What Genetic Tests Told Me About My Health & Longevity

Table of Contents

Most centenarians today are centenarians because of their exceptional genes.

A couple of years ago I decided to get my genetics tested. I bought kits from 23andMe, My Heritage, and Ancestry. I briefly looked at their reports but found them worthless. However, all three companies provide access to the raw data, which I then merged into a single file. I uploaded this to various online services, the most important of which was Promethease.

Obviously, genetic tests are to be taken with a huge grain of salt because the association between allele and phenotype often has a lot of confounding variables. Nonetheless, I found out a couple of interesting things, some of which had actionable insights.

Longevity

I have good versions of SIRT1 (hype created by David Sinclair), FOXO3 (common in centenarians), and CDK2ND (cyclin-dependent kinases are important in cell division), all of which are uncommon in the Caucasian general population, and all of which are associated with longevity.

Self-decode puts my genome-wide association longevity score at the 99th percentile, so I was ultra-lucky in this department (given that their percentiles have actual predictive power). Last year, my grandpa died at the age of 96 with no hint of dementia, cancer, or heart attack.

According to another genome-wide association study (GWAS), I am at the 97th percentile for genes associated with long-standing health without frailty.

Dementia

I have no APOE4 allele but two APOE3 alleles. A single copy of that gene increases the risk of Alzheimer’s by 300%. Two copies by roughly 1500%. Individuals with two copies get AD almost 90% of the time. Conversely, individuals with two E2 alleles get AD less than 1% of the time. Furthermore, I am homozygous for a “good” version of CETP (cholesterol-ester transfer protein) that is associated with a markedly reduced risk for dementia (20% of the population).

This means that my genetic risk for Alzheimer’s disease (the most common form of dementia) is somewhat low. I discuss my dementia prevention protocol here.

Cardiovascular disease

No adverse polymorphism in any lipoprotein-associated genes (e.g., Lp(a), LDL-R, PCSK9 function, HMG-Co-Reductase), which means that my risk for heart disease is not artificially elevated. Genetically, I am at the 15th percentile of Lp(a) levels. Lp(a) is the particle of death, and is highly associated with heart attack, stroke, and amputations.

Unfortunately, I have a Factor V Leiden mutation, which means that my risk for thromboembolism is higher than the general population. I discuss my atherosclerosis prevention protocol here.

Cancer

I have no deleterious polymorphisms in JAK2 (tyrosine kinase important in cell division), AKT1 (upstream of mTOR), and a beneficial polymorphism in p53 (cell cycle break; associated with a three-year longer lifespan; elephants have dozens of copies and thus get less cancer despite greater cell mass), which means that my genetic risk of cancer is on the lower end. However, my mum had breast cancer, and my dad had prostate cancer, so I do not know how much of this is true. Cancer prevention protocol here.

Diet

I have “normal” PPAR alpha and PPAR gamma alleles, which are important for fatty acid metabolism and insulin sensitivity. Polymorphisms with these genes are associated with a poor tolerance of high-fat diets from a metabolic standpoint.

Autoimmune disease

I do not have the dreaded HLAB27 polymorphism (allele important for presenting “foreign” peptide fragments to the immune system), an allele often associated with a large number of of autoimmune diseases.

Inflammation

I am homozygous for a gene associated with low CRP, another gene associated with low IL-6 levels, and a gene associated with low IL-23 levels. I am not sure of its real-world significance. Article on how I combat inflammation here.

“Bad genes”

I was quite lucky in that department. No APOE4, bad CETP, bad genes associated with high Lp(a) or bad lipid markers, or bad genes associated with cancer or autoimmunity. No monogenic diseases. The only really bad gene I have is a factor V Leiden mutation, meaning that my risk of clotting is considerably higher than the rest of the population – about 5% of Europeans have that gene. However, on blood tests, my clotting times are usually slower than the end of the reference range, which is weird.

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Other interesting or actionable insights

  • I have a couple of “adverse” polymorphisms in the SLC2A9 gene coding for the urate transporter, which is associated with high uric acid levels. This was no surprise, as my uric acid levels were always on the higher end, and for which I had been taking 150mg of allopurinol already.

  • I have a couple of polymorphisms associated with low vitamin D levels, and therefore increased my intake of vitamin D from 2000IU/d to 4000IU/d.

  • I have two versions of the “sprinter gene” (ACTN3), which is uncommon in Caucasians (25%) but very common in people of African origin. It is associated with an increased number of fast-twitch muscle fibers and with a lower risk of muscle injury.

  • I have a potentially deleterious allele in a NAC-transferase, which is associated with a 7x elevated risk for hearing loss. Therefore, I started to supplement with 300mg N-acetyl cysteine per day. My supplement protocol here.

  • I am homozygous for three genes associated with a reduced ability to detect bitter, which means that I like vegetables more than people without these SNPs (all else being equal), which in turn is associated with a lower risk of obesity.

  • I have a “bad” version of MTRR and two bad SNPS in MTHFR, both of which are associated with a “bad” methylation phenotype. Therefore, I supplement with 1mg L-methyl folate, and 1g TMG.

  • I have a gene associated with poor conversion of ALA. Therefore, I increased my omega-3 fatty acid intake.

  • I have a gene associated with a low synthesis of coenzyme Q10, which I now supplement with (60mg/d).

  • I have a couple of genes associated with less hairiness. I have little body hair, so that checks out. Not even a year of TRT increased my body hair by any significant degree.

  • I am homozygous for an allele (ABCC11) associated with less body odor and dry ear wax, which means that my risk for infections of my outer ear canal is low when I wear ear plugs.

  • I have two interesting SNPs associated with interleukins. Firstly, I have a SNP that is strongly associated with low IL-6 levels. I am also homozygous for an SNP (1%) associated with low IL-23 levels, which are associated with lower CRP levels.

  • I am homozygous for a version of CETP (cholesterol-ester transfer protein) that is associated with a markedly reduced risk for dementia (20% of the population). CETP inhibitors are currently being developed for atherosclerosis.

  • I have a normal MAO-A gene (so no “warrior gene”), but with moclobemide, I can mimic the phenotype.

  • I have normal JAK2 versions (leukemia/lymphoma risk). Janus kinase inhibitors are drugs that are used for autoimmune diseases or leukemia/lymphoma.

  • I have multiple genes associated with an increased risk of prostate cancer. My use of finasteride is thus not just good for reducing my rate of cosmetic aging but also for reducing my risk of prostate cancer.

I discuss the influence of genetics in more detail here: Biohacking Can’t Beat Genetics

My Longevity Protocol (Long & Technical Version)

This article is part of a much larger post describing my complete longevity blueprint. For my full protocol, read here.

Sources & further information

Disclaimer

The content on this website represents the opinion and personal experience of the author and does not constitute medical advice. The author does not endorse the use of supplements, pharmaceutical drugs, or hormones without a doctor’s supervision. The content presented is exclusively for informational and entertainment purposes. Never disregard professional medical advice or delay in seeking it because of something you have read on the internet.

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