Healthcare professionals commonly give nutritional recommendations based on an entire population, only sometimes changing these according to age, sex, and pregnancy. Over the last 20 years, however, an increase in research studies has demonstrated that epigenetics can ultimately affect nutrition and even increase the risk of developing a variety of health issues, including oxidative stress and inflammation. Recent advances in technology are also currently being used to help healthcare professionals understand how nutrigenomics can affect an individual’s overall health and wellness.
Several research studies have also demonstrated that single nucleotide polymorphisms can explain the risk for individual complex disease traits. A single-nucleotide polymorphism, or SNP, is a substitution of a nucleotide that happens in the genome. Moreover, further research studies can be utilized to explain the variation in health issue risk based on nutrition and genome. The purpose of the following article is to discuss recent developments in the field of epigenetics and personalized nutrition as well as to consider the contribution of research studies to nutritional recommendations.
Table of Contents
Epigenetics is a collection of changes that affect chromatin structure, without altering our DNA sequence, while allowing transcriptional regulation over a range of timescales. Common epigenetic processes include histone modification, non-coding RNAs, and DNA methylation. Many research studies on how epigenetics affects personalized nutrition focus on DNA methylation, however, research findings have demonstrated other epigenetic marks. DNA methylation inside a dinucleotide is a well-known modification in the genome of a variety of mammals in DNA replication and cell division.
Methylation of dinucleotides is shown by DNA methyltransferases, or Dnmts, and is regulated by mitosis. DNA methylation can trigger transcriptional silencing by blocking and/or promoting the connection of transcription factors in the methyl CpG-binding protein MeCP2 which activates histone-modifying complexes to the DNA. MeCP2 activates what is frequently referred to as histone deacetylases, or HDACs, and histone methyltransferases, or HMTs, resulting in a closed chromatin structure and transcriptional silencing. These have been demonstrated to be associated with various health issues.
Dnmt1 is activated by HDACs and HMTs which suggests that chromatin structure may also affect the status of DNA methylation in the regulation of genes associated with nutrition. According to healthcare professionals, epigenetic marks are essentially maintained throughout an individual’s life. However, recent research findings show that epigenetic plasticity can be affected in early development, including in stages of increased physiological changes, such as puberty and aging. This ultimately suggests the possibility that epigenotypes associated with the increased risk of developing health issues can change.
Research studies have demonstrated that our early life environment can affect our epigenetic process and the origins of health issues. Healthcare professionals also believe that nutrition in our early life can affect our epigeno- and phenotype in the future. Pregnant rat groups given a diet with corn oil resulted in hypermethylation and decreased gene expression in the offspring, causing mature osteoblasts. This is the first research study to find how maternal diet affects epigenetic processes by altering morphogenesis and changing non-imprinted gene expression in pregnant rat groups.
Pregnant rat groups given a diet with an undisclosed type of fat had increased fetal blood glucose concentration and increased mRNA expression of gluconeogenic genes in the fetal liver. A recent research study found that the amount of fat in the maternal diet was one of the major factors resulting in epigenetic changes in the offspring of pregnant rat groups. The diets given to the pregnant rat groups including fat derived from safflower oil, butter, hydrogenated soybean oil, or fish oil caused hypermethylation in the offspring compared with those where pregnant rat groups were only given 7 percent fat.
Furthermore, one research study found that pregnant rat groups given a protein-restricted, or PR, diet developed epigenetic silencing in both histone modifications and DNA methylation which was followed by progressive transcriptional suppression as the offspring aged. The research findings suggest that nutrition during early development can ultimately cause long-term changes in phenotype. Pregnant rat groups given a PR diet also developed hypomethylation of specific dinucleotides in the adipose tissue leptin promoter and in the heart PPARa promoter in adult offspring.
For more information regarding how epigenetics affects personalized nutrition, please review this article:
Epigenetics: Are There Implications for Personalised Nutrition?
Healthcare professionals have demonstrated that we can change gene expression and improve the risk of developing a variety of health issues, including oxidative stress and inflammation which can cause chronic pain, by controlling the food we eat. Starting in the kitchen and then taking it to the genes, if we follow a balanced nutrition, we will see a considerable change in our overall health and wellness. We have the ability to assess your specific genetic factors and what dietary guidelines are best for you to follow. One test we use is from DNA life called DNA Diet. A sample of this report is shown below:
Research studies have demonstrated how epigenetics affect personalized nutrition. The same research studies have also demonstrated that a balanced nutrition can change our gene expression to improve how good food affects our overall health and wellness. While following a proper diet can help improve the risk of developing a variety of health issues, including oxidative stress and inflammation associated with chronic pain, eating good food may be difficult for some people. That’s why drinking smoothies or juices can be easy ways to include the balanced nutrition we need to promote our well-being. In the section below, I’ve provided a smoothie recipe so you can take your health and wellness from the kitchen to your genes. – Dr. Alex Jimenez D.C., C.C.S.T. Insights
Servings: 1
Cook time: 5-10 minutes
• 1/2 cup cantaloupe, cubed
• 1/2 banana
• 1 handful of kale or spinach
• 1 handful of Swiss chard
• 1/4 avocado
• 2 teaspoons spirulina powder
• 1 cup water
• 3 or more ice cubes
Blend all ingredients in a high-speed blender until completely smooth and enjoy!
The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues or functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or disorders of the musculoskeletal system. Our office has made a reasonable attempt to provide supportive citations and has identified the relevant research study or studies supporting our posts. We also make copies of supporting research studies available to the board and or the public upon request. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900.
Curated by Dr. Alex Jimenez D.C., C.C.S.T.
1. Rimbach G, Minihane AM. Nutrigenetics and personalized nutrition: how far have we progressed and are we likely to get there? Pro Nutr Soc 2009; 68:162 – 172.
2. Manolio TA, Collins FS, Cox NJ, et al. Finding the missing heritability of complex diseases. Nature 2009; 461:747–753.
3. Slatkin M. Epigenetic inheritance and the missing heritability problem. Genetics 2009; 182:845–850.
4. GoldbergAD,AllisCD,BernsteinE.Epigenetics:alandscapetakesshape. Cell 2007; 128:635 – 638.
5. BirdA.DNAmethylationpatternsandepigeneticmemory.GenesDev2002; 16:6 – 21.
6. Razin A, Szyf M. DNA methylation patterns. Formation and function. Biochim Biophys Acta 1984; 782:331–342.
7. Strahl BD, Ohba R, Cook RG, et al. Methylation of histone H3 at lysine 4 is highly conserved and correlates with transcriptionally active nuclei in Tetrahymena. Proc Natl Acad Sci USA 1999; 96:14967–21472.
8. Lachner M, O’Carroll D, Rea S, et al. Methylation of histone H3 lysine 9 creates a binding site for HP1 proteins. Nature 2001; 410:116 – 120.
9. Zegerman P, Canas B, Pappin D, et al. Histone H3 lysine 4 methylation disrupts binding of nucleosome remodeling and deacetylase (NuRD) repressor complex. J Biol Chem 2002; 277:11621–11624.
10. Nakayama J, Rice JC, Strahl BD, et al. Role of histone H3 lysine 9 methylation in epigenetic control of heterochromatin assembly. Science 2001; 292:110 –113
11. Fuks F, Burgers WA, Brehm A, et al. DNA methyltransferase Dnmt1 associates with histone deacetylase activity. Nature Gen 2000; 24:88–91.
12. Rountree MR, Bachman KE, Baylin SB. DNMT1 binds HDAC2 and a new co-repressor, DMAP1, to form a complex at replication foci. Nature Gen 2000; 25:269–277.
13. Vire ́ E, Brenner C, Deplus R, et al. The Polycomb group protein EZH2 directly controls DNA methylation. Nature 2006; 439:871–874.
14. SzyfM.Thedynamicepigenomeanditsimplicationsintoxicology.ToxicolSci 2007; 100:7 – 23.
15. Gluckman PD, Hanson MA, Cooper C, et al. Effect of in utero and early-life conditions on adult health and disease. N Engl J Med 2008; 359:61–73.
16. Burdge GC, Lillycrop KA. Bridging the gap between epigenetics research and nutritional public health interventions. Genome Med 2010; 2:80.
17. Chen J-R, Zhang J, Lazarenko OP, et al. Inhibition of fetal bone development & through epigenetic down-regulation of HoxA10 in obese rats fed high-fat diet.
FASEB J 2012; 26:1131–1141. This article shows a link between a high-energy diet and bone development through global hypermethylation and decreased HoxA10 expression.
18. Temple IK. Imprinting in human disease with special reference to transient neonatal diabetes and Beckwith-Wiedemann syndrome. Endo Dev 2007; 12:113 – 123.
19. Strakovsky RS, Zhang X, Zhou D, et al. Gestational high fat diet programs hepatic phosphoenolpyruvate carboxykinase gene expression and histone modification in neonatal offspring rats. J Physiol 2011; 589:2707– 2717.
20. Kelsall C, Hoile SP, Irvine N, et al. Vascular dysfunction induced in offspring by & maternal dietary fat involves altered arterial polyunsaturated fatty acid biosynthesis. PloS One 2012; 7:e34492. This study shows that amount of fat in the maternal diet significantly altered vascular function, via altered epigenetic regulation of the fads2 pathway.
21. Sandovici I, Smith NH, Nitert MD, et al. Maternal diet and aging alter the & epigenetic control of a promoter-enhancer interaction at the Hnf4a gene in rat
pancreatic islets. Proc Natl Acad Sci USA 2011; 108:5449–5454. This articled shows both altered methylation and histone modifications at the HNF4a promoter in pancreatic islet cells and suggested a link to T2DM risk.
22. Zheng S, Rollet M, Pan Y-X. Protein restriction during gestation alters histone modifications at the glucose transporter 4 (GLUT4) promoter region and induces GLUT4 expression in skeletal muscle of female rat offspring. J Nutr Biochem 2011; 6:161–170.
23. Zheng S, Rollet M, Pan Y-X. Maternal protein restriction during pregnancy & induces CCAAT/enhancer-binding protein (C/EBPb) expression through the regulation of histone modification at its promoter region in female offspring rat skeletal muscle. Epigenetics 2011; 6:161–170. Showed that maternal protein restriction led to sex-specific differences in the C/EBPb expression, which were associated with histone modifications.
24. Jousse C, Parry L, Lambert-Langlais S, et al. Perinatal undernutrition affects the methylation and expression of the leptin gene in adults: implication for the understanding of metabolic syndrome. FASEB J 2011; 25:3271–3278.
25. Slater-Jefferies JL, Lillycrop KA, Townsend PA, et al. Feeding a protein-restricted diet during pregnancy induces altered epigenetic regulation of peroxisomal proliferator-activated receptor-a in the heart of the offspring.
J Dev Origins Health Dis 2011; 2:250–255.
26. McKay JA, Williams EA, Mathers JC. Effect of maternal and postweaning folate supply on gene-specific DNA methylation in the small intestine of
weaning and adult APC and wild type mice. Frontiers Gen 2011; 2:23.
27. McKay JA, Wong YK, Relton CL, et al. Maternal folate supply and sex influence gene-specific DNA methylation in the fetal gut. Mol Nutr Food Res 2011;
55:1717 – 1723.
28. McKay JA, Waltham KJ, Williams EA, et al. Folate depletion during pregnancy & and lactation reduces genomic DNA methylation in murine adult offspring. Genes Nutr 2011; 6:189 – 196. This study shows that low folate diets results led to global hypomethylation in the small intestine of 100-day old offspring, in mice.
29. Hoile SP, Lillycrop KA, Grenfell LR, et al. Increasing the folic acid content of && maternal or postweaning diets induces differential changes in phosphoenol-pyruvate carboxykinase mRNA expression and promoter methylation in rats. Br J Nutr 2011; 10.1017/S0007114511006155.
This is the first study to show both time and sex-related differences in DNA methylation following folic acid supplementation in the rat. Altered methylation of a specific CpG of the PEPCK was associated with altered transcription factor binding.
30. Schaible TD, Harris RA, Dowd SE, et al. Maternal methyl-donor supplementation induces prolonged murine offspring colitis susceptibility in association with mucosal epigenetic and microbiomic changes. Human Mol Gen 2011; 20:1687 – 1696.
31. Roseboom TJ, Van Der Meulen JH, Ravelli AC, et al. Effects of prenatal exposure to the Dutch famine on adult disease in later life: an overview. Mol
Cell Endocrinol 2001; 185:93 – 98.
32. Heijmans BT, Tobi EW, Stein AD, et al. Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proc Natl Acad Sci USA 2008; 105:17046 – 17049.
33. Tobi EW, Lumey LH, Talens RP, et al. DNA Methylation differences after exposure to prenatal famine are common and timing- and sex-specific. Hum Mol Genet 2009; 18:1460 – 2083.
34. Talens RP, Jukema JW, Trompet S, et al. Hypermethylation at loci sensitive to the prenatal environment is associated with increased incidence of myocardial infarction. Int J Epidemiol 2011; 41:106 – 115.
35. Godfrey KM, Sheppard A, Gluckman PD, et al. Epigenetic gene promoter & methylation at birth is associated with child’s later adiposity. Diabetes 2011;
60:1528 – 1534. This study used Sequenom Mass Array to show umbilical RXRA promoter methylation at specific loci accounted for variation in childhood adiposity.
36. Harvey NC, Lillycrop KA, Garratt E, et al. Evaluation of methylation status of the eNOS promoter at birth in relation to childhood bone mineral content. Cal
Tissue Int 2012; 90:120 – 127.
37. Relton CL, Groom A, St. Pourcain B, et al. DNA methylation patterns in cord & blood DNA and body size in childhood. PLoS One 2012; 7:e31821. Using two birth cohorts, showed a link between methylation of a single CpG in the alkaline phosphatase gene in umbilical cord was associated with childhood body size.
38. Jablonka E, Raz G. Transgenerational epigenetic inheritance: prevalence, mechanisms, and implications for the study of heredity and evolution. Q Rev
Biol 2009; 84:131 – 176.
39. Burdge GC, Hoile SP, Uller T, et al. Progressive, transgenerational changes in & offspring phenotype and epigenotype following nutritional transition. PLoS
One 2011; 6:e28282. This study is the first to provide a mechanism by which offspring can adjust to transient environmental stimuli across multiple generations, through de-novo methylation of the epigenome in each generation.
40. Li CCY, Cropley JE, Cowley MJ, et al. A sustained dietary change & increases epigenetic variation in isogenic mice. PLoS Gen 2011;
7:e1001380. A six-generation mouse study, using methyl donors, which suggests that the environmental has an effect on epigenetic variation.
41. Ling C, Del Guerra S, Lupi R, et al. Epigenetic regulation of PPARGC1A in human type 2 diabetic islets and effect on insulin secretion. Diabetologia 2008; 51:615–622.
42. Toperoff G, Aran D, Kark JD, et al. Genome-wide survey reveals predisposing && diabetes type 2-related DNA methylation variations in human peripheral blood. Human Mol Gen 2012; 21:371 – 383. This is one of the first human genome-wide association studies to identify specific loci in blood leukocytes with links to T2DM risk. Methylation of the FTO gene was 3.4% lower in adults with T2DM, compared with those without.
43. Bell CG, Finer S, Lindgren CM, et al. Integrated genetic and epigenetic analysis identifies haplotype-specific methylation in the FTO type 2 diabetes
and obesity susceptibility locus. PloS One 2010; 5:e14040.
44. Yang BT, Dayeh TA, Kirkpatrick CL, et al. Insulin promoter DNA methylation correlates negatively with insulin gene expression and positively with HbA(1c)
levels in human pancreatic islets. Diabetologia 2011; 54:360 – 367.
45. Volkmar M, Dedeurwaerder S, Cunha DA, et al. DNA methylation profiling & identifies epigenetic dysregulation in pancreatic islets from type 2 diabetic
patients. EMBO J 2012; 31:1405 – 1426. This is another human genome-wide association study, which has identified loci, with links to T2DM, which appear specific to pancreatic islets.
46. Zhao J, Goldberg J, Bremner JD, et al. Global DNA methylation is associated with insulin resistance: a monozygotic twin study. Diabetes 2012; 61 :542-546.
47. Zhang FF, Cardarelli R, Carroll J, et al. Physical activity and global genomic & DNA methylation in a cancer-free population. Epigenetics 2011; 6:293 – 299. This article shows a link between acute exercise and global levels of methylation.
48. Barre` s R, Yan J, Egan B, et al. Acute exercise remodels promoter methylation && in human skeletal muscle. Cell Met 2012; 15:405 – 411. This study provides a more specific link between exercise and methylation, through investigation of specific gene promoters. Incremental acute exercise to fatigue was used to show PGC-1a, PDK4, and PPAR-d hypomethylation.
49. Burdge GC, Lillycrop KA, Jackson AA. Nutrition in early life, and risk of cancer and metabolic disease: alternative endings in an epigenetic tale? Br J Nutr
2009; 101:619 – 630.
50. Wong EM, Southey MC, Fox SB, et al. Constitutional methylation of the BRCA1 promoter is specifically associated with BRCA1 mutation-associated
pathology in early-onset breast cancer. Cancer Prev Res 2011; 4:23 – 33.
51. Papoutsis AJ, Borg JL, Selmin OI, et al. BRCA-1 promoter hypermethylation and silencing induced by the aromatic hydrocarbon receptor-ligand TCDD are prevented by resveratrol in MCF-7 Cells. J Nutr Biochem 2011; 10.1016/
j.jnutbio.2011.08.001.
52. Junaid MA, Kuizon S, Cardona J, et al. Folic acid supplementation dysregulates gene expression in lymphoblastoid cells–implications in nutrition. Bio-
chem Biophys Res Comm 2011; 412:688 – 692.
53. Ceccarelli V, Racanicchi S, Martelli MP, et al. Eicosapentaenoic acid de- & methylates a single CpG that mediates expression of tumor suppressor
CCAAT/enhancer-binding protein delta in U937 leukemia cells. J Biol Chem 2011; 286:27092 – 27102. This study shows a direct link between eicosapentaenoic acid supplementation and methylation of a single CpG in the C/EBPd promoter in vitro.
54. Piyathilake CJ, Macaluso M, Alvarez RD, et al. A higher degree of LINE-1 methylation in peripheral blood mononuclear cells, a one-carbon nutrient-related epigenetic alteration, is associated with a lower risk of developing cervical intraepithelial neoplasia. Nutri 2011; 27:513 – 519.
55. Zeng H, Irwin ML, Lu L, et al. Physical activity and breast cancer survival: an epigenetic link through reduced methylation of a tumor suppressor gene L3MBTL1. Breast Cancer Res Treat 2012; 133:127 – 135.
Professional Scope of Practice *
The information herein on "How Epigenetics Affects Personalized Nutrition" is not intended to replace a one-on-one relationship with a qualified health care professional or licensed physician and is not medical advice. We encourage you to make healthcare decisions based on your research and partnership with a qualified healthcare professional.
Blog Information & Scope Discussions
Our information scope is limited to Chiropractic, musculoskeletal, physical medicines, wellness, contributing etiological viscerosomatic disturbances within clinical presentations, associated somatovisceral reflex clinical dynamics, subluxation complexes, sensitive health issues, and/or functional medicine articles, topics, and discussions.
We provide and present clinical collaboration with specialists from various disciplines. Each specialist is governed by their professional scope of practice and their jurisdiction of licensure. We use functional health & wellness protocols to treat and support care for the injuries or disorders of the musculoskeletal system.
Our videos, posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate to and directly or indirectly support our clinical scope of practice.*
Our office has reasonably attempted to provide supportive citations and has identified the relevant research study or studies supporting our posts. We provide copies of supporting research studies available to regulatory boards and the public upon request.
We understand that we cover matters that require an additional explanation of how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez, DC, or contact us at 915-850-0900.
We are here to help you and your family.
Blessings
Dr. Alex Jimenez DC, MSACP, RN*, CCST, IFMCP*, CIFM*, ATN*
email: coach@elpasofunctionalmedicine.com
Licensed as a Doctor of Chiropractic (DC) in Texas & New Mexico*
Texas DC License # TX5807, New Mexico DC License # NM-DC2182
Licensed as a Registered Nurse (RN*) in Florida
Florida License RN License # RN9617241 (Control No. 3558029)
License Compact Status: Multi-State License: Authorized to Practice in 40 States*
Presently Matriculated: ICHS: MSN* FNP (Family Nurse Practitioner Program)
Dr. Alex Jimenez DC, MSACP, RN* CIFM*, IFMCP*, ATN*, CCST
My Digital Business Card
Could learning to apply healthy sleep hygiene habits help improve sleep and overall health for… Read More
Can incorporating natural probiotic foods help improve many people's gut health and restore functionality to… Read More
Experiencing a whiplash injury can be disorienting and painful. Can recognizing the signs of more… Read More
Individuals dealing with fibromyalgia can find natural remedies to reduce the pain-like symptoms and provide… Read More
For individuals who are looking for a whipped cream substitute for a dairy-free alternative, what… Read More
Can modified workouts and/or having a personal trainer design an alternate fitness routine while in… Read More