Southlake Psychiatric & Counseling Center

10/08/2025

https://apple.news/AiJ1IQni4TKWbRaeni__1lQ

What if a protein could be injected to help heal both "leaky gut" and severe depression? New research from the University of Victoria (UVic), published in Chronic Stress, shows that a glycoprotein called reelin may one day be able to do just that.

10/08/2025

https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3003399

Sleep can be a marker of health but is often only investigated from a single dimension such as sleep duration or cognitive performance. This study identifies five sleep-biopsychosocial profiles that link self-reported sleep patterns to inter-individual variability in health, cognition and lifestyle....

09/17/2025

Ketamine repairs reward circuitry to reverse stress-induced anhedonia

by Eric W. Dolan July 9, 2025in Depression, Ketamine

A single low dose of the anesthetic ketamine restored the ability to enjoy sweet treats and social contact in mice that had been made apathetic by long-term stress, according to new research published in Neuron. The same injection also repaired weakened connections onto a specific group of reward-related brain cells. When those repaired connections were blocked, the animals’ recovery disappeared—suggesting the synaptic fix is a key part of ketamine’s sustained antidepressant effects.

Originally developed as an anesthetic in the 1960s, ketamine has more recently drawn attention for its fast-acting antidepressant properties. Over the past two decades, clinicians have found that sub-anesthetic doses can lift mood within hours in many people with major depression who do not respond to conventional medications. That rapid action stands in contrast to commonly prescribed drugs like selective serotonin reuptake inhibitors, which often take weeks to alleviate symptoms.

One symptom of depression that appears to respond especially well to ketamine is anhedonia—the loss of pleasure in normally rewarding experiences. Yet it remains unclear which brain circuits are responsible for the drug’s lasting effects on mood and motivation. The new study set out to identify those changes down to the level of individual synapses.

“Depression is a leading cause of morbidity and mortality worldwide, and it is projected to become the second leading cause of disability by 2030,” said study author Marco Pignatelli, an assistant professor of psychiatry at Washington University School of Medicine in St. Louis.

“Despite the urgent need to address depression as a public health priority, current pharmacotherapies require prolonged administration—weeks, if not months—for clinical improvement, and are often associated with high non-response rates. In contrast, a single sub-anesthetic dose of ketamine induces a rapid antidepressant effect in about 70% of treatment-resistant patients.”

“Importantly, this improvement often occurs within the context of anhedonia,” he added. “Conventional antidepressants do poorly in relieving anhedonia, which is one of the two core symptoms used to diagnose major depression. That makes ketamine a promising and unique pharmacological option. However, without understanding the circuits and synapses that support this effect, our ability to design safer, more targeted medications is limited.”

To model anhedonia in mice, the researchers implanted slow-release corticosterone pellets under the animals’ skin to mimic chronic stress. Over three weeks, the hormone reduced the animals’ interest in sweetened water, decreased time spent with other mice, and lowered their willingness to work for rewards in a progressive ratio task where nose-pokes earned sugar pellets.

Twenty-four hours before each test, half the stressed mice received a single injection of ketamine at 10 milligrams per kilogram—a dose well below what’s used for anesthesia. The rest received saline, as did a group of unstressed control mice. Ketamine restored reward-seeking behavior across all tasks, while saline had no effect. The drug did not increase overall activity levels, ruling out general stimulation as an explanation.

To uncover what had changed in the brain, the researchers prepared thin slices from another group of similarly treated mice and recorded electrical activity in the nucleus accumbens, a key hub for processing reward. They focused on medium spiny neurons that express dopamine receptor type 1, a subtype linked to motivation and approach behavior.

Chronic stress reduced the strength and frequency of excitatory inputs to these neurons, but ketamine reversed this effect within a day—possibly as soon as one hour after injection. These changes were not observed in neighboring neurons that express dopamine receptor type 2, highlighting the cell-type specificity of the effect.

To test whether these restored synapses were necessary for ketamine’s behavioral benefits, the researchers used a molecular technique to block them. They introduced a HaloTag protein into dopamine receptor type 1 neurons, allowing them to tether a glutamate receptor blocker to just those cells. Delivering the blocker into the nucleus accumbens 24 hours after ketamine erased the previously observed improvements in sugar preference, sociability, and motivation. Blocking the same receptors on dopamine receptor type 2 neurons had no effect, pinpointing the importance of the type 1 cells.

The team then asked whether strengthening the same synapses—without ketamine—would be enough to reverse anhedonia. They inserted a light-sensitive version of Rac1, a protein that clusters glutamate receptors, into the dopamine receptor type 1 neurons. Mice exposed to blue light showed restored motivation and sociability, while exposure to red light had no effect. The findings suggest that targeted synaptic enhancement alone can substitute for ketamine in relieving anhedonia.

To identify where the restored signals were coming from, the researchers injected a light-activated protein into several brain areas that send input to the nucleus accumbens. They found that chronic stress weakened glutamatergic connections from the medial prefrontal cortex and ventral hippocampus—regions involved in decision-making and memory. Ketamine restored both pathways but did not affect inputs from the amygdala, thalamus, or ventral tegmental area.

Further analysis revealed distinct mechanisms for each pathway. The prefrontal input gained stronger unitary synaptic responses, while the hippocampal input showed both stronger responses and increased release events. These changes indicate different modes of adaptation at the two inputs.

To confirm that both inputs were required for ketamine’s effects, the team used a two-virus strategy to express a designer inhibitory receptor specifically in either the prefrontal or hippocampal projection to the nucleus accumbens. Administering a drug that silenced the targeted neurons before ketamine blocked the behavioral rescue.

Interestingly, the type of failure depended on which pathway was silenced. Turning off the ventral hippocampal input delayed the animals’ first approach to a social partner and the first attempt to obtain a reward. In contrast, silencing the prefrontal input did not affect initiation, but reduced overall engagement. These results suggest that hippocampal input helps trigger reward-seeking, while prefrontal input helps sustain it.

“We’ve uncovered a brain mechanism through which ketamine restores reward-related behavior after chronic stress in mice, and we believe these mechanisms are likely conserved across species,” Pignatelli said. “That makes this discovery relevant for clinical applications.”

But, as with all research, there are limitations. “It is always important to highlight that our mechanistic studies are taking place by using murine animal models,” Pignatelli noted. “In general, the findings of a study in mice may not directly translate to humans or other species, but they offer valuable insights into biological processes within that model.”

Future studies could use brain imaging to examine whether similar changes occur in patients who recover from anhedonia after ketamine treatment. Identifying specific synapses that support antidepressant effects may eventually allow researchers to design drugs that improve motivation without the dissociative side effects associated with ketamine.

“I hope that results from this body of work will have a sustained impact on the field by propelling the rational design of more targeted treatments, thereby facilitating more effective and safer therapies aiming at alleviating anhedonia,” Pignatelli said.

The study, “Ketamine rescues anhedonia by cell-type- and input-specific adaptations in the nucleus accumbens,” was authored by Federica Lucantonio, Jacob Roeglin, Shuwen Li, Jaden Lu, Aleesha Shi, Katherine Czerpaniak, Francesca R. Fiocchi, Leonardo Bontempi, Brenda C. Shields ,Carlos A. Zarate, Jr., Michael R. Tadross, and Marco Pignatelli.

09/17/2025

Psychiatric Disorders and Brain Structure Connected via Genetic Mapping
August 12, 2025


Researchers have long hypothesized that the genes influencing the architecture of the brain also play a role in determining mental health; however, the precise relationship between genetic predisposition for mental illness and the brain’s physical structure remains ambiguous. A recent study in Nature Mental Health, utilizing extensive datasets in genetics and neuroimaging, has elucidated connections in remarkable detail, uncovering a genetic network that associates psychiatric disorders with the structural composition of the cerebral cortex.

Genetic untangling of psychiatric disorders and brain structure

Psychiatric disorders are significantly impacted by genetics and frequently correlate with observable alterations in brain anatomy—variations evident not only in patients but also in their unaffected relatives and individuals with elevated genetic susceptibility. Extensive genome-wide association studies (GWAS) have demonstrated that brain structure is significantly heritable, with attributes like cortical surface area and thickness influenced by specific genetic mechanisms.

Surprisingly, only a limited number of genetic loci have been identified that affect both psychiatric risk and brain morphology, and conventional analytical techniques may overlook significant overlaps. This discrepancy arises because common methodologies, such as global genetic correlation or polygenic risk scoring, may underestimate shared influences when genetic variants affect the two traits in opposing directions. Standard statistical tools often miss shared genetic influences if the effects move in opposite directions. A variant might, for example, increase the thickness of one brain region while decreasing it in another.

To explore these associations, researchers from the University of Pennsylvania and the Children’s Hospital of Philadelphia examined genome-wide association study (GWAS) results from nearly 900,000 individuals of European ancestry, incorporating data from the Psychiatric Genomics Consortium on eight disorders: attention deficit hyperactivity disorder, alcohol use disorder, anxiety, autism, bipolar disorder, major depression, post-traumatic stress disorder, and schizophrenia.

Utilizing high-resolution MRI measurements from the UK Biobank and the Adolescent Brain Cognitive Development (ABCD) Study—the most extensive longitudinal investigation of brain development and child health in the United States—they quantified two critical attributes of the cortex: surface area, indicative of the cortex’s expanse across the skull, and cortical thickness, denoting the depth of the gray matter layer. These two measures possess unique biological origins and lack genetic correlation, indicating that the genes affecting one are frequently dissimilar to those affecting the other.

Seeing genetic and structural patterns

To accommodate bidirectional values, the researchers employed a Bayesian-based “conjunctional false discovery rate” methodology, capable of identifying shared variants regardless of whether their effects coincide or diverge. This strategy identified 55 genetic loci associated with psychiatric disorders and cortical surface area and 29 associated with psychiatric disorders and cortical thickness.

Not all genetic effects moved in the same direction. For most disorders, risk alleles were associated with either greater cortical thickness or smaller surface area, but this relationship was not universal. In schizophrenia, for example, there was a balanced mix: some variants tied to greater thickness, others to less, even within the same brain region. This bidirectionality may help explain why previous studies found low overall genetic correlation between psychiatric disorders and brain measures. By treating all variants as moving in the same direction, those earlier analyses may have missed the genetic tug-of-war happening beneath the surface.

The shared genetic loci were enriched in genomic regions active in the brain and involved in processes such as synaptic organization, neuronal development, and metabolism. Many overlapped with genes differentially expressed in the postmortem brains of people with psychiatric disorders. Still, the overlap was not uniform. Autism and PTSD, for example, sometimes showed opposite genetic effects on the same brain structures, such as the dorsal prefrontal cortex, echoing earlier neuroimaging findings that the two conditions can be associated with different patterns of cortical change. While the research identifies genetic variants linked to both brain structure and psychiatric disorders, it does not prove that one causes the other. Both may arise from overlapping mechanisms acting through shared molecular pathways during brain development.

To further delineate the neuroanatomical profile of shared genetic influences between regional brain structure and risk for psychiatric disorders, the researchers turned to an approach called FUMA. This integrative web-based platform facilitates functional annotation of GWAS results, gene prioritization, and interactive visualization while accommodating positional, expression quantitative trait loci (eQTL) and chromatin interaction mappings, and provides gene-based pathway and tissue enrichment results.

Shared genetic influences were distributed along a hierarchical axis of the cortex. At one end lay the primary sensorimotor and visual cortices, regions specialized for basic perception and movement, which showed strong links with genetic risk for conditions like ADHD, bipolar disorder, and schizophrenia. At the other end sat the association cortex, involved in more complex and internally focused thought, which showed different patterns of overlap, particularly for surface area in depression, ADHD, and bipolar disorder. This organization mirrors known gradients in cortical gene expression and neural connectivity seen across species.

Limitations and future directions

These findings offer one of the clearest pictures yet of how shared genetics can shape both mental illness risk and brain anatomy—and why the relationship is anything but straightforward. They also underscore the need for more nuanced genetic tools. Instead of boiling down risk to a single polygenic score, future research could develop pleiotropy-enriched scores that account for both converging and diverging effects. While the research identifies genetic variants linked to both brain structure and psychiatric disorders, it does not prove that one causes the other. Both may arise from overlapping mechanisms acting through shared molecular pathways during brain development.

The study’s scope was limited to individuals of European ancestry, meaning it remains unclear whether the same patterns hold across more diverse populations. Extending the research to encompass global datasets is essential to facilitate the equitable dissemination of genetic insights. By pinpointing these shared genetic factors, scientists may eventually uncover biological targets for prevention or treatment and better understand why some genetic risks manifest differently in different people. For now, these results serve as a reminder that the relationship between mental illness and brain structure is not linear, but rather a complex web of connections, which genetics is gradually unraveling.

09/17/2025

Genetic link found between su***de risk and brain structure in large-scale study

by Eric W. Dolan August 13, 2025in Mental Health, Neuroimaging


People with a higher genetic predisposition to attempting su***de tend to show differences in brain structure, according to a new study published in the journal Human Brain Mapping. The researchers found that specific genetic markers associated with su***de attempt risk also overlap with those related to brain volume, particularly in subcortical regions involved in emotion, reward, and cognitive control.

The findings point to a small but statistically meaningful genetic correlation between su***de attempts and total brain volume, and suggest that shared genetic influences may be expressed in distinct ways across development. While previous studies have independently tied suicidal behavior and brain structure to genetic factors, this new research indicates that they may be more intertwined than previously understood.

Su***de attempt is one of the strongest predictors of su***de death and remains a pressing global health concern. Although environmental stressors, psychiatric conditions, and trauma history contribute to risk, there is growing recognition that su***de also has biological underpinnings. Large-scale genetic studies have identified heritable components of suicidal behavior, and structural brain changes have been reported in individuals with a history of su***de attempts.

However, researchers have yet to fully determine whether these biological features share a common genetic basis. If su***de risk and variations in brain morphology stem from overlapping genetic pathways, identifying those regions and gene sets could help reveal new targets for intervention or prediction. The new study aimed to clarify the degree to which the genetic architecture of su***de attempt overlaps with regional brain volume in both adults and adolescents.

“My colleagues and I were specifically interested in determining whether genetic risk for su***de behaviors could be reflected in neurodevelopmental differences early in life. Su***de behavior is very difficult to predict, and understanding risk factors for suicidal behavior early in development prior to the emergence of these behaviors could be one avenue towards prevention,” said study author Jill A. Rabinowitz, an assistant professor at Robert Wood Johnson Medical School at Rutgers University.

The research team used data from two of the largest genome-wide association studies available: one on su***de attempts, including nearly one million individuals, and one on brain imaging, which included structural MRI data from approximately 75,000 participants. The su***de attempt dataset included both people who had made nonfatal attempts and those who had died by su***de. The brain imaging data included measurements of total brain volume and nine subcortical regions, such as the caudate, putamen, amygdala, hippocampus, and thalamus.

To examine shared genetic factors, the researchers first applied a statistical technique known as linkage disequilibrium score regression, which estimates genome-wide genetic correlations between traits. Then, to look for specific areas of the genome influencing both su***de attempts and brain volumes, they used GWAS-pairwise analysis, which examines smaller segments of the genome to detect local genetic overlap. These segments were then mapped to genes using functional annotation tools.

To explore how these genetic relationships might emerge during adolescence, the researchers also examined data from over 5,000 European-ancestry participants in the Adolescent Brain Cognitive Development (ABCD) study. Using polygenic scores for su***de attempt—scores that summarize the cumulative effect of thousands of genetic variants—they tested whether higher genetic risk was associated with differences in brain volume in this younger cohort.

The strongest genome-wide genetic correlation emerged between su***de attempt risk and intracranial volume. The correlation was modest (r = -0.10) but statistically significant, suggesting that genetic factors associated with a higher likelihood of su***de attempt are also linked to smaller overall brain volume. This aligns with earlier neuroimaging research indicating that individuals with a history of su***de attempt tend to have smaller intracranial volume.

Zooming in on specific brain regions, the researchers identified ten genomic segments that appeared to influence both su***de attempt risk and at least one subcortical brain structure. Seven of these were associated with the thalamus, two with the putamen, and one with the caudate nucleus. These areas are involved in various cognitive, emotional, and motor processes, and have been implicated in psychiatric conditions such as depression and schizophrenia.

Several genes were mapped to these overlapping genomic segments. One of the most prominent was DCC, a gene involved in axonal guidance and synaptic development, which was associated with both su***de risk and volume of the caudate and putamen. Other implicated genes, including members of the histone cluster (e.g., HIST1H2BN and HIST1H4L), were located in a highly complex region of the genome known as the major histocompatibility complex, which is involved in immune function and has also been linked to psychiatric disorders.

In conditional analyses, the researchers found that associations between su***de risk and thalamic volume within this region were likely due to separate genetic signals rather than a single shared variant. This suggests that while the same region of the genome may influence both traits, it may do so through distinct genetic mechanisms.

In the adolescent sample from the ABCD study, higher polygenic risk for su***de attempt was significantly associated with smaller volume of the right nucleus accumbens, a brain region involved in reward sensitivity and motivation. This association remained significant even after correcting for multiple comparisons. Notably, the nucleus accumbens did not show overlap in the adult genomic segment analyses, suggesting that different brain regions may reflect genetic vulnerability at different stages of development.

“We found that people with higher genetic risk for su***de attempt tend to have smaller overall brain volume and differences in specific brain regions like the thalamus and caudate nucleus,” Rabinowitz told PsyPost. “In adolescents, a higher genetic risk for su***de attempt was also associated with a smaller volume in the nucleus accumbens, a region involved in reward and motivation. These findings suggest that certain brain structures may help explain how genetic risk for su***de is expressed in the brain early in life, offering insight for future prevention efforts.”

There are some limitations to consider. The genetic analyses were based exclusively on individuals of European ancestry, which means the results may not generalize to other populations. Future studies should aim to replicate these findings in more diverse samples.

Additionally, while the study identifies genetic overlap, it cannot determine whether these shared genetic factors causally influence both su***de risk and brain structure. It’s possible that genes influence one trait, which in turn affects the other. Future research using causal inference methods like Mendelian randomization could help clarify the direction of these relationships.

“It is important to note that findings are not causal; that is, we did not find that genetic risk causes brain structure differences, but rather that an association exists between genetic liability for su***de attempt and neurodevelopment,” Rabinowitz explained. “It will be important to consider third variables in future research, such as environmental exposures, that may be potential pathways through which genetic propensity for suicidal behavior is linked to brain structure differences. I look forward to continuing to conduct research that incorporates genetic and novel biobehavioral and neural phenotypes that may be associated with suicidal behavior across the lifespan.”

The study, “Genetic Links Between Subcortical Brain Morphometry and Su***de Attempt Risk in Children and Adults,” was authored by Zuriel Ceja, Luis M. García-Marín, I-Tzu Hung, Sarah E. Medland, Alexis C. Edwards, Miguel E. Rentería, and Jill A. Rabinowitz.

09/07/2025

L*D Could Offer a Next-Gen Treatment for Anxiety
In a new trial, people who took L*D experienced a reduction in anxiety symptoms compared to placebo.
Read in Gizmodo:

In a new trial, people who took L*D experienced a reduction in anxiety symptoms compared to placebo.

09/07/2025

Health. 13 August 2025

ADHD drugs reduce risk of criminal behaviour, drug abuse and accidents

A study of 150,000 people with ADHD in Sweden confirms that drugs taken to manage the condition have wider benefits beyond improving immediate symptoms

People with ADHD who take drugs to manage their symptoms have a lower risk of suicidal behaviours, criminal convictions, drug abuse, being accidentally injured or being in a road accident, according to a study of 150,000 people in Sweden. Previous research has suggested this is the case, but the researchers behind the latest study say this is the most reliable evidence so far.

“This is the best approach, the closest to a randomised trial,” says Zheng Chang at the Karolinska Institute in Sweden.

Read more ADHD: What's behind the recent explosion in diagnoses?

When drugs are considered for managing ADHD, the wider consequences of not taking them can be overlooked, says team member Samuele Cortese at the University of Southampton in the UK. For instance, parents tend to focus on the immediate issues their children are having at school, he says, but they should also be informed about the longer-term outlook.

“If you don’t treat ADHD, there are risks,” he says. “Now we have evidence that treatment reduces these risks.”

People with ADHD often have trouble paying attention and may make impulsive decisions. Randomised controlled trials show that drugs are effective for managing these immediate symptoms.

These kinds of trials involve randomly assigning people to get a treatment or not, and they are regarded as the gold standard in medicine. But no randomised trials have looked at the wider effects of taking ADHD drugs. Instead, researchers have had to rely on observational studies, which aren’t set up to show whether taking the drugs actually cause the observed changes in symptoms or behaviour.

Now, Chang, Cortese and their colleagues have done what is known as target trial emulation, which involves analysing observational data as if it were from a randomised trial. They used data from Sweden’s medical and legal records to see how people fared in the two years following an ADHD diagnosis.

Compared with those who did not get medication during this time, those who started taking ADHD drugs within 3 months were 25 per cent less likely to get criminal convictions or have an issue with drugs or alcohol. They were also 16 per cent less likely to be involved in a road accident, 15 per cent less likely to attempt su***de and 4 per cent less likely to have accidental injuries.

We're finally pinning down the mechanisms that drive obsessive-compulsive disorder, revealing a complex combination of imbalanced brain networks, the immune system and even gut microbes

“It’s always helpful to know if medications can impact daily life beyond reducing symptoms,” Adam Guastella at the University of Sydney in Australia told the Science Media Centre in the UK. “This information is also important for governments to help policy-makers understand the potential benefits of treatment for broader society, such as mental health or criminal outcomes.”

Need a listening ear? UK Samaritans: 116123 (samaritans.org); US 988 Su***de & Crisis Lifeline: 988 (988lifeline.org). Visit bit.ly/Su***deHelplines for other countries.

Journal reference: The BMJ DOI: 10.1136/bmj-2024-083658

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09/07/2025

Alzheimer's disease: lithium may help slow cognitive decline – new research in mice

A new study has found lithium acts as a natural defender against the harmful proteins that are linked with cognitive decline.
Read in The Conversation US:

A new study has found lithium acts as a natural defender against the harmful proteins that are linked with cognitive decline.

09/07/2025

WELLNESS. 08/24/2025 07:00AM EDT

You Might Have A 'Depression Room' In Your House And Not Even Realize It

Usually, people wake up one day and feel totally depressed, but it doesn’t happen overnight. Here's what you need to know.

It’s well-known that depression takes a toll on physical and mental health as feelings of isolation, loneliness, despair and low energy prevail.

One area that doesn’t get as much attention? Depression’s impact on your physical space, like your home or bedroom —but a conversation about this is starting on social media.

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Folks on platforms like Instagram and TikTok are posting videos of their “depression rooms” — spaces filled with old laundry, trash, dirty dishes, takeout boxes and more that weren’t attended to when someone was feeling low. The videos show people cleaning their (or their loved ones’) “depression homes” or “depression rooms.”

“‘Depression room’ is this term that has entered into the pop psychology lexicon lately, and it refers to the living space of a person in the grips of a depressive episode,” said Dayton Olsen, a licensed professional counselor with Thriveworks in Roanoke, Virginia.

“A ‘depression room’ describes a living space that has become noticeably cluttered or chaotic because the person living in it is experiencing depression,” said Kobe Campbell, a licensed clinical mental health counselor in North Carolina.

“It’s not about laziness or lack of care, it’s a sign that the inner world has become so heavy or disorganized that maintaining the outer world feels impossible,” Campbell added.

There’s a clear reason “depression rooms” happen.

“The state of the room becomes a mirror of what is happening internally,” Campbell noted.

“It’s amazing what even just a brief glance into someone’s living space can say about how that person’s doing,” Olsen said. A picture — or video, in this case — speaks 1,000 words, he added.

“These awful depressive episodes, they do to a person’s living space what they do to a person. They rob them of the ability to just care for themselves, to tend to themselves and their space,” Olsen noted.

“Depression impairs executive function, which is the area of the brain that helps us plan, prioritize and follow through on tasks,” said Campbell.

When you’re depressed, everyday tasks and chores feel overwhelming, Campbell added.

People who’ve dealt with depression describe it as a period of timelessness “where they can’t remember back, necessarily, to a time where they didn’t feel depressed, and they can’t imagine a future where they feel differently,” Olsen said.

“They’re just frozen in this awful emotional pain, and what that translates to so often is this difficulty to do what so many of us typically do when we’re well, which is to make small investments in our future — brushing our teeth, vacuuming, folding laundry, bathing, eating regularly, all of these things that don’t necessarily require a ton of energy or mental bandwidth but they do require looking ahead to the future and investing in that. And depression robs us of that,” Olsen explained.

Depression also robs folks of their energy and motivation, which can make things like doing the dishes or hanging up your clothes feel impossible.

“Depression room” cleaning is a way to break the depression feedback loop.

“When you think about psychology and mental health, there’s this feedback loop between your thoughts, your feelings and your behaviors,” explained Taisha Caldwell-Harvey, a psychologist and the founder and CEO of The Black Girl Doctor, an online therapy and wellness platform.

When your behavior changes, and you’re no longer cleaning your bedroom or letting dishes pile up, it also influences how you think, talk to yourself and how you feel, she said.

“It’s all a circle, it’s all a loop, and so you might look around and say, ‘Oh, I’m gross, I’m lazy,’ and then if you say that, now you’re going to have [thoughts like] ‘I shouldn’t be doing this,’ ‘I’m a bad person,’ and that’s going to trigger emotions that are connected to that — now I’m sad, I feel guilty, I feel bad,” Caldwell-Harvey said.

If you feel bad, why would you do anything around your house? If you tell yourself you’re lazy, why would you pick up after yourself?

The clean-up depression room videos on social media are a way to break this feedback loop and make people feel better, Caldwell-Harvey said.

“Most of the times, we can’t just tell ourselves ‘feel better,’ right? The feeling [aspect] is the hardest one to try to interrupt ... we usually let that one be for a minute and start with something that is an easier place, and so behavior activation is a big one that is usually easier for people to do,” Caldwell-Harvey said.

“So, while you feel like crap, while you’re still telling yourself these negative things, you can force yourself to do a behavior. We call it behavior activation. And so it could be something like clean up your room, [or] it can be something as small as clean up this corner of your room,” she added.

If you don’t have it in you to clean your whole kitchen, set a timer for five minutes and clean for just that amount of time.

“So, you clean for five minutes, and now you think, ‘Oh, I did one small thing,’” she said. Being able to say to yourself, “I did one small thing” can lead to a tiny bit of hope and even a commitment to do five more minutes of cleanup the next day, she added.

This breaks the cycle and interrupts the pattern, she explained.

You can also always use your home as a visual mental health check.

“Our environment influences our emotional health. A 2010 study published in Personality and Social Psychology Bulletin found that women who described their homes as cluttered or unfinished had higher levels of cortisol and more feelings of fatigue and depression compared to those who described their spaces as restful and restorative,” said Campbell.

“So, even small acts of tidying can help signal safety to the nervous system,” Campbell noted.

Beyond signaling safety, your home can give you a peek into your emotional and mental health, which is important as it’s hard to keep tabs on the small mental health changes that lead to big declines.

Usually, people wake up one day and feel totally depressed, but it doesn’t happen overnight, Caldwell-Harvey said. “You actually have a decline,” she said.

One way to keep tabs on your mental health and be aware of the decline is by using your bedroom or home as a mental health check, Caldwell-Harvey added.

“A lot of times, your environment really is telling you how you’re doing, and so it’s a good question to ask — ‘What is my environment telling me about what’s happening right now?’” she said.

If you do have a depression room, don’t be ashamed.

Depression is heavy, isolating and scary. If you have a depression room during times of low mood, that’s OK. “If you have a ‘depression room,’ you are not alone,” said Campbell.

“Feeling shame about it is understandable, but misplaced. Clutter isn’t a character flaw, it’s a flag signaling that you need more support than you can offer yourself,” she added.

It’s also a sign that you’re struggling and need additional care, Campbell noted.

Beyond taking a few minutes to clean your depression room, make social plans and create structure for yourself within your home, added Olsen, whether that’s waking up at the same time, logging on to work at a certain time or simply having a glass of water before bed.

And know when you need extra support.

“I always want to be really careful when we talk about stuff like this,” said Caldwell-Harvey.

While content about “depression rooms” can help people feel less alone and increase conversations about depression, “I also am really cautious that we’re not glamorizing suffering, and that we’re not further stigmatizing people that are in a clinical depression that needs treatment,” she said.

You can have symptoms of depression and not have clinical depression, Caldwell-Harvey explained. But for those with clinical depression, things like room cleaning, behavior changes or daily mantras aren’t going to be enough to boost your mood.

If two weeks go by and you still aren’t feeling good, you may need more support, she noted.

“If you’re struggling and you are trying this stuff, and you’re just like, ‘Yeah, this ain’t doing it,’ that’s when we want you to reach out for help,” she said. “That is what therapists are for. Medication is really effective for depression — medication and talk therapy are both extremely effective for depression,” Caldwell-Harvey added.

For some people, a depression room — and depression — may be a short-lived occurrence, but for others, it’ll be a longer challenge.

“Cleaning your room is not going to take away grief. It might make you feel better for a minute, and that’s great if it does, but again, you probably need to talk to somebody and process it and do all the things that are going to give you the long-term relief from what you’re going through,” she said.

“Not all messy rooms are depression rooms. Not all depression shows up that way,” she added. Some depressed people have spotless homes, and some nondepressed folks have cluttered, messy spaces, Caldwell-Harvey added.

But if you know your depression room is just that, be sure to take care of yourself and be kind to yourself.

“The goal isn’t to flip a switch that changes you immediately. Healing requires tiny, consistent acts of kindness toward yourself, because caring for your space is caring for yourself, said Campbell.