The effects of rhythmic input on breath period (TT) under constant metabolic drive were assessed in 10 musically trained and 10 untrained subjects. They tapped to a metronome and then to four musical segments, each for 5 min. Ten of these subjects (5 from each group) also listened to the selections without tapping. TT, beat period (TB), and phase coupling (PC) were assessed during the last 20 breaths of each presentation. TT coefficient of variation decreased significantly (P less than 0.001) in all subjects (base line = 23%; listening = 15%; listening and tapping = 10%). Significant correlation between rhythm and TT, indicating relative entrainment, was found in half of the subjects (r greater than 0.45; P less than 0.01). Significant integer TT/TB ratio and PC, both indicating tight entrainment between rhythm and breathing, were observed in 12 subjects (though not consistently in each one). These data advance the following hypothesis: musical rhythm can be a zeitgeber (i.e., pacemaker), with its ability to entrain respiration dependent on the strength of its signal relative to spurious signals from the higher neural centers that introduce noise into the central pattern generator. Tapping reinforces the zeitgeber, increasing its signal-to-noise ratio and thereby promoting entrainment.

OBJECTIVE:To assess the effect of weight change on the relationship between coffee and tea consumption and diabetes risk. DESIGN: Prospective cohort study, using data from the First National Health and Nutrition Examination Survey Epidemiologic Follow Up Study. Survival analyses were conducted using 301 selfreported cases of diabetes and eight documented diabetes deaths during an 8.4-y follow-up. SUBJECTS: A total of 7006 subjects aged 32-88 y with no reported history of diabetes were included in the study. RESULTS: For all subjects combined, increases in consumption of ground-caffeinated coffee and caffeine at baseline were followed by decreases in diabetes risk during follow-up. There were significant statistical interactions between age and consumption of caffeine (P ¼ 0.02) and ground-caffeinated coffee (P ¼ 0.03). Age-stratified analysis showed that the decrease in diabetes risk only applied to r60-y-old subjects, for whom the decrease in diabetes risk also obtained for ground-decaffeinated coffee and regular tea. The multivariate hazard ratio (HR) and 95% confidence interval for a 2 cups/day increment in the intake of ground-caffeinated coffee, ground-decaffeinated coffee and regular tea was 0.86 (0.75-0.99), 0.58 (0.34-0.99) and 0.77 (0.59-1.00), respectively. The diabetes risk was negatively related to the consumption in a dose-response manner. There were strong statistical interactions between prior weight change and beverage consumption for r60-y-old subjects. Further analysis revealed that the decrease in diabetes risk only applied to those who had lost weight, and that there was a positive doseresponse relationship between diabetes risk and weight change. For example, the multivariate HR and 95% confidence interval for 40 vs 0 cups/day of ground-decaffeinated coffee was 0.17 (0.04-0.74), 0.52 (0.19-1.42), 0.77 (0.30-1.96) and 0.91 (0.39-2.14) for subgroups with weight change of r0, 0-10, 10-20 and 420 lbs, respectively. There was no significant association between diabetes risk and consumption of instant-caffeinated coffee, instant-decaffeinated coffee or herbal tea. Caffeine intake appeared to explain some, but not all, of the diabetes-risk reduction and weight change. CONCLUSION: The negative relationship between diabetes risk and consumption of ground coffee and regular tea, observed for all NHEFS subjects, actually only applied to nonelderly adults who had previously lost weight.

Maternal obesity increases placental transport of macronutrients, resulting in fetal overgrowth and obesity later in life. Choline participates in fatty acid metabolism, serves as a methyl donor, and influences growth signaling, which may modify placental macronutrient homeostasis and affect fetal growth. Using a mouse model of maternal obesity, we assessed the effect of maternal choline supplementation on preventing fetal overgrowth and restoring placental macronutrient homeostasis. C57BL/6J mice were fed either a high-fat (HF, 60% kcal from fat) diet or a normal (NF, 10% kcal from fat) diet with a drinking supply of either 25 mM choline chloride or control purified water, respectively, beginning 4 weeks prior to mating until gestational day 12.5. Fetal and placental weight, metabolites, and gene expression were measured. HF feeding significantly (P < 0.05) increased placental and fetal weight in the HF-control (HFCO) versus NF-control (NFCO) animals, whereas the HF choline-supplemented (HFCS) group effectively normalized placental and fetal weight to the levels of the NFCO group. Compared to HFCO, the HFCS group had lower (P < 0.05) glucose transporter 1 (GLUT1) and fatty acid transport protein 1 (FATP1) expression as well as lower accumulation of glycogen in the placenta. The HFCS group also had lower (P < 0.05) placental 4E-binding protein 1 and ribosomal protein s6 phosphorylation, which are indicators of mechanistic target of rapamycin complex 1 (mTORC1) activation favoring macronutrient anabolism. In summary, our results suggest that maternal choline supplementation prevented fetal overgrowth in obese mice at mid-gestation and improved biomarkers of placental macronutrient homeostasis.