Tag Archives: brain damage

Going green – why envy is an adaptive process

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The Bible says, in Job 5:2, “For wrath kills a foolish man, And envy slays a simple one.”

A German proverb goes, “Envy eats nothing, but its own heart.”

Dr Caroline Leaf, communication pathologist and self-titled cognitive neuroscientist, posted today on her social media feeds, “Jealousy and envy creates damage in the brain … but … celebrating others protects the brain!”

Yes, sometimes envy isn’t good for us. Emotions guide our thought process, and like all emotions that are out of balance, too much envy can cloud our better rational judgement and bias our perception of the world. Thankfully, envy doesn’t literally eat out our hearts or literally cause brain damage.

If anything, envy when experienced in a balanced way can actually improve our brain functioning. According to real cognitive neuroscientists, envy and regret are emotions that help us because they both fulfil the role of effectively evaluating our past actions, which improves our choices in the future. As Coricelli and Rustichini noted, “envy and regret, as well as their positive counterparts, share the common nature that is hypothesized in the functional role explanation: they are affective responses to the counterfactual evaluation of what we could have gotten had we made a different choice. Envy has, like regret, a functional explanation in adaptive learning.” [1]

When it comes to the human psyche, there is no black or white, good vs evil distinction between different feelings or emotions. B-grade life coaches and slick pseudoscience salespeople dumb down our emotions into a false dichotomy because it helps sell their message (and their books). Every emotion can be either helpful or unhelpful depending on their context in each individual.

As Skinner and Zimmer-Gembeck wrote, “Emotion is integral to all phases of the coping process, from vigilance, detection, and appraisals of threat to action readiness and coordinating responses during stressful encounters. However, adaptive coping does not rely exclusively on positive emotions nor on constant dampening of emotional reactions. In fact, emotions like anger have important adaptive functions, such as readying a person to sweep away an obstacle, as well communicating these intentions to others. Adaptive coping profits from flexible access to a range of genuine emotions as well as the ongoing cooperation of emotions with other components of the action system.” [2]

If you find your thoughts and feelings tinged by the greenish hue of envy, don’t worry, it’s not necessarily a bad thing. Your heart isn’t going to consume itself and you won’t sustain any brain damage. Use envy or regret as tools of learning, tools to help you evaluate your choices so that you make a better choice next time. Having balanced emotions is the key to learning and growing, coping with whatever obstacles life throws at us.

References

  1. Coricelli, G. and Rustichini, A., Counterfactual thinking and emotions: regret and envy learning. Philos Trans R Soc Lond B Biol Sci, 2010. 365(1538): 241-7 doi: 10.1098/rstb.2009.0159
  2. Skinner, E.A. and Zimmer-Gembeck, M.J., The development of coping. Annu Rev Psychol, 2007. 58: 119-44 doi: 10.1146/annurev.psych.58.110405.085705

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.