There is no single obesity gene. The reach of genetics extends far beyond body size and encompasses numerous compounding factors including appetite control, addictive tendencies, efficiency of fat metabolism, and exercise responsiveness to name a few.
Genetics determines obesity susceptibility. However, seeing that a myriad of environmental factors can change the expression of our genes, obesity susceptibility can be manipulated by changing the environment.
An obesogenic environment is defined as the sum of external influences that promote obesity. However, the evolving study of nutrigenomics has offered incredible insights into environmental adaptations which can manipulate gene expression. Such adaptations are extremely individualised – disregarding any preconceived ‘one-size-fits-all’ approach to obesity management.
Decoding DNA
As Homo sapiens, we all carry the same DNA sequence, but -due to variations within the code at each gene location- we will have variable genetic susceptibilities. This variation of code is called our genotype. Identical twins carry the same genotype.
Whilst your genotype can be described as ‘what you inherit,’ your phenotype is the actual observable outcome or ‘what you look like’. The critical point of influence here is that the translation of genotype to phenotype can be affected by the environment.
In other words, susceptibility may only become an eventuality under specific environmental conditions. By manipulating external conditions, we can prevent the expression of certain genes and thereby manipulate our phenotype. Although identical twins will have the same genotype, they may have different phenotypes (physical traits) as a result of contrasting environmental influences.
Understanding your genotype can provide invaluable information to assist in impactful environmental change. To order a 3X4 Genetics Test and discover your unique genotype, click here.
When genotype + environment = phenotype
The following examples highlight the potential impact of the environment on various genes linked to obesity:
- FABP2: FATTY ACID BINDING PROTEIN 2
This gene decodes the rate of fat absorption from a meal. Certain genotypes are more susceptible to hypertriglyceridemia (increased circulating fat) and increased abdominal fat storage from high intakes of dietary fat, especially saturated fat. Therefore, changing the environment by limiting total - and saturated fat intake, would consequently disrupt the potential for fat storage, despite genetic risk.
- PPARG: PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR GAMMA
This gene influences the response potential of different genotypes to caloric restriction and diabetes risk. Although an energy-controlled diet and reduction of refined carbohydrates may be beneficial for everyone, for some genotypes these are essential requirements to mitigate obesity risk.
- ADRB2: BETA 2 ADRENERGIC RECEPTORS
These genes decode the genetic variability of waist-to-hip ratio, and variability in the ability to mobilise fat stores from exercise. Depending on the specific codes of genotype, it is possible to predict the inclination for rebound weight gain; ascertain meaningful exercise guidelines and distinguish whether the focus of weight loss should prioritise diet or physical activity.
- ADRB3: BETA 3 ADRENERGIC RECEPTOR
Depending on gene variation, a sedentary lifestyle may compound obesity risk. Some gene variants at this locus are also associated with reduced fat loss responsiveness to exercise; increased risk for abdominal obesity and a lower metabolic rate. However, this does not mean that exercise would be fruitless. On the contrary, it means that a much greater intensity of exercise would be required for certain genotypes to achieve weight loss.
- FTO: FAT MASS AND OBESITY ASSOCIATED GENE
This gene plays a role in regulating energy homeostasis by increasing appetite and decreasing metabolism. Certain genotypes have a reduced satiety threshold and inherent tendencies for overconsumption of high-fat foods. A high-fat diet and sedentary lifestyle would therefore precipitate obesity, whilst a low-fat diet and active lifestyle would mitigate genetic risk.
- MC4R: MELANOCORTIN – 4 RECEPTOR
Certain variants of this gene are associated with increased hunger and the tendency for overeating. Studies have suggested that adherence to an energy-restricted eating plan that includes small, regular meals (five meals per day) is likely to result in better weight loss outcomes than meal skipping- which has been suggested to exacerbate hunger, binge eating and BMI.
This gene plays a role in the behaviour patterns of eating that are linked to psychological reward. Some genotypes have weaker dopamine signalling mechanisms and are thereby less sensitive to reward stimuli. This often results in compensatory behaviours (such as binge eating) as a means to achieve psychological comfort.
Useful intervention strategies would include emotional eating counselling; mindfulness; the use of exercise-induced serotonin uptake and the implementation of non-food dopamine rewards.
The fact remains that some people will have to work harder than others to achieve weight loss and weight loss maintenance. However, decoding your DNA will allow you to work smarter, with a specific direction and a greater understanding of different obesity intervention strategies.