Scientifically Speaking: Do firstborns really do better because of germs?

What is new, and where a biologist has to slow down and catch his breath, is the claim that this may help explain why an adult earns more 25 years later.

I first heard this question on The Economist’s podcast, framed around a well-known puzzle. Firstborns tend to do a little better in school and earn a little more as adults. As a firstborn, I enjoy this fact more than I should, though the scientist in me knows it applies only at a population level. But I still have to ask why.

For representational purposes only.

A new study offers an unexpected answer: the older sibling is a vector. She comes home from playschool with a nose full of viruses and passes them on to her baby brother during the most vulnerable months of his life. Decades later, the baby brother earns a little less and leaves school a little earlier, and the birth-order gap we have been puzzling over becomes, in this saga, the long shadow of an infant chest infection.

The hypothesis is in a working paper of the National Bureau of Economic Research and is now listed as forthcoming in the American Economic Review. It is the kind of study that economists have mastered and that biologists are rarely audacious enough to attempt.

The paper uses Danish population registers covering births from 1981 to 2017, linked across hospital, tax, and education records, to ask whether infants in families with heavier local respiratory disease burden do worse in adulthood than their older siblings. The answer is yes.

Children exposed to higher levels of respiratory disease in their first year go on, on average, to earn about 0.8 per cent less as adults, are slightly less likely to finish school, and have somewhat higher rates of chronic respiratory illness and psychiatric care. The effects are small but, the authors argue, meaningful.

The headline has travelled well in the general and business press. Business Insider has written about it, as has The Economist.

What I find striking is who has not. I looked for substantial news coverage or commentary in Nature and Science, the two journals I read every week, and found none. I looked for engagement in the clinical infectious disease journals, and it hasn’t made its way there yet.

A paper that points to a lifelong population-level consequence of early respiratory disease exposure is being explained by economists and explained to the public by business magazines, while the biologists and clinicians who would have to validate how these are connected have barely entered the conversation.

It is worth looking more closely at what the paper actually shows. At its core, the findings are elegant. Younger siblings in Denmark are hospitalised for acute respiratory illness in the first year of life at two to three times the rate of their older siblings at the same age. The gap is largest in the first three months, in winter, with short birth spacing, and when the older sibling is in group childcare. Every one of those patterns is what a paediatric infectious disease clinician would predict. Toddlers are viral chimneys, infant immune systems are still calibrating, and respiratory syncytial virus is nastier in a three-month-old than in a three-year-old. We have known this for a long time.

What is new, and where a biologist has to slow down and catch his breath, is the claim that this may help explain why an adult earns more 25 years later.

The authors build a municipality-level index of respiratory hospitalisations among slightly older children as a proxy for local viral pressure, and they ask whether heavier pressure harms the younger sibling more than the older one. The design goes a long way toward controlling for shared family background, local conditions, and seasonality, and uses local epidemic waves as the source of variation.

But the readout is not an infection. It is a municipality-level count of hospital admissions, assembled from administrative codes, serving as a proxy for something a biologist would actually want to measure. It is not viral load, not immune activation, not cytokine profile, not microbiome disruption, nor airway epithelial damage. Hospitalisation is only the visible tip of a much larger iceberg of respiratory infection, as the authors themselves note, and the index is several steps removed from the biological event.

If severe respiratory infection in infancy can dent adult earnings a quarter of a century later, we would want to know how. Severe viral lower respiratory infection in the first months of life has long been linked to later wheeze and asthma, which fits the paper’s own finding of more chronic respiratory illness in adulthood. It is also biologically plausible that inflammation during a period of rapid brain development leaves some footprint on later cognition. And severe infant illness can lead to early antibiotic exposure, which might harm the gut microbiome with implications for long-term immunity and metabolism.

None of these mechanisms are tested yet.

Or there may be no single mechanism at all. The adult earnings gap may be a composite of small biological effects and small social ones. That story may be closer to the truth, but it is more complicated and harder to tell on a magazine cover.

So, do firstborns really do better because of germs? Younger siblings do catch more severe respiratory infections in infancy, and on average they do a little worse as adults. But the effect is small, the mechanism is not pinned down, and the distance between a baby’s chest infection and a thirty-year-old’s paycheck is filled with biology that has not yet been measured. Until it is, I would not go much further than that.

Anirban Mahapatra is a scientist and author. His most recent book is When the Drugs Don’t Work. The views expressed are personal.