outsourced to “inevitably present” microorganisms. The classic example is a laboratory experiment where a culture of amoebae became infected with a bacterium. At
first, both species in this mixed culture were handicapped but after 5 years the two
organisms became mutually dependent and could no longer survive alone (Jeon
1972). Each of them had lost some crucial genes because the encoded functions
could be outsourced to the other organism, which was inevitably present. However,
evolved dependence can clearly arise in two different ways. First, a species might
evolve in the presence of something (our need for oxygen for example), and so
incorporate that something into its physiology from the start. Alternatively, as in the
experiment with the amoeba described above, something might appear later and
cause the pre-existing germ line-encoded function to become redundant. For example, most mammals can synthesise vitamin C, but in humans and some other species
the gene encoding an essential enzyme is corrupted (Nishikimi and Yagi 1991). We
lost an enzyme required for making vitamin C because the diet of evolving humans
“inevitably” contained adequate supplies of it. Unfortunately, for sailors on long sea
voyages before vitamin C was recognised, the presence of vitamin C in the diet
turned out not to be inevitable after all and scurvy was common.
Both mechanisms apply to the human need for collaboration with, and exposure
to microorganisms. Genetic analyses indicate that about 65% of our genes originated
with the Bacteria, Archaea, and unicellular eukaryotes (Domazet-Loso and Tautz
2008), and we evolved in a world in which Bacteria, Archaea, and eukaryotic
microbes are dominant life forms (Bar-On et al. 2018). Thus, it is well-established
that we evolved from some microorganisms, and that we have incorporated others
into our physiology as symbionts, especially in the gut. But as will be described
below, we have also evolved dependence on continued exposure to microbes that
were, at least in the past, inevitably present in the environment.
So evolution turns the inevitable into a necessity, but it is equally important to
take note of the reverse concept: evolution tends not to turn the non-inevitable into a
necessity because obviously this can lead to gene–environment mismatch. Sometimes human development results in lifestyle changes that evolution could not
“predict” (such as the long sea voyages without sources of vitamin C), but sometimes we scientists assume inevitability that was not there. For example, the belief
that we are in a state of evolved dependence on infection with helminths seems to be
an error of this type. Helminths need to keep the host alive, so they downregulate
inflammation in order to avoid fatal immunopathology. So, it was argued that
humans accumulated mutations to partly offset the immunoregulatory strategies of
helminths, with the consequence that without helminths our immune systems are too
pro-inflammatory (Bilbo et al. 2011). But different helminth species live in blood,
tissues, bladder or gut, and each species downregulates inflammatory responses via a
different mechanism. Moreover, the loads of helminths differ wildly between individuals, even when they live in similar geographical locations. So there is no
constant “inevitable” factor that could drive germ line-encoded dependence on
helminths (discussed in Rook et al. 2017). Rather than becoming written into
germline mutations, intermittent or temporary environmental or infectious stresses
are coped with via epigenetic adaptations that can fade over several generations, or
18 Darwinian Medicine: We Evolved to Require Continuing Contact with the. . .
331
first, both species in this mixed culture were handicapped but after 5 years the two
organisms became mutually dependent and could no longer survive alone (Jeon
1972). Each of them had lost some crucial genes because the encoded functions
could be outsourced to the other organism, which was inevitably present. However,
evolved dependence can clearly arise in two different ways. First, a species might
evolve in the presence of something (our need for oxygen for example), and so
incorporate that something into its physiology from the start. Alternatively, as in the
experiment with the amoeba described above, something might appear later and
cause the pre-existing germ line-encoded function to become redundant. For example, most mammals can synthesise vitamin C, but in humans and some other species
the gene encoding an essential enzyme is corrupted (Nishikimi and Yagi 1991). We
lost an enzyme required for making vitamin C because the diet of evolving humans
“inevitably” contained adequate supplies of it. Unfortunately, for sailors on long sea
voyages before vitamin C was recognised, the presence of vitamin C in the diet
turned out not to be inevitable after all and scurvy was common.
Both mechanisms apply to the human need for collaboration with, and exposure
to microorganisms. Genetic analyses indicate that about 65% of our genes originated
with the Bacteria, Archaea, and unicellular eukaryotes (Domazet-Loso and Tautz
2008), and we evolved in a world in which Bacteria, Archaea, and eukaryotic
microbes are dominant life forms (Bar-On et al. 2018). Thus, it is well-established
that we evolved from some microorganisms, and that we have incorporated others
into our physiology as symbionts, especially in the gut. But as will be described
below, we have also evolved dependence on continued exposure to microbes that
were, at least in the past, inevitably present in the environment.
So evolution turns the inevitable into a necessity, but it is equally important to
take note of the reverse concept: evolution tends not to turn the non-inevitable into a
necessity because obviously this can lead to gene–environment mismatch. Sometimes human development results in lifestyle changes that evolution could not
“predict” (such as the long sea voyages without sources of vitamin C), but sometimes we scientists assume inevitability that was not there. For example, the belief
that we are in a state of evolved dependence on infection with helminths seems to be
an error of this type. Helminths need to keep the host alive, so they downregulate
inflammation in order to avoid fatal immunopathology. So, it was argued that
humans accumulated mutations to partly offset the immunoregulatory strategies of
helminths, with the consequence that without helminths our immune systems are too
pro-inflammatory (Bilbo et al. 2011). But different helminth species live in blood,
tissues, bladder or gut, and each species downregulates inflammatory responses via a
different mechanism. Moreover, the loads of helminths differ wildly between individuals, even when they live in similar geographical locations. So there is no
constant “inevitable” factor that could drive germ line-encoded dependence on
helminths (discussed in Rook et al. 2017). Rather than becoming written into
germline mutations, intermittent or temporary environmental or infectious stresses
are coped with via epigenetic adaptations that can fade over several generations, or
18 Darwinian Medicine: We Evolved to Require Continuing Contact with the. . .
331