Wave of Tide theft possibly connected to production of meth?

The recent news coverage of theft involving Tide liquid detergent has involved speculation about why thieves are targeting laundry soap. The reports suggest that laundry soap is such a commodity that it can be easily resold, and that perhaps it is being used in exchange for drugs. But, no report has suggested that liquid Tide is being used to make drugs.

To further confuse matters, Fox News is running an article that says the Tide theft wave is a mere rumor, and that there is no evidence of an increase in theft of Tide.

My immediate (and seemingly obvious) suspicion is that something in the liquid soap is being used to make methamphetamine, and if so, I have to wonder why this possibility has not been raised by the reports. So, I set out in hope of finding some answers online.

I first thought of phosphorus. It appears that Tide's original formula was changed from sodium tripolyphosphate because it was causing environmental concerns, and that a red phosphorus does not pose the same concerns and has been used since. Apparently, red phosphorus is a controlled substance in Russia because it is used to produce amphetamines, but I am unclear about whether or not liquid Tide contains red phosphorus (see links and excerpts below).

Perhaps more relevant, other ingredients listed in liquid Tide are sodium hydroxide and diethyl phthalate, which are also associated with production of methamphetamine:

http://health.utah.gov/meth/html/ToxicologyofMeth/SodiumHydroxide.html

http://gradworks.umi.com/14/97/1497207.html

So, unless I'm completely off track or missing information, it seems likely that liquid Tide could possibly be used to produce meth, in which case I wonder whether the media is avoiding liability for connecting the Tide brand with drug production, or possibly avoiding spreading the idea of using it. We know that the sale of products like cold medicine (Nyquil) containing acetaminophen are monitored, sometimes with an ID check. I can imagine how the monitoring of laundry soap sales might create a logistic nightmare.

The situation reminds me of my other question in regard to birth control. Older women have been warned about taking estrogen due to a threat of breast cancer, but no warning was ever suggested for younger women who take birth control pills - a warning that would pose an enormous logistic problem.

When the issue came about, I was also noticing how older couples who rely on fertility drugs were having smaller and sometimes multiple babies. I wondered whether a long history of birth control use would make it harder for older women to get pregnant, and I wondered whether there is now a higher number of women requiring fertility drugs, and therefore lowering the average birth rate - all due to the use of birth control pills. At one point, I sought to compare average birth weights between the time of the introduction of the pill and today, and I was unable to find the information.

Do these kinds of problems create such huge liability for public administration that prevent discussion or cause avoidance?


More background about laundry detergent contents and methamphetamine:

http://en.wikipedia.org/wiki/Allotropes_of_phosphorus#Red_phosphorus

Red phosphorus may be formed by heating white phosphorus to 250 °C (482 °F) or by exposing white phosphorus to sunlight. Red phosphorus exists as an amorphous network. Upon further heating, the amorphous red phosphorus crystallizes. Red phosphorus does not ignite in air at temperatures below 240 °C, whereas white phosphorus ignites at about 30 °C. Red phosphorus can be converted to white phosphorus upon heating to 260 °C, as can be seen when one strikes a match.
It is a controlled substance (precursor) in Russia and much of the rest of the former Soviet Union, due to its use in illicit amphetamine production.

http://chemistry.about.com/od/medicalhealth/a/crystalmeth.htm

Where Does Crystal Meth Come From?

Methamphetamine is available with a prescription for obesity, attention deficit hyperactivity disorder, and narcolepsy, but crystal meth is a street drug, made in illegal labs by chemically altering over-the-counter drugs. Making crystal meth usually involves reducing ephedrine or pseudoephedrine, found in cold and allergy medicine. In the US, a typical meth lab employs something called the 'Red, White, and Blue Process', which entails hydrogenation of the hydroxyl group on the ephedrine or pseudoephedrine molecule. The red is red phosphorus, white is the ephedrine or pseudoephedrine, and blue is iodine, used to make hydroiodic acid. Making crystal meth is dangerous to the people making it and dangerous to the neighborhood where it's being made. White phosphorus with sodium hydroxide can produce poisonous phosphine gas, usually as a result of overheating red phosphorus, plus white phosphorus can autoignite and blow up the meth lab. In addition to phosphine and phosphorus, various hazardous vapors may be associated with a meth lab, such as chloroform, ether, acetone, ammonia, hydrochloric acid, methylamine, iodine, hydroiodic acid, lithium or sodium, mercury, and hydrogen gas.

About Phosphorus and Laundry Detergent

http://www.chemistryexplained.com/elements/L-P/Phosphorus.html

The second most important use of phosphate compounds is in making detergents. The compound most often used in detergents is called sodium tripolyphosphate, or STPP (Na ₅ P ₃ O ₁₀ ).
STPP adds a number of benefits to a detergent. For example, it can kill some bacteria and prevent washers from becoming corroded (rusted) and clogged. The most important function in detergents, however, is as a water-softening agent.

Natural water often contains chemicals that keep soaps and detergents from sudsing. They reduce the ability of soaps and detergents to clean clothes. STPP has the ability to capture these chemicals. It greatly improves the ability of soaps and detergents to make suds and clean clothes. The first detergent to use STPP was Tide, in 1947. The introduction of Tide brought about a revolution in clothes cleaning.

But STPP can create problems for the environment. After detergents have been used, they often end up in rivers and streams and, eventually, in lakes from waste water. And that's just fine for the algae that live in those lakes. Algae are tiny green plants that use phosphorus as they grow. As more detergents get into lakes, the amount of STPP increases. That means there is more phosphorus in a lake and that, in turn, means that algae begin to grow much faster.

In some cases, there is so much STPP and phosphorus in a lake that algae grow out of control, clogging the lake with algae and other green plants. The lake slowly turns into a swamp, and finally into a meadow. The lake disappears!

Many people became concerned about this problem in the 1960s. They demanded that less STPP be used in detergents. A number of cities and states banned the sale of STPP detergents. STPP production had grown rapidly from 1.10 billion pounds in 1955 to 2.44 billion pounds in 1970. But then production began to drop off. By the mid-1990s, production had dropped well below a billion pounds a year.

Interestingly, red phosphorus does not have the same effects. It is considered to be relatively safe. It is dangerous only if it contains white phosphorus mixed with it.

Google AR

 Here it comes...as per previous posts (seach the blog for 'glasses'), and as I speculated in an email I sent around 12/10:

"...glasses might be used in combination with several other technologies. If the kinect could somehow move with the player (maybe through a local area network GPS) it could open up a lot of major possibilites - it might be a matter of rigging up some kind of central point that tracks the orientation of the head and limb points more like a motion capture flock system, and transmits the data back to the network  - I have an idea for playing games whereby the players would view their environment through glasses with built in headphones and microphones, the kinect could allow for avatars to be superimposed over the players, and other elements could be projected into the environment, using the local area network and localized GPS to track the players. So the result would be a mixed reality of actual physical involvement by the player (running and spatial relations), with superimposed elements (the avatar/appearance of other players, AI elements, effects, etc.) and sounds would be blended into the actual surrounding sounds and voices of other players around the person as well.

The same combo of glasses and sound could be used in real world wifi environments for navigating any space, marketing, etc. - the information could appear on the glasses - you look at a building and the information can appear and also be narrated via audio - users would set up preferences or maybe toggle preferences via mobile devices. I have thought to illustrate/animate an explanatory demo of the concept."


the article:

What will the Google AR Glasses be Like?
Sunday, February 26, 2012 - Iddo Genuth

http://thefutureofthings.com/news/11429/what-will-the-google-ar-glasses-be-like.html

Google is reportedly working on digital sunglasses with advanced capabilities. Among other things the Google glasses will supposedly allow users to use GPS while walking the street add visual information in the form of Augmented Reality as well as give you many of the capabilities current smartphones do. When should we expect these wonder glasses? keep on reading.

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Google AR Glasses?

The first leaks about Google secret plan to develop advanced digital eyewear didn't start yesterday. In fact in mid December 2011 the New York Times reported that both Apple and Google are working on advanced wearable projects. But while Apple is supposedly working on a watch like computer, Google has been working on advanced glasses.
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The idea of a personal heads up display isn't new. On July 2007 we had a chance to visit visited the offices of Lumus - an Israeli startup located near the Weizmann Institute of Science in the city of Rehovot. The company developed what was supposedly the first see-through head-mounted display.  Since 2007 Lumus was not able to bring a product to the market but continued to develop its technology and recently a new generation of prototype see through glasses was unveiled.
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It's not clear wheatear or not there is any connection between what Lumus has been developing and what has been going on in Google's secret labs but even if they are based on different technology (some claim the Google  eyewear uses a form of transparent OLED technology) they both have lots of potential. Google of course is especially poised to make something of this potential using many of its current technologies.

It is highly likely that the Google  eyewear will use some sort of Android OS and will be connected to the web using WIFI or 3G and giving it access to a variety of Google services including all types of location based searches, social networks (where you can see where you friends are on a map in relation to your position) as well as various levels of augmented reality.
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So far augmented reality was mostly restricted to fairly cumbersome use as well as cell phones which are not typically held in front of the eyes for long periods of time and are not transparent. Google  eyewear might change all that by adding virtual information in front of a person that is relevant to his location.

Another potential use for augmented reality based Google  eyewear might be gaming. Playing first person shooters in a real world environment with both real and virtual players and enemies might be the ultimate gaming experience. This might get gamers to get up from their chairs and move into the real world looking for their next adrenalin rush.
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Its not exactly clear when are all these amazing technologies going to be realized but what seems quite clear at this point is that Google is serious about its plans to launch a product in 2012 for between $250 and $600.

Keeping up with the Kardashians

Whew, this is a relief. I was beginning to worry that the mechas had finally begun making their way in amongst us.
Soon, everyone will be wiping their nose this way.

A momentary lapse of pleasin'.

Facebook one-page cheat sheet lays out exactly what must be confirmed and deleted

http://cache.gawkerassets.com/assets/images/7/2012/02/88e77406de7ac8efad90dc5d096deaa2.jpg

Interface scaffolds" could wire prosthetics directly into amputees' nervous systems

http://www.gizmag.com/nerve-prostheses-interface-scaffolds/21646/

By David Szondy

Scientists at Sandia National Laboratories have announced a breakthrough in prosthetics that may one day allow artificial limbs to be controlled by their wearers as naturally as organic ones, as well as providing sensations of touch and feeling. The scientists have developed a new interface consisting of a porous, flexible, conductive, biocompatible material through which nerve fibers can grow and act as a sort of junction through which nerve impulses can pass to the prosthesis and data from the prosthesis back to the nerve. If this new interface is successful, it has the potential to one day allow nerves to be connected directly to artificial limbs.
It all sounds very simple as an idea, but attaching nerves to a mechanical limb isn't like securing a wire to a terminal with a spot of solder. For one thing, you need a very special type of "solder" and that's what organic materials chemist Shawn Dirk and robotics engineer Steve Buerger, working in collaboration with teams at the University of New Mexico and MD Anderson Cancer Center in Houston, are trying to create.
The interface that they are working on must be biocompatible. In other words, it mustn't harm the nerves, which are notoriously delicate. The interface must also be able to interact with the nerves and that's very difficult to engineer because, unlike in electronics, the nerves' specs cannot be in any way changed, so the interface material has to carry the burden. The interaction has to be very subtle and has to carry thousands of nerve impulses of all kinds every second and it must do so accurately. While it is doing this, it also has to be very flexible, very fluid and very conductive.
This is a very tall order.

Creating the interface

The interface came about through Buerger's original attempt to produce implantable neural electronic interfaces as part of a robotics approach to the problem. It soon became apparent that the heart of the problem was how to form an interface with the nerves themselves, so Dirk and his team were brought in. They took this problem down to the level of the material itself and turned to a technique called projection microstereolithography. This involves projecting a pattern of ultraviolet light on to a wafer coated with Polydimethylsiloxane (PDMS). This is a silicon-based organic polymer more commonly known as dimethicone, which is used in contact lenses, medical devices, shampoos, play putty and other products.
When subjected to microstereolithography, the PDMS forms a thin, porous membrane with holes only 79 microns in diameter. This provides a mechanically compatible scaffolding through which nerve fibers can grow. The addition of carbon nanotubes to the PDMS makes it conductive in a way that is highly controllable, so the basic interface could be formed.
All this talk about putty and nanotubes may seem a long way from anything practical, but it's the final link in a very important story. The number of amputees in the world is unknown, but in the United States alone there are some two million people living with the loss of one or more limbs. Of these, 1,400 were US soldiers fighting in the recent wars in Iraq and Afghanistan. It's a curious paradox that as advances in medicine and surgery save more lives, they leave behind more amputees who would previously have died of their diseases or injuries, especially among military and civilian casualties in wartime. However, thanks to advances in prosthetics, the loss of a limb does not automatically mean a life of confinement and dependence.

Recent developments

Modern prostheses have come a long way since the days when the best that could be hoped for was a carved wooden leg. Modern artificial limbs benefit from a wide variety of lightweight plastics and composite materials that make them lighter, stronger and more comfortable, with custom-fitted attachments that fit the prosthetic to the body so closely that they're often held by suction alone. Some have sophisticated joints that, for example, mimic the movements of the human knee. Others use electronics, hydraulics, pneumatics or the wearer's own muscles to power motors and gears that can make limbs flex and turn or fingers grasp with such precision that they can pick up an egg without cracking it.
Some artificial arms can be covered with cosmetic skin so lifelike that it's almost unnerving to realize that it's made of metal and plastic rather than flesh and bone. There are even specialized limbs, such as curved springs made out of composite materials that can turn a man with no legs into an Olympic-level sprinter.
All of this is remarkable, but at the end of the day, these incredible bits of engineering aren't much more advanced than Captain Hook's hook or Long John Silver's peg leg. That's because no matter how exotic the materials or clever the design, they are still worn by the amputee while the arm and the leg they replace was an integral part of that person. While the prosthetic is worn by the amputee, it is ultimately still separate from them.
The difference between a real limb and a prosthesis is that a living arm or leg does what the person wants. We could say that it "responds to commands," but that isn't quite true. Because our limbs are connected directly to our nervous systems, we don't need conscious thought to make them go. The nervous system is like a series of extremely sophisticated triggers that set off complex actions with little more than intent on our part. Sometimes, when we touch a hot stove, for instance, intention isn't even needed as the nervous system yanks the burned hand away before we're even aware. It allows us to do things without thinking about it. I'm typing these words, but I'm thinking about what I'm writing, not what my fingers are doing at the keyboard. The nervous system does the hard work of moving the fingers to the right keys in the right order.
Artificial limbs don't have that sort of direct command. Worse, they have no sense of feeling. There's no touch. If a prosthesis is to be truly successful, it needs these attributes. That's why scientists an engineers have been working on the problem for decades. There have been a lot of advances and, from an engineering point of view, the artificial limbs of today are very good, but the tricky bit is providing them with the necessary degree of natural control and sensation. And it isn't a question of having one or the other. Both are necessary for the artificial limb to work as it should.
A way of understanding what's involved is to look at one of the early attempts at direct control, the Boston Arm, which was developed in 1969 by Dr. Melvin J. Glimcher, professor of orthopedic surgery at Harvard University and Prof. Robert W. Mann of the Massachusetts Institute of Technology. This was an artificial arm for above the elbow amputees with a motorized elbow joint and an articulated hook for grasping things. What made the Boston Arm novel was that it had sensors that attached to the stump of the wearer's upper arm. When the wearer flexed his bicep, the arm would pick up the electrical impulse the muscle made as it flexed and the arm would bend and rise. If the wearer flexed his triceps, the arm would straighten and drop.

We can rebuild him ...

So far so good, but the problem is, it's one thing to get the arm moving, it's another thing to get it moving the right way. Too little power and the arm won't move, too much and you'll smack yourself in the face picking up a spoon. Glimcher and Mann solved this by introducing a forced feedback system into the arm. There were strain gauges installed that told the arm how much effort was involved in lifting something. If the object being lifted was heavy, the voltage to the motors would drop and the wearer would have to flex his muscles harder to compensate by ordering the arm to increase the voltage. In this way, the wearer could learn how to lift anything from a cup to at ten-pound weight with confidence.
This early arm showed the importance of sensation. The simple feedback system of the Boston Arm was very successful and it even inspired the television series The Six Million Dollar Man, but it also paved the way for the artificial limbs of tomorrow. Already DARPA and scientists in U.S. and the U.K. are working on developing nanosensors that can provide sensations far beyond earlier, cruder attempts using micro-switches and the like. Eventually, it's hoped that these will lead to remote presence devices and artificial limbs, but the key to the entire problem is how to connect the nerves to the machines. Once that is licked, the rest follows. It will then be possible to build limbs that have a much more natural means of control and the necessary senses to allow the user to experience touch and the feedback needed to accurately control the device.
The current work at Sandia Laboratories is still in the proof of concept stage, but the stakes are very high. If they pan out and the gap between man and machine can be bridged, we could see the first true cyborg produced. Or, at the very least, the liberation of hundreds of thousands of people from physical limitations.

The Forgetting Pill Erases Painful Memories Forever

http://www.wired.com/magazine/2012/02/ff_forgettingpill/all/1

By Jonah Lehrer

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 Department of Defense, the Federal Emergency Management Agency, the Israeli army, the United Nations, and the American Red Cross. Each year, more than 30,000 people are trained in the technique. (After the September 11 attacks, 2,000 facilitators descended on 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.

Photo illustration: Curtis Mann; Photo: Owen Franken/Corbis

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, realized that no one knew. “My big advantage was that I wasn’t trained in memory,” Nader says. “I was very naive about the subject. Even though the field wasn’t that interested in the mechanisms of recall, it struck me as a mystery worth pursuing.”
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 done this experiment before,” he says. “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.
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, called PKMzeta. 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.

Illustration: Teagan White

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, identified 19 patients who had been suffering for several years from serious stress and anxiety disorders such as PTSD. (Their traumas included sexual assaults, car crashes, and violent muggings.) People in the treatment group were given the drug propranolol, a beta-blocker that has long been used for conditions like high blood pressure and performance anxiety; it inhibits norepinephrine, a neurotransmitter involved in the production of strong emotions. Brunet asked subjects to write a detailed description of their traumatic experiences and then gave them a dose of propranolol. While the subjects were remembering the awful event, the drug suppressed the visceral aspects of their fear response, ensuring that the negative feeling was somewhat contained.
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.”

Photo illustration: Curtis Mann; Photo: Ed Andrieski/AP

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. (She asked that I not use her last name.) When Lois describes the tragic arc of her life, she sounds like a cursed character in the Old Testament. Sexually molested as a child, she married an abusive man, who would later hang himself at home. Years after that, her teenage daughter was hit by a truck and died. “I’d been holding it together my entire life,” she says. “But when I heard my child was gone I just started sobbing and couldn’t stop. I felt this pain that I thought was going to kill me.”
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 once a week. The routine was always the same: A nurse would give her propranolol, wait for the drug to take effect, and then have her read her life story out loud. The first few weeks were excruciating. “I was a mess for days afterward,” she says. “I couldn’t believe I’d signed up for this.” But then, after five weeks of therapy, Lois felt herself slowly improve. She would still cry when describing the death of her daughter—Lois cried during our interview—but now she could stop crying. “That was the difference,” she says. “I still remembered everything that happened, and it still hurt so much, but now I felt like I could live with it. The feelings were just less intense. The therapy let me breathe.”
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 neurologist named Todd Sacktor became obsessed with this mental mystery. His breakthrough came from an unlikely source. “My dad was a biochemist,” Sacktor says. “He was the one who said I should look into this molecule, because it seems to have some neat properties.” Sacktor’s father had suggested a molecule called protein kinase C, an enzyme turned on by surges of calcium ions in the brain. “This enzyme seemed to have a bunch of properties necessary to be a regulator of long-term potentiation,” Sacktor says. “But so did a bunch of other molecules. It took me a few years to figure out if my dad was right.”
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.

Photo illustration: Curtis Mann; Photo: Doug Kanter/Getty

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, the overall cost of substance abuse exceeds $600 billion a year. Previous attempts to treat drug addiction with drugs have largely failed; methadone is among the best, and it’s not that good. But addiction is driven by memory—associating the high with a crack pipe, or the buzz of nicotine with the smell of smoke—which means that reconsolidation therapy offers some hope. Studies of morphine-addled rats have found that a few doses of a PKMzeta inhibitor can eliminate their cravings. Nader, meanwhile, has just begun a trial in which cocaine addicts are given propranolol and then shown a drug-related cue, such as a video of people shooting up. Because the blood-pressure medicine dials down their basic emotional response to the world—it reduces symptoms of stress but also inhibits expressions of pleasure—Nader believes it can slowly diminish the desire for illicit substances. “The craving is a learned association,” he says. “We’re hoping to weaken that association over time.”
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.

World's first biodegradable joint implant grows new joints

http://www.gizmag.com/regjoint-biodegradable-joint-implant/21655/

By Ben Coxworth

Joint implants should always be made of materials like titanium, so they can last the lifetime of the patient ... right? Well, not according to researchers at Finland's Tampere University of Technology. They've developed a product known as RegJoint, which is reportedly the world's first biodegradable joint implant. Unlike permanent implants, it allows the patient's bone ends to remain intact, and it creates a new joint out of their own tissue.
In arthritic joints, the cartilage that protects the connecting ends of the bones has become compromised. This allows the bones themselves to grate against one another, causing pain and reducing the joint's range of movement. A traditional permanent implant replaces the ends of the affected bones with low-friction man-made material.
RegJoint, however, takes a different approach.
The implant has been in development since the mid 90s, and is intended for use in the small finger and toe joints of osteoarthritis and rheumatoid arthritis patients. It is made from a polylactide copolymer, and is inserted within the joint capsule of the affected digit.
Once in place, it reduces pain by acting as a cushioning spacer between the exposed bone ends, while also also restoring a reasonable range of movement, and keeping the already-compromised cartilage from being damaged further. Additionally, however, it triggers the body to produce new fibrous tissue, which proceeds to gradually replace the implant. According to the university, all that's left eventually is a fully-functioning "neojoint," made from the body's own cells.
Recently, RegJoint received CE Mark approval, which will allow it to be sold within Europe - it has already been used in over 200 patients, in clinical trials. Assisting in its development were Conmed Linvatec Biomaterials and Scaffdex Ltd., which is now bringing the implant to market.
Source: Tampere University of Technology