Bereavement is a severe stressor that typically incites painful and debilitating symptoms of acute grief that commonly progresses to restoration of a satisfactory, if changed, life. Normally grief does not need clinical intervention. However, sometimes acute grief can gain a foothold and become a chronic debilitating condition called complicated grief. Moreover, the stress caused by bereavement, like other stressors, can increase the likelihood of onset or worsening of other physical or mental disorders. Hence some bereaved people need to be diagnosed and treated. A clinician evaluating a bereaved person is at risk for both over-and under-diagnosis, either pathologizing a normal condition or neglecting to treat an impairing disorder. The authors of DSM IV focused primarily on the problem of over-diagnosis, and omitted complicated grief because of insufficient evidence. We revisit bereavement considerations in light of new research findings. This paper focuses primarily on a discussion of possible inclusion of a new diagnosis and dimensional assessment of complicated grief. We also discuss modifications in the bereavement V code and refinement of bereavement exclusions in major depression and other disorders.

Behavioral scientists have increasingly included inflammatory biology as mechanisms in their investigation of psychosocial dynamics on the pathobiology of disease. However, a lack of standardization of inclusion and exclusion criteria and assessment of relevant control variables impacts the interpretation of these studies. The present paper reviews and discusses human biobehavioral factors that can affect the measurement of circulating markers of inflammation. Keywords relevant to inflammatory biology and biobehavioral factors were searched through PubMed. Age, sex, and hormonal status, socioeconomic status, ethnicity and race, body mass index, exercise, diet, caffeine, smoking, alcohol, sleep disruption, antidepressants, aspirin, and medications for cardiovascular disease are all reviewed. A tiered set of recommendations as to whether each variable should be assessed, controlled for, or used as an exclusion criteria is provided. These recommendations provide a framework for observational and intervention studies investigating linkages between psychosocial and behavioral factors and inflammation.

Complicated grief (CG) occurs when an individual experiences prolonged, unabated grief. The neural mechanisms distinguishing CG from noncomplicated grief (NCG) are unclear, but hypothesized mechanisms include both pain-related activity (related to the social pain of loss) and reward-related activity (related to attachment behavior). Bereaved women (11 CG, 12 NCG) participated in an eventrelated functional magnetic resonance imaging scan, during grief elicitation with idiographic stimuli. Analyses revealed that whereas both CG and NCG participants showed pain-related neural activity in response to reminders of the deceased, only those with CG showed reward-related activity in the nucleus accumbens (NA). This NA cluster was positively correlated with self-reported yearning, but not with time since death, participant age, or positive/negative affect. This study supports the hypothesis that attachment activates reward pathways. For those with CG, reminders of the deceased still activate neural reward activity, which may interfere with adapting to the loss in the present.

Grief is mediated by a distributed neural network that subserves affect processing, mentalizing, episodic memory retrieval, processing of familiar faces, visual imagery, autonomic regulation, and modulation/coordination of these functions. This neural network may account for the unique, subjective quality of grief and provide new leads in understanding the health consequences of grief and the neurobiology of attachment.

Summary Repeated interactions between infant and caregiver result in either secure or insecure relationship attachment patterns, and insecure attachment may affect individual emotion-regulation and health. Given that oxytocin enhances social approach behavior in animals and humans, we hypothesized that oxytocin might also promote the experience of attachment security in humans. Within a 3-week interval 26 healthy male students classified with an insecure attachment pattern were invited twice to an experimental session. Within each session, a single dose of oxytocin or placebo was administered, using a double-blind, placebo-controlled within-subject design. In both conditions, subjects completed an attachment task based on the Adult Attachment Projective Picture System (AAP). Thirty-two AAP picture system presentations depicted attachment-related events (e.g. illness, solitude, separation, loss), and were each accompanied by four prototypical phrases representing one secure and three insecure attachment categories. In the oxytocin condition, a significant proportion of these insecure subjects (N = 18; 69%) changed their rankings of “secure attachment” phrases towards the more appropriate for the AAP picture presentation, and the same subjects decreased in overall rating of the “insecure attachment” phrases. In particular, there was a significant decrease in the number of subjects ranking the pictures with “insecure-preoccupied” phrases from the placebo to the oxytocin condition. We find that a single dose of intranasally administered oxytocin is sufficient to induce a significant increase in the experience of attachment security in adults classified previously as insecure.

Background The hippocampus is likely involved in mood disorders but in vivo evidence for the role of anatomically distinct hippocampal subregions is lacking. Multiple sclerosis (MS), an inflammatory disease of the CNS, is linked to a high prevalence of depression as well as hippocampal atrophy and may thus provide important insight into the pathological correlates of medical depression. Here, we examine the role of subregional hippocampal volume for depression in relapsing-remitting (RR) MS. Methods Anatomically defined hippocampal subregional volumes (Cornu Ammonis 1 (CA1), CA2–CA3 and the Dentate Gyrus (CA23DG), Subiculum, Entorhinal Cortex) were measured using a high resolution T2-weighted magnetic resonance imaging (MRI) sequence in 29 RRMS patients and 20 matched healthy controls. Diurnal salivary cortisol was assessed at awakening, 4pm and 9pm on two consecutive days. Subjects also completed the Beck Depression Inventory (BDI-II). Results MS patients showed smaller hippocampal volumes compared to controls, particularly in the CA1 and Subiculum subregions. In addition, MS patients with depressive symptoms (BDI-II > 13) also showed smaller CA23DG volumes and higher cortisol levels. Within the MS group, CA23DG volume was correlated with depressive symptoms and cortisol levels. There were no associations with number of previous steroid treatments, global atrophy, or disease duration. Conclusions This report provides in vivo evidence for selective association of smaller CA23DG subregional volumes in the hippocampus with cortisol hypersecretion and depressive symptoms in MS.

Similar to non-Hispanic Blacks, Hispanics/Latinos experience a range of psychosocial and physical health challenges, including high rates of poverty, neighborhood segregation, discrimination, poor healthcare access, and high rates of obesity, diabetes, and undiagnosed and late-stage diagnosed diseases. Despite such risks, Hispanics generally experience better physical health and lower mortality than non-Hispanic Whites, an epidemiological phenomenon commonly referred to as the Hispanic or Latino health paradox. With the basic phenomenon increasingly well-established, attention now turns to the sources of such resilience. The current aims are to briefly examine the epidemiological paradox and highlight potential sociocultural resilience factors that may contribute to the paradoxical effects. We conclude with presentation of a framework for modeling sociocultural resilience and discuss future directions for psychological contributions.

Background-Pro-inflammatory cytokines are associated with sickness behaviors, a set of behaviors including low mood, which are orchestrated by the brain and described as shift in motivational state. The present study investigated the hypothesis that local inflammation is associated with greater subgenual anterior cingulate cortex (sACC) activation in persons undergoing chronic stress.