by Nina van Santvoort, Research Intern Resist Project

Over the course of the last decades, a paradigm shift has occurred in how antisocial behavior is generally perceived. Whilst before a social-cultural approach was used to explain antisocial behavior, it is now viewed in a more holistic light, focusing on social, and genetic and biological components. Dissecting how all these different factors combine and interact in the development of antisocial behavior, however, remains a challenge. Looking through a lens of biology, it has been establish that brain development plays a role in the predisposition to engage in externalizing , aggressive, and antisocial behaviors. But by taking a biological view on antisocial behavior, caution is warranted that the pendulum of antisocial behavior is not slowly swinging us back to Lombroso; heading toward a fatalistic adage that people who show an inclination to antisocial behavior were simply ‘born this way’.
The environment can shape one’s biological infrastructure. Through a process called epigenetics, the environment can affect a person’s genetic make-up and alter biological and neural structures, which in turn increases the chance of antisocial development. Be that as it may, the environment can also act as a protective factor, decreasing this chance. To understand the development of antisocial behavior it is therefore crucial to view antisocial behavior, and its biological correlates, holistically and as malleable, alterable phenomena.

As Told by Genes
Genes are short segments of DNA. The genome contains all these genetic parts and forms the “blueprint” for our features and characteristics. The human genome is similar in every human being, but not completely the same; genetic polymorphisms (variants) determine the diversity between different individuals due to distinct DNA sequence variations. Studies investigating the role of genotypes in the development of antisocial behavior suggest that particular genes may contribute to the development and maintenance of antisocial behavior. This means that, having a particular gene, or set of genes, could increase a person’s susceptibility to develop antisocial behavior. Take for instance, the MAOA gene. MAOA is an enzyme that breaks down serotonin. It appears that different levels of MAOA, which are caused by different genetic polymorphisms, either increase or decrease the risk of aggressive behavior. It was shown that low levels of MAOA are associated with later antisocial behavior. Moreover, a study by Guo et al. (2008) demonstrated that a very specific MAOA gene variant called VNTR, which causes extremely low levels of MAOA, even results in twice as much violence in adolescence and young adulthood compared to control subjects without the VNTR variant.

Serotonin has an inhibitory function on the brain and is involved in the regulation of impulsive and aggressive behavior. Like MAOA, other genetic variations also appear to play a role in the serotonergic contribution to aggression and antisocial behavior. For example, the short allele version of 5-HTTLPR has been linked to low serotonin production. Studies indeed show that antisocial groups demonstrate significantly lower levels of serotonin metabolite 5HTT compared to non-antisocial controls. These findings may be interpreted as such that low serotonin is associated with antisocial behavior as it results in dysfunctional emotion regulation and impaired impulse control. Interestingly though, since antisocial behavior is very heterogeneous and manifests itself differently in different individuals, it is believed distinct variations in genes that result in altered neurotransmitter systems underlie distinct subtypes of antisocial behavior. Referring back to the previous example, a divergent pattern of 5-HTTLPR genes has been found based on the level of callous-unemotional traits: whilst the short allele has often been implicated in increased impulsivity, a link was shown between the long allele and youths with conduct disorder high on callous-unemotional traits. These findings emphasize the significance of understanding different etiologies, neural bases, and behavioral indices.

However, attention must be paid to the interpretation of these findings. Meta-analyses show that the association between specific genes independently and aggression are too weak to be utilized as predictors of violent behavior. As we will see, the genetic contribution to antisocial behavior must be seen in a much wider context.

A Plastic Genome
Thus, genetic influences on antisocial behavior are not that simple. Firstly, the magnitude of the expression of genes depend heavily on many more factors, including a ton of environmental ones as well. As an example, let’s go back to MAOA; the gene that has been linked to antisocial behavior. What if this genetic risk factor were to be combined with adverse social-environmental factors? A longitudinal study by Caspi and Moffitt (2002) showed that children who were maltreated and simultaneously showed low levels of MAOA were more likely engage in antisocial behavior than maltreated children with high levels of MAOA. However, children who were not maltreated but did have low levels of MAOA showed no higher inclination to antisocial behavior. That is, MAOA alone cannot predict antisocial behavior. Only in tandem with adverse environmental factors does there appear to be an association. The results of the study indicate that individual genes are indeed important, but more so in a particular context.
Moreover, heritability estimates are statistical descriptions of variances based on group level findings. Meaning, when genetic risks are calculated for an entire group, it cannot be used as a predictor for the risk of one specific individual’s propensity to antisocial behavior. Lastly, whilst gene studies can inform about what proportion of antisocial is explained by genetic factors, twin and adoption studies show that genetic factors can only explain 50% of the variance in antisocial behavior. This means that the other 50% must be attributed to environmental factors.

Hence, heritability does not imply genetic determinism. Studies investigating the effects of genetic, biological, and environmental factors within the development of antisocial behavior indicate that all factors interact in predisposing a person to antisocial behavior. This means that, although certain genetic and biological make-ups may naturally lead to a higher propensity to antisocial behavior, it also works the other way around: the environment can actually alter gene expression through DNA modification. Thus, whilst we tend to conceive genes as fixed and static, they are very malleable.
The process of the environment modifying genetic expression is called epigenetics. Generally, epigenetics plays a central role in the adaptation of humans to their environments. For the development of antisocial behavior, this means that experiences in the environment may modify the gene expression, so that it could result in the generation of new neural trajectories that can increase someone’s susceptibility to develop antisocial behavior. A multitude of research studies suggest that external factors such as early post-natal and childhood adversities interfere with neural development, affecting biochemical pathways. Take for example, maternal care. Research suggests that maternal responsiveness in early childhood could have a big effect of later outcomes through the mechanisms of epigenetics. A study by Provenzi et al. (2019) demonstrated that appropriate maternal caregiving affected DNA methylation in infants. Maternal touch appeared to be an environmental proxy that could protect the child by affecting genes such as SCL6A4 (the serotonin transporter gene of formerly discussed polymorphism 5-HTTLPR).

Risk and Protective Factors
These modifications of gene expression can be placed in a much wider context of how different kinds of factors may give rise to the development of antisocial behavior or protect against it. It is clear that the social environment is a vital agent in shaping the brain toward or away from antisocial behavior. The developmental stage during which youth are exposed to certain risk factors that could result in the onset of antisocial behavior is important in order to identify corresponding protective factors that may prevent its onset. Family factors such as birth complications, inconsistent responsiveness from parents, and parental substance abuse matter the most in early childhood. During adolescence it is important that the person has access to healthy peer relationships and is provided with the appropriate responsiveness from the school and the community. In fact, lower affiliation with delinquent peers even resulted in a heightened resilience to the exposure to family adversity. But also nutrition may offset the development of antisocial behavior amongst youth. For example, a nutritional intervention rich in omega-3 has been linked to reduced levels of aggression. Results showed a long-and short-term decline of aggression in a sample of youth aged 8-16 after 3 months of omega-3 supplementation. This was also the case for youth characterized by callous-unemotional traits. However, the exact mechanisms on why this works are yet to be investigated.

Conclusion
Genetic and biological research can contribute to the understanding of the development of antisocial behavior. Yet, what ought to be prevented is that it creates a defeatist attitude. Research demonstrates that one should not turn a blind eye to the social and environmental factors affecting a developmental predisposition to antisocial behavior. Taking into account social factors will also prevent ethical quandaries stemming from an inaccurate and defeatist ‘biology equals destiny’ attitude.
Though, a pre-emptive strike can be made with the further investigation of the biological and genetic correlates of antisocial behavior and the development of neuro-treatment. Still, the social environment is key in understanding, preventing, and altering the trajectory toward antisocial behavior. Given the heterogeneity of youths affected by antisocial behavior, it is crucial to understand the influence of particular social-environmental effects per developmental stage on the specific neurochemical and neurobiological correlates that tend to typify certain subgroups of youths with antisocial behavior. Understanding the specificities of antisocial behavior, and paying attention to the differentiated genetic, biological, social-environmental effects on its development, will also aid in the development of targeted intervention efforts that may increase resilience and decrease vulnerability of youth prone to maladaptive antisocial development.

by Nina van Santvoort, Research Intern Resist Project

Adopted into a loving home in Oklahoma, Jeffrey Landrigan was provided a safe and nurturing environment. Yet, at 11 years of age Jeffrey was already arrested for burglary. Nine years later, Jeffrey was sentenced for second-degree murder of his childhood friend. What dark shadows cast over Jeffrey, resulting in his rapid path to violence?

On any given day, you may encounter such news stories about violent acts committed by youth. An extraordinary portion of these violent acts, however, can be accounted for by only small number of youths. What produces this type of behavior? Why do some youths commit violent acts whilst others do not? Research now shows that the roots of pervasive and continuous externalizing behavior amongst youth may be partially explained by underlying neurodevelopmental markers. Jeffrey met his biological father, who killed twice, in prison. Given Jeffrey’s adoption, may there be a biological contribution to his antisocial behavior? Research shows that a various set of brain regions, if dysfunctional, could predispose a person to antisocial behavior. Abnormal responsivity in the amygdala as triggered by provoking cues, and the failure of the frontal regions to exert regulatory control appear to play a vital role in the display of aggressive acts.

The Brain’s Homeland Security System
The amygdala, which stems from the Greek word amýgdalo, is an almond-shaped structure in the medial temporal lobes of the brain. When the sensory areas of the brain sense something in the environment, the amygdala receives a rough copy of whatever it is that the brain is sensing and subsequently checks whether it is threatening or not. Consequently, it may send out a flight or fight response. Additionally, the amygdala is involved in the ability to recognize when someone else is in a state of fear. Yet, for this almond-like structure in the brain to appropriately support emotional learning, this burglar alarm cannot run all by itself.

Hence, whilst the visual or auditory sensory system is further processing a signal, and thus attaining more detail, another note is send up to the frontal cortex. As the name implies, the frontal cortex is positioned at the very front of the brain. One of the tasks of the frontal cortex is help to coordinate your behavior. It makes sure that you behave appropriately in the current context. If the situation is safe, it can tell the amygdala to calm down; it can, so to speak, turn off the brain’s homeland security system and stop the flight or fight response originating from the amygdala. The connections between the amygdala and the prefrontal cortex (PFC) are believed to form the foundation of emotional regulation behaviors. In maturity, the amygdala has very strong bi-directional connections with the PFC that by and large facilitate coordination of its inputs; often for the purposes of regulating its signals.

A brainy bias to antisocial behavior
So, why is it that adolescents characterized by conduct problems find it particularly difficult to regulate and control their emotional responses? Neuroimaging research on the neurobiology of antisocial behavior discovered that the parts of the brain that are normally involved in emotion regulation, such as the amygdala and areas of the prefrontal cortex, are atypical in these youths. An imbalance between these two regions could impair emotion regulation. If functioning properly, the frontal cortex keeps a lid on the amygdala, making sure that the emotions do not boil over. Reduced frontal functioning results in a lack of control over the amygdala, resulting in extreme emotions such as anger, rage and fear; increasing the likelihood of one behaving aggressively.

Recently, researchers have investigated the functional coupling between the amygdala and the frontal cortex. It was shown that the strength of the connectivity between the amygdala and the frontal regions of the brain could predict successful emotion regulation. This suggests a top-down regulatory effect of the prefrontal cortex on the amygdala. Extending this to antisocial behavior, fMRI results of a study investigating the connectivity in a sample of violent offenders found a significant decrease in amygdala-frontal cortex connectivity and increased connectivity between the amygdala and other limbic areas. The opposite was found for non-offender controls. Complementary, Passamonti and colleagues (2012) found that the uncinate fascicle, which is a bundle of white matter tracts that connect the amygdala to the frontal areas (particularly the orbitofrontal cortex), shows structural abnormalities in adolescents with conduct disorder, further indicating atypical communication between the areas. 

Taken together, research demonstrates that abnormalities in communication between the amygdala and the frontal cortex could disrupt emotion regulation, and may therefore predispose an individual to antisocial behavior.

Heterogeneity in conduct disorder
Whilst advances in brain imaging technology have thus allowed neuroscientists and neuropsychologists to look under the hood of aggressive juveniles, the (neural) roadmap to antisocial behavior and aggressive acts may be different per individual.

Different forms of antisocial behavior seem to coincide with different neural bases. For example, a body of imaging research demonstrates that youths with conduct disorder high on callous-unemotional traits are typified by low reactivity to negative emotional cues, as signified by low amygdala activity. These youths also show an attenuated response in the pain-processing network of the brain, including the insula, anterior cingulate cortex, amygdala, and prefrontal cortex. This may imply an impairment in the ability to recognize the emotional states of others. Compared to youths without conduct disorder or youths with conduct disorder but without callous-unemotional traits, they also tend to engage in proactive (pre-planned and intentional) aggression significantly more often.

Conversely, youths diagnosed with conduct disorder yet low in callous-unemotional traits, showed high emotional reactivity to these negative emotional cues and also scored high on reactive aggression as compared to youths characterized by callous-unemotionality and controls. The increase in the use of reactive aggression is associated with increased activity in the limbic areas of the brain, where the amygdala is positioned, and decreased activation in the prefrontal cortex. Thus, it seems that unique etiological factors contribute to the heterogeneous pathogeneses of conduct disorder and antisocial behavior.

Implications
The findings regarding the communication between the amygdala and frontal cortex in youths with conduct disorder suggest some errors in the Homeland Security System of the brain: the alarm may be harder to turn off, or might not be sensitive enough, with different atypical neural processes underlying each impairment. Important to realize, however, is that the antisocial brain is a complex puzzle consisting of different brain areas and multiple dysfunctional neural networks. By putting together the pieces, one must refrain from glossing over these complexities.

Crucially, although there are biological components that may negatively affect the neurological development of emotion regulation abilities and could consequently predispose a person to antisocial behavior, it is not the full story. The connection between the amygdala and the PFC takes a long time to develop. Because of the prolonged plasticity of the amygdala and prefrontal cortex, the link between the areas is also mediated by early experiences and its association with later emotional functioning and must hence be viewed in a developmental context. The brain is sculpted by one’s experiences. Understanding conduct disorder holistically, meaning in light of genetic, biological, social, and environmental etiological contributors is crucial for understanding the developmental trajectory to antisocial behavior. Furthermore, it may aid in the possibility to shape treatment to target the specific neural atypicality that fits the antisocial individual. Detecting developmental markers that predispose an individual to antisocial behavior augurs well for early intervention: stepping in during a phase of life where antisocial traits are more malleable may prevent many adversities in a young person’s future whilst additionally protecting the society around them.

The RESIST project of Erasmus University’s SYNC lab aims to better understand individual trajectories that lead to antisocial behavior, investigating this from a psychological- and neurodevelopmental perspective.

Health care organizations, governments, and policymakers are facing social and economic challenges as the global population has been aging very rapidly the past few years. With aging comes the risk of developing health issues, like neurodegenerative disorders. In 2015, 46 million individuals worldwide were suffering from dementia. By 2050, it is expected that this number will increase to 131.5 million, mainly due to the growth of the number of older adults. So what are the determinants of healthy cognitive aging and, by consequence, how can age-associated neurodegenerative diseases like dementia be attenuated? One of the many approaches that might bring us a step closer, is the work on the relationship between bilingualism and aging.

Enhanced executive functions among bilinguals
In the past two decades studies have accumulated information that has provided comprehensive, yet inconsistent, evidence regarding the advanced cognitive control among healthy bilingual individuals. However despite the ongoing debate, those studies that have found a bilingualism effect point to it positively contributing to cognitive processes like attentional conflict, inhibitory control, and goal maintenance. These studies are not limited to older adults, but target bilingual speakers from different ages. The origin of the bilingual advantage presumably follows the experience of monitoring and switching between two or more languages on a regular basis. For example, researchers have found reduced switching costs and enhanced flexibility in mental shifting in non-verbal executive tasks for bilinguals compared to monolinguals, that form the support for the idea that managing and frequently switching between two languages affects the executive control system.

The ability to control and switch between multiple languages involves the recruitment of various components of the executive system. It follows that lifelong experience of bilingualism or multilingualism may modify the neural representation and/or brain activity of regions and circuits associated with executive control. Executive control processes are supported by a frontoparietal network in the brain. Among children and young adults, neuroimaging studies on bilingualism in connection to nonlinguistic cognitive control revealed that, compared to their monolingual peers, bilinguals show a more distributed network of brain activation, including the involvement of brain regions associated with language control. Comparable results are seen in adult bilinguals, who show similar and distinct task-related functional networks when engaged in executive control processes. The functional difference in relation to executive functioning is characterized by the additional activation of areas primarily recruited during linguistic processes (i.e. left inferior frontal gyrus (IFC), anterior cingulate cortex (ACC), left inferior parietal lobule (IPL), and left basal ganglia) by bilinguals but not monolinguals.

Brain reserve vs. cognitive reserve
Could the enhanced executive control processes play a key role in the neuroprotective effects of bilingualism on cognitive decline via preserved and stronger frontoparietal pathways? Well, it is known that even in the presence of pathological brain changes, which are expected to result in dysfunctional behavior, some individuals exhibit significantly fewer and less severe symptoms or even no clinical symptoms at all. The epidemiological evidence suggests that these so-called protective factors act as a ‘reserve’, and can explain the inter-individual variability in symptom onset and severity. There is a distinction between brain reserve and cognitive reserve, two concepts which in the past have been used interchangeably. Stern defines the former as the individual differences in the brain itself (e.g. volume, number of neurons or synapses) that allow some people to cope better than others with brain pathology. Although predominantly hard-wired, brain anatomy can be influenced by life experience via several processes including neurogenesis, up-regulating receptors that promote neural plasticity, and resistance to apoptosis. By contrast to brain reserve, cognitive reserve postulates that individual differences in mental processing allow some people to cope better than others with brain pathology. Stern further subdivides cognitive reserve in neural reserve, i.e. the heterogeneity in brain networks (e.g. efficiency, capacity, or flexibility), which might explain why some people are better capable of coping with the effects of neuropathology, and neural compensation. The latter is defined as the heterogeneity in the ability to compensate for the disrupted brain networks by utilizing brain regions and networks which, in the absence of brain pathology, are normally not associated with that particular mental process.

The potential neuroprotective effects of bilingualism
The process of aging is characterized by complex and heterogenous alterations across the brain and in cognitive performance. In a MRI-study from 2015, the authors examined global and local differences in volume and cortical thickness of regions associated with aging and dementia (i.e. temporal pole, entorhinal cortex, and hippocampus) in healthy monolingual and bilingual seniors. Monolinguals and bilinguals did not differ on measures of global gray matter volume, nor in their rate of age-related decline in relation to white or gray matter in one of the lobar regions. However, strikingly, bilinguals showed significantly greater white matter volume in the frontal lobe, and marginally greater white matter volume in the temporal lobe than monolinguals. This correlated with better executive functioning, as measured with a Stroop task. The study also exhibited that cortical thickness within the temporal lobe decreases as a function of age in monolinguals, but not in bilinguals. Collectively, these findings demonstrate that bilingualism may have  neuroprotective effects, in terms of brain reserve, providing evidence for the assumption that over time the bilingual advantage of executive control might result in stronger and longer preserved pathways in the brain. At the same time, another study found evidence pointing more towards bilingualism as cognitive reserve. The authors examined white matter integrity and gray matter volume between healthy older monolinguals and bilinguals, and found that bilinguals showed more neural signs of an aging brain regions involved in memory processes compared to the monolinguals. Crucially, on a behavioral level the bilinguals did not underperform in relation to the monolinguals despite suffering greater brain atrophy. This led the authors to assume that bilinguals are flexible in using other intact (frontal) pathways, such as those involved in executive control as a way to compensate for the affected areas.

The protective effects of bilingualism upon cognitive decline have been found to reach further than healthy aging, extending to neurodegenerative diseases like Alzheimer’s Disease (AD). In one of the first studies it was revealed that (lifelong) experience of bilingualism does not lower the incidence or prevalence of dementia, but that the beneficial outcome of bilingualism is rather embedded in a delay in the onset of the symptoms.  Within a sample of non-specified demented individuals, the age at onset of clinical symptoms reported by family members, was on average 4 years later than for bilingual individuals compared to monolingual individuals. The decline rates, however, did not differ between the two groups, which suggests a shift in onset only and not altered progression. These findings have led to the thought that that bilinguals deal with greater brain atrophy than monolinguals but still manage to cognitively perform on a similar level. As expected, researchers have found that bilingual AD patients showed greater atrophy in the medial temporal lobe (a well-known brain region affected by AD) than monolinguals, supporting the view that benefits of bilingualism do not directly operate by protecting against structural disruptions of AD related regions, but rather act on maintenance of cognition (via intact pathways) in the presence of brain burden. As already mentioned before, bilingualism may exert an influence on the preserved executive control pathways in the brain in both healthy and pathological aging. A recent study on metabolic connectivity in monolingual and bilingual AD patients revealed more severe left hemispheric hypometabolism among bilinguals than monolinguals (e.g. IPL, IFG, parrahippocampal gyrus, insula, putamen, and cerebellum). Interestingly, the bilinguals did show increased metabolic activity in the executive control (specifically frontoparietal networks) and default mode network compared to the monolinguals. This implies that the neuroprotective effect of bilingualism indeed involves compensatory strategies associated with the intact executive control pathways, making it possible to have a mismatch between brain damage and cognitive performance.

The precise mechanisms underlying the neuroprotective effect remain unclear. It could be that the bilingual advantage is primarily the result of neural compensation, via frontoparietal connections, when other brain regions are disrupted. At the same time, there is also evidence for better preservation of structural and functional integrity in bilinguals compared to monolinguals. It would be interesting to know whether these different protective effects of bilingualism (brain vs. cognitive reserve) are associated with individual variability in type of bilingualism language use, proficiency, or amount of switching between first and second language. Till then the bilingual brain will continue to be both fascinating and mysterious.

This blog is a shortened version of an unpublished writing assignment by Green (2016) as part of a master programme at Utrecht University.

The current generation of adolescents has to stay at home with parents most of the time and follow online lessons instead of going to school. They are forced to stay physically distant from peers during a period of life in which they crave friends and social interactions the most. Fortunately, teens today have the chance to turn to technology to stay socially connected. Why are teens in particular suffering from the radical change in social environment? And what solutions does the use of social media offer?

From a biological perspective, turning to digital social spaces makes sense. Especially in the absence of social interactions elsewhere. Adolescents (between 10 and 24 years) go through a uniquely sensitive phase of development in which almost every activity is focused on fitting in. Changes in the brain and the hormonal system shape the process of breaking free from primary caregivers and form the strong desire to feel accepted and belong to peer groups. In the past decennia, neuroscientists have been discovering that the typical adolescent brain is actually equipped to process social experiences as extremely valuable. By comparing the brains of adolescents with those of children and adults, we measure that being judged by peers is eliciting a stronger reaction in teens. When adolescents just look at pictures of facial expressions in a lab setting, their brains get more active.

Researchers have been keeping track of the growth of neural connections between specific brain areas while teenagers get older. What they find: brain areas that are involved in social behaviour grow relatively fast in comparison to other parts of the brain. This specific pattern of brain development highly influences adolescents’ behaviour and goals: they naturally become more motivated to engage in social activities with peers.

The natural urge to spend time with peers is much needed at a young age. Socially orienting yourself independent from parents trains you to be an autonomous social adult. On the downside however, feeling lonely or socially isolated during this formative period of life is shown to be uniquely damaging for the development of structures in the brain. It may even trigger psychological problems and depression. Being active on social media may help teens to overcome a sense of social isolation.

Scholars from various research disciplines emphasise that social media is indeed fitting in adolescents’ developmental processes. The routine of chatting, updating, and sharing via social media platforms gives the levers to manage self-presentation, learning to express oneself and to develop one’s own identity. Researchers that measure brain activity patterns even show us that teens experience the social stimuli hosted by social media as evenly gratifying as when they engage in offline interaction.

Digital spaces can be a lifesaver on a much broader scale. LGBTQ youths for instance, who often lack confidence to express themselves in their physical surroundings or struggle to belong, turn to safe spaces on the internet. When I was exploring my sexual orientation as a teenager, social media was my biggest support. The LGBTQ-corner of the internet encouraged me to eliminate doubts and allowed me to feel more comfortable about my sexuality in online and offline surroundings.

Over the last decades, the online world as well as safe spaces for LGBTQ identifying youths have been expanding drastically. LGBTQ teens today take to the video-sharing app TikTok to share feelings and struggles or to seek for recognition in content uploaded by others. On such a platform, they can encounter like-minded peers whom they may not easily find in their physical environment. While there is still a lack of positively reflected queer representation in the mainstream media, various social media platforms offer a place for self-discovery, social connection and support.

Although the impact of enforced physical distancing may not be completely comparable with the struggles that marginalized groups of youths might face, it does show what the online social environment is capable of. Social media has the potential to stretch a safety net below teenagers in a formative period of social development. Digital spaces provide a crucial tool to connect and support each other while physically distant or when lacking a sense of normality elsewhere.

At the same time, however, some concerned voices claim that constantly being online might be rather unfavourable for teenagers well-being. Considering the average of six to seven hours spend on digital devices on a weekday (reported by Dutch adolescents during corona times), these concerns are not at all surprising. Even adolescents themselves are questioning whether they spend too much time behind their screens. Among Dutch adolescents, 60% report to feel uncomfortable with the number of hours they are online.

The concerns seem legitimate. The extend to which technology can assist in adolescents’ social development has its boundaries. Socializing with a screen in between is essentially different from its real-life counterpart, resulting in inevitable negative consequences on the flip side of the coin. Photo-sharing platforms such as Instagram entail an uncanny great emphasis on quantifiability of social endorsement. Many teens suffer from the pressure to portray an unrealistic self-image on their online profiles, or to achieve social standards that may be displayed on social media.

Of course, text-based communicating contains less social cues and an asynchrony of interaction. This might make social experiences in the online world challenging and less fulfilling. Algorithms continue to ensure you mainly encounter what you already like, imposing anyone who uses social media with the limitations of engaging in your online social bubble. Face-to-face social interactions with peers and the spontaneity of socializing in physic social events or in school surroundings are still necessities.

It is, on the one hand, more important than ever to focus psychological and brain research on the opportunities of the online world to assist in youths’ social development. On the other hand, although youths experience positive social support in many online settings, we still need more research into the limitations of social media’s role in the development of teens. We need experimental studies to find out to what extend social media is sufficient to fulfil adolescents’ social needs. How should we approach social media to support a healthy and responsible social environment? For both adolescents during physical distancing, but also for adolescents who already find less connection in their offline surroundings, these questions are of vital importance.