![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 11 of 11. This is the beginning of the thread.
Posted by pelorojo on November 4, 2002, at 19:38:32
Hi all,
I'm new : ) I've been doing a ton of research on the neurophysiology of PTSD and am looking for others that may be able to share resources and discuss the topic. In particular, I'm interested in-
-natural/alternative/herbal therapies. In particular: TMG, SAMe, Licorice Root, Rhodiola Rosea, Ashwagandha, and some of the new herbal cortisol reduction pills
-the neurophysiology of PTSD
-the connection between PTSD and social anxiety and the neurophysiology of social anxiety
-herbal/medication known or theoretical interactions (esp. related to klonopin, Neurontin, Wellbutrin, and Lexapro)
Any thoughts, experiences, resources (studies, websites), etc. are greatly appreciated. I'm wondering if there is a way that I can get to the PTSD at one of its sources-the HPA axis-through the use of herbals. I'm also real interested in the new cortisol reducing supplements (i.e., Relora or Pharmanex's "cortitrol").
thanks. Best to all-
Austin, TX
Posted by Larry Hoover on November 5, 2002, at 9:05:22
In reply to PTSD/Social Anxiety-Herbals, posted by pelorojo on November 4, 2002, at 19:38:32
I'm really interested in the topic; chronic PTSD underlies my own difficulties. Your inquiry is overwhelming in scope. Why don't you share some of your research findings, and let's see where that takes us?
BTW, I'm very surprised to not see St. John's wort among your listed interventions. It seems tailor-made for PTSD.
Regards,
Larry
Posted by Tabitha on November 5, 2002, at 15:38:47
In reply to PTSD/Social Anxiety-Herbals, posted by pelorojo on November 4, 2002, at 19:38:32
Hi,
You might also look into EMDR therapy. I've seen reports that it's particularly good for PTSD, and faster than standard talk therapy. I'm a little skeptical myself, but my therapist has had success with EMDR.
Posted by pelorojo on November 6, 2002, at 14:05:53
In reply to Re: PTSD/Social Anxiety-Herbals, posted by Larry Hoover on November 5, 2002, at 9:05:22
hey thanks for the replies.
Here's my favorite article on the neurophysiology of PTSD. It's labeled "speculative" but jives with what I've read elsewhere ... my psychologist & psyhciatrist indicated it's consistent with their knowledge of PTSD. More later.
The Neurophysiology of Dissociation and Chronic Disease
Robert C. Scaer
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Abstract
Dissociation as a clinical psychiatric condition has been defined primarily in terms of the fragmentation and splitting of the mind, and perception of the self and the body. Its clinical manifestations include altered perceptions and behavior, including derealization, depersonalization, distortions of perception of time, space and body and conversion hysteria. Using examples of animal models, and the clinical features of the whiplash syndrome, we have developed a model of dissociation linked to the phenomenon of freeze/immobility. Also employing current concepts of the psychobiology of posttraumatic stress disorder (PTSD), we propose a model of PTSD linked to cyclical autonomic dysfunction, triggered and maintained by the laboratory model of kindling, and perpetuated by increasingly profound dorsal vagal tone and endorphinergic reward systems. These physiologic events in turn contribute to the clinical state of dissociation. The resulting autonomic dysregulation is presented as the substrate for a diverse group of chronic diseases of unknown origin.
Key Words:
Autonomic nervous system
Conversion
Dissociation
Kindling
RSD (reflex sympathetic dystrophy)
Author’s note:Published in: Applied Psychophysiology and Biofeedback, (2001), 26(1), 73-91, based on a Keynote Address presented at the 31st annual meeting of the Association for Applied Psychophysiology and Biofeedback, March 29-April 2, 2000, Denver, CO.
Please address correspondence to:Robert C. Scaer, MD
372 Brook Circle
Boulder, CO 80302
Tel (303) 544-0717
Email: scaermdpc@aol.com
--------------------------------------------------------------------------------THE NEUROPHYSIOLOGY OF DISSOCIATION
AND CHRONIC DISEASE
Robert C. Scaer, M.D.
During the last two decades of the 19th century, psychiatrists in Europe began to explore and define the peculiar behavior manifested by patients of theirs who fell under the diagnostic category of hysteria. Pierre Janet at the Salpetriere` described dissociation as phobias of memories, in the form of expressions of excessive or inappropriate physical responses to thoughts or memories of old traumas (Janet, 1920). After visiting Janet, Freud adopted many of these concepts of dissociation as a splitting of consciousness, often associated with bizarre physical symptoms and manifestations, and ultimately attributed such symptoms in his hysterical patients to a history of childhood sexual abuse (Freud, 1896). Evolution of the concept of dissociation led to the description of a constellation of varied clinical manifestations attributed to it, including altered perceptions of physical sensation, time, memory, and the perceptions of self and reality. Complex expressions of these states came to include conversion disorder, fugue states and multiple personalities (dissociative identity disorder) (Freud & Breur, 1953, Mayer-Gross, W., 1935, Spiegal & Cardena, 1991, Bremner, et al, 1992). Thus the concept of dissociation evolved to include not only mental and emotional aberrations, but also stereotyped and unusual somatic perceptual and motor experiences and expressions.
All of these symptoms and behaviors were felt to be the sequellae of prior life trauma. The basic mechanism of dissociation was felt to involve the splitting off of parts of memory or perception in order to escape intolerable anxiety triggered by those areas of the mind that retained elements of the traumatic conflict. Relief from that conflict through hysterical dissociation resulted in relief from anxiety, resulting at times in the seemingly blasé acceptance of disabling physical conditions (la belle indifference`).
Freud, however, soon began revising his concepts of hysteria, and by 1925 had recanted his theories of the relationship of hysteria and dissociation to prior childhood trauma (Freud, 1959). He ultimately attributed the stories of childhood sexual abuse in his hysterical patients to fabrication, based on unacceptable sexual wishes and fantasies that they could not acknowledge. As a result, the role of childhood trauma in the etiology of dissociation was basically ignored for decades.
The introduction of the diagnosis of Post Traumatic Stress Disorder (PTSD) into the Diagnostic and Statistical Manual of Mental Disorders, 3rd edition (DSM III) in 1980 also resulted in the reclassification of many of the conditions formerly attributed to trauma and dissociation, and in some cases, ignored their association with prior life trauma (American Psychiatric Association, 1980). Van der Kolk et al (1998) note that in the DSM IV, dissociative symptoms are included under the diagnostic categories of not only Post Traumatic Stress Disorder, but also of Acute Stress Disorder, Somatization Disorder and Dissociative Disorders themselves (van der Kolk, et al, 1998). In fact, in the DSM IV, Dissociative Disorders do not include Conversion Disorder, which has now been placed under the Somatiform Disorders. Since the DSM III, the diagnosis of hysteria is nowhere to be found. Van der Kolk et al (1998) make a strong case for the consideration of dissociation, somatization and affect dysregulation as late expressions of trauma even in the absence of continuing criteria for the diagnosis of PTSD. In doing so, they echo the concerns of Nemiah (1995), who notes that the diagnoses of PTSD, conversion disorder and dissociation are connected by the common process of dissociation itself, whereas their disparate placement in different categories of the DSM IV inhibits investigation of the psychodynamics of trauma.
This attempt to return to the concepts of a relatively broadly-based response of the organism to traumatic stress is critical to our consideration of the neurophysiology of trauma and its effects not only on systems of the brain and endocrine systems, but also on the body itself. When one accepts the tenet that the clinical expressions of a multitude of psychiatric syndromes derive not only de novo or through gene expression, but perhaps also through life experience and its lasting effects on brain physiology, one must return to the concept of a physiological continuum between many psychiatric diagnoses.
CLINICAL TYPES OF DISSOCIATION
One of the dilemmas of classification of symptoms of dissociation is that these symptoms assume many and varied forms and expressions. They may be emotional, perceptual, cognitive or functional. They may involve altered perception of time, space, sense of self and reality. Emotional expressions may vary from panic to numbing and catatonia. Altered sensory perceptions may vary from anesthesia to analgesia to intolerable pain. Motor expressions frequently involve weakness, paralysis and ataxia, but may also present as tremors, dysarthria, shaking and convulsions (Please see discussion of conversion reaction later). Cognitive symptoms may involve confusion, dysphasia, dyscalculia and severe deficits in attention. Perceptual symptoms include ignoral and neglect. Memory alteration may appear as hypermnesia in the form of flashbacks, or as amnesia in the form of fugue states or more selective traumatic amnesia. The varied symptoms of dissociation therefore mimic the intrinsic bipolar nature of the defining symptoms of PTSD (arousal, reexperiencing, avoidance).Time perception is often greatly altered, most commonly characterized by a sense of slowing of time (Terr, 1983). Altered perception of self (depersonalization) may manifest as an out-of body experience, or a sense of intense familiarity (de ja` vu) (Pynoos, et al, 1987). In its most extreme expression, depersonalization may encompass perception of several separate states of self in the form of distinct and separate personalities (dissociative identity disorder), each with distinct personality characteristics and even physical attributes (Mayer-Gross, 1935). Strange persons or events may appear familiar, whereas familiar faces and scenes may appear alien and strange.
Abnormal memories also constitute a significant dissociative phenomenon. Simple amnesia for the traumatic event is common, and may present as complete amnesia, or as distorted or inaccurate memory content (Torrie, 1944, Terr, 1983). Fugue states present an extreme state of amnesia, characterized by periods of time for which the dissociative patient has no memory, often triggered by exposure to cues reminiscent of prior trauma. During that time, the person may appear distracted and may not remember personal facts. More often, they may appear confused, histrionic, socially inappropriate or bizarre (Fisher, 1945).
Perhaps the most unique symptom of dissociation is that of flashbacks. These episodes are distinctive in that they involve intense arousal and reexperiencing, symptoms more related to acute PTSD than to dissociation (Mellman, & Davis, 1985). During these episodes, which may last briefly or for several hours or even days, the person will also usually experience more typical dissociative experiences such as depersonalization. Sensory processing and perception may be greatly distorted. During flashbacks, the person may appear confused and detached, but later may report vivid sensory and memory experiences, often associated with intense emotions and states of arousal. The accuracy of the associated memories may be variably valid or distorted.
Conversion reaction and hysteria no longer are described in the DSM IV under dissociation (American Psychiatric Association, 1994). In fact the DSM IV goes so far as to assert that if dissociative and conversion-based symptoms occur in the same patient, both diagnoses must be made. The neurophysiological and pathophysiological basis for dissociation proposed in this paper, however, demands that conversion be reintroduced as a specific form of dissociation, one that is closely linked to somatic perceptual alterations that are an acceptable and in fact intrinsic feature of the dissociative process. The model presented proposes that the atypical neurologic symptoms and signs that characterize conversion constitute perceptual alterations based on prior trauma, and represent the same splitting of consciousness that produces disorders of perception of time, space, reality and self presented above. As such, conversion may be associated with the same spectrum of positive and negative phenomena as PTSD as well as other symptoms of dissociation (analgesia/pain, paralysis/seizures).
MEMORY, TRAUMA AND DISSOCIATION
Disorders of memory constitute one of the diagnostic categories for PTSD in the form of reexperiencing. As noted above, this may be in the form of hypermnesia, amnesia or distortion of memory. Trauma-based memory phenomena often involve declarative (explicit, semantic) memory in the form of variably accurate verbal and imaginal recall of the traumatic event. Declarative memory, the form of memory that relates to facts and events, initially involves hippocampal and prefrontal cortical pathways and plays an important role in conscious recall of trauma-related events. It also is notoriously inaccurate, and subject to decay. Procedural memory relates to acquisition of motor skills and habits, to the development of emotional memories and associations, and to the storage of conditioned sensorimotor responses. Procedural memory is unconscious, implicit and extremely resistant to decay, especially if it is linked to information of high emotional or threat-based content (van der Kolk, 1994). Although declarative memory may account for much of the arousal-based cognitive symptoms of PTSD, procedural memory provides the seemingly unbreakable conditioned link that perpetuates the neural cycle of trauma and dissociation.Endogenous opiate reward systems very likely contribute to the establishment of conditioned procedural memory in trauma. Researchers have known for decades that exposure to overwhelming trauma in combat often results in a sustained period of analgesia. Soldiers wounded in battle frequently require much lower doses of morphine than in other types of incidental injury (Beecher, 1946). Stress-induced analgesia is a well-documented phenomenon in many forms of traumatic stress (van der Kolk, Greenberg, Orr & Pittman, 1989). Release of endorphins at the time of acute stress has a distinct survival benefit. An animal ministering to his wounds due to pain at the time of aggressive, life-threatening injury would suffer significant compromise of his defensive capabilities. Endorphins also persist during freeze/immobility, rendering the animal analgesic in the face of the injury from the attack. This also has potential survival value, since the persistence of immobility in the face of painful injury might serve to end the predator’s attack behavior. In the event of lack of completion of the freeze/immobility response, however, persistent recurrent dissociation with associated endophinergic reward might well potentiate the kindled trauma reflex. Endorphinergic influences might also contribute to the phenomenon of compulsive trauma reenactment (van der Kolk, 1989).
THE ANIMAL MODEL
The behavior and physiology of the freeze response have been studied for decades. Freezing of course is routinely seen in the wild, initially as a state of alert immobility, as in the fawn that assumes an immobile state in the presence of a predator. This state may proceed to sudden flight, or if the fawn is attacked and captured by the predator, to a deeper state of freeze, one associated with apparent unresponsiveness, and associated with marked changes in basal autonomic state. Early immobility has the advantage for the prey animal of remaining hidden, especially since movement cues often are necessary to elicit attack by the predator. All animals manifest alert immobility, a state termed "animal hypnosis" by Krystal (1988).In the event of attack, when the creature is rendered helpless, a different state of freezing is elicited, as noted above. Laboratory studies of this phenomenon yield interesting results. Hofer (1970) exposed rodents to a variety of predator-related stimuli in an open space with no means of escape. All rodents entered a deep phase of freeze, persisting for up to 30 minutes. This state was associated with marked bradycardia associated with cardiac arrythmias, suggesting a pronounced state of vagal or parasympathetic tone.
Ginsberg (1974) immobilized chicks, and then allowed one group to recover spontaneously, and one to recover, but with prodding and stimuli to terminate the freeze. These groups, along with a third group of chicks that had not been immobilized, were then tested for resiliency to avoid death by drowning. The group that had not been allowed to complete recovery from immobility died first, the group not exposed to immobility next, and the group that had spontaneously recovered from the freeze survived the longest. Clearly the experience of and the spontaneous recovery from freezing carries survival benefits, whereas not being allowed to go through this recovery process seemed to reduce resiliency to life threat.
The key to this process appears to revolve around the state of helplessness, or lack of control. In drowning experiments, wild rats will swim for up to 60 hours before dying from exhaustion. If these rats experience immobility in the hands of the investigator, and then are placed into the water, they will drown in minutes. Some rats experience sudden death during induced immobility (Richter, 1957). The freeze response clearly is associated with high risk to the creature if it is not allowed to dissipate spontaneously.
Studies in animals with inescapable shock (IS) further illustrate this dilemma. Animals exposed to significant shock stimuli in an escape-proof environment predictably freeze with subsequent shock exposure. Subsequent introduction of routes of escape in these animals do not elicit escape behavior- the animals remain frozen, and continue to exhibit helplessness (Seligman, 1975). They appear to be unable to learn from new experiences, even from those experiences that promote escape or survival. Animals exposed to escapable shock (ES), however, soon learn to use the escape route and do not freeze (Fanselow & Lester, 1988). The critical factor in trauma therefore appears to be controllability of the outcome of the threat vs. a state of helplessness. Van der Kolk, et al, have noted the remarkable similarities between the human response to trauma, and the animal response to inescapable shock (IS), and have suggested that IS may be a biological model for PTSD (van der Kolk, et al,1985). Nijenhuis, et al (1998) have presented the novel model of dissociation in humans as an analogy to the alteration in defensive and recuperative behaviors in animals exposed to IS (Nijenhuis, et al, 1998). Threat-associated conditioned stimuli (CS) in this model would automatically elicit a dissociative or freeze response, rather than a conditioned response more specific to the stimulus. Persistent dissociation would therefore prompt the animal, or human, to be sensitized to continue to freeze, or dissociate, to a wide range of stimuli that might be associated with threat.
Levine (1997) takes the phylogenetic model a step further, by equating the lack of recovery from the freeze, or immobility response with retention of the stored and undissipated energy of the truncated fight/flight response. This sustained state of sympathetic arousal serves as the drive for the memory and arousal-based symptoms of trauma and PTSD. He attributes the tendency for traumatization in the human species to the inhibitory influence of selected neocortical centers that block the instinctual capability that other wild animal species possess, to "discharge" this retained energy. Noting that animals emerging from immobility often manifest repetitive, almost seizure-like motor activity, he postulates that these stereotyped motor responses are able to allow completion of the motor sequences of successful escape or defense, and therefore to effect an energetic discharge.
Dissociation in the animal model, then, appears to have many similarities to behavior in animals in whom freezing has been elicited in a state of helplessness with subsequent prevention of spontaneous recovery from immobility. Furthermore, dissociation also may be associated with predominantly parasympathetic tone, impaired cognition and learning behavior and a tendency for conditioned perpetuation.
TRAUMA AND DISSOCIATION: THE WHIPLASH MODEL
We have previously presented an hypothesis that the Whiplash Syndrome constitutes a model for traumatization rather than physical injury, and that many of its symptoms and clinical manifestations are in fact a universal response to a life threat in the face of helplessness (Scaer, 1997, 1999, 2001). This hypothesis is based on the occurrence of dissociation at the time of the motor vehicle accident (MVA) in the form of numbing and the altered state of awareness often attributed to concussion. Subsequent clinical symptoms are based on theories of limbic kindling in the development of the arousal-memory cycle in PTSD (Goddard, et al, 1969, Post, Weiss & Smith, 1995, Miller, 1997). Kindling is the name given to the phenomenon in rats of the progressive development of self-perpetuating neural circuits produced by repetitive time- and frequency-contingent regional electrical brain stimulation (Goddard, et al, 1969). The behavioral expression of kindling may include epileptic seizures, but kindling is also widely felt to be a model for a number of clinical syndromes, including PTSD.The neural pathways involved in the process of acquisition of this kindled physiologic response to threat probably involve a series of events involving primarily the locus ceruleus, amygdala, thalamus, hippocampus and right orbitofrontal cortex (van der Kolk, 1994). Arousal-based input from a variety of sensory organs, especially those of the head and neck, is transmitted to the thalamus and locus ceruleus. The locus ceruleus then provides input to the thalamus and to the amygdala, which evaluates this input for its emotional content. The amygdala then transmits this information to the hippocampus, the center for declarative memory, which establishes a cognitive context to the information. This data is then transmitted to the right orbitofrontal cortex (OFC), which organizes the appropriate cortical and autonomic response based on the implications of the sensory information for survival. The OFC therefore functions as a master regulator for organization of the brain’s response to threat. Inadequate development of the OFC resulting from a maladaptive childhood experience, or from prior brain injury may result in faulty modulation of this arousal response (Schore, 1994).
Further regulatory control is provided by the anterior cingulate cortex, a center that may provide a gating function inhibiting fear conditioning by inhibitory input to the amygdala ( Morgan, et al, 1995). The locus ceruleus, through intense adrenergic input triggered by an acute arousal stimulus, inhibits both the anterior cingulate and the OFC, thereby inhibiting the gating and modulation functions of these two centers. This in turn would allow exposure of the amygdala to overwhelming internal and external arousal cues, thereby promoting the kindled development of pathways producing the clinical syndrome of PTSD (Hamner, 1999).
Dissociation at the time of trauma is the primary predictor for the later development of PTSD (van der Kolk & van der Hart, 1989). Individuals who actively dissociate at the time of a traumatic event are much more likely to develop subsequent symptoms of PTSD than those who do not (Bremner, et al, 1992, Holen, 1993, Cardena & Spiegel, 1993). Children are especially prone to dissociate at the time of a traumatic experience, and therefore people with a history of past trauma, especially child abuse, are more susceptible to arousal, freezing and retraumatization after exposure to even non-specific arousal or traumatic stimuli (Kolb, 1987).
In the whiplash hypothesis, spontaneous recovery from dissociation, or freeze/immobility at the moment of traumatic impact often will not occur, based on the premise that involvement in an MVA is by its very nature a model of helplessness. The potential for dissociation to occur will predictably be greatly enhanced by a prior history of trauma and dissociation. This state of altered memory, perception and autonomic function may potentiate kindling between centers for memory and arousal (amygdala, hippocampus, locus ceruleus) that we have described above. The resulting self generated and maintained kindled loop will then serve as the substrate for development of clinical PTSD.
From a somatic standpoint, procedural or conditioned memory for sensory input and motor responses to the physical events associated with the actual accident will also be incorporated into this kindled trauma response. In an event of great arousal and threat, only one trial may be necessary for a conditioned response to be established. Thus vestibular, ocular, and sensorimotor experiences of the accident will be imprinted on procedural memory through traumatic operant conditioning. These perceptions will then subsequently be elicited in exact form by memories, flashbacks, nightmares as well as internal and external cues reminiscent of the MVA. All of the elements of the post-concussion syndrome - vertigo, blurring of vision, tinnitus, headache, myofascial pain - now constitute symptoms precipitated by cue- and memory-based stimuli, and eventually by a wider and wider range of nonspecific arousal-based events. Myofascial pain probably represents procedural memory for the specific defensive motor stretch reflex and its proprioceptive template precipitated by the movement of the body in the MVA, thereafter elicited by stress or any movement pattern reminiscent of the accident, in the form of bracing and muscle spasm. Cognitive impairment may appear and in fact worsen based on well-documented attention and memory deficits in dissociation and PTSD (Gill, et al, 1990, Alexander, 1992, Miller, 1992, Bremner, et al, 1993, Grigsby, et al, 1995). None of this diverse array of symptoms would therefore require tissue injury to produce them.
This hypothesis is dependent on the occurrence of dissociation contributing to an unresolved freeze response as a result of life threat in the face of helplessness. Resulting kindling would then incorporate not only the centers for memory and arousal noted above, but also the centers providing the sensory information of the MVA (visual, auditory, vestibular, proprioceptive sensory receptors), and the motor centers that organized the defensive response (cerebellum, brainstem, basal ganglia, motor cortex). Kindling and dissociation would explain the vexing tendency for whiplash symptoms to be resistant to most forms of physical therapy, to persist indefinitely in many cases and to worsen dramatically in situations of ambient life stress. The proposal also incorporates somatic symptoms into the basic theories of PTSD and dissociation, leading to a somatic definition of dissociation that is the core of this paper.
THE AUTONOMIC NERVOUS SYSTEM IN DISSOCIATION
Patients with chronic PTSD cycle in and out of exaggerated levels of arousal and avoidance, of panic and numbing, of terror and confusion. The panorama of autonomic symptoms includes pallor and flushing, nausea, abdominal cramps and diarrhea, tachycardia and light-headedness, diaphoresis and shivering. The DSM IV criteria for PTSD (arousal, reexperiencing, avoidance) reflect dramatic cycling of mood from panic, hypervigilence and irritability, to numbing, withdrawal and flattened affect. Physiologic markers of PTSD referenced in the DSM IV include measurements of pulse rate, electromyographic and electrodermal responses, all primarily measures of sympathetic tone. The role of the cyclical increase in parasympathetic tone or function in trauma, however, has been largely neglected. PTSD is in fact a bipolar syndrome, one that reflects remarkable cyclical autonomic instability, with patterns of heightened sympathetic arousal alternating at times with clear and dramatic parasympathetic dominance.Oscillatory phenomena in a variety of biological systems have been studied and documented in a number of settings. Many physiologic subsystems (endocrine, autonomic, neurohumoral) operate in a bimodal fashion based on a variety of rhythmic environmental and internal physiologic influences. Antelman et al (1997) propose that exposure of such systems to chemical or behavioral stressors of sufficient intensity can induce cyclical patterns of increase and decrease in response to each subsequent exposure (Antelman, et al, 1996, Antelman & Caggiula, 1996). This phenomenon seems to be applicable to such a variety of physiological systems that the authors conclude that oscillation in response to chemical or behavioral input may represent a general principle of biological functioning (Antelman, et al, 1997). This may well be an innate biological reflex designed to reestablish homeostasis, the rhythmic and balanced fluctuation of all biological systems, be they endocrinological, neurophysiological, metabolic or immunological (Antelman et al, 1997).
In PTSD, through unresolved peritraumatic dissociation, internal and external stimuli impacting the central neural circuits mediating memory and arousal will contribute to kindling, leading to internally-based stressors of associated neural subsystems, especially the autonomic nervous system. By this model, cyclical autonomic dysfunction will result, leading to many of the divergent but dramatic autonomic symptoms of the traumatized victim. Thus periods of sympathetic arousal will include symptoms of muscle bracing, bruxism, ocular divergence, tachycardia, diaphoresis, pallor, tremor, startle, hypervigilence, panic, rage and constipation. These states will alternate with parasympathetic dominance, including symptoms of palpitations, nausea, dizziness, indigestion, abdominal cramps, diarrhea and incontinence. Although many of these symptoms are often attributed to somatization disorder, they in fact represent the extremes of the cyclical autonomic dysfunction seen in trauma, are inherently self-perpetuating, and contribute to continued abnormal autonomic oscillation. The syndrome of trauma has now literally taken control of the body.
As the kindled cycle of PTSD continues and becomes chronic, avoidance and withdrawal become increasingly prominent, often with subsidence of symptoms of arousal, hypervigilence and phobia. At this point, the DSM IV-based criteria of PTSD no longer specifically justify the diagnosis, and patients are usually given diagnoses of somatization disorder, dissociative disorder, conversion or depression. With time, the role of trauma in the patient’s syndrome may be ignored. Although autonomic oscillation is still apparent, it is clear that the prevailing symptom complex reflects a state of parasympathetic dominance. Endocrinological measures now tend to show a state of low serum cortisol (Mason, et al, 1986, Yehuda et al, 1990), also commensurate with evolving parasympathetic tone. This trend is associated with behavioral responses including social isolation and withdrawal, substance abuse, constricted affect, denial, cognitive impairment and dissociation, all relatively parasympathetic states.
Another compelling rationale for this process may be drawn from the phylogenetic role of the parasympathetic nervous system, specifically the vagal system, as presented in the Polyvagal Theory of Emotion by Porges (1995). Porges emphasizes the phylogenetic layering of arousal responses in mammals, based on the varied functions of the vagal nuclei. The dorsal vagal complex (DVC), composed of the dorsal motor nucleus of the vagus and nucleus tractus solitarius, is a vestigial and primitive center, primarily useful in reptiles for energy conservation. In the low oxygen-demand system of the reptile, the DVC shuts down the energy-use system by inducing marked bradycardia and apnea, as in the reptilian dive reflex. The ventral vagal complex (VVC), unique to mammals, is a recent adaptation to the high oxygen need of this class of animals, and finely tunes energy utilization by subtle and flexible influences on heart rate. The early alerting response seen in animals consists of raising the head from grazing, orienting with the head to the source of the new, potentially threatening stimulus, widening of palpebral fissures, and sniffing for scents. This energy-conserving reflex is mediated by the VVC, and employs the locus ceruleus, which has rich connections with sense organs of the head, as well as the muscles of the head and neck. If sufficient information of threat is attained through this reflex, the VVC response is inhibited and the animal will progress to the neuromuscular and cardiovascular mechanisms of the epinephrine-based fight/flight response. If deterrence of the threat through defense or flight fails, the animal enters a state of helplessness, associated by a marked increase in DVC tone, initiating the freeze/immobility response. This state of deep parasympathetic tone is associated with marked bradycardia, apnea, sphinctor relaxation and gastrointestinal activation.
A persistent state of DVC activation, however, is common to reptiles, but in fact dangerous for mammals due to its association with marked bradycardia and life-threatening arrythmias. The spontaneous death of wild animals during induced states of immobility in the laboratory setting attests to this danger, as does the remarkable mortality rate of wild mammals introduced to the zoo environment (Seligman, 1987). In humans, this state of immobility and "suspended animation" perhaps has its most extreme expression in the phenomenon of Voodoo death, as described by Cannon (1942). The study of death in the freeze/immobility response in animals reveals that death occurs by cardiac arrest during diastole, or relaxation of the heart, in a state of complete cardiac flaccidity and engorgement with blood (Richter, 1957, Hofer, 1970). The extremes of vagal parasympathetic tone as manifested in the state of DVC activation therefore contribute greatly to the generation of severe emotions, especially those of terror and helplessness. Although freeze/ immobility states in mammals may be useful for short-term survival, prolongation or repeated activation of that state clearly has serious implications for health and long-term survival. The model of disease presented here suggests that the gradual descent into dissociation and parasympathetic dominance in chronic unresolved PTSD constitutes just such a state of peril.
SOMATIC DISSOCIATION
As suggested earlier, dissociation may be accompanied by split or altered perceptions not only of self and reality, but also of parts or regions of the body. The clinical impairment experienced by the dissociated individual under those circumstances will almost always present as physical deficits that defy physiologic explanation by examination, laboratory tests or imaging studies. Diagnoses entertained by physicians in these states include hysteria, conversion and psychosomatic disorders. The cause for these states is uniformly assumed to be psychological, and the common factor to be stress. Almost all of the deficits have a neurological nature, and may affect any system, including visual, auditory, vestibular, speech, balance, sensation and motor function. Seizures and fainting are common expressions of this state.Symptoms associated with conversion may appear to be exaggerated, and findings do not conform to those objectively seen in actual disease or injury of the nervous system. Thus, sensory loss usually presents in a "stocking/glove" distribution, rather than the layered dermatomal loss seen is lesions of the spinal cord. Weakness is diffuse and inconsistent, with a "give-away" quality. Symptoms are often one-sided, and findings may fluctuate in time, with ambient stress often enhancing the symptoms. Conversion symptoms occur more commonly in lower socioeconomic and less developed countries and cultures, and in women (American Psychiatric Association, 1994). From patient to patient and culture to culture, however, the seemingly varied syndromes of conversion have a remarkably constant theme that demands consideration of a common and as yet undefined neurophysiologic mechanism.
The medical literature does not address this attempted crossover between psychological and physiological factors in conversion and related disorders. Concepts presented in this model are based on the evaluations of thousand of patients who have experienced physical trauma in motor vehicle and other types of accidents, and who, to a varying degree, have also manifested symptoms of having been traumatized as well. Many of these patients have presented with symptoms and signs of conversion, and with minute observation of their physical states and behavioral symptoms, several conclusions appear to be inescapable.
Patients with conversion in this setting seldom present with la belle indifference, but rather exhibit early symptoms of arousal and distress consistent with PTSD. Their symptoms are remarkably common from patient to patient. Difficulties with speech elocution and mechanics are common, with word blocking, stutter and unusual dysarthric patterns of speech. One-sided or one upper extremity sensory loss is almost universal, associated with severe problems with dexterity on the same side. This sensory loss is invariably "non-physiological", often stocking and glove in distribution. Balance is impaired with variable swaying and staggering patterns not consistent with impairment of intrinsic brainstem balance centers. With careful observation, many such patients experience a physical sensation of arousal if the examiner presents a visual stimulus to them from a part of the room on the same side as their predominant non-physiologic symptoms. This pattern of arousal is most commonly experienced as nausea or dizziness, and may be associated with flushing, suggesting the influence of VVC activation as part of the early response to threat.
The concept of peripheral perceptual boundaries in psychological terms relates primarily to subtle areas of our sense of self that we perceive in relationship to others, the regions of appropriate limitations in personal and social interaction. In the model of somatic dissociation presented here, this concept of boundaries relates to an actual physical perceptual whole, or continuity of self, that represents the limits of the unconscious but perceived area defining the safe extent of our physical expression. The area comprising this space is directly proportional to the experience of previously unresolved life threats, and the continuity of the perceptual boundaries surrounding this space is dependant on the perceptual experience of severe threat within a specific boundary sector. Findings in testing the boundaries of a traumatized patient reveals that the area of a person’s perception where they first experienced the warning of the impending threat (eg – the approaching automobile) will thereafter be an area where accessing any stimulus is intrinsically threatening. As a result, passing a hand around the periphery of that person’s visual field at the distance of 3-4 feet will often produce an arousal response in the region of perception of prior threat. Such patients have developed a conditioned arousal reflex within areas of their perceptual surround, or boundary. Predictably, persistent ambient subliminal sensory perceptual experiences within that region, whether visual, tactile or proprioceptive in nature, will result in conditioned arousal and will perpetuate the kindled trauma reflex. Just as the chronic victim of PTSD will freeze or dissociate in the face of familiar threat, the part or region of the body representing the proprioceptive and somatic procedural memory for the threat experience will be selectively dissociated, leading to the nonphysiological signs of conversion. It will come as no surprise, therefore, that many patients with localized signs of conversion will experience symptoms of discomfort and arousal with presentation of visual or other seemingly benign stimuli within those regions of their boundary perception that now possess the sensory perception of threat.
In addition, with further close observation of such patients, one may detect unusual but reproducible physical changes in the dissociated portions of their body. My awareness of these physical phenomena began when one patient with "hysterical" right sided hemianesthesia, weakness and clumsiness related that her hairdresser had noted that her hair grew much more slowly on the right side, and was of a different texture. Close observation revealed that in addition, her hair was more sparse on the right side of her head. Examination of the patient’s right hand and arm then revealed that her fingernails were broken and ridged, the hand was cooler than on the left, and finger hair growth was diminished. Close observation of other similar patients subsequently documented signs of dystrophic skin, hair and nail changes in many patients in parts of the body manifesting signs of conversion. Finally, several of these patients proceeded to develop clear-cut signs of sympathetically maintained pain, or reflex sympathetic dystrophy (RSD).
REFLEX SYMPATHETIC DYSTROPHY
Sympathetically maintained pain, complex regional pain syndrome, and RSD comprise fairly common, well recognized but controversial and poorly understood pain syndromes, by definition associated with vasomotor autonomic symptoms and signs in the affected body parts. The extremities, especially their distal portions, are predominantly affected. Described by S. Wier Mitchell in the Civil War, the syndrome perhaps is most common in traumatic injuries of the extremities, but also may follow seemingly trivial injuries such as minor bruises or overuse injuries (Mitchell, et al, 1864, Schwartzman & McLellan, 1987). The syndrome is characterized by severe, often burning pain in the affected area, associated with variable signs of vasomotor dysfunction, both parasympathetic and sympathetic. These signs may include abnormal hair growth or loss, erythema and warmth, or pallor and coolness. With unsuccessful treatment and progression of the syndrome, signs of vasoconstriction and dystrophy predominate, hence the term sympathetic. Attribution of the syndrome to abnormal sympathetic autonomic tone is supported at least in part by the fact that the injection of related ganglia of the sympathetic nervous system may provide variable relief of pain. Many investigators feel that the central nervous system may be involved. Dystonic postures of the affected limbs are common. Electromyographic and nerve conduction studies of RSD reveal that the character of this dystonia is more typical of voluntary holding of the posture than of comparable dystonias in patients with brain lesions (Koelman, et al, 1999). The authors go so far as to say, "In causalgia-dystonia, central motor control may be altered by a trauma in such a way that the affected limb is dissociated from normal regulatory mechanisms" (p. 2198).The model presented here proposes that regional somatic dissociation exposes the dissociated member or region of the body to selective vulnerability to the effects of existing cyclical and oscillatory autonomic dysfunction associated with the neurophysiological changes of unresolved trauma. In this state, that region or part may then be vulnerable to vasomotor oscillation, with vasoconstriction and functional reduction in blood flow ultimately creating the ischemic tissue pathology characteristic of RSD. This syndrome, as often is the case, comprises a continuum, or spectrum of clinical expression, from the subtle signs seen in most patients, to the full-blown pain, dystrophic changes and dystonia of RSD. Dissociation, by this model, is a neurophysiological syndrome of central nervous system origin. It is initiated by a failed attempt at defensive/escape efforts at the moment of a life threat, and is perpetuated if spontaneous recovery from the resulting freeze response is blocked or truncated. Lack of recovery from this freeze response results in conditioned association of all sensorimotor information assimilated at the time of the traumatic event into procedural memory, to be resurrected at times of subsequent perceived threat as a primitive conditioned survival reflex. This procedural memory acquisition initially is elicited by internal and external cue-specific stimuli, but because the threat itself has not been resolved, internal cues persist without inhibition from external messages of safety, and kindling is triggered in the cortical, limbic and brainstem centers previously discussed. Recurrent dissociation in response to arousal accompanies this cycle and facilitates the development of pathologic autonomic oscillation. Physiologic inhibition of perception of those parts or regions of the body for which the brain holds procedural memory of their sensory input at the time of the threat results in the syndrome of conversion and regional somatic dissociation. Divorced from the normal trophic benefits of cerebral perception, these regions are subject to the extremes of vasomotor instability of late trauma, and develop syndromes of pathologic vasoconstriction and ischemia, leading to RSD.
THE DISEASES OF TRAUMA
Selye (1936) has generally been credited with the concept that prolonged or excessive exposure to stress could contribute to the development of a group of specific diseases. These diseases predominantly reflected exposure to elevated levels of adrenal cortical hormones as part of the modulating role of cortisol on the hypothalamic/pituitary/adrenal (HPA) axis in stress. Thus rats exposed to prolonged and excessive stress developed erosion of the gastric mucosa, atherosclerosis and adrenal cortical atrophy. Other specific pathologic effects of excessive cortisol exposure include immune suppression, elevated serum lipids and atherosclerosis, diabetes, osteoporosis, hypertension, peptic ulcer disease, obesity and cognitive/emotional impairment. Many of these effects are now well described in the medical and lay literature as "diseases of stress".The relationship of the long-term effects of trauma (as opposed to stress) and disease are less well documented. Whereas ongoing stress is easily identified, the past experience of traumatization is masked by the evolution of the resulting syndrome into experiences, symptoms and behaviors that ultimately are attributed to characterological and psychological causes – i.e. – that are due to internal rather than external events. This perception is basically correct in that the internal events in trauma are self-driven and capable of changing somatic physiology in the absence of external influences. This concept is also in keeping with the physiologic effects of somatic dissociation, which are driven by internal brain-based mechanisms that are self-perpetuating. Therefore, one would not expect the diseases of trauma to reflect the generally cortisol-based syndromes of acute and even chronic exogenous stress. Rather, one would predict that diseases of trauma would reflect autonomic regulatory impairment, both sympathetic and parasympathetic, with a predominance of vagal and parasympathetic syndromes in the later stages.
This model of disease in trauma would predict that vasomotor symptoms and signs would be likely, with both trophic and dystrophic components, the latter reflecting vasoconstriction and ischemia. Cardiac, pulmonary, bowel and exocrine gland dysfunction should be predictable. Abnormalities of strength, muscle tone and endurance should be common. Lowering of serum cortisol in late stages of trauma might lead to relative lack of immune inhibition, and therefore to hyperimmune syndromes. One would also expect these syndromes in some cases to manifest remarkable periods of exacerbation and remission based on autonomic oscillation, and to be specifically sensitive to exacerbation by external stress. Fluctuating symptoms of cognitive impairment especially related to attention and memory would be common in many of these conditions. One would expect an unusual association of the emotional symptoms of late trauma, including affect dysregulation, dissociation, somatization, depression, hypervigilance and denial/avoidance. A psychosocial trauma history in many cases might reflect a history of substantial life trauma, especially in childhood.
Among other manifestations, these diseases would at least in part show evidence of abnormal parasympathetic tone, perhaps along with sympathetic vasoconstrictive dystrophic and ulcerative phenomenona. Diseases and syndromes of the gastrointestinal system that fall into this general concept of diseases of trauma include peptic ulcer and gastroesophageal reflux disease, irritable bowel syndrome, Crohn’s disease (regional ileitis) and ulcerative colitis. All reflect organ hypermotility, excessive glandular secretion and in some, ulcerative features. Cardiac syndromes would likely reflect the cardiac abnormalities associated with DVC dominance, and be associated with a variety of tachy- and bradyarrythmias, including those seen in mitral valve prolapse. Bronchial asthma, a syndrome primarily manifested by stress and hyperimmune-induced abnormal organ-specific parasympathetic events (bronchospasm and hypersecretion) has many of the criteria predictable in diseases of trauma. Interstitial cystitis is a condition characterized by pain, spasm and ulceration of the bladder wall, combining the parasympathetic/dystrophic elements of many of these syndromes.
One of the most perplexing and controversial chronic syndromes that may fall into this category is that of fibromyalgia/chronic fatigue. Protean symptoms include diffuse and severe musculoskeletal pain, impaired and nonrestorative sleep with chronic fatigue, stiffness, headaches, anxiety, hypervigilance, cognitive impairment, ocular and vestibular symptoms and paresthesias. Associated syndromes include irritable bowel syndrome, interstitial cystitis, mitral valve prolapse, and esophageal dysfunction (Clauw, 1995). Low serum cortisol and HPA axis dysfunction similar to that in late PTSD have been documented (Crofford, 1996). Fibromyalgia syndrome primarily affects women, and controversial but suggestive evidence for an increased incidence of childhood sexual and physical trauma in fibromyalgia patients has been documented (Boisset, et al, 1995). Fibromyalgia arising de novo from a traumatic experience has been well-documented (Waylonis & Perkins, 1994). While recognizing that overwhelming circumstantial evidence does not constitute medical scientific proof, fibromyalgia/chronic fatigue syndrome appears to present a prototypic syndrome for the model of the diseases of autonomic dysfunction seen in late trauma.
The rationale for RSD as a dissociative/autonomic posttraumatic disease has been presented. Chronic pain in instances where documented structural pathology is not apparent very likely represents another syndrome of late trauma. Phantom limb pain appears to represent the prototype for this model. This syndrome occurs much more commonly when the amputation was associated with a traumatic injury. Persisting representation of pain in an absent organ or body part suggests procedural memory for that pain as a conditioned response. The critical element for that memory to be conditioned, of course, is the unresolved threat associated with the injury producing the pain itself. One must remember that severe pain itself may be traumatizing, and that the medical system in which that pain was managed has many potential sources of traumatic stress (Scaer, 2001, Chapter 9). Conditioned imprinting of pain in procedural memory of course implies that trauma will have occurred in a state of helplessness without opportunity for spontaneous resolution of a freeze response. Under those circumstances, the specific pain will continue to represent the threat, and be retained for late survival purposes in conditioned procedural memory.
An underlying state of vulnerability to traumatization would also be a predictable substrate for the development of chronic pain in the injured individual. Victims of child abuse or multiple prior traumatic events clearly possess this vulnerability, and would be predicted to be susceptible to the incorporation of a newly painful experience into procedural memory in the model described above. The trauma literature amply documents the high incidence of chronic pain of many types seen in victims of child abuse relative to the general population. Types of pain represented in these studies include pelvic, back, abdominal, head, orofacial pain, and chronic pain in general. Also documented is the extremely high incidence of childhood abuse in patients referred to centers for chronic pain treatment (Rapkin, et al, 1990, Wurtele, et al, 1990, Toomey, et al, 1993, Walling, et al, I, 1994,Walling, et al, II, 1994).
A number of studies and proposed models of disease suggest that trauma may in part contribute to the autoimmune diseases. As noted, the lower serum cortisol documented in late PTSD might be related to increased immune activities in vivo (Yehuda, et al, 1993). Indeed, Watson et al (1993) have documented increased reactivity of skin to antigens in combat-related PTSD (Watson, et al, 1993). Other authors have specifically proposed that the low cortisol state of late PTSD might well present the substrate for a hyperimmune state (Friedman, & Schnurr, 1995, p. 518). More recently, the ratio of lymphocytic phenotypes documented in victims of childhood sexual abuse with PTSD showed a pattern indicative of lymphocytic activation. This finding supports the likelihood of increased immune activity in these patients, suggesting the potential for a hyperimmune state in late PTSD (Wilson, et al, 1999). Supported by an exhaustive literature review, Rothschild and Masi present a strong argument for a vascular hypothesis for rheumatoid arthritis (RA) incorporating as a cardinal feature vasoconstriction and tissue hypoxia, both of which have been well-documented in RA. Hypoxia of the arteriolar wall leads to vascular permeability with release of antigens into surrounding tissues. The resulting immune response therefore represents a relatively secondary feature of RA (Rothschild, & Masi, 1982). This theory, supported by an extensive array of studies, is in keeping with the model of autonomic and vasomotor dysfunction presented previously as a template for trauma-related disease processes. Such findings by no means provide a specific link between prior trauma and the autoimmune diseases, but suggest an avenue for further investigation of a possible relationship between trauma and autoimmune processes.
Perhaps a more compelling and immediate avenue for investigation relates to the studies of morbidity and mortality in trauma. Victims of trauma have long been known to experience increased morbidity and mortality rates (Friedman & Schnurr, 1995). Many of these studies focus on the late health problems of former prisoners of war (POW’s) (Beebe, 1975, Page, 1992). Cardiovascular and gastrointestinal diseases predominate in this group of late trauma victims, although emotional sequellae related to depression and cirrhosis of the liver associated with alcoholism contributed significantly to mortality. When the diagnosis of PTSD is added to the equation, however, the health effects of trauma are noted to increase substantially, with the cardiovascular diseases predominating (Friedman & Schnurr, 1955, Wolff, et al, 1994).
From the early morbidity intrinsic to Selye’s model of stress, to the late effects of autonomic dysregulation, and pathologic vagal dominance, the potential and real health effects of trauma are clear. Unfortunately, the trauma necessary to place the individual at risk may be as subtle as adverse childhood experiences. Felitti et al, (1998) found a strong graded relationship between the breadth of exposure to abuse or family dysfunction during childhood and multiple risk factors for several of the leading causes of death in adults (Felitti, et al, 1998). Adult diseases that were endemic in those who had experienced childhood abuse or family dysfunction included ischemic heart disease, cancer, chronic lung disease, skeletal fractures, obesity and liver disease. Additional diseases attributable to risk exposure and behavior included sexually transmitted disease, alcoholism, drug abuse, depression and suicide. This study is particularly disturbing in that it shows that the "trauma" of childhood in these high-morbidity cases was often as indirect as living with family members who were mentally ill or substance abusers. The sensitivity and vulnerability of the developing child to a loss of nurturing and safe boundary structure, and the adverse effects of this loss throughout life on emotional and physical health appear to be frighteningly clear.
CONCLUSION
We have presented a model of altered brain function precipitated by a traumatic event whose completion or resolution was truncated or aborted by lack of spontaneous resolution of a freeze/immobility response, a phenomenon closely allied to the clinical psychological state of dissociation. In addition to the arbitrary psychiatric diagnosis of PTSD, this state is associated with a complex set of somatic pathologic events characterized by cyclical autonomic dysregulation, and an evolving state of vagal dominance involving primarily the dorsal vagal nucleus. The sympathetic portion of this cyclical physiologic complex primarily involves vasoconstriction, with dystrophic and ischemic regional changes, especially in regions of the body that have been subject to dissociation due to their residual representation of sensory messages of threat stored in procedural memory. The experimental model of kindling is intrinsic to the self-perpetuation of this pathologic process, driven by internal cues derived from unresolved procedural memory of threat, and enhanced by endorphinergic mechanisms inherent to both the initial response to threat, and to subsequent freeze/dissociation.In this context, a variety of chronic diseases are postulated to represent late somatic expressions of traumatic stress. These diseases are of remarkably varied expression, but with a common thread of autonomic cyclical instability, frequently subtle vasoconstrictive/ischemic features, and usually pain. They are generally distinct from those diseases frequently attributed to stress, although these "stress-related" diseases often occur simultaneously and are definitely also more frequent in the adult population of those persons who have experienced trauma.
This model rejects the concept that the terms "somatization", "conversion", "hysterical", "psychological", or "psychosomatic" have any viable meaning in the definition of a symptom complex or disease state. It places all of these terms in a pathologic somatic context associated with subtle, but definable and objective clinical findings and manifestations of disease. It moves beyond the concept of mind/body medicine to the concept of a mind/brain/body continuum.
By attempting to isolate psychosomatic disease processes into a distinct category, we are ignoring perhaps the major cause for the group of diseases that members of the healing professions probably understand the least, and treat the most ineffectively – chronic diseases of unknown cause. Many of these diseases are due to impairment of regulation, rather than due to the invasion of microbes, toxins or other extrinsic agents. As such, they present a unique opportunity for those practitioners, researchers and teachers in the area of applied psychophysiology and biofeedback who have dealt with concepts of self-regulation and healing for the past 40 years. If one accepts the concepts of myofascial pain, visceral dysfunction, chronic pain and systemic diseases such as fibromyalgia presented above, it quickly becomes apparent that biofeedback practitioners have been treating symptoms and conditions primarily driven by past trauma in most of their patients. Not surprisingly, their techniques have often been more effective than polypharmacy and many medical/surgical techniques. Application of advanced techniques such as cerebral regulation through neurofeedback and autonomic regulation through control of heart rate variability (HRV) may have profound implications for healing trauma by providing a unique means of access to the conditioned autonomic responses that drive the trauma reflex.
Finally, as clinicians, we must look beyond the dysfunctional behavior apparent in many of these patients, to the neurophysiological and autonomic dysregulation that is the source of their symptoms and eventually their disease. Medical science must shed the concept that a symptom not measurable by current technology is "psychological", and therefore invalid. And physicians must reject the pejorative implications of the term somatization, and stop further traumatization of patients by subtly implied rejection.
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Wurtele, S., Kaplan, G., Keairnes, M. (1990). Childhood sexual abuse among chronic pain patients, The Clinical Journal of Pain, 6:110-113.
Yehuda, R., Southwick, S., Nussbaum, G et al. (1990). Low urinary cortisol excretion in patients with posttraumatic stress disorder, Journal of Nervous and Mental Diseases, 178:366-369.
Posted by pelorojo on November 6, 2002, at 17:58:08
In reply to Re: PTSD/Social Anxiety-Herbals, posted by Larry Hoover on November 5, 2002, at 9:05:22
After reading that article on the neurophysiology of PTSD and many others, I've been wondering:
-is an SSRI really the answer in such a complicated physiological chain of events? It seems like some way to go to the root of the problem would be better
-do the "adaptogenic" herbs, which claim to "modulate" or "normalize" the stress response, have any role here? I'm thinking of ashwagandha, astragalus, reishi, shiitake/maitake, rhodiola rosea, adapton, suma, cordyceps, licorice, etc., etc. Might they help "normalize" cortisol?
- could a cortisol-reducer (such as Relora or cortitrol) help in acute situations of stress when PTSD is triggered? I have "complex" PTSD and know of some (but not all) situations that trigger it. Perhaps a cortisol-reducer would help?
-what neurotransmitters are most important in PTSD? My limited reading on social anxiety suggests that they may be similar and the prime suspects are dopamine, serotonin, and gaba.
-could amino acid precursors be effective? L-tyrosine, 5-htp, etc.
-are other amino acids useful for other reasons? D,L-phenylalanine, L-theanine come to mind here.
-I had largely given up on St. John's Wort because of the studies that questioned its efficacy and showed potential interactions (in the form of reduced effectiveness) of other drugs..but is there something I'm missing? There's also a herbal SSRI, sceletium (sp?)...
-finally is there a creative approach that might work best? For example, taking certain amino acids on certain days, certain herbs for a period of time, etc. etc. Instead of chronically taking something taking them on cycles or "pulsing" them (i.e., L-Tyrosine Monday, SAMe Tuesday, herbal L-dopa Wednesday, etc).
No one can probably answer these questions for certain but is anyone thinking along these lines? Any resources to bear on it?I've been on SSRIs for 2 long cycles. They work in that they make me less depressed and less anxious but it seems like the underlying issues remain unaddressed. I'm working on them in therapy as well but that is very slow going ... I guess I'm a little desperate to find things that help.
thanks
Ken
Austin, TX
Posted by pelorojo on November 6, 2002, at 18:29:07
In reply to Re: PTSD/Social Anxiety-Herbals, posted by Tabitha on November 5, 2002, at 15:38:47
thanks - I had thought of that and discussed it with my therapist. He's seeing varying rates of success (i.e., 0 to 80% improvement). He thought I could try it but that it seems to work best in "standard" PTSD rather than "complex" PTSD (my diagnosis). I may still give it a try tho I've read that it is essentially exposure therapy with finger-tapping.
Posted by Larry Hoover on November 7, 2002, at 9:05:07
In reply to Re: PTSD/Social Anxiety-Herbals, posted by pelorojo on November 6, 2002, at 17:58:08
> After reading that article on the neurophysiology of PTSD and many others, I've been wondering:
>
> -is an SSRI really the answer in such a complicated physiological chain of events? It seems like some way to go to the root of the problem would be betterYes, but the beginning of the healing journey may begin with medication which facilitates e.g. cognitive-behavioural therapy. If your thinking is distorted by chronic or recurrent dysthymia or depression, you have to address the symptoms in order to permit useful insight.
> -do the "adaptogenic" herbs, which claim to "modulate" or "normalize" the stress response, have any role here? I'm thinking of ashwagandha, astragalus, reishi, shiitake/maitake, rhodiola rosea, adapton, suma, cordyceps, licorice, etc., etc. Might they help "normalize" cortisol?
There is some evidence that adaptogens may have much lesser effect the longer the chronic stress has continued. The HPA can become 'locked in' to a vicious cycle caused by what some call burn-out.
That said, gingko or Siberian ginseng have quite different modes of action when compared to e.g. rhodiola or witheria or licorice root. For example, licorice root blocks liver enzymes affecting interconversion of some of the steroids. I don't like the 'lumping together' of herbs like this.
> - could a cortisol-reducer (such as Relora or cortitrol) help in acute situations of stress when PTSD is triggered? I have "complex" PTSD and know of some (but not all) situations that trigger it. Perhaps a cortisol-reducer would help?I've never even heard of these drugs before (but I'll certainly look into it). You need to do a 24-hour cortisol/DHEA/DHEA-S to determine your circadian secretion level/pattern. Before you muck around with your hormones, you need both baselines and justification.
> -what neurotransmitters are most important in PTSD? My limited reading on social anxiety suggests that they may be similar and the prime suspects are dopamine, serotonin, and gaba.I think norepinephrine (noradrenaline) is actually the key player. It's secreted by the adrenals, and in some respects, dysregulates all the others.
Whatever. Theories aren't going to make you well. What I'm getting at is that you need to do a series of trials with n=1. You have to try interventions, assess the outcome, go off the intervention, re-assess, and go on it again. That's the only way to know what works for you. I tried rhodiola after someone I knew had astounding results, including sleep normalization. It exacerbated *my* insomnia, and made *me* more anxious. No thought experiment will tell you anything with any certainty.
> -could amino acid precursors be effective? L-tyrosine, 5-htp, etc.
I'd stay away from 5-HTP. You bypass the rate-limiting step, which your body uses to limit the amount of serotonin in general circulation. You don't want serotonin in your blood, but 5-HTP will do that, because the aromatic-decarboxylase enzyme is found in every organ compartment.
You can buy tryptophan for veterinary purposes. It is of equal quality to pharma grade.
> -are other amino acids useful for other reasons? D,L-phenylalanine, L-theanine come to mind here.I forget what theanine does, but DLPA gives two bangs for the buck. It's a precursor to the feel-good PEA, as well as being converted into tyrosine.
> -I had largely given up on St. John's Wort because of the studies that questioned its efficacy and showed potential interactions (in the form of reduced effectiveness) of other drugs..but is there something I'm missing? There's also a herbal SSRI, sceletium (sp?)...You're probably referring to this study, which also showed that sertraline (Zoloft) doesn't work. I'm surprised that the press didn't run with the 'proof' that a pharmaceutical drug failed this test. If you read the full-text, you'll see that the SJW they used was not standardized to contain the industry-standard minimum level of active ingredients. The study was methodologically flawed, and therefore, worthless.
Or perhaps you're thinking of this one, declaring SJW infeffective for major depression, despite the finding that, "The number reaching remission of illness was significantly higher with St John's wort than with placebo (P =.02)", and that SJW doses routinely used in Europe for more severe depressive symptoms were not emloyed in this study (funded by a major pharmaceutical corporation).
Funny, but a recent report in Am. J. Psych. showing the effectiveness of SJW gets no press.
Nor does this one:
Here's the most recent meta-analysis, demonstrating the effectiveness of SJW:
> -finally is there a creative approach that might work best? For example, taking certain amino acids on certain days, certain herbs for a period of time, etc. etc. Instead of chronically taking something taking them on cycles or "pulsing" them (i.e., L-Tyrosine Monday, SAMe Tuesday, herbal L-dopa Wednesday, etc).
I take many of my supplements in pulses. My intuition guides me on this, and I just let it happen that way. Your brain/body may vary.
Some supplements need to be taken daily to have maximum effect, like SJW. It takes eight weeks on SJW for significant changes in the biochemistry of the hypothalamus and hippocampi.
>
>
> No one can probably answer these questions for certain but is anyone thinking along these lines? Any resources to bear on it?I'm trying to keep my answer short. I've been studying this for years, but you have raised ideas I have not yet considered. I'll have to get back to you on some of this.
> I've been on SSRIs for 2 long cycles. They work in that they make me less depressed and less anxious but it seems like the underlying issues remain unaddressed. I'm working on them in therapy as well but that is very slow going ...
I think you may need a slight adjustment in attitude. Rhetorically, why do you think it is that Olympic teams are largely composed of athletes in their late teens and early twenties? There are changes which come with age, and PTSD might well 'age' some parts of us a little faster than we'd like. Comparisons of your 'now' self to your past self may be maladaptive.
>I guess I'm a little desperate to find things that help.
Just so long as you're not thinking 'cure'.
> thanks
> Ken
> Austin, TXLar
Posted by pelorojo on November 7, 2002, at 18:39:17
In reply to Re: PTSD/Social Anxiety-Herbals, posted by Larry Hoover on November 7, 2002, at 9:05:07
I'm happy to meet someone so knowledgeable! Thanks for your reply. Some comments/questions below:
>
> Yes, but the beginning of the healing journey may begin with medication which facilitates e.g. cognitive-behavioural therapy. If your thinking is distorted by chronic or recurrent dysthymia or depression, you have to address the symptoms in order to permit useful insight.
>Of course. I've stabilized and the pharmaceuticals I've used so far have leveraged me about as far as I think they can. So I'm looking for next step on this front.
>
> There is some evidence that adaptogens may have much lesser effect the longer the chronic stress has continued. The HPA can become 'locked in' to a vicious cycle caused by what some call burn-out.Interesting, I had never read that. I thought the adaptogens were especially useful for chronic stress - it didn't occur to me that long-term stress would reduce their effectiveness.
>
> That said, gingko or Siberian ginseng have quite different modes of action when compared to e.g. rhodiola or witheria or licorice root. For example, licorice root blocks liver enzymes affecting interconversion of some of the steroids. I don't like the 'lumping together' of herbs like this.
>Oh yeah - 'adaptogen' encompasses a large number of herbs with different modes of action and presumed benefits. I listed some of those I had identified as potentially useful. It's a tremendous amount of information to swallow at once so I'm hoping to gain some insight about the options on this board.
>
> I've never even heard of these drugs before (but I'll certainly look into it). You need to do a 24-hour cortisol/DHEA/DHEA-S to determine your circadian secretion level/pattern. Before you muck around with your hormones, you need both baselines and justification.
>
Are there other tests that would be especially useful? Is the test reliable? (I've read some conflicting views on how effective hormone testing is -- especially cortisol -- since being tested itself can alter your cortisol). I've read that many supplements/drugs/herbs affect cortisol, either directly or indirectly. Gosh even caffeine. The substances you take in your body - probably even some foods - are going to alter your cortisol levels. On some level mucking with your hormones is unavoidable. I agree that being reckless or taking other hormones into your body is not to be taken lightly. On the other hand, given the wide range of things that can affect hormones like cortisol, a little experimentation and non-chronic, informed use of herbs like this could be useful.
>
> I think norepinephrine (noradrenaline) is actually the key player. It's secreted by the adrenals, and in some respects, dysregulates all the others.Ahh--do you have any recommended reading? I had picked up the serotonin/gaba/DA concept from this website: http://www.socialfear.com/
But it sounds like you're saying NE is at the core of the problem by dysregulating the others. Do you have any favorite references on the topic you could point me to?
>
> Whatever. Theories aren't going to make you well. What I'm getting at is that you need to do a series of trials with n=1. You have to try interventions, assess the outcome, go off the intervention, re-assess, and go on it again. That's the only way to know what works for you. I tried rhodiola after someone I knew had astounding results, including sleep normalization. It exacerbated *my* insomnia, and made *me* more anxious. No thought experiment will tell you anything with any certainty.
>
Oh I agree -- trying is the only way to know. I want to use the theory though to help me choose what to try in what order -- in the hopes it will be quicker or more cost-effective. Is there another, more rational approach?
>
> I'd stay away from 5-HTP. You bypass the rate-limiting step, which your body uses to limit the amount of serotonin in general circulation. You don't want serotonin in your blood, but 5-HTP will do that, because the aromatic-decarboxylase enzyme is found in every organ compartment.
>
> You can buy tryptophan for veterinary purposes. It is of equal quality to pharma grade.
>
What is inherently bad about serotonin in the blood? Also, isn't it possibly good that 5-HTP skips the rate-limiting step (and that's why it works)? I mean if you are stuck at a suboptimal homeostasis in re: serotonin levels, wouldn't you want to "nudge" that homeostasis to a different level? Could you use the 5-HTP in a pulse fashion (instead of chronically) to help that along? Any favorite resources on this topic?
>
> I forget what theanine does, but DLPA gives two bangs for the buck. It's a precursor to the feel-good PEA, as well as being converted into tyrosine.
>Could DLPA conceivably increase cortisol if it raises tyrosine & DA (i.e., DLPA-tyrosine-DA-NE-adrenalin/epinephrine-cortisol)? It seems like anything that raises dopamine or norepinephrine secretion would raise cortisol, wouldn't it? I don't know if that's a good or bad thing, just trying to get a handle on it.
You seem very knowledgeable about SJW! I've been trying to find extract WS 5570 (the one standardized to 4% hyperforin) but I don't think it's available in the U.S. Would you know where to locate it ?
>
>
>>
> I think you may need a slight adjustment in attitude. Rhetorically, why do you think it is that Olympic teams are largely composed of athletes in their late teens and early twenties? There are changes which come with age, and PTSD might well 'age' some parts of us a little faster than we'd like. Comparisons of your 'now' self to your past self may be maladaptive.
>
Oh I need a huge adjustment in attitude! But I'm not getting your point here.
>
> Just so long as you're not thinking 'cure'.I rely on my tenacious desire to get better. I don't expect a cure but I don't expect no cure, either.
>
thanks so much for your thoughts! I'm impressed by your knowledge and look forward to learning more from you.regards
Ken
Posted by Larry Hoover on November 8, 2002, at 8:55:29
In reply to Re: PTSD/Social Anxiety-Herbals » Larry Hoover, posted by pelorojo on November 7, 2002, at 18:39:17
> I'm happy to meet someone so knowledgeable!
I'm not so sure about that, but I have been spending a lot of time trying to make sense of the situation.
Thanks for your reply. Some comments/questions below:
> > There is some evidence that adaptogens may have much lesser effect the longer the chronic stress has continued. The HPA can become 'locked in' to a vicious cycle caused by what some call burn-out.
>
> Interesting, I had never read that. I thought the adaptogens were especially useful for chronic stress - it didn't occur to me that long-term stress would reduce their effectiveness.You've probably come across the three-stage model proposed by Hans Selye, called the GAS model. It's useful, but I find it does not account for some of the characteristics of chronic PTSD.
Theories and models are simplifications, abstractions which connect observations together. It's kind of like a connect-the-dots picture, except the theory forces you to fit the dots to the abstraction. Consider the constellations. For the life of me, I don't see a bear when I look at the Big Dipper.
The theoretical underpinnings of the GAS model, and the effect of adaptogens, presume that it is possible to normalize glandular communications (endocrine and exocrine). However, studies on lab animals clearly show that stressors can permanently change the pattern and extent of hormonal responses to subsequent stressors. Such, I believe, is the case with PTSD.
That's what I was trying to suggest in my mention of Olympic athletes. There's a window of opportunity for optimizing how the body functions, which once passed, cannot be re-obtained. Call it aging. Call it a disease syndrome. Call it what you want. You can't go back.
> >
> > That said, gingko or Siberian ginseng have quite different modes of action when compared to e.g. rhodiola or witheria or licorice root. For example, licorice root blocks liver enzymes affecting interconversion of some of the steroids. I don't like the 'lumping together' of herbs like this.
> >
>
> Oh yeah - 'adaptogen' encompasses a large number of herbs with different modes of action and presumed benefits. I listed some of those I had identified as potentially useful. It's a tremendous amount of information to swallow at once so I'm hoping to gain some insight about the options on this board.Options I understand. The issue is also one of interpretation. It is my belief (and I encourage you to come clearly to your own) that adaptogens ought not to be considered to be maintenance therapy. They can be helpful in short-term use, but should not be used beyond 3-4 weeks at a time.
If a particular adaptogen is chosen, and it seems to help, it then provides a guide for understanding just what it is in our body which is functioning at a non-optimal level. Then a strategy to augment the bodily function through dietary/supplemental nutrition manipulations should be sought out. I believe that goes to causation, rather than symptom-management. But you see, that is *my* model.
I mentioned licorice root. It has powerful impacts on some core liver enzyme functions, and both increases circulating cortisol while decreasing conversion to testosterone. Clearly, you don't want those changes to be permanent. But, they may serve to inform, if one listens to the language of the body.
If licorice root makes you feel better, you may want to consider adrenal fatigue. Temporarily increasing cortisol (which flies in the face of the GAS model) will inhibit ACTH secretion via the feedback modulation of the hypothalamus on the pituitary. Which then implies other interventions.
It's all exceedingly complex, but that's just how it is. I inform the mind, then let my intuition have a go at it. That's just what works for me.
Here's a little bit of science on licorice root:
Life Sci 1998;62(6):571-82
Effect of licorice and glycyrrhizin on murine liver CYP-dependent monooxygenases.Paolini M, Pozzetti L, Sapone A, Cantelli-Forti G.
Department of Pharmacology, University of Bologna, Italy. paolini@biocfarm.unibo.it
This study is aimed to investigate the effect of the prolonged intake of conspicuous amounts of licorice (LE), or its natural constituent glycyrrhizin (G) on murine liver CYP-catalyzed drug metabolism. For this purpose the modulation of the regio- and stereo-selective hydroxylation of testosterone, together with the use of highly specific substrates as probes for different CYP isoforms such as ethoxyresorufin (CYP1A1), methoxyresorufin (1A2), pentoxyresorufin (2B1), p-nitrophenol (2E1) and aminopyrine (3A), were investigated. Daily doses of licorice root extract (3,138 or 6,276 mg/kg b.w. per os), or G (240 or 480 mg/kg b.w. per os), were administered to different groups of Swiss Albino CD1 mice of both sexes for 1, 4 or 10 consecutive days. While a single LE or G dose was unable to affect the multienzymatic CYP-system, using both schedules of repeated treatment, either LE or G were able to significantly induce hepatic CYP3A- and, to a lesser extent, 2B1- and 1A2-dependent microsomal monooxygenase activities, as well as 6beta- (mainly associated to CYP3A), 2alpha-, 6alpha- (CYP2A1, 2B1), 7alpha-, 16alpha- (CYP2B9) and 16beta-testosterone hydroxylase (TH) activities in male and female mice. Data on CYP3A modulation, the major isoform present in human liver, was confirmed by using Western immunoblotting with anti-CYP3A1/2 rabbit polyclonal antibodies raised against purified rat CYP3A. Northern blotting analysis using CYP3A cDNA biotinylated probe showed that the expression of such isozyme is regulated at the mRNA level. These results suggest that the induction of cytochrome P450-dependent activities by the prolonged intake of high LE or G doses, may result in accelerated metabolism of coadministered drugs with important implications for their disposition. The adverse effects associated with CYP changes such as toxicity/cotoxicity and comutagenicity may also have clinical consequences.
Exp Clin Endocrinol Diabetes 2002 Sep;110(6):257-61
History of the endocrine effects of licorice.Armanini D, Fiore C, Mattarello MJ, Bielenberg J, Palermo M.
Department of Medical and Surgical Sciences -Endocrinology University of Padua.
Summary. The history of licorice as an officinal plant dates back thousands of years, and licorice is still appreciated as a medicinal root. Many of its endocrine properties can be derived from observations of Authors of the ancient world, when hormones were not known. Inappropriate use of licorice can produce pseudoaldosteronism, by inactivating 11beta-hydroxysteroiod-dehydrogenase and by binding to mineralocorticoid receptors. Licorice possesses many other therapeutic properties as to potentiate the action of cortisol, to reduce testosterone synthesis, especially in women, to exert an estrogen-like activity and to reduce body fat mass. The chronological development of research on these effects is described.
Yakugaku Zasshi 2000 Oct;120(10):849-62A drug over the millennia: pharmacognosy, chemistry, and pharmacology of licorice.
Shibata S.
Shibata Laboratory of Natural Medicinal Materials, C/o Minophagen Pharmaceutical Co., Ltd., Tokyo, Japan.
Licorice, the root of Glycyrrhiza spp. (Fabaceae), has been used since ancient Egyptian, Greek, and Roman times in the West and since the Former Han era (the 2nd-3rd century B.C.) in ancient China in the East. In traditional Chinese medicine, licorice is one of the most frequently used drugs. In Japan, the oldest specimen of licorice introduced from China in the middle of the 8th century still exists in Shosoin, the Imperial Storehouse, in Nara. Extracts of licorice were recommended as a remedy for gastric ulcer by Revers of the Netherlands in 1946, which was soon withdrawn owing to its side effects. Carbenoxolon sodium, glycyrrhetinic acid (GA) hemisuccinate Na, was prepared from licorice to treat peptic ulcer in the UK. In Japan for the past 60 years, a glycyrrhizin (GL) preparation under the name of Stronger Neo-Minophagen C (SNMC) has been used clinically as an antiallergic and antihepatitis agent. GL and GA sometimes induce edema, hypertension, and hypokalemia in patients treated with higher doses and long-term administration. The mechanism of this side effect, pseudoaldosteronism, has been explained as due to the 11-hydroxy-steroid dehydrogenase inhibitory activity of GL and GA. The excess of endogenous cortisol produced combines with the renal mineral corticoid receptor, which promotes an aldosterone-like action. GL and GA reduce alanine transaminase (ALT) and aspartate transaminase (AST) values in the serum. This hepatoprotective effect has recently been explained as the inhibitory effects of GL and GA on immune-mediated cytotoxicity against hepatocytes and on nuclear factor (NF)-kappa B, which activates genes encoding inflammatory cytokines in the liver. To exclude the side effects and enhance the therapeutic activities, chemical modification of GL and GA has been performed. Deoxoglycyrrhetol (DG), homo- and heteroannular diene homologs of dihemiphthalates, showed a remarkable improvement in antiinflammatory, antiallergic, and antiulcer activities in animal experiments. Immunomodulating effects of GL, GA, and DG derivatives, which induce interferon-gamma and some other cytokines, have been demonstrated in relation with their antiviral activities. Antiinflammatory, antitumorigenic, and antimalarial effects of licorice flavonoids have also been investigated.
Posted by Larry Hoover on November 8, 2002, at 9:20:39
In reply to Re: PTSD/Social Anxiety-Herbals » Larry Hoover, posted by pelorojo on November 7, 2002, at 18:39:17
>>You need to do a 24-hour cortisol/DHEA/DHEA-S to determine your circadian secretion level/pattern. Before you muck around with your hormones, you need both baselines and justification.
> >
> Are there other tests that would be especially useful? Is the test reliable? (I've read some conflicting views on how effective hormone testing is -- especially cortisol -- since being tested itself can alter your cortisol).There's pretty good agreement between saliva cortisol and blood cortisol. I don't think it would be too stressful spitting into a container.
The typical cortisol test is a morning fasting blood level, but that's just a 'snapshot' reading. Or, you might do a 24-hour urine collection, but that doesn't assess the variation throughout the day.
There's pretty good evidence that those with PTSD (and chronic fatigue) have disordered diurnal (day and night) secretion of cortisol, so you want to assess how cortisol varies througout the day, as well as the total amount.
DHEA is a precursor to other steroids. It also assesses adrenal function. The term cortico-steroid derives from the term adrenal cortex. Adrenal dysfunction is associated with many of the physical symptoms of PTSD.
>I've read that many supplements/drugs/herbs affect cortisol, either directly or indirectly. Gosh even caffeine. The substances you take in your body - probably even some foods - are going to alter your cortisol levels.Ya, so we all muck about with our hormone levels. What else is new? What you want is to assess your functioning, mucking being a normal part of everyone's day.
The distinctions between food, culinary herbs, medicinal herbs, and drugs, are arbitrary. Do you think there are no health benefits accruing from the use of rosemary or parsley? I can't imagine the taste of valerian soup. Who wants soup that tastes like gym socks? So, if you use valerian, you want to use it differently. It's still a drug.
You are what you eat.
>On some level mucking with your hormones is unavoidable. I agree that being reckless or taking other hormones into your body is not to be taken lightly.
First, assess your own bodily function. Then manipulate. Don't expect too much support from your doctors, though. At least, not until you've got some evidence to present.
>On the other hand, given the wide range of things that can affect hormones like cortisol, a little experimentation and non-chronic, informed use of herbs like this could be useful.
Exactly. Go cautiously, but go.
Posted by Larry Hoover on November 8, 2002, at 9:52:11
In reply to Re: PTSD/Social Anxiety-Herbals » Larry Hoover, posted by pelorojo on November 7, 2002, at 18:39:17
> > I think norepinephrine (noradrenaline) is actually the key player. It's secreted by the adrenals, and in some respects, dysregulates all the others.
>
> Ahh--do you have any recommended reading? I had picked up the serotonin/gaba/DA concept from this website: http://www.socialfear.com/> But it sounds like you're saying NE is at the core of the problem by dysregulating the others. Do you have any favorite references on the topic you could point me to?
http://www.psych.org/pnews/00-05-19/stress.html
http://www.biopsychiatry.com/noradanx.htm
http://www.ncptsd.org/treatment/cq/v7/n4/southwick.html
If you can modulate noradrenaline (norepinephrine), you reduce CRF, and all that flows from that.
> > Whatever. Theories aren't going to make you well. What I'm getting at is that you need to do a series of trials with n=1. You have to try interventions, assess the outcome, go off the intervention, re-assess, and go on it again. That's the only way to know what works for you. I tried rhodiola after someone I knew had astounding results, including sleep normalization. It exacerbated *my* insomnia, and made *me* more anxious. No thought experiment will tell you anything with any certainty.
> >
> Oh I agree -- trying is the only way to know. I want to use the theory though to help me choose what to try in what order -- in the hopes it will be quicker or more cost-effective. Is there another, more rational approach?Although we share patterns with one another, we remain unique. That's why you can't apply statistics to individuals.
> >
> > I'd stay away from 5-HTP. You bypass the rate-limiting step, which your body uses to limit the amount of serotonin in general circulation. You don't want serotonin in your blood, but 5-HTP will do that, because the aromatic-decarboxylase enzyme is found in every organ compartment.
> >
> > You can buy tryptophan for veterinary purposes. It is of equal quality to pharma grade.
> >
> What is inherently bad about serotonin in the blood?Phen/fen (the diet prescription combo) and carcinoid tumours are pretty good arguments against serotonin in the blood. Also, do a google search on Steve Harris, 5-HTP in the newsgroup sci.med.nutrition
>Also, isn't it possibly good that 5-HTP skips the rate-limiting step (and that's why it works)? I mean if you are stuck at a suboptimal homeostasis in re: serotonin levels, wouldn't you want to "nudge" that homeostasis to a different level?
Yes, but you don't want to bypass normal feedback modulation. Encourage your body to do better, but don't use a sledgehammer.
>Could you use the 5-HTP in a pulse fashion (instead of chronically) to help that along?
I suppose. Still, I'd stick with tryptophan.
>Any favorite resources on this topic?
See the Harris thread on 5-HTP.
>
> >
> > I forget what theanine does, but DLPA gives two bangs for the buck. It's a precursor to the feel-good PEA, as well as being converted into tyrosine.
> >
>
> Could DLPA conceivably increase cortisol if it raises tyrosine & DA (i.e., DLPA-tyrosine-DA-NE-adrenalin/epinephrine-cortisol)? It seems like anything that raises dopamine or norepinephrine secretion would raise cortisol, wouldn't it?You actually want cortisol's feedback inhibition of CRF. CRF does a lot of nasty things, if it is secreted at high levels. So does ACTH, quite separately from CRF.
>I don't know if that's a good or bad thing, just trying to get a handle on it.
It's exceedingly complex, because the body doesn't do things in a vacuum. Changing one parameter always changes others. That's where we retreat to art and intuition. You become an artist by doing.
>
> You seem very knowledgeable about SJW! I've been trying to find extract WS 5570 (the one standardized to 4% hyperforin) but I don't think it's available in the U.S. Would you know where to locate it ?WS 5572 is sold in the United States as Nature's Way brand called Perika. It's standardized at 3% hyperforin.
> >
> >
> >>
> > I think you may need a slight adjustment in attitude. Rhetorically, why do you think it is that Olympic teams are largely composed of athletes in their late teens and early twenties? There are changes which come with age, and PTSD might well 'age' some parts of us a little faster than we'd like. Comparisons of your 'now' self to your past self may be maladaptive.
> >
> Oh I need a huge adjustment in attitude! But I'm not getting your point here.PTSD changed you. It's permanent. Your adaptability has been used up. That said, you still have manipulations which will help.
> >
> > Just so long as you're not thinking 'cure'.
>
> I rely on my tenacious desire to get better. I don't expect a cure but I don't expect no cure, either.Tenacity is a great attribute. I see overcoming PTSD like the effect of compounding interest. Little bits of invested capital, over time, with interest, accruing substantial benefit. Over time, bit by bit.
> >
> thanks so much for your thoughts! I'm impressed by your knowledge and look forward to learning more from you.
>
> regards
> KenIt's a work in progress. Glad to interact with you.
Lar
This is the end of the thread.
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