The world’s population has increased by more than 2.6-fold in the last 60 years. The growing trend continues — projections indicate that the number of people living on our planet will grow to 9 billion by 2037 from 8 billion in 2022. These numbers underscore the need for considering family planning; however, there have been limited breakthroughs in contraception in recent decades. Specifically for men, there are no oral contraceptive pills available.
In a study published in the journal Science, researchers at Baylor College of Medicine and collaborating institutions show in animal models that a novel, non-hormonal sperm-specific approach offers a promising option for reversible human male contraception.
“Although researchers have been investigating several strategies to develop male contraceptives, we still do not have a birth control pill for men,” said corresponding author Dr. Martin Matzuk, director of the Center for Drug Discovery and chair of the Department of Pathology and Immunology at Baylor. “In this study we focused on a novel approach — identifying a small molecule that would inhibit serine/threonine kinase 33 (STK33), a protein that is specifically required for fertility in both men and mice.”
Previous research has shown that STK33 is enriched in the testis and is specifically required for the formation of functional sperm. In mice, knocking out the Stk33 gene renders the mice sterile due to abnormal sperm and poor sperm motility. In men, having a mutation in the STK33 gene leads to infertility caused by the same sperm defects found in the Stk33 knockout mice. Most importantly, mice and men with these mutations have no other defects and even have normal testis size.
“STK33 is therefore considered a viable target with minimal safety concerns for contraception in men,” said Matzuk, who has been on faculty at Baylor for 30 years and is Baylor’s Stuart A. Wallace Chair and Robert L. Moody, Sr. Chair of Pathology and Immunology. “STK33 inhibitors have been described but none are STK33-specific or potent for chemically disrupting STK33 function in living organisms.”
Finding an effective STK33 inhibitor
“We used DNA-Encoded Chemistry Technology (DEC-Tec) to screen our multi-billion compound collection to discover potent STK33 inhibitors,” said first author Dr. Angela Ku, staff scientist in the Matzuk lab. “Our group and others have used this approach before to uncover potent and selective kinase inhibitors.”
The researchers uncovered potent STK33-specific inhibitors, from which they successfully generated modified versions to make them more stable, potent and selective. “Among these modified versions, compound CDD-2807 turned out to be the most effective,” Ku said.

“Next, we tested the efficacy of CDD-2807 in our mouse model,” said co-author Dr. Courtney M. Sutton, postdoctoral fellow in the Matzuk lab. “We evaluated several doses and treatment schedules and then determined sperm motility and number in the mice as well as their ability to fertilize females.”
Compound CDD-2807 effectively crossed the blood-testis barrier and reduced sperm motility and numbers and mice fertility at low doses. “We were pleased to see that the mice did not show signs of toxicity from CDD-2807 treatment, that the compound did not accumulate in the brain, and that the treatment did not alter testis size, similar to the Stk33 knockout mice and the men with the STK33 mutation,” Sutton said. “Importantly, the contraceptive effect was reversible. After a period without compound CDD-2807, the mice recovered sperm motility and numbers and were fertile again.”
“In our paper, we also present the first crystal structure for STK33,” said co-author Dr. Choel Kim, associate professor of biochemistry and molecular pharmacology and member of the Dan L Duncan Comprehensive Cancer Center at Baylor. “Our crystal structure showed how one of our potent inhibitors interacts with STK33 kinase in three dimensions. This enabled us to model and design our final compound, CDD-2807, for better drug-like properties.”
“This study was a tour de force by our team in the Center for Drug Discovery at Baylor and our collaborators,” said co-author Dr. Mingxing Teng, assistant professor of pathology and immunology and of biochemistry and molecular pharmacology at Baylor. Teng also is a Cancer Prevention Research Institute of Texas Scholar and a member of the Dan L Duncan Comprehensive Cancer Center at Baylor. “Starting with a genetically validated contraceptive target, we were able to show that STK33 is also a chemically validated contraceptive target.”
“In the next few years, our goal is to further evaluate this STK33 inhibitor and compounds similar to CDD-2807 in primates to determine their effectiveness as reversible male contraceptives,” Matzuk said.
Additional co-authors of the paper affiliated with Baylor College of Medicine are Kiran L. Sharma, Hai Minh Ta, Kurt M. Bohren, Yong Wang, Srinivas Chamakuri, Ruihong Chen, John M. Hakenjos, Ravikumar Jimmidi, Katarzyna Kent, Feng Li, Jian-Yuan Li, Lang Ma, Chandrashekhar Madasu, Murugesan Palaniappan, Stephen S. Palmer, Xuan Qin, Zhi Tan, Yasmin M. Vasquez, Jian Wang, Zhifeng Yu, Qiuji Ye and Damian W. Young. Co-authors Matthew B. Robers and Jennifer Wilkinson are affiliated with Promega Corp., and Banumathi Sankaran is affiliated with Lawrence Berkeley National Laboratory.

Anew analysis has revealed detailed information about genetic variation in brain cells that could open new avenues for the targeted treatment of diseases such as schizophrenia and Alzheimer’s disease.
The findings, reported May 23 in Science, were the result of a multi-institutional collaboration known as PsychENCODE, founded in 2015 by the National Institutes of Health, which seeks new understandings of genomic influences on neuropsychiatric disease. The study was published alongside related studies in Science, Science Advances, and Science Translational Medicine.
Previous research has established a strong link between a person’s genetics and their likelihood of developing neuropsychiatric disease, says Mark Gerstein, the Albert L. Williams Professor of Biomedical Informatics at Yale School of Medicine and senior author of the new study.
“The correlations between genetics and your susceptibility to disease are much higher for brain diseases than for cancer or heart disease,” said Gerstein. “If your parents have schizophrenia, you’re much more likely to get it than you are to get heart disease if your parents have the disease. There is a very large heritability for these brain-related conditions.”
What’s less clear, however, is how this genetic variation leads to disease.
“We want to understand the mechanism,” said Gerstein. “What is that gene variant doing in the brain?”
For the new study, researchers set out to better understand the genetic variation across individual cell types in the brain. To do so, they performed several types of single-cell experiments on more than 2.8 million cells taken from the brains of 388 people, including healthy individuals and others with schizophrenia, bipolar disorder, autism spectrum disorder, post-traumatic stress disorder, and Alzheimer’s disease.

From that pool of cells, the researchers identified 28 different cell types. Then they examined gene expression and regulation within those cell types.
In one analysis, the researchers were able to link gene expression to variants in “upstream” regulatory regions, bits of genetic code situated before the gene in question that can increase or decrease the gene’s expression.
“That’s useful because if you have a variant of interest, you can now link it to a gene,” said Gerstein. “And that’s really powerful because it helps you interpret the variants. It helps you understand what effect they’re having in the brain. And because we looked across cell types, our data also allow you to connect that variant to an individual cell type of action.”
The researchers also assessed how particular genes, such as those associated with neurotransmitters, varied across individuals and cell types, finding variability was usually higher across cell types than across individuals. This pattern was even stronger for genes that code for proteins targeted for drug treatment.
“And that’s generally good for a drug,” Gerstein said. “It means that those drugs are homing in on particular cell types and not affecting your whole brain or body. It also means those drugs are more likely to be unaffected by genetic variants and work in many people.”
Using the data generated by the analysis, the researchers were able to map out within-cell type genetic regulatory networks and between-cell communication networks, and then plug those networks into a machine learning model. Then, using an individual’s genetic information, the model could predict whether they had a brain disease.

“Because these networks were hard coded in the model, when the model made a prediction we could see which parts of the network contributed to it,” said Gerstein. “So we could identify which genes and cell types were important for that prediction. And that can suggest candidate drug targets.”
In one example, the model predicted an individual with a particular genetic variant might have bipolar disorder, and the researchers could see that prediction was based on two genes in three cell types. In another, the researchers identified six genes in six cell types that contributed to a schizophrenia prediction.
The model also worked in the opposite direction. The researchers could introduce a genetic perturbation and see how that might affect the network and an individual’s health. This, Gerstein says, is useful for drug design or previewing how well drugs or drug combinations might fare as treatments.
Together, the findings could help facilitate precision-medicine approaches for neuropsychiatric disease, said the researchers.
To further this work, the consortium has made its results and model available to other researchers.
“Our vision is that researchers interested in a particular gene or variant can use our resources to better understand what it’s doing in the brain or to perhaps identify new candidate drug targets to investigate more,” said Gerstein.

The legislation would make possession of the drugs without a prescription a crime in Louisiana, punishable with jail time.Louisiana lawmakers passed legislation on Thursday to make the state the first in the nation to designate abortion pills as dangerous controlled substances. Possession of the drugs without a prescription would be a crime punishable with jail time and thousands of dollars in fines.The legislation, which passed the State Senate by a vote of 29 to 7, now goes to Gov. Jeff Landry, a Republican who previously defended the state’s stringent abortion ban in court as attorney general. He is widely expected to sign it.By classifying the abortion pills mifepristone and misoprostol as Schedule IV drugs — a category of medicines with some potential for abuse or dependence that includes Ambien, Valium and Xanax, among others — lawmakers in the state say they aim to curb the illicit distribution of the drugs for abortions. But the Food and Drug Administration does not consider the two medications to have potential for abuse or dependence, and years of research have overwhelmingly shown both pills to be safe.Because Louisiana already bans most abortions, and because the two drugs are also prescribed for other uses — both can be used during miscarriages, and misoprostol is often used to prevent ulcers and help during childbirth — hundreds of doctors in the state strenuously opposed the legislation.“I understand that it may give some in this body some heartburn,” State Senator Thomas Pressly, who championed the bill, said to other lawmakers on Thursday. “But I truly believe this is the right step for making sure that the criminal action on the front end is stopped.”Doctors and other medical professionals warned lawmakers that the bill would send the false message that the drugs are dangerous, and that it could cause delays in treatment for patients with medical needs not related to abortion.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

15 hours agoJoanna Morris

For two weeks at the 140-hospital system, doctors and nurses have had little access to digital records for patient histories, resorting to paper and faxes to treat people.In more than a dozen states, doctors and nurses have resorted to paper and handwritten treatment orders to chart patient illnesses and track them, unable to access the detailed medical histories that have long been available only through computerized records.Patients have waited for long stints in emergency rooms, and their treatments have been delayed while lab results and readings from machines like M.R.I.s are ferried through makeshift efforts lacking the speed of electronic uploads.For more than two weeks, thousands of medical personnel have turned to manual methods after a cyberattack on Ascension, one of the nation’s largest health systems with about 140 hospitals in 19 states and the District of Columbia.The large-scale attack on May 8 was eerily reminiscent of the hack of Change Healthcare, a unit of UnitedHealth Group that manages the nation’s largest health care payment system. The assault shut down Change’s digital billing and payment routes, leaving hospitals, doctors and pharmacists without ways to communicate with health insurers for weeks. Patients were unable to fill prescriptions, and providers could not get paid for care.While some earlier cyberattacks affected a single hospital or smaller medical networks, the breakdown at Change, which handles a third of all U.S. patient records, underscored the dangers of consolidation when one entity becomes so essential to the nation’s health system.Ascension systems remain down indefinitely, but doctors and nurses are working to find ways of getting access to some information about patients’ medical histories by looking at health records kept by other providers. Ascension is also telling doctors and nurses that they will soon be able to see existing digital records.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

New research from Flinders University has revealed that feeling a sense of belonging to a social group can have a significant impact on our food choices, potentially nudging us towards healthier options.
“Social groups, such as one’s nationality or university, provide group members with a shared social identity, or a sense of belonging, and can influence their behaviour,” says Professor Eva Kemps, from the College of Education, Psychology and Social Work.
“Accordingly, when someone sees themselves as belonging to a group, and feels that their membership to the group is an important part of their identity, they are more likely to bring their behaviour in line with what is perceived as the ‘norm’ for that group.
“This has shown to be true in influencing what we eat and the food choices we make, and could have implications for the development of health campaigns and interventions that aim to promote healthier food choices,” she says.
Researchers say making healthier food choices is vital, with 65 per cent of Australians aged 15 and over being overweight or obese. Furthermore, 92 per cent of adults do not meet the recommended five-six daily servings of vegetables and 49 per cent do not eat the recommended two servings of fruit.
A diet that is high in unhealthy foods and low in nutrition is a major contributor to the prevalence of diseases such as diabetes, heart disease and cancer, which are the leading causes of death worldwide.
The new study tested the idea that people are more likely to adopt healthy food choices if they feel like they belong to the same group or community as those who are promoting healthy eating habits.

Study recipients were undergraduate students, and their university affiliation was used as the example of their valued group membership, meaning that they were either part of the same university group (in-group) or not (out-group).
Conducted using Facebook groups — a popular platform for university community pages — students either felt an affinity to, or indifference to, a group and were then presented with healthy and less healthy food options and assessed on their choices.
“When people are exposed to social norms on Facebook such as what others eat, they are more likely to be influenced by someone in the same group with them than by someone who isn’t. This builds on the age-old adage of the ‘herd mentality’,” says Professor Kemps.
“This is because people are more likely to identify with and internalise the behaviours of someone who shares a common group interest or affiliation with them, which can lead to changes in their own behaviour.
“We found that when people felt a sense of connection or belonging, they were more likely to be influenced one way or the other.
“This builds on the growing literature that shared group membership can affect someone’s behaviour, particularly when it is applied to food choices.
“Whilst the results are promising, further research is required to explore our understanding of social influence and its role in shaping people’s behaviour, especially in the context of food and how we can influence people to make healthier choices,” she adds.
“Our study demonstrates that people within a ‘group’ are more likely to view the behaviour of other perceived group members as an appropriate or relevant guide. Therefore, seeing fellow group members make healthy choices — or receiving a healthy food recommendation from them — may promote healthier eating habits,” says study lead-author Juliana Gleaves.
“We hope the outcomes of our findings will lead to further research in this area that ultimately generates improved communications and support materials for health campaigns and interventions that promote healthier food choices in social media settings and beyond,” she adds.

A new study led by UC Davis researchers finds widespread differences in brain development between autistic boys and girls ages 2-13. The study, published recently in Molecular Psychiatry, found sex-specific changes in the thickness of the outer layer of the brain, called the cortex.
The findings are notable because so few studies have addressed cortical development in autistic girls, who are diagnosed with autism less often than males. Nearly four males are diagnosed with autism for every one female.
“It is clear that this sex bias is due, in part, to underdiagnosis of autism in females,” said Christine Wu Nordahl, a professor in the Department of Psychiatry and Behavioral Sciences and the UC Davis MIND Institute and a senior author on the paper. “But this study suggests that differences in diagnosis are not the full story — biological differences also exist.”
The brain’s outer layer, the cortex, is made up of distinct layers comprised of millions of neurons. These fire in sync together, allowing us to think, learn, solve problems, build memories, and experience emotions. Until about age 2, the cortex rapidly thickens as new neurons are created. After this peak, the outer cortical layer thins. Previous studies have found that this thinning process is different in autistic children than non-autistic children, but whether autistic boys and girls share the same differences had not been examined.
“It’s important to learn more about how sex differences in brain development may interact with autistic development and lead to different developmental outcomes in boys and girls,” explained Derek Andrews, lead author on the study and an assistant project scientist in the Department of Psychiatry and Behavioral Sciences and at the MIND Institute.
A changing cortex in childhood
The research team studied the brain scans of 290 autistic children — 202 males and 88 females, and 139 non-autistic, typically developing individuals — 79 males and 60 females. They used sex assigned at birth to categorize the children.

All participants were in the MIND Institute’s Autism Phenome Project (APP), one of the largest longitudinal autism studies in the world. The project includes the Girls with Autism Imaging of Neurodevelopment (GAIN) study, launched to increase the number of females represented in research. The researchers took MRI scans at up to four time periods between the ages of 2 and 13.
They found that at age 3, autistic girls had a thicker cortex than non-autistic girls of the same age, comprising about 9% of the total cortical surface. Differences in autistic males when compared to non-autistic males of the same age were much less widespread.
In addition, when compared to males, autistic females had faster rates of cortical thinning into middle childhood. The cortical differences were present across multiple neural networks.
“We found differences in the brain associated with autism across nearly all networks in the brain,” Andrews said.
He noted that it was a surprise at first that the differences were greatest at younger ages. Because autistic girls had a more rapid rate of cortical thinning, by middle childhood, the differences between autistic males and females were much less pronounced.
“We typically think of sex differences as being larger after puberty. However, brain development around the ages of 2-4 is highly dynamic, so small changes in timing of development between the sexes could result in large differences that then converge later,” Andrews explained.

The importance of long-term studies of both sexes
These findings make it clear that longitudinal studies that include both sexes are necessary, Nordahl said.
“If we had only looked at boys at age 3, we may have concluded that there were no differences. If we had both boys and girls, but only investigated differences at 11 years of age, we may have concluded that there were very few sex differences in the cortex. We needed to follow both boys and girls across development to see the full picture,” she explained.
This was why Nordahl, who now directs the APP, launched the GAIN study in 2014. “The APP had a wonderfully large sample of about 150 autistic boys, but only about 30 autistic girls. This was too few autistic girls to really examine how they might be similar or different to boys, so we worked to increase the representation of autistic females in our research,” she said.
GAIN is unique, and Andrews said he hopes other researchers will follow suit in including more autistic girls in autism research. “Autistic females represent about 20% of the autistic population. Any successful effort to understand autism will need to include autistic females.”
Co-authors on the study include Kersten Diers and Martin Reuter of the German Center for Neurodegenerative Diseases; Devani Cordero of Massachusetts General Hospital; and Joshua K. Lee, Danielle J. Harvey, Brianna Heath, Sally J. Rogers, Marjorie Solomon and David Amaral of UC Davis.
The study was supported by the National Institute of Mental Health (R01MH127046, R01MH128814 and R01MH103284), the National Institute of Child Health and Development (P50 HD093079) and the MIND Institute Intellectual and Developmental Disabilities Research Center (P50 HD103526)

An exploration into the national U.S. dataset on children ever diagnosed with ADHD has revealed an “ongoing and ever-expanding” public health issue.
Findings published in the peer-reviewed Journal of Clinical Child & Adolescent Psychology uncover that approximately one million more children, aged 3-17, had received an ADHD diagnosis in 2022 than in 2016.
The paper reveals around one in nine children have ever received an ADHD diagnosis — 11.4%, or 7.1 million children. Some 6.5 million children (10.5%) currently live with ADHD.
Among children currently living with ADHD, 58.1% have moderate or severe ADHD. 77.9% have at least one co-occurring disorder, approximately half of children with current ADHD (53.6%) received ADHD medication, and 44.4% had received behavioral treatment for ADHD in the past year. Nearly one third (30.1%) did not receive any ADHD-specific treatment.
The results follow an analysis of the 2022 National Survey of Children’s Health (NSCH) dataset. They demonstrate that the estimated prevalence of ADHD (based on a parent report) is higher in the United States than comparable estimates from other countries.
The expert team of authors come from institutions including the Centers for Disease Control and Prevention, the Oak Ridge Institute for Science and Education, and the Health Resources and Services Administration.
In the paper, the team explains the increase of ADHD prevalence can partially be explained by “sociodemographic and child characteristics,” whilst they state societal context can also “contribute to the overall trends in the diagnosis of ADHD.” These include the context around children’s mental health before and during the COVID-19 pandemic.

“Public awareness of ADHD has changed over time. ADHD was historically described as an externalizing disorder with a focus on easily observable hyperactive-impulsive symptoms, and was thought to primarily affect boys,” the authors say.
“With increased awareness of symptoms related to attention regulation, ADHD has been increasingly recognized in girls, adolescents, and adults.
“Moreover, ADHD has previously been diagnosed at lower rates among children in some racial and ethnic minority groups. With increased awareness, such gaps in diagnoses have been narrowing or closing.
“Circumstances related to the pandemic may also have increased the likelihood that a child’s ADHD symptoms could cause impairment. For example, in families where children needed to engage in virtual classroom learning while parents were also working from home, previously manageable ADHD symptoms may have become more impairing or symptoms that were previously unobserved by parents may have become recognizable.”
The aim of this new paper was to provide updated U.S. prevalence estimates of diagnosed ADHD; ADHD severity; co-occurring disorders; and receipt of ADHD medication and behavioral treatment.
The team assessed 45,483 completed interviews, monitoring, as well, differences in demographic and clinical subgroups. Questions asked parents for details such as the severity of the condition.

Findings highlight how socioeconomic and geographic factors play a part in diagnosis/prevalence of ADHD.
For example: Asian and Hispanic/Latino children had a lower prevalence of diagnosed ADHD than White children. Children living in households with high school as the highest level of education and lower-income households had a higher prevalence than children living in households with more education and with income ≥200% of the federal poverty level, respectively. Children with public insurance (with or without private insurance) had a higher prevalence than children with private insurance alone. Prevalence was also higher for children living in the Northeast, Midwest, or South compared to those living in the West and for children living in rural or suburban areas compared to children living in urban areas.The results also demonstrated how such factors impacted upon medicated treatment: Hispanic children and children living in non-English-speaking households had a lower prevalence of taking ADHD medication than non-Hispanic children and children living in primarily English-speaking homes, respectively. A higher prevalence of children with both public and private insurance were taking ADHD medication than children with private insurance only. A higher prevalence of children living in the Midwest and South were taking ADHD medication compared to children in the West.Other behavioral treatments, such as mental health counseling, also followed similar patterns. Explaining the findings further, the authors state: “Shifts in patterns of treatments may also be affected by changes in the demographic distribution of who receives ADHD diagnoses.
“There is evidence that the sex difference for diagnosis of ADHD may be narrowing; in prior years, the ratio of boys to girls diagnosed with ADHD was more than 2:1.”
Concluding, the team state that they hope their findings can be used by clinicians to understand diagnosis and treatment patterns to better inform clinical practice. As well, they hope it could be used by policymakers, government agencies, health care systems, public health practitioners, and other partners to plan for the needs of children with ADHD, such as by ensuring access to care and services for ADHD.
Future research, the team states, could investigate patterns of service delivery during and after the pandemic; as well as modes of ADHD service delivery; uptake and discontinuation of ADHD medication; and receipt of evidence-based behavioral treatment and other recommended services such as school services.
This study is subject to a number of limitations, including it being based on a survey of parent recall and reporting decisions and have not been validated against medical records or clinical judgment.

Novel real-time PCR method might become diagnostic tool targeting emerging bacterium responsible for food poisoning outbreaks.
The prevalence of pathogenic E. coli has meant the frequent misidentification of a similar bacterium of the Escherichia genus. E. albertii is an emerging zoonotic foodborne pathogen, first isolated in Bangladesh in 1991. Large-scale outbreaks of food poisoning caused by E. albertii have since been reported especially in Japan, causing severe symptoms in both children and adults.
In the hopes of establishing a diagnostic method, a joint research group led by Professor Shinji Yamasaki and Dr. Sharda Prasad Awasthi, a specially appointed associate professor, from the Graduate School of Veterinary Science at Osaka Metropolitan University, have developed a way to detect E. albertii more accurately using a quantitative real-time PCR method.
Specimen examination using this technique showed that E. albertii survived in the human intestinal tract for approximately four weeks and continued to be found in feces. The identical genotype of the bacterial DNA of E. albertii that infected siblings also suggested that intrafamilial transmission may have occurred.
“These results and a novel real-time PCR developed in this study are expected to contribute not only to the selection of appropriate treatment for E. albertii gastroenteritis, but also to the elucidation of the source and route of infection,” Professor Yamasaki declared.

Using population-wide registry data, researchers from the University of Helsinki, the Finnish Institute for Health and Welfare, the University of Jyväskylä and the University of Manchester investigated whether mental disorders can be transmitted within social networks formed by school classes.
The study is the largest and most comprehensive so far on the spread of mental disorders in social networks, with more than 700,000 ninth-grade pupils from 860 Finnish schools participating. The adolescents were followed from the end of ninth grade for a median of 11 years.
The researchers demonstrated that the number of classmates diagnosed with a mental disorder was associated with a higher risk of receiving a mental disorder diagnosis later in life.
“The observed link was the strongest during the first year of follow-up in the study. This was not explained by a number of factors related to parents, school and residential area. The link was most pronounced in the case of mood, anxiety and eating disorders,” says Associate Professor Christian Hakulinen of the University of Helsinki.
Research enabled by comprehensive Finnish registers
According to Hakulinen, prior studies have yielded similar results: for example, American researchers have observed indications of depressive symptoms potentially being transmitted from one individual to another in social networks.
In prior research, however, social networks have typically been chosen independently by the research subjects, which may result in bias in the data. Hakulinen points out that school classes are social networks well suited to research, as people are usually not able to choose their classmates.

“Defining the social networks and following adolescents were made possible by extensive Finnish registers. The findings significantly deepen our understanding of how mental health problems develop and affect other people in our social networks,” he says.
Hakulinen nevertheless notes that the connection observed in the study is not necessarily causal. Furthermore, the study did not investigate how mental disorders can potentially be transmitted between individuals.
“It may be possible, for instance, that the threshold for seeking help for mental health issues is lowered when there are one or more people in your social network who have already sought help for their problems. In fact, this kind of normalisation of diagnosis and treatment can be considered beneficial contagion of mental disorders,” Hakulinen says.
More preventive measures?
Mental disorders are a significant global challenge, adversely affecting individuals, society and the economy. According to Hakulinen, anxiety and mood symptoms in particular have in recent years increased among young people.
Previous studies have shown that, in roughly half of all cases, the onset of mental disorders in adulthood occurs when people are under 18. In fact, Hakulinen emphasises the importance of preventive measures and early intervention.
“When taking preventive measures, it’s worthwhile considering that mental disorders can spread from one adolescent to another,” Hakulinen says.
The study involved a total of 713,809 Finnish citizens born between 1985 and 1997. The adolescents were investigated from the end of comprehensive school until they received their first mental disorder diagnosis, relocated from the country or died. At the latest, the follow-up was discontinued at the end of 2019, resulting in a median follow-up period of 11.4 years.
The study received funding from the European Research Council (ERC) and the Research Council of Finland.