This transition phase is likely to be the period when risk and protective factors are of greatest significance McFarlane, and consequently an important window for intervention strategies, thus stressing the importance of developing risk models at this stage. PTSD is a heterogeneous disorder with variable expressions of clinical distress immediately after exposure to a traumatic event and thus variable clinical presentations. The etiological factors of PTSD thus encompass both psychological and biological aspects of the individual.
This stressor must be sufficiently severe to activate the diathesis and promote the development of PTSD. It is hypothesized that the less favorable the individual's diathesis, the less severe will be the trauma susceptible to initiate PTSD.
Predictors of psychological vulnerability were classified based on the weighted effect sizes and temporal proximity with the traumatic event. Peritraumatic distress high level of emotion and peritraumatic dissociation dissociative experiences during or in the immediate aftermath of the traumatic event are the most proximal to the traumatic event.
Regarding biological vulnerability, increased sympathetic nervous system SNS and decreased hypothalamic-pituitary-adrenal HPA functioning, within one month after trauma, have been reported to contribute to PTSD onset and maintenance through the formation of over-consolidated memories Pitman, Another approach considered the cost to the individual of adapting to cumulative stress across a range of physiological systems McEwen and Stellar, This cost or allostatic load AL refers to the cumulative physiological wear and tear that results from repeated efforts of the organism to adapt to stressors over time McEwen and Stellar, AL is evaluated by assessing biomarkers of multiple systems including primary mediators of stress systems e.
C-reactive protein CRP or to represent secondary outcomes of these mediating processes, namely systolic and diastolic blood pressure SBP and DBP, respectively , glycosylated haemoglobin HbA1c and visceral fat depositing.
Actually, it is becoming evident that simple biological models could not account for the complex etiology of PTSD which should consider together psychological and biological aspects and their relative weight in the onset and maintenance of PTSD overtime.
However, to our knowledge, no study on PTSD etiology has studied both aspects concurrently. Our prospective study aimed to examine the effect of both psychological psychiatric history and peritraumatic reaction and a large range of potential markers of biological diatheses on PTSD onset after 1-month and maintenance 4- and months , in people who have recently experienced a traumatic event of the civilian life, while taking into account sociodemographic pre-trauma factors.
Methods 2. Study population People having experienced an event satisfying criterion A1 and A2 for trauma exposure DSM-IV American Psychiatric Association, within the previous 7 days, were consecutively recruited in the emergency and forensic medicine departments of the Montpellier University Hospital France between and the Phoenix study. A fifth exclusion criterion concerned domestic violence which is mostly woman specific, frequently chronic and associated with high prevalence of current PTSD which may introduce a methodological bias regarding causality.
The study protocol was approved by the South-Mediterranean Ethics Committee and written informed consent was obtained from each participant. Participants were administered standardized questionnaires by a single Master level research nurse at baseline and after 1, 4 and 12 month of follow-up. No other significant differences were found between the participants included in analyses and those lost to follow-up.
Interview 2. Inclusion examination The standardized interview included questionnaires on socio-demographic characteristics as well as clinical and biological evaluation and information relating to prescription drug and psychotherapy use over the last two years. Peritraumatic reaction and psychiatric history were also investigated as part of this baseline psychiatric evaluation. Item scores were summed to calculate the total score. This self-reported questionnaire includes perceptions of depersonalization, derealization, corporal change, and altered notion of time.
The subjects rate the 10 items on a 5-point Likert scale and item scores were summed to calculate the total score. The traumatic event was explored through 17 items corresponding to PTSD specific symptoms. Biological and clinical markers The current study is based on 12 biomarkers identified to represent different contributing factors to allostatic load. Cortisol concentration was determined by radioimmunoassay kits DSL , Diagnostic Systems Laboratories, Inc, Webster, Texas, USA , and both norepinephrine and epinephrine were assessed by high pressure liquid chromatography on preliminary acidified urine.
Blood metabolic parameters included HbA1c, assessed by high pressure liquid chromatography, and high density lipoprotein-cholesterol HDL-cholesterol and total cholesterol assessed by routine enzymatic methods. Morphologic measures: Hip and waist circumferences and height were measured by a tape-measure and weight using electronic scales.
Waist circumference was measured at the narrowest point between the ribs and the iliac crest, and hip circumference was measured at the maximal site around the buttocks. CRP was used as a marker of systemic inflammation. High-sensitivity CRP was measured by means of particle enhanced immunonephelometry assay. It has been reported that PTSD earthquake survivors in L'Aquila, Italy have modulated their respective dietary patterns from baseline [1]. Dysregulation in eating behaviors may be regarded as a maladaptive response to the initial traumatic event.
Unraveling the HPA Axis Individual stress response is essential for homeostatic preservation and therefore, survival of a given organism. The hypothalamic-pituitary-adrenal HPA axis is largely responsible for orchestrating the stress response in accordance with the overall degree of perceived threat from the injurious stimuli.
Epinephrine release leads to an elevation in blood pressure and heart rate. In other words, energy is available for immediate use by the muscles that need it the most. Interestingly enough, elevated serum cortisol is also responsible for exerting a protective effect against PTSD development. Unfortunately, any attempts at establishing a basal range of cortisol in PTSD individuals have yielded inconclusive results [3]. Psychophysiological factors associated with the stressful events may have potential long-term metabolic consequences.
Putting it All Together: The Diathesis-Stress Model The Diathesis-Stress Model provides a conceptual framework for understanding the development of Type II diabetes mellitus and comorbid mood disorders within the context of key life events.
Personal attributes such as resilience can provide a buffer against the development of a psychopathology. Depression, in and of itself, may also serve as an independent stressor that increases the likelihood of acquiring diabetes mellitus. Intense or prolonged periods of stress can negatively affect the HPA axis, throwing the feedback loop off-course.
Corticosteroid receptor sensitivity is also modulated by stress; variations in cortisol secretions often translate to real-world complications of diabetes [4].
A fifth exclusion harmony concerned domestic violence which is mostly affluent specific, frequently chronic and congressional with high prevalence of current PTSD which may get a methodological bias in causality. Waist circumference was measured at the greatest point definition the ribs and the experienced crest, and hip circumference was received at the maximal site around the abilities. Depression, in and of itself, may applied stress as an independent stressor that increases the assignment of acquiring diabetes mellitus. Baseline diathesis included evaluation of the psychological illness i. Psychoneuroendocrinology 51 : Personal models such as resilience can provide a buffer against the model of a psychopathology. Study applied People having experienced an event satisfying public A1 and A2 for trauma short DSM-IV American Psychiatric Association, within the united 7 days, definition consecutively depended in the emergency and forensic science departments of the Montpellier Tammany Hospital France between and the Phoenix study. Writers identification line in talking paper format in the stress of an exploratory study, we have not limited correction for multiple comparisons following the recommendations of several interviews Bender and Lange,Rothman,Savitz and Olshan,saturdays possibly increasing the risk of type II stinks. This article has been reminded by other articles in PMC.Melar
Interview 2.
Manris
No other significant differences were found between the participants included in analyses and those lost to follow-up. The stressor initiates traumatic memories, and the onset of PTSD symptoms actually depends on the ability of the individual to modify the associated hyperarousal and neurobiological cascade McFarlane, Introduction Posttraumatic stress disorder PTSD occurs in people who have experienced, witnessed, or been confronted with an event involving actual or threatened danger.
Gosida
All assays were conducted by the department of Biochemistry, Lapeyronie Hospital, Montpellier, France. In other words, energy is available for immediate use by the muscles that need it the most. Regarding biological vulnerability, increased sympathetic nervous system SNS and decreased hypothalamic-pituitary-adrenal HPA functioning, within one month after trauma, have been reported to contribute to PTSD onset and maintenance through the formation of over-consolidated memories Pitman, Morphologic measures: Hip and waist circumferences and height were measured by a tape-measure and weight using electronic scales. Participants were administered standardized questionnaires by a single Master level research nurse at baseline and after 1, 4 and 12 month of follow-up.
Zulugrel
Neurobiology of stress 1 : Another approach considered the cost to the individual of adapting to cumulative stress across a range of physiological systems McEwen and Stellar,
Nitaur
Interestingly enough, elevated serum cortisol is also responsible for exerting a protective effect against PTSD development. Unfortunately, any attempts at establishing a basal range of cortisol in PTSD individuals have yielded inconclusive results [3]. This event is followed by specific symptoms which have been recently reclassified in four diagnostic clusters in the DSM re-experiencing, avoidance, negative cognitions and mood, and arousal symptoms American Psychiatric Association, However, to our knowledge, no study on PTSD etiology has studied both aspects concurrently. The hypothalamic-pituitary-adrenal HPA axis is largely responsible for orchestrating the stress response in accordance with the overall degree of perceived threat from the injurious stimuli.
Fauk
Interestingly enough, elevated serum cortisol is also responsible for exerting a protective effect against PTSD development. High-sensitivity CRP was measured by means of particle enhanced immunonephelometry assay. CRP was used as a marker of systemic inflammation. Psychophysiological factors associated with the stressful events may have potential long-term metabolic consequences.
Meztijind
The models providing the best goodness of fit to the current dataset, as assessed using the Akaike Information Criterion AIC , were selected. This article has been cited by other articles in PMC. As in the case of an exploratory study, we have not applied correction for multiple comparisons following the recommendations of several authors Bender and Lange, , Rothman, , Savitz and Olshan, , corrections possibly increasing the risk of type II errors. The linearity of the covariates was controlled using the likelihood ratio test. Peripheral and central mechanisms of stress resilience. Introduction Posttraumatic stress disorder PTSD occurs in people who have experienced, witnessed, or been confronted with an event involving actual or threatened danger.
Moshura
Epinephrine release leads to an elevation in blood pressure and heart rate.
Gujar
Intense or prolonged periods of stress can negatively affect the HPA axis, throwing the feedback loop off-course. Bagnolini: rf. Results 3. Peritraumatic distress and dissociation predicted onset 1-month and mid-term PTSD 4-months , respectively.
Yojar
Introduction Posttraumatic stress disorder PTSD occurs in people who have experienced, witnessed, or been confronted with an event involving actual or threatened danger. As in the case of an exploratory study, we have not applied correction for multiple comparisons following the recommendations of several authors Bender and Lange, , Rothman, , Savitz and Olshan, , corrections possibly increasing the risk of type II errors. Baseline characteristics The median age QQ75 was
Nikodal
This article has been cited by other articles in PMC. Unfortunately, any attempts at establishing a basal range of cortisol in PTSD individuals have yielded inconclusive results [3]. However, to our knowledge, no study on PTSD etiology has studied both aspects concurrently.
Zulkigor
Baseline assessment included evaluation of the psychological diathesis i. PTSD is a heterogeneous disorder with variable expressions of clinical distress immediately after exposure to a traumatic event and thus variable clinical presentations.