Does Junk Food increase the risk of Allergies and IBD?

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As discussed here on many occasions it is well recognised that developed countries are suffering from an epidemic rise in immunologic disorders, such as allergy-related diseases and certain auto-immunities. One of the proposed explanations and one that I feel most convinced about is the changing composition of our intestinal microflora and parasite burden. Our intestinal ecological changes  appear to be altering our ability to manage appropriate immunomodulatory responses to various ingested and inhaled antigens.

The Proceedings of The National Academy of Science Journal published a paper this June 2010 exploring the differences in the microbial communities between those children on a western style diet and those from a rural African community whose diet reflected that of a the early humans – high in fibre.[1]

Key Findings:

  • African children had increased levels of Bacteroides, and depletion in Firmicutes Bacteria, and a unique range of bacteria for fibre degradation absent in the EU children. They also had higher levels of short chain fatty acids. In particular, propionic and butyric acids are nearly four times more abundant in BF than in EU faecal samples
  • EU children had higher levels of shigella and Escherichia and fewer of the immune modulating and fibre degrading bacteria

Microbiologists and immunologists see the changing of the supply of our food from the Neolithic Revolution forward (approx 10,000 years ago) as a significant event in terms of bacterial transformation in our guts.[2] More recently, based on the germ theory and an almost zealous use of antibiotics and vaccines has produced a conflicting outcome. Infectious diseases have declined dramatically and acute emergency orientated infections have largely been controlled, but the emergence of allergy, autoimmune diseases and inflammatory bowel diseases have increased in the developed worlds.[3]

This study took 15 children aged between 1-6 living in Burkina Faso – where their diet is low in fat and animal protein and rich in starch, fibre, and plant polysaccharides, and is predominantly vegetarian. Children are breast-fed up to the age of 2 y as a complement to a mixed diet. Then ran a comparrison investigation against 14 EU children who were breast-fed for up to 1 y of age. They were eating a typical western diet high in animal protein, sugar, starch, and fat and low in fibre and this included ‘Junk Food’.

The diet of the African children consisted mainly of cereals, black-eyed peas and vegetables. The Italians, by contrast, ate higher quantities of meat, fat and sugar.

The authors suggest that the difference in fibre intake of around 8.4 g/d (EU -2-6yrs) vs 14.2 g/d (African 2-6 yrs) provides the explanation for the bacterial diversity, and that this combined with higher caloric intake from the EU diet leads to higher levels of obesity due to the changes in Firmicutes to Bacteroides ratio.[4]

So was Burkitt right?[5] This paper indicates that exposure to the large variety of environmental microbes associated with a high-fibre diet could increase the potentially beneficial bacterial genomes, enriching the microbiome. Reduction in microbial richness is possibly one of the undesirable effects of globalisation and of eating generic, nutrient-rich, uncontaminated foods. Both in the Western world and in developing countries diets rich in fat, protein, and sugar, together with reduced intake of unabsorbable fibres, are associated with a rapid increase in the incidence of non-infectious intestinal diseases.

The results suggest that diet has a dominant role over other possible variables such as ethnicity, sanitation, hygiene, geography, and climate, in shaping the gut microbiota.

The African experience of increased gut microbial diversity and reduced quantities of potentially pathogenic strains supports the “old friend” hypothesis, indicating a role of microbiota in protecting children from pathogens as well as from gastrointestinal diseases.[6]

Comments

We have much to learn yet about the mechanisms employed by our commensal bacterial species, but what we do know is that they are capable of significant effects both good and bad on human health. If we look at recent experimentation using bacterial translocation to treat IBD, the potential for extracting bacterial species from the commensals of the traditional fibre rich diets for probiotic therapy is very appealing.

In the meantime we know that fibre has a direct impact on inflammation as well as providing raw materials for bacterial growth, but we may yet have to work hard on providing adequate quantities of live bacteria to support a substantive bacterial relationship change in the damaged or healthy gut.

In terms of assisting the reduction in allergies, the bacterial inhabitants and their role was explored in a recent post.

References


[1] De Filippo C, Cavalieri D, Di Paola M, Ramazzotti M, Poullet JB, Massart S, Collini S, Pieraccini G, Lionetti P. Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa. Proc Natl Acad Sci U S A. 2010 Aug 2 View Full Paper

[2] Mira A, Pushker R, Rodríguez-Valera F (2006) The Neolithic revolution of bacterial genomes. Trends Microbiol 14:200–206. View Abstract

[3] Strachan DP (1989) Hay fever, hygiene, and household size. BMJ 299:1259–1260. View Full Paper

[4] Ley RE, Turnbaugh PJ, Klein S, Gordon JI (2006) Microbial ecology: Human gut microbes associated with obesity. Nature 444:1022–1023. View Abstract

[5] Burkitt DP (1973) Epidemiology of large bowel disease: The role of fibre. Proc Nutr Soc 32:145–149. View Ref

[6] Rook GAW, Brunet LR (2005) Microbes, immunoregulation, and the gut. Gut 54: 317–320. View Abstract

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