GERD (gastroesophageal reflux disease) remains extremely common, affecting an estimated 40% of Americans on at least a weekly basis, despite widespread use of acid-suppressing therapies such as antacids, H2 blockers, and proton-pump inhibitors (PPIs). I have written previously (1) about my concerns regarding long-term use of these medications, particularly the decreased absorption of critical minerals and other nutrients caused by lack of adequate stomach acid. In this article I would like to highlight some evidence-based non-pharmacologic treatment options that improve normal function of the esophagogastric junction and may therefore decrease reflux occurrence and symptoms and ultimately the need for PPIs.
Over the past 10 years or so there has been increasing recognition within the medical literature that the diagnosis of GERD actually consists of a spectrum of conditions. (2, 3, 4, 5) The classic symptom picture of erosive esophagitis (with reflux of stomach acid into the esophagus that causes tissue damage over time) appears to describe a minority of patients with chronic heartburn, while non-erosive reflux (NERD) subtypes account for 50-85% of cases. Most NERD patients are only identified when their symptoms fail to improve on empiric PPI therapy.
“True” NERD involves abnormal acid exposure within the lower esophagus but no mucosal tissue changes (such as erosions or ulcerations) are visible on upper endoscopy. The other subtypes of NERD are designated as esophageal hypersensitivity and “functional” heartburn; these do not involve abnormal acid exposure but likely involve increased chemical and mechanical sensitivity within the esophagus for a variety of reasons including altered mucosal integrity and/or immunity, increased nerve density, and central sensitization. (6, 7, 8, 9, 10, 11, 12)
Proper workup and diagnosis of reflux symptoms is therefore essential for individualized treatment. At minimum, I prefer to have all patients with GERD undergo an upper endoscopy procedure. EGD (esophagogastroduodenoscopy) examines the health of the mucosa in the esophagus, stomach, and duodenum. This technique identifies erosive esophagitis when it is present (so we can use acid-suppressing medications when they are most needed) and allows biopsy of tissue samples to assess for conditions that can mimic or exacerbate reflux such as eosinophilic esophagitis, atrophic gastritis, H. pylori infection, etc.
The best test for diagnosing the subtypes of NERD seems to be combined impedance and pH testing, which measures the frequency and duration of reflux episodes as well as the acidity of the refluxate fluid. Currently this technique is used mostly in research studies but I expect it will become more common in clinical practice over the next few years.
The normal anatomy at the junction of the esophagus and stomach is intended to prevent reflux. The stomach should sit in the abdomen below the diaphragm, positioned so the lower esophageal sphincter (LES) muscle is reinforced by the crural section of the diaphragm. Resting pressure within the LES is normally maintained at 10-30 mmHg, with fluctuations throughout the day (lowest after meals and highest at night). Pressure at the esophagogastric junction (EGJ) also varies with breathing; during inhalation the contraction of the crural diaphragm increases EGJ pressure up to 3-4x. (13)
Gastroesophageal reflux occurs when either or both parts of this muscle barrier become weakened, thereby allowing frequent transient LES relaxations (TLESRs). This phenomenon is a normal venting mechanism (i.e. to allow belching) when the stomach is distended by food or gas. However, in GERD patients the baseline LES pressure tends to be much lower than normal, often below 10 mmHg. (14)
Not all the reasons for EGJ hypotonia are well understood, but parasympathetic nervous system dysfunction appears to be a major underlying cause. The crural diaphragm and much of the esophagus are innervated by the vagus nerve in addition to spinal nerves. (15) Since the parasympathetic nervous system is responsible for “rest and digest” functions, it makes sense that chronic activation of the sympathetic nervous system (“fight or flight”) would have numerous negative impacts on digestive function:
- altered gastrointestinal motility;
- increased visceral perception;
- decreased gastrointestinal secretion;
- increased esophageal and intestinal permeability; and
- decreased regenerative capacity of gastrointestinal mucosa and mucosal blood flow. (16, 17)
Chronic stress has been shown to aggravate GERD symptoms due to inhibition of the LES, increased esophageal sensitivity to acid reflux (18), impaired ability of the stomach to accommodate and mechanically digest food, and delayed gastric emptying. (19)
Weakness of the crura combined with chronic or episodic increases in intra-abdominal pressure (such as from obesity, pregnancy, exertion while holding the breath, weightlifting, jumping on a trampoline, etc.) allow stretching of the fascial attachments between the esophagus and diaphragm and eventually the protrusion of the stomach through the hiatus (opening) of the diaphragm, creating a hiatal hernia. When this occurs, the diaphragm no longer acts as part of the anatomical reflux barrier but rather contributes to reflux as it compresses the upper part of the stomach. A “sliding” type of hiatal hernia is most common and may occur in 40% of the general population. (20) Hiatal hernia can often be identified by tenderness at the Riddler hiatal hernia reflex point located just below and just to the left of the xyphoid process at the base of the sternum. (21) Although some hernias may be identified on EGD, the best test to detect a hiatal hernia remains a barium swallow x-ray. (22) A large number of hiatal hernias may never be diagnosed until found incidentally during abdominal surgery – as many as 43% in one case series. (23)
From the above discussion, we see that an optimal treatment approach for GERD would attempt to improve the normal structure and function of the esophagogastric junction. The plan would:
- soothe, protect, and stimulate regeneration of the esophageal mucosa;
- improve the muscle tone of the LES and crural diaphragm and promote downward GI motility; and
- identify and address dietary and lifestyle factors that aggravate reflux.
(Disclaimer: please note that none of these recommendations should be considered a substitute for your individualized medical evaluation and treatment).
Part 1: Soothe, protect, and stimulate
- Acid-suppressing medications as needed for short-term use (ideally ≤ 2 weeks), particularly when erosive esophagitis or severe hypersensitivity are present
- Demulcent herbs to soothe irritated mucosa (24)
- Hyaluronic acid and chondroitin to accelerate tissue healing (25, 26)
- Melatonin to stimulate mucosal blood flow (27)
- Zinc carnosine to support mucosal cell repair (28, 29)
- Probiotics to support mucosal immunity and parasympathetic nervous system tone (30, 31)
Part 2: Improve EGJ pressure and promote downward GI motility / energy flow
- Visceral manipulation of the stomach can sometimes be used to reduce a hiatal hernia. (32) Unfortunately, this technique may not be permanent for patients with a sliding hiatal hernia but it may become more useful over time.
- Chiropractic evaluation and treatment often reveals muscle tightness and bony restrictions in the lower thoracic spine. Thoracolumbar kyphosis and scoliosis can negatively impact diaphragm function and increase intra-abdominal pressure with compression of the esophagus and stomach. (33)
- Myofascial release of the diaphragm may be useful, especially following chiropractic care. (34)
- Acupuncture has been shown to promote downward/forward motility through the digestive tract in animals and humans. (35, 36)
- In Chinese medicine, GERD is considered a manifestation of qi that has become stagnant; this is often associated with holding things in on an emotional level. Counseling and journaling may be useful ways of learning to “let it go, let it go!” (37)
- Deep breathing exercises should be performed to engage the diaphragm. Slow abdominal breathing improves parasympathetic nervous system tone (38) and decreases esophageal sensitivity. (39) There is also exciting research which suggests that the diaphragm can be strengthened like any other muscle and therefore breathing training may improve GERD symptoms by increasing muscle tone in the LES and crural diaphragm. (40) Several studies have used a Threshold IMT device for progressive resistance breathing training (like lifting weights for your diaphragm). (41, 42)
- Supine bilateral leg raises have been shown to increase LES pressure; (43) they also build core strength.
Part 3: Address diet and lifestyle habits
A study by Yuan et al. determined the major lifestyle risk factors among 699 patients with GERD. These are tabulated here both by significance (P values < 0.05, which are underlined) and likelihood (odds ratio > 1.0): eating too quickly (< 10 minutes per meal and chewing < 10 times per bite) (OR 4.06), eating beyond fullness (2.85), wearing restrictive clothing (eg. corset, girdle) (2.19), obesity with BMI > 24 (1.81), eating very hot foods (> 60 °C) (1.81), lying down after eating (1.54), smoking (at least one cigarette per day) (1.52). (44)
The 699 patients were followed for 6 months. All participants were treated with PPI therapy (20 mg omeprazole) and counseled on 20 lifestyle factors. Of the 464 patients who followed all lifestyle recommendations, 56.9% had substantial improvement and 41.4% had moderate improvement; only 1.7% had no improvement. (By contrast, of the 235 patients who did not follow lifestyle recommendations, 26.4% had substantial improvement, 59.6% had moderate improvement, and 14.0% had no improvement).
From this list we can easily observe that relatively simple changes may have a big impact. General dietary recommendations as supported by the most recent research literature are as follows:
- Eat slowly and chew food thoroughly. This is probably the single most important modifiable risk factor for most patients. Eating too quickly encourages overeating which distends the stomach (increasing TLESRs and reflux episodes) and slows digestion and therefore delays gastric emptying. Swallowing large mouthfuls of rough, half-chewed food or very hot food may damage mucous membranes. Habitual rapid food intake may eventually cause ineffective esophageal motility; chewing gum may strengthen weakened esophageal muscles. (45)
- Limit snacking between meals; after every feeding, gastric acid is secreted and the acid pocket reforms. (46) Eating only two meals per day has been shown to decrease symptoms in GERD patients with reflux esophagitis within 2 weeks. (47)
- Avoid drinking more than a few ounces of fluids during mealtime (30 minutes before food and 60-120 minutes after) to avoid over-filling the stomach and diluting stomach acid. (48)
- Limit coffee, tea, and soda (or similar carbonated beverages) which are associated with increased reflux; replacing 2 servings of these beverages with water can decrease GERD symptoms. (49)
- The best food choices will vary person to person. Acidic and spicy foods tend to be most problematic due to direct irritation of the mucosa; alcohol, coffee, chocolate, and mint decrease LES muscle tone. (50) Food intolerance testing or an elimination diet may be helpful for identifying food triggers. Almost all patients in one retrospective study were intolerant to at least 5 food items; milk, lettuce, coffee, yeast, pork, tuna, sole, rice, asparagus, and eggs were most common. (51)
- Fatty foods can trigger reflux in some patients. (52) However, high carbohydrate intake can also contribute. A study by Pointer et al. of dietary habits among 144 overweight women with GERD revealed that sugar intake was significantly associated with reflux symptoms, with the odds increasing by 13% for every additional teaspoon (4.2 g) of sugars consumed. Over the 16 weeks of the study, carbohydrate intake was decreased from 45 to 35% of total calories (1/2 complex carbs and 1/2 simple carbs) and fat intake was increased from 38 to 48% of total calories (1/3 saturated, 1/3 monounsaturated, 1/3 polyunsaturated), while keeping protein intake the same at 17% of total calories. All of the women with GERD had resolution of their symptoms and were able to discontinue PPI medications within 10 weeks! (53) Other studies have shown that very-low carbohydrate diets (< 20 grams per day) also reduce distal esophageal acid exposure and improve heartburn symptoms. (54, 55) GERD triggered by carbohydrate intake is typically related to the effects of bacterial fermentation of undigested starches in the large intestine; studies by Piche et al. have shown that consumption of fermentable starches and the presence of short-chain fatty acids in the colon dramatically decreases LES pressure by 10 mmHg, increasing the number of TLESRs and reflux episodes. (56, 57) Anywhere from 2-20% of dietary starches may remain undigested in healthy people; malabsorption conditions may increase this percentage, and dysbiosis conditions (such as SIBO) may increase the rate of fermentation within the intestines. Interestingly, increased intake of non-fermentable fiber such as psyllium 5 grams 2-3x per day can decrease GERD symptoms comparable to omeprazole. (58, 59)
- Weight loss resulting in a decrease of ≥ 2 kg/m2 BMI and ≥ 2 inches waist circumference improves GERD sxs in obese patients with baseline BMI > 25 by decreasing intra-abdominal pressure. (60)
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