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kiss health goodnightNote: this is the sixth and final article in a series about heartburn and GERD. If you haven’t done so already, you’ll want to read Part I, Part II, Part III, and Part IVa, and Part IVb before reading this article.

In this final article of the series, we’re going to discuss three steps to treating heartburn and GERD without drugs. These same three steps will also prevent these conditions from developing in the first place, and keep them from returning once they’re gone.

To review, heartburn and GERD are not caused by too much stomach acid. They are caused by too little stomach acid and bacterial overgrowth in the stomach and intestines. Therefore successful treatment is based on restoring adequate stomach acid production and eliminating bacterial overgrowth.

This can be accomplished by following the “three Rs” of treating heartburn and GERD naturally:

  1. Reduce factors that promote bacterial overgrowth and low stomach acid.
  2. Replace stomach acid, enzymes and nutrients that aid digestion and are necessary for health.
  3. Restore beneficial bacteria and a healthy mucosal lining in the gut.

  1. Reduce factors that promote bacterial overgrowth and low stomach acid

Carbohydrates

As we saw in Part II and Part III, a high carbohydrate diet promotes bacterial overgrowth. Bacterial overgrowth – in particular H. pylori – can suppress stomach acid. This creates a vicious cycle where bacterial overgrowth and low stomach acid reinforce each other in a continuous decline of digestive function.

It follows, then, that a low-carb (LC) diet would reduce bacterial overgrowth. To my knowledge there have only been two small studies done to test this hypothesis. The results in both studies were overwhelmingly positive.

The first study was performed by Professor Yancy and colleagues at Duke University. They enrolled five patients with severe GERD that also had a variety of other medical problems, such as diabetes. Each of these patients had failed several conventional GERD treatments before being enrolled in the study. In spite of the fact that some of these patients continued to drink, smoke and engage in other GERD-unfriendly habits, in every case the symptoms of GERD were completely eliminated within one week of adopting a very low carbohydrate (VLC) (<20 grams/day) diet! The patients were able to stop all antacids and prescription stomach medicines and this improvement continued even after they liberalized their carbohydrate intake to a more tolerable 70 grams per day.

The second study (PDF) was performed by Yancy and colleagues a few years later. This time they examined the effects of a VLC diet on eight obese subjects with severe GERD. They measured the esophageal pH of the subjects at baseline before the study began using something called the Johnson-DeMeester score. This is a measurement of how much acid is getting back up into the esophagus, and thus an objective marker of how much reflux is occurring. They also used a self-administered questionnaire called the GSAS-ds to evaluate the frequency and severity of 15 GERD-related symptoms within the previous week.

At the beginning of the diet, five of eight subjects had abnormal Johnson-DeMeester scores. All five of these patients showed a substantial decrease in their Johnson-DeMeester score (meaning less acid in the esophagus). Most remarkably, the magnitude of the decrease in Johnson-DeMeester scores is similar to what is reported with PPI treatment. In other words, in these five subjects a very low carbohydrate diet was just as effective as powerful acid suppressing drugs in keeping acid out of the esophagus.

All eight individuals had evident improvement in their GSAS-ds scores. The GSAS-ds scores decreased from 1.28 prior to the diet to 0.72 after initiation of the diet. What these numbers mean is that the patients all reported significant improvement in their GERD related symptoms. Therefore, there was both objective (Johnson-DeMeester) and subjective (GSAS-ds) improvement in this study.

It’s important to note that obesity is an independent risk factor for GERD, because it increases intra-abdominal pressure and causes dysfunction of the lower esophageal sphincter (LES). The advantage to a low-carb diet as a treatment for GERD for those who are overweight is that LC diets are also very effective for promoting weight loss.

I don’t recommend VLC diets for extended periods of time, as they are unnecessary for most people. Once you have recovered your digestive function, a diet low to moderate in carbohydrates should be adequate to prevent a recurrence of symptoms.

An alternative to a VLC is something called a “specific carbohydrate diet” (SCD), or the GAPS diet. In these two approaches it is not the amount of carbohydrates that is important, but the type of carbohydrates. The theory is that the longer chain carbohydrates (disaccharides and polysacharides) are the ones that feed bad bacteria in our guts, while short chain carbohydrates (monosacharides) don’t pose a problem. In practice what this means is that all grains, legumes and starchy vegetables should be eliminated, but fruits and certain non-starchy root vegetables (winter squash, rutabaga, turnips, celery root) can be eaten. These are not “low-carb” diets, per se, but there is reason to believe that they may be just as effective in treating heartburn and GERD. See the resources section below for books and websites about these diets, which have been used with dramatic success to treat everything from autism spectrum disorder (ASD) to Crohn’s disease.

Be careful to avoid the processed low-carb foods sold in supermarkets. Instead, I suggest what is known as a “paleolithic” or “primal” approach to nutrition. Mark’s Daily Apple is a great online resource for this approach, and his book “Primal Blueprint” is a good summary of the principles.

Fructose and artificial sweeteners

As I pointed out in Part II, fructose and artificial sweeteners have been shown to increase bacterial overgrowth. Artificial sweeteners should be completely eliminated, and fructose (in processed form especially) should be reduced.

Fiber

High fiber diets and bacterial overgrowth are a particularly dangerous mix. Remember, Almost all of the fiber and approximately 15-20% of the starch we consume escape absorption. Carbohydrates that escape digestion become food for intestinal bacteria.

Prebiotics, which can be helpful in re-establishing a healthy bacterial balance in some patients, should probably be avoided in patients with heartburn and GERD. Several studies show that fructo-oligosaccharides (prebiotics) increase the amount of gas produced in the gut.

The other problem with fiber is that it can bind with nutrients and remove them from the body before they have a chance to be absorbed. This is particularly problematic in GERD sufferers, who may already be deficient in key nutrients due to long term hypochlorydria (low stomach acid).

H. pylori

In Part III we looked at the possible relationship between H. pylori and GERD. While I think it’s a contributing factor in some cases, the question of whether and how to treat it is less clear. There is some evidence that H. pylori is a normal resident on the human digestive tract, and even plays some protective and health-promoting roles. If this is true, complete eradication of H. pylori may not be desirable. Instead, a LC or specific carbohydrate diet is probably a better choice as it will simply reduce the bacterial load and bring the gut flora back into a state of relative balance.

The exception to this may be in serious or long-standing cases of GERD that aren’t responding to a VLC or LC diet. In this situation, it may be worthwhile to get tested for H. pylori and treat it more aggressively.

Dr. Wright, author of Why Stomach Acid is Good For You, suggests using mastic (a resin from a Mediterranean and Middle Eastern variety of pistachio tree) to treat H. pylori. A 1998 in vitro study in the New England Journal of Medicine showed that mastic killed several strains of H. pylori, including some that were resistant to conventional antibiotics. Studies since then, including in vivo experiments, have shown mixed results. Mastic may be a good first-line therapy for H. pylori, with antibiotics as a second choice if the mastic treatment isn’t successful.

  1. Replace stomach acid, enzymes and nutrients that aid digestion and are necessary for health

HCL with Pepsin

If you have an open-minded doctor, or one that is aware of the connection between low stomach acid and GERD, ask her to test your stomach acid levels. The test is quite simple. A device called a Heidelberg capsule, which consists of a tiny pH sensor and radio transmitter compressed into something resembling a vitamin capsule, is lowered into the stomach. When swallowed, the sensors in the capsule measure the pH of the stomach contents and relay the findings via radio signal to a receiver located outside the body.

In cases of mild to moderate heartburn, actual testing for stomach acid production at Dr. Wright’s Tahoma clinic shows that hypochlorydria occurs in over 90 percent of thousands tested since 1976. In these cases, replacing stomach acid with HCL supplements is almost always successful.

Although testing actual stomach acid levels is preferable, it is not strictly necessary. There is a reasonably reliable, “low-tech” method that can be performed at home to determine whether HCL supplementation will provide a benefit. To do this test, pick up some HCL capsules that contain pepsin. HCL should always be taken with pepsin because it is likely that if the stomach is not producing enough HCL, it is also not producing enough pepsin.

Note: HCL should never be taken (and this test should not be performed) by anyone who is also using any kind of anti-inflammatory medication such as corticosteroids (e.g. predisone), aspirin, Indocin, ibuprofen (e.g. Motrin, Advil, etc.) or other NSAIDS. These drugs can damage the GI lining that supplementary HCL might aggravate, increasing the risk of gastric bleeding or ulcer.

To minimize side effects, start with one 650 mg capsule of HCL w/pepsin in the early part of each meal. If there are no problems after two or three days, increase the dose to two capsules at the beginning of meals. Then after another two days increase to three capsules. Increase the dose gradually in this stepwise fashion until you feel a mild burning sensation. At that point, reduce the dosage to the previous number of capsules you were taking before you experienced burning and stay at that dosage. Over time you may find that you can continue to reduce the dosage, or you may also find that you may need to increase the dosage.

In Dr. Wright’s clinic, most patients end up at a dose of 5-7 650 mg capsules. In my more limited experience, 3-4 capsules is the norm.

Bitters

Another way to stimulate acid production in the stomach is by taking bitter herbs. “Bitters” have been used in traditional cultures for thousands of years to stimulate and improve digestion. More recently, studies have confirmed the ability of bitters to increase the flow of digestive juices, including HCL, bile, pepsin, gastrin and pancreatic enzymes. 1

Unsurprisingly, there aren’t many clinical studies evaluating the therapeutic potential of unpatentable and therefore unprofitable bitters. However, in one uncontrolled study in Germany, where a high percentage of doctors prescribe herbal medicine, gentian root capsules provided dramatic relief of GI symptoms in 205 patients.

The following is a list of bitter herbs commonly used in Western and Chinese herbology:

  • Barberry bark
  • Caraway
  • Dandelion
  • Fennel
  • Gentian root
  • Ginger
  • Globe artichoke
  • Goldenseal root
  • Hops
  • Milk thistle
  • Peppermint
  • Wormwood
  • Yellow dock

Bitters are normally taken in very small doses – just enough to evoke a strong taste of bitterness. Kerry Bone, a respected Western herbalist, suggests 5 to 10 drops of a 1:5 tincture of the above herbs taken in 20 mL of water.

An even better option is to see a licensed herbalist who can prescribe a formula containing several of the herbs above as appropriate for your particular condition.

Apple cider vinegar, lemon juice, raw (unpasteurized) sauerkraut and pickles are other time-tested, traditional remedies that often relieve the symptoms of heartburn and GERD. However, although these remedies may resolve symptoms, they do not increase nutrient absorption and assimilation to the extent that HCL supplements do. This may be important for those who have been taking acid suppressing drugs for a long period.

It is also important to avoid consuming liquid during meals. Water is especially problematic, because it literally dilutes the concentration of stomach acid. A few sips of wine is probably fine, and may even be helpful.

Finally, for those who have been taking acid stopping drugs for several years, it may be necessary to replace the nutrients that are not absorbed without sufficient stomach acid. These include B12, folic acid, calcium, iron and zinc. It’s best to get your levels tested by a qualified medical practitioner, who can then help you replace them through nutritional changes and/or supplementation.

  1. Restore beneficial bacteria and a healthy mucosal lining in the gut

Probiotics

Because bacterial overgrowth is a major factor in heartburn and GERD, restoring a healthy balance of intestinal bacteria is an important aspect of treatment. Along with performing several other functions essential to digestive health, beneficial bacteria (probiotics) protect against potential pathogens through “competitive inhibition” (i.e. competing for resources).

While I haven’t seen any specific research on probiotics in the treatment of GERD, numerous studies have demonstrated their effectiveness in treating a variety of G.I. conditions.

Researchers in Australia have shown that probiotics are effective in reducing bacterial overgrowth and altering fermentation patterns in the small bowel in patients with IBS. Probiotics have also been shown to be effective in treating Crohn’s disease, ulcerative colitis, and other digestive conditions.

I am often asked what type of probiotics I recommend. First, I am not a big believer in supplements. I think we should always attempt to get the nutrients we need from food. This is also true for probiotics. Fermented foods have been consumed for their probiotic effects for thousands of years. What’s more, contrary to popular belief and the marketing of commercial probiotic manufacturers, foods like yogurt and kefir generally have a much higher concentration of beneficial microorganisms than probiotic supplements do.

For example, even the most potent commercial probiotics claim to contain somewhere between one and five billion microorganisms per serving. (I say “claim” to contain because independent verification studies have shown that most commercial probiotics do not contain the amount of microorganisms they claim to.) Contrast that with a glass of homemade kefir, a fermented milk product, contains as many as 5 trillion beneficial microorganisms!

What’s more, fermented milk products like kefir and yogurt offer more benefits than beneficial bacteria alone, including minerals, vitamins, protein, amino acids, L-carnitine, fats, CLA, and antimicrobial agents. Studies have even shown that fermented milk products can improve the eradication rates of H. pylori by 5-15%.

The problem with fermented milk products in the treatment of heartburn and GERD, however, is that milk is relatively high in carbohydrates. This may present a problem for people with severe bacterial overgrowth. However, relatively small amounts of kefir and yogurt are therapeutic and may be well tolerated. It’s best to make kefir and yogurt at home, because the microorganism count will be much higher. Lucy’s Kitchen Shop sells a good home yogurt maker, and Dom’s Kefir site has exhaustive information on all things kefir. If you do buy the home yogurt maker, I suggest you also buy the glass jar that Lucy’s sells to make it in (rather than using the plastic jar it comes with).

Another option is to eat non-dairy (and thus lower-carb) unpasteurized (raw) sauerkraut and pickles and/or drink a beverage called kombucha. Raw sauerkraut can easily be made at home, or sometimes found at farmer’s markets. Bubbies brand raw pickles are sold at health food stores, as is kombucha, but both of these can also be made quite easily at home.

If you do choose to take capsules, make sure the brand you choose is reputable and the viability of their product has been independently verified. Natren is such a brand in the US.

Bone broth and DGL

Restoring a healthy gut lining is another important part of recovering from heartburn and GERD. Chronic stress, bacterial overgrowth, and certain medications such as steroids, NSAIDs and aspirin can damage the lining of the stomach. Since it is the mucosal lining of the stomach that protects it from its own acid, a damaged stomach lining can cause irritation, pain and ultimately, ulcers.

Homemade bone broth soups are effective in restoring a healthy mucosal lining in the stomach. Bone broth is rich in collagen and gelatin, which have been shown to benefit people with ulcers. It’s also high in proline, a non-essential amino acid that is an important precursor for the formation of collagen. Bone broth also contains glutamine, an important metabolic fuel for intestinal cells that has been shown to benefit the gut lining in animal studies. See this article and this one for more information about the healing power of bone broth, and how to make it.

Although I’m not big on supplements, as I explained above, I’m not averse to using them when they can be helpful – especially for short periods. Deglycyrrhizinated licorice (DGL) has been shown to be effective in treating gastric and duodenal ulcers, and works as well in this regard as Tagamet or Zantac, with far fewer side effects and no undesirable acid suppression. In animal studies, DGL has even been shown to protect the stomach lining against damage caused by aspirin and other NSAIDs.

DGL works by raising the concentration of compounds called prostaglandins, which promote mucous secretion, stabilize cell membranes, and stimulate new cell growth – all of which contributes to a healthy gut lining. Both chronic stress and use of NSAIDs suppress prostaglandin production, so it is vital for anyone dealing with any type of digestive problem (including GERD) to find ways to manage their stress and avoid the use of NSAIDs as much as possible.

When natural treatments may not be enough

There may be some cases when an entirely natural approach is not enough. When there is tissue damage in the esophagus, for example, a surgical procedure called “gastroplication” which repairs the LES valve may be necessary. These procedures don’t have the potential to create nutrient deficiencies and disease the way acid blockers do. It is advisable for anyone suffering from a severe case of GERD to consult with a knowledgeable physician.

Conclusion

The mainstream medical approach to treating heartburn and GERD involves taking acid stopping drugs for as long as these problems occur. Unfortunately, because these drugs not only don’t address the underlying cause of these problems but may make it worse, this means that people who start taking antacid drugs end up taking them for the rest of their lives.

This is a serious problem because acid stopping drugs promote bacterial overgrowth, weaken our resistance to infection, reduce absorption of essential nutrients, and increase the likelihood of developing IBS, other digestive disorders, and cancer. The manufacturers of these drugs have always been aware of these problems. When acid-stopping drugs were first introduced, it was recommended that they not be taken for more than six weeks. Clearly this prudent advice has been discarded, as it is not uncommon today to encounter people who have been on these drugs for decades – not weeks.

What is especially disturbing about this is that heartburn and GERD are easily prevented and cured by making simple dietary and lifestyle changes, as I have outlined in this final article.

Unfortunately, the corruption of our “disease-care” system by the financial interests of the pharmaceutical companies virtually guarantees that this crucial information will remain obscure. Drug companies make more than $7 billion a year selling acid suppressing medications. The last thing they want is for doctors and their patients to learn how to treat heartburn and GERD without these drugs. And since 2/3 of all medical research is sponsored by drug companies, it’s virtually guaranteed that we won’t see any large studies on the effects of a low-carb diet on acid reflux and GERD.

So once again it’s up to us to discover the truth and be our own advocates. I hope this series of articles has served you in that goal.

I have created a “myth busing report” page for heartburn and GERD which contains an index of these articles, as well links to books and other offsite resources. If anyone you know is suffering from heartburn and GERD, please direct them to http://thehealthyskeptic.org/heartburn.

  1. Wright, Jonathan M.D. Why Stomach Acid is Good For You. M Evans 2001. p.142

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picture of H. pyloriNote: this is the third article in a series about heartburn and GERD. If you haven’t done so already, you’ll want to read Part I and Part II before reading this article.

Right after publishing yesterday’s article (The hidden causes of heartburn and GERD), I came across a new research (PDF) study hot off the presses that adds support to the theory that GERD is caused in part by bacterial overgrowth. Before moving on to my next planned article in the series, I want to take some time to review this study and discuss its implications.

Malekzadeh & Moghaddam performed a retrospective study to investigate the prevalence of GERD in patients with IBS and vice versa. The data comes from a very large number of patients (6,476). To my knowledge it’s the largest data set that has been reported about the overlap between GERD and IBS.

The authors found that 64% of IBS subjects studied also had GERD, whereas 34% of the GERD patients also had IBS. They also found that the prevalence of all functional symptoms (such as nausea, changes in bowel movement, headache, etc.) was higher in overlapping GERD and IBS subjects than the prevalence in GERD subjects without IBS or IBS subjects without GERD.

Implications of the connection between GERD and IBS

What this correspondence suggests, of course, is exactly what I argued in the last article: that IBS and GERD may very well share a common etiology and underlying mechanism. From the conclusion:

This finding shows that in overlapping GERD and IBS, other functional abnormalities of the GI tract are also highly prevalent, suggesting a common underlying dysfunction.

The authors even speculate that the underlying cause may be an overgrowth of bacteria. Specifically, they mention H. pylori as a possible culprit. I think they’re on to something!

Assessing the role of H. pylori infection in GERD and IBS patients could be a target of future research, as in the present study the prevalence of H. pylori infection in GERD patients was found to be greater than in non- GERD patients.

The role of H. pylori in GERD

I believe that H. pylori infection plays a significant role in the pathogenesis of GERD and other digestive disorders.

H. pylori is the most common chronic bacterial pathogen in humans. Statistics indicate that more than 50% of the world population is infected. Infection rates increase with age. In general, the prevalence of infection raises 1% with every year of life. So we can expect that approximately 80% of 80 year-olds are infected with H. pylori.

Second, we know that H. pylori suppresses stomach acid secretion. In fact, this is how it survives in the hostile acidic environment of the stomach, which would ordinarily kill all bacteria. Treating an asymptomatic H. pylori infection with antibiotics increases stomach acidity and eradicating H. pylori with antibiotics improves nearly all patients suffering from hypochlorhydria.

Although it is commonly assumed that stomach acid production declines with age, recent studies suggest that the secretion of stomach acid doesn’t decrease with age and that the trend is actually to increase, especially in men.

However, this tendency for acid secretion to increase with age is completely nullified by the corresponding increase in H. pylori infection. Since the incidence of H. pylori infection increases with age, it follows that hypochlorhydria also increases with age.

Acid suppressing drugs increase risk of H. pylori infection

Perhaps most importantly for those taking acid suppressing drugs, researchers now believe that the initial infection with H. pylori can only take place when the acidity level in the stomach is decreased (albeit on a temporary basis). In two human inoculation experiments, infection could not be established unless the pH of the stomach was raised by use of histamine agonists. (1, 2)

If low stomach acid is a prerequisite to H. pylori infection, we might expect acid suppressing drugs to worsen current H. pylori infections and increase rates of infection. That’s exactly what studies suggest. Prilosec and other acid suppressing drugs increase gastritis (inflammation of the stomach) and epithelial lesions in the corpus of the stomach in people infected with H. pylori.

A 1996 article published in the New England Journal of Medicine followed two groups of people who were being treated for reflux esophagitis for a period of five years. One group took Prilosec (20-40 mg/day) and the other underwent surgical repair of the LES. Among those who had documented H. pylori infections at the start of the study and who were treated with Prilosec, the rate of atrophic gastritis increased from 59 percent at the beginning of treatment to 81 percent by the end of the study. Among those who had no atrophic gastritis at the beginning of the study, 30 percent of those who took Prilosec later developed it. By contrast, just 4 percent of the surgically treated group developed atrophic gastritis.

Another vicious cycle you’d be smart to avoid

The connection between low stomach acid, h. pylori and acid suppressing drugs kicks off another nasty vicious cycle, similar to the one we discussed in the previous article.

Low stomach acid >>> heartburn >>> acid suppressing drugs >>> H. pylori infection >>> further reduction of stomach acid >>> chronic heartburn & GERD

The increased risk of H. pylori infection caused by acid suppressing drugs is especially significant because H. pylori infection is associated with a small but significant increase in the risk of stomach cancer. I’ll have more to say about this in the next article.

As I mentioned in the last article, fermentation of malabsorbed carbohydrates produces hydrogen gas in the intestines. Hydrogen gas is the preferred energy source for H. pylori. Elevated levels of hydrogen gas are also associated with other nasty bugs such as Salmonella, E. coli and Campylobacter jejuni, the leading cause of bacterial human diarrhea illnesses in the world.

Excessive fructose, certain types of fiber and starch, and particularly wheat increase hydrogen production, and thus increase the risk of infection by H. pylori and other pathogenic bacteria. If you’d like to avoid heartburn, GERD and the many other unpleasant symptoms associated with bacterial overgrowth, it follows that you should minimize your intake of sugars, starches and grains.

In the next article we’ll examine the many important roles of stomach acid and the significant risks of long term hypochlorhydria.

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bread and other high carbohydrate foodsThis is the second article in a series on heartburn and GERD. If you haven’t read the first one, I’d suggest doing that first.

The idea that heartburn is caused by too much stomach acid is still popular in the media and the public. But as Daniel pointed out in the comments section of the last post, anyone familiar with the scientific literature could tell you that heartburn and GERD are not considered to be diseases of excess stomach acid.

Instead, the prevailing scientific theory is that GERD is caused by a dysfunction of the muscular valve (sphincter) that separates the lower end of the esophagus and the stomach. This is known as the lower esophageal valve, or LES.

The LES normally opens wide to permit swallowed food and liquids to pass easily into the stomach. Except for belching, this is the only time the LES should open.

If the LES is working properly, it doesn’t matter how much acid we have in our stomachs. It’s not going to make it back up into the esophagus. But if the LES is malfunctioning, as it is in GERD, acid from the stomach gets back into the esophagus and damages its delicate lining.

Here’s the key point. It doesn’t matter how much acid there is in the stomach. Even a small amount can cause serious damage. Unlike the stomach, the lining of the esophagus has no protection against acid.

We’ve been asking the wrong question

In a recent editorial published in the journal Gastroenterology, the author remarked:

Treating gastroesophageal reflux disease with profound acid inhibition will never be ideal because acid secretion is not the primary underlying defect.

I couldn’t agree more. For decades the medical establishment has been directing its attention at how to reduce stomach acid secretion in people suffering from heartburn and GERD, even though it’s well-known that these conditions are not caused by excess stomach acid.

Instead, the question researchers should have been asking is, “what is causing the LES to malfunction?” Since it is universally agreed upon that this is the underlying mechanism producing the symptoms of GERD, wouldn’t it make sense to focus our efforts here?

That’s exactly what we’re going to do in this article.

GERD is caused by increased intra-abdominal pressure

It is well accepted in the literature that GERD is caused by an increase in intra-abdominal pressure (IAP). Acid reflux occurs when pressure causes gastric distention (stomach bloating) that pushes the stomach contents, including acid, through the LES into the esophagus.

According to current thought, factors contributing to this include overeating, obesity, bending over after eating, lying down after eating, and consuming spicy or fatty foods.

For example, several studies have indicated an association between obesity and GERD, and this recent paper in Gastroenterology concluded that increased intra-abdominal pressure was the causative mechanism.

But while I agree that all of the currently accepted factors play a role, I do not think they are the primary causes of the increased IAP seen in GERD.

The two primary causes of increased intra-abdominal pressure

Instead, I believe the primary causes of IAP (and thus heartburn and GERD) are bacterial overgrowth and maldigestion of carbohydrates – both of which are caused at least in part by low stomach acid.

In a nutshell, the process looks like this:

diagram of what causes gerd

Let’s look at each step in turn.

Low stomach acid causes bacterial overgrowth

As I will explain in the next article, one of the chief roles of stomach acid is to inhibit bacterial overgrowth. At a pH of 3 or less (the normal pH of the stomach), most bacteria can’t survive for more than 15 minutes. But when stomach acid is insufficient and the pH of the stomach rises above 5, bacteria begin to thrive.

The gastrin knockout mouse, which is incapable of producing stomach acid, suffers from bacterial overgrowth – as well as inflammation, damage and precancerous polyps in its intestines. It is also well documented that acid-suppressing drugs promote bacterial overgrowth. Long-term use of Prilosec, one of the most potent acid suppressing drugs, reduces the secretion of hydrochloric acid (HCL) in the stomach to near zero. In one trial, 30 people with GERD were treated with a high dose of Prilosec (40g/day) for at least 3 months. 11 of the 30 Prilosec-treated people had developed significant bacterial overgrowth, compared with only one of the ten people in the control group.

Low stomach acid causes maldigestion of carbohydrates

Stomach acid (HCL) supports the digestion and absorption of carbohydrates by stimulating the release of pancreatic enzymes into the small intestine. If the pH of the stomach is too high (due to insufficient stomach acid), the pancreatic enzymes will not be secreted and the carbohydrates will not be broken down properly.

Bacterial overgrowth + maldigested carbohydrates = GAS!

Though microbes are able to metabolize proteins and even fats, their preferred energy source is carbohydrate. The fermentation of carbohydrates that haven’t been digested properly produces gas. The resulting gas increases intra-abdominal pressure, which is the driving force behind acid reflux and GERD.

When stomach acid is sufficient and carbohydrates are consumed in moderation, they are properly broken down into glucose and rapidly absorbed in the small intestine before they can be fermented by microbes. However, if stomach acid is insufficient and/or carbohydrates are consumed in excess, some of the carbs will escape absorption and become available for intestinal microbes to ferment.

A nasty vicious cycle: the role of hydrogen gas

Hydrogen (H2) is one of the gases produced by bacterial fermentation of carbohydrates. In fact, there have been explosions during intestinal surgery due to the high amounts of hydrogen gas production in the gut. This is significant because a recent landmark study demonstrated that pathogenic bacteria feed on hydrogen gas.

So, the more undigested carbohydrate you have in your gut, the more hydrogen gas bacteria will produce. The more hydrogen gas is produced, the more bacterial overgrowth will occur. And the more bacteria you have in your gut, the more gas will be produced by fermentation of undigested carbohydrate. This becomes a nasty vicious cycle.

There is significant evidence that the carbohydrates consumed in the “standard American diet” contribute to this phenomenon. Fructose is a particular problem. In one study researchers fed fructose to 15 normal adults. They found that more than half of the 15 adults showed evidence of fructose malabsorption after just 25g of fructose, and greater than two-thirds showed malabsorption after 50g of fructose. To put this in perspective, one 12 oz. can of Coca-Cola contains 30g of fructose.

One of the measures of malabsorption used in the study was a hydrogen breath test. Both the 25g and the 50g doses caused a large increase in H2, especially the 50g dose (a 5-fold increase). Bacterial fermentation of carbohydrate is the only source of hydrogen in the human body. This means that the hydrogen measured in the study indeed came from the undigested fructose in the gut.

Certain type of fiber and starch also promote hydrogen production. Almost all of the fiber and approximately 15-20% of the starch we consume escape absorption. The amount of gas that can be produced by undigested carbohydrates is almost hard to believe. According to Suarez and Levitt, just 30g of carbohydrate (equivalent to 1/2 of a small muffin) that escapes absorption in a day could produce more than 10,000 mL of hydrogen gas. That’s equivalent to ten large one-liter water bottles full of intestinal gas!

Finally, a recent study showed that ingestion of lactose (the carbohydrate found in milk) results in an increased number of transient lower esophageal sphincter relaxations (TSELRs), increased reflux episodes, higher esophageal acid exposures, and more severe GERD symptoms. Another study showed that oral administration of fructo-oligosaccharides (FOS) produces similar findings. Together these studies suggest that colonic fermentation of malabsorbed carbohydrates contributes to the pathogenesis of GERD.

Other supporting evidence

If gas produced by microbial fermentation of carbohydrates causes acid reflux, we might expect that reflux could be treated by either 1) reducing bacterial overgrowth or 2) reducing carbohydrate intake.

In fact, that’s exactly what we see. In a study by Pehl, administration of erythromycin (an antibiotic) significantly decreased esophageal reflux. In another study by Pennathur, erythromycin strengthened the defective lower esophageal sphincter in patients with acid reflux.

To my knowledge there have only been two small trials performed to test the effects of carbohydrate restriction on GERD. Both had positive results. A small case series showed a significant, almost immediate resolution of GERD symptoms in obese individuals initiating a very low-carb diet. A more recent study found that a very low-carb diet decreased distal esophagus acid exposure and improved the symptoms of GERD. Perhaps most importantly, the magnitude of the improvement was similar to what has been reported with treatment with proton-pump inhibitors (acid suppressing drugs).

Many researchers now believe that Irritable Bowel Syndrome (IBS) is caused by bacterial overgrowth in the small intestine (SIBO). A study performed at the GI Motility Center in Los Angeles in 2002 found that 71% of GERD patients tested positive for IBS – double the percentage seen in non-GERD patients being examined.

The high prevalence of IBS in GERD patients combined with the recognition that bacterial overgrowth causes IBS is yet another line of evidence suggesting that bacterial overgrowth is also a causative factor in GERD.

A unified theory

To summarize, GERD is caused by increased pressure in the stomach resulting in a malfunction of the lower esophageal sphincter (LES). The increase in pressure is caused by bacterial overgrowth and malabsorption of carbohydrates, both of which are precipitated by low stomach acid. Reducing bacteria loads and limiting carbohydrate intake have both been shown to greatly improve, and in some cases completely cure, acid reflux and GERD.

In the Part III of the series I discuss the connection between GERD and H. pylori, and further evidence supporting the theory that GERD is caused by bacterial overgrowth. Read on!

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