9 research outputs found

    Sleep and glycemic control in type 1 diabetes

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    Objective Our aim in the present study was to elucidate how type 1 diabetes mellitus (T1DM) and sleep parameters interact, which was rarely evaluated up to the moment. Materials and methods Eighteen T1DM subjects without chronic complications, and 9 control subjects, matched for age and BMI, were studied. The following instruments used to evaluate sleep: the Epworth Sleepiness Scale, sleep diaries, actimeters, and polysomnography in a Sleep Lab. Glycemic control in T1DM individuals was evaluated through: A1C, home fingertip glucometer for 10 days (concomitant with the sleep diary and actimeter), and CGM or concomitant with continuous glucose monitoring (during the polysomnography night). Results Comparing with the control group, individuals with diabetes presented more pronounced sleep extension from weekdays to weekends than control subjects (p = 0.0303). Among T1DM, glycemic variability (SD) was positively correlated with sleep latency (r = 0.6525, p = 0.0033); full awakening index and arousal index were positively correlated with A1C (r = 0.6544, p = 0.0081; and r = 0.5680, p = 0.0272, respectively); and mean glycemia values were negatively correlated with sleep quality in T1DM individuals with better glycemic control (mean glycemia < 154 mg/dL). Conclusion Our results support the hypothesis of an interaction between sleep parameters and T1DM, where the glycemic control plays an important role. More studies are needed to unveil the mechanisms behind this interaction, which may allow, in the future, clinicians and educators to consider sleep in the effort of regulating glycemic control. Arch Endocrinol Metab. 2015;59(1):71-

    Different Craniofacial Characteristics Predict Upper Airway Collapsibility in Japanese-Brazilian and White Men.

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    BackgroundOSA pathogenesis is complex and may vary according to ethnicity. The anatomic component predisposing to OSA is the result of the interaction between bony structure and upper airway soft tissues and can be assessed using passive critical closing pressure (Pcrit). We hypothesized that Japanese-Brazilians and whites present different predictors of upper airway collapsibility, suggesting different causal pathways to developing OSA in these two groups.MethodsMale Japanese-Brazilians (n = 39) and whites (n = 39) matched for age and OSA severity were evaluated by full polysomnography, Pcrit, and upper airway and abdomen CT scans for determination of upper airway anatomy and abdominal fat, respectively.ResultsPcrit was similar between the Japanese-Brazilians and the whites (-1.0 ± 3.3 cm H2O vs -0.4 ± 3.1 cm H2O, P = .325). The Japanese-Brazilians presented smaller upper airway bony dimensions (cranial base, maxillary, and mandibular lengths), whereas the whites presented larger upper airway soft tissue (tongue length and volume) and a greater imbalance between tongue and mandible (tongue/mandibular volume ratio). The cranial base angle was associated with Pcrit only among the Japanese-Brazilians (r = -0.535, P &lt; .01). The tongue/mandibular volume ratio was associated with Pcrit only among the whites (r = 0.460, P &lt; .01). Obesity-related variables (visceral fat, BMI, and neck and waist circumferences) showed a similar correlation with Pcrit in the Japanese-Brazilians and the whites.ConclusionsJapanese-Brazilians and whites present different predictors of upper airway collapsibility. Although craniofacial bony restriction influenced Pcrit only in the Japanese-Brazilians, an anatomic imbalance between tongue and mandible volume influenced Pcrit among the whites. These findings may have therapeutic implications regarding how to improve the anatomic predisposition to OSA across ethnicities

    Different Craniofacial Characteristics Predict Upper Airway Collapsibility in Japanese-Brazilian and White Men.

    No full text
    BackgroundOSA pathogenesis is complex and may vary according to ethnicity. The anatomic component predisposing to OSA is the result of the interaction between bony structure and upper airway soft tissues and can be assessed using passive critical closing pressure (Pcrit). We hypothesized that Japanese-Brazilians and whites present different predictors of upper airway collapsibility, suggesting different causal pathways to developing OSA in these two groups.MethodsMale Japanese-Brazilians (n = 39) and whites (n = 39) matched for age and OSA severity were evaluated by full polysomnography, Pcrit, and upper airway and abdomen CT scans for determination of upper airway anatomy and abdominal fat, respectively.ResultsPcrit was similar between the Japanese-Brazilians and the whites (-1.0 ± 3.3 cm H2O vs -0.4 ± 3.1 cm H2O, P = .325). The Japanese-Brazilians presented smaller upper airway bony dimensions (cranial base, maxillary, and mandibular lengths), whereas the whites presented larger upper airway soft tissue (tongue length and volume) and a greater imbalance between tongue and mandible (tongue/mandibular volume ratio). The cranial base angle was associated with Pcrit only among the Japanese-Brazilians (r = -0.535, P &lt; .01). The tongue/mandibular volume ratio was associated with Pcrit only among the whites (r = 0.460, P &lt; .01). Obesity-related variables (visceral fat, BMI, and neck and waist circumferences) showed a similar correlation with Pcrit in the Japanese-Brazilians and the whites.ConclusionsJapanese-Brazilians and whites present different predictors of upper airway collapsibility. Although craniofacial bony restriction influenced Pcrit only in the Japanese-Brazilians, an anatomic imbalance between tongue and mandible volume influenced Pcrit among the whites. These findings may have therapeutic implications regarding how to improve the anatomic predisposition to OSA across ethnicities

    Different Craniofacial Characteristics Predict Upper Airway Collapsibility in Japanese-Brazilian and White Men

    No full text
    BACKGROUND: OSA pathogenesis is complex and may vary according to ethnicity. The anatomic component predisposing to OSA is the result of the interaction between bony structure and upper airway soft tissues and can be assessed using passive critical closing pressure (Pcrit). We hypothesized that Japanese-Brazilians and whites present different predictors of upper airway collapsibility, suggesting different causal pathways to developing OSA in these two groups. METHODS: Male Japanese-Brazilians (n = 39) and whites (n = 39) matched for age and OSA severity were evaluated by full polysomnography, Pcrit, and upper airway and abdomen CT scans for determination of upper airway anatomy and abdominal fat, respectively. RESULTS: Pcrit was similar between the Japanese-Brazilians and the whites (−1.0 ± 3.3 cm H(2)O vs −0.4 ± 3.1 cm H(2)O, P = .325). The Japanese-Brazilians presented smaller upper airway bony dimensions (cranial base, maxillary, and mandibular lengths), whereas the whites presented larger upper airway soft tissue (tongue length and volume) and a greater imbalance between tongue and mandible (tongue/mandibular volume ratio). The cranial base angle was associated with Pcrit only among the Japanese-Brazilians (r = −0.535, P < .01). The tongue/mandibular volume ratio was associated with Pcrit only among the whites (r = 0.460, P < .01). Obesity-related variables (visceral fat, BMI, and neck and waist circumferences) showed a similar correlation with Pcrit in the Japanese-Brazilians and the whites. CONCLUSIONS: Japanese-Brazilians and whites present different predictors of upper airway collapsibility. Although craniofacial bony restriction influenced Pcrit only in the Japanese-Brazilians, an anatomic imbalance between tongue and mandible volume influenced Pcrit among the whites. These findings may have therapeutic implications regarding how to improve the anatomic predisposition to OSA across ethnicities
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