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Daily RC Article 360

Unveiling the Bittersweet Truth: The Neuroscience of Sugar Addiction


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“The first few days are a little rough,” Andrew told me about his sugar-free adventure. “It almost feels like you’re detoxing from drugs. I found myself eating a lot of carbs to compensate for the lack of sugar.” There are four major components of addiction: bingeing, withdrawal, craving, and cross-sensitisation (the notion that one addictive substance predisposes someone to becoming addicted to another). All of these components have been observed in animal models of addiction – for sugar, as well as drugs of abuse. A typical experiment goes like this: rats are deprived of food for 12 hours each day, then given 12 hours of access to a sugary solution and regular chow. After a month of following this daily pattern, rats display behaviours similar to those on drugs of abuse. They’ll binge on the sugar solution in a short period of time, much more than their regular food. They also show signs of anxiety and depression during the food deprivation period. Many sugar-treated rats who are later exposed to drugs, such as cocaine, demonstrate dependent behaviours towards the drugs compared to rats who did not consume sugar beforehand.

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Like drugs, sugar spikes dopamine release in the brain. Over the long term, regular sugar consumption actually changes the gene expression and availability of dopamine receptors in the brain. Specifically, sugar increases the concentration of a type of excitatory receptor called D1, but decreases another receptor type called D2, which is inhibitory. In short, this means that repeated access to sugar over time leads to prolonged dopamine signalling, greater excitation of the brain and a need for even more sugar to activate all of the dopamine receptors like before. The brain becomes tolerant to sugar – and more is needed to attain the same “sugar high.” In a related study, rats that had undergone a typical sugar dependence protocol then underwent “sugar withdrawal.” This was facilitated by either food deprivation or treatment with naloxone, a drug used for treating opiate addiction which binds to receptors in the brain. Both withdrawal methods led to physical problems, including teeth chattering, paw tremors, and head shaking. Naloxone treatment also appeared to make the rats more anxious, as they spent less time on an elevated apparatus that lacked walls on either side.

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Another study reports that sugar withdrawal is also linked to impulsive behaviour. Initially, rats were trained to receive water by pushing a lever. After training, the animals returned to their home cages and had access to a sugar solution and water, or just water alone. After 30 days, when rats were again given the opportunity to press a lever for water, those who had become dependent on sugar pressed the lever significantly more times than others. These are extreme experiments, of course. We humans aren’t depriving ourselves of food for 12 hours and then allowing ourselves to binge on sugar at the end of the day. However, it’s not far-fetched to say that the same primitive processes are occurring in the human brain, too. They certainly give us insight into the neuro-chemical underpinnings of sugar dependence, withdrawal, and behaviour.

Sugar addiction shares striking parallels with drug addiction, as evidenced by animal studies. Rats subjected to sugar binges exhibit behaviors akin to drug dependence, including bingeing, withdrawal symptoms, cravings, and cross-sensitization. Sugar consumption triggers dopamine release, altering brain chemistry and gene expression, leading to tolerance and increased cravings. Withdrawal from sugar induces physical symptoms and impulsive behavior in rats. While human sugar consumption differs from these extreme experiments, the neuroscience sheds light on the mechanisms of sugar dependence and withdrawal.
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