An Examination of Sugar Addiction as aSubstance Use DisorderAbstractIn the last decade, many studies have supported the addictive nature of sugar. In this examination of sugar addiction, we explore the parallels with substance abuse disorder and highlight the effects on the brain and body as well as the psychological and biological risk factors that may make an individual vulnerable to sugar addiction. We theorize that defining sugar addiction as a substance abuse disorder in a future version of the Diagnostic and Statistical Manual of Mental Disorders (DSM) will change policy to improve public health, and minimize the costs of metabolic disorders like diabetes, obesity, and heart disease on the economy.Keywords: sugar addiction, substance use disorder, dopamine,impulsivity, obesityWorldwide obesity rates are rapidly rising. In 2016, an estimated30% of Americans over the age of 18, and almost 20% of young adults were overweightor obese, as defined by a body mass index (BMI) greater than 30 (Centers forDisease Control and Prevention, 2016); and they are projected to increase to80% by 2023 (Wang, Beydoun, Liang, Caballero, & Kumanyika, 2008). Between 29%and 47% of obese individuals meet the criteria for binge eating disorders (BED)(McCuen-Wurst, Ruggieri, & Allison, 2017). However, we suggest in this reviewof the literature that the food addiction model is a more appropriate mechanismwhen looking at correlates and causes of the development of eating disordersand metabolic disorders, including insulin resistance, diabetes, and obesity. TheDSM-5 criteria for BED is limited in that it focuses largely on behavior, distressand shame caused by the eating disorder, and lacks acknowledgment of theneurobiological vulnerabilities and effects (American Psychiatric Association,2013a). Alternatively, the food addiction model proposes that food, especiallyhighly palatable, processed foods that are high in sugar, fat and/or salt areaddictive (Davis & Carter, 2014), and therefore may be the underlying causeof BED and metabolic disorders, including obesity. For this examination, we mainlyfocus on the addictive nature of sugar, as the majority of food addictionstudies have shown that sugar intake is more addictive than fat or salt, and highlightthe numerous biological and psychological parallels to substance (Avena,Bocarsly, Rada, Kim, & Hoebel, 2008; Avena, Rada, & Hoebel, 2008; Davis,Loxton, Levitan, Kaplan, Carter, & Kennedy, 2013; Hoebel, Avena, Bocarsly,& Rada, 2009; Hone-Blanchet & Fecteau, 2014; Ifland, Preuss, Marcus,Rourke, Taylor, Burau, Jacobs, Kadish, & Manso, 2009; Page & Melrose,2016; Tran & Westbrook, 2017; Wong, Dogra, & Reichelt, 2017).It is well known that addictive drugs activate thedopaminergic reward pathway. The mesocorticolimbic pathway, which includes theventral tegmental area (VTA), nucleus accumbens (NAc) and the frontal cortex,is especially implicated in the reinforcement of the use of these substances.These areas release high levels of dopamine, which produce a euphoric state,and help form “liking” motivations and positive associations toward theaddictive substances. However, as the drug is repeatedly consumed, tolerancebuilds in the body, and “liking” becomes “wanting,” resulting in reducedpleasure, and physiological dependence that necessitates increased consumption(Reeve, 2015). Food addiction studies have shown that while a variety offoods lead to the release of dopamine, sugar activates the dopaminergic pathwayin a way that mirrors addictive substances, and leads to bingeing, tolerance, cravings,dependence, and subsequent withdrawal symptoms when deprived (AmericanPsychiatric Association, 2013b; Avena et al., 2008; Davis & Carter, 2014;Davis et al., 2013). As sugar is over-consumed, tolerance grows and bingeingwith increased amounts of sugar are needed to obtain the same pleasurableeffect. This is suggested to be due to the down-regulation of dopaminereceptors (Avena et al., 2008; Davis, Patte, Levitan, Reid, Tweed, &Curtis, 2007; Hoebel et al., 2009; Ifland et al., 2009, Loxton & Tipman,2017). Thereafter, “wanting” or cravings are suggested to be due to theimbalance of hormone signals that results in high anticipation and highsensitivity to sugar when it is consumed. In a study conducted by Lindqvist,Baelemans, and Erlanson-Albertsson (2008), rats that were given a sugarsolution showed a 40% increase in ghrelin, the hormone that triggers appetite;in contrast to a significant decrease in leptin and peptide YY, two hunger-suppressinghormones; and a significant down-regulation in mRNA expression of additional hunger-suppressingpeptides. This imbalance of appetite hormones and gene expression werehypothesized to have resulted in bingeing and tolerance, as demonstrated by a doublingof the drink consumption compared to control-group rats given water. Lastly, animalstudies on sugar addiction have shown that sugar withdrawal mimics opioidwithdrawal, and presents with depression and anxiety when deprivation of sugaroccurs (Avena et al., 2008; Avena, Rada, & Hoebel, 2008; Hoebel et al.,2009; Hone-Blanchet & Fecteau, 2014; Ifland et al., 2009). The numerousstudies in sugar addiction that overlap with the different stages of substanceuse disorders provide strong biological support for sugar addiction to be classifiedas a substance use disorder.Further adding to the biological susceptibility of sugaraddiction, Davis et al. (2013) found enhanced dopamine transmission was due tosix genetic mutations linked to the dopamine reward pathway; and that associationbetween increased dopamine signaling and multilocus genetic profile scores wassignificantly higher in participants with high reward sensitivity and high riskfor food addiction. These neurological changes and genetic vulnerabilities supporttolerance and dependence that may result from a frequent flooding of dopamine anda reduction of receptors as seen in substance use disorders. Likewise, psychological traits like impulsivity and pooremotional regulation, have been found in both substance use disorders and sugaraddiction. Impulsivity, as it relates to immediate gratification and deficitsin behavioral inhibition, was positively correlated with sugar addiction.However, sensation-seeking, as an impulsive personality trait, was negativelyassociated with sugar addiction, and theorized to be due to the lack of arousaland stimulation from eating food; “those who are risk seeking and reward-drivenmight seek out experiences involving greater levels of arousal and stimulation(Pivarunas & Connor, 2015; VanderBroek-Stice, Stojek, Beach, vanDellen,& MacKillop, 2017). Poor emotional regulation and low distress tolerancewere also positively associated with sugar addiction, and the consumption ofsugar was hypothesized to activate the pleasure center countering the negativeemotional state and further reinforcing the reward of sugar intake behavior (Kozak& Fought, 2011; Pivarunas & Connor, 2015).Equally important in the comparison between sugar addictionand substance use disorders are the detrimental effects on the brain and body’sfunctions, such as cognitive impairment and metabolic disorders. Reversible cognitiveimpairments in decision-making, motivation, spatial or place-recognition memorywere recently identified in studies with rats (Tran & Westbrook, 2017; Wong,Dogra, & Reichelt, 2017). However, in a study conducted by Page and Melrose(2016), high levels of circulating sugar and insulin levels dulled food cues, reducinghypothalamic activity, and negatively affecting neural food processing, whichover time increased the risk for insulin resistance, type 2 diabetes, andobesity. A separate study found that the overconsumption of sugar increasedlevels of free fatty acids, triglycerides and cholesterol in the blood (Lindqvist,Baelemans, & Erlanson-Albertsson, 2008), which are confirmed risk factors fordeveloping in heart disease and strokes in humans (National Institute ofHealth, 2005; American Heart Association, 2017). The relationship between sugaraddiction’s detrimental effects and long-term illness are apparent in theliterature, and is analogous to the relationship between substance use anddisease.Current treatment options for food or sugar addiction arelimited to exercise, which addresses biological pathways; and mindfulness,which emphasizes psychological processes. Exercise serves as a protectivetreatment against metabolic disorders and food addiction via increases in brain-derivedneurotropic factor (BDNF), a neurotransmitter that plays a major role inneuroplasticity, and in the regulation of food intake, physical activity, andglucose metabolism (Codella, Terruzzi, & Luzi, 2017). Whereas, mindfulnessaddresses the dual process model of health behavior, which states that thereare interactive automatic (implicit) and controlled (explicit) psychological processesthat result in addictive behavior. Implicit, automatic processes includeintentions, approach and avoidance tendencies, and emotions, meanwhile explicit,controlled processes include reflective action (Hagger, Trost, Keech, Chan,& Hamilton, 2017; Tang, Posner, Rothbart, & Volkow, 2015). In 2017, Kakoschke,Kemps, & Tiggemann showed that a two-pronged approach-modification protocolsuccessfully retrained participants to avoid unhealthy food by 1) reducing theapproach bias toward unhealthy food, and 2) increasing the approach bias towardhealthy food. Another study showed a high approach tendency for healthy foodbuffered against the stress of hunger and wanting for unhealthy food (Cheval,Audrin, Sarrazin, & Pelletier, 2017). Mindfulness was also found toregulate emotional reactivity to internal and external cues (Fisher, Mead,Lattimore, Malinowski, 2017). Unfortunately, available treatment options havelow generalizable, replicable success as they fail to provide a streamlined approachto sugar addiction and/or address neurobiological vulnerabilities and negativeeffects.Neither sugar nor food addiction is currently defined in theDSM-5. The only consistent measure of food addiction is the Yale Food AddictionScale (YFAS), a survey developed in 2009, and it is used in studies reliably asits questions are based on DSM-IV addiction criteria (Gearhardt, Corbin,Brownell, 2009; Gearhardt, Corbin, Brownell, 2016). As mentioned earlier, foodaddiction and BED are not reciprocal disorders, therefore acknowledging sugaraddiction as a substance use disorder in a future DSM may increase evidence-basedresearch that strongly implicates genetic and brain pathways, which may lead toearly prevention, reduced stigmatization and diverse treatment options that addressthe psychological as well as neurobiological vulnerabilities throughmedication, and even gene therapy. Further research and government regulation canalso limit the pseudo-science funded by sugar and packaged goods companies. Forexample, in reviewing the literature, two studies were found that denied sugarand its addictive properties (Benton, 2010; Markus, Rogers, Brouns, &Schepers, 2017); they were funded by Coca-Cola and the World Sugar ResearchOrganization. Similar to the studies conducted by the tobacco industry, theinformation countering sugar addiction can be confusing and deceptive toconsumers. Government regulation of the sugar industry, like the tobaccoindustry can result in a decrease of sugar addiction and its harmful health effects.Lastly, there is also a large benefit to public health and the economic costs in treating sugar addiction like a substance use disorder. The costs to treat diabetes, a disease directly related to increased blood sugar levels and insulin resistance was $245 billion in 2012 (Centers for Disease Control and Prevention, 2017). These costs do not include comorbid diseases like obesity, hypertension, and hyperlipidemia. 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High-sucrose diets in male rats disrupt aspects of decision-making tasks,motivation and spatial memory, but not impulsivity measured by operantdelay-discounting. Behavioural BrainResearch, 327, 144-154. doi:10.1016/j.bbr.2017.03.029Get Help With Your EssayIf you need assistance with writing your essay, our professional essay writing service is here to help!Find out more