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.
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