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Co-Enzyme Q10 Study Stopped Because of Lack of Evidence that It Delays Progression of Early PD

New York, NY - Jun 06 2011

On May 27, the National Institute of Neurological Diseases and Stroke (NINDS) announced the halt of a large clinical trial conducted by the Parkinson Study Group (PSG) on the potential beneficial effects of the dietary supplement coenzyme Q10 (CoQ10) on reducing the progression of early Parkinson’s disease (PD). Their reason: a mid-study analysis suggested that there is no improvement in the CoQ10-treated individuals in comparison to those receiving placebo (empty tablet) treatment and that continuing the program would have a very low likelihood of demonstrating any benefit from coenzyme Q10 usage in delaying the progression of early PD.
For this reason, the Data Safety Monitoring Board of the program recommended stopping the study. Individuals currently enrolled in the program have been notified and the study sites are in the process of meeting with all participants.
For the PD community, both scientists and people with Parkinson’s and their care partners, this outcome is disappointing. In an earlier, far smaller study, there was preliminary evidence that people taking CoQ10 at 1200 mg/daily appeared to slow disease progression. For this reason, the current study focused on the effects of CoQ10 at 1200 and 2400 mg daily. The study involved the participation of 600 individuals with early Parkinson’s in 67 North American study centers. To date, there were no reported safety concerns related to CoQ10 at dosages of 1200 mg/day and 2400 mg/day for up to 16 months of treatment.
Christopher G. Goetz, M.D., Chair of the Parkinson's Disease Foundation Medical Policy Subcommittee comments:
“While a final judgment on the efficacy of CoQ10 must await full analysis of the data and peer review, PDF trusts the conclusion of the study sponsors that there is no evidence that CoQ10 reduces the progression of Parkinson’s disease. The action taken on May 27 shows the vigilance of NINDS and PSG in assuring that individuals in the study are kept well informed throughout the duration of a study, and are advised immediately in the event that an investigative treatment is found to have little likelihood of success.
“People with PD who are receiving CoQ10, and who feel they have been substantially helped while taking this over-the-counter product, may wish to discuss with their physician whether the group results should lead them to stop CoQ10 treatment or to continue treatment because of their individual response.
“Fortunately, there are several new and on-going programs that are studying the same question of whether early treatment of PD can positively delay clinical decline. These agents work differently from CoQ10 and they offer individuals in the current CoQ10 program – as well as other people with early PD – key opportunities for potential enrollment to continue our quest to delay the clinical decline of PD.”

Parkinson's Disease May Boost Melanoma Risk: Study

Patients with the brain disorder should get checked annually for the skin cancer, expert advises

By Steven Reinberg
HealthDay Reporter
MONDAY, June 6 (HealthDay News) -- People with Parkinson's disease may have twice the risk of developing the deadly skin cancer melanoma, a new report confirms.
Parkinson's disease, which affects about one million people in the United States, is a progressive neurological disorder that causes tremors, stiffness and difficulty with movement, coordination and walking. Melanoma, with nearly 70,000 new cases diagnosed each year in the United States, is the most dangerous type of skin cancer.
"Over the past decade there has been accumulating evidence that Parkinson's disease patients are less likely to have most types of cancers, particularly smoking-related cancers; however, they were more likely to have melanoma," said lead researcher Dr. Honglei Chen, head of the Aging & Neuroepidemiology Group at the U.S. National Institute of Environmental Health Sciences.
Not only are people with Parkinson's disease more likely to develop melanoma, but people with melanoma are more likely to develop Parkinson's disease. "It appears the association is bidirectional," he said.
Scientists have theories about why these conditions seem to co-occur, but no firm answers. They know it's not the drugs Parkinson's patients take, Chen said.
"Both conditions may have common genetic pathways or environmental factors or both," he said. "We understand very little about this possible relationship."
Ultraviolet radiation from the sun can cause skin cancer, including melanoma. No association was found between Parkinson's disease and skin cancers other than melanoma, however, the investigators said.
The report, which was supported by the National Institute of Environmental Health Sciences, is published in the June 7 issue of Neurology.
For the study, Chen's team analyzed 12 epidemiologic studies dating from 1965 through 2010 that looked at a possible association between Parkinson's disease and melanoma. This is a process called a meta-analysis, in which data from various studies are pooled together to try to find a consistent statistical pattern.
While most of these studies reported fewer than 10 cases where both conditions occurred, the researchers found that men with Parkinson's disease were twice as likely to develop melanoma as men without Parkinson's disease.
For women, the risk of melanoma was one-and-a-half times greater if they had Parkinson's disease than if they didn't, Chen's group found.
However, since both conditions are relatively rare, the odds of having Parkinson's disease and melanoma are only about 4 percent, Chen said. "The absolute risk is not that high," he added.
Still, "it is prudent for Parkinson's disease patients to be a little cautious about their skin health," Chen said. "Be prudent, but do not be alarmed."
Limitations of the study include the fact that most of the studies were not originally designed to evaluate the association between melanoma and Parkinson's disease, and the analysis is based on a very small number of cases, the authors noted.
The authors also acknowledged that their research is preliminary and said more studies are needed to explore the relationship between the brain disorder and the potentially lethal skin cancer.
Joyce Oberdorf, CEO of the National Parkinson's Foundation, said an association between the two conditions is becoming increasingly evident, but most patients and doctors are unaware of the possible connection.
"Drawing attention to the risk is definitely required," Oberdorf said, adding that the foundation is launching a campaign to alert patients.
"We are making the recommendation that every person with Parkinson's wear sunscreen and receive an annual screening by a dermatologist for melanoma," she added.
More information
For more information on Parkinson's disease, visit the U.S. National Institute of Neurological Disorders and Stroke.
SOURCES: Honglei Chen, M.D., Ph.D., head, Aging & Neuroepidemiology Group, U.S. National Institute of Environmental Health Sciences; Joyce Oberdorf, CEO, National Parkinson's Foundation; June 7, 2011, Neurology
Last Updated: June 06, 2011
Copyright © 2011 HealthDay. All rights reserved.

 

 

Drifting Pesticides May Endanger People in Nearby Workplaces

California study finds higher Parkinson's risk among non-agricultural workers

FRIDAY, June 3 (HealthDay News) -- People who work near fields sprayed with pesticides face an increased risk for Parkinson's disease, a new study has found.
Not just agricultural workers but teachers, firefighters, clerks and others whose workplaces are near fields in California's Central Valley are at greater risk for the degenerative disorder of the central nervous system, according to researchers from the University of California, Los Angeles.
"This stuff drifts," the study's senior author, Dr. Beate Ritz, an epidemiology professor at the UCLA School of Public Health, said in a university news release. "It's borne by the wind and can wind up on plants and animals, float into open doorways or kitchen windows -- up to several hundred meters from the fields."
The study focused on three pesticides used on the fields: the fungicides maneb and ziram and the herbicide paraquat. The researchers estimated the exposure of 703 people who lived or worked in the area over a 25-year span, taking into account how far they were from the fields sprayed with the chemicals. About half of the people in the study had Parkinson's.
The risk for Parkinson's rose threefold for those who worked near fields sprayed with the three pesticides, the study found. Exposure to just ziram and paraquat raised risk by 80 percent. Earlier analysis by the researchers had found a 75 percent jump in risk for people who lived near fields where maneb and paraquat were sprayed.
The findings suggest that the chemicals act together in increasing the risk for Parkinson's, according to the study, published online in the European Journal of Epidemiology.
"Our estimates of risk for ambient exposure in the workplaces were actually greater than for exposure at residences," said Ritz. "And, of course, people who both live and work near these fields experience the greatest ... risk. These workplace results give us independent confirmation of our earlier work that focused only on residences, and of the damage these chemicals are doing."
More information
The U.S. Environmental Protection Agency offers tips on reducing pesticide risk.

-- Mary Elizabeth Dallas

SOURCE: University of California, Los Angeles, news release, May 26, 2011

ANTI-OXIDANTS LESSEN THE RISK OF PARKINSON'S DISEASE

1st June
2011 - New research

ANTI-OXIDANTS LESSEN THE RISK OF PARKINSON'S DISEASE

European Journal of Neurology [2011] 18 (1) : 106-113 (Y.Miyake, W.Fukushima, K.Tanaka, S.Sasaki, C.Kiyohara, Y.Tsuboi, T.Yamada, T.Oeda, T.Miki, N.Kawamura, N.Sakae, H.Fukuyama, Y.Hirota, M.Nagai)
Antioxidant vitamins are expected to protect cells from oxidative damage in Parkinson's Disease by neutralizing the effects of reactive oxygen. However, evidence regarding the association between antioxidant vitamin intake and Parkinson's Disease is limited and inconsistent. So researchers investigated the relationship between the dietary
intake of selected antioxidant vitamins, vegetables and fruit and the risk of Parkinson's Disease. Higher consumption of vitamin E and ß-carotene (a form of vitamin A) were significantly associated with a reduced risk of Parkinson's Disease - down to only 45% for vitamin E, and down to 56% for ß-carotene. However, this relationship was only significant in women. The lesser likelihood of Parkinson's Disease was not related to the intake of vitamin C, a-carotene, cryptoxanthin, green and yellow vegetables, other vegetables, or fruit.

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Dietary intake of antioxidant vitamins and risk of Parkinson's disease: a case-control study in Japan.

Miyake Y, Fukushima W, Tanaka K, Sasaki S, Kiyohara C, Tsuboi Y, Yamada T, Oeda T, Miki T, Kawamura N, Sakae N, Fukuyama H, Hirota Y, Nagai M; Fukuoka Kinki Parkinson's Disease Study Group.

Source: Department of Public Health, Faculty of Medicine, Fukuoka University, Fukuoka Department of Public Health, Osaka, Japan. miyake-y@fukuoka-u.ac.jp

BACKGROUND: antioxidant vitamins are expected to protect cells from oxidative damage by neutralizing the effects of reactive oxygen species. However, epidemiological evidence regarding the associations between antioxidant vitamin intake and Parkinson's disease (PD) is limited and inconsistent. We investigated the relationship between dietary intake of selected antioxidant vitamins, vegetables and fruit and the risk of PD in Japan using data from a multicenter hospital-based case-control study.

METHODS: included were 249 patients within 6 years of onset of PD. Controls were 368 inpatients and outpatients without a neurodegenerative disease. Information on dietary factors was collected using a validated self-administered diet history questionnaire. Adjustment was made for sex, age, region of residence, pack-years of smoking, years of education, body mass index, dietary intake of cholesterol, alcohol, total dairy products, and coffee and the dietary glycemic index.

RESULTS: higher consumption of vitamin E and β-carotene was significantly associated with a reduced risk of PD after adjustment for confounders under study: the adjusted odds ratio in the highest quartile was 0.45 (95% confidence interval [CI]: 0.25-0.79, P for trend = 0.009) for vitamin E and 0.56 (95% CI: 0.33-0.97, P for trend = 0.03) for β-carotene. Stratified by sex, such inverse associations were significant only in women. No material relationships were shown between intake of vitamin C, α-carotene, cryptoxanthin, green and yellow vegetables, other vegetables, or fruit and the risk of PD.

CONCLUSIONS: higher intake of vitamin E and β-carotene may be associated with a decreased of PD.

NLX-P101 CLINICAL TRIAL DATA FOR PARKINSON'S DISEASE

NLX-P101 CLINICAL TRIAL DATA FOR PARKINSON'S DISEASE

Neurologix have provided details of a Phase 2 clinical trial of NLX-P101 in Parkinson's Disease. NLX-P101 is a gene therapy under investigation for the treatment of Parkinson's Disease. NLX-P101 increases the level of GABA, a substance involved in muscular movement that is naturally produced in the brain. In a one-year follow-up, patients treated with NLX-P101 who achieved clinically-meaningful symptom improvements increased from 50% at six months to 63% after one year. No serious adverse events related to the therapy or surgical procedure were reported.

NLX-P101 led to an average improvement of 23% in those people treated, which is an 8 point reduction from their symptom questionnaire score. Those patients undergoing sham surgery (those that were untreated) had an average improvement of nearly 13%, which is nearly a 5 point reduction from their symptom questionnaire score. Therefore the average improvement beyond that of doing nothing was only actually 10% and occurred in only just over half of patients.

PROSAVIN CLINICAL TRIAL DATA FOR PARKINSON'S DISEASE

25th May 2011 - News release

PROSAVIN CLINICAL TRIAL DATA FOR PARKINSON'S DISEASE

Oxford BioMedica, a leading gene therapy company, have announced clinical data from a Phase I/II clinical trial of ProSavin for the treatment of Parkinson’s Disease. They claim : an average improvement in motor function of 43%, a maximum improvement of 61%, an increase in "on" time of 3 hours, and an decrease in "off" time of 4 hours. Two doses have been tested. For more information go to the News release. ProSavin uses Oxford BioMedica's own LentiVector gene delivery technology to deliver the genes for three enzymes that are required for the formation of dopamine. The product is administered locally to the relevant region of the brain in order to increase the brain's own capacity for the formation of dopamine. For more information go to ProSavin.

However, only nine patients have so far been tested, and only for part of the intended duration of the clinical trial. The claim of increased "on" time and decreased "off" time has come only from two patients, and had been entirely self reported by the patients themselves. The claim of an average improvement in motor function of 43%, and a maximum improvement of 61% comes from only three of the patients who have been tested for the least time. It was not the actual average improvement of the patients, which was much less. Those patients tested for the longest actually declined in their improvement as time wore on.

Eli Lilly and Medtronic Announce New Preclinical Partnership to Develop GDNF for Parkinson's Disease

April 26, 2011

News in Context: Eli Lilly and Medtronic Announce New Preclinical Partnership to Develop GDNF for Parkinson's Disease

 From: Michael J. Fox Foundation:

Pharmaceutical giant Eli Lilly and Company and Medtronic, Inc. today announced a new Parkinson’s drug-device collaboration. According to both groups, the goal of the collaboration is to move the needle toward an effective GDNF-based treatment for PD through the combination of Lilly’s modified form of the neurotrophic factor GDNF and Medtronic’s implantable drug infusion system technology.
MJFF’s Chief Program Officer Todd Sherer, PhD, explains what this initiative could mean to ongoing efforts to treat the symptoms and possibly even the progression of Parkinson’s by introducing neurotrophic factors into the right areas of the brain at the appropriate levels. But he warns that there is still much work to do, and many hurdles to overcome, before this treatment approach can realistically be considered a viable one to treating Parkinson’s.
NOTE: The medical information contained in this article is for general information purposes only. The Michael J. Fox Foundation has a policy of refraining from advocating, endorsing or promoting any drug therapy, course of treatment, or specific company or institution. It is crucial that care and treatment decisions related to Parkinson’s disease and any other medical condition be made in consultation with a physician or other qualified medical professional.
MJFF: Let’s begin with the basics. What are trophic factors?
Sherer: Trophic factors are proteins that are naturally found in the brain. The analogy we often use at our Foundation is to think of trophic factors as fertilizer for the brain that keeps brain cells alive and functioning well.
Researchers have demonstrated in pre-clinical models of neuronal injury and neurodegenerative diseases that increasing the levels of trophic factors can serve to protect the cells in these model systems. From a Parkinson’s drug discovery and development standpoint, this is exciting because in theory, trophic factors could protect the dopamine cells that die in Parkinson’s disease.
MJFF: Is this how trophic factors could lead to a breakthrough treatment for Parkinson’s disease?
Sherer: Yes, again, in theory. One of the main goals we are working toward at MJFF is to find a disease-modifying therapy for PD. This means a treatment that would target and affect the underlying processes related to the onset and progression of Parkinson’s, not just treat the symptoms. Treatments available today only treat the symptoms.
Because trophic factors have shown potential to keep brain cells alive and functioning properly, they are potentially very important to R&D experts in Parkinson’s who are looking for the breakthroughs that will lead to disease-modifying therapies.
MJFF: What are some of the challenges, then, in trophic factor therapeutic development?
Sherer: The biggest challenge to the viability of trophic factors as treatment relates to the delivery of the therapy. Trophic factors can’t be given orally — for example, in pill form — because they can’t easily get into the brain, where they need to go. They are large proteins, and because of their size, they cannot penetrate the blood-brain barrier — a membrane that surrounds the brain. The blood-brain barrier is actually a very important mechanism, because it protects molecules of a certain size from entering into the brain including disease-causing pathogens and viruses. However, the blood-brain barrier also represents a challenge for finding new and better ways to treat neurological disease, because in addition to keeping out the bad stuff, it blocks many potential therapies, including trophic factors, from entering the brain.
For this reason, and also because it is probably preferable to have these trophic factors only target the area that has become susceptible to the disease, it is critical to develop innovative means for delivering them to the right areas and at the right levels to have a therapeutic effect. The two most common approaches to do this that are currently in development are direct protein therapy and gene therapy:
• In direct protein therapy, a catheter is used to directly infuse the trophic factor into the part of the brain affected by the disease.
• In gene therapy, the brain is genetically modified in order to produce the therapy itself within the brain tissue. This is achieved through the injection of a genetic vector in order to allow the brain to produce the trophic factor.
There are pros and cons to each method. With direct protein therapy you have the ability to better regulate dosing and stop the flow of the protein. The negative would be the constant presence of the catheter and the attached equipment that goes with it.
For gene therapy, the advantage is that it is a one-time surgery. Once the genetic vector itself is implanted the brain itself produces the therapy. The negative here is that it is impossible to turn the therapy off once it has begun, because once a gene is introduced into our bodies, we do not yet have a way to regulate it (turn it off and on again).
Both therapies have thus far proven to be safe. However, while both techniques have been shown to protect dopamine neurons in pre-clinical models, no one has yet successfully demonstrated this effect in a clinical trial in Parkinson’s patients.
MJFF: What exactly are Lilly and Medtronic announcing today and how might this announcement stand to shape future neurotrophic factor research?
Sherer: Most researchers believe there are a couple of high priority issues to focus on, one being the selection of the neurotrophic factor that might give the greatest potential biological benefit, and the other being improved delivery of these molecules at the right levels to the right regions of the brain.
Lilly and Medtronic are announcing new preclinical work that could potentially lead to progress on both the biology and the delivery fronts. Lilly has biosynthetically engineered a new GDNF variant with the goal of achieving increased distribution in targeted brain regions. They are pairing this with Medtronic’s drug pump and specially designed catheter that have been designed to hopefully enable precise delivery of the GDNF variant into a targeted area of the brain consistently over time. While it’s early days, the hope is that this combination of a novel GDNF variant, paired with an optimized delivery system, could help overcome some of the technical hurdles that have affected earlier trophic research.
Most importantly, it is encouraging to see well-established companies reaffirming a commitment to trophic factor research. MJFF has long been a leader in supporting trophic factor development and we continue to believe in their promise to yield a next-generation therapy for PD. But given the many challenges, the more shots on goal that are being taken, the better.
MJFF: What other trophic factor research is under way?
Sherer: MJFF is currently funding a Phase 1/2 clinical trial of a trophic factor called neurturin, which is closely related to GDNF. This trial is sponsored by the San Diego-based biotech Ceregene. We have been working with them on the development of their neurturin therapeutic since 2005. Another company, MedGenesis, is working on an approach called convection-enhanced delivery, or CED, to deliver GDNF to the putamen through an integrated approach based on four components, including a catheter system and MRI technology.
We are also funding a researcher named Mart Saarma who is working with a different neurotrophic factor called conserved dopamine neurotrophic factor (CDNF) in order to compare the effects between this protein and GDNF. The idea is to begin to prioritize which one might be most effective in the regions of the brain affected by Parkinson’s.
Of these projects, currently only Ceregene is in the clinic. Saarma and MedGenesis are still preclinical, but with short time horizons to the clinic if all goes well. Another GDNF study funded by the National Institute of Neurological Disorders and Stroke (NINDS) at the National Institutes of Health expects to enter the clinic in short order.
It is important to recognize that these are different, yet complementary efforts. Most Parkinson’s researchers believe that trophic factors hold a great deal of potential to improve treatment of PD, and what’s exciting is that there is now a wealth of studies intent on finding the best ways to implement them in the fight against Parkinson’s. Hopefully, if one such project is successful, there will be synergy among all of them. It is our hope that we can ultimately work together to successfully develop a disease-modifying therapy that would impact millions of lives.

IRON IS ASSOCIATED WITH REDUCED PARKINSON'S DISEASE

21st April 2011 - New research
IRON IS ASSOCIATED WITH REDUCED PARKINSON'S DISEASE

The Journal of  Neurological Science [2011] Apr 15. [Epub ahead of print] (Miyake Y, Tanaka K, Fukushima W, Sasaki S, Kiyohara C, Tsuboi Y, Yamada T, Oeda T, Miki T, Kawamura N, Sakae N, Fukuyama H, Hirota Y, Nagai M) Complete abstract

In some people, metals such as iron and zinc have been claimed to be increased in the substantia nigra, which is the part of the brain most involved in Parkinson's Disease. Copper is sometimes decreased in the same part of the brain. It has consequently often been claimed that iron may contribute to Parkinson's Disease. However, instead of being a toxic substance, iron is a nutrient required for normal function in the brain. Iron is essential for the formation of L-dopa, whose deficiency causes Parkinson's Disease. So its deficiency rather than excess would be likely to cause Parkinson's Disease. Evidence for the association of the dietary intake of metals with the risk of Parkinson's Disease is limited. So researchers investigated the relationship between metal consumption and the risk of Parkinson's Disease using a self administered dietary questionnaire. Instead of causing Parkinson's Disease, higher intake of iron, magnesium, and zinc was actually associated with a reduced risk of Parkinson's Disease. The lowest risk of Parkinson's Disease was associated with increased intake of iron, then magnesium, then zinc. There were no relationships between the intake of copper or manganese and the risk of Parkinson's Disease.

INTESTINAL BACTERIA IS HIGHLY PREVALENT IN PARKINSON'S DISEASE

27th April 2011 - New research
INTESTINAL BACTERIA IS HIGHLY PREVALENT IN PARKINSON'S DISEASE

Movement Disorders [2011] 26 (5) : 889-892 (Gabrielli M, Bonazzi P, Scarpellini E, Bendia E, Lauritano EC, Fasano A, Ceravolo MG, Capecci M, Rita Bentivoglio A, Provinciali L, Tonali PA, Gasbarrini A.) Complete abstract

Small intestinal bacterial overgrowth has been found to be highly prevalent in Parkinson's Disease. Parkinson's Disease is associated with gastrointestinal motility abnormalities that could favour the occurrence of small intestinal bacterial overgrowth. The aim of this study was to assess the prevalence of small intestinal bacterial overgrowth in people with Parkinson's Disease. The prevalence of small intestinal bacterial overgrowth was far higher in people with Parkinson's Disease. It occurred in over half (54%) of all people with Parkinson's Disease, in contrast to only 8% of people that do not have Parkinson's Disease. The severity of Parkinson's Disease was also very significantly related to small intestinal bacterial overgrowth.

This can lead to the following symptoms : excess gas, abdominal bloating and distension, abdominal pain, and diarrhea or in some cases chronic constipation.

What is small intestinal bacterial overgrowth (SIBO)?

What is small intestinal bacterial overgrowth (SIBO)?

The small bowel, also known as the small intestine, is the section of the gastrointestinal tract that connects the stomach with the colon. The main purpose of the small intestine is to digest and absorb food into the body. The small intestine is approximately 21 feet in length and begins in the duodenum (into which food from the stomach empties), followed by the jejunum, and then the ileum (which empties the food that has not been digested into the large intestine or colon).

The entire gastrointestinal tract, including the small intestine, normally contains bacteria. The number of bacteria is greatest in the colon (at least 1,000,000,000 bacteria per milliliter (ml) of fluid) and much lower in the small intestine (less than 10,000 bacteria per ml of fluid). Moreover, the types of bacteria within the small intestine are different than the types of bacteria within the colon. Small intestinal bacterial overgrowth (SIBO) refers to a condition in which abnormally large numbers of bacteria (at least 100,000 bacteria per ml of fluid) are present in the small intestine and the types of bacteria in the small intestine resemble more the bacteria of the colon than the small intestine.

Small intestinal bacterial overgrowth (SIBO) is also known as small bowel bacterial overgrowth (SBBO).

What causes small intestinal bacterial overgrowth?

The gastrointestinal tract is a continuous muscular tube through which digesting food is transported on its way to the colon. The coordinated activity of the muscles of the stomach and small intestine propels the food from the stomach, through the small intestine, and into the colon. Even when there is no food in the small intestine, muscular activity sweeps through the small intestine from the stomach to the colon.

The muscular activity that sweeps through the small intestine is important for the digestion of food, but it also is important because it sweeps bacteria out of the small intestine and thereby limits the numbers of bacteria in the small intestine. Anything that interferes with the progression of normal muscular activity through the small intestine can result in SIBO. Simply stated, any condition that interferes with muscular activity in the small intestine allows the bacteria to stay longer and multiply in the small intestine. The lack of muscular activity also may allow bacteria to spread backwards from the colon and into the small intestine.

Many conditions are associated with SIBO. A few are common.

• Neurologic and muscular diseases can alter the normal activity of the intestinal muscles. Diabetes mellitus damages the nerves that control the intestinal muscles. Scleroderma damages the intestinal muscles directly. In both cases, abnormal muscular activity in the small intestine allows SIBO to develop.
• Partial or intermittent obstruction of the small intestine interferes with the transport of food and bacteria through the small intestine and can result in SIBO. Causes of obstruction leading to SIBO include adhesions (scarring) from previous surgery and Crohn's disease.
• Diverticuli (out-pouchings) of the small intestine that allow bacteria to multiply inside diverticuli.