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Insufficient sleep predicts poor weight loss maintenance after 1 year.
Bogh, AF, Jensen, SBK, Juhl, CR, Janus, C, Sandsdal, RM, Lundgren, JR, Noer, MH, Vu, NQ, Fiorenza, M, Stallknecht, BM, et al
Sleep. 2023;46(5)
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Short sleep duration, defined as less than 6 hours/night, is associated with all-cause mortality, cardiovascular diseases, hypertension, diabetes, and obesity. Sleep restriction causes metabolic and behavioural changes suggesting that short sleep duration may contribute to the development of obesity. The aim of this study was to investigate associations between short sleep duration or poor sleep quality and weight regain after weight loss. This study is based on data from the S-LiTE randomised, controlled trial. Participants followed a low-calorie diet (800 kcal/day) for eight weeks prior to randomisation. Those who lost at least 5% of initial weight were randomised to the control or intervention group. Results showed that participants with objectively measured short sleep duration after a diet-induced weight loss had less success during weight loss maintenance than those with longer sleep duration. Worse sleep quality was associated with less weight loss during a low-calorie diet and subsequent weight maintenance. Authors conclude that insufficient sleep predicts weight regain during interventional efforts to maintain weight loss. Exercise maintained low-calorie diet-induced improvements in sleep quality during 1 year of weight loss maintenance, and liraglutide transiently increased sleep duration.
Abstract
STUDY OBJECTIVES Insufficient sleep may attenuate weight loss, but the role of sleep in weight loss maintenance is unknown. Since weight regain after weight loss remains a major obstacle in obesity treatment, we investigated whether insufficient sleep predicts weight regain during weight loss maintenance. METHODS In a randomized, controlled, two-by-two factorial study, 195 adults with obesity completed an 8-week low-calorie diet and were randomly assigned to 1-year weight loss maintenance with or without exercise and liraglutide 3.0 mg/day or placebo. Sleep duration and quality were measured before and after the low-calorie diet and during weight maintenance using wrist-worn accelerometers (GENEActiv) and Pittsburgh Sleep Quality Index (PSQI). To test associations between insufficient sleep and weight regain, participants were stratified at randomization into subgroups according to sleep duration (≥6 h/night) or sleep quality (PSQI score ≤/>5). RESULTS After a diet-induced 13.1 kg weight loss, participants with short sleep duration at randomization regained 5.3 kg body weight (p = .0008) and had less reduction in body fat percentage compared with participants with normal sleep duration (p = .007) during the 1-year weight maintenance phase. Participants with poor sleep quality before the weight loss regained 3.5 kg body weight compared with good quality sleepers (p = .010). During the weight maintenance phase, participants undergoing liraglutide treatment displayed increased sleep duration compared with placebo after 26 weeks (5 vs. -15 min/night) but not after 1 year. Participants undergoing exercise treatment preserved the sleep quality improvements attained from the initial weight loss. CONCLUSIONS Short sleep duration or poor sleep quality was associated with weight regain after weight loss in adults with obesity.
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Trial of the MIND Diet for Prevention of Cognitive Decline in Older Persons.
Barnes, LL, Dhana, K, Liu, X, Carey, VJ, Ventrelle, J, Johnson, K, Hollings, CS, Bishop, L, Laranjo, N, Stubbs, BJ, et al
The New England journal of medicine. 2023;389(7):602-611
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Lifestyle interventions targeting diet are a possible approach that could affect public health. Most clinical trials have investigated comprehensive diets, in contrast to dietary manipulation of single foods or nutrients. The aim of this study was to evaluate the effects of a 3-year dietary intervention on cognitive decline and brain-imaging markers of dementia and Alzheimer’s disease in older, cognitively unimpaired adults at risk for dementia because of family history. This study was a 3-year, two-site, randomised, controlled trial. The participants were randomly assigned to follow the MIND diet with mild caloric restriction for weight loss or their usual diet with the same mild caloric restriction for weight loss (control diet). Participants were randomly assigned in a 1:1 ratio. Results showed that the participants who followed the MIND diet had small improvements in a global measure of cognition that were similar to those who followed a control diet with mild caloric restriction. Authors concluded that brain health, cognitive function and brain imaging outcomes (after 3 years) did not differ significantly between participants who followed the MIND diet and those who followed a control diet with a mild caloric restriction.
Abstract
BACKGROUND Findings from observational studies suggest that dietary patterns may offer protective benefits against cognitive decline, but data from clinical trials are limited. The Mediterranean-DASH Intervention for Neurodegenerative Delay, known as the MIND diet, is a hybrid of the Mediterranean diet and the DASH (Dietary Approaches to Stop Hypertension) diet, with modifications to include foods that have been putatively associated with a decreased risk of dementia. METHODS We performed a two-site, randomized, controlled trial involving older adults without cognitive impairment but with a family history of dementia, a body-mass index (the weight in kilograms divided by the square of the height in meters) greater than 25, and a suboptimal diet, as determined by means of a 14-item questionnaire, to test the cognitive effects of the MIND diet with mild caloric restriction as compared with a control diet with mild caloric restriction. We assigned the participants in a 1:1 ratio to follow the intervention or the control diet for 3 years. All the participants received counseling regarding adherence to their assigned diet plus support to promote weight loss. The primary end point was the change from baseline in a global cognition score and four cognitive domain scores, all of which were derived from a 12-test battery. The raw scores from each test were converted to z scores, which were averaged across all tests to create the global cognition score and across component tests to create the four domain scores; higher scores indicate better cognitive performance. The secondary outcome was the change from baseline in magnetic resonance imaging (MRI)-derived measures of brain characteristics in a nonrandom sample of participants. RESULTS A total of 1929 persons underwent screening, and 604 were enrolled; 301 were assigned to the MIND-diet group and 303 to the control-diet group. The trial was completed by 93.4% of the participants. From baseline to year 3, improvements in global cognition scores were observed in both groups, with increases of 0.205 standardized units in the MIND-diet group and 0.170 standardized units in the control-diet group (mean difference, 0.035 standardized units; 95% confidence interval, -0.022 to 0.092; P = 0.23). Changes in white-matter hyperintensities, hippocampal volumes, and total gray- and white-matter volumes on MRI were similar in the two groups. CONCLUSIONS Among cognitively unimpaired participants with a family history of dementia, changes in cognition and brain MRI outcomes from baseline to year 3 did not differ significantly between those who followed the MIND diet and those who followed the control diet with mild caloric restriction. (Funded by the National Institute on Aging; ClinicalTrials.gov number, NCT02817074.).
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The effect of weight loss following 18 months of lifestyle intervention on brain age assessed with resting-state functional connectivity.
Levakov, G, Kaplan, A, Yaskolka Meir, A, Rinott, E, Tsaban, G, Zelicha, H, Blüher, M, Ceglarek, U, Stumvoll, M, Shelef, I, et al
eLife. 2023;12
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Obesity is linked to premature brain ageing and subsequent development of diseases such as dementia and Alzheimer’s disease. Weight loss through lifestyle modifications may be able to attenuate brain ageing. This sub-study of 102 individuals from a randomised control trial known as the Dietary Intervention Randomised Controlled Trial Polyphenols Unprocessed Study (DIRECT-PLUS), aimed to determine the effect of 18 months lifestyle modifications and weight loss on brain age. The results showed that a decrease in BMI attenuated brain ageing and that 1% body weight loss reduced brain ageing by 8.9 months. Reduced brain age was also associated with decreased waist circumference and fat mass. Interestingly, reduced consumption of processed foods was also associated with reduced brain age. It was concluded that weight loss can be of benefit to brain health. This study could be used by healthcare professionals to understand that people with obesity are at a higher risk of brain related diseases, and that weight loss may be an effective way to prevent their development.
Abstract
BACKGROUND Obesity negatively impacts multiple bodily systems, including the central nervous system. Retrospective studies that estimated chronological age from neuroimaging have found accelerated brain aging in obesity, but it is unclear how this estimation would be affected by weight loss following a lifestyle intervention. METHODS In a sub-study of 102 participants of the Dietary Intervention Randomized Controlled Trial Polyphenols Unprocessed Study (DIRECT-PLUS) trial, we tested the effect of weight loss following 18 months of lifestyle intervention on predicted brain age based on magnetic resonance imaging (MRI)-assessed resting-state functional connectivity (RSFC). We further examined how dynamics in multiple health factors, including anthropometric measurements, blood biomarkers, and fat deposition, can account for changes in brain age. RESULTS To establish our method, we first demonstrated that our model could successfully predict chronological age from RSFC in three cohorts (n=291;358;102). We then found that among the DIRECT-PLUS participants, 1% of body weight loss resulted in an 8.9 months' attenuation of brain age. Attenuation of brain age was significantly associated with improved liver biomarkers, decreased liver fat, and visceral and deep subcutaneous adipose tissues after 18 months of intervention. Finally, we showed that lower consumption of processed food, sweets and beverages were associated with attenuated brain age. CONCLUSIONS Successful weight loss following lifestyle intervention might have a beneficial effect on the trajectory of brain aging. FUNDING The German Research Foundation (DFG), German Research Foundation - project number 209933838 - SFB 1052; B11, Israel Ministry of Health grant 87472511 (to I Shai); Israel Ministry of Science and Technology grant 3-13604 (to I Shai); and the California Walnuts Commission 09933838 SFB 105 (to I Shai). Obesity is linked with the brain aging faster than would normally be expected. Researchers are able to capture this process by calculating a person’s ‘brain age’ – how old their brain appears on detailed scans, regardless of chronological age. This approach also helps to monitor how certain factors, such as lifestyle, can influence brain aging over relatively short time scales. It is not clear whether lifestyle interventions that promote weight loss can help to slow obesity-driven brain aging. To answer this question, Levakov et al. studied 102 individuals who met the criteria for obesity and took part in a lifestyle intervention aimed to improve diet and physical activity levels over 18 months. The participants received a brain scan at the beginning and the end of the program; additional tests and measurements were also conducted at these times to capture other biological processes impacted by obesity, such as liver health. Levakov et al. used the brain scans taken at the start and end of the study to examine the impact of the lifestyle intervention on the aging trajectory. The results revealed that a reduction in body weight of 1% led to the participants’ brain age being nearly 9 months younger than the expected brain age after 18 months. This attenuated aging was associated with changes in other biological measures, such as decreased liver fat and liver enzymes. Increases in liver fat and production of specific liver enzymes were previously shown to negatively impact brain health in Alzheimer’s disease. Finally, examining more closely the food consumption reports completed by participants showed that reduced consumption of processed food, sweets and beverages were linked to attenuated brain aging. The findings show that lifestyle interventions which promote weight loss can have a beneficial impact on the aging trajectory of the brain observed with obesity. The next steps will include determining whether slowing down obesity-driven brain aging results in better clinical outcomes for patients. In addition, the work by Levakov et al. demonstrates a potential strategy to evaluate the success of lifestyle changes on brain health. With global rates of obesity rising, identifying interventions that have a positive impact on brain health could have important clinical, educational and social impacts.
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The consequences of exercise-induced weight loss on food reinforcement. A randomized controlled trial.
Flack, KD, Hays, HM, Moreland, J
PloS one. 2020;15(6):e0234692
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Exercise is a long-standing remedy for nearly all of obesity’s comorbidities and often recommended as an economical and health-promoting option for weight loss and weight loss maintenance. The aim of this study was to investigate the effect of exercise on food reinforcement (reward-driven feeding), and to examine whether changes in body composition would be correlated with changes in food reinforcement. This study is randomized controlled trial with a total of 52 participants aged 18 to 40 years. Participants were randomly assigned to one of the three groups (six exercise sessions per week, two sessions per week, and sedentary control). Results indicate that there is great variability in individuals’ change in food reinforcement after a 12-week aerobic exercise intervention. Furthermore, those who did increase their food reinforcement were also those who lost the greatest amount of fat-free mass post-intervention. Authors conclude that preventing the loss of fat-free mass may be a valuable piece to a weight loss programme (with resistance training or dietary protein intake as adjunct therapy).
Abstract
BACKGROUND Obesity remains a primary threat to the health of most Americans, with over 66% considered overweight or obese with a body mass index (BMI) of 25 kg/m2 or greater. A common treatment option many believe to be effective, and therefore turn to, is exercise. However, the amount of weight loss from exercise training is often disappointingly less than expected with greater amounts of exercise not always promoting greater weight loss. Increases in energy intake have been prescribed as the primary reason for this lack of weight loss success with exercise. Research has mostly focused on alterations in hormonal mediators of appetite (e.g.: ghrelin, peptide YY, GLP-1, pancreatic polypeptide, and leptin) that may increase hunger and/or reduce satiety to promote greater energy intake with exercise training. A less understood mechanism that may be working to increase energy intake with exercise is reward-driven feeding, a strong predictor of energy intake and weight status but rarely analyzed in the context of exercise. DESIGN Sedentary men and women (BMI: 25-35 kg/m2, N = 52) were randomized into parallel aerobic exercise training groups partaking in either two or six exercise sessions/week, or sedentary control for 12 weeks. METHODS The reinforcing value of food was measured by an operant responding progressive ratio schedule task (the behavioral choice task) to determine how much work participants were willing to perform for access to a healthy food option relative to a less healthy food option before and after the exercise intervention. Body composition and resting energy expenditure were assessed via DXA and indirect calorimetry, respectively, at baseline and post testing. RESULTS Changes in fat-free mass predicted the change in total amount of operant responding for food (healthy and unhealthy). There were no correlations between changes in the reinforcing value of one type of food (healthy vs unhealthy) to changes in body composition. CONCLUSION In support of previous work, reductions in fat-free mass resulting from an aerobic exercise intervention aimed at weight loss plays an important role in energy balance regulation by increasing operant responding for food.
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Effects of 3-week total meal replacement vs. typical food-based diet on human brain functional magnetic resonance imaging food-cue reactivity and functional connectivity in people with obesity.
Kahathuduwa, CN, Davis, T, O'Boyle, M, Boyd, LA, Chin, SH, Paniukov, D, Binks, M
Appetite. 2018;120:431-441
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Weight loss diets that use total meal replacement shakes have been shown to reduce food cravings compared to typical reduced-calorie diets. The mechanism for this is unclear. This study examined the effects of a 3-week 1120 kcal per day meal replacement diet compared to a reduced calorie diet on activity in areas of the brain associated with food cravings. Thirty-two obese adults participated in the study. Before and after the study, the participants were given magnetic resonance imaging (MRI) scans to measure activity in different areas of the brain. They were also questioned on food cravings and weighed. The group following the meal replacement diet experienced a significant weight loss of 4.87 kg, a reduction in body fat of 2.19 kg and reduced their overall food cravings. The reduced calorie diet group also experienced significant weight loss and a reduction in body fat (2.37kg and 1.64kg, respectively) but less than the meal replacement group. The meal replacement group experienced reduced cravings compared to the reduced calorie diet group. MRI scans suggested that this was due to changes in activity in the food reward related regions in several areas of the brain, resulting in an increase in executive control. The authors concluded that meal replacement diets may increase executive control within the brain, leading to a reduction in food cravings and weight loss.
Abstract
OBJECTIVES Calorie restriction via total meal replacement (TMR) results in greater reduction of food cravings compared to reduced-calorie typical diet (TD). Direct evidence of the impact of these interventions on human brain fMRI food-cue reactivity (fMRI-FCR) and functional connectivity is absent. We examined the effects of a 3-week 1120 kcal/d TMR intervention as compared to an iso-caloric TD intervention using an fMRI-FCR paradigm. METHODS Thirty-two male and female subjects with obesity (19-60 years; 30-39.9 kg/m2) participated in a randomized two-group repeated measures dietary intervention study consisting of 1120 kcal/d from either 1) TMR (shakes), 2) TD (portion control). Pre-intervention and following the 3-week diet fMRI-FCR, functional connectivity, food cravings (Food Craving Inventory) and weight were considered. RESULTS Compared to TD, TMR showed increased fMRI-FCR of the bilateral dorsolateral prefrontal (dlPFC), orbitofrontal, anterior cingulate, primary motor and left insular cortices and bilateral nucleus accumbens regions in the post-intervention state relative to the pre-intervention state. Compared to TD, TMR was also associated with negative modulation of fMRI-FCR of the nucleus accumbens, orbitofrontal cortex and amygdala by dlPFC. Reduced body weight (4.87 kg, P < 0.001), body fat (2.19 kg, P = 0.004) and overall food cravings (0.41, P = 0.047) were seen in the TMR group. In the TD group reduced body weight (2.37 kg, P = 0.004) and body fat (1.64 kg, P = 0.002) were noted. Weight loss was significantly greater in TMR versus TD (2.50 kg, P = 0.007). CONCLUSIONS Greater weight loss and reduced cravings, coupled with stronger activations and potential negative modulation of the food reward related regions by the dlPFC during exposure to visual food cues is consistent with increased executive control in TMR vs. TD.
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Zinc supplementation in the treatment of anorexia nervosa.
Brazilian Association of Nutrology
Revista da Associacao Medica Brasileira (1992). 2013;59(4):321-4
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Anorexia nervosa (AN) is a disorder characterised by significant weight loss, restrictive diets, a search for thinness and a distortion of body image. Zinc is a key micronutrient that plays essential roles in the body including in gene transcription regulation and enzyme reactions. There is a similarity between symptoms of zinc deficiency and AN; namely weight loss, changes in appetite and sexual dysfunction. This review aims to provide healthcare professionals with insight into the nutritional recommendations for zinc in patients with AN. The review suggests that there are clinical studies demonstrating a strong association between AN and low levels of serum zinc and low levels of urinary zinc suggesting a micronutrient deficiency in these individuals. The severity of zinc deficiency is associated with greater weight deficits and longer AN duration. It is also associated with higher levels of anxiety and depression in AN individuals. Zinc is key in smell and taste perception and the brain regions associated with interpreting eating as pleasurable. Reduced food intake and practices like purging and low-zinc diets may exacerbate any low levels and impair zinc absorption. A controlled study showed that oral supplementation resulted in a higher rate of body mass index (BMI) increase and an improvement in neurotransmitters. The review recommends: 1. Check serum levels of zinc in AN patients as it may be low. Zinc status may contribute to eating behaviour including gaining pleasure from eating, smell and taste. 2. Zinc supplementation of 15mg/daily for preventative purposes and 15-20mg/daily if zinc deficiency is identified after testing. The review recommends supplementation for a minimum of 2 months.