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. 2017 Apr 18;40(6):zsx055. doi: 10.1093/sleep/zsx055

Table 4.

Heritability estimatesa of heart rate response to arousal measures in twins.

Measure Unadjusted Adjustedb
ICCMZc ICCDZc H2d C2e ICCMZc ICCDZc H2d C2e
Arousal Index 0.628 0.438 0.380 0.248 0.594 0.443 0.300 0.293
Average arousal duration 0.473 0.204 0.538 −0.065 0.465 0.249 0.433 0.032
Average arousal intensity scale 0.689 0.202 0.972 −0.284 0.663 0.146 1.035 −0.372
Slope of ΔHR per arousal intensity 0.456 0.562 −0.211 0.667 0.306 0.237 0.139 0.167
Arousal intensity threshold of ΔHR 0.533 0.000 1.065 −0.533 0.449 0.000 0.899 −0.449
Average ΔHR 0.660 0.557 0.208 0.453 0.548 0.240 0.616 −0.068
ΔHR at arousal intensity scale 4 0.621 0.547 0.148 0.472 0.529 0.342 0.372 0.156
ΔHR at arousal intensity scale 5 0.600 0.636 −0.071 0.671 0.489 0.388 0.203 0.286
ΔHR at arousal intensity scale 8 0.541 0.672 −0.262 0.803 0.399 0.376 0.047 0.352

Abbreviations: ICC, Intraclass Correlation Coefficient; H2, classical broad-sense heritability; C2, estimated proportion of phenotypic variability explained by common environmental factors; PGM, preferred genetic model; ΔHR, heart rate response to arousal.

aNegative values of H2 or common environment (C2) suggest genetic or environment effects are likely not important, respectively, while values greater than 1 suggest strong genetic or environmental effects.

bAdjusted for race, age, sex, and age by sex interaction.

cICC: Intraclass Correlation Coefficient, equal to σ2B / (σ2W + σ2B).

dH2: classical, broad-sense heritability estimate, equal to 2(ICCMZ – ICCDZ).

eC2: Estimated proportion of phenotypic variability explained by common environmental factors, equal to 2(ICCDZ) – ICCMZ. C2 estimates < 0 suggest that an ADE inheritance model may be more appropriate and C2>0 imply an ACE model may better represent the inheritance pattern, where A = additive genetic effects, C = common environmental effects, D = dominant genetic effects, and E = unique individual effects. Thus, ACE models additive genetic, common environment and individual effects, whereas ADE models additive and dominant genetics and individual effects.