The Truth Behind Genes And Bodyweight

The Truth Behind Genes And Bodyweight

We know by now that we need to eat the right foods, need to work out, and do stuff that is healthy for us. Because maintaining good health does not happen by accident, it requires work and smart lifestyle choices. But sometimes when we wake up at 6 am to hit the gym before work or shunning the donuts in breakfast, it’s easy to lose sight of for what are we doing all these. So here are some top articles choices that can keep you motivated to lead a healthy lifestyle and keep diseases at bay.

The Truth Behind Genes And Bodyweight

, The Truth Behind Genes And BodyweightWhen I ask (as I frequently do) a group students to rate on a scale of one to ten their view on how much of weight is genetic and how much is behaviour (where one is entirely behaviour and ten is entirely genetic) the consensus among the group normally settles for around four.  A combination of genes and lifestyle 60/40 in favour of lifestyle.  This of course is the big question: What is the actual contribution of each?

Geneticists have recently updated the human obesity gene map and they have documented 14 single gene mutations in seven genes, which, together with other markers have been associated or linked with human obesity [1]. According to Timothy Frayling at the University of Exeter, people who carried a variant gene known as FTO faced a 30 percent higher risk of obesity if they had one copy of the variant; 60 percent if they had two [2]However, readers may recall the recent series of “Embarrassing Fat Bodies” where they asked Frayling’s lab to test for fat-promoting genes, and the results showed one very overweight family did not have the FTO gene whilst the lean researcher conducting the study did!

It has also been proposed that children with two obese parents have an approximate 80% risk of becoming obese compared to only 20% in children with two lean parents [3].  Critically though, the unanswered question of how much of this is genetic and how much is behavioural is not yet resolved to any satisfactory conclusion [4].

Bouchard and colleagues [5] propose that about 40% of the variance in energy management may be explained by inherited characteristics.  In addition, significant similarities in levels of physical activity (PA) has been reported in twin studies [6]. Other studies have suggested that response to dieting is also heritable. When identical twins share identical diets there is great variance in changes in body weight between pairs of twins, but within each pair, weight loss is comparable [7, 8].

Nonetheless, whilst genes clearly have influence over weight, they are far from certain to determine our fat mass and no single gene is responsible for the current pandemic of obesity.  Each obesity gene makes only a small contribution but collectively the action may be substantial [9]. Currently far too little is known about how genes interact with environmental forces to determine an absolute effect. In humans it has been difficult to separate genetic and environmental factors and assign the relative contribution of each to the development of obesity and therefore much is still guesswork [10].

For this reason, animal models are often used though clearly this is less satisfactory and caution should be applied when interpreting data from animal studies. For instance, in genetically modified mice (bred to be lean or fat) some have failed to display the expected phenotype, or have even been obese when leanness was expected [11].

Looking at the other side of the equation (lifestyle, behaviour and environment) several studies have shown genes to be far less influential than our lifestyle choices.  These studies mainly looked at identical twins whose weight was significantly different and asked each to compare their own eating and activity patterns with their twin.  The lean twins consistently reported that their obese twin siblings ate more food overall, consumed less healthy foods and exercised less. The obese twins however suggested that they behaved in a similar way to their lean twins.  But data from the scientific study controls proved the overweight twins had eaten significantly more (760kcal ± 262kcal/day) and undertaken significantly less PA (429kcal ± 200kcals/day) [12]. Therefore the differences in these cases were entirely behavioural.

One thing that is often overlooked in the genes debate is the influence of genes on behaviour.  Most studies and scientific enquiries into the genetic impact on weight tend to examine the physiological determinants of genes on the way the body manages energy.  However genes will influence whether you are going to be a highly motivated individual, diligent and hard-working, or whether you are likely to be a de-motivated, disengaged and disinterested layabout.

Genes are also likely to influence your preference for certain foods and to some degree your relationship with physical activity and strenuous exercise, and how you perceive each.  Consider the impact then that each of these character profiles may have on weight and it may well be that the behavioural impact of genes far outweighs the physiological effects (if indeed these do exist).

On balance then, it appears that my students are correct.  Genes do influence weight and this is fairly certain.  However the strength of association (by how much) is far less certain and at this moment in time, behaviour and lifestyle choices appear significantly more influential. I think my students have it about right at 60/40 in favour of lifestyle.

Alan Jackson is the founder of Discovery Learning and Weight Management centre which are educational establishments offering courses for fitness, gym instructors and personal trainers.  Alan is also a leading weight management and obesity tutor and lecturer in the UK.


1.     Speliotes, E.K., et al., Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index. Nat Genet, 2010. 42(11). 937-948.

2.     Freathy, R.M., et al., Common Variation in the FTO Gene Alters Diabetes-Related Metabolic Traits to the Extent Expected Given Its Effect on BMI. Diabetes, 2008. 57(5). 1419-1426.

3.     Thirlby, R.C. and J. Randall, A genetic “obesity risk index” for patients with morbid obesity. Obes Surg, 2002. 12(1). 25-9.

4.     Anderssen, N., B. Wold, and T. Torsheim, Are parental health habits transmitted to their children? An eight year longitudinal study of physical activity in adolescents and their parents. Journal of Adolescence, 2006. 29(4). 513-524.

5.     Bouchard, C., et al., The response to long-term overfeeding in identical twins. New England Journal of Medicine, 1990. 322(21). 1477-1482.

6.     Samaras, K., et al., Genetic and Environmental Influences on Total-Body and Central Abdominal Fat: The Effect of Physical Activity in Female Twins. Annuals of Internal Medicine, 1999. 130(11). 873-882.

7.    Bouchard, C., et al., The response to exercise with constant energy intake in identical twins. Obes Res, 1994. 2. 400-410.

8.    Hainer, V., et al., Intrapair resemblance in very low calorie diet-induced weight loss in female obese identical twins. Int J Obes Relat Metab Disord, 2000. 24. 1051-1057.

9.    Lyon, H.N. and J.N. Hirschhorn, Genetics of Common Forms of Obesity: A Brief Overview. American Journal of Clinical Nutrition, 2005. 82(1). 215S-17S.

10.   Farooqi, I.S. and S. O’Rahilly, Genetic factors in human obesity. Obesity Reviews, 2007. 8(s1). 37-40.

11.   Arch, J.R.S., Lessons in obesity from transgenic animals. Journal of Endocrinological Investigation. Vol., 2002. 25(10). 867-875.

12.   Pietilainen, K.H., et al., Inaccuracies in food and physical activity diaries of obese subjects: complementary evidence from doubly labeled water and co-twin assessments. Int J Obes, 2010. 34(3). 437-445.

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