Nutrigenomics for Prostate Health
Written by Mille Lytle, ND, MPH, CNS
The field of nutrigenomics is a subfield of epigenetics. These are big words but their concepts are relatively simple.
What is Epigenetics?
Epigenetics is the study of the behavior of genetic material (RNA and DNA) through variations in the cellular environment. Epigenetics fundamental principle states that the cellular environment of the gene determines how the gene behaves, rather than the mere presence of the gene code itself. Therefore the health of the organism, as a whole, is directly affected by the expression of the gene, not just its presence. This is known as gene behavior.1 For example, just because you are born with the genetic predisposition to develop prostate cancer, does not mean that you will. Like a light switch, genes can be turned in one direction toward health and youth or “expressed” in the opposite direction towards illness and aging. What determines the expression of the genes, is the environment of the cell. The cellular environment is a combination of many factors, which include thoughts and emotions, detoxification and the nutrients present. This latter field of research is called nutrigenomics.
What is Nutrigenomics?
Nutrigenomics is the study of the relationship between nutrients and the genes.2 It acknowledges that genetic expression of the cell, be it towards vitality or cancer, is in part determined by the presence of specific nutritional components surrounding the DNA and RNA. The degree of methylation, the ability of the cell to reject and detoxify old harmful material, antioxidant activity and the cell's ability to replicate normally without mutation are all components of nutrigenomics, which is measured over generations of cell cycles. If you think this does not apply to you, think again! While medical research continues to advance, this area of research, called Nutrigenomic testing, is moving into the clinical and even the commercial realm. It is even possible for the average consumer to have their DNA sequenced for the low cost of $99!
Cells of the body are differentiated according to the organs and function. Prostate cells are specific in their own way. Some lifestyle factors have consistently shown to be negatively correlated with prostate cancer risk. Increasing age, smoking and low serum selenium levels are significantly associated with an increased risk for prostate disease at the epigenetic level.3 Alcohol consumption increased the glutathione peroxidase (GPx) activity, as well.
I decided to review some ongoing information and studies regarding specific nutrients and their protection of prostate cells according to nutrigenomic theories. This is what I have discovered:
Twenty men with diagnosed prostate cancer adhered to a Mediterranean diet, with specific adaptations, for three months. Prostate-specific antigen (PSA), C-reactive protein (CRP) and DNA damage were evaluated at baseline and after three months of following the diet. Dietary data was collated from diet diaries and an adaptation of a validated Mediterranean diet questionnaire. A significant reduction in DNA damage compared to baseline was apparent, with particular benefit noted for overall adherence to the diet, increased intake of folate, vitamin, legumes and green tea. Higher intakes of red meat and dairy products were inversely associated with DNA damage, meaning higher red meat and dairy consumption was associated with abnormal cells. The results from this small feasibility study suggest that a high-antioxidant diet, modelled on Mediterranean traditions, may be of benefit for men with prostate cancer. Protection against DNA damage appears to be associated with the diet implemented, theorized to be due to reduction in free radical damage from Reactive Oxygen Species.
One clinical trial indicated that men who consume more superfoods such as broccoli, pomegranate, green tea and turmeric, have a short-term, favorable effect on the percentage rise in PSA following ingestion of this well-tolerated, specific blend of concentrated food. Its influence on decision-making suggests that this intervention is clinically meaningful, but further trials will evaluate longer term clinical effects, and other makers of disease progression.5
Despite public health and animal studies strongly supporting a relationship between eating soy isoflavone and protection of breast and prostate cancer, results are confusing. The body’s processes modulated by isoflavones, and especially by genistein, have been extensively studied. Studies have found that study results have not often taken all the information into account. Too often knowledge on isoflavone bioavailability or absorbability is not considered. Sometimes higher levels of Isoflavones are given in order to compensate for low levels of microflora (good bacteria) in the gut. Not only is it important to consider the individual strains and levels of available gut bacteria, but genetic variations may also help to explain the discrepancies observed so far in the clinical studies. Finally, the relationships between the type of cell and the metabolism of the nutritional Isoflavones are required in order to understand when these helpful phytoestrogens are helpful for prostate cells.6
Selenium may affect prostate cancer risk via its plasma carrier selenoprotein P, which shows dramatically reduced expression in prostate cancer tumors and cell lines. The selenoprotein P (SEPP1) Ala234 single nucleotide polymorphism (SNP) allele is associated with lower plasma selenoprotein P in men, reducing the concentration/activity of other antioxidant selenoproteins. Selenium status also modifies the effect of the mitochondrial superoxide dismutase (SOD) on prostate cancer risk. Researchers in this study measured the relationship of SNPs, genetic variations and prostate cancer. DNA from 2,975 men with prostate cancer were genotyped and allocated to aggressive or non-aggressive prostate cancers. From the population-based Prostate Cancer study in Sweden, 1,896 age-matched controls were compared. Those men who were positive with the genetic variation were at a greater risk of prostate cancer as well as aggressive prostate cancer. This interaction was stronger in men who had ever smoked, having an almost doubled risk of prostate cancer. In a low-selenium population without prostate cancer, an increased risk of prostate cancer/aggressive prostate cancer was especially present if ever-smokers, because they are likely to produce more mitochondrial hydrogen peroxide, a Reactive Oxygen Species, that they cannot remove, thereby promoting prostate tumor cell proliferation and migration.7
Omega-3 Fatty Acids
The type of dietary fat matters for prostate cells. Low intakes of Omega 3 fatty acids (EPA and DHA) combined with polymorphisms at inflammatory enzyme COX-2 increase the risk for prostate cancer.8 The literature suggests that fish, and particularly long-chain omega-3 PUFAs, may have a more pronounced protective effect on biologically aggressive tumors or on their progression, and less on early steps of cancer cell promotion. Moreover, the impact of Long Chain Pmega-3 Poly Unsaturated Fatty Acids (PUFAs) may be modified by variation of the COX-2 gene. Overall, results to date support the hypothesis that long-chain omega-3 PUFAs may impact prostate inflammation and carcinogenesis via the COX-2 enzymatic pathway.9 In contrast, DNA damage was correlated with various dietary fat sources and types of dietary fat.10 In another study blood fatty acid levels, PSA, C-reactive protein and DNA damage were assessed pre- and post-intervention. DNA damage was inversely correlated with dietary adherence and whole blood monounsaturated fatty acids and Omega-9. DNA damage was positively correlated with the intake of dairy products, red meat, and whole blood omega-6 polyunsaturated fatty acids. Both the source and type of dietary fat changed significantly over the course of the dietary intervention.10
While this research, that shows why some people do better with some nutrients than others,is a great start, it is suggested by nutrigenomic researchers that genome-wide association studies need to include environmental exposures as well as dietary nutrients in the interaction between genetic variation and prostate disease association.
- Science Daily. Epigenetics: DNA isn't everything. accessed July 14, 2015 http://www.sciencedaily.com/releases/2009/04/090412081315.htm
- University of California, Davis. Center of Excellence for Nutritional Genomics (CENG) accessed July 14, 2015 http://ghs.ucdavis.edu/
- Karunasinghe N, Han DY, Goudie M, Zhu S, Bishop K, Wang A, et al.Prostate disease risk factors among a New Zealand cohort. J Nutrigenet Nutrigenomics. 2012;5(6):339-51.
- Erdrich S, Bishop KS, Karunasinghe N, Han DY, Ferguson LR.A pilot study to investigate if New Zealand men with prostate cancer benefit from a Mediterranean-style diet PeerJ. 2015 Jul 2;3:e1080.
- Thomas R, Williams M, Sharma H, Chaudry A, Bellamy P. A double-blind, placebo-controlled randomised trial evaluating the effect of a polyphenol-rich whole food supplement on PSA progression in men with prostate cancer--the U.K. NCRN Pomi-T study. Prostate Cancer Prostatic Dis. 2014 Jun;17(2):180-6.
- Steiner C, Arnould S, Scalbert A, Manach C.Br J Nutr. Isoflavones and the prevention of breast and prostate cancer: new perspectives opened by nutrigenomics. 2008 May;99 E Suppl 1:ES78-108.
- Cooper ML, Adami HO, Grönberg H, Wiklund F, Green FR, Rayman MP. Interaction between single nucleotide polymorphisms in selenoprotein P and mitochondrial superoxide dismutase determines prostate cancer risk. Cancer Res. 2008 Dec 15;68(24):10171-7.
- Simopoulos AP. Genetic variants in the metabolism of omega-6 and omega-3 fatty acids: their role in the determination of nutritional requirements and chronic disease risk. Exp Biol Med (Maywood). 2010 Jul;235(7):785-95.
- Reese AC, Fradet V, Witte JS. Omega-3 fatty acids, genetic variants in COX-2 and prostate cancer. J Nutrigenet Nutrigenomics. 2009;2(3):149-58.
- Bishop KS, Erdrich S, Karunasinghe N, Han DY, Zhu S, Jesuthasan A, Ferguson LR.An investigation into the association between DNA damage and dietary fatty acid in men with prostatecancer. Nutrients. 2015 Jan 8;7(1):405-22.
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