Looks good on paper…

Home » science » health and wellbeing » The ultimate QS data: DNA?

The ultimate QS data: DNA?


So, in a sort of tedious but inevitable way, I did one of those DNA tests not so long back with 23andme. I was curious about the ancestry reports — no real surprises that I am 100% European — but was disappointed that they are no longer producing health reports. Another website, Promethease, will produce them, though, or at least pull together the literature regarding your genome and classify it as “good news”, “bad news”, or simply “interesting”.

It’s pretty cheap to run once you have the 23andme data, so costs perhaps $100 in total. I did mine mainly out of curiosity, and I don think DNA is the ‘ultimate’ QS data, but having got the report, I think it’s worth analysing a little more. Here is a quick review of the “news” that it gave me, what I make of it, what it means for me in trying to live an active and health life, and other bits that are just entertaining!


This is the biggie. The one that almost everyone wants to know the ‘answer’ to. Inevitably, there are no clear-cut answers, but there are plenty of genes that have been linked to higher or lower incidences of particular cancers. This is an aggregate of what I found out from my report, omitting prostate cancer as a non-issue in my case:

  • Slightly lower risk of bladder cancer according to one gene, but two others linked to an increased (3x or 1.4x) risk
  • 0.87x decreased risk for ovarian cancer according to one gene
  • Three genes linked to an increased (1.17x or 1.4x) risk of colorectal cancer, but also one linked to a ‘normal, risk and one linked to a decreased (0.73x) risk
  • Half the risk of endometrial cancer
  • Increased (1.64x, 1.6x, or 1.4x) risk of breast cancer according to four genes (two of which are themselves linked)
  • An increased (2.6x) risk of thyroid cancer
  • An increased risk (1.17x) of gastric cancer
  • One gene linked to an increased risk of lung cancer in non-smokers (which I am), and up to a 1.5x increased risk according to other genes.
  • “Generally more cancer prone”

So what do I take from this rather scary list of numbers?

First and foremost, I think genes linked to an increased risk of cancer are more likely to be sought out — and found — than those linked to a decreased risk. So there’s a real risk of ‘What a You See Is All There Is’ thinking arising out of receiving this list.
Second, cancer is always likely to touch one’s life at some point. Both of my maternal grandparents have had cancer, and they are non-smoking, light-drinking vegetarians. Shit happens. So, these may be interesting numbers, but I can’t put much store in them, except to keep an eye out for other studies that are shown to decrease rates of some of the cancers I might be most prone to (e.g. links between fibre intake and colorectal cancer).
Mental health and capacity

  • I have a “warrior” geneversus the “worrier” gene — whereby I lose dopamine more quickly than others. I am likely to have a higher pain threshold, better stress resiliency, but a “modest reduction in executive cognition performance under most conditions”; i.e. less good concentration and a less well-functioning prefrontal cortex in circumstances where I’m not under stress. The placebo effect is also apparently less effective on me.
This is interesting. Apparently, I should work best under stress, and this is probably true. I don’t know about the placebo effect being more or less effective (how would I tell?!), but making it easy for me to perform well in day-to-day life, e.g. by understanding and working with my working patterns, is something I need to give some though to.
  • I have a gene correlated with a 0.84x decreased risk of Alzheimer’s disease, and another with a 0.85x decreased risk, but another with a 3x increased risk. With one gene I have a reduced memory capacity, but with another I have a decreased (0.76x) risk of cognitive impairment as I age. Another indicates a higher dementia risk, especially amongst Ashkenazi Jews.
Tant pis? A bit like the cancer results, really. The picture is mixed, and genetic links to common ailments of ageing are something I cannot control. I’ll keep being vigilant about my sugar intake, given the current research suggesting that Alzheimer’s is Type-3 diabetes. My Ashkenazi Jewish heritage is quite far back in the family tree, but it’s interesting evidence in favour of being more vigilant about lifestyle factors implicated in dementia.
  • 1.29x increased risk for depression or 1.3x, or 1.4x. Another gene associated with impaired remission from depression. 7x less likely to respond to certain antidepressants, and 18% less likely to respond to citalopram. 
This is not a mixed picture. And it’s absolutely no surprise. We’re depressives in my family. I’ve never come anywhere near antidepressants medication (I’m generally opposed and I’ve written on the subject before), but this is useful information in case I ever have to…
  • I have an increased (2-5x or 3-5x) risk of dyslexia according to two genes.
I’m not dyslexic. So, increased risk is just increased risk. Interesting, perhaps, if I ever have children, though.
  • I have one gene that may be correlated with a reduced risk of bipolar disorder, two correlated with an increased (1.51x and 1.32x) and another correlated with a generally increased risk. I have a gene that is correlated with a “normal” risk of schizophrenia, and three with increased (1.58x, 1.1x, and generally) risk of schizophrenia. I have a gene that may render me more prone to less favourable clinical outcomes on antipsychotics.
I’ve grouped bipolar and schizophrenia together here because they seem to be reported on together for several of the genes, and the general picture seems to be ‘increased’. Again, this is not a wild surprise. There’s some incidence of both in my family. It’s interesting that there are genes connected to decreased responsiveness to psych meds generally (see above on depression). 
  • I have a gene linked to an “increased susceptibility to novelty seeking” and less efficient serotonin processing (although apparently parenting can help!)
I do get bored easily! I do prefer to start projects than finish them. This suggests an interesting link here between brain chemistry and personality traits, I think, but the information is no more than I have gleaned having lived with myself for so many years! It is at least heartening that the information provided by the report doesn’t pathologise this trait by correlating it with a specific ‘disorder’ from the DSM (although I’ve no doubt this has been done in the medical literature and in the press).
  • I have an allele combination that means I am “optimistic and empathetic” and handle stress well, being less likely to be startled by a loud noise and better able to judge the emotions of others by their faces. The combination is apparently also correlated with lower rates of autism, feeling less lonely, and employing more sensitive parenting techniques. However, another four genes were affiliated with increased risk of autism (varying levels up to 2x, with one associated with a 1.19x risk due to worse brain-cell adhesion) and a higher “insistence on sameness”. Conduct disorder is more likely in adolescents with my genotype. 
There’s a lot to unpack here, and I’ve grouped several results together, as I think they can be analysed as a bundle. I do tend to do well at the ’empathy test’ where one judges emotional states by pictures of people’s eyes. I’m not sure I’d be described as optimistic, but there is a lot of nuture there, I think. I do like ‘sameness’, but my position on the spectrum is not, I think, especially high! I was never diagnosed with conduct disorder, but I wasn’t exactly a model child. In a more psychiatrist-friendly home, I might have ended up with a label something like it, although actually I have a bit of a fixation on social rules (the breaking of which is a conduct disorder criteria). The entanglement with nurture is profound, here, I think, and in my view this would be an example of the ‘bad’ medical tendency to find fixed, biological reasons for complex social behaviours. I’m going to leave this here…
  • I am apparently likely to be “bad at avoiding errors” and learning from mistakes and have fewer dopamine receptors. My genotype is correlated with a 0.5x lower OCD risk, but a higher ADHD risk and a greater risk of alcohol dependence or smoking addiction. However, another gene has been linked to higher scores on anxiety-related personality traits, OCD, panic disorder, and other related disorders.
Again, there are a few related issues here. It is interesting to see the tension between being bad at learning from the past and accurately predicting consequences (I’m not that bad at it anymore, but I think increased experience and self-awareness may overwrite this natural balance; I remain rubbish at chess, however) and a predisposition towards anxiety that might lead to obsessive-compulsive behaviours. I am a natural worrier, always anxious about doing the wrong thing (hence my particular fixation on social rules, mentioned above), always early for things, and a bit of a precrastinator. The predisposition to find a crutch — implicit in the statements about alcohol and nicotine addition, I think — is not a surprise, although I think food would actually be my drug of choice, and I’m working on that! What these results confirm for me is that I’m on the right track in terms of self-management and self-knowledge. Keeping my sugar intake down (which in turn strongly discourages drinking alcohol in any significant quantities!), using exercise to help structure my day and keep myself feeling happy and strong, making sure that I get enough sleep (lack of sleep being correlated with higher anxiety and higher calorie intake): all of these things are helpful for me. If they are a little bit obsessive-compulsive, so be it!

More general health and fitness

This section is mainly about physical traits. Many of these are useful for me in thinking long-term about what I’m aiming to get out of any health and fitness regime.

  • I have the genotype that indicates better performing muscles, in the sense of likely being a sprinter, rather than an endurance athlete.
This is a surprise to me, as I was never a particular good sprinter and always made excuses for myself at school for being slow in races. This will make me even more inclined to try to include speedwork in my runs and plyometrics in my cross-training, though. Work with what you’ve (probably) got, right?
  • I have genes correlated with an increased (1.2-1.8x) risk of tuberculosis.
I don’t really think this is going to be a huge issue, but should I ever wish to feign consumption, I’ll keep this in mind!
  • I probably have an increased (1.9x or 2.3x) risk of developing rheumatoid arthritis, although another gene is correlated with normal risk, and another still with a decreased (0.89x) risk. I have genes correlated with an increased (1.16x or 1.45x) risk of osteoarthritis. I also have three genes associated with weaker bones.
Both my grandmothers had arthritis, so this is not new information, but knowing that there is a substantial increases risk (2.3x) will make me more careful about this, keeping an eye out for research about how to strengthen my body against it through diet and exercise, which are also key for maintaining strong bones later in life. It’ll also keep me thinking about my calcium and vitamin D intakes, and sometimes my desire to avoid too much sugar might take a backseat ad I might just have to have a whole-milk latte, rather than soy!
  • I have a 10x risk of endometriosis.
That’s a big number! Again, an increased risk, but I don’t have this, so…
  • Heart and cardiovascular diseases: Although the results here a bit mixed, the key take-home is that I am at increased risk here. I am at an increased (1.2x, 1.5x, 1.54x, 1.9x, or 7x with a history of high blood sugar!) risk for coronary artery disease. I have an increased (1.6x, 1.7x, 2x, and 2.2x) risk of heart disease, although some studies have shown that ‘regularly eating raw vegetables and fruit’ can decrease this.
So. There is no real family history of this here, but I think it would be silly not to take these results seriously. Again, increased risk is just increased risk, but it would be foolish to not give careful thought to the lifestyle factors that can bring down my risk of these diseases. Upping my fruit and veg intake, keeping my sugar intake down, and maintaining an active lifestyle — including trying to avoid being an ‘active couch potato’ — will be key. When thinking about dietary and lifestyle changes, health impacts are a major influence in maintaining changes over the long-term (versus, say, weight loss). These figures will stick in my mind, and I’ll use them as motivation, even whilst I repeat that biology is not destiny!
  • Increased risk of ischemic stroke based on two genes.
My maternal (maternal) great-grandmother had several strokes before she died. Again, this is not new information, but it reinforces the need to be careful about making choices that promote health.
  • I have several genes associated with higher HDL cholesterol, but one associated with lower HDL, particularly amongst Ashkenazi Jews.
I’ve never had a cholesterol check but keep meaning to! Perhaps I will try to get one done, just to see the lie of the land. As mentioned above, my Ashkenazi heritage is some generations back, so I won’t put too much store in that result.
  • I have a gene associated with “impaired NSAID drug metabolism“, which is a risk factor for GI bleeds when taking ibuprofen and other such drugs. I also have “probably impaired Warfarin metabolism”, with another gene correlated with an average 40% reduction in warfarin metabolism. This would mean I would need a reduced dose if treated for VTE. Another gene is associated with an “ultra-fast drug metabolism”. 
This is quite interesting. My mother takes warfarin, and she as told that she s responding very quickly to it when she first started. I’m not exceptionally likely to have the same condition as she, but drug metabolism more generally is interesting to me. I need to think more carefully about the painkillers I would naturally turn to (aspirin in particular) and take account of the increased GI risk in deciding how regularly to take them. I would try to avoid taking painkillers much now, but have been known to take an aspirin post-run, and certainly to take one or more when flying. As I don’t find painkillers exceptionally effective, I’ve also taken more than the recommended dose (or, more accurately. Played fast and loose with the minimum time intervals). I’ll think more carefully next time I’m inclined to do that. 
  • I have an increased (1.4x) risk of hypertension
As I typically have low blood pressure, like my mother and maternal grandmother, I’m not sure I will see this manifested…
  • I have genes correlated with an Increased risk of gluten intolerance and coeliac disease
I don’t have coeliac. I have some scepticism about gluten intolerance, and I avoid eating bread mainly because it’s not very nutritious, not for any other reason. My partner tries to avoid gluten for GI reasons (he’s not strictly intolerant), so avoiding high-gluten foods suits our lifestyles well, but I do often wonder whether not consuming the protein will, in turn, increase intolerance because the body modifies its enzyme production to be most efficient… This is something I’m ambivalent about. Perhaps I will just deliberately eat seitan when I can. It’s high in protein, after all!
  • My genotype has been linked to an increased risk of developing Parkinson’s (according to several genes).
This is not so surprising, given the other result regarding decreased dopamine levels. Aside from avoiding pesticides and Agent Orange, I’ll also pay more heed to research into the disease.
  • I have a higher risk of alcoholic liver disease, and alcohol is 3x more damaging to my liver.

This is yet another piece of information that will motivate me to keep my alcohol consumption low (see above about alcohol dependence, and my avoidance of alcohol because of sugar content!).

  • I am more likely (1.5-2.7x) to live to 100, and have a gene associated with living 3 years longer than others and another associated with longer telomeres. However, I have a gene associated with faster ageing and increased dementia risk, particularly amongst Ashkenazi Jews.

This is no real surprise, as it’s a running joke that the women on my mother’s side seem to live forever! I’m not sure whether I necessarily want to live to 100, but if I can keep myself in good health, it might not be so bad. Mark this up to another good reason to take care of my health and wellbeing! 

  • I am less stimulated by caffeine. I am probably a fast-caffeine metaboliser, so it will have less effect on me. This may decrease the risk of heart attack but caffeine will be less effective at preventing breast cancer, Parkinson’s and Alzheimer’s.  
I do drink a heck of a lot of coffee. Sometimes the people in Starbucks try to inform me of the caffeine content of the beverage I’ve requested. I’ve stopped going to one particular shop because I got sick of the bloke in there making fun of the number of espresso shots I ordered (he was flirting, but it was grating). I have reminders daily on my phone about the times when drinking coffee is most effective (time when your cortisol levels aren’t peaking naturally anyway). Enough said? Bit of a bummer about the breast cancer/Parkinson’s/Alzheimer’s point, though, given the results above…
  • I have “decreased high myopia risk”.
I’m pretty darn myopic! I’m not sure how to take this result…
  • I probably have a lower (’much lower’ or 0.87x) risk of Type-1 diabetes, a normal risk based on yet another, but another gene suggests a much higher (18.5x!) risk. Two genes indicate a lower risk of Type-2, but two others indicate an increased risk (1.2x or 1.4x), and a gene that indicates an increased (1.32x) risk of early-onset Type-2. Another gene is associated with a lower fasting blood glucose level.
Okay. Diabetes is something I am anxious about, mainly Type-2 (and 3!). There is no family history of Type-1, and I don’t have it. However, I do have to be careful of my blood sugar. I can have some serious lows, and high-sugar food and drink doesn’t sit well with me. I avoid high-sugar foods now (I remain sceptical about glycemic load analyses), and I think that’s the right approach for me. Note that an 18.5x increase only takes the risk of Type-1 up to 0.75%, though, so it’s still pretty low!  
  • I have a lower risk of obesity based on one gene, but a higher risk based on another (and am likely to be 0.22 BMI units higher). I am not one of the lucky 12% who find it easy to maintain weight loss without plenty of cardio exercise, but I have a gene affiliated with less weight-gain on high-fat diets and greater weight loss on a low-fat diet.
This is interesting. The message is mixed, but suggests that exercise is the best approach for me. I don’t subscribe to low-fat diets, preferring to focus on keeping my sugar intake down, but it’s nice to know that a low-fat diet could be effective for me, and that eating lots of nuts and full-fat Greek yoghurt isn’t a complete own-goal for me.
  • I have a 1.74x increased risk of gout.
Again, a good reason to keep an eye on my diet!
  • I have an increased (2-6x) risk for cluster headaches.
My father has migraines. I don’t have migraines or cluster headaches at the moment, but I’ll keep an eye out for them!
  • Reduced beta-carotene conversion to retinol.
This is interesting. Conversion is generally low (less than 22%) in the human body, but knowing hat mine is likely to be even lower will make me more conscious of my intake of retinol versus relying simply on orange vegetables. As retinol is fat-soluble and requires some fat in order to be stored in the body, I will also take this as an endorsement of my refusal to adopt a low-fat diet!

Miscellaneous “fun” facts

  • I have a combination of genes that are associated with a lower viral load and slower progression towards AIDs, should I ever contract HIV.
  • I have a resistance to prion disease.
  • I have the highest odds for a photic sneeze reflex.
  • Larger mosquito bites.
Definitely. My mother and I have tasty blood, and the last bite I had took about three weeks to go away (and there’s still a blemish there on my leg).
  • Possibly unable to taste bitter in some foods.
I’m not sure whether this is true. I will keep in mind that I might be safe to try new foods that others might find bitter.
  • Early riser, by about an hour.

Hell yes! Early morning FTW. I will keep running in the morning, then.


Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s

%d bloggers like this: