By Gabi Giacomin
You can’t believe how fascinating it is when you get your child’s stool results back and there is a bacteria you’ve never heard of showing high levels – Bacteroides Dorei. According to research from Mexico (2015) a gut which is dominated by Bacteroides produces more acetate, propionate and succinate which lead to mucin breakdown, gut permeability and development of autoimmunity. The two species which drive the increase in Bacteroides are B. Dorei and B. Vulgatus, predictors of Type 1 Diabetes (T1D).
A quick search on google suggests that Bacteroides Dorei has been found in the microbiome of children who develop Type 1 Diabetes, an autoimmune condition commonly found in children.
Levels of beneficial butyrate forming bacteria – Roseburia, and Ruminococcus were by contrast low in my daughters report, almost non-existent, wiped out from antibiotics given at birth.
Butyrate protects us against developing T1D and is also found to be low in the microbiome of children who develop this. Low levels of butyrate forming bacteria are also thought to be a cause of Sleep Apnea linked to hypertension. My daughter was diagnosed with Pulmonary Hypertension postnatally and has had Apnea since birth.
The study goes on to reveal that fat and protein intake from cow’s milk products further increase the development of T1D. Gluten is also mentioned as a cause of increased gut permeability which leads to autoimmunity and T1D.
Breasfeeding is encouraged to increase the diversity of lactic acid bacteria necessary for gut health. And avoidance of baby formula which encourages growth of pathogenic species such as Staphylococcus aureus, Clostridium difficile, Bacteroides spp.
In conclusion I’m relieved to say that despite my daughters initial exposure to antibiotics at birth which I believe has initiated an Autoimmune/ Sleep Apnea/ Hypertension/ T1D type profile we are having success with treatment.
Intuitively we have avoided gluten, dairy, and sugar since birth and she was breastfed for 3 years. Coincidentally, I was diagnosed with gestational diabetes during my pregnancy which could be a driving factor.
Specific substrates like Beta Glucans and Bitter Melon inhibit the expression of B. Dorei and my daughters body composition has improved since taking these. I am taking these as well as I have moderate levels of B. Dorei in my gut microbiome.
We are now starting a butyrate supplement as well as using foods to enhance the production of Roseburia and Ruminococcus butyrate forming species species.
I’m hopeful we have found the root cause of my daughters health issues and holistic treatment means she will avoid developing T1D in the future.
“The gut microbiota could be the link between environmental factors and the development of autoimmunity and T1D. This has led to the proposal of a possible intestinal origin of T1D [9], and has placed the microbiota as the central factor for its study.
T1D development involves genetic and environmental factors, such as birth delivery mode, use of antibiotics, and diet. Gut microbiota could be the link between environmental factors, the development of autoimmunity, and T1D. In this review, we will focus on the dietary factor and its relationship with the gut microbiota in the complex process involved in autoimmunity and T1D.
In addition to genetics, other factors such as birth delivery mode, diet, infections, and the use of antibiotics have been associated with T1D development [7].
In Finnish children from the Diabetes Prediction and Prevention (DIPP) study [33] and in Americans from the Diabetes Autoimmunity Study in the Young (DAISY) study [34], it has been found that fat intake from bovine milk products as well as proteins from fresh milk presented an increase in the risk of advanced β-cell autoimmunity and subsequent progression to T1D.
Breastfeeding increases the diversity of lactic acid bacteria, while infant formulas contribute to the acquisition of bacterial communities such as Staphylococcus aureus, Clostridium difficile, Bacteroides spp., and other pathogenic communities.
The effects of gluten on intestinal homeostasis are multiple. Gluten increases gut permeability, affecting the tight junctions, which is well described in celiac disease patients and recently in T1D.
Among them, the experiment by Brugman et al. [40], performed in Bio-Breeding diabetes prone (BB-DP) rats, proved that antibiotic treatment had an effect on the incidence of diabetes, and that the differences in gut bacterial composition were detectable before the rats developed disease. In another work by Wen et al. [8], the interaction between intestinal microbiota and the innate immune system was recognized as an epigenetic factor which can modify predisposition to T1D.
An interesting finding of Davis-Richardson et al. [47] was the identification of two specific species causing the increase in gut abundance of Bacteroides: B. dorei and B. vulgatus, with B. dorei significantly increased before seroconversion.
This suggests that the high fat diet may be maintaining the Bacteroides levels, limiting the full recovery of the microbiotal balance.
In contrast, when microorganisms such as Bacteroides and Veillonella are harbored in abundance, this substrate follows the pathway to succinate, acetate, and propionate. These products compromise mucin synthesis and increase paracellular permeability by altering the tight junctions [50].
Butyrate has been associated with the expression of cathelicidin-related antimicrobial peptide (CRAMP) in the β-cells of NOD mice. This peptide has been shown to protect against the development of T1D by inducing a regulatory response and suppressing the inflammatory process in the pancreatic islets of prediabetic mice [55].
Thus, decreased production of butyrate in children with low levels of Prevotella in their gut microbiota could be contributing to T1D development.”

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