Meredith C. Peddie

Breaking prolonged sitting reduces postprandial glycemia in healthy, normal-weight adults: a randomized crossover trial

BACKGROUND Sedentary behavior is a risk factor for cardiometabolic disease. Regularly interrupting sedentary behavior with activity breaks may lower this risk. OBJECTIVE We compared the effects of prolonged sitting, continuous physical activity combined with prolonged sitting, and regular activity breaks on postprandial metabolism. DESIGN Seventy adults participated in a randomized crossover study. The prolonged sitting intervention involved sitting for 9 h, the physical activity intervention involved walking for 30 min and then sitting, and the regular-activity-break intervention involved walking for 1 min 40 s every 30 min. Participants consumed a meal-replacement beverage at 60, 240, and 420 min. RESULTS The plasma incremental area under the curve (iAUC) for insulin differed between interventions (overall P < 0.001). Regular activity breaks lowered values by 866.7 IU · L(-1) · 9 h(-1) (95% CI: 506.0, 1227.5 IU · L(-1) · 9 h(-1); P < 0.001) when compared with prolonged sitting and by 542.0 IU · L(-1) · 9 h(-1) (95% CI: 179.9, 904.2 IU · L(-1) · 9 h(-1); P = 0.003) when compared with physical activity. Plasma glucose iAUC also differed between interventions (overall P < 0.001). Regular activity breaks lowered values by 18.9 mmol · L(-1) · 9 h(-1) (95% CI: 10.0, 28.0 mmol · L(-1) · 9 h(-1); P < 0.001) when compared with prolonged sitting and by 17.4 mmol · L(-1) · 9 h(-1) (95% CI: 8.4, 26.3 mmol · L(-1) · 9 h(-1); P < 0.001) when compared with physical activity. Plasma triglyceride iAUC differed between interventions (overall P = 0.023). Physical activity lowered values by 6.3 mmol · L(-1) · 9 h(-1) (95% CI: 1.8, 10.7 mmol · L(-1) · 9 h(-1); P = 0.006) when compared with regular activity breaks. CONCLUSION Regular activity breaks were more effective than continuous physical activity at decreasing postprandial glycemia and insulinemia in healthy, normal-weight adults. This trial was registered with the Australian New Zealand Clinical Trials registry as ACTRN12610000953033.

Long-term vitamin D 3 supplementation is more effective than vitamin D 2 in maintaining serum 25-hydroxyvitamin D status over the winter months

Public health recommendations do not distinguish between vitamin D2 and vitamin D3, yet disagreement exists on whether these two forms should be considered equivalent. The objective of the present study was to evaluate the effect of a daily physiological dose of vitamin D2 or vitamin D3 on 25-hydroxyvitamin D (25(OH)D) status over the winter months in healthy adults living in Dunedin, New Zealand (latitude 46°S). Participants aged 18-50 years were randomly assigned to 25 μg (1000 IU) vitamin D3 (n 32), 25 μg (1000 IU) vitamin D2 (n 31) or placebo (n 32) daily for 25 weeks beginning at the end of summer. A per-protocol approach, which included ≥ 90 % supplement compliance, was used for all analyses. Serum 25-hydroxyvitamin D3 (25(OH)D3), 25-hydroxyvitamin D2 (25(OH)D2) and parathyroid hormone (PTH) were measured at baseline and at 4, 8, 13 and 25 weeks. Geometric mean total serum 25(OH)D concentrations (sum of 25(OH)D2 and 25(OH)D3) at baseline was 80 nmol/l. After 25 weeks, participants randomised to D2 and placebo had a significant reduction in serum 25(OH)D3 concentrations over the winter months compared with vitamin D3-supplemented participants (both P< 0.001). Supplementation with vitamin D2 increased serum 25(OH)D2 but produced a 9 (95 % CI 1, 17) nmol/l greater decline in the 25(OH)D3 metabolite compared with placebo (P< 0.036). Overall, total serum 25(OH)D concentrations were 21 (95 % CI 14, 30) nmol/l lower in participants receiving vitamin D2 compared with those receiving D3 (P< 0.001), among whom total serum 25(OH)D concentrations remained unchanged. No intervention-related changes in PTH were observed. Daily supplementation of vitamin D3 was more effective than D2; however, the functional consequence of the differing metabolic response warrants further investigation.

Physical activity and postprandial lipidemia: Are energy expenditure and lipoprotein lipase activity the real modulators of the positive effect?

Historically, the link between elevated cholesterol and increased risk of cardiovascular disease has been based on fasting measurements. This is appropriate for total, low-density lipoprotein and high-density lipoprotein cholesterol. However, triglyceride concentrations vary considerably throughout the day in response to the regular consumption of food and drink. Recent findings indicate that postprandial triglyceride concentrations independently predict future cardiovascular risk. Potential modulators of postprandial lipidemia include meal composition and physical activity. Early cross sectional studies indicated that physically active individuals had a lower postprandial lipidemic response compared to inactive individuals. However, the effect of physical activity on postprandial lipidemia is an acute phenomenon, which dissipates within 60 h of a single bout of exercise. Total exercise induced energy expenditure, rather than duration or intensity of the physical activity is commonly reported to be a potent modulator of postprandial lipidemia. However, the pooled results of studies in this area suggest that energy expenditure exerts most of its influence on fasting triglyceride concentrations rather than on the incremental change in triglyceride concentrations seen following meal consumption. It seems more likely that energy expenditure is one component of a multifactorial list of mediators that may include local muscle contractile activity, and other yet to be elucidated mechanisms.

Estimation of usual intake and food sources of choline and betaine in New Zealand reproductive age women

Recently, choline has been associated with neurodevelopment, cognitive function and neural tube defect incidence. However, data on usual intakes are limited, and estimates of dietary intakes of choline and its metabolite betaine, are not available for New Zealanders. The objective of the present study was to determine usual intake and food sources of choline and betaine in a group of New Zealand reproductive age women. Dietary intake data were collected from a sample of 125 women, aged 18-40 years, by means of a 3-day weighed food record, and usual choline and betaine intake distributions were determined. The mean (SD) daily intakes of choline and betaine were 316 (66) mg and 178 (66) mg, respectively. The total choline intake relative to energy intake and body weight was 0.18 mg/kcal and 5.1 mg/kg, respectively. Only 16% of participants met or exceeded the Adequate Intake (AI) for adult women of 425 mg of choline. The top five major food contributors of choline were eggs, red meat, milk, bread and chicken; and of betaine were bread, breakfast cereal, pasta, grains and root vegetables (carrots, parsnips, beetroot, swedes). Our findings contribute towards the recent emergence of published reports on the range of dietary choline and betaine intakes consumed by free-living populations. In our sample of New Zealand women, few participants were meeting or exceeding the AI level. Given recent epidemiological evidence suggesting health benefits of increased choline and betaine intakes, recommendations should be made to encourage the consumption of choline and betaine-rich foods.

Effect of increasing voluntary folic acid food fortification on dietary folate intakes and adequacy of reproductive-age women in New Zealand.

OBJECTIVE Mandatory folic acid fortification of breads in New Zealand was put on hold in 2009. At this time, bread manufacturers were requested to adopt greater voluntary fortification and agreed to add folic acid to approximately one-third of their bread range. We sought to evaluate the impact of increased voluntary fortification of bread and the proposed mandatory fortification programme on folate intake adequacy of reproductive-age women. DESIGN Cross-sectional study conducted in 2008. Dietary data were collected using 3 d weighed food records and usual folate intakes were generated by modifying the food composition table as follows: (i) voluntary fortification of bread as of 2008 (six breads); (ii) increased voluntary fortification of bread as of 2011 (thirty-four breads); and (iii) mandatory fortification of all breads. The prevalence of inadequate folate intake was calculated for all three scenarios using the Estimated Average Requirement (320 μg dietary folate equivalents/d) cut-point method. SETTING New Zealand. SUBJECTS Healthy non-pregnant women (n 125) aged 18-40 years. RESULTS Usual folate intake in 2008 was 362 μg dietary folate equivalents/d. Increased voluntary bread fortification led to a marginal increase in folate intakes (394 μg dietary folate equivalents/d) and a decline in inadequacy from 37 % to 29 %. Mandatory fortification resulted in an increase of 89 μg folic acid/d, which substantially shifted both the proportion of women with folic acid intakes above 100 μg/d and the distribution of overall folate intakes, producing a marked reduction in inadequacy to 5 %. CONCLUSIONS Increased voluntary bread fortification efforts are far inferior to mandatory fortification as a reliable public health intervention.

Interrupting Prolonged Sitting with Regular Activity Breaks does not Acutely Influence Appetite: A Randomised Controlled Trial

Regular activity breaks increase energy expenditure; however, this may promote compensatory eating behaviour. The present study compared the effects of regular activity breaks and prolonged sitting on appetite. In a randomised, cross-over trial, 36 healthy adults (BMI (Body Mass Index) 23.9 kg/m2 (S.D. = 3.9)) completed four, two-day interventions: two with prolonged sitting (SIT), and two with sitting and 2 min of walking every 30 min (RAB). Standardized meals were provided throughout the intervention, with an ad libitum meal at the end of Day 2. Appetite and satiety were assessed throughout both days of each intervention using five visual analogue scales. The five responses were combined into a single appetite response at each time point. The area under the appetite response curve (AUC) was calculated for each day. Intervention effects for appetite response AUC and ad libitum meal intake were tested using linear mixed models. Appetite AUC did not differ between interventions (standardised effect of RAB compared to SIT: Day 1: 0.11; 95% CI: −0.28, 0.06; p = 0.212; Day 2: 0.04; 95% CI: −0.15, 0.24; p = 0.648). There was no significant difference in energy consumed at the ad libitum lunch meal on Day 2 between RAB and SIT. Interrupting prolonged sitting with regular activity breaks does not acutely influence appetite or volume of food consumed, despite inferred increases in energy expenditure. Longer-term investigation into the effects of regular activity breaks on energy balance is warranted.

Postprandial Metabolic Effects of Accelerometer Measured Spontaneous Low-Level Activity.

BACKGROUND Interrupting sedentary time induces improvements in glucose metabolism; however, it is unclear how much activity is required to reduce the negative effects of prolonged sitting. METHODS Sixty-six participants sat continuously for 9 hours except for required bathroom breaks. Participants were fed meal replacement beverages at 60, 240 and 420 min. Blood samples were obtained hourly for 9 hours, with additional samples collected 30 and 45 min after each feeding. Responses were calculated as incremental area under the curve (iAUC) for plasma glucose, insulin and triglyceride. Participants wore a triaxial accelerometer and a heart rate monitor. Energy expenditure was estimated using indirect calorimetry. RESULTS After controlling for age, sex and BMI, every 100 count increase in accelerometer derived total movement was associated with a 0.06 mmol·L-1·9 hours decrease in glucose iAUC (95% CI 0.004-0.1; P = .035), but not associated with changes in insulin or triglyceride iAUC. Every 1 bpm increase in mean heart rate was associated with a 0.76 mmol·L-1·9 hours increase in triglyceride iAUC (95% CI 0.13-1.38). CONCLUSION Accelerometer measured movement during periods of prolonged sitting can result in minor improvements in postprandial glucose metabolism, but not lipid metabolism.

Sedentary behavior: Is it time to break up with your chair?

60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 In the past 70 years there have been dramatic increases in time spent engaging in activities usually performed in a seated position. Take, for example, the reading of the latest issue of a journal (such as this one). Twenty years ago, for many, reading this issue would have involved a walk across campus to the medical library, climbing several flights of stairs to the floor where the journal was located, carrying a weighty volume to the photocopier for copying, and then a return trip made to the office. This trip may have taken 20 minutes, during which time the potential reader would have been walking or standing, chatting with students or colleagues they met along the way, or making a side trip to a colleague’s office. Today, we stay firmly seated in our chair, using only the muscles in our index finger to click a button. Perhaps that means we have time to read another article in the issue, or write a letter to the editor, but how are these more prolonged bouts of sitting impacting our heath? A growing body of evidence indicates that sedentary behavior, activities associated with low energy expenditure performed in a seated position, is associated with increased morbidity—particularly cardiovascular and diabetic—and mortality. For example, the highest quintile of sedentary time was been associated with a hazard ratio of 1.143 (95% confidence interval [CI] 1.002–1.729) for cardiovascular disease incidence, 1.910 (95% CI 1.642–2.222) for type II diabetes incidence, and 1.240 (95% CI 1.090–1.257) for all-cause morality. This association appears to be more strongly expressed when TV viewing is used as a proxy measure of sedentary behavior (compare a hazard ratio all-cause mortality of 1.27 (95% CI 1.22–1.32) for the highest category of sitting (.8 h/d) to 1.44 (95% CI 1.34–1.56) for the highest category of TV viewing (

Sedentary Behavior and Body Weight and Composition in Adults: A Systematic Review and Meta-analysis of Prospective Studies

5 h/ d)), possibly because TV viewing is often accompanied by snack consumption. However, it exists for most measures of sedentary behavior such as occupational sitting time, sedentary commuting, and objectively measured total sedentary behavior. Many of the individual observational studies find that this association holds when controlling