New research has demonstrated that both apple pectin and polyphenol-rich apple juice components actually enhance biological mechanisms that produce anticarcinogenic compounds during the fermentation process.
Using human fecal matter as the test substance, German researchers Dr. Dieter Schrenk, M.D. and his colleagues hypothesized that the compound butyrate could be increased in the presence of apple pectin and apple juice extracts.
Butyrate has been suggested to be a chemopreventative metabolite that might prevent the occurrence of colorectal cancer, which is very common in Western industrialized countries. It is a short chain fatty acid which is seen as a major factor contributing to healthy colon mucosa. The research notes, Butyrate not only serves as a major nutrient for the colon epithelia but is also thought to play an important role in the protective effect of natural fiber against colorectal cancer.
So how do apple pectin and apple juice extracts play a role in increasing amounts of butyrate? The laboratory tests performed by Schrenk found that by the increased production of butyrate via the addition of apple components, histone deacetlyases (HDAC) were inhibited. With slowed production of HDAC, there would be significantly less growth of precancerous and tumor cells.
The research, published in the April 2008 issue of Nutrition, notes, apples are a major source of natural fiber and of low molecular weight plan polyphenols in the Western diet. The researchers conclude, Pectin-rich apple products can thus be expected to exert anticarginogenic effects in the colon.
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Dr Stockinger explains: The AhR system can potentially react to an astounding range of factors, from environmental pollutants to particular foods or even hormone levels. So here we have identified a molecular mechanism that shows how such a wide range of environmental factors could be directly linked to the cells that cause autoimmune reactions.''In comparison, mice that lack AhR still develop Th17 cells and T helper cell responses but they don't have enhanced numbers of these cells. This suggests that AhR interaction with environmental factors leads to an increase in the number of Th17 cells and may contribute to the onset or development of autoimmune diseases in genetically susceptible individuals. In addition, the research showed that stimulation of AhR resulted in faster development of autoimmunity with greater severity. This means that environmental factors are interacting with genetic factors to generate a detrimental autoimmune reaction.
Dr Stockinger concludes: The discovery that the stimulation of AhR by environmental pollutants can accelerate the development of autoimmune reactions and the severity of symptoms raises intriguing possibilities and warrants closer examination of a possible role of AhR in human autoimmune diseases."
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