Lab animals fed a diet containing either broccoli or blueberries displayed significant decrease in gut levels of E. coli and other bacterial strains associated with IBD, according to findings published in Nutrition.
Researchers from the New Zealand Institute for Plant and Food Research indicate that their results deserve “further investigation through clinical studies to establish whether the consumption of blueberries and/or broccoli is able to alter the composition and metabolism of large intestine microbiota and promote colon health in humans”.
Bowel disease
Chronic inflammatory bowel disease (IBD) is a multi factorial disease with an unknown cause.
The prevalence of IBD rapidly increased in Europe and North America in the second half of the twentieth century, and is becoming more common in the rest of the world as countries adopt a Western lifestyle.
“Currently, there is insufficient literature to propose an association between diet and IBD; polyphenols and dietary polysaccharides in fruit and vegetables can be effective in promoting [gastrointestinal] health benefits,” explained the New Zealand-based researchers.
“Dietary blueberries and/or broccoli altered cecal microbiota composition and metabolism, and colon morphology. Future studies are necessary to unravel the underlying mechanisms by which broccoli, and to a lesser extent blueberries, were beneficial to intestinal inflammation.”
Study details
For their new study, the researchers used a strain of mice that is susceptible to intestinal damage and can therefore act as an animal model of IBD. Animals were fed a control diet, or diets supplemented with 10% blueberry or broccoli for 21 weeks.
Results showed a significant reduction in inflammation of the colon in the broccoli-fed mice, and a trend towards lower inflammation in the blueberry-fed animals, compared with the control mice.
In addition, the intestinal microbiota of the animals fed broccoli or blueberries was different from the control animals, with similar results for both broccoli and blueberry groups except for Faecalibacterium prausnitzii, which were much less in the broccoli group.
Both supplemented groups displayed significant reductions in C. perfringens and Enterococcus spp., said the researchers, but the link between these bugs and reducing inflammation in the intestine “needs further investigation”.
Interestingly, E. coli was significantly reduced in both groups, with the greatest reductions observed in the broccoli group.
“The influence of these diets (blueberry and broccoli) n lowering E. coli may be beneficial to the host,” wrote the researchers.
The blueberry- and broccoli-fed animals showed no change in levels of Bifidobacterium spp. and a decrease in levels of Lactobacillus spp. While both species are often considered beneficial to the host, a decrease in Lactobacillus spp. in IBD may be positive, argued the researchers.
“The decrease in lactic acid concentration can be considered beneficial to the host during intestinal inflammation due to the role of lactic acid as a favored cosubstrate for sulfate-reducing bacteria, which release hydrogen sulfide known to be toxic for intestinal epithelial cells,” said the researchers.
Blueberries and gut health
This is not the first time that blueberries have been linked to changes in gut health. A human study performed in Italy revealed that a daily drink of juice containing wild blueberry powder may boost the levels of beneficial bifidobacteria in the gut (Journal of Agricultural and Food Chemistry, doi: 10.1021/jf2028686).
In a addition, a 2009 study by scientists from Massey University in New Zealand and the University of Illinois in Urbana concluded that blueberry extracts “could modify the bacterial profile by increasing the numbers of beneficial bacteria and thereby improving gut health”.
Source: Nutrition
Published online ahead of print, doi:
“Influence of dietary blueberry and broccoli on cecal microbiota activity and colon morphology in mdr1a(-/-) mice, a model of inflammatory bowel diseases”
Authors: G. Paturi, T. Mandimika, C.A. Butts, S. Zhu, N.C. Roy, W.C. McNabb, J. Ansell