The Biology of Resilience
Currently, our local e-media is doing a series of articles on resilience. Many of the stories are quite uplifting – about people who have overcome adversity and are using their experiences to influence outcomes for other people.
With the input of psychologists, other professionals, and recovered traumatised individuals, we are presented with a very evidential explanation for resilience.
What interests and fascinates me is what’s happening behind the scenes in the trillions of neurons that are processing the information and allowing us to make conscious decisions.
Our phenotype – how we appear in the physical world – is the outcome of three major contributing factors. One is our individual variable gene code; the second is our nutrition in the wider sense of the word; and, the third is our environment, again in the wider sense of the word.
Since the unravelling of the human genome in early 2000 and the understanding of the variations within the gene code that exist and that are epigenetically triggered, one can start to formulate a systems biology approach to the understanding of resilience.
There is one major driver in the crucible that nurtures DNA, and that is the persistence of DNA. The ongoing attempt to avoid the final mortality of DNA has yet to be understood; however, DNA’s ease of multiplication is not only demonstrated within our populations but also in the PCR reactions that we see on the lab bench.
Protection of this ability to replicate is the one critical feature that is paramount for its survival.
In the physical world, we have our HPA axis that allows us to recognise environmental hazards, and through biochemically internalised advice from experience and innate ability, we avoid destruction.
The cerebral structure’s ability to incorporate life events – both in utero and in the physical world after birth – is very plastic. This plasticity can also be viewed as adaptability. At a molecular level, through genetic guidance, the ability to activate adrenaline, cortisol, dopamine, and other neurotransmitters involved in the HPA axis allows us to understand our environment at a subconscious level.
From a medical point of view, physical illness (this is the whole body; there is no reason to separate the head as in pre-Newtonian times driven by religious dictum) has proven to be modifiable – in many cases very effectively – through the use of a number of behavioural interventions and biochemical interventions.
Every neurone, in fact nearly every cell in the body involved in survival, has the ability to respond to the chemicals released as a response to an environmental signal.
On every cell, there is a receptor called the glucocorticoid receptor, which is very responsive to environmental events. From intrauterine times through to puberty (during which the preparation of an individual to pass on the baton of DNA and be protective of their progeny happens), the glucocorticoid receptor is set up to respond to what the environment has taught the HPA axis – from memory within the cortex and immune system – allowing a complex presumptive forward ability to plan, identify and manage future cortical stimulating events.
ACE (acute corticosteroid events) can induce a change in the responsiveness to future episodes, priming the individual to respond in a certain format.
There is no doubt that many genetic processes are involved in the survival of the individual; however, one subject that appears to be dominating the literature currently is that of the genes that manage adrenaline and dopamine.
A fascinating study done on the war veterans from the Middle East wars showed that there was a considerable amount of predictability of post-traumatic stress disorder (PTSD) in those individuals who had the less favourable/productive Co-methyltransferase gene (COMt) gene. There are many influences on this gene or group of genes, including the nutritional, social, and psychosocial. It would be naive to believe that one element of the whole can be used to predict outcomes – in this case, the COMt gene, which manages dopamine, adrenaline, cortisol, and other hormones. When the individual with the less functioning SNP variant appears, under excessive adverse stimuli, not to be able to degrade the excitatory neurohormones in a timely fashion generated by this type of situation; this leads to a distorted view of threat with a wide range of dysfunctional behavioural variations.
In my clinical work, the range of conditions generated from this can trouble, terrorise, and distort the consciousness of the individual – putting them in a state of hypervigilance, which is not only pretty inappropriate at solving the perceived crisis but is also exhausting.
When considering resilience, the genetic variances of the individual have a large part to play, as does the nutritional environment for the genes.
Understanding this gives a broader array of solutions.