Long-term exposure to common air pollutants may significantly raise the risk of developing substance use disorders, while living surrounded by greenery appears to offer a measure of protection, according to a large new population-based study drawing on nearly a quarter of a million participants from the UK Biobank.

The research, published in BMC Psychiatry, analyzed data from 247,138 UK Biobank participants who were free of substance use disorders at baseline, tracking them over a median follow-up period of 10.9 years. During that time, 4,982 participants went on to develop a substance use disorder, providing the researchers with a robust dataset to examine the relationship between environmental exposures and mental health outcomes.

The study, led by Huan Liu and Bolun Cheng of Xi’an Jiaotong University in China, along with colleagues including Feng Zhang, represents one of the most comprehensive investigations to date into how the air people breathe and the greenness of their neighborhoods may influence vulnerability to addiction. The findings arrive at a moment when urban planners and public health officials are increasingly recognizing that the built and natural environments shape health in ways that extend well beyond respiratory and cardiovascular disease.

To assess air pollution exposure, the team employed Land Use Regression modeling to estimate concentrations of five pollutants at each participant’s residential address: fine particulate matter known as PM2.5, coarse particulate matter classified as PM2.5−10, the larger particulate fraction PM10, nitrogen dioxide (NO2), and nitrogen oxides (NOX). These pollutants, produced primarily by traffic, industry, and combustion sources, have long been associated with a range of physical health problems, but their role in psychiatric and behavioral conditions has remained far less certain.

For residential greenness, the researchers turned to the 2005–2007 Land Cover Map, measuring three distinct aspects of the environment within a 300-meter buffer around each home: the proportion of green space, the presence of a domestic garden, and the extent of natural environment. This tripartite approach allowed the investigators to distinguish between different types of vegetation and their potentially different effects on health.

Using Cox proportional hazards models, the team calculated hazard ratios with 95 percent confidence intervals to quantify the association between each exposure and the risk of developing a substance use disorder. The results were striking in their consistency. All five air pollutants were positively associated with incident SUD in fully adjusted models that controlled for a wide range of potential confounders.

Fine particulate matter, or PM2.5, showed the strongest effect, with a hazard ratio of 1.111 (95 percent CI: 1.081–1.142), followed by PM10 with a hazard ratio of 1.070 (95 percent CI: 1.054–1.086). These figures indicate that higher exposure to particulate pollution was associated with a measurable increase in the likelihood of developing a substance use disorder over the follow-up period, even after accounting for demographic, socioeconomic, and behavioral factors.

On the protective side of the ledger, two of the three greenness measures emerged as significant. Green space was inversely associated with SUD risk, showing a hazard ratio of 0.997 (95 percent CI: 0.996–0.998), and the natural environment measure produced an identical finding, with a hazard ratio of 0.997 (95 percent CI: 0.995–0.998). While these effect sizes appear modest on a per-unit basis, they represent population-level signals across a very large cohort, suggesting that even incremental increases in neighborhood greenness may contribute to reduced vulnerability.

Perhaps the most intriguing finding of the study concerns the interaction between pollution and greenery. The researchers tested whether residential greenness modified the association between air pollutants and SUD risk by introducing cross-product terms into their models and evaluating them with likelihood-ratio tests. The results pointed to a buffering role for domestic gardens specifically. Among participants in the high-exposure subgroup, the presence of a domestic garden attenuated the positive associations between pollutants and SUD, with cross-product terms of 0.979 (95 percent CI: 0.963–0.996) for PM2.5 and 0.987 (95 percent CI: 0.980–0.995) for PM10.

In practical terms, this suggests that having access to a private garden may partially offset some of the harm associated with living in areas of elevated particulate pollution, offering a form of environmental resilience that public health advocates have long hypothesized but rarely demonstrated with prospective cohort data.

The associations were not uniform across the population. The positive relationships between air pollution and substance use disorder risk were most pronounced among males, participants aged 65 and older, and individuals with a history of smoking. These findings highlight the importance of considering demographic and behavioral modifiers when assessing the health consequences of environmental exposures, and they suggest that certain subgroups may benefit disproportionately from interventions aimed at reducing pollution or increasing green cover.

To ensure the robustness of their findings, the team conducted a series of sensitivity analyses. These included restricting the sample to long-term residents to minimize exposure misclassification from relocation, using alternative outcome definitions based on ICD-10 codes F10-F19 and F11-F19 to capture different ranges of substance-related diagnoses, and recomputing greenness measures at a wider 1000-meter buffer around each residence. The core conclusions held across these variations, strengthening confidence in the results.

The study was performed in accordance with the ethical principles of the Declaration of Helsinki and was registered with the UK Biobank under application number 46478. Ethical approval for the UK Biobank was granted by the North West Multi-centre Research Ethics Committee under approval reference 11/NW/0382. All participants provided written informed consent before any study-related procedures were initiated.

The work was supported by the China Postdoctoral Science Foundation, the Natural Science Basic Research Plan in Shaanxi Province of China, and the Fundamental Research Funds for the Central Universities. Corresponding authors are Bolun Cheng and Feng Zhang, both affiliated with Xi’an Jiaotong University, with Zhang also holding a position in the Department of Psychiatry at the First Affiliated Hospital of Xi’an Jiaotong University.

The findings come amid growing scientific interest in the neurological and psychiatric consequences of air pollution. Particulate matter, particularly PM2.5, is small enough to cross the blood-brain barrier and has been implicated in neuroinflammation, oxidative stress, and alterations in brain structure and function. These biological mechanisms could plausibly influence reward processing, impulse control, and stress reactivity, all of which are central to the development and perpetuation of substance use disorders.

Conversely, greenness has been associated with stress reduction, improved mental well-being, greater opportunities for physical activity and social interaction, and lower levels of psychological distress, each of which may buffer against the onset of addictive behaviors. The current study adds a significant piece of evidence to this emerging picture by demonstrating the relationship prospectively in one of the world’s largest and most deeply phenotyped biobanks.

The authors conclude that long-term exposure to ambient air pollutants was associated with a higher risk of incident substance use disorders and that residential greenness showed protective associations, with the most pronounced patterns observed among older males and individuals with a smoking history. They argue that the findings support integrating greenness exposure into environmental frameworks for the prevention of substance use disorders, a recommendation that carries implications for urban design, housing policy, and environmental regulation.

As cities around the world continue to grapple with the twin challenges of air quality and mental health, studies of this scale provide an evidence base for interventions that address both simultaneously. The prospect that something as tangible as a garden could offer measurable protection against the psychiatric consequences of polluted air adds a compelling dimension to ongoing debates about how the environments we build shape the minds that inhabit them.

The article is published open access under a Creative Commons Attribution 4.0 International License, permitting broad sharing and adaptation with appropriate credit to the original authors and source. It was received on 08 December 2025, accepted on 28 August 2026, and published on 09 September 2026.

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In one of the most comprehensive investigations of its kind, researchers have taken a major step toward untangling the biology underlying suicide risk, moving the field beyond long-standing debates about whether suicidal behavior is simply a consequence of psychiatric illness. By integrating large-scale genetic data with cutting-edge approaches that map how genes act in specific brain cells and circuits, an international team has identified shared genetic liability that cuts across psychiatric diagnoses while also pinpointing druggable biological pathways that could one day inform prevention strategies. The study, published in Translational Psychiatry, offers a sweeping synthesis of how inherited risk factors may translate into molecular vulnerabilities, and it does so with a level of resolution that previous candidate-gene approaches could never achieve.

Suicide remains one of the leading causes of death worldwide, claiming more than 700,000 lives each year according to global health estimates. Despite decades of research, clinical prediction remains stubbornly imprecise, and biological models of suicidal behavior have historically been hampered by small sample sizes, inconsistent findings, and a tendency to conflate suicide risk with the psychiatric disorders with which it so often co-occurs. Major depression, bipolar disorder, schizophrenia, and substance use disorders all carry elevated suicide risk, yet most people with these conditions never attempt suicide, while some individuals who die by suicide have no diagnosed psychiatric illness at all. This paradox has long suggested to researchers that suicidal behavior may possess partially distinct biological underpinnings, and the new study set out to test that hypothesis with unprecedented statistical power.

At the heart of the work lies genome-wide association study methodology, or GWAS, which scans hundreds of thousands to millions of genetic variants spread across the entire genome in very large groups of people, comparing individuals who have experienced suicidal thoughts or behaviors with those who have not. Each variant is tested for statistical association with the outcome, and the results can be combined into polygenic risk scores, numerical summaries of a person’s inherited liability based on the cumulative small effects of thousands of variants. Because no single common variant exerts a large effect, the field depends on aggregating data across massive biobanks and cohorts, a strategy that has only become feasible in the past decade as datasets containing hundreds of thousands of individuals became available.

The research team took particular care to address a central confound: psychiatric disorders themselves are highly heritable, and any genetic signal linked to suicide could simply reflect inherited liability to depression or schizophrenia rather than to suicide specifically. To disentangle this, the investigators applied sophisticated statistical techniques, including genetic correlation analysis and conditional modeling, which allow researchers to ask how much genetic overlap remains between suicidal behavior and psychiatric conditions after accounting for their shared heritability. Their findings revealed a complex architecture. Substantial genetic correlations confirmed that suicide risk shares a meaningful fraction of its inherited basis with major psychiatric disorders, supporting the idea of a common pool of genetic liability. Yet the analyses also uncovered signals that persisted beyond what could be explained by those disorders, pointing to biological mechanisms that may be more specific to the emergence of suicidal thoughts and actions.

A key conceptual innovation of the study is its framing of “shared genetic liability” as a bridge between diagnoses. Rather than treating suicide as an epiphenomenon of any single disorder, the researchers modeled it as a transdiagnostic phenomenon, one whose risk emerges partly from inherited vulnerabilities that cut across diagnostic categories. This perspective aligns with a growing movement in biological psychiatry that emphasizes symptom dimensions and mechanisms over traditional diagnostic boundaries. From this vantage point, the genetic variants that raise risk for depression, PTSD, and schizophrenia may do so partly because they converge on shared molecular pathways, and those same pathways may govern an individual’s threshold for suicidal crises regardless of which diagnosis they carry.

Identifying genetic variants, however, is only the first step. A GWAS signal typically points to a genomic region rather than a specific causal gene or mechanism, since many associated variants fall in non-coding stretches of DNA that regulate gene activity from a distance. To translate statistical associations into biological insight, the team deployed a battery of functional genomics approaches. Transcriptome-wide association studies, known as TWAS, integrate gene expression data to identify genes whose genetically predicted expression levels are linked to suicide risk. Tissue and cell-type enrichment analyses then ask whether the implicated genes are unusually active in particular organs or cell populations. The results converged strikingly on brain tissue, and more specifically on neuronal populations, providing support for the idea that inherited suicide risk is mediated largely through gene regulation within the central nervous system.

The study’s most clinically provocative findings concern druggable biology. Using databases that catalog the protein targets of approved and investigational medications, the researchers examined whether genes implicated in suicide risk were over-represented among known drug targets. The analysis identified several classes of candidate targets, including components of neurotransmitter signaling systems, ion channels, and intracellular signaling cascades that are already the focus of pharmacological development for other conditions. This “druggable genome” approach, which has gained traction in genetics research across many diseases, offers a pragmatic shortcut for translational science: rather than waiting decades for entirely new therapeutic classes to be invented, researchers can prioritize existing or in-development compounds whose molecular targets intersect with genetically implicated pathways.

Among the pathways receiving attention in the analysis were those involving glutamatergic and GABAergic neurotransmission, the primary excitatory and inhibitory systems of the brain, which have repeatedly surfaced in studies of mood disorders and stress response. The endocannabinoid system and inflammatory signaling pathways also appeared in the convergent analyses, consistent with a broader literature linking immune dysregulation and allostatic load to suicidal ideation. Importantly, the authors emphasize that these findings identify hypotheses rather than ready-made treatments. Genetic association with a drug target does not guarantee that modulating that target will reduce suicide risk, and any therapeutic application would require extensive preclinical validation and carefully designed clinical trials. Nevertheless, the work provides a principled, data-driven map for where to look, replacing decades of largely failed candidate-gene speculation with a genome-wide evidence base.

The methodological rigor underpinning the study deserves emphasis, because the genetics of suicidal behavior has a troubled history. Early candidate-gene studies, which typically examined a handful of variants in genes related to serotonin signaling, produced findings that largely failed to replicate and in some cases were later shown to reflect statistical artifacts, small samples, and publication bias. The field has since undergone a reckoning, and modern efforts adhere to far stricter standards: preregistered analyses, very large and ancestrally diverse cohorts, replication in independent samples, and conservative multiple-testing corrections that demand genome-wide significance thresholds on the order of five times ten to the negative eighth power. The new study reflects these lessons, applying sensitivity analyses to guard against confounding from psychiatric comorbidity and examining whether findings generalize across ancestral groups, an issue of considerable importance given that most genetic discovery to date has been conducted in populations of European ancestry.

The implications for clinical practice, while still distant, are worth considering. Polygenic risk scores for suicide-related outcomes currently explain only a small fraction of individual differences in risk, far too little to be used as stand-alone screening tools, and their predictive performance is degraded in populations not represented in the discovery data. Researchers in the field are careful to stress that genetic risk is not destiny: suicidal behavior arises from an intricate interplay of inherited vulnerability, mental illness, trauma, substance use, social isolation, access to lethal means, and the availability of support. What genetics offers is not a crystal ball but a window into mechanism, and mechanistic knowledge is the raw material from which better biomarkers, risk stratification tools, and ultimately targeted interventions are built. In the near term, the druggable pathway findings are most valuable as a guide for laboratory science, directing neurobiologists toward molecular systems whose manipulation might alter suicide-relevant phenotypes in animal models and cellular assays.

Looking forward, the study signals where the field must go next. Sample sizes for suicide-specific genetic analyses remain smaller than those for major psychiatric disorders, and expanding representation across ancestries is essential if the benefits of this research are to be shared equitably. Integrating genetic data with longitudinal measures of life stress, neural imaging, and digital phenotyping may eventually allow researchers to model how inherited liability interacts with environmental triggers across the lifespan. Functional experiments in induced pluripotent stem cell-derived neurons and brain organoids could test whether the implicated genes genuinely alter stress-response circuitry or resilience. And randomized trials in patients carrying high genetic liability, though ethically and logistically complex, represent the logical endpoint of the druggable-target approach.

What the study ultimately delivers is a reframe. Suicide risk, in this analysis, is not an amorphous clinical outcome but a measurable, partly heritable trait whose genetic architecture is now being resolved with the same tools that have transformed our understanding of heart disease, diabetes, and schizophrenia. By demonstrating that shared genetic liability links suicide risk across diagnostic boundaries and by mapping that liability onto specific, pharmacologically tractable biology, the researchers have converted a long-standing clinical puzzle into a concrete research agenda. The path from genetic correlation to effective prevention is long, and no genetic finding will soon replace the human work of crisis intervention, connection, and care. But for a problem that has defied biological explanation for generations, the identification of shared, druggable mechanisms represents a genuine and hard-won advance, one that may shape suicide research for years to come.

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Nearly every displaced woman in Gaza surveyed in a new study screened positive for severe post-traumatic stress symptoms, a finding researchers describe as an unprecedented psychological toll linked directly to hunger, overcrowded displacement, and the collapse of everyday life under war.

The study, published in the International Journal for Equity in Health, assessed 503 displaced women in the Gaza Strip during the 2023–2025 war using a mixed-methods design that combined a structured quantitative survey with in-depth qualitative interviews. The average participant was 29.4 years old, with a standard deviation of 7.3 years, and the majority were married, unemployed, and living below the deep poverty line. Most had been displaced for nearly a year, and the overwhelming majority were sheltering in tents under conditions of severe overcrowding and acute food shortage.

When researchers measured post-traumatic stress symptoms using the Impact of Event Scale–Revised, a widely used screening instrument that evaluates intrusion, avoidance, and hyperarousal symptoms following traumatic exposure, they found that 98.2 percent of participants scored in the severe range. The mean IES-R score across the sample was 61.5, with a standard deviation of 9.5 — a figure far above the thresholds typically used to flag clinically significant trauma-related distress. The authors are careful to note that because symptoms were assessed with a screening tool rather than a formal diagnostic clinical interview, the results should be interpreted as reflecting an extremely high burden of trauma-related distress within the study sample rather than confirmed clinical diagnoses. Even with that caveat, the near-universality of severe scores stands out even against the backdrop of other conflict-affected populations, where severe symptom prevalence rarely approaches such levels.

Food emerged as one of the strongest statistical correlates of psychological suffering. Severe food insecurity, measured with the Food Insecurity Experience Scale developed by the Food and Agriculture Organization, affected approximately 71 percent of participants. Women experiencing severe food insecurity had significantly higher PTSD symptom severity scores, an association that held at a p-value below 0.001. The researchers also identified a cluster of socioeconomic and living-condition factors associated with worse outcomes: being divorced or widowed, living in an extended-family household, sheltering in a tent or collective shelter during displacement, and reporting that food was simply unavailable were all significantly linked to elevated symptom scores.

These quantitative patterns were given texture and depth by the qualitative arm of the study, in which trained researchers conducted semi-structured, face-to-face interviews in Arabic with 34 of the women. Analysis of the transcripts revealed five overarching themes: poverty and inequity; food as a luxury; wounds you cannot see; on the move, nowhere to belong; and small acts of resilience. Together, the themes trace an arc from material deprivation to psychological injury and, ultimately, to the fragile coping strategies women deployed to keep themselves and their families functioning.

The theme of food as a luxury captured how a basic biological need had been transformed into an object of obsession and grief. Women described rationing scraps, skipping meals so children could eat, and the humiliating experience of standing in lines for aid that never arrived. The researchers note that this chronic preoccupation with food security operated on two fronts — it was simultaneously a source of traumatic stress in its own right and an amplifier of existing war trauma, since hunger stripped away one of the last remaining domains in which mothers could still protect their children.

The “wounds you cannot see” theme speaks directly to the invisible nature of psychological injury in wartime. Women recounted nightmares, intrusive memories of bombings and the deaths of relatives, hypervigilance, emotional numbness, and an inability to feel safe even in moments of quiet. Several described the stigma of admitting psychological suffering, or the sense that mental distress was a luxury they could not afford to acknowledge while survival demanded constant action. The researchers interpret these accounts as illustrating how trauma in this context is not a discrete event but a continuous condition, woven into the fabric of daily life.

Displacement itself — the theme of being “on the move, nowhere to belong” — emerged as a distinct psychological stressor. Women described repeated forced evacuations, the loss of homes that anchored family identity and memory, and the corrosive instability of living in tents that leaked in rain, baked in heat, and offered no privacy for grieving or for motherhood. The loss of place, the authors suggest, compounds the loss of people, producing a grief that has nowhere to settle.

Yet the final theme, small acts of resilience, complicates a narrative of pure victimhood. Women described prayer, mutual aid among neighbors, storytelling with children, and small rituals of domesticity — making tea, arranging a tent, celebrating a birthday with almost nothing — as deliberate acts of psychological resistance. The researchers frame these behaviors as adaptive coping mechanisms that, while insufficient to protect against severe trauma symptoms, sustained a sense of agency and dignity under conditions designed to strip both away.

Methodologically, the study relied on a convenience sample recruited through structured surveys administered via Google Forms, a pragmatic choice given the destruction of infrastructure and the impossibility of random sampling in an active war zone. The authors acknowledge this limitation, along with the screening-based measurement of PTSD and the absence of consistent formal referral pathways for psychological care during data collection, which meant that women who became distressed during interviews could not always be directed to clinical services. Interviews followed strict ethical protocols approved by the Institutional Review Board at An-Najah National University, with verbal informed consent, anonymization, and trained interviewers instructed to pause or terminate any conversation that caused visible distress.

The demographic profile of the sample underscores the socioeconomic dimension of psychological vulnerability. That most participants were unemployed and living below the deep poverty line before and during the war reflects broader patterns in which economic deprivation and mental health outcomes are tightly intertwined in conflict settings. Divorced and widowed women — those without a partner’s social and economic support — fared significantly worse, as did women in extended-family households, possibly reflecting crowded conditions and multiplied caregiving burdens.

The study carries a sobering human footnote. The acknowledgments honor the memory of co-author Ayman S. Abutair, a clinical nutrition researcher at Al-Azhar University-Gaza, who lost his life during the war before the paper’s publication. His death stands as a stark reminder that the researchers documenting these invisible wounds were themselves living within the same catastrophe.

The authors argue that their findings demonstrate an urgent and unmet need for comprehensive humanitarian and psychosocial support tailored to displaced women — support that integrates mental health care with food assistance, shelter improvement, and protection for female-headed households. They emphasize that because caregiving responsibilities fall disproportionately on women during war and displacement, their psychological deterioration radiates outward to children and entire family systems, making women’s mental health a strategic priority for any humanitarian response rather than an afterthought.

What the study ultimately documents is the entanglement of hunger and trauma at a scale rarely captured in research. Where most studies of conflict-related PTSD examine populations after violence has subsided, this research measured psychological injury while bombs were still falling, while displacement was ongoing, and while food systems had collapsed. The result is a portrait of a population in which severe trauma symptoms are not an unfortunate consequence of war but, in effect, a near-universal condition — visible not in wounds, but in sleepless nights, interrupted meals, and the quiet endurance of half a million women carrying burdens that remain, for now, largely untreated.

Police have finally dropped a year-long investigation into three hero passengers who tackled a man exposing himself in front of children on a train – though only because the CPS has refused to take the case forward.

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The science of getting Z’s has progressed rapidly in recent years. A growing body of research links poor sleep to increased risk of cognitive decline, a higher likelihood of Alzheimer’s disease, and even greater chances of developing heart problems. At the same time, wearables, like smart rings and watches, are transforming the way everyday people view sleep, turning their resting hours into rich datasets to pore over, sometimes to unhealthy obsessive levels. 

What’s still less understood, is how the subtle, everyday fluctuations in sleep quality that come from simply living a normal life can alter brain chemistry. People don’t live in controlled lab settings, and even the most avid bio-optimizer still has nights where quality sleep takes a backseat. Actually understanding how someone’s day-to-day sleep patterns affect their brain chemistry would require putting them in an MRI machine and collecting data over and over again, over long stretches of time to get a more holistic view. 

That’s exactly what Auburn University electrical and computer engineering graduate student Joshita Majumdar signed up for. Over 76 weeks, Majumdar slipped into the university’s 7-Tesla MRI scanner 104 times. That’s a level of commitment that would make even a stalwart Zen meditator fidget with frustrated boredom. Thankfully, Majumdar had a special companion to accompany her during the loud, cramped, 90-minute sessions: the hit television sitcom Friends.

Majumdar recalls how a screen in the machine would cycle through four 10-minute videos of the staple from the 90’s and early 2000’s, each made up of several different scenes clipped together. The idea was twofold. Majumdar needed something playing during the sessions that would keep her from getting bored, and Friends just happens to be her self-described “guilty pleasure.” It was also one of the first shows she connected with as an international student adjusting to her early days in the United States, so some scenes strike particularly nostalgic, emotional notes. And like any great sitcom, Friends runs the gamut from numbing brain-rot to tear-jerking sentimentality. That’s potentially a great backdrop for a study analyzing changes in brain chemistry.  

“If you’re happy, you watch Friends. If you’re sad, you watch Friends,” Majumdar tells Popular Science. “So all times [are] a good time to watch Friends, right?”

Past studies have looked at the way sleep variability affects brain chemistry, but many of those involve intentionally depriving the subject of sleep. This longer-term approach takes a more subtle approach that should better reflect the nuances of everyday life. 

“This is a person living her life, going through normal ups and downs and we are seeing how brain chemistry responds to that,” Majumdar’s advisor and Auburn University Electrical and Computer Engineering Professor Gopikrishna Deshpande said.  “That’s what makes this dataset so powerful. It’s not artificial. It’s not forced. It’s real.”

The journey to 104 brain scans 

Majumdar grew up in Kolkata, West Bengal, India, and moved to the U.S. in 2016 to pursue a master’s degree in engineering at the University of Georgia, with an emphasis on mechanical engineering. Early on, she became interested in how different environmental factors affect brain function. And while she was busy pushing forward with her rigorous academic work, she also dealt with occasional homesickness, living in a new country thousands of miles away from friends and relatives. 

Around that same time, Majumdar says she started watching Friends to see what all the fuss was about. People around her seemed obsessed with the show, but she hadn’t seen it, and initially didn’t really understand the hype. Eventually, she went back to the show with fresh eyes and everything clicked. The sarcastic Chandler Bing (Matthew Perry) and affable actor Joey Tribbiani (Matt LeBlanc) are among her favorite characters.

“I gave it another try, and then I was like, oh no, this is fun,” Majumdar said. “And then it became a guilty pleasure.” 

When it came time to pick a test subject for this new, lengthy MRI study, Majumdar says Dr. Deshpande asked her if she’d be up for volunteering. Majumdar has some experience with MRI machines from past projects, enough to know that she wasn’t prohibitively claustrophobic or bothered by the machine’s loud industrial noises. Still, nothing she’d done before this could compare to the endurance and commitment it would take to see this through. The team decided not to commit to a set number of scans at the onset, and took it day by day to see how much the grad student could handle. 

“We said, like, ‘Okay, we’ll take one day at a time, one week at a time, and see how far we can pull it through,” Majumdar explained. 

Don’t sleep on Friends  

Majumdar was the one who pitched playing Friends episodes in the machine. She compiled four 10-minute videos, each made up of different scenes from various episodes. The material ran the gamut in tone, with the goal of eliciting a range of brain responses. One particularly strategic choice was to include clips of episodes aired around Thanksgiving. These fan-favorites tend lean heavily on themes of family, friendship, and camaraderie. Friends, in other words, was meant to roughly simulate the backdrop for Majumdar’s everyday life brain state. 

“In a task-based MRI, we are giving a particular stimulus, so we kind of have an idea what we are trying to activate in the brain,”  Majumdar said. “But in a naturalistic run, it’’s kind of like you’re putting yourself into a real-world situation.” 

But that wasn’t all. Every session, the team would also play a roughly four-minute music video to the song “Love You Zindagi,” from the 2016 Bollywood film Dear Zindagi. Similar to the Thanksgiving episodes, this video was thoughtfully selected for its depiction of friends and family. It also helps remind Majumdar of home. 

“I have left my friends and family back in India,” Majumdar said. “So depending upon what my emotions are on that day, I used to really connect to it differently each day.”

Majumdar and her colleagues quickly settled into a routine for their MRI odyssey. She would come to the university’s neuroimaging center on Tuesdays and Thursdays, typically around 7:30 in the evening. She had the choice of that later time slot or first thing in the morning, but chose the former because she says she isn’t really a morning person. That choice came with some trade-offs, though. 

Early on, she discovered that eating a meal immediately before entering the machine made her feel dizzy. After one fraught experience, she made a point of giving herself a gap of 90 minutes to two hours after eating before going into the scanner. Coming in later at night, especially after a long day of PhD work, also meant she sometimes had to fight the urge to fall asleep. Even though she was stuck in the machine for 90 minutes at a time, the tests required that she keep her eyes open for the vast majority of it. That struggle is partly what makes subsequent findings all the more interesting. 

“Sometimes I was a little bit sleepy, but that’s part of it,” Majumdar said. “And that’s the thing that we wanted to bring out through this research: that you are in a very natural setting. You’re not in a kind of a forced experiment where you are either sleep-deprived or put under some conditions that might evoke a different brain response. We really wanted to look at the real-world condition where I’m just living my life, and in parallel I’m getting scanned and seeing how the brain chemistry responds to it.”

In addition to sitting in the MRI machine, Majumdar logged everything she ate and wore a sleep-tracking ring. With all of that data, the team was able to match each night’s sleep metrics with the next day’s scan and compare patterns over time. Though there’s still data being combed through, they’ve already found an important connection: across the 104 sessions collected over 76 weeks, nights with less deep sleep and more light sleep tended to be followed by higher glutamate levels the next day. Glutamate is an amino acid that acts as a kind of chemical messenger in the brain. In a previous university blog post, Majumdar compared this finding to the brain flushing out byproducts that build up during active, wakeful moments, allowing for a more restful night’s sleep.

“You wake up with a fresh mind,” she said. “But if that process is blocked, it’s going to hamper you the next day.”

But is she sick of sipping coffee at Central Perk?

Majumdar’s work in this area has only just begun. Moving forward, she and her colleagues hope to bring on more study participants  to make the dataset even richer, though they’ll likely make adjustments so that each participant doesn’t have to go in for scans quite as often as she did. 

Eventually, she says she also hopes to use AI and other tools to try and extract the feelings and emotions experienced during those MRI sessions (and during certain Friends’ moments) to get a better sense of what’s happening in the brain when certain feelings are evoked. 

Miraculously, even after watching the show in a cramped, rumbling tube for 18 months, Majumdar says she still isn’t sick of Friends. When asked if she can still watch the silly sitcom without getting bored, Majumdar responds with an emphatic, 

“Yes, definitely.”

The post Classic sitcom ‘Friends’ helps grad student endure 104 brain scans appeared first on Popular Science.

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