By Kelley Herring
Of course, you know that every human being looks different on the outside. But it’s easy to assume that we all work the same way on the inside. After all, we have the same organs and our bodies function in the same basic way.
Yet, that’s where the similarity ends…
You see, your biology and genetics are unique… and that means so are your dietary requirements. This is why two people can follow the same diet and achieve very different results. It is also why a healthy food for someone else… could actually make YOU sick!
In today’s article, you’ll discover how your specific genetics impact your risk for disease. More importantly, you will learn how to personalize your diet to optimize your genes, including:
- The specific “autoimmune gene” that increases your risk for diseases like lupus and rheumatoid arthritis – plus four foods and seven nutrients to inhibit it
- The specific foods and nutrients you need to boost methylation – the critical biological process that helps repair DNA, regulates hormones, supports detoxification, strengthens your nervous system and protects against cancer and other chronic disease.
- Whether you have the “alcohol flush-reaction gene” – and how this impacts your risk for certain cancers (and the specific foods and supplements that can help)
… plus dozens of simple dietary tricks you can use to “hack” your genes to optimize their expression!
First, however, let’s learn the basics of genetics…
Genetics 101
Inside all of your cells – with the exception of your red blood cells – is a nucleus containing DNA, or deoxyribonucleic acid. This double-helix strand of DNA holds the blueprint… for YOU!
Your DNA is made up of over three billion pairs of nucleotide bases which include: A (adenine), C (cytosine), G (guanine), and T (thymine). You have three billion base PAIRS (or bases) that bond to one another. And these bases pair up such that C bonds to G and A bonds to T.
Your three billion base pairs are organized into chromosomes. Humans all have 23 pairs of chromosomes, referred to as chromosomes 1-22 and the sex chromosomes X and Y. We get one set of chromosomes from Mom and the other from Dad.
Within these 23 chromosomes are 20,000+ regions that make up our genes. That may sound like a lot of genes… until you realize that a mouse has 30,000 different genes and rice has over 50,000!
So what do these 20,000 human genes do?
It’s pretty simple, actually:
1. Your DNA makes RNA.
2. Your RNA makes proteins.
Proteins are the building blocks for all of the cellular components and enzymes in your body. For example, melanin is the protein that gives skin and hair its color. We all have a gene that codes for the production of melanin. And it is the variable amount of melanin made by cells that cause variations in skin and hair color.
Single Nucleotide Polymorphisms (SNPs): The Genetic Differences that Make You Unique
Genetically speaking, humans are 99.9% alike. It’s the 0.1% difference that makes us unique!
The acronym you will see when reading about these differences is “SNP”, which stands for Single Nucleotide Polymorphism. This simply means there is a change in one (single) DNA base (the A, C, G, T) and that change occurs in more than 1% of the population.
What can a SNP do? Sometimes changing just one amino acid building block can affect the structure of a protein in a way that it doesn’t function as well. Other SNPs can be in a region on the gene that controls how much of a protein is made.
Research shows that some SNPs can cause a real impact on our risk for chronic disease, and that diet can play a role in mitigating this risk.
For example, consider the LCT (lactase enzyme) gene…
One genetic variant of the LCT gene allows people to still produce lactase (the enzyme that breaks down milk) as an adult. However, if you don’t carry the variant to produce lactase as an adult, you may find that dairy causes digestive problems. Knowing this, you can omit milk, switch to lactose-free milk, or add helper enzymes to your diet, like lactobacillus probiotics or lacto-fermented foods (like kimchi, kefir).
Let’s recap the science so far:
1. Genes code for proteins (and enzymes) that make our body function
2. SNPs can cause an increase, decrease or no effect on those proteins / enzymes
3. We all have lots of SNPs that make us unique!
Keep in mind that SNPs won’t cause you to suddenly develop a disease. They simply indicate that you may be at an increased risk.
But here’s the great news…
There’s a LOT you can do with your diet to mitigate those risks!
In the remainder of this guide, you’ll discover the specific SNPs and how you can use diet to optimize them.
(NOTE: If you have taken a 23andMe panel, simply log into your account and go to the Tools section to look up these SNPs. There you will find an option to “Browse Raw Data”. Just plug in the numbers listed below – starting with “rs” – and you will be able to see your genotype for that SNP.)
Inflammation Response: TNF-α (TNFA) Genetic Variants
Tumor necrosis factor alpha is a type of cell-signaling molecule known as a cytokine. It signals to the immune system that a response is needed.
TNF-α acts as an immunoregulator, increasing the inflammatory response when needed. Genetic variants of TNF-α can leading to over-activation of the immune response, which has been linked to an increased risk of rheumatoid arthritis, lupus,1 ulcerative colitis,2 Hashimoto’s thyroiditis, Graves’ disease,3 periodontitis,4 and diabetic foot ulcers.5
However, increased TNF-α can be a positive factor when dealing with pathogens. In fact, the genetic variants that increase its function are actually protective against the recurrence of malaria,6 leprosy,7and dengue fever.8 Increased TNF also signals the body for increased bone turnover, which decreases the risk of osteoporosis.9
rs1800629 (23andMe v4, v5 and AncestryDNA)
- AA: Increased TNF-α levels
- AG: Moderately increased TNF-α levels
- GG: Normal TNF-α levels
Your Personalized TNF-α Diet
Several spices and herbs used traditionally in cooking are effective inhibitors of TNF-α. Let’s take a look at the natural ways to reduce TNF α:
- Curcumin (found in turmeric), has been shown to block inflammation by reducing TNF-α.10
- Rosmarinic acid (found in rosemary, basil, holy basil, lemon balm and perilla oil) is another natural TNF-α inhibitor.11
- Glycine (an important amino acid abundant in bone broth, gelatin, and collagen) helps decrease the inflammation signaled by TNF-α.12
- Magnesium has also been shown in studies to decrease TNF levels.13 Spinach, almonds, and quinoa are good food sources of magnesium.
Alcohol Flush Reaction: ALDH2 – Acetaldehyde Dehydrogenase Gene
Alcohol is initially broken down in the liver and converted into acetaldehyde – a compound that is fairly toxic to your body. The enzyme acetaldehyde dehydrogenase then converts the acetaldehyde into acetate. It is the intermediate step – the acetaldehyde – that can make your face flush and cause you to feel poorly when drinking alcohol.
A genetic variant in the ALDH2 gene causes a decrease in function of the enzyme, thus causing an increased flushing reaction to alcohol – not to mention, worse hangovers! The variant is fairly rare in Caucasian populations, but it is found in up to 40 percent of people with Asian backgrounds.
Unfortunately, recent research from the MRC Laboratory of Molecular Biology at Cambridge found a link between acetaldehyde and damage to DNA in blood stem cells. Researchers also discovered that those with ALDH2 deficiency were subject to 4 times more DNA damage than subjects without the deficiency.14
Given this, it is unsurprising that those with the ALDH2 gene are at increased risk for cancers of the esophagus, head and neck, breast, colon and rectum.15,16
Acting Director of National Institute on Alcohol Abuse and Alcoholism (NIAAA), Dr. Kenneth R. Warren, Ph.D. says:
“It is very important for clinicians who treat patients of East Asian descent to be aware of the risk of esophageal cancer from alcohol consumption in their patients who exhibit the alcohol flushing response, so they can counsel them about limiting their drinking“
Here’s what to look for in your genetics:
rs671 (23andMe v4, v5 and AncestryDNA)
- AA: Alcohol flush reaction
- AG: Alcohol flush reaction
- GG: normal acetaldehyde metabolism
Your ALDH2 Personalized Diet
If you carry the genetic variant for alcohol flush reaction, the simple solution is to not drink very much (if any) alcohol.
Also, it is important to note that white wine tends to be very high in acetaldehyde – almost double that of red wine! While all alcohol metabolism will produce acetaldehyde (and more acetaldehyde is produced as consumption goes up), some alcohols are naturally higher in acetaldehyde.
So, if you are sensitive to these compounds, take note of how you feel after consuming different types of alcoholic beverages.17
Further, boosting glutathione – your body’s master antioxidant and detoxifier – is very important if you carry the ALDH2 gene. In fact, the cysteine component of glutathione has been found to reduce acetaldehyde in the stomach after alcohol consumption.18
In addition to eating cysteine-rich foods like eggs, whey protein, pastured meats and broccoli sprouts, consider taking N-Acetyl-Cysteine (NAC) – a simple amino acid supplement that can boost your body’s natural production of glutathione.19,20
Folate Metabolism: The MTHFR Gene
The MTHFR gene codes for an enzyme (methlenetetrahydrofolate reductase) that is important for folate metabolism. It takes the folate from foods and transforms it into the active version that your body needs for many processes in the methylation cycle. The C677t genetic variant caused a reduction in the enzyme availability. This is linked to an increased risk of higher levels of homocysteine (a marker of inflammation) as well as heart disease. 21
rs1801133 MTHFR C677T (23andMe v4, v5 and AncestryDNA)
- GG: normal folate metabolism
- AG: one copy of C677T allele (heterozygous), MTHFR efficiency reduced by 40%
- AA: two copies of C677T (homozygous), MTHFR efficiency reduced by 70 – 80%
rs1801131 MTHFR A1298C (23andMe v4, v5 and AncestryDNA)
- TT: normal folate metabolism
- GT: one copy of A1298C allele (heterozygous), MTHFR efficiency slightly reduced
- GG: two copies of A1298C (homozygous), MTHFR efficiency reduced
*Note that both of these are flipped to be the plus orientation to match up with 23andMe and AncestryDNA results.
Your MTHFR Personalized Diet
Getting enough folate is important for everyone. But it is particularly important if you have one of the MTHFR genetic variants. Good food sources of folate include legumes and dark green leafy vegetables.
Within the methylation cycle, choline and its metabolite betaine also play an important role. If your folate is less than optimal due to an MTFHR variant, supporting methylation by getting enough choline is important.i Foods that are high in choline include beef liver and egg yolks. Foods high in betaine include beets, quinoa, and spinach.
Finally, it’s important to note that if you take vitamins, the specific form of B vitamins is very important for those with MTHFR variants. Methylated vitamins – such as methylcobalamin – are a better choice than what you will find in cheap, commercial vitamin brands.
Please stay tuned for Part II of this article. You will continue to learn how to optimize your genetics, by making wise (and informed) choices about your diet and lifestyle! Here’s a small taste of what you’ll discover…
- How to know if you are a “slow metabolizer” of caffeine (and what it means for heart)
- Three “bio-hacks” if you lack the enzymes to digest milk
- Discover how many carbs your body is designed to handle (plus, how to personalize your macronutrient ratio to your genes!)
Part II – Create The Perfect Personalized Diet For Your Genetics can be found HERE. Read more of Kelley Herring’s Health & Wellness articles on our Discover Blog.
Ed Note: Need some kitchen inspiration? Grab Kelley’s free guide – Instant Pot Keto Dinners – made exclusively with Paleo-and-Keto ingredients, for quick and delicious meals that taste just as good – of not better – than your restaurant favorites. Get your free guide here.
References
-
-
- Postal M, Appenzeller S. The role of Tumor Necrosis Factor-alpha (TNF-α) in the pathogenesis of systemic lupus erythematosus. Cytokine. 2011 Dec;56(3):537-43. doi: 10.1016/j.cyto.2011.08.026. Epub 2011 Sep 9. PMID: 21907587. https://www.ncbi.nlm.nih.gov/pubmed/21907587.
- Tavares M, de Lima C, Fernandes W, Martinelli V, de Lucena M, Lima F, Telles A, Brandão L, de Melo Júnior M. Tumour necrosis factor-alpha (-308G/A) promoter polymorphism is associated with ulcerative colitis in Brazilian patients. Int J Immunogenet. 2016 Dec;43(6):376-382. doi: 10.1111/iji.12289. Epub 2016 Aug 16. PMID: 27528546. https://www.ncbi.nlm.nih.gov/pubmed/27528546
- Durães C, Moreira CS, Alvelos I, Mendes A, Santos LR, Machado JC, Melo M, Esteves C, Neves C, Sobrinho-Simões M, Soares P. Polymorphisms in the TNFA and IL6 genes represent risk factors for autoimmune thyroid disease. PLoS One. 2014 Aug 15;9(8):e105492. doi: 10.1371/journal.pone.0105492. PMID: 25127106; PMCID: PMC4134306. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4134306/ e
- Ding C, Ji X, Chen X, Xu Y, Zhong L. TNF-α gene promoter polymorphisms contribute to periodontitis susceptibility: evidence from 46 studies. J Clin Periodontol. 2014 Aug;41(8):748-59. doi: 10.1111/jcpe.12279. Epub 2014 Jul 2. PMID: 24905365. https://www.ncbi.nlm.nih.gov/pubmed/24905365 .
- Viswanathan V, Dhamodharan U, Srinivasan V, Rajaram R, Aravindhan V. Single nucleotide polymorphisms in cytokine/chemokine genes are associated with severe infection, ulcer grade and amputation in diabetic foot ulcer. Int J Biol Macromol. 2018 Oct 15;118(Pt B):1995-2000. doi: 10.1016/j.ijbiomac.2018.07.083. Epub 2018 Jul 14. PMID: 30009916. https://www.ncbi.nlm.nih.gov/pubmed/30009916
- Gichohi-Wainaina WN, Melse-Boonstra A, Feskens EJ, Demir AY, Veenemans J, Verhoef H. Tumour necrosis factor allele variants and their association with the occurrence and severity of malaria in African children: a longitudinal study. Malar J. 2015 Jun 20;14:249. doi: 10.1186/s12936-015-0767-3. PMID: 26088606; PMCID: PMC4474355. https://www.ncbi.nlm.nih.gov/pubmed/26088606.
- Cardoso CC, Pereira AC, Brito-de-Souza VN, Duraes SM, Ribeiro-Alves M, Nery JA, Francio ÂS, Vanderborght PR, Parelli FP, Alter A, Salgado JL, Sampaio EP, Santos AR, Oliveira ML, Sarno EN, Schurr E, Mira MT, Pacheco AG, Moraes MO. TNF -308G>A single nucleotide polymorphism is associated with leprosy among Brazilians: a genetic epidemiology assessment, meta-analysis, and functional study. J Infect Dis. 2011 Oct 15;204(8):1256-63. doi: 10.1093/infdis/jir521. PMID: 21917899. https://www.ncbi.nlm.nih.gov/pubmed/21917899.
- Oliveira M, Saraiva DP, Cavadas B, Fernandes V, Pedro N, Casademont I, Koeth F, Alshamali F, Harich N, Cherni L, Sierra B, Guzman MG, Sakuntabhai A, Pereira L. Population genetics-informed meta-analysis in seven genes associated with risk to dengue fever disease. Infect Genet Evol. 2018 Aug;62:60-72. doi: 10.1016/j.meegid.2018.04.018. Epub 2018 Apr 17. PMID: 29673983. https://www.ncbi.nlm.nih.gov/pubmed/29673983.
- Kotrych D, Dziedziejko V, Safranow K, Sroczynski T, Staniszewska M, Juzyszyn Z, Pawlik A. TNF-α and IL10 gene polymorphisms in women with postmenopausal osteoporosis. Eur J Obstet Gynecol Reprod Biol. 2016 Apr;199:92-5. doi: 10.1016/j.ejogrb.2016.01.037. Epub 2016 Feb 8. PMID: 26914399. https://www.ncbi.nlm.nih.gov/pubmed/26914399
- Aggarwal BB, Gupta SC, Sung B. Curcumin: an orally bioavailable blocker of TNF and other pro-inflammatory biomarkers. Br J Pharmacol. 2013 Aug;169(8):1672-92. doi: 10.1111/bph.12131. PMID: 23425071; PMCID: PMC3753829.
https://www.ncbi.nlm.nih.gov/pubmed/23425071. - Shao N, Jia H, Li Y, Li J. Curcumin improves treatment outcome of Takayasu arteritis patients by reducing TNF-α: a randomized placebo-controlled double-blind clinical trial. Immunol Res. 2017 Aug;65(4):969-974. doi: 10.1007/s12026-017-8917-z. PMID: 28349250. https://www.ncbi.nlm.nih.gov/pubmed/28349250.
- Blancas-Flores G, Alarcón-Aguilar FJ, García-Macedo R, Almanza-Pérez JC, Flores-Sáenz JL, Román-Ramos R, Ventura-Gallegos JL, Kumate J, Zentella-Dehesa A, Cruz M. Glycine suppresses TNF-α-induced activation of NF-κB in differentiated 3T3-L1 adipocytes. Eur J Pharmacol. 2012 Aug 15;689(1-3):270-7. doi: 10.1016/j.ejphar.2012.06.025. Epub 2012 Jun 23. PMID: 22732655. https://www.ncbi.nlm.nih.gov/pubmed/22732655.
- Yu X, Guan PP, Zhu D, Liang YY, Wang T, Wang ZY, Wang P. Magnesium Ions Inhibit the Expression of Tumor Necrosis Factor α and the Activity of γ-Secretase in a β-Amyloid Protein-Dependent Mechanism in APP/PS1 Transgenic Mice. Front Mol Neurosci. 2018 May 30;11:172. doi: 10.3389/fnmol.2018.00172. PMID: 29899688; PMCID: PMC5988891.
https://www.ncbi.nlm.nih.gov/pubmed/29899688 . - Garaycoechea, J., Crossan, G., Langevin, F. et al. Alcohol and endogenous aldehydes damage chromosomes and mutate stem cells. Nature 553, 171–177 (2018). https://doi.org/10.1038/nature25154
- Grewal P, Viswanathen VA. Liver cancer and alcohol. Clin Liver Dis. 2012 Nov;16(4):839-50. doi: 10.1016/j.cld.2012.08.011. PMID: 23101985. https://pubmed.ncbi.nlm.nih.gov/23101985/
- Hamajima N, Hirose K, Tajima K, Rohan T, et al.; Collaborative Group on Hormonal Factors in Breast Cancer. Alcohol, tobacco and breast cancer–collaborative reanalysis of individual data from 53 epidemiological studies, including 58,515 women with breast cancer and 95,067 women without the disease. Br J Cancer. 2002 Nov 18;87(11):1234-45. doi: 10.1038/sj.bjc.6600596. PMID: 12439712; PMCID: PMC2562507. https://pubmed.ncbi.nlm.nih.gov/12439712/
- Kim SH, Jung HJ, Lee JH. Changes in the levels of headspace volatiles, including acetaldehyde and formaldehyde, in red and white wine following light irradiation. J Food Sci. 2021 Mar;86(3):834-841. doi: 10.1111/1750-3841.15642. Epub 2021 Feb 13. PMID: 33580549. https://pubmed.ncbi.nlm.nih.gov/33580549/
- Linderborg K, Marvola T, Marvola M, Salaspuro M, Färkkilä M, Väkeväinen S. Reducing carcinogenic acetaldehyde exposure in the achlorhydric stomach with cysteine. Alcohol Clin Exp Res. 2011 Mar;35(3):516-22. doi: 10.1111/j.1530-0277.2010.01368.x. Epub 2010 Dec 8. PMID: 21143248. https://pubmed.ncbi.nlm.nih.gov/21143248/
- Vanduchova A, Anzenbacher P, Anzenbacherova E. Isothiocyanate from Broccoli, Sulforaphane, and Its Properties. J Med Food. 2019 Feb;22(2):121-126. doi: 10.1089/jmf.2018.0024. Epub 2018 Oct 27. PMID: 30372361. https://pubmed.ncbi.nlm.nih.gov/30372361/
- Bumrungpert A, Pavadhgul P, Nunthanawanich P, Sirikanchanarod A, Adulbhan A. Whey Protein Supplementation Improves Nutritional Status, Glutathione Levels, and Immune Function in Cancer Patients: A Randomized, Double-Blind Controlled Trial. J Med Food. 2018 Jun;21(6):612-616. doi: 10.1089/jmf.2017.4080. Epub 2018 Mar 12. PMID: 29565716. https://pubmed.ncbi.nlm.nih.gov/29565716/
- Liew SC, Gupta ED. Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism: epidemiology, metabolism and the associated diseases. Eur J Med Genet. 2015 Jan;58(1):1-10. doi: 10.1016/j.ejmg.2014.10.004. Epub 2014 Nov 4. PMID: 25449138. https://pubmed.ncbi.nlm.nih.gov/25449138/
- Ganz AB, Shields K, Fomin VG, Lopez YS, Mohan S, Lovesky J, Chuang JC, Ganti A, Carrier B, Yan J, Taeswuan S, Cohen VV, Swersky CC, Stover JA, Vitiello GA, Malysheva OV, Mudrak E, Caudill MA. Genetic impairments in folate enzymes increase dependence on dietary choline for phosphatidylcholine production at the expense of betaine synthesis. FASEB J. 2016 Oct;30(10):3321-3333. doi: 10.1096/fj.201500138RR. Epub 2016 Jun 24. PMID: 27342765; PMCID: PMC5024689. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5024689/
-