Nutrigenomics: Can we change our genetics with nutrition?

Nutrigenomics: Can we change our genetics with nutrition?

Nutrigenomics is the next great scientific discipline that can change the healthcare metric. Bill Sardi explains how nutrition can influence the switching on and off of genes and improve health outcomes.

Conventional medicine may not be ready to fully embrace nutritional medicine, but the widespread adoption of nutraceuticals would certainly spare the medical world from its current misdirection and rescue it from its impending insolvency. Through nutrigenomics, we can even make healthcare affordable for many low-income groups. How? Natural molecules influence hundreds, even thousands, of genes, while pharmaceuticals narrowly target a specific gene or cell surface receptor.

Nutrigenomics refers to processes that regulate when certain genes are turned on and off. These can be triggered by environmental influences such as temperature, radiation exposure and diet. A major reason we are mired in the genetic slow lane of progress is that the public is misdirected. While it is true that we inherit our genetic makeup, only about two percent of diseases can be attributed to locked-in single-gene mutations. Incredibly, some inherited diseases due to gene mutations can also be remedied by nutrients via epigenetics.

Contrary to common belief, our genetic makeup is dynamic rather than static. It’s true that there is a permanence to inherited gene mutations—substitutions or deletions of nucleotides (adenine, guanine, cytosine, thymine) on the DNA ladder are permanent. But epigenetics refers to the protein-making capacity of genes.1 Our genetic makeup doesn’t necessarily determine our biological fate. Even inherited gene mutations such as those for progeria, a disease of premature aging, or Huntington’s disease, a brain-deteriorating disease, may be overcome with nutrition.


Nutrients, genes and aging

Dipak Das, PhD, at the University of Connecticut, in a paper published in the January 2011 Annals of the New York Academy of Sciences, documented how just one natural molecule, resveratrol (found in red wine), exhibits anti-inflammatory, antidepressant, cholesterol-lowering, anti-bacterial, anti-viral, anti-fungal, anti-brain plaque, anti-coagulant, and liver-detoxifying effects, all while elevating the production of internal antioxidants (glutathione, heme oxygenase).1,2 These wide-ranging benefits stem from resveratrol’s wide-ranging effect on the human genome, or library of genes.

Every cell in the human body houses a library of about 25,000 human genes. A recent study shows that only about 295 genes out of the 16,571 (or 2 percent) screened are significantly involved in the aging of human white blood cells—as measured by microRNA analysis—which suggests control of age-related diseases may be within reach.3

Here is where natural molecules shine—in particular a class of small molecules called polyphenols that can exert influence over many hundreds of genes.4 Polyphenols can be sourced from grapes (resveratrol, quercetin), berries (ellagic acid from raspberries), pomegranates (punicalagin, gallic acid), olives (hydroxytyrosol), green tea (EGCG) and spices (curcumin from turmeric).

Of course, natural medicines might pose a threat to modern pharmacology simply by virtue of their ability to reduce the number of required medicines. Also, natural medicines more appropriately address the rate of aging.5 This is particularly true for age-related illnesses, which comprise the vast majority of treated chronic disease today.

Recent revelations in the field of genetics may tip in favor of natural molecules, which more favorably influence the broader genome. The genomic impact of natural molecules on laboratory animals most closely mimicked a calorie-restricted diet—considered an unequivocal practice that nearly doubles the lifespan of all living organisms. Short-term provision of a modest dose of this matrix of natural molecules switched 677 of 831 known longevity genes in the same direction as long-term calorie restriction.6 Results like this suggest that a true anti-aging pill may not be far off.

In contrast, researchers at the University of Pittsburgh revealed, based upon genetic analysis, that prescription drugs unfavorably alter genes and provoke rather than avert disease.7 Researchers at the University of Pittsburgh Medical Center write:

It is becoming clear that a wide variety of common illnesses, behaviors, and other health conditions may have at least a partial epigenetic etiology, including cancer, respiratory, cardiovascular, reproductive, and autoimmune diseases, neurological disorders such as Parkinson’s, Alzheimer’s, and other cognitive dysfunctions, psychiatric illnesses, obesity and diabetes, infertility and sexual dysfunction. Effectors of epigenetic changes include many agents, such as heavy metals, pesticides, tobacco smoke, polycyclic aromatic hydrocarbons, hormones, radioactivity, viruses, bacteria, basic nutrients, and the social environment, including maternal care. It has even been suggested that our thoughts and emotions can induce epigenetic changes.
[Medical Hypotheses. 2009 Jun 4]

While aging affects many genes, there still may be a master gene that controls aging, since a single gene may control or be a marker for a whole gene pathway or network of genes. Early on, researchers thought they had found the holy grail of anti-aging in a single master gene, called Sirtuin1, a so-called survival gene that partially mimics the genetic action of a calorie-restricted diet,8 but this later proved to be misdirection.9

More recently, researchers have begun to investigate a related gene called Sirtuin3, and have discovered that mice bred to develop hearing loss by 12 months of age are completely resistant to this problem if they are placed on a calorie-restricted diet. But if the Sirtuin3 gene is removed from these animals, the protective effect is abolished.10 SIRT3 is the big gene involved in mitochondrial health and renewal. These results have little to do with hearing loss, per se. SIRT3 activation provokes aged mitochondria back to youthful function. This suggests molecules that activate the SIRT3 gene, such as the red wine molecule resveratrol, may be the true anti-aging agents.11


MicroRNA: The guiding hand of the human genome

MicroRNA are a newer way of measuring the on-off switches in the human genome and can be used as a measure of human aging.12 These small snippets of messenger RNA that escape from the cell nucleus may interlock with messenger RNA itself to stop the gene-activated synthesis of proteins, or what is called gene expression.13 MicroRNA lace on top of messenger RNA, thus shutting off genes. Imagine this for cancer genes or viral genes. There is great interest now in microRNA analysis of anti-viral therapy.14 MicroRNA are controlled by environmental factors, such as temperature, radiation and diet—the latter meaning molecular control of the genome with natural molecules is a reality.15

Everyone has the same 25,000 genes. You can globally improve gene expression in a broad array of genes involved inaging and disease without testing everyone for gene sensitivity; society doesn’t have money for personalized medicine. These small natural molecules work for all, not like man-made drugs that work only for a few. Personalized medicine has resulted in fewer drugs being utilized and paid for by insurance, an admission that many cancer chemotherapies are totally worthless.

Polyphenols are undergoing microRNA analysis, and the first studies are promising. One such study showed that resveratrol, and more so a resveratrol matrix combined with other small, natural molecules, restored the microRNA profile in post–heart attack animal hearts to near-normal pre–heart attack patterns.16

Personalized medicine: is it relevant?

We’re hearing more and more about personalized medicine—gene therapy tailored to your genetic makeup. There are now more than 1,700 tests for gene mutations that are linked to specific diseases.17 But wait a moment. Are the people with these single-gene mutations doomed to a fateful biological future? Not necessarily. There are many examples of gene mutations that can be overcome with nutritional medicines.18 In fact, single gene mutations that affect large portions of humanity call for widespread nutritional fortification and supplementation could have widespread benefits.

For example, all humans have a defective gulonolacone oxidase gene mutation that blocks the natural synthesis or handling of vitamin C. Animals produce vitamin C endogenously—not so in mutated humans. This is why ensuring adequate vitamin C in our diets is so important. Some East Asian populations have an additional genetic defect that interferes in their production of haptoglobin (Hp gene), an iron-binding protein that helps maintain adequate levels of vitamin C.19 Asians need even more vitamin C because of this genetic flaw.20

However, it should be noted the current recommended dietary intake for vitamin C is not sufficient to fully rectify either of the inherited problems noted above.21

Millions of people around the globe are also affected by the inability to properly metabolize folic acid, which can result in birth defects (spina bifida, anencephaly) and other health problems. This is due to mutations in two enzyme-producing genes (cystathionine-beta-synthase (CBS) and 5,10-methylenetetrahydrofolate reductase). There are many causes—radiation and toxins among them—but even modest nutrient shortages over the long term can result in gene mutations and pre-disease states. Folic acid supplementation overrides this inherited problem.22 Again, recommended daily allowances may not be effective in overcoming this inborn defect in folic acid metabolism.23

It seems obvious that public health authorities are asleep at the switch and that massive numbers of people with genetically inherited abnormalities in nutrient metabolization are left in an avoidable nutrient-deficient state. If we can fix common health problems simply by addressing nutrient-deficiency, we should be doing that.

Oddly, while commercialized tests to determine genetic susceptibility for disease are now being widely marketed, these tests often address gene mutations that affect a small portion of human populations (~1–2 percent), while gene mutations that broadly affect 40–100 percent of humanity are ignored. Such prevalent gene mutations should require no testing because they are so common that they call for mass food fortification programs.

At a recent symposium on nutrigenomic applications, it was said: “Dietary reference values, e.g. recommended dietary allowance (RDA) or safe upper limits, which are designed for the general population and based on different metabolic outcomes, are not optimized for genetic subgroups.”24 This should spell opportunity for the food and nutrition industry.


Nutrients to overcome obesogens

Another application for nutrigenomics is to overcome the many “obesogens”—chemicals that genetically induce obesity—that now are spread throughout the human diet and environment and have helped to spawn the current diabesity epidemic across the globe. This is especially true in developed countries where processed foods are abundant. One such chemical obesogen that genetically alters the control of hormones such as estrogen is bisphenol A—used to line the inside of tin cans and in some plastic bottles.25 By their epigenetic action, dietary flavonoids such as genistein (fava beans, soybeans), quercetin (onions, apple peel) and luteolin (olive oil, peppermint, rosemary, navel oranges and oregano) may counter the adverse effects posed by environmental estrogens.26

As one recent report concluded, “It is becoming increasingly evident that nutrigenetics and nutrigenomics are taking a central stage in the investigation of the effect of nutrition on health outcomes.”24 When the pharmaceutical drug patents all expire, natural molecules may rise to the top of the remedies humans employ to favorably influence their genome. In the long run, we can all hope for that day.





1 Kode A, et al, Resveratrol induces glutathione synthesis by activation of Nrf2 and protects against cigarette smoke-mediated oxidative stress in human lung epithelial cells. Am J Physiol Lung Cell Mol Physiol. 2008 Mar;294(3):L478-88. PMID: 18162601

2 Das DK, Maulik N, Resveratrol in cardioprotection: a therapeutic promise of alternative medicine. Mol Interv. 2006 Feb;6(1):36-47. PMID:16507749

3 Lorna W. Harries, Human aging is characterized by focused changes in gene expression and deregulation of alternative splicing. Aging Cell June 13, 2011 early onlinedoi: 10.1111/j.1474-9726.2011.00726.x

4 McKay JA, Mathers JC, Diet induced epigenetic changes and their implications for health. Acta Physiol (Oxf). 2011 Jun;202(2):103-18. doi: 10.1111/j.1748-1716.2011.02278.x. PMID: 21401888

5 Cherniack EP, The potential influence of plant polyphenols on the aging process.
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6 Barger JL, et al, Short-term consumption of a resveratrol-containing nutraceutical mixture mimics gene expression of long-term caloric restriction in mouse heart. Exp Gerontol. 2008 Sep;43(9):859-66. PMID: 18657603

7 Csoka AB, Szyf M, Epigenetic side-effects of common pharmaceuticals: a potential new field in medicine and pharmacology. Med Hypotheses. 2009 Nov;73(5):770-80. PMID: 19501473

8 Howitz KT, et al. Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan. Nature 2003 Sep 11;425(6954):191-6.

9 Pearson KJ, et al. Resveratrol delays age-related deterioration and mimics transcriptional aspects of dietary restriction without extending life span. Cell Metab. 2008 Aug;8(2):157-68. PMID: 18599363

10 Guarente L, Sirtuins, Aging, and Medicine. N Engl J Med 2011;364:2235-44.

11 Mukherjee S, et al, Effects of Longevinex (modified resveratrol) on cardioprotection and its mechanisms of action. Can J Physiol Pharmacol. 2010 Nov;88(11):1017-25. PMID:21076489

12 Kashyap L, Can microRNAs act as biomarkers of aging? Bioinformation. 2011 Feb 7;5(9):396-7. PMID: 21383908

13 Dennis C, Small RNAs: the genome's guiding hand? Nature. 2002 Dec 19-26;420(6917):732. PMID:12490907


15 Link A, Balaguer F, Goel A, Cancer chemoprevention by dietary polyphenols: promising role for epigenetics. Biochem Pharmacol. 2010 Dec 15;80(12):1771-92. Epub 2010 Jun 26. PMID: 20599773

16 Mukhopadhyay P, et al, Restoration of altered microRNA expression in the ischemic heart with resveratrol. PLoS One. 2010 Dec 23;5(12):e15705. PMID: 21203465


18 Jirtle RL, Skinner MK, Environmental epigenomics and disease susceptibility. Nat Rev Genet. 2007 Apr;8(4):253-62. PMID: 17363974

Kaput J, Diet-disease gene interactions. Nutrition. 2004 Jan;20(1):26-31.

PMID: 14698010

19 Cahill LE, El-Sohemy A, Haptoglobin genotype modifies the association between dietary vitamin C and serum ascorbic acid deficiency. Am J Clin Nutr. 2010 Dec;92(6):1494-500. PMID: 20926521

20 Soejima M, et al, The distribution of haptoglobin-gene deletion (Hpdel) is restricted to East AsiansTransfusion Volume 47, Issue 10 pages 1948–1950, October 2007  DOI: 10.1111/j.1537-2995.2007.01467.x

21 Carr AC, Frei B, Toward a new recommended dietary allowance for vitamin C based on antioxidant and health effects in humans. Am J Clin Nutr. 1999 Jun;69(6):1086-107. Review. PMID: 10357726

22 Boyles AL, et al, Folate and one-carbon metabolism gene polymorphisms and their associations with oral facial clefts. Am J Med Genet A. 2008 Feb 15;146A(4):440-9. PMID: 18203168

23 Fenech M, Recommended dietary allowances (RDAs) for genomic stability. Mutat Res. 2001 Sep 1;480-481:51-4. PMID: 11506798

24 Fenech M, et al, Nutrigenetics and Nutrigenomics: Viewpoints on the Current Status and Applications in Nutrition Research and Practice. J Nutrigenet Nutrigenomics. 2011 May 28;4(2):69-89. PMID: 21625170

25 Grün F, Obesogens. Curr Opin Endocrinol Diabetes Obes. 2010 Oct;17(5):453-9.
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26 Han DH, Denison MS, Tachibana H, Yamada K, Relationship between estrogen receptor-binding and estrogenic activities of environmental estrogens and suppression by flavonoids. Biosci Biotechnol Biochem. 2002 Jul;66(7):1479-87. PMID: 12224631

27 Martín-Subero JI, Esteller M, Profiling epigenetic alterations in disease. Adv Exp Med Biol. 2011;711:162-77. PMID: 21627049


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