Nature Reviews Disease Primers published a 2024 review on ADHD. B/c only the abstract is publically available, here are points of possible interest.
Introduction: “…we know the disorder’s core symptoms (inattention, hyperactivity and impulsivity), impairments (for example, school and occupational failure, poor socialization, and accidental injuries) and comorbidities (for example, anxiety and mood disorders).
Epidemiology (distribution and determinants): “In school-aged children, the prevalence of ADHD based on epidemiological samples representative of the general population is 5.3%…. In some individuals, symptom severity declines during adolescence but two-thirds of children…retain impairing symptoms…. In early adulthood, the prevalence of ADHD is ~2.5% with a gradual decrease to 1% at older ages.
“Only 56.8% of individuals with ADHD are diagnosed before 14…73.0% are diagnosed by 18 years and 91.8% by 25 years.”
“ADHD symptoms and impairments tend to worsen under certain conditions…increased self-regulation challenges, weak support systems, intensification of comorbid conditions and poor fit between individuals and their environment.”
Co-travelers: “ADHD often coexists with other psychiatric disorders.” “ADHD is also often comorbid with somatic conditions.” In children, these somatic conditions are dermatitis, obesity, asthma and rhinitis. In adults, this includes type 2 diabetes mellitus. ” “ADHD is also associated with vision problems….” “Children with ADHD have many sleep difficulties, including bedtime resistance, late sleep onset, night awakenings, morning awakenings, sleep disordered breathing and daytime sleepiness.”
Mechanisms/Pathophysiology, Genetics: “Meta-analyses…have shown…heritability of ADHD is ~80%.”
“[S}hared genetic factors partly explain the co-occurrence of ADHD with other psychiatric disorders …anxiety, major depressive, bipolar, conduct, autism spectrum and substance use disorders…and some somatic conditions. …ADHD is genetically associated with measures of cognition, electroencephalographic (EEG) variability and subtle structural brain differences.”
“The largest genome-wide association studies (GWAS) of ADHD found 27 genome-wide significant loci implicating 76 genes, many…upregulated during early brain development.” (upregulated: increased expression/activation) “ADHD genetic risk is enriched for genes associated with several brain-specific neuronal subtypes and midbrain dopaminergic neurons.”
Mechanisms/Pathophysiology, Environmental Correlates: “…strong evidence that rare events…traumatic brain injury…extreme emotional…nutritional deprivation…can cause ADHD….” “[M]any other environmental events are associated with ADHD. Most…events or complications…during pregnancy, delivery or early after birth (for example, low birthweight, perinatal hypoxia and advanced paternal age), although all have low risk ratios for ADHD.
Electrophysiology and brain imaging: “The most recent mega-analysis included five cohorts with almost 7,000 participants, and found reduced fractional anisotropy.” Where? The “inferior longitudinal and left uncinate fasciculi.” (The UF connects the temporal lobe with the medial orbitofrontal cortex, per articles cited here. Animal studies show its disconnection “causes impairment of object-reward association learning” and reduced memory performance “involving temporally complex visual information.” Studies on neurodevelopmental and neurological disorders show UF damage correlates with emotional processing deficits, “behavioral inhibition…and impaired object naming….
In meta-analyses of fMRI studies of cognitive control, the most consistent finding “is under-activation of the inferior frontal cortex (IFC) and the insula” among people with ADHD compared to controls.
Tonya Lippert 
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