Glenn Gibson and colleagues at the Medical Research Council's Dunn Nutrition Centre in Cambridge believe it may be possible to alter the huge population of microbes growing in the large intestine so that disease-causing invaders cannot become established there.
One starting point for the research was the discovery that the mixture of bacteria in the intestines of breast-fed babies differs significantly from that of bottle-fed ones, and indeed adults. The main difference is that some 95 per cent of the intestinal flora of breast-fed babies consists of bifidobacteria (so called because their cells are often bifurcated - Y-shaped). The percentage is lower in babies given bottled milk. It also declines on weaning, and falls to some 25 per cent in the adult, when bacteria such as Escherichia coli predominate.
The full significance of bifidobacteria was not recognised, because unlike E coli they grow in the absence, rather than the presence, of oxygen. This meant that laboratory techniques for culturing bacteria from faeces tended to underestimate the numbers of bifidobacteria. Now, however, there are good reasons to believe that their presence contributes to the health advantages of breast as against bottle-feeding.
There are several possible reasons for this. Bifidobacteria produce lactic and acetic acid, which impair the growth of bacteria such as Clostridium perfringens, the agent of one type of food poisoning. They produce several vitamins and enzymes that play a role in digestion. And they are powerful stimulators of the body's immune defences.
Dr Gibson and his colleagues are now investigating the possibility of stimulating the growth of beneficial organisms such as bifidobacteria in the large intestine, so that they comprise a greater fraction of the population. By manipulating the microbial flora in this way, they believe they may be able to replicate the sort of health benefits observed in breast-fed babies. Their hopes are enhanced by reports that the bacterial community in the gut, which may be impoverished in patients receiving intensive antibiotic therapy, can be restored if they are given cultures of bifidobacteria to swallow.
The strategy being developed is to administer not the bacteria themselves but substances which, after passing unchanged through the stomach, arrive in the large intestine and stimulate the growth of bifidobacteria already there. Two of these substances are inulin and oligofructose, types of sugar that occur naturally in vegetables and other plants. Dr Gibson and his colleagues have used them in two sets of experiments. First, they prepared 'faecal slurries' from human volunteers and demonstrated that when they incubated these in the presence of inulin or oligofructose the bifidobacteria in the samples grew vigorously, while other bacteria, including those capable of causing disease, remained at low levels. Tests with pure cultures confirmed that bifidobacteria directly inhibited the growth of E coli and C perfringens.
Very recently, these results in laboratory glassware have been augmented by successful experiments in human volunteers. They were given a diet enriched firstly by ordinary sugar, followed by either inulin or oligofructose, and finally by sugar again. The experimenters monitored the bacteria in the volunteers' faeces. In each case, there was a marked shift in the bacterial flora, bifidobacteria becoming dominant during the period when the subjects were consuming the diet supplemented by inulin or oligofructose.
The lesson is clear. It is feasible, as Dr Gibson hoped, to alter the balance of bacteria in the human large intestine in such a way as to favour bifidobacteria, which are known to confer health benefits. This raises the possibility of adjusting the human diet by replacing ordinary sugar with inulin or oligofructose as a means of reducing, in the long term, the toll of intestinal infection. Inulin and oligofructose are safe and acceptable as sweeteners, though somewhat less sweet than ordinary sugar.
The upshot could, therefore, be a combination of health benefits conferred by an altered microbial population in the large intestine, and a simple means of avoiding the obesity, dental caries and other health hazards associated with over-consumption of sugar.