32 results for “gednet”
Genetic study shows the first Hawai'ians came from Easter Island and arrived around 1200 A.D. This work clashes with traditional scholarship, which estimated the first Hawai'ians arrived centuries earlier from the Marquesas and Tahiti.
I expected to find robust discussion of this in some Hawaii forums but haven't really seen any.
Genetic study links Native Hawaiians to Easter Island seafarers
New genetic research indicates Native Hawaiians are most closely related to people from Easter Island, suggesting a founding population arrived from Rapa Nui. The study also highlights significant disease risks due to genetic bottlenecks.
https://hermes-vector.buzz/posts/genetic-study-links-native-hawaiians-to-easter-island-seafarers
📰 Conexión genética entre Rapa Nui y Hawái llega a la portada de Science
🔗 https://www.elmostrador.cl/cultura/ciencia-cultura/2026/10/22/conexion-genetica-entre-rapa-nui-y-hawai-llega-a-la-portada-de-science/
With the advent of custom-made genetically engineered cures for all diseases, scientists warn of the possibility of an extinction-level mutated disease that would wipe out all life on Earth
The Woolly Mammoth Billionaire's New Startup Is Genetically Engineering War Dogs For The Military (Forbes)
https://www.forbes.com/sites/amyfeldman/2026/10/22/the-woolly-mammoth-billionaires-new-startup-is-genetically-engineering-war-dogs-for-the-military/
http://www.memeorandum.com/261022/p137#a261022p137
David Sabatini, reconhecido cientista na área da edição genética, recebeu uma indemnização de cinco milhões de euros após júri ter deliberado que colega que o acusou de assédio sexual o difamou.
https://www.publico.pt/2026/10/20/ciencia/noticia/cientista-afastado-mit-vence-processo-difamacao-apos-acusado-assedio-2191974 #notícias
LRBA deficiency is a rare and severe autoimmune disorder caused by a genetic mutation that disrupts crucial protein recycling pathways within the cell, leading to the accumulation of enlarged endolysosomes and subsequent immune dysfunction.
#MolecularBiology #CellularBiology #Immunology #Genetics #Pathology #sflorg
https://www.sflorg.com/2026/10/mbio10202601.html
The Kremlin appears to be pitching American Eagle with an exciting new denim ad campaign: Putin claimed today that "recent genetic studies" show Russians and Ukrainians are “one people.” Eat your heart out, Sydney Sweeney's genes/jeans! https://t.me/bbbreaking/240648
La llegada de suevos, alanos y visigodos no borró la profunda huella genética de la Hispania romana
La llegada de suevos, alanos y visigodos no borró la... #tardigram #suevos #alanos #visigodos #genética #hispania #Cultura
¡Hermanos de sangre separados por el océano! Investigación internacional revela conexión genética entre Rapa Nui y Hawái
¡Hermanos de sangre separados por el océano!... #tardigram #rapa #nui #hawaii #genética #conexión #Ciencia
https://www.europesays.com/es/828642/ Kira Miró: “Tengo una dulzura genética y a veces siento que esa dulzura y esa amabilidad extrema me convierten en invisible» #Celebrities #Entertainment #Entretenimiento #ES #España #Famosos #Spain
Researchers identify new depression subtype linked to the body clock
Research by experts at the University of Sydney has identified a new subtype of depression called “circadian depression”. …
#NewsBeep #News #Mentalhealth #Brain #depression #Genetic #Genetics #Health #lighttherapy #melatonin #MentalHealth #Psychiatry #research #serotonin #Sleep #Therapy #UK #UnitedKingdom
https://www.newsbeep.com/uk/810748/
Researchers have characterized the "average" human genome using whole-genome sequencing from nearly one million individuals, revealing that extensive genetic variation, including the presence of disease-associated mutations, is a universal biological baseline rather than a physiological anomaly.
#Genomics #HumanGenetics #MolecularBiology #Bioinformatics #sflorg
https://www.sflorg.com/2026/10/geno10222601.html
`Using whole-genome sequences spanning Polynesia, we show that two of the most bottlenecked populations are Hawaiʻi and Easter Island (Rapa Nui) and that these two most closely genetically related yet geographically distant islands were likely settled by the same ultravoyagers with earlier ancestral roots in Mangareva.` https://www.science.org/doi/10.1126/science.aec7662
The news at 03:49:01 is: Title: The tech helping crack decades-old cold cases, Description: Investigative genetic genealogy can help hunt down criminals but raises worries over privacy., https://www.bbc.co.uk/news/articles/c370pzdkw77jo?at_medium=RSS&at_campaign=rss #news #headlines
Asimov Announces Adoption of Its AI-Driven Cell Line Development Platform by LG Chem
Asimov’s CHO Edge System, including the recently announced Chrysalis transposase and Kernel, Asimov’s AI-driven genetic design software, will…
#EuropeSays #Korea #KR #LG #adoption #AI-driven #Announces #Asimov #by #cell #Chem #development #its #LGGroup #line #of #platform
https://www.europesays.com/korea/197368/
Despite the extraordinary advances of the past hundred years or so, the twentieth and twenty-first centuries by no means have a monopoly on genetic insight.... The single greatest application of genetics to human well-being was carried out eons ago by anonymous ancient farmers. Almost everything we eat -- cereals, fruit, meat, dairy products -- is the legacy of that earliest and most far-reaching application of genetic manipulations to human problems.
-- James D. Watson (DNA: The Secret of Life)
https://www.europesays.com/ie/744495/ Researchers identify new depression subtype linked to the body clock #Brain #Depression #Éire #Genetic #Genetics #Health #IE #Ireland #LightTherapy #melatonin #Psychiatry #Research #Serotonin #Sleep #therapy
Callipyge Genetics says genomic test identifies cattle for beef tenderness
Agricultural biotechnology company Callipyge Genetics made a genomic discovery in 2018 that identified the genetic basis for the…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Genetics #beeftenderness #Science #tenderness
https://www.newsbeep.com/us/889172/
https://www.europesays.com/gbr/ham/2165/ Hampshire mother says life of daughter could’ve been different with genetic screening #Hampshire
En Guápiles, provincia de Limón, Costa Rica, fue fotografiado un tucán pico castaño apodado cariñosamente «Tuki». Su aspecto llamó la atención porque, en lugar del plumaje oscuro habitual de su especie, presenta plumas blancas y anaranjadas.
Esta apariencia se atribuye al leucismo, una condición genética que reduce la pigmentación de las plumas.
😍🥰🤩
#Naturaleza #Nature #MedioAmbiente #Environment #VidaSilvestre #Wildlife #MadreNaturaleza #MotherNature
DATE: October 20, 2026 at 06:00PM
SOURCE: PSYPOST.ORG
** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
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TITLE: Early-life pain led to lasting social deficits in mice, and brain stimulation reversed them
Deep brain stimulation may reverse social deficits caused by early-life pain, mouse study suggests
A study on mice found that inflammatory pain early in life led to lasting deficits in social behavior, along with an imbalance between excitatory and inhibitory activity in a brain region called the anterior cingulate cortex. Boosting the region’s excitatory neurons, quieting its inhibitory neurons, or applying deep brain stimulation reversed the social deficits. The paper was published in Translational Psychiatry.
The human brain develops through a complex interaction between genetic instructions and experiences from the environment. This interaction is especially important in early years of life, when the developing brain is highly plastic and particularly sensitive to outside influences. Adverse experiences during childhood, such as abuse, neglect, social isolation, or chronic stress, can interfere with normal brain development and leave lasting changes in both brain structure and function.
Research has linked such experiences to alterations in areas involved in memory, emotional regulation, decision-making, and responses to stress, including the hippocampus, amygdala, and prefrontal cortex. These changes may help explain why early-life adversity is associated with a greater risk of psychological and behavioral difficulties later in life.
Pain experienced during childhood or adolescence can also act as a powerful and persistent source of stress during sensitive stages of development. When pain becomes chronic, its consequences may extend far beyond physical discomfort and affect education, social relationships, later employment, and overall quality of life. Despite this, much less is known about how painful experiences early in life influence the development of brain systems responsible for complex social behavior.
Study author Xiangdong Wan of Xuanwu Hospital, Capital Medical University, in Beijing and colleagues set out to examine the long-term effects of early-life pain on social behavior. They focused on the anterior cingulate cortex, a region toward the front of the brain that is involved both in processing social information and in the emotional, unpleasant side of pain. The region’s normal function depends on a precise balance between excitatory neurons, which increase activity in the networks they connect to, and inhibitory neurons, which dampen it. The researchers hypothesized that early-life pain disrupts this balance, leading to social deficits.
The researchers used male and female laboratory mice, including genetically modified strains that allowed them to target excitatory or inhibitory neurons specifically. In these mice, the researchers could make one type of neuron glow so it could be counted, record its activity, or switch it on or off using light (optogenetics) or a designer drug that acts only on engineered receptors (chemogenetics).
When the mice were 10 days old, the researchers injected a substance called Complete Freund’s Adjuvant into one hind paw of mice in one group, producing inflammation that made the paw more sensitive to pressure and heat. A control group received a saline injection instead. To find out whether timing mattered, the researchers also gave the injection to other groups of mice at 6, 9, 12, 15, 18, or 21 days of age.
By adulthood, the mice’s sensitivity to pressure and heat had returned to normal, but those that had experienced early-life pain showed social deficits. Unlike control mice, which preferred a chamber containing an unfamiliar mouse over one containing an empty cage, they showed no preference between the two. The deficit appeared in both males and females, persisted to at least 16 weeks of age, and occurred only when the injection was given at 12 days of age or younger.
The mice that had experienced early-life pain still showed normal interest in a newly introduced mouse, and they did not show more anxiety-like behavior than control mice. The authors suggest this points to a specific loss of social motivation rather than general anxiety or memory problems.
When the pain-exposed mice approached an unfamiliar mouse, excitatory neurons in their anterior cingulate cortex became less active than those of control mice. In control mice, inhibitory neurons in the region normally quieted down during social approach, but this drop was smaller in pain-exposed mice, leaving the region relatively more inhibited. Measurements of chemical messengers showed a matching pattern, with less release of the excitatory messenger glutamate and a smaller drop in the inhibitory messenger GABA during social approach, and the pain-exposed mice also had fewer excitatory and more inhibitory neurons in the region.
Boosting the activity of excitatory neurons or dampening the activity of inhibitory neurons, using light or designer drugs, rescued the social deficit in pain-exposed mice. In healthy mice, the opposite manipulations produced social deficits. Infusing drugs that enhance glutamate signaling or block GABA receptors directly into the region also improved social behavior, although not fully.
Finally, the researchers implanted an electrode in the anterior cingulate cortex to deliver deep brain stimulation, a technique already in clinical use in humans. At the setting they selected, stimulation increased the activity of excitatory neurons while only mildly activating inhibitory ones, and applying it during testing reversed the social deficit in pain-exposed mice. A higher setting caused seizure-like reactions in some mice.
“This study unveils a core mechanism whereby early-life pain impairs social function by inducing a state of hypoexcitation [reduced activation] and hyperinhibition [increased inhibition] in the ACC [anterior cingulate cortex]. Furthermore, we establish that DBS [deep brain stimulation] can effectively rectify this ACC imbalance, providing a novel theoretical basis and a potential translational strategy for intervening in social deficits associated with developmental trauma,” study authors concluded.
The study contributes to the scientific understanding of the importance of early experiences for adult life. However, it should be noted that the study was conducted on mice, not on humans. Although mice and humans share many genetic and physiological similarities, they are still very different species, and a brief inflammatory injury in mouse pups is not the same as chronic pain in children.
In addition, the researchers were not blinded to which mice were in which group during testing, and the stimulation was tested only while it was switched on, so it is not known whether its benefits last. The researchers also did not track the estrous cycle in female mice, which can affect social behavior.
The paper, “Deep brain stimulation ameliorates social deficits from early-life pain by restoring excitatory/inhibitory balance in the anterior cingulate cortex,” was authored by Xiangdong Wan, Tao Du, Dou Yang, Zaiying Jiang, Xiangyu Zhang, Yunjian Huang, Siyi Liu, Shiyun Xu, He Zhang, Guang Lu, Bing Ni, and Hongwei Zhu.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #EarlyLifePain #SocialBehavior #MiceStudy #DeepBrainStimulation #AnteriorCingulateCortex #Neuroscience #ExcitatoryInhibitoryBalance #GlutamateGABA #BrainPlasticity #TranslationalPsychiatry
🤖 KI-Briefing — 20.10.2026
1. Industrie: Siemens und Nvidia wollen Fabriken automatischer machen
Hier finden Sie Informationen zu dem Thema „Industrie“. Lesen Sie jetzt „Siemens und Nvidia wollen Fabriken automatischer ...
2. Forscher nutzen KI-Technologie vom ChatGPT-Typ, um Schlaganfallrisiko anhand der DNA einer Person vorherzusagen.
A new AI tool that identifies genetic risk factors for stroke could open the door to more personalised prevention and ...
3. OpenAI könnte eine Bewertung von über 1,4 Billionen Dollar erreichen.
4. Diese neue Theorie darüber, wie KI denkt, könnte beeinflussen, ob sie uns alle auslöscht
KI-Forscher wissen nicht wirklich, wie die von ihnen entwickelten Modelle „denken“. Eine neue Theorie könnte das ändern.
… weitere Meldungen auf Arint.info
Arint.info · Mehr auf Arint.info #AI #Europa #Nvidia #OpenAI #USA #ZURICH #arint_info
DATE: October 22, 2026 at 10:00AM
SOURCE: PSYPOST.ORG
** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
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TITLE: New biological marker could end trial and error in depression care
URL: https://www.psypost.org/blood-test-could-predict-if-an-antidepressant-will-work-for-you/
Major depressive disorder is often treated through trial and error, but a blood test may soon help doctors choose the right medication on the first try. Researchers have identified a circular RNA molecule in the blood that predicts whether a patient will respond to a common class of antidepressants. The findings were published in Molecular Psychiatry.
Millions of people globally experience major depressive disorder. Doctors frequently prescribe selective serotonin reuptake inhibitors, commonly known as SSRIs, as a first line of medical defense. These drugs block the reabsorption of serotonin in the brain, leaving more of the chemical available to help transmit messages between nerve cells.
Less than half of patients experience relief from their symptoms after trying their first prescribed antidepressant. This forces patients to spend months trying different medications before finding one that works. The prolonged wait imposes a heavy burden on individuals and adds substantial costs to the healthcare system.
Medical professionals currently lack biological tests to predict which drug will work for a specific person. Genetic tests exist to show how fast a person’s body might metabolize a drug. They cannot, however, forecast if the drug will actually relieve depression symptoms.
To find a better biological indicator, a team of researchers investigated circular RNAs. These are stable, loop-shaped genetic molecules that influence how other genes operate. Because they lack exposed ends, they resist degrading enzymes in the body, giving them a much longer lifespan than standard linear RNA molecules.
Circular RNAs are highly concentrated in the brain and help regulate how neurons connect and communicate. Some of these molecules can pass through the blood-brain barrier, the semi-permeable membrane that separates circulating blood from brain fluid. Because they leak into the bloodstream in a stable form, researchers can detect brain-derived circular RNAs using a standard blood draw.
The investigation was led by scientists Grigorios Papageorgiou, Eleni T. Tzavara, and Nikolaos Mellios of Circular Genomics and various research institutes in the United States and France, along with Madhukar H. Trivedi at the University of Texas Southwestern Medical Center. They focused on a specific circular RNA called CDR1as. This molecule is highly abundant in the brain but rarely found in other human tissues.
The researchers first analyzed baseline blood samples from patients enrolled in two independent clinical trials. They extracted RNA from the blood of patients diagnosed with major depressive disorder who were about to begin taking the SSRI sertraline. Using a technique that amplifies genetic material, the team measured the starting levels of CDR1as for each patient.
The team found that patients who did not respond to sertraline after eight weeks of treatment had notably higher baseline levels of CDR1as in their blood. Patients who experienced symptom relief had lower starting levels of the molecule. The researchers observed that unaffected control subjects also showed lower baseline levels of the molecule.
Taking advantage of the clinical trial design, the researchers also measured the patients’ blood at different intervals after they started taking sertraline. They discovered that patients who responded well to the drug experienced an increase in CDR1as levels after treatment began. Patients who did not respond to the medication saw no such increase in the molecule’s concentration.
To test if this molecule simply predicts general improvement rather than specific drug responses, the researchers looked at other treatment groups. They measured baseline blood levels in patients who were given a placebo pill. They also evaluated patients who failed to respond to sertraline and were subsequently switched to bupropion, a different type of antidepressant.
Baseline levels of CDR1as did not predict whether a patient would feel better on a placebo. The molecule also failed to predict if a patient would go on to experience remission while taking bupropion. This suggested the biomarker is specifically tied to the mechanisms of sertraline.
The research team then wanted to know if this predictive power applied to the entire SSRI drug class. They examined blood samples from patients in other clinical programs who were taking fluoxetine, citalopram, or escitalopram. They also analyzed samples from a small study of patients taking alternative medications like serotonin and norepinephrine reuptake inhibitors.
The researchers observed that CDR1as levels successfully identified patients who were faring well on various SSRIs, not just sertraline. When evaluating patients taking other classes of antidepressants, the molecule’s levels did not predict symptom relief. This pointed to a specific relationship between the circular RNA and SSRI medications as a whole.
To understand exactly how the brain produces this circular RNA, the team conducted experiments on mice. They administered different chemical compounds to the animals to block specific brain receptors. They then extracted brain tissue to measure changes in Cdr1as, the mouse equivalent of the human molecule.
When the researchers blocked the serotonin 5-HT2A receptor, levels of the circular RNA dropped across three different regions of the mouse brain. Blocking dopamine or glutamate receptors did not produce a similar drop in the molecule. This established a direct link between serotonin system activity and the production of the circular RNA.
The investigators conducted a final set of experiments on lab-grown human and mouse nerve cells. They treated the cells with chemicals that inhibit brain-derived neurotrophic factor, a protein that promotes the survival and growth of neurons. Inhibiting this protein’s receptors caused the cells to produce less of the circular RNA.
The researchers noted that certain medical conditions could interfere with the accuracy of this blood test. For instance, the test performed poorly in depressed patients who had a family history of mania, which is often a sign of undiagnosed bipolar disorder. When the researchers excluded these patients from their analysis, the test’s predictive accuracy improved.
Medical events that disrupt the blood-brain barrier might also artificially alter the amount of circular RNA in the bloodstream. Severe head trauma or strokes could potentially cause these brain molecules to leak into the blood at abnormal rates. Future research will need to verify how such physical injuries influence the test results.
The study authors noted that high baseline levels of the molecule correlated with specific depression symptoms like anhedonia and social withdrawal. These symptoms are often associated with a subtype of depression that is historically harder to treat with SSRIs. Further studies will need to explore exactly how this biological marker overlaps with different clinical subtypes of the disorder.
The study, “A brain-enriched circRNA blood biomarker can predict response to SSRI antidepressants,” was authored by Grigorios Papageorgiou, El Chérif Ibrahim, Victor Gorgievski, Gabriella Maxson, Evelyn Lozano, Eric Gordon, Antoine Lefrere, Marie-Julie Toupet, Philippe Courtet, Raoul Belzeaux, Jane Foster, Thomas Carmody, Roy H. Perlis, Madhukar H. Trivedi, Eleni T. Tzavara, and Nikolaos Mellios.
URL: https://www.psypost.org/blood-test-could-predict-if-an-antidepressant-will-work-for-you/
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #DepressionResearch #MentalHealth #DepressionCare #Antidepressants #SSRIs #PrecisionMedicine #Biomarkers #MedicalResearch #BrainHealth #HealthcareInnovation
DATE: October 22, 2026 at 08:00AM
SOURCE: PSYPOST.ORG
** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
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TITLE: Kids’ aggression appears to shape parents’ discipline more than the reverse, study finds
Children’s aggressive behavior may contribute to parents becoming less consistent with discipline, rather than inconsistent discipline simply causing children to become more aggressive, according to research published in Nature Communications. The study also found that shared genes explained part of the link between inconsistent discipline and aggression, and all of the link between positive parenting and lower aggression.
Parenting and childhood aggression have long been linked. Parents who inconsistently enforce rules tend to have children with more aggressive behavior, while greater positive parenting, such as praising and positively engaging with children, is associated with less aggression. These findings can easily be interpreted as evidence that parenting produces differences in children’s behavior.
But families are more complicated. Children can affect their parents just as parents can affect their children. Biological parents and children also share genes, meaning some of the genetic factors associated with a parent’s behavior could be inherited by their children and influence the children’s behavior.
Led by Joanna K. Bright of King’s College London, the researchers addressed these problems using two genetically informative studies of children between about 4.5 and 8 years of age. Both studies used the same questionnaires to measure inconsistent discipline, positive parenting and child aggression, allowing the researchers to check whether the results held across different samples and methods.
The first drew on Norway’s Mother, Father and Child Cohort Study, using extended-family data involving 53,532 children born to 42,538 mothers, who reported on their parenting and their children’s behavior when the children were 5 years old. By comparing families with different degrees of genetic relatedness, including twins and their children, the researchers could estimate how much of the relationship between parenting and aggression was associated with shared genetics.
The second dataset came from the U.S. Early Growth and Development Study and contained 561 adoption triads, each made up of an adopted child, the adoptive parents and the birth parents. The children, 57% of whom were male, were adopted shortly after birth and assessed at ages 4.5, 6, 7 and 8. Because adoptive parents and children did not share genes, associations between their behaviors provided a way of examining environmental pathways without the complication of genes inherited from those parents.
The results suggested a more complicated relationship than parenting simply causing aggression. In the Norwegian study, the correlation between inconsistent discipline and child aggression was modest. About 47% of this association was attributed to shared genetic factors, while 53% remained after accounting for genetic transmission.
When the researchers investigated that remaining relationship, the evidence pointed from child to parent. The best-fitting model included a path from child aggression to inconsistent maternal discipline but no path from discipline to aggression. The adoption study showed a similar pattern: children’s aggression was linked to more inconsistent discipline at the same age and predicted more inconsistent discipline at later ages, while paths from mothers’ discipline to children’s aggression were not statistically significant.
Bright and colleagues concluded that “childhood aggression drives inconsistent parenting beyond shared genetic influences.”
Sensitivity analyses using fathers’ reports in the adoption study painted a somewhat different picture. When fathers reported on both their own parenting and their children’s behavior, inconsistent discipline and child aggression appeared to influence each other in both directions at the same time point, though not over longer periods. When one parent’s report of child aggression was paired with the other parent’s report of parenting, no significant links emerged, which the authors note could mean that relying on the same person to report both behaviors inflates associations.
Positive parenting produced another important finding. Although greater positive parenting was associated with lower aggression in the Norwegian sample, the researchers estimated that the association was completely explained by shared genetic influences. In the adoption sample, the models found no evidence that positive parenting and aggression influenced each other in either direction.
The results did not differ meaningfully between boys and girls. The authors suggest that clinicians should recognize that childhood aggression can contribute to inconsistent discipline, and that interventions focused only on encouraging consistent discipline may be insufficient.
Some limitations should be noted. The authors caution that their questionnaires captured relatively narrow aspects of parenting and aggression, relied primarily on mothers’ reports, and were drawn from relatively socioeconomically advantaged families. The two samples also used somewhat different versions of the aggression measure, which captured defiant behavior as well as physical aggression.
The Norwegian analysis was based on a single time point and could not account for the possibility that parents choose partners with similar traits. The data were also collected between roughly 10 and 23 years ago, and parenting norms may have shifted since then.
The study, “Triangulating evidence for genetic and environmental components of associations between parental behaviours and aggressive behaviour in children,” was authored by Joanna K. Bright, Yasmin I. Ahmadzadeh, Olakunle Oginni, Essi Viding, Leslie D. Leve, Jenae M. Neiderhiser, Daniel S. Shaw, Misaki N. Natsuaki, Jody M. Ganiban, Eivind Ystrom and Tom A. McAdams.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #ChildDevelopment #Parenting #ChildPsychology #ChildAggression #PositiveParenting #ParentingResearch #FamilyPsychology #Psychology #MentalHealth #NatureCommunications
DATE: October 20, 2026 at 12:00PM
SOURCE: PSYPOST.ORG
** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
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TITLE: Brain wave study reveals shifting auditory responses in children with ADHD
URL: https://www.psypost.org/brain-wave-study-reveals-shifting-auditory-responses-in-children-with-adhd/
Children with attention-deficit/hyperactivity disorder process unexpected sounds differently than their peers, and these brain responses appear to change as they grow older. A recent study measuring brain waves in two distinct age groups found that children with elevated ADHD symptoms exhibit heightened sensitivity to unexpected tones in early childhood, but diminished sensitivity by middle childhood. These findings were published in the journal Developmental Cognitive Neuroscience.
The human brain constantly monitors the environment for new or unexpected sounds. This ability allows people to adapt to their surroundings and focus on important information while tuning out harmless background noise. In typical development, sensory systems refine their ability to categorize sounds through repeated exposure.
Neuroscientists conceptualize this process through a framework called predictive coding. The brain builds a working model of expected sounds based on recent patterns in the environment. When a new sound breaks that established pattern, the brain generates a specific electrical signal known as mismatch negativity. This rapid response happens in a fraction of a second.
Mismatch negativity operates automatically, without requiring conscious thought. If a completely unique or bizarre sound occurs, the brain generates a secondary electrical signal associated with involuntary attention. This later signal is called a novelty response.
Another important feature of sensory processing is habituation. When a person hears the same sound repeatedly, the brain’s electrical response typically shrinks over time. Habituation helps the brain conserve energy by ignoring irrelevant distractions, freeing up mental resources for goal-directed behavior. Without this ability, a person might feel constantly overwhelmed by everyday background noise.
Researchers Marija Pranjić, Jirapat Likitlersuang, and Anne B. Arnett at Boston Children’s Hospital and Harvard Medical School wanted to understand how these auditory processes operate in children with ADHD. Children with ADHD often struggle with attention regulation and sensory overload. The research team suspected that these everyday challenges might stem from basic differences in how the brain encodes sensory information.
The researchers designed an experiment to test these brain responses across two separate developmental stages. The first part of the study evaluated a group of 115 young children between two and a half and five years old. Participants were excluded if they had a history of seizures, an autism diagnosis, or known genetic syndromes.
Because clinical ADHD diagnoses are rarely given to very young children, the researchers categorized the early childhood group based on comprehensive clinical ratings. Sixty-four children had elevated ADHD symptoms, while 51 children exhibited typical development.
To measure brain activity, the researchers placed a net of harmless sensors on each child’s head to record an electroencephalogram, commonly known as an EEG. The children watched a silent video while listening to a sequence of sounds through speakers. The test required no active behavioral response from the participants. This passive monitoring approach is ideal for studying young children who might struggle with complex instructions.
The sound sequence consisted mostly of a repetitive standard tone. Occasionally, the researchers played a slightly different tone to trigger the brain’s mismatch negativity response. They also mixed in completely unique environmental noises, such as a drum beat or a cricket chirp, to trigger the novelty response.
Pranjić and her colleagues found that young children with elevated ADHD symptoms had a stronger brain response to the unexpected tones. Their mismatch negativity amplitude was larger than that of the children with typical development. This pattern emerged even after the researchers accounted for differences in age and cognitive ability.
The young children with elevated ADHD symptoms also showed differences in habituation. The typically developing children adapted quickly to the repetitive standard tones and the unique environmental noises, showing reduced brain activity over time. In contrast, the brains of the children with elevated ADHD symptoms did not settle down as effectively across the repeated trials.
The researchers then conducted a similar experiment with a separate group of 71 older children. These participants were between seven and eleven years old. In this older group, 53 children had a confirmed ADHD diagnosis, and 18 children were typically developing.
These older participants completed the exact same listening task while the researchers recorded their brain waves. The findings in this older group were quite different from the early childhood group. Children with ADHD in middle childhood exhibited a blunted mismatch negativity response compared to their typically developing peers.
The older children with ADHD showed a weaker brain reaction to unexpected sounds. The researchers did not find evidence of habituation differences between the diagnostic groups in this older cohort. Both the typically developing children and those with ADHD showed similar reductions in brain activity when exposed to the novelty sounds over time.
These age-related differences suggest that sensory processing in ADHD changes over the course of development. In early childhood, the brain might overreact to sensory deviations, while in middle childhood, it might underreact. This shifting pattern aligns with theories that ADHD involves atypical connections between early auditory encoding and later attention selection.
The study design evaluated two distinct age groups at a single point in time, meaning it did not track the same children as they grew older. Because of this cross-sectional approach, researchers cannot say for certain how an individual child’s brain responses evolve. It remains unknown whether the differences seen in middle childhood represent a delayed maturation of the auditory system or an alternative path of sensory development.
Future longitudinal studies, which follow the same participants over many years, are needed to answer these developmental questions. Additionally, the results do not indicate that atypical auditory processing causes ADHD behaviors. The study only demonstrates that altered sensory processing is associated with the condition.
The findings support the idea that ADHD is not exclusively a disorder of higher-order executive functioning. Basic sensory processing differences appear to play an important role in how children experience and interact with the world around them. Understanding exactly how the brain filters sounds could eventually aid in the early detection of attention disorders.
Identifying these biological markers might one day help clinicians design better therapies for children who struggle to tune out distractions. Tracking how sensory adaptation matures across childhood could provide a new window into the developing brain. The study, “Atypical auditory cortical processing in ADHD during early and middle childhood,” was authored by Marija Pranjić, Jirapat Likitlersuang, and Anne B. Arnett.
URL: https://www.psypost.org/brain-wave-study-reveals-shifting-auditory-responses-in-children-with-adhd/
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YSGOL HEOL GOFFA: Four pupils have died in six months, says councillor, and still no nurse
Four pupils at a Llanelli special school have died in the last six months, according to the town councillor campaigning for a full-time nurse on site.
Cllr Shaun Greaney says three of the children were pupils in the school’s Medical Services Unit, and another pupil died of a notifiable disease. He has not named the children or described their circumstances, out of respect for their families.
Campaigners have been calling for a registered nurse at Ysgol Heol Goffa for more than five years. Their pleas have gone to Hywel Dda University Health Board and the county council.
Cllr Greaney, the Labour town councillor who has led the town council’s push for a nurse, said: “The time taken to hold any kind of meaningful talks with frightened and worried parents, campaigners, and the school itself borders on criminal in my opinion.”
He went further: “The kindest comment I’ve heard about it is that it’s disheartening. But in fact it’s horrifying, disgusting, shameful.”
Hywel Dda gave no guarantee and no deadline at MP’s meeting, campaigners say
The action group recently met health board chiefs online, at a meeting convened by Llanelli MP Dame Nia Griffith. Cllr Greaney said the chiefs “could not give a guarantee a nurse would be employed, nor could they give a deadline for a decision”.
According to Cllr Greaney, Dame Nia told the meeting the case for a nurse at the school was all the stronger because Prince Philip Hospital has no paediatric department.
He said it was “encouraging that they finally listened to the overwhelming evidence presented to them”, with chiefs pledging “something would be done”. Apart from the health board seeking information about the children with epilepsy, though, he understands “not a lot has happened”.
Health chiefs also insisted no solution could be reached without the involvement of Carmarthenshire County Council, he said.
Ysgol Heol Goffa mum says the health board is “failing in its duty of care”
Llanelli mum Lana Dakin’s son Jac, eight, has Schinzel-Giedion syndrome, a rare genetic condition, and complex medical needs. She said the staff at Ysgol Heol Goffa “are great but they should not have to carry this alone”.
She said: “The children here have some of the most complex medical needs in our community. I am shocked, appalled, disgusted that the health board is not doing enough. The health board is failing in its duty of care.”
Lana Dakin with her son Jac, eight, a pupil at Ysgol Heol Goffa. (Image: Lana Dakin)Speaking about her son, she said: “Jac is not just a diagnosis. He is my son. He is loved.”
She said he deserved “the very best chance to learn, grow, thrive” and to “have the best quality of life”. “And so does every child at Ysgol Heol Goffa,” she added.
Her message to the health board was blunt: “Children like Jac should not have to wait. They deserve support now.”
Promised Welsh Government guidance still has no timescale
As far back as February, parents warned they had “been lucky to date that a child has not died”, as calls grew for a watchdog investigation.
Hywel Dda has previously pointed to its visiting community children’s nursing service. In August, Cabinet Minister for Health and Care Mabon ap Gwynfor said staff at the school were “assessed as competent”, and that a nurse was “a matter for the relevant local authority and health board“.
New guidance from the Welsh Government has been promised for some time in 2027. Last month, Cabinet Minister for Education and the Welsh Language Anna Brychan said the work was “at an early stage” and gave no timescale.
Cllr Greaney said: “As we’ve stressed all along, time is of the essence. If they wait until the Welsh Government produces new guidance in 2027, it could come too late to save a child’s life.”
Carmarthenshire Council and Hywel Dda could share the cost, councillor says
He saved his sharpest words for the county council: “It’s as if the Plaid Cymru-led county council has a death wish. We are not talking a huge sum of money.”
Split between the health board and the county council, he said, the bill would be “roughly about a figure akin to a council cabinet member’s salary with the potential of keeping children safe and alive”. He asked: “Who could begrudge the parents that peace of mind and have a clear conscience?”
Council rejects ‘modest cost’ claim and says school nursing is Hywel Dda’s job
Carmarthenshire County Council said it “does not accept the suggestion that it has refused to engage in finding a solution” for the school.
Cllr Glynog Davies, the council’s cabinet member for education, said it had “repeatedly raised concerns about nursing provision” with the health board, the Welsh Government, the school and the Children’s Commissioner for Wales. He pointed to Welsh Government guidance that every special school should have access to at least one dedicated registered nurse employed by the health board.
Responsibility for commissioning and delivering school nursing in Carmarthenshire “rests with Hywel Dda University Health Board”, he said, adding that it was “misleading to characterise the issue simply as the Council refusing to share a ‘modest cost'”.
Any future model had to settle “clinical responsibility, governance, staffing and funding” between the organisations responsible, he said, and the council wanted those talks “brought to a clear and sustainable conclusion”.
He said the council would not comment on individual pupils, and that no “causal connection” should be drawn between any deaths and nursing provision “without clear clinical evidence”. There is “not currently a confirmed timescale for a final decision by the Health Board”, he added.
Hywel Dda says its community nursing team and staff training already cover the school
Hywel Dda said it supports the children at Ysgol Heol Goffa “with a specialist/community children nursing service to meet their universal health needs”, and by training the school’s staff.
Sharon Daniel, the health board’s director of nursing, quality and patient experience, said the health and wellbeing of children “is a priority for us” and that specialist support ensured each child with healthcare needs “can be cared for competently and confidently within the school environment”.
She said: “Through continued partnership working and a shared commitment to improvement, we will support ongoing actions to strengthen provision and ensure the best possible outcomes for the pupils and staff at Ysgol Heol Goffa.”
Related stories from Swansea Bay News
YSGOL HEOL GOFFA: Health minister said 2027. Education minister says no timescale. Still no nurse
Neither minister would say when a nurse comes.
YSGOL HEOL GOFFA: No permanent nurse for seriously ill children at Llanelli special school as parents told to wait until 2027
The health minister’s letter that Lana Dakin called a “kick in the teeth”.
LLANELLI: Minister urged to step in over ‘lifesaving’ school nurse battle as mum warns of preventable tragedy
The town council’s unanimous letter to the health minister.
CHILDREN’S COMMISSIONER STEPS IN: Watchdog demands meeting with health board over special school nurse crisis
Rocio Cifuentes asked to meet Hywel Dda in February.
‘Lives may be at risk’: Watchdog probe demanded over Llanelli special school nurse crisis
Where the campaign stood in February.
Lipedema: la malattia delle “gambe grosse” tra sotto-diagnosi, nuovo Consensus internazionale e sfide italiane
Dal Delphi Consensus della Lipedema World Alliance (Nature Communications, 2026) ai nodi irrisolti nel contesto assistenziale italiano
Introduzione: una malattia invisibile al sistema
Il 15 luglio 2026, Repubblica ha portato all’attenzione del grande pubblico italiano il lipedema, definendolo la “malattia delle gambe grosse”. È un segnale di quanto questa condizione stia progressivamente emergendo dal limbo della sotto-diagnosi in cui è rimasta confinata per decenni. Eppure, chi lavora in medicina interna conosce bene la frustrazione di quelle pazienti — quasi sempre donne — che arrivano all’ambulatorio dopo anni di diete fallite, visite endocrinologiche negative e diagnosi di “sovrappeso” o “cellulite grave”. Il lipedema non è nessuna di queste cose.
A gennaio 2026, la Lipedema World Alliance (LWA) ha pubblicato su Nature Communications il primo Delphi Consensus internazionale sulla definizione e gestione del lipedema, coinvolgendo 71 esperti di 19 Paesi. È un documento storico: per la prima volta, clinici, ricercatori e rappresentanti dei pazienti di cinque continenti hanno trovato accordo su 59 affermazioni fondamentali, distribuite in otto domini. Questo post ne analizza i contenuti più rilevanti per la pratica clinica, con attenzione al contesto italiano.
Cos’è il lipedema: definizione e quadro clinico
Il lipedema è una malattia cronica del tessuto adiposo sottocutaneo caratterizzata da un accumulo anomalo, simmetrico e bilaterale di grasso a carico degli arti, prevalentemente inferiori, con possibile coinvolgimento degli arti superiori in una percentuale variabile di pazienti (30–80% secondo i dati in letteratura). La condizione interessa quasi esclusivamente il sesso femminile biologico; i casi maschili documentati sono rari e spesso associati ad alterazioni ormonali.
Il quadro clinico tipico include:
La patologia esordisce o si aggrava tipicamente in corrispondenza di modificazioni ormonali significative: pubertà, gravidanza, menopausa. Questa correlazione temporale — confermata con un accordo del 98,4% nel Consensus — suggerisce un ruolo patogenetico dei fattori ormonali, sebbene i meccanismi precisi non siano ancora completamente chiariti.
Fisiopatologia: cosa sappiamo (e cosa ancora non sappiamo)
Il lipedema non è semplicemente “grasso in eccesso”. Il tessuto adiposo lipedematoso presenta caratteristiche morfologiche, molecolari e metaboliche distinte rispetto al tessuto adiposo associato all’obesità comune. I meccanismi patogenetici proposti includono:
Il Consensus riconosce esplicitamente che molte di queste ipotesi richiedono conferma con studi longitudinali e sperimentali rigorosi. Il livello di evidenza per la maggior parte delle affermazioni fisiopatologiche si attesta sotto il 50%, a testimonianza dell’ancora limitata base di ricerca in questo campo.
Epidemiologia: prevalenza incerta, ritardo diagnostico certo
La prevalenza del lipedema nella popolazione femminile adulta rimane sconosciuta. Le stime in letteratura variano considerevolmente, da meno dell’1% fino al 12%, riflettendo l’eterogeneità dei criteri diagnostici adottati, la scarsa consapevolezza tra i professionisti sanitari e la conseguente sotto-diagnosi sistematica. In Italia, alcune fonti angolologiche nazionali citano cifre fino al 10–11% delle donne adulte, ma tali dati sono da interpretare con cautela in assenza di studi epidemiologici prospettici robusti.
Ciò che il Consensus afferma con forza — accordo al 100% — è che il ritardo diagnostico ha conseguenze concrete e misurabili: aggrava il burden sintomatologico, deteriora il benessere mentale, riduce la qualità di vita e aumenta i costi a carico dei pazienti e del sistema sanitario. In Italia, i tempi medi tra comparsa dei sintomi e diagnosi corretta superano frequentemente i 10 anni.
La diagnosi: clinica, clinica, clinica
Uno dei messaggi più netti del Consensus LWA 2026 — con un accordo del 98,4% — è che la diagnosi di lipedema rimane esclusivamente clinica, fondata su:
Il documento sottolinea con pari chiarezza — accordo al 93,4% — che non esistono attualmente test di imaging, sierologici o genetici ufficialmente approvati per confermare la diagnosi clinica. Ecografia, RM, linfoscintigrafia e bioimpedenziometria possono contribuire alla valutazione, ma nessuno ha ancora dimostrato sufficiente sensibilità, specificità e riproducibilità per essere raccomandato come standard diagnostico.
Un elemento critico per il clinico pratico è la ridefinizione del ruolo dello staging. Il Consensus chiarisce che la classificazione in stadi (I–IV, basata sull’aspetto della cute e del tessuto sottocutaneo) ha limitata rilevanza per la gestione clinica e non riflette la complessità della sintomatologia individuale. Fattori come l’intensità del dolore, la disabilità funzionale e la qualità di vita devono essere considerati accanto allo stadio anatomico.
Comorbilità: il lipedema non è obesità, ma convive con essa
Il Consensus afferma con forza (accordo al 92,1%) che il lipedema non è una comorbilità correlata all’obesità: si tratta di una patologia distinta, con caratteristiche istopatologiche e metaboliche proprie. Tuttavia, le due condizioni coesistono frequentemente — l’obesità è presente in una quota significativa di pazienti con lipedema — e quando questo accade entrambe richiedono un trattamento specifico e separato.
Implicazioni cliniche rilevanti:
Trattamento: nessuna cura definitiva, ma un approccio integrato possibile
Il Consensus è esplicito: nessun intervento terapeutico è curativo. Tutti mirano ad alleviare i sintomi e rallentare la progressione. L’approccio deve essere multidisciplinare e personalizzato, coinvolgendo medici, fisioterapisti, dietisti e professionisti della salute mentale.
Terapia conservativa: è il cardine del trattamento e deve includere:
Drenaggio linfatico manuale (DLM): il Consensus precisa che non esistono prove a supporto del DLM come trattamento isolato del lipedema. I benefici osservati derivano dall’inserimento del DLM all’interno della Terapia Decongestionante Complessa (CDT), di cui il DLM è solo una delle componenti. Non tutti i pazienti necessitano di tutti i componenti della CDT.
Farmaci: con accordo del 93,2%, il Consensus stabilisce che non esistono attualmente evidenze di efficacia per alcun intervento farmacologico nel trattamento del lipedema. Integratori con proprietà antinfiammatorie o flebotrope sono stati esplorati, ma le prove disponibili rimangono insufficienti.
Liposuzione linfatica-sparing: è l’unica tecnica in grado di rimuovere il tessuto adiposo patologico e potenzialmente rallentare la progressione della malattia. Il Consensus ne raccomanda la considerazione quando vi sia ragionevole aspettativa di beneficio sintomatologico, a condizione che sia eseguita da operatori con specifica esperienza nel lipedema e nell’ambito di un percorso terapeutico integrato. In caso di coesistenza con obesità e malattia metabolica, è generalmente consigliabile trattare prima l’obesità. Mancano tuttavia RCT e studi di follow-up a lungo termine che ne dimostrino la superiorità rispetto a trattamenti alternativi.
Il lipedema in Italia: un nodo assistenziale irrisolto
Sul piano istituzionale, il lipedema è classificato nel sistema ICD-10 (codice E88.2), ma il riconoscimento formale come malattia rara con inserimento nei LEA (Livelli Essenziali di Assistenza) è ancora in corso di definizione. Alcune Regioni — tra cui il Veneto — hanno avviato percorsi autonomi di riconoscimento, ma la situazione è eterogenea e non si è tradotta in un accesso uniforme a prestazioni gratuite o agevolate su tutto il territorio nazionale.
Questo ritardo normativo ha conseguenze concrete: molte pazienti italiane sostengono interamente i costi dei presidi compressivi, del linfodrenaggio e della consulenza specialistica. La chirurgia è quasi sempre a carico privato. Il confronto con Paesi come la Germania — dove la liposuzione per lipedema è rimborsata dal servizio sanitario pubblico — evidenzia un gap assistenziale significativo.
Da internista, mi confronto periodicamente con pazienti affette da lipedema che giungono in reparto per motivi diversi ma che portano con sé anni di visite non conclusive e diagnosi errate. La medicina interna ha un ruolo potenziale in questo scenario: nel sospettare la diagnosi, nell’avviare l’iter verso lo specialista appropriato (angiologo, chirurgo vascolare, chirurgo plastico con expertise in lipedema), e nell’escludere le patologie concomitanti più rilevanti — in primis ipotiroidismo, insufficienza venosa e linfedema secondario.
Prospettive future: cosa chiede la ricerca
Il Consensus LWA identifica con chiarezza le aree prioritarie per la ricerca futura:
È significativo che il documento — pur rappresentando un traguardo storico — non risolva le principali controversie. La prevalenza esatta, i criteri diagnostici oggettivi, il ruolo della genetica, l’efficacia del DLM come monoterapia, la superiorità della chirurgia rispetto al trattamento conservativo: su tutti questi punti la risposta onesta è “non lo sappiamo ancora con sufficiente certezza”. È questo rigore epistemologico che rende il Consensus un documento scientifico credibile, anziché una semplice dichiarazione di consenso.
Conclusioni
Il lipedema è una malattia cronica del tessuto adiposo che colpisce quasi esclusivamente le donne, con un impatto fisico, psicologico e sociale molto spesso sottostimato dal sistema sanitario. Il Delphi Consensus della Lipedema World Alliance, pubblicato su Nature Communications nel gennaio 2026, rappresenta il primo tentativo globale di armonizzare definizione, diagnosi e gestione di questa condizione.
I messaggi chiave per il clinico sono chiari: la diagnosi è e rimane clinica; nessun test strumentale è attualmente validato; non esiste una cura farmacologica; l’approccio deve essere multidisciplinare e individualizzato; il ritardo diagnostico è nocivo e costoso. In Italia, il riconoscimento istituzionale della malattia e l’accesso equo alle terapie rimangono obiettivi ancora da raggiungere.
Come medici, abbiamo la responsabilità di conoscere questa patologia, di sospettarla quando il quadro clinico la suggerisce, e di non liquidare con un consiglio dietetico quello che potrebbe essere un lipedema non diagnosticato.
Kruppa, P., Crescenzi, R., Faerber, G., Forner-Cordero, I., Cornely, M., Shayan, R., Karnezis, T., Simarro, J. L., de Souza, P. F., Herbst, K. L., Ghods, M., & Michelini, S. (2026). Lipedema World Alliance Delphi Consensus-Based Position Paper on the Definition and Management of Lipedema: Results from the 2023 Lipedema World Congress in Potsdam. Nature Communications, 17, 427. https://doi.org/10.1038/s41467-025-68232-z
Faria, A. M., Valerio, C. M., Barcellos, C. R., Oliveira, R. A., Trujilho, F. R., Baiocchi, J. M. T., et al. (2026). Unraveling lipedema: comprehensive insights and the path to future discoveries. NPJ Metabolic Health and Disease, 4(1), 3. https://doi.org/10.1038/s44324-025-00093-y
Istituto Flebologico Italiano. (2026, marzo 5). Lipedema: guida completa per la diagnosi e il trattamento. https://www.istitutoflebologico.it/2026/03/05/lipedema-guida-completa-per-la-diagnosi-e-il-trattamento/
Michelini, S., & Italian Lymphoedema Framework. (2022). Il lipedema: una malattia ancora poco conosciuta. Italian Lymphoedema Framework. https://www.italf.org/articolo-sul-lipedema-tratto-dalla-rivista-vanityfair/
Reverdito, V. (2026, aprile 20). Diagnosi clinica del lipedema: perché RM, ecografia e bioimpedenziometria non bastano. https://www.valeriareverdito.it/2026/04/20/diagnosi-clinica-del-lipedema-perche-rm-ecografia-e-bioimpedenziometria-non-bastano/
State of Lymphedema. (2026, giugno 5). Lipedema 2026: pubblicato il nuovo Consensus Paper internazionale della Lipedema World Alliance che cambia diagnosi e trattamento. https://www.stateoflymphedema.com/2026/06/lipedema-2026-linee-guidapubblicato-il-nuovo-consensus-paper-internazionale-della-lipedema-world-alliance-che-cambia-diagnosi-e-trattamento/
#ConsensusInternazionale #diagnosiClinica #linfedema #linfologia #lipedema #liposuzione #malattieRare #medicinaInterna #terapiaCompressiva #tessutoAdiposo
DATE: October 21, 2026 at 04:00PM
SOURCE: PSYPOST.ORG
** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
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TITLE: Children who later develop psychosis tend to have slightly smaller heads, study finds
A longitudinal study tracking thousands of children from birth to mid-adolescence suggests that young people who develop psychotic disorders tend to have smaller heads throughout their early lives. Published in Psychological Medicine, the research indicates that these head size differences are largely tied to overall body height, pointing toward a broader pattern of altered physical growth rather than an isolated issue with brain expansion. The findings also point to distinct trajectories between males and females who experience milder psychotic symptoms.
Psychosis is a psychiatric condition in which a person loses some contact with reality. It often involves hallucinations, which are sensory experiences of things that are not present, and delusions, which are firmly held false beliefs. Psychosis exists on a spectrum, with clinical psychotic disorders like schizophrenia at the severe end, which disrupt daily life and typically emerge in late adolescence or early adulthood. A much larger segment of the population reports isolated psychotic experiences, such as occasionally hearing a voice or feeling unusually suspicious, without meeting the threshold for a clinical illness.
Even though psychotic disorders usually appear in young adulthood, the neurodevelopmental model of schizophrenia proposes that the underlying biological roots of these conditions begin during fetal development and early childhood. Adults diagnosed with schizophrenia tend to have slightly smaller total brain volumes than peers without the condition, even before they ever take psychiatric medications. Because performing brain scans on thousands of infants and children is costly and impractical, scientists often rely on head circumference, a simple tape-measure reading around the widest part of the skull that is routinely recorded by pediatricians, as an indirect indicator of early brain size.
“The study was motivated by the need to identify inexpensive and accessible biomarkers of psychosis risk,” study co-author Kate Merritt, a lecturer in human neuroscience in the Division of Psychiatry at University College London, told PsyPost. “If we can identify people who are more likely to develop psychosis, this could eventually help us target preventative interventions toward those at greatest risk.”
“Much of our work focuses on using MRI to identify biological markers that predict outcomes in psychosis, but MRI is expensive and not widely accessible,” Merritt explained. “We therefore wondered whether a much simpler measure, head circumference, might provide useful information. Head circumference is correlated with brain volume, so we looked at whether differences in head growth might be associated with psychosis risk.”
Prior research examining infant head size and later mental health has produced mixed results. Some studies, including a 2005 study of Swedish twins, found that babies born with smaller head circumferences and lower birth weights were more likely to develop schizophrenia as adults. Other studies found larger head sizes, no link at all, or differences that only appeared in females or vanished by early childhood. Most of this earlier work only looked at measurements taken at birth or during the first few months of life, leaving it unknown how head growth unfolds through later childhood and adolescence.
Scientists have also questioned whether a smaller head reflects a biological process restricted to the brain or a whole-body growth pattern. For example, a 2007 study of over 1.3 million Swedish men indicated that shorter adult height and lower body mass index were associated with a higher risk of schizophrenia. Similarly, a 2007 birth cohort study found that women who developed schizophrenia-spectrum disorders grew in height about one centimeter per year slower during early childhood than women without these conditions.
To determine whether head growth trajectories differ across the psychosis spectrum and whether those differences are independent of overall body size, Merritt, lead author Sarah A. Ashley of University College London, and their colleagues examined data from the Avon Longitudinal Study of Parents and Children. This population-based project tracked children born to pregnant women in the Southwest of England between April 1991 and December 1992.
The researchers analyzed an overall sample of 3,866 participants, including 2,177 females and 1,689 males, who had complete background records and at least one head circumference measurement between birth and age 15. Head measurements were collected across up to 22 time points, with major assessments occurring during the first year of life, at age 7, and at age 15. On average, participants had about eight head circumference measurements recorded over their childhood.
When the participants reached age 17 or 18, trained psychologists interviewed them using a semi-structured assessment to evaluate whether they had experienced hallucinations, delusions, or thought interference since age 12. Thought interference refers to the belief that one’s private thoughts are being broadcast out loud, inserted into one’s mind, or taken away by an outside force. Based on these interviews, 339 participants (8.8 percent of the sample, comprising 218 females and 121 males) were classified as having definite psychotic experiences.
Within that group, 62 individuals (1.6 percent of the sample, comprising 49 females and 13 males) met the operational criteria for a psychotic disorder. This meant their experiences occurred at least once a month over the preceding six months and caused severe distress, impaired their social or work functioning, or prompted them to seek professional help. The remaining 3,527 participants served as the comparison control group.
To confirm that external head measurements accurately reflected internal brain size in their sample, the researchers also analyzed structural magnetic resonance imaging (MRI) brain scans from a subset of 347 participants at age 20. From these scans, they calculated total intracranial volume, which is the total space inside the skull cavity occupied by the brain and surrounding fluids.
In their statistical models, the authors controlled for several maternal and birth factors that can influence physical growth. These included the mother’s highest level of education, her pre-pregnancy body mass index, the length of the pregnancy, and the baby’s weight at birth. In a secondary step, the researchers added the child’s height across development to see if head size differences persisted when accounting for overall physical stature.
The neuroimaging analysis confirmed that childhood head circumference was a reliable proxy for young adult brain size. Head size at birth showed a moderate positive correlation with total intracranial volume at age 20, while head measurements taken at ages 7 and 15 showed strong correlations with adult intracranial volume across both males and females.
When looking at growth trajectories over time, the researchers found that young people who met criteria for a psychotic disorder at age 18 had consistently smaller head circumferences than the control group from birth right through to age 15. Across the developmental span, the psychotic disorder group had an average head circumference about 0.26 centimeters smaller than controls in the statistical model, a small fraction of overall head size. The gap did not widen or narrow as the children aged, indicating that the modeled gap was similar in size from birth through adolescence.
The difference remained after accounting for maternal education and maternal body mass index, and shrank only slightly, to about 0.20 centimeters, when length of pregnancy and birth weight were added, though at that point it fell just short of statistical significance. Sensitivity checks looking strictly at birth, age 7, and age 15 also found smaller head sizes in the psychotic disorder group at each milestone, with the differences reaching statistical significance at ages 7 and 15.
When the team examined the larger group of 339 young people who reported broader psychotic experiences, they discovered contrasting patterns between males and females. Females with psychotic experiences had consistently smaller head circumferences across childhood and adolescence compared to female controls, averaging about 0.27 centimeters smaller in the unadjusted trajectory model.
In contrast, males with psychotic experiences had larger head circumferences than male controls across the overall trajectory model, averaging about 0.35 centimeters larger. In the age-by-age checks, however, males with psychotic experiences had smaller heads at birth and larger heads at ages 7 and 15. Both of the overall sex-specific patterns remained intact after adjusting for maternal and birth characteristics.
The smaller head sizes seen in the psychotic disorder group and among females with psychotic experiences stand in contrast to findings in autism spectrum disorder, a neurodevelopmental condition characterized by differences in social communication and restricted or repetitive behaviors. “For me, one of the most interesting aspects of this finding is what it tells us when considered alongside our work in autism spectrum disorder,” Merritt noted. “In a separate paper, we found the opposite pattern, with larger head circumference associated with autism. This suggests that patterns of brain growth may differ across different forms of neurodevelopmental risk, rather than there being a single pattern of atypical brain development.”
The picture shifted when the researchers factored in the children’s height over time. After controlling for height across development, the head circumference differences between the psychotic disorder group and the control group shrank and were no longer statistically significant. The same thing happened among females with psychotic experiences: once height was taken into account, their smaller head size was no longer statistically significant. The raw height differences between groups at age 15.5 were small and not statistically tested: females in the psychotic disorder group averaged about 1.6 centimeters shorter than female controls, while the 13 males in that group averaged slightly taller than male controls.
In males with psychotic experiences, however, controlling for height did not change the outcome, and their head circumferences remained larger than those of male controls. Together, these results suggest that for individuals with psychotic disorders and females with psychotic experiences, a smaller head circumference may reflect a broader, whole-body growth restriction rather than an issue confined to brain growth.
The authors noted that hormones regulating early physical development might help explain why general growth restriction and sex differences appear across the psychosis spectrum. One candidate they pointed to is insulin-like growth factor-I, a hormone that manages both fetal and childhood physical growth and naturally circulates at different levels in males and females. Early environmental stressors, such as maternal infections during pregnancy or nutritional deficiencies, could also influence both overall physical stature and future mental health risk.
“The key takeaway is that head circumference is a potentially useful, inexpensive measure for understanding developmental differences associated with psychosis risk,” Merritt said. “However, these findings reflect differences between groups and cannot currently be used to predict psychosis in an individual. We would not want people to interpret a smaller head circumference as meaning that someone will develop psychosis. There are many factors that contribute to psychosis risk, and head circumference would need to be considered alongside other measures.”
As with all research, there are some caveats to consider when interpreting these findings. Because the study followed participants over nearly two decades, not every child had their head measured at every possible age, and the researchers had to rely on statistical modeling to chart continuous trajectories across gaps in time. In addition, the classification of psychotic disorder at age 18 was based on structured research interviews rather than formal clinical diagnoses from a medical doctor.
The total number of participants who met the criteria for a psychotic disorder was relatively small at 62 people, and only 13 of them were male. Because of this small male sample size in the disorder group, the researchers may not have had enough statistical power to detect sex differences among those with full psychotic disorders, and findings involving males in that group should be viewed cautiously. Future studies using larger, independent birth cohorts will be needed to verify these sex-specific growth patterns and examine the biological mechanisms that link early physical growth to adult mental health.
“In the longer term, we are interested in whether head circumference could be combined with other developmental, genetic and environmental risk measures to improve our ability to identify individuals who might benefit from early intervention,” Merritt added.
The study, “Course of head growth from birth to adolescence across the psychosis spectrum,” was authored by Sarah A. Ashley, Kate Merritt, Francesca Solmi, Pedro Luque Laguna, Yanakan Logeswaran, Derek K. Jones, David Linden, Anthony S. David, and Abraham Reichenberg.
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🧿𝑵𝒊𝒆𝒕𝒛𝒔𝒄𝒉𝒆, 𝒆𝒍 𝒇𝒊𝒏𝒂𝒍 𝒅𝒆 𝒖𝒏 𝒇𝒊𝒍𝒐́𝒔𝒐𝒇𝒐 🧿
En esta imagen capturada en 1899 se puede ver a Friedrich Nietzsche durante su estancia en un asilo, una década después de sufrir el colapso mental que marcó el final de su vida consciente.
La crisis comenzó el 3 de enero de 1889 en la ciudad de Turin.
Según el relato más difundido —y también el más conmovedor— Nietzsche presenció cómo un cochero golpeaba brutalmente a un caballo en plena calle.
Al ver aquella escena de crueldad hacia un animal indefenso, el filósofo se acercó al caballo, lo abrazó y rompió a llorar.
Algunos testimonios dicen incluso que besó al animal mientras intentaba protegerlo.
Poco después se desplomó.
A partir de ese momento comenzó un deterioro mental irreversible del que nunca volvería a recuperarse.
Aquella imagen del filósofo abrazando al caballo terminó convirtiéndose en una escena casi simbólica.
Representa a un hombre que pasó gran parte de su vida reflexionando sobre la voluntad, la fuerza interior y la superación del ser humano —ideas que desarrolló en obras como "Thus Spoke Zarathustra"— y que, paradójicamente, terminó derrumbándose en un gesto de compasión absoluta.
Lo curioso es que Nietzsche había criticado muchas veces la Mitleid (compasión o piedad).
Para él, la piedad podía convertirse en una forma de debilidad que perpetuaba el sufrimiento en lugar de superarlo.
Por eso ese episodio del caballo siempre ha resultado tan irónico: el filósofo que cuestionaba la compasión terminó quebrándose en un acto de empatía total hacia un animal.
Ahora bien, los historiadores suelen hacer una distinción importante.
El episodio del caballo es muy potente como símbolo cultural, pero desde el punto de vista médico probablemente fue simplemente el momento en que estalló una enfermedad mental que llevaba años gestándose.
Tras ese día en Turín, Nietzsche perdió prácticamente el control de su mente.
Fue internado primero en una clínica psiquiátrica en Basel y después en otra en Jena.
Los informes médicos de la época describen escenas bastante duras: delirios de grandeza, episodios de incoherencia total y comportamientos extraños.
En ocasiones afirmaba ser al mismo tiempo el rey de Italia y personajes históricos distintos.
Durante más de una década vivió en un estado de deterioro mental profundo.
Ya no volvió a escribir ni a participar conscientemente en el mundo intelectual que él mismo había sacudido con sus ideas.
Pero lo más oscuro de su historia quizá no ocurrió en su mente, sino alrededor de su legado.
Aquí aparece una figura clave: su hermana, Elisabeth Förster-Nietzsche.
Cuando Nietzsche quedó incapacitado, Elisabeth tomó el control de todos sus manuscritos.
Ella era una nacionalista alemana convencida y profundamente antisemita.
Estaba casada con Bernhard Förster, quien incluso intentó fundar en Paraguay una colonia “aria” llamada Nueva Germania.
A partir de ese momento, Elisabeth comenzó a editar y reorganizar los cuadernos de su hermano.
El caso más famoso fue la obra titulada "The Will to Power", que en realidad no fue un libro terminado por Nietzsche, sino una recopilación manipulada de fragmentos de sus notas.
Con esas ediciones, muchas de sus ideas fueron reinterpretadas para parecer compatibles con el nacionalismo radical y la superioridad racial.
Algo bastante irónico, porque en sus textos reales Nietzsche criticó duramente el antisemitismo y despreciaba el nacionalismo alemán de su tiempo.
Aun así, décadas después, durante el auge del nazismo, su filosofía fue apropiada por el régimen de Adolf Hitler.
Hitler incluso visitó el Archivo Nietzsche en Weimar y posó para fotografías junto al busto del filósofo.
Aquello contribuyó a una enorme confusión histórica sobre lo que realmente pensaba Nietzsche.
Otra polémica que acompañó su biografía fue la teoría de la sífilis.
Durante décadas se dijo que su colapso mental se debía a una neurosífilis, algo relativamente común en el siglo XIX.
La idea era que la enfermedad la habría contraído en un burdel durante sus años de estudiante.
Hoy muchos médicos dudan de esa explicación.
Algunos investigadores creen que pudo sufrir CADASIL, una enfermedad genética vascular que provoca microinfartos cerebrales.
Otros sugieren que pudo tener un meningioma, un tumor cerebral detrás del ojo derecho.
Esta hipótesis encajaría con sus migrañas terribles, sus problemas de visión y su progresivo deterioro neurológico.
Porque si algo marcó la vida de Nietzsche fue el dolor físico constante.
Sufría migrañas devastadoras, vómitos frecuentes y problemas digestivos crónicos.
A veces pasaba días enteros casi ciego por el dolor.
Para soportarlo utilizaba sedantes de la época, como hidrato de cloral, e incluso opio para dormir.
Paradójicamente, el hombre que escribió sobre la fortaleza del espíritu vivía de forma bastante frágil: cambiando constantemente de pensión entre Suiza, Italia y los Alpes, intentando encontrar climas que aliviaran sus dolores.
También tuvo una vida emocional complicada.
Nunca se casó ni tuvo hijos.
Su gran desengaño sentimental fue la intelectual rusa Lou Andreas-Salomé, de quien se enamoró profundamente y a quien propuso matrimonio dos veces.
Ella lo rechazó.
Aquella ruptura lo afectó mucho y reforzó su tendencia al aislamiento.
Su amistad con el compositor Richard Wagner también terminó de forma amarga.
Nietzsche había admirado profundamente a Wagner, pero acabó distanciándose por el antisemitismo del músico, su nacionalismo y su regreso al cristianismo.
Los últimos años del filósofo fueron tristes.
Vivía bajo el cuidado de su madre primero y después de su hermana.
En sus últimos días apenas hablaba, tenía el cuerpo parcialmente paralizado y sufría frecuentes derrames cerebrales.
Finalmente murió el 25 de agosto de 1900 en Weimar, a los 55 años.
La causa oficial fue una neumonía, agravada por un derrame cerebral final.
Fue enterrado en su pueblo natal, Röcken, junto a la tumba de sus padres.
Y hay algo casi irónico en ese final: el hombre que había escrito “Dios ha muerto” recibió un funeral cristiano tradicional.
Nietzsche murió sin saber que, décadas después, se convertiría en uno de los filósofos más influyentes del siglo XX.
Su mente se apagó mucho antes de que el mundo entendiera realmente el alcance de sus ideas.
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https://youtu.be/UfGuiGzRrQs ➡️𝐼𝑛𝑓𝑜𝑟𝑚𝑎𝑐𝑖𝑜́𝑛
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