Gastroesophageal Reflux Disease (GERD)
The Development of GERD
Occasionally, increased pressure within the abdomen or a momentary relaxation of the esophageal sphincter can force some stomach contents back into the esophagus. Everyone experiences occasional reflux, which can result from a large meal, physical activity, or reclining after a meal. Other physiological conditions, both normal (pregnancy) and pathological (obesity) can also increase the likelihood of reflux. As long as gastric reflux is occasional, and promptly cleared from the esophagus, there is little risk of damage (Kuo 2006).
Prolonged reflux, however, can present serious health concerns. Repeated exposure of the esophagus to the harsh chemistry of the stomach can have deleterious effects on esophageal tissue (Stefanidis 2010).
It is important to note that while stomach acid is most often associated with reflux disease, there are other compounds, such as bile acids, that may be present in refluxed digestive juices. This is an important consideration in the diagnosis and treatment of GERD, especially when the disease is resistant to acid-suppression therapy. Many patients with treatment-resistant GERD (despite use of acid-blocking pharmaceutical therapy) may have bile in their reflux (Bredenoord 2012; McQuaid 2011). In one study, over half of the patients with reflux symptoms had 24-hour esophageal pH measurements within normal limits (Martinez 2003; Shi 1995). In some cases, stomach acid may partially neutralize damaging alkaline reflux from lower parts of the digestive tract, thus protecting the esophagus. In an animal model of small intestinal reflux, rats on acid-blocking therapy demonstrated more esophageal damage and Barrett’s esophagus (see below) than control animals, a finding consistent with some human observational studies (Nasr 2012).
A functional (transient LES relaxation) or mechanical (hypotensive LES) problem of the LES are the most common causes of GERD. Transient relaxation of the LES can be caused by foods (coffee, alcohol, chocolate, fatty meals), medications (beta-agonists, nitrates, calcium channel blockers, anticholinergic drugs), hormones (e.g., progestins), and nicotine (Tutuian 2010).
Allergy is not a risk for progression to GERD, but it can increase the incidence of a related condition - eosinophilic esophagitis (EE). EE is characterized by upper gastrointestinal symptoms (some of which resemble GERD such as food impaction, heartburn, or difficulty swallowing) as well as the presence of eosinophils (a type of white blood cell often involved in allergic immune responses) in the esophagus (Arora 2004). Individuals with EE often have normal levels of acidity in the esophagus. Children with EE appear to be unresponsive to acid-blocking therapies. Once thought a rare condition, it is being increasingly recognized as a cause of GERD-like symptoms in adults and, especially children (Gonsalves 2009; Foroutan 2010). Inhaled and food allergens are thought to be responsible for the progression of EE. As such, it is commonly managed by either eliminating the source of the allergen or with steroids (Arora 2004). For individuals with GERD-like symptoms that have been unresponsive to conventional GERD treatments, an elimination diet based upon IgE food allergy testing may be useful (Spergel 2005).
Previous evidence indicates that food sensitivities may contribute to GERD-related irritation of the esophagus (Price 1978). Since immunoreactivity to certain foods is linked with GERD, especially in children (Semeniuk 2009), then using a convenient blood test to assess IgG antibodies against specific foods may prove to be a useful tool for those whose GERD symptoms fluctuate with diet. While clinical studies have yet to evaluate the potential of an elimination diet based upon IgG antibody testing for the relief of GERD symptoms, similar approaches have been successful (Gonsalves 2012).
For more information about food allergy and/or sensitivity testing, refer to the Allergies protocol.
H. pylori Infection Infection with the bacteria Helicobacter pylori, which resides in the stomach and is associated with ulcers of the gastric lining, has been observed in up to 40% of GERD cases; though it is unclear whether H. pylori infection causes GERD (O’Connor 1999; Ferri 2012). Until recently some experts believed that H. pylori infection possibly conferred some protection against development of GERD (Haruma 2007). However, more recent research suggests that this is likely not the case (Saad 2012; Yaghoobi 2010). Furthermore, upon conducting a review of randomized controlled trials, Saad (2012) and colleagues uncovered a significantly lower incidence of GERD symptoms in patients who had undergone H. pylori eradication compared to those who had not.