scholarly journals Reward Region Responsivity Predicts Future Weight Gain and Further Evidence that the TaqIA Allele Moderates these Predictive Effects

2017 ◽  
Author(s):  
Kyle Stanley Burger
Keyword(s):  
Weight Gain ◽  
Body Fat ◽  
Neural Response ◽  
Monetary Reward ◽  
Healthy Weight ◽  
Vulnerability Factors ◽  
Allele Status ◽  
Increase Risk ◽  
Dopamine Signaling

As no large prospective study has evaluated neural vulnerability factors that predict future weight gain we tested whether neural response to receipt and anticipated receipt of palatable food and monetary reward predicted weight gain over 3-year follow-up in originally healthy-weight adolescents and whether relations were moderated by the TaqIA polymorphism, which affects dopamine signaling capacity. 153 adolescent humans completed functional magnetic resonance imaging (fMRI) paradigms assessing response to these four events; body fat was assessed yearly over follow-up. Split half analyses indicated that elevated orbitofrontal cortex response to cues signaling impending milkshake receipt predicted future body fat gain (r = .32), which is a novel finding that provides support for the incentive sensitization theory of obesity. Neural response to receipt and anticipated receipt of monetary reward did not predict body fat gain, which has not been tested previously. Replicating an interaction reported previously (Stice et al., 2008a), elevated caudate response to milkshake receipt predicted future body fat gain for youth with a genetic propensity for greater dopamine signaling by virtue of possessing the TaqIA A2/A2 allele, but lower caudate response predicted body fat gain for youth with a genetic propensity for less dopamine signaling by virtue of possessing a TaqIA A1 allele, though this interaction was only marginal (pFWE = .06). Parental obesity, which correlated with TaqIA allele status (OR = 2.7), similarly moderated the predictive effects of caudate response to milkshake receipt to body fat gain, which is also a novel finding. The former interaction implies that too much or too little dopamine signaling capacity and reward region responsivity may increase risk for overeating, suggesting the possibility of qualitatively distinct reward surfeit and reward deficit pathways to obesity.

scholarly journals Relation of FTO to BOLD response to receipt and anticipated receipt of food and monetary reward, food images, and weight gain in healthy weight adolescents

2019 ◽  
Vol 15 (10) ◽  
pp. 1135-1144 ◽  
Author(s):  
Eric Stice ◽  
Sonja Yokum ◽  
Pascale Voelker
Keyword(s):  
Weight Gain ◽  
Body Mass ◽  
Parietal Lobe ◽  
Monetary Reward ◽  
Healthy Weight ◽  
Palatable Food ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging ◽  
Food Images

Abstract Although the fat mass and obesity-associated gene (FTO) correlates with elevated body mass, it is unclear how it contributes to overeating. We tested if individuals with the A allele show greater reward region responsivity to receipt and anticipated receipt of food and money and palatable food images. We also tested if these individuals show greater future weight gain. Initially healthy weight adolescents (Study 1, N = 162; Study 2, N = 135) completed different functional magnetic resonance imaging paradigms and had their body mass measured annually over 3 years. Adolescents with the AA or AT genotypes showed less precuneus and superior parietal lobe response and greater cuneus and prefrontal cortex response to milkshake receipt and less putamen response to anticipated milkshake receipt than those with the TT genotype in separate analyses of each sample. Groups did not differ in response to palatable food images, and receipt and anticipated receipt of money, or in weight gain over 3-year follow-up. Results suggest that initially healthy weight adolescents with vs without the FTO A allele show differential responsivity to receipt and anticipated receipt of food but do not differ in neural response to palatable food images and monetary reward and do not show greater future weight gain.

Fitness Level and Risk of Weight Gain in Middle-Age Women: A Prospective Cohort Study

2010 ◽  
Vol 7 (3) ◽  
pp. 308-315 ◽  
Author(s):  
Larry Tucker ◽  
Travis Peterson
Keyword(s):  
Weight Gain ◽  
Energy Intake ◽  
Middle Age ◽  
Treadmill Test ◽  
Fitness Level ◽  
Food Records ◽  
Increase Risk ◽  
A Prospective Study ◽  
Risk Ratios

Background:This study was conducted to determine if cardiorespiratory fitness at baseline, and changes in fitness, influence risk of weight gain (≥3 kg) over 20 months. Another aim was to ascertain if potential confounding factors, including age, education, strength training, energy intake, and weight, influence risk of weight gain.Methods:In a prospective study of 257 women, fitness (VO2max) was assessed using a graded, maximal treadmill test at baseline and follow-up. Energy intake was measured using 7-day, weighed food records. Subjects were divided into quartiles based on fitness. Risk ratios were used to show the risk of weight gain among those who were fit at baseline compared with their counterparts.Results:Most women gained weight and 23% gained ≥3 kg. Mean VO2max was 35.7 ± 7.2 mL·kg−1·min−1. Women with low-fitness at baseline had 3.18 times (95% CI: 1.46 to 6.93) greater risk, and moderately fit women had 2.24 times (95% CI: 1.04 to 4.82) greater risk of weight gain than women in the high-fitness quartile. Adjusting for potential confounders had little effect on results.Conclusions:High levels of fitness seem to help protect middle-aged women against weight gain, whereas low and moderate fitness increase risk of weight gain over time.

scholarly journals Weight gain is associated with changes in neural response to palatable food tastes varying in sugar and fat and palatable food images: a repeated-measures fMRI study

2019 ◽  
Vol 110 (6) ◽  
pp. 1275-1286 ◽  
Author(s):  
Sonja Yokum ◽  
Eric Stice
Keyword(s):  
Weight Gain ◽  
Cingulate Cortex ◽  
Neural Response ◽  
Group Differences ◽  
Healthy Weight ◽  
Palatable Food ◽  
High Fat ◽  
Low Fat ◽  
High Sugar ◽  
Food Images

ABSTRACT Background Emerging data suggest that weight gain is associated with changes in neural response to palatable food tastes and palatable food cues, which may serve to maintain overeating. Objective We investigated whether weight gain is associated with neural changes in response to tastes of milkshakes varying in fat and sugar content and palatable food images. Methods We compared changes in neural activity between initially healthy-weight adolescents who gained weight (n = 36) and those showing weight stability (n = 31) over 2–3 y. Results Adolescents who gained weight compared with those who remained weight stable showed decreases in activation in the postcentral gyrus, prefrontal cortex, insula, and anterior cingulate cortex, and increases in activation in the parietal lobe, posterior cingulate cortex, and inferior frontal gyrus in response to a high-fat/low-sugar compared with low-fat/low-sugar milkshake. Weight gainers also showed greater decreases in activation in the anterior insula and lateral orbitofrontal cortex in response to a high-fat/high-sugar compared with low-fat/low-sugar milkshake than those who remained weight stable. No group differences emerged in response to a low-fat/high-sugar compared with a low-fat/low-sugar milkshake. Weight gainers compared with those who remained weight stable showed greater decreases in activation in the middle temporal gyrus and increases in cuneus activation in response to appetizing compared with unappetizing food pictures. The significant interactions were partially driven by group differences in baseline responsivity and by opposite changes in neural activation in adolescents who remained weight stable. Conclusions Data suggest that weight gain is associated with a decrease in responsivity of regions associated with taste and reward processing to palatable high-fat- and high-fat/high-sugar food tastes. Data also suggest that avoiding weight gain increases taste sensitivity, which may prevent future excessive weight gain. This trial was registered at clinicaltrials.gov as NCT01949636.

scholarly journals Neural vulnerability factors that increase risk for future weight gain.

2016 ◽  
Vol 142 (5) ◽  
pp. 447-471 ◽  
Author(s):  
Eric Stice ◽  
Sonja Yokum
Keyword(s):  
Weight Gain ◽  
Vulnerability Factors ◽  
Increase Risk

scholarly journals Anticholinergic Medication Use, Dopaminergic Genotype, and Recurrent Falls

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 756-756
Author(s):  
Andrea Rosso ◽  
Xiaonan Zhu ◽  
Zachary Marcum ◽  
Nico Bohnen ◽  
Briana Sprague ◽  
...  
Keyword(s):  
Generalized Estimating Equations ◽  
Fall Risk ◽  
Medication Use ◽  
Effect Modification ◽  
Anticholinergic Medication ◽  
Anticholinergic Medications ◽  
Recurrent Falls ◽  
Increase Risk ◽  
Dopamine Signaling

Abstract Anticholinergic medications (A-chol) increase risk for falls; higher dopaminergic signaling may provide resilience to these effects. In 2489 older adults (mean age=74; 52% women) with 10 years of data on medication use, falls, and dopaminergic genotype (catechol-O-methyltransferase (COMT)), we assessed the association of A-chol use with recurrent falls (≥2) over the subsequent 12 months using generalized estimating equations. Effect modification by COMT (met/met, higher dopamine signaling, n=473 vs val carriers, lower dopamine signaling, n=2016) was tested; analyses were then stratified by COMT and adjusted for demographics and A-chol use indicators. During follow-up, 843 people reported recurrent falls. A-chol use doubled the odds of recurrent falls (OR [95%CI]=2.13[1.74, 2.60]), with a suggested effect modification by COMT (p=0.1). The association was present in val carriers (adjusted OR [95%CI]=1.93[1.36, 2.73]) but not in met/met (adjusted OR [95%CI]=1.30[0.53, 3.22]). Higher dopaminergic signaling may provide protection against the effects of A-chol use on fall risk.

scholarly journals In search of the most reproducible neural vulnerability factors that predict future weight gain: analyses of data from six prospective studies

2021 ◽  
Author(s):  
Sonja Yokum ◽  
Ashley N Gearhardt ◽  
Eric Stice
Keyword(s):  
Weight Gain ◽  
Body Fat ◽  
Orbitofrontal Cortex ◽  
Fat Studies ◽  
Palatable Food ◽  
Vulnerability Factors ◽  
Main Effect ◽  
Limited Support ◽  
Food Images ◽  
High Calorie

Abstract We tested if we could replicate the main effect relations of elevated striatum and lateral orbitofrontal cortex (OFC) response to high-calorie food stimuli to weight gain reported in past papers in six prospective datasets that used similar functional MRI (fMRI) paradigms. Participants in Study 1 (N = 37; M (mean) age = 15.5), Study 2 (N = 160; M age = 15.3), Study 3 (N = 130; M age = 15.0), Study 4 (N = 175; M age = 14.3), Study 5 (N = 45; M age = 20.8) and Study 6 (N = 49; M age = 31.1) completed fMRI scans at the baseline and had their body mass index (BMI) and body fat (Studies 4 and 6 only) measured at the baseline and over follow-ups. Elevated striatal response to palatable food images predicted BMI gain in Studies 1 and 6 and body fat gain in Study 6. Lateral OFC activation did not predict weight gain in any of the six studies. The result provide limited support for the hypothesis that elevated reward region responsivity to palatable food images predicts weight gain. Factors that make replication difficult are discussed and potential solutions considered.

scholarly journals The Use of Continuous Glucose Monitoring System in Combination with Individualized Lifestyle and Therapeutic Recommandations on Glycemic Control of Type 2 Diabetes Patients

2014 ◽  
Vol 21 (4) ◽  
pp. 291-299
Author(s):  
Anca-Elena Crăciun ◽  
Cornelia Bala ◽  
Cristian Crăciun ◽  
Gabriela Roman ◽  
Carmen Georgescu ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Weight Gain ◽  
Glycemic Control ◽  
Insulin Therapy ◽  
Body Fat ◽  
Visceral Fat ◽  
Glucose Monitoring ◽  
Visceral Fat Area

Abstract Background and aims. The aim of our research was to evaluate the impact of short-time continuous glucose monitoring (CGM) on glycemic control evaluated by HbA1c and within-day glucose variability. We also assessed if the initiation of insulin therapy in conjunction with lifestyle recommendations may prevent the weight gain. Materials and method. We included 28 patients with type 2 diabetes with 2 consecutive CGMS recordings available (baseline and follow-up) and for which were collected data on weight, body mass index (BMI), percentage (%) of body fat, visceral fat area, HbA1c and glycemic variability. Results. The HbA1c decreased significantly from 8.8% at baseline to 7.3% at follow-up (p <0.0001) in the whole group, and from 10.5% to 7.5% in the subgroup for which the insulin therapy was initiated at baseline (p=0.011). The BMI, % body fat and visceral fat area decreased significantly from 29.2 kg/m2 to 28.4 kg/m2; from 32.3% to 30.4%; and from 141.6 to 129.3 (cm2), respectively. No increase of these parameters was observed in the subgroup for which the insulin therapy was initiated at baseline. Conclusion. The use of CGMS in combination with individualized lifestyle and therapeutic recommendations may have a beneficial effect on glycemic control and may prevent the weight gain associated with insulin initiation.

scholarly journals Postdiagnosis Body Mass Index, Weight Change, and Mortality From Prostate Cancer, Cardiovascular Disease, and All Causes Among Survivors of Nonmetastatic Prostate Cancer

2020 ◽  
Vol 38 (18) ◽  
pp. 2018-2027 ◽  
Author(s):  
Alyssa N. Troeschel ◽  
Terryl J. Hartman ◽  
Eric J. Jacobs ◽  
Victoria L. Stevens ◽  
Ted Gansler ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cardiovascular Disease ◽  
Body Mass Index ◽  
Weight Gain ◽  
Body Mass ◽  
Weight Change ◽  
Cox Proportional Hazards ◽  
Healthy Weight ◽  
All Cause Mortality

PURPOSE To investigate the association of postdiagnosis body mass index (BMI) and weight change with prostate cancer–specific mortality (PCSM), cardiovascular disease–related mortality (CVDM), and all-cause mortality among survivors of nonmetastatic prostate cancer. METHODS Men in the Cancer Prevention Study II Nutrition Cohort diagnosed with nonmetastatic prostate cancer between 1992 and 2013 were followed for mortality through December 2016. Current weight was self-reported on follow-up questionnaires approximately every 2 years. Postdiagnosis BMI was obtained from the first survey completed 1 to < 6 years after diagnosis. Weight change was the difference in weight between the first and second postdiagnosis surveys. Deaths occurring within 4 years of the follow-up were excluded to reduce bias from reverse causation. Analyses of BMI and weight change included 8,330 and 6,942 participants, respectively. RESULTS Postdiagnosis BMI analyses included 3,855 deaths from all causes (PCSM, n = 500; CVDM, n = 1,155). Using Cox proportional hazards models, hazard ratios (HRs) associated with postdiagnosis obesity (BMI ≥ 30 kg/m2) compared with healthy weight (BMI 18.5 to < 25.0 kg/m2) were 1.28 for PCSM (95% CI, 0.96 to 1.67), 1.24 for CVDM (95% CI, 1.03 to 1.49), and 1.23 for all-cause mortality (95% CI, 1.11 to 1.35). Weight gain analyses included 2,973 deaths (PCSM, n = 375; CVDM, n = 881). Postdiagnosis weight gain (> 5% of body weight), compared with stable weight (± < 3%), was associated with a higher risk of PCSM (HR, 1.65; 95% CI, 1.21 to 2.25) and all-cause mortality (HR, 1.27; 95% CI, 1.12 to 1.45) but not CVDM. CONCLUSION Results suggest that among survivors of nonmetastatic prostate cancer with largely localized disease, postdiagnosis obesity is associated with higher CVDM and all-cause mortality, and possibly higher PCSM, and that postdiagnosis weight gain may be associated with a higher mortality as a result of all causes and prostate cancer.

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