Don’t stress about stress, part 2

ThatWhichDoesNotKillUs

In the last blog post, we looked at some of the different ways of looking at stress outside of the medical field – the stress on a guitar string, the power band of the car engine, and the action of gravity on our bodies. In this post, I want to expand on those metaphors, using them to help us understand how we can respond to stress, and why stress isn’t our enemy, but it actually brings out our best if managed in the right way.

One of the reasons why gravity gives you strong muscles and bones, and zero gravity gives you weak muscles and bones, is because of resistance.

Movement involves work. We do “work” everyday in simple everyday activities, because our muscles and bones have to apply a certain amount of force in order to overcome gravity. Our muscles adapt by growing the muscle fibres to provide that force, and bones remodel themselves to provide the maximum resistance to the loads that gravity and the muscles put through them. We’re not aware of this day-to-day because we never experience prolonged changes in our gravitational fields.

But when we need to do more work than our muscles are accustomed to, our muscle fibres increase in strength, first as the nerve networks that supply the muscles become more efficient, after about two weeks of ongoing training, the fibres themselves increase in size [1, 2]. The growth in muscle fibres is caused by three related factors: mechanical tension, muscle damage and metabolic stress [2]. Mechanical tension involves “force generation and stretch”. In other words, the muscle fibres are stretched just beyond their usual capacity, and they actively fight against the resistance. This damages the weaker muscle fibres, which are repaired. The remaining muscle fibres are forced to adapt by growing larger because of the stimulation of growth factors [2].

One of my favorite “Demotivator” posters says, “That which does not kill me postpones the inevitable” [3]. Of course, the phrase that they’ve parodied is, “That which does not kill us makes us stronger.” Why is there truth to that idiom? Adversity occurs when life circumstances come against us. In other words, adversity resists us. In the arm wrestle between adversity and overcoming, work is involved. We have to fight back.

In a similar way, we grow when adversity pushes us just beyond what we have done before, stretching us. We may sustain some damage in the process, but that helps to reduce our weaknesses, and forces us into growth as we heal. When we push back against adversity, the “cells” of our character grow.

Of course, we all know examples where muscles fail under intense or prolonged loads. I vividly remember the pictures of the UK’s Paula Radcliffe, succumbing to the grueling hills and scorching Athens heat with only four miles left in the 2004 Olympic Marathon. Muscle failure from excessive stretch or excessive endurance parallels the allostatic load response, which is what people commonly referred to as ‘stress’.

Scientific evidence that stress is positive

There have been recent studies in animals that demonstrate that stress is physically as well as mentally enhancing.

Neurogenesis is the process of new nerve cell formation. Studies of rodents placed under intermittent predictable stressors showed an increase in neurogenesis within the hippocampus, which is the part of the brain related to learning and memory. Along with this enhancement of neurogenesis, the function of the hippocampus increased, specifically hippocampal-dependent memory, with a reduction in depression and anxiety-like behaviours.

As Petrik et al noted in their review, “Contrary to stress always being ‘bad’, it has long been appreciated that stress has an important biological role, and recent research supports that some amount of stress at the right time is actually useful for learning and memory.” [4]

Lessons from stress

So what can we learn from stress? How do we use the stress that we are exposed to every day to make us grow strong and durable?

Firstly, like the guitar string, we need to learn when we are in tune, at the peak of our productivity. Or like the car engine, what it feels like to be in the power band. When we know where our sweet spot is, we can operate within it, achieving our best in life without doing ourselves harm. This is the first point that we need to identify on our own personal stress/productivity curve. This is the point of maximum productivity.

The other life principle to be gained from the car engine analogy is that not all of us are high performance engines. I would love to think that I’m a F1 racing engine – highly tuned, supreme power – but I recognise my limitations. I would even settle for a 5-litre V8, but I know that I’m probably more like a well-tuned V6. We are what we are. Sometimes we apply the most stress to ourselves when we try to drive in the power band of someone else’s engine. We need to accept who we are.

It seems logical that if too much stress is bad for us, then having little or no stress is good for us. But like the new guitar string, minimal stress makes us unproductive. Like zero gravity on the body, little or no stress makes us weak.

And we need to understand that a bit more stress is ok. It’s inevitable that we are going to be stressed beyond what we usually cope with at times. But without that challenge, there would be no growth. Challenges usually hurt. You can’t have growth without pain. In the muscle analogy, at the stretch at which peak growth occurs, muscle fibres tear and the lactic acid build up in the remaining cells can be very uncomfortable. The key is learning how far we can push ourselves before we start to falter and fail. This is the second point we need to discover on our personal stress/productivity curve. This is the point of maximum growth.

Once we understand our own individual points of maximum productivity and growth, we can use them as guides to our personal growth and achievement. Actually, I should specify that these are our starting points, since as we face challenges and experience growth, the points will change slightly. We can remap those points and continue in our pattern of growth and development.

Pushing ourselves into just enough stress to achieve growth, then pulling back to rest and restore, is a pattern of growth that is seen in many facets of the natural world and the human body. Body builders and athletes use this method all the time in their training. They push themselves with more repetitions and heavier weights, or longer or faster runs, then they pull back to consolidate their gains. During our adolescence, our bodies naturally go through growth spurts – periods of rapid growth followed by a plateau, before the next burst of growth hormone hits us again. Even tree rings demonstrate that growth and consolidation occur all the way through the natural world.

This is the Stressed-Rest cycle. The studies in animals on neurogenesis strengthen the theory, because it was the animals that experienced bursts of stress that showed enhanced neurogenesis, memory and reduced depression/anxiety behaviours.

If you want maximum personal growth, constant stress does not help. There has to be times of rest. Some people think that rest time is wasted time, reducing productivity. But as explained, without rest time, productivity rapidly falls away. Without rest, stress goes bad, leading to allostatic overload.

So in summary, excessive stress is bad. But if all stress were bad, then we would all crumple any time that something became difficult. So stress is not a force for evil. Stress is part of our normal everyday lives, and is vital if we are to see ongoing personal growth.

We know from living life that we all don’t fall in a heap when things go wrong. We have in-built ways of coping that help us to absorb troubles and adversities and like emotional photosynthesis – turn them into fuel for growth.

This is the science of resilience, the counterbalance to the forces of stress that help us cope and adapt in a rapidly changing natural and social environment, the Yang to allostatic overload’s Yin. A discussion on the science of stress is not complete without a discussion of resilience, which I’ll discuss in the next blog in this series.

References

  1. Hortobagyi, T. and Maffiuletti, N.A., Neural adaptations to electrical stimulation strength training. Eur J Appl Physiol, 2011. 111(10): 2439-49 doi: 10.1007/s00421-011-2012-2
  2. Schoenfeld, B.J., The mechanisms of muscle hypertrophy and their application to resistance training. J Strength Cond Res, 2010. 24(10): 2857-72 doi: 10.1519/JSC.0b013e3181e840f3
  3. Adversity. Demotivators [cited July 2013]; Available from: http://www.despair.com/adversity.html.
  4. Petrik, D., et al., The neurogenesis hypothesis of affective and anxiety disorders: are we mistaking the scaffolding for the building? Neuropharmacology, 2012. 62(1): 21-34 doi: 10.1016/j.neuropharm.2011.09.003

Dr Caroline Leaf and the chemistry of perceptions

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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

Dr Caroline Leaf and the tongues trivia tall tales

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In every day life, if someone started talking in strings of indecipherable, chaotic syllables, you’d be giving them quite a lot of space, concerned about how much methamphetamine they’d been using.

In the average charismatic church, it’s just another service (the speaking in tongues, not the meth).

I’ve grown up in Pentecostal churches, and was baptised in the Holy Spirit when I was a child, so I forget how freaky it is for those who’ve never seen a whole church start talking or singing in tongues. For the uninitiated, the Bible talks about speaking in other tongues, which is a “New Testament phenomena where a person speaks in a language that is unknown to him. This language is either the language of angels or other earthly languages (1 Cor. 13:1). It occurred in Acts 2 at Pentecost and also in the Corinthian church as is described in 1 Corinthians 14. This New Testament gift was given by the Holy Spirit to the Christian church and is for the purpose of the edification of the Body of Christ as well as for glorifying the Lord.” (http://carm.org/speaking-in-tongues)

In scientific terms, speaking in tongues is referred to as “Glossolalia”, from the Greek, ‘glosso-‘ ~ ‘the tongue’ and ‘-lalia’ ~ ‘to speak, to chat’. Scientists who initially studied it in the 60’s and 70’s drew the conclusion that glossolalia was related to psychopathology (that people who spoke in tongues were crazy) [1, 2], and in later decades, it was thought to be caused by a form of temporal lobe epilepsy [3].

Earlier today, Dr Caroline Leaf, a communication pathologist and self-titled cognitive neuroscientist, declared that, “When we speak in tongues, research shows that the areas involved in discernment in the brain increase in activity, which means we increase in wisdom.”

I was fascinated to find this research for myself. Dr Leaf never references her social media memes, so I started looking through the medical literature on the subject from respected databases like PubMed, and search engines like Google Scholar.

Despite a thorough search, I was only able to find one article that studied the pattern of brain activity during speaking in tongues. The article, “The measurement of regional cerebral blood flow during glossolalia: A preliminary SPECT study” [4] took five healthy women, psychiatrically stable, long term members of their churches, who had all spoken in tongues for many years. They scanned their brain activity after a period of singing to gospel songs in English and compared it to their brain activity after the same amount of time praying in tongues (while listening to the same music as before).

What they found was that the brain was more active in the left superior parietal lobe, while there was a decrease in brain activity in the prefrontal cortices, left caudate nucleus and left temporal pole. There was a trend for an increase in the activity of the right amygdala, but this may have just been chance.

So are any of those brain regions responsible for discernment as Dr Leaf suggested?

Well, that all depends on how you define “discernment”. “Discernment” is not really a common neurobiological term. The standard term in the literature is “judgement”. The brain regions that are associated with evaluation and judgement are the amygdala and ventral portions of the striatum as well as the ventromedial prefrontal cortex (vmPFC), orbitofrontal cortex (OFC), the insula, the dorsal anterior cingulate cortex (dACC), and the periaqueductal gray (PAG) [5].

Are there any parts of the brain that match in the two lists? Only one – the ventromedial prefrontal cortex, or vmPFC for short. The prefrontal cortex is important in reasoning and decision-making, especially if there is uncertainty or novelty, while the vmPFC in particular is involved in the use of goal-relevant information in guiding responses, e.g., assigning value to choice options [6].

According to Dr Leaf, “When we speak in tongues, research shows that the areas involved in discernment in the brain increase in activity”. But that’s certainly not what the research paper said. The actual research is entirely the opposite.

Again, there are really only two reasonable explanations as to why the research contradicts Dr Leaf; either there is another piece of research which supports Dr Leaf’s assertion, or Dr Leaf is simply wrong.

At the risk of repeating myself, Dr Leaf needs to quote her sources when she is writing her little social media memes. Her meme may be perfectly justified by robust scientific evidence, but if she isn’t willing to share her sources, we’ll never know, and the only conclusion remaining is that Dr Leaf can’t interpret simple research.

So as it stands, there really isn’t any evidence that speaking in tongues makes you more discerning. By trying to claim otherwise, Dr Leaf further undermines her own reputation and credibility as an expert.

References

  1. Hine, V.H., Pentecostal glossolalia: towards a functional reinterpretation. Journal for the Scientific Study of Religion, 1969. 8: 212-26
  2. Brende, J.O. and Rinsley, D.B., Borderline disorder, altered states of consciousness, and glossolalia. J Am Acad Psychoanal, 1979. 7(2): 165-88 http://www.ncbi.nlm.nih.gov/pubmed/370074
  3. Persinger, M.A., Striking EEG profiles from single episodes of glossolalia and transcendental meditation. Perceptual and Motor Skills, 1984. 58: 127-33
  4. Newberg, A.B., et al., The measurement of regional cerebral blood flow during glossolalia: a preliminary SPECT study. Psychiatry Res, 2006. 148(1): 67-71 doi: 10.1016/j.pscychresns.2006.07.001
  5. Doré, B.P., et al., Social cognitive neuroscience: A review of core systems, in APA Handbook of Personality and Social Psychology, Mikulincer, M., et al., (Eds). 2014, American Psychological Association: Washington, DC. p. 693-720.
  6. Nicolle, A. and Goel, V., What is the role of ventromedial prefrontal cortex in emotional influences on reason?, in Emotion and Reasoning, Blanchette, I., (Ed). 2013, Psychology Press.

STOP THE PRESSES! Dr Leaf releases a new meme based on my correction, still doesn’t acknowledge source. (13 November 2014)

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So, I can’t find fault on what Dr Leaf said here.  It fits with the paper I quoted from Newberg et al (2006).  Still, it begs the question of why Dr Leaf couldn’t have said this in the first place, and why she still isn’t willing to share her citations?

It also raises the other obvious question, why is it important to know what our brain does in glossolalia?  It’s only a study of 5 patients, and I’m sure that not all episodes of speaking in tongues is associated with decreased intentionality.  The research, being so small, isn’t a true reflection of the practice of speaking in tongues.  Lets hope that the future will bring more funding to better study this central tenet to the charismatic faith.

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 mins 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 (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.

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. 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

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

In chapter one we discussed the conscious broadcast model of thought. 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.

Dr Caroline Leaf and the matter of mind over genes

Screen Shot 2014-11-07 at 8.13.45 pm

I think I might have to throw away my genetics textbook.

I was always taught that genes were the main driver behind health and disease, and I always thought it was a pretty good theory.

But not according to Dr Caroline Leaf, communication pathologist and self-titled cognitive neuroscientist, who said on her social media feeds today, “Our health is not controlled by genetics – our health is controlled by our mind.”

Taking her statement at face value, she appears to be saying that genes have nothing to do with our health. Dr Leaf has made some asinine statements in the past, but to suggest that genes are irrelevant to human health seemed so stupid that no one in their right mind would suggest such a thing.

Perhaps I was taking her statement the wrong way? I wanted to make sure I didn’t jump to any rash conclusions about Dr Leaf’s statement, so I pondered it at length. Could she be referring to ‘control’ in the absolute sense? How much control do genes have on our health? What about the mind?

After deliberating for a while, I still came to the conclusion that Dr Leaf’s statement was nonsense.

Unfortunately, Dr Leaf’s statement is, like so many of her previous Facebook memes, so vague as to be misleading. The meaning of ‘health’ and ‘controlled’ could be taken so many ways … which part of our health? How much regulation constitutes ‘control’? What about genetics?

Looking at her statement in more depth, it becomes clear that no matter which way Dr Leaf meant it, it’s still wrong. For example, all of human health is controlled, in part, by genetics. That’s because life itself is controlled by genetics. The human genome provides a blueprint for the construction of all of the proteins in all of the cells in our entire body. The expression of those genes determines exactly how our body will run. If the genes are wrong, if the translation of the gene code into a protein is wrong, or if too much or too little of a protein is made, all determines whether our body is functioning at its optimum level or not.

The stimulus for the expression of our genes is influenced by the environment in which we live. If I go out into the sun a lot, the UV light triggers my skin cells to make the protein melanin, which makes my skin go darker and helps to provide some protection against the damaging effects of the UV light.

While the environment plays a part of the expression of some genes, it’s wrong to say that genetics doesn’t control the process. If I go into the sun too much, I risk developing a melanoma, because the sun damages the genes in some of my skin cells, causing them to grow without control.

Genes are still responsible for the disease itself. Sometimes the trigger is from the environment, sometimes it’s not. There are some people with genes for melanoma who don’t need an environmental trigger, because they develop melanoma on skin that’s exposed to very little UV light, like the genital skin.

So fundamentally, even taking the environment into account, our health is controlled by our genetics.

The other part of Dr Leaf’s meme is also wrong. Our health is not controlled by our mind. Our genes are influenced by “the environment”, which according to the seminal paper by Ottman, “The environmental risk factor can be an exposure, either physical (e.g., radiation, temperature), chemical (e.g., polycyclic aromatic hydrocarbons), or biological (e.g., a virus); a behavior pattern (e.g., late age at first pregnancy); or a “life event” (e.g., job loss, injury). This is not intended as an exhaustive taxonomy of risk factors, but indicates as broad a definition as possible of environmental exposures.” [1]

Even if one considers the mind as part of the sub classification of “a behavior pattern”, it’s still pretty clear that most of the factors that make up our environment are not related to our mind at all but are related to the external world, of which we have minimal or no control over. Sure, we make choices, but our choices aren’t truly free. They’re constrained by the environment in which we find ourselves. In the same way, our mind may have some tiny influence on our health, but only insofar as our environment and our genes will allow.

When it all boils down, this meme of Dr Leaf’s is rested on her foundational presumption that our mind can control matter, a very strong theme throughout her most recent book [2], but which is still preposterous. Our thoughts are simply a function of our brain, which is in turn determined by the function of our nerve cells, which is in turn a function of our genes and their expression.

Our mind doesn’t control matter. Matter controls our mind.

I can keep my genetics textbooks after all.

References

  1. Ottman, R., Gene-environment interaction: definitions and study designs. Prev Med, 1996. 25(6): 764-70 http://www.ncbi.nlm.nih.gov/pubmed/8936580
  2. Leaf, C.M., Switch On Your Brain : The Key to Peak Happiness, Thinking, and Health. 2013, Baker Books, Grand Rapids, Michigan:

Understanding Thought – Part 3

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’ve looked at some basic neurobiology and the neurobiology of thought itself. Today we’ll discuss some psychological models of our thought processing, and the common brain states and functions that are usually confused with thought.

Other cognitive frameworks of thought

Dual Systems

A number of models of thought use a dual systems approach, explaining our cognitive process in terms of two systems.

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” as people typically think about it. It is both conscious and reflective in character, and proceeds in a slow, serial manner, according to principles that vary among both individuals and cultures [1]. This system is in harmony with the Global Workspace/LIDA concept of the cognitive cycle.

System 2 is generally held to be subject to intentional control, hence why thoughts can be volitional. System 2 can be guided by normative beliefs about proper reasoning methods. In other words, we can learn ways of thinking about our thoughts to handle them better. And one of the principal roles often attributed to system 2 is to override the unreflective responses that are issued automatically by system 1 in reasoning tasks, when these fall short of appropriate standards of rationality. We can use thought to modulate or suppress our intuitive responses, the concept of “think before you act”.

Neuroscience research confirms the neural networks involved with the dual systems, and have taken the theory further [2]. Not only can stimuli that are emotionally significant activate the lower, emotional parts of our brain, they can do so without us ever being consciously aware they were detected. For example, when test subjects had their visual cortex temporarily stunned by a transcranial magnetic stimulator, they could detect whether a face was happy or sad and even where it was on a grid without consciously sensing that they had “seen” a face [3]. Subconscious emotional stimuli can modulate our attention before we are aware of their perception [4].

Relational Frame Theory / Acceptance And Commitment Therapy

Relational frame theory, and the clinical approach based on it called Acceptance and Commitment Therapy, sees thoughts as contextual. This is interesting, as new neurobiological approaches such as neurocognitive networks are also girded by the developing view of cognition which is that cognition “is marked by both dynamic flexibility and context sensitivity.” [5]

Relational frame theory posits that “the core of human language and cognition is learning to relate events mutually and in combination not simply on the basis of their formal properties (e.g., size, shape) but also on the basis of arbitrary cues.” [6] Basically, we understand things in both concrete and abstract ways. “The gold coin is small” is referring to the tangible properties of the gold coin. “The gold coin is very valuable” is referring to the arbitrary properties of the gold coin, which are values that we define in our minds.

Hayes states, “A key RFT insight of clinical importance is that relational framing is regulated by two distinguishable features: the relational context and the functional context … The relational context determines what you think; the functional context determines the psychological impact of what you think.” [6]

So in terms of thought, what we think isn’t necessarily reliable. It’s contextual, and often abstract and arbitrary. The meanings and values that are placed on our thoughts are related to the context in which they came to us, and the impact is also arbitrary, a function of our minds and our language.

As William Shakespeare wrote, “for there is nothing either good or bad, but thinking makes it so.” [7] Thoughts are just that – thoughts. So while there is a mountain of published literature on “negative” or “positive” thoughts, such distinctions are subjective, arbitrary, and often entirely unhelpful.

We often become fused to the meaning of our thoughts. We begin to take them literally, without noticing the process of thinking itself. When the thoughts become painful, we don’t know how to handle them, and we run from them, or try to suppress them. But in fighting with the thoughts, we actually draw attention to them and make them more powerful. This makes them even more painful, and makes the avoidance worse. We then lose flexible contact with the present moment, as we become more and more consumed with the internal battle with our painful thoughts and subsequent emotions. Rather than looking around us, all we can do is focus on the pain or be anywhere else where difficult events are not occurring. [6]

The key in this battle is not to engage with the “negative” thoughts by pushing them away or trying to change them. Pushing the painful thoughts away makes them go away for a while, but it takes a lot of effort. The thoughts return as we tire, but we have less energy to resist them.

Try holding a fully inflated basketball under water. It’s possible, but the basketball wants to get back to the surface. Holding it down is hard work. You usually can’t do it for long. Fighting our thoughts is the same.

Harris describes the focus of Acceptance and Commitment Therapy, “around two main processes: developing acceptance of unwanted private experiences which are out of personal control, commitment and action towards living a valued life … In ACT, there is no attempt to try to reduce, change, avoid, suppress, or control these private experiences. Instead, clients learn to reduce the impact and influence of unwanted thoughts and feelings, through the effective use of mindfulness.” [8]

The first principle of ACT is to start treating thoughts as what they really are … just thoughts. This is simply done by learning to observe the process of thinking again, to realise that the words going through our minds are just words. They only have the meaning that we give to them. They only have the power that we allow them to have.

The key to overcoming thought patterns we don’t want isn’t to change them, it’s to remove their power. Trying to change them means engaging with them, which only makes them stronger. Disempowering them means seeing them for what they are. They may sound like Rottweiler’s but when you actually look, they’re more like Chihuahua’s with megaphones. When you understand that your thoughts are not in control, you can move forward into the actions that really bring change.  If you want to know more about ACT, or you would like to use ACT to help stop fighting your thoughts, there are a number of free resources that are a great starting point = http://www.actmindfully.com.au/free_resources

What is, and is not, a thought?

Thought, therefore, is simply a broadcast of one part of a deeper flow of information. Thought is not a controlling force. It’s not a case of, “I think, therefore, I am”, but, “I am, therefore, I think.”

Thoughts are often described in the peer-reviewed publications as the “stream of thought” or the “stream of consciousness”. According to Baars and Franklin, thoughts arise from the broadcast step of multiple cognitive cycles, but the conscious broadcast of our thought stream is limited to a single cognitive cycle at any given instant. Thus, even though it is considered a “stream”, our awareness of our thought is in a serial, sometimes disparate, sequence of frames [9].

There are some features of our stream of thought that differentiate it from other brain activity. We have a level of voluntary control over our stream of thought, even if it’s not direct [10]. It is also characterized by a metacognitive level – we have “thinking about thinking” [1, 11], and we have “awareness of awareness” [12].

Yet there are still many neurological functions that are confused with thoughts.

Brain activity

“Thoughts” are often confused for any brain activity. The stream of thought is sometimes referred to as the “stream of consciousness” but that’s a misnomer.

Consciousness has varying levels (coma, deep sleep, lucid dreaming, awake, and alert). Only some of these levels of consciousness allow thought. Therefore, it would be fair to say that thoughts are a form of activity of the brain, just like Toyotas are a form of car.

Brain activity is largely subconscious. It carries on in the background without our awareness [2]. There are multiple simultaneous streams of data being perceived all the time – sensation from our ears, skin, eyes and internal organs – that our brain filters out before it reaches our awareness. Background traffic noise, the pressure of your clothes on your skin, joint position, heart rate and breathing, for example. It’s not that these sensations are not present, but you only become aware of them when your attention is drawn to them. Those data streams are not thoughts in and of themselves because we lack awareness of them. They only become part of our thoughts when attention is paid to them. Since thoughts are characterized by metacognition, “awareness of awareness”, then neural activity we aren’t aware of cannot be considered thoughts.

The other problem with defining all brain activity as “thought” is that such as definition would also mean that seizures were thoughts, or brainstem reflexes were thoughts. We intuitively know that’s not the case.

Dreams

So what about dreams? We’re aware of dreams, aren’t we? Could dreams be considered thoughts?

Dreams are awareness of perception and emotion, similar to our state of awareness when we’re awake. But dreams occur in an altered state of consciousness (that is, we are asleep). Dreams also lack self-awareness. When you dream, you don’t realise that you’re dreaming. Secondary consciousness, the level of consciousness that we possess when we are awake, is defined in part as having awareness of awareness. It is more than just having awareness of perception and emotion. It is “self-reflection, insight, judgment or abstract thought that constitute secondary consciousness.” [12]

Memories

As I wrote earlier, memories aren’t just simple recall, but a complex system involving both conscious and unconscious elements. The conscious elements of memory are simply stored representations of events and experiences. They may become part of a thought broadcast, but they are not thoughts per se.

References

  1. Fletcher, L. and Carruthers, P., Metacognition and reasoning. Philos Trans R Soc Lond B Biol Sci, 2012. 367(1594): 1366-78 doi: 10.1098/rstb.2011.0413
  2. 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
  3. Jolij, J. and Lamme, V.A., Repression of unconscious information by conscious processing: evidence from affective blindsight induced by transcranial magnetic stimulation. Proc Natl Acad Sci U S A, 2005. 102(30): 10747-51 doi: 10.1073/pnas.0500834102
  4. Ohman, A., et al., Emotion drives attention: detecting the snake in the grass. J Exp Psychol Gen, 2001. 130(3): 466-78 http://www.ncbi.nlm.nih.gov/pubmed/11561921
  5. 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
  6. Hayes, S.C., et al., Acceptance and commitment therapy and contextual behavioral science: examining the progress of a distinctive model of behavioral and cognitive therapy. Behav Ther, 2013. 44(2): 180-98 doi: 10.1016/j.beth.2009.08.002
  7. Shakespeare, W., Hamlet, Act II, Scene 2.
  8. Harris, R., Embracing Your Demons: an Overview of Acceptance and Commitment Therapy. Psychotherapy In Australia, 2006. 12(6): 1-8 http://www.actmindfully.com.au/upimages/Dr_Russ_Harris_-_A_Non-technical_Overview_of_ACT.pdf
  9. Franklin, S., et al., Conceptual Commitments of the LIDA Model of Cognition. Journal of Artificial General Intelligence, 2013. 4(2): 1-22
  10. 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
  11. Scott, B.M., Levy, M. G., Metacognition: Examining the components of a fuzzy concept. Educational Research eJournal, 2013. 2(2): 120-31 doi: 10.5838/erej.2013.22.04
  12. Hobson, J.A., REM sleep and dreaming: towards a theory of protoconsciousness. Nat Rev Neurosci, 2009. 10(11): 803-13 doi: 10.1038/nrn2716