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Books on the topic 'Metabolic interventions'

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Published: 10 December 2022
Last updated: 29 January 2023

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1

Beard, Jonathan C. Illicit drug use: Acute and chronic pharmacological intervention. Salisbury, Wiltshire: Quay Books, 1995.

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2

Shattock, Paul. Autism as a metabolic disorder: Guidelines for gluten and casein- free dietary intervention. 2nd ed. Sunderland: Autism Research Unit, 2001.

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3

Nadjmi, Maschallah, ed. Imaging of Brain Metabolism Spine and Cord Interventional Neuroradiology Free Communications. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74337-5.

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4

George, Weinbaum, Giles Ralph E, Krell Robert D, New York Academy of Sciences., and American Thoracic Society, eds. Pulmonary emphysema: The rationale for therapeutic intervention. New York, N.Y: New York Academy of Sciences, 1991.

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5

Nordin, B. E. C. Metabolic consequences of the menopause a cross-sectional, longitudional, and intervention study on 557 normal postmenopausal women. New York: Springer, 1987.

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6

1921-, Kinney John M., Tucker Hugh N, and Clintec International Horizons Conference (3rd : 1996 : Amsterdam, Netherlands), eds. Physiology, stress, and malnutrition: Functional correlates, nutritional intervention. Philadelphia: Lippincott-Raven, 1997.

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7

Management of lipid disorders: A basis and guide for therapeutic intervention. Baltimore, MD: William & Wilkins, 1997.

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8

Congress, European Society of Neuroradiology. Imaging of brain metabolism, spine and cord interventional neuroradiology free communications: XVth Congress of the European Society of Neuroradiology, Würzburg, September 13th-17th, 1988. Berlin: Springer-Verlag, 1989.

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9

Ken'ichi, Kitani, Goto S, and Aoba A, eds. Pharmacological intervention in aging and age-associated disorders: Proceedings of the Sixth Congress of the International Association of Biomedical Gerontology. New York: New York Academy of Sciences, 1996.

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10

The packaging designer's book of patterns. Hoboken: Wiley, 2012.

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11

Mukhopadhyay, Satinath, and Sunetra Mondal. Metabolic Syndrome: From Mechanisms to Interventions. Elsevier Science & Technology Books, 2022.

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12

Mukhopadhyay, Satinath, and Sunetra Mondal. Metabolic Syndrome: From Mechanisms to Interventions. Elsevier Science & Technology, 2022.

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13

Castle, David J., Peter F. Buckley, and Fiona P. Gaughran. Interventions for metabolic problems in people with schizophrenia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198811688.003.0008.

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To address the risk factors associated with early death in people with schizophrenia, a comprehensive framework is required. This is required to address individuals, systems, and the community. A number of specific frameworks are available to provide better physical health treatments for people with schizophrenia. The most effective of these embrace elements of self-management and self-efficacy. The engagement of patients, carers, and clinicians requires concerted work and effective communication. Peer workers can play a particular role. Various medications can also be used to address specific aspects of the metabolic syndrome in particular, and care should be taken to try to choose (where feasible) antipsychotic medications with the lowest possible risk of metabolic syndrome.
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14

Nutritional and Therapeutic Interventions for Diabetes and Metabolic Syndrome. Elsevier Science & Technology Books, 2018.

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15

Nutritional And Therapeutic Interventions For Diabetes And Metabolic Syndrome. Academic Press, 2012.

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16

Bagchi, Debasis, and Sreejayan Nair. Nutritional and Therapeutic Interventions for Diabetes and Metabolic Syndrome. Elsevier Science & Technology Books, 2018.

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17

Nutritional and Therapeutic Interventions for Diabetes and Metabolic Syndrome. Elsevier, 2012. http://dx.doi.org/10.1016/c2010-0-66168-2.

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18

Nutritional and Therapeutic Interventions for Diabetes and Metabolic Syndrome. Elsevier, 2018. http://dx.doi.org/10.1016/c2016-0-01904-6.

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19

Bagchi, Debasis, Sreejayan Nair, and Nair Sreejayan. Nutritional and Therapeutic Interventions for Diabetes and Metabolic Syndrome. Academic Press, 2012.

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20

Bagchi, Debasis, and Sreejayan Nair. Nutritional and Therapeutic Interventions for Diabetes and Metabolic Syndrome. Elsevier Science & Technology Books, 2012.

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21

Ostojic, Sergej M. Molecular Nutrition and Mitochondria: Metabolic Deficits, Whole-Diet Interventions, and Targeted Nutraceuticals. Elsevier Science & Technology, 2022.

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22

Ostojic, Sergej M. Molecular Nutrition and Mitochondria: Metabolic Deficits, Whole-Diet Interventions, and Targeted Nutraceuticals. Elsevier Science & Technology Books, 2022.

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23

Fugmann, Andreas. Effects of Acute Metabolic Interventions on Hemodynamics, Endothelial Function and Forearm Glucose Uptake. Uppsala Universitet, 2001.

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24

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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25

Weekers, Frank. Study of the Endocrine & Metabolic Dysfunction & Assessment of Hormonal Interventions in a Novel in Vivo Experimental Model of Critical Illness. Leuven Univ Pr, 2003.

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26

Brown, Sharon Ann. THE EFFECTS OF EDUCATIONAL INTERVENTIONS ON KNOWLEDGE, SELF-CARE BEHAVIORS, AND METABOLIC CONTROL IN DIABETIC ADULTS: A META-ANALYSIS OF FINDINGS. 1987.

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27

Dichi, Isaias, and Andrea Name Colado Simao. Nutritional Intervention in Metabolic Syndrome. Taylor & Francis Group, 2015.

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28

Dichi, Isaias, and Andrea Name Colado Simao. Nutritional Intervention in Metabolic Syndrome. Taylor & Francis Group, 2015.

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29

Dichi, Isaias, and Andrea Name Colado Simao, eds. Nutritional Intervention in Metabolic Syndrome. CRC Press, 2015. http://dx.doi.org/10.1201/b19099.

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30

Dichi, Isaias, and Andréa Name Colado Simão. Nutritional Intervention in Metabolic Syndrome. Taylor & Francis Group, 2021.

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31

Ellenstein, Aviva, Christina Prather, and Mikhail Kogan. Neurodegenerative Diseases: Parkinson’s and Alzheimer’s Diseases. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190466268.003.0020.

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Neurodegenerative diseases increase in prevalence with aging. This chapter begins with a discussion of Parkinson’s disease. Optimally individualized treatment includes dopaminergic medications, physiotherapy, and multidisciplinary care. Evidence for integrative approaches is limited. Advances in genetics and biomarkers hold promise for subtype-specific, precision treatment in the near future. The second part of this chapter focuses on Alzheimer’s disease. Standard evaluation includes assessment for possible contributing factors that may worsen cognition, and management includes optimizing factors that may improve cognitive function. No disease-modifying medical approaches yet exist, but increasing emphasis on interventions to limit chronic inflammation and optimize brain metabolism remain fundamental in the integrative approach to Alzheimer’s disease. The new metabolic approach first described by Dr. Dale Bredesen is summarized and the importance of multidisciplinary care, with emphasis on early transition to palliative care when appropriate, is reviewed.
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32

Golper, Thomas A., Andrew A. Udy, and Jeffrey Lipman. Drug dosing in acute kidney injury. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0364.

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Drug dosing in acute kidney injury (AKI) is one of the broadest topics in human medicine. It requires an understanding of markedly altered and constantly changing physiology under many disease situations, the use of the drugs to treat those variety of diseases, and the concept of drug removal during blood cleansing therapies. Early in AKI kidney function may be supraphysiologic, while later in the course there may be no kidney function. As function deteriorates other metabolic pathways are altered in unpredictable ways. Furthermore, the underlying disorders that lead to AKI alter metabolic pathways. Heart failure is accompanied by vasoconstriction in the muscle, skin and splanchnic beds, while brain and cardiac blood flow proportionally increase. Third spacing occurs and lungs can become congested. As either kidney or liver function deteriorates, there may be increased or decreased drug sensitivity at the receptor level. Acidosis accompanies several failing organs. Protein synthesis is qualitatively and quantitatively altered. Sepsis affects tissue permeability. All these abnormalities influence drug pharmacokinetics and dynamics. AKI is accompanied by therapeutic interventions that alter intrinsic metabolism which is in turn complicated by kidney replacement therapy (KRT). So metabolism and removal are both altered and constantly changing. Drug management in AKI is exceedingly complex and is only beginning to be understood. Thus, we approach this discussion in a physiological manner. Critically ill patients pass through phases of illness, sometimes rapidly, other times slowly. The recognition of the phases and the need to adjust medication administration strategies is crucial to improving outcomes. An early phase involving supraphysiologic kidney function may be contributory to therapeutic failures that result in the complication of later AKI and kidney function failure.
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33

Vitor, Cohen Ricardo, ed. Metabolic and systemic responses following interventional laparoscopy. Austin: R.G. Landes, 1994.

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34

Muñoz, George E., and Isabella Leoni Garcia. Functional Medicine Approach to Addiction. Edited by Shahla J. Modir and George E. Muñoz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190275334.003.0018.

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The functional medicine protocol complements and enhances the traditional approach to recovery. Seen from a functional medicine perspective, the path to substance/and or food addiction recovery involves a multimodal approach. It shifts the focus from the imbalances in the brain and neurotransmitters to treat the whole person. It does so by considering the metabolic, hormonal, psychologic, immunologic, and neurologic functions that have been disturbed by addiction and that further perpetuate the inflammatory state of active addiction and during recovery phases. The gut-brain axis is reviewed from all aspects. Specific microbiome interventions, micronutrient, and vitamin deficiency support is reviewed. These interventions can be addressed through lifestyle modifications (including stress-reduction techniques), nutrition, supplementation, and in-depth case protocols, which will be further reviewed in the chapter.
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35

Strasburger, Victor C., and Susan M. Coupey, eds. AM:STARs: Metabolic Challenges to Adolescent Health, Vol. 19, No. 3. American Academy of Pediatrics, 2005. http://dx.doi.org/10.1542/9781581104103.

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This widely respected resource includes "The Adolescent Obesity Epidemic," "Adolescent Obesity: Etiology, Office Evaluation, and Treatment," "Medical Intervention in Adolescent Obesity," "Dietary Approaches to Healthy Weight Management for Adolescents," "Does Adolescent Media Use Cause Obesity and Eating Disorders?" "Bariatric Surgery in Adolescents: Mechanics, Metabolism, and Medical Care," "The Metabolic Syndrome: A Gathering Challenge in a Time of Abundance," "Type 2 Diabetes Mellitus," "Screening Adolescents for Lipid Disorders: What Is the Best Approach?" "Body Image, Eating Disorders, and the Media," "Eating Disorders," and "Bone Metabolism During Adolescence: The Known, the Unknown, and the Controversial."
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36

Dichi, Isaias, and Andrea Name Colado Simao. Nutritional Intervention in Metobolic Syndrome. Taylor & Francis Group, 2015.

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37

Stafstrom, Carl E. Dietary Therapy for Neurological Disorders. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0018.

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Dietary and metabolic therapies such as the high-fat, low-carbohydrate ketogenic diet (KD) are best known for the treatment of intractable epilepsy. Yet, dietary and metabolic approaches have also found some efficacy in a wide variety of other neurological diseases, including autism spectrum disorder, brain trauma, Alzheimer’s disease, sleep disorders, brain tumors, pain, and multiple sclerosis, as discussed in other chapters of this volume. This chapter provides an overview of clinical and experimental studies using the KD in an array of other neurologic disorders: amyotrophic lateral sclerosis, Parkinson’s disease, mood disorders, and migraine. Despite the wide spectrum of pathophysiological mechanisms underlying these disorders, it is possible that one or more final common metabolic pathways might be influenced by dietary intervention. There is compelling albeit preliminary evidence that correction of aberrant energy metabolism through dietary manipulation could favorably influence diverse neurological diseases.
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38

Gaspar, Joana M., Humberto M. Carvalho, and Alberto Camacho-Morales, eds. Metabolic Disorders Associated with Autism Spectrum Disorders: Approaches for Intervention. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-116-8.

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39

Molecular Interventions and Local Drug Delivery (Frontiers in Cardiology). W.B. Saunders Company, 1995.

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40

Fischer, Kevin M., and Shannon S. Carson. Chronic Multiple Organ Dysfunction. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0013.

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This chapter reviews the clinical syndrome of chronic multiple organ dysfunction (MOD) following acute critical illness. Chronic MOD, also referred to as chronic critical illness, occurs in patients who have survived the acute phase of their illness or injury but remain dependent on life support for weeks or months. This condition presents unique physiologic and metabolic abnormalities distinct from those encountered in the acute illness. These include neuroendocrine and immune dysregulation, ICU-acquired weakness, persistent respiratory failure, and brain dysfunction. The symptom burden for these patients is high, and long-term survival is limited for elderly patients and those for whom MOD persists for weeks. Comprehensive and systematic programmes will need to be designed and implemented involving bundled best-practice interventions in order to reduce the incidence and treat the consequences of chronic MOD.
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41

Lin, Eric, and John Cahill. Switching Antipsychotics to Reduce Metabolic Risk. Edited by Ish P. Bhalla, Rajesh R. Tampi, Vinod H. Srihari, and Michael E. Hochman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190625085.003.0043.

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This chapter provides a summary of the landmark Comparison of Antipsychotics for Metabolic Problems trial on schizophrenia treatment. This trial was designed to help clarify some of the clinical considerations in choosing antipsychotics. Does switching to aripiprazole from olanzapine, quetiapine, or risperidone confer metabolic benefits? Does the switch to aripiprazole cause clinical destabilization? Starting with these questions, it describes the basics of the study, including funding, study location, study population characteristics, how many patients, study design, study intervention, follow-up, endpoints, results, and criticism and limitations. The chapter briefly reviews other relevant studies and information, discusses implications, and concludes with a relevant clinical case.
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42

Levy, David. Macrovascular complications, hypertension, and lipids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198766452.003.0008.

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Premature vascular disease is common in Type 1 diabetes, especially in women and those with long duration. Many studies have identified early vascular involvement, using carotid Doppler and coronary artery calcification. Symptoms of coronary heart disease are often absent or muted, and the best methods for identifying occult coronary heart disease in Type 1 patients are not known. The concept of ideal cardiovascular health is valuable in planning preventive lifestyle and medical interventions. ‘Essential’ hypertension in young Type 1 patients is common, and reflects increased arterial stiffness. Hypertension is invariable in patients with any degree of albuminuria or renal impairment. Statin treatment in patients over 40 years old is recommended, but the evidence base is weak. Statins and ezetimibe are the only agents of prognostic value currently available for prevention of vascular events. Primary prevention with aspirin needs individual assessment. Insulin resistance/metabolic syndrome is frequent in Type 1 diabetes.
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43

van den Boogaard, Mark, and Paul Rood. Delirium in Critically Ill Patients. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199398690.003.0002.

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This chapter addresses delirium in critically ill patients in the intensive care unit (ICU), especially the mixed subtype (alternating hyperactivity and hypoactivity). The Confusion Assessment Method for the ICU and the Intensive Care Delirium Screening Checklist are discussed as useful delirium assessment tools in this setting. Several neurotransmitter pathways have been implicated in delirium, including cholinergic, GABAergic, and serotonergic pathways; cytokines and glucocorticoids also appear relevant. Risk factors for delirium in the ICU include older age, prior cognitive impairment, worse illness severity, recent delirium or coma, mechanical ventilation, admission category (especially trauma or neurological/neurosurgical admission), infection, metabolic acidosis, morphine and sedative administration, urea concentration, respiratory failure, and admission urgency. Prevention and treatment of delirium are discussed, including nonpharmacological interventions (frequent reorientation, providing eyeglasses and hearing aids if needed, promoting nighttime sleep, and early mobilization) and judicious use of opiate, sedative, and antipsychotic medications.
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44

Rancaño, Rocío Santos, Andrés Sánchez Pernaute, and Antonio José Torres Garcia. Single-Anastomosis Malabsorptive Procedures. Edited by Tomasz Rogula, Philip Schauer, and Tammy Fouse. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190608347.003.0039.

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Malabsorptive interventions are recognized as the procedure of choice in metabolic surgery and as the best strategy for re-do surgery when restriction fails. This chapter describes the most recently published single-anastomosis malabsorptive procedures: the one-anastomosis gastric bypass (OAGB), the single-anastomosis duodenoileal anastomosis with sleeve (SADIS), the duodenojejunal omega switch (DJOS), the duodenoileal omega switch (DIOS), the ileal food diversion (IFD), and the sleeve gastrectomy with loop bipartition (SG + LB). These procedures are effective and safe and may be regarded as an option, although no consensus exists as to which procedure offers the best option overall, nor is there an established criterion or algorithm for a made-to-measure procedure for a given patient. The use of a single anastomosis is the most important part of the techniques. All the procedures are relatively new and their safety should be evaluated in bigger randomized trials.
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45

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0032.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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46

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_001.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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47

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_002.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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48

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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49

Golier, Julia A., Andreas C. Michaelides, Maya Genovesi, Emily Chapman, and Rachel Yehuda. Pharmacological Treatment of Posttraumatic Stress Disorder. Oxford University Press, 2015. http://dx.doi.org/10.1093/med:psych/9780199342211.003.0019.

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Although psychotherapy is considered first-line treatment for posttraumatic stress disorder (PTSD), advances have been made in pharmacological treatment. Based on controlled clinical trials, antidepressants remain the first-line pharmacological treatment. Studies suggest that selective serotonin reuptake inhibitors reduce PTSD-specific symptoms and improve global outcome. Emerging evidence suggests efficacy for venlafaxine. Other individual agents found to be efficacious include imipramine and phenelzine. Prazosin is emerging as a beneficial adjunct for PTSD-related sleep disturbances and nightmares. Some evidence suggests that atypical antipsychotics may be efficacious against a broad range of symptoms, although the risk of metabolic side effects may limit widespread use. Trials are needed to assess whether anticonvulsants, cortisol-based treatments, sympatholytics, or other novel approaches are efficacious, and how pharmacotherapy can enhance psychotherapy outcomes. These studies should consider the goals of pharmacotherapy in PTSD and the subgroups of patients or clinical presentations most likely to benefit from pharmacological interventions.
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50

Nadjmi, Maschallah. Imaging of Brain Metabolism Spine and Cord Interventional Neuroradiology Free Communications. Springer-Verlag, 1990.

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