If you are obese, can you blame it on your genes?

If you are obese, can you blame it on your genes?

Last Updated on April 19, 2017 by Joseph Gut – thasso

February 13, 2017 – If you are obese (or plain out fat), can you blame it on your genes? Actually, in very many cases, the answer is a qualified yes. Or a maybe. Under certain circumstances. Researchers are moving towards a better understanding of some of the roots of obesity.

In fact, a research team at the Mc-Gill University has recently discovered that for girls who are carriers of a particular gene variant (DRD4 VNTR with 7 repeats), the crucial element that influences a child’s fat intake is not the gene variant itself. Instead, it is the interplay between the gene and girls’ early socio-economic environment that may determine whether they have increased fat intake OR healthier than average eating compared to their peers from the same socio-economic background. The DRD4 repeat 7 is found in approximately 20 per cent of the population and is known to be associated with obesity, especially in women.

“We found that among girls raised in poorer families, those with DRD4 repeat 7 had a higher fat intake than other girls without DRD4 repeat 7 from the same socio-economic background,” stated Laurette Dubé, the lead researcher on the study and Scientific Director of the McGill Centre for the Convergence of Health and Economics. “But we also found that girls with exactly the same DRD4 repeat 7 gene variant who came from wealthier families, compared to those with the same socio-economic conditions, had a lower fat intake. This suggests that it’s not the gene or its variant solely acting by itself, but rather how the gene makes an individual more sensitive to environmental conditions that determines “for better or worse” a child’s preference for fat and consequent obesity as the years pass by”.

How the research was done.

The researchers used food diaries kept by the parents of close to 200 young Canadian children (average age of four) from the MAVAN birth cohort in Montreal, Quebec and Hamilton, Ontario. They calculated the percentages of fat, protein and carbohydrates the children were taking in. They also measured the body mass index (BMI) of the children, and used saliva tests to identify which of the children were carriers of the DRD4 repeat 7 gene. They then used the family income as a way of measuring the quality of the socio-economic environment in which the children were being raised, and an indirect marker of the food environment as well (availability of fruits and vegetables or fast food in the neighborhood, for instance).

Certain gene variants make some people more susceptible to their environment. 

The research, which was published in JAMA Pediatrics in 2016, builds on work by others which suggests that certain genes or their allelic variants, including DRD4 7 repeat, function as “plasticity genes“. This means that those with these gene variants may be more “open” to their environment, in general, than those without them, meaning that, depending on the environment in which the individual with the gene or its variant lives can either increase OR decrease the risk for certain neurobehavioral conditions.

Because carriers of the DRD4 repeat 7 were already reported to have an increased risk of obesity, the researchers wondered whether this variant of DRD4 was, instead of a strict risk allele for obesity, a plasticity gene, whose effects would vary depending on environment.

Thus, the researchers wondered if the higher fat intake already reported previously in girls with the DRD4 repeat 7 allelic variant could be modified by the social environment. In fact, it can, as the fat intake will increase or decrease in girls with the DRD4 repeat 7 allelic variant according to their socio-economic status, said Dr. Patricia Silveira, based in the Faculty of Medicine at the Universidade Federal do Rio Grande do Sul in Brazil, the first author on the study done in collaboration with McGill, University of Toronto and McMaster University. According to Dr. Silveira’s statement, this is important because the focus from the gene, previously “blamed” for the risk for increased fat preference is shifted to the environment in which you find the gene (or its variant in question), since the effects of the DRD4 gene (0r better perhaps its DRD4 repeat 7 variant) will vary according to the environmental conditions in which a child is raised.

Boys at the same age don’t show the same clear pattern of food preferences.

Interestingly, the researchers found this effect to be true only in the girls that they tested. They speculate that this may be because, from an evolutionary standpoint, it may have been more important for girls to be able to gain weight easily to adapt to adverse conditions in order to reproduce. Another possibility they advance is that at age four, it may simply be too early to see these effects in boys since boys and girls gain weight at different stages at this age, and may also have different behavioural responses to hunger and feelings of satiety.

These results underscore the importance of moving beyond a ‘one-size-fits-all’ approach to childhood obesity prevention, said Dubé, the lead author of this study. It seems that a  move towards targeted approaches that focus on populations that are particularly vulnerable to both genetic and environmental factors is needed; those who are biologically more vulnerable under adverse environments are those likely to be more responsive to improvements in their conditions.

Further reading in this context: A brain reward gene influences food choices in the first years of life

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Ph.D.; Professor in Pharmacology and Toxicology. Senior expert in theragenomic and personalized medicine and individualized drug safety. Senior expert in pharmaco- and toxicogenetics. Senior expert in human safety of drugs, chemicals, environmental pollutants, and dietary ingredients.