Published in PLoS ONE in 2025, researchers conducted the first comprehensive meta-analysis pooling data from 11 studies involving 3,177 total participants to quantitatively assess the immune effects of cold-water immersion.

The pooled analysis found no statistically significant effects on immune function markers either immediately after cold-water immersion or 1 hour post-immersion. Furthermore, the meta-analysis found a significant acute increase in inflammation markers, suggesting that cold exposure initially triggers an inflammatory stress response rather than an immune-boosting effect.

The authors concluded that purported immune benefits of cold-water immersion "remain unsubstantiated" by the pooled quantitative evidence. They noted that while the Buijze 2016 study showed 29% fewer sick days, this appeared only in narrative synthesis and could not be confirmed in quantitative meta-analysis because it measured work absence rather than actual immune function.

The Buijze 2016 cold shower trial (N=3,018) is the most cited evidence for cold-boosting immunity, but a critical detail is often overlooked: while sickness absence from work decreased by 29%, the number of self-reported illness days (days participants actually felt sick) was not significantly different between groups.

This means cold shower participants still got infections at the same rate and felt sick for the same duration as the control group. They simply chose to go to work despite feeling ill. The study authors themselves acknowledged they could not distinguish between actual immune enhancement and psychological effects such as improved perceived energy, increased mental toughness, or a sense of invigoration that made participants more willing to work while sick.

This distinction is critical because "fewer sick days off" is not the same as "fewer infections." If cold showers boosted immune function, we would expect fewer infections or shorter illness duration. Finding neither suggests the benefit is perceptual rather than immunological.

Published in Wilderness and Environmental Medicine in 2011, researchers reviewed the immune effects of exercising in cold environments, combining data from military, athletic, and laboratory studies.

Cold exposure combined with physical exertion caused increased cortisol secretion (an immunosuppressive hormone), decreased lymphoproliferative responses (reduced ability of immune cells to multiply when challenged), decreased TH1 cytokines (the pro-inflammatory signals needed to fight infections), and decreased salivary IgA (the antibody that protects against respiratory infections).

At the Winter Olympics, 45% of Finnish athletes (20 of 44) and 32% of staff (22 of 68) developed upper respiratory tract infections during a median 21-day stay. The combination of cold exposure and physical stress amplified immune suppression beyond either stressor alone. This evidence suggests that prolonged cold exposure, particularly when combined with physical demands, impairs rather than enhances immune defense.

Published in PLoS ONE in 2014, Lithuanian researchers measured immune cell populations before, during, and after single cold-water immersion at 14 degrees Celsius to determine whether the observed changes represent genuine immune enhancement or merely redistribution.

Cold immersion caused increased neutrophil proportion, decreased lymphocyte proportion, and reduced monocyte proportion. However, all leukocyte counts fully recovered to pre-exposure baseline levels within 6 to 12 hours after immersion ended.

The complete recovery indicates that cold exposure causes temporary redistribution of existing immune cells between blood, lymph tissue, and peripheral compartments rather than stimulating the production of new immune cells. This is analogous to how exercise transiently moves immune cells into the bloodstream from tissue reservoirs. A genuine immune boost would require either more immune cells being produced or existing cells becoming more effective at killing pathogens, neither of which was demonstrated.

Published in Rhinology in 2002, Cardiff University researcher Ron Eccles reviewed the mechanisms by which body surface cooling affects upper respiratory tract defense against viral infections.

Acute cooling of the body surface causes reflex vasoconstriction in the nasal passages, reducing blood flow to the nasal mucosa. This inhibits local immune defense by reducing mucociliary clearance (the mechanism that traps and expels pathogens) and impairing phagocytic activity of resident immune cells that require adequate blood supply to function.

The review proposed that cold does not directly cause infection but may activate latent subclinical viral infections that the body was successfully suppressing. By temporarily weakening local nasal immune defense, cooling may tip the balance from asymptomatic carriage to symptomatic clinical infection. This provides a mechanism for the common observation that people get more colds in winter and after cold exposure.

The Costello 2025 meta-analysis in PLoS ONE identified critical methodological weaknesses across the cold exposure literature that undermine confident conclusions about immune benefits.

Of the 11 studies included in quantitative synthesis, 5 combined cold-water immersion with exercise, making it impossible to isolate the effect of cold alone from the well-established immune effects of physical activity. Only 1 of the included studies had female participants (44 of 52 total studies reviewed were male-only), severely limiting generalizability.

The review also identified strong evidence for placebo contributions to reported improvements. People who choose to practice cold exposure tend to be healthier, more physically active, and more health-conscious at baseline than the general population. This selection bias means observational studies of winter swimmers or cold shower enthusiasts may be measuring pre-existing health advantages rather than effects of the cold exposure itself.

Published in Comprehensive Physiology in 2015, military physiologists John Castellani and Michael Tipton reviewed the effects of cold stress on human physiology, drawing on decades of military research with soldiers in cold environments.

Prolonged cold stress activates the hypothalamic-pituitary-adrenal axis, producing sustained elevations in cortisol, norepinephrine, and epinephrine. While brief elevations of these hormones can stimulate immune cell mobilization, sustained elevations suppress the immune system by reducing pro-inflammatory cytokine release, decreasing adhesion molecules (preventing immune cells from reaching infection sites), and altering immune cell trafficking patterns.

The review emphasized a critical distinction: brief voluntary cold exposure (cold showers, short swims) produces different physiological effects than chronic involuntary cold stress (prolonged outdoor exposure, hypothermia). Most immune-boosting claims extrapolate from the brief voluntary category, while military and occupational data consistently show that sustained cold exposure leads to immunosuppression and increased infection rates.

Published in the New England Journal of Medicine in 1968, researchers at Baylor University College of Medicine inoculated 44 antibody-free volunteers with rhinovirus Type 15 (a common cold virus) and then exposed them to 4 degrees Celsius cold environments at various timepoints.

The study found "no effect of exposure to cold on host resistance to rhinovirus infection and illness." People exposed to cold after inoculation developed colds at the same rate as those kept warm. Cold exposure did abolish the normal neutrophil increase seen during illness, but this did not translate into any difference in infection rates or symptom severity.

This foundational study demonstrated that being cold does not make you more likely to catch a cold if exposed to a virus. However, it also shows no protective effect: cold exposure did not prevent infection or reduce symptoms. The finding challenges both the folk belief that cold causes illness and the modern claim that cold exposure prevents illness by boosting immunity.