- BCM7: beta-casomorphin-7
- C. albicans: Candida albicans
- FOS: fructooligosaccharide
- GERD: gastroesophageal reflux disease
- GI: gastrointestinal
- H. pylori: Helicobacter pylori, aka Campylobacter pylori
- IBS: irritable bowel syndrome
- LES: lower esophageal sphincter
- LPSs: lipopolysaccharides
- NBS: narcotic bowel syndrome
- OIBD: opioid-induced bowel dysfunction
- PPIs: proton pump inhibitors
- PUFAs: polyunsaturated fatty acids
- SIBO: small intestinal bacterial overgrowth
- SIFBO: small intestinal fungal and bacterial overgrowth
At the end of the last post, I went over some popular theories used to explain GERD, while also noting why most of them are incomplete. Today’s post will cover what I believe to be the best explanation for why acid reflux bedevils so many. In order to spare you some page hopping, I’ve re-printed the stomach illustration for your reference. And as in the first installment, an abbreviation index has also been included.
Delayed Stomach Emptying
In my estimation, delayed stomach emptying appears to be the best explanation for why so many suffer from gastroesophageal reflux disease or GERD. In support of this hypothesis, I’ll be writing about several different groups of people who suffer from acid reflux because of this.
As mentioned in part one, delayed stomach emptying will always increase the risk of acid reflux. If stomach contents are not periodically released by the opening of the pyloric sphincter, acid-laden contents many times swollen by the addition of certain foods that I’ll cover below, will cause stomach contents to move from the antrum of the stomach to the fundus. Once this happens, the risk of undigested food pushing through the lower esophageal sphincter (LES) and into the esophagus increases dramatically.
As in many medical conditions, delayed stomach emptying comes in varying degrees of intensity, ranging from mild to severe. The severe form of delayed stomach emptying is known by the medical term gastroparesis.
Gastroparesis is characterized by acid reflux, heartburn, chronic nausea, vomiting of undigested food, stomach bloating, stomach pain, palpitations and a consistent feeling of fullness even after eating a few bites of food. This condition is particularly prevalent in diabetics, especially type 2 diabetics.
In this latter group, the prevailing theory has been that chronically elevated glucose levels lead to nerve damage, especially in the vagus nerve thus accounting for this disorder. However, you’ll read later how certain simple dietary changes in this group resolves this condition, calling into question this nerve-damage hypothesis.
Elevated insulin levels are also thought to be a causal agent for delayed stomach emptying in diabetics. Insulin is a satiety hormone, meaning that insulin signals fullness to the brain and delays stomach emptying after a meal containing carbohydrates.
However, insulin is far from the only hormone to delay gastric emptying. Nor can insulin explain GERD in those with proper blood glucose control.
Known causes of delayed stomach emptying include connective tissue disorders like scleroderma and Ehlers-Danlos syndrome, Parkinson’s disease, previous abdominal surgery, chronic renal failure and high levels of progesterone during pregnancy. However, in a large number of cases there is no known cause for delayed stomach emptying.
Delayed stomach emptying affects women more often than men. There are a few hypotheses that solely reference differences in hormones between the sexes to explain this phenomenon, but as you’ll soon see, there are other explanations that may better account for these observations.
My take on why delayed stomach emptying is experienced more often in women than in men is explained by a combination of hormonal differences between genders, and how these differences impact opioid receptor function. The consistent variability seen in responses to opioids between the sexes is well documented in the scientific literature. (1) (2) (3) (4)
Apart from differences in gender responses to opioids, women as a group are more likely to experience pain, especially past the age of 50. (5) And they are also more apt to visit doctors than men. So as a group, they are more likely to be prescribed opioid-based pain medications. As you’ll soon see, this carries significant ramifications for gastrointestinal (GI) function.
So the first group I want to discuss who consistently experience slow stomach emptying and GERD are those on opioid drugs, both legal and illegal.
The digestive tract is very rich in opioid receptors. (6) For those unfamiliar with what a receptor is, think of it as a biological “lock” that can only be activated by a particular “key”, in this case opioid compounds that either the body itself produces (endogenous) or are taken in from the outside (exogenous).
There are three different types of opioid receptors in the GI tract: mu(μ), kappa(κ) and delta(δ). Of the three, mu receptors are most prevalent. These receptors are located throughout the digestive tract, but are found in the greatest number in the colon, stomach and ileum, which is the section of the small intestine closest to the colon.
Mu receptors in the brain depress the perception of pain and are capable of depressing respiratory function when opioids are given in large doses. In the digestive tract, activated mu receptors consistently and reliably inhibit motility, a fancy medical term for intestinal movement. Therefore, opioids always have the potential to negatively impact stomach function, including functioning of the pyloric sphincter at the base of this organ.
In times of acute stress or trauma, endogenous opioids are released by the body that activate these receptors and slow GI movement. This makes perfect sense as the GI tract is a very energy-intensive system. In an emergency that provokes the fight or flight system or causes trauma, energy needs to be quickly redirected away from digestion to the brain and muscles to prepare for fighting or fleeing or to deal with injury.
Exogenous opioids, say from drugs, have the same effect on these receptors as endogenous opioids. The activation of these receptors can lead to a condition known as opioid-induced bowel dysfunction (OIBD). Symptoms of OIBD are:
- stomach swelling
- stomach growling
- stomach pain
- acid reflux
- delayed stomach emptying
- feeling full for long periods of time after eating
- chronic burping
- decreased appetite
- sour stomach
- constipation alternating with diarrhea
- dry, hard to pass stools
- impacted colon
- feeling as if you have not completely evacuated your bowels after going to the toilet
- rectal pain when passing stools
- straining while going to the bathroom
- anal fissures
If many of these symptoms sound suspiciously to you like irritable bowel syndrome (IBS), congratulations! You can now advance to the head of the class.
Please keep in mind that not all symptoms may be experienced by everyone. And if all are experienced, they may not be experienced at the same time. And how people react to opioids is not only dependent on gender differences, but also individual genetic susceptibility.
These symptoms are well-known to anyone who is now on opioid-based painkillers. They are also intimately known to anyone abusing illegal opioids like heroin.
Now, how much of this is due solely to opioids and how much can be attributed to small intestinal fungal and bacterial overgrowth (SIFBO)? I haven’t a clue, and nor for that matter does anyone else.
As I wrote in my SIBO series, delayed intestinal movement always predisposes to contracting SIFBO by inhibiting the peristalsis that keeps colonic gram-negative bacteria from migrating into the small intestine and colonizing it. It is disturbances in intestinal movement that is the most common cause of SIFBO. Be sure to keep that little tidbit of information filed away for when you read the next post.
It is therefore not only conceivable, but highly probable, that opioid ingestion from whatever source will over time cause development of SIFBO.
In very severe forms of opioid-induced bowel dysfunction, fecal impaction is a distinct possibility necessitating medical intervention. The most severe form of OIBD goes by the name of narcotic bowel syndrome (NBS). (7)
Paradoxically, NBS is often accompanied by increasing stomach and intestinal pain. Why?
Because opioid receptors in the brain naturally build up tolerance to these substances over time, necessitating even greater doses to have the same pain-numbing effect. However, the opioid receptors in the stomach and intestines continue to respond to these opioids by paralyzing the gut.
Because many patients complain of stomach and intestinal pain when visiting their doctors, many primary-care physicians respond by prescribing painkillers ultimately making the problem worse. This scenario is also seen in opioid addicts who increase their dose to counteract similar GI pain.
Kurt Cobain, the now-deceased lead singer of the rock band Nirvana, was a heroin addict. When I read one of the biographies written about him, it became clear that one of the reasons for his continuing heroin habit, apart from addiction, was to self medicate against recurring stomach pain that had plagued him much of his life. This was obviously a self-defeating strategy that only ended when he died.
The following two case studies illustrate what can happen when doctors and patients are unaware of these opioid-induced side effects (7):
“A 42 year old female with a history of three caesarean deliveries, laparoscopy for lyses of adhesions [surgical removal of intestinal scar tissue] and irritable bowel syndrome for 23 years [emphasis mine], was referred for treatment for increasing pain. The mild and occasional post-prandial [after meal] cramping became associated over 3 years with another more persistent chronic lower abdominal pain that seemed different from her more typical IBS symptom. The new pain was not relieved by defecation, though there was associated abdominal bloating, nausea, vomiting and depressive symptoms. Notably, during these 3 years her primary care physician prescribed oxycodone 10 mg TID for the pain. Other medications included clonazepam 0.5mg TID and paroxetine 60 mg QD for anxiety and depressive symptoms.
On two occasions she tried to stop the narcotics, but was unsuccessful due to worsening pain. She was referred to UNC [University of North Carolina] gastroenterology clinic for consultation and agreed to withdraw the narcotic. She continued with clonazepam and paroxetine and was placed on a clonidine 0.1 mg 3/day for one week, with the oxycodone titrated to 5 mg twice a day for one week and discontinued. She then switched from the clonidine patch clonidine pills 0.1mg 3/day. One year later she was [sic] remained off narcotics with no reports of abdominal pain.”
Here we see that her primary-care physician, responding to the very real pain complaints of their patient, made the situation worse by prescribing oxycodone. I truly believe her doctor thought he or she was doing the right and compassionate thing for the patient, even though the outcome was the opposite. This scenario is sadly all too common in medical care.
Here’s another case study:
“A 37 year old female was referred to UNC GI clinic for treatment of chronic abdominal pain, nausea, vomiting and alternating diarrhea and constipation that began after a salmonella infection 15 years earlier. Increasing abdominal pain led to frequent emergency room visits, hospitalizations and 4 abdominal surgeries to diagnose or treat the abdominal pain. In addition, multiple CT scans, barium enemas, colonoscopy and abdominal/pelvic ultrasounds were also negative. Her physicians prescribed increasing dosages of narcotics for pain control over a 2- year period, and when seen in the UNC GI clinic she was taking 90mg/day of morphine sulfate.”
Lucky for her, the doctors at the University of North Carolina were able to wean her off the morphine after she unsuccessfully tried to do so on her own. They go on to say:
“Nine months later she reported only 3 episodes of mild abdominal pain and diarrhea that was consistent with her IBS. Several years later she graduated from law school and is currently in practice with no reports of abdominal pain.”
While no mention of GERD was made in either case, I think it’s safe to assume that both patients also suffered from recurring acid reflux during their ordeals.
Of course, going off narcotics would only be the start of curing their GI issues. That would entail clearing up SIFBO, making dietary modifications and replenishing their guts with beneficial bacteria via probiotics, fermented food and prebiotics. There is no indication in this paper that any of this was suggested so God only knows how well their digestive systems are doing.
This problem continues to get worse as more and more people are prescribed painkillers by their doctors for a variety of reasons, including relief from gastrointestinal distress. The following illustration summarizes what is likely to happen once someone gets on this opioid merry-go-round:
This issue is especially relevant to healthcare in the United States. With just 4.6% of the world’s population, the U.S. is responsible for 80% of the world’s opioid use. (8) And you wonder why gastrointestinal issues are such a huge health burden for the U.S. medical system?
Between 1997 and 2002, there was a more than 400% increase in the sales of oxycodone and methadone. (9) And between 1993 and 1999, there was a 100% increase in hydrocodone emergency room visits. These figures are somewhat stale, so you can imagine how much worse the statistics have become in the interim.
So what is a person to do who suffers from GERD because of the delayed stomach emptying caused by these drugs? There is no easy answer I can give apart from some dietary modifications I’ll be covering shortly.
The reality is that even if you change your dietary habits, that is not going to resolve your dilemma. And while proton pump inhibitors do offer relief, they do so at a cost that will become clearer in the next post.
I recognize that many, many people suffer from debilitating chronic pain. This can make life very miserable.
Sadly, some of this pain is often caused by the very medications many are taking to deal with it. Any hope of resolving GERD or any other GI disturbance due to these drugs is slim unless a pain sufferer can find other non-narcotic ways to deal with it.
In certain cases that may involve utilizing physical therapy, Pilates, yoga, tai chi, weight loss, massage, etc. In other cases, as in post-operative surgery or end-stage cancer treatment, opioids are the only viable means of controlling pain. Yet even here, cancer patients have been known to refuse to take these drugs because the cancer pain is more bearable than the resulting GI side effects.
At the very least, any changes to pain medications to relieve OIBD should be discussed with your physician. And if your doctor is ignorant of OIBD, then find another who will work with you to deal with its symptoms or find alternatives for managing pain in a non-narcotic way.
And as for addicts who take these opioid drugs recreationally, all I can say is that the problem is staring back at you in the mirror. As these drugs are extraordinarily addictive, it is imperative you seek help in kicking your addiction if you want any hope of conquering your stomach and intestinal issues.
Opioids, however, are not only generated endogenously by the body or the result of drug use. Some foods also form opioids upon their digestion, bringing me to the next group of GERD sufferers: celiacs.
Those with celiac disease experience an autoimmune destruction of the absorptive brush border in their small intestine. This reaction is triggered by the presence of the protein gluten which is found in wheat, barley and rye.
For many years it was generally accepted that celiac disease was mainly a disorder of malabsorption, which it obviously is. Hard to be healthy if you can’t properly digest and absorb the food you eat.
However, in the last ten years or so, celiac disease is gaining a reputation as a disorder that can, and often does manifest in ways that have seemingly nothing to do with GI function. In an editorial that appeared in the medical journal Clinical Gastroenterology and Hepatology, the author had this to say about the disease:
“During the past decade, we have become increasingly aware of the myriad possible presenting features of celiac disease. Indeed, it has reached the point at which listings of the signs, symptoms, and associated disorders of celiac disease overfill lecture slides, even at the smallest font. They also challenge the diagnostic acumen of clinicians when attempting to decide who should be tested for celiac disease. Considering gastrointestinal manifestations alone, the widely known and commonly accepted symptoms of celiac disease include diarrhea, constipation, abdominal pain and discomfort, bloating, increased gas, lactose intolerance, and irritable bowel–like symptoms.
Gastroesophageal reflux disease (GERD) symptoms including heartburn and acid regurgitation are unusual in that they are generally reliable and specific indicators of gastric acid reflux. They are also among the few gastrointestinal symptoms missing from the list of common manifestations of celiac disease. In this issue, however, Nachman et al from the celiac research group at Dr C. Bonorino Udaondo Gastroenterology Hospital in Buenos Aires report a striking association between untreated celiac disease and GERD symptoms. Their aims were to determine the prevalence of GERD symptoms in newly diagnosed celiac disease and to evaluate the effects of a gluten-free diet on those symptoms. They evaluated 133 adults with newly diagnosed and untreated celiac disease and 70 healthy controls using the GERD subscale of the Gastrointestinal Symptom Rating Scale (GSRS)….
…In this cohort of celiac patients, 30% had GERD scores of 3 or greater compared with less than 6% of controls. Results were similar using a more stringent cut-off value of 4 or higher. The prevalence of GERD symptoms in patients with classic manifestations of celiac disease, defined in this study as gastrointestinal symptoms, was particularly high at 35%. Even in those patients with atypical or silent celiac disease, GERD was more frequent (15%) than in controls. Interestingly, however, the prevalence of patients taking proton pump inhibitors (PPI) was similar in patients with celiac disease and controls.” (10)
So clearly, celiac disease is significantly associated with the risk of GERD. And going gluten-free appears to resolve the issue in many newly diagnosed celiacs.
An Italian study published in 2008 tracked what effect going gluten-free would have on GERD incidence in a group of 29 confirmed celiacs. (11) All celiacs had non-erosive esophageal disease.
These subjects were paired against an age and sex matched non-celiac group that also suffered from non-erosive GERD. Both groups were instructed to take proton pump inhibitors (PPI) once a day to control their symptoms. Additionally, the celiacs were told to start a gluten-free diet.
At eight weeks, those in either group who positively responded to PPI treatment were asked to stop the drug, while the celiacs were also instructed to continue with their gluten-free diet.
At this time, 25 out of 29 celiac patients (86.2%) and 20 out of 30 controls (66.7%) reported no acid reflux. Those that still reported symptoms were excluded from further study.
Six months later, the remaining 20 celiacs reported satisfactory or complete resolution of their GERD. In contrast, only 14 of the original 20 from the control group reported the same.
At one year, the same 20 celiac patients still reported satisfactory or complete resolution. In the control group, however, only 8 now reported the same.
By the end of the 2 year evaluation period, the same 20 celiacs were reporting resolution of their GERD, while only 3 were reporting the same in the control group. So of the original 20 members in the control group, 17 or 85% reported that their GERD had returned.
Now why would this be? The researchers had this to say in their summary:
“The improvement of GERD-related symptoms observed in CD [celiac disease] patients could be explained by the effect of gluten exorphins [gluten opioids] on gastric emptying, since, in 1989 Morley et al reported that pepsin hydrolyzed gluten prolongs gastrointestinal transit time which is prevented by simultaneous oral administration of naloxone [a drug that blocks the effect of opioids]. Therefore, although the effects of gluten exorphins still remain to be fully elucidated, it could be argued that the gluten exorphins, opioid peptides identified in the enzymatic digests of gluten, could exert a morphine-like activity on esophageal and gastric motility.”
These opioids are what put comfort into comfort foods. And the fear of doing without them causes unwavering terror in many who are told they may be better off if they avoided eating these grains.
I suspect that the major reason the majority of controls in this study relapsed was because like everyone else, they react to opioids in a similar manner. Given that everyone produces opioid peptides when eating foods containing gluten, it should come as no surprise why delayed stomach emptying and the GERD that often results from that should be so common in populations where eating wheat, barley and rye is the norm.
So for those of you out there popping acid-suppressing drugs to control your reflux, my advice is to severely limit or remove gluten grains entirely from your diet to see if that has any beneficial effect on your GERD.
Did you hear that sound? That’s the sound of readers clicking away from this post muttering to themselves “I’ll be damned if I’m going to give up eating [insert favorite gluten-containing food here]. This is total bullshit! Now where online did I see those cheap prices for Nexium?”
And to those people I say, good riddance. Don’t let the Googles hit you on the ass on your way out. However, do try to come back for part three of this series when I discuss the side effects of those proton pump inhibitors you love so much.
Gluten opioids aren’t the only things formed by the digestion of this protein. Gluten also increases levels of adenosine, a nueroinhibitory transmitter that also slows gastrointestinal function. (14)
Now, to what extent do these substances slow stomach emptying? Well, as the saying goes: the dose makes the poison. The more ingested, the more formed, and the more formed, the more effect it will have on stomach function.
However, dose alone cannot account for the wide variability in response to gluten. For that the nature of the gluten eaten (Was it in a food that was fermented? How long was it fermented?) along with individual genetic variability must also be factored in.
I bring up the issue of fermentation because all fermentation denatures or predigests protein. All things being equal, a baked gluten food that has undergone some fermentation will produce fewer of these opioid peptides upon digestion than a gluten food that hasn’t.
However, a lengthy fermentation that would thoroughly digest gluten to the point that no opioid peptides are formed after eating would result in a product that would be very dense and unpleasant to eat. It’s doubtful such a food would gain much acceptance in the marketplace.
Some people react to very small amounts of dietary opioids, while others can tolerate larger quantities before it begins to affect GI function. Tolerance also plays a role here. Someone who eats wheat often will develop some tolerance to its gut-stopping effects in contrast to someone else who rarely eats it. And there is evidence that as we age, amounts that at one time caused no appreciable impact on gastrointestinal motility begin to do so as we get older.
This probably is due to shifts in gut bacterial populations as we age. Just as opioid drugs predispose to SIFBO by slowing intestinal movement, it would be expected that the longer and more often someone eats food that forms opioids upon digestion, the more likely they are to develop SIFBO.
However, gluten opioids and adenosine aren’t the only dietary substances impacting stomach emptying and GERD incidence. Another class of opioid is formed from the digestion of a certain type of dairy:
This is an illustration of one section of the milk protein casein found in two different types of dairy. The casein at the top is derived from A2 dairy. The milk protein below from A1 dairy.
Each of these circles represents the different amino acids that make up this protein. Both are identical except for position 67. In A2 dairy, this position is occupied by the amino acid proline. In A1 dairy, this position is occupied by the amino acid histidine.
As humans, we are quite adept at producing enzymes capable of breaking apart or cleaving histidine bonds. Not so proline, which is why gluten, being very rich in this amino acid, is so difficult for us to digest into harmless peptides or individual amino acids.
The seven amino acid structure formed by the cleaving of the histidine bond in A1 dairy forms an opioid by the name of beta-casomorphin-7 (BCM7). The number seven refers to the number of amino acids in this peptide.
Just as gluten opioid peptides would be expected to have an effect on gastrointestinal function, including stomach emptying, so too BCM7. A1 dairy is derived from the milk of cows that originated in Europe. Although it contains the number 1 in its name, it’s actually a more recent evolutionary variant of older A2 cattle.
A1 dairy comes from the milk of Holstein and Frisian cows. These are the predominant dairy animals found in North America. A2 dairy is derived from Jersey cows, Asian and African cattle, goats and sheep. Milk and milk byproducts from A2 dairy sources do not form opioids.
Anyone trying to resolve GERD via dietary change needs to reassess their intake of A1 dairy casein. Because butter and cream contain negligible amounts of protein, both should be well tolerated regardless of which dairy source they are derived from.
Fermentation would be expected to have the same effect on A1 casein as it does on gluten. Therefore, fermented A1 dairy will tend to form less BCM7 than unfermented dairy. However, I caution anyone reading this that it may still contain enough BCM7 to affect GI function.
The harder the cheese, the more casein it tends to contain. Fermented soft cheeses are the best bet for GERD sufferers unless hard cheeses are made from A2 dairy sources.
As always, the dose makes the poison. Eating a small amount of A1 dairy will be a different experience than eating a large amount. Lactose intolerance will also be a different can of worms depending on which type of dairy is eaten.
Lactose intolerance results in lots of gas as colonic bacteria ferment undigested milk sugar that reaches the colon. In the presence of a colon also paralyzed by dairy or gluten opioids, this gas is likely to stay trapped for an extended period resulting in painful bloating.
The American habit of starting the day with a big bowl of wheat cereal soaked with A1 casein milk goes a long way in explaining the heartburn and acid reflux many report even before lunch time has rolled around.
Changing nutritional recommendations over the last forty years have made the problem worse. The advice by dietitians, nutritionists, government officials and physicians to cut dairy fat intake has led to the unintended consequence of more children and adults ingesting more A1 dairy protein.
Because casein is found in the non-fat portion of milk, the lower the level of fat, the higher its protein content.
According to the USDA food database, one cup of whole milk (244 g) has 7.69 grams of protein. One cup of non-fat milk contains 8.75 grams of protein and would therefore result in the formation of more BCM7 opioids upon digestion.
So if you are looking to get more bang out of the gut-paralyzing effects of A1 dairy-derived opioids, then by all means avoid butter, cream and whole milk, and choose non-fat or reduced-fat milk. You’re welcome!
Alcohol is another drug that reliably delays stomach emptying when over imbibed, so it shouldn’t come as much of a shock that alcoholics and binge drinkers often suffer from heartburn and GERD. Here are some of my musings from the post Alcohol and the Gastrointestinal Tract:
“Alcohol affects the esophagus in several ways. Alcohol always diminishes the wave-like motions that propel food along the digestive tract, and this is also true of the peristaltic movements that shuttle food from the throat to the stomach via the esophagus.
Alcohol also weakens the lower esophageal sphincter that exists to prevent stomach acid from entering the esophagus after food has passed. As a result, alcohol always predisposes to gastric reflux. This is dose dependent, so the more you drink, the more likely you are to experience this.
Drink enough and often, and you too may experience the joys of what is known as “nutcracker esophagus,” a lovely sensation that mimics a heart attack! Fun times!
Alcoholics and binge drinkers make up a large part of those suffering from Barrett’s esophagus. This condition is characterized by changes in the epithelial lining of the esophagus that results in mucosal inflammation. Barrett’s often precedes esophageal cancer, which isn’t surprising as chronic inflammation is a precursor to many cancers.
Another disorder of the esophagus experienced by alcoholics and binge drinkers is Mallory-Weiss syndrome. This condition involves bleeding caused by tears in the mucosal layer at the junction of the stomach and esophagus. Mallory-Weiss syndrome accounts for between 5% to 15% of upper GI bleeding episodes; and in 20% of these cases, the direct cause is repeated retching and vomiting from a night of binge drinking….
….High alcohol consumption, regardless of type, results in an increase in stomach alkalinity that compromises not only your ability to kill swallowed pathogens, but also your capacity to properly digest protein.
While small quantities of alcohol decrease the time food sits in the stomach, large quantities inhibit stomach emptying. The more you drink at any one sitting, the longer food will stay in the stomach.
Pair this with the relaxing of the lower esophageal sphincter, and you can soon experience the unbridled joy of heartburn, acid reflux, and re-tasting the food you ate hours earlier. And if you are in just the right position when you finally pass out, choking to death on your own vomit becomes a distinct possibility as was the unfortunate case for John Bonhom.”
The delayed stomach emptying effects of alcohol are amplified by the addition of opioids, dietary or otherwise. Finishing your evening of painting the town red with a greasy cheese burger stuck in the middle of extra large hamburger buns is as good a recipe as any to experience acid reflux and/or vomiting in your sleep when you finally go horizontal for the night. Just make sure to sleep on your side to avoid John Bonhom’s fate.
Low Thyroid Function
Another population that often complains of GERD and gastroparesis are those suffering from low thyroid function. Common causes of low thyroid function are the autoimmune disorder Hashimoto’s thyroiditis and euthyroid sick syndrome.
As you may recall from my post Thyroid Function And Gastrointestinal Distress, GERD is a common manifestation of this disorder because depressed thyroid function slows down all gastrointestinal movement, including stomach emptying. Constipation is a common complaint in ketogenic dieters for the same reason.
Note to physicians: please screen for thyroid disorders in your patients who present with GERD. That also includes asking your patients if any of them are on a ketogenic diet to screen for the presence of euthyroid sick syndrome.
Much has been said of fat’s ability to slow stomach emptying. And it does so by stimulating the release of the hormone cholecystokinin from the brush border of the small intestine in response to fat being present in this part of the digestive tract. So too much fat in a meal can easily delay emptying and predispose to GERD.
However, there is often a double standard applied to fat when it comes to explaining GERD. Those who point to fat’s ability to slow gastric emptying are typically the same people who tell us how absolutely wondrous fiber is because—–wait for it—–it reliably delays stomach emptying! This is claimed to be a joyous thing you see, because it will help you lose weight by decreasing your appetite.
But if feeling full to reduce appetite is such a wonderful ideal when it comes to fiber, why would it be a horrible ideal when it comes to fat? And indeed, many people who go on restricted carb diets credit their intake of fat along with protein for keeping hunger at bay and causing their weight loss.
Nevertheless, fat will delay stomach emptying so I don’t recommend overdoing fatty foods when trying to deal with GERD. The situation is of course made far worse when opioids are involved, binge drinking is engaged in, thyroid dysfunction is present and as you’ll read shortly, insoluble fiber is sopping up gastric juices in the stomach.
But as I extensively detailed in this post, the type of fat you eat also has impacts on gastrointestinal health separate and apart from delayed stomach emptying.
Given the pro-inflammatory and easily oxidizable nature of omega 6 polyunsaturated fatty acids (PUFAs), and their propensity to form lipid peroxidation byproducts, these fats would be expected to have a negative impact in those afflicted by recurring acid reflux by increasing oxidative stress in the cells lining the esophagus, the stomach and the pyloric sphincter.
And this also applies to omega 6 PUFAs that are sold as cold-pressed. Many believe they can skirt the issue of lipid peroxidation if they restrict themselves to purchasing these types of PUFAs. This is a delusion.
Digestion does not resemble a Disney movie where blue birds of happiness serenade digested food as it merrily makes its way through the gastrointestinal tract escorted by seven dwarfs. No, digestion is more akin to life inside a chemical plant.
It is an extremely volatile process where ingested food is subjected to a slurry of enzymes, hydrochloric acid, hormones, mucus, bicarbonate, the detergent action of bile, wild swings in pH, churning, pressure (as food is squirted past various sphincters) and high temperatures. Long before virgin PUFAs are incorporated into chylomicrons or make their way to the liver, oxidation and lipid peroxidation has already set in.
I can only tip my hat at the marketing genius of those who convinced hordes of health-conscious consumers that it was a privilege to pay extra for these inherently toxic oils. It certainly is a monetary privilege for places like Whole Foods and other “health food” stores who sell these fats to unsuspecting shoppers, including myself before I knew any better.
Fiber is the indigestible portion of fruits, vegetables, legumes, grains, nuts, seeds, etc.
Because fiber is not typically fermented in the small intestine unless a person suffers from SIFBO, it reaches the colon intact where it is set upon by gut flora and fermented. The results of this fermentation become readily apparent when you eat lots of beans, for example, and were spoofed in the classic campfire scene from the movie Blazing Saddles.
Fiber can be subdivided into soluble and insoluble fiber. Soluble fiber dissolves in water. Prebiotics are composed of soluble fiber. When properly mixed with water, they dissolve leaving no visible trace behind.
Insoluble fiber, also known as bulking fiber, does not disappear when mixed with liquid. It swells and creates a mixture that some would liken to sludge. Metamucil, which is composed of psyllium seed husks, is an insoluble fiber.
The recommendation to increase fiber consumption, especially from whole grains, has been beaten into the skulls of the American public since at least the mid 1970s and many have heeded the call. Lots of health claims are made for fiber supported not by findings from controlled clinical trials, but from confounder-prone nutritional epidemiology.
As I and others have repeatedly stated, epidemiology is inherently incapable of ever proving causation. At best, all it can show are statistical associations that need to be verified in trials capable of controlling for confounding variables.
Regardless of the delusions held by nutritional epidemiologists, no amount of statistical manipulation of the data derived from these studies can ever entirely control for these variables. Unsurprisingly then, nutritional advice derived from these exercises in mathematical masturbation are not only unscientific, they can be downright harmful to health.
For a refutation of the many supposedly health-promoting benefits attributed to consuming fiber from whole grains, I’ll direct you to Anthony Colpo’s website. Anthony takes special glee in destroying what he terms the whole-grain scam. I couldn’t agree with him more.
My focus today is a bit narrower than Anthony’s, however. I want to concentrate on fiber’s well documented ability to delay stomach emptying.
Now, delaying stomach emptying isn’t an issue if acid reflux or gastroparesis does not impact your life. Mild forms of delayed stomach emptying are normal and natural after you eat any meal. However, in those suffering from GERD, large amounts of dietary fiber can most definitely exacerbate the problem.
One way fiber slows gastric emptying is by its actions in the colon. I realize that sounds strange, but as I said in the last post, you can’t understand gastrointestinal function without taking into account how different sections of this complex system interact.
In a study published in 2003, nine people complaining of acid reflux participated in a cross-over study to determine if increasing fiber intake would lead to a higher incidence of GERD. (15) A cross-over study involves the same study participants undergoing the intervention, in this case supplementing with fiber, as well as taking the placebo during a different phase of the trial.
The fiber used in this study was good old fructooligosaccharide (FOS), a prebiotic. In this study, participants were asked to take 6.6 grams of FOS three times a day with each meal. As the dose recommended by me is 3 grams once a day, that works out to 6.6 times my recommended daily dose.
I can only assume that not only were their bifidobacteria extremely happy fermenting all of this FOS, many of these subjects were doing their best to recreate the Blazing Saddles campfire scene. I wouldn’t advise trying this near any open flames.
One result of all this FOS supplementation, in combination with their other sources of dietary fiber, was relaxation of the lower esophageal sphincter (LES). This, in turn, led to more acid reflux in those taking in this much soluble fiber.
The mechanisms behind this curious observation were theorized to be the result of increased production of a hormone called glucagon-like peptide 1 as a result of the bacterial fermentation of FOS. How exactly this hormone affects LES function is not entirely clear, although the researchers did offer a few theories that I won’t go into here. Regardless, the fermentation of fiber in the colon did increase GERD in these subjects.
Now, how realistic are these results outside of a clinical trial where study participants feel obligated to continue with an experiment regardless of side effects?
Well, it certainly is conceivable if you are taking in way too much prebiotic powder. I definitely don’t advise taking six times the recommended daily dosage of FOS no matter how beneficial it proves to be for colonic gut flora.
Getting this much FOS from eating a whole-food diet would typically be pretty hard to do unless you’re eating lots of bananas, raw onions, raw chicory root, raw garlic, raw asparagus, barley, raw jícama, raw leeks, raw Jerusalem artichokes or whole wheat. That said, of the items listed, the last one is often eaten not only daily, but multiple times during the day by many, many people. Combined with the gluten opioids released upon its digestion, the effects of this one food would of course increase the risk of acid reflux apart from its FOS content.
So yes, too much fiber reaching the colon can increase GERD incidence. However, I consider fermentation of fiber as more of an ancillary cause of GERD, not the main attraction.
The real culprit, in my estimation, occurs in the stomach due to the over consumption of insoluble fiber. This type of fiber, apart from not dissolving in gastric juice, is quite adept at acting like a sponge to absorb it.
For example, take a handful of crackers, especially whole-wheat crackers, crush them in a bowl and add liquid. You’ll soon see how the fiber absorbs the liquid and swells in volume. Anyone who has soaked beans overnight to neutralize the phytic acid contained in them before cooking has also observed this effect. Look in the container the next day, and where there was once water, there is now a mass of swollen legumes.
Insoluble fiber is unique in this ability to absorb liquid and increase in volume. This characteristic means that meals rich in this type of fiber are more likely to expand and push acid-laden stomach contents towards the fundas and LES resulting in acid reflux.
Insoluble fiber also has a tendency to form what are broadly defined as bezoars. Bezoars are stomach and intestinal obstructions.
Bezoars formed from insoluble fiber are called phytobezoars and even have their own entry on Wikipedia. Those who preach the gospel of plant-based nutrition rarely, if ever, bring up this unfortunate potential side-effect of eating the dietary equivalent of twigs and bark.
As I wrote in the last post, the pyloric sphincter will not open unless food is reduced to a diameter of 2 mm or less. Because fiber readily clumps together and expands in the stomach, it takes longer for it to be broken down and exit this organ.
If you’re a typical dietitian or nutritionist, this is considered cause for shouting hosannas to the heavens! But if you’re a GERD sufferer, this will be a consistent bane of your existence.
Confirmation for how fiber can cause the very gastropareris and GERD that afflict so many type 2 diabetics comes from a recently published doctoral theses out of the University of Gothenburg, Sweden. What this researcher discovered was nicely summarized in the Science Daily article that covered it:
“In the study, which involved 56 diabetes patients with gastroparesis, the subjects who were put on a small particle diet (smaller than 2 mm in diameter) experienced significantly less severe gastrointestinal symptoms than those who ate a conventional diabetes diet, which tends to focus on large particle foods. [foods high in insoluble fiber are large particle foods]
Small particle foods can be defined as food items that fall apart like a boiled potato when mashed with a fork. Examples include boiled, baked and mashed potatoes, fish gratin, meat loaf and thin soups. [Do note that the potatoes were all served without their skins.]
Patients who were put on this type of diet for at least 20 weeks experienced considerably fewer gastrointestinal symptoms such as vomiting, nausea, regurgitation, inability to finish a meal, bloating and lack of appetite.
The study shows that particle size is directly correlated with the process of gastric emptying: the patients who were put on the small particle diet showed the same rates of gastric emptying as the healthy control group.
They also displayed more normal blood sugar responses than those found for large particle meals.”
So banishing high particle foods from their diet resolved not only their gastrointestinal issues, but also helped normalize their blood sugar. But wait! Haven’t we been told repeatedly that because fiber slows gastric emptying, it leads to better blood sugar control than if diabetics ate mashed potatoes or pureed carrots?
Why yes we have. And so has every doctor under the sun, which is why they continue to erroneously recommend eating lots of insoluble fiber to their hapless patients suffering from delayed stomach emptying and GERD.
Sadly, I don’t expect this paper to have much impact in changing guidelines for fiber intake anytime soon. This dogma is firmly entrenched in the halls of academic nutrition, especially in the English-speaking world.
Just how much insoluble fiber will cause delayed stomach emptying and increase the risk of heartburn and acid reflux? Well, as before, that mostly depends on how much was eaten, what was eaten with it and the unique makeup of each individual.
For example, insoluble fiber from food that is devoid of gluten opioids will present less of an issue than insoluble fiber from whole-wheat, barley or rye. A bowl of cereal containing lots of insoluble fiber and A1 casein milk will cause more problems than one eaten with A2 dairy.
Now, by no stretch of the imagination am I recommending avoiding dietary fiber. I’ve spent a good chunk of my time on this website blogging about the importance of feeding beneficial colonic bacteria, in particular bifidobacteria, with prebiotic soluble fibers from both supplements and whole foods.
I have absolutely no issue with fiber derived from fruits and vegetables. There is little doubt in my mind that fiber from these sources is extremely important for health precisely because they feed beneficial gut flora.
Most people can handle both types of fiber contained in vegetables and fruit quite well, although there is wide individual variability here as well. For some, failing to peel an apple before eating it, or eating the skin off a baked potato, can present problems with acid reflux and gastrointestinal bloating, so your mileage may vary. In most circumstances, soluble fiber will be far better tolerated than insoluble fiber in susceptible individuals.
Unlike Paul Jaminet, co-author of the Perfect Health Diet book, I consider beans a harmless and nutritious food as long as phytic acid is neutralized and lectins are inactivated by long cooking times. The resistant starch they contain are known to feed beneficial bacteria. A meal of rice and beans also offers complete protein, is very inexpensive for those on a tight budget and can be extremely tasty.
That said, legumes are very rich in insoluble fiber, so if you suffer from GERD, you may need to cut back on your portions or avoid them altogether until you get a handle on your problem. Only you can determine what level of insoluble fiber intake causes acid reflux and heartburn.
Small Intestinal Fungal and Bacterial Overgrowth (SIFBO)
There is little doubt that SIFBO has a role in GERD. This isn’t surprising as some of the aforementioned foods, drugs and hormonal changes predispose to developing gut dysbiosis.
While there is no evidence consuming non-gluten fiber causes dysbiosis per se, the taking of acid-lowering medications to deal with resulting GERD can certainly initiate gut dysbiosis by compromising gastric-barrier defenses. And an abnormal fermentation of fiber in the small intestine is liable to lead to the same delay in stomach emptying as it does in the colon.
Of course, there are other causes of disturbed gut flora. Infections derived from eating improperly handled foods, overuse of antibiotics, chemotherapy, radiation, steroid medications, stress, excess refined fructose consumption–all can cause gut dysbiosis.
As I wrote in the last post, the majority of people who present to a doctor with GERD also suffer from other GI complaints like bloating, diarrhea alternating with constipation, gas, abdominal pain, etc. I believe that well before these people begin taking acid-lowering drugs, many are already afflicted by SIFBO. And a certain percentage of those with SIFBO are also suffering from undiagnosed celiac disease and/or undetected thyroid disorders.
Confirmation for this belief comes from a 2009 study that found that 60% of patients with confirmed gastroparesis tested positive for SIBO when administered a hydrogen and methane breath test. (16) However, I believe these figures grossly understate the true incidence of SIFBO.
Breath tests are notorious for under diagnosing bacterial overgrowth in the small intestine. About 20% to 30% of patients who test negative on these tests are later found to have a bacterial and/or fungal overgrowth when examined using endoscopy.
And even endoscopy, considered the gold standard of SIFBO diagnosis, is not foolproof if the sample aspirate is collected from an area that happens to be clear of pathogens. Intestinal infections can be quite localized and patchy, which is why the gut wall must be sampled from various locations.
Unlike endoscopy, a breath test is also incapable of determining yeast overgrowth in the small bowel. As many of you know, it has long been my contention that it is unlikely that any disturbance to beneficial gut flora is not simultaneously accompanied by disturbances in native yeast species like Candida albicans (C. albicans).
Now, the ability of pathogens, whether bacterial or fungal, to impact gastrointestinal function must be understood from the perspective of the organism causing the problem. Pathogens always create environments that benefit them, not us.
Cholera, for example, causes profuse diarrhea. And the reason it does so is because water is the way it spreads. By being partly washed out in diarrhea, it has a better chance of entering the water supply where it can infect more people. In areas where sanitation is poor, there is no need for the victim to be ambulatory in order to transmit the disease to others. Diarrhea and water are all the vectors needed to infect the next victim.
H. pylori has a unique ability to establish itself in the highly acidic environment of the stomach. However, its chances for survival are increased if it can reduce stomach acid by destroying the parietal cells responsible for its production, which is precisely what H. pylori proceeds to do. In doing so, it gains a survival advantage much to the detriment of the human who happens to be infected by it.
Other gut pathogens paralyze gut function, much as opioids do, through the release of toxic byproducts generated as a result of their metabolism. Again, from the perspective of the pathogen, this makes perfect sense. As periodic movement of the intestinal tract prevents pathogens from attaching to the gut wall, preventing this helps keep these organisms from being incorporated into feces and flushed down the toilet.
Gut pathogens like certain strains of E. coli, Klebsiella, Clostridia, etc., are well suited to thriving in inflamed environments. Beneficial gut flora do not do well in these conditions so their numbers decline.
As beneficial bacteria are the only things standing between a person and these pathogens, their decreasing numbers guarantee conditions that allow these organisms to bloom. And as there is no such thing as a healthy digestive tract without friendly gut flora, dysbiosis reliably leads to gastrointestinal dysfunction.
Another way pathogens disrupt GI function, and in particular stomach function, is by displacing histamine producing beneficial bacterial species like Lactobacillus casei from the small intestine. Recall that histamine is an important promoter of acid secretion in the stomach.
A class of acid-suppressive drugs by the name of histamine 2 blockers (or H2 blockers or H2-receptor antagonists) work because they block the receptors that these beneficial Lactobacillus bacteria utilize to maintain proper stomach acid levels.
By displacing these histamine-producing bacteria, gut pathogens that have taken up residence in the small intestine ensure that more swallowed pathogens survive transit through the stomach by lowering the production of stomach acid. It’s conceivable that the organisms responsible for displacing these Lactobacillus species can communicate with H. pylori to maintain an environment conducive to the survival of both H pylori and the pathogens that have settled in the small intestine.
That a certain segment of the “alternative health” community is choosing to avoid taking probiotics containing histamine-producing strains, thereby unintentionally undermining their gastric-barrier defenses, displays a level of ignorance that would make Thomas Jefferson shake his head in despair were he alive today. Not only are these people confusing H1 histamine receptors with H2 receptors, they lack a holistic understanding of the myriad ways beneficial bacteria work to keep us healthy.
I mentioned in the last post that obesity is typically associated with GERD, although there are plenty of people who are not overweight and also suffer from this problem. Nonetheless, GERD is often experienced by the obese who also have metabolic syndrome.
As I’ve written over the past year or so, the translocation of bacteria, especially lipopolysaccharide (LPS) containing gram-negative bacteria, across the gut wall and into the liver and systemic circulation, always provokes an inflammatory immune response. And this endotoxemia also provokes the release of the stress hormone cortisol via activation of the hypothalamic-pituitary-adrenal axis.
This makes perfect sense as LPSs are innately perceived by the body as a threat, one that can potentially cause death if their numbers multiply unchecked. It is LPSs, and the intense immune response to them, that dispatches patients to the hereafter who are unfortunate enough to contract sepsis.
Chronic endotoxemia, and the stress response it induces, always results in depressed GI function. In my post Endotoxemia, Stress and Metabolism I wrote:
“It is well documented that acute cortisol release as occurs in sepsis, can directly depress secretion of TSH [thyroid stimulating hormone] from the pituitary gland and suppress downstream thyroid hormone release and conversion. While chronic endotoxemia appears to spare direct damage to the hypothalamic-pituitary-thyroid axis, at least initially, it does lower metabolism by promoting euthyroid sick syndrome (ESS).
In this syndrome, levels of both TRH [thyroid releasing hormone] and TSH are normal, as are production of both T3 and T4 by the thyroid gland. In fact, clinical tests that fail to directly measure levels of serum T3 or reverse T3 will typically show no abnormalities in someone experiencing ESS.
The mechanism for metabolic derangement in euthyroid sick syndrome appears to be two-fold. First, translocating LPSs will directly down-regulate thyroid receptor activity. All hormones require properly functioning receptors to affect biological processes. By interfering with receptor activity in the liver, lipopolysaccharides prevent these thyroid hormones from carrying out their functions even when their levels are in the normal range.
Secondly, stress hormones directly reduce the conversion of T4 to T3 in the liver, kidneys, and other peripheral organs. They do so because one of the functions of glucocorticoids is to shuttle energy to the brain and the heart in emergencies. Chronic stress, however, is a never-ending “emergency” that causes chronic stimulation of the HPA axis and cortisol release.”
So endotoxemia and the cortisol release it stimulates slows GI function, predisposing to conditions like GERD and constipation. And chronic cortisol release tends to depress the motivation to move while simultaneously increasing an appetite for refined carbohydrates and fat. (17) (18) (19) (20) (21) This is a perfect recipe for weight gain, and a major reason why being metabolically unhealthy and obese is often associated with GERD.
Putting it all together
The dramatic increase in GERD incidence in the Western world is not due to one cause. Rather, through a confluence of different factors, many of them unintended, GERD has come to impact a growing percentage of the population in developed countries.
The first factor involves the overall decrease in H. pylori infection rates in the developed world as a direct result of antibiotic use. This has led to a normalization in stomach acid levels that can elevate acid reflux risk if certain foods and/or drugs, including alcohol, are ingested.
With normalized stomach acid production, foods that were better tolerated in past generations, like those forming gluten and dairy opioids, are now causing more and more people trouble. Concurrent with successful eradication of H. pylori infection, has been a push by nutritional experts and the medical professionals gullible enough to believe them, to encourage the overconsumption of insoluble fiber from whole gluten grains.
For many of these nutritional advisors, concerns about gluten are routinely dismissed as irrelevant for anyone other than the 1% or so who are believed to have celiac disease. I say believed because while this statistic is usually trotted out to silence people like myself who warn against the habitual consumption of these grains, no one has any real ideal how many people actually have this disease.
In order to arrive at a true figure, every man, woman and child would have to be tested, yet clearly they are not. And since this disease can develop later in life in those who are genetically susceptible to getting it (estimated to be about 50% of the U.S. population), a negative test result only confirms that the individual hasn’t developed celiac disease up to that point, not that they never will.
But even if this 1% estimate were valid, there are an increasing number of people reporting some form of gluten intolerance, with or without genetic predisposition to celiac disease. This is now a recognized disorder going under the name of non-celiac gluten sensitivity. There are still others who suffer from wheat allergies. So the soothing reassurances offered by many nutritionists and dietitians about the wholesomeness of eating whole-gluten grains are beginning to ring increasingly hollow.
This colorful flow chart is from a paper published earlier this year in the American Journal of Gastroenterology titled Dietary Proteins and Functional Gastrointestinal Disorders. (22) It depicts the many ways wheat and/or gluten can impact a patient suffering from GI upset.
It is meant as a helpful guide for the clinician to help him or her determine what it is about these grains that may be causing the patient gastrointestinal distress. I shook my head when I saw this thinking how much simpler the chart would be if it just said in big bold letters: LIMIT OR ELIMINATE GLUTEN GRAINS OR ANYTHING THAT CONTAINS GLUTEN FROM YOUR DIET!
But that would seriously piss off the North American wheat barons, the congressmen and senators that represent them, the fast-food and restaurant industry and processed food manufacturers everywhere. Such advice would also put a serious crimp in the balance of trade of the United States as this country is currently one of the reigning champs of wheat exports.
So many continue to be afflicted with delayed stomach emptying, gastroparesis and acid reflux as they continue to eat loads of insoluble, bulking fiber, often replete with gluten. Why? Because they continue to drink the fiber-from-whole-grains-is-always-good-for-you Kool-Aid.
On the other end, these same people suffer when they nearly faint trying to squeeze out bulked-up turds resembling dildos modeled after a well-endowed male porn star. They strain mightily to expel these enormous feces, many times hard and dry, through a rectal opening that measures only 1.37″ (3.5cm) in diameter at its widest.
And people wonder why they suffer from anal fissures and hemorrhoids? For more on the “blessings” of over consuming insoluble dietary fiber, especially from whole grains, I again refer you to the book Fiber Menace by Konstantin Monastyrsky.
At the same time the “experts” were trying to convince us all to eat more like a cow with four stomachs than a human with just one, a simultaneous push was made to lower animal fat consumption, supposedly to avoid developing diseases claimed to be caused by consuming these types of fat. In the case of dairy, that meant advising the public against consuming high fat, yet low casein butter and cream, and instead recommending their replacement with their higher protein, lower fat alternatives.
Consumers were encouraged to switch from whole milk to skim or non-fat dairy. This advice oftentimes coming from the same people who love to prattle on about the importance of eating whole foods, blind to their own hypocrisy in advocating the consumption of a food that is anything but.
This shift in dairy consumption has, of course, increased exposure to dairy opioids as very little dairy available for sale in the United States comes from A2 casein sources like Jersey cows or goats.
Along with these dietary changes, shifts in drug habits have also occurred over the last few decades. I’ve already mentioned the huge increase in the use of opioid-based pain medications in the United States.
This has paralleled an alarming increase in opioid abuse for recreational purposes estimated at over 12 million people in the U.S. alone. (23) Whole swaths of this country are now inundated with oxycodone (Oxycontin) addicts all looking for their next fix, and wondering why oh why they suffer so horribly from GERD and other gastrointestinal complaints.
Then there is the issue of binge drinking, a habit that is especially popular in Northern Europe, Eastern Europe and the English-speaking world. Rather than seeing any improvement, many governments now report increases in this behavior, especially among the young and those newly retired. (24)
Coupled with all of this is the increasing prevalence of gut dysbiosis manifested by soaring rates of IBS, Crohn’s disease, allergies, ulcerative colitis and more. Dysbiosis is more than capable of causing GERD even in the absence of opioids, binge drinking or excessive fat and fiber intake.
The rise in dysbiosis is partly explained by the overuse of antibiotics. These drugs have saved millions of lives, and I wouldn’t want to live in a world without them.
However, their indiscriminate use has not only led to the development of antibiotic-resistant bacterial strains, but to a multi-generational shift in beneficial gut flora populations. While the eradication of strains like H. pylori is net positive, the devastation of other commensal bacteria and overall disturbances in gut flora communities is not.
Finally, we have a medical profession seemingly entranced by the copious amounts of junk research findings flowing from the hallowed halls of academic nutrition, much of it happily funded by the generous financial contributions of food conglomerates. But lack of basic nutritional knowledge is not the only problem afflicting modern medicine.
There is often a cavalier disregard for the importance of our beneficial gut bacteria from many medical practitioners. While there is a growing cohort of physicians who appreciate how vital gut flora is to health and well-being, there are still a large number of doctors who consider the entire topic to be nothing more than another form of woo.
Because of this attitude, there is often a gross under appreciation for the damage that can be caused to their patients by the long-term use of proton pump inhibitors or histamine-2 blockers to control GERD. There is little doubt in my mind that the perception of these drugs as being relatively harmless has been fostered by the pharmaceutical companies that manufacture them, and for good reason. Proton pump inhibitors and histamine-2 blockers are some of the biggest selling drugs on the market.
In the next and final installment in this series, I’ll detail what research is now revealing about the disturbing side effects that can be expected from the long-term use of these very popular and widely prescribed drugs.