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A Straightforward, Drug-free and Effective Solution
• Western allopathic medicine blames GERD on the flawed and outdated theory of stomach acid overproduction, but GERD is actually due to a lack of stomach acid, which can arise in response to multiple triggers.
• Hydrochloric acid plays a critical role in maintaining the stomach’s pH, which enables the first phase of digestion to occur efficiently.
• GERD symptoms vary widely in both presentation and severity.
• Incorrectly addressing the early stages of GERD as a problem of too much stomach acid turns it into something far more deleterious.
• Antacids, histamine 2 (H2) antagonists and proton pump inhibitors (PPIs) all have serious long-term risks and side effects.
• Factors that can trigger GERD include gut dysbiosis, medications, hiatal hernias, the standard American diet (SAD) and stress.
• Diagnosis of GERD requires a thorough health history and assessment of digestive function and inflammation.
• Treatment of GERD may involve correction of hiatal hernias, enzymes, selected supplements and a healing diet that emphasizes bone broth and lacto-fermented foods.
Gastroesophageal reflux disease, better known by its catchy acronym GERD, is a growing health epidemic in the United States and worldwide. GERD costs U.S. taxpayers billions of dollars each year and accounts for hundreds of deaths.1
Historically, the very first “blockbuster” drug was Tagamet (cimetidine), developed in the 1960s by researchers looking for a “solution” for heartburn. Currently, the proton pump inhibitors (PPIs) often used to treat GERD are one of the best-selling classes of drugs in the U.S., with sales of nine and a half billion dollars in 2012. Nexium, one of the more well known PPIs, was the top-selling of all drugs that year, raking in nearly six billion dollars.2 Americans also spend over two billion dollars annually on liquid and tablet antacids. In 2016, U.S. private-label sales of antacids reached almost eight hundred and sixty million dollars, and sales of Nexium 24HR and Zantac totaled over half a billion dollars more.3
Think about these facts for a moment and let them sink in. Then consider the fact that in my small private practice in Bergen County, New Jersey, I see on average two new patients a week with GERD symptoms. These patients range in age from as young as twenty to the elderly. Almost all have sought medical treatment before coming to me, and one after the other ends up on my office doorstep looking for a better answer for their problem than the prescription medications and over-the-counter (OTC) antacids they have come to rely on.
One glaring problem with the status quo is that most patients are very unsuspecting when it comes to the risks associated with long-term use of the various OTC and prescription drugs recommended for GERD. For all that these patients know (or are told by their physicians), their problem is caused by too much stomach acid, and neutralizing that acid with OTC antacids or shutting down acid production (as is the case with PPIs and H2 antagonist medications) just seems to make logical and harmless sense. What I hope to prove in this article is that the standard allopathic medical approach to the treatment of GERD is not only fundamentally flawed, it actually makes the problem worse, not better, and can set a person up for a lifetime of health problems. But before I expound further on the dangers presented by the allopathic medical treatment of GERD, let’s take a look at what exactly GERD is.
OVERVIEW OF GERD
The esophagus is the tube that carries food from the mouth to the stomach. GERD occurs when the stomach contents move retrograde back up through the esophageal sphincter up into the esophagus and, at times, all the way back up into the mouth. GERD symptoms vary widely in both presentation and severity, from a subtle chronic cough or pain in the abdomen to ulcers and even erosion of the esophagus.
A discussion of the stomach’s anatomy and function can provide a better understanding of just what is occurring in GERD. The stomach is a muscular organ, somewhat J-shaped, which lies in the upper left quadrant of the abdominal cavity. It is closed off at the uppermost section from the esophagus by the lower esophageal sphincter (LES), a muscular ring responsible for opening and closing to allow passage of food into the stomach and prevent it from moving back up into the esophagus. The esophagus must first pass through the diaphragm in order to enter the abdominal cavity. It does so with the help of the LES, which forms the “door” between the esophagus and the stomach (Figure 1, left).
The stomach’s lining is made up of specialized cells known as goblet cells, which secrete a protective coating of mucous. This smooth lining is interspersed with millions of deep gastric pits where specialized glands produce the gastric juices. Within these pits are parietal cells and chief cells. The parietal cells pump hydrogen ions (H+) and chloride ions (Cl-) into the lumen (cavity) of the stomach, making hydrochloric acid (HCl), a very strong acid that helps to liquefy the ingested food and begin the digestion of protein. It does the latter by creating the strong acid environment needed to convert inactive pepsinogen into the powerful protein-digesting enzyme pepsin. (The chief cells have primary responsibility for production of pepsinogen.) Protein digestion, therefore, is initiated in the stomach and is essentially the only type of enzymatic digestion that occurs there.4 Hydrochloric acid plays a critical role in maintaining the stomach’s pH between 1.8 and 3.5, which not only enables the first phase of digestion to occur efficiently, but also helps kill any bacteria we are exposed to through the oral route. Parietal cells also produce intrinsic factor, a carrier protein responsible for ensuring that vitamin B12 is picked up and carried to the small intestine, where it is absorbed.
Generally, three distinct stimuli regulate gastric secretions. Although the three vary in mechanism and location, all three target the stomach either to stimulate or inhibit gastric secretory activity. The first is the cephalic reflex/phase, whereby the mere smell, taste, sight or thought of food triggers neural reflexes (via input from the olfactory nerve, optic nerve, taste, etc.) to the hypothalamus (a portion of the brain whose most important function is to link the nervous system to the endocrine system via the pituitary gland). The hypothalamus then relays these “digestive” signals to the medulla, causing motor impulses to be transmitted via the vagus nerve (the fifth cranial nerve) to the parasympathetic (stimulatory) enteric ganglia.4 This creates a stimulatory effect on the glands in the stomach and, therefore, an increase in gastrin and hydrochloric acid production.
The second stimulus, known as the gastric phase, is characterized by food entering the stomach and initiating local neural and hormonal mechanisms. This phase is responsible for the bulk of gastric juices stimulation. The two most important factors here are the stretching of the stomach wall as food enters and the rising pH created by the food. Stretch receptors in the wall of the stomach are triggered as the stomach fills with food. These receptors initiate reflexes that culminate in the increased production of gastric juices. The presence of partially digested protein, combined with a rising pH (created by protein in the meal entering the stomach and binding up free H+) trigger the gastrin-secreting enteroendocrine cells found in the gastric mucosa. Gastrin then stimulates the release of enzymes (pepsinogen) and the production of hydrochloric acid. Interestingly, anything that triggers the “fight or flight” sympathetic response—including emotional upset, fear or anxiety—will inhibit gastrin production, thereby halting or slowing digestion in the stomach.
The third and final phase, known as the intestinal phase, is characterized primarily by the inhibitory effects set in motion when partially digested food begins to enter the duodenum (the first section of the small intestine connected to the stomach). As the intestine begins to distend with chyme (the liquefied food produced by the stomach), this triggers the enterogastric reflex, the result of which is inhibitory to the stomach’s production of gastric juices. Furthermore, the intestinal distention triggers the release of intestinal hormones collectively called the enterogasterones—made up of secretin, cholecystokinin (CCK), vasoactive intestinal peptide (VIP) and gastric inhibitory peptide (GIP)—all of which further inhibit gastric secretion.4
ALLOPATHIC TREATMENT CASCADE
Western allopathic medicine blames GERD on two theories that are, in my opinion, flawed and outdated—the main one being the production of too much stomach acid. Interestingly, I’ve yet to see proof of how the stomach, whose job it is to produce acid for digestion, suddenly and without warning begins producing “too much.” The second faulty theory states that certain foods can “relax” the LES, thereby allowing stomach contents to enter the esophagus. Top on the list of apparent offenders are tomatoes, citrus fruits, garlic, onions, “deadly” animal fats, coffee or other caffeinated products, alcohol and peppermint. Smoking also is considered a contributor to GERD. Aside from three items on that list (alcohol, caffeinated beverages and smoking), you’re going to be hard pressed to convince me that the blame for GERD’s rise is due to garlic, oranges or, for that matter, animal fats. However, these theories do fit perfectly with the pharmaceutical industry’s agenda to sell you antacids, PPIs or H2 receptor antagonists—to the tune of billions of dollars each year.
Let’s take a closer look at what happens when the average person faces GERD (or the early stages leading up to GERD) and its varying symptoms. Unfortunately, many people with GERD symptoms choose to self medicate with antacids like Rolaids, Tums or the like. In my opinion, it is here that the first mistake is made by addressing a straightforward problem incorrectly and turning it into something far more deleterious. For the most part, all of these products serve one purpose, neutralizing the hydrochloric acid inherent in the stomach and relieving the “burn” of heartburn. I’ve met people who pop these acid-sopping medications like they’re candy without even thinking twice.
Sadly, most people I encounter in my practice have self medicated with antacids for years and sometimes decades, damaging their digestive system immensely, before seeking further help. Because the antacids initially seem to ameliorate their symptoms, they never think that anything more serious is occurring or that they are making a simple problem far worse. The reality is that antacids are doomed to fail and, over time, stomach symptoms inevitably will worsen.
It is at that point—often after years of OTC antacid use—that a person may visit their medical doctor with more pronounced symptoms of GERD. Because on the surface the problem logically seems to be one of hyperacidity, the doctor will continue on the same treatment path, recommending a protocol centered around nullifying the acid, even though hydrochloric acid is a crucial part of the stomach’s normal function.
Often, the next class of drugs along the conventional GERD treatment pathway will be the H2 (histamine 2) antagonists, named for their ability to bind to and block the type-2 histamine receptor site. Common H2 antagonist brand names are Axid, Pepcid, Tagamet and Zantac. These drugs work by reversibly blocking the H2 receptors of the gastric parietal cells responsible for acid secretion and, in doing so, preventing the production of hydrochloric acid.
They accomplish this through two mechanisms. First, histamine released by enterochromaffin-like cells in the stomach is blocked from binding on the parietal cell H2 receptors that stimulate acid secretion; secondly, when the H2 receptors are blocked, other substances that promote acid secretion (such as gastrin and acetylcholine) also will have a reduced effect on parietal cells.5 According to the National Institutes of Health, H2 receptor blockers decrease stomach acid secretions over a twenty-four-hour period by 70 percent.6 Any hope of actually digesting your food with these bad boys is slim to none—but hey, at least your heartburn and reflux will be gone.
One very serious problem with H2 antagonists is that they have been shown, albeit in rare instances, to be toxic to the liver. This is bad news if you value your liver (and I’d say that most of us should). The H2 antagonists also can cause diarrhea, muscle pain, fatigue, drowsiness, constipation and headache. Even worse, they can react with other drugs to cause more deleterious effects.
Researchers from as far back as the 1990s have questioned the safety of long-term H2-receptor antagonist therapy, stating that it needs to be considered in relation to the potential consequences of prolonged acid suppression. These include the risk of proliferation of gastric flora and the risk of developing enterochromaffin-like cell hyperplasia, which could, theoretically, lead to gastric malignancy.7 Yes, you read that correctly—not only can these drugs interact in unknown ways with other medications, they also can lead to proliferation of bacteria in your stomach, which is normally a sterile environment. In fact, the normal highly acidic environment of the stomach is our body’s first line of defense against any pathogens we are exposed to through the oral route. Bacterial proliferation in the stomach and the potential for gastric malignancy do not sound to me like reasonable solutions for GERD.
When H2 antagonists no longer work, or if the person’s GERD symptoms are more severe, PPIs will be the last option before more invasive surgical procedures. PPIs work by irreversibly blocking the hydrogen-potassium adenosine triphosphatase enzyme system (the H+/K+ ATPase, or, more commonly, the gastric proton pump) of the gastric parietal cells.8 Stated another way, PPIs essentially shut down the pumps that make hydrochloric acid for the stomach. In doing so, however, PPIs can lead to bacterial overgrowth just like H2 antagonists. One trial of the very popular PPI Prilosec (omeprazole) showed that the drug blocked stomach acid production so effectively that a majority of the subjects developed significant bacterial overgrowth as compared to the control group.9
The truth is that PPIs and other medications used to treat GERD all come with long-term risks and side effects, which are all too often brushed under the carpet. Numerous studies have reported that the use of PPIs is associated with negative health effects that include kidney disease; decreased calcium, iron and vitamin B12 absorption; magnesium deficiency; fractures of the wrist, hip and spine; pneumonia; dementia; life threatening Clostridium difficile infections; and cardiovascular disease. An October, 2015 article in The New York Times emphasized these very facts, quoting a Harvard Medical School doctor as saying that PPIs “are not the benign drugs the public thinks they are.”10
A 2016 study published in JAMA Neurology found that PPIs were associated with an increased risk for dementia in older patients.11 The study used data from the largest mandatory public health insurer in Germany, which covers roughly one-third of the population and includes information on both diagnoses and drug prescriptions. The analysis included over seventy thousand elderly subjects (aged seventy-five or older) who, at the outset of the study, did not have dementia. After following the subjects from 2004-2011, nearly 60 percent of the subjects had dementia, but there was a significantly higher risk of dementia in the nearly three thousand patients who regularly used PPIs, compared to patients not taking any PPIs. This is very important information if we consider that PPI usage has been steadily increasing, not just in the elderly but in an ever growing population of younger people who potentially will take these drugs for decades.
An even more recent observational study published in 2017 in The British Medical Journal Open found that PPIs increased the risk of premature death. Compared to individuals exposed to PPIs for a month or less, the risk of death increased by 17 percent for those using the drugs for three to six months, by 31 percent in people on the drugs for six months to a year and by 51 percent in those using PPIs for more than a year.12
Where can we turn if we hope to avoid the pitfalls of Western medicine’s dangerous approach to GERD? First, we must understand what is really going on in the stomach (and in the intestinal tract as well) that creates this problem in the first place. As laid out above, mainstream medicine considers GERD to be a problem of hyperacidity (too much acid) and treats it accordingly, but in fact, it is almost always the complete opposite. I am certainly not the first to put forth the notion that GERD is actually a problem of hypochlorhydria (lack of stomach acid), which can arise in response to multiple triggers.
THE GUT FLORA
The first causative factor linked to GERD—supported in the medical literature yet seldom discussed—is dysbiosis (abnormal intestinal flora). Disruption of the human intestinal tract’s normal healthy flora is a well known link to irritable bowel syndrome (IBS), and research has concluded that there is a “higher prevalence of IBS in subjects with GERD compared with subjects without GERD.”13 A study published in Digestion likewise has noted that GERD, dyspepsia and IBS commonly overlap in the general population.14 Interestingly, these overlaps are most likely to occur in individuals with anxiety.14 One reason for this may be the fact that protein breakdown cannot occur properly without correct stomach function and adequate hydrochloric acid—and without proper protein digestion, we cannot liberate and absorb the amino acids needed to build neurotransmitters like dopamine and serotonin. Symptoms like insomnia and anxiety (as well as many others) can result from improper protein digestion, sometimes even before any major symptoms of GERD appear.
Jonathan V. Wright and Lane Lenard have come to similar conclusions in their book, Why Stomach Acid is Good for You, a must read for anyone having symptoms or facing a diagnosis of GERD.15 I will take it one step further and note that when dysbiosis is present, proteins that are not digested serve as “dinner” for many opportunistic bacteria. The caustic fermentation products produced when these bacteria break down protein then lead to further stomach and intestinal (colon) irritation.
Current research highlighted by Dr. David Perlmutter in his book Brain Maker: The Power of Gut Microbes to Heal and Protect Your Brain—for Life describes how our gut microbiome develops from birth and evolves, for better or worse, based on our diet and lifestyle choices—and discusses how this microbiome can even affect our brain.16 Perlmutter makes a point that is even more critical to the GERD discussion when he states:
The research is clear: your gut’s bugs may as well be considered an organ in their own right. And they are just as vital to your health as your own heart, lungs, liver and brain. The latest science tells us that the intestinal flora that take up residence on the delicate folds of your intestinal walls aid in digestion and absorption of nutrients [and] create a physical barrier against potential invaders such as bad bacteria (pathogenic flora), harmful viruses and injurious parasites.16
A simple search on PubMed will produce a bevy of research papers that speak to this point. Whether the diagnostic label is dysbiosis, IBS or small intestine bacterial overgrowth (SIBO), we know that there is a link between the changes in the natural flora of the intestinal tract and our digestion, specifically with regard to GERD.
In some patients, another common causative factor for GERD can be, at least in part, taking prescription medications that delay gastric emptying (gastroparesis).17 Gastroparesis leads to an overall reduction in gastric acids and a rise in pH, which allows for fermentation of ingested food from the bacterial proliferation that occurs now that the stomach’s pH is no longer low enough (due to the hypochlorhydria) to inhibit the overgrowth. (Remember, bacteria are not supposed to grow in the stomach.) The classic example of this is overgrowth of Helicobacter pylori (H. pylori), often blamed for causing ulcers. This bacterium normally cannot grow in the highly acidic environment of the stomach, but when the stomach becomes hypochlorhydric for any of the reasons outlined throughout this paper, H. pylori can thrive. The sinister part of this problem is that H. pylori has the ability to further shut down stomach acid production. The resultant fermentation of foods in the stomach then leads to gas production (and the bloated or full feeling with which many GERD sufferers are familiar), as well as production of caustic organic acids. As a result of these gases, which naturally want to rise, pressure builds in the stomach, putting further pressure on the LES and opening the door for reflux.
The many drugs known to cause GERD include anticholinergics, bronchodilators for asthma, calcium channel blockers for high blood pressure, dopamine-active drugs for Parkinson’s disease, progestin for abnormal menstrual bleeding and birth control, sedatives for insomnia and anxiety, and tricyclic antidepressants.18 The culprit also can be more common “everyday” medications that directly damage the gastric lining, including aspirin, naproxen, ibuprofen and other anti-inflammatory drugs. With all of these, the end result is the same—damage to and spasm of the stomach wall and refluxing of food back up into the esophagus, which weakens the stomach’s ability to produce acid and digest food effectively. The pressure from the spasm and fermentation also weakens the LES, as noted previously, setting the stage for passage of acids up into the esophagus. Therefore, the first variable I rule in or out when examining a patient with GERD is medication. I believe this should be standard protocol because without it, any intervention to assuage the GERD will be negated by medication side effects.
A third variable when examining a GERD patient is evaluation of whether a hiatal hernia exists. A hiatal hernia occurs when the uppermost portion of the stomach, termed the fundus, herniates up through the LES (Figure 1). According to the Cleveland Clinic, the most common cause of hiatal hernia is an increase in the pressure in the abdominal cavity. Pressure can come from coughing, vomiting, straining during bowel movements, heavy lifting or physical strain.19 It is my opinion that the increased intra-abdominal pressure caused from SIBO and bacterial dysbiosis and the resultant gas production also is a leading cause of LES weakening, increasing the likelihood of hiatal hernia formation. This condition will often create the feeling of fullness that patients with GERD complain of, or the inability to eat even a modest amount of food without becoming full very quickly. The most common allopathic medical tests used to confirm hiatal hernia are a barium swallow followed by an X-ray or endoscopy. It is always prudent for the physician to consider this when evaluating a patient with GERD.
FIGURE 1: Normal esophageal opening versus opening with hiatal hernia. Copyright Kansas Medical Clinic, used with permission.
In my clinical practice, I use a very special chiropractic adjustment approach (see Figure 2) combined with a manual adjustment of the stomach to treat a hiatal hernia when it is involved in GERD. Yes, you read that correctly—I manually adjust the stomach. In fact, I have seen cases of hiatal hernia where, despite strict dietary changes and compliance, a patient could not get off of their medication (without exacerbation of symptoms) until this adjustment was performed to pull the stomach back down through the LES into its natural abdominal position.
FIGURE 2: Manual adjustment for hiatal hernia patients: hand positioning
The adjustment is done with the patient upright. I use my adjustment table, which can be raised to a near vertical position, and the patient simply lies back while in a somewhat standing position (Figure 3). I position myself on the patient’s left side and gently place my hands (using the first four digits of each hand aligned from left to right horizontally and in the shape of an upside down “V”) just lateral to and below the xiphoid process (lower sternum) and rib cage. I then tell the patient to follow my instructions regarding breathing so that we are in sync with each other. This is very important, because the adjustment can be a bit uncomfortable, and tenseness in a patient can prevent the procedure from being effective.
FIGURE 3: Manual adjustment of the stomach for hiatal hernia patients
As the patient breathes diaphragmatically in through their nose and releases the air out through their mouth, I begin to apply firm pressure from anterior to posterior and cephalad to caudad (down toward the floor with the patient vertical). I then hold this firm pressure for approximately thirty seconds while instructing the patient to continue breathing with his diaphragm. I will often instruct the patient as he is breathing to attempt to push the abdomen out as if to push my hands off of the abdomen. Doing so will encourage patients to breathe with their diaphragm (something most people do not do anymore) and help to squeeze or push the fundus of the stomach back down through the LES. It works remarkably well and is usually only necessary one or two times to achieve success. Many times during this procedure, the patient and the practitioner will feel the stomach release back down into the abdomen.
STANDARD AMERICAN DIET
Most Americans, whether they know it or not, are eating a diet of “dead” foods. The caustic, highly processed standard American diet (SAD) is overloaded with refined, highly processed pseudo-foods that are devoid of the natural enzymes present in whole, unadulterated foods. This lack of life-giving enzymes places a larger burden on the entire digestive tract, and especially the stomach, gallbladder, small intestine and pancreas. When someone consuming the SAD also overuses antibiotics, birth control pills, cortisone or other medications and thereby alters the natural probiotic flora that inhabit the human intestine, these two factors go hand-in-hand to create the perfect GERD storm. An altered gut flora, combined with overconsumption of refined carbohydrates, creates the ideal environment for fermentation, leading to bloating, distention of the abdomen and a weakening of the abdominal wall, which limits the patient’s ability to breathe diaphragmatically. The toxins and organic acids produced by opportunistic bacteria also further damage the stomach and intestinal lining.
Although practitioners rarely discuss food combining when treating gastrointestinal problems like GERD, I have found it to be very effective and have used food combining principles in my practice for many years to simplify the digestive process for my patients (see sidebar). The reason for streamlining digestion is to minimize the likelihood that foods will irritate the gastric lining. By paying attention to the foods one puts together at any one meal, it is possible to avoid putting extra demands on the stomach, enabling it to function more efficiently and with ease.
Another consideration when treating a patient with GERD should be to limit the consumption of water and other beverages with meals. Drinking copious amounts of water during meals serves to dilute the stomach’s hydrochloric acid, thereby raising the stomach’s pH. In much the same way as the other factors described above, this creates relative hypochlorhydria and, therefore, poorly digested food. Ultimately, this can aggravate the stomach lining and lead to GERD.
STRESS AND GERD
Stress (especially emotional upset) is another variable that cannot be overlooked as a causative factor in GERD. Stress activates the sympathetic nervous system, and in doing so overrides parasympathetic control of digestion, signaling the stomach to decrease stomach secretory activity.4 In today’s modern world, stress is everywhere we look, in the way we drive, the way we rush to work and even in the words we use. Stress causes us to rush our meals, lose sleep, hardly take the time to chew our food (certainly another factor in and of itself since chewing signals the stomach to increase gastric juices) and eat on the run instead of sitting down with our families to enjoy our meal and our time together. Having patients work on stress reduction using meditation and other techniques can be very helpful in eliminating this contributing factor. I also encourage all of my patients to take time to sit down for at least thirty minutes and enjoy each meal in a peaceful, calm environment.
To diagnose GERD properly and treat it naturally, we must start by taking a thorough history, one that includes a patient’s habits. Does she smoke? Drink alcohol? Rest adequately? Eat on the run? Eat fast food often? Take medications? Getting a complete history of the individual’s symptoms and habits can go a long way in identifying her particular causative factors with regard to GERD. For some, stress will be a big factor, while for others, medication or diet may be the main culprits. More often than not, it is a combination of these and other factors.
Secondly, we must examine overall digestive wellbeing. For this, I rely on a test known as a Complete Digestive Stool Analysis (CDSA). There are many labs that now offer some variation of this test. I use Genova Diagnostics’ GI Effects Stool Profile,20 which offers a look at what the company calls the four functional pillars of gastrointestinal health: infection, inflammation, insufficiency and imbalance. Although a detailed discussion of the test is beyond the scope of this article, I would like to highlight the main factors that this particular test allows us to assess.
First, and perhaps most importantly, it gives us the opportunity to screen for dysbiosis using a PCR (polymerase chain reaction) DNA analysis of the microbiome. We can then evaluate some of the major flora that constitute a healthy gastrointestinal tract, like the different lactobacillus and bifidobacterial species. Conversely, it also allows us to test for common pathogens as well as more nefarious critters like clostridia or H. pylori. From here, we get a glimpse of whether or not a condition of dysbiosis is present. The test also affords the opportunity to see drug and botanical resistance based on any pathogens present so as to customize our natural antibiotic approach using the most potent botanicals for that particular pathogen. We can also assess the need for probiotics and what type of probiotic is best suited for the particular patient.
A second feature of the CDSA is the assessment of the patient’s digestive function by looking at carbohydrate, protein and fat breakdown products present in the stool. This allows us to glean information about specific enzymes that may be necessary to support their particular situation. Most GERD patients will need a form of hydrochloric acid known as betaine hydrochloride to increase the acidity of the stomach (that is, to lower pH) and ensure proper protein breakdown. In many cases, pancreatic support is also necessary for fat and carbohydrate digestion. Thus, a quality comprehensive digestive enzyme is preferable in most cases of GERD.
The GI Effects Stool Profile assesses inflammation (one of the four pillars) using several well studied markers, including eosinophil protein X (EPX), calprotectin and fecal secretory IgA. Along with these inflammatory markers, we can use the serum zonulin test to assess the integrity of the intestinal tight junctions and screen for leaky gut. When combined, all of these markers (and more) give us a look at the severity of the situation for each person, allowing the treatment plan to be tailored to the individual.
TREATING GERD NATURALLY
The protocol I use to treat GERD is common sense, straightforward and effective. My first step is to prescribe a digestive enzyme based on the patient’s test results and specific needs. At a minimum, the enzyme must contain betaine hydrochloride as well as pepsin. However, a more complete enzyme offering digestive support for a full range of foods is almost always needed.
Secondly, I typically prescribe Gastrex by Standard Process. Gastrex is a whole food supplement consisting of okra, chlorophyll, bentonite and Tillandsia usneoides (Spanish moss), along with other synergistic ingredients to support digestion and the body’s normal tissue repair process. The dose is two capsules, fifteen minutes prior to meals, two to three times per day. I often combine Gastrex with a product by Designs for Health called GastroMend-HP, especially if the patient has tested positive for H. pylori or has an active gastric or peptic ulcer. GastroMend-HP contains deglycyrrhizinated licorice root (excellent at helping heal the mucous lining of the stomach); “vitamin U” (methymethionine sulfonium chloride), a cabbage extract useful for healing ulcers; and zinc carnosine (effective at killing off H. pylori).
The diet for GERD uses the traditional healing foods outlined in Sally Fallon Morell’s classic book Nourishing Traditions. It must be kept somewhat bland (nothing hot or spicy for now!) and should be focused around two key components: homemade bone broth (chicken or fish to start) and lacto-fermented foods, especially sauerkraut. Meals should be eaten in smaller portions more frequently, perhaps up to six smaller meals throughout the day. Bone broth is rich in gelatin; as Fallon Morell notes, it is “an aid to digestion and has been used successfully in the treatment of many intestinal disorders, including hyperacidity, colitis and Crohn’s disease.”21 Lacto-fermented foods are a rich source of probiotics as well as enzymes, vitamins and minerals.
I usually start the patient off the first week on nothing but cups of healing broth and ample amounts of meat, skin and marrow from making the broth. Vegetables should be cooked when making the broth and preferably should be non-fibrous at first. Too much fiber can cause gas and bloating in patients who have dysbiosis or leaky gut, as most GERD patients do. One must have good intestinal flora to digest fiber-rich vegetables. Typically, I will have patients blend the meat or fish, marrow, vegetables and broth into a puréed soup to aid digestion. Puréeing the soup increases the surface area of the food for contact with enzymes, while liquefying it makes it easier to digest. I also instruct them to add ample amounts of sauerkraut juice and eventually the sauerkraut itself to provide probiotic bacteria, vitamins and enzymes. Sauerkraut is well known for its wonderful healing qualities for stomach dysfunction. Adding ghee and fermented raw dairy (goat or sheep is best for GERD patients) to the soups after they have cooled to lukewarm also provides nourishing fats, which are critical to the healing process.
Breakfast will often consist of stewed apples or pears, cooked in raw ghee and sprinkled with some Celtic sea salt and a touch of cinnamon. They can alternate these fruits throughout the morning with soft cooked eggs cooked in ghee or lard and vegetable omelets. It is very important that a digestive enzyme is taken with each meal, although not with stewed fruit.
Once the healing process has begun, usually within the first two weeks, we begin teaching the patient the principles of the Weston A. Price Foundation’s Wise Traditions diet. Doing so allows the patient to slowly introduce more and more foods, properly prepared and rich in nutrition. Getting patients back in touch with the spiritual connection to their food and the world around them can go a long way toward promoting the healing process.
What are some of the consequences of living with GERD? According to the Mayo Clinic, GERD can lead to a long list of symptoms, including chronic coughing, asthma, recurrent sore throat, recurrent laryngitis, dental enamel loss, globus sensation (the feeling of having a lump in your throat), subglottic stenosis (narrowing of the airway above the trachea and below the vocal cords), chest pain, pounding of the heart (especially when reclining) and many others.22 GERD also can affect a person’s ability to sleep (as symptoms are often worse while reclining) and can severely impair normal day-to-day functioning.
When untreated and allowed to progress, GERD can lead to dysphagia (difficulty swallowing); odynophagia (painful swallowing); gastrointestinal bleeding; iron-deficiency anemia; pernicious anemia; folate, calcium and zinc deficiency; vomiting; early satiety; erosions of the esophagus; and weight loss. About 10 percent of people with chronic symptoms of GERD go on to develop Barrett’s Esophagus, where the normal tissue lining the esophagus changes to tissue that resembles the lining of the intestine.23 This increases the risk of developing esophageal adenocarcinoma, which is a serious, potentially fatal cancer of the esophagus.23 Overall, this is quite a list of problems.
Interpreting GERD as a problem of too little (rather than too much) stomach acid makes it a far different problem that actually has a much easier and more common sense solution. I watched my father treat GERD effectively in this manner over his more than fifty years of practice. I have done so myself with great success—and for far less cost to my patient’s pocketbooks and to their long-term health.
WHAT’S IN THAT ANTACID?
Most people don’t know what is in their over-the-counter candy-like antacids. The active ingredients in Rolaids, as one example, are calcium carbonate (550 mg) and magnesium hydroxide (110 mg); the inactive ingredients are dextrose, flavoring, magnesium stearate, polyethylene glycol, pre-gelatinized starch, sucralose and sucrose. Nothing like a dose of chalk, artificial sweeteners, refined sugars, aluminum and other Franken-gredients to start one’s day right! Moreover, antacids come in many varieties and cool “flavors,” many of which contain artificial colorings like FD&C lake #6 (aluminum), which imparts a reddish-yellow color to medicines and foods (because, let’s face it, it has to have a cool color, doesn’t it?). The frightening fact is that this very same aluminum may play a role in Alzheimer’s disease as well as some forms of cancer.24 Further discussion of the myriad harmful ingredients in over-the-counter antacids is beyond the scope of this article, but much of this information is easily available to those willing to search it out.
FOOD COMBINING PRINCIPLES FOR GERD PATIENTS
Three main rules form the foundation of proper food combining:
1. Because starches and proteins are the two more complex and difficult foods to break down, they should be kept separate when planning meals. In other words, GERD patients should not eat animal proteins with starches. These foods generally take three hours to empty from the stomach.
2. Non-starchy vegetables combine well with either starches or proteins. These include green vegetables, salads and many others.
3. Ripe fruit, which is digested and leaves the stomach very quickly (usually in under an hour), should be eaten alone. This can either be an hour or so before a meal or three to four hours after meals.
1. Digestive diseases statistics for the United States. http://digestive.niddk.nih.gov/statistics/statistics.aspx#specific.
2. Proton pump inhibitors (PPI) medicines review: our review of these drugs shows all are similar but there are big differences in price. Consumer Reports, July 2013. https://www.consumerreports.org/cro/2013/07/best-drugs-to-treat-heartburn-and-gerd/index.htm.
3. Leading antacid tablet brands in the United States in 2017, based on sales (in million U.S.
4. Marieb EN. Human Anatomy and Physiology. Menlo Park, CA: Benjamin/Cummings Science Publishing, 1998.
5. H2 antagonist. https://en.wikipedia.org/wiki/H2_antagonist.
6. Drug record: histamine H2 receptor antagonists/blockers (H2 blockers). https://livertox.nih.gov/H2ReceptorBlockers.htm.
7. Sabesin SM. Safety issues relating to long-term treatment with histamine H2-receptor antagonists. Aliment Pharmacol Ther 1993;7(suppl 2):35-40.
8. Sakai H, Fujii T, Takeguchi N. “Proton-potassium (H+/K+) ATPases: properties and roles in health and diseases.” Chapter 13 in Sigel A, Sigel H, Sigel RKO (eds). The Alkali Metal Ions: Their Role for Life. Metal Ions in Life Sciences (MILS) series, vol. 16. Springer International Publishing, 2016, pp. 459–483.
9. Theisen J, Nehra D, Citron D et al. Suppression of gastric acid secretion in patients with gastroesophageal reflux disease results in gastric bacterial overgrowth and deconjugation of bile acids. J Gastrointest Surg 2000;4(1):50-54.
10. Rabin RC. Ask well: taking heartburn drugs long-term. The New York Times, Oct. 15, 2015.
11. Gomm W, von Holt K, Thomé F et al. Association of proton pump inhibitors with risk of dementia: a pharmacoepidemiological claims data analysis. JAMA Neurol 2016;73(4):410-416.
12. Xie Y, Bowe B, Li T, Xian H, Yan Y, Al-Aly Z. Risk of death among users of proton pump inhibitors: a longitudinal observational cohort study of United States veterans. BMJ Open 2017;7(6):e015735.
13. Pimentel M, Rossi F, Chow EJ et al. Increased prevalence of irritable bowel syndrome in patients with gastroesophageal reflux. J Clin Gastroenterol 2002;34(3):221–224.
14. Lee SY, Lee KJ, Kim SJ, Cho SW. Prevalence and risk factors for overlaps between gastroesophageal reflux disease, dyspepsia, and irritable bowel syndrome: a population-based study. Digestion 2009;79(3):196–201.
15. Wright JV, Lenard L. Why Stomach Acid Is Good for You: Natural Relief from Heartburn, Indigestion, Reflux & GERD. Lanham, MD: Rowman & Littlefield Publishing Group, Inc, 2001, pp. 165-167.
16. Perlmutter D. Brain Maker: The Power of Gut Microbes to Heal and Protect Your Brain—for Life. New York, NY: Little, Brown and Company, 2015, pp. 24-25.
17. Nichols TW, Faass N. Optimal Digestion: New Strategies for Achieving Digestive Health. Acton, MA: Quill Press, 2000, pp. 580-581.
18. Gastroesophageal reflux disease. https://medlineplus.gov/ency/article/000265.htm.
19. Hiatal hernia. https://my.clevelandclinic.org/health/articles/hiatal-hernia.
21. Fallon S, with Enig MG. Nourishing Traditions: The Cookbook that Challenges Politically Correct Nutrition and the Diet Dictocrats. White Plains, MD: New Trends Publishing, 2001, p. 116.
22. Gastroesophageal reflux disease (GERD). http://www.mayoclinic.org/diseases-conditions/gerd/basics/symptoms/con-20025201.
23. Barrett’s esophagus: symptoms, causes, and treatments. http://www.webmd.com/heartburn-gerd/guide/barretts-esophagus-symptoms-causes-and-treatments#1.
24. First case study to show direct link between Alzheimer’s and aluminum toxicity. Mercola.com, March 22, 2014.
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Summer 2018.
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