This preprint reports a quantitative genetic and association analysis of daily feeding rhythms in pigs. The authors aimed to quantify circadian feeding rhythmicity across a large commercial dataset, estimate genetic contributions to variation in feeding rhythms, identify genomic loci associated with rhythmicity, and examine phenotypic consequences for feed efficiency and resilience. The study uses data from automated feeders and integrates wavelet-based phenotyping with genome-wide association testing.
Hourly feed intake data were collected from automated feeding systems, totaling approximately 40.5 million records. The dataset comprised 3,470 Swiss Landrace and 15,181 Swiss Large White pigs. The focal phenotype was defined as the proportion of days per animal that exhibited a statistically significant feeding rhythm across the 24-hour cycle, as determined by wavelet analysis. This approach captures the day-to-day organization of feeding and quantifies whether animals show recurrent daily feeding–fasting cycles.
Genome-wide analyses were performed using imputed sequence variants. Two variant sets were reported for association testing: 15.7 million and 23.1 million imputed sequence variants. Variance component models were used to partition phenotypic variance and estimate additive genetic contributions and heritability for circadian feeding rhythmicity.
The authors observed systematic effects of sex and age on feeding rhythmicity. Females exhibited higher rhythmicity than males, and older animals showed greater rhythmicity compared with younger ones. These findings indicate that both biological sex and developmental stage contribute to the organization of daily feeding behavior in pigs.
Variance components analysis revealed a substantial additive genetic contribution to circadian feeding rhythmicity. Reported heritability estimates ranged between 0.53 and 0.57, indicating that more than half of the observed variation in rhythmicity is attributable to additive genetic effects in the studied populations. This high heritability supports the view that feeding rhythm organization is a genetically influenced trait amenable to further genetic mapping and potential selection.
Genome-wide association testing detected a quantitative trait locus (QTL) on chromosome 4 associated with circadian feeding rhythmicity. The QTL explained 5.3% of the phenotypic variance in Swiss Landrace pigs and 2.9% in Swiss Large White pigs. The associated region overlaps the genes OPRK1 and NPBWR1, both of which have prior implication in the regulation of feeding behavior, reward pathways, and energy homeostasis. The authors highlight these genes as plausible candidates that could mediate the link between genetic variation and the timing of food intake.
Phenotypic analyses indicated that pigs with higher circadian feeding rhythmicity had reduced nocturnal intake, an improved feed conversion ratio, and lower day-to-day variability in feed intake. These associations suggest that stronger daily organization of feeding is linked to improved feed efficiency and greater short-term stability in intake, traits that the authors interpret as improved resilience. The reported relationships align behavioral rhythmicity with economically and biologically relevant production traits.
Because circadian feeding rhythmicity is both heritable and associated with feed efficiency and intake stability, the authors propose that this behavioral trait could be considered in breeding programs aimed at enhancing feed utilization and resilience. The identification of a relatively large-effect QTL on chromosome 4 offers a concrete genomic target for follow-up functional studies and potential marker-assisted selection. The overlap with OPRK1 and NPBWR1 provides testable hypotheses about molecular mechanisms linking circadian organization and metabolic regulation.
The article is a bioRxiv preprint and has not been peer reviewed. The authors report that SUISAG, a pig breeding company, provided most of the data; one author is an employee of SUISAG and declared no competing interests related to the manuscript. The Swiss National Science Foundation supported the work. Details beyond what is reported in the preprint (for example, replication in independent populations or functional validation of candidate genes) were not presented in the source and therefore are not summarized here.