It may well be true that if we had listened better to what our grandparents and parents taught us about the importance of eating fruit and vegetables, we would be living healthier and perhaps longer lives. Research is beginning to show us that aging, and the diseases that accompany that process, may well be the result of the decreasing ability of our bodies to deal with oxidative stress. There is also substantial evidence showing that eating adequate amounts of fruits and vegetables de-creases our chances of developing can-cer, high blood pres-sure, heart disease, stroke and diabetes. A complex network of
By: Dr. Robyn Murphy, ND
The verdict is in, your genes are not your destiny. Advances in genetics and epigenetics have evolved through observations that environmental factors influence genetic expression to directly impact an individual’s health. Epigenetic changes are reversible while effects of genetic variations are modifiable. 1,2
Today, in the midst of personalized medicine, understanding an individual’s genetic blueprint provides simple yet powerful strategies to significantly make a difference in one’s health. While science reveals how general lifestyle strategies in diet, exercise and stress reduction significantly impacts epigenetic modifications and thus gene expression and risk for disease; it is important to know how specific gene variations interact with an individual’s wellbeing to influences their response to these lifestyle interventions. Generational studies prove that these lifestyle changes not only reduce the prevalence of disease within one’s lifetime, but that these changes are heritable, modifying the health of generations to come. 3
“Understanding an individual’s genetic blueprint provides simple
yet powerful strategies to significantly impact health.”
Nutrients and Epigenetics
Nutri-epigenomics is an emerging discipline examining the role of dietary influences on gene expression.2 Particular interest is with dietary practices and micronutrients that affect DNA methylation, such as; B vitamins, including folate and vitamin B12, choline, betaine and micronutrients magnesium, zinc and copper. 2 These vitamins are crucial for the production of SAMe, which influences epigenetic modification through DNA methylation and thus gene expression. DNA methylation and its relationship to disease follows the Goldilocks effect, where both too little (hypomethylation) and too much (hypermethylation) have damaging effects. It is important to have just the right amount to ensure the activation of genes that promote health, and the inactivation of those that promote disease.
In a study, women between the ages of 20 and 30 with a reduction in dietary choline and folate saw a decrease in global methylation of DNA within the white blood cell (WBC). However, these effects were reversible. Dietary re-supplementation with folate lead to widespread improvements in DNA re-methylation. What is interesting, is the strength of the association was more robust in individuals with the T/T variation in the gene, MTHFR C677T. This suggests that folate supplementation may be more crucial for methylation maintenance in individuals with MTHFR polymorphisms.2
Other genetic variations impact susceptibility to not only folate deficiency but choline, betaine, vitamin B12 and vitamin B6, all important in the production of SAMe. SAMe is imperative for hundreds of other biochemical pathways, such DNA repair, elimination of toxic chemicals, hormone balance, mood, energy production, and cellular replication. Studies show that by supplementing mothers susceptible to low SAMe with a diet rich in methyl donors, protects the baby from epigenetic changes due to chemical exposure, such as bisphenol A (BPA). 2 The mother’s at-risk for high BPA, are those with genetic variations in genes responsible for detoxification and antioxidation (GSTT1, GSTM1, SOD2).4 By identifying those mothers who are sensitive to depletion of SAMe or the effects of BPA, appropriate dietary and lifestyle interventions can be implemented preventatively, improving the health of her and her future baby.
Exercise and Epigenetics
Regular exercise positively impacts epigenetics and reduces the development of chronic diseases, including cardiovascular disease, obesity, hypertension, and type 2 diabetes. 5 Nonetheless, genetic variations influence individual response to exercise.
For long-term benefits of exercise, the key is consistency. Intellectually, most know that exercise is good for them; however, while some seem to carry an innate motivation for regularity, others are lacking. The BDNF gene not only affects the likelihood for one to continue exercising when given the option to stop, it also moderates benefits of exercise.5 In a randomized trial, those with the ‘met’ allele had a more positive mood and the largest increase in aerobic tolerance following a series of exercises. 5
Predisposition towards power exercises versus endurance is modified by genetics. Endurance athletes more commonly carry certain versions of the ACTN3 and ACE genes. 6 Those with the T/T version of the SOD2 gene are more prone to exercise associated oxidative stress. 7
Knowing these individual tendencies towards exercise, changes in motivational strategies, choice of activities and supplementation to improve aerobic capacity during exercise training, such as ginseng or NAC, may improve training outcomes. 7
Stress and Epigenetics
Stress has numerous long-lasting consequences to a person’s health. Not only does it lead to short term consequences of fatigue and insomnia, it also produces lifelong epigenetic alterations, resulting in changes in gene expression within the brain implicated in a host of neural conditions, from Alzheimer’s-related memory loss to depression.8,9
Variations in the COMT gene influence one’s response to stress. Those with the ‘met’ version, known as the ‘worriers’, have a greater HPA activity (i.e., cortisol) in response to stressful stimuli; while those with the ‘val’ version are ‘warriors’, who typically perform better under stress. 10,11 Several studies show the impact of COMT gene variations on the risk for developing mental health disorders, including, generalized anxiety disorder (GAD), PTSD, depression and ADHD.12,13,14 Furthermore, COMT modifies treatment response. Warriors have a higher response to, placebo in those with IBS, CBT in those with addiction and exposure-based CBT in those with panic disorder. 15,16,17 In addition, they perform better in reducing stress hormones during meditation.18 Support for the ‘worriers’ could therefore include L-theanine or ashwagandha, to reduce HPA-axis stimulation and stress hormones and improve the outcome of their meditation practices.
Overall, knowing your individual genetic susceptibility not only unveils predispositions to disease, it also guides strategic interventions to modify the impact on health. Scientific and technological innovations now make it possible for the public to access the key for us all to unlock our genetic potential.
- Hou L, Zhang X, Wang D, Baccarelli A. Environmental chemical exposures and human epigenetics. Int J Epidemiol. 2012;41(1):79-105. doi:10.1093/ije/dyr154
- Anderson OS, Sant KE, Dolinoy DC. Nutrition and epigenetics: An interplay of dietary methyl donors, one-carbon metabolism, and DNA methylation. J Nutr Biochem. 2012;23(8):853-859. doi:10.1016/j.jnutbio.2012.03.003
- Kanherkar RR, Stair SE, Bhatia-Dey N, Mills PJ, Chopra D, Csoka AB. Epigenetic Mechanisms of Integrative Medicine. Evid-Based Complement Altern Med ECAM. 2017;2017. doi:10.1155/2017/4365429
- Kim JH, Lee M-R, Hong Y-C. Modification of the association of bisphenol A with abnormal liver function by polymorphisms of oxidative stress-related genes. Environ Res. 2016;147:324-330. doi:10.1016/j.envres.2016.02.026
- Caldwell Hooper AE, Bryan AD, Hagger MS. What keeps a body moving? The brain-derived neurotrophic factor val66met polymorphism and intrinsic motivation to exercise in humans. J Behav Med. 2014;37(6):1180-1192. doi:10.1007/s10865-014-9567-4
- Contrò V, Schiera G, Abbruzzo A, et al. An innovative way to highlight the power of each polymorphism on elite athletes phenotype expression. Eur J Transl Myol. 2018;28(1):7186. doi:10.4081/ejtm.2018.7186
- Sen CK, Rankinen T, Vaisanen S, Rauramaa R. Oxidative stress after human exercise: effect of N-acetylcysteine supplementation. J Appl Physiol. 1994;76(6):2570-2577. doi:10.1152/jappl.1918.104.22.16870
- Stankiewicz AM, Swiergiel AH, Lisowski P. Epigenetics of stress adaptations in the brain. Brain Res Bull. 2013;98:76-92. doi:10.1016/j.brainresbull.2013.07.003
- Qigong Institute – Epigenetics and Psychoneuroimmunology. https://www.qigonginstitute.org/category/15/epigenetics-and-psychoneuroimmunology. Accessed May 1, 2017.
- Cao C, Cao L, Chen J. Differences in Sensitivity to Environment Depending on Catechol-O-Methyltransferase (COMT) Gene? A Meta-analysis of Child and Adolescent Gene-by-Environment Studies. J Youth Adolesc. 2019;48(4):655-667. doi:10.1007/s10964-019-01004-3
- Stein DJ, Newman TK, Savitz J, Ramesar R. Warriors Versus Worriers: The Role of COMT Gene Variants. CNS Spectr. 2006;11(10):745-748. doi:10.1017/S1092852900014863
- Bieliński M, Jaracz M, Lesiewska N, et al. Association between COMT Val158Met and DAT1 polymorphisms and depressive symptoms in the obese population. Neuropsychiatr Dis Treat. 2017;13:2221-2229. doi:10.2147/NDT.S138565
- Jung M, Mizuno Y, Fujisawa TX, et al. The Effects of COMT Polymorphism on Cortical Thickness and Surface Area Abnormalities in Children with ADHD. Cereb Cortex N Y N 1991. December 2018. doi:10.1093/cercor/bhy269
- Walder DJ, Trotman HD, Cubells JF, Brasfield J, Tang Y, Walker EF. Catechol-O-Methyltransferase (COMT) Modulation of Cortisol Secretion in Psychiatrically At-risk and Healthy Adolescents. Psychiatr Genet. 2010;20(4):166-170. doi:10.1097/YPG.0b013e32833a1ff3
- Hall KT, Lembo AJ, Kirsch I, et al. Catechol-O-Methyltransferase val158met Polymorphism Predicts Placebo Effect in Irritable Bowel Syndrome. PLOS ONE. 2012;7(10):e48135. doi:10.1371/journal.pone.0048135
- Carroll KM, Herman A, DeVito EE, Frankforter TL, Potenza MN, Sofuoglu M. Catehol-o-methyltransferase gene Val158met polymorphism as a potential predictor of response to computer-assisted delivery of cognitive-behavioral therapy among cocaine-dependent individuals: Preliminary findings from a randomized controlled trial. Am J Addict. 2015;24(5):443-451. doi:10.1111/ajad.12238
- Lonsdorf TB, Rück C, Bergström J, et al. The COMTval158met polymorphism is associated with symptom relief during exposure-based cognitive-behavioral treatment in panic disorder. BMC Psychiatry. 2010;10:99. doi:10.1186/1471-244X-10-99
- Jung Y-H, Kang D-H, Byun MS, et al. Influence of brain-derived neurotrophic factor and catechol-O-methyl transferase polymorphisms on effects of meditation on plasma catecholamines and stress. Stress. 2012;15(1):97-104. doi:10.3109/10253890.2011.592880