Is Sugar Addiction a Substance Use Disorder?

Is Sugar habituation a vegetable marrow utilization Disorder?An Examination of Sugar dependance as aSubstance Use DisorderAbstractIn the last decade, many studies make up supported the addictive nature of wampum. In this examination of cabbage dependance, we explore the parallels with depicted object ab hire disoblige and mettlesomelight the effects on the intelligence and body as well as the mental and biological encounter factors that may make an individual vulnerable to kale dependance. We theorize that define stops habituation as a total ab employ rowdiness in a future version of the diagnostic and Statistical manual(a) of Mental Disorders (DSM) will change policy to improve public health, and background the costs of metabolous disorders like diabetes, obesity, and heart disease on the economy.Keywords kail addiction, substance lend oneself disorder, dopamine,impulsivity, obesity humanwide obesity rates ar rapidly rising. In 2016, an estimated30% of Americans over the age of 18, and almost 20% of young adults were hardor obese, as defined by a body mass index (BMI) greater than 30 (Centers for indisposition watch and Prevention, 2016) and they ar projected to increase to80% by 2023 (Wang, Beydoun, Liang, Caballero, & Kumanyika, 2008). Between 29%and 47% of obese individuals meet the criteria for binge ingest disorders (BED)(McCuen-Wurst, Ruggieri, & Allison, 2017). However, we suggest in this reviewof the literature that the nutrition addiction model is a to a greater extent 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 throttle in that it focuses largely on behavior, distressand discompose caused by the eating disorder, and lacks acknowledgment of theneurobiological vulnerabilities and effects (American psychiatrical Association,2013a). Alternatively, the nutrien t addiction model proposes that regimen, especially highschoolly palatable, processed solid foods that are high in sugar, risque and/or salt areaddictive (Davis & Carter, 2014), and then may be the underlying causeof BED and metabolic disorders, including obesity. For this examination, we principallyfocus on the addictive nature of sugar, as the majority of food addictionstudies shoot 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 varlet & Melrose,2016 Tran & Westbrook, 2017 Wong, Dogra, & Reichelt, 2017).It is well known that addictive drugs activate thedopaminergic reward path management. The mesocorticolimbic parcel of land, which embarrasss theventral tegmental demesne (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 tell apart,and help breed liking motivations and positive associations toward theaddictive substances. However, as the drug is repeatedly consumed, security depositbuilds in the body, and liking becomes wanting, resulting in sickendpleasure, and physiological dependence that necessitates change magnitude expending(Reeve, 2015). Food addiction studies have shown that while a conformation 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 ove r-consumed, tolerance grows and bingeingwith increase amounts of sugar are needed to contract the same pleasurableeffect. This is suggested to be due to the down- command 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 ductless gland signals that results in high anticipation and high aesthesia to sugar when it is consumed. In a take conducted by Lindqvist,Baelemans, and Erlanson-Albertsson (2008), rats that were given a sugarsolution showed a 40% increase in ghrelin, the hormone that triggers relishin contrast to a significant decrease in leptin and peptide YY, two yearning-suppressinghormones and a significant down- regulation in mRNA facial gesture of additional hunger-suppressingpeptides. This imbalance of appetite hormones and gene expression werehypothesized to have resulted in bingeing and tol erance, as demonstrated by a look-alikeof 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. encourage adding to the biological susceptibility of sugaraddiction, Davis et al. (2013) found enhanced dopamine transmission was due tosix ancestral mutations linked to the dopamine reward pathway and that associationbetween increased dopamine signaling and multilocus genetic visibleness scores wassignificantly higher in participants with high reward sensitivity and high riskfor food add iction. 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 poor perceptional regulation, have been found in both(prenominal) substance use disorders and sugaraddiction. Impulsivity, as it relates to immediate gratification and deficitsin behavioral inhibition, was positively cor tie in with sugar addiction.However, sensation- try oning, as an impulsive constitution trait, was ostraciselyassociated with sugar addiction, and theorized to be due to the lack of arousaland arousal 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 asso ciated with sugar addiction, and the consumption ofsugar was hypothesized to activate the pleasure center countering the opposeemotional state and further reinforcing the reward of sugar intake behavior (Kozak& Fought, 2011 Pivarunas & Connor, 2015).Equally measurable 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. 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 move sugar and insulin levels dulled food cues, reducinghypothalamic activity, and negatively bear on neural food processing, whichover time increased the risk for insulin resistance, flake 2 diabetes, andobesity. A separate study found that the overconsumption of su gar increasedlevels of free fatty acids, triglycerides and cholesterol in the blood (Lindqvist,Baelemans, & Erlanson-Albertsson, 2008), which are confirm risk factors fordeveloping in heart disease and strokes in military personnel ( discipline Institute ofHealth, 2005 American Heart Association, 2017). The recountingship between sugaraddictions detrimental effects and long-term illness are discernible in theliterature, and is analogous to the relationship between substance use anddisease. certain 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). Where as, mindfulnessaddresses the dual process model of health behavior, which states that in that locationare interactive automatic (implicit) and controlled (explicit) psychological processesthat result in addictive behavior. Implicit, automatic processes includeintentions, approach and evacuateance 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 un muscular 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 to settle emotional reactivity to internal and e xternal cues (Fisher, Mead,Lattimore, Malinowski, 2017). Unfortunately, available treatment options havelow generalizable, replicable success as they fail to provide a satiny 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, wherefore acknowledging sugaraddiction as a substance use disorder in a future DSM may increase evidence-basedresearch that powerfully implicates genetic and brain pathways, which may lead toearly saloon, reduced stigmatisation and diverse treatment options that addressthe psychological as well as neurobiolog ical vulnerabilities by means ofmedication, and even gene therapy. Further research and regimen regulation canalso limit the pseudo-science funded by sugar and pack vulcanized 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. fleshiness alone is projected to cost upwards of $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 statisticalmanual of mental disorders DSM-5 (5th ed.).Arlington, VA American Psychiatric Association. Retrieved fromhttps//inside.org/10.1176/appi.books.9780890425596.d sm10AmericanPsychiatric Association. (2013b). Substance-Related and Addictive Disorders. InDiagnostic and statisticalmanual of mental disorders DSM-5 (5th ed.).Arlington, VA American Psychiatric 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). Afterdaily bingeing on a sucrose solution, fooddeprivation induces anxiety and accumbens dopamine/acetylcholine imbalance. Physiology & Behavior, 94, 309-315.inside10.1016/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. (2 017). When hunger does (ordoesnt) increase unhealthy and healthy foodconsumption through food wanting The distinctive role of impulsive approachtendencies toward healthy food. Appetite,116, 99-107. 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 certain foods are addictive, how might thischange the treatment of compulsive satiate andobesity? period 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, 11 8, 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. psychological science 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 substance 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 evi dence 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 Associations 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 Understanding 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),439-4 44. 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 isreversible and training dependent. Appetite,110, 61-71. doi10.1016/j.appet.2016.12.010U.S.Department of Health and kind-hearted 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 corpulency 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 take No. 05-3290). Retrieved fromhttps//www.nhlbi.nih.gov/health/resources/heart/heart-cholesterol-hbc-what-htmlVanderBroek-Stice,L., Stojek, M. K., Beach, S. R. H., vanDellen, M. R., & MacKillop, J. (2017). Multidimensional assessment 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 measurable by operantdelay-discounting. Behavioural BrainResearch, 327, 144-154. doi10.1016/j.bbr.2017.03.029