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Biomedical subjects

R Yehuda

Publications and source records attributed to R Yehuda.

At least 19 recordsLinked to original sources
PubMed2006

Clinical correlates of DHEA associated with post-traumatic stress disorder.

OBJECTIVE: Increased plasma dehydroepiandrosterone (DHEA) and dehydroepiandrosterone-sulfate (DHEAS) have been demonstrated in post-traumatic stress disorder (PTSD), but the documented beneficial effects of these steroids in enhancing mood and cognition, as well as neuroprotection, suggest their presence in PTSD may be associated with defensive rather than maladaptive effects. METHOD: We, therefore, examined plasma DHEA, DHEAS, cortisol, and the DHEA/cortisol ratio in 40 male veterans with or without PTSD, and determined their relationships to PTSD symptom severity and symptom improvement. RESULTS: The PTSD group showed significantly higher plasma DHEA and non-significantly higher DHEAS levels as well as a significantly lower cortisol/DHEA ratio, controlling for age. Regression analyses demonstrated that DHEA and DHEAS levels could be predicted by symptom improvement and coping, whereas the cortisol/DHEA ratio was predicted by severity of childhood trauma and current symptom severity. CONCLUSION: That greater symptom improvement was related to DHEA levels may suggest for a role for these hormones in modulating recovery from PTSD.

Adaptation, Psychological↗
PubMed2005

Neuroendocrine aspects of PTSD.

This chapter discussed how neuroendocrine findings in posttraumatic stress disorder (PTSD) potentially inform hypothalamic-pituitary-adrenal (HPA) alterations in PTSD and highlight alterations relevant to the identification of targets for drug development. Most studies demonstrate alterations consistent with an enhanced negative feedback inhibition of cortisol on the pituitary, an overall hyperreactivity of other target tissues (adrenal gland, hypothalamus), or both in PTSD. However, findings of low cortisol and increased reactivity of the pituitary in PTSD are also consistent with reduced adrenal output. The observations in PTSD are part of a growing body of neuroendocrine data providing evidence of insufficient glucocorticoid signaling in stress-related neuropsychiatric disorders.

Adrenal Cortex Hormones↗
PubMed2005

Influence of visible light and ultraviolet irradiation on motility and fertility of mammalian and fish sperm.

OBJECTIVE: The effects of visible light irradiation on sperm motility, fertility, and reactive oxygen species (ROS) formation were investigated and compared in ram and fish (tilapia). BACKGROUND DATA: Low-energy visible light has previously been found to modulate various processes in different biological systems. In the literature, it is accepted that the first step following visible light irradiation is the formation of ROS by endogenous cellular photosensitizers. METHODS: Sperm of ram and tilapia were irradiated with various light sources (400-800 nm white light, 660 nm red light, 360 nm blue light, 294 nm UV), and their motility and fertility rates were measured. The amount of ROS generated by irradiation was estimated using electron paramagnetic resonance (EPR) technique. RESULTS: Sperm taken from tilapia showed higher motility and fertility following red and white light irradiation. In contrast, the motility and fertility of ram sperm were slightly increased only by red light. A negative effect on motility and fertility of sperm of both species was obtained following irradiation with UV and blue light. The amount of ROS produced in irradiated tilapia sperm was much higher than that of ram sperm. CONCLUSIONS: The results show that different wavelengths differentially affect tilapia and ram sperm motility and fertilization. The difference in response to the various light sources might be explained by the different amounts of ROS formation by ram and tilapia, which are in agreement with the physiology of fertilization appropriate to each of these species. Based on these results, it is suggested that in vitro fertilization in mammals should be performed in darkness or at least under red light.

Animals↗
PubMed2001

Variability and severity of depression and anxiety in post traumatic stress disorder and major depressive disorder.

In order to better characterize the similarities in and differences between the nature of the affective disturbance associated with Posttraumatic Stress Disorder (PTSD) and with Major Depressive Disorder (MDD), self-reported mood and anxiety ratings were examined in PTSD subjects, MDD subjects, and subjects without a psychiatric disorder while they were undergoing a chronobiologic study. Based on serial ratings on visual analogue scales over a 24 hr period, PTSD subjects showed comparable levels of depression as the MDD group, as measured by the mean and maximum levels of mood; however, they had greater mood variability, as measured by the range and coefficients of variation of the mood ratings. The MDD but not the PTSD group had significantly lower mood variability than the non-psychiatric group, as measured by the coefficients of variation. The PTSD group reported higher levels of anxiety than the non-psychiatric or MDD group but showed no differences in any measure of variability of anxiety. These findings suggest there are phenomenologic differences in the affective symptoms experienced by patients with PTSD and with MDD and that mood variability may distinguish between them.

Adult↗
PubMed2001

Childhood trauma and risk for PTSD: relationship to intergenerational effects of trauma, parental PTSD, and cortisol excretion.

Among the adverse mental health consequences of childhood trauma is the risk related to the development of posttraumatic stress disorder (PTSD) in adulthood. Other risk factors for PTSD. including parental trauma exposure and parental PTSD, can also contribute to the experience of child trauma. We examined associations between childhood trauma and PTSD in 51 adult children of Holocaust survivors and 41 comparison subjects. in consideration of parental trauma exposure and parental PTSD. We also examined these variables in relation to 24-hr urinary cortisol levels. Adult offspring of Holocaust survivors showed significantly higher levels of self-reported childhood trauma, particularly emotional abuse and neglect. relative to comparison subjects. The difference was largely attributable to parental PTSD. Self-reported childhood trauma was also related to severity of PTSD in subjects, and emotional abuse was significantly associated with 24-hr mean urinary cortisol secretion. We conclude that the experience of childhood trauma may be an important factor in the transmission of PTSD from parent to child.

Adult↗
PubMed2001

CSF norepinephrine concentrations in posttraumatic stress disorder.

OBJECTIVE: Despite evidence of hyperresponsive peripheral and central nervous system (CNS) noradrenergic activity in posttraumatic stress disorder (PTSD), direct measures of CNS norepinephrine in PTSD have been lacking. The goal of this study was to determine serial CSF norepinephrine levels in patients with PTSD. METHOD: CSF samples were obtained serially over a 6-hour period in 11 male combat veterans with chronic PTSD and eight healthy men through an indwelling subarachnoid catheter. Thus the authors were able to determine hourly CSF norepinephrine concentrations under baseline (unstressed) conditions. Severity of the patients' PTSD symptoms was assessed with the Clinician-Administered PTSD Scale. RESULTS: CSF norepinephrine concentrations were significantly higher in the men with PTSD than in the healthy men. Moreover, CSF norepinephrine levels strongly and positively correlated with the severity of PTSD symptoms. Plasma norepinephrine concentrations showed no significant relationship with the severity of PTSD symptoms. CONCLUSIONS: These findings reveal the presence of greater CNS noradrenergic activity under baseline conditions in patients with chronic PTSD than in healthy subjects and directly link this pathophysiologic observation with the severity of the clinical posttraumatic stress syndrome.

Adult↗
PubMed2001

Paroxetine in the treatment of chronic posttraumatic stress disorder: results of a placebo-controlled, flexible-dosage trial.

BACKGROUND: The objective of this double-blind, placebo-controlled study was to investigate the efficacy and safety of paroxetine in outpatients with posttraumatic stress disorder (PTSD). METHOD: Male and female outpatients 18 years and older who met DSM-IV criteria for PTSD and had baseline scores of 50 or greater on the Clinician Administered PTSD Scale (CAPS-2) were randomly assigned to treatment with paroxetine (20-50 mg/day) or placebo for 12 weeks. The primary efficacy variables were the change from baseline to the 12-week endpoint in the CAPS-2 total score and the proportion of responders on the Clinical Global Impressions-Global Improvement scale (CGI-1). Additional key outcome measures were the change from baseline in the reexperiencing, avoidance/ numbing, and hyperarousal scores of the CAPS-2 and in the total scores of the Treatment Outcome PTSD Scale and the patient-rated Davidson Trauma Scale and Sheehan Disability Scale (SDS). Depressive symptoms were assessed with the Montgomery-Asberg Depression Rating Scale. The proportion of patients achieving response and remission was also determined. RESULTS: 307 patients constituted the intent-to-treat population. At week 12, compared with the placebo group (N = 156), the paroxetine group (N = 151) showed significantly greater reduction of PTSD symptoms on both of the primary and all of the secondary outcome measures. Significantly greater improvement on the CAPS-2 total score was observed for paroxetine compared with placebo from week 4 (p < .05), and significantly greater proportions of paroxetine-treated patients achieved response (p < .001) and remission (p = .008) by week 12. The improvement in PTSD symptoms was similar in male and female patients. Functional improvement at the study endpoint was significantly greater (p < .05) in the paroxetine group in all 3 domains of the SDS (work, social life, family life). Treatment with paroxetine was well tolerated, with the frequency and type of adverse events recorded for the paroxetine group corresponding to the known safety profile of this medication. CONCLUSION: Paroxetine in doses of 20 to 50 mg once daily is effective as a treatment for chronic PTSD. Improvement is obtained for all 3 symptom clusters (reexperiencing, avoidance/numbing, hyperarousal) and is associated with significant reduction in disability after 12 weeks of treatment.

Adolescent↗
PubMed2001

Biology of posttraumatic stress disorder.

Most biological findings in posttraumatic stress disorder (PTSD) are compatible with those of the chronic stress response, such as increased corticotropin-releasing factor (CRF) concentrations, catecholamine depletion within the central nervous system, and reduced hippocampal volume. However, over the last 10 years, biological observations have been made in PTSD that are different from what has been typically associated with chronic stress, notably certain hypothalamic-pituitary-adrenal (HPA) axis findings. In particular, urinary and plasma cortisol levels are considerably lower in PTSD patients than in non-PTSD trauma survivors and normal controls. Furthermore, the circadian pattern of cortisol release from the adrenal glands follows a greater dynamic range in PTSD than in patients with major depression or in normal controls. The reduction in cortisol levels results from an enhanced negative feedback by cortisol, which is secondary to an increased sensitivity of glucocorticoid receptors in target tissues. This HPA axis alteration contrasts with the well-known chronic stress cascade in which CRF release results in erosion of negative feedback and down-regulation of glucocorticoid receptors. Sensitization of the HPA axis is consistent with the clinical picture of hyperreactivity and hyperresponsiveness in PTSD.

Adrenocorticotropic Hormone↗
PubMed2000

Behavioral and endocrine response to cholecystokinin tetrapeptide in patients with posttraumatic stress disorder.

BACKGROUND: Given the relationship between posttraumatic stress disorder (PTSD) and panic, it was of interest to examine whether panic provoking agents affect PTSD symptoms. We therefore investigated the behavioral and endocrine response of PTSD patients to the panicogen cholecystokinin tetrapeptide (CCK-4). METHODS: Eight patients with PTSD (DSM-IV) received 50 micrograms CCK-4 intravenously in a placebo-controlled, double-blind balanced design. Provocation of panic, anxiety, and flashbacks was assessed. Plasma adrenocorticotropin (ACTH) and cortisol levels after CCK-4 were measured and compared to healthy subjects matched for age, gender, and provoked symptoms. RESULTS: Despite significant effects of CCK-4 on anxiety and panic symptoms, no significant provocation of flashbacks emerged. CCK-4-induced panic symptoms showed an inverse correlation to trait dissociation. The ACTH response after CCK-4 was significantly lower in PTSD patients than in controls. Cortisol was similarly increased in both groups after CCK-4, but PTSD patients showed a more rapid decrease of stimulated cortisol concentrations. CONCLUSIONS: Panic symptoms or heightened anxiety are not necessarily conditioned stimuli for the provocation of posttraumatic flashbacks. Further studies in PTSD with different panicogens should be controlled for the potential interference of trait dissociation. Our hormone data show further evidence for a corticotropin-releasing hormone (CRH) overdrive and enhanced negative glucocorticoid feedback in PTSD patients.

Adrenocorticotropic Hormone↗
PubMed2000

Clinical treatment of posttraumatic stress disorder: conceptual challenges raised by recent research.

OBJECTIVE: This paper highlights some of the recent findings in the field of posttraumatic stress disorder (PTSD) and examines their impact on conceptions of trauma-focused clinical treatment. METHOD: A series of research findings in the area of epidemiology, phenomenology, neurobiology and treatment are summarised. RESULTS: The findings from these studies present critical challenges for clinicians who wish to treat trauma survivors using specialised trauma treatments. The major challenge is one of avoiding a simplistic view of PTSD as a singular response to trauma, as this perception may result in an underestimation of the complexity and disabling quality of the disorder, and lead to the formulation of treatment plans that are simplistic or incomplete. CONCLUSIONS: A more precise characterisation of the nature and range of the stress responses of trauma victims will significantly improve treatments of trauma survivors.

Combined Modality Therapy↗
PubMed2000

Low cortisol and risk for PTSD in adult offspring of holocaust survivors.

OBJECTIVE: The study examined the association between cortisol and putative risk factors for posttraumatic stress disorder (PTSD) in a sample of subjects at increased risk for the development of PTSD. METHOD: Twenty-four-hour urinary cortisol excretion was measured in 35 adult offspring of Holocaust survivors and 15 healthy comparison subjects who were not offspring of Holocaust survivors. Subjects were also characterized with regard to clinical symptoms, presence or absence of psychiatric diagnoses including PTSD, and presence or absence of PTSD in their parents. RESULTS: Low cortisol levels were significantly associated with both PTSD in parents and lifetime PTSD in subjects, whereas having a current psychiatric diagnosis other than PTSD was relatively, but nonsignificantly, associated with higher cortisol levels. Offspring with both parental PTSD and lifetime PTSD had the lowest cortisol levels of all study groups. CONCLUSIONS: Parental PTSD, a putative risk factor for PTSD, appears to be associated with low cortisol levels in offspring, even in the absence of lifetime PTSD in the offspring. The findings suggest that low cortisol levels in PTSD may constitute a vulnerability marker related to parental PTSD as well as a state-related characteristic associated with acute or chronic PTSD symptoms.

Adult↗
PubMed2000

Biology of posttraumatic stress disorder.

An understanding of the biological basis of posttraumatic stress disorder (PTSD) requires an examination of the underlying neurobiology of fear and the factors that might contribute to an unsuccessful termination of the fear response in some individuals. Several factors may lead to an inadequate termination of a stress response, and the failure to contain the biological alterations initiated by stress may have long-term adverse consequences. In particular, a prolonged continuation of biological responses following stress may lead to an inappropriate pairing of the traumatic memory with distress and may then initiate a cascade of secondary biological alterations. This article examines some of the biological alterations in PTSD and develops a framework for understanding the development progression of the neurobiology of this disorder.

Adaptation, Psychological↗
PubMed1999

Biological factors associated with susceptibility to posttraumatic stress disorder.

Because only a proportion of persons exposed to traumatic events develop posttraumatic stress disorder (PTSD), it has become important to elucidate the factors that increase the risk for the development of PTSD following trauma exposure as well as the factors that might serve to protect individuals from developing this condition. Putative risk factors for PTSD may describe the index traumatic event or characteristics of persons who experience those events. Recent data have implicated biological and familial risk factors for PTSD. For example, our recent studies have demonstrated an increased prevalence of PTSD in the adult children of Holocaust survivors, even though these children, as a group, do not report a greater exposure to life-threatening (Diagnostic and Statistical Manual of Mental Disorders [DSM-IV] Criterion A) events. These studies are reviewed. It is difficult to know to what extent the increased vulnerability to PTSD in family members of trauma survivors is related to biological or genetic phenomena, as opposed to experiential ones, because of the large degree of shared environment in families. In particular, at-risk family members, such as children, may be more vulnerable to PTSD as a result of witnessing the extreme suffering of a parent with chronic PTSD rather than because of inherited genes. But even if the diathesis for PTSD were somehow "biologically transmitted" to children of trauma survivors, the diathesis is still a consequence of the traumatic stress in the parent. Thus, even the most biological of explanations for vulnerability must at some point deal with the fact that a traumatic event has occurred.

Adaptation, Psychological↗
PubMed1999

Linking the neuroendocrinology of post-traumatic stress disorder with recent neuroanatomic findings.

It has been hypothesized that stress damages the hippocampus and results in myriad other deleterious consequences owing to the toxic effects of cortisol, presumed to be released in excess in response to traumatic stress. Several studies have now demonstrated that hippocampal volumes of trauma survivors with post-traumatic stress disorder (PTSD) are reduced compared to those of nontraumatized persons. Interestingly, however, there is little evidence of increased cortisol release in either the acute or chronic aftermath of stress in trauma survivors who develop this disorder, raising questions about the etiology of the smaller hippocampal volumes as well as the relationship between the neuroendocrine and neuroanatomic alterations in PTSD. This article will review hypothalamic-pituitary-adrenal alterations in PTSD in an attempt to link the neuroendocrine findings with the observation of reduced hippocampal volume. It will be argued that the resolution of the neuroendocrine and neuroanatomic alterations in PTSD depends on understanding the pivotal role of glucocorticoids and their action at glucocorticoid receptors at target brain areas in response to stress and in PTSD.

Animals↗
PubMed1999

Managing anger and aggression in patients with posttraumatic stress disorder.

Posttraumatic stress disorder was categorized as a clinical entity in 1980 in response to assertions by trauma survivors (particularly Vietnam veterans) and their clinicians that existing diagnostic categories failed to adequately describe their symptoms. The diagnostic features of the current DSM-IV diagnosis have been expanded, and the concept of the disorder is still evolving. Posttraumatic stress disorder rarely occurs in "pure" form, and individuals suffering from the disorder commonly meet criteria for Axis I and Axis II disorders. Research is now emerging that supports the prevalence of aggression in posttraumatic stress disorder. Treatment approaches vary, but pharmacotherapy aimed at targeting individual symptoms or clusters can promote mood stabilization. This article discusses the evolving concept of posttraumatic stress disorder as a clinical entity, the association of anger and aggression with the disorder, and the psychopharmacologic approaches to treatment.

Aggression↗
PubMed1998

Predicting the development of posttraumatic stress disorder from the acute response to a traumatic event.

Posttraumatic stress disorder (PTSD) is a psychiatric condition that is directly precipitated by an event that threatens a person's life or physical integrity and that invokes a response of fear, helplessness, or horror. In recent years it has become clear that only a proportion of those exposed to fear-producing events develop or sustain PTSD. Thus, it seems that an important challenge is to elucidate aberrations in the normal fear response that might precipitate trauma-related psychiatric disorder. This paper summarizes the findings from recent studies that examined the acute and longer term biological response to traumatic stress in people appearing to the emergency room immediately following trauma exposure. In the aggregate, these studies have demonstrated increased heart rate and lower cortisol levels at the time of the traumatic event in those who have PTSD at a follow-up time compared to those who do not. In contrast, certain features associated with PTSD, such as intrusive symptoms and exaggerated startle responses, are only manifest weeks after the trauma. The findings suggest that the development of PTSD may be facilitated by an atypical biological response in the immediate aftermath of a traumatic event, which in turn leads to a maladaptive psychological state.

Animals↗