A new review and analysis of several studies has found that probiotics do not improve self-reported anxiety symptoms in humans, although there was evidence of minor improvements in rodents.
The study reviewed 36 preclinical studies in total, 14 involving humans and 22 involving rats and mice. That’s a decent-sized sampling of the research covering a variety of probiotic strains, and it turned up zero evidence that humans with self-reported anxiety symptoms benefited from taking any of them.
“Probiotics did not significantly reduce symptoms of anxiety in humans and did not differentially affect clinical and healthy human samples,” the study concluded.
One of the strains, Lactobacillus (L.) rhamnosus, did appear to reduce anxiety symptoms in rodents, but further analysis showed that effects were most pronounced only for the sickest of the specimens, and even in those animals the results weren’t dramatic.
Probiotics are one of the strongest selling nutritional products in the world, with annual US sales exceeding $3.3 billion in 2016. That market size is predicted to more than double by 2025. Clearly a large chunk of the supplement-buying public has confidence in these products, and the marketing push is only intensifying. But this study, like others turning up similar findings, suggests caution is warranted.
“I think people should wait — that’s the best takeaway here,” said lead study author Daniel J. Reis, a doctoral student of clinical psychology at the University of Kansas. “We’re in the early days of this research into probiotics. I’ve seen a lot of stories hyping probiotics as helpful for anxiety. We’re not saying they do nothing, but we have a lot to figure out before we know if they can be used therapeutically.”
Why some effects were found in rodents and not in humans isn’t clear, but the researchers noted that the differences in dosage between humans and rodents were significant.
“If you control for the weights of animals versus humans, animals are getting much larger doses of probiotics in these experiments by one or two orders of magnitude. Sometimes the doses were hundreds of times higher than we see in human studies,” said Reis in a press statment.
The researchers also noted that while this study didn’t find anxiety-reducing benefits for humans, it’s still possible that a pathway exists for certain strains to yield therapeutic effects. And they were clear that the anxiety levels among the human participants in the reviewed studies weren’t necessarily “clinically elevated.” Future research has an opportunity to delve more deeply among that expanding population.
“We see a lot of pathways between our digestive systems and our brains,” Reis said. “We see nervous system connections, the inflammation response — these microorganisms seem to be able to influence the human brain through this gut-brain axis. We wanted to know if changes to the microbiota could improve mental health. But in terms of research, it’s all at a very preliminary stage.”
And that, for the moment, is the big takeaway on probiotics – the research is still very preliminary, despite marketing claims of conclusive results. Evidence supporting the claims just isn’t there, at least not yet.
Scientific research is nearing a consensus that bacteria in our digestive systems affect our brains. The microbiome in our guts, populated by billions of bacteria, appears to play a significant role not only in our digestive health, but also our mental health. Exactly how this happens is still being worked out, with each new study turning over another proverbial rock of possibilities. Despite these advances, we don’t yet know how, or if, probiotic supplements can improve our mental health by influencing gut bacteria. The marketing of these products is far ahead of the facts, as a quick review of what we know will show.
First, a brief sampling of the latest bacteria-brain research, which includes a study that found specific hormonal exchanges enabling communication between gut bacteria and the brain. This is especially noteworthy because the hormone in question is cortisol, the so-called “stress hormone”– a well-established indicator of stress levels in humans and other mammals. The study was conducted in pigs, which share several physiological similarities with humans, and it identified a possible communication pathway between gut bacteria and the brain that uses cortisol as a channel to send “messages.” The implications of this research will take some time to unravel, but one initial takeaway is that our stress-response system may play a key role in how gut bacteria communicate with the brain.
Another recent study suggests that gut bacteria may influence anxiety and depression. This study was conducted with mice raised in a sterile, germ-free environment devoid of bacterial influence. Researchers exposed these mice to gut bacteria and watched what happened compared to mice that were raised in a normal, germy environment. The germ-free mice exposed to bacteria developed anxiety and depression symptoms on par with the human equivalent. The researchers identified a specific brain region influenced by the bacteria, and suspect that our early-life exposure to bacteria may predispose us one way or another to anxiety and depression later on. Again, the conclusions are speculative, but the research is exciting because it moves us a little closer to figuring out what’s going on.
More studies like these are underway and another wave is in the planning phase. So why, with all of this research, can’t we make grand claims for the promise of probiotics? After all, if we have even an inkling that gut bacteria affect our brains (and we certainly have more than an inkling at this point) then why not jump onboard the probiotic supplement express?
The reasons can be boiled down to a few big ones.
The probiotic philosophy is to blast the gut with billions of allegedly “good” bacteria, in hopes of populating out the bad ones. While re-populating the gut with good bacteria sounds plausible, there’s little scientific clarity around which gut bacteria are objectively “good” or if that qualification is even valid. Bacteria can be “good” or “bad” depending on a slew of variables. Even less clear is which bacteria influence the brain and how they’re exerting their influence.
But let’s say we could achieve perfect clarity on that point, there’s still an enormous gastric obstacle ahead. Whether you’re ingesting a probiotic with one billion or 30 billion live bacterial cultures, they still have to survive your stomach acid to do anything worthwhile. Only a couple types of bacteria have proven resistant enough to survive that peril (lactobacillus and bifidobacteria), which means almost everything else in your pricey probiotic capsule is toast.
But let’s say that problem is solved by a fantastic pill coating – what will this army of bacteria do once they arrive in your gut? We simply don’t know enough to know for sure. Last year a review of probiotic trials in humans concluded that the research “demonstrates a lack of evidence for an impact of probiotics on fecal microbiota composition in healthy adults.” In other words, we don’t know precisely what probiotics are doing in the gut – and there’s at least a possibility that they aren’t doing much to make a difference.
Given how little we understand about what probiotics can accomplish in our guts, jumping to a further conclusion that they can improve our mental health is really reaching. That hasn’t stopped those marketing these products from making outlandish claims, but that’s standard operating procedure for a large chunk of supplement marketing.
Where actual science is concerned, we don’t yet know if probiotics can achieve the promises made for them, or what sort of probiotic formula will prove effective. We may eventually find out that probiotics need to be tailored to a given person’s microbiome like bespoke clothing. Once that’s established (if it can be established), then perhaps we’ll have a better opportunity to understand how probiotics might improve our mental health – assuming the underlying theory holds up over time.
Right now, we don’t know enough to justify the claims made for probiotic supplements. The marketing is leagues ahead of the evidence, and we’d do well to view these claims with skepticism. Perhaps one day probiotics will give our brains a boost, but we’re just not there yet.
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We rely on energy to get through the day, the week, the year. We know that losing out on sleep can leave us feeling drained, but sleep deprivation is only one of a long list of possible reasons behind feeling exhausted.
The following are some of the typical pitfalls which will cause chronic fatigue:
You don’t drink water. Even slight dehydration will cause a drop in energy level. This may be surprising, but dehydration actually makes your blood thicker, meaning your heart has to work harder to pump oxygen and nutrients to your muscles and organs, ultimately slowing you down.
You don’t eat breakfast. It’s not called the most important meal of the day for nothing! Skipping breakfast can often leave you feeling lifeless the rest of the day. We rely on breakfast to kickstart our metabolism after a goodnight’s sleep. The body continues to burn through food and nutrients even as we sleep, leaving our stores depleted by morning. A meal shortly after waking up is important to replenish these depleted energy stores and re-energize the body.
You have a drink to unwind. Many adults enjoy an alcoholic beverage after a long day of work, to help them unwind before bed. However alcohol can actually interrupt your sleep at night. Initially, the alcohol will depress the nervous system and produce a tranquilizing effect helping you to fall asleep. But as it breaks down while you sleep, it gives your body a surge of energy, likely to wake you up at night.
You stay up late on weekends. Altering your sleep cycle on the weekends can leave you feeling tired by the time Monday rolls around. It is unrealistic to expect people to stay in on the weekends to avoid a case of the “Mondays,” but trying to stay close to your regular bed time, or at least wake time, is essential for your body. Keeping your sleep patterns regular will keep you feeling fresh throughout the day.
You check your phone in bed. The light given off by your most prized electronics – phones, TVs and tablets – can actually throw off your sleep cycles. Your body typically follows the rule of if it’s bright it’s time to get up, if it’s dark it’s time for sleep. The glow from the modern tech devices that surround us can keep us awake for longer, and make it difficult for our bodies to wind down.
So you know what you are doing wrong, but what can you do to boost your energy levels throughout the day? The best way to keep energy up is to eat well. The general rule of thumb for high-energy foods is to eat those high in fiber, but low in glycemic index.
Glycemic index (GI) measures the variation in blood sugar levels according to foods consumed. Foods with carbohydrates that break down more slowly, releasing glucose more gradually into the bloodstream, tend to have a low GI. Consuming foods with high GI will cause a spike in blood sugar and energy, translating to a jolt of energy followed by a crash. This constant up and down will leave you exhausted. For this reason we look to foods with low GI to create a sustained level of energy.
Here are some foods that will give you that much-needed boost:
It is important to remember that energy not only refers to physical strength and alertness, but mental health as well. Whether the issue is committing yourself to too many social obligations, or always saying yes to a new project at work (even during your time off), it is important to take time for yourself. It is easy to overlook stress and anxiety as a cause of prolonged fatigue, but this can be both physically and emotionally taxing.
Getting outdoors, meditating, and regular exercise boosts strength, endurance, and energy. This movement not only delivers oxygen and nutrients to your tissues, but provides an influx of endorphins, boosting both your energy and mood!
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Despite the spread of nearsightedness among U.S. schoolchildren, nearly 1 in 3 has not had a vision screening in at least two years, according to a new Education Week Research Center analysis of federal data, and research suggests several ways schools may help reduce children’s risk of bad eyesight.
Myopia, or nearsightedness, means that a person has good vision for close objects but difficulty seeing things farther away. The problem, caused when the eyeball grows too long from back to front, can in more severe cases mean that a student cannot see clearly even a foot in front of her face.
In 2017, the National Eye Institute, part of the National Institutes of Health, reported that nearly 42 percent of Americans are nearsighted, compared with only 25 percent in the 1970s. About 4 percent have severe, or “high” myopia, which can lead to blindness.
The problem is just as bad or worse in some other industrialized countries. Australia and Great Britain have seen similar increases in myopia. In China, India, and throughout industrialized Asia, the National Eye Institute reported that 80 percent to 90 percent of all high school graduates are nearsighted, and 20 percent have high myopia.
“The rate of children needing glasses is so much greater than I ever imagined,” said Carolyn Amberry, who is in her 17th year as a school nurse at Long Beach Unified schools in California. At Lincoln Elementary, one high-poverty school where Amberry worked, “I couldn’t believe at a school of 1,200 kids, I had more than 300 needing glasses.”
Natural Light Helps
Nearsightedness does run in families, but the spread of the vision problems has raised concerns among educators and researchers. Studies have pointed to both the rise of computer and mobile use and the reduction of recess in schools as potentially contributing to the problem.
“With technology nowadays, [students’] faces are always in a screen,” said Leila Bajarin, who coordinates vision screenings for students at Kalihi Waena Elementary in Hawaii. “I think that makes [eyesight] deteriorate a lot quicker at a young age.”
She’s not wrong, research says, but longitudinal studies suggest that reading and studying either on computers or in print—so-called “near work”—do not fully explain the rapidly rising rates of nearsightedness.
“There’s no question that the [electronic] devices and students starting to use them so early contributes to the earlier onset of myopia we’re seeing,” said optometrist Amanda Hikin, “but a lot of the kids we are seeing are [in poverty] and may not have as much access to some of those things. But still we see quite a lot of myopia and astigmatism.”
Instead, researchers including Donald Mutti, an optometry professor at Ohio State University in Columbus, have found what children do inside is less important a predictor of myopia than the time children spend outside. Young children’s eyes grow quickly in infancy and toddlerhood, but that growth slows during the school years. If instead, the eye continues to lengthen at its early pace, light coming through the lens will not focus correctly, creating myopia. Mutti and other researchers have suggested exposure to natural light in the elementary years helps to trigger the slower pace of growth—so being outside less during and after school also may boost the risk of nearsightedness.
Spotting Vision Problems
The American Association for Pediatric Ophthalmology and Strabismus recommends children have their vision checked at least every other year after age 5, but states differ widely in whether and how often students are screened. In Connecticut and New Jersey, for example, just over 23 percent of children younger than 18 have not had a vision check in the past two years; in Idaho and Nevada, that share is more than 40 percent, according to the research center analysis of data from the National Survey of Children’s Health, an ongoing federal study of children in more than 364,000 households across the country. Children in poverty also were more likely than their wealthier peers to go two years or more without screening, the analysis showed.
At Kalihi Waena Elementary, Bajarin recalled one child, who was among the more than 32 percent of schoolchildren in Hawaii who hadn’t had their eyes tested in two years. The 5th grader’s teachers noticed she had trouble seeing two years ago—”She was moved up [in the classroom], but even at the front of the class, there is information up on all walls” that she couldn’t see, Bajarin said—but for two years, her father argued he didn’t have time to take his daughter for an eye exam. “Thankfully, we convinced him before she aged out of our school.”
The 5th grader ultimately got an exam and free glasses during a screening event by Vision to Learn, a nonprofit that works with schools in 12 states to identify and correct vision problems among students in poverty. In the group’s first screening of about 200 of Kalihi Waena’s 480 P-5 students, 75 students needed glasses, including several older elementary students.
“It helped a lot, behaviorally, in the classroom with a lot of the kids,” said Bajarin, the school’s parent-community networking coordinator. “Some of [the students], they won’t speak up, because they don’t know that they have an actual vision problem. When they can see better, they don’t feel so insecure and that they have to act up, … and getting glasses, it was something for them that boosted their confidence because they could take ownership of it.”
Nationwide, 70 percent of the children for whom Vision to Learn provides glasses had never had their vision corrected before, and another 20 percent have outdated prescriptions, according to Damian Carroll, the group’s national director.
“When the children finally get to the eye exam and are told they needed glasses, it is often just such a shock,” Carroll said. “The kid doesn’t realize there’s a problem because it’s the way the world has always looked, and it’s just not something parents first think of when the child is struggling in school.”
Long Beach’s Amberry agreed; on her own, she said, she was only able to get follow-up exams and glasses for 50 percent to 70 percent of students who failed their initial vision screenings before the school began working with nonprofits to provide on-campus exams and fittings.
Hikin, the optometrist, said Vision to Learn and other groups that work with schools also increasingly are moving away from testing vision using the traditional letter-and-shape eye charts (which were the focus of the national survey), and toward using auto-refractors, handheld machines that gauge vision by measuring how light changes as it enters a person’s eye. That sort of testing can be done on less verbal and younger children.
Mary Beth Thurston, a school nurse at Long Beach Unified, said her district also works with the local Lion’s Club to get 3- and 4-year-olds in its preschool programs tested for glasses. Last year, she said about eight out of the 200 students tested ended up needing new glasses. Next year, the district will try to pair students’ medical physicals and vision screenings, to encourage more families to get their children tested.
Screening and getting glasses to students, while important, is only a start, Amberry said. Lincoln Elementary in Long Beach made a photo gallery of students wearing their glasses to boost their confidence and held popsicle parties for those who wore their glasses regularly, both to encourage students to wear them and to report quickly if they were lost or broken. Reading teachers also began referring struggling students for vision screenings earlier, at the same time they tried academic interventions.
Other studies suggest getting children outside more can lower their risk of developing vision problems. Mutti of OSU found that for children of nearsighted parents, about 20 percent of those who spent at least 14 hours a week outside developed nearsightedness, compared to 60 percent of children with the same genetic risk who spent less time outdoors. Similarly, large randomized-controlled studies in Australia and China found primary schoolchildren who got more than 40 minutes a day of outdoor activities were more than 20 percent less likely to develop nearsightedness. But getting outside more did not necessarily slow the progression of myopia in students who had already developed deteriorating vision.
In a separate 2017 study in China, a team of researchers from that country as well as from Australia, the United Kingdom, and the United States tested a so-called “bright classroom,” built with wall-sized clear and light-diffusing glass and intended to provide more access to natural light while reducing glare or distractions from outside the classroom. The study found over the course of a year, light from the blue-green part of the spectrum—which has been associated with lower risk of nearsightedness—was significantly higher in the prototype classroom than traditional classrooms, and a group of 230 students and teachers testing the room reported it was more comfortable for reading than a typical classroom.
However, the yearlong pilot was too short to tell whether students who used the bright classroom actually became less likely to develop myopia than those in regular classrooms.
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Stephen has been married twice. Two wedding days. Two “I do”s. Yet Stephen has no happy memories from either – or, in fact, from the marriages or any of his relationships.
He met his first wife on a pre-nursing course when he was just 16. Six years later, they were married. Three years after that, they got divorced; she was never really the right one for him, he says.
Almost two decades on, in 2009, he met his second wife through a dating site. He threw himself into the relationship and, the following year, with his father and her two adult siblings present, they married at the registrar’s office in Sheffield, where they both live.
He put on smiles for the wedding photos because he recognized that they were expected but, as he explains: “From an inner feeling point of view, anything I do that requires an emotional response feels like a fake.
“Most of my responses are learned responses. In an environment where everyone is being jolly and happy, it feels like I’m lying. Acting. Which I am. So it is a lie.”
Happiness isn’t the only emotion that Stephen struggles with. Excitement, shame, disgust, anticipation, even love… he doesn’t feel these, either. “I feel something but I’m unable to distinguish in any real way what that feeling is.” The only emotions he is familiar with are fear and anger.
Such profound problems with emotion are sometimes associated with autism, which Stephen does not have, or with psychopathy, which he doesn’t have, either.
Last year, at the age of 51, he finally learned what he does have: a little-known condition called alexithymia, a word made from Greek parts meaning, roughly, “no words for emotion”.
Despite the name, the real problem for people with alexithymia isn’t so much that they have no words for their emotions, but that they lack the emotions themselves. Still, not everyone with the condition has the same experiences. Some have gaps and distortions in the typical emotional repertoire.
Some realise they’re feeling an emotion, but don’t know which, while others confuse signs of certain emotions for something else – perhaps interpreting butterflies in the stomach as hunger pangs.
Surprisingly, given how generally unrecognised it is, studies show that about one in 10 people fall on the alexithymia spectrum. New research is now revealing what’s going wrong – and this work holds the promise not only of novel treatments for disorders of emotion, but of revealing just how the rest of us feel anything at all.
After working as a nurse for 10 years, Stephen decided he wanted to do something different. A two-year Access to University course led to a degree in astronomy and physics, and then to a job testing computer games.
He built a successful career for himself, working for various companies in their computer testing departments, managing teams, and travelling around the world to speak at conferences. He had no problem conveying facts to colleagues.
It was in the context of more personal relationships – or any other scenario that would typically involve expressions of emotion – that he felt things were “wrong”.
“At the beginning of a relationship, I’m totally into who that person is,” he explains. “I’ve been told I’m very good at maintaining a honeymoon period for ‘longer than expected’. But after a year it takes a massive turn. It all falls apart. I’ve put myself on a pedestal to be this person which I’m really not. I react mostly cognitively, rather than it being emotions making me react. Obviously, that is not valid. It’s not real. It seems fake. Because it is fake. And you can only pretend for so long.”
He and his current wife stopped living together in 2012. He saw a GP and was prescribed antidepressants. Though he was still in contact with his wife, it was clear that the relationship was no longer working. In June 2015, he attempted suicide.
“I had actually been posting on Facebook and Twitter regarding killing myself and someone – I’ve never found out who – contacted the police. I was taken to hospital and treated.”
A psychiatrist referred Stephen for a series of counselling sessions and then a course of psychodynamic psychotherapy, a type of Freudian-based therapy that, in trying to uncover unconscious drivers of thoughts and behaviour, is similar to psychoanalysis.
It was in a book called Why Love Matters by Sue Gerhardt, which his therapist recommended, that he first came across the concept of alexithymia.
“I brought it up in therapy, and that’s when we started talking about how I was very alexithymic. Obviously, I’ve got a vocabulary. I’ve got words for emotions. But whether they’re the right words for the right emotion is a different point altogether… I just thought that I wasn’t good at talking about how I feel and emotions and stuff like that. But after a year of therapy, it became apparent that when I talk about emotions I don’t actually know what I’m talking about.”
The term “alexithymic” dates from a book published in 1972 and has its origins in Freudian psychodynamic literature.
Freudian ideas are now out of favour with most academic psychologists, as Geoff Bird, a professor of psychology at the University of Oxford explains. “Not to disrespect those traditions, but in the cognitive, neuro, experimental field, not so many people are really very interested in anything associated with Freud any more.”
But when Bird read about alexithymia, he found the descriptions intriguing. “Actually, it’s really quite amazing.” For most people, “at a low level of emotion, you might be a bit unsure about exactly what you’re feeling, but if you have a strong emotion, you know what it is”. And yet somehow, here were people who simply did not know.
Bird started his academic career studying autism spectrum disorder, empathy and emotional awareness, which led to his interest in alexithymia.
In one of his first studies in this field, he linked alexithymia, as measured with a 20-item checklist developed at the University of Toronto, with a lack of empathy. If you can’t feel your own emotions in the typical way, it makes sense that you can’t identify with those of others, either.
But what really drew Bird into alexithymia research were his interactions with people with autism. “There has been this perception that people with autism don’t have empathy. And that’s rubbish. And you can see that immediately as soon as you meet some autistic people.”
In a series of studies, Bird has found that about half of people with autism have alexithymia – it’s these people who struggle with emotion and empathy, while the rest do not. In other words, emotion-related difficulties are intrinsic to the alexithymia, not to the autism.
Bird is passionate about spreading this message. He talks with feeling about one particular autistic study volunteer who did not have alexithymia: “A lovely guy with an IQ we couldn’t measure, it’s that good. He couldn’t hold down a job. But he volunteered to work at a care home because he wanted to do something productive with his time.
“They said, ‘Oh because you’ve got a diagnosis of autism you can’t do empathy, therefore you can’t look after our elderly people.’ Which is just ridiculous.”
Bird has since run a series of studies exploring alexithymia outside the context of autism. He has found, for example, that people with the condition have no trouble recognising faces, or distinguishing pictures of people smiling and frowning.
“But for a few of our really alexithymic people, while they can tell a smile and a frown apart, they have no idea what they are. That is really quite strange.”
Many of the people with the condition who Bird has met talk about being told by other people that they’re different, though some do recognise it in themselves early on.
“I guess it’s a bit like not being able to see colour, and everybody’s always banging on about how red this is or how blue, and you come to realise there’s an aspect of human experience that you’re just not participating in.”
As well as better characterising alexithymia, Bird and his colleagues have also dug into what explains it, taking what could seem to be a circular argument – Stephen has problems with emotion because he has alexithymia, which is characterised by problems with emotion – and blowing it right apart.
In situations that Stephen recognises as being in theory highly emotional – like telling someone “I love you” – he experiences changes inside his body. “I feel my heart race and this rush of adrenaline, but to me that feeling is always scary. I don’t know how to react. It makes me want to either run away or react verbally aggressively.”
Fear and anger – and confusion – he understands. “Everything else just feels all the same… it’s this feeling of, ‘Errrr, I’m not quite comfortable with this – it’s not quite right’.”
For Rebecca Brewer, a former student of Bird’s and now a lecturer at Royal Holloway, University of London, this makes sense. “With alexithymia, people often know that they are experiencing an emotion but don’t know which emotion it is,” she explains. “This means they could still experience depression, possibly because they struggle to differentiate between different negative emotions, and struggle to identify [positive] emotions.
“Similarly with anxiety, it might be that someone experiences an emotional response associated with a fast heartbeat – which might be excitement – but they don’t know how to interpret that, and they could panic about what’s happening in their body.”
The ability to detect changes inside the body – everything from a racing heart to a diversion of blood flow, from a full bladder to a distension of the lungs – is known as interoception. It’s your perception of your own internal state.
Different emotions are associated with different physical changes. In anger, for example, the heart rate rises, blood rushes to the face, and fists clench. In fear, the heart rate also rises but blood drains from the face.
It’s generally thought that these changes are not entirely specific to individual emotions, and so context is also important: if you feel your heart racing and you’re looking at a spider, you know it’s fear that you’re feeling, not sexual arousal.
What Bird, Brewer and others have found in people with alexithymia is a reduced ability, sometimes a complete inability, to produce, detect or interpret these internal bodily changes. People with the condition have normal-range IQs.
They can understand as well as anyone else that they’re seeing a spider, rather than an attractive potential partner. But either their brains aren’t triggering the physical changes that it seems are needed for the experience of an emotion, or other regions of their brains aren’t reading these signals properly.
In 2016, Bird and Brewer, along with Richard Cook at City University in London, published a research paper that characterised alexithymia as a “generalised deficit of interoception”.
Here, then, was an explanation for these people’s problems with emotion – but also, in effect, a manifesto stating that the perception of a range of bodily signals is important for the experience of emotion in the rest of us.
It’s an idea that we already express in everyday language: in English, for an apology to mean anything, it has to be “heartfelt”. If you truly love someone, it’s with “all your heart”.
When you’re really angry, your “blood boils”. Instead of saying that you’re anxious, you might talk about having “butterflies in your stomach” (thought to be caused by a diversion of blood flow away from the digestive system).
While most people may not be familiar with alexithymia, there is a different disorder involving flat emotions and poor empathy that seems to fascinate us, even more than it repels us: psychopathy. Can we learn more about how we feel by understanding psychopaths?
Lieke Nentjes is in her early thirties. She’s slender and softly spoken; it’s hard to picture her spending countless hours in small rooms with incarcerated, unshackled psychopaths, including serially violent men who have committed murder.
As Nentjes talks, though, she reveals her confidence. “One time, there was this pretty big fella with wild, long hair sat across from me, and he suddenly said [raising her voice and half getting up from her chair]: ‘Aren’t you afraid of me?’ I was surprised. I didn’t see that coming. And I went: ‘Why – are you afraid of me?’ And he sat back down.
“Then he explained that he was at the end of his therapy and was ‘resocialising’ and no one would hire him because they were intimidated by him. He wasn’t really angry. He was frustrated.”
While the nature of psychopathy is still debated, psychologists generally agree that it entails, among other things, a lack of empathy or guilt, shallow emotions, and antisocial behaviour – treating other people badly and, in some cases, engaging in criminal acts.
It has certainly been suggested that the reason some psychopaths are able to torture or murder people is that they don’t process emotions properly – they don’t feel fear, for example, and they don’t recognise it in others.
Nentjes is based at the University of Amsterdam. Here in the Netherlands, if a criminal is found to have a psychological condition that relates to the crime, he or she is deemed to be only partially responsible.
Such criminals might spend a few years in a regular jail before being sent to a secure treatment centre, or they may be sent straight for treatment.
Nentjes decided to assess a range of criminals from these centres and from jails to find out just how psychopathic they were (with particular attention to different aspects of psychopathy), to learn about their lives – their upbringing, and their criminal behaviour – and also to measure their interoceptive ability.
“Emotion is very central when you look at psychopathy – or rather, lack of emotion,” she says. So could it be that psychopathic offenders just aren’t very in touch with their bodies?
In the course of the interviews, Nentjes asked questions to probe their levels of empathy, and how much remorse they felt about what they had done to their victims. “Some were just completely honest, and would say, ‘I don’t care,’” she says.
“Others who were psychopathic would say, ‘Oh, but I’m very empathic.’ They had learned the lingo to describe feelings very accurately and they could talk about compassionate, empathic feelings towards others – but then when you look at the crimes they have committed…” Her sentence trails off.
“There is research finding that psychopathic offenders can describe emotions in terms of words, but they lack the inner experience of the emotion,” she adds.
Since assessing a person’s ability to detect a range of bodily signals is tricky, the most commonly used measures of interoceptive sensitivity are based on judgements of heart rate. One test involves asking participants to count their heartbeats over varying periods – 25 or 50 seconds, perhaps – multiple times.
About 10 per cent of us are good at counting heartbeats, 5 to 10 per cent are very bad, and the rest fall somewhere in between.
In another test, volunteers are played a series of beeps that are either in sync or out of sync with their heartbeat, and asked which it is. On this type of task, about 10 per cent of the general population can do it really well, and 80 per cent can’t do it at all.
Nentjes brought the necessary equipment for the heartbeat synch task with her into the interview rooms, and took measures for 75 offenders. She found a clear link: the higher an offender’s score on the antisocial aspect of psychopathy, the poorer their performance on the heart-rate task.
This does at least suggest that psychopaths who are poorer at detecting bodily signals feel less emotion and therefore less empathy for others.
Psychopathic criminals are sometimes divided into the “white-collar” type, who tend to commit non-violent crimes such as fraud, and the violent type. In her interviews with this violent group, Nentjes was struck by one similarity, in particular, compared with the white-collar group.
“That was their upbringing. Or rather lack of it. Emotional abuse. Sexual abuse. Neglect. A lot of physical abuse. I’ve heard people literally say that emotion is not of use to them. All they felt during their upbringing was fear.”
As a child, Stephen suffered extreme emotional neglect. When he was six, his mother intentionally set fire to their home in Nottingham while she, Stephen, his younger brother and even younger sister were all inside. Fortunately, the children’s father, who had left for work, realised that he’d forgotten his packed lunch and came home.
Looking back, Stephen says it’s clear that his mother was suffering from post-natal depression. But she received no treatment, “and all I knew was anxiety and being worried”. After the fire, his mother went to prison. His father was a steelworker, who worked all kinds of shifts.
“A neighbour contacted social services and Dad was told to sort it out or they’d take us away. None of my dad’s brothers or sisters wanted me or my brother because we were little shits. We were always in trouble. Robbing shops. All kinds of stuff. So we went into care.”
For the rest of his childhood, Stephen was in and out of care homes. The only emotions he remembers feeling, even then, are fear, anger and confusion. “Christmas, birthdays, people out of the blue at care homes being nice to me… I never really got used to it. I always felt uncomfortable. There’s just a mess of feelings inside me that I don’t interpret properly, or respond to properly.”
Alexithymia is often associated with trauma and neglect from a young age, explains Geoff Bird. Twin studies have suggested a genetic component, too. And it’s also linked to certain types of brain damage, particularly to the insula, the region that receives interoceptive signals.
As Rebecca Brewer notes, the kind of anxiety that Stephen experiences is common in people with poor interoception. At the University of Sussex, Hugo Critchley and Sarah Garfinkel, who have expertise in psychiatry and neuroscience, are looking at ways to alter interoception, to bring anxiety down.
Garfinkel has put forward a three-dimensional model of interoception that has been well received by others in the field. First, objective accuracy at perceiving interoceptive signals – how good you are at counting heartbeats, for example.
Second, subjective report – how good you think you are. And third, metacognitive accuracy – how good you are at knowing how good you actually are.
The third dimension is important because various studies have found that the gap between how good someone thinks they are at counting heartbeats, for example, and how good they actually are predicts their levels of anxiety.
Lisa Quadt, a research fellow with the Sussex group, is now running a clinical trial with the aim of testing whether reducing this gap for people with autism can reduce their anxiety.
In a pilot study, Critchley, Garfinkel and MSc student Abigail McLanachan recruited a group of students who came into the lab for six training sessions. In each session, they first did the heartbeat-counting task.
The volunteer sat at rest, with a loose rubber pulse oximeter on their forefingers, and reported how many beats they’d counted. Then McLanachan told them how they’d done so that they got a better sense of how accurate they were.
McLanachan then got them to do a few minutes of jumping jacks or walking fast up the steep hill outside the building – whatever was necessary to raise their heart rate, to make it easier to detect. (“Because some people really can’t feel their heartbeat at all. I can’t,” Quadt explains.)
Then they went back into the lab, did the tasks again and, as before, were given feedback each time.
This was just a pilot study on a general student population. But after three weeks, not only had the students’ accuracy improved on all three dimensions of interoception, but they also reported reductions in anxiety of around 10 per cent.
For the main trial, volunteers diagnosed with autism spectrum disorder will complete the same tasks as in the pilot, but once at the start and once at the end they’ll do them inside an MRI scanner.
This will allow the team to monitor activity in the insula, which receives heart-rate data, and look at how changes in that activity may correspond to connections between the amygdala, which detects threats, and the prefrontal cortex, which can work out whether a potential threat really is or is not dangerous and so whether anxiety is warranted.
The hope, Critchley explains, is to see improved connectivity between these two regions, which previous studies have linked to reduced anxiety.
In Oxford, meanwhile, Geoff Bird wants to look at the idea that there are two different types of alexithymia. People with one type don’t produce enough of the bodily signals necessary for the experience of an emotion, so would be unlikely to benefit from the Sussex group’s kind of training.
People with the other type produce all kinds of bodily sensations but their brains don’t process these signals in the typical way. This second group, which includes Stephen, might benefit more.
Bird stresses that, although people with alexithymia struggle to understand emotion, that doesn’t mean they don’t care about other people. “For the most part, individuals with alexithymia can recognise that others are in a negative state, and this makes them distressed.
“The problem is that they can’t work out what the other person is feeling, and what they are feeling, and therefore how to make the other person feel better or how to reduce their own distress. I think that’s important because alexithymia is different from psychopathy in that respect.”
Stephen says that for him, this is certainly true. And in theory, an emotional training technique is something he would welcome. “I’ve got several books about emotions and feelings and they don’t make a jot of difference because they’re not talking specifically enough about what you actually feel within your body is which emotion.”
For now, given the absence of available treatments for alexithymia, Stephen plans to use his newfound understanding of himself, gained through therapy, to try to move forwards. At first, he says, he hoped that therapy would fix everything.
“I thought every day would be perfect, brilliant… and I’ve come to realise that’s not going to happen. I’m always going to have problems, always going to have issues.”
He’s learned valuable lessons, he says. Though he and his wife are still separated, they talk regularly and now he tries not to reject her views on his anxiety. “Rather than go, ‘No,’ I will listen. I think, ‘Well, you know what emotions are about and I don’t, so I’m going to listen to you and I’ll either take it on board or I’ll find a way to deal with it’.”
He’s also thinking about moving to work with people who are struggling with substance abuse, because he’d like to be back in a career where he can help people.
Most of all, he’s determined to use his diagnosis of alexithymia. “For me, it empowers me – now I know about it, I can read about it. I can find out more about it. And I can develop certain tools that enable me to combat it.”
People without alexithymia could probably use such tools as well. Bird has led work showing that people who are more aware of their own heartbeat are better able to recognise others’ emotions, a crucial first step in being empathetic.
He’s planning studies to investigate whether heartbeat training might therefore increase empathy.
Those who want to reduce feelings of stress and anxiety in daily life, but who either can’t or don’t want to change the sources of stress, could focus on changing the signals coming from their bodies instead.
Regular physical exercise should dampen down the kinds of bodily signals (from the heart and circulation, for example) that the brain could interpret as being anxious – so it should dampen down feelings of anxiety, too.
Knowing that signals from our bodies underpin our emotions could be empowering for all of us. Now, how does that make you feel?
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In the morning of June 24, 2014, a Tuesday, Vanessa Johnson Brandon awoke early in her small brick house in North Baltimore and felt really sick. At first, she thought she had food poisoning, but after hours of stomach pain, vomiting and diarrhea, she called her daughter, Keara Grade, who was at work. “I feel like I’m losing it,” said the woman everyone called Miss Vanessa. Keara begged her to call an ambulance, but her mother wanted to wait until her husband, Marlon, got home so he could drive her to the emergency room. Doctors there took a CT scan, which revealed a large mass in her colon.
Hearing about the mass terrified her. Her own mother had died of breast cancer at the age of 56. From that point on, Miss Vanessa, then 40, became the matriarch of a large family that included her seven younger siblings and their children. Because she knew how it felt to have a loved one with cancer, she joined a church ministry of volunteers who helped cancer patients with chores and doctor visits. As she prepared meals for cancer patients too weak to cook for themselves, she couldn’t know that the disease would one day come for her, too.
The ER doctors told Miss Vanessa she wouldn’t get the results of follow-up tests—a colonoscopy and a biopsy—until after the July 4 weekend. She had to smile her way through her own 60th birthday on July 6, stoking herself up on medications for nausea and pain to get through the day.
At 9:30 the next morning, a doctor from the Greater Baltimore Medical Center called. He didn’t say, “Are you sitting down?” He didn’t say, “Is there someone there with you?” Later Miss Vanessa told the doctor, who was on the young side, that when he delivers gut-wrenching news by telephone, he should try to use a little more grace.
It was cancer, just as Miss Vanessa had feared. It was in her colon, and there also was something going on in her stomach. The plan was to operate immediately, and then knock out whatever cancer still remained with chemotherapy drugs.
Thus began two years of hell for Miss Vanessa and her two children—Keara, who is now 45, and Stanley Grade, 37—who live nearby and were in constant contact with their mother and her husband. The surgery took five hours. Recovery was slow, leading to more scans and blood work that showed the cancer had already spread to the liver. Her doctors decided to start Miss Vanessa on as potent a brew of chemotherapy as they could muster.
Every two weeks, Miss Vanessa underwent three straight days of grueling chemo, administered intravenously at her home. Keara and her two teenage sons came around often to help out, but the older boy would only wave at Miss Vanessa from the doorway of her bedroom as he rushed off to another part of the house. He just couldn’t bear to see his grandmother so sick.
Miss Vanessa powered on for 11 months, visualizing getting better but never really feeling better. Then, in July 2015, the doctor told her there was nothing more he could do for her.
“My mom was devastated,” Keara says. Keara told her mother not to listen to the doctor’s dire prediction. “I said to her, ‘The devil was a liar—we are not going to let this happen.’”
So Keara—along with Miss Vanessa’s husband, brother and brother’s fiancée—started Googling like mad. Soon they found another medical center that could offer treatment. But it was in Illinois, in the town of Zion—a name Miss Vanessa took as a good omen, since it was also the name of her 5-year-old grandson. In fact, just a few days earlier little Zion had asked his grandmother if she believed in miracles.
Based entirely on interviews with the investigators, this book is the story of the immuno-oncology pioneers. It’s a story of failure, resurrection, and success. It’s a story about science, it’s a story about discovery, and intuition, and cunning. It’s a peek into the lives and thoughts of some of the most gifted medical scientists on the planet.
The family held a fund-raiser for Stanley to get on a plane to Chicago with his mother every two weeks, drive her to Zion and stay with her at the local Country Inn & Suites hotel for three days of outpatient chemotherapy. It felt like a replay of her treatment in Baltimore—worse, since the drugs were delivered in a hotel instead of in her bedroom, and the chemotherapy caused nerve damage that led to pain, tingling and numbness in Miss Vanessa’s arms and legs.
And then, in May 2016, the Illinois doctor, too, said there was nothing more he could do for her. But at least he offered a sliver of hope: “Go get yourself on a clinical trial.” Weeks later, desperate, Miss Vanessa and Keara grew hopeful about a treatment involving mistletoe. They attended an information session at a Ramada extolling the plant extract’s anti-cancer properties. But when they learned that it would cost $5,000 to enroll, they walked out dejected.
Finally, Miss Vanessa’s husband stumbled onto a website for a clinical trial that seemed legit, something underway at the Johns Hopkins Bloomberg-Kimmel Institute for Cancer Immunotherapy, just down the road from their home. This new treatment option involved immunotherapy, something markedly different from anything she had gone through. Rather than poisoning a tumor with chemotherapy or zapping it with radiation, immunotherapy kills cancer from within, recruiting the body’s own natural defense system to do the job. There are a number of different approaches, including personalized vaccines and specially engineered cells grown in a lab. (See “A Cancer Vaccine?” and “A DNA-Based Attack”)
The trial at Hopkins involved a type of immunotherapy known as a checkpoint inhibitor, which unlocks the power of the immune system’s best weapon: the T-cell. By the time Miss Vanessa made the call, other studies had already proved the value of checkpoint inhibitors, and the Food and Drug Administration had approved four of them for use in several cancers. The Hopkins researchers were looking at a new way of using one of those drugs, which didn’t work at all for most patients but worked spectacularly well for some. Their study was designed to confirm earlier findings that had seemed almost too good to be true.
“With the very first patient who responded to this drug, it’s been amazing,” says Dung Le, a straight-talking Hopkins oncologist with long dark hair and a buoyant energy. Most of her research had been in desperately ill patients; she wasn’t used to seeing her experimental treatments do much good. “When you see multiple responses, you get super-excited.”
Immunotherapy is poised to become the standard of care for a variety of cancers. The work being done now is forcing a reconsideration of basic tenets of clinical oncology—for instance, whether surgery should be a first line of treatment or should come after drugs like Keytruda.
Many questions still remain. Elizabeth Jaffee, a member of the “cancer moonshot” panel convened by then-Vice President Joseph Biden in 2016, says she’s conscious of the danger of overselling a treatment. While the effect of checkpoint inhibitors can be “exciting,” she says, “you have to put it in perspective. A response doesn’t mean they’re cured. Some may have a year of response,” but the cancer might start growing again.
When Miss Vanessa paid her first visit to Le in August 2016, the physician explained that not every patient with advanced colon cancer qualified for the trial. Investigators were looking for people with a certain genetic profile that they thought would benefit the most. It was a long shot—only about one person in eight would fit the bill. If she had the right DNA, she could join the trial. If she didn’t, she would have to look elsewhere.
About a week later, Miss Vanessa was in her kitchen, a cheery room lined with bright yellow cabinets, when her telephone rang. Caller ID indicated a Hopkins number. “I didn’t want anyone else to call you but me,” said the study’s principal investigator, Daniel Laheru. He had good news: her genes “matched up perfectly” with the criteria for the clinical trial. He told her to come in right away so they could get the blood work done, the paperwork signed and the treatment started. Miss Vanessa recalls, “I cried so hard I saw stars.”
The trial was part of a string of promising developments in immunotherapy—an apparent overnight success that was actually more than 100 years in the making. Back in the 1890s, a New York City surgeon named William Coley made a startling observation. He was searching medical records for something that would help him understand sarcoma, a bone cancer that had recently killed a young patient of his, and came upon the case of a house painter with a sarcoma in his neck that kept reappearing despite multiple surgeries to remove it. After the fourth unsuccessful operation, the house painter developed a severe streptococcus infection that doctors thought would kill him for sure. Not only did he survive the infection, but when he recovered, the sarcoma had virtually disappeared.
Coley dug deeper and found a few other cases of remission from cancer after a streptococcus infection. He concluded—incorrectly, it turned out—that the infection had killed the tumor. He went around promoting this idea, giving about 1,000 cancer patients streptococcus infections that made them seriously ill but from which, if they recovered, they sometimes emerged cancer-free. He eventually developed an elixir, Coley’s Toxins, which was widely used in the early 20th century but soon fell out of favor as radiation and then chemotherapy began to have some success in treating cancer.
Then, in the 1970s, scientists looked back at Coley’s research and realized it wasn’t an infection that had killed the house painter’s tumor; it was the immune system itself, stimulated by the bacterial infection.
In a healthy body, T-cells activate their weaponry whenever the immune system detects something different or foreign. This might be a virus, a bacterium, another kind of disease-causing agent, a transplanted organ—or even a stray cancer cell. The body continuously generates mutated cells, some of which have the potential to turn cancerous, but current thinking is that the immune system destroys them before they can take hold.
Once scientists recognized the cancer-fighting potential of the immune system, they began to look for ways to kick it into gear, hoping for a treatment that was less pernicious than chemotherapy, which often uses poisons so toxic the cure may be worse than the disease. This immune-based approach looked good on paper and in lab animals, and showed flashes of promise in people. For instance, Steven Rosenberg and his colleagues at the National Institutes of Health’s National Cancer Institute made headlines when they removed a patient’s white blood cells, activated them in the lab with the immune system component known as interleukin-2, and infused the cancer-fighting cells back into the patient in hopes of stimulating the body to make a better supply of cancer-fighting cells. Rosenberg ended up on the cover of Newsweek, where he was hailed for being on the cusp of a cancer cure. That was in 1985.
The FDA did approve interleukin-2 for adults with metastatic melanoma and kidney cancer. But immunotherapy remained mostly on the fringes for decades, as patients continued to go through rounds of chemotherapy and radiation. “We’ve been curing cancer in mice for many, many years . . . but the promise was unfulfilled for a very long time in people,” says Jonathan Powell, associate director of the Bloomberg-Kimmel Institute at Hopkins.
Meanwhile, Topalian is continuing to work with Hopkins experts in genetics, metabolism, bioengineering and other areas. One of her colleagues, Cynthia Sears, recently received a grant to study biofilms—the colonies of bacteria that grow in the colon and can either promote or prevent cancer growth. Sears is looking at how a particular “tumor microbial environment” affects the way a patient responds—or fails to respond—to cancer immunotherapy.
“The immune system is the most specific and powerful killing system in the world,” says Pardoll, summing up the state of immunotherapy in early 2018. “T-cells have an amazingly huge diversity, and 15 different ways to kill a cell. The basic properties of the immune system make it the perfect anti-cancer lever.” But science won’t be able to fully mobilize that system without the help of myriad specialists, all working from different angles to piece together the incredibly complex puzzle of human immunity.
Indeed, many cancer experts lost faith in the approach over the next decade. “Nobody believed in immunotherapy except our own community,” says Drew Pardoll, the director of the BKI. The lack of support was frustrating, but Pardoll says it did have one salutary effect: It made immunotherapy more collegial and less back-biting than a lot of other fields of science. “When you’re a little bit ostracized I think it’s just a natural part of human nature…to sort of say, ‘Well, look, our field is going to be dead if we don’t work together, and it shouldn’t be about individuals,’” Pardoll said. He calls the recent explosion of successes “sort of like Revenge of the Nerds.”
In keeping with this collaborative spirit, immunotherapy researchers from six competing institutions have formed a cover band known as the CheckPoints, which performs at the annual meeting of the American Society of Clinical Oncology and in other venues. The band’s harmonica player, James Allison of the M.D. Anderson Cancer Center in Houston, helped set immunotherapy on its current course with his work on checkpoint inhibitors in 1996, when he was at Berkeley. He was the first to prove that blocking the checkpoint CTLA-4 (shorthand for “cytotoxic T-lymphocyte antigen”) with an antibody would generate an anti-tumor response. As Pardoll puts it, once Allison demonstrated that first checkpoint system, “we had molecular targets. Before that, it was a black box.”
The checkpoint system, when it’s working as it should, is a simple one: invader is detected, T-cells proliferate. Invader is destroyed, T-cells are deactivated. If T-cells were to stay active without an invader or a rogue cell to fight, they could create collateral damage to the body’s own tissues. So the immune system contains a braking mechanism. Receptors on the surface of the T-cells look for binding partners on the surfaces of other cells, indicating that those cells are healthy. When these receptors find the proteins they’re looking for, they shut the T-cells down until they spot a new invader.
Cancer cells are able to do their damage partly because they co-opt these checkpoints—in effect, hacking the immune system by activating the brakes. This renders the T-cells impotent, allowing the cancer cells to grow unimpeded. Now scientists are figuring out how to put up firewalls that block the hackers. Checkpoint inhibitors deactivate the brakes and allow the T-cells to get moving again. This lets the body kill off the cancer cells on its own.
Suzanne Topalian, who is Pardoll’s colleague at the Bloomberg~Kimmel Institute (and also his wife), played a key role in identifying another way the immune system could be used to fight cancer. After working as a fellow in Rosenberg’s lab, she became the head of her own NIH lab in 1989 and moved to Johns Hopkins in 2006. At Hopkins, she led a group of investigators who first tested drugs blocking the immune checkpoint receptor PD-1—short for “programmed death-1”—and the proteins that trigger it, PD-L1 and PD-L2.
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Newswise — WINSTON–SALEM, N.C. – May 16, 2018 – They’re actors, but they don’t perform on stage or in front of cameras. And they don’t do drama or comedy. Rather, they specialize in injuries and illnesses.
“I’ve had every disease you can imagine,” said Donna Sparks, a retired teacher who, along with her husband, Jeff, has been acting sick for 10 years at Wake Forest School of Medicine.
Donna and Jeff Sparks are among the role-players known as standardized patients. They are people who have been trained to accurately and consistently portray the physical signs or symptoms of medical conditions and the emotional characteristics and everyday concerns of actual patients in simulated clinical sessions with medical students, physician assistant students and others who are pursuing health care professions.
The purpose of these encounters is both simple and important: to give prospective providers the opportunity to develop both clinical skills and “bedside manner” before they begin to practice medicine for real.
“It’s definitely valuable,” said Lauren West-Livingston, a third-year student at Wake Forest School of Medicine. “We get to practice with these patients in a controlled environment so that when we go on to see real patients in the hospital or in clinic we have some experience, and some confidence.”
Standardized patients – also referred to as simulated patients or patient actors – are employed at most medical schools and teaching hospitals in the United States. The concept was introduced at the University of Southern California in 1963, more fully developed at the University of Arizona in the 1970s and widely adopted by medical schools – including Wake Forest School of Medicine – in the 1980s.
“Standardized patients are vital in helping us prepare our students for their future careers in health care,” said Mary Claire O’Brien, M.D., the Wake Forest medical school’s senior associate dean for health care education. “Our students are able not only to practice their clinical work but also to learn the importance of building relationships with their patients, empathizing with them and doing what’s best for them physically, emotionally and financially.”
Wake Forest medical students have clinical sessions with standardized patients – SPs for short – during all four of their years at the school. To give the students the most realistic experience possible, the sessions are held in specially equipped examination rooms at the Bowman Gray Center for Medical Education and cover a wide variety of medical scenarios – such as conducting a routine physical examination, diagnosing a minor ailment or delivering a negative prognosis about a life-threatening disease – with all types of people.
Wake Forest School of Medicine currently has a roster of 85 patient actors, said Kendall Freeman, manager of the Standardized Patient Program, which is part of the school’s Center for Experiential and Applied Learning. These men and women range in age from 20 to 75, have body types spanning the spectrum from athletic to obese, are members of different racial and ethnic groups and come from diverse socioeconomic, educational and occupational backgrounds.
“Right now we have pretty much everybody,” Freeman said.
To maintain that mix, hiring is done on the basis of demographic need, Freeman said. Otherwise, there are no requirements for becoming a standardized patient, and acting experience is definitely not necessary. That’s because SPs are obliged to strictly stick to the script in the clinical sessions, for which the medical aspects are standardized to allow for direct comparison and consistent evaluation of the students’ clinical skills.
At Wake Forest School of Medicine, newly hired standardized patients undergo a full day of training. To prepare for sessions with students, all SPs receive, usually one or two weeks in advance, detailed instructions and, if needed, additional training for the particular medical scenario.
And while emoting and improvisation are taboo, the SPs are, in addition to presenting a specific medical condition, sometimes called on to portray patients with assorted attitudes, behaviors or issues related to or independent of their health status.
“There are patients who intentionally make it difficult for us to get the information we need,” said West-Livingston, who is pursuing a Ph.D. along with her medical degree. “The sessions also can include what are called opportunities for empathy, where they’ll say ‘I’m worried about my job’ or ‘My insurance doesn’t cover that’ and we have to take a break from the diagnostic side and focus on the human aspect.”
Faculty members evaluate the students’ performances in the simulations but the SPs also have input, submitting a written evaluation sheet after each session.
“One thing we evaluate the students on is how comfortable we feel with them,” Donna Sparks said. “Do they listen to us? Do they show empathy and concern? Do they use layman’s terms instead of medical jargon?”
Being a standardized patient is not, it must be said, a regular part-time job. The hours are not steady, the need for SPs varies throughout the year and each actor is by nature ineligible to participate in more than half of the simulated clinical sessions. (“I don’t qualify for ectopic pregnancy,” Jeff Sparks noted.) But the position does have its rewards beyond the pay, which at Wake Forest is $20 an hour.
“It’s very gratifying to see how the students progress from their first year to their fourth year,” Jeff Sparks said. “It’s quite a change.”
“For me, this is another way that I can continue teaching and keep myself busy during retirement,” Donna Sparks said. “The students are so appreciative of what we do, and we really enjoy working with them.”
That feeling extends both ways. The sessions with the standardized patients, West-Livingston said, “are most people’s favorite part of the curriculum.”
Over the last decade, the Center for Medicare and Medicaid Services (CMS) has created both mandatory and voluntary programs designed to move healthcare providers from fee-for-service payment models to those that are value-based. Some of the most well-known programs are bundled payments.
Bundled payments have proven challenging for providers to address, as oftentimes they are unsure where or how to start. The shift towards value-based programs like BPCI (voluntary bundled payment program) and CJR (mandatory bundled payment program) have become a dividing issue amongst healthcare executives as some doubt the programs will drive desired success. More often than not, forward-thinking and progressive providers are already positioning themselves for the future by putting into place the right processes and structures for success.
Common Challenges in Succeeding Under Bundled Payment Programs The purpose of bundled payments is to promote high-quality care, and the system is meant to reward providers that care for patients during the entire care episode at a predetermined cost. Conversely, if a provider goes over the predetermined budget or target price, it is required to pay the difference back to CMS.
The challenge for providers is that bundled payments require more coordination that is tailored to individual patient preferences than traditional fee-for-service models. Scaling this type of care management is typically a new process that will require better reporting, communication, and engagement workflows. Additionally, many providers do not have consistent processes around communicating with patients prior to their arrival or after they have left the facility.
By capitating episode-based payments, providers across the care continuum must work more closely together to understand and act upon patient needs. From gathering patient outcomes information at the physician office to proactive rounds in a rehab facility, if processes are not efficient and systems don’t communicate with each other, there is a greater risk of poor patient outcomes and of losing money. So, the question is, how can healthcare providers realize success under bundled payments? The answer lies in creating efficient and consistent patient engagement programs.
Utilizing Patient Engagement Strategies to Maximize Bundled Payment Rewards
As with any value-based initiative, involving patients in their care is critical to success. This is especially true of bundled payments. Under most CJR and BPCI models, providers are accountable for the patient for the entire care episode, which can include up to 90-days post-discharge. To ensure success, patients should be engaged prior to their scheduled appointment, educated while in the facility, and contacted throughout their recovery.
With proactive engagement strategies such as pre-op education and post-op follow up, providers can identify and prevent potentially costly events such as an infection or a readmission. There are many engagement strategies that can help providers achieve bundled payment goals and KPIs. For example, programs like CJR require providers to collect patient-reported outcomes. To do this, providers can implement kiosks at physician offices or they can proactively reach out to patients via call or text to capture the information. Additionally, clinical follow-up calls or wearable fitness trackers can be used to monitor patients post-discharge and determine if patients are experiencing any issues.
To further engage patients in the hospital or post-acute healthcare facility, rounds are a great way to track progress and leverage best practices such as teach-back to help prepare patients for their transition home and recovery. The bottom line is that there are countless interaction points where providers can engage patients in their own care to lower costs, improve outcomes, and enhance experiences.
Achieving Success with Bundled Payments Whether you are a believer in bundled payments or a vocal skeptic, putting the right processes and technologies in place to drive patient engagement is proving to have a positive impact. Several hospitals in the U.S. are already meeting bundled program KPIs (key performance indicators) such as reduced readmissions with effective patient engagement and scalable patient engagement processes are what can drive long-term success.
The hospitals leverage the patient information they have to deploy automated calls and text messages, cross-continuum care management, and point-of-care data collection. By using technology, the team is able to leverage one orthopedic care coordinator to manage the day-to-day workflow associated with all total hip and knee replacement patient episodes.
By implementing patient engagement processes that leverage technology for efficiency, providers are creating a better experience throughout the entire care episode, all while reducing the overall cost of care. It is evident that risk-based models are here to stay with the launch of new programs such are BPCI Advanced, which is set to go live this year. As CMS and commercial payers continue to leverage value-based payments, patient engagement will play a critical role in improving quality and driving financial success.
John Banks Powell is the Vice President of Post-Acute Strategy at CipherHealth. Powell spearheads CipherHealth’s post-acute and bundled payment initiatives by partnering with providers across the care continuum who leverage CipherHealth’s patient engagement and care coordination solutions to meet quality initiatives. Powell holds a BA from the University of North Carolina at Chapel Hill, and a Masters degree from the Fuqua School of Business at Duke University.
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Medications are totally avoided, sparing the system from chemical formulations.
The spread of vitiligo is contained almost immediately.
Enhanced skin color visible in four days, with total cure guaranteed in three to eight weeks.
Improved immunity and general health.
Boost of self-confidence.
Support From The Author
If you’re looking for additional assistance, all you need to do is send him an email and he will reply to you. You can voice your queries, clarifications, or even ask for advice about your vitiligo.
You’ll also have access to the findings of ongoing research on vitiligo treatments as part of the “Free Lifetime Updates” and three months of free consultation from Michael Dawson himself.
This e-book offers a permanent, scientifically-proven, holistic and 100% natural treatment for vitiligo, which is bound to get the glow and smile back on your face. Simply follow the instructions and prescribed lifestyle/dietary changes highlighted in the book, and you won’t need the two-month money-back guarantee. This ebook definitely gets a huge thumbs up!
(Source: sg.news.yahoo.com) A Mediterranean diet involves eating little red meat, and lots of fruit and veggies, legumes such as peas and beans, unrefined cereals, fish, and vegetable oil Women who follow a diet rich in fresh fruit and vegetables, fish, and olive oil may stand a better chance of falling pregnant through in-vitro fertilisation (IVF), […]