Why do we dream?

You’d think we’d know by now. Everyone dreams, and people have been fascinated by dreams throughout recorded history. But scientifically, their origin and importance remain uncertain. Do they serve some vital psychological or physiological function? Or are they just meaningless accidents of our brain’s wiring?

A few years ago, Finnish psychologist Antti Revonsuo theorized that dreams evolved as a way to rehearse threatening situations.

Silvio Scarone of the Universita degli Studi de Milano in Milan, Italy, explains it this way: “The environment in which the human brain evolved included frequent dangerous events that posed threats to human reproduction. These would have been a serious selection pressure on ancestral human populations and would have fully activated the threat simulation mechanisms.”

For most of the time humans have been evolving, the most common threatening situation was a wild animal attack, and it’s interesting to note that children, often viewed as being closer to their evolutionary ancestors than grown-ups, dream particularly often of animal or monster attacks.

Another bit of evidence is the fact that people who suffer from REM Sleep Behavior Disorder (RBD), who lack the mechanism that normally immobilizes the body during the dreaming stages of sleep, often act out violently: patients flail, kick and punch in their sleep; kick holes in walls; try to jump out windows or set fire to things, or even try to choke those sleeping with them—and often report they were dreaming of fending off attackers, protecting their families, or fleeing a threat.

A 2005 study of 98 patients with RBD showed that they reported having violent dreams more than four times as often as healthy people. In other words, their “threat-simulation system” seems to be hyperactive.

But threat simulation doesn’t completely explain dreaming, which after all isn’t completely focused on threatening situations. Dreams also seem to have a role in the learning process, helping you integrate information your brain absorbed while you were awake. You can often remember things better the day after you learned them than you could at first…which is why “Let’s sleep on it” is valuable advice before making decisions of any sort.

It’s hard to pin down the psychological reasons for dreaming because you can read just about anything you want into dreams (which is why interpreting them has been such a profitable occupation for charlatans for most of human history). Studies show that people attribute more meaning to dreams when it corresponds with their pre-existing beliefs and desires.

So, people consider pleasant dreams about people they like more significant than pleasant dreams about people they dislike, and vice versa—that is, they ascribe more significance to unpleasant dreams about people they dislike than unpleasant dreams about people they like.

Similarly, people who believe in God are more likely to consider any dream in which God speaks to them as meaningful than agnostics, who tend to consider dreams in which God speaks to them more meaningful when God commands them to take a pleasant vacation than when He commands them to engage in self-sacrifice.

In other words, dreams feel meaningful, but the meaning is one we impose based on our waking personalities rather than anything arising from the dreams themselves.

Now a Harvard psychiatrist and sleep researcher says that while there may be psychological value to dreams, their more important function may be physiological.

Dr. J. Allan Hobson holds that during REM sleep the brain is essentially just “warming its circuits” by anticipating the sights, sounds and emotions of the waking state. The metaphor he uses is jogging: just as the body does not remember every step of a jog, but knows it has exercised, so we don’t remember many of our dreams, but our brain has nevertheless been exercised so that it’s ready for the rigors of waking life once more.

In this view, dreams represent a parallel state of consciousness that’s always running, but which is suppressed while we’re awake. When both states of consciousness are in play at once, Hobson says, we get lucid dreaming, the ability to watch a dream as an observer without waking up.

The arguments and research will no doubt continue indefinitely…as, too, will the dreams.

Sleep tight!

Well, you get the idea. Fact is, you’re lucky to be getting this column at all.

Which is ironic, because my jumping-off point is an article from Slate, written by Emily Yoffe, titled “Seeking: How the brain hard-wires us to love Google, Twitter, and texting. And why that’s dangerous.”

There’s no doubt that the seeking out of information online is an addictive pastime. I’ve more than once sat up way past bedtime pursuing essentially useless bits of knowledge through the information labyrinth (remember when they used to call it a highway?)…and regretted it when the alarm rang the next morning.

Blame my brain.

Washington State University neuroscientist Jaak Panksepp, writes Yoffe in Slate, says this is an example of “seeking,” what he calls “the granddaddy” of the emotional systems hard-wired into all mammalian brains.

“What’s my motivation?” Method actors stereotypically demand of directors. For mammals, Panksepp believes, it’s seeking, which is so strongly innate that animals in captivity prefer to search for their food rather than have it delivered to them.

But unlike most animals, humans seek out not just concrete physical rewards, but abstract mental rewards such as new ideas and connections.

At the heart of this system is the neurotransmitter dopamine, which, Panksepp says, promotes “states of eagerness and directed purpose,” states that feel so good to us we want as much of them as we can get…and sometimes turn to cocaine, amphetamines and other drugs to stimulate them.

When I burn away an hour at the computer without meaning to, then, it’s not my fault, it’s dopamine’s (the stuff also controls our internal sense of time).

At the University of Michigan, psychology professor Kent Berridge and co-researchers use the term “wanting,” instead of seeking, companion to another system they call “liking.”

Berridge says that whereas “wanting” is driven by dopamine, “liking” is driven by our opioid system, providing a feeling of fulfillment and contentment and temporarily removing the desire to seek. Eat a big meal, and the thought of even a dinner mint no longer appeals.

But, notes Berridge, our brains are “more stingy with mechanisms for pleasure than for desire,” so that we spend much more time in the “wanting” mode than in the “liking” mode.

Evolutionarily speaking, that’s important (which is why it’s so). If we did not want and seek, we would be like the rats whose dopamine neurons have been destroyed: they’ll starve to death in a cage full of food because they’ve lost the desire to go get it.

But if these systems get out of whack, we end up in trouble. Berridge believes addiction results when the wanting, rather than the liking, takes precedence, so that addicts are driven to continually seek out the whatever-it-is-they’re-addicted-to, even though the pleasure of actually having that thing becomes progressively less rewarding.

Which brings us back to Google, Twitter, “push” emails (thanks, Blackberry!), etc., etc. We’re addicted to the search for novelty, victims of our dopamine-drugged brains.

The dopamine system, Yoffe notes, can be activated by cues that a reward is coming. When your computer dings to tell you you’ve got mail, or your phone buzzes on your belt, it’s triggering your brain to expect a reward, just like Pavlov’s famous ringing bell triggered the brains of conditioned dogs to salivate on cue.

Trouble is, when we respond, we only receive a tiny bit of information—an email, a text message, a Tweet—which is not enough to satisfy. We’re like rats who, given just a little bit of sugar, end up in a state of “panting appetite,” searching frantically for more.

Yoffe quotes Temple Grandin, author of the book Animals in Translation, who writes of driving cats crazy by flicking an uncatchable point of laser light around a room. They’ll chase it for hours, she notes; and yet, if they were in the wild, this kind of “mindless chasing” could prove fatal, “because it short-circuits intelligent stalking behavior.”

Hmm. Sounds like an interesting book. Think I’ll Google it.

Be right back…

Now, the writing of fiction is a very odd thing, in that it involves the making up of characters: people who don’t really exist, but for whom the illusion of existence is created by the words the author puts on the page.

Quite often, these people are very different from the author. I recently interviewed renowned Canadian science fiction writer Robert J. Sawyer for FreeLance, the magazine of the Saskatchewan Writers’ Guild. The main character in his latest book, Wake, is a blind teenage girl, Caitlin Decter. Now, although Sawyer can draw on some experience at the age of 12 of being blind (eyes bandaged) for a few days, he has never been, nor will he ever be, a teenage girl.

But as he puts it, “The most interesting thing as a writer is to try to put yourself in somebody else’s shoes, get inside somebody who is not like you. It’s like being an actor. No ambitious actor wants to play the part that’s closest to who he or she actually is. They want to play the part that’s the biggest stretch for them.

“I’m writing my 20th novel. I’ve written a hundred significant characters. If they were all middle aged bald white guys who watched way too much Star Trek when they were young, they’d be boring.”

In a way, it sounds impossible, to “get inside somebody who is not like you.” But in fact, we all do it all the time, predicting how other people will react to a given situation, even if it isn’t one we’ve experienced ourselves…and scientists have just begun to figure out the brain mechanisms that enable us to do so.

And interestingly enough, the work is based on the study of people who are congenitally blind…like Caitlin Decter.

Our ability to figure out what other people are thinking is called “theory of mind,” and there are two main theories about how it works.

One, called simulation, suggests that when we try to figure out other people’s mental reactions to an event, we try to match experiences we’ve had to the experience the other person is having.

The other theory proposes that we each carry within our brains an abstract model of how minds work, just as we have a model of how the physical world works. Just as we know that if we drop a watermelon from a ten-story building it will splatter, even though we’ve never actually done it, we can figure out how other people will react to an experience even if we’ve never had a similar experience ourselves.

MIT neuroscientists Marina Bedny and Rebecca Saxe decided to test these competing theories by studying congenitally blind people who, since they’ve never had visual input, can’t reason about the visual experiences of others the way sighted people do. The example they give is that while a blind person could understand the experience of being happy at seeing a love letter from a boyfriend, she would have no memories of that exact experience herself.

However, Bedny and Saxe found that blind people performed just as well in predicting the feelings of other people as sighted people did. Not only that, fMRI (functional magnetic resonance imaging) brain scans revealed that blind people and sighted people used the same brain regions when predicting other people’s mental states—even though other studies have shown that the brains of blind people can reorganize themselves, giving over the cortex that normally processes visual information to language processing, for example.

All of which seems to indicate that we can understand other people’s experiences because we carry a model of how human brains work within our own brain, not because we’ve necessarily shared similar experiences.

Which brings me back to writing. There’s an old adage to “write what you know,” and yet writers—especially science fiction writers—often write about things they could never possibly experience, and readers are quite capable of understanding and enjoying those impossible experiences.

It seems to me that if we could only understand other people’s experiences if we’d had similar experiences ourselves, writing fiction—especially science fiction—would be impossible.

In other words, Bedny and Saxe, nice study—but I could have told you that.

Um, not so fast.

A year and a half ago, scientists at the Blue Brain Project in Switzerland announced they had successfully created an extremely detailed—down to the molecular level—model of the neurocortical column of a two-week-old rat…and that was just Phase 1 of their ambitious research effort aimed at nothing less than reverse-engineering the mammalian brain and recreating it in a computer.

The neurocortical column (NCC) is the basic unit of the neocortex, which in mammals is responsible for higher brain functions and thought.

“The thing about the neocortical column is that you can think of it as an isolated processor,” Blue Brain Project founder Henry Markram of the Brain and Mind Institute at the École Polytechnique (EPFL) in Lausanne, recently told BBC News. “It is very much the same from mouse to man—it gets a bit larger and a bit wider in humans, but the circuit diagram is very similar.”

At the Science Beyond Fiction conference in Prague last month Markram said the researchers are now taking their simulated NCC and inserting it into a “virtual reality agent”—a computer simulation of an animal. As the virtual animal moves around a virtual space, the researchers will observe the detailed activities in the column, and closely compare the results of their model with what is known about real NCCs in real rats, to ensure their model is accurate.

Once they’re satisfied with their model rat NCC, they can use it as a basic template on which to build models of NCCs from other species.

The computing power involved is, of course, immense. For its first phase, Blue Brain used an IBM Blue Gene supercomputer with more than 8,000 processors. It provided “only just enough” power: Markram estimates it can probably simulate about 50,000 fully complex neurons (brain cells) in close to real time. The rat NCC has about 10,000 neurons; at the upper end of the scale—that would be us—the NCC has 100,000 neurons.

And remember that the NCC is only the most basic element of the neocortex. The human neocortex has millions of NCCs. The hope is, however, that by creating an extremely detailed, accurate copy of a simple NCC at the molecular level, the researchers will then learn to create a simplified version that performs the same way but doesn’t require as much computing power.

However you slice it, they’re a long way now from where they’d like to get to…but remember, since 1958, computer power has doubled approximately every two years, and that trend is continuing. (This is called Moore’s Law, after Intel co-founder Gordon E. Moore, who noted the trend in 1965.)

Blue Brain is moving up to the next generation of supercomputer—and with it will be able to add in all the molecules and biochemical pathways in their model NCC, something they couldn’t do with their first machine.

All well and good, but what’s the point? After all, humans are already pretty good at making copies of the human brain: every child has one.

True, but it’s impossible to study a real human brain at this level. A computer simulation, unlike a brain, can be slowed down or even stopped so processes can be observed in detail. From that basic knowledge all sorts of benefits could flow.

For example, Markram believes that in a decade or two doctors may be able to draw on an enormous database to simulate patients individually to better predict how they’ll respond to a given drug or treatment.

More excitingly, Markram believes that as the computer simulation of the brain grows in complexity, “emergent properties” may arise…things like thought and creativity.

Will a computer-simulated brain someday create a new work of art or scientific invention?

Markram has a straightforward answer. “It’s not a question of years, it’s one of dollars. The psychology is there today and the technology is there today.

“It’s a matter of if society wants this. If they want it in 10 years, they’ll have it in 10 years. If they want it in 1,000 years, we can wait.”

Lovely lyrics. But as a kid, I thought it would have made more sense for Denver to sing, “Sunlight in my eyes can make me sneeze.” Because for somewhere between one in 10 and one in three people, sunlight has exactly that effect.

It’s called “photic sneezing,” and it’s nothing new: Aristotle wondered about it in the 4th century BC (although he thought it was brought on by heat, not light). But millennia later, we still don’t know exactly why it happens, as New Scientist writer Richard Webb recently discovered.

The usual explanation for regular sneezing is that it serves to expel unwanted material from the airway. A regular sneeze begins with an irritation in your nose. This excites the trigeminal nerve, which sends impulses to the “sneezing center” in the brainstem, the primitive part of the brain that triggers our involuntary reflexes.

The sneezing center sends impulses along the facial nerve ordering the nasal passages to secrete fluid, and simultaneous impulses along the spinal cord to the respiratory muscles, prompting them to take a quick, deep breath (“Ah-”), then expel it with great force (a 150-kph “Choo!”). The abdominal, chest, vocal cord and throat muscles are all in on the act, as is your diaphragm and even your eyelids (you always close your eyes when you sneeze).

Sneezing is, as Webb notes in his article, “one of the most violent actions your body will ever perform,” so violent that cases of sneezing-caused whiplash are not unknown.

With today’s sensitive brain-scanning equipment, you’d think it would be a simple matter to track down the precise location of the “sneezing center.” But you’d be wrong. And since we can’t pin down the specific neurons involved, we can’t pin down how photic sneezing arises, either.

We do know a few things about it. In 1964 Henry Everett, a consulting psychiatrist at the Johns Hopkins University Hospital in Baltimore, Maryland, made one of the first systematic studies of the condition, questioning 75 of his patients and 169 of his students in detail about their sneezing habits. Among other things, he asked those with photic sneezing (18 percent of the patients and 24 percent of the students) if they had any close relatives who reacted to sunlight the same way, and found that 80 percent of the sneezers said they did, compared to only 20 percent of the non-sneezers.

This strongly indicated that photic sneezing has a genetic component, and further studies have borne that out. In fact, its inheritance is consistent with transmission via a dominant gene, meaning you only need one copy of it from either parent. This is known as autosomal dominant transmission, so photic sneezing now has the irresistible scientific name of “autosomal-dominant compelling helio-opthalmic outburst,” the acronym for which is, of course, ACHOO.

But that still doesn’t answer the question of why sunlight should make us sneeze, and as Webb found, at the moment nobody actually has an answer.

Not that there aren’t theories. Other things unrelated to nasal irritation can cause sneezing, after all. A study last year revealed there are patients who sneeze when they have an orgasm—or even simply in response to sexual thoughts.

Maybe all of these strange causes of sneezing come about because of a kind of short-circuit in the brainstem, where all kinds of reflex actions are triggered, so that various stimuli that trigger unrelated reflexes such as blood flow to the genitals or squinting against a bright light also trigger, quite by accident, a sneeze. The genes that create these short-circuits are more nuisances than threats to survival, and so have been preserved by evolution.

Which sounds plausible, but there isn’t actually any solid evidence for it. Or as Webb quotes Louis Ptácek, a neurogeneticist at the University of California in San Francisco, as saying, “People speak as if they know what the hell’s going on. In reality, we don’t.”

As our tools for studying the brain improve, maybe we’ll figure it out. In the meantime, if sunlight makes you sneeze, try to follow Aristotle’s example:

Just be philosophical about it.

Until recently the only way to measure an emotion scientifically was to focus physiological changes such as an increased heart rate, a change in body temperature, or enhanced (or inhibited) activity on the part of certain glands. But new technology, such as positronic emission tomography (PET) and functional magnetic resonance imaging (MRI), has enabled scientists to see which parts of the brain are most active when subjects are feeling various emotions.

Dr. Richard Davidson, director of the Laboratory for Affective Neuroscience at the University of Wisconsin, has discovered that positive and negative emotions produce activity in very different parts of the brain.

His research reveals that people experiencing anxiety, anger or depression show the most brain activity in the right prefrontal cortex (just behind the forehead), while those experiencing positive, outward-reaching emotions show more activity in the left prefrontal cortex. Not only that, people seem to be disposed, both genetically and by their formative experiences, toward being either more left-brained or right-brained–i.e., more cheerful or morose.

Hundreds of readings have shown that the general population forms a standard bell-curve distribution, with the relatively few who tilt farthest toward the right-brain end of the curve more likely to suffer clinical depression or an anxiety disorder, while those few on the far left end of the curve less likely to suffer from negative moods and more likely to recover from them rapidly.

One of the people Dr. Davidson scanned was a senior Tibetan lama, who turned out to have the most extreme value to the left–“happy”–side of the brain of the 175 people he had studied to that point. The question was, did the lama’s meditative training produce that value, or was it just an individual quirk?

In collaboration with Dr. Jon Kabat-Zinn, founder of the Mindfulness-Based Stress Reduction Clinic at the University of Massachusetts Medical School in Worcester, Mass., Dr. Davidson conducted a small study on the effects of training in mindfulness meditation. Based on the Buddhist meditation practiced by Tibetan lamas, but stripped of its religious context, mindfulness meditation involves learning to monitor sensations and thoughts, both while sitting quietly and during activities like yoga exercises, and to drop those that might lead to a negative mood.

Workers in a high-pressure biotech business, who started out, on average on the right-brain side of the emotional distribution, and complained of feeling highly stressed, studied mindfulness meditation for three hours a week over two months.

The results were promising. After the training, on average the workers’ emotions ratio had shifted leftward, and their moods had improved: they reported feeling more engaged in their work, more energized and less anxious. (And as an added benefit, their immune systems seemed stronger: they had more flu antibodies in their blood after they received flu shots than a control group.)

Dr. Davidson and other scientists in this field met with the Dalai Lama in India in March 2000, and with his blessing, Dr. Davidson is now studying other Tibetan lamas who have completed at least three years of solitary meditative retreat.

Even if you’re not prepared to sit in the lotus position and chant “om,” you may be able to improve your mood. Three related studies conducted by Will Fleeson, associate professor of psychology at Wake Forest University in North Carolina, have shown that if you’re feeling unhappy, you can make yourself happier simply by acting as if you’re happy.

In each study, about 50 randomly selected university students carried handheld computers for up to 10 weeks, regularly recording their answers to a set of questions about their mood and activities.

The study showed the subjects invariably felt happier when they were acting extroverted: singing aloud with a song, walking over and talking to someone, asking a question in class. Further studies showed that subjects who were asked to be assertive and energetic during group discussions were then judged, both by themselves and by others, to be significantly happier afterward then those who were asked to be passive and reserved.

In other words, the mere act of pursuing happiness may make you happier–maybe even happier than catching the thing you began to pursue in the hope it would make you happy!

Good hunting!

Why do we crave this unique food? It’s not just the taste. As new research has shown, a lot of the pleasure we get out of eating chocolate is purely in our heads.

First, we should abolish some of the most pernicious myths about chocolate. Eating chocolate does not cause acne, nor does it aggravate existing acne. Studies at both the Pennsylvania School of Medicine and the U.S. Naval Academy showed that eating chocolate or not eating chocolate had no impact on acne. (Additional studies have found that diet in general is not linked to acne.)

Second, chocolate has not been proven to cause cavities or tooth decay, and in fact there are indications that the cocoa butter in chocolate coats the teeth and may even prevent plaque from forming. Yes, the sugar in chocolate can contribute to calories, but no more than the sugar in any other food.

I can’t, alas, say that chocolate is not fattening. It is a high-calorie food, and you will gain weight if you take in more calories than you’re expending in exercise, but that’s not a fault in chocolate per se; the solution to that “problem” is simply to eat it in moderation.

The cocoa butter in chocolate contains saturated fat, which can increase blood cholesterol levels. However, recent research at the University of California, Davis, shows that chocolate also contains lots of antioxidant chemicals called phenolics, which may help lower the risk of heart disease (coffee and tea also contain high levels of phenolics). Phenolics are also found in red wine. The plants from which these foods (and others) are derived probably make the phenolics to protect themselves against insects and disease, but in our bodies phenolics apparently prevent fat-like substances in the bloodstream from oxidizing and clogging the arteries.

“May” help lower the risk of heart disease is the important qualifier to note in the paragraph above. Phenolics are definitely anti-oxidants, but so far there aren’t any really compelling, large-scale human studies to show if consuming them is beneficial. Still, it’s nice to think that eating a piece of chocolate might be as helpful as it is harmful, isn’t it?

All of this is very interesting, but it still doesn’t explain exactly why we like to eat chocolate so much. For answers to that question, we need to move from the bloodstream to the brain.

Chocolate contains more than 300 known chemicals, and many more unknown ones. Scientists have already found several chemicals that alone and in combination definitely have an impact on the way we feel.

One of the most obvious is caffeine, but there’s not that much of it in chocolate–certainly nothing like the amount found in coffee. However, there is another weak stimulant, called theobromine, present in slightly higher amounts, and these two working together could be enough to give us a lift when we eat chocolate–especially in conjunction with another chemical found in chocolate called phenylethylamine, a substance related to amphetamines. All three of these stimulants make us more alert by increasing the activity of neurotransmitters, the chemicals our brain uses to communicate with itself.

But we could be getting more out of chocolate than just a mild mental stimulation. Researchers at the Neurosciences Institute in San Diego think chocolate has an effect on the brain related to the effect of marijuana.

Brain cells have a receptor–a structure on their surface that can lock onto certain molecules–for a neurotransmitter called anandamide, which is produced naturally in the brain. When this receptor was first located, however, it wasn’t because it locks onto anandamide–it was because it also locks onto a substance called THC (well, actually it’s called tetrahydrocannabinol, but THC is much easier), the active ingredient for marijuana.

Anandamide, researchers speculate, may play a role in natural feelings of euphoria, those moments when everything feels wonderful and five minutes can seem like an hour–which is why THC, when it locks onto the anandamide receptor, makes us feel “high.”

THC isn’t found in chocolate (much to the relief of chocolate makers); however, chocolate does contain two chemicals that inhibit the natural breakdown of anandamide. That could mean that when we’re already feeling good, chocolate makes us feel even better by prolonging the euphoria.

Another study seems to indicate that eating chocolate causes the brain to produce more “opioid” chemicals. “Opioid” chemicals also make us feel good–the similarity to the word “opiate” is intentional. Adam Drewnowski of the University of Michigan found that chemically blocking receptors for opioid chemicals in the brain decreased the consumption of high-fat chocolates by compulsive eaters by more than half.

It’s a fascinating field of study. In fact, I think it’s so fascinating that, if anyone in Saskatchewan is currently pursuing chocolate research, I would like to offer myself up right here and now as a test subject. I pledge to eat as much chocolate as is necessary to get to the bottom of this.

It’s the least I can do.

Okay, so forgetting whether a dog was an Afghan or a St. Bernard isn’t a big deal. But all of us can cite similar experiences. We remember things that never happened, forget things we shouldn’t, and yet, for some reason, can still sing jingles to TV commercials from when Pearson was prime minister.

Still, the fact our memories are sometimes unreliable isn’t nearly as remarkable as the fact that we have memories at all: that somehow, we can call up sights, sounds and feelings from months, years, or decades ago. It’s almost like time travel!

There are three main types of memory: short-term, middle-term, and long-lasting. Short-term memory lasts just a few seconds, long enough for us to dial a number we looked up in the phone book, for example

Middle-term memory lasts a few hours. It reminds us whether we’ve had lunch yet or that we’re supposed to take the kids to the dentist this afternoon. But it fades; by Thursday, you will have forgotten most of Monday.

Sometimes, middle-term memory becomes long-lasting memory, which remind us of what we’ve done in the past, of goals we’ve set for ourselves, of joys and disappointments. Our long-lasting memories are, in a sense, ourselves: they’re inextricably intertwined with our identities.

Whenever any new information enters the brain–say, somebody’s name–it does so in the form of electric impulses, passed from neuron to neuron (the nerve cells that are the brain’s basic building blocks). These impulses die away in milliseconds, but their passage reinforces a particular pattern of connections among a particular set of neurons, making it possible for the brain to recreate the name. The more often that pattern is reinforced, from hearing the name again or thinking about it, the more likely it will become a long-lasting memory. Whereas short-term and middle-term memory involve only chemical changes in the neurons, long-lasting memory is “hard-wired”–the synapses that link the neurons involved grow thicker and stronger.

Most of us constantly edit, ignore and overlook information, rather than committing it all to memory. A few people remember everything, and they find the enormous flood of memories associated with every person, event and object makes it difficult for them to interact normally with people or hold down a job. The best known example, a Russian named Shershevsky, ended up as a Vaudeville act.

The editing and sorting process, however, leaves us open to false memories. Several studies have shown just how easy it easy to create these. For example, volunteers who listen to a list of related words, such as “bed,” “dream,” “blanket,” “doze” and “pillow,” when later asked to recall the words they heard, will often include another related word, “sleep,” which wasn’t on the list.

Then there’s “hindsight bias.” Suppose you see a picture of a politician and you think, “He has shifty eyes.” If that politician is later convicted of misusing public funds (not that THAT would ever happen), you’re likely to be convinced that the first time you laid eyes on him, you thought, “What a crook.” Since later events proved your initial negative reaction to be justified, you become convinced you were much more perceptive than you really were.

Entire events can also be created out of nothing. In another study, college students were prompted on two consecutive days to imagine having spilled a bowl of punch at a wedding as a child. The next day, several of those students were convinced they really had spilled a bowl of punch at a wedding. Typically, they inserted the false memory into a larger, more accurate memory of a particular wedding…just as my friend inserted a St. Bernard into a scene that really involved an Afghan.

We may eventually be able to distinguish between false memories and real ones: recent research with PET scans shows that real memories activate regions of the brain related to sensory input, whereas false memories do not.

Someday, we may be able to settle the St. Bernard/Afghan question–or your personal equivalent–once and for all.