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Temporal Change in Biomarkers of Bone Turnover Following Late Evening Ingestion of a Calcium-Fortified, Milk-Based Protein Matrix in Postmenopausal Women with Osteopenia.
Hettiarachchi, M, Cooke, R, Norton, C, Jakeman, P
Nutrients. 2019;11(6)
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Low bone mineral density (bone mineral content) and a diminution in bone quality (bone microarchitecture) are attributes of risk of fracture in people with osteopenia. The aim of this study was to investigate the effect of feeding a milk protein-based matrix (MBPM) fortified with calcium and vitamin D prior to bedtime on the biomarkers of bone remodelling in postmenopausal women with osteopenia. The study is a block-randomised cross-over design which recruited a sample of 41 postmenopausal women aged 50 to 70 years. Out of the 24 participants classified as osteopenic, 16 volunteers progressed to the RCT and randomly assigned to receive either a milk-based protein supplement (MBPM) or an isoenergetic, control. Results indicate that a dairy-based protein supplement fortified with calcium (MBPM) fed at bedtime has a potent effect on nocturnal rates of bone resorption in healthy osteopenic postmenopausal women. Furthermore, the synergistic, pluripotent quality of a milk-based protein matrix and timing of ingestion to the nocturnal, peak rate of bone remodelling transiently depressed bone turnover. Authors conclude that a late-evening supplement of calcium-fortified milk protein affects a beneficial decrease in the homeostatic rate of bone remodelling in persons at risk of degenerative bone disease.
Abstract
The diurnal rhythm of bone remodeling suggests nocturnal dietary intervention to be most effective. This study investigated the effect of bedtime ingestion of a calcium-fortified, milk-derived protein matrix (MBPM) or maltodextrin (CON) on acute (0-4 h) blood and 24-h urinary change in biomarkers of bone remodeling in postmenopausal women with osteopenia. In CON, participants received 804 ± 52 mg calcium, 8.2 ± 3.2 µg vitamin D and 1.3 ± 0.2 g/kg BM protein per day. MBPM increased calcium intake to 1679 ± 196 mg, vitamin D to 9.2 ± 3.1 µg and protein to 1.6 ± 0.2 g/kg BM. Serum C-terminal cross-linked telopeptide of type I collagen (CTX) and procollagen type 1 amino-terminal propeptide (P1NP), and urinary N-telopeptide cross-links of type I collagen (NTX), pyridinoline (PYD) and deoxypyridinoline (DPD) was measured. Analyzed by AUC and compared to CON, a -32% lower CTX (p = 0.011, d = 0.83) and 24% (p = 0.52, d = 0.2) increase in P1NP was observed for MBPM. Mean total 24 h NTX excreted in MBPM was -10% (p = 0.035) lower than CON. Urinary PYD and DPD were unaffected by treatment. This study demonstrates the acute effects of bedtime ingestion of a calcium-fortified, milk-based protein matrix on bone remodeling.
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Sleep restriction increases the neuronal response to unhealthy food in normal-weight individuals.
St-Onge, MP, Wolfe, S, Sy, M, Shechter, A, Hirsch, J
International journal of obesity (2005). 2014;38(3):411-6
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Sleep patterns influence eating behaviour and the body’s response to food. Previous studies suggest that short sleep duration leads to increased caloric intake and a desire for high-fat foods, however the specific neural mechanisms explaining how sleep restriction modulates this response is unknown. The aim of this study was to determine whether a specific area of the brain is activated in response to unhealthy compared with healthy foods. 25 participants were included, all of which were normal weight and had normal sleeping patterns. Each participant was tested after five nights of either 4 or 9 hours in bed by functional magnetic resonance imaging (fMRI). The test was performed while the participant was shown healthy and unhealthy food photos in the fasted state. This study found that after a period of restricted sleep compared with habitual sleep, unhealthy foods led to greater activation in brain regions associated with reward compared with healthy foods. This finding provides a model of neuronal mechanisms relating short sleep duration to obesity and cardio-metabolic risk factors and warrants further investigation.
Abstract
CONTEXT Sleep restriction alters responses to food. However, the underlying neural mechanisms for this effect are not well understood. OBJECTIVE The purpose of this study was to determine whether there is a neural system that is preferentially activated in response to unhealthy compared with healthy foods. PARTICIPANTS Twenty-five normal-weight individuals, who normally slept 7-9 h per night, completed both phases of this randomized controlled study. INTERVENTION Each participant was tested after a period of five nights of either 4 or 9 h in bed. Functional magnetic resonance imaging (fMRI) was performed in the fasted state, presenting healthy and unhealthy food stimuli and objects in a block design. Neuronal responses to unhealthy, relative to healthy food stimuli after each sleep period were assessed and compared. RESULTS After a period of restricted sleep, viewing unhealthy foods led to greater activation in the superior and middle temporal gyri, middle and superior frontal gyri, left inferior parietal lobule, orbitofrontal cortex, and right insula compared with healthy foods. These same stimuli presented after a period of habitual sleep did not produce marked activity patterns specific to unhealthy foods. Further, food intake during restricted sleep increased in association with a relative decrease in brain oxygenation level-dependent (BOLD) activity observed in the right insula. CONCLUSION This inverse relationship between insula activity and food intake and enhanced activation in brain reward and food-sensitive centers in response to unhealthy foods provides a model of neuronal mechanisms relating short sleep duration to obesity.
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Nighttime snacking reduces whole body fat oxidation and increases LDL cholesterol in healthy young women.
Hibi, M, Masumoto, A, Naito, Y, Kiuchi, K, Yoshimoto, Y, Matsumoto, M, Katashima, M, Oka, J, Ikemoto, S
American journal of physiology. Regulatory, integrative and comparative physiology. 2013;304(2):R94-R101
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Night eating syndrome (NES) is defined by night time eating (25% or more of the total energy of the day is consumed after the evening meal or by waking up in the middle of the night to eat at least three times per week). Research suggests that it is associated with obesity and a higher BMI. Those with NES may have higher glucose and insulin levels, and lower levels of ghrelin during the night compared to those without NES. This randomised crossover study aimed to explore the impact of nighttime eating on energy, glucose and lipid metabolism in normal weight young women. Participants were asked to either complete a 2 week nighttime snacking intervention or a daytime snacking intervention. The snack represented 10% of the average energy requirement (1950 k/cal per day) with a protein:fat:carbohydrate ratio of 5:50:45. The study found no impact of nighttime snacking on body weight, energy expenditure or glucose metabolism compared to daytime snacking. However, it did find a decrease in fat oxidation and increases in total and LDL cholesterol. Hunger levels before lunch were also higher during the nighttime snacking intervention.
Abstract
The increase in obesity and lipid disorders in industrialized countries may be due to irregular eating patterns. Few studies have investigated the effects of nighttime snacking on energy metabolism. We examined the effects of nighttime snacking for 13 days on energy metabolism. Eleven healthy women (means ± SD; age: 23 ± 1 yr; body mass index: 20.6 ± 2.6 kg/m(2)) participated in this randomized crossover trial for a 13-day intervention period. Subjects consumed a specified snack (192.4 ± 18.3 kcal) either during the daytime (10:00) or the night time (23:00) for 13 days. On day 14, energy metabolism was measured in a respiratory chamber without snack consumption. An oral glucose tolerance test was performed on day 15. Relative to daytime snacking, nighttime snacking significantly decreased fat oxidation (daytime snacking: 52.0 ± 13.6 g/day; nighttime snacking: 45.8 ± 14.0 g/day; P = 0.02) and tended to increase the respiratory quotient (daytime snacking: 0.878 ± 0.022; nighttime snacking: 0.888 ± 0.021; P = 0.09). The frequency of snack intake and energy intake, body weight, and energy expenditure were not affected. Total and low-density lipoprotein (LDL) cholesterol significantly increased after nighttime snacking (152 ± 26 mg/dl and 161 ± 29 mg/dl; P = 0.03 and 76 ± 20 mg/dl and 83 ± 24 mg/dl; P = 0.01, respectively), but glucose and insulin levels after the glucose load were not affected. Nighttime snacking increased total and LDL cholesterol and reduced fat oxidation, suggesting that eating at night changes fat metabolism and increases the risk of obesity.