This 2017 Penn State simulation found:

“By taking advantage of the natural variation in genetic relatedness among identical (monozygotic: MZ) and fraternal (dizygotic: DZ) twins, twin studies are able to estimate genetic and environmental contributions to complex human behaviors.

In the standard biometric model when MZ or DZ twin similarity differs from 1.00 or 0.50, respectively, the variance that should be attributed to genetic influences is instead attributed to nonshared environmental influences, thus deflating the estimates of genetic influences and inflating the estimates of nonshared environmental influences.

Although estimates of genetic and nonshared environmental influences from the standard biometric model were found to deviate from “true” values, the bias was usually smaller than 10% points indicating that the interpretations of findings from previous twin studies are mostly correct.”

The study model’s input was five phenotypes that varied the degrees of:

1. Genetic and epigenetic heritability;
2. Shared environmental factors; and
3. Nonshared environmental factors.

Item 1 above was different than the standard model’s treatment of heritable factors, which considers only additive genetic influences.

The authors cited studies for moderate and significant shared environmental influences in child and adolescent psychopathology and parenting to support the model’s finding that overall, item 2 above wasn’t underestimated.

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I wasn’t satisfied with the simulation’s description of item 1 above. With

1. Environmental influences accounted for elsewhere, and
2. No references to transgenerational epigenetic inheritance,
3. Randomness seemed to be the only remaining explanation for an epigenetic heritability factor.

Inserting the model’s non-environmental randomness explanation for epigenetic heritability into the abstract’s statement above exposed the non sequitur:

In the standard biometric model when MZ or DZ twin similarity differs from 1.00 or 0.50, respectively, the variance that should be attributed to genetic [and non-environmental stochastic heritability] influences is instead attributed to nonshared environmental influences, thus deflating the estimates of genetic [and non-environmental stochastic heritability] influences and inflating the estimates of nonshared environmental influences.

Why did the researchers design their model with an adjustment for non-environmental epigenetic heritability? Maybe it had something to do with:

“Estimates of genetic and nonshared environmental influences from the standard biometric model were found to deviate from “true” values.”

In any event, I didn’t see that this simulation was much more than an attempt to reaffirm a belief that:

“The interpretations of findings from previous twin studies are mostly correct.”

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Empirical rather than simulated findings in human twin study research are more compelling, such as The primary causes of individual differences in DNA methylation are environmental factors with its finding:

“Differential methylation is primarily non-genetic in origin, with non-shared environment accounting for most of the variance. These non-genetic effects are mainly tissue-specific.

The full scope of environmental variation remains underappreciated.”

https://link.springer.com/article/10.1007/s10519-017-9875-x “The Impact of Variation in Twin Relatedness on Estimates of Heritability and Environmental Influences” (not freely available)