I have been an athlete my entire life, and in being one, I have always justified my high-sugar diet. I ate the cupcake, candy bar, or brownie because on a given day, I had either already “earned it” or was going to make sure I “burned it off”. I thought that because I didn’t gamble, drink heavily, or smoke, I was clear from the risk of addiction. However, as both research and personal anecdotes can conclude, sugar and processed food addiction is very real.
It all comes down to the dopamine rush experienced when we eat ultra-processed foods (UPFS) or foods high in sugar. Although a shot of sugar is much less extreme than a kick from a drug, the neurological processes that are involved are still similar. Typically, a drug provides a euphoric feeling through an intense dopamine rush which activates our brain’s reward system. Sugar, to a much lesser extent (nobody gets high from sugar) has a similar effect. One theory for why this is the case was discussed in Dr. Hampton’s PSYC 110 – because our ancestors received an extremely beneficial energy rush from naturally occurring sugars, genes which expressed sugar-seeking and sugar-rewarding behaviors were more likely to be passed on to following generations. This results in the sugar reward pathways we as humans have now. Like with reward pathways in other vices, continued use of the stimulus desensitizes the pathway, leading to cravings and more intense use.
To investigate these questions behind sugar, Elsevier published a research paper in which rats were exposed to a human-like sugar consumption schedule, with binge and access restriction periods. There was also a control group and “amphetamine group”, included to see if sugar could produce drug-like addictive tendencies. The dopamine was measured in their brains using microdialysis, and the results show that sugar rats had similar behavior and dopamine fluctuations as the amphetamine group, but to a lesser extent. This proves that sugar intake can trigger neurochemical changes similar to those seen in drug addiction, particularly in the dopamine system. Repeated sugar intake leads to increased dopamine release in the nucleus accumbens, and the brain’s reward system adapts to excessive sugar intake.
The University of Michigan posed a similar question of whether abstaining from sugar could cause drug-like withdrawal, this time using self-reported data from humans. They selected 231 volunteers to participate in a study in which all UPFs (including most forms of sugar) were eliminated, even including many sugar-dense fruits, to increase difficulty. Participants self-reported their following symptoms on the ProWS, a food withdrawal scale that the paper introduced. The results of the study had clear implications – 82% of participants felt strong withdrawal symptoms, including headaches, anxiety, intense cravings, mood swings, nausea, and fatigue.
However, the paper introduced a second complexity – those who endured the symptoms for over a week reported them as beginning to fade and eventually going away entirely. This points to an interesting idea of how the symptoms specifically can be interpreted. By withholding energy in the form of UPFs, the brain (which has been regulated to its presence) enters a state of dopamine dysregulation and confusion. The brain activates our sympathetic nervous system, a neural alarm, resulting in activation of some “fight or flight” symptoms and lower dendritic release of dopamine. However, as we adjust to our body’s new equilibrium state, the neural alarm turns off, and symptoms fade.
The science is clear – sugar can be addictive and produce withdrawal symptoms. Understanding this fact can have major implications on our health, including the way we approach our diet and treat obesity.
Sources:
Rada, P., et al. “Daily Bingeing on Sugar Repeatedly Releases Dopamine in the Accumbens Shell.” Neuroscience, vol. 134, no. 3, Jan. 2005, pp. 737–744, doi.org/10.1016/j.neuroscience.2005.04.043.
Parnarouskis, Lindsey, et al. “Withdrawal: A Key Consideration in Evaluating Whether Highly Processed Foods Are Addictive.” Obesity Reviews, vol. 23, no. 11, 5 Oct. 2022, https://doi.org/10.1111/obr.13507
Ford, C. P., et al. “Control of Extracellular Dopamine at Dendrite and Axon Terminals.” Journal of Neuroscience, vol. 30, no. 20, 19 May 2010, pp. 6975–6983, www.ncbi.nlm.nih.gov/pmc/articles/PMC2883253
Cleveland Clinic. “Parasympathetic Nervous System (PSNS): What It Is & Function.” Cleveland Clinic, Cleveland Clinic, 6 June 2022, my.clevelandclinic.org/health/body/23266-parasympathetic-nervous-system-psns.