Fiber and Probiotics as a possible way to control inflammatory responses

Hi All, I just heard the following on an Australian news site (a well respected news site and the research published in Nature). It talks about the possible benefits of a high fiber diet and probiotics in helping reduce inflammatory response like asthma and auto-immune diseases. It is just early research, but I thought people may find it interesting.

(http://www.abc.net.au/am/content/2009/s2727183.htm)

TONY EASTLEY: Eating fibre is already thought to reduce the risk of heart disease and some cancers. Now Australian researchers have found a new benefit.

The scientists from the Garvan Institute have found fibre boosts the immune system, keeping a lid on inflammatory diseases such as asthma and type 1 diabetes that has become so prevalent.

Professor Charles Mackay is the lead author of the paper which has been published in the journal Nature. Professor Mackay is speaking here with AM's Barbara Miller.

CHARLES MACKAY: The important finding is that we provide a direct link between what we eat and the breakdown of this food in the gut by micro-organisms and immune responses, particularly inflammatory responses like asthma and auto-immune diseases.

BARBARA MILLER: And the key is fibre, is that right?

CHARLES MACKAY: Yes, fibre. We can't digest fibre ourselves but our bacteria can and the products of this metabolism in the gastrointestinal tract are substances called short-chain fatty acids. And these directly stimulate immune cells and keep a lid on inflammatory responses like asthma and type 1 diabetes and colitis and so forth.

And so what we believe is that our changes in diet in Western countries have led to this increase in inflammatory diseases.

BARBARA MILLER: Wasn't that known already that changes in diet are impacting on these diseases?

CHARLES MACKAY: Yes, there was very strong evidence. It was certainly the main suspect.

But what was really lacking were the molecular explanations for what is it in diets, what particular food stuff and what molecular mechanism could explain these changes.

We don't claim to have the final answer but at least we now have a candidate that might explain it and for which we can do future studies.

BARBARA MILLER: If we wanted therefore to decrease the prevalence of these diseases, would it be as simple as saying we need to eat more fibre?

CHARLES MACKAY: It could be. I think these are the sort of things that we need to study.

I personally believe that fibre is the likely cause and I think these sorts of studies are going to need careful clinical trials to ascertain whether it is fibre.

BARBARA MILLER: What else could it be?

CHARLES MACKAY: Well I mean other candidates that have been suggested is that types of saturated fats that have changed over the years in Western societies. There are vitamins that have been suggested. So it could be any number of things.

BARBARA MILLER: You did your research on mice. Is it reasonable to assume that the results can be transferred to humans?

CHARLES MACKAY: I think it's reasonable. It's not an absolute given, but it's reasonable that we'll see the same effects in other animals and in humans.

What is also important is the makeup of the bacteria in our gastrointestinal tract. And so I think this is one of the claims of the probiotic industry - that there are good healthy bacteria that promote good immune function.

And so our results could explain the beneficial effects of probiotics.

BARBARA MILLER: Your results would seem to back up the claims by the manufactures of probiotic yoghurts and drinks?

CHARLES MACKAY: I wouldn't want to endorse an industry without any evidence but at least it provides a molecular explanation why good bacteria might be providing an immune benefit.

BARBARA MILLER: Have you changed the way you're eating since getting your results?

CHARLES MACKAY: Yes, I've tried, but it's very difficult with all this tempting food out there to be good.

TONY EASTLEY: So true. Professor Charles Mackay who's now at Monash University, speaking to Barbara Miller.

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