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1
Dhungel, Sanat K. Ecology of hog deer in Royal Chitwan National Park, Nepal. [Bethesda, MD?]: Wildlife Society, 1991.
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Dhungel, Sanat K. Ecology of the hog deer in Royal Chitwan National Park, Nepal. Blacksburg, VA: Wildlife Society, 1991.
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Dhungel, Sanat K. Ecology of the hog deer in Royal Chitwan National Park, Nepal. [s.l.]: Wildlife Society, 1991.
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Dhungel, Sanat K. Ecology of the hog deer in Royal Chitwan National Park, Nepal. [Bethesda, MD?]: Wildlife Society, 1991.
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5
Patisaul, Heather B., and Scott M. Belcher. The Neuroendocrine System and General Mechanisms of Endocrine Disruption. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199935734.003.0004.
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The neuroendocrine system is the interface between the endocrine and nervous systems. This chapter presents an overview of the neuroendocrine system and endogenous hormones, with a primary focus on the hypothalamic-pituitary-gonadal (HPG) axis, the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-thyroid axis (HPT). The importance of impacts of exogenous compounds, both natural and man-made, on the neuroendocrine system is discussed, with a focus on endocrine-disruptive actions of plant-derived phytoestrogens and the role of the aryl hydrocarbon receptor as an environmental sensor. The impacts of EDCs on feed-forward and negative feedback regulation of neuroendocrine functions, including those mediated by estrogen, androgen, and thyroid pathways, as well as other less studied pathways of hormonal signaling that involve disruption of neurosteroids, peptide hormones, and adrenal hormone signaling are also presented.
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Patisaul, Heather B., and Scott M. Belcher. Receptor and Enzyme Mechanisms as Targets for Endocrine Disruptors. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199935734.003.0005.
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In this chapter, the current understanding of the mechanisms of endocrine disruption on the brain and nervous system are presented. Because the overwhelming majority of mechanistic studies on EDCs have focused on the actions mediated by nuclear hormone receptors, this mechanisms is described in detail. The chapter also discusses the classic transcriptional mechanisms of steroid action and the impact of EDCs on rapid signaling (non-genomic) mechanisms. It presents an overview of the enzymes and pathways involved in the biosynthesis of steroid hormones, which are critical to proper functioning of the HPA and HPG axis, and the neuroactive steroids synthesized and active in the mammalian brain. The potential for EDCs to alter metabolic enzymes, with a focus on possible targets in the metabolic blood-brain barrier, is presented as a potential, though largely unexplored, mode of EDC action in the brain.
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Herman, James P. Limbic Pathways to Stress Control. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0008.
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Appropriate control of the HPA (hypothalamo-pituitary-adrenocortical axis) is required for adaptation to physiological and environmental challenges. Inadequate control is linked to numerous stress-related pathologies, including PTSD, highlighting its importance in linking physiological stress responses with behavioral coping strategies. This chapter highlights neurocircuit mechanisms underlying HPA axis adaptation and pathology. Control of the HPA stress response is mediated by the coordinated activity of numerous limbic brain regions, including the prefrontal cortex, hippocampus, and amygdala. In general, hippocampal output inhibits anticipatory HPA axis responses, whereas amygdala subnuclei participate in stress activation. The prefrontal cortex plays an important role in inhibition of context-dependent stress responses. These regions converge on subcortical structures that relay information to paraventricular nucleus corticotropin-releasing hormone neurons, controlling the magnitude and duration of HPA axis stress responses. The output of these neural networks determines the net effect on glucocorticoid secretion, both within the normal adaptive range and in pathological circumstances.
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Young, Allan H., and Mario F. Juruena. Hypothalamic–pituitary–adrenal axis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0006.
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Increased adrenocortical secretion of hormones, primarily cortisol in depression, is one of the most consistent findings in neuropsychiatry. The maintenance of the internal homeostatic state of an individual is facilitated by the ability to circulate glucocorticoids to exert negative feedback on the secretion of hypothalamic–pituitary–adrenal (HPA) hormones through binding to mineralocorticoid and glucocorticoid receptors, thus limiting the vulnerability to diseases related to psychological stress in genetically predisposed individuals. The HPA axis response to stress can be thought of as a crucial part of the organism’s response to stress: acute responses are generally adaptive, but excessive or prolonged responses can lead to deleterious effects. A spectrum of conditions may be associated with increased and prolonged activation of the HPA axis, including depression, poorly controlled diabetes mellitus, and metabolic syndrome. HPA axis dysregulation and hypercortisolaemia may further contribute to a hyperglycaemic or poorly controlled diabetic state.
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Schulkin, Jay. Conservation of CRF in Brains and its Regulation by Adrenal Steroids. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780198793694.003.0003.
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The regulation of the HPA axis has been categorized as the classical mechanism of slow-acting genomic regulation of gene products, but this has given way to both slow and fast regulation of the HPA axis. We do not know how cortisol restrains the production of CRF in the paraventricular nucleus, thereby directly decreasing ACTH and, subsequently, cortisol; we know the classical negative-feedback regulatory system, which provides a mechanism, but how it works, well, that is another thing. Glucocorticoids restrain the HPA axis, but not other regions of the brain, such as the central nucleus of the amygdala and bed nucleus of the amygdala. But we now know that both chemically and electrically, these regions are not the same (equal).
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Butler, Gary, and Jeremy Kirk. Adrenal gland disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199232222.003.0068.
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Physiology 236Adrenal insufficiency 238Adrenal steroid excess 246Further reading 247The adrenal cortex, which produces steroid hormones, is under the control of both the hypothalamo–pituitary–adrenal (HPA) endocrine axis, which regulates cortisol secretion, and the renin–angiotensin system, which regulates aldosterone secretion (Figs 8.1 and ...
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Lightman, Stafford. Can neurobiology explain the relationship between stress and disease? Oxford University Press, 2015. http://dx.doi.org/10.1093/med:psych/9780198530343.003.0006.
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This chapter explores if neurobiology can explain the relationship between stress and disease. It considers if events that occurred early in life, perhaps during a period of prolonged stress, may affect biological processes, sometimes permanently, through changes in the midbrain neurotransmitter concentrations, the hypothalamic-pituitary-adrenal (HPA) axis, and the central nervous system (CNS). Animal models of stress are used to demonstrate these changes.
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Nielsen, David A., Dmitri Proudnikov, and Mary Jeanne Kreek. The Genetics of Impulsivity. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0080.
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Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.
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Yehuda, Rachel. Neuroendocrinology of PTSD. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0020.
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Initial studies on the neuroendocrine basis of post-traumatic stress disorder (PTSD) showed a biological dysregulation of stress response systems that appeared to be incompatible with the stress response theories that had prevailed when PTSD was first established as a diagnosis. Cortisol levels were found to be lower and catecholamine higher in patients with PTSD than in those with major depression and other psychiatric disorders. There was no explanation for why levels of two stress hormones that are generally correlated—cortisol and norepinephrine—would be different, and it was also not clear why cortisol levels would be on the low end of the normal spectrum, when the classic stress response paradigms suggested stress results in elevated cortisol. The study of neuroendocrinology and hypothalamic–pituitary–adrenal (HPA) axis alterations in PTSD provides an object lesson in how paradoxical observations might be pursued toward a better understanding of the pathophysiology of a disorder. This chapter reviews HPA findings in PTSD in cross-sectional and prospective longitudinal studies.
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Schulkin, Jay. Introduction. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780198793694.003.0001.
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CRF is well known and studied as a hypothalamic-releasing factor. It, along with ACTH and cortisol, are mobilized under diverse conditions, including adversity, and are often thought of as part of the stress axis. CRF, however, is much more than this. One aim of this book is pushing the conception of CRF beyond the HPA axis, and what most people know about CRF. Since its original discovery, research has shown that this molecule is much broader than a hypothalamic-releasing factor. It took a while to discern CRF and its properties outside of its role as an ACTH-releasing factor. Now, the scientific community knows that CRF is a dynamic and diversely widespread peptide hormone with many roles and functions, beyond its role as a releasing factor in the brain. CRF in invertebrates is linked to basic regulatory functions such as osmotic regulation, food intake, learning, and circadian rhythmicity.
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Hodgkiss, Andrew. Introduction to biological and molecular psychiatry. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0002.
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An introduction to biological and molecular psychiatry is offered, intended for oncology and palliative medicine clinicians. A recent historical perspective is used, beginning with a summary of monoaminergic and cholinergic neurotransmission as understood in the 1980s. One endocrine theory of depression, based on HPA axis dysfunction, is described. Recognition of the limits of these models has led to a deeper molecular psychiatry ‘beyond the synapse’ and to an appreciation of the importance of amino acid neurotransmission. Selective expression of proteins, and their covalent and allosteric modification, is now seen as central to neuroplasticity. The NMDA receptor and excitotoxicity are introduced. The chapter closes with an overview of the amygdala and of hippocampal neurogenesis.
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Hodgkiss, Andrew. Psychiatric consequences of particular cancers. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0004.
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Certain tumour types can cause psychopathology through direct biological mechanisms such as metastatic spread to the brain, release of onconeuronal antibodies, ectopic hormone secretion, or release of pro-inflammatory cytokines. Lung cancers, adenocarcinoma of the pancreas, brain tumours, and ovarian tumours are considered in detail. Confusional states due to brain metastases, syndrome of inappropriate ADH secretion, hypercalcaemia of malignancy, and anti-Hu encephalitis are found in lung cancers. Severe depression, due to interleukin-6 release and its actions on the HPA axis and tryptophan metabolism, is common in adenocarcinoma of the pancreas. Anti-NMDA-receptor limbic encephalitis, clinically indistinguishable from acute schizophrenia, can complicate teratomas. Gliomas, pituitary tumours, and thyroid, adrenal, and testicular tumours can also disrupt mental health through various biological mechanisms described here.
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Schulkin, Jay. Evolution and Diversification of Function of an Information Molecule. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780198793694.003.0002.
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Chapter 2 begins with a depiction of the evolutionary origins of CRF in living things. CRF appears to date back hundreds of millions of years. It is found in diverse invertebrates, including flies and bees. Invertebrates’ brains look nothing like those of vertebrates except for the diverse information molecules that underlie both brain systems. There is no clear anatomical organ like the HPA axis in invertebrates, yet information molecules, including CRF, are just as important to invertebrate functioning as they are to vertebrates. CRF in invertebrates is linked to basic regulatory functions such as osmotic regulation, food intake, learning, and circadian rhythmicity. There are many examples of regulatory molecules that, over time, become adapted to serve multiple functions. Once a gene for a potent regulatory molecule exists, the potential for the differentiation of function, regulation, and mode of action exist as well.
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Geracioti, Thomas D., Jeffrey R. Strawn, and Matthew D. Wortman. Mechanisms of Action in the Pharmacology of PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0020.
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This chapter reviews medications currently available for PTSD in the context of their mechanisms of action, pathophysiological relevance, and clinical efficacy data. It systematically reviews aminergic mechanisms in PTSD pharmacology, including commonly used serotonin and norepinephrine agents, selective reuptake inhibitors and receptors drugs, as well as dopaminergic agents and psychostimulants. It also discusses the use of anticonvusants and antianxiety agents that modulate GABAergic and glutamatergic signaling, such as carbamazepine, VPA, benzodiazepines, gabapentine, and others. It also reviews other clinically available agents as well as HPA axis-modulating compounds, both for treatment and secondary prevention of PTSD. It concludes with the suggestion that clinical selection of one or more of these medications for PTSD should be based on individual patient considerations, including target symptoms, PTSD subtype, post-traumatic interval, comorbidities, genotypes for CYP450 enzymes, and genetic polymorphisms of clinical relevance.
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Dutton, Garreth R., and Belinda L. Needham. Obesity. Edited by C. Steven Richards and Michael W. O'Hara. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199797004.013.021.
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Cross-sectional and longitudinal studies indicate a positive association between obesity and depression. While some evidence suggests that depression is a risk factor for obesity, other findings indicate that obesity is a risk factor for depression. Therefore the directionality of this relationship remains unclear. Alternatively, there may be common mediating biological or environmental contributors accounting for this association. Potential biological mediators include dysregulation of the HPA axis, leptin resistance, and inflammatory immune responses. Environmental and psychological mediators may include a history of abuse and binge eating. It is also possible that the association between obesity and depression is most pronounced among particular subsets of individuals (e.g., women, those with more severe obesity). A better understanding of this depression-obesity association is needed to guide treatment recommendations for obese clients with comorbid depression. Future research is also needed to determine who is most vulnerable to experiencing comorbid depression and obesity.
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Yang, James. Endocrine Disorders: Integrative Treatments of Hypothyroidism, Diabetes, and Adrenal Dysfunction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190466268.003.0014.
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Thyroid function, glucose metabolism, and an adaptive hypothalamic–pituitary–adrenal (HPA) axis are critical determinants of health and wellness. This chapter highlights the integrative physiology and interactions between these three systems and an integrative medicine approach to these conditions. Integrative medicine expands the evaluation of endocrine dysfunction through a person-centered approach. Patients’ overall symptoms and physiological function should be taken into account in evaluating thyroid function and planning treatment. Our approach to diabetes focuses on the importance of lifestyle changes and nutrition. Our perspective of the effects of chronic stress has been informed by current perspectives on neurobiology and neuroplasticity; chronic stress leaves its mark on the brain through changes in structure as well as its function in adapting to further stress. We present an integrative approach to manage and improve these three endocrine systems to address disease and improve patients’ energy and health.
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Naninck, E. F. G., P. J. Lucassen, and Aniko Korosi. Consequences of Early-Life Experiences on Cognition and Emotion. Edited by Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.003.
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Perinatal experiences during a critical developmental period program brain structure and function “for life,” thereby determining vulnerability to psychopathology and cognition in adulthood. Although these functional consequences are associated with alterations in HPA-axis activity and hippocampal structure and function, the underlying mechanisms remain unclear. The parent-offspring relationship (i.e., sensory and nutritional inputs by the mother) is key in mediating these lasting effects. This chapter discusses how early-life events, for example, the amount of maternal care, stress, and nutrition, can affect emotional and cognitive functions later in life. Interestingly, effects of perinatal malnutrition resemble the perinatal stress-induced long-term deficits. Because stress and nutrition are closely interrelated, it proposes that altered stress hormones and changes in specific key nutrients during critical developmental periods act synergistically to program brain structure and function, possibly via epigenetic mechanisms. Understanding how the adult brain is shaped by early experiences is essential to develop behavioural and nutritional preventive therapy.
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Cohen, Hagit, and Joseph Zohar. The Role of Glucocorticoids in the (Mal)adaptive Response to Traumatic Experience. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0038.
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Glucocorticoids (GCs) play a major role in orchestrating the complex physiological and behavioral reactions essential for the maintenance of homeostasis. These compounds enable the organism to prepare for, respond to, and cope with the acute demands of physical and emotional stressors and enable a faster recovery with passage of the threat. A timely and an appropriate GC release commensurate with stressor severity enables the body to properly contain stress responses so as to promote recovery by rapidly restoring homeostasis. Inadequate GC release following stress not only delays recovery by disrupting biological homeostasis but can also interfere with the processing or interpretation of stressful information that results in long-term disruptions in memory integration. A salient example of such an impaired post-traumatic process is post-traumatic stress disorder (PTSD). The findings from recent animal models and translational and clinical neuroendocrine studies summarized in this chapter provide insights shedding light on the apparently contradictory studies of the HPA-axis response to stress. Also included is a review of the basic facts about PTSD and biological data.
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Perkins, Elizabeth C., Shaun P. Brothers, and Charles B. Nemeroff. Animal Models for Post-Traumatic Stress Disorder. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0024.
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Animal models of post-traumatic stress disorder (PTSD) provide a wellspring of biological information about this complex condition by providing the opportunity to manipulate trauma exposure and measure biological outcomes in a systematic manner that is not possible in clinical studies. Symptoms of PTSD may be induced in animals by physical (immobilization, foot shock, underwater stress) and psychological stressors (exposure to predator, social defeat, early life trauma) or a combination of both. In addition, genetic, epigenetic and transgenic models have been created by breeding animals with a behavioral propensity for maladaptive stress response or by directly manipulating genes that have been implicated in PTSD. The effect of stressors in animals is measured by a variety of means, including observation of behavior, measurement of structural alterations in the brain and of physiological markers such as HPA axis activity and altered gene expression of central nervous system neurotransmitter system components including receptors. By comparing changes observed in stress exposed animals to humans with PTSD and by comparing animal response to treatments that are effective in humans, we can determine the validity of PTSD animal models. The identification of a reliable physiological marker of maladaptive stress response in animals as well as standard use of behavioral cutoff criteria are critical to the development of a valid animal model of PTSD.
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Schulkin, Jay. The CRF Signal. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780198793694.001.0001.
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This book discusses just how diverse a peptide corticotrophin-releasing factor (CRF) is, as demonstrated by its presence in various tissues in the body, including the skin, the placenta, and various regions of the brain. As Dobzhansky (1962) noted, in light of Darwin (1874), and beyond, CRF must be placed in the larger world of regulatory biology. Evolutionary trends do not proceed in a continuous one-dimensional direction; there are starts, turns, and abrupt ends. The study of CRF is mostly about diverse functions in physiological and behavioral regulation of the internal milieu and adapting to an ecological and or social context. The book begins with a depiction of the evolutionary origins of CRF in living things, dating back hundreds of millions of years. The book pushes the conception of CRF beyond the HPA axis and common knowledge. We study the role of CRF in metamorphosis and parturition. Further, CRF is a contributor to fear and anxiety, and the book explains how excessive fear is tied to anxiety disorders and vulnerability to the breakdown of mental and physical health. Also discussed is CRF in approach/avoidance behaviors across pre- and postnatal events. CRF is intimately involved in organ development, but it is also linked to devolution of function and conditions of danger. Cravings, addictions, and how CRF is tied both to the ingestion of diverse drugs and to withdrawal are explored. CRF is considered as an epistemic object, addressing what constitutes an information molecule, in general, and CRF, in particular.