Association of small intestinal bacterial overgrowth with Parkinson’s disease: a systematic review and meta-analysis

Li, Xiaoqing; Feng, Xin; Jiang, Zhongxiang; Jiang, Zheng

doi:10.1186/s13099-021-00420-w

Cited by 34 publications

(42 citation statements)

References 31 publications

(17 reference statements)

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“…SIBO is relatively common in people with PD, including those with recent onset of motor symptoms, around half of the patients with PD testing positive for SIBO, compared with only up to a quarter in the general population [ 42 , 43 , 44 , 45 ]. Notably, however, the prevalence may be as low as 14%, or as high as 67%, depending on the demographic and clinical characteristic of the population included in the study, as well as on the testing method that has been used (i.e., small intestine fluid bacterial count, H 2 glucose breath testing, or H 2 and methane lactulose breath testing, the highest percentages being reported in studies using both glucose and lactulose H 2 and methane breath testing and the lowest in studies using H 2 glucose testing alone) [ 43 , 62 , 63 , 64 , 65 , 66 ].…”

Section: Sibo and Pdmentioning

confidence: 99%

“…Notably, however, the prevalence may be as low as 14%, or as high as 67%, depending on the demographic and clinical characteristic of the population included in the study, as well as on the testing method that has been used (i.e., small intestine fluid bacterial count, H 2 glucose breath testing, or H 2 and methane lactulose breath testing, the highest percentages being reported in studies using both glucose and lactulose H 2 and methane breath testing and the lowest in studies using H 2 glucose testing alone) [ 43 , 62 , 63 , 64 , 65 , 66 ]. Additional conditions and medications interfering with the gut microbiota also need to be excluded for a reliable account of the direct association between SIBO and PD [ 45 , 62 ]. Despite this variability, a recently published meta-analysis found a strong association between SIBO and PD when compared to healthy controls, with a pooled prevalence of SIBO in patients with PD of 47% (95% confidence interval 36–56), higher in Western countries (i.e., 52%, compared to 33% in Eastern countries), and an overall odds ratio of SIBO in patients with PD of 5.22 (95% confidence interval 3.33–8.19, p < 0.00001) [ 45 ].…”

Section: Sibo and Pdmentioning

confidence: 99%

“…Additional conditions and medications interfering with the gut microbiota also need to be excluded for a reliable account of the direct association between SIBO and PD [ 45 , 62 ]. Despite this variability, a recently published meta-analysis found a strong association between SIBO and PD when compared to healthy controls, with a pooled prevalence of SIBO in patients with PD of 47% (95% confidence interval 36–56), higher in Western countries (i.e., 52%, compared to 33% in Eastern countries), and an overall odds ratio of SIBO in patients with PD of 5.22 (95% confidence interval 3.33–8.19, p < 0.00001) [ 45 ].…”

Section: Sibo and Pdmentioning

confidence: 99%

“…There have been inconsistent findings regarding the association of SIBO with more advanced PD or longer disease duration [ 42 , 43 , 44 , 45 ]. The above-mentioned meta-analysis failed to identify any statistically significant differences of SIBO prevalence in people with PD and constipation, bloating, diarrhea, or longer disease duration [ 45 ].…”

Section: Sibo and Pdmentioning

confidence: 99%

“…SIBO-related symptoms typically disappear after one or several courses of antibiotics but recur if the predisposing condition persists [ 22 , 40 , 41 ]. Considering the potential immunomodulatory/proinflammatory effects of SIBO, its impact on intestinal barrier permeability and the potential effects on the levels of the microbial gases and other microbial products that are produced in the small intestine, the involvement of SIBO in the etiopathogeneses of neurodegenerative disorders seems plausible [ 42 , 43 , 44 , 45 ]. In this review we discuss the possibility that SIBO could contribute to the progression of PD, by promoting or preventing neurodegeneration, thus being a potential therapeutic target not only for symptomatic management (i.e., by improving gastrointestinal symptoms and increasing the efficacy of the oral medication used for the symptomatic treatment of PD) but also for delaying or stopping disease progression.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Small Intestinal Bacterial Overgrowth as Potential Therapeutic Target in Parkinson’s Disease

Dănău

Dumitrescu

Lefter

et al. 2021

IJMS

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Increasing evidence suggests that the gut microbiota and the brain are closely connected via the so-called gut–brain axis. Small intestinal bacterial overgrowth (SIBO) is a gut dysbiosis in which the small intestine is abundantly colonized by bacteria that are typically found in the colon. Though not a disease, it may result in intestinal symptoms caused by the accumulation of microbial gases in the intestine. Intestinal inflammation, malabsorption and vitamin imbalances may also develop. SIBO can be eradicated by one or several courses of antibiotics but reappears if the predisposing condition persists. Parkinson’s disease (PD) is a common neurodegenerative proteinopathy for which disease modifying interventions are not available. Sporadic forms may start in the gut years before the development of clinical features. Increased gastrointestinal transit time is present in most people with PD early during the course of the disease, predisposing to gut dysbiosis, including SIBO. The role that gut dysbiosis may play in the etiopathogenesis of PD is not fully understood yet. Here, we discuss the possibility that SIBO could contribute to the progression of PD, by promoting or preventing neurodegeneration, thus being a potential target for treatments aiming at slowing down the progression of PD. The direct symptomatic impact of SIBO and its impact on symptomatic medication are also briefly discussed.

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Section: Sibo and Pdmentioning

confidence: 99%

Section: Sibo and Pdmentioning

confidence: 99%

Section: Sibo and Pdmentioning

confidence: 99%

Section: Sibo and Pdmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Small Intestinal Bacterial Overgrowth as Potential Therapeutic Target in Parkinson’s Disease

Dănău

Dumitrescu

Lefter

et al. 2021

IJMS

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Infectious Agents as Potential Drivers of α‐Synucleinopathies

Linard

Ravier

Mougué³

et al. 2022

Movement Disorders

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α‐synucleinopathies, encompassing Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, are devastating neurodegenerative diseases for which available therapeutic options are scarce, mostly because of our limited understanding of their pathophysiology. Although these pathologies are attributed to an intracellular accumulation of the α‐synuclein protein in the nervous system with subsequent neuronal loss, the trigger(s) of this accumulation is/are not clearly identified. Among the existing hypotheses, interest in the hypothesis advocating the involvement of infectious agents in the onset of these diseases is renewed. In this article, we aimed to review the ongoing relevant factors favoring and opposing this hypothesis, focusing on (1) the potential antimicrobial role of α‐synuclein, (2) potential entry points of pathogens in regard to early symptoms of diverse α‐synucleinopathies, (3) pre‐existing literature reviews assessing potential associations between infectious agents and Parkinson's disease, (4) original studies assessing these associations for dementia with Lewy bodies and multiple system atrophy (identified through a systematic literature review), and finally (5) potential susceptibility factors modulating the effects of infectious agents on the nervous system. © 2022 International Parkinson and Movement Disorder Society

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Microbiome–gut–brain dysfunction in prodromal and symptomatic Lewy body diseases

et al. 2022

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Lewy body diseases, such as Parkinson’s disease and dementia with Lewy bodies, vary in their clinical phenotype but exhibit the same defining pathological feature, α-synuclein aggregation. Microbiome–gut–brain dysfunction may play a role in the initiation or progression of disease processes, though there are multiple potential mechanisms. We discuss the need to evaluate gastrointestinal mechanisms of pathogenesis across Lewy body diseases, as disease mechanisms likely span across diagnostic categories and a ‘body first’ clinical syndrome may better account for the heterogeneity of clinical presentations across the disorders. We discuss two primary hypotheses that suggest that either α-synuclein aggregation occurs in the gut and spreads in a prion-like fashion to the brain or systemic inflammatory processes driven by gastrointestinal dysfunction contribute to the pathophysiology of Lewy body diseases. Both of these hypotheses posit that dysbiosis and intestinal permeability are key mechanisms and potential treatment targets. Ultimately, this work can identify early interventions targeting initial disease pathogenic processes before the development of overt motor and cognitive symptoms.

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Association of small intestinal bacterial overgrowth with Parkinson’s disease: a systematic review and meta-analysis

Cited by 34 publications

References 31 publications

Small Intestinal Bacterial Overgrowth as Potential Therapeutic Target in Parkinson’s Disease

Small Intestinal Bacterial Overgrowth as Potential Therapeutic Target in Parkinson’s Disease

Infectious Agents as Potential Drivers of α‐Synucleinopathies

Microbiome–gut–brain dysfunction in prodromal and symptomatic Lewy body diseases

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