Imperial College London
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Dr Benjamin Mullish

Faculty of Medicine, Department of Metabolism, Digestion and Reproduction

IPPRF Research Fellow
 
 
 
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Contact

 

b.mullish

 
 
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Location

 

Queen Elizabeth the Queen Mother Wing (QEQM)St Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Augustin:2023:10.1002/ctm2.1152,
author = {Augustin, A and Le, Guennec A and Umamahesan, C and Kendler-Rhodes, A and Tucker, RM and Chekmeneva, E and Takis, P and Lewis, M and Balasubramanian, K and DeSouza, N and Mullish, BH and Taylor, D and Ryan, S and Whelan, K and Ma, Y and Ibrahim, M and Bjarnason, I and Hayee, BH and Charlett, A and Dobbs, SM and Dobbs, RJ and Weller, C},
doi = {10.1002/ctm2.1152},
journal = {Clinical and Translational Medicine},
title = {Faecal metabolite deficit, gut inflammation and diet in Parkinson’s disease: integrative analysis indicates inflammatory response syndrome},
url = {http://dx.doi.org/10.1002/ctm2.1152},
volume = {13},
year = {2023}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Background:Gut-brain axis is widely implicated in the pathophysiology of Parkinson's disease (PD). We take an integrated approach to considering the gut as a target for disease-modifying intervention, using continuous measurements of disease facets irrespective of diagnostic divide.Methods:We characterised 77 participants with diagnosed-PD, 113 without, by dietary/exogenous substance intake, faecal metabolome, intestinal inflammation, serum cytokines/chemokines, clinical phenotype including colonic transit time. Complete-linkage hierarchical cluster analysis of metabolites discriminant for PD-status was performed.Results:Longer colonic transit was linked to deficits in faecal short-chain-fatty acids outside PD, to a ‘tryptophan-containing metabolite cluster’ overall. Phenotypic cluster analysis aggregated colonic transit with brady/hypokinesia, tremor, sleep disorder and dysosmia, each individually associated with tryptophan-cluster deficit. Overall, a faster pulse was associated with deficits in a metabolite cluster including benzoic acid and an imidazole-ring compound (anti-fungals) and vitamin B3 (anti-inflammatory) and with higher serum CCL20 (chemotactic for lymphocytes/dendritic cells towards mucosal epithelium). The faster pulse in PD was irrespective of postural hypotension. The benzoic acid-cluster deficit was linked to (well-recognised) lower caffeine and alcohol intakes, tryptophan-cluster deficit to higher maltose intake. Free-sugar intake was increased in PD, maltose intake being 63% higher (p = .001). Faecal calprotectin was 44% (95% CI 5%, 98%) greater in PD [p = .001, adjusted for proton-pump inhibitors (p = .001)], with 16% of PD-probands exceeding a cut-point for clinically significant inflammation compatible with inflammatory bowel disease. Higher maltose intake was associated with exceeding this calprotectin cut-point.Conclusions:Emerging picture is of (i) clinical phenotype being described by deficits in microbial metabolites essenti
AU  - Augustin,A
AU  - Le,Guennec A
AU  - Umamahesan,C
AU  - Kendler-Rhodes,A
AU  - Tucker,RM
AU  - Chekmeneva,E
AU  - Takis,P
AU  - Lewis,M
AU  - Balasubramanian,K
AU  - DeSouza,N
AU  - Mullish,BH
AU  - Taylor,D
AU  - Ryan,S
AU  - Whelan,K
AU  - Ma,Y
AU  - Ibrahim,M
AU  - Bjarnason,I
AU  - Hayee,BH
AU  - Charlett,A
AU  - Dobbs,SM
AU  - Dobbs,RJ
AU  - Weller,C
DO  - 10.1002/ctm2.1152
PY  - 2023///
SN  - 2001-1326
TI  - Faecal metabolite deficit, gut inflammation and diet in Parkinson’s disease: integrative analysis indicates inflammatory response syndrome
T2  - Clinical and Translational Medicine
UR  - http://dx.doi.org/10.1002/ctm2.1152
UR  - http://hdl.handle.net/10044/1/102187
VL  - 13
ER  -
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