近幾年有許多研究發現:腸道菌叢健康或者平衡與否,會直接影響大腦健康,不管是憂鬱症、巴金森氏症、失智症甚至是自閉症等等。

然而腸道菌道到底是怎樣和大腦溝通的呢?最近一項發表的研究結果揭開了這個謎題,答案是腎上腺分泌的壓力荷爾蒙可體松cortisol,這對於自閉症患者,往往有嚴重的腸道功能問題提供了可能的致病原因解答。

嬰兒期大腦得發展,有一個關鍵的影響因素,那便是腸道菌叢的生態,不只是一般厭氧或者嗜氧細菌,還包含黴菌、酵母菌甚至是芽孢梭狀桿菌等等綜合的影響,但這些腸道菌叢如何跟大腦溝通,之前鮮少有研究來解釋明確的機轉。

這項新研究透過一個月大的幼豬(等同人類嬰兒期,方便大腦發展及腸道菌叢得觀察),開始先透過蒐集昇結腸內含相關的腸道菌叢分析,然而檢測血液以及大腦中一些特定檢測物質的濃度。研究發現,糞便中擬桿菌( Bacteroides)以及縮狀菌(Clostridium)濃度比較高的,血液中的肌醇(myo-inositol)濃度就比較高。而Butyricimonas這種桿菌濃度高的,n-乙醯天門冬胺酸(n-acetylaspartate ,簡稱NAA)這種神經傳導物質(與興奮有關),就會高些。但瘤胃球菌(Ruminococcus )濃度高的,NAA濃度比較低。

被診斷自閉症的患者分析其神經代謝物會與一般人有差異,之前鮮少有研究針對不同的微生物可能會以想哪些神經傳導物質的濃度做過分析。

然而要做檢測,血液還是比較直接且容易蒐集的檢體,因此研究人員想了解血液濃度得哪些代謝物質與腸道菌的多寡有關,結果發現,可體松以及血清素與腸道菌的關連比較明顯。數據顯示擬桿菌( Bacteroides)濃度高者,血清素濃度會比較高。瘤胃球菌(Ruminococcus )濃度高的,血清素和可體松的濃度都會比較低。許多自閉症患者,其血清素和可體松的濃度都呈現異常。

最後研究人員以瘤胃球菌(Ruminococcus ),也就是腸道菌部分,可體松(血液部分)以及NAA(腦部神經傳導物質)部分來做分析,研究人員發現彼此的相關性,也就是腸道菌,透過可體松去影響神經傳導物質的濃度。研究人員希望未來鹽就能夠把這發現做為自閉症診斷甚至是治療的重要環節。

這研究也提醒我們:自閉症患者的治療,最好不要輕忽腸道菌叢失衡的影響。

參考文獻:

 

  1. Austin T. Mudd, Kirsten Berding, Mei Wang, Sharon M. Donovan, Ryan N. Dilger. Serum cortisol mediates the relationship between fecal Ruminococcus and brain N-acetylaspartate in the young pigGut Microbes, 2017; 1 DOI: 10.1080/19490976.2017.1353849

 

 

 

 

 

The researchers found predictive relationships between the fecal microbiota and serotonin and cortisol, two compounds in the blood known to be influenced by gut microbiota. Specifically, Bacteroideswas associated with higher serotonin levels, while Ruminococcuspredicted lower concentrations of both serotonin and cortisol. Clostridium and Butyricimonas were not associated strongly with either compound.

Again, Mudd says, the results supported previous findings related to ASD. "Alterations in serum serotonin and cortisol, as well as fecal Bacteroides and Ruminococcus levels, have been described in ASD individuals."

Based on their initial analyses, the researchers wanted to know if there was a three-way relationship between Ruminococcus, cortisol, and NAA. To investigate this further, they used a statistical approach known as "mediation analysis," and found that serum cortisol mediated the relationship between fecal Ruminococcus abundance and brain NAA concentration. In other words, it appears that Ruminococcus communicates with and makes changes to the brain indirectly through cortisol. "This mediation finding is interesting, in that it gives us insight into one way that the gut microbiota may be communicating with the brain. It can be used as a framework for developing future intervention studies which further support this proposed mechanism," Dilger adds.

"Initially, we set out to characterize relationships between the gut microbiota, blood biomarkers, and brain metabolites. But once we looked at the relationships identified in our study, they kept leading us to independently reported findings in the autism literature. We remain cautious and do not want to overstate our findings without support from clinical intervention trials, but we hypothesize that this could be a contributing factor to autism's heterogenous symptoms," Mudd says. Interestingly, in the time since the researchers wrote the paper, other publications have also reported relationships between Ruminococcus and measures of brain development, supporting that this might be a promising area for future research.

Dilger adds, "We admit this approach is limited by only using predictive models. Therefore, the next step is to generate empirical evidence in a clinical setting. So it's important to state that we've only generated a hypothesis here, but it's exciting to consider the progress that may be made in the future based on our evidence in the pre-clinical pig model."

 

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