Part 2. The Mind in Motion: Evolution, Cognition, and the Future of Thought

To change the way we think, first change the way we feel. Kevin Rigley

Cognitive Epigenetics: The Biology of Thought Selection

Give me a child until he is seven, and I will show you the man. — Attributed to Aristotle & the Jesuits.

Cognition is often viewed as an inherent trait; some people naturally maintain focus, while others may easily get distracted. Yet, it’s worth contemplating that focus, attention, and cognitive style might not be fixed characteristics but flexible biological responses shaped by environmental influences.

Think about this: Every one of the 8 billion individuals on Earth starts as a single fertilized cell called a zygote, which holds a full set of DNA. As this initial cell divides, it generates more than 200 distinct cell types—such as neurons, muscle cells, and immune cells—all sharing the same DNA yet undertaking vastly different roles. What factors decide whether a cell develops into a neuron rather than a liver cell?

To understand this impressive concept, we examine epigenetics, the process that controls gene activation. While DNA remains unchanged, epigenetic modifications direct cellular development by selectively activating or deactivating genes.

This process extends beyond birth. Epigenetics continues to influence us throughout our lives, affecting physical traits, metabolism, cognition, and behaviour. However, genes do not all react to their environment uniformly. Some adhere to a fixed blueprint, while others engage in an ongoing conversation with their surroundings.

To make sense of this, I have categorised epigenetic modifications into three broad domains:

Developmental Epigenetic Modification (DEM) refers to genes that construct the body according to a precise developmental blueprint.

Metabolic Epigenetic Modification (MEM) involves genes that manage metabolism and respond to environmental changes.

Cognitive Epigenetic Modification (CEM) – Genes that influence thought, learning, and attention, dynamically responding to experience.

Each category varies in how much the environment dictates the outcome.

DEM: The High-Fidelity Blueprint of Life

During embryonic development, epigenetic mechanisms orchestrate every stage, ensuring that A heart cell forms a heart, not a neuron. A bone cell produces bone, not insulin. A child with DNA for blue eyes will develop blue eyes regardless of environmental differences.

At first glance, these processes seem entirely deterministic. This sense of predictability arises from the significant stability of the uterine environment across different populations. Whether a child is conceived in a bustling city or a tranquil village in India, the fundamental biological conditions required for foetal development remain constant.

However, this stability is not absolute. External environmental disruptions can undermine this precision, resulting in severe consequences. For example, the thalidomide disaster—a drug once prescribed for morning sickness—led to widespread limb malformations, proving that even tightly regulated developmental pathways can be altered by environmental exposure.

Nutrient deficiencies, such as maternal folate deficiency, can increase the risk of neural tube defects, showing that DEM still relies on a controlled environment.

Therefore, although DEM adheres to a detailed script, it is still susceptible to environmental disruptions.

The Shift in Environmental Control: Pre- vs. Post-Birth

Before birth, the mother’s body provides a controlled environment—temperature, oxygen levels, and nutrients are carefully regulated to optimise foetal development. This is why DEM outcomes appear primarily predetermined.

After birth, environmental control significantly lessens. Newborns are exposed to a range of sensory, social, and metabolic environments, which fosters increased individual variability. This is the point where MEM and CEM influence metabolism, cognition, and behavior based on external experiences.

MEM: The Adaptive Engine of Metabolism

Unlike structural development, metabolism must remain flexible to meet changing demands. Epigenetic modifications in MEM regulate how the body responds to diet, stress, and lifestyle:

Nutrient availability can epigenetically shape fat metabolism. The diet during early childhood may determine the activation of genes related to insulin resistance later in life. Chronic stress modifies HPA axis regulation, consequently impacting cortisol production and overall metabolic health over the long term. MEM responds more to environmental factors than DEM, while still functioning within biological limits.

CEM: The Most Plastic, the Most Malleable

Cognition is the least constrained by genetics and is most influenced by epigenetics. In contrast to traits like eye colour or metabolism, cognitive processes such as thought selection, attention, and learning form through experience-driven neural pathways. A child nurtured in a stable and stimulating environment will likely cultivate strong cognitive flexibility. Conversely, a child subjected to chronic stress and unpredictability may develop an enhanced threat-detection mechanism. Additionally, a child frequently engaging with rapid digital media may possess an attention system tailored for processing fragmented, fast-paced information. Within CEM, cognition remains fluid—a balance refined by environmental influences.

Cognition as an Adaptive Equilibrium

The subconscious does not generate thoughts randomly; rather, it filters, reinforces, and selects them based on past experiences and contributions from levels 1 and 2 of conscious input. This leads us to a different viewpoint: all cognitive states, such as ADHD, ASD, and anxiety, are not genetic defects. Instead, they represent stable cognitive equilibriums influenced by environmental factors. This leads to the logical conclusion that if neurodiversity represents every individual, then every individual is also neurodivergent.

Implications for Education and Cognitive Interventions

If cognition is malleable, interventions should focus on changing environmental inputs rather than merely managing symptoms. Rather than viewing neurodivergence as a fixed deficit or natural variation, cognitive epigenetics suggests that all neurotypes are dynamic responses to experience.

Experience-Expectant Learning and Critical Periods

“What if the way you think today was shaped before you even knew what thinking was?”

Many believe personality, intelligence, and cognitive style evolve gradually throughout life. However, consider that the foundations of your thinking might have been largely established before you even noticed. The principle of experience-expectant learning indicates that the brain is biologically inclined to develop in particular ways, depending on the type and timing of sensory input it receives in early life. Thus, neurodevelopment is an active interplay between genetic factors and environmental conditions. Key experiences—whether present or absent—during critical periods shape which cognitive traits surface and to what extent they manifest.

The developing brain expects certain sensory, social, and emotional inputs at specific times. During critical periods, when these inputs are present, the brain reinforces connections related to those experiences. However, if these inputs are missing, excessive, or distorted, it may lead to various cognitive effects. For example, infants are inherently equipped to learn language, but a lack of spoken word exposure in early childhood can reduce their chance of achieving full linguistic fluency. Likewise, face-to-face interactions boost social communication pathways, while limited engagement (like excessive screen use) can impair attention to social signals and emotional regulation. Additionally, early sensory experiences play a role in regulating attention. A child who encounters rapid, fragmented stimuli (for instance, from digital media overstimulation) may develop an overly active attention system, while a child with minimal sensory stimulation might show decreased cognitive flexibility.

Early sensory inputs can significantly influence which neurodevelopmental patterns become more dominant. When early sensory experiences are unpredictable or fast-paced, the brain often develops a heightened responsiveness, rapid idea generation, and impulsivity—traits associated with ADHD. Conversely, if these sensory inputs are overwhelming or processed inconsistently, the brain might selectively filter information, leading to rigid thinking and deep-focus cognition typical of ASD. Moreover, if early experiences are marked by stress or unpredictability, the brain tends to overemphasize threat detection, resulting in increased vigilance and fear-driven cognition, as seen in anxiety. These developmental patterns arise not randomly but through the interplay of genetic predispositions and environmental factors during growth.

If initial sensory experiences shape cognition, then cognitive flexibility—the ability to adapt to new information and direct thought processes—could primarily be established before conscious thought emerges. This implies that interventions in later life aimed at altering cognition should prioritize changes in sensory experiences rather than solely teaching cognitive control methods. Possible strategies may include structured sensory exposure to align attention systems, physical activity and embodied learning to improve the SNS-PNS balance, and engaging in social or imaginative play to enhance cognitive adaptability.

Instead of seeing neurotypes as static characteristics, this viewpoint posits that ADHD, ASD, and anxiety-related traits are influenced by developmental factors rather than solely by genetics. The following section examines how contemporary environmental shifts—especially in the Anthropocene—are altering cognitive balances worldwide.

Inflammation and the Shift in Cognitive Outcomes

“Could stress and diet rewire your brain without you realising it?”

Cognition is often viewed as reliant on neurons and synaptic connections. Nevertheless, recent research reveals that the immune system plays a substantial role in influencing thought processes, attention, and emotional regulation. Since inflammation can alter brain function, it’s plausible that factors such as stress, diet, and digital overload may modify cognition in ways we are beginning to comprehend. Inflammation acts as the body's natural defense mechanism against injury or infection. However, persistent low-grade inflammation, fueled by modern environmental influences, could disrupt cognitive balance and impact neurodevelopment. Studies indicate that key inflammatory markers—such as IL-6, TNF-α, and CRP—are elevated in individuals with ADHD, ASD, and anxiety, suggesting that both neural signaling and immune responses are involved in shaping cognition.

Various environmental elements contribute to chronic inflammation. Diets rich in ultra-processed foods, sugars, and industrial seed oils foster systemic inflammation, which impacts neural plasticity and cognitive abilities. Ongoing psychological stress raises cortisol levels, disturbing the balance of the autonomic nervous system and causing the release of inflammatory cytokines. Excessive digital exposure, particularly screen time, disrupts sleep, overstimulates the sympathetic nervous system, and is associated with higher pro-inflammatory markers, leading to cognitive dysregulation. If cognition is regulated by the autonomic nervous system, an inflamed nervous system may alter cognitive balance, affecting neurodevelopmental characteristics in particular ways. In terms of ADHD, increased inflammation raises SNS activity, which can result in greater impulsivity, distractibility, and sensory-seeking behaviours. For individuals with ASD, neuroinflammation may cause greater synaptic rigidity, strengthening hyper-focused thinking and a resistance to cognitive flexibility. In cases of anxiety, chronic stress-related inflammation can prepare the brain for heightened threat detection, increasing fear-driven thoughts and emotional sensitivity. These insights indicate that cognitive diversity is influenced not only by genetics but also by immune reactions to environmental factors.

If inflammation disrupts cognitive balance, interventions that aim to reduce inflammation could help restore cognitive flexibility. Anti-inflammatory diets high in omega-3 fatty acids, polyphenols, and fibres beneficial for gut health can decrease systemic inflammation and enhance neuroplasticity. Techniques such as meditation, breathwork, and organized physical activity stimulate the parasympathetic nervous system, mitigating inflammation driven by the sympathetic nervous system (SNS). Strategies for digital detox and increased nature exposure encourage autonomic balance and support neuroimmune regulation. Instead of perceiving ADHD, ASD, and anxiety as immutable traits, they might be seen as various cognitive balances influenced by inflammatory conditions. If contemporary lifestyles contribute to neuroinflammation, society should reconsider how it organises education, diet, and digital use to foster an environment that enhances cognitive flexibility rather than limits it.

Click for Part 1

Click for Part 2

Click for Part 3