Monday 13 July 2015

Sugar


 

 

It is now widely agreed that consumption of sugar in substantial quantities is a major cause of obesity and a major threat to public health.  This is not a finding which I accept fully.  However, it is a more complicated statement than is usually appreciated.  The great majority of the carbohydrate that we eat is starch which is the major constituent of potatoes and wheat. We absorb this as glucose, the monosaccharide sugar formed from starch when it is digested in the intestinal tract.  Why therefore is eating sugar – a disaccharide made up of glucose and fructose – so much more harmful as a cause of obesity than eating starch?  I can think of three reasons which are not mutually exclusive but which do give rise to the possibility of addressing the problem in different ways.

 

The first is that it is the fructose which does the damage.  At first sight this seems slightly unlikely since fructose is less well absorbed than glucose but it is a possible explanation and corn syrup, which contains high levels of fructose, is regarded as particularly prone to give rise to obesity.  One way of seeing whether fructose is particularly harmful would be to feed people with a polyfructose polysaccharide analogous to starch.  This is Inulin which is the main polysaccharide in Jerusalem artichokes.  Few people eat these as a major component of their diet and the well known complication of eating them is that much of the fructose is fermented by gut bacteria and this gives rise to the production of excessive amounts of flatus.  However, it would be interesting to know in experimental situations whether feeding Inulin causes obesity.  If fructose were to be found to be one of the reasons why sugar is harmful, this could be resolved by eliminating it from the sugar component of the diet by going over to glucose.  This could presumably be done by genetic modification of sugar cane and sugar beet or otherwise by removing the fructose by fractionation and using it to generate alcohol as a car fuel and using the glucose only as food.  There are already glucose only sugary drinks on the market, for example Lucozade, so this is not an impractical solution.

 

The second possibility is concerned with the rate of absorption and that it is the rapid rise of glucose levels in the circulation which stimulates insulin production and interferes with the insulin signalling pathways and that this produces obesity.  This is entirely plausible.  If that were the case, then forms of sugar that are rapidly absorbed should be more harmful than those which are more slowly absorbed.  This would be consistent with the idea that fizzy sugary drinks are particularly harmful since they are very rapidly absorbed and would support the contention that these should perhaps be banned.  On the other hand, sugar in chocolate or in cakes that are more slowly digested and absorbed would be relatively less harmful and there is some suggestive evidence that this may be the case. It should be possible to modify the preparation of cakes and chocolate in ways to make the sugars even more slowly absorbed, perhaps by associating the sugar with other molecules that are slowly absorbed. 

 

The third possibility is that the harmful effect of sugar results from its property as an appetite stimulant.  If that is a major factor, it may well be that the sugar substitutes such as aspartame which industry now puts into some fizzy drinks and other foods, may similarly stimulate appetite and may not be particularly effective in reducing this aspect of sugar’s activity. One might then have to persuade people to eschew things that taste sweet as well as, or rather than, things that contain sugar. 

 

Having answers on the relative importance of these three mechanisms might enable more logical and effective campaigns to be put in place to reduce the effects of sugar on obesity.  HH

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