Tag Archives: DSM5

Dr Caroline Leaf – Increasing the stigma of mental illness again

Posted on by
6

Screen Shot 2016-03-19 at 9.02.05 PM

Let me tell you a story.

A couple of years ago, one of my patients was an elderly gentleman in his late seventies.  He was living in a nursing home at the time, but because of his history of psychosis, he remained on a treatment order – a requirement by law that if he was to remain outside of a mental facility, he had to have regular anti-psychotic medication every few weeks.

This man was on a treatment order because his disease caused him to have delusions.  He misinterpreted what was going on around him, and would not consider that he could be wrong.  In his particular case, he was convinced that his next-door neighbour was a paedophile, and he was planning to ambush his neighbour and castrate him.  Luckily the police had taken my patient into custody before he got the opportunity.  With treatment, my patient had clear thoughts, although needed close supervision.  Without his medication, he became confused and violent.

According to a post on the blog Mad in America and promoted by Dr Caroline Leaf, my patient’s diagnosis was spurious, and he was denied his basic human rights by being forced to take medications.

Dr Caroline Leaf is a communication pathologist and self-titled cognitive neuroscientist.  She is also a self-declared expert in mental health, despite not having any professional training in medicine, psychiatry, psychology or even cognitive neuroscience for that matter.

Indeed, if she had any experience or expertise in mental health, she would have recognised the basic factual errors and logical fallacies that riddled the post she quoted from.

Take the quote that Dr Leaf posted on social media.  The full quote from the Mad in America post is:

“Despite the fact that no one in history, not even the omnipotent American Psychiatric Association – which produces and profits mightily from the ‘Bible’ of mental disorders — has come up with a halfway good definition of “mental illness,” and despite the fact that the process of creating and applying the labels of mental illness is unscientific, any of those labels can be used to deprive the person so labeled of their human rights. This is terrifying. It ought to terrify those who are so labeled and those who are not, because deprivation of human rights on totally arbitrary grounds is inhumane and immoral.”

This is the same tired, emotionally laden and misleading rhetoric that’s so often barked in fervent paroxysms through the foaming lips of those opposed to modern psychiatric practice:

  1. There is no good definition of ‘mental illness’
  2. The American Psychiatric Association is just a profit-driven cabal
  3. The DSM5 (which the author alludes to as the ‘Bible’ of mental disorders) is unscientific
  4. Psychiatric diagnoses are unscientific
  5. Any psychiatric diagnosis can be used as a trigger to force people into unwanted treatments or incarceration
  6. Therefore psychiatric diagnosis and treatment is against basic humans rights and is inhumane and immoral.

Inhumane and immoral hey?  Tell that to my patients neighbour who almost became a eunuch except for that “inhumane and immoral treatment” of my former patient.

Caplan claims just don’t stand up to any rational scrutiny.

  1. There are lots of good definitions of mental illness … modern psychiatry critics just don’t like them. But take the definition used by the CDC, “Mental illness is defined as … ‘health conditions that are characterized by alterations in thinking, mood, or behavior (or some combination thereof) associated with distress and/or impaired functioning.’” There’s nothing wrong with this definition. It describes mental illness and helps differentiate mental illness from variations of mood, thought and behaviour that are part of the everyday human experience.
  1. The American Psychiatric Association isn’t the only group to have created a classification of psychiatric illnesses. The World Health Organisation publishes the International Classification of Diseases, or the ICD, which is also used for psychiatric diagnosis. Is the WHO an evil profit-driven junta too?
  1. The DSM, the ICD, and any other system of diagnosis, are simply different classification systems. Over the last century, clinicians have noted clusters of symptoms and have tried to classify them into common groups. How is that unscientific?  It’s no different to scientists looking at the different characteristics of various animals and creating a taxonomy, to provide a common system and language for clinicians and researchers across disciplines and across countries.The DSM system isn’t perfect, but what system ever is?  As knowledge of neuroscience grows, the classifications are reviewed and tightened in an ongoing process of improvement.  If those who oppose the DSM want to come up with something better, they’re welcome to put something forward.
  1. The old saying goes that medicine is an art and a science. Human beings, as nuanced as we are, often don’t fit into diagnostic criteria as easily as we would like. That doesn’t invalidate the diagnostic criteria or make the process unscientific as critics of modern psychiatry would have us believe, just like an unusual and hard-to-classify form of cancer doesn’t invalidate the other cancer classifications that are well defined.  Psychiatry, by it’s nature, relies on verbal report from patients rather than a clean-cut blood test or piece of tissue under a microscope, so at this stage in history, it seems imprecise.  That doesn’t make it any less scientific.
  1. The allegation that any psychiatric diagnosis can any be used to deprive the person so labeled of their human rights is utter nonsense. It’s a giant scarecrow – it seems really scary, but on closer inspection, it’s just a tarted-up mound of straw.People are never forced into treatments unless they really are “dangerous to themselves and/or others”.  This rule can’t be invoked willy-nilly.  There are multiple checks and balances, and a whole school of civil rights lawyers expectantly circling, ready for the whiff of blood in the water (http://www.mhrt.qld.gov.au/?page_id=2 is an example of the process in my home state, but each jurisdiction has their own version).

Caplan rightly pointed out that those with mental illness were less likely to be the perpetrators of violence and more likely to be the victims, but that doesn’t negate the need for protection of the community from those with mental illness who have shown violent intent and no capacity to control their behaviour.

If you want to find a group that really are suffering from inhumane and immoral deprivations of their human rights, then that would be Christians.  Around the globe, millions of Christians are oppressed, imprisoned, tortured, raped, and murdered every year.

Time and space preclude a full analysis of Caplan’s post, but what’s really important is that both the American Psychiatric Association and the U.S. Department of Health and Human Services’s Office of Civil Rights, an independent ombudsman, dismissed formal appeals by Caplan relating to her hysterical claims of inhumane forced psychiatric treatment.  Dr Leaf conveniently left that out of her social media post.

Instead, Dr Leaf chose to publish one of the most alarming quotes from an article heavy on scaremongering, from a disaffected author on an extremist blog.  If Dr Leaf was a real expert on mental health instead of being a self-declared one, she would have easily seen how nonsensical Caplan’s post was.

By posting this quote on social media today, it’s highly likely that Dr Leaf has caused harm to thousands of vulnerable Christians by unnecessarily increasing the stigma and fear of a mental health diagnosis.  This, in turn, is likely to lead to these same vulnerable Christians missing out on (drug and non-drug) treatment which would help them rise to their true potential in God and in life, leaving them trapped and suffering in their mental destitution.

Dr Leaf has a track record of misinformation when it comes to mental health.  Christians suffering mental illness need more support, not more stigma.  It’s time Dr Leaf stepped aside, and stopped making things worse.

The Prospering Soul – Christians and Depression Part 1

Posted on by
1

In the average charismatic church, from the time you park your car in the parking lot, to the time the music starts at the beginning of the service, the smiles of at least a hundred people beam at you, and at least one third of those smiles are also attached to enthusiastic handshakes and exhortations like, “Isn’t it great to be in church this morning!”

When you’re a Christian, especially at the happy-clappy end of the church spectrum, you’re supposed to be constantly full of the Holy Spirit and experiencing the joy of the Lord.

Which is why for most church-goers, putting the terms “Christian” and “depression” in the same sentence just doesn’t seem natural, even though depression affects a lot more of the church than the church is aware of.

So, how much of the church is affected by depression? The lifetime prevalence (how likely you are to suffer from depression at one stage through your life) is about twenty-five percent, or about one in four people. The point prevalence (those who are suffering from clinical depression at any particular time) is about six percent.

I used to attend a church which had a regular congregation of about 2500 people. So statistically, one hundred and fifty people in that congregation are suffering from depression every Sunday, and more than 600 will experience depression in their lifetime.

And by ‘depression’, we’re not talking about feeling a little sad … that Bill Shorten might become Prime Minister one day, or Ben Hunt can’t catch, or that One Direction isn’t the same without Zayn. Sadness for genuine reasons … you broke up with a long term partner, someone stole your purse out of your bag, or there’s the threat of redundancies at your office … also doesn’t mean you’re depressed.

The DSM5 is the current standard for psychiatric diagnoses around the world. I’ve included the full definition of depression at the end of this blog, but suffice to say, depression is more than just unhappiness. Proper depression symptoms “cause clinically significant distress or impairment in social, occupational or other important areas of functioning.” In other words, you’re so low that your social life or work is affected, and for more than two whole weeks. It’s also important to know that depression isn’t just low mood but can also be experienced as “Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day”.

Depression has a number of causes and correlations. People who are chronically unwell, be that from chronic pain, long term illness such as cancer or autoimmune disease, or life threatening illnesses such as those who’ve suffered from heart attacks or meningitis, have a higher rate of depression. People who have experienced significant physical or psychological trauma also have a higher rate of depression. In fact, stress of any form is highly correlated with depression (that is, people who suffer from any severe stress are more likely to develop depression).

This observation led to a theory about the development of depression, called the Stress Exposure Model of depression [1] – You develop depression because you’ve suffered from stress. This is one of the most common assumptions about depression in our society, and there are some important consequences from this line of thinking. Like, if being stressed is the cause of depression then the cure for depression is simply reducing stress. This is probably why most people assume that depression is a choice, or a simple weakness, and why depressed people are often told just to snap out of it.

But there’s more to depression than just better dealing with stress. Fundamentally, I understand depression as the end result of the brains capacity to deal with the demands of life. Too many demands or not enough resources overwhelms the brain and low mood is the end result.

Some depression is predominantly biological. People with biological depression can’t effectively deal with even a normal amount of demand on their system, because their brain doesn’t have the resources to process the incoming signals correctly or efficiently. The main biological cause is a deficiency of a growth factor called BDNF, which is needed for the nerve cells to grow new branches, which enable the brain to process new information. This theory is called the Neurotrophic Hypothesis of Depression [2] (‘neuro’ = nerve and ‘trophic’ = growth). BDNF isn’t the only critical factor in the biological story of depression. There are many others, including the stress hormone system [3], the serotonin system [4] and the dopamine/rewards system [5].

Some depression is predominantly psychological. There are certain situations in which there’s so much going on and so much change and adaptation is required, and the brains coping systems simply can’t cope. So, severe and sudden stressors would fit into this category. For example, people trying to cope with natural disasters, or a tragedy like a massive house fire.

Most of the time, depression is a combination of both biological and psychological. Genetic factors change our capacity to handle the incoming. The nerve cells don’t have enough BDNF and are slow to grow new branches. Genetics are also important in determining other mechanisms of resilience, and people with poor resilience are also more prone to depression [6-8]. Genetic factors also determine other factors involved in the way we process the incoming stream of sensory input – our personality. People with the neurotic personality type, the classical introverts/pessimists, are more prone to depression, because of the way their brain naturally biases the flavour of the incoming information [9]. What’s also very interesting is that these tendencies to depression also tend to create more stress [1, 10]. So stress is important to the risk of depression, but ironically, it is the risk of depression which influences the risk of stress.

The risk of depression is related to an increased tendency towards stress, and poor processing of that stress because of personality factors and a reduced capacity to cope. All three of these factors are influenced by a broad array of genetic factors.

What’s also important to see here is that being depressed isn’t because of “toxic thinking” or because of “negative confessions”. What we say and what we think are signs of what is going on underneath, not the cause of it. And more importantly, you can make as many faith-filled confessions as you like, but if they don’t help you to change your capacity to cope, then they’re just hot air.

In the next instalment, we’ll look at ways to handle depression, and what the Bible says about being depressed.

References

[1]        Liu RT, Alloy LB. Stress generation in depression: A systematic review of the empirical literature and recommendations for future study. Clinical psychology review 2010 Jul;30(5):582-93.
[2]        Duman RS, Li N. A neurotrophic hypothesis of depression: role of synaptogenesis in the actions of NMDA receptor antagonists. Philosophical transactions of the Royal Society of London Series B, Biological sciences 2012 Sep 5;367(1601):2475-84.
[3]        Hauger RL, Risbrough V, Oakley RH, Olivares-Reyes JA, Dautzenberg FM. Role of CRF receptor signaling in stress vulnerability, anxiety, and depression. Annals of the New York Academy of Sciences 2009 Oct;1179:120-43.
[4]        Caspi A, Hariri AR, Holmes A, Uher R, Moffitt TE. Genetic sensitivity to the environment: the case of the serotonin transporter gene and its implications for studying complex diseases and traits. The American journal of psychiatry 2010 May;167(5):509-27.
[5]        Felten A, Montag C, Markett S, Walter NT, Reuter M. Genetically determined dopamine availability predicts disposition for depression. Brain and behavior 2011 Nov;1(2):109-18.
[6]        Karatsoreos IN, McEwen BS. Resilience and vulnerability: a neurobiological perspective. F1000prime reports 2013;5:13.
[7]        Wu G, Feder A, Cohen H, et al. Understanding resilience. Frontiers in behavioral neuroscience 2013;7:10.
[8]        Russo SJ, Murrough JW, Han M-H, Charney DS, Nestler EJ. Neurobiology of resilience. Nature neuroscience 2012 November;15(11):1475-84.
[9]        Hansell NK, Wright MJ, Medland SE, et al. Genetic co-morbidity between neuroticism, anxiety/depression and somatic distress in a population sample of adolescent and young adult twins. Psychological medicine 2012 Jun;42(6):1249-60.
[10]      Boardman JD, Alexander KB, Stallings MC. Stressful life events and depression among adolescent twin pairs. Biodemography and social biology 2011;57(1):53-66.

The DSM5 Formal Diagnostic Criteria for Depression

A. Five (or more) of the following symptoms have been present during the same 2- week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.

(Note: Do not include symptoms that are clearly due to a general medical condition, or mood-incongruent delusions or hallucinations.)

  • Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad or empty) or observation made by others (e.g., appears tearful). Note: In children and adolescents, can be irritable mood.
  • Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation made by others).
  • Significant weight loss when not dieting or weight gain (e.g., a change of more than 5 percent of body weight in a month), or decrease or increase in appetite nearly every day. Note: In children, consider failure to make expected weight gains.
  • Insomnia or hypersomnia nearly every day.
  • Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down).
  • Fatigue or loss of energy nearly every day.
  • Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick).
  • Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others).
  • Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.

B. The symptoms cause clinically significant distress or impairment in social, occupational or other important areas of functioning.
C. The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hypothyroidism).

Putting thought in the right place, part 2

Posted on by
1

CAP v2.1.2

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

Small changes in the early processes within the Cognitive-Action Pathway model can snowball to effect every other part of the process. A real life example of this is ASD, or Autism Spectrum Disorder.

ASD has been present since time immemorial. Numerous bloggers speculate that Moses may have had ASD, while a couple of researchers proposed that Samson was on the spectrum (although their evidence was tenuous [1]). Thankfully, autism is no longer considered a form of demon possession or madness, or schizophrenia, or caused by emotionally distant “refrigerator mothers”, nor treated with inhumane experimental chemical and physical “treatments” [2, 3].

The autism spectrum is defined by two main characteristics: deficits in social communication and interaction, and restricted repetitive patterns of behaviour. People on the autism spectrum also tend to have abnormal sensitivity to stimuli, and other co-existing conditions like ADHD. The full diagnostic criteria can be found in DSM5. The new criteria are not without their critics [4-6], but overall, reflect the progress made in understanding the biological basis of autism.

ASD is recognized as a pervasive developmental disorder secondary to structural and functional changes in the brain that occur in the womb, and can be detected as early as a month after birth [7]. In the brain of a foetus that will be born with ASD, excess numbers of dysfunctional nerve cells are unable to form the correct synaptic scaffolding, leaving a brain that is large [8, 9], but out-of-sync. The reduced scaffolding leads to local over-connectivity within regions of the brain, and under-connectivity between the regions of the brain [10]. The majority of the abnormal cells and connections are within the frontal lobe, especially the dorsolateral prefrontal cortex and the medial prefrontal cortex [11], as well as the temporal lobes [12]. The cerebellum is also significantly linked to the autism spectrum [13]. There is also evidence that the amygdala and hippocampus, involved in emotional regulation and memory formation, are significantly effected in ASD [10].

There is also strong evidence for an over-active immune system in an autistic person compared to a neurotypical person, with changes demonstrated in all parts of the immune system, and the immune system in the brain as well as the rest of the body [14]. These immune changes contribute to the reduced ability of the brain to form new branches as well as develop new nerve cells or remove unnecessary cells.

There are a number of environmental and epigenetic associations linked to autism. These include disorders of folate metabolism [15, 16], pollutants [17], fever during pregnancy [18] and medications such as valproate and certain anti-depressants [19, 20] which are linked with an increase in autism[1]. Supplements such as folate [15, 21], omega-6 polyunsaturated fatty acids [22] and the use of paracetamol for fevers in pregnancy [18] have protective effects.

Although these factors are important, genes outweigh their influence by about 4:1. Twin studies suggest that between 70-90% of the risk of autism is genetic [23, 24]. Individual gene studies have only shown that each of the many single genes carry about a one percent chance each for the risk of autism [10]. It’s been proposed that the hundreds of genes linked with autism [10, 25] are not properly expressed (some are expressed too much, some not enough). The resulting proteins from the abnormal gene expression contribute to a different function of the cell’s machinery, altering the ability of a nerve cell to fully develop, and the ability of nerve cells to form connections with other nerve cells [26]. The effects are individually small, but collectively influential [24]. Autism is considered a complex genetic disorder involving rare mutations, complex gene × gene interactions, and copy number variants (CNVs) including deletions and duplications [27].

According to the Cognitive-Action Pathways model, the triad of the environment, epigenetics, and genes influence a number of processes that feed into our actions, thoughts, perceptions, personality and physiology. In ASD, the starting place is language processing.

New born babies from as young as two days old prefer listening to their own native language [28], which suggests that we are born already pre-wired for language. Auditory stimuli (sounds) are processed in the temporal lobes, including language processing. In neurotypical people, language processing is done predominantly on the left side, with some effect from the right side. But in people with autism, because of the abnormal wiring, there is only significant activity of the right temporal lobe [12]. Even more, from data so recent that it’s pending publication, loss of the processing of information of the left temporal lobe reversed the brains orientation to social and non-social sounds, like the sound of the babies name [7].

The change in the wiring of the left and right temporal lobes then alters the processing of language, specifically the social significance of language and other sounds. So already from a young age, people with autism will respond differently to environmental stimuli compared to a neurotypical person.

In the same way, the fusiform gyrus is part of the brain that processes faces. It’s quite specific to this task in a neurotypical person. However, the altered wiring of the brain in someone with autism causes a change, with different parts of the brain having to take up the load of facial processing [29].

Each time that one part of the brain can’t perform it’s normal function, the other parts take up the load. However that reduces the capacity for those parts of the brain to perform their own normal functions. In the case of the temporal lobes and the fusiform areas, this results in a reduced ability to discern subtleties especially those related to recognizing social cues. A neurotypical person and an autistic person could be standing in front of the same person, listening to the same words, and seeing the same facial expressions, but because of the way each persons brain processes the information, the perception of those words and cues can be completely different. This demonstrates how genetic changes can lead to changes in the perception of normal sensory input, resulting in differences in the physiological response, emotions, feelings, thoughts and actions, despite identical sensory input.

Physiology

The same changes that effect the cerebral cortex of the brain also have an influence on the deeper structures such as the hippocampus and the amygdala. The hippocampus is largely responsible for transforming working memory into longer term declarative memory. Studies comparing the size of the hippocampus in ASD children have shown an increase in size compared with typical developing children [30]. Combined with the deficits in the nerve cell structure of the cerebellum [13], autistic children and adults have a poor procedural memory (action learning, regulated by the cerebellum) and an overdeveloped declarative memory (for facts, regulated by the hippocampus). This has been termed the “Mnesic Imbalance Theory” [31].

The amygdala is also functionally and anatomically altered because of the changes to the nerve cells and their connections. The amygdala is larger in young children with ASD compared to typically developing children. As a result, young ASD children have higher levels of background anxiety than do neurotypical children [32]. It’s proposed that not only do ASD children have higher levels of background anxiety, they also have more difficulty in regulating their stress system, resulting in higher levels of stress compared to a neurotypical child exposed to the same stimulus [33].

Personality

On a chemical level, autism involves genes that encode for proteins involved in the transport of key neurotransmitters, serotonin and dopamine. Early evidence confirms the deficits of the serotonin and dopamine transporter systems in autism [34]. These neurotransmitters are integral to processing the signals of mood, stress and rewards within the brain, and as discussed in the last chapter, are significantly involved in the genesis of personality.

The abnormal neurotransmitter systems and the resulting deficiencies in processing stress and rewards signals contribute to a higher correlation of neuroticism and introverted personality styles in children with autism symptoms [35, 36].

So people with autism genes are going to process stress and rewards in a different way to the neurotypical population. As a result, their feelings, their thoughts and their resulting actions are tinged by the differences in personality through which all of the incoming signals are processed.

Actions

The underlying genes and neurobiology involved in autism also effect the final behavioural step, not only because genes and sensory input influence the personality and physiology undergirding our feelings and thoughts, but also because they cause physical changes to the cerebellum, the part of the brain involved in fine motor control and the integration of a number of higher level brain functions including working memory, behaviour and motivation [13, 37].

When Hans Asperger first described his cohort of ASD children, he noted that they all had a tendency to be clumsy and have poor handwriting [38]. This is a good example of how the underlying biology of ASD can effect the action stage independently of personality and physiology. The cerebellum in a person with ASD has reduced numbers of a particular cell called the Purkinje cells, effecting the output of the cerebellum and the refined co-ordination of the small muscles of the hands (amongst other things). Reduced co-ordination of the fine motor movements of the hands means that handwriting is less precise and therefore less neat.

A running joke when I talk to people is the notoriously illegible doctors handwriting. One of the doctors I used to work with had handwriting that seriously looked like someone had dipped a chicken’s toes in ink and let it scratch around for a while. My handwriting is messy – a crazy cursive-print hybrid – but at least it’s legible. I tell people that our handwriting is terrible because we spent six years at medical school having to take notes at 200 words a minute. But it might also be that the qualities that make for a good doctor tend to be found in Asperger’s Syndrome, so the medical school selection process is going to bias the sample towards ASD and the associated poor handwriting (Thankfully, those that go on to neurosurgery tend to have good hand-eye coordination).

But if your educational experience was anything like mine, handwriting was seen as one of the key performance indicators of school life. If your handwriting was poor, you were considered lazy or stupid. Even excluding the halo effect from the equation, poor handwriting means a student has to slow down to write neater but takes longer to complete the same task, or writes faster to complete the task in the allotted time but sacrificing legibility in doing so.

Either way, the neurobiology of ASD results in reduced ability to effectively communicate, leading to judgement from others and internal personal frustration, both of which feedback to the level of personality, molding future feelings, thoughts and actions.

Thought in ASD

By the time all the signals have gone through the various layers of perception, personality and physiology, they reach the conscious awareness level of our stream of thought. I hope by now that you will agree with me that thought is irrevocably dependent on all of the various levels below it in the Cognitive-Action Pathways Model. While thoughts are as unique as the individual that thinks them, the common genetic expression of ASD and the resulting patterns in personality, physiology and perception lead to some predictable patterns of thought in those sharing the same genes.

As a consequence of the differences in the signal processing, the memories that make their way to long-term storage are also going to be different. Memories and memory function are also different in ASD for other neurobiological reasons, as described earlier in the blog with the Mnesic Imbalance Theory.

Summary

The Cognitive-Action Pathways model is a way of describing the context of thoughts to other neurological processes, and how they all interact. It shows that conscious thoughts are one link of a longer chain of neurological functions between stimulus and action – simply one cog in the machine. The autistic spectrum provides a good example of how changes in genes and their expression can dramatically influence every aspect of a person’s life – how they experience the world, how they feel about those experiences, and how they think about them.

I used autism as an example because autism is a condition that’s pervasive, touching every aspect of a person’s life, and provides a good example of the extensive consequences from small genetic changes. But the same principles of the Cognitive-Action Pathways Model apply to all aspects of life, including conditions that are considered pathological, but also to our normal variations and idiosyncrasies. Small variations in the genes that code for our smell sensors or the processing of smells can change our preferences for certain foods just as much as cultural exposure. Our appreciation for music is often changed subtly between individuals because of changes in the structure of our ears or the nerves that we use to process the sounds. The genetic structure of the melanin pigment in our skin changes our interaction with our environment because of the amount of exposure to the sun we can handle.

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

References

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

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