Genetic control of methylation can affect your health

With the holiday season ending so does a peak travel period, as friends, family, and coworkers return from holiday getaways. In addition to stories of family celebration or tropical paradises visited, the travel experience can also bring stories of layovers, cancelled flights, and lost luggage. As annoying as such experiences can be, it is quite profound how much actually goes right during these chaotic times given the amount of information that needs to be kept straight. A series of tickets, tags, scanners, and check points coordinate information to transport millions of people and their belongings all around the world.

The body has a similar information system to instruct molecules where they should be, when they should be there, and what they should be doing. One part of this system involves methylation. The methylation pathway, which is the result of close communication between the methionine, folate, and biopterin cycles, plays a vital role in many biological processes (Figure 1).

Figure 1. Methylation biochemistry is the result of close communication between the methionine, folate, and biopterin cycles and plays a role in many biological processes.

Figure 1. Methylation biochemistry is the result of close communication between the methionine, folate, and biopterin cycles and plays a role in many biological processes.

The methylation pathway affects inflammation, detoxification, DNA and cellular repair, as well as maintenance of proper levels of neurotransmitters which can influence energy levels, mood, and cognitive function. This is due, in part, to the effect of methylation on gene expression. Proper function of the methylation cycle is needed for gene expression, as methyl groups on regions of DNA serve as markers for when to turn a gene on and off.  Different methylation patterns in a variety of genes can result in many poor physical and mental health outcomes, including cardiovascular and metabolic issues, as well as depression, psychiatric disorders, and other mental health conditions. DNA methylation is also becoming increasingly important in understanding the pathology of many types of cancer, as tumor cells may shift methylation patterns in a way that favors inactivation of tumor suppressor genes.

Since methylation plays such an important role in gene expression, mutations in genes within the methylation cycle can alter normal biological processes. One important gene in this cycle is for the enzyme methylenetetrahydrofolate reductase (MTHFR). This gene is responsible for an important step in the metabolism of folate (a B-Vitamin). A variety of mutations in the MTHFR gene can interfere with this process.

A common variant in this gene includes the C677T polymorphisms. These polymorphisms result in an amino acid substitution that causes a significant decrease in enzymatic function at elevated temperatures. Mutations like this in the MTHFR gene can interact with other genetic or environmental components and possibly contribute to a variety of conditions, including Alzheimer’s disease, Parkinson’s disease, autism, diabetes, arthritis, cardiovascular issues, chronic fatigue, and many types of cancer.

As many of us return from our holiday travels, we transition from feasting to considering New Year’s Resolutions that often include improvements in our health.  The good news is that we may not have to struggle as much with these goals as we have in the past.  It is now possible to test our genes for mutations that increase our risk for many health conditions.  Gaining this insight into which genes we actually carry and how to best support proper function of these genes can help ensure we experience many more happy holiday travels to come.

Guest author: Curtis Christian is a member of the Clinical Support & Education Department at NeuroScience, Inc. and the resident expert in genetics.

References:
Bai, J. L., Zheng, M. H., Xia, X., Ter-Minassian, M., Chen, Y. P., & Chen F. (2008). MTHFR C677T polymorphism contributes to prostate cancer risk among Caucasians: A meta-analysis of 3511 cases and 2762 controls. European Journal of Cancer, 45, 1443-1449.
Botto, L. D., & Yang, Q. (2000). 5, 10-Methylenetetrahydrofolate reductase gene variants and congenital anomalies: A huge review. American Journal of Epidemiology, 151(9), 862-877.
Carvalho, D. D., et al. (2012). DNA methylation screening identifies driver epigenetics events of cancer cell survival. Cancer Cell, 21, 655-667.
Coppede, F. (2014). Epigenetics biomarkers of colorectal cancer: Focus on DNA Methylation. Cancer Letters, 342, 238-247.
Phillips, T. (2008). The role of methylation in gene expression. Nature Education, 1(1), 116.
Szyf, M. (2013). DNA methylation, behavior and early life adversity. Journal of Genetics and Genomics, 40, 331-338.
Wu, Y. L., Ding, X. X., Sun, Y. H., & Sun, L. (2013). Methylenetetrahydrofolate reductase (MTHFR) C677T/A1298C polymorphisms and susceptibility to Parkinson’s disease: A meta-analysis. Journal of Neurological Sciences, 335, 14-21.
Wang, W. Hou, Z., Wang, C., Wei, C., Li, Y, & Jiang, L. (2013). Association between 5, 10-methylenetetrahydrofolate reductase (MTHFR) polymorphisms and congenital heart  disease: A meta-analysis. Meta Gene, 1, 109-125.
Yang, S., Zhang, J., Feng, C. & Huang G. (2013). MTHFR 677 T variant contributes to diabetic nephropathy risk in Caucasian individuals with type 2 diabetes: A meta-analysis. Metabolism Clinical and Experimental, 62, 586-594.
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