Going outside with wet hair will make you catch a cold.

For most of recorded medical history, the question of what caused respiratory illness had a common-sense answer: cold. The very name suggested as much. Hippocrates had observed that respiratory diseases clustered in winter. Centuries of common experience reinforced the connection. Mothers who sent children outside with wet hair noticed, or believed they noticed, that colds followed. The theory was not absurd, it was an inference from genuine correlation, drawn before anyone had the tools to distinguish correlation from cause.

The discovery that colds have microbial origins began unraveling the cold-weather theory before most people had heard of a rhinovirus. In 1914, the German physician Walther Kruse demonstrated that filtered nasal secretions from patients with colds, secretions small enough to pass through a filter that stopped bacteria, could induce colds in healthy volunteers, indicating a viral agent. The work was extended at the Medical Research Council's Common Cold Unit in Salisbury, England, established in 1946. Volunteer subjects were inoculated with nasal washings from cold sufferers, then observed under controlled conditions. The colds that resulted had nothing to do with whether the subjects were warm or cold.

The definitive experimental evidence came in 1968. R. Gordon Douglas, Keith Lindgren, and Robert Couch recruited forty-four antibody-free volunteers and exposed some of them to a 4°C environment, near freezing, at various points during experimentally induced rhinovirus infections. Others were placed in a 32°C water bath. The temperature exposures produced no significant difference in infection rates, symptom severity, or duration. The paper appeared in the New England Journal of Medicine in October 1968 under the flat, categorical title "Exposure to Cold Environment and Rhinovirus Common Cold: Failure to Demonstrate Effect." The conclusion required no elaboration.

Ron Eccles, who directed the Common Cold Centre at Cardiff University, complicated the picture somewhat in a 2002 review in the journal Rhinology. Eccles reviewed the epidemiological literature and proposed a physiological mechanism by which acute cooling might matter after all, not by initiating viral infection, but by triggering symptoms in people who already carry rhinovirus subclinically. Cooling causes reflex vasoconstriction in the nasal mucosa, which may suppress local immune defense enough to allow a silent infection to cross into clinical illness. In a controlled experiment, Eccles's research group found that subjects who immersed their feet in cold water for twenty minutes developed cold symptoms at twice the rate of controls, but the operative word is developed, not contracted. The virus was already there.

The distinction is small, but it is the right distinction to make. Winter does bring more colds. The correlation is real, and several factors explain it: people congregate indoors where air is shared; low humidity dries the nasal lining and may impair mucus clearance; school calendars concentrate children in close contact precisely when temperatures drop. Cold, damp air is part of the season in which rhinoviruses thrive. But it is a feature of the ecological context, not an independent causal agent. No virus has ever been produced by a wet scalp.

The belief that wet hair causes colds survived in households throughout the twentieth century, impervious to the accumulating virological literature, because it seemed to explain something real. The correlation was real. The causal mechanism was not. The difference between colds happening more when the weather turns and cold weather causing colds is exactly the kind of distinction that requires controlled experiments to untangle, experiments that cannot be conducted by observing one's own family across a single winter. The theory persisted not because it was immune to disproof but because disproving a folk belief requires more than publishing a paper in a journal most households have never read.