Anxiety is a multifaceted phenomenon that can manifest itself in a beneficial way, when it acts as an adaptive mechanism, or in a harmful way, when it interferes with well-being and cognitive functioning. Within this spectrum, “subjective anxiety” can be distinguished – a particular type of anxiety that differs from pathological and somatic anxiety, and even from transient anxiety states. This state is characterized by an internal overload caused by high cognitive demands and the speed of information processing, factors common among people with high intellectual capacity, as is often the case with gifted individuals.
Defining Subjective Anxiety
Subjective anxiety is essentially an exacerbated response to the accumulation of information and accelerated processing by the prefrontal cortex, especially in the areas that govern attentional control and emotional regulation. Unlike pathological anxiety, which is sustained by dysfunction in neural circuits and, often, by ineffective regulation of neurotransmitters, subjective anxiety is more easily modulated, due to the functional integrity of these networks in individuals with greater cognitive efficiency. This type of anxiety manifests itself particularly in contexts of cognitive overload, where the processing of multiple pieces of information overwhelms the attention system.
In neurobiological terms, subjective anxiety has a distinct etiology from physical or pathological anxiety, which can be induced by dysfunctions in the dopaminergic and serotonergic systems, often associated with the nucleus accumbens and the amygdala. In subjective anxiety, the prefrontal cortex, especially the dorsolateral prefrontal cortex (DLPFC) and the anterior cingulate cortex (ACC), plays a crucial role in attempting to maintain attentional control under conditions of information overload. These areas are responsible for organizing and prioritizing information, processes that in individuals with high cognitive capacity can reach extreme efficiency, but which, at the same time, become vulnerable to subjective anxiety due to the constant demand on cognitive resources.
The Role of Brain Subregions and Neurotransmitters
The DLPFC, which acts as a cognitive “executive,” is essential for processing complex information and planning. In situations of overload, it activates mechanisms to manage high cognitive demand. However, the ACC, which mediates the emotional response to mental effort, can signal this overload to the limbic system, particularly the amygdala, inducing a feeling of alertness and internal tension, which is the basis of subjective anxiety.
The regulation of neurotransmitters such as dopamine and glutamate is essential in this process. In the DLPFC, dopamine modulates cognitive flexibility and control, while glutamate supports the synaptic activation required for rapid information processing. Hyperactivity in these pathways can result in an acceleration of processing, which, in high-demand contexts, contributes to a subjective feeling of anxiety. Furthermore, norepinephrine, a key neurotransmitter in the stress response, can exacerbate the feeling of cognitive overload by sensitizing the ACC and intensifying the emotional response of the limbic system.
Cell Types and Intracellular Signaling
The regulation and balance between excitatory (mainly glutamatergic) and inhibitory (GABAergic) neurons in the DLPFC and ACC are essential for the modulation of subjective anxiety. In individuals with high cognitive ability, GABAergic interneurons, especially those expressing parvalbumin, play a crucial role in modulating neuronal excitability, helping to maintain focus and avoid information overload. Intracellular signaling mediated by dopaminergic D1 and D2 receptors influences synaptic plasticity and the stress response, facilitating or hindering adaptation to new information as cognitive demand increases.
Furthermore, the NMDA receptor, which is critical for synaptic plasticity and working memory, plays a role in rapid information processing in the DLPFC. In high-demand situations, overactivation of these receptors can lead to exhaustion of neural resources and the consequent feeling of subjective anxiety. The interplay between intracellular signaling pathways, including the MAPK (mitogen-activated protein kinase cascade) system and the cAMP/PKA pathway, are also crucial for the adjustment of the neuronal response to cognitive stress.
Genetic and Molecular Aspects
Studies on genetic polymorphisms suggest that variants in genes related to the dopaminergic system, such as COMT (catechol-O-methyltransferase), which regulates dopamine degradation in the prefrontal cortex, may influence the predisposition to subjective anxiety. The Val158Met polymorphism, for example, is known to affect dopamine availability and, consequently, the efficiency of the DLPFC in high-demand contexts. Individuals with the Met variant tend to have higher levels of dopamine in the DLPFC, which may favor cognitive processing but also increase the likelihood of subjective anxiety by accelerating internal processes.
Another relevant genetic factor is the expression of the SLC6A3 gene, which encodes the dopamine transporter. Variants of this gene can alter the regulation of dopamine in the central nervous system and influence attentional control and the response to stress. Genes involved in synaptic plasticity and control of the glutamatergic system, such as GRIN2B (an NMDA receptor), have also been associated with the modulation of information processing and predisposition to subjective anxiety.
Conclusion
Subjective anxiety is a complex phenomenon, distinctly regulated by neurobiological processes involving the prefrontal cortex, the ACC and the interaction of dopaminergic and glutamatergic neurotransmitters. In individuals with high cognitive ability, subjective anxiety results from a specific neurobiological dynamic that, although intense in situations of high cognitive demand, is easier to control due to the integrity and efficiency of frontal circuits. A detailed understanding of the cellular, molecular and genetic bases of this form of anxiety allows us to explore differentiated approaches to modulating this state, without the stigma and limitations often associated with pathological anxiety.
This perspective leads us to reconsider anxiety not just as a problem, but as an expression of the complex interactions between cognition and emotion in an efficient nervous system, but sensitive to cognitive stress.
