A new study from the University of Bergen shows an association between breastfeeding up to 6 months of age and a reduced risk of ADHD symptoms from ages 3 to 8.

Breast milk is the primary source of nutrition for infants. It is uniquely tailored for the child and contains numerous components beneficial for growth and brain development, including long-chain fatty acids, amino acids, antibodies and beneficial bacteria.

“It is well established that psychiatric symptoms and disorders can be influenced by both genetic and environmental factors,” says Berit Skretting Solberg, psychiatrist and researcher at the Department of Biomedicine, University of Bergen, and senior consultant at Betanien Hospital.

Researchers stimulated human neurons and tracked gene activity. Activation exposed hidden variants and epigenetic changes linked to schizophrenia and autism, explaining disease risk missed in resting brain studies.

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, impulsivity and/or hyperactivity. In recent years, metabolic alterations, primarily obesity, insulin resistance, and diabetes, have emerged as frequent comorbidities in individuals with ADHD, suggesting a bidirectional relationship between neurodevelopmental and metabolic dysfunctions. Emerging evidence indicates that dysregulation of dopaminergic signaling, disturbances in the hypothalamic-pituitary-adrenal (HPA) axis, and chronic low-grade inflammation are central to both ADHD symptomatology and metabolic impairments. For instance, alterations in dopamine-related genes (e.g., DRD4, DAT1) not only affect cognitive and behavioral functions but also play a role in appetite regulation and glucose homeostasis. Epidemiological studies further demonstrate that individuals with ADHD exhibit poorer glycemic control and a higher prevalence of both type 1 and type 2 diabetes, while early-life metabolic challenges such as maternal diabetes may predispose offspring to ADHD. This review aims to comprehensively synthesize the epidemiological, genetic, and pathogenetic evidence linking ADHD to metabolic alterations. We discuss key pathophysiological pathways—including dopaminergic dysregulation, HPA axis disturbances, inflammation, and oxidative stress—and evaluate their contributions to the co-occurrence of ADHD and metabolic disorders. In addition, we explore the clinical implications and integrated treatment approaches that encompass lifestyle modifications, pharmacological therapies, and multidisciplinary care. Finally, we outline future research directions to develop personalized and holistic interventions.

A new study from the Knight Initiative for Brain Resilience researchers may help explain an enduring mystery about amyotrophic lateral sclerosis (ALS): why the disease kills off some of the brain and spinal cord’s movement-controlling neurons while others show greater resilience.

As ALS progresses, more and more of those motor neurons degenerate and die. As a result, patients lose control of their bodies and become unable to breathe. Many people are diagnosed in middle to late adulthood, and most survive only three to five years after diagnosis.

“It’s a cruelly rapid disease,” said Olivia Gautier, a postdoctoral scholar in the lab of Knight Initiative researcher Aaron Gitler, the Stanford Medicine Basic Science Professor and a professor of genetics at Stanford Medicine.