The Effects of Physical and Psychological Stress on the Gastrointestinal Tract: Lessons from Animal Models
Sección de Gastroenterología, Servicio de Aparato Digestivo, Hospital General Universitario "Gregorio Marañón", C/ Dr Esquerdo 46. 28007 Madrid, Spain. Current Molecular Medicine
(Impact Factor: 3.62).
07/2008; 8(4):299-312. DOI: 10.2174/156652408784533751
Physical and psychological stresses are widely accepted as triggers and / or modifiers of the clinical course of diverse gastrointestinal disorders such as peptic ulcer, irritable bowel syndrome or inflammatory bowel disease. Growing experimental evidence from a variety of models such as immobilization, thermal injury or early maternal deprivation in laboratory animals uniformly supports the ability of stress to induce the development of gastric ulcers, altered gastrointestinal motility and ion secretion, and increased intestinal permeability leading to the passage of antigens to the lamina propria and bacterial translocation. Stress can also synergize with other pathogenic factors such as Helicobacter pylori, non-steroidal anti-inflammatory drugs or colitis-inducing chemicals to produce gastrointestinal disease. The brain-gut axis provides the anatomical basis through emotions and environmental influences modulate the gastrointestinal function through the regulation of gastrointestinal immune system and mucosal inflammation; in this sense, mucosal mast cells - at cellular level - and corticotropin releasing factor (CRF) - at molecular level - seem to play a crucial role. On the other hand, an array of adaptive responses have been evolved in order to maintain the homeostasis and to ensure the survival of the individual. In the gut mucosa anti-inflammatory pathways counteract the deleterious effect of the stressful stimuli on the gastrointestinal homeostasis. In the present review we discuss the several experimental approaches used to mimic human stressful events or chronic stress in laboratory animals, the evidence of stress-induced gastrointestinal inflammation and dysfunction derived from them, and the involved cellular and molecular mechanisms that are being discovered during the last years.
Available from: ps.oxfordjournals.org
- "Production stressors have been shown to be a major factor in the inflammatory changes in gut architecture and ecology that are moderated through the use of AGP. Because both physical and psychological stressors have been shown to affect gastrointestinal barrier functions and increase intestinal inflammation (Caso et al., 2008; Gareau et al., 2008; Lambert, 2009), it is necessary find cost-effective replacements for AGP that can consistently function to modulate the stress response in poultry production environments. "
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ABSTRACT: Prebiotics consisting of resistant starch may alter intestinal ecology, thus modulating inflammation and increasing intestinal health through increased cecal production of short-chain fatty acids (SCFA). Probiotics may directly alter the intestinal microbiome, resulting in the same effects. We hypothesize that adding prebiotics and probiotics to feed may protect the gut of young chicks under stress. Studies 1, 2, and 3 evaluated treatments in a cold stress (CS) and Escherichia coli (EC) oral challenge to 430 day-old broiler chicks for 3 wk. In study 1, prebiotics were administered as 15% of the diet during the first week only and consisted of the following: Hi-Maize resistant starch (HM), potato starch (PS), or raw potato (RP). In studies 2 and 3, the PS treatment was identical to study 1, and an additional probiotic treatment (PRO) was administered in feed and water. In study 1, PS protected BW during the first week and decreased the mortality of CS/EC-challenged birds during the first week and wk 3, while RP decreased the mortality of warm-brooded birds challenged with EC during the first week. In study 2, PS decreased and PRO increased the main effect mean (MEM) of the first week BW. PS and PRO numerically decreased the feed conversion ratio (FCR) by 23 and 29 points, respectively, in CS/EC-challenged birds with no effects on mortality. In study 3, PS decreased and PRO increased the first week and wk 3 MEM BW. PS numerically increased FCR by 16 points, while PRO decreased FCR by 2 points. Both PS and PRO tended to increase overall mortality, and PRO significantly increased mortality in the CS/EC challenge. These results suggest that the effects of PS may be too variable in this challenge model for further study; however, the PRO treatment improved production values and may have potential as an alternative to antibiotics during the first weeks after hatch.
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Available from: Muriel Larauche
- "Corticosterone (rodent)/cortisol (human) exert a negative feedback on the paraventricular nucleus of the hypothalamus and pituitary gland ultimately contributing to the termination of the response (Turnbull and Rivier, 1997). Far beyond an exclusive neuroendocrine role, CRF, which is widely distributed outside of the hypothalamus (De Souza and Grigoriadis, 2002), also acts as a neurotransmitter/ neuromodulator to coordinate the behavioral, autonomic, immune, and visceral efferent limbs of the stress response (Bale and Vale, 2004; Caso et al., 2008; Friedman and Irwin, 1995; Taché et al., 2001). For instance brain CRF activates the sympathetic nervous system inducing the systemic release of catecholamines (adrenaline and noradrenaline) involved in the " fight or flight " response (Tsatsanis et al., 2007; Usui et al., 2009; Yorimitsu et al., 2008). "
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ABSTRACT: Epidemiological studies have implicated stress (psychosocial and physical) as a trigger of first onset or exacerbation of irritable bowel syndrome (IBS) symptoms of which visceral pain is an integrant landmark. A number of experimental acute or chronic exteroceptive or interoceptive stressors induce visceral hyperalgesia in rodents although recent evidence also points to stress-related visceral analgesia as established in the somatic pain field. Underlying mechanisms of stress-related visceral hypersensitivity may involve a combination of sensitization of primary afferents, central sensitization in response to input from the viscera and dysregulation of descending pathways that modulate spinal nociceptive transmission or analgesic response. Biochemical coding of stress involves the recruitment of corticotropin releasing factor (CRF) signaling pathways. Experimental studies established that activation of brain and peripheral CRF receptor subtype 1 plays a primary role in the development of stress-related delayed visceral hyperalgesia while subtype 2 activation induces analgesic response. In line with stress pathways playing a role in IBS, non-pharmacologic and pharmacologic treatment modalities aimed at reducing stress perception using a broad range of evidence-based mind-body interventions and centrally-targeted medications to reduce anxiety impact on brain patterns activated by visceral stimuli and dampen visceral pain.
Available from: I.D. Wijnberg
- "An organism develops defence and adaptive mechanisms in order to ensure survival in response to stress. Some adaptive responses directed towards the restoration of gastrointestinal functional homeostasis and physical integrity have been described including the sensory neurons of the enteric nervous system (their role in enhancing mucosal defence and regulation of mucosal blood flow) and the hormones vasopressin and prolactin which seem to induce protective mechanisms, although the responsible mechanisms are not understood (Caso et al. 2008). Overtraining is a stress-related disease probably caused by a neuro-endocrine imbalance. "
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ABSTRACT: Gastric ulceration can be caused by different pathophysiological mechanisms including dietary factors, psychological stress and exercise. Overtraining is a medical syndrome in performance horses associated with altered hormone levels, altered feed intake, altered behaviour and decreased performance. These components might lead to a higher incidence of gastric ulceration in overtrained horses.
To investigate whether the incidence of gastric ulceration is increased in overtrained compared to control horses.
A longitudinal training study with twelve 1.5 years old Standardbred horses was performed on a treadmill for a total of 32 weeks. Training was divided into 4 periods: (1) acclimatisation (2) training (3) intensified training, and (4) detraining. In period 3, the horses were randomly divided into 2 groups: control (C) and intensified trained group (IT). At the end of each period, gastroscopy was performed in conscious horses after withholding feed for 12 h and water for 6 h using a 3.5 m video gastroendoscope. Lesion scores were assigned to areas of the stomach and graded 1-4. Logistic regression was used for statistical calculations.
Evaluation of the stomach revealed only minor changes (grades 1 or 2) on each occasion. There were no significant differences in gastric lesion scores between groups or periods. Most lesions (70%) were found around the minor curvature. After detraining no lesions (0%) were found in contrast to periods 1 (40%, P = 0.056), 2 (30%) and 3 (30%).
Experimentally-induced overtraining does not increase the incidence of gastric ulceration in normally fed Standardbred horses and detraining appears to reduce gastric ulceration.
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