Tag Archives: ASD

Should pregnant women still take antidepressants if they’re depressed? – SSRI’s and the risk of autism

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As is my usual habit, I sat down tonight to do something useful and wound up flicking though Facebook instead.  Procrastination … avoidance behaviour … yeah, probably.  But at least this time it turned out to be rather useful procrastination, because I came across a science news story on Science Daily about a study linking the use of anti-depressants in pregnancy with an 87% increased risk of autism.

Actually, this is old news.  Other studies have linked the use of some anti-depressants with an increased risk of autism, such as Rai et al in 2013 [1].

The latest study to come out used data from a collaboration called the Quebec Pregnancy Cohort and studied 145,456 children between the time of their conception up to age ten.  In total, 1,045 children in that cohort were diagnosed with autism of some form, which sounds like a lot, but it was only 0.72%, which is actually lower than the currently accepted prevalence of autism in the community of 1%.

What the researchers got excited about was the risk of developing autism if the mother took an antidepressant medication at least at one time during her pregnancy.  Controlling for other variables like the age, wealth, and other health of the mothers, a woman who took an anti-depressant during pregnancy had a 1.87 times greater chance that her baby would end up with ASD, compared to women who did not take an anti-depressant [2].

An 87% increase sounds like an awful lot.  In fact, it sounds like another reason why anti-depressants should be condemned … right?

Well, like all medical research, you’ve got to consider it all in context.

First, you’ve always got to remember that correlation doesn’t always equal causation.  In this particular study, there was a large number of women being followed, and their children were followed for a long enough time to capture all of the likely diagnoses.  So that’s a strength.  They also tried to control for a large number of variable when calculating the risk of anti-depressants, which also adds more weight to the numbers.

Although the numbers are strong, studies like these can’t prove that one thing causes another, merely that they’re somehow linked.  It might be that taking anti-depressants causes the brain changes of autism in the foetus, but this sort of study can’t prove that.

Even if the relationship between anti-depressants and ASD was cause-and-effect, what’s the absolute risk?  Given the numbers in the study, probably pretty small.  With a generous assumption that ten percent of the study population was taking anti-depressants, the increase in the absolute risk of a women taking anti-depressants having a child with ASD is about 0.5%.  Or, there would be one extra case of autism for every 171 that took anti-depressants.

Hmmm … when you think of it that way, it doesn’t sound as bad.

You also have to consider the increase in risk to women and their offspring when they have depression that remains untreated, or in women that stop their anti-depressant medications.  There is some evidence that babies born to women with untreated depression are at risk of prematurity, low birth weight, and growth restriction in the womb, as well as higher impulsivity, poor social interaction, and behavioural, emotional and learning difficulties.  For the mother, pregnant women with depression are more at risk of developing postpartum depression and suicidality, as well as pregnancy complications such as preeclampsia, and an increase in high-risk health behaviour such as smoking, drug and alcohol abuse, and poor nutrition.  Women who discontinued their antidepressant therapy relapsed significantly more frequently compared with women who maintained their antidepressant use throughout pregnancy (five times the rate) [3].

So the take home messages:

  1. Yes, there’s good evidence that taking anti-depressants in pregnancy is linked to an increased risk of a child developing autism.
  2. But the overall risk is still small. There is one extra case of autism for every 171 women who take anti-depressants through their pregnancy.
  3. And this should always be balanced out by the risks to the mother and child by not adequately treating depression through pregnancy.
  4. If you are pregnant or you would like to become pregnant, and you are taking anti-depressants, do not stop them suddenly. Talk to your GP, OBGYN or psychiatrist and work out a plan that’s best for you and your baby.

References

[1]       Rai D, Lee BK, Dalman C, Golding J, Lewis G, Magnusson C. Parental depression, maternal antidepressant use during pregnancy, and risk of autism spectrum disorders: population based case-control study. Bmj 2013;346:f2059.
[2]       Boukhris T, Sheehy O, Mottron L, Bérard A. Antidepressant use during pregnancy and the risk of autism spectrum disorder in children. JAMA Pediatrics 2015:1-8.
[3]       Chan J, Natekar A, Einarson A, Koren G. Risks of untreated depression in pregnancy. Can Fam Physician 2014 Mar;60(3):242-3.

Putting thought in the right place, part 2

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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.

Hold That Thought – Reappraising the work of Dr Caroline Leaf

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Hold That Thought Cover

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

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

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

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

Dr Caroline Leaf, Dualism, and the Triune Being Hypothesis

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Executive Summary

The idea that humans have an immaterial soul, separate to the body, has spanned history and culture. This idea is known as dualism. The concept of the spirit is fundamental to the Christian church. Christians are usually taught that humans are a spirit, having a soul and living in a body (the Triune Being Hypothesis). The concept permeates the work of Dr Caroline Leaf, forming the basis for her assumptions that our minds can control matter.

However, the Bible does not state that the spirit and soul are separate to the body, only that they are linked in the earthly and supernatural realms. Over the last few decades, cognitive neuroscience has demonstrated that definable neural networks within the human brain mediate the components of the traditional soul. Religious belief and spiritual experiences are also heavily reliant on the human brain.

These findings, along with a number of other philosophical objections, prove that dualism is not compatible with science or philosophy. Dr Leaf’s reliance on the concept of dualism creates an intellectual dissonance between her teaching and neuroscience.

The notion that the soul and the spirit are separate to the body is also incorrect. However, quantum physics, and String Theory in particular, suggest that other dimensions and other universes exist, which may provide a scientifically plausible explanation of both natural and supernatural realms. It may be that our earthly body houses our natural spirit and soul within the brain, but that these are translocated to the celestial realm upon death. The challenge for the Christian church now is to unite the evidence of cognitive neuroscience with the description of the spirit, soul and body from scripture and further delineate the doctrine of humans as triune beings.

(Word count: 7256, including references)

Introduction

Are we a body with a mind, or a mind with a body?

It sounds a bit like the age-old chicken and the egg conundrum. In Ancient Greece, Plato proposed that human beings have an immaterial soul distinct from the material body while Descartes reinvigorated the idea in the 17th century. But the idea of the distinct immaterial soul is also found throughout different religions, and seems to be interwoven through the Bible as well.

For Dr Caroline Leaf, Communication Pathologist and self-titled Cognitive Neuroscientist, dualism is fundamental to her theory of “Mind over Matter”. In her 2013 book, “Switch On Your Brain”, Dr Leaf states that, “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.” [1: p33] She has also made several similar public statements via her social media feeds, such as, “Don’t blame your physical brain for your decisions and actions. You control your brain!” (6/6/2014) and “Your mind is all powerful! Your brain simply captures what your mind dictates! 2 Timothy 1:7.” (11/5/2014)

I have previously blogged about the scriptural and scientific voracity of Dr Leaf’s various statements on the Mind-Body problem (see also “Dr Caroline Leaf and the Myth of the Blameless Brain“, and others). But when she published, “Your mind will adjust your body’s biology and behaviour to fit with your beliefs” (21/6/2014) I thought enough was enough. The concept of dualism not only permeates the teachings of Dr Leaf, but also significantly influences the current understanding of the Biblical principles of the soul and spirit. So, this topic deserves an in-depth review, to ensure that the thinking within the church aligns with both scripture and science.

The Triune Being Hypothesis

On the 9th of June 2014, Dr Leaf published another meme on her social media feeds, “We are triune beings designed to be lead by the Holy Spirit … who speaks to our spirit. Our spirit controls our soul/mind and our soul/mind controls our body.”

By virtue of growing up in a Christian family, going to a Christian school, and digesting thousands of sermons during my lifetime, I’m very familiar with the concept of humans as a triune being (“triune”, meaning “three in one”). The concept I’ve been taught is similar to Dr Leaf’s view: that humans consist of three separate but interlinked components, the ethereal spirit and soul, and the physical body. The soul, in turn, consists of the mind, will and emotions. The three-part design reflects the image of God who is, of course, a triune being (the Holy Trinity: Father, Son and Holy Spirit). The hypothesis proposes that the body is just an earthly dwelling for a being that is fundamentally spirit in nature, the soul being the intermediary between the two.

In keeping with the theme, this essay will be in three parts! First, I review the Biblical evidence relating to the body, soul and spirit. Second, I review the scientific evidence relating to the spirit and soul. And finally, I discuss how the scriptural and scientific evidence relates to our current understanding of dualism, the triune being hypothesis and the implications for Dr Leaf and Christianity more broadly.

The Bible on the Triune Being Hypothesis

One of the fundamental arguments used by those who support the idea of man as a triune being is the way the Apostle Paul used distinct words to describe body, soul and spirit within the same sentence. For example, in 1 Thessalonians 5:23, Paul wrote, “And the very God of peace sanctify you wholly; and I pray God your whole spirit and soul and body be preserved blameless unto the coming of our Lord Jesus Christ” (emphasis added).

The three words used in ancient Greek were pneuma (‘spirit’), psyche (‘soul’) and soma (‘body’). According to Thayer’s Greek Lexicon, the words pneuma (‘spirit’) and psyche (‘soul’) were often used indiscriminately. So although the Apostle Paul distinctly used the word pneuma separately to the word psyche as in 1 Thessalonians 5:23, most of the other New Testament writers weren’t so precise.

James wrote that without the spirit (pneuma), the body (soma) would die (James 2:26). This also suggests that the spirit is different to the body, but still integral to the whole person, although given the interchangeable use of the terms, James may have also been referring to the soul.

However, Jesus told the disciples in Matthew 10:28, “And fear not them which kill the body (soma), but are not able to kill the soul (psyche): but rather fear him which is able to destroy both soul (psyche) and body (soma) in hell.” This suggests that both the soul and the body maybe found in hell, a post-death spiritual dimension (see also Luke 12:5). So it seems that at least in some form, our supernatural selves also possess a body and mind.

This idea seems to have some backing in the form of the description given in the Bible of the resurrected body of Jesus. After Jesus was crucified and buried, scripture describes the empty tomb, and the multiple sightings of Jesus by the disciples up until the time that he ascended into heaven (Luke 24). He walked along the road to Emmaus with two disciples, Cleopas and probably Cleopas’ wife Mary (see also John 19:25). He then appeared in the middle of the group of disciples within an instant. He still possessed the defects caused by the crucifixion. He ate some broiled fish and some honeycomb (see Luke 24:42-43). He said to the disciples at this meeting with them, “Behold my hands and my feet, that it is I myself: handle me, and see; for a spirit hath not flesh and bones, as ye see me have.” (Luke 24:39) Not only did he have the same physical characteristics as his pre-resurrected body (same appearance, same gender etc), but he also had similar mental traits, such as self-awareness, memory of his pre-resurrection life, and emotions and connection to the people around him. However, he was not subject to the natural laws of physics, twice suddenly appearing in a closed room (John 20:19 and 26).

Therefore it appears that rather than being a spirit housed in a body and furnished with a soul, we are instead an inseparable combination of body, soul and spirit – three unique but indivisible parts – but in different dimensions depending on which side of eternity we currently reside.

1 Thessalonians 5:23 confirms, rather than precludes, this view. Reviewing the scripture again, Paul wrote, “And the very God of peace sanctify you wholly; and I pray God your whole spirit and soul and body be preserved blameless unto the coming of our Lord Jesus Christ.” Paul chooses to emphasize all three components of our triune being equally in his prayers and wishes. If only our spirit was to pass into the celestial realm, then Paul wouldn’t have needed to delineate the three parts of our triune composition, but could have instead written “And the very God of peace sanctify you wholly; and I pray God your whole spirit be preserved blameless unto the coming of our Lord Jesus Christ”. By penning, “whole spirit and soul and body be preserved blameless”, Paul seems to treat all three parts as equally important to our future with Christ.

It follows that if we believe that our heavenly body is an integral part with our spirit and soul on the celestial side of eternity, then it should follow that our spirit and our soul are part of, and dependent on, our earthly body on this side of eternity.

This proposal differs from the conventional wisdom at two fundamental points:

1. I suggest that the spirit is integral to, and dependent on our earthly body whilst we live on the earth,
and
2. I suggest that the whole person is translated across from the earthly realm to the celestial, rather than just the spirit.

Such suggestions are compatible with current scientific understanding. There is ample evidence of spiritual neural networks that complement the emotional and moral parts of our brain (this will be discussed further in a future section).

String Theory provides a plausible explanation of other dimensions and worlds in parallel with our own which could very easily explain a spiritual dimension. String Theory is the theory that the very fabric of the cosmos is made up of tiny vibrating loops of energy, which physicists call “strings”. These strings are almost impossibly small. Physicist Brian Greene said that, “Each of these strings is unimaginably small. In fact, if an atom were enlarged to the size of the solar system, a string would only be as large as a tree!” [2] It’s the shape and vibrational pattern of each of these strings that gives subatomic particles their properties, which in turn combine to make up everything we see in the universe, including ourselves.

In order for these strings to vibrate and move the way they are predicted to, String Theory postulates that there are actually 11 dimensions of space. In one of these dimensions, a string could become stretched out into a membrane, or a “brane” for short. I’ll let Brian Greene and colleagues explain it further.

“BRIAN GREENE: The existence of giant membranes and extra dimensions would open up a startling new possibility, that our whole universe is living on a membrane, inside a much larger, higher dimensional space. It’s almost as if we were living inside … a loaf of bread? Our universe might be like a slice of bread, just one slice, in a much larger loaf that physicists sometimes call the “bulk.” And if these ideas are right, the bulk may have other slices, other universes, that are right next to ours, in effect, “parallel” universes. Not only would our universe be nothing special, but we could have a lot of neighbours. Some of them could resemble our universe, they might have matter and planets and, who knows, maybe even beings of a sort. Others certainly would be a lot stranger. They might be ruled by completely different laws of physics. Now, all of these other universes would exist within the extra dimensions of M-theory, dimensions that are all around us. Some even say they might be right next to us, less than a millimetre away. But if that’s true, why can’t I see them or touch them?
BURT OVRUT: If you have a brane living in a higher dimensional space, and your particles, your atoms, cannot get off the brane, it’s like trying to reach out, but you can’t touch anything. It might as well be on the other end of the universe.
JOSEPH LYKKEN: It’s a very powerful idea because if it’s right it means that our whole picture of the universe is clouded by the fact that we’re trapped on just a tiny slice of the higher dimensional universe.” [3]

Although it sounds preposterous, String Theory isn’t a fantasy of a few physicists who have watched too many sci-fi shows. String Theory is mathematically proven, and accepted by the majority of scientists.

What if our physical reality was one brane, the supernatural realm was a different brane, and heaven was another? Angels could be all around us, in a different dimension of space that we cannot ordinarily perceive, but who have the ability to move into our dimension if required. When we die, it’s possible that our whole person is transformed into a different dimension – the supernatural or celestial brane. The physical body remains like a snakeskin left after the snake has shed it.

My theory is only one of many possible theories. Ultimately, they all remain scientifically unprovable. While String Theory is well accepted by physicists all over the world, and the predictions of extra dimensions and branes are mathematically robust, my hypothesis that the supernatural realm is a dimension of space on a brane is conjecture, and would be impossible to test mathematically or scientifically. The concept of extra dimensions and branes is one way of explaining the Bible’s description that our spirit, soul and body remain together, but in a different realm to the physical reality that we currently experience.

Science on the Triune Being Hypothesis

So if it’s possible that we can live as a whole person, spirit, soul and body, in a celestial dimension, what makes up our spirit, soul and body in the physical dimension?

Biological science and neuroscience have uncovered many of the previously mysterious qualities that define us as human beings, although there is still much more to be uncovered.

  1. THE BODY

The body is our physical selves – our flesh and blood, sealed by our coating of skin. The body is so ultimately universal, I don’t want to waste space justifying the case for the normal. The obvious physical separation makes each person easy to delineate, although there are rare exceptions that challenge the division of body and soul/spirit.

In May 2014, Faith and Hope Howie were born in Sydney (Australia) [4]. They were born with two separate faces and two brains which merged into one brain stem. They had one body. While they were considered to be conjoined twins, in the strictest medical sense, they had a condition called disrosopus, resulting from the over-expression of a protein involved in the formation of the cranial structures [5]. The condition is extremely rare, and most children with the condition are either stillborn, or don’t survive for more than 24 hours after birth. That Faith and Hope survived for 19 days is a miracle in itself.

Strictly speaking, Faith and Hope were one baby that developed two brains, rather than being twins who failed to adequately separate. So did they have two souls or one? I don’t propose to answer this question here, but it will be worth pondering as we review the concept of the soul.

  1. THE SOUL

The soul is traditionally considered to consist of the mind, will and emotions. In the earthly realm, there is overwhelming evidence that all the parts of the traditional soul are found in the human brain.

a. The Mind

The mind is considered to be “a person’s ability to think and reason; the intellect.” [6] As we will discuss in more detail later, dualism suggests that the mind is an ethereal force separate to the body. But modern neuroscience has accumulated decades of evidence to the contrary. Our stream of consciousness is linked to the function of our working memory [7, 8]. Working memory in turn is heavily dependent on the part of the brain called the pre-frontal cortex and on a neurotransmitter called dopamine [9]. When dopamine-secreting nerve cells are damaged in the pre-frontal cortex, conditions involving disordered thought such as schizophrenia occur [9, 10]. Schizophrenia is best known for hallucinations, essentially hearing and/or seeing things that are not there. These symptoms are reversed by medications that enhance the dopamine response [11]. Lesions of the frontal lobe can also result in the loss of abstract thinking [9]. So it is fair to say that the function of the mind is dependent on the brain, specifically the pre-frontal cortex. If the function of the pre-frontal cortex is disrupted, either by damage to a group of cells, or by impairment of the signaling of those cells via disruption of the neurotransmitter dopamine, the patterns of thought change. These changes in the patterns of thought can be reversed if the impairment can be reversed. Therefore the mind is dependent on the brain. If the mind were independent of the brain, then the function of the mind would not be affected by damage or impairment to the physical brain.

Our stream of thought is a function of our working memory utilizing a wider area of the brains cortex to better process important information. Baars [7, 12] noted that the conscious broadcast comes into working memory which then engages a wider area of the cerebral cortex necessary to most efficiently process the information signal.

We perceive thought most commonly as either pictures or sounds in our head (“the inner monologue”), which corresponds to the slave systems of working memory. When you “see” an image in your mind, that’s the visuospatial sketchpad. When you listen to your inner monologue, that’s your phonological loop. When a song gets stuck in your head, that’s your phonological loop as well, but on repeat mode.

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

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

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

So our mind, also called our stream of thought, is simply a projection of information from our working memory, broadcast to our cerebral cortex, and our consciousness, for extra processing power. It is dependent on our pre-frontal cortex. When the pre-frontal cortex is damaged, our mind can experience defective output, as is the case in thought disorders such as schizophrenia.

b. The Will

The second part of our soul is our will, “the faculty by which a person decides on and initiates action.” [6] Like our mind, the feeling that we have free will is a ubiquitous human trait. Haggard observed, “Most adult humans have a strong feeling of voluntary control over their actions, and of acting ‘as they choose’. The capacity for voluntary action is so fundamental to our existence that social constraints on it, such as imprisonment and prohibition of certain actions, are carefully justified and heavily regulated.” [14]

Again, like the mind, our feeling of our will comes from our brain. Over three decades ago, Libet performed an experiment that demonstrated measurable neural activity occurring up to a full second before a test subject was consciously aware of the intention to act [15]. More recently, a study by Soon et al showed that predictable brain activity occurred up to eight seconds before a person was aware of their intention to act [16].  Haggard again, “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.” [14]

These brain networks initially involve the basal ganglia deep in the brain along with the dopamine rewards system, which provide a flexible interaction between the person’s current situation and the memory of previous similar situations. Also important are the frontal lobes in general, and the pre-Supplementary Motor Area (pre-SMA) in particular, which have crucial roles in keeping actions focused and ‘on task’, or in “binding intention and action”. Parts of the pre-SMA are also active in voluntary selection between alternative tasks and in switching between the selections. An area of the anterior frontomedian cortex, near the pre-SMA, was activated in veto trials more than in trials on which participants made an action. This brain activity might have a key role in self-control [14].

Damage to different areas of the frontal cortex and the other parts of the motor system can result in a number of different conditions, highlighting the role of the brain in our “voluntary” actions. For example, blockage of a small artery in the brain called the artery of Huebner may cause a stroke of the head of the Caudate Nucleus, resulting in the loss of voluntary movement, loss of motivation and loss of speech [17]. Psychosis and ADHD are also disorders of action output of the brain, both of which improve with medications that improve the function of the frontal lobes of the brain. In children with ADHD, the change can be dramatic in a short space of time, and research across the last few decades proves the effect is more than placebo [18, 19].

The feelings of intention and the sense of agency (planning to do or being about to do something, and the sense that one’s action has indeed caused a particular external event) are so fundamental to human experience that it’s hard to consider the alternative: that our ‘free will’ is by-and-large an illusion. Our brain has already reviewed a number of alternative actions for any particular situation, and by the time that our consciousness becomes aware of the decision our brain has made, our motor area of our brain has already primed the neuromuscular circuit in preparation to perform the action. At best, our ‘free will’ is more like a veto function rather than a full conscious control of our behaviour [20]. Multiple parts of our brain are involved in the planning and execution of our actions, especially the basal ganglia and the pre-SMA.

c. The Emotions

Emotions are a difficult concept to define. Despite being studied as a concept for more than a century, the definition of what constitutes an emotion remains elusive. Some academics and researchers believe that the term is so ambiguous that it’s useless to science and should be discarded [21]. I use a concept of emotions described by Dr Alan Watkins [22], which thinks of our emotional state as the sum total of the state of our different physiological systems, while feelings are the awareness, or the perception of our emotional state. However, I should stress that this is only one concept. Often the terms “emotion” and “feelings” are used interchangeably.

That said, neurobiology has still mapped specific feelings/emotions to different parts of the brain. The amygdala is often considered the seat of our fears, the anterior insula is responsible for the feeling of disgust, and the orbitofrontal and anterior cingulate cortex are involved in a broad range of different emotions [23].

Different moods have been linked to specific neurotransmitter systems in the physical brain. A predisposition to anxiety is often linked to variations in the genes for serotonin transport [24] while positive and negative affect (“joy / sadness”) are linked to the dopaminergic system [25].

What is clear is that scientifically speaking, our emotions and the perception of them is dependent on our physical brain.

Summarizing the Soul

Dualism’s view that the soul is an ethereal force separate to the body is redundant. The evidence from the scientific study of the brain makes it clear that every aspect of the traditional ‘soul’ – the mind, will and emotions – is housed in the brain.

3. THE SPIRIT

The scientific study of spirituality is on the leading edge of scientific progress.

Whether a spiritual realm exists is not something that can be tested scientifically. I’ve discussed the Biblical view of the triune being hypothesis earlier in this essay, and suggested that a spiritual realm is at least scientifically plausible depending on your interpretation of String Theory. Ultimately, it remains a matter of faith.

The existence of the spiritual realm may be debatable, but what’s well accepted is that human beings are fundamentally spiritual. Spiritual or mystical experiences are reported across all cultures [26], and throughout history, religions in various forms have spanned the globe, integral to civilizations and the forming of cultural identity. It’s therefore not surprising to find that the brain is a focal point for spiritual experience. Just as hunger, laughter, anger and many other characteristic human traits have their own unique pathways in the brain, so does the experience of the divine.

Spirituality can be defined as “an individual’s experience of and relationship with a fundamental, nonmaterial aspect of the universe that may be referred to in many ways – God, Higher Power, the Force, Mystery and the Transcendent and forms the way by which an individual finds meaning and relates to life, the universe and everything.” [27] On consideration, spirituality encompasses both episodic mystical experiences and ongoing religious beliefs.

Spiritual experiences involve multiple brain regions, and are mediated by a number of different neurotransmitters. In a study of Carmelite Nuns reliving a spiritual experience, Beauregard and Paquette observed activation of the right medial orbitofrontal cortex, the right medial prefrontal cortex, the right dorsal anterior cingulate cortex, the right middle temporal cortex and the left superior and inferior parietal lobes [26]. There is also evidence that dopamine and serotonin are important neurotransmitters in the religious experience [27]. More recent work on the function and connectivity of the medial orbitofrontal cortex shows all of these brain regions have strong connections to each other [28], and that together they function to encode and determine the predicted and real values of our choices. In particular, the medial orbitofrontal cortex helps to encode the anticipated rewards of incoming stimuli. The anticipated and actual values for the perceived stimuli are compared to give a prediction error, which serves as a teaching signal that can be used to improve future value assignments at the time of decision-making [29]. This is intrinsically linked to the limbic rewards system via dopamine, which partially explains the increase in dopamine during intense religious experiences.

Yet spiritual experiences are more than the rewards processing of incoming stimuli. Intense religious experiences have been reported during the aura of temporal lobe epilepsy, especially on the right side [27, 30]. It maybe that the right temporal lobe is largely responsible for the sensed presence of a higher being, and for the more intense religious experiences. Some scientists even went so far as to claim that complex weak magnetic stimulation of the right temporal cortex produced intense religious experiences [31], although this maybe more related to the suggestibility of the subjects rather than the temporal lobe “stimulation” [32]. Therefore, while it is likely that the right temporal lobe is involved in experiences of spirituality, there is no lab-based repeatable evidence to confirm or delineate it.

However, the cognitive and neuroanatomical correlates of religious belief have been delineated. Kapogiannis and colleagues summarized their work by stating that, “religious belief engages well-known brain networks performing abstract semantic processing, imagery, and intent-related and emotional theory of mind, processes known to occur at both implicit and explicit levels. Moreover, the process of adopting religious beliefs depends on cognitive-emotional interactions within the anterior insulae, particularly among religious subjects. The findings support the view that religiosity is integrated in cognitive processes and brain networks used in social cognition, rather than being sui generis.” [33]

If spirituality is indeed solely based on the structure and function of the human brain, what are the implications for organized religion?

To start with, it would mean that those with deficits in certain cognitive functions would experience spirituality to a lesser degree, or at least experience it to a different degree. In keeping with this hypothesis, Canadian researchers have shown that those people with mentalization deficits (reduction in the ability to understand the mental state of oneself and others which underlies overt behaviour), such as people on the Autism spectrum, are less likely to believe in a personal God [34]. On the flipside, other people would be naturally wired to the divine: intuitive and sensitive to the experience of the spiritual.

Moreover, even if a person is not naturally spiritual, one can train oneself to become more spiritual. The brain increases the neural connections within regions that are recurrently stimulated, which leads to expertise. For example, the mid-posterior hippocampus of London taxi drivers is much larger compared to London bus drivers. London taxi drivers are required to drive anywhere in London without maps, and so develop a much larger region of spatial knowledge than the bus drivers, who drive pre-determined routes [35]. Similarly, novices who meditate show increased growth of neural networks involved in the regulation of emotion [36]. It would follow that brain regions involved in the processing of spiritual experience would increase with regular spiritual practice, resulting in a greater sense of the presence of God and his joy.

On the other hand, if acceptance of God is dependent on the function of certain networks within our brain, then how does that affect the foundational principle of salvation? Is it justice if one is condemned to eternal damnation when one has less capacity to believe in the first place?

I cannot offer a definitive answer to that question. Maybe there is no definitive answer? Given that Jesus told Nicodemus, “For God sent not his Son into the world to condemn the world; but that the world through him might be saved” (John 3:17), and that Peter says about God, “The Lord is not slow in keeping his promise, as some understand slowness. Instead he is patient with you, not wanting anyone to perish, but everyone to come to repentance” (2 Peter 3:9), I trust that God will judge everyone fairly, but I’m not sure how the capacity of a person to accept salvation is judged. Perhaps that’s something that someone who’s theologically trained can comment on.

The Triune Being Hypothesis – A New Approach

In summary, while the Bible makes a distinction between body, soul and spirit, it maintains that they are inseparable parts of the same whole person. In the earthly realm, our spirit and the various aspects that traditionally constitute our soul are all enabled though various networks within our physical brain. The Bible also offers evidence that in the transition from the terrestrial to the celestial dimensions, the whole person is translocated and transformed, not just the spirit or soul. Like a reptile shedding its skin, our earthly body and brain remain after death but the person has been translocated into the celestial realm.

Dualism

Psychoneural or Cartesian dualism is the premise that matter and mind are distinct entities or substances; that the one can exist without the other; and that they may interact, but that neither can help explain the other.

Dualism appears self-evident. It seems to explain behavior; and it accounts for the survival of the soul after death. Our mind and our body also appear separate. We have direct knowledge of our mental states, but we do not have direct knowledge of our brain states, so by simple logic, our mental states are not identical with our brain states. Dualism seems to be the obvious model of choice.

Despite claiming to be a cognitive neuroscientist, Dr Leaf embraces dualism, expanding the original concept of a soul into the broader idea of the soul and spirit of the triune being hypothesis, complete with its own hierarchy, “We are triune beings designed to be lead by the Holy Spirit … who speaks to our spirit. Our spirit controls our soul/mind and our soul/mind controls our body.” (Dr Leaf social media post, 9/6/2014)

However, we know that executive functions, emotions and even spiritual experiences can be induced or improved by stimulating the responsible brain networks (electrically in the lab, or with medications). And pathological changes to the brain, such as tumours, strokes, or brain injuries, all have the capacity to change the emotional or cognitive function of the sufferer, depending on the location of the lesion within the brain. If the mind were truly separate to the brain, then changes to the physical brain would not influence the mind or soul. Therefore, medicine and cognitive neuroscience have shown that dualism is false.

Philosophically, dualism is also fatally flawed. According to Bunge [37], dualism fails on a number of counts:

1. Dualism is conceptually fuzzy: “the expression ‘mind-body interaction’ is an oxymoron because, by hypothesis, the immaterial mind is impregnable to physical stimuli, just as matter cannot be directly affected by thoughts or emotions. The very concept of an action is well defined only with reference to material things.”
2. Dualism is experimentally irrefutable: “since one cannot manipulate a nonmaterial thing, as the soul or mind is assumed to be, with material implements, such as lancets and pills.”
3. Dualism considers only the adult mind: “Hence it is inconsistent with developmental psychology, which shows how cognitive, emotional and social abilities develop (grow and decay) along with the brain and the individual’s social context.”
4. Dualism is inconsistent with cognitive ethology: “in particular primatology … comparative psychology and cognitive archaeology”.
5. Dualism violates physics: “in particular the law of conservation of energy. For instance, energy would be created if a decision to take a walk were an event in the nonmaterial soul. Moreover, dualism is inconsistent with the naturalistic ontology that underpins all of the factual sciences.”
6. Dualism confuses even investigators who are contributing to its demise: “in the cognitive, affective and social neuroscience literature one often reads sentences of the forms ‘N is the neural substratum (or correlate) of mental function M,’ and ‘Organ O subserves (or mediates, or instantiates) mental function M’ – as if functions were accidentally attached to organs, or were even prior to them, and organs were means in the service of functions … Why not say simply that the brain feels, emotes, cognizes, intends, plans, wills, and so on? Talk of substratum, correlate, subservience and mediation is just a relic of dualism, and it fosters the idea (functionalism) that what matters is function, which can be studied independently of stuff. But there is neither walking without legs nor breathing without lungs. In general, there is neither function without organ nor organ without functions.”
7. Dualism isolates psychology from most other disciplines: “insofar as none of them admits the stuff/function dichotomy.”
8. Dualism is barren at best, and counterproductive at worst, “In fact, it has spawn superstitions and pseudosciences galore … (and) has slowed down the progress of all the disciplines dealing with the mind.”

Bunge sums up the concept of dualism, “In short, psychoneural dualism is scientifically and philosophically untenable. Worse, it continues to be a major obstacle to the scientific investigation of the mind, as well as to the medical treatment of mental disorders.”

In short, dualism is dead.

Dualism and Dr Leaf

This damning evaluation of dualism poses significant ongoing problems for Dr Leaf and her teaching. Her proposition that “Our spirit controls our soul/mind and our soul/mind controls our body” is not supported by either science or by scripture. This significantly weakens her standing as a biblical and scientific authority, and highlights an intellectual dissonance between science, scripture, and her published work.

Unless Dr Leaf is prepared to review her position and change her teaching on the subject, the gap between her teaching and the accepted scientific position will only continue to widen, and her authority and respect will continue to weaken.

The New Triune Being Hypothesis and the Christian Church

For the Christian church, the Triune Being Hypothesis in its current form is now redundant. The review of the biblical evidence, and the current evidence from neuroscience, has disproven the triune being hypothesis insofar as there is no Biblical or scientific proof that the spirit, soul and body are separate entities. However, it’s reasonable to consider the spirit, soul and body as inseparable parts of the whole being, which are translocated together into the celestial realm upon death.

At the very least, the position of the Christian church on the nature of the soul/spirit requires review, and topic should be brought back to the table to be appropriately debated. It’s clear that the old, generally accepted hypothesis of the separate, immaterial soul/spirit is untenable with current scientific evidence. In this essay, I have proposed one theory which is at least plausible with current scientific understanding. However, there are many other theories that may be just as valid, and warrant consideration.

It’s my hope that with academic honesty and divine guidance, the truth of our triune nature can be further delineated.

References

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  17. Espay, A.J. Frontal Lobe Syndromes. Medscape eMedicine 2012 [cited 2014, July 1]; Available from: http://emedicine.medscape.com/article/1135866-clinical – showall.
  18. Castells, X., et al., Amphetamines for Attention Deficit Hyperactivity Disorder (ADHD) in adults. Cochrane Database Syst Rev, 2011(6): CD007813 doi: 10.1002/14651858.CD007813.pub2
  19. Hodgkins, P., et al., The Pharmacology and Clinical Outcomes of Amphetamines to Treat ADHD. CNS drugs, 2012. 26(3): 245-68
  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. Dixon, T., “Emotion”: The History of a Keyword in Crisis. Emot Rev, 2012. 4(4): 338-44 doi: 10.1177/1754073912445814
  22. Watkins, A. Being brilliant every single day – Part 1. 2012 [cited 2 March 2012]; Available from: http://www.youtube.com/watch?v=q06YIWCR2Js.
  23. 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
  24. 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
  25. Felten, A., et al., Genetically determined dopamine availability predicts disposition for depression. Brain Behav, 2011. 1(2): 109-18 doi: 10.1002/brb3.20
  26. Beauregard, M. and Paquette, V., Neural correlates of a mystical experience in Carmelite nuns. Neurosci Lett, 2006. 405(3): 186-90 doi: 10.1016/j.neulet.2006.06.060
  27. Mohandas, E., Neurobiology of spirituality. Mens Sana Monogr, 2008. 6(1): 63-80 doi: 10.4103/0973-1229.33001
  28. Kahnt, T., et al., Connectivity-based parcellation of the human orbitofrontal cortex. J Neurosci, 2012. 32(18): 6240-50 doi: 10.1523/JNEUROSCI.0257-12.2012
  29. Plassmann, H., et al., Appetitive and aversive goal values are encoded in the medial orbitofrontal cortex at the time of decision making. J Neurosci, 2010. 30(32): 10799-808 doi: 10.1523/JNEUROSCI.0788-10.2010
  30. Devinsky, O. and Lai, G., Spirituality and religion in epilepsy. Epilepsy Behav, 2008. 12(4): 636-43 doi: 10.1016/j.yebeh.2007.11.011
  31. Persinger, M.A., et al., The electromagnetic induction of mystical and altered states within the laboratory. Journal of Consciousness Exploration & Research, 2010. 1(7)
  32. Granqvist, P., et al., Sensed presence and mystical experiences are predicted by suggestibility, not by the application of transcranial weak complex magnetic fields. Neurosci Lett, 2005. 379(1): 1-6 http://www.ncbi.nlm.nih.gov/pubmed/15849873
  33. Kapogiannis, D., et al., Cognitive and neural foundations of religious belief. Proc Natl Acad Sci U S A, 2009. 106(12): 4876-81 doi: 10.1073/pnas.0811717106
  34. Norenzayan, A., et al., Mentalizing deficits constrain belief in a personal God. PLoS One, 2012. 7(5): e36880 doi: 10.1371/journal.pone.0036880
  35. Maguire, E.A., et al., London taxi drivers and bus drivers: a structural MRI and neuropsychological analysis. Hippocampus, 2006. 16(12): 1091-101 doi: 10.1002/hipo.20233
  36. Holzel, B.K., et al., Mindfulness practice leads to increases in regional brain gray matter density. Psychiatry Res, 2011. 191(1): 36-43 doi: 10.1016/j.pscychresns.2010.08.006
  37. Bunge, M., The Mind-Body Problem, in Matter and Mind. 2010, Springer Netherlands. p. 143-57.

Postscript: There is a lot more to String Theory, and anyone interested in knowing more would be well served by reviewing the transcripts or watching the PBS series “The Elegant Universe”, hosted by Brian Greene.

The Discovery of Aspie

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The Discovery of Aspie

Carol Gray and Tony Attwood

Some of this century’s best discoveries were creative and determined efforts to answer “What if…?” questions. What if people could fly? What if electrical energy could be harnessed to produce light? What if there was an easily accessible, international communication and information network? The answers have resulted in permanent changes: air travel, light bulbs, the Internet. These discoveries have rendered their less effective counterparts to relative extinction from use: gone is the stagecoach, gas lighting, and multi-volume hardbound encyclopedias. These improvements remind us of our option and ability to experiment, re-mold, re-think, and imagine. In that spirit, this article submits a new question: What if Asperger’s Syndrome was defined by its strengths? What changes might occur?

Moving from diagnosis to discovery
Making any diagnosis requires attention to weaknesses, the observation and interpretation of signs and symptoms that vary from typical development or health. Certainly it would be a little disarming to visit a doctor for a diagnosis, only to have her inquire, “So, what feels absolutely great?” The DSM 5 (American Psychiatric Association, 2013) assists in the identification of a variety of disorders. It is used by psychiatrists and psychologists to match observed weaknesses, symptoms and behaviors to text. In DSM 5 Autism Spectrum Disorder, which includes Asperger’s Syndrome, is identified by specific diagnostic criteria, a constellation of observed social and communication characteristics. Once diagnosed, a child or adult with the diagnosis is referred to with politically correct “people first” terminology, i.e. a person with Autistic Spectrum Disorder.

Unlike diagnosis, the term discovery often refers to the identification of a persons strengths or talents. Actors are discovered. Artists and musicians are discovered. A great friend is discovered. These people are identified by an informal combination of evaluation and awe that ultimately concludes that this person – more than most others – possesses admirable qualities, abilities, and/or talents. It’s an acknowledgment that, “… you know, he’s better than me at …”. In referring to people with respect to their talents or abilities, politically correct “people first” terminology is not required; labels like musician, artist, or poet are welcomed and considered complimentary.

If Asperger’s syndrome was identified by observation of strengths and talents, it would no longer be in the DSM 5, nor would it be referred to as a syndrome. After all, a reference to someones special strengths or talents does not use terms with negative connotations (it’s artist and poet, not Artistically Arrogant or Poetically Preoccupied), nor does it attach someones proper name to the word syndrome (it’s vocalist or soloist, not Sinatra’s Syndrome).

New ways of thinking of thinking often lead to discoveries that consequently discard their outdated predecessors. It could result in typical people rethinking their responses and rescuing a missed opportunity to take advantage of the contributions of those with autism to culture and knowledge.

Discovery Criteria for Aspergers Syndrome, by Attwood and Gray

A. A qualitative advantage in social interaction, as manifested by a majority of the following:

1. peer relationships characterised by an absolute loyalty and impeccable dependability
2. free of sexist, “age-ist”, or cultural biases; ability to regard others at “face value”
3. speaking one’s mind irrespective of social context or adherence to personal beliefs
4. ability to personal theory or perspective despite conflicting evidence
5. seeking an audience or friends capable of: enthusiasm for unique interests and topics; consideration of details; spending time discussing a topic that may not be of primary interest to others
6. listening without continual judgement or assumption
7. Interested primarily in significant contributions to conversation; preferring to avoid “ritualistic small talk” or socially trivial statements and superficial conversation
8. seeking sincere, positive, genuine friends with an unassuming sense of humour.

B. Fluent in autism, a social language characterised by at least three of the following:

1. a determination to seek the truth
2. conversation free of hidden meaning or agenda
3. advanced vocabulary and interest in words
4, fascination with word-based humour, such as puns
5. advanced use of pictorial metaphor

C. Cognitive skills characterised by at least four of the following:

1. strong preference for detail
2. original, often unique perspective in problem solving
3. exceptional memory and/or recall of details often forgotten or disregarded by others, for example: names, dates, schedules, routines
4. avid perseverance in gathering and cataloguing information on a topic of interest
5. persistence of thought
6. encyclopaedic or digital knowledge of one or more topics
7. knowledge of routines and a focused desire to maintain order, consistency and accuracy
8. clarity of values/decision making unaltered by political or financial factors

D. Additional possible features

1. acute sensitivity to specific sensory experiences and stimuli, for example: hearing, touch, vision, and/or smell
2. strength in individual sports and games, particularly those involving endurance, visual accuracy or intellect, including rowing, swimming, bowling or chess
3. “social unsung hero” with trusting optimism: frequent victim of social weakness and prejudices other others, while steadfast in the belief of the possibility of genuine friendship
4. increased probability over general population of attending university after high school
5. often take care of others outside the range of typical development

Perhaps we have discovered the next stage of human evolution?

(c) Tony Attwood and Carol Gray 2014 All Rights Reserved
Republished with permission from the author (TA)

Autism Series 2013 – Part 3: The Autism “Epidemic”

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Weintraub, K., Autism counts. Nature, 2011. 479(7371): 22-4.

Weintraub, K., Autism counts. Nature, 2011. 479(7371): 22-4.

It seems that autism is on the rise.  Once hidden away in institutions or just dismissed as odd, society is now faced with a condition that it is yet to come to grips with.  Some out in the community believe that it must be a toxin, or vaccines or mercury.  Others accuse doctors of simply giving in to the unreasonable demands of pushy parents to defraud the system of money – “Things have reached the point these days where any kid that’s not a charming little extrovert will be accused of being, ‘on the spectrum.’”[1]

So is there an epidemic of kids who are “not charming little extroverts”?  It depends on who you ask.

Take, for example, two articles written in the year 2000.  In the first, titled “The autism epidemic, vaccinations, and mercury”, Rimland said,

“While there are a few Flat-Earthers who insist that there is no real epidemic of autism, only an increased awareness, it is obvious to everyone else that the number of young children with autism spectrum disorders (ASD) has risen, and continues to rise, dramatically.”[2]

The other, written by Professor Tony Attwood, a world authority on Aspergers Syndrome, said,

“… is there an epidemic of people being diagnosed as having Asperger’s Syndrome? At present we cannot answer the question, as we are unsure of the diagnostic criteria, the upper and lower levels of expression and the borders with other conditions. Nevertheless, we are experiencing a huge increase in diagnosis but this may be the backlog of cases that have been waiting so long for an explanation.”[3]

I don’t think it’s very often Prof Attwood is lumped with ‘flat-earthers’.  But you can see the change in perspective from one side looking objectively to the other who need for there to be an “epidemic” of autism in order to strengthen their case.

So who’s right?  To see if this autism “epidemic” hypothesis has any real merit, we need to delve into some numbers.

First, some basic epidemiology – because part of the confusion in looking at the autism numbers is defining exactly what those numbers represent.  Here are some important epidemiology terms from the “Physicians Assistant Exam for Dummies”[4]:

Incidence: For any health-related condition or illness, incidence refers to the number of people who’ve newly acquired this condition.

Prevalence: Prevalence concerns the number of people who have this condition over a defined time interval.

Most autism figures are for prevalence, or often more specifically, point prevalence – “the number of people who have this condition at any given point in time.”

The other thing to remember from my last blog is that initially autism was only diagnosed on the strict rules of Kanner, and was considered to be a single disease caused mainly by bad parenting [5].  So through the 1960’s and 1970’s, only the most severe children were diagnosed as having autism because the high-functioning autism would not have met Kanners criteria, and even if they did, most parents didn’t want the label for fear of the social stigma.

So then, what are the numbers?  The early prevalence was estimated to be less than 5/10,000 or 1 in 2000[6], although in surveys done after 1987, the numbers began to rise past 7/10,000[7].  In the 1990’s, Autism prevalence climbed into the teens and the latest prevalence has been documented for autism is 20.6/10,000[7].

But that’s only about 1 in 485.  The CDC estimated a prevalence of 1 in 88 (113/10,000)[8].  Where did the other 400 people go?

This is where the importance of definitions is highlighted.  Autism is considered part of a spectrum, and at the time of the surveys reviewed by Fombonne, DSM III then DSM IV considered conditions like Pervasive Developmental Disorder and then Aspergers Disorder to be part of that spectrum.  Adding in the rate of PDD and you have a figure of 57.7/10,000 and adding in Aspergers gives you a combined rate of 63.7/10,000, or 1 in 157 people surveyed[7].

And yet even then, who you measure and how you measure makes much more of a difference, because a recent, rigorous study targeting all 7 to 12 year old children in a large South Korean populous found a prevalence of 2.64%, which is 264/10,000 or 1 child in every 38.  The authors noted that, “Two-thirds of ASD cases in the overall sample were in the mainstream school population, undiagnosed and untreated. These findings suggest that rigorous screening and comprehensive population coverage are necessary to produce more accurate ASD prevalence estimates and underscore the need for better detection, assessment, and services.”[9]

So if there has been a fifty-fold change in prevalence (from 5 to 264 cases per 10,000 people) in just thirty years, isn’t that an epidemic?

Well, no.  As much as some might ignorantly deny it, there is no real evidence for it.  Remember the definitions from the “Physicians Assistant Exam for Dummies”[4]:

Incidence: For any health-related condition or illness, incidence refers to the number of people who’ve newly acquired this condition.

Prevalence: Prevalence concerns the number of people who have this condition over a defined time interval.

It’s the rapid rise in the number of new cases diagnosed that defines an epidemic, which is the incidence and not the prevalence[10].  While the prevalence has changed a lot, the incidence has been fairly stable.  From Nature, “Christopher Gillberg, who studies child and adolescent psychiatry at the University of Gothenburg in Sweden, has been finding much the same thing since he first started counting cases of autism in the 1970s. He found a prevalence of autism of 0.7% among seven-year-old Swedish children in 1983 and 1% in 1999. ‘I’ve always felt that this hype about it being an epidemic is better explanation’, he said.”[11]

Fombonne agrees. “As it stands now, the recent upward trend in estimates of prevalence cannot be directly attributed to an increase in the incidence of the disorder.”[7]  He said later in the article that a true increase in the incidence could not be ruled out, but that the current epidemiological data which specifically studied the incidence of autism over time was not strong enough to draw conclusions.

While there’s no epidemic, there is the real issue of the genuinely increasing prevalence.  Why the rise in those numbers?  Fombonne went on to explain, “There is good evidence that changes in diagnostic criteria, diagnostic substitution, changes in the policies for special education, and the increasing availability of services are responsible for the higher prevalence figures.”[7]  Nature published a graph from the work of Professor Peter Bearman, showing that 54% of the rise in the prevalence of autism could be explained by the refining of the diagnosis, greater awareness, an increase in the parental age, and clustering of cases in certain geographic areas.

Weintraub, K., Autism counts. Nature, 2011. 479(7371): 22-4. (Adapted from King, M. and Bearman, P., Diagnostic change and the increased prevalence of autism. International Journal of Epidemiology, 2009. 38(5): 1224-34 AND King, M.D. and Bearman, P.S., Socioeconomic Status and the Increased Prevalence of Autism in California. Am Sociol Rev, 2011. 76(2): 320-46.)

Weintraub, K., Autism counts. Nature, 2011. 479(7371): 22-4. (Adapted from King, M. and Bearman, P., Diagnostic change and the increased prevalence of autism. International Journal of Epidemiology, 2009. 38(5): 1224-34 AND King, M.D. and Bearman, P.S., Socioeconomic Status and the Increased Prevalence of Autism in California. Am Sociol Rev, 2011. 76(2): 320-46.)

From Nature: “The fact that he still cannot explain 46% of the increase in autism doesn’t mean that this ‘extra’ must be caused by new environmental pollutants, Bearman says. He just hasn’t come up with a solid explanation yet. ‘There are lots of things that could be driving that in addition to the things we’ve identified,’ he says.”[11]

There is no autism epidemic, just medical science and our population realising just how common autism is as the definition becomes more refined, people become more aware, and some other biosocial factors come into play.

What can we take from the numbers?  That we’re being overtaken by Sheldon clones?  That soon there will be no more “charming little extroverts”?  If the CDC figure is accurate, then one person in every hundred is on the spectrum, so the world is hardly being overtaken by autism.  But the take home message is that Autism Spectrum Disorders are more common that we ever thought, and there are more people on the spectrum “hiding in plain sight”.  If the study from South Korea is accurate then one person in every thirty-eight is on the spectrum, but two thirds of them are undiagnosed.

Should there be more funding, more resources, or more political representation for people on the spectrum?  Perhaps, although the public and research funds are not unlimited, and other health concerns should also be treated fairly.  But since autism is life long and impacts on so many areas of mental health and education, understanding autism and managing it early could save governments billions of dollars into the future.

Rather, I think that the climbing prevalence of ASD is a clarion call for understanding and tolerance.  If we learn to tolerate differences and practice discretionary inclusion, then both the autistic and the neuro-typical can benefit from the other.  That’s a world which we’d all like to live.

REFERENCES

1. Bolt, A. If the autistic don’t get full cover, where’s the money going? 2013  2013 May 11]; Available from: http://blogs.news.com.au/heraldsun/andrewbolt/index.php/heraldsun/comments/if_the_autistic_dont_get_full_cover_wheres_the_money_going/.

2. Rimland, B., The autism epidemic, vaccinations, and mercury. Journal of Nutritional and Environmental Medicine, 2000. 10(4): 261-6.

3. Attwood, T., The Autism Epidemic: Real or Imagined, in Autism Aspergers Digest2000, Future Horizons Inc: Arlington, TX.

4. Schoenborn, B. and Snyder, R., Physician Assistant Exam For Dummies. 2012: John Wiley & Sons.

5. Pitt, C.E. Autism Series 2013 – Part 2: The History Of Autism. 2013  [cited 2013 2013 Aug 15]; Available from: https://cedwardpitt.com/2013/08/15/autism-series-2013-part-2-the-history-of-autism/.

6. Rice, C.E., et al., Evaluating Changes in the Prevalence of the Autism Spectrum Disorders (ASDs). Public Health Reviews. 34(2).

7. Fombonne, E., Epidemiology of pervasive developmental disorders. Pediatric research, 2009. 65(6): 591-8.

8. Baio, J., Prevalence of Autism Spectrum Disorders: Autism and Developmental Disabilities Monitoring Network, 14 Sites, United States, 2008. Morbidity and Mortality Weekly Report. Surveillance Summaries. Volume 61, Number 3. Centers for Disease Control and Prevention, 2012.

9. Kim, Y.S., et al., Prevalence of autism spectrum disorders in a total population sample. American Journal of Psychiatry, 2011. 168(9): 904-12.

10. “Epidemic vs Pandemic”. 2013  [cited 2013 Sept 03]; Available from: http://www.diffen.com/difference/Epidemic_vs_Pandemic.

11. Weintraub, K., Autism counts. Nature, 2011. 479(7371): 22-4.

 

Dr Caroline Leaf – Contradicted by the latest research

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This is my most popular post by far.  I truly appreciate the support and interest in this post, but I’ve discovered and documented a lot more about Dr Leaf’s ministry in the last two years.  I welcome you to read this post, but if you’d like a more current review of the ministry of Dr Caroline Leaf, a new and improved version is here:
Dr Caroline Leaf – Still Contradicted by the Latest Evidence, Scripture & Herself

* * * * *

Mr Mac Leaf, the husband of Dr Caroline Leaf, kindly took the time to respond to my series of posts on the teachings of Dr Leaf at Kings Christian Centre, on the Gold Coast, Australia, earlier this month. As I had intended, and as Mr Leaf requested, I published his  reply, complete and unabridged (here).

This blog is my reply.  It is heavily researched and thoroughly referenced.  I think it’s fair to say that while Dr Leaf draws her conclusions from some scientific documents, there is more than enough research that contradicts her statements and opinions.  I have only listed a small fraction, and only on some of the points she raised.

In fairness, the fields of neurology and neuroscience are vast and rapidly expanding, and it is impossible for one person to cover all of the literature on every subject.  This applies to myself and Dr Leaf.  However, I believe that the information I have read, and referenced from the latest peer-reviewed scholarly works, do not support Dr Leaf’s fundamental premises.  If I am correct, then the strength and validity of Dr Leaf’s published works should be called into question.

As before, I welcome any reply or rebuttal that Dr Leaf wishes to make, which I will publish in full if she requests.  In the interests of healthy public debate, and encouraging people to make their own informed decisions on the teachings of Dr Leaf, any comments regarding the response of Mr Leaf, Dr Leaf or myself, are welcome provided they are constructive.

This is a bit of a lengthy read, but I hope it is worthwhile.

Dear Mr Leaf,

Thank you very much for taking the time out to reply to some of the points raised in my blog.  I am more than happy to publish your response, and to publish any response you wish to make public.

ON INFORMED DECISIONS

I published my blog posts to open up discussion on the statements made by Dr Leaf at the two meetings that I attended at Kings Christian Centre on the Gold Coast.  As you rightly point out, people should be able to make informed decisions.  A robust discussion provides the information required for people to make an informed choice.  Any contributions to this discussion from either yourself or Dr Leaf would be most welcome.

I apologise if you interpreted my blogs as judgemental, or if you believe there are any misunderstandings.  You may or may not have read my final two paragraphs from the third post, in which I acknowledged that I may have misunderstood where she was coming from, but that I would welcome her response.  If there were any misunderstandings, it is likely because Dr Leaf did not make any attempt to reference any of the statements she made on the day.  You may argue that she was speaking to a lay audience, and referencing is therefore not necessary.  However, I have been to many workshops for the lay public by university professors, who have extensively referenced their information during their presentations.  A lay audience does not preclude providing references.  Rather, it augments the speakers authority and demonstrates the depth of their knowledge on the subject at hand.

YOUR DEFENCE

It’s interesting that you feel the need to resort to defence by association, and Ad Hominem dismissal as your primary counter to the points I raised.

Can you clarify how attending the same university as Dr Christaan Barnard, or a Nobel laureate, endorses her arguments or precludes her from criticism?  I attended the University of Queensland where Professor Ian Frazer was based.  He developed the Human Papilloma Virus vaccine and was the 2006 Australian of the Year.  Does that association enhance my argument?

Can you also clarify why a reference from a colleague was preferred to letting Dr Leaf’s statements and conclusions speak for themselves?  Dr Amua-Quarshie’s CV is certainly very impressive, no doubt about that, although he doesn’t list the papers he’s published.  (I’m assuming that to hold the title of Adjunct Professor, he’s published peer-reviewed articles.  Is he willing to list them, for the record?)

Whatever his credentials, his endorsement means very little, since both Dr Leaf and Dr Amua-Quarshie would know from their experience in research that expert opinion is one of the lowest forms of evidence, second worst only to testimonials [1].  Further, both he and Dr Leaf are obviously close friends which introduces possible bias.  His endorsement is noteworthy, but it can not validate every statement made by Dr Leaf.  Her statements should stand up on their own through the rigors of critical analysis.

On the subject of evidence, disparaging your critics is not a substitute for answering their criticism.  Your statement, “By your comments it is obvious that you have not kept up to date with the latest Scientific research” is an assumption that is somewhat arrogant, and ironic since Dr Leaf is content to use superseded references dating back to 1979 to justify her current hypotheses.

DR LEAF’S EVIDENCE

In the blog to which you referred, Dr Leaf makes a number of statements that are intended to support her case.  These include the following.

“A study by the American Medical Association found that stress is a factor in 75% of all illnesses and diseases that people suffer from today.”  She fails to reference this study.

“The association between stress and disease is a colossal 85% (Dr Brian Luke Seaward).”   But again, she fails to reference the quote.

“The International Agency for Research on Cancer and the World Health Organization has concluded that 80% of cancers are due to lifestyles and are not genetic, and they say this is a conservative number (Cancer statistics and views of causes Science News Vol.115, No 2 (Jan.13 1979), p.23).”  It’s good that she provides a reference to her statement.  However, referencing a journal on genetics from 1979 is the equivalent of attempting to use the land-speed record from 1979 to justify your current preference of car.  The technology has advanced significantly, and genetic discoveries are lightyears ahead of where they were more than three decades ago.

“According to Dr Bruce Lipton (The Biology of Belief, 2008), gene disorders like Huntington’s chorea, beta thalassemia, cystic fibrosis, to name just a few, affect less than 2% of the population. This means the vast majority of the worlds population come into this world with genes that should enable the to live a happy and healthy life. He says a staggering 98% of diseases are lifestyle choices and therefore, thinking.”  Even if it’s true that Huntingtons, CF etc account for 2% of all illnesses, they account for only a tiny fraction of genetic disease.  And concluding that the remaining 98% must therefore be lifestyle related is overly simplistic.  It ignores the genetic influence on all other diseases, other congenital, and environmental causes of disease.  I will fully outline this point soon.

Similarly, “According to W.C Willett (balancing lifestyle and genomics research for disease prevention Science (296) p 695-698, 2002) only 5% of cancer and cardiovascular patients can attribute their disease to hereditary factors.”  Science is clear that genes play a significant role in the development of cardiovascular disease and most cancers, certainly greater than 5%.  Again, I will discuss this further soon.

“According to the American Institute of health, it has been estimated that 75 – 90% of all visits to primary care physicians are for stress related problems (http://www.stress.org/americas.htm). Some of the latest stress statistics causing illness as a result of toxic thinking can be found at: http://www.naturalwellnesscare.com/stress-statistics.html”  These websites not peer-reviewed, and both suffer from a blatant pro-stress bias.

You’ll also have to forgive my confusion, but Dr Leaf also wrote, “Dr H.F. Nijhout (Metaphors and the Role of Genes and Development, 1990) genes control biology and not the other way around.”  So is she saying that genes DO control development?

EVIDENCE CONTRADICTING DR LEAF

Influence Of Thought On Health

Dr Leaf has categorically stated that “75 to 98% of all illnesses are the result of our thought life” on a number of occasions.  She repeated the same statement in her most recent book so it is something she is confident in.  However, in order to be true, this fact must be consistent across the whole of humanity.

And yet, in a recent peer-reviewed publication, Mara et al state, “At any given time close to half of the urban populations of Africa, Asia, and Latin America have a disease associated with poor sanitation, hygiene, and water.” [2]  Bartram and Cairncross write that “While rarely discussed alongside the ‘big three’ attention-seekers of the international public health community—HIV/AIDS, tuberculosis, and malaria—one disease alone kills more young children each year than all three combined. It is diarrhoea, and the key to its control is hygiene, sanitation, and water.” [3]  Hunter et al state that, “diarrhoeal disease is the second most common contributor to the disease burden in developing countries (as measured by disability-adjusted life years [DALYs]), and poor-quality drinking water is an important risk factor for diarrhoea.” [4]

Toilets and clean running water have nothing to do with stress or thought.  We live in a society that essentially prevents more than half of our illnesses because of internal plumbing, with additional benefits from vaccination and population screening.  If thoughts have any effect on our health, they are artificially magnified by our clean water and sewerage systems.  Remove those factors and any effects of thought on our health disappear from significance.  Dr Leaf’s assertion that 75 to 98% of human illness is thought-related is a clear exaggeration.

Let me be clear – I understand the significance of stress on health and the economy, but it is not the cause of 75-98% of all illnesses.  I’m not sure if there is a similar study in the US, but the latest Australian data suggests that all psychological illness only counts for 8% of visits to Australian primary care physicians [5].

In terms of cancer, I don’t have time to exhaustively list every cancer but of the top four listed in the review “Cancer Statistics 2013” [6] , here are the articles that list the gene x environment interactions:

  1. PROSTATE – There are only two risk factors for prostate cancer, familial aggregation and ethnic origin. No dietary or environmental cause has yet been identified [7].  It is most likely caused by multiple genes at various loci [8].
  2. BREAST – Genes make up 25% of the risk factors for breast cancer, and significantly interacted with parity (number of children born) [9].
  3. LUNG/BRONCHUS – Lung cancer is almost exclusively linked to smoking, but nicotine addiction has a strong hereditary link (50-75% genetic susceptibility) [10].
  4. COLORECTUM – Approximately one third of colorectal cancer is genetically linked [11].

So the most common cancer is not linked to any environmental factors at all, and the others have genetic influences of 25% to more than 50%.  This is far from being 2% or 5% as Dr Leaf’s sources state.

Also in terms of heart disease, the INTERHEART trial [12] lists the following as significant risk factors, and I have listed the available gene x environment interaction studies that have been done on these too:

  1. HIGH CHOLESTEROL – Genetic susceptibility accounts for 40-60% of the risk for high cholesterol [13].
  2. DIABETES – Genetic factors account for 88% of the risk for type 1 diabetes [14].  There is a strong genetic component of the risk of type 2 diabetes with 62-70% being attributable to genetics [15, 16].
  3. SMOKING – nicotine addiction has a strong hereditary link (50-75% genetic susceptibility) [10].
  4. HYPERTENSION – While part of a much greater mix of variables, genetics are still thought to contribute between 30% and 50% to the risk of developing high blood pressure [17].

So again, while genes are a part of a complex system, it is clear from the most recent evidence that genetics account for about 50% of the risk for cardiovascular disease, which again is a marked difference between the figures that Dr Leaf is using to base her assertions on.

Atrial Natriuretic Peptide

I am aware of research that’s studied the anxiolytic properties of Atrial Natriuretic Peptide.  For example, Wiedemann et al [18] did a trial using ANP to truncate panic attacks.  However, these experiments were done on only nine subjects, and the panic attacks were induced by cholecystokinin.  As such, the numbers are too small to have any real meaning.  And the settling is completely artificial.  Just as CCK excretion does not cause us all to have panic attacks every time we eat, ANP does not provide anxiolysis in normal day to day situations.  Besides, if ANP were really effective at reducing anxiety, then why do people suffering from congestive cardiac failure, who have supraphysiological levels of circulating ANP [19] , also suffer from a higher rate of anxiety and panic disorders than the general population? [20]

The Heart As A Mini-Brain

As for Heartmath, they advance the notion of the heart being a mini-brain to give themselves credibility.  It’s really no different to an article that I read the other day from a group of gut researchers [21] – “‘The gut is really your second brain,’ Greenblatt said. ‘There are more neurons in the GI tract than anywhere else except the brain.’”  The heart as a mini-brain and the gut as a mini-brain are both figurative expressions.  Neither are meant to be taken literally.  I welcome Dr Leaf to tender any further evidence in support of her claim.

Hard-Wired For Optimism

As for being wired for optimism, the brain is likely pre-wired with a template for all actions and emotions, which is the theory of protoconsciousness [22].  Indeed, neonatal reflexes often reflect common motor patterns.  If this is true, then the brain is pre-wired for both optimism and love, but also fear.  This explains the broad role of the amygdala in emotional learning [23] including fear learning.  It also means that a neonate needs to develop both love and fear.

A recent paper showed that the corticosterone response required to learn fear is suppressed in the neonate to facilitate attachment, but with enough stress, the corticosterone levels build to the point where amygdala fear learning can commence [24].  The fear circuits are already present, only their development is suppressed.  Analysis of the cohort of children in the Bucharest Early Intervention Project showed that negative affect was the same for both groups.  However positive affect and emotional reactivity was significantly reduced in the institutionalised children [25].  If the brain is truly wired for optimism and only fear is learned, then positive emotional reactivity should be the same in both groups and the negative affect should be enhanced in the institutionalised cohort.  That the result is reversed confirms that neonates and infants require adequate stimulation of both fear and love pathways to grow into an emotionally robust child, because the brain is pre-wired for both but requires further stimulation for adequate development.

The Mind-Brain Link

If the mind controls the brain and not the other way around as Dr Leaf suggests, why do anti-depressant medications correct depression or anxiety disorders?  There is high-level evidence to show this to be true [26-28].  The same can be said for recent research to show that medications which enhance NDMA receptors have been shown to improve the extinction of fear in anxiety disorders such as panic disorder, OCD, Social Anxiety Disorder, and PTSD [29].

If the mind controls the brain and not the other way around as Dr Leaf suggests, why do some people with acquired brain injuries or brain tumours develop acute personality changes or thought disorders?  Dr Leaf has done PhD research on patients with closed head injuries and treated them in clinical settings according to her CV.  She must be familiar with this effect.

One can only conclude that there is a bi-directional effect between the brain and the stream of thought, which is at odds with Dr Leaf’s statement that the mind controls the brain and not the other way around.

FURTHER CLARIFICATION

One further thing.  Can you clarify which of Dr Leaf’s peer-reviewed articles have definitively shown the academic improvement in the cohort of 100,000 students, as you and your referee have stated?  And can you provide a list of articles which have cited Dr Leaf’s Geodesic Information Processing Model?  Google Scholar did not display any articles that had cited it, which must be an error on Google’s part.  If her theory is widely used as you say, it must have been extensively cited.

I understand that you are both busy, but I believe that I have documented a number of observations, backed by recent peer-reviewed scientific literature, which directly contradict Dr Leaf’s teaching.  I have not had a chance to touch on many, many other points of disagreement.

For the benefit of Dr Leaf’s followers, and for the scientific and Christian community at large, I would appreciate your response.

I would be grateful if you could respond to the points raised and the literature which supports it, rather than an Ad Hominem dismissal or further defense by association.

Dr C. Edward Pitt

REFERENCES

1. Fowler, G., Evidence-based practice: Tools and techniques. Systems, settings, people: Workforce development challenges for the alcohol and other drugs field, 2001: 93-107.

2. Mara, D., et al., Sanitation and health. PLoS Med, 2010. 7(11): e1000363.

3. Bartram, J. and Cairncross, S., Hygiene, sanitation, and water: forgotten foundations of health. PLoS Med, 2010. 7(11): e1000367.

4. Hunter, P.R., et al., Water supply and health. PLoS Med, 2010. 7(11): e1000361.

5. FMRC. Public BEACH data. 2010  16JUL13]; Available from: <http://sydney.edu.au/medicine/fmrc/beach/data-reports/public&gt;.

6. Siegel, R., et al., Cancer statistics, 2013. CA Cancer J Clin, 2013. 63(1): 11-30.

7. Cussenot, O. and Valeri, A., Heterogeneity in genetic susceptibility to prostate cancer. Eur J Intern Med, 2001. 12(1): 11-6.

8. Alberti, C., Hereditary/familial versus sporadic prostate cancer: few indisputable genetic differences and many similar clinicopathological features. Eur Rev Med Pharmacol Sci, 2010. 14(1): 31-41.

9. Nickels, S., et al., Evidence of gene-environment interactions between common breast cancer susceptibility loci and established environmental risk factors. PLoS Genet, 2013. 9(3): e1003284.

10. Berrettini, W.H. and Doyle, G.A., The CHRNA5-A3-B4 gene cluster in nicotine addiction. Mol Psychiatry, 2012. 17(9): 856-66.

11. Hutter, C.M., et al., Characterization of gene-environment interactions for colorectal cancer susceptibility loci. Cancer Res, 2012. 72(8): 2036-44.

12. Yusuf, S., et al., Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet, 2004. 364(9438): 937-52.

13. Asselbergs, F.W., et al., Large-scale gene-centric meta-analysis across 32 studies identifies multiple lipid loci. Am J Hum Genet, 2012. 91(5): 823-38.

14. Wu, Y.L., et al., Risk factors and primary prevention trials for type 1 diabetes. Int J Biol Sci, 2013. 9(7): 666-79.

15. Ali, O., Genetics of type 2 diabetes. World J Diabetes, 2013. 4(4): 114-23.

16. Murea, M., et al., Genetic and environmental factors associated with type 2 diabetes and diabetic vascular complications. Rev Diabet Stud, 2012. 9(1): 6-22.

17. Kunes, J. and Zicha, J., The interaction of genetic and environmental factors in the etiology of hypertension. Physiol Res, 2009. 58 Suppl 2: S33-41.

18. Wiedemann, K., et al., Anxiolyticlike effects of atrial natriuretic peptide on cholecystokinin tetrapeptide-induced panic attacks: preliminary findings. Arch Gen Psychiatry, 2001. 58(4): 371-7.

19. Ronco, C., Fluid overload : diagnosis and management. Contributions to nephrology,. 2010, Basel Switzerland ; New York: Karger. viii, 243 p.

20. Riegel, B., et al., State of the science: promoting self-care in persons with heart failure: a scientific statement from the American Heart Association. Circulation, 2009. 120(12): 1141-63.

21. Arnold, C. Gut feelings: the future of psychiatry may be inside your stomach. 2013  [cited 2013 Aug 22]; Available from: http://www.theverge.com/2013/8/21/4595712/gut-feelings-the-future-of-psychiatry-may-be-inside-your-stomach.

22. Hobson, J.A., REM sleep and dreaming: towards a theory of protoconsciousness. Nat Rev Neurosci, 2009. 10(11): 803-13.

23. Dalgleish, T., The emotional brain. Nat Rev Neurosci, 2004. 5(7): 583-9.

24. Landers, M.S. and Sullivan, R.M., The development and neurobiology of infant attachment and fear. Dev Neurosci, 2012. 34(2-3): 101-14.

25. Bos, K., et al., Psychiatric outcomes in young children with a history of institutionalization. Harv Rev Psychiatry, 2011. 19(1): 15-24.

26. Arroll, B., et al., Antidepressants versus placebo for depression in primary care. Cochrane Database Syst Rev, 2009(3): CD007954.

27. Soomro, G.M., et al., Selective serotonin re-uptake inhibitors (SSRIs) versus placebo for obsessive compulsive disorder (OCD). Cochrane Database Syst Rev, 2008(1): CD001765.

28. Kapczinski, F., et al., Antidepressants for generalized anxiety disorder. Cochrane Database Syst Rev, 2003(2): CD003592.

29. Davis, M., NMDA receptors and fear extinction: implications for cognitive behavioral therapy. Dialogues Clin Neurosci, 2011. 13(4): 463-74.

Autism Series 2013; Part 1 – Why it matters.

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What do you think of when you think about autism?  Is it a TV character like Jake, from Kiefer Sutherland’s recent series ‘Touch’, or perhaps Sheldon from ‘The Big Bang Theory’?  Or is it a movie character like the savant that Dustin Hoffman played in ‘Rain Man’? They are common stereotypes, but they only depict a tiny fraction of the autism that is all around us every day.  Chances are, you would run into people every day who have autism.  Would you be able to pick them?

The current point prevalence rate of autism is given by various international health bodies including the World Health Organization, as one person in a hundred.  With a prevalence of one percent of the population as having autism, you would think it would be better known, better dealt with by teachers, better handled by public officials, better screened and managed by health workers, and better resourced in terms of assistance to families and in terms of research dollars.

But while funding and recognition are important, the greatest impact that the lack of autism awareness has is the human cost.  It is the cost that can’t be measured in terms of dollars, caused by the maligned stigma that having autism brings.

Autism at the less severe end, what used  to be called ‘high functioning’ autism, or what I prefer to classify as (the now unofficial diagnosis of) Aspergers Syndrome, doesn’t make a person look that much different on the outside.  But it makes their behaviour somewhat odd to everyone else.  They have quirks.  They have strange mannerisms.  They have rigid ways of doing things.  They have very narrow interests.  They misread social cues.

“Normal” people don’t like odd.  Especially children.  If you don’t fit in to their particular group-think view of the world, their intolerant tormenting can be merciless and unrelenting.  Some people never grow up though, and many adults with autism can be marginalised by their adult peers. Every barb, joke and isolating experience eroding at the soul of a person with autism until there is nothing left.

This is the most destructive of all. It is death by a thousand insults.

I am writing this series of blogs because I want to help assist in whatever way I can to reduce the ignorance surrounding autism.  There is still so much ignorance out there – simple ignorance because the message is still diffusing through our social networks, and  obstinate ignorance, by people who use pseudoscientific scare mongering to promote their views, or promote bogus treatments for the sole purpose of taking advantage of the desperation of some of those who live with autism.

No matter which form of ignorance is out there, ignorance is ignorance and it does the same damage.  It needs to be stopped.

When I was a little boy, I was odd.  It took me a while before I started talking.  I had an obsession with vacuum cleaners and watches.  I was the misfit, or the loner.  I was incessantly bullied in the latter half of primary school and almost all the way through high school.  I didn’t want to go out and be with large groups of other kids.  My parents made me go to marshall arts training, cub scouts, church groups and school holiday excursions.

I hated those social outings.  I had huge anxiety being in these large groups.  Even when I wasn’t being mocked or belittled, I still felt anxious because I didn’t naturally fit in with the other kids.  The leaders of the group would go out of their way to include me but that had the opposite effect of highlighting how much of a social misfit I was.  The anxiety was disabling when I was in middle high school.

Thankfully I was smart, mainly in maths and science.  Academic achievement was my only positive, so I took refuge in studying.  I graduated in the top percentile in my state, and made it into medical school.  I did a whole medical degree, five years in hospitals including several in subspecialty paediatrics, and a fellowship in General Practice, and another eight years of GP experience, before my son was diagnosed as being on the autistic spectrum.

Despite years of medical training, It’s only been since my son’s diagnosis that I have been realising just how much of my quirky behaviour and social dysfunction was due to the fact that I’m on the spectrum too.  All those years, I thought I was retarded, socially incompetent, a freak.  All those years, I was bullied, harassed and made to think I was stupid, just because I didn’t naturally understand the unspoken social codes , but no one explained them to me.

That’s nearly forty years of living with self-doubt, low self-esteem, low self-confidence, and various mental health issues, because I never knew, because no one else knew, because of ignorance and intolerance.

So it stings when I hear people spread mistruths about ASD, and it pains me when the mistruths are spread by people who should know better.  It makes me mad when the mistruths come from self-titled ‘experts’.

I don’t want my son going through the same stigma and denigration, or anyone else on the spectrum for that matter.  The truth about autism – what it is, what it is caused by, and what strengths autism bestows, need to hold sway so that death by a thousand insults is no longer tolerable in our progressive society.

I will publish further blog posts over the coming days to weeks on what autism is, on why it seems to be increasing, and the latest scientific evidence on what autism may be caused by.  I will devote a whole blog (or two) to the misinformation surrounding vaccines and autism.  So stay tuned.

Dr Caroline Leaf – Serious questions, few answers (Part 2)

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Yesterday I published the first part of an essay discussing the presentation of Dr Caroline Leaf, Audiologist, Communication Pathologist, and self-titled cognitive neuroscientist, at Kings Christian Church, Gold Coast.

Tonight I want to continue dissecting some of the more pertinent statements that she made, including her view of the mind-brain connection, a smattering of smaller issues, her over-reliance on case studies, and her opinion on the cause and treatment of ADHD.

Tomorrow I will publish the last, and most important part of my essay – That Dr Leaf believes that ‘toxic’ thoughts are sinful, and why this single statement unravels her most fundamental premise.

THE MIND IS IN CHARGE OF THE BRAIN

A large part of her sermon was based on her next premise, that the mind changes the brain, and not the other way around. That is half true. The mind influences the brain, and how we think will have effects on neural pathways within the brain. But for a cognitive neuroscientist to state that the brain does not influence the mind is somewhat concerning.

There are several reasons why her assertion is deeply flawed. For starters, where else does the mind or thought come from other than our neural networks? Thought is built on our neural connections. To say that the brain does not influence thought is like saying that the foundation of a building doesn’t influence the bricks.

There are clinical reasons as well. These come from a few areas – firstly the research that showed that newborn babies (who do not have thought like we have thoughts) are pre-wired for emotions which are refined as we learn. There is no time for neonates to have enough stimulation to form those emotions and reactions if it was from our mind.

Secondly, people with brain injuries or tumours can have personality or mood changes. The most famous was a man in the 1800’s called Phineas Gage, who on 13 September 1848 was packing explosives into rock with a tamping iron (a long, tapered, smooth crow-bar). History says that the explosives sent the tamping iron through his left face and skull, taking a fair chunk of his frontal lobe with it. Depending on who you believe, Gage’s personality changed after his physical recovery, reportedly from a moral, respectful man into a cursing, angry one (Kihlstrom 2010). Some reports of his story were that Gage made an almost full recovery, but assuming that some of the historical record is true, changes to his brain changed his mental function, ie: his thoughts.

Further, I have personally seen two patients with personality changes secondary to brain tumours. The first was a woman in her late 20’s who had six months of worsening anxiety, who did not seek help despite my referrals, until she had a seizure and the diagnosis was made. Then there was the sad case of a girl in her pre-teens who had only two weeks of rapidly escalating sullenness then aggression then violence. Her parents initially thought she was moody, and when they brought her into the Emergency Department they thought she was perhaps in the middle of a psychotic episode. It turned out that she had a very aggressive tumour near her frontal lobe.

It is clear from these cases, and from a basic understanding of the concept of thought, that changes to the brain result in changes to thoughts and the mind, and vice versa.

SOME MISCELLANEOUS ISSUES

If I had the time I would like to look at many others issues that she raised, but this isn’t a book. Suffice it to say that she claimed that stress prunes our “thought trees” although the evidence is only in animal models and only related to severe stress (Karatsoreos and McEwen 2011). She also stated that EVERY thought we EVER have is stored in ALL of our cells (so some random fibroblast in my big toe is somehow affected by my thought about tonights dinner), and that ALL our thoughts are stored in our gametes (our sperm and eggs) and are passed down to our 4th generation (but packed, like in a metaphysical zip-lock bag, and only opened if we choose to have the same thoughts.) And here I was thinking that nurture had something to do with learned behaviour.

ASD/ADHD – MORE OPINION THAN FACT?

She also claimed that 55-70% of ASD/ADHD cases are over-referred and the problem is in educational modeling. This one made me mad.

Not even professorial level researchers know exactly what’s going on in ASD/ADHD, so her statement is a brave one to make, especially without referencing her evidence.

She then espoused the party line of ADHD ignorance – that Ritalin is evil and all you need to do is stop their sugar intake and feed them organic foods and give them supplements. Ritalin isn’t perfect, to be sure, but it is the most effective treatment that’s currently available. If dietary measures and educational measures were effective, then ritalin wouldn’t be prescribed. I have never met a parent that has wanted their child on ritalin. Most of them have tried educational/psychological measures or dietary controls first. The reason why ritalin is prescribed is because dietary and psychological interventions on their own do not adequately control the symptoms, or fail altogether.

To confirm that I’m not just having a rant, there is published scientific literature to back me up. In their recently published meta-analysis, Nigg et al (2012) state, “An estimated 8% of children with ADHD may have symptoms related to synthetic food colors.” Eight percent. That’s all! That’s ninty-two percent of children with ADHD (real ADHD, not just rambunctious children with lots of energy) DID NOT have symptoms due to food colourings. Their conclusions: “A restriction diet benefits some children with ADHD. Effects of food colors were notable but susceptible to publication bias or were derived from small, nongeneralizable samples.” In terms of sugar, Kim and Chang (2011) note that, “children who consumed less sugar from fruit snacks or whose vitamin C intake was less than RI was at increased risks for ADHD (P < 0.05).” (emphasis added) The study was only of about 100 children, but the result was statistically significant. It wasn’t a chance effect.

The misinformation she stated as fact from the pulpit promotes scare-mongering and ignorance throughout the church, which has flow on effects. Church members with children with ADHD or ASD will avoid standard medical treatment on Dr Leaf’s advice. When her treatments fail in the majority of cases, those parents will either live with unnecessarily heightened stress because of their child’s poorly controlled condition, or the guilt of using ritalin, all the while believing that they are ruining their childs brain.

This also places the hosting church in a bind. Do they stand behind their guest speaker, or do they support the advice of the medical community? Is their duty of care to the reputation of the guest speaker or to the congregation under their protection? What would happen if Dr Leaf’s advice lead to the death or disability of a person in their congregation? Would they be libel?

CASE STUDIES – INSPIRATIONAL STORIES, BUT POOR SCIENTIFIC EVIDENCE

Dr Leaf also told a lot of stories of how everyone afflicted came to her and how she healed them all. If you took her at face value, she would have you believe that people with ASD, ADHD, anorexia, OCD, depression etc, just needed a glimpse of their self-worth and their inner gift and they would be cured. While her stories were inspirational, the world of scientific research demands more. If Dr Leaf’s insights are worth more than the hot air she produces when espousing them, then they should be put to the wider research community so they can pass through the fire of peer review. If peer review prove her insights to be valid, I would be happy to apply them and promote them.

Tomorrow, I will publish the last, and probably the most important part of my essay – that Dr Leaf believes that ‘toxic’ thoughts are sinful, and why this single statement unravels her most fundamental premise.

REFERENCES

Crum, A. J., P. Salovey and S. Achor (2013). “Rethinking stress: the role of mindsets in determining the stress response.” J Pers Soc Psychol 104(4): 716-733.

Karatsoreos, I. N. and B. S. McEwen (2011). “Psychobiological allostasis: resistance, resilience and vulnerability.” Trends Cogn Sci 15(12): 576-584.

Kihlstrom, J. F. (2010). “Social neuroscience: The footprints of Phineas Gage.” Social Cognition 28: 757-782.

Kim, Y. and H. Chang (2011). “Correlation between attention deficit hyperactivity disorder and sugar consumption, quality of diet, and dietary behavior in school children.” Nutr Res Pract 5(3): 236-245.

Leaf, C. (2009). Who Switched Off My Brain? Controlling toxic thoughts and emotions. Southlake, TX, USA, Inprov, Ltd.

Nigg, J. T., K. Lewis, T. Edinger and M. Falk (2012). “Meta-analysis of attention-deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms, restriction diet, and synthetic food color additives.” J Am Acad Child Adolesc Psychiatry 51(1): 86-97 e88.