1200 words

Introduction

Heritability estimates have been used as a cornerstone and psychology and genetic research. They are designed to quantify the proportion of phenotypic variance in a population that can be attributed to genetic differences among individuals. We’ve known for a while now that heritability isn’t a measure of genetic strength (Moore and Shenk, 2016), but it’s a population-specific estimate of variance. Here I will provide two a priori arguments (one methodological on twins and the EEA and one theoretical based on Noble’s biological relativity argument). The twin critique shows that the twin researcher’s main assumption (equal environments) does not hold while the biological relativity critique shows that h2 is conceptually invalid. This is why there is a missing heritability problem—it never existed in the first place, and the assumptions twin researchers have are false.

The classical twin method

The CTM compares MZ and DZ twins to attempt to quantify the relative contributions of genes and environment in relation to the origin of trait differences between individuals. Perhaps the biggest assumption of the twin researcher is the equal environments assumption (EEA). The EEA assumes that MZ and DZ twins experience equivalent shared environments.

The EEA seems plausible enough: twins reared together should experience compatible environments, regardless of zygosity. But since DZ twins are more genetically similar than DZ twins so they’ll be more phenotypically similar as well. MZ twins are dressed alike, mistaken for one another, or placed in similar social roles compared to DZ twins which leads to more similar environments. So the shared environmental variance for MZ twins exceeds that for DZ twins, violating the EEA.

Clearly this violation throws a wrench into the logic of the CTM. The formula assumes that the greater similarity in MZ twins stems solely from their genetic identity. But if MZ twins experience more similar environments due to their phenotypic similarity (Fosse, Joseph and Richardson, 2015; Joseph et al, 2015), the difference in correlations between MZs and DZs captures genetic variance and excess environmental similarity. Thus, heritability is overestimated (see eg Bingley, Cappellari, and Tatsiramos, 2023) increasing the effect of genes while masking the effects of the environment—in effect, environment is made to look like genes. Thus, h2 fails to isolate genetic influence as intended. (Note that Grayson 1989 explains this as well, but it seems that it’s just ignored.) Here’s the argument:

(1) The classical twin method assumes that its heritability (h2) estimate (Falconer’s formula) isolates the proportion of phenotypic variance due solely to genetic variance.

(2) For the h2 estimate to isolate genetic variance, the shared environmental variance must be equal for MZ and DZ twins.

(3) MZ twins are more genetically similar than DZ twins.

(4) Genetic similarity between individuals leads to greater similarity in their expressed phenotypic traits, and this phenotypic similarity results in greater similarity in their environmental experiences.

(5) Because MZ twins have greater genetic similarity than DZ twins, and genetic similarity leads to phenotypic similarity, which in turn results in environmental similarity, the shared environmental variance is greater for MZ twins compared to DZ twins.

(6) If the shared environmental variance for MZ twins is greater than that for DZ twins, then the EEA is false because it requires that shared environmental variance be equal for both twin types.

(7) If the EEA is false, then we cannot logically infer genetic conclusions from h2, and thus h2 reflects shared environmental variance (c2), rather than genetic variance.

(8) Any method that relies on an assumption that’s logically inconsistent with the principles governing it’s variables – like the relationship between genetic similarity, environmental similarity and phenotypic similarity – cannot accurately isolate its intended causal component and is therefore conceptually untenable.

(9) Thus, the classical twin method is conceptually and logically untenable since it depends on the EEA which, when false, renders h2 a measure of environmental—not genetic—variance.

The biological relativity critique against h2

This argument is theoretical as opposed to methodological, and it relies on Noble’s (2012) biological relativity argument, where there is no privileged level of causation in biological systems. Genes, cells, tissues, organs, organisms, and the environment form an interdependent network where each level influences and is influenced by the other levels. Phenotypes arise from the interaction between all of these levels, not just due to the independent action of any one of the resources.

Heritability rests on a reductionist assumption—that phenotypic variance can be neatly partitioned into genetic and environmental components with genetic effects isolated as a distinct and quantifiable entity. This framework, clearly, privileges the genetic level treating it as separate from the broader biological and ecological context. But Noble’s argument directly contradicts this view. Genes don’t operate in a vacuum and do nothing on their own.

So by attempting to isolate genetic variance, heritability imposed an artificial simplicity on a complex reality (Rose, 2006). Noble’s principle suggests that separation isn’t just an approximation but a fundamental conceptual flaw. Phenotypic variation emerges from the integrated functioning of all biological levels, which then makes it impossible to assign causation to genes alone.

Thus, h2 is conceptually flawed, since it seeks to measure a genetic contribution that cannot be meaningfully disentangled from the holistic system in which it operates. Obviously the conceptual foundation of h2 contradicts the principle of biological relativity. Since h2 attempts to assign a specific portion of trait variance to genes alone, h2 implicitly privileges the genetic level, suggesting that it can be disentangled from the broader biological system. Noble’s argument denies that this is possible while emphasizing holism and rejecting reductionism. Thus, a priori, h2 estimates are fundamentally flawed because they rest on a reductionist framework which assumes a separability of causes which is incompatible with the holistic, relativistic nature of biological causation. Here’s the argument:

(1) Biological relativity holds that there is no privileged level of causation in biological systems: all levels (genes, cells, tissues, organs, organisms, environments) are interdependent in producing phenotypes.

(2) h2 assumes that genetic variance can be isolated and quantified as a distinct contributor to phenotypic variance.

(C) Since biological relativity rejects the isolation of genetic effects, h2 is conceptually invalid as a measure of genetic influence.

Conclusion

Both of these arguments show the same thing—h2 is a deeply flawed concept. The EEA critique exposes a methodological weakness: since MZ twins experience more similar environments than DZ twins, the excess environmental similarity experienced by MZs masquerades as genetic influence, leaving h2 incapable of isolating genetic variance.

But Noble’s biological relativity argument strikes at a deeper conceptual flaw in this practice, since it challenges the theoretical aspects of h2 itself. Since it highlights the interdependence of biological systems, it dismantles the reductionist notion that genetic effects can be separated from other levels of causation. The gene-centric assumption is at ends with the reality of phenotypes being emergent properties of multi-level interactions, which then renders the concept of h2 conceptually incoherent. Therefore, h2 isn’t only empirically questionable but it is theoretically untenable. The conceptual model is just not sound due to how genes really work (Burt and Simon, 2015)

Thus, again, hereditarianism fails conceptually. Even their main “tool” fails for a modicum of reasons not least the main theoretical killshot for heritability estimates—the principle of biological relativity. The reductionist hereditarian paradigm is conceptually and logically untenable, it’s time to throw it away, it’s time to throw it to the dustbin of history.