Ning Leow
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Ning Leow
@whatnowning.bsky.social
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Neuroscientist / Post-Doctoral Fellow @ IMCB, A*STAR 🇸🇬/ Formerly @MITBrainandCog 🇺🇸& @uclnpp 🇬🇧 / recovering revenge bedtime procrastinator

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Reposted by Ning Leow
carlbergstrom.com
Since people expressed curiosity, here's an excerpt from my textbook Evolution (coauthored with Lee Dugatkin) that addresses fever as an evolved defense and why we can treat it safely nonetheless.
The proximate mechanisms responsible for triggering mammalian fever are relatively well understood. When immune cells recognize the presence of a pathogen, they release signaling chemicals known as cytokines. Among many other functions, cytokine signals stimulate the brain region known as the hypothalamus, which is responsible for regulating many of the body’s physiological systems (Figure 20.2). The signals induce a shift in the body’s thermal setpoint for temperature regulation, promoting warmth-seeking behavior while driving an endogenous increase in body temperature and inducing fever (Osterhout et al. 2022). For example, when components of the bacterial cell wall are bound by immune cells known as macrophages, the macrophages produce the fever-inducing signals. The presence of bacterial cell wall components is a strong indicator of bacterial infection, and thus this pathway illustrates a mechanistic coupling between indications of pathogen challenge and the fever response. Consequences of Fever In humans, higher fevers are associated with more severe infections. A number of studies of human patients have shown that patients who receive fever- reducing antipyretic drugs such as aspirin, acetaminophen, or ibuprofen recover less quickly from viral infection (Hasday et al. 2000). These observations indicate that fever may play a beneficial role in shortening the duration of infection. Studies of patients with bacterial sepsis (a severe and very dangerous full-body inflammatory response induced by bacterial infection) have often, but not always, revealed a higher survival rate in patients that exhibit fever than in patients without fever. It is important to recognize that this observed correlation does not provide direct evidence of causation. Survival rates could be lower in patients without fever because, for example, the inability to mount a fever response could be indicative of more severe illness. As we described in the introduction of this chapter, numerous nonhuman species exhibit a fever response as well (Figure 20.3). In many of the species, manipulative studies are possible. Animals infected with bacterial pathogens and then treated with antipyretic drugs have more rapid bacterial proliferation and higher mortality rates than individuals allowed to develop a normal fever response. Similar results have been observed for viral infections. Because manipulating temperature by pharmaceutical means may cause additional side effects that make it hard to interpret the experimental results, researchers have also conducted experiments in which they manipulate body temperature directly. These studies tend to show comparable benefits to elevated body temperature. Taken together, the correlational studies in humans and manipulative studies in … of bacterial cell wall components is a strong indicator of bacterial infection, and thus this pathway illustrates a mechanistic coupling between indications of pathogen challenge and the fever response. Consequences of Fever In humans, higher fevers are associated with more severe infections. A number of studies of human patients have shown that patients who receive fever- reducing antipyretic drugs such as aspirin, acetaminophen, or ibuprofen recover less quickly from viral infection (Hasday et al. 2000). These observations indicate that fever may play a beneficial role in shortening the duration of infection. Studies of patients with bacterial sepsis (a severe and very dangerous full-body inflammatory response induced by bacterial infection) have often, but not always, revealed a higher survival rate in patients that exhibit fever than in patients without fever. It is important to recognize that this observed correlation does not provide direct evidence of causation. Survival rates could be lower in patients without fever because, for example, the inability to mount a fever response could be indicative of more severe illness. As we described in the introduction of this chapter, numerous nonhuman species exhibit a fever response as well (Figure 20.3). In many of the species, manipulative studies are possible. Animals infected with bacterial pathogens and then treated with antipyretic drugs have more rapid bacterial proliferation and higher mortality rates than individuals allowed to develop a normal fever response. Similar results have been observed for viral infections. Because manipulating temperature by pharmaceutical means may cause additional side effects that make it hard to interpret the experimental results, researchers have also conducted experiments in which they manipulate body temperature directly. These studies tend to show comparable benefits to elevated body temperature. Taken together, the correlational studies in humans and manipulative studies in … downtime—is far less than the cost of failing to produce a fever when it is needed to clear an infection. Thus, we might expect that fevers should be relatively common, and most should be unnecessary. If so, this means that in most cases, we should be able to intervene safely, reducing fever with antipyretic drugs. Medical technologies—most notably antibiotics and rehydration therapy—and improvements in nutritional status further reduce the risk of death by infection relative to what it would have been throughout much of our evolutionary history. Even many of those infections that might historically have been lethal without a fever response can now be safely controlled without fever. This is not to say that treating most fevers with antipyretic drugs is necessarily a good idea. Further research will be needed to resolve that issue. But it does provide an explanation for why we can often safely interfere with fever, despite its role as an evolved defense against pathogens.
April 13, 2025 at 7:39 PM