A recent article on PLoS One by a research team from the Benson-Henry Institute for Mind/Body Medicine at Massachusetts General Hospital (MGH) and the Genomics Center at Beth Israel Deaconess Medical Center (BIDMC) discusses the genetic effects of the relaxation response, a widespread bodily state induced by different mind-body techniques (such as meditation).
The relaxation response is a bodily state, found in a variety of contexts, characterized by ‘decreased oxygen consumption, increased exhaled nitric oxide, and reduced psychological distress.’ Long-term effects of relaxation exercises include decreased oxygen intake and carbon dioxide elimination; reductions in blood pressure, heart and respiration rate; prominent low frequency heart rate oscillations; and some changes in cortical and subcortical brain regions, including increased thickness of the cortex (see NeuroReport and here also on the effect of meditation on aging).
For about three decades, dependable clinical studies have shown that relaxation response-producing exercises have a range of positive health benefits. What makes the current research distinctive (at least in my reading) is that the team traced this metabolic process to its genetic effects. As the authors write:
This study provides the first compelling evidence that the RR elicits specific gene expression changes in short-term and long-term practitioners. Our results suggest consistent and constitutive changes in gene expression resulting from RR may relate to long term physiological effects. Our study may stimulate new investigations into applying transcriptional profiling for accurately measuring RR and stress related responses in multiple disease settings.
Narrative and memory are interwoven in our consciousness, and thus explorations into trauma from both humanities and social science perspectives almost invariably discuss narrative in one form or another.An ongoing debate within psychological research, for example, ponders whether the coherence of trauma stories is correlated to the amount of emotional distress associated with a given traumatic memory.It is hypothesized that the greater the distress, the less organized the narrative.If this were the case, we might expect that the coherence with which an individual is able to talk about the trauma would increase as the memory is processed and resolved, a finding for which we have some evidence.
We do know – when it comes to Post-Traumatic Stress Disorder (PTSD) – that narrative matters.As I wrote in an earlier post, the most effective therapies yet proven for reducing PTSD symptoms are the exposure therapies, particularly Prolonged Exposure (PE) therapy.These therapies are more effective for reducing the full range of PTSD symptoms than any pharmaceutical yet identified.And the crux of these therapies rests on telling the story of the trauma, sometimes over and over again.This simple practice, this process of speaking, has been reliably demonstrated to result in an improvement of PTSD symptoms for many patients.
But for all its clinical benefit, this extraordinary observation tells us very little about the mechanisms of psychic healing after trauma.Instead, it points to a growing body of evidence that suggests it is not just narrative that matters in PTSD, but, more intriguingly, that it is the type of narrative that matters.Unstructured psychodynamic therapies, for example, have not been demonstrated to lessen the severity of PTSD, even among patients who continue in therapy for years.And yet certain ways of narrating memory do make a difference, and this phenomenon once again points to a role for anthropologists and other culturally-minded researchers in exploring the cultural-emotional-physiological-environmental interactions at play in post-traumatic processing.
Over the past year and a half, I have been conducting research among male U.S. veterans who have served combat tours in Iraq and Afghanistan, most of whom have been diagnosed with Post-Traumatic Stress Disorder (PTSD). An anthropologist myself, I planned to follow the trail originally blazed by Victor Frankl and Robert Jay Lifton, psychotherapists who wrote a great deal about meaning in their descriptions of trauma and PTSD.
Early on, however, a psychiatrist whose work on trauma I admire opined to me that crises of meaning belong to the realm of depression rather than PTSD. He suggested that combat PTSD was best thought of as the physiological effects of living under conditions of extreme stress, while more meaning-related struggles were best understood as a symptom of depression. Given the frequency of comorbidity between PTSD and depression, I was for some time inclined to go along with his analysis.
Then two things happened. First, I began the work of talking with veterans themselves about their stories of trauma and PTSD, listening to how they describe their own experiences. And second, I began to explore the increasingly dominant Prolonged Exposure model of PTSD, which views the disorder as a pathology that develops when individuals fail to process their traumatic memories in the normal way.
Some background is important here. A recent RAND report suggests that as many as 18.5% of combat troops have gone on to develop PTSD after serving in Iraq or Afghanistan; alarming as that number is, it nonetheless demonstrates that the vast majority of combat-exposed individuals do not develop PTSD. However, most of the veterans I’ve spoken with – even those without a formal PTSD diagnosis – report experiencing some PTSD symptoms for a period of time following their combat deployment. Many of them dealt with such symptoms for a while – a month, three months, a year – before passing through this period of processing their memories and going on with their lives. They may be changed by their experiences in the war zone, but they are not broken by them, and may even describe them as resulting in personal growth and other positive effects.
I just read a fascinating piece by Clayton Dach, America’s Chemically Modified 21st Century Soldiers, on Alternet. Although there’s a sense in which Mr. Dach jumps to some of the worst possible outcomes when he looks at technology in the pipeline, on the whole, it’s a pretty well thought and concerned-but-not-hysterical account of some of the technology being brought to bear on soldiers, including the possibility of removing humans further from the ‘loop’ in combat decisions. I’m less interested with the latter — the robot warriors angle — not only because I think it’s been done better in science fiction movies, but also because I think it’s simply a more remote technology than some of the pharmaceutical work he discusses.
In particular, I found the discussion of ‘psychological kevlar’ to be interesting for neuroanthropology:
In the U.S., where roughly two-fifths of troops returning from combat deployments are presenting serious mental health problems, PTSD has gone political in form of the Psychological Kevlar Act, which would direct the Secretary of Defense to implement “preventive and early-intervention measures” to protect troops against “stress-related psychopathologies.”
Proponents of the “Psychological Kevlar” approach to PTSD may have found a silver bullet in the form of propranolol, a 50-year-old beta-blocker used on-label to treat high blood pressure, and off-label as a stress-buster for performers and exam-takers. Ongoing psychiatric research has intriguingly suggested that a dose of propranolol, taken soon after a harrowing event, can suppress the victim’s stress response and effectively block the physiological process that makes certain memories intense and intrusive. That the drug is cheap and well tolerated is icing on the cake.
With PTSD so prevalent among soldiers, can it be better treated, even if that means blocking the formation of traumatic memories? Daniel did a piece on PTSD rates in soldiers in April, Invisible Wounds of War, and he discussed a RAND Corporation estimate that treatment of soldiers with PTSD would cost ‘6.2 billion dollars in the first two years after returning from deployment.’ (Daniel also provided links to a number of articles on Iraq and its psychological effects in Wednesday Round Up #7.) The potential to use drugs to stop the development of PTSD, even if it also blocks normal memory formation, raises a number of ethical and moral questions as well as some interesting neuroanthropological ones.
By Jessica Peyton, Jen Hames, Rebecca Llontop, and Mike Many
Meeting deadlines. A family crisis. Juggling social obligations. We all have responsibilities that demand effort. Given all this, who isn’t stressed?
While most people are aware that stress can be a factor in how much and how often you choose to drink, the term “stress related drinking” remains ambiguous. Here we use it to discuss the consumption of alcohol or drugs in response to environmental stressors. For example, a college student is overwhelmed with needing to finish two papers by the end of the week, upcoming exams, and a fight she had with her roommate. Then her mother calls to let her know that her grandfather is sick. This student, extra anxious come Friday, might agree to go out with her friends to forget about her problems for a while. Once out, the alcohol flows – a temporary release from what feels like continual stress.
But what happens when someone habitually uses alcohol or drugs as a means of coping with stressful situations? Studies show that the substance abuse itself becomes a stressor, triggering a cycle of use that can ultimately result in the development of an addiction. As Enoch Gordis, M.S. states in his commentary Drinking and Stress, “Why people should engage in an activity that produces effects similar to those that they are trying to relieve is a paradox we do not yet understand.”
Today, new research offers some insights regarding the cyclical nature of stress and addiction. Returning to the example of a college student, stress related drinking is primarily social in origin. According to Wesley H. Perkins (1999) students are constantly bombarded by academic, social, and family stressors. Particularly at the nation’s top institutions, the student body is characterized by perfectionist personalities, people who are acutely aware of the expectations for them to be straight-A scholars, winning athletes, and socially popular. Substance use, particularly alcohol, is one potent option to relieve anxieties and forget disappointments. Moreover, you are also being social by getting out and commiserating with people experiencing the same stressors.
My mind raced for potential titles to a post when I read the recent report from Science, ‘The Antidepressant Fluoxetine Restores Plasticity in the Adult Visual Cortex,’ by a team headed by José Fernando Maya Vetencourt (abstract), but I’ve opted to be demure, rather than go with some of my other options (like ‘Anti-depressants the “Cocoon” pool for brain?’ or something similarly outrageous).
The research team investigated wither fluoxetine, a selective serotonin reuptake inhibitor (SSRI), could restore plasticity in the visual system of adult rats. They chose fluoxetine because long-term regimens of the drug promote neurogenesis and synaptogenesis in the hippocampus and increased activity of neurotrophin brain-derived neurotrophic factor (BDNF) and its primary receptor, TrkB (close paraphrase to the original article). These effects have been shown essential to the drug’s effect; block one of these processes, and the anti-depressant doesn’t work nearly as well. In order to test plasticity, the team studied how rats responded to monocular deprivation — covering one eye — both the initial shift in ocular dominance and then the recovery of visual function after long-term monocular deprivation. In general, the fluoxetine-treated rats responded in exaggerated fashion to both conditions, suggesting that plasticity was greater with long-term administration of the drug. From the abstract:
We found that chronic administration of fluoxetine reinstates ocular dominance plasticity in adulthood and promotes the recovery of visual functions in adult amblyopic animals, as tested electrophysiologically and behaviorally. These effects were accompanied by reduced intracortical inhibition and increased expression of brain-derived neurotrophic factor in the visual cortex. Cortical administration of diazepam prevented the effects induced by fluoxetine, indicating that the reduction of intracortical inhibition promotes visual cortical plasticity in the adult. Our results suggest a potential clinical application for fluoxetine in amblyopia as well as new mechanisms for the therapeutic effects of antidepressants and for the pathophysiology of mood disorders.