ABSTRACT
OBJECTIVE: Shorter sleep duration predisposes to obesity, but the mechanisms whereby sleep deprivation affects body weight are poorly understood. We tested whether this association is modulated by the obesity genes FTO, TMEM18 and NRXN3. SUBJECTS: Body mass index (BMI), waist circumference, visceral fat (abdominal ultrasound), homeostasis model assessment for insulin resistance (HOMA-IR), systolic blood pressure (SBP) and sleep time per 24 h were assessed in 297 asymptomatic children (151 boys, 146 girls; age range 5-9 years; BMI s.d. score range -2.0-4.0). Associations between sleep duration and the abovementioned outcomes were tested for three common single-nucleotide polymorphisms (SNPs), namely FTO (rs9939609), TMEM 18 (rs4854344) and NRXN3 (rs10146997), as well as for their combination. RESULTS: TT homozygotes (but not A(*) carriers) for the FTO SNP, exhibited nominal associations between decreasing sleep duration and increasing BMI, waist circumference, visceral fat and HOMA-IR (all P<0.05). Similar associations were observed in children with risk alleles (but not in those without risk alleles) for the TMEM18 and NRXN3 SNPs (P<0.05 to P<0.0001). The three SNPs had additive effects on the negative associations between sleep and, respectively, BMI (P<0.001), waist (P<0.005), visceral fat (P<0.001), HOMA-IR (P=0.010) and SBP (P<0.0005). The combined effects on obesity measures and SBP remained significant after correction for multiple testing. On average, 2 h of sleep less per night was associated with an increase in BMI of 1.0 s.d. (95% confidence interval 0.5-1.6 s.d.) and with 8.0 cm (95% confidence interval 3.6-12.2 cm) more waist circumference in genetically susceptible children. CONCLUSION: By age 7, common variations in FTO, TMEM18 and NRXN3 influence the vulnerability to metabolic complications of sleep deprivation. Further genetic studies are warranted to replicate these findings in other populations.
Subject(s)
Membrane Proteins/metabolism , Nerve Tissue Proteins/metabolism , Obesity/metabolism , Polymorphism, Single Nucleotide , Proteins/metabolism , Sleep Wake Disorders/metabolism , Alpha-Ketoglutarate-Dependent Dioxygenase FTO , Body Mass Index , Child , Child, Preschool , Female , Genetic Predisposition to Disease , Genotype , Humans , Insulin Resistance , Intra-Abdominal Fat , Male , Membrane Proteins/genetics , Nerve Tissue Proteins/genetics , Obesity/genetics , Proteins/genetics , Sleep Wake Disorders/genetics , Waist Circumference , Weight GainABSTRACT
OBJECTIVE: To assess the monitoring of arterial pressure (AP) in non-hypertensive patients at a health centre and to compare the results of two types of consultations. DESIGN: A retrospective observation study over 5 years. SETTING: Urban health care. PATIENTS: After the exclusion of hypertensive patients, 337 medical records, which were active over the period under assessment, were chosen by systematic sampling of the adult population. Consultation types were: CT1 (stable staff, MIR training, habitual development of the PAPPS); CT2 (staff not stable, training uneven, without systematic development of the PAPPS). Records were considered indicated when they contained symptoms suggestive of AHT or when AP had been measured because the patients had been included in a health programme; the rest of the records were considered not indicated. Data were analysed using the Chi-squared test. MEASUREMENTS AND RESULTS: 152 of the 337 records belonged to CT1 and 185 to CT2. In 151 records there was no measurement of AP: 50 belonging to CT1 and 101 to CT2. 508 measurements of AP were performed, 274 in CT1 and 234 in CT2. Of the 151 cases where measurements were not indicated (64 in CT1 and 87 in CT2. CONCLUSIONS: The percentage of patients without any monitoring is high (44.8%), similar to the percentage of AP measurements not indicated, which would imply the need to rationalise use of the sphygmomanometer in the consulting-room. CT1 consultations seem to have the most rational measurements of AP.
