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Negative Thinking: Today's Prescription for Tomorrow's Dysfunction

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Abstract

Meade’s work on ‘reactivity’ continues to ripple through the psychology world via his professional practice and his pen. His tenth book, Negative Thinking: Today’s Prescription for Tomorrow’s Dysfunction, retraces his ongoing focus on Executive Function and parenting but specifically addresses the contribution of negative thinking to the HPA axis delivery of cortisol via cerebral blood flow. His mix of practical examples from his professional role as a school psychologist blends with his controversial insights and challenging of many of today’s standard practices in psychology, encourages the reader to step out of their comfort zone and question accepted offerings from their allied health and academic professionals.
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The global focus on Executive Function has resulted in large volumes of research and psychological intervention presenting many (often divergent) views of this elusive neural construct. Researchers, Ostrosky and Gurtierrez stated in their 2019 paper, ‘Neurological Assessment of Executive Function’, that the accurate measuring of Executive Function is not drawing unified consensus or definition due to a diversity of conceptual and theoretical approaches. Steve Meade has been addressing the foundations of Executive Function in his private practice since 2011, and in his growing compendium of books on ‘Reactivity’. As he disseminates current explanations of the topic, readers can expect to be challenged on their current views of Executive Function development, as well as the societal and familial contributors necessary for it to effectively control and regulate behaviour.
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Steve Meade’s work in schools for over ten years has furnished him with exposure to the challenges faced by students, teachers, and parents. As a practicing psychologist, his focus on reactivity has equipped with insights that have directed his efforts away from more traditional psychological approaches and interventions toward a broader view of human behaviour, particularly the behaviours of students that directs their life efforts. Part of this evolution has been to shift his intervention from problem presentation toward a more ‘origin’ focus of reactive behaviour. Meade’s revealing account opens up a distinctly different view of reactivity, but also challenges those implicated in that endeavour. Despite that uncomfortable dissemination, a trademark of his work, school staff and the broader academic community need to better support parents and their children in the real world challenges that many are desperately trying to retreat from somatically and emotionally. More than a ‘must read’, this latest book in Meade’s growing catalogue provides a template which addresses the foundational issues continuing to plague school settings, and ultimately society.
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“Reactivity: An Evolutionary Solution to a Biogeographical Dilemma” synthesises ingredients from Meade’s previous trilogy, The Reactive Alien series. Focussing on reactivity as being merely a symptom of a topological dilemma faced by the neural system for millions of years, enables more detailed insights into reactivity and behaviour. Meade’s writing remains unswerving in addressing society’s biggest social, familial, and academic challenges. Underpinned by a number of theorists and models, his expose on behaviour platforms the inner workings of human reactivity. Unlike his previous works, this book offers a more accessible entry point for the general reader to gain insight into the complexity (and often misunderstood functioning) of the brain, while simultaneously reducing that complexity down to its simplest expressions. His theories on Executive Function continue to challenge traditional views on neural network maturation while offering evolutionary explanations for today’s human experiences and direction.
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Better executive functioning may be associated with more adaptive stress responses than worse executive functioning, potentially due to less propensity for rumination. In this study, we tested the hypothesis that better executive functioning would be associated with decreased total cortisol output (AUCg) and cortisol sensitivity with respect to increase/decrease (AUCi) in response to a stressor, and that this association is mediated by stress task rumination. Participants completed measures of inhibition, updating/monitoring, and cognitive flexibility, a social-evaluative stressor, and a self-report measure of rumination about the stressor. Participants provided saliva samples at six time points to measure cortisol output and sensitivity. Cognitive flexibility was negatively associated with stress task rumination (r = -0.30, p < .05); however, this association was no longer significant when adding covariates (i.e., participant age, sex, highest education, and body mass index) to a regression model. Cognitive flexibility was also associated with AUCg (r = -.28, p < .05), while rumination was associated with AUCi in non-adjusted (r = .28, p < .05) and adjusted (b = .81, p < .05) analyses. Furthermore, females demonstrated better cognitive flexibility (r = .26, p < .05) and lower AUCg (r = - .45, p < .05) compared to males. Findings demonstrate the importance of cognitive flexibility and rumination when predicting dynamic measures of stress-induced cortisol over time.
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Major depressive disorder (MDD) is a very common stress-related mental disorder that carries a huge burden for affected patients and the society. It is associated with a high mortality that derives from suicidality and the development of serious medical conditions such as heart diseases, diabetes, and stroke. Although a range of effective antidepressants are available, more than 50% of the patients do not respond to the first treatment they are prescribed and around 30% fail to respond even after several treatment attempts. The heterogeneous condition of MDD, the lack of biomarkers matching patients with the right treatments and the situation that almost all available drugs are only targeting the serotonin, norepinephrine, or dopamine signaling, without regulating other potentially dysregulated systems may explain the insufficient treatment status. The hypothalamic-pituitary-adrenal (HPA) axis is one of these other systems, there is numerous and robust evidence that it is implicated in MDD and other stress-related conditions, but up to date there is no specific drug targeting HPA axis components that is approved and no test that is routinely used in the clinical setting identifying patients for such a specific treatment. Is there still hope after these many years for a breakthrough of agents targeting the HPA axis? This review will cover tests detecting altered HPA axis function and the specific treatment options such as glucocorticoid receptor (GR) antagonists, corticotropin-releasing hormone 1 (CRH1) receptor antagonists, tryptophan 2,3-dioxygenase (TDO) inhibitors and FK506 binding protein 5 (FKBP5) receptor antagonists.
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There are no specific structural neuropathological hallmarks found in the brain of mood disorders. Instead, there are molecular, functional and structural alterations reported in many brain areas. The neurodevelopmental underpinning indicated the presence of various genetic and developmental risk factors. The effect of genetic polymorphisms and developmental sequalae, some of which may start in the womb, result in functional changes in a network mediated by neurotransmitters and neuropeptides, which make the emotion- and stress-related brain systems more vulnerable to stressful events. This network of stress-related neurocircuits consists of, for instance, brainstem nuclei, the amygdala, habenula, prefrontal cortex and hypothalamus. Various nuclei of the hypothalamus form indeed one of the crucial hubs in this network. This structure concerns not only the hypothalamo-pituitary-adrenal (HPA) axis that integrate the neuro-endocrine-immune responses to stress, but also other hypothalamic nuclei and systems that play a key role in the symptoms of depression, such as disordered day-night rhythm, lack of reward feelings, disturbed eating, sex, and disturbed cognitive functions. The present review will focus on the changes in the human hypothalamus in depression, with the HPA axis in the center. We will discuss the inordinate network of neurotransmitters and neuropeptides involved, with the hope to find the most vulnerable neurobiological systems and the possible development of tailor-made treatments for mood disorders in the future.
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Maintenance of adequate tissue perfusion through a dense network of cerebral microvessels is critical for the perseveration of normal brain function. Regulation of the cerebral blood flow has to ensure adequate delivery of nutrients and oxygen with moment-to-moment adjustments to avoid both hypo- and hyper-perfusion of the brain tissue. Even mild impairments of cerebral blood flow regulation can have significant implications on brain function. Evidence suggests that chronic stress and depression elicits multifaceted functional impairments to the cerebral microcirculation, which plays a critical role in brain health and the pathogenesis of stress-related cognitive impairment and cerebrovascular events. Identifying the functional and structural changes to the brain that are induced by stress is crucial for achieving a realistic understanding of how related illnesses, which are highly disabling and with a large economic cost, can be managed or reversed. This overview discusses the stress-induced alterations in neurovascular coupling with specific attention to cerebrovascular regulation (endothelial dependent and independent vasomotor function, microvessel density). The pathophysiological consequences of cerebral microvascular dysfunction with stress and depression are explored.
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A medical approach towards behavioural problems could make professionals without a medical background, like teachers and other educational professionals feel inapt. In this article, we raise six scientifically grounded considerations regarding ADHD, currently the most prevalent childhood psychiatric diagnosis. These “need to knows” show just how misguided and potentially stigmatizing current conceptualizations of unruly behaviour have become. Some examples are given of how teachers are misinformed, and alternative ways of reporting about neuropsychological research are suggested. A reinvigorated conceptual understanding of ADHD could help educational institutions to avoid the expensive outsourcing of behavioural problems that could also—and justifiably better—be framed as part of education’s primary mission of professionalized socialization.
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Evolution is the process in which traits such as physiological stress response systems (SRSs) are shaped by natural selection. A full understanding of any trait requires knowing its evolutionary history, how it has given a selective advantage, and the trade-offs and costs involved. Stress-related mechanisms emerged early in the history of life. Like all traits, they have costs as well as benefits. Because the stress response is so often associated with negative events, its utility has often been neglected. This chapter reviews the phylogeny and functional significance of the SRS, with a special focus on how selection has shaped the mechanisms that process environmental information to regulate the stress response, and how the stress response influences other traits such as risk-taking and sexual behavior.
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This randomized within-subject, double blind study aimed to compare the effects of a single dose of two different antipsychotics (haloperidol and aripiprazole) on cortisol, interleukin (IL)-6 and hippocampal regional Cerebral Blood Flow (rCBF) in the same 17 healthy male individuals. Subjects received a single dose of haloperidol (3mg), aripiprazole (10mg) and placebo, in a randomized order on three study appointments. We measured salivary cortisol levels at multiple time points, IL-6 levels from plasma samples, and resting cerebral blood flow (rCBF), using a pulsed continuous arterial spin labeling (pCASL) sequence (1.5T). We found significantly lower cortisol levels in the haloperidol condition (F(2,32)=5.78, p=0.007), than in either placebo (p=0.013; CI=0.45, 0.406) or aripiprazole (p=0.037; CI=-0.520, -0.014). Interleukin-6 levels were also lower following haloperidol (F(2,22)=4.19, p=0.048) in comparison with placebo (p=0.02; CI=0.14, 1.8), but not with aripiprazole. Finally, we found a greater rCBF in the right (peak voxel: T=6.47, p<0.0001) and left (peak voxel T=5.17, p<0.01) hippocampus following haloperidol compared with placebo, and at trend level also in the left hippocampus following aripiprazole compared with placebo (T=4.07, p=0.057). These differences in hippocampal rCBF after both antipsychotics were no longer evident (haloperidol) or present at trend level (aripiprazole), after controlling for cortisol and IL-6 levels. Our findings suggest that haloperidol can directly regulate the hypothalamic-pituitary-adrenal (HPA) axis and immune system through a pharmacological action via D2 receptor antagonism. Finally, our data suggest that the increased hippocampal rCBF is a manifestation of the reduction in IL-6 and cortisol which follows the administration of haloperidol.