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Power is an all-pervasive, and fundamental force in human relationships and plays a valuable role in social, political, and economic interactions. Power differences are important in social groups in enhancing group functioning. Most people want to have power and there are many benefits to having power. However, power is a corrupting force and this has been a topic of interest for centuries to scholars from Plato to Lord Acton. Even with increased knowledge of power's corrupting effect and safeguards put in place to counteract such tendencies, power abuse remains rampant in society suggesting that the full extent of this effect is not well understood. In this paper, an effort is made to improve understanding of power's corrupting effects on human behavior through an integrated and comprehensive synthesis of the neurological, sociological, physiological, and psychological literature on power. The structural limits of justice systems' capability to hold powerful people accountable are also discussed. [ABSTRACT FROM AUTHOR]

We live in times when our culture is obsessed with happiness. The value of almost every aspect of our lives is increasingly judged in terms of their contribution to our happiness. Happiness has become the ultimate goal by which values and priorities are constructed and the only thing for which any action in pursuit of does not require justification. In contrast, sadness is increasingly abnormalized and pathologized. In this paper, an effort is made to counteract the narrative that sadness, a critical aspect of human life is abnormal or a pathological condition. The evolutionary benefits of sadness and its place in human flourishing are discussed. A rebranding of sadness is proposed that emphasizes the free expression of sadness in everyday greetings to remove it from its current negative state and promote many of its benefits including post-traumatic growth and resilience. [ABSTRACT FROM AUTHOR]

A person trapped in a building engulfed in a raging fire, a person dealing with severe chronic disease, people dealing with a virus pandemic, and people fighting in a protracted war may appear dissimilar but are fundamentally in a similar situation and their behaviors follow a predictable and similar pattern. In this paper, the behaviors of rational people dealing with a significant persistent unpleasant, or dangerous stimulus that is inescapable are elucidated. The unique modulatory effects of stimulus persistence on human behavior as well as the role of means and interest are discussed. [ABSTRACT FROM AUTHOR]

Understanding the mechanisms behind memory, learning, and behavior is crucial to human development and significant research has been done in this area. Classical and operant conditioning and other theories of learning have elucidated different mechanisms of learning and how it modulates behavior. Even with advances in this area, questions remain on how to unlearn faulty ideas or extinguish maladaptive behaviors. In this paper, a novel theory to improve our understanding of this area is proposed. The theory proposes that as a consequence of the brain's energy efficiency evolutionary adaptations, all learning following memory consolidation, reconsolidation, and repeated reinforcements or strengthening over time, results in a phenomenon called mental representation block. The implications of this block on learning and behavior are significant and broad and include cognitive biases, belief in a creator or God, close-mindedness, dogmatism, physician misdiagnosis, racism, homophobia, and transphobia, susceptibility to deception and indoctrination, hate and love, artificial intelligence and creativity. [ABSTRACT FROM AUTHOR]

Background: Multiple sclerosis (MS) is a neurodegenerative disease caused by dysfunction of the immune system that affects the central nervous system (CNS). It is characterized by demyelination, chronic inflammation, neuronal and oligodendrocyte loss and reactive astrogliosis. It can result in physical disability and acute neurological and cognitive problems. Despite the gains in knowledge of immunology, cell biology, and genetics in the last five decades, the ultimate etiology or specific elements that trigger MS remain unknown. The objective of this review is to propose a theoretical basis for MS etiopathogenesis. Methods: Search was done by accessing PubMed/Medline, EBSCO, and PsycINFO databases. The search string used was "(multiple sclerosis* OR EAE) AND (pathophysiology* OR etiopathogenesis)". The electronic databases were searched for titles or abstracts containing these terms in all published articles between January 1, 1960, and June 30, 2019. The search was filtered down to 362 articles which were included in this review. Results: A framework to better understand the etiopathogenesis and pathophysiology of MS can be derived from four essential factors; mitochondria dysfunction (MtD) & oxidative stress (OS), vitamin D (VD), sex hormones and thyroid hormones. These factors play a direct role in MS etiopathogenesis and have a modulatory effect on many other factors involved in the disease. Conclusions: For better MS prevention and treatment outcomes, efforts should be geared towards treating thyroid problems, sex hormone alterations, VD deficiency, sleep problems and melatonin alterations. MS patients should be encouraged to engage in activities that boost total antioxidant capacity (TAC) including diet and regular exercise and discouraged from activities that promote OS including smoking and alcohol consumption. [ABSTRACT FROM AUTHOR]

The brain has been described as very resistant to change. However, why it does this has not been fully explained. In this paper, I propose that resilience to the disruption of consolidated memory is at the heart of the brain's resistance to change, and this resilience is a consequence of its energy efficiency evolutionary adaptations. I discussed the implications of this energy efficiency adaptation on dogmatism, close-mindedness, and artificial intelligence. [ABSTRACT FROM AUTHOR]

Objectives: Alcohol abuse is known to result in behavioral impairments (such as increased impulsivity, aggressive, and suicidal behavior), but the neurobiological basis for these behavioral impairments remains unknown. The objective of this review is to propose a neurobiological basis for alcohol-induced aggression, impulsivity, and suicidal behavior. Methods: Search was done by accessing PubMed/Medline, EBSCO, and PsycINFO databases. The search string used was "(Alcohol OR Alcoholism* OR Alcohol Abuse) AND (Behavior* OR Behavioral Impairment or Disorder) AND (Oxidative Stress OR Reactive Oxygen Species)." The electronic databases were searched for titles or abstracts containing these terms in all published articles between January 1, 1960, and May 31, 2019. The search was limited to studies published in English and other languages involving both animal and human subjects. Articles selected included randomized clinical trials (RCTs), observational studies, meta-analyses, and both systemic and narrative reviews, providing both quantitative and qualitative information with a measure of alcohol abuse or alcoholism as an outcome. Exclusion criteria were unpublished data of any form, including conference proceedings and dissertation. New key terms were identified (new term included: "Antioxidants, Neurotransmitters, Dopamine, Serotonin, GABA, Glutamate. Aggression, Impulsivity, Suicidal Behavior, hippocampus, prefrontal cortex, limbic system, psychiatric disorders, PTSD, Anxiety, Depression. These new terms were searched with Alcohol or Alcoholism or Alcohol Abuse and Oxidative Stress separately resulting in the identification of over 3000 articles. 196 were included in this article. Results: Multiple lines of evidence indicate that oxidative stress (OS) plays a critical underlying role in alcohol toxicity and behavioral impairments. Conclusions/Importance: People diagnosed with PTSD, anxiety disorder, depression, and those with a personality high in psychoticism as measured by the P Scale of the Eysenck Personality Questionnaire, with comorbid alcohol abuse or alcohol use disorder (AUD), may display increased impulsivity, aggression, and suicidal behavior because of the potentiating effect of alcohol-induced OS on their elevated brain oxidative status. Antioxidant therapy should be an integral part of acute alcohol intoxication and AUD treatment. Further research is necessary to fully understand the relationship between OS and alcohol-induced behavioral impairments. [ABSTRACT FROM AUTHOR]

Multiple sclerosis (MS) is a complex human neurodegenerative dysimmune disease of the central nervous system (CNS) which is characterized by chronic inflammation, demyelination, loss of blood‐brain barrier (BBB) integrity, neuronal loss, reactive astrogliosis, and oligodendrocyte depletion. It can result in physical disability and severe neurological and cognitive deficits. Research indicates that MS prevalence has significantly increased in many regions around the world since 1990. The specific elements that trigger MS remain unknown. In this paper, the critical role played by mitochondria dysfunction and oxidative stress in MS pathogenesis, progression, and clinical symptoms are elucidated. Their interactions with the key factors in the disease, as well as treatment strategies, are discussed. [ABSTRACT FROM AUTHOR]

Introduction: Evidence suggests that in convenience stores across the United States (U.S), sales of e-cigarettes (EC) continue to grow, indicating their rising popularity. ECs have been touted as a means for traditional cigarette (TC) smokers to quit smoking. However, the dramatic increase in the number of adolescents and young adults using e-cigarettes (vaping) in America is a cause for concern as their long-term effects remain unknown.Methods: Search was done by accessing PubMed/Medline, EBSCO, and PsycINFO databases. The search string used was "(Cigarettes OR E-Cigarettes* OR Vaping) AND (Oxidative Stress* OR Reactive Oxygen Species (ROS)) AND (Adolescents OR Teens OR Young Adults)". The electronic databases were searched for titles or abstracts containing these terms in all published articles between January 1, 1970, and June 30, 2019. Over 3000 articles were found in the first round of search which was filtered to 129 articles.Results: Oxidative Stress is a critical underlying molecular factor that drives the harmful effects of traditional cigarettes. The developing brain is particularly vulnerable to the harmful effects of oxidative stress and e-cigarettes just like traditional cigarettes induces oxidative stress. Many e-cigarette components including the flavoring, vapor, e-liquids and metallic coil, trigger oxidative stress, indicating that both nicotine and non-nicotine e-cigarette use may be harmful.Conclusions: E-cigarettes use could potentially play a role in adolescent/young adults social maladjustments including poor learning and academic performance, increased aggressive and impulsive behavior, poor sleep quality, attention deficits, impaired memory, and cognition, and increased depression and suicidal ideation. The government, parents, school authorities and clinicians should be advised on these potentially harmful effects. [ABSTRACT FROM AUTHOR]

Background: Alzheimer's disease (AD) is the commonest cause of dementia, with approximately 5 million new cases occurring annually. Despite decades of research, its complex pathophysiology and etiopathogenesis presents a major hindrance to the development of an effective treatment and prevention strategy. Aging is the biggest risk factor for the development of AD, and the total number of older people in the population is going to significantly increase in the next decades, suggesting that AD incidence and prevalence is likely to increase in the future. This makes the need for a better understanding of the disease to be extremely urgent.Methods: A search was done by accessing PubMed/Medline, EBSCO, and PsycINFO databases. The search string used was "(dementia* OR Alzheimer's) AND (pathophysiology* OR pathogenesis)". New key terms were identified (new term included "vitamin D, thyroid hormone, mitochondria dysfunction, oxidative stress, testosterone, estrogen, melatonin, progesterone, luteinizing hormone, amyloid-β (Aβ), and hyperphosphorylated tau"). The electronic databases were searched for titles or abstracts containing these terms in all published articles between January 1, 1965, and January 31, 2019. The search was limited to studies published in English and other languages involving both animal and human subjects.Results: Mitochondria dysfunction and oxidative stress play a critical role in AD etiopathogenesis and pathophysiology.Conclusion: AD treatment and prevention strategies must be geared towards improving mitochondrial function and attenuating oxidative stress. [ABSTRACT FROM AUTHOR]

Alzheimers' disease (AD) is the most common cause of dementia, with an estimated 5 million new cases occurring annually. Among the elderly, AD shortens life expectancy, results in disability, decreases quality of life, and ultimately, leads to institutionalization. Despite extensive research in the last few decades, its heterogeneous pathophysiology and etiopathogenesis have made it difficult to develop an effective treatment and prevention strategy. Aging is the biggest risk factor for AD and evidence suggest that the total number of older people in the population is going to increase astronomically in the next decades. Also, there is evidence that air pollution and increasing income inequality may result in higher incidence and prevalence of AD. This makes the need for a comprehensive understanding of the etiopathogenesis and pathophysiology of the disease extremely critical. In this paper, a quintuple framework of thyroid dysfunction, vitamin D deficiency, sex hormones, and mitochondria dysfunction and oxidative stress are used to provide a comprehensive description of AD etiopathogenesis and pathophysiology. The individual role of each factor, their synergistic and genetic interactions, as well as the limitations of the framework are discussed. [ABSTRACT FROM AUTHOR]

• Vitamin D deficiency, Oxidative stress, Thyroid dysfunction, and Hormonal alterations play a major role in maternal postpartum depression (PPD) etiopathogenesis and pathophysiology. • Better awareness and antenatal, perinatal, and postnatal screening for PPD is crucial to reducing the incidence and severity of the disease. • Treatment strategies should include an integrated approach Maternal Postpartum (PPD) or Postnatal Depression (PND) is believed to be the commonest medical complication postpartum. Evidence suggests a significantly higher prevalence of the disease compared to the often reported 10-15%. Studies were identified by accessing several databases including PubMed/Medline, PubMed Central, EBSCO, and PsycINFO. Vitamin D (VD) deficiency, hormonal levels alteration (estrogen, progesterone, testosterone, oxytocin, and prolactin), thyroid dysfunction, and increased oxidative stress, play a critical role in PPD etiopathogenesis and pathophysiology. Treatment strategies should include an integrated approach of antidepressants and psychotherapy, melatonin, diet, sleep improvement, exercise, VD and antioxidants supplementation, and economic and social support. [ABSTRACT FROM AUTHOR]

Obesity is a major public health problem whose prevalence has been rapidly increasing in the United States (U.S), and globally. It is one of the leading causes of preventable deaths globally and contributes to the development of many diseases. The search was limited to studies published in English and other languages involving both animal and human subjects. Articles selected included preclinical studies, randomized clinical trials RCTs, observational studies, meta-analyses, narrative and systemic reviews providing primary quantitative data with a measure of obesity or food addiction as an outcome. Over 5000 articles were found in the first round of search which was filtered to 506 articles. Oxidative stress plays a critical role in food addiction and is both a cause and mediator of obesity. Reactive oxygen species play a direct role in adipogenesis and oxidative stress modulates all factors involved in obesity including genetics, sleep, gut microbiome, insulin, ghrelin, inflammation, adipokines, leptin, stress, HPA axis, and the hypothalamus. The idea of thinking of combating obesity from the lens of calorie count, low carbohydrate, high or low-fat, vegetarian, vegan, plant-based, or animal-based diet is fundamentally wrong. The best way to look at obesity is through the framework of systemic redox homeostasis. Since redox homeostasis is tilted towards increased reactive oxygen species production, and excessive antioxidant intake can result in oxidative stress, an antioxidant and prooxidant food ratio of 2:3 per meal is the ideal nutritional ratio for good health and ideal weight. A ratio of 3:4 is ideal for obese individuals because of their state of chronic oxidative stress and inflammation. Physical activity, sleep quality, psychological stress, maternal prenatal diet and oxidative stress promoting disease conditions are important modulators of oxidative stress and obesity. [ABSTRACT FROM AUTHOR]

Alcohol use is known to result in disinhibition. However, evidence suggests that alcohol consumption could also result in inhibition. Several hypotheses have been proposed for this confounding alcohol-induced behavior, but none explains it adequately at the level of the brain. In this paper, oxidative stress is put forth as the underlying molecular cause of alcohol induced behavioral impairments. The implications of this understanding and how oxidative stress may modulate behavior in obesity, diabetes, psychiatric and neurodegenerative diseases and during hot weather are discussed. [ABSTRACT FROM AUTHOR]