The United States is one of the few developed countries in the world with a fertility rate close to the replacement rate – that is, the rate of fertility required to maintain existing population levels. The two reasons most often cited for this is are high levels of fertility in the Hispanic immigrant population and the high level of fertility of religious people. Even when you control for income and education, religious people have more children than non-religious people (on average).
The higher fertility among religious people raises a couple of questions. As religion is heritable (that is, the predisposition to be religious and not the specific religion itself), will religion spread through society and what will the consequences of this be? What will happen to the underlying alleles (alleles are the different variants of a particular gene)?
If we had a situation where the religious have higher fertility and a religious genotype is determinative, it is clear that they will eventually form the largest group in the population and the religiosity allele will dominate the gene pool. However, what if there are more complicated dynamics such as defections between groups, with the religiosity allele(s) giving a predisposition as opposed to being determinative?
Robert Rowthorn addressed this question in a paper published earlier this year in which he explored the dynamic consequences of heritable religiosity and the higher fertility of religious people. Razib at Gene Expression wrote a great post on this paper when it was first released, but as is often the case, writing a blog post myself is the best way to get my head around it.
Rowthorn noted that a natural result of defections from a high-fertility religious group is that the religious group would be smaller than it would otherwise be. However, he also points out that defection from the religious group allows the religious allele(s) to spread to and within the non-religious group. If this religiosity allele affects the number of people from the non-religious group who become religious and as a result, boosts their fertility, the religious allele may come to dominate the population regardless.
To explore this issue, Rowthorn constructed two models (one haploid, in which predisposition is determined by a single gene, one diploid, in which predisposition is determined by two genes, one from each parent). In these models, culture (religion) determined fertility, while religious predisposition has a genetic component. On becoming an adult, one can defect from their religious or non-religious group, with their underlying genotype giving the probability of switching.
Some of the outcomes of the model are unsurprising. Firstly, the pace of evolution is heavily dependent on the fertility differential between religious and non-religious types. With a differential of two or three to one, large changes in population structure occur within five to 10 generations. Where the fertility differential is 1.3 to one, it might take several hundred generations for the share of the religious gene in the population to dominate from a low base.
With defection added, there are two main results. First, the speed of the spread of the religiosity allele is reduced, although it still spreads through the population. Second, the total number of religious people in the population is reduced, possibly significantly. Defection changes the expression of religiosity, but not the eventual spread of the gene.
For high fertility sects such as the Amish, with fertility rates two to three times above the national average, this would imply that they would come to dominate the population in five to ten generations, unless there is a particularly high level of defection. If they do have a high defection rate, while reducing the size of the Amish population, the religious gene will still spread. Even with a 50 per cent defection rate, the religious gene still spread to most of the population within 20 generations in Rowthorn’s model. From this, Rowthorn notes that while secularisation might reduce the growth of high-fertility sects, the importing of the religious gene into the non-religious population results in the religious allele ultimately spreading through the entire population.
Rowthorn does not venture far into the implications of his findings beyond the spread of religion. In the last paragraph, he makes the following observation:
It is interesting to speculate how such a predisposition might manifest itself in a secular context. The findings of Koenig & Bouchard suggest that a genetic predisposition towards religion is associated with obedience to authority and conservatism. If this is correct, then the diffusion of religiosity genes into the rest of society should see an increase in the number of secular people who are genetically inclined towards such values. The implications of such a development are beyond the scope of this paper to consider.
Is the growing conservatism among youth, which seems to be a common media topic in recent years, an early reflection this effect?
Rowthorn does not specifically explore the question of overall population size. If the religious allele(s) spread through society, fertility would be expected to be higher and overall population higher. This could have significant implications for the debate on population size I have posted about in the last week (such as here, here and here).
Further, Rowthorn’s findings show the general result that any genetically based predisposition that increases fertility can be expected to spread through the population. Whether that predisposition is religion, dislike of contraception, urge to have a larger family or some other trait, the effect is the same. The alleles responsible for higher fertility spread and, barring further environmental shocks, population growth increases. The only question is how long this will take.
*As an extension to this idea, I have a working paper that examines the consequences of heritability of fertility more generally.
Rowthorn, R. (2011). Religion, fertility and genes: a dual inheritance model Proceedings of the Royal Society B: Biological Sciences DOI: 10.1098/rspb.2010.2504