Future science OA · 2026
Causal effects of basal metabolic rate and adiposity on obstructive sleep apnea: univariable, multivariable, and bidirectional Mendelian randomization evidence.
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Zhang Mengjie, Li Chao, Wang Xiaoe, Liu Ruirui, Chen Qingge, Wu Chaomin
Аннотация
BACKGROUND: Obstructive sleep apnea (OSA) is a common disorder strongly associated with obesity, yet the causal contribution of basal metabolic rate to OSA and the directionality of the OSA-metabolism relationship remain unclear. The objective of this study was to evaluate the independent and potential bidirectional causal relationships between basal metabolic rate and adiposity-related traits with obstructive sleep apnea using Mendelian randomization.
METHODS: Two-sample Mendelian randomization (MR) was performed using genome-wide association study data from predominantly European populations to evaluate the causal effects of basal metabolic rate, body mass index, and whole-body fat mass on OSA risk and to assess the reverse effects of genetic liability to OSA on basal metabolic rate. Genetic instruments were derived from the UK Biobank genome-wide association study, and the OSA outcome was obtained from a large meta-analysis genome-wide association study. Univariable MR, multivariable MR, reverse MR, and extensive sensitivity analyses (MR-Egger, weighted median, MR-PRESSO, and leave-one-out analyses) were performed.
RESULTS: Univariable MR showed that higher genetically predicted basal metabolic rate, body mass index, and whole-body fat mass were each associated with increased OSA risk (IVW odds ratio per SD: basal metabolic rate 1.85, 95% CI 1.62-2.10; body mass index 2.27, 95% CI 2.07-2.49; whole-body fat mass 2.05, 95% CI 1.85-2.28; all p < 0.05). In multivariable MR, the association between basal metabolic rate and OSA was fully attenuated after adjusting for adiposity (p > 0.05), whereas body mass index and whole-body fat mass retained strong independent causal effects (both p < 0.05), indicating that the apparent basal metabolic rate-OSA association is entirely mediated by fat mass. Reverse MR suggested that genetic liability to OSA modestly increases basal metabolic rate (OR = 1.08, 95% CI 1.04-1.12, p < 0.05), although this estimate showed partial sensitivity to pleiotropy.
CONCLUSION: Elevated adiposity is the primary causal driver of OSA. Although basal metabolic rate does not independently influence OSA risk, OSA may increase resting energy expenditure, suggesting a bidirectional relationship. These findings highlight adiposity reduction as a central target for preventing and treating OSA.
METHODS: Two-sample Mendelian randomization (MR) was performed using genome-wide association study data from predominantly European populations to evaluate the causal effects of basal metabolic rate, body mass index, and whole-body fat mass on OSA risk and to assess the reverse effects of genetic liability to OSA on basal metabolic rate. Genetic instruments were derived from the UK Biobank genome-wide association study, and the OSA outcome was obtained from a large meta-analysis genome-wide association study. Univariable MR, multivariable MR, reverse MR, and extensive sensitivity analyses (MR-Egger, weighted median, MR-PRESSO, and leave-one-out analyses) were performed.
RESULTS: Univariable MR showed that higher genetically predicted basal metabolic rate, body mass index, and whole-body fat mass were each associated with increased OSA risk (IVW odds ratio per SD: basal metabolic rate 1.85, 95% CI 1.62-2.10; body mass index 2.27, 95% CI 2.07-2.49; whole-body fat mass 2.05, 95% CI 1.85-2.28; all p < 0.05). In multivariable MR, the association between basal metabolic rate and OSA was fully attenuated after adjusting for adiposity (p > 0.05), whereas body mass index and whole-body fat mass retained strong independent causal effects (both p < 0.05), indicating that the apparent basal metabolic rate-OSA association is entirely mediated by fat mass. Reverse MR suggested that genetic liability to OSA modestly increases basal metabolic rate (OR = 1.08, 95% CI 1.04-1.12, p < 0.05), although this estimate showed partial sensitivity to pleiotropy.
CONCLUSION: Elevated adiposity is the primary causal driver of OSA. Although basal metabolic rate does not independently influence OSA risk, OSA may increase resting energy expenditure, suggesting a bidirectional relationship. These findings highlight adiposity reduction as a central target for preventing and treating OSA.