In the obesogenic environment that we live in, not everyone
becomes obese. To the high priests of nutrition, that variability is put down
to variation in self-control and self-discipline and that in turn relates to
level of education and social class. The idea that this variation might be
genetically based is dismissed with the old reliable falsism that since our
genes have not changed during the recent epidemic of obesity, it’s the
environment that counts. Well, yet another twin study shows that this is
nonsense and this twin study is somewhat special since it pooled data from 23
twin cohorts from four countries: Denmark, Australia, Canada and Sweden
involving just over 24,000 children[1].
Moreover, this pooling study was able to provide data on twins from birth
through 19 years of age. By comparing variation within and between both
identical and non-identical twins, it is possible to distinguish the effect of
genes from the effect of the environment and the latter can be split into common
and unique environments. At birth, only 8% of variation in weight or body mass
index (BMI) could be explained by genetic factors. By 5 months this had
increased to 65% and rose into the 70% decile up to 9 years of age. In the
early teens the genetic variation had reached into to 80% decile and by late
teens it had hit 90%. As children got
older, the environmental explanation of obesity had fallen from 74% at birth,
to 25% at 6 years and down to about 10% in late teens. While this study clearly
shows the powerful effect of genetic factors on obesity, it does raise the
question as to why this genetic dimension increased with age. Clearly, the
genetic make up remained constant so most likely, changes in gene expression
were the contributory factor. Growth in childhood and especially in adolescence
is associated with significant biological adjustments, which could create the
environment for altered gene expression.
One of the reasons which I personally think public health
nutritionists are wary of the genetic influence on obesity is that the subject
is strongly orientated toward basic biology, effectively, the digestion,
absorption, transport, distribution and utilisation of calories from fat,
carbohydrate, protein and alcohol. However, genetic influences on behaviour are
to my mind far more important than the
genetics of basic biological elements. A recent twin study has looked at the
heritability of taste[2]. Subjects were given a strawberry jelly with
or without the hot spice capsaicin derived from chili peppers. They were also
asked questions on their liking or otherwise of spicy foods and spices and of
foods that have mild, strong and extremely strong pungency properties. 50% of
the variation in preference for spicy foods and spices and 58% of the variation
in “pleasantness of strong pungency” was explained by genetic factors. Another
twin study looked at food neophobia in a group of children aged 8 to 11 years,
comprising 5,390 pairs of identical and non-identical twins[3]. Parents were asked about their children’s
attitude to foods with four statements: “My child is constantly sampling new
and different foods”, “My child doesn’t trust new foods,” “My child is afraid
to eat things/he has never had before.” and “If my child doesn’t know what’s in
a food s/he won’t try it.” A food neophobia score was worked out and the highly
robust finding of the study was that a staggering 78% of variation in food
neophobia was genetic in origin. Only 22% was learned from the environment.
These studies show that the genetic component of obesity need not be related to
the biochemistry of energy metabolism, but rather to more complex behavioural
traits such as food choice.
Twin studies of obesity always raise the question of
assortative mating, that is fat partners mating with other fat partners and
similarly for slim partners. Assortative mating has been shown to occur in
personality type, education, religion, politics, age, smoking habits and
anti-social behaviour. Researchers at the Rowett Institute in Aberdeen used
DEXA scans to accurately measure body fat levels in 42 couples[4].
Strong evidence for assortative mating in relation to body fat was found. For
example, subjects with disproportionately large arms assortatively mated with
like partners. Given the high heritability of the propensity to develop obesity,
assortative mating will accelerate the incidence of obesity sine the children
of such parents are likely to inherit genetic patterns from both parents.
The high priests of public health nutrition may dislike the
implications of a genetic dimension to obesity but they are being increasingly
isolated from the scientific truth.
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