Behavioral and molecular genetics of dissociation: the role of the serotonin transporter gene promoter polymorphism (5-HTTLPR).

We evaluated the role of the serotonin transporter gene promoter polymorphism (5-HTTLPR) in the etiology of dissociation. Adult twin pairs (N = 184 pairs; mean age 33.0 years, SD = 10.8) completed measures for dissociation and trauma. The DNA samples were genotyped for 5-HTTLPR adjusted for rs25531 alleles. Behavioral genetic analyses showed that genetic factors explained 45% of the variance in dissociative symptoms, while 55% of the variance was explained by unique environment and measurement error. Participants with the SS genotype of 5-HTTLPR reported more dissociative symptoms compared to participants with the other genotypes (p = .02), and they showed more pathological dissociative symptoms than the other participants (p = .04) when they reported more depressive symptoms and when they had experienced trauma.

Oxytocin modulates amygdala, insula, and inferior frontal gyrus responses to infant crying: a randomized controlled trial.

BACKGROUND: Oxytocin facilitates parental caregiving and mother-infant bonding and might be involved in responses to infant crying. Infant crying provides information about the physical status and mood of the infant and elicits parental proximity and caregiving. Oxytocin might modulate the activation of brain structures involved in the perception of cry sounds-specifically the insula, the amygdala, and the thalamocingulate circuit-and thereby affect responsiveness to infant crying. METHOD: In a randomized controlled trial we investigated the influence of intranasally administered oxytocin on neural responses to infant crying with functional magnetic resonance imaging. Blood oxygenation level-dependent responses to infant crying were measured in 21 women who were administered oxytocin and 21 women who were administered a placebo. RESULTS: Induced oxytocin levels reduced, experimentally, activation in the amygdala and increased activation in the insula and inferior frontal gyrus pars triangularis. CONCLUSIONS: Our findings suggest that oxytocin promotes responsiveness to infant crying by reducing activation in the neural circuitry for anxiety and aversion and increasing activation in regions involved in empathy.

Oxytocin receptor gene and depressive symptoms associated with physiological reactivity to infant crying.

Both the oxytocin receptor (OXTR) gene and depressive symptoms have been associated with parenting behaviour. The OXTR GG genotype has been suggested to be related to more sensitive parenting, whereas depressive symptoms may affect sensitivity negatively. We examined the role of OXTR and the influence of depressive symptoms in explaining differences in physiological reactivity to infant crying. Heart rate responses of 40 healthy females without children (age 19-47 years, randomly selected half of twin pairs) were measured during the presentation of three episodes of infant cry sounds. Participants with the presumably more efficient variant of the oxytonergic system gene (OXTR GG) had more pronounced physiological reactivity to repeated cry sounds, except when they showed more symptoms of depression. Results were replicated in the second half of the twin sample. This is the first study to suggest effects of OXTR genotype on physiological reactivity to infant crying. Depressive symptoms may however suppress the effect of the OXTR GG genotype.

Intended sensitive and harsh caregiving responses to infant crying: the role of cry pitch and perceived urgency in an adult twin sample.

OBJECTIVE: To examine the underlying mechanisms of adults' intended caregiving responses to cry sounds in a behavioral genetic design and to investigate the role of cry pitch and perceived urgency in sensitive and harsh caregiving responses. METHODS: The sample consisted of 184 adult twin pairs (18-69 years), including males and females, parents and nonparents. In an experimental design we presented cry sounds varying in pitch and measured adults' perception and their intended caregiving responses. Cry stimuli were based on a 10-second cry sample of a 2-day-old infant with a fundamental frequency averaging 500 Hz. Two additional cry sounds were created by digitally increasing the fundamental frequency to 700 and 900 Hz. RESULTS: Individual differences in the perceived urgency of infant crying and intended sensitive caregiving responses were explained by genetic factors (38% and 39%, respectively), while the variance in harsh caregiving responses was due to shared (31%) and unique (69%) environmental influences. Adults were more likely to indicate sensitive caregiving responses to higher-pitched cry sounds and when they perceived the cries as more urgent, while high-pitched cry sounds were also directly associated with harsh caregiving responses. CONCLUSIONS: The influence of genetic factors on intended caregiving responses to infant crying is substantial for normal variations in sensitive caregiving, but absent for harsh caregiving responses. The findings suggest that the perception of infant crying as urgent paves the way for more immediate and affectionate caregiving responses, while an extreme increase in cry pitch may present a direct risk factor for more irritated, negative and even harsh parenting. PRACTICE IMPLICATIONS: Infants who display abnormal cry acoustics such as extreme increases in pitch may be at risk for harsh parenting. Interventions should promote parental sensitive response to distress vocalizations to prevent harsh parenting in case of at-risk infants.

Prolonged cardiac effects of momentary assessed stressful events and worry episodes.

OBJECTIVES: To test the hypothesize that increased heart rate (HR) and decreased heart rate variability (HRV) are not only due to concurrent stressful events and worries but also to stressors and worries occurring in the preceding hours or stressors anticipated to occur in the next hour. Worry was expected to mediate at least part of the prolonged effects of stressors. METHODS: Ambulatory HR and HRV of 73 teachers were recorded for 4 days, during which the participants reported occurrence and duration of worry episodes and stressful events on an hourly basis, using computerized diaries. Multilevel regression models were used, accounting for effects of several biobehavioral variables. RESULTS: Stressful events were not associated with changes in HR or HRV. However, worry episodes had effects on concurrent HR and HRV (2.55 beats/minute; -5.76 milliseconds) and HR and HRV in the succeeding hour (3.05 beats/minute; -5.80 milliseconds) and 2 hours later (1.52 beats/minute; -3.14 milliseconds). These findings were independent of emotions, physical activity, posture, and other biobehavioral factors. CONCLUSION: Worry has effects on cardiac activity, and these effects were still visible after 2 hours. The latter finding suggests that a considerable part of prolonged activation may be induced by unconscious stress-related cognition.

Cardiac effects of momentary assessed worry episodes and stressful events.

OBJECTIVE: To hypothesize that increased heart rate (HR) and decreased heart rate variability (HRV) occurs not only during stressful events but also during episodes in which stress is cognitively represented, but not necessarily present, i.e., during worry. METHODS: Ambulatory HR and HRV of 73 female and male teachers were recorded for 4 days, during which they reported, on an hourly basis using computerized diaries, the number and characteristics of worry episodes and stressful events. Multilevel regression models were used, controlling for biobehavioral variables. RESULTS: Compared with neutral periods, worry episodes and stressful events had independent effects on HR (2.00 beats/min and 2.75 beats/min, respectively) and HRV (-1.07 ms and -1.05, respectively). Neither psychological traits nor biobehavioral variables influenced these results. Effects were most pronounced for work-related worry on HR (9.16 beats/min) and HRV (-1.19 ms), and for worry about anticipated future stress on HR (4.79 beats/min). CONCLUSIONS: Worry in daily life might have substantial cardiac effects in addition to the effects of stressful events, especially in the form of work-related and anticipatory stress, the latter being a type of stress that has been largely neglected in stress research.

Prolonged stress-related cardiovascular activation: Is there any?

BACKGROUND: Prolonged physiological activation before or after stressors has gained recognition as a decisive element in theories that explain the link between stress and disease, specifically cardiovascular (CV) disease. This view is opposed to the conventional reactivity hypothesis that emphasizes responses during stressors. PURPOSE: Prolonged activity has not often been an explicit research goal of real-life stress studies. Nevertheless, a growing number of these studies have provided evidence for prolonged activity, often as a secondary research goal. METHODS: An overview of this evidence is lacking and is provided in this article. RESULTS: The combined data from the reviewed studies suggest that discrete and chronic stress sources, as well as negative emotional episodes and dispositions, are related to prolonged CV activity of various durations, including sleep periods. On the other hand, evidence supporting the assumption that prolonged stress-related activation predicts disease is still very modest. CONCLUSIONS: In this article we suggest that future research of prolonged activation should give priority to (a) the establishment of clear beginnings and endings of stressful events, (b) the prediction of disease by prolonged activation, and (c) potential psychological mediators of stress-related prolonged activation. These mediators may include, for example, worry and rumination, or other processes characterized by perseverative cognition, including unconscious processes.

Expanding stress theory: prolonged activation and perseverative cognition.

Several theories of the stress-disease link have now incorporated prolonged activation. This article argues that these theories still lack an important element, that is, the cognitive nature of the mechanism that causes stress responses to be sustained. The perception of stress and the initial response to it do not automatically lead to prolonged activation. The active cognitive representations of stressors need to be prolonged in order to extend their physiological concomitants. We call this mediating process perseverative cognition, and it is manifested in phenomena such as worry, rumination, and anticipatory stress. We summarize evidence suggesting that these phenomena are indeed associated with physiological activation, including cardiovascular, endocrinological and immunological parameters. This evidence is still far from sufficient, due to the many methodological insufficiencies in the studies involved. Nevertheless, it makes clear that cognitive phenomena characterized by perseverative cognition may be likely candidates to mediate the effects of stress sources on somatic disease. We also argue that there is a dearth of evidence supporting the role of prolonged activation. There are a limited number of studies demonstrating prolonged activity related to stressors and emotional episodes, and their methodologies often do not allow unambiguous conclusions. Even more important, the crucial assumption that prolonged activation actually leads to pathogenic states and disease has received hardly any attention yet and therefore is still largely unsupported. There are only a few studies that showed that anticipatory responses and slow recovery from stress predicted disease states.