In the midst of a pandemic, social networking sites (SNS) have been pivotal in maintaining our social lives, but offer convenient distractions that drain productivity and deteriorate mental health. Yet, even before the pandemic, social media addiction, characterized by the uncontrollable use of social media, has been a prevalent yet mysterious problem due to unknown neurobiological mechanisms. Much like the parallels observed between drug addictions and other behavioral addictions, there is a clear link between dopamine, triggered by rewards such as “likes,” reinforcing the irresistible draw towards social media. Scientists speculate that social media addiction can lead to a decrease in dopamine receptor density, release, and binding. By understanding the changes to the dopaminergic pathway, scientists can promptly point out more effective treatments to guide individuals in regulating healthy social media usage.
From an evolutionary perspective, seeking social interactions is classified as a primary drive. The drive to maintain social bonds is a type of goal-oriented social behavior, regulated by the neurotransmitter dopamine secreted in the nucleus accumbens (NAcc), a region in the ventral striatum and a major aspect of the 37 reward system. Dopamine released from the striatum mediates the conditioned response after repeated exposure to social stimuli, which produces a positive emotion that motivates continued social behaviors [1]. Through sharing aspects of our lives, we find that doing the same to connect on social media platforms not only conveniently satisfies our fundamental social needs, but also easily reinforces continued use.
Maintaining reputation in society is also considered a social reward-driven by natural selection. “Likes” on SNS platforms easily become a form of currency that quantifies online popularity and delineates social reputation. Across all age groups, the instant gratification received from each “like'' increases activity in the striatum [2]. A “like” provides positive feedback for the recipient, thus indicating a positive view for the particular user and their reputation. This can also be seen in how individuals tend to give “likes” to popular posts, even to those portraying illegal behaviors, suggesting that the number of ‘likes’ can change the other’s perception of a post [3]. In other words, “likes” are strong social rewards that can reinforce social behavior by signifying acceptance from others in society. Because the striatum also encodes for habitual behavior, when “likes” activate the reward system encompassing the NAcc and the striatum, the positive feedback loop that drives social interactions is initially enhanced, eventually shifting to neural circuits that reinforce habitual use in the same region [4]. Knowing the reward circuitry is mediated by dopamine, excessive social media use may thereby have significant effects on dopamine function.
To better understand social media addictions, compulsive behavior can be drawn in parallel to other addictions, the most well-known being substance abuse. Disrupted dopamine function has been reported through a series of PET scans that consistently demonstrate at least a 20% decrease in D2 dopamine release and receptors in addicts’ striatum [5, 6]. Yet, these results are repeatedly demonstrated with other various behavioral addictions without the influence of chemical substances. Both internet addicts and patients with morbid overeating tendencies were found to have a lower D2 dopamine receptor density [7, 8]. Moreover, PET scans in pathological gamblers reveal decreased dopamine binding potential in the ventral striatum [9]. Thus, these findings, when taken together, suggest how behavioral addictions are also similar to substance addiction, especially via alterations in dopamine function. Because striatal dopamine regulates the saliency and motivation for rewards, the reduced striatal dopamine release along with decreased dopamine receptors may overall account for decreased sensitivity of the reward circuit to other “natural” reinforcers in addicted patients [5]. Therefore, this could explain why the subject will continually seek the ‘reward’ despite the detrimental effects to stimulate the same pleasurable “high” in the disrupted dopaminergic pathways. Seeing how social media addiction is also a form of behavioral addiction characterized by tolerance and withdrawal symptoms, long-term excessive social media usage may also lead to the same lowered dopamine release, binding, and receptor density.
Thus, altered dopamine function may affect projections to other components in the reward system that explain the increasing correlation with mental health disorders such as depression and anxiety. Catalyzed by the pandemic, some may start prioritizing the virtual media platform instead of in-person interactions as a coping mechanism [10]. Furthermore, there is an increased fear of missing out (FOMO), leading to anxiety whenever one is disconnected from the virtual world [11]. By finding out how longterm social media addiction affects dopamine neurologically, scientists can point to more effective treatments to prevent the commonly experienced symptoms. As society increases the reliance on social media, understanding the neurological impacts becomes even more important to guide healthy social media usage and bring awareness to our wellbeing.
References:
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