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Stress, which is defined as an acute threat to homeostasis, shows both short- and long-term effects on the functions of the gastrointestinal tract.
One of the important coordinators of the endocrine, behavioural and immune response to stress is corticotrophin releasing factor (CRF). The topic of the brain-gut axis has recently received even more attention due to the discovery of the bidirectional interaction between the brain-gut axis and gut microbiota. There is also an evidence that gut bacteria helps to keep the bidirectional contact between the components of the brain and gut axis.
Concerning the translation of the stress signals to the gut, mast cells play an important role.
Finally, the exposure to chronic stress is associated with prolonged and excessive activation of stress response areas within the CNS. Gastroesophageal reflux disease (GERD) represents one of the most important manifestations of stress exposure to GI tract. There is also evidence that stress may have a profound effect on bacterial flora leading to increased adhesion and translocation of bacteria due to increased barrier permeability. One of the most important diseases of the GI tract that is linked to stress exposure to gut is IBS, which represents a common, but heterogeneous gastrointestinal disorder with a worldwide prevalence of between 10-20%. Among important risk factors is genetic susceptibility and chronic stress (life events) while the key trigger factors include psychosocial factors and exposure of the gut to infections or overuse of antibiotics leading to negative alterations in gut flora.
Diagnostic approach to the potential IBS patient includes obtaining a full medical history, physical examination, laboratory testing and operative diagnostic procedures. Finally, the alarm symptoms ("red flags") such as unintentional weight loss, nocturnal diarrhoea, anaemia, bloody stools, onset of symptoms at 50 years or older should immediately prompt the physician to consider an alternative diagnosis, such as colon cancer.
The differential diagnosis of IBS symptoms is broad and can lead to multiple, but often unnecessary, diagnostic tests. A lot of patients believe that diet plays an important role in the exacerbation of symptoms.
In IBS patients with bloating and pain the recommended first line of therapy is a antispasmodics such as hyoscamine sulphate (0.125 up to four times daily) or dicyclomine (10-10 mg twice daily up to four times daily). Recently, an increasing number of studies indicates the positive effect of probiotics IBS on symptoms. Complementary or alternative approaches includes cognitive behavioural therapy (CBT), dynamic psychotherapy, stress management, hypnotherapy, relaxation therapy and even acupuncture represent further important treatment approaches to reduce the symptoms of IBS (64, 65). Science, Technology and Medicine open access publisher.Publish, read and share novel research.
Irritable bowel syndrome (IBS) affects as many as 5%-20% of individuals worldwide and has a significant impact on quality of life. The reaction of IBS patients to certain food items has been attributed to a number of short-chain carbohydrates called FODMAPs that are poorly digested and absorbed so that a significant portion of the ingested carbohydrates do not get digested properly and enter the small intestine and colon.
A recent systematic review with meta-analysis published in a worldwide gastroenterology journal examined the efficacy of probiotics in the treatment of IBS.  A total of 1,793 patients were included in the meta-analysis. There are several pieces of evidence showing that inflammation and immune cells affect the neuroendocrine system (NES) of the gut, which controls and regulates GI motility and sensitivity.
Treatment for diarrhea-predominant IBS (IBS-D) include anti-diarrheals (loperamide), 5-HT3 antagonists or serotonin-blockers (alosetron, cilansetron, ramosetron), anti-inflammatory drugs (mesalamine) and antibiotic drugs (rifaximin).  The potential use of antibiotics in IBS treatment has been supported by a growing body of evidence showing the important role that intestinal bacterial overgrowth plays in the development of IBS. Treatment for constipation-predominant IBS (IBS-C) include laxative-based treatments (osmotic agents, and stool softeners), prokinetics (drugs to stimulate movement of bowels), prosecretory agents (drugs that augment intestinal secretion, thus acting as a stool lubricant and facilitating its evacuation, such as lubiprostone and linaclotide), serotonin-boosting drugs (serotonin receptor modulators and 5-HT4 agonists such as tegaserod) and bile acid modulators (CDC and elobixibat). However, these drugs have limited effects in their use due to their symptomatic approach and risk of various side effects.
Dietary compounds can induce immune responses in the GI tract and contribute to low-grade inflammation, particularly in gut permeability issues, therefore food sensitivity testing can be of value in IBS patients. 365. Spiller R, Aziz Q, Creed F, Emmanuel A, Houghton L, Hungin P, Jones R, Kumar D, Rubin G, Trudgill N, et al.
369. Sandler RS, Everhart JE, Donowitz M, Adams E, Cronin K, Goodman C, Gemmen E, Shah S, Avdic A, Rubin R. 376. Austin GL, Dalton CB, Hu Y, Morris CB, Hankins J, Weinland SR, Westman EC, Yancy WS, Drossman DA. 377. Simren M, Mansson A, Langkilde AM, Svedlund J, Abrahamsson H, Bengtsson U, Bjornsson ES.
379. Austin GL, Dalton CB, Hu Y, Morris CB, Hankins J, Weinland SR, Westman EC, Yancy WS, Drossman DA. 380. Ford AC, Talley NJ, Spiegel BM, Foxx-Orenstein AE, Schiller L, Quigley EM, Moayyedi P.
384. Kassinen A, Krogius-Kurikka L, Makivuokko H, Rinttila T, Paulin L, Corander J, Malinen E, Apajalahti J, Palva A. It’s critical that you remove the inflammatory foods such as grains, sugar, dairy, and processed foods and add in healing, anti-inflammatory foods.
Below are just a few foods that can aid greatly in reducing inflammation, soothing your digestive system, and healing your gut. Animal protein, preferably organic, grass-fed, pasture-raised, wild-caught, is extremely healing to the gut.
Bitter, astringent foods like lemon are great for stimulating bile production, which aids in digestion. Aromatic herbs like oregano, ginger, cloves and rosemary are great for digestive health because they possess antibacterial properties. Fermented foods are great for gut health because they are a fantastic source of good bacteria, or probiotics. NOTE: if you suffer from SIBO (small intestinal bacterial overgrowth) prebiotics might worsen symptoms.
Now that you have an extensive list of gut-healing foods, try incorporating these options on a consistent basis.
PS: If you’d like more information on steps you can take to heal your gut, sign up for your FREE Digestion Guide- 3 Simple Ways to Improve Your Digestion in 30 Days or Less at Jen Broyles. 11 Best Breakfast Foods for Digestive HealthDo you bloat out like a hot air balloon after every meal?
6 Ab Exercises That Are Better Than CrunchesCrunches seem to be everyone’s go-to exercise for a flat stomach and toned midsection.
Oh yeah, and when you sign up, we'll also give you some neat free bonuses like our Paleo for Beginners guide, with 15 extra delicious recipes! Neither Valley Medical Weight Loss nor any of its affiliates, directors, officers or employees warrant the accuracy, responsibility for errors, omissions or completeness of the information, text, graphics, links or other items contained within these materials. The information, including but not limited to, text, graphics, images and other material, contained on this website is for educational purposes only. Exposure to stress results in alterations of the brain-gut interactions ("brain-gut axis") ultimately leading to the development of a broad array of gastrointestinal disorders including inflammatory bowel disease (IBD), irritable bowel syndrome (IBS) and other functional gastrointestinal diseases, food antigen-related adverse responses, peptic ulcer and gastroesophageal reflux disease (GERD).
Especially the focus is addressed to the role of stress in the pathophysiology of the most common diseases of the gastrointestinal tract and to the diagnostic and therapeutic options to prevent stress-related disorders. The CRF family of peptides are expressed in the CNS and within the gut and displays potent biologic actions. The cross talk between gut microbiota, the immune system and the brain-gut axis plays an important role in the modulation of the stress response of the gut in the context of the development of different gut disorders (13). In other words exposure to stress modifies the bacterial flora, but also the opposite is true that the gut bacteria, which may have a profound effect on the BGA and may modulate motility, permeability and visceral sensitivity. Interestingly, these cells secrete a number of important mediators and have on their surface the receptors for the CRF indicating an important link between stress and these cells (16, 17). This exposure may cause even irreversible changes in the brain areas responsible for the perception of pain in the gut. It has been shown that stress causes the aggravation of GERD symptoms due to inhibition of the lower esophageal sphincter and increased sensitivity to acid i.e. This may be an important factor leading to the activation of the immune system resulting in the exacerbation or induction of acute colitis (39). There is a strong evidence of the putative role of gut microbiota in the disturbance of brain-gut axis in IBS. With concerns to taking the medical history, the physician should focus on the predominant bowel disorder for example diarrhoea, constipation, pain, bloating.
One of the most important aspects in the management of IBS is the development of positive physician-patient relationship. Dietary assessment plays important role, and the symptoms may improve after avoiding of following: milk products, some carbohydrates (sorbitol, fructose), caffeine and alcohol.
Antispasmodics act predominantly as antagonists at cholinergic receptors and thereby reduce contraction of the GI tract. However, a physician combining different types of drugs should be aware of possible side effects and interactions.
These forms of therapy should not only be used in refractory forms of disease, but also used as useful adjunctive therapy. Restraint stress stimulates colonic motility via central corticotropin-releasing factor and peripheral 5-HT3 receptors in conscious rats. Corticotropin-releasing factor receptors and stress-related alterations of gut motor function.
Probiotic bacteria Escherichia coli strain Nissle 1917 attenuates acute gastric lesions induced by stress.
Mucosal mast cells are pivotal elements in inflammatory bowel disease that connect the dots: stress, intestinal hyperpermeability and inflammation. Corticotropin-releasing hormone (CRH) regulates macromolecular permeability via mast cells in normal human colonic biopsies in vitro. Affective disturbances modulate the neural processing of visceral pain stimuli in irritable bowel syndrome: an fMRI study. Do interactions between stress and immune responses lead to symptom exacerbations in irritable bowel syndrome? The effects of psychological stress on the esophagogastric junction pressure and swallow-induced relaxation. Physiological, immunohistochemical and molecular aspects of gastric adaptation to stress, aspirin and to H. Importance of brain-gut axis in the gastroprotection induced by gastric and remote preconditioning.
Psychological stress and inflammatory bowel disease: a follow-up study in parents who lost a child in Denmark.
The effect of restraint stress on the normal colon and on intestinal inflammation in a model of experimental colitis. Exposure to a social stressor alters the structure of the intestinal microbiota: implications for stressor-induced immunomodulation. Extraintestinal symptoms in irritable bowel syndrome and inflammatory bowel diseases: nature, severity, and relationship to gastrointestinal symptoms.
S3 guideline of the German Society for Digestive and Metabolic Diseases (DGVS) and the German Society for Neurogastroenterology and Motility (DGNM) to the definition, pathophysiology, diagnosis and treatment of intestinal motility. Current and emerging therapies in irritable bowel syndrome: from pathophysiology to treatment. Alosetron for severe diarrhea-predominant irritable bowel syndrome: improving patient outcomes. Alosetron for severe diarrhoea-predominant irritable bowel syndrome: safety and efficacy in perspective. Pharmacologic and complementary and alternative medicine therapies for irritable bowel syndrome. A randomized, double-blind, placebo-controlled trial of polyethylene glycol effects on fasting and postprandial rectal sensitivity and symptoms in hypersensitive constipation-predominant irritable bowel syndrome.
Alpha 2 delta (a(2)d) ligands, gabapentin and pregabalin: what is the evidence for potential use of these ligands in irritable bowel syndrome.
Probiotics and prebiotics in the management of irritable bowel syndrome: a review of recent clinical trials and systematic reviews.

Risk factorsSo far, four major risk factors for NEC have been defined with prematurity being the most consistent. IBS symptoms range from diarrhea to constipation, or a combination of the two, with abdominal pain or discomfort and gas or bloating, referred to as “abdominal distension”.  The degree of symptoms varies in different patients from tolerable to severe, and the time pattern and discomfort varies immensely from patient to patient. Up to 33% of patients with IBS had a family history of IBS compared to 2% of the controls in one study.[370] In another study of a family cluster, a significant association was reported between having a first degree family member with bowel symptoms and presenting with IBS. Once there, these unabsorbed carbohydrates provide a substrate for bacterial fermentation with the production of gas and distension of the intestinal tract and an increase in intra-abdominal pressure (IAP). Prevalence of gastrointestinal symptoms six months after bacterial gastroenteritis and risk factors for development of the irritable bowel syndrome: postal survey of patients. Increased rectal mucosal enteroendocrine cells, T lymphocytes, and increased gut permea-bility following acute Campylobacter enteritis and in post-dysenteric irritable bowel syndrome.
Serotonin, inflammation, and IBS: fitting the jigsaw together? J Pediatr Gastroenterol Nutr. Increased gastrointestinal permeability and gut inflammation in children with functional abdominal pain and irritable bowel syndrome. J Pediatr.
Small intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome. Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome.
The mast cell stabiliser ketotifen decreases visceral hypersensitivity and improves intestinal symptoms in patients with irritable bowel syndrome. Gut. Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome.
Desperately seeking serotonin… A commentary on the withdrawal of tegaserod and the state of drug development for functional and motility disorders. All disease begins in the gut and spreads to other areas of the body (see: 7 Signs Your Gut Bacteria Are Out of Whack). You might be thinking that I’m going to talk about bone broth, but I’m going to provide some other options for you. If you’re following a Paleo diet, I imagine you’ve taken many of these inflammatory foods out.
It’s a fantastic source for dietary amino acids such as glutamine, glutamate, and arginine, which optimize the immune functions of the intestine. Cooking with these delicious herbs not only provides flavor to your meals, but helps heal and protect your gut too. For me, I’ve found it to be pretty easy to get most of these foods into my diet on a regular basis.
If you liked that article, you'll absolutely LOVE our daily newsletter -- with more recipes, workouts, and tips and tricks to be the healthiest version of yourself. Detox supports hepatic and gastrointestinal detoxification by providing nutrients and botanical extracts that enhance toxin elimination, digestion, intestinal motility, gut integrity, and cell function.
Neither Valley Medical Weight Loss nor any of its affiliates, directors, officers or employees shall be liable for any special, indirect, incidental, or consequential damages, including without limitation, lost revenues or lost profits, which may result from the use of these materials. The content is not intended in any way as a substitute for professional medical advice, diagnosis or treatment. CRF has a potent effects on gut via modulation of inflammation, increase of gut permeability, contribution to visceral hypersensitivity (increased perception to pain) and modulation of the gut motility. Microbiota communicate with the BGA through different mechanisms: 1) direct interaction with mucosal cells (endocrine message), 2) via immune cells (immune message) and finally 3) via contact to neural endings (neuronal message) (13). These changes can be shown using so called functional magnetic resonance imaging (MRI) techniques (18). IBS is a functional disease and its diagnosis is mainly based on the exclusion of organic disease.
Later during the course of this disease due to anxiety and the upregulation of immune system an irreversible state of self-perpetuation takes place (42). From a diagnostic point of view, it is very important to associate the symptoms to an exposure to stress.
After taking a complete medical history of the patient, a through physical examination of the patients should be performed (45-47). The impact of IBS symptoms on patients is often associated with feelings of shame, fearfulness or embarrassment, which patients perceive to be poorly understood by physicians or family.
The recent advances in the elucidation of the pathogenesis of IBS have resulted in the development of novel therapies. In addition to reduction of colonic contraction by antispasmodics, tricyclic antidepressants (TCA) and selective serotonin reuptake inhibitors SSRI such as fluoxetine (10-40 mg daily), citalopram (20 mg daily), sertraline (25-100 mg daily) and escitalopram (10 mg daily) are effective in the treatment of chronic pain in IBS patients. Despite the high number of studies using probiotics in IBS patients, a lot of new questions have been left unanswered such as the optimal dose, its role in combination therapy, strain specific activity, stability within GI tract, possible development of antibiotic resistance and the duration of therapy. The role of psychological stress in inflammatory bowel disease: quality assessment of methods of 18 prospective studies and suggestions for future research.
Toll-like receptors (TLR) and nucleotide-binding oligomerisation domain-like (NOD) receptors recognise patterns of bacterial signals.
At 36 weeks gestation there is a sharp decrease in the incidence of NEC, supporting the concept that gut maturation provides significant protection against development of the disease [4].
Effectiveness of probiotics in irritable bowel syndrome: Updated systematic review with meta-analysis. Constipation-predominant irritable bowel syndrome: a review of current and emerging drug therapies. So, whether you’re suffering from chronic headaches, skin conditions, depression, joint pain, or digestive issues, you must first put out the fire in your gut. However, there are some specific Paleo-friendly foods that you can focus on consuming on a regular basis to promote healing. Adding turmeric to your food or taking it in capsule form can help reduce the inflammation in your gut and promote healing. Examples of fermented foods are apple cider vinegar, kefir (coconut, dairy, or water versions), yogurt, kimchi, and sauerkraut.
Examples of foods rich in prebiotics are sweet potatoes, winter squash, pumpkin, cantaloupe, honeydew, honey, zucchini, and artichokes. She dealt with chronic digestive issues for over 10 years, and it was significantly affecting her quality of life.
But have you considered the actual close connection…Continue reading40 Turmeric Recipes, The Ultimate Paleo SpiceTurmeric is known as one of the healthiest natural foods on Earth. Goitrogens get…Continue reading3 Sweet Potato Toast RecipesThe best thing to hit the toaster since sliced bread. Valley Medical Weight Loss may make changes to these materials, or to the products described therein, at any time without notice.
Always seek the advice of your physician or other qualified health care provider with any questions you may have regarding a medical condition or treatment.
Mast cells (MC) are important effectors of brain-gut axis that translate the stress signals into the release of a wide range of neurotransmitters and proinflammatory cytokines, which may profoundly affect the gastrointestinal physiology. It may be real (physical) or perceived (psychological) and posed by events in the outside world or from within.
CRF release in the hypothalamus is the first step in activation of HPA involved in stress response. On the other side the reduction of stress may lead to an improvement of GERD symptoms (22). Different stressors (physiological or physical like infection) may lead to flare-up or exacerbation of complaints. The positive physician-patient relationship can significantly increase the efficiency of the therapy.
At the molecular level, TCA inhibit the re-uptake of both serotonin and norepinephrine, increasing the bioavailability of these neurotransmitters in the synaptic cleft. Probiotics may vary in species, strains, preparation and doses, what makes the interpretation of the efficacy difficult. Scanty mucus and reduced antimicrobial factors allow bacteria to adhere to enterocytes, activating NFKB via TRL leading to enterocyte apoptosis, necrosis and loosening of tight junctions. Broadbent2[1] Department of Microbiology and Immunology, Otago School of Medical Sciences, University of Otago, New Zealand[2] Department of Women and Children’s Health, Dunedin School of Medicine, University of Otago, New Zealand1. Nevertheless, NEC in term and high birth-weight infants is not unknown, although the risk factors appear to be somewhat different [4,6,13]. Try cooking with coconut oil, adding it to your smoothies, or eating a tablespoon by itself. She returned to school to study nutrition, started doing her own research, and trained with functional medicine practitioners.
IBS represents the most important gastrointestinal disorder in humans, and is characterized by chronic or recurrent pain associated with altered bowel motility.
Importantly, stress evokes adaptive responses that serve to defend the stability of the internal environment and to ensure the survival of the organism (1).
Interestingly, during stress exposure the amount of reflux does not always increases, but the probability of a feeling of reflux as heartburn increase. In other words, providing more information to the patient and reassuring that IBS represents a functional disease of the gut, and may play an important role in the therapy of IBS. Patients with IBS have increased prevalence of lactose, fructose or sorbitol intolerance (49). Bacterial translocation may be increased by presence of enteric viruses or microbial and other toxins. IntroductionNecrotising enterocolitis (NEC) is a progressive disease of the neonatal intestine beginning in the distal ileum and proximal colon and characterised by inflammatory necrosis [1,2]. The introduction of enteral feeds, particularly formula milk, and subsequent colonisation of the neonatal intestinal tract with bacteria are believed to be significant risk factors in the development of NEC [4,6,19].
She now helps clients restore their health naturally through diet and lifestyle changes and necessary diagnostic testing to uncover the root cause.
The diagnostic testing for IBS patients include routine blood tests, stool tests, celiac disease serology, abdominal sonography, breath testing to rule out carbohydrate (lactose, fructose, etc.) intolerance and small intestinal bacterial overgrowth. The pituitary gland responds to CRF by releasing of adrenocorticotropic hormone (ACTH) to stimulate adrenal glands secretion of the stress hormone cortisol (12).
Generally, the treatment for GERD, especially in those who are not responsive to anti-reflux therapy (PPI), requires further evaluation of potential effect of stress on patients subjected to PPI therapy (23). Serotonin stored in enterochromaffin cells (ECC) plays a crucial role in the motility, visceral sensitivity and secretion.
In recent years alpha 2 delta (a2d) ligands, gabapentin and pregabalin have been shown to reduce visceral pain perception in IBS patients (61).
It typically affects low birth-weight, preterm infants who account for the majority (70–90%) of cases [3–5]. Not only does formula milk lack the gastrointestinal protective, anti-inflammatory and maturation factors present in breast milk, it can be a source of Cronobacter sakazakii, a neonatal pathogen implicated in some cases of NEC [19].
She is a firm believer in the role that real food, a balanced lifestyle, and a positive attitude plays on overall health. These materials are provided as is without warranty of any kind, expressed or implied, including but not limited to the implied warranties of merchantability, for any particular purpose or non-infringement.
Colonoscopy is recommended if alarming symptoms are present or to obtain colonic biopsies especially in patients with diarrhoea predominant IBS. Since gastroenteritis may play an important role as a trigger in the development of IBS, the physician should ask whether the patient had the gastroenteritis in the past history. Further drugs effective in IBS treatment include antimuscarinic agents, µ-opioid antagonists, CRF antagonists, chloride channel opener and even melatonin (50).
Finally, pre- and probiotics may positively influence the visceral hypersensitivity and reduce bloating in IBS patients. Diversity of enteric microbiota and normal gut motility prevent a bloom of one type of bacteria.

Since the 1960s, advances in medical care have raised the survival rate for preterm infants with increasingly shortened gestation periods, resulting in a concomitant surge in NEC cases. Early research concentrated on the role of hypoxia and ischaemia, with the idea that the subsequent mucosal injury due to lack of oxygenation initiates NEC through promotion of bacterial translocation and the inflammatory cascade [1]. You can visit her website and blog for FREE digestive wellness tips, recipes, and healthy living advice. The management of IBS is based on a multifactorial approach and includes pharmacotherapy targeted against the predominant symptom, behavioural and psychological treatment, dietary alterations, education, reassurance and effective patient-physician relationship.
A careful history and physical examination may reveal clues that suggest a coexistence or alternative diagnosis, such as small intestinal bacterial overgrowth or celiac disease (CD). For moderate symptoms, identification and modification of exacerbating factors, psychotherapeutic and behavioural techniques aimed at the predominant symptoms are recommended. This last group of drugs show a positive effect on IBS via antioxidative, anti-inflammatory and anti-motility effects.
The overall incidence of NEC is generally accepted as ranging from <1% to 5% of neonatal intensive care unit (NICU) admissions, or up to 5 cases per 1,000 live births [4–6].
Many animal models of NEC have subsequently relied on reproducing this type of damage [5,20,21]. Jen offers private health coaching to individuals who are struggling with chronic digestive problems as well as an exclusive online program designed to Heal Your Digestion. When evaluating for the stress-induced condition in the upper GI tract, the diagnostic testing includes mainly blood tests and gastroscopy to rule out GERD and peptic ulcer disease. Melatonin strongly prevents the exacerbation of colitis caused by stress as shown in appropriate animal models (51).
Kosloske et al suggested the ‘dive reflex’, whereby blood flow is diverted away from the GI tract to vital organs, as one mechanism of intestinal injury but current opinion, based on analyses of risk factors over several decades, favours a secondary role for hypoxia-ischaemia [5]. The therapy for these conditions is mainly based on the inhibition of gastric acid by proton pump inhibitors and eradication of Helicobacter pylori-infection.
Caplan reported NEC rates for VLBW infants vary greatly across countries, ranging from 1.5% in Japan to 28% in Hong Kong, with racial disparity apparent in VLBW black infants who have an increased risk and greater associated mortality [5,8].
Nevertheless, the fact that NEC most commonly occurs in the distal ileum and proximal colon, the watershed areas of the mesenteric arteries, suggests inadequate or disordered blood circulation constitutes a risk factor in some circumstances [1,22].
Additionally, melatonin an important mediator of brain gut axis has been shown to exhibit important protective effects against stress-induced lesions in the gastrointestinal tract. Despite advances in neonatal care, the overall mortality remains high at around 20–30% [3,8-10]. Prenatal circulatory events, umbilical and aortic catheterisation with dispersion of small emboli and congenital heart disease have been linked to NEC, but occur in a minority of cases [2,4].
Finally, probiotics may profoundly affect the brain-gut interactions ("microbiome-gut-brain axis") and attenuate the development of stress-induced disorders in both the upper and lower gastrointestinal tract. An estimated 20-40% of infants with NEC require surgery, which has a case fatality rate of up to 50%, the smallest, least mature infants having the worst prognosis [5].
Preterm neonates are more susceptible to hypoxia and intestinal ischaemia than term neonates because of poor vascular resistance [1,4,22].
Further studies on the brain-gut axis are needed to open new therapeutic avenues in the future.
Most cases of NEC are sporadic with no clear seasonal distribution, but outbreaks have been documented [5].
However, there is a stronger association between NEC, prematurity, enteral feeding and the presence of bacteria in the GI tract than hypoxia-ischaemia [1,5,22]. Treatment of NEC is mainly supportive with the administration of broad-spectrum antibiotics while surgery is indicated for intestinal perforation or removal of necrotic bowel segments. NEC complications and sequelae include serious neurodevelopmental delay, poor growth, intestinal obstruction due to scarring, short bowel syndrome, and liver failure due to prolonged hyperalimentation [6,9].
The terms TANEC (Transfusion Associated NEC) and TRAGI (Transfusion-Related Acute Gut Injury) have been coined, referring to this association [25,31].
Clinical classificationThe classification system of Bell has historically proved important in defining three main stages: suspected, definite and advanced NEC [11]. A recent meta-analysis examining evidence for the association concludes that recent transfusion is associated with NEC, and that transfusion-associated NEC has a higher risk of mortality than NEC which was not preceded by transfusion [25].
Modifications to Bell’s criteria have provided a more detailed system of clinical staging as shown in Table 1 [12,13]. However, Gordon et al and others have challenged the belief that NEC is a single entity, preferring to view it as an umbrella term for a number of separate diseases with some common features [13,14]. Prior to concern about TRAGI, Doppler studies have shown a decrease in neonatal superior mesenteric blood flow during and after blood transfusion [32]. Although relatively uncommon, conditions, which mimic neonatal NEC, such as focal bowel perforation, intussusception, ecchymotic colitis, appendicitis and shigellosis, have been reported and may complicate the clinical diagnosis [14-18]. The reason for this is not clear, but blood transfusion appears to have wide-ranging effects on haemodynamics, possibly as a result of changes in the microcirculation.
Digestion of food requires a major increase in gut blood supply and it has been suggested that limiting or ceasing milk feeds before, during and after a blood transfusion in susceptible babies may decrease the risk of TRAGI. Any trial of an intervention for TRAGI prophylaxis would need large numbers, requiring a multicentre approach.There are other characteristics of the preterm infant favouring the development of NEC. The combination of poor gut motility and under-production of mucous decreases clearance and increases exposure of the epithelium to potentially harmful components of the luminal contents [1,5,19]. Moreover, induction of foetal hypoxia can further reduce postnatal intestinal motility [1].
Bacterial overgrowth, as indicated by a positive hydrogen breath test, is considered to be a further consequence of delayed transit time and may promote NEC through increasing bacterial translocation from the intestinal lumen into the tissues or through exposure to high concentrations of bacterial antigens [33,34]. More recently, it has been proposed that genetic polymorphisms in the genes encoding the interleukin (IL) 4 binding receptor alpha chain and the chemokine IL-8 may also be a risk factor for NEC [35].
Breastfeeding, handling by the mother and exposure to environmental bacteria create further opportunities for gaining new species [6]. Colonisation takes place in the first few days of life and is influenced by a multitude of factors such as mode of delivery, type of feeding (breast milk or formula), gestation age, hospitalisation, the surrounding environs, maternal infection and antibiotic therapy, with mode of delivery and type of feeding considered the most significant [36]. Whereas breast fed infants are regarded as having an enteric microbiota rich in bifidobacteria, a more diverse microbiota, including potentially pathogenic groups such as Clostridium and Enterobacteriaceae, has been traditionally associated with formula fed infants.
However, modern infant formulas more closely represent breast milk, shifting the gut microbiota towards beneficial species such as lactobacilli [19,36]. Breast-fed infants are less likely to develop NEC as breast milk contains many protective bioactives [1].
The initial neonatal microbiota consists of facultative anaerobic bacteria such as Enterobacteriaceae, enterococci, streptococci and staphylococci, which are present within days of birth [33].
These bacteria consume oxygen providing the reducing conditions required for the growth of obligate anaerobes, typically bifidobacteria, clostridia and Bacteroides, appearing one to two weeks later [33,36]. It is well established that the intestinal microbiota has a profound effect on gut health, influencing physiology and metabolism, as well as maturing the infant immune system and protecting against pathogens [19,33]. However, in the preterm infant, the normal succession of bacterial colonisers may be interrupted by the administration of broad-spectrum antibiotics, gut immaturity, acquisition of nosocomial bacteria in the NICU and placement of orogastric or nasogastric feeding tubes, resulting in a more restricted enteric microbiota with delayed colonisation with bifidobacteria and without the individual differences seen in the healthy, term neonate [6,33,37].
The relationship between delayed succession, bacterial overgrowth and NEC is discussed in more detail elsewhere in this chapter.2.
The role of microbes in NECThe belief bacteria are crucial for the development of NEC stems from a number of clinical and experimental findings. In two studies totalling over 100 infants, Santulli et al and Schullinger et al were the first to credibly establish bacterial colonisation of the neonatal intestine was a requirement for this disease [38,39]. NEC does not usually occur immediately post-partum but some days later, when feeding has usually commenced and there is ample opportunity for substantial intestinal colonisation. The reason for this difference is not entirely clear, but it may relate to a difference in pathophysiology, with bowel ischaemia being the predominant factor in early-onset NEC and cytokine priming being the predominant factor in late-onset NEC.
The case for bacterial colonisation is further strengthened by the absence of NEC in ischaemic, ileal segments of germ-free rats and in infants who are stillborn [42,43]. Regardless of the initiating factors, pathological changes certainly involve bacteria as the intramural gas produced in pneumatosis intestinalis contains hydrogen of bacterial origin [44]. Demonstration of bacteria and bacterial DNA in the intestinal wall of resected segments from NEC infants supports this finding [45,46]. Epidemiological studies also indicate NEC has an infectious origin as it may occur in clusters of related cases which are amenable to infection control measures [47]. Moreover, prevention of NEC has been achieved through the administration of enteral antibiotics [48]. Bacteraemia and endotoxinaemia are frequent complications of NEC but are more likely to be sequelae rather than the actual cause [49,50]. Microbes implicated in the aetiology of NECEnteric anaerobesAmong the enteric anaerobes, Clostridium species are notorious for their proteolytic, saccharolytic, toxin and gas producing activities, making them ideal candidate microorganisms for the specific pathogen theory.
Pederson et al emphasised the similarities between neonatal NEC and gas gangrene of the bowel, suggesting that ischaemic lesions were ideal sites for clostridial invasion, the anaerobic conditions of the bowel favouring conversion of the spores to toxin-producing bacteria [51].
Studying the histology of resected intestinal segments from NEC infants led these researchers to conclude Clostridium perfringens (C. Parallels were drawn with pigbel, an acute necrotising enterocolitis common in older children and adults in Papua New Guinea, caused by type C porcine Clostridium perfringens [52,53]. As the oxygen tension of healthy tissue is likely to inhibit growth of clostridia, pre-existing tissue necrosis may be exigent. The hypothesis that clostridial alpha-toxin plays a major role in NEC has never been proven [57].C. Somewhat surprisingly, colonisation with this microbe seems not to be a risk factor for NEC, probably because the neonatal bowel is tolerant to C. Other intestinal anaerobic genera have not been fully investigated, probably due to the difficulty of culturing under strict anaerobic conditions.
Despite the prevailing view that non-sporing anaerobes are frequently absent in the intestinal tract of preterm infants, a DNA-based study indicated Bacteroides were abundant, and a review of anaerobic bacteraemia in a NICU carried out by Noel et al indicated anaerobic bacteraemia was frequently linked to NEC [63,64]. It is likely that further culture-independent studies will be able to better define the contribution these bacteria make to the pathogenesis of NEC.StaphylococciCoagulase negative staphylococci (CoNS) are commonly found in the stools of NEC infants and have been associated with significant disease [65,66]. The role of staphylococcal delta(?)-toxin was examined by Scheifele et al and Scheifele and Bjornson, who believed that toxin positive CoNS were enteropathic [67,68]. Moreover, it could be detected in the stools of infants colonised with ?-toxin producing CoNS [67,68].We investigated 25 CoNS isolates from the stools of six NEC and six control infants in Dunedin Hospital NICU. A diagnosis of NEC was made on the basis of clinical indications and pneumatosis intestinalis or peritonitis on X-ray as described previously [69]. PCR primers for the ?-toxin gene were based on sequence data published by Tegmark et al and PCR conditions were as described by McIntosh [70,71]. The results, summarised in Table 2, suggest that the ?-toxin gene was frequently present in CoNS isolated from the infants (23 of 25 isolates) but that insufficient toxin was produced to cause a CPE in either of the cell lines tested compared to the Staphylococcus aureus control, which induced cell death.
The toxic strain was positive for the ?-toxin gene by PCR and Southern hybridisation, although we lacked the specific antibody required to ultimately prove the cytopathic activity was ?-toxin mediated. The ?-toxin theory has been largely dismissed, but our research suggests there may be occasional strains of S.
The findings of Scheifele et al may reflect the dominance of such strains at a particular time in their NICU. There is one instance of a small outbreak of NEC and bacteraemia associated with a ?-toxin-producing methicillin resistant S. In addition, preterm infants exhibit deficiencies in immune responses to CoNS, suggesting they may cause more aggressive infections in this group compared to term neonates [75]. Large, relatively stable reservoirs of CoNS have been identified in the faces, ear region, axillae and nares of preterm infants, with smaller, less stable populations elsewhere on the skin, indicating the widespread presence of this group of bacteria and their easy access to the GI tract [76].

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