PSYC2500: Introduction to Mental Disorders (Wk 10-12)

Alcohol use and burden of disease

Alcohol use represents 5.1% total burden of disease and across all adult age groups, alcohol use ranks within top 10 risk factors contributing to disease burden

Substance use disorder

Substance use causes clinically and functionally significant impairment involving the development of tolerance and withdrawal. The DSM-IV-TR had two broad categories (substance abuse & dependence) while DSM-V has only SUD

Commonality of substance use

People frequently use drugs to wake up (coffee, tea), to stay alert (cigarettes, soft drinks), to relax (alcohol), and reduce pain (paracetamol)

Tolerance

Person requires a larger dose of a substance to get the desired effect or that the effects are less than what they once were for the same amount of drug taken.

Withdrawal

Person experiences physical and psychological effects that develop when person stops taking the substance or reduces the amount of substance they are using.

Stigma of substance use disorder

Terms such as addict or alcoholic are commonly used to characterise people by the disorder and perpetuate the idea that someone IS the disorder and that they were predisposed and can’t recover from that disorder (e.g. disease model of addiction). Ad campaigns and other media depictions can encourage the idea that people with SUD are dangerous or violent. Clinicians should not use the term alcoholic or drunk as a noun.

Alcohol consumption and misuse

Alcohol consumption = drinking at least one serve/standard drink of alcohol

Alcohol misuse = drinking over the amount suggested by the risk minimisation guidelines

*problematic drinking can include alcohol misuse repeatedly (important to remember it doesn’t have a certain look)

Alcohol use disorder (DSM criteria)

A problematic pattern of alcohol use leading to clinically significant impairment or distress demonstrated by 2+ symptoms:

• Large amounts or long periods of alcohol use, unsuccessful effort to reduce/control use, time spent to obtain, use, or recover from alcohol use, cravings, failure to fulfil major role obligations, social, interpersonal, physical or psychological problems, recurrent alcohol use in hazardous situations and giving up important activities

Must include tolerance and withdrawal

Severity characterised by no. of criteria: mild = 2-3, moderate = 4-5, and severe = 6+

Standard drink

• Light beer = 425ml (2.7% alcohol/volume)

• Full beer = 285ml (4.9%)

• Cider = 285ml (4.9%)

• Fortified wine = 60ml (20%)

• Sparkling and normal wine = 100ml (13%)

• Spirits = 30ml (40%)

Australian alcohol guidelines to reduce risk

These guidelines are only to reduce risk as there is no “safe” drinking

• To reduce lifetime risk = drink no more than 10 standard drinks per week

• To reduce single occasion risk = drink no more than 4 standard drink per day

• Don’t drink if you are under 18 or are pregnant/breastfeeding

Proportion of alcohol abstinence

Alcohol abstinence is gradually increasing but most people still consume alcohol. Abstinence is mostly in younger age groups as older people’s alcohol use is either stable or increasing.

Proportion of risky alcohol use

• 31% people consumed alcohol above recommendations (stable). 25% consumed more than 10 drinks per week and 24% consumed more than 4 drinks per day (decrease).

• Young people were more likely to exceed daily guidelines while older people exceeded weekly guidelines.

• People who consumed alcohol riskily were more likely to be aware of guidelines (69%).

• Fewer males had risky alcohol consumption than ever at 39%

Proportion of underage drinking (14-17yr)

Significantly decreased from 69% → 31% with increasing proportion of young women drinking 29% → 35%. Decline in risky drinking 9.5% → 5.5%. 32 of ppl believe 16-17 yr old can drink 1 to 2 standard drinks without risking health.

Proportion of harm caused by someone under the influence

21% of people were verbally/physically abused or scared by someone under the influence. This increased for women from 2.2-2.4 ml and decreased for men.

WHO ranking of alcohol use

Australia = 21st, New Zealand = 31st, USA = 38th, Canada = 41st, UK = 24th, Germany = 12th, France = 8th, and Ireland = 7th

Harms associated with alcohol misuse

Alcohol contributes to 40% of burden to liver cancer, 30% burden due to road injuries, 28% due to chronic liver disease, and 15% due to suicide and self harm. 5.5% of ppl who exceed lifetime risk required hospital admission/medical attention due to intoxication related injuries.

Short term impacts of alcohol use

Alcohol enters bloodstream through small intestine and is metabolised by liver. Effects depend on concentration and concentration depends on gender, height, weight and liver efficiency. Produces the biphasic effect. Large amounts of alcohol impairs speech/vision, inhibits PFC (complex thought), loss of balance/coordination and depression

Alcohol interactions with neural system

Stimulates GABA receptors, increases dopamine/serotonin, and inhibits glutamate receptors

Biphasic effect

Alcohol initially stimulates (buzz) → producing sociability and well being → later alcohol depresses → increases negative emotions

Long term impact of alcohol use

• Malnutrition and B complex deficiency (amnestic syndrome and memory loss) because alcohol interferes with digestion and absorption of vitamins

• Cirrhosis of liver, endocrine and pancreas damage, heat failure, erectile dysfunction, hypertension, capillary haemorrhage (facial swelling and redness especially in nose), stroke, and destruction of brain cells

Vaping use

Increase in use of e-cigarettes daily from 0.5% (2016) to 3.5% in 2023 however daily tobacco use as decrease from 12% to 8.3%. Vaping is more common in younger ppl (9.3%) and higher SES ppl while smoking is more common in older and lower SES groups. Vaping is only beneficial if you are trying to quit smoking as it is less harmful however there are 40 cigarettes in one vape so still bad.

Foetal alcohol syndrome (FAS)

Heavy alcohol intake during pregnancy = slowed foetal growth and cranial, facial, and limb abnormalities including epicanthal folds, railroad track ears, thin upper lip, and small palpebral fissures

Moderate alcohol intake (1 drink/day) = learning and memory impairments and growth deficits

Withdrawal from heavy alcohol use

Anxiety, depression, weakness, restlessness, difficulty sleeping, elevated BP, pulse and temp. Muscle tremors and delirium tremens which occur when blood alcohol levels drop suddenly causing delirium, tremors, and hallucinations (usual visual e.g. little blue men)

Impaired control vs choice theory of addiction

Impaired control theory = Used within the disease model of addiction where addiction is characterised by brain impairment which impairs control

Impaired choice theory = maladaptive substance use reflects a rational choice by the individual

Biological factors of SUD

Addiction substances act of brains reward systems including the dopaminergic reward system (most important), endogenous opioid system and inhibitory system (impairs it)

Genetic factors of SUD

SUD’s cluster in families with higher-risk for relatives and children. Greater concordance in monozygotic than dizygotic twins which support heritability however this is non-substance specific (e.g. general SUD not specific alcohol or heroin). Alcohol tolerance may have a genetic origin e.g. asian ppl have higher tolerance and lower rates of alcohol abuse bc they have CYP2A6 gene.

Psychological factors of SUD

Mood alteration during substance use and withdrawal. Personality can affect substance use e.g. impulsivity and low self-esteem might increase use. Expectancies can alter substance effects e.g. if you expect to have a bad trip or have increased aggression.

Socio-cultural factors of SUD

Many cultural commonalities in alcohol use but some cross-cultural differences due to availability of substance, family factors, and social setting.

Process of dependence and neurobiological factors

Positive attitude towards substance → experimentation → regular use → heavy use → dependence or abuse. Problems in the dopamine pathways since drug use results in rewarding feelings might account for why people become dependent on drugs.

Treatments of AUD

1 in 5 people who met AUD criteria in previous 12 months had sought treatment. Treatments include withdrawal management, cognitive behavioural treatments, couples therapy, motivational interviewing, moderation in drinking, alcoholic anonymous, SMART recovery and medication e.g. makes ppl sick if they drink (conditioning). Most frequent services are counselling, withdrawal management and assessment. Withdrawal from alcohol can kill people meaning it requires professional treatment.

Treatments of smoking and vaping

Pick a day to quit → make a plan → get rid of vapes and triggers → tell friends/support network → quit with supportive friend → know what help is available e.g. psychological treatments and nicotine replacement treatment/medications. Manage cravings by avoiding triggers during first 2 weeks, carry a snack, exercise, use distractions, and meditate/deep breathing

National alcohol strategy (2018-2026)

Aims to address risky alcohol use and related harm in community using law enforcement, prevention, early intervention and health care strategies. Centres around harm minimisation and being a people centred, collaborative, innovative and evidence/practice based approach. Has four strategies including promoting healthy communities, improving community safety/amenity, managing availability, price, and promotion, and supporting individuals to get help and systems to respond.

National alcohol strategy: Improving community safety and amenity

Harmful alcohol and drug consumption has adverse impacts through violence, assault, crime, additional social costs, lost productivity and reduced capacity within community services e.g. emergency and police department.

Objectives = less injury/violence, safer drinking settings, and better offender treatments and rehabilitation

National alcohol strategy: Managing availability, price, and promotion

Alcohol has been became more readily available/affordable over last decade which correlates with increased alcohol-related problems. WHO identified that taxation, restricting availability and implementing bans on advertising are the most effective strategies in harmful alcohol use minimisation

Objectives = strength controls on access/availability, pricing and taxation and minimise promotion of risky drinking

National alcohol strategy: Supporting individuals to obtain help and systems to respond

Treatment is crucial in reducing harm and services need to be ready to respond in a timely matter including for family and friends of someone with a SUD who might need support.

Objectives = promote evidence-based info and services, deliver a quality, responsive, safe, and effective treatment system and reduce the impact of FASD

National alcohol strategy: Promoting healthier communities

Regular repetition of evidence-informed messages to encourage cultural/attitude shift and target at-risk populations.

Objectives = improve awareness and understanding of harm + improve communication to target certain groups (specific intervention)

Three pillars of harm minimisation

Demand reduction = prevent uptake and delay first use, reduce harmful use and support recovery

Harm reduction = reduce risk behaviours and provide safer settings

Supply reduction = control illicit drug and precursor availability + reduce illicit drug use, availability and accessibility

Median delay before treatment for SUD

18 years

Most common psychoactive substance in general population

Caffeine then tobacco

Effects of opiates

Euphoria, drowsiness, reverie, and lack of coordination

Types of addictive behaviours

Sex, gambling, Internet/screen, gaming, shopping, thrill-seeking, binge eating/food, and plastic surgery addiction. Often involves an  inability to stop or control addictive behaviours e.g. can't stop gambling, feeling shame or embarrassment, increasing risk-taking behaviours, engaging in addictive behaviours while engaging in substance use, loneliness, stress, and decreased functioning

Decriminalisation

Drug use and possession is illegal however it doesn't involve criminal charges (e.g. criminal record/jail) but may involve civil penalties e..g education and treatment programs or fines. Focus on improving health and social outcomes, increase likelihood people will seek help, avoid negative social outcomes resulting from criminalisation, reduce strain on criminal justice system, and reduce stigma

Legalisation

Removal of all penalties for the possession and personal use of a drug within the drug regulations e.g. alcohol is a legal drug. The regulations may include certain age groups, quantities, business licenses, etc.

Stages of change model (Transtheoretical)

Pre-contemplation, contemplation, preparation, action, maintenance and relapse. 

Delirium

Disturbance in attention that develops in a short period. Represents a change from usual behaviour and often fluctuates in severity. Has an additional distance in cognition e.g. disorientation or memory deficit. Disturbance is caused by another medical condition, substance intoxication or withdrawal

Biological and sociological ageing

Biological ageing = progressive and generalised deterioration in function from post-maturity until death

Sociological ageing = changes in assumed social roles, attitudes and beliefs about ageing and older people

Normal ageing

Distractible (attention), slower encoding and retrieval (memory), word finding and complex syntax difficulties (language), slower processing speed (first thing to decline), spatial relationships and rotation ability reduces (visuospatial), and poorer decision making and judgements (frontal lobe and executive function decline)

• No necessarily memory loss or forgetting but slower retrieval and less attentional resources

• Vocab often improves and word comprehension is stable

• Basic perceptual abilities are stable

Brain changes with ageing

Changes in cognition results from structural and functional brain changes mostly relating to volume decrease. Not all brain areas change and this is dependent on what cognitive abilities decline or remain stable during ageing e.g. hippocampus volume decreases but primary visual cortex doesn’t.

Age-related cognitive decline

Decrease in processing speed, reasoning, memory and executive functions. Verbal abilities and general knowledge are less affected or even increase. Primary prevention stage.

Mild cognitive impairment (MCI)

More extensive cognitive changes and preserved functional abilities with varying presentations of principal cognitive impairment: amnestic (memory), non-amnestic or multiple cognitive domains. Main assessed cognitive areas = complex attention, executive function, learning and memory, language, perceptual-motor or social cognition. Secondary prevention stage.

Dementia

Marked impairment in cognitive AND functional abilities which progresses to the point where the person is dependent. DSM doesn’t use the term dementia and moved to neurocognitive disorder due to stigma. Over 100 types of dementia with the most common being Alzheimer’s then vascular.

Mild neurocognitive disorder (MND) DSM-5 Criteria

A. Evidence of modest cognitive decline in 1+ domains based on individuals concern, knowledgeable informant or clinician AND modest impairment in cognitive performance demonstrated by testing or clinical assessment

B. Cognitive deficits don’t interfere with independence in everyday activity but greater effort, compensatory strategies or accommodations may be required

C & D. cognitive deficits don’t only occur during delirium and aren’t better explained by another mental disorder

Neuropsychological assessment for MND

• Establish clinical history = get context, details regarding change, premorbid ability, time course, mood, and life events

• Cognitive testing = 1-1.5 SD’s below mean cognitive ability for age across attention, visuospatial, language & executive function

• Validated measure of mood

• Repeat assessment 6-12 months later to measure progression

Clinical course of MND

10-15% of patients seen in memory clinics will progress to dementia each year with 70% to progress to dementia in 5-6 years and 30% may not progress. Currently not possible to predict with certainty whether someone will develop dementia as there are differing rates of progression.

MCI progression depending on principal impairment

• MCI amnestic → Alzheimer’s disease

• MCI multiple domains → Alzheimers and Vascular dementia and normal ageing

• MCI non-amnestic → Frontotemporal, Lewy and Vascular dementia, Parkinsons, Alzheimers, and primary progressive aphasia

Prevalence of dementia

411,000 Australians are living with dementia with half of people being undiagnosed. Over 25%of people aged 95+ have dementia with 28,000 ppl under 65 have dementia (young onset). Seemingly increase in people living with dementia which potentially could be linked to a larger elderly population due to ppl living longer or increases in population.

• Prevalence = % of ppl with dementia in a define population

Incidence and mortality of dementia

• Incidence = occurrence of new dementia cases in a population within a specific period

• Mortality = occurrence of death cases in a population within a specific period

Non-modifiable risk factors for dementia

Family history of dementia, older age, being a woman, and certain genes

Modifiable risk factors for dementia

Biological = physical inactivity, traumatic brain injury, hypertension, cardiovascular disease, hearing loss, obesity, diabetes, smoking, and excessive alcohol consumption

Psychological = depression, stress, cognitive inactivity, and anxiety

Social = low education, social isolation, air pollution,

Cognitive health environment life course model (CHELM)

Independent variables (genetics, environment, demography and lifestyle) → disease risk factors (stress and cardio metabolic risk factors) → diseases (depression, diabetes, cardiovascular disease) → neuropathology (amyloid deposition, tau aggregation, microbleed, atrophy) → cognitive function

A clinical diagnosis of dementia can be made by considering which combination of evidence:

Client and informant reported history of symptoms, cognitive testing, functional disability

The reason why dementia incidence is falling in some high-income countries is best explained by:

Control of hypertension and cardiovascular health

Major neurocognitive disorder (mNCD) DSM-5 criteria

A. Significant cognitive decline in 1+ cognitive domains based on individuals concern, knowledgeable informant or clinician AND modest impairment in cognitive performance demonstrated by testing or clinical assessment

B. Cognitive deficits interfere with independence in everyday activity (with severity based on the level it interferes)

C & D. cognitive deficits don’t only occur during delirium and aren’t better explained by another mental disorder

The inevitability/avoidability of dementia

The functional disability of dementia can be avoided, although you may still have the disease pathology

Subtypes of dementia

Alzheimer, Huntington, Lewy body, Parkinson, Prion, and Vascular disease. Frontotemporal degeneration, traumatic brain injury, substance/medication use, HIV infection, another medical condition, multiple aetiologies, and unspecified.

Alzheimers disease

A. criteria met for major or mild neurocognitive disorder

B. Insidious onset (due to gradual progression, forgotten or not wanting to disclose)

C. Evidence of causative Alzheimers genetic mutation (family history or genetic testing), clear evidence of cognitive decline or gradual decline

Types: amnestic and non-amnestic

Amnestic and non-amnestic types of Alzheimers Disease

Amnestic = impairment in learning and recall of recently learned info

Non-amnestic = affects domains other than memory

• I. language presentation: word finding

• II. visuospatial presentation: spatial cognition, object agnosia, impaired face recognition, simultagnosia, and alexia

• III. executive dysfunction: impaired reasoning, judgement, and problem solving

Simultagnosia

Neurological condition where individuals are unable to perceive more than one object in their visual field at a time

Pathology for Alzheimers disease

Presence and accumulation of amyloid (AB) plaques and neurofibrillary (Tau) tangles. Decreased brain structure volume which progresses i.e. early stages have changes in deep structures e.g. hippocampus while later stages show widespread change and reduction e.g. cortex. MRI scans show show shrunken cortical tissue and increase in ventricle and fluid (black) area.

Atypical Alzheimer’s disease

People with alzheimers pathology e.g. amyloid can have different clinical presentation including no memory related problems. Atypical forms of AD have an early onset with distinguishing clinical variants = pathological biomarkers, neuroimaging, neuropsychological performance, and reported behaviour/psychiatric symptoms. Atypical AD don’t follow progressive worsening of episodic memory.

Subtypes of atypical AD

• Primary progressive aphasia (PPA) logopenic variant = primarily affects language ability

• Posterior cortical atrophy (PCA) = primarily affects visual ability

• Frontotemporal variant/behaviour dysexecutive variant = primarily affects executive ability

Primary progressive aphasia (PPA)

Neurodegenerative condition which causes progressive change to language abilities including 3 main subtypes:

• Progressive non-fluent aphasia (PNFA) = difficulties with language production and grammar but can understand others

• Semantic variant/dementia (SD) = difficulty understanding and naming words but no difficulty in producing language

• Logopenic progressive aphasia (LPA) = tangential speech and memory problems

Initial brain changes are in the left hemisphere with PNFA & SD not having presence of amyloid while LPA does

Neuropsychological assessment for PPA

Determine if it’s PPA → determine which subtype it is. This process involves measuring performance in language skills i.e. naming, speech (repetition), grammar and comprehension to distinguish between semantic and non-fluent. Example: cookie theft task shows that ppl with PPA understand image but stutter/struggle with grammar while SD don’t struggle speaking but actually understanding the story and naming the words.

Posterior cortical atrophy (PCA)

Difficulties with higher order visual processing abilities including visual agnosia, simultagnosia, prosopagnosia, reductions in visual fields, anxiety and difficulty with praxis skills e.g. dressing and eating. Age onset is 50-65 years with the clinical course being that memory and other cognitive functions can become increasingly compromised and ppl can become cortically blind with widespread atrophy in cortex and medial temporal lobe after 5 years.

Posterior cortical atrophy diagnostic criteria

Core features = insidious onset, gradual progression, visual deficits in absence of ocular disease, preserved episodic memory, verbal fluency, insight, visual agnosia, simultagnosia, optic ataxia and apraxia, dyspraxia, environmental disorientation and absence of stroke/tumour

Supportive features = alexia, ideomotor apraxia, agraphia, onset before 65 yrs, and neuroimaging evidence

Clinical interview for PCA

Person often has insight about difficulties, feel anxious and commonly report difficulties reading lines of text, judging distances, identifying static objects and problems with stairs and escalators. When further probed people report difficulties with posterior functions e.g. using common objects and making calculations.

Neuropsychological testing for PCA

Visuospatial skills (basic visual perceptual), verbal and visual language (reading and description/picture naming), verbal and visual memory, posterior brain function (arithmetic WAIS), working memory and executive function

Lewy body disease (LBD)

Onset between 60-90 years. Includes dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD) which have related clinical pathological features including the accumulations of Lewy bodies, combination of cognitive and motor dysfunction, fluctuations n arousal (e.g. incoherent/disorganised speech), visual hallucinations, and REM sleep disorder.

Neuropsychological assessment for LBD

Presentation = behavioural symptoms e.g. apathy, sleepiness and reduced alertness (fluctuations)

Testing = digit span (attention), verbal fluency (executive function), clock drawing, 3D cube, intersecting pentagons (visuospatial), verbal memory and language (naming tests)

• Recognition memory is better than recall and language is mostly preserved

Frontotemporal dementia (bvFTD)

Behavioural variant of dementia with onset of 45-64 years. Presenting features include progressive deterioration of personality, social cognition including early apathy, uninterested in previous hobbies, impulsive/disinhibited, loses interest/appreciation of appearance, reduced empathy, rude or blunt, disorganised, stereotyped speech, mental rigidity, changes in early behaviour and lack of insight. Median survival = 3 - 4.5 years

Discriminating factors from bvFTD and AD

Frontotemporal dementia distinguishing characteristics include early apathy, changes in eating behaviour e.g. craving sweet food, stereotyped speech and disinhibited

Pathological characteristics of bvFTD

Hyperphosphorylated tau (40-50% of patients), TAR DNA binding protein (40-50%), and ubiquitnated fused in sarcoma (5-10%). Primary frontal lobe deficits and decrease in cortical volume.

Neuropsychological assessment of bvFTD

Early stages = may be difficult to detect any impairments on testing instruments however usually attention and executive functioning deficits with intact language, perception and visuospatial abilities

Demonstrates memory impairment, verbal repeating, pacing, tapping, and picking. Emotion processing tests show generalised deficits in facial emotion recognition

Limitations of the mild cognitive impairment diagnosis

Lacks consensus, depends on cognitive tests, overlaps with early dementia, based on subjective complaints (depending on personality and psychological state), doesn’t include clear biomarkers or underlying pathology, and limited clinical usefulness.

APA definition of resilience

Process of successfully adapting to difficult/challenging experiences through mental, emotional, and behavioural flexibility/adjustment to external and internal experiences which considers the factors that contribute to ppls adaptability e.g. social resources, perspectives, etc. Resilience is a process and an outcome.

Is resilience a trait or a skill

There is a genetic basis in resilience e.g. certain genes and heritability, but it isn’t a trait you have to be born with as resources and skills associated with resilience can be practiced and it involves behaviours, thought, and actions that anyone can develop

Resilience and mental health

Resilience is not the absence of mental disorders as becoming resilient often involves experiencing difficulty or distress as resilience helps people overcome adversity. People with high resilience are less likely to develop mental disorders and have exisiting disorder get worse + recover faster from adversity related problems

Covid-19 and resilience (Understanding America study)

Pre-pandemic resilience levels predict how well people coped through Covid-19 i.e. probability of mental distress. People with high levels of resilience pre-pandemic had lower levels of mental distress during the pandemic and people with low levels of resilience pre-pandemic had significantly higher levels of mental distress

Four pillars of resilience + 10 tips

Connection

1. Build strong social connections
Well-being: 2. Stay physically active, 3. Eat a healthy diet, 4. Be sleep smart, and 5. Stay mindful

Purpose:

Healthy thinking:

Four pillars of resilience + 10 tips

Connection

1. Build strong social connections

Well-being

2. Stay physically active

3. Eat a healthy diet

4. Be sleep smart

5. Stay mindful

Purpose and Meaning

6. Help others

7. Find your ‘why’

Healthy thinking

8. Adopt a flexible thinking style

9. Make room for unpleasant feelings

10. Keep the faith

Connection

Social connections are causal components of resilience and in stressful situations our social connections reduce the effects of stress. Rich social networks lead to less risky behaviours, more optimistic, increase treatment adherence, more adaptive coping styles and increase help seeking.

Social support

Refers to quality and function of social relationships e.g. social interactions, emotional support, material support, etc. Strong social support is linked to better mental health for uni students, widows, new mothers, and unemployed adults. Social support also reduces exposure and adverse psychological effects during disasters leading to greater reduced depression and psychological distress.

Trier social stress test

Study tells participants that they are taking a job interview. The interviewer shows no positive reinforcement and surprises them with a maths test to increase stress. Found that when people were allowed to have a friend waiting for them after the interview they had lower levels of cortisol in saliva i.e. stress due to the social buffer

Social isolation

Loneliness and social isolation has the same impact on life expectancy as obesity, smoking, high BP and physical inactivity + people are 2-3x more likely to die. Poor social support is linked to onset and relapse of depression, seasonal mood disorder, and presence of co-occurring depression with other illnesses

Physical activity (well-being)

Physical activity is beneficial for all-cause mortality, academics, heart/bone health, mental health, gestational diabetes, etc. It is the single best thing for your health especially for mental health as PA is as effective for depression as therapy and medication especially dance. Study found that university students who exercised regularly before an exam had much lower levels of stress

Cross Stressor Adaption Hypothesis

Demonstrates that your body reacts to all stressors the same way e.g. stress hormones, heart rate and alertness. Physical activity puts the body under varying degrees of stress which trains the sympathetic nervous system to avoid overacting and switch off when stressor is gone

Eat a healthy diet (Well-being)

Diet is now recognised as one of the most modifiable factor in prevention and a non negotiable step in treatment of mental illness. A healthy diet helps optimise the gut microbiota which plays a role in cognitive and mental health (e.g. by regulating serotonin) and reduce inflammation. Study at UON found an association between resilience and dietary behaviours.

Be sleep smart (Well-being)

Sleep is essential for emotional functioning e.g. empathy, self-control, calmness, flexibility, motivation, and optimism. We need sleep for energy conservation, tissue growth,, memory encoding, reorganisation of neurons, muscle repair, enhanced immunity, emotional stability and clears waste from the brain (linked to neurodegenerative conditions).

Stay mindful (Well-being)

Mindfulness is the full awareness (open mind) + attentional control (focused mind) and can include mindful journalling, yoga, meditation and other spiritual practices builds connections, restores hope and primes you to deal with situations needing resilience.

Mindfulness study on firefighters

Found that mindfulness techniques superior to relaxation techniques for increasing resilience