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Effects of acute sleep loss on leptin, ghrelin, and adiponectin in adults with healthy weight and obesity: A laboratory study.
van Egmond, LT, Meth, EMS, Engström, J, Ilemosoglou, M, Keller, JA, Vogel, H, Benedict, C
Obesity (Silver Spring, Md.). 2023;31(3):635-641
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Plain language summary
A lack of sleep may be a risk factor for weight gain. Leptin is an adipocyte-derived hormone that activates satiety networks within the brain. Ghrelin, as opposed to leptin, is mainly produced by the stomach and it acts as a hunger hormone, signalling fuel status to the central nervous system. Some studies have found either no alterations or higher leptin and lower ghrelin blood levels following experimental sleep deprivation. The aim of this study was to investigate whether blood concentrations of leptin, ghrelin, and adiponectin are affected by acute total sleep deprivation in a sex- and weight-specific manner. This study is a laboratory study based on blood samples from 44 participants, mainly university students. Results show that: - acute total sleep deprivation is linked to lower serum levels of the adipokine leptin and higher blood levels of ghrelin. - following sleep deprivation, serum adiponectin levels were elevated. - the drop in serum leptin was larger in women after total sleep deprivation; however, there wasn’t a significant association between biological sex and experimental condition. - the increase in blood levels of adiponectin was slightly more pronounced among women, whereas there weren’t any differences in the effects of sleep loss on plasma ghrelin. Authors conclude that acute total sleep deprivation shifts the endocrine balance from the satiety hormone leptin toward the hunger-promoting hormone ghrelin. However, further investigation in larger samples focusing on their findings linked to sex- and weight-specific differences in leptin, ghrelin, and adiponectin are needed.
Expert Review
Conflicts of interest:
None
Take Home Message:
Sleep deprivation may shift the balance of appetite controlling hormones causing an increase in hunger and decreased satiety and therefore resulting in increased food intake. These changes may be more pronounced in biological females.
Evidence Category:
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A: Meta-analyses, position-stands, randomized-controlled trials (RCTs)
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B: Systematic reviews including RCTs of limited number
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C: Non-randomized trials, observational studies, narrative reviews
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D: Case-reports, evidence-based clinical findings
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E: Opinion piece, other
Summary Review:
Introduction
Sleep deprivation may contribute to weight gain and obesity through its effect on the hormonal pathways promoting hunger and satiety. Research has also linked chronic sleep loss with an increase in the brain reward response to food, thus driving an increase in daily food intake. Leptin and ghrelin are hormones involved in the control of food intake. Some research has associated alterations in these hormones following sleep loss, whilst others have not.
This study aimed to investigate whether biological sex and weight status affect fasting serum levels of leptin, ghrelin and adiponectin following chronic sleep deprivation in a supervised laboratory setting.
Methods
This randomised crossover design study included n=44 mixed sex participants with a mean age of 24.9 years. A total of 19 of the participants were classed as obese, with the remaining n= 25 participants were considered normal weight. Participants completed 2 nights in experimental sessions under continuously supervised conditions in a laboratory. One night was spent awake and the other asleep. Fasting blood samples were taken the morning after each session to measure levels of leptin, ghrelin and adiponectin.
Results
Serum levels of leptin after one night’s sleep loss were around 7% lower than those measured after sleep (17.3 = +/-2.6 vs 18.6 +/- 2.8 ng/mL, p = 0.037). Adjustments using sex-stratified analysis showed significantly lower levels of serum leptin in women (25.8 +/_4.3 vs 28.1 +/_ 4.7 ng/mL, p = 0.030) but not for men (10.1 +/_ 2.4 vs 10.6 +/_ 2.3 ng/mL, p = 0.458). However, when comparing individual participant differences between sleep and wake sessions, the results were not significant. Additionally, no significant differences were found between normal weight and obese participants.
Higher levels of ghrelin were found following sleep deprivation in both sexes and weight sub-groups (839.4 +/-77.5 vs 741.4+/-63.2 pg/mL, p= 0.003). Adiponectin was also found to be elevated in all participants regardless of biological sex or weight status (7.5 +/- 0.6 vs 6.8 +/- 0.6ug/mL, p= 0.003). However, ghrelin was observed to increase slightly more in participants with obesity, whereas elevations in adiponectin were slightly greater in those of normal weight.
Conclusion
In this study, sleep loss was associated with lowered levels of leptin and higher levels of ghrelin. Analysis between biological sexes indicated that there may be a greater decrease in leptin in females. Serum levels of adiponectin were also found to be elevated after sleep deprivation for both sexes with a slightly larger increase in women. These changes may result in increased hunger and food intake and decreased satiety. No significant differences were found between normal weight and obese participants.
Notes: The authors reported no conflicts of interest.
Clinical practice applications:
Sleep deprivation may lead to lower levels of leptin in both sexes with a greater decrease for females. Ghrelin and adiponectin levels may be increased in both men and women after sleep loss with a slightly larger increase in adiponectin for women. This could lead to an increase in appetite, food consumption and therefore weight gain, particularly in women.
Considerations for future research:
- Larger studies are needed to investigate sex and weight status related differences in serum levels of ghrelin, leptin and adiponectin.
- It may be beneficial for blood samples to be taken at different points during the day to allow for fluctuations in hormone levels.
- Food intake should be measured to monitor any increases in food intake.
Abstract
OBJECTIVE This study investigated whether blood concentrations of leptin, ghrelin, and adiponectin are affected by acute total sleep deprivation in a sex- and weight-specific manner. METHODS A total of 44 participants (mean age 24.9 years; 20 women; 19 with obesity) participated in a crossover design, including one night of sleep deprivation and one night of sleep in the laboratory. After each night, fasting blood was collected. RESULTS After sleep deprivation, fasting levels of leptin were lower (mean [SE], vs. sleep: 17.3 [2.6] vs. 18.6 [2.8] ng/mL), whereas those of ghrelin and adiponectin were higher (839.4 [77.5] vs. 741.4 [63.2] pg/mL and 7.5 [0.6] vs. 6.8 [0.6] μg/mL, respectively; all p < 0.05). The changes in leptin and adiponectin following sleep loss were more pronounced among women. Furthermore, the ghrelin increase was stronger among those with obesity after sleep loss. Finally, the sleep loss-induced increase in adiponectin was more marked among normal-weight participants. CONCLUSIONS Acute sleep deprivation reduces blood concentrations of the satiety hormone leptin. With increased blood concentrations of ghrelin and adiponectin, such endocrine changes may facilitate weight gain if persisting over extended periods of sleep loss. The observed sex- and weight-specific differences in leptin, ghrelin, and adiponectin call for further investigation.
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Association between Sleep Disturbances and Liver Status in Obese Subjects with Nonalcoholic Fatty Liver Disease: A Comparison with Healthy Controls.
Marin-Alejandre, BA, Abete, I, Cantero, I, Riezu-Boj, JI, Milagro, FI, Monreal, JI, Elorz, M, Herrero, JI, Benito-Boillos, A, Quiroga, J, et al
Nutrients. 2019;11(2)
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Inadequate sleep has been associated with poor health outcomes such as obesity and type 2 diabetes. The relevance of sleep patterns in the onset or progression of non-alcoholic fatty liver disease (NAFLD) is poorly understood. The aim of this cross-sectional study was to investigate the association between sleep characteristics and liver health in obese people with NAFLD compared to normal weight people without NAFLD. 94 overweight or obese patients with NAFLD and 40 normal weight people without NAFLD were enrolled in the study. Measures of liver health such as liver stiffness and levels of liver enzymes were assessed, along with sleep features evaluated using a Sleep Quality Index (SQI). A higher prevalence of short sleep duration and poor sleep quality were found in people with NAFLD. Sleep disturbance or sleep quality predicted up to 20.3% and 20.4% of the variability of liver stiffness, respectively, after adjusting for other factors. The authors of the study suggest that sleep disruption may be contributing to the development of NAFLD, and/or the alteration of the liver may be affecting sleep patterns. Consequently, sleep may be a modifiable behaviour to consider in the prevention and management of NAFLD.
Abstract
The relevance of sleep patterns in the onset or evolution of nonalcoholic fatty liver disease (NAFLD) is still poorly understood. Our aim was to investigate the association between sleep characteristics and hepatic status indicators in obese people with NAFLD compared to normal weight non-NAFLD controls. Ninety-four overweight or obese patients with NAFLD and 40 non-NAFLD normal weight controls assessed by abdominal ultrasonography were enrolled. Hepatic status evaluation considered liver stiffness determined by Acoustic Radiation Force Impulse elastography (ARFI) and transaminases. Additionally, anthropometric measurements, clinical characteristics, and biochemical profiles were determined. Sleep features were evaluated using the Pittsburgh Sleep Quality Index (PSQI). Hepatic status parameters, anthropometric measurements, and clinical and biochemical markers differed significantly in NAFLD subjects compared to controls, as well as sleep efficiency, sleep disturbance score, and sleep quality score. In the NAFLD group, a higher prevalence of short sleep duration (p = 0.005) and poor sleep quality (p = 0.041) were found. Multivariate-adjusted odds ratio (95% confidence interval) for NAFLD considering sleep disturbance was 1.59 (1.11⁻2.28). Regression models that included either sleep disturbance or sleep quality predicted up to 20.3% and 20.4% of the variability of liver stiffness, respectively, and after adjusting for potential confounders. Current findings suggest that sleep disruption may be contributing to the pathogenesis of NAFLD as well as the alteration of the liver may be affecting sleep patterns. Consequently, sleep characteristics may be added to the list of modifiable behaviors to consider in health promotion strategies and in the prevention and management of NAFLD.
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The relationship between the leptin/ghrelin ratio and meals with various macronutrient contents in men with different nutritional status: a randomized crossover study.
Adamska-Patruno, E, Ostrowska, L, Goscik, J, Pietraszewska, B, Kretowski, A, Gorska, M
Nutrition journal. 2018;17(1):118
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Obesity is a chronic disease caused mostly by an excessive supply of energy delivered with food in relation to energy expenditure, which leads to fat accumulation. The aim of the study was to investigate the leptin/ghrelin ratio (appetite-regulating hormones) in response to meal intake with various macronutrient contents, and to assess the fasting and postprandial (after meal) differences between normal and overweight or obese men. The study is a crossover designed study which was conducted among 46 non-diabetic men. The participants were randomly divided into two groups. Each group included men with normal weight and overweight/obesity. Results indicate that in normal body weight men, a more beneficial leptin/ghrelin ratio was noted after the high-carbohydrate fat-free meal intake, compared to the normal-carbohydrate/high-protein and high-fat/low-carbohydrate meal. Furthermore, overweight/obese men presented with a significantly higher leptin/ghrelin ratio in a fasting state and after intake of each of the three meals. Authors conclude that overweight/obese individuals can be recommended to chose meals with lower carbohydrate content.
Abstract
BACKGROUND Hormones, which influence satiety and hunger, play a significant role in body energy balance regulation. Ghrelin is a peptide that plays an important role in short-term appetite regulation, whereas leptin is a factor that controls long-term energy balance and is considered as a satiety hormone. The aim of this study was to evaluate the leptin/ghrelin ratio in a fasting state and after the intake of meals with varying macronutrient contents and to assess the possible differences between normal body weight and overweight/obese men. METHODS We examined 46 healthy adult men (23 with normal body weight and 23 overweight/obese) aged 21-58, who were divided into two groups. In the crossover study, participants received isocaloric (450 kcal) meals with different macronutrient contents: men from the first group received high-carbohydrate (HC) and normo-carbohydrate (NC) meals, and in the second group, participants received high-carbohydrate and high-fat (HF) meals. The ratio of leptin/ghrelin levels was calculated from leptin and total ghrelin serum concentrations in a fasting state and 30, 60, 120, 180 and 240 min after meal intake. One-way ANOVA and Wilcoxon signed-rank tests were carried out. The normality of the variable distribution was checked with the Shapiro-Wilk test, the homogeneity of variances was verified with the Levene test, and the false discovery rate p-value adjustment method was used. RESULTS The leptin/ghrelin ratio was significantly higher in overweight/obese men than individuals with normal body weight in a fasting state, as well as postprandially. We observed trends towards a higher leptin/ghrelin ratio values from the 60 min after HC-meal intake compared to the NC- and HF-meals in normal body weight participants, while in overweight/obese men, we did not note any significant differences dependent on the meal type. CONCLUSIONS We have observed a significantly different postprandial leptin/ghrelin ratio in normal body weight and overweight/obese men, and our results suggest that in men with normal body weight, a greater feeling of satiety may occur after high-carbohydrate meal intake, which was not noted in the overweight/obese individuals.
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Comparison of low calorie high protein and low calorie standard protein diet on waist circumference of adults with visceral obesity and weight cycling.
Witjaksono, F, Jutamulia, J, Annisa, NG, Prasetya, SI, Nurwidya, F
BMC research notes. 2018;11(1):674
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Obesity has become one of the world’s biggest health problem. Obese individuals with a history of repeated weight loss and regain (called weight cycling) have a higher risk of developing chronic disease and increased fat mass in every cycle. The objective of the study was to evaluate the effect of a low calorie high protein diet compared to a low calorie standard protein diet on waist circumference in adults with visceral obesity. The open, randomised clinical trial recruited 61 obese subjects who are older than 20 years of age and had a history of weight cycling. Participants were randomly assigned to one of the two diet groups; high protein or standard protein. Results showed that following a low-calorie diet resulted in waist circumference reduction thus reducing visceral fat. However, protein composition in the diet plan did not affect waist circumference reduction. Authors conclude that calorie restricted diets could be suggested in the treatment of visceral obesity. Macronutrient composition can be adjusted to meet the patient’s individual needs.
Abstract
OBJECTIVES Many individuals with visceral obesity who previously had succeeded in reducing body weight regain and this loss-gain cycle repeats several times which is called as weight cycling. We aimed to evaluate the effect of a low calorie high protein diet (HP) compared to a low calorie standard protein diet (SP) on waist circumference of visceral obese adults with history of weight cycling. RESULTS In this open-randomized clinical trial, participants were asked to follow dietary plan with reduction in daily caloric intake ranging from 500 to 1000 kcal from usual daily amount with minimum daily amount of 1000 kcal for 8 weeks and were divided in two groups: HP group with protein as 22-30% total calorie intake; and SP group with protein as 12-20% total calorie intake. There was a statistically significant difference (P < 0.001) between waist circumference before and after the dietary intervention among both groups. Meanwhile, there was no statistically significant difference in the mean reduction of waist circumference between HP and SP groups (P = 0.073). Taken together, the protein proportion does not significantly affected waist circumference. Trial registration ClinicalTrials.gov NCT03374150, 11 December 2017.
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Gut microbiota varies by opioid use, circulating leptin and oxytocin in African American men with diabetes and high burden of chronic disease.
Barengolts, E, Green, SJ, Eisenberg, Y, Akbar, A, Reddivari, B, Layden, BT, Dugas, L, Chlipala, G
PloS one. 2018;13(3):e0194171
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Obesity and type 2 diabetes (T2D) can lead to alterations of the composition of the gut microbiota. The gut microbiota, in turn, has been suggested to play a role in the development of psychological conditions, such as anxiety, depression and drug addiction. This cross-sectional study included 99 mostly overweight/obese African American men, with or without T2D, and with or without opioid addiction and other psychiatric disorders. The aim of the study was to determine, whether the gut microbiota composition was linked to T2D and the use of opioids in these patients. Furthermore, the researchers looked at the associations between leptin and oxytocin levels in the blood and the gut microbiota, and whether these hormone biomarkers could be indicative of obesity and psychosocial behaviour, such as opioid addiction. The authors found that some bacterial species in the gut were affected by T2D, diabetes medication and opioid use in the studied subjects. A relationship was also observed between leptin and oxytocin levels and the abundance of certain bacteria in the gut in subjects without T2D. The authors conclude that targeting the gut microbiota could be used for the management of T2D and associated psychiatric disorders. However, more studies are needed to provide further understanding of the connections between the gut microbiota and the brain.
Abstract
OBJECTIVE The gut microbiota is known to be related to type 2 diabetes (T2D), psychiatric conditions, and opioid use. In this study, we tested the hypothesis that variability in gut microbiota in T2D is associated with psycho-metabolic health. METHODS A cross-sectional study was conducted among African American men (AAM) (n = 99) that were outpatients at a Chicago VA Medical Center. The main outcome measures included fecal microbiota ecology (by 16S rRNA gene sequencing), psychiatric disorders including opioid use, and circulating leptin and oxytocin as representative hormone biomarkers for obesity and psychological pro-social behavior. RESULTS The study subjects had prevalent overweight/obesity (78%), T2D (50%) and co-morbid psychiatric (65%) and opioid use (45%) disorders. In the analysis of microbiota, the data showed interactions of opioids, T2D and metformin with Bifidobacterium and Prevotella genera. The differential analysis of Bifidobacterium stratified by opioids, T2D and metformin, showed significant interactions among these factors indicating that the effect of one factor was changed by the other (FDR-adjusted p [q] < 0.01). In addition, the pair-wise comparison showed that participants with T2D not taking metformin had a significant 6.74 log2 fold increase in Bifidobacterium in opioid users as compared to non-users (q = 2.2 x 10-8). Since metformin was not included in this pair-wise comparison, the significant 'q' suggested association of opioid use with Bifidobacterium abundance. The differences in Bifidobacterium abundance could possibly be explained by opioids acting as organic cation transporter 1 (OCT1) inhibitors. Analysis stratified by lower and higher leptin and oxytocin (divided by the 50th percentile) in the subgroup without T2D showed lower Dialister in High-Leptin vs. Low-Leptin (p = 0.03). Contrary, the opposite was shown for oxytocin, higher Dialister in High-Oxytocin vs. Low-Oxytocin (p = 0.04). CONCLUSIONS The study demonstrated for the first time that Bifidobacterium and Prevotella abundance was affected by interactions of T2D, metformin and opioid use. Also, in subjects without T2D Dialister abundance varied according to circulating leptin and oxytocin.
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Melatonin Supplementation Lowers Oxidative Stress and Regulates Adipokines in Obese Patients on a Calorie-Restricted Diet.
Szewczyk-Golec, K, Rajewski, P, Gackowski, M, Mila-Kierzenkowska, C, Wesołowski, R, Sutkowy, P, Pawłowska, M, Woźniak, A
Oxidative medicine and cellular longevity. 2017;2017:8494107
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Obesity is one of the major global health problems. Melatonin is a hormone which regulates wakefulness, functions as an antioxidant and plays a role in the immune system. Previous research suggests that melatonin deficiency is associated with obesity. The aim of this study was to estimate the effect of melatonin on oxidative stress and levels of cell signalling proteins released by fat cells (adipokines) in obese patients on a calorie-restricted diet. Thirty obese patients were supplemented with a daily dose of 10 mg of melatonin or placebo for 30 days with a calorie-restricted diet. Blood levels of melatonin, adipokines and markers of oxidative stress were measured at baseline and after supplementation. Significant body weight reduction (7%) was observed only in the melatonin group. After melatonin supplementation, the adiponectin and omentin-1 levels and glutathione peroxidase activities statistically increased, whereas the malondialdehyde concentrations were reduced. In the placebo group, a significant rise in 4-hydroxynonenal and a drop in the melatonin concentrations were found. The results show evidence of increased oxidative stress accompanying calorie restriction. The authors concluded that melatonin supplementation facilitated body weight reduction, improved the antioxidant defence, and regulated adipokine secretion. The findings suggest that melatonin should be considered in the management of obesity.
Abstract
Obesity is one of the major global health problems. Melatonin deficiency has been demonstrated to correlate with obesity. The aim of the study was to estimate the effect of melatonin on oxidative stress and adipokine levels in obese patients on a calorie-restricted diet. Thirty obese patients were supplemented with a daily dose of 10 mg of melatonin (n = 15) or placebo (n = 15) for 30 days with a calorie-restricted diet. Serum levels of melatonin, 4-hydroxynonenal (HNE), adiponectin, omentin-1, leptin, and resistin, as well as erythrocytic malondialdehyde (MDA) concentration and Zn/Cu-superoxide dismutase, catalase, and glutathione peroxidase (GPx) activities, were measured at baseline and after supplementation. Significant body weight reduction was observed only in the melatonin group. After melatonin supplementation, the adiponectin and omentin-1 levels and GPx activities statistically increased, whereas the MDA concentrations were reduced. In the placebo group, a significant rise in the HNE and a drop in the melatonin concentrations were found. The results show evidence of increased oxidative stress accompanying calorie restriction. Melatonin supplementation facilitated body weight reduction, improved the antioxidant defense, and regulated adipokine secretion. The findings strongly suggest that melatonin should be considered in obesity management. This trial is registered with CTRI/2017/07/009093.
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In a randomized trial in prostate cancer patients, dietary protein restriction modifies markers of leptin and insulin signaling in plasma extracellular vesicles.
Eitan, E, Tosti, V, Suire, CN, Cava, E, Berkowitz, S, Bertozzi, B, Raefsky, SM, Veronese, N, Spangler, R, Spelta, F, et al
Aging cell. 2017;16(6):1430-1433
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Obesity and insulin resistance are associated with accelerated aging and increased risk of many age-related diseases. The risk of many cancers, including prostate cancer, increases with age and being overweight further increases the risk. The aim of the study is to investigate the inhibition of tumour growth through the effect of protein restriction diets and hence, levels of circulating amino acids. The participants of the study were men (n=38) with prostate cancer awaiting prostatectomy surgery. Most of the subjects were overweight with a BMI of 30.45 ± 5.8. They were randomly assigned to either a control diet or a protein restricted diet. In comparison to the control diet, results show that protein restriction increased the levels of receptors (a protein molecule that receives chemical signals from outside a cell) responsible of leptin, the hormone that controls hunger. The results also show that protein restriction can improve the body’s sensitivity to the effects of the insulin in neurons (a nerve cell specialised to transmit information throughout the body). Authors conclude that protein restriction can counteract major age-related diseases.
Abstract
Obesity, metabolic syndrome, and hyperleptinemia are associated with aging and age-associated diseases including prostate cancer. One experimental approach to inhibit tumor growth is to reduce dietary protein intake and hence levels of circulating amino acids. Dietary protein restriction (PR) increases insulin sensitivity and suppresses prostate cancer cell tumor growth in animal models, providing a rationale for clinical trials. We sought to demonstrate that biomarkers derived from plasma extracellular vesicles (EVs) reflect systemic leptin and insulin signaling and respond to dietary interventions. We studied plasma samples from men with prostate cancer awaiting prostatectomy who participated in a randomized trial of one month of PR or control diet. We found increased levels of leptin receptor in the PR group in total plasma EVs and in a subpopulation of plasma EVs expressing the neuronal marker L1CAM. Protein restriction also shifted the phosphorylation status of the insulin receptor signal transducer protein IRS1 in L1CAM+ EVs in a manner suggestive of improved insulin sensitivity. Dietary PR modifies indicators of leptin and insulin signaling in circulating EVs. These findings are consistent with improved insulin and leptin sensitivity in response to PR and open a new window for following physiologic responses to dietary interventions in humans.
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Inflammation as a predictive biomarker for response to omega-3 fatty acids in major depressive disorder: a proof-of-concept study.
Rapaport, MH, Nierenberg, AA, Schettler, PJ, Kinkead, B, Cardoos, A, Walker, R, Mischoulon, D
Molecular psychiatry. 2016;21(1):71-9
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This study investigated whether Omega 3 (n-3) fatty acids had a clinical effect on five inflammatory biomarkers on individuals diagnosed with Major Depressive Disorder (MDD). Individuals were randomised into 3 groups, each of which took 8 weeks of double blind treatment with either eicosapentaenoic acid enriched n-3 fatty acids (EPA), docosahexaenoic acid enriched n-3 fatty acids (DHA), or placebo. There were no significant differences in the outcomes of the groups. However, it was noted that individuals with higher levels of inflammatory markers who took EPA improved more than those on placebo, and less on DHA than placebo. he larger the number of high inflammatory markers, the wider the gap between the improvements of the EPA versus placebo. Individuals with high hs-CRP, IL-6 or leptin responded less well to placebo than those with lower levels of these biomarkers. EPA was less effective than placebo or DHA if subjects had low levels of all 5 biomarkers. The five biomarkers were strongly influenced by gender and weight. The majority of obese women and men had at least one high marker of inflammation, and many of these had 2 high markers. There was no difference in treatment patterns for men and women. This is consistent with literature that suggests that inflammation is associated with obesity. Results suggest that it is important to look at more than one marker of inflammation, and that subjects with a specific combination inflammation markers were more likely to respond to EPA treatment. The authors concluded that anti-inflammation therapy was only beneficial for those with inflammation related MDD, and not helpful and possibly harmful for those with physiologically derived MDD.
Abstract
This study explores whether inflammatory biomarkers act as moderators of clinical response to omega-3 (n-3) fatty acids in subjects with major depressive disorder (MDD). One hundred fifty-five subjects with Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV) MDD, a baseline 17-item Hamilton Depression Rating Scale (HAM-D-17) score ⩾ 15 and baseline biomarker data (interleukin (IL)-1ra, IL-6, high-sensitivity C-reactive protein (hs-CRP), leptin and adiponectin) were randomized between 18 May 2006 and 30 June 2011 to 8 weeks of double-blind treatment with eicosapentaenoic acid (EPA)-enriched n-3 1060 mg day(-1), docosahexaenoic acid (DHA)-enriched n-3 900 mg day(-1) or placebo. Outcomes were determined using mixed model repeated measures analysis for 'high' and 'low' inflammation groups based on individual and combined biomarkers. Results are presented in terms of standardized treatment effect size (ES) for change in HAM-D-17 from baseline to treatment week 8. Although overall treatment group differences were negligible (ES=-0.13 to +0.04), subjects with any 'high' inflammation improved more on EPA than placebo (ES=-0.39) or DHA (ES=-0.60) and less on DHA than placebo (ES=+0.21); furthermore, EPA-placebo separation increased with increasing numbers of markers of high inflammation. Subjects randomized to EPA with 'high' IL-1ra or hs-CRP or low adiponectin ('high' inflammation) had medium ES decreases in HAM-D-17 scores vs subjects 'low' on these biomarkers. Subjects with 'high' hs-CRP, IL-6 or leptin were less placebo-responsive than subjects with low levels of these biomarkers (medium to large ES differences). Employing multiple markers of inflammation facilitated identification of a more homogeneous cohort of subjects with MDD responding to EPA vs placebo in our cohort. Studies are needed to replicate and extend this proof-of-concept work.
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A comparative controlled trial comparing the effects of yoga and walking for overweight and obese adults.
Telles, S, Sharma, SK, Yadav, A, Singh, N, Balkrishna, A
Medical science monitor : international medical journal of experimental and clinical research. 2014;20:894-904
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Walking and yoga are types of exercise that may be useful for weight loss. The aim of this study was to compare the effects of yoga and walking on the biochemistry, body composition, balance and strength in overweight people. 68 Indian adults who were overweight or obese were allocated to either yoga or walking twice a day for 15 days. Both groups were given the same plant-based diet providing 1,650 kcal/day Both groups showed similar and significant decreases in body mass index (BMI), waist and hip circumference, lean mass, body water and total cholesterol over the 15 days. The yoga group increased serum leptin and decreased LDL cholesterol. The walking group decreased serum adiponectin and triglycerides. Since there was no control group, it was not possible to attribute the changes to the yoga or walking, rather than the diet. The authors concluded that both yoga and walking improved anthropometric variables and serum lipid profile in overweight and obese people, and that these interventions may be useful in treating obesity.
Abstract
BACKGROUND Walking and yoga have been independently evaluated for weight control; however, there are very few studies comparing the 2 with randomization. MATERIAL AND METHODS The present study compared the effects of 90 minutes/day for 15 days of supervised yoga or supervised walking on: (i) related biochemistry, (ii) anthropometric variables, (iii) body composition, (iv) postural stability, and (v) bilateral hand grip strength in overweight and obese persons. Sixty-eight participants, of whom 5 were overweight (BMI ≥25 kg/m2) and 63 were obese (BMI ≥30 kg/m2; group mean age ±S.D., 36.4±11.2 years; 35 females), were randomized as 2 groups - (i) a yoga group and (ii) a walking group - given the same diet. RESULTS All differences were pre-post changes within each group. Both groups showed a significant (p<0.05; repeated measures ANOVA, post-hoc analyses) decrease in: BMI, waist circumference, hip circumference, lean mass, body water, and total cholesterol. The yoga group increased serum leptin (p<0.01) and decreased LDL cholesterol (p<0.05). The walking group decreased serum adiponectin (p<0.05) and triglycerides (p<0.05). CONCLUSIONS Both yoga and walking improved anthropometric variables and serum lipid profile in overweight and obese persons. The possible implications are discussed.
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A decline in inflammation is associated with less depressive symptoms after a dietary intervention in metabolic syndrome patients: a longitudinal study.
Perez-Cornago, A, de la Iglesia, R, Lopez-Legarrea, P, Abete, I, Navas-Carretero, S, Lacunza, CI, Lahortiga, F, Martinez-Gonzalez, MA, Martinez, JA, Zulet, MA
Nutrition journal. 2014;13:36
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Metabolic syndrome (defined as a cluster of cardiovascular risk factors including central obesity, glucose intolerance, hypertension and lipid disorders) is rising rapidly worldwide. Certain features of metabolic syndrome including adiposity, glucose intolerance and lipid disorders have also been linked to depression, another burden on healthcare worldwide. The exact pathways linking these diseases are unclear but appear to be bidirectional and dependent on biological and behaviour factors. This study hypothesises that hypo caloric treatment may have a positive impact on both metabolic syndrome and depression, and explores the possible mechanisms for this effect. The sample included 60 subjects with a BMI of at least 36.1 and aged over 50 years. These were a subsample of the RESMENA-S study which involved a 6 month weight loss intervention (either RESMANA-S or a control both with the same energy restrictions). This study found a reduction in depressive symptoms, alongside a reduction in CRP and leptin following the diet. Previous research has found a relationship between weight loss and reduced depression, but this study specifically found the decrease in CRP and leptin with a reduction of depression. The precise mechanism between CRP and depression remains unclear but the authors suggest that inflammation may be responsible. Theoretically, the association between leptin and depression may be related to its metabolic properties and neurobiological activity (it may relate to mood and cognition).
Abstract
BACKGROUND Metabolic syndrome (MetS) and depression have become two prevalent diseases worldwide, whose interaction needs further investigation. Dietary treatment for weight loss in patients with MetS may improve depressive manifestations, however, the precise interactive pathways remain uncertain. Therefore, the aim of this study was to examine the effects of a hypocaloric diet designed to reduce MetS features on self-perceived depression and the possible underlying factors. METHODS Sixty subjects (Age: 50 ± 1 y; BMI: 36.1 ± 0.6 kg/m(2)) with MetS were selected from the RESMENA study (control and intervention) after they completed the 6-months hypocaloric treatment and rated for depressive symptoms using the Beck Depression Inventory (BDI). Anthropometric and biochemical measurements including leptin, C-reactive protein (CRP) and insulin levels were evaluated. RESULTS Depressive symptoms decreased during the weight loss intervention, with no differences between both dietary groups (control group -4.2 ± 0.8 vs RESMENA group -3.2 ± 0.6, P = 0.490). The number of criteria of the MetS was higher among subjects with more somatic-related depressive symptoms at baseline (B = 1.032, P-trend = 0.017). After six months of dietary treatment, body weight decreased in all subjects (-8.7%; confidence interval (95% CI) = 7.0-9.7) and also self-perceived depression (-37.9%; 95% CI = 2.7-4.9), as well as circulating leptin (-20.1%; 95% CI = 1.8-6.8), CRP (-42.8%; 95% CI = 0.6-3.0) and insulin (-37.7%; 95% CI = 4.1-7.2) concentrations. The decrease in BDI was significantly associated with declines in body fat mass (B = 0.34, 95% CI = 0.11-0.56) and also with the decrease in leptin (B = 0.16, 95% CI = 0.04-0.28) and CRP (B = 0.24, 95% CI = 0.01-0.46) concentrations. CONCLUSIONS The decrease in depressive manifestations after a weight loss intervention was related with adiposity, CRP and leptin in subjects with MetS. TRIAL REGISTRATION ClinicalTrials.gov: NCT01087086.