The lost art of joy – Joy blindness

Light at the end of the tunnel …

Joy is a ubiquitous human experience, almost an innate function of the human brain.

Joy is a bit like vision for the soul.

Writing an entire months worth of blog posts on joy, then, is a little writing series of blog posts on art appreciation. The readers of a blog on art appreciation will be able to see the art, the blog helping them to better understand the art. The vast majority of people who will be reading these blogs on joy will be able to experience joy and (hopefully) the posts will help them better understand joy.

But what happens if you can’t experience joy in the first place? What about those people who have ‘joy blindness’, so to speak?

As I’ve been writing this blog every day, I’ve been mindful of those people who struggle to experience joy. For the most part, growing joy in our life is related to our actions or decisions, such as learning acceptance, aligning our direction in life with our values, forgiving ourselves and others etc. Hence why I have been exploring these concepts in my blogs thus far. But there are some people who will read these blogs and say, “But I’ve tried to do all these things, and nothing has worked. I want to experience joy like everyone else but all I have is sadness, anger, loneliness, mourning … I must be doing something wrong … it’s all my fault that I can’t experience joy … I don’t deserve to be happy.”

Remember yesterday when I talked about the work of Sonja Lyubomirsky and her colleagues who estimated that that intentional actions can contribute as much as 40% to a person’s feeling of happiness, where as circumstances could only contribute 10%? In their estimates, our genetics contributed to the other 50% of our overall happiness. Yesterday I made the comment that, even allowing for the generous estimations that were used to come to those final numbers, our actions were of much greater importance in our overall level of happiness than our circumstances.

But there was a second point to come out of the work of Lyubomirsky et al, that our happiness is related to factors beyond our control more than it is related to factors within our control.

For the vast majority of people, our genes, the biggest contributing factor to our joy, work fine. But there are some people whose genes do not work the same way, which makes them much more vulnerable to the effects of circumstances or personal actions. These are the people with major depression, who do not feel joy like the everyday person. There may be sources of joy all around them, but try as they might, they can not perceive it. They have ‘joy blindness’.

Depression is an abnormally low mood for an abnormally long time. Major depression sucks. Major depression is not just letting yourself feel miserable. So often, those without depression think that those with depression are weak, malingering, or wallowing in child-like self-pity. Despite the enormous strides in mental health education and awareness that have been made in the last couple of decades, there’s still a strong current of stigma that flows through our society, adding an additional barrier to improvement for anyone living with or recovering from depression.

Depression affects a lot of people too. About one in ten people will suffer from an episode of major depression in their lifetime.

There’s a lot of good and easily accessible information already available about depression, from organisations like Black Dog Institute or Beyond Blue. I’ve also written about depression and Christianity (Part 1 and Part 2). I don’t want to try and repeat all of that information here.

Rather, I wanted to say just a couple of things. Firstly, if you’re suffering from ‘joy blindness’ – if you long to experience joy in your life but all you feel is sadness, please don’t blame yourself or beat yourself up. It’s not your fault.

And you’re not alone. The depth of despair is so lonely, so isolating. But there are others out there who have gone what you’re going through and have come out the other side. And there are people around you to help you through – whether they’re friends, family, or professionals who can help, like your GP or a psychologist. Those suffering from depression benefit from specific counselling, or talking therapies, and occasionally those suffering from depression might need medication to assist them in their recovery.

For most people who suffer it, ’joy blindness’ isn’t permanent. It’s more like walking through a long dark tunnel rather than being trapped in a cave. If you can keep moving forward, you will eventually get through the other side. I know it’s hard, because I’ve been there myself. I know that in the middle of the tunnel, it feels like there is no end, that you’ll never experience joy again.

The key is hope. Hope keeps us moving forward. If you can keep moving forward, you will overcome the joy blindness of major depression and you will experience joy again.

Don’t lose hope, and you will experience joy again.

If you are struggling with mental illness and you need urgent assistance, please talk to someone straight away:

In Australia:
Lifeline ~ 13 11 14
BeyondBlue ~ 1300 22 4636 or https://www.beyondblue.org.au/about-us/contact-us
Suicide Callback Service ~ 1300 659 467 or https://www.suicidecallbackservice.org.au

USA:
National Suicide Prevention Lifeline ~ 1-800-273-TALK (8255)

New Zealand:
Lifeline Aotearoa 24/7 Helpline ~ 0800 543 354

UK:
Samaritans ~ 116 123

For other countries: Your Life Counts maintains a list of crisis services across a number of countries: http://www.yourlifecounts.org/need-help/crisis-lines.

Dr Caroline Leaf – Not a mental health expert

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Dr Caroline Leaf is a communication pathologist and self-titled cognitive neuroscientist.  She wrote a PhD on a learning program developed for an educational setting.  She is not a medical doctor.  She is not a psychologist.  She has no experience or training in the diagnosis and management of mental illness.  She is no more qualified to give advice on mental illness than my hairdresser is.

And it shows in her latest social media post: “Lets really start loving as a church- true unconditional non judgmental love – pushing people away and locking them up and drugging them against their will is not the solution to the the problems of life.”

Her statements is a nonsense, nothing more than a scarecrow fallacy.  Yes, pushing people away and locking them up and drugging them against their will is not the solution to the problems of life, that’s why no one does it.  If people were locked up or drugged against their will because of “the problems of life” then we’d all be locked up and drugged.

The only people that are forcibly treated are those with the most serious of mental illnesses whose condition has deprived them of the insight they need to make the decision for themselves.  Even then, the consent for treatment is given by the next of kin, and if no next of kin can provide consent, then the consent is usually made by a independent statutory body so there’s no conflict of interest.

That Dr Leaf continues to make such inane statements about mental illness confirms that she is not fit to give the church, or anyone else for that matter, any advice on mental health.  She may have a PhD in communication pathology but that is a highly specialised field that doesn’t even begin to cross over to clinical knowledge of mental illness.

Dr Leaf has chosen to fill her vacuum of mental health experience with the opinions of Mad In America, a group that’s irrationally biased against modern mental health care.  She regurgitates their creed almost verbatim – mental illness is over diagnosed, psychiatric medications are useless and dangerous, and Dr Leaf also claims that psychiatric medications are only prescribed to bring the cabal of the American Psychiatric Association and the pharmaceutical companies more power and money.

Psychiatric medications are more helpful than harmful (Leucht et al, 2012, Torniainen et al, 2015).  I’ve discussed this in blog posts in the past.  Yes, they’re not without their side effects, and they’re not for every patient, but they have their place in psychiatric care.  That Dr Leaf can’t or won’t review this evidence is just another indictment against her ministry.  That she actively promotes the idea that pharmaceutical companies and the APA are actively attempting to harm people for their own power and riches is scandalous.

If Dr Leaf was serious about promoting good mental health through the church, she should stop promoting baseless anti-psychiatric propaganda, and start encouraging Christians with mental illness to seek the best treatment available, whether that be medications or counselling or both.  She should also start teaching the church the truth about mental illness … That mental illness isn’t caused by poor choices or toxic thoughts, but because of genetic abnormalities that make the affected persons brain more vulnerable to external stress.

Because to stop turning pain and trauma into shame, anger, fear and then hate, people need correct information to allow them to offer real loving understanding and nonjudgmental support to move through the pain.  At the moment, Dr Leaf isn’t offering the church anything even close to that.

References

Leucht S, Tardy M, Komossa K, et al. Antipsychotic drugs versus placebo for relapse prevention in schizophrenia: a systematic review and meta-analysis. Lancet 2012 Jun 2;379(9831):2063-71.
Torniainen M, Mittendorfer-Rutz E, Tanskanen A, et al. Antipsychotic treatment and mortality in schizophrenia. Schizophrenia bulletin 2015 May;41(3):656-63.

Dr Caroline Leaf and the can of worms – UPDATE

Yesterday, Dr Leaf opened a proverbial can of worms with her quote from Gøtzsche, that “Psychiatric Drugs are the third leading cause of death, after heart disease and cancer.”

Dr Caroline Leaf is a communication pathologist and a cognitive neuroscientist. Clearly scrambling, she attempted to placate her growing number of detractors with an unprecedented explanatory statement. But rather than distancing herself from her comments, she still chose to portray psychiatric medications as harmful and ungodly.

Instead of quelling the fire, this seems to have thrown fuel on it. Dr Leaf has continued to try and justify her comments with a further two statements today. Neither of them contain a retraction or an apology.

Earlier today, she wrote:

Screen Shot 2015-10-19 at 7.02.14 pm

Dear all, regarding the recent two posts I put up on mental health and medications and the flood of positive and negative responses that followed, I would love you to hear my heart: all my posts are lovingly crafted, designed to help, based on my years of extensive research and experience in the field of mind, learning and mental health, including within my immediate and extended family..and {sic} most importantly, they are Holy Spirit led. I work with a team of professionals, that include medical doctors, neurosurgeons, neurologists, neuroscientists, theologians, pastors and historians in order to provide excellent information. I am a messenger: I teach and provide information and encourage you, in turn, not to be reactive, but to read, do your own research and think. To this end, I provide as much help as I can on my web page and TV shows and resources with information and research links and citations. I DO believe in using general medications and surgeries when managed correctly and not abused, I myself have been helped by surgery and used medications when necessary, as have my family. I DO NOT judge anyone. I believe in your right to choose; I DO NOT tell anyone to go off their meds, I recommend supported and supervised withdrawal if this is what you choose; I DO encourage you to make Holy Spirit led educated choices about your choices, I DO encourage you to use your love, power and sound mind – your intellect, will and emotions, the way God designed these to be used – led by Him continuously. Please watch this incredible and touching video by Laura Delano on You Tube, which highlights why I do what I do. https://m.youtube.com/watch?list=PLK_W1lA1BNLk2vbBH2XetI80LDpmaGTUG&params=OAFIAVgF&v=b6ZljUs4Xos&mode=NORMAL Many blessings to you all and my prayer for you is: “Beloved, I pray that you may prosper in every way and [that your body) may keep well, even as [I know) your soul keeps well and prospers.” 3 John 1:2 AMP see http://www.drleaf.com scientific FAQ’s for more information, citations and links

then later in the day:

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Dear all, some of you have questioned whether or not I have ever dealt with people experiencing severe mental health issues. As someone who has specialized in the mind over the past 30 years, I have been given the opportunity to work, first hand, with people experiencing mental and physical pain in the most terrible life situations, from severe traumatic brain injuries to rape, murder and abysmal poverty. I have seen these individuals choose with their minds not to allow their life circumstances to take control over their identity… through the power of God, love and community they overcame what life threw their way. But, on a more personal level, my eldest daughter (@therascalcook) was severely bulimic, suicidal and depressed for most of her early years due to a chronic illness and traumatic bullying. I have been in hospitals, crying beside her bed when she nearly died. I have experienced her pain…I am crying as I write this. But as a family we supported her and loved her through it, as did her friends and many of our loved ones, (it was not easy but it was worth it!). She never took a single medication nor was she institutionalized, even though doctors were telling me she would never recover if she didn’t. Yet today, after rejecting God and life for many years, she is a graduate student in historical theology, whose life goal is to bring a piece of heaven to earth through sustainable farming communities in disadvantaged areas. There is hope, God is greater than anything, and magic bullets are never the answer. You are not a label or a faulty biological machine. You are a child of God, as we all are. Unless all of us realize what it truly means to be the church, to bring heaven to earth as we love our God and people, to be the community of love that this world is so desperately crying out for, people will continue to have mental health issues, be labeled {sic}, face stigma and suffer. We all have this responsibility, and none of us can do it alone. We were created by God to help each other. Jessica used to call me her Sam. We all need a Sam, because we all know what it is like to be Frodo.

Kudos to Dr Leaf for the bravery and vulnerability that sharing such a personal story took. I’m genuinely happy that Jessica found her way through those dark and distressing days and has once again found peace and success. I have been through the same dank and destructive times of depression, and I know what it feels like. I wouldn’t wish it on anyone. When I hear stories of people who have overcome, I truly appreciate their joy.

I also recovered from my depression without ever using medications. What helped me enormously was a psychologist who listened to me without judgement as I unloaded years of emotional turmoil and distress. To this day, I don’t remember what we actually talked about in my first session with him. All I remember is getting ten minutes in and then crying almost uncontrollably for the next forty. Thankfully, I did more talking and less crying over the few months as my mood lifted and I grew to accept my brokenness, just like God does.

Clearly, the story of Jessica Leaf is heart-warming and uplifting. Dr Leaf clearly understands the pain and distress that severe mental illness brings to those who suffer with it, and their families. But all emotions aside, Dr Leaf has still left important issues unresolved. Indeed, those who are more cynical might see such an emotional recollection as a play for sympathy and a distraction from the lingering questions surrounding Dr Leaf’s handling of this issue, and of her expertise in mental health.

Dr Leaf’s expertise, revisited.

Dr Leaf’s experience during those darkest of times may give her a legitimate platform to discuss what worked for her daughter and her family, but however moving, it does not qualify her as an expert in mental health more broadly. Science isn’t about generalising from your personal experience. It’s about looking at the evidence from a number of rigorously designed trials with a minimum of bias, conducted across a broad range of participants.

When women come to see me in the few weeks after giving birth, they’re usually confused. Nearly every woman that’s ever given birth sometime in the last century believes their experience automatically qualifies them as experts in breast feeding and infant health. But their ‘helpful’ advice, given with the best of intentions, often conflicts with the opinion of every other self-proclaimed motherhood expert. By the time the poor new mother comes to see me, they’ve been given so many pieces of conflicting advice that they’re completely lost.

Just living through an experience doesn’t qualify you as an expert. So I don’t claim to be an expert in mental health just because I’ve lived through prolonged periods of anxiety and depression. Nor should Dr Leaf.

Dr Leaf can’t use the fact that she has worked with people who have mental health problems as a claim to expertise either. She may been given the opportunity to work, first hand, with “people experiencing mental and physical pain in the most terrible life situations, from severe traumatic brain injuries to rape, murder and abysmal poverty.” That doesn’t make her an expert in mental health any more than seeing female patients makes me a gynaecologist.

That’s because expertise in medical fields requires specific training. You can read surgical textbooks for thirty years but that doesn’t quality you as a surgeon. You can learn a bit of anatomy and physiology in the same lab as some medical students, but that doesn’t make you equivalent to a medical doctor. You might do some research involving some neurobiology, but that doesn’t make you a neuroscientist.

Dr Leaf is a communication pathologist who completed a PhD which included some educational psychology. She is not a counsellor, she is not a psychologist, she is not a medical doctor and she isn’t even a cognitive neuroscientist. Dr Leaf is not qualified to provide an expert opinion on the risks and harms of psychiatric medication.

Dr Leaf’s heart

Coming back to Dr Leaf’s first statement today, Dr Leaf said that she wanted to share her heart:

all my posts are lovingly crafted, designed to help, based on my years of extensive research and experience in the field of mind, learning and mental health, including within my immediate and extended family..and {sic} most importantly, they are Holy Spirit led

If I were Dr Leaf, I’d be careful about blaming the Holy Spirit for her posts. I have rebutted and debunked scores of Dr Leaf’s memes over the last couple of years. The Holy Spirit is the ‘Spirit of all truth’, not of half-baked facts and misquotes.

Dr Leaf goes on to say

I teach and provide information and encourage you, in turn, not to be reactive, but to read, do your own research and think. To this end, I provide as much help as I can on my web page and TV shows and resources with information and research links and citations.

I respectfully disagree. Dr Leaf rarely references her social media memes, and until recently, her website was bereft of citations. I have never seen her encourage critical thinking before. And if Dr Leaf really wanted to encourage thinking amongst her followers, then why does her team actively block people on social media who dare to disagree with her? That’s not encouraging free thinking, that’s presenting an illusion of conformity.

Dr Leaf’s Do’s and Don’ts

To clarify her position on several issues, Dr Leaf stated:

I DO believe in using general medications and surgeries when managed correctly and not abused, I myself have been helped by surgery and used medications when necessary, as have my family. I DO NOT judge anyone. I believe in your right to choose; I DO NOT tell anyone to go off their meds, I recommend supported and supervised withdrawal if this is what you choose; I DO encourage you to make Holy Spirit led educated choices about your choices, I DO encourage you to use your love, power and sound mind – your intellect, will and emotions, the way God designed these to be used – led by Him continuously.

Dr Leaf may say that she doesn’t tell anyone to go off their meds, but I think that’s a little disingenuous.

Sure, Dr Leaf never directly said to stop taking their medications. She just said that psychiatric medications were unscientific and unbiblical [1: p31-32], that psychiatric medications are the third most common cause of death after heart disease and cancer, and admonished her followers to “Take all thoughts into captivity, not drug all thoughts into captivity.” And just yesterday, she also linked psychiatric medications with evolutionary theory and said that they strip 15-25 years off your lifespan.

So it’s more like, “I DO NOT tell anyone to go off their meds, I just scare them by telling them the drugs are unholy poison”.

That’s not encouraging “Holy Spirit led educated choices”, it’s encouraging fear-driven poor choices.

Dr Leaf’s support team

One last point. Dr Leaf stated,

I work with a team of professionals, that include medical doctors, neurosurgeons, neurologists, neuroscientists, theologians, pastors and historians in order to provide excellent information.

Really? Dr Leaf’s work consistently conflicts with basic medical and psychological science, and she regularly misquotes scripture. Would they be willing to be named? Because either they’re providing Dr Leaf with terrible oversight or Dr Leaf is ignoring everything they say.

Dr Leaf still hasn’t apologised for, or retracted her statements

It’s no secret that I disagree with Dr Leaf’s teaching, and I have outlined why I think some of her statements today are disingenuous. You may agree with me, or not. I don’t mind. Hey, I could be wrong.

Though when you get down to brass tacks, the most important issue is that Dr Leaf remains legally vulnerable.

Since she opened up the can of worms with her Gøtzsche quote, she has made three separate statements, none of which apologise for potentially misleading nearly 150,000 people about the true risks and benefits of psychiatric medications. Nor has she issued any retraction or taken the posts down.

When Dr Leaf says that psychiatric medications are unbiblical and poisonous, people on psychiatric medications will want to come off them. She may not have said the words “Stop your medications”, but people will still want to come off them because they’re afraid, or because of the stigma, or because of their desire to live true to God. And as I discussed yesterday, there is a very real chance that some of those people who were stable on their medications but who unnecessarily cease them because Dr Leaf told them to, may harm themselves or take their own life, since that’s what the studies tell us [2, 3]. At the very least, they are likely to have a shorter life expectancy because of it [4, 5]. This may open Dr Leaf to law suits, as well as the possibility of having someone’s death on her conscience.

No one wants that scenario. But the only way to avoid it is to:

  1. Take the offending posts down
  2. Issue an apology
  3. Specifically direct those of her followers on psychiatric medications to stay on them until they have spoken to their doctors,
  4. In future, provide a balanced view of the benefits of psychiatric medications as well as their harms.
  5. Better yet, unless Dr Leaf gets a medical degree, it may be better not to publically discuss psychiatric medication at all.

Again, I implore Dr Leaf, for her sake and for the sake of her ministry and those who follow her, please unequivocally apologise, retract your statement, and encourage people to see their doctors if they have concerns about their medication, or their mental health.

This is not a game: people’s lives are at stake. I hope that Dr Leaf sees this before it’s too late.

References
[1]        Leaf CM. Switch On Your Brain : The Key to Peak Happiness, Thinking, and Health. Grand Rapids, Michigan: Baker Books, 2013.
[2]        Correll CU, Detraux J, De Lepeleire J, De Hert M. Effects of antipsychotics, antidepressants and mood stabilizers on risk for physical diseases in people with schizophrenia, depression and bipolar disorder. World psychiatry : official journal of the World Psychiatric Association 2015 Jun;14(2):119-36.
[3]        Tiihonen J, Suokas JT, Suvisaari JM, Haukka J, Korhonen P. Polypharmacy with antipsychotics, antidepressants, or benzodiazepines and mortality in schizophrenia. Archives of general psychiatry 2012 May;69(5):476-83.
[4]        Tiihonen J, Lonnqvist J, Wahlbeck K, et al. 11-year follow-up of mortality in patients with schizophrenia: a population-based cohort study (FIN11 study). Lancet 2009 Aug 22;374(9690):620-7.
[5]        Torniainen M, Mittendorfer-Rutz E, Tanskanen A, et al. Antipsychotic treatment and mortality in schizophrenia. Schizophrenia bulletin 2015 May;41(3):656-63.

Remember: This article is a rebuttal of Dr Leaf’s opinion regarding psychiatric medication.  This blog doesn’t constitute individual medical advice.  If you do not like your medication or think you should come off it, please talk to your own GP or psychiatrist.  Do not stop it abruptly or without adequate medical advice.

Don’t stress about stress – Part 3: Coping

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

  1. Wu, G., et al., Understanding resilience. Front Behav Neurosci, 2013. 7: 10 doi: 10.3389/fnbeh.2013.00010
  2. 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
  3. 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
  4. 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
  5. 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
  6. 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
  7. 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
  8. 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
  9. 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
  10. Felten, A., et al., Genetically determined dopamine availability predicts disposition for depression. Brain Behav, 2011. 1(2): 109-18 doi: 10.1002/brb3.20
  11. 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
  12. Russo, S.J., et al., Neurobiology of resilience. Nature neuroscience, 2012. 15(11): 1475-84
  13. 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

Putting thought in the right place, part 2

CAP v2.1.2

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

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

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

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

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

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

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

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

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

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

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

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

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

Physiology

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

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

Personality

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

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

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

Actions

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

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

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

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

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

Thought in ASD

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

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

Summary

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

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

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

References

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

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

Dr Caroline Leaf and the shotgun approach

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“It has been collectively demonstrated by researchers around the world that just about every aspect of our brainpower, intelligence and control – in normal, and psychiatrically and neurologically impaired individuals – can be improved by intense, efficient, organised and appropriately direct mind training … thank you Jesus.”

Sounds impressive doesn’t it.

Unfortunately for Dr Caroline Leaf, communication pathologist and self-titled cognitive neuroscientist, grandstanding does not equate to authority.  It’s all very well and good to publish broad, sweeping generalisations, but it’s like firing a shotgun at a cork from thirty paces.  Sure, you might hit your target, but the scatter pattern of the ammunition misses more times than it hits.

If Dr Leaf wants her statement to be taken seriously, then she needs to do a couple of small things.
(1) Reference her statement.  This should be fairly easy if “researchers around the world” really have demonstrated the power of mind training.  To sum it up more effectively, perhaps Dr Leaf could cite a meta-analysis that proves the value of mind training.
(2) Stop confusing the mind with the brain. This is the biggest problem with her statement. The mind does not control the brain.  If Dr Leaf produced any references in support of her statement, they would be along the lines of training or retraining the brain, not the mind.

It may seem trivial, because most people think the mind and the brain are the same, but they’re two distinct things.  Old psychological therapies were based upon the notion that fixing your thoughts was the key to improving your mental health, but this notion is now outdated, considered part of “Western folk psychology” [1]. By using the concept of “mind” and “brain” interchangeably, Dr Leaf confuses the issue for the average person trying to come to grips with modern science.

I’d be grateful if Dr Leaf could publish some evidence to support her claim, because I’m unfamiliar with research showing that things like intelligence can be improved with brain training. Sure, there’s good evidence for the improvement in the damaged brain with specific physical exercises – it’s one of the primary tools in Rehabilitation Medicine. There is also good evidence for psychological therapies such as ACT, or Acceptance and Commitment Therapy, in improving mood amongst other things [2, 3]. Though I’ve read a recent meta-analysis of multiple studies that suggests “brain training” for working memory offers minimal benefit which is not maintained and not transferable across categories [4], which means there’s no proof that “brain training” improves intelligence.

In future posts, I hope that Dr Leaf provides something more accurate instead of grandiose shotgun statements.

References

  1. Herbert, J.D. and Forman, E.M., The Evolution of Cognitive Behavior Therapy: The Rise of Psychological Acceptance and Mindfulness, in Acceptance and Mindfulness in Cognitive Behavior Therapy. 2011, John Wiley & Sons, Inc. p. 1-25.
  2. Harris, R., Embracing Your Demons: an Overview of Acceptance and Commitment Therapy. Psychotherapy In Australia, 2006. 12(6): 1-8 http://www.actmindfully.com.au/upimages/Dr_Russ_Harris_-_A_Non-technical_Overview_of_ACT.pdf
  3. Harris, R., The happiness trap : how to stop struggling and start living. 2008, Trumpeter, Boston:
  4. Melby-Lervag, M. and Hulme, C., Is working memory training effective? A meta-analytic review. Dev Psychol, 2013. 49(2): 270-91 doi: 10.1037/a0028228

 

Dr Caroline Leaf – Exacerbating the Stigma of Mental Illness

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It was late in the afternoon, you know, that time when the caffeine level has hit critical and the only way you can concentrate on the rest of the day is the promise you’ll be going home soon.

The person sitting in front of me was a new patient, a professional young woman in her late 20’s, of Pakistani descent. She wasn’t keen to discuss her problems, but she didn’t know what else to do. After talking to her for a few minutes, it was fairly obvious that she was suffering from Generalised Anxiety Disorder, and I literally mean suffering. She was always fearful but without any reason to be so. She couldn’t eat, she couldn’t sleep, her heart raced all the time.

I was actually really worried for her. She let me do some basic tests to rule out any physical cause that was contributing to her symptoms, but that was as far as she let me help her. Despite talking at length about her diagnosis, she could not accept the fact that she had a psychiatric condition, and did not accept any treatment for it. She chose not to follow up with me either. I only saw her twice.

Perhaps it was fear for her job, social isolation, or a cultural factor. Perhaps it was the anxiety itself. Whatever the reason, despite having severe ongoing symptoms, she could not accept that she was mentally ill. She was a victim twice over, suffering from both mental illness, and its stigma.

Unfortunately, this young lady is not an isolated case. Stigma follows mental illness like a shadow, an extra layer of unnecessary suffering, delaying proper diagnosis and treatment of diseases that respond best to early intervention.

What contributes to the stigma of mental illness? Fundamentally, the stigma of mental illness is based on ignorance. Ignorance breeds stereotypes, stereotypes give rise to prejudice, and prejudice results in discrimination. This ignorance usually takes three main forms; people with mental illness are homicidal maniacs who need to be feared; they have childlike perceptions of the world that should be marveled; or they are responsible for their illness because they have weak character [1].

Poor information from people who claim to be experts doesn’t help either. For example, on her social media feed today, Dr Caroline Leaf said, “Psychiatric labels lock people into mental ill-health; recognizing the mind can lead us into trouble and that our mind is powerful enough to lead us out frees us! 2 Timothy1:7 Teaching on mental health @TrinaEJenkins 1st Baptist Glenardin.”

Dr Caroline Leaf is a communication pathologist and self-titled cognitive neuroscientist. It’s disturbing enough that Dr Leaf, who did not train in cognitive neuroscience, medicine or psychology, can stand up in front of people and lecture as an “expert” in mental health. It’s even more disturbing when her views on mental health are antiquated and inane.

Today’s post, for example. Suggesting that psychiatric labels lock people in to mental ill-health is like saying that a medical diagnosis locks them into physical ill-health. It’s a nonsense. Does diagnosing someone with cancer lock them into cancer? It’s the opposite, isn’t it? Once the correct diagnosis is made, a person with cancer can receive the correct treatment. Failing to label the symptoms correctly simply allows the disease to continue unabated.

Mental illness is no different. A correct label opens the door to the correct treatment. Avoiding a label only results in an untreated illness, and more unnecessary suffering.

Dr Leaf’s suggestion that psychiatric labels lock people in to their illness is born out of a misguided belief about the power of words over our thoughts and our health in general, an echo of the pseudo-science of neuro-linguistic programming.

The second part of her post, that “recognizing the mind can lead us into trouble and that our mind is powerful enough to lead us out frees us” is also baseless. Her assumptions, that thought is the main driving force that controls our lives, and that fixing our thought patterns fixes our physical and psychological health, are fundamental to all of her teaching. I won’t go into it again here, but further information on how Dr Leaf’s theory of toxic thinking contradicts basic neuroscience can be found in a number of my blogs, and in the second half of my book [2].

I’ve also written on 2 Timothy 1:7 before, another of Dr Leaf’s favourite scriptures, a verse whose meaning has nothing to do with mental health, but seized upon by Dr Leaf because one English translation of the original Greek uses the words “a sound mind”.

So Dr Leaf believes that labelling someone as having a mental illness will lock them into that illness, an outdated, unscientific and purely illogical notion that is only going to increase the stigma of mental illness. If I were @TrinaEJenkins and the good parishioners of 1st Baptist Glenardin, I would be asking for my money back.

With due respect, and in all seriousness, the stigma of mental illness is already disproportionate. Mental illness can cause insurmountable suffering, and sometimes death, to those who are afflicted by it. The Christian church does not need misinformation compounding the suffering for those affected by poor mental health. Dr Leaf should not be lecturing anyone on mental health until she has been properly credentialed.

References

  1. Corrigan, P.W. and Watson, A.C., Understanding the impact of stigma on people with mental illness. World Psychiatry, 2002. 1(1): 16-20 http://www.ncbi.nlm.nih.gov/pubmed/16946807
  2. Pitt, C.E., Hold That Thought: Reappraising the work of Dr Caroline Leaf, 2014 Pitt Medical Trust, Brisbane, Australia, URL http://www.smashwords.com/books/view/466848

Hold That Thought – Reappraising the work of Dr Caroline Leaf

Hold That Thought Cover

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

REFERENCES

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

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

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

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

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

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

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

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

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

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

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

 

Dr Caroline Leaf – Contradicted by the latest research

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

* * * * *

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

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

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

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

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

Dear Mr Leaf,

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

ON INFORMED DECISIONS

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

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

YOUR DEFENCE

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

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

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

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

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

DR LEAF’S EVIDENCE

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

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

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

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

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

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

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

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

EVIDENCE CONTRADICTING DR LEAF

Influence Of Thought On Health

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

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

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

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

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

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

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

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

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

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

Atrial Natriuretic Peptide

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

The Heart As A Mini-Brain

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

Hard-Wired For Optimism

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

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

The Mind-Brain Link

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

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

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

FURTHER CLARIFICATION

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

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

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

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

Dr C. Edward Pitt

REFERENCES

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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