with increases in exposure to psychological stressors, a paucity of studies has addressed HPA axis response to this class of stimuli among depressed children and adolescents.
Recall that in normative populations, childhood has been hypothesized to be a period of hyporesponsivity to psychological stressors, relative to adolescence Gunnar et al. For example, Stroud et al. These investigators found that adolescents exhibited significantly greater reactivity across several physiological indices relative to children for both tasks. Only four such reports have been published Hankin et al. Although these few published data reflect the smallest body of literature examining pediatric HPA axis dysregulation associated with early-onset depression, it is intriguing to note that the patterns of findings are by far the most consistent.
All four studies reported significant findings related to cortisol hypersecretion of depressed juveniles in response to acute, laboratory-induced psychological stress relative to non-depressed psychiatric controls or normative volunteers. Given the small number of published reports, a brief review of each is provided below.
The two studies by Luby et al. The evidence from these studies suggests continuities of HPA axis dysfunction in depressive disorders across early development and into adulthood. Both studies drew upon data from a relatively large sample of depressed preschoolers together with age-matched psychiatric and normative comparison groups. The investigators collected multiple salivary samples before and after stressors that involved separation from parents and frustrating tasks e. The study revealed that whereas all groups of children displayed heightened cortisol response to frustrating tasks relative to baseline, depressed preschoolers were the only group to show significantly augmented cortisol levels in response to a separation stressor, as well as an overall pattern of increasing mean cortisol secretion throughout the 2-h assessment.
Importantly, in comparison with both control groups, depressed children displayed higher cortisol levels subsequent to their arrival at the laboratory, perhaps indicating heightened emotional reactivity to the novel experimental paradigm or chronically elevated basal cortisol levels. Additional subgroup analyses of these data presented in the study indicated that depressed preschoolers experiencing significant symptoms of anhedonia tended to exhibit the greatest cortisol reactivity to acute psychological stress.
The authors argued that, as with adults, anhedonia in children may represent a marker of a more severe, biologically, and genetically based depressive subtype. This pattern of more consistent and pronounced patterns of HPA hyperactivity corresponding to more severe depressive symptomatology parallels findings from studies using DST and CRH probes. Rao and colleagues study of adolescents utilized the Trier Social Stress Test TSST , a standardized and validated psychosocial stress protocol that has been shown to reliably induce HPA activity in adolescents and adults Gunnar et al.
The TSST is an interpersonal stressor that involves the participant being challenged to perform well on evaluative tasks by an unsupportive examiner. The TSST was administered to 30 depressed adolescents and 25 healthy volunteers and systematically measured both baseline and post-TSST samples of salivary cortisol.
Consistent with their hypothesis, the authors found that although both groups of adolescents exhibited significantly elevated cortisol response to the TSST relative to their respective baseline levels, depressed participants showed significantly higher and more prolonged cortisol secretion following psychosocial stress induction when compared with control subjects.
In Search of HPA Axis Dysregulation in Child and Adolescent Depression
Parallel findings were reported by Hankin et al. Prepubertal children with current MDD had higher initial cortisol levels, but they did not differ from comparison children in reactivity min post-stress or recovery min post-stress saliva samples. Conversely, post-pubertal youths with current MDD evidenced stronger reactivity to the task than did comparison youths.
Intriguingly, in a parallel analysis of children and youths with remitted MDD, no differences from the comparison groups were noted. Given the limited literature on response to psychological stressors in depressed children and adolescents, perspective is gained from examining studies of cortisol reactivity in children and adolescents with subclinical levels of depression Gunnar et al.
In the former study, older adolescent boys showed the strongest reactivity to the task, but it was only for adolescent girls that having a stronger reaction to the TSST larger increase in cortisol from pre-task to min post-task samples was associated with having more internalizing problems Klimes-Dougan et al.
In subsequent analyses, youths with early pubertal maturation were found to have more internalizing problems, and again for girls only, stronger HPA reactivity to the TSST mediated the association between early pubertal maturation and internalizing problems Natsuaki et al. Thus, adolescent girls, and particularly early-maturing girls, appear to show heightened physiological reactivity to interpersonal stressors that might increase their risk for developing depression-related problems. Analogous findings were reported by Gunnar et al. Together, these findings of gender differences in the links between HPA axis response to psychological stressors and severity of affective problems echo other literature that has hypothesized that HPA dysregulation might function as one mechanism underlying sex differences in depression Stroud et al.
Finally, in addition to studying pediatric depression, Hankin et al.
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They distinguished subclinical dysphoric children from children with low negative affect, measured temperament and recent stressful life events and, in the three older groups, assessed pubertal maturation. The dysphoric preschoolers and third-graders did not show cortisol increases to the stressors, whereas the non-dysphoric children had significant cortisol elevations. No group differences were evident for sixth-graders, but the dysphoric youths in ninth grade showed stronger cortisol elevations than did the non-dysphoric youths.
Group differences in temperament and life stressors could not account for these findings, but pubertal maturation explained the age effects. Regardless of puberty, non-dysphoric children and youth showed the expected pattern of moderate HPA reactivity, whereas prepubertal dysphoric children were relatively hyporesponsive and post-pubertal dysphoric children were relatively hyper-reactive. Studies have provided consistent evidence that the offspring of depressed parents are themselves at increased risk for developing depression Beardslee et al.
Should the children of depressed parents demonstrate adrenocortical dysregulation prior to evidencing their own depressive symptoms, this could be taken as further evidence that atypical HPA axis activity is a precursor of, and possibly contributing factor to, pediatric depression. There have been 13 papers that specifically examined the relations between parental depression and cortisol levels in offspring, with children ranging in age from neonates through young adults Ashman et al. Most studies included only depressed mothers, although some included both depressed mothers and depressed fathers.
All of the papers included non-depressed comparison families and, strikingly, all of the investigations identified elevated cortisol levels in one or more measures of HPA axis activity in the offspring of depressed parents. For example, in several reports, Field and her colleagues , ; Diego et al. Similarly, Brennan et al. They found that, relative to infants of mothers without depression, there were elevated basal cortisol levels in the infants of mothers with perinatal or postnatal depression.
Infants of mothers who had experienced depression only prior to conception did not differ from infants of non-depressed mothers, suggesting that genetic transference of risk for depression alone cannot account for the elevated cortisol levels in offspring. Although Brennan et al. They reported that 9-month-old infants of depressed mothers had greater elevations in cortisol in response to a fear-induction paradigm than did infants of mothers without psychopathology.
Several of the studies of children and youths included measurements of family functioning, stressful life events, temperament or personality, and similar factors to determine whether these accounted for differences in cortisol levels between depressed and non-depressed groups. For example, Halligan et al. It is not clear that disruptions to the diurnal rhythm of basal HPA activity in the children of depressed parents are specific to the morning period, however.
As did Halligan et al. Mannie et al. Essex et al. Young et al. The children of depressed parents also were less responsive to the DST, evidencing higher waking and afternoon cortisol levels the day after receiving dexamethasone. Conversely, maternal depression during infancy was unrelated to morning, evening, or reactive cortisol levels in 7- to 8-year-old children in a study by Ashman et al.
Considered together, these studies present singularly consistent evidence that parental depression, and particularly maternal depression in the prenatal and postnatal periods, is associated with atypical HPA axis functioning in offspring. This is evidenced across developmental periods and principally in disruptions to basal cortisol levels.
Yet in the two samples that were followed longitudinally Ashman et al. Important, if preliminary, observations can be offered from this review of the emerging body of literature examining various components of HPA axis functioning among depressed children and adolescents.
The principal conclusion, drawing from a number of experimental approaches and findings, is that there is good evidence that HPA dysfunction plays a role in depressive syndromes in populations of young people. First, this conclusion derives from the broad similarity of findings from studies in young populations with the results observed in research with adults. Studies of the dexamethasone suppression test DST in pediatric depressed samples have revealed robust rates of cortisol non-suppression that are comparable to those found in studies of depressed adults.
These data suggest that at least some forms of child and adolescent depression are characterized by abnormal stress system functioning i. Moreover, the pediatric DST data appear to mirror adult findings of greater HPA axis dysregulation associated with inpatient when compared with outpatient status. It is likely that inpatient status serves as a proxy for more serious depressive symptomatology, heightened stress exposure, or a combination of both factors.
Third, results from research assessing basal HPA axis functioning and diurnal variation among child and adolescent samples show some continuity with corresponding work in adults. On the whole, the evidence supports a developmental pattern in which basal HPA axis dysfunction becomes increasingly associated with pediatric depression with advancing age. Further, emerging longitudinal research provides strong evidence that overall dysregulated basal HPA activity precedes and predicts the development of depression in adolescence and early adulthood.
Consistent with the conclusion made by Lopez-Duran et al. Rather, depressed children and youth manifest slightly elevated circulating cortisol levels across the diurnal cycle. Fourth, initial evidence supports the observation that depressed children and adolescents demonstrate increasing cortisol hyper-reactivity with age in response to developmentally appropriate psychological stressors.
Indeed, relative to non-depressed controls, all of the germane studies reported significantly elevated cortisol levels subsequent to acute psychosocial stress induction in depressed children and adolescents. These results may also point to the primary importance of abnormalities in the functions of brain regions involved in processing or evaluating stressful events and affective information i. Such abnormalities suggest a neuropathological mechanism of initial stress system dysregulation among at least some depressed young people.
This still untapped area represents an important direction for future multidisciplinary research with depressed children and adolescents. Fifth, studies that have examined HPA axis functioning in asymptomatic children and adolescents of depressed parents provide consistent evidence that parental depression, and particularly maternal depression, is associated with elevated HPA axis functioning in offspring. This finding has been observed across developmental periods and appears to be principally manifested by disruptions to basal cortisol functioning, which might precede the onset of symptoms of depression.
Interestingly, this HPA dysregulation in offspring tends to be associated with maternal depression occurring during the prenatal and postnatal periods rather than with a history of maternal depression prior to conception. This pattern of results, together with the scarce longitudinal data available, suggests that genetic risk for depression alone cannot account for the elevated cortisol levels in offspring and provides further evidence that HPA axis dysregulation precedes and predicts the development of depression in young people.
The second principal conclusion that can be drawn from investigations of HPA axis functioning in pediatric depression is the centrality of a developmental perspective. Children and adolescents are not just small adults. For instance, relative to their adult counterparts, depressed young people appear to have somewhat lower rates of cortisol non-suppression following the DST. Additionally, in contrast to the adult data, there were generally smaller differences between depressed children and adolescents and control participants on such HPA indices as overall basal cortisol secretion and natural diurnal variation, as well as cortisol and ACTH secretion following the administration of the CRH challenge.
Above all, there is a pressing need for research aimed at identifying these and other possible mechanisms of HPA axis dysfunction among depressed young people. Two broad conclusions emerge from developmentally oriented research examining HPA axis irregularities associated with child and adolescent depression. First, the differences in HPA axis functioning that exist among depressed young people relative to non-depressed individuals appear to be smaller in scale than those found between their adult counterparts, but these disruptions to normative HPA axis functioning might emerge prior to evidence of symptoms of depression.
Second, differences in HPA axis functioning are found most consistently and prominently in the context of increased exposure to psychological stress, whether that is a brief, acute stress e. The ostensible discontinuities between the data on the HPA axis in pediatric populations and those more consistent and pronounced findings from adult depression literature may reflect important developmentally associated patterns.
Rather than a simple dichotomous transition from absence to presence of HPA axis dysregulation when one compares child versus adult manifestations of depression, the consideration of longitudinal data across developmental periods suggests more subtle, progressive changes in HPA axis functioning. Indeed, research conducted with depressed adults has found a positive correlation between age and basal cortisol hypersecretion Asnis et al.
Other cross-sectional studies—which have included samples of participants ranging from infancy to adulthood—have also supported the possibility of a developmental increase in cortisol levels over the pubertal and especially post-pubertal periods in adolescence Kenny et al. Although longitudinal evidence is exceedingly scarce, Shirtcliff et al. There is a pressing need for more prospective, longitudinal research to determine whether developmental changes in HPA functioning could account in part for the dramatic increases in the rates of depression from childhood to adolescence.
Regrettably, a salient omission from the extant pediatric literature is information related to stage of illness i. It is possible that the observed differences from adult studies may be primarily attributable to systematically differences in the proportion of depressed patients experiencing recurrent as opposed to first-onset episodes of the disorder. Accordingly, it will be critical for future work to consider the relative contribution of developmental changes in neurobiology e. Finally, given the robust and troubling gender differences in the rates of depression that also emerge in the context of the transition from childhood to adolescence, it will be essential to further examine gender differences in stress system functioning.
This notion is supported by the emerging empirical work indicating that adolescent girls, and particularly early-maturing girls, without a history of depression exhibit heightened HPA axis reactivity to interpersonal stressors. Although this research requires replication, these findings closely parallel earlier work using subjective measures of stress response. Similarly, there is a critical need for additional investigations that utilize a developmental psychopathology perspective to determine whether and how aberrant physiological stress system reactions may interact with other, possibly gender-specific sources of physiological, psychological, cognitive, and social vulnerabilities.
Multidisciplinary, methodologically rigorous particularly with respect to subject selection, power, and the nature and timing of biological sampling and longitudinal research designs are needed to further elucidate the role of the HPA axis in depression, as well as likely transactions between biological and psychological stress system functioning across development.
For example, future prospective research might benefit from the examination of possible HPA axis changes associated with certain cognitive vulnerabilities to depression e. Another future avenue of investigation might utilize an epidemiological approach incorporating psychological, neurological, and endocrinological measures in depressed, high-risk, and control samples. There are four salient conclusions from the present review. First, the extant research clearly supports the presence of HPA dysregulation in pediatric depression, and it appears this association strengthens with age.
Second, based on studies examining the DST among depressed samples of children and adolescents, pediatric depression may involve particular disruption to higher regulatory inhibitory auto-feedback. Third, available data suggest that HPA dysregulation may precede and predict the onset of depression in individuals, regardless of age. Fourth and finally, HPA dysregulation is evident in acute stress responses and might result from exposure to chronic early stressors or perturbations to normal infant care experiences.
Although adopting a developmental psychopathology perspective has helped to shed light on the ontogenesis of the relation between HPA axis function and depression, continued child clinical research is needed to further this understanding with the aim of informing diagnosis, prognostication, and intervention. This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author s and source are credited.
Skip to main content Skip to sections. Advertisement Hide. Download PDF. Open Access. First Online: 03 February The Problem of Child and Adolescent Depression Depression is among the most prevalent of psychological disorders. This still nascent and heterogeneous literature can be summarized as follows. The remaining studies, which recruited depressed participants referred either to outpatient evaluation or to treatment, were mostly composed of children. Only two studies by Birmaher et al. Second, the majority of studies utilized non-depressed control groups which were nonetheless composed of individuals who met criteria for other psychiatric conditions.
Only six studies included normative control samples Birmaher et al. Third, the vast majority of studies used a standardized experimental protocol, namely the oral administration of dexamethasone to depressed participants and non-depressed controls at or around 11 p. As with the body of work investigating the DST, basal cortisol secretion and diurnal rhythms associated with child and adolescent depression are similarly incomplete.
Here again, approximately equal numbers of published reports utilized child and adolescent samples. The average sample size in studies of diurnal cortisol is larger than that of studies of response to DST, but about half the studies included fewer than 40 patients with depression and a comparable number of control participants. In contrast to the DST literature, all but four studies of child and adolescent basal HPA axis functioning included normative control samples.
A synthesis of findings across this preliminary research is difficult due to the wide array of basal cortisol measures that have been indexed e. For example, nine studies employed the use of an indwelling venous catheter to collect unbound plasma cortisol samples from blood at various, unstandardized times throughout the day, whereas seven studies collected samples either from repeated venipuncture or from saliva. Assays of saliva samples assess only the levels of unbound active cortisol, whereas assays of serum assess both unbound and bound inactive cortisol.
However, there is high correspondence between serum and saliva assays of cortisol in children Bober et al. Equivalent Equivalent Goodyer et al. Equivalent Equivalent Kutcher et al. Equivalent Higher Car. Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author s and source are credited. References marked with an asterisk indicates those reviewed in the included tables Abela, J. Depression in children and adolescents: Causes, treatment, and prevention.
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Electronic industries. ISBN : cloth : alk. Includes index. Browse by Subject. Explore More. Summary A hotbed of activity for far-sighted thinkers and determined doers, the high technology industry has given rise to a pioneering group of entrepreneurs and executives which is not only behind today's most innovative technological advances, but at the forefront of a dynamic new movement in business. Armed with groundbreaking management philosophies and practices, the members of this visionary group are changing the way corporate structures are modeled and altering conventional conceptions of how companies should be run.
Having helped their own organizations survive and thrive in a highly competitive, pressure-filled arena, they offer invaluable lessons for executives and managers in all industries. Now, in Silicon Gold Rush, their inspirational stories are told and their strategies for success revealed. Written by Karen Southwick, editor of Upside Magazine's book division, this enlightening behind-the-scenes account spans the gamut of emerging technology management styles, from proven successes such as Cisco Systems to new kids on the block like Crossworlds Software.
Providing valuable insights into a myriad of key issues, from nurturing creativity and motivating employees to finding new markets and weathering tough times, Silicon Gold Rush examines the modi operandi of the technology world's emerging stars and heavyweights. The book reveals the maverick leadership techniques that are finding their way into mainstream corporate culture with far-reaching consequences. As Southwick points out: "Everywhere you look today, you will see older companies and those in traditional industries adopting the organizational structures, business strategies, and operational methods of the Silicon Valley gang.
To illustrate the dynamics of the technology industry that make it so exciting and instructive to watch-the scramble for financing, the feverish move of product from design to delivery, the constant risk of failure-it tracks the progress of CrossWorlds Software Inc. Delivering insider analysis of the thinking and motivations that drive today's cyber-Powerhouses, this eye-opening volume presents illuminating interviews with more than twenty trailblazing CEOs and senior executives, including Yahoo! A one-of-a-kind book that delves into the management ideas and strategies of high-tech leaders who are "rewriting the rules of business," Silicon Gold Rush is essential reading for anyone-in any industry-seeking the inside track on contemporary business transformations.
A hotbed of activity for far-sighted thinkers and determined doers, the high technology industry has given rise to a pioneering group of entrepreneurs and executives which is not only behind today's most innovative technological advances, but at the forefront of a dynamic new movement in business. Armed with groundbreaking management philosophies and practices, the members of this visionary read more. Video And Music.
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Video Games. About The Author. Formerly executive editor of Upside Magazine, she is currently editor of Upside's book division.
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