Is Sugar Addiction a Substance Use Disorder?

Is loot Addiction a Substance Use Disorder?An Examination of Sugar Addiction as aSubstance Use DisorderAbstractIn the last decade, many studies consecrate supported the habit-forming nature of peag. In this examination of cole colony, we explore the parallels with way ab do disorder and senior highlight the effectuate on the brain and body as substantially as the mental and biological risk factors that may make an individual vulnerable to borecole addiction. We theorize that defining kale 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 decrease the costs of metabolic disorders equal diabetes, obesity, and heart disease on the economy.Keywords sugar addiction, substance use disorder, dopamine,impulsivity, obesityWorldwide obesity rates argon chop-chop rising. In 2016, an estimated30% of Americans over the age of 18, and almost 20% of young a dults were overweightor obese, as defined by a body jackpot index (BMI) capitaler 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 sate the criteria for binge eating disorders (BED)(McCuen-Wurst, Ruggieri, & Allison, 2017). However, we suggest in this reviewof the literature that the feed addiction fashion 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 effect (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 reinforcing stimulus roadway. The mesocorticolimbic pathway, which overwhelms 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 purpose(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, 2014Davis 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 appetitein contrast to a significant decrease in leptin and peptide YY, dickens hunger-suppressinghormones and a significant down-regulation in template RNA 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 add iction 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 patrimonial 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 an da 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 behavioural 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 stimulantand 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 plaza 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 bodysfunctions, such as cognitive impairment and metabolic disorders. correctable 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 go 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 f or exploitation in heart disease and strokes in humans (National Institute ofHealth, 2005 American Heart Association, 2017). The relationship between sugaraddictions 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 a pull aheadst 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 r esult in addictive behavior. Implicit, automatic processes includeintentions, come near 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 sunburnt food by 1) reducing theapproach bias toward unhealthy food, and 2) change magnitude 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 reciprocative disorders, therefore acknowledging sugaraddiction as a substance use disorder in a future DSM may increase evidence-basedresearch that potently implicates genetic and brain pathways, which may lead toearly legal community, 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 co mpanies. 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. Obesity alone is projected to cost upwards o f $957 billion by 2030 (Wang et al., 2008). Therefore, prevention of these life-long metabolic disorders by addressing the addictive properties of sugar can potentially reduce the burden on global health and economic systems in a great way. ReferencesAmericanHeart Association. (2017). Prevention andTreatment of High Cholesterol (Hyperlipidemia). Retrieved from http//www.heart.org/HEARTORG/Conditions/Cholesterol/PreventionTreatmentofHighCholesterol/Prevention-and-Treatment-of-High-Cholesterol-Hyperlipidemia_UCM_001215_Article.jsp.WhoJdNy1uUlAmericanPsychiatric Association. (2013a). Feeding and Eating Disorders. In Diagnostic and statistical manual(a) of mental disorders DSM-5 (5th ed.).Arlington, VA American Psychiatric Association. Retrieved fromhttps//inside.org/10.1176/appi.books.9780890425596.dsm10AmericanPsychiatric Association. (2013b). Substance-Related and Addictive Disorders. InDiagnostic and statisticalmanual of mental disorders DSM-5 (5th ed.).Arlington, VA American Psychi atric Association. Retrieved from https//inside.org/10.1176/appi.books.9780890425596.dsm16Avena,N. M., Bocarsly, M. E., Rada, P., Kim, A., & Hoebel, B. G. (2008). After daily bingeing on a sucrose solution, fooddeprivation induces anxiety and accumbens dopamine/acetylcholine imbalance. Physiology & Behavior, 94, 309-315.doi10.1016/j.physbeh.2008.01.008Avena,N. M., Rada, P., & Hoebel, B. G. (2008). Evidence for sugar addictionBehavioral and neurochemical effects ofintermittent, excessive sugar intake. Neuroscienceand Biobehavioral Reviews, 32, 20-39. doi10.1016/j.neubiorev.2007.04.019Benton,D. (2010). The plausibility of sugar addiction and its role in obesity andeating disorders. Clinical Nutrition, 29, 288-303. doi10.1016/j.clnu.2009.12.001Cheval,B., Audrin, C., Sarrazin, P., & Pelletier, L. (2017). When hunger does (ordoesnt) increase unhealthy and healthy foodconsumption through food wanting The distinctive role of impulsive approachtendencies toward healthy food. Appetite,116, 9 9-107. doi10.1016/j.appet.2017.04.028Codella,R., Terruzzi, I., & Luzi, L. (2017). Sugars, exercise and health. Journal of Affective Disorders, 224, 76-86. doi10.1016/j.jad.2016.10.035Davis,C., & Carter, J. C. (2014). If definite foods are addictive, how might thischange the treatment of compulsive overeating andobesity? Current Addiction Reports, 1,89-95. doi10.1007/s40429-014-0013-zDavis,C., Loxton, N. J., Levitan, R. D., Kaplan, A. S., Carter, J. C., & Kennedy,J. L. (2013). Food addiction and itsassociation with a dopaminergic multilocus genetic profile. Physiology & Behavior, 118, 63-69.doi10.1016/j.physbeh.2013.05.014Fisher,N. R., Mead, B. R., Lattimore, P., & Malinowski, P. (2017). Dispositionalmindfulness and reward motivated eating The role of emotion regulation andmental habit. Appetite, 118, 41-48. doi10.1016/j.appet.2017.07.019Gearhardt,A. N., Corbin, W. R., & Brownell, K. D. (2009). Preliminary validation ofthe Yale Food Addiction Scale. Appetite,52, 430-436. doi10.1016/ j.appet.2008.12.003Gearhardt,A. N., Corbin, W. R., & Brownell, K. D. (2016). Development of the Yale Food Addiction Scale Version 2.0. Psychology of Addictive Behaviors, 30,113-121. doi10.1037/adb0000136Hagger,M. S., Trost, N., Keech, J. J., Chan, D. K. C., & Hamilton, K. (2017).Predicting sugar consumption Application of an integrateddual-process, dual-phase model. Appetite,116, 147-156. doi10.1016/j.appet.2017.04.032Hoebel,B. G., Avena, N. M., Bocarsly, M. E., & Rada, P. (2009). A behavioral andcircuit model based on sugar addiction inrats. Journal of Addiction Medicine, (3)1,33-41. doi10.1097/ADM.0b013e31819aa621Hone-Blanchet,A., & Fecteau, S. (2014). Overlap of food addiction and substance usedisorders definitions Analysis of animal and human studies.Neuropharmacology, 85, 81-90.doi10.1016/j.neuropharm.2014.05.019Ifland,J. R., Preuss, H. G., Marcus, M. T., Rourke, K. M., Taylor, W. C., Burau, K., Jacobs, W. S., Kadish, W., &Manso, G. (2008). Refined food addiction A classic subs tance use disorder. Medical Hypotheses, 72, 518-526. doi10.1016/j.mehy.2008.11.035Kakoschke,N., Kemps, N., & Tiggemann, M. (2017). Impulsivity moderates the effect of approach bias modification on healthy foodconsumption. Appetite, 117, 117-125.doi10.1016/j.appet.2017.06.019Kozak,A. T., & Fought, A. (2011). Beyond alcohol and drug addiction. Does thenegative trait of low distress tolerance have anassociation with overeating? Appetite, 57,578-581. doi10.1016/j.appet.2011.07.008Lindqvist,A., Baelemans, A., & Erlanson-Albertsson, C. (2008). Effects of sucrose,glucose and fructose on peripheral and centralappetite signals. Regulatory Peptides,150, 26-32. doi10.1016/j.regpep.2008.06.008Markus,C. R., Rogers, P. J., Brouns, F., & Schepers, R. (2017). Eating dependenceand weight gain no human evidence for a sugar-addiction model of overweight.Appetite, 114, 64-72. doi10.1016/j.appet.2017.03.024 McCuen-Wurst,C., Ruggieri, M., & Allison, K. C. (2017). Disordered eating and obesity Association s between binge-eating disorder,night-eating syndrome, and weight-related comorbities. Annals of the New York Academy of Sciences, 1-10.doi10.1111/nyas.13467Page,K. A., & Melrose, A. J. (2016). Brain, hormone and appetite responses toglucose versus fructose. Current Opinion in Behavioral Sciences, 9, 111-117.doi10.1016/j.cobeha.2016.03.002Pivarunas,B., & Conner, B. T. (2015). Impulsivity and emotion dysregulation aspredictors of food addiction. EatingBehaviors, 19, 9-14. doi10.1016.j.eatbeh.2015.06.007Reeve,J. M. (2015). The Motivated and Emotional Brain. In instinct Motivation and Emotion (6th ed.). Hoboken, NJ Wiley.Tang,Y., Posner, M. I., Rothbart, M. K., & Volkow, N. D. (2015). Circuitry ofself-control and its role in reduction addiction. Trends in Cognitive Sciences, 19(8),439-444. doi10.1016/j.tics.2015.06.007Tran,D. M. D., & Westbrook, R. F. (2017). A high-fat high-sugar diet-inducedimpairment in place-recognition memory is bilateral and training dependent. Appetite,110, 61- 71. doi10.1016/j.appet.2016.12.010U.S. segment of Health and clement Services, Centers for Disease Control andPrevention. (2017). National DiabetesStatistics Report, 2017 Estimates of Diabetesand its Burden in the United States. Retrieved fromhttps//www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdfU.S.Department of Health and Human Services, Centers for Disease Control andPrevention. (2016). Nutrition, PhysicalActivity, and Obesity Behavioral Risk Factor Surveillance SystemPercent of adults aged 18 and older who have obesity. Retrieved from https//chronicdata.cdc.gov/Nutrition-Physical-Activity-and-Obesity/Percent-of-adults-aged-18-and-older-who-have-obesi/cwdv-83miU.S.Department of Health and Human Services, National Institutes of Health,National Heart, Lung, and Blood Institute. (2005). High blood cholesterol What you need toknow. (NIH Publication No. 05-3290). Retrieved fromhttps//www.nhlbi.nih.gov/health/resources/heart/heart-cholesterol-hbc-wha t-htmlVanderBroek-Stice,L., Stojek, M. K., Beach, S. R. H., vanDellen, M. R., & MacKillop, J. (2017). Multidimensional mind ofimpulsivity in relation to obesity and food addiction. Appetite, 112, 59-68. doi10.1016/j.appet.2017.01.009Wang,Y., Beydoun, M. A., Liang, L., Caballero, B., & Kumanyika, S. K. (2008).Will all Americans become overweight or obese? Estimating the progression andcost of the U.S. obesity epidemic. Obesity, 15(10),2323-2330. doi10.1038/oby.2008.351Wong,A., Dogra, V. R., & Reichelt,A. C. (2017). 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. doi10.1016/j.bbr.2017.03.029