FAQ

hydrogen breath test

What is the hydrogen breath test?

The hydrogen breath test is a test that uses the measurement of hydrogen in the breath to diagnose several conditions that cause gastrointestinal symptoms. In humans, only bacteria – specifically, anaerobic bacteria in the colon – are capable of producing hydrogen. The bacteria produce hydrogen when they are exposed to unabsorbed food, particularly sugars and carbohydrates, not proteins or fats. Although limited hydrogen is produced from the small amounts of unabsorbed food that normally reach the colon, large amounts of hydrogen may be produced when there is a problem with the digestion or absorption of food in the small intestine, that allows more unabsorbed food to reach the colon.

Large amounts of hydrogen also may be produced when the colon bacteria move back into the small intestine, a condition called bacterial overgrowth of the small bowel. In this latter instance, the bacteria are exposed to unabsorbed food that has not had a chance to completely traverse the small intestine to be fully digested and absorbed. Some of the hydrogen produced by the bacteria, whether in the small intestine or the colon, is absorbed into the blood flowing through the wall of the small intestine and colon. The hydrogen-containing blood travels to the lungs where the hydrogen is released and exhaled in the breath where it can be measured.

 

When is hydrogen breath testing used?

Hydrogen breath testing is used in the diagnosis of three conditions.

  • The first is a condition in which dietary sugars are not digested normally. The most common sugar that is poorly digested is lactose, the sugar in milk. Individuals who are unable to properly digest lactose are referred to as lactose intolerant. Testing also may be used to diagnose problems with the digestion of other sugars such as sucrose, fructose and sorbitol.
  • The second condition for which hydrogen breath testing is used is for diagnosing bacterial overgrowth of the small bowel, a condition in which larger-than-normal numbers of colonic bacteria are present in the small intestine.
  • The third condition for which hydrogen breath testing is used is for diagnosing rapid passage of food through the small intestine. All three of these conditions may cause abdominal pain, abdominal bloating and distention, flatulence (passing gas in large amounts), and diarrhea.
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Sphincter of Oddi (SOD)

The sphincter of Oddi is a muscular valve that controls the flow of digestive juices (bile and pancreatic juice) through ducts from the liver and pancreas into the first part of the small intestine (duodenum). Sphincter of Oddi dysfunction (SOD) describes the situation when the sphincter does not relax at the appropriate time (due to scarring or spasm). The back-up of juices causes episodes of severe abdominal pain.

The sphincter of Oddi is a muscular valve that controls the flow of digestive juices (bile and pancreatic juice) through ducts from the liver and pancreas into the first part of the small intestine (duodenum). Sphincter of Oddi dysfunction (SOD) describes the situation when the sphincter does not relax at the appropriate time (due to scarring or spasm). The back-up of juices causes episodes of severe abdominal pain.

Doctors often consider SOD in patients who experience recurrent attacks of pain after surgical removal of the gallbladder (cholecystectomy). More than half a million of these surgeries are performed annually in the United States, and 10–20% of these patients present afterwards with continuing or recurrent pains. SOD is also considered in some patients who suffer from recurrent attacks of unexplained inflammation of the pancreas (pancreatitis).

About half of these patients will have findings on laboratory studies or imaging (blood test, ultrasound, CT scan, or MRCP) to suggest a definite abnormality, such as a stone in the bile duct. MRCP (magnetic resonance cholangiopancreatography) is nowadays a good non-invasive test for checking on the biliary and pancreatic drainage systems.

Based on patients histories, physical examinations, and other clinical data, doctors can categorize these patients as having SOD Types I and II. The categories help guide treatment of the disease. They are based on a system called the Milwaukee criteria.

When symptoms are severe, standard treatment is to perform an endoscopic procedure called ERCP (endoscopic retrograde cholangiopancreatography). ERCP is a procedure for the examination or treatment of the bile duct and pancreatic duct. The procedure carries a risk of serious complications and is done under sedation by experts trained in the technique. It combines the use of x-rays and an endoscope that is passed down to the duodenum, where the bile duct and pancreatic ducts drain, and a dye that is injected into the ducts.

An additional procedure, sphincter of Oddi manometry (SOM), involves passing a catheter into the bile and/or pancreatic duct during ERCP to measure the pressure of the biliary and/or pancreatic sphincter. It is considered the gold standard diagnostic modality for SOD.

Treatment depends on what is found. It may often involve cutting the muscular sphincter (sphincterotomy) to remove any stones or to relieve any scarring or spasm of the sphincter.

As noted above, a very important problem in this context is that these ERCP procedures carry a significant risk of complications. In particular, ERCP (with or without sphincter of Oddi manometry) can cause an attack of pancreatitis in 5–10% of cases. While most of these result in a few days in the hospital, about 1% of patients suffer a major attack, with weeks or months in the hospital. Sphincterotomy also carries a small risk of other severe complications such as bleeding and perforation, and the possibility of delayed narrowing of a duct (stenosis) due to scarring.

Functional SOD

Patients with a similar pain problem, but who have little or no abnormalities on blood tests and standard scans (including MRCP), are categorized as having SOD Type III. The episodes of pain are assumed due to intermittent spasm of the sphincter. It is very difficult to effectively evaluate and manage patients with Type III SOD. Some physicians are skeptical of its existence, or assume that it is a part of a broader problem of a functional digestive disturbance such as irritable bowel syndrome.

Because of the risks of ERCP, patients with suspected SOD III are usually advised to try medical treatments first. Some respond to the use of antispasmodic drugs and/or antidepressants that may help decrease pain.  There have been studies of other medical therapies, such as calcium channel blocking drugs. Despite a few encouraging reports, these methods have not proven to be effective generally, and are not widely used.

Patients who fail these approaches (at least those with severe symptoms) are usually advised to see specialists at referral centers. Further evaluation may involve additional or more specialized tests to help guide treatment options.

Clinical Research Study

The uncertainties in how best to diagnose and to treat “suspected” sphincter of Oddi dysfunction (and the risks involved) mandate further scientific investigation. The National Institutes of Health has recently funded an important study called “EPISOD” in 6 major Gastroenterology centers in USA.

The studies are being conducted at centers located in:

  • Johns Hopkins Hospital, Baltimore, MD
  • University of Alabama at Birmingham, Birmingham, AL
  • Medical University of South Carolina Digestive Disease Center, Charleston, SC
  • Indiana University, Indianapolis, IN
  • Hennepin County Medical Center, Minneapolis, MN
  • Virginia Mason Medical Center, Seattle, WA

Additional details are available at the NIH website at http://clinicaltrials.gov/ by searching: sphincter of Oddi dysfunction III.

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IBD versus IBS

Is inflammatory bowel disease (IBD) the same thing as Irritable Bowel Syndrome (IBS)?

No. Inflammatory bowel disease, including UC and CD, is different from irritable bowel syndrome (IBS). Unlike IBD, IBS does not cause inflammation, ulcers or other damage to the bowel. Instead, IBS is a much less serious problem called a functional disorder. This means that the digestive system looks normal but doesn’t work as it should. Symptoms of IBS may include crampy pain, bloating, gas, mucus in the stool, diarrhea and constipation. IBS has also been called spastic colon or spastic bowel

Source: http://www.webmd.com/ibd-crohns-disease/crohns-disease/ibd-versus-ibs

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Bloating

For further information see related separate article Irritable Bowel Syndrome.

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Ursodeoxycholic acid
Aust Prescr 1999;22:95-8

Ursofalk (Orphan Australia)
250 mg capsules
Approved indication: chronic cholestasis
Australian Medicines Handbook Section 12

In primary biliary cirrhosis, there is chronic inflammation which destroys the intrahepatic bile ductules. At first, patients may be asymptomatic, but the reduced excretion of bile can cause steatorrhoea. The disease slowly progresses and death can result from hepatic failure or the complications of cirrhosis. Primary biliary cirrhosis is now a common indication for a liver transplant. Although there is no effective drug treatment, some patients will benefit from ursodeoxycholic acid.

Ursodeoxycholic acid is a bile acid which is synthesised from its precursor by intestinal bacteria. Its mechanism of action in primary biliary cirrhosis is uncertain. Ursodeoxycholic acid may have an effect by increasing the flow and altering the composition of bile. It has also been used in the treatment of gallstones.

In clinical trials with at least two years of follow up, patients who took ursodeoxycholic acid had improved liver function tests. This may not always improve the patient’s symptoms or the histology of the liver.

Ursodeoxycholic acid has few known adverse effects. Diarrhoea is the main adverse reaction. Patients can complain of an increase in itching when they begin treatment. This may respond to a reduction in the dose. Ursodeoxycholic acid is contraindicated if there is acute inflammation of the gall bladder or obstruction of the common bile duct.

Ursodeoxycholic acid will probably have a role in delaying the need for liver transplantation. A placebo-controlled study of 145 patients with primary biliary cirrhosis found that the disease progressed more slowly in patients given ursodeoxycholic acid. This group also had a significantly lower probability of transplantation or death during the two-year study.1

Reference

. Poupon RE, Poupon R, Balkau B. Ursodiol for the long-term treatment of primary biliary cirrhosis. The UDCA-PBC Study Group. N Engl J Med 1994;330:1342-7.

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Celecoxib
Aust Prescr 1999;22:147-51

Celebrex (Searle)
100 mg and 200 mg capsules
Approved indication: arthritis
Australian Medicines Handbook Section 15.1

Non-steroidal anti-inflammatory drugs act by inhibiting the enzyme cyclo-oxygenase(COX).1 This enzyme is required for the synthesis of prostaglandins and its activity increases in inflammation. It has two isoforms, COX-1 andCOX-2, both of which are blocked to varying degrees by non-steroidal anti-inflammatory drugs. As COX-1 may produce protective prostaglandins in the stomach, its inhibition could be responsible for some of the adverse effects of the drugs. Celecoxib is much more selective for COX-2, so it may cause fewer adverse effects than the older drugs.

Patients with symptoms of rheumatoid arthritis take celecoxib in two divided doses. A single daily dose may be used in osteoarthritis. The drug is quickly absorbed. Although taking the capsules with food delays absorption, the bioavailability is increased. Celecoxib is metabolised in the liver by cytochrome P450 CYP2C9so there is a potential for interactions with drugs such as fluconazole.

In studies lasting up to 12 weeks, celecoxib has reduced the pain of osteoarthritis more effectively than placebo. Trials, of up to 24 weeks, in patients with rheumatoid arthritis have found the efficacy of celecoxib to be similar to that of naproxen 500 mg twice daily.

The effect of celecoxib on the gut has been assessed by endoscopy. Gastric ulcers were seen significantly less frequently during treatment with celecoxib, than they were in patients taking naproxen or diclofenac. Celecoxib, however, is not free of gastrointestinal adverse effects. Dyspepsia, abdominal pain and diarrhoea occur more frequently than with placebo. In animal studies, COX-2inhibitors retard ulcer healing.1

Most of the enzyme activity in platelets is COX-1, so celecoxib should have little effect on bleeding time. The potential of COX-2 inhibitors to cause fluid retention, renal impairment or hypertension is unknown. In clinical trials peripheral oedema occurred with equal frequency (2.1%) in patients taking celecoxib or naproxen. Celecoxib is not recommended for patients with aspirin-sensitive asthma.

The COX-2 inhibitors have the potential to replace non-steroidal anti-inflammatory drugs for the relief of arthritic symptoms. Whether or not they fulfill this potential will depend on their long-term safety. For example, will they cause fewer gastrointestinal haemorrhages than the non-steroidal anti-inflammatory drugs?

Reference

1. Hawkey CJ. COX-2 inhibitors. Lancet 1999;353:307-14.

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Postcholecystectomy Syndrome

The laparoscopic cholecystectomy is considered the “gold standard” in chronic calculous cholecystitis treatment. After the gallbladder removal the physiology of gallbladder bile formation is changed.

Absence of the gallbladder leads to development of functional biliary hypertension and dilatation of common bile duct and the common hepatic duct. The dilatation of right and left hepatic ducts may be formed within 3-5 years after cholecystectomy. Functional hypertension in the common bile duct leads to development of functional hypertension in Wirsung’s pancreatic duct accompanied by chronic pancreatitis symptoms.

During this period in some patients this is accompanied by chronic pancreatitis progression, dysfunction of the sphincter of Oddi and duodeno-gastral reflux. Duodeno-gastral reflux causes the development of atrophic (bile-acid-depen­dent) antral gastritis . After cholecystectomy 40% to 60% of patients suffer from dyspeptic disorders, 5% to 40% from pains of different localizations. Up to 70% of patients show symptoms of chronic “bland” intrahepatic cholestasis, chronic cholestatic hepatitis and compensatory bile-acid-dependent apoptosis of hepatocytes. In some of cholecystectomized patients with high concentration of hydrophobic hepatotoxic co-cancerogenic deoxycholic bile acid in serum and/or feces high risk of the colon cancer is found.

Therefore, depending on dysfunction (hyper tonus) or relaxation (hypo tonus) of the sphincter of Oddi, pathology in hepato-biliary-pancreato-duodenal-gastral zone will form after cholecystectomy.

Postcholecystectomy syndrome is a dysfunction of the sphincter of Oddi, caused by noncalculous obstructive disorder, which decrease bile passage and pancreatic juice outflow into the duodenum.

More reading

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Gastroparesis

CDR0000428446_largeGastroparesis, also called delayed gastric emptying, is a disorder in which the stomach takes too long to empty its contents. Normally, the stomach contracts to move food down into the small intestine for digestion. The vagus nerve controls the movement of food from the stomach through the digestive tract. Gastroparesis occurs when the vagus nerve is damaged and the muscles of the stomach and intestines do not work normally. Food then moves slowly or stops moving through the digestive tract.

What causes gastroparesis?

The most common cause of gastroparesis is diabetes. People with diabetes have high blood glucose, also called blood sugar, which in turn causes chemical changes in nerves and damages the blood vessels that carry oxygen and nutrients to the nerves. Over time, high blood glucose can damage the vagus nerve.

Some other causes of gastroparesis are

  • surgery on the stomach or vagus nerve
  • viral infections
  • anorexia nervosa or bulimia
  • medications-anticholinergics and narcotics-that slow contractions in the intestine
  • gastroesophageal reflux disease
  • smooth muscle disorders, such as amyloidosis and scleroderma
  • nervous system diseases, including abdominal migraine and Parkinson’s disease
  • metabolic disorders, including hypothyroidism

Many people have what is called idiopathic gastroparesis, meaning the cause is unknown and cannot be found even after medical tests.

What are the symptoms of gastroparesis?

Signs and symptoms of gastroparesis are

  • heartburn
  • pain in the upper abdomen
  • nausea
  • vomiting of undigested food-sometimes several hours after a meal
  • early feeling of fullness after only a few bites of food
  • weight loss due to poor absorption of nutrients or low calorie intake
  • abdominal bloating
  • high and low blood glucose levels
  • lack of appetite
  • gastroesophageal reflux
  • spasms in the stomach area

Eating solid foods, high-fiber foods such as raw fruits and vegetables, fatty foods, or drinks high in fat or carbonation may contribute to these symptoms.

The symptoms of gastroparesis may be mild or severe, depending on the person. Symptoms can happen frequently in some people and less often in others. Many people with gastroparesis experience a wide range of symptoms, and sometimes the disorder is difficult for the physician to diagnose.

What are the complications of gastroparesis?

If food lingers too long in the stomach, it can cause bacterial overgrowth from the fermentation of food. Also, the food can harden into solid masses called bezoars that may cause nausea, vomiting, and obstruction in the stomach. Bezoars can be dangerous if they block the passage of food into the small intestine.

Gastroparesis can make diabetes worse by making blood glucose control more difficult. When food that has been delayed in the stomach finally enters the small intestine and is absorbed, blood glucose levels rise. Since gastroparesis makes stomach emptying unpredictable, a person’s blood glucose levels can be erratic and difficult to control.

How is gastroparesis diagnosed?

After performing a full physical exam and taking your medical history, your doctor may order several blood tests to check blood counts and chemical and electrolyte levels. To rule out an obstruction or other conditions, the doctor may perform the following tests:

  • Upper endoscopy. After giving you a sedative to help you become drowsy, the doctor passes a long, thin tube called an endoscope through your mouth and gently guides it down the throat, also called the esophagus, into the stomach. Through the endoscope, the doctor can look at the lining of the stomach to check for any abnormalities.
  • Ultrasound. To rule out gallbladder disease and pancreatitis as sources of the problem, you may have an ultrasound test, which uses harmless sound waves to outline and define the shape of the gallbladder and pancreas.
  • Barium x ray. After fasting for 12 hours, you will drink a thick liquid called barium, which coats the stomach, making it show up on the x ray. If you have diabetes, your doctor may have special instructions about fasting. Normally, the stomach will be empty of all food after 12 hours of fasting. Gastroparesis is likely if the x ray shows food in the stomach. Because a person with gastroparesis can sometimes have normal emptying, the doctor may repeat the test another day if gastroparesis is suspected.

Once other causes have been ruled out, the doctor will perform one of the following gastric emptying tests to confirm a diagnosis of gastroparesis.

  • Gastric emptying scintigraphy. This test involves eating a bland meal, such as eggs or egg substitute, that contains a small amount of a radioactive substance, called radioisotope, that shows up on scans. The dose of radiation from the radioisotope is not dangerous. The scan measures the rate of gastric emptying at 1, 2, 3, and 4 hours. When more than 10 percent of the meal is still in the stomach at 4 hours, the diagnosis of gastroparesis is confirmed.
  • Breath test. After ingestion of a meal containing a small amount of isotope, breath samples are taken to measure the presence of the isotope in carbon dioxide, which is expelled when a person exhales. The results reveal how fast the stomach is emptying.
  • SmartPill. Approved by the U.S. Food and Drug Administration (FDA) in 2006, the SmartPill is a small device in capsule form that can be swallowed.The device then moves through the digestive tract and collects information about its progress that is sent to a cell phone-sized receiver worn around your waist or neck. When the capsule is passed from the body with the stool in a couple of days, you take the receiver back to the doctor, who enters the information into a computer.

How is gastroparesis treated?

Treatment of gastroparesis depends on the severity of the symptoms. In most cases, treatment does not cure gastroparesis-it is usually a chronic condition. Treatment helps you manage the condition so you can be as healthy and comfortable as possible.

Medication

Several medications are used to treat gastroparesis. Your doctor may try different medications or combinations to find the most effective treatment. Discussing the risk of side effects of any medication with your doctor is important.

  • Metoclopramide (Reglan). This drug stimulates stomach muscle contractions to help emptying. Metoclopramide also helps reduce nausea and vomiting. Metoclopramide is taken 20 to 30 minutes before meals and at bedtime. Side effects of this drug include fatigue, sleepiness, depression, anxiety, and problems with physical movement.
  • Erythromycin. This antibiotic also improves stomach emptying. It works by increasing the contractions that move food through the stomach. Side effects include nausea, vomiting, and abdominal cramps.
  • Domperidone. This drug works like metoclopramide to improve stomach emptying and decrease nausea and vomiting. The FDA is reviewing domperidone, which has been used elsewhere in the world to treat gastroparesis. Use of the drug is restricted in the United States.
  • Other medications. Other medications may be used to treat symptoms and problems related to gastroparesis. For example, an antiemetic can help with nausea and vomiting. Antibiotics will clear up a bacterial infection. If you have a bezoar in the stomach, the doctor may use an endoscope to inject medication into it to dissolve it.

Dietary Changes

Changing your eating habits can help control gastroparesis. Your doctor or dietitian may prescribe six small meals a day instead of three large ones. If less food enters the stomach each time you eat, it may not become overly full. In more severe cases, a liquid or pureed diet may be prescribed.

The doctor may recommend that you avoid high-fat and high-fiber foods. Fat naturally slows digestion-a problem you do not need if you have gastroparesis-and fiber is difficult to digest. Some high-fiber foods like oranges and broccoli contain material that cannot be digested. Avoid these foods because the indigestible part will remain in the stomach too long and possibly form bezoars.

Feeding Tube

If a liquid or pureed diet does not work, you may need surgery to insert a feeding tube. The tube, called a jejunostomy, is inserted through the skin on your abdomen into the small intestine. The feeding tube bypasses the stomach and places nutrients and medication directly into the small intestine. These products are then digested and delivered to your bloodstream quickly. You will receive special liquid food to use with the tube. The jejunostomy is used only when gastroparesis is severe or the tube is necessary to stabilize blood glucose levels in people with diabetes.

Parenteral Nutrition

Parenteral nutrition refers to delivering nutrients directly into the bloodstream, bypassing the digestive system. The doctor places a thin tube called a catheter in a chest vein, leaving an opening to it outside the skin. For feeding, you attach a bag containing liquid nutrients or medication to the catheter. The fluid enters your bloodstream through the vein. Your doctor will tell you what type of liquid nutrition to use.

This approach is an alternative to the jejunostomy tube and is usually a temporary method to get you through a difficult period with gastroparesis. Parenteral nutrition is used only when gastroparesis is severe and is not helped by other methods.

Refractory Gastroparesis

Gastric Electrical Stimulation

Neurostimulator Device

When gastroparesis does not respond to standard medical management including drugs and dietary changes, the condition is said to “refactory”. For patients who have documented delayed gastric emptying with no evidence of abnormal obstruction, a gastric neurostimulator may be implanted to reduce or eliminate nausea and other symptoms.

A gastric neurostimulator is a surgically implanted battery-operated device that releases mild electrical pulses to help control nausea and vomiting associated with gastroparesis. This option is available to people whose nausea and vomiting do not improve with medications. Further studies will help determine who will benefit most from this procedure, which is available in a few centers across the United States.

Implanted neurostimulator device

Gastric electrical stimulation uses a device, surgically implanted in the abdomen, to deliver mild electrical pulses to the nerves and smooth muscle of the lower part of the stomach. This stimulation may reduce chronic nausea and vomiting in patients with gastroparesis resulting from diabetes (diabetic gastropathy) or ideopathic gastroparesis (unknown cause).

 

Pyloroplasty

If gastroparesis is related to an injury of the vagus nerve, patients may benefit from a procedure called pyloroplasty. This procedure widens and relaxes the valve separating the stomach from the upper part of the small intestine, called the pyloric valve. This permits the stomach to empty more quickly.

In some cases,before deciding to perform the procedure, botulinum toxin (Botox) will be injected at the pyloric valve to temporarily paralyze and relax it. The purpose is to determine if the patient would benefit from a pyloroplasty. While use of botulinum toxin has been associated with improvement in symptoms of gastroparesis in some patients, further research is required to validate its efficacy.

Treatment Goals

The primary treatment goals for gastroparesis related to diabetes are to improve stomach emptying and regain control of blood glucose levels. Treatment includes dietary changes, insulin, oral medications, and, in severe cases, a feeding tube and parenteral nutrition.

Dietary Changes

The doctor will suggest dietary changes such as six smaller meals to help restore your blood glucose to more normal levels before testing you for gastroparesis. In some cases, the doctor or dietitian may suggest you try eating several liquid or pureed meals a day until your blood glucose levels are stable and the symptoms improve. Liquid meals provide all the nutrients found in solid foods, but can pass through the stomach more easily and quickly.

Insulin for Blood Glucose Control

If you have gastroparesis, food is being absorbed more slowly and at unpredictable times. To control blood glucose, you may need to

  • take insulin more often or change the type of insulin you take
  • take your insulin after you eat instead of before
  • check your blood glucose levels frequently after you eat and administer insulin whenever necessary

Your doctor will give you specific instructions for taking insulin based on your particular needs.


 

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Small Intestine Bacterial Overgrowt

Simply put, Small Intestine Bacterial Overgrowth is a chronic bacterial infection of the small intestine.  The infection is of bacteria that normally live in the gastrointestinal tract but have abnormally overgrown in a location not meant for so many bacteria.  

The Problem
The bacteria interfere with our normal digestion and absorption of food and are associated with damage to the lining or membrane of the SI (leaky gut syndrome, which I prefer to call leaky SI in this case). 

  • They consume some of our food which over time leads to deficiencies in their favorite nutrients such as iron and B12, causing anemia.
  • They consume food unable to be absorbed due to SI lining damage, which creates more bacterial overgrowth (a vicious cycle).
  • After eating our food, they produce gas/ expel flatus, within our SI.  The gas causes abdominal bloating, abdominal pain, constipation, diarrhea or both (the symptoms of IBS).  Excess gas can also cause belching and flatulence.
  • They decrease proper fat absorption by deconjugating bile leading to deficiencies of vitamins A & D and fatty stools.
  • Through the damaged lining, larger food particles not able to be fully digested, enter into the body which the immune system reacts to.  This causes food allergies/ sensitivities.
  • Bacteria themselves can also enter the body/bloodstream.  Immune system reaction to bacteria and their cell walls (endotoxin) causes chronic fatigue and body pain and burdens the liver.
  • Finally, the bacteria excrete acids which in high amounts can cause neurological and cognitive symptoms.
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