Posts Tagged ‘ drugs ’

Drugs, Neuroscience, and You

Let’s be honest here: if a person really wants to try an illegal drug, he or she is going to find a way to try it. To me, the most reasonable response to this fact seems to be to share clear, science-backed explanations of the effects and risks involved with each drug.

So today, I’m going to take a little break from my usual newsy reporting, and provide a condensed rundown on some drugs, in the style of my Memory Menagerie write-up.

First, just a couple quick notes about this summary. For one thing, it’s going to focus on drugs that are illegal in many places, for the simple reason that it’s (understandably) not easy to get clear scientific info about them. (If you’re interested in a similar write-up about psychiatric prescription drugs, though, drop me a comment and I’ll happily write one.) Anyway, my goal here is to inform and educate – not to advise or condone anything. To be annoyingly literal about this: I’m not suggesting that you take illegal drugs.

Second, I also can’t cover every drug that’s available today – spend a few minutes on, and you’ll see that there are dozens, if not hundreds of them. So I’m going to stick to the ones you’re most likely to hear about. And that brings up my final note: my main goal here isn’t to be exhaustive or in-depth, but to provide a quick overview of major “street drugs” on a single page, simply because one-page collections of quick scientific info on illegal substances are (oddly enough) hard to come by.

And now, without further ado…let’s talk about some drugs.

Cannabis (marijuana)1

What it is: A resin that grows on the female buds of plants in the genus Cannabis. The word “marijuana” seems to have first come into use as a slang term (of unknown origin) in Mexico in the 1800s.
What it does: Physically, ingestion of the drug causes bloodshot eyes, dry mouth, increased heart rate, and muscle relaxation. Mentally, it produces a “high” – a feeling of euphoria. Beyond this, its psychological effects vary widely from user to user. Some common effects, though, include reduction of stress-related feelings, increased appreciation of art and music, increased tendency to laugh, increased appetite, a distorted sense of time, a variety of degrees of amnesia, and a tendency toward metacognition (thinking about thinking) and introspection. Another notable aspect of the high is that certain internal thoughts – especially those linked with strong emotion – seem extraordinarily vivid. If someone with an anxiety-related disorder uses cannabis, these effects can become tinged with negativity, and paranoia may set in, sometimes leading to a panic attack. As with many drugs, the boundary between positive and negative effects is easily crossed, and constant careful monitoring of one’s set and setting is crucial. Depending on the dose, effects can last from 30 minutes to eight hours. Though this drug is not chemically addictive, a large number of users develop a psychological dependency on it.
How it does this: A variety of cannabinoids bind to a range of receptors involved in the body’s natural endocannabinoid system, which blocks communication between neurons within their own areas.  Most prominent among the cannabinoids in cannabis is Δ9tetrahydrocannabinol, often known as THC. It binds to CB1 and CB2 endocannabinoid receptors in a wide range of brain areas, including the amygdala, the hippocampus, and the nucleus accumbens. The exact relationship between the neurochemistry of the “high” and many of the side effects above remains poorly understood.

Cocaine (coke)

What it is: A crystalline alkaloid, a chemical compound found in the leaves of the Coca plant. It was first isolated by the chemist Friedrich Gaedcke in 1855.
What it does: Physically, cocaine acts as a stimulant, raising heart rate, increasing feelings of energy, raising confidence and enthusiasm, and providing an otherwise euphoric and alert “high.” Cocaine also acts as a mild to moderate local anesthetic. In many users, the drug also greatly reduces patience and attention span, and contributes to feelings of anxiety or paranoia, especially after repeated use. Effects usually last from 15 minutes to an hour. This drug is highly addictive – withdrawal symptoms can include irritability, anxiety, fatigue, anhedonia (inability to feel pleasure) and insomnia.
How it does this: Cocaine molecules bind to sites on neurons called dopamine transporters, which normally help reabsorb dopamine – a neurotransmitter involved in feelings of reward – for future use. When the cocaine molecules bind to the dopamine transporters, they block these transporters’ function, keeping dopamine in the synaptic clefts much longer than usual. The result is that many brain pathways – in regions like the nucelus accumbens, the ventral tegmental area, and the prefrontal cortex – are bathed in dopamine, raising reward feelings far above the norm.

Psilocybin (mushrooms)

What it is: A chemical produced by more than 200 species of mushrooms – but mainly associated with the mushroom Psilocybe mexicana.
What it does: Physically, the drug tends to cause lethargy and drowsiness, disorientation, intensified reflexes, pupil dilation, and increased heart rate. As with most psychedelics, psychological effects vary widely from person to person, and depend heavily on set and setting. Feelings of euphoria or depression are common, as are enhanced appreciation of colors or shapes, and a distorted sense of time. Closed- and open-eye hallucinations vary from mild to intense depending on the dose, and can range from simple moving colors, shapes and patterns all the way to entheogenic experiences and dialogues with hallucinated beings. Effects can last from six to twelve hours, or possibly longer.
How it does this: The human body rapidly converts psilocybin to psilocin, a chemical that acts as a partial agonist to several types of serotonin receptors, especially the 5-HT2A receptor (serotonin is also known as 5-hydroxytryptamine, or 5-HT). Serotonin’s exact role in psychedelic effects remains poorly understood, but it’s known that this neurotransmitter is involved in regulating moods, and increasing feelings of well-being.

LSD (acid)

What it is: A semi-synthetic chemical originally derived from ergotamine, a substance found in ergot, a fungus that often grows on rye grain. It was first synthesized by the chemist Albert Hofmann in 1938, but he didn’t make his first (self-administered) test of LSD until 1943.
What it does:
Physically, the drug raises alertness, causes pupil dilation, raises or lowers body temperature, and increases or decreases appetite. As with most psychedelics, LSD’s psychological effects vary widely from person to person, and depend heavily on set and setting. Many users perceive movement of static surfaces like walls, as well as intensified perception of colors, brightness, iridescence, and shininess. Higher doses can trigger closed- or open-eye hallucinations of geometric patterns, echo-like distortion of sounds, and synaesthesia. Because the drug often intensifies emotions, some users can descend into “bad trips” involving panic attacks or even fragmentation of identity. However, the overall euphoric “high” sustained by LSD means a calming friend can sometimes help turn a bad trip back into a positive one. Effects usually last from four to twelve hours.
How it does this: LSD binds to many types of serotonin receptors, including 5-HT1A, 5-HT2A, 5-HT2C, 5-HT5A, and 5-HT6. At 5-HT2A, in particular, it acts as a strong partial agonist, helping trigger the release of glutamate throughout the cerebral cortex. Some research suggests that LSD may preferentially bind to less-used 5-HT receptors, triggering synaptic activity along little-used pathways. Exactly how all this contributes to the drug’s psychedelic effects remains poorly understood, but it’s likely to be linked with serotonin’s excitatory effects in the prefrontal cortex.

Salvinorin A (salvia)

What it is: A chemical found in the plant Salvia divinorum, a member of the sage family.
What it does: As with most psychedelics, salvinorin’s psychological effects vary widely from person to person, and depend heavily on set and setting. Some common effects include uncontrollable laughter, sensations of movement, distortions of time, distortions of body boundaries and perceived location, closed- or open-eye hallucinations of membranes or geometric patterns, vivid reliving of memories, synaesthesia, and glossolalia. Some users report feelings of euphoria, while others descend into fits of rage or panic attacks. Length of effects varies widely depending on the dose and method of ingestion – the experience can last from one minute to several hours.
How it does this: Salvinorin is a strong agonist for the κ-opioid receptor, and an even stronger partial agonist for the D2 dopamine receptor – thus, it increases availability of opioids and dopamine. Research on where this activity is mainly targeted, and what its relationship is to salvinorin’s psychedelic effects, remains in very early stages. Interestingly, though, salvinorin has no affinity for the 5-HT2A serotonin receptor, which is heavily affected by drugs like psilocybin, LSD, and mescaline – so salvinorin’s effects may be produced via entirely different neurochemical pathways.

MDMA (ecstasy)

What it is: A chemical first synthesized in 1912 by Merck chemist Anton Köllisch; its original intended use was to stop abnormal bleeding. It was derived from safrole, an oil extracted from the sassafras plant.
Important note: The term “MDMA” refers to the pure chemical; many tablets described as “ecstasy” also contain other substances, such as dextromethorphan or amphetamine.
What it does: Both physically and psychologically, the effects of the drug are more similar from user to user than those of many psychedelic drugs. Physically, it causes loss of appetite and exerts tension on muscles, which often results in behaviors like mild twitching or jaw-grinding. Psychologically, its most notable effect is that it raises alertness and produces a euphoric mental state, characterized by high energy, strong feelings of empathy and intimacy, heightened self-confidence, and sexual arousal. Effects last from 1.5 to 3 hours. The “comedown,” (i.e., aftereffects) of ecstasy can include dysphoria (feelings of unpleasantness), anxiety, and – in some cases – even prolonged depression.
Why it does this: MDMA triggers neurons to release serotonin, dopamine and norepinephrine. By blocking the actions of the vesticular monoamine transporter protein, which normally would help reabsorb norepinephrine, MDMA prolongs and heightens the availability of this neurotransmitter. It also acts as a weak agonist at 5-HT1 and 5-HT2 serotonin receptors, which increases the concentration and availability of serotonin – LSD acts as a partial agonist at some of these same receptors. Some scientists have suggested that MDMA also increases availability of oxytocin, the hormone present in high concentrations in a mother’s body during childbirth.

Nitrous oxide (balloons)

What it is: A chemical compound composed of sets of two nitrogen atoms bonded to one oxygen atom, usually in gas form.
What it does: At low doses, nitrous oxide has an anti-anxiety effect. It also produces dizziness, euphoria, and a feeling of being intensely in tune with somatosensory sensations. Effects often last only a few minutes, though they can be prolonged by repeated doses over a given time period.
How it does this: Nitrous oxide activates dopaminergic neurons in the ventral tegmental area and nucleus accumbens – areas known to be involved in addiction and reward. It also moderately blocks NMDA glutamate receptors, which play crucial roles in memory and learning, as well as β2-subunit-containing nicotinic acetylcholine (ACh) channels,which respond to nicotine-like chemicals. Meanwhile, it weakly inhibits AMPA and kainate glutamate receptors, GABAC receptors, and 5-HT3 serotonin receptors, while potentiating GABAA and glycine receptors – all of which modify synaptic likelihood and range in a wide variety of ways.


What it is: An acid that naturally occurs in small amounts in the central nervous systems of most animals. Synthesis of the chemical was first reported in 1874 by chemist Alexander Zaytsev.
What it does: Though it’s sometimes described as “liquid ecstasy” (i.e., MDMA), GHB can produce a much broader range  of effects than MDMA does, depending on the dosage. At low to moderate doses, its effects are indeed very similar to MDMA: it acts as a stimulant and produces euphoria, decreased anxiety, and increased sociability – often with a more serene emotional tenor than the typical MDMA experience. At higher doses, though, it can act as a dissociative or a sedative, and has even been reported to trigger “blackout” fugue states in some users. Depending on the dose, effects may last from 1 to 5 hours.
How it does this: GHB is an agonist at the excitatory GHB receptor, and it’s a weak agonist at the GABAB receptor, which is inhibitory. GHB induces the accumulation of either a derivative of tryptophan or tryptophan itself in the extracellular space, possibly by increasing tryptophan transport across the blood-brain barrier. Activation of the GHB receptor in some brain areas seems to contribute to the release of the excitatory neurotransmitter glutamate. Interestingly, low concentrations stimulate dopamine release via the GHB receptor, while higher concentrations inhibit dopamine release via GABA(B) receptors.

2C-B (nexus)

What it is: A chemical first synthesized as an anesthetic by chemist Alexander Shulgin in 1974.
What it does: At low doses, many users experience aphrodisiac effects, increased energy, and euphoria. Moderate to high doses can result in jittery feelings, a tendency toward “giggliness,” increased attention to one’s body and thought processes, and difficulty holding one’s concentration on a task (executive attention). Higher doses can produce unique visual and auditory hallucinations – objects can take on “runny” shapes or “watercolor-like” colors. At high doses, these may become full-blown hallucinations; i.e., independent of the user’s actual visuals. Depending on the dose, these effects can last from 1 to 5 hours – but the drug is known to leave residual effects with some users (i.e., the effects of the drug may still be experienced for several hours after the user’s body has metabolized the entire dose); this seems to be more common with higher doses. The “comedown” period has been associated with irritability, headaches, etc., but not all users report these symptoms.
Why it does this: Unlike most hallucinogens, 2C-B has been shown to be a low efficacy serotonin 5-HT2A receptor partial agonist or even full antagonist. This means its effects are produced by other neurochemical pathways than the serotonin pathway used by drugs like LSD and mescaline. Though it’s known that 2C-B contributes to the formation of several chemicals in the liver, their role in its effects is still poorly understood.

Ketamine (special K)

What it is: A chemical first synthesized as an anesthetic by pharmaceutical company Parke-Davis in 1962.
What it does: The drug produces a feeling of “dissociative anesthesia” – a sense of depersonalization or detachment from one’s body. As with other dissociatives, this state is often accompanied by a feeling of euphoria – the tendency of users in dissociative states to report decreased fear responses may also contribute to this feeling. At higher doses, ketamine can result in hallucinations (typically simple closed- or open-eye visuals), and sometimes in the strong dissociation commonly known as a “K-hole,” which is thought to mimic the psychological effects of schizophrenia. Effects often last 60 minutes or shorter.
How it does this: Ketamine acts as an NMDA receptor antagonist. At high, fully anesthetic level doses, ketamine has also been found to bind to type 2 opioid μ receptors, both of which contribute (along with its general tendency to block sodium channels) to its anaesthetic and analgesic effects. It acts as a dopamine reuptake inhibitor, increasing the availability of that neurotransmitter. Effects seem to be primarily focused in the hippocampus and the prefrontal cortex.

PCP (angel dust)

What it is: A chemical first synthesized as a surgical anesthetic in 1926.
What it does: Physically, low doses produce numbness, loss of balance, and slurred speech, while higher doses have analgesic and even anesthetic effects. Psychologically, users report euphoria, increased self-confidence, feelings of invulnerability, changes in body image, and loss of ego boundaries. Higher doses have been reported to lead to paranoia, hallucinations, depersonalization, and suicidal impulses. Depending on the dose, effects may last from 1 to 6 hours.
How it does this: PCP’s primary action is as an antagonist at on glutamate receptors, such as the NMDA receptor – this inhibits the release of the excitatory neurotransmitter glutamate, which is likely a cause of effects like loss of ego boundaries and depersonalization. PCP also inhibits nicotinic acetylcholine receptors – and, like ketamine, it acts as a partial agonist at D2 dopamine receptor sites, contributing to feelings of reward and euphoria.

Mescaline (peyote)

What it is: An alkaloid that occurs naturally in several types of cactus, most notably the peyote cactus (Lophophora williamsii).
Important note: the terms “mescaline” and “peyote” aren’t strictly synonymous; the peyote cactus contains a large spectrum of psychoactive  phenethylamine alkaloids, of which the principal one is mescaline.
What it does: The visual distortions produced by mescaline are somewhat different from those of LSD – rather than perceptions of non-existent objects or persons, they tend to enhance subjective perceptions and modify them in ways that many users find difficult to describe in words. Color and shape are greatly enhanced, and users report experiencing an overwhelming sense of the unique “is-ness” of individual objects. As with LSD, synesthesia is also common. Effects typically last for 12-18 hours.
How it does this: Neurochemically, mescaline acts similarly to other psychedelic drugs like LSD and DMT – it binds to and activates the serotonin 5-HT2A receptor with a high affinity as a partial agonist. How this leads to psychedelic effects is still poorly understood, but it likely involves excitation of neurons in the prefrontal cortex. Mescaline also activates the 5-HT2C serotonin receptor. In addition to serotonin receptor activity, the drug also stimulates dopamine receptors.


What it is: A chemical compound that naturally occurs in small quantities in the central nervous systems of many animals, and is often made from the bark resin of Virola trees. It was first synthesized in 1936 by chemist Richard Manske.
Important note: Although 5-Me-O DMT is often referred to as “DMT,” the two terms are actually not synonymous: 5-Me-O DMT is a close relative  of the chemical DMT, but it’s approximately 4 times as potent. Still, the pharmacology and range of potential effects for both chemicals are highly similar.
What it does: At low doses, DMT and its relatives produce somewhat similar effects to those of psychedelics like LSD and 2C-B – increased appreciation for light, color, and sound, and enhanced brightness and “watercolor-like” colors. At higher doses, the drug can produce powerful entheogenic experiences including intense visuals, euphoria and hallucinations. Effects often last only 5 to 10 minutes, but users have reported that a full-blown “trip” can be shocking in its alienness and intensity.
How it does this: Like other hallucinogens such as LSD and mescaline, a large part of DMT’s psychedelic effects are linked to the drug’s activation of the 5-HT2A serotonin receptor – though, as with these other drugs, the exact linkage between 5-HT receptors and psychedelic effects is poorly understood. Psilocin, an active chemical in many psychedelic mushrooms, is structurally similar to DMT.


What it is: A chemical stew of various psychoactive substances prepared from the South American Banisteriopsis caapi jungle vine. Its usage in certain tribal rituals dates back hundreds – if not thousands – of years.
What it does: Ayahuasca is essentially a preparation specially crafted to allow DMT to be deliverable to the brain when taken orally – so most of its effects are highly similar to those listed in the “5-MeO-DMT” entry above. The chemicals harmine and harmaline – other ingredients in the brew – can cause severe nausea and vomiting, which some users say enhances the intensity of the psychedelic experience.
How it does this: Ordinarily, the chemical MAO-A prevents DMT from crossing the blood-brain barrier – but the chemicals harmine and harmaline are selective and reversible inhibitors of MAO-A, while tetrahydroharmine is a weak serotonin uptake inhibitor. This inhibition of MAO-A allows DMT to diffuse unmetabolized past the membranes in the stomach and small intestine and eventually get through the blood-brain barrier (which, by itself, requires no MAO-A inhibition) to activate receptor sites in the brain.

Methamphetamine (meth)

What it is: A chemical first synthesized from the herb ephedrine by chemist Nagai Nagayoshi in 1893. Fun fact: in World War II, the Japanese military stockpiled vast amounts of this drug, and handed it out to soldiers before battles.
What it does: Physically, the drug often increases heart rate, raises body temperature, and causes tremors or twitching. Psychologically, it creates euphoria and aids concentration – especially on menial and repetitive tasks – increases libido, and raises self-confidence and feelings of power. Higher and/or repeated doses can lead to dermatillomania (compulsive skin picking), hallucinations, paranoia, and sometimes even psychosis. Depending on the dose, effects can last from 3 to 12 hours. This drug is highly addictive, and many former users experience anhedonia (inability to feel pleasure).
How it does this: Methamphetamine causes the norepinephrine, dopamine, and serotonin (5HT) transporters to reverse their direction of flow, leading to a release of these neurotransmitters into the synaptic cleft. The drug also indirectly prevents the reuptake of these neurotransmitters, causing them to remain available for a prolonged period. This leads to feelings of euphoria and reward – and, over time, also contributes to paranoia and addiction.


What it is: A chemical first synthesized from the opioid drug morphine by C. R. Alder Wright in 1874. The usage of opium dates back at least to the third millennium BCE, if not earlier.
What it does: Because heroin is essentially a concentrated form of morphine, which in turn is essentially a concentrated form of opium, this entry will deal with the similar effects of these three related drugs. Users of all three report an intense “rush,” and an acute, transcendent state of euphoria. Many users also report anesthetic and analgesic effects. Depending on the dose and the method of administration, effects may last from 30 minutes to 3 hours. This drug is highly addictive – withdrawal symptoms include dysphoria (feelings of displeasure), anxiety, nausea, diarrhea, fever, restlessness, and insomnia.
How it does this: When taken orally, heroin is metabolized in the digestive tract, delivering morphine to the body and brain. When injected, the drug quickly crosses the blood-brain barrier and is converted into morphine there. In either case, morphine binds to μ-opioid receptors, creating euphoria, analgesia, and anti-anxiety effects. It also stimulates histamine release, leading to a “body high” for many users.

…and there you have it. I’ll do my best to keep updating, refining, and adding to this over time; but for now, I just wanted to make sure it’s available.


1. For all these drugs, I’m going to provide the “real” name, and the most common “unofficial” name. Every drug is known by loads of other slang terms, and more are being coined all the time. My goal isn’t to list them, but simply to make it clear what drug I’m talking about.

Perfect Memory and the Ten Percent Myth

This story begins in a bar.

On the wall-mounted TV, the popular channel Sports Channel was taking a break from the popular show Men in Suits Awkwardly Attempting Rapport to show a trailer for the movie Limitless.

"I haven't seen a shot like that since the last time a sports player took a shot like that!"

I’m not gonna lie – I was intrigued by the plot at first; and not only because literally anything on TV is made more awesome by alcohol consumption.

Plus, I’ve always been fascinated by Flowers for Algernon-type stories, where human minds contain vast potential for genius, just waiting to be unleashed by the right combination of drugs or electrical signals or meditation techniques. As you might guess, it’s one of the major reasons why I like to study the human mind so much – and why I launched this blog.

But a few seconds into the trailer, I heard a line that makes me cringe (or do a whisky-spitting double-take) every time I hear it: “You know, they say we only use ten percent of our brains.” Then the narrator explains he’s taking pills that give him super-human intelligence, which boils down to an ability to remember everything he’s ever seen or heard.

[SCIENCE UPDATE! #1 – I watched Limitless this weekend, and it turns out I wasn’t quite right about that last point. At one point, the movie’s narrator/protagonist describes his experience on the pill by saying that his memories of everything he’d ever seen or heard were incredibly accessible and organized. So presumably the drug did act as a sort of associative and attentive filter (see #2 below).]

Now, I understand that a movie is a work of fiction. But Limitless provides a great opportunity to clear up some confusion that surrounds this ten percent myth. I also want to talk about why the idea that a flawless memory leads to a genius intellect is… well, not so flawless.

Not to point fingers, but psychics are mainly the ones behind this “ten percent” nonsense. The claim seems to have originated in a 1997 book called Reasons to Believe: A Practical Guide to Psychic Phenomena. Since I know this thanks to Benjamin Radford of, I’ll let him tell the rest:

Author Michael Clark mentions a man named Craig Karges. Karges charges a lot of money for his “Intuitive Edge” program, designed to develop natural psychic abilities. Clark quotes Karges as saying: “We normally use only 10 to 20 percent of our minds. Think how different your life would be if you could utilize that other 80 to 90 percent known as the subconscious mind.”

I don’t want to put words in anyone’s mouth, but think what Karges may have been trying to say is that the majority of the human mind’s processing takes place outside the “spotlight” of the subjective consciousness – in other words, that at any given time, we’re only consciously devoting around ten percent of our connectome’s total processing capacity to cognitive tasks, while the rest is being used by the unconscious for its own ends.

Now, at the conceptual level, there’s probably some merit in considering an idea like this. Studying dreams and other subconscious processes can help us acknowledge and confront our true desires and feelings. It’s also important, I think, to acknowledge the authority that emotions and other semi-conscious feelings often hold over our cognitive minds.

But the problem is, a confusion tends to sneak in when people repeat the claim: instead of Karges’ rather vague word “mind,” the word “brain” is usually the one that ends up in the statement – and that’s a more serious inaccuracy. None of this Freudian theory has anything to do with what percent of our brain our conscious mind is capable of using. Nor does it have anything to do with any hidden abilities that can be unleashed with the right code-words or pills. And on a neurophysiological level, such a statement reveals a major lack of understanding about how the human brain actually works.

Now that we’ve got a better grip on what the ten percent myth is, I’m going to explain two reasons why any claims of this nature are just untrue. I’m also going to explain why a perfect memory isn’t as great as it might sound. But I’m going to end on a hopeful note, by talking about how every connectome actually does contain untapped potential – for those willing to put in the effort.

So to start, let’s talk about some reasons why this ten percent idea makes no sense neurologically.

1. There’s no such thing as an “unused part” of the brain.
Brain scanning technologies like functional magnetic resonance imaging (fMRI) show that throughout an ordinary day, every structure in the brain is active in some kind of processing. Although various kinds of tasks are related to increased activity in certain areas of the brain, there are no areas that just sit around unused. And processing-heavy tasks like social interaction bring vast regions of the brain together at once in a synchronized symphony, often many times a day.

Now, this is not to say there’s no signal redundancy built into the nervous system – on the contrary, there’s quite a bit. Even so, every single neuron in your connectome plays a part in some function or other, on a daily basis. Well, in normal, healthy human brains, anyway – and that’s what I’m going to talk about next.

2. If a part of the brain does fall out of use temporarily, it gets reconnected.
There’s another important reason we know the ten percent myth can’t be true: the scientific literature is full of examples of patients who were temporarily using less than 100 percent of their brains – those with severe cerebral damage, or who received a lack of sensory stimulation during their developmental years – and scientists have watched as those brains either quickly recruited the unused neurons for other purposes, or allowed them to die off and free up space.

Neurons bein' all friendly.

You can imagine the neurons in your connectome as little social-butterfly cells, because they’re always looking for new connections to make – and gradually ignoring the ones they don’t talk to much. This process is called  synaptic plasticity. In some cases, neurons can form whole new pathways when they’re craving some interaction.

This works because every neuron has a response threshold – a level of a certain neurotransmitter chemical it needs to receive in order to pass a signal on.*  When a neuron sits around unstimulated for a while, it eventually downregulates its own threshold, allowing it to receive signals from neurons that used to be too “quiet” or distant for it to sense. This means that even in those rare cases where some neurons aren’t receiving or responding to signals, they’ll start to look for new connections – and if they can’t find any, they’ll typically die. “Unemployed” neurons never stay unemployed for more than a few weeks, at most.

“OK,” you might say, “so every neuron in the brain has a use, and no neuron stays unstimulated for long. I’m with you so far. But what if our brains are so used to being ten-percent effective, they’ve learned to rewire themselves that way? What if those connections could be somehow… perfected?”

Well, that’s pretty close to the claim made in Limitless: that a near-perfect memory equates to super-intelligence. At first glance, this seems like it must be true – after all, wouldn’t we all be better at our jobs or classes if we never forgot anything we saw or heard? Not so much.

3. “Perfect” memory ain’t so perfect.
Actually, scientists have found that the reverse is more accurate: intelligence has less to do with the ability to remember, and more to do with the ability to distinguish between relevant and irrelevant details, and forget the irrelevant ones. If you read my post on magical mice, you’ll remember the story of the patient Sherashevsky:

Sherashevsky had such a perfect memory that he often struggled to forget irrelevant details. For instance, [he] was almost entirely unable to grasp metaphors, since his mind was so fixated on particulars.

He tried to read poetry, but the obstacles to his understanding were overwhelming. Each expression gave rise to a remembered image; this, in turn, would conflict with another image that had been evoked.

In short, a good memory is only as helpful as the filters applied to it. As a matter of fact, that’s how drugs like Adderall help memory and concentration – by helping the brain filter out irrelevant input and focus on what’s important to the task at hand. Without the ability to selectively forget, a “perfect” memory is as likely to cause total confusion as it is to offer up useful details.

“OK,” you might say, “but what if you had a super memory and took a drug like Adderall?”

Well, even that wouldn’t be much of a help if your mind wasn’t well-practiced at correlating and iterating your thoughts. If you’ve got a few minutes, check out the short story “Understand” by Ted Chiang. Its plot emphasizes that brilliance has less to to with physical synaptic connectivity (or perfect memory, which quickly becomes a burden), and much more to do with conceptual connectivity – the ability of a mind to form creative connections between abstract concepts – and iterative reasoning – the ability to view complex systems as elements within an even more complex system, which is itself an element within an even more complex system, and so on.

[SCIENCE UPDATE! #2 – The protagonist of Limitless actually does exhibit (or reference) most of these abilities throughout the course of the plot. He describes a clarity of purpose, and a level of correlative and sequential planning cognition that seem… exhausting. Still, as with the protagonist of “Understand,”  synaptic ultraplasticity and manic energy seem to work out fine for Our Hero – for a few Ferris Bueller-esque weeks, anyway. Also, despite a (presumably) more precise grasp of his place within the universe as a whole, his new-found sense of purpose seems to direct him toward life goals that are distinctly, shall we say, American. I found myself wondering what Bertrand Russell, or Isaac Newton, or the Dalai Lama (or, hell, Muhammar Qaddafi) might accomplish on these pills. In that sense, it’s actually kind of a thought-provoking movie.]

In “Understand,” the patient gains both these abilities through an experimental brain treatment that’s never explained in much detail. But the upshot of all this is that both those abilities can be learned and practiced by anyone. All it takes is dedication. It might come as a surprise to some people that intelligence can be improved with practice, but the fact is, it’s just another set of skills, like those that contribute to physical fitness, or mastery of a musical instrument. We might not all have the potential to be Einsteins – or Olympic athletes or award-winning composers – but any skill-set can be improved with practice.

So it is true that some people only realize ten percent of their connectome’s cognitive potential – just as many people only realize a fraction of the athletic or musical potential they could develop if they chose to put in years of practice.

On the other hand, it’s easy to see why the “ten percent of the brain” myth has such an enduring popularity – it’s sort of like telling a crowd of people that they each have the potential to turn into Professor X, if they just… concentrate really hard, or something. As Dr. Barry Beyerstein puts it in this article, “It would be so darn nice if it were true.” But intelligence isn’t a box of magic that can just be opened with some secret key – it’s a reward that can only be earned through years of practice.

That may be a harder pill to swallow, but it’s the one that actually contains medicine.

* This is one of the reasons neural signals are more like “fuzzy” analog signals, like radio, than “on/off” digital signals. Another reason is that even when the threshold is reached, the neuron doesn’t automatically fire – it just becomes more likely to.


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