Posts Tagged ‘brain’

Meet Helen Lavretsky, Professor of Psychiatry at UCLA, recently completed a pilot study of Kundalini yoga vs memory training in older adults with subjective memory complaints and mild cognitive impairment.

Patients assigned to yoga practice for 12 weeks with daily meditation for 12 minutes in weekly one hour classes did better than those who participated in memory training classes in verbal and visual memory, executive function, mood resilience, anxiety, and connectivity of the brain.

Results suggest that yoga can be a cognitive enhancement or brain fitness exercise that can confer similar or even more extensive cognitive resilience than memory training—the gold standard—in older adults.

Meditation in this study was practiced with music recorded on the White Sun album, which received a Grammy award this year.

Dr Lavretsky is Professor of Psychiatry at UCLA. She also directs the Late Life Mood, Stress, and Wellness Research Program at the Semel Institute at UCLA.

http://www.psychiatrictimes.com/geriatric-psychiatry/cognitive-enhancement-with-yoga?GUID=C523B8FD-3416-4DAC-8E3C-6E28DE36C515&rememberme=1&ts=17082017

Eyre HA1, Siddarth P1, Acevedo B1, et al. A randomized controlled trial of Kundalini yoga in mild cognitive impairment. Int Psychogeriatr. 2017;29:557-567. https://www.cambridge.org/core/journals/international-psychogeriatrics/article/randomized-controlled-trial-of-kundalini-yoga-in-mild-cognitive-impairment/138A3EB97520CE72B01D17059B7AA286.

Yang H, Leaver AM, Siddarth P, et al. Neurochemical and Neuroanatomical Plasticity Following Memory Training and Yoga Interventions in Older Adults with Mild Cognitive Impairment. Front Aging Neurosci. 2016;8:277. eCollection 2016. http://journal.frontiersin.org/article/10.3389/fnagi.2016.00277/full.

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By Ashley P. Taylor

During adulthood, the mouse brain manufactures new neurons in several locations, including the hippocampus and the subventricular zone of the forebrain. The hypothalamus, previously identified as an area with an important role in aging, also generates new neurons from neural stem cells. In a study published July 26 in Nature, Dongsheng Cai and his team at the Albert Einstein College of Medicine in New York connect the dots between these two observations, reporting that hypothalamic neural stem cells have widespread effects on the rate of aging in mice.

In what David Sinclair, who studies aging at Harvard Medical School and who was not involved in the work, calls a “Herculean effort,” the researchers “discovered that stem cells in the hypothalamus of the mouse play a role in overall health and life span,” he tells The Scientist.

Cai and his team found that killing hypothalamic neural stem cells accelerates aging, and transplantation of additional neural stem cells into the same brain region slows it down. Further, the stem cells’ anti-aging effects could be reproduced simply by administering the cells’ secreted vesicles, called exosomes, containing microRNAs (miRNAs).

“If this is true for humans, one could imagine a day when we are treated with these small RNAs injected into our bodies or even implanted with new hypothalamic stem cells to keep us younger for longer,” Sinclair adds.

Researchers who study aging have long been searching for a central location that controls the process system-wide. In a 2013 paper, Cai and his team reported aging-associated inflammation in the hypothalamus of the mouse, which they could experimentally manipulate to speed up or slow down various types of aging-related decline, from muscle endurance to cognitive skills.

This study, Cai says, suggested the hypothalamus might be that central locus in control of aging. The researchers wanted to understand more about how this region of the brain drives aging and what role hypothalamic neural stem cells might play in that process, so they undertook a series of experiments.

Age-defying stem cells

The researchers first confirmed that cells bearing protein markers of neural stem cells (Sox2 and Bmi1) were present in the hypothalamus of early-to-middle-aged mice (11 to 16 months old) and that the number of those cells decreased in older mice.

Next, they destroyed neuronal stem cells in the hypothalamus by injecting the third ventricle, adjacent to the hypothalamic region where the stem cells are found, with a lentivirus that converted an administered compound into a toxin in cells expressing the stem-cell marker Sox2. Three or four months later, the researchers compared a variety of aging-related measures, including muscle endurance, coordination, social behaviors, novel object recognition, and cognitive performance, between mice injected with the virus and various control groups of mice that received a brain injection of some sort but in which the toxin could not be produced and the hypothalamic stem cells were consequently not ablated.

The mice in the experimental group lost 70 percent of their hypothalamic stem cells and, based on results of the physiological tests, had accelerated aging. Mice with ablated hypothalamic stem cells also died earlier than control mice.

Next, the researchers implanted middle-aged mice with neural stem cells derived from newborn mice to see if the additional stem cells would slow aging. But the implanted stem cells almost all died, which the researchers believe was a result of the inflammatory environment of the aging hypothalamus. Newborn neuronal stem cells genetically engineered to withstand that environment, on the other hand, did survive, and mice implanted with those cells lived longer and performed better on aging-related measures than control mice.

“What’s cool about this study is that they specifically delete a population of cells in the hypothalamus of the brain . . . and they show pretty striking alterations in whole-body aging,” says Anna Molofsky, a psychiatrist at the University of California, San Francisco, who studies glial cells and whose graduate work focused on neuronal stem cells and aging. “That’s really showing that there’s a mechanism within the brain that’s regulating whole-body organismal aging,” she adds. Molofsky, who was not involved in the work, says that these results support the idea of the hypothalamus as a central regulator of aging.

Anti-aging mechanism

Although neural stem cells are known for their ability to produce new neurons, that doesn’t seem to be their primary method for protecting against aging. The anti-aging effects of these hypothalamic stem cells were visible at around four months—not long enough, the authors write, for significant adult neurogenesis to have taken place.

The authors looked instead for some other factor that might be responsible for the stem cells’ effects. In the hypothalamic neural stem cells, the researchers detected exosomes—secreted vesicles that can contain RNA and proteins—containing a variety of miRNAs, short RNA molecules that inhibit the expression of targeted genes. These exosomes were not present in non-stem cells of the hypothalamus.

To test the effects of the exosomes alone on aging, the researchers purified the vesicles from cultured hypothalamic neural stem cells and transplanted them into middle-aged mice, finding that the exosome-treated mice aged more slowly than vehicle-treated controls. They also found that the exosomes could ameliorate the aging symptoms of mice whose hypothalamic neurons had been ablated.

Cai says microRNAs could be a potential mechanism by which hypothalamic neural stem cells have such wide-ranging effects on aging, yet he believes that neurogenesis may also be involved.

Regardless of the mechanism, Molofsky says, “the medical applications could be pretty profound.” The phenotypes, such as muscle mass and skin thickness, affected by these stem cells are the same ones that cause age-related disease, she notes. “The fact that you can reverse that with a brain-specific modulation, potentially, in a cell type that one could pharmacologically target, I think potentially that could be very profound, assuming that the mouse work translates to humans.”

Y. Zhang et al., “Hypothalamic stem cells control ageing speed partly through exosomal miRNAs,” Nature, doi:10.1038/nature23282, 2017.

By Bradley J. Fikes

A diabetes drug developed by a San Diego biotech company from a venomous lizard’s saliva reduces Parkinson’s disease symptoms, according to a study published Thursday.

The placebo-controlled study of 62 patients found the drug, exenatide, provided statistically significant effectiveness in preserving motor control. It may actually slow down disease progression, although this has to be confirmed with more research.

For Parkinson’s patients, the trial represents stronger grounds to expect more effective treatments. For San Diego’s life science community, it represents another example of the benefits of original research and innovation.

The study was published in The Lancet by researchers led by Thomas Foltynie and Dilan Athauda, both of University College London in London, England. While the study wasn’t particularly large, with 62 patients, it was placebo-controlled, and is in line with a previous clinical study published in 2014.

Exenatide was found in Gila monster saliva by Dr. John Eng, an endocrinologist at Bronx Veterans Affairs Medical Center in New York. The venomous lizard, native to the Southwestern United States and northwestern Mexico, delivers excruciating pain with its bite.

San Diego’s Amylin Pharmaceuticals licensed the discovery in 1996. Further development yielded exenatide, sold under the brand name Byetta.

The drug became a hit, providing a major reason for Amylin’s 2012 purchase for $7 billion by Bristol-Myers Squibb. As for Amylin, the company was disbanded and no longer exists.

Exenatide/Byetta reduces insulin resistance in Type 2 diabetes, allowing for better control of blood glucose. There’s evidence that Parkinson’s disease is also related to problems with insulin signaling.

The new clinical study improves on the previous study because it is placebo-controlled, according to an accompanying commentary in The Lancet. But the study has limitations that prevent it from being considered definitive.

“Whether exenatide acts as a novel symptomatic agent or has neuroprotective effects on the underlying Parkinson’s disease pathology remains unclear, but Athauda and colleagues’ study opens up a new therapeutic avenue in treatment of Parkinson’s disease,” the commentary stated.

Christian Weyer, M.D., a former Amylin executive, said one of the most interesting parts of the study was exenatide’s potential for modifying the course of Parkinson’s disease. Weyer is now president of Chula Vista’s ProSciento, a clinical services provider.

Patients were measured on motor skills after getting 48 weeks of injections, either with exenatide or placebo. The treated group showed an advantage of 4 points on a 132-scale test, which was statistically significant.

Exenatide mimics the action of a hormone, and such drugs often show disease-modifying properties, said Weyer, who was Amylin’s Senior Vice President of Research and Development.

“It’s not conclusive that exenatide has the potential for disease-modification, but I was impressed by the fact that the endpoint of the test was in the off-medication period, so you actually assess whether there’s an effect even after the treatment had been stopped,” Weyer said.

Amylin had performed early preclinical research on exenatide for Parkinsons’ disease, Weyer said. The research was funded by a small grant from the Michael J. Fox Foundation.

In chronic diseases such as Type 2 diabetes and Parkinson’s, finding disease-modifying therapies is the “Holy Grail,” Weyer said.

“These are life-long diseases, and anything you can do to either delay or prevent the onset of the disease, or to slow its progression over a long period of time” has great benefit, Weyer said.

Insulin has many biological roles in the body, so it’s not surprising that an abnormal response to insulin could play a role in Parkinson’s disease as well as diabetes, Weyer said.

http://www.sandiegouniontribune.com/business/biotech/sd-me-exenatide-parkinsons-20170803-story.html

That warm, fuzzy feeling you get when you’re being generous or charitable happens when the brain areas involved in generosity and in happiness synchronise.

No one likes a Scrooge. It’s been shown that generous people make more popular partners, and researchers have also honed in on the brain areas linked to generosity.

But fundamentally, being generous means spending resources – be they time, energy or money – on another person that you could be spending on yourself. According to conventional economic theory, this is very surprising: prioritising others over yourself might leave you with fewer resources.

Now neuroscientists have pinpointed how generosity is linked to happiness on a neural level, in a study in the journal Nature Communications.

In a study of 50 people, half were given the task of thinking about how they’d like to spend 100 Swiss Francs (£80) on themselves over the next four weeks. The other half were told to think about how they’d like to spend it on someone else – for example, a partner, friend or relative. They took a test to measure their subjective level of happiness before and after the experiment.

The people who were told to spend the money on others had a bigger mood boost than the group who had planned more treats for themselves.

Immediately after this test, the participants took part in another one. They were put in an fMRI scanner and their brain activity was measured while they were asked questions about how to distribute money between themselves and someone else they knew.

They were given the chance to accept offers such as giving their chosen person a present of 15 Swiss Francs even if it cost them 20 Francs. The people who had been in the ‘generous’ group in the first experiment tended to be more generous in this activity.

The decisions people made in the experiment weren’t just hypothetical, they had real consequences.

“The people were told that one of those options would be randomly chosen and then realised. So, for example they would have to pay 20 Francs and we would send other person the 15 Francs with a letter explaining why they were receiving it,” study author Soyoung Park of the University of Lübeck, Germany, told IBTimes UK.

The scans revealed the brain areas that were most active during the acts of generosity. The area associated with generosity – the temporo-parietal junction – and an area associated with happiness – the ventral striatum – both lit up particularly strongly during the fMRI scans. In addition, the activity of the two regions synchronised.

People tend not to realise how happy generous giving will make them, the researchers conclude.

“In everyday life, people underestimate the link between generosity and happiness and therefore overlook the benefits of prosocial spending. When asked, they respond that they assume there would be a greater increase in happiness after spending money on themselves and after spending greater amounts of money,” the authors write in the study.

“Our study provides behavioural and neural evidence that supports the link between generosity and happiness. Our results suggest that, for a person to achieve happiness from generous behaviour, the brain regions involved in empathy and social cognition need to overwrite selfish motives in reward-related brain regions. These findings have important implications not only for neuroscience but also for education, politics, economics and health.”

http://www.ibtimes.co.uk/warm-glow-you-get-generosity-real-scientific-phenomenon-1629891

by Jerry Useem

If power were a prescription drug, it would come with a long list of known side effects. It can intoxicate. It can corrupt. It can even make Henry Kissinger believe that he’s sexually magnetic. But can it cause brain damage?

When various lawmakers lit into John Stumpf at a congressional hearing last fall, each seemed to find a fresh way to flay the now-former CEO of Wells Fargo for failing to stop some 5,000 employees from setting up phony accounts for customers. But it was Stumpf’s performance that stood out. Here was a man who had risen to the top of the world’s most valuable bank, yet he seemed utterly unable to read a room. Although he apologized, he didn’t appear chastened or remorseful. Nor did he seem defiant or smug or even insincere. He looked disoriented, like a jet-lagged space traveler just arrived from Planet Stumpf, where deference to him is a natural law and 5,000 a commendably small number. Even the most direct barbs—“You have got to be kidding me” (Sean Duffy of Wisconsin); “I can’t believe some of what I’m hearing here” (Gregory Meeks of New York)—failed to shake him awake.

What was going through Stumpf’s head? New research suggests that the better question may be: What wasn’t going through it?

The historian Henry Adams was being metaphorical, not medical, when he described power as “a sort of tumor that ends by killing the victim’s sympathies.” But that’s not far from where Dacher Keltner, a psychology professor at UC Berkeley, ended up after years of lab and field experiments. Subjects under the influence of power, he found in studies spanning two decades, acted as if they had suffered a traumatic brain injury—becoming more impulsive, less risk-aware, and, crucially, less adept at seeing things from other people’s point of view.

Sukhvinder Obhi, a neuroscientist at McMaster University, in Ontario, recently described something similar. Unlike Keltner, who studies behaviors, Obhi studies brains. And when he put the heads of the powerful and the not-so-powerful under a transcranial-magnetic-stimulation machine, he found that power, in fact, impairs a specific neural process, “mirroring,” that may be a cornerstone of empathy. Which gives a neurological basis to what Keltner has termed the “power paradox”: Once we have power, we lose some of the capacities we needed to gain it in the first place.

That loss in capacity has been demonstrated in various creative ways. A 2006 study asked participants to draw the letter E on their forehead for others to view—a task that requires seeing yourself from an observer’s vantage point. Those feeling powerful were three times more likely to draw the E the right way to themselves—and backwards to everyone else (which calls to mind George W. Bush, who memorably held up the American flag backwards at the 2008 Olympics). Other experiments have shown that powerful people do worse at identifying what someone in a picture is feeling, or guessing how a colleague might interpret a remark.

The fact that people tend to mimic the expressions and body language of their superiors can aggravate this problem: Subordinates provide few reliable cues to the powerful. But more important, Keltner says, is the fact that the powerful stop mimicking others. Laughing when others laugh or tensing when others tense does more than ingratiate. It helps trigger the same feelings those others are experiencing and provides a window into where they are coming from. Powerful people “stop simulating the experience of others,” Keltner says, which leads to what he calls an “empathy deficit.”

Mirroring is a subtler kind of mimicry that goes on entirely within our heads, and without our awareness. When we watch someone perform an action, the part of the brain we would use to do that same thing lights up in sympathetic response. It might be best understood as vicarious experience. It’s what Obhi and his team were trying to activate when they had their subjects watch a video of someone’s hand squeezing a rubber ball.

For nonpowerful participants, mirroring worked fine: The neural pathways they would use to squeeze the ball themselves fired strongly. But the powerful group’s? Less so.

Was the mirroring response broken? More like anesthetized. None of the participants possessed permanent power. They were college students who had been “primed” to feel potent by recounting an experience in which they had been in charge. The anesthetic would presumably wear off when the feeling did—their brains weren’t structurally damaged after an afternoon in the lab. But if the effect had been long-lasting—say, by dint of having Wall Street analysts whispering their greatness quarter after quarter, board members offering them extra helpings of pay, and Forbes praising them for “doing well while doing good”—they may have what in medicine is known as “functional” changes to the brain.

I wondered whether the powerful might simply stop trying to put themselves in others’ shoes, without losing the ability to do so. As it happened, Obhi ran a subsequent study that may help answer that question. This time, subjects were told what mirroring was and asked to make a conscious effort to increase or decrease their response. “Our results,” he and his co-author, Katherine Naish, wrote, “showed no difference.” Effort didn’t help.

This is a depressing finding. Knowledge is supposed to be power. But what good is knowing that power deprives you of knowledge?

The sunniest possible spin, it seems, is that these changes are only sometimes harmful. Power, the research says, primes our brain to screen out peripheral information. In most situations, this provides a helpful efficiency boost. In social ones, it has the unfortunate side effect of making us more obtuse. Even that is not necessarily bad for the prospects of the powerful, or the groups they lead. As Susan Fiske, a Princeton psychology professor, has persuasively argued, power lessens the need for a nuanced read of people, since it gives us command of resources we once had to cajole from others. But of course, in a modern organization, the maintenance of that command relies on some level of organizational support. And the sheer number of examples of executive hubris that bristle from the headlines suggests that many leaders cross the line into counterproductive folly.

Less able to make out people’s individuating traits, they rely more heavily on stereotype. And the less they’re able to see, other research suggests, the more they rely on a personal “vision” for navigation. John Stumpf saw a Wells Fargo where every customer had eight separate accounts. (As he’d often noted to employees, eight rhymes with great.) “Cross-selling,” he told Congress, “is shorthand for deepening relationships.”

Is there nothing to be done?

No and yes. It’s difficult to stop power’s tendency to affect your brain. What’s easier—from time to time, at least—is to stop feeling powerful.

Insofar as it affects the way we think, power, Keltner reminded me, is not a post or a position but a mental state. Recount a time you did not feel powerful, his experiments suggest, and your brain can commune with reality.

Recalling an early experience of powerlessness seems to work for some people—and experiences that were searing enough may provide a sort of permanent protection. An incredible study published in The Journal of Finance last February found that CEOs who as children had lived through a natural disaster that produced significant fatalities were much less risk-seeking than CEOs who hadn’t. (The one problem, says Raghavendra Rau, a co-author of the study and a Cambridge University professor, is that CEOs who had lived through disasters without significant fatalities were more risk-seeking.)

But tornadoes, volcanoes, and tsunamis aren’t the only hubris-restraining forces out there. PepsiCo CEO and Chairman Indra Nooyi sometimes tells the story of the day she got the news of her appointment to the company’s board, in 2001. She arrived home percolating in her own sense of importance and vitality, when her mother asked whether, before she delivered her “great news,” she would go out and get some milk. Fuming, Nooyi went out and got it. “Leave that damn crown in the garage” was her mother’s advice when she returned.

The point of the story, really, is that Nooyi tells it. It serves as a useful reminder about ordinary obligation and the need to stay grounded. Nooyi’s mother, in the story, serves as a “toe holder,” a term once used by the political adviser Louis Howe to describe his relationship with the four-term President Franklin D. Roosevelt, whom Howe never stopped calling Franklin.

For Winston Churchill, the person who filled that role was his wife, Clementine, who had the courage to write, “My Darling Winston. I must confess that I have noticed a deterioration in your manner; & you are not as kind as you used to be.” Written on the day Hitler entered Paris, torn up, then sent anyway, the letter was not a complaint but an alert: Someone had confided to her, she wrote, that Churchill had been acting “so contemptuous” toward subordinates in meetings that “no ideas, good or bad, will be forthcoming”—with the attendant danger that “you won’t get the best results.”

Lord David Owen—a British neurologist turned parliamentarian who served as the foreign secretary before becoming a baron—recounts both Howe’s story and Clementine Churchill’s in his 2008 book, In Sickness and in Power, an inquiry into the various maladies that had affected the performance of British prime ministers and American presidents since 1900. While some suffered from strokes (Woodrow Wilson), substance abuse (Anthony Eden), or possibly bipolar disorder (Lyndon B. Johnson, Theodore Roosevelt), at least four others acquired a disorder that the medical literature doesn’t recognize but, Owen argues, should.

“Hubris syndrome,” as he and a co-author, Jonathan Davidson, defined it in a 2009 article published in Brain, “is a disorder of the possession of power, particularly power which has been associated with overwhelming success, held for a period of years and with minimal constraint on the leader.” Its 14 clinical features include: manifest contempt for others, loss of contact with reality, restless or reckless actions, and displays of incompetence. In May, the Royal Society of Medicine co-hosted a conference of the Daedalus Trust—an organization that Owen founded for the study and prevention of hubris.

I asked Owen, who admits to a healthy predisposition to hubris himself, whether anything helps keep him tethered to reality, something that other truly powerful figures might emulate. He shared a few strategies: thinking back on hubris-dispelling episodes from his past; watching documentaries about ordinary people; making a habit of reading constituents’ letters.

But I surmised that the greatest check on Owen’s hubris today might stem from his recent research endeavors. Businesses, he complained to me, had shown next to no appetite for research on hubris. Business schools were not much better. The undercurrent of frustration in his voice attested to a certain powerlessness. Whatever the salutary effect on Owen, it suggests that a malady seen too commonly in boardrooms and executive suites is unlikely to soon find a cure.

https://www.theatlantic.com/magazine/archive/2017/07/power-causes-brain-damage/528711/

by Daniel Oberhaus

Amanda Feilding used to take lysergic acid diethylamide every day to boost creativity and productivity at work before LSD, known as acid, was made illegal in 1968. During her downtime, Feilding, who now runs the Beckley Foundation for psychedelic research, would get together with her friends to play the ancient Chinese game of Go, and came to notice something curious about her winning streaks.

“I found that if I was on LSD and my opponent wasn’t, I won more games,” Feilding told me over Skype. “For me that was a very clear indication that it improves cognitive function, particularly a kind of intuitive pattern recognition.”

An interesting observation to be sure. But was LSD actually helping Feilding in creative problem solving?

A half-century ban on psychedelic research has made answering this question in a scientific manner impossible. In recent years, however, psychedelic research has been experiencing something of a “renaissance” and now Feilding wants to put her intuition to the test by running a study in which participants will “microdose” while playing Go—a strategy game that is like chess on steroids—against an artificial intelligence.

Microdosing LSD is one of the hallmarks of the so-called “Psychedelic Renaissance.” It’s a regimen that involves regularly taking doses of acid that are so low they don’t impart any of the drug’s psychedelic effects. Microdosers claim the practice results in heightened creativity, lowered depression, and even relief from chronic somatic pain.

But so far, all evidence in favor of microdosing LSD has been based on self-reports, raising the possibility that these reported positive effects could all be placebo. So the microdosing community is going to have to do some science to settle the debate. That means clinical trials with quantifiable results like the one proposed by Feilding.

As the first scientific trial to investigate the effects of microdosing, Feilding’s study will consist of 20 participants who will be given low doses—10, 20 and 50 micrograms of LSD—or a placebo on four different occasions. After taking the acid, the brains of these subjects will be imaged using MRI and MEG while they engage in a variety of cognitive tasks, such as the neuropsychology staples the Wisconsin Card Sorting test and the Tower of London test. Importantly, the participants will also be playing Go against an AI, which will assess the players’ performance during the match.

By imaging the brain while it’s under the influence of small amounts of LSD, Feilding hopes to learn how the substance changes connectivity in the brain to enhance creativity and problem solving. If the study goes forward, this will only be the second time that subjects on LSD have had their brain imaged while tripping. (That 2016 study at Imperial College London was also funded by the Beckley Foundation, which found that there was a significant uptick in neural activity in areas of the brain associated with vision during acid trips.)

Before Feilding can go ahead with her planned research, a number of obstacles remain in her way, starting with funding. She estimates she’ll need to raise about $350,000 to fund the study.

“It’s frightening how expensive this kind of research is,” Feilding said. “I’m very keen on trying to alter how drug policy categorizes these compounds because the research is much more costly simply because LSD is a controlled substance.”

To tackle this problem, Feilding has partnered with Rodrigo Niño, a New York entrepreneur who recently launched Fundamental, a platform for donations to support psychedelic research at institutions like the Beckley Foundation, Johns Hopkins University, and New York University.

The study is using smaller doses of LSD than Feilding’s previous LSD study, so she says she doesn’t anticipate problems getting ethical clearance to pursue this. A far more difficult challenge will be procuring the acid to use in her research. In 2016, she was able to use LSD that had been synthesized for research purposes by a government certified lab, but she suspects that this stash has long since been used up.

But if there’s anyone who can make the impossible possible, it would be Feilding, a psychedelic science pioneer known as much for drilling a hole in her own head (https://www.vice.com/en_us/article/drilling-a-hole-in-your-head-for-a-higher-state-of-consciousness) to explore consciousness as for the dozens of peer-reviewed scientific studies on psychedelic use she has authored in her lifetime. And according to Feilding, the potential benefits of microdosing are too great to be ignored and may even come to replace selective serotonin reuptake inhibitors, or SSRIs as a common antidepressant.

“I think the microdose is a very delicate and sensitive way of treating people,” said Feilding. “We need to continue to research it and make it available to people.”

https://motherboard.vice.com/en_us/article/first-ever-lsd-microdosing-study-will-pit-the-human-brain-against-ai

Look at a photo of yourself as a teenager and, mistaken fashion choices aside, it’s likely you see traces of the same person with the same personality quirks as you are today. But whether or not you truly are the same person over a lifetime—and what that notion of personhood even means—is the subject of ongoing philosophical and psychology debate.

The longest personality study of all time, published in Psychology and Aging and recently highlighted by the British Psychological Society, suggests that over the course of a lifetime, just as your physical appearance changes and your cells are constantly replaced, your personality is also transformed beyond recognition.

The study begins with data from a 1950 survey of 1,208 14-year-olds in Scotland. Teachers were asked to use six questionnaires to rate the teenagers on six personality traits: self-confidence, perseverance, stability of moods, conscientiousness, originality, and desire to learn. Together, the results from these questionnaires were amalgamated into a rating for one trait, which was defined as “dependability.” More than six decades later, researchers tracked down 635 of the participants, and 174 agreed to repeat testing.

This time, aged 77 years old, the participants rated themselves on the six personality traits, and also nominated a close friend or relative to do the same. Overall, there was not much overlap from the questionnaires taken 63 years earlier. “Correlations suggested no significant stability of any of the 6 characteristics or their underlying factor, dependability, over the 63-year interval,” wrote the researchers. “We hypothesized that we would find evidence of personality stability over an even longer period of 63 years, but our correlations did not support this hypothesis,” they later added.

The findings were a surprise to researchers because previous personality studies, over shorter periods of time, seemed to show consistency. Studies over several decades, focusing on participants from childhood to middle age, or from middle age to older age, showed stable personality traits. But the most recent study, covering the longest period, suggests that personality stability is disrupted over time. “The longer the interval between two assessments of personality, the weaker the relationship between the two tends to be,” the researchers write. “Our results suggest that, when the interval is increased to as much as 63 years, there is hardly any relationship at all.”

Perhaps those who had impulsive character flaws as a teenager would be grateful that certain personality traits might even out later in life. But it’s disconcerting to think that your entire personality is transformed.

“Personality refers to an individual’s characteristic patterns of thought, emotion, and behavior, together with the psychological mechanisms—hidden or not—behind those patterns,” note the authors, quoting psychology professor David Funder’s definition.

If your patterns of thought, emotions, and behavior so drastically alter over the decades, can you truly be considered the same person in old age as you were as a teenager? This question ties in with broader theories about the nature of the self. For example, there is growing neuroscience research that supports the ancient Buddhist belief that our notion of a stable “self” is nothing more than an illusion.

Perhaps this won’t surprise you if you’ve had the experience of running into a very old friend from school, and found a completely different person from the child you remembered. This research suggests that, as the decades go by, your own younger self could be similarly unrecognizable.

You’re a completely different person at 14 and 77, the longest-running personality study ever has found