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Published: 4 June 2021
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1

Farooqui, Akhlaq A. Metabolic syndrome: An important risk factor for stroke, Alzheimer disease, and depression. New York, NY: Springer, 2013.

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2

Jay, Lombard, and Monte Tom, eds. Freedom from disease: The breakthrough approach to preventing cancer, heart disease, alzheimer's, and depression by controlling insulin. New York: St. Martin's Griffin, 2009.

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3

Jay, Lombard, and Monte Tom, eds. Freedom from disease: The breakthrough approach to preventing cancer, heart disease, Alzheimer's, and depression by controlling insulin. New York: St. Martin's, 2008.

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4

Osher, Susan. One-carbon metabolism in adults with major depression. Ottawa: National Library of Canada, 1999.

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5

Jones, Shirley Anne. Tetrahydrobiopterin metabolism in depression and senile dementia of Alzheimer type. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1988.

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6

1935-, Takada Akikazu, and Curzon G. 1928-, eds. Serotonin in the central nervous system and periphery: Proceedings of the Symposium on Serotonin in the Central Nervous System and Periphery, April 1-2, 1995, Nagoya, Japan. Amsterdam: Elsevier, 1995.

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7

Gissey, Lidia Castagneto, James R. Casella Mariolo, Geltrude Mingrone, and Francesco Rubino. Metabolic surgery and depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0012.

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The incidence of obesity is rising worldwide and so are its comorbidities: type-2 diabetes mellitus (T2DM), dyslipidaemia, hypertension, cardiovascular disease, sleep apnoea, and depression. Bariatric/metabolic surgery has established itself over the past several years as an effective treatment not only for morbid obesity but also for its associated morbidities. The effects of bariatric/metabolic surgery on depression are controversial, with some studies showing improvement and others demonstrating a worsening. However, a major drawback of these studies is that they do not compare patients with the same baseline psychiatric disorders. In fact, mild to severe depressive symptoms are observed in most candidates for bariatric/metabolic surgery. Preoperative evaluation of the patient’s mental state would enable identification of the appropriate interventions, enhancing long-term compliance and weight maintenance. It could also leverage psychological support in case the patient’s disorder relapses postoperatively. Preoperative evaluation should detect potential psychological contraindications to surgery, such as severe eating disorders.
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8

Bertocci, Michele A., and Mary L. Phillips. Neuroimaging of Depression. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0025.

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This chapter illustrates the historical progression, methodological approaches, and current neurobiological understanding of depression, the first leading cause of mental and behavioral disorder disability in the United States. We describe and position, in relation to depressive symptoms, the complex abnormalities that depressed adults and youth show concerning neural function during tasks and at rest, structural abnormalities, as well as key neurotransmitter, neuroreceptor, and metabolic abnormalities that have been examined in the literature. We also describe newer findings and methods such as differentiating between unipolar and bipolar depression and applying machine learning to individual prediction. Finally, we provide suggestions for future study.
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9

Farooqui, Akhlaq A. Metabolic Syndrome: An Important Risk Factor for Stroke, Alzheimer Disease, and Depression. Springer, 2013.

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10

Farooqui, Akhlaq A. A. Metabolic Syndrome: An Important Risk Factor for Stroke, Alzheimer Disease, and Depression. Springer, 2015.

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11

Goldstein, Jill M., L. Holsen, S. Cherkerzian, M. Misra, and R. J. Handra. Neuroendocrine Mechanisms of Depression. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0029.

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Studies have demonstrated that major depressive disorder (MDD) is intimately tied to neuroendocrine dysregulation. This arises, in part, from the fact that brain regions that regulate mood also regulate primary neuroendocrine axes and metabolic functions. We and others demonstrated that the origin of MDD-neuroendocrine deficits begins in fetal development, is sex-dependent, emerges just post-puberty, and can be catalyzed by pregnancy (postpartum) and menopause. Here, we critically review clinical and preclinical studies to argue that higher MDD risk in women may arise, in part, from hormone-dependent pathogenic processes initiated during fetal development that drive sex-dependent developmental alterations of HPA circuitry emerging post-puberty with lifelong consequences.
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12

Ismail, Khalida, Andreas Barthel, Stefan R. Bornstein, and Julio Licinio, eds. Depression and Type 2 Diabetes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.001.0001.

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Type 2 diabetes is predicted to affect between 10% and 25% of the world population in the next 20 years. Depression is a common comorbid condition in those affected with type 2 diabetes, and the combination of these conditions is associated with a poorer prognosis, including earlier mortality. Genetic and epigenetic predisposition and overlap of risk factors related to our modern lifestyle seem to drive the shared biology of diabetes and depression. This book aims to provide an understanding of the sequelae of events leading to the frequent comorbidity of diabetes and depression. This book project has been supported by the transCampus of Kings College London and Technical University of Dresden. Chapter by chapter, internationally recognized clinicians and scientists have summarized the state of the art and outstanding controversies of the epidemiology, mechanisms, and treatment of the depression–type 2 diabetes comorbidity. This book is relevant for all health professionals including the general practitioner and specialist clinicians in internal medicine, endocrinology, diabetes and metabolic diseases, neurology, psychiatry, and psychology as well as students interested in this topic.
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13

Lebovitz, Harold E., and Shlomo Ben-Haim. Novel technologies: What does gastric electrical stimulation offer to the patient with type 2 diabetes and depression? Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0014.

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Owing to the epidemiologic dimensions of type 2 diabetes, obesity, and depression, the development of novel and effective treatment options for these conditions is of great importance. One of the major challenges in this field is that many antidiabetic and antidepressive drugs may have disadvantageous metabolic effects by increasing weight and worsening insulin resistance. Novel technologies more effectively considering the pathophysiological changes related to this entity are needed. The DIAMOND electrical stimulation device improves glycaemic control, causes weight loss and decreases systolic blood pressure in overweight and obese patients with type 2 diabetes. The DIAMOND device detects food ingestion and automatically activates its postprandial metabolic effects. It does so with minimal side effects, no hypoglycaemia, modest weight loss, minimal requirement for self-blood glucose monitoring, and improvement in eating behaviour. The properties of DIAMOND treatment suggest that it may have merit for treating patients with comorbid diabetes and depression.
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14

Waldemar, Gunhild. Diagnosing Alzheimer’s disease in clinical practice. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199569854.003.0005.

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• In the current clinical criteria, the diagnosis of Alzheimer’s disease (AD) is a clinical diagnosis based on characteristic symptoms and signs, and the exclusion of other causes.• AD must be differentiated from cognitive impairment due to depression, metabolic conditions, substance abuse, and other neurodegenerative or vascular brain diseases...
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15

Potter, Gregory D. M., and Eleanor M. Scott. Targeting the circadian system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0016.

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Circadian (approximately 24-hour) rhythms are generated by a hierarchical system responsible for coordinating behaviour and physiology throughout the 24-hour day. Increasing evidence supports roles for disruption of the circadian system in the development of type 2 diabetes (T2DM) and depression. We outline the key aspects of circadian system regulation, discuss the findings indicating that biological disruption of the circadian system produces various behavioural and metabolic abnormalities, and review human studies which show that environmental disruption of the circadian system contributes to T2DM and depression. Finally, we will summarize the therapeutic potential of restoring circadian system organization to manage these diseases.
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16

Donard, Dwyer, ed. Glucose metabolism in the brain. Amsterdam: Academic Press, 2002.

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17

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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18

Landsbergis, Paul A., Marnie Dobson, Anthony D. LaMontagne, BongKyoo Choi, Peter Schnall, and Dean B. Baker. Occupational Stress. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0017.

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This chapter describes sources of stress in the work environment, their adverse effects on the health of workers, and how they are influenced by economic globalization, political systems, laws, government policies, and the changing labor market. Models of occupational stress, in particular job strain and effort-reward imbalance, are presented. Additional occupational stressors are described, including long work hours, shift work, precarious work and job insecurity, work-family conflict and organizational injustice, including discrimination, harassment, and bullying. The health and safety consequences of exposure to occupational stressors are detailed, including musculoskeletal disorders, acute traumatic injuries, mental disorders (such as depression), health behaviors, and cardiovascular disease and its risk factors (including hypertension, obesity, diabetes, and the metabolic syndrome). Finally, there is a discussion of efforts on work reorganization and job redesign, workplace policies and programs, and laws and regulations designed to reduce occupational stress and improve the health and safety of workers.
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19

McEwen, Bruce S., and Natalie L. Rasgon. The Brain and Body on Stress. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0002.

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Neuroscientists have treated the brain in isolation from the rest of the body, while endocrinology and general medicine have viewed the body largely without regard to the influence of systemic physiology and pathophysiology on higher brain centers outside of the hypothalamus and pituitary gland. But now there is greater recognition of brain–body interactions affecting the limbic and cognitive systems of brain and altering systemic physiology; these are conceptualized as allostasis and allostatic load and overload. These concepts look at both the interactions of brain and body to stressors and health-promoting and health-damaging behaviors, and they help integrate behavior and mood with systemic functions. These interactions involve genetic predispositions and epigenetic alterations mediated by circulating steroid and metabolic hormones. Comorbidity and multi-morbidity of disorders will be illustrated by the relationship of systemic and brain insulin resistance to the psychopathology of depression and to the increased risk for dementia.
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20

Sousa Alves, Gilberto, Felipe Kenji Sudo, and Johannes Pantel. The treatment of bipolar disorder in the elderly. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0022.

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Bipolar disorder (BD) is an extremely disabling condition characterized by mood switches, and cognitive and functional impairment. The current chapter discusses the updated review on pharmacological and non-pharmacological interventions targeting BD in the elderly. The risk of concurrent medical diseases (eg, metabolic syndrome) and relatively lower tolerability than young BD make the patient safety a major concern in most cases. Evidence-based guidelines, although useful for promoting rational and effective therapy, are generally lacking in elderly BD. Current recommendations for acute mania include atypical antipsychotics, careful use of lithium, and election of valproate as the gold-standard therapy. In acute BD depression, first-line agents in monotherapy may include lithium, lamotrigine, quetiapine, and quetiapine extended release (XR). Electroconvulsive therapy may be an option for severe/refractory cases. Family members or caregivers should be encouraged to support the patient, since potential ethical issues involving patrimony or profession may arise during the treatment.
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21

Kliger, Alan S., and Rita Suri. Frequent haemodialysis. Edited by Jonathan Himmelfarb. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0262_update_001.

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Haemodialysis is a renal replacement treatment, an ‘artificial kidney’ that performs some of the functions of the normal kidney. It is an inelegant device, providing only a fraction of native kidney’s ability to filter toxins from the blood, but with none of the responsiveness to volume, fine feedback control to regulate solute concentrations, or endocrine functions of the healthy organ. Conventional haemodialysis performed three times a week for 4 hours per treatment filters the blood for only 12 of 168 hours each week, and removes less than 10 per cent of small solutes like urea than does the normal kidney. It is therefore not surprising that haemodialysis patients suffer high morbidity and mortality. A dialysis patient’s expected remaining lifetime is substantially shorter than a comparable person with normal kidney function. For example, a woman aged 40–44 years old in the general population can expect on average 40 more years of life, but if she is on dialysis her life expectancy is only 8.1 years. She is also more likely to have co-morbid disease, including hypertension, cardiovascular disease, metabolic bone disease, anaemia, sepsis, depression, malnutrition and inflammation, and physical and cognitive impairment.
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22

Cozza, Kelly L., Rita Rein, Gary H. Wynn, and Eric G. Meyer. Psychopharmacology of Depression as a Systemic Illness for Primary and Specialty Care Clinicians. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0010.

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There are nearly 4 million patients with depression followed by primary care in the United States, with nearly 80% of prescriptions for antidepressants written by non-psychiatrists (Mark et al. 2009). Understanding and utilizing psychopharmacology is a critical skill for primary care physicians, who are often initial or sole prescribers. Persons with medical illnesses and depression are often prescribed a multitude of medications, necessitating attention to pharmacodynamic, pharmacokinetics, and an understanding of intended effects, side effects, toxicities, and drug interactions. This chapter begins with a brief review of drug mechanisms of action, metabolism, and interaction principles; addressing the interplay between depression, the medications used to treat depression, co-prescribed medications, and medical illness. The chapter includes a discussion of drugs used to treat depression in text and table format, highlighted with case examples. Details about mechanism of action, common side effects and adverse reactions, drug interactions, and other clinical implications are provided.
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23

Nixon, Heather C. Voltage Disturbances During Pregnancy. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0052.

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This chapter covers the incidence, etiology, and treatment of the most common electrocardiogram and rhythm disturbances encountered during pregnancy. Baseline electrocardiogram changes associated with pregnancy include left ventricular hypertrophy and ST segment depressions secondary to anatomic and metabolic changes of pregnancy. The most common arrhythmias include atrial and ventricular ectopy, which are usually benign in nature. Supraventricular and ventricular tachycardia are also discussed in detail, along with the impact of antiarrhythmic and electrical conversion therapy on fetal and maternal well-being. An understanding of the pathophysiology, assessment, and treatment of these rhythm disturbances is requisite knowledge for all anesthesiologists to provide optimal and timely care to parturients.
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24

Nuno, Azóia, and Dobreiro Pedra, eds. Treadmill exercise and its effects on cardiovascular fitness, depression, and muscle aerobic function. Hauppauge, N.Y: Nova Science Publisher, 2009.

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25

Cavacuiti, Christopher. The Pharmacology of Opioids (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190265366.003.0008.

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This chapter focuses on the attributes of and component medications within the class of opioids, emphasizing kinetics, dynamics, and therapeutic and adverse effects. To help patients make informed decisions about opioid use, the clinicians prescribing these medications must be able to explain when opioids are likely to help and when they are likely to do harm. Subclasses of opioids include phenanthrenes, benzomorphans, phenylpiperidines, and diphenylheptanes; examples are given of each, with respective utilities and limitations. A discussion then follows of pharmacodynamics, pharmacokinetics, opioid receptor affinity, metabolism, and drug interactions. Tables and figures amplifying the text include: opioid class by synthetic method (Table 8.1); common physiological effects by opioid receptor subtypes (Table 8.2); opioid activity (Table 8.3); and a listing of figures and tables located in Appendix B (opioid receptor affinity, respiratory depression with opioids, adverse effects, metabolism, pharmacogenetics, extended release/long-acting opioids, abuse deterrent formulations). A text box provides supplemental resources.
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26

B, Matchar David, United States. Agency for Healthcare Research and Quality., and Duke University Evidence-based Practice Center., eds. Testing for cytochrome P450 polymorphisms in adults with non-psychotic depression treated with selective serotonin reuptake inhibitors (SSRIs). Rockville, MD: Agency for Healthcare Research and Quality, 2007.

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27

Testing for cytochrome P450 polymorphisms in adults with non-psychotic depression treated with selective serotonin reuptake inhibitors (SSRIs). Rockville, MD: AHRQ, 2007.

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28

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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29

The LDN book: How a little-known generic drug, low dose naltrexone, could revolutionize treatment for autoimmune diseases, cancer, autism, depression, and more. 2016.

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30

Sedel, Frédéric, and Yann Nadjar. Neurological and Psychiatric Symptoms. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0067.

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Late-onset forms of inborn errors of metabolism (IEM) first presenting in adulthood often display psychiatric or neurological manifestations, including atypical psychosis or depression, unexplained coma, peripheral neuropathy, cerebellar ataxia, spastic paraparesis, dementia, movement disorders, or epilepsy. With the exception of several review articles, most if not all existing books and diagnostic algorithms refer to pediatric forms of these diseases. Late-onset forms of IEM always display attenuated phenotypes, which in some instances are associated with one or more clinical manifestations that differ from the classic clinical picture described in children. Although the limited information available about adult forms of IEM makes the specialty new and quite exploratory, the diagnostic approach in adults is facilitated by the fact that the nervous system is already mature. Therefore, clinical presentations are more homogeneous than in children, in whom clinical signs usually differ depending on their stage of maturation.
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31

Alavi, Abass, and Andrew B. Newberg. Functional Neuroimaging: A Transformative Tool for Integrative Psychiatry. Edited by Anthony J. Bazzan and Daniel A. Monti. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190690557.003.0014.

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Functional neuroimaging with positron emission tomography (PET), single photon emission computed tomography (SPECT), and functional magnetic resonance imaging (fMRI) can be highly useful in the evaluation and management of patients with psychiatric disorders. PET and SPECT imaging typically evaluate cerebral metabolism and blood flow, respectively, and can determine patterns associated with different disorders such as depression or schizophrenia. PET and SPECT imaging can also evaluate neurotransmitter changes such as dopamine or serotonin associated with different psychiatric disorders. fMRI is an excellent tool for studying the effects of psychiatric disorders on specific brain processes related to cognition and mood. fMRI activations studies allow researchers to present various stimuli to a subject in order to determine how the brain reacts and whether psychiatric disorders are associated with different brain reactivity patterns. Functional neuroimaging with PET, SPECT, and fMRI can be highly useful in the investigation of the mechanism of action of integrative therapies for psychiatric disorders.
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32

Clare, Stanford S., ed. Selective serotonin reuptake inhibitors (SSRIs): Past, present, and future. Austin: R.G. Landes, 1999.

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33

Brown, Malcomb R. trends in bipolar disorder research. Nova Science Publishers, 2004.

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34

Brüne, Martin, and Wulf Schiefenhövel, eds. Oxford Handbook of Evolutionary Medicine. Oxford University Press, 2019. http://dx.doi.org/10.1093/oxfordhb/9780198789666.001.0001.

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Medicine is grounded in the natural sciences, among which biology stands out with regard to the understanding of human physiology and conditions that cause dysfunction. Ironically, evolutionary biology is a relatively disregarded field. One reason for this omission is that evolution is deemed a slow process. Indeed, macroanatomical features of our species have changed very little in the last 300,000 years. A more detailed look, however, reveals that novel ecological contingencies, partly in relation to cultural evolution, have brought about subtle changes pertaining to metabolism and immunology, including adaptations to dietary innovations, as well as adaptations to exposure to novel pathogens. Rapid pathogen evolution and evolution of cancer cells cause major problems for the immune system to find adequate responses. Moreover, many adaptations to past ecologies have turned into risk factors for somatic disease and psychological disorder in our modern world (i.e. mismatch), among which epidemics of autoimmune diseases, cardiovascular diseases, diabetes, and obesity, as well as several forms of cancer stand out. In addition, depression, anxiety, and other psychiatric conditions add to the list. The Oxford Handbook of Evolutionary Medicine is a compilation of up-to-date insights into the evolutionary history of ourselves as a species, and how and why our evolved design may convey vulnerability to disease. Written in a classic textbook style, emphasising the physiology and pathophysiology of all major organ systems, the book addresses students as well as scholars in the fields of medicine, biology, anthropology, and psychology.
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35

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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