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Tuesday, December 11, 2012

Obesity and Nature v Nurture re-visited

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.

[1] Dubois et al (2012) PLoS ONE 7, e30153
[2] Tornwall et al (2012) Physiology & Behaviour, 107, 381-389
[3] Cooke et al (2007) Am J Clin Nutr 86, 428-433
[4] Speakman et al(2007) Am J Clin Nutr 86, 316-323

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