Sugar “addiction.” Its an attractive concept to the ‘Cult of Wellness‘ and their social media accounts, aided and abetted by supermodels claiming sugar is “toxic.”
The issue, common to the entire landscape of nutrition currently, is that anyone with good looks and a penchant for food photos becomes a “guru”, and with massive reach to the population at large, is capable of spreading food-fear using nebulous, unscientific terms that elicit emotive responses – and precipitate eating disorders. Like “clean eating.”
Sure, if sugar was a substantive aspect to anyones diet, and they cut it out, they will lose weight. Because the maths adds up – they’ve just eliminated a food group that was substantially contributing to their diet, reducing their overall energy intake and creating a calorie deficit in the process. But don’t tell the Instafabulous sugar zealots that. Calorie deficit? Don’t be silly. They lost weight because they were once addicted to sugar, overcame their addiction, “cleansed” their body of the “toxin”, and hey presto!, the fat fell off.
Ok, in all seriousness – can sugar be addictive? Let’s appraise the evidence, for and against, the issue.
First, we need to understand how addiction is defined in relation to food.
The concept of food addiction was originally defined by reference to the diagnostic criteria that define substance addiction, the Diagnostic and Statistical Manual of Mental Disorders 4th ed. or “DSM-IV.” Adapting the DSM-IV criteria to food palatability provided a framework within which to contrast substance abuse addiction [SUD] with eating behaviour, but the overlap failed to translate certain addictive criterion to food behaviour (Meule & Gearhardt, 2014). As a result, the DSM-IV criteria were modelled into the Yale Food Addiction Scale [YFAS], which expanded to include distress as a consequence of overeating (Gearhardt, Corbin & Brownell, 2009).
The DSM-IV was updated and revised in 2013 to the DSM-V, which has certain parallels to overeating (Meule & Gearhardt, 2014). In particular, there is an overlap between the criteria for binge eating disorder [BED] diagnosis and the DSM-V criteria; craving/compulsion to consume, loss of control over the eating episode, and aversive emotional state (Silverstein, Silverstein & Nunn, 2009; Avena, 2007).
There is also up to a 50% correlation between high YFAS scores and BED (Meule & Gearhardt, 2014). This overlap between a high YFAS and BED, and the association with sugar intake do suggest that sugar may be addictive (Davis, 2013). However, given the neuronal circuitry involved in addiction and food intake, it is also plausible that we are biologically hardwired to overconsume when energy is freely available.
There is an argument that our species may be biologically predisposed to overconsume when energy is easily available (Avena, 2007). The scare availability of energy-dense, highly digestible foods in natural environments may have precipitated adaptations toward increasing consumption beyond daily energy requirements for future energy storage (Milton, 2000).
In relation to the addictive criteria of craving, both drugs and sugar can trigger cravings (Davis, 2013). This does not, however, mean sugar is addictive and it is arguable that sugar is distinguishable from substance abuse: an evolutionary adaptation to increase energy intake in unpredictable natural environments, rather than a consequence of addiction (Gerber, Williams & Gray, 1999). As the incubation period for sugar craving in animal models of addiction differs to drugs, it is difficult to assess the criteria of craving between sugar and drugs in a comparative context (Counotte et al., 2014).
Drugs are a more potent trigger of motivational/seeking behaviour than food cues are for eating (Kearns, Gomez-Sorrano & Tunstall, 2011); the reinforcing addictive response is 10-times greater with drugs than the response to consuming a normal meal while hungry (Volkow & Wise, 2005). The fact, however, that the neuronal circuitry activated in response to drugs and sugar overlap is indicative of addictive potential in sugar (Volkow et al., 2013). This has been consistently demonstrated in animal models.
In rats, sugar is a potent hedonic reward that promotes overconsumption in the absence of an energetic requirement, and triggers learned associations with the food reward (Lenoir, 2007). When rats are exposed to sugar on an intermittent daily basis, they reliably and predictably escalate consumption over time, which is indicative of cravings and of the criteria for escalating consumption in addiction (Rada, Avena & Hoebel, 2005; Widemam, Nadzam & Murphy, 2005).
Such behaviour mirrors tolerance in drug addiction, as dopaminergic reward circuitry decreases in sensitivity to the rewarding effect of sugar, such that the actual reward does not fulfil the expectation (Volkow, Wang & Baler, 2011; Davis, 2013). This effect can be evidenced by neuroimaging showing decreases in dopamine D2 receptors in the brain (Volkow et al., 2013). The decrease in dopamine sensitivity favours overconsumption to compensate for decreased reward-saliency from the substance (Volkow et al., 2013).
The fact that rats will overconsume in a fed, sated state (Alsiö et al., 2009) is consistent with addiction criterion of consuming more than intended. Deprivation of sugar precipitates withdrawal symptoms in rodents, and adverse psychological affects are observed in the form of anxiety and depression* (Avena, 2007; Colantuoni et al., 2002).
Thus, in an animal model of sugar, these characteristics closely resemble the neuro-behavioural patterns that define drug addiction (Davis, 2013). But animal model evidence does not always correspond to human evidence. The question is whether these patterns are features of the human data?
*How are anxiety and depression measured in rodents? A few tests are commonly used. One is an elevated, exposed runway in a T shape. If a rodent is anxious, they won’t venture out in the exposed space, while a happy out mouse will get curious and go walkabout. Another is a swim test to measure depression – the rodents are dropped into water. The happy ones will keep swimming trying to survive. The depressed ones will immobilise in the water and except their imminent demise. Moral of the story is, we owe a lot to these lil’ guys.
If we look at sugar addiction purely through the mechanisms of reward circuitry activation in the brain, there is substantial evidence of neurobiological similarities with drug addiction (Volkow et al., 2013; Hone-Blanchet & Fecteau, 2014). Decreased dopamine D2 receptors are observed both in drug addiction, and in persons with obesity (Wang et al., 2001), but these data do not separate cause from consequence. It remains a strong possibility that decreased dopaminergic sensitivity is a neurological adaptation to excessive stimulation by sugar (Davis, 2013).
A pattern of enhanced anticipation for sweet food, coupled with a corresponding decrease in satisfaction from consumption, is reflective of the neuronal activation in substance abuse (Hone-Blanchet & Fecteau, 2014). In animal models of bingeing, the dopamine response to standard rodent chow becomes blunted once novelty erodes, but both sugar and drugs elicit a response each time (Rada, Avena & Hoebel, 2005). The promotion of a positive feedback mechanism, in which sugar craving precipitates overeating, can result in that mechanism becoming resistant to change, and prone to relapse if sugar is refrained from for a time (Davis, 2013).
The difficulty with these neurobiological overlaps is that the behavioural patterns reflecting addiction are most compelling in the animal research, and do not overlap as clearly with the human data (Hone-Blanchet & Fecteau, 2014). Tolerance in drug addiction is assessed through intoxication, which is incomparable to aspects of food behaviour, in particular satiety (Hone-Blanchet & Fecteau, 2014). Indeed, a “low-satiety phenotype” has been identified in the literature, for whom increased consumption and loss of control may reflect impaired satiety mechanisms, and is thus distinguishable from a model of addiction (Dalton et al., 2015).
There is an absense of human data to support the existence of withdrawal symptoms from sugar (Hone-Blanchet & Fecteau, 2014). One of of the other criterion of addiction, increasing time spent seeking and acquiring a substance, is inapplicable to sugar due to its ubiquity in the food environment (Hone-Blanchet & Fecteau, 2014). Thus in comparing neurobiological changes to behaviours by reference to established models of addiction, there is a compelling argument for addictive properties of sugar, but key features of the addiction model are incomplete and/or weakly supported in human data (Avena, Rada & Hoebel, 2008; Avena, 2007; Hone-Blanchet & Fecteau, 2014).
A feature of drugs is that they undergo processing to increase concentrations of the addictive substance (Schulte, Avena & Gearhardt, 2015). The use of faster delivery methods is also a factor that increases the likelihood of abuse (Schulte, Avena & Gearhardt, 2015). Looking at sugar from a pharmacokinetic perspective, glycaemic load [GL] is strongly associated with problematic eating in individuals with a high YFAS score, reflecting both an increased quantity (dose) and absorption rate (delivery) that is consistent with an addictive pharmacokinetic profile (Schulte, Avena & Gearhardt, 2015).
It may be that individuals with a high YFAS score are more susceptible to addictive properties of sugar (Gearhardt, Corbin & Brownell, 2009). Subjects with a high YFAS demonstrate emotional dysregulation and high levels of depression, consistent with the relationship between addiction and adverse psychological outcomes (Gearhardt et al., 2013).
There are two sides to the brain reward system, which act in concert and may underlie the addictive potential of sugar. ‘Wanting’, driven by the neurotransmitter dopamine, and ‘liking’, driven by opioids and cannabinoids (Berridge, 2009). ‘Wanting’ triggers the intense urge for the food reward, while the opioid-driven ‘liking’ response conveys hedonic properties of food (Peciña & Berridge, 2013; Volkow, Wang & Baler, 2011).
In both lean and obese subjects with BED, ‘wanting’ is higher when already in the fed state, triggering increased consumption of sugar despite there being no self-perceived differences in appetite compared to non-binge eating controls (Dalton, Blundell & Finlayson, 2013). The low-satiety phenotype may thus be driven by ‘wanting’, as reward-motivated eating can override satiation (Berthoud & Morrison, 2008).
This favours overconsumption, as enhanced ‘liking’ is consistently associated with binge tendencies and increased energy consumption from sweet foods (Dalton, Blundell & Finlayson, 2013). In subjects with a high YFAS, sugar appears to disturb these control mechanisms resulting in a conditioned impulsive response, and lack of inhibitory control precipitates compulsive food intake (Schulte, Avena & Gearhardt, 2015; Dalton, Blundell & Finlayson, 2013; Volkow, Wang & Baler, 2011).
Not all obese persons with BED exhibit psychopathology different from obese non-binge types, other than enhanced responsiveness to hyper-palatability, while others fit a clinical profile resembling drug addiction by reference to the YFAS (Davis, 2013). Subjects with both BED and a high YFAS demonstrate emotional, cue-driven overeating, more severe binges and cravings, greater hedonic responsiveness, impulsivity and addictive personality traits (Davis, 2013b).
This profile does appear to be particularly sensitive to, and driven by, sugary foods (Schulte, Avena & Gearhardt, 2015; Dalton, Blundell & Finlayson, 2013). But a sensitivity or susceptibility to sugary foods does not by implication mean addictive. Despite neurobiological overlap with traditional models of addiction, and strong animal model data, current human evidence makes it difficult to differentiate addiction to sugar per se from a severe phenotype of BED (Hone-Blanchet & Fecteau, 2014; Davis, 2013).
This means, ultimately, that the potential for sugar to be considered addictive is at present confined to a severe manifestation of a very serious behavioural eating disorder. Not Instababes evangelically pushing “clean eating” on their hapless followers.
If sugar contributes a substantial proportion of your overall calories, then your health and body composition is definitely best served by making reductions.
But it is not inherently “toxic.” Nor does the evidence at present support that it is of itself addictive in humans. And this distinction is important, because BED is a serious, debilitating condition.
Sugar may drive overconsumption. It may be easy to consume in large amounts. It is certainly ubiquitous in the food environment.
But the chocolate brownie isn’t going to lead you to pour the Caster into your mouth. The important take-home message is this: as a small proportion of a well-balanced diet, some sugar intake is fine.
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