Viewing Diseases As Adaptations

An error that is as natural as it is serious

By Randolph M. Nesse
October 13, 2025 on Nessays.com

Viewing Diseases As if they are Adaptations shaped by natural selection (VDAA) is increasingly recognized as an error, but it remains common. Diseases are not traits shaped by natural selection. They don’t have evolutionary explanations based on their adaptive functions. The correct objects of explanation are, instead, universal traits that make all individuals in a species vulnerable to a disease.

Does the creativity of some individuals who have schizophrenia give selective advantages that explains the persistence of the responsible genes? Can the special abilities of some individuals with autism explain its persistence? Are cystic fibrosis alleles selected for because they prevent fatal diarrhea? Is anorexia nervosa a facultative adaptation that responds to famine by inducing some individuals to run many miles looking for food to benefit the group? Was ADHD selected for because it increases curiosity or creativity? Published articles advocate for each of those hypotheses, but they are inconsistent with evolutionary theory. Genes and traits that reduce average inclusive fitness tend to be selected out, even if they benefit some individuals or groups. With only a few exceptions, uncommon traits are not adaptations. The default evolutionary explanation for diseases is not that they are somehow useful, it is instead that natural selection’s power is limited, and it shapes traits that maximize gene transmission at the expense of robustness

VDAA persists nonetheless, like a mutation that arises again as fast as it is selected out. I think it is a product of deep human cognitive tendencies. When George Williams and I first tackled the mystery of why natural selection leaves organisms vulnerable to disease, we spent hours speculating about ways that atherosclerosis, cancer, and schizophrenia could give advantages. Only after a month of frustrating discussions did we finally recognize our mistake: diseases don’t have direct evolutionary explanations. The correct objects of explanation are, instead, universal traits that make all individuals in a species vulnerable to a disease. Examples include immune cells in the endothelium, the ability of liver cells to multiply, the narrow bh canal, and the body’s limited abilities to prevent mutations, cancer, and infection.

That crucial insight spurred us to describe six possible evolutionary explanations for traits that cause disease vulnerability. The first three reflect the limitations of natural selection:

• it can’t get to or preserve optimal designs ,

• it is too slow to keep up with shifting environments, and

• it is far too slow to keep up with fast-evolving pathogens.

The other three arise instead from the power of natural selection:

• it shapes tradeoffs that compromise individual robustness in the service of increased performance,

• it maximizes reproduction at the expense of health and longevity, and

• it shapes costly painful defensives that impose substantial risks.

Those six categories have been widely used to understand universal traits that make bodies vulnerable to disease. Multiple explanations usually apply, but the tendency to emphasize only one is a topic for a different essay.

Why do efforts to explain diseases as adaptations continue when a framework is available for understanding traits that make a species vulnerable? I see two main possibilities: 1) humans cognition is predisposed to find functions, and 2) many diseases are associated with benefits.

Battles about adaptationism still smoulder despite consuming gigawatts of emotion and thinking. Gould and Lewontin’s 1979 spandrels article attacked speculations about adaptations effectively, but it said little about how to frame and test hypotheses. Forty-four years later, the phrase “just-so-stories” still suffices as a critique in some circles, as if the fields of evolutionary physiology and behavioral ecology did not exist. Such global criticism does little to address a problem that remains real and large. Decades of teaching evolutionary medicine gradually forced me to recognize that the tendency to adaptationist thinking about disease results runs deep. I began each course by warning students not to make the mistake of thinking that diseases are traits that give selective advantages. At the end of each term, despite more warnings and many examples, I received term papers proposing that schizophrenia, epilepsy, or anorexia nervosa were somehow useful.

The tendency to excess adaptationism may have an adaptationist explanation. Imagining possible functions for an object can give big advantages. Humans carve branches into digging sticks and they flake sharp stones into knives. Our words organize experience into categories based on function. Chairs come in diverse shapes and sizes, but they all are all for sitting, just as knives of many shapes are for cutting, and bags of many designs are for carrying. Because so much human cognition is organized around function, our minds are primed to pair traits with functions, even when that is not appropriate.

Educational traditions also contribute. Natural selection is taught by describing how a rare trait become common, the exemplar being the transition of the peppered moth (Biston betularia) from white to dark wings as tree trunks were increasingly stained by Victorian era-soot. The focus on how variations influence fitness is entirely appropriate; that is the process by which natural selection changes a species. However, that framework encourages viewing uncommon traits as if they are adaptations and it distracts from the vastly more common effect of natural selection to keep traits the way they are.

The second explanation for VDAA arises because many diseases have associated benefits. Those benefits do not give net advantages that can explain the trait, but they are nonetheless relevant. Cystic fibrosis alleles decrease the risk of death from cholera, but that does not mean they give a net advantage, it just means that they are selected out more slowly than they would be otherwise. The characteristics of low mood are useful in certain situations, but that does not mean that major depression is an adaptation.

Other benefits are associated with tradeoffs. Most traits reflect a compromise among multiple costs and benefits. In a stable environment, fitness tends to be highest for individuals with the average value of a trait. Although individuals with values away from the mean will have lower fitness on average, they will also experience some benefits. Individuals with more anxiety than average get protection against dangers along with larger costs from lost opportunities. Individuals with less anxiety than average benefit from risk-taking along with larger costs from harm. The wide range of most personality characteristics suggests that fitness does not vary much across the mid-range of the distribution. Individuals with traits far from the mean are, however, sometimes viewed as if they are special types selected for because they have advantages. This is usually an error. For instance, it has been repeatedly suggested that tendencies to ADHD gave selective advantages in the past, but individuals in ancestral environments who had lower-than-average ability to focus attention would be expected to have lower than average fitness in ancestral environments; the disadvantages are magnified in modern environments.

Defenses against pathogens are particularly likely to cause problems because arms races create fitness functions with steep slopes and high costs, even at the peak. So, individuals with immune systems of optimal aggressiveness are vulnerable to both infection and inflammation. Adaptive responses with flatter fitness functions also result in advantages and net disadvantages for individuals away from the mean. So, individuals with tendencies to sweat profusely get protection against overheating at the risk of dehydration, while those who sweat less than average get the opposite benefits and costs. In modern environments such costs and benefits may be shifted markedly, often creating new selection forces that shift the population mean. These observations suggest ways to consider the adaptive significance of advantages associated with disease without falling into VDAA.

In the spirit of trying to provide guidance instead of just criticism, here are three principles that can help guide attempts to find evolutionary explanations for disease vulnerability.

1. The appropriate object of explanation in evolutionary medicine is usually a shared trait that makes all members of a species vulnerable to the disease, not the disease itself.

2. Multiple explanations are usually relevant.

3. Uncommon genes or traits are usually products of mutation, migration, genetic drift, or stochasticity more generally. They are selected for only in special circumstances including:

   1. Being selected in or out. (ApoE4)

   2. Geographically separate subgroups exposed to different environments. (skin color)

   3. Effects of adaptive plasticity and facultative adaptations. (skin tanning, anxiety)

   4. Trade-offs: Individuals with trait values away from the mean are expected to have some advantages along with net disadvantages. (more than average sweating prevents heat stroke at the risk of dehydration)

   5. Balancing selection maintains genetic variations when the fitness effects of an allele vary depending on the external environment or the genomic ground. (polymorphic shell patterns in grove snails)

   6. Heterozygote advantage is a subtype of balancing selection in which the superior fitness of heterozygote individuals maintains the variation by frequency dependent selection. Heterozygote advantage is rare because the costs to homozygotes are high. (sickle cell hemoglobin)

   7. Antagonistic pleiotropy maintains alleles that cause aging because the benefits they give in youth when selection is strong are greater than the costs in late life when selection is weak. lifetime. (senescence)

   8. Morphs can persist if each has equal fitness maintained by negative frequency dependent selection of distinct separate types. (fish mating types)

   9. Bet hedging increases gene transmission in wildly varying environments at the expense of individual survival. (seed coat variation in desert plants)