This article is about theories and studies that we are doing to better understand PTSD. It is part of a thesis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4520791/
PTSD can develop in the aftermath of traumatic incidents like combat, sexual abuse, or life-threatening accidents. Unfortunately, there are still no biomarkers for PTSD. We have to talk about it, listen, observe and be empathetic.
Often the best persons for this when it comes to religious abuse are others that have been within the same religiously abusive system. There is no blood test, SCAT scan MRI or App to diagnose PTSD. So we have Thursday and Saturday night sessions to help.
{A biomarker or biological marker is a measurable indicator of some biological state or condition. Biomarkers are often measured and evaluated to examine normal biological processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention.} We use talk therapy, interactions, and watch for the response.
Post-traumatic stress disorder (PTSD) is a severe psychiatric disorder that occurs after a psychological traumatic life event and increases individual vulnerability to adverse health outcomes. PTSD is heterogeneous, often presenting across different symptom domains, including re-experiencing, avoidance/numbing, and hyperarousal symptoms. While extensive work has successfully identified psychological, genomic, and biological risk factors that are associated with PTSD in trauma survivors, the identification of discrete diagnostic biomarkers for PTSD remains elusive. The lack of diagnostic biomarkers for PTSD is not due to a lack of intensive study, but rather likely due to the complexity of PTSD and the complex set of rules by which we classify individuals according to the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), as illustrated by the recent description of 636,120 different ways in which an individual can be diagnosed with PTSD. Furthermore, PTSD is associated with significant mental health (e.g., major depression, substance and alcohol abuse, panic disorder, suicide) and general medical (e.g., diabetes, cardiovascular disease comorbidities, which can obscure the search for diagnostic biomarkers for PTSD.
Given that DSM criteria are not based on the underlying biology, PTSD research could benefit significantly from the new approach to mental health diagnoses using symptoms and actually discussing and speaking to clients, rather than diagnostic classification.
Abstract: Bio-Markers
Posttraumatic stress disorder (PTSD) is a heterogeneous disorder that affects individuals exposed to trauma (e.g., combat, interpersonal violence, and natural disasters). Although its diagnostic features have been recently re-classified with the emergence of the Diagnostic and Statistical Manual for Mental Disorders, Fifth Edition (DSM-5), the disorder remains characterized by hyperarousal, intrusive reminders of the trauma, avoidance of trauma-related cues, and negative cognition and mood. This heterogeneity indicates the presence of multiple neurobiological mechanisms underlying the etiology and maintenance of PTSD. Translational research spanning the past few decades has revealed several potential avenues for the identification of diagnostic biomarkers for PTSD. These include, but are not limited to, monoaminergic transmitter systems, the hypothalamic-pituitary-adrenal (HPA) axis, metabolic hormonal pathways, inflammatory mechanisms, psychophysiological reactivity, and neural circuits.
I personally use Massage therapy, Far infrared light, intense heat and water therapies.
The vast heterogeneity inherent in PTSD symptom presentation makes it highly unlikely that a valid, singular biomarker will be identified for PTSD However, comprehensive biological phenotyping of the factors associated with PTSD may yield a parsimonious diagnostic model with which to diagnose PTSD in the future. The current review will highlight several biomarkers associated with PTSD symptomatology and vulnerability, in addition to underscoring how individual factors, such as one’s co-morbid diagnoses and gender, must be considered as they can profoundly influence biology and thus influence our search for true biomarkers of PTSD. Specifically, we will emphasize monoamine, neuroendocrine, inflammatory, genetic, epigenetic, psychophysiologial, neuroanatomical and neuroactivational phenotypes associated with PTSD to illustrate the potential efficacy of using multi-dimensional phenotypic data to characterize unique profiles of PTSD.
Monoamine Systems in PTSD
PTSD is characterized by increased sympathetic nervous system (SNS) tone that is coincident with augmented levels of catecholamine secretion . Urinary and central levels of norepinephrine (NE) are heightened in individuals with PTSD and in child trauma victims, and peripheral and central levels of NE in response to threatening stimuli are also elevated in PTSD. Recent evidence suggests that this increase in NE in PTSD is due to attenuated levels of the NE transporter within the brainstem locus coeruleus . PTSD has also been associated with decreased expression of peripheral α2-adrenergic receptors; receptors that underlie an autoreceptor-driven mechanism that serves to inhibit synaptic transmitter release. Further, facilitation of NE release via blockade of pre-synaptic α2-adrenergic receptors with the antagonist, yohimbine, can produce panic attacks and an increase in anxiety- and trauma-related symptoms in individuals with PTSD. A prospective study of motor vehicle accident survivors indicates that urinary levels of NE were associated with increased development of PTSD one-month following trauma, but only in men, indicating that gender may be important for characterizing catecholaminergic biomakers of PTSD. Increased catecholamines, however, are also coincident with panic attacks and other fear-related psychopathology , indicating that increased sympathetic activation is not a specific biomarker of PTSD, but rather of a common neurobiological feature of fear- and anxiety-related disorders.
Alterations in the serotonergic system have also been implicated in the pathophysiology of PTSD. Individuals with PTSD show decreased levels of paroxetine binding, suggesting that levels of the serotonin (5-HT) transporter (5-HTT) are attenuated in PTSD and involved in the manifestation of arousal and avoidance symptoms . Empirical evidence has shown that 5-HTT expression within the amygdala is attenuated in PTSD, and is significantly associated with higher anxiety and depressive symptoms. Brainstem and forebrain levels of the 5-HT1A receptor are higher in individuals with PTSD , similar to what has been described in depression . Likewise, reductions in central 5-HT1B receptors in trauma-exposed individuals are associated with increased PTSD and depression symptoms. Taken together, these data indicate that alterations within serotonergic system could reveal putative biomarkers for depressive symptoms common to both PTSD and major depression. The effectiveness of selective serotonin reuptake inhibitors (SSRIs; e.g., sertraline) for reducing the symptoms of PTSD, major depression, and other psychiatric conditions with which PTSD is highly comorbid , further suggest that more careful examination of serotonergic phenotypes is warranted to better disentangle the specificity of biomarkers for PTSD- and depression-specific phenotypes.
One way in which to elucidate the specificity of monoaminergic biomarkers on PTSD symptomology is to concurrently characterize sympathetic and serotonergic function within the same individuals. Using a repeated-measures design, Southwick and colleagues (1997) found that both yohimbine and meta-Chlorophenylpiperazine (m-CPP) treatment increased panic attacks, anxiety, and trauma-related symptoms in veterans diagnosed with PTSD in a manner that suggested at least two different biological sub-types of PTSD; thus, underscoring the need for more robust phenotyping of biological factors including the monoaminergic transmitter systems.
Hopefully, this article will shed more light on what is being done to better understand PTSD.
Rene and I are embarking on a project to test touch modalities for PTSD.
we will have more on that in a later post.