How British Food Environments Changed the Link Between Genes and Weight

A person born in Britain in 1946 spent their childhood under food rationing, which did not end completely until they were roughly eight years old.

Someone born in 2001, by contrast, was raised amid inexpensive takeaways, processed snacks and a fast-food outlet on almost every corner.

In terms of weight-related genetic variants, their DNA was strikingly alike. Their bodies were not.

A new study set out to follow that divide – and its findings question a long-standing belief about the way inherited traits and body weight interact between generations.

How genes changed

The research was led by Liam Wright of University College London (UCL). His team compared four long-running studies that have followed British people from birth.

These studies repeatedly recorded the height and weight of people born in 1946, 1958, 1970 and around 2001 throughout their lives.

Researchers also gave every participant’s DNA a polygenic index score – one figure combining hundreds of small genetic variations, each known to raise body weight slightly.

The team created two forms of the score: one matched to adult body size and another to childhood body size. They then tested how closely each score corresponded with participants’ measured size at equivalent ages.

The same broad pattern emerged in each of the four cohorts. Higher genetic scores were generally associated with greater weight. The difference was in how strong that association became.

Among the youngest participants, genes seemed to exert a much greater influence than they had for their grandparents’ generation, even when compared at the same age.

What the numbers show

The most straightforward comparison is at age 16. For people born in 1946, a standard rise in the adult genetic score was linked to around half a kilogram of additional body weight.

Among teenagers born in 2001, that identical genetic rise was associated with almost twice as much extra weight. Nearly twice as much – at the same age and for the same scale of genetic difference.

The first three cohorts, born in 1946, 1958 and 1970, appeared unexpectedly alike throughout childhood and adolescence.

Their differences emerged only in adulthood, at about the period when obesity rates in Britain started to rise.

The youngest cohort departed from this pattern completely: its separation from older generations was evident during childhood rather than appearing decades afterwards.

That timing sits at the heart of the finding. Genes did not alter between 1946 and 2001 – too little time has elapsed for that to happen.

Instead, something changed in the environment surrounding these children, apparently allowing the same inherited tendencies greater scope to show themselves.

Where it hits hardest

A further level of analysis brings the result into clearer focus. Rather than examining average weight alone, the researchers assessed the entire range, from the lightest individuals to the heaviest.

At the lower end, genetic scores made little difference. At the upper end, however, the pattern split apart.

At age 10 or 11, a higher genetic score added only a small part of a kilogram among the leanest children, and this remained broadly consistent across all four generations.

For children at the heavier end of the range at the same age, the youngest cohort separated sharply from the rest.

In that group, a higher genetic score corresponded with well over a kilogram of extra weight – considerably more than in any preceding cohort.

This may help resolve a question that has troubled body mass index researchers for years. Average weight has risen only modestly, while severe obesity rates have increased sharply.

The analysis indicates that genetic effects may be becoming concentrated among those already most susceptible to weight gain, widening the divide instead of raising everyone’s weight equally.

Why genes need a setting

This does not mean earlier generations did not possess these genetic variants. They had them as well. They were simply raised in a world that gave those variants less opportunity to act.

The oldest cohort lived through early childhood under post-war food rationing, which did not end in Britain until they were around eight years old.

Wright and his colleagues believe the explanation may lie in the transformation of the food environment over those decades.

Cheaper processed foods, a greater number of fast-food outlets and the gradual removal of physical effort from daily routines all arrived together.

The opportunity to eat more

Variants that may subtly promote a larger appetite or reduce feelings of fullness seem likely to have more chance to operate in an environment filled with cheap, calorie-dense food.

The researchers stress, however, that the precise mechanism has not yet been confirmed.

In practical terms, a genetic tendency towards hunger has relatively little effect in a kitchen where food is limited.

Place that same tendency in an environment where energy-dense meals are affordable and ubiquitous, and it may become far more significant. The DNA remained unchanged, but the chance to act on it increased.

What stayed the same

There is an important complication to the story. Although the direct association between genes and weight strengthened between generations, a different measure remained largely unchanged.

The proportion of overall weight variation explained by genetics did not rise in a clear, consistent pattern.

Both findings can coexist. As average body weight increases, the range of weights also becomes wider, meaning a stronger genetic influence can still account for about the same proportion of a larger, more varied whole.

The researchers also acknowledged that some measures did not have sufficient statistical power to answer the question definitively. A study using Norwegian data produced broadly similar findings.

One result was particularly notable. When the team applied a much more powerful genetic score, developed using more than five million people, genetics explained a greater proportion of weight in the youngest cohort than in the older groups.

This suggests there may be a genuine relative increase, although larger samples will be needed to confirm it.

What it means now

Before this research, most scientific understanding of genes, environment and weight came from older adults, largely Americans, assessed at one point in their lives.

Following entire British generations from early childhood onwards breaks new ground.

It shows that the connection between genes and weight becomes strongest, and does so earliest, among children at the upper end of the weight range – the group in which obesity rates have risen most dramatically.

If genetic risk leads to high body weight only where the surrounding environment allows it, then that environment is a lever worth changing.

Genes are fixed. Their effects may not be.

This directs doctors and policymakers towards the food and activity environment in which children grow up, instead of viewing genetic predisposition as an inescapable destiny.