Thursday, 24 April 2014

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.

Monday, 21 April 2014

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.

Saturday, 19 April 2014

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. 

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

Friday, 18 April 2014

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.

Psychological Therapies for Depression

 Beck's Cognitive Behavioural Therapy (CBT) aims to challenge and alter negative thoughts and beliefs through changing dysfunctional behaviours that are affecting the client and maintaining their depression.
 The therapy is separated into two parts: The cognitive part involves identifying faulty cognitions or irrational thinking processes that are affecting the client. This is done through the client giving examples of situations and what they would think and do in each. The therapist will then develop ideas on how to challenge and alter these irrational thoughts. The behavioural part involves setting homework for the client designed to help them challenge their own irrational beliefs. For instance, someone with anxiety disorder may not be able to cope in a certain situation; the homework would involve putting themselves in this situation in order to prove themselves wrong. This is known as 'thought stopping', where the client will identify the negative thoughts, challenge them, and replace them with positive thoughts. The client may also be asked to keep a journal during the therapy to monitor their thoughts, which would be reviewed in later sessions. 

 CBT has shown to be highly effective, with recovery rates of 60% for a 12 week programme. However, the success rate may depend on the skill of the therapist, as well as the type of person receiving the therapy. It is very time consuming and those with rigid attitudes who are resistant to change may not have such an effective outcome.
 CBT is often combined with drug therapy, and whilst drugs are said to be more effective in the acute phase of depression, CBT is more effective in the latter phase. To validate this, psychologist Keller analysed  the effect of CBT and found that drugs alone had a 55% success rate in the reduction of symptoms, whereas CBT alone had a 52% success rate. Both used in conjunction with one another however resulted in an 85% success rate, which is a remarkably clear improvement. Even so, an important issue to consider from this is that, considering CBT is often undertake after drug therapy, or possibly something else, it is hard to determine how much of the success and effectiveness is purely due to the therapy rather than any other treatment. Nevertheless, studies have shown it to be very effective in reducing symptoms of depression and preventing relapse.

 Rational Emotive Behavioural Therapy (REBT) builds on the methods of CBT and is very similar. It is an attempt to replace irrational thoughts with rational thoughts. The therapists task is to make the client aware of the irrational, negative or self-defeating ways of thinking. The therapist will challenge negative thoughts through argument and confrontation to defeat these irrational thoughts, and the result should be a significant increase in self-esteem. 

 The issues surrounding REBT are very similar to those surrounding CBT. Like CBT its effectiveness may be due to the skill of the therapist and the client's attitude towards the therapy, rather than the therapy itself.
 Furthermore, the success of REBT may also be due to the 'Hawthorne effect'; when people are being studied they may alter and improve their behaviour due to the increased attention. This may therefore change the end results and account for the success of the treatment. 
 There are several factors that make CBT a more appropriate treatment than REBT. In CBT, the client plays a more active role, and must gradually take control in order to manage things, whereas in REBT the therapist will play a more active, controlling role and the client is more passive, which may not be preferable to many undertaking or considering to undertake the treatment.
 Moreover, a major and concerning weakness with REBT is that those doing the evaluation of the clinical trials supporting or going against the therapy may have a biased view of the treatment. This therefore makes the findings potentially unreliable and forces one to question the overall effectiveness of the therapy.

 Interpersonal Therapy (IPT) is a psychodynamic therapy for depression which was devised by Harry Sullivan in the 1970s, and focuses on the individual's relationships with others, communication difficulties and how ones mood can influence how they relate to people close to them. 

 IPT aims to treat depressive symptoms by resolving interpersonal conflicts and to encourage the individual to make the best use of any available social support. 
 The first stage of IPT involves identifying the client's major problems in order to create a treatment contract. Clear measurable goals are then set by the therapist for the client to fulfil by the end of the treatment.
 Secondly comes the intermediate stage which involves working through the problems identified with the therapist, and resolving the conflict which is stopping the person from moving on. Similar to the other therapies the patient will also be set homework to complete.
 Lastly comes the termination stage, which involves consolidating what has been learnt and looking forward to how these techniques and coping strategies will be applied in the future.

 Overall, a problem with these psychological therapies is that it is often difficult to measure the progress a patient is making. To increase access to more psychological therapies, the NHS is aiming to make practice more measurable and objective. Patient reported outcome measures (PROMs) have been introduced which involve patients completing a questionnaire based measure at each session, which records their current mental and physical state. This will lead to a clearer indication of the patient's progress, as well as the effectiveness of the therapies they are undertaking.

(For the exam, you'll probably only need to know two of these therapies at max if a question about this comes up, which is why I've spent less time on IPT, that and because I find it hardest to remember.) 

Psychological Explanations of Depression

"Unexpressed emotions will never die. They are buried alive 
and will come forth later in uglier ways."

Sigmund Freud 
 The psychological explanation of depression centres around Freud's Theory of The Unconscious Mind and Structures of Personality. His original view linked depression to the oral stage of development (0-18 months old). Children whose needs are not met by their parents at this stage can become over dependant, making them more vulnerable to depression because they spend a lot of time seeking approval.
 Freud further argued that depression is like grief, as it occurs as a reaction to the loss of an important relationship. The difference is that depressed people regard themselves as worthless. According to Freud, the individual will identify with the lost person, and the repressed anger towards the person will be directed at the face. This will reduce the individual's self-esteem and thus make him or her more vulnerable to depression.

 Freud's idea of depression occurring due to the loss of an important relationship can be supported by studies from Weller et al, who found that men who had lost their fathers during childhood scored higher on the depression scale than those who did not lose their fathers. 
 Similar to this, psychologist Bifulco found evidence 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. 

 Freud also distinguished between actual and symbolic loss; both can cause depression by causing an individual to re-experience childhood episodes, where they experienced the loss of affection from a significant person. This is supported by Kendler et al, who found 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. 

 In order to avoid loss leading to depression, one must engage in a period of mourning whilst recalling the memories of the lost one. The individual must separate themselves from the lost one, in order to reduce the inner-directed anger.

 The psychological/psychodynamic explanation has high face validity, as even if it is not favoured it is widely accepted that childhood experiences can predispose an individual to mental illness in adulthood. However, early loss of course does not always predict depression. In fact, fewer than 10% of individuals who experience major losses go on to develop depression, making the findings of studies used to support Freud's theory difficult to generalise to the wider population.

 [Freud predicts that the individual's anger is turned inwards on themselves, yet often it is turned outwards on those closest to them instead.]

 A major weakness in Freud's theory regarding psychological explanations of depression is that it still severely lacks empirical support, therefore making it neither verifiable or falsifiable. 

Biological Therapies for Depression

 SSRIs are said to be the most commonly prescribed antidepressants. This can include drugs such as Sertraline and Citalopram.  Monamine Oxidase Inhibitors (MAOIs)  control the activity of certain neurotransmitters; chemicals in the brain which allow brain cells to communicate  with one another. The main neurotransmitters thought to be involved in depression are serotonin and noradrenaline.

 MAOIs are first-generation antidepressants which inhibit the production of monoamine oxidase, an enzyme which breaks down neurotransmitters. Through hindering the process it allows them to stay in the body longer, and thus increase the levels of serotonin and noradrenaline in the synapse. 

 Tricyclic drugs prevent the uptake of both serotonin and noradrenaline by the presynaptic neurone after it has been fired. This leaves more neurotransmitters in the synapse, in order for the next impulse to be made much easier. Cost effectiveness can also be taken into account with these antidepressants, as tricyclic drugs are just as effective as SSRIs, but less expensive, however SSRIs are said to be far more effective in very severe cases of depression.

 A concerning issue underlying the use of antidepressants is that they take a significantly long time to take effect (around 2-4 weeks), which weakens the effectiveness of the drug. Furthermore, they do not produce a cure for depression, as they only seem to treat the symptoms rather than the cause of the disorder. On the other hand, recent tests have shown 50-65% of patients given antidepressants showed signs of improvement, compared to a success rate of 25-30% for those in the same test given a placebo. Arguably these results highlight that antidepressants are in fact very effective, however they may force one to consider that due to placebo effects, the success of the drug may be psychological as well as pharmacological. 
 Additionally, antidepressants can cause a wide variety of side effects, ranging from dry mouth to suicidal thoughts, which may encourage the patient to stop taking the medication. MAOIs have proven to be very effective for many patients suffering from depression, however are problematic because out of all antidepressants they are said to have the most side effects. It is therefore debatable whether or not this is an appropriate drug to be prescribed to patients suffering from depression if the drug violates the 'protection from harm' ethical guideline. Speaking of which, there are ethical arguments that drug therapy is dehumanising and takes away the sense of personal responsibility and freedom. However, a short course of anti-depressants offer people a relief from depression and can allow them to regain the motivation to engage with other therapies to help overcome their disorder. 

 Electro Convulsive Therapy (ECT) may be advised if an individual has a very severe case of depression, however it should only be used if antidepressants have not worked.
 The modern technique involves putting the patient under a short-acting anaesthetic and muscle relaxant  before the shock is given, oxygen is also administered. A small amount of current around 6 amps is then passed through the brain, lasting around half a second, which results in a seizure roughly lasting a minute. This is usually given 3 times a week for up to 5 weeks.

 ECT appears to be highly successful for severe cases of depression. Psychologists have reviewed studies on ECT and have found it to be effective in over 60% of psychotic depressed patients, and researchers have also found that it seems to work where drugs don't. Psychologist Janicack found that around 80%of severely depressed patients responded positively to ECT, compared to 64% to drug therapy. 
 On the other hand, psychologists have found ECT to have a high relapse rate within a year of treatment, suggesting that it is only a temporary relief rather than a cure. Recent tests have found it to be very effective in the short-term, but smaller than the effect obtained by drugs.
 A primary disadvantage with ECT are the ethical issues surrounding its use and the extent to which the patient is protected from harm. Many patients dislike it as it is potentially dangerous, and their consent is problematic because they are forced to have the treatment. The Debt of Health checked 700 patients who had been sectioned and 59% of them had not been consented to treatment.
 Another issue igniting the debate on ECT's appropriateness is that doctors still have very little idea how it works. However, it is quick compared to drug therapy, and is sometimes the only option. 

Biological Explanations of Depression

 According to psychologists from a biological perspective, individuals may develop depression due to genetic inheritanceChildren can inherit different types of the 5H77 gene from their parents, which is responsible for the transmission of serotonin, therefore having a history of depression in the family can increase ones chance of developing it. This is known as genetic predisposition.  In support of this Harrington et al found that people who share a 50% genetic relationship with someone with depression have a 20% of developing the disorder, compared to 50% of the general population. This highlights strong evidence confirming the biological explanation of depression, since it supports the basic prediction of genetic theory. However, although the genetic explanation makes sense at face value, many people who have a family history of depression never go on to develop it, and people with no family history of the disorder can develop it, therefore genetics cannot be the sole explanation for depression.   

 Nonetheless, the findings from Adoption Studies can be applied to support the genetic argument. Wender et al studied adopted children with depression and found that their biological relatives were 7 times more likely to have depression than the adoptive relatives. This further suggests that there is a genetic factor in depression, and although other adoptive studies have found a relatively weak correlation when studying this they have found a similar result. 
 Additionally, twin studies have proven to be effective in investigating the possible link between genetics and depression, where one twin would have the disorder and to investigate the likelihood (concordance rate) of the other twin having it. McGuffin et al found a 46% concordance rate among Mz (identical) twins, compared to 20% among Dz (non-identical). Both these rates are dramatically higher than the general life time risk of developing depression, applied to the general population, however due to the fact that the concordance rate is not 100% this study therefore again highlights that genetics cannot be the sole explanation for depression. One must also consider the environment the twins were raised in, which could be a contributory factor to why they may develop depression.

 Neurotransmitters can play a significant role on the development of depression; dopamine and noradrenaline are said to be the main ones involved in depression. It has been found that low levels of noradrenalin can lead to depression, and high levels can lead to the mania's depressive symptoms and suicidal tendencies. Additionally, the serotonin theory suggests that high levels of serotonin can lead to depression.
 In support of this, Martin et al found impaired serotonin levels transmitting in people with depression, which of course accepts the basic predictions of the serotonin theory. 
 Rosen et al presented evidence supporting biochemical theory through comparing the substances found in urine samples of depressed people and a control group. It was found that compounds produced as a by-product of the action of enzymes activating serotonin and noradrenalin were present in smaller amounts of the depressed urine. This shows the impact neurotransmitters can have in depression.

 Depression can also occur due to hormonal imbalance. Depressed people tend to have high levels of cortisol, which can lead to depressive symptoms such as suicidal thoughts, and low levels of noradrenalin means that the hypothalamus is unable to regulate these levels. If these levels are not lowered by the means of drugs, the depression lifts.  
 In support of this, psychologist Suomi has been studying rhesus monkeys in order to measure the effect of genes on depression. Through this he has found that 20% of monkeys are born with a genetic tendency to depression and anxiety, and in a laboratory environment they produce cortisol when experiencing stress. On the other hand, whether or not these monkeys develop depression in later life depends on the attachment formed with their mothers. 
 Unfortunately this study holds several weaknesses which make it difficult to apply to humans as well as the real world. Firstly the fact that much of the research was conducted under artificial settings in a laboratory gives it low ecological validity due to the control over extraneous variables, making the findings inapplicable to a real life situation. Furthermore, a huge disadvantage within this study, and the biochemical explanation of depression in general, is that 
much of the studies used to support its proposals are not only unethical due to the use of animals but also anthropomorphic. It is therefore difficult to extrapolate the findings in hormonal imbalance from non-human animals 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. 

(I've highlighted the bit on anthropomorphism because its key to learn when writing an essay. Loads of research studying loads of different approaches use animals, which you'll see through further reading and revision, so remembering this sentence can significantly maximise your Ao2, as well as make your essay sound a lot more fluent and sophisticated.)