Psychosocial Perspectives on Pregnancy: Prenatal Maternal Stress and Coping

Pregnancy is a momentous life event experienced by most women that involves biomedical and psychosocial changes that are potentially stressful. High levels of maternal stress in pregnancy contribute to adverse fetal, infant, child, and adult outcomes, including cognitive, emotional, neurodevelopmental, and physical health effects. This article discusses definition, measurement, and effects of stress in pregnancy and describes current research questions such as whether the timing or pattern of prenatal stress accentuates its effects and whether prenatal stress accounts for ethnic disparities in adverse birth outcomes in the United States. We review research on the ways that women cope with prenatal stress and research examining associations of coping with maternal emotional state, health, and birth outcomes. Additionally, we describe important factors that improve women's psychosocial adaptation to pregnancy, their health, and their birth outcomes, specifically trait optimism, social support, and physical activity, and we emphasize interventions that utilize these factors.     

Emergent Values and the Experience of Aging

This study examined the role of values or guiding principles emerging from the life histories and reflections of 111 older adults as predictors of the experience of aging. Participants completed a detailed life history interview in which they described themselves on 10 major life dimensions. They also completed standardized questionnaires of well-being, personality traits, and intolerance of uncertainty. Participants expressed a mix of prosocial and self-interest values in their interviews. Multiple regression analyses indicated that social support and intolerance of uncertainty positively predicted the extent of values articulated in the interviews. Better quality of aging was predicted positively by extent of emergent values and greater well-being and negatively by age. The results indicate that an examination of values provides a unique contribution to the understanding of the experience of aging.     

Does natural law have non-normative foundations?

This paper addresses one aspect of the natural law theory of Germain Grisez. According to Grisez, practical reason identifies the goods of human life prior to the invocation of any moral or normative notions. It can thus provide a non-normative foundation for moral theory. I present Grisez’s position and argue that the apparently non-normative aspect of natural law cannot support the moral position built upon it. I argue, in particular, that practical principles, as Grisez understands them, are best understood as speech acts. If this is correct, it is possible to develop a sceptical challenge to Grisez’s position. I am grateful to Michael Frede, Robert George, Richard Holton, Philip Pettit, and two anonymous reviewers for many helpful comments on this paper. This paper was presented at a seminar in the Department of Philosophy at Princeton University in November 1987, and I am grateful for the comments I received from the audience—in particular, Germain Grisez—on that occasion.     

Measured Gene–Environment Interactions and Mechanisms Promoting Resilient Development

ABSTRACT— Childhood maltreatment elevates risk for antisocial behavior, depression, and other problems over the life span, but a subset of maltreated individuals avoids maladaptive development and shows resilience. Resilience reflects a dynamic confluence of factors that promotes positive adaptation despite exposure to adverse experiences. Recent replicated findings of gene–environment interactions (abbreviated G × E) involving maltreatment have identified two genes, monoamine oxidase A ( MAOA ) and serotonin transporter ( 5-HTT ), that moderate the association between childhood maltreatment and psychopathology. Accordingly, G × E raise new questions about potential biological mechanisms by which some individuals are able to cope adaptively and function relatively well despite experiencing early adversity. We summarize advances toward greater specification of G × E mechanisms, including genetic and environmental moderation of G × E effects and imaging genomics that provide clues regarding resilience processes in development.     

Intrahippocampal infusions of anisomycin produce amnesia: Contribution of increased release of norepinephrine,dopamine, and acetylcholine

Intra-amygdala injections of anisomycin produce large increases in the release of norepinephrine (NE), dopamine (DA), and serotonin in the amygdala. Pretreatment with intra-amygdala injections of the β-adrenergic receptor antagonist propranolol attenuates anisomycin-induced amnesia without reversing the inhibition of protein synthesis, and injections of NE alone produce amnesia. These findings suggest that abnormal neurotransmitter responses may be the basis for amnesia produced by inhibition of protein synthesis. The present experiment extends these findings to the hippocampus and adds acetylcholine (ACh) to the list of neurotransmitters affected by anisomycin. Using in vivo microdialysis at the site of injection, release of NE, DA, and ACh was measured before and after injections of anisomycin into the hippocampus. Anisomycin impaired inhibitory avoidance memory when rats were tested 48 h after training and also produced substantial increases in local release of NE, DA, and ACh. In an additional experiment, pretreatment with intrahippocampal injections of propranolol prior to anisomycin and training significantly attenuated anisomycin-induced amnesia. The disruption of neurotransmitter release patterns at the site of injection appears to contribute significantly to the mechanisms underlying amnesia produced by protein synthesis inhibitors, calling into question the dominant interpretation that the amnesia reflects loss of training-initiated protein synthesis necessary for memory formation. Instead, the findings suggest that proteins needed for memory formation are available prior to an experience, and that post-translational modifications of these proteins may be sufficient to enable the formation of new memories.A dominant view of the molecular basis for memory is that the formation of long-term memory for an experience depends on de novo protein synthesis initiated by that experience (Davis and Squire 1984; Frey and Morris 1998; Kandel 2001; Dudai 2002; Nader 2003; Alberini 2008). This view is supported by numerous studies showing that drugs that interfere with protein synthesis by inhibiting translational processes near the time of training produce later amnesia.Despite the centrality of experience-induced protein synthesis in contemporary models of memory formation, the necessity of protein synthesis for memory consolidation and long-term potentiation (LTP) stabilization has been questioned since the beginning of experiments of this type (e.g., Flexner and Goodman 1975; Barraco and Stettner 1976; Flood et al. 1978; Martinez et al. 1981), and continues to be questioned in several recent reviews (Routtenberg and Rekart 2005; Gold 2006, 2008; Radulovic and Tronson 2008; Routtenberg 2008; Rudy 2008). There are many instances of intact memories formed in the presence of extensive inhibition of protein synthesis, and a wide range of behavioral and pharmacological manipulations can rescue memory impaired by protein synthesis inhibitors. For example, amnesia is attenuated in a graded manner by increasing the training trials and foot shock intensity in avoidance tasks (Flood et al. 1975, 1978). Moreover, a wide range of stimulants, such as amphetamine, strychnine, corticosteroids, and caffeine, block amnesia induced by anisomycin (Flood et al. 1978). Like memory, LTP is sometimes insensitive to protein synthesis inhibitors. Simultaneous inhibition of both protein synthesis and degradation does not interfere with induction and maintenance of LTP (Fonseca et al. 2006a). Also, the specific schedule and frequency of test pulses after induction of LTP determine the vulnerability of LTP to anisomycin-induced impairment; anisomycin treatment does not impair LTP unless test pulses at a rate of 1/10 sec were administered during the anisomycin exposure (Fonseca et al. 2006b).Findings that memory and LTP can survive the inhibition of protein synthesis challenge the necessity of specific training- or stimulation-initiated protein synthesis for memory formation and synaptic plasticity. Several actions of protein synthesis inhibitors offer alternative accounts for amnesia produced by these drugs. These include cell sickness (Rudy et al. 2006; Rudy 2008), activation of protein kinases and superinduction of immediate early genes (Radulovic and Tronson 2008), abnormal neural electrical activity (Agnihotri et al. 2004; Xu et al. 2005), and intrusion of neural “noise” that masks the primary changes representing memory formation (Gold 2006). Neural responses to inhibition of protein synthesis such as these may impair memory either secondary to or independent of interference with protein synthesis.Another example of the mechanisms by which inhibition of protein synthesis might impair memory is by altering neurotransmitter functions. This possibility was suggested in early studies (e.g., Flexner and Goodman 1975; Quartermain et al. 1977) and has recently been supported by studies of neurotransmitter release at the site of intra-amygdala injections of anisomycin (Canal et al. 2007). In addition to impairing later memory after inhibitory avoidance training, pretraining injections of anisomycin into the amygdala produced rapid and dramatic increases in release of norepinephrine (NE), dopamine (DA), and serotonin (5-HT) at the sites of injection. The release of NE and DA then plummeted below baselines from 2 to 6 h after anisomycin injections, recovering within 48 h after anisomycin injection. The possibility that these neurochemical changes contribute to anisomycin-induced amnesia was supported by studies showing attenuation of amnesia in rats pretreated with intra-amygdala injections of the β-adrenergic receptor antagonist propranolol, apparently acting to blunt the effects of the large increases in release of NE after anisomycin injection. In addition, amnesia was produced by injections of high doses of norepinephrine into the amygdala.In addition to amnesias produced by anisomycin injections into the amygdala, as above, anisomycin also impairs memory when administered to other memory systems, including the hippocampus, where anisomycin impairs inhibitory avoidance memory (Quevedo et al. 1999; Debiec et al. 2002; Milekic et al. 2006). The present study extends the prior findings (Canal et al. 2007) in several respects. Experiments presented here determine whether anisomycin injections into the hippocampus result in changes in release of the catecholamines, NE and DA, at the site of injection, as seen previously in the amygdala. Additionally, the present experiments determine whether intrahippocampal injections of anisomycin result in increased release of acetylcholine, a neurotransmitter not examined in the previous study. To examine parallels with earlier amygdala findings, a further experiment determines whether intrahippocampal pretreatment with propranolol is effective in attenuating anisomycin-induced amnesia.     

How need for cognition and perceived control are differentially linked to emotional outcomes in the transition to retirement

This study contrasts how need for cognition and perceived control relate to positive and negative affect in 351 adults experiencing the transition to retirement (age range 44–79 years, M = 60). Structural equation modeling was used to identify significant pathways between exogenous variables of conscientiousness, openness, and education to need for cognition, and between neuroticism and health to perceived control. Need for cognition and perceived control emerged as separate and distinct forms of motivation, contributing to positive and negative affect in this model through differing patterns and to different degrees. Mediators between need for cognition and positive affect were frequency of cognitive activity and problem-focus coping. Perceived control had direct effects on positive and negative affect and indirect effects through cognitive activity on positive affect. The model helps to explain some of the psychological mechanisms instrumental in successful adaptation to change in adulthood. The dispositional motivation of need for cognition is described as a character strength with unique predictive value for older adults.     

An evaluation of recollection and familiarity in Alzheimer’s disease and mild cognitive impairment using receiver operating characteristics

There is a need to investigate exactly how memory breaks down in the course of Alzheimer’s disease (AD). Examining what aspects of memorial processing remain relatively intact early in the disease process will allow us to develop behavioral interventions and possible drug therapies focused on these intact processes. Several recent studies have worked to understand the processes of recollection and familiarity in patients with mild cognitive impairment (MCI) and very mild AD. Although there is general agreement that these patient groups are relatively unable to use recollection to support veridical recognition decisions, there has been some question as to how well these patients can use familiarity. The current study used receiver operating characteristic (ROC) curves and a depth of processing manipulation to understand the effect of MCI and AD on the estimates of recollection and familiarity. Results showed that patients with MCI and AD were impaired in both recollection and familiarity, regardless of the depth of encoding. These results are discussed in relation to disease pathology and in the context of recent conflicting evidence as to whether familiarity remains intact in patients with MCI. The authors highlight differences in stimuli type and task difficulty as possibly modulating the ability of these patients to successfully use familiarity in support of memorial decisions.     

PSYCHOLOGICAL OUTCOMES AMONG LESBIAN SEXUAL ASSAULT SURVIVORS: AN EXAMINATION OF THE ROLES OF INTERNALIZED HOMOPHOBIA AND EXPERIENTIAL AVOIDANCE

This study explored the relations among internalized homophobia (IH), experiential avoidance, and psychological symptom severity in a community sample of 72 lesbian sexual assault survivors. Results indicated that IH is associated with both experiential avoidance and posttraumatic stress disorder (PTSD) symptom severity. In addition, experiential avoidance is related to both PTSD and depression symptom severity. Finally, experiential avoidance completely mediated the relation between IH and PTSD symptom severity. The implications of these findings are discussed and suggestions for future research are provided.     

The influence of emotional awareness and expressiveness on care-giving burden and health complaints in women and men

This study was designed to investigate the role of emotional awareness and expressiveness as influences on the experience of burden and impaired health for women and men maintaining a spouse or relative at home who had been diagnosed as having dementia. One hundred and thirty-one Caucasian care givers, 41 males and 90 females, participated in the study. Multivariate analysis of variance indicated that women scored higher than men on measures of burden, health complaints, and awareness of others' emotions. Regression analysis indicated that self-awareness of emotions interacted with care-giver gender to decrease health complaints for female care givers but increased health complaints for male care givers. Self-awareness of emotions also increased feelings of burden for male care givers in general and for female care givers experiencing low levels of burden. Awareness of others' emotions tended to reduce feelings of burden. Emotional expressiveness did not influence burden or health complaint scores.This research was funded by grants from the Health Research Funds of Quebec, the Quebec Council for Social Research, and the Montreal Alzheimer Society. The authors would like to express their gratitude to Valerie Takeda, Charlene Stamegna, and Helene Fyfe for their work on the project, and to the families, patients, and staff of the various referral agencies for their cooperation with the study.To whom reprint requests should be addressed at Centre for Research in Human Development, Concordia University, 1455 de Maisonneuve Boulevard West, Montreal, Quebec, Canada, H3G 1M8.