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Here’s a fewEVOLUTION 44 REASONS WHY EVOLUTION IS A FAIRY TALEFROM; Exposing The Truth One Story At A Time…Because anti-faith folk have taken over our educational system these days. Most Americans would be absolutely shocked to learn that most of what is taught as “truth” about evolution is actually the product of the overactive imaginations of members of the scientific community. They so badly want to believe that it is true that they will go to extraordinary lengths to defend their fairy tale. They keep insisting that the theory of evolution has been “proven” and that it is beyond debate. Meanwhile, most average people are intimidated into accepting the “truth” about evolution because they don’t want to appear to be “stupid” to everyone else.In this day and age, it is imperative that we all learn to think for ourselves. Don’t let me tell you what to think, and don’t let anyone else tell you what to think either. Do your own research and come to your own conclusions. The following are 44 reasons why evolution is just a fairy tale for adults…#1 If the theory of evolution was true, we should have discovered millions upon millions of transitional fossils that show the development of one species into another species. Instead, we have zero.#2 When Charles Darwin came up with his theory, he admitted that no transitional forms had been found at that time, but he believed that huge numbers certainly existed and would eventually be discovered…“Lastly, looking not to any one time, but to all time, if my theory be true, numberless intermediate varieties, linking closely together all the species of the same group, must assuredly have existed. But, as by this theory, innumerable transitional forms must have existed, why do we not find them embedded in countless numbers in the crust of the earth?”#3 Even some of the most famous evolutionists in the world acknowledge the complete absence of transitional fossils in the fossil record. For example, Dr. Colin Patterson, former senior paleontologist of the British Museum of Natural History and author of “Evolution” once wrote the following…“I fully agree with your comments about the lack of direct illustration of evolutionary transitions in my book. If I knew of any, fossil or living, I would certainly have included them …. I will lay it on the line – there is not one such fossil for which one could make a watertight argument.”#4 Stephen Jay Gould, Professor of Geology and Paleontology at Harvard University, once wrote the following about the lack of transitional forms…“The absence of fossil evidence for intermediary stages between major transitions in organic design, indeed our inability, even in our imagination, to construct functional intermediates in many cases, has been a persistent and nagging problem for gradualistic accounts of evolution.”#5 Evolutionist Stephen M. Stanley of Johns Hopkins University has also commented on the stunning lack of transitional forms in the fossil record…“In fact, the fossil record does not convincingly document a single transition from one species to another.”#6 If “evolution” was happening right now, there would be millions of creatures out there with partially developed features and organs. But instead there are none.#7 If the theory of evolution was true, we should not see a sudden explosion of fully formed complex life in the fossil record. Instead, that is precisely what we find.#8 Paleontologist Mark Czarnecki, an evolutionist, once commented on the fact that complex life appears very suddenly in the fossil record…“A major problem in proving the theory has been the fossil record; the imprints of vanished species preserved in the Earth’s geological formations. This record has never revealed traces of Darwin’s hypothetical intermediate variants – instead species appear and disappear abruptly, and this anomaly has fueled the creationist argument that each species was created by God.”#9 The sudden appearance of complex life in the fossil record is so undeniable that even Richard Dawkins has been forced to admit it…“It is as though they [fossils] were just planted there, without any evolutionary history. Needless to say this appearance of sudden planting has delighted creationists. Both schools of thought (Punctuationists and Gradualists) despise so-called scientific creationists equally, and both agree that the major gaps are real, that they are true imperfections in the fossil record. The only alternative explanation of the sudden appearance of so many complex animal types in the Cambrian era is divine creation and both reject this alternative.”#10 Nobody has ever observed macroevolution take place in the laboratory or in nature. In other words, nobody has ever observed one kind of creature turn into another kind of creature. The entire theory of evolution is based on blind faith.#11 Evolutionist Jeffrey Schwartz, a professor of anthropology at the University of Pittsburgh, openly admits that “the formation of a new species, by any mechanism, has never been observed.”#12 Even evolutionist Stephen J. Gould of Harvard University has admitted that the record shows that species do not change. The following is how he put it during a lecture at Hobart & William Smith College…“Every paleontologist knows that most species don’t change. That’s bothersome….brings terrible distress. ….They may get a little bigger or bumpier but they remain the same species and that’s not due to imperfection and gaps but stasis. And yet this remarkable stasis has generally been ignored as no data. If they don’t change, its not evolution so you don’t talk about it.”#13 Anyone that believes that the theory of evolution has “scientific origins” is fooling themselves. It is actually a deeply pagan religious philosophy that can be traced back for thousands of years.#14 Anything that we dig up that is supposedly more than 250,000 years old should have absolutely no radiocarbon in it whatsoever. But instead, we find it in everything that we dig up – even dinosaur bones. This is clear evidence that the “millions of years” theory is simply a bunch of nonsense…It’s long been known that radiocarbon (which should disappear in only a few tens of thousands of years at the most) keeps popping up reliably in samples (like coal, oil, gas, etc.) which are supposed to be ‘millions of years’ old. For instance, CMI has over the years commissioned and funded the radiocarbon testing of a number of wood samples from ‘old’ sites (e.g. with Jurassic fossils, inside Triassic sandstone, burnt by Tertiary basalt) and these were published (by then staff geologist Dr Andrew Snelling) in Creation magazine and Journal of Creation. In each case, with contamination eliminated, the result has been in the thousands of years, i.e. C-14 was present when it ‘shouldn’t have been’. These results encouraged the rest of the RATE team to investigate C-14 further, building on the literature reviews of creationist M.D. Dr Paul Giem.In another very important paper presented at this year’s ICC, scientists from the RATE group summarized the pertinent facts and presented further experimental data. The bottom line is that virtually all biological specimens, no matter how ‘old’ they are supposed to be, show measurable C-14 levels. This effectively limits the age of all buried biota to less than (at most) 250,000 years.#15 The odds of even a single sell “assembling itself” by chance are so low that they aren’t even worth talking about. The following is an excerpt from Jonathan Gray’s book entitled “The Forbidden Secret“…Even the simplest cell you can conceive of would require no less than 100,000 DNA base pairs and a minimum of about 10,000 amino acids, to form the essential protein chain. Not to mention the other things that would also be necessary for the first cell.Bear in mind that every single base pair in the DNA chain has to have the same molecular orientation (“left-hand” or “right hand”)? As well as that, virtually all the amino acids must have the opposite orientation. And every one must be without error.“Now,” explained Larry, “to randomly obtain those correct orientations, do you know your chances? It would be 1 chance in 2110,000, or 1 chance in 1033,113!“To put it another way, if you attempted a trillion, trillion, trillion combinations every second for 15 billion years, the odds you would achieve all the correct orientations would still only be one chance in a trillion, trillion, trillion, trillion … and the trillions would continue 2755 times!“It would be like winning more than 4700 state lotteries in a row with a single ticket purchased for each. In other words…impossible.”#16 How did life learn to reproduce itself? This is a question that evolutionists do not have an answer for.#17 In 2007, fishermen caught a very rare creature known as a Coelacanth. Evolutionists originally told us that this “living fossil” had gone extinct 70 million years ago. It turns out that they were only off by 70 million years.#18 According to evolutionists, the Ancient Greenling Damselfly last showed up in the fossil record about 300 million years ago. But it still exists today. So why hasn’t it evolved at all over the time frame?#19 Darwinists believe that the human brain developed without the assistance of any designer. This is so laughable it is amazing that there are any people out there that still believe this stuff. The truth is that the human brain is amazingly complex. The following is how a PBS documentary described the complexity of the human brain: “It contains over 100 billion cells, each with over 50,000 neuron connections to other brain cells.”#20 The following is how one evolutionist pessimistically assessed the lack of evidence for the evolution of humanity…“Even with DNA sequence data, we have no direct access to the processes of evolution, so objective reconstruction of the vanished past can be achieved only by creative imagination.”#21 Perhaps the most famous fossil in the history of the theory of evolution, “Piltdown Man”, turned out to be a giant hoax.#22 If the neutron were not about 1.001 times the mass of the proton, all protons would have decayed into neutrons or all neutrons would have decayed into protons, and therefore life would not be possible. How can we account for this?#23 If gravity was stronger or weaker by the slimmest of margins, then life sustaining stars like the sun could not exist. This would also make life impossible. How can we account for this?#24 Why did evolutionist Dr. Lyall Watson make the following statement?…“The fossils that decorate our family tree are so scarce that there are still more scientists than specimens. The remarkable fact is that all of the physical evidence we have for human evolution can still be placed, with room to spare, inside a single coffin!”#25 Apes and humans are very different genetically. As DNA tests prove Darwin Was Wrong explains, “the human Y chromosome has twice as many genes as the chimpanzee Y chromosome and the chromosome structures are not at all similar.”#26 How can we explain the creation of new information that is required for one animal to turn into another animal? No evolutionary process has ever been shown to be able to create new biological information. One scientist described the incredible amount of new information that would be required to transform microbes into men this way…“The key issue is the type of change required — to change microbes into men requires changes that increase the genetic information content, from over half a million DNA ‘letters’ of even the ‘simplest’ self-reproducing organism to three billion ‘letters’ (stored in each human cell nucleus).”#27 Evolutionists would have us believe that there are nice, neat fossil layers with older fossils being found in the deepest layers and newer fossils being found in the newest layers. This simply is not true at all…The fossil layers are not found in the ground in the nice neat clean order that evolutionists illustrate them to be in their textbooks. There is not one place on the surface of the earth where you may dig straight down and pass through the fossil layers in the order shown in the textbooks. The neat order of one layer upon another does not exist in nature. The fossil bearing layers are actually found out of order, upside down (backwards according to evolutionary theory), missing (from where evolutionists would expect them to be) or interlaced (“younger” and “older” layers found in repeating sequences). “Out of place” fossils are the rule and not the exception throughout the fossil record.#28 Evolutionists believe that the ancestors of birds developed hollow bones over thousands of generations so that they would eventually be light enough to fly. This makes absolutely no sense and is beyond ridiculous.#29 If dinosaurs really are tens of millions of years old, why have scientists found dinosaur bones with soft tissue still in them? The following is from an NBC News report about one of these discoveries…For more than a century, the study of dinosaurs has been limited to fossilized bones. Now, researchers have recovered 70 million-year-old soft tissue, including what may be blood vessels and cells, from a Tyrannosaurus rex.#30 Which evolved first: blood, the heart, or the blood vessels for the blood to travel through?#31 Which evolved first: the mouth, the stomach, the digestive fluids, or the ability to poop?#32 Which evolved first: the windpipe, the lungs, or the ability of the body to use oxygen?#33 Which evolved first: the bones, ligaments, tendons, blood supply, or the muscles to move the bones?#34 In order for blood to clot, more than 20 complex steps need to successfully be completed. How in the world did that process possibly evolve?#35 DNA is so incredibly complex that it is absolutely absurd to suggest that such a language system could have “evolved” all by itself by accident…When it comes to storing massive amounts of information, nothing comes close to the efficiency of DNA. A single strand of DNA is thousands of times thinner than a strand of human hair. One pinhead of DNA could hold enough information to fill a stack of books stretching from the earth to the moon 500 times.Although DNA is wound into tight coils, your cells can quickly access, copy, and translate the information stored in DNA. DNA even has a built-in proofreader and spell-checker that ensure precise copying. Only about one mistake slips through for every 10 billion nucleotides that are copied.#36 Can you solve the following riddle by Perry Marshall?…1) DNA is not merely a molecule with a pattern; it is a code, a language, and an information storage mechanism.2) All codes are created by a conscious mind; there is no natural process known to science that creates coded information.3) Therefore DNA was designed by a mind.If you can provide an empirical example of a code or language that occurs naturally, you’ve toppled my proof. All you need is one.#37 Evolutionists simply cannot explain why our planet is so perfectly suited to support life.#38 Shells from living snails have been “carbon dated” to be 27,000 years old.#39 If humans have been around for so long, where are all of the bones and all of the graves? The following is an excerpt from an article by Don Batten…Evolutionists also claim there was a ‘Stone Age’ of about 100,000 years when between one million and 10 million people lived on Earth. Fossil evidence shows that people buried their dead, often with artefacts—cremation was not practised until relatively recent times (in evolutionary thinking). If there were just one million people alive during that time, with an average generation time of 25 years, they should have buried 4 billion bodies, and many artefacts. If there were 10 million people, it would mean 40 billion bodies buried in the earth. If the evolutionary timescale were correct, then we would expect the skeletons of the buried bodies to be largely still present after 100,000 years, because many ordinary bones claimed to be much older have been found. However, even if the bodies had disintegrated, lots of artefacts should still be found.#40 Evolutionists claim that just because it looks like we were designed that does not mean that we actually were. They often speak of the “illusion of design”, but that is kind of like saying that it is an “illusion” that a 747 airplane or an Apple iPhone were designed. And of course the human body is far more complex that a 747 or an iPhone.#41 If you want to be part of the “scientific community” today, you must accept the theory of evolution no matter how absurd it may seem to you. Richard Lewontin of Harvard once made the following comment regarding this harsh reality…We take the side of science in spite of the patent absurdity of some of its constructs, . . . in spite of the tolerance of the scientific community for unsubstantiated commitment to materialism. . . . we are forced by our a priori adherence to material causes to create an apparatus of investigation and set of concepts that produce material explanations, no matter how counterintuitive, no matter how mystifying to the uninitiated. Moreover, that materialism is absolute, for we cannot allow a Divine Foot in the door.#42 Time Magazine once made the following statement about the lack of evidence for the theory of evolution…“Yet despite more than a century of digging, the fossil record remains maddeningly sparse. With so few clues, even a single bone that doesn’t fit into the picture can upset everything. Virtually every major discovery has put deep cracks in the conventional wisdom and forced scientists to concoct new theories, amid furious debate.”#43 Malcolm Muggeridge, the world famous journalist and philosopher, once made the following statement about the absurdity of the theory of evolution…“I myself am convinced that the theory of evolution, especially the extent to which it’s been applied, will be one of the great jokes in the history books of the future. Posterity will marvel that so very flimsy and dubious an hypothesis could be accepted with the incredible credulity that it has.”#44 In order to believe the theory of evolution, you must have enough blind faith to believe that life just popped into existence from nonlife, and that such life just happened to have the ability to take in the nourishment it needed, to expel waste, and to reproduce itself, all the while having everything it needed to survive in the environment in which it suddenly found itself. Do you have that much blind faith?For years, I have been looking for someone that can explain to me the very best evidence for the theory of evolution in a systematic way. My challenge has been for someone to lay out for me a basic outline of the facts that “prove” that evolution is true.

Small Intestinal Bacterial OvergrowthA Comprehensive ReviewAndrew C. Dukowicz, MD, Brian E. Lacy, PhD, MD,AbstractSmall intestinal bacterial overgrowth (SIBO), defined as excessive bacteria in the small intestine, remains a poorly understood disease. Initially thought to occur in only a small number of patients, it is now apparent that this disorder is more prevalent than previously thought. Patients with SIBO vary in presentation, from being only mildly symptomatic to suffering from chronic diarrhea, weight loss, and malabsorption. A number of diagnostic tests are currently available, although the optimal treatment regimen remains elusive. Recently there has been renewed interest in SIBO and its putative association with irritable bowel syndrome. In this comprehensive review, we will discuss the epidemiology, pathogenesis, clinical manifestations, diagnosis, and treatment of SIBO.Keywords: Bacterial overgrowth, small intestinal bacterial overgrowth, diarrhea, bloating, motility disorders, antibioticsSmall intestinal bacterial overgrowth (SIBO) is defined as the presence of excessive bacteria in the small intestine. SIBO is frequently implicated as the cause of chronic diarrhea and malabsorption. Patients with SIBO may also suffer from unintentional weight loss, nutritional deficiencies, and osteoporosis. A common misconception is that SIBO affects only a limited number of patients, such as those with an anatomic abnormality of the upper gastrointestinal (GI) tract or those with a motility disorder. However, SIBO may be more prevalent than previously thought. This apparent increase in prevalence may have occurred, in part, because readily available diagnostic tests have improved our ability to diagnose SIBO. This comprehensive review will discuss the epidemiology and pathophysiology of SIBO; review common clinical presentations, diagnostic tests, and their limitations; and discuss currently available treatment options.Go to:MethodsOvid MEDLINE and PubMed databases were used to search the published literature. For Ovid MEDLINE (1966 to December 2006, English language only) three primary search terms (bacterial overgrowth, small intestine overgrowth, and small intestine bacterial overgrowth) were individually coupled with a larger number of secondary search terms (epidemiology, incidence, prevalence, populations at risk, symptoms, pathogenesis, pathophysiology, inflammation, malabsorption, complications, vitamin deficiency, motility disorders, scleroderma, gastroparesis, chronic intestinal pseudo-obstruction, celiac disease, irritable bowel syndrome, renal failure, cirrhosis, alcohol abuse, elderly, aging, diabetes, hypochlorhydria, surgery, malnutrition, diarrhea, evaluation, diagnosis, breath testing, duodenum, jejunum, aspirates, breath tests, lactulose, treatment, antibiotics, rifaximin, tetracycline, metronidazole, ciprofloxacin, amoxicillin/clavulanate, probiotics, duration, resistance). For PubMed (no time limit), a similar search process was followed. All identified articles were then manually searched for other relevant studies. Only published manuscripts are included in this review; abstracts are not included.Go to:DefinitionSIBO is defined as a bacterial population in the small intestine exceeding 105–106organisms/mL.1,2Normally, less than 103organisms/mL are found in the upper small intestine, and the majority of these are Gram-positive organisms.3In addition to the absolute number of organisms, the type of microbial flora present plays an important role in the manifestation of signs and symptoms of overgrowth.4For example, a predominance of bacteria that metabolize bile salts to unconjugated or insoluble compounds may lead to fat malabsorption or bile acid diarrhea. In contrast, microorganisms that preferentially metabolize carbohydrates to short-chain fatty acids and gas may produce bloating without diarrhea because the metabolic products can be absorbed. Gram-negative coliforms, such as Klebsiella species, may produce toxins that damage the mucosa, interfering with absorptive function and causing secretion, thereby mimicking tropical sprue.Go to:PrevalenceAn extensive literature search was unable to identify a study evaluating the incidence of SIBO in healthy volunteers. Only limited data are available regarding the prevalence of SIBO in healthy populations. In a study of 294 nonhospitalized older adults in which 34 younger adults (mean age 33.6 years) served as healthy controls, the prevalence of SIBO, as determined by glucose breath test, was 5.9% in the control group versus 15.6% in the older group.5A study of healthy older adults from Japan (mean age 74.7 years) found no patient with SIBO using a glucose breath test;6an Australian study detected SIBO from duodenal aspirates in 0% of healthy controls (mean age 59), although 13% were positive for SIBO using a lactulose breath test.7Healthy elderly volunteers from the United Kingdom had a 14.5% prevalence rate for SIBO based on a positive glucose breath test.8Finally, in a study of 111 patients with irritable bowel syndrome (IBS), 20% of healthy age- and sex-matched controls were found to have an abnormal lactulose breath test suggestive of SIBO.9In summary, although data are limited, the prevalence rates of SIBO in young and middle-aged adults appear to be low, whereas prevalence rates appear to be consistently higher in the older patient (14.5–15.6%); these rates, however, are dependent upon the diagnostic test used (see below).Go to:PathogenesisSIBO develops when the normal homeostatic mechanisms that control enteric bacterial populations are disrupted. The two processes that most commonly predispose to bacterial overgrowth are diminished gastric acid secretion and small intestine dysmotility. Disturbances in gut immune function and anatomical abnormalities of the GI tract also increase the likelihood of developing SIBO. Once present, bacterial overgrowth may induce an inflammatory response in the intestinal mucosa, further exacerbating the typical symptoms of SIBO. Although not universally seen,10overgrowth of small bowel intestinal flora may result in microscopic mucosal inflammation. Analysis of small bowel biopsies in elderly patients with bacterial overgrowth revealed blunting of the intestinal villi, thinning of the mucosa and crypts, and increased intraepithelial lymphocytes, all of which reversed with antibiotic treatment.11Gastric AcidGastric acid suppresses the growth of ingested bacteria, thereby limiting bacterial counts in the upper small intestine. Diminished acid production (hypochlorhydria) is a risk factor for SIBO, and can develop after colonization with Helicobacter pylori or as a consequence of aging.12–14Interestingly, bacterial overgrowth can lead to a false positive H. pylori diagnosis using urea-based testing given the presence of urease-positive bacterial strains.15Inhibition of acid secretion via histamine type 2 receptor blockers (H2RAs) or proton-pump inhibitors (PPIs) may predispose to SIBO, although conflicting results are found in the published literature. Treatment with H2RAs led to SIBO in 18 adult patients, as measured by bile acid breath tests and jejunal aspirates.16A prospective study of 47 outpatients treated with either omeprazole (20 mg/day) or cimetidine (800 mg/day) found that bacterial overgrowth was present in 53% of patients who received omeprazole, compared to 17% who received cimetidine (P<.05).17Twenty patients treated with 4 weeks of omeprazole had a significant increase in duodenal bacterial counts (compared to baseline) as measured by endoscopic aspirate.18These disparate results may represent a true medication effect or, alternatively, reflect the small number of patients studied and differences in assay techniques.Motility DisordersNormal GI motility involves a complex, tightly coordinated series of events designed to move material through the GI tract. During periods of fasting, a migrating motor complex (MMC) develops approximately every 90-120 minutes to sweep residual debris through the GI tract. Several studies have demonstrated that abnormalities in the MMC may predispose to the development of SIBO.19–21Postprandial peristalsis includes irregular, high-amplitude contractions in the stomach (to assist with trituration and gastric emptying).22Gastroparesis, a chronic disorder of delayed gastric emptying, can develop secondary to long-standing diabetes, connective tissue disorders, a prior viral infection, and ischemia.23Impaired gastric peristalsis can lead to SIBO due to stasis of food and bacteria in the upper GI tract.Small bowel motility disorders also predispose to the development of SIBO, because bacteria may not be effectively swept from the proximal bowel into the colon. Disruption of the MMC is associated with bacterial overgrowth in an experimental model.24Patients with cirrhosis and portal hypertension (compared to patients without portal hypertension) had retrograde pressure waves in the proximal duodenum, clustered contractions, and abnormalities of the MMC leading to a greater prevalence of SIBO.25Patients with chronic renal failure have neuropathic-like motor abnormalities in the small intestine and are more likely to develop bacterial overgrowth.26Neuropathic processes, such as chronic intestinal pseudo-obstruction (CIP), and myopathic processes, such as scleroderma and polymyositis, are likely to be associated with SIBO.27In a small group of systemic sclerosis patients with greater than 105 colony-forming units/pL via duodenal aspiration, 7 out of 8 patients had positive lactulose breath tests.28Other conditions that affect small bowel motility, which predispose patients to develop SIBO, are shown in Table 1.Table 1Risk Factors for the Development of Small Intestinal Bacterial OvergrowthStructural Abnormalities of the GI TractStructural abnormalities in the GI tract provide an ideal environment for bacterial colonization and overgrowth. GI tract surgeries that create a blind loop (eg, a Billroth II procedure or a Roux-en-Y anastomosis; Figures ​Figures11 and ​and2)2) predispose to bacterial stasis and overgrowth due to abnormal motility and ineffective clearance of retained food and secretions.29Patients who have undergone jejunoileal bypass, an end-to-side enteroenteric anastomosis, or the creation of a Koch distal ileal pouch, are also at risk to develop SIBO.Figure 1Billroth II anatomy that may predispose some patients to small intestinal bacterial overgrowth.Figure 2Roux-en-Y anastomosis that may predispose some patients to small intestinal bacterial overgrowth.Small bowel diverticula occur in approximately 1—6% of the population, based on autopsy studies and a variety of radiographic studies. They are generally incidental, asymptomatic, and small in size.30However, large duodenal and jejunal diverticula can harbor bacteria and lead to symptoms of SIBO. Strictures of the small intestine, which can develop after surgery, after radiation, in association with Crohn's disease, or secondary to medication use, also predispose to the development of SIBO.31Finally, resection of the ileocecal valve increases the risk of developing SIBO, because retrograde movement of bacteria from the colon into the small intestine can now readily occur. One study of Crohn's patients found that resection of the ileocecal valve significantly increased the prevalence of SIBO from 18% to 30%.32Immune FunctionPatients who are immunodeficient, whether due to an abnormal antibody response or T-cell response, are prone to bacterial overgrowth.33Patients with SIBO (compared to those with normal jejunal aspirates) were more likely to have abnormalities in intestinal mucosal immunity (evidenced by increased luminal immunoglobulin A [IgA] concentrations and lamina propria IgA plasma cell counts).34,35Patients with deficiencies in humoral or cellular immunity do not appear to be predisposed to SIBO, as they have normal intestinal microflora.36,37Go to:Populations at RiskSIBO can develop in a variety of patient populations (Table 1). Risk factors are reviewed below, along with a discussion of the prevalence of SIBO in these specific situations, where data are available. A review of the literature failed to identify any study evaluating the incidence of SIBO in specific populations.Irritable Bowel SyndromeThere is a significant amount of interest on the possible role of SIBO in the generation of IBS. Many IBS symptoms are nonspecific (bloating, distention, cramping, abdominal discomfort) and can mimic symptoms of SIBO.38In an uncontrolled study, Pimentel and colleagues found that 78% of 202 patients who met the Rome I criteria for IBS had an abnormal lactulose breath test suggestive of SIBO.39A blinded, randomized study found that 84% of patients who met Rome I criteria for IBS had an abnormal lactulose breath test consistent with SIBO, compared to 20% of healthy volunteers,9while another group reported a prevalence rate of 65% in 98 consecutive IBS patients.40In contrast, other research groups have failed to replicate these interesting findings. In 85 consecutive patients meeting the Rome II criteria for IBS, none had SIBO using glucose breath testing;41Walters and Vanner reported that only 10% of their IBS patients (Rome II criteria) had SIBO using the lactulose breath test.42Given these widely discordant results, there is considerable debate in the scientific community about the potential relationship between IBS and SIBO. Delayed transit, disordered motility, or abnormalities in the MMC, all of which can occur in IBS patients, could potentially predispose these patients to SIBO.36,43Metabolic DisordersLong-standing and poorly controlled diabetes can injure the enteric nervous system leading to disordered GI motility. Diabetic gastroparesis and neuropathic small bowel motility disorders are both associated with SIBO (see above). A recent study found that SIBO was present in 43% of diabetic patients with chronic diarrhea, and 75% had a significant improvement in their symptoms after being treated with antibiotics.44Additionally, in a group of 82 diabetic patients, of those who had carbohydrate malabsorption on an oral glucose tolerance test, 75% were diagnosed with SIBO.45AgingMitsui and colleagues, using a glucose breath test, found that 33% of disabled older adults had SIBO.6Parlesak and coworkers, also using a glucose breath test, showed that 15.6% of older, nonhospitalized adults had SIBO;5Lewis and associates reported similar data (14.5%).8Although it is commonly believed that SIBO develops in the elderly because of age-associated decline in GI tract motility, most studies have not shown a significant decrease in GI motility with aging.46,47Rather, other pathophysiologic processes likely play a role, including medications and agents 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.Celiac DiseaseLong-standing celiac disease can disturb gut motility, leading to small intestine dysmotility.48A study of 15 celiac patients with persistent symptoms despite adherence to a strict gluten-free diet found that 66% had bacterial overgrowth on lactulose breath testing.49All of these patients noted a resolution of their symptoms after being treated for bacterial overgrowth.Chronic DiarrheaA recent study evaluated the role of SIBO in 87 consecutive patients with chronic diarrhea. All patients underwent extensive testing to exclude structural, metabolic, inflammatory, and acute infectious processes. In addition, celiac disease and inflammatory bowel disease were ruled out by both laboratory and endoscopic testing. The authors reported that SIBO was present in 33% of the patients using small bowel culture, compared to 0% in healthy controls.7Other Organ DysfunctionGI symptoms are common in patients with renal failure and include nausea, early satiety, bloating, and abdominal pain. Although often attributed to uremia, these symptoms may reflect altered gut motility and SIBO. A study of 22 patients with chronic renal failure found that 50% had evidence of a neuropathic motility disorder, as measured by antroduodenojejunal manometry.25SIBO was more prevalent in patients with neuropathic motility disorders (55%) compared to those without (18%; P=.07).Surgically induced obstructive jaundice can lead to bacterial overgrowth and increased bacterial translocation from the GI tract in laboratory animals.50Clinical studies have shown that patients with advanced liver disease are more likely to have abnormalities in gut motility compared to those with lower Child-Pugh scores.24,51,52These include abnormalities in the MMC and an increase in the frequency of clustered contractions—both of which may promote bacterial stasis and the development of SIBO—in 31–68% of patients.53–56SIBO does not appear to be an independent risk factor for liver injury, however.Recent animal studies have demonstrated that acute pancreatitis can alter the MMC57and that acute necrotizing pancreatitis disturbs the jejunal MMC leading to SIBO.58A study of 35 patients with chronic pancreatitis and pancreatic insufficiency found that 34% had SIBO, as determined by a glucose breath test.59Chronic alcohol use may predispose patients to SIBO. A study from Sweden compared 22 alcoholics with epigastric pain and nausea to 12 nonalcoholic patients with dyspeptic symptoms.60Using both gastric and duodenal biopsies and aspirates, bacterial overgrowth was identified in 90% of alcoholics compared to 50% of controls (P<.01). Of note, 7 of the control patients had used acid suppressants, which may explain the high rate of bacterial overgrowth in the control population.Finally, antibiotics can alter the normal balance of gut flora leading to changes in the population of bacteria within the GI tract. No prospective studies in this area were identified in the literature.Go to:Clinical ManifestationsSymptoms of SIBO are nonspecific and include bloating, abdominal distension, abdominal pain or discomfort, diarrhea, fatigue, and weakness. The frequency and severity of symptoms likely reflect both the degree of bacterial overgrowth along with the extent of mucosal inflammation. However, symptoms may also reflect the underlying cause of SIBO (eg, small bowel dysmotility). Other symptoms can reflect complications of SIBO, including malabsorption, nutritional deficiencies, and metabolic bone disorders (Table 2).61The nonspecific nature of these complaints makes SIBO difficult to distinguish clinically from other disease entities, such as IBS, lactose intolerance, or fructose intolerance. No study has evaluated the specificity of these symptoms; therefore, objective testing is recommended.Table 2Symptoms Associated With Bacterial OvergrowthGo to:ComplicationsComplications of SIBO range from mild, including diarrhea and minimal vitamin deficiencies, to severe, including malabsorption and neuropathies due to fat-soluble vitamin deficiencies. The nutritional consequences of SIBO result from maldigestion and malabsorption of nutrients in the intestinal lumen (Table 3).62The latter occurs secondary to microscopic damage to the small intestinal mucosa which diminishes the absorptive capacity of the microvilli.Table 3Clinical Manifestations of Small Intestinal Bacterial OvergrowthFat malabsorption occurs as a result of bacterial deconjugation of bile salts. In addition, free bile acids are toxic to the intestinal mucosa, resulting in mucosal inflammation and malabsorption.63,64Deconjugated bile salts are reabsorbed in the jejunum rather than the ileum, leading to impaired micelle formation, fat malabsorption, and deficiencies in fat-soluble vitamins (A, D, E, and K). Fortunately, symptoms rarely develop; however, in severe cases night blindness (vitamin A), osteomalacia and tetany due to hypocalcemia (vitamin D), prolonged prothrombin times (vitamin K), or neuropathy, retinopathy, and impairments in T-cell function can occur.59Carbohydrate malabsorption develops as a result of premature breakdown of sugars by bacteria in conjunction with decreased disaccharidase activity secondary to disruption of the intestinal brush border.65Protein malabsorption can occur because of digestion by bacteria, whereas protein-losing enteropathies can develop as a result of mucosal damage.66A common complication of bacterial overgrowth is cobalamin (vitamin B12) deficiency. Patients with normal intestinal enteric flora rely on gastric intrinsic factor to bind to vitamin B12to permit absorption in the ileum. An animal model of SIBO demonstrated competitive uptake of vitamin B12by bacteria (especially aerobes).67Human subjects with atrophic gastritis and bacterial overgrowth absorbed significantly less protein-bound vitamin B12compared to controls, although this was reversed with antibiotic therapy.68Folate levels can be normal but frequently are elevated due to increased synthesis of folate by small bowel bacteria.69,70Go to:DiagnosisThe diagnosis of SIBO is controversial. There is substantial disagreement in the literature regarding which test is the most appropriate in either the clinical or research setting. Two tests are commonly employed: bacterial culture and breath tests.The most direct method of assessing the bacterial population is to perform anaerobic and aerobic colony counts of small bowel luminal contents;2however, this method is saddled with several technical hurdles. First, the small bowel must be intubated. In years past, a long tube was passed under fluoroscopic guidance and fluid aspirated through the tube. Today, few diagnostic centers use this cumbersome, time-consuming method, and instead, a catheter is passed into the distal duodenum through an endoscope and fluid aspirated for culture. The cost of endoscopy, as well as its low but measurable risk, makes this approach less than ideal. Second, many bacterial species do not grow in routine culture media, and quantitative culture may underestimate the bacterial population. Third, there are multiple problems inherent in performing this procedure including contamination of the endoscope and catheter as the instrument is passed through the GI tract, difficulty aspirating a sufficient sample, and insufflation of air into the lumen, which prevents accurate sampling. Finally, regardless of which approach is used to culture luminal contents, prompt and proper specimen handing poses yet another hurdle.The challenges of directly measuring small bowel bacterial contamination led to the development of several indirect tests to diagnose SIBO.71Breath testing is now the predominant method to evaluate patients for potential overgrowth because of its simplicity, safety, and lack of invasiveness. These methods all rely on the modification of a substrate by bacteria. The substrate most commonly used is a readily metabolized carbohydrate, such as lactulose, glucose, sucrose, or xylose. Complex carbohydrates, such as rice, are neither sensitive nor specific.72Other investigators have used bile salt cogeners as substrates for bacterial modification; however, these are less sensitive and specific when compared to xylose.73All breath tests rely on the recovery and quantification of an exhaled gas produced by the bacterial metabolism of the ingested substrate. The development of inexpensive, commercially available gas chromatographs to measure exhaled hydrogen and/or methane has led to the widespread use of breath testing for the diagnosis of bacterial overgrowth.Another method of breath sample analysis utilizes substrates such as xylose or glycocholic acid labeled with13C and14C isotopes followed by mass spectrographic or scintillation counting of breath samples for isotopic CO2.74–76Obviously,14C-labeled substrates are not appropriate for testing children and pregnant women. The use of a bile salt cogener,75Se homocholic-tauro acid, has been proposed but is expensive and not proven to be of value.77There are several points that deserve mention regarding the accuracy and utility of breath testing. First, there is no consensus regarding a gold standard for diagnosing SIBO. Most experts advocate bacterial culture as the benchmark; however, as noted, there are multiple problems inherent to this technique. Second, several substrates have been studied, but none has been identified as being superior to another. Third, differences in bacterial flora among patients can determine their response to breath testing. For example, about 10% of adults and 15% of children may not be colonized with bacteria capable of producing hydrogen. These individuals have flora-pro ducing methane from hydrogen.78Fourth, the optimum protocol for the administration, timing, and collection of breath specimens is not known. Fifth, proper interpretation of results in the setting of rapid or delayed gastric emptying has not been validated. Sixth, special populations of patients (eg, postgastrectomy, obesity surgery, advanced age) may require different standards.79,80Seventh, recent antibiotic use may alter the results, although the ideal antibiotic-free interval prior to testing is not known.2Lastly, the effects of H2RAs and PPIs on breath test results remain controversial.81All the caveats outlined above make breath testing an easy procedure to perform but a difficult procedure to interpret. At present, the lactulose or glucose hydrogen breath test is the most commonly performed. The collection of the samples relies on collecting alveolar air samples. Patients are generally instructed to avoid ingesting unfermentable carbohydrates (eg, whole grain breads, pasta). After an overnight fast, a baseline hydrogen sample is collected and then 10 g of lactulose, or 50–80 g of glucose, is administered in 120–200 mL of water. Serial end-expiratory breath samples are collected every 15–30 minutes for a total of 3–4 hours (Figure 3). Results from patients with chronic obstructive pulmonary disease or those who cannot cooperate in breath sample collection may be invalid. Smokers are advised not to smoke for 1-2 hours prior to testing.Figure 3Lactulose breath test in a patient without evidence of small intestinal bacterial overgrowth.At present, there are no accepted criteria for what constitutes a positive hydrogen breath test. Generally, an increase from the baseline fasting hydrogen concentration to a value greater than 10–-12 parts per million (ppm) after a 50-g glucose load5,82or greater than 20 ppm following lactulose,83during the first 90 minutes of the test has been accepted as proof of SIBO (Figure 4). Higher cutoff values increases the specificity at a loss of sensitivity. A second criteria often accepted as proof of overgrowth is a double peak (Figure 5). This consists of an initial hydrogen peak prior to 90 minutes, followed by a fall of more than 5 ppm over two consecutive samples, and then a second peak in breath hydrogen as the substrate enters the cecum.37Figure 4Lactulose breath test in a patient with small intestinal bacterial overgrowth—note the elevated fasting hydrogen level and subsequent rise greater than 20 ppm.Figure 5Lactulose breath test with a double peak seen in some patients with small intestine bacterial overgrowth.King and colleagues found that 1 g of xylose labeled with 1 μCi14C xylose was superior to hydrogen breath testing for the diagnosis of (culture-proven) SIBO.72The xylose test had a 95% sensitivity compared to less than 50% sensitivity for lactulose and 25% for glucose breath testing. However, others have not been able to confirm the superiority of the14C xylose test, instead reporting that the 50-g glucose hydrogen test is superior in patients with more than 105coliform bacteria/mL.84,85Corazza and colleagues reported that the glucose and lactulose breath tests have sensitivities of 60–70%, with specificities of 40–80%.2However, a recent study reported that glucose and lactulose breath tests, when compared to culture of an endoscopic small bowel aspirate, have lower sensitivities (glucose 44%, lactulose 31%) but higher specificities (glucose 80%, lactulose 86%) than previously thought.86Studies have found that the specificity of the 10-g lactulose breath test and the14C-labeled 1-g xylose test were 100% when radionuclide scintigraphy was done during the test to assess gastric emptying.87,88Elevated fasting breath hydrogen (>19 ppm or methane >10 ppm) are excellent predictors of overgrowth, being highly specific (>90%) but not sensitive (<30%).89However, a normal fasting value should not obviate performing a complete test.Go to:TreatmentThe goals of treatment for SIBO are threefold: 1) correct the underlying cause; 2) provide nutritional support, if necessary; and 3) treat the overgrowth.Treatment aimed at correcting the underlying cause includes dietary, surgical, and medical therapies. Strict adherence to diet may lead to symptom improvement in patients with celiac disease and bacterial overgrowth. Surgical revision of altered small bowel anatomy may be beneficial in patients with SIBO secondary to small bowel diverticulosis, fistulas, or strictures. Medications should be reviewed to determine if they are playing a role in the development of symptoms. Patients with gastroparesis or small bowel dysmotility as the underlying cause of SIBO may benefit from the use of prokinetic agents. Patients with cirrhosis and SIBO (demonstrated with hydrogen breath testing) and small bowel dysmotility (manometry-proven) had an improvement in overgrowth and manometric parameters after treatment with cisapride, as compared to placebo.90Their improvement was comparable to that found in patients treated with alternating neomycin and norfloxacin. Octreotide improves small bowel dysmotility and, in a small group of patients, decreased SIBO.91,92Larger trials have not yet confirmed these findings.Nutritional support, particularly in those patients with weight loss or vitamin and mineral deficiencies, is an important component of SIBO treatment. Supplementation and maintenance of vitamin B12and fat-soluble vitamins, with correction of calcium and magnesium deficiencies, are key components of treatment. Lactase and fructase deficiency may develop due to inflammation of the small bowel brush border, and dietary restrictions are often advocated, although this has not been pro