Such an effect may indeed be real, as higher mobility has increased opportunities for mating between individuals from distant locations. However, the paper is completely ignoring an alternative explanation which may contribute, at least in part, to the observed data.
The authors studied the genomes of individuals of different ages for runs of homozygosity (ROH), i.e., continuous regions of DNA where the two strands are identical to each other. Such regions are typical of inbred individuals, who inherit identical big chunks of genetic material from both parents -- these chunks can be traced to recent common ancestors shared by these parents.
They were able to discover that older individuals had more significant ROHs than younger ones. Ergo -according to them- older generations had more inbred individuals than more recent ones: inbreeding has decreased over time.
There is, however, one catch to this whole argument: older individuals (and they tested individuals up to 99 years of age) are not a random sample of their generations: they are the survivors, the people whose genetic makeup allowed them to reach old age.
Is there any reason to think that surviving older people are similar in terms of their ROHs to the now-dead members of their generation? Here are some relevant data:
Increase of homozygosity in centenarians revealed by a new inter-Alu PCR technique
a significant increase in homozygote genotypes frequency was observed in centenarians. These counterintuitive results suggest that increased homozygosity contributes to human longevity.
The Unusual Genetics of Human Longevity
In no species other than humans do cultural, social, and biological factors interact with each other in modulating complex phenotypes. Thus, the identification of genetic factors that affect human longevity is a true challenge. The model of centenarians provides us a unique opportunity to tackle this challenge. In this Perspective, we discuss some recent findings (the impact of geography and demography on the longevity phenotype, the relationship between longevity and homozygosity, the role of the nuclear-mitochondrial genome cross-talk) by which new ideas are suggested, such as the concept of a complex allele timing as a pivotal process in modulating the probability of achieving longevity.
Homozygosity - not always a bad thing
“Longevity seems to be linked to homozygosity,” Passarino says. This may be because certain copies of some genes boost lifespan, and carrying two of them doubles the effect. A number of DNA analyses have located regions of the genome where centenarians show an unusually high level of homozygosity, he says.The conclusion: inbreeding may have decreased over time, but testing the homozygosity of people who are alive today is no way to demonstrate it. Direct genomic testing of people from 100 years ago seems plausible, and may disclose whether increase of autozygosity with age is due to reduced inbreeding over time, or to increased lifespan of homozygous individuals.
PLoS Genetics doi:10.1371/journal.pgen.1000415
Measures of Autozygosity in Decline: Globalization, Urbanization, and Its Implications for Medical Genetics
Michael A. Nalls et al.
This research investigates the influence of demographic factors on human genetic sub-structure. In our discovery cohort, we show significant demographic trends for decreasing autozygosity associated with population variation in chronological age. Autozygosity, the genomic signature of consanguinity, is identifiable on a genome-wide level as extended tracts of homozygosity. We identified an average of 28.6 tracts of extended homozygosity greater than 1 Mb in length in a representative population of 809 unrelated North Americans of European descent ranging in chronological age from 19–99 years old. These homozygous tracts made up a population average of 42 Mb of the genome corresponding to 1.6% of the entire genome, with each homozygous tract an average of 1.5 Mb in length. Runs of homozygosity are steadily decreasing in size and frequency as time progresses (linear regression, p less than 0.05). We also calculated inbreeding coefficients and showed a significant trend for population-wide increasing heterozygosity outside of linkage disequilibrium. We successfully replicated these associations in a demographically similar cohort comprised of a subgroup of 477 Baltimore Longitudinal Study of Aging participants. We also constructed statistical models showing predicted declining rates of autozygosity spanning the 20th century. These predictive models suggest a 14.0% decrease in the frequency of these runs of homozygosity and a 24.3% decrease in the percent of the genome in runs of homozygosity, as well as a 30.5% decrease in excess homozygosity based on the linkage pruned inbreeding coefficients. The trend for decreasing autozygosity due to panmixia and larger effective population sizes will likely affect the frequency of rare recessive genetic diseases in the future. Autozygosity has declined, and it seems it will continue doing so.