Is Sugar Addiction a Substance Use Disorder?

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An Examination of Sugar Addiction as a Substance Use Disorder

Abstract

In 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, obesity


Worldwide obesity rates are rapidly rising. In 2016, an estimated 30% of Americans over the age of 18, and almost 20% of young adults were overweight or obese, as defined by a body mass index (BMI) greater than 30 (Centers for Disease Control and Prevention, 2016); and they are projected to increase to 80% 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 review of the literature that the food addiction model is a more appropriate mechanism when looking at correlates and causes of the development of eating disorders and metabolic disorders, including insulin resistance, diabetes, and obesity. The DSM-5 criteria for BED is limited in that it focuses largely on behavior, distress and shame caused by the eating disorder, and lacks acknowledgment of the neurobiological vulnerabilities and effects (American Psychiatric Association, 2013a). Alternatively, the food addiction model proposes that food, especially highly palatable, processed foods that are high in sugar, fat and/or salt are addictive (Davis & Carter, 2014), and therefore may be the underlying cause of BED and metabolic disorders, including obesity. For this examination, we mainly focus on the addictive nature of sugar, as the majority of food addiction studies have shown that sugar intake is more addictive than fat or salt, and highlight the 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 the dopaminergic reward pathway. The mesocorticolimbic pathway, which includes the ventral 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 the addictive substances. However, as the drug is repeatedly consumed, tolerance builds in the body, and “liking” becomes “wanting,” resulting in reduced pleasure, and physiological dependence that necessitates increased consumption (Reeve, 2015).

Food addiction studies have shown that while a variety of foods lead to the release of dopamine, sugar activates the dopaminergic pathway in a way that mirrors addictive substances, and leads to bingeing, tolerance, cravings, dependence, and subsequent withdrawal symptoms when deprived (American Psychiatric Association, 2013b; Avena et al., 2008; Davis & Carter, 2014; Davis et al., 2013). As sugar is over-consumed, tolerance grows and bingeing with increased amounts of sugar are needed to obtain the same pleasurable effect. This is suggested to be due to the down-regulation of dopamine receptors (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 the imbalance of hormone signals that results in high anticipation and high sensitivity to sugar when it is consumed. In a study conducted by Lindqvist, Baelemans, and Erlanson-Albertsson (2008), rats that were given a sugar solution showed a 40% increase in ghrelin, the hormone that triggers appetite; in contrast to a significant decrease in leptin and peptide YY, two hunger-suppressing hormones; and a significant down-regulation in mRNA expression of additional hunger-suppressing peptides. This imbalance of appetite hormones and gene expression were hypothesized to have resulted in bingeing and tolerance, as demonstrated by a doubling of the drink consumption compared to control-group rats given water. Lastly, animal studies on sugar addiction have shown that sugar withdrawal mimics opioid withdrawal, and presents with depression and anxiety when deprivation of sugar occurs (Avena et al., 2008; Avena, Rada, & Hoebel, 2008; Hoebel et al., 2009; Hone-Blanchet & Fecteau, 2014; Ifland et al., 2009). The numerous studies in sugar addiction that overlap with the different stages of substance use disorders provide strong biological support for sugar addiction to be classified as a substance use disorder.

Further adding to the biological susceptibility of sugar addiction, Davis et al. (2013) found enhanced dopamine transmission was due to six genetic mutations linked to the dopamine reward pathway; and that association between increased dopamine signaling and multilocus genetic profile scores was significantly higher in participants with high reward sensitivity and high risk for food addiction. These neurological changes and genetic vulnerabilities support tolerance and dependence that may result from a frequent flooding of dopamine and a reduction of receptors as seen in substance use disorders.

Likewise, psychological traits like impulsivity and poor emotional regulation, have been found in both substance use disorders and sugar addiction. Impulsivity, as it relates to immediate gratification and deficits in behavioral inhibition, was positively correlated with sugar addiction. However, sensation-seeking, as an impulsive personality trait, was negatively associated with sugar addiction, and theorized to be due to the lack of arousal and stimulation from eating food; “those who are risk seeking and reward-driven might 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 tolerance were also positively associated with sugar addiction, and the consumption of sugar was hypothesized to activate the pleasure center countering the negative emotional state and further reinforcing the reward of sugar intake behavior (Kozak & Fought, 2011; Pivarunas & Connor, 2015).

Equally important in the comparison between sugar addiction and substance use disorders are the detrimental effects on the brain and body’s functions, such as cognitive impairment and metabolic disorders. Reversible cognitive impairments in decision-making, motivation, spatial or place-recognition memory were 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, reducing hypothalamic activity, and negatively affecting neural food processing, which over time increased the risk for insulin resistance, type 2 diabetes, and obesity. A separate study found that the overconsumption of sugar increased levels of free fatty acids, triglycerides and cholesterol in the blood (Lindqvist, Baelemans, & Erlanson-Albertsson, 2008), which are confirmed risk factors for developing in heart disease and strokes in humans (National Institute of Health, 2005; American Heart Association, 2017). The relationship between sugar addiction’s detrimental effects and long-term illness are apparent in the literature, and is analogous to the relationship between substance use and disease.

Current treatment options for food or sugar addiction are limited to exercise, which addresses biological pathways; and mindfulness, which emphasizes psychological processes. Exercise serves as a protective treatment against metabolic disorders and food addiction via increases in brain-derived neurotropic factor (BDNF), a neurotransmitter that plays a major role in neuroplasticity, and in the regulation of food intake, physical activity, and glucose metabolism (Codella, Terruzzi, & Luzi, 2017). Whereas, mindfulness addresses the dual process model of health behavior, which states that there are interactive automatic (implicit) and controlled (explicit) psychological processes that result in addictive behavior. Implicit, automatic processes include intentions, 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 protocol successfully retrained participants to avoid unhealthy food by 1) reducing the approach bias toward unhealthy food, and 2) increasing the approach bias toward healthy food. Another study showed a high approach tendency for healthy food buffered against the stress of hunger and wanting for unhealthy food (Cheval, Audrin, Sarrazin, & Pelletier, 2017). Mindfulness was also found to regulate emotional reactivity to internal and external cues (Fisher, Mead, Lattimore, Malinowski, 2017). Unfortunately, available treatment options have low generalizable, replicable success as they fail to provide a streamlined approach to sugar addiction and/or address neurobiological vulnerabilities and negative effects.

Neither sugar nor food addiction is currently defined in the DSM-5. The only consistent measure of food addiction is the Yale Food Addiction Scale (YFAS), a survey developed in 2009, and it is used in studies reliably as its questions are based on DSM-IV addiction criteria (Gearhardt, Corbin, Brownell, 2009; Gearhardt, Corbin, Brownell, 2016). As mentioned earlier, food addiction and BED are not reciprocal disorders, therefore acknowledging sugar addiction as a substance use disorder in a future DSM may increase evidence-based research that strongly implicates genetic and brain pathways, which may lead to early prevention, reduced stigmatization and diverse treatment options that address the psychological as well as neurobiological vulnerabilities through medication, and even gene therapy. Further research and government regulation can also limit the pseudo-science funded by sugar and packaged goods companies. For example, in reviewing the literature, two studies were found that denied sugar and its addictive properties (Benton, 2010; Markus, Rogers, Brouns, & Schepers, 2017); they were funded by Coca-Cola and the World Sugar Research Organization. Similar to the studies conducted by the tobacco industry, the information countering sugar addiction can be confusing and deceptive to consumers. Government regulation of the sugar industry, like the tobacco industry 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 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.

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