Nutrigenomics

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Not to be confused with Nutrigenetics.

Nutrigenomics is a branch of nutritional genomics and is the study of the effects of foods and food constituents on gene expression.[1] It is a field of research focusing on identifying and understanding molecular-level interaction between nutrients and other dietary bioactives with the genome.[2] Nutrigenomics studies the influence of genetic variation on nutrition by correlating gene expression or SNPs with a nutrient's absorption, metabolism, elimination or biological effects. The field aims to enhance rational means to optimize nutrition with respect to an individual's genotype.

By determining the mechanism of the effects of nutrients or the effects of a nutritional regime, nutrigenomics tries to define the causality or relationship between these specific nutrients and specific nutrient regimes (diets) on human health. Nutrigenomics has been associated with the idea of personalized nutrition based on genotype. While there is hope that nutrigenomics will ultimately enable such personalised dietary advice, it is a science still in its infancy and its contribution to public health over the next decade is thought to be major.[citation needed] Whilst nutrigenomics is aimed at developing an understanding of how the whole body responds to a food via systems biology, research into the effect of a single gene/single food compound relationships is known as nutrigenetics.[3]

Definitions

Nutrigenomics is an emerging field of research that expands upon the existing field of nutritional science using genomic data.[citation needed] Certain advances in the field such as microarrays, and high throughput sequencing allow for expansive analysis of the genome and in-vivo experiments in knockout mice are major sources of genomic based data.[citation needed] This type of genomic data collection can be applied to view the effects that certain nutrients or foods may have on large portions or different locales of the genome rather than one specific location.[4]

Nutrigenomics is also defined as a field that examines "effect of nutrients on genome, proteome, metabolome and explains the relationship between these specific nutrients and nutrient-regimes on human health".[5] In other words, a nutrigenomics approach is a holistic one that examines the effect of nutrients at all levels, from gene expression to metabolic pathways.[5]

Background and preventive health

Nutritional science originally emerged as a field that studied individuals lacking certain nutrients and the subsequent effects,[5] such as the disease scurvy which results from a lack of vitamin C. As other diseases closely related to diet (but not deficiency), such as obesity, became more prevalent, nutritional science expanded to cover these topics as well.[5]  Nutritional research typically focuses on preventative measure, trying to identify what nutrients or foods will raise or lower risks of diseases and damage to the human body.

Nutrigenomics emerged as a possible way to fix gaps in the current field of nutritional science. The development of technology to analyze the genome such as different types of sequencing and different microarrays suggest a new way to reinforce current theories or hypotheses. Existing information from genetic research directs emerging research in nutrigenomics. Individuals within the same population or even the same family have genetic variability.[4] There is a lack of consistent relationships between certain foods and nutrients and increased disease risk, most likely due to this type of variation.[6]  Nutrigenomics is highly personalized because it looks at biomarkers within each individual.[6] One group of researchers suggest that current technology can be used to build an ideal diet/intake of certain nutrients, or a 'nutriome.'[7] A 'nutriome' would ensure proper function of all pathways involved in genome maintenance.[7]

Research has already provided evidence identifying potential genetic origins of metabolic disorders or compromised phenotypes.[4] Disorders that scientists previously thought to be heritable, can be identified as genetic disorders with set pathological effects.[4] For example, Prader-Willi syndrome, a disease whose most distinguishing factor is insatiable appetite, has been specifically linked to an epigenetic pattern in which the paternal copy in the chromosomal region is erroneously deleted, and the maternal loci is inactivated by over methylation.[8] Yet, although certain disorders may be linked to certain single nucleotide polymorphisms (SNPs) or other localized patterns, variation within a population may yield many more polymorphisms.[9] Each may have a negligible effect by itself, yet the cumulative effects may be significant.Now, with advances that have been made, these small changes and additive effects are possible to study.[9]  Small epigenetic changes such as methylation patterns or phosphorylation can be determined.

Rationale and aims

Cell signaling is an important component of regulation of gene expression and metabolism, relying on both internal and external signals to ensure the body is maintaining homeostasis. Individual nutrients can each be considered signals, with the summation of their effects being the diet.[4] The effort of nutrigenomics is to identify this "dietary signature", or pattern of effects ranging from effects at the cellular level to entire body systems.[4] However it is often hard to monitor the diet of an individual, and current protocols should be improved.[10] The desired outcome from this type of research is to identify genetic factors for chronic diseases and conditions, whether it be a certain gene itself or an epigenetic marker, and how foods influence it. Nutrigenomics looks mainly to be a way of identifying individuals predisposed for conditions and preventing onset.[4]  First, genes with regulation influenced must be identified, and then more focused studies may emerge.[4]

In addition, nutrigenomics also looks to identify certain compounds that are bioactive, and other foods that are of particular benefit to health.[4] This knowledge can be personalized to produce specific diet plans and functional foods to both prevent predisposed conditions and maximize health.[4]

Application

Anti-aging

Aging of cells occur because of the accumulation of excess free radicals formed due to the lack of proper nutrition to the cells and external factors like UV rays, pollution, stress, food, etc. DNA analysis is instrumental in identifying the right concoction of nutrients needed to eliminate the excess free radicals present in the cell.

The science of nutrigenomics studies the interaction between dietary components of food and genes.[11] Scientific advances have now made it possible to apply nutrigenomics in the field of anti ageing and customize nutritional solutions in the form of supplements to meet the optimal nutrition required by the body to prevent aging of cells by the formation of excess free radicals.[12][13]

Obesity

Obesity is one of the most widely studied topics in nutrigenomics. Due to genetic variations among individuals, each person could respond to diet differently. By exploring the interaction between dietary pattern and genetic factors, nutrigenomics aim to suggest prevention measures and/ or treatment to obesity via personal nutrition.[14]

There are studies suggesting genetic factors account for a fair proportion of inter-individual BMI (body mass index).[14] Among different types of genetic variation between humans, SNPs are suggested to be the most important marker for the study of nutrigenomics.[14]

Multiple studies have found association between SNPs and obesity. One of the most well known obesity associating gene is the FTO gene. Among studied individuals, it was found that those with AA genotype showed a higher BMI compared those with TT genotype when having high fat or low carbohydrate dietary intake.[14][15]

The APO B SNP rs512535 is another obesity related variation. It was found that the A/G heterozygous genotype was found to have association with obesity (in terms of BMI and waist circumference). The same study also found that for individuals with habitual high fat diet (>35% of energy intaken), individuals with GG homozygotes genotype showed higher BMI compared to AA allele carriers. However, this difference is not found in low fat consuming group (<35% of energy intaken).[14][16]

Besides the FTO genes and APO B, SNPs in various genes such as MC4R, SH2B1, MTCH2, SEC16B etc. have been found to be associated with obesity.[14] Although many of these genetic variations are found in populations all over the world, there are also variations unique to certain races or populations.[14]

Cancer

Nutrigenomics may be able to supplement current oncology. There is a wealth of information about processes that occur within genome maintenance that prevent cell abnormalities linked to cancer and certain nutrients that play a role as cofactors.[7] Genome damage caused by micronutrient deficiency may be just as severe as damage owed to exposure to certain environmental carcinogens.[7] If these micronutrients can be identified, with concrete evidence, the risk for cancer in some individuals could be significantly reduced. One such micronutrient may be folate. In one experiment, folate was given to cells in different concentrations and those with less folate exhibited as much damage to their chromosomes as they would have exhibited with a heavy amount of radiation.[7]  Likewise, dietary supplementation using the cinnamon-derived food factor cinnamaldehyde prevented colon cancer in a chemical exposure-induced mouse model of the human disease, an effect dependent on expression of the cytoprotective transcription factor Nrf2.[17] Nutrigenomics can be used to develop new, alternative treatments that target the altered cancer cell metabolism.[10] The alternative way of energy production in cancer cell metabolism, the Warburg effect, in which glycolysis and lactic acid fermentation are the main means of energy production opposed to oxidative reduction. Certain nutrients may provide ways to starve or inhibit this type of metabolism. Polyunsaturated fatty acids (PUFA) which affect gene expression related to inflammation and other nutrients that have displayed potential in repressing cancer cell metabolism.[10] Another practical application of nutrigenomics to cancer may be identifying nutrient that is a cofactor of a compromised pathway where consuming a surplus of could potentially reduce the compromised pathway's negative consequences.[7] A nutrigenomics approach could provide a safe, holistic model to mitigate tumor growth in place of existing cancer treatments that often have harsh side effects and are not always effective.[10]

Companies involved

Across the globe, there are companies who are not only working towards personalized nutrition but also personalized medicine. Few companies like GeneSupport [18] in India, GeneticHealing [19] in India, DNAfit[20] in London, 23andMe[21] in the United States, Genecorp[22] in India and HiMyDna[23] in HongKong.

Ethics

To put nutrigenomics into practice, genetic testing is required as the test results act as the reference for diagnosis. Genetic testing has been met with many concerns surrounding ethics and regulations. These concerns inherently become a part of, if not augmented by Nutrigenomics, a field that looks to provide highly personalized information.

Consent

One of the major concerns regarding genetic tests would be privacy issue. To perform any type of genetic testing, consent is need directly by the individual who provides the sample. However, if an individual has results that indirectly tie family members to it, by identifying information about a genetic predisposition or condition, information about that family member has been inadvertently revealed.[24] Thus, this type of genetic testing would require consent from a network of individuals. For some sets of the population such as mentally impaired adult or children, it is not possible to obtain direct consent.[24]'The best interest' of the patient must be determined by close family members, care takers and professionals, leaving room for discrepancy.[24] Tissue samples obtained from patients, particularly those who are deceased are also a source of controversy.[24] There is no established ethical code to suggest if data from these patients should be allowed to be published, or if they should remain only as sources of validation for lab techniques. There also exists no regulation for releasing information about heritable condition to family members. The stances on how to approach these situations are arbitrary and regulation provides few guidelines to direct them.

Distribution of tests

As the subject is recently commercialized by companies which sell direct to customer (DTC) genetic tests, as well as being applied by related professionals (such as dietetic practitioners), there has been increased awareness in the use of this information.

Validity

Nutrigenomics is still a new field. There are no set guidelines on how to interpret data from genetic testing. Without a validated way to produce accurate results, there exist concern about how valid results produced are. In 2005-6, the US Government Accountability Office (GAO) attempted to check the validity of numerous DTC tests by sending out information and samples of sham identities.[25] The information they received was varied and not medically verified, and two companies tried to market general supplements as 'individualized'.[25] The GAO study was also rudimentary, without taking into concern that differing environmental factors may affect results.[25]

At that time, DTC genetics was a relatively new business model and was lightly regulated in the US.[26] The first warnings to nutrigenomics companies came in June 2008 when the California Department of Public Health issued cease-and-desist notices to 13 DTC genetics companies, including nutrigenomics startup Salugen.[27][28]

Quackwatch has cautioned that DTC genetic tests marketed by companies marketing dietary supplements have no credible evidence of validity and should be avoided.[29]

One suggestion to try and minimize fraud is to channel distribution of genetic testing to healthcare professionals.[25] American College of Medical Genetics(ACMG) has taken a stance that healthcare professionals should be involved for proper implementation of information from genetic testing.[24]  Healthcare professionals are not necessarily qualified to properly interpret and distribute this information as it is not currently required that they have an in-depth knowledge of genetics.[30] There are a sheer 45 genetic residencies in the US, with a low number of individuals who have completed training per year.[30]  Practitioners often focus on acute medical conditions and do not spend much of their time making health recommendations to each patient.[30] It is suggested that nutritionists and genetic counselors may be the best choice to ensure proper distribution of genetic tests' results.[30]

Privacy

One of the major concerns regarding genetic tests would be privacy issue. There are concerns on who has the right to have access to test results. Abuse of these tests could result in discrimination. For example, genetic information might be used by insurance companies to risk rate their clients or assess how likely their clients are to be costly.[25] Other examples of privacy concerns include disclosure to the workplace that may led to discrimination in employment.[24] Social concerns exist as certain conditions may be stigmatized by the general population.

See also

References

  1. ^ Rawson, N. (October 24, 2008). "Nutrigenomics Boot Camp: Improving Human Performance through Nutrigenomic Discovery. A Supply Side West VendorWorks Presentation". Las Vegas, Nevada. {{cite journal}}: Cite journal requires |journal= (help)
  2. ^ Braicu C, Mehterov N, Vladimirov B, Sarafian V, Nabavi SM, Atanasov AG, Berindan-Neagoe I. Nutrigenomics in cancer: Revisiting the effects of natural compounds. Semin Cancer Biol. 2017 Jul 1. doi:10.1016/j.semcancer.2017.06.011. Review. PMID 28676460.
  3. ^ Astley, Sian B. (Oct 2007). "An introduction to nutrigenomics developments and trends". Genes Nutr. 2 (1): 11–13. doi:10.1007/s12263-007-0011-z. PMC 2474912. PMID 18850130.
  4. ^ a b c d e f g h i j Aglave, B.A.; Mahajan, V.A.; Lokhande, M.O. (April–September 2009). "Nutritional Genomics" (PDF). International Journal of Medical Sciences. 2.1: 90–92.
  5. ^ a b c d Neeha, V. S.; Kinth, P. (2013). "Nutrigenomics research: a review". Journal of Food Science and Technology. 50 (3): 415–428. doi:10.1007/s13197-012-0775-z. PMC 3602567.
  6. ^ a b Ardekani, A.M., & Jabbari, S. (2009). Nutrigenomics and Cancer. Avicenna Journal of Med Biotechnology, 1(1), 9-17. 
  7. ^ a b c d e f Bull, C., & Fenech, M. (2008) Genome-health nutrigenomics and nutrigenetics: nutritional requirements or ‘nutriomes’ for chromosomal stability and telomere maintenance at the individual level. Proceedings of the Nutrition Society, 67, 146-156. doi:10.1017/S0029665108006988
  8. ^ Xia, Q; Grant, SF (2013). "The genetics of human obesity". Ann N Y Acad Sci. 1281: 178–90. doi:10.1111/nyas.12020. PMC 3717174. PMID 23360386.
  9. ^ a b Bisen, Prakash A.; Debnath, Mousumi; Prasad, Godavarthi B.K.S. (2010). Molecular Dianostics: Promises and Possibilities. Springer Science & Business Media. p. 26. ISBN 9048132614.
  10. ^ a b c d Kang, J.X. (2013). Nutrigenomics and Cancer Therapy. Journal of Nutrigenetics and Nutrigenomics, 6, I-II. doi:10.1159/000355340
  11. ^ Simopoulos, A. P., & Ordovás, J. M. (Eds.). (2004). Nutrigenetics and nutrigenomics (Vol. 93). Karger Medical and Scientific Publishers.
  12. ^ Van Ommen, B.; Stierum, R. (2002). "Nutrigenomics: exploiting systems biology in the nutrition and health arena". Current Opinion in Biotechnology. 13 (5): 517–521. doi:10.1016/s0958-1669(02)00349-x.
  13. ^ Müller, M.; Kersten, S. (2003). "Nutrigenomics: goals and strategies". Nature Reviews Genetics. 4 (4): 315–322. doi:10.1038/nrg1047.
  14. ^ a b c d e f g Doo, Miae; Kim, Yangha (2015-03-01). "Obesity: interactions of genome and nutrients intake". Preventive Nutrition and Food Science. 20 (1): 1–7. doi:10.3746/pnf.2015.20.1.1. ISSN 2287-1098. PMC 4391534. PMID 25866743.
  15. ^ Sonestedt, Emily; Roos, Charlotta; Gullberg, Bo; Ericson, Ulrika; Wirfält, Elisabet; Orho-Melander, Marju (2009-11-01). "Fat and carbohydrate intake modify the association between genetic variation in the FTO genotype and obesity". The American Journal of Clinical Nutrition. 90 (5): 1418–1425. doi:10.3945/ajcn.2009.27958. ISSN 1938-3207. PMID 19726594.
  16. ^ Phillips, Catherine M.; Goumidi, Louisa; Bertrais, Sandrine; Field, Martyn R.; McManus, Ross; Hercberg, Serge; Lairon, Denis; Planells, Richard; Roche, Helen M. (2011-02-01). "Gene-nutrient interactions and gender may modulate the association between ApoA1 and ApoB gene polymorphisms and metabolic syndrome risk". Atherosclerosis. 214 (2): 408–414. doi:10.1016/j.atherosclerosis.2010.10.029. ISSN 1879-1484. PMID 21122859.
  17. ^ Long M, Tao S, Rojo de la Vega M, Jiang T, Wen Q, Park SL, Zhang DD, Wondrak GT (May 2015). "Nrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde". Cancer Prevention Research. 8 (5): 444–54. doi:10.1158/1940-6207.CAPR-14-0359. PMC 4417412. PMID 25712056.
  18. ^ "GeneSupport". www.genesupport.in/.
  19. ^ "GeneticHealing". www.genetichealing.in/.
  20. ^ "DNAFit - Genetic Information for Fitness & Nutrition". www.dnafit.com.
  21. ^ 23andMe. "DNA Genetic Testing & Analysis - 23andMe". www.23andme.com.{{cite web}}: CS1 maint: numeric names: authors list (link)
  22. ^ "Homepage - Genecorp". Genecorp.
  23. ^ "myDNA - the Industry's 1st Nutrigenomics-based Mobile Health Coach". himyDNA.
  24. ^ a b c d e f Williams, J.; Skirton, H.; Masny, A. (2006). "Ethics, Policy and Educational Issues in Genetic Testing". Journal of Nursing Scholarship. 38(2): 119–125 – via Wiley Online Library.
  25. ^ a b c d e Castle, David; Ries, Nola M. (2007-09-01). "Ethical, legal and social issues in nutrigenomics: The challenges of regulating service delivery and building health professional capacity". Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. Nutrigenomics. 622 (1–2): 138–143. doi:10.1016/j.mrfmmm.2007.03.017.
  26. ^ Kaye, Jane (2008). "The Regulation of Direct-to-Consumer Genetic Tests". Hum Mol Genet. 17 (R2): R180–R183. doi:10.1093/hmg/ddn253.
  27. ^ "Genetic Test Cease-And-Desist Notices". California Department of Public Health. 24 June 2008. Archived from the original on 2 July 2008. Retrieved 27 June 2018. {{cite web}}: Unknown parameter |dead-url= ignored (|url-status= suggested) (help)
  28. ^ Johnson, Steve (24 June 2008). "Five California gene testing firms among 13 suspended". Mercury News. Retrieved 27 June 2018.
  29. ^ Barrett, Stephen; Hall, Harriet (24 November 2008). "Dubious Genetic Testing". Quackwatch. Retrieved 24 June 2018.
  30. ^ a b c d Ries, Nola M. (2008). "Nutrigenomics and Ethics Interface: Direct-to-Consumer Services and Commercial Aspects". OMICS: A Journal of Integrative Biology. 12: 245–250. doi:10.1089/omi.2008.0049.

Further reading

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