-
1.
Changes in eating patterns in response to chronic insufficient sleep and their associations with diet quality: a randomized trial.
Barragán, R, Zuraikat, FM, Tam, V, RoyChoudhury, A, St-Onge, MP
Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine. 2023;(11):1867-1875
Abstract
STUDY OBJECTIVES Insufficient sleep leads to overconsumption, but the factors contributing to this effect are poorly understood. Therefore, we assessed the influence of prolonged curtailment of sleep on free-living eating patterns linked with overconsumption and explored associations of these eating patterns with diet quality under different sleep conditions. METHODS Sixty-five adults (47 females) participated in outpatient randomized crossover studies with two 6-week conditions: adequate sleep (7-9 h/night) and sleep restriction (-1.5 h/night relative to screening). Food records were collected over 3 nonconsecutive days, from which we ascertained data on eating frequency, midpoint, and window and intakes of energy and nutrients. Linear mixed models were used to assess the impact of sleep condition on change in eating pattern (sleep × week interaction) and the relation between eating patterns and dietary intakes (sleep × eating pattern interaction). RESULTS Sleep condition impacted the change in eating frequency across weeks, with eating frequency increasing in sleep restriction relative to adequate sleep (β = 0.3 ± 0.1; P = .046). Across conditions, eating more frequently tended to relate to higher energy intakes (β = 60.5 ± 34.6; P = .082). Sleep also influenced the relation of variability in eating midpoint with intakes of saturated fat (β = 6.0 ± 2.1; P = .005), polyunsaturated fat (β = -3.9 ± 2.0; P = .051), and added sugar (β = 17.3 ± 6.2; P = .006), with greater midpoint variability associated with more adverse changes in these diet quality components in sleep restriction vs adequate sleep. CONCLUSIONS Chronic short sleep increases eating frequency and adversely influences associations of variability in meal timing with components of diet quality. These findings help to explain how short sleep leads to overconsumption and obesity. CLINICAL TRIAL REGISTRATION Registry: ClinicalTrials.gov; Name: Impact of Sleep Restriction in Women; URL: https://clinicaltrials.gov/ct2/show/NCT02835261; Identifier: NCT02835261 and Name: Impact of Sleep Restriction on Performance in Adults; URL: https://clinicaltrials.gov/ct2/show/NCT02960776; Identifier: NCT02960776. CITATION Barragán R, Zuraikat FM, Tam V, RoyChoudhury A, St-Onge M-P. Changes in eating patterns in response to chronic insufficient sleep and their associations with diet quality: a randomized trial. J Clin Sleep Med. 2023;19(11):1867-1875.
-
2.
Comparisons of electrophysiological markers of impaired executive attention after traumatic brain injury and in healthy aging.
Kim, N, Jamison, K, Jaywant, A, Garetti, J, Blunt, E, RoyChoudhury, A, Butler, T, Dams-O'Connor, K, Khedr, S, Chen, CC, et al
NeuroImage. 2023;:120126
Abstract
Executive attention impairments are a persistent and debilitating consequence of traumatic brain injury (TBI). To make headway towards treating and predicting outcomes following heterogeneous TBI, cognitive impairment specific pathophysiology first needs to be characterized. In a prospective observational study, we measured EEG during the attention network test aimed at detecting alerting, orienting, executive attention and processing speed. The sample (N = 110) of subjects aged 18-86 included those with and without traumatic brain injury: n = 27, complicated mild TBI; n = 5, moderate TBI; n = 10, severe TBI; n = 63, non-brain-injured controls. Subjects with TBI had impairments in processing speed and executive attention. Electrophysiological markers of executive attention processing in the midline frontal regions reveal that, as a group, those with TBI and elderly non-brain-injured controls have reduced responses. We also note that those with TBI and elderly controls have responses that are similar for both low and high-demand trials. In subjects with moderate-severe TBI, reductions in frontal cortical activation and performance profiles are both similar to that of controls who are ∼4 to 7 years older. Our specific observations of frontal response reductions in subjects with TBI and in older adults is consistent with the suggested role of the anterior forebrain mesocircuit as underlying cognitive impairments. Our results provide novel correlative data linking specific pathophysiological mechanisms underlying domain-specific cognitive deficits following TBI and with normal aging. Collectively, our findings provide biomarkers that may serve to track therapeutic interventions and guide development of targeted therapeutics following brain injuries.
-
3.
Extracranial Carotid Plaque Calcification and Cerebrovascular Ischemia: A Systematic Review and Meta-Analysis.
Homssi, M, Saha, A, Delgado, D, RoyChoudhury, A, Thomas, C, Lin, M, Baradaran, H, Kamel, H, Gupta, A
Stroke. 2023;(10):2621-2628
Abstract
BACKGROUND Although coronary calcification quantification is an established approach for cardiovascular risk assessment, the value of quantifying carotid calcification is less clear. As a result, we performed a systematic review and meta-analysis to evaluate the association between extracranial carotid artery plaque calcification burden and ipsilateral cerebrovascular ischemic events. METHODS A comprehensive literature search was performed in the following databases: Ovid MEDLINE(R) 1946 to July 6, 2022; OVID Embase 1974 to July 6, 2022; and The Cochrane Library (Wiley). We performed meta-analyses including studies in which investigators performed a computed tomography assessment of calcification volume, percentage, or other total calcium burden summarizable in a single continuous imaging biomarker and determined the association of these features with the occurrence of ipsilateral stroke or transient ischemic attack. RESULTS Our overall meta-analysis consisted of 2239 carotid arteries and 9 studies. The presence of calcification in carotid arteries ipsilateral to ischemic stroke or in stroke patients compared with asymptomatic patients did not demonstrate a significant association with ischemic cerebrovascular events (relative risk of 0.75 [95% CI, 0.44-1.28]; P=0.29). When restricted to studies of significant carotid artery stenosis (>50%), the presence of calcification was associated with a reduced risk of ischemic stroke (relative risk of 0.56 [95% CI, 0.38-0.85]; P=0.006). When the analysis was limited to studies of patients with mainly nonstenotic plaques, there was an increased relative risk of ipsilateral ischemic stroke of 1.72 ([95% CI, 1.01-2.91]; P=0.04). Subgroup meta-analyses of total calcium burden and morphological features of calcium showed wide variability in their strength of association with ischemic stroke and demonstrated significant heterogeneity. CONCLUSIONS The presence of calcification in carotid plaque confers a reduced association with ipsilateral ischemic events, although these results seem to be limited among carotid arteries with higher degrees of stenosis. Adoption of carotid calcification measures in clinical decision-making will require additional studies providing more reproducible and standardized methods of calcium characterization and testing these imaging strategies in prospective studies.
-
4.
Effect of vitamin D3 and calcium carbonate supplementation on muscle strength in postmenopausal women living with HIV.
Yin, MT, Bucovsky, M, Williams, J, Brunjes, D, RoyChoudhury, A, Colon, I, Ferris, DC, Olender, S, Schulze, PC, Sharma, A, et al
Antiviral therapy. 2020;(8):411-418
-
-
Free full text
-
Abstract
BACKGROUND Both falls and fractures are increased in older persons living with HIV (PLWH). Low serum total 25-hydroxyvitamin D (25-OHD) levels have been associated with falls, fractures and poor muscle strength. We hypothesized that vitamin D (VitD) supplementation would improve muscle strength in postmenopausal PLWH. METHODS In a 12-month prospective, randomized, double-blind, study of 69 African American and Hispanic postmenopausal PLWH on antiretroviral therapy with 25-OHD ≥10 ng/ml and ≤32 ng/ml, we investigated the effects of daily low (1,000 IU; n=31) and moderate (3,000 IU; n=38) cholecalciferol doses on lean mass and strength. Change in lean body mass was assessed by dual-energy X-ray absorptiometry (DXA), and isometric and isokinetic muscle strength in the dominant lower extremity was assessed using the Biodex System 4 Pro. RESULTS Mean age was 56 ±5 years, median CD4+ T-cell count 722 cells/mm3 and 74% had HIV RNA≤50 copies/ml. Serum 25-OHD did not differ at baseline, but was higher in the moderate than low VitD group at 6 and 12 months. In both groups, there were significant increases in lower extremity isokinetic torque, work and power at 12 months, with no change in lean mass. CONCLUSIONS VitD supplementation was associated with a modest increase in lower extremity strength in postmenopausal PLWH, without a concomitant increase in muscle mass. Magnitude of increase in strength were similar with 3,000 IU and 1,000 IU daily. Future larger studies will be required to determine the optimal dose of VitD to improve muscle strength and to determine whether supplementation reduces the risk of falls and fractures in PLWH.
-
5.
Mild sleep restriction increases 24-hour ambulatory blood pressure in premenopausal women with no indication of mediation by psychological effects.
St-Onge, MP, Campbell, A, Aggarwal, B, Taylor, JL, Spruill, TM, RoyChoudhury, A
American heart journal. 2020;:12-22
-
-
Free full text
-
Abstract
BACKGROUND Studies assessing the impact of sleep restriction (SR) on blood pressure (BP) are limited by short study length, extreme SR (<4 hours a night), and lack of attention to psychological distress as a possible mediator. METHODS A community-based cohort was assembled with 237 women (age 34.1 ± 13.5 years; body mass index 25.4 ± 5.4 kg/m2), and a randomized, crossover, intervention study was conducted in 41 women (24 completed: age 30.2 ± 6.5 years; body mass index 24.3 ± 2.8 kg/m2) to determine the causal effect of SR on BP. Sleep was maintained as usual (HS) or reduced by 1.5 hours a night (SR) for 6 weeks. In the cohort, associations between sleep and psychosocial factors were evaluated using multivariable models adjusted for demographic and clinical confounders. In the intervention study, in-office BP was measured weekly; ambulatory BP was measured at end point. Psychological factors were assessed at baseline and end point. Mixed-model analyses with total sleep time (TST, main predictor), week and fraction of time spent in physical activity (covariates), and subject (random effect) were performed. RESULTS Among the community cohort, higher perceived stress, stressful events and distress, and lower resilience were associated with shorter sleep, worse sleep quality, and greater insomnia symptoms (P < .05). In the intervention, systolic BP increased as TST decreased (TST × week interaction, [coefficient ± standard error] -0.0097 ± 0.0046, P = .036). Wake ambulatory diastolic blood pressure (-0.059 ± 0.022, P = .021) and mean arterial pressure (-0.067 ± 0.023, P = .018) were higher after SR versus HS. Psychological distress variables were not affected by TST and did not mediate the effects of SR on BP. CONCLUSIONS These results suggest that SR influences CVD risk in women via mechanisms independent of psychological stressors.
-
6.
Sleep restriction and testosterone concentrations in young healthy males: randomized controlled studies of acute and chronic short sleep.
Smith, I, Salazar, I, RoyChoudhury, A, St-Onge, MP
Sleep health. 2019;(6):580-586
-
-
Free full text
-
Abstract
OBJECTIVE Low testosterone in men increases the risk for various disorders. Severe sleep restriction (SR) may reduce testosterone, but the effects of long-term short sleep are unknown. This study tested the effects of SR on circulating testosterone in healthy young men. DESIGN Randomized controlled studies of SR vs habitual sleep (HS) in inpatient (study 1, n=14) and outpatient (study 2, n=13) settings. METHODS Study 1 involved severe, acute SR (4 hours time in bed [TIB]) vs HS (9 hours TIB) for 5 nights; study 2 consisted of mild, long-term SR (HS 1.5 hours of sleep/night) vs HS for 6 weeks. Plasma testosterone levels were measured at baseline and end point (study 1) or baseline, week 3, and week 6 (study 2) of each phase. Linear model analyses to assess the effects of SR on testosterone were performed separately for each study. RESULTS Study 1: There were no significant sleep-time interaction on testosterone concentrations (change in testosterone levels during HS = 22.86 ± 163.79 ng/dL; SR = 43.73 ± 159.96 ng/dL, P = .41) and no main effect of sleep duration (P = .13). Study 2: There were a trend for a sleep-time interaction (P = .067) and a main effect of sleep on testosterone concentrations from 6 weeks of SR (P = .0046). Testosterone concentrations were slightly lower but increased over time with SR relative to HS. CONCLUSIONS Sleep restriction does not adversely affect plasma testosterone levels in healthy young men. Given prior contradicting evidence, confirmatory studies should be done to ascertain the influence of sleep duration and quality on testosterone concentrations in men throughout life.
-
7.
A Randomized Placebo-Controlled Trial of Low- Versus Moderate-Dose Vitamin D3 Supplementation on Bone Mineral Density in Postmenopausal Women With HIV.
Yin, MT, RoyChoudhury, A, Bucovsky, M, Colon, I, Ferris, DC, Olender, S, Agarwal, S, Sharma, A, Zeana, C, Zingman, B, et al
Journal of acquired immune deficiency syndromes (1999). 2019;80(3):342-349
-
-
-
Free full text
-
Plain language summary
Prevalence of fracture is 2 to 3-fold higher in women with HIV over age 50 than in the general population. The aim of this study was to compare the effects of two doses of vitamin D3 repletion (3000 IU Vs 1000 IU) on bone turnover and change in bone mass and microarchitecture in postmenopausal women with HIV. The study is a randomised placebo-controlled study which recruited women with HIV aged between 40 and 70 years. The participants were randomised to 3000 vs 1000 IU vitamin D3 daily together with 500mg calcium carbonate twice daily. Results indicate that moderate dose vitamin D3 (3000 IU) supplementation in minority postmenopausal women with HIV on established antiretroviral therapy (treatment for HIV) did not appear to have a greater impact on bone mineral density or bone turnover than low dose vitamin D3 supplementation (1000 IU). Authors conclude that further studies are required to determine whether vitamin D3 supplementation is beneficial in this patient population, and if so, what dose provides the maximum benefit in terms of musculoskeletal health in persons aging with HIV.
Abstract
BACKGROUND Prevalence of osteoporosis and fracture is increased among older people with HIV. We compared the effects of low (1000 IU) vs moderate (3000 IU) vitamin D3 (VitD) supplementation on areal bone mineral density (aBMD) and volumetric bone mineral density (vBMD) in African American and Hispanic postmenopausal women with HIV on antiretroviral therapy. METHODS We performed a 12-month prospective, randomized, double-blind, placebo-controlled study with primary outcomes of change in aBMD by dual-energy X-ray absorptiometry (DXA) and secondary outcomes of change in vBMD by quantitative computed tomography and bone turnover markers. An intent-to-treat analysis was performed on 85 randomized subjects (43 low and 42 moderate) for primary DXA outcomes, and complete case analysis was performed for secondary outcomes. RESULTS Mean age was 56 ± 5 years, median CD4 count was 722 cells/mm, and 74% had HIV RNA ≤ 50 copies/mL. Serum 25-OHD was higher in the moderate than low VitD group at 6 months (33.1 ± 10.3 vs 27.8 ± 8.1 ng/mL, P = 0.03) and 12 months, but parathyroid hormone levels remained similar. Percent change in aBMD, vBMD, and bone turnover markers did not differ between low and moderate VitD groups before or after adjustment for baseline aBMD. CONCLUSIONS VitD supplementation at 3000 IU daily increased mean total 25-OHD levels in postmenopausal women with HIV, but we did not find evidence of an effect on BMD beyond those observed with 1000 IU daily. Future studies are necessary to determine whether VitD supplementation is beneficial in this patient population, and if so, what dose is optimal for skeletal health.
-
8.
Sleep and meal timing influence food intake and its hormonal regulation in healthy adults with overweight/obesity.
St-Onge, MP, Pizinger, T, Kovtun, K, RoyChoudhury, A
European journal of clinical nutrition. 2019;(Suppl 1):76-82
-
-
Free full text
-
Abstract
BACKGROUND Studies associate sleeping and eating late in the day with poor dietary quality and higher obesity risk but differences in sleep duration confound this association. We aimed to determine whether sleep and meal timing, independent of sleep duration, influenced food intake in healthy adults. METHODS This was a controlled, 2 × 2 inpatient crossover study with normal (0000-0800 h) or late (0330-1130 h) sleep and normal (1, 5, 11, and 12.5 h after awakening) or late (4.5, 8.5, 14.5, and 16 h after awakening) meals. Food intake was controlled while blood samples were obtained for determination of appetite-regulating hormones on days 3-4. Self-selected food intake was assessed on day 5. Data were analyzed using linear mixed model analysis with sleep, meal, and sleep x meal interaction as dependent variables. RESULTS Five participants completed all phases (mean age 25.1 ± [SD] 3.9 y, body mass index 29.2 ± 2.7 kg/m2). There was a significant sleep x meal interaction on energy intake (P = 0.035) and trends on fat and sodium intakes (P < 0.10). Overnight ghrelin concentrations were higher under normal sleep and meal conditions relative to late (P < 0.005) but lower when both were combined (P < 0.001). Overnight leptin concentrations were higher under normal meal conditions (P = 0.012). There was a significant sleep x meal interaction on ghrelin (P = 0.032) and glucagon-like peptide 1 (P = 0.041) concentrations, but not leptin (P = 0.83), in response to a test meal. CONCLUSIONS Our results suggest that alignment of sleep and meals may influence food choice and energy balance. Additional research is necessary to expand and confirm our findings.
-
9.
Pilot study of sleep and meal timing effects, independent of sleep duration and food intake, on insulin sensitivity in healthy individuals.
Pizinger, T, Kovtun, K, RoyChoudhury, A, Laferrère, B, Shechter, A, St-Onge, MP
Sleep health. 2018;(1):33-39
-
-
Free full text
-
Abstract
This pilot study tested the independent and interactive effects of sleep and meal times, under identical sleep duration and feeding conditions, on insulin sensitivity (Si) in overweight adults. Participants underwent a 4-phase randomized crossover inpatient study differing in sleep times: normal (Ns: 0000-0800 hours) or late (Ls: 0330-1130 hours); and in meal times: normal (Nm: 1, 5, 11, and 12.5 hours after awakening) or late (Lm: 4.5, 8.5, 14.5, and 16 hours after awakening). An insulin-modified frequently sampled intravenous glucose tolerance test, at scheduled breakfast time, and a meal tolerance test, at scheduled lunch time, were performed to assess Si after 3 days in each condition. Six participants were enrolled (4 men, 2 women; mean age 25.1±[SD] 3.9 years, body mass index 29.2±2.7 kg/m2); only 1 failed to complete her last study phase. There were no effects of sleep and meal times or sleep × meal time interaction on Si (all P>.35), acute insulin response to intravenous glucose (all P>.20), and disposition index (all P>.60) after adjusting for sex and body mass index. Meal tolerance test glucose and insulin areas under the curve were lower during Nm (glucose P=.11; insulin P=.0088). There were a sleep × meal interaction and an effect of meal times on overnight glucose (P=.0040 and .012, respectively) and insulin (P=.0075 and .067, respectively). Sleep timing, without concomitant sleep restriction, does not adversely affect Si and glucose tolerance, but meal times may be relevant for health. Our results should be confirmed in a larger sample.
-
10.
Sleep architecture following a weight loss intervention in overweight and obese patients with obstructive sleep apnea and type 2 diabetes: relationship to apnea-hypopnea index.
Shechter, A, St-Onge, MP, Kuna, ST, Zammit, G, RoyChoudhury, A, Newman, AB, Millman, RP, Reboussin, DM, Wadden, TA, Jakicic, JM, et al
Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine. 2014;(11):1205-11
Abstract
STUDY OBJECTIVES To determine if weight loss and/ or changes in apnea-hypopnea index (AHI) improve sleep architecture in overweight/ obese adults with type 2 diabetes (T2D) and obstructive sleep apnea (OSA). METHODS This was a randomized controlled trial including 264 overweight/ obese adults with T2D and OSA. Participants were randomized to an intensive lifestyle intervention (ILI) or a diabetes and support education (DSE) control group. Measures included anthropometry, AHI, and sleep at baseline and year-1, year-2, and year-4 follow-ups. RESULTS Changes in sleep duration (total sleep time [TST]), continuity [wake after sleep onset (WASO)], and architecture stage 1, stage 2, slow wave sleep, and REM sleep) from baseline to year 1, 2, and 4 did not differ between ILI and DSE. Repeated-measure mixed-model analyses including data from baseline through year-4 for all participants demonstrated a significant positive association between AHI and stage 1 sleep (p < 0.001), and a significant negative association between AHI and stage 2 (p = 0.01) and REM sleep (p < 0.001), whereas changes in body weight had no relation to any sleep stages or TST. WASO had a significant positive association with change in body weight (p = 0.009). CONCLUSIONS Compared to control, the ILI did not induce significant changes in sleep across the 4-year follow-up. In participants overall, reduced AHI in overweight/ obese adults with T2D and OSA was associated with decreased stage 1, and increased stage 2 and REM sleep. These sleep architecture changes are more strongly related to reductions in AHI than body weight, whereas WASO may be more influenced by weight than AHI. CLINICAL TRIAL REGISTRATION NUMBER NCT00194259.