Losing one’s virginity – specifically, the age at which one does so – has become something of a hot topic among adolescents in the 21st century. Most research on sexual behaviour so far has concentrated on socioeconomic and cultural factors; perhaps unsurprisingly, many such correlations have been established.

Younger age at first sexual intercourse has been linked to social disadvantage, family instability, and lack of religious affiliation, not to mention the strong influence of one’s peers. However, analysis of genomic data published in Nature Genetics this week points to considerable chromosomal sway over such milestones.

Researchers at the University of Cambridge’s Medical Research Council Epidemiology Unit surveyed the DNA of over 125,000 people in the UK aged 40 to 69, and found 38 gene variants associated with the age of first sexual intercourse.

These so-called Single Nucleotide Polymorphisms (SNPs – alterations to just one unit of the genetic blueprint) affected two broad types of gene. The first group encoded substances with roles in the onset of puberty and reproductive development in general, including the oestrogen receptor. This might have been expected, given that sexual activity typically follows pubescence.

Interestingly, the second set contained a number of genes involved in brain development and thus personality. CADM2, for instance, is involved in adhesion between neuronal cells and linked to a propensity for risk-taking.

This week’s paper demonstrated significant correlation between the population distribution of an SNP in CADM2 and the number of sexual partners, number of children, and the age at which virginity was lost. Conversely, an SNP in MRSA, a gene implicated in levels of irritability, was observed to delay an individual’s first act of intercourse. The links here seem plausible: engaging in sexual activity with more people and at a younger age could indeed be described as ‘risky’ behaviour, and a short temper is unlikely to get one’s cherry popped.

The team ultimately concluded that roughly 25 per cent of the observed variation in sexual behaviour could be attributed to these genetic differences.

Nevertheless, Dr John Perry, a lead author of the paper, stressed that environmental factors were still extremely important and proposed more research “to show exactly how these genes help regulate the timing of the reproductive milestones”.

Crucially, the large-scale study was made possible through UK Biobank, a registered charity based in Greater Manchester that was set up in 2006 to monitor physical and genetic changes in around 500,000 volunteers over the course of several decades. The researchers at Cambridge obtained their DNA samples from UK Biobank and were also able to verify their findings using similar databases in Iceland and the US.

As such, their study is representative of a wider movement in science and healthcare to isolate the root causes of an individual’s well-being or illness from a wealth of confounding factors by looking at broad epidemiological patterns.

Perry’s investigations have revealed “that individuals who go through puberty at younger ages have higher risks of many diseases of old age, such as diabetes, heart disease and breast cancer”. Similarly, he writes, “first sexual intercourse at an earlier age is linked to a number of adverse behavioural, educational and health outcomes.”

He supports the notion of future efforts to prevent early puberty, which is often brought on by poor nutrition and childhood obesity. Such views, backed up by meticulous research, herald a new era of medicine that is anticipatory rather than solely remedial, and personalised rather than prescriptive.