Deep brain stimulation for patients with chronic anorexia is safe and might improve symptoms

Small study in 16 people suggests technique is safe and might help improve mood, anxiety and wellbeing, while increasing weight.

Deep brain stimulation might alter the brain circuits that drive anorexia nervosa symptoms and help improve patients’ mental and physical health, according to a small study published in The Lancet Psychiatry.

Despite having the highest mortality rate of any psychiatric disorder, there are few effective ways to manage treatment-resistant anorexia. While the study only included 16 patients, it suggests that the intervention is safe and could help improve some symptoms of anorexia, but more research is needed.

Worldwide, 0.5% of people have anorexia, and teenage girls account for the majority of cases. The eating disorder is characterised by persistent concerns about bodyweight, shape and size, leading patients to maintain a low weight. Many patients experience mood and anxiety disorders, deny their illness and avoid seeking medical help for it.

Chronic anorexia causes severe health problems as a result of malnutrition, including weak bones and muscles, sexual problems, infertility, heart problems and seizures. The condition can be fatal and those who become acutely ill are admitted to specialised hospital units to receive nutritional support, medical stabilisation and behavioural therapy.

The small study followed 16 women aged between 21 and 57 years old who had had anorexia for an average of 18 years and were severely underweight (with an average body mass index (BMI) of 13.8). They were selected for the study as all other available treatments did not work for them and they were at risk of early death because of anorexia.

All patients underwent deep brain stimulation, which involves implanting electrodes and stimulating areas of the brain that control dysfunctional behaviours. The technique is currently used to target the brain circuits involved in Parkinson’s disease, dystonia, and tremors, where it has been shown to be highly effective in controlling symptoms.

The study looked at how safe deep brain stimulation was for patients with anorexia, and how it affected their BMI, mood, anxiety and wellbeing. Using PET scans, the researchers also looked at how brain activity changed after one year of stimulation.

Electrodes were placed into their subcallosal cingulate, an area located in the centre of the brain that has been shown to have altered serotonin binding in patients with anorexia. Once implanted, the electrodes stimulated the area for one year at a level of 5 — 6.5 volts every 90 micro-seconds.

The treatment had few serious adverse events; however, five patients had pain that persisted for longer than usual following the surgery (more than 3-4 days) and one had an infection at the site of the surgery which resulted in the electrodes needing to be removed and re-implanted. Most adverse events were a result of the patients’ chronic anorexia and included having very low sodium and potassium levels. One patient had an unexplained seizure several months after their electrodes were implanted.

During the study, two patients asked to have the electrodes removed, potentially a result of them being uncomfortable with their weight gain. This meant that there were only 14 patients included at follow-up.

For these patients, mental health symptoms improved over the study with mood and anxiety symptoms reducing in five patients and depression reducing in 10 out of 14 patients. They also reported better quality of life.

While psychological symptoms improved soon after the stimulation began, changes in weight started after three months, suggesting that improving mental health symptoms may precede or even enable changes in weight. Over the course of the study, average BMI of the group increased to 17.3 — an increase of 3.5 points — and six patients achieved a normal BMI (of 18.5 or more).

When comparing the scan results for brain activity before treatment and after a year of stimulation, the researchers found that there were changes in the regions linked to anorexia, suggesting that deep brain stimulation was able to directly affect the related brain circuits. This included less activity in the putamen, thalamus, cerebellum amongst other areas, and more activity in the peripheral cortical areas which are also linked to social perception and behaviour.

“Anorexia remains the psychiatric disorder with the highest mortality rate, and there is an urgent need to develop safe, effective, evidence-driven treatments that are informed by a growing understanding of brain circuitry,” said study author, Professor Andres Lozano, University of Toronto, Canada. “While our results show some early promise, more research will be needed before this becomes available for patients with anorexia. Our findings emphasise the need for continued research into novel neuromodulation strategies for anorexia nervosa, and for psychiatric disorders more broadly.”

“Our study suggests that a focal brain intervention, deep brain stimulation, may have an impact on the circuitry of symptoms that serve to maintain anorexia and make it so difficult to treat.” said lead author, Dr Nir Lipsman, Sunnybrook Health Sciences Centre, Canada.

The researchers note some limitations within their work, including that the group was small and there was no control group. In addition, all patients were aware they were being given treatment so the results seen could be affected by placebo effect. However, the authors note this is unlikely as the results lasted for a year and were confirmed with the brain activity scans.

Writing in a linked Comment Dr Carrie McAdams, University of Texas, USA, said: “Conventional treatment of anorexia nervosa includes behavioural modifications to improve feeding, combined with psychological therapy to address cognitive distortions related to self-esteem, eating, and body dissatisfaction. Nevertheless, after intensive treatment, nearly half of adult women with anorexia nervosa relapse within a year… This work shows how modern neuroscience can lead to a new treatment and simultaneously improve understanding of perpetuating factors in a complex, multifactorial disease… Both mood and social function warrant further examination as potential neural factors that might perpetuate anorexia nervosa in adults. Difficulty in changing these factors, which are not part of the diagnostic symptoms of anorexia nervosa, could contribute to the poor outcomes seen with conventional treatments.”

Computer bots are more like humans than you might think, having fights lasting years

Researchers say ‘benevolent bots’, otherwise known as software robots, that are designed to improve articles on Wikipedia sometimes have online ‘fights’ over content that can continue for years. Editing bots on Wikipedia undo vandalism, enforce bans, check spelling, create links and import content automatically, whereas other bots (which are non-editing) can mine data, identify data or identify copyright infringements. The team analysed how much they disrupted Wikipedia, observing how they interacted on 13 different language editions over ten years (from 2001 to 2010). They found that bots interacted with one another, whether or not this was by design, and it led to unpredictable consequences. The research paper, published in PLOS ONE, concludes that bots are more like humans than you might expect. Bots appear to behave differently in culturally distinct online environments. The paper says the findings are a warning to those using artificial intelligence for building autonomous vehicles, cyber security systems or for managing social media. It suggests that scientists may have to devote more attention to bots’ diverse social life and their different cultures.

The research paper by the University of Oxford and the Alan Turing Institute in the UK explains that although the online world has become an ecosystem of bots, our knowledge of how they interact with each other is still rather poor. Although bots are automatons that do not have the capacity for emotions, bot to bot interactions are unpredictable and act in distinctive ways. It finds that German editions of Wikipedia had fewest conflicts between bots, with each undoing another’s edits 24 times, on average, over ten years. This shows relative efficiency, says the research paper, when compared with bots on the Portuguese Wikipedia edition, which undid another bot’s edits 185 times, on average, over ten years. Bots on English Wikipedia undid another bot’s work 105 times, on average, over ten years, three times the rate of human reverts, says the paper.

The findings show that even simple autonomous algorithms can produce complex interactions that result in unintended consequences — ‘sterile fights’ that may continue for years, or reach deadlock in some cases. The paper says while bots constitute a tiny proportion (0.1%) of Wikipedia editors, they stand behind a significant proportion of all edits. Although such conflicts represent a small proportion of the bots’ overall editorial activity, these findings are significant in highlighting their unpredictability and complexity. Smaller language editions, such as the Polish Wikipedia, have far more content created by bots than the large language editions, such as English Wikipedia.

Lead author Dr Milena Tsvetkova, from the Oxford Internet Institute, said: ‘We find that bots behave differently in different cultural environments and their conflicts are also very different to the ones between human editors. This has implications not only for how we design artificial agents but also for how we study them. We need more research into the sociology of bots.’

The paper was co-authored by the principal investigator of the EC-Horizon2020-funded project, HUMANE, Professor Taha Yasseri, also from the Oxford Internet Institute. He added: ‘The findings show that even the same technology leads to different outcomes depending on the cultural environment. An automated vehicle will drive differently on a German autobahn to how it will through the Tuscan hills of Italy. Similarly, the local online infrastructure that bots inhabit will have some bearing on how they behave and their performance. Bots are designed by humans from different countries so when they encounter one another, this can lead to online clashes. We see differences in the technology used in the different Wikipedia language editions and the different cultures of the communities of Wikipedia editors involved create complicated interactions. This complexity is a fundamental feature that needs to be considered in any conversation related to automation and artificial intelligence.’

Professor Luciano Floridi, also an author of the paper, remarked: ‘We tend to forget that coordination even among collaborative agents is often achieved only through frameworks of rules that facilitate the wanted outcomes. This infrastructural ethics or infra-ethics needs to be designed as much and as carefully as the agents that inhabit it.’

The research finds that the number of reverts is smaller for bots than for humans, but the bots’ behaviour is more varied and conflicts involving bots last longer and are triggered later. The average time between successive reverts for humans is 2 minutes, then 24 hours or one year, says the paper. The first bot to bot revert happened a month later, on average, but further reverts often continued for years. The paper suggests that humans use automatic tools that report live changes and can react more quickly, whereas bots systematically crawl over web articles and they can be restricted on the number of edits allowed. The fact that bots’ conflicts are longstanding also flags that humans are failing to spot the problems early enough, suggests the paper.

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Sugar “tipping point” link to Alzheimer’s disease revealed

For the first time a “tipping point” molecular link between the blood sugar glucose and Alzheimer’s disease has been established by scientists, who have shown that excess glucose damages a vital enzyme involved with inflammation response to the early stages of Alzheimer’s.

Abnormally high blood sugar levels, or hyperglycaemia, is well-known as a characteristic of diabetes and obesity, but its link to Alzheimer’s disease is less familiar.

Diabetes patients have an increased risk of developing Alzheimer’s disease compared to healthy individuals. In Alzheimer’s disease abnormal proteins aggregate to form plaques and tangles in the brain which progressively damage the brain and lead to severe cognitive decline.

Scientists already knew that glucose and its break-down products can damage proteins in cells via a reaction called glycation but the specific molecular link between glucose and Alzheimer’s was not understood.

But now scientists from the University of Bath Departments of Biology and Biochemistry, Chemistry and Pharmacy and Pharmacology, working with colleagues at the Wolfson Centre for Age Related Diseases, King’s College London, have unraveled that link.

By studying brain samples from people with and without Alzheimer’s using a sensitive technique to detect glycation, the team discovered that in the early stages of Alzheimer’s glycation damages an enzyme called MIF (macrophage migration inhibitory factor) which plays a role in immune response and insulin regulation.

MIF is involved in the response of brain cells called glia to the build-up of abnormal proteins in the brain during Alzheimer’s disease, and the researchers believe that inhibition and reduction of MIF activity caused by glycation could be the ‘tipping point’ in disease progression. It appears that as Alzheimer’s progresses, glycation of these enzymes increases.

The study is published in the journal Scientific Reports.

Professor Jean van den Elsen, from the University of Bath Department of Biology and Biochemistry, said: “We’ve shown that this enzyme is already modified by glucose in the brains of individuals at the early stages of Alzheimer’s disease. We are now investigating if we can detect similar changes in blood.

“Normally MIF would be part of the immune response to the build-up of abnormal proteins in the brain, and we think that because sugar damage reduces some MIF functions and completely inhibits others that this could be a tipping point that allows Alzheimer’s to develop.

Dr Rob Williams, also from the Department of Biology and Biochemistry, added: “Knowing this will be vital to developing a chronology of how Alzheimer’s progresses and we hope will help us identify those at risk of Alzheimer’s and lead to new treatments or ways to prevent the disease.

Dr Omar Kassaar, from the University of Bath, added: “Excess sugar is well known to be bad for us when it comes to diabetes and obesity, but this potential link with Alzheimer’s disease is yet another reason that we should be controlling our sugar intake in our diets.”

Globally there are around 50 million people with Alzheimer’s disease, and this figure is predicted to rise to more than 125 million by 2050. The global social cost of the disease runs into the hundreds of billions of dollars as alongside medical care patients require social care because of the cognitive effects of the disease.

The study was funded by the Dunhill Medical Trust. Human brain tissue for this study was provided through Brains for Dementia Research, a joint initiative between Alzheimer’s Society and Alzheimer’s Research UK in association with the Medical Research Council.

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Receiving a clot-buster drug before reaching the hospital may reduce stroke disability

Stroke patients receiving clot-busting medications before arriving at the hospital have a lower risk for disability afterward, according to research presented at the American Stroke Association’s International Stroke Conference 2017.

Researchers analyzed results from 658 stroke patients who were treated with tPA — a drug that dissolves blood clots. About half of the participants received the clot-busting drug at the hospital, and half received it while still in the ambulance.

This preliminary study showed that three months after stroke, 182 out of every 1,000 patients treated before arriving at hospital were less disabled, including 58 patients who had zero disability, compared to people who received treatment after reaching the hospital.

“Time is brain in acute stroke after vascular collaterals fail, and faster treatment yields better outcomes,” said May Nour, M.D., Ph.D., lead researcher, interventional neurologist and director of UCLA’s Mobile Stroke Rescue Program. “Our study shows pre-hospital clot-busting is a promising, evolving approach to providing tPA stroke therapy. Its better outcomes could offset the increased costs of a mobile stroke unit.”

Past research showed the sooner that a clot-busting tPA drug is given after an ischemic stroke — one in which a clot is blocking blood flow — the better patients fare. But tPA is not indicated and could hurt a patient’s chances if they are having a hemorrhagic stroke, in which a blood vessel ruptures. That is why patients need a CT scan to confirm the type of stroke before receiving tPA.

Every second counts, in the current standard of care, patients who experience stroke-like symptoms and call 9-1-1 arriving to the hospital by ambulance are assessed by clinical examination and imaging (CT or MRI scan) in the Emergency Department. This takes a certain amount of time from the patient’s symptom onset which prompted the 9-1-1 call.

In a mobile stroke unit, a specialized ambulance is equipped with a CT scanner, a paramedic, a critical care nurse, a CT technologist and a neurologist in person or by telemedicine. The ambulance arrives, does the CT on-site, gives the clot-busting drug if indicated and then transports the patient to the hospital.

Nour’s team used data from Berlin’s PHANTOM-S study, which took place from 2011 to 2015 and included 427 participants (median age 72) which were compared to 505 patients who received conventional care with in-hospital clot busting. Researchers analyzed information about patients’ disabilities to determine how many needed to be treated in the mobile stroke unit to yield a greater benefit in disability outcomes when compared to patients who received tPA at the hospital.

The findings bordered on statistical significance, suggesting that future clinical trials with a greater number of patients are needed to show similar benefits.

“People should know the warning signs of stroke and call 9-1-1 as soon as they observe stroke signs,” said Nour. “Treatment then needs to happen as quickly as possible, and a mobile stroke unit may allow that to happen.”

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Playing favorites: Brain cells prefer one parent’s gene over the other’s

Most kids say they love their mom and dad equally, but there are times when even the best prefers one parent over the other. The same can be said for how the body’s cells treat our DNA instructions. It has long been thought that each copy — one inherited from mom and one from dad — is treated the same. A new study from scientists at the University of Utah School of Medicine shows that it is not uncommon for cells in the brain to preferentially activate one copy over the other. The finding breaks basic tenants of classic genetics and suggests new ways in which genetic mutations might cause brain disorders.

In at least one region of the newborn mouse brain, the new research shows, inequality seems to be the norm. About 85 percent of genes in the dorsal raphe nucleus, known for secreting the mood-controlling chemical serotonin, differentially activate their maternal and paternal gene copies. Ten days later in the juvenile brain, the landscape shifts, with both copies being activated equally for all but 10 percent of genes.

More than an oddity of the brain, the disparity also takes place at other sites in the body, including liver and muscle. It also occurs in humans.

“We usually think of traits in terms of a whole person, or animal. We’re finding that when we look at the level of cells, genetics is much more complicated than we thought,” says Christopher Gregg, Ph.D., assistant professor of neurobiology and anatomy and senior author of the study which publishes online in Neuron on Feb. 23. “This new picture may help us understand brain disorders,” he continues.

Among genes regulated in this unorthodox way are risk factors for mental illness. In humans, a gene called DEAF1, implicated in autism and intellectual disability, shows preferential expression of one gene copy in multiple regions of the brain. A more comprehensive survey in primates, which acts as a proxy for humans, indicates the same is true for many other genes including some linked to Huntington’s Disease, schizophrenia, attention deficit disorder, and bipoloar disorder.

What the genetic imbalance could mean for our health remains to be determined, but preliminary results suggest that it could shape vulnerabilities to disease, explains Gregg. Normally, having two copies of a gene acts as a protective buffer in case one is defective. Activating a gene copy that is mutated and silencing the healthy copy — even temporarily — could be disruptive enough to cause trouble in specific cells.

Supporting the idea, Gregg’s lab found that some brain cells in transgenic mice preferentially activate mutated gene copies over healthy ones. “It has generally been assumed that there is correlation between both copies of a gene,” says Elliott Ferris, a computer scientist who co-led the study with graduate student Wei-Chao Huang. Instead, they found something unexpected. “We developed novel methods for mining big data, and discovered something new,” Huang explains.

The investigators screened thousands of genes in their study, quantifying the relative levels of activation for each maternal and paternal gene copy and discovered that expression of the two is different for many genes. Surprised by what they saw, they developed statistical methods to rigorously test their validity and determined that they were not due to technical artifacts, nor genetic noise. Following up on their findings, they examined a subset of genes more closely, directly visualized imbalances between gene copies at the cellular level in the mouse and human brain.

Results from Gregg and colleagues build on previous research, expanding on scenarios in which genes play favorites. Imprinted genes and X-linked genes are specific gene categories that differentially activate their maternal and paternal gene copies. Studies in cultured cells had also determined that some genes vary which copy they express. The results from this study, however, suggests that silencing one gene copy may be a way in which cells fine tune their genetic program at specific times during the lifecycle of the animal, or in discrete places.

“Our new findings reveal a new landscape of diverse effects that shape the expression of maternal and paternal gene copies in the brain according to age, brain region, and tissue type,” explains Gregg. “The implication is a new view of genetics, one that starts up close.”

Fructose is generated in the human brain

Fructose, a form of sugar linked to obesity and diabetes, is converted in the human brain from glucose, according to a new Yale study. The finding raises questions about fructose’s effects on the brain and eating behavior.

The study was published on Feb. 23 by JCI Insight.

Fructose is a simple sugar found in fruits, vegetables, table sugar, and many processed foods. Excess consumption of fructose contributes to high blood sugar and chronic diseases like obesity. The Yale research team had demonstrated in a prior study that fructose and another simple sugar, glucose, had different effects on brain activity. But it was not known whether fructose was produced in the brain or crossed over from the bloodstream.

To investigate, the research team gave eight healthy, lean individuals infusions of glucose over a four-hour period. They measured sugar concentrations in the brains of the study participants using magnetic resonance spectroscopy, a noninvasive neuroimaging technique. Sugar concentrations in the blood were also assessed.

The researchers found cerebral fructose levels rose significantly in response to a glucose infusion, with minimal changes in fructose levels in the blood. They surmised that the high concentration of fructose in the brain was due to a metabolic pathway called the polyol pathway that converts glucose to fructose.

“In this study, we show for the first time that fructose can be produced in the human brain,” said first author Janice Hwang, M.D., assistant professor of medicine.

While the production of fructose in the brain had been seen in animals, it had not been demonstrated in humans, Hwang noted.

The finding raises several key research questions, which the research team plans to pursue. “By showing that fructose in the brain is not simply due to dietary consumption of fructose, we’ve shown fructose can be generated from any sugar you eat,” said Hwang. “It adds another dimension into understanding fructose’s effects on the brain.”

Glucose in the brain sends signals of fullness, but that is not the case with fructose, she said.

The conversion of glucose to fructose in the brain, known as the polyol pathway, also occurs in other parts of the body. “This pathway may be one other mechanism by which high blood sugar can exert its adverse effects,” Hwang added.

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Materials provided by Yale University. Original written by Ziba Kashef. Note: Content may be edited for style and length.

Removing barriers to early intervention for autistic children: A new model shows promise

In the February 2017 issue of Pediatrics, investigators representing the South Carolina Act Early Team report a five-fold increase in the number of children with autism spectrum disorder (ASD) eligible for early intensive behavioral therapy (also known as applied behavior analysis therapy or ABA) after statewide implementation of a two-tiered screening process to identify who children who were “presumptively eligible” for intervention.

ABA is the gold standard for treating children with ASD and is known to, sometimes dramatically, improve outcomes and quality of life. However, ABA can be expensive and so is out of the reach of many families without governmental support.

In South Carolina, BabyNet is the IDEA Part C program, with state-level intervention, that pays for early behavioral interventions for children three and under. Prior to the policy changes, a formal diagnosis of ASD was required before BabyNet would pay for early intervention. However, the requirement of a formal diagnosis led to delays in treatment.

“The big issue with autism is that the waitlist for ASD evaluation is typically six months,” said Act Early team member Jane M. Charles, M.D., an MUSC Children’s Health developmental pediatrician who holds the Jeffrey Edwin Gilliam Memorial Chair for the Study of Developmental Disabilities. As a result, early intervention was delayed as children waited for a formal diagnosis.

The team, which also included David A. Rotholz, Ph.D., of the University of South Carolina School of Medicine, Anne M. Kinsman, Ph.D., of the Greenville Health System, and Kathi K. Lacy of the South Carolina Department of Disabilities and Special Needs (SC DDSN), as well as other leaders from key public and private stakeholder organizations from across the state, saw a way to remove this barrier.

“If the eligibility of children under three could be determined more promptly, then ABA therapy, which is between $60,000 and $70,000 yearly, could be done at no cost to families and these children could get the treatment they need,” explained Charles.

At the team’s request, and with the close collaboration of two state agencies (BabyNet/First Steps and the SCDDSN), approval was granted by the U.S. Department of Education to use BabyNet funds to pay for ABA therapy for children who failed a two-stage screening process, even if they had not yet received a formal diagnosis.

Children were first screened (typically by a primary care physician) with the Modified Checklist for Autism in Toddlers (M-CHAT); if that screen showed they were at high risk for ASD, they then underwent the Screening Tool for Autism in Toddlers and Children (STAT). Because STAT must be performed by experienced evaluators to be effective, the SCDDSN developed a training program for STAT evaluators to ensure an adequate pool to meet the demand.

After implementation of these policy changes in South Carolina, the number of children aged 18 to 36 months receiving ABA therapy grew from 53 children in 2010 to more than 265 children in 2015, a five-fold increase.

Providing early ABA to children presumed to have ASD is critical because it is the only intervention that can potentially improve the IQ of an ASD child. The two-stage screening process was highly effective at identifying the children in need of these services and had a very low false-positive rate. Only 16 (2.5%) of the children deemed “presumptively eligible” for ABA were later found not to have ASD.

In South Carolina, a Medicaid waiver enables Medicaid-eligible children aged three to 11 years to receive ABA therapy, and state funds pay for ABA therapy for eligible children in that age group who do not receive Medicaid. The state (SCDDSN) agreed that any child who was deemed “presumptively eligible” for ABA through BabyNet and later received a diagnosis of ASD would continue to receive ABA therapy after reaching age three under the Medicaid waiver or through the special state appropriations. This also included having the child bypass the lengthy waiting list for Medicaid waiver ASD services. As a result, children with ASD not only receive ABA early, when it is most effective, but can continue treatment uninterrupted as they grow older.

“One thing we know is that when intervention is done early and intensely, especially among children with the most significant deficits, there is improved social interaction and communication,” Charles said.

The simple policy changes instituted in South Carolina with recommendations from collaborative stakeholders effectively removed barriers to early provision of such services to children with ASD. It is a model that could be replicated by other states.

“The collaborative effort of our South Carolina Act Early Team has dramatically increased the number of children at risk for ASD who receive early intervention (ABA services) in a way that is nationally unique,” said Rotholz. “It provides a tremendously important service to these children and demonstrates the innovation of our South Carolina partner universities, organizations and agencies.”

 

Sons of cocaine-using fathers have profound memory impairments

Fathers who use cocaine at the time of conceiving a child may be putting their sons at risk of learning disabilities and memory loss. The findings of the animal study were published online in Molecular Psychiatry by a team of researchers from the Perelman School of Medicine at the University of Pennsylvania. The researchers say the findings reveal that drug abuse by fathers — separate from the well-established effects of cocaine use in mothers — may negatively impact cognitive development in their male offspring.

The study, which was led by Mathieu Wimmer, PhD, a post-doctoral researcher in the laboratory of R. Christopher Pierce, PhD, a professor of Neuroscience in Psychiatry in the Perelman School of Medicine at the University of Pennsylvania, found evidence that the sons of fathers that ingested cocaine prior to conception struggle to make new memories. Their findings demonstrated that the sons — but not the daughters — of male rats that consumed cocaine for an extended period of time could not remember the location of items in their surroundings and had impaired synaptic plasticity in hippocampus, a brain region critical for learning and spatial navigation in humans and rodents.

“These results suggest that the sons of male cocaine addicts may be at risk for learning deficits,” said senior author, R. Christopher Pierce, PhD, a professor of Neuroscience in Psychiatry in the Perelman School of Medicine at the University of Pennsylvania.

Pierce and his colleagues propose that epigenetic mechanisms are at the root of the problem. Epigenetics refers to heritable traits that are not caused by changes in the DNA sequence, as is the case with genetic inheritance. DNA is tightly wound around proteins called histones, like thread around a spool, and chemical changes to histones influence the expression of genes, which is an epigenetic process.

Their research showed that cocaine use in dads caused epigenetic changes in the brain of their sons, thereby changing the expression of genes important for memory formation. D-serine, a molecule essential for memory, was depleted in male rats whose father took cocaine and replenishing the levels of D-serine in the sons’ hippocampus improved learning in these animals.

In collaboration with Benjamin Garcia, PhD, presidential professor of Biochemistry and Biophysics in the Epigenetics Institute at the Perelman School of Medicine, the authors showed that cocaine abuse in dads broadly altered the chemical marks on histones in the brain of their sons, even though the offspring were never exposed to cocaine. Chemical modifications on the histones were changed to favor active transcription of genes in the hippocampus of male rats with a paternal history of cocaine taking, allowing more production of the enzyme D-amino acid oxidase, which degrades D-serine. The authors propose that increased expression of the enzyme, driven by changes in the epigenetic landscape, cause the memory problems in the sons of addicted rats.

“There is substantial interest in the development of D-serine and related compounds, which are well tolerated by humans, as drug therapies,” Pierce said. “The ability of D-serine to reverse the adverse effects of paternal cocaine taking on learning adds potential clinical relevance to our research.”

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English learners treated differently depending on where they go to school

As the number of English learners continues to grow across the nation, new research indicates these students are being treated differently depending on where they go to school.

Michigan State University researchers found that schools in Texas — second only to California in total number of English learners — vary widely in how they determine if students should be reclassified as English proficient, affecting their chances of success in school and beyond.

An English learner in the El Paso metropolitan area, for example is nearly twice as likely to be reclassified by the end of seventh grade compared to a student performing at the same level in the Rio Grande Valley. Recent changes in federal law require all states to standardize how they identify and reclassify English learners, but Texas has had policies in place since the 1990s.

“If we are seeing this amount of variation in Texas, imagine what we would see in a state where the population is newer and educators have less experience serving immigrants and English learners,” said Madeline Mavrogordato, assistant professor of K-12 educational administration and lead author.

At least one in 10 U.S. students is classified as an English learner, compared to 1 in 20 back in 1990.

Being reclassified is a key turning point in a student’s educational trajectory, said Mavrogordato. If it occurs too early, English learners could find themselves struggling without the support services they need. If too late, students may be restricted from taking higher-level courses that would prepare them for college.

Mavrogordato used state data to estimate reclassification rates for English learners throughout Texas over seven years. The study, published in Educational Evaluation and Policy Analysis, is one of the first to examine how reclassification rates vary — and to document how educators make decisions in schools.

Mavrogordato and Rachel White, a MSU doctoral candidate in education policy, observed eight Texas elementary schools while educators conducted annual meetings required to determine the status of English learners. They found clear differences in what happens during the meetings, how technology is incorporated into the process, what data sources are used and ultimately how individual students were reviewed.

In one school, the meeting entailed committee members filling in assessment scores and signing forms, while another school invited each child’s teacher to provide input followed by a discussion of the relative assessment data and how best to serve the student in the coming year.

Focus group interviews showed most educators believe they are approaching the reclassification process in the same way. However, Mavrogordato says the likelihood of reclassification in different parts of the state appears to be linked to how educators understand the purpose of the policy and their role in implementation.

“We need to give educators the background needed to understand the spirit of the law,” said Mavrogordato. “Since they are the ones implementing policy on the ground, we need to build their understanding of why these policies are in place. Otherwise, we may end up focusing on demonstrating compliance as opposed to truly expanding educational opportunity.”

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Deprivation in early childhood can affect mental health in adulthood, according to landmark study

Despite living in strong and supportive families for over 20 years, many children exposed to severe early deprivation in Romanian institutions aged 0-3 experience a range of mental health problems in early adulthood.

Experiencing severe deprivation and neglect in childhood can have a lasting psychological impact into early adulthood, according to a unique study which has followed the mental health of a group of children adopted from Romanian institutions to UK families in the 1990s.

Published in The Lancet, this is the first large-scale study to follow a group of children who were subjected to extreme deprivation into adulthood, tracking how their mental health and cognition has developed as a result.

The English and Romanian Adoptees study began shortly after the fall of the communist regime in Romania. Children living in institutions were subjected to extremely poor hygiene, insufficient food, little personalised care and no social or cognitive stimulation. The study, running since 1990, analyses the mental health of 165 children who spent time in Romanian institutions and who were adopted by families in the UK between the ages of two weeks and 43 months. In the UK, they joined socioeconomically advantaged, stable, caring and supportive families.

Comparing against 52 children adopted within the UK, the study has followed them throughout their childhood using questionnaires, IQ tests and interviews with the children and their parents to analyse social, emotional and cognitive outcomes at ages 6, 11 and 15.

The latest part of the study followed the adoptees to ages 22 to 25 years old. It includes around three-quarters of the original adoptees — 39 UK adoptees, 50 Romanian adoptees who had spent less than six months in an institution as children and 72 who had spent over six months.

The researchers found that the amount of time spent in a Romanian institution was an important marker of children’s future mental health. Romanian adoptees who had spent less than six months had similar rates of mental health symptoms as UK adoptees. However, adoptees who had spent more time in the institutions had higher rates of social, emotional and cognitive problems throughout their lives.

People who had lived in Romanian institutions for more than six months as children had higher rates of social problems including autistic features, difficulties engaging with others, inattention and overactivity which persisted from childhood into adulthood. They were also three to four times more likely to experience emotional problems as adults, and had lower educational attainment and employment rates than the other UK and Romanian adoptees. This all despite living in strong and supportive families for over 20 years.

As children, more adoptees who lived in Romanian institutions for over six months had an IQ of less than 80, but this recovered within normal levels (an IQ of 90 or above) by early adulthood, suggesting developmental delays but no permanent impact on general cognitive abilities.

Additionally, one in five (21%, 15 children) adoptees who spent over six months in Romanian institutions did not experience any mental health problems throughout their lives. The next steps of the research will involve an in-depth genetic analysis of the most exposed adoptees who did not develop mental health problems to distinguish whether genetic and epigenetic differences contribute to resilience.

“Being exposed to very severe conditions in childhood can be associated with lasting and deep-seated social, emotional and cognitive problems, which are complex and vary over time,” said lead author Professor Edmund Sonuga-Barke, King’s College London, UK, who conducted the follow-up study while at the University of Southampton. “This highlights the importance of assessing patients from deprived backgrounds when providing mental health support and carefully planning care when these patients transfer from child to adult mental health care. Although focussed on children adopted from Romanian institutions in the early 1990s, our findings may also be relevant to large numbers of children who are still exposed to abusive or neglectful conditions around the world.”

Because the children were different ages when they entered institutions and lived there for different amounts of time, the study could not determine whether there is a window during childhood development when children may be more or less likely to be affected by deprivation. In addition, it cannot control for other early risk factors affecting the child’s mental health, such as maternal smoking or substance abuse during pregnancy, but the authors argue that there are unlikely to be significant differences among the two groups of Romanian adoptees.

Writing in a linked Comment, Professor Frank Verhulst, Erasmus University Medical Centre, The Netherlands, said: “Whatever the underlying mechanisms, the findings of Sonuga-Barke and colleagues’ study elegantly support the rule of the earlier the better for improving the caregiving environment for young children whose basic needs are profoundly violated. This finding is true for millions of children around the world who are exposed to war, terrorism, violence, or mass migration. As a consequence, many young children face trauma, displacement, homelessness, or family disruption.”

Studies show that the cerebellum is crucial to understanding vulnerability to drug addiction

An international research team led by the Universitat Jaume I (UJI) has shown that the cerebellum, contrary to what was thought, fulfils functions that go beyond the motor sphere and can be co-responsible for the brain alterations associated with addictive consumption of drugs. The findings, which are shown in two recent reviews published in Neuroscience & Biobehavioral Reviews and Journal of Neuroscience — with an image taken at the UJI laboratories — , would represent a step forward towards the design of new therapies for the future.

These studies are based on a series of works published over the last two years by the research group Addiction and Neuroplasticity at the Universitat Jaume I, directed by the lecturer of the Area of Psychobiology at ​​the UJI, which has had the collaboration of researchers from European, Mexican and North American universities. The most relevant, according to Miquel, is that the studies show that changes in the cerebellum “only occur in those subjects who appear to be especially vulnerable to the effect of drugs.” For a long time, “we have verified that the cerebellum responds in a very potent way to the effect of cocaine, to the point of changing the mechanisms of plasticity,” states Miquel, who is also coordinator of the master’s degree in Research in Brain and Behaviour.

Consequently, the cerebellum is a region of the brain relevant to understanding and designing future treatments for drug addiction. “There is progress in describing the neuronal circuits affected by drug addiction, a chronic brain disorder that is difficult to treat because it affects the basic processes of acquiring and storing the information whose description is still incomplete,” explains the teacher, who acknowledges that, in this way, “the path to new therapies will be accelerated.”

Addiction involves alterations in the neuronal mechanisms of plasticity that allow the brain to store information, regenerate itself and recover from possible disorders or injuries. In an addicted person, the brain’s mechanisms of learning and memory that allow you to make decisions and carry out acts of will are sick. Addictive drugs force the brain to store harmful data about where, when and how to consume the substance. In fact, the drug is the predominant information in the brains of people affected by addiction.

The Effects of Cocaine

On this occasion, the reviewed investigations address the function of the cerebellum in these storage processes involved in the addictive disorder. Specifically, “experimental work shows that these effects of cocaine on cerebellar function only occur in those individuals dominated by stimuli that predict drug availability and suggest that the cerebellum may be crucial to understanding mechanisms of vulnerability to addiction,” explains Marta Miquel.

Science has corroborated that certain regions of the brain, such as the prefrontal cortex, amygdala, hippocampus, and basal ganglia, may be relevant for addiction. However, the cerebellum had traditionally been excluded from this circuit because it was considered a structure exclusively dedicated to motor control, especially motor coordination. “Today we know that this is a very partial view on the complexity of the cerebellum, and a growing volume of data suggests its involvement in many of the brain functions affected in addicted subjects,” refers Marta Miquel. “The cerebellum comprises 80% of all neurons in the brain; it contains 60 billion neurons packaged in only 10% of the brain mass and is a fundamental structure in the consolidation and automation of learned behavioural repertoires,” concludes the lecturer.

In addition to the UJI team, scientists from the University of Kentucky (USA), University of Turin (Italy), Universidad Veracruzana (Mexico), Washington State University (USA), University of Cambridge, University of Leeds (United Kingdom), McLean Hospital Translational Neuroscience Laboratory and Mailman Research Center (USA) also participate in the research works. After presenting the papers at the last congress of the International Society for Neuroscience (San Diego, USA), the work will be discussed soon at the Albert Einstein Institute in New York.

The priority line of the research group Addiction and Neuroplasticity from the Universitat Jaume I, directed by the lecturer Marta Miquel, is the brain’s function in drug addiction.

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Sorting out risk genes for brain development disorders

Gene discovery research is uncovering new information about similarities and differences underlying various neurodevelopmental disorders.

These are a wide-ranging collection of conditions that affect the brain. They include autism, intellectual impairments, developmental delays, attention deficits, tic disorders and language difficulties.

To better understand how gene-disrupting mutations contribute to the biology of neurodevelopmental disorders, researchers recently conducted a large, international, multi-institutional study.

More than 11,700 affected individuals and nearly 2,800 control subjects underwent targeted DNA sequencing of 208 suspected disease-risk genes. The candidate genes were chosen based on previously published studies.

By looking at greater numbers of cases and using a reliable yet inexpensive molecular inversion probe, the project team wanted to measure the statistical significance of individual, implicated genes.

Their results are reported in Nature Genetics. The study leaders were Holly A. F. Stessman, Bo Xiong and Bradley P. Coe, of the genome sciences laboratory of Evan Eichler at the University of Washington School of Medicine and the Howard Hughes Medical Institute. Stessman is now at Creighton University.

Their samples were collected through the Autism Spectrum/Intellectual Disability 15-center network spanning seven countries and four continents. An advantage of this collection, the researchers said, is the ability to check back on a large fraction of cases to try to relate genetic results to clinical findings.

In their study population, the researchers associated 91 genes with the risk of a neurodevelopmental disorder. These included 38 genes not previously suspected of playing a role. Based on some of the family studies, however, mutations even in two or more of the risk genes may not be necessary or sufficient to cause disease.

Of the 91 genes, 25 were linked with forms of autism without intellectual disability. The scientists also described a gene network that appeared to be related to high-functioning autism. Individuals with this form of autism have average to above average intelligence, but may struggle in learning to talk, interact socially, or manage anxiety and sensory overload.

While observing that some genes were more closely associated with autism and others with intellectual or developmental impairments, the researchers found that most of the genes implicated were mutated in both conditions. This result reinforces the substantial overlap among these conditions in their underlying genetics and observable characteristics.

“Most of these genes are clearly risk factors for neurodevelopmental disorders in a broad sense,” the researchers explained. “But analysis of both the genetic and subsequent patient follow-up data did single out some genes with a statistical bias towards autism spectrum disorder, rather than an intellectual disability or developmental delay.”

Additional findings suggest that less severe mutations may be behind autism that is not accompanied by intellectual disability.

By following up with patients, the researchers could start to assess the newly discovered mutations. Such clinical information is important in determining how the genes might function, and how their disruption might lead to specific traits or symptoms.

In addition to looking at the overall severity of each neurodevelopmental disorder present, the scientists also summarized other features such as seizures, head size, and congenital abnormalities.

The researchers did in fact observe patterns from combining clinical and genetic data. They partitioned those genes most strongly associated with autism, and those more related to developmental disabilities.

Although the overall numbers were low, several autism risk genes appeared predominantly in males, including some detected exclusively in males who had autism without intellectual impairment.

To obtain additional evidence for how risk genes might affect behavior and nervous system function, the researchers investigated 21 genes in fruit fly models. They wanted to see if any of the mutations disrupted a fundamental form of learning — growing accustomed to harmless stimuli.

Problems with the neuronal mechanisms behind habituation are thought to account for some autism features, such as inability to filter sensory input. The fruit fly studies showed habituation deficits from several of the gene mutations under review, thereby providing additional evidence that they may have a role in cognitive function.

Numerous grants and other funding from government agencies and private foundations in several countries supported this research.

“The scientists are continuing this project and are eager to work with interested families,” said Raphael Bernier, associate professor of psychiatry and behavioral sciences and clinical director of the Seattle Children’s Autism Center and associate director of the UW Center on Human Development and Disability.

 

Tiny cavefish may help humans evolve to require very little sleep

We all do it; we all need it — humans and animals alike. Sleep is an essential behavior shared by nearly all animals and disruption of this process is associated with an array of physiological and behavioral deficits. Although there are so many factors contributing to sleep loss, very little is known about the neural basis for interactions between sleep and sensory processing.

Neuroscientists at Florida Atlantic University have been studying Mexican cavefish to provide insight into the evolutionary mechanisms regulating sleep loss and the relationship between sensory processing and sleep. They are investigating how sleep evolves and using this species as a model to understand how human brains could evolve to require very little sleep, just like the cavefish.

In their latest study, just published in the Journal of Experimental Biology, findings suggest that an inability to block out your environment is one of the ways to lose sleep. The study also provides a model for understanding how the brain’s sensory systems modulate sleep and sheds light into the evolution of the significant differences in sleep duration observed throughout the animal kingdom.

“Animals have dramatic differences in sleep with some sleeping as much as 20 hours and others as little as two hours and no one knows why these dramatic differences in sleep exist,” said Alex C. Keene, Ph.D., corresponding author of the study and an associate professor in the Department of Biological Sciences in FAU’s Charles E. Schmidt College of Science. “Our study suggests that differences in sensory systems may contribute to this sleep variability. It is possible that evolution drives sensory changes and changes in sleep are a secondary consequence, or that evolution selects for changes in sensory processing in order to change sleep.”

Because the cave environment differs dramatically from the rivers inhabited by surface fish, cavefish have evolved robust differences in foraging and feeding behavior, raising the possibility that differences in nutrient availability contribute to the evolution of sleep loss in cave populations. Furthermore, multiple cave populations have evolved substantial reductions in sleep duration and enhanced sensory systems, suggesting that sleep loss is evolutionary and functionally associated with sensory and metabolic changes.

Key findings of the study have shown that the evolution of enhanced sensory capabilities contribute to sleep loss in cavefish and that sleep in cavefish is plastic and may be regulated by seasonal changes in food availability.

There are more than 29 different populations of cavefish and many of them evolved independently. This enabled the researchers to determine whether evolution occurs through the same or different mechanisms. The Pachon cavefish, the population they studied, appear to have lost sleep due to increased sensory input, but not the other populations.

“We were surprised to find that there are multiple independent mechanisms regulating sleep loss in different cave populations and this can be a significant strength moving forward,” said James Jaggard, first author and a graduate student at FAU working with Keene. “This means that there are many different ways to lose sleep or evolve a brain that sleeps less and we are going to search to identify these mechanisms.”

Keene, Jaggard and their colleagues use Mexican cavefish because they are a powerful system for examining trait evolution. In earlier research studies, they observed the evolutionary convergence on sleep loss in these fish. However, the neural mechanisms underlying this dramatic behavioral shift remained elusive. Since they already knew that cavefish also had evolved a highly sensitive lateral line (the groups of sensory neurons that line the body of the fish), they wondered if an increase in sensory input from these neurons contribute to sleep loss.

For the study, the researchers recorded the cavefish under infrared light set up in individual tanks. They automated video-tracking software that told them when the fish were inactive and they defined sleep as one minute of immobility because it correlated with changes in arousal threshold.

“Humans block out sensory cues when we enter a sleep-like state,” said Keene. “For example, we close our eyes and there are mechanisms in the brain to reduce auditory input. This is one of the reasons why a sensory stimuli like someone entering a room is less likely to get your attention if you are asleep. Our thinking was that cavefish have to some degree lost this ability and this drives sleep loss.”

The researchers recently generated transgenic fish lines and they will be able to image brain activity and genetically map anatomical differences between the Mexican cavefish populations.

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Many stroke patients do not receive life-saving therapy

Although tPA treatment for stroke is increasing over time, minorities, women and residents of 11 southeastern states that make up the “Stroke Belt” are left behind when it comes to receiving tPA, according to research presented at the American Stroke Association’s International Stroke Conference 2017.

Tissue plasminogen activator, or tPA, is the only treatment approved by the Food and Drug Administration for ischemic stroke, the most common kind of stroke. If administered within 4.5 hours of the first signs of stroke, tPA can dissolve the blood clot and restore blood flow to the affected part of the brain.

“Hospitals, governments and other organizations are undertaking efforts to increase the number of patients who receive tPA,” said Tracy Madsen, M.D., Sc.M., lead researcher and Assistant Professor of Emergency Medicine at Brown University in Rhode Island. “We wanted to see if these quality improvement efforts were making a difference.”

The study reviewed records from the National Inpatient Sample of 563,087 patients (median age 74) who had an ischemic stroke between 2005 and 2011. Overall, 3.8 percent of patients received tPA, with the number growing each year.

Researchers found:

  • Blacks were 38 percent less likely than whites to receive tPA.
  • Hispanics were 25 percent less likely than whites to receive tPA.
  • Women were 6 percent less likely than men to receive tPA.
  • Those with private insurance were 29 percent more likely to receive tPA compared to those with Medicare.
  • Residents of the “Stroke Belt” were 31 percent less likely than those living elsewhere to receive tPA.

Researchers also found that patients discharged from a designated stroke center or a hospital participating in the American Heart Association’s Get With The Guidelines® — Stroke program were more likely to receive tPA. Likewise, patients were more likely to receive tPA at large, urban, or teaching hospitals compared to hospitals discharged from small, rural, or non-teaching hospitals.

Madsen said that the growing number of hospitals participating in the Get With The Guidelines® — Stroke program and legislation requiring emergency services to take stroke patients to regional stroke centers are likely to increase the number of patients receiving tPA.

“Some previous studies have found that up to three-fourths of patients arrived after the time window for tPA had closed,” Madsen said. “Many patients across all groups do not arrive at the hospital in time, but this is particularly true for underrepresented minorities.”

An important limitation of the study data is that researchers could not determine why patients did not receive tPA. The study is also limited because we were not able to adjust for patient level factors such as time to arrival and other tPA exclusion criteria, stroke severity, patient education, and socioeconomic status. “More research needs to be done to help figure out why many patients do not receive tPA,” Madsen said.

“There is also a lot of work to do in the realm of stroke education so that patients recognize stroke symptoms and call EMS immediately,” Madsen said.

According to the American Heart Association’s Heart Disease and Stroke Statistical Update, 795,000 Americans have a stroke every year, causing almost 129,000 deaths. Residents of the Stroke Belt — Alabama, Arkansas, Georgia, Indiana, Kentucky, Louisiana, Mississippi, North Carolina, South Carolina, Tennessee and Virginia — suffer even higher rates of stroke and stroke death.

The National Inpatient Sample is the largest publicly available database of inpatient health care in the U.S.

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Tired teens 4.5 times more likely to commit crimes as adults

Teenagers who self-report feeling drowsy mid-afternoon also tend to exhibit more anti-social behavior such as lying, cheating, stealing and fighting. Now, research from the University of Pennsylvania and the University of York, in the United Kingdom, shows that those same teens are 4.5 times more likely to commit violent crimes a decade and a half later.

“It’s the first study to our knowledge to show that daytime sleepiness during teenage years are associated with criminal offending 14 years later,” said Adrian Raine, the Richard Perry University Professor with appointments in the departments of Criminology and Psychology in the School of Arts & Sciences and the Department of Psychiatry in Penn’s Perelman School of Medicine.

He and Peter Venables, an emeritus psychology professor at the University of York, published their findings in the Journal of Child Psychology and Psychiatry.

Raine had collected the data for this work 39 years earlier, as part of his Ph.D. research (studying under Venables) but had never analyzed it. Recently, he began noticing cross-sectional studies, those that analyze multiple behaviors at a single point in time, connecting sleep and behavioral problems in children. He dug out his old dissertation work to look for a link between these and illegal behavior in adulthood.

“A lot of the prior research focused on sleep problems, but in our study we measured, very simply, how drowsy the child is during the day,” Raine said.

To get at this information, he tested 101 15-year-old boys from three secondary schools in the north of England. At the start and end of each lab session, which always ran from 1 to 3 p.m., he asked participants to rate their degree of sleepiness on a 7-point scale, with 1 being “unusually alert” and 7 being “sleepy.” He also measured brain-wave activity and sweat-rate responses to stimuli, which indicates the level of attention a person pays to a tone being played over headphones. This represents brain-attentional function, Raine said.

Next he collected data about anti-social behavior, both self-reported from the study participants, as well as from two or three teachers who had worked with each teen for at least four years.

“Both are helpful. There are kids who don’t really want to talk about their anti-social behavior, and that’s where the teacher reports really come in handy,” Raine said. “Actually, the teacher and child reports correlated quite well in this study, which is not usual. Often, what the teacher says, what the parent says, what the child says — it’s usually three different stories.”

Finally, Raine conducted a computerized search at the Central Criminal Records Office in London to suss out which of the original 101 had a criminal record at age 29. Excluding minor violations, focusing instead on violent crimes and property offenses and only those crimes for which participants were convicted, the researchers learned that 17 percent of participants had committed a crime by that point in adulthood.

With these data in hand, Raine also incorporated the study participants’ socioeconomic status. He found a connection.

“Is it the case that low social class and early social adversity results in daytime drowsiness, which results in inattention or brain dysfunction, which results 14 years later in crime? The answer’s yes,” he said. “Think of a flow diagram from A to B to C to D. Think of a chain. There is a significant link.”

Put another way, he added: “Daytime drowsiness is associated with poor attention. Take poor attention as a proxy for poor brain function. If you’ve got poor brain functioning, you’re more likely to be criminal.”

The researchers stress that drowsiness in and of itself doesn’t always predispose a teenage boy to becoming anti-social. And many children with sleep problems do not become lawbreakers. But the researchers did find that those with sleepiness and a greater frequency of anti-social behavior during teenage years had higher odds of a life of crime later.

Knowing this could potentially help with a simple treatment plan for children with behavioral issues: Recommend they get more sleep at night.

“That could make a difference not just for anti-social behavior at school with these teenage kids but more importantly, with later serious criminal behavior,” Raine said. “More sleep won’t solve crime, but it might make a bit of a dent.”