Category: Behavior genetics

As a story in the New York Times reports, some people respond well to aerobic exercise, while others seem to benefit less or not at all. There are studies that show there is a genetic component to this: various exercise traits (and the drive to exercise at all) do certainly run in families. A new study has scanned to genomes of 473 individuals subjected to the same 5-month exercise regime and found that particular SNPs (pronounced “snips;” we’ve talked about these before, see this post) are associated with a robust response to exercise. From the New York Times story:

The researchers looked at 324,611 individual snippets over all. Each of the volunteers had already completed a carefully supervised five-month exercise program, during which participants pedaled stationary bicycles three times a week, at controlled and identical intensities. Some wound up much fitter, as determined by the increase in the amount of oxygen their bodies consumed during intense exercise, a measure called maximal oxygen capacity, or VO2 max. In others, VO2 max had barely budged. No obvious, consistent differences in age, gender, body mass or commitment marked those who responded well and those who continued to huff and struggle during their workouts, even after five months.

But there was a divergence in their genomes. The researchers identified 21 specific SNPs, out of the more than 300,000 examined, that differed consistently between the two groups. SNPs come in pairs, since each of us receives one paternal copy and one maternal copy. So there were 42 different individual versions of the 21 SNPs. Those exercisers who had 19 or more of these SNPs improved their cardiorespiratory fitness three times as much as those who had nine or fewer.

One interesting question that is raised by this research is: if one finds that they do not have the advantageous SNPs, will they simply not try to exercise at all?

Our keynote speaker John Hawks describes this study and harps on the New York Times reporting on his blog.


Bouchard, C., et al. Genomic predictors of maximal oxygen uptake response to standardized exercise training programs. Journal of Applied Physiology in press.

Ok, let’s start off with the basics:

Parkinson’s disease is a neurological disorder where nerve cells that make dopamine are destroyed. Dopamine is an important neurotransmitter and without it, nerve cells are unable to properly send messages to other parts of the body. Eventually, the destruction of dopamine-producing cells leads to a loss of muscle function that gets worse over time. The typical symptoms of Parkinson’s are shaking and difficulty with walking, movement, and muscle coordination.  Unfortunately, not a lot is known about why these nerve cells waste away in the first place.

In gene therapy, a gene variant is used to alter the function of a cell or an organ. The way that genes are transferred into cells is pretty interesting: the gene is put into an inert virus, which is then injected into the target cell to deliver the gene.

Now, a new large-scale study suggests that a type of gene therapy (called NLX-P101) may be able to improve Parkinson’s symptoms. The gene that was targeted is called GAD (stands for glutamic acid decarboxylase). This gene produces a chemical called GABA (stands for Gamma-aminobutyric acid), which is a neurotransmitter than inhibits the excessive firing of neurons seen among Parkinson’s patients. From an interview in ScienceDaily with one of the researchers, Dr. Matthew During:

“In Parkinson’s disease, not only do patients lose many dopamine-producing brain cells, but they also develop substantial reductions in the activity and amount of GABA in their brains. This causes a dysfunction in brain circuitry responsible for coordinating movement,” explains Dr. During.

So, what they’ve done is inject a fully-functioning GAD gene into the brains of Parkinson’s patients. Those that were injected showed substantial improvement compared to individuals that did not receive the treatment.  


LeWitt, P.A. et al. (2011). AAV2-GAD gene therapy for advanced Parkinson’s disease: a double-blind, sham-surgery controlled, randomised trial. Lancet Neurology in press.

Robert Rowthorn, a professor emeritus of economics at Cambridge University, published a study that models population genetics scenarios based on the observation that religious individuals have, on average, higher fertility than non-religious individuals. In an extreme example, Rowthorn cites studies that show Amish and ultra-orthodox Jews have fertility rates 3 to 4 times higher than the secular average. Rowthorn goes on to build mathematical models that show how religiosity can spread throughout the population. From the paper’s abstract:

The paper considers the effect of religious defections [i.e., abandoning one’s religion] and exogamy [i.e., marrying outside one’s religious denomination or marrying a non-religious individual] on the religious and genetic composition of society. Defections reduce the ultimate share of the population with religious allegiance and slow down the spread of the religiosity gene. However, provided the fertility differential persists, and people with a religious allegiance mate mainly with people like themselves, the religiosity gene will eventually predominate despite a high rate of defection. This is an example of ‘cultural hitch-hiking’, whereby a gene spreads because it is able to hitch a ride with a high-fitness cultural practice.    

This models assumes, of course, that there is some sort of genetic underpinning for religious belief or, as Rowthorn puts it “[b]elief in the supernatural, obedience to authority, and affinity for ceremony and ritual depend on genetically based features of the human brain.” Naturally, there is a lot of debate on the biological foundation of religious belief. A great place to start is Carl Zimmer’s review of Dean H. Hamer’s “The God Gene.”

What do you think? What are some of the problems inherent in this debate?


Rowthorn, R. (2011). Religion, fertility, and genes: a dual inheritance model. Proceedings of the Royal Society B

Hamer, D.H. (2005). The God Gene: How Faith is Hardwired into Our Genes. Doubleday: New York.

A gambling gene?

Not exactly, but a new study by Cary Frydman and colleagues published in the Proceedings of the Royal Society examine variation in MAOA, DRD4, and 5-HTT, which are genes that affect either the breakdown or transport of the neurotransmitters serotonin and dopamine (both of which can affect things like aggression, risk-taking and risk aversion, and anxiety). As laid out in the summary of the study in the journal Nature, Frydman and colleagues found that individuals with a particular variant of the MAOA gene were more likely to make better finanical decisions in risky circumstances.

It would be interesting to screen World Series of Poker winners for MAOA gene variants…


Frydman, C., Camerer, C., Bossaerts, P., Rangel, A. (in press). MAOA-L carriers are better at making optimal financial decisions under risk. Proceedings of the the Royal Society (Biological Sciences).