Previous studies have shown that quantitative electroencephalography (qEEG) provides measures of brain wave voltage and symmetry within each of the standard bandwidths. These qEEG measures are neurophysiological correlates of brain wave signatures for various aspects of cognition and behavior and are susceptible to neurofeedback training for improving human performance. Using exam scores and an individualized self-inventory (ISI) of psychosocial interactions, we provide unique data for probing behavioral and cognitive performance of medical students. Increments in voltage within the standard theta (4–7 Hz) and beta (15–20 Hz) frequencies and decrements in the theta–beta ratio (TBR) suggest improvements in attentional control. Associations between right-sided frontal alpha asymmetry (fAA) and ISI scores for negative self-perceptions suggest a novel qEEG signature for emotional balance. These findings suggest that changes in qEEG voltages and asymmetries may be predictive of improvements in attentional control, cognitive performance, and psychosocial skills, as well as serving as surrogate markers for neurofeedback training-related changes in neuroplasticity.
Part of the book: Neurophysiology
COVID-19 is a highly contagious viral illness that has claimed millions of lives worldwide. Since its emergence, it has exerted a negative impact on many sectors globally without the exception of frontline COVID-19 healthcare providers. Specifically, in frontline COVID-19 healthcare workers, occupational stress-related sleep disorders such as insomnia and daytime somnolence have been extensively reported and were characterized by neuro-immunological changes. However, the possible mechanisms that underlie the sleep disorders have not been elucidated. The review was designed to highlight possible sleep mechanisms responsible for insomnia and daytime somnolence reported in frontline COVID-19 health workers. Available evidence shows that emotional perturbation, hypertension, chronobiological disruption and prolonged exposure to artificial light are among the events orchestrating occupational-stress-related sleep disorders in frontline COVID-19 healthcare workers. Anxiety-associated sleep anomaly is attributable to stimulation of the reticular activating system which occurs as a result of activation of noradrenergic fiber and sympatho-adrenal axis. Another mechanism includes depletion of hippocampal and brain glycogen by anxiety-induced activation of corticotropin releasing hormone (CRH)-secreting brain neurons and hypothalamic-corticotropic-adrenal cortex axis. Spontaneous discharge of noradrenergic fiber during basal state and changes in normal secretory rhythm of hypnosis-related chemical messengers may be responsible for hypertension- and chronobiological disruption-induced sleep disorders, respectively. Lastly, prolonged light exposure-induced suppression of melatonin secretion may elicit disruption of normal circadian sleep.
Part of the book: Identifying Occupational Stress and Coping Strategies
Physiological processes exhibit distinct rhythmic patterns influenced by external cues. External cues such as photic signal play an important role in the synchronization of physiological rhythms. However, excess of or indiscriminate exposure to photic signals exerts profound effects on physiological processes, disrupting normal hormonal secretory rhythms, altering sleep/wakefulness cycle, and impairing reproductive function. Alteration in sleep/wakefulness cycle, impairment in reproductive cycle, and disruption of normal hormonal secretory rhythms characterize risk groups for photic stress such as night workers, trans-meridian travelers, and night-active people. Evidence from primary studies is increasing on the tendency of selenium to reset internal biorhythms by targeting circadian proteins and melatonin. The review highlights the chronobiological roles of selenium.
Part of the book: Selenium and Human Health
Statins remain the most efficient hypolipidemic agent and their use is pivotal in primary, secondary, and tertiary treatment of cardiovascular disease, reducing both morbidity and mortality. Statins target 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the enzyme that catalyzes conversion of HMG-CoA to mevalonate, the “committed and rate limiting step” in hepatic production of cholesterol. Genetic predilections for hypercholesterolemia are known to be responsible for substantial morbidity and mortality from cardiovascular disease. Environmental or lifestyle factors such as dietary fat and carbohydrate may also contribute to cardiovascular disease mortality by both genetic and epigenetic mechanisms. Besides lipid-lowering, statins have pleiotropic effects which may contribute to their protection against cardiovascular and several other diseases wherein hypercholesterolemia is a risk factor. Evidence is emerging that the clinical outcomes of many diseases are improved when modifications of environmental or lifestyle factors play integral roles in treatment and preventive prescriptions. This chapter is, therefore, intended to inform physicians and other health care professionals about the environment-gene interactions underlying the main and pleiotropic effects of statins which may be employed to improve the efficacy of statin therapies.
Part of the book: Statins