Reflux (GERD)

Reflux, or Gastroesophageal reflux disease (GERD), is a chronic condition in which contents of the stomach flow back (`reflux`) into the esophagus potentially causing symptoms (e.g., heartburn) and injury to esophageal tissue. GERD is one of the most common health conditions of the gastrointestinal tract.

Common conventional treatment uses proton pump inhibitors (PPIs) but long-term use of acid-blocking drugs can impair nutrient absorption and may lead to deficiencies with dangerous consequences. For example, chronic, high-dose therapy with proton pump inhibitors and histamine-2 receptor blockers can significantly increase the risk of hip fracture (Corley 2010).

In addition to robbing your body of critical nutrients like calcium, magnesium and vitamin B12, PPIs can also cause a rebound effect when they are discontinued, potentially exacerbating GERD symptoms (Khalili 2012; Sheen 2011; Roulet 2012).

Furthermore, conventional treatment strategies call for increasing the dosage or adding another acid blocking drug when PPIs fail to relieve GERD symptoms.

 

Basics about the Esophagus and Digestive Tract

The esophagus connects the mouth to the stomach. After food has travelled down the esophagus, they are emptied into the acidic environment of the stomach for chemical and mechanical digestion.

While the thick cellular layer of the stomach is a suitable barrier against stomach acid, the thinner mucous membrane of the esophagus was not designed to withstand such harsh conditions. To protect the esophagus from the potential back-flow of stomach contents (reflux), a sphincter is located at the junction between the esophagus and stomach, called the gastroesophageal or lower esophageal sphincter (LES). This sphincter, a circular band of thickened muscle, surrounds the lower esophagus and pinches it closed. The LES is usually closed. It opens to allow swallowed food or drink to enter the stomach, a reflex that is triggered by the act of swallowing.

 

GERD Symptoms & Complications

Aside from heartburn, other symptoms associated with GERD include nausea, increased saliva production, globus (the sensation of a constant lump in the throat), trouble swallowing, bad breath, and dental erosion (Stanghellini 2004). Sleep disturbances and nocturnal choking are also possible (Kamal 2010).

Prolonged exposure of the esophagus to gastric reflux can result in dramatic alterations to its function. Serious complications of GERD include:

Peptic Stricture – healing of ulcerations can lead to the deposit of fibrous scar tissue as well as a stricture (i.e., narrowing) of the esophagus (Rosemurgy 2011). Segments of the esophagus with stricture are usually thickened, stiff, and may be shortened. As the esophagus shortens, it can pull the stomach up through the esophageal hiatus, resulting in hiatal hernia (Horvath 2000).

Barrett’s Esophagus – a change in the cellular makeup of the mucous membrane of the esophagus. The reversible replacement of one differentiated cell type with another mature differentiated cell type is called metaplasia, and is distinct from the cellular transformation that occurs during cancer progression.

Esophageal Cancer – 2 major types of esophageal cancer are esophageal squamous cell carcinoma and esophageal adenocarcinoma. Esophageal adenocarcinoma EAC arises from metaplasia of tissue in the lower part of the esophagus, and is thought to develop as a result of long-term GERD and Barrett’s esophagus (Siersema 2007). 

 

 

Everyone experiences occasional reflux, which can result from a large meal, physical activity, or reclining after a meal. Other physiological conditions, such as pregnancy and 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).

A functional (transient LES relaxation) or mechanical (hypotensive LES) problem of the LES (lower esophageal sphincter) 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).

Previous evidence indicates that food sensitivities may contribute to GERD-related irritation of the esophagus (Price 1978).  Using a convenient blood test to assess IgG antibodies against specific foods may be a useful for those whose GERD symptoms fluctuate with diet.

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).

 

An Alternative Theory on the Cause of GERD

Hypochlorhydria – Alternative medical practitioners suggest that, rather than too much stomach acid, it may be too little acid that causes GERD (Wright 2001). The proposed etiology involving hypochlorhydria argues that just because acid is being refluxed does not necessarily mean that there is too much in the stomach to begin with. The hypochlorhydria theory suggests that inadequate stomach acid reduces lower esophageal sphincter tone, thereby allowing stomach contents to be refluxed giving rise to GERD symptoms.

Hydrochloric acid (HCl) in the stomach activates enzymes that help break down proteins and stimulates other digestive processes. The hypochlorhydria theory of GERD proposes increasing stomach acidity to alleviate symptoms, as opposed to lowering it, which is the conventional approach. To do this, betaine HCl is used to deliver additional hydrochloric acid to the stomach. This therapy is sometimes preceded by the Heidelberg test to measure the pH of the stomach.

 

 

Up to 50% of patients with GERD experience persistent symptoms, despite taking PPIs regularly (Dibley 2010). Diet and lifestyle interventions are therefore an important adjunct to standard drug therapy. Education on managing stress, proper diet and physical activity has been shown to promote significant improvement in patient’s well-being.

Some diet and lifestyle modifications commonly suggested for GERD patients include:

1. Avoid foods and beverages associated with GERD symptoms. Common dietary components associated with increases in GERD symptoms are:

• Coffee (Bhatia 2011)
• Chocolate (Bujanda 2007)
• Spicy foods (Song 2011)
• Carbonated beverages (Hamoui 2006)
• Alcohol (Grande 1996; Song 2011)

Additional foods that may cause symptoms include tomatoes (cooked and raw), milk, cheese, citrus foods, cakes and pastries (Dibley 2010).

2.Quit Smoking. Smoking increases GERD symptoms by reducing 1) the ability of the LES to remain closed against increases in gastric pressure, and 2) the clearance of reflux from the esophagus (Kaltenbach 2006). The incidence of GERD increases with the duration of smoking. Based upon data from a large population study, long term (> 20 years) daily smoking resulted in a 70% increase in the occurrence of reflux episodes compared to those who have smoked for less than one year (Nilsson 2004).

3.Lose weight. Increased body mass and abdominal adiposity increases pressure on the stomach and lower esophagus. This can stress the lower esophageal valve, hampering its ability to maintain a seal against gastric reflux. Sustained abdominal pressure can also increase the risk of hiatal hernia (Festi 2009).

4.Monitor meal size and macronutrient composition. Fatty foods delay gastric emptying, which may increase the probability of reflux in patients. High-fat meals are also associated with increased risk of esophageal cancer (De Ceglie 2011).  Aside from their direct effects on GERD, limitation of fat, carbohydrate, and total calorie intake are effective methods for weight reduction, which itself is an effective anti-reflux strategy.

5.Avoid eating close to bedtime. GERD patients have long been advised to avoid eating close to bedtime in order to give the stomach adequate time to empty before lying down (DeVault 1999).

6.Elevate the head of the bed while sleeping. Several studies have suggested that raising the head of the bed 8-11 inches, or sleeping on a “wedge”, can reduce the number and duration of reflux episodes (Kaltenbach 2006). This approach uses gravity to help keep stomach contents out of the esophagus. Left lateral recumbency (sleeping on one’s left side) may also reduce GERD symptoms by potentially keeping the LES above the level of the stomach and reducing pressure on the valve (Kaltenbach 2006 ).

7.Limit aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs). Some evidence suggests that NSAID use is associated with GERD (Kotzan 2001). NSAIDs exert their anti-inflammatory activity by inhibiting the activity of pro-inflammatory cyclooxygenase (COX) enzymes. However, the COX-1 enzyme is also important for promoting the formation of the protective mucus lining of the stomach.

 

Nutritional Interventions

Raft-Forming Agents

Raft-forming reflux suppressants have been used to treat GERD for more than 30 years (Hampson 2010). Raft-formers are combinations of a gel-forming fiber (e.g., alginate or pectin) with an antacid buffer (commonly sodium or potassium bicarbonate). When the combination reaches the stomach, chemical reactions cause the release of carbon dioxide bubbles. These bubbles become trapped in the gelled fiber, converting it into a foam that floats on the surface of the stomach contents (hence “raft-forming” agent). Several studies have demonstrated that rafts reduce GERD symptoms by mechanisms independent of acid reduction. They can either move into the esophagus ahead of the stomach contents during reflux (protecting it from exposure) or may act as a barrier to reflux episodes (Mandel 2000). A recent multicenter study of patients with mild to moderate GERD symptoms demonstrated that an alginate-based raft-forming agent was as effective as the PPI omeprazole at reaching an initial heartburn-free period and reducing reflux pain (Pouchain 2012).

The properties of raft-forming agents can be modified by adding calcium salts, which can cross-link fibers and form stiffer gels (Mandel 2000). Raft-formers are most effective when taken after the heaviest meal of the day.

 

Melatonin

Melatonin is a hormone most often associated with the sleep cycle, but is found at levels hundreds of times higher in the gut than in the brain (Werbach 2008). Animal trials of melatonin for GERD symptoms have found it to be not only effective in preventing acid-induced esophageal damage, but also damage caused by digestive enzymes and bile (Konturek 2007). Two human trials have investigated supplemental melatonin on GERD symptoms. In the first, 176 patients on a 6 mg melatonin /multi-nutrient combination were compared to 175 patients on a PPI (20 mg omeprazole). The effects were measured by the length of time it took for the patients to become asymptomatic (defined as no heartburn or regurgitation) for 24 hours. All patients in the melatonin group reported improvement in GERD symptoms compared to two-thirds in the PPI group. Relief was reached faster in the melatonin (7 days) vs. PPI (9 days) group, with a much lower incidence of side effects (Pereira 2006). A second study compared 3 groups of 9 GERD patients, each on a different regimen (3 mg melatonin, 20 mg omeprazole, or both) to a group of healthy control subjects. Heartburn and gastric pain were decreased after four weeks and completely resolved after eight weeks in all treatment groups. However, only the two melatonin groups had significant improvements in LES function (Kandil 2010).

 

Deglycyrrhizinated Licorice (DGL)

Licorice extracts have been shown to support the health of the stomach lining and combat H. pylori – bacterium that can cause ulcers (Wittschier 2009). This may convey benefits to those suffering from GERD, since recent evidence indicates that H. pylori eradication appears to improve GERD symptoms (Saad 2012). Unlike whole licorice, deglycyrrhizinated licorice (DGL) extracts provide beneficial licorice compounds without glycyrrhizin (a component of whole licorice that has been shown to cause side effects). While published, peer-reviewed literature supporting the use of DGL in GERD is lacking, some innovative doctors employ DGL with positive results (Martin 2011).

 

Slippery Elm

Slippery Elm bark (ulmus rubra) contains mucilage, a substance that becomes a slick gel when mixed with water. It has been used traditionally as a demulcent to soothe mucous membranes, especially in the gastrointestinal tract.

It coats and soothes the mouth, throat, stomach, and intestines. It also contains antioxidants that help relieve inflammatory bowel conditions. Slippery elm causes stimulation of nerve endings in the gastrointestinal tract, leading to increased mucus secretion. The increased mucus production may support and protect the gastrointestinal tract against ulcers and excess acidity.

 

 

The following ingredients may promote a healthy chemical environment within the esophagus:

• Raft-forming alginate: Per label instructions
• Melatonin: 0.3 – 5 mg before bed (sometimes up to 10 mg)
• Deglycyrrhizinated licorice (DGL): 760 mg as chewable tablets before each meal
• Slippery elm: 1000 mg, up to 3 times daily

 

The following ingredients may combat side effects of conventional treatments:

• Probiotics: Per label instructions
• Comprehensive multivitamin (containing B-complex vitamins): Per label instructions
• Vitamin B12: 1000 mcg – 5000 mcg daily
• Iron: If deficient
• Calcium: 200 - 1200 mg daily
• Magnesium: 140 mg daily as magnesium-L-threonate; 320 mg daily as magnesium citrate

 

 

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