under / standings

Dan Chalykoff

danchalykoff@hotmail.com

Resilience, Consilience, & Allostasis II

Last week, we met young Alice, who was awakened by the sound of plates, utensils, and a soup pot being thrown while her parents’ angry and intoxicated voices shrieked mutual hatred.  At seven years of age, Alice went down to see what was happening. 

What she saw was her mother with blood on her face, blouse torn open, lying on the kitchen floor, while her usually quiet father screamed and kicked her mother’s legs.  Both of their voices were distorted by alcohol, which Alice had heard before. 

When her father saw Alice, his face kind of collapsed and he told her, “Go back to your room. Now.”

Alice turned and began the short walk to the stairs.  But she turned again and asked, “What about Mommy?  Are you alright?”

Her mother was crying loudly now and sitting up hugging herself.  “I’m so sorry, Alice.  I’m alright, I’ll be fine, please, dear, go to bed.”  So, Alice did return to her bed, but it took a long, long time before she slept. Alice was a different girl when she rose the next morning.

Adverse Childhood Experiences (ACE, e.g., poverty, neglect, trauma) decrease resilience and increase vulnerability through the “biological embedding of trajectories of response to stressful life events” (Shonkoff, 2003 in Hunter et al., 2018, p. 310).  Spelled out, that sentence says that our internal systems, in body and brain, have ways of laying down pathways that make our reactions to stressful events automatic.  This is not a moral or personal failing because, when we meet setbacks, unless we stop to take an almost superhuman pause, we follow automatized neural and behavioural patterns of response.

Over a lifetime, these unchallenged automatic responses can contribute to disorders such as depression, dementia, and diabetes.  This happens through allostatic overload.  We defined allostasis (last week), as adaptation through change.  Overload is too much pressure to change, resulting in pathological or disordered adaptation, causing the ailments cited above (Rasgon & McEwen, 2016, in Hunter et al. 2018, p. 310).  Too much pressure to change, resulting in maladaptation, is the opposite of resilience.

What about Alice?  What is a child to do with such data as Alice has involuntarily gathered from her homelife?  Chances are high that the maladaptive responses described herein will take hold of Alice.  To emote healthfully, to respond to life with healthful hopefulness, Alice will need assistance.  But we’re not abandoning her.  We’ll keep looking at causes today and next week work out how Alice can be made whole again. 

Resilience is defined as the ability to achieve a successful outcome in the face of adversity (Hunter et al., 2018, p. 310).  One of Hunter’s main points is that rodents, through experimental exposure to threatening conditions, can become passive and fearful in their avoidance of harmful environments.  Crucially, anxiety- and depression-reducing medications have been shown to reverse that fear and avoidance.  And this is my understanding of Hunter in a nutshell: medication can facilitate and increase the chances of building more resilience through making neuroplastic adaptation more probable. 

One of the more convincing arguments, presented by Hunter, is that stress and trauma shrink the volume of the hippocampus.  (Remember the three-in-one hand last week?  The hippocampus is part of the emotional seat represented by the thumb—in those photographs.)  Lost hippocampal volume is associated with increased susceptibility to post-traumatic stress disorder (PTSD).  Interestingly, when “hippocampus” is Googled, the first of the 154,000,000 results states that the “Hippocampus is a complex brain structure embedded deep into temporal lobe.  It has a major role in learning and memory. It is a plastic and vulnerable structure that gets damaged by a variety of stimuli. Studies have shown that it also gets affected in a variety of neurological and psychiatric disorders” (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3548359/).

There’s a theme here that I want to emphasize: lost hippocampal volume means a lesser ability to emote = a lesser self.  Put another way, shrinkage in heart is shrinkage in self.  And if you envision that shrinkage combined with resistant internal responses, imagine the body language of a person unable to feel or express feelings.  What I see is fear, avoidance, isolation, and social withdrawal.  If the opposite of addiction is connection, how different is a loss of self from addiction? 

To understand causes, we return to ACEs and attachment.  Attachment is the study of how young children, from in-utero forward, bond with their caregivers. That ability, or inability, to bond is crucial to how one’s life unfolds. Hunter et al. (2018, p. 313, citing Meany et al., 1985) reinforce that finding stating that, “High levels of maternal care have been shown to decrease later stress reactivity…”  This is important.  If people from the addictive or traumatized communities know they had troubled youths, sorting those issues, in a manageable and open-eyed manner, can make the difference between being able to get along with others versus isolation. 

And sadly, it can get worse.  If your childhood wasn’t so troubled, but one or both of your parents’ childhoods were troubled, that trouble can be transmitted through behaviour and biology but, again, with help and work, this too can be reversed and healthfully managed, if attended to in an attentive and straight-up manner. 

Hunter also noted that stress has not been precisely defined, suggesting two definitions to fill that void. Toxic stress describes levels of stress that produce maladaptation and pathology (p. 8) and tolerable stressors are varieties of stress that produce adaptive outcomes.  For regular readers of this blog, there’s an etymological overlap that may interest some: the Greek word for what English speakers call happiness is eudaimonia or well-spiritedness; the word for productive stress is eustress.  This is helpful in that it may encourage those who know this history to see many stressors in a motivational or growth-inducing light rather than in a more painful pathological light.

Hunter’s (2018, p. 312) paper went into some detail about brain systems described as reward-seeking centres.  The key takeaway is that when this system is damaged, a person is more susceptible to PTSD and depression as those are associated with low motivation and low ability to enjoy life.  That’s the bad news.  The good news is that neuroplasticity, whether through self-care, talk therapy, pharmacology, or a combination of these, can return those hurt in youth—like Alice—to a life with goals, meaning, and pleasure. 

That return route (to wellness) is the subject of next week’s blog.

Dan Chalykoff is working toward an M.Ed. in Counselling Psychology and accreditation in Professional Addiction Studies.  He writes these blogs to increase (and share) his own evolving understandings of ideas.  Since 2017, he has facilitated two voluntary weekly group meetings of SMART Recovery.  Please email him (danchalykoff@hotmail.com) to be added to or removed from the Bcc’d emailing list.

References

Hunter, R. G., Gray, J. D. & McEwen, B. S. (2018). The neuroscience of resilience. Journal of the Society of Social Work and Research, Vol. 9: 2.

McEwen, B. S. (2000). Allostasis and allostatic load: Implications for neuropsychopharmacology.  Neuropsychopharmacology 2000-Vol. 22, No.2, Elsevier Science Inc.

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