The population genomic legacy of the second plague pandemic

Human populations have been shaped by catastrophes that may have left long-lasting signatures in their genomes. One notable example is the second plague pandemic that entered Europe in ca. 1,347 CE and repeatedly returned for over 300 years, with typical village and town mortality estimated at 10%–40%.1 It is assumed that this high mortality affected the gene pools of these populations. First, local population crashes reduced genetic diversity. Second, a change in frequency is expected for sequence variants that may have affected survival or susceptibility to the etiologic agent (Yersinia pestis).2 Third, mass mortality might alter the local gene pools through its impact on subsequent migration patterns. We explored these factors using the Norwegian city of Trondheim as a model, by sequencing 54 genomes spanning three time periods: (1) prior to the plague striking Trondheim in 1,349 CE, (2) the 17th–19th century, and (3) the present. We find that the pandemic period shaped the gene pool by reducing long distance immigration, in particular from the British Isles, and inducing a bottleneck that reduced genetic diversity. Although we also observe an excess of large FST values at multiple loci in the genome, these are shaped by reference biases introduced by mapping our relatively low genome coverage degraded DNA to the reference genome. This implies that attempts to detect selection using ancient DNA (aDNA) datasets that vary by read length and depth of sequencing coverage may be particularly challenging until methods have been developed to account for the impact of differential reference bias on test statistics.publishedVersio

The population genomic legacy of the second plague pandemic

Human populations have been shaped by catastrophes that may have left long-lasting signatures in their genomes. One notable example is the second plague pandemic that entered Europe in ca. 1,347 CE and repeatedly returned for over 300 years, with typical village and town mortality estimated at 10%-40%.1 It is assumed that this high mortality affected the gene pools of these populations. First, local population crashes reduced genetic diversity. Second, a change in frequency is expected for sequence variants that may have affected survival or susceptibility to the etiologic agent (Yersinia pestis).2 Third, mass mortality might alter the local gene pools through its impact on subsequent migration patterns. We explored these factors using the Norwegian city of Trondheim as a model, by sequencing 54 genomes spanning three time periods: (1) prior to the plague striking Trondheim in 1,349 CE, (2) the 17th-19th century, and (3) the present. We find that the pandemic period shaped the gene pool by reducing long distance immigration, in particular from the British Isles, and inducing a bottleneck that reduced genetic diversity. Although we also observe an excess of large FST values at multiple loci in the genome, these are shaped by reference biases introduced by mapping our relatively low genome coverage degraded DNA to the reference genome. This implies that attempts to detect selection using ancient DNA (aDNA) datasets that vary by read length and depth of sequencing coverage may be particularly challenging until methods have been developed to account for the impact of differential reference bias on test statistics

Effects of Long-Term Physical Activity and Diet on Skin Glycation and Achilles Tendon Structure

Advanced glycation end-products (AGEs) accumulate with aging and have been associated with tissue modifications and metabolic disease. Regular exercise has several health benefits, and the purpose of this study was to investigate the effect of regular long-term exercise and diet on skin autofluorescence (SAF) as a measure of glycation and on Achilles tendon structure. In connection with the 2017 European Masters Athletics Championships Stadia, high-level male athletes (n = 194) that had regularly trained for more than 10 years were recruited, in addition to untrained controls (n = 34). SAF was non-invasively determined using an AGE Reader. Achilles tendon thickness and vascular Doppler activity were measured by ultrasonography, and diet was assessed by a questionnaire. There was no significant difference in SAF between the athletes and controls. However, greater duration of exercise was independently associated with lower SAF. Diet also had an effect, with a more “Western” diet in youth being associated with increased SAF. Furthermore, our data demonstrated that greater Achilles tendon thickness was associated with aging and training. Together, our data indicate that long-term exercise may yield a modest reduction in glycation and substantially increase Achilles tendon size, which may protect against injury.publishedVersio

Effects of Long-Term Physical Activity and Diet on Skin Glycation and Achilles Tendon Structure

Advanced glycation end-products (AGEs) accumulate with aging and have been associated with tissue modifications and metabolic disease. Regular exercise has several health benefits, and the purpose of this study was to investigate the effect of regular long-term exercise and diet on skin autofluorescence (SAF) as a measure of glycation and on Achilles tendon structure. In connection with the 2017 European Masters Athletics Championships Stadia, high-level male athletes (n = 194) that had regularly trained for more than 10 years were recruited, in addition to untrained controls (n = 34). SAF was non-invasively determined using an AGE Reader. Achilles tendon thickness and vascular Doppler activity were measured by ultrasonography, and diet was assessed by a questionnaire. There was no significant difference in SAF between the athletes and controls. However, greater duration of exercise was independently associated with lower SAF. Diet also had an effect, with a more “Western” diet in youth being associated with increased SAF. Furthermore, our data demonstrated that greater Achilles tendon thickness was associated with aging and training. Together, our data indicate that long-term exercise may yield a modest reduction in glycation and substantially increase Achilles tendon size, which may protect against injury