Reducing Addictive Behaviour - Psychology / Cognitive Interventions

  In Cognitive Behavioural Therapy (CBT), the client is trained in social skills and developing strategies, which involve the behaviour of both cognitive and behavioural assumptions in order to challenge the client's faulty thinking.
  According to the therapy, behaviour can be unlearnt, and correcting faulty thinking will help abstain addiction. CBT programmes often ask the addicts partner to help them improve their social skills and problems.

  In support of this intervention, Well et al researched CBT and found it to be highly effective, however no more effective than other psychological therapies. Nonetheless in 2003, CBT appeared a more preferable treatment by therapists in the addiction field. An advantage of the intervention is that it helps the individual gain control of their behaviour, even if it doesn't help them cease to perform it.
  Further research has also found that people with low levels of addiction responded in a more favourable manner towards CBT. It is also even more effective when used in conjunction with biological interventions, such as drug therapy, however, this makes it hard to measure CBT's individual effectiveness.


  Motivational Interviewing (MI) is an intervention which focuses on trying to help addicts find motivation to quite their addiction (obv). The therapist will try to encourage the addict to review their addictive habits, and weigh up the pros and cons it has on their life. The aim is to get the addict to give their own reasons for making a change to their addictive habit 

 MI assumes that issues with motivation are not due to personality, but that motivation is something that can be readily damaged. Research has shown MI to be highly effective in helping those with substance abuse issues. Moreover, Research from Burk, who conducted a meta-review on MI, found that it led 56% decrease in alcohol consumption, further confirming it to be a very effective intervention for reducing addictive behaviour.

The Cognitive Model of Addiction - Applied to Smoking

  ▲ Initiation   ▲ Maintenance   ▲ Relapse

  The concepts of of coping and expectancy can be applied to this model.
 Perhaps people begin to smoke because they are bored and it relieves their mood. The smoker's expectancies of smoking can be wide-ranging. It may facilitate social interaction, make them look more attractive or perhaps control their appetite and weight. Regardless if these are true these expectancies may motivate someone to initiate a smoking addiction.
  Self efficacy can also be applied to initiating smoking; the smoker may in fact know their habit is dangerous and addictive however believe they are totally in control of their behaviour.

  Maintenance can be addressed through reference to 'Beck's Vicious Circle' of addiction. 
 The individual may be unhappy or lead a stressful life and may therefore start smoking. However this may lead to the ill-health problems associated with smoking, as well as financial difficulties and social isolation. All these problems may result in a negative mood; the person will then reach for a cigarette to relieve this negativity, and thus the cycle continues.
  The concepts of coping may also explain the maintenance of smoking.
 People will continue to smoke because they believe it enhances their ability to concentrate for longer, or carrying out repetitive tasks without getting bored.
  Self efficacy is also an issue in the maintenance of smoking.
 The individual may feel they can give up whenever they feel like doing so, however it could that once initiated they are unable to cope with the side effects of withdrawal, and therefore not give up.

  A smoker may relapse due to due to coping, expectancy and self efficacy. 
 The negative feelings of withdrawal can easily be relieved if the person smoked a cigarette. Relapsed smokers may also feel that if they have given up once, they are able to whenever they want. They may therefore believe that a return to smoking won't be permanent because they have had the experience of quitting before.

Reducing Addictive Behaviour - Biological Interventions

 Nicotine Replacement Therapy (NRT) includes devices such as gum and patches, which help reduce the symptoms associated with withdrawal from nicotine, through stress relieving effects that provide a positive reinforcement. 

 Nicotine gum and spray give an almost immediate hit of nicotine. Patches on the other hand release a gradually sustaining amount of nicotine throughout the day, and therefore do not provide as much positive reinforcement. 

 NRTs appear to desensitise the brain's nicotine receptors, which makes smoking whilst on one of the drugs a lot less satisfying. 

 NRT has proven to be very effective in relieving withdrawal symptoms from tobacco, even in small doses. However, it only seems to treat the biological side of  the addiction, and does not target the associations smokers have with certain times of the day and places with smoking.

 Smokers are also very prone to relapse whilst on NRT, as it delivers nicotine to the bloodstream at a much slower rate than a cigarette does. On the other hand, it is a much healthier alternative to smoking, and is considered less harmful. 

 Nonetheless, nicotine still has its limitations on health; it increases heart rate and blood pressure, and can aggravate diabetes. Additionally, although it is not a direct cancer causing chemical, animal research has suggested that it promotes tumour growth. 

 Bupropion is an antidepressant which increases the levels of dopamine and noradrenalin in the brain. This stimulates the effect of nicotine on the neurotransmitters, which is thought to block the nicotine receptors in the brain.

 Effectively this makes the person taking the drug less likely to experience positive effects from smoking.

 Psychologists such as Watts have found this to be a very successful method in treating smoking addicts.

 Champix is another antidepressant, which works exactly the same way as Bupropion by increasing the levels of dopamine and thus reducing nicotine levels in the brain.

 Clinical trials have found this to be even better than Bupropion in helping people stop smoking. It has also shown to reduce the likelihood of relapse in smokers who had been abstinent after 2 weeks of therapy.

 Overall, all biological interventions have shown to be more effective than a placebo in clinical trials. However, these types of medical treatments usually only treat withdrawal symptoms rather than the cause of the addiction.

 Furthermore, they assume that addiction is a disease, which grants a more humane understanding on addiction, as it takes away individual blame. 

 On the contrary this also takes away the individual's free will,  suggesting that they have no control over their addiction. A person may be fully capable of changing their addictive habits by themselves, but biological interventions rely on the deterministic assumption that this is not possible.

The Biological Model of Addiction - Applied to Smoking

▲ Initiation  ▲ Maintenance  ▲ Relapse

 - The biological model of smoking proposes that people will initially take up smoking due to genetics. Studies from Lerman et al have shown that people who inherit the SLC 63A-9 gene are less likely to take up smoking than those without it. This gene is responsible for controlling levels of dopamine in the brain.


 - According to the physical dependance theory, people can become addicted to smoking through developing a tolerance to nicotine. As a person begins to smoke they need to smoke more and more in order to maintain the pleasurable feeling it gives them. Stopping this activity therefore may well result in unpleasant withdrawal symptoms, unpleasant side effects ranging from shaking and sweating to increased heart-rate and blood pressure. 
 Psychologists have found evidence showing how extremely addictive nicotine is. Schachter studied the effects of nicotine and found that smokers with low-nicotine cigarettes smoked more than smoked more than smokers with high-nicotine cigarettes. The higher content allowed smokers to reach the required level of nicotine with fewer cigarettes. This was referred to as the 'nicotine regulation model'. 

 Smoking nicotine activates of the 'pleasure centres'  in the brain which enhances the reward value of other stimuli, making the reward gained from things much better. Stimulation procedures from Harrison et al can be used to support this. Through training rats to self-administer a small electrical stimulation to the reward centre of the brain, whilst injecting some of them with nicotine, he found that rats with nicotine needed a lower electrical stimulation to have the same level of reward. When the nicotine exposure was stopped, withdrawal symptoms occurred and the self-stimulation increased. This of course supports that people will maintain their smoking addiction because it makes everything else seem a lot more enjoyable. 
 However this study comes with major limitations. Not only is it unethical due to the use of animals and their lack of protection from harm, but it is also ratomorphic. It is therefore difficult to extrapolate the findings in addiction from rats to that of humans, as we are said to have a far more complex brain structure and live in a more social and emotional world. Contrary, some psychologists, particularly from an evolutionary perspective, would argue that the same characteristics apply across species. 

(For those who might not know - Ratomorphism = anthropomorphism but strictly regarding the use of rats)

 There is also a genetic factor in the maintenance of smoking, as Sabol et al showed that the SLC 63A-9 was also extremely important in enhancing people's ability to stop smoking.

 - Relapse also refers to the physical dependance theory as previously mentioned regarding the maintenance of the addiction. Stopping smoking after developing a high tolerance to nicotine can result in high withdrawal symptoms, which can easily be avoided if the individual continues to smoke.

 In support of this, Lerman et al showed that smokers deprived of nicotine during withdrawal showed increased blood flow in certain parts of the brain. The findings also suggests that certain people are more prone to craving due to changes in brain chemistry. This research is useful in helping us understand what encourages a smoker to relapse and why some are more likely to relapse than others.  

 Overall the biological model of smoking appears to see the addiction as a disease, emphasising the idea that it is the fault of the individual alone and that regardless the treatment it is irreversible. This leads to the issue of it being a deterministic approach, in the sense that the cause is specifically pinpointed to a specific set of genetic factors, and if someone has these they will have the addiction, thus it does not scope for the individual's free will. Furthermore, the fact that it reduces the complex idea of addiction strictly down to genetics and brain chemistry leads to the issue of it being a reductionist approach to addictive behaviour.

 Nonetheless, there is much research and empirical evidence to support the proposals of the biological model of smoking, much which has been conducted in recent years, allowing for high temporal validity with findings that are applicable to modern-day society.

So I've finished the topic of Depression and thought I'd end it with this video, which I strongly recommend be shown to anyone who may be suffering from depression. 

Cute

The next topic will be Addiction, I'll start uploading stuff on that as soon as I can but it might take a while so bare with me if you still give a shit, or start your own blog.

I've had an attempt at doing a 24 mark essay condensing and integrating all the explanations of depression together in the unlikely event that a question like this might come up in the exam. I've basically repeated everything I've already posted about the explanations but shortened and combined it together, as well as adding a paragraph on the cognitive explanations of depression at the end. I'm assuming this is enough Ao1 and Ao2 for 24 marks:

Explanations of Depression using Empirical Evidence (8+16)

▲ Biological   ▲ Psychological   ▲ Cognitive

 Biological explanations of depression explain how children can inherit different types of the 5H77 gene, which is responsible for the transmission of serotonin. Therefore, having a history of depression in the family can increase ones chance of getting it. This is known as Genetic Predisposition.
 Much research has been conducted to support the biological explanation that depression can develop due to genetic inheritance. Wender et al studied adopted children and found that their biological relatives were 7 times more likely to develop depression than the adoptive relatives. These findings suggest that there is a genetic factor in depression, and although other adoptive studies have found a relatively weak correlation studying this, they have found a similar result.
 Additionally, Harrington et al has presented supporting research, finding that people who share a 50% genetic relationship with someone who has depression have a 20% chance of developing the disorder. This shows strong evidence to confirm the proposals of the genetic explanation of depression, as like Wender it accepts the basic prediction of genetic theory. Nevertheless, Harrington et al's  study was compared to only 5% of the general population, therefore making it hard to generalise as a whole. 
 Using twins has also proven to be very effective in investigating how genetic factors link to depression, where one twin has the disorder and to investigate the likelihood (concordance rate) of the other twin having it. Supporting evidence comes from McGuffin et al, who found a 46% concordance rate in Mz twins, compared to 20% among Dz. Both these rates are dramatically higher than the general life time risk of developing depression, and highlight strong indications that depression can be genetically inherited. However the fact that these concordance rates are not 100% shows that genetics cannot be the sole explanation of depression.

 Psychological explanations of depression centre around Freud's Theory of The Unconscious Mind and The Structures of Personality. His original view linked depression to the oral stage of development (0-18 months); children whose needs are not met by their parents at this stage can become over-dependant on people, which makes them more vulnerable to experiencing depression late in life. Freud further argued that depression is like grief as it occurs as a reaction to the loss of an important relationship. He distinguished between 'actual' and 'symbolic' loss, which can both lead to depression by causing an individual to re-experience childhood episodes where they experienced the loss of affection from a significant individual.
 This theory can be supported by studies from Waller et al, who found that men who had lost their fathers during childhood scored higher on the depression scale than those whose father did not pass away. Similar to this Bifulco found  that children whose mothers died during childbirth were more likely to experience depression in later life.  Although this study cannot support that depression occurs due to the loss of an important relationship (it is not possible for a child to develop an emotional bond with their mother during childbirth), it does however support Freud's theory that unmet needs from the parent during the oral stages of development can root to depression.  
 Furthermore, Kendler et al can be used to support Freud's assumptions, finding that female twins who had experienced parental loss through separation had an above average tendency to experience depression in later life, confirming the basic predictions of Freud's theory that symbolic loss can lead to depression. 

 The cognitive explanation of focuses on Beck's Cognitive Triad, which suggests that depression is caused by faulty cognitions; negative thoughts about ones self, the world and the future. The individual can become trapped by these negative thoughts, which can eventually lead to depression. It is also thought that we can develop cognitive distortions, such as overgeneralising things and 'selective abstraction' where an individual will focus only on one single aspect of a situation and ignore the others.
 Beck developed his theory into two schemas to characterise depression: sociotropy,  which involves basing self-esteem on the approval of others, and autonomy, which involves basing self-esteem on success and achievements.
 In support of this explanation, Evans et al conducted a prospective study and found that women with the highest scores for negative beliefs were more likely to become depressed than those with lower scores. This of course accepts the assumption from Beck that faulty cognitions are a factor of depression.
  Practical applications from Butler and Beck can also be used to support this approach. Through reviewing 14 meta-analyses on Beck's cognitive behavioural therapy they concluded that 80% of adults benefitted from it. It was also found to be more effective than drug therapy, and had a low relapse rate. This supports the predisposition that depression has a cognitive bias, and therefore suggests that knowledge of the cognitive explanation of depression can improve the quality of people's lives. 

The Classification and Diagnosis of Depression

 Clinical Characteristics  

 According to the DSM-V, one must show at least 5 specific symptoms over a period of two weeks in order to be clinically diagnosed with  major depressive disorder. One in particular that is absolutely essential to be shown in order for an individual to be diagnosed is of course a depressed mood, all day and nearly every day. Other symptoms may include Insomnia or hypersomnia nearly everyday/night and significant weight loss or gain; a 5% change in body weight must be seen in the space of a month. The individual may also have a diminished interest in pleasure nearly everyday, as well as feelings of worthlessness and excessive guilt. If an individuals shows less than 5 symptoms, they may be diagnosed with minor depressive disorder. 

 Reliability in Diagnosis

 Diagnosis is made more reliable if more than one psychiatrist gives the same diagnosis to an individual, which is known as inter-rater reliability.  

 The most reliable diagnostic instruments are SCID-I/Ps, 60-90 minute semi-structured clinical interviews which start with open-ended questioning and gradually move to more systematic questioning regarding symptoms and current lifetime disorders. Clinical judgement is also required in order to interpret the patient's answer and to make a decision on the diagnosis.

 Studies from Williams et al have found inter-rater reliability and diagnostic accuracy to be high, even when used by inexperienced interviewers.  On the contrary, Beck studied 2 psychiatrists with 153 patients to diagnose, and found that inter-rater reliability was as low as 54%, suggesting that the diagnostic tool is not always reliable. Although SCID-I/Ps assess whether or not the patient scores on 5 or more of the DSM-V symptoms of depression, it does not assess the severity of those symptoms. Furthermore, each symptom is said to have a threshold, and therapists may disagree on whether or not this has been exceeded for a given patient.

 As a result of these various issues a new method has recently been devised in order to improve the reliability of diagnosis, known as test-retest reliability. This refers to the same individual being tested at a later a date, by the same measure and receiving the same diagnosis. 

 One of the measures which has been tested is the Beck Depression Inventory (BDI), a 21-item self-report questionnaire. This method of test-retest reliability has been confirmed to be very effective by Beck himself, who found a significant correlation level of 0.93 using BDI for test-retest reliability. However, the reliability of these findings must be questioned due to the possibility of investigator bias, as Beck would of course be in favour of a method he created himself, and would therefore perhaps purposely highlight it to be highly effective in his own study.

 There is also a possibility that the classification and diagnosis of depression is gender biased, as it has been proposed that there is no real difference between men and women suffering from depression. This is because while women are more likely to seek help for depression, men rarely do so and are therefore never included in the statistics. To support this, Bertakis et al found that clinicians in the Yale Family Study were more likely to diagnose women as depressed, even when the level of severity was equal to a man. This of course highlights that there may be a gender bias in diagnosis.

 Additionally, knowing that both diagnostic systems were initially devised by white middle-class males indicates that they are potentially ethnocentric, as they are rooted in western societies. The characteristics for a person to be diagnosed as depressed are of course totally different across cultures. This was shown by Davidson and Neale, who found that Asian cultures encouraged individuals to show no emotion whilst experiencing turmoil, whilst Arabian cultures encouraged the outpouring of emotion at difficult times. Without this knowledge, individuals showing overt emotional behaviour in western societies may be deemed abnormal in this context.

 Labelling and stigmatisation also appears to be a prevailing issue in the classification and diagnosis of depression.  Psychiatrist Thomas Szasz argued that diagnosis is made on political and social backgrounds, and that this then leads to those who differ from society's norms being excluded from the mainstream population. Those with depression are therefore stigmatised by society once they are diagnosed, and will act in accordance to the label they are given in order to fit in.