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

Author(s):  
Sonja Yokum ◽  
Ashley N Gearhardt ◽  
Eric Stice

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.

2019 ◽  
Vol 15 (10) ◽  
pp. 1135-1144 ◽  
Author(s):  
Eric Stice ◽  
Sonja Yokum ◽  
Pascale Voelker

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.


2019 ◽  
Vol 110 (6) ◽  
pp. 1275-1286 ◽  
Author(s):  
Sonja Yokum ◽  
Eric Stice

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.


1990 ◽  
Vol 259 (6) ◽  
pp. R1096-R1102 ◽  
Author(s):  
B. Graham ◽  
S. Chang ◽  
D. Lin ◽  
F. Yakubu ◽  
J. O. Hill

Weight cycling, defined as repeated episodes of weight loss followed by weight regain, has been suggested to make rats more energy efficient and produce a state of energy balance favoring accumulation of excess body fat. In addition, weight cycling may favor accumulation of fat in central vs. peripheral adipose depots. In the present study, we gave two groups of female Wistar rats ad libitum access to an obesity-producing high-fat diet (60% of calories from fat). Both groups had previously eaten a low-fat stock diet, but one group had been subjected to three bouts of weight cycling. Rats that were previously weight cycled gained less body weight and body fat when given the high-fat diet than did controls. The lower rate of weight gain was due to a lesser increase in food intake, since daily energy expenditure was significantly lower in previously cycled rats than in controls. In summary, weight cycling does not appear to predispose rats to becoming obese on a high-calorie diet and apparently produces some effect on food intake that reduces, at least in the short run, weight gain on the high-calorie diet.


2017 ◽  
Author(s):  
Kyle Stanley Burger

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.


2020 ◽  
Vol 36 (2) ◽  
pp. 410-420 ◽  
Author(s):  
Anthony M. Gibson ◽  
Nathan A. Bowling

Abstract. The current paper reports the results of two randomized experiments designed to test the effects of questionnaire length on careless responding (CR). Both experiments also examined whether the presence of a behavioral consequence (i.e., a reward or a punishment) designed to encourage careful responding buffers the effects of questionnaire length on CR. Collectively, our two studies found (a) some support for the main effect of questionnaire length, (b) consistent support for the main effect of the consequence manipulations, and (c) very limited support for the buffering effect of the consequence manipulations. Because the advancement of many subfields of psychology rests on the availability of high-quality self-report data, further research should examine the causes and prevention of CR.


Author(s):  
Mercedes Díaz-Rodríguez ◽  
Celia Pérez-Muñoz ◽  
Jesús Carretero-Bravo ◽  
Catalina Ruíz-Ruíz ◽  
Manuel Serrano-Santamaría ◽  
...  

(1) Background: Obesity is defined as an excessive accumulation of body fat. Several early developmental factors have been identified which are associated with an increased risk of childhood obesity and increased adiposity in childhood. The primary objective of the present study is to analyse the effect of various early risk factors on Body Mass Index (BMI) and body fat percentage at 2 years of age. (2) Methods: A prospective cohort study design was used, with the sample consisting of 109 mother-child pairs from whom data were collected between early pregnancy and 2 years old. Adiposity was determined based on skinfold measurements using the Brooks and Siri formulae. Mean comparison tests (Student’s t-test and ANOVAs) and multiple linear regression models were used to analyse the relationship between early programming factors and dependent variables. (3) Results: Maternal excess weight during early pregnancy (β = 0.203, p = 0.026), gestational smoking (β = 0.192, p = 0.036), and accelerated weight gain in the first 2 years (β = − 0.269, p = 0.004) were significantly associated with high body fat percentage. Pre-pregnancy BMI and accelerated weight gain in the first 2 years were associated with high BMI z-score (β = 0.174, p = 0.047 and β = 0.417, p = 0.000 respectively). The cumulative effect of these variables resulted in high values compared to the baseline zero-factor group, with significant differences in BMI z-score (F = 8.640, p = 0.000) and body fat percentage (F = 5.402, p = 0.002) when three factors were present. (4) Conclusions: The presence of several early risk factors related to obesity in infancy was significantly associated with higher BMI z-score and body fat percentage at 2 years of age. The presence of more than one of these variables was also associated with higher adiposity at 2 years of age. Early prevention strategies should address as many of these factors as possible.


1975 ◽  
Vol 84 (2) ◽  
pp. 353-364 ◽  
Author(s):  
C. Thomas ◽  
J. M. Wilkinson ◽  
J. C. Tayler

SUMMARYFifty-four British Friesian castrated male calves, initially 3, 6 or 9 months of age (107, 180 and 249 kg initial live weight, respectively), were individually fed for 83 days on maize silage (27·9% dry matter (D.M.), 10·7% crude protein in D.M.), offeredad libitum. Silage was offered either alone or supplemented with cobs of dried lucerne (21% of total D.M. intake). Three levels of urea (0, 1 and 2% of silage D.M.) were added to the silage before feeding.Total D.M. intakes averaged 23·0, 23·4 and 21·6 g/kg live weight (LW) for the 3-, 6- and 9-month-old animals, respectively. Addition of urea increased silage intake by 11% in the 6-month-old group but there was little effect in the 3- and 9-month-old groups. Lucerne supplementation reduced silage D.M. intake from 22·0 to 18·4 g/kg LW (P< 0·001) and increased total D.M. intake by 1·4 g/kg LW (P< 0·001).Live-weight gain (LWG) of the cattle fed on silage alone increased (P< 0·001) with increasing age of animal. The main effect of urea was to elevate (P< 0·001) LWG from an average of 0·79 (no urea) to 0·94 kg/head/day (2% urea). However, it appeared that most of this effect was confined to the 6-month-old group. The effect of lucerne on LWG decreased with increasing age of animal (P< 0·001). Inclusion of lucerne in the diet significantly reduced the response to urea (P< 0·05).Feed conversion efficiency (LWG/100 Mcal DE intake) decreased (P< 0·01) with increasing age of animal but increased with urea addition from an average of 4·7 (no urea) to 5·3 kg LWG/100 Meal DE intake (2% urea). The response to lucerne supplementation in terms of efficiency was greatest in the 3-month-old group and thereafter declined markedly with increasing age of animal.The results of this experiment indicated that cattle older than 6 months of age (180 kg LW) could achieve a rate of growth of 1·0 kg/head/day on maize silage supplemented solely with urea, but that younger animals required supplementary lucerne to support a high rate of live-weight gain.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Katherine H Ingram ◽  
Roxanna Lopez

An association between abdominal adiposity and insulin resistance is well-established. Recent research indicates that subcutaneous fat accumulation in the lower body may be associated with higher levels of insulin sensitivity. Hypothesis: This pilot study tested the hypothesis that the distribution of body fat in the lower body after pregnancy is negatively associated with gestational insulin resistance. Methods: In 32 nulliparous pregnant women (age 27±4.5, BMI 29.5±7.9, 69% non-hispanic white), the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) was computed from fasting glucose and insulin at 24-28 weeks gestation. Body composition was assessed at mid-gestation (18-20 weeks) and at four weeks post-partum. Total body fat was estimated via bioelectrical impedance (InBody 720) and skinfold thicknesses were measured at seven sites. Dual-energy xray absorptiometry (DXA) measures of regional fat (gynoid, visceral, and leg) were obtained post-partum only. Gestational weight gain was monitored by medical records. Partial correlation analyses were controlled for age and race and then analyses were repeated controlling for baseline (mid-gestation) body fat percent. HOMA-IR was log-transformed for normality. Results: HOMA-IR was associated with post-partum body fat ( r =0.45, p < .05) and adiposity in the trunk region ( r =0.58, 0.57 and 0.52 for DXA visceral fat, suprailiac skinfold, and abdominal skinfold, respectively, p < .01), but not with gestational weight gain ( r =.07, p = ns), DXA gynoid region ( r = 0.26, p = ns), or any other leg measure. When analyses were further controlled for baseline body fat, post-partum measures of lower-body adiposity were strongly and negatively correlated with HOMA-IR ( r = -0.66, -0.48, and -0.48 for thigh skinfold, DXA gynoid, and DXA leg, respectively, p < .05 for all). Neither DXA visceral fat ( r = .23; p = ns) nor any other post-partum fat measures were associated with HOMA-IR when controlling for baseline body fat. Conclusions: Gestational insulin resistance was negatively associated with post-partum thigh fat accumulation, independent of overall body fat. These data indicate that insulin sensitivity may be associated with the ability to store fat in the lower body and should warrant further study of subcutaneous leg fat as a metabolically “healthy” storage depot.


1987 ◽  
Vol 117 (12) ◽  
pp. 2127-2134 ◽  
Author(s):  
Israel Ramirez

2007 ◽  
Vol 292 (5) ◽  
pp. R1834-R1838 ◽  
Author(s):  
Christopher L. Gentile ◽  
Jeb S. Orr ◽  
Brenda M. Davy ◽  
Kevin P. Davy

We tested the hypothesis that modest, overfeeding-induced weight gain would increase sympathetic neural activity in nonobese humans. Twelve healthy males (23 ± 2 years; body mass index, 23.8 ± 0.7) were overfed ∼1,000 kcal/day until a 5-kg weight gain was achieved. Muscle sympathetic nerve activity (MSNA, microneurography), blood pressure, body composition (dual energy X-ray absorptiometry), and abdominal fat distribution (computed tomography) were measured at baseline and following 4 wk of weight stability at each individual's elevated body weight. Overfeeding increased body weight (73.5 ± 3.1 vs. 78.4 ± 3.2 kg, P < 0.001) and body fat (14.9 ± 1.2 vs. 18 ± 1.1 kg, P < 0.001) in 42 ± 8 days. Total abdominal fat increased (220 ± 22 vs. 266 ± 22 cm2, P < 0.001) with weight gain, due to increases in both subcutaneous (158 ± 15 vs. 187 ± 12 cm2, P < 0.001) and visceral fat (63 ± 8 vs. 79 ± 12 cm2, P = 0.004). As hypothesized, weight gain elicited increases in MSNA burst frequency (32 ± 2 vs. 38 ± 2 burst/min, P = 0.002) and burst incidence (52 ± 4 vs. 59 ± 3 bursts/100 heart beats, P = 0.026). Systolic, but not diastolic blood pressure increased significantly with weight gain. The change in MSNA burst frequency was correlated with the percent increase in body weight ( r = 0.59, P = 0.022), change in body fat ( r = 0.52, P = 0.043) and percent change in body fat ( r = 0.51, P = 0.045). The results of the current study indicate that modest diet-induced weight gain elicits sympathetic neural activation in nonobese males. These findings may have important implications for understanding the link between obesity and hypertension.


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