To our knowledge, this is the first study of the relationship between OSA severity and the macronutrient content associated with individuals’ dietary choices. Severity of OSA correlated with calories ordered for dinner, and especially with the fat and carbohydrate content of that meal. These relationships persisted after covarying for age- and gender-corrected BMI, so they can not be explained by a confounding relationship with obesity severity.
This novel finding has important potential implications. If OSA induces changes in diet, this would represent a potentially modifiable behavior that could contribute to a spiral of worsening obesity and sleep-disordered breathing [5
]. A causal link between OSA and diet also would support aggressive screening and treatment for OSA. An alternative explanation would be a reverse causal sequence, in which dietary choices alter nocturnal respiration, independent of BMI. Acute dietary changes can alter sleep architecture in humans [11
] and ventilation control in rats [12
]. Such an effect could have implications for the conduct of PSG. Even in the absence of a clear causal sequence, the co-occurrence of OSA with a diet high in fats and refined carbohydrates may increase morbidity. In an animal model, such a diet worsened the impact of intermittent hypoxia on learning and neural tissue [13
Although links between OSA and carbohydrate content fit with prior reports of increased craving for carbohydrate-rich foods following experimental sleep restriction [4
], fat content also was associated with OSA in our sample. Prior research did not specify macronutrient content, and the greatest craving increase was for “salty” foods, including high-fat foods. In our study, similar items (e.g., “french fries”) were ordered by 75% of subjects with an AHI>3, compared to 14% of those with AHI≤3. Methodological factors may also explain the discrepancy between present findings and past reports that (a) sleep duration correlates with weight status [14
] or dietary patterns [15
] and (b) experimental sleep restriction heightens food cravings [4
]. The current study was not well-powered to detect the small correlations that have been reported in epidemiological studies, and experimental work to date has limited sleep to far less than that experienced by our subjects.
Several limitations temper the conclusions that can be drawn from present results, which reflect food choices, not food consumption. We could not control for activity level or food consumption prior to the appointment, and subjects may have ordered atypically in anticipation of a hospital stay. However, if anything, this unmeasured variability might attenuate correlations, not result in spuriously inflated findings. Our sample size did not allow us to explore gender as an effect moderator, and the study lacked the hunger ratings and physiological measures needed to address the mechanisms that might underlie a relationship between OSA and food choices. Detailed PSG data were available, but no variable surpassed AHI as a correlate of dietary data; the rate of desturation events correlated with fat grams only (r=.32, p=.04; all others p>.05), and frequency of arousals, average O2, and nadir O2 failed to correlate with any dietary index (p>.05). As an additional limitation, BMI does not index fat distribution on the body. Finally, our recruitment of obese subjects ensured a broad range of breathing functioning during sleep, but the generalizability of findings to other populations, including non-obese individuals, remains to be seen. Taken together, these limitations suggest that findings be viewed as intriguing, but preliminary, warranting replication and extension in future work.