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Toddlers’ food fussiness is heavily influenced by genes

By rmjlad3, on 14 October 2016

Written by Andrea Smith, Alison Fildes and Clare Llewellyn

In early childhood, children are gradually introduced to an increasingly varied diet. While some children happily accept new foods and enjoy eating lots of different kinds of foods, many are hesitant. Food avoidant behaviour can be broadly classified into two traits: ‘Food Fussiness’ and ‘Food Neophobia’. Food Fussiness is the tendency to be highly selective about the textures, taste and smell of foods you are willing to eat and is often seen as a consequence of inadequate parenting. However, Food Neophobia – the refusal to try new foods – is often seen as a normal development stage experienced by most young children regardless of the way their parents feed them. Fussy and neophobic eating behaviours typically emerge in toddlerhood and commonly peak between two and six years of age; but for some children these traits persist into later childhood.

Food avoidant behaviour can be both frustrating and worrying for parents; children who eat only a restricted range of foods might miss out on key dietary nutrients essential for healthy development. In particular, fussy eaters tend to reject nutrient-dense foods such as vegetables. Early childhood is also an important period during which food preferences develop; learning to like a range of healthy foods requires the child to try a wide variety of different foods. Researchers have therefore been interested in finding out what shapes food avoidant behaviour in early life. Some research has suggested that children who are breastfed for longer and whose parents use less persuasive feeding practices (e.g. rewarding with food) are less likely to display fussy eating behaviours; suggesting that there are important environmental shapers of this behaviour. On the other hand, Food Neophobia is associated with temperamental traits such as shyness or inhibition; these characteristics have an established genetic influence, indicating that neophobia might also have a strong genetic basis.

In a new study published in the Journal of Child Psychology and Psychiatry we used data from the Gemini twin cohort to investigate the extent to which genes and environmental factors influence children’s food fussiness and food neophobia. Gemini is a large study of 2400 pairs of twins that was set up in 2007 to explore early life growth and behaviour. Twin studies are useful for investigating the relative importance of genetic- and environmental factors on individual differences in traits such as food avoidant behaviours. The current study was based on data from 1,932 families collected when the twins where 16 months old.

We found that both food fussiness and food neophobia have a strong genetic basis, with 46% and 58% of the variation in each trait explained by genetic influences respectively. The shared home environment (which includes factors such as parental feeding practices) was a more important influence on Food Fussiness than Food Neophobia; but overall, these environmental factors were less important than a child’s genetic predisposition towards these behaviours.

The finding that there is substantial genetic influence on fussy eating behaviour in early childhood might be quite a relief for some parents who can often feel judged or guilty about their children’s fussy eating. Understanding that these traits are largely innate might help to deflect this blame.

However, our genes are not our destiny. Establishing the importance of genetic influences on fussy eating behaviours in early childhood does not imply that these behaviours cannot be changed. An effective intervention to overcome food rejection is through repeated exposure to the problem food; the more a child tries a food, the more familiar it becomes and the more they learn to like it. In our group we have developed a tasting game called ‘Tiny Tastes’ to help families introduce foods to reluctant and fussy eaters. This is an avenue through which parents might be able to positively change fussy or neophobic eating behaviours.

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Food fussiness and food neophobia share a common etiology in early childhood

Andrea D. Smith, Moritz Herle, Alison Fildes, Lucy Cooke, Silje Steinsbekk, and Clare H. Llewellyn

Article link: http://onlinelibrary.wiley.com/doi/10.1111/jcpp.12647/epdf

Tell me about your family and I can tell you about your weight?

By Susanne F Meisel, on 4 October 2011

Mentioning genetics in the context of weight is like treading into a minefield; those who are brave enough to approach the topic need to don their hard hats and be prepared to take hits by followers in the ‘eat-less-and-move-more’ camp. Accusations of laziness, lack of willpower, making excuses and just looking for an easy way out are common responses to the genetic argument of obesity.

However, to ignore genetics when talking about obesity is somewhat confusing when considering how keen people are to attribute skinniness to ‘good genes’, ‘fast metabolism’, and ‘being naturally active’. Nobody seems to notice that skinniness and fatness are two sides of the same coin.

As so often in life, the truth lies somewhere in between. While behaviour is certainly not to be ignored when searching for the root cause of the obesity epidemic, neither should the heritability of body weight. Two recent studies from our research group add evidence to the idea that the predisposition to thinness, as well as to overweight, is transmitted across generations. Researchers used data from the Health Survey for England, which included a large sample of families with children aged 2-15 years to see whether thin children were more likely to have thin parents. Of the thousands of families included in the first study, it was shown that thin children were almost twice as likely to have 2 thin parents.  Furthermore, as parents’ weight decreased, children likewise got progressively lighter.

But, what about the reverse side of the coin – parental weight of children who were overweight? Here, exactly the same pattern was found, but it was even more apparent. Children, who had 2 obese or severely obese parents, were approximately 12 times more likely to be overweight and again the likelihood of obesity gradually decreased with decreased parental body weight. In both studies, findings were unrelated to other factors such as age, sex, social status or ethnicity. Interestingly, the mothers’ weight seemed to be more predictive of a child’s than the father’s, but only among those children that were overweight. For thin children, mothers’ and fathers’ genes appeared to contribute equally to being thin.

Two things are important here. Firstly, weight is governed in part by genetic factors; but, and this is the second important conclusion to take away, there are environmental factors involved that influence a child’s weight – otherwise all children would have had parents that fully resembled their weight status. Influences seem to come especially from the mother’s side, which may be, because the foetus receives nutrients from the maternal diet in the womb and after birth when the infant is breast-fed. In addition, maternal environmental influences may be stronger because the mother is usually in charge of food preparation.

Unfortunately, dietary records of participants were not available, so it was not possible to investigate how diets between underweight and overweight children and their parents differed.

Genes do not always act in the same way; their activity is influenced by the environment. This flexibility allowed our species to adapt well to changing environmental conditions, which made it possible to survive and evolve.  Variation is the key. And this is why it is easier for some than for others to (not) have their cake and eat it, too.

 

References:

Whitaker KL, Jarvis MJ, Boniface D, Wardle J. Inter-generational transmission of thinness. Archives of Pediatrics and Adolescent Medicine. http://archpedi.ama-assn.org/cgi/content/full/165/10/900

Whitaker KL, Jarvis, MJ, Beeken RJ, Boniface D, Wardle J. Comparing maternal and paternal intergenerational transmission of obesity risk in a large population-based sample. American Journal of Clinical Nutrition. 91, 2010, 1560-1567. http://asn-cdn-remembers.s3.amazonaws.com/f8ee4cfad55bd34900cff3371b9a146d.pdf