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Gastrointestinal Disorders and the Nervous System.
White, H
Continuum (Minneapolis, Minn.). 2020;(3):577-590
Abstract
PURPOSE OF REVIEW This article describes the neurologic sequelae of various nutritional micronutrient deficiencies, celiac disease, inflammatory bowel disease, and liver disease. Where relevant, appropriate treatments for these conditions are also discussed. The developing field of the microbiome and nervous system interaction is also outlined. RECENT FINDINGS Pathology in the gastrointestinal system can affect the nervous system when it causes micronutrient deficiency, when immune responses created by the gastrointestinal system affect the nervous system, when toxins caused by gastrointestinal organ failure harm the nervous system, and when treatments aimed at a gastrointestinal medical condition cause damage to the nervous system as a side effect. SUMMARY This article addresses familiar concepts and new developments in the treatment and understanding of diseases that affect the gut and nervous system simultaneously.
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2.
Impact of gut microbiota on neurological diseases: Diet composition and novel treatments.
Larroya-García, A, Navas-Carrillo, D, Orenes-Piñero, E
Critical reviews in food science and nutrition. 2019;(19):3102-3116
Abstract
Gut microbiota has significant effects on the structure and function of the enteric and central nervous system including human behaviour and brain regulation. Herein, we analyze the role of this intestinal ecosystem, the effects of dietary changes and the administration of nutritional supplements, such as probiotics, prebiotics, or fecal transplantation in neuropsychiatric disorders. Numerous factors have been highlighted to influence gut microbiota composition, including genetics, health status, mode of birth delivery and environment. However, diet composition and nutritional status has been repeatedly shown to be one of the most critical modifiable factors of this ecosystem. A comprehensively analysis of the microbiome-intestine-brain axis has been performed, including the impact of intestinal bacteria in alterations in the nervous, immune and endocrine systems and their metabolites. Finally, we discuss the latest literature examining the effects of diet composition, nutritional status and microbiota alterations in several neuropsychiatric disorders, such as autism, anxiety, depression, Alzheimer's disease and anorexia nervosa.
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3.
Copper Deficiency: Causes, Manifestations, and Treatment.
Altarelli, M, Ben-Hamouda, N, Schneider, A, Berger, MM
Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition. 2019;(4):504-513
Abstract
BACKGROUND The metabolism of the essential trace element copper remains incompletely understood and, until recently, nearly ignored in acute medicine. Menkes disease was for long the only known copper deficiency condition, but several case reports and investigations conducted over the last 2 decades have shown that deficiency is more frequent than previously suspected, with devastating individual consequences and potential public health consequences. The copper needs in healthy individuals are 0.9 mg/d, which translates to 0.3 mg/d intravenously in parenteral nutrition; the present review aims at gathering actual knowledge. METHOD AND RESULTS A review of literature was conducted in PubMed and Cochrane systematic reviews to identify the most recent information about copper deficiency and generate a narrative review. Copper deficiency has hereditary and acquired origins, the latter being the most frequent. Clinical manifestations are nonspecific but affect all organs and systems, particularly the hematologic (anemia) and the neurologic (myeloneuropathy) systems. Deficiency also affects the cardiovascular, cutaneous, and immune systems. Severe copper deficiency due to reduced absorption after bariatric bypass surgery has become frequent. CONCLUSION Deficiency is more frequent than previously recognized, probably because of changing nutrition patterns but also because of some treatments that have become very common such as bypass bariatric surgery and, in acute medicine, prolonged continuous renal replacement therapy. The patients may present with severe hematologic and neurologic complications that go untreated because copper deficiency was not considered in the differential diagnosis: These complications often need active intravenous repletion with doses 4-8 times the usual nutrition recommendations.
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4.
Nutritional Modulation of Immune and Central Nervous System Homeostasis: The Role of Diet in Development of Neuroinflammation and Neurological Disease.
Estrada, JA, Contreras, I
Nutrients. 2019;(5)
Abstract
The gut-microbiome-brain axis is now recognized as an essential part in the regulation of systemic metabolism and homeostasis. Accumulating evidence has demonstrated that dietary patterns can influence the development of metabolic alterations and inflammation through the effects of nutrients on a multitude of variables, including microbiome composition, release of microbial products, gastrointestinal signaling molecules, and neurotransmitters. These signaling molecules are, in turn, implicated in the regulation of the immune system, either promoting or inhibiting the production of pro-inflammatory cytokines and the expansion of specific leukocyte subpopulations, such as Th17 and Treg cells, which are relevant in the development of neuroinflammatory and neurodegenerative conditions. Metabolic diseases, like obesity and type 2 diabetes mellitus, are related to inadequate dietary patterns and promote variations in the aforementioned signaling pathways in patients with these conditions, which have been linked to alterations in neurological functions and mental health. Thus, maintenance of adequate dietary patterns should be an essential component of any strategy aiming to prevent neurological pathologies derived from systemic metabolic alterations. The present review summarizes current knowledge on the role of nutrition in the modulation of the immune system and its impact in the development of neuroinflammation and neurological disease.
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5.
Neurological manifestations of excessive alcohol consumption.
Planas-Ballvé, A, Grau-López, L, Morillas, RM, Planas, R
Gastroenterologia y hepatologia. 2017;(10):709-717
Abstract
This article reviews the different acute and chronic neurological manifestations of excessive alcohol consumption that affect the central or peripheral nervous system. Several mechanisms can be implicated depending on the disorder, ranging from nutritional factors, alcohol-related toxicity, metabolic changes and immune-mediated mechanisms. Recognition and early treatment of these manifestations is essential given their association with high morbidity and significantly increased mortality.
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6.
Role of Omega-3 PUFAs in Neurobiological Health.
Grant, R, Guest, J
Advances in neurobiology. 2016;:247-74
Abstract
The importance of the essential, dietary-derived, polyunsaturated fatty acids (PUFAs) omega-6 and omega-3 to human health was first reported over 85 years ago. Subsequent research has revealed many beneficial effects of the omega-3 PUFAs in particular. This has been linked to their involvement in multiple biochemical functions, including synthesis of inflammatory mediators, cell membrane fluidity, intracellular signalling and gene expression. Through these pathways, the omega-3 PUFAs help modulate aspects of inflammation and immunity, cell growth and tissue repair. While a detailed understanding of the mechanisms involved in the role of omega-3 PUFAs to health in the central nervous system (CNS) is still to be elucidated, a role for both inflammatory modulation and a direct impact on neuronal membrane fluidity and receptor function is apparent. At least partially through these mechanisms, low omega-3 levels have been associated with CNS-linked disorders such as poor cognition, depression, anxiety disorders, poor anger control, attention deficit hyperactivity disorder (ADHD) and accelerated neurodegeneration in the elderly.Following a brief introduction to the history and chemistry of the omega-3 family of PUFAs, this chapter will provide an overview of the omega-3 fatty acids and how various members of this PUFA family influence central nervous system function leading towards either health or disease.
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7.
Neurologic manifestations of malabsorption syndromes.
Pfeiffer, RF
Handbook of clinical neurology. 2014;:621-32
Abstract
Although malabsorption is generally considered to be a gastrointestinal problem, the effects of malabsorption extend far beyond the gastrointestinal tract and can include neurologic dysfunction. Malabsorption may occur by a variety of mechanisms, both genetic and acquired, that interfere with the absorption of basic nutrients, vitamins, minerals, and trace elements. Disorders that interfere with fat absorption can lead to neurologic dysfunction as a consequence of associated impairment of fat-soluble vitamin absorption. Thus, individuals with genetic vitamin E deficiency and the familial hypocholesterolemias may develop symptoms of peripheral neuropathy, cerebellar ataxia, and other neurologic signs and symptoms. Disease processes that damage the enteric mucosa and produce malabsorption can trigger neurologic dysfunction both by immune-related processes, as in celiac disease, and by impairing absorption of essential vitamins and other nutrients, as in tropical sprue. Deficiencies of water-soluble vitamins, such as thiamine and niacin, can also develop in the setting of malabsorption and lead to neurologic dysfunction. Neurologists are aware of the neurologic damage that copper excess can cause in Wilson's disease, but copper deficiency due to malabsorption can also produce neurologic dysfunction in the form of myelopathy. It is vitally important for neurologists to be aware of the potential for malabsorptive processes to produce neurologic dysfunction, because effective treatment for such disorders is often available.
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8.
Extragastric diseases and Helicobacter pylori.
Roubaud Baudron, C, Franceschi, F, Salles, N, Gasbarrini, A
Helicobacter. 2013;:44-51
Abstract
In the last year, several diseases from outside of the gastrointestinal tract have been associated with Helicobacter pylori infection. Indeed, this bacterium produces a low-grade inflammatory state, induces molecular mimicry mechanisms, and interferes with the absorbance of nutrients and drugs possibly influencing the occurrence or the evolution of many diseases. In addition to its role in some hematologic conditions, such as immune thrombocytopenic purpura, idiopathic sideropenic anemia, and vitamin B12 deficiency, which were included in the current guidelines, several other conditions such as cardiovascular diseases, diabetes mellitus, hepatobiliary diseases, and neurologic disorders have also shown promising results.
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9.
[Neurological and psychiatric aspects of some gastrointestinal diseases].
Aszalós, Z
Orvosi hetilap. 2008;(44):2079-86
Abstract
The gastrointestinal tract is controlled by the independent enteric nervous system. It is also closely connected to the central nervous system, and bi-directional communication exists between them. The communication involves neural pathways as well as immune and endocrine mechanisms. The brain-gut axis plays a prominent role in the modulation of gut functions. Signals from different sources (e.g. sound, sight, smell, somatic and visceral sensations, pain) reach the brain. These inputs are modified by memory, cognition and affective mechanisms and integrated within the neural circuits of the central nervous system, spinal cord, autonomic and enteral nervous systems. These inputs can have physiologic effects, such as changes in motility, secretion, immune function, and blood flow to the gastrointestinal tract. One of the most important neurotransmitters is serotonin that plays a key role in the pathogenesis of the most common chronic functional gastrointestinal disorder: the irritable bowel syndrome. It is a biopsychosocial disease, resulting from the dysregulation of the brain-gut axis. Endogenous pain facilitation rather than inhibition, pathologic gradation of visceral perception and reduced threshold for pain are all evident in these patients. Abuse history is common in their anamnesis. Exaggerated conscientiousness, perfectionism, oversensitivity, feeling of deficiency in effectiveness, and higher demand for social parity, neuroticism and alexithymia have been detected among their constant personality features. Females are also characterized by gender role conflict and low assertiveness. Antidepressants and psychotherapy have important roles in their treatment. Also patients with inflammatory bowel disease are characterized by neuroticism and alexithymia and altered mother-child attachment is often described in their anamnesis. Autonomic neuropathy is a frequent and early neurological complication. Reflux disease and obstructive sleep apnea mutually generate each other and their severities significantly correlate. In the celiac disease the most common neurological manifestations are ataxia, peripheral neuropathy and myopathy. Up to 85% of patients with histologically proven coeliac disease have no gastrointestinal symptoms; consequently, measurement of antigliadin antibody titre is therefore vital in all cases of idiopathic ataxia. Complete resolution of neurological symptoms is the result of gluten-free diet.
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10.
Neurological complications of coeliac disease: what is the evidence?
Grossman, G
Practical neurology. 2008;(2):77-89
Abstract
Coeliac disease is a chronic immune-mediated disorder that primarily affects the gastrointestinal tract. There is an inflammatory response in the intestine to the ingestion of gluten which improves with a gluten-free diet. Many patients, especially adults, may be asymptomatic or have only extraintestinal symptoms at onset without any of the classical coeliac symptoms. In the last two decades there have been increasing numbers of reports describing neurological complications of coeliac disease, especially ataxia, peripheral neuropathy and epilepsy. This literature has become quite controversial, with disputes over the definition of coeliac disease and gluten sensitivity, whether neurological complications are caused by coeliac disease or are epiphenomena, and whether the proposed complications respond to a gluten-free diet. This review uses an evidence-based approach to critically assess this literature and provides guidelines for the evaluation and management of these patients.