Cracking the Genetic Code: Nutrigenomics and Fertility

Nutrigenomics, an emerging field of nutritional science, integrates genomics, epigenomics, transcriptomics, proteomics, and metabolomics to understand the interaction between diet and genes and their subsequent effects on health. In the scope of fertility issues, nutrigenomics provides valuable insights that can inform personalized nutritional strategies, helping you and your partner increase your chances to overcome infertility and conceive successfully.

Nutrigenomics: An Overview

At the core of nutrigenomics is the principle that nutrients and other bioactive components in foods can influence health by interacting with our genome, thereby altering gene expression and/or the structure of an individual's genome. The genome encodes all the information necessary for the function and structure of living organisms. It is a sophisticated system that uses approximately 25,000 genes to manufacture proteins that perform myriad functions, from providing structural support to cells, to acting as enzymes that catalyze life-sustaining chemical reactions.

In addition to encoding life's instruction manual, the genome also comes equipped with a highly responsive system that regulates gene expression in response to internal and external environmental signals. This gene regulatory system allows the body to adapt to ever-changing environments by altering the production of proteins encoded by the genome. One of the most critical environmental signals that affects gene expression is diet. Certain nutrients can activate or inhibit the transcription of genes, which influences protein synthesis and, consequently, bodily functions.

Nutrigenomics and Infertility

Infertility, defined as the inability to conceive after a year of regular unprotected intercourse, is a common reproductive issue affecting approximately 15% of couples globally. Infertility can be due to male factors, female factors, or a combination of both. Recent studies suggest that diet and lifestyle, interacting with an individual's unique genetic makeup, may play a significant role in fertility. This is where the utility of nutrigenomics comes into play.

Nutrigenomic testing provides comprehensive insights into an individual's genetic variations, which can influence various biological processes involved in fertility. These include metabolic processes like methylation, hormonal regulation, nervous system function, and detoxification pathways. The knowledge obtained from such testing can help you and your partner follow a completely personalized, gene-based nutritional protocol to address underlying issues, optimize fertility, and improve pregnancy outcomes.

Methylation SNPs and Fertility

Methylation, a biochemical process essential to numerous cellular functions, is one such area where genetic variations can influence fertility. It involves the addition of a methyl group (a carbon atom linked to three hydrogen atoms) to DNA molecules, proteins, or neurotransmitters. Methylation is involved in DNA synthesis and repair, gene expression, detoxification processes, and the regulation of neurotransmitters. It also plays a crucial role in embryonic development, making it critical for fertility.

Single Nucleotide Polymorphisms (SNPs), which are variations at a single position in a DNA sequence, can affect the efficiency of methylation. For instance, the methylenetetrahydrofolate reductase (MTHFR) gene, which codes for an enzyme critical for folate metabolism and methylation, has two well-known SNPs: MTHFR/ rs1801133 and MTHFR/ rs1801131. Both can reduce the enzyme's activity, thereby impairing methylation. Impaired methylation has been associated with an increased risk of recurrent miscarriages, neural tube defects, pre-eclampsia, and other pregnancy complications.

Another critical gene in methylation and fertility is the methionine synthase reductase (MTRR) gene. An SNP (MTRR/ rs1801394) in this gene, which helps maintain adequate levels of vitamin B12 (a critical nutrient for methylation), can impair its function. This impairment can lead to elevated homocysteine levels, associated with miscarriages and pregnancy complications.

By identifying such SNPs and understanding their implications, you and your partner can take proactive steps - such as dietary modifications or supplementation - to support optimal methylation processes and enhance fertility outcomes.

Hormones SNPs and Fertility

Hormonal regulation is another key aspect of fertility, and genetic variations can significantly impact hormone production and function. Hormones such as estrogen, progesterone, follicle-stimulating hormone (FSH), luteinizing hormone (LH), and thyroid hormones play critical roles in the menstrual cycle, ovulation, and pregnancy.

The estrogen receptor 1 (ESR1) gene, which codes for the primary estrogen receptor, contains several SNPs that have been associated with fertility issues. For example, the ESR1/ rs2234693 and ESR1/ rs9340799 polymorphisms have been linked to endometriosis and polycystic ovary syndrome (PCOS), both common causes of female infertility.

In the context of thyroid hormones, an SNP DIO2/ rs225014 in the deiodinase 2 (DIO2) gene, which converts the inactive thyroid hormone (T4) to the active form (T3), can affect thyroid function and, therefore, fertility. Hypothyroidism or subclinical hypothyroidism can lead to ovulatory disorders and an increased risk of recurrent miscarriage or recurrent pregnancy loss.

The detection of these SNPs via nutrigenomic testing can guide nutritional interventions to support hormonal balance, such as emphasizing foods rich in phytoestrogens for ESR1 SNPs or optimizing selenium and iodine intake for thyroid health in the case of DIO2 SNPs.

Nervous System SNPs and Fertility

The nervous system, particularly the hypothalamic-pituitary-adrenal (HPA) axis, plays a crucial role in stress response and fertility. Chronic stress can disrupt the HPA axis and impair fertility by altering gonadotropin-releasing hormone (GnRH) secretion, which regulates the production of fertility hormones like FSH and LH.

An SNP FKBP5/ rs1360780 in the FK506 binding protein 5 (FKBP5) gene, which regulates stress response by modulating the sensitivity of the glucocorticoid receptor, has been linked to a heightened stress response and may negatively impact fertility. Identification of such SNPs can lead to stress management strategies, including nutritional approaches like emphasizing magnesium-rich foods or B-vitamins to support the nervous system and reduce stress impact. Personalised lifestyle modifications are also shown positive results in regulating stress hormones.

Detoxification SNPs and Fertility

Detoxification is a vital bodily process that eliminates waste products and toxins. Efficient detoxification is crucial for overall health, including reproductive health. Genetic variations can affect the activity of detoxification enzymes, potentially leading to an accumulation of harmful substances that can impact fertility.

For instance, the glutathione S-transferase mu 1 (GSTM1) gene, which codes for an enzyme involved in phase II detoxification, can have a null variation where the entire gene is missing. Individuals with this null variation have reduced detoxification capacity, which may increase oxidative stress and contribute to fertility issues.

Another gene, the cytochrome P450 1B1 (CYP1B1), is involved in estrogen metabolism. An SNP CYP1B1/ rs1056836 can increase the enzyme's activity, leading to a higher production of potentially harmful estrogen metabolites, which can contribute to conditions like endometriosis and infertility.

Through nutrigenomic testing, the identification of such SNPs can help you and your partner adjust your dietary and lifestyle habits to support detoxification processes. This could include increasing intake of cruciferous vegetables for their beneficial compounds that support detoxification or managing exposure to environmental toxins.

Conclusion

Nutrigenomics represents a revolutionary approach in understanding and addressing fertility issues. It acknowledges the complexity of fertility and appreciates the multitude of factors, including genetic variations and dietary habits, that influence reproductive outcomes. Through nutrigenomic testing, you can gain deeper insights into your genetic predispositions and how you can modify your diet to support fertility-related biological processes, providing a beacon of hope on the challenging journey of trying to conceive.

References

Afman, L., & Müller, M. (2006). Nutrigenomics: From molecular nutrition to prevention of disease. Journal of the American Dietetic Association, 106(4), 569-576. doi: 10.1016/j.jada.2006.01.001

Blesa, D., Ruiz-Alonso, M., Simon, C. (2014). Clinical management of endometrial receptivity. Seminars in Reproductive Medicine, 32(5), 410–413. doi: 10.1055/s-0034-1383955

Collins, F. S. (2004). What we do and don't know about 'race', 'ethnicity', genetics and health at the dawn of the genome era. Nature Genetics, 36, S13-S15. doi: 10.1038/ng1436

Frosst, P., Blom, H. J., Milos, R., Goyette, P., Sheppard, C. A., Matthews, R. G., Boers, G. J., den Heijer, M., Kluijtmans, L. A., van den Heuvel, L. P., & Rozen, R. (1995). A candidate genetic risk factor for vascular disease: a common mutation in methylenetetrahydrofolate reductase. Nature Genetics, 10(1), 111–113. doi: 10.1038/ng0595-111

Gharagozloo, P., Aitken, R. J. (2011). The role of sperm oxidative stress in male infertility and the significance of oral antioxidant therapy. Human reproduction, 26(7), 1628-1640. doi: 10.1093/humrep/der132

Infertility. (2021). World Health Organization. Retrieved from: https://www.who.int/health-topics/infertility#tab=tab_1

Khatami, F., Larijani, B., Tavangar, S. M. (2016). The presence of tumor extrachomosomal circular DNA (ecDNA) as a component of liquid biopsy in blood. Medical Hypotheses, 89, 14-17. doi: 10.1016/j.mehy.2016.02.004

Matsuzaka, Y., Kikuti, Y. Y., Goya, K., Suda, T., Izumi, T., Hiramoto, M., Tomita, K., Sugita, Y., Nakamura, H., Takagi, K., Shinohara, T., Kashiwase, K., Tadokoro, K., Juji, T., Akaza, T. (1997). CYP1B1 gene in endometrial cancer. Molecular Carcinogenesis, 18(3), 130–137. doi: 10.1002/(sici)1098-2744(199703)18:3<130::aid-mc1>3.0.co;2-i

van der Put, N. M., Gabreëls, F., Stevens, E. M., Smeitink, J. A., Trijbels, F. J., Eskes, T. K., van den Heuvel, L. P., & Blom, H. J. (1998). A second common mutation in the methylenetetrahydrofolate reductase gene: an additional risk factor for neural-tube defects?. American Journal of Human Genetics, 62(5), 1044–1051. doi: 10.1086/301825

Ruder, E. H., Hartman, T. J., Blumberg, J., Goldman, M. B. (2008). Oxidative stress and antioxidants: exposure and impact on female fertility. Human Reproduction Update, 14(4), 345–357. doi: 10.1093/humupd/dmn011

Vanhees, K., Coort, S., Ruijters, E. J., Godschalk, R. W., van Schooten, F. J., Barjesteh van Waalwijk van Doorn-Khosrovani, S. (2014). Epigenetics: prenatal exposure to genistein leaves a permanent signature on the hematopoietic lineage. The FASEB Journal, 28(1), 83-92. doi: 10.1096/fj.13-235440

Zintzaras, E. (2006). Methylenetetrahydrofolate reductase gene and susceptibility to breast cancer: a meta-analysis. Clinical Genetics, 69(4), 327–336. doi: 10.1111/j.1399-0004.2006.00596.x

 

Related Posts

 
 
 

Instagram

 
Previous
Previous

Male Factor Infertility: Causes and Implications

Next
Next

Take charge of your fertility journey today!