A population-based analysis demonstrates that surviving twins who lose their co-twins by death are at considerably elevated risks of developing psychiatric disorders.

Findings of this population-based sibling-matched cohort study corroborate an association of loss of a co-twin at birth with risk of psychiatric disorders, supporting the hypothesis of twin-bond development in utero.

Analysis of data from monozygotic twins reveals that DNA methylation level in human blood cells is reactive to cigarette smoking.

Unhealthy lifestyle habits in adolescence associate with accelerated biological aging in young adulthood, but shared genetic factors underlying both lifestyle and biological aging may largely explain the observed associations.

Prospective, cross-sectional, and intra-twin study designs identify skewed X chromosome inactivation is associated with cardiovascular disease risk and future cancer diagnosis in the TwinsUK population cohort.

A minor subset of plasma lipids are heritable, and this is associated with gene expression of transcripts related to roles beyond lipid metabolism, including immune function and cell signalling.

Multiple replicated examples of epistasis affecting gene expression in humans are identified, some explaining a substantial proportion of the variation in expression.

Genetics and biochemical analyses reveal an evolutionarily conserved mechanism to regulate gene isoform expression by mTORC1 and implicate possible gene isoform imbalance in cancer and neurological disorders with mTORC1 pathway dysregulation.

RNA sequencing reveals the finer details of circadian variation in the mammalian master pacemaker over 24 hours, which suggests that transcriptional timing influences clock resetting mechanisms.

Greater early developmental growth, as indexed by birth weight, relates to greater cortical volume and area in a stable way through the human lifespan.