Research led by Si-Qiong June Liu, MD, PhD, Professor of Cell Biology and Anatomy at LSU Health New Orleans School of Medicine, discovered a surprising reciprocal interaction between chemicals in the brain resulting in accelerated loss of molecules that regulate brain cell communication. The research team’s findings are published online in Nature Communications, available here.
Working in a rodent model, the researchers showed that the release of Gamma-Aminobutyric acid (GABA), an amino acid that acts as a neurotransmitter, hastens the breakdown of endocannabinoids in the brain. Endocannabinoids are naturally produced molecules that regulate how brain cells communicate, and their dysfunction can lead to neurological disorders. Endocannabinoids are produced “on-demand” and are removed when they are no longer needed. The researchers found that GABA upsets this delicate balance. Endocannabinoids are critically involved in several aspects of emotional memory processing, and the researchers found that memory formation through fear conditioning selectively speeds up their decline in the cerebellum. The findings reveal a potential therapeutic target to regulate the rate of degradation of endocannabinoids and provide an effective way to alter behavior.
“Endocannabinoids control emotional behavior,” notes Dr. Liu. “Learning increased the release of the inhibitory neurotransmitter, GABA, and this was responsible for driving the change in endocannabinoid degradation. This form of plasticity is responsible for the formation of fear memory. Our findings suggest a novel mechanism for the physiological regulation of endocannabinoid signaling and for modulating emotional behavior.”
Other members of the LSU Health New Orleans research team included Dr. Christophe J. Dubois, graduate student Jessica Fawcett-Patel and undergraduate student Paul A. Katzman.
This work was supported by National Science Foundation Grant IBN-0344559, Veterans Administration Grant BX003893 and National Institutes of Health Grants NS58867, R01NS106915, and MH095948, as well as an NIH COBRE grant, P30 GM106392.
AboutLSU Health Sciences Center New Orleans: LSU Health New Orleans educates Louisiana’s health care professionals. The state’s health sciences university leader, LSU Health New Orleans includes a School of Medicine with branch campuses in Baton Rouge and Lafayette, the state’s only School of Dentistry, Louisiana’s only public School of Public Health, and Schools of Allied Health Professions, Nursing, and Graduate Studies. LSU Health New Orleans faculty take care of patients in public and private hospitals and clinics throughout the region. In the vanguard of biosciences research, the LSU Health New Orleans research enterprise generates jobs and enormous annual economic impact. LSU Health New Orleans faculty have made lifesaving discoveries and continue to work to prevent, advance treatment or cure disease. To learn more, visit http://www.lsuhsc.edu, http://www.twitter.com/LSUHealthNO, or http://www.facebook.com/LSUHSC.
Misperceptions most prevalent in insomnia patients
People with sleep disorders commonly have a misperception about their actual sleep behaviour. A research group led by Karin Trimmel and Stefan Seidel from MedUni Vienna’s Department of Neurology (Outpatient Clinic for Sleep Disorders and Sleep-Related Disorders) analysed polysomnography results to identify the types of sleep disorder that are associated with a discrepancy between self-reported and objective sleep parameters and whether there are any factors that influence this. The main finding: irrespective of age, gender or screening setting, insomnia patients are most likely to underestimate how long they sleep. The study has been published in the highly regarded Journal of Clinical Sleep Medicine.
Patients’ misperceptions about the actual time that they sleep is a well-known phenomenon in sleep research. Their own impression of their sleep behaviour is often quite different from that demonstrated by clinical measurements. Nonetheless, until now there had been no scientific comparison between patients’ actual total sleep time and their self-reported sleep time that also analysed the associated factors.
A research group led by neurologists Karin Trimmel and Stefan Seidel from MedUni Vienna’s Outpatient Clinic for Sleep Disorders and Sleep-Related Disorders has now retrospectively analysed patient consultations from between 2012 and 2016 and polysomnograms (PSG) of a representative group of 303 sleep clinic patients, 49% of whom were women. 32% were suffering from the commonest sleep disorder, insomnia, 27% from sleep-related breathing disorders, 15% from sleep-related movement disorders, 14% from hypersomnia/narcolepsy and 12% from parasomnias. A PSG measures depth of sleep, muscle activity and breathing over the course of the night. It can be performed in the sleep lab or as ambulatory tests, where the patients sleep at home.
There was found to be a discrepancy between self-reported perception and objective readings in all sleep disorders, although it was largest in the case of insomnia, irrespective of age, sex or whether the monitored night was spent in the sleep lab or at home. Insomnia patients overestimate their sleep latency, that is to say the time it takes them to fall asleep, and significantly underestimate the amount of total sleep time. A constantly elevated level of background stress (hyperarousal) could be a factor in this, since this would result in disrupted sleep architecture (increased number of microarousals), as well as the fact that insomnia is often associated with psychiatric comorbidities. In contrast to insomnia patients, patients with other sleep disorders tended to underestimate their sleep latency and overestimate their total sleep time.
The study corroborates the clinical observation that sleep misperception occurs in all forms of sleep disorder but is most prevalent in insomnia. The treatment of choice in this instance is cognitive behavioural therapy. Karin Trimmel explains: “By incorporating this misperception into behavioural therapy, we can significantly improve treatment outcomes, so that polysomnography is highly recommended for patients with treatment-resistant insomnia.”
Reference: Trimmel K, Eder HG, Böck M, Stefanic-Kejik A, Klösch G, Seidel S. The (mis)perception of sleep: factors influencing the discrepancy between self-reported and objective sleep parameters. J Clin Sleep Med. 2021 Jan 4. doi: 10.5664/jcsm.9086. Epub ahead of print. PMID: 33393901. https://pubmed.ncbi.nlm.nih.gov/33393901/
The presence of particular memory cells in the skin could explain why atopic dermatitis keeps recurring
Researchers from the Meduni Vienna and the CeMM were able to show that certain populations of immune cells settle in the skin of atopic dermatitis sufferers and are still present even after one year of successful therapy. These cells from the group of dendritic cells and T helper cells are characterized by the production of certain inflammatory messenger substances that fuel the activity of neurodermatitis.
Atopic dermatitis, also known as neurodermatitis or atopic eczema, is currently the most common chronic inflammatory skin disease in humans. It usually begins in early childhood and can be accompanied by food allergies, hay fever and allergic asthma. In many cases, the disease disappears again in late childhood or early adulthood, but a not inconsiderable proportion suffer from this very itchy skin disease for a lifetime. In these patients there are a number of therapy options to alleviate the skin symptoms or to bring them to healing, but atopic dermatitis usually returns very soon after the end of therapy.
Researchers at the University Clinic for Dermatology at MedUni Vienna (first author: Christine Bangert, project leader: Patrick M. Brunner), in collaboration with Thomas Krausgruber and Christoph Bock from CeMM, were able to show that certain populations of immune cells settle in the skin of atopic dermatitis sufferers, and these too cannot be eliminated after one year of successful therapy.
These cells, which belong to the group of dendritic cells and T helper cells, are characterized by the production of certain inflammatory messengers, which fuel the activity of neurodermatitis.
In the study, now published in the top journal Science Immunology, the authors examined skin samples from patients whose skin lesions had completely healed under therapy with the monoclonal antibody dupilumab, which blocks the interleukin-4 receptor. Despite the successful therapy, certain inflammatory cells, namely the dendritic and T-helper memory cells mentioned, were still detectable. Interestingly, these cells were not found in healthy volunteers.
“The fact that these cells do not appear to be found in healthy skin makes them an attractive target for new therapeutic approaches that could possibly lead to a long-term healing of this skin disease beyond active therapy,” explains Patrick Brunner. The so-called Th2A cells, which also occur in the blood of allergy sufferers and which disappear after successful immunotherapy, are of particular interest here. These cells have certain receptors on their surface that enable them to react quickly to inflammatory stimuli that are typical for diseases of the so-called atopic type (atopic dermatitis, asthma, allergic rhinitis). These cells could also contribute to why atopic dermatitis resolves spontaneously in adolescence in some patients, but persists for a lifetime in others.
Interestingly, increased inflammation signals were not only detectable in the skin, but also in the blood of successfully treated patients. “This result shows us that patients with severe atopic dermatitis also show systemic involvement due to successful therapy, despite the absence of appearance,” adds Christine Bangert.
Copyright of this article (English version) belongs to aur author S. Aman. One is allowed to reuse it only by giving proper credit either to him of to us.
Reference: Christine Bangert, Katharina Rindler, Thomas Krausgruber, Natalia Alkon, Felix M. Thaler, Harald Kurz, Tanya Ayub, Denis Demirtas, Nikolaus Fortelny, Vera Executive Lechner, Wolfgang M. Bauer, Tamara Quint, Michael Mildner, Constanze Jonak, Adelheid Elbe-Bürger, Johannes Griss, Christoph Bock, Patrick M. Brunner, “Persistence of mature dendritic cells, Th2A and Tc2 cells characterize clinically resolved atopic dermatitis under IL-4R-alpha blockade”, Science Immunology, Vol. 6, Issue 55, eabe2749 2021. DOI: 10.1126/sciimmunol.abe2749 https://immunology.sciencemag.org/content/6/55/eabe2749
In a lab in Amsterdam, arachnophobes have volunteered to encounter their eight-legged nemeses to help researchers hoping to conjure and obliterate fear memories. These studies, as well as new understanding of overlooked brain regions, are revealing how fears linked to PTSD or phobias work, and how they may be treated.
In upcoming clinical trials, Professor Merel Kindt at the University of Amsterdam, the Netherlands, plans to expose volunteers to fleet-footed spiders and tarantulas to provoke their fear memory. Afterwards, they will receive an approved drug to try to thwart their spider fears. She believes that her ‘recall and erase’ strategy can be used to treat all sorts of phobias, but also life-changing clinical conditions such as post-traumatic stress disorder (PTSD).
Through a project called ErasingFear, her Emotional Memory Lab will shortly also begin clinical trials with Dutch war veterans and medical staff traumatised by experiences during the COVID-19 pandemic.
Prof. Kindt is a clinical psychologist who began her research on modifying fear in 2008, inspired by earlier work with lab animals. That research convinced her that it was possible to trigger fear memories and destabilise them using certain drugs.
The strategy is different from cognitive behavioural therapy where people who fear spiders, for example, are exposed to a fear cue, and learn through direct experience that their fear is not realistic. But the relapse rate is relatively high, says Prof. Kindt.
‘During and after exposure, people form a new memory, an inhibitory memory that competes with the original fear memory, but the fear memory remains intact,’ she explained. Prof. Kindt’s approach is different. She aims to recall the original memory and destabilise it, the drug propranolol interferes with the otherwise resaving – or rewriting of the same memory for long-term storage in the brain.
‘It seems possible to target fear memory itself so as to weaken the root of the anxiety disorder by weakening or even erasing the fear memory,’ said Prof. Kindt.
She does this by giving the beta-blocker drug propranolol in conjunction with the fear memory being triggered. This approved drug slows down heart rate and is prescribed to people with high blood pressure or anxiety, usually before a stressful situation. Prof. Kindt is using it in an entirely different way for phobias – by administering it after someone is exposed to a fear stimulus in order to interfere with the restabilisation of their fear memory.
If propranolol is given two hours or more after a brief exposure to a spider, this does not work. ‘Timing is important, and we only give the drug once,’ Prof. Kindt said.
It seems possible to target (the) fear memory itself so as to weaken the root of the anxiety disorder by weakening or even erasing the fear memory.
— Prof. Merel Kindt, University of Amsterdam, the Netherlands
The idea of recalling and then eliminating a memory came from research that Prof. Kindt noted in animals more than a decade ago. Drugs that blocked protein synthesis were used to erase memories, but these are too toxic for people. Propranolol, an approved drug, has few side effects. It blocks adrenoceptors in the brain. These are docking sites for neuro-adrenaline, a chemical messenger involved in memory-making. By blocking them, the drug interferes with stabilisation of the memory and dulls the strength of the memory and therefore the fear response underpinned by that memory.
In other words, memories are not being wiped out. People will still recall that they were afraid of spiders, but the idea is that by weakening the memory we erase or weaken the bodily fear response next time the person encounters a spider, she explains. ‘After 24 hours, the drug completely washes out. If you then observe a striking reduction in fear, this is not because that drug is still onboard,’ said Prof. Kindt, referring to the weakened memory reducing fear. So far, since she first started testing it with spider phobias in 2013, the treatment is an all or nothing affair – it either works or it doesn’t work at all for spider phobias in individuals.
If the fear is gone a day later, they know the procedure has worked, she says.
She has video recorded sessions and taken physiological measures, such as heart rate, to try to discover a predictor of treatment success, one that can tell her whether a fear memory has re-stabilised or not.
She is now doing several trials with spider phobias to better understand optimal conditions to ensure memory triggering and rebuilding.
Prof. Kindt has also begun pilot studies of Dutch veterans who served in Afghanistan – using burning smells and battlefield noises to recall the memories that underpin a soldier’s PTSD. This is more difficult than spider phobias, because usually there are highly specific memories that underpin such complex traumas.
She will also begin a clinical trial with medical personnel who had to deal with the psychological difficulties of patients passing away without the support of family and friends during the COVID-19 pandemic.
The brain is such a complex organ that scientists still struggle with basic questions about what is happening where inside our brain, and why. To better understand how fear works, scientists are attempting to map out what fear looks like inside the brain, an extremely challenging task.
Scientists can scan the human brain using magnetic resonance imaging (MRI), to see where blood flows. This can highlight which areas of the brain are most active when a person looks at a fearful picture, for example.
But these brain images do not have the resolution to peer into the most ancient and mysterious parts that lie deep at the bottom of our brain, says Professor Cornelius Gross, neurobiologist at the European Molecular Biology Laboratory (EMBL) in Rome, Italy.
His COREFEAR project sought to find which brain circuits were activated when mammals face predators or stressful social situations, such as encounters with bullies.
This, he suggested, would be very different from many fear experiments. Historically, experiments usually involved rodents being conditioned to expect (and fear) a brief electric shock each time they heard a buzzer sound. These experiments pointed to the epicentre for fear and anxiety as the amygdala, two almond-shaped structures found in the relatively recently evolved forebrain of mammals. But Prof. Gross thinks the textbooks need to be amended.
‘We argue that the amygdala is just a gateway to real fear centres deep in the brain,’ said Prof Gross. ‘The part of the amygdala that has been most studied for fear in the lab is irrelevant for fear of a predator or social threat.’
His research results suggest that the hypothalamus has been overlooked in human fear and anxiety. This is a deep brain region the size of your thumb that’s most well known for releasing hormones.
He notes that in an experiment where the part of the hypothalamus that controls predator fear was stimulated, a person had a full-on panic attack. ‘They had a conscious experience of fear and dread and a feeling like they were going to die,’ explained Prof. Gross, who was not involved in this study.
Still, other areas of the brain, such as the seahorse-shaped hippocampus, are probably also involved in our innate and learnt fears. Human behaviour is also complicated by our having a much more developed cerebral cortex, which makes up the largest part of our brains and allows us to suppress our fear responses.
The EMBL lab in Rome recently released a preprint study showing that the mouse cortex can dampen inbuilt defensive behaviours of the rodent to threats. Our own highly developed cortex allows us to consciously control our own behaviours.
Prof. Gross also recently reported on special hypothalamus cells that can map the spatial coordinates of where an animal encountered an intimidating rival. These cells fired whenever the animal returned to that spot, a social fear memory that encodes context and spatial memory. This was the major discovery he made in the COREFEAR project.
Such memories and fear of social defeats by rivals are likely to be important in territorial animals, which includes many rodents and also primates. Prof. Gross now plans to pursue these findings to fill in the many blanks in our understanding of how fear is stamped onto human brains. This could eventually help patients with behavioural and psychological disorders, including anxiety.
Featured image: By triggering original fear memories, a researcher hopes to weaken them to help treat phobias. Image credit – Islander Images/Unsplash
New research highlights the social side of self-control.
Self-control plays an important role in achieving our personal goals. Yet, self-control is hard and prone to failure – whether we’re trying to stick to a workout regimen, to reduce alcohol consumption, or to limit air travel to protect the environment. Fortunately, there are strategies we can adopt to make self-control slightly less difficult.
Social Self-Control Strategies
Self-control is sometimes mistakenly thought of as an entirely individual enterprise. However, self-control decisions and their success can be strongly influenced by other people – for good or bad.
Picture the following scenario: You have just decided to become a vegetarian after learning about the environmental and animal-welfare consequences of animal agriculture. Your partner, on the other hand, doesn’t want to follow suit and will continue to eat meat (something you still like the taste of). It’s not hard to imagine how, in this scenario, you will be regularly tempted to eat meat – either when your partner prepares delicious-looking meat dishes or when dining at a restaurant. The need for self-control in order to stick to your vegetarian diet thus seems never-ending, and the odds of successfully maintaining the diet are undoubtedly slimmer than had your partner made the same dietary change as you.
This scenario illustrates how our goals and self-control may be challenged by other people, including those dearest to us. Though we’re especially sensitive to the opinions, preferences, and behavior of close others, even unfamiliar encounters can elicit temptations and lead us astray (e.g., a former smoker seeing someone on the street smoke a cigarette).
But rest assured, other people can also be a force for good and support our self-control. For example, they can help ensure that temptations are not elicited (thereby circumventing the need for self-control in the first place). They can also help monitor our behavior and provide feedback if we’re straying off course, act as models of good behavior, and encourage us to exert self-control when temptations become overwhelming.
While many self-control strategies exist, below are two promising and interconnected social strategies that may help boost your self-control.
Leverage Goal Support. Goal support involves receiving support from another person in relation to a particular goal in a certain situation or across situations. Goal support is thus a specific type of social support, and one that research suggests can promote goal progress and effective self-control. There are at least two types of goal support. The first is passive goal support whereby support is received automatically, often resulting from simply being around people who generally support your goals (e.g., partner, friends, or family). The second is active goal support where goal support is not automatically available to you, thus requiring you to seek it out deliberately. A well-known example of active goal support is getting a goal buddy or team (e.g., a fitness or running buddy), which research has shown to promote self-control success. So, if you struggle with self-control or staying on track for a certain goal, asking for other people’s support may be an effective strategy.
Avoid Tempting Social Situations. One of the most illuminating findings in recent self-control research is that people who are generally good at self-control more often find themselves in situations that support their goals and limit the risk of temptation. Indeed, they also tend to find themselves in goal-supportive social environments compared to people who generally struggle with self-control. By being mindful of your social environments you can identify specific people and/or social situations that may lead you into temptation and try to avoid them. For example, if you’re trying to quit smoking, going out with all your friends who smoke may not be the wisest decision (perhaps unless you are also joined by a supportive non-smoking friend). Opting yourself into social environments that are goal-supportive and out of those that aren’t may therefore be a sound self-control strategy.
Although we sometimes cannot change our social environments (or don’t want to), becoming more attentive to them and seeking out goal support may just provide that boost in self-control so many of us desire.
Reference: 1. vanDellen MR, Shah JY, Leander NP, Delose JE, Bornstein JX. In Good Company: Managing Interpersonal Resources That Support Self-Regulation. Personality and Social Psychology Bulletin. 2015;41(6):869-882. doi:10.1177/0146167215580778 (2) 1. Duckworth AL, Milkman KL, Laibson D. Beyond Willpower: Strategies for Reducing Failures of Self-Control. Psychological Science in the Public Interest. 2018;19(3):102-129. doi:10.1177/1529100618821893 (3) 1. Nielsen KS, Bauer JM. The Merits of Goal Support as a Self-Control Strategy. Social Psychological and Personality Science. 2019;10(5):671-680. doi:10.1177/1948550618780729 (4) Leahey, T.M., Kumar, R., Weinberg, B.M. and Wing, R.R. (2012), Teammates and Social Influence Affect Weight Loss Outcomes in a Team‐Based Weight Loss Competition. Obesity, 20: 1413-1418. https://doi.org/10.1038/oby.2012.18 (5) Hofmann, Wilhelm,Baumeister, Roy F.,Förster, Georg,Vohs, Kathleen D., “Everyday temptations: An experience sampling study of desire, conflict, and self-control.”, Journal of Personality and Social Psychology, Vol 102(6), Jun 2012, 1318-1335.
Copyright of this article totally belongs to Kristian Steensen Nielsen, who is a Research Associate at the University of Cambridge. This article is republished here from psychology today under common creative licenses
Why do people think autistic people don’t have empathy when in some ways they have more than most people? It’s worth understanding.
There’s a myth that autistic people don’t have empathy, that they’re too self-absorbed or uncaring. That’s simply false. They do have empathy. I’d like to raise the issue of “double empathy,” and the additional question (generally unasked) as to whether non-autistic people, “neurotypicals,” have empathy for autistic people.
There’s at least two kinds of empathy, cognitive empathy and emotional empathy. Cognitive empathy is seeing the perspective of someone else; emotional empathy is having feelings for the feelings of someone else. They don’t necessarily go together. A narcissist can have cognitive empathy – see another person’s perspective – but not care how that person feels. Research has shown that autistic people do more poorly than neurotypicals on tests of cognitive empathy but score the same or even have more emotional distress at the distress of others than neurotypical people.
One reason why autistic people are seen as lacking emotional empathy is that autistic people don’t generally express their empathy in the expected way, with body language, gesture, and statements such as “I’m sorry” or “I understand.” An autistic person might express empathy by offering a solution to a problem, or by sharing a similar experience. Both of these can be seen as not validating the feelings of the other person. Autistic people may not have empathy for every situation. (Neither do neurotypicals.) However, autistic adults often express their support and concern directly when posting online in response to someone sharing distress. It may be that it’s difficult for autistic adults to find the right words to say in the moment, and it helps to have time as one does online.
In a recent court case, the prosecutor argued that the autistic defendant didn’t show remorse because of his lack of facial expression or tears. This was despite the fact that the defendant had said that he was devastated by the impact of his inadvertently causing an accident in which someone was badly hurt, and that he would do everything he could to help the person and his family.
Nonverbal communication accounts for well over half of social/emotional communication, and this young man’s words were dismissed as inauthentic since they weren’t matched by expressive body language. Actually, as someone autistic, this young man was much less likely than a neurotypical person to say something untrue just because it benefited him.
An autistic person often has such a strong feeling for what’s right that he would put that before his own interests. A research study examined whether individuals would incur a personal cost for supporting a morally good cause or support a morally bad cause to receive personal gain. The study found that autistic people were much more likely than neurotypical people to reject the opportunity to support a bad cause even at a cost to themselves. “ASD individuals are more inflexible when following a moral rule even though an immoral action can benefit themselves and suffer an undue concern about their ill-gotten gains and the moral cost. These findings deepen our understanding of the neurobiological roots that underlie atypical moral behaviors in ASD patients.” (Hu et al, 2000) The researchers seemed to conclude that the consistently moral behavior of autistic people and their strong concern about whether they had done anything “ill-gotten” signaled atypical behavior and inflexibility rather than admirable commitment to good causes. I question whether neurotypicals who consistently put doing what’s right over their self interest would be described as inflexible.
Like emotional empathy, cognitive empathy is also complex and worth exploring. In studies, autistic people show less cognitive empathy or ability to take the perspective of others than neurotypicals. It is possible that black and white thinking tends to frame things as right or wrong so a different perspective might be dismissed. I find using Ross Greene’s approach can be helpful in seeing different perspectives; it is described on his website, Lives in the Balance. However, let’s accept the idea that autistic people don’t do as well as neurotypicals at understanding the perspective of others.
Dr. Damian Milton raised the idea of double empathy – that empathy and understanding go two ways. I’m not aware of studies exploring whether neurotypicals have cognitive empathy for autistic people. Neurodiverse and neurotypical people have different ways of thinking and processing their experience. They notice (or don’t notice) different things and express themselves in different ways. Are neurotypical people any better at understanding the perspective of an autistic person than autistic people are at understanding the perspective of a neurotypical person?
Based on my experience, neurotypicals often see explanations of an autistic person’s perspective as an excuse. A mother of one of my clients was angry that her son didn’t carry in the groceries when she commented that they were heavy. She felt he was selfish, that he lacked empathy for her needs. She rejected my explanation that he needed a direct request (“Can you help me carry the groceries?”) instead of a hint as “making excuses for him.” Autistic people take language literally. Her son took her statement at face value and didn’t understand the implied but unstated meaning. She didn’t think his perspective was valid, feeling he “should” have understood if he cared.
In another case, a girl was not participating in an interactive exercise of having a conversation in French in her French class. She was drawing instead. Her behavior was labeled avoidant and attention-seeking. The autistic student was overwhelmed by the noise in the class, the new fluorescent lighting in the room and the social demand to interact with someone she didn’t know, so she was calming herself by drawing. A behavior plan that simply prevented her from drawing did not take into account her perspective and needs.
One could take the idea of double empathy and failure of cognitive empathy further. It may be that many people don’t have cognitive empathy for people whose life experience is fundamentally different from their own, whether this difference is neurotype, racial, ethnic, religious, cultural, gender-related, or some other kind of difference. For example, there are many books and classes currently addressing the difficulty for white people of understanding the perspective of Black people.
It makes sense that people have more accurate cognitive empathy with people like themselves than they do for people whose experience of the world and processing of what happens is different from their own. Research studies have found that autistic people better understand other autistic people, and neurotypical people understand other neurotypical people, and the problems occur when different neurotypes need to understand each other. Since the majority of the world are neurotypical people, it falls upon autistic people to develop some understanding of the perspective of a different neurotype in order to navigate daily life.
The myth that all autistic people lack empathy is just that, a myth, and the whole business of empathy is much more complex than a superficial assumption of who does and doesn’t have it. Autistic people can be more empathic in some ways than neurotypicals; in the area that’s considered their deficit—being able to see the perspective of others—autistic people aren’t the only ones with challenges. There certainly is variability within groups. Seeing perspectives, emotionally connecting to feelings, and empathy in general are much more complex than they seem.
References: (1) Hu Y, Pereira AM, Gao X, Campos BM, Derrington E, Corgnet B, Zhou X, Cendes F, Dreher JC. Right temporoparietal junction underlies avoidance of moral transgression in Autism Spectrum Disorder. J Neurosci. 2020 Nov 6:JN-RM-1237-20. doi: 10.1523/JNEUROSCI.1237-20.2020. Epub ahead of print. PMID: 33158960. (2) Damian, M. (2012) On the ontological status of the double empathy problem Disability and Society 27 (6) 883-887. (3) Crompton, C, Hallett, S, Roper, D, Flynn, E & Fletcher-Watson, S. (2020) “I never realized everybody felt as happy as I do when I am around autistic people.” A thematic analysis of autistic adults’ relationships with autistic and neurotypical friends and family Autism 24 (6) 1438 – 1448.
Copyright of this article totally belongs to Marcia Eckerd, who is a licensed psychologist. This article is republished here from psychology today under common creative licenses
Fragile sense of masculinity, or reliance on others’ views, triggers a macho response
When their manhood is threatened, some men respond aggressively, but not all. New research from Duke University suggests who may be most triggered by such threats – younger men whose sense of masculinity depends heavily on other people’s opinions.
“Our results suggest that the more social pressure a man feels to be masculine, the more aggressive he may be,” said Adam Stanaland, a Ph.D. candidate in psychology and public policy at Duke University and the study’s lead author.
“When those men feel they are not living up to strict gender norms, they may feel the need to act aggressively to prove their manhood — to ‘be a man’.”
The pair of studies considered 195 undergraduate students and a random pool of 391 men ages 18 to 56.
Study participants were asked a series of questions about “gender knowledge.” For men, these included questions on such stereotypical topics such as sports, auto mechanics and home repair. After answering, participants were randomly told their score was either higher or lower than that of an average person of their gender.
To simulate real-world threats to manhood, men who received a low score were also told they were “less manly than the average man.”
After receiving their quiz scores, study participants were asked to complete a series of word fragments by adding missing letters, in order to reveal their state of mind. The results were striking, revealing aggressive thoughts among certain men but not others.
Men whose sense of masculinity came from within seemed unruffled by receiving a low score. It was a different story for men with a more fragile sense of masculinity, whose feelings of masculinity relied on others. That group included men who said they behaved “like a man” due to social pressures such as the desire to fit in, be liked or get dates.
Men with a more fragile sense of masculinity responded to the word fragments by creating words with violent associations rather than neutral meanings. For instance, when provided with the letters “ki” and asked to complete the word, they wrote “kill” rather than, say, “kiss.” When given the letters “blo,” they typed “blood” instead of a word such as “blow” or “bloom.”
Those aggressive responses were strongest among the youngest study participants, men between 18 and 29 years old. The response was milder among middle-aged men between ages 30 and 37, and milder still among the oldest group of participants, men ages 38 years old and older.
“It’s clear that younger men are more sensitive to threats against their masculinity,” Stanaland said.
“In those years, as men attempt to find or prove their place in society, their masculine identity may be more fragile. In many places, this means that younger men are hit constantly with threats to their manhood. They have to prove their manhood every day of their lives.”
Female students did not display a similar aggressive response when their gender was threatened.
Men’s aggressive responses didn’t end with the study questionnaire, the researchers noted. The study designers received violent threats from some men who received low scores – further evidence that the study hit a nerve.
Stanaland said he hopes to delve further into the forces that shape men’s aggression.
“Men report aggressive behavior in all sorts of domains,” Stanaland said. “Some of them are trying to prove their own manhood by being aggressive.
“Men’s violence, terrorism, violence against women, political aggression – fragile masculinity may explain many of these behaviors. It’s in everyone’s interest to understand this phenomenon better.”
The research was funded by the Charles Lafitte Foundation Program in Psychological Research at Duke University.
Nagoya University researchers and colleagues have revealed that colorectal cancer tissues contain at least two types of fibroblasts (a type of cells found in connective tissue), namely, cancer-promoting fibroblasts and cancer-restraining fibroblasts, and that the balance between them is largely involved in the progression of colorectal cancer. Their findings, recently published in the journal Gastroenterology, suggest that artificially altering the balance between the two types of cells could curb the spread of colorectal cancer tumors, which may become an effective strategy for preventing cancer progression.
Cancer tissues comprise both cancer cells and non-malignant cells such as fibroblasts. Previous studies have suggested that the proliferation of fibroblasts is largely involved in the progression of colorectal cancer, the most common cancer in Japan. Fibroblasts within cancer tissues, called cancer-associated fibroblasts (CAFs), are considered to be divided into at least two populations: those that promote cancer progression and those that restrain it. Impeding the function of cancer-promoting CAFs could be a promising method to prevent cancer progression, but a lack of understanding of the mechanism underlying heterogeneity of CAFs has hampered its development.
In normal colon tissues, proteins called bone morphogenetic proteins (BMPs), which are secreted by stromal cells, are known to play a critical role in regulating intestinal homeostasis, whereas in cancerous colon tissues, they are considered to be associated with cancer progression. In this context, the research team led by Professors Atsushi Enomoto and Masahide Takahashi of the Graduate School of Medicine at Nagoya University in Japan conducted a study to determine how stroma cells lead BMPs to be involved in the progression of colorectal cancer.
The team first analyzed comprehensive gene expression profiling data to identify BMP-related genes that are specifically expressed in colorectal CAFs. Two types of proteins, meflin and gremlin 1, were identified to be encoded by such genes. Next, to investigate the relevance of these proteins in colorectal cancer progression, Prof. Enomoto and his colleagues, who had previously shown that meflin plays a role in restraining the progression of pancreatic cancer, conducted a study in collaboration with researchers from the University of Adelaide and the South Australian Health and Medical Research Institute, who have conducted studies focusing on the role of gremlin 1 as a BMP inhibitor in the intestine.
The joint research group examined the prognostic significance of the expression of meflin and gremlin 1 in colorectal cancer patients and found that, interestingly, those with a high expression of meflin have a favorable prognosis, whereas those with a high expression of gremlin 1 have an unfavorable prognosis. In addition, experiments using a mouse model revealed that the proliferation of colorectal cancer cells can be suppressed through administration of a gremlin 1-neutralizing antibody or overexpression of meflin.
Regarding the role of BMP signaling mediated by stromal gremlin 1 and meflin in colorectal cancer, Prof. Enomoto explains, “We hypothesize that CAFs mediated by gremlin 1 promote cancer progression by decreasing BMP signaling, whereas CAFs mediated by meflin restrain the growth of the cancer by reinforcing BMP signaling.” Therefore, intensifying stromal BMP signaling, either by using a gremlin 1-neutralizing antibody or by overexpressing meflin, could be an attractive therapeutic strategy to treat colorectal cancer.
The study, “The balance of stromal BMP signaling mediated by GREM1 and ISLR drives colorectal carcinogenesis,” was published online in the journal Gastroenterology on November 14, 2020 at DOI 10.1053/j.gastro.2020.11.011.
Featured image:Representative images of human colon cancer tissue showing the localization of gremlin 1-positive (left) and meflin-positive (right) cancer-associated fibroblasts (CAFs) in the stroma. Brown denotes CAFs that are positive for gremlin 1 or meflin T, tumor cells. (Credit: Atsushi Enomoto)