The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress-Driven Mucus Depletion and Exacerbates Intestinal Inflammation.
Federica Laudisi, Davide Di Fusco, Vincenzo Dinallo, Carmine Stolfi, Antonio Di Grazia, Irene Marafini, Alfredo Colantoni, Angela Ortenzi, Claudia Alteri, Francesca Guerrieri, Maria Mavilio, Francesca Ceccherini-Silberstein, Massimo Federici, Thomas Thornton MacDonald, Ivan Monteleone
May 2019Synopsis of Social media discussions
The discussions reflect a high level of agreement on the harmful effects of maltodextrin, with users advocating for bans and switching to natural alternatives, as seen in messages like 'Can we get Maltodextrin banned?' and references to replacing ingredients with FOS. The tone combines concern and urgency, emphasizing both scientific details and practical implications, contributing to a sense of impact and engagement.
Agreement
Strong agreementMost postings strongly endorse the findings, emphasizing that maltodextrin negatively affects gut health and should be reconsidered or banned.
Interest
Moderate level of interestDiscussions show moderate interest, with some users expressing concern and calling for action, though not all are deeply engaged with the science.
Engagement
High engagementMany discussions reference specific mechanisms like ER stress and mucus depletion, indicating a desire to understand and deliberate on the implications.
Impact
High level of impactThe posts suggest the research could have significant influence on consumer choices and policy debates, especially regarding food additive regulation.
Social Mentions
YouTube
3 Videos
3 Posts
11 Posts
Blogs
2 Articles
News
3 Articles
Metrics
Video Views
2,939
Total Likes
94
Extended Reach
30,560
Social Features
22
Timeline: Posts about article
Top Social Media Posts
Posts referencing the article
Impact of Dietary Maltodextrin on Gut Bacteria and Crohn's Disease Risk
This video explores how the common food additive maltodextrin influences gut bacteria, particularly adherent invasive E. coli, potentially contributing to Crohn's disease development by enhancing bacterial adhesion and biofilm formation.
Potential Risks of Maltodextrin in Gut Health and Disease Development
Maltodextrin is a caloric sweetener which may provoke inflammatory intestinal diseases and can contribute to weight gain and obesity. Recent research indicates it enhances the adhesion and biofilm formation of bacteria associated with Crohn's disease, potentially worsening condition.
The Dangers of Maltodextrin in Food Products and Health Risks
Today we discuss a carbohydrate more dangerous than sugar, maltodextrin. It can lead to abdominal fat, diabetes, and intestinal inflammation. Found in many processed foods, this additive promotes bacterial adhesion linked to Crohn's disease development.
-
Food additives chronically messing with Ur gut. I avoid this in supplements/powders. https://t.co/2m3mxeCE7Z https://t.co/DpThy5oHkb
view full postJuly 25, 2025
1
-
Type4_Nickel_Sensitivity
@type4_nickel (Twitter)@TeamTrump @RobertKennedyJr Can we get Maltodextrin banned? https://t.co/wmyjkUygfR
view full postDecember 24, 2024
-
Type4_Nickel_Sensitivity
@type4_nickel (Twitter)@solarayvitamins Your Baby Me Now Bifidobacterium longum powder contains maltodextrin, which causes gut inflammation https://t.co/wmyjkUygfR Please go back to FOS. I'm pretty sure that's what you guys wete using 10 years ago.
view full postDecember 24, 2024
-
BANT
@BANTonline (Twitter)@thelowcarb_rd @MaritKolby https://t.co/dKDsXvgH9J
view full postApril 10, 2024
2
-
DrDawnSherling
@dharrissherling (Twitter)@england_cy @KevinH_PhD Laudisi F, Di Fusco D, Dinallo V, et al. The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress-Driven Mucus Depletion and Exacerbates Intestinal Inflammation. Cell Mol Gastroenterol Hepatol. 2019;7(2):457-473. doi: 10.1016/j.jcmgh.2018.09.002. Epub 2018 Sep 11.
view full postSeptember 8, 2023
-
Joe B
@JBianco215 (Twitter)https://t.co/UsZdeNXHeH Food additive Maltodextrin increases Endoplasmic Reticulum stress in gut epithelial cells with the downstream effect of reducing mucus production and enhancing colitis susceptibility.
view full postJanuary 22, 2023
1
-
Jerome Craig, CHPC, CFMP, DC
@CHPCJeromeCraig (Twitter)The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress-Driven Mucus Depletion and Exacerbates Intestinal Inflammation. https://t.co/TSV4HIwZCb
view full postFebruary 26, 2020
-
Dr. Suzana Mantovani
@Tweet_Nutrition (Twitter)The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress–Driven Mucus Depletion and Exacerbates Intestinal Inflammation https://t.co/7pNwLBG30W
view full postMarch 4, 2019
-
Mucus papers
@mucuspapers (Twitter)Pubmed: The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress-Driven Mucus Depletion and Exacerbates Intestinal Inflammation. https://t.co/n0vpMUvb9y
view full postFebruary 16, 2019
-
Steven M. Weil
@smweilhermes (Twitter)The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress–Driven Mucus Depletion and Exacerbates Intestinal Inflammation https://t.co/68PRuvFMpq
view full postFebruary 16, 2019
1
-
Symbiosis papers
@Symbiosispapers (Twitter)The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress-Driven Mucus Depletion and Exacerbates Intestinal Inflammation. https://t.co/FDYB24yr9c
view full postFebruary 16, 2019
Abstract Synopsis
- Maltodextrin (MDX), a common food additive, worsens intestinal inflammation by causing stress in the cells’ endoplasmic reticulum, leading to a decrease in protective mucus and increased gut inflammation in mice.
- The study found that MDX triggers ER stress by activating specific cellular pathways (like inositol requiring protein 1 and p38 MAP kinase), which results in less mucin2, a key mucus protein, without significantly changing gut microbiota.
- Using an ER stress inhibitor (TUDCA) in mice reduced mucus depletion and inflammation, suggesting that MDX’s harmful effects are linked to ER stress pathways in gut cells, making it a potential target to lessen diet-related intestinal issues.]
✨Reina Nakamoto✨
@mindstatex (Twitter)