Like theoretical physics theories, evolutionary theories are difficult to test experimentally. You can’t conduct experiments as you can in most other branches of science.

However, they can be validated by looking at whether they can make accurate predictions.

One obvious prediction from the Red King Theory is that if shorter lifespans help reduce pathogen and parasite load, then there should be some pathogens and parasites that extend the lifespan of their hosts. By extending the host lifespan, the pathogens can increase the transmission of its progeny. We would expect a battle between hosts and pathogens over lifespan, in which sometimes hosts win and sometimes parasites win. So while in many or most cases we would expect hosts that have pathogens or parasites to accelerate programmed aging (and this is generally the case), we would expect to see that some would demonstrate longer lifespans when infected by a parasite that is winning the battle over lifespan.

The great thing about this prediction is that mainstream theories would predict that pathogens generally reduce the survival and lifespan of its hosts. So this prediction is unusual, and contrary to what would be expected. So it’s a good prediction to test because if it is borne out by observations then not a lot of competing theories would be consistent with that.

So are there pathogens or parasites that increase host lifespan?

Yes. Many.

One example is the Xenos vesparum that infects Polistes dominnula wasps. These paper wasps are eusocial wasps that have several castes. The workers and males generally only live 30-40 days and never survive beyond the summers, while the queens survives over the winter and can live up to a year.

The workers that are parasitized by the parasite don’t die at the end of the summer. Instead, they survive over the winter, until the next generation of wasp larvae are ready to be infected. Furthermore, the male parasites don’t affect the lifespan. Only the female parasites do. All this points to manipulation of the lifespan by the parasite.

There are other examples, even though this is not a phenomena that has been well-studied. For example, Hymenolepis diminuta that infect Tenebrio molitor beetles increase host lifespan by up to 40%.

As another example, workers of the ant Temnothorax nylanderi infected by a tapeworm (Anomotaenia brevis) show extreme lifespan extension. Infected workers live as long as the colony’s queens (who can survive decades), whereas normal uninfected workers have lifespans as short as few weeks. The parasite appears to secrete factors that keep the host in a juvenile-like state – infected ants remain yellowish and continue to be fed and groomed by nest-mates as if they were young, avoiding risky foraging . Their metabolism is altered and they experience low wear-and-tear, allowing them to survive far beyond a worker’s normal span. This prolonged host survival presumably aids the parasite, giving it more time to complete development and eventually spread .

Symbiotic Bacteria Wolbachia bacteria can positively affect host longevity in some cases. Not only that, certain Wolbachia strains in Drosophila melanogaster were shown to increase female fly lifespan (and fertility) with no obvious trade-offs . In one study, females harboring the wMel or wMelCS Wolbachia variants lived longer and laid more eggs than Wolbachia-free flies . (Not all Wolbachia are beneficial – some shorten lifespan – but these findings suggest specific symbiont–host genotypes can be mutualistic.) Wolbachia infections in insects can block certain viruses, indirectly improving host survival . Thus, in some insects a bacterial “parasite” effectively acts as a longevity-promoting symbiont.

Even in mammals, there is some evidence that parasites may have longevity effects. A striking example is the nematode worm product ES-62 (a secreted glycoprotein from Acanthocheilonema viteae). In a mouse model of diet-induced aging, weekly ES-62 treatments reduced chronic inflammation (“inflammaging”) and improved metabolic health, resulting in a 12% extension of median lifespan in treated mice. Helminth infections are known to dampen pro-inflammatory cytokines and can protect tissue integrity (e.g. maintaining gut lining and preventing fat accumulation) . This immune modulation relieves age-accelerating inflammation and may mimic effects of caloric restriction or anti-aging pathways (indeed, worm infections have been noted to suppress the pro-aging mTOR pathway in host cells) . Such cases support the idea that a parasite can prolong host life by attenuating immunopathology and preserving organ function, effectively keeping the host alive longer as a hospitable environment.

There is a small body of data that certain parsites, such as instestinal worms, can have anti-inflammatory effects, including lowering the incidence of diabetes, lowering the risk of cancer, and decreasing atherosclerotic plaque size (reviewed here).

Some parasites manipulate plant physiology to keep host tissues alive longer. Leaf-miner moths in the genus Phyllonorycter are herbivorous insect parasites whose larvae tunnel within leaves. Remarkably, these larvae induce localized “green islands” – patches of leaf that stay green and photosynthetically active even as the rest of the leaf yellows and dies in autumn . Research shows this effect is mediated by bacterial endosymbionts (Wolbachia) inside the insect: the symbiotic bacteria manipulate plant hormones (cytokinins) to prevent the leaf segment from senescing . When the bacteria are removed (antibiotically “cured”), the leaf-miner can no longer create green islands; the leaf dies normally and the larvae have reduced survival . In essence, the microbe helps the insect parasite extend the lifespan of the host leaf tissue, maintaining a fresh food supply. This three-way interaction (bacteria–insect–plant) is a striking example of a parasite prolonging the life of part of its host for its own benefit via hormonal manipulation of host cells.

In the roundworm Caenorhabditis elegans, which is a model for aging studies, certain bacterial strains can dramatically affect longevity. For instance, feeding worms a diet of probiotic Pediococcus bacteria instead of the standard E. coli can extend the worms’ lifespan and improve health markers. One study found that Pediococcus acidilactici prolonged C. elegans lifespan by activating the worm’s stress resistance pathways (insulin/IGF-1 and JNK/MAPK signaling) and reducing fat accumulation and reactive oxygen species in the worm . Essentially, the bacterium triggers a mild stress response or improved metabolic profile in the host, akin to dietary or genetic anti-aging interventions. Other commensal bacteria produce metabolites (e.g. indoles, short-chain fatty acids) that signal the host to enhance tissue maintenance and immune balance, thereby slowing aging in the worm .

Parasitologists have noted that “parasitic castrators” (parasites that stop host reproduction) often lead to increased host longevity as a side-effect. For instance, certain larval trematode worms infecting snails prevent the snail from reproducing and can cause the snail to grow larger and live longer than normal, thereby providing a longer-lived vessel for the parasite’s asexual multiplication .