Even before he was born, it was clear that the boy’s brain was unusual—so much so that his expecting parents flew from rural Alaska to Seattle, where specialists could attend to their son from birth. That is how James Bennett first met the boy, then a days-old infant struggling to breathe. The baby’s head was too big. The structures in his brain looked wrong. Bennett, a pediatric geneticist at Seattle Children’s, was tasked with figuring out why.
Microglia make up 10 percent of the brain’s cells, but they are not neurons and therefore have long been overlooked. The boy’s case makes their importance unmistakable. In the absence of microglia, the boy’s neurons still grew to fill his skull, but they ended up in the wrong places and made the wrong connections. Microglia, scientists have started to realize, guide the development of the brain.
“There wasn’t any part of the brain that wasn’t involved and affected in this child,” Bennett says. A part of the baby’s cerebellum jutted at an odd angle. His ventricles, normally small fluid-filled cavities in the brain, were too large. And a dense bundle of nerves that is supposed to connect the brain’s left and right hemispheres, called the corpus callosum, had entirely failed to develop.
In petri dishes and in animals, scientists had previously observed how microglia guide developing neurons to the right locations, creating the highly organized layers that make up the brain. They also prune connections between neurons. “Things get off track pretty quickly when you start manipulating the functions of microglia,” says Stephen Noctor, a developmental neurobiologist at the University of California at Davis who was not involved in examining the boy. To better understand the CSF1R gene, Bennett teamed up with zebra-fish biologists. In fish, turning off the gene disrupts a cellular pathway necessary for corpus-callosum neurons to grow in humans.
Kim Green, a neurobiologist at the University of California at Irvine, notes that mutant mice lacking microglia have broadly similar patterns of disorganization in their brains. These mice models essentially predicted what would happen in a human. Green had just never expected to see a person without microglia. “It’s absolutely remarkable,” he says.
The boy’s brain helped unlock these scientific mysteries. But he was ultimately still a boy, a very sick one with worried young parents. Their son’s condition was so severe, it turns out, because he had inherited two faulty copies of the CSF1R gene—one from each parent. His parents happened to carry the same rare mutation because they are cousins.
In adults, just one copy of a CSF1R mutation can lead to a brain disorder called adult-onset leukoencephalopathy with axonal spheroids and pigmented glia, which causes memory loss and eventually dementia beginning in one’s 40s. When the boy’s DNA-sequencing results came back, Bennett realized that he had to explain to the parents their own CSF1R mutation and their risks of developing the disorder. They were relieved, he says, to understand what was wrong with their child, but perhaps too overwhelmed to fully take in what it meant for their lives. The couple spoke with a genetic counselor before their son’s DNA sequencing, and Bennett says he arranged to have them meet with another genetic counselor back in Alaska, where they returned home.
This story has no miracle cure or happy ending. The boy died in Alaska at 10 months old of likely related causes, and Bennett says the family agreed to an autopsy. They have since lost touch. The phone numbers he has for them no longer work. He told me that he recently got hold of the mother’s sister, in an attempt to tell the family about the research made possible by their child. It’s a delicate balance: He feels a duty to inform, but he understands that the parents might not want to be reminded of their dead son.
A pediatric geneticist’s job, Bennett said, is often to diagnose extremely rare conditions, which push up against the limits of the human body. “On any day, you can find a patient you spend the rest of your career thinking about,” he said. The boy is one of them.
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You make countless decisions every day that range from mundane to incredibly important, but what part of you is actually making those decisions? We all assume that our brains are focused on whatever task we’re tackling, but a new study suggests that your brain is usually working a few steps ahead all on its own, and it makes your decisions long before you consciously think about them.
The study, which was published in Scientific Reports, reveals that what we often think of as free will and our ability to make decisions on the fly isn’t nearly as cut-and-dry. Your brain, it turns out, might be running the show largely in the background.
The experiment was fairly straightforward, tasking volunteers to decide between two patterns with different colors and orientations. Their brains were being monitored in an fMRI machine while the images flashed before their eyes, and the researchers were able to match brain activity patterns with whatever choice the subject was making.
That part isn’t particularly surprising, since scientists have long known that repeatable brain patterns can correlate with decision making. But what’s interesting about this research is that the team found the participants brain activity could predict their eventual choices before the individual was even asked to make a choice.
“We believe that when we are faced with the choice between two or more options of what to think about, non-conscious traces of the thoughts are there already, a bit like unconscious hallucinations,” Professor Joel Pearson, co-author of the study, said in a statement. “As the decision of what to think about is made, executive areas of the brain choose the thought-trace which is stronger. In, other words, if any pre-existing brain activity matches one of your choices, then your brain will be more likely to pick that option as it gets boosted by the pre-existing brain activity.”
Put simply, the path you’re about to choose when you make a decision can sometimes be pre-determined before you even actively consider your options. The researchers found that they could predict the outcome up to 11 seconds before the subject began to weigh their decision.
“This would explain, for example, why thinking over and over about something leads to ever more thoughts about it, as it occurs in a positive feedback loop,” Pearson said.
Because sleep often becomes increasingly lighter and more disrupted as we get older, the study reinforces and potentially explains the links among aging, sleep deprivation, and heightened risk for Alzheimer’s disease.
“Sleep is critical to the function of the brain’s waste removal system and this study shows that the deeper the sleep the better,” says Maiken Nedergaard, codirector of the Center for Translational Neuromedicine at the University of Rochester Medical Center (URMC) and lead author of the study.
“These findings also add to the increasingly clear evidence that quality of sleep or sleep deprivation can predict the onset of Alzheimer’s and dementia.”
The study, which appears in the journal Science Advances, indicates that the slow and steady brain and cardiopulmonary activity associated with deep non-REM sleep are optimal for the function of the glymphatic system, the brain’s unique process of removing waste. The findings may also explain why some forms of anesthesia can lead to cognitive impairment in older adults.
WASHING AWAY WASTE
Nedergaard and her colleagues first described the previously unknown glymphatic system in 2012. Prior to that point, scientists didn’t fully understand how the brain, which maintains its own closed ecosystem, removed waste. The study revealed a system of plumbing which piggybacks on blood vessels and pumps cerebral spinal fluid (CSF) through brain tissue to wash away waste. A subsequent study showed that this system primarily works while we sleep.
Because the accumulation of toxic proteins such as beta amyloid and tau in the brain are associated with Alzheimer’s disease, researchers have speculated that impairment of the glymphatic system due to disrupted sleep could be a driver of the disease. This squares with clinical observations which show an association between sleep deprivation and heightened risk for Alzheimer’s.
In the current study, researchers conducted experiments with mice anesthetized with six different anesthetic regimens. While the animals were under anesthesia, the researchers tracked brain electrical activity, cardiovascular activity, and the cleansing flow of CSF through the brain.
The team observed that a combination of the drugs ketamine and xylazine (K/X) most closely replicated the slow and steady electrical activity in the brain and slow heart rate associated with deep non-REM sleep. Furthermore, the electrical activity in the brains of mice administered K/X appeared to be optimal for function of the glymphatic system.
“The synchronized waves of neural activity during deep slow-wave sleep, specifically firing patterns that move from front of the brain to the back, coincide with what we know about the flow of CSF in the glymphatic system,” says Lauren Hablitz, a postdoctoral associate in Nedergaard’s lab and first author of the study.
“It appears that the chemicals involved in the firing of neurons, namely ions, drive a process of osmosis which helps pull the fluid through brain tissue.”
The study raises several important clinical questions. It further bolsters the link between sleep, aging, and Alzheimer’s disease. Researchers have known that as we age it becomes more difficult to consistently achieve deep non-REM sleep, and this study reinforces the importance of deep sleep to the proper function of the glymphatic system.
The study also demonstrates that enhancing sleep can manipulate the glymphatic system, a finding that may point to potential clinical approaches, such as sleep therapy or other methods to boost the quality of sleep, for at-risk populations.
Furthermore, because several of the compounds used in the study were analogous to anesthetics used in clinical settings, the study also sheds light on the cognitive difficulties that older patients often experience after surgery and suggests classes of drugs that could help avoid this phenomenon. Mice in the study that researchers exposed to anesthetics that did not induce slow brain activity saw diminished glymphatic activity.
“Cognitive impairment after anesthesia and surgery is a major problem,” says coauthor Tuomas Lilius with the Center for Translational Neuromedicine at the University of Copenhagen in Denmark. “A significant percentage of elderly patients that undergo surgery experience a postoperative period of delirium or have a new or worsened cognitive impairment at discharge.”
Additional researchers from the University of Rochester and the University of Copenhagen contributed to the study. The National Institute of Neurological Disorders and Stroke, the National Institute on Aging, the Adelson Foundation, the Sigrid Juselius Foundation, the Novo Nordisk Foundation, and the Lundbeck Foundation supported the research.
Unlike a bicep or a quadricep, we can’t see or feel when our brain is turning into mush through either disuse or misuse. Instead, any atrophy will instead make itself known when we’re struggling to remember a very common word, getting hopelessly lost in a part of town we’re intimately familiar with, or being driven to tears trying to figure out how to set up a personal hotspot. That last one happened to me about 90 minutes ago.
While the brain isn’t literally a muscle, its function can be positively and negatively affected by the behaviors we engage in—and ones that we don’t—each and every day. Below is a litany of habits you can pick up that could help you stop fucking with your grey matter and help enhance its function instead. If you change your ways, your chances of regaining your sparkle are good.
As I’m sure you’ve noticed, sleep is extremely important to all aspects of our health. Unfortunately, we’re getting less of it than ever. As recently as the mid-1900s, people slept around nine hours per night. In 1970, that number had fallen to around 7.5 hours per night. According to the CDC, over a third of American adults getting less than seven hours shut-eye per night. “Sleep is essential for optimal neuropsychological ability,” says Virginia-based neurologist and sleep specialist W. Christopher Winter. He elaborates on this in his book, The Sleep Solution: Why Your Sleep is Broken and How to Fix It. “From interpreting nonverbal cues and emotional content to managing concentration and organizing information in our minds, sleep is vital—and restricted sleep can dramatically impact cognitive performance.”
Another sleep-related thing to consider: naps are not just for cranky toddlers. A small study from 2010 looked at the academic performance of two groups of young adults: nappers and non-nappers. In the experiment, every participant completed a rigorous learning task. After the first task, one group took a 90-minute nap while the other stayed awake until a second task was administered hours later. The participants who napped in between tasks did significantly better on the second task and also showed signs of improvement and learning.
The non-nappers, on the other hand, became worse at learning and their ability to retain information decreased. “Napping helps raise levels of alertness and can help with memory,” says clinical psychologist and sleep specialist Michael Breus. He explains that a 20 to 25 minute cat nap can help you to stay sharp when you just didn’t get enough sleep the night before, but that getting more nighttime sleep is the best solution.
Caffeinate (in moderation)
Many of us are well acquainted with coffee’s ability to get us moving in the morning, but it can also help you process things more quickly. Winter says that caffeine’s role as a performance-enhancing drug has long been known. “It helps with concentration, focus, and memory processing as well as recall,” he says. According to a study from 2012, 200 mg of caffeine (about as much as you’d find in a 12-ounce cup of coffee) can improve a person’s verbal processing speed. By providing a group of adults a 200 mg caffeine pill in the morning and then asking them to complete word-recognition tasks, researchers discovered improved speed and accuracy compared to when they completed these tasks without caffeine.
Put the bottle down once in a while
In a study in the British Medical Journal, researchers looked at the impact of moderate alcohol consumption on the brain through the cognitive ability of more than 500 adults over 30 years. It was demonstrated that people who drank between 15 and 20 standard drinks per week were three times more likely to suffer from hippocampal atrophy—damage to the area of the brain involved in memory and spatial navigation.
Overall, drinking doesn’t “kill your brain cells,” but drinking too much too often can damage the part of your brain responsible for remembering things, which is almost as bleak. That actually leads me to my next suggestion.
Give Google a break
If you’re older than say, 35, you can probably remember a time when you had at least a dozen phone numbers committed to memory. You may also recall certain mental tricks you may have employed to help you do so, such as associating certain number sequences with the location of their keys on the dial pad, or “clustering” the numbers into groups to help you retain them. Guess what? That’s called using your brain.
In today’s connected world, we’re storing information basically everywhere else. In a 2011 paper entitled Google Effects on Memory: Cognitive Consequences of Having Information at Our Fingertips, college students were shown to recall less information when they knew they could search for it instead. Winter says that stress can be helpful in memory formation. Knowing that you have access to all the information you’ll need “might reduce memory capacity,” he says.
Have more sex
Sometimes, after a long, hard day, the thought of energetic humping can seem so daunting that you and your partner agree to a half-assed snuggle instead. But if you’re not making sex a priority at all, it might be worth checking out some of the research that touts the benefits it might have on our brain function.
In a small 2017 study published in the Journals of Gerontology, researchers asked a group of older adults questions about their sex lives and then had them to take a standardized test. This revealed a link between sex frequency and intelligence: People who claimed to engage in sexual activity weekly wound up having higher test scores than people who did not. It’s important to note that we can’t be certain of the direction of this effect—people who feel sharper might be more likely to be having more sex.
Still, other recent research has demonstrated a strong link between getting wild and getting smart. In 2017, another study published in the Archives of Sexual Behavior looked at the effect of sex on the cognitive abilities of 78 women aged between 18 and 29. Controlled for other factors such as menstrual phase and relationship length, researchers found that women who had sex more often had better recall of abstract words on a memory test. In fact, the bulk of research done on the benefits of sex on the brain revolves around memory. People who are getting some on a regular basis may be less depressed and more emotionally satisfied too, Winter says. This, he adds, could line up with sex being cognitively beneficial and helpful with focus.
A new study finds that “night owls” — those whose internal body clock dictates they go to bed and wake up very late — appear to have fundamental differences in their brain function compared to “morning larks.”
This suggests that night owls could be disadvantaged by the constraints of a normal working day.
Researchers at the University of Birmingham discovered that night owls, who typically have an average bedtime of 2:30 am and a wake-up time of 10:15 am, have lower resting brain connectivity in many of the brain regions associated with the maintenance of consciousness.
Importantly, this reduced brain connectivity was tied to poorer attention, slower reactions and increased sleepiness throughout the hours of a typical working day.
According to the Office for National Statistics, around 12 percent of employees work night shifts. It is well-established that night-shift workers often face huge negative health consequences due to the constant disruption to sleep and body clocks.
However, this type of disruption can also result from being forced to fit into a societal 9-5 working day if those timings do not align with one’s natural biological rhythms. Since around 40-50 percent of the population identify as having a preference for later bedtimes and for getting up after 8:20 a.m., the researchers say much more work needs to be done to investigate any negative implications for this group.
“A huge number of people struggle to deliver their best performance during work or school hours they are not naturally suited to,” said lead researcher Dr. Elise Facer-Childs, from the University of Birmingham’s Centre for Human Brain Health. “There is a critical need to increase our understanding of these issues in order to minimize health risks in society, as well as maximize productivity.”
For the study, the researchers looked at brain function at rest and linked it to the cognitive abilities of 38 individuals who were identified as either night owls or morning larks using physiological rhythms (melatonin and cortisol), continuous sleep/wake monitoring and questionnaires.
The participants underwent MRI scans and then completed a series of tasks, with testing sessions being undertaken at a range of different times during the day from 8 a.m. to 8 p.m. They were also asked to report on their levels of sleepiness.
Self-identified morning larks reported being least sleepy with their fastest reaction time during the early morning tests, which was significantly better than night owls. Night owls, however, were least sleepy and had their fastest reaction time at 8pm in the evening, although this was not significantly better than the larks, highlighting that night owls are most disadvantaged in the morning.
Interestingly, the brain connectivity in the regions that could predict better performance and lower sleepiness was much higher in larks at all time points, suggesting that the resting state brain connectivity of night owls is impaired throughout the whole day (8 a.m.-8 p.m.).
“This mismatch between a person’s biological time and social time, which most of us have experienced in the form of jet lag, is a common issue for night owls trying to follow a normal working day. Our study is the first to show a potential intrinsic neuronal mechanism behind why ‘night owls’ may face cognitive disadvantages when being forced to fit into these constraints,” said Facer-Childs, who is now based at the Monash Institute for Cognitive and Clinical Neurosciences in Melbourne, Australia.
“To manage this, we need to get better at taking an individual’s personal body clock into account — particularly in the world of work. A typical day might last from 9 a.m.-5 p.m., but for a night owl, this could result in diminished performance during the morning, lower brain connectivity in regions linked to consciousness and increased daytime sleepiness.”
“If, as a society, we could be more flexible about how we manage time we could go a long way towards maximizing productivity and minimizing health risks.”
Invariably, a hoard of studies exploring the famously ambiguous hormone knows as oxytocin begin to pepper the internet around Valentine’s Day. What we do know about the pituitary function however-its profound effect on childbearing, empathy and social interaction, is more than enough to warrant its dubbing as “The Love Hormone.”Tend and defendThe endocrinology is simultaneously a punch to the gut and a pat on the back.On one hand, it’s a little underwhelming to know that all of the things that make us feel warm and husky can be traced to a gland residing in the rotting meat in our heads. But it’s somehow concurrently comforting to know why and how we love someone can be vividly sketched by neurology.
As it turns out love is encouraged and mediated by a temperate-mathematic entity; every kiss and hug funded by a network of hypothalamic animations. But oxytocin doesn’t retire once bonds have been successfully established between mates.
The neuropeptide is expressed primarily in women as it helps with increasing uterine contractions during labor and cervical dilation. It promotes the nurturing maternal link by surging in accordance with things like a child’s cry and suckling.
More grimly, the neurotransmitter has been proven to inspire intolerance. A study conducted back in 2014, examined two groups of Dutch men: one group given oxytocin, the other given placebos.
Both groups were tasked with choosing five men they would give lifeboats to. The ones on oxytocin were found to be more likely to reject Muslim or German-sounding names, while the placebo group’s decisions were notably less informed by superficial factors.
The hormone’s mission to tend and defend makes us more prone to form allegiances towards those with similar characteristics and just as well more readily aware of distinctions.
We are genetically presupposed to crumble in the presence of tribalism.
There are less obvious by-products of the hypothalamus as well. Because oxytocin impacts our ability to process social cues, it indirectly correlates to our productivity in the workplace.
In an attempt to better comprehend the effect neurology has on a healthy corporate community, neuroeconomist Paul J. Zak, successfully administered synthetic oxytocin into living brains during an experiment in the early 2000s. His team of researchers found increased levels of the hormones to have a clear effect on the firm’s profitability and the feelings of fulfillment in those cohabiting it.
According to Zak, productivity lives and dies by one stipulation: a strong community composed of members that have a clear understanding of their purpose within it.
Being rewarded trust by another increases levels of oxytocin significantly. Individuals with higher levels of oxytocin are found to have lower levels of stress, depression and be more apt at social interaction.
The same tend and defend mechanic can apply to a corporation. Employers are biologically incentivized to work harder for those they feel bonded towards.
Zak remarks: “These laboratory studies showed that when trust between team members is high, oxytocin flows and work feels less like, well, work, and more like doing interesting things with friends. ”
Organic methods of raising oxytocin
The production of oxytocin is all about catering to all the things that bring you joy. Considering the intimate things that make us happy is sort heretical in the corporate world, but it has an undeniable affect on its ability to thrive. Pet a dog, listen to music, copulate, take a bubble bath, hug a baby, (your own baby please).
The great thing about oxytocin though is that it responds equally to feeling good as it does to making others feel good. Giving gifts has been studied to raise levels of the hormone. Perfect timing too. People that receive chocolate and flowers exhibit higher levels of oxytocin, as do people that bequeath them.
It’s an evolutionary mistake not to revel in love and empathy.
You know the feeling. The alarm goes off and before you’ve found the button, your brain is already in the shower, fretting over the day ahead. So much work to do. How will you get it all done? Will you do OK in that big presentation? So many meetings you aren’t looking forward to. You want to pick up your daughter after school but secretly know you hardly have the time to do so.
Dread kicks in. What’s wrong with my life?
This is the scenario neuroscientist Lisa Feldman Barrett paints in an interesting TED talk she gave in December 2017 and in her book How Emotions Are Made.
The good news is that you don’t have to be held hostage by this spiraling A.M. anxiety. Barrett’s research points to a surprising finding about our emotions: they’re linked to physical sensations your body is feeling. That’s right, your brain reacts to physical sensations you’re feeling in the form of emotions.
In other words, you might be feeling that sense of dread as soon as you wake up because you simply didn’t sleep well, because you’re hungry, or because you feel dehydrated.
As Barrett explains:
“Your brain is searching to find an explanation for those sensations in your body that you experience as wretchedness. But those sensations might not be an indication that anything is wrong with your life.”
So before you go off the deep end with your morning mental swim, Barrett says ask yourself one question about what you’re feeling, just seven words:
“Could this have a purely physical cause?”
I tried this and found that quite often the answer is, yes. For me, I often wake up parched and, like most of us, have nights where I just didn’t sleep well. I paid attention to this and noticed whenever I felt that sense of dread, it went away as I woke up, drank water, and had breakfast.
But I’d like to add another seven-word question to the mix that you can use when you’re feeling that morning dread; in case your emotions aren’t just based on a physical sensation you’re experiencing in the moment.
“Could this be a signal for change?”
Some have called it Sunday Night Dread–that pit in your stomach you feel as you wind down on Sunday night and think about the day ahead tomorrow. A general unease and unhappiness nags at you. That’s the front line. Ground zero is when you wake up in the morning and the dread is instant and intensified as you face the immediate prospects of the day ahead.
Experiencing this over and over may be a sign that it’s time to make a change and engage in a different line of work or make dramatic changes at the job you’re in.
I experienced this towards the end of my corporate days. I ignored the feeling at first, and then for too long, frankly. Eventually, I let it trigger deep introspection, which ultimately led me to leave corporate behind and embark on my current entrepreneurial journey. I’m so glad I didn’t ignore the signals my morning routine was sending me.
So don’t accept that feeling of morning dread as “just the way it is”. Use Barrett’s question to discern if there’s an underlying physical cause based on what you’re feeling that morning. Use my question so that you’re not just brushing off that dread as you’re brushing your hair. Instead, look in the mirror and get honest with yourself.
When we hear someone is psychotic, we automatically think of psychopaths and cold-blooded criminals. We automatically think “Oh wow, they’re really crazy!” And we automatically think of plenty of other myths and misconceptions that only further the stigma surrounding psychosis.
In other words, the reality is that we get psychosis very wrong.
For starters, psychosis consists of hallucinations and/or delusions. “You can have one or both at the same time,” said Devon MacDermott, Ph.D, a psychologist who previously worked in psychiatric hospitals and outpatient centers, treating individuals experiencing psychosis in various forms.
“Hallucinations are sensory perceptions in the absence of external triggers,” MacDermott said. That is, “the trigger comes from inside [the person’s] own mind,” and involves one of their five senses. The most common is hearing voices, she said. People also can “see or feel things that aren’t there.”
“Delusions are persistent beliefs without sufficient evidence to back up those beliefs—and often with substantial evidence to refute the belief,” said MacDermott, who’s now in private practice where she specializes in trauma and OCD.
Psychologist Jessica Arenella, Ph.D, describes psychosis as a disruption in meaning-making: “The person may be finding meaning in otherwise random or inconsequential things (e.g., license plate numbers, TV ads), while minimizing or failing to grasp the importance of basic needs (e.g., showing up for work, changing one’s clothes).”
The signs of a psychotic episode differ depending on the person, because the symptoms are “an extension of each person’s unique thinking patterns,” MacDermott said.
Generally, people’s speech can be tough to follow or not make sense (because the person’s thoughts are disorganized); they might mutter or talk to themselves; say extraordinary, often unlikely things (e.g., “An actor is in love with me”), she said.
During a psychotic episode, it’s common for individuals to act in ways that are strange or out of character for them, MacDermott said. “This can range from something small like wearing more layers of clothes than is appropriate for the temperature all the way to sudden bursts of emotion that seem to come out of nowhere.”
What Psychotic Episodes Feel Like
“[During a psychotic episode], I zone out. I’m gone. I leave reality,” said Michelle Hammer, who has schizophrenia. She’s the co-host of Psych Central’s A Bipolar, a Schizophrenic, and a Podcast and founder of Schizophrenic.NYC, a clothing line with the mission of reducing stigma by starting conversations about mental health. “I can be thinking of anything. A past conversation. A made-up conversation. A weird dreamlike situation. I lose reality of where I actually physically am.”
“I mainly just feel ‘off,’ Things just aren’t right,” said Rachel Star Withers, who has schizophrenia and is an entertainer, speaker and video producer. She creates videos documenting her schizophrenia and ways to manage it, and aims to let others like her know they are not alone and can still live an amazing life.
“The biggest tell for me is that I start talking to myself and thinking in third person,” Withers said. She’ll tell herself things like:”OK Rachel, just walk; be normal.”
A patient once described psychosis in this way to MacDermott: “Imagine that you summon a picture in your mind like, say, a baseball. Imagine a baseball. Now imagine what it would be like to have the knowledge that you put that image in your mind taken away. Now, all you are left with is a thought having no idea how it got there. That’s what it’s like to be psychotic.”
MacDermott’s patients also have told her that they struggle with interpreting situations and see special meaning in everyday things. “That same patient once saw a family member put a knife down while they were cooking and had the thought that the family member was trying to send the patient a message that they were going to be killed because a knife represents death.”
In this piece on The Mighty individuals shared what it’s like to experience psychosis. One person wrote, “For me, it felt like I was watching a movie that was my life. I knew bad things were happening and I couldn’t stop it.” Another person described having an “out of body experience,” along with “excruciating sensations amplified by 1,000 at the tip of every sensor in my body.”
Someone else explained it in this way: “Every sense is heightened and colors are especially bright. The world is on a giant flat screen TV. Everything seems more crystal clear than you ever knew, but then it all becomes confused and muddled. You make your own realities, constantly decoding messages that seem extremely important, but are ultimately meaningless. They further the storyline in your head that seems so real.”
Arenella’s clients have described their psychotic episodes as “disorienting, overwhelming, frightening and isolating. They often describe heightened sensitivity, believing that there are no boundaries, that everything is related and transparent, and there is no privacy.”
Some might believe that they’re part of, or at the center of, a critical life-altering mission or plan, Arenella said. Which might lead to intense activity or the complete opposite: a feeling of paralysis.
Myths about Psychotic Episodes
One of the biggest and most harmful myths about psychosis is that people are dangerous and violent. Both MacDermott and Arenella emphasized that individuals in the throes of psychosis are much more likely to be victimized than to victimize.
Similarly, psychosis is not the same as psychopathy, MacDermott said. “Psychopaths are people who don’t feel empathy, are thrill seeking, and often are parasitic, aggressive, or manipulative to others. Psychosis is completely different and unrelated.”
Another misconception is that psychosis is always indicative of schizophrenia. Sometimes, psychotic episodes occur on their own, or as part of a different mental illness, such as depression, Arenella said. Most people only experience one or a handful of psychotic episodes in their lifetime, she said. (“Only approximately one third of people who experience psychotic episodes go on to have persistent psychotic states.”)
And if someone’s psychotic episodes are part of schizophrenia, it’s important to understand that people can and do recover from this illness, Arenella said.
Arenella, a founding board member of Hearing Voices NYC, also noted that eliminating voice hearing isn’t an essential part of treatment. “How a person interprets and interacts with their voices is more important for recovery than hearing them or not hearing them.” (This TED talk from Eleanor Longden, who has schizophrenia, provides more insight.)
Moreover, even many mental health professionals believe the widespread myth that medication successfully treats psychosis, said Arenella, the president of the United States chapter of the International Society for Psychological and Social Approaches to Psychosis. While medication can decrease the intensity of symptoms, many people still hear voices and have difficulty in social relating, she said. Many also experience bothersome or serious side effects.
“Medication works for some people, some of the time, but it is not a cure all.” Psychosocial treatments, such as cognitive behavioraltherapy for psychosis (CBT-p), have been shown to be effective in treating psychosis.
What Causes Psychotic Episodes
MacDermott noted that there’s a lot we still don’t know about psychosis, and that includes its causes. Genetics likely plays a role. “People with an immediate family member with schizophrenia are much more likely to have schizophrenia themselves than someone who doesn’t have an immediate family member with the disorder,” she said.
Adverse childhood events and trauma can contribute to psychosis, as well, even though the episode can occur years later, Arenella said. She also identified other common factors: loss, social rejection, insomnia, illegal and prescribed drugs and hormonal changes.
“A lot of antipsychotic medication reduces the amount of certain neurotransmitters, like dopamine, in the brain,” MacDermott said. This suggests that too much dopamine (and other neurotransmitters) might be involved in psychosis. But, as MacDermott noted, “People and brains are so complicated that we can’t know for sure exactly what triggers psychosis in each person.”
A big reason psychosis scares and confuses us is because it seems so out of the realm of “normal.” But in actuality, “psychosis is part of the normal range of human experience,” Arenella said. “While it is unusual, it is not fundamentally different from other human experience.”
That is, she said, “people who hear voices actually hear them and they sound just as real as all of the other voices of people. Imagine if someone were talking to you all day long while you’re trying to have a conversation with someone else; you might be distracted, confused, irritable, and want to avoid conversations. This is a normal response, albeit to an unusual stimuli.”
Also, many people hear voices, and aren’t having a psychotic episode. Arenella noted that after a loved one dies, some people report hearing the person talking to them. “Musicians and poets often hear tunes and verses in their heads and may not feel as if they created them, but more like they received them somehow.” Many people also talk about hearing the voice of God or Jesus during pivotal moments in their lives.
We tend to be taught, both implicitly and explicitly, that psychosis is unlike any other mental health issue—such as anxiety or depression, and “is not amenable to regular therapeutic techniques,” Arenella said. “This fosters a profound othering and harmful stigma toward people who experience psychosis.”
And such teachings simply couldn’t be further from the truth.
Good Reasons for Bad Feelings: Insights From the Frontier of Evolutionary PsychiatryRandolph M. Nesse Dutton (2019)
Globally, the burden of depression and other mental-health conditions is on the rise. In North America and Europe alone, mental illness accounts for up to 40% of all years lost to disability. And molecular medicine, which has seen huge success in treating diseases such as cancer, has failed to stem the tide. Into that alarming context enters the thought-provoking Good Reasons for Bad Feelings, in which evolutionary psychiatrist Randolph Nesse offers insights that radically reframe psychiatric conditions.
In his view, the roots of mental illnesses, such as anxiety and depression, lie in essential functions that evolved as building blocks of adaptive behavioural and cognitive function. Furthermore, like the legs of thoroughbred racehorses — selected for length, but tending towards weakness — some dysfunctional aspects of mental function might have originated with selection for unrelated traits, such as cognitive capacity. Intrinsic vulnerabilities in the human mind could be a trade-off for optimizing unrelated features.
Similar ideas have surfaced before, in different contexts. Evolutionary biologists Stephen Jay Gould and Richard Lewontin, for example, critically examined the blind faith of ‘adaptationist’ evolutionary theorizing. Their classic 1979 paper ‘The spandrels of San Marco and the Panglossian paradigm’ challenged the idea that every aspect of an organism has been perfected by natural selection (S. J. Gould et al. Proc. R. Soc. Lond. B205, 581–598; 1979). Instead, like the curved triangles of masonry between arches supporting domes in medieval and Renaissance architecture, some parts are contingent structural by-products. These might have no discernible adaptive advantage, or might even be maladaptive. Gould and Lewontin’s intuition has, to some extent, been vindicated by molecular genetics. Certain versions of the primitive immune-system protein complement 4A, for instance, evolved for reasons unrelated to mental function, and yet are associated with an increased risk of schizophrenia.
Decades earlier, the evolutionary theorist George C. Williams explored perhaps the most perplexing aspect of human biology: our inconvenient tendency to age and die. He suggested in 1957 that some of the genes that cause ageing evolved because they enhanced fitness early in life (G. C. Williams Evolution11, 398–411; 1957). Such ‘antagonistic pleiotropy’ — in which a single gene controls at least one beneficial and one detrimental trait — suggests that the design of biological structures is a complex optimization problem involving multiple trade-offs. Emotions and other aspects of mental function are not like machine components, each with a set function; instead, they are embedded in complex overlapping biochemical pathways.
In 1994, Nesse teamed up with Williams for Why We Get Sick, a manifesto for “Darwinian medicine”. Their insights opened up new perspectives on the origins of diseases, arguing for ‘proximate’ causes (driven by anatomy, biochemistry and physiology) and higher-level ‘ultimate’ (evolutionary) causes. They noted that evolution selects for reproductive success rather than for health and happiness; hence, the existence of human diseases and disorders. They also detailed the contingent and sometimes ‘irrational’ nature of biological legacies, such as the nerves and blood vessels that run across the human eye’s retinal surface. Cephalopod eyes don’t have this ‘flaw’.
Good Reasons for Bad Feelings builds on these insights. Adopting an “engineers’ point of view” on mental illnesses, Nesse suggests that anxiety, although apparently undesirable, is a design component with utility in certain situations — for instance, as a “smoke detector” for potentially life-threatening events. Depression might also perform adaptive functions. The psychiatrist Aubrey Lewis argued that by signalling distress, depression could prompt others into providing assistance through foraging and other activities. It has even been suggested that depressive behaviour in vervet monkeys (Chlorocebus pygerythrus) evolved to signal loss of status, deflecting attacks from dominant males.
Yet, however functional its components when appropriately regulated, mental illnesses cause suffering, and evidence-based treatments are sparse. Indeed, the field has seen no significant pharmaceutical breakthroughs for many years. Biological causes remain elusive, and biomarkers non-existent.
Psychiatry as a field, meanwhile, quivers with theoretical uncertainty. It has not become a sub-speciality of neurology, as one might have expected if mental illness mapped directly to neural behaviour. And common genetic variations with large effects on mental disorders are elusive. The various incarnations of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders(DSM) have enabled diagnostic consistency and the objectification of mental illnesses. But the DSM has resulted in overlapping diagnoses, and contrived symptom-cluster checklists. At times, it impinges on the territory of healthy mental function. Allen Frances, chair of the task force that wrote the manual’s fourth edition in 1994, revolted against out-of-control mental diagnosis in his 2013 book DSM: Saving Normal.
From adaptive to maladaptive
Nesse argues that evolutionary theory could foster therapeutic breakthroughs by providing a robust theoretical foundation for psychiatry. He posits that it might also help to prevent people from equating psychiatric symptoms with diseases and viewing extremes of emotion such as anxiety as disorders. Nesse also suggests that mental illnesses might result from the disruption of regulators that maintain equilibrium in the body, such as the endocrine system. The normally adaptive function of thoughts and emotions could, in such instances, become maladaptive.
The future success of clinical psychiatry might depend on an evolutionary framework being integrated with whole-genome sequence-data analysis; this could help to identify mutations predisposing people to mental illness. Given the small contributions of individual genes and the diverse mechanisms involved, this will demand analysis of the genomes of hundreds of thousands of people. As a result of the extensive and often paradoxical entanglement of genetic networks, future treatments might, by necessity, require mental circuits to be engineered to release them from hard-wired evolutionary constraints.
In Theodicy (1710), German philosopher Gottfried Leibniz argued that God, being omniscient, must have created the best of all possible worlds. (Fifty years later, in his novel Candide, Voltaire lampooned Leibniz as Doctor Pangloss, who opined that faults in the world are necessary, like contrasting shadows in a painting.)
Ironic readings aside, the philosopher’s optimism might now be shown to have rational echoes in contemporary science. As Good Reasons for Bad Feelings boldly posits, many of the core dysfunctional components of mental illness ultimately help to make us human.