Tag Archives: anxiety

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

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.

The end of the sugar obsession?

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I was flicking through Facebook this evening as I usually do, hoping to vicariously share someone else’s joy in life, when I came across this little tidbit, “You know what? Don’t quit sugar.”

The link was to a blog on mamamia.com.au (http://www.mamamia.com.au/health-wellbeing/you-know-what-dont-quit-sugar/) which asked if the tide of the quit sugar obsession was starting to recede.  It discussed the recent post of Sarah Wilson, a journalist for Fairfax and the author of several books on quitting sugar, which have become immensely popular by tagging on the coat-tails of David Gillespie’s “Sweet Poison” books.

In her blog, Wilson confessed to a barely forgivable sin of giving in to peer pressure and eating two chocolate croissants, then emotionally self-flagellating for the rest of the day.  That the symptoms that she described fitted nicely into the category of an anxiety neurosis didn’t seem to register with Wilson, who carried on like she had ingested a large goblet of hemlock.

Credit to the mammamia team who published some of the comments of real nutritionists like Cassie Platt, and eating-disorder counsellors like Paula Kotowitz, who said,

“Being harsh on ourselves, not only does not help, but makes us feel so much worse in the long run because it deconstructs our sense of self and causes us to beat up on ourselves. Isn’t it possible that there is a happy medium in there somewhere? It’s not crack. Just food.”

Platt, who is about to release a book titled, “Don’t Quit Sugar”, says,

“Your food choices should be based on biological and metabolic needs. What we eat should fuel our cells, facilitate growth, repair and reproduction and, most importantly, enable your body to function at its very best.”

Platt said that she has previously tried removing sugar from her diet and that she had to “claw” her way back to health.

The mamamia writing team summed up by saying,

“The benefits of reducing sugar intake are widely accepted in the scientific community but the idea of avoiding it altogether remains an issue of serious contention. And the possibility that these sorts of diet programs can mask dangerous eating disorders, is particularly worrying.”

They asked the question, “Has the sugar-quitting backlash begun?”  For the love of all things sacred, I seriously hope so.

About a month ago I wrote a piece about the quit sugar fad, and posted evidence that eating an extremely low carbohydrate diet is no better than eating a low fat diet, because it’s calories, not sugar, that makes all the difference to weight gain or loss.

A balanced, low calorie diet has been pushed by nutritionists and doctors ad nauseum for decades, but consistently neglecting to use words like “poison”, “toxin” or “death” has meant that the message is nowhere near as stimulating as the current whim.

Is it possible to have your cake and eat it too?  Absolutely.  My hero of nutritional science, Dr Rosemary Stanton, spoke at a Brisbane conference a couple of years ago and succinctly debunked Gillespie, Wilson and their ilk.  She also explained the concept of feasting, the long forgotten art form of having exceptionally good food once in a while, and enjoy it with friends, rather than eating substandard food every day by yourself, which is the modern trend.

Rather than gorging on sugar every day to compensate for your loneliness and despair, Dr Stanton advocated a diet high in vegetables and little or no processed food on a daily basis.  But then once a month or two, she advised to enjoy your favourite food, no matter what it might happen to be – cheesecake, ice cream, chocolate croissants – anything you like.  The only rules were to make sure that it is really good quality, the best that you can afford, so that it is worth savouring and looking forward to next time, and enjoy it with friends, since the social aspects of the food we eat are as important as the nutritional value.  Sage advice from someone who has been researching nutrition for longer than I’ve been alive.

I’m sure that by now, Sarah Wilson will have got over her sugar intoxication.  She may not have enjoyed it, but I hope that ends up being a pivotal moment in correcting the imbalance in our relationship to sugar, and living by the facts, not the latest fad.

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.

Fear: Friend or Foe?

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Fear.  Should we run, fight, or think?

I was lazily wasting time at Zarraffas this afternoon, and while I was savouring the richness and depth of my triple masai mocha, I was filling the time by flicking through Facebook.

I came upon a blog post by one of the best thinkers and writers I’m personally acquainted with, one Ruth Limkin, who shared the story of how she was given an opportunity to snorkel in a pristine area of ocean in the South Pacific that is limited to only a handful of people, such is the fragile beauty of the ecosystem there.  As she started swimming into the warm, calm, azure waters, she felt this sudden dread.

Five years ago in a similar situation, she misjudged the current, was swept into some coral, and sustained a laceration to her knee.  This left a lot of blood in the water which, quite reasonably, made her think that she had suddenly become shark bait.  She made it back to shore otherwise unscathed. But it left her with the implicit memory of that event.

This year, despite the obviously calm surroundings, she recalled that fear. Her brain told her to get out of there.  She did manage to overcome her fear though, and enjoyed the snorkelling!

Her lesson was that the pain of yesterday can become todays fear, which robs tomorrow of its promise.

I don’t disagree with Ruth.  I’m not intelligent enough to do that.  But I guess I come from a more medical and analytical perspective of this phenomenon, and I wanted to flesh out her point a bit further.

We all feel it at sometime or another – your heart pounds faster and heavier in your chest. Your breathing gets faster. Your muscles tighten. And your brain either says, “Run” or “Fight”, or sometimes it says nothing at all and we simply freeze up.

The human fear response is both rational and irrational.  We usually don’t understand why we are faced with conflicting realities of internal anxiety and external tranquility, feeling scared while looking at calm clear waters.  Sometimes when we take a step back, we can gain some understanding of why we have reacted the way we did, and cognitively overcome our fear.

B-grade pop-psychologists make us believe that courage is the absence of fear, and that the way to move forward is to eliminate or repress your fears.  But that approach is wrong for a couple of reasons.

There is a good reason why we have fear conditioning.  There is a part of the brain called the limbic system, which is integral to emotional processing.  Central to this is the amygdala, which is responsible for adding emotions to our experiences, especially fear and anger.  When something happens that has real or perceived negative consequences (we experience pain, or we think that there is a high chance that we will experience pain) the amygdala pairs that aversive sensation with the memory of the total experience.  This helps us learn from our mistakes [1].

For example, if a pre-historic man was walking through a forest and came across a sabre-toothed tiger, the fight-or-flight response would help him escape.  But the amygdala would attach the memory of the emotion to the memory of the event itself.  Next time the man walked through a similar forest, or even recalled that event in his mind, the emotion of the memory would also be recalled.  This is why Ruth felt uneasy despite the lack of danger.  Her surroundings triggered the emotional memory of the previous snorkelling experience.

But while unpleasant, fear does confer a survival advantage.  Without the same emotion being recalled, we wouldn’t remember what situations were dangerous and which were safe.  Recalling the emotion and realising there may be sabre-toothed tigers around, or strong currents and sharks, means that there is a much smaller chance of us becoming lunch.

There are two pathways in the brain that are involved in the fear response.  The direct pathway goes from the senses to the amygdala, bypassing the thinking parts of our brain entirely.  Again, this confers a survival advantage as the quicker you can prepare yourself for danger, the more likely you are to survive it.  The signal is not properly analysed, but it doesn’t need to be.  It is better to be wrong and live than to be right and eaten by something.

The second pathway from the senses to the cerebral cortex then back to the amygdala is more precise, but it is slower than the direct path.  It can downgrade the fear response if it is not appropriate.  Well, it can in most people.  Anxiety and panic disorders arise when the balance between the direct and indirect pathways is skewed in the direction of the amygdala.

If you think you may have an anxiety disorder or panic disorder, you should see a good GP.  There are specific forms of psychological therapy that you may need to engage with.  Some people also need medications to assist with the process.

For most people though, we can simply allow the recalled feeling of fear stop us from engaging in life.  When we sense fear, the natural reaction is to run or fight.  That is the direct pathway talking in our brain. The lesson from our neurobiology is that we have another choice.  We can let our cerebral cortex do its job, we can think about the situation, and allow our higher functions to downgrade our primitive reactions.

We also need to understand that fear is ok.  It is necessary, in fact.  Without it, we wouldn’t adapt to our surroundings or learn from our mistakes.  We should not avoid fear.  We should not fight fear.  But we should not let fear control us.

Nelson Mandela, a man who experienced great fear but greater hope, sums it up beautifully, and so gets the final word, “Courage is not the absence of fear, but the triumph over it.”

References
[1] Dalgleish, T., The emotional brain. Nat Rev Neurosci, 2004. 5(7): p. 583-9.