Tag: Anxiety

Posted on

Awakening from the Trance

This blog was originally posted by the TLC Foundation for BFRBs

Trichotillomania touches on all levels of human experience, from the neurological to the spiritual. It represents the interactions of brain chemistry, but also habituated physiological responses, sensory processing, behavior patterns, characteristic emotional states, perceptual styles and beliefs, and the sense of interconnectedness with others and the experience of faith. It is more than just a behavior, although it is most apparent when it manifests itself in that way.

Trichotillomania can be treated at all of these levels through different treatment approaches: medication, relaxation and response prevention, behavior modification, hypnotherapy, psychotherapy, cognitive therapy and visualization, group therapy and spiritual practices. The most effective approach will depend on the specific needs and circumstances of each individual at specific times, as well as on the compatibility of the personalities of the treatment provider and patient/participant.

In this article I will present my own view of treatment with a particular focus on how to understand and address the aspect of trance.

“Trance” is not a clinical term, but it is one which most pullers seem to recognize immediately as a significant part of the hair pulling experience: particularly when reading or watching TV. However, I believe that any time one is pulling, one has entered a trance state and that trance states occur with great frequency even at other times. To look at how to make use of this concept I will first describe what I think treatment needs to address.

Trichotillomania as a symptom: My approach is to look at what the behavior of pulling means to a particular person, and what it means about them. I view pulling as a symptom which indicates something about what is going on in that person’s life and can be best understood if we look at the context in which it occurs – both over time (how did it evolve), and ecologically (how does it fit into the network of the person’s relationships, commitments, self-perceptions, experiences of their own body and emotional states, etc.).

Symptoms are an indication of the existence of some other process. Just as a fever may reflect a viral infection, a repetitive behavior reflects an underlying mental activity. The symptom develops in response to the activity and one of its functions is to achieve some control over the consequences of that mental activity. I believe that trichotillomania indicates an attempted solution to a psychological challenge (or opportunity) one is facing in one’s life. However, it is an ineffective solution for two reasons. Firstly, it doesn’t alter the situation which has become challenging, and so the underlying causes remain unchanged. Secondly, by drawing attention onto itself it obscures those underlying causes. It distracts attention from them.

But the behavior, none the less, does have some purpose and utility. It relieves the anxiety of becoming too aware that there are challenges and opportunities which one feels unprepared to confront.

The role of emotions:

The mechanism which could be drawing one’s attention to these challenges and opportunities is the experience of emotional reaction. Emotions serve to amplify our perceptions of situations by making the good seem better and the bad seem worse. In that way, they lead us to focus on what is important to us so that we will take action. Being able to notice and interpret our emotions is something we learn as we grow up. Emotions represent a kind of language for helping us make meaningful choices as we engage with life.

But if these emotions were felt to be too overwhelming – if what they indicated felt too bad to be tolerated because we did not learn how to resolve the situations they drew attention to – then we eliminated them from our emotional vocabulary and we restricted our awareness of them. Now, when those situations reoccur, rather than notice our feelings of hopelessness and helplessness, we may turn to other mechanisms, more basic ones rooted in physical sensations, to occupy ourselves and restore some sense of order to the world.

So, in this model, the behavior of hair pulling is not an indicator of psychological inadequacy, but rather a lack of awareness. It reflects a split between awareness/thoughts and sensations/feelings. It is the result of an unknown mental process, something one has not been able to assimilate into one’s conscious thought, for which no words or language have been developed.

If this could be understood then I believe there would be less justification for feelings of shame connected with Trichotillomania, because Trichotillomania represents an underlying process outside of personal awareness, and thus is not something voluntarily chosen. (It would also answer the following disturbing statement frequently made to hair pullers: “You could stop if you really wanted to.”)

I have so far described how emotional activity and unconscious thoughts affect us in ways which we do not recognize. Despite this lack of recognition, we still need to adjust to them and regulate or organize ourselves. A good example of this is the way in which a fussy baby, if not picked up or fed when it wants to be, learns to get its thumb into its mouth and suck on it. It is finding a way to organize its reactions to its world by retreating into an attitude of self-sufficiency. In this way it solves the problems of the conflict it experiences between the emotions it feels and the lack of a way to take effective action about them in the outside world. It restores order by returning to a sensation-based activity which it has control over. It has learned to retreat into a trance.

The similarities between this example and the experience of hair pulling are striking. So how is Trichotillomania like a trance, exactly?

Trance:

The (Oxford) dictionary defines “trance” in these ways: a suspension of consciousness; a state of mental abstraction from external things; absorption, exaltation, rapture, ecstasy. Going into a trance is turning away from the world, suspending engagement with it, and entering a twilight zone of self-enchantment. The experience is one of being in between states: neither in one’s own mind, nor aware of one’s body. One has turned away, both from the rest of the world and from the rest of oneself.

It is a state in which one doesn’t think about what one feels, and doesn’t act on what one feels. One has turned away from the parts of the self which are concerned with action and purposefulness. In the trance state, a part of the personality takes over which doesn’t care about anything (except the act of pulling) and ignores the existence of time or consequences to one’s actions. It is the opposite of the perfectionist attitude so common to many hair pullers. Becoming entranced in the act of reading, for example, one detaches from the here and now, and allows this part of the personality to “come out”: while the cat’s away, the mouse plays. It is a secure, dependable, magical place in which one can avoid dealing with the stimulation of one’s spontaneous emotional responses to life.

If we look again at the role of emotions as amplifiers of perceptions, we see that what is happening in this state is that one is neither thinking about, nor acting on, what the emotions could be indicating. And as they indicate what is important so that action can be taken, the trance state eliminates the possibility of taking the action required.

How does this detaching process become chronic?

I believe it is the result of repeated experiences of failing to take effective action on what one’s emotions tell one is important. This failure can have many causes, but the result is that these important situations become perceived as challenging and threatening because they are felt as over stimulating. To protect oneself from discomfort, one disassociates from the situation. The part of oneself which perceives or feels what is going on is split off from consciousness. What remains conscious is the part which doesn’t feel and which preserves a sense of order and calm. Gradually, a gap develops between this external presentation of the self – as coherent, caring, positive – and an inner state of feeling confused, frustrated, and overwhelmed.

A false self develops, a self which appears to be more in control than is actually felt, and which one tries to believe in. The fear of having this façade penetrated adds greatly to the level of stress felt by hair pullers. Because this false self cannot be dropped when one’s gut reactions tell one to, one becomes trapped in a vicious circle that leaves one over stimulated (including the times when one merely seems to be bored), detaching from one’s body, and trying to regain control. A strong need is felt to reconnect to the body and feel grounded.‍

Trichotillomania as a return to the body:

The route to feeling in one’s body again is through becoming hyperaware and hypersensitive to sensation. This is a more basic and elementary experience of oneself: one cannot think or feel what is happening, so one uses a physical behavior to establish a link between unconscious inner experience and being in the real, physical world. This provides a solution to the twilight state of feeling detached. The sensation-focused behavior provides a substitute sense of being connected, and its ritualistic aspect creates a sense of soothing order rather than chaos.

So, looked at in this way, the act of pulling a hair actually represents the second stage of entering into a trance. The trance is triggered by the habitual reaction of disassociating rather than facing a situation which one perceives as overwhelming. But while an attitude of order and calm is being adopted (a state of “mental abstraction”), the experience of being detached from the feelings in the body becomes disorienting and the urgent need is felt to focus on the sensation of touching, playing with, and pulling hair. This provides the experience of concreteness and connectedness which allows the trance to continue.

Awakening:

What is needed is a process for regaining consciousness and turning back to engaging with life. How does one wake up? How can one build a sort of observational platform from which to watch the process of entering into a trance; one which can be separate from the process itself? I would suggest that rather than start with the ultimate goal of avoiding trance states altogether (which may be unreachable), a more pragmatic approach would be to learn how to wake up once one starts.

When we drive long distances on freeways and our attention wanders, we sometimes find ourselves drifting over into the next lane. If there were raised lane markers on the road, they would then alert us by causing a noise and a vibration as the car drove over them. That is the kind of alarm system we are looking for. It doesn’t prevent our minds from wandering, but it brings us back to the here-and-now experience before we get into trouble.

Such a system does exist: it is the sensation of a hair being pulled out. Once one hair is pulled, the opportunity exists to break the trance. That hair can be a signal to come back to the here and now rather than getting into the trouble of starting a pulling binge. (The goal of stopping at one hair pulled would also very likely include the benefit of making it much easier to commit to a realistic process of bringing the behavior within tolerable limits.)

How can one learn to stop at just one? Setting such a goal becomes much more possible if one understands one’s reasons for avoiding the goal until now. I have discussed in this article how Trichotillomania is a process which provides an attempted solution to an underlying tension. There is an inevitable anxiety about relinquishing a familiar, dependable behavior. A part of oneself therefore resists changing it and depends on the benefits it brings. This part has no intention of allowing any changes to occur unless one is prepared for the emotional experiences that follow, and it protects one from them.

A way to understand this resistance to change would be to think of the patterns of our behavior as a balanced mobile hanging from the ceiling. All its parts are interconnected and form a stable pattern. If we remove one of the parts, all of the others start to swing wildly until they settle into a new, substantially different formation. The intermediate stage of unbalanced, indeterminate movement could be likened to the feeling of overstimulation from one’s emotions when the ritualistic trance is denied.

To prepare for this change, an expanded awareness of emotional experience and what it teaches is indispensable. The remainder of this article offers some suggestions for work that can be done alone to expand this ability. This task is made much easier and more effective, however, when it is done in the context of a healing dialogue: either in individual or group therapy, or in a support group. This option deserves serious consideration because the act of communicating to another person helps bring one’s inner experiences into focus. Additionally, when there is the trust that the other person is willing not only to listen but to actively attempt to grasp what the speaker means from the speaker’s own point of view, the feeling of validation and recognition received makes awareness of the emotional states more bearable.

Reading the signals:

Part of the personal preparation which can be done is to establish intent to learn from what is found when one tries to read the signals. This would require a willingness to recognize that there are good reasons for what one feels rather than prejudging emotions as wrong, inappropriate, or proof of all the “bad” things one has come to believe about oneself. It also requires a willingness to feel discomfort, hurt, and vulnerability so that there can be a return to wholeness and the sense of being fully alive.

1. The most direct step is simply to ask yourself questions such as: What am I feeling? What is on my mind? Is something bothering me? What do I want right now? Is there something I should be doing? Special attention should be paid to the first answer that comes to mind, even if it very quickly disappears or seems insignificant. You should have an open mind and be prepared to be surprised. Before asking yourself these questions, stop the activity you are doing, if possible. If answers do not emerge the following techniques can be tried.

2. Let your body speak. Allow yourself to become aware of where you feel tension or discomfort. Imagine that that part of you has a voice and can answer the questions in Step One. Try asking follow-up questions to learn more.

3. Try exaggerating the physical state that you are in. That is, whatever movement your body is making or would like to make, take it to an extreme as if you were a very melodramatic actor or dancer who had no inhibitions. Again, think about how your body is expressing answers to the questions in Step One.

4. Visualize yourself as a child of about five and ask the questions of her or him. The answers should seem to be in the language of a 5-year-old. It might help to hold an object such as a cushion or stuffed animal to you as you try to make contact with yourself in this way. It also might help to combine this with some exaggeration of body expression. Additional questions you might ask could be: What do you need from me? Is somebody upsetting you? (See Reference 1.)

5. Write a question to the child, then switch your pen to your other hand and write the answer with that hand. You should write very quickly and with no attempt to make the writing more legible. Then switch your pen back to your original hand for a further question. Continue the dialogue, and the switching of hands, until no further clarification is necessary. The purpose of this technique is to facilitate the spontaneous flow of ideas. (See Reference 2.)

6. Write out the questions as complete sentences to be completed and complete the same question five times as quickly as possible. The questions would be rewritten as follows: Right now, I want….; or: I am upset because…. Allow any response to come forward. Often, a few unrevealing responses will be followed by one unexpected and more valuable one. (See Reference 3.)

7. Hold the hair which has just been pulled out and ask yourself: What did this hair give itself up for? A significant reason for the failure to stop hair pulling is the frequent presence of trance states, which enable one to deny the consequences of the behavior. Additionally, the experience of trance encourages one to focus on physical sensations such as the feeling of a hair being pulled, so as to achieve a greater sense of being connected to reality.

I have described how one enters a trance when certain situations trigger a habituated expectation of becoming overwhelmed. In self-defense one suspends consciousness of the challenge and retreats into a state of emotional detachment. The alternative to the trance, then, is to identify and assimilate the emotional cues about the situation so that appropriate action can be taken. The sensation of the first hair being pulled can serve as an alarm to awaken one from the trance and begin this process of self-evaluation and a return to an alert engagement with life.

Reference 1: Margaret Paul. Inner Bonding. San Francisco: Harper Collins, 1990.Reference 2: Lucia Cappachione. The Power of Your Other Hand. North Hollywood, CA: Newcastle Publishing, 1988.Reference 3: Nathaniel Branden. How to Raise Your Self-Esteem. New York: Bantam, 1987.

The post Awakening from the Trance appeared first on International OCD Foundation.

Posted on

Drug Target for Fragile X Syndrome Identified Through Preclinical Study

UCLA Health researchers have identified a potential drug target for treating fragile X syndrome (FXS), the most common genetic cause of intellectual disability and autism that affects roughly one in 2,000 boys.

Fragile X syndrome is caused by a mutation in a single gene, FMR1, that results in the loss of a protein critical for normal brain development and function. Headed by Carlos Portera-Cailliau, MD, PhD, professor of neurology at UCLA and member of the UCLA Brain Research Institute, the researchers, the team’s work in genetically engineered mice lacking the Fmr1 gene identified the synaptic protein EPAC2 as a potential therapeutic target for fragile X syndrome. Their study showed that blocking EPAC2 in the fragile X mouse model restored abnormal patterns of brain activity and improved several FXS-associated behavioral symptoms.

Pertera-Cailliau is senior and corresponding author of the researchers published paper in Neuron, titled “Translatome profiling reveals opposing alterations in inhibitory and excitatory neurons of fragile X mice and identifies EPAC2 as a therapeutic target.”

Fragile X syndrome is a prototypical neurodevelopmental disorder (NDD) characterized by intellectual disability, social anxiety, atypical sensory processing characterized heightened sensitivity to sensory input such as sound and touch, and a higher risk of seizures. Many also meet the criteria for an autism spectrum disorder diagnosis. “Symptoms of fragile X syndrome (FXS), the leading monogenic cause of intellectual disability and autism, are thought to arise from an excitation/inhibition (E/I) imbalance,” the authors stated.

FXS is caused by mutations in the FMR1 gene, resulting in near complete loss of the fragile X messenger ribonucleoprotein (FMRP), an RNA-binding protein in neurons that plays different roles in cell compartments including the nucleus, axons and dendrites, including regulating mRNA translation at synapses, they explained. As it is caused by a change in a single gene, fragile X syndrome has long been considered a promising candidate for targeted therapies yet clinical trials to date have not produced an effective treatment. “Since the discovery of the genetic basis of FXS in 1991, several clinical trials have been undertaken—without success—and no specific treatments for FXS are currently available,” the investigators continued. “Thus, there is an urgent need to rethink therapeutic strategies for FXS.”

For their newly reported study the researchers used genetically engineered knockout (KO) mice that lack Fmr1 to simulate fragile X syndrome. Using genetic sequencing, they found that levels of the gene EPAC2 were increased in the brain of fragile X mice. This was of potential interest as a target for therapy because the gene’s protein, EPAC2, is localized to synapses and is known to be important for learning and memory.

The researchers then demonstrated that blocking EPAC2 in the fragile X mouse model, either genetically, or using an EPAC2 inhibitor compound, restored cortical circuit function and improved multiple behavioral symptoms associated with fragile X syndrome, including heightened sensitivity to touch, difficulties with social interaction and their susceptibility for seizures. “Perhaps the most exciting result is that treatment with an EPAC2 antagonist can rescue several behavioral phenotypes in Fmr1 KO mice,” the authors stated.

“EPAC2 emerged as an attractive target because it was consistently altered across multiple types of brain cells in our analysis,” said the study’s first author Anand Suresh, PhD, a post-doctoral fellow in the laboratory of Portera-Cailliau. “When we blocked it, either genetically or with a drug compound, we saw meaningful improvements in both brain circuit function and behavior.”

EPAC2 is expressed almost exclusively in the brain, which means drugs targeting it are less likely to cause unwanted effects elsewhere in the body. Suresh said this is an important consideration as researchers continue preclinical studies. “This bodes well for future preclinical trials and safety studies in humans, as compounds that target EPAC2 should not have off-target effects,” the authors stated in their report.

For their study the UCLA investigators used an RNA sequencing technique to examine gene activity separately in two major classes of brain cells: those that excite and those that inhibit neural activity. Fragile X syndrome is thought to arise from an imbalance between these two systems. The analysis revealed striking differences in how the genetic mutation underlying Fragile X syndrome affects each cell type but also identified a small set of genes, including the one that encodes EPAC2, that were dysregulated in both.

The researchers also found that EPAC2 levels appear to rise gradually as the brain matures, suggesting it may be a particularly relevant target for older children and adults with Fragile X syndrome, rather than only in early development. They concluded, “Our results should encourage the development of novel EPAC2 inhibitors for the treatment of FXS. More generally, our study exemplifies how transcriptomic approaches in animal models of neuropsychiatric conditions can be used to prioritize potential novel therapeutic targets.”

The post Drug Target for Fragile X Syndrome Identified Through Preclinical Study appeared first on GEN – Genetic Engineering and Biotechnology News.

Posted on

Neurocognitive function among individuals with problematic social media use

BackgroundWith the development of technology and the internet, social networks gained momentum quickly and play a central role in daily activities. Despite this, there is a public health concern over excessive or problematic social media use. There is also a debate whether excessive social media use should be considered as a behavioral addiction characterized by impulsivity or an impulse control disorder characterized by compulsivity. The goal of this study is to use neurocognitive tasks to investigate impulsivity and compulsivity among excessive social media users compared with non-excessive users.MethodThe study included 79 participants (age range 18 to 37), divided into two groups: 34 participants who excessively use social media (Mean Age = 23.03, SD = 2.71) and 45 participants who do not excessively use social media (Mean Age = 25.47, SD = 4.3). Participants filled out a demographic questionnaire, questionnaires on social media use, impulsivity, compulsivity, anxiety, and depression. They performed computerized cognitive tasks: GO/NO-GO (with Facebook and traffic sign pictures), Experimental Delay Discounting (EDT), and the Wisconsin Card Sorting Test (WCST).ResultsExcessive users of social media exhibited a lower ability to delay gratification on the EDT, indicating impulsivity. They made fewer non-perseverative errors on the WCST, which indicated high flexibility and test shifting, which is a contradicting evidence for compulsivity. Furthermore, on the GO/NO-GO task, individuals who excessively use social media made more omission errors in response to the “Facebook” sign compared to traffic signs (GO condition), indicating impaired selective attention. Finally, they also showed higher subjective ratings of anxiety, depression, impulsivity, and compulsivity.DiscussionThe results of this study provide evidence for impulsivity indicated by delay discounting tendency, which supports the behavioral addiction model, impaired selection attention and lack of evidence for compulsivity in excessive social media users. Further research on neurocognitive function in excessive social media users is required in order to determine whether it should be considered a behavioral addiction or an impulse control disorder.
Posted on

Reducing Intrusive Trauma Memories Using a Brief Mental Imagery Competing Task Intervention: Case Series of Trauma-Exposed Women in Iceland

Background: There is a need for scalable and simple interventions for trauma-exposed people. In this case series, we built on our previous case study and case series findings and further explored the use and potential effectiveness of a brief novel intervention to reduce the number of past intrusive memories of trauma. The imagery competing task intervention consists of a memory reminder and the visuospatial task Tetris played with mental rotation, targeting 1 intrusive memory at a time. Here, we test remote delivery of the intervention, including guidance from researchers without specialist mental health training, in a sample of women in Iceland with current intrusive memories from trauma. Objective: In a case series of trauma-exposed women, we aimed to explore whether this brief novel intervention reduces the number of established intrusive memories (primary outcome) and improves general functioning and symptom reduction in posttraumatic stress, depression, and anxiety (secondary outcomes). The acceptability of the intervention along with adaptations, that is, delivery by psychology students without specialist mental health training and digital delivery, was explored. Methods: Participants (N=8) monitored the number of intrusive memories from an index trauma (occurring 3‐16 years previously) in a daily diary at baseline, during the intervention, and postintervention at 1-month and 3-month follow-ups. The intervention was delivered digitally with guidance from clinical psychologists or psychology students. A repeated AB design was used (“A”: preintervention baseline, “B”: intervention phase). Intrusions were targeted one by one, creating repetitions of an AB design (ie, length of baseline “A” and intervention “B” varied for each memory). Results: The number of intrusive memories reduced for all participants from the baseline phase compared with the intervention phase, although the reduction was minimal for 2 participants (6.3%‐93%). The number of intrusive memories continued to reduce for 6 out of 8 participants (58%‐100% reduction at 1-month follow-up; 72%‐100% reduction at 3-month follow-up). Symptoms of posttraumatic stress, depression, and anxiety were reduced for most participants postintervention and continued to decrease during the follow-up periods. Functioning was improved for 7 of the 8 participants from baseline to postintervention and continued to improve at the follow-up assessments for 3 participants. The intervention delivered digitally and partly by students was perceived to be an acceptable way to reduce the frequency of intrusive memories by all participants (mean rating 9.5 out of 10). Conclusions: Data from this case series of traumatized women provide preliminary evidence for the effectiveness of this novel brief intervention in reducing intrusive memories of trauma occurring several years ago and in improving functioning and reducing core symptom burden. This study will inform a randomized controlled trial of this novel intervention, which may have considerable implications for large-scale clinical management of traumatized populations. Trial Registration: ClinicalTrials.gov NCT04209283; https://clinicaltrials.gov/study/NCT04209283 International Registered Report Identifier (IRRID): RR2-10.2196/29873
<img src="https://jmir-production.s3.us-east-2.amazonaws.com/thumbs/0ee87211be76a539e221eafe3d6346f8" />

Posted on

Context-dependent interaction between oxytocin gene polymorphisms and alcohol dependence in modulating negative emotions during acute alcohol withdrawal in adult males

ObjectiveThe importance of multiple gene-environment interaction (G × E) has been highlighted in understanding the etiology of negative emotions. This study examines the impact of oxytocin (OXT) polymorphisms (rs2740210, rs6133010, and rs2740209) in combination with alcohol dependence on anxiety and depression symptoms during acute alcohol withdrawal under different social and environmental contexts.MethodA total of 414 Chinese Han male adults undergoing acute alcohol withdrawal were recruited. Participants provided blood samples for genotyping, self-reported measures of depression and anxiety, assessments of alcohol dependence severity, and demographic information regarding social and environmental contexts.ResultsResults revealed a positive correlation between severity of alcohol dependence and symptoms of depression and anxiety, while oxytocin polymorphism did not have a direct effect on depressive and anxiety symptoms. A significant interaction between OXT polymorphism (rs2740210 and rs2740209) and alcohol dependence in relation to anxiety symptoms solely among adults living with family and/or those who were married was observed. Further analyses indicate that the GG and CC genotypes are risk genotypes, while the T allele (rs2740210) and G allele (rs2740209) are non-risk alleles in the interaction between OXT genotypes (rs2740210, rs2740209) and alcohol dependence on anxiety among the aforementioned participants.ConclusionsThese findings provide evidence for distinct G × E interaction effects on anxiety and depression symptoms during acute alcohol withdrawal, supporting the weak diathesis-stress model. Furthermore, the study highlights the importance of considering environmental factors when investigating the role of oxytocin as a biological substrate underlying social bonding and the regulation of negative emotions.
Posted on

Contact Lenses Show Promise for Depression

Using specialized contact lenses to stimulate the brain could offer a novel route to treating depression, preclinical research suggests.

The research, in mice, demonstrates how wearable neuromodulation devices can provide a versatile platform for mood and other brain disorders.

It brings eye-based neurotherapies a step closer towards clinical reality and reveals the feasibility of using contact lenses as a bioelectronic strategy for the treatment of depression.

The findings appear in the latest issue of Cell Reports Physical Science.

“Our work opens up an entirely new frontier of treating brain disorders through the eye,” said lead author Jang-Ung Park, PhD, from Yonsei University.

“We believe this wearable, drug-free approach holds tremendous promise for transforming how depression and other brain conditions are treated, including anxiety, drug addiction, and cognitive decline.”

Depression is increasingly recognized as a disorder involving structural and functional abnormalities in brain networks.

Conventional treatments—such as pharmacological therapy, electroconvulsive therapy, and deep brain stimulation—target these abnormalities but can be invasive and are often limited in their efficacy or tolerability.

Park and team note that the eye provides a compelling gateway for indirect brain modulation due to its embryological derivation from the brain and extensive connectivity.

Studies also suggest that visual impairment with higher prevalence of depression, further recognizing the importance of the eye-brain axis.

To investigate this avenue further, the researchers developed a contact lens that uses transcorneal electrical stimulation (TES) based on temporal interference (TI) to stimulate the brain. This delivers two electrical signals to the retina, which only become active where they intersect, allowing specific areas of the brain to be targeted.

The platform circumvents the invasiveness and limited tolerability of conventional brain stimulation therapies by using the retina as a precise interface for the eye-brain axis.

Electrodes made from ultrathin layers of gallium oxide and platinum allow the lens to be flexible and transparent, conforming to the cornea and preserving natural vision.

The researchers examined the efficacy of the lenses in a stress-induced mouse model that recapitulated key behavioral and biological features associated with depression.

Depressed mice received either no intervention, temporal interference, or the SSRI fluoxetine and were compared with control mice that were not depressed before and after treatment. Machine learning was applied for comprehensive efficacy evaluation.

The team reported that the lenses restored behavioral, neural, and biological deficits in depression.

TI-TES enhanced behavioral resilience, restored prefrontal-hippocampal oscillatory synchrony, and normalized depression-related biomarkers.

When machine-learning integration was used to integrate behavior, brain activity, and biomarkers, it consistently grouped the mice with lenses with the non-depressed control mice rather than the untreated depressed mice.

The researchers acknowledge their research is in its early stages, and that the current study employed a wired configuration to ensure precise waveform control and stimulation stability during proof-of-concept validation.

“Like any new medical technology, our contact lenses will need to go through rigorous clinical evaluation in patients before reaching the market,” said Park.

“Next, we plan to make the lens fully wireless, test it for long-term safety in larger animals, and personalize the stimulation for each user before advancing into clinical trials in patients.”

The post Contact Lenses Show Promise for Depression appeared first on Inside Precision Medicine.

Posted on

I’m scared of everything — what does it mean and how do I get over it?

What you’re describing sounds really overwhelming. I’m glad you reached out. The fears you mention — being scared of doing something against your will, worrying you might not have control, and feeling intensely concerned about being judged — are patterns I often see in people with anxiety and, sometimes, people with obsessive-compulsive disorder (OCD). A hallmark of OCD is a deep doubt about control: the fear that you might act in a way that goes against your values, even though you don’t want to. These kinds of fears are called intrusive thoughts. While intrusive thoughts can feel very real and frightening, they are not things you actually intend to do or predictions of things that you will do — they’re unwanted experiences that don’t define you.

Avoiding sports and other things for fear of being judged is also a symptom of anxiety. I can understand how hard it is to tell your family what you’re going through, especially if you have felt ignored in the past. At the same time, your pain deserves to be heard and taken seriously. I encourage you to try talking to your parents again, but if you truly feel like you can’t, consider telling one safe person — whether that’s another family member, a school counselor, or even a teacher you trust. You can write how you’re feeling in a note if speaking feels too hard.

The physical symptoms you mentioned — neck and shoulder pain, fidgeting — are also common in anxiety because our bodies can hold tension when our brains are on high alert. What this likely means is that your brain is caught in a fear loop, constantly scanning for danger around control and judgment.

The good news is that this is very treatable. A mental health professional may recommend a type of cognitive behavioral therapy called exposure and response prevention (ERP). ERP helps you gradually face the situations or thoughts you fear instead of looking for reassurance from someone else or avoiding those situations or thoughts altogether. Over time, ERP teaches your brain that thoughts are just thoughts, not actions, and that you can tolerate uncertainty without something bad happening.

For now, you might try gently labeling upsetting thoughts as anxiety, not facts, and practicing not accepting them as true when they show up. Taking small steps toward what you’ve been avoiding can help you rebuild your confidence, even if it feels uncomfortable at first.

While you can practice managing anxiety or intrusive thoughts on your own, it’s better to have help. Once you talk to someone you know and trust, have them help you reach out to a mental health professional who can provide a more thorough assessment and the appropriate treatment for you. You don’t have to go through this alone, and with the right support, this can get much better.

The post I’m scared of everything — what does it mean and how do I get over it? appeared first on Child Mind Institute.

Posted on

Direct modulation of human GABA-A α1β2γ2 receptors by the endocannabinoid 2-arachidonoylglycerol: implications for cannabinoid-related ligands and limitations for anxiolytic drug development

Anxiety disorders are associated with impaired inhibitory neurotransmission mediated by γ-aminobutyric acid type A (GABA-A) receptors. Although benzodiazepines remain effective anxiolytics, their clinical utility is limited by sedation, cognitive impairment, tolerance, and dependence, prompting the search for mechanistically distinct GABAergic modulators. Among cannabinoid-related molecules, the strongest evidence for direct GABA-A receptor modulation concerns the endocannabinoid 2-arachidonoylglycerol (2-AG), which potentiates recombinant human α1β2γ2 receptors through residues located in the M4 helix of the β2 subunit. Here, we review the structural architecture, biophysical properties, and pharmacological profile of the human GABA-A α1β2γ2 isoform as the relevant molecular framework for evaluating this mechanism, while discussing the broader relevance of cannabinoid-related ligands and selected phytocannabinoids without assuming mechanistic equivalence. We further assess the hypothesis that 2-AG reaches the β2-M4 site through a membrane-access route and identify five conceptual barriers that currently limit translation of this mechanism into anxiolytic drug development: supraphysiological effective concentrations, unresolved synaptic-versus-extrasynaptic actions, uncertain subtype selectivity, incomplete validation of lipid-environment effects, and lack of clinical evidence linking this mechanism to anxiolysis in humans. We conclude that direct modulation through β2-M4 defines a mechanistically intriguing allosteric pathway distinct from benzodiazepine action; however, its location on a shared β2 subunit and the micromolar concentrations required for modulation represent substantial obstacles to the rational design of anxioselective agents based on this mechanism.
Posted on

Internalizing and externalizing pathways to internet gaming disorder: the roles of anger and social anxiety

BackgroundInternet Gaming Disorder (IGD) represents a significant behavioral health concern, yet the roles of internalizing and externalizing psychological vulnerabilities in its development remain underexplored, particularly in Arabic-speaking populations.ObjectiveThis study examined anger and social anxiety as distinct externalizing and internalizing predictors of IGD severity in a Saudi Arabian community sample.MethodsA cross-sectional survey was administered to 303 participants (60.1% female; estimated mean age = 29.79 years, SD = 8.83) across five regions of Saudi Arabia. Participants completed the Internet Gaming Disorder Scale–Short Form (IGDS9-SF), a three-item Anger Screening Scale, and a two-item Social Anxiety screener. Hierarchical linear regression and structural equation modeling (SEM) were conducted to examine unique and incremental contributions of anger and social anxiety to IGD symptoms.ResultsAnger and social anxiety were strongly intercorrelated (r = .86, p <.001) but demonstrated divergent patterns in multivariate models. Hierarchical regression indicated that both predictors contributed unique variance when entered simultaneously, with anger positively and social anxiety negatively predicting IGD after controlling for shared variance. However, SEM clarified that only social anxiety significantly predicted latent IGD severity (β = .32, p = .027), whereas anger did not (β = .07, p = .68). The final model explained approximately 13% of variance in IGD symptoms.ConclusionsSocial anxiety was associated with IGD severity as a distinct internalizing correlate, consistent with avoidance-based coping and online social preference accounts. These preliminary, cross-sectional findings suggest that social anxiety warrants consideration in future IGD screening and research efforts in Arabic-speaking contexts.