The science of sugar addiction

The science of sugar addiction?

There are some reservations surrounding sugar addiction. Some wonder if habitual overconsumption of sugar-rich food is an actual behavioural addiction similar to compulsive gambling or sexual perversion. Furthermore, unlike substance addiction, it is impossible to completely gear away from sugar because it is an essential source of energy.

However, it is important to take note of the fact that a diet high in sugar or carbohydrates has been associated with myriads of health issues ranging from changes in brain structure and function and accelerated aging or development of age-related diseases.

Sugar addiction, as demonstrated by compulsive sugar overconsumption, is still a possibility according to experts. A study and literature review by researchers N. M. Avena, P. Rada, and B. G. Hoebel explored and discussed the behavioural and neural mechanisms underlying strong urges to eat sugar-rich foods.

Accordingly, food addiction seems probable because food consumption activates neural systems or brain pathways that previously evolved to respond to natural rewards. Addictive drugs such as cocaine and heroin activate these same pathways. Furthermore, take note that the consumption of sugar-rich food releases opioids and dopamine. Thus, it seems reasonable to argue for the addictive potential of sugar.

Similarities between sugar addiction and drug addiction

Researchers Avena et al summarised the evidence for sugar addiction using an animal model. They also referenced and analysed four known components of addiction: bingeing, withdrawal, craving, and cross-sensitisation. This analysis drew comparison between sugar addiction and drug addiction.

The animal model involved depriving rats of food for a 12-hour period before giving them a 12-hour access to a sugar solution and chow after a 4-hour delay based on their circadian-driven active period. This cycle of deprivation and overconsumption or intermittent feeding schedule lasted for a month. Results demonstrated that rats learned to drink the sugar solution copiously, particularly when it first became available each day.

Using the four components of addiction as basis of analysis, the researchers found that the rats also demonstrated behaviours similar to the effects of drug abuse. Bingeing was indicative of unusually large bouts of sugar intake and opioid-like withdrawal by the presence of anxiety and behavioural depression. The researchers also determined craving by observing response to sugar after abstinence while they also observed signs of both locomotor and consummatory cross-sensitisation from sugars to addictive drugs.

The four components of addiction were nonetheless present in rats that underwent a sugar-based intermittent feeding schedule. To a certain extent, there are similarities between sugar addiction and drug addiction.

Avena et al further explored why these behaviours emerged from the experimented animals by reviewing similar studies undertaken in the past. The literature review revealed that lab rats with intermittent access to sugar were more likely to drink a sugar solution in a binge-like manner. This feeding behaviour triggered the release of the neurochemical dopamine.

Take note that addictive drugs have the capacity to cause a repeated and intermittent increase in extracellular dopamine level in the nucleus accumbens—a region in the basal forebrain rostral to the preoptic area of the hypothalamus that plays a critical role in the cognitive processing of aversion, motivation, pleasure, reward, and reinforcement learning. In other words, this region of the brain plays a significant role in addiction.

The same intermittent sugar intake results in changes in the opioid systems of rats as demonstrated by a decrease in encephalin mRNA expression in the accumbens. The researchers noted that sugar deprivation is also sufficient to trigger signs of opiate-like withdrawal as determined by at least two neurochemical manifestations. The first is a decrease in extracellular dopamine in accumbens and the second is the release of acetylcholine from accumbens interneurons. These neurochemical manifestations in response to intermittent sugar intake are nonetheless similar to the effects of opiates.

Based from their findings, Avena et al theorised that the intermittent and excessive intake of sugar can have a dopaminergic, cholinergic, and opioid effects. These effects are similar with the neurochemical mechanisms triggered by psychoactive drugs. However, the researchers noted that the effects of intermittent overconsumption of sugar are smaller in magnitude compared to the effects of addictive drugs.

Sweet addiction rather than sugar addiction

There are indeed evidences that intermittent overconsumption of sugar results in behaviours and neurochemical mechanisms that are similar with the effects of addictive drugs. However, it is still unclear whether the chemical composition of sugar causes these addiction-like behavioural and neural manifestations.

A study by Magalie Lenoir et al reported that it is not sugar that is addictive but rather the sweet taste. Their study involved rats that were free to choose between a calorie-free water solution artificially sweetened with saccharin and intravenous cocaine. Results revealed that 90 percent of the studied rats preferred the sweet taste of saccharin. The researchers noted that this preference was also similar to options between a sucrose water solution and intravenous cocaine.

Based on their findings,Lenoir et al concluded that intense sweetness surpasses cocaine reward. This is also true even in drug-sensitised and drug-addicted subjects.

The predisposition toward addiction to sweetness might have an evolutionary underpinning according to the researchers. In addition, they hypothesised that the addictive potential of intense sweetness could have come from an inborn hypersensitivity to sweet taste.

Most mammals including humans and rodents have sweet receptors that evolved from environments that lacked easy access to sugars or carbohydrates. This made them poorly adapted to food with high sugar tastants. Because high-sugar food and sweet additives have bombarded the diet of modern societies, high-sugar consumption produces a supranormal reward signal in the brain.

The neural response produced by overconsumption of sugar has a potential to override the self-control mechanisms and thereby lead to addiction. Remember that common notions about addiction centre on habits or behaviours characterised by compulsive engagement in rewarding stimuli, despite adverse consequences.

Further details of the study of Avena et al are in the article “Evidence of Sugar Addiction: Behavioural and Neurochemical Effects of Intermittent, Excessive Sugar Intake” published in 2008 in the journal Neuroscience Behavioural Review. Details of the study of Lenoir et al are in the article “Intense Sweetness Surpasses Cocaine Reward” published in 2007 in the journal PLOS One.

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