Perceived Stress and Weight Gain in Adolescence: A Longitudinal Analysis

Perceived Stress and Weight Gain in Adolescence: A Longitudinal Analysis

Cornelia H.M. van Jaarsveld1, Jennifer A. Fidler1, Andrew Steptoe2, David Boniface1 and Jane Wardle1
1Health Behaviour Research Centre, Department of Epidemiology and Public Health, University College London, London, UK
2Psychobiology Group, Department of Epidemiology and Public Health, University College London, London, UK

Abstract

Although perceived stress has been hypothesized to be a risk factor for obesity, epidemiological studies relating stress to weight gain have shown mixed results. We examined prospective associations between perceived stress and changes in waist circumference and BMI in a large study of adolescents. As part of the Health and Behaviour in Teenagers Study (HABITS), height, weight, and waist circumference were measured annually in 4,065 adolescents aged from 11 to 16. Waist and BMI standard deviation scores (SDS) were used as indices of adiposity. Adolescents completed a measure of perceived stress each year, from which mean stress scores over the 5-year period were also calculated and divided by tertile into lower, moderate, and higher stress. Associations between perceived stress at each year and adiposity 1–4 years later and also adiposity trajectories over the whole period in relation to mean stress were investigated. Analyses were adjusted for age, sex, ethnicity, socioeconomic deprivation, pubertal timing, and smoking. Perceived stress in any year was not related prospectively to increases in waist or BMI SDS 1–4 years later, nor was there any evidence that higher stress over the whole period was associated with greater gains in waist or BMI SDS. However, waist and BMI SDS were significantly higher in the moderate- and higher-stress groups than the lower-stress group across the whole 5-year period. Persistent stress was associated with higher waist circumference and BMI in adolescence, but did not lead to differential changes over 5 years.

Antiobesity Effects of yerba maté Extract (Ilex paraguariensis) in High-fat Diet–induced Obese Mice

Antiobesity Effects of yerba maté Extract (Ilex paraguariensis) in High-fat Diet–induced Obese Mice

Demétrius P. Arçari1,2, Waldemar Bartchewsky1, Tanila W. dos Santos1, Karim A. Oliveira1, Alexandre Funck1, José Pedrazzoli1, Marina F.F. de Souza2, Mario J. Saad3, Deborah H.M. Bastos2, Alessandra Gambero1, Patricia de O. Carvalho4 and Marcelo L. Ribeiro1
1Unidade Integrada de Farmacologia e Gastroenterologia, Universidade São Francisco, Bragança Paulista, Brazil
2Departamento de Nutrição, Faculdade de Saúde Publica, Universidade de São Paulo, São Paulo, Brazil
3Departamento de Medicina Interna UNICAMP, Campinas, Brazil
4Laboratório Multidisciplinar de Pesquisa, Universidade São Francisco, Bragança Paulista, Brazil

Abstract

Because the potential of yerba maté (Ilex paraguariensis) has been suggested in the management of obesity, the aim of the present study was to evaluate the effects of yerba maté extract on weight loss, obesity-related biochemical parameters, and the regulation of adipose tissue gene expression in high-fat diet–induced obesity in mice. Thirty animals were randomly assigned to three groups. The mice were introduced to standard or high-fat diets. After 12 weeks on a high-fat diet, mice were randomly assigned according to the treatment (water or yerba maté extract 1.0 g/kg). After treatment intervention, plasma concentrations of total cholesterol, high-density lipoprotein cholesterol, triglyceride, low-density lipoprotein (LDL) cholesterol, and glucose were evaluated. Adipose tissue was examined to determine the mRNA levels of several genes such as tumor necrosis factor- (TNF-), leptin, interleukin-6 (IL-6), C-C motif chemokine ligand-2 (CCL2), CCL receptor-2 (CCR2), angiotensinogen, plasminogen activator inhibitor-1 (PAI-1), adiponectin, resistin, peroxisome proliferator-activated receptor-2 (PPAR-2), uncoupling protein-1 (UCP1), and PPAR- coactivator-1 (PGC-1). The F4/80 levels were determined by immunoblotting. We found that obese mice treated with yerba maté exhibited marked attenuation of weight gain, adiposity, a decrease in epididymal fat-pad weight, and restoration of the serum levels of cholesterol, triglycerides, LDL cholesterol, and glucose. The gene and protein expression levels were directly regulated by the high-fat diet. After treatment with yerba maté extract, we observed a recovery of the expression levels. In conclusion, our data show that yerba maté extract has potent antiobesity activity in vivo. Additionally, we observed that the treatment had a modulatory effect on the expression of several genes related to obesity.

A Meta-Analysis Evaluating the Impact of Chitosan on Serum Lipids in Hypercholesterolemic Patients

A Meta-Analysis Evaluating the Impact of Chitosan on Serum Lipids in Hypercholesterolemic Patients

William L. Bakera, c, Alix Terciusb, Moise Angladeb, C. Michael Whitea, c, Craig I. Colemana, c

University of Connecticut Schools of
aPharmacy and
bMedicine, Storrs, Conn. and Farmington, Conn., and
cEvidence-Based Practice Center at Hartford Hospital, Hartford, Conn., USA

Address of Corresponding Author

Ann Nutr Metab 2009;55:368-374 (DOI: 10.1159/000258633)

Key Words
Chitin
Chitosan
Hypercholesterolemia
Meta-analysis

Abstract

Background/Objective: Chitosan is increasingly being used in the United States as an over-the-counter cholesterol-lowering agent. The positively charged amino groups of chitosan may have the ability to bind negatively charged molecules such as lipids and bile acids, inducing a greater fractional excretion in the feces. To better characterize the impact of chitosan on serum lipids in hypercholesterolemic patients, we performed a meta-analysis of randomized controlled trials. Methods: A systematic literature search of Medline, Embase, Cochrane Central and the Natural Medicines Comprehensive Database was conducted from the earliest possible date through May 2008. Trials were included in the analysis if they were randomized, placebo-controlled trials of chitosan in hypercholesterolemic patients and reported efficacy data on total, low-density lipoprotein (LDL), high-density lipoprotein (HDL) cholesterol or triglycerides. The weighted mean difference (WMD) of the change from baseline (in milligrams per deciliter) with 95% confidence interval was calculated as the difference between the mean in the chitosan and placebo groups using a random-effects model. Results: Six studies (n = 416 patients) met the inclusion criteria. Upon meta-analysis, the use of chitosan significantly lowered total cholesterol [WMD, -11.59 mg/dl (-21.45 to -1.73), p = 0.02] but not LDL cholesterol, HDL cholesterol or triglycerides.

Conclusions: Based upon the currently available literature, we can only say that chitosan beneficially affects total cholesterol with 95% confidence. Additional, larger randomized controlled trials are needed to better characterize the effect of chitosan on other lipoproteins.

Sustained participation in youth sport decreases metabolic syndrome in adulthood

Sustained participation in youth sport decreases metabolic syndrome in adulthood

X Yang1, R Telama2, M Hirvensalo2, J S A Viikari3 and O T Raitakari4
1LIKES Research Center for Sport and Health Sciences, Jyväskylä, Finland
2Department of Sport Sciences, University of Jyväskylä, Jyväskylä, Finland
3Department of Medicine, University of Turku, Turku, Finland
4Department of Clinical Physiology, University of Turku, Turku, Finland

Correspondence: Dr X Yang, LIKES Research Center for Sport and Health Sciences, Yliopistonkatu 20, Jyväskylä 40100, Finland. E-mail: xiaolin.yang@likes.fi

Received 13 May 2009; Revised 18 June 2009; Accepted 28 June 2009; Published online 1 September 2009.

Abstract
Objective: to explore the effect of organized youth sport on metabolic syndrome (MetS) in adulthood.
Design: Longitudinal study data from the cardiovascular risk in young Finns study.
Subjects: A total of 1493 males (n=704) and females (n=789) aged 3, 6, 9, 12, 15 and 18 years were randomly selected from five university towns and their rural surroundings in 1980. They were followed up for 21 years. In 2001 they were 24, 27, 30, 33, 36 and 39 years old.
Measurements: Youth sports participation data (participation in sport-club training and competitions) were assessed in 1980 and 1983 using a self-report questionnaire completed in connection with a medical examination. Participants were divided into athletes and non-athletes at each measurement point, and then classified into four groups: Persistent athlete, Starter, Leaver and Non-athlete. A mean score of youth sport was assessed by calculating the average of four consecutive measurements (1980–1989). MetS risk in 2001 was defined as a categorical variable based on the guidelines of the European Group for the Study of Insulin Resistance (EGIR) and as a continuous MetS-score variable by summing the z-scores of individual metabolic variables.
Results: In males and females, intense participation in youth sports over 3 years was inversely and significantly associated with clustered MetS score and prevalence of MetS defined by EGIR in adulthood (P<0.05). The association remained significant after adjustment for age, baseline clustered MetS score, smoking and total caloric intake and after additional adjustments for adult leisure-time physical activity. Starters during 3 years were less likely to have MetS than non-athletes. Leavers were at a higher risk for MetS than persistent athletes. These associations were attenuated in males by adjustment for all potential confounders. Similar associations were found using EGIR MetS as an outcome.
Conclusions: Sustained participation in organized sport lasting at least 3 years in youth is associated with reduced risk for developing MetS in adulthood.

Alcohol as a Risk Factor for Type 2 Diabetes: A systematic review and meta-analysis

Alcohol as a Risk Factor for Type 2 Diabetes: A systematic review and meta-analysis

by Baliunas, D. O., Taylor, B. J., Irving, H., Roerecke, M., Patra, J., Mohapatra, S., Rehm, J.

OBJECTIVE 

To clarify the dose-response relationship between alcohol consumption and type 2 diabetes.

RESEARCH DESIGN AND METHODS 

A systematic computer-assisted and hand search was conducted to identify relevant articles with longitudinal design and quantitative measurement of alcohol consumption. Adjustment was made for the sick-quitter effect. We used fractional polynomials in a meta-regression to determine the dose-response relationships by sex and end point using lifetime abstainers as the reference group.

RESULTS 

The search revealed 20 cohort studies that met our inclusion criteria. A U-shaped relationship was found for both sexes. Compared with lifetime abstainers, the relative risk (RR) for type 2 diabetes among men was most protective when consuming 22 g/day alcohol (RR 0.87 [95% CI 0.76–1.00]) and became deleterious at just over 60 g/day alcohol (1.01 [0.71–1.44]). Among women, consumption of 24 g/day alcohol was most protective (0.60 [0.52–0.69]) and became deleterious at about 50 g/day alcohol (1.02 [0.83–1.26]).

CONCLUSIONS 

Our analysis confirms previous research findings that moderate alcohol consumption is protective for type 2 diabetes in men and women.

Sleep Duration, Lifestyle Intervention, and Incidence of Type 2 Diabetes in Impaired Glucose Tolerance: The Finnish Diabetes Prevention Study

Sleep Duration, Lifestyle Intervention, and Incidence of Type 2 Diabetes in Impaired Glucose Tolerance: The Finnish Diabetes Prevention Study

by Tuomilehto, H., Peltonen, M., Partinen, M., Lavigne, G., Eriksson, J. G., Herder, C., Aunola, S., Keinanen-Kiukaanniemi, S., Ilanne-Parikka, P., Uusitupa, M., Tuomilehto, J., Lindstrom, J., on behalf of the Finnish Diabetes Prevention Study Group

OBJECTIVE 

Both short and long sleep duration have frequently been found to be associated with an increased risk for diabetes. The aim of the present exploratory analysis was to examine the association between sleep duration and type 2 diabetes after lifestyle intervention in overweight individuals with impaired glucose tolerance in a 7-year prospective follow-up.

RESEARCH DESIGN AND METHODS 

A total of 522 individuals (aged 40–64 years) were randomly allocated either to an intensive diet-exercise counseling group or to a control group. Diabetes incidence during follow-up was calculated according to sleep duration at baseline. Sleep duration was obtained for a 24-h period. Physical activity, dietary intakes, body weight, and immune mediators (C-reactive protein and interleukin-6) were measured.

RESULTS 

Interaction between sleep duration and treatment group was statistically significant (P = 0.003). In the control group, the adjusted hazard ratios (HRs) (95% CI) for diabetes were 2.29 (1.38–3.80) and 2.74 (1.67–4.50) in the sleep duration groups 9–9.5 h and ?10 h, respectively, compared with for that of the 7–8.5 h group. In contrast, sleep duration did not influence the incidence of diabetes in the intervention group; for sleep duration groups 9–9.5 h and ?10 h, the adjusted HRs (95% CI) were 1.10 (0.60–2.01) and 0.73 (0.34–1.56), respectively, compared with that in the reference group (7–8.5 h sleep). Lifestyle intervention resulted in similar improvement in body weight, insulin sensitivity, and immune mediator levels regardless of sleep duration.

CONCLUSIONS 

Long sleep duration is associated with increased type 2 diabetes risk. Lifestyle intervention with the aim of weight reduction, healthy diet, and increased physical activity may ameliorate some of this excess risk.

Eat less and exercise more - is it really enough to knock down the obesity pandemia?

Eat less and exercise more - is it really enough to knock down the obesity pandemia?

Hubácek JA.

Institute for Clinical and Experimental Medicine-CEM-LMG, Prague, Czech Republic. jahb@ikem.cz.

Reduced physical activity and abundant energy intake are two most common factors leading to uncontrolled body weight gain. But these factors are not under entire internal consciousness control; they are also partially genetically determined and are affected by for example food marketing practices. In addition to these two widely accepted factors, there are some other factors, whose could also contribute to the recent increase of obesity prevalence. For example, non-exercise activity thermogenesis, sleeping habits, more stable inside room temperatures (using of heating and air conditioning), high prescription of medications with weight gain as side effect, psychosocial factors, unfavourable socioeconomic status and unpleasant urban environment are the background factors which should not be omitted if obesity/BMI determination should be fully understood and kept under control. In conclusion, unhealthy life style is necessary, but not sufficient for obesity development.

Viral obesity: fact or fiction?

Viral obesity: fact or fiction?

Mitra AK, Clarke K.

Department of Community Health Sciences, The University of Southern Mississippi, Hattiesburg, MS, USA.

Summary The aetiology of obesity is multifactorial. An understanding of the contributions of various causal factors is essential for the proper management of obesity. Although it is primarily thought of as a condition brought on by lifestyle choices, recent evidence shows there is a link between obesity and viral infections. Numerous animal models have documented an increased body weight and a number of physiologic changes, including increased insulin sensitivity, increased glucose uptake and decreased leptin secretion that contribute to an increase in body fat in adenovirus-36 infection. Other viral agents associated with increasing obesity in animals included canine distemper virus, rous-associated virus 7, scrapie, Borna disease virus, SMAM-1 and other adenoviruses. This review attempted to determine if viral infection is a possible cause of obesity. Also, this paper discussed mechanisms by which viruses might produce obesity. Based on the evidence presented in this paper, it can be concluded that a link between obesity and viral infections cannot be ruled out. Further epidemiologic studies are needed to establish a causal link between the two, and determine if these results can be used in future management and prevention of obesity.

Eating Slowly Increases the Postprandial Response of the Anorexigenic Gut Hormones, Peptide YY and Glucagon-Like Peptide-1.

Eating Slowly Increases the Postprandial Response of the Anorexigenic Gut Hormones, Peptide YY and Glucagon-Like Peptide-1.

Kokkinos A, le Roux CW, Alexiadou K, Tentolouris N, Vincent RP, Kyriaki D, Perrea D, Ghatei MA, Bloom SR, Katsilambros N.

First Department of Propaedeutic Medicine (A.K., K.A., N.T., D.K., D.P., N.K.), Athens University Medical School, Laiko General Hospital, 11527 Athens, Greece; and Department of Metabolic Medicine (C.W.l.R., R.P.V., M.A.G., S.R.B.), Hammersmith Hospital, Imperial College, London W12 ONN, United Kingdom.

Context: The rate at which people eat has been suggested to be positively associated with obesity, although appetite and related gut hormones have not been measured. Objective: The objective of the study was to determine whether eating the same meal at varying speeds elicits different postprandial gut peptide responses. Design and Setting: This was a crossover study at a clinical research facility. Study Participants: Seventeen healthy adult male volunteers participated in the study. Intervention: A test meal consisting of 300 ml ice cream (675 kcal) was consumed in random order on two different sessions by each subject: meal duration took either 5 or 30 min. Main Outcome Measures: The postprandial response of the orexigenic hormone ghrelin and the anorexigenic peptides peptide YY and glucagon-like peptide-1 over 210 min was assessed. Visual analog scales for the subjective feelings of hunger and fullness were completed throughout each session. Results: Peptide YY area under the curve (AUC) was higher after the 30-min meal than after the 5-min meal (mean +/- SEM AUC 5 min meal: 4133 +/- 324, AUC 30 min meal: 5250 +/- 330 pmol/liter . min, P = 0.004), as was glucagon-like peptide-1 AUC (mean +/- SEM AUC 5 min meal: 6219 +/- 256, AUC 30 min meal: 8794 +/- 656 pmol/liter . min, P = 0.001). There was a trend for higher visual analog scale fullness ratings immediately after the end of the 30-min meal compared with immediately after the 5-min meal. There were no differences in ghrelin response. Conclusions: Eating at a physiologically moderate pace leads to a more pronounced anorexigenic gut peptide response than eating very fast.

The energy expenditure of using a "walk-and-work" desk for office workers with obesity.

The energy expenditure of using a "walk-and-work" desk for office workers with obesity.

Levine JA, Miller JM.

Endocrine Research Unit, Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA. levine.james@mayo.edu

OBJECTIVE: For many people, most of the working day is spent sitting in front of a computer screen. Approaches for obesity treatment and prevention are being sought to increase workplace physical activity because low levels of physical activity are associated with obesity. Our hypothesis was that a vertical workstation that allows an obese individual to work while walking would be associated with significant and substantial increases in energy expenditure over seated work. METHODS: The vertical workstation is a workstation that allows an office worker to use a standard personal computer while walking on a treadmill at a self-selected velocity. 15 sedentary individuals with obesity (14 women, one man; 43 (7.5) years, 86 (9.6) kg; body mass index 32 (2.6) kg/m(2)) underwent measurements of energy expenditure at rest, seated working in an office chair, standing and while walking at a self-selected speed using the vertical workstation. Body composition was measured using dual x ray absorptiometry. RESULTS: The mean (SD) energy expenditure while seated at work in an office chair was 72 (10) kcal/h, whereas the energy expenditure while walking and working at a self-selected velocity of 1.1 (0.4) mph was 191 (29) kcal/h. The mean (SD) increase in energy expenditure for walking-and-working over sitting was 119 (25) kcal/h. CONCLUSIONS: If sitting computer-time were replaced by walking-and-working, energy expenditure could increase by 100 kcal/h. Thus, if obese individuals were to replace time spent sitting at the computer with walking computer time by 2-3 h/day, and if other components of energy balance were constant, a weight loss of 20-30 kg/year could occur.