Here's a report I wrote in 2013 about sugar addiction. And if you can't be bothered reading there's a video below summing it all up that my mate David Schaaf helped put together. As you can see we kind of got over it half way through... Enjoy!
There is a growing body of research around the affects of sugar on health. Sugar consumption has been linked to a number of chronic health problems, including obesity, diabetes, and cardiovascular disease (Alpert, 2012) as well as inducing all the diseases linked with metabolic syndrome (Lustig, Schmidt, & Brindis, 2012).
Several studies have associated the rapidly increasing rates of obesity and other non-communicable diseases with the rapidly increasing rates of sugar consumption. Lustig et al. (2012) state that sugar consumption has tripled worldwide over the past 50 years. In New Zealand the obesity rate has almost tripled over the past 35 years. In 1977, 10% of adults were obese, and a further 32% were already overweight (Ministry of Health [MoH], 2004). This increased to 29% of adults in 2011/2012, with a further 35% overweight (MoH, 2012). In other words, last year, 64% of the adult population in New Zealand was either overweight or obese.
Despite the knowledge that sugar, along with foods high in sugar, has the potential to lead to adverse health affects, sugar consumption continues to increase globally (Lustig et al., 2012). This has lead to the hypothesis that sugar may be capable of triggering an addictive process (Gearhardt, Roberts, & Ashe, 2013). In 1998, DesMaisons conceptualized the idea of sugar addiction and was later able to show sugar mimicked an analgesic drug (Alpert, 2012). Since then further studies have been executed indicating similarities between sugar, drug and alcohol addiction.
A number of neurochemical and behavioural commonalities between the consumption of sugar and substance abuse, such as cocaine, methamphetamine, nicotine and alcohol, have been established. This report will expand on the chief similarities in a means to answer the question; is sugar addictive?
The term “addiction” is often used synonymously with the term “dependence,” both of which do not have a universal agreement of the definitions. Addiction traditionally focused on substance abuse such as morphine, cocaine, nicotine and alcohol. However recently the term has shifted to include non-substance entities such as gambling, sex (Avena, Rada, & Hoebel, 2007), and in this report, sugar.
Potenza (2006) cites that “the core elements of addiction includes (1) craving state prior to behavioural engagement, or a compulsive engagement; (2) impaired control over behavioural engagement; and (3) continued behavioural engagement despite adverse consequences” (p. 143).
Sugar: What is it?
Carbohydrates are essentially sugars composed of carbon, hydrogen and oxygen molecules. Simple carbohydrates containing one to two sugar units include the monosaccharide’s glucose, fructose and galactose, and the disaccharides, formed when glucose bonds with another monosaccharide and produces either sucrose (glucose and fructose), lactose (glucose and galactose), or maltose (glucose and glucose). Polysaccharides are a form of complex carbohydrates as they can contain 1000 or more glucose units and are also referred to as starch. Another complex carbohydrate made up of polysaccharides includes fibre, however unlike the other monosaccharides, disaccharides and polysaccharides, fibre is indigestible in the human body (Wardlaw & Smith, 2013).
During digestion enzymes and gastric acid break down carbohydrates into their simplest form (Alpert, 2012) to be absorbed into the blood for use as energy, or to be stored as glycogen in the liver for the regulation of blood glucose levels (Wardlaw & Smith, 2013). Glucose is the body’s key source of energy, providing around 4 kilocalories or 16 kilojoules of energy per gram and is the main fuel source for some cells and tissues in the brain, nervous system and red blood cells (Wardlaw & Smith, 2013). Through glycolysis and eventually through the Krebs cycle glucose is oxidized to produce energy in the form of adenosine tri-phosphate (Alpert, 2012), a form of energy in which the body can utilize.
In this report the focus is on added sugars rather than all components of carbohydrates. The use of the term sugar will be referred to as sugars and/or syrups such as table sugar that is added to foods during preparation and processing as opposed to sugars naturally occurring in foods such as in fruit, vegetables and milk.
One of the strongest similarities between sugar consumption and drugs of abuse is the release of dopamine, a neurotransmitter that promotes pleasure, within the nucleus accumbens (Avena et al., 2007). This system is responsible for behavioural reinforcement and plays an important role in mediating reward-seeking effects to increase pleasure and/or decrease pain (Fortuna & Smelson, 2008).
Research using positron emission tomography (PET) scans show that drug abuse significantly increases dopamine turnover, that is, elevate extracellular dopamine levels in the nucleus accumbens, in cocaine dependent, methamphetamine dependent and alcohol dependent subjects (Fortuna & Smelson, 2008). Studies on obese subjects have shown a parallel dopamine response when bingeing on foods high in sugar (Fortuna & Smelson, 2008), that is excessively indulging on high sugary foods in a short time frame.
A decrease in dopamine turnover can occur after prolonged periods of bingeing on drugs in which the number of dopamine-2 receptors deplete (Fortuna & Smelson, 2008), a form of neurochemical sensitization to the substance. Individuals with low levels of dopamine and dopamine-2 receptors are known to have difficulty feeling good from normal life events, this is often “referred to as reward deficiency syndrome” (Fortuna & Smelson, 2008). It is suggested that drug-dependant individuals may self-administer the drug of choice to compensate for an underactive dopamine system. Which brings about the conclusion that any substance that causes the release of dopamine and thus a down regulation of dopamine-2 receptors has the potential for abuse (Fortuna, 2010). This is due to an increased state of pleasure from consuming the substance of abuse and compelling the individual to consume more (Lustig et al., 2012), generally in a binge like manner.
A lab study carried out on rats given 12 hour access to a sugar solution followed by 12 hours of deprivation (intermittent access), showed similar bingeing characteristics when sugar became accessible after the deprivation period, in particular, they would consume a large quantity of the sugar solution within the first hour of access (Avena et al., 2007). This bingeing behaviour resulted in an increase in dopamine release (Fortuna, 2010), mimicking the dopamine response seen in drug dependent subjects following a period of withdrawal.
The same dynamic has been seen in obese individuals that continuously binge on sugar; dopamine-2 receptors down regulate to lower than normal levels which predisposes the individual to self-medicate with sweets in order to reobtain a pleasurable state (Fortuna & Smelson, 2008). Sugar also increases central production of serotonin, a neurotransmitter that has an antidepressant and calming effect, which can contribute to the act of searching-of and self-medicating with ‘comfort foods’ (Fortuna, 2010) to elevate ones mood in a means to counterbalance a reduction of dopamine turnover.
Another interesting result in the study on rats found that one of the control groups, fed sugar ad libitum, developed a blunted dopamine response to the sugar solution as the novelty of sugar became ordinary (Avena et al., 2007). The exception to this was if the animal was food deprived, in which the dopamine response would again pick up during sugar consumption (Avena et al., 2007). In contrast, drugs of abuse exert their effects on dopamine release each time they are administered. This suggests that unlike drugs of abuse, the dopamine response phases out during sugar consumption parallel to the novelty of the food, unless in a state of starvation (Avena et al., 2007).
An increase of acetylcholine within the nucleus accumbens simultaneously lowers dopamine (Avena et al., 2007). This dopamine-acetylcholine seesaw is associated with behavioural depression, that is, when acetylcholine levels are high and dopamine levels are low, a sense of depression is expressed, and when acetylcholine levels are low and dopamine levels are high there is a sense of satiety (Avena et al., 2007). The withdrawal of addictive substances such as morphine, nicotine and alcohol on dependent individuals, result in an increase of acetylcholine release, consequently decreasing dopamine and causing behavioural depression (Avena et al., 2007).
This dopamine-acetylcholine imbalance has been studied in rats forced to abstain from morphine or alcohol, which resulted in increased acetylcholine and a decreased dopamine levels within the nucleus accumbens (Avena et al., 2007). Another study with rats given intermittent access to sugar also resulted in alterations in the dopamine-acetylcholine balance during withdrawal, of which food was deprived for 36 hours (Avena et al., 2007).
Avena et al. (2007) cites that there are three distinct behavioural stages in which dependence is diagnosed; this includes bingeing, withdrawal and craving. Bingeing on sugar has a drug-like effect in the nucleus accumbens due to the acute effects of dopamine release and chronic changes with the sensitisation of dopamine-2 receptors (Fortuna & Smelson, 2008). Both acute and chronic effects lead to individuals craving their substance of choice. Craving is personally perceived following a period of abstinence or involuntary withdrawal of the substance (Avena et al., 2007), resulting in an increase of acetylcholine and decreased dopamine turnover (Fortuna, 2010). This places the individual in a state of depression (Avena et al., 2007). Craving triggers compulsive behaviour to use the substance again to resecure a positive state (Fortuna & Smelson, 2008). This becomes a vicious cycle where the individual binges on the substance, builds up tolerance to the effects and becomes sensitised to dopamine-2 receptors, therefore needing more of the substance to recreate the same sensations, followed by craving and compulsion to use the substance again (Avena et al., 2007; Fortuna & Smelson, 2008).
Food is essential for survival and does not normally resemble a substance of abuse. However, the creation of refined sugar has exploited a natural substance present in food, to stimulate neurochemical changes within the brain, thereby acting more like an addictive drug. Studies have shown similarities in both neurochemical and behavioural effects between intermittent sugar consumption and drug and alcohol abuse. Sugar meets many of the criteria to be classified for a substance of abuse and can be addictive to some individuals when consumed in a binge-like manner, triggering the binging-withdrawal-craving cycle. Due to studies looking at sugar addiction chiefly involving animal subjects, it is unclear how these results would translate to humans. Further studies involving human subjects would need to be carried out to provide sufficient evidence in this area. However, it has been demonstrated that rats with intermittent access to sugar show behavioural and neurochemical commonalities that parallel substance dependent rats that voluntarily self-administer addictive drugs. In conclusion, these animal models provide evidence that sugar can be addictive.
Alpert, P. T. (2012). Sugar: The Good, the Bad, and the Ugly Facts. Home Health Care Management & Practice, 24 (4), 208-210. DOI: 10.1177/1084822312441703
Avena, N. M., Rada, P., & Hoebel, B. G. (2007). Evidence for Sugar Addiction: Behavioural and Neurochemical Effects of Intermittent, Excessive Sugar Intake. Neuroscience and Biobehavioral Reviews, 32, 20-39. DOI: 10.1016/j.neubiorev.2007.04.019
Fortuna, J. L. (2010). Sweet Preference, Sugar Addiction and the Familial History of Alcohol Dependence: Shared Neural Pathways and Genes. Journal of Psychoatic Drugs, 42 (2), 147-151. DOI: 10.1080/02791072.2010.10400687
Fortuna, J. L., & Smelson, D. A. (2008). The Phenomenon of Drug Craving. Journal of Psychoactive Drugs, 40 (3), 255-261. DOI: 1080/02791072.2008.10400640
Gearhardt, A., Roberts, M., & Ashe, M. (2013). If Sugar Is Addictive...What does It Mean for the Law? Journal of Law, Medicine & Ethics, 41, 46-49. DOI: 10.1111/jlme.12038
Lustig, R. H., Schmidt, L. A., & Brindis, C. D. (2012). The Toxic Truth About Sugar. Nature, 482 (7383), 27-29. DOI: 10.1038/482027a
Ministry of Health. (2012). The Health of New Zealand Adults 2011/12: Key findings of the New Zealand Health Survey. Wellington: Ministry of Health.
Ministry of Health. (2004). Tracking the Obesity Epidemic: New Zealand 1977-2003. Wellington: Ministry of Health.
Potenza, M. N. (2006). Should Addictive Disorders Include Non-Substance-Related Conditions? Addiction, 101 (Suppl. 1), 142-151. DOI: 10.1111/j.1360-0443.2006.01591.x
Wardlaw, G. M., & Smith, A. M. (2013). Wardlaw's Nutrition. NSW: Mc-Graw-Hill Australia
Just another health and fitness professional putting in their 2 cents. 2 cents may be all you need one day.