It is increasingly well understood that the countless microbes in our guts help us to digest our food, to absorb and produce essential nutrients, and to prevent harmful organisms from settling in. Less intuitive — perhaps even outlandish — is the idea that those microbes may also affect our mood, our mental health and how we perform on cognitive tests. But there is mounting evidence that they do.

For nearly two decades, neuroscientist John Cryan of University College Cork in Ireland has been uncovering ways in which intestinal microbes affect the brain and behavior of humans and other animals. To his surprise, many of the effects he’s seen in rodents appear to be mirrored in our own species. Most remarkably, research by Cryan and others has shown that transplanting microbes from the guts of people with psychiatric disorders like depression to the guts of rodents can cause comparable symptoms in the animals.

These effects may occur in several ways — through the vagus nerve connecting the gut to the brain, through the influence of gut bacteria on our immune systems, or by microbes synthesizing molecules that our nerve cells use to communicate. Cryan and coauthors summarize the science in a set of articles including “Man and the Microbiome: A New Theory of Everything?,” published in the Annual Review of Clinical Psychology. Cryan told Knowable Magazine that even though it will take much more research to pin down the mechanisms and figure out how to apply the insights, there are some things we can do already.

This conversation has been edited for length and clarity.

“Man and the Microbiome: A New Theory of Everything?” — with all due respect, isn’t that a wee bit ambitious?

That title is admittedly a bit overstated. But the point we are trying to make is that it isn’t really so odd that the microbiome is involved in everything, because the microbes were there first, and so our species has evolved in their presence. We have been able to show that growing up in a germ-free environment really affects the development of the mouse brain, for example, in a variety of ways.

Our immune system is also completely shaped by microbial signals. Via that route, inflammation in our gut can affect our mood and cause symptoms of sickness behavior that are quite similar to important aspects of depression and anxiety. Many psychiatric disorders are also known to be associated with various gastrointestinal issues, though cause and effect often aren’t clear yet. So if you study the body, including the brain, you ignore microbes at your own peril.

Most people are on board with the idea that gut microbes affect our health, but it may be more difficult to accept that they also influence how we feel and think. How did you convince yourself this was true?

I’m a stress neurobiologist, so I was trained in stress-related disorders like depression and anxiety, and my interest was really in using animal models of stress to look for novel therapeutic strategies.

When I moved to University College Cork in 2005, I met a clinical researcher, Ted Dinan, and we started working together to study irritable bowel syndrome, a very common disorder that is characterized by alterations in bowel habits and abdominal pain.

That was interesting to me, as it had become very clear that this is also a stress-related disorder. So we started working on an animal model called the maternal separation model, where rat pups are separated from their moms early in life and develop a stress-like syndrome when they grow up.

Siobhain O’Mahony, a graduate student at the time, also wanted to look at the microbiome, and I remember telling her, “No! Focus, focus!” But she went ahead anyway and found a signature of this early-life stress in the microbiome of adult rats. That was kind of a eureka moment for me.

The next part of the puzzle came when we showed that mice born in a germ-free environment have an exaggerated stress response when they grow up. So we’d already shown that stress was affecting the microbiome, and now we’d shown that the microbiome is regulating how a mouse responds to stress. It turned out that a very nice study from Japan had already shown this.

The third part of the puzzle for me was to ask whether we could alter the microbiome to alleviate some of the effects of stress. In 2011, we were able to show that a specific strain of the bacterium Lactobacillus, when given to normal, healthy mice in a stressful situation, was able to dampen down the stress response, and that the vagus nerve connecting the gut to the brain was required for that.

These three things together, from 2006 to 2011, really crystallized my interest in the link between the gut microbiome, brain and behavior. Since then, we’ve been on this magical journey to try and understand these discoveries, uncover the mechanisms and find how they translate to humans.

Can you explain what a depressed or anxious mouse looks like, and how you quantify that?

One way to look at fear is to quantify how often mice venture into wide open areas, which they normally avoid. If we give a mouse Valium or another anxiety-reducing drug, it will go out and explore and be carefree, not to say a bit reckless. Depression is often studied by looking at mice in a cylinder of water. They are good swimmers, but they don’t like swimming, so after a while, they’ll stop and adopt an immobile posture. Yet if you give them antidepressant drugs, they keep going.

These types of paradigms have shown their validity in studies of pharmacological agents used in human psychiatry, and so they’re ideal to explore whether microbiome manipulations have similar effects. This can be done by transplanting the microbes from a mouse model for a psychiatric disease to a healthy mouse to see whether that creates similar issues, or vice versa, to see if it can resolve them.

Following a similar logic, we have shown that the microbiome can be important in brain aging and cognitive decline. We took the microbiome from eight-week-old mice and gave it to 22-month-old animals — these are very old mice. And we were able to show wide-scale changes across the body — in the microbiome and the immune system, but also in the hippocampus, a brain structure involved in memory.

In the old animals that received the microbiome from young ones, the hippocampus looked completely rejuvenated in its chemical composition. They also performed significantly better in mazes designed to test their memory. This finding has now been replicated in two other labs, giving it further credence.

Such experiments are difficult if not impossible to do in people. How to make that jump?

One thing we can do is to transplant microbes from the guts of people with psychiatric disorders to rodents, to see if they cause comparable behaviors. This has now been done for depression, anxiety, schizophrenia, social anxiety disorder and even Alzheimer’s disease. In one of our own studies, we transferred fecal microbiota from depressed patients to a rat model. This resulted in behavior reminiscent of that in rat models for depression, such as increased anxiety and an uninterest in rewards, in addition to inflammation.

In addition, we can see if bacterial strains we’ve identified as troublemakers in rodents also occur in people with psychiatric issues, and if strains that are beneficial in rodents can help humans as well.

What I’d really like to do is follow a large group of healthy people for a couple of years and track their mental and brain health as well as the changes in their microbiome, and regularly transplant their gut microbes into mice. This would give us a much better view on how this relationship evolves.

Do you think some of the probiotics available in stores today might be helpful, or not quite?

In my opinion, many so-called probiotics aren’t probiotics at all. Probiotics, per definition, are live microorganisms that, when taken in adequate amounts, can confer a health benefit. Most of what’s for sale in shops would never meet that criterion. To demonstrate that something confers a health benefit, you need clinical trials to show it is more effective than a placebo. That’s the first thing. Second, you have to show that the microbes are alive, and that they can survive the stomach acid.

There have been properly randomized controlled trials for some products. But for most products available over the counter today, such studies haven’t been done, because the regulatory authorities do not require them for probiotics as they would for medicines.

There’s a lot of snake oil out there. For most people, it’s probably harmless, but if you are immunosuppressed, it could be dangerous: Even beneficial bacteria can cause great harm if your immune system does not function properly.

Don’t get me wrong, I think there are many promising findings, but this field is very much in its infancy. I’m much more enthusiastic right now about whole-food approaches that adjust people’s diets to include more fermented foods — a source of beneficial bacteria — and the fibers that many beneficial members of our microbiome need to survive. And this, everyone can already do.

Have you done any experiments that show such a diet can improve mental health?

We’ve just done a small study with what we call a psychobiotic diet. Kirsten Berding, a German dietician who did a post-doc in my group, took a group of people with bad diets who were stress-sensitive — namely, our student population — and put them on a one-month diet to really ramp up fermented foods and fibers to the benefit of the microbiome. What we showed was that the better individuals followed the diet, the greater the reduction in stress.

The study wasn’t perfectly blinded, because people knew what they were eating, but they didn’t know what they were eating it for. And this was just the beginning: We’re now doing a much longer study trying to really untangle this.

We’ve also done a small randomly controlled study with a polydextrose fiber that was shown to improve the performance of healthy volunteers on a range of cognitive tests.

Obviously, more work of this kind is necessary. But in this case, I don’t think we should wait for that. Think about the experiment where we’ve transplanted microbes from young to old mice, for example: I’m not advertising poop transplants for aging adults. What we’ve found is that the more diverse your diet, the more diverse your microbiome, and the better your health when you get old. If you look at the beige, bland food served in many nursing homes and hospitals today, that is not the kind of diet that helps people to maintain a healthy microbiome and therefore a healthy brain.

We’ve done a study in mice where we adjusted their diet to contain much more inulin, a fiber that we know supports the growth of beneficial bacterial strains, and found we could dampen down the neuroinflammation that is often associated with cognitive decline in aging. This fiber is present in our everyday diet — there is a lot of it in vegetables like leeks, artichokes and chicory. So perhaps if you’re thinking of having a midlife crisis, forget about the motorbike and start growing vegetables.

This is all in healthy patients. Do you think the diet might also help people with mental health issues?

I do, but we need to test it, of course. An earlier study of ours showed that students born by C-section, who missed out on some of the microbes that newborns acquire during vaginal birth, had an elevated immune and psychological response to both chronic and acute stress, in line with our findings in mice. It would be very interesting to test if a psychobiotic diet might benefit them.

As I said, many psychiatric disorders are also associated with inflammation and other problems in the gut. Of course, this relationship works both ways, and it’s not always clear to what extent the irregularities in the gut are the cause or the result of the mental issues — or whether it’s a bit of both. But if we can show a healthier microbiome can improve mental health, that would be great news.

This is what’s appealing about the microbiome: It’s probably more modifiable than the rest of our body. If we understand how it works, that might give people more options to improve their health, even if they didn’t have the best start, microbially speaking. That’s what we hope to achieve.

This article The growing link between microbes, mood, and mental health is featured on Big Think.

Global suicide rates have steadily increased during the 21st century. Every year, more than 700,000 people die by suicide worldwide, and for every death, many more people attempt to end their own lives. Suicide is the fourth leading cause of death among 15- to 29-year-olds, and suicidal behavior in people of this age appears to have increased during the COVID-19 pandemic.  

Suicide and suicidal behavior have multiple complex causes that include social, cultural, and economic factors. Psychology and biology also play a role. Suicidal behavior is heritable and is more prevalent in people with major depressive disorder, with more than half of those who die by suicide having previously been diagnosed. 

Suicidal behavior and inflammation

At the molecular level, suicidal behavior and various psychiatric disorders are increasingly being linked to elevated levels of inflammatory biomarkers. Research now shows that the brains of people who died by suicide have reduced levels of a “master” control gene that regulates inflammation.   

Qiong Sha of the Van Andel Institute in Grand Rapids, Michigan, and her colleagues examined brain tissue from 29 people who had died by suicide and 32 controls who had died of other causes. Using molecular profiling techniques, they measured DNA modifications at more than 850,000 sites across the genome, and expression levels of the inflammatory regulator gene NPAS4.  

They found that NPAS4 was significantly down-regulated in the tissues of the people who had died by suicide compared to those from the controls. This was associated with increased expression levels of multiple genes linked to inflammatory processes. Also down-regulated were genetic pathways linked to the development and plasticity of neuronal circuits. Genes known to be involved in the function of oligodendrocytes were also suppressed in the tissues from the suicide group.  

Consequently, the tissues obtained from those who had died by suicide contained significantly fewer mature oligodendrocytes, as well as their precursors, than those from the controls. These cells, which synthesize the fatty myelin sheath that insulates nerve fibers in the brain, are known to be susceptible to inflammation and to be dysfunctional in schizophrenia and bipolar disorder, though the significance of this is still unclear. 

We know from animal studies that NPAS4 has a neuroprotective effect. In rodents, its expression in the prefrontal cortex plays a role in fear memory and depression-like symptoms, and reduction of it results in increased nerve cell death, inflammation, and the size of brain lesions following ischemia. There are only a few studies of NPAS4 expression in humans; one shows that its expression in the prefrontal cortex is downregulated in people who died from opioid overdose.   

As well as contributing to our knowledge of NPAS4 expression in humans, these new findings add to the growing body of evidence linking suicide and its associated behaviors to brain inflammation. The authors say that the findings “validate NPAS4‘s as a potential biomarker or therapeutic target in suicidality.” 

This article Brain inflammation linked to increased suicidal behaviors is featured on Big Think.

Hana K.’s third LSD experience was terrifying. Initially, the images that flashed before her eyes were beautiful: fountains of colors, fields of tulips, peacock feathers. Then they turned dark: monsters, claws, demonic eyes, vampires. She saw kings and beggars dead, buried, eaten by worms, providing food for animals and eventually for other people. “Imagine the countless atoms of our ancestors in this perpetual motion!” she cried aloud, describing everything she saw to another patient, sitting beside her bed.

Hana had a troubled life. Born in 1949, she grew up in a town south of Prague, in a family crushed by poverty. When Hana was a child, her father drank and her spiteful mother often hit her for wetting the bed. At school, classmates teased her for wearing secondhand clothes, which were often damp because she was too shy to ask permission to go to the bathroom. In her teens, she was lonely and angry, so tormented by vivid dreams of murdering her enemies that she asked to be hospitalized. At 18, she married a boy she barely knew, separated from him after four months, and then tried to kill herself by swallowing 30 sleeping pills.

After that, Hana’s existence was a series of mind-numbing jobs, more suicide attempts, and stays in the massive, 2,000-patient Dobřany mental hospital, 60 miles southwest of Prague. Although intelligent, she was also considered hopelessly psychotic. But in 1969, when she faced another return to Dobřany, Hana told her family doctor she would rather kill herself — and this time the doctor referred her to the 112-bed clinic at Sadská, a facility east of Prague specializing in repeated sessions of LSD psychotherapy, directed by the psychiatrist Milan Hausner (1929–2000).

Hana K. (left) with poet Karel Šebek (right) in 1970, during the time they were both patients undergoing LSD therapy at Sadská. (Source: Wikimedia Commons)

Hausner originally doubted that she could be helped. But as he listened to a recording of Hana’s third LSD session, he saw some hope. “The most pronounced aspect of this session is her archetypal regression into the realm of antiquity and to the very beginnings of humanity,” Hausner later wrote. “Hana is beginning to formulate a new attitude toward death and eternity.”

Over the next six months, Hana had 20 more sessions of LSD. Hausner told her that she might need 60 to be cured.

As Sarah Marks and others have detailed, psychiatry in communist Europe was not merely an obedient lapdog to the Pavlovian conditioning promoted by the Soviet Union. It was far more varied and complex — and certainly one of its most unusual chapters concerns the use of LSD psychotherapy in 1960s Czechoslovakia, when that country’s progression to a more humane government, its increasing openness to Western Europe, and its developments in psychiatry and pharmacology all coincided with a worldwide curiosity about psychedelic drugs.

Until recently, LSD therapy in Czechoslovakia was known mainly through the work of Stanislav Grof (1931–), who practiced at Prague’s Psychiatric Research Institute, moved to the U.S. in 1967, and is today celebrated as one of the founders of transpersonal psychology. But dozens of other Czech and Slovak psychiatrists also used LSD in psychotherapy, and the most dedicated and outspoken of them was Hausner, who supervised more than 3,000 LSD sessions, published research in more than 100 articles and books, and yet remains largely unknown, even in his homeland.

Hausner grew up in Prague, the only child of an insurance clerk and a pharmacist. He was drawn to the healing arts early: In May 1945, during the uprising against Nazi Germany’s occupation of Czechoslovakia, he cared for fighters at Prague’s barricades. Germany had closed Czech universities during the six-year occupation, so after the war, the need for young doctors was acute, and in 1948 — the same year the communists seized control of Czechoslovakia’s government — Hausner enrolled in medicine at Prague’s Charles University. After graduating in 1953, he practiced psychiatry in various places around the country, including a children’s hospital. He married Zdena Procházková, a medical statistician, completed his compulsory military service, and by 1958 was back in Prague, busily working on several psychiatric wards, often traveling from one hospital to another on the same day.

Hausner first experienced LSD in experiments conducted by Jiří Roubíček, likely in 1954. Roubíček, a neurologist, was interested in comparing the brain-wave patterns of schizophrenic patients with those of healthy subjects undergoing a “model psychosis” induced by LSD, which he obtained from Sandoz and started experimenting with in 1952. Since LSD produces mind-altering effects in tiny amounts without inflicting physical harm, Roubíček’s superiors considered it safe, and many young psychiatrists became his test subjects. (Czech doctors have a tradition of self-experimentation: The Czech medical society is named after Jan Evangelista Purkyně, a 19th-century physiologist who asserted that one learns best from direct experience and studied the effects that he underwent after ingesting such substances as digitalis and belladonna.) Unfortunately, it’s not known what Hausner thought of his own LSD experiences, as he did not describe them in his writings.

In the late 1950s, Hausner started conducting his own medical research, publishing a study of his application of the new antipsychotic drug chlorpromazine combined with electroconvulsive therapy (ECT). Increasingly, however, he was interested less in biological psychiatry and more in psychotherapy — a controversial discipline, as it was often associated with Freudian psychoanalysis, which communists considered unscientific, individualistic, and likely to bankrupt national health insurance programs. In 1959, Czech ideologues denounced Ferdinand Knobloch (1916–2018), the head of psychiatry at Charles University’s medical-faculty polyclinic, for advocating the use of psychotherapy to treat neuroses, and Hausner came to his defense. In the journal Czechoslovak psychiatry, Knobloch assured his readers that he was developing a “materialistic” psychotherapy, with measurable results, and Hausner provided a survey of recent Soviet medical literature showing that Russian doctors already were practicing psychotherapy in various forms, using suggestion (often with hypnosis) and persuasion, in an effort to fully understand “the personality of socialist man in unity with the socialist environment.” (Hausner read and spoke Russian, along with English and German.) Czechoslovakia held an international congress on treating neuroses later that year, so a wider acceptance of psychotherapy was already underway. But Knobloch likely appreciated Hausner’s support, because he soon hired Hausner to work at the university polyclinic.

Between seeing patients, Hausner wrote his first book, “The Mentally Ill Among Us” (1961), a guide to the mental-health system for patients and their families that told the story of a young man’s psychotic break, his treatment through medication and psychotherapy, and his return to work. In the preface, Hausner noted that Czechoslovakia’s third Five-Year Plan (1961–1965) called for wider treatment of “nervous diseases,” and he hoped that his readers would learn that “mental illness does not equal disgrace, but can be successfully treated like any other physical illness.” (Hausner’s compassionate book was so popular that it was republished in 1969, 1978, and 1981.) During this time, he also began paying privately to undergo psychoanalysis, perhaps with Knobloch, as part of his training to become a psychoanalyst himself. Most fatefully, though, he became interested in treating patients with LSD, newly available from Czechoslovakia’s government laboratories.

In 1956, chemists at the Research Institute for Pharmacy and Biochemistry in Prague filed a patent for a new process for making LSD, and in 1959, the ministry of health gave the institute permission to begin producing the drug, trademarked Lysergamid, “primarily for experimental purposes.” So Hausner devised an experiment. In 1954, R. A. Sandison and other British doctors had reported benefits in neurotic patients who received small-to-substantial doses of LSD (25 to 400 µg, or micrograms) in conjunction with individual psychotherapy, applied repeatedly over several months — a method that Sandison later called “psycholytic” therapy. Hausner wondered if this would work in groups. Through the university, he knew Vladimír Doležal, a medical doctor and chemist specializing in toxicology, and they proposed using LSD in a therapeutic community established by Hausner’s boss.

Even under communism, Czechs with “bad nerves” were typically treated with baths at the country’s opulent 19th-century spa resorts.

At the polyclinic, Knobloch had become intrigued by the self-defeating behavior of his neurotic patients, so he’d developed a retreat for them on a state farm in Lobeč (35 miles north of Prague), modeled on the therapeutic community for traumatized soldiers that Maxwell Jones had established near London in 1947. Even under communism, Czechs with “bad nerves” were typically treated with baths at the country’s opulent 19th-century spa resorts, and Knobloch wanted to prove that he could help more people at less cost. At Lobeč, 15 men and 15 women spent several hours every day working on the farm, and several additional hours with a rehabilitation aide engaged in group discussions or various types of therapy, producing art or music or acting out events from their lives via psychodrama or “psychogymnastics,” a nonverbal exercise incorporating movement and mime. A psychiatrist from Prague visited to direct individual and group psychotherapy only once or twice a week, so the patients effectively became cotherapists, a design that Hausner tried to duplicate at Sadská.

In their experiment, Hausner and Doležal gave 11 neurotic patients 100 µg of LSD in conjunction with six hours of individual psychotherapy; seven got 50 µg and group therapy, and seven got saline as a control. After several weeks, the patients who’d received LSD and individual therapy showed the most improvement, displaying new insights and changed attitudes in their relationships with staff and other patients. Those who received LSD in the group had the worst results: “Patients were more concerned about their unusual experiences than to expose them to the therapeutic effect of the collective.” It was a modest study, but the first on LSD psychotherapy to appear in the Czech medical literature.

Other Czech doctors were starting to use the drug. Stanislav Grof began psycholytic therapy with neurotic patients at the Psychiatric Research Institute in 1961, and that year the authorities approved Lysergamid for outpatient psychiatry, encouraging other doctors around Czechoslovakia to test it in their own practices. Individual psychotherapy expanded, and soon it was possible to discuss concepts that were essentially Freudian: In 1963, Hausner and Doležal published a remarkable how-to guide for hallucinogens in the journal Czechoslovak psychiatry, citing the West German psychiatrist Hanscarl Leuner’s contention that such drugs “reawakened psychic dynamics” by evoking “age regression going to the first years of life,” “re-living of forgotten traumatic events,” and providing “abreactive emotional release with subsequent insight.” They outlined radical techniques, some borrowed from Leuner and other Western LSD doctors, that they used at Lobeč: getting patients to write out their autobiographies, using family photos to encourage associations, having the doctor play characters perceived in patients’ hallucinations, and even recruiting other patients to assist with the sessions. Hausner and Doležal quoted their patients endorsing LSD therapy, included samples of patients’ artwork, and claimed that after a year, 75 percent of their patients receiving LSD and individual therapy had improved, although the best results were in those who’d combined such therapy with a stay at Lobeč, where they could practice insights acquired from their LSD experience.

Through such research, Hausner established contact with Leuner, who became the principal advocate for psycholytic therapy after Sandison moved on from LSD in 1964. Hausner started getting published in international journals, Czechoslovakia began permitting academics to travel to capitalist countries, and in August 1964, Hausner summarized his Lobeč work at the Sixth International Congress of Psychotherapy in London. By 1965, Czechoslovakia’s authorities had approved commercial production of its LSD, and Hausner wrote a paper — published in English — for the state pharmaceutical export firm, noting that Lysergamid was indistinguishable from Sandoz’s product and describing its effectiveness in outpatient psychiatry. He would run 104 sessions with 65 patients, using doses of 50 to 300 µg, and found LSD was “a valuable means for deepening and accelerating the psychotherapy.” (Perhaps reluctant to limit foreign interest in Lysergamid to therapeutic communities, Hausner downplayed his Lobeč research, writing that he’d seen “no impressive differences” in results with outpatients.)

Hausner had credentials, contacts, and a steady supply of LSD. He was ready to apply everything that he’d learned at a clinic of his own.

The psychiatric clinic at Sadská, a town of 3,000 residents 40 miles east of Prague, consisted of a pair of two-floor pavilions originally constructed in the 1920s as a retreat for postal employees to enjoy a nearby lake and mineral spa, or walk along the Elbe River and through the Kersko forests. To meet the growing demand for psychiatric care, the ministry of health acquired the facility and began admitting patients in 1962. But by the autumn of 1965, Sadská’s chief physician was losing his eyesight. The clinic was affiliated with Charles University’s faculty of medicine, so Hausner, then 36, got the job, and he quickly made changes.

Pavilion A remained devoted to standard psychiatry for inpatients suffering issues from hysteria to psychosis. But Hausner had Pavilion B remodeled as an open ward to suit a therapeutic community. He selected some 50 inpatients for it, to stay six to eight weeks, and from them, he chose one or two groups of 12 to 14 patients who he thought were most likely to benefit from LSD, to stay six months. As at Lobeč, the patients spent mornings laboring in the forest or in the clinic’s garden and workshop, afternoons in group discussions, and evenings hearing lectures, creating dances or plays, or watching films. But with his own facility, Hausner could fully implement psycholytic therapy, and every day several patients underwent LSD.

The drug was usually delivered by injection to control the dosage, and before breakfast so the patients wouldn’t be hungry in the middle of their trip. Sessions were conducted in the patients’ rooms — LSD groups were on the ground floor — and the patients were accompanied by a sitter. Outpatients also came to Sadská for “weekend therapy,” undergoing LSD and individual or group analysis and returning to work on Monday. Like the inpatients, these visitors underwent dozens of treatments: one 42-year-old male received 300 µg 37 times in 18 months.

Hausner wrote up a guide for patients, introducing them to psycholytic therapy. Many instructions were typical of clinics elsewhere — he advised patients to keep their eyes closed while on LSD and to accept unpleasant or frightening episodes, as they might reveal the sources of their psychological difficulties — but others seemed worded to reassure patients who had lived under totalitarianism. “Talk openly about everything that comes to mind while using the substance,” Hausner advised. “The purpose of sitting is not to ‘extract’ experiences that you would not discuss in a completely awake state.”

He also wrote detailed instructions for the staff. Nurses were to supervise patients filling out the numerous questionnaires, to conduct art and occupational therapy, and to sit with patients during LSD sessions. Some patients might undergo psychotic episodes, he warned: “Remember that kindness, an effort to understand seemingly bizarre behavior, and minimal restraints can usually eliminate even the most violent manifestations.” Any doctor or therapist working with LSD was required to have at least three experiences with the drug themselves so that they could better understand their patients, and nurses had the option to undergo LSD as well. “When work started at Sadská, the personnel took a very skeptical attitude to the whole undertaking,” Hausner told a reporter, but most employees came around. “Their first eye-opener is that as ‘normal’ people they are not so very different from the patients under LSD intoxication. This discovery breaks down the barrier of prejudice in them.”

The LSD therapy at Sadská was also greatly influenced by Zbyněk Havlíček (1922–1969), a psychologist and surrealist poet who had worked at the Dobřany mental hospital in the 1950s and was at Sadská when Hausner arrived. Fascinated by psychoanalysis, Havlíček considered LSD a “miracle” compared to the mind-numbing drugs issued by most psychiatrists, and he ran many of the early psycholytic groups at Sadská, interviewing patients while they were hallucinating.

In letters to his girlfriend, Havlíček described his method in detail, playing with patients’ symptoms “like a bullfighter, waving a red cloth to their statements,” probing their visions and memories and finding connections in their biographies and patterns of behavior. This LSD analysis apparently worked: Hausner reported that 80 hospitalized patients underwent psycholytic therapy at Sadská in 1966, mainly suffering from neuroses, sexual disorders, and psychosomatic syndromes that hadn’t responded to other treatments for years, and 47 of them improved enough to be discharged. “The more sessions, the better the results,” Hausner said: patients who improved significantly had an average of 12 sessions (average dose 250 µg), while those showing no improvement had an average of six.

This was good news at a time when moral panic about LSD was cresting elsewhere. In April 1966, a few days after the New York Times reported that a man claiming to be “flying” on LSD had stabbed his mother-in-law to death, Sandoz announced that it was stopping all distribution of its product, and therapists from the U.S., the UK, Italy, and other countries started visiting the Sadská clinic, hoping to buy Lysergamid. Stanislav Grof knew many prominent LSD doctors after presenting his own psycholytic research at a conference in New York, and he brought several of them to Sadská, including Harvard’s Walter Pahnke. But the panic elsewhere reached Czechoslovakia, too: The communist daily Rudé Právo ran an article denouncing LSD as a “new god” that had unleashed madness in the West, and Hausner had to respond. No misuse of Lysergamid had occurred in Czechoslovakia, he assured readers; only trained psychiatrists could request the drug after approval by a special committee of the ministry of health. (Hausner was the committee secretary, and he directed foreigners’ inquiries to the state export company.) Besides, LSD was too valuable a tool to be outlawed. The drug was a “probe into the subconscious,” Hausner wrote — and “the probe goes very deep, often into the first days of life, if not further.”

This was an extraordinary claim, especially for the pages of the official Communist Party newspaper, but it did reflect what the doctors were seeing. Hausner reported elsewhere that two-thirds of his LSD patients “relived phantasies concerning their birth, intrauterine life, ‘birth trauma,’ [or] first events of the sucking age.” At an October 1966 conference in Amsterdam, Grof theorized that LSD brought forth constellations of emotionally charged, condensed experiences (COEX), individual to each patient’s life, and these earliest memories or fantasies lay at the core of each COEX system, providing a key to understanding the patient’s problems. Havlíček, the Freudian, disagreed, arguing that such experiences were merely “a retroprojection of later conflicts” onto the richly symbolic moment of birth. To Hausner, these were theoretical differences; he was focused on managing his clinic, and he instructed Sadská’s nurses to comfort patients in a “pediatric regression” by “stroking, taking a hand, etc.” — which required “a certain skill” in distinguishing regression from “adult manifestation on an erotic level.”

Havlíček argued that the psychedelic experience was essentially narcissistic and typically American — a retreat into a “luxurious uterus.”

The most fundamental dispute between the doctors, however, occurred over how LSD therapy should be conducted. In 1967, Grof got a fellowship to work at Baltimore’s Spring Grove State Hospital, which used “psychedelic” therapy, giving alcoholics one huge dose of LSD (400 µg or more) to induce a life-changing spiritual experience. Grof started thinking that Europe’s psycholytic advocates were on the wrong track: Repeated sessions of psychoanalysis were time-consuming and couldn’t grasp the profound sensations of ego death, rebirth, or cosmic unity that LSD patients often experienced at higher doses, which he saw could be beneficial. Havlíček had none of it: He argued that the psychedelic experience was essentially narcissistic and typically American — a retreat into a “luxurious uterus,” providing feelings of divine exaltation but socially worthless, separating the patient from the real world where their problems began, and where they had to learn to survive. Hausner, who’d been elected vice president of the European Association for Psycholytic Therapy, agreed: “In my experience,” he later wrote, “achieving true transcendental insight is rare unless the subject succeeds in discarding the negative aspects of his unconscious and erases the faulty programming that is causing the problem.” (To avoid confusion with psychedelic therapy, Hausner usually referred to the drugs as “psychodysleptics,” meaning that they induced a dreamlike state.)

Grof prepared a response, proposing a way to integrate psycholytic and psychedelic techniques at an international LSD congress to be held in Prague in September 1968, but the paper was never heard. On August 20, Soviet troops invaded Czechoslovakia to crush the democratic progress emerging during the Prague Spring. Then, on January 7, 1969, Havlíček died of leukemia. Sadská’s fortunes were destined to change after that.

When Hana K. arrived at Sadská in 1970, she spent four months in group therapy while Hausner assessed her. She answered questionnaires and wrote her autobiography, read books by Freud and Erich Fromm, and sat in on discussions about relationships — many of the patients were young and had family conflicts because the state wouldn’t assign them apartments of their own unless they were married. Then Hana started the LSD treatments, and by sharing work and experiences with other patients, for the first time in her life she made some friends.

After 22 sessions, Hausner decided that Hana had improved enough to join a group psycholytic session. Although his early research suggested that group LSD sessions had little value, Hausner found that low doses of the drug helped some patients see their own “faulty, unbalanced behavior” when interacting with others. Hana received 100 µg with half the patients in her group. At first, the experience was unpleasant, like she was being watched on a stage. But soon members of the community started violently arguing with each other — and Hana was flooded with empathy.

“I am actually beginning to understand and to relate to people,” Hana wrote in her diary. “I can see and understand the reason for the things they do, and I don’t hate them anymore! Poor doctor. He’s got so many children. How can he cope with it all?”

After the 1968 invasion, it took Czechoslovakia’s new Soviet-backed government several years to replace key officials with hardline communists, and during that time Hausner was able to continue LSD therapy. Newcomers joined Sadská, including a psychoanalyst from Poland and a group therapist from Barcelona, and foreigners continued to tour the clinic — R. A. Sandison visited in 1970 — but increasingly from the Soviet bloc, curious about methods unavailable in their own countries. “We have found your system of contacting LSD group’s therapy very fascinating,” two Polish psychologists wrote in Sadská’s guestbook after staying several weeks in the summer of 1969. “We have seen wonderful results. We have taken LSD ourselves and experienced that it helps very much in speeding up psychotherapy. We would like to arrange LSD group’s psychotherapy in Poland.”

To hear the people who worked there describe it, Sadská was more like an offbeat arts college than a Soviet medical facility. Hausner brought his three children to the clinic, and sculptors and dream interpreters came from Prague to give classes to the patients. Some evenings, they held masquerades or parties; the doctors and nurses and patients would dance together, and the next day, they would discuss in group how they had interacted. There were a few suicide attempts, but there were also romances: one older LSD patient, who had spent his youth in a Nazi concentration camp and suffered from depression, was so impressed by Sadská that after his discharge, he became a therapist at the clinic and married one of the psychiatrists. As one patient later wrote, “At Sadská, it was Freud and love.”

There were a few suicide attempts, but there were also romances.

Sadly, that love wasn’t felt in the Czech capital. Communists feared that the Western scourge of narcotics addiction was leaking into Czechoslovakia, and in December 1969, the popular magazine Květy ran an article about drug abuse by Prague youths, opening with a rumor that LSD could be bought in front of a downtown cinema from a car with Austrian license plates. Hausner increasingly had to defend the psychiatric use of LSD and the distribution scheme that he helped administer. At the prestigious Collegium Internationale Neuropsychopharmacologicum, held in Prague in 1970, he spoke on the “therapeutic and illegal use of Lysergamide”: After some 3,000 sessions with 300 patients at Sadská, he reported that general health improved for 60 percent of them, and life satisfaction increased for 70 percent. “Nobody of these 300 patients became habituated to LSD,” he asserted; distribution of the drug was under “rigorous governmental control,” and “no misuse has been observed.” But he was swimming against the tide. In February 1971, 34 countries adopted the UN Convention on Psychotropic Substances, classifying LSD as a drug of abuse with no therapeutic value. Czechoslovakia was only an observer of the proceedings, but the Soviet Union soon signed on, and Sadská came under scrutiny.

In May of that year, a panel of doctors conducted a comprehensive audit of the clinic “due to frequent negative comments” from the regional health authority. Hausner prepared a table showing that LSD patients were a small percentage of Sadská’s admissions, and the time they spent there was decreasing.

Sadská’s admissions and the time patients spent at the clinic.

The panel commended Hausner for fulfilling the planned number of treatments, his focus on “modern currents” in psychiatry, such as “group psychotherapy and active pursuit of cooperation of the patient,” and his “progressive efforts” to reduce hospitalization via his “weekend” LSD therapy. But, “[a]s far as LSD treatment is concerned, we reiterate the fact that this method is not generally accepted. The number of patients treated in this way needs to be limited as much as possible, or to stay with LSD for a few cases that would only go to outpatient treatment.”

Every third or fourth weekend, about 40 patients would endure a “psycholytic marathon,” taking turns sitting for each other and heading back to work on Monday.

Hausner complied, increasingly putting new LSD patients on weekend therapy. Every third or fourth weekend, about 40 patients would endure a “psycholytic marathon,” taking turns sitting for each other and heading back to work on Monday. Each of them would have been hospitalized an average of 64 days without the program, Hausner calculated, so it saved the state 1.34 million Crowns per year. (At the time, the average salary in Czechoslovakia was 26,844 Crowns per year.) To save more money, Hausner recruited psychology students to assist on weekends, and many underwent a “training intoxication” with LSD for university credit.

Hausner continued to publish articles internationally, including one comparing the symbology of dreams to LSD hallucinations that was subsequently reprinted in a Czech journal for general practitioners. In March 1973, he chaired a conference on psychotherapy in socialist countries that was attended by experts from across the Soviet bloc — although he was careful to mention psycholytic therapy only once in his own paper, surveying the range of techniques used in Czechoslovakia at the time. (For example, Hausner, then president of the psychotherapeutic section of Czech Psychiatric Society, noted that 250 of its 300 members used hypnosis.) In June, he traveled to Oslo for the 9th International Congress of Psychotherapy, where he identified his practice as “dynamic confrontation therapy,” in which a patient faces the problems of past, present, and future (!) in a controlled environment, with psychodysleptic drugs targeting the “neurochemical, intrapsychic, interpersonal, psychosomatic and the valuation system area[s],” and ultimately providing a corrective emotional experience.

But officials back in Prague were likely suspicious of the relative freedom that Hausner enjoyed without a Communist Party membership. Drug abuse was becoming a problem in Czechoslovakia, and though nearly all the cases involved prescription medicines, often containing ephedrine or codeine, the bureaucrats feared that LSD was next. In October 1973, they inspected the Sadská clinic, and in its safe, they found 619 ampoules of LSD that had expired in 1969. In January 1974, they consulted the pharmacy that distributed the drug and learned it had another 2,400 ampoules that Hausner had ordered in 1971 and were about to expire. In a series of letters, Hausner apologized. Supplies from the factory had been unpredictable, he said, and LSD remained stable in glass ampoules for many years. Besides, the drug hadn’t been stolen or turned up on the black market, so what was the harm?

Hausner needed some good press, so he invited journalists from Květy to visit Sadská. The resulting article described a traumatized 18-year-old girl arriving at the clinic, and Hausner’s plans to treat her with LSD, accompanied by a full-page color photo of Hausner ministering to a female patient lying on a wildly patterned couch in his office under a wall of primitive masks. The deputy director of the regional health authority demanded that LSD therapy be stopped. Hausner apologized again, admitting the photo was “too provocative,” and he got letters from other doctors supporting the continued use of LSD. But the health authority ordered Hausner to send reports on every patient receiving the drug, and it started conducting spot checks of the clinic’s supply.

In the late summer of 1974, Hausner’s father died, and Hausner had a nervous breakdown. “He had the worst fears for the future, he was anxious about his family, and concerned about material security,” one of his colleagues later said. Hausner admitted that he’d considered suicide and was hospitalized in Prague for several months. The regional pharmacist came to Sadská, collected all the ampoules of LSD, and stomped on them in Hausner’s office.

“They took away all his appetite for work,” a nurse said years after this incident. Hausner suffered another breakdown and received treatments from his Prague colleagues that he’d tried to avoid in his own practice, including ECT, antidepressants, and lithium. When he finally returned to Sadská in 1975, he was emotionally flattened, a changed man. A nearby hospital took over administration of the Sadská clinic and converted the psychotherapeutic pavilion into a ward for chronic psychiatric patients. LSD was still theoretically available with permission from the health ministry, but nobody risked ordering it.

Hausner left Sadská in 1981, after he and Zdena divorced. Czechoslovakia drifted into a stultifying political “normalization,” and Hausner ended up in the industrial north, providing psychiatry to the employees of a uranium mine. When he died in 2000, Czech medical journals did not mention his passing.

For many decades, even after the communist regime fell in 1989, Czech medical authorities resisted any talk of reviving LSD therapy, and the few doctors interested in the drug were limited to conducting animal studies. But possibilities are beginning to reopen. Prague psychiatrists are studying the neurobiological effects of psilocybin — in a suite designed to resemble Hausner’s office as it appeared in Květy — and have established a private clinic offering ketamine-assisted psychotherapy, the first in central Europe, although such treatments are not yet covered by Czech medical insurance.

Hausner’s correspondence, patient files, and hundreds of pieces of artwork reside in the Czech Academy of Sciences archive, but they are currently inaccessible to the public. Thanks to the growing interest in psychedelics, a book that Hausner wrote in 1997 about psycholytic therapy at Sadská has finally been published, but to get a more complete picture of what happened at the clinic, I also sought out people who were there. Some 30 psychiatrists and psychologists worked or trained at the clinic; my colleagues and I interviewed nine of them, and while many said that Hausner was a superb administrator and psychiatrist, they also said that LSD didn’t “accelerate” psychotherapy because so much time was spent in sessions and analyzing the patients’ experiences. Several said that therapists were overwhelmed by the volume of material that LSD evoked and Hausner tried to do too much: Many of the LSD patients had neuroses or depression, but the conditions of others ranged from alcoholism to schizophrenia to psychopathy. I also interviewed five Sadská nurses, all of whom said that it was the most interesting period of their careers, and the clinic was “like a big family.” But did LSD therapy help the patients? “Well, they did not come back,” one nurse said. “They went back to life and everything was OK,” said another. “It is true that it was a half-year-long treatment. But it was successful, at least according to me.”

One woman said that she felt “broken” after every session and experienced unnerving flashbacks years later.

I also interviewed 15 former Sadská patients. Three said that psycholytic therapy hadn’t substantially changed their condition, and four said that it made their condition worse. One woman said that she felt “broken” after every session and experienced unnerving flashbacks years later. A man who suffered sexual neuroses said that he didn’t consider LSD useful because “it opened everything in allegorical terms” and confused the therapeutic relationship: In one session, he tried to rest his head in his doctor’s lap, and she rejected him, which took him a long time to overcome. But eight thought that Sadská’s therapy had helped. A woman who suffered from posttraumatic stress disorder (PTSD) and sexual dysfunction said that she was “newly born” after her third session; she had been raised Catholic, and she said that LSD showed her “what belief really is.” A male alcoholic said that “LSD made the first step” to his sobriety and inspired him to become a therapist for other alcoholics.

Hana K. was discharged not long after her group LSD session. In 1972, she married a fellow Sadská patient, and eventually they had two sons. Today, she says that she’s become happier as she gets older, and the worst time of her life was just before she went to Sadská.

“A home, and kind people around me, that is something I never had before,” she said of the clinic nearly 50 years later. “And with LSD they taught me things I never came across anywhere else. But whether the treatment would be equally as successful without LSD I cannot say.”

Ross Crockford is an award-winning journalist based on Vancouver Island who has written about the medical use of psychedelic drugs for publications in Europe and North America. He is currently preparing a book about the history of LSD in communist Czechoslovakia. A version of this article with a complete list of notes and resources can be downloaded here. This story was excerpted from the volume “Expanding Mindscapes.”

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We all want to be happy — and for decades, psychologists have tried to figure out how we might achieve that blissful state. The field’s many surveys and experiments have pointed to a variety of approaches, from giving stuff away to quitting Facebook to forcing one’s face into a toothy grin.

But psychology has undergone serious upheaval over the last decade, as researchers realized that many studies were unreliable and unrepeatable. That has led to a closer scrutiny of psychological research methods, with the study of happiness no exception. So — what really makes us happy? Under today’s more careful microscope, some routes to happiness seem to hold up, while others appear not to, or have yet to re-prove themselves. Here’s what we know so far, and what remains to be reassessed, according to a new analysis in the Annual Review of Psychology.

Put on a happy face

One long-standing hypothesis is that smiling makes you feel happier. In a classic 1988 study, researchers asked 92 Illinois undergraduates to hold a felt tip pen in their mouth either with their teeth, forcing an unnatural grin, or with their lips, making them pout. The students then looked at four examples of The Far Side comics. On average, those with the forced smiles found the one-panel comics slightly funnier than those with the forced pouts.

But when 17 different research labs got together to retest the pen-clench smile’s effects on 1,894 new participants, the finding failed to hold up, the researchers reported in 2016.

The repetition study was part of a broader effort to counter psychology’s reproducibility crisis, which in part has been attributed to the variety of ways in which researchers could examine and reanalyze their data until they arrived at publishable results. “It’s kind of like shooting a bunch of arrows at the wall and drawing the bullseye on after,” says Elizabeth Dunn, a social psychologist at the University of British Columbia in Vancouver and coauthor of the new Annual Review of Psychology paper.

One solution has been for scientists to publicly declare, or preregister, their analysis plans before they conduct their experiments. In other words, they draw the bullseye first. Dunn and her graduate student, Dunigan Folk, homed in on such preregistered studies in their analysis, which narrowed the vast field of happiness research to just 48 published papers. Even that small number is encouraging, says Brian Nosek, a psychologist at the University of Virginia in Charlottesville and executive director of the Center for Open Science, which aims to improve research reproducibility. “I was actually surprised that there were as many papers that qualified,” he says. “That really demonstrates that this area of research has adopted a lot of these new rigor-enhancing practices.”

Preregistration alone doesn’t guarantee that results will be correct, nor does it solve all of psychology’s reproducibility problems. Quality studies also require sound methods and large and diverse sets of participants, for example. And indeed, most of the papers reviewed were high quality in those features beyond just preregistration, Dunn says. Even under the regimen of renewed scrutiny, some of the paths to happiness held up, the researchers found — including practicing gratitude, acting sociable and spending money on other people.

Take gratitude. In one of the recent studies, researchers asked hundreds of parents to either write about how they spent their week, or pen a gratitude letter to someone they knew. Expressing gratitude resulted in more positive moods. In another recent study, scientists asked more than 900 undergraduates to express gratitude in letters, texts or social media, or to list their daily activities. Those in the gratitude group scored as happier and more satisfied with their lives the following day. In both cases, it’s unclear how long these effects would persist.

Three different preregistered studies pointed to sociability as beneficial. In one, scientists assigned 71 adults to act extroverted — “bold, talkative, outgoing, active and assertive” — for a week, and another 76 to be “unassuming, sensitive, calm, modest and quiet.” Participants in the extroverted condition reported better moods during the study week, though the benefits were less for those who were naturally introverted.

And surprise! Smiling to promote happiness was also supported by new, preregistered research — once scientists switched to more natural grins. About two dozen labs from 19 different countries worked together to test the instruction to grip a pen in the teeth or to mimic the expression of a smiling person in nearly 4,000 subjects. The pen clenching still didn’t work, but people who were told to copy a smile did report better moods. Remarkably, this was true even if the subjects didn’t believe it would work, another team reported in 2023.

Researchers have also found that external agencies can promote people’s happiness. Giving people cash promoted life satisfaction, as did workplace interventions such as naps.

Dunn cautions, however, that participation in preregistered studies tends to yield small effects on happiness overall, in part because scientists can’t massage the data to get bigger numbers. If the interventions were a diet program, she says, users might drop about four pounds.

Nice ideas, poor results

Other well-known happiness approaches haven’t measured up to Dunn and Folk’s standards — at least, not yet. The researchers didn’t find clear evidence of benefits for volunteering, performing random acts of kindness or meditation. For example, a recent, preregistered study asked participants to perform acts of kindness for others, or for themselves, or simply to list what they did each day. Being kind to others over a four-week period made no difference to well-being.

Dunn and Folk didn’t find any preregistered studies at all on exercising or spending time in nature, two oft-recommended strategies. That doesn’t mean those strategies don’t or can’t work, Dunn says — just that as the preregistered landscape now stands, research hasn’t weighed in. The pair considered only two preregistered studies on meditation, and did not include meditation research on people with diagnosed mental health problems.

Such rigor is admirable, but it also means one can miss things, says Simon Goldberg, a psychologist at the University of Wisconsin-Madison. He studies the effects of meditation, including research among people who have psychological problems such as depression and anxiety. He noted that because of Dunn and Folk’s strict criteria, they omitted hundreds of studies on meditation’s benefits. “It’s, in the spirit of rigor, throwing lots of babies out with the bathwater,” he says. “It’s really very obvious that meditation training reduces symptoms of anxiety and depression.”

Dunn agrees that the review only covered the tip of the iceberg of happiness research. But that tip should expand as more psychologists preregister their science as part of what some call a renaissance in the field. As Dunn and Folk conclude, “happiness research stands on the brink of an exciting new era.”

This article Scientists scrutinize happiness research is featured on Big Think.

One of the most difficult questions for the science of memory deals with the most obvious fact about memories: We can, well, recollect them. The problem is that no one knows exactly how we call to mind, and with such ease, that party last weekend, with all the samba dancing and clinking of ice in glasses, the scent of circulating hors d’oeuvres, the jolt up the spine from catching a lover’s eye across a crowded room. All these emotional and sensory elements, we know, are registered in distinct areas of the brain—but how is it that we can reminisce and conjure them all up at once, recalling the mental event as a single experience?

A group of scientists based at the University of California, San Diego, have found a promising mechanism that may explain not just how recollection works, but also, more broadly, conscious experience itself.

In a recent paper published in the Proceedings of the National Academy of Sciences, lead author and neurophysiologist Charles Dickey identified patterns of ripples—brief high frequency oscillations in neural activity—that synchronize across the human brain during spontaneous waking and memory recall.¹ These ripples fan out across distant areas of the cerebral cortex (the wrinkly surface of the brain) that are responsible for the sensory elements involved in any mental event, and extend to the hippocampus, a seahorse-shaped structure key to memory. Many studies had previously investigated ripples in the rat hippocampus and their relationship to memory, but Dickey only recently identified ripples in the human cortex.

There are several competing theories about networks of neuronal activity that may facilitate communication between different areas of the brain to give rise to conscious experience.² But this may be the first observed mechanism that could potentially solve the so-called “soft problem” of consciousness—the quest to identify the physical processes in the brain that underpin mental events. The soft problem is in contrast to the so-called “hard problem” of consciousness, the question of how something physical like the brain can possibly generate the rich, clearly mental quality of lived experience.

“We have to solve the soft problem of consciousness first, and the hard problem doesn’t really impede that search,” said Eric Halgren, senior author of the paper and director of the UC San Diego lab where Dickey did his graduate research.

The difficulty behind the soft problem of consciousness is that there isn’t a readily identifiable locus of consciousness, though many possibilities have been proposed over the centuries. Rene Descartes, the 17th-century philosopher, thought the seat of consciousness was the pineal gland, a small gland in the center of the brain, but we now realize it’s probably responsible for producing and regulating melatonin for our sleep cycles instead. Two hundred years later a German physiologist named Johannes Müller suggested the medulla oblongata, the stem-like structure at the bottom of the brainstem, was responsible for consciousness. (We now know it’s chiefly responsible for involuntary functions like heartbeat, breathing, vomiting, and sneezing.)

This mechanism could solve the “soft problem” of consciousness.

Later, the English physiologist William B. Carpenter nominated the thalamus, a boot-shaped structure in the middle of the brain, as the hub of consciousness, and then celebrated biologist Francis Crick considered the claustrum, a neural structure that appears like a crown of thorns around the cortex. It turns out that both the claustrum and the thalamus may indeed play important roles in certain features of consciousness, but their candidacies as coordinating centers for consciousness remains largely conjectural.

The largest hurdle for the search for consciousness in the brain was somewhat inadvertently discovered by 20th-century neurosurgeon Wilder Penfield, who was treating patients with severe epilepsy by lesioning the malfunctioning areas of the brain that were instigating seizures. During his surgical procedures, Penfield noticed that certain movements or perceptions could be manufactured by stimulating different areas of the cortex; stimulation via an electrode on your forehead could produce the smell of a bandage, while one on the back of your head might make you see the Buddha and wiggle your pinky. This presented a problem of brain geography that is sometimes called “the binding problem”: How do distant areas—the ones involved in, say, the smell of bandages and the ones involved in the throbbing pain of the wound under the bandage—communicate with one another to produce a seamless experience? Enter brain ripples.

Brain ripples are so named because these high-frequency oscillations of neural activity appear as ripples on stereogram readouts of the cortex called electroencephalograms.

“The cortex is where we have all our sensory areas, so experiences are primarily a cortical phenomenon,” Dickey said. “The idea is that an experience happens, and this affects the firing of synapses between specific sets of sensory neurons, strengthening their connections.” He added, “Ripples may modulate this synaptic activity to consolidate the memory within the cortex.”

Ripples unify our experience by the moment, playing a memory like a song.

“What’s really interesting about brain ripples as a mechanism for studying consciousness and memory is that they’re primarily temporal,” Halgren said. Ripples emanate and multiply across the cortex spatially, but in the way that music fills a room. Ripples form fleeting but repeated patterns. They come and go like memories and experiences themselves.

While these specific kinds of human cortical brain ripples are newly discovered, the purely theoretical underpinnings of them have been around since the late 1970s. One popular theory of consciousness is known as “binding-through-synchrony,” which postulates that a synchronization of neural activity is what organizes different sensory cues from different regions of the cortex into coherent experience. The theory has been  around for decades, but evidence for it (beyond some experiments with the visual systems of cats) was limited.³ Brain ripples are the first observable and testable mechanism that could corroborate the binding-through-synchrony hypothesis.

What could this mean for consciousness and the study of the mind? The mechanism of brain ripples seems to suggest that consciousness may not have a center, or a fixed unifying organ controlling it. Instead, they suggest a decentralized consciousness, where frequencies accompany and hold our thoughts like ghostly electrical consorts, appearing and disappearing as quickly as they do. Instead of a single ghost in the machine, we may host an infinite number of ghosts, in the form of an incredible procession of ripples, unifying the entirety of our experience by the moment, playing a memory like a song, taking its notes from the distributed and diverse functions of our sensory apparatuses.

In the end, perhaps the search for consciousness was impeded for so long because we were searching for the wrong kind of thing, something physical or structural rather than phenomenal—a pineal gland instead of an electric signature, a neuro-chemical ghost that pulses across the cortex.

The real test for whether brain ripples underpin conscious experience might include cortical stimulation experiments in humans to test if certain kinds of experiences can be induced by ripples (or, conversely, if conscious experiences can be interrupted by disrupting cortical ripples). If further research concludes that ripples do in fact coordinate the communication of all the different parts of the brain responsible for an experience of, say, a beach in August (with its hot sand everywhere, the blazing sun and cooling ocean, and drying off while waves whoosh nearby), then Dickey’s study could be an immense step forward for solving the soft problem of consciousness.

This article How we remember last weekend is featured on Big Think.

Mental problems are commonly blamed for extremist violence—radicals and terrorists appear by definition to be selfish psychopaths. Yet research finds that no single psychological profile leads to violent extremism. And while depression is sometimes correlated with political violence, these links are not always reliable and may only occur when combined with environmental factors like recent life stressors. Instead, most research finds that radicalization and political violence stem from environmental factors like marginalization, oppression, and perceived injustice.

“Clinical traits that might seem obvious are actually often unrelated,” Jaïs Adam-Troïan, Assistant Professor of Psychology at Heriot-Watt University, told Big Think. “So for a long time, researchers assumed that mental health was unimportant for predicting political violence.”

That is, until recently. Work by Adam-Troïan and his colleague Jocelyn Bélanger (2023), Assistant Teaching Professor at Carnegie Mellon University in Qatar, finds that obsessive-compulsive disorder (OCD) symptoms are reliably linked with political violence intentions. 

Yes, the same disorder associated with washing your hands until they bleed or checking the stove nine times before bed is also correlated with extremism and political violence. 

A little background on obsessions

OCD is not normally associated with extremism or violence. The disorder—characterized by strong, uncontrollable thoughts and urges—is a maladaptive coping mechanism. It causes patients significant distress and rarely eradicates the underlying anxiety or belief. But usually, these thoughts and behaviors are nonviolent. A prototypical person with OCD, for example, might be extremely afraid of getting into an accident and feel a compulsion to follow a specific time-consuming (and unreasonable) routine to ignore or suppress their fear.

But Adam-Troïan and Bélanger noticed some similarities between OCD and what researchers call obsessive passion (OP), which relates to political or religious activities. Unlike harmonious passion (HP), which allows for flexibility in when and how to help one’s cause, OP is rigid and makes it difficult for people to consider alternatives. People high in OP tie their sense of self-worth to their cause. They are so consumed with their cause that it conflicts with other life goals like social relationships and work. 

Whereas HP predicts nonviolent political activism, OP predicts radicalization and support for violent political behaviors. “Harmonious passion is consistent with functional, proportional behavior, like street demonstrations or defending oneself when needed,” explained Adam-Troïan. “Obsessive passion, on the other hand, appears to relate to pathological and unhelpful behavior, like disproportionate retaliation and torture.”

And because both OP and OCD involve cognitive rigidity, self-regulatory deficiencies, and a sense of losing control, Adam-Troïan and Bélanger hypothesized that people with higher OCD symptoms might be more likely to experience obsessive passion and in turn violent intentions.

Obsessive passion

The researchers recruited 1,120 US citizens online who had previously identified as environmental activists, Democrats, Republicans, or Muslims. Participants filled out surveys about their ideology including:

• level of passion, both harmonious and obsessive (e.g., how much “My involvement in the Democratic Party is the only thing that really captivates me.”)
• activism support, both violent and non-violent (e.g., how much they agree with “doing risky or illegal actions to prevent [the other political party] from winning the next election.”)
• OCD symptoms (e.g., “Time spent on obsessions” and “Distress from compulsions.”)

They also reported other factors that might be relevant, like commitment, depression, and gender. 

Across all groups, people who reported higher levels of OCD symptoms also reported higher levels of OP and support for radical activism, but not peaceful activism. These relationships were substantial: Compared to people with low OCD and OP, people with high OCD symptoms and OP reported nearly twice as high scores in radical intention. 

“I was surprised by the weight of the differences,” said Adam-Troias. “In social psychology, we often view violence as provoked, but this shows the importance of proactive motivation to engage in violence.”

Because the data was collected at the same time and is correlational, they cannot establish whether OCD causes OP, or vice versa, or whether some third factor is involved.  However, mediation analysis, which statistically evaluates how well the data fits certain models, supported the hypothesis that OCD symptoms lead to OP (rather than OP leading to OCD), which in turn affects radical endorsements. Moreover, these relationships held even after controlling for anxiety, depression, commitment, substance use, childhood experiences, loss of significance, and gender. 

Potential treatments

In short, OCD predicts obsessive passion, which in turn appears to predict endorsement of violent activism. This holds across different political and religious groups, and after controlling for other relevant factors like depression and commitment. 

This helps explain why only a small proportion of people who face injustice engage in radical behavior. “Most people, even if they are strongly committed to their causes, only endorse functional, goal-oriented behavior,” explains Adam-Troias. “But high levels of OCD symptoms may impair self-regulation and compel people to behave in ways they would normally consider horrific.” 

Interestingly, Adam-Troias pointed out, people with OCD generally find their obsessions and the resulting compulsive behavior distressing. So people with OCD may be more willing to change their OCD-related symptoms rather than their political or religious values and beliefs. He hopes future research will examine whether OCD treatments—like teaching people skills for how to effectively respond to threats and how to separate emotions from behavior—may reduce OP and extremist violence.

Many people with high levels of OCD symptoms may not be diagnosed or receiving treatment. So large-scale campaigns targeting the general population may be needed. For example, researchers have had some success with online interventions and mass media education-entertainment shows to reduce other problematic behaviors like hate speech and violence against women. 

“It’s really hard to change someone’s core beliefs and values,” Adam-Troias says. “But we do have effective treatments for OCD.” 

By furthering our understanding of what leads to political violence—whether terrorizing innocent civilians, bombing government buildings, or torturing prisoners of war—we may one day be able to stop such abhorrent behavior at its source. 

This article “Obsessive passion”: The surprising links between OCD and radicalization is featured on Big Think.

I’m lying down in a white cylinder barely wider than my body, surrounded on all sides by a mass of sophisticated machinery the size of a small camper van. It’s an fMRI machine, one of the technological marvels of modern neuroscience. Two small inflatable cushions squeeze my temples, keeping my head still. 

“We are ready to begin the next batch of exercises,” I hear Dr. Horikawa’s gentle voice saying. We’re underground, in one of the laboratories of Tokyo University’s Faculty of Medicine, Hongo Campus. “Do you feel like proceeding?”

“Yes, let’s go,” I answer. 

The machine sets in motion again. A powerful current grows inside the cryogenically cooled wires that coil around me, showering my head with radio waves, knocking the hydrogen atoms inside my head off their original spin axis, and measuring the rate at which the axis recovers afterward. To the sensors around me, I’m now as transparent as a glass of water. Every tiny change of blood flow anywhere inside my brain is being watched and recorded in 3-D.

A few seconds pass, then a synthetic female voice speaks into my ears over the electronic clamor: “top hat.” I close my eyes and I imagine a top hat. A few seconds later a beep tells me I should rate the quality of my mental picture, which I do with a controller in my hand. The voice speaks again: “fire extinguisher,” and I repeat the routine. Next is “butterfly,” then “camel,” then “snowmobile,” and so on, for about 10 minutes, while the system monitors the activation of my brain synapses. 

Understanding aphantasia means learning something more about what it means to be human.

For most people, this should be a rather simple exercise, perhaps even satisfying. For me, it’s a considerable strain, because I don’t “see” any of those things. For each and every one of the prompts, I rate my mental image “0” on a 0 to 5 scale, because as soon as I close my eyes, what I see are not everyday objects, animals, and vehicles, but the dark underside of my eyelids. I can’t willingly form the faintest of images in my mind. And, although it isn’t the subject of the current experiment, I also can’t conjure sounds, smells, or any other kind of sensory stimulation inside my head. I have what is called “aphantasia,” the absence of voluntary imagination of the senses. I know what a top hat is. I can describe its main characteristics. I can even draw an above-average impression of one on a piece of paper for you. But I can’t visualize it mentally. What’s wrong with me?

My whole life, I’ve been aware—sometimes painfully so—of my own peculiarities, strengths, and weaknesses: A terrible memory, a good sense of direction, and what I felt was a lack of “visual creativity,” among others. I always thought these were just random, disconnected traits, and didn’t think much about them. Who doesn’t have their quirks?

Then, some time in 2021 (not coincidentally, I forget exactly where or when) I read about aphantasia for the first time, and it hit me hard: When people say “picture this scene in your head,” they aren’t speaking metaphorically! People can actually invoke shapes and colors in their minds. The shock of this realization was followed by a piecing together of many of those little idiosyncrasies of mine into a single, coherent phenomenon that fit with the scientific description of the condition. By the time my formal diagnosis came, I was already quite sure I was aphantasic.

I share this trait with many people. Occasional reports of people claiming to be without a “mind’s eye” go back to the 1800s, with several cases briefly mentioned in the scientific literature throughout the 20th century. Yet these cases were ignored by the broader scientific community, relegated to the fringes of the field as outliers or misunderstandings.

It was only in the 2010s that the topic began to attract attention. A man approached Adam Zeman, professor of cognitive and behavioral neurology at the University of Exeter, in the United Kingdom, claiming to have lost his mind’s eye following a heart surgery. In 2010, Zeman published a study showing that the man had different brain activation patterns from other subjects when trying to imagine things.¹

This was an interesting case study on its own, but something more surprising followed the publication of Zeman’s paper: Several people contacted him claiming to have had that same condition for as long as they could remember. Zeman and his collaborators assessed their claims using the Vividness of Visual Imagery Questionnaire (VVIQ), a popular measure of internal visualization quality, and found that these individuals indeed seemed to have little to no ability to visualize at will. The researchers published these findings in 2015, and proposed to call the condition “aphantasia”—literally “the absence of images” in Greek.²

With this new label, word about aphantasia finally started to spread within the neuroscience community and the broader public. More groups of researchers around the world began studying it, and every year a larger number of papers on the topic reaches scientific journals. We now know that roughly 1 out of 25 people are “aphantasics” (or “aphants,” in internet slang)—a rare condition, but common enough that each of us must know several people in the category.

For those equipped with a trusty inner eye, hearing about aphantasia can be a puzzling experience. How can someone even function as a human being without the ability to imagine pictures and sounds?

The biggest source of confusion with aphantasia comes from the assumption that “imagination” and “forming mental images” are one and the same thing. This is, of course, incorrect. I’m able to imagine anything, except it is all devoid of sensory representations. The imagined objects exist in my mind as interconnected concepts, like bullet lists of facts about things. For example, when I reread the scene in Ernest Hemingway’s The Old Man and the Sea where the protagonist battles a giant marlin, I’m able to take in a large amount of information: We’re on his skiff, bobbing on the waves of the deep waters of the Gulf of Mexico, the sun hammering mercilessly on the poor man while he pulls on the line for hours on end. I can reason about the situation, try to predict what could happen next, and relate with the character’s plight.

None of this requires having a picture of the scene in my head. This way of imagining is, perhaps, more abstract than what most people are used to, but not significantly less useful.

A surprising aspect of this is that, for me, the physical “bullet-list concepts” don’t just float haphazardly in nothingness, but are embodied in coherent three-dimensional structures that I can manipulate in my mind. In the scene of the old fisherman, I can imagine moving around the small boat, sitting down next to Santiago, and I can “feel” the monstrous mass of the fish floating near the vessel. This spatial awareness might be what allows me to find my way around my bedroom in darkness: I know where the furniture is and the rough distances between things even without seeing them. The science is still unclear as to why someone like me can form spatial thoughts without the accompanying imagery, but some speculate that it might have something to do with a separation of these functions in and around the visual cortex.

For non-aphants, it’s also hard to imagine how those of us without this sensory mind’s eye remember events if we can’t call to mind images, smells, or sounds. Scientists have begun trying to untangle this difficult question about the brain as well. In a 2015 paper, a group of researchers from the University of Toronto led by psychologist Daniela Palombo identified a new syndrome they called “Severely Deficient Autobiographical Memory,” or SDAM for short.³ People with SDAM lack the ability to relive past experiences in their minds. While this condition is rare among the general population, a preliminary survey hints at a link with aphantasia, with as many as 51 percent of a sample of 2,000 SDAM individuals also having aphantasia.

My own experience is similar. Past episodes of my life—when I can recall them at all—feel distant and non-sensory. SDAM is a new discovery, still unknown to most practicing psychiatrists, so people like me have to rely on self-diagnosis for the time being. But the symptoms described by the researchers match with what I’ve always taken for granted. I would describe my recollections as summaries of key facts rather than first-person “mind movies.” When asked, out of the blue, about an experience I’ve surely had—say, any childhood birthday party—my mind first responds by drawing a blank. It feels as if my episodic memories were filed into a “mental cabinet” without an index. Many memories are in there, somewhere, but retrieving them is a daunting task unless I’m provided with very specific prompts. With some groping work of deduction (where did I live at the time? Who did I hang out with?) I can gather enough hints to bring out some locations and non-visual facts: I had a big party in our countryside garden when I was 11 or 12; there was cake; a lot of kids running around and … that’s about it.

How does all of this affect my life? The surprising answer is that it doesn’t, at least not in any debilitating way. To my great relief, people rarely ask me what happened at parties held decades ago. But even when there is a need to describe scenes or people visually, I usually have enough “verbal facts” and eloquence to give a satisfying answer, without the need to replicate the actual pictures in my head.

Among researchers, the consensus seems to be that aphantasia doesn’t meet the criteria to be called a disability, and that aphantasic individuals, in general, are fully functional and just as successful at living their lives and performing in their careers as the rest of the population. This seems to be further supported by a new paper published by two researchers at Sorbonne University.⁴ They presented their participants, including many aphantasics, with a series of tasks involving the comparison of shapes, colors, words, faces, and spatial relations in one’s head. Aphantasics were as accurate as the other participants in all the tests, although they took longer to solve the imagery-based tasks, presumably because they used different, less-direct strategies to complete them.

Yet, some of those who discover they have aphantasia despair at the news. I’ve seen people make claims like “my whole life was a lie” and “this must be what ruined my marriage.” While I’m not quite as pessimistic, I can relate with that minority of fellow aphants. Sure, aphantasia and SDAM may not be causing major problems in our daily lives, but wouldn’t their subtle effects compound over time? And could they not be the cause of many of our other more embarrassing weaknesses and shortcomings?

For many of us, the aftermath of learning about one’s aphantasia leads to some sort of self-consciousness crisis. Suddenly, your performance in every other aspect of life comes under scrutiny, and blaming your congenital aphantasia for it is almost irresistible. Is drawing without a reference so difficult because of my aphantasia? Could SDAM be why I’m so bad at keeping in touch with people? Would I be less socially awkward without it? Very few of these supposed connections have been tested yet, let alone confirmed by solid scientific studies. Yet almost every aphantasic I’ve talked to does this. But everyone seems to focus their self-doubt on whatever they don’t like about themselves, scapegoating different shortcomings.

I have learned to embrace the diversity of aphantasia, and I hope to spread the word about it. And so does Junichi Takahashi, the first researcher I talked to about my condition. Takahashi is a psychologist at Fukushima University and was one of the first scientists to pay attention to aphantasia in Japan, where I’ve lived since 2011. He set up a website with the VVIQ survey, which is what led me to confirm my suspicions of having aphantasia. I got in touch with him directly and began to learn more about the science behind mental visualization and its absence.

Rather than studying aphantasia as a single phenomenon, Takahashi is trying to bring clarity to its diversity. In July 2023, he and several co-authors published a paper examining subtypes of aphantasia.⁵While most previous studies relied solely on the VVIQ questionnaire to identify aphantasic individuals, Takahashi and his team administered a battery of additional psychological question-sets to the same subjects and analyzed their correlations.

One of these questionnaires probed the vividness of multi-sensory mental imagery, including the sense of hearing, smell, and so on. Can aphantasics mentally replay their parents’ voices or the unique taste of cheesecake? Another questionnaire tested the tendency toward verbally oriented (relying more on words to figure out things) or visually oriented (relying more on images) thinking styles. Yet another one was used to detect “face blindness,” the inability to recognize faces.

Their statistical analysis revealed that all of these factors are somewhat correlated, but none fully. For instance, many of their aphantasic subjects lacked all of their “mind senses,” but some did have the ability to imagine sounds, flavors, or other non-visual sensations. The paper also found that face blindness did occur more often among people with aphantasia (40 percent) than in the control group (20 percent), but is far from being a universal aphantasic trait.

But all this talk of questionnaires and self-reports brings us to the age-old question: How do we know that aphantasia really exists, as opposed to being a form of psychological denial or simply a different interpretation of the same inner experience?

When aphantasia was first formally proposed, some researchers wondered whether the purported lack of visualization ability might in many cases be, not a congenital trait, but a psychopathological issue, such as neurosis or a defensive response against trauma. A kind of “philosophical language barrier” further complicates the issue: We might be talking about the same thing with different words and, language being the only medium we have to compare inner experiences, we have (or, rather, had) no way of confirming that. Even Ludwig Wittgenstein, one of the great philosophers of the 20th century, wondered about this very scenario more than 60 years before aphantasia got its name: If a person claimed they can’t imagine a picture but is still able to draw one, he asked, should we believe that something different is really going on in their head?

Scientists are now finding ways to answer these questions with hard, objective data. “Even before aphantasia became a thing, researchers tried separating people with low VVIQ from those with high VVIQ, and found that the performance at certain tasks is different between the two groups,” Takahashi explained to me. “There is also a lot of research showing a good correlation between VVIQ scores and fMRI scans.” The way the questions are posed in the questionnaire seems to work well enough to pick out individuals with demonstrably different visualization abilities.

Of the groups working on this front, Joel Pearson’s is one of the most active. His team at the University of New South Wales, in Australia, has been researching mental imagery since long before aphantasia became widely known. In 2022, his team even found a measurable physical characteristic of aphantasics.⁶ They discovered that, while the pupils of typical people involuntarily contracted when imagining bright shapes, no such response happened to the aphantasic group. In other words, Pearson’s team showed the first physiological difference confirming the reports of people claiming to have aphantasia. It looks like, at least in most cases, something different is happening inside our heads.

Aphantasia is turning out to be a little cornucopia of scientific insights.

And some are trying to go even further. That’s why I periodically get into the fMRI machine in Dr. Horikawa’s lab to get my brain scanned. A researcher at NTT Communication Science Laboratories in Japan, Tomoyasu Horikawa specializes in using AI to decipher the contents of the human visual cortex. He has recently turned his attention to aphantasia. I connected with him in April 2023, when Takahashi suggested I join Horikawa’s new research project. Horikawa is still collecting data from me and several other people, but preliminary, unpublished analysis indeed shows a quantitative difference in brain activity when aphantasic and typical subjects imagine things. When measuring the “distinctness” of brain activation patterns—how accurately the same patterns are repeated in a subject’s brain when imagining the same object, and how reliably different when imagining different objects—aphantasic subjects seem to score a bit lower. But he says that much more data is necessary to definitely tell. That may turn out to be the best proof of the neural differences between people with and without the condition.

All things considered, learning about my aphantasia made me doubly optimistic, both at the collective and personal levels.

In terms of social impact, aphantasia is turning out to be a little cornucopia of scientific insights. Already scientists are working with aphantasics not only to understand the condition itself, but also to shed light on the intricate workings of the human brain in general.

Rebecca Keogh, a cognitive neuroscientist at Macquarie University, in Australia, for example, has looked into the mechanisms of PTSD by comparing the occurrence of intrusive thoughts between aphantasics and people who can visualize. For Horikawa, aphantasia is a way to isolate the precise neural processes that create mental imagery in the general population. And researchers from the universities of Calgary and Radboud in the Netherlands recently published an article in Nature Reviews Psychology arguing for the use of aphantasia to resolve long-running debates about “embodied cognition”—a theory that treats thinking as a process involving mental simulations of one’s body and sensations, as opposed to only abstract concepts and symbols. The absence of something—like the lack of “inner senses” in aphantasics—can teach us much about the presence of it. This might be the biggest reason why I participate in these experiments: Understanding aphantasia means learning something more about what it means to be human.

In a sense, discovering aphantasia as a scientific topic is a bit like landing on a beach on an unknown continent. We know it’s new, but we have no idea of its geography and size. The binary division between “aphantasic” and “everyone else” might be a short-lived one. The subtype studies of Takahashi and others may lead to a more detailed map of the myriad ways a lack of visualization manifests in people and how they work around it. The brain seems to always have more surprises in store for us, more facets and inter-connections where we previously expected simplicity. We now have an even more interesting landscape to explore.

I would not want to remove the aphantasia even if it were possible.

And as this additional diversity comes into focus, it is easier for us to marvel at the paradox of human cooperation. What would seem like fundamental differences in the way we think—some with pictures, others without—do not lead to fundamental barriers in the way we talk to, connect with, and love each other. We are able to form societies and, through struggle and errors, build thriving communities despite these cognitive differences, and maybe because of them.

On the personal level, my “self-consciousness crisis” is eclipsed by a more powerful “self-knowledge renaissance.” Learning that I have aphantasia gave me the habit of carefully observing my inner experience. It led, among other things, to realizing that I may also have SDAM and mild synesthesia, something that I had never paid any attention to before. It also honed my ability to explain to others what goes on inside me. Armed with these new skills, I can say that I am better at managing myself and at picking the battles that I am best at. I feel like I have gained much and lost nothing.

Some people ask me if my aphantasia can be cured. The easy answer is no, because you can’t cure what isn’t a disease, and anyway we don’t know enough about it yet to influence it. The more sincere answer is that I would not want to remove the aphantasia even if it were possible. Temporary visualization tools? Sure. But not permanent changes to my brain. Whatever compounding effects it had on me over the decades, it helped produce the person I am today. I’m glad it did, even counting all the flaws. The question I started with—what’s wrong with me?—was both rhetorical and itself wrong. The better question is one we all ask ourselves at some point: “What makes me who I am?”

This article My brain doesn’t picture things. What’s wrong with me? is featured on Big Think.

Young jumping spiders dangle by a thread through the night, in a box, in a lab. Every so often, their legs curl and their spinnerets twitch — and the retinas of their eyes, visible through their translucent exoskeletons, shift back and forth.

“What these spiders are doing seems to be resembling — very closely — REM sleep,” says Daniela Rößler, a behavioral ecologist at the University of Konstanz in Germany. During REM (which stands for rapid eye movement), a sleeping animal’s eyes dart about unpredictably, among other features.

In people, REM is when most dreaming happens, particularly the most vivid dreams. Which leads to an intriguing question. If spiders have REM sleep, might dreams also unfold in their poppy-seed-size brains?

Rößler and her colleagues reported on the retina-swiveling spiders in 2022. Training cameras on 34 spiders, they found that the creatures had brief REM-like spells about every 17 minutes. The eye-darting behavior was specific to these bouts: It didn’t happen at times in the night when the jumping spiders stirred, stretched, readjusted their silk lines or cleaned themselves with a brush of a leg.

Though the spiders are motionless in the run-up to these REM-like bouts, the team hasn’t yet proved that they are sleeping. But if it turns out that they are — and if what looks like REM really is REM — dreaming is a distinct possibility, Rößler says. She finds it easy to imagine that jumping spiders, as highly visual animals, might benefit from dreams as a way to process information they took in during the day.

Rößler isn’t the only researcher thinking about such questions in animals distantly removed from ourselves. Today, researchers are finding signs of REM sleep in a broader array of animals than ever before: in spiders, lizards, cuttlefish, zebrafish. The growing tally has some researchers wondering whether dreaming, a state once thought to be limited to human beings, is far more widespread than once thought.

REM sleep is generally characterized by a suite of features in addition to rapid eye movements: the temporary paralysis of skeletal muscles, periodic body twitches, and increases in brain activity, breathing and heart rate. Observed in sleeping infants in 1953, REM was soon identified in other mammals such as cats, mice, horses, sheep, opossums and armadillos.

Events in the brain during REM have been well-characterized, at least in humans. During non-REM periods, also known as quiet sleep, brain activity is synchronized. Neurons fire simultaneously and then go quiet, especially in the brain’s cortex, making swells of activity known as slow waves. During REM, by contrast, the brain displays bursts of electrical activity that are reminiscent of waking.

Even across mammals, REM sleep doesn’t all look the same. Marsupial mammals called echidnas show characteristics of REM and non-REM sleep at the same time. Reports on whales and dolphins suggest that they may not experience REM at all. Birds have REM sleep, which comes with twitching bills and wings and a loss of tone in the muscles that hold up their heads.

Still, researchers are starting to find similar sleep states across many branches of the animal tree of life.

Researchers are finding different phases of sleep in more and more creatures across the animal kingdom. In mammals, sleep is divided into active, rapid-eye-movement (REM) sleep and quiet, non-REM sleep, and these phases are associated with specific patterns of brain activity. Though such brain activity patterns haven’t been investigated in many animals, researchers have documented active sleep phases, wherein animals experience jerky movements such as twitches or rapid eye movements, interspersed with quiet (quiescent) sleep, when those behaviors aren’t present. The growing tally suggests an evolutionary importance for multiple types of sleep. (Adapted from N.C. Rattenborg and G. Ungurean / Trends in Ecology & Evolution 2023 / Knowable Magazine)

In 2012, for example, researchers reported a sleep-like state in cuttlefish, as well as a curious, REM-like behavior during that state of putative sleep: Periodically, the animals would move their eyes rapidly, twitch their arms and alter the coloring of their bodies. During a fellowship at the Marine Biological Laboratory in Woods Hole, Massachusetts, behavioral biologist Teresa Iglesias investigated the phenomenon further, collecting terabytes of video of half a dozen cuttlefish.

All six showed bouts of REM-like activity that repeated roughly every 30 minutes: bursts of arm motions and eye movements during which their skin put on a show, jumping through a variety of colors and patterns. The creatures flashed camouflage signals and attention-grabbing ones, both of which are displayed during waking behaviors. Since the cephalopod’s brain directly controls this skin patterning, “that kind of suggests that the brain activity is going a bit wild,” says Iglesias, now at the Okinawa Institute of Science and Technology in Japan.

Researchers have since observed a similar state in octopuses. If octopuses and cuttlefish dream, “it just kind of blows down the walls of what we think about humanity being so special,” Iglesias says. 

Researchers have also observed a REM-like stage in bearded dragons by recording signals from electrodes in their brains. And they have reported at least two sleep states in zebrafish based on the fishes’ brain signatures. In one of the states, neural activity synced up like it does in a non-REM stage of mammals. In another state, the fish showed neural activity reminiscent of a waking state, as happens in REM. (The fish didn’t show rapid eye movements.)

Observing multiple sleep stages in such an evolutionarily distant relative from ourselves, the authors suggested that different sleep types arose hundreds of millions of years ago. It’s now known that flies, too, may flit between two or more sleep states. Roundworms appear to have one sleep state only.

Researchers consider the possibility of nonhuman animals dreaming during REM-like sleep because creatures act out waking-like behaviors in this state — like the cephalopods’ pattern-flashing or the spiders’ spinneret-shaking. In pigeons, sleep scientist Gianina Ungurean of the Max Planck Institute for Biological Intelligence in Munich and the University Medicine Göttingen has observed, with colleagues, that pupils constrict during REM as they do during courtship behavior. That evokes the question of whether the pigeons are dreaming or in some way re-experiencing what happened during their waking courtship instances, she says.

REM sleep also has been linked to the replay of experiences in some animals. For instance, when researchers looked at the brain electrical activity of sleeping mice that had earlier run a maze, they saw the firing of neurons that help with navigation and are linked with the head’s direction, even though the heads of the mice weren’t moving. They also saw activity in neurons associated with eye movement. The combination suggests that the mice may have had a dreamlike experience in which they were scanning the environment, Ungurean says.

With all these signs, it’s fair to posit that animals could be dreaming, Ungurean says. “However, if we take these reasons one by one, it turns out that none of them is sufficient.” The brain activity associated with replay, like that of the maze-running mice, doesn’t occur only during REM or sleeping, Ungurean says. It can also occur during planning or daydreaming. And the link between REM and dreaming isn’t absolute: Humans dream in non-REM too, and when drugs are used to suppress REM sleep, human study participants can still have lengthy and bizarre dreams.

Ultimately, people know they are dreaming because they can report it, Ungurean says. “But animals cannot report, and this is the biggest problem that we have in purely scientifically and robustly establishing this.”

There’s still debate over what REM is even for. “No one really knows what the function of sleep is — non-REM or REM,” says Paul Shaw, a neuroscientist at Washington University in St. Louis. One of the most accepted ideas is that REM helps the brain to form and reorganize memories; other theories are that REM supports brain development, aids in developing the body’s movement systems, maintains the circuitry needed for waking activities so they don’t degrade during sleep, or boosts brain temperature.

But if REM turns out to be present in far-flung species within the animal kingdom, that suggests its role, whatever it may be, could be very important, Iglesias says.

Not all scientists believe that researchers are seeing REM. They may simply be fulfilling preconceived notions that all animals have two sleep states and interpreting one of those as REM, says Jerome Siegel, a neuroscientist who studies sleep at UCLA. Some of these animals — such as the spiders — may not even be asleep, he argues. “Animals may do things that look the same, but the physiology isn’t necessarily the same,” he says.

Researchers continue to look for clues. Rößler’s team is trying to develop stains that would allow them to image spider brains — this might reveal activation in areas that are functionally analogous to the ones that we use when we dream. Iglesias and others have implanted electrodes in cephalopods’ brains and captured their electrical activity during two sleep states — one that shows waking-like activity, and another that’s a quiet state, with neural signatures similar to ones observed in mammals. And Ungurean has trained pigeons to sleep in an MRI machine and found that many of the brain areas that light up in human REM sleep also activate in birds.

If cuttlefish and spiders and a broad array of other critters dream, it raises interesting questions about what they experience, says David M. Peña-Guzmán, a philosopher at San Francisco State University and author of the book When Animals Dream: The Hidden World of Animal Consciousness. Since dreams unfold from the viewer’s perspective, dreaming animals should have the capability to see the world from their point of view, he says.

Dreaming would also hint that they have imaginative capabilities, he adds. “We want to think that humans are the only ones who can enact that break from the world,” he says. “We might have to think a little bit more about other animals.”

This article Do spiders dream? What about cuttlefish? Bearded dragons? is featured on Big Think.

Jason was a man in need of a fleece, but not just any boutique fleece. This being ancient Greece, and Jason being an Argonautic hero with divine blood coursing his princely veins, he was searching for the golden fleece. And after years of questing, battling, and rowing, he arrived in Colchis to claim his gilded prize.

There were the usual kinds of challenges, such as plowing a field with fire-breathing oxen, and Jason handled them all heroically. One challenge, though, proved too much. He couldn’t get past a scaly and sleepless dragon. Lucky, then, that he fell in love with a princess and sorceress named Medea. Medea gave Jason a magic potion to drug the insomniac leviathan, and the two hot-footed it away with his shiny new cardigan to live happily ever after.

Except not quite. When the young couple found themselves in Corinth as poor and insignificant civilians, the honeymoon ended. Jason got itchy feet and decided it was far more glorious and worthy of a hero to marry a princess. He abandoned Medea and their two young children. Medea was spurned, proud, and furious. She wanted desperately to hurt Jason for the pain he caused her. But how? Jason was courting a princess in a guarded castle, sipping wine and eating grapes. So, Medea did something monstrous. In a mad-hot rage over the betrayal, she killed her own children. She loved her children, but retribution mattered more.

In those last few lines, the story comes down to Earth. The millennia melt away, and we have here the all-too-familiar story of a family broken by betrayal, pride, and spite. This is known in psychotherapy as the Medea effect.

The Medea effect

There are two ways to view the Medea effect. The first is when we encounter those devastating stories of a mother killing her children because they got in the way of her other life plans. They occasionally pop up on the news, and they elicit a surge of anger and indignation. Susan Smith, for instance, drowned her two children in a car because she was obsessed with a man who didn’t want kids.

Carl Jung theorized that the reason we find these stories so much more disturbing than other cases of infanticide is that they invert the “Mother” archetype. For Jung, a mother is supposed to be the embodiment of care and love. They are the rock for any child; however, when a mother abandons that role — by neglect or murder — we rage about the cruelty and the “Terrible Mother” inversion.

While stories of maternal infanticide are heartbreaking, the more common version of the Medea effect is when a mother harms a child to “get back” at an old partner or spouse. A typical way this is done is when a mother fights tooth and nail in court to deprive a father of any form of custody. In cases where the father is a caring parent, the act harms the child to hurt the father. This version of the Medea effect is known as “parental alienation syndrome.”

Learning to hate dad

In the 1980s, child psychologist Richard Gardner coined the term “parental alienation” to refer to an indoctrination strategy in which one parent portrays the other as evil. Over time, the child’s relationship with the other parent frays, and they learn to avoid, shun, or even hate them. In the case of the Medea effect, the mother vilifies the father, but parental alienation more broadly can go either way.

Here are three examples of such strategies:

False narratives. In some cases, one parent will fabricate stories or exaggerate situations to paint the other in a negative light. This could involve unproven, unsubstantiated accusations of neglect, abuse, or other harmful behaviors.

Undermining. A parent might belittle or criticize everything the other one does in front of their children, hoping the children learn to disrespect them. For instance, a father might undermine the character of a mother with lines like, “Oh, mommy wouldn’t be able to do that” or “You can’t expect any better from your mom.”

Restricted communication. In a household setting, one parent might insist on taking on certain emotionally important roles. A mother might claim “only she” can nurse a sick child. A father might refuse a mother the right to take the child to some sports events. In a divorced context, one parent can limit the phone time a child has with the other. They might say a child can “only” meet a parent in a certain setting, for a certain time, and with specific supervision.

Long-lasting harm

All of which can cause deep-rooted harm and lifelong trauma for the child. The psychiatrist Robert M. Gordon wrote a paper called “The Medea Complex and the parental alienation syndrome” about his experiences witnessing divorce proceedings as a court-appointed child custody evaluator. He noted: “It is not only cruel to the alienated parent, but it produces life-long harm to the child. It is psychological child abuse … Such brainwashing and alienation usually lead to a lifelong problem with establishing and maintaining healthy intimacy.”

Gordon’s paper is full of case studies about such lifelong harm. Today, parental alienation is well documented and has proven harmful to children.

For Gardner, parental alienation tactics are born of Medea-type powerlessness. As he put it in the 1980s: “Because these mothers are separated and cannot retaliate directly at their husbands, they wreak vengeance by attempting to deprive their former spouses of their most treasured possessions, the children.” And both Gardener and Gordon assumed parental alienation tactics to be the main reserve of mothers. Gordon argued, “I believe that brainwashing by a mother is more powerful than that of a father, since the child’s bond with the mother is usually more primitive.”

Even if we disagree with those gender roles and Jungian archetypes, we can appreciate the huge damage parental alienation can have on children. As is often the case in psychotherapy, when we have a name for something, we can better inoculate against it. Knowing some parents can and do harm their children, let us call it out.

This article The Medea effect: When a parent harms their child to get back at someone else is featured on Big Think.

One sunny day this fall, I caught a glimpse of the new psychiatry. At a mental hospital near Yale University, a depressed patient was being injected with ketamine. For 40 minutes, the drug flowed into her arm, bound for cells in her brain. If it acts as expected, ketamine will become the first drug to quickly stop suicidal drive, with the potential to save many lives. Other studies of ketamine are evaluating its effect as a vaccination against depression and post-traumatic stress. Between them, the goal is nothing less than to redefine our understanding of mental illness itself.

Depression is the most common mental illness in the United States, affecting 30 percent of Americans at some point in their lives. But despite half a century of research, ubiquitous advertising, and blockbuster sales, antidepressant drugs just don’t work very well. They treat depression as if it were caused by a chemical imbalance: Pump in more of one key ingredient, or sop up another, and you will have fixed the problem.

But the correspondence between these chemicals (like serotonin) and depression is relatively weak. An emerging competitive theory, inspired in part by ketamine’s effectiveness, has it that psychiatric disease is less about chemical imbalance than structural changes in the brain—and that a main cause of these changes is psychological stress. “I really do think stress is to mental illness as cigarettes are to heart disease,” says Gerard Sanacora, the psychiatry professor running the ketamine trial at Yale.

The theory describes stress grinding down individual neurons gradually, as storms do roof shingles. This, in turn, changes the nature of their connections to one another and the structure of the brain. Ketamine, along with some similar molecules, acts to strengthen the neuron against that damage, affecting not just the chemistry of the brain but also its structure.

Mental hospitals don’t usually see patients until they break: a brain shaped by vulnerable genes, wrecked by the stress of loss or trauma. This isn’t how it works with other sicknesses: heart disease, cancer, AIDS. Detected early, these conditions can often be managed. Crises averted.

If Sanacora and like-minded researchers are right, we may be on the cusp of a sea change that allows for a similar approach to mental health. The new approaches may prevent mental illness before it hits, by delivering a vaccination for the mind.

The need for progress could hardly be more urgent: Of all illnesses, neuropsychiatric diseases are estimated to put the heaviest burden on society. Nearly half of Americans are affected by some sort of mental disorder at some point in life. Suicides, 90 percent of them among the mentally ill, take 40,000 Americans every year—more than murder or car crashes. Since 2005, the suicide rate among U.S. war veterans has nearly doubled; in the first half of 2012, more service members died by suicide than in combat. Few medical failures are more flagrant than psychiatry’s impotence to save these people.

At the same time, treatment can be woefully ineffective. Less than a third of depression patients respond to a drug within 14 weeks, according to the 2006 STAR*D trial, the largest clinical test of antidepressants. After six months and multiple drugs, only half of patients recovered. Thirty-three percent don’t respond to any drug at all. When the pills do work, they are slow—a deadly risk, given that people with mood disorders kill themselves more often than anyone else.

Our treatments work so poorly in part because we don’t really understand what they do. Serotonin, the most common target for current antidepressants, is a neurotransmitter, a chemical that carries messages in the brain. But it was first found, in 1935, in the gut. Serotonin’s name comes from blood serum, where Cleveland Clinic scientists discovered it in 1948, noting that the chemical helps with clotting.

When Betty Twarog, a 25-year-old Ph.D. student at Harvard, later found serotonin in neurons, she wasn’t taken seriously. At that time, brain signals were thought to be purely electrical impulses that leapt between cells. Twarog called this old idea “sheer intellectual idiocy,” as Gary Greenberg reports in his book Manufacturing Depression. Working at the Cleveland Clinic in 1953, she found serotonin in the brains of rats, dogs, and monkeys.

Twarog didn’t know yet what serotonin was doing there, but a clue came soon from D.W. Woolley, a biochemist at Rockefeller University, in New York. In 1954 Woolley pointed out in a paper that lysergic acid diethylamide, or LSD, is chemically similar to serotonin and is processed similarly in the brain. Since LSD “calls forth in man mental disturbances resembling those of schizophrenia,” he wrote, another drug affecting serotonin might be used to treatschizophrenia. Twarog’s original paper would take years to percolate through the male-dominated field, but her work and Woolley’s would become accepted as evidence of how important chemicals like serotonin could be to brain signaling. The discovery was a breakthrough for neuroscience—but it also birthed a misleading, long-lived belief about mental illness. “The thesis of this paper,” Woolley wrote, “is that … serotonin has an important role to play in mental processes and that the suppression of its action results in a mental disorder. In other words, it is the lack of serotonin which is the cause of the disorder.”

Around the same time, other researchers stumbled on the first antidepressants, iproniazid and imipramine. Intended to treat tuberculosis and schizophrenia, respectively, these drugs also happened to make some patients “inappropriately happy.” Researchers found that the drugs elevated levels of serotonin, along with related neurotransmitters.¹ This began a huge search to find chemically similar drugs that worked better as antidepressants.

Iproniazid was the first of a class of medicines that block an enzyme from breaking down serotonin, as well as dopamine and norepinephrine, two other neurotransmitters. The chief downside of these drugs, called monoamine oxidase inhibitors (MAOIs), is that they require a strict diet: no aged cheeses, wine, beer, or cured meats. Combined with these foods, the drugs can cause deadly spikes in blood pressure, a hassle that often inclines patients to ditch them. (The novelist David Foster Wallace took an MAOI for decades; in part to escape the food restrictions, he got off the drug months before his suicide.) On the other hand, tricyclic antidepressants, like imipramine, work by blocking the re-absorption of serotonin and norepinephrine. The cost is a host of side effects, from dry mouth to weight gain to erectile dysfunction and loss of libido.

The next generation of drugs focused on fine-tuning the same mechanisms, and had somewhat improved side effects. A new class of drugs known as selective serotonin reuptake inhibitors, or SSRIs, arrived in the ’80s, bringing huge commercial successes like Prozac, Zoloft, and Paxil. Since SSRIs are more specifically focused on serotonin, they were heralded as cleaner options; but they are not much more effective at lifting mood than the older drugs. We often take for granted the diabetes analogy for depression: If you are depressed, it is because you need serotonin, just as a diabetic person needs insulin. Drug companies often say that mood disorder is caused by a “chemical imbalance” in serotonin or a signal like it. One ad for Zoloft, the blockbuster antidepressant, featured a sad white circle crawling cutely beneath a gray cloud; the voice-over boasted that depression may be “related to an imbalance of natural chemicals in the brain. Zoloft works to correct this imbalance.”

But the evidence for this story is slim. Prozac raises serotonin levels within hours yet doesn’t change mood for weeks. When scientists deplete serotonin in healthy people, it does not make them sad. And when doctors measure serotonin levels in the cerebrospinal fluid of depressed people, they do not find a consistent deficiency; one 2008 study even found increased levels of serotonin in depressed people’s brains. The drug tianeptine, discovered in the late ‘80s, decreases serotonin levels yet relieves depression. And studies have shown that people falling in love show lower, not higher, levels of serotonin.

Serotonin is clearly not just a feel-good chemical. If a serotonin-based drug like Zoloft makes you happier, it works in some other, indirect way. As psychiatrist Ronald Pies, editor of Psychiatric Times, put it in 2011, “The ‘chemical imbalance’ notion was always a kind of urban legend—never a theory seriously propounded by well-informed psychiatrists.”

Meanwhile, as serotonin falls far short of explaining depression, a more likely candidate is emerging.

Stress in moderation is not harmful, but motivating. Cortisol, a stress hormone, cycles daily; synchronizing with sunlight, it helps arouse us for the day. In health, the hormone spikes when we need to pay attention: a test, a job interview, a date. Studies on rodents and humans confirm that brief, mild increases in stress are good for the brain, particularly for memory. During these spikes, neurons are born and expand in the hippocampus, the seahorse-shaped finger of tissue responsible for forming new memories and understanding three-dimensional space, and rodents learn better. The student who gets stressed while studying is more alert and remembers more than the one who feels no urgency—up to a point. The problem comes when stress is either too intense at one moment, as in a rape or violent attack, or too sustained, as in long-term poverty, neglect, or abuse.

Stress changes brain architecture differently, depending on how long it lasts. After chronic stress, like childhood trauma, the effect of hormones on brain cells inverts: Neurons in the hippocampus and the prefrontal cortex, which is responsible for mood and impulse control, start to shrink, while those in the amygdala, the almond-shaped seat of fear and anxiety, expand like overgrown shrubbery. But people are differently vulnerable, depending on genes and on prior life experience. “If you take two people and subject them to the same stressful event, for one of them it will be harmful and for the other, no,” says Maurizio Popoli, a professor of pharmacology at the University of Milan. “It is because they perceive the stress differently.”

Stress hormones’ most important effect is to flood parts of the brain with glutamate, the brain’s “go” signal. Used by 80 percent of neurons in the cortex, this key neurotransmitter drives mental processes from memory to mood. Glutamate triggers neurons to generate sudden bursts of electricity that release more glutamate, which can in turn trigger electrical bursts in nearby neurons.

This cellular signaling is called excitation and is fundamental to how information is processed in the brain. Like sexual excitability, it ebbs and flows; a “refractory period” follows each neural firing, or spike, during which the neuron cannot be excited. Other neurotransmitters, like serotonin, are called “modulatory,” because they change the sensitivity of neurons that secrete glutamate (among others). Less than 1 percent of neurons in the cortex signal with these modulators. As Popoli puts it, these modulators are “very important for fine-tuning the machine. But the machine itself is an excitatory machine,” driven by glutamate.

Glutamate moves like a ship between neurons. The sea it sails is called the synapse, the shore it departs from is the presynaptic neuron, and the destination, on the synapse’s far side, is the postsynaptic neuron. Another component, called a glial cell, works to remove glutamate ships from the synapse and recycle them. The glutamate system is affected at each of these points by stress hormones: They push the first neuron to send more ships, interfere with the glial cell’s recycling, and block the docks on the distant shore. All of these changes increase the number of glutamate ships left in the synapse, flooding the cell with aberrant signals. Indeed, depressed people’s brains, or at least animal models of depression, show all three of these problems, leading to long-lasting excesses of glutamate in key portions of the brain.

This superabundance of glutamate makes a neuron fire sooner than it should and triggers a cascade of signals inside the cell, damaging its structure. Glutamate binds to the neuron and allows in a flood of positively charged particles, including calcium, which are vital to making a neuron fire. But in excess, calcium activates enzymes that break down the neuron. Each neuron has tree-like branches, called dendrites, which are used to communicate with other neurons. When overdosed in glutamate, this canopy of branches shrinks, like a plant doused with herbicide. First the “twigs,” called spines, disappear. After prolonged stress, whole branches recede.

This harmful process, called excitotoxicity, is thought to be involved in bipolar disorder, depression, epilepsy, and neurodegenerative diseases like Alzheimer’s, Huntington’s, and Parkinson’s. In depressed brains, many areas are shrunken and underactive, including part of the prefrontal cortex and the hippocampus. The brain changes that cause mood disorders, Sanacora and his colleagues believe, come in part from chronic stress overexciting neurons with glutamate.

We usually think of our brains’ adaptability as a good thing. Just as neurons grow during development, the wiring in the adult brain can change. After strokes or other brain injuries, neural signals re-route themselves around damage, allowing even very old people to re-learn lost skills. Psychotherapy and meditation can change patterns of brain activity in ways that persist after treatment.²

But the neuroplasticity hypothesis of mental disorder highlights the drawback of such neural liberalism: The human brain’s flexibility allows regeneration, but also renders it vulnerable to being altered by stress. Subjected to the trauma of war, a bad breakup, or a bout of homelessness, a person with a genetic predisposition may find his mind stuck in a loop of chronic fear or depression.

The mood drugs in wide use now focus on modulatory neurotransmitters like serotonin. Ketamine, however, works directly on glutamate signaling. If ketamine is tapping into the root of the problem, this might explain why it works faster, better, and more often than more popular antidepressants.

Not everybody accepts the idea that glutamate and stress are central to depression. Some experts see the effects of stress as downstream effects, not the root cause of mood disorder. “The mechanism of action of a good treatment does not have to be the inverse of a disease mechanism,” says Eric Nestler, an expert on addiction and depression at Mt. Sinai Hospital. Serotonin drugs and ketamine may affect depression indirectly, without a serotonin or glutamate abnormality at the root of depression. Nestler also points out that depression probably includes a diversity of subtypes, without any single cause. He treats depression not as a unified disease, but a constellation of symptoms, each with discrete neural roots.

Even so, we do know that ketamine works faster than any other drug, and for up to 65 percent of patients who don’t respond to existing treatments.

If ketamine turns out to be a psychiatric savior, it will be one with a surprising history. Since 1962 it has been a go-to anesthetic for children in emergency rooms, because it kills pain, muffles consciousness, and rarely causes breathing or heart problems. Children given ketamine enter “a trance like state of sensory isolation” free of pain, memory, and awareness, as one review put it. Emergency room doctors rely on ketamine to make sure kids have no awareness or memory of, say, the trauma of having a shattered arm set back into place.

On the other hand, ketamine is a well-known recreational drug with potential for abuse. The dissociative trip caused by a moderate dose of ketamine has made it popular in clubs and raves since the 1970s, especially in Asian cities like Hong Kong. Its sedative effect made “special K” a date-rape drug. Doctors, patients, and the government agencies that fund research are often suspicious of a drug known to cause hallucinations, as they have been of psychedelics like psilocybin and ecstasy, despite their potential for treating depression or anxiety. Each tends to show fast results after a single dose, like ketamine.

In 1999, the same year ketamine was declared a controlled substance in the United States, Yale researchers happened upon its antidepressant power. A team co-led by Dennis Charney, now dean of the Icahn School of Medicine at Mt. Sinai, in Manhattan, and John Krystal, now chair of the department of psychiatry at Yale, used ketamine to study glutamate: Since ketamine was known to block glutamate receptors, it might show what role the excitatory neurotransmitter plays in the depressed brain. To their surprise, they found that the drug made patients feel better, often within hours. A single dose, much smaller than what’s used for anesthesia, tended to last for weeks.

Since 1999, a dozen studies have replicated the results, often on patients who failed to respond to other drugs. Ketamine also works for bipolar people in depressive phases, without triggering mania, as classic antidepressants sometimes do. The majority of depressed people studied have responded to ketamine. For patients who are often suicidal, this fast response can be lifesaving. Some 50 doctors in the U.S. now offer ketamine infusions for depression.

Many leaders in the field see the emergence of ketamine, and future fast antidepressants based on glutamate, as a great leap forward for the field. “In my mind,” Sanacora told NPR recently, “it is the most exciting development in mood-disorder treatment in the last 50 years.”

Ketamine and the old antidepressants both result in fuller neural “trees,” but by different routes, at different speeds. Prozac and other serotonin-based drugs take four to six weeks to kick in. A landmark 2003 Science study by Columbia University’s René Hen and Ronald Duman, now at Yale, found that serotonin-based antidepressants only work if they spur birth of new neurons in the hippocampus.³ These new neurons take four to six weeks to mature, roughly the same amount of time that conventional antidepressants take to lift a depressed person’s spirits. A 2010 paper argued that SSRIs like Prozac may work by dampening glutamate release in response to stress. So even old-school antidepressants, when they work, may act on the glutamate system.

Ketamine, on the other hand, seems to act directly on mature neurons, fertilizing them to grow branches more robustly, or protecting them against damage. Ketamine’s key effect is to block glutamate receptors of one type. This causes less calcium to flow into the neuron, reducing the risk of the neuron shrinking or self-destructing.

Today ketamine is offered by psychiatrists and anesthesiologists, at prices ranging from $300 to $1,000 per dose, for people who are morbidly depressed or have chronic pain. Insurance doesn’t usually cover the cost of an infusion, because even though it is FDA approved as an anesthetic, it has not been approved as an antidepressant. Each new use of a drug requires multiphase clinical trials for FDA approval, usually funded by pharmaceutical companies, which have little incentive to invest in a drug they can’t monetize. Ketamine got its original patent in 1966, and that expired long ago. So even if drug companies steered ketamine through the expensive approval process as an antidepressant, doctors could still prescribe the cheap, generic versions already available for anesthesia instead of pricier, patented versions intended for depression. This is an old story. Lithium carbonate, which also acts on glutamate receptors, is still one of the most reliable drugs for treating bipolar disorder. But lithium, which is an element, can’t be patented. So, despite their effectiveness, these generic pills do not attract many corporate dollars.

One tough truth about mood disorder is that not all forms may ever be curable. Brain-imaging studies have shown structural differences between the white matter in healthy versus bipolar brains. Differences in personality and sleep patterns also persist in bipolar people, even between manic or depressed episodes. The structural changes likely have genetic roots, and once they arise, are difficult or impossible to reverse.

Nevertheless, if a drug prevents a mood disorder from manifesting, it might prevent harmful anatomical changes from ever taking place. Just as a vaccine triggers the body to arm itself against a particular virus, a drug like ketamine, given before the crisis that triggers a breakdown, might protect the brain against the effects of stress. Like a vaccine, the drug might only need to be given once for lasting resilience.

The first evidence in humans that ketamine might work to prevent mood disorder, not just treat it, came from the battlefield. U.S. soldiers injured in Iraq were treated with various anesthetics, including ketamine. Since ketamine can cause hallucinations, surgeons worried that it might make trauma worse: Scary combat-related hallucinations could put soldiers at higher risk of mental illness.

But they found the opposite. Out of 25,000 service members wounded in Iraq between 2002 and 2007, the data showed, veterans treated with ketamine for burns had lower rates of post-traumatic stress disorder. Among civilians and soldiers hospitalized for burns, as many as 45 percent end up with PTSD. But soldiers treated with ketamine on the battlefield got PTSD about half as often—even though they had more severe burns requiring more surgeries and longer hospital stays.

Rebecca Brachman, a neuroscientist and recent doctoral graduate from Columbia University, and her supervisor, Christine Denny, tried giving ketamine to mice and then exposing them to stressors.⁴ The researchers tested several types of stress, including one in which subject mice are “bullied” by more aggressive mice for two weeks. After this daily hazing, mice ordinarily develop the rodent equivalent of PTSD and depression: freezing in a new space, refusing to interact with other mice, and not moving in a forced swim test. But the mice “vaccinated” before the bullying fared far better: They didn’t act depressed afterward. Brachman and Denny found that the protection from a single dose lasted for weeks, even though ketamine only stays in the body for a few hours. Though they haven’t tested it yet, it is possible that, like a vaccine, this protection could last for much longer. Their rodent research suggests ketamine may work even better as a prophylactic than as an antidepressant.

Denny says that we may eventually routinely use ketamine to prevent PTSD in combat veterans, rape victims, or survivors of car crashes or mass shootings. Ketamine seems to be most strongly protective in mice when given before stressful events, Brachman says. Since we can’t predict most traumatic life events, this would limit the drug’s utility. But if injected after a trauma yet before the psychological damage sets in—as with the burned soldiers—ketamine may still be protective. Denny is investigating this possibility now. 

And in some situations, violent shock is predictable. “You don’t know when an earthquake will happen,” Brachman says, “but we do know when we’re about to send U.N. workers into an area devastated by a disaster.” When people know they are going into an acutely traumatic situation, she imagines, a preventive drug given ahead of time might protect their brains from the long-lasting effects of stress. Think of earthquake aid workers, fire fighters, or rescue workers in Syria, dragging mangled people from rubble.

The idea that a single injection could prevent mood disorders is a radical departure from current psychiatric thinking. But there are some precedents: Talk therapy and mindfulness meditation have long focused on building resilience to stress. Bipolar patients take “neuroprotective” drugs like lithium not to treat current symptoms, but as a protection against future breakdowns, for instance.

Not everyone is confident that ketamine is a safe bet, to be sure. Ketamine’s long-term safety is not known, says Nestler. No lasting ill effects are seen in anesthesia patients, who take much larger doses, but they haven’t received routine treatments, the way it is administered as an antidepressant.

Plus, ketamine’s reputation as a street drug is tough to shake. Many doctors consider the hallucinogenic an unacceptable risk for patients, who they fear may develop a taste for the high. Yale’s Sanacora points out that patients in his trial, who are screened for drug or alcohol abuse, often find the trip feeling unpleasant or disturbing. The psychedelic experience is surreal, he points out, not the mellowing pleasure of a drug like alcohol, Xanax, or heroin. Extreme ketamine trips, referred to as falling in a “K-hole,” are often compared to near-death or unsettling out-of-body experiences; they hardly sound like fun to most people.

But since the antidepressant dose is far lower than the one taken to get high, many patients don’t even notice. Drug companies are also competing to develop a less trippy alternative. Johnson & Johnson is testing a nasal spray form of esketamine, a version of ketamine with less psychoactive impact. A company called Naurex has finished phase II trials of Rapastinel, an injected drug that partially blocks the same glutamate receptors as ketamine, but is not psychedelic.

The ketamine pioneers emphasize that their prevention research is the beginning of a new road, raising hopes, rather than offering an immediate cure. Brachman and Denny stress that ketamine may not be the drug that ultimately makes it into widespread use; like the anti-tubercular drugs in the 1950s that spawned the antidepressant era, it is the first to trail-blaze this new class of psychiatric prophylactics. “What this work shows us is that we can intervene beforehand and create some sort of self-reinforcing stress resilience,” Brachman says. “We didn’t know that before; that’s what’s important. Everything else—should we use it, how should we use it—that all comes later.”

Taylor Beck is a journalist based in Brooklyn. Before writing, he worked in brain imaging labs studying memory, aging, and dreams.

References

1. Maxwell, R.A. & Eckhardt, S.B. Drug Discovery Humana Press, New York, NY (1990).

2. Kennedy, S.H., et al. Differences in brain glucose metabolism between responders to CBT and venlafaxine in a 16-week randomized controlled trial. American Journal of Psychiatry 164, 778-788 (2007).

3. Vogel, G. Depression drugs’ powers may rest on new neurons. Science 301, 757 (2003).

4. Brachman, R.A., et al. Ketamine as a prophylactic against stress-induced depressive-like behavior. Biological Psychiatry (2015). Retrieved from DOI: http://dx.doi.org/10.1016/j.biopsych.2015.04.022

This article A vaccine for depression is featured on Big Think.

A new biohybrid computer combining a “brain organoid” and a traditional AI was able to perform a speech recognition task with 78% accuracy — demonstrating the potential for human biology to one day boost our computing capabilities.

The background: The human brain is the most energy efficient “computer” on Earth — while a supercomputer needs 20 megawatts of power to process more than a quintillion calculations per second, your brain can do the equivalent with just 20 watts (a megawatt is 1 million watts).

This has given researchers the idea to try boosting computers by combining them with a three-dimensional clump of lab-grown human brain cells, known as a brain organoid.

The human brain is the most energy efficient “computer” on Earth.

What’s new? A team from the University of Indiana Bloomington (UIB) has now unveiled a new one of these hybrid systems, which it calls “Brainoware.”

After growing a brain organoid from stem cells, the UIB team placed the tissue on a plate covered in thousands of electrodes. They could then use traditional computing hardware to deliver electrical pulses to the organoid and record its responding neural activity.

To demonstrate how such a system might be used, the team converted 240 recordings of 8 Japanese speakers saying vowel sounds into electrical pulses. They then trained an AI to predict which person was speaking based on the neural activity of the brain organoid in response to the electrical stimulation.

Brainoware’s predictions improved steadily during the training, and after 2 days, it could predict the speaker with 78% accuracy.

The big picture: Brainoware was less accurate at speech recognition than a traditional computing system running an AI, and keeping the organoid alive required a CO2 incubator and other power-hungry resources.

In other words, the system isn’t an improvement on the tech we already have — but it could prove to be a key stepping stone on the path to more advanced biocomputing systems in the future.

“We wanted to ask the question of whether we can leverage the biological neural network within the brain organoid for computing,” lead researcher Feng Guo told Tech Xplore. “This is just proof-of-concept to show we can do the job.”

This article Cyborg computer combining AI and human brain cells really works is featured on Big Think.

The heart is a fickle thing, but it may be best to keep it that way. In a recent preprint article, still awaiting peer review, Imperial College London researchers Fernando Rosas and Pedro Mediano reveal how the heart behaves under psychedelics, dynamically interacting with the brain in unique ways that may promote well-being. Drawing on multiple data sets for psilocybin, ketamine, DMT, and LSD, the researchers analyzed correlations between brain activity, subjective effects, and three measures of cardiac activity in humans: heart rate, heart-rate variability, and heart-rate entropy. Their findings suggest that by knowing the heart, we can better know the mind.  

The vocabulary of the heart

When it comes to modeling psychedelic brain effects, neuroscientists tend to view heart rate and other peripheral physiological changes as mere byproducts of the experience, irrelevant to understanding how altered states of consciousness are constructed, let alone how psychedelics might improve mental health. After all, it’s common knowledge that many psychoactive drugs, including psychedelics, can increase heart rate (the number of beats per minute), so why should the line of inquiry go any further?  

For good reason, as it turns out. Thanks to advances in neuroscience, we now know that the heart can influence cognition, including emotion, time perception, social interaction, and sense of self. In fact, selfhood itself may be grounded in the integration of internal signals, especially heartbeats, into the brain’s representation of the body. And when it comes to influencing selfhood, not all beats are created equal.   

In order to support the body in balancing “fight or flight” with “rest and digest,” one important thing the heart does under normal conditions is behave erratically. Although it may feel like your heart beats rather consistently, it actually varies by a fraction each time, even when you’re at rest. This variation in time between beats is called heart rate variability (HRV), and it’s important for adapting to change. The pattern of HRV differs for each person, like a fingerprint, and can shift depending on the time of day, season, and other factors. Overall higher HRV has been firmly linked to greater health, as it seems to reflect the ability of an organism to flexibly adapt to complex environmental circumstances. Meanwhile, lower variability has been linked to illness. Good sleep, physical exercise, and positive social interaction have been shown to increase HRV, while depression, schizophrenia, and other conditions have been associated with reduced HRV. The heart, it seems, is fundamental to conscious experience. 

Still, most theories of how psychedelics work have focused on the brain, broadly neglecting the rest of the body. Another view, Rosas and Mediano write, is that autonomic changes (i.e. changes in involuntary bodily functions) are part of the experience itself, and therefore “bearers of signal rather than noise.” 

It was on this basis that Rosas and his team — which includes University College London neuroscientist and cardiac researcher Sarah Garfinkel — sought to investigate the link between brain and heart in psychedelic experience. They wanted to know: Do psychedelics increase HRV as well as heart rate, or do something else to the heart entirely? Even more intriguingly, would these cardiac markers predict subjective experience? They already had a few clues to work with. Since previous research has shown that psychedelics increase “brain entropy,” which is a measure of the variability of conscious states (more diverse and less typical patterns of activity), they wondered whether psychedelics might also diversify patterns of heart activity. This variability of HRV — variability of variability, if you will — is called heart-rate entropy (HRE). 

“Entropy measures not the prevalence of specific patterns, but the diversity of patterns in heart rate fluctuations,” Rosas told Big Think. “I like thinking that entropy doesn’t look for patterns but looks for patterns of patterns.”

To measure HRV, you need to identify the “shape” of the pattern. To measure HRE, you don’t necessarily need to know what the HRV pattern looks like exactly — just how diverse it is.

“Two subjects may display entirely different shapes in their patterns of fluctuation, but for the entropy this is not a problem, as it just assesses how broad the repertoire of patterns of each subject are.”

If psychedelics increased heart-rate entropy, the team wondered, would these changes be correlated with increases in brain entropy, and could that tell them something about the therapeutic effects of psychedelics?

The heart of the trip

First, the research team showed that, compared to placebo, all psychedelic compounds — ketamine, psilocybin, LSD, and DMT — did, in fact, increase HR, HRV, and HRE. 

Next, to take a closer look at the dynamic relationship between heart activity, brain activity, and subjective experience, they pulled aside the DMT data set for analysis. They chose this data set for two reasons. Because a DMT trip takes less than 20 minutes, the data set gave Rosas and his team a good glimpse of what high variability over a relatively short time could look like. This set also provided them with rich psychological ratings associated with various subjective dimensions of the experience, gathered from questionnaires. (As a side note, the psilocybin and ketamine data sets were excluded from the following analyses as they couldn’t provide the same insight into the dynamics of a trip, covering only a small portion of what is a much longer trip.)

The researchers found that heart-rate entropy predicted changes in brain entropy much better than HR and HRV, with substantial correlation 0 to 5 minutes (peak experience) and 9 to 12 minutes after injection. “Although heart-rate entropy waxes and wanes similarly to the mean heart rate, it has very distinctive predictive properties,” Rosas says. “Even if their dynamics may look similar, they seem to be capturing rather different processes.” 

In fact, each autonomic marker had very distinctive predictive power over dimensions of the DMT experience as it unfolded, explaining up to 70% of the variation between subjects. For example, the intensity of experience was dominated by HR, challenging experience by HR entropy, and complex imagery alternating between HRV, HR, and entropy at different times. 

That said, Rosas cautions against over-interpreting the findings. 

“This is an explorative analysis on a small sample size, which we think should be taken as a proof of principle that this works,” he says. “Larger studies should be carried out to find out what autonomic feature is most associated with what psychological dimension.”

Next, they examined the LSD data set, which was larger (20 subjects under drug and placebo in four different environmental conditions), to see whether heart-rate entropy and brain entropy were simply co-occurring phenomena, or whether they each contributed in their own way to the subjective experience. As the LSD dataset used MEG and structural MRI rather than the low-density EEG of the DMT data set, they were also able to extract spatial information to tell them which parts of the brain showed this entropic link (as it turns out, the precuneus, mid cingulate, and sensorimotor areas, specifically). 

What they found is that different features of the LSD experience — simple and complex imagery, positive mood, intensity of the experience, ego dissolution, and emotional arousal — correlated in distinct ways with different biomarkers (heart and brain). For example, brain entropy was the strongest predictor of simple and complex imagery, while HR entropy was the strongest predictor of positive mood. But when taken together, positive correlations between heart and brain biomarkers were even more predictive of various states, suggesting that knowing the state of the autonomic system substantially increases predictive power over subjective scores.

“The predictive power of autonomic markers is not redundant with the predictive power of brain entropy,” Rosas says, “but seems to be synergistic.” In other words, heart activity doesn’t just reflect brain activity — it’s an integral part of the picture, contributing its own pieces to the puzzle of the psychedelic state. “Better predictions of the psychological effects of LSD can be attained by considering models which include both brain and heart signatures, and their interactions.” 

Entropy and health

So, what could all this mean for mental health? For starters, you might say hearts were behaving rather strangely in these data sets, and that’s a good thing.

“The patterns of heart activity we were seeing with psychedelics was quite special,” Dr. Garfinkel told Big Think. “To get such striking rises in both heart rate and heart rate variability together is an unusual profile, typically only seen under conditions of intense joy and euphoria.”

In most cases, if heart rate increases, HRV decreases. This happens every time you exercise, for example. What’s more, in schizophrenia and some cases of depression, brain entropy is increased while HRV is reduced. To see simultaneous increases in brain entropy, heart rate, and heart entropy was fairly remarkable.

“As we are increasingly recognizing that cardiac signatures and their interactions with the brain are potentially pivotal for guiding emotional states,” Garfinkel said, “this relatively unique signature may be integral in helping us understand the body-brain dynamics underscoring the therapeutic and beneficial effects of psychedelics.” 

The next obvious step would be to disentangle the relationship between brain effects and HRV — for example, by determining whether the heart itself could be driving, not just responding to, psychedelic states. Motivated by this possibility, Rosas said, “I don’t like the simplistic view that the heart is nothing more than a blood pump, but I’d like to be able to support counter-arguments on empirical evidence.” 

In future studies, Rosas believes causality could first be investigated without psychedelics by “employing animal models to perform pharmacological or other interventions, altering one system or the other to see what happens with the coupling.” What’s most exciting to him, for now, is that focusing on the heart could change the way psychedelic scientists work: “Collecting large samples of ECG data related to psychedelics is far easier, less invasive, and more cost-effective than brain imaging.” 

While the team acknowledges that the uniqueness of this “entropic heart effect” could be partly due to its difficulty to elicit in a laboratory setting (thus making it relatively absent from the research literature), they also offer another — more heartening — possibility: “This peculiar autonomic signature may be associated with the very special state of mind often associated with psychedelic experiences, related to expansion, connection, and meaning.”

This article The psychedelic heart: Scientists predict DMT effects from cardiac activity is featured on Big Think.

There’s nothing so beloved by filmmakers as the near-death experience scene. You know the one: It happens when the hero is bleeding out, drowning, or staggering through a heat-warped desert. Suddenly, the screen turns a pure, calming white, and there’s a saccharine scene between the hero and their dead loved ones, or perhaps a wise old person with a kind face. After some heart-warming back and forth, it ends with something like, “It’s not your time,” or, “You don’t belong here.” Then, the hero jerks awake and goes on to defeat anything and everything.

As it turns out, these near-death experiences (NDEs) are not just a box office trope. They’re unusually common in the general public. Roughly 9 million Americans claim to have had an NDE. It’s thought that roughly five percent of the general population, and 15-20 percent of critical patients (that is, those in critical care) have had an out-of-body experience. It’s likely that someone in your life has had one. Perhaps you have?

So, what philosophical or religious conclusions can we draw from this? To paraphrase C.S. Lewis, if we have an experience which cannot be satisfied by this world, does that point to another world? An afterlife, perhaps? Well… it’s complicated.

A different kind of experience, entirely

In the scientific or philosophical literature, a near-death experience is not a misunderstanding or misrepresentation of some other cognitive phenomenon. As one leading author on the topic, Pim van Lommel, describes them, “the NDE is an authentic experience that cannot be simply reduced to imagination, fear of death, hallucination, psychosis, the use of drugs, or oxygen deficiency.” NDEs need to be examined as their own thing — a separate experience, that millions of people around the world encounter, and which is irreducible to any other (existing) neuroscientific explanation.

Lommel’s landmark paper reveals several interesting things. First, NDEs have been shown to occur some minutes after the heart of a critical patient has stopped, and at a time when “the brain ordinarily stops functioning and cortical activity becomes isoelectric.” This implies that whatever the source or reason for these NDEs, it does not lie in normal, understood brain processes. Second, our recollection of NDEs is much more like real memories than imagined memories. As a research team from the University of Padova showed, “NDE memories and the real memories had the same amount of mnesic characteristics and both were more complex and richer than imagined memories.” That is to say, NDEs cannot be immediately dismissed as the fictional nonsense of near-death — at least in terms of memory and recollection.

Finally, and perhaps most shockingly, people who have had an NDE can often recount things that actually happened while they were unconscious, such as an open-heart operation taking place. Even more oddly, in a point considered by psychiatrist Dr. Bruce Greyson in a video for Big Think, sometimes NDEs feature events that the experiencers couldn’t even have known about. In Greyson’s case, a patient could “see” him talking to a colleague a corridor away from where her bed lay. He could think of no other explanation for how she knew that fact.

Heaven exists because I’ve seen it

The Swedish philosopher, Jens Ambers, in his book, Why an Afterlife Obviously Exists, believes that NDEs make an interesting case for the existence of an afterlife.

He argues, first, that NDEs can happen to anyone — atheists, believers, and everyone in between. And yet, people who have these experiences are much more likely to come away from an NDE believing in the presence of an afterlife. Between 76 and 100 percent of those who have an NDE end up agreeing with the statement, “An afterlife definitely exists.” These experiences are so profoundly vivid and so moving, that they serve to utterly reorient people in regard to their beliefs. The existence of experiencers is the reason for non-experiencers to believe. For Ambers, an NDE acts as self-justifying, “empirically certain” proof for God, gods, and the afterlife. Given that these experiences are coherent, structured, and detailed, they are valid and justified grounds for these beliefs (as much as any “real” experience is).

That’s all good and well, for them, but it’s hardly going to convince everyone else, right? For Ambers, it certainly should. If up to 15 percent of the general population claims to have first-hand, indisputable proof of an afterlife, surely that adds weight to its probable existence? If millions of otherwise rational, reputable, and reliable people tell you something is true, isn’t that good grounds for believing so?

Not quite seeing the light

There’s a lot to be said for this argument. It is certainly compelling insofar that it utilizes some of the most modern research we have into neuroscience and NDEs. But, there are still at least four issues it needs to address.

First, using NDEs in this way is essentially a reworking of the “god of the gaps” fallacy. This is an argument that falls under the category, “We do not know how something works, so therefore it must be god/the mystical.” Yes, it might be, but until we have ruled out all other natural explanations, there is little philosophical reason to recourse to the supernatural. Our understanding of the brain still has a lot of gaps in it, so it is unclear why we need to assume God as the explanation.

Second, the problem with any study involving human consciousness is that it relies on self-reporting. And, the problem with self-reporting is that it cannot be corroborated by any objective tool. For instance, if someone says that they floated above their body at a certain time, that cannot be independently verified. There is a difference between when someone thinks they had an experience and when they actually did. It’s a bit like asking someone when in the night they had a particular dream.

Third, while a great weight of reputable and reasonable testimony lends itself to something being true, it is not clear that the threshold has been met for NDEs. As is commonly ascribed to Carl Sagan, “extraordinary claims require extraordinary evidence.” When we’re dealing with the afterlife, gods, the supernatural, or the one-of-a-kind, we require more than the “usual” standards for justification. Seven percent of Britons and a tenth of all Americans (including our own astrophysicist!) claim to have seen a UFO. Does that count for evidence of their existence? In the U.S., nearly 20 percent of people claim to have seen a ghost. But do ghosts exist?

What kind of afterlife?

Even if we were to assume NDEs did prove an afterlife, there is a fourth issue yet. Ambers refers to NDEs as being coherent and consistent, not to mention common across all peoples and all ages. This is likely true for the existence of NDEs but says nothing of their content. As Dr. Greyson tells us, how people “describe these phenomena is influenced by their cultural background.”

A Christian in America will see Jesus or the God of the Bible. A Buddhist or Hindu almost certainly will see it differently. While we can form broad categories of NDEs, each are personal and unique to the experiencer. So, rather than saying “we have a million sources that point to a single conclusion,” we ought to be saying “we have a million sources pointing to a million conclusions.”

Start of something new

Near-death experiences often have been dismissed by the philosophical literature as being the byproduct of a malfunctioning brain. But in recent years, the sheer depth and variety of NDE studies mean they can no longer be ignored. They are common enough, and abnormal enough, to require our attention.

At the very least, NDEs reveal our brain (again) to be a mysterious, complicated puzzle that we are only just starting to unravel. At the most, they might allow us to peak behind the curtain to see the spiritual world first-hand.

This article Can near-death experiences prove the afterlife? is featured on Big Think.

There’s a common perception that entrepreneurs and small business owners are overworked and stressed out. Both of those things can be true on occasion. At the same time, 94% of small business owners say they are happy with their lives, and 81% attribute this happiness to their entrepreneurship. The former value easily tops employees’ self-reported happiness. In a 2012 survey of 11,000 graduates of the Wharton MBA program, respondents running their own businesses ranked themselves the most content. “Entrepreneurship” even dominated “income” as a predictor of happiness.

The reason for this may be that entrepreneurship stokes a type of happiness called “eudaimonic happiness.”

There are two popular conceptions of happiness in psychology, hedonic and eudaimonic. You experience hedonic happiness through pleasure and enjoyment, like when scarfing down your favorite dessert, watching your beloved sports team win a big game, or hitting a jackpot in the casino. On the other hand, eudaimonic happiness is derived from activities that provide meaning or purpose, like volunteering for a cause you care about, raising children, or striving to make your business a success.

Both eudaimonic and hedonic happiness contribute to overall life satisfaction, but eudaimonic seems to provide a far more sustained effect. That’s because hedonic forms of happiness tend to provide only fleeting bursts of well-being, and the more hedonic activities you engage in, the more their positive effect on mood becomes muted. This partly explains why lottery winners generally aren’t significantly happier than people who have never won. After the initial excitement of winning life-changing wealth, their happiness mostly returns to baseline unless they utilize their newfound wealth to engage in eudaimonic pursuits — such as nurturing a hobby, starting an exercise program, or learning a language. These sorts of goal-driven activities, which realize personal talents and potential, evoke happiness that tends to stick around, raising overall well-being.

Again, all this isn’t to say that hedonic happiness is worthless. For a quick, mood-boosting pick-me-up, partying with friends or playing hours of mindless video games is fantastic. On the other hand, basing one’s well-being purely around hedonic happiness requires repeated, and often more stimulating, triggers. This is one aspect of what researchers term the “hedonic treadmill,” the observed tendency of humans to return to a fairly stable level of happiness despite experiencing positive or negative events.

Interestingly, cues of hedonic and eudaimonic happiness seem to stimulate different parts of the brain. In a 2019 study, researchers found that subjects in an fMRI brain scanner cued with hedonic events “showed enhanced activity in frontal medial/middle regions and anterior cingulate cortex.” On the other hand eudaimonic events prompted “increased activity in the right precentral gyrus.”

“Hedonic and eudaimonic happiness activate similar neural correlates. However, both kinds of happiness are also associated with distinctive brain areas serving distinctive functions,” the researchers wrote.

Another fascinating physiological difference between eudaimonic and hedonic happiness may arise in the immune system. In a 2013 study published to the Proceedings of the National Academy of Sciences, subjects who characterized their lives as having “a sense of direction and meaning” had lower expression of genes tied to inflammation and higher expression of antibody and antiviral genes compared to subjects who described their happiness as more founded in hedonic pursuits.

Lead author Barbara Fredrickson of the University of North Carolina, Chapel Hill, told Greater Good Magazine that there may be an evolutionary explanation:

“My guess is that eudaimonic pursuits build more and more helpful social resources relative to hedonic pursuits. So perhaps when hedonic pursuits become unbalanced by [too few] eudaimonic pursuits, our immune systems gear up for the same immune threats we’d encounter if we were lonely or otherwise socially isolated.”

This article Is eudaimonic happiness the best kind of happiness? is featured on Big Think.

In a systematic review published last year in the journal Psychophysiology, researchers from Monash University in Australia swept through the scientific literature, seeking to summarize how the connectivity of the human brain changes over our lifetimes. The gathered evidence suggests that in the fifth decade of life (that is, after a person turns 40), the brain starts to undergo a radical “rewiring” that results in diverse networks becoming more integrated and connected over the ensuing decades, with accompanying effects on cognition.

Since the turn of the century, neuroscientists have increasingly viewed the brain as a complex network, consisting of units broken down into regions, sub-regions, and individual neurons. These units are connected structurally, functionally, or both. With increasingly advanced scanning techniques, neuroscientists can observe the parts of subjects’ brains that “light up” in response to stimuli or when simply at rest, providing a superficial look at how our brains are synced up.

The Monash University team pored over 144 studies that used these imaging techniques to probe the brains of tens of thousands of subjects. From this analysis, the researchers gleaned a general trend in how the networked brain changes over our lifetimes.

Early on, in our teenage and young adult years, the brain seems to have numerous, partitioned networks with high levels of inner connectivity, reflecting the ability for specialized processing to occur. That makes sense, as this is the time when we are learning how to play sports, speak languages, and develop talents. Around our mid-40s, however, that starts to change. Instead, the brain begins becoming less connected within those separate networks and more connected globally across networks. By the time we reach our 80s, the brain tends to be less regionally specialized and instead broadly connected and integrated.

This “rewiring” has tangible effects on cognition.

“Older adults tend to show less flexible thinking, such as forming new concepts and abstract thinking, lower response inhibition, as well as lower verbal and numeric reasoning,” the reviewers noted. “These executive function changes can be seen first in adults in their fifth decade of life, consistent with the findings of the systematic review that functional network connectivity changes reach their inflection point in the fourth and fifth decade.”

But the news isn’t all bad for the aging brain. “Tasks relying on predominantly automatic or well-practiced processes are less impacted by age or may even increase slightly across the lifespan, such as vocabulary and general knowledge,” the authors wrote.

So why do these brain networking changes even occur in the first place? The reviewers offered some learned speculation. They noted that the brain is a resource-hungry organ, ravenous for the simple sugar glucose. “The adult brain accounts for approximately 2% of total body weight but requires approximately 20% of total glucose supply,” they wrote.

But as we get older, our bodies tend to slow down and the brain becomes less efficient. So not only is the brain getting less glucose, it’s also not putting the fuel to good use. Thus, the networking changes likely result from the brain reorganizing itself to function as well as it can with dwindling resources and aging “hardware.”

Proper diet, regular exercise, and a healthy lifestyle can keep the mind in good working order and put networking changes on hold, sometimes well into old age.

The brain’s inner workings are mysterious indeed, but with this grand systematic review comprising hundreds of studies and tens of thousands of brain scans, we are at least starting to get a surface view of how it changes across our lifetimes.

“During the early years of life, there is a rapid organization of functional brain networks. A further refinement of the functional networks then takes place until around the third and fourth decade of life. A multi-faceted interplay of potentially harmful and compensatory changes can follow in aging,” the reviewers concluded.

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In the 1950s, Noam Chomsky proposed his theory of universal grammar, which argued that language acquisition is biologically determined and that children have an innate ability to acquire language. The idea revolutionized the field of linguistics and changed the way psychologists view language development.

Universal grammar challenged the prevailing view that language development is due solely to environmental factors, instead proposing that newborns are equipped with brain circuits that contain information about the structure of language. We still know very little about the neurological basis of how newborns so easily acquire language.

New research published in the journal Science Advances now shows that exposure to language in the womb begins to influence brain function before birth, enhancing a newborn’s sensitivity to the language they have previously heard.

Early exposure

Benedetta Mariani of the University of Padua in Italy and her colleagues hypothesized that the brain activity of newborn babies could provide evidence of language learning; specifically, that exposure to language in the womb would have a lasting effect on neural processes after birth.

To test this, they used electroencephalography (EEG) to monitor brain wave activity in 49 one- to five-day-old infants born to French-speaking mothers, before, during, and after they heard recordings of the children’s story “Goldilocks and the Three Bears” in French, Spanish, and English. The recordings were presented in a semi-random order, such that only some of the babies heard the French version of the story last.

“We measured how much newborns’ brain activity remained high and complex not only during, but even after stimulation with different languages,” says senior author Judit Gervain. “We found that for several minutes after stimulation with the native language French, but not the unfamiliar languages English and Spanish, newborns’ brain responses remained high and had an organization that resembled that seen during stimulation.”

The researchers conclude that language experienced in the womb alters the functional organization of the brain before birth, increasing the newborn’s sensitivity to previously heard sounds. The amount or quality of prenatal speech exposure is not likely to be important, says Gervain, because “everything the mother says is transmitted to the fetus… so [they] naturally produce enough speech for babies to learn from.”

Linguistic stimulation

A mother’s voice is transmitted to the fetus as both sounds and vibrations, while other sounds, including the father’s voice, are more strongly filtered by the environment in the uterus, and thus transmitted less effectively.

The results of the new study are consistent with earlier findings that newborns prefer their mothers’ voices, and that two-day-old infants prefer their native language. They also highlight the importance of linguistic stimulation during early life, as this “lays the foundation for further language development.”

The researchers are now following up their findings by investigating preterm and deaf or hard-of-hearing infants to see how these atypical experiences might influence language development.

This article How exposure to language in the womb shapes the brain is featured on Big Think.

Christof Koch, a leading researcher on consciousness and the human brain, has famously called the brain “the most complex object in the known universe.” It’s not hard to see why this might be true. With a hundred billion neurons and a hundred trillion connections, the brain is a dizzyingly complex object.

But there are plenty of other complicated objects in the universe. For example, galaxies can group into enormous structures (called clusters, superclusters, and filaments) that stretch for hundreds of millions of light-years. The boundary between these structures and neighboring stretches of empty space called cosmic voids can be extremely complex.¹ Gravity accelerates matter at these boundaries to speeds of thousands of kilometers per second, creating shock waves and turbulence in intergalactic gases. We have predicted that the void-filament boundary is one of the most complex volumes of the universe, as measured by the number of bits of information it takes to describe it.

This got us to thinking: Is it more complex than the brain?

So we—an astrophysicist and a neuroscientist—joined forces to quantitatively compare the complexity of galaxy networks and neuronal networks. The first results from our comparison are truly surprising: Not only are the complexities of the brain and cosmic web actually similar, but so are their structures. The universe may be self-similar across scales that differ in size by a factor of a billion billion billion.

The task of comparing brains and clusters of galaxies is a difficult one. For one thing it requires dealing with data obtained in drastically different ways: telescopes and numerical simulations on the one hand, electron microscopy, immunohistochemistry, and functional magnetic resonance on the other.

It also requires us to consider enormously different scales: The entirety of the cosmic web—the large-scale structure traced out by all of the universe’s galaxies—extends over at least a few tens of billions of light-years. This is 27 orders of magnitude larger than the human brain. Plus, one of these galaxies is home to billions of actual brains. If the cosmic web is at least as complex as any of its constituent parts, we might naively conclude that it must be at least as complex as the brain.

The total number of neurons in the human brain falls in the same ballpark of the number of galaxies in the observable universe.

But the concept of emergence makes the comparison possible. Many natural phenomena are not equally complex at all scales. The majestic network of the cosmic web becomes evident only when the sky is surveyed over its largest extent. On smaller scales, with matter locked into stars, planets, and (probably) dark matter clouds, this structure is lost. An evolving galaxy does not care about the dance of electron orbitals within atoms, and electrons move around their nuclei without regard to the galactic system they reside in.

In this way, the universe contains many systems nested into systems, with little to no interaction across different scales. This scale segregation allows us to study physical phenomena as they emerge at their own natural scales.

The building blocks of the cosmic web are the self-gravitating halos of stars, gas, and dark matter (whose existence has yet to be definitively proved). In total, the number of galaxies within the observable universe should be on the order of 100 billion. The balance between the accelerating expansion of the fabric of spacetime and the pull of self-gravity gives this network its spider-web-like pattern. Ordinary and dark matter condense into string-like filaments, and clusters of galaxies form at filament intersections, leaving most of the remaining volume basically empty. The resulting structure looks vaguely biological.

A direct estimate of the number of cells or neurons in the human brain was not available in the literature until recently. Cortical gray matter (representing over 80 percent of brain mass) contains about 6 billions neurons (19 percent of brain neurons) and nearly 9 billion non-neuronal cells. The cerebellum has about 69 billion neurons (80.2 percent of brain neurons) and about 16 billion non-neuronal cells. Interestingly enough, the total number of neurons in the human brain falls in the same ballpark of the number of galaxies in the observable universe.

The eye immediately grasps some similarity between images of the cosmic web and the brain. We showed a simulated distribution of cosmic matter in a slice 1 billion light-years across, along with a real image of a 4 micrometers (µm)-thick slice through the human cerebellum.

Cross section of the brain showing the cerebellum. (Public domain)

Is the apparent similarity just the human tendency to perceive meaningful patterns in random data (apophenia)? Remarkably enough, the answer seems to be no: Statistical analysis shows these systems do indeed present quantitative similarities. Researchers regularly use a technique called power spectrum analysis to study the large-scale distribution of galaxies. The power spectrum of an image measures the strength of structural fluctuations belonging to a specific spatial scale. In other words, it tells us how many high-frequency and low-frequency notes make the peculiar spatial melody of each image.

A stunning message emerges: The relative distribution of fluctuations in the two networks is remarkably similar, over several orders of magnitude.

An evolving galaxy does not care about the dance of electron orbitals within atoms.

The distribution of fluctuations in the cerebellum at 0.1-1 mm scales is reminiscent of the galaxy distribution on hundreds of billions of light-years. At the smallest scales available to microscopic observation (about 10 µm), it is the morphology of the cortex that more closely matches the one of galaxies, on scales of a few hundreds of thousands of light-years.

By comparison, the power spectra of other complex systems (including projected images of clouds, tree branches, and plasma and water turbulence) are quite dissimilar from that of the cosmic web. The power spectra of these other systems display a steeper dependence on scale, which may be a manifestation of their fractal nature. This is particularly striking for the distribution of branches in trees and in the pattern of clouds, both of which are well known for being fractal-like systems with self-similarity across a large variety of scales. For the complex networks of the cosmic web and of the human brain, on the other hand, the observed behavior is not fractal, which can be interpreted as evidence of the emergence of scale-dependent, self-organized structures.

As remarkable as the power spectrum comparison is, it doesn’t tell us whether the two systems are equally complex. A practical way of estimating the complexity of a network is to measure how difficult it is to predict its behavior. This can be quantified by counting how many bits of information are necessary for building the smallest possible computer program that can perform such a prediction.

One of us has recently measured how difficult it is to predict how the cosmic network evolves, based on the digital evolution of a simulated universe.¹ This estimate suggests that about 1 to 10 petabytes of data are needed to describe the evolution of the entire observable universe at the scale where its self-organization emerges (or at least of its simulated counterpart).

Estimating the complexity of the human brain is much more difficult, because global simulations of the brain remain an unmet challenge. However, we can argue that complexity is proportional to intelligence and cognition. Based on the latest analysis of the connectivity of the brain network, independent studies have concluded that the total memory capacity of the adult human brain should be around 2.5 petabytes, not far from the 1-10 petabyte range estimated for the cosmic web!

Roughly speaking, this similarity in memory capacity means that the entire body of information that is stored in a human brain (for instance, the entire life experience of a person) can also be encoded into the distribution of galaxies in our universe. Or, conversely, that a computing device with the memory capacity of the human brain can reproduce the complexity displayed by the universe at its largest scales.

It is truly a remarkable fact that the cosmic web is more similar to the human brain than it is to the interior of a galaxy; or that the neuronal network is more similar to the cosmic web than it is to the interior of a neuronal body. Despite extraordinary differences in substrate, physical mechanisms, and size, the human neuronal network and the cosmic web of galaxies, when considered with the tools of information theory, are strikingly similar.

Does this fact tell us something profound about the physics of emergent phenomena in the two systems? Maybe. But we must take these findings with a grain of salt. Our analysis has been limited to small samples taken with very different measurement techniques.

Also, our analysis doesn’t point to a dynamical similarity among these systems. A model of how information flows across spatial scales and time in the two systems will be the crucial test. This is already feasible for the cosmic web through numerical simulations. For the human brain we have to rely on more global estimates, usually derived from smaller portions that are then scaled upward. In the near future we aim at testing these concepts in more sophisticated numerical models of the human brain.

Programs like the Human Brain Project, designed to simulate an entire human neuronal network, and the Square Kilometer Array, the biggest enterprise ever in radio astronomy, will help us fill in some of these details and understand whether the universe is even more surprising than we thought.

1. Vazza, F. On the complexity and the information content of cosmic structures. Monthly Notices of the Royal Astronomical Society 465, 4942-4955 (2017).

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Trauma is not merely a phenomenon of the mind but also a condition physically embedded in the body, often eluding our conscious awareness and affecting our overall health. That was the main argument in psychiatrist Bessel van der Kolk’s 2014 bestseller The Body Keeps the Score, which quickly became a modern classic among trauma researchers, clinicians, and survivors. The book shifted how many in the West view psychiatric illness, which was often viewed solely through a psychological or neurochemical lens, and it sparked new interest in more holistic treatments for trauma that had long been considered alternative: yoga, eye movement desensitization and reprocessing therapy (EMDR), the performing arts, and psychedelics, to name a few.

But what does it really mean for the body to “keep the score”? Is it biologically possible for the viscera to actually store and release trauma? In his book, van der Kolk writes:

“The body keeps the score. If the memory of trauma is encoded in the viscera, in heartbreaking and gut-wrenching emotions, in autoimmune disorders and skeletal/muscular problems, and if mind/brain/visceral communication is the royal road to emotion regulation, this demands a radical shift in our therapeutic assumptions.”

Can the body “keep score”?

Recently, neuroscientists have expressed skepticism over the notion that the body can “keep score” of anything. In a 2023 Big Think video, Lisa Feldman Barrett argued that everything, including trauma, is in our heads, and that “the brain keeps the score and the body is the scorecard.” In her view, everything we experience is constructed by the brain, which learns to predict how we will feel based on past experiences, issues, and sensations that seem to come from our body but actually come from our brain.

“When you feel your heart beating, you are not feeling it in your chest, you are feeling it in your brain,” she said. “Your body is always sending sensory signals to the brain, of course, but emotions are made in the brain, not in the body. They are experienced in the brain, like everything else you experience, not in the body. If you experience a trauma, you experience it in your brain.”

Bottom-up treatments like yoga, massage, and breathwork would then serve to override predictions and provide the brain with a different experience of the body.

“It’s not your body that needs to heal,” she said. “It’s your brain’s predictions that need to change. It’s not biologically possible for the body to keep score of anything.”

The line between scorekeeper and scorecard, however, may not be so clear. While the conscious experience of trauma may be constrained to the brain, there is a mountain of evidence that trauma impacts the physiological systems of the body, which can set off a cascade of bodily processes that in turn impact the brain.

“It’s entirely likely that the viscera ‘record’ stress and carry a lingering memory of such,” Paul Kenny, PhD, an addiction researcher and professor of neuroscience at the Icahn School of Medicine at Mount Sinai, told Big Think.

“For example, the immune system, which interacts with both sensory and autonomic neurons, is highly stress-responsive. Also, stress profoundly modifies the function of peripheral organs (e.g. release of glucoregulatory hormones from pancreas; liver storage and release of glucose). Adipocytes are also stress-responsive, and stress remodels the way that fat is stored in the body. So, indeed, the viscera are likely highly sensitive to both acute and chronic stressors.”

These processes may rely on interactions with the brain, but if some of them originate in peripheral systems, can we really say the body isn’t keeping score? If trauma can result in chronic inflammation or autoimmune disease, one might argue that the expression of these conditions itself is no less valid than the brain’s construction of an emotionally triggering experience. The question then becomes semantic: “Keeping the score” doesn’t have to mean being conscious of keeping the score. Lymphocytes, white blood cells that promote adaptive immunity, “keep score” of every antigen they’ve encountered, forming memory cells in the immune system. The heart and enteric system can function independently of the brain, keeping their own score of metabolic processes. More often than not, what happens inside us is a two-way partnership between the brain and viscera, but it’s not always clear who’s in charge.

Who’s in charge?

When it comes to treatment, physical therapists and bodyworkers who work with trauma patients are well-acquainted with this partnership. Scroll any bodyworker’s website and you’ll read testimonies and descriptions of how “emotional energy” gets stuck in the body. No one actually knows how deep tissue massage leads to emotional catharsis, but the fact that it can seems to align with van der Kolk’s claims, as well as those of medical celebrities like Gabor Mate, author of When the Body Says No.

There’s growing evidence that such treatments have a direct effect on the brain. Cynthia Price, a research professor at the University of Washington who runs Seattle’s Center for Mindful Body Awareness, has found in her own work that body-oriented interventions such as Mindful Awareness in Body Oriented Therapy (MABT) can change the plasticity of the brain in areas related to self-awareness.

“It is quite possible that there are physiological changes in the body related to interoception,” she told Big Think. (Interoception is the sense that allows an individual to perceive the internal state of their body.) “We certainly notice shifts in bodily tissue/musculature in response to MABT processes of sustained interoceptive attention.”

How emotional energy might be “stored” in the body — for instance, in patterns of tension that contribute to the way the brain represents the body, and therefore the self — is an open question. In framing trauma as blockages in the viscera, are we oversimplifying bidirectional processes that are valuable to understand on a deeper level? And in relegating the body to a scorecard, are we defining intelligence too narrowly? These are urgent questions as we reconceptualize wellness, healing, and mental health according to the complex connections between the brain and body.

This article Does the body really “keep the score” of trauma? is featured on Big Think.

When I visited Buenos Aires last year, I thought the six semesters of Spanish I took in school would pay dividends. The fast flow of Spanish from Argentinians quickly killed that delusion. I realized I had forgotten most conjugation rules and vocabulary, and I was able to formulate only simple, stilted sentences: “I can have a beer?” 

So it was admittedly encouraging to hear that Arieh Smith, a New York City-based polyglot who runs the popular language-learning YouTube channel Xiaomanyc, didn’t leave his first foreign language classes with much proficiency either.

“In high school, I was actually terrible at learning languages,” he said. “I spent years learning Latin and Greek and Hebrew, and it just never clicked. I would be just very confused why, year in and year out, I would have no understanding of this material despite pretty good grades and, you know, continually doing the work.”

It finally clicked when he entered a one-year immersion program, through Princeton University, to learn Chinese in Beijing. Students had to sign a pledge: If you speak English at any time during the program, you get kicked out (a policy that had been enforced at least once, he said). Smith eventually became fluent in Chinese, partly through the constant immersion in a Chinese-speaking environment, and partly through language-learning software that utilizes spaced repetition, a technique where review intervals are progressively increased to enhance long-term retention.

Practical phrases and comprehensible input

But neither of those is necessary for learning a language. Studying Chinese helped Smith develop more straightforward learning strategies he would later apply while learning dozens of other languages over the following years. One key strategy: Instead of memorizing a long list of random words, he studied practical phrases that he was likely to use in conversation, such as “Does this cost $1.50 or $2?” or “Do you have coffee?”

“[Words] don’t have as much meaning as when they’re put into useful, chunkable phrases that are relevant to you and your day-to-day life,” Smith said. “It just hooks in with the way our brains naturally learn languages.”

There is also the fact that the phrases you use in, say, the grocery store are probably pretty simple. Case in point: The Oxford English Corpus, the largest record of English words, contains more than 600,000 entries, but an analysis of thousands of English texts found that just 100 lemmas (the base form of a word, like “climb” is to “climbing”) accounted for half of all words used in those writing samples.

Smith said he keeps a document of English phrases he commonly uses in conversation so he can translate them into whatever language he wants to learn when starting a new one. The idea is to start using these phrases in real conversations as soon as possible, not spending too much time learning vocabulary. “There’s no way to get high fluency in a language without speaking,” Smith said. “For practical purposes, it’s impossible.”

Still, fluency also requires learning vocabulary. One concept that has helped Smith and many others efficiently learn languages is comprehensible input, first developed in the 1970s by linguist Stephen Krashen. Comprehensible input refers to listening or reading the target language at a difficulty slightly above your current level of proficiency. It’s a process that mirrors how children learn languages: They might not understand every word in a sentence, but they can use context clues to derive the meaning, and over time they accumulate more and more words.

The key is finding the sweet spot.

“I can’t tell you how much time I’ve wasted [earlier in my language-learning career] trying to immerse myself in media that was way above my level,” Smith said, bringing up the time he made a YouTube video where he tried to learn Japanese by watching hours of the TV show Naruto with Japanese audio and subtitles. “The end result of that was I learned almost no Japanese.”

What better helps you find comprehensible input is through conversation with a friend or tutor. “They’re tailored to your level,” Smith said. “You start from a basic point, you get more and more complex, and you build over time.”

Misconceptions about learning languages

Smith said it is a misconception that learning new languages is only for smart people or those naturally gifted in linguistics. Natural talent does exist, but it’s not everything. Smith brought up an analogy he heard from another language-learning YouTuber, Matt vs Japan, which is that learning a language is like losing weight: It’s hard but not in the same way that learning calculus is hard. “Everybody can understand how a language works,” Smith said. “It’s not a problem.”

Consistent effort is probably more important.

I asked Smith about the awkwardness people might feel when speaking a new language with native speakers.

“I’m not really a natural extrovert, so it’s also something I’ve had to overcome,” he said. “One thing that I realized, even before doing any of this as a business, is also that people really appreciated it when I spoke even a little Chinese.”

This phenomenon might not be universal: An American touring Paris probably won’t amuse the waiter by ordering in French. Still, Smith said that learning languages, even on a very basic conversational level (which is his level of proficiency in most of the languages he has studied), helps you learn about the cultures in which they developed — both through the idiosyncrasies of the language and the people those languages enable you to speak with.

“It just forced me to, go to like, Little Haiti in Brooklyn and try to speak in Haitian Creole, which is probably something I’d have never done. And the same for Punjabi or Vietnamese.”

As for whether some languages are inherently more useful or beautiful than others? “Personally I would say I prefer the sound of certain languages,” Smith said, noting that Welsh, to his ears, is more beautiful than most other languages. “Ultimately, the way that I really see languages is as a tool… I’ve always been skeptical of the idea that some languages are better at communicating ideas. I think that, fundamentally, whatever any language can express has to be able to be expressed by another language.”

This article A polyglot explains the tips (and myths) of learning new languages is featured on Big Think.

Once upon a time, people believed you could ascertain a person’s character and personality traits by examining the bumps and shapes of their skull. Such study was called phrenology and its proponents were not just people on the fringe; established scientists beieved such a “science” had merit.

“In origin [phrenology] was distinctly medical,” writes Robert E. Riegel in a 1933 article published in The American Historical Review. “Its originators being the doctors François Joseph Gall and John Gaspar Spurzheim, who did the greater part of their work in the first two decades of the century.”

Gall received his doctorate in 1785 and became “a successful, well-connected, private physician in Vienna,” writes John Van Wyhe in an article in The British Journal for the History of Science. He supposedly rejected an offer to become the personal physician to Emperor Franz II to “preserve his independence,” and found inspiration in a theory on “mind-body dualism” put forward by philosopher Johann Gottfried von Herder. Subsequently, Gall set out to prove this theory—that the mind and body are linked—and collected human and animal skulls, made wax molds of brains and skull surfaces, and became something of a “local celebrity” owing to his skull collection (some 300 in number). Before long, the government accused Gall of endangering morality and religion, and forbade him from lecturing on the subject. It was at one such lecture that Spurzheim met Gall. Starting in 1804, for about eight years the two collaborated until Spurzheim started offering his own take on the system and called it “phrenology” from phren, the Greek word for “mind.”

While Spurzheim toured Britain—a celebrity lecture series of sorts—phrenology found a new home. Everyone from Charlotte Brontë and George Eliot to Arthur Conan Doyle bought into it. Between 1823 and 1836, phrenologists established twenty-four dedicated societies with 1,000 members, and published a whopping fifty-seven books and pamphlets, amounting to 64,250 volumes.

In 1836, Hewett Watson, a prominent botanist (and, later, phrenologist) foresaw that future naysayers would be laughed at. “Public pity will be freely bestowed upon the anti-phrenologists,” Watson wrote. “[A]nti-phrenology will exist in the last decrepitude of age […] it will be a subject for the historians of things that have ceased to be.”

What’s more, phrenology was supported by people Watson esteemed, including the Anglican Archbishop of Dublin, Richard Whately, who declared “Phrenology is true as…the sun is now in the sky.”

The irony is delicious.

For a while though, phrenology thrived. In 1850, even Queen Victoria and Prince Albert invited phrenologist George Combe to the palace to read the heads of their children. Combe—who introduced phrenology to the British middle classes in the 1820s through his lecture tours—examined the Prince of Wales, Edward VII. Then aged 9, the Prince was doing poorly in his studies. Later still, a phrenologist was appointed as tutor to Prince Alfred, Queen Victoria’s second son.

For their part, phrenologists believed abstract behavioral attributes including, firmness, hope, sublimity, destructiveness “could be localized to specific convolutions on the brain surface and that the representation of these attributes could be inferred by palpation of the skull,” writes James Ashe in The Quarterly Review of Biology.

Although phrenology was largely spread through glorified lecture tours, it wasn’t long before university professors taught this pseudoscience to medical students alongside anatomy. Phrenologists primarily used tape measures and craniometers—semi-circular tools to measure the cranium–as well as calipers to reach their diagnoses. With the advent of electricity, some phrenologists used “psychographs,” circuited helmets that would take “readings” of skulls.

George Combe divided the skull into 33 “organs,” or regions, each associated with a different attribute. For instance, organ one—the back of your neck—Informed sex drive, while region 23—above your brow—indicated skin color and tone. It’s from this that the term “highbrow” came to reflect intellectual superiority.

It’s also why the study of the shapes, bumps, and curvature of people’s heads is tied to racist, sexist, and classist beliefs. Phrenology thrived during the height of the British Empire, a power defined largely by its dependence on servility and enslavement. Employing a “science” that perpetuated myths about white supremacy helped justify its imperialism.

According to an article in The Atlantic, other words that originated in phrenology include “shrink” (as in, to get one’s head shrunk to manage or reduce “undesirable” traits), “stuck up” (snobby) and “hard headed.”

Eventually, phrenology crumbled owing to its lack of scientific rigor. “After the passing of the early figures of the movement…little time was spent on the necessary scientific research,” writes Robert E. Reigel. “Much time was spent [by phrenologists] in elaborating phrenological doctrines and in applying them to education, marriage, [and] racial relations.”

In marriage, for instance, it was noted that the “devoted wife and mother” had a pronounced curve to the back of her head and neck, where the “childless lover of children” did not. Interestingly, this gave rise to various trends in hairstyles and overexaggerations of phrenologically appealing features in art, including the works of sculptor Hiram Powers.

Still, as it waned in England, it found new life in the United States. In as early as the 1830s, Harriet Martineau noted that when Spurzheim came to New England, “the mass of society became phrenologists in a day.”

Given the claims phrenology made about white racial superiority, phrenology was embraced in antebellum America, writes Peter McCandless in The Journey of Southern History. “One of [Spurzheim’s] disciples, Dr. Jonathon Barber, soon took the gospel to Charleston and other southern cities.” By the 1830s and 1840s the city’s bookshops sold the works of Spurzheim and Combe as an ode to their own appetite for intellectualism in the subject.

Phrenology would soon find mentions across American literature, from Whitman to Poe whose Fall of the House of Usher is peppered with phrenological double entendres: Roderick’s “ inordinate expansion above the regions of the temple,” for instance, reflects his ideality and cautiousness accounting for his melancholy, writes Brett Zimmerman.

In the United States phrenology was considered a tool for self-improvement. Celebrated American phrenologists included the Fowler Brothers, Walt Whitman, Lorenzo Niles and Orson Squire, the former of whom “phrenologized” young Clara Barton. Of Barton, who would later become a nurse and the founder of the American Red Cross, L. N. Fowler said: “She will never assert herself for herself . . . but for others she will be perfectly fearless. Throw responsibility upon her.” The phrenologized diagnosis would go on to be quoted in magazine articles and Barton’s own memoir.

As in England, however, phrenology’s success in the States rapidly declined “undermined by science’s popular successes,” notes McCandless. Developing and evolving scientific methodologies required more than a map of the skull. While science prevailed, phrenologists persisted to a degree writes Riegel, preying on the desperate and impressionable. The end of phrenology gave rise to the “practical phrenologist,” he notes.

“This practitioner, frequently without training, sought to capitalize the new science and make it pay dividends,” Riegel says. “He was a fortune teller.”

This article The lies that skulls told us is featured on Big Think.

Several years ago, a British man named Harry picked his nose. A hidden camera recorded him in this private moment, then someone uploaded the video to the internet, and soon Harry’s pratfall exploded into a worldwide meme. Millions of people—most of them in the United States—became obsessed with the video. Everywhere Harry went, strangers shot significant looks at him and touched their nostrils, as if to say, “Hey, you’re that nose-picking guy!”

Harry loved the attention—he described his fame as a “safety blanket” and said he felt as if everyone on the street had become his friend. But there was a problem with Harry’s internet stardom: No one else could perceive it.

In a parallel reality where most of us live, Harry had been diagnosed with psychotic delusions, many of them seemingly borrowed from the YouTube videos he obsessively watched.

If lining a hat with tinfoil gives a person a sense of power, wonderful. Let’s do it.

His family convinced him to visit a mental health clinic affiliated with the University of Birmingham. There, he enthused to his clinician—Rosa Ritunnano—that he was “the happiest man in the world.” Harry told Ritunnano that he could read and control other people’s thoughts; he deployed his telepathy to battle the lizard-humans and the Illuminati at the center of a web of power. These enemies, for their part, surveilled him through hidden cameras and telepathic spies.

As nightmarish as that all might sound, Harry relished the attention from the imaginary conspirators who monitored him. “If I found out that they [were] not watching me and reading my mind, I would feel alone and crazy,” he explained to Ritunnano.¹

Though he was engaged in an apocalyptic psi war, Harry was also a remarkably pleasant fellow who seemed to pose no threat to anyone. He did refuse his prescribed antipsychotic medications, but when Ritunnano and her colleagues asked him whether he would submit to a battery of pencil-and-paper tests, he cheerfully agreed. And so the doctors administered some whimsically named tools that are used to measure self-worth, including the Purpose in Life Test, the Life Regard Index and the Existential Meaning Scale. Harry aced them all.

In the past decade, the Hearing Voices Movement, a federation of people who experience auditory hallucinations, has pushed the medical community to acknowledge that their symptoms can be a meaningful adaptation to trauma.²Ritunnano belongs to a compatible movement among caregivers—when she met Harry a few years ago, she had just started her Ph.D. in a field known as phenomenological psychopathology, which puts the doctor’s sense of reality on an equal footing with the patient’s.

In Harry, Ritunnano saw a teacher. She thought she could “learn something about what it means to be happy” from him. At the same time, she struggled with her obligations as his clinician: How was she supposed to help a man like Harry?

Clearly, his psychosis had cost him some heartbreaking losses. Due to Harry’s odd behavior, and concerns that his children might be at risk, he was barred from seeing them for a period. Even when he was able to see his children more regularly, Harry often spent his days glued to YouTube, addicted to videos about the flat Earth and other conspiracies, making it impossible for him to work and damaging his family life. And yet he reveled in his imaginary superpowers, which he told Ritunnano connected him to all of humanity. Now, he said, all “people are like a family for me.”

They are always struggling to find human connection.

Ritunnano isn’t the only one asking such questions. Louise Isham—a research clinical psychologist at the University of Oxford—told me that she first began to grapple with ethical dilemmas connected with delusions after she met a female patient who believed she worked undercover as an MI5 spy. The patient’s “missions” let her imagine that she was rushing around the world to battle villains and gave her a sense that she was serving her country. So even if doctors could find a way to bring the patient back to reality, would that be the right thing to do?

This question inspired Isham to scour the psychiatric literature for guidelines on how to treat patients with “grandiose delusions.” (The term is psychology-speak for delusions involving fantastical powers or secret knowledge.) As it turned out, there were no clear guidelines. Isham realized, “this is an area that’s massively under-researched.” She told me, “there is a genuine problem that I’ve witnessed in clinical services, where you can see the harm that’s coming from a patient’s grandiose delusions, but there’s also a clear benefit to the belief, and there is a real lack of empirical literature that tells us what to do about that.”

Patients with “superpowers” might decide to fly off the top of a building or to baptize strangers—and often they may be so busy with their imaginary role that they lose their real-life jobs and become socially isolated. And yet, “given the benefits that people can get” from their delusions, Isham said, “you have to be really careful not to go in and make things worse.”

In order to learn more about this condition, Isham and her colleagues identified patients with grandiose delusions and polled them about their experiences as messiahs, secret agents, and conspiracy-investigators. You might think people described as “grandiose” would dream themselves into the billionaire class and indulge selfish desires—if you have godlike superpowers then why not sail an imaginary yacht to Macau and win every hand of blackjack? But Isham and her coauthors found that most of the patients had created a fantasy world where they performed selfless acts, even miracles, to help others.³ About 70 percent of these patients reported that their “special powers” helped them to make other people happy and to protect others from harm.

Perhaps the inner life of these patients tells us something more universal about the search for meaning: For most of us, self-worth depends on being useful to others. And we, like Harry, are always struggling to find human connection—but he and others with psychosis might get that need met more easily by communicating telepathically with fictional strangers than in person with family or friends.

As Isham said, “This is a very misunderstood group of people.”

aroline Mazel-Carlton would agree with that. She told me that she heard her first disembodied voice after being abused by a daycare worker. The woman—who had hit young Caroline and scalded her with chemical cleaners—was chatting with another adult, and said, “It’s such a nice day. Not a cloud in the sky.”

That’s when the voice in young Caroline’s head spoke up: “She’s lying. I hate her.” Mazel-Carlton told me that the voice—she would later name it “Frank”—didn’t frighten her at first. If anything, he seemed to be coming to her defense. But later, voices turned into a swarm of tormentors. As a teenager and young woman, Mazel-Carlton bounced from mental hospitals to jail cells, where doctors numbed her with pills.

In her late 20s, Mazel-Carlton detoxed from psych meds and learned how to tame and soothe even the most frightening voices in her head, including “Frank.” If Frank orders her to throw a chair across the room, for instance, she can “satisfy” him, by simply touching the chair or turning it over.

Like an improv actor, she jumps into their stories with them.

Nowadays, Mazel-Carlton uses her lived experience to guide other people—she’s the director of training for the Wildflower Alliance in Western Massachusetts. A support network that’s aligned with the Hearing Voices Movement, the Wildflower Alliance brings together a community of peers to cope with voices, visions, and other “extreme states.”

Years ago, when Mazel-Carlton was on the other side of the consulting table, the doctors would ask her whether she was hearing voices, yes or no? And the conversation would usually end there—with a diagnosis and a prescription for meds. But now, as a caregiver, she explores her clients’ hallucinations with probing questions that her own doctors never bothered to ask: “Do you want to share what your voices say? How do they make you feel? Do your voices remind you of anyone you’ve known in the past?”

Mazel-Carlton said that “as mental health professionals, we’re not really doing our job if we’re not looking for meaning,” and she emphasized that caregivers should recognize that psychosis can be a survival tool. As an example of that, she told me about a man she’d met in a locked psychiatric ward who announced that he was the president of the United States. The patient “had been through horrific institutional trauma. He was once stripped naked and handcuffed to a sink by police,” she said. And now the psychiatrists on the ward wanted to drug the “president” back into painful reality.

They identified patients with experiences as secret agents and conspiracy-investigators.

Mazel-Carlton had a different idea. She invited the patient to walk the halls of the locked ward with her, and then she asked him, “How does it feel to be the president of the United States?” She wondered if he regretted becoming the most powerful person in the world. Wasn’t he overwhelmed by his responsibilities?

He told her, no, he loved being president. “He shared with me that he was reflecting on who his cabinet members would be, and he asked me if I wanted to serve on the cabinet,” she said. “He wanted Beyoncé to serve in another position in the cabinet, and that gave him so much joy.” For Mazel-Carlton, the patient’s fantasy seemed an act of heroism—he’d recaptured his own human dignity and found a reason to keep on living.

Mazel-Carlton believes that the last thing you should do is to tell someone that their voices and visions aren’t real. “If I were to do that, I’d sever my connection with them,” she said. “If I don’t validate their own fears and concerns, why would they turn to me as a source of support?” And so, like an improv actor, she jumps into their stories with them. This allows her to help the patient change a potentially dangerous narrative to one that’s benign. “If the CIA is asking them to monitor their neighborhood and they’re ending up in people’s yards or looking in mailboxes, that’s when I ask them to imagine other ways to complete their mission. Like, could you get to know your neighbors?” And if Jesus or Allah feels the need to cut out their own eyes as a sacrifice, then Mazel-Carlton suggests other ways of performing the holy ritual. She might encourage the client to make a drawing of the sacrifice, or to say a prayer.

“Anything that gives someone the sense of power and won’t hurt them is great,” she says. “If lining a hat with tinfoil gives a person a sense of power, wonderful. Let’s do it. Buying a cell phone jammer for the room? Great. Let’s do it. Because when we can give a little bit of power, then we can often have the conversation about the deeper seed of truth and meaning.”

She acknowledges that her methods are out of sync with mainstream psychiatry. She and others in the Hearing Voices Movement are “throwing ourselves bodily at the Overton Window,” she said, meaning that they want to expand the spectrum of acceptable treatments for people who struggle with mental-health problems.

This seemingly radical approach has its critics. Ian Gold, a professor of philosophy and psychiatry at McGill University, told me that clinicians may need to make judgment calls on behalf of patients who are suffering. “There’s a spectrum of patients,” he pointed out. “Somebody might say, ‘I’m happy and I have this delusion.’ But really they’ve got an illness that is not severe.” He noted that if a patient is struggling with depression or feels tormented by their voices, then the clinician may need to treat the underlying pathology that causes their pain.

Ritunnano made much the same point. She told me, “It’s not about the actual belief, it’s about the individual and their social context.” If a patient with severe bipolar disorder suddenly becomes terrified of black cats, that might be “a harbinger of serious decline, and they will need intense support to avoid hospital admission.” On the other hand, she said, when a patient with a long-time delusion that he’s being tormented by aliens suddenly stops talking about spaceships, that may be a sign that he has slid into depression and needs medication for that—rather than for his delusion.

Still, many clinicians are now embracing methods that empower patients to live with their voices and visions if they so choose, including a form of cognitive-behavioral therapy in which patients learn to cope with hallucinations. In one recent paper, for instance, researchers pointed out that clinical guidelines from countries around the world suggest that people with psychosis should have a say in their own therapy—even if that involves refusing to take medications.

And that brings us back to Ritunnano’s question: What can we learn from Harry’s happiness? She told me that working with Harry challenged her to think differently as a clinician. “With Harry, it was mostly about being able to sit with the uncertainty,” she said. “While our job as clinicians is often focused on treating ‘symptoms’ and managing risk, Harry’s case reminded me that we are also always confronted with the existential struggles that accompany health and illness alike. What do you do when eliminating ‘illness’ also means eliminating meaningfulness?”

Harry had no complaints, and there were no immediate concerns about harm coming to him or others. So, as long as his joy lasted, Ritunnano’s job was to believe in it, rather than treating it as a symptom to be snuffed out. Harry had discovered that his best life could be in his fantasies. As he once told Ritunnano, “I feel like Jesus. Of course I’m not [Jesus.] But why not believe?”

1. Ritunnano, R., Humpston, C., & Broome, M.R. Finding order within the disorder: A case study exploring the meaningfulness of delusions. British Journal of Psychiatry Bulletin 46, 109-115 (2022).

2. Corstens, D., Longden, E., McCarthy-Jones, S., Waddingham, R., & Thomas, N. emerging perspectives from the Hearing Voices movement: Implications for research and practice. Schizophrenia Bulletin 40, S285-S294 (2014).

3. Isham, L., et al. The meaning in grandiose delusions: Measure development and cohort studies in clinical psychosis and non-clinical general population groups in the U.K. and Ireland. The Lancet 9, 792-803 (2022).

This article The happiest man in the world has psychotic delusions is featured on Big Think.

Several years ago, my father died as he had done most things throughout his life: without preparation and without consulting anyone. He simply went to bed one night, yielded his brain to a monstrous blood clot, and was found the next morning lying amidst the sheets like his own stone monument.

It was hard for me not to take my father’s abrupt exit as a rebuke. For years, he’d been begging me to visit him in the Czech Republic, where I’d been born and where he’d gone back to live in 1992. Each year, I delayed. I was in that part of my life when the marriage-grad-school-children-career-divorce current was sweeping me along with breath-sucking force, and a leisurely trip to the fatherland seemed as plausible as pausing the flow of time.

Now my dad was shrugging at me from beyond— “You see, you’ve run out of time.”

His death underscored another loss, albeit a far more subtle one: that of my native tongue. Czech was the only language I knew until the age of 2, when my family began a migration westward, from what was then Czechoslovakia through Austria, then Italy, settling eventually in Montreal, Canada. Along the way, a clutter of languages introduced themselves into my life: German in preschool, Italian-speaking friends, the francophone streets of East Montreal. Linguistic experience congealed, though, once my siblings and I started school in English. As with many immigrants, this marked the time when English became, unofficially and over the grumbling of my parents (especially my father), our family language—the time when Czech began its slow retreat from my daily life.

Many would applaud the efficiency with which we settled into English—it’s what exemplary immigrants do. But between then and now, research has shown the depth of the relationship all of us have with our native tongues—and how traumatic it can be when that relationship is ruptured. Spurred by my father’s death, I returned to the Czech Republic hoping to reconnect to him. In doing so, I also reconnected with my native tongue, and with parts of my identity that I had long ignored.

While my father was still alive, I was, like most young people, more intent on hurtling myself into my future than on tending my ancestral roots—and that included speaking the language of my new country rather than my old one. The incentives for adopting the culturally dominant language are undeniable. Proficiency offers clear financial rewards, resulting in wage increases of 15 percent for immigrants who achieve it relative to those who don’t, according to economist Barry Chiswick. A child, who rarely calculates the return on investment for her linguistic efforts, feels the currency of the dominant language in other ways: the approval of teachers and the acceptance of peers. I was mortally offended when my first-grade teacher asked me on the first day of school if I knew “a little English”—“I don’t know a little English,” was my indignant and heavily accented retort. “I know a lot of English.” In the schoolyard, I quickly learned that my Czech was seen as having little value by my friends, aside from the possibility of swearing in another language—a value I was unable to deliver, given that my parents were cursing teetotalers.

But embracing the dominant language comes at a price. Like a household that welcomes a new child, a single mind can’t admit a new language without some impact on other languages already residing there. Languages can co-exist, but they tussle, as do siblings, over mental resources and attention. When a bilingual person tries to articulate a thought in one language, words and grammatical structures from the other language often clamor in the background, jostling for attention. The subconscious effort of suppressing this competition can slow the retrieval of words—and if the background language elbows its way to the forefront, the speaker may resort to code-switching, plunking down a word from one language into the sentence frame of another.

Meanwhile, the weaker language is more likely to become swamped; when resources are scarce, as they are during mental exhaustion, the disadvantaged language may become nearly impossible to summon. Over time, neglecting an earlier language makes it harder and harder for it to compete for access.

His death underscored another loss, albeit a far more subtle one: that of my native tongue.

According to a 2004 survey conducted in the Los Angeles metropolitan area, fewer than half of people belonging to Generation 1.5—immigrants who arrive before their teenage years—claimed to speak the language they were born into “very well.” A 2006 study of immigrant languages in Southern California forecast that even among Mexican Americans, the slowest group to assimilate within Southern California, new arrivals would live to hear only 5 out of every 100 of their great-grandchildren speak fluent Spanish.

When a childhood language decays, so does the ability to reach far back into your own private history. Language is memory’s receptacle. It has Proustian powers. Just as smells are known to trigger vivid memories of past experiences, language is so entangled with our experiences that inhabiting a specific language helps surface submerged events or interactions that are associated with it.

Psychotherapist Jennifer Schwanberg has seen this firsthand. In a 2010 paper, she describes treating a client who’d lived through a brutal childhood in Mexico before immigrating to the United States. The woman showed little emotion when talking about events from her early life, and Schwanberg at first assumed that her client had made her peace with them. But one day, the woman began the session in Spanish. The therapist followed her lead and discovered that “moving to her first language had opened a floodgate. Memories from childhood, both traumatic and nontraumatic, were recounted with depth and vividness … It became clear that a door to the past was available to her in her first language.”

A first language remains uniquely intertwined with early memories, even for people who fully master another language. In her book The Bilingual Mind, linguist Aneta Pavlenko describes how the author Vladimir Nabokov fled the Russian revolution in 1919, arriving in the United Kingdom when he was 20. By the time he wrote his memoir Conclusive Evidence in 1951, he’d been writing in English for years, yet he struggled writing this particular text in his adopted language, complaining that his memory was tuned to the “musical key” of Russian. Soon after its publication, he translated the memoir into his native tongue. Working in his first language seems to have prodded his senses awake, leading him to insert new details into the Russian version: A simple anecdote about a stingy old housekeeper becomes perfumed with the scents of coffee and decay, the description of a laundry hamper acquires a creaking sound, the visual details of a celluloid swan and toy boat sprout as he writes about the tub in which he bathed as a child. Some of these details eventually made it into his revised English memoir, which he aptly titled Speak, Memory. Evidently, when memory speaks, it sometimes does so in a particular tongue.

Losing your native tongue unmoors you not only from your own early life but from the entire culture that shaped you. You lose access to the books, films, stories, and songs that articulate the values and norms that you’ve absorbed. You lose the embrace of an entire community or nation for whom your family’s odd quirks are not quirks all. You lose your context. This disconnection can be devastating. A 2007 study led by Darcy Hallett found that in British Columbian native communities in which fewer than half of the members could converse in their indigenous language, young people killed themselves six times more often than in communities where the majority spoke the native language. In the Midwestern U.S., psychologist Teresa LaFromboise and her colleagues found that American-Indian adolescents who were heavily involved in activities focused on their traditional language and traditions did better at school and had fewer behavior problems than kids who were less connected to their traditional cultures—in fact, cultural connectedness buffered them against adolescent problems more than having a warm and nurturing mother. Such benefits appear to span continents: In 2011, the Australian Bureau of Statistics reported that aboriginal youth who spoke their traditional language were less likely to binge drink or use illegal drugs.

Why is a heritage language so conducive to well-being? Michael Chandler, one of the authors of the suicide study, emphasizes that a sense of cultural continuity makes people resilient by providing them with a cohesive self-concept. Without that continuity, he warns, aboriginal youth, who have typically experienced plenty of turbulence, are in grave existential danger. They risk losing “the thread that tethers together their past, present, and future.”

As my siblings and I distanced ourselves from the Czech language in our youth, a space widened between us and our parents—especially my father, who never wore English with any comfort. Memories of our early family life, along with its small rituals and lessons imparted, receded into a past that drifted ever further out of reach. It was as if my parents’ life in their home country, and the values that defined that life, didn’t translate credibly into another language; it was much easier to rebel against them in English. Even the English names for our parents encouraged dissent: The Czech words we’d used—Maminka, Tatinek—so laden with esteem and affection, impossible to pronounce with contempt, had no corresponding forms. In English, the sweet but childish Mommy and Daddy are soon abandoned for Mom and Dad—words that, we discovered, lend themselves perfectly well to adolescent snark.

I watched as my father grew more and more frustrated at his powerlessness to pass on to his children the legacy he most longed to leave: a burning religious piety, the nurturing of family ties, pleasure in the music and traditions of his region, and an abiding respect for ancestors. All of these became diluted by the steady flow of new memories narrated in English, laced with Anglophone aspiration and individualism. As we entered adulthood and dispersed all over North America into our self-reliant lives, my father gave up. He moved back home.

For the next two decades, I lived my adult life, fully absorbed into the English-speaking universe, even adding American citizenship to my Canadian one. My dad was the only person with whom I regularly spoke Czech—if phone calls every few months can be described as “regularly,” and if my clumsy sentences patched together with abundant English can be called “speaking Czech.” My Czech heritage began to feel more and more like a vestigial organ.

You lose the embrace of an entire community. You lose your context.

Then my father died. Loss inevitably reveals that which is gone. It was as if the string section of the orchestra had fallen silent—not carrying the melody, it had gone unnoticed, but its absence announced how much depth and texture it had supplied, how its rhythms had lent coherence to the music. In grieving my father, I became aware of how much I also mourned the silencing of Czech in my life. There was a part of me, I realized, that only Czech could speak to, a way of being that was hard to settle into, even with my own siblings and mother when we spoke in English.

After my father’s death, my siblings and I inherited a sweet little apartment in a large compound that has been occupied by the Sedivy family since the 1600s, and where my uncle still lives with his sprawling family. This past spring, I finally cleared two months of my schedule and went for a long visit, sleeping on the very same bed where my father and his brothers had been born.

I discovered that, while I may have run out of time to visit my father in his homeland, there was still time for me to reunite with my native tongue. On my first day there, the long drive with my uncle between the airport and our place in the countryside was accompanied by a conversation that lurched along awkwardly, filled with dead ends and misunderstandings. Over the next few days, I had trouble excavating everyday words like stamp and fork, and I made grammar mistakes that would (and did) cause a 4-year-old to snicker. But within weeks, fluency began to unspool. Words that I’m sure I hadn’t used in decades leapt out of my mouth, astounding me. (Often they were correct. Sometimes not: I startled a man who asked about my occupation by claiming to be a savior—spasitelka. Sadly, I am a mere writer—spisovatelka.) The complicated inflections of Czech, described as “character-building” by an acquaintance who’d learned the language in college, began to assemble into somewhat orderly rows in my mind, and I quickly ventured onto more and more adventurous grammatical terrain. Just a few weeks into my visit, I briefly passed as a real Czech speaker in a conversation with a stranger. Relearning Czech so quickly felt like having linguistic superpowers.

Surprised by the speed of my progress, I began to look for studies of heritage speakers relearning childhood languages that had fallen into disuse. A number of scientific papers reported evidence of cognitive remnants of “forgotten” languages, remnants that were visible mostly in the process of relearning. In some cases, even when initial testing hinted at language decay, people who’d been exposed to the language earlier in life showed accelerated relearning of grammar, vocabulary, and most of all, of control over the sounds of the language.

One of the most remarkable examples involved a group of Indian adoptees who’d been raised from a young age (starting between 6 and 60 months) in English-speaking families, having no significant contact with their language of origin. The psychologist Leher Singh tested the children when they were between the ages of 8 and 16. Initially, neither group could hear the difference between dental and retroflex consonants, a distinction that’s exploited by many Indian languages. After listening to the contrasting sounds over a period of mere minutes, the adoptees, but not the American-born children, were able to discriminate between the two classes of consonants.

This is revealing because a language’s phonology, or sound structure, is one of the greatest challenges for people who start learning a language in adulthood. Long after they’ve mastered its syntax and vocabulary, a lifelong accent may mark them as latecomers to the language. Arnold Schwarzenegger was the star of many American movies and the governor of the country’s biggest state, but his Austrian accent is a constant reminder that he could never run for president. The crucial timing of exposure for native-like speech is evident in my own family: I can pronounce the notoriously difficult “ř” sound in Czech—as in the name of the composer Dvořák—but my brother, born three years after me, in Vienna, cannot.

Phonology’s resistance to both attrition and later learning may be due to the fact that the sound structure of a language is fixed in a child’s mind very early. Before 6 months of age, infants can distinguish most subtle differences in speech sounds, whether their language makes use of those distinctions or not. But over the second half of their first year, they gradually tune their perception to just the sounds of the language they hear around them. Children who hear only English lose the ability to distinguish between dental and retroflex sounds. Children learning Japanese begin to hear “r” and “l” as variants of the same sound. Linguist Pat Kuhl, who has studied this phenomenon for decades, describes the process as one of perceptual narrowing and increasing neural commitment, eventually excluding native-like perception of other languages.

One of the most striking examples of the brain’s attunement to native sounds is apparent in languages such as Mandarin, where varying the tone of an utterance can produce entirely different words. (For instance, the syllable ma can mean “mother,” “hemp,” “horse,” or “scold,” depending on the pitch contour you lay over it.) When Mandarin speakers hear nonsense syllables that are identical except for their tones, they show heightened activity in the left hemisphere of the brain, where people normally process sounds that signal differences in meaning—like the difference between the syllables “pa” and “ba.” But speakers of non-tonal languages like English have more activity in the right hemisphere, showing that the brain doesn’t treat tone as relevant for distinguishing words. A recent study found that Chinese-born babies adopted into French homes showed brain activity that matched Chinese speakers and was clearly distinct from monolingual French speakers—even after being separated from their birth language for more than 12 years.

he brain’s devotion to a childhood language reminds me of a poem by Emily Dickinson:

The Soul selects her own Society—
Then—shuts the Door—
To her divine Majority—
Present no more—

Unmoved—she notes the Chariots—pausing—
At her low Gate—
Unmoved—an Emperor be kneeling
Upon her Mat—

I’ve known her—from an ample nation—
Choose One—
Then—close the Valves of her attention—
Like Stone—

Those of us who received more than one language before the valves of our attention closed may find, to our surprise, that our earliest language lingers on in our soul’s select society, long after we thought it had faded.

I’ve become aware of the deep sense in which I belong to the Czech language, as well as the extent to which my formative memories are tinged by its “musical key.” For me, the English phrase “pork with cabbage and dumplings” refers to a concept, the national dish of the Czechs. But hearing the Czech phrase vepřo-knedlo-zelo evokes the fragrance of roasting meat, pillowy dumpling loaves being pulled steaming out of a tall pot and sliced with sewing thread, and the clink of the nice china as the table is dressed for Sunday dinner, the fulcrum of every week.

Since coming back from the Czech Republic, I’ve insisted on speaking Czech with my mother. Even though it’s more effortful for both of us than speaking in English, our conversation feels softer, more tender this way. English was the language in which I forged my independence, the language of my individuation—but it was in Czech that I was nurtured, comforted, and sung to.

It has also gotten easier to hear the timbre of my father’s voice in my mind’s ear, especially when working in my garden. It’s no accident that many of my conversations with him, and more recently with my uncle, have been on the subject of horticulture. My father’s family has lived for centuries in the fertile wine and orchard region of Moravia, and on my recent visit, I saw my relatives gaze out at their land with an expression usually reserved for a beloved spouse or child. Throughout my own life, I’ve given in to the compulsion to fasten myself to whatever patch of land I happened to be living on by growing things on it, an impulse that has often conflicted with the upwardly and physically mobile trajectory of my life. It’s an impulse I submit to once again, living now in the lee of the Rocky Mountains; neither grapes nor apricots will thrive in the brittle mountain air, but I raise sour cherries and saskatoons, small fruits native to western Canada. As I mulch and weed and prune, I sometimes find myself murmuring to my plants in Czech as my father did, and the Moravian homestead doesn’t seem very far away.

My newly vocal native tongue, and along with it, the heightened memory of my father’s voice, does more than connect me to my past: It is proving to be an unexpected guide in my present work. I’ve recently left my job as an academic linguist to devote more time to writing, and I often find myself these days conjuring my father’s voice by reading a passage in Czech. Like many Czechs I’ve met, my father treated his language like a lovely object to be turned over, admired, stroked with a fingertip, deserving of deliberate and leisurely attention. He spoke less often than most people, but was more often eloquent. I may never regain enough of my first language to write anything in it worth reading, but when I struggle to write prose that not only informs but transcends, I find myself steering my inner monologue toward Czech. It reminds me of what it feels like to sink into language, to be startled by the aptness of a word or the twist of a phrase, to be delighted by arrangements of its sounds, and lulled by its rhythms. I’ve discovered that my native language has been sitting quietly in my soul’s vault all this time.

Julie Sedivy has taught linguistics and psychology at Brown University and the University of Calgary. She is the co-author of Sold on Language: How Advertisers Talk to You and What This Says About You and more recently, the author of Language in Mind: An Introduction to Psycholinguistics.

This article The strange persistence of first languages is featured on Big Think.

You’re lying in bed, staring at the ceiling, listening to cars go by. You have no idea how long you have been like this, but it must be a few hours, at least. Go to sleep, you tell yourself. Just close your eyes and: Go. To. Sleep. You shut your eyes tight, force your body to relax, and wait for the blissful slumber to come. But, nothing happens. More minutes pass and… nothing happens. It’s 3 a.m., and you’re still staring at the ceiling.

We have all been in this situation. Try as we might, it is nearly impossible to consciously will yourself to sleep. Sleep comes to those who let their mind wander and focus on anything other than sleep itself. Count sheep, control your breathing, listen to an audiobook, or whatever — so long as it turns your mind from wanting to sleep.

This is a common and familiar example of the “law of reversed effort.”

The law of reversed effort

The Law of Reversed Effort was first coined by the author Aldous Huxley, who wrote:

“The harder we try with the conscious will to do something, the less we shall succeed.

“Proficiency and the results of proficiency come only to those who have learned the paradoxical art of doing and not doing, or combining relaxation with activity, of letting go as a person in order that the immanent and transcendent unknown quantity may take hold.”

It’s the idea that the more we try to do something, the worse we become at it. Suppose, for instance, that you are learning how to ride a bike for the first time. You are told to hold the handlebars a certain way, to push off with this foot, to pedal at that speed, to sit in a specific position, to hold your balance here, and so on. There is a small book’s worth of micro-instructions when learning to ride a bike. When we ride a bike, we know all these things, but we do not try to do them. They just happen. In Huxley’s words, it’s “combining relaxation with activity.”

But, there’s a spiritual or holistic way of viewing the “law of reversed effort” as well. It’s something that has a much longer history than Aldous Huxley — it’s the Daoist idea of “Wu Wei.”

Wu Wei

The word “surrender” comes laden with negative connotation. Surrender is cowardly or weak. Heroes are ones who never back down, and no great story begins with the good guys just giving up. And yet, there is a lot of arrogance in this.

To surrender to a greater power — or a nobler, righteous one — is not an act of cowardice. It is an act of profound wisdom. There is nothing praiseworthy about swimming in a storm or punching a bear in the face. There is wisdom in knowing our limits, in embracing humility, and even in being pushed around.

This is the meaning of Wu Wei. It is not some lazy torpor, or an excuse for a duvet day and Netflix binge. In fact, it is often the very opposite. Wu Wei is to appreciate, recognize, and accept the pull of forces far greater than us. It is to walk the path that opens up and push the door that gives. Call it gut-feeling, intuition, fate, divine calling, or whatever, but Wu Wei is to stop doing what you think is right, and to let yourself be pulled by some other power.

Wu Wei is the reed bending in the wind. It’s the stick riding the current. It’s surrender and humility. It is, in short, the law of reversed effort — to recognize that some things need patience and space.

Practical applications

That’s nice, you might think, but how does that actually translate to real life? The problem with a lot of philosophy of this kind is that it rather leaves us no better off than before. How can Huxley’s law of reversed effort be seen not as an ideology but as a practical guide? The fact is that “not doing” is fundamental to the nature of many tasks. Here are just a few examples.

Writing: For an author, there is nothing so terrifying as the blank page. If you have been told you have to write something, especially on a deadline, the mind often can go into meltdown grasping for something — anything — to write. It’s much better to let ideas come and write them in a notebook so they don’t get lost.

Technical skills: When you are learning a new sport or skill, you have to learn the technique. You go through the motions, ticking off steps in your head, and eventually end up succeeding. But there comes a point when overthinking is detrimental. It’s probably why your favorite team are rubbish at penalty shoot-outs.

Stress and anxiety: We all get stressed about things. All jobs involve bottlenecks and crunch points. Life has good days and bad days. But when we obsessively run things over in our heads, we actually make anxiety worse. There is a reason why “mindfulness” is such a breakaway phenomenon, and why Headspace is a $250-million business. Stepping away, taking a breath, and doing nothing are good for you.

Conversations: When it comes to how we talk to people, less really is more. A bad conversation involves you talking too much and your “listening” consisting of simply waiting to talk again. Yet research shows that active listening gives more “conversational satisfaction” and leaves the partner feeling more understood.

You can’t force it

There are many moments in life when trying harder makes things worse. When you have a mosquito bite, a broken bone, or a nosebleed, you leave it be. Picking, prodding, and probing only exacerbate the problem. So, too, with a lot of life’s major moments.

Perhaps it is time to step away from what you are doing and enjoy Wu Wei or inaction. After all, if I tell you not to think of pink elephants, there’s only one way to do it.

Jonny Thomson runs a popular Instagram account called Mini Philosophy (@philosophyminis). His first book is Mini Philosophy: A Small Book of Big Ideas.

This article The law of reversed effort: The harder you try, the harder you fall is featured on Big Think.

Adolescence, defined as the transitional period between puberty and adulthood, is characterized by major changes in psychological, emotional, and social processes, and is often associated with challenging behavior. Teenagers can be moody, defiant, and may engage in substance use and other risky behaviors. It is during this stage of life that people are most vulnerable to developing mental health conditions such as schizophrenia.  

According to neuroscientific theory, adolescence is characterized by the gradual maturation of executive function and development of higher-order cognitive skills, such as decision-making and planning, with which we coordinate other cognitive abilities and behaviors. But at what point in adolescence is this maturation process complete?  

A new “big data” study shows precisely when executive function matures. The results, published in the journal Nature Communications, demarcate the boundary between adolescence and adulthood, to reveal when adolescents begin to think like adults. 

Just in time to vote

Studies of the development of executive function typically examine how processes such as working memory, inhibitory control, and task switching change with age, but most use either small numbers of children and teenagers performing a wide range of these tasks, or large numbers performing just a few. Brenden Trevo-Clemmens of the University of Minnesota and his colleagues aggregated the results from four large independent studies to create one data set comprising the performance of nearly 10,800 individuals aged between 8 and 35 years on 23 different measures of executive function from 17 distinct tasks. They were thus able to chart the maturation of executive function throughout adolescence. 

Analysis of the data revealed that performance on almost all the tasks improved with age, with the biggest improvements occurring between early to middle adolescence (10-15 years of age), and smaller but still significant improvements from middle to late adolescence (15-18 years). Performance on all the measures stabilized to adult levels between 18 and 20 years of age. 

The authors say that their findings confirm, and provide rare direct evidence for, the idea that adolescence is a distinct transitional phase during which goal-directed executive functioning reaches maturity.

The brain keeps changing

Executive function depends largely on a brain structure called the prefrontal cortex (PFC), which undergoes protracted maturation during adolescence. Numerous brain imaging studies show, however, that PFC maturation continues well into the third decade of life — far later than the maturation of executive function observed here.

“The PFC is clearly relevant for executive function, and both brain processes and cognitive performance may be used to demarcate the boundaries of adolescence,” says Tervo-Clemmens. “Our work focuses on behaviors as defined by computerized cognitive tasks, and we did not measure brain processes themselves.” 

“One idea we have is that brain maturation in the 20s may be important for fine tuning variability from day-to-day or across contexts, which isn’t well captured by lab-based computerized cognitive assessments,” he adds.

“Likewise, we think cognitive charting and brain changes are just one part of the puzzle when it comes to determining when adolescents reach adulthood, and should be used in parallel to emotional responses and sociocultural frameworks to discuss and consider the bounds of adolescence.” 

Tervo-Clemmens says that he and his colleagues are planning to investigate the matter in contexts that more closely resemble the real world, by assessing executive function in participants’ day-to-day lives using, for example, smartphone apps, rather than relying only on lab-based tasks.  

“This will help us better understand multiple sources of variability, both within and between individuals, and get closer to real-world outcomes,” he says. “We also plan to continue to develop these insights to inform the emergence of mental health presentations, which typically first emerge during adolescence, that may be associated with executive function.”

This article At what age do adolescents and teenagers begin to think like adults? is featured on Big Think.

There is a school cross-country competition. It happens every year, on a muddy track on a dreary, foggy day. Almost all the students hate it. But not Mike. He has spent every day for the past six months training for this. He finished last the year before and is determined to do better this year. Mike wakes at 6 a.m. each day and runs the cross-country route. He eats well and gets lean. Mike’s life is a Rocky training montage. 

The day arrives. Mike is nervous. He walks up to the starting line, his heart thundering in his ears, and the gun fires to start the race. Mike finishes in 12th place. He’s nowhere near first. The winner, Jules, finishes so far ahead that Mike couldn’t even see him. Jules has never trained in his life. He doesn’t even like running. Jules was just born with the natural, muscular physique of someone who can lope their way to victory. 

Whose run do you appreciate more? Whom do we value more? According to several notable research papers, people will tend to vote for Mike. 

Effort bias 

We tend to respect effort. When we find out that someone has spent a lot of time on a project, we value that work more. This is known as the “effort heuristic.” People will rate a product more highly if more effort has gone into it. In 2004, Kruger et al. gave participants a poem and told half of them that it took only four hours to write, and they told the other half it took 18 hours to write. Participants ended up rating the 18-hour poem more highly and also placing it at a higher monetary value. The team repeated a similar thing for a painting and got the same outcome. 

An interesting point raised by the paper is the role of art and the artist. When Jackson Pollock first appeared on the art scene in the 1930s with his paint-splattered canvases, the art world was torn. Some were unimpressed by the random, seemingly nonsense drips. Others thought it was genius. At the time, and now, Pollock was defended based on the effort heuristic. The work was a slow, deliberate, and exhausting process, often requiring weeks or even months of hard work. When we appreciate art, we do so, at least in part, with the effort heuristic in mind. 

Severity of initiation 

The effort heuristic also pops up in initiations or rites of passage. In 1959, psychologists Elliot Aronson and Judson Mills argued and proved that the more severe an initiation, the more favorably an initiate views the group they join. If you have to endure some kind of pain, embarrassment, or long waiting period, then you value the membership more. Aronson and Mills argued that it resulted from “cognitive dissonance” — which is to say, we don’t like to believe we tried hard or suffered deeply for something of little worth. So, if you wait in line for a long time, you are more likely to tell yourself that the thing at the end of the line is amazing. 

The Aronson and Mills experiment has been reproduced and corroborated since (not least to iron out some problems in the original study). More recently, in 2010, Lydall et al. showed that a similar effort bias seems to exist in animals. 

Harness the bias 

Beyond psychological studies, it is not hard to imagine how the effort heuristic manifests in everyday life. Here we can look at three common examples of the bias at play: 

Relationships. “Treat them mean; keep them keen.” Or so it goes. If you want someone to fall madly in love with you, then you need to appear aloof and hard to get. It turns out that there might be some truth to that. If someone devotes a lot of time, effort, and money to win you over, they are more likely to value the subsequent relationship more highly. 

Weight loss. The more effort and discipline you exert on losing weight and being healthier, the more likely you are to carry it on. Let’s suppose you have a New Year’s resolution: “I will eat no chocolate.” The hardest month will be the first. The average American will give up their resolution in just 32 days. But the longer you work at it — the longer you go without — the more steadfast is your determination. 

Luxury goods. In 2020, a team from South Korea showed that if you earn a coupon (as opposed to being given it through little or no effort), you are more likely to rate it highly and, therefore, use it. A similar phenomenon is seen in the pricing of luxury goods. We value items more when they have a higher price tag — more money, more effort, more value. 

This article Effort bias: Why we overvalue fraternities, exclusive clubs, and Taylor Swift tickets is featured on Big Think.

Do you have an uncle who believes vaccines cause autism but refuses to study the reams of research showing them to be safe? What about a friend who avoids information about factory animal farming so they can eat cheap meat guilt-free? Or how about that CEO who claims their business is ethically minded, yet doesn’t investigate its supply chain for exploitation of the environment or the impoverished?

Each is an example of what psychologists call willful ignorance — the intentional act of avoiding information that reveals the negative consequences of one’s actions. Not to judge: We all have a place in our lives where we look the other way and pretend everything is fine. It may be personal, political, or professional in nature, but just below the conscious surface, we know our actions don’t align with our stated values.

“Examples [of] willful ignorance abound in everyday life,” Linh Vu, a doctoral candidate at the University of Amsterdam, said. “We wanted to know just how prevalent and how harmful willful ignorance is, as well as why people engage in it.”

To find out, Vu and a team of researchers performed the first meta-analysis on the current empirical evidence of willful ignorance, and it was published in the Psychological Bulletin, a peer-reviewed journal published by the American Psychological Association. They compared the results of 22 studies with a total of more than 6,000 participants. Here’s what they found. 

Moral wiggle room

The classic experiment for studying willful ignorance is known as the moral wiggle room task. It was designed by Jason Dana, an associate professor of marketing and management at Yale. Participants are randomly assigned the role of decision-maker or recipient. The decision-maker is given a choice: They can take either a $5 or $6 payout. If they take the $5 payout, the recipient will receive $5 as well. If they take the $6 payout, the recipient will receive $1.

When provided with this information by a researcher, the majority of decision-makers act altruistically. They sacrifice the slightly larger payout for themselves to give the recipient more money. On average, only about a quarter of decision-makers act selfishly. But this full-information condition is simply the control. The experiment really begins when the researchers become less forthcoming.

In the experimental condition, the decision-makers can still choose between the $5 or $6 payouts, but this time they are not told what the recipient will receive. There’s a 50-50 chance the recipient will receive $5 or $1. Importantly, the decision-makers can ask the researchers what payout the recipient will receive, and they can do so at no cost to themselves. In other words, while the decision-makers start out blind to the consequences of their actions, they don’t have to stay that way if they don’t want to.

In Dana’s original 2007 study, 44% of decision-makers in the experimental condition chose to remain willfully ignorant and took the selfish option.

Some studies in the meta-analysis were variations on this original design. For instance, one version of the game included ultimatum bargaining where the recipient could accept or reject the decision-maker’s offer. If they reject it, both participants walk away empty-handed. Another version had group members vote on payouts for the group and an unknown recipient.

But across all the studies, the researchers found Dana’s original split to be fairly consistent. On average, 40% of people chose not to learn about the consequences of their actions, and such ignorance was associated with less altruism compared to those who became informed.

Ignorance as an excuse

The researchers hypothesized two potential motivations for willful ignorance. First, they thought willful ignorance may offer a built-in excuse for not acting generously. If a person doesn’t know the consequences of their actions, the internal logic goes, then they still can consider themselves a morally upstanding individual even if they decide to act selfishly. Willful ignorance serves to protect their self-image.

The second potential motivation is known as “cognitive inattentiveness.” That is, people dislike thinking more than they have to. It may stem from laziness, not paying attention, or not wanting to take the time to learn more. Whatever the case, they favor the quick-and-easy decision — even if they would have acted altruistically had they been informed upfront. 

To test this, the researchers compared the choices of participants who chose to inform themselves with those who learned about the consequences by default. The researchers reasoned that if the driver was cognitive inattentiveness, then the percentage of altruism would be roughly the same between the two. 

On the other hand, if those who chose to learn about the consequences acted more generously, this would suggest that those informed by default would have “self-selected” to remain ignorant if given the option. And that’s what they found. Across the studies, participants who chose to be informed of the consequences were 7% more likely to make the altruistic choice. 

“The findings are fascinating as they suggest a lot of the altruistic behaviors we observe are driven by a desire to behave as others expect us to,” Shaul Shalvi, co-author and a professor of behavioral ethics at the University of Amsterdam, said in a statement.

He added: “A part of the reasons why people act altruistically is due to societal pressures as well as their desire to view themselves in a good light. Since being righteous is often costly, demanding people to give up their time, money, and effort. Ignorance offers an easy way out.”

With that said, the analysis couldn’t eliminate cognitive inattentiveness as a potential motivation. In fact, willful ignorance could be the cumulative effect of many motivations, including those not considered in the meta-analysis, such as reputation. The data simply suggest that maintaining a positive self-image is one of those motivations.

A little less ignorant about willful ignorance

The meta-analysis does have limitations that should be mentioned. To start, participants overwhelmingly came from Europe and the U.S., meaning the results may not be replicated in other cultures. The studies also looked at willful ignorance in the lab versus actual decisions in the real world. Finally, they focused on discrete tasks, meaning they were only performed once. It’s possible that continuous rounds of give-and-take between decision-maker and recipient would yield different results (like in many game theory games).

Still, the authors conclude that “taken together, the aggregate evidence suggests ignorance is indeed in part ‘willful’ and driven by excuse-seeking and self-image maintenance motives.” Thanks to them, we are all a little less ignorant about ignorance.

This article 40% of people willfully choose to be ignorant. Here’s why is featured on Big Think.

It is generally assumed that sleep is a state of unconsciousness, during which we disconnect from, and become completely unresponsive to, our surroundings. Recent research shows, however, that we can process information while we sleep, and that this sleep-learning can exert implicit influences on our behavior when we are awake.

Most of this research demonstrates that the processing of sensory information during sleep occurs automatically and unconsciously. Several years ago, however, Başak Türker of the Paris Brain Institute and her colleagues showed that they could initiate two-way communication with lucid dreamers. Their findings, published in 2021, showed that lucid dreamers were able to answer yes-or-no questions, discriminate between sights, sounds and textures, and perform mathematical calculations during the rapid eye movement (REM) stage of sleep. 

The same research team now shows that their earlier findings extend not only to non-lucid dreamers, but also to other sleep stages. In a new study published in the journal Nature Neuroscience, they report that people can also perceive and respond to verbal instructions while they sleep. 

You are getting sleepy

For this latest study, Türker and her colleagues recruited 49 participants, 27 of whom have narcolepsy, and played them a series of words and “pseudo-words,” presented in semi-random order, while they napped in a sound-proof room. The participants were required to decide if each word was real or made up, and respond with facial expressions: smile if the word was real one, frown if it was made up. During the experiment, the researchers used electrodes to measure the electrical activity of each participant’s brain, heart, and facial muscles. 

The electrode recordings showed that all the participants were significantly more responsive during those periods in which they heard words and pseudo-words than during the “off” periods when they heard nothing. They responded to the verbal stimuli during all sleep stages, with their responsiveness increasing with the depth of sleep. 

Responsiveness was also associated with, and preceded by, increased neural activity in regions of the brain linked to high cognitive states, such that the researchers could predict when the participants would respond to the verbal stimuli by surges in brain activity. 

After waking from each nap, the participants were asked to describe any mental content they experienced while they slept, whether they had a lucid dream, and whether they recalled performing the task. Only those participants with narcolepsy, which is characterized by excessive daytime sleepiness and increased lucid dreaming, reported having lucid dreams. Interestingly, lucid dreaming was associated with an increase in the neural activity associated with cognition, above and beyond that seen with the responses that occurred during non-lucid dreaming.

Talking to sleepers

The researchers conclude that “transient windows of reactivity to external stimuli exist during bona fide sleep,” and that lucid dreamers may have “privileged access to their inner world,” with “heightened awareness… to the outside world.” They also suggest that these windows could offer a way of communicating with sleepers to study sleep-related mental problems.    

This article You can respond to verbal instructions in your sleep is featured on Big Think.

What image does the number 693 produce in your mind? For Katie Kermode, who holds four world records in memory championships, the answer is a theatrical showman. She has a mental image handy for all numbers between 1 and 999. The number 522, for instance, makes her visualize red lentils “spilling everywhere.” And 711 conjures a cat. 

These images aren’t arbitrarily selected. If you’ve ever wondered how it’s humanly possible for someone to recite 70,030 digits of pi from memory, as Suresh Kumar Sharma did in 2015, the answer is that they’re almost certainly using a mnemonic technique — a strategy that helps you remember and retrieve long lists of information by simplifying it into more relatable or easily visualized concepts.

To memorize numbers, for example, Kermode uses the Ben System (a variation of the widely used Major System), in which each digit represents a particular consonant or vowel sound. These form words when combined: 7 (kuh) 1 (ah) 1 (tuh) gives you “cat.” 

Why convert numbers into mental images? The brain has a much easier time recalling images over words, a phenomenon known as the picture superiority effect. “Numbers are just hard to remember naturally because they’re very abstract,” Kermode said. So, if you tried to memorize and recall the first 100 digits of pi, “You might see a row of digits, but I’m seeing ‘tree,’ ‘cat,’ whatever. [I wouldn’t] remember the order without some sort of technique.” 

That’s for digits, however. Years before learning her first memory technique (a grade school mnemonic trick to remember the names of the planets), Kermode had a knack for memorization. At three years old, her parents found that she could easily recall the names of football players and the clubs they played for, and later, she was able to easily recall license plates, phone numbers, and the names of kids in school.

In 2008, Kermode competed in her first memory competition, landing a world record for memorizing 84 unfamiliar names and faces in five minutes. (She later topped that with a new world record of 105.) Today, with numerous records and awards under her belt, Kermode is one of the world’s top competitors for names-and-faces and word competitions. 

But, perhaps surprisingly, she doesn’t use mnemonic techniques for every memory task. “Especially for names, there’s literally no technique that I use,” Kermode said. “I try not to even think about it.”

But that’s not to say that performing wild feats of memory is only possible for those who are naturally gifted. Kermode said many memory athletes never felt they had a strong memory, and some competitors might have a hard time remembering faces and names yet do very well in other competitions, like numbers. Ultimately, anybody can get to a high level in memory sports, Kermode said.

“You have to train, but also ability helps. I think it’s like with any sport: It’s a mixture of the two.”

So where should you start if you want to improve your memory abilities? The answer is likely with the strategy used by virtually every memory athlete whom Kermode knows: the method of loci.

The method of loci

Also called the “memory palace” technique, the method of loci was developed by the ancient Greek polymath Simonides of Ceos, who narrowly avoided being crushed to death by a building collapse during a dinner party in the 5th century BC. Simonides came up with the technique after finding he was able to identify the dead by thinking about where each person was seated at the banquet. Spatial location, he realized, is a powerful memory aid.

In 2020, Big Think interviewed the English illusionist Derren Brown about how he uses the technique in his performances to count cards and do other tricks. In essence, the method involves creating a mental map of a familiar place (your house or your neighborhood) and then pairing the information you want to remember with specific locations within that place. 

But Kermode, like many memory athletes, uses a modified version of the method. When she wants to remember a long list of digits — like the 1,080 numbers she memorized over 30 minutes in a 2017 competition, for example — she breaks the numbers into groups of three. Using the phonetic-based Ben System, she converts these three-digit numbers into words and corresponding images: a cat, lentils, a showman. She then visualizes walking through a familiar route within her mental map (she often uses her home) and “places” two images in each predetermined spot along this imaginary stroll. 

“I actually do something a little bit different [from] most people, which is [that] I’ve got a fixed person in each location,” Kermode said. “So, in my driveway it’s this guy called Ben, who’s a memory competitor. In my hallway, it’s my nephew… It just helps me link the objects to something rather than just putting them in a location.”

Why add people to the mix? 

“It’s much more meaningful to have a person to link them to,” Kermode said. “It’s like if you find out a fact about your friend — like a certain friend owns a snake — you know, you’ll remember it. ‘Oh, they own a snake? That’s kind of odd.’ You won’t have to visualize the snake in their house. You’ll just remember it.”

Kermode said other competitors use different variations. For example, some people use the scenes of a movie instead of a familiar area. “That’s something that’s not quite the method of loci but it essentially is.” Other memory athletes might not use any version of the Major System to convert the numbers they want to remember into images, or they’ll arbitrarily assign images to certain numbers. “I find that strange, but everybody’s got different brains, different ways of coming up with these strategies.”

Cognition and memory sports

When Kermode encounters the number 711, an image of a cat appears in her mind — the result of training through the Ben System. But Kermode said words and numbers can also spark visualizations and other perceptions completely organically, without any intention or prior training. This seems to be a product of synesthesia, the perceptual phenomenon that blends the senses in unusual ways, such as “seeing colors” when hearing music. 

The number 2, for example, presents itself as blue. Meanwhile, certain names have different “textures”: The name Penelope comes off as “rounded” while Ethan is “harsh” and “sounds like scratching nails on a fence.” Kermode said she’s only met one or two memory athletes with synesthesia, but noted that “people talk a lot about it” in the memory sports world. 

In recent decades, researchers have been investigating synesthesia and its relationship to memory. Some studies (though not all) suggest that synesthetes have better memory abilities than the general population, at least in certain memory tasks. Why? It’s not completely clear, but one explanation may be that synesthetes naturally form the kind of vivid, multisensory mnemonic associations that others have to cultivate to enhance memory. 

Beyond questions over synesthesia or inherent abilities, Kermode noted that there’s a big push in the memory sports world to emphasize that “anybody can do this.” And she agrees, mentioning that she knows memory athletes who have built up their abilities “from scratch.” A 2017 study published in Neuron supports this idea, noting that high-level memory abilities “do not seem to be associated with extraordinary brain anatomy or general cognitive superiority, but they are acquired through deliberate training in mnemonic strategies.”

“[Especially for] memorizing numbers — there are techniques you can use,” Kermode said. “It’s not really something you need natural ability for.”

But like any sport, Kermode believes natural advantage is not a factor to be ignored, in part because she hopes researchers will continue to study the mechanisms behind memory. 

“Because I was able to get a world record on my first competition, it’s never really been a doubt in my mind that I must have some sort of natural ability,” she said. “Of course, I don’t like to go around saying, ‘Hey, I’ve got some natural ability!’ But it’s just a fact.”

Kermode, who works as a software developer in England and created the memorization and recall software used at IAM World Memory Championships and other competitions, hopes to compete in more face-to-face memory competitions soon, noting that the pandemic had halted many in-person contests. In the meantime, she’s working on a four-digit system that pairs specific images with all numbers up to 10,000. 

As for what people often get wrong or might not know about memory sports?

“I think one misconception that people have is they think it’s really boring — sitting looking at a row of digits, for instance,” Kermode said. “But what perhaps people don’t realize is we’re turning them into objects and people, and we’re making these really cool stories… When I’m going through my locations, they’re usually places I’ve been on holiday or vacation. I’m thinking of these really amazing places and sort of making things happen in those locations and it’s very creative. It’s actually quite fun.”

This article Memory champion explains how she memorizes 1,080 numbers in 30 minutes is featured on Big Think.

In the mid-20th century, scientific research suggested that psychedelic drugs could be beneficial in the treatment of alcoholism and psychiatric disorders. Soon enough, however, LSD was outlawed in a knee-jerk response to the hippie counterculture, and studies of the therapeutic potential of psychedelics were abandoned.

Psychedelic research resumed about 30 years ago and has blossomed ever since. There are dozens of labs in leading academic institutions investigating the potential benefits of these substances, and a search for the term “psychedelic” on ClinicalTrials.gov, the U.S. National Library of Medicine’s registry of human clinical trials, produces more than 500 results. 

Psychedelic renaissance

Today, we are at the peak of the so-called “psychedelic renaissance.” Psychedelics are touted as wonder drugs; Silicon valley CEOs espouse the benefits of LSD “microdosing“; various companies offer luxury psychedelic retreats in the Caribbean; and numerous startups are in the process of developing psychedelics-based pharmaceutical compounds. The psychedelics industry, which had an estimated market value of $4.9 billion in 2022, is anticipated to grow to nearly $12 billion by 2029. 

The consciousness altering effects of psychedelics are well documented. Their purported therapeutic benefits may be linked to their ability to induce existential experiences, but robust evidence for these benefits is still thin on the ground. Psychedelics are also known to have negative effects, but these too are under-studied and under-reported. The evidence for “bad trips” remains largely anecdotal.

What a long strange trip it’s been

Now, new research published in the open access journal PLoS ONE provides fresh insights into the long-term difficulties that can follow a psychedelic experience, and it reveals factors that can accurately predict extended difficulties.

Jules Evans of Queen Mary University in London and his colleagues used social media, email lists, and a newsletter and newspaper advertisement to recruit 608 participants who had problems that lasted more than one day after using a psychedelic, and asked them to complete an online survey about their experience. As well as providing details about the type of drug they used and its dosage, most of the participants also provided detailed written accounts of their psychedelic trip and the difficulties they experienced afterward.

According to the results of the survey, emotional difficulties were the most common problems experienced. About two-thirds (67%) of participants reported experiencing anxiety, fear, anger, low mood or depression, paranoia, panic attacks, shame or guilt, or resurfaced trauma, among other things, after taking the psychedelic. 

Social difficulties were the next most commonly reported, with just over one quarter (27%) saying that they felt a sense of disconnection from others, had difficulties communicating, or experienced social anxiety or withdrawal after their trip.

About one fifth (21%) of the participants reported experiencing perceptual problems such as visual or auditory hallucinations, “flashbacks,” or time distortions, and a slightly smaller proportion (18%) of them reported cognitive problems such as difficulty thinking clearly or concentrating, intrusive thoughts, forgetfulness, or difficulty making decisions.  

For about one-third of those surveyed, the difficulties persisted for more than one year. For one-sixth, they persisted for more than three years after the psychedelic experience. The survey results showed that the more challenging a psychedelic experience was, the longer the negative effects lasted, and that taking a psychedelic in an unpredictable or unguided setting was associated with a wider range of negative effects. They also show that psilocybin and LSD are more frequently associated with long-term difficulties, but the authors suggest that this may be because they are more readily available than other psychedelics such as ayahuasca and DMT. 

Psychedelic medicine

The authors acknowledge that their results may not be universally applicable, because their respondents consisted mostly of white English speakers. Also, people in countries where psychedelics are legal, or where they are used in a cultural or religious context, could experience them differently. Nevertheless, they say their results suggest that taking psychedelics, even in a clinical setting, is not entirely risk-free.

This article Bad trips: Study examines the long-term adverse effects of psychedelic drugs is featured on Big Think.

Psychonaut turned scientific researcher Josie Kins has personally tried over 200 psychedelic compounds and had hundreds of psychedelic experiences. But she no longer takes them herself. “I’ve already explored them so thoroughly,” she says. Over the past 12 years, Kins has compiled a list of 233 effects people experience under the influence of psychedelic drugs, drawn from online accounts and her own experience, called the Subjective Effect Index.

In 2021, she began working for a startup drug company called Mindstate Design Labs to make the classification system more precise and comprehensive, under the advisement of renowned psychedelic researchers Thomas Ray and Andy Newburg. That work could double the total number of entries on the list, she says. But it’s the cognitive and emotional effects that seem to elude categorization and need the most refining. “The visual effects are already rigorous,” says Kins.

Below, a selection of some of the 52 visual effects on her list.

Diffraction

Diffraction is the experience of seeing rainbows and spectrums of color embedded within the brighter parts of a person’s visual field. It is most commonly induced under the influence of mild dosages of psychedelic compounds, such as LSD, psilocybin, and mescaline.

Increased pareidolia

Increased pareidolia is an increase in a person’s ability and tendency to recognize patterns (usually faces) within vague stimuli. It is most commonly induced under the influence of mild dosages of psychedelic compounds, such as LSD, psilocybin, and mescaline.

Machinescapes

Machinescapes are a complex visual and tactile experience where one perceives hallucinatory mechanical landscapes that are vast in both size and intricacy. They are most commonly induced under the influence of heavy dosages of Salvia divinorum. However, they can also occur less commonly under the influence of psychedelic compounds, such as LSD, psilocybin, and 2C-P.

Object activation

Object activation is the experience of looking at an object and perceiving it to move, become alive, or become fully animated and autonomous of its own accord. It is most commonly induced under the influence of heavy dosages of deliriant compounds, such as DPH, datura, and benzydamine.

Scenery slicing

Scenery slicing is the experience of a person’s visual field appearing to split into separate, cleanly cut sections. These individual slices then proceed to drift slowly away from their original position before disappearing and resetting to normal. It is most commonly induced under the influence of moderate dosages of dissociative compounds, such as ketamine, PCP, and DXM.

Texture liquidation

Texture liquidation is the experience of the texture, shape, and general structure of objects and scenery appearing progressively simplified, smudged, and stylized in such a way that one’s external environment begins to take on the aesthetic of a painting or cartoon. It is most commonly induced under the influence of moderate dosages of psychedelic compounds, such as LSD, psilocybin, and mescaline.

Unspeakable horrors

Unspeakable horrors describe the experience of prolonged exposure to indescribable scenarios and hallucinatory content of a scary and disturbing nature, which are often directly influenced by a person’s fears. They are most commonly induced under the influence of heavy dosages of psychedelic compounds, such as LSD, psilocybin, and 2C-P.

Visual exposure to inner mechanics of consciousness

Visual exposure to inner mechanics of consciousness is the experience of being exposed to a mass of visual geometry comprised entirely of innately readable representations which subjectively feel as if they convey the inner mechanics that compose all underlying neurological processes.

This article 8 ways psychedelics distort our vision is featured on Big Think.