By Dr. Fabiano de Abreu Agrela Rodrigues
The idea that people with a high Intelligence Quotient (IQ) make better, faster and more assertive decisions is a simplistic generalization that lacks neuroscientific support. Logical reasoning, analytical ability and memory capacity do not, by themselves, guarantee decision-making efficiency. In many cases, the opposite is observed: highly intelligent individuals present recurring blocks when making decisions, especially when the context involves emotional variables, ambiguity or unpredictability.
This difficulty is not necessarily linked to cognitive limitations, but to the *functional disorganization between three essential neurobiological axes: **dopaminergic regulation* in the prefrontal cortex, the *balance between glutamatergic excitation and serotonergic inhibition, and **neuroplasticity linked to motivation and the need for achievement*. The decision-making system does not depend exclusively on the volume of brain processing, but on the way in which the fronto-limbic networks communicate and respond to the individual’s internal and external reality.
For example, in the *COMT (catechol-O-methyltransferase) gene, variants such as the Met allele (present in Met/Met heterozygotes and homozygotes) reduce the degradation of dopamine in the prefrontal cortex, leading to **greater cognitive efficiency, but also to **greater sensitivity to stress and indecision when faced with complex stimuli*. Excess dopamine can inhibit action instead of promoting it, resulting in excessive analysis, rumination and behavioral paralysis. In the case of the COMT GG (Val/Val) genotype, there is a more accelerated degradation of dopamine, which can act as an inhibitory brake — useful for quick decisions, but limiting when flexibility and depth are required.
Furthermore, people with greater emotional intensity or high sensitivity tend to have greater synaptic density mediated by glutamate, the main excitatory neurotransmitter. When there is no serotonergic balance, this state of hyperarousal can become dysfunctional, reducing the emotional stability necessary for well-informed choices. In these profiles, basal dopamine in Brodmann areas 9, 10, 11, 24, 25, 32, 46 and 47 — all associated with judgment, anticipation, executive control and affective processing — becomes critical. The absence of this basal tone prevents the system from fluidly activating the circuits necessary for coordinated action.
*Neuroplasticity*, in turn, represents a dual factor: when well regulated, it promotes adaptation and creative problem-solving; but when focused on the incessant search for novelty or narcissistic achievements, it can generate chronic dissatisfaction and decision-making blocks. The need for constant challenge, typical of individuals with high cognitive potential, can become a factor of vulnerability when there is no meaning attached to the action.
Therefore, the difficulty in making decisions in people with high IQs should not be interpreted as an inconsistency between intelligence and behavior, but as the reflection of a highly sophisticated neurocognitive system that, at the slightest imbalance, enters a state of *analytical, sensory and emotional overload*. Decision-making requires more than knowledge — it requires biochemical regulation, emotional structure and clarity of purpose.
Diagram for interpretation with case study example
In individuals with variants of the COMT gene (catechol-O-methyltransferase), especially heterozygotes (Val/Met) or homozygotes Met/Met, there is less dopamine degradation in the prefrontal region. This condition favors an increase in basal dopaminergic levels, which is associated with greater cognitive efficiency, especially in tasks that require abstract reasoning and working memory. However, this same genetic profile can result in a lower capacity for rapid and effective decision-making, due to excess dopaminergic signaling in the prefrontal cortex, which compromises cognitive flexibility and behavioral selection on demand. When the genotype is COMT GG (Val/Val), there is greater enzymatic activity and, consequently, less dopamine availability, which acts as a functional brake. However, when this genetic pattern coexists with variants associated with greater emotional intensity, such as polymorphisms in genes related to limbic reactivity, there is an increased demand for basal dopamine in specific regions, such as the dorsolateral prefrontal cortex (BA 9 and 46), frontopolar cortex (BA 10), orbitofrontal cortex (BA 11 and 47), anterior cingulate cortex (BA 24 and 32) and subgenual cortex (BA 25). In parallel, genes such as SNAP25, linked to synaptic efficiency, and ADAM12, associated with neuroplasticity, can contribute to a state of glutamatergic hyperexcitation. This increase in excitatory activity tends to reduce serotonin levels, generating a condition of homeostatic dysfunction that leads to the compulsive search for rewarding stimuli, as a way to reestablish frontal dopaminergic tone. The result can be a cognitive profile with high global intelligence, heightened creativity and, paradoxically, greater vulnerability to decision-making blocks and emotional swings.
The solution to this dysfunction does not lie in generic motivational techniques, but in the *recognition and conscious management of one’s own neural mechanisms*. Interventions based on applied neuroscience, self-knowledge, and practices that rebalance dopaminergic tone and the reward circuit, such as purposeful projects, tasks guided by intrinsic value, and reorganization of choice environments, can restore decision-making flow.
Intelligence, when not accompanied by *emotional regulation and neurofunctional harmony*, runs the risk of becoming a burden. Thinking well does not guarantee acting well. And acting well often depends on being able to not think too much.
References
* Diamond, A. (2013). Executive Functions. Annual Review of Psychology.
* Goriounova, N. A., & Mansvelder, H. D. (2019). Genes, Cells and Brain Areas of Intelligence. Frontiers in Human Neuroscience.
* Abreu Agrela Rodrigues, F. de. (2023). Neurobiology and Foundations of Intelligence. CPAH.
* Meyer-Lindenberg, A., & Weinberger, D. R. (2006). Intermediate Phenotypes and Genetic Mechanisms of Psychiatric Disorders. Nature Reviews Neuroscience.
Dr. Fabiano de Abreu Agrela Rodrigues MRSB holds a post-PhD in Neuroscience and is an elected member of Sigma Xi – The Scientific Research Honor Society (more than 200 members of Sigma Xi have received the Nobel Prize), as well as being a member of the Society for Neuroscience in the United States, the Royal Society of Biology and The Royal Society of Medicine in the United Kingdom, the European Society of Human Genetics in Vienna, Austria, and the APA – American Philosophical Association in the United States. He holds a Master’s degree in Psychology and a Bachelor’s degree in History and Biology. He is also a Technologist in Anthropology and Philosophy, with several national and international degrees in Neuroscience and Neuropsychology. Dr. Fabiano is a member of prestigious high IQ societies, including Mensa International, Intertel, ISPE High IQ Society, Triple Nine Society, ISI-Society, and HELLIQ Society High IQ. He is the author of more than 300 scientific studies and 30 books. He is currently a visiting professor at PUCRS in Brazil, UNIFRANZ in Bolivia and Santander in Mexico. He also serves as Director of CPAH – Centro de Pesquisa e Análises Heráclito and is the creator of the GIP project, which estimates IQ through the analysis of genetic intelligence. Dr. Fabiano is also a registered journalist, having his name included in the book of records for achieving four records, one of which is for being the greatest creator of characters in the history of the press.