“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 . 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.” 
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.”  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.”  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.” 
It’s more accurate to think that chronic stress causes dendritic remodeling in animals , 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 . 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  (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 . 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.
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
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