Maternal obesity (MO) impairs maternal and offspring health. Mechanisms and interventions to prevent adverse maternal and offspring outcomes need to be determined. Human studies are confounded by socio-economic status providing the rationale for controlled animal data on effects of maternal exercise (MEx) intervention on maternal (F0) and offspring (F1) outcomes in MO.
MO produces metabolic and endocrine dysfunction, increases maternal and offspring glucocorticoid exposure, oxidative stress and adverse offspring outcomes by postnatal day (PND) 36. MEx prevents these outcomes.
F0 female rats ate either control or obesogenic diet from weaning through lactation. Half of each group wheel ran (from day ninety of life through pregnancy beginning day 120) providing four groups (n=8/group) – i) controls, ii) obese, iii) exercised controls and iv) exercised obese. After weaning, PND 21, F1 offspring ate a control diet. Metabolic parameters of F0 prepregnancy and end of lactation and F1 offspring at PND 36 were analyzed.
Exercise did not change maternal weight. Before breeding, MO elevated F0 glucose, insulin, triglycerides, cholesterol, leptin, fat and oxidative stress. Exercise completely prevented the triglyceride rise and partially glucose, insulin, cholesterol and oxidative stress increases. MO decreased fertility, recovered by exercise. At the end of lactation, exercise returned all metabolic variables except leptin to control levels. Exercise partially prevented MO elevated corticosterone. F1 Offspring weights were similar at birth. At PND 36 MO increased F1 male but not female offspring leptin, triglycerides and fat mass. In controls exercise reduced male and female offspring glucose, prevented the offspring leptin increase and partially the triglyceride rise.
MEx before and during pregnancy has beneficial effects on maternal and offspring metabolism and endocrine function occurring with no weight change in mothers and offspring indicating the importance of body composition rather than weight in evaluations of metabolic status.
Maternal obesity; exercise; programming
3T3-L1 cells have been widely used as a model for adipogenesis.
However, despite its popularity, differentiation of this cell line has been
reported to be inconsistent with low efficiency.
To investigate the effect of media height during adipocyte
differentiation on lipid accumulation and adipokine secretion in mature
Three cell lines (3T3-L1, OP9, and ChubS7) were used to test the
influence of media volume on adipogenesis. Total lipid content and lipid
droplet size and number were quantified. Adipocyte related gene expressions
were quantified during the course of differentiation. Secretion of leptin
and adiponectin from mature adipocytes were measured using Enzyme-Linked
Immunosorbent Assays. The influence of oxygen partial pressure on
adipogenesis was investigated using three oxygen percentages: 5%,
21%, and 30%. Insulin sensitivity was measured by insulin
inhibition of isoproterenol-induced lipolysis and phosphorylation of Insulin
Receptor Substrate-1 (IRS-1).
A lower media height during adipogenesis increased total lipid
accumulation, NEFA release and leptin and adiponectin secretion in mature
adipocytes. Insulin sensitivity was not affected by media height during
Media height during adipogenesis was inversely correlated with lipid
content in mature adipocytes. To achieve a high lipid content and greater
adipokine secretion, it is best to use a low media volume during
3T3-L1; OP9; adipogenesis; lipid; hypoxia; media volume
Epidemiological evidence shows an inverse relationship between sleep duration and overweight/obesity risk. However, there are few polysomnographic studies that relate the organization of sleep stages to pediatric overweight (OW). We compared sleep organization in otherwise healthy OW and normal weight (NW) 10-year-old children.
Polysomnographic assessments were performed in 37 NW and 59 OW children drawn from a longitudinal study beginning in infancy. Weight and height were used to evaluate body-mass index (BMI) according to international criteria. Non-REM (NREM) sleep (stages N1, N2 and N3), rapid eye movement (REM) sleep (stage R), and wakefulness (stage W) were visually scored. Sleep parameters were compared in NW and OW groups for the whole total sleep period (SPT) and for each successive third of it using independent student t-tests or non-parametric tests. The relationship between BMI and sleep variables was evaluated by correlation analyses controlling for relevant covariates.
The groups were similar in timing of sleep onset and offset, and sleep period time. BMI was inversely related to total sleep time (TST) and sleep efficiency. OW children showed reduced TST, sleep efficiency, and stage R amount, but higher stage W amount. In analysis by thirds of the SPT, the duration of stage N3 episodes, was shorter in the first third and longer in the second third in OW children, compared with NW children.
Our results show reduced sleep amount and quality in otherwise healthy OW children. The lower stage R amount and changes involving stage N3 throughout the night suggest that OW in childhood is associated with modifications not only in sleep duration, but also in the ongoing nighttime patterns of NREM sleep and REM sleep stages.
Overweight; Sleep duration; NREM sleep; REM sleep; Children
Previous studies have found greater adiposity and cardiovascular risk in first born children. The causality of this association is not clear. Examining the association in diverse populations may lead to improved insight.
We examine the association between birth order and body mass index (BMI), systolic and diastolic blood pressure (SBP/DBP) in the 2004 Pelotas cohort from southern Brazil and the Avon Longitudinal Study of Parents and Children (ALSPAC) from Bristol, south west England, restricting analysis to families with two children in order to remove confounding by family size.
No consistent differences in BMI, SBP or DBP were observed comparing first and second born children. Within the Pelotas 2004 cohort, first born females were thinner, with lower SBP and DBP; e.g. mean difference in SBP comparing first with second born was -0.979 (95% confidence interval -2.901 to 0.943). In ALSPAC, first born females had higher BMI, SBP and DBP. In both cohorts, associations tended to be in the opposite direction in males, although no statistical evidence for gender interactions was found.
The findings do not support an association between birth order and BMI or blood pressure. Differences to previous studies may be explained by differences in populations and/or confounding by family size in previous studies.
ALSPAC; birth order; blood pressure; body mass index; cardiovascular; obesity; Pelotas; siblings
Background & Objectives
Shorter sleep is associated with higher weight in children, but little is known about the mechanisms. The aim of this study was to test the hypothesis that shorter sleep was associated with higher energy intake in early childhood.
Participants were 1303 families from the Gemini twin birth cohort. Sleep duration was measured using the Brief Infant Sleep Questionnaire (BISQ) when the children were 16 months old. Total energy intake (kcal/day) and grams/day of fat, carbohydrate and protein were derived from 3-day diet diaries completed by parents when children were 21 months old.
Shorter nighttime sleep was associated with higher total energy intake (p for linear trend=0.005). Children sleeping <10 hours consumed around 50 kcals/day more than those sleeping 11-<12 hours a night (the optimal sleep duration for children of this age). Differences in energy intake were maintained after adjustment for confounders. As a percentage of total energy intake, there were no significant differences in macronutrient intake by sleep duration. The association between sleep and weight was not significant at this age (p=0.13).
This study provides the first evidence that shorter nighttime sleep duration has a linear association with higher energy intake early in life. That the effect is observed before emergence of associations between sleep and weight indicates that differences in energy intake may be a mechanism through which sleep influences weight gain.
sleep; diet; obesity; child
We investigate whether differences in sleep duration help explain ethnic disparities in body mass index (BMI) among U.S. adolescents. We also evaluate the functional form of the association between sleep duration and BMI, and investigate whether this association varies by sex and ethnicity.
Participants and Methods
We analyzed restricted-use data from the first 2 waves of the National Longitudinal Study of Adolescent Health (n=30 133) to evaluate linear and quadratic associations between sleep duration and BMI. Through a series of models that incorporated interaction terms between sex, ethnicity and sleep duration, we also assessed whether (1) sleep duration mediates associations between ethnicity and BMI, and (2) associations between sleep duration and BMI differ for girls and boys from different ethnic groups.
A linear association between sleep duration and BMI best fits the data in this large sample of U.S. adolescents. We find no evidence that sleep duration contributes substantially to ethnic disparities in BMI. However, we detect significant differences in the association between sleep duration and BMI by sex and ethnicity. Sleep duration is negatively associated with BMI among white, Hispanic and Asian boys, positively associated with BMI among black girls, and not related to BMI among black boys or girls from white, Hispanic or Asian ethnic groups.
Despite significant associations between sleep duration and BMI for certain groups of adolescents, we find no evidence that ethnic differences in sleep duration exacerbate ethnic disparities in BMI. Future research should explore mechanisms that underlie ethnic differences in the association between sleep and BMI.
Adolescent Health; Body Mass Index-BMI; Ethnicity; Health Disparities; Sleep
To examine nine-year trends and relationships regarding misperceptions of body size and dieting for weight loss among adolescents from 24 countries, and explore the influence of country-level overweight prevalence.
Socio-demographic characteristics, body size perception, and dieting for weight loss were assessed in the Health Behaviour in School-aged Children survey conducted in 24 countries cross-sectionally at three time points (2001/02, 2005/06, 2009/10). Logistic regression models examined change over time in overestimation of body size in non-overweight adolescents, underestimation of body size in overweight adolescents, dieting for weight loss in non-overweight and overweight adolescents, and relationships between body size perception and dieting. Analyses were stratified by weight status and sex. Covariates included country-level overweight prevalence, family affluence, and country level of development. Body mass index was only included in models examining dieting for weight loss.
Country-level overweight prevalence increased over time (11.6% to 14.7%). Compared to Time 1, overweight adolescents had greater odds of body size underestimation at Time 3 (OR=1.68 for girls, OR=1.10 for boys), while non-overweight adolescents had lower odds of body size overestimation at Time 3 (OR=0.87 for girls, OR=0.89 for boys). Controlling for country-level overweight prevalence attenuated these relationships. Compared to Time 1, overweight and non-overweight boys were 10% more likely to diet at Time 3, while overweight and non-overweight girls were 19% and 16%, respectively, less likely to diet at Time 3. Controlling for country-level overweight prevalence did not impact trends in dieting for weight loss. Additionally, the association of self-perceived overweight with increased odds of dieting diminished over time.
Body size perceptions among adolescents may have changed over time concurrent with shifts in country-level body weight. However, controlling for country-level overweight prevalence did not impact trends in dieting for weight loss, suggesting a potentially stronger impact of social comparison on weight-related perceptions than on behavior.
Adolescents; body image; dieting; weight perceptions; overweight; development
Obesity and Major Depressive Disorder (MDD) are associated, but evidence about how they relate over time is conflicting. The goal of this study was to examine prospective associations between depression and obesity from early adolescence through early adulthood.
Participants were drawn from a statewide, community-based, Minnesota sample. MDD and obesity with onsets by early adolescence (by age 14), late adolescence (between 14 and 20), and early adulthood (ages 20 to 24) were assessed via structured interview (depression) and study-measured height and weight.
Cross-sectional results indicated that depression and obesity with onsets by early adolescence were concurrently associated, but the same was not true later in development. Prospective results indicated that depression by early adolescence predicted the onset of obesity (odds ratio=3.76, confidence interval= 1.33–10.59) during late adolescence among females. Obesity that developed during late adolescence predicted the onset of depression (odds ratio=5.89, confidence interval= 2.31–15.01) during early adulthood among females.
For girls, adolescence is a high risk period for the development of this comorbidity, with the nature of the risk varying over the course of adolescence. Early adolescent-onset depression is associated with elevated risk of later onset obesity, and obesity, particularly in late adolescence, is associated with increased odds of later depression. Further investigation into the mechanisms of these effects and the reasons for the observed gender and developmental differences is needed. Prevention programs focused on early-onset cases of depression and adolescent-onset cases of obesity, particularly among females, may help in reducing risk for this form of comorbidity.
obesity; depression; comorbidity; prospective; adolescence
Basal Metabolic Rate (BMR) represents the largest component of total energy
expenditure and is a major contributor to energy balance. Therefore, accurately estimating
BMR is critical for developing rigorous obesity prevention and control strategies. Over
the past several decades, numerous BMR formulas have been developed targeted to different
population groups. A comprehensive literature search revealed 248 BMR estimation equations
developed using diverse ranges of age, gender, race, fat free mass, fat mass, height,
waist-to-hip ratio, body mass index, and weight. A subset of 47 studies included enough
detail to allow for development of meta-regression equations. Utilizing these studies,
meta-equations were developed targeted to twenty specific population groups. This review
provides a comprehensive summary of available BMR equations and an estimate of their
accuracy. An accompanying online BMR prediction tool (available at http://www.sdl.ise.vt.edu/tutorials.html) was developed to automatically
estimate BMR based on the most appropriate equation after user-entry of individual age,
race, gender, and weight.
Basal Metabolic Rate; Resting Metabolic rate; Prediction; Meta-Analysis; Review; Meta-Regression
The Wnt/β-catenin signalling network offers potential targets to diagnose and uncouple obesity from its metabolic complications. Here we investigate the role of the Wnt antagonist, secreted Frizzled related protein 1 (SFRP1) in promoting adipogenesis in vitro and adipose tissue expansion in vivo.
We use a combination of human and murine, in vivo and in vitro models of adipogenesis, adipose tissue expansion and obesity-related metabolic syndrome to profile the involvement of SFRP1.
Secreted Frizzled related protein 1 (SFRP1) is expressed in both murine and human mature adipocytes. The expression of SFRP1 is induced during in vitro adipogenesis and SFRP1 is preferentially expressed in mature adipocytes in human adipose tissue. Constitutive ectopic expression of SFRP1 is proadipogenic and inhibits the Wnt/β-catenin signalling pathway. In vivo endogenous levels of adipose SFRP1 are regulated in line with proadipogenic states. However, in longitudinal studies of high fat diet-fed mice we observed a dynamic temporal but biphasic regulation of endogenous SFRP1. In agreement with this profile we observed that SFRP1 expression in human tissues peaks in patients with mild obesity and gradually falls in morbidly obese subjects.
Our results suggest that SFRP1 is an endogenous modulator of Wnt/β-catenin signalling and participates in the paracrine regulation of human adipogenesis. The reduced adipose expression of SFRP1 in morbid obesity and its knock-on effect to prevent further adipose tissue expansion may contribute to the development of metabolic complications in these individuals.
Obesity; Metabolic syndrome; Adipose tissue; Adipogenesis; Wnt Signalling
Breakfast skipping (BS) is closely associated with overeating (in the evening), weight gain and obesity. It is unclear whether the addition of breakfast, with emphasis on dietary protein, leads to better appetite and energy intake regulation in adolescents.
The purpose of the study was to examine the impact of addition of a normal-protein (PN) breakfast vs protein-rich (PR) breakfast on appetite and food intake in ‘breakfast-skipping’ adolescents.
Subjects and Design
A total of 13 adolescents (age 14.3 ± 0.3 years; body mass index percentile 79 ± 4 percentile; skipped breakfast 5 ± 1× per week) randomly completed 3 testing days that included a PN (18 ± 1 g protein), PR (48 ± 2 g protein) or BS. Breakfast was 24% of estimated daily energy needs. Appetite, satiety and hormonal responses were collected over 5 h followed by an ad libitum lunch and 24-h food intake assessments.
Perceived appetite was not different following PN vs BS; PR led to greater reductions vs BS (P<0.01) and PN (P< 0.001). Fullness was greater following both breakfast meals vs BS (P<0.01) but was not different between meals. Ghrelin was not different among treatments. Greater PYY concentrations were observed following both breakfast meals vs BS (P<0.01) but was not different between meals. Lunch energy intake was not different following PN vs BS; PR led to fewer kcal consumed vs BS (P<0.01) and PN (P<0.005). Daily food intake was not different among treatments.
Breakfast led to increased satiety through increased fullness and PYY concentrations in ‘breakfast skipping’ adolescents. A breakfast rich in dietary protein provides additional benefits through reductions in appetite and energy intake. These findings suggest that the addition of a protein-rich breakfast might be an effective strategy to improve appetite control in young people.
breakfast skipping; appetite; ghrelin; PYY; increased dietary protein
Several epidemiologic, longitudinal studies have reported that short sleep duration is a risk factor for the incidence of obesity. However, the vast majority of these studies used self-reported measures of sleep duration and did not examine the role of objective short sleep duration, subjective sleep disturbances, and emotional stress.
Longitudinal, population-based study.
We studied a random sample of 815 non-obese adults from the Penn State Cohort in the sleep laboratory for one night using polysomnography (PSG) and followed them up for a mean of 7.5 years. Subjective and objective measures of sleep as well as emotional stress were obtained at baseline. Obesity was defined as a body mass index (BMI) ≥ 30kg/m2.
The incidence of obesity was 15% and it was significantly higher in women and in individuals who reported sleep disturbances, shorter sleep duration, and higher emotional stress. Significant mediating effects showed that individuals with subjective sleep disturbances who developed obesity reported the shortest sleep duration and the highest emotional stress and that subjective sleep disturbances and emotional stress were independent predictors of incident obesity. Further analyses revealed that the association between short sleep duration, subjective sleep disturbances, and emotional stress with incident obesity was stronger in young and middle-age adults. Objective short sleep duration was not associated with a significantly increased risk of incident obesity.
Self-reported short sleep duration in non-obese individuals at risk of developing obesity is a surrogate marker of emotional stress and subjective sleep disturbances. Objective short sleep duration is not associated with a significant increased risk of incident obesity. The detection and treatment of sleep disturbances and emotional stress should become a target of our preventive strategies against obesity.
Incidence; Obesity; Polysomnography; Poor sleep; Sleep duration; Stress
We examined whether deficiency of Shp2 signaling in forebrain neurons alters metabolic and cardiovascular regulation under various conditions and if it attenuates the anorexic and cardiovascular effects of leptin. We also tested whether forebrain Shp2 deficiency alters blood pressure (BP) and heart rate (HR) responses to acute stress.
Forebrain Shp2-/- mice were generated by crossing Shp2flox/flox mice with CamKIIα-cre mice. At 22 to 24 weeks of age, mice were instrumented for telemetry for measurement of BP, HR and body temperature (BT). Oxygen consumption (VO2), energy expenditure and motor activity were monitored by indirect calorimetry.
Shp2/CamKIIα-cre mice were heavier (46±3 vs 32±1 g), hyperglycemic, hyperleptinemic, hyperinsulinemic, and hyperphagic compared to Shp2flox/flox control mice. Shp2/CamKIIα-cre mice exhibited reduced food intake responses to fasting/refeeding and impaired regulation of BT when exposed to 15°C and 30°C ambient temperatures. Despite being obese and having many features of metabolic syndrome, Shp2/CamKIIα-cre mice had similar daily average BP and HR compared to Shp2flox/flox mice (112±2 vs 113±1 mmHg and 595±34 vs 650±40 bpm), but exhibited increased BP and HR responses to cold exposure and acute air-jet stress test. Leptin's ability to reduce food intake and to raise BP were markedly attenuated in Shp2/CamKIIα-cre mice.
These results suggest that forebrain Shp2 signaling regulates food intake, appetite responses to caloric deprivation, and thermogenic control of body temperature during variations in ambient temperature. Deficiency of Shp2 signaling in the forebrain is associated with augmented cardiovascular responses to cold and acute stress but attenuated BP responses to leptin.
Energy expenditure; food intake; blood pressure; heart rate; acute stress; thermoneutrality
To evaluate the geographic concentration of adult obesity prevalence by census tract (CT) in King County, WA, in relation to social and economic factors.
Methods and Design
Measured heights and weights from 59 767 adult men and women enrolled in the Group Health (GH) health care system were used to estimate obesity prevalence at the CT level. CT-level measures of socioeconomic status (SES) were median home values of owner-occupied housing units, percent of residents with a college degree, and median household incomes, all drawn from the 2000 Census. Spatial regression models were used to assess the relation between CT-level obesity prevalence and socio-economic variables.
Smoothed CT obesity prevalence, obtained using an Empirical Bayes tool, ranged from 16.2% to 43.7% (a 2.7-fold difference). The spatial pattern of obesity was non-random, showing a concentration in south and southeast King County. In spatial regression models, CT-level home values and college education were more strongly associated with obesity than household incomes. For each additional $100 000 in median home values, CT obesity prevalence was 2.3% lower. The three SES factors together explained 70% of the variance in CT obesity prevalence after accounting for population density, race/ethnicity, age and spatial dependence.
To our knowledge, this is the first report to show major social disparities in adult obesity prevalence at the CT scale that is based, moreover, on measured heights and weights. Analyses of data at sufficiently fine geographic scale are needed to guide targeted local interventions to stem the obesity epidemic.
obesity; health status disparities; geography; socioeconomic factors; cross-sectional studies
Despite theoretical evidence that the model commonly referred to as the 3500 kcal rule grossly overestimates actual weight loss, widespread application of the 3500 kcal formula continues to appear in textbooks, on respected government and health related websites, and scientific research publications. Here we demonstrate the risk of applying the 3500 kcal rule even as a convenient estimate by comparing predicted against actual weight loss in seven weight loss experiments conducted in confinement under total supervision or objectively measured energy intake. We offer three newly developed, downloadable applications housed in Microsoft® Excel and Java which simulates a rigorously validated, dynamic model of weight change. The first two tools available at www.pbrc.edu/sswcp, provide a convenient alternative method for providing patients with projected weight loss/gain estimates in response to changes in dietary intake. The second tool which can be downloaded from the URL, www.pbrc.edu/mswcp, projects estimated weight loss simultaneously for multiple subjects. This tool was developed to inform weight change experimental design and analysis. While complex dynamic models may not be directly tractable, the newly developed tools offer the opportunity to deliver dynamic model predictions as a convenient and significantly more accurate alternative to the 3500 kcal rule.
3500 kcal Rule; Wishnofsky’s Rule; Dynamic Model; Energy Balance; First Law of Thermodynamics
Obesity is a risk factor for congenital heart defects (CHD), but whether risk is independent of abnormal glucose metabolism is unknown. Data on whether overweight status increases risk is also conflicting.
Research Design and Methods
We included 121815 deliveries from a cohort study, the Consortium on Safe Labor, after excluding women with pregestational diabetes as recorded in the electronic medical record. CHD were identified via medical record discharge summaries. Adjusted odds ratios (OR) for any CHD were calculated for prepregnancy body mass index (BMI) categories of overweight (25 to <30 kg/m2), obese (30 to <40 kg/m2), and morbidly obese (≥40 kg/m2) compared to normal weight (18.5 to <25 kg/m2) women, and for specific CHD with obese groups combined (≥30 kg/m2). A sub-analysis adjusting for oral glucose tolerance test (OGTT) results where available was performed as a proxy for potential abnormal glucose metabolism present at the time of organogenesis.
There were 1388 (1%) infants with CHD. Overweight (OR=1.15 95% CI: 1.01–1.32), obese (OR=1.26 95% CI: 1.09, 1.44), and morbidly obese (OR=1.34 95% CI: 1.02–1.76) women had greater odds of having a neonate with CHD than normal weight women (P< 0.001 for trend). Obese women (BMI ≥30 kg/m2) had higher odds of having an infant with conotruncal defects (OR=1.34 95%CI: 1.04–1.72), atrial septal defects (OR =1.22 95% CI: 1.04–1.43), and ventricular septal defects (OR=1.38 95% CI: 1.06–1.79). Being obese remained a significant predictor of CHD risk after adjusting for OGTT.
Increasing maternal weight class was associated with increased risk for CHD. In obese women, abnormal glucose metabolism did not completely explain the increased risk for CHD; the possibility that other obesity-related factors are teratogenic requires further investigation.
Prepregnancy BMI; Obesity; Congenital Heart Defects
Although overweight and obesity are less prevalent among active-duty military personnel compared with similar persons not serving in the military, no such differences have been observed between veterans and nonveterans.
To assess the magnitude of weight changes before, concurrent with, and following discharge from the military, relative to weight during service, and to determine the demographic, service-related, and psychological characteristics associated with clinically-important weight gain among those who were discharged from military service during follow-up.
Eligible Millennium Cohort Study participants (n=38,686) completed questionnaires approximately every three years (2001, 2004, and 2007) that were used to estimate annual weight changes, as well as the percentage experiencing clinically-important weight gain, defined as ≥10%. Analyses were stratified by sex.
Weight gain was greatest around the time of discharge from service and in the 3 years prior to discharge (1.0–1.3 kg/year), while it was nearly half as much during service (0.6–0.7 kg/year) and three or more years after service ended (0.7 kg/year). Consequently, 6-year weight gain was over 2 kg greater in those who were discharged compared to those who remained in the military during follow-up (5.7 vs. 3.5 kg in men; 6.3 vs. 4.0 kg in women). In those who were discharged, younger age, less education, being overweight at baseline, being in the active duty component (vs. Reserve/National Guard), and having experienced deployment with combat exposures (vs. non-deployment) were associated with increased risks of clinically-important weight gain.
This study provides the first prospectively-collected evidence for an increased rate of weight gain around the time of military discharge that may explain previously reported higher rates of obesity in veterans, and identifies characteristics of higher risk groups. Discharge from military service presents a window of risk and opportunity to prevent unhealthy weight gain in military personnel and veterans.
Military veterans; weight gain; prospective; cohort; posttraumatic stress disorder; obesity; military deployment
The Delboeuf Illusion affects perceptions of the relative sizes of concentric shapes. This study was designed to extend research on the application of the Delboeuf illusion to food on a plate by testing whether a plate’s rim width and coloring influence perceptual bias to affect perceived food portion size.
DESIGN AND METHODS
Within-subjects experimental design. Experiment 1 tested the effect of rim width on perceived food portion size. Experiment 2 tested the effect of rim coloring on perceived food portion size. In both experiments, participants observed a series of photographic images of paired, side-by-side plates varying in designs and amounts of food. From each pair, participants were asked to select the plate that contained more food. Multi-level logistic regression examined the effects of rim width and coloring on perceived food portion size.
Experiment 1: Participants overestimated the diameter of food portions by 5% and the visual area of food portions by 10% on plates with wider rims compared to plates with very thin rims (P<0.0001). The effect of rim width was greater with larger food portion sizes. Experiment 2: Participants overestimated the diameter of food portions by 1.5% and the visual area of food portions by 3% on plates with rim coloring compared to plates with no coloring (P=0.01). The effect of rim coloring was greater with smaller food portion sizes.
The Delboeuf illusion applies to food on a plate. Participants overestimated food portion size on plates with wider and colored rims. These findings may help design plates to influence perceptions of food portion sizes.
portion size; visual illusions; mindless eating; perceptual bias; dishware; plate
While several studies have found an association between excessive gestational weight gain and obesity later in life, to the best of our knowledge, no studies have explored the role of gestational weight gain events across the life course.
Design and Methods
We describe how the prevalence of mid-life obesity (BMI≥30 at age 40 or 41) among women varies by life course patterns of gestational weight gain (using 2009 IOM guidelines) in the USA’s National Longitudinal Survey of Youth 1979 cohort.
Among women who reported 1–3 births before age 40, the prevalence of mid-life obesity increased with a rising number of excessive gestational weight gain events: from none (23.4%, n=875), to one (37.6%, n=707), to two (46.8%, n=427), and to three (54.6%, n=108), p<0.00005 for trend. Obesity prevalence was similar for the same number of excessive gestational weight gain events, regardless of parity. No clear pattern emerged for the sequencing of excessive gestational weight gain event(s) and later obesity.
In our descriptive exploratory study, excessive gestational weight gain events appear to be associated with increased prevalence of obesity for parous women, suggesting the importance of preventive interventions regardless of timing of pregnancy-related weight changes over the life course.
gestational weight gain; life course; obesity; pregnancy; women
Obesity, which is frequently associated with diabetes, hypertension, and cardiovascular diseases, is primarily the result of a net excess of caloric intake over energy expenditure. Human obesity is highly heritable, but the specific genes mediating susceptibility in non-syndromic obesity remain unclear. We tested candidate genes in pathways related to food intake and energy expenditure for association with body mass index (BMI).
We re-analyzed 355 common genetic variants of 30 candidate genes in 7 molecular pathways related to obesity in 1,982 unrelated European Americans from the New York Health Project. Data were analyzed by using a Bayesian hierarchical generalized linear model. The BMIs were log-transformed and then adjusted for covariates including age, age2, gender, and diabetes status. The single nucleotide polymorphisms (SNPs) were modeled as additive effects.
With the stipulated adjustments, nine SNPs in eight genes were significantly associated with BMI: GHRL (rs35683), AGRP (rs5030980), CPE (rs1946816 and rs4481204), GLP1R (rs2268641), HTR2A (rs912127), NPY5R (Y5R1c52), SOCS3 (rs4969170), and STAT3 (rs4796793). We also found a gender-by-SNP interaction (rs1745837 in HTR2A), which indicated that variants in the gene HTR2A had a stronger association with BMI in males. In addition, NPY1R was detected as having a significant gene effect even though none of the SNPs in this gene was significant.
Variations in genes AGRP, CPE, GHRL, GLP1R, HTR2A, NPY1R, NPY5R, SOCS3, and STAT3 showed modest associations with BMI in European Americans. The pathways in which these genes participate regulate energy intake and thus these associations are mechanistically plausible in this context.
Obesity; genetic association; single nucleotide polymorphism (SNP); Bayesian hierarchical generalized linear model (BhGLM)
To determine whether the mRNA concentrations of inflammation response genes in isolated adipocytes and in cultured preadipocytes are related to adipocyte size and in vivo insulin action in obese individuals.
Cross-sectional inpatient study.
Obese Pima Indians with normal glucose tolerance.
Adipocyte diameter (by microscope technique; n=29), expression of candidate genes (by quantitative real-time PCR) in freshly isolated adipocytes (monocyte chemoattractant protein [MCP] 1 and MCP2, macrophage inflammatory protein [MIP] 1α, MIP1β and MIP2, macrophage migration inhibitory factor [MIF], tumor necrosis factor alpha, interleukin [IL] 6 and IL8; n=22) and cultured preadipocytes (MCP1, MIP1α, MIF, IL6 and matrix metalloproteinase 2; n=33) from subcutaneous abdominal adipose tissue (by aspiration biopsy, n=34), body fat by dual-energy X-ray absorptiometry, glucose tolerance by 75-gram oral glucose tolerance test, and insulin action by euglycemic-hyperinsulinemic clamp (insulin infusion rate 40 mU/m2.min)(all n=34).
MIF was the only gene whose expression in both freshly isolated adipocytes and cultured preadipocytes was positively associated with adipocytes diameter and negatively associated with peripheral and hepatic insulin action (all P<0.05). In multivariate analysis, the association between adipocyte MIF mRNA concentrations and adipocytes diameter was independent of percent body fat (P=0.03), whereas adipocyte MIF mRNA concentrations but not adipocytes diameter independently predicted peripheral insulin action. The mRNA expression concentrations of MIF gene in adipocytes were not associated with plasma concentrations of MIF, but were negatively associated with plasma adiponectin concentrations (P=0.004). In multivariate analysis, adipocyte MIF RNA concentrations (P=0.03) but not plasma adiponectin concentrations (P=0.4) remained a significant predictor of insulin action.
Increased expression of MIF gene in adipose cells may be an important link between obesity characterized by enlarged adipocytes and insulin resistance in normal glucose tolerant people.
adipocytes; preadipocytes; MIF; insulin action; inflammation; adiponectin
Evidence is mixed regarding sugar-sweetened beverage (SSB) intake and adiposity among adults, perhaps due to reporting bias.
To determine the impact of reporting bias on any associations between increased SSB intake and overweight/obesity.
Beverage intake and overweight/obese status (BMI ≥25 kg/m2) was examined among adults from a dietary assessment and doubly labeled water study (n=250). Four web-based, 24-hour recalls assessed dietary intake. SSB intake was categorized as no intake, 1–99 kcals per day, and >99 kcals per day. Logistic regression models adjusted for total caloric intake, age, race, education and diet quality compared SSB intake to overweight/obese status. To investigate dietary self-reporting bias, analyses were replicated in a subset of “true reporters”: those with self-reported total caloric intake within 25% of total energy expenditure per doubly labeled water assessments (n=108).
One-half of participants were overweight/obese; more overweight/obese participants consumed SSB than normal weight participants (69% vs. 47%; p<0.001). Intake of other beverages did not differ by adiposity. Less White participants (48%) consumed SSB compared to African-American participants (68%; p=0.002). Compared to no intake, SSB intake up to the median intake doubled the risk of being overweight/obese (OR: 2.1, 95% CI: 1.0–4.3; p=0.046), and SSB intake over the median more than doubled the risk (OR: 2.6, 95% CI: 1.2–6.0; p=0.018). When limited to true reporters, SSB intake significantly increased the risk of being overweight/obese by nearly 4 fold.
Underreporting of SSB intake may be attenuating true associations of SSB intake and the risk of being overweight/obese.
Sugar-sweetened beverages; obesity; African-American; high-fructose corn syrup