<![CDATA[Lawsuits, research, and clinicians clash over youth screen addiction—learn more about how problematic social platform use evades diagnosis and how we can curb harm.]]>
STAT+: UnitedHealthcare’s lactation billing feud, and fake strokes
This is the online version of STAT’s weekly email newsletter Health Care Inc. Sign up here.
I live in northwest Indiana, and it appears the Chicago Bears are going to put the team’s new stadium here, well outside the actual city of Chicago with almost no public transit and financed completely by Indiana taxpayers. The Bears are successfully pissing off just about everyone — no small feat. Send all Bears thoughts and health care tips my way! bob.herman@statnews.com.
The breastfeeding billing battle
UnitedHealthcare is cutting back on paying for lactation counseling, and the clinicians who provide those services are up in arms, another example of the deepening rifts between providers and insurers.
STAT+: Novo underwhelmed by drug it once fought Pfizer for
Want to stay on top of the science and politics driving biotech today? Sign up to get our biotech newsletter in your inbox.
Gene therapies can now cure disease, but America still hasn’t figured out how to pay for them. Is there a better way? Also, Novo executives are downplaying a once-coveted obesity drug, Incyte is making a $2 billion blood disease bet, and new data suggest Boehringer’s obesity contender may struggle to stand out in an increasingly crowded market.
The need-to-know this morning
- Roche is partnering with Nurix Therapeutics to co-develop an experimental antibody treatment that works by degrading, or eliminating, a protein called BTK that is associated with blood cancer and other diseases.
- Treeline Biosciences, the developer of early-stage cancer medicines co-founded by biotech entrepreneur Josh Bilenker, is going public via a reverse merger with Standard BioTools.
Combination of pancreatic cancer drugs from Tango, Revolution leads to high response rate
Revolution Medicines’ experimental pancreatic cancer drug has been the star of the oncology field in recent weeks, with new data showing the medicine produced unprecedented outcomes for patients.
STAT+: Pharmalittle: We’re reading about Lilly and Pfizer obesity drug data, Roche and J&J deals, and more
Good morning, everyone, and welcome to another working week. We hope the weekend respite was relaxing and invigorating because that oh-too-familiar routine of meetings, deadlines, and the like has returned with a vengeance. You knew this would happen, yes? To cope, we are relying, as always, on cups of stimulation. Our choice today is laced with chocolate raspberry. Feel free to join us. Remember, no prescription is required. Meanwhile, here are some tidbits to help you along. Best of luck accomplishing your goals today, and of course, do keep in touch. …
Revolution Medicines’ experimental pancreatic cancer drug has been the star of the oncology field in recent weeks, with new data showing the medicine produced unprecedented outcomes for patients, but its next act — this time as a co-lead — was just revealed, STAT points out. Tango Therapeutics said that in an early-stage clinical trial, a combination of its drug vopimetostat and Revolution’s daraxonrasib led to durable responses in the large majority of pancreatic cancer patients who received both medicines. Tango’s strategy of testing the two targeted drugs is notable because combination approaches in pancreatic cancer often include chemotherapy. The recent successful Revolution trial that has upended the specialty tested daraxonrasib versus chemotherapy as a second-line treatment.
Eli Lilly has already established that its next-generation obesity drug can lead to rapid weight loss, but researchers disclosed new data that provide more details on the safety and tolerability of the closely watched therapy, STAT writes. Lilly previously said that in one late-stage study, retatrutide helped people with diabetes lower blood sugar and lose a significant amount of weight, which is notable since those who have diabetes tend to lose less weight on treatment than those who do not. New data showed seven out of the 403 participants who received retatrutide experienced arrhythmias, and three treated participants experienced major cardiovascular complications, compared with none in the placebo group.
Divergent dFC stability of DMN and SMN in narcolepsy
Narcolepsy type 1 (NT1) is characterized by profound sleep-wake state instability, pointing to a fundamental dysregulation of large-scale brain network dynamics. To elucidate this, we assessed whole-brain dynamic functional connectivity (dFC) stability using resting-state fMRI in 27 patients with NT1 and 25 matched healthy controls. Our analysis revealed a pattern of opposing alterations: patients exhibited significantly increased dFC stability within the bilateral somatomotor network (SMN), concurrent with decreased stability in the medial prefrontal default mode network (Default_PFCm). These opposing alterations were clinically relevant, as increased SMN stability correlated with poorer objective sleep efficiency, and decreased Default_PFCm stability was similarly associated with lower objective sleep efficiency. Here, we identify for the first time this coexisting neural signature of SMN hyper-stability and Default_PFCm instability in NT1. By simultaneously destabilizing higher-order cognitive networks and disinhibiting primary sensorimotor processing, orexin deficiency may contribute to a synergistic dysregulation that blurs sleep-wake boundaries. The divergence in dynamic network stability provides a novel systems-level framework for understanding state instability in NT1.
Gut microbiome dynamics in autism: a prospective nested case–control study demonstrates microbial-clinical associations following rehabilitation interventions
BackgroundChildren with autism spectrum disorder (ASD) commonly exhibit gut microbiota dysbiosis and metabolic abnormalities, yet the mechanisms linking these changes to clinical symptoms remain unclear.ObjectiveThis study employed a nested case–control design and multi-omics approaches to evaluate the effects of rehabilitation intervention on clinical symptoms and gut microbiota in children with ASD, identify distinct microbial-metabolic signatures, and explore their mechanistic links with sleep disorders and developmental abilities.MethodsWithin a prospectively established pediatric cohort (n = 45), we implemented a nested case–control design including 26 ASD children (18 males, 8 females; mean age 61.79 ± 11.15 months) and 19 age- and sex-matched healthy controls. All ASD participants received standardized rehabilitation therapy (2 h/day, 5 days/week for 6 months) comprising occupational therapy and cognitive-linguistic training. Primary outcomes included comprehensive clinical assessments [Griffiths Development Scales-Chinese (GDS-C), Children’s Sleep Habits Questionnaire (CSHQ), Autism Behavior Checklist (ABC), Childhood Autism Rating Scale (CARS)] and longitudinal multi-omics analysis (metagenomic sequencing and LC–MS-based metabolomics). Association analyses were performed with FDR correction (q < 0.05).ResultsFollowing the 6-month rehabilitation intervention, significant clinical improvements were observed in sleep quality (CSHQ total and subscores) and developmental performance (GDS-C). Multi-omics profiling revealed distinct biological signatures in ASD children compared to healthy controls, characterized by elevated Intestinibacter_bartlettii and reduced levels of ornithine and siderophore nonribosomal peptide biosynthesis. Crucially, correlation analysis demonstrated that, after FDR correction, ornithine levels were significantly positively correlated with multiple GDS-C developmental domains, while tyrosine was associated with parasomnias. These findings establish a potential mechanistic link where amino acid metabolism connects gut microbial shifts to clinical phenotypes.ConclusionThis study demonstrates that rehabilitation intervention synchronously ameliorates clinical symptoms and modulates the gut-metabolic profile in ASD. The identified associations between specific metabolites (ornithine and tyrosine) and clinical outcomes suggest a metabolic mechanism underlying the gut-brain axis, highlighting the potential of these metabolites as biomarkers for therapeutic monitoring. Further large-scale studies are needed to validate these findings.
Postnatal maternal mental health-related hospitalisation and its association with adverse child health and maltreatment outcomes: narrative review
BackgroundMaternal mental health conditions within the postnatal period can have long-lasting consequences on a child’s well-being. This study synthesises current evidence on the association between postnatal maternal mental health-related hospitalisation (MHrH) and adverse child health and maltreatment outcomes.MethodsWe conducted an inclusive search across multiple databases, including MEDLINE, PsycINFO, CINAHL, Scopus, Embase, Google Scholar, and the reference list of eligible papers. Studies that used standardised outcome measures were included. Study selection and data extraction were made using a standardised Joanna Briggs Institute (JBI) tool. The quality of the studies was assessed using the Newcastle-Ottawa Scale (NOS). Descriptive vote counting to map the direction of effects, alongside narrative thematic synthesis, was used to summarise the findings from the included studies.ResultsFour studies (n = 1,020,342) were included in the review. Three of these studies suggest a possible association between postnatal maternal MHrH and adverse child health outcomes (growth failure, respiratory and gastrointestinal infection) or maltreatment (sexual, physical, and emotional abuse). One study did not find a statistically significant association between postnatal maternal MHrH and infant growth.ConclusionThe available evidence suggests a possible association between postnatal maternal MHrH and adverse child health and maltreatment outcomes. However, given the small number of studies and methodological heterogeneity, these findings should be interpreted cautiously and highlight the need for further high-quality longitudinal research.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD42023446155.
Disruption of a GalR2–mitochondrial axis in the ventral hippocampus contributes to depression-like phenotypes after prenatal stress
BackgroundPrenatal stress (PS) is a major risk factor for depression later in life, yet the cellular mechanisms linking early-life adversity to long-term affective vulnerability remain incompletely understood. Neuropeptide receptors have emerged as important modulators of stress-related psychopathology, but their roles in mitochondrial regulation within limbic circuits remain largely unexplored.MethodsA rat model of PS was established to assess depression-like behaviors in adulthood. Mitochondrial ultrastructure, ATP production, and the expression of Galanin receptor 2 (GalR2) and key components of the PINK1/Parkin mitochondrial quality control machinery were examined in the ventral hippocampus (vHPC). The effects of intranasal administration of the GalR2 agonist AR-M1896 on behavioral and mitochondrial alterations were evaluated in vivo. To directly test whether the vHPC mediates these effects, we performed unilateral intra−vHPC infusion of AR−M1896. In vitro, glucocorticoid exposure and pharmacological manipulation of GalR2 were used to assess their impact on mitochondrial function and PINK1/Parkin signaling.ResultsPS induced persistent anhedonia-like behavior and behavioral despair phenotypes in adult offspring, accompanied by marked mitochondrial structural abnormalities, reduced ATP production, and downregulation of GalR2 and PINK1/Parkin-associated mitochondrial quality control signaling in the vHPC. Intranasal AR-M1896 partially normalized reward-related behavioral deficits and ameliorated mitochondrial dysfunction. Importantly, direct intra−vHPC infusion of AR−M1896 elevated ATP, PINK1 and Parkin levels in the ipsilateral vHPC, providing causal evidence that the vHPC is a critical site for GalR2−mediated PINK1/Parkin-related mitophagy−restoring effects. In cell-based assays, glucocorticoid exposure suppressed, whereas GalR2 activation enhanced, mitochondrial membrane potential and PINK1/Parkin-related signaling.ConclusionThese findings identify a GalR2–mitochondrial axis in the ventral hippocampus that is disrupted by PS and associated with vulnerability to depression-like phenotypes. The complementary intra−vHPC infusion experiments establish a causal role for vHPC GalR2 signaling in rescuing mitochondrial deficits, directly demonstrating that intranasal AR−M1896 acts at least in part via the vHPC. This receptor–organelle pathway may represent a neurobiological mechanism linking early-life adversity to long-term affective dysfunction.
Integrative mechanisms and intervention targets of the microbiota–gut–brain axis in depressive disorders: advances across immune, endocrine, and central nervous system pathways
Depressive disorders are highly heterogeneous syndromes characterized not only by depressed mood but also by cognitive impairment, sleep–circadian rhythm disturbances, altered appetite, somatic discomfort, and metabolic or gastrointestinal comorbidities. In recent years, the microbiota–gut–brain axis (MGBA) has been increasingly recognized as an integrative biological framework linking abnormalities in mood regulation, immune responses, endocrine function, metabolism, and neuroplasticity. This review provides a systematic synthesis of gut microbial ecology and host phenotypic features associated with depressive disorders, with particular emphasis on the depletion of short-chain fatty acid-producing commensals, the enrichment of potentially pro-inflammatory taxa, and the functional remodeling of key metabolic pathways, including the tryptophan–kynurenine pathway, short-chain fatty acids, bile acids, and trimethylamine N-oxide. We further discuss how bidirectional gut-to-brain and brain-to-gut communication may contribute to the onset and progression of depressive disorders through intestinal barrier disruption, low-grade systemic inflammation, hypothalamic–pituitary–adrenal axis activation, vagal signaling, and dysregulation of neurotransmitter and neurotrophic pathways. Current interventional evidence suggests that dietary and lifestyle modification, psychobiotics, and fecal microbiota transplantation may exert antidepressant potential in selected populations; however, the overall effect sizes remain limited and between-study heterogeneity is substantial. Patients with prominent gastrointestinal symptoms, metabolic abnormalities, or low-grade inflammatory states may represent priority candidates for MGBA-targeted interventions; nevertheless, a putative microbiota-responsive phenotype should not be simply equated with high stress exposure alone, and its definition requires prospective validation integrating stress burden, host responses, and microbial/metabolic readouts. Overall, MGBA research is gradually moving beyond descriptive profiling of microbial composition toward functional integration and clinical translation; however, causal inference, multi-omics standardization, and the identification of stratification biomarkers remain major challenges. Future studies should incorporate phenotype-based stratification, strengthened functional readouts, and precision intervention designs to determine which patients are most likely to benefit from microbiota-targeted therapies.
Feasibility study examining the short-term effects of Sonic Augmentation Technology™
BackgroundThe current study evaluated Sonic Augmentation Technology™ (SAT), a novel, Polyvagal-informed probe that incorporates continuously varying and acoustic features modeled on patterns of autonomic regulation into musical soundscapes. Specifically, the study examined whether SAT led to improvements in self-reported biobehavioral state (e.g. relaxation, breathing slowly, interoceptive clarity), and whether individuals with poorer baseline functioning (i.e., increased autonomic reactivity and anxiety/depression symptoms) reported greater improvements in biobehavioral state following SAT. It also sought to determine whether there would be changes in endogenous oxytocin level, and whether individuals who exhibit larger gains in biobehavioral state would show greater increases in oxytocin.MethodsThe current study examined data obtained from four samples, with 72 participants providing data virtually and 41 participants providing data in-person. Participants completed self-report measures of biobehavioral state, autonomic reactivity, and psychiatric symptomatology (i.e. anxiety and depression). Salivary oxytocin (pg/mL) was assessed via enzyme immunoassay in the participants who completed the study in person, with samples collected pre-and post-SAT.ResultsFollowing SAT, participants reported significant improvements in total biobehavioral state and the low and high arousal subscales. We also found that participants scoring above the cutoff for autonomic reactivity, anxiety, and depression reported greater increases in total biobehavioral state and decreases in the high arousal subscale. Greater decreases in the low arousal subscale were observed in the participants with increased anxiety. The subset of participants with salivary oxytocin samples exhibited increases in salivary oxytocin.ConclusionsThus, our results support the potential of SAT as a low-cost, non-invasive auditory probe for improving wellbeing, especially for clinical populations experiencing autonomic dysregulation and psychiatric difficulties, such as anxiety and depression.Clinical trial registrationClinicalTrials.gov, identifiers NCT06710886, NCT06902506, NCT06580119, and NCT07065227.