The biomedical model and biopsychosocial model of health have some similarities as they both aspire to treat the illness to aid recovery but their approach and understanding of disease and illness differs. The biomedical model looks at the disease but the biopsychosocial model incorporates social and psychological factors. Taylor (2006) states ‘that the biomedical model is a reductionist model as it reduces illness to low level processes rather than recognising the role of social and psychological processes’. Walker et al (2004) states the biopsychosocial model is seen as a more comprehensive approach to investigating and treating conditions such as rheumatic arthritis.
Whilst on placement on a medical ward a gentleman named Jack, a 38 year old man was brought in to hospital by the police after they found him unconscious with lacerations to his forehead and face. Jack is dependent on alcohol and has had several admissions due to alcohol related accidents. Jack first started drinking at the age of 15 when his mother died, his relationship with his father broke down shortly after that and Jack was often referred to as a failure by his father due to his excessive drinking. After being kicked out of the family home Jack went on to meet his wife, they were married for about 10 years in the meantime having 2 children, he had cut down his alcohol intake during his married years but when the marriage started to deteriorate he started depending on alcohol again and eventually found himself homeless, living in a hostel with no contact with his family and unable to keep his job because of drinking. Jack has had several admissions in the past with alcohol related accidents. Jack finds he will black out and wake up with lacerations, bruising or worse with no knowledge of how they had happened. This assignment will now focus on the biopsychosocial model to explain and understand Jack’s health and alcoholism. A look into the biological consequences of how alcohol affects the body and how Jack’s cognitive process and his blackouts have been affected due to his alcohol dependency.
The Department of Health (DoH) recommends that adult men should not regularly drink more than four units of alcohol per day. (DoH, 1995). Drinking between 22–50 units per week for men is defined as ‘hazardous’ drinking, with increased risk of developing physical harm, and drinking over these levels is considered as ‘harmful’ drinking (otherwise known as alcohol misuse), which is the pattern of drinking associated with the development of physical damage (Morgan & Ritson, 2009). For a diagnosis of alcohol dependency, the alcohol dependent person must present with 3 or more symptoms such as ‘neglect of activities, excessive use of alcohol, impaired control of alcohol consumption, persistence of alcohol use, large amounts of time spent in alcohol-related activities, withdrawal symptoms and tolerance of alcohol’ (Medline Plus 2011). In the UK 1 in 20 are alcohol dependent (Royal College of Physicians 2005).
Alcohol is a depressant which affects the central nervous system; its behavioural effects are a result of its influence on the response in the nervous tissue. Alcohol acts as a general anaesthetic with high concentrations of alcohol and at very low doses, it can appear to be a stimulant by suppressing certain inhibitory brain functions. ( 2009) However, as concentration increases, further suppression of nervous tissue functions produce the classic symptoms of intoxication: slurred speech, unsteady gate, disturbed sensory perceptions, and inability to react quickly ( 2009) When alcohol is ingested it is absorbed through the stomach and small intestine, and enters into the bloodstream through the small intestine, about 20% of the alcohol is absorbed in the stomach and 80% in the small intestine (Goodwin 1995). As the alcohol is water soluble, the alcohol is transported via the bloodstream throughout the body absorbing into the body tissues except body fat as these have a poor blood supply. Alcohol is metabolized in the liver which eliminates about 90% of ingested alcohol from the body. For the alcohol to be metabolized two enzymes are needed alcohol dehydrogenase which is mainly found in the liver which metabolizes the alcohol and aldehyde dehydrogenase which is the second enzyme and very toxic. Acetic acid which can be found throughout the body quickly turns the aldehyde into harmless acetic acid, it is then fed into the body’s metabolic system where the acetic acid becomes carbon dioxide and water either burning or storing seven calories per gram of alcohol in the process (Goodwin 1995). Through oxidation by the liver, alcohol is detoxified and removed from the blood preventing it from accumulating in the tissues and destroying cells and tissues ( 2009). The liver manages to breakdown alcohol at a fairly constant rate at 15mg of alcohol per 100ml of blood per hour so regardless of how much is drunk within an hour the body continues to breakdown alcohol at the same rate (Plant et al 2000). A minute amount of alcohol escapes metabolism in the liver and is excreted unchanged through urine, breath and sweat. The alcohol in breath can be detected and measured to calculate a person’s blood alcohol concentrations (BAC). ( 2009.)
The effect of alcohol on the body and the absorption rate depends on how much alcohol has been consumed; the presence of food in the stomach and the concentration of the alcohol (Hanson et al 2010) The blood alcohol concentration level largely determines behavioural and physical responses to alcoholic beverages (Hanson et al 2010). The higher the BAC level the more impaired a person can be although Levinthal (2002) states that ‘those who drink heavily, more regularly, and have longer drinking histories are likely to experience impairment at higher BAC levels than those who are light, or inexperienced drinkers’. This adaption is called tolerance (Manzardo 2008). Plant et al states that tolerance is an indication that the alcohol is beginning to take hold of the individual and that the drinker gets used to the effects of intoxication and is more adept at disguising or handling it. This occurs as regular alcohol intake reduces sensitivity, requiring higher quantities of alcohol to be consumed in order to achieve the same effects as before tolerance was established (NIAAA, 1995) Guthrie et al. (2008) states that tolerance develops as continued alcohol use depletes the neurotransmitters and the dopaminergic receptors become less responsive (O’Brien, 2008). Tolerance levels can also be influenced by socio-economic and cultural difference including diet, average body weight and patterns of consumption (Waldram et al. 2005). Jack had been drinking for about 20 years since the death of his mother, he had built up his tolerance to alcohol and was able to disguise his drinking habit until it had got worse and eventually was drinking every day. People who are alcohol dependent are often unable to take care of their health during drinking periods and are at high risk of developing a wide range of health problems because of their drinking (Rehm et al., 2003).
Jack has been suffering from blackouts due to his alcoholism and will now focus on the effects alcohol has on the brain and what maybe causing his blackouts. Alcohol absorption begins immediately in the mouth and oesophagus with small quantities entering directly into the blood system; the effects on the brain are almost immediate. (Insel et al 2011). Heavy drinking over many years may result in serious mental disorders and irreversible damage to the brain and peripheral nervous system leading to permanently compromised mental function and memory and alterations in other brain systems (Baxamusa 2010). Alcohol produces both stimulant and depressant effects within the brain and interacts with various chemical messengers (neurotransmitters) such as dopamine, serotonin, GABA, and the endorphins. Its main direct effect is probably upon the channels which permit charged chemicals to pass in and out of nerve cells, blocking or generating impulses, alcohol powerfully inhibits glutamate receptors and this is probably an important source of the impaired co-ordination and cognitive function (Robson 2002). Glutamate is a major neurotransmitter responsible for brain stimulation, and alcohol affects glutamate through its inhibitory action on N-methyl D-aspartate (NMDA)-type glutamate receptors, producing amnesia (for example, blackouts) and sedation (Krystal et al., 1999).
There are several parts of the brain that are affected by alcohol which in turn have an effect on the rest of the body. The cerebellum co-ordinates muscle movement and the cerebral cortex initiates the muscular movement by sending a signal through the medulla and spinal cord to the muscles. As the nerve signals pass through the medulla, they are influenced by nerve impulses from the cerebellum, which controls the fine movements, including those necessary for balance. When alcohol affects the cerebellum, muscle movements become uncoordinated. (). The cerebral cortex processes information from your senses, processes thoughts, initiates the majority of voluntary muscle movements and has some control over lower order brain centres. In the cerebral cortex, alcohol can affect thought processes, leading to potentially poor judgement, depresses inhibition, leading one to become more talkative and more confident and blunts the senses and increases the threshold for pain (). The medulla (brain stem) influences or controls body functions that occur automatically, such as your heart rate, temperature and breathing. When alcohol affects the medulla, a person will start to feel sleepy, increased consumption can lead to unconsciousness and can be fatal if it is excessive. (). The hypothalamus controls and influences many automatic functions of the brain (through the medulla), and co-ordinates hormonal release (through the pituitary gland). By inhibiting the pituitary secretion of anti-diuretic hormone (ADH), alcohol also affects urine excretion. ADH acts on the kidney to reabsorb water, so when it is inhibited, ADH levels drop, and the kidneys don't reabsorb as much water and the kidneys produce more urine. ()
A Blood alcohol concentration in excess of 150mg is associated with periods of impairment or total absent memory, these memory blanks may last several hours and are commonly known as alcoholic blackouts (Plant et al 2000) Schuckit (2008) states that because alcohol is a central nervous system depressant, people who consume large quantities of alcohol frequently experience blackouts or acute retrograde amnesia during periods of intoxication and should be viewed as an important warning sign of problem drinking whilst Goodwin (1995) states that blackouts represent episodes of amnesia during which subjects are capable of participating even in salient, emotionally charged events as well as the mundane events that they cannot remember. Jack had frequent blackouts while he was drinking and this would often be the cause of his injuries as he would not be able to understand how he got his injuries. White (2004) states that there are two types of blackouts partial (fragmentary) or complete (en bloc) blackouts, people who experience en bloc blackouts are unable to recall any details whatsoever from events that occurred whilst they were intoxicated. Fragmentary blackouts involve partial blocking of memory formation. Goodwin (1995) states that people with fragmentary blackouts often become aware that they are missing pieces from events only after being reminded that the events occurred. Heavy chronic alcohol consumption has been linked to structural and functional changes in the medial temporal lobes and fronto-striatal circuits, brain regions known to mediate higher cognitive function (Berman 2007) The Hippocampal anterior thalamic circuitry is thought to be critical for recollection, whereas familiarity can be supported by medial temporal lobe regions outside the hippocampus, such as the rhinal cortices and their thalamic projection regions in the mediodorsal nucleus Eichenbaum (2007) Both acute and chronic alcohol consumption are detrimental to hippocampus-based learning and memory mechanisms Herrera (2003).
In 2009/10 there were around 1,057,000 admissions related to alcohol consumption where an alcohol-related disease, injury or condition was the primary reason for hospital admission or a secondary diagnosis costing around 3 billion pound a year equivalent to 12% of NHS expenditure (Alcohol Concern 2010).
PSYCHOLOGICAL
Jack could not cope, he drank to forget and to help him relax and cope better with stresses of everyday life, although Jack was not suicidal he would often say that he did not care if the alcohol killed him as he would not have to deal with his problems and would see his mum again. Jack started drinking at the age of 15 when his mother died in a car crash, his relationship with his father broke down as soon as he started drinking and was often referred to as a failure. NICE 2011 guidelines on alcohol dependence and alcohol abuse state that adverse life events can trigger excessive drinking and may predispose to the development of alcohol dependence, this is particularly apparent following a bereavement or job loss. Thompson et al (2008) suggested that there are two distinct types of alcoholism. Type 1 alcoholism affects both men and women and requires the presence of a genetic as well as an environmental predisposition and can start later on in life and can take on either a mild or severe form. Type II alcoholism, affects mainly sons of male alcoholics, is influenced only weakly by environmental factors, often begins during adolescence or early adulthood, is characterized by moderate severity, and usually is associated with criminal behaviour and that additional studies have demonstrated that type I and type II alcoholics also differ in characteristic personality traits (e.g., harm avoidance and novelty seeking respectively. Jack’s drinking would correspond with Type 1 alcoholism as he mainly drank as a coping mechanism, although started at an early age but am unsure of any genetic connection with alcoholism and would not like to assume otherwise.
Khantzian (1997) states that individuals become addicted as the result of their attempts to adapt their heightened reactions to stress and alleviate their feelings, while attempting to block out negative emotions or use avoidance as their sole coping strategies. Folkman and Lazarus have defined coping as ‘the person’s cognitive and behavioural efforts to manage the internal and external demands of the person–environment transaction that is appraised as taxing or exceeding the resources of the person’ (Folkman et al., 1986), this could mean that the stressfulness of a situation is dependent on the person and how they cope with the environment and resources around them. Moos (2002) defined two basic modes of coping. Approach: adolescents with an approach coping style are more likely to resolve their stressors and experience more self confidence, less depression and dysfunction and then avoidance: adolescents who depend more on avoidance coping tend to experience maladjustment and continued difficulties (Holahan and Moos 2002). The approach and avoidance systems are associated with a distinct profile of brain regions and emotional states, facilitating different behavioural outcomes (Friedman and Forster 2005). Jack had a lot of stress from the death of his mum, his divorce, losing his home and job and instead of approaching his problems; he turned to avoidance and turned to drinking to cope. Friedman and Forester state that avoidance could be turned into approach as people turn a negative situation and gain something positive out of the situation. In Jack’s case he did find a positive as after being kicked out of the family home he married and went on to have children but then it turned into a negative as when things started going wrong in his marriage he started drinking again.
The health belief model was developed initially by Rosenstock in 1966 and further by Becker, it is a useful framework to predict preventative health behaviours and also the behavioural response to treatment in acutely and chronically ill patients (Ogden 2007). Edelman 2000 states that a given health behaviour is a function of demographic and socio-cultural variables as well as four factors: perceived susceptibility; perceived severity; perceived benefits/barriers and cues to action and that these core beliefs should be used to predict the likelihood that a behaviour will occur, each of these perceptions either individually or combined can be used to explain health behaviours. Perceived susceptibility: In regard to susceptibility, individuals vary greatly in terms of
their perceived vulnerability. Perceptions range from total denial of susceptibility to perceptions of imminent risk (Strecher & Rosenstock 1997). For instance, people without a family history of diabetes may not perceive themselves to be susceptible to this condition. Alternatively, those who have a strong family history of diabetes may believe that they are highly likely to develop it. (Strecher & Rosenstock 1997). Perceived severity: Perceived severity is thought to influence health related behaviour and refers to the supposed consequences of contracting a health problem or leaving it untreated. Consequences may involve physical as well as a psychosocial outcomes (Strecher & Rosenstock 1997). This could mean that unless a person feels threatened by an illness they are likely to leave it untreated and as such, the perceived benefits of their behaviours must outweigh the presumed costs (Strecher & Rosenstock 1997). Perceived benefits/barriers: another factor that influences behaviour is perceived barriers, or the negative aspects of particular actions. Barriers may include financial costs, inconvenience, or pain (Strecher & Rosenstock 1997). A person may find it difficult changing from oral medications to insulin and believe the discomfort of injections will outweigh the benefits of improved health. (Strecher & Rosenstock 1997). Positive changes such as guidance and education can be implemented to allow barriers to come down to allow for the benefits. Cues to action was added to the health belief model at a later date and is a cue to action to help a person from wanting to make a change to their health to actually making the change. . (Strecher & Rosenstock 1997). This health change could be because of a related death which could increase a person’s perception of the illness or disease which could run in the family.
Rosenstock (1974) states that health behaviour change is initiated by readiness to take action, which is based on a balance of multiple beliefs and involves the balancing of beliefs regarding susceptibility, severity, behaviour efficacy, barriers and cues to action. Alongside the health belief model a looking into Jack’s locus of control could be considered. The term locus of control was coined by Rotter(1966) to encapsulate the idea of perceived control Rotter (1966), the notion underlying the term that individuals come to expect that things that happen to them are determined either by their own actions or beliefs or factors external to themselves as a result of luck or chance (Rodham 2010) For people who believe they have control over their lives and health have an internal locus of control and those that feel their lives are governed by chance or luck and have no control over their health have an external locus of control. When considering the health belief model with the locus of control theory a person with an internal locus of control would be more likely to benefit as they have control over their health and are in general positive people and succeed in achieving a positive outcome.
In view of this Jack appears to have an external locus of control as he has lost control of his drinking and health and is quite a negative person, he has lost everyone that is dear to him and continues on with his life feeling that he is not able to control what happens. Jack also suffers from low self esteem due to not having much confidence in himself and from the negativity in his life, this has contributed to Jack having feelings of hopelessness and feeling helpless which could be a contributory factor for his depression, this in turn can lead to a theory called "Learned Helplessness". Martin Seligman (1975) developed a model of depression based on the theory of learned helplessness. Over a long period of time a lack of personal control can affect a person’s health, negative situations and having no control can lead to learned helplessness.
Learned helplessness is a learned behaviour and can have the same feature and characteristics of depression, when a person is placed in a situation where a particular outcome is or appears to be independent of his responses, he learns that his responses are ineffective (Seligman 1975). The individual with learned helplessness will assume that any responses he makes will be ineffective and will not change the outcome. Learned helplessness also affects other psychological processes: motivation is reduced with no incentive to try new coping responses. Lack of motivation can cause feelings of hopelessness which makes them believe they are unable to do better for themselves and feel inadequate in themselves; all these feelings lead to depression and are related to learned helplessness. Seligman (1975). Other characteristics similar to depression are lack of positivity; creativity and healthy self image.
Jack, before his mother’s death may have been an outgoing person who had never experienced stress or bereavement and found that when it did happen he was unable to cope with his emotions and found solace in alcohol which caused a numbing effect “Learned helplessness is the giving-up reaction, the quitting response that follows from the belief that whatever you do doesn’t matter.” Seligman (1975). With the loss of his mother and breakdown with his relationship of his father, Jack may have reached the point where he could not control his drinking and did not care that he had.
SOCIOLOGY
Drinking alcohol is widely socially accepted and associated with relaxation and pleasure, and some people drink alcohol without experiencing harmful effects. However, a growing number of people experience physical, social and psychological harmful effects of alcohol (NICE 2011). Alcoholism, like all addictions has been long considered a ‘social disease’ caused by weakness of will, poor self control or lack of faith but has now been recognised as a biological disease (Gifford 2010). The effects of alcohol on body functions potentially can be so profound and destructive that alcoholism (severe addiction) is now considered a disease (NIAAA 2010). The World Health Organisation (1992) recognises alcohol dependence as a disease and a mental health disorder, it defines alcohol dependence or dependence syndrome as:
‘a cluster of behavioural, cognitive, and physiological phenomena that develop after repeated substance use and that typically include a strong desire to take the drug, difficulties in controlling its use, persisting in its use despite harmful consequences, a higher priority given to drug use than to other activities and obligations, increased tolerance, and sometimes a physical withdrawal state’. (WHO, 2011 pg 33).
Whilst the American Medical Association (2002) defines alcohol dependence as “a primary, chronic disease with genetic, psychosocial, and environmental factors influencing its development and manifestations." The WHO definition describes the effects the dependence a person will have for alcohol whilst the American Medical Association describes the disease and its influences which could have been based on the principles of the Biopsychosocial model of health, but both are classed as a disease, although there is an ongoing dispute as to whether this title is appropriate. The Baldwin Research Institute (2006) states that ‘the disease concept strips the substance abuser of responsibility and a disease cannot be cured by force of will; however, alcohol misuse can’. Alcoholics anonymous do not describe alcoholism as a disease they describe it as an illness; a progressive illness that can never be "cured" but which, like some other illnesses, can be arrested, they describe the addiction to be a ‘physical compulsion coupled with mental obsession’. (Alcoholics Anonymous 2010) but a study by McLellan et al (2000) called Drug dependence: a chronic medical illness, disagrees as his study goes on to look the diagnoses and comparing them to others, heritability, aetiology, pathophysiology and response to treatments of alcohol dependence and compared them with Type 2 diabetes mellitus, systemic hypertension and asthma, and concluded that genetic heritability, personal choice and environmental factors are comparably involved in the aetiology and cause of all of these disorders. The authors state that this provides evidence that alcohol (and other drug) dependency can be classified as a chronic disease. (McLellan et al, 2000)
Goffman (1963) argues that every society has stereotypical expectations of its members and stigmas occur when social norms are not being followed; and those who do not conform to social norms are referred to as a deviance (Goffman 1990) Deviance can be defined as not following a set of values and rules set by society, (Giddens, 2009). he also believes there are three distinct types of stigmas ‘‘Abominations of the body,’’ which referred to physical deformities; ‘‘blemishes of individual character for example weak will, dishonesty, mental disorders, addictions and unemployment (deviant individuals) and lastly ‘‘Tribal identities’’ referred to stigmatized conditions of race, sex, religion and national origin. Jack falls under the stigma referring to as ‘blemishes of individual character’ due to his alcoholism and unemployment. Denzin (1995) states the stigmatized alcoholic self may suffer from the imposition of a double, contradictory identity: ‘perceived as being sick, as suffering from an illness or a disease, but lacking will power and self-will’. Cumming et al states that whether it is an invisible mark or invisible stain, stigma acquires its meaning through the emotion it generates within the person bearing it and the feeling and behaviour toward him and those affirming it. These two aspects are indivisible since they each act as a cause or effect of the other
CONCLUSION
The biopsychosocial model of health was used to explore Jack’s health and wellbeing as this gave us an insight into his alcoholism. We were able to take a look at the biological damage that has been done to his body, the psychological reasons as to why he began drinking and the social influences that affected Jack and his drinking. With alcoholism on the increase, it is important to understand the reasons why people turn to alcohol, to help them through difficult times and understand that alcoholism is not a choice but a way of escaping or as a coping mechanism.
The biopsychosocial model is a great way of making patient care more holistic and realistic; there are often reasons why people do what they do. Jack did not seek any help when his mother died and turned to alcohol as a coping mechanism, which eventually took over his life. His alcoholic blackouts were a result of his chronic drinking but because of his external locus of control and learned helplessness took no control over his drinking.
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