Genes and Environment

January 27, 2012

In my Biology and Cognitive Science of Communication course last year, one of the #1 themes–one of perhaps 5 ideas that I really hoped students would understand by the end of the course and take away with them–is the notion that genes/innate biology and environment have, for the most part, mutual effects on outcomes (including/especially behavior) that cannot be parceled out in to X% and Y%.  That is, the interaction between genes and environment is usually much more important than either by itself.

Of course, this is not always true.  There are extreme versions of both–single-gene traits (e.g., color blindness, Huntington’s Disease, many others) and trisomies (e.g., Down Syndrome) obviously have a very large, direct effect on outcomes.  Likewise, extreme environmental circumstances (e.g., Fetal Alcohol Syndrome, head trauma, sensory deprivation) can have large, direct effects.

But for the most part, it’s an interaction–and that’s an easy, glib line to memorize, but I think it took students awhile (and, for that matter, it took me a long time) to really grasp what that means.  But this morning I was perusing my new* results and I came across a good example.  Below the cut is copy pasta of one of my results, “Response to Diet.”  This result reports on 3 SNPs (essentially, genes) that research shows to be associated with the link between diet and obesity.

Now, calls these “preliminary results” because each link only has one approved study that goes with it, and there are a host of statistical issues with the way that much research is done on gene effects (basically, it’s correlational data mining, so unless you have MANY studies showing the same association repeatedly, there’s always the possibility that a given result is a chance fluke rather than an actual relationship).  But let’s pretend for a moment that they’re associations that can be taken at face value.

Each of these genes has 3 known variants (this is not the only way it can happen, but it’s usual for the SNPs that 23andme reports).  Scientists doing gene studies compute odds of whatever outcome they’re interested in (e.g., obesity, Parkinson’s Disease, etc.), comparing the less usual variants (i.e., mutations) to the most common variant (i.e., “normal”).  Sometimes the mutation seems to be protective–it does better than the most common variant (e.g., it is correlated with lower odds of heart disease than the general population), but often the mutation is associated with higher odds of things you don’t want.

The results below the cut are interesting because they specifically relate to response to diet–that is, how my body interacts with the environment. Thus, these aren’t “obesity” genes in the simplistic sense–having a given variant causes obesity–but they are (perhaps) genes that determine how I metabolize different kinds of foods, and thus what kinds of foods are likely to help me lose weight or make me gain weight.**

So the genes themselves are not causing weight loss/gain.  Neither is my diet alone.  You can’t say it’s 30% genes and 70% environment.  It’s genes AND diet (environment).  The effects of the genes are conditional upon what food I eat, and the effect of food I eat is conditional upon my genes.  Their effects cannot be separated.

I think this is also interesting to interpret the wide variety of fad diets out there, and how so many people can swear that a given fad diet is THE way to lose weight because it worked very, very well for them.  How can Atkins work for some people, and low-fat diets work for other people?  I suggest that those people have different genes like the ones below (assuming this research pans out).  This isn’t even that earth-shattering of an idea–maybe some people store carbs more easily than others, whereas some people store fats more easily than others.  Human metabolism is ridiculously complex–you learn the Krebs cycle in high-school or freshman Bio and think that’s complex?  That’s just baby stuff, and really scientists have only scratched the surface of figuring out how we do the biochemical wonders that we do.***  It’s no surprise, to me at least, that the wide range of individual differences in diet efficacy could have some underlying genetic cause.

And my particular results affirm why I have personally had success with low-fat diets and not with low-carb diets (that, and I’m also a carrier for MCAD deficiency–which apparently even carriers have lower-than-typical MCAD levels, so eating very few carbs tends to do things like make me faint).

* If you are not familiar, is a company that, for a fee and a container of spit, tells you about your genes.  They only provide results that are based on some baseline level of expert-vetted (as well as peer-reviewed, published) research.  For that reason, though their information about my genes doesn’t change, they periodically update what given results MEAN based on new research.  You can also download the full result that lists every gene that they genotyped, which despite the fact that it is not a full sequence, is 8MB of text–that’s a lot.

** I phrase things this way because I am currently, um, larger than I would prefer to be–curse you, baby weight that never left!!–but the reverse is obviously also true if you are one of those folks who have trouble keeping weight on.

*** You know what’s scary, that I did not know prior to being married to someone in Big Pharma?  A great many drugs on the market have unknown or only theorized mechanisms.  They don’t really know how they work.  Drugs are developed by testing a bunch of molecules (usually, ones that have something in common with another drug/compound that is already known to work) to see which ones are biologically active, and out of those which ones do the things that we want with the fewest side effects (in a very simplistic nutshell).  It’s very much “throw stuff, see what sticks.”

[See below for my 23andme “Response to Diet” results]

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