Wikipedia: Dr. Stephen Porges' Polyvagal Theory

The Polyvagal Theory (gr. 'polus', “‘many’” + 'vagal', "'Vagus Nerve'") was proposed and developed by Dr. Stephen Porges, Director of the Brain-Body Center at the University of Illinois at Chicago.

The theory specifies two functionally distinct branches of the vagus, or tenth cranial nerve. The branches of the vagal nerve serve different evolutionary stress responses in mammals: the more primitive branch elicits immobilization behaviors (e.g., feigning death), whereas the more evolved branch is linked to social communication and self-soothing behaviors.

These functions follow a phylogenetic hierarchy, where the most primitive systems are activated only when the more evolved structures fail. These neural pathways regulate autonomic state and the expression of emotional and social behavior.

Thus, according to this theory, physiological state dictates the range of behavior and psychological experience. Polyvagal theory has many implications for the study of stress, emotion, and social behavior, which has traditionally utilized more peripheral indices of arousal, such as heart rate and cortisol level.

The measurement of vagal tone in humans has become a novel index of stress vulnerability and reactivity in many studies of populations with affective disorders, such as children with conduct problems and those suffering from borderline personality disorder.

Phylogenetic Subsystems/Stages

The vagus nerve is a primary component of the autonomic nervous system. Polyvagal theory outlines the structure and function of the two distinct branches of the vagus, both of which originate in the medulla.

More specifically, each branch is associated with a different adaptive behavioral strategy, both of which are inhibitory in nature via the parasympathetic nervous system (PNS).

The vagal system is in opposition to the sympathetic-adrenal system, which is involved in mobilization behaviors. According to polyvagal theory, these opposing systems are phylogenetically arranged.

The Dorsal Vagal Complex

The dorsal branch of the vagus originates in the dorsal motor nucleus and is considered the phylogenetically older branch. This branch is unmyelinated and exists in most vertebrates. This branch is also known as the “vegetative vagus” because it is associated with primal survival strategies of primitive vertebrates, reptiles, and amphibians. Under great stress, these animals freeze when threatened, conserving their metabolic resources.

The DVC provides primary control of subdiaphragmatic visceral organs, such as the digestive tract. Under normal conditions, the DVC maintains regulation of these digestive processes. However, prolonged disinhibition can be lethal for mammals, as it results in apnea and bradycardia.

The Ventral Vagal Complex

With increased neural complexity seen in mammals (due to phylogenetic development) evolved a more sophisticated system to enrich behavioral and affective responses to an increasingly complex environment.

The ventral branch of the vagus originates in the nucleus ambiguus and is myelinated to provide more control and speed in responding. This branch is also known as the “smart vagus” because it is associated with the regulation of sympathetic “fight or flight” behaviors in the service of social affiliative behaviors.

These behaviors include social communication and self-soothing and calming. In other words, this branch of the vagus can inhibit or disinhibit defensive limbic circuits, depending on the situation.

The VVC provides primary control of supradiaphragmatic visceral organs, such as the esophagus, bronchi, pharynx, and larynx. The VVC also exerts important influence on the heart.

When vagal tone to the heart’s pacemaker is high, a baseline or resting heart rate is produced. In other words, the vagus acts as a restraint, or brake, limiting heart rate. However, when vagal tone is removed, there is little inhibition to the pacemaker, and so rapid mobilization (“fight/flight”) can be activated in times of stress, but without having to engage the sympathetic-adrenal system, as activation comes at a severe biological cost.

Vagal Tone: A Physiological Marker of Stress

In order to maintain homeostasis, the central nervous system responds constantly, via neural feedback, to environmental cues.

Stressful events disrupt the rhythmic structure of autonomic states, and subsequently, behaviors. Since the vagus plays such an integral role in the PNS via regulation of heart rate, it follows that the amplitude of respiratory sinus arrhythmia (RSA) is a good index of PNS activity via the cardiac vagus.That is, RSA is a measurable, noninvasive way to see how the vagus modulates heart rate activity in response to stress. This method is useful to measure individual differences in stress reactivity.

RSA is the widely used measure of the amplitude of heart rate rhythm associated with rate of spontaneous breathing. Research has shown that amplitude of RSA is an accurate indicator of the efferent influence of the vagus on the heart. Since inhibitory effects of the VVC branch of the vagus allow for a wide range of adaptive, prosocial behaviors, it has been theorized that individuals with greater vagal tone are able to exhibit a greater range of such behaviors.

On the other hand, decreased vagal tone is associated with illnesses and medical complications that compromise the CNS. These complications may reduce one's capacity to respond to stress appropriately.

Clinical Applications of Polyvagal Theory and Vagal Tone

Vagal tone has been used in medical and psychological research to better understand the physiological underpinnings of various disorders.

For example, healthy human fetuses have a high variability in heart rate, which is mediated by the vagus. On the other hand, heart rate decelerations, which are also mediated by the vagus, are a sign of fetal distress.

More specifically, prolonged withdrawal of vagal influence on the heart creates a physiological vulnerability to the influence of the DVC, which in turn produces clinically relevant bradycardia. However, the onset of this deceleration is commonly preceded by transitory tachycardia, which is reflective of the immediate effects of VVC withdrawal.

For more:

"How your nervous system sabotages your ability to relate" an interview with Stephen Porges about his polyvagal theory by Ravi Dykema

http://www.nexuspub.com/articles_2006/interview_porges_06_ma.php

Luminita Daniela Saviuc Blog: Seven Ways To Release Negative Emotions

Do you get easily angered, stressed, frustrated? How often do you get caught up in other people's drama or your own drama? Are there any toxic emotions present in your body right now?

Whether there is any negativity in your life right now or not, it is wise to know what would be the best way to release the toxic emotions from your life when they arise, because in the end we are all human and we will all experience negative emotions at one point or another.

1. Awareness

Firstly, we need to understand that the first person who will get hurt by holding on to the toxic emotions is us and not so much the person, event or situation who triggered the toxic emotions in us.

Let us not look back in anger, nor forward in fear, but around in awareness. -- James Thurber

2. Take Responsibility

Even though it may not always be easy, it is very important to stop blaming others for how we feel and to take 100 percent responsibly for our own thoughts, emotions, action or inaction, to take 100 percent responsibility for our life, and by doing so we will claim back our own power.
When you blame some outside forces for whatever you are feeling, you give away any power you may have to change the negative situation and your feelings about it, and you allow yourself to be the victim.

Take your life in your own hands, and what happens? A terrible thing: no one to blame. -- Erica Jong

3. Don't Believe Everything You Think

The next wise thing to do is question your own thoughts. Don't believe everything you think, especially if your thoughts are creating even more stress, anxiety, frustration, anger and all kind of other negative emotions in your life.

The world we have created is a product of our thinking; it cannot be changed without changing our thinking. -- Albert Einstein

4. Acceptance vs. Resistance

Don't resist the pain these toxic emotions are causing you, for resistance would only make things even worse. What you want to do is to act as if whatever you are feeling right now is there because you chose to. Accept it and allow the pain to just be and by doing so you will help release and heal the pain.

Acceptance of what has happened is the first step to overcoming the consequences of any misfortune. -- William James

5. Let Go

Let go of the need to blame others for your anger, let go of the need to put yourself down for feeling the way you are feeling and let go of all the toxic emotions you are holding on to. It is as easy as holding tightly a rotten apple -- toxic emotions -- and then letting that apple go. It's that simple.

Holding on to anger is like grasping a hot coal with the intent of throwing it at someone else; you are the one who gets burned. -- Buddha

6. Shift From Negative To Positive

If you focus too much on what seems to be wrong, you will not be able to release the negative emotions. Shift your focus from negative to positive, focus on the things you want to attract in your life and the feelings you want to feel and not on what you don't want -- very important! By doing so, you will allow the dark clouds to pass and the sun to shine through.

I can feel guilty about the past, apprehensive about the future, but only in the present can I act. The ability to be in the present moment is a major component of mental wellness. -- Abraham Harold Maslow

7. Show Gratitude

Now that you released all the toxicity from your body, why not express your gratitude for all the amazing things you have learned along the way? Express your gratitude toward all those people/events that triggered all kind of negative emotions in you, and thank them for helping you become a happier, wiser and confident person.

I have learned silence from the talkative, toleration from the intolerant, and kindness from the unkind; yet, strangely, I am ungrateful to those teachers. -- Khalil Gibran

Hermona Soreq Blog: Stress Reactions: Acetylcholine

by Hermona Soreq, Professor of Molecular Neuroscience, The Hebrew University’s Edmond and Lily Safra Center for Brain Sciences

Do the Stress Reactions of Our Brain Control the Immune System -- Or Is It the Other Way Around?

In the well-known 17th-century text Le Malade Imaginaire, Molière (Jean-Baptiste Poquelin) wrote, "the mind has great influence over the body, and maladies have their origin there."

Since Molière, we now know that a diseased body and malfunctioning immune system also affect the mind.

Inflammation of the nervous system has been increasingly recognized as an important factor in multiple conditions, including Alzheimer's and Parkinson's disease. New technologies in genetic engineering and drug development are rapidly progressing to implement this knowledge for early diagnosis and creative treatment strategies that take into consideration both the brain and the body.

One area that has benefited considerably from these developments is the study of anxiety.

Historically, human stress reactions enabled our ancestors to survive attacks and protect the body from injury. But even though these reactions aren't necessities like they were for our ancestors, the same response patterns have continued to the present. An unpleasant discussion at work rarely leads to physical attacks, but our body nevertheless prepares for such attacks; it elevates the blood pressure to prepare for running, and produces more white blood cells as protection from anticipated injury.

While such reactions are useful for immediate protection -- since alertness can assist us in reacting to stressful experiences faster and more efficiently -- the consequences of stress responses may also entail long-term damages spanning muscle and nerve cells malfunctions, neurodegenerative diseases like Alzheimer's and Parkinson's, and inflammatory diseases.

The long-term and disease-provoking consequences of stress responses may take years to develop. This was not a concern for early humans, whose life span was shorter than ours (by the time stress could take its toll, they were no longer alive). But today, humans live much longer, and as a result, stress-associated diseases -- especially in the elderly -- have become a major social and financial burden.
***Over the past two decades, I, along with my colleagues at the Edmond and Lily Safra Center for Brain Sciences (ELSC) at The Hebrew University of Jerusalem, have pioneered and developed innovative strategies for investigating the consequences of traumatic experiences and designed new strategies to combat neurodegenerative diseases.

Our work has proven that in both brain neurons and blood cells, the genetic information that processes events are vulnerable to changes under stress. Moreover, we've discovered that both inherited and acquired defects in neurons, as well as traumatic experiences or exposure to a contaminated environment, contribute to delayed susceptibilities to stress-associated diseases.

The consequences may be seriously harmful, affect seemingly unrelated functions (e.g. learning and memory, the day-and-night cycle, muscle fatigue, inflammation), and last over the life spans of individuals and communities.

A good portion of our research has been devoted to a small chemical called acetylcholine, the first known neurotransmitter (a small chemical compound which is capable of activating neurons to send electrical signals) and the primary communicator between the body and the brain.

Discovered 100 years ago by the Nobel laureate Otto Loewi, acetylcholine comes from the brain through the vagus nerve and is responsible for muscle twitching. We've discovered that acetylcholine signals produced in the brain affect psychological stress responses, inflammation, aging, and the recovery from acute ischemic stroke.

As part of our research, we isolated the genes controlling acetylcholine degradation in humans and identified stress-induced changes in their expression in brain neurons and blood cells alike.

To pinpoint the physiological role of these genes, we engineered mice with excess or deficient amounts of the genes' protein products and watched their learning, muscle functioning and behavior. We learned three basic things:

1) Either too much or too rapid degradation of acetylcholine may cause cognitive deterioration, which intensifies anxiety reactions and can also intensify them, creating a vicious cycle;

2) The mice with excess breakdown of acetylcholine suffer constant inflammation, demonstrating the power of brain-to-body communication for our immune system and showing that individuals who carry inherited small changes in these genes are at increased risks for Parkinson's and Alzheimer's disease;

3) Different products of these genes may either enhance the progression of brain pathology in Alzheimer's and Parkinson's disease or help protect against them, and they also determine one's prospects to survive and recover from ischemic stroke. Measuring such changes by a simple blood test can hence predict one's prospects for recovery and the risks for post-traumatic stress disorder.

New discoveries in stress-related pathologies are occurring at a quickening pace. Just recently, we've developed a synthetic DNA-based drug for treating patients with inflammatory bowel disease.

With the help of a $5 million grant approved by the Leona M. and Harry B. Helmsley Charitable Trust, we hope that such developments will bring us closer to finding more permanent treatments for neurodegenerative and other diseases that have, unfortunately, become all too common.

Steven M. Southwick M. D. :The Science of Resilience

For nearly twenty years my colleagues and I studied post-traumatic stress disorder and the profound negative psychological, social, and neurobiological impact of traumas such as child abuse, natural disasters, physical and sexual abuse, and combat. We often wondered why some survivors succeeded in overcoming adversity, bouncing back, and continuing on with purposeful lives, while others didn't. Some individuals were clearly more resilient than others.

The American Psychological Association defines resilience as "the process of adapting well in the face of adversity, trauma, tragedy, threats or even significant sources of threat." To answer our question, we turned to three groups of highly resilience individuals: former Vietnam prisoners of war, Special Forces instructors, and civilian men and women who had endured and even thrived after surviving harrowing traumas.

In our book, Resilience: The Science of Mastering Life's Greatest Challenges, Dennis Charney M. D. and I systematically address the topic of resilience. Because resilience is the complex product of genetic, psychological, biological, social and spiritual factors, we investigate resilience from multiple scientific perspectives. We synthesize the latest scientific and popular literature on the topic, describe our own psychological and neurobiological research on resilience, and quote from our in-depth interviews with a large number of highly resilient people.

When we began our study, we assumed that resilience was rare and resilient people were somehow special, perhaps genetically gifted. It turns out, we were wrong. Resilience is common and can be witnessed all around us. Even better, we learned that everyone can learn and train to be more resilient. The key involves knowing how to harness stress and use it to our advantage. After all, stress is necessary for growth. Without it the mind and body weaken and atrophy.

Let's take a quick look at some genetic and biological factors that have been associated with resilience. While no one gene or gene variation explains resilience, genetic factors do play an important role in determining how an individual responds to stress and trauma. For example, DNA studies have found that polymorphisms (i.e., variations) of genes that regulate the sympathetic nervous system, the hypothalamic-pituitary-adrenal axis, and the serotonin system partially determine whether our biological response to stress is too robust, too muted, or within a range that is optimal for adaptive functioning. In addition, studies of identical twins, where one twin has been exposed to a traumatic stressor such as combat but the other twin has not, have estimated an overall heritability of posttraumatic stress disorder ranging from 32-38%. This means that genes are important but that they are only part of the story.

A host of neurobiological factors and systems have been associated with resilience including a sympathetic nervous system (i.e., epinephrine and norepinephrine) and a hypothalamic-pituitary-adrenal axis (i.e., cortisol) that respond rapidly to stress and danger but that are well regulated and shut off once the danger has passed; a dopamine reward system that continues to fuel positive emotions even during periods of chronic stress; intact hippocampi that allow us to form new memories, to differentiate between dangerous and safe environments, and help to regulate our stress response; and a highly developed prefrontal cortex that can regulate emotional and behavioral reactivity to stress by inhibiting the amygdala, which plays a central role in processing and triggering raw emotions related to the fight-flight response.

Emerging scientific research has begun to show that neurobiological systems associated with resilience can be strengthened to respond more adaptively to stress. For example, research using EEG and fMRI technology has shown that mindfulness meditation and training in cognitive reappraisal can increase activation of the left prefrontal cortex. This is important because people with greater activation of the left prefrontal cortex recover more rapidly from negative emotions such as anger, disgust, and fear. University of Wisconsin researcher Richard Davidson has proposed that resilience is largely related to activation of the left prefrontal cortex and the strength of neural connections between the prefrontal cortex and the amygdala. Robust activation of the PFC inhibits the amygdala, quiets associated anxiety and fear-based emotions, and allows the PFC to facilitate rational planning and behavior.

As a second example, the hippocampus is another brain region that is critically involved in resilience and how we respond to stress. It is well known that unremitting stress with prolonged elevation of cortisol can damage neurons in the hippocampus. Because the hippocampus helps to regulate the hypothalamic-pituitary-adrenal axis, damage to its neurons can decrease their ability to dampen the stress response. The result may be even greater damage to hippocampal neurons. Fortunately, recent research has found that nerve growth factors, like brain-derived neurotrophic factor, enhance the growth of brain cells, prolong cell survival, and repair damaged nerve cells. In animal studies, vigorous voluntary aerobic exercise increases levels of nerve growth factor and appears to protect against some of the negative effects of stress. This may also be true in humans where research has shown that aerobic exercise can increase hippocampal volume, raise serum levels of BDNF, and improve spatial memory, and that physically active subjects show lower cortisol and SNS responses to psychological laboratory stress compared to less physically active subjects.

As scientists learn more about the complex interplay of genetics, development, cognition, environment, and neurobiology, it will be possible to develop behavioral, social and pharmacological interventions and training programs to enhance resilience to stress.

Steven M. Southwick, MD, a recognized expert on the psychological and neurobiological effects of extreme psychological trauma, is the co-author of Resilience: The Science of Mastering Life's Greatest Challenges (Cambridge University Press 2012). Dr. Southwick is the inaugural Greenberg Professor of Psychiatry, Post-Traumatic Stress Disorder, and Resilience at the Yale Medical School and the Yale Child Study Center, adjunct professor of psychiatry at the Mt. Sinai School of Medicine, and medical director of the Clinical Neurosciences Division of the National Center for Posttraumatic Stress Disorder.

In the News: Work Stress 'Raises Heart Risk'

Is this really news? It seems pretty well known and obvious to me.

Work stress 'raises heart risk'

By James Gallagher Health and science reporter, BBC News

Having a highly demanding job, but little control over it, could be a deadly combination, UK researchers say.

They analysed 13 existing European studies covering nearly 200,000 people and found "job strain" was linked to a 23% increased risk of heart attacks and deaths from coronary heart disease.

The risk to the heart was much smaller than for smoking or not exercising, the Lancet medical journal report said.

The British Heart Foundation said how people reacted to work stress was key.

Job strain is a type of stress. The research team at University College London said working in any profession could lead to strain, but it was more common in lower skilled workers.

Doctors who have a lot of decision-making in their jobs would be less likely to have job strain than someone working on a busy factory production line.

Freedom

There has previously been conflicting evidence on the effect of job strain on the heart.

In this paper, the researchers analysed combined data from 13 studies.

At the beginning of each of the studies, people were asked whether they had excessive workloads or insufficient time to do their job as well as questions around how much freedom they had to make decisions.

They were then sorted into people with job strain or not and followed for an average of seven and a half years.

One of the researchers, Prof Mika Kivimaki, from University College London, said: "Our findings indicate that job strain is associated with a small but consistent increased risk of experiencing a first coronary heart disease event, such as a heart attack."

The researchers said eliminating job strain would prevent 3.4% of those cases, whereas there would be a 36% reduction if everyone stopped smoking.

'Unable to change'

Prof Kivimaki said the evidence of a direct effect of job strain on the heart was mixed.

He told the BBC job strain was linked to other lifestyle choices that were bad for the heart: "We know smokers with job strain are more likely to smoke a bit more, active people with job strain are more likely to become inactive and there is a link with obesity.

"If one has high stress at work you can still reduce risk by keeping a healthy lifestyle."
Prof Peter Weissberg, medical director at the British Heart Foundation, said: "We know that being under stress at work, and being unable to change the situation, could increase your risk of developing heart disease.

"This large study confirms this, but also shows that the negative effect of workplace strain is much smaller than, for example, the damage caused by smoking or lack of exercise.

"Though stresses at work may be unavoidable, how you deal with these pressures is important, and lighting up a cigarette is bad news for your heart. Eating a balanced diet, taking regular exercise and quitting smoking will more than offset any risk associated with your job."

Dr Bo Netterstrom, from Bispebjerg Hospital in Denmark, said other stresses at work such as job insecurity "are likely to be of major importance".

He said job strain was "a measure of only part of a psychosocially damaging work environment".

Wray Herbert: Having Heart Can We Rethink Life's Stresses?

Eustress is the "good stress."

From Wray Herbert's blog
Author, 'On Second Thought: Outsmarting Your Mind's Hard-Wired Habits'

Imagine that you are at the top of a ski slope, about to make a run. It's a challenging slope, black diamond--steep and narrow, lots of trees. Plus it's windy, and there's that treacherous drop-off on the right. You're an inexperienced skier, not a novice but not at all confident that you belong in such extreme terrain. Your heart is pounding and your gut is tight.

Now imagine that you're on top of the very same slope, but you are a skilled downhill racer, an Olympic contender. You're sure you know how to attack this slope--you've done it many times before--but even so, your heart is pounding and butterflies are fluttering in your gut.

Both of these hypothetical skiers are under stress, and feeling the arousal that comes with stress. But one is experiencing good stress, the other bad stress. They are both looking at the same slope, but one sees it as a threat, the other as a challenge. The expert knows that his skills are more than sufficient for the situation. The nervous learner has no such confidence.

Psychological scientists are interested in this contrast, as are health professionals. We tend to think of stress as negative, and arousal as harmful, and indeed we spend lots of time and money--on vacations, fitness clubs, bar tabs--trying to minimize stress. But is it possible that stress is not all that bad, that in fact it may be tonic at times?

The key is how we think about stress and arousal. Those two skiers are in fact experiencing different bodily changes. Though both are feeling activation of the sympathetic nervous system, the fearful skier is feeling constriction of the vessels, which makes the heart work harder. The expert is actually experiencing more sympathetic arousal as he contemplates the challenge ahead, but the blood vessels are dilating, increasing cardiac efficiency. But they don't know or care what's going on inside them. They both simply feel edgy and aroused.

What if the learner's fear could be construed as a positive challenge? What a skier--or anyone--could be made to believe that the pounding and fluttering were actually a resource, tools for enhanced performance? That's the question that University of Rochester scientist Jeremy Jamieson wanted to explore in the laboratory. Working with UCSF's Wendy Berry Mendes and Harvard's Matthew Nock, he has run a series of experiments to see if bad stress can be transformed into good stress in the mind.

Here's an example. The researchers took physiological measurements on a group of volunteers, who were told that they would have to make a public speech--a stressful prospect for most people. Just prior to this event, some were instructed about the value of human stress response in high-level performance. They were encouraged to interpret any signs of arousal as a positive thing, a tool that would aid them in making a confident speech. The others were told to ignore their stress arousal, or they were told nothing at all.

The findings were clear. During the speech, those instructed in reappraisal were much more like the Olympian skier, showing what Jamieson calls "physiological toughness": They experienced less blood vessel constriction and more cardiac output, as if they were attacking the slope. What's more, immediately after the speech, these volunteers were less vigilant. In other words, they felt confident, not threatened.

Think about this. It wasn't an elaborate intervention. They were merely encouraged to reappraise their gut feelings. The scientists decided to test this simple idea again, in the context a high-stress real-life event: a high-stakes examination. They recruited students who were already preparing to take the Graduate Record Examination (GRE), guaranteeing that their performance was genuinely important to them. The students came into the lab to take a practice version of the exam. As before, only some were told that their nervous stomachs and pumping hearts were known to improve, not worsen, performance. Right before the test, all the students gave saliva samples for analysis.

Those who were taught to reappraise their arousal--to see it as a benefit--had higher levels of alpha amylase, an indicator of nervous system arousal, and they performed better on the practice GRE. But here's the really interesting part: One to three months later, when they took the actual GRE under regular testing conditions, these students had higher math scores than the controls. And they also reported that their test-day arousal had helped them with the exam. This brief and simple intervention had sustained effects on both stress appraisal and test performance.

These are just a couple examples on ongoing research that the Jamieson and his colleagues will describe in a forthcoming issue of the journal Current Directions in Psychological Science. The findings may change the way that clinicians think about acute, everyday stress and a variety of ills. Much valuable work has shown that we can regulate our emotions and mitigate our stress arousal--through mindfulness mediation, for example. But there are many times when it's impossible, or inadvisable, to dampen the body's arousal signals. Reappraisal may offer an additional tool to cope with bodily stress in an adaptive way.

Relaxation Technique: Autogenic Training

From yee Wiki,

"Autogenic training is a relaxation technique developed by the German psychiatrist Johannes Heinrich Schultz and first published in 1932. The technique involves the daily practice of sessions that last around 15 minutes, usually in the morning, at lunch time, and in the evening. During each session, the practitioner will repeat a set of visualisations that induce a state of relaxation. Each session can be practiced in a position chosen amongst a set of recommended postures (for example, lying down, sitting meditation). The technique can be used to alleviate many stress-induced psychosomatic disorders.

Schultz emphasized parallels to techniques in yoga and meditation. It is a method for influencing one's autonomic nervous system. Abbe Faria and Emile Coue were the forerunners of Schultz. There are many parallels to progressive relaxation. In 1963 Wolfgang Luthe discovered the significance of "autogenic discharges", paroxistic phenomena of motor, sensorial, visual and emotional nature related to the traumatic history of the patient, and developed the method of "Autogenic Abreaction". His disciple Luis de Rivera, a McGill trained psychiatrist, introduced psychodynamic concepts into Wolfgang Luthe's approach, developing "Autogenic Analysis" as a new method for uncovering the unconscious.

Herbert Benson, MD, a Harvard professor also did significant research in the area. He called it the Relaxation Response and wrote an influential book with that same title.

Example of an autogenic training session

1. Sit in the meditative posture and scan the body
2. "My right arm is heavy"
3. "My arms and legs are heavy and warm" (repeat 3 or more times)
4. "My heartbeat is calm and regular" (repeat 3 times)
5. "My solar plexus is warm" (repeat 3 times)
6. "My forehead is cool"
7. "My neck and shoulders are heavy" (repeat 3 times)
8. "I am at peace" (repeat 3 times)

9. Finish Part One by cancelling

10. Start Part Two by repeating from step 2 on to cancelling

11. Start Part Three by repeating from step 2 on to cancelling

When you end your practice, it is a good idea to cancel, to avoid your thoughts from inadvertently materializing. To cancel say "arms firm," and move your arms vigorously; say "breathe deeply," and breathe deeply; and say "open eyes," and open your eyes.

Many practitioners will choose not to cancel between the three iterations, in order to maintain a deeper relaxation.

Quite often, one will ease themselves into the "trance" by counting to ten, and exit by counting backwards from ten. This is another practice taken from progressive relaxation.

Effects of autogenic training

Autogenic training restores the balance between the activity of the sympathetic (flight or fight) and the parasympathetic (rest and digest) branches of the autonomic nervous system. This has important health benefits, as the parasympathetic activity promotes digestion and bowel movements, lowers the blood pressure, slows the heart rate, and promotes the functions of the immune system.

Contraindications

Autogenic training is contraindicated for people with heart conditions or psychotic disorders.

Clinical evidence

Autogenic training has been subject to clinical evaluation from its early days in Germany, and from the early 1980s worldwide. In 2002, a meta-analysis of 60 studies was published in Applied Psychophysiology and Biofeedback, finding significant positive effects of treatment when compared to normals over a number of diagnoses; finding these effects to be similar to best recommended rival therapies; and finding positive additional effects by patients, such as their perceived quality of life.

In Japan, four researchers from the Tokyo Psychology and Counseling Service Center have formulated a measure for reporting clinical effectiveness of autogenic training.

Autogenic training was popularized in North America particularly among practitioners by Wolfgang Luthe, who co-authored, with Schultz, a multi-volume tome on Autogenic Training. Luthe was a firm believer that autogenic training was a powerful approach that should only be offered to patients by qualified professionals.

Like many techniques (progressive relaxation, yoga, qigong, varieties of meditation) which have been developed into advanced, sophisticated processes of intervention and learning,

Autogenic training, as Luthe and Schultz wrote in their master tome, took well over a year to learn to teach and over a year to learn. But some biofeedback practitioners took the most basic elements of autogenic imagery and developed "condensed" simplified versions that were used in combination with biofeedback.

This was done at the Menninger foundation by Elmer Green, Steve Fahrio, Patricia Norris, Joe Sargent, Dale Walters and others, where they took the hand warming imagery of autogenic training and used it as an aid to develop thermal biofeedback."