Adolescence is a particularly vulnerable neurodevelopmental period marked by high rates of engagement with risky alcohol use. This review summarizes the cognitive and neural consequences following alcohol use during adolescence from longitudinal design studies in humans and animals. Findings from human adolescent studies suggest that binge drinking and heavy alcohol use is associated with poorer cognitive functioning on a broad range of neuropsychological assessments, including learning, psychomotor speed, attention, executive functioning, and impulsivity. adolescence is memory, visuospatial functioning, Alcohol use during associated with accelerated decreases in gray matter and attenuated increases in white matter volume, and aberrant neural activity during executive functioning, attentional control, and reward sensitivity tasks, when compared to non-drinking adolescents. Animal studies in rodents and nonhuman primates have replicated human findings, and suggest cognitive and neural consequences of adolescent alcohol use may persist into adulthood. Novel rodent studies demonstrate that adolescent alcohol use may increase reward responsiveness of the dopamine system to alcohol later in life, as well as disrupt adolescent neurogenesis, potentially through neuroinflammation, with long-lasting neural and behavioral effects into adulthood. Larger longitudinal human cognitive and neuroimaging studies with more diverse samples are currently underway which will improve understanding of the impact of polysubstance use, as well as the interactive effects of substance use, physical and mental health, and demographic factors on cognition and neurodevelopment.

Magnesium is well known for its diverse actions within the human body. From a neurological standpoint, magnesium plays an essential role in nerve transmission and neuromuscular conduction. It also functions in a protective role against excessive excitation that can lead to neuronal cell death (excitotoxicity), and has been implicated in multiple neurological disorders. Due to these important functions within the nervous system, magnesium is a mineral of intense interest for the potential prevention and treatment of neurological disorders. Current literature is reviewed for migraine, chronic pain, epilepsy, Alzheimer’s, Parkinson’s, and stroke, as well as the commonly comorbid conditions of anxiety and depression. Previous reviews and meta-analyses are used to set the scene for magnesium research across neurological conditions, while current research is reviewed in greater detail to update the literature and demonstrate the progress (or lack thereof) in the field. There is strong data to suggest a role for magnesium in migraine and depression, and emerging data to suggest a protective effect of magnesium for chronic pain, anxiety, and stroke. More research is needed on magnesium as an adjunct treatment in epilepsy, and to further clarify its role in Alzheimer’s and Parkinson’s. Overall, the mechanistic attributes of magnesium in neurological diseases connote the macromineral as a potential target for neurological disease prevention and treatment.

Lagging behind rapid changes to state laws, societal views, and medical practice is the scientific investigation of cannabis’s impact on the human brain. While several brain imaging studies have contributed important insight into neurobiological alterations linked with cannabis use, our understanding remains limited. Here, we sought to delineate those brain regions that consistently demonstrate functional alterations among cannabis users versus non-users across neuroimaging studies using the activation likelihood estimation meta-analysis framework. In ancillary analyses, we characterized task-related brain networks that co-activate with cannabis-affected regions using data archived in a large neuroimaging repository, and then determined which psychological processes may be disrupted via functional decoding techniques. When considering convergent alterations among users, decreased activation was observed in the anterior cingulate cortex, which co-activated with frontal, parietal, and limbic areas and was linked with cognitive control processes. Similarly, decreased activation was observed in the dorsolateral prefrontal cortex, which co-activated with frontal and occipital areas and linked with attention-related processes. Conversely, increased activation among users was observed in the striatum, which co-activated with frontal, parietal, and other limbic areas and linked with reward processing. These meta-analytic outcomes indicate that cannabis use is linked with differential, region-specific effects across the brain.

Gulf War Illness (GWI) is a multisymptom disorder including widespread chronic pain, fatigue and gastrointestinal problems. The objective of this study was to examine the low glutamate diet as a treatment for GWI. Forty veterans with GWI were recruited from across the US. Outcomes included symptom score, myalgic score, tender point count, dolorimetry and the Chalder Fatigue Scale. Subjects were randomized to the low glutamate diet or a wait-listed control group, with symptom score being compared after one month. Subjects then went onto a double-blind, placebo-controlled crossover challenge with monosodium glutamate (MSG)/placebo to test for return of symptoms. Symptom score was compared between diet intervention and wait-listed controls with an independent t-test and effect size was calculated with Cohen’s d. Change scores were analyzed with Wilcoxon Signed Rank tests. Crossover challenge results were analyzed with General Linear Models and cluster analysis. The diet intervention group reported significantly less symptoms (p = 0.0009) than wait-listed controls, with a very large effect size, d = 1.16. Significant improvements in average dolorimetry (p = 0.0006), symptom score, tender point number, myalgic score and the Chalder Fatigue Scale (all p < 0.0001) were observed after the 1-month diet. Challenge with MSG/placebo resulted in significant variability in individual response. These results suggest that the low glutamate diet can effectively reduce overall symptoms, pain and fatigue in GWI, but differential results upon challenge suggest that other aspects of the diet, or underlying differences within the population, may be driving these changes. Future research is needed to identify potential nutrient effects, biomarkers, and underlying metabolic differences between responders and non-responders.

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Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, hyperactivity, and/or impulsivity with associations to short- and long-term aversive life events. The exact etiology of the disorder is still unknown. ADHD is heterogeneous in symptomology and a single consistent, reliable biomarker has not been found. Quantitative electroencephalography (EEG) has been proposed as a potential way to differentiate those with ADHD from typically developing controls; however, the data on the diagnostic utility of this approach have been variable. Quantitative EEG has been employed in prognostic ways to assess differences in baseline spectral power profiles and pharmacological and nonpharmacological treatment effects on electrocortical activity within the ADHD population. The aim of this review is to summarize the literature investigating the degree of normalization of resting-state EEG profiles in individuals with ADHD through various interventions, including stimulant and nonstimulant medication, exercise, and diet.

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Current research has demonstrated the definitive presence of oxidative stress in multiple sclerosis (MS). This finding has led to clinical trial research which has indicated that specific antioxidants have the ability to effectively reduce markers of oxidative stress. However, few interventions testing antioxidant supplements have shown efficacy for reducing the symptom burden in the disorder. This paper quickly reviews what is currently known about oxidative stress and antioxidants in MS, explains which nutrients are critical for the creation and maintenance of the myelin sheath, describes potential negative effectors in the diet which may be contributing to oxidative stress, and how these aspects of diet, combined with current knowledge on antioxidants, may be able to be combined into a whole food dietary intervention which can be tested for efficacy in MS.