Category Archives: Psychological

Dr Caroline Leaf and the 98 Percent Myth

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Dr Caroline Leaf believes that nearly all our diseases come from our thoughts.

Dr Caroline Leaf believes that nearly all our diseases come from our thoughts.

In the hustle and bustle of daily life, most people wouldn’t stop to consider what makes people sick.  In my profession, I get a front row seat.

In the average week, I get to see a number of different things.  Mostly “coughs, colds and sore holes” as the saying goes, although there are some rarer things too.  And sometimes, people present with problems that aren’t for the faint of heart (or stomach – beware of nail guns is all I can say).

Normally, the statistics of who comes in with what doesn’t make it beyond the desk of the academic or health bureaucrat.  The numbers aren’t as important as the people they represent.

But to Dr Caroline Leaf, Communication Pathologist and self-titled Cognitive Neuroscientist, the numbers are all important.  To support her theory of toxic thoughts, Dr Leaf has stated that “75 to 98% of mental and physical (and behavioural) illness comes from one’s thought life” [1: p37-38].  She has repeated that statement on her website, on Facebook, and at seminars.

As someone with a front row seat to the illnesses people have, I found such a statement perplexing.  In the average week, I don’t see anywhere near that number.  In general practices around Australia, the number of presentations for psychological illnesses is only about eight percent [2].

But Australian general practice is a small portion of medicine compared to the world’s total health burden.  Perhaps the global picture might be different?  The World Health Organization, the global authority on global health, published statistics in November 2013 on the global DALY statistics [3] (a DALY is a Disability Adjusted Life Year).  According to the WHO, all Mental and Behavioural Disorders accounted for only 7.2% of the global disease burden.

You don’t need a statistics degree to know that seven percent is a long way from seventy-five percent (and even further from 98%).

Perhaps a large portion of the other ninety-three percent of disease that was classified as physical disease was really caused by toxic thoughts?  Is that possible?  In short: No.

When considered in the global and historical context, the vast majority of illness is related to preventable diseases that are so rare in the modern western world because of generations of high quality public health and medical care.

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.” [4] 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.” [5] 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.” [6]

Diarrhoeal disease in the developing world – the second most common contributor to disease in these countries, afflicting half of their population – has nothing to do with thought.  It’s related to the provision of toilets and clean running water.

We live in a society that prevents half of our illnesses because of internal plumbing.  Thoughts seem to significantly contribute to disease because most of our potential illness is prevented by our clean water and sewerage systems.  Remove those factors and thought would no longer appear to be so significant.

In the same manner, modern medicine has become so good at preventing diseases that thought may seem to be a major contributor, when in actual fact, most of the work in keeping us all alive has nothing to do with our own thought processes.  Like sanitation and clean water, the population wide practices of vaccination, and health screening such as pap smears, have also significantly reduced the impact of preventable disease.

Around the world, “Recent estimates of the global incidence of disease suggest that communicable diseases account for approximately 19% of global deaths” and that “2.5 million deaths of children annually (are) from vaccine-preventable diseases.” [7] Again, that’s a lot of deaths that are not related to thought life.

Since 1932, vaccinations in Australia have reduced the death rate from vaccine-preventable diseases by 99% [8].  Epidemiological evidence shows that when vaccine rates increase, sickness from communicable diseases decrease [9: Fig 2, p52 & Fig 8, p67].

Population based screening has also lead to a reduction in disease and death, especially in the case of population screening by pap smears for cervical cancer.  Canadian public health has some of the best historical figures on pap smear screening and cervical cancer. In Canada, as the population rate of pap smear screening increased, the death rate of women from cervical cancer decreased.  Overall, pap smear screening decreased the death rate from cervical cancer by 83%, from a peak of 13.5/100,000 in 1952 to only 2.2/100,000 in 2006, despite an increase in the population and at-risk behaviours for HPV infection (the major risk factor for cervical cancer) [10].

And around the world, the other major cause of preventable death is death in childbirth.  The risk of a woman dying in childbirth is a staggering one in six for countries like Afghanistan [11] which is the same as your odds playing Russian Roulette.  That’s compared to a maternal death rate of one in 30,000 in countries like Sweden.  The marked disparity is not related to the thought life of Afghani women in labour.  Countries that have a low maternal death rate all have professional midwifery care at birth.  Further improvements occur because of better access to hospital care, use of antibiotics, better surgical techniques, and universal access to the health system [11].  Again, unless one’s thought life directly changes the odds of a midwife appearing to help you deliver your baby, toxic thoughts are irrelevant as a cause of illness and death.

Unfortunately for Dr Leaf, her statement that “75 to 98 percent of mental, physical and behavioural illnesses come from toxic thoughts” is a myth, a gross exaggeration of the association of stress and illness.

In the global and historical context of human health, the majority of illness is caused by infectious disease, driven by a lack of infrastructure, public health programs and nursing and medical care.  To us in the wealthy, resource-rich western world, it may seem that our thought life has a significant effect on our health.  That’s only because we have midwives, hospitals, public health programs and internal plumbing, which stop the majority of death and disease before they have a chance to start.

Don’t worry about toxic thoughts.  Just be grateful for midwives and toilets.

References

1.         Leaf, C.M., Switch On Your Brain : The Key to Peak Happiness, Thinking, and Health. 2013, Baker Books, Grand Rapids, Michigan:

2.         FMRC. Public BEACH data. 2010  [cited 16JUL13]; Available from: <http://sydney.edu.au/medicine/fmrc/beach/data-reports/public%3E.

3.         World Health Organization, GLOBAL HEALTH ESTIMATES SUMMARY TABLES: DALYs by cause, age and sex, GHE_DALY_Global_2000_2011.xls, Editor 2013, World Health Organization,: Geneva, Switzerland.

4.         Mara, D., et al., Sanitation and health. PLoS Med, 2010. 7(11): e1000363 doi: 10.1371/journal.pmed.1000363

5.         Bartram, J. and Cairncross, S., Hygiene, sanitation, and water: forgotten foundations of health. PLoS Med, 2010. 7(11): e1000367 doi: 10.1371/journal.pmed.1000367

6.         Hunter, P.R., et al., Water supply and health. PLoS Med, 2010. 7(11): e1000361 doi: 10.1371/journal.pmed.1000361

7.         De Cock, K.M., et al., The new global health. Emerg Infect Dis, 2013. 19(8): 1192-7 doi: 10.3201/eid1908.130121

8.         Burgess, M., Immunisation: A public health success. NSW Public Health Bulletin, 2003. 14(1-2): 1-5

9.         Immunise Australia, Myths and Realities. Responding to arguments against vaccination, A guide for providers. 5th ed. 2013, Commonwealth of Australia, Department of Health and Ageing, Canberra:

10.       Dickinson, J.A., et al., Reduced cervical cancer incidence and mortality in Canada: national data from 1932 to 2006. BMC Public Health, 2012. 12: 992 doi: 10.1186/1471-2458-12-992

11.       Ronsmans, C., et al., Maternal mortality: who, when, where, and why. Lancet, 2006. 368(9542): 1189-200 doi: 10.1016/S0140-6736(06)69380-X

Bad choices cause brain damage?

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“To err is human; to forgive, divine.”  Alexander Pope.

I’m not perfect.  At least, not the last time I checked.  And we’re all the same, aren’t we.  We all know through experience that we all stuff things up on a fairly regular basis.  We make bad choices.  We’re human!

Dr Caroline Leaf, Communication Pathologist and self-titled Cognitive Neuroscientist, believes that these bad choices literally cause brain damage.  Her fundamental assumption is that our thoughts control our brain [1: p33].  These thoughts can be healthy or they can be toxic.  Toxic thoughts “are thoughts that trigger negative and anxious emotions, which produce biochemicals that cause the body stress.” [2: p19]

Dr Leaf’s assumption is that thoughts and bad choices cause our brain cells to shrivel or die. “Once your body is truly in stress mode and the cortisol is flowing, dendrites start shrinking and even ‘falling off’” [2: p32].  She also says that, “We have two choices, we can let our thoughts become toxic and poisonous or we can detox our negative thoughts which will improve our emotional wholeness and even recover our physical health.” [2: p21]

It sounds a little extreme.  We all make bad choices, and we all experience stress.  When we’re stressed, do our memories really go missing, or the dendrites of nerve cells shake and fall like tree branches in a storm?  If we make a bad choice, do we really get brain damage?  Lets see what the scientific literature has to say.

Imagine walking along a path in a forest and you see a snake, only inches in front of you on the path.  What do you do? When faced with a high level of acute stress, the brain switches into a binary mode – fight/flight or freeze. Self-preservation has to kick in.  The only decision you have to make then and there is whether to run, to try and kill the snake before it kills you, or stop dead still and hope that the snake ignores you and slithers away.

At that point, most memory is redundant, as is a high-level analysis of snake species, or any other cognitive pursuit.  The brain doesn’t need them at that precise moment.  If they did engage, they would just get in the way.  Switching the thinking parts of your brain off focuses your attention on the immediate danger.  It’s an adaptive survival response.  Meantime, your memories and your theoretical knowledge about snakes don’t disappear.  They are still there, unchanged.  It is false to suggest that the memories “shrink”.

We’ve all experienced “mental block”.  Sometimes when we get into a situation, like an exam or a business meeting, our stress levels are high, and binary mode kicks in again, although this time it can be a hindrance.  This phenomenon of mental block under high stress was first proposed in 1908 and is currently known as the Yerkes-Dodson Law, a fundamental principle of the behavioural sciences [3].  Similar to the stress-productivity curve, Yerkes and Dodson proposed a U-shaped curve to represent the relationship between arousal (which could be either level of consciousness or stress) and behavioural performance.  At low arousal, there is poor performance.  At the mid-point of arousal, there is peak performance, and at high arousal, performance diminishes.

But again, our memories don’t shrink, and our nerve cell branches don’t fall off.  Once we reduce our level of arousal, we move away from the fight/flight/freeze mode, and everything is still there (and we perform better, according to Yerkes-Dodson).

Dr Leaf has a favourite analogy of “neurons as trees”.  And if neurons are trees, then the branches can “fall off”.  But neurons are not trees and dendrites are not tree branches.  The dendrites do not ‘fall off’ the neuron.  The neurons in the brain have mechanisms for ongoing brain plasticity – the ability of the brain to adapt to the challenges and changes in its internal and external environment that are constantly occurring.  If the brain needs to build a new circuit to encode a new piece of information, then it grows new dendrites and creates new synapses.  But the brain is limited by the amount of energy it can consume, and therefore the number of synapses it can maintain.  So the brain trims unnecessary dendrites, a process called “synaptic pruning”.

Synaptic pruning is a normal process. Chechik and Meilijson confirm that, “Human and animal studies show that mammalian brains undergoes massive synaptic pruning during childhood, removing about half of the synapses until puberty.” [4]

Synaptic pruning is not deleterious, but beneficial.  Chechik and Meilijson also note that, “synaptic overgrowth followed by judicial pruning along development improves the performance of an associative memory network with limited synaptic resources.” [4] So synaptic pruning is a normal physiological process, and occurs in all of us for many reasons, predominantly to improve the efficiency of our neural networks.  Perhaps synaptic pruning associated with the stress response is also an adaptive process?

Synaptic pruning also occurs in other physiological states that have nothing to do with stress or thought, such as the effects of oestrogen during the menstrual cycle and at menopause [5, 6].

A link between stress and dendrite loss has been discovered, but it is not consistent.  Some authors like Kopp and Rethelyi suggest that “severe stress for a prolonged period causes damage in hippocampal pyramidal neurons, especially in the CA3 and CA4 region and reductions in the length and arborization of their dendrites.” [7] However, Chen et al writes, “Whereas hippocampus-mediated memory deficits commonly were associated with—and perhaps result from—loss of synapse-bearing dendrites and dendritic spines, this association has not been universal so that the structure–function relationship underlying the effects of stress on hippocampal neurons has not been resolved.” [8]

It’s more accurate to think that chronic stress causes dendritic remodeling in animals [9], in which some nerve cells prune their synapses, which others grow them, and energy is diverted away from new nerve cell formation to the new synapses that are needed to cope with the stress.

A number of scientists have pointed out that patients with depression or anxiety, who normally have high levels of stress, have a smaller hippocampus and larger amygdala, so stress and depression must cause the smaller brain regions [9].  There may be some reduction in the number of synapses within the hippocampus and the frontal lobes of the brain, which may account for the change in size observed by a number of researchers.  But the modern thinking on these changes is that they are associated with depression, not caused by depression [10] (Correlation does not equal causation).

So, stress is associated with depression, but this is because genetic defects in one or multiple genes reduce the ability for the brain cells to produce synaptic branches.  It’s this decrease in the number of synapses that contributes to the typical changes in the brain seen at autopsy of patients who suffered from depression or anxiety [11].  The reduced ability of the nerve cells to grow synapses means that new branches can’t grow fast enough to process the stress signals properly [11, 12].  The poor signal transmission leads to a predisposition towards mood disorders like anxiety and depression [10, 11, 13-15], and less synaptic branches means both a smaller volume of the hippocampus, and an inability to process stress signals leads to a larger, overactive amygdala.

In summary, synaptic pruning is not due to toxic thinking or bad choices, unless every one of us engages in nothing but toxic thinking from early childhood to puberty, and menopause causes bad choices and toxic thoughts.  Stress doesn’t cause dendrites to fall off, but causes a reorganization of the dendrites to adapt to the new signals. The reduced capacity to form new dendrites makes those prone to mood disorders more vulnerable to stress, and depression or anxiety is the end result.

We are all bound to make bad choices and to have stress.  They don’t cause brain damage.  Which if you’re not perfect like me, is good news.

References

1.         Leaf, C.M., Switch On Your Brain : The Key to Peak Happiness, Thinking, and Health. 2013, Baker Books, Grand Rapids, Michigan

2.         Leaf, C., Who Switched Off My Brain? Controlling toxic thoughts and emotions. 2nd ed. 2009, Inprov, Ltd, Southlake, TX, USA:

3.         Cohen, R.A., Yerkes–Dodson Law, in Encyclopedia of Clinical Neuropsychology, Kreutzer, J.S., et al., Editors. 2011, Springer Science+Business Media LLC: New York ; London. p. 2737-8.

4.         Chechik, G., et al., Neuronal regulation: A mechanism for synaptic pruning during brain maturation. Neural Comput, 1999. 11(8): 2061-80  http://www.ncbi.nlm.nih.gov/pubmed/10578044

5.         Chen, J.R., et al., Gonadal hormones modulate the dendritic spine densities of primary cortical pyramidal neurons in adult female rat. Cereb Cortex, 2009. 19(11): 2719-27 doi: 10.1093/cercor/bhp048

6.         Dumitriu, D., et al., Estrogen and the aging brain: an elixir for the weary cortical network. Ann N Y Acad Sci, 2010. 1204: 104-12 doi: 10.1111/j.1749-6632.2010.05529.x

7.         Kopp, M.S. and Rethelyi, J., Where psychology meets physiology: chronic stress and premature mortality–the Central-Eastern European health paradox. Brain Res Bull, 2004. 62(5): 351-67 doi: 10.1016/j.brainresbull.2003.12.001

8.         Chen, Y., et al., Correlated memory defects and hippocampal dendritic spine loss after acute stress involve corticotropin-releasing hormone signaling. Proc Natl Acad Sci U S A, 2010. 107(29): 13123-8 doi: 10.1073/pnas.1003825107

9.         Karatsoreos, I.N. and McEwen, B.S., Psychobiological allostasis: resistance, resilience and vulnerability. Trends Cogn Sci, 2011. 15(12): 576-84 doi: 10.1016/j.tics.2011.10.005

10.       Palazidou, E., The neurobiology of depression. Br Med Bull, 2012. 101: 127-45 doi: 10.1093/bmb/lds004

11.       Karatsoreos, I.N. and McEwen, B.S., Resilience and vulnerability: a neurobiological perspective. F1000Prime Rep, 2013. 5: 13 doi: 10.12703/P5-13

12.       Russo, S.J., et al., Neurobiology of resilience. Nature neuroscience, 2012. 15(11): 1475-84

13.       Felten, A., et al., Genetically determined dopamine availability predicts disposition for depression. Brain Behav, 2011. 1(2): 109-18 doi: 10.1002/brb3.20

14.       Bradley, R.G., et al., Influence of child abuse on adult depression: moderation by the corticotropin-releasing hormone receptor gene. Arch Gen Psychiatry, 2008. 65(2): 190-200 doi: 10.1001/archgenpsychiatry.2007.26

15.       Hauger, R.L., et al., Role of CRF receptor signaling in stress vulnerability, anxiety, and depression. Ann N Y Acad Sci, 2009. 1179: 120-43 doi: 10.1111/j.1749-6632.2009.05011.x

Dr Caroline Leaf and the myth of optimism bias

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“What are little girls are made of?  Sugar and spice, and all things nice.”

It sounds sweet doesn’t it?  We like to connect with these rosy little memes that warm our cockles and make us feel good about the world and ourselves.  We think of all of the examples in our own experience, which seems to confirm the saying.  We may think of a few examples that don’t quite fit, but they’re just the exception that proves the rule.

It doesn’t seem to matter what the saying or proverb is, we usually just assume it’s true.  Think of some other examples:
“Blondes have more fun.”
“Women can’t read maps.”
“White guys can’t dance.”

In all of these things, we tend to experience what psychologists call confirmation bias (Princeton University, 2014), our own mini-delusion in which we fool ourselves into believing a half-truth.  It looks right on first glance, and we can easily think of a few confirming examples, so without deeper inspection, we assume it must be true.

When Dr Leaf proclaims that,

“Science shows we are wired for love with a natural optimism bias”

the same process kicks in.  But in truth, science doesn’t show anything of the sort.  What science shows is that we learn love and fear, and our genetics influences the way we see the world, our personality.

We are prewired to LEARN to love and fear.  It doesn’t come naturally.  We require exposure to both love and to fear for these emotions to develop.  The Bucharest Early Intervention Project is a study looking at the long-term psychological and physical health of children in Bucharest, one group who remained in an orphanage, and the other, a group of children that were eventually adopted.  Analysis of the cohort of the two groups of children showed that negative affect was the same for both groups.  However positive affect and emotional reactivity was significantly reduced in the institutionalised children (Bos et al., 2011).  This shows that children who lived in an institution all of their lives and given limited emotional stimulation had lower levels of positive affect (ie: love, happiness) compared to a child that was adopted.

The children in the institution did not have high positive affect because they were not shown love.  Those children who were adopted were higher on positive affect because they were shown love by their adopted parents.  Both groups were exposed to distress and fear during their time in the orphanage, so their negative affect was the same across both groups.  Thus, love and fear don’t come naturally.  They need to be learned.

Personality is “the combination of characteristics or qualities that form an individuals distinctive character.” (“Oxford Dictionary of English – 3rd Edition,” 2010) As Professor Greg Henriques wrote in psychology today, “Personality traits are longstanding patterns of thoughts, feelings, and actions which tend to stabilize in adulthood and remain relatively fixed. There are five broad trait domains, one of which is labeled Neuroticism, and it generally corresponds to the sensitivity of the negative affect system, where a person high in Neuroticism is someone who is a worrier, easily upset, often down or irritable, and demonstrates high emotional reactivity to stress.” (Henriques, 2012) Personality is heavily influenced by genetics, with up to 60% of our personality pre-determined by our genes (Vinkhuyzen et al., 2012), expressed through the function of the serotonin and dopamine transporter systems in our brain (Caspi, Hariri, Holmes, Uher, & Moffitt, 2010; Chen et al., 2011; Felten, Montag, Markett, Walter, & Reuter, 2011).

So some people *ARE* natural optimists – their genetic heritage blessed them with a rosy outlook and their early life experiences cemented it in.  These naturally optimistic people, and the people who know them, are the ones who take Dr Leaf’s word as truth because they see it in themselves or their friends.  But the fact that some people are naturally wired for pessimism or a neurotic personality disproves Dr Leaf’s assertion.

Its important that Dr Leaf’s misleading meme is seen for what it is.  If we assume that we’re all pre-wired for love and optimism, then those who are pessimistic must be deficient or deviant, and the fact they can’t change must mean they are incompetent or lazy.  If we know the truth, those who are less optimistic won’t be unnecessarily judged or marginalised.

I should point out that what I’ve said isn’t a free licence to be cranky or sullen all the time.  The natural pessimist still needs to be able to negotiate their way through life, and being a misery-guts makes it hard to get what you need from other people in any business, social or interpersonal relationship.  We have the ability to learn, and the person with a neurotic personality can still learn ways of dealing with people in a positive way.

But if you naturally see the glass half-empty, don’t tell yourself that you’re abnormal, or that you aren’t good enough.  You are who you are.  Accept who you are, because while there are weaknesses inherent to having neurotic personality traits, there are also strengths, such as the enhanced awareness of deception, or protection from gullibility (Forgas & East, 2008).

A good thing to have when searching for the truth.

 References

Bos, K., Zeanah, C. H., Fox, N. A., Drury, S. S., McLaughlin, K. A., & Nelson, C. A. (2011). Psychiatric outcomes in young children with a history of institutionalization. Harv Rev Psychiatry, 19(1), 15-24. doi: 10.3109/10673229.2011.549773

Caspi, A., Hariri, A. R., Holmes, A., Uher, R., & Moffitt, T. E. (2010). Genetic sensitivity to the environment: the case of the serotonin transporter gene and its implications for studying complex diseases and traits. Am J Psychiatry, 167(5), 509-527. doi: 10.1176/appi.ajp.2010.09101452

Chen, C., Chen, C., Moyzis, R., Stern, H., He, Q., Li, H., . . . Dong, Q. (2011). Contributions of dopamine-related genes and environmental factors to highly sensitive personality: a multi-step neuronal system-level approach. PLoS One, 6(7), e21636. doi: 10.1371/journal.pone.0021636

Felten, A., Montag, C., Markett, S., Walter, N. T., & Reuter, M. (2011). Genetically determined dopamine availability predicts disposition for depression. Brain Behav, 1(2), 109-118. doi: 10.1002/brb3.20

Forgas, J. P., & East, R. (2008). On being happy and gullible: Mood effects on skepticism and the detection of deception. Journal of Experimental Social Psychology, 44, 1362-1367.

Henriques, G. (2012). (When) Are You Neurotic?  Retrieved from http://www.psychologytoday.com/blog/theory-knowledge/201211/when-are-you-neurotic

Oxford Dictionary of English – 3rd Edition. (2010)   (3rd edition ed.). Oxford, UK: Oxford University Press.

Princeton University. (2014). Confirmation bias.   Retrieved January 10, 2014, from http://www.princeton.edu/~achaney/tmve/wiki100k/docs/Confirmation_bias.html

Vinkhuyzen, A. A., Pedersen, N. L., Yang, J., Lee, S. H., Magnusson, P. K., Iacono, W. G., . . . Wray, N. R. (2012). Common SNPs explain some of the variation in the personality dimensions of neuroticism and extraversion. Transl Psychiatry, 2, e102. doi: 10.1038/tp.2012.27

My patient, Kev

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I meet a lot of people in my job. Some are not particularly memorable, and some I truly wish to forget. But every now and then, I meet a person who’s memorable for all the right reasons. Kev was one of those people.

Once upon a time, Kev was a business man, a corporate manager who started in the postal service in his late teens, but got more experience and moved into the Commonwealth Bank, where he quickly moved through their ranks and became a regional manager. Towards the end of his career, he moved industries to become the CEO of one of the smaller private hospitals in Brisbane in the 1980’s.

After he retired, his wife developed dementia, and he cared for her at home for many years, before he became too weak. They both moved into a nursing home, but his wife succumbed a couple of years later.

When I met Kev in early 2013, he was dying. His heart and his lungs were failing, and he couldn’t walk ten metres without gasping or needing oxygen. He was gaunt and frail, and extremely thin. I was worried that if he fell, he might snap.

But his intellect remained untouched by the disease ravaging the rest of his body. He was quick-witted, jovial, and always polite. He was the consummate professional – always showing respect, and earning it. I could see why he was so good as a businessman. He was a pleasure to be around – so much so that I spent extra time with him every week just chatting, when I should have been finishing off my work.

In the week before he died, the last time I saw him, as I sat in his room listening to some more of his stories, he looked me in the eye and said,

“Don’t sweat the small stuff. You don’t have to do everything. Let people flow in the things they can do. There are more important things in life.”

He smiled as he looked at the photos on his wall of his wife and kids.

I smiled and shook his hand. “I’ll see you later, Kev”, I said. I never did see him again.

I still remember him now, skinny and breathless, but with a big smile on his face and a sparkle in his eyes every time I entered his room. And I remember his advice on living a life driven by values.

New Years Day is a time to start afresh, a celebration of new beginnings, a focal point to take stock and refocus. But if we’ve learnt anything at all from our previous attempts at New Years resolutions, it is that they don’t work. Don’t be mislead by the occasional partial successes. I sometimes hit a golf ball straight, but that still doesn’t mean my golf swing is any good. New Years resolutions are the same – they are fundamentally flawed, in spite of the accidental successes that we sometimes have.

The truth is that etherial statements, or short term goals for self-improvement don’t help us. We don’t need New Years resolutions, we need New Years re-evaluations.

Values are different to goals. A goal is like a destination, where as a value is like a direction. Our individual values are like the direction of the breeze. It’s easier to sail with the breeze of our values than against it.

We often get goals and values confused. Goal orientation means that we move from place to place, sometimes travelling in the same direction as our values, but sometimes against them. When we live according to our values, the goals seem to set themselves as we live according to what we truly believe in, what truly motivates us.

A few things can acts as guides to help us learn what our values are. What are your passions or what makes you mad? Is it justice, or injustice? Is it relationships? Is it children, or family? The environment? What is it that gets your juices flowing?

Another way of understanding your values is to do the eulogy exercise. It’s a little morbid, perhaps. But simply, the eulogy exercise involves writing your own eulogy. What is it that you want others to remember you for? What do you want your epitaph to say?

The eulogy exercise helps us to plan our lives with the end in mind. When you’re on your death bed, will you regret not finishing that report, or will you regret whether you lived according to your values, your deepest desires. Putting your values into perspective makes it much easier to let things go that aren’t truly important. It’s a lesson I’m continually working at too.

May 2014, and the rest of your life, be about the important things. Don’t sweat the small stuff.

I hope you have a happy new year.

Cheers, Kev.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

REFERENCES

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

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

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

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

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

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

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

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

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

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

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

 

Dr Caroline Leaf – Contradicted by the latest research

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

* * * * *

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

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

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

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

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

Dear Mr Leaf,

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

ON INFORMED DECISIONS

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

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

YOUR DEFENCE

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

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

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

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

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

DR LEAF’S EVIDENCE

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

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

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

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

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

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

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

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

EVIDENCE CONTRADICTING DR LEAF

Influence Of Thought On Health

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

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

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

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

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

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

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

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

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

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

Atrial Natriuretic Peptide

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

The Heart As A Mini-Brain

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

Hard-Wired For Optimism

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

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

The Mind-Brain Link

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

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

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

FURTHER CLARIFICATION

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

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

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

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

Dr C. Edward Pitt

REFERENCES

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Mac Leaf responds to “Dr Caroline Leaf – Serious Questions, Few Answers”

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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, here is his reply, complete and unabridged.  My further response is posted here.

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 or my reply are welcome provided they are constructive.

Hi Dr C. Pit,

It is a pity you did not seek to clarify the comments you have posted above with us before you posted them. We hope you allow our comments to be displayed so that your readers can make informed decisions and not to judge Dr Leaf as you have done without getting accurate information. By your comments it is obvious that you have not kept up to date with the latest Scientific research.

Dr Leaf can call herself a Cognitive Neuroscientist because of her field research (published in peer evaluated Journals) …see the Science articles in the media/downloads section at drleaf.com. If you require, we can also send letters from her peers in the field of Neuroscience

She also developed the Geodesic Information Processing model theory.

Yes she does read a lot as the field of Neuroscience is constantly evolving and one has to be as informed as possible.

Some research links re the correlation between illness and thought are presented in Dr Leaf’s November the 30th blog at drleaf.com…blog. There are many more statistic correlation research links.

Dr Leaf has listed references differently in the different books and has a full list of references in the ‘thought life’ section at drleaf.com. The references were listed simply in that book for the lay person. This is an accepted literary format for the lay person. Subsequent books have fuller references.

The mini brain in the heart research can be found at Heartmath.org

Heartmath and Dr Don Colbert both reference the effect of ANF

The wired for optimism bias research has been evidenced by various scientific researchers
For easy access to this research please see the Google links to TED talks and Time Magazine’s article.

Please send us your E-mail address so that we can send you further documentation.

BELOW IS A LETTER OF REFERENCE FROM A MEDICAL PROFESSIONAL ENDORSING DR CAROLINE LEAF
My name is Dr Peter Amua-Quarshie and I am presently a full-time Adjunct Professor (lecturer) at the University of Wisconsin-Stout in Menomonie, Wisconsin. I have a B.Sc (Hons) in Medical Sciences (specializing in Neuropathology) and a Masters of Public Health (MPH), both degrees from the University of Leeds (UK). Additionally I have a medical degree (MB ChB) from the University of Ghana Medical School, Accra, Ghana, and a Master’s of Science (MS) in Behavioral and Neural Sciences from Rutgers University, Newark, New Jersey. I started teaching anatomy in the University of Leeds Medical School in 1996. I have taught Neurochemistry to graduate students and Neuroscience to undergraduates at Delaware State University and the University of Wisconsin respectively. I have known Dr. Caroline Leaf since 2006 and have worked closely with her since 2008 on various projects in the field of cognitive neuroscience.
Caroline Leaf received her training in Communication Pathology (BSC Logopaedics) at the University of Cape Town, South Africa. The University of Cape Town has produced many outstanding graduates, including Max Theiler, a Nobel Prize laureate in Physiology or Medicine and Christaan Barnard, the first person to successfully transplant a human heart. Caroline Leaf was a contemporary to the eminent neuroscientist Henry Markram, director of the Blue Brain Project and the new one billion Euro European Union Flagship Project, the Human Brain Project. As well having to study the cognition, she had to endure the rigor of the first 2 years of the medical course, in which she had to study neuroanatomy and neurophysiology. Dr. Leaf also holds a Master’s degree and PhD in Communication Pathology from the University of Pretoria, South Africa. In her Master’s degree her dissertation concentrated on cognitive neuroscience of Traumatic Brain Injury (Closed Head Injury). In developing her groundbreaking Geodesic Learning™ Theory (brain-compatible learning) in her ground breaking PhD thesis, she examined cognition and neurobiology of thinking. The Geodesic Learning™ Theory has been implemented among approximately 100,000 students in South Africa with great success. I have personally helped implement her Geodesic Learning™ Theory in a School District in the USA and was able to demonstrate quantitative improvement in scholastics across the board among the students. She is widely published in journal, book, DVD, television and the internet in the field of cognitive neuroscience in South Africa, USA and other parts of the world.
I have discussed neuroscientific subjects with her for multiple hours many times and have been thoroughly impressed with her knowledge and insight in neurobiology. However what really thrills me is revelation God gives her about the brain. She is an example to me of a neuroscientist who glorifies God in her pursuit of understanding the brain, and who is able to demonstrate that we are truly fearfully and wonderfully made (Psalm 139:14).

DR LEAF’s BIOGRAPHY

Since 1985, Dr Caroline Leaf, a Communication Pathologist and Audiologist, has worked in the area of Cognitive Neuroscience. She holds a Bsc Logopaedics with focus on in Neuroscience, Neuronanatomy and anatomy, Communication Pathology, Psychology, linguistics and audiology) , Masters in Communication Pathology She specialized in Traumatic Brain Injury and PhD in Communication Pathology (TBI) and Learning Disabilities focusing specifically on the Science and neuroscience of Thought as it pertains to thinking and learning. She developed a Cognitive Neuroscientific theory called the Geodesic Information Processing Theory for her PhD research and did some of the initial research back in the 1990’s showing how using non-traditional techniques, based on neuroscientific principles of neuroplasticity and neuropsychological principles, that the mind can change the brain and can effect behavioural change as seen academically, behaviorally and emotionally. A large part of her research in recent years has been to link scientific principles with scripture showing how science is catching up with the bible.

She applied the findings of her statistically proven research in clinical practice for nearly 20 years and now lectures and preaches around the world on these topics. She is a prolific author of many books, articles and scientific articles. She has been a featured guest of Enjoying Everyday Life with Joyce Meyer, and LIFE TODAY with James and Betty Robison, Marilyn Hickey, Sid Roth and TBN Doctor to Doctor, amongst many others. She has her own show on TBN called Switch on Your Brain.

Her passion is to help people see the link between science and scripture as a tangible way of controlling their thoughts and emotions, learning how to think and learn and finding their sense of purpose in life.

Caroline and her husband, Mac, live in Dallas, Texas with their four children.

Dr Leaf’s Qualifications

Web page: http://www.drleaf.com has my full qualifications and links to the Universities where I studied

Dr Leaf’s Reference list

1. Leaf, C.M. 1985. “Mind Mapping as a Therapeutic Intervention Technique”. Unpublished workshop manual.

2. Leaf, C.M. 1989. “Mind Mapping as a Therapeutic Technique” in Communiphon, South African Speech-Language-Hearing Association, 296, pp. 11-15.

3. Leaf, C.M. 1990. “Teaching Children to Make the Most of Their Minds: Mind Mapping” in Journal for Technical and Vocational Education in South Africa, 121, pp. 11-13.

4. Leaf, C.M. 1990. “Mind Mapping: A Therapeutic Technique for Closed Head Injury”. Masters Dissertation, University of Pretoria.

5. Leaf, C.M. 1992. “Evaluation and Remediation of High School Children’s Problems Using the Mind Mapping Therapeutic Approach” in Remedial Teaching, Unisa, 7/8, September 1992.

6. Leaf, C.M., Uys, I.C. and Louw, B. 1992. “The Mind Mapping Approach(MMA): A Culture and Language-Free Technique” in The South African Journal of Communication Disorders, Vol. 40, pp. 35-43.

7. Leaf, C.M. 1993. “The Mind Mapping Approach (MMA): Open the Door to Your Brain Power; Learn How to Learn” in Transvaal Association of Educators Journal (TAT).

8. Leaf, C.M. 1997. “The Mind Mapping Approach: A Model and Framework for Geodesic Learning”. Unpublished D.Phil Dissertation, University of Pretoria.

9. Leaf, C.M. 1997. “The Development of a Model for Geodesic Learning: The Geodesic Information Processing Model” in The South African Journal of Communication Disorders, Vol. 44, pp. 53-70.

10. Leaf, C.M. 1997. “The Move from Institution Based Rehabilitation (IBR) to Community Based Rehabilitation (CBR): A Paradigm Shift” in Therapy Africa, 1 (1) August 1997, p. 4.

11. Leaf, C.M. 1997. ‘”An Altered Perception of Learning: Geodesic Learning” in Therapy Africa, 1 (2), October 1997, p. 7.

12. Leaf, C.M., Uys, I. and Louw. B., 1997. “The Development of a Model for Geodesic Learning: the Geodesic Information Processing Model” in The South African Journal For Communication Disorders, 44.

13. Leaf, C.M. 1998. “An Altered Perception of Learning: Geodesic Learning: Part 2” in Therapy Africa, 2 (1), January/February 1998, p. 4.

14. Leaf, C.M., Uys, I.C. and Louw, B. 1998. “An Alternative Non-Traditional Approach to Learning: The Metacognitive-Mapping Approach” in The South African Journal of Communication Disorders, 45, pp. 87-102.

15. Leaf. C.M. 2002. Switch on Your Brain with the Metacognitive-Mapping Approach. Truth Publishing.

16. Leaf, C.M. 2005. Switch on Your Brain. Understand Your Unique Intelligence Profile and Maximize Your Potential. Tafelberg, Cape Town, SA

17. Leaf, C.M. 2008. Switch on Your Brain 5 Step Learning Process. Switch on Your Brain USA, Dallas.

18. Leaf, C.M. 2007. Who Switched Off My Brain? Controlling Toxic Thoughts and Emotions. Switch on Your Brain USA, Dallas.

19. Leaf, C.M. 2007. “Who Switched Off My Brain? Controlling Toxic Thoughts and Emotions”. DVD series. Switch on Your Brain, Johannesburg, SA.

20. Leaf, C.M., Copeland M. & Maccaro, J. 2007. “Your Body His temple. God’s Plan for Achieving Emotional Wholeness”. DVD series. Life Outreach International, Dallas.

Autism Series 2013 – Part 2: The History Of Autism

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“We can chart our future clearly and wisely only when we know the path which has led to the present.” Adlai E. Stevenson

I always thought history was boring, and I must admit, If you want to put me to sleep, start reading early Australian history to me. “Convicts … first fleet … zzzzzz.”

But as Stevenson wrote, the key to the future is the past. With autism, I don’t want to see a future as checkered as its past. In this series of essays, I want to help our community see a future in which autism is recognised and appreciated for its strengths. To properly lay the groundwork, I want to look at the history of autism. This will help provide context for the current understanding of autism, which will then give a framework for understanding the autistic person, and for a glimpse into the future as new research unfolds.

The autistic spectrum has been present for as long as humans have. But to our knowledge, one of the first specific descriptions of someone who met the characteristics of the autistic spectrum was in the mid 1700’s. In 1747, Hugh Blair was brought before a local court to defend his mental capacity to contract a marriage. Blair’s younger brother successfully had the marriage annulled to gain Blair’s share of inheritance. The recorded testimony describes Blair as having the classic characteristics of autism, although the court described him at the time as lacking common sense and being afflicted with a “silent madness”.[1]

Isolated case reports appeared sporadically in medical journals. John Haslam reported a case in 1809, although with modern interpretation, the child probably had post-encephalitis brain damage rather than true autism. Henry Maudsley described a case of a 13 year old boy with Aspergers traits in 1879. There were no other reports of children with autism in the early literature, although at the turn of the 19th century, Jean Itard reported on the case of an abandoned child found roaming in the woods like a wild animal. This child, called Victor, displayed many features of autism, although he may have simply had a speech disorder. Either diagnosis was obscured by the effects of severe social isolation.[1]

Others described syndromes which shared autistic features, but without describing autism itself. The names given to each syndrome reveals how autistic features were regarded in the 19th century: Dementia Infantalis, Dementia Praecocissima, Primitive Catatonia of Idiocy.[1]

Around 1910, Eugen Bleuger was a Swiss psychiatrist who was researching schizophrenic adults (and as an aside, Bleuger was the person to first use the term ‘schizophrenia’). Bleuger used the term ‘autismus’ to refer to a particular sub group of patients with schizophrenia, from the Greek word “autos,” meaning “self”, describing a person removed from social interaction, hence, “an isolated self.”[2]

But it wasn’t until the 1940’s that the modern account of autism was articulated, when two psychiatrists in different parts of the world first documented a handful of cases. Leo Kanner documented eleven children who, while having variable presentations, all shared the same pattern of an inability to relate to people, a failure to develop speech or an abnormal use of language, strange responses to objects and events, excellent rote memory, and an obsession with repetition and sameness[3].

Kanner thought that the condition, which he labelled ‘infantile autism’, was a psychosis[1] – in the same family of disorders as schizophrenia, although separate to schizophrenia itself[2]. He also observed a cold, distant or anti-social nature of the parents relationship towards the child or the other parent. He thought this may have contributed (although he added that the traits of the condition were seen in very early development, before the parents relationship had time to make an impact)[3]. True to the influence of Freud on early 20th century psychiatry, Kanner said of the repetitive or stereotyped movements of autistic children, “These actions and the accompanying ecstatic fervor strongly indicate the presence of masturbatory orgastic gratification.”[3]

Despite the otherwise reserved, cautious discussion of possible causes of this disorder, the link with schizophrenia and “refrigerator mothers” took hold in professional and lay communities alike. In the 1960s and 70s, treatments for autism focused on medications such as LSD, electric shock, and behavioral change techniques involving pain and punishment. During the 1980s and 90s, the role of behavioral therapy and the use of highly controlled learning environments emerged as the primary treatments for many forms of autism and related conditions.[2]

Unbeknown to Kanner, at the same time as his theory of ‘infantile autism’ was published in an English-language journal, a German paediatrician called Hans Asperger published a descriptive paper of four boys in a German language journal. They all shared similar characteristics to the descriptions of Kanner’s children, but were functioning at a higher level. They shared some aggression, a high pitched voice, adult-like choice of words, clumsiness, irritated response to affection, vacant gaze, verbal oddities, prodigious ability with arithmetic and abrupt mood swings. Asperger was the first to propose that these traits were the extreme variant of male intelligence[4].

But the full impact of Asperger wasn’t felt until 1981, when British psychiatrist Lorna Wing translated Aspergers original paper into English. By this time, autism had become a disorder of its own according to the DSM-III, the gold-standard reference of psychiatric diagnosis, but it was still largely defined by the trait of profound deficit. Aspergers description of a ‘high-functioning’ form of autism resonated amongst the autism community, and a diagnosis of Aspergers Syndrome became formally recognised in the early 1990’s with the publication of the DSM-IV.

The most recent history of autism comes in two parts. The first was the revision of the DSM-IV. For the first time, rather than two separate diagnoses, Autism and Aspergers have been linked together as a spectrum and collectively known as the Autism Spectrum Disorders (although autism self-advocates prefer the term ‘conditions’ to ‘disorders’).

The second part is a highly controversial chapter that will stain the history of autism research and scientific confidence, into the next few decades. Chris Mooney, in a piece for Discover Magazine, sums it up nicely:

“The decade long vaccine-autism saga began in 1998, when British gastroenterologist Andrew Wakefield and his colleagues published evidence in The Lancet suggesting they had tracked down a shocking cause of autism. Examining the digestive tracts of 12 children with behavioral disorders, nine of them autistic, the researchers found intestinal inflammation, which they pinned on the MMR (measles, mumps, and rubella) vaccine. Wakefield had a specific theory of how the MMR shot could trigger autism: The upset intestines, he conjectured, let toxins loose in the bloodstream, which then traveled to the brain. The vaccine was, in this view, effectively a poison.”[5]

Inflamed by a post-modern distrust of science and a faded memory of what wild-type infectious diseases did to children, the findings swept through the internet and social media and lead to a fall in vaccination rates (from about 95% to below 80% at its lowest)[6].

But the wise words, “Be sure your sins will find you out”, still hold true, even in modern science. In 2010, Wakefield was found guilty of Serious Professional Misconduct by the British General Medical Council, and was struck off the register of medical practitioners in the UK. In the longest ever hearing into such allegations, the GMC considered his conduct surrounding the research project, the medical treatment of his child subjects, and his failure to disclose his various conflicts of interest to be dishonest and professionally and clinically unethical[7]. There is evidence that he also selectively chose his subjects to confound the results, misrepresented the time course of their symptoms related to the vaccinations, misrepresented their diagnosis of autism, and altered the reports of their bowel tests[8, 9].

For the record, this isn’t a comment on the science of Wakefield’s rise and fall, but the history. I am not suggesting that the proposed autism/vaccination link should be discounted solely on the basis of Wakefield’s scientific fraud. Rigorous science has already done that. The science for and against the proposed link between autism and vaccinations deserves special attention, and will be discussed in a future post. Rather, lessons need to be learned from what is one of the most destructive cons in the recent history of medicine.

The losers of this hoax are twofold. Thousands of children have unnecessarily suffered from preventable infectious disease because of a fear of vaccines that has turned out to be unfounded, and those who actually have autism miss out on actual funding because it was syphoned off into Wakefield’s pockets and into research disproving his rancid theory. As the editorial in the BMJ stated, “But perhaps as important as the scare’s effect on infectious disease is the energy, emotion, and money that have been diverted away from efforts to understand the real causes of autism and how to help children and families who live with it.”[6]

As with all good history, there are lessons for the future. Autism is still largely misunderstood. The vacuum of definitive scientific knowledge is slowly being filled, gradually empowering people with autism and the people that interact with them to truly understand and communicate. Each breakthrough and revision of the diagnosis has lead to more sophisticated and more humane ways of living with autism. But there is still a need for caution – people will use the gaps in knowledge and the pervasive distress that can come from the diagnosis, to manipulate and exploit for their own ends.

I’ll continue with the series in the next week or so, looking at the modern “epidemic” of autism.

REFERENCES:

1. Wolff, S., The history of autism. Eur Child Adolesc Psychiatry, 2004. 13(4): 201-8.
2. WebMD: The history of autism. 2013  [cited 2013 August 14]; Available from: http://www.webmd.com/brain/autism/history-of-autism.
3. Kanner, L., Autistic disturbances of affective contact. Acta Paedopsychiatr, 1968. 35(4): 100-36.
4. Draaisma, D., Stereotypes of autism. Philos Trans R Soc Lond B Biol Sci, 2009. 364(1522): 1475-80.
5. Mooney, C., Why Does the Vaccine/Autism Controversy Live On?, in Discover2009, Kalmbach Publishing Co: Waukesha, WI.
6. Godlee, F., et al., Wakefield’s article linking MMR vaccine and autism was fraudulent. BMJ, 2011. 342: c7452.
7. General Medical Council. Andrew Wakefield: determination of serious professional misconduct, 24 May 2010. http://www.gmc-uk.org/Wakefield_SPM_and_SANCTION.pdf_32595267.pdf
8. Deer, B., How the case against the MMR vaccine was fixed. BMJ, 2011. 342: c5347.
9. Deer, B., More secrets of the MMR scare. Who saw the “histological findings”? BMJ, 2011. 343: d7892.

Autism Series 2013; Part 1 – Why it matters.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

TOXIC THOUGHTS ARE SIN

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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