“We look for medicine to be an orderly field of knowledge and procedure. But it is not. It is an imperfect science, an enterprise of constantly changing knowledge, uncertain information, fallible individuals, and at the same time lives on the line. There is science in what we do, yes, but also habit, intuition, and sometimes plain old guessing. The gap between what we know and what we aim for persists. And this gap complicates everything we do.”
Atul Gawande, Complications: A Surgeon’s Notes on an Imperfect Science
- AC: adenocarcinomas
- BE: Barrett’s esophagus
- EC: esophageal cancer
- GERD: gastroesophageal reflux disease
- H. pylori: Helicobacter pylori, aka Campylobacter pylori
- IBS: irritable bowel syndrome
- IF: intrinsic factor
- LES: lower esophageal sphincter
- SCC: squamous cell carcinomas
- SIBO: small intestinal bacterial overgrowth
- SIFBO: small intestinal fungal and bacterial overgrowth
As you’ve no doubt figured out from reading the title of today’s post, I’ll be tackling the very large subject of gastroesophageal reflux disease or GERD. And as in all my posts dealing with the gastrointestinal system, it will be impossible to talk about GERD or any other stomach disorder without referring to other areas of the gastrointestinal tract.
What occurs, or doesn’t occur, in the stomach has knock-on effects for the small intestine and colon. And what occurs or doesn’t occur in the small or large intestine can, and often does, react back on stomach function.
Gastrointestinal functioning is dependent on the unique state of each person’s gut flora. It is also influenced by a wide variety of ingested dietary ingredients, stress and drugs. Couple all this with the fact that the gut is in intimate communication with the brain, and that this communication flows in both directions, and you begin to realize just how difficult it can be to resolve gastrointestinal issues.
Today is the first part of what will be a multi-part series. However, please be patient if forthcoming posts don’t come as quickly as you’d like.
Today I’ll cover what GERD is, complications arising from it if left untreated and some popular theories used to explain it.
However, I need to emphasize some points before I get started. First and foremost, I once again remind everyone reading this that I am not a medical doctor, nor do I play one online.
A second point I want to emphasize is that serious medical conditions can cause recurring acid reflux. For example, there is a disease called Zollinger-Ellison syndrome that results in increased production of stomach acid. This disorder involves having small tumors in the pancreas or small intestine or both. This is a very serious medical disorder necessitating competent medical treatment.
And by competent medical treatment, I’m not talking about your acupuncturist, chiropractor, nutritionist or homeopath. No, I’m referring to a licensed medical doctor who can screen for this disease.
Another medical condition closely associated with GERD is hiatal hernia. This is the protrusion of the upper stomach through a weak or torn diaphragm into the chest cavity. Other disorders that can lead to intractable acid reflux are Barrett’s esophagus, as well as tumors in the esophagus, stomach and intestines.
I suspect that many people who visit this blog are engaging in self-diagnosis and treatment, and quite frankly that scares the hell out of me. That works out OK if you’ve already visited a physician who has administered a series of tests and found no obvious cause for your problems. Otherwise, you risk suppressing symptoms that may be masking a more serious condition.
Sadly, this prudent advice is complicated by the fact that patients aren’t the only ones guilty of just treating symptoms. Many doctors do the same with disastrous consequences. That will become all too clear when I discuss both pain- and acid-suppressing medications.
I’ve included an index at the top of this post. I get tired typing long medical terms, so I’ll be resorting to using abbreviations for many of them. This index should make reading easier for those who forget where in the post I began using them.
So what is GERD? According to Taber’s Medical Dictionary, GERD is:
“A common condition in which acid from the stomach (gastric and/or duodenal) flows back into the esophagus, causing discomfort and, in some instances, damage to the esophageal lining.”
Notice that nowhere in this definition does it state that GERD is caused by too much stomach acid. Rather, the condition is caused by stomach acid reaching a part of the digestive tract, the esophagus to be precise, that is not equipped to handle it.
Too many laypeople, not to mention their physicians, convince themselves that the problem is caused by excess stomach acid and treat it accordingly. In the case of Zollinger-Ellison syndrome that is true. However, in all other cases, save one that I’ll be covering in-depth in a future post, that is not the proximate cause.
Continuing on with Taber’s definition, we learn that symptoms often include:
“…heartburn, indigestion, and noncardiac chest pain (which may mimic angina pectoris by radiating to the neck, jaw, and/or arms.) Patients occasionally experience asthma, cough, hoarseness, difficulty in swallowing, or nocturnal regurgitation [vomiting].”
Those of you who suffer from acid reflux, and I used to be one of them by the way, know how unpleasant all of this is. For me, the worst symptom was waking up in the middle of the night with a mouth full of partially digested, acid-laden food and scurrying my middle-aged man butt as quickly as I could to the nearest sink or toilet to unload it. I still remember with revulsion the lingering burning sensation in the back of my throat that no amount of water seemed to counteract.
For most, GERD is coupled with digestive problems further down the old food chute. In fact, it is exceedingly rare for anyone to present with GERD and not also complain of diarrhea and/or constipation, bloating or other symptoms that are typically classified under the designation irritable bowel syndrome (IBS). It also often affects those with either Crohn’s or inflammatory bowel disease.
Risks Associated with GERD
Apart from decidedly unpleasant symptoms, there are some very serious risks involved if the problem persists. Chief among them is the possibility of developing esophageal cancer (EC). (1)
EC is not a cancer medicine has had much luck treating. In fact, very little progress has been made in the last twenty-five years in mortality rates.
EC can be subdivided into two main types: squamous-cell carcinomas (SCC) or adenocarcinomas (AC). Esophageal tumors are mostly of the SCC type as they are the type of tumor most likely to result in cancer–between 60% to 70% of all cases. AC make up between 30% to 40% of all EC diagnoses.
SCC happens most often in people with a history of cigarette use and/or heavy alcohol intake. Another risk factor includes previous radiation therapy for those who’ve undergone breast cancer treatment or treatment for lymphoma. In these cases, SCC can develop ten or more years after treatment. It’s important to note that SCC are not considered an outcome of GERD, so this is the last time I’ll be referring to this particular type of esophageal tumor.
However, AC is a risk for those with GERD who go on to develop another disorder known as Barrett’s esophagus (BE). BE is characterized by an abnormal change to the cells lining the lower esophagus due to repeated contact with stomach acid.
In this condition, normal squamous cells are replaced by columnar cells, cells that are taller than they are wide. These types of cells are common throughout the body and their main function is protective. While normal in the stomach and intestine, they are not normal in the esophagus.
BE develops in about 10% to 20% of those afflicted with GERD. Read another way, 80% to 90% of those with GERD never develop Barrett’s, so just because you suffer from acid reflux doesn’t mean you have BE.
As for cancer risk, a Danish study that collected data on 11,028 patients with BE between 1992 and 2009 found that the actual rate of cancer development was much lower than previously assumed. (2) This study found that for every 860 people with confirmed Barrett’s, only one went on to develop esophageal cancer.
So while BE does predispose some to developing cancer of the esophagus, they are decidedly in the minority. As in the development of BE itself, there are obviously other factors driving the formation of adenocarcinomas, including genetic predisposition, dybiosis of the esophagus (yes, the esophagus has bacteria that is native to it and these populations can become pathogenic) and dietary factors.
People who typically go on to develop BE are male, with an average age of 55, white and overweight. The most common symptoms of BE are abnormal amounts of acid reflux, heartburn, regurgitation, indigestion and what is termed epigastric pain, which is pain that emanates from the upper stomach and chest area.
Now, as much as I’d like to jump right in and discuss possible causes of GERD, it really is impossible for any of you to get a handle on this disorder without discussing how the stomach is supposed to work in a normal, healthy person. You can’t figure out what is wrong with something unless you understand how it’s supposed to work.
Take a refrigerator, for example. If you don’t know that its main function is to keep food either cold or frozen, how could you possibly know if it’s broken? And even if you were told it wasn’t working properly, by what possible criteria could you gauge your success in fixing it?
To that end, I’m going to cover how the stomach functions, and for that there is just no way to avoid a short course in anatomy. I beg you not to skip this section unless you’re a physician who knows, or should know, what I’m about to cover. And even then, some doctors may benefit from sticking around if for nothing else than as a refresher.
Subsequent installments of this series will sail right over your pretty little heads if you skip reading this. I suspect many will do so anyway, but I’m old enough to recognize that there’s just no way to fix stupid.
As always, I hope to make this as simple as I can without sacrificing medical accuracy. This may prove too simple for some of you medical professionals reading this. However, please understand that I have to balance the desire that some have for scientific complexity with the reality that a good chunk of my readership is not interested in the nitty-gritty of how the exchange of potassium ions with hydrogen drives acid production.
And for the purposes of this series such minutiae is just not necessary, although like many of you I too find all of this immensely fascinating. So please forgive me in advance if what follows is too oversimplified for your nerdy tastes.
Alrighty then, let’s dive in, shall we?
Courtesy: Johns Hopkins
When you eat, food is mixed with saliva in the mouth while chewing. This saliva has enzymes that begin breaking down the food.
A principal enzyme found in the mouth is amylase, a substance that specifically acts on starches. This makes evolutionary sense since our hunter-gatherer ancestors not only subsisted on the wild game they killed, but also glucose-rich plants like starchy tubers.
Another enzyme found in oral saliva is lingual lipase that acts on fats. Both amylase and lingual lipase retain some function even after reaching the stomach. Both are joined by gastric lipase, an enzyme produced by cells of the stomach. Gastric lipase breaks apart short- and medium-chain fatty acids and is responsible for up to 20% of fat digestion in humans.
Swallowed food travels from the mouth to the back of the throat or pharynx. Here, food enters the esophagus after the upper esophageal sphincter opens.
A sphincter is a circular muscle that constricts an orifice. It’s normal condition is to remain closed, and it must relax in order to open.
When this mass of food, now called a bolus, enters the esophagus involuntary muscle contractions begin to propel the bolus down and through the lower esophageal sphincter (LES) and into the stomach.
The primary location of acid reflux and heartburn is at this junction of the esophagus and the stomach. In the illustration above, this junction is located just above the area labeled cardia.
In a normal, healthy stomach this sphincter closes to prevent acid from refluxing back into the esophagus. Unlike the lining of the stomach, the cells lining the esophagus are not designed to handle the very low pH of stomach acid. Apart from heartburn, repeated contact of cells with stomach acid can lead to the cellular changes I’ve already mentioned.
The volume of the stomach when completely empty is about 50 ml or about 2 oz. However, once food begins to enter, folds in the stomach called rugae begin to expand much like an accordion. Once expanded, the stomach can hold between 1 to 1.5 L (37 to 52 ounces), although this is just an approximation.
Some people have smaller stomachs, while others can handle a lot more food. This latter group is poised for either a bright future participating in food-eating contests and/or obesity.
As illustrated, the stomach is divided into three sections. The section closest to the LES is called the fundus. The middle third of the stomach is called the body. And the part nearest the pyloric sphincter (aka pylorus), is called the antrum.
These divisions are not arbitrary, but dependent upon the type of glands that line the stomach cavity. Cardiac glands are found in the fundus. Oxyntic glands are found in the body. And plyloric glands are located mainly in the antrum.
These glands secrete different substances. For example, cells located close to the surface secrete mucus and bicarbonate. Parietal cells located in oxyntic glands secrete hydrochloric acid and a substance known as intrinsic factor (IF).
Other cells called chief cells secrete pepsinogens. Enteroendocrine cells secrete a variety of hormones.
So gastric juice contains a mixture of these substances along with water and electrolytes. As many of you know all too well, gastric juice has an abundance of hydrochloric acid produced by the parietal cells.
The elevated amount of hydrochloric acid in gastric juice means that this juice has a very low pH. For those of you new to the concept of pH, just be aware that the lower the number, the more acidic the solution. The pH scale runs from 0 (the most acidic) to 14 (the most alkaline). 7 being right in the middle of both extremes is unsurprisingly considered neutral pH.
Gastric juice has a pH of around two. Few acids go lower than that. This is about the same pH as lemon juice. Vinegar is a more alkaline 3, orange juice 4 and coffee comes in at about 5.
Baking soda neutralizes acid by increasing its pH and comes in at about 9. Ammonia is quite alkaline and registers at 11.
Now I’m sure many of you are wondering why nature designed us this way, especially those of you bedeviled by acid reflux. Why have stomachs that produce such an acidic substance?
Well, there are three major reasons for this evolutionary outcome. The first involves converting pepsinogen into its active form known as pepsin. Recall that pepsinogen is secreted by chief cells.
Pepsin is absolutely vital for the pre-digestion of protein. Without it, you risk not only having protein-rich meals just sit in your stomach for extended periods of time, but also risk failing to properly digest and assimilate protein in the small intestine. This can lead to protein malnourishment, a problem especially common in the frail and elderly.
The ability to produce pepsin from its precursor, pepsinogen, is reliant on the acidity of stomach acid. The ideal conversion to pepsin occurs at a pH of around 3.5. Therefore, anything that makes stomach acid more alkaline, or prevents its production, will impair the proper digestion and assimilation of protein.
Another major function of stomach acid is its role in the proper assimilation of various nutrients. Chief among these are calcium, iron and B12. Low stomach acid levels consistently and reliably impairs the absorption of these important substances. It should therefore not be surprising to anyone that persons with inadequate stomach acid tend to suffer disproportionately from thinning bones and anemia.
I mentioned that parietal cells also release intrinsic factor (IF). IF is necessary for the proper absorption of vitamin B12 in the small intestine. The state of a person’s B12 status depends on how much they get in their diet, coupled with how well it is absorbed with the aid of intrinsic factor.
A B12 deficiency, like an iron or calcium deficiency, is not something you want in your life. Common symptoms of B12 deficiency include:
- a type of anemia known as megaloblastic macrocytic anemia
- skin pallor
- shortness of breath
- tingling and numbness in the extremities
- abnormal gait
- loss of concentration
- memory loss
- elevated homocysteine levels, a risk factor for heart disease
Finally, one of the most important functions of stomach acid, if not the most important, is to guard against colonization of the small intestine and colon by swallowed bacterial pathogens. Therefore, the very low pH of stomach acid is one of the most important front-line defenses against infection of the intestinal tract.
Each and every time you swallow, whether you are eating or not, you swallow bacteria. The source of this bacteria comes from the oral cavity and the respiratory tract.
While many of these bacteria are commensal, or friendly bacteria there to aid in keeping you healthy, many others are pathogens that can make you quite ill should they survive transit through the stomach. This is especially true in those with rotting teeth and gums, and no doubt explains the consistant association seen between those with periodontal disease and a whole host of other disorders including heart disease. (3)
Because stomach acid is such a formidable barrier to bacterial survival, certain probiotic manufacturers have devised ingenious ways to thwart this defensive barrier so as to effectively deliver beneficial organisms to where they will do the most good.
As I wrote in my small intestinal bacterial overgrowth (SIBO) series, anything that compromises this gastric barrier increases the risk of developing disturbed gut flora (gut dysbiosis). I need to again remind you that this dysbiosis can affect not only the small intestine, but the colon and rectum, potentially leading to some very serious diseases as extensively explained in over a year of writing posts on this blog.
Not all of this swallowed bacteria is native to your mouth or respiratory tract, however. A lot of the food we eat, especially if improperly handled or insufficiently cooked, also contains bacteria.
A stomach with correct levels of stomach acid at the right pH will kill many of these ingested pathogens well before they have the opportunity to take up residence in your gut. Conversely, a stomach without sufficient stomach acid will fail to protect you from intestinal infections. I’ll have more to say about this in a subsequent post.
Returning to the digestion of food, pepsin pre-digests protein. I was very careful to choose my words here, and that’s because very little actual digestion occurs in the stomach.
This part of the digestive system should be regarded, like the mouth, as initiating but not completing the digestion of food. The only absorption that occurs in the stomach is of water, alcohol, some fat-soluble drugs like aspirin and a few minerals.
It is the small intestine where most digestion and absorption occurs, and for this to happen you must have a small intestine that is populated with beneficial bacteria and free of colonization by pathogens.
Now, how exactly are stomach secretions regulated? Well, many different substances are responsible.
Among these are gastrin, acetycholine, histamine, motilin, secretin, cholecystokinin, enterogastrone, peptide YY, somatostatin, substance P, glucagon-like peptide, etc. Obviously, it would take an entire book to explain the mechanisms involved here so lucky for you I won’t be covering most of these in-depth today.
However, I do want to briefly discuss the first three members on the list: gastrin, acetycholine and histamine.
Gastrin is a hormone produced in enteroendocrine G-cells in the stomach, pancreas and the duodenum. Gastrin acts on parietal cells to stimulate the release of hydrochloric acid.
Gastrin also stimulates stomach emptying and gastrointestinal motility or movement. High gastrin levels can cause chronic diarrhea.
Gastrin also increases the growth of the parietal cells responsible for stomach acid secretion. I’ll be returning to this growth-promoting or trophic action in a future post.
What’s important to remember is that the more gastrin released, all other things being equal, the more hydrochloric acid generated. Gastrin release occurs in response to stimulation of the vagus nerve, distension of the stomach by food, epinephrine and the ingestion of certain substances like coffee, alcohol, calcium and protein.
At the top of this post, I mentioned Zollinger-Ellison syndrome. What occurs in this disorder is that small tumors located in the pancreas and/or small intestine cause large amounts of gastrin to be released into the blood in a condition known as hypergastrinemia. This then causes hyper secretion of hydrochloric acid that results in the formation of multiple ulcers in the stomach and small intestine.
Thankfully, Zollinger-Ellison syndrome has a relatively low occurrence rate in the United States, affecting only between 1 to 3 patients per million. And in those diagnosed with a small intestinal ulcer, this syndrome accounts for only 1% of all cases.
In addition to gastrin, the release of acetylcholine by the vagus nerve stimulates the release of histamine. Histamine also stimulates acid secretion. Gastrin, by the way, also stimulates histamine release so you could say that gastrin is the master hormone of the two.
Now, nothing that I’ve mentioned about the workings of gastrin, acetycholine or histamine is abnormal outside of Zollinger-Ellison syndrome. That is how the system is designed to work.
These substances are important because by increasing acid secretion, they make sure that 1) we properly digest our food, 2) correctly metabolize calcium, iron, and B12 and 3) maintain our defenses against potentially troublesome bacterial pathogens.
Now once proper acid levels are reached, a feedback mechanism is initiated to shut down the production of gastrin, acetycholine and histamine. The body innately understands just how important proper levels of stomach acid are for its survival, both nutritionally and as a defense against intestinal infection. So when stomach acid production is impeded for whatever reason, it continues to produce both gastrin and histamine to overcome this deficiency.
Once food enters the stomach, apart from being combined with gastric juice, it is also subjected to mechanical action resulting in the mixing and churning of stomach contents. This is necessary not only to move the food towards the pylorus before emptying into the small intestine, but also to break food down into small particles.
The phyloric sphincter at the base of the stomach will typically not open unless solid food has been reduced to a diameter of about 2 mm (.07 inches). Therefore, food that is very difficult for your stomach to break down will consistently delay stomach emptying.
Anything that delays stomach emptying increases the risk of GERD. Why? Because the longer it takes to empty the stomach of acid-laden food, the greater the chance that the highly acidic contents of the stomach will slosh back up into the esophagus, especially when bending over or lying down.
OK, that ends our anatomy lesson for the day. That wasn’t too horrible was it? Let’s now explore some popular theories about what causes GERD.
Explanations for GERD
It’s a common misconception that GERD is always caused by too much stomach acid. It’s an easy assumption to make given the symptoms.
However, as I already hinted, unless you have Zollinger-Ellison syndrome, or are trying to wean yourself from proton pump inhibitors, this isn’t the true cause of GERD.
Ray, what do you mean if I try to wean myself from proton pump inhibitors?
What? Your doctor didn’t tell you that one of the most common side effects of stopping proton pump inhibitors is elevated acid production for one to three months after? Oops!
But gentle reader, I’m getting way ahead of myself here. This and other side effects of acid-suppressive drugs are for the future, so let’s get back to the topic at hand, shall we?
So if elevated acid is not the issue prior to treatment with proton pump inhibitors, what is? Well, what we do know with any certainty is that hydrochloric acid is reaching an esophagus that is not designed to handle it. Nevertheless, that begs the question as to why this is happening.
Some have speculated that high rates of antibiotic use are behind the rise of GERD seen in the West. How so?
Because an increasing number of people in developed countries are no longer infected with Helicobacter pylori (H. pylori). For those of you who’ve been living under a rock, H. pylori is a gram-negative bacteria that makes its home in the human stomach and is a major cause of stomach inflammation (gastritis). It is also an important risk factor for peptic ulcers and stomach cancer.
H. pylori reduces stomach acid production to ensure its survival, resulting in a condition that goes by the medical term aclorhydria (aka hypochlorhydria).(4) In populations living outside of the developed world where infection rates are high, GERD incidence is typically low and this is part of the reason why.
I say part of the reason because there are plenty of people who don’t have H. pylori, myself included, and who don’t or no longer suffer from GERD. So while infection with H. pylori no doubt decreases the incidence of GERD by suppressing acid secretion, much like any acid-suppressing drug, this hypothesis can’t totally account for these exceptions.
Of course, there is a downside to carrying around a bacteria that damages the cells of the stomach responsible for hydrochloric acid production. I’ve already mentioned three: gastritis, ulcers and stomach cancer. This is a major reason stomach cancer rates are much higher in underdeveloped countries.
It should go without saying that aclorhydria increases the risk of developing both SIBO and small intestinal fungal overgrowth, or as I will term it going forward, small intestinal fungal and bacterial overgrowth (SIFBO). And because it does, it should not be at all surprising that many of these populations also suffer from severe nutritional deficiencies even in cases where nutritional intake is adequate.
Low stomach acid also results in high gastrin release. High gastrin release typically results in diarrhea. In a population afflicted with H. pylori, high rates of SIFBO, combined with faster intestinal transit due to chronic diarrhea, is not a recipe for nutritional health.
Another interesting corollary to this hypothesis is the contention that the increasing incidence of obesity seen in Western populations over the past thirty to forty years may be partly explained by the eradication of this bacteria. The rationale behind believing this centers around the fact that low stomach acid increases feelings of satiety (stomach fullness) and typically causes someone to eat less.
And this is very true. A common outcome of aclorhydria is feeling very full after any meal, especially one containing protein.
Stomach acid acts on proteins by opening up their complex folded structures (denaturing) in order to prepare for further protein digestion in the small intestine. Low stomach acid will cause protein to sit longer in the stomach and make you feel full, which would be expected to cut caloric intake as this sensation can oftentimes be less than pleasant.
Moreover, as SIFBO consistently interferes with nutrient absorption, it is not uncommon in those with gut dysbiosis caused by low stomach acid to have undigested fat and protein appear in their stool. Calories that are not absorbed can never be stored as fat in conditions of food excess.
For example, not all celiacs are thin. However, most are because both the destruction of the brush border in their small intestine by their reaction to gluten, coupled with the concurrent SIFBO that afflicts most if not all untreated celiacs, ensures that calories pass through them like crap through a goose. Another marvelous illustration of the truism that thinness is no guarantee of health.
As H. pylori infection can also lead to gastritis and ulcers, separate and apart from small and large intestinal dysbiosis, eating anything can be a decidedly unpleasant experience in infected groups. While acid reflux in this population remains low, feelings of abdominal fullness, bloating, intestinal pain and diarrhea with alternating constipation are all too common.
So yes, there is something to the hypothesis that increased caloric intake may partly be explained by lower H. pylori infection rates in the developed world. If eating has morphed from being a joy into a living hell, then it’s not at all surprising if people choose to eat less to avoid the misery.
However, given the many unfortunate side effects of having H. pylori, purposely infecting yourself with this pathogen as a means to control your weight is, to put it as mildly as I can, the dumbest f**king thing you could do.
Now, as intriguing as this hypothesis is for explaining the higher incidence of GERD and Barrett’s esophagus in developed countries, it still can’t account for the large number of people who do not have this pathogen and yet experience no acid reflux. Nor is everyone who is thin or normal weight walking around with a belly full of H. pylori. At best, H. pylori infection, just like acid-suppressive drugs, prevents damage to the esophagus by inhibiting stomach acid production. But like these drugs, it does not cure the underlying disorder.
Another hypothesis holds that GERD can be explained by dysfunction in the lower esophageal sphincter. And like many of these hypotheses, there is some truth in this belief.
Certainly, a LES that fails to close will also fail to prevent stomach acid from sloshing back up into the esophagus. So any physical abnormality in this muscle can most certainly cause recurring problems. Nevertheless, there is an issue identifying the direction of causation.
Is the abnormality, should one be found, the cause of the GERD? Or does the GERD lead to the abnormality? That’s a good question that no one has the answer to. That said, there is very little proof that malfunctioning of the LES is a major cause of GERD in the overwhelming majority of cases.
Another hypothesis holds that certain foods cause the LES to weaken. Foods that have been identified to have this effect are coffee, chocolate, tea, alcohol, citrus and spices (red and black pepper, nutmeg, cloves, chili powder). Another class of foods that have relaxing effects on the lower esophageal sphincter are the carminatives such as peppermint and spearmint.
Now, what do I think of this hypothesis? Well, there’s little doubt in my mind that these foods can cause relaxation of the LES, and may be best avoided in those suffering from GERD.
However, not everyone who eats these foods suffers from acid reflux. And there is absolutely no proof that these foods exclusively act upon the LES and nothing else. What do I mean by this?
Take peppermint, for example. When I suffered from IBS, the absolute worst symptom I endured was painful bloating brought about because I could not pass trapped gas. This condition typically would wake me up at night and keep me up for hours.
The only remedy that gave me consistent relief was drinking two large mugs of peppermint tea. Before I would finish the second mug, the tea would relax the muscles and nerves in my intestines enough to allow me to finally, and gratefully, expel the gas that up to that point made a restful night’s sleep a cruel mirage.
So yes, peppermint and these other foods do have the ability to affect nerves and muscles, including sphincters in the digestive tract. But recall from our little anatomy lesson that the stomach has two, not one, sphincters: the LES and pylorus.
The rate at which a stomach fills raising acid-laden, partially-digested food towards the fundus, cardia and LES is dependent on three things: the amount eaten, the type of food eaten and the rate the stomach empties its contents.
Big meals are always going to predispose to acid reflux because the greater the amount of food in a stomach, the longer it will take to empty through the pylorus and the more likely it is to sit in close proximity to the LES.
Food that swells when in contact with liquid will also increase the volume of stomach contents and the risk of acid reflux. All things being equal, eating foods that don’t expand when mixed with gastric juice and ingested liquids will tend to lessen the risk of acid reflux. Conversely, foods that swell when immersed in liquid, like insoluble dietary fiber, will increase the volume of stomach contents and push acidified food back up towards the LES.
A pyloric sphincter that rapidly releases food into the small intestine drains the stomach faster than a pylorus that for whatever reason doesn’t open often or in severe cases, not at all. As I said before, delayed stomach emptying always increases the risk of acid reflux.
Now it should be clear that if the above-mentioned foods have a relaxing effect on the LES, they also have a similar effect on the phyloric sphincter, thus accelerating stomach emptying. So this hypothesis makes me doubtful that relaxation of the LES is a major culprit in GERD.
This isn’t to say that other side effects like burping are not caused by these foods. I’ve noticed that if I have coffee or chocolate on a empty stomach, I burp more often. However, I never experience acid reflux unless stomach emptying has been delayed after eating.
Still another hypothesis holds that the cause of GERD is due not to too much stomach acid, but to too little. This theory is popular in “alternative” medical circles.
It’s based on the reality that as we age, we become less capable of producing stomach acid than in our youth. Our ability to produce hydrochloric acid begins to gradually decline past the age of 40 or so. (4)
This reduction is especially acute in older people who at a younger age were infected with H. pylori. As a matter of course, these people need to be especially vigilant about compounding their problem by adding acid-suppressive medications to the mix. Alas, that is precisely what many of these people are doing, with the active collusion of their physicians, I might add.
For most people, supplementing with HCI Betaine can help retard this normal part of aging. For purposes of full disclosure, I take these pills before each meal containing protein.
Yes, that’s right. While many of you are trying to lower your stomach acid, I’m trying to raise or maintain mine. But then again, you could say I have an acute appreciation for how incredibly important stomach acid is for proper digestion and in keeping my intestine free of harmful pathogens.
However, care must be exercised when recommending acid supplementation. There are a couple of instances where hyper secretion of stomach acid is the issue and where further augmentation would prove counterproductive.
Finally, being overweight is often associated with GERD. Many people, therefore, assume that being overweight is the cause of the disorder and dispense the advice that simply losing weight will resolve the issue.
However, this hypothesis cannot account for why people who take opioids, have depressed thyroid function, celiac disease, or SIFBO suffer disproportionately from GERD even if thin or normal weight. Nor can this hypothesis explain the many overweight people who never experience acid reflux, or the scores of normal-weight individuals popping antacids or proton-pump inhibitors to deal with their acid reflux.
That brings me to the end of today’s post. In the next installment, I’ll give you explanations for what I believe is causing GERD in most cases…