Nutrigenetics is defined as the science that studies the effect that our genes have on the response to various dietary components. Therefore, a nutrigenetic study will allow us to adapt the food we eat to our needs.
The fundamental hypotheses on which the science of nutrigenetics is based are the following:
❖ The health effects of nutrients depend on inherited genetic variants that alter the absorption and metabolism of nutrients and, therefore, the activity of biochemical reactions.
❖ Better health outcomes can be achieved if nutritional requirements are personalized for each individual considering their genetic characteristics, both inherited and acquired, throughout their different life stages, dietary preferences and health status.1
This science should not be confused with nutrigenomics, which analyzes the direct influence of nutrients on gene expression and health. You can learn more about the difference between nutrigenetics and nutrigenomics in our blog.
Food problems and their associated pathologies on a global level
Intensive animal husbandry, crop manipulation and food processing have altered the qualitative and quantitative balance of nutrients in the food consumed by Western society. This change, to which human physiology and biochemistry are not currently adapted, is believed to be responsible for the chronic diseases that are rampant in industrialized western countries.2
On the other hand, in most developing countries, agricultural production and food processing practices, as well as Western dietary habits and lifestyles, are promoted without considering the health implications. As a result, there is an upward trend in the incidence of obesity, type 2 diabetes, hypertension, cardiovascular disease and dental caries.3
In recent decades, a nutritional transition has resulted in a global shift away from the consumption of minimally processed foods and towards ultra-processed alternatives, away from home-prepared dishes and towards ready-to-eat meals and snacks. The same period has seen a rapid increase in the global prevalence of obesity in children and adults.4
The importance of nutrigenetic testing
In a world characterized by an overwhelming increase in the prevalence of obesity and associated metabolic disorders and cardiovascular disease, personalized nutrition represents a promising approach to both the prevention and treatment of these diseases. However, in order to assess the nutritional needs of each individual, it is recommendable to carry out a prior nutrigenetic study.
From a nutrigenetic perspective, there are many factors to be considered when designing personalized and unbiased nutritional solutions for individuals or population subgroups. Also, a joint effort between nutritionists, scientists, clinicians, and health professionals is needed to establish a comprehensive framework to enable the application of these new findings at the population level.5
Nutrigenetics and its role in obesity.
The increasing quest for individualization and optimization of consumer goods, as well as a willingness to pay a premium price, suggests that the market may be ready to embrace personalized nutrition to prevent, manage or treat specific diseases.
Obesity is one of many diseases with great potential for improved prevention using nutrigenetic testing. It is estimated that 40-70% of the variation in susceptibility to obesity observed in the population is due to interindividual genetic differences.
Arkadianos et al.6 developed a personalized calorie-controlled diet using 24 variants in 19 genes involved in metabolism for a weight reduction program. These authors6 compared weight loss and weight maintenance in 50 individuals who received genotype-tailored dietary and exercise advice to optimize nutrient intake during weight loss and 43 control individuals who received only generic diet and exercise advice. The results of the study showed that individuals who received personalized dietary advice not only performed better during the weight loss period, but also in weight loss stabilization over the following year.
The FTO gene is an example of a gene in which certain polymorphisms have been linked to an increased predisposition to develop obesity. This FTO-obesity association has been observed in populations of diverse ancestry and across the life course, with the greatest effect observed in young adulthood.7
Nutrigenetics in cancer control and treatment.
Many lifestyle-related factors affect the development of cancer through oxidative stress that occurs because of damage induced by reactive oxygen and nitrogen species (RONS), which produce potentially mutagenic DNA damage.8 Cellular oxidative stress is a process that occurs in our cells due to an excess of free radicals and a lack of antioxidants to counteract them. The increase of these oxygen and nitrogen free radicals in our body results in our cells becoming oxidized, affecting their functions and damaging them.
An example of an everyday habit with a potent pro-oxidant capacity is smoking. Inhaled tobacco smoke is considered a potent exogenous prooxidant, as high concentrations of RONS are present in both their tar and gas phases. The direct increase in oxidative burden from inhaled tobacco smoke can be further increased through secondary oxidative stress due to inflammation. However, there are nutrients with high antioxidant power that have been shown to play a significant role in cancer prevention. These include vitamin C, vitamin E and vitamin B2.8
In this context, nutrigenetic testing becomes a helping tool in cancer prevention. An example of this is seen in people who possess a certain variant in the SLC23A1 gene. A study carried out by Timpson et al9 showed that people with this variant had lower circulating levels of vitamin C. This population not only had lower circulating levels of vitamin C, but also lower levels of vitamin C in the blood, a higher risk of developing cancer and other chronic complex diseases, such as arteriosclerosis or type 2 diabetes.
Nutrigenetics in the prevention and control of cardiovascular diseases.
Throughout the last century, research established that lifestyle, including diet, greatly affects the risk of cardiovascular disease (CVD). For this reason, dietary recommendations have been the focus of public health campaigns aimed at reducing CVD risk. Despite this effort, the expected reduction in CVD mortality does not occur consistently, and this failure has been attributed, at least in part, to individual variability in response to dietary recommendations and different genetics, or possibly to bidirectional interactions between the two factors.10
Altered lipid metabolism and inflammation, both strongly associated with dietary patterns, are key factors in the development of atherosclerosis. In fact, many of the identified genetic variants associated with CVD are directly or indirectly involved in the regulation of these two central pathways.
Particularly relevant, both in terms of lipid profile regulation and reduction of inflammation, is the intake of polyunsaturated fatty acids or PUFA, such as omega-6 and omega-3. Intake of these PUFA has been associated with decreased risk of CVD. In addition, omega-3 fatty acids have been widely shown to exert cardioprotective effects by lowering triglyceride levels.10
An important example of a genetic variant associated with reduced fatty acid processing and thus an increased predisposition to the development of CVD is in the FADS gene. Numerous large-scale studies have shown that certain polymorphisms in the FADS gene cause carriers to have lower omega-6 and omega-3 levels. 11
The future of nutrigenetics and implications for nutritional recommendations and dietary practice
The role that this science plays in investigating the effects of nutrition on health is becoming increasingly evident, as is the importance of conducting nutrigenetic studies. It is not only naïve, but also probably dangerous, to assume that all individuals will respond identically to the foods they consume.
The development of a personalized approach to nutrition for disease prevention and treatment will require a much more complete understanding of nutrient-gene interactions and their impact on phenotype in order to identify, evaluate, and prioritize appropriately targeted dietary intervention strategies.
While the challenges associated with unraveling the nutrigenetics-disease interrelationship will not be easy, the implications for public health are enormous.1
24Genetics and its nutrigenetics study
At 24Genetics, thanks to our DNA diet test and the report with your results, you will be able to know your genetic predisposition to correctly metabolize various dietary components, to have higher or lower levels of different nutrients, to respond positively or negatively to certain diets, and your sensitivity to certain flavors.
1. Fenech, M. et al. Nutrigenetics and Nutrigenomics: Viewpoints on the Current Status and Applications in Nutrition Research and Practice. Lifestyle Genomics 4, 69–89 (2011).
2. de Araújo, T. P. et al. Ultra-Processed Food Availability and Noncommunicable Diseases: A Systematic Review. Int. J. Environ. Res. Public. Health 18, 7382 (2021).
3. Popkin, B. M., Adair, L. S. & Ng, S. W. Global nutrition transition and the pandemic of obesity in developing countries. Nutr. Rev. 70, 3–21 (2012).
4. Dicken, S. J. & Batterham, R. L. The Role of Diet Quality in Mediating the Association between Ultra-Processed Food Intake, Obesity and Health-Related Outcomes: A Review of Prospective Cohort Studies. Nutrients 14, 23 (2021).
5. de Toro-Martín, J., Arsenault, B., Després, J.-P. & Vohl, M.-C. Precision Nutrition: A Review of Personalized Nutritional Approaches for the Prevention and Management of Metabolic Syndrome. Nutrients 9, 913 (2017).
6. Arkadianos, I. et al. Improved weight management using genetic information to personalize a calorie controlled diet. Nutr. J. 6, 29 (2007).
7. Loos, R. J. F. & Yeo, G. S. H. The bigger picture of FTO—the first GWAS-identified obesity gene. Nat. Rev. Endocrinol. 10, 51–61 (2014).
8. Goodman, M., Bostick, R. M., Kucuk, O. & Jones, D. P. Clinical trials of antioxidants as cancer prevention agents: Past, present, and future. Free Radic. Biol. Med. 51, 1068–1084 (2011).
9. Timpson, N. J. et al. Genetic variation at the SLC23A1 locus is associated with circulating concentrations of l-ascorbic acid (vitamin C): evidence from 5 independent studies with >15,000 participants. Am. J. Clin. Nutr. 92, 375–382 (2010).
10. Barrea, L. et al. Nutrigenetics—personalized nutrition in obesity and cardiovascular diseases. Int. J. Obes. Suppl. 10, 1–13 (2020).
11. Guan, W. et al. Genome-Wide Association Study of Plasma N6 Polyunsaturated Fatty Acids Within the Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium. Circ. Cardiovasc. Genet. 7, 321–331 (2014).