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Excess weight is correlated with an elevated susceptibility to acute ailments that can necessitate hospital care and culminate in death. However, researchers are still trying to understand the reasons behind this correlation. (Image credit: Witthaya Prasongsin via Getty Images)
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According to a recent study involving over half a million participants, individuals dealing with obesity face a 70% greater likelihood than individuals without this issue to require hospitalization or perish due to critical infections.
The investigation determined that 1 in 10 deaths around the globe resulting from infections happened in obese individuals. This association remained even among those with obesity who didn’t have metabolic syndrome or diabetes. It was apparent across different socioeconomic backgrounds and physical activity habits, the researchers stated on Feb. 9 in the journal The Lancet.
“Individuals with obesity may struggle more in their fight against infections,” said study lead author Mika Kivimäki, an epidemiologist working at University College London, when speaking to Live Science. “Excess body mass can impact the immune system through several mechanisms, such as affecting lymphatic system performance, diminishing lung function, and raising the risk of persistent, low-level inflammation.” The lymphatic system is responsible for preserving fluid equilibrium in the body, plus guiding and carrying immune cells.
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A prior study, led by separate researchers and appearing in August 2025, indicated that semaglutide — the key component in prescription medications like Ozempic and Wegovy — decreased the likelihood of users getting severe infections by 10%. That discovery might also imply that obesity and vulnerability to infection are related, suggesting that this risk may be diminished.
The connection between obesity and hazardous infections was underscored during the COVID-19 pandemic, this study noted. In 2021, 15% of all hospitalizations and deaths due to infection had connections to obesity. That association linking obesity and COVID-19 severity encouraged Kivimäki and his team to examine if the coronavirus was specifically perilous for individuals with obesity, or whether the risk applied across diverse infection categories.
They referred to the UK Biobank, a major database of genetic sequencing and associated medical documents from UK adults, and also similar large-scale studies from Finland, like the Finnish Public Sector study, and the Health and Social Support study. In total, over 540,000 individuals were included in these databases.
Within the Finnish cohorts, individuals recorded their heights and weights, which enabled calculation of their body mass index (BMI). BMI delivers a general assessment of body composition that is frequently utilized in expansive population analyses. The participants in the UK Biobank underwent more accurate assessments using a body-composition analysis tool and also had measurements of their waist sizes. (Some researchers have suggested that such metrics should substitute BMI, as they more effectively predict health outcomes.)
For this study, obesity included those registering a BMI of 30 or greater; waist measurements exceeding 40 inches (102 centimeters) for men and 35 inches (88 cm) for women; or a waist-to-height ratio hitting 0.6 or higher. Obesity correlated with a 70% surge in the odds of hospitalization and death resulting from infection, after making allowances for age and gender. This correlation held for varying definitions of obesity and across diverse bacterial, viral, fungal, and parasitic infections.
The outcomes also indicated that the greater the degree of obesity, the greater the risk involved.
Obesity is connected to a heightened chance of grave illness and death resulting from COVID-19.
Individuals reporting a BMI ranging from 30 to 34.9 faced a 50% increased hazard of infection, hospitalization, or fatality, compared to those with BMI values below 30. However, those showing a BMI of 35 to 39.9 had double the risk, and those registering a BMI of 40 or more had triple the risk. Within the sample of individuals with obesity follow-up measurements after initial evaluation, those who shed or gained pounds showed proportional declines or increases in their severe infection risk.
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The study’s design didn’t empower researchers to determine causality or to precisely isolate how obesity may elevate such risks, according to Kivimäki.
Nevertheless, available data indicates that fat tissue and the immune response are intertwined; cells that can morph into fat cells can act similarly to immune cells, and select fat cells emit pro-inflammatory chemicals, stated Nikhil Dhurandhar, a nutrition professor at Texas Tech University, who was not involved in the recent analysis.
It’s a chronic disease. It’s not a matter of willpower; it’s not a matter of discipline.
Nikhil Dhurandhar, Texas Tech University
Previous studies have uncovered not only that weight impacts the risk of infection, but also some specific pathogens are associated with the progression of obesity, Dhurandhar informed Live Science. The support for the argument that some pathogens accelerate fat gain has primarily been gathered from animal studies, and information relating to humans is less conclusive.
Dhurandhar noted that obesity may play a role in immune dysfunction that makes it more taxing for the body to combat infection. As a result of this dysfunction, obese individuals might not have as strong of a response to vaccination as those with body mass designated as overweight or within normal ranges, which leaves them prone to infections. Obesity has connections with deficient sensitivity to the hormone leptin, which contributes to controlling appetite and body mass, while also functioning as an immune protector, he stated.
Dhurandhar conveyed that the connection of 1 in 10 infection deaths to obesity, as uncovered in the study, shouldn’t be regarded as easily avoided by shedding weight, given that it is quite challenging to both reduce weight and prevent its return.
“Obesity is a disease,” he said. “It’s a chronic disease. It’s not a matter of willpower; it’s not a matter of discipline.”
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However, the development of drugs, like semaglutide, that are recognized collectively as GLP-1 agonists, could potentially make weight loss more manageable for some. The effects of such pharmaceuticals on infection risks remains to be verified, Kivimäki stated.
Even though initial tests suggest these drugs may lessen risk, those consuming these drugs commonly also lose muscle in addition to fat, possibly yielding detrimental impacts on the immune defenses. Muscle provides an amino acid called glutamine that strengthens specific immune cells and also releases the anti-inflammatory ingredient interleukin-6.
“In our coming research, we aim to enhance our understanding of why obesity escalates the likelihood of severe infections,” stated Kivimäki, “and, critically, what interventions can diminish that risk.”
Disclaimer
This article is for informational purposes only and is not meant to offer medical advice.
Article Sources
Nyberg, S. T., Frank, P., Ahmadi-Abhari, S., Pentti, J., Vahtera, J., Ervasti, J., Suominen, S. B., Strandberg, T. E., Sipilä, P. N., Meri, S., Sattar, N., & Kivimäki, M. (2026). Adult obesity and risk of severe infections: A multicohort study with Global Burden Estimates. The Lancet. https://doi.org/10.1016/s0140-6736(25)02474-2
Stephanie PappasSocial Links NavigationLive Science Contributor
Stephanie Pappas writes for Live Science as a contributing author, covering topics ranging from geoscience and archaeology to human brain science. She was a senior writer for Live Science formerly but now is a freelancer from Denver, Colorado, and adds content regularly to Scientific American and The Monitor, a monthly publication by the American Psychological Association. Stephanie secured a bachelor’s degree in psychology from the University of South Carolina, together with a graduate certificate in science communication from the University of California, Santa Cruz.
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Insomnia and anxiety come with a weaker immune system — a new study starts to unravel why