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  • What is Nutrigenetics and what are its benefits?

What is Nutrigenetics and what are its benefits?

Dr. David DiesNovember 4, 2022November 6, 2022

This scientific discipline is revolutionizing the way we understand and intervene in our health.

What is nutrigenetics? In a more academic way, we could say that it is a discipline of nutritional genomics, specifically the part that is responsible for studying how genetic variants influence the effect of nutrients on our health.So that we understand each other, nutrigenetics observes how, depending on the genetics of each one of us, we can be recommended to encourage or reduce the consumption of different foods , to control, reduce and/or avoid different pathologies, see overweight/obesity, hypertension , vitamin deficiency, etc. [1-2], offers the possibility of personalizing the diet based on individual genetics, and this is really interesting because, as we well know from popular wisdom, not all of us get fat the same way, we all have that friend who he eats “what he wants” and does not gain weight.

Going back to the beginning, it is also interesting to define nutritional genomics, this is a branch of science that studies how genes and nutrients interact in general. It also includes nutrigenomics (not to be confused) (figure 1)[3], another discipline within nutritional genomics that investigates how the different nutrients contained in food can cause us to express some genes or others, for example, the role of polyunsaturated fatty acids in the expression of genes related to thermogenesis and obesity [4].

Table of Contents

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  • How does Nutrigenetics work?
  • What are these small differences between individuals?
  • Does it conflict with population or community nutrition?
      • Bibliographic references

How does Nutrigenetics work?

How does it work? To understand it, perhaps we should establish some previous concepts of genetics, such as the genotype and phenotype of a person. Well, the genotype is the set of genes that define us and our individual variations, our genetic pantry, in this sense our genotype may have, for example, the appropriate genes to have an ideal weight, or perhaps have the most obesogenic variants (they cause obesity ).

On the other hand, the phenotype is what in the end is shown to the outside, in the case of obesity, being thin or overweight, and no, this phenotype is not 100% determined by the genotype, it greatly influences the environment ( culture, diet, habits and lifestyles, sports, even pollution, etc.), if you lead a life far from healthy habits, balanced diets and of course appropriate to those genes , no matter how many “healthy” genes are have, in the end they will develop overweight, obesity, diabetes and perhaps other associated pathologies.

Let’s not be discouraged, one should never give up on the purpose of reaching your ideal weight because your genetic inheritance is prone to developing obesity, you can always modulate a high percentage through diet , and in general healthy and personalized habits, and that This is what this discipline teaches us, nutrigenetics [5].

What are these small differences between individuals?

These small differences also known as polymorphisms , SNP or snip, are small variations in the DNA (molecular mutations) with which nutrigenetics mainly works, the change of a nitrogenous base in the DNA causes that in the end you and I do not metabolize the In the same way, polyunsaturated fatty acids, or we do not absorb certain vitamins in the same way, or we do not appreciate some flavors in the same way [6-8]. Another characteristic is that this variation must be present in at least 1% of the population, this less frequent variant will be known as “mutant” and the most common variant as the wild variant.

Metaphorically speaking, our genome is the book of our life, the genes are the words that form it, and the nitrogenous bases are the 4 letters (molecules) with which these words are written (A, T, G and C), like this Well, if between two people where one person has A, another person had C, that word no longer says the same thing, “where I said I say, I say Diego”. Let us say, for example, that this protein, which would have the function of correctly transporting HDL cholesterol and improving the “good/bad” cholesterol profile, after an intake of monounsaturated fatty acid [9], will no longer be doing it correctly, or perhaps it is doing just otherwise, increase its levels, so the correct and personalized dietary recommendation for the person who has C will in no case be the same as the one with the letter A.

There are some flagrant cases in which a disease is determined by the mutation of a single gene, for example; phenylketonuria, galactosemia, some intolerances and familial cholesterolemia, among others [10]. These cases are the least frequent, the most common are usually multifactorial diseases, in which numerous genes (and their variants) are involved in addition to the environment and other external factors, as is the case of obesity without going any further, as already we had commented

With a bit of perspective, a large part of the current nutritional recommendations were based on population, epidemiological, analytical and observational studies such as case/control or cohort studies, which are easy to introduce bias (error), and draw conclusions from the results very heterogeneous.

Usually the individuals that escape the normal behavior of the population (which are the most interesting) are considered deviations from the mean that can be assumed by the statistical model used, or they are simply within the normality of a somewhat heterogeneous response, but it has gone Observing over time that, in many cases, individual polymorphisms could explain a large percentage of these variations, thus, as shown in the example in Figure 2, if we wanted to minimize the appearance of a particular disease, the individual AA and AG (orange and blue) we would recommend encouraging the consumption of nutrient X, but we would not recommend it to individual GG (green), in order to keep their risks in the lower part of the graph for all of them.Classical nutrition would recommend everyone an intermediate consumption for the “general” population.

These same conclusions were reached in a study (figure 3) [11], in which a group of 74 people after administering 2.5 milligrams a day of an omega-3 (EPA, eicosapentaenoic fatty acid) for 6 weeks , very heterogeneous results were observed, explained in part by inter-individual genetics. Chronic consumption of omega 3 was not beneficial to all individuals in the study in terms of lowering “bad” cholesterol levels.

Does it conflict with population or community nutrition?

Not at all, as we have commented, it is true that a large part of the recommendations and health claims that we all hear on TV, or the radio, in the written press (promoting olive oil, polyunsaturated fats, fiber, reducing saturated fats, less salt, etc) are based on observations of the population, with a scientific basis without a doubt, but generalist after all, all of them are true and important, but they do not have to be personalized to each one of us.

Even so, community nutrition has in fact one of the greatest challenges in public health in recent decades, correcting the pandemic of this century, obesity. This objective is reached without a doubt, with general advice based on science, with nutritional education from an early age, with self-control in the media, with legislation in accordance with the health objectives that we want to achieve in the medium and long term, and with a lot of work and effort on the part of all the parties involved, research centers, private companies, governments, etc.

Without conflicting with the above, in clinical and personalized nutrition, the future is already the use of this nutrigenetic tool, and many other tools and technologies , such as epigenetics , precision nutrition, omics techniques, artificial intelligence, and more. that they will arrive

Personalized nutrition at Meyo® makes use of this knowledge with a simple saliva sample (because each person’s DNA is the same in all its cells), analyzes the numerous variants of genes of interest (FTO, MC4R, etc.) with a genetic predisposition to obesity and/or related diseases. With this information and artificial intelligence and machine learning techniques that are used precisely in mobile applications, it allows defining more personalized dietary, sports and lifestyle guidelines to achieve specific objectives, for each specific person.

To conclude, with a reflection, would we buy an electronic device without knowing its characteristics, the manufacturer, price, guarantees, etc…? Or maybe if all my neighbors have found it useful, yes? Then why do we eat without knowing the “technical characteristics” of our genetics? Or without knowing if it will be beneficial to me in particular?

  • Download Meyo now for Android and for iOs .

Bibliographic references

  • [1] Franzago M, Santurbano D, Vitacolonna E, Stuppia L. Genes and Diet in the Prevention of Chronic Diseases in Future Generations. Int J Mol Sci. 2020;21(7):2633. Published 2020 Apr 10. doi:10.3390/ijms21072633
  • [2] Ordovas, J.M., Corella, D. Genetic variation and lipid metabolism: Modulation by dietary factors. Curr Cardiol Rep 7, 480–486 (2005). https://doi.org/10.1007/s11886-005-0067-6
  • [3] Adela Emily Gomez Ayala. Nutrigenomics and nutrigenetics. Offarm Vol. 26. Num. 4. pages 78-85 (April 2007)
  • [4] Palou A, Bonet ML, Picó C, Rodríguez AM. Nutrigenomics and obesity. Rev Med Univ Navarra. 2004;48:36-48
  • [5] Arkadianos I, Valdes AM, Marinos E, Florou A, Gill RD, Grimaldi KA. Improved weight management using genetic information to personalize a calorie controlled diet. Nutr J. 2007;6:29. Published 2007 Oct 18. doi:10.1186/1475-2891-6-29
  • [6] Piroddi M, Albini A, Fabiani R, et al. Nutrigenomics of extra-virgin olive oil: A review. Biofactors. 2017;43(1):17‐41. doi:10.1002/biof.1318
  • [7] Galmés S, Serra F, Palou A. Vitamin E Metabolic Effects and Genetic Variants: A Challenge for Precision Nutrition in Obesity and Associated Disturbances. Nutrients. 2018;10(12):1919. Published 2018 Dec 4. https://doi.org/doi:10.3390/nu10121919
  • [8] Vesnina A, Prosekov A, Kozlova O, Atuchin V. Genes and Eating Preferences, Their Roles in Personalized Nutrition. Genes (Basel). 2020;11(4):E357. Published 2020 Mar 27. doi:10.3390/genes11040357
  • [9] de Luis Román DA, Izaola Jáuregui O, Primo D, Aller R. Influence of the rs670 variant of the APOA1 gene on serum HDL response to a hypocaloric diet enriched with polyunsaturated fats versus one enriched with monounsaturated fats [Influence of rs670 variant of APOA1 gene on serum HDL response to an enriched-polyunsaturated vs. an enriched-monounsaturated fat hypocaloric diet]. Nutr Hosp. 2019;36(6):1288‐1295. doi:10.20960/nh.02390
  • [10] Scriver CR, Waters PJ. Monogenic traits are not simple: lessons from phenylketonuria. Trends Genet. 1999;15(7):267‐272. doi:10.1016/s0168-9525(99)01761-8
  • [11] Lovegrove JA, Rachel Gitau. Nutrigenetics and CVD: What does the future hold? Proceedings of The Nutrition Society 67(2):206-13 · June 2008.
Dr. David Dies
Dr. David Dies
Website |  + postsBio

To the classic question “what do you do?” I always answer “basically I am a psychologist”. In fact, my academic training has revolved around the psychology of development, education and community, a field of study influenced my volunteer activities, as well as my first work experiences in personal services.

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