Exploring the mutual regulation between oxytocin and cortisol as a marker of resilience (2024)

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Arch Psychiatr Nurs. Author manuscript; available in PMC 2020 Apr 1.

Published in final edited form as:

Arch Psychiatr Nurs. 2019 Apr; 33(2): 164–173.

Published online 2018 Nov 20. doi:10.1016/j.apnu.2018.11.008

PMCID: PMC6442937

NIHMSID: NIHMS1514230

PMID: 30927986

Yang Li,^a,^* Afton L. Hassett,^b and Julia S. Seng^c

Author information Copyright and License information PMC Disclaimer

The publisher's final edited version of this article is available at Arch Psychiatr Nurs

Abstract

Early trauma can increase the risk for developing posttraumatic stress disorder (PTSD) in adulthood. Early trauma has also been associated with the dysregulation between the hypothalamic-pituitary-adrenal (HPA) and oxytocin systems and may influence the co-regulation between these two systems. But whether the mutual regulation of the two systems represents a sign of resilience and/or mutual dysregulation could be a sign of vulnerability to PTSD and the dissociative subtype of PTSD (PTSD-D) is unknown. The study aims to synthesize and conduct a preliminary test of a conceptual model of the mutual regulation between these two systems as a marker of resilience. We analyzed a pilot data with 22 pregnant women in 3 groups (PTSD only, PTSD-D, and trauma-exposed resilient controls) and repeated measures of plasma oxytocin and cortisol. Oxytocin and cortisol seemed reciprocal in all three groups, but both levels were relatively high in women with PTSD-D and low in those with PTSD compared with controls. This suggests that both hormones in women with PTSD-D and PTSD only are dysregulated, but not lacking in reciprocity.

Keywords: Oxytocin, cortisol, resilience, dissociation, posttraumatic stress disorder

Introduction

A substantial amount of research has focused on alteration in the hypothalamic-pituitary-adrenal (HPA) axis as a potential underpinning for posttraumatic stress disorder (PTSD; ; ). Many of the most chronic and complex cases of PTSD are those with roots in childhood maltreatment trauma. Cascade theory posited that there are three pillars of stress response dysregulated as consequences of attachment trauma in early development: cortisol, catecholamines, and oxytocin (). Those stress response hormones might be associated with psychopathological vulnerabilities, including PTSD and other manifestations of early developmental trauma, including dissociation and the dissociative subtype of PTSD (PTSD-D; ; Olff et al., 2013; Seng et al., 2013; Simeon et al., 2007).

Oxytocin as a neuropeptide hormone, can not only regulate the smooth muscle contractility for reproductive and lactation processes, but also plays a role in attachment and social affiliation such as mother-child interaction and parenting (Feldman, 2012; ; ; Orsucci, Paoloni, Conti, Reda, & Fulcheri, 2013). Oxytocin has also received increasing attention for its role in stress regulation and related psychopathology, including PTSD. The oxytocin and HPA systems are mutually regulating (Dabrowska et al., 2011). Oxytocin can inhibit the stress-induced activity of the HPA axis to promote the return of cortisol levels to normal levels after stress is experienced (; ; ). A variety of stressors could induce oxytocin secretion in both blood and brain. Brain oxytocin plays a role in the control of neuroendocrine stress responses by inhibiting the secretion of adrenocorticotropic hormone (ACTH) and thus decreasing the production and release of cortisol. Oxytocin release, oxytocin receptor expression, and oxytocin binding exist in many brain regions that are rich in glucocorticoid receptors and thus oxytocin can have an effect on the inhibition of neuroendocrine stress responses. Maltreated children have been reported to have decreased urinary oxytocin levels () and women with a history of childhood abuse showed reduced cerebrospinal fluid oxytocin concentrations (Heim et al., 2009). Childhood trauma may alter the development of the oxytocin system as well as the connectivity with other systems (Buisman-Pijlman et al., 2014). A study found increased cortisol reactivity in subjects with early life stress while attenuated cortisol reactivity in subjects without early life stress after oxytocin administration (Grimm et al., 2014). Early parental separation stress has been studied to decrease the suppressing effect of oxytocin on cortisol levels (). These findings suggest that oxytocin and cortisol systems may be mutually dysregulated as a consequence of traumatic stress.

There is a growing consensus that altered reactivity of the oxytocin system can contribute to enhanced vulnerability to the development of psychiatric disorders and reduced resilience to stress (Buisman-Pijlman et al., 2014; ). Mutual dysregulation between oxytocin and cortisol as a consequence of traumatic stress could contribute to individual vulnerability to the psychopathologic effects of stress (e.g., PTSD). Conversely, the mutual regulation between these two hormones may be a sign of resilience to stress (). This hypothesis has not been considered; there is not yet a theoretical basis or empirical evidence to support mutual dysregulation between these two hormones as a sign of the susceptibility to PTSD and PTSD-D or conversely mutual regulation as a sign of resilience.

The concept of resilience

Resilience is a dynamic, interactive concept that refers to the overcoming of traumatic stress, decreased vulnerability to environmental risk experiences, and maintenance of relatively normal physical and psychological function (Rutter, 2006). In contrast, vulnerable individuals can be defined as exhibiting detrimental physiological and psychological consequences as a result of trauma exposure, including serious stress-related psychiatric disorders (e.g., PTSD). Thus, from the resilience perspective, the development of psychopathology such as PTSD can be explained by individual variability in stress vulnerability (). Studies have established models of resilience to stress from a psychosocial perspective (; ; Woodgate, 1999). For example, in the resiliency model proposed by Woodgate (1999) for adolescent cancer patients, whether adolescent cancer patients adapt successfully to their stressors (e.g., cancer diagnosis, hair loss) depends on the interaction between vulnerability (e.g., disabling) and protective (e.g., self-understanding) factors on stress response.

Increasing attention has also been paid to the neurobiological features of resilience (Rutter, 2013). Individuals who successfully adapt to traumatic stress may exhibit changes in biological processes that differ from those found in stress-vulnerable individuals (). Many biomarkers, including oxytocin and cortisol typically considered separately, have been suggested to represent the biological basis for resilience to stress (; Ozbay et al., 2008). For example, among police officers routinely exposed to potentially traumatic events and routine life stressors, those who followed trajectories of resilience and recovery over 4 years had significantly increased cortisol levels in response to the experimental stressor, while those following a trajectory of chronic increasing distress had a blunted cortisol response to the challenge (Galatzer-Levy et al., 2014). This finding suggests that individual differences in cortisol stress response may be related to the development and long-term course of stress pathology and resilience. The anxiolytic effects of oxytocin have been seen through reducing anxiety and increasing the effects of social support in individuals exposed to psychosocial stress (). Dysregulated oxytocin system may be a biological underpinning for the elevated risk for psychiatric disorders and decreased resilience to stress (Buisman-Pijlman et al., 2014; Ozbay et al., 2008).

It has been noted that resilience to stress cannot be fully accounted for by a single neurobiological marker, but rather the interaction of multiple biomarkers (Osorio et al., 2016; Ozbay et al., 2008). Tops and colleagues (2007) suggested that stress-related health outcomes might rely on the balance between oxytocin and cortisol stress responses (). This is biologically plausible because oxytocin could inhibit the stress-induced cortisol levels that play a protective role in maintaining normal HPA stress regulation (Neumann, Kromer, et al., 2000; Neumann, Torner, et al., 2000; Pierrehumbert et al., 2012). The fight/flight system––HPA axis and the stress-buffering oxytocin system, tends to operate in balance, reaching a homeostasis state (Moberg, 2003). But when the oxytocin system is affected by early attachment trauma, the connectivity with the HPA axis may also be influenced (Buisman-Pijlman et al., 2014). This could affect the stress response activity of the HPA axis, contributing to HPA dysregulation. Thus, the mutual regulation between oxytocin and cortisol may play a significant role in an individual’s resilience to stress, while the mutual dysregulation between these two hormones may reflect the susceptibility to PTSD. The resilience concept can serve as a conceptual basis for understanding the balance between oxytocin and cortisol stress responses as a sign of resilience to stress and the imbalance between these two systems as a marker of susceptibility to PTSD.

Despite a growing body of research on the neurobiological underpinnings of resilience, no resilience models have been constructed that focuses on the reciprocal relationship between oxytocin and cortisol. Therefore, it is essential to build a conceptual model with oxytocin and cortisol and their mutual regulation and/or dysregulation as a potential biological pathway for resilience to stress and/or vulnerability to the development of PTSD. We posit that, in addition to individual variability in oxytocin and cortisol levels, their interactions can affect resilience to stress. The purpose of this paper is to propose a conceptual model that can be considered as a guide for future research on the neurobiological mechanism of PTSD and to put it to a very preliminary test-of-concept using archived data from a small clinical study.

Literature on oxytocin and cortisol in relation to PTSD and its dissociative subtype

Numerous studies have investigated cortisol in relation to PTSD, but the findings have been varied. Two meta-analyses indicated that PTSD was not associated with basal cortisol levels (Klaassens et al., 2012; Meewisse et al., 2007), while the other two meta-analyses found lower daily cortisol output in relation to PTSD (; ). Oxytocin administration has been recently suggested as a potential therapeutic intervention for alleviating psychiatric disorders (). However, high oxytocin levels are not always associated with the beneficial conditions. In a study with 26 adults exposed to child abuse, 25 adult survivors of childhood cancer and 39 healthy controls, the adults who experienced life-threatening illnesses in childhood had higher oxytocin secretion in response to the psychosocial stress test compared to the other two groups (Pierrehumbert et al., 2010). A study with a highly traumatized sample in Atlanta reported the highest basal levels in those who had a history of childhood maltreatment as well as a current PTSD diagnosis while the lowest levels of oxytocin in individuals without child maltreatment and current PTSD (Olff et al., 2013). Given the mixed the findings, studies are still needed to test the direction of the relationships between cortisol, oxytocin and PTSD.

Explication of the conceptual model

The conceptual model was constructed by synthesizing the resilience concept, the resilience model by Woodgate (1999), and evidence from the literature (Figure 1). The model posits that when stressors occur, the activity of the HPA axis is initiated, which produces cortisol in response to stress. Oxytocin exerts stress-buffering effects to inhibit the stress-induced HPA activity and decrease cortisol levels. When cortisol stress responses and the protective stress-buffering effects of oxytocin reach a balance, homeostasis is preserved. Oxytocin level and its connectivity with the HPA axis might be affected by severe or chronic stressors, including early trauma in attachment relationships. Severe or chronic stressors could also cause dysregulation of the HPA axis, including abnormal basal cortisol levels and/or elevated or weak cortisol stress reactivity. The mutual regulation between these two systems would thus be considered as a sign of resilience to stress, while the mutual dysregulation between these two systems would be a sign of vulnerability to PTSD and especially PTSD-D. There likely would be a continuum or dynamic process from the mutual regulation to the mutual dysregulation.

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Figure 1.

The bio-behavioral resilience model for understanding the mutual regulation between oxytocin and cortisol as a marker of resilience. Note. * The dashed line indicates a continuum of mutual regulation and dysregulation. HPA=hypothalamic-pituitary-adrenal; PTSD=posttraumatic stress disorder; PTSD-D=the dissociative subtype of PTSD.

The main components of the model are stressors, HPA axis, oxytocin system, mutual regulation, mutual dysregulation, resilience, and vulnerability. Stressors include acute (e.g., traumatic life events, catastrophic events) and chronic (e.g., childhood maltreatment and sociodemographic and environmental) stressors, with stressors to attachments plausibly taking both acute and chronic forms. Cortisol and oxytocin are primary physiological indicators of the HPA axis and oxytocin system, respectively. The mutual regulation is defined as a homeostasis state in which HPA axis and oxytocin reach a balance within their normal range. The mutual dysregulation can be classified into three types: both oxytocin and cortisol in extremely high levels; both hormones in extremely low levels; and the ratio of these two hormones out of proportion (one in extremely high levels and the other in extremely low levels). For the first two types of dysregulation, the two hormones may lack reciprocity, while they are still reciprocal for the last type. Resilience refers to a healthy state in which an individual remains after exposure to stressors, while vulnerability is more specific to the risk for developing PTSD and PTSD-D.

The test-of-concept

To provide a very preliminary test of this bio-behavioral resilience model, we conducted secondary analysis of data to answer the question: Do differences in mutual regulation of oxytocin and cortisol (a) distinguish women with posttraumatic psychopathology from trauma-exposed resilient controls and (b) distinguish PTSD-D from women with PTSD only? Based on the results of the analysis, we would revise or refine the model to advance it toward further testing.

Methods

Study design and data suitability

To conduct a theory-testing secondary analysis, we needed, at a minimum, repeated measures of oxytocin and cortisol in a sample well-characterized in terms of PTSD and dissociation. We used the archived data from the co-author’s pilot study of oxytocin and the severe vomiting of pregnancy, PTSD, and dissociation. The original study was a test of concept about the extent to which PTSD-related oxytocin dysregulation might be a mechanism of hyperemesis via its role in smooth muscle peristalsis (Seng, 2010; Seng et al., 2013). That study demonstrated oxytocin differences in PTSD and PTSD-D but did not examine relationship with cortisol or consider their mutual regulation. Thus, this dataset was well-suited to being extended into this resilience theory test-of-concept purpose. It contained the necessary series of repeated measures of both oxytocin and cortisol collected under a strict in-patient research protocol. It characterized the women with standardized measures of PTSD and dissociation. As oxytocin is sexually dimorphic, testing the concept in a sample of females only is a reasonable starting point. However, there were some shortcomings, including small sample size and the fact that all are pregnant and affected to a greater or lesser extent by nausea and vomiting. The previously published pilot report contains descriptions of the study sample recruitment, data collection, and assay methods (Seng et al., 2013). Here we present an overview of those methods and our analysis plan for the test-of-concept.

Sample and Setting

In the pilot study, pregnant women who met diagnostic criteria for the severe nausea and vomiting of pregnancy (hyperemesis gravidarum) were recruited during their first emergency department visit, and pregnant women with more normal levels of pregnancy nausea and vomiting were recruited via community fliers. Exclusion criteria were smoking, non-English speaking, more than sixteen weeks of gestational age, histories of psychotic disorder, acute illness, molar pregnancy or multiple gestations, both of which raise oxytocin levels. A total of twenty-five pregnant women were included in the pilot study.

Participants completed data collection in the inpatient General Clinical Research Center at the medical center of the University of Michigan with approval of the Institutional Review Board, a confidentiality certificate, and written informed consent. In the original protocol (“24-hour protocol”), fifteen participants had blood specimens for oxytocin and cortisol collected every four hours for 24 hours. No diurnal pattern for oxytocin was observed, so 10 more women were enrolled in a revised protocol (“90-minute protocol”) and had blood specimens for oxytocin drawn every 10 minutes between 10:30 am and noon, based on Nyquist’s Sampling Theorem (Nyquist, 1928) to detect pulsatility; cortisol was measured in the first, fifth, and last of these specimens.

In this secondary analysis of the data, the PTSD diagnosis and a dissociative symptom score cutoff were used to classify participants into three groups: the PTSD-D group who had the dissociative symptoms as well as PTSD, the PTSD only group who met the diagnosis for PTSD but did not have dissociative symptoms, and trauma-exposed resilient controls with neither dissociative symptoms nor PTSD. Three women in the 90-minute protocol had dissociative symptoms but did not meet the PTSD diagnosis and were excluded because of the small group size and because this study focused on PTSD-D rather than the dissociation per se. Thus, the total sample size included in the present study is twenty-two, with fifteen women in the 24-hour protocol and seven women in the 90-minute protocol. The participant flow is shown in Figure 2.

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Figure 2.

Participant flow chart. Note. PTSD=posttraumatic stress disorder; PTSD-D=the dissociative subtype of PTSD.

Measures

The Life Stressor Checklist was used to assess lifetime exposure to 30 potentially traumatic events with a yes/no response format (). The 30 traumatic events includes disasters, accidents, being sent to jail, parental separation or divorce, physical or mental illness, emotional abuse or neglect, physical neglect, physical abuse, sexual assault, and other events. Respondents are asked to provide ages when events occurred and when they ended. The questionnaire has shown high sensitivity to trauma among women (). In this study, child abuse was defined as any “yes” response to physical abuse, physical neglect, emotional abuse or neglect, and sexual assault before age 16. Adult abuse was defined as any “yes” response to physical abuse, physical neglect, emotional abuse or neglect, and sexual assault after age 16. The sum of lifetime trauma exposures was the total number of “yes” responses to the 30 traumatic events.

The National Women’s Study PTSD Module was used to yield a 0–17 count of symptoms and a current PTSD case variable based on the DSM-IV symptom clusters criteria. The measure had sensitivity of 0.99 and specificity of 0.79 compared to the Structured Clinical Interview for DSM-III-R (Kilpatrick DG et al., 1998; ).

The 8-item taxon version of the Dissociative Experiences Scale (DES-T) was used to measure dissociative symptoms (). In clinical and community samples, test-retest reliability was .84 to .96, alpha was .95, sensitivity was .80, and specificity was .80 (; Waller et al., 1996). The 75th percentile of the DES-T score was used as the cutoff to make the dissociation cases.

The Pregnancy Unique Quantification of Emesis (PUQE) includes 3 questions to assess the severity of nausea and vomiting (Koren et al., 2002). The number of hours of nausea and the number of times of vomiting and retching/dry heaves were asked on a 1 to 5 scale. The nausea and vomiting severity score was computed by summing up the scores of the 3 questions, ranging from 3 to 15.

Statistical analysis

The demographic characteristics, gestational weeks, nausea and vomiting severity score, trauma history, PSTD symptom count, DES-T score and group membership were compared for the total, 24-hour protocol, and 90-minute protocol samples using chi-squares and ANOVAs. Due to the small sample size in each protocol, and the availability of noon oxytocin and cortisol in both protocols, we combined the samples and used the noon blood specimens. Moreover, we calculated the mean of the repeated measures for oxytocin in the 24-hour protocol, as well as the area under the curve (AUC) for the cortisol levels across the 24-hour protocol since there was a diurnal pattern for cortisol. However, the 90-minute protocol for this pilot has only 7 women. Given this small sample size in the 90-minute protocol, we did not conduct any inferential statistical analysis, but we did depict their levels in the graphs.

We analyzed the hormone patterns with descriptive statistical and basic visualizing approaches. Although the sample size is small, we used independent samples t-tests and ANOVAs to describe group differences in terms of noon oxytocin and cortisol levels for both protocols combined, mean oxytocin levels for the 24-hour protocol, and cortisol AUC for the 24-hour protocol. These statistical methods were used to test hypothesis 1a, that oxytocin and cortisol patterns among women with PTSD would differ from healthy controls and to test hypothesis 1b that patterns would also differ between women with PTSD and PTSD-D. We interpreted the tests to be statistically significant if P was <.05 (two-tailed), which is stringent for this sample size. Linear regressions were done to estimate effect size of significant relationships in terms of variance explained. When oxytocin and cortisol levels were not log-transformed, the ANOVA and linear regression results were similar with the results with oxytocin and cortisol levels log-transformed. Thus, the non- transformed oxytocin and cortisol levels were used for analysis to show the natural units of oxytocin and cortisol. To test hypothesis 2, Pearson’s correlations were used to examine the correlations between oxytocin and cortisol levels within the three groups. We graphically depicted hormone levels by group for each hormone separately. Then we juxtaposed the oxytocin and cortisol levels within each group to explore the appearance of reciprocity. SPSS v.22 was used for all analyses.

Results

Sample characteristics

There were no significant differences in the demographic characteristics, gestational weeks, nausea and vomiting severity, trauma history, PTSD symptom count, DES-T score, or group membership across the total, 24-hour protocol, and 90-minute protocol samples (P>.05). The results can be seen in Table 1.

Table 1.

Sample characteristics.

Characteristic	Total Sample	24-hour protocol	90-minute protocol
	(n=22)	(n=15)	(n=7)
Demographics, n
African American race	8	6	2
Pregnant as a teen (20 years old or less)	4	2	2
Living in poverty (income < $15,000)	3	3	0
High school education or less	15	11	4
Gestational Weeks, M (SD)	12.27 (2.51)	11.67 (2.74)	13.57 (1.27)
Nausea and vomiting severity, M (SD)	8.07 (3.66)	8.20 (4.07)	8.20 (4.07)
Trauma History
Childhood abuse/neglect, n	7	5	2
Adult abuse/assault, n	9	5	4
Trauma exposure sum, M (SD)	6.27 (3.59)	6.86 (4.74)	6.00 (3.07)
Mental Health, M (SD)
PTSD symptom count	5.55 (4.95)	5.07 (4.98)	6.57 (5.13)
DES-T score	9.64 (2.92)	9.27 (2.58)	10.43 (3.64)
Group Membership, n
PTSD-D	4	2	2
PTSD only	6	3	3
Resilient controls	12	10	2

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PTSD=posttraumatic stress disorder; DES-T=the taxon version of the Dissociative Experiences Scale; PTSD-D=the dissociative subtype of PTSD.

Oxytocin and cortisol levels across groups

Independent samples t-tests showed no significant differences between PTSD group and resilient controls in noon oxytocin and cortisol levels from both protocols combined and mean oxytocin and cortisol AUC from the 24-hour protocol (P>.05).

ANOVA tests showed that there were significant differences in noon oxytocin levels and mean oxytocin levels for the 24-hour protocol among the three groups (F (2, 19)=18.74, P < .001, partial η²=0.66; F (2, 12)=4.34, P=.038, partial η²=0.42). Post hoc analyses revealed that the significant difference was between the PTSD-D group compared to both the PTSD only group and resilient controls (P < .05). No significant group differences were observed for either noon cortisol levels or cortisol AUC from the 24-hour protocol (P>.05). The results can be seen in Table 2 and Figure 3. Following up this finding with linear regression showed that the PTSD-D group’s higher noon oxytocin levels and mean oxytocin levels (β = 0.79; β = 0.62) explained 66% of the noon oxytocin variance and 42% of the mean oxytocin levels. However, there were no significant associations of group with noon cortisol levels and cortisol AUC from the 24-hour protocol (P >.05). No significant associations of PTSD only with any oxytocin and cortisol levels were detected (P >.05). The results can be seen in Table 3.

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Figure 3.

Changes in oxytocin and cortisol levels across time by group. Note. PTSD=posttraumatic stress disorder; PTSD-D=the dissociative subtype of PTSD.

Table 2

Means and standard deviations of the oxytocin (pg/mL) and cortisol levels (ug/dL) among the three groups.

	PTSD-D ^a	PTSD only ^b	Resilient controls ^c	F	P	η²	Post hoc comparison
Noon Oxytocin for both	619.75	72.00	118.67	18.74	<.001	0.66	a>b
protocols combined, n=22	(290.00)	(41.78)	(130.08)				a>c
Mean Oxytocin for 24- hour protocol, n=15	477.50 (423.09)	78.28 (52.90)	125.10 (124.02)	4.34	.038	0.42	a>b a>c
Noon Cortisol for both protocols combined, n=22	9.58 (2.41)	9.12 (3.68)	11.78 (4.68)	1.00	.388	0.10	-
Cortisol AUC for 24- hour	51.65	35.83	49.68	1.15	.349	0.16	-
protocol, n=15	(15.56)	(3.62)	(15.91)

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PTSD=posttraumatic stress disorder; PTSD-D=the dissociative subtype of PTSD; AUC=Area under the curve.

Table 3.

Linear regressions for the associations of oxytocin and cortisol levels with the dissociative subtype of PTSD and PTSD only.

	Predictor ^a	β	F	P	R²
Noon Oxytocin for both protocols combined			18.74	<.001	0.66
	PTSD-D	0.79^***
	PTSD only	−0.09
Mean Oxytocin for 24-hour protocol			4.34	.038	0.42
	PTSD-D	0.62^*
	PTSD only	−0.10
Noon Cortisol for both protocols combined			1.00	.388	0.10
	PTSD-D	−0.21
	PTSD only	−0.29
Blood Cortisol AUC for 24-hour protocol			1.15	.349	0.16
	PTSD-D	0.05
	PTSD only	−0.39

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PTSD=posttraumatic stress disorder; PTSD-D=the dissociative subtype of PTSD; AUC=Area under the curve.

^aThe reference group is the resilient controls.

^*P< .05.

^***P< .001.

Correlation and reciprocity between oxytocin and cortisol levels among the three groups

Coefficients for correlations between the hormones within groups were weak, ranging from −.26 to .06, and none were statistically significant.

Figure 4 depicts the inter-relationships between oxytocin and cortisol levels across time for each group. Figure 4A, ,4B,4B, and and4C4C described changes in oxytocin and cortisol levels across 24 hours for PTSD-D, PTSD only and resilient controls. In the PTSD-D group, oxytocin levels decrease as cortisol levels increase before 8 AM and then oxytocin levels rise as cortisol levels go down. The oxytocin and cortisol levels seem reciprocal, but both levels are relatively high. In the PTSD-only group, both hormones are at relatively low levels and appear to be consistently lower than resilient controls. Figure 4D, ,4E,4E, and and4F4F depict changes in oxytocin and cortisol levels across 90 minutes for PTSD-D, PTSD only and controls. The oxytocin and cortisol levels seem reciprocal among all three groups. The PTSD-D group exhibited the most obvious reciprocity, but both hormones are at relatively high levels. The revised bio-behavioral resilience model based on the preliminary test (Figure 5) aligns with the specific finding that patterns of cortisol and oxytocin appear to distinguish the PTSD-D group from those with PTSD only.

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Figure 4.

The inter-relationships between oxytocin and cortisol levels across time within each group. Note. PTSD=posttraumatic stress disorder; PTSD-D=the dissociative subtype of PTSD.

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Figure 5.

The revised bio-behavioral resilience model. Note. * The dashed line indicates a continuum of mutual regulation and dysregulation. HPA=hypothalamic-pituitary-adrenal; PTSD=posttraumatic stress disorder; PTSD-D=the dissociative subtype of PTSD

Discussion

This study developed a conceptual model to guide future research on the mutual dysregulation between oxytocin and cortisol as a potential sign of the susceptibility to PTSD and PTSD-D, as well as tested the model via secondary analysis of data from a small sample of pregnant women. The test-of-concept graphic analysis partially supported the conceptual model that oxytocin and cortisol co-varied in higher patterns with the PTSD-D group and lower patterns with the PTSD only group and appeared to be especially dysregulated (significantly higher oxytocin levels) in women with PTSD-D. However, this co-variance suggests that reciprocity is maintained.

As reported in relation to the parent study, PTSD-D was found in relation to higher oxytocin levels, indicating that elevated oxytocin concentrations may be a marker for the subtype of PTSD. This is consistent with another pilot study including 15 women, where the presence of dissociative symptoms was correlated with higher oxytocin levels in response to a laboratory provocation (Munro et al., 2013). Although oxytocin administration has been demonstrated to have treatment effects on psychiatric disorders such as anxiety (), our finding suggests that it may not be effective in treating individuals with PTSD-D as those individuals already have high basal oxytocin levels. The overall lower levels of oxytocin in pregnant women with PTSD only compared to resilient controls was not statistically significant, but it may still suggest that PTSD-D and PTSD diagnosis only may have a distinct biological basis in the oxytocin regulation system. In individuals with PTSD-D, the enhanced oxytocin levels may serve as a signal for a need to seek social affiliation (Olff et al., 2013). However, the lower levels of oxytocin in those with PTSD diagnosis only are in line with the understanding of PTSD as an anxiety disorder since it appears in these data that they have low plasma oxytocin levels. An experiment study demonstrated greater anxiety-related behavior in transgenic mice that lacked oxytocin ().

We did not find significant differences in cortisol levels among the three groups, which is inconsistent with studies reporting the associations of cortisol levels with PTSD or dissociation (; ; Simeon et al., 2007). No correlations between oxytocin and cortisol were observed for any group. Among women with PTSD-D, the higher levels of oxytocin might inhibit the stress response and thus the release of cortisol is decreased. Such a process may explain our finding that cortisol levels in women with PTSD-D was not significantly higher than the other two groups. But the small sample size used in the pilot study makes it challenging to determine whether the non-significant findings are also not clinically significant. Another possible explanation for the non-significant findings is that study subjects included pregnant women with nausea and vomiting. Since numerous physiological changes occur throughout pregnancy () and nausea and vomiting have been reported in relation to higher cortisol levels (), it may lead to the non-significant associations between cortisol levels and PTSD or dissociation, as well as between oxytocin and cortisol levels.

Despite our hypothesis was that mutual regulation of oxytocin and cortisol would be a sign of resilience to stress, the graphs revealed that all three groups exhibited reciprocity. But oxytocin levels were the highest in women with PTSD-D. Although no statistical significances were reached, women with PTSD-D had slightly higher cortisol levels and women with PTSD diagnosis only had relatively lower oxytocin and cortisol levels compared to resilient controls. Thus, the most succinct statement of the findings might be that both hormones in women with PTSD-D and PTSD only are mutually dysregulated, but not lacking in reciprocity. To some extent, the findings support our conceptual model that the two forms of mutual dysregulation (i.e., both hormones in extremely high levels or low levels) can be considered as a sign of vulnerability to PTSD and PTSD-D.

Based on the findings, we revised the proposed conceptual model. The first type of mutual dysregulation we defined is that both oxytocin and cortisol are at very high levels compared to the healthy group, which may be associated with the vulnerability to developing PTSD-D. The second type of mutual dysregulation is that both hormones are lower than healthy group levels, which may be the biological basis for the risk of developing PTSD. But for these two types of dysregulations, the two hormones still remain reciprocal, which is opposite to our initial hypothesis. The regulating functions of each hormone system may be impaired by chronic or severe stress, but the inhibiting effect of oxytocin on cortisol levels is not influenced. We initially defined the ratio of these two hormones being out of proportion (one in extremely high levels and the other in extremely low levels) as the last type of mutual dysregulation. Although our findings did not identify this type, it did not mean this type does not exist. Future studies need to explore if this type of mutual dysregulation is associated with other trauma-related psychopathology (e.g., depression, anxiety).

This test-of-concept secondary analysis had several limitations inherent in the pilot study database available for the purpose. First, the sample size is relatively small, limiting the power to detect significant differences in cortisol levels among the three groups, as well as significant correlations between oxytocin and cortisol levels. Second, as our sample size was small, we were unable to control for confounding factors such as demographic characteristics, gestational weeks, nausea and vomiting severity, trauma history, and comorbid depression that may influence our main findings. Third, our sample included pregnant women who had 16 weeks or less gestation, as well as had hyperemesis gravidarum, nausea, or vomiting. Pregnancy physiological changes and hyperemesis gravidarum, nausea, and vomiting may influence our findings. Fourth, PTSD-D was measured based on the self-rating DES-T score. The lack of clinical diagnosis may underestimate the severity of the dissociative symptoms. Fifth, due to the small sample size, the numbers of participants who reported child maltreatment was very small. Thus, we did not examine the effects of child maltreatment as the attachment trauma on the risk for PTSD and PTSD-D as well as the mutual regulation between oxytocin and cortisol. Lastly, the study lacked attachment measures, as well as a stress provocation test specific to attachment trauma during the blood specimen collection. Measuring attachment and oxytocin and cortisol levels in response to attachment trauma would contribute to better understanding of the oxytocin and cortisol regulating mechanisms for PTSD-D and PTSD diagnosis only.

Implications for research and clinical practice

The study has implications for future research. Since the conceptual model was tested based on a secondary analysis of data from a pilot study with some limitations, the model needs to be further developed and tested to better understand the mutual regulation between oxytocin and cortisol as a potential sign of resilience to stress. Future studies need to have a larger female representative or clinical sample, attachment measures, and a stress-provocation test specific to attachment trauma. Oxytocin and cortisol need to be collected multiple times using a protocol to detect the pulsatility. The different oxytocin and cortisol patterns for the PTSD only and the dissociative subtype of PTSD suggest that researchers need to pay attention to this subtype of PTSD and further investigate the specific biological basis for the subtype. These findings may also have implications for psychiatric nursing practice. The bio-behavioral model may help psychiatric nurses better understand the neurobiological role in vulnerability to trauma-related psychopathology, as well as the neurobiological mechanisms for resilience to stressful life events, which could promote nursing care for patients with trauma exposures. Additionally, interventions that could facilitate the mutual regulation of oxytocin and cortisol may be effective treatment strategies to enhance resilience to stress. Identifying biomarkers of trauma-related psychopathology could assist in recognizing at–risk populations.

Conclusion

This study is the first to explore a conceptual model that considers the mutual dysregulation of oxytocin and cortisol as a sign of vulnerability to PTSD and PTSD-D. Our study filled a gap in exploring Cascade theory’s view that more than one stress response system is dysregulated by childhood maltreatment trauma. The parent pilot study had already shown that oxytocin levels were elevated in the presence of high levels of dissociation (Seng et al., 2013); and this test-of-concept extends that finding by focusing on the relationship between the two systems to show that reciprocity appears to be maintained, but that both oxytocin and HPA systems appear to be similarly dysregulated – either both are elevated or diminished. Future studies are still needed to modify and validate the conceptual model to better understand the biological basis for the vulnerability to PTSD and its dissociative subtype.

Highlights

Both oxytocin and cortisol levels were relatively high in women with PTSD-D.
Both hormones were relatively low in women with PTSD only.
Both hormones in women with PTSD-D and PTSD only are dysregulated.
Both hormones in women with PTSD-D and PTSD only are not lacking in reciprocity.

Acknowledgments

Funding: Funding for this project was from the National Institutes of Health grant M01RR00042 to the University of Michigan General Clinical Research Center, grant U013786 to the University of Michigan Office of the Vice President for Research, and grant 1P20 NR008367 from the National Institute of Nursing Research.

Footnotes

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Declarations of interest: None.

References

Agaibi CE, & Wilson JP (2005). Trauma, PTSD, and resilience: a review of the literature.Trauma Violence Abuse, 6(3), 195–216. doi: 10.1177/1524838005277438 [PubMed] [CrossRef] [Google Scholar]
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (DSM-5): American Psychiatric Publication.
Amico JA, Mantella RC, Vollmer RR, & Li X (2004). Anxiety and stress responses in female oxytocin deficient mice.Journal of Neuroendocrinology, 16(4), 319–324. doi: 10.1111/j.0953-8194.2004.01161.x [PubMed] [CrossRef] [Google Scholar]
Bernstein EM, & Putnam FW (1986). Development, reliability, and validity of a dissociation scale.The Journal of Nervous and Mental Disorder, 174(12), 727–735. [PubMed] [Google Scholar]
Bremner D, Vermetten E, & Kelley ME (2007). Cortisol, dehydroepiandrosterone, and estradiol measured over 24 hours in women with childhood sexual abuse-related posttraumatic stress disorder.The Journal of Nervous and Mental Disorder, 195(11), 919–927. doi: 10.1097/NMD.0b013e3181594ca0 [PubMed] [CrossRef] [Google Scholar]
Buisman-Pijlman FT, Sumracki NM, Gordon JJ, Hull PR, Carter CS, & Tops M (2014). Individual differences underlying susceptibility to addiction: Role for the endogenous oxytocin system.Pharmacology Biochemistry and Behavior, 119, 22–38. doi: 10.1016/j.pbb.2013.09.005 [PubMed] [CrossRef] [Google Scholar]
Dabrowska J, Hazra R, Ahern TH, Guo JD, McDonald AJ, Mascagni F, … Rainnie DG (2011). Neuroanatomical evidence for reciprocal regulation of the corticotrophinreleasing factor and oxytocin systems in the hypothalamus and the bed nucleus of the stria terminalis of the rat: Implications for balancing stress and affect.Psychoneuroendocrinology, 36(9), 1312–1326. doi: 10.1016/j.psyneuen.2011.03.003 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
de Weerth C, & Buitelaar JK (2005). Physiological stress reactivity in human pregnancy--a review.Neuroscience & Biobehavioral Reviews, 29(2), 295–312. doi: 10.1016/j.neubiorev.2004.10.005 [PubMed] [CrossRef] [Google Scholar]
Delahanty DL, Nugent NR, Christopher NC, & Walsh M (2005). Initial urinary epinephrine and cortisol levels predict acute PTSD symptoms in child trauma victims.Psychoneuroendocrinology, 30(2), 121–128. doi: 10.1016/j.psyneuen.2004.06.004 [PubMed] [CrossRef] [Google Scholar]
Feldman R (2012). Oxytocin and social affiliation in humans.Hormones and Behavior, 61(3), 380–391. doi: 10.1016/j.yhbeh.2012.01.008 [PubMed] [CrossRef] [Google Scholar]
Fries ABW, Ziegler TE, Kurian JR, Jacoris S, & Pollak SD (2005). Early experience in humans is associated with changes in neuropeptides critical for regulating social behavior.Proceedings of the National Academy of Sciences of the United States of America, 102(47), 17237–17240. doi: 10.1073/pnas.0504767102 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Galatzer-Levy IR, Steenkamp MM, Brown AD, Qian M, Inslicht S, Henn-Haase C, … Marmar CR (2014). Cortisol response to an experimental stress paradigm prospectively predicts long-term distress and resilience trajectories in response to active police service.Journal of Psychiatric Research, 56, 36–42. doi: 10.1016/j.jpsychires.2014.04.020 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Galbally M, Lewis AJ, Ijzendoorn M, & Permezel M (2011). The role of oxytocin in mother-infant relations: a systematic review of human studies.Harvard Review of Psychiatry, 19(1), 1–14. doi: 10.3109/10673229.2011.549771 [PubMed] [CrossRef] [Google Scholar]
Gordon I, Zagoory-Sharon O, Leckman JF, & Feldman R (2010). Oxytocin and the development of parenting in humans.Biological Psychiatry, 68(4), 377–382. doi: 10.1016/j.biopsych.2010.02.005 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Grimm S, Pestke K, Feeser M, Aust S, Weigand A, Wang J, … Bajbouj M (2014). Early life stress modulates oxytocin effects on limbic system during acute psychosocial stress.Social Cognitive and Affective Neuroscience, 9(11), 1828–1835. doi: 10.1093/scan/nsu020 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Heim C, Young LJ, Newport DJ, Mletzko T, Miller AH, & Nemeroff CB (2009). Lower CSF oxytocin concentrations in women with a history of childhood abuse.Molecular Psychiatry, 14(10), 954–958. doi: 10.1038/mp.2008.112 [PubMed] [CrossRef] [Google Scholar]
Heinrichs M, & Domes G (2008). Neuropeptides and social behaviour: effects of oxytocin and vasopressin in humans.Progress in Brain Research, 170, 337–350. doi: 10.1016/S0079-6123(08)00428-7 [PubMed] [CrossRef] [Google Scholar]
Jewell D, & Young G (2003). Interventions for nausea and vomiting in early pregnancy.Cochrane Database Systematic Review(4), CD000145. doi: 10.1002/14651858.CD000145 [PubMed] [CrossRef]
Koren G, Boskovic R, Hard M, Maltepe C, Navioz Y, & Einarson A (2002). MotheriskPUQE (pregnancy-unique quantification of emesis and nausea) scoring system for nausea and vomiting of pregnancy.American Journal of Obstetrics and Gynecology, 186(5 Suppl Understanding), S228–231. [PubMed] [Google Scholar]
Kilpatrick DG, Resnick HS, Freedy JR, Pelcovitz D, Resick PA, Roth S, & van der Kolk B (1998). The posttraumatic stress disorder field trial: Emphasis on Criterion A and overall PTSD diagnosis (Vol. 4). Washington, DC: American Psychiatric Press. [Google Scholar]
Klaassens ER, Giltay EJ, Cuijpers P, van Veen T, & Zitman FG (2012). Adulthood trauma and HPA-axis functioning in healthy subjects and PTSD patients: a meta-analysis.Psychoneuroendocrinology, 37(3), 317–331. doi: 10.1016/j.psyneuen.2011.07.003 [PubMed] [CrossRef] [Google Scholar]
Lanius RA, Bluhm R, Lanius U, & Pain C (2006). A review of neuroimaging studies in PTSD: Heterogeneity of response to symptom provocation.Journal of Psychiatric Research, 40(8), 709–729. doi: 10.1016/j.jpyschires.2005.07.007 [PubMed] [CrossRef] [Google Scholar]
Lanius RA, Vermetten E, Loewenstein RJ, Brand B, Schmahl C, Bremner JD, & Spiegel D (2010). Emotion modulation in PTSD: Clinical and neurobiological evidence for a dissociative subtype.The American Journal of Psychiatry, 167(6), 640–647. doi: 10.1176/appi.ajp.2009.09081168 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Liberzon I, & Knox D (2012). Expanding Our Understanding of Neurobiological Mechanisms of Resilience by Using Animal Models (vol 37, pg 317, 2012).Neuropsychopharmacology, 37(6), 1558–1558. doi: 10.1038/npp.2012.9 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Luecken LJ, Dausch B, Gulla V, Hong R, & Compas BE (2004). Alterations in morning cortisol associated with PTSD in women with breast cancer.Journal of Psychosomatic Research, 56(1), 13–15. doi: 10.1016/S0022-3999(03)00561-0 [PubMed] [CrossRef] [Google Scholar]
Macdonald K, & Feifel D (2013). Helping oxytocin deliver: considerations in the development of oxytocin-based therapeutics for brain disorders.Frontiers in Neuroscience, 7, 35. doi: 10.3389/fnins.2013.00035 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Meewisse ML, Reitsma JB, de Vries GJ, Gersons BP, & Olff M (2007). Cortisol and post-traumatic stress disorder in adults: systematic review and meta-analysis.The British Journal of Psychiatry, 191, 387–392. doi: 10.1192/bjp.bp.106.024877 [PubMed] [CrossRef] [Google Scholar]
Meinlschmidt G, & Heim C (2007). Sensitivity to intranasal oxytocin in adult men with early parental separation.Biological Psychiatry, 61(9), 1109–1111. doi: 10.1016/j.biopsych.2006.09.007 [PubMed] [CrossRef] [Google Scholar]
Miller GE, Chen E, & Zhou ES (2007). If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans.Psychological Bulletin, 133(1), 25–45. doi: 10.1037/0033-2909.133.1.25 [PubMed] [CrossRef] [Google Scholar]
Moberg KU (2003). The oxytocin factor: Tapping the hormone of calm, love, and healing: Da Capo Press. [Google Scholar]
Morris MC, Compas BE, & Garber J (2012). Relations among posttraumatic stress disorder, comorbid major depression, and HPA function: a systematic review and metaanalysis.Clinical Psychology Review, 32(4), 301–315. doi: 10.1016/j.cpr.2012.02.002 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Munro ML, Brown SL, Pournajafi-Nazarloo H, Carter CS, Lopez WD, & Seng JS (2013). In search of an adult attachment stress provocation to measure effect on the oxytocin system: a pilot validation study.Journal of American Psychiatric Nurses Association, 19(4), 180–191. doi: 10.1177/1078390313492173 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Neumann ID, Kromer SA, Toschi N, & Ebner K (2000). Brain oxytocin inhibits the (re)activity of the hypothalamo-pituitary-adrenal axis in male rats: involvement of hypothalamic and limbic brain regions.Regulatory Peptides, 96(1–2), 31–38 [PubMed] [Google Scholar]
Neumann ID, Torner L, & Wigger A (2000). Brain oxytocin: differential inhibition of neuroendocrine stress responses and anxiety-related behaviour in virgin, pregnant and lactating rats.Neuroscience, 95(2), 567–575 [PubMed] [Google Scholar]
Norris FH, & Hamblen JL (2004). Standardized self-report measures of civilian trauma and PTSD.Assessing psychological trauma and PTSD, 2, 63–102 [Google Scholar]
Nyquist H (1928). Certain topics in telegraph transmission theory.trans AIEE, 47, 617–644 [Google Scholar]
Olff M, Frijling JL, Kubzansky LD, Bradley B, Ellenbogen MA, Cardoso C, … van Zuiden M (2013). The role of oxytocin in social bonding, stress regulation and mental health: an update on the moderating effects of context and interindividual differences.Psychoneuroendocrinology, 38(9), 1883–1894. doi: 10.1016/j.psyneuen.2013.06.019 [PubMed] [CrossRef] [Google Scholar]
Osorio C, Probert T, Jones E, Young AH, & Robbins I (2016). Adapting to Stress: Understanding the Neurobiology of Resilience.Journal of Behavioral Medicine, 1–16. doi: 10.1080/08964289.2016.1170661 [PubMed] [CrossRef]
Ozbay F, Fitterling H, Charney D, & Southwick S (2008). Social support and resilience to stress across the life span: a neurobiologic framework.Current Psychiatry Reports, 10(4), 304–310 [PubMed] [Google Scholar]
Pierrehumbert B, Torrisi R, Ansermet F, Borghini A, & Halfon O (2012). Adult attachment representations predict cortisol and oxytocin responses to stress.Attachment & Human Development, 14(5), 453–476. doi: 10.1080/14616734.2012.706394 [PubMed] [CrossRef] [Google Scholar]
Pierrehumbert B, Torrisi R, Laufer D, Halfon O, Ansermet F, & Beck Popovic M (2010). Oxytocin response to an experimental psychosocial challenge in adults exposed to traumatic experiences during childhood or adolescence.Neuroscience, 166(1), 168–177. doi: 10.1016/j.neuroscience.2009.12.016 [PubMed] [CrossRef] [Google Scholar]
Resnick HS, Kilpatrick DG, Dansky BS, Saunders BE, & Best CL (1993). Prevalence of civilian trauma and posttraumatic stress disorder in a representative national sample of women.Journal of Consulting and Clinical Psychology, 61(6), 984–991 [PubMed] [Google Scholar]
Rutter M (2006). Implications of resilience concepts for scientific understanding.Annals of the New York Academy of Sciences, 1094, 1–12. doi: 10.1196/annals.1376.002 [PubMed] [CrossRef] [Google Scholar]
Rutter M (2013). Annual Research Review: Resilience--clinical implications.Journal of Child Psychology and Psychiatry, 54(4), 474–487. doi: 10.1111/j.1469-7610.2012.02615.x [PubMed] [CrossRef] [Google Scholar]
Sandler IN, Wolchik SA, & Ayers TS (2008). Resilience rather than recovery: A contextual framework on adaptation following bereavement.Death Studies, 32(1), 59–73. doi: 10.1080/07481180701741343 [PubMed] [CrossRef] [Google Scholar]
Seng JS (2010). Posttraumatic oxytocin dysregulation: is it a link among posttraumatic self disorders, posttraumatic stress disorder, and pelvic visceral dysregulation conditions in women?Journal of Trauma & Dissociation, 11(4), 387–406. doi: 10.1080/15299732.2010.496075 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Seng J, Miller J, Sperlich M, van de Ven CJ, Brown S, Carter CS, & Liberzon I (2013). Exploring dissociation and oxytocin as pathways between trauma exposure and trauma-related hyperemesis gravidarum: a test-of-concept pilot.Journal of Trauma & Dissociation, 14(1), 40–55. doi: 10.1080/15299732.2012.694594 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Simeon D, Knutelska M, Yehuda R, Putnam F, Schmeidler J, & Smith LM (2007). Hypothalamic-pituitary-adrenal axis function in dissociative disorders, post-traumatic stress disorder, and healthy volunteers.Biological Psychiatry, 61(8), 966–973. doi: 10.1016/j.biopsych.2006.07.030 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Teicher MH, Andersen SL, Polcari A, Anderson CM, & Navalta CP (2002). Developmental neurobiology of childhood stress and trauma.Psychiatric Clinics of North America, 25(2), 397–426, vii-viii [PubMed] [Google Scholar]
Tops M, van Peer JM, Korf J, Wijers AA, & Tucker DM (2007). Anxiety, cortisol, and attachment predict plasma oxytocin.Psychophysiology, 44(3), 444–449. doi: 10.1111/j.1469-8986.2007.00510.x [PubMed] [CrossRef] [Google Scholar]
Waller N, Putnam FW, & Carlson EB (1996). Types of dissociation and dissociative types: A taxometric analysis of dissociative experiences.Psychological Methods, 1(3), 300–321 [Google Scholar]
Wolfe J, & Kimerling RGender issues in the assessment of posttraumatic stress disorder. In: Wilson JP, Keane TM, eds. Assessing psychological trauma and PTSDNew York, NY: Guilford Press;1997:192–238. [Google Scholar]
Woodgate RL (1999). Conceptual understanding of resilience in the adolescent with cancer: Part I.Journal of Pediatric Oncology Nursing, 16(1), 35–43. [PubMed] [Google Scholar]

Exploring the mutual regulation between oxytocin and cortisol as a marker of resilience (2024)

FAQs

What is the relationship between oxytocin and cortisol? ›

Oxytocin exerts stress-buffering effects to inhibit the stress-induced HPA activity and decrease cortisol levels. When cortisol stress responses and the protective stress-buffering effects of oxytocin reach a balance, homeostasis is preserved.

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What are the roles of oxytocin in stress responses allostasis and resilience? ›

Various factors including environment and early life adversity plastically modulate activity of the endogenous oxytocin system. Oxytocin influences behavioral and neuroendocrine responses to stress (to maintain homeostasis) and plays a role in the inhibition of allostatic load/overload.

What role does oxytocin primarily play in emotional processing? ›

To summarize, OXT exerts its effects on different information processing levels associated with social anxiety via a more general stress-dampening effect during social stress, modulation of fear conditioning, and modulation of attentional processes associated with social anxiety.

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Is cortisol also known as the motivational hormone? ›

Cortisol belongs to a class of hormones known as glucocorticoids. It helps regulate a person's motivation, mood, fear, and fight-or-flight response. Stress causes the body to produce an abundance of cortisol, which can slow some bodily functions.

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How do you increase oxytocin and decrease cortisol? ›

Yoga, Meditation, and Mindfulness

Researchers have investigated yoga for its ability to stimulate the vagus nerve and produce oxytocin. Plus, being mindful throughout your day can help reduce stress, increase oxytocin levels, and improve overall well-being.

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What emotions are linked to oxytocin? ›

Euphoria and feelings of relaxation are the most common effects of oxycodone on the brain, which explains its high potential for abuse.

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What is oxytocin trying to tell you in its stress response? ›

It has been hypothesized that oxytocin release during stressful situations serves to dampen physiological stress levels, for it has also been observed that high basal plasma oxytocin levels are associated with low norepinephrine levels, blood pressure and heart rate (Light et al., 2004).

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What 3 hormones are involved in the stress response? ›

As an adaptive response to stress, there is a change in the serum level of various hormones including CRH, cortisol, catecholamines and thyroid hormone. These changes may be required for the fight or flight response of the individual to stress.

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What kind of behavior does oxytocin facilitate? ›

A plethora of studies have uncovered a role for oxytocin in intimacy, social recognition, pair bonding, and anxiety, among others. Oxytocin acts centrally within the brain to control behavior, as opposed to its well-known peripheral role in parturition and lactation.

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What are signs of low oxytocin? ›

What happens if I have too little oxytocin?

irritability and inability to feel affectionate.
increased feelings of anxiety.
difficulty achieving org*sm.
disturbed sleep.

What can too much oxytocin do to the brain? ›

Our study proves that the hormone ramps up innate social reasoning skills, resulting in an emotional oversensitivity that can be detrimental in those who don't have any serious social deficiencies.”

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What does oxytocin do mentally? ›

Oxytocin fuels maternal instincts, tells us who brings us the most joy, helps us make friends, and is associated with the development of empathy but also hatred and prejudice. The same hormone that makes us warm and fuzzy can also stoke the fires of aggression under the right circ*mstances.

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What does a cortisol belly look like? ›

The adrenal glands are part of your endocrine system and release cortisol into your bloodstream. It then flows throughout your body and can lead to a specific appearance and feel in your abdominal area. A stress belly will likely appear more “saggy” than the rest of the fat on your body.

What is the difference between oxytocin and cortisol? ›

Whereas cortisol mediates energy mobilization during stress, oxytocin has anti-inflammatory, anxiolytic, and analgesic effects that support social connection and survival across the lifespan.

Why cortisol is called stress combat hormone? ›

Regulating your body's stress response: During times of stress, your body can release cortisol after releasing its “fight or flight” hormones, such as adrenaline, so you continue to stay on high alert. In addition, cortisol triggers the release of glucose (sugar) from your liver for fast energy during times of stress.

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What hormone triggers oxytocin? ›

The release of oxytocin can be stimulated by hormones such as estrogen. In addition oxytocin can be released in response to various types of sensory stimulation.

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What is the role of oxytocin in the stress response? ›

Oxytocin administration prior to stress inhibits this neuroendocrine response, reducing the secretion of CRF and glucocorticoids. In the CNS, oxytocin administration attenuates stress-related activity within the amygdala and appears to protect against stress-induced alterations in hippocampal synaptic plasticity.

What hormone is the opposite of cortisol? ›

Morning light also signals the brain to release cortisol, which is our awake hormone. Cortisol wakes us and should be at its peak in the morning. Melatonin and cortisol are in an opposite relationship; when melatonin is high, cortisol should be low and vice versa.

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What is the relationship between oxytocin and adrenaline? ›

Moderate doses of adrenaline (5–25 μg) did not inhibit the effect of simultaneously administered oxytocin on the uterus. The effect of oxytocin appears superimposed upon the uterine response to adrenaline. When low doses of oxytocin are used a delay of the oxytocic effect occurs.