Don’t stress about stress – Part 3: Coping

In our last two blogs, we’ve been looking at stress, and why stress is usually more helpful than harmful.

It’s not that stress can never be harmful. Stress can be a trigger to some illnesses (although not as many as the popular media often portrays). What is it that makes the difference between helpful and harmful? What is it that causes one person to surf the tsunami of sewerage that often confronts us in life, while another person sinks?

The answer lies in resilience.

WHAT IS RESILIENCE?

Resilience is the term given to the individual’s capacity to cope.

Researchers in the field of psychiatry often use the term resilience, which “is the capacity and dynamic process of adaptively overcoming stress and adversity while maintaining normal psychological and physical functioning” [1] although psychologists and social science researchers would use the term “coping”, which is defined by Compas et al as, “conscious and volitional efforts to regulate emotion, cognition, behavior, physiology, and the environment in response to stressful events or circumstances.” [2] Skinner and Zimmer-Gembeck define coping as, “action regulation under stress.” [3]

Considering the definitions used, the terms are essentially interchangeable. The other observation to be made here is that coping/resilience is an active process. It’s not something that happens despite of us – we actively cope with stress. In the face of a situation involving emotional arousal (danger or stress), we take steps to deal with our inner and outer environments (the physiological processes of our body, as well as the environment around us). Sometimes these steps are conscious and/or under our control. But theorists also consider automatic, unconscious, and involuntary responses to also be part of the coping spectrum [4].

WHAT CONTRIBUTES TO RESILIENCE?

Coping Strategies

What makes up those actions? What influences the action steps?

Psychologists have described hundreds of individual methods of coping through recent research, although there have been efforts to consolidate the plethora of individual coping strategies into “family” clusters, based on function. For example, a primary tier is to “Coordinate actions and contingencies in the environment” which involves “finding additional contingencies” which on the third level involves “reading, observation, and asking others.” [3] Table 1 in the paper by Skinner and Zimmer-Gembeck [3] summarize the many ways of coping and how they can be grouped together into families, and their corresponding adaptive process.

Personality factors

Coping strategies follow along the lines of personality type [5], as well as the stage of development in children [3]. Personality types such as Neuroticism and Openness have been well studied, with Neuroticism associated with maladaptive coping strategies, and Openness correlated with adaptive coping (in marital relationships [6] and in public speaking tasks [5]).

Further research has shown how personality significantly influences coping, with the severity of the stress, and the age and culture of a person influencing the strategy and strength of the coping response [4]. Of course, personality traits like neuroticism sound bad, but they confer their own strengths. For example, negative affect has protective benefits by enhancing the detection of deception [7].

Biological factors

The shared connection that personality types and coping responses have is in their shared genetics, with personality and coping styles influenced by common genes [8]. This makes perfect sense as it has been shown that changes in individual genes effect the ability of the brain to associate the correct value to rewards [9], which then influences both mood [10], and learning [11]. Even though environmental variables are important in determining personality and learning aspects of coping with stress, the brains underlying capacity to process the incoming signals correctly will significantly influence the direction and outcome of the learning process, which includes learning which coping strategies work best for each individual.

On a deeper level, there are several biological processes that make up the features of resilience. Animal studies on resilience, as a whole, have shown that resilience “is mediated not only by the absence of key molecular abnormalities that occur in susceptible animals to impair their coping ability, but also by the presence of distinct molecular adaptations that occur specifically in resilient individuals to help promote normal behavioral function.” [12] That is, resilient individuals have the full complement of critical components in the resilience pathway, and have some extra tools too.

Human studies thus far have shown strong links to genetic changes that affect the proteins in the stress system. Epigenetic mechanisms are involved, and the role of the environment is also significant, especially uncontrollable early childhood trauma. Wu et al list the current studies of genetic changes that effect resilience in humans [1: Table 1]. The proteins involved are responsible for the growth of new nerve pathways (BDNF), and for their function, especially within the stress system (CRHR1, FKBP5) and in control of mood and reward systems (COMT, DAT1, DRD2/4, 5-HTTLPR, the HTR group).

Wu et al [1] also summarised the currently known facts about epigenetic factors in resilience. Interestingly, they noted an animal study in which chronic stressors increased an epigenetic marker called histone acetylation in the hippocampus in mice, which enhanced the protective effects of the stress (epigenetics will be the subject of a future blog)

Resilience on a personal level

So coping and resilience are known protective factors for stress, and are more commonly deployed than most people realize. Despite all of the publicity that stress has generated, human beings remain remarkably unscathed. It’s estimated that, “in the general population, between 50 and 60% experience a severe trauma, yet the prevalence of illness is estimated to be only 7.8%.” [12] (Note: By ‘illness’, the authors were referring to Post Traumatic Stress Disorder, not all of human sickness).

But when it comes to recommending different coping strategies on an individual level, it is a much harder thing to do. What is adaptive in some situations and for some people is maladaptive in other situations and for other people.

For example, in animal studies, “stressed females tend to perform better than males on non-aversive cognitive or memory tasks … Conversely, in tests of acute stress or aversive conditioning, stress enhances learning in males and impairs it in females … the literature suggests that in cognitive domains females cope better with chronic forms of stress, whereas males tend to cope better with acute stress.” [12] So animal studies confirm a difference in the biological stress response between men and women. If these studies in animals can be extended to humans, it may explain the tendency for men to engage in “fight-or-fight” responses to stress where women usually move to “tend-and-befriend” mode [13].

Human studies on coping also demonstrate that what is good for one is not necessarily good for another. Connor-Smith and Flachsbart confirm that, “In particular, daily report and laboratory studies suggest that individuals high in sensitivity to threat may either benefit from disengagement or be harmed by engagement in the short term, with the opposite pattern appearing for individuals low in threat sensitivity.” [4]

So in other words, just because engaging may be a positive method of coping does not mean that it should be recommended to everyone. Some people will have more harm from trying to engage. Care should be taken when giving people advice about how to manage their stress. Ill-informed instructions can actually make things worse.

SUMMARY

It’s well established that stress can have negative impacts on your physical and mental health. But contrary to the popular view, stress is not always bad. As a number of authors point out, most people go through significant stress at some point in their lives, but only a fraction succumb to that stress.

The difference is the factors that make up resilience. Where we are along the stress spectrum (that is, whether you are wired to be more stressed, or more resistant to stress) depends on our genetic predisposition, which determines the physiology of our stress system and our personality, and the ways we learn to cope.

How we cope best depends on our individual traits and the situation. There is no one-size-fits-all. Pushing a person into a form of coping that’s not suitable can actually cause a lot of harm.

Remember, we normally find what coping strategies work for us automatically as our resilience is mostly innate, and we all go through severe stress at some point or another in our lives, but only a small fraction of us will succumb to that stress.

In the last blog in the series, we’ll have a brief look at what happens when stress overwhelms us … when stress is breaking bad.

References

  1. Wu, G., et al., Understanding resilience. Front Behav Neurosci, 2013. 7: 10 doi: 10.3389/fnbeh.2013.00010
  2. Compas, B.E., et al., Coping with stress during childhood and adolescence: problems, progress, and potential in theory and research. Psychol Bull, 2001. 127(1): 87-127 http://www.ncbi.nlm.nih.gov/pubmed/11271757
  3. Skinner, E.A. and Zimmer-Gembeck, M.J., The development of coping. Annu Rev Psychol, 2007. 58: 119-44 doi: 10.1146/annurev.psych.58.110405.085705
  4. Connor-Smith, J.K. and Flachsbart, C., Relations between personality and coping: a meta-analysis. Journal of personality and social psychology, 2007. 93(6): 1080
  5. Penley, J.A. and Tomaka, J., Associations among the Big Five, emotional responses, and coping with acute stress. Personality and individual differences, 2002. 32(7): 1215-28
  6. Bouchard, G., Cognitive appraisals, neuroticism, and openness as correlates of coping strategies: An integrative model of adptation to marital difficulties. Canadian Journal of Behavioural Science/Revue canadienne des sciences du comportement, 2003. 35(1): 1
  7. Forgas, J.P. and East, R., On being happy and gullible: Mood effects on skepticism and the detection of deception. Journal of Experimental Social Psychology, 2008. 44: 1362-7 http://bit.ly/Jm66a7
  8. Kato, K. and Pedersen, N.L., Personality and coping: A study of twins reared apart and twins reared together. Behavior Genetics, 2005. 35(2): 147-58 http://link.springer.com/article/10.1007%2Fs10519-004-1015-8
  9. Dreher, J.-C., et al., Variation in dopamine genes influences responsivity of the human reward system. Proceedings of the National Academy of Sciences, 2009. 106(2): 617-22
  10. Felten, A., et al., Genetically determined dopamine availability predicts disposition for depression. Brain Behav, 2011. 1(2): 109-18 doi: 10.1002/brb3.20
  11. Ullsperger, M., Genetic association studies of performance monitoring and learning from feedback: the role of dopamine and serotonin. Neuroscience & Biobehavioral Reviews, 2010. 34(5): 649-59
  12. Russo, S.J., et al., Neurobiology of resilience. Nature neuroscience, 2012. 15(11): 1475-84
  13. Verma, R., et al., Gender differences in stress response: Role of developmental and biological determinants. Ind Psychiatry J, 2011. 20(1): 4-10 doi: 10.4103/0972-6748.98407
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Dr Caroline Leaf and the chemistry of perceptions

Screen Shot 2014-11-16 at 3.19.48 pm

On her social media feed just now, Dr Caroline Leaf, communication pathologist and self-titled cognitive neuroscientist, said, “Your perceptions adjust your brain chemistry”.

Hmmm … yes and no.

I’m not really sure what Dr Leaf is trying to suggest with this statement, because it’s so vague. The brain works through the passage of an electrical current travelling along a nerve cell, and being passed to the next nerve cell by the release of a “chemical” neurotransmitter that floats across the space between the nerve cells.  If that’s what Dr Leaf is referring when she talks about our brain chemistry, then sure, our perceptions adjust our brain chemistry. But then again, so does everything else that our brain does. In this sense, perception is nothing special.

What I think Dr Leaf was trying to suggest is that our mind influences our brain chemistry, following along with her “mind controls matter” theme. But perception is the process of translating the raw data into a signal that the brain can process, for example, the light coming into your eye is translated into the electrical impulses your brain can utilise. It’s not an explicit process. It has nothing to do with our consciousness or our volition.

Also, our “brain chemistry” as it’s considered in neuroscience is usually referring to the neurotransmitters and their function, which is often determined by our genetics and influences how we perceive and understand our environment [1].

So if anything, it’s not our perception altering our brain chemistry, but rather it’s our brain chemistry that alters our perceptions.

Our mind does not control our brain. Our brain is responsible for the function of our mind.

References

  1. Caspi, A., et al., Genetic sensitivity to the environment: the case of the serotonin transporter gene and its implications for studying complex diseases and traits. Am J Psychiatry, 2010. 167(5): 509-27 doi: 10.1176/appi.ajp.2010.09101452

Putting thought in the right place, part 2

CAP v2.1.2

In the last blog post, I discussed the Cognitive Action Pathways model, a schematic conceptual representation of the hierarchy of key components that underpin human thought and behaviour.

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 [1]). 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” [2, 3].

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. The full diagnostic criteria can be found in DSM5. The new criteria are not without their critics [4-6], 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 [7]. 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 [8, 9], 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 [10]. The majority of the abnormal cells and connections are within the frontal lobe, especially the dorsolateral prefrontal cortex and the medial prefrontal cortex [11], as well as the temporal lobes [12]. The cerebellum is also significantly linked to the autism spectrum [13]. There is also evidence that the amygdala and hippocampus, involved in emotional regulation and memory formation, are significantly effected in ASD [10].

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 [14]. 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 [15, 16], pollutants [17], fever during pregnancy [18] and medications such as valproate and certain anti-depressants [19, 20] which are linked with an increase in autism[1]. Supplements such as folate [15, 21], omega-6 polyunsaturated fatty acids [22] and the use of paracetamol for fevers in pregnancy [18] 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 [23, 24]. 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 [10]. It’s been proposed that the hundreds of genes linked with autism [10, 25] 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 [26]. The effects are individually small, but collectively influential [24]. Autism is considered a complex genetic disorder involving rare mutations, complex gene × gene interactions, and copy number variants (CNVs) including deletions and duplications [27].

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 [28], 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 [12]. 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 [7].

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 [29].

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.

Physiology

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 [30]. Combined with the deficits in the nerve cell structure of the cerebellum [13], 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” [31].

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 [32]. 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 [33].

Personality

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 [34]. 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 [35, 36].

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.

Actions

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 [13, 37].

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 [38]. 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 blog with the Mnesic Imbalance Theory.

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. 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 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.

So in summary, this blog was to set out the place that our thoughts have in the grand scheme of life. Thought is not the guiding or controlling force, it is simply a product of a number of underlying functions and variables.

References

  1. Mathew, S.K. and Pandian, J.D., Newer insights to the neurological diseases among biblical characters of old testament. Ann Indian Acad Neurol, 2010. 13(3): 164-6 doi: 10.4103/0972-2327.70873
  2. Wolff, S., The history of autism. Eur Child Adolesc Psychiatry, 2004. 13(4): 201-8 doi: 10.1007/s00787-004-0363-5
  3. WebMD: The history of autism. 2013 [cited 2013, August 14]; Available from: http://www.webmd.com/brain/autism/history-of-autism.
  4. Buxbaum, J.D. and Baron-Cohen, S., DSM-5: the debate continues. Mol Autism, 2013. 4(1): 11 doi: 10.1186/2040-2392-4-11
  5. Volkmar, F.R. and Reichow, B., Autism in DSM-5: progress and challenges. Mol Autism, 2013. 4(1): 13 doi: 10.1186/2040-2392-4-13
  6. Grzadzinski, R., et al., DSM-5 and autism spectrum disorders (ASDs): an opportunity for identifying ASD subtypes. Mol Autism, 2013. 4(1): 12 doi: 10.1186/2040-2392-4-12
  7. Pierce, K. Exploring the Causes of Autism – The Role of Genetics and The Environment (Keynote Symposium 11). in Asia Pacific Autism Conference. 2013. Adelaide, Australia: APAC 2013.
  8. Courchesne, E., et al., Evidence of brain overgrowth in the first year of life in autism. JAMA, 2003. 290(3): 337-44 doi: 10.1001/jama.290.3.337
  9. Shen, M.D., et al., Early brain enlargement and elevated extra-axial fluid in infants who develop autism spectrum disorder. Brain, 2013. 136(Pt 9): 2825-35 doi: 10.1093/brain/awt166
  10. Won, H., et al., Autism spectrum disorder causes, mechanisms, and treatments: focus on neuronal synapses. Front Mol Neurosci, 2013. 6: 19 doi: 10.3389/fnmol.2013.00019
  11. Courchesne, E., et al., Neuron number and size in prefrontal cortex of children with autism. JAMA, 2011. 306(18): 2001-10 doi: 10.1001/jama.2011.1638
  12. Eyler, L.T., et al., A failure of left temporal cortex to specialize for language is an early emerging and fundamental property of autism. Brain, 2012. 135(Pt 3): 949-60 doi: 10.1093/brain/awr364
  13. Fatemi, S.H., et al., Consensus paper: pathological role of the cerebellum in autism. Cerebellum, 2012. 11(3): 777-807 doi: 10.1007/s12311-012-0355-9
  14. Onore, C., et al., The role of immune dysfunction in the pathophysiology of autism. Brain Behav Immun, 2012. 26(3): 383-92 doi: 10.1016/j.bbi.2011.08.007
  15. Schmidt, R.J., et al., Maternal periconceptional folic acid intake and risk of autism spectrum disorders and developmental delay in the CHARGE (CHildhood Autism Risks from Genetics and Environment) case-control study. Am J Clin Nutr, 2012. 96(1): 80-9 doi: 10.3945/ajcn.110.004416
  16. Mbadiwe, T. and Millis, R.M., Epigenetics and Autism. Autism Res Treat, 2013. 2013: 826156 doi: 10.1155/2013/826156
  17. Volk, H.E., et al., Residential proximity to freeways and autism in the CHARGE study. Environ Health Perspect, 2011. 119(6): 873-7 doi: 10.1289/ehp.1002835
  18. Zerbo, O., et al., Is maternal influenza or fever during pregnancy associated with autism or developmental delays? Results from the CHARGE (CHildhood Autism Risks from Genetics and Environment) study. J Autism Dev Disord, 2013. 43(1): 25-33 doi: 10.1007/s10803-012-1540-x
  19. Rai, D., et al., Parental depression, maternal antidepressant use during pregnancy, and risk of autism spectrum disorders: population based case-control study. BMJ, 2013. 346: f2059 doi: 10.1136/bmj.f2059
  20. Christensen, J., et al., Prenatal valproate exposure and risk of autism spectrum disorders and childhood autism. JAMA, 2013. 309(16): 1696-703 doi: 10.1001/jama.2013.2270
  21. Suren, P., et al., Association between maternal use of folic acid supplements and risk of autism spectrum disorders in children. JAMA, 2013. 309(6): 570-7 doi: 10.1001/jama.2012.155925
  22. Lyall, K., et al., Maternal dietary fat intake in association with autism spectrum disorders. Am J Epidemiol, 2013. 178(2): 209-20 doi: 10.1093/aje/kws433
  23. Abrahams, B.S. and Geschwind, D.H., Advances in autism genetics: on the threshold of a new neurobiology. Nature Reviews Genetics, 2008. 9(5): 341-55
  24. Geschwind, D.H., Genetics of autism spectrum disorders. Trends Cogn Sci, 2011. 15(9): 409-16 doi: 10.1016/j.tics.2011.07.003
  25. Chow, M.L., et al., Age-dependent brain gene expression and copy number anomalies in autism suggest distinct pathological processes at young versus mature ages. PLoS Genet, 2012. 8(3): e1002592 doi: 10.1371/journal.pgen.1002592
  26. O’Roak, B.J., et al., Sporadic autism exomes reveal a highly interconnected protein network of de novo mutations. Nature, 2012. 485(7397): 246-50 doi: 10.1038/nature10989
  27. Stankiewicz, P. and Lupski, J.R., Structural variation in the human genome and its role in disease. Annu Rev Med, 2010. 61: 437-55 doi: 10.1146/annurev-med-100708-204735
  28. Moon, C., et al., Two-day-olds prefer their native language. Infant behavior and development, 1993. 16(4): 495-500
  29. Pierce, K., et al., Face processing occurs outside the fusiform `face area’ in autism: evidence from functional MRI. Brain, 2001. 124(10): 2059-73 doi: 10.1093/brain/124.10.2059
  30. Schumann, C.M., et al., The amygdala is enlarged in children but not adolescents with autism; the hippocampus is enlarged at all ages. J Neurosci, 2004. 24(28): 6392-401 doi: 10.1523/JNEUROSCI.1297-04.2004
  31. Romero-Munguía, M.A.n., Mnesic Imbalance and the Neuroanatomy of Autism Spectrum Disorders, in Autism – A Neurodevelopmental Journey from Genes to Behaviour, Eapen, V., (Ed). 2011 Edition 1st, InTech. p. 425-44.
  32. Bal, E., et al., Emotion recognition in children with autism spectrum disorders: relations to eye gaze and autonomic state. J Autism Dev Disord, 2010. 40(3): 358-70 doi: 10.1007/s10803-009-0884-3
  33. Harms, M.B., et al., Facial emotion recognition in autism spectrum disorders: a review of behavioral and neuroimaging studies. Neuropsychol Rev, 2010. 20(3): 290-322 doi: 10.1007/s11065-010-9138-6
  34. Nakamura, K., et al., Brain serotonin and dopamine transporter bindings in adults with high-functioning autism. Arch Gen Psychiatry, 2010. 67(1): 59-68 doi: 10.1001/archgenpsychiatry.2009.137
  35. Austin, E.J., Personality correlates of the broader autism phenotype as assessed by the Autism Spectrum Quotient (AQ). Personality and Individual Differences, 2005. 38(2): 451-60
  36. Wakabayashi, A., et al., Are autistic traits an independent personality dimension? A study of the Autism-Spectrum Quotient (AQ) and the NEO-PI-R. Personality and Individual Differences, 2006. 41: 873-83
  37. De Sousa, A., Towards an integrative theory of consciousness: part 1 (neurobiological and cognitive models). Mens Sana Monogr, 2013. 11(1): 100-50 doi: 10.4103/0973-1229.109335
  38. Wing, L., Asperger’s syndrome: a clinical account. Psychol Med, 1981. 11(1): 115-29 http://www.ncbi.nlm.nih.gov/pubmed/7208735

[1] 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.

Dr Caroline Leaf: Putting thought in the right place

Following hard on the heels of her false assumption that our minds control our health, not our genes, and following the same theme, Dr Leaf had this to say today, “Everything is first a thought; the brain is being controlled with EVERY thought you think!”

Dr Caroline Leaf is a communication pathologist and a self-titled cognitive neuroscientist. Reading back through my blogs, this “thought controls the brain / mind controls matter” is a recurrent theme of hers. It is repeated multiple times in her books, like when she writes, “Thoughts influence every decision, word, action and physical reaction we make.” [1: p13] and “Our mind is designed to control the body, of which the brain is a part, not the other way around. Matter does not control us; we control matter through our thinking and choosing” [2: p33] just as a couple of examples.

So how does thought relate to the grand scheme of our brain and it’s processing? Does our thought really control our brain, or is it the other way around. Through all of the reading that I have done on neuroscience, I propose a model of the place of thought in relation to the rest of our brains information processing. It is based on the LIDA model, dual systems models, and other neuroscientific principles and processes.

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 [3].

CAP v2.1.2
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 (I discuss this in more detail in chapter 12 of my book, https://www.smashwords.com/books/view/466848). 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.

Perception
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.

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
Personality is “the combination of characteristics or qualities that form an individual’s distinctive character” [4]. 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.” [5]

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.” [6] 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 [7], predominantly through genes involved in the serotonin [8] and dopamine systems [9, 10]. The “non-shared environment” (influences outside of the home environment) contributes heavily to the remainder [11, 12].

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.

Physiology
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 [13].

Emotion
According to Watkins, “emotion” is the sum of all the data streams of physiology, or what he described as “E-MOTIONEnergy in MOTION.” [13] 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 [14].

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

Feelings
“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 [11, 12]. 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 [15]. 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 [16] 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.

Thoughts
Thoughts are essentially a stream of data projected into our conscious space. Baars [17, 18] 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.” [19]

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
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[1] 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 [20], 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 [21], with some assistance from working memory.

So as you can see, according to the CAP model, conscious thoughts are one link of a longer chain of neurological functions between stimulus and action – simply one cog in the machine. Thoughts are dependent on a number of processes that are both genetically and environmentally determined, beyond our conscious control. It’s simply wrong to assume that thoughts control the brain.

Dr Leaf is welcome to her opinion, but it is in contradiction to the overwhelming majority of neuroscientific knowledge

References

  1. Leaf, C., Who Switched Off My Brain? Controlling toxic thoughts and emotions. 2nd ed. 2009, Inprov, Ltd, Southlake, TX, USA:
  2. Leaf, C.M., Switch On Your Brain : The Key to Peak Happiness, Thinking, and Health. 2013, Baker Books, Grand Rapids, Michigan:
  3. Hao, X., et al., Individual differences in brain structure and resting brain function underlie cognitive styles: evidence from the embedded figures test. PLoS One, 2013. 8(12): e78089 doi: 10.1371/journal.pone.0078089
  4. Oxford Dictionary of English – 3rd Edition, 2010, Oxford University Press: Oxford, UK.
  5. De Pauw, S.S., et al., How temperament and personality contribute to the maladjustment of children with autism. J Autism Dev Disord, 2011. 41(2): 196-212 doi: 10.1007/s10803-010-1043-6
  6. Henriques, G. (When) Are You Neurotic? Theory of Knowledge: Psychology Today; 2012, 23 Nov 2012 [cited 2013 23 Nov 2012]; Available from: http://www.psychologytoday.com/blog/theory-knowledge/201211/when-are-you-neurotic.
  7. Vinkhuyzen, A.A., et al., Common SNPs explain some of the variation in the personality dimensions of neuroticism and extraversion. Transl Psychiatry, 2012. 2: e102 doi: 10.1038/tp.2012.27
  8. Caspi, A., et al., Genetic sensitivity to the environment: the case of the serotonin transporter gene and its implications for studying complex diseases and traits. Am J Psychiatry, 2010. 167(5): 509-27 doi: 10.1176/appi.ajp.2010.09101452
  9. Felten, A., et al., Genetically determined dopamine availability predicts disposition for depression. Brain Behav, 2011. 1(2): 109-18 doi: 10.1002/brb3.20
  10. Chen, C., et al., Contributions of dopamine-related genes and environmental factors to highly sensitive personality: a multi-step neuronal system-level approach. PLoS One, 2011. 6(7): e21636 doi: 10.1371/journal.pone.0021636
  11. Krueger, R.F., et al., The heritability of personality is not always 50%: gene-environment interactions and correlations between personality and parenting. J Pers, 2008. 76(6): 1485-522 doi: 10.1111/j.1467-6494.2008.00529.x
  12. Johnson, W., et al., Beyond Heritability: Twin Studies in Behavioral Research. Curr Dir Psychol Sci, 2010. 18(4): 217-20 doi: 10.1111/j.1467-8721.2009.01639.x
  13. Watkins, A. Being brilliant every single day – Part 1. 2012 [cited 2 March 2012]; Available from: http://www.youtube.com/watch?v=q06YIWCR2Js.
  14. Dixon, T., “Emotion”: The History of a Keyword in Crisis. Emot Rev, 2012. 4(4): 338-44 doi: 10.1177/1754073912445814
  15. Elliott, R., Executive functions and their disorders Imaging in clinical neuroscience. British Medical Bulletin, 2003. 65(1): 49-59
  16. Marien, H., et al., Unconscious goal activation and the hijacking of the executive function. J Pers Soc Psychol, 2012. 103(3): 399-415 doi: 10.1037/a0028955
  17. Baars, B.J. and Franklin, S., How conscious experience and working memory interact. Trends Cogn Sci, 2003. 7(4): 166-72 http://www.ncbi.nlm.nih.gov/pubmed/12691765 ; http://bit.ly/1a3ytQT
  18. Baars, B.J., Global workspace theory of consciousness: toward a cognitive neuroscience of human experience. Progress in brain research, 2005. 150: 45-53
  19. Repovs, G. and Baddeley, A., The multi-component model of working memory: explorations in experimental cognitive psychology. Neuroscience, 2006. 139(1): 5-21 doi: 10.1016/j.neuroscience.2005.12.061
  20. Bonn, G.B., Re-conceptualizing free will for the 21st century: acting independently with a limited role for consciousness. Front Psychol, 2013. 4: 920 doi: 10.3389/fpsyg.2013.00920
  21. Beste, C., et al., Response inhibition subprocesses and dopaminergic pathways: basal ganglia disease effects. Neuropsychologia, 2010. 48(2): 366-73 doi: 10.1016/j.neuropsychologia.2009.09.023

[1] 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.

Understanding Thought – Part 1

WHAT IS THOUGHT?

We’re all familiar with thought, to be sure, just like we’re familiar with our own bodies. But just because we know our own bodies doesn’t make us all doctors. In the same way, we might know our own thoughts well, but that doesn’t make us experts in the science of thought.

But understanding thought is important. If we don’t know what thoughts are, then it’s very easy to be conned into believing the myriad of myths about thought perpetuated about them by every pop-psychologist and B-grade life coach.

This series of blogs is taken from my book Hold That Thought: Reappraising the work of Dr Caroline Leaf. We will look at some basic neurobiology first, then look at the neurobiology of thought itself. We’ll discuss some psychological models of our thought processing, and finally we’ll discuss the common brain states and functions that are usually confused with thought.

Neurobiology 101

The nerve cell

At the most fundamental level of our thought process is the nerve cell, also called a neuron. Nerve cells, like all cells in the body, have a nucleus containing the genetic material. The nucleus is surrounded by cytoplasm, a watery chemical soup that contains the functional proteins that make the cell run. A thin lipid layer called the cell membrane envelopes the nucleus and cytoplasm. The cell membrane contains important protein structures such as receptors that help the cell receive signals from other cells, and ion channels, which help the cell regulate its internal chemistry.

Compared to other cells, nerve cells have three unique structures that help them do their job. First are dendrites, which are spiny branches that protrude from the main cell body, which receive the signals from other nerve cells. Leading away from the cell body is a long thin tube called an axon which helps carry electrical signal from the dendrites, down to the some tentacle-like processes that end in little pods. These pods, called the terminal buttons of the axon, and then convey the electrical signal to another nerve cell by directing a burst of chemicals towards the dendrites of the next nerve cell in the chain.

In order for the signal to be successfully passed from the first nerve cell to the second, it must successfully traverse a small space called the synapse.

The synapse

Despite being very close to each other, no nerve cell touches another. Instead, the spray of chemicals that’s released from the terminal button of the axon floats across a space of about 20-40nM (a nanometre is one billionth of a metre).

There are a number of different chemicals that traverse synapses, but each terminal button has its own particular one. The most well known are serotonin, noradrenaline and dopamine.

If the signal from the first nerve is strong enough, then a critical amount of the chemical is released and will make it across the gap to the dendrites of the second nerve cell on the other side. The chemical interacts with specific receptors on the new dendrites, which cause them to open up to certain salts like sodium and potassium. As sodium and potassium move in and out of the cell, a new electrical current if formed in the second nerve cell, passing the signal down the line.

To prevent the chemicals in the synapse from over-stimulating the second nerve cell, enzymes breakdown the chemicals to clear the space before the next signal comes past.

Nerve pathways

Combining nerve cells and synapses together creates a nerve pathway, where the input signal is received by specialised nerve endings and is transmitted down the nerve cell across a synapse to the next nerve cell, across the next synapse to the next nerve cell, and on and on until the signal has reached the destination for the output of that signal.

And that’s it. The entire nervous system is just a combination of nerve cells and the synapses between them.

What gives the nervous system and brain the near-infinite flexibility, and air of mystery, is that there are eighty-six billion nerve cells in the average adult (male) brain. Each nerve cell has hundreds to thousands of synapses. It’s estimated that there are about 0.15 quadrillion (that’s 150,000,000,000,000) synapses throughout the average brain [1]. And that’s not including the nerve cells and synapses in the spinal cord, autonomic nervous system and throughout the body. Each of these cells and synapses connect in multiple directions and levels, and transmit signals through the sum of the exciting or inhibiting influences they receive from, and pass on to, other nerve cells.

Single nerve cells may have the appearances of trees with their axon trunks and dendritic branches. But altogether, the billions of connections would more resemble a box of cobwebs.

Higher order brain structures

But unlike a box of cobwebs, the brain has precise organisation to the myriad of connections. These areas can be defined either by their structure, or by their function.

Structurally, there are areas in the brain that are dominated by nerve cell bodies, formed into a little cluster, called a nucleus (different from the nucleus of each cell). Then there are groups of axons bundled together, called a tract, which behave like a data cable for your computer. Nuclei process multiple sources of signal and refine them. The refined signals are sent into the appropriate tract to be transmitted to either another set of nuclei for further refinement, or to distant structures to carry out their effect. The axons of the nerve cells that make up the tracts are usually covered in a thick white material called myelin. Myelin acts like insulation on a wire, improving the speed and accuracy of the communicated signal. Parts of the brains with lots of myelinated cells are described as “white matter”. The nuclei and the cerebral cortex (the outer covering of the brain) are unmyelinated cells, and are referred to as “grey matter”.

On a functional level, the brain is divided into parts depending on what information is processed, and how it gets processed. For example, the cerebral cortex is divided into primary areas for the senses and for motor functions, secondary areas and tertiary association areas. The primary sensory areas detect specific sensations, whereas the secondary areas make sense out of the signals in the primary areas. Association areas receive and analyze signals simultaneously from multiple regions of both the motor and sensory areas, as well as from the deeper parts of the brain [2]. The frontal lobe, and specifically pre-frontal cortex, is responsible for higher brain functions such as working memory, planning, decision making, executive attention and inhibitory control [3].

Everything our senses detect is essentially deconstructed, processed then reconstructed by our brains. For example, when reading this page, the image is decoded by our retina and sent through a number of pathways to finally reach the primary visual cortex at the back of our brain. The primary visual cortex has 6 layers of nerve cells which simultaneously encode the various aspects of the image (especially colour, intensity and movement of the signals) and this information is sent to the secondary association areas that detect patterns, both basic (lines are straight, curved, angled) and complex (two diagonal intersecting lines form an ‘x’). One part of the secondary association areas in the visual cortex (the Angular Gyrus) processes these patterns further into the patterns of written words. The information on the various patterns that were discerned by the secondary association areas then get sent to the tertiary association area for the senses where those visual patterns are combined with patterns processed from other sensory areas (hearing, touch and internal body sensations) to form a complex pattern of multimodal association [2]. In the case of reading, the tertiary association area allows comprehension of the written words that were previously only recognised as words by the secondary association areas.

In the recent decades, with the widespread adoption of non-invasive methods of studying the active living brain such as PET scanning and fMRI, researchers have discovered that rather than discrete parts of the brain lighting up with a specific task, entire networks involving multiple brain regions are activated. This has lead to the paradigm of neurocognitive networks, in which the brain is made up of multiple interconnected networks that “are dynamic entities that exist and evolve on multiple temporal as well as spatial scales” and “by virtue of both their anatomical and functional architectures, as well as the dynamics manifested through these architectures, large-scale network function underlies all cognitive ability.” [4]

Emotions and feelings

Emotions are a difficult concept to define. Despite being studied as a concept for more than a century, the definition of what constitutes an emotion remains elusive. Some academics and researchers believe that the term is so ambiguous that it’s useless to science and should be discarded [5].

I’ll discuss emotions further in chapter 2, but for now, it’s easiest to think of our emotional state as the sum total of our different physiological systems, and feelings are the awareness, or the perception of our emotional state.

Different parts of the brain are responsible for the awareness of these feelings. The amygdala is often considered the seat of our fears, the anterior insula is responsible for the feeling of disgust, and the orbitofrontal and anterior cingulate cortex are involved in a broad range of different emotions [6].

Different emotional states are linked with different neurotransmitters within the brain. For example, a predisposition to anxiety is often linked to variations in the genes for serotonin transport [7] while positive and negative affect (“joy / sadness”) are linked to the dopaminergic system [8].

Memories

Memories, like thoughts, are something that we’re all familiar with in our own way.

Memory is quite complicated. For a start, there’s more than one form of memory. You’ve probably heard of short term and long term memory. Short term memory is further thought of as sensory memory and working memory. Long term memory is divided into semantic and episodic memory. Memory is also classified as either declarative memory, also called explicit memory, and nondeclarative memory, also called implicit memory.

Squire and Wixted explain, “Nondeclarative memory is neither true nor false. It is dispositional and is expressed through performance rather than recollection. These forms of memory provide for myriad unconscious ways of responding to the world. In no small part, by virtue of the unconscious status of the nondeclarative forms of memory, they create some of the mystery of human experience. Here arise the dispositions, habits, and preferences that are inaccessible to conscious recollection but that nevertheless are shaped by past events, influence our behavior and mental life, and are an important part of who we are.” [9]

On the other hand, declarative memory “is the kind of memory that is referred to when the term memory is used in everyday language. Declarative memory allows remembered material to be compared and contrasted. The stored representations are flexible, accessible to awareness, and can guide performance in a variety of contexts. Declarative memory is representational. It provides a way of modeling the external world, and it is either true or false.” [9]

Working memory is a central part of the memory model. Information from feelings, stored memories and actions all converge in working memory. The model of working memory initially proposed by Baddeley involves a central executive, “a control system of limited attentional capacity that is responsible for the manipulation of information within working memory and for controlling two subsidiary storage systems: a phonological loop and a visuospatial sketchpad.”[10] Baddeley later added a third subsidiary system, the episodic buffer, “a limited capacity store that is capable of multi-dimensional coding, and that allows the binding of information to create integrated episodes.” [10]

Working memory is known to be distinct from other longer term memories that are dependent on part of the brain called the hippocampus, because patients with severe damage to the hippocampus can remember a small amount of information for a short time, but are not able to push that information into longer term memory functions to retain that information. Information in working memory doesn’t last for any more than a few minutes [9].

So, there are many forms of memory that are important to our lives and influence our behaviour that are “inaccessible to conscious recollection”. But even declarative memory, which is accessible to thought, doesn’t actually make up the thought itself. Memories are stored representations.

When memories are formed or retrieved, the information is processed in chunks. As Byrne pointed out, “We like to think that memory is similar to taking a photograph and placing that photograph into a filing cabinet drawer to be withdrawn later (recalled) as the ‘memory’ exactly the way it was placed there originally (stored). But memory is more like taking a picture and tearing it up into small pieces and putting the pieces in different drawers. The memory is then recalled by reconstructing the memory from the individual fragments of the memory.” [11] Recalling the original memory is an inaccurate process, because sometimes these pieces of the memory are lost, faded or mixed up with another [12]. This is why what we perceive and what we recall are often two different things entirely.

Why do we have memory then, if it’s so flawed at recalling information? Because memory is less about recalling the past, and more about imagining and planning the future. As Schacter writes, “The constructive episodic simulation hypothesis states that a critical function of a constructive memory system is to make information available in a flexible manner for simulation of future events. Specifically, the hypothesis holds that past and future events draw on similar information and rely on similar underlying processes, and that the episodic memory system supports the construction of future events by extracting and recombining stored information into a simulation of a novel event. While this adaptive function allows past information to be used flexibly when simulating alternative future scenarios, the flexibility of memory may also result in vulnerability to imagination-induced memory errors, where imaginary events are confused with actual events.” [13]

References

  1. Sukel, K. The Synapse – A Primer. 2013 [cited 2013, 28/06/2013]; Available from: http://www.dana.org/media/detail.aspx?id=31294.
  2. Hall, J.E. and Guyton, A.C., Guyton and Hall textbook of medical physiology. 12th ed. 2011, Saunders/Elsevier, Philadelphia, Pa.:
  3. Stuss, D.T. and Knight, R.T., Principles of frontal lobe function. 2nd ed. 2013, Oxford University Press, Oxford ; New York:
  4. Meehan, T.P. and Bressler, S.L., Neurocognitive networks: findings, models, and theory. Neurosci Biobehav Rev, 2012. 36(10): 2232-47 doi: 10.1016/j.neubiorev.2012.08.002
  5. Dixon, T., “Emotion”: The History of a Keyword in Crisis. Emot Rev, 2012. 4(4): 338-44 doi: 10.1177/1754073912445814
  6. Tamietto, M. and de Gelder, B., Neural bases of the non-conscious perception of emotional signals. Nat Rev Neurosci, 2010. 11(10): 697-709 doi: 10.1038/nrn2889
  7. Caspi, A., et al., Genetic sensitivity to the environment: the case of the serotonin transporter gene and its implications for studying complex diseases and traits. Am J Psychiatry, 2010. 167(5): 509-27 doi: 10.1176/appi.ajp.2010.09101452
  8. Felten, A., et al., Genetically determined dopamine availability predicts disposition for depression. Brain Behav, 2011. 1(2): 109-18 doi: 10.1002/brb3.20
  9. Squire, L.R. and Wixted, J.T., The cognitive neuroscience of human memory since H.M. Annu Rev Neurosci, 2011. 34: 259-88 doi: 10.1146/annurev-neuro-061010-113720
  10. Repovs, G. and Baddeley, A., The multi-component model of working memory: explorations in experimental cognitive psychology. Neuroscience, 2006. 139(1): 5-21 doi: 10.1016/j.neuroscience.2005.12.061
  11. Byrne, J.H. Learning and Memory (Section 4, Chapter 7). Neuroscience Online – an electronic textbook for the neurosciences 2013 [cited 2014, Jan 3]; Available from: http://neuroscience.uth.tmc.edu/s4/chapter07.html.
  12. Bonn, G.B., Re-conceptualizing free will for the 21st century: acting independently with a limited role for consciousness. Front Psychol, 2013. 4: 920 doi: 10.3389/fpsyg.2013.00920
  13. Schacter, D.L., et al., The future of memory: remembering, imagining, and the brain. Neuron, 2012. 76(4): 677-94 doi: 10.1016/j.neuron.2012.11.001

Dr Caroline Leaf and the Profound Simplicity Paradox

It was a guy called Charles Bukowski that said once, ‘Genius might be the ability to say a profound thing in a simple way’. It always grabs our attention when something is said that’s easy to understand, yet deeply meaningful. The simple yet profound juxtaposition draws our attention and exercises our cognition in a way that nothing else seems to match. Those that are able to utter pervasive truth in a few syllables are elevated to gurus, and their pearls of wisdom are endlessly reposted on Pinterest and Facebook.

Of course, for something to be profound, it doesn’t just need to be deep, but also true.

Dr Caroline Leaf is a communication pathologist and self-titled cognitive neuroscientist. Her social media feeds are littered with Pinterest profundities, and she adds her own sometimes for good measure. Today, she shared something which I’m sure she thinks is one of those strokes of genius that Charles Bukowski was talking about,

“What we say and do is based on what we have already built into our minds.”

Well, her statement is simple, but it’s certainly not profound. It’s a paint-by-numbers version of the neuroscience of behaviour, based on her underlying assumption that we are in full control of every thought and action that we ever have or do.

It’s nice story to tell. It seems to fit with our experience of our thoughts and of the attribution of every action we take with our feeling of conscious volition. It’s just that it’s not what real neuroscientists actually tell us is going on in our brain.

Our thoughts and our actions are based on a number of things, mostly beyond our conscious control. This is because our perception, physiological responses, and personalities are all strongly genetically determined, our memory systems are predominantly subconscious, and so is the vast majority of the processing our brain does on a second-by-second basis. Our thoughts and our feeling of our conscious ‘free will’ are the subconscious brain simply projecting a small sliver of that information stream to a wider area of the cerebral cortex for fine-tuning (I discuss this in much more detail in chapters 1, 2 and 6 of my book).

So what we say and do is not based on just based on what we have already built into our minds, because our actions are largely built on our genetics and our subconscious memories, which we don’t necessarily have control over either.

There will be some people who think that this sounds like a cop-out, just an excuse to avoid responsibility for our own actions. I would argue that this actually refines our responsibility to that which we can change, taking the focus away from those things that we cannot change. For example, there’s no point in suggesting that I’m a bad father because I can’t breastfeed my children. This is an extreme example of course, but chiding someone for not doing something that they can’t do because of their genetic predisposition is no different.

Rather than focusing unnecessary effort on trying to change what cannot be changed, we should look to work on the things that can be changed. Even then, we all have different strengths and weaknesses. Some people will take a long time to learn something that another person might pick up straight away.

It’s also important for people to understand that not everything you struggle with is related to your poor choices. There’s no point in wrestling with something that isn’t going to move. All you do is tire yourself, sapping you of energy that you could be using to effect change on the things you do have power over.

So on the surface, Dr Leaf’s statement may be simple, but it’s ultimately erroneous. Instead of being liberating, it can actually be oppressing. Those who are looking for something profound would be better served looking somewhere else on Pinterest.

Reference:
Pitt, C.E., Hold That Thought: Reappraising the work of Dr Caroline Leaf, 2014 Pitt Medical Trust, Brisbane, Australia, URL www.smashwords.com/books/view/466848

Hold That Thought – Reappraising the work of Dr Caroline Leaf

Hold That Thought Cover

It’s been more than a few late nights in the making, but sixteen months and 68,000 words on, the early release of my new book is now available on line through Smashwords: https://www.smashwords.com/books/view/466848.  Apple iBook, Kindle, and a number of other platforms will come online soon.

Dr Caroline Leaf is a South African communication pathologist and self-titled cognitive neuroscientist, now based in the USA.  This book is an in-depth look at the current scientific understanding of thought, stress, free will and choice, as well as a thorough critique of Dr Leaf’s foundational teachings and the evidence she provides as proof of her hypotheses.

In the coming few days, I will make the text of the book available on this blog as well.  If you have any questions, send them in.  I’m happy to put up a FAQ page.  And as always, I’m happy to answer any legitimate criticism of my work, so long as it’s constructive and evidence based, not personal.

And as always, Dr Leaf herself is welcome to comment.  Indeed, I would value her feedback, and I’m sure any comment she wishes to make would be welcome by the Christian community as a whole.