Is Sugar Addiction a Substance Use Disorder?

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).

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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. References
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