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Anxiety & Stress

Anxiety & Stress


Today's society is ever driven by demands on our limited resources resulting in stress and anxiety in less well prepared groups.

 

What is Stress

For students of physics, stress simply is defined as load or force exerted per unit area. And the response or resulting strain is change per unit length. The elements in this definition are mass, duration and surface area. 

This definition gives a fair picture of how stress can affect biological systems where stress may be defined as any uncomfortable "emotional experience accompanied by predictable biochemical, physiological and behavioural changes."  Simply it is an individual's response to environmental and psychosocial conditions that demand change.

 

Human Capacity

Resources could be internally preset in other words biologically determined by multiple innate factors. This include our inherited gene pool otherwise referred to as nature, or acquired environmental factors such as early adaptive resilience by positive nurturing. Good enough parenting and adequate prosocial and learning abilities in combination with a healthy brain help set the stage for stable and positive neurocognitive development conferring resilience. 

These conditions are essential plateau for a normative development. It forms the template for embedding sequential information that is, memory, over time. 

Objects are critical in the process of learning. They form 'wrap around' for for us to attach meaningful information. Like the proverbial baobab tree travellers inscribe or stick messages to as compasses, we rely on the longevity of brain networks to remember where we have been, what we did and what was done to us. Transitional objects and significant others reinforce our human experiences and inadvertently shape our reaction in times of stress. What attachment figures we register and how we related to them 'prime' our future reactions in a stressful world.

 

Origins of stress

The origins of stress predates modern man. It can be found in other vertebrates and indeed all mammals. Incidentally the development of a large frontal lobe loaded with conscious awareness increases our vulnerability to stress. Actions and reactions of the primitive reptilian brain are determined by reflexes that do not necessarily advance to consciousness. Though they may experience stress, evidenced by neurochemical changes, this itself is accepted as 'fait de vie'
At cellular level apoptosis or cell death represents the most primitive response to stress. Experts have argued that major depression and its involutory reaction may represent a biological response to overwhelming demands on the organism in this case man. 

The response of humans to stress may be acute and evidenced by a flight or fright reaction as commonly known. There is usually an accompanying slow and chronic reaction that continues as a lag phase following the initial acute response. The total duration of the acute and chronic stress response is determined by a number of parameters.

 

Acute stress

A typical picture is when we experience a potentially dangerous situation. Escaping a ferocious  dog or being chased by a lion in our dream!  We reflexly engage all available resources to execute an escape. This action is often energy intense as subcortical processes driven by the amygdala 'emotive' centres triggers a flight response. Overcoming the threat, leads to relief and 'phew all good', signal to the brain. The neurochemicals are reset, and yes, we may be exhausted or tired and have to catch our breath, but we are safe and can go to sleep rest assured that the danger is gone.

The neurochemical processes at play in an acute stress response are specific and time bound. They draw from stores of neurotransmitters in neurones, the functional unit of the brain, spinal cord and ganglion. Stored in neuronal cell bodies these chemicals primarily adrenaline and noradrenaline forming the sympathetic system, rely on signalling processes modulated across the central and peripheral nervous system.
Energy substrates comprising glycogen in muscle (more rapidly metabolised) and glucose in brain provides resource for sequentially generating signalling molecules that trigger action potentials. Excitatory neurotransmitters act in a cascade to ensure various pathways work in tandem to effect the necessary outcome.

Cardiac output, respiration and all other physiological processes required for sustaining the necessary flight response increases. Non-essential organs such as the guts and genitourinary systems which are largely vegetative or parasympathetic are by-passed.

This acute stress reaction is primordial and innate. 

Whatever the trigger, the ability of the individual to overcome an acute stress is critical to longer term prospects.

Chronic stress

The neurochemical picture in persistent and continuous stress relies on available resources and individual resilience. A process of neuroadaptation is triggered as the body tries to predict the duration of the stress. Early resolution of the stress in the short term may restore normal function with little or no adverse sequel. Persistent stress however results in a shift in the equilibrium with disruption of feedback inhibition of hypothalamic regulatory mechanisms such as the Hypothalamic-Pituitary-Adrenal (HPA) axis. The consequences on interconnected brain pathways such as those controlling cognition, motivation and reward, emotional regulation, long term memory and indeed sleep, interests and appetite to mention a few, are immense. 

Persistent sympathetic activation of adrenal system triggers a glucocorticoid hormone response in adrenal cortex of the kidneys. This is in an attempt to restore homeostatic equilibrium by inhibiting HPA regulation of glucocorticoid mechanisms in other to sustain the required cardiac output. 

 

Neurobiological mechanisms in anxiety and depression

Studies have demonstrated that individuals with depressive disorders have very low amounts of serum catecholamines and serotonin. Treating clinical depression with antidepressants does bring about significant improvement in majority of patients with major depression. 

However various observations including the delayed onset of improvement informs the understanding that other mechanisms are involved in the longer term effect of antidepressants.  The increase in serum levels of cortisol a glucocorticoid hormone in depressive disorder offered further insight into the link between depression and a number of metabolic and immune dysfunction. Cortisol mediates numerous neuroendocrine, metabolic, immune processes but also inhibits neurogenesis required in fighting infection or recovery from stress and depression. 

Chronically elevated cortisol level is toxic and has been shown to be implicated in a number of long term changes in a number of disorders - stress and depression, alcohol dependency, poorly controlled diabetes in addition to other diseases of the adrenal cortex such as Cushing's syndrome.

Cortisol is normally secreted in a circadian (night/day) rhythm in response to 'stressful' wakening response. Cortisol in physiological states regulates its serum level via negative feedback activation of intracellular second messenger systems, glucocorticoid receptors(MR) and mineralocorticoid receptors(MR). It's serum level peaks about half-hour after waking up and troughs at around midnight. Cortisol secretion and release by the adrenal cortex is modulated by feedback mechanisms that trigger the HPA axis and causes release of Corticotrophin Releasing Factor (CRF) from the hypothalamus. CRF stimulates the anterior pituitary to synthesis a precursor hormone to ACTH. ACTH released in circulation acts on adrenal cortex triggering release of mineralocorticoid hormone from the zona glomerulosa and glucocorticoid hormone from zona fasciculata predominantly.   

In chronic stress, the normal circadian response is blunted due to loss of negative feedback of the Glucocorticoid receptor inhibition. Further increases in cortisol results in persistent toxic effects. This essentially means the individual is unable to respond effectively to the stress by adequate release of catecholamines and serotonin.  

 

Effect of Prolonged stress

Anxiety which is an undue trigger of the flight or fright response in the absence of objective threats is a feature of maladaptive reaction to stress. Studies have shown that over 50 per cent of individuals with depression have at one time or another being exposed to stressful events.  Childhood reaction to adverse events have been categorised into major loss events, neglect or experience of violence or abuse. Insecure and disorganised attachment in early childhood predisposes to various forms of anxiety disorders. Early exposure to violence and trauma and indeed increases risks of post traumatic stress disorder and depression in adults. Prolonged stress in the form of acute on chronic (persistent and continuous) adverse events modulate neuroadaptive mechanisms priming future extreme reaction to perceived threats. This is referred to as kindling or sensitization where individuals become predisposed to internalizing or externalising maladaptive responses to negative life events.

Depression, anxiety, irritability and (negative) apathy or inhibition have been shown to be a result of adverse psychological stressors described as internalizing behaviours while aggression, delinquency and ‘acting out’ behaviours are often related to early physical abuse.  

Prolonged activation of sympathetic systems due to effect of cortisol on mineralocorticoids potentially increases risk from hypertension, heart disease and stroke. Arteriosclerotic changes predisposis to small vessel diseases affecting organs such as the eyes and kidneys in addition to stress ulcers. 

Individuals able to mobilize internal mechanisms to combat stress are at better stead to overcome the stressful event.

Managing stress 

Prevention

  • Lifestyle choices - exercises, play therapy (especially children), structured regular activities, music therapy, join a band or a choir!
  • Supportive network of friends, confiding relationships, get advice if not sure. Two good heads better than one.
  • Learn a life skill and create a job or find one. Doing nothing is recipy for stress.
  • Healthy diets and fluid intake - you are what you eat!
  • Avoid harmful substances - nicotine dependence, drug and alcohol or gambling, all potentially  predisposing to addictive behaviours. They potentially would lead to reduced capacity to cope with stress due to blunting of normal patterns.

Early recognition 

  • Early recognition of symtoms of stress in yourself or a friend is critical to good outcomes.
  • Young mothers especially with two or more children below age 10 and with unstable supportive relationships may be vulnerable.
  • If sudden and unexpected change in personal circumstances, explore problem solving strategies with support from a friend.

 

Treatment

  • Remove the source of stress if possible. e.g if in a toxic relationship, seek to end it or get counselling, do not        continue in a job that does not make ends meet.
  • Counselling - talk to a therapist
  • Mindfulness - self guided mastery, Mindfulness Based Therapy
  • Psychology - self help CBT for managing anxiety and emotions
  • Relaxation therapy
  • Consultant your doctor

 

DO NOTs    

DO NOT add petrol to fire by relying on alcohol or illicit drugs.
DO NOT let yourself slip into contemplating ending your life. 

Doing the right thing! 

Whatever you are going through is not new. Help may just be round the corner! Ask. People have turned things around with the right support and made adversities into success. 

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