Obesity and the Neurocognitive Basis of Food Reward and the Control of Intake

Ziauddeen, Hisham; Alonso‐Alonso, Miguel; Hill, James O.; Kelley, Michael J.; Khan, Naiman A.

doi:10.3945/an.115.008268

Cited by 122 publications

(85 citation statements)

References 183 publications

(192 reference statements)

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“…In agreement with our hypothesis, the present investigation evidenced associations of DA gene methylation patterns with BMI, AO, and carbohydrate intake, which might serve as epigenetic biomarkers of feeding behavior attitudes, excessive adiposity, and fat deposition. These results are consistent with the fact that disruptions in dopaminergic synapse may lead to overconsumption by altering the rewarding effects elicited by palatable foods (Ziauddeen et al., 2015). In this sense, it has been reported that high‐carbohydrate diets can trigger addictive‐like neurochemical and behavioral responses in vulnerable individuals, contributing to weight gain (Lennerz & Lennerz, 2018).…”

Section: Discussionmentioning

confidence: 99%

“…Besides homeostatic processes concerning energy and nutrient metabolic control, eating behavior is also regulated by hedonic (nonhomeostatic) mechanisms (Hernández Ruiz de Eguilaz et al., 2018), which are thought to be driven by the rewarding properties of foods and specific nutritional and behavioral afferent signals (Ziauddeen, Alonso‐Alonso, Hill, Kelley, & Khan, 2015). In this context, it has been reported that similar to alcohol and other drugs of abuse, highly palatable foods (rich in sugars and fat) can trigger neuroadaptive responses in brain reward circuitries (Alonso‐Alonso et al., 2015).…”

Section: Introductionmentioning

confidence: 99%

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Dopamine gene methylation patterns are associated with obesity markers and carbohydrate intake

et al. 2018

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IntroductionDopamine (DA) is a neurotransmitter that regulates the rewarding and motivational processes underlying food intake and eating behaviors. This study hypothesized associations of DNA methylation signatures at genes modulating DA signaling with obesity features, metabolic profiles, and dietary intake.MethodsAn adult population within the Methyl Epigenome Network Association project was included (n = 473). DNA methylation levels in white blood cells were measured by microarray (450K). Differentially methylated genes were mapped within the dopaminergic synapse pathway using the KEGG reference database (map04728). Subsequently, network enrichment analyses were run in the pathDIP portal. Associations of methylation patterns with anthropometric markers of general (BMI) and abdominal obesity (waist circumference), the blood metabolic profile, and daily dietary intakes were screened.ResultsAfter applying a correction for multiple comparisons, 12 CpG sites were strongly associated (p < 0.0001) with BMI: cg03489495 (ITPR3), cg22851378 (PPP2R2D), cg04021127 (PPP2R2D), cg22441882 (SLC18A1), cg03045635 (DRD5), cg23341970 (ITPR2), cg13051970 (DDC), cg08943004 (SLC6A3), cg20557710 (CACNA1C), cg24085522 (GNAL), cg16846691 (ITPR2), and cg09691393 (SLC6A3). Moreover, average methylation levels of these genes differed according to the presence or absence of abdominal obesity. Pathway analyses revealed a statistically significant contribution of the aforementioned genes to dopaminergic synapse transmission (p = 4.78E−08). Furthermore, SLC18A1 and SLC6A3 gene methylation signatures correlated with total energy (p < 0.001) and carbohydrate (p < 0.001) intakes.ConclusionsThe results of this investigation reveal that methylation status on DA signaling genes may underlie epigenetic mechanisms contributing to carbohydrate and calorie consumption and fat deposition.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dopamine gene methylation patterns are associated with obesity markers and carbohydrate intake

et al. 2018

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“…To protect children and those vulnerable to obesity, clinicians and others working with young people should make consistent, comprehensive concerted efforts to discourage hedonic eating [43], especially given that eating can become an addiction under certain circumstances, as with other behaviors [44]. Some consideration that the brain is either impaired to start off with, or undergoes structural changes must be considered in light of the finding that despite it becoming increasingly known that added sugars can have detrimental effects on health, people persist in consuming them in excess [45].…”

Section: Resultsmentioning

confidence: 99%

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2016

AOWMC

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Obesity is a worldwide health issue that shows no signs of abating despite concerted efforts in the past decade to understand the determinants of this growing problem, as well as efforts to prevent or reduce the problem. Associated with high rates of morbidity, and lower than anticipated life quality and years of life, as well as significant impacts in middle life on working ability, the costs to the individual and society are increasingly exorbitant, with no respite in sight. This brief was designed to examine the most recent data in PUBMED and Web of Science that discusses the possible role played by foods that can become addictive in the context of obesity, and to examine the evidence base linking food addiction and obesity. Results show that despite the absence of an extensive research base, and clear differences between addictive drugs and foods, there is increasing evidence from human and animal-based research that food addictions can occur in the same way individuals can become addicted to chemical substances, and that a linkage to obesity in some cases cannot be overlooked.

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“…Fourth, obesity is not caused by a single behavior, for example, overeating (Elman et al, 2006;Stice et al, 2011b;Ziauddeen et al, 2015), but falls into different behavioral categories. One example comes from binge-eating disorder with and without obesity.…”

Section: Obesity-related Changes In Striatal Reward Processingmentioning

confidence: 99%

Altered reward anticipation: Potential explanation for weight gain in schizophrenia?

Grimm

Kaiser

Plichta

et al. 2017

Neuroscience & Biobehavioral Reviews

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a b s t r a c tObesity and weight gain are severe complications of mental illness, especially schizophrenia. They result from changes in lifestyle and nutrition, side effects of medication and other, less well-understood factors. Recent studies suggest that obesity and weight gain are linked to psychopathology. Specifically, severe psychopathology is associated with greater weight dysregulation, typically weight gain. However, our knowledge about the neuroscientific basis of weight gain in schizophrenia is currently limited. We propose that altered reward anticipation, which in turn is related to striatal dopaminergic dysregulation, may explain why obesity is more prevalent in individuals with mental illness. We review evidence that reward anticipation and weight change are linked by a core deficit in dopaminergic striatal circuits. Several lines of evidence, running from animal studies to preclinical and clinical studies, suggest that striatal dopaminergic neurotransmission is a major hub for the regulation of eating behavior and that dopamine links eating behavior to other motivated behavior. From this perspective, the present review outlines a unifying perspective on dopaminergic reward anticipation as a theoretical frame to link weight gain, medication effects and psychopathology. We derive important but open empirical questions and present perspectives for new therapeutic concepts.

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Obesity and the Neurocognitive Basis of Food Reward and the Control of Intake

Cited by 122 publications

References 183 publications

Dopamine gene methylation patterns are associated with obesity markers and carbohydrate intake

Dopamine gene methylation patterns are associated with obesity markers and carbohydrate intake

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Altered reward anticipation: Potential explanation for weight gain in schizophrenia?

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