F3. Functional defecation disorders F3a. Inadequate defecatory propulsion F3b. Dyssynergic defecation G. Childhood functional GI disorders: Neonate/Toddler G1. Infant regurgitation G2. Rumination syndrome G3. Cyclic vomiting syndrome (CVS) G4. Infant colic G5. Functional diarrhea G6. Infant dyschezia G7. Functional constipation H. Childhood functional GI disorders: Child/Adolescent H1. Functional nausea and vomiting disorders H1a. Cyclic vomiting syndrome (CVS) H1b. Functional nausea and functional vomiting H1b1. Functional nausea H1b2. Functional vomiting H1c. Rumination syndrome H1d. Aerophagia H2. Functional abdominal pain disorders H2a. Functional dyspepsia H2a1. Postprandial distress syndrome H2a2. Epigastric pain syndrome H2b. Irritable bowel syndrome (IBS) H2c. Abdominal migraine H2d. Functional abdominal pain ‒ NOS H3. Functional defecation disorders H3a. Functional constipation H3b. Nonretentive fecal incontinence Causes FGIDs share in common any of several physiological features including increased motor reactivity, enhanced visceral hypersensitivity, altered mucosal immune and inflammatory function (associated with bacterial dysbiosis), and altered central nervous system and enteric nervous system (CNS-ENS) regulation. The pathophysiology of FGID has been best conceptualized using biopsychosocial model help to explain the relationships between an individual factors in their early life that in turn can influence their psychosocial factor and physiological functioning. This model also shows the complex interactions between these factors through the brain-gut axis. These factors affect how FGID manifest in terms of symptoms but also affect the clinical outcome. These factors are interconnected and the influences on these factors are bidirectional and mutually interactive. Early life factors Early life factors include genetic factors, psychophysiological and sociocultural factors, and environmental exposures. Genetics – Several polymorphisms and candidate genes may predispose individuals to develop FGID. These include alpha-2 adrenergic and 5-HT receptors; serotonin and norepinephrine transporters (SERT, NET); inflammatory markers interleukin-(IL)10, tumor necrosis factor-(TNF) alpha, and TNF super family member 15 (TNF-SF15); intracellular cell signaling (G proteins); and ion channels (SCN5A). However, the expression of a FGID requires the influence of additional environmental exposures such as infection, illness modeling and other factors. Psychophysiological factors may affect the expression of these genes, thus leading to symptoms production associated with FGID. Sociocultural factors and family interactions have been shown to shape later reporting of symptoms, the development of FGIDs, and health care seeking. The expression of pain varies across cultures as well including denial of symptoms to dramatic expression. Environmental exposures – Prior studies have shown the effect of environmental exposures in relation to the development of FGIDs. Environmental exposures such as childhood salmonella infection