There are a multitude of studies in the last few years on sugar and its additive nature. I found one particularly useful because it discusses addiction properties and mechanisms as well as presents evidence on sugar. Like I have done it the past, I am going to summarize key points in bullet format. Hope this is useful for you!
* The researches wanted to explore whether or not sugar intake could cause an addiction by analyzing standard mechanisms behind addiction and comparing those to the effects of sugar. They look at 4 components of addiction (binging, withdrawal, cravings, and cross-sensitization) and compare these to sugar affected behavior since these behaviors are related to neurochemical changes in the brain that also happen with addictive drugs.
* The neural systems involved in food intake are also involved in drug-seeking.
* Rats were fasted for 12hrs daily then given access to a sugar solution and rat chow. The rats learn to drink the sugar solution in large amounts, especially when they first receive it. After 1 month, the rats showed signs of addictive behaviors. First, binging is displayed, followed by an opiate-like withdrawal which included anxiety, depression signs, and craving.
* One property of addictive drugs is their ability to increase extracellular dopamine. Sugar causes changes similar to opiates in the brain, and food withdrawal can lead to opiate-like withdrawal signs which include: a decrease in extracellular dopamine and and the release of acetylcholine.
* The researchers note that there is not a universal agreement of the definition of addiction, and traditional addiction research focused on “hard drugs”, but now research is being done on non-drug addictions such as gambling and sex. They mention that often, “addiction” is often used synonymously with “dependence”, which includes a psychological aspect and not just a physiological one.
* Diagnostic criteria for addiction includes three stages: binging, withdrawal, and craving. Also, behavioral sensitization is though to contribute.
* Addictive drugs activate dopamine containing neurons in the brain thus inducing behavioral reinforcement. Any substance that consistently causes a dopamine release or inhibits dopamine uptake may be a candidate for abuse. Foods or food products that cause dopamine release include: sugar, saccharin, and corn oil.
* Interesting to note that in satiated animals only experience this dopamine release in situations of novelty, but deprived animals who are fed sugar intermittently experience these dopamine releases consistently.
* Endogenous opioid systems interact with dopamine systems. Repeated use of opiates, and some non-opiate drugs, can cause a sensitivity with opiate receptor regions. Upon injection of opiate agonist, intake of food rich in fat and sugar increases, but when injected with an opiate antagonist, ingestion of sweet and palatable foods decreases.
* Also, several cholingergic systems are involved with food and drug intake and are involved with dopamine and endogenous opiate systems. Morphine, alcohol, and nicotine withdrawal all increase extracellular acetylcholine while decreasing dopamine. The researchers in this paper have concluded that acetylcholine acts as a “brake” causing a feeling of satiety when dopamine is high and behavioral depression when dopamine is low.
* Even though the idea of sugar addiction has been in the media for almost 20 years and there are numerous reports of people describing withdrawal symptoms from sugar rich foods, this phenomenon has only recently been studied in the laboratory.
* With addictive drugs, the length of daily access affects the rate of amount of self-administration, and those with limited access began to display compulsive behaviors and will binge on the substance upon first daily contact. Similarly with the sugar rats, even though the limited access sugar group and the ad lib sugar group both increased sugar intake (compared to control), the limited access group would binge on the sugar at first access and consume as much sugar in 12hrs as their ad lib counterparts did over a 24hr period. The rats with limited access would also consume less rat chow in favor of sugar calories.
* Opiate withdrawal in rats produces physical symptoms that include: decreased body temp, aggression, anxiety, and depression. These symptoms have also been observed when rats with intermittent sugar access have their sugar/food removed or they receive an opioid antagonist. Observations include: teeth chattering, fore paw tremor, head shakes, anxiety, behavioral depression, decreased body temp, and aggressive behaviors.
* Cravings in lab animals is determined by an enhanced motivation to obtain the substance is question, and animals will sometimes even face adverse consequences and abuse to obtain the substance. Not only did the researchers find that the motivation to obtain sugar continued through a two week period, but also the desire to obtain the sugar appeared to increase as as the abstinence period lengthened.
* Cross-sensitization is the increased sensitivity to substances other than the original substance, and this has been observed in drugs of abuse such as cocaine cross-sensitizing with alcohol and heroin with cannabis. This paper and others have report sugar cross-sensitizing with drugs of abuse, specifically amphetamines and cocaine.
* Drugs of abuse can not only alter dopamine and opioid receptors in regions of the brains, but also cause changes in gene expression of dopamine receptors. Similar brain changes were observed in rats given intermittent access to sugar.
* The researchers wanted to distinguish between dopamine release from food vs. sugar vs. drugs of abuse since dopamine is one of the strongest commonalities between sugar and drugs of abuse. When fed palatable food, dopamine increase wanes with repeated access when the food is no longer novel (unless food deprived), but this does not occur with sugar or drugs of abuse as dopamine is released every take of intake without waning. So, the researchers conclude that sugar acts more like a drug of abuse than a food.
* The researchers note that food does not normally act like a substance of abuse, but even though sugar is very common, it meets the criteria for a substance of abuse and could be addictive if consumed in a binge like manner.
* The researchers also mention there are some similarities between the intermittent sugar fed rats and people with binge-eating disorder and bulimia. They attempted to mimic the purging seen in bulimia by emptying the contents of the rats stomachs and observed that while there was a increase in dopamine, the acetylcholine “buffering” satiety response was eliminated, which caused the binging/purging to produce effects even more like a drug of addiction.
* Another important point is that several studies have correlated the surge in obesity to increased sugar intake. Sugar intake may increase the affinity/number of opioid receptors, leading to increased sugar intake, which may leads to obesity.
* All sugars are not created equal. The rats in this study were fed sucrose or glucose, but the same results may not happen with all sugars. Fructose is metabolized differently, being adsorbed lower in the intestine. While glucose causes an insulin release from the pancreas, fructose only stimulates the production of insulin but does not cause a release. Since insulin can inhibit eating, fructose intake may not result in the satiety than an equal amount of sucrose/glucose would, possible leading to a higher food intake.
In conclusion, the researchers point out that while desire for food is inherently related to survival from an evolutionary perspective, it can go awry, especially in obese or eating disordered people. Under certain circumstances, the behavioral and neurochemical changes of intermittent sugar access can resemble those brought about by substances of abuse. They hesitate in actually calling those with binge eating disorder or bulimia “food addicts”, and simple state that sugar can be an addictive substance.