Don’t stress about stress – Part 3: Coping

Posted on November 23, 2014 by cedwardpitt

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

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

The answer lies in resilience.

WHAT IS RESILIENCE?

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

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

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

WHAT CONTRIBUTES TO RESILIENCE?

Coping Strategies

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

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

Personality factors

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

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

Biological factors

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

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

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

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

Resilience on a personal level

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

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

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

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

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

SUMMARY

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

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

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

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

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

References

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

Dr Caroline Leaf and the chemistry of perceptions

Posted on November 16, 2014 by cedwardpitt

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

Hmmm … yes and no.

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

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

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

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

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

References

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

Putting thought in the right place, part 2

Posted on November 11, 2014 by cedwardpitt

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

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

Dr Caroline Leaf: Putting thought in the right place

Posted on November 8, 2014 by cedwardpitt

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

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

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

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

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

What’s going on under the surface is a complex interplay of our genes and their expression which controls the structure and function of our brains, which effects how we perceive information, how we process that information and combine it into our memories of the past, predictions of the future, and even the further perception of the present [3].

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

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

Epigenetics and the environment contribute to the way genes are expressed. Epigenetics are “tags” on the strand of DNA that act to promote or silence the expression of certain genes (I discuss this in more detail in chapter 12 of my book, https://www.smashwords.com/books/view/466848). Environmental factors (the components that make up the world external to our bodies) can influence genes and epigenetic markers. The environment can cause genetic mutations or new epigenetic marks that change the function of a particular gene, and depending on which cell they effect (a very active embryonic cell or a quiet adult cell) will largely determine the eventual outcome. The environment is more influential to our genetic expression than epigenetics.

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

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

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

Different organs are needed to translate the optical, chemical or mechanical signals into electrical signals. Different parts of our brain then interpret these signals and their patterns.

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

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

Personality
Personality is “the combination of characteristics or qualities that form an individual’s distinctive character” [4]. Formally speaking, personality is, “defined as constitutionally based tendencies in thoughts, behaviors, and emotions that surface early in life, are relatively stable and follow intrinsic paths of development basically independent of environmental influences.” [5]

Professor Gregg Henriques explained it well in Psychology Today, “Personality traits are longstanding patterns of thoughts, feelings, and actions which tend to stabilize in adulthood and remain relatively fixed. There are five broad trait domains, one of which is labeled Neuroticism, and it generally corresponds to the sensitivity of the negative affect system, where a person high in Neuroticism is someone who is a worrier, easily upset, often down or irritable, and demonstrates high emotional reactivity to stress.” [6] The other four personality types are Extraversion, Agreeableness, Conscientiousness, and Openness to Experience.

Gene x environment studies suggest that personality is highly heritable, with up to 60% of personality influenced by genetics [7], predominantly through genes involved in the serotonin [8] and dopamine systems [9, 10]. The “non-shared environment” (influences outside of the home environment) contributes heavily to the remainder [11, 12].

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

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

All of these signals are constantly being generated, and collated in different parts of the brain. Some researchers consider them positive and negative depending on the data stream and the signal its providing. They coalesce into emotion [13].

Emotion
According to Watkins, “emotion” is the sum of all the data streams of physiology, or what he described as “E-MOTION … Energy in MOTION.” [13] In this context, think of emotion as a bulls-eye spirit-level of our body systems. The different forces of our physiology change the “level” constantly in different directions. Emotion is the bubble that marks the central point, telling us how far out of balance we are.

In the interest of full disclosure, I should mention that although emotion is a familiar concept, the work of literally thousands of brilliant minds has brought us no closer to a scientifically validated definition of the word “emotion”. Some psychologists and researchers consider it vague and unscientific, and would prefer that it not be used altogether [14].

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

Feelings
“Feelings” are the perception of emotion.

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

As I wrote earlier, personality is largely determined by our genetics with contributions from our environment [11, 12]. The emotional signal is filtered by our personality to give rise to our feelings. Classically, an optimistic personality is going to bias the emotional input in a positive, adaptive way while a pessimist or neurotic is going to bias the emotional signal in a maladaptive way

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

Executive Functions
Executive function of the brain is defined as a complex cognitive process requiring the co-ordination of several sub-processes to achieve a particular goal [15]. These sub-processes can be variable but include working memory, attention, goal setting, maintaining and monitoring of goal directed action and action inhibition. In order to achieve these goals, the brain requires flexibility and coordination of a number of networks and lobes, although mainly the prefrontal cortex, parietal cortex, anterior cingulate and basal ganglia, and the while matter tracts that connect them.

Executive functions process the incoming information and decide on what goals are best given the context, then plan the goals, execute them to the motor cortices, and monitor the action. Research work from Marien et al [16] demonstrates that unconscious/implicit goals can divert resources away from conscious goals especially if it is emotionally salient or otherwise strongly related. They also confirm that conscious awareness is not necessary for executive function but that implicit goals can be formed and executed without conscious involvement.

Thoughts
Thoughts are essentially a stream of data projected into our conscious space. Baars [17, 18] noted that the conscious broadcast comes into working memory which then engages a wider area of the cerebral cortex necessary to most efficiently process the information signal. We perceive thought most commonly as either pictures or sounds in our head (“the inner monologue”), which corresponds to the slave systems of working memory. When you “see” an image in your mind, that’s the visuospatial sketchpad. When you listen to your inner monologue, that’s your phonological loop. When a song gets stuck in your head, that’s your phonological loop as well, but on repeat mode.

There is another slave system that Baddeley included in his model of working memory called the episodic buffer, “which binds together complex information from multiple sources and modalities. Together with the ability to create and manipulate novel representations, it creates a mental modeling space that enables the consideration of possible outcomes, hence providing the basis for planning future action.” [19]

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

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

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

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

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

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

According to the model proposed by Bonn [20], the conscious network has some feedback from the control network of our brain, providing real time context to actions about to be executed, and a veto function, stopping some actions at the last minute before they are carried out. This is largely a function of the basal ganglia [21], with some assistance from working memory.

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

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

References

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

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

Understanding Thought – Part 1

Posted on October 23, 2014 by cedwardpitt

WHAT IS THOUGHT?

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

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

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

Neurobiology 101

The nerve cell

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

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

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

The synapse

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

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

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

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

Nerve pathways

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

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

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

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

Higher order brain structures

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

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

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

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

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

Emotions and feelings

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

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

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

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

Memories

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

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

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

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

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

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

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

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

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

References

Sukel, K. The Synapse – A Primer. 2013 [cited 2013, 28/06/2013]; Available from: http://www.dana.org/media/detail.aspx?id=31294.
Hall, J.E. and Guyton, A.C., Guyton and Hall textbook of medical physiology. 12th ed. 2011, Saunders/Elsevier, Philadelphia, Pa.:
Stuss, D.T. and Knight, R.T., Principles of frontal lobe function. 2nd ed. 2013, Oxford University Press, Oxford ; New York:
Meehan, T.P. and Bressler, S.L., Neurocognitive networks: findings, models, and theory. Neurosci Biobehav Rev, 2012. 36(10): 2232-47 doi: 10.1016/j.neubiorev.2012.08.002
Dixon, T., “Emotion”: The History of a Keyword in Crisis. Emot Rev, 2012. 4(4): 338-44 doi: 10.1177/1754073912445814
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
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
Felten, A., et al., Genetically determined dopamine availability predicts disposition for depression. Brain Behav, 2011. 1(2): 109-18 doi: 10.1002/brb3.20
Squire, L.R. and Wixted, J.T., The cognitive neuroscience of human memory since H.M. Annu Rev Neurosci, 2011. 34: 259-88 doi: 10.1146/annurev-neuro-061010-113720
Repovs, G. and Baddeley, A., The multi-component model of working memory: explorations in experimental cognitive psychology. Neuroscience, 2006. 139(1): 5-21 doi: 10.1016/j.neuroscience.2005.12.061
Byrne, J.H. Learning and Memory (Section 4, Chapter 7). Neuroscience Online – an electronic textbook for the neurosciences 2013 [cited 2014, Jan 3]; Available from: http://neuroscience.uth.tmc.edu/s4/chapter07.html.
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
Schacter, D.L., et al., The future of memory: remembering, imagining, and the brain. Neuron, 2012. 76(4): 677-94 doi: 10.1016/j.neuron.2012.11.001

Dr Caroline Leaf and the Profound Simplicity Paradox

Posted on September 23, 2014 by cedwardpitt

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

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

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

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

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

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

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

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

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

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

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

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

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

Hold That Thought – Reappraising the work of Dr Caroline Leaf

Posted on August 13, 2014 by cedwardpitt

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 and the Mixed Message Memes

Posted on July 5, 2014 by cedwardpitt

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

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

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

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

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

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

The storage of memories within declarative memory is also done piecemeal, by breaking down the information stored into chunks. Byrne notes, “We like to think that memory is similar to taking a photograph and placing that photograph into a filing cabinet drawer to be withdrawn later (recalled) as the ‘memory’ exactly the way it was placed there originally (stored). But memory is more like taking a picture and tearing it up into small pieces and putting the pieces in different drawers. The memory is then recalled by reconstructing the memory from the individual fragments of the memory.” [4] Retrieving the original memory is an inaccurate process, because sometimes pieces of the memory are lost, faded or mixed up with another [5]. What the memory systems lose in accuracy of recall is more than made up for by the flexibility of the information stored in memory to plan current action, and to imagine possible future scenarios.

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

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

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

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

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

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

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

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

References

Berns, G., Iconoclast : a neuroscientist reveals how to think differently. 2008, Harvard Business School Press, Boston:
Squire, L.R. and Zola, S.M., Structure and function of declarative and nondeclarative memory systems. Proceedings of the National Academy of Sciences, 1996. 93(24): 13515-22 http://www.pnas.org/content/93/24/13515.abstract
Binder, J.R. and Desai, R.H., The neurobiology of semantic memory. Trends Cogn Sci, 2011. 15(11): 527-36 doi: 10.1016/j.tics.2011.10.001
Byrne, J.H. Learning and Memory (Section 4, Chapter 7). Neuroscience Online – an electronic textbook for the neurosciences 2013 [cited 2014, Jan 3]; Available from: http://neuroscience.uth.tmc.edu/s4/chapter07.html.
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
Haggard, P., Human volition: towards a neuroscience of will. Nat Rev Neurosci, 2008. 9(12): 934-46 doi: 10.1038/nrn2497
Libet, B., et al., Time of conscious intention to act in relation to onset of cerebral activity (readiness-potential). The unconscious initiation of a freely voluntary act. Brain, 1983. 106 (Pt 3): 623-42 http://www.ncbi.nlm.nih.gov/pubmed/6640273
Soon, C.S., et al., Unconscious determinants of free decisions in the human brain. Nat Neurosci, 2008. 11(5): 543-5 doi: 10.1038/nn.2112
Leaf, C.M., Switch On Your Brain : The Key to Peak Happiness, Thinking, and Health. 2013, Baker Books, Grand Rapids, Michigan:

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

Dr Caroline Leaf – Contradicted by the latest research

Posted on August 29, 2013 by cedwardpitt

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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:

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].
BREAST – Genes make up 25% of the risk factors for breast cancer, and significantly interacted with parity (number of children born) [9].
LUNG/BRONCHUS – Lung cancer is almost exclusively linked to smoking, but nicotine addiction has a strong hereditary link (50-75% genetic susceptibility) [10].
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:

HIGH CHOLESTEROL – Genetic susceptibility accounts for 40-60% of the risk for high cholesterol [13].
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].
SMOKING – nicotine addiction has a strong hereditary link (50-75% genetic susceptibility) [10].
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>.

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.

Dr Caroline Leaf – Serious questions, few answers (Part 3) – “Flirting with heresy”

Posted on August 6, 2013 by cedwardpitt

Following on from the last 2 posts discussing the various teaching points of Dr Caroline Leaf at Kings Christian Church, here is my final post on the points that she raised. Tonight, I conclude by proposing that in equating ‘toxic’ thoughts with sin, she seriously weakens her own argument, or she flirts with heresy.

TOXIC THOUGHTS ARE SIN

Probably the most disturbing of all she discussed was her point blank statement that, “Toxic thoughts are sin.”

This is an astounding claim, and it was said in such an off-handed manner. It was like she threw a grenade and calmly moved on. Her claim not only has psychological ramifications, but deep theological connotations.

Her statement has the effect of ADDING to the stress response of her audience. Indeed, it sets up a feedback loop of self-perpetualising existential distress – the spiritual struggle switch. Crum et al (2013) showed that negatively framing the concept of stress leads to an increase in the subjects stress response. What could be more stressing that telling a christian that they have sinned every time that have had a persistent stress? More stress is then equated with more ‘sin’ which then gives rise to even more stress. And so the cycle continues.

She then attempted to redeem her statement by declaring that we can transcend the guilt from the sin of stress, because her 21-day brain detox program would fix it. But on the surface, it seems an arbitrary premise. Inducing guilt to then offer to fix it is like a supermarket marking up a price so they can claim to offer a discount when they reduce it again.

More importantly though, in making the link between stress and sin, she brings herself undone. She either unravels her entire argument, or she flirts with heresy. Because if a thought process which results in prolonged or severe fear/stress is a sin, then Jesus himself sinned.

In the Garden of Gethsemane, the gospels record that Jesus, the spotless lamb of God, about to be crucified for the sins of all mankind, was “overwhelmed with sorrow to the point of death” (Mark 14:34, Matthew 26:38), and became so distressed by the ordeal he was about to endure that he literally sweat drops of blood (Luke 22:44).

Where do you think Jesus was on the stress spectrum according to those accounts? I’d wager that it wasn’t “healthy stress”.Rev Bob Deffinbaugh wrote that,

“Jesus spent what appears to be at least three agonizing hours in prayer.” He also noted that, “Never before have we seen Jesus so emotionally distraught. He has faced a raging storm on the Sea of Galilee, totally composed and unruffled. He has faced demonic opposition, satanic temptation, and the grilling of Jerusalem’s religious leaders, with total composure. But here in the Garden, the disciples must have been greatly distressed by what (little) they saw. Here, Jesus cast Himself to the ground, agonizing in prayer.” (https://bible.org/seriespage/garden-gethsemane-luke-2239-46)

There is no other way to explain it – Jesus suffered severe and prolonged mental anguish to the point that it had physical effects. By Dr Leaf’s definition (Leaf 2009, p19), Jesus had “toxic” thoughts. So the crux is: either toxic thoughts and emotions are sinful, in which case Jesus was a sinner and our salvation is invalid, or toxic thoughts and emotions are not sinful, which directly contradicts her teaching.

There is at least one further example from the life of Jesus that significantly weakens Dr Leafs definition of ‘toxic’ thoughts. In her book, Dr Leaf states, “hostility and rage are at the top of the list of toxic emotions”, and that “Stress is the direct result of toxic thinking.” (Leaf 2009, p29-30)

In John 2:13-17, it says, “When it was almost time for the Jewish Passover, Jesus went up to Jerusalem. In the temple courts he found people selling cattle, sheep and doves, and others sitting at tables exchanging money. So he made a whip out of cords, and drove all from the temple courts, both sheep and cattle; he scattered the coins of the money changers and overturned their tables. To those who sold doves he said, “Get these out of here! Stop turning my Father’s house into a market!” His disciples remembered that it is written: “Zeal for your house will consume me.”

So Jesus saw the sellers and the money exchangers, then in a pre-meditated way, took small cords and fashioned a whip out of them, then proceeded to use that whip to violently and aggressively overturn the tables of the merchants and spill the money of the money changers. John adds a post-script – “Zeal for your house will consume me.” So Jesus wasn’t mincing words. He drove them out of the temple in a rage.

Again, was Jesus acting in sin? Of course not. Instead, perhaps God has designed normal human beings to experience rage, anger and stress – emotions that are not curses passed down in genetic material and are not learned behaviours as a result of our sin nature.

Further, God himself displayed anger. God also made us in his image, and in his likeness. Dr Leaf stated that we were designed to function in optimism and love, and again, negative emotions like anger and fear are learnt from living in sin. Yet it is interesting that God the Father regularly kindled his wrath, and smote Israelites or their enemies (Numbers 11:33, Deuteronomy 11:16-17, and in 2 Kings 23:25-27, “Notwithstanding the Lord turned not from the fierceness of his great wrath, wherewith his anger was kindled against Judah, because of all the provocations that Manasseh had provoked him withal.”)

If God regularly displayed anger throughout the Old Testament, and Jesus displayed it in the New Testament, then anger and rage can not be the perversion of God’s ultimate design as Dr Leaf proposes.

Therefore, ‘toxic’ thought is NOT sin, because Jesus suffered prolonged mental stress and anguish and he did not sin. Emotions that are deemed to be toxic by Dr Leaf and her definition are not toxic, since both God and Jesus displayed them and they did not and do not sin. Such a suggestion is incongruent with the Christian faith.

We were made in the image of God, so therefore we mirror all the emotions of God, which includes anger. This shows that Dr Leaf’s proposals and the assumptions on which they are based, are incongruent with a logical interpretation of scripture.

In conclusion, Dr Leaf has been gathering quite a following. From the pulpit at least, her claims of evidence of studies from peer-reviewed sources have been lacking. From what I saw on Sunday last, her reputation is excessive, her arguments unsupported and her theology is questionable at best, dangerous at worst.

Personally, I would welcome Dr Leaf’s response to these posts. I have written these posts over a few days from her teaching at one church, so perhaps I have misunderstood her. I have not been able to go through all of her books in such a short time, so she may have references to her teaching. But she needs to clarify each question that I’ve raised and respond with current peer-reviewed science and sound theological resources.

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.

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

Dr C. Edward Pitt

Faith, Hope, Love, Science.

Tag Archives: implicit memory

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