A Swedish team of scientists led by Dr. Karl Mårild, recently reported a link between taking antibiotics and the development of celiac disease[i]. Note: You can download the entire article free.
Celiac disease is an autoimmune reaction to gluten proteins contained in wheat, rye and barley. The disease process causes inflammation and villus atrophy (which means the little hair-like projections in the small intestine that allow us to absorb nutrients become flattened and loose function). People who express the certain proteins (HLA-DQ2 or –DQ8) on the surface of their white blood cells are genetically predisposed to the disease. The condition affects approximately one percent of the population and is linked to numerous other autoimmune diseases, neurological disorders, cancers, anemia, osteoporosis, itchy dermatitis, digestive damage and digestive malabsorption.
In my book, Fast Tract Digestion IBS, I talk about the connection between celiac disease, IBS and SIBO. People with celiac disease more often diagnosed with IBS[ii] or SIBO.[iii],[iv] The question is why? What do these conditions have in common that could explain this connection? In both each case the small intestine becomes inflamed, the absorptive surface of the small intestine is damaged and foods, especially carbohydrates, are poorly digested leading to bacterial overgrowth. Like celiac disease, antibiotics can also increase the risk developing IBS.
What happens to the digestive tract and gut microbiome when people take antibiotics certainly deserves much more attention. Antibiotics dramatically change the gut microbiome by killing off many healthy bacteria. This puts people at increased risk for C diff infection, SIBO and IBS. Leaning more about the role of antibiotics in changing the gut microbiome may lead to a better overall understanding of the cause of celiac disease, SIBO and IBS leading to better treatments.
We know that gluten-free diets don’t correct the problem in approximately one third of cealics. Are there other aspects of this condition that we need to understand to help these individuals? I wouldn’t be surprised if fermentable carbs such as resistant starch and fiber – not limited in gluten free diets – is part of the answer. But avoiding antibiotics when they are not absolutely needed should be standard practice to maintain our diverse gut microbiome providing more protection against celiac, IBS and other SIBO-related conditions.
BMC Gastroenterol. 2013 Jul 8;13:109. doi: 10.1186/1471-230X-13-109.
Antibiotic exposure and the development of coeliac disease: a nationwide case-control study.
Abstract
BACKGROUND:
Theintestinal microbiota has been proposed to play a pathogenic role in
coeliac disease (CD). Although antibiotics are common environmental
factors with a profound impact on intestinal microbiota, data on
antibiotic use as a risk factor for subsequent CD development are
scarce.
METHODS:
In this population-based case-controlstudy we linked nationwide histopathology data on 2,933 individuals with
CD (Marsh stage 3; villous atrophy) to the Swedish Prescribed Drug
Register to examine the association between use of systemic antibiotics
and subsequent CD. We also examined the association between antibiotic
use in 2,118 individuals with inflammation (Marsh 1-2) and in 620
individuals with normal mucosa (Marsh 0) but positive CD serology. All
individuals undergoing biopsy were matched for age and sex with 28,262
controls from the population.
RESULTS:
Antibiotic use wasassociated with CD (Odds ratio [OR] = 1.40; 95% confidence interval
[CI] = 1.27-1.53), inflammation (OR = 1.90; 95% CI = 1.72-2.10) and
normal mucosa with positive CD serology (OR = 1.58; 95% CI = 1.30-1.92).
ORs for prior antibiotic use in CD were similar when we excluded
antibiotic use in the last year (OR = 1.30; 95% CI = 1.08-1.56) or
restricted to individuals without comorbidity (OR = 1.30; 95% CI = 1.16 -
1.46).
CONCLUSIONS:
The positive association betweenantibiotic use and subsequent CD but also with lesions that may
represent early CD suggests that intestinal dysbiosis may play a role in
the pathogenesis of CD. However, non-causal explanations for this
positive association cannot be excluded.
