pic. Biopsy of the small bowel in bacterial overgrowth (SIBO) can mimic celiac disease, with partial villous atrophy.
Small intestinal bacterial overgrowth (SIBO), defined as excessive bacteria in the small intestine, remains a poorly understood disease within the allopathic community. Initially thought to occur in only a small number of patients, it is now apparent that this disorder is far more prevalent than previously thought. Patients with SIBO vary in presentation, from being only mildly symptomatic to suffering from chronic diarrhea, moderate to severe bloating, weight loss, and malabsorption. This post will focus on some of the predisposing factors for the development of SIBO.
SIBO develops when the normal checks and balances that control intestinal bacterial populations are disrupted. The two processes that most commonly predispose one to develop small intestinal bacterial overgrowth (SIBO) are DIMINISHED STOMACH ACID (HCl, potassium and sodium chloride) secretion and small intestine DYSMOTILITY – basically increased transit time, of food, through the small intestine – not caused by SIBO itself.
Other potential causes of SIBO are immune disturbances within the small intestine (multiple-causes), anatomical abnormalities of the GI tract, chronic antibiotic use, and poorly controlled diabetes. These are worth looking into even if the above two predisposing factors have been ruled in or out.
So we now know that small intestinal dysmotility and reduced stomach acid are the two most common predisposing factors, but what are their predisposing factors? That is the most important question and of more importance than treating only the symptoms – dysmotility and low stomach acid (hypochlorhydria).
Important Note: In order to receive SIBO protocol information or help, you will need to become a distance patient – DISTANCE CLIENT PROGRAM revised 08-22-17. I truly do want to help any and all who are interested, but it’s finally gotten to the point where too many people want free advice, treatment plans, personalized protocols…. I’m a firm believer in fair exchange and I feel I have done that by providing the information in this post. I will help you and I can create a tailor-made protocol for your individual situation. Please fill out the distance patient application (link above) or if you have questions about the program, please call me at 714-639-4360nt goes here
Low Stomach Acid (Hypochlorhydria)
The four most common causes of low stomach acid production are antacid or PPI use, H. pylori infection, electrolyte balance (sodium, chloride, and potassium), and aging. The interesting thing here is that they all can, and usually, overlap.
1. Chronic Exposure to PPI’s or Acid Blockers, such as Prilosec, Zantac or Tagamet. An overabundance of native or non-native bacteria within the small intestine can occur in as little as four weeks of PPI exposure. Zantac, an H2 blocker, from my research is the safest and the least likely to contribute to SIBO. PPI’s, especially omeprazole, are the worst offenders. Omeprazole is also a prescribed component, of the Triple Therapy, used for H. pylori eradication.
A simple experiment to see where your natural level of stomach acid (HCl) is, is to drink 1 tsp of Baking Soda in 3-4 ounces of water. The experiment should be done right when you wake up and once before bed – 1 tsp of Baking Soda each time. No matter what this should be done on an empty stomach for optimum results. If your stomach acid levels are normal you should get 1-3 good burps within 60-90 seconds after drinking the mixture – both times. If your morning drink does not produce 1-3 good burps than your AM level of stomach acid is low. If both your bedtime and morning mixtures don’t produce 1-3 good burps, find a local functional medicine doctor who can help you to diagnose the cause and get you going on a restoration protocol, as you have low stomach acid production.
2. H. pylori Bacterial Infection. When this infection is in the body of the stomach (The body of the stomach makes up the majority of the familiar kidney-bean-shaped portion of the organ) it can cause hypochlorhydria due to the inflammation impairing the function of the parietal cells (which make HCl) and atrophy reducing their number. On the other hand, H. pylori infection of the pyloric antrum (opening to the body of the stomach) can cause the opposite effect, with too much gastric acid. A biopsy or Heidelberg test can help make this determination.
H. pylori can also neutralize stomach acid by producing large amounts of urease, which breaks down the urea present in the stomach to carbon dioxide and ammonia. The ammonia, which has a very high pH, neutralizes stomach acid.
If H. pylori is also present than it needs to be treated before or concurrently with a SIBO protocol.
3. Aging. Under normal circumstances, total gastrointestinal transit time in the elderly is that of a younger individual. It’s more likely that medications that slow GI motility, a decline in mobility, the onset of new diseases (eg, diabetes), dietary changes that lead to malnutrition, and changes in gut immune function are the primary triggers of SIBO as we age.
4. Other Causes of SIBO.
- Food poisoning causing an acute autoimmune within the small intestine. Food poisoning caused by any of these bacteria (E. coli, Salmonella, Shigella or Campylobacter) produce a common toxin called Cdt-B toxin (Cytolethal Distending Toxin B). Once exposed to this toxin, susceptible individuals will produce antibodies to the Cdt-B toxin. This leads to an acute reduction in intestinal motility leading to the development of SIBO.
- Acute or chronic exposure to antibiotics.
- Chronic stress which leads to a sympathetic nervous system dominant state, (flight-flight response. This leads to increased GI transit time, a decrease in nutrient absorption, a decrease in nutrient assimilation, leaky gut, and intestinal dysbiosis.
- A high FODMAP diet in suitable individuals.
Bacterial overgrowth in the small intestine commonly occurs in association with hypochlorhydria caused by atrophic gastritis (AG) or during treatment with PPI’s. AG can be caused by persistent infection with H. pylori or can be autoimmune in origin. Those with the autoimmune version of atrophic gastritis are statistically more likely to develop gastric carcinoma, Hashimoto’s thyroiditis, and achlorhydria (lack of stomach acid).
Dysmotility (prior to SIBO)
Brain-Gut Dysfunction occurs when there is the altered interpretation of neurologic messages from the GI tract to the brain, and back to the GI tract. Both the central and peripheral nervous system tone* can be altered resulting in decreased function to the entire GI tract and glands associated with digestion. *In this context, tone specifically refers to the continual nature of baseline parasympathetic action that the vagus nerve and central nervous system exerts.
Gut-Brain Connection Imbalance is a stress-adaptation phenomenon. There are too many factors that may contribute to this. Below is a common list of physical, behavioral and emotional symptoms liked to stress. If you have any of these symptoms then stress may be contributing to your SIBO or other GI-related symptoms. Here is a link to the full article from Harvard Health Publishing – Gut-Brain Connection.
- Stiff or tense muscles, especially in the neck and shoulders
- Sleep problems
- Shakiness or tremors
- The recent loss of interest in sex
- Weight loss or gain
- Grinding teeth
- Difficulty completing work assignments
- Changes in the amount of alcohol or food you consume
- Taking up smoking, or smoking more than usual
- Increased desire to be with or withdraw from others
- Rumination (frequent talking or brooding about stressful situations)
- An overwhelming sense of tension or pressure
- Trouble relaxing
- Quick temper
- Poor concentration
- Trouble remembering things
- Loss of sense of humor
If you experience any of the symptoms above and they are of a long-standing nature, a stress management coach should be part of your health-restoration team. Exercise, yoga, tai chi, and other stress-reduction techniques should be implemented.
Certain nutritional support products may be indicated to help facilitate repair and/or increased intestinal motility* or act as a stress-support crutch until other measures kick-in. Please talk to your health coach before starting any nutritional protocol.
- Mucuna pruriens is a natural source of L-dopa. Its deficiency, for whatever reason, is a primary cause the physical, behavioral, or emotional symptoms, such as those listed within the Gut-Brain Connection site.
- 5-HTP* is a precursor to serotonin, a happy neurotransmitter, and melatonin. 95% of the body’s serotonin lies within the GI tract.
- Lithium orotate at 5-10mg’s is a phenomenal product to keeping your brain’s lines of communication open and healthy.
- Pantothenic acid (vitamin B5) is known as “the anti-stress vitamin.” B5 works with your LDL cholesterol to help make pregnenolone, DHEA, progesterone, cortisol, estrogen, testosterone. and aldosterone.
Note: 5-HTP may act as a mild prokinetic, meaning it helps movement through the small intestine. 5-HTP supplementation is well tolerated by the GI tract and does not induce perpetual or excessive motility. Those with diarrhea should watch to see if 5-HTP increases bowel movements.
Alteration of The Migrating Motor Complexes (MMC). MMC are waves of electrical activity that regulate stomach emptying and move the contents down through the small intestine and into the large bowel. Every 90 minutes, during fasting, the MMC sweeps through the intestines triggering peristaltic waves, which facilitates transportation of chyme (digested food), and indigestible substances such as bone, fiber, and foreign bodies from the stomach, through the small intestine, past the ileocecal sphincter, and into the colon. The MMC is thought to be partially regulated by motilin and ghrelin, which is initiated in the stomach as a response to vagus nerve (fight/flight nerve) stimulation.
Note: when you experience stomach noise (hunger pains) about 4-5 hours after eating it’s the MMC at work. If you do not get movement just below the breast-bone (sternum), at the margin of your left rib cage, then your MMC may need some tonifying.
Help: In omnivores and carnivores the origin of the (MMC) is suppressed by the ingestion (eating) of a meal and returns after complete stomach emptying. Since most people are snaking or eating more than 2-3 meals a day, this complex may lose some of its integrity (tone). The key, in my opinion, is to eat just 2-3 meals per day with at least 12 hours in between dinner and breakfast. I have seen this reestablish proper MMC integrity.
Help: Box Breathing (reproduced with grateful acknowledgment to Mark Divine and Sealfit)
Deep diaphragmatic breathing
Breathing is both a conscious and unconscious process. When unconscious we tend be do what is called “chest breathing.” This type of breathing is inefficient and labor intensive in that it requires more effort for the same amount of oxygen intake, lowering energy stores and increasing anxiety.
Facing a stressful event, we should switch to a deep diaphragmatic breathing pattern.
We can practice a deep diaphragmatic breathing pattern through a discipline we call Box Breathing at SEALFIT Academy. Box breathing is meant to be done in a quiet and controlled setting, not while you are in the fight. The pattern is simply a box, whereby you inhale to a count of 5, hold for a count of 5, exhale to the same 5 count and hold again for 5. You can start at 3 if this is difficult, or take it up a notch if easy. You should be uncomfortable on the exhale hold and be forced to fill the entirety of your lung capacity on the inhale hold.
The benefits of deep diaphragmatic box breathing include:
- Reduction of performance anxiety
- Control of the arousal response
- Increasing brain elasticity – flexibility through enhanced blood flow and reduced mental stimulation
- Enhancing learning and skill development
- Increasing capacity for focused attention and long-term concentration
- Saltzman JR, Kowdley KV, Pedrosa MC, et al. Bacterial overgrowth without clinical malabsorption in elderly hypochlorhydric subjects. 1994;106:615–623. [PubMed]
- Dukowicz AC, Lacy BE, Levine GM. Small Intestinal Bacterial Overgrowth, A Comprehensive Review. Gastroenterol Hepatol (N Y). 2007 Feb; 3(2): 112–122. [PubMed]
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