This is a long article but it is
worth reading. We rethink the whole
issue of memory and it appears that PTSD will soon be generally curable. This
is hugely important and shows us a way forward with treating shock generally.
What is also important is that it
can all be done without necessarily destroying the memory itself. It is enough to eliminate the emotional
loading.
As this article points out, this
will be the first real cure in the field of psychiatric medicine.
The Forgetting Pill Erases Painful Memories Forever
By Jonah Lehrer
February 17, 2012 |
Photo: Dwight Eschliman
Jeffrey Mitchell, a volunteer firefighter in the suburbs of
Baltimore, came across the accident by chance: A car had smashed into a pickup
truck loaded with metal pipes. Mitchell tried to help, but he saw at once that
he was too late.
The car had rear-ended the truck at high speed, sending a pipe through
the windshield and into the chest of the passenger—a young bride returning home
from her wedding. There was blood everywhere, staining her white dress crimson.
Mitchell couldn’t get the dead woman out of his mind; the tableau was
stuck before his eyes. He tried to tough it out, but after months of suffering,
he couldn’t take it anymore. He finally told his brother, a fellow firefighter,
about it.
Pushing to remember a traumatic event soon after it occurs doesn’t
unburden us—it reinforces the fear and stress.
Miraculously, that worked. No more trauma; Mitchell felt free.
This dramatic recovery, along with the experiences of fellow first responders,
led Mitchell to do some research into recovery from trauma. He eventually
concluded that he had stumbled upon a powerful treatment. In 1983, nearly a
decade after the car accident, Mitchell wrote an influential paper in the Journal
of Emergency Medical Services that transformed his experience into a
seven-step practice, which he called critical incident stress debriefing, or CISD. The central
idea: People who survive a painful event should express their feelings soon
after so the memory isn’t “sealed over” and repressed, which could lead to
post-traumatic stress disorder.
In recent years, CISD has become exceedingly popular, used by the US New York
City
Even though PTSD is
triggered by a stressful incident, it is really a disease of memory. The
problem isn’t the trauma—it’s that the trauma can’t be forgotten. Most
memories, and their associated emotions, fade with time. But PTSD memories
remain horribly intense, bleeding into the present and ruining the future. So,
in theory, the act of sharing those memories is an act of forgetting them.
A typical CISD session lasts about three hours and involves a trained
facilitator who encourages people involved to describe the event from their
perspective in as much detail as possible. Facilitators are trained to probe
deeply and directly, asking questions such as, what was the worst part of the
incident for you personally? The underlying assumption is that a way to ease
a traumatic memory is to express it.
The problem is, CISD rarely helps—and recent studies show it often
makes things worse. In one, burn victims were randomly assigned to receive
either CISD or no treatment at all. A year later, those who went through a
debriefing were more anxious and depressed and nearly three times as likely to
suffer from PTSD. Another trial showed CISD was ineffective at preventing
post-traumatic stress in victims of violent crime, and a US Army study of 952
Kosovo peacekeepers found that debriefing did not hasten recovery and led to
more alcohol abuse. Psychologists have begun to recommend that the practice be
discontinued for disaster survivors. (Mitchell now says that he doesn’t think
CISD necessarily helps post-traumatic stress at all, but his early papers on
the subject seem clear on the link.)
Mitchell was right about one thing, though. Traumatic, persistent
memories are indeed a case of recall gone awry. But as a treatment, CISD
misapprehends how memory works. It suggests that the way to get rid of a
bad memory, or at a minimum denude it of its negative emotional connotations,
is to talk it out. That’s where Mitchell went wrong. It wasn’t his fault,
really; this mistaken notion has been around for thousands of years.
Since the time of the ancient Greeks, people have imagined memories to
be a stable form of information that persists reliably. The metaphors for this
persistence have changed over time—Plato compared our recollections to
impressions in a wax tablet, and the idea of a biological hard drive is popular
today—but the basic model has not. Once a memory is formed, we assume that it
will stay the same. This, in fact, is why we trust our recollections. They feel
like indelible portraits of the past.
None of this is true. In the past decade, scientists have come to
realize that our memories are not inert packets of data and they don’t remain
constant. Even though every memory feels like an honest representation, that
sense of authenticity is the biggest lie of all.
When CISD fails, it fails because, as scientists have recently learned,
the very act of remembering changes the memory itself. New research is showing
that every time we recall an event, the structure of that memory in the brain
is altered in light of the present moment, warped by our current feelings and
knowledge. That’s why pushing to remember a traumatic event so soon after it
occurs doesn’t unburden us; it reinforces the fear and stress that are part of
the recollection.
This new model of memory isn’t just a theory—neuroscientists actually
have a molecular explanation of how and why memories change. In fact, their
definition of memory has broadened to encompass not only the cliché cinematic
scenes from childhood but also the persisting mental loops of illnesses like
PTSD and addiction—and even pain disorders like neuropathy. Unlike most brain
research, the field of memory has actually developed simpler explanations.
Whenever the brain wants to retain something, it relies on just a handful of
chemicals. Even more startling, an equally small family of compounds could turn
out to be a universal eraser of history, a pill that we could take whenever we
wanted to forget anything.
And researchers have found one of these compounds.
In the very near future, the act of remembering will become a
choice.
Every memory begins as a changed set of connections among cells in
the brain. If you happen to remember this moment—the content of this
sentence—it’s because a network of neurons has been altered, woven more tightly
together within a vast electrical fabric. This linkage is literal: For a memory
to exist, these scattered cells must become more sensitive to the activity of
the others, so that if one cell fires, the rest of the circuit lights up as
well. Scientists refer to this process as long-term potentiation, and it
involves an intricate cascade of gene activations and protein synthesis that
makes it easier for these neurons to pass along their electrical excitement.
Sometimes this requires the addition of new receptors at the dendritic end of a
neuron, or an increase in the release of the chemical neurotransmitters that
nerve cells use to communicate. Neurons will actually sprout new ion channels
along their length, allowing them to generate more voltage. Collectively this
creation of long-term potentiation is called the consolidation phase, when the
circuit of cells representing a memory is first linked together. Regardless
of the molecular details, it’s clear that even minor memories require major
work. The past has to be wired into your hardware.
That understanding of how memories are created emerged in the 1970s.
But what happens after a memory is formed, when we attempt to access it, was
much less well understood. In the late 1990s, Karim
Nader, a young neuroscientist studying emotional response at New York University
He began with the simplest question he could think of. While it was
clear that new proteins were needed for the making of memories—proteins are
cellular bricks and mortar, the basis of any new biological construction—were
additional proteins made when those memories were recalled? Nader hypothesized
that they were, and he realized that he could test his notion by temporarily
blocking protein synthesis in a brain and looking to see if that altered
recall. “This is the kind of question you ask when you don’t know how else to
approach the subject,” Nader says. “But I had to do something, so why not
this?”
His boss, the famed neuroscientist Joseph
LeDoux, couldn’t have been more discouraging. “I told Karim he was wasting
his time,” LeDoux says. “I didn’t think the experiment would work.” To LeDoux,
the reason was obvious: Even if Nader blocked protein synthesis during recall,
the original circuitry would still be intact, so the memory should be too. If Nader
could induce amnesia, it would be temporary. Once the block was removed, the
recall would return as strong as ever. And so LeDoux and Nader made a bet: If
Nader failed to permanently erase a set of fear memories in four lab animals,
he had to buy LeDoux a bottle of tequila. If it worked, drinks were on LeDoux.
“I honestly assumed I’d be spending a bunch of money on alcohol,” Nader says.
“Everyone else knew a lot more about the neuroscience of memory. And they all
told me it would never work.”
He taught several dozen rats to associate a loud noise with a mild but
painful electric shock. It terrified them—whenever the sound played, the rats
froze in fear, anticipating the shock. After reinforcing this memory for
several weeks, Nader hit the rats with the noise once again, but this time he
then injected their brains with a chemical that inhibited protein synthesis.
Then he played the sound again. “I couldn’t believe what happened,” Nader says.
“The fear memory was gone. The rats had forgotten everything.” The absence of
fear persisted even after the injection wore off.
The secret was the timing: If new proteins couldn’t be created
during the act of remembering, then the original memory ceased to exist. The
erasure was also exceedingly specific. The rats could still learn new
associations, and they remained scared of other sounds associated with a shock
but that hadn’t been played during the protein block. They forgot only what
they’d been forced to remember while under the influence of the protein
inhibitor.
The disappearance of the fear memory suggested that every time we think
about the past we are delicately transforming its cellular representation in
the brain, changing its underlying neural circuitry. It was a stunning
discovery: Memories are not formed and then pristinely maintained, as
neuroscientists thought; they are formed and then rebuilt every time they’re
accessed. “The brain isn’t interested in having a perfect set of memories about
the past,” LeDoux says. “Instead, memory comes with a natural updating
mechanism, which is how we make sure that the information taking up valuable
space inside our head is still useful. That might make our memories less
accurate, but it probably also makes them more relevant to the future.”
After collecting his tequila, Nader hit the library in an attempt to
make sense of his bizarre observations. “I couldn’t believe that no one had
ever I thought, there’s no way I’m this lucky.” Nader was right. He had
unknowingly replicated a 44-year-old experiment performed by a Rutgers
psychologist named Donald Lewis, in which rats had been trained to be afraid of
a sound—associating it, again, with an electric shock—and then had those
memories erased by a separate electroconvulsive shock. Lewis had discovered
what came to be called memory reconsolidation, the brain’s practice
of re-creating memories over and over again.done this experiment before,” he
says. “
But by the mid-1970s, neuroscientists had largely stopped investigating
reconsolidation. Other researchers failed to replicate several of Lewis’
original experiments, so the phenomenon was dismissed as an experimental error.
“These guys had discovered it all way before me,” Nader says. “But they had
been left out of all the textbooks.”
Nader was convinced that Lewis’ work had been rejected unjustly. But no
one wanted to hear it. “Man, it was brutal,” Nader says. “I couldn’t get
published anywhere.” He was shunned at conferences and accused in journal
articles of “forgetting the lessons of the past.” By 2001, just a few years
after his experimental triumph, he was on the verge of leaving the field. He
thought of Thomas Kuhn, the philosopher of science who famously
observed that overturning paradigms is always a fearsome task. “Why put up with
this shit?” Nader says. “I finally understood what Kuhn was talking about. I’d
run straight into a very stubborn paradigm.”
But Nader was so angry at his scientific opponents that he refused to
let them win, and by 2005 other researchers had started to take his side.
Multiple papers demonstrated that the act of recall required some kind of
protein synthesis—that it was, at the molecular level, nearly identical to the
initial creation of a long-term recollection.
To be more specific: I can recall vividly the party for my eighth
birthday. I can almost taste the Baskin-Robbins ice cream cake and summon the
thrill of tearing wrapping paper off boxes of Legos. This memory is embedded
deep in my brain as a circuit of connected cells that I will likely have
forever. Yet the science of reconsolidation suggests that the memory is less
stable and trustworthy than it appears. Whenever I remember the party, I
re-create the memory and alter its map of neural connections. Some details are
reinforced—my current hunger makes me focus on the ice cream—while others get
erased, like the face of a friend whose name I can no longer conjure. The memory
is less like a movie, a permanent emulsion of chemicals on celluloid, and more
like a play—subtly different each time it’s performed. In my brain, a network
of cells is constantly being reconsolidated, rewritten, remade. That two-letter
prefix changes everything.
Memory Erasure: How It Works
For years scientists have been able to change the emotional tone of a
memory by administering certain drugs just before asking people to recall the
event in detail. New research suggests that they’ll be able to target and erase
specific memories altogether. Here’s how.
1/ Pick a memory.
It has to be something deeply implanted in the brain, a long-term
memory that has undergone a process called consolidation—a restructuring of
neural connections.
2/ Recall requires neural connections by protein synthesis.
To remember something, your brain synthesizes new proteins to stabilize
circuits of neural connections. To date, researchers have identified one such
protein, calledPKMzeta. Before trying to erase the targeted memory,
researchers would ensure that it was ensconced by having the patient write down
an account of the event or retell it aloud several times.
3/ Nuke the memory.
To delete the memory, researchers would administer a drug that
blocks PKMzeta and then ask the patient to recall the event again. Because the
protein required to reconsolidate the memory will be absent, the memory will
cease to exist. Neuroscientists think they’ll be able to target the
specific memory by using drugs that bind selectively to receptors found only in
the correct area of the brain.
4/ Everything else is fine.
If the drug is selective enough and the memory precise enough, everything
else in the brain should be unaffected and remain as correct—or incorrect—as
ever.
Once you start questioning the reality of memory, things fall
apart pretty quickly. So many of our assumptions about the human mind—what it
is, why it breaks, and how it can be healed—are rooted in a mistaken belief
about how experience is stored in the brain. (According to a recent survey, 63
percent of Americans believe that human memory “works like a video camera,
accurately recording the events we see and hear so that we can review and
inspect them later.”) We want the past to persist, because the past gives us
permanence. It tells us who we are and where we belong. But what if your most
cherished recollections are also the most ephemeral thing in your head?
Consider the study of flashbulb memories, extremely vivid, detailed
recollections. Shortly after the September 11 attacks, a team of psychologists
led by William Hirst and Elizabeth
Phelps surveyed several hundred subjects about their memories of that
awful day. The scientists then repeated the surveys, tracking how the stories
steadily decayed. At one year out, 37 percent of the details had changed. By
2004 that number was approaching 50 percent. Some changes were innocuous—the
stories got tighter and the narratives more coherent—but other adjustments
involved a wholesale retrofit. Some people even altered where they were when
the towers fell. Over and over, the act of repeating the narrative seemed to
corrupt its content. The scientists aren’t sure about this mechanism, and they
have yet to analyze the data from the entire 10-year survey. But Phelps expects
it to reveal that many details will be make-believe. “What’s most troubling, of
course, is that these people have no idea their memories have changed this
much,” she says. “The strength of the emotion makes them convinced it’s all
true, even when it’s clearly not.”
Reconsolidation provides a mechanistic explanation for these errors.
It’s why eyewitness testimony shouldn’t be trusted (even though it’s central to
our justice system), why every memoir should be classified as fiction, and why
it’s so disturbingly easy to implant false recollections. (The psychologist Elizabeth
Loftus has repeatedly demonstrated that nearly a third of subjects can
be tricked into claiming a made-up memory as their own. It takes only a single
exposure to a new fiction for it to be reconsolidated as fact.)
And this returns us to critical incident stress debriefing. When we
experience a traumatic event, it gets remembered in two separate ways. The
first memory is the event itself, that cinematic scene we can replay at will.
The second memory, however, consists entirely of the emotion, the negative
feelings triggered by what happened. Every memory is actually kept in many
different parts of the brain. Memories of negative emotions, for instance, are
stored in the amygdala, an almond-shaped area in the center of the brain.
(Patients who have suffered damage to the amygdala are incapable of remembering
fear.) By contrast, all the relevant details that comprise the scene are kept
in various sensory areas—visual elements in the visual
cortex, auditory elements in the auditory cortex, and so on. That filing system
means that different aspects can be influenced independently by
reconsolidation.
The larger lesson is that because our memories are formed by the act of
remembering them, controlling the conditions under which they are recalled can
actually change their content. The problem with CISD is that the worst time to
recall a traumatic event is when people are flush with terror and grief.
They’ll still have all the bodily symptoms of fear—racing pulse, clammy hands,
tremors—so the intense emotional memory is reinforced. It’s the opposite
of catharsis.
But when people wait a few weeks before discussing an event—as Mitchell, the
inventor of CISD, did himself—they give their negative feelings a chance to
fade. The volume of trauma is dialed down; the body returns to baseline. As a
result, the emotion is no longer reconsolidated in such a stressed state.
Subjects will still remember the terrible event, but the feelings of pain
associated with it will be rewritten in light of what they feel now.
LeDoux insists that these same principles have been used by good
therapists for decades. “When therapy heals, when it helps reduce the impact of
negative memories, it’s really because of reconsolidation,” he says. “Therapy
allows people to rewrite their own memories while in a safe space, guided by
trained professionals. The difference is that we finally understand the neural
mechanism.”
But competent talk therapy is not the only way to get at those
mechanisms. One intriguing approach to treating PTSD that emerged recently
involves administering certain drugs and then asking patients to recall their
bad memories. In one 2010 clinical trial, subjects suffering from PTSD were
given MDMA(street
name: ecstasy) while undergoing talk therapy. Because the drug triggers a rush
of positive emotion, the patients recalled their trauma without feeling
overwhelmed. As a result, the remembered event was associated with the positive
feelings triggered by the pill. According to the researchers, 83 percent of
their patients showed a dramatic decrease in symptoms within two months. That
makes ecstasy one of the most effective PTSD treatments ever devised.
Other scientists have achieved impressive results with less extreme
drugs. In 2008, Alain Brunet, a clinical psychologist at McGill University
One week later, all the patients returned to the lab and were exposed
once again to a description of the traumatic event. Here’s where things got
interesting: Subjects who got the placebo demonstrated levels of arousal
consistent with PTSD (for example, their heart rate spiked suddenly), but those
given propranolol showed significantly lower stress responses. Although they
could still remember the event in vivid detail, the emotional memory located in
the amygdala had been modified. The fear wasn’t gone, but it no longer seemed
crippling. “The results we get sometimes leave me in awe,” Brunet says. “These
are people who are unable to lead normal lives, and yet after just a few
sessions they become healthy again.”
Recoveries are possible, but they aren’t necessarily neat. One of
Brunet’s patients was Lois, a retired member of the Canadian military living in
Kingston , Ontario
Lois coped by drinking. She would start around noon and keep going
until she went to bed. “I lost four years to alcohol,” she says. “But if I
wasn’t drunk then I was crying. I knew I was killing myself, but I didn’t know
what else to do.”
“Psychiatry never cures anything—all we do is treat the worst symptoms.
But this new treatment could be the first psychiatric cure ever.”
In early 2011, Lois learned about the experimental trials being
conducted by Brunet. She immediately wrote him an email, begging for help. “I’d
spent a lot of my life in standard talk therapy,” she says. “It just didn’t do
it for me. But this seemed like it might actually work.” Last spring Lois began
reconsolidation treatment at Brunet’s hospital, driving to Montreal
Such improvements, small though they may seem, are almost unheard of
in psychiatry. “We never cure anything,” Brunet says. “All we do is try to
treat the worst symptoms. But I think this treatment has the potential to be
the first psychiatric cure ever. For many people, the PTSD really is gone.”
Propranolol, of course, is an imperfect drug, a vintage tool
commandeered for a new purpose. Despite Brunet’s optimistic assessment, many of
his patients remain traumatized, albeit perhaps less so. While he is currently
conducting a larger-scale, randomized PTSD trial with the beta-blocker, future
therapies will rely on more targeted compounds. “These norepinephrine
inhibitors are just what’s available right now,” LeDoux says. “They work OK,
but their effect is indirect.” What reconsolidation therapy really needs is a
drug that can target the fear memory itself. “The perfect drug wouldn’t just
tamp down the traumatic feeling,” he says. “It would erase the actual
representation of the trauma in the brain.”
Here’s the amazing part: The perfect drug may have already been found.
The chemistry of the brain is in constant flux, with the typical
neural protein lasting anywhere from two weeks to a few months before it breaks
down or gets reabsorbed. How then do some of our memories seem to last forever?
It’s as if they are sturdier than the mind itself. Scientists have narrowed
down the list of molecules that seem essential to the creation of long-term
memory—sea slugs and mice without these compounds are total amnesiacs—but until
recently nobody knew how they worked.
In the 1980s, a Columbia
University
In fact, it took Sacktor more than a decade. (He spent three years just
trying to purify the molecule.) What he discovered is that a form of protein
kinase C called PKMzeta hangs around synapses, the junctions where neurons
connect, for an unusually long time. And without it, stable recollections start
to disappear. While scientists like Nader had erased memories using chemicals
that inhibited all protein synthesis, Sacktor was the first to target a single
memory protein so specifically. The trick was finding a chemical that inhibited
PKMzeta activity. “It turned out to be remarkably easy,” Sacktor says. “All we
had to do was order this inhibitor compound from the chemical catalog and then
give it to the animals. You could watch them forget.”
What does PKMzeta do? The molecule’s crucial trick is that it increases
the density of a particular type of sensor called an AMPA receptor on the
outside of a neuron. It’s an ion channel, a gateway to the interior of a cell
that, when opened, makes it easier for adjacent cells to excite one another.
(While neurons are normally shy strangers, struggling to interact, PKMzeta
turns them into intimate friends, happy to exchange all sorts of incidental
information.) This process requires constant upkeep—every long-term memory is
always on the verge of vanishing. As a result, even a brief interruption of
PKMzeta activity can dismantle the function of a steadfast circuit.
If the genetic expression of PKMzeta is amped up—by, say, genetically
engineering rats to overproduce the stuff—they become mnemonic freaks, able to
convert even the most mundane events into long-term memory. (Their performance
on a standard test of recall is nearly double that of normal animals.)
Furthermore, once neurons begin producing PKMzeta, the protein tends to linger,
marking the neural connection as a memory. “The molecules themselves are always
changing, but the high level of PKMzeta stays constant,” Sacktor says. “That’s
what makes the endurance of the memory possible.”
For example, in a recent experiment, Sacktor and scientists at
the Weizmann Institute of Science trained
rats to associate the taste of saccharin with
nausea (thanks to an injection of lithium). After just a few trials, the rats
began studiously avoiding the artificial sweetener. All it took was a single
injection of a PKMzeta inhibitor called zeta-interacting protein, or ZIP,
before the rats forgot all about their aversion. The rats went back to guzzling
down the stuff.
By coupling these amnesia cocktails to the memory reconsolidation
process, it’s possible to get even more specific. Nader, LeDoux, and a
neuroscientist named Jacek Debiec taught rats elaborate sequences of
association, so that a series of sounds predicted the arrival of a painful
shock to the foot. Nader calls this a “chain of memories”—the sounds lead to
fear, and the animals freeze up. “We wanted to know if making you remember that
painful event would also lead to the disruption of related memories,” Nader
says. “Or could we alter just that one association?” The answer was clear. By
injecting a protein synthesis inhibitor before the rats were exposed to only
one of the sounds—and therefore before they underwent memory
reconsolidation—the rats could be “trained” to forget the fear associated with
that particular tone. “Only the first link was gone,” Nader says. The other
associations remained perfectly intact. This is a profound result. While
scientists have long wondered how to target specific memories in the brain, it
turns out to be remarkably easy: All you have to do is ask people to remember
them.
This isn’t Eternal Sunshine of the Spotless
Mind-style mindwiping. In some ways it’s potentially even more effective
and more precise. Because of the compartmentalization of memory in the
brain—the storage of different aspects of a memory in different areas—the
careful application of PKMzeta synthesis inhibitors and other chemicals that
interfere with reconsolidation should allow scientists to selectively delete
aspects of a memory. Right now, researchers have to inject their obliviating
potions directly into the rodent brain. Future treatments, however, will
involve targeted inhibitors, like an advanced version of ZIP, that become
active only in particular parts of the cortex and only at the precise time a
memory is being recalled. The end result will be a menu of pills capable of
erasing different kinds of memories—the scent of a former lover or the awful
heartbreak of a failed relationship. These thoughts and feelings can be made to
vanish, even as the rest of the memory remains perfectly intact.
“Reconsolidation research has shown that we can get very specific about which
associations we go after,” LeDoux says. “And that’s a very good thing. Nobody
actually wants a totally spotless mind.”
The astonishing power of PKMzeta forces us to redefine human
memory. While we typically think of memories as those facts and events from the
past that stick in the brain, Sacktor’s research suggests that memory is
actually much bigger and stranger than that. In fact, PTSD isn’t the only
disease that’s driven by a broken set of memories—other nasty afflictions,
including chronic pain, obsessive-compulsive disorder, and drug addiction, are
also fueled by memories that can’t be forgotten.
Sacktor is convinced that the first therapeutic use of PKMzeta
inhibitors will involve making people forget not an event but physical pain.
For reasons that remain mysterious, some sensory nerves never recover from
bodily injury; even after a wound heals, the hurt persists. The body remembers.
Because these memories are made of the exact same stuff as every other kind of
memory, injecting an inhibitor near the spinal cord—where, presumably, the
sensation of pain is being stored—and then somehow inducing or focusing on the
pain could instantly erase the long-term suffering, as if the nerves themselves
were reset. “It’s hard to argue against this form of memory alteration,”
Sacktor says. “It might be the only way to treat neuropathic pain.” PTSD is the
emotional version of this problem. Instead of the pain coming from the spinal
cord, it comes from the amygdala, where a trauma is encoded and just won’t let
go. For many reconsolidation researchers, there is little difference among
categories of hurt. It doesn’t matter if the tragedy is physical or psychic:
The treatment is the same.
There is perhaps no societal plague more expensive than drug addiction.
In the US
Being able to control memory doesn’t simply give us admin access to our
brains. It gives us the power to shape nearly every aspect of our lives.
There’s something terrifying about this. Long ago, humans accepted the
uncontrollable nature of memory; we can’t choose what to remember or forget.
But now it appears that we’ll soon gain the ability to alter our sense of the
past.
The problem with eliminating pain, of course, is that pain is often
educational. We learn from our regrets and mistakes; wisdom is not free. If our
past becomes a playlist—a collection of tracks we can edit with ease—then how
will we resist the temptation to erase the unpleasant ones? Even more
troubling, it’s easy to imagine a world where people don’t get to decide the
fate of their own memories. “My worst nightmare is that some evil dictator gets
ahold of this,” Sacktor says. “There are all sorts of dystopian things one
could do with these drugs.” While tyrants have often rewritten history books,
modern science might one day allow them to rewrite us, wiping away genocides
and atrocities with a cocktail of pills.
Those scenarios aside, the fact is we already tweak our memories—we
just do it badly. Reconsolidation constantly alters our recollections, as we
rehearse nostalgias and suppress pain. We repeat stories until they’re stale,
rewrite history in favor of the winners, and tamp down our sorrows with
whiskey. “Once people realize how memory actually works, a lot of these beliefs
that memory shouldn’t be changed will seem a little ridiculous,” Nader says.
“Anything can change memory. This technology isn’t new. It’s just a better
version of an existing biological process.”
It’s a pretty notion—hey, this memory-alteration stuff is totally
natural, man—but some ethicists and clinicians dispute whether this kind of
therapy is acceptable. Researchers in the field counter that not treating
suffering is cruel, regardless of the type of pain involved. We have a duty,
they say, to take psychological pain seriously. We can no longer ignore people
like Lois. “If you’re in a car accident and you break your leg, everyone agrees
we need to give you treatment and painkillers,” Nader says. “But if something
terrible happens and your mind breaks, people conclude that treatment is a
dangerous idea, at least if it’s effective. But what’s the difference?” Just
think of all the poor souls in therapy, trying to talk themselves into a better
place. These scientists point out that memory tweaks will one day be used in the
same way—except that unlike CISD or Jungian analysis or selective serotonin
reuptake inhibitors, these therapies could put permanent recovery just one pill
away.
At the moment, of course, such treatments remain entirely hypothetical,
an avant-garde limited to the lab. PKMzeta inhibitors can zap rodent memories,
but we can’t ask the rats how they feel afterward. Maybe they feel terrible.
Maybe they miss their fear. Maybe they miss their morphine. Or maybe all they
know is that they miss something. They just can’t remember what.
Contributing editor Jonah Lehrer (jonah.lehrer@gmail.com) is the
author of the new book Imagine: How Creativity Works, out in March.
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