Posts Tagged ‘PTSD’


Brains of individuals with PTSD and suicidal thoughts (top) show higher levels of mGluR5 compared to healthy controls (bottom).

By Bill Hathawaymay

The risk of suicide among individuals with post-traumatic stress disorder (PTSD) is much higher than the general population, but identifying those individuals at greatest risk has been difficult. However, a team at Yale has discovered a biological marker linked to individuals with PTSD who are most likely to think about suicide, the researchers report May 13 in the journal Proceedings of the National Academy of Sciences.

Researchers used PET imaging to measure levels of metabotropic glutamatergic receptor 5 (mGluR5) — which has been implicated in anxiety and mood disorders — in individuals with PTSD and major depressive disorder. They found high levels of mGluR5 in the PTSD group with current suicidal thoughts. They found no such elevated levels in the PTSD group with no suicidal thoughts or in those with depression, with or without current suicidal thoughts.

There are two FDA approved treatments for PTSD, both of which are anti-depressants. It can take weeks or months to determine whether they are effective. That can be too late for those who are suicidal, note the researchers.

“If you have people who suffer from high blood pressure, you want to reduce those levels right away,” said Irina Esterlis, associate professor of psychiatry at Yale and senior author of the study. “We don’t have that option with PTSD.”

Esterlis said testing for levels of mGluR5 in people who have experienced severe trauma might help identify those at greatest risk of harming themselves and prompt psychiatric interventions. Also, researchers might investigate ways to regulate levels mGluR5 with hopes of minimizing suicide risk in PTSD patients, she said.

https://news.yale.edu/2019/05/13/biomarker-reveals-ptsd-sufferers-risk-suicide

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Summary: Newly identified ‘extinction neurons’ in the hippocampus suppress fearful memories when activated, and allow the memories to return when deactivated. The findings may provide new treatment avenues for PTSD, phobias, and anxiety.

Neuroscientists at The University of Texas at Austin have discovered a group of cells in the brain that are responsible when a frightening memory re-emerges unexpectedly, like Michael Myers in every “Halloween” movie. The finding could lead to new recommendations about when and how often certain therapies are deployed for the treatment of anxiety, phobias and post-traumatic stress disorder (PTSD).

In the new paper, out today in the journal Nature Neuroscience, researchers describe identifying “extinction neurons,” which suppress fearful memories when they are activated or allow fearful memories to return when they are not.

Since the time of Pavlov and his dogs, scientists have known that memories we thought we had put behind us can pop up at inconvenient times, triggering what is known as spontaneous recovery, a form of relapse. What they didn’t know was why it happened.

“There is frequently a relapse of the original fear, but we knew very little about the mechanisms,” said Michael Drew, associate professor of neuroscience and the senior author of the study. “These kinds of studies can help us understand the potential cause of disorders, like anxiety and PTSD, and they can also help us understand potential treatments.”

One of the surprises to Drew and his team was finding that brain cells that suppress fear memories hid in the hippocampus. Traditionally, scientists associate fear with another part of the brain, the amygdala. The hippocampus, responsible for many aspects of memory and spatial navigation, seems to play an important role in contextualizing fear, for example, by tying fearful memories to the place where they happened.

The discovery may help explain why one of the leading ways to treat fear-based disorders, exposure therapy, sometimes stops working. Exposure therapy promotes the formation of new memories of safety that can override an original fear memory. For example, if someone becomes afraid of spiders after being bitten by one, he might undertake exposure therapy by letting a harmless spider crawl on him. The safe memories are called “extinction memories.”

“Extinction does not erase the original fear memory but instead creates a new memory that inhibits or competes with the original fear,” Drew said. “Our paper demonstrates that the hippocampus generates memory traces of both fear and extinction, and competition between these hippocampal traces determines whether fear is expressed or suppressed.”

Given this, recommended practices around the frequency and timing of exposure therapy may need revisiting, and new pathways for drug development may be explored.

In experiments, Drew and his team placed mice in a distinctive box and induced fear with a harmless shock. After that, when one of the mice was in the box, it would display fear behavior until, with repeated exposure to the box without a shock, the extinction memories formed, and the mouse was not afraid.

Scientists were able to artificially activate the fear and suppress the extinction trace memories by using a tool called optogenetics to turn the extinction neurons on and off again.

“Artificially suppressing these so-called extinction neurons causes fear to relapse, whereas stimulating them prevents fear relapse,” Drew said. “These experiments reveal potential avenues for suppressing maladaptive fear and preventing relapse.”

The studies were led by graduate student Anthony Lacagnina of The University of Texas at Austin, with contributions from Emma Brockway, Chelsea Crovetti, Francis Shue, Meredith McCarty and Kevin Sattler of The University of Texas; and Sean Lim, Sofia Leal Santos and Christine Denny of Columbia University.

https://neurosciencenews.com/ptsd-hippocampus-fear-10966/

by PETER DOCKRILL

When bad things happen, we don’t want to remember. We try to block, resist, ignore – but we should perhaps be doing the opposite, researchers say.

A new study led by scientists in Texas suggests the act of intentionally forgetting is linked to increased cerebral engagement with the unwanted information in question. In other words, to forget something, you actually need to focus on it.

“A moderate level of brain activity is critical to this forgetting mechanism,” explains psychologist Tracy Wang from the University of Texas at Austin.

“Too strong, and it will strengthen the memory; too weak, and you won’t modify it.”

Trying to actively forget unwanted memories doesn’t just help prevent your brain from getting overloaded.

It also lets people move on from painful experiences and emotions they’d rather not recall, which is part of the reason it’s an area of active interest to neuroscientists.

“We may want to discard memories that trigger maladaptive responses, such as traumatic memories, so that we can respond to new experiences in more adaptive ways,” says one of the researchers, Jarrod Lewis-Peacock.

“Decades of research has shown that we have the ability to voluntarily forget something, but how our brains do that is still being questioned.”

Much prior research on intentional forgetting has focussed on brain activity in the prefrontal cortex, and the brain’s memory centre, the hippocampus.

In the new study, the researchers monitored a different part of the brain called the ventral temporal cortex, which helps us process and categorise visual stimuli.

In an experiment with 24 healthy young adults, the participants were shown pictures of scenes and people’s faces, and were instructed to either remember or forget each image.

During the experiment, each of the participants had their brain activity monitored by functional magnetic resonance imaging (fMRI) machines.

When the researchers examined activity in the ventral temporal cortex, they found that the act of forgetting effectively uses more brain power than remembering.

“Pictures followed by a forget instruction elicited higher levels of processing in [the] ventral temporal cortex compared to those followed by a remember instruction,” the authors write in their paper.

“This boost in processing led to more forgetting, particularly for items that showed moderate (vs. weak or strong) activation.”

Of course, forgetting specific images on demand in a contrived laboratory experiment is very different to moving on from painful or traumatic memories of events experienced in the real world.

But the mechanisms at work could be the same, researchers say, and figuring out how to activate them could be a huge benefit to people around the world who need to forget things, but don’t know how.

Especially since this finding in particular challenges our natural intuition to suppress things; instead, we should involve more rather than less attention to unwanted information, in order to forget it.

“Importantly, it’s the intention to forget that increases the activation of the memory,” Wang says.

“When this activation hits the ‘moderate level’ sweet spot, that’s when it leads to later forgetting of that experience.”

The findings are reported in JNeurosci.

https://www.sciencealert.com/to-forget-something-you-need-to-think-about-it-neuroscientists-reveal


Pinpoint stimulation of a cluster of nerve cells in the brains of mice encouraged timid responses to a perceived threat, whereas stimulation of an adjacent cluster induced boldness and courage.

Researchers at the Stanford University School of Medicine have identified two adjacent clusters of nerve cells in the brains of mice whose activity level upon sighting a visual threat spells the difference between a timid response and a bold or even fierce one.

Located smack-dab in the middle of the brain, these clusters, or nuclei, each send signals to a different area of the brain, igniting opposite behaviors in the face of a visual threat. By selectively altering the activation levels of the two nuclei, the investigators could dispose the mice to freeze or duck into a hiding space, or to aggressively stand their ground, when approached by a simulated predator.

People’s brains probably possess equivalent circuitry, said Andrew Huberman, PhD, associate professor of neurobiology and of ophthalmology. So, finding ways to noninvasively shift the balance between the signaling strengths of the two nuclei in advance of, or in the midst of, situations that people perceive as threatening may help people with excessive anxiety, phobias or post-traumatic stress disorder lead more normal lives.

“This opens the door to future work on how to shift us from paralysis and fear to being able to confront challenges in ways that make our lives better,” said Huberman, the senior author of a paper describing the experimental results. It was published online May 2 in Nature. Graduate student Lindsey Salay is the lead author.

Perilous life of a mouse
There are plenty of real threats in a mouse’s world, and the rodents have evolved to deal with those threats as best they can. For example, they’re innately afraid of aerial predators, such as a hawk or owl swooping down on them. When a mouse in an open field perceives a raptor overhead, it must make a split-second decision to either freeze, making it harder for the predator to detect; duck into a shelter, if one is available; or to run for its life.

To learn how brain activity changes in the face of such a visual threat, Salay simulated a looming predator’s approach using a scenario devised some years ago by neurobiologist Melis Yilmaz Balban, PhD, now a postdoctoral scholar in Huberman’s lab. It involves a chamber about the size of a 20-gallon fish tank, with a video screen covering most of its ceiling. This overhead screen can display an expanding black disc simulating a bird-of-prey’s aerial approach.

Looking for brain regions that were more active in mice exposed to this “looming predator” than in unexposed mice, Salay pinpointed a structure called the ventral midline thalamus, or vMT.

Salay mapped the inputs and outputs of the vMT and found that it receives sensory signals and inputs from regions of the brain that register internal brain states, such as arousal levels. But in contrast to the broad inputs the vMT receives, its output destination points were remarkably selective. The scientists traced these outputs to two main destinations: the basolateral amygdala and the medial prefrontal cortex. Previous work has tied the amygdala to the processing of threat detection and fear, and the medial prefrontal cortex is associated with high-level executive functions and anxiety.

Further inquiry revealed that the nerve tract leading to the basolateral amygdala emanates from a nerve-cell cluster in the vMT called the xiphoid nucleus. The tract that leads to the medial prefrontal cortex, the investigators learned, comes from a cluster called the nucleus reuniens, which snugly envelopes the xiphoid nucleus.

Next, the investigators selectively modified specific sets of nerve cells in mice’s brains so they could stimulate or inhibit signaling in these two nerve tracts. Exclusively stimulating xiphoid activity markedly increased mice’s propensity to freeze in place in the presence of a perceived aerial predator. Exclusively boosting activity in the tract running from the nucleus reuniens to the medial prefrontal cortex in mice exposed to the looming-predator stimulus radically increased a response seldom seen under similar conditions in the wild or in previous open-field experiments: The mice stood their ground, right out in the open, and rattled their tails, an action ordinarily associated with aggression in the species.

Thumping tails

This “courageous” behavior was unmistakable, and loud, Huberman said. “You could hear their tails thumping against the side of the chamber. It’s the mouse equivalent of slapping and beating your chest and saying, ‘OK, let’s fight!’” The mice in which the nucleus reuniens was stimulated also ran around more in the chamber’s open area, as opposed to simply running toward hiding places. But it wasn’t because nucleus reuniens stimulation put ants in their pants; in the absence of a simulated looming predator, the same mice just chilled out.

In another experiment, the researchers showed that stimulating mice’s nucleus reuniens for 30 seconds before displaying the “looming predator” induced the same increase in tail rattling and running around in the unprotected part of the chamber as did vMT stimulation executed concurrently with the display. This suggests, Huberman said, that stimulating nerve cells leading from the nucleus reunions to the prefrontal cortex induces a shift in the brain’s internal state, predisposing mice to act more boldly.

Another experiment pinpointed the likely nature of that internal-state shift: arousal of the autonomic nervous system, which kick-starts the fight, flight or freeze response. Stimulating either the vMT as a whole or just the nucleus reuniens increased the mice’s pupil diameter — a good proxy of autonomic arousal.

On repeated exposures to the looming-predator mockup, the mice became habituated. Their spontaneous vMT firing diminished, as did their behavioral responses. This correlates with lowered autonomic arousal levels.

Human brains harbor a structure equivalent to the vMT, Huberman said. He speculated that in people with phobias, constant anxiety or PTSD, malfunctioning circuitry or traumatic episodes may prevent vMT signaling from dropping off with repeated exposure to a stress-inducing situation. In other experiments, his group is now exploring the efficacy of techniques, such as deep breathing and relaxation of visual fixation, in adjusting the arousal states of people suffering from these problems. The thinking is that reducing vMT signaling in such individuals, or altering the balance of signaling strength from their human equivalents of the xiphoid nucleus and nucleus reuniens may increase their flexibility in coping with stress.

Reference:
Salay, L. D., Ishiko, N., & Huberman, A. D. (2018). A midline thalamic circuit determines reactions to visual threat. Nature. doi:10.1038/s41586-018-0078-2

http://med.stanford.edu/news/all-news/2018/05/scientists-find-fear-courage-switches-in-brain.html

mdma

By DAVE PHILIPPS

After three tours in Iraq and Afghanistan, C. J. Hardin wound up hiding from the world in a backwoods cabin in North Carolina. Divorced, alcoholic and at times suicidal, he had tried almost all the accepted treatments for post-traumatic stress disorder: psychotherapy, group therapy and nearly a dozen different medications.

“Nothing worked for me, so I put aside the idea that I could get better,” said Mr. Hardin, 37. “I just pretty much became a hermit in my cabin and never went out.”

Then, in 2013, he joined a small drug trial testing whether PTSD could be treated with MDMA, the illegal party drug better known as Ecstasy.

“It changed my life,” he said in a recent interview in the bright, airy living room of the suburban ranch house here, where he now lives while going to college and working as an airplane mechanic. “It allowed me to see my trauma without fear or hesitation and finally process things and move forward.”

Based on promising results like Mr. Hardin’s, the Food and Drug Administration gave permission Tuesday for large-scale, Phase 3 clinical trials of the drug — a final step before the possible approval of Ecstasy as a prescription drug.

If successful, the trials could turn an illicit street substance into a potent treatment for PTSD.

Through a spokeswoman, the F.D.A. declined to comment, citing regulations that prohibit disclosing information about drugs that are being developed.

“I’m cautious but hopeful,” said Dr. Charles R. Marmar, the head of psychiatry at New York University’s Langone School of Medicine, a leading PTSD researcher who was not involved in the study. “If they can keep getting good results, it will be of great use. PTSD can be very hard to treat. Our best therapies right now don’t help 30 to 40 percent of people. So we need more options.”

But he expressed concern about the potential for abuse. “It’s a feel-good drug, and we know people are prone to abuse it,” he said. “Prolonged use can lead to serious damage to the brain.”

The Multidisciplinary Association for Psychedelic Studies, a small nonprofit created in 1985 to advocate the legal medical use of MDMA, LSD, marijuana and other banned drugs, sponsored six Phase 2 studies treating a total of 130 PTSD patients with the stimulant. It will also fund the Phase 3 research, which will include at least 230 patients.

Two trials here in Charleston focused on treating combat veterans, sexual assault victims, and police and firefighters with PTSD who had not responded to traditional prescription drugs or psychotherapy. Patients had, on average, struggled with symptoms for 17 years.

After three doses of MDMA administered under a psychiatrist’s guidance, the patients reported a 56 percent decrease of severity of symptoms on average, one study found. By the end of the study, two-thirds no longer met the criteria for having PTSD. Follow-up examinations found that improvements lasted more than a year after therapy.

“We can sometimes see this kind of remarkable improvement in traditional psychotherapy, but it can take years, if it happens at all,” said Dr. Michael C. Mithoefer, the psychiatrist who conducted the trials here. “We think it works as a catalyst that speeds the natural healing process.”

The researchers are so optimistic that they have applied for so-called breakthrough therapy status with the Food and Drug Administration, which would speed the approval process. If approved, the drug could be available by 2021.

Under the researchers’ proposal for approval, the drug would be used a limited number of times in the presence of trained psychotherapists as part of a broader course of therapy. But even in those controlled circumstances, some scientists worry that approval as a therapy could encourage more illegal recreational use.

“It sends the message that this drug will help you solve your problems, when often it just creates problems,” said Andrew Parrott, a psychologist at Swansea University in Wales who has studied the brains of chronic Ecstasy users. “This is a messy drug we know can do damage.”

Allowing doctors to administer the drug to treat a disorder, he warned, could inadvertently lead to a wave of abuse similar to the current opioid crisis.

During initial studies, patients went through 12 weeks of psychotherapy, including three eight-hour sessions in which they took MDMA. During the sessions, they lay on a futon amid candles and fresh flowers, listening to soothing music.

Dr. Mithoefer and his wife, Ann Mithoefer, and often their portly terrier mix, Flynn, sat with each patient, guiding them through traumatic memories.

“The medicine allows them to look at things from a different place and reclassify them,” said Ms. Mithoefer, a psychiatric nurse. “Honestly, we don’t have to do much. Each person has an innate ability to heal. We just create the right conditions.”

Research has shown that the drug causes the brain to release a flood of hormones and neurotransmitters that evoke feelings of trust, love and well-being, while also muting fear and negative emotional memories that can be overpowering in patients with post-traumatic stress disorder. Patients say the drug gave them heightened clarity and ability to address their problems.

For years after his combat deployments, Mr. Hardin said he was sleepless and on edge. His dreams were marked with explosions and death. The Army gave him sleeping pills and antidepressants. When they didn’t work, he turned to alcohol and began withdrawing from the world.

“I just felt hopeless and in the dark,” he said. “But the MDMA sessions showed me a light I could move toward. Now I’m out of the darkness and the world is all around me.”

Since the trial, he has gone back to school and remarried.

The chemist Alexander Shulgin first realized the euphoria-inducing traits of MDMA in the 1970s, and introduced it to psychologists he knew. Under the nickname Adam, thousands of psychologists began to use it as an aid for therapy sessions. Some researchers at the time thought the drug could be helpful for anxiety disorders, including PTSD, but before formal clinical trails could start, Adam spread to dance clubs and college campuses under the name Ecstasy, and in 1985, the Drug Enforcement Administration made it a Schedule 1 drug, barring all legal use.

Since then, the number of people seeking treatment for PTSD has exploded and psychiatry has struggled to keep pace. Two drugs approved for treating the disorder worked only mildly better than placebos in trials. Current psychotherapy approaches are often slow and many patients drop out when they don’t see results. Studies have shown combat veterans are particularly hard to treat.

In interviews, study participants said MDMA therapy had not only helped them with painful memories, but also had helped them stop abusing alcohol and other drugs and put their lives back together.

On a recent evening, Edward Thompson, a former firefighter, tucked his twin 4-year-old girls into bed, turned on their night light, then joined his wife at a backyard fire.

“If it weren’t for MDMA … ” he said.

“He’d be dead,” his wife, Laura, finished.

They both nodded.

Years of responding to gory accidents left Mr. Thompson, 30, in a near constant state of panic that he had tried to numb with alcohol and prescription opiates and benzodiazepines.

By 2015, efforts at therapy had failed, and so had several family interventions. His wife had left with their children, and he was considering jumping in front of a bus.

A member of a conservative Anglican church, Mr. Thompson had never used illegal drugs. But he was struggling with addiction from his prescription drugs, so he at first rejected a suggestion by his therapist that he enter the study. “In the end, I was out of choices,” he said.

Three sessions with the drug gave him the clarity, he said, to identify his problems and begin to work through them. He does not wish to take the drug again.

“It gave me my life back, but it wasn’t a party drug,” he said. “It was a lot of work.”

http://mobile.nytimes.com/2016/11/29/us/ptsd-mdma-ecstasy.html

by Lauren Gravitz

Imagine you’re the manager of a café. It stays open late and the neighbourhood has gone quiet by the time you lock the doors. You put the evening’s earnings into a bank bag, tuck that into your backpack, and head home. It’s a short walk through a poorly lit park. And there, next to the pond, you realise you’ve been hearing footsteps behind you. Before you can turn around, a man sprints up and stabs you in the stomach. When you fall to the ground, he kicks you, grabs your backpack, and runs off. Fortunately a bystander calls an ambulance which takes you, bleeding and shaken, to the nearest hospital.

The emergency room physician stitches you up and tells you that, aside from the pain and a bit of blood loss, you’re in good shape. Then she sits down and looks you in the eye. She tells you that people who live through a traumatic event like yours often develop post-traumatic stress disorder (PTSD). The condition can be debilitating, resulting in flashbacks that prompt you to relive the trauma over and over. It can cause irritation, anxiety, angry outbursts and a magnified fear response. But she has a pill you can take right now that will decrease your recall of the night’s events – and thus the fear and other emotions associated with it – and guard against the potential effects of PTSD without completely erasing the memory itself.

Would you like to try it?

When Elizabeth Loftus, a psychologist at the University of California, Irvine, asked nearly 1,000 people a similar question, more than 80 per cent said: ‘No.’ They would rather retain all memory and emotion of that day, even if it came with a price. More striking was the fact that 46 per cent of them didn’t believe people should be allowed to have such a choice in the first place.

Every day, science is ushering us closer to the kind of memory erasure that, until recently, was more the province of Philip K Dick. Studies now show that some medications, including a blood-pressure drug called propranolol, might have the ability to do just what the ER doctor described – not just for new traumas, but past ones too.

Granted, that future is not yet here. Most of the time, we’re still better at subconsciously editing our own recollections than any new technology is. But with researchers working on techniques that can chisel, reconstruct and purge life’s memories, it becomes crucial to ask: do we need our real memories? What makes us believe that memory is so sacrosanct? And do memories really make us who we are?

Many would argue that humans are driven by their stories. We create our own narratives based on the memories we retain and those we choose to discard. We use memories to build an understanding of self. We lean on them to make decisions and direct our lives.

But what happens to our sense of self if we purge the most distasteful memories and cherry-pick the good ones? When some things are hard to think about, or so injurious to our self-image, are we better off creating a history in which they no longer exist? And if we do, are we doomed to repeat our mistakes without learning from them, doomed to fight the same wars? By finding ways to erase our memories, are we erasing ourselves?

Our memories aren’t fixed. We already edit them: sometimes intentionally, sometimes not. Sometimes by ourselves, and sometimes when other people’s recollections filter into our own. We forget. We ‘remember’ incorrectly. We can even train our brains to remember facts and moments with greater acumen.

Think about your first kiss. No, go back further, to the first time you rode a bike. How clear is that memory? Is it picture-perfect or has it acquired a sepia tint and become a bit tattered around the edges?

The first time I balanced on a two-wheeler was in front of our little ranch-style house on a quiet street in northern California. I was perched proudly, if hesitantly, on the flowered banana seat of a shiny purple Schwinn that my father had just separated from its training wheels. ‘Don’t let go,’ I told my mom before we pushed off. She nodded and I started peddling as she grasped the rounded chrome handle on the back of the seat. ‘Don’t let go!’ I yelled again, and glanced back to find that she had, in fact, let go and was now half a block away, laughing and looking oh-so proud. I promptly fell. And then, because I’d scraped my knees, I started to cry. She came running up and I screamed at her, feeling betrayed.

At least, I think that’s what happened. Thirty-five years later I’m not so sure. Perhaps adult-me has re-interpreted what five-year-old me was feeling. Or perhaps, over the years, every time I pulled this memory up to the surface and told the story, I changed it ever so slightly, until what I remember now is more fiction than fact.

For decades, most memory researchers compared memories to photographs, and our brains to albums or filing cabinets stuffed full of them. They believed that each photo required an initial development period – much the way that pictures are processed in a darkroom – and then was filed away for future reference.

But in the past few decades, scientists have discovered that memory is far more plastic than that. It doesn’t just fade like a photograph tucked away in an album. The details subtly morph and shift. It’s malleable. And some research suggests it might be erasable.

Individual neurons communicate using chemicals called neurotransmitters, which flow from one neuron to the next across synapses – small gaps between the nerve cells. When memories are formed, protein changes at the nerve synapses must be consolidated and translated into long-term circuits in the brain. If consolidation is interrupted, the memory dissolves.

Different types of memories are stored in different places in the brain, and each memory has a dedicated network of neurons. Short-term memories such as a grocery list or an address live, briefly, in the pre-frontal cortex – the foremost area of the folded grey matter that encases the brain. Fear and other intensely emotional memories exist in the amygdala, while facts and autobiographical events are located in the hippocampus. But memories aren’t isolated in these different areas – they overlap and intertwine and connect and diverge like the tangled branches of an old lilac tree. Even when a factual memory fades it can leave an emotional trace behind.

In 2000, two neuroscientists at New York University, Karim Nader and Joseph LeDoux were studying memory in rats when they discovered that the very act of recalling a memory puts it at risk of being altered or possibly erased. When a rat is afraid, it freezes in its tracks. Nader trained his rats to associate a particular tone with a mild electrical shock – every time he played it for them, they froze. As much as a year later, they still froze whenever they heard it, proof that the memory had consolidated and remained intact. Then, he injected a drug that blocked protein formation into each rat’s amygdala, the brain’s emotional strongbox, and played them the same sound but this time without the shock. The next day, the animals had no reaction at all to the tone.

The results were the first to prove how it might be possible to alter a memory that had already been stored, says Nader, who’s now at McGill University in Montreal. ‘We showed that just by recalling a year-old memory, a circuit can go back to being unstored and has to be stored again.’ With each recall, the memory was being reconsolidated – a process akin to pulling a picture out of that album, telling a story about it, then trying to reposition it exactly as it was. But the drug disrupted that process, as though someone had closed the album and spirited it away before the photo could be replaced. Now, with nothing to reinforce the rats’ memories upon recall, the memories appeared to evaporate as though they had never existed.

Upon hearing about Nader’s research, one of his colleagues at McGill, the psychologist Alain Brunet, began looking into whether the finding could be applied to people with PTSD. This condition is less a problem of remembering and more of not-forgetting, when the mind repeatedly plays back a disturbing chain of events, each time prompting the same feelings of fear and distress that were present the moment it happened.

The drug that Nader injected into his rats isn’t approved for most uses in humans. But another one that blocks protein formation in the amygdala is inexpensive, safe, and readily available: the blood pressure-lowering drug, propranolol.

Brunet has now performed a number of trials in people with PTSD – with as few as one session and as many as six – and seen some intriguing results. By administering the pill, waiting an hour, then asking his subjects to write down the traumatic story in as much detail as they could remember, Brunet found that some who had suffered PTSD for years began to look back at the event and remember most of the details while feeling… well, not much at all.

Scientists think it might work like this: norepinephrine is a stress hormone, a neurotransmitter that enhances emotional learning in the brain. Propranolol blocks its effects, preventing its involvement in reconsolidation of the retrieved memory. ‘The reconsolidation blockade has potential to become a universal treatment for PTSD. And PTSD is a universal problem,’ Brunet told me.

Other researchers have tried to repeat Brunet’s work, with greater or lesser success. In two separate studies, led by Brunet and the Harvard psychiatrist Roger Pitman, ER patients who took propranolol within six hours after a trauma appeared protected from experiencing intensely physical reactions when they recalled the event a few months later. It was these studies that Loftus referenced when she created her thought experiment – and that her subjects believed should not be allowed to go any further.

Because propranolol can seemingly erase emotional fear without affecting factual memory, it also holds promise for other anxiety-related disorders. Last year, Merel Kindt, a psychology researcher at the University of Amsterdam, used the drug to help people with arachnophobia to overcome their fear of spiders. Although they clearly remembered being afraid, Kindt’s subjects could now touch and even hold a tarantula.

New studies continue to reveal ways in which memory reconsolidation might be helpful, and multiple mechanisms that could be exploited for memory editing. By disassociating addicts’ memories of being high from their fond feelings toward the experience, scientists have looked at the potential of propranolol to cure alcohol addiction in people, and have even tested it for treating heroin and cocaine addiction in rats. Others are interested in a different drug, called Blebb, to slice out methamphetamine-related memories.

If this same memory-dampening pill could be used to help addicts, would Loftus’s subjects feel differently about its value? Could a judge ethically order this kind of therapy for chronically troubled addicts? When is memory expendable for the good of an individual or of society? And why is it less tolerable to use medication to erase or suppress a memory than it is to rely on our own brains to do the work?

The human brain is remarkably flexible. Its ability to selectively prune our memories’ errant branches is a necessary adaptation. If we remembered every moment of every day, most of us would get too bogged down in our own minds to be functional. Psychologists believe that the human brain has evolved to forget the trivial stuff and highlight important episodes, especially negative ones, so that we might better predict future events and know how to handle them.

That can make trauma harder to expunge, perhaps for good reason. ‘Traumatic experiences give you an opportunity to think about who you are in the moment that life really disrupts you. They make you ask: “What kind of person am I? How did I get out of it?”’ says Kate McLean, a psychologist who specialises in narrative identity at Western Washington University in Bellingham.

‘Dealing with trauma is like strengthening a muscle. If you’ve done your bicep curls, the next time you have to lift a heavy box you can do it more easily,’ she says. ‘People who don’t deal with or who forget [trauma] are not necessarily less happy, but will they be able to deal with the challenges that come next?’ She postulates that they might. But, she says, they could also discover that this kind of temporary coping strategy has consequences up the road.

I have no need to remember what I had for lunch last Wednesday, nor what I wore to that REM concert in 1995 (and I probably don’t want to). I do, however, clearly remember how I lost my footing at the top of the 57th Street subway entrance and bumped down a flight of stairs to land in a wet, embarrassed heap. I will never again forget that metal stair treads get slippery in the rain.

As mortified as I felt, however, the experience doesn’t seem like something I’d want to erase from my memory. Even the most red-faced, shameful moments of my life aren’t something I want to forget: they make me who I am. They are my cautionary tales, my forehead wrinkles. They help me navigate relationships more tactfully and better predict potential outcomes.

If someone were to ask me how I felt about scrubbing away emotional memories, I’d advise them to think hard about it. After all, that’s what I did, and I might never forgive myself.

I am one of the people McLean’s warning is meant for, one of those people who at some point made a conscious decision not to deal with one of life’s challenges. I have a gaping hole in my memory where my father should be, the result of a particularly effective attempt at not dealing by my adolescent brain.

My father had multiple sclerosis. It wasn’t something I thought much about growing up, other than dedicating a sixth-grade science-fair project to describing the disease. It’s an autoimmune disorder of the central nervous system, in which damage to the protective nerve sheaths disrupts neural signalling. It can cause everything from vision problems to paralysis. For my dad, at first, it mostly meant bouts of dizziness and occasional weakness.

One January afternoon when I was 12, however, I walked in after school to see both of my working parents at home in the middle of the day. Something was clearly wrong. My father had caused a car accident that morning and, while both he and the person he’d hit were uninjured, he had no memory of how he got there – a neighbourhood in the opposite direction from his office – and remained confused about the gender of the other driver. It was our first clue that his disease was about to take a rare, devastating turn, and steal not only his mobility but his mind.

In a way, it stole my mind, too.

Within six months, my father – a toxicologist and epidemiologist with a PhD in biochemistry – was spending his workdays staring vacantly out of his office window. He went from a sharp and quick-witted (if occasionally acerbic) debate partner to someone who was dull and vacuous (if mostly pleasant). He displayed all the joy and petulance of a four-year-old and had trouble holding up his end of anything but the simplest conversations.

His body soon followed. The medications he took to help him walk caused terrible convulsions that left him shaking on the floor. A lifelong smoker, he’d light a cigarette and then forget he was holding it, sometimes singeing the tips of his fingers or, once, dropping it in the bathroom where it melted a hole in the linoleum. Within months, he progressed from cane to walker to wheelchair, and eventually had so much trouble swallowing he required a gastric feeding tube for nutrition and a Styrofoam cup to spit into so he wouldn’t choke on his own saliva.

I remember all of this quite clearly. I remember that damned Styrofoam cup, the shiny blue of his wheelchair, the glassy look in his eyes. I remember how he hardly recognised me but how he lit up with the purest smile when my mother entered the room. And despite the fact that I was almost a teenager when the disease began to ravage my father, despite 12 years of prior history dense with family trips and holidays, despite a nightly tradition reading The Hobbit and other books aloud together before bed, I do not remember what my dad was like before he lost his mind.

It’s not that I don’t remember doing all those things – I do. I just can’t remember him. On the day of that first bike ride, even though he had just taken the training wheels off my purple Schwinn, I have no idea if he was standing next to my mother when I fell or if he was even there at all. It’s as if I have taken a scissor to my memories and sliced him right out of the photographs.

At the time, I did it quite intentionally. Every time my mother started to ask: ‘Do you remember when your father…’ I would cut her off abruptly. ‘I don’t want to talk about it,’ I’d say. Then I’d force my brain to bounce past it like a stone skipping off a pond and focus instead on something less painful, usually the man he had become. Rather than dwelling on the father I’d lost, my teenage brain lessened the heartbreak by replacing him with the man who sat in that blue wheelchair. Decades later, I can’t remember him as anything else, no matter how hard I’ve tried.

According to Michael Anderson, a neuroscientist at the University of Cambridge, I did something called ‘retrieval suppression’, in which someone intentionally takes mental action to prevent remembering something unpleasant – a process facilitated by the prefrontal cortex. So far, the emotional stronghold of the amygdala is what researchers understand best when it comes to memory suppression. Yet it’s my hippocampus, the area where factual memory lies, that seems to have the (figurative) holes. Intentional suppression works because we engage the brain’s prefrontal cortex to help us temporarily interrupt hippocampal function, briefly preventing it from encoding or consolidating memories.

Psychologists have long suggested that this kind of memory suppression takes a toll. According to Freud, memories pushed deep into the subconscious mind continue to influence a person’s thoughts and actions long into the future.

But Anderson has found that suppressing a memory also suppresses its subconscious effect on behaviour. He uses a procedure dubbed ‘think/no-think’ to better understand suppression in his study volunteers: first he shows them a picture or a word, then he directs them to either think about it or to intentionally shut down the retrieval process. To look specifically at its effect on behaviour, he and his colleagues asked volunteers to learn a set of word-picture pairs so that a word would prompt them to think of the coupled object (be it a motorcycle or a potted plant). But if the word itself was in red, they told participants to intentionally suppress any thought of the associated object when it popped to mind. When the researchers later showed them pictures of the objects, their subjects had a slightly harder time identifying them.

Some clinicians take the stance that memory suppression can be unhealthy, but this may be based on false assumptions, Anderson says. ‘Maybe it’s not a bad idea to suppress them after all. By giving unwanted memories undue attention, you could ensure they continue to stick around.’

Earlier this year, using the same think/no-think technique, he found that intentional suppression creates what he calls an ‘amnesic shadow’, one that spreads beyond the unwanted memory like a tree pruned a bit too enthusiastically. Participants in Anderson’s trial found that not only were they unable to remember objects they were trying to suppress, they were also less likely to remember objects they learned shortly before or after one they tamped down. It’s a finding that helps explain why people who experience harrowing car crashes and other distressing events often can’t remember what immediately preceded the trauma. It could also help explain why I have so few memories of doing anything at all with my father.

Those memories might not be gone forever. A recent study in the neurologically simple sea slug indicates that interrupting reconsolidation might not be erasing memories but instead simply blocking our access to them. David Glanzman, a neurobiologist at the University of California, Los Angeles, has found that when neurons of the sea hare known as Aplysia californica are transferred to a petri dish, they can be trained much like Nader’s shocked rats. And as with those rats, when Glanzman and his colleagues triggered a memory of the shock and then dosed them with a drug that blocks protein formation, a number of synapses disappeared. But the synapses that dissolved appeared to be random – they weren’t necessarily those associated with the shock. When the researchers went back to the intact animals to see if they could reinstate the shock memory, they found that just a few shocks were enough to restore memories that should have been completely erased. This told them that the memory was located outside the synapses; they traced it to the cell’s nucleus, a part of the neuron that remains intact even as synapses come and go. Deep within the brain, or at least in the brain cells of a sea hare, memories persist.

Yet knowing this, knowing someone could one day tell me that they had found a way to grant me access to my memories of my father, I’m no longer certain I would try.

I spent years trying to find those memories. I asked relatives and friends for stories. I stared at faded family pictures trying to infuse them with the personality and warmth that comes only from the act of reminiscing. But perhaps all this time I’ve been looking for the wrong thing. Perhaps it’s okay to let the memories go. Over time, my sliced-up memories have defined my personal understanding of self and have, ever so gradually, become part of a narrative I’m no longer sure I want to change.

Yes, my over-pruned tree is missing some branches and appears rather lopsided. Its flowers don’t always open the way they should. But it’s also sprouting new leaves in places I never expected, and its crooked visage is simply part of who I am. Rather than trying to fill those empty holes, I can now look at the negative space and see it – all of it – as a part of me.

By Supriya Venkatesan

At 19, I enlisted in the U.S. Army and was deployed to Iraq. I spent 15 months there — eight at the U.S. Embassy, where I supported the communications for top generals. I understand that decisions at that level are complex and layered, but for me, as an observer, some of those actions left my conscience uneasy.

To counteract my guilt, I volunteered as a medic on my sole day off at Ibn Sina Hospital, the largest combat hospital in Iraq. There I helped wounded Iraqi civilians heal or transition into the afterlife. But I still felt lost and disconnected. I was nostalgic for a young adulthood I never had. While other 20-somethings had traditional college trajectories, followed by the hallmarks of first job interviews and early career wins, I had spent six emotionally numbing years doing ruck marches, camping out on mountaintops near the demilitarized zone in South Korea and fighting someone else’s battle in Iraq.

During my deployment, a few soldiers and I were awarded a short resort stay in Kuwait. There, I had a brief but powerful experience in a meditation healing session. I wanted more. So when I returned to the United States at the end of my service, I headed to Iowa.

Forty-eight hours after being discharged from the Army, I arrived on campus at Maharishi University of Management in Fairfield, Iowa. MUM is a small liberal arts college, smack dab in the middle of the cornfields, founded by Maharishi Mahesh Yogi, the guru of transcendental meditation. I joked that I was in a quarter-life crisis, but in truth my conscience was having a crisis. Iraq left me with questions about the world and grappling with my own mortality and morality.

Readjustment was a sucker punch of culture shock. While on a camping trip for incoming students, I watched girls curl their eyelashes upon waking up and burn incense and bundles of sage to ward off negative energy. I was used to being in a similar field environment but with hundreds of guys who spit tobacco, spoke openly of their sexual escapades and played video games incessantly. Is this what it looked like to be civilian woman? Is this what spirituality looked like?

Mediation was mandatory for students on campus, and the rest of the town was composed mainly of former students or longtime followers of the maharishi. Shortly after arriving, I completed an advanced meditator course and began meditating three hours a day — a habit that is still with me five years later. Every morning, I went to a dome where students, teachers and the people of Fairfield gathered to practice meditation. In the evening, we met again for another round of meditation. During my time in Fairfield, even Oprah came to meditate in the dome.

I was incredibly lucky to have supportive mentors in the Army, but Fairfield embraced me in a maternal way. I cried for hours during post-meditation reflection. I released the trauma that is familiar to every soldier who has gone to war but is rarely discussed or even acknowledged. I let go, and I blossomed. I was emancipated of the unhealthy habits of binge-drinking and co-dependency in romantic interludes, as well as a fear that I didn’t know controlled me.

Suicide and other byproducts of post-traumatic stress disorder plague the military. In 2010, a veteran committed suicide every 65 minutes. In 2012, there were more deaths by suicide than by combat. In Iraq, one of my neighbors took his M16, put it in his mouth and shot himself. Overwhelmed with PTSD-related issues from back-to-back deployments and with no clear solution to the problem, in 2012, the Defense Department began researching meditation practices to see whether they would affect PTSD. The first study of meditation and the military population, done with Vietnam veterans in 1985, had shown 70 percent of veterans finding relief, but meditation never gained in popularity nor was it offered through veterans’ services. Even in 2010, when I learned TM, the military was alien to the concept.

But today, the results of the studies showcase immense benefits for veterans. According to the journal Military Medicine, meditation has shown a 40 percent to 55 percent reduction in symptoms of PTSD and depression among veterans. Furthermore, studies show that meditation correlates with a 42 percent reduction in insomnia and a 25 percent reduction in the stress hormone cortisol in the veteran population. To complement meditation, yoga has also been embraced as a tool for treatment by the military. With the growing acceptance of holistic approaches, psychological wounds are beginning to heal.

The four-day training course to learn TM is now available at every Veterans Affairs facility for those who have PTSD or traumatic brain injury. Even medical staff and counselors who help veterans at the VA are offered training in both TM and mindfulness meditation. Additionally, Norwich University, the oldest military college in the country, has done extensive research on TM and incoming cadets, and many military installations have integrated meditation programs into their mental health services. When I had first learned to meditate, many of my active-duty friends found it a bit too crunchy. But with the military’s recent efforts at researching meditation and funding it for all veterans, the stigma is gone, and my battle buddies see meditation as a tool for building resilience.

For me, meditation has created small but significant changes. One day, while going for a walk downtown, I stopped and patted a dog. A few minutes later, I came to a halt. I realized what I had done. While in Iraq, during a month when we were under heavy mortar attack, a bomb-sniffing K-9 had become traumatized and attacked me. This, coupled with a life-long fear of dogs, had left me guarded around the canines. I touched the scar on my elbow from where the K-9 had latched on and could no longer find the fear that had been there. Soon I was shedding all the things that held me back from living my life in an entirely unforeseen way.

For the first time in my life, I found forgiveness for those who had wronged me in the past. I literally stopped to smell the flowers on my way to work every day. And I smiled. All the freaking time. I even felt smarter. Research shows that meditation raises IQ. I’m not surprised. After graduation, I went on to complete my master’s at Columbia University.

Fairfield is also home to generations of Iowans who are born there, brought up there and die there. Many of these blue-collar Midwesterners have had animosity toward the meditators. Locals felt as if their town had been overtaken. They preferred steak to quinoa, beers at the bar to yoga and pickup trucks to carbon-reducing bicycles. And with MUM having a student body from more than 100 countries, the ethnic differences were a challenge. However, things are changing. Meditators and townspeople now fill less stereotypical roles. And with the economic boom that meditating entrepreneurs have provided the town, the differences are easier to ignore.

It was strange for me to live removed from the local Iowans. When I went shopping at the only Walmart the town had, I’d see the “Wall of Heroes” — a wall of photos of veterans from Fairfield. One day, I noticed a familiar face — a soldier from my last assignment. Fairfield and other socioeconomically depressed areas are where most military recruits come from. Here I was living among them, but not moving in step with them. Having that synchronous experience made me come back full circle. When I had first learned to meditate, my teacher had asked me what my goal was. I told her, “I want to be in the world, but not of it.” And that’s exactly what I got.

For me, this little Iowan town provided a place of respite and rejuvenation. It was easy for me to trade one lifestyle of order and discipline for another, and this provided me with nourishment and an understanding of self. Nowhere else in America can you find an entire town living and breathing the principles of Eastern mysticism. It goes way beyond taking a yoga class or going to the Burning Man festival. I continue my meditation practice and am grateful for the gifts it has provided me. But in the end, my time had come, and I had to leave. As residents would say, that was just my karma.

https://www.washingtonpost.com/posteverything/wp/2016/04/06/how-meditating-in-a-tiny-iowa-town-helped-me-recover-from-war/