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 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

Dr Caroline Leaf and the Mixed Message Memes

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If you were talking to your doctor, and she said, “Smoking is bad for you”, while lighting a cigarette for herself, would you be confused? Bit of a mixed message, don’t you think?

When I got back to Facebook last night, I found this interesting post from Dr Leaf: “If you have just spoken or done something … It means you have the physical root thought in your brain.” Perhaps not interesting in an I-never-knew-that sort of way … more interesting in a yet-another-mixed-message sort of way.

Dr Caroline Leaf is a Communication Pathologist and a self-titled Cognitive Neuroscientist. She has a habit of posting fluffy pseudoscientific memes to her social media feeds, which sound plausible at face value, but look a little closer, and they crumble like a sand castle at high tide.

Her current post is actually a bit sturdier than usual. We do use information we’ve learned to guide our ultimate behaviour, which include our words and our actions. But that’s not the whole story.

Our brain is an amazing organ. It processes a torrent of incoming information, compares it to previous experience stored in memory, and then delivers real-time instructions to the rest of the body, whilst updating the memory systems with the new information received. However, the brain also has a limited amount of energy that it can utilise – the brain only runs on about 40 watts of power [1: p7] (the same as a low power light bulb). In order to use this limited energy efficiently, the brain automates certain actions, like skills or habits, while retaining the flexibility to handle situations or to perform different actions than the skills or habits that we have developed.

The brain achieves this feat of brilliance by having a number of different types of memory [2] – procedural memory, priming, classical conditioning and non-associative learning make up implicit memory (memory not available to conscious awareness). Declarative memory is the fifth type of memory, which has two sub-components: episodic memory, which is the recallable memory of specific events (that you had coffee and eggs for breakfast), which itself is heavily dependent on semantic memory, the recallable memory for concepts (the abstract concepts of coffee, eggs, and breakfast) [3].

The storage of memories within declarative memory is also done piecemeal, by breaking down the information stored into chunks. Byrne notes, “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.” [4] Retrieving the original memory is an inaccurate process, because sometimes pieces of the memory are lost, faded or mixed up with another [5]. What the memory systems lose in accuracy of recall is more than made up for by the flexibility of the information stored in memory to plan current action, and to imagine possible future scenarios.

Each time the brain decides on an action, it subconsciously performs five different steps to determine the best action to take, although the best way to consider the process is simply to say that “voluntary” action is a flexible and intelligent interaction with the subject’s current and historical context (present situation and past experience) [6].

In a new situation, the brain takes the information from the senses (sight, hearing etc) and compares it with the necessary pieces of information recalled from memory, including previous actions taken in similar situations and their outcome. It then decides on the best course of action, plans what to move, when to move, how to move, and then performs one more final check before proceeding. If the situation is familiar, and the brain has a previous script to follow, like a skill or a habit, it will perform those actions preferentially because it’s more efficient in terms of brain energy used, but if there is no previous script, the brain will plan a novel set of actions appropriate to the situation.

The best example of this is driving a car. I learnt to drive in my parents’ 1970-something, 4-to-the-floor Chrysler Galant. The skills required to handle a manual transmission car with an old clutch was challenging to learn, but once those skills were mastered and road rules learnt, I could drive successfully. But I didn’t need to learn evasive maneuvers. When confronted with an emergency situation for the first time, my brain moved my body very quickly to control the car in ways I’d not practiced, before my conscious mind had a chance to process the incident. So my brain used skills I had learnt in ways that I had not learnt, independent of my conscious will.

Dr Leaf’s underlying assumption is that we are in full control of our thoughts and actions. Unfortunately for Dr Leaf, neuroscience proves that predictable brain activity occurs several seconds before a person is aware of their intention to act [7, 8], which runs counter to her presupposition. To try and patch the enormous hole in her argument, she contends that the brain activity that occurs before we are consciously aware of our intentions is just our non-conscious brain accessing our stored, previously conscious thoughts (see also [9], page 42). The implication is that anything you do is still a choice that you made in either the present, or your past. As she said in the Facebook post, “Everything you say and do is first a thought that you have built in your brain.”

Unfortunately for Dr Leaf, cognitive neuroscience disproves her folk-science. It’s way oversimplified to suggest that everything we do is based on our thought life. There are many chunks of our memory that don’t come from a willful, conscious input of information (acquired fear is one example). And the brain can use chunks of memory, often from memory systems not accessible by our conscious awareness, to produce complex actions that are completely new, without needing our conscious input.

Even though cognitive neuroscience disproves her meme, which is embarrassing enough for a woman who calls herself a cognitive neuroscientist, the bigger problem for this meme is that Dr Leaf is again contradicting herself.

About a month ago, Dr Leaf published on her social media feeds, “Don’t blame your physical brain for your decisions and actions. You control your brain!” Now she says that your words and actions are the result of a hardwired “physical root thought”, so your decisions and actions ARE the result of your physical brain. Which is it Dr Leaf? For the sake of her followers, her clarification would be welcome. After all, the more she contradicts herself, the more doubt she casts over the validity of the rest of her writing and teaching. Is she accurately interpreting research, and drawing valid conclusions? Dr Leaf is welcome to comment.

But one thing’s for sure; her mixed message memes are certainly not doing her any favours.

References

  1. Berns, G., Iconoclast : a neuroscientist reveals how to think differently. 2008, Harvard Business School Press, Boston:
  2. Squire, L.R. and Zola, S.M., Structure and function of declarative and nondeclarative memory systems. Proceedings of the National Academy of Sciences, 1996. 93(24): 13515-22 http://www.pnas.org/content/93/24/13515.abstract
  3. Binder, J.R. and Desai, R.H., The neurobiology of semantic memory. Trends Cogn Sci, 2011. 15(11): 527-36 doi: 10.1016/j.tics.2011.10.001
  4. 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.
  5. 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
  6. Haggard, P., Human volition: towards a neuroscience of will. Nat Rev Neurosci, 2008. 9(12): 934-46 doi: 10.1038/nrn2497
  7. Libet, B., et al., Time of conscious intention to act in relation to onset of cerebral activity (readiness-potential). The unconscious initiation of a freely voluntary act. Brain, 1983. 106 (Pt 3): 623-42 http://www.ncbi.nlm.nih.gov/pubmed/6640273
  8. Soon, C.S., et al., Unconscious determinants of free decisions in the human brain. Nat Neurosci, 2008. 11(5): 543-5 doi: 10.1038/nn.2112
  9. Leaf, C.M., Switch On Your Brain : The Key to Peak Happiness, Thinking, and Health. 2013, Baker Books, Grand Rapids, Michigan:

(PS: And happy Independence Day, USA! #4thofjuly )

Dr Caroline Leaf and the Myth of the Blameless Brain

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When I came back to Facebook this morning, I found this from Dr Leaf on my feed,

“Don’t blame your physical brain for your decisions and actions. You control your brain!”

Dr Caroline Leaf is a Communication Pathologist and a self-titled Cognitive Neuroscientist. Her post follows her theme of the last couple of weeks, the premise that the mind is the dominant cognitive force, controlling the physical brain, and indeed, all matter. I have written about the Myth of Mind Domination in a previous blog. But Dr Leaf’s latest offering here deserves special attention.

Lets think about her statement in more detail:

“Don’t blame your physical brain for your decisions and actions.”

What Dr Leaf is really saying is that the physical brain has no role in your choices or behaviour whatsoever, because if your physical brain had a role in the decisions and actions you make, it would also carry some blame for your poor decisions and actions.

“You control your brain.”

The question to ask here is, “Which part of ‘you’ controls your brain?” Her answer would be, “Your mind”, although she never says where the mind is. Certainly not in the physical brain or even in our physical body, since “Our mind is designed to control the body, of which the brain is a part, not the other way around.” [1: p33].

So an ethereal, disembodied force is in full control of our physical body, such that our brain has no role in the decisions we make or actions we take. Even at this stage of analysis, Dr Leaf’s statement is ludicrous. But wait, there’s more.

Dr Leaf’s statement puts her at odds with real Cognitive Neuroscientists. Professor Patrick Haggard is the Deputy Director of the Institute of Cognitive Neuroscience at the University College London. He has authored or co-authored over 350 peer-reviewed articles on the neuroscience of making choices. He writes, “Modern neuroscience rejects the traditional dualist view of volition as a causal chain from the conscious mind or ‘soul’ to the brain and body. Rather, volition involves brain networks making a series of complex, open decisions between alternative actions.” [2] Strike one for Dr Leaf.

Dr Leaf’s statement puts her at odds with herself. Two weeks ago when misinterpreting James 1:21, Dr Leaf wrote, “How you react to events and circumstances of your life is based upon your perceptions.” Perception is classically defined in neurobiology as conscious sensory experience [3: p8] although the work of cognitive neuroscientists has shown that perception can also be non-conscious [4, 5]. Either way, perception is based entirely on processing within the brain [3: p6-11]. So one week, Dr Leaf is saying that our brain determines how we behave, and then ten days later, she is telling us that our brain does not determine how we behave. Which is it? Strike two for Dr Leaf.

Finally, Dr Leaf’s statement is borderline insulting to the sufferers of congenital or acquired brain disorders. Would you tell a stroke patient that they shouldn’t blame their physical brain for their immobility, because they’re mind is in control of their brain? What about a child with Cerebral Palsy? Would you tell a mother of a child with Downs Syndrome that their child is having recurrent seizures because they aren’t using their mind properly to control their brain? Dr Leaf is doing exactly that. I find it incredible that she could be so insensitive, given her background as a speech pathologist working with patients with Acquired Brain Injury.

I imagine that her defence would be something along the lines of, “What I meant was, ‘don’t blame your normal physical brain for your decisions and actions. You control your functional brain.’” That sort of explanation would be less insulting to people with strokes or brain injuries, but it then undermines her whole premise. The hierarchy of the brain and the mind doesn’t change just because a part of the brain is damaged.

Besides, changes to brain function at any level can change the way a person thinks and behaves. The classic example was Phineas Gage, who in 1848, accidentally blasted an iron rod through his skull, damaging his left frontal lobe. History records that Gage’s well-mannered, pleasant demeanour changed suddenly into a fitful, irreverent, obstinate and capricious man whose workmates could no longer stand him [6]. Medical science has documented numerous cases of damage to the right ventromedial prefrontal cortex causing acquired sociopathy [7]. How can the mind be in control of the brain when an injury to the brain causes a sudden change in thought pattern and behaviour? Clearly one CAN blame the physical brain for one’s decisions and actions. Strike three. You’re out.

Dr Leaf is welcome to comment here. Perhaps she meant something completely different by her post, although there’s only so many ways that such a statement can be interpreted.

Ultimately, Dr Leaf’s love of posting pithy memes of dubious quality is now getting embarrassing. Being so far behind the knowledge of a subject in which she claims expertise is ignominious. Undermining her own premise and contradicting herself is just plain embarrassing. But to be so insensitive to some of the most vulnerable is poor form. I think she’d be well served by re-examining her facts and adjusting her teaching.

References

  1. Leaf, C.M., Switch On Your Brain : The Key to Peak Happiness, Thinking, and Health. 2013, Baker Books, Grand Rapids, Michigan:
  2. Haggard, P., Human volition: towards a neuroscience of will. Nat Rev Neurosci, 2008. 9(12): 934-46 doi: 10.1038/nrn2497
  3. Goldstein, E.B., Sensation and perception. 8th ed. 2010, Wadsworth, Cengage Learning, Belmont, CA:
  4. Kouider, S. and Dehaene, S., Levels of processing during non-conscious perception: a critical review of visual masking. Philos Trans R Soc Lond B Biol Sci, 2007. 362(1481): 857-75 doi: 10.1098/rstb.2007.2093
  5. 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
  6. Fumagalli, M. and Priori, A., Functional and clinical neuroanatomy of morality. Brain, 2012. 135(Pt 7): 2006-21 doi: 10.1093/brain/awr334
  7. Mendez, M.F., The neurobiology of moral behavior: review and neuropsychiatric implications. CNS Spectr, 2009. 14(11): 608-20 http://www.ncbi.nlm.nih.gov/pubmed/20173686