CHAPTER 2 - The Cognitive-Action Pathways Model

Models.  From the "really, really ridiculously good looking", to the little ones of cars and planes that I was never able to build, there are lots of models in the world.

A model in science is not quite as interesting as Zoolander, and definitely not ridiculously good looking, but they are a lot smarter.  A scientific model simplifies a complex process to assist with understanding and making predictions.

In the last chapter I described the current concept of thought, based on evidence from modern neuroscience: Our thoughts are a conscious broadcast of a small segments of the much larger cycle of information processing going on in our subconscious brain.  But what makes up that larger cycle of information processing?  What are the different components that influence the flashes of light on the dark recesses of our brain?

The Cognitive-Action Pathways model combines a number of different cognitive models and other biological influences, into a schematic conceptual representation of the pathways that feed our thoughts and actions.

Using this model, I want to demonstrate how small changes in the processes underlying our thinking can radically change the way people perceive and interact with the world around them, and explain why understanding this knowledge doesn’t take our power to change away from us, but empowers us to make real changes.

The tip of the iceberg

We’ve all heard the phrase, “It’s just the tip of the iceberg.”  It comes from the fact that icebergs are made of fresh water, which is nine-tenths less dense than seawater.  As a result, ten percent of an iceberg sits above the waters surface with most of it hiding beneath.

The information processing of our brains is much the same.  We may be aware of our conscious stream of thought, but there is a lot going on under the surface that makes our thoughts what they are, even though we can’t see the process underneath.

What’s going on under the surface is a complex interplay of our genes and their expression which controls the structure and function of our brains, which effects how we perceive information, how we process that information and combine it into our memories of the past, predictions of the future, and even the further perception of the present [40].

The Cognitive-Action Pathways Model

The CAP model describes the process leading to our thoughts and our behaviours.  It is formed by a number of loops, or 'pathways', that lead to our cognition and our action.

In formulating the CAP model, I incorporated some well-known and accepted models of cognition, including the Dual Systems Model, and the Cognitive Cycle as described in the Global Workspace/IPA model.  I also incorporated concepts not described in other cognitive models, namely the triad of genes, epigenetics and the environment, and the filters of perception and personality[1].

The CAP Model - Explained

Genes, epigenetics and the environment

We start with the most fundamental level of our biological system, which is genetics.  It becomes clear from looking at any textbook of biological sciences that genes are fundamental to who we are.  From the simplest bacteria, fungi, protozoans and parasites, through to all plants, all animals and all of human kind - EVERY living thing has DNA.  DNA is what defines life in the broadest sense.

Proteins are responsible for the size, shape and operation of the cell.  They make each tissue structurally and functionally different, but still work together in a highly precise electrochemical synchrony.  But ultimately, it’s our genes that hold all of the instructions to make every one of the proteins within our cells.  Without our genes, we would be nothing more than a salty soup of random amino acids.

Epigenetics and the environment contribute to the way genes are expressed.  Epigenetics are “tags” on the strand of DNA that act to promote or silence the expression of certain genes (this will be discussed in more detail in chapter 12).  Environmental factors (the components that make up the world external to our bodies) can influence genes and epigenetic markers.  The environment can cause genetic mutations or new epigenetic marks that change the function of a particular gene, and depending on which cell they effect (a very active embryonic cell or a quiet adult cell) will largely determine the eventual outcome.  The environment is more influential to our genetic expression than epigenetics. 

Still, on average only about 25% of the expression of a complex trait is related to environmental factors.  So while the environment is important, it is still outdone 3:1 by our genome.

Yes, epigenetics and the environment are important, but they influence, not control, the genome.


We live in a sensory world.  The five senses are vital in providing the input we need for our brain to understand the world and meaningfully interact with it.

Different organs are needed to translate the optical, chemical or mechanical signals into electrical signals.  Different parts of our brain then interpret these signals and their patterns.  We discussed this in more detail in chapter 1.

Our genes significantly influence this process.  For example, if someone is born with red-green colour blindness then how he or she interprets the world will always be subtly different to someone with normal vision.  Or a person born with congenital deafness will always interpret his or her environment in a different way to someone with full hearing.  I’ve highlighted these two conditions because they provide stark examples to help demonstrate the point, but there are many unique genetic expressions in each of the five senses that subtly alter the way each of us perceives the world around us.

So while we may all have the same photons of light hitting our retinas, or the same pressure waves of sound reaching our ears or touch on our skin, how our brains receive that information is slightly different for every individual.  The information from the outside world is received by our sensory organs, but it is perceived by our brain, and even small differences in perception can have a big impact on the rest of the system.


Personality is “the combination of characteristics or qualities that form an individual's distinctive character” [3].  Formally speaking, personality is, “defined as constitutionally based tendencies in thoughts, behaviors, and emotions that surface early in life, are relatively stable and follow intrinsic paths of development basically independent of environmental influences.” [41]

Professor Gregg Henriques explained it well in Psychology Today, “Personality traits are longstanding patterns of thoughts, feelings, and actions which tend to stabilize in adulthood and remain relatively fixed. There are five broad trait domains, one of which is labeled Neuroticism, and it generally corresponds to the sensitivity of the negative affect system, where a person high in Neuroticism is someone who is a worrier, easily upset, often down or irritable, and demonstrates high emotional reactivity to stress.” [42] The other four personality types are Extraversion, Agreeableness, Conscientiousness, and Openness to Experience.

Gene x environment studies suggest that personality is highly heritable, with up to 60% of personality influenced by genetics [43], predominantly through genes involved in the serotonin [10] and dopamine systems [11, 44].  The “non-shared environment” (influences outside of the home environment) contributes heavily to the remainder [45, 46].

Personality is like a filter for a camera lens, shaping the awareness of our emotional state for better or worse, thus influencing the flow on to our feelings (the awareness of our emotions), our thoughts, and our actions.


Watkins describes physiology as streams of data that are provided from the different parts of your body, like the heart rate, your breathing rate, the oxygen in your blood, the position of your joints, the movement of your joints, even the filling of your bladder telling you that you need a break soon.

All of these signals are constantly being generated, and collated in different parts of the brain.  Some researchers consider them positive and negative depending on the data stream and the signal its providing.  They coalesce into emotion [47].


According to Watkins, “emotion” is the sum of all the data streams of physiology, or what he described as “E-MOTION ... Energy in MOTION.” [47] In this context, think of emotion as a bulls-eye spirit-level of our body systems.  The different forces of our physiology change the “level” constantly in different directions.  Emotion is the bubble that marks the central point, telling us how far out of balance we are.

In the interest of full disclosure, I should mention that although emotion is a familiar concept, the work of literally thousands of brilliant minds has brought us no closer to a scientifically validated definition of the word “emotion”.  Some psychologists and researchers consider it vague and unscientific, and would prefer that it not be used altogether [8].

I’ve retained it because I think it’s a well-recognised word that conceptually describes the balance of physiological forces.


“Feelings” are the perception of emotion.

I discussed earlier in the chapter that what we perceive is different to what we “see” because the subtle genetic differences in our eyes and brains causes the information to be processed differently between individuals.  The same applies to the perception of our emotion.

As I wrote earlier, personality is largely determined by our genetics with contributions from our environment [45, 46].  The emotional signal is filtered by our personality to give rise to our feelings.  Classically, an optimistic personality is going to bias the emotional input in a positive, adaptive way while a pessimist or neurotic is going to bias the emotional signal in a maladaptive way.

That’s not to say that an optimist can’t have depressed feelings, or a neurotic can’t have happy feelings.  In the same way that a coloured lens will allow a lot of light through but filter certain wavelengths out, most of our emotional state of being will come through the filter of our personality but the feelings will be subtly biased one way or another.

Executive Functions

Executive function of the brain is defined as a complex cognitive process requiring the co-ordination of several sub-processes to achieve a particular goal [48].  These sub-processes can be variable but include working memory, attention, goal setting, maintaining and monitoring of goal directed action and action inhibition.  In order to achieve these goals, the brain requires flexibility and coordination of a number of networks and lobes, although mainly the prefrontal cortex, parietal cortex, anterior cingulate and basal ganglia, and the while matter tracts that connect them.

Executive functions process the incoming information and decide on what goals are best given the  context, then plan the goals, execute them to the motor cortices, and monitor the action.  Research work from Marien et al [49] demonstrates that unconscious/implicit goals can divert resources away from conscious goals especially if it is emotionally salient or otherwise strongly related.  They also confirm that conscious awareness is not necessary for executive function but that implicit goals can be formed and executed without conscious involvement.


In chapter one we discussed the conscious broadcast model of thought.  Baars [18, 20] noted that the conscious broadcast comes into working memory which then engages a wider area of the cerebral cortex necessary to most efficiently process the information signal.  We perceive thought most commonly as either pictures or sounds in our head (“the inner monologue”), which corresponds to the slave systems of working memory.  When you “see” an image in your mind, that’s the visuospatial sketchpad.  When you listen to your inner monologue, that’s your phonological loop.  When a song gets stuck in your head, that’s your phonological loop as well, but on repeat mode.

There is another slave system that Baddeley included in his model of working memory called the episodic buffer, “which binds together complex information from multiple sources and modalities. Together with the ability to create and manipulate novel representations, it creates a mental modeling space that enables the consideration of possible outcomes, hence providing the basis for planning future action.” [13]

Deep thinking is a projection from your brains executive systems (attention or the default mode network) to the central executive of working memory, which then recalls the relevant information from long-term memory and directs the information through the various parts of the slave systems of working memory to process the complex details involved.  For example, visualizing a complex scene of a mountain stream in your mind would involve the executive brain directing the central executive of working memory to recall information about mountains and streams and associated details, and project them into the visuospatial sketchpad and phonological loop and combine them via the episodic buffer.  The episodic buffer could also manipulate the scene if required to create plans, or think about the scene in new or unexpected ways (like imagining an elephant riding a bicycle along the riverbank).

Even though the scene appears as one continuous episode, it is actually broken up into multiple cognitive cycles, in the same way that images in a movie appear to be moving, but are really just multiple still frames played in sequence.


Action is the final step in the process, the output, our tangible behaviour.

Our behaviour is not the direct result of conscious thought, or our will (as considered in the sense of our conscious will).

We discussed this before when we talked about our choices in chapter 1.  There are two main pathways that lead from sensory input to tangible behaviour – various automated pathways that take input from the thalamus, deep in the brain, and sent to motor circuits in the supplementary motor area and motor cortex of the brain.  These can be anything from evasive “reflex” actions[2] to rehearsed, habituated motor movements, like driving.  Then there is the second pathway, coming from the executive areas of our brain, that plan out options for action, which are reviewed by the pre-supplemental motor area and the default mode network.

This second pathway is amenable to conscious awareness.  Like thought, the projection of different options for action into our consciousness helps to engage a wider area of cerebral cortex to process the data.  Most of the possible plans for action have already been rejected by the implicit processing of our executive brain before consciousness is brought in to help.  Once an option has been selected, the action is sent to the pre-supplementary motor area, the supplementary motor area, the basal ganglia and finally the motor cortex.

According to the model proposed by Bonn [15], the conscious network has some feedback from the control network of our brain, providing real time context to actions about to be executed, and a veto function, stopping some actions at the last minute before they are carried out.  This is largely a function of the basal ganglia [50], with some assistance from working memory.

CBT and the CAP

Cognitive behavioural therapy is the most successful psychological therapy in the history of mankind, at least in terms of published data.  Originally developed by Beck in the mid-60’s [51], it has been applied to more and more conditions, with ongoing success.

CBT relies on the part of the CAP model involving feelings, thoughts and actions.  According to the original theory of Beck [51, 52], the input of thoughts is more powerful than feelings, and thus, changing your thoughts is the first step in the process of behavioural change.  This is the basis of Cognitive Behavioural Therapy – that changing your maladaptive patterns of thinking will change your behaviour and also the way you feel.  Dr Leaf’s interventions, such as her 21-day Brain Detox and her Brain Sweep, are loosely built on the same principles as CBT.

But CBT remains the original therapy based on the thoughts/actions/feelings loop, and has been proven to be effective in a wide range of psychological dysfunctions including depression [53: p215-38], anxiety [54] and chronic pain [55] to name a few.  As research has progressed, Beck’s original theory - that a change in thinking is required for a change in behaviour - has fallen off its pedestal.  The cognitive part of Cognitive Behavioural Therapy has been found to be much less important to the process than first proposed.  This will be discussed further in chapter 7.

Other feedback loops within the CAP model

There are other feedback loops as well, from action back to sensory input as our sensors in our muscles, joints, ears, eyes and skin detect the actions that we make as we perform them (ie: we hear ourselves speak, or we feel ourselves move).

The High and Low Roads

In chapter 1, I talked about a model of thought called the Dual Systems Model - the high and low roads of thought processing.

System 1 involves a set of different subsystems that operate in parallel, delivering swift and intuitive judgments and decisions in response to our perceptions. System 1 is unconscious, automatic and guided by principles that are, to a significant extent, innately fixed and universal among humans. System 2 is the system that involves “thought” in relation to my working definition. It is conscious and reflective in character, and proceeds in a slow, serial manner, according to principles that vary among both individuals and cultures [28].

In terms of the Cognitive-Action Pathways Model, System 1 (the “Low Road”), travels directly between perception and action, bypassing the filtering of the several cognitive steps in between.  It’s much faster because it involves less processing, but it’s also less refined.  It’s a pathway of stimulus-response, what makes up our instincts and raw reflexes.

System 2, the “High Road”, is the other pathway taken through the steps of physiology, emotion, feelings and thoughts.  System 2 is much slower, although it’s more refined and has much more power, because each step in the system hones the raw data to produce an output that is more specific to the context of the stimulus in terms of both space and time.

Thought Independent Action, Stimulus Independent Thought, and Parasomnias

System 1 of the Dual Systems Model describes our reflexes, our habits and our instincts, which I categorize into a group called Thought Independent Actions.  These are actions in which our cognitive functions are bypassed.

Another variation within the Cognitive-Action Pathways Model is the concept of Stimulus Independent Thought.

The two different systems can run at the same time.  In the example I used in chapter 1, sometimes I can be driving home at the end of a long day and find myself drifting off into thinking about something inane, then realise I’ve driven a couple of kilometres on autopilot.  When performing a menial, routine task, (or even a reasonably complex habituated task, like driving), our sensory signals are passing through the deeper parts of our brain and surfacing as actions while our Default Mode network and working memory are on a completely different tangent.

Dreaming is a different state altogether, in which our brain initiates a self-generated program of reorganizing the stored memories in our brain.  The characteristic of dreaming as opposed to waking consciousness is that dreaming lacks awareness, it is incoherent, and it is diminished in thought and memory.  Whenever we sleep, we dream, but we rarely remember dreams or have awareness of them [35].  If we wake up during a dream, some of what we dreamt will be left over in our short-term memory system and becomes available to our thoughts.  But more often, we simply don’t remember them.

Parasomnia is a medical description for a condition in which the inhibitory reflexes that are normally applied when we are in a state of NREM sleep are missing, which means that what we dream about can move to the Action step.  They are more commonly referred to as sleep-walking and sleep-talking, although sometimes the parasomnias can be complex motor patterns like eating [56].  One of my patients once had a parasomnia in which she drove her car.

In summary, the Cognitive-Action Pathways Model is a way of describing the context of thoughts to other neurological processes, and how they all interact.  It shows that conscious thoughts are one link of a longer chain of neurological functions between stimulus and action - simply one cog in the machine.  Thoughts are an important cog, but they are dependent on a number of other processes or they can be bypassed altogether.  Thoughts are not the driver of our consciousness or our free will, but merely a bit player.

Autism Spectrum Disorder – a real life example of the Cognitive-Action Pathways model

Small changes in the early processes within the Cognitive-Action Pathway model can snowball to effect every other part of the process.  A real life example of this is ASD, or Autism Spectrum Disorder.

ASD has been present since time immemorial.  Numerous bloggers speculate that Moses may have had ASD, while a couple of researchers proposed that Samson was on the spectrum (although their evidence was tenuous [57]).  Thankfully, autism is no longer considered a form of demon possession or madness, or schizophrenia, or caused by emotionally distant “refrigerator mothers”, nor treated with inhumane experimental chemical and physical “treatments” [58, 59].

The autism spectrum is defined by two main characteristics: deficits in social communication and interaction, and restricted repetitive patterns of behaviour.  People on the autism spectrum also tend to have abnormal sensitivity to stimuli, and other co-existing conditions like ADHD.  It’s hard to fully explain these definitions in a paragraph, but for completeness, I’ve listed the full DSM-5 diagnostic criteria for ASD in appendix A.  The new criteria are not without their critics [60-62], but overall, reflect the progress made in understanding the biological basis of autism. 

ASD is recognized as a pervasive developmental disorder secondary to structural and functional changes in the brain that occur in the womb, and can be detected as early as a month after birth [63].  In the brain of a foetus that will be born with ASD, excess numbers of dysfunctional nerve cells are unable to form the correct synaptic scaffolding, leaving a brain that is large [64, 65], but out-of-sync.  The reduced scaffolding leads to local over-connectivity within regions of the brain, and under-connectivity between the regions of the brain [66].  The majority of the abnormal cells and connections are within the frontal lobe, especially the dorsolateral prefrontal cortex and the medial prefrontal cortex [67], as well as the temporal lobes [68].  The cerebellum is also significantly linked to the autism spectrum [69].  There is also evidence that the amygdala and hippocampus, involved in emotional regulation and memory formation, are significantly effected in ASD [66].

There is also strong evidence for an over-active immune system in an autistic person compared to a neurotypical person, with changes demonstrated in all parts of the immune system, and the immune system in the brain as well as the rest of the body [70].  These immune changes contribute to the reduced ability of the brain to form new branches as well as develop new nerve cells or remove unnecessary cells.

There are a number of environmental and epigenetic associations linked to autism.  These include disorders of folate metabolism [71, 72], pollutants [73], fever during pregnancy [74] and medications such as valproate and certain anti-depressants [75, 76] which are linked with an increase in autism[3].  Supplements such as folate [71, 77], omega-6 polyunsaturated fatty acids [78] and the use of paracetamol for fevers in pregnancy [74] have protective effects.

Although these factors are important, genes outweigh their influence by about 4:1.  Twin studies suggest that between 70-90% of the risk of autism is genetic [79, 80].  Individual gene studies have only shown that each of the many single genes carry about a one percent chance each for the risk of autism [66].  It’s been proposed that the hundreds of genes linked with autism [66, 81] are not properly expressed (some are expressed too much, some not enough).  The resulting proteins from the abnormal gene expression contribute to a different function of the cell’s machinery, altering the ability of a nerve cell to fully develop, and the ability of nerve cells to form connections with other nerve cells [82].  The effects are individually small, but collectively influential [80]. Autism is considered a complex genetic disorder involving rare mutations, complex gene × gene interactions, and copy number variants (CNVs) including deletions and duplications [83].

According to the Cognitive-Action Pathways model, the triad of the environment, epigenetics, and genes influence a number of processes that feed into our actions, thoughts, perceptions, personality and physiology.  In ASD, the starting place is language processing.

New born babies from as young as two days old prefer listening to their own native language [84], which suggests that we are born already pre-wired for language.  Auditory stimuli (sounds) are processed in the temporal lobes, including language processing.  In neurotypical people, language processing is done predominantly on the left side, with some effect from the right side.  But in people with autism, because of the abnormal wiring, there is only significant activity of the right temporal lobe [68].  Even more, from data so recent that it’s pending publication, loss of the processing of information of the left temporal lobe reversed the brains orientation to social and non-social sounds, like the sound of the babies name [63].

The change in the wiring of the left and right temporal lobes then alters the processing of language, specifically the social significance of language and other sounds.  So already from a young age, people with autism will respond differently to environmental stimuli compared to a neurotypical person. 

In the same way, the fusiform gyrus is part of the brain that processes faces.  It’s quite specific to this task in a neurotypical person.  However, the altered wiring of the brain in someone with autism causes a change, with different parts of the brain having to take up the load of facial processing [85].

Each time that one part of the brain can’t perform it’s normal function, the other parts take up the load.  However that reduces the capacity for those parts of the brain to perform their own normal functions.  In the case of the temporal lobes and the fusiform areas, this results in a reduced ability to discern subtleties especially those related to recognizing social cues.  A neurotypical person and an autistic person could be standing in front of the same person, listening to the same words, and seeing the same facial expressions, but because of the way each persons brain processes the information, the perception of those words and cues can be completely different.  This demonstrates how genetic changes can lead to changes in the perception of normal sensory input, resulting in differences in the physiological response, emotions, feelings, thoughts and actions, despite identical sensory input.


The same changes that effect the cerebral cortex of the brain also have an influence on the deeper structures such as the hippocampus and the amygdala.  The hippocampus is largely responsible for transforming working memory into longer term declarative memory.  Studies comparing the size of the hippocampus in ASD children have shown an increase in size compared with typical developing children [86].  Combined with the deficits in the nerve cell structure of the cerebellum [69], autistic children and adults have a poor procedural memory (action learning, regulated by the cerebellum) and an overdeveloped declarative memory (for facts, regulated by the hippocampus).  This has been termed the “Mnesic Imbalance Theory” [87].

The amygdala is also functionally and anatomically altered because of the changes to the nerve cells and their connections.  The amygdala is larger in young children with ASD compared to typically developing children.  As a result, young ASD children have higher levels of background anxiety than do neurotypical children [88].  It’s proposed that not only do ASD children have higher levels of background anxiety, they also have more difficulty in regulating their stress system, resulting in higher levels of stress compared to a neurotypical child exposed to the same stimulus [89].


On a chemical level, autism involves genes that encode for proteins involved in the transport of key neurotransmitters, serotonin and dopamine.  Early evidence confirms the deficits of the serotonin and dopamine transporter systems in autism [90].  These neurotransmitters are integral to processing the signals of mood, stress and rewards within the brain, and as discussed in the last chapter, are significantly involved in the genesis of personality. 

The abnormal neurotransmitter systems and the resulting deficiencies in processing stress and rewards signals contribute to a higher correlation of neuroticism and introverted personality styles in children with autism symptoms [91, 92].

So people with autism genes are going to process stress and rewards in a different way to the neurotypical population.  As a result, their feelings, their thoughts and their resulting actions are tinged by the differences in personality through which all of the incoming signals are processed.


The underlying genes and neurobiology involved in autism also effect the final behavioural step, not only because genes and sensory input influence the personality and physiology undergirding our feelings and thoughts, but also because they cause physical changes to the cerebellum, the part of the brain involved in fine motor control and the integration of a number of higher level brain functions including working memory, behaviour and motivation [26, 69].

When Hans Asperger first described his cohort of ASD children, he noted that they all had a tendency to be clumsy and have poor handwriting [93].  This is a good example of how the underlying biology of ASD can effect the action stage independently of personality and physiology.  The cerebellum in a person with ASD has reduced numbers of a particular cell called the Purkinje cells, effecting the output of the cerebellum and the refined co-ordination of the small muscles of the hands (amongst other things).  Reduced co-ordination of the fine motor movements of the hands means that handwriting is less precise and therefore less neat.

A running joke when I talk to people is the notoriously illegible doctors handwriting.  One of the doctors I used to work with had handwriting that seriously looked like someone had dipped a chicken’s toes in ink and let it scratch around for a while.  My handwriting is messy - a crazy cursive-print hybrid - but at least it’s legible.  I tell people that our handwriting is terrible because we spent six years at medical school having to take notes at 200 words a minute.  But it might also be that the qualities that make for a good doctor tend to be found in Asperger’s Syndrome, so the medical school selection process is going to bias the sample towards ASD and the associated poor handwriting (Thankfully, those that go on to neurosurgery tend to have good hand-eye coordination).

But if your educational experience was anything like mine, handwriting was seen as one of the key performance indicators of school life.  If your handwriting was poor, you were considered lazy or stupid.  Even excluding the halo effect from the equation, poor handwriting means a student has to slow down to write neater but takes longer to complete the same task, or writes faster to complete the task in the allotted time but sacrificing legibility in doing so.

Either way, the neurobiology of ASD results in reduced ability to effectively communicate, leading to judgement from others and internal personal frustration, both of which feedback to the level of personality, molding future feelings, thoughts and actions.

Thought in ASD

By the time all the signals have gone through the various layers of perception, personality and physiology, they reach the conscious awareness level of our stream of thought.  I hope by now that you will agree with me that thought is irrevocably dependent on all of the various levels below it in the Cognitive-Action Pathways Model.  While thoughts are as unique as the individual that thinks them, the common genetic expression of ASD and the resulting patterns in personality, physiology and perception lead to some predictable patterns of thought in those sharing the same genes.

As a consequence of the differences in the signal processing, the memories that make their way to long-term storage are also going to be different.  Memories and memory function are also different in ASD for other neurobiological reasons, as described earlier in the chapter with the Mnesic Imbalance Theory.


The Cognitive-Action Pathways model is a way of describing the context of thoughts to other neurological processes, and how they all interact.  It shows that conscious thoughts are one link of a longer chain of neurological functions between stimulus and action - simply one cog in the machine.  The autistic spectrum provides a good example of how changes in genes and their expression can dramatically influence every aspect of a person’s life - how they experience the world, how they feel about those experiences, and how they think about them. 

I used autism as an example for this chapter because autism is a condition that’s pervasive, touching every aspect of a person’s life, and provides a good example of the extensive consequences from small genetic changes.  But the same principles of the Cognitive-Action Pathways Model apply to all aspects of life, including conditions that are considered pathological, but also to our normal variations and idiosyncrasies.  Small variations in the genes that code for our smell sensors or the processing of smells can change our preferences for certain foods just as much as cultural exposure.  Our appreciation for music is often changed subtly between individuals because of changes in the structure of our ears or the nerves that we use to process the sounds.  The genetic structure of the melanin pigment in our skin changes our interaction with our environment because of the amount of exposure to the sun we can handle.

This chapter was about setting out the place that our thoughts have in the grand scheme of life.  It’s not a plug for genetic pre-determination.  We are not a victim of our genes, but at the same time, we are not the master and commander either.

In the next chapter, I want to explain why the Cognitive-Action Pathways Model provides real truth, and why it’s liberating rather than debilitating.


[1] In the interests of full disclosure, I make no specific claim that this model is unique, although I’m unaware of other models incorporating all of these specific elements.

[2] We often describe rapid unconscious movements, especially to evade danger or to protect ourselves, as “reflexes”.  Medically speaking, a true reflex is a spinal reflex, like the knee-jerk reflex.  When a doctor taps the knee with the special hammer, the sudden stretch of the tendon passes a nerve impulse to the spinal cord, which is then passed to the muscle, which makes it contract.  A true reflex doesn’t go to the brain at all.

[3] A word of caution: While there’s good evidence that valproate increases the risk of autism, and a possible link between some anti-depressants and autism, that risk has to be balanced with the risk to the baby of having a mother with uncontrolled epilepsy or depression, which may very well be higher.  If you’re taking these medications and you are pregnant, or want to become pregnant, consult your doctor BEFORE you stop or change your medications.  Work out what’s right for you (and your baby) in your unique situation.