Monday, 11 June 2012

HG Library: Cannabis induced caetextia, explaining the paradoxical effects of cannabis

We are delighted to mark the launch of our new HG Library with the release of this fascinating article, originally published in Vol 18, No 4 of the Human Givens Journal and the first of many in the new HG Library series.

The paradox that cannabis can both exacerbate and alleviate mental health problems such as depression, schizophrenia, paranoia and anxiety whilst giving rise to imagination and creativity has never been resolved. However, a new theory which places the human givens model for psychosis in a wider context could offer an explanation for the conflicting effects.

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Cannabis-induced caetextia: exploring whether the organising idea of caetextia can help resolve confusion about the effects of cannabis misuse and point towards better treatments.

Author: Ezra Hewing is a coordinator for Suffolk Mind’s Community Resource Service and also acts as a training consultant on mental health and wellbeing issues. Previously, he was a substance misuse worker and, before that, a coordinator, curriculum designer and teacher of personal, social, health and economic education (PSH E), emotional wellbeing and social skills, and offending behaviour courses in young offenders institutes, prisons and community centres. He occasionally works as a counsellor in private practice and gained the Human Givens Diploma in 2006.

When I was working as a substance misuse worker with 15–18-year-old males in a young offenders institute, cannabis use was a daily topic of conversation among them, as they yearningly recalled the last time that they had smoked or how much they looked forward to smoking it again on their release.

Intervention work with people who are at the ‘pre-contemplative stage’1 in their thinking about their substance use (ie they don’t even consider it a problem) tends to focus on raising awareness of the associated health (mental and physical) and legal risks. But the young men we were working with were at an age when the effects on physical health (such as heart and lung diseases and cancers, arising from smoking tobacco with cannabis) were not yet apparent; they were also heavily involved in subcultures where illegal behaviour might be perceived as a badge of honour or indicative of status, so neither of these areas of risk held much significance for them. Indeed, researchers have identified how using illicit drugs, and the culture that surrounds their use, can meet emotional needs 2 – as we might well expect, taking a human givens perspective.

When it comes to discussing the risks to mental health, there is even less to work with and workers are often reduced to falling back on citing statistical evidence for harm – for instance that users of the skunk form of cannabis are x times more likely to develop psychosis or are at x times greater risk of developing memory loss, etc. Human givens practitioners will know how empowering explanatory models for addiction and depression can be when they accord with a client’s model of reality but, to date, there is no such equivalent for explaining what is currently just a statistical link between cannabis use and mental health issues. Without a coherent explanation, statistical evidence is often met with cynicism: “doesn’t that only happen to people who already have mental health problems” and “isn’t cannabis sometimes legally prescribed as a painkiller?” Far from experiencing mental health issues as a result of cannabis use, many of the young people who spoke to me about it reported that cannabis helped them to relax and to feel less stressed or took their minds off their problems; those involved with musical subcultures claimed, further, that cannabis use boosted their creativity.

Some advocates for the legalisation of cannabis echo these claims, arguing that the mental health problems associated with cannabis arise only because of social stigma and persecution. Government changes made in recent years to the legal classification of cannabis have not brought clarity to the debate around possible links between cannabis use and mental ill health, and the increase in the potency of cannabis over recent years means that different generations of users do not share the same experiences of cannabis use. Media attention has predictably focused on headline-grabbing stories about the ill effects of cannabis and so has not aided public understanding in a balanced way. Even among professionals who subscribe to the view that cannabis use increases the risk to mental health, there is still a lack of agreement on a number of issues. For instance, does a discrete ‘cannabis psychosis’ exist? Can cannabis use actually cause schizophrenia? Does it contribute to the exacerbation of existing mental health problems? And, conversely, can cannabis really be used, as some pharmacologists are seeking to demonstrate, to alleviate the symptoms of mental health issues?

Despite the need for some clear answers, very many researchers seem still to be focused on gathering statistical data and only some researchers acknowledge the need to develop explanatory models and identify ‘mechanisms’ which might, in turn, lead to novel strategies for the treatment of psychoses attributed to cannabis use.3 Clearly, to use human givens terminology, a larger organising idea is needed, which would be able to explain the apparent contradiction of statistical evidence showing cannabis use increases the risk of mental health problems and reports of cannabis alleviating the symptoms of mental health problems. It should also be able to explain the diverse range of reported effects of cannabis use, including changes in mood and thinking style, increased creativity, relaxation and relief from the symptoms of mental distress and increased risk of developing depression and schizophrenia.



The pioneers of the human givens approach have already introduced a model which offers a highly plausible explanation for psychosis, and contends that waking reality is processed through the REM state, a state of consciousness with dreamlike qualities, the most prominent form of which is the dream state itself; unmet needs put so much strain on the REM state mechanism for discharging unexpressed emotional arousals through dreaming that it breaks into waking consciousness.4 Anybody who is familiar with the reported effects of cannabis use and the phenomena associated with the REM state will have noticed the correlation between the two, but just noting the similarities is not an explanation in itself. For a long time, whilst puzzling over the connection between the REM state and cannabis use, I assumed that cannabis must provide users with a short cut for accessing the REM state. Paradoxically, using cannabis suppresses REM sleep – which may be one reason why the development of cannabis as an antidepressant is being pursued, as sufferers from depression experience excess REM sleep. However, the state induced by cannabis is not the same as a psychotic episode.

I am going to suggest that an organising idea which places the human givens explanatory model for psychosis in a wider context can reconcile the apparent contradictions between the findings of researchers and the reports of users. Its central plank is caetextia, the term devised by Joe Griffin and Ivan Tyrrell to express an inability to appreciate context, which compels sufferers to fall back on one of two modes of thinking, designated leftor right-brained caetextia.5

Left- and right-brained caetextia

In caetextia sufferers who are left-brain dominant, caetextia manifests as a dependence on logical, straight-line thinking, better than average powers of concentration on external tasks, difficulties with communication and a reduced capacity to take into consideration the feelings of others – typical characteristics of Asperger’s syndrome. In those who are right-brain dominant, caetextia is expressed through “thinking by associations and a strong undisciplined imagination” which is left to “run free, making directionless, random associations”.5

There are a number of parallels between cannabis-induced behaviour and right-brained caetextia:
  • associative thinking style
  • lack of reasoning capacity
  • increased access to the imagination
  • loss of motivation (increasing the likelihood of needs not being met)
  • inability to distinguish quality of ideas
  • short-term memory loss
  • difficulty with maintaining attention
  • extreme mood swings and difficulty with regulating emotions
  • paranoia 
  • increased vulnerability to depression and psychosis
  • disassociation/loss of sense of self
  • increased appetite (hunger or ‘munchies’)
  • inability to discipline association of ideas and a dependency on black-and-white thinking
  • lack of reasoning capacity
  • difficulty with concentration
  • difficulty with the further development of a sense of self
Cannabis users often report enhanced creativity while under the influence of cannabis, producing ideas which seem profound and original to them at the time but not so impressive when reviewed in a down-to-earth state. The correlation between this phenomenon and Griffin and Tyrrell’s description of right-brained caetextia, as observed in clients, is striking: “Despite showing undoubted signs of creativity, they might not be able to discriminate good work from bad and can take their work intensely seriously, even if it isn’t particularly good”.5

Griffin and Tyrrell also assert that “undoubtedly, many highly imaginative right-brained people, who may be vulnerable to psychotic thinking, display caetextic tendencies that compromise their ability to connect to the ‘ordinary’ world … they spend much of the time disconnected from reality… .”5 If cannabis has the potential to induce right-brained caetextia, then users may also exhibit psychotic, disconnected thinking.

Right-brained caetextia sufferers and those under the influence of cannabis also exhibit the same deficits in focusing their attention. Attention capacity is shared between both hemispheres of the brain, but focused attention is largely located in the left anterior cingulate6 and is therefore difficult for right-brained caetextia sufferers to access. Laboratory researchers and users agree that, while the effects of cannabis are dose dependent (that is, the larger the dose the stronger the effect, and experienced users require larger doses than inexperienced users), cannabis use “impairs focused, sustained and divided attention”.7 It is the ability to divide and manage multiple streams of attention which is missing in both left- and right-brained caetextia sufferers, and which can result in increased vulnerability to mood swings, extreme anxiety and anger.5 Of course, not all cannabis users report equivalent effects on their emotions but, if this ability to manage multiple streams of attention becomes impaired as a result of cannabis use over a period of time, and in people less resistant to its effects, it might explain why some users experience the same vulnerabilities.

In a right-brained caetextic state, there is less access to the prefrontal cortex which is responsible for focusing on tasks, cognition and movement. 8 Researchers report that cannabis use impairs cognition and psychomotor functioning.7 The prefrontal cortex is also where self-will and determination are located9 and the inhibition of these functions could account for the loss of motivation associated with regular cannabis use.

The increased appetite observed both in users of cannabis and in right-brained caetextics is interesting. Research into what has been termed the default network setting (the ‘relaxed’ or idling state, which human givens practitioners will recognise as the REM state) shows that it requires 20 per cent more calories than when the brain is focused outwards, for example on a task.10

Another reaction to cannabis use, admittedly rarely reported, is the loss of a sense of self. This also has a parallel with right-brained caetextic states. Griffin and Tyrrell describe how it is normal to engage in daydreaming (the REM state in which we can imagine and rehearse other realities) but “if we were to become absorbed to the same extent as when we are dreaming, our sense of reality would disappear. While daydreaming, our brains are still contextually aware, so that, when we stop introspecting, we know very quickly where we are and can reorient ourselves. Whereas, in the dream state, we are totally ‘associated’: completely lost in the dream.”5

Evidence from neurobiology

If cannabis has the potential, at least temporarily, to induce right-brained caetextia, then can findings from neurobiological research enable us to identify the underlying mechanisms? Researchers have identified at least 60 active ingredients present in cannabis and research still needs to be conducted into how those ingredients act upon the user. There is, however, agreement about the action of the psychoactive components delta- 9 tetrahydrocannabinol and cannabinol (the latter being the weaker of the two) and how they bind – or find their match – to cannabinoid receptors, which form part of the body’s relatively recently identified endogenous (innate) cannabinoid system. (Research is still in early stages but it appears possible that this system is involved in diverse functions of the body, including immunological, gastrointestinal, reproductive and cardiovascular, as well as the nervous system.) The cannabinoid receptors located in the brain are called CB1 receptors and have a role in mediating the production and transmission of messages sent by neurotransmitters.11,12 However, rather than having an excitatory effect, the active ingredients in cannabis have an inhibitory effect.11 In other words, taking cannabis prevents activity along neural pathways where CB1 receptors are present at the synapses that connect neurons to one another.11

There are several neurotransmitters which are inhibited. These include glutamate, the brain’s major excitatory neurotransmitter, vital for forging links between neurons concerned with learning and long-term memory;13 gamma-amino butyric acid (GABA), which regulates the responses of cannabinoid receptors;14 noradrenalin, which triggers physical and mental arousal and heightens mood;9 acetylcholine, which controls activity connected with attention, learning and memory;9 and dopamine, which drives motivation13 – human givens practitioners will be familiar with dopamine’s role in emotional hijacking and addiction15 – although it has also been suggested that delta-9 tetrahydrocannabinol may increase dopamine levels.

We have seen that there is an overlap between the thinking styles and behaviours associated with a right-brained caetextic state and the effects of cannabis use. And we know that cannabis use inhibits brain activity in parts of the brain where CB1 receptors are located. We should therefore expect CB1 receptors to be most prevalent in areas of the brain associated with logical, linear, left-brained cognition and an external focus of attention, and this is indeed the case: high densities of CB1 receptors are found in the forebrain in general, and in the prefrontal cortex16 which, as mentioned before, is concerned with focusing on external reality, concentration on tasks and logical thinking.9 Inhibition of these areas of the brain would surely lead to a greater reliance on the capacities associated with the right hemisphere: creativity, imagination and associative thinking.

Attention, memory and fear

CB1 receptors are also densely located along the pathways which run between the brain structures that are critical for processing emotion (the amygdala and the medial frontal cortex).17 There are CB1 receptors located in the anterior cingulate cortex, as we might expect, given the effects of cannabis on attention capacity, and also in the limbic system, where there are high densities in the hypothalamus, the hippocampus, responsible for short-term memory, and the amygdala.16 In other words, the activity of those parts of the brain that are involved in ‘emotional hijacking’, and which are vulnerable to the kinds of harmful conditioning that accompany traumatic experience, are inhibited by cannabis use. Suppression of activity in the hippocampus as a result of cannabis ingestion would explain the short-term memory loss reported by cannabis users and demonstrated by researchers. Taking cannabis would also have the effect of relieving users temporarily from the symptoms of post-traumatic stress, as the activity of the amygdala, involved in fear responses, and the hippocampus, involved in emotional memory formation, would both be inhibited, along with the transmission of glutamate and GABA, which have an important role in learning and the process of conditioning fear.13,17

With an understanding of how the amygdala, when sufficiently emotionally aroused, can send us into survival ‘fight or flight’ mode, which distorts our thinking, it is easy to see why using cannabis, which suppresses areas of the brain that process emotion and emotionally charged memories, would temporarily lower emotional arousal and provide relief to those suffering from depression, anxiety and the symptoms of trauma, as has been claimed.18 The temporary release from external problems and an easy retreat into the imagination may provide some relief for cannabis users, the nature of whose lives may not be enabling them to get their needs met in healthier ways. However, accessing the creativity of the REM state without the balance provided by contextual thinking also increases the potential for the misuse of imagination.

If cannabis does inhibit dopamine production and high dopamine levels are associated with psychosis (antipsychotic medication reduces dopamine levels), it would seem more likely that using cannabis would be protective against psychosis rather than a risk factor. However, it makes sense that, as cannabis wears off, there would be a dopamine rebound, and that paranoid and psychotic symptoms would be exacerbated at that time by chaotic imaginings recently experienced while under the influence of the drug.

Another possibility is that cannabidiol – a component in cannabis which is held to counteract the effects of delta-9 tetrahydrocannabinol, including the psychotic symptoms associated with its use19 – may bind more effectively to receptors in the limbic system, which would explain its antipsychotic qualities, while delta-9 tetrahydrocannabinol may bind more effectively with receptors in the prefrontal cortex, thereby having a stronger inhibitory effect on the lefthemisphere capacities that would normally prevent an individual slipping into a dissociated right hemisphere caetextic state. (Cannabidiol has attracted interest as a potential antipsychotic; its concentration in cannabis can vary from zero to 40 per cent and it is either not present at all or only in low amounts in stronger ‘skunk’ varieties of the drug.20)

Why adolescents are so vulnerable

Statistically, adolescents and young adults who use cannabis are more likely to develop psychotic symptoms and psychosis than those who started using cannabis in adulthood or those who don’t use cannabis at all;19 this may be connected with brain maturation and the coinciding with the peak period for the onset of psychosis.20 Sarah Jayne-Blakemore, a neuroscientist at the forefront of studies into adolescent brain development, has speculated that there may be a relationship between adolescent cannabis use, the pruning back of neural pathways in the neocortex (which starts happening around the onset of puberty and slows capacity to focus on and carry out cognitive tasks) and the increased risk of developing schizophrenia at a later stage.21,22, 23

Perhaps the relaxing effects of cannabis and the short-cut retreat it facilitates into the imagination would make it attractive to young people experiencing the emotional turmoil of adolescence. Learning how to regulate emotion and the development of self-awareness require the forming of new connections between synapses in the brain24 but, as we have seen, the activity of neurotransmitters involved in this process are inhibited by cannabis use. In this case, so-called Hebbian learning, the wiring together of cells that fire together, doesn’t take place. The resulting arrested development of those areas of the left hemisphere which provide a balance for the right hemisphere makes the user more prone to psychotic thinking.

Addictions arise initially from unmet needs and fade away when needs are met.25 But that is not the case if cannabis use, by impairing the left hemisphere’s capacity to focus outside of ourselves and to regulate emotions, hijacks the internal guidance system we depend upon to secure our needs. Those who work with people suffering addictions have noticed that drug users are often lacking in maturity – childlike or adolescent behaviours do not seem to have been superseded by adult patterns of behaviour. It makes sense that adolescent cannabis users emerging into their 20s without having fully developed the cognitive skills of their non-using peers would be left at an earlier stage in their development, less able to regulate and manage their emotions, less resilient to stress and therefore more vulnerable to mental health problems.

Strange dreams

Because cannabis inhibits dopamine production and transmission it should come as no surprise that it suppresses expectation (motivation). A widely reported cannabis withdrawal symptom is the occurrence of strange dreams. An explanation could be that, with cannabis no longer inhibiting dopamine production and transmission, overemotional arousal may occur, as the prefrontal cortex, which has the role of regulating and inhibiting inappropriate emotional responses, may, as we have seen, be impaired, ‘out of practice’ or not fully developed in the former cannabis user. Unexpressed emotional arousal will need to be discharged through dream sleep, in the normal way, using metaphorical representations, which, in the circumstances, might be extra vivid or lurid.4

It has been suggested by some researchers that larger than usual amounts of dopamine production in schizophrenia sufferers, attributed to malfunctions in dopamine production, pathways and/or receptors, might be the cause of psychosis, rather than a symptom.26 The ability of the active ingredients in cannabis to inhibit the production and transmission of dopamine has attracted interest in its potential use as a medication for people who have been diagnosed with psychotic illnesses. Given the lack of explanatory models for the wideranging effects of cannabis use, this should, surely, give cause for concern. With an understanding of the inhibitory effects of cannabis use, we can predict some of the less desirable results of using cannabis as a medication. While it would provide relief from stress, anxiety and the symptoms of post-traumatic stress, it would also, depending on developmental maturation, inhibit the further development of the ability to regulate emotion. This might result in mood swings, paranoia and vulnerability to depression and psychotic symptoms. Either as a prescribed antipsychotic or as illicit self-medication, we would also expect users to exhibit some of the ‘zombie’ side effects associated with both existing antipsychotics and cannabis use. As previous research has shown, it may be that users would resort to illicit stimulants to counter the inhibiting effects of cannabis-based antipsychotics.2

How practitioners could put this understanding to a practical use

I would like to suggest that an understanding of how cannabis inhibits the processing of emotion and induces a right-brained caetextic state could be enormously helpful in developing effective therapeutic approaches for supporting people who have decided that they want to abstain from cannabis use, and also those still at a pre-contemplative stage in their thinking. These are my ideas for what substance misuse workers might choose to do, in the light of this understanding, to work more effectively with cannabis users:

• Recognise and accept that using cannabis can help people to relax and provide relief from stress and difficult feelings. Explaining why cannabis has this effect will help to build rapport, give the practitioner credibility and give the user a better understanding of why they may be drawn to use cannabis.

• Recognise and accept that using cannabis helps people to access their imaginations and be able to explain how this works, and how it can sometimes give rise to unusual thoughts and, in some cases, paranoia.

• Be able to explain why sometimes creative ideas which occur when people are ‘stoned’ may seem to be better than they are.

• Enable understanding that we all have two innate thinking styles, logical thinking and associative thinking, and how we need both, to balance and complement one other.

• Enable understanding that overreliance on associative thinking can lead us to make connections between events, feelings and thoughts that may be inaccurate. Without access to logic to ‘check things out’, we are less able to recognise when our thoughts are paranoid or when we are ‘blowing things out of proportion’

• Be able to alert people to what to expect when they stop using cannabis: the return of strong emotions and dreams that seem unusual; be able to explain why this happens and help people anticipate such sudden changes, which provide additional challenges during abstinence.

• Be able to teach people the skills they will need to manage their lives without cannabis, such as the ability to relax, to develop and/or use thinking skills to check out feelings, to reframe thoughts instead of, say, jumping to conclusions, and to access the imagination naturally – all within the human givens practitioner’s toolbox of techniques.

• Be aware that people may have been using cannabis to self-medicate against the distressing symptoms of stress, anxiety, depression and post-traumatic stress and be able to treat (or at least refer to somebody that can treat) these symptoms of stress, anxiety, depression and post-traumatic stress and be able to treat (or at least refer to somebody that can treat) these conditions.

The explanatory model I am presenting here for what I am calling cannabis-induced caetextia does not suggest that cannabis use is a direct cause of mental health problems: what it attempts to do is explain how cannabis use can condition our innate guidance system in such a way as to make us more vulnerable to developing mental health problems, particularly if cannabis is used during adolescence. At the same time, it explains why some users report that cannabis can help to alleviate the symptoms of mental distress. It also accounts for the other reported effects of use, including changes in mood, thinking style and, in particular, increased creativity – a human given which is associated with a vulnerability to mental health problems. It can thus successfully explain the apparent contradictions surrounding the use of cannabis.

I hope that the core idea, as it is presented here, together with the suggested therapeutic applications, may point towards a better understanding of how to educate people about the risks associated with cannabis use and how to equip them with the skills needed to secure better mental health. If the idea finds resonance and helps to advance thinking, then it also highlights the power of the human givens perspective to bring clarity to a field of study that has become clouded and confused. We might wonder what other problems might be seen afresh, if looked at through the lens of new organising ideas.

How cannabis might affect different people differently

I would like to make a few speculations about how cannabis use might affect people according to their individual make-up. Amongst people who already have a genetic disposition towards rightbrained caetextia, the effects of cannabis on thinking and behaviour may be less noticeable. One cannabis user I knew met all the criteria for right-brained caetextia yet seemed almost unaffected by her daily use of very potent ‘skunk’ cannabis.

High-functioning, left-brained caetextia sufferers or those who display classic Asperger’s traits, however, might require stronger doses just to suppress their already strong left-brain capacities. But, given that they may have poor right-brained capacity or difficulty accessing the REM state, it is possible that, for first-time users, whose need for control is usually met through routine and familiarity, the experience of unusual, out-ofcontrol feelings or thoughts might trigger anxiety or panic attacks. Also, the inhibition of their natural left-hemisphere strengths might leave them in a kind of distressing no-man’s land: with limited access to either left- or right-hemisphere capacities, continuing to develop a coherent sense of self could become increasingly difficult. They might, however, find that the inhibitory effect of cannabis on emotional activity in the brain helps them to manage the stress which arises from their already reduced access to contextual thinking; this may increase the likelihood of dependency.

Those who are not caetextic but strongly righthemisphere dominant – young people who have some access to logic and reason but are also highly creative and imaginative – might be the most vulnerable to experiencing a loss of a sense of self. Sufficiently strong doses of cannabis might imbalance their already well-developed right hemisphere abilities to such a degree that they begin to exhibit psychotic symptoms, experience significant distress and, in rare cases, become totally dissociated. It is also possible that users who pattern match to previous experiences of psychotic symptoms – whether as a result of cannabis use or not – may be vulnerable to reexperiencing trauma even after limited exposure to the effects of cannabis.

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REFERENCES

1- DiClemente, C C and Prochaska, J O (1985). Processes and stages of self-change. In S Shiffman and T A Wills (eds) Coping and Substance Use. Academic Press.

2 - Asher, C J and Gask, L (2010). Reasons for illicit drug use in people with schizophrenia. BMC Psychiatry, 10, 94, doi:10.1186/ 1471-244X-10-94. Cited in Human Givens, 18, 1, 6–7.

3 - D’Souza, D C, Hyun-Sang, C, Perry, E B and Krystal, J H (2004). Cannabinoid ‘model’ psychosis, dopaminecannabinoid interactions and implications for schizophrenia. In D Castle and R Murray (eds) Marijuana and Madness. Cambridge University Press, Cambridge.

4 - Griffin, J and Tyrrell, I (2004). Dreaming Reality. HG Publishing, East Sussex.

5 - Griffin, J and Tyrrell, I (2008). Parallel Processing. Human Givens, 15, 4, 11–17.

6 - Cited in McGilchrist, I (2009). The Master and his Emissary. Yale University Press.

7 - Castle, D J. and Salowij, N (2004). Acute and subacute psychomimetic effects of cannabis in humans. In D Castle and R Murray (eds) Marijuana and Madness. Cambridge University Press, Cambridge.

8 - Griffin, J (2009). Presentation to the Human Givens Institute Conference 2009: http://vimeo.com /6007673

9 - Carter, R (2004). Mapping the Mind. Phoenix.

10 - Raichle, M E, MacLeod, A M, Snyder, A Z, Powers, W J, Gusnard, D A and Schulman, G L (2001). A default mode of brain function. Proceedings of the National Academy of Sciences USA, 98, 2, 676–82.

11 - Iversen, L (2004). How cannabis works in the brain, In D Castle and R Murray (eds) Marijuana and Madness. Cambridge University Press, Cambridge.

12 - Toole, G and S (2004). Essential Biology. Nelson Thornes Ltd.

13 - Le Doux, J (1999). The Emotional Brain. Phoenix.

14 - Pagotto, U, Marsicano, G, Cota, D, Lutz, B and Pasquali, R (2006). The emerging role of the endocannabinoid system in endocrine regulation and energy balance. Endocrine Reviews, 27, 1, 73–100. The Endocrine Society.

15 - Griffin, J (2004). Great Expectations. Human Givens, 11, 1, 12–19.

16 - Herkenham, M, Lynn, A B, Little M D, Johnson, M R, Melvin, L S, de Costa B R and Rice K C (1990). Cannabinoid receptor localization in the brain. Proceedings of the National Academy of Sciences USA, 87, 5, 1932–6.

17 -Tan, H, Lauzon, N M, Bishop, S F, Bechard, M A and Laviolette, S R (2009). Integrated cannabinoid CB1 receptor transmission within the amygdala-prefrontal cortical pathway modulates neuronal plasticity and emotional memory encoding. Cerebral Cortex, 20, 6, 1486–96.

18 - Caldwell, I. (2007). Talking Point. Human Givens, 14, 3, 30.

19 - DiForti, M, Morgan, C et al (2009). High potency cannabis and the risk of psychosis. British Journal of Psychiatry, 195, 488–91.

20 - Morgan, C J A, Schafer, G, Freeman, TP and Curran, H V (2010). Impact of cannabidiol on the acute memory and psychomimetic effects of smoked cannabis: naturalistic study. British Journal of Psychiatry, 197, 285–90.

21 - Blakemore, S-J (2007). Brain Development during Adolescence and Beyond. Institute for Cultural Research.

22 - Hall, W D and Pacula, R L (2003). Cannabis use and dependence: public health and public policy. Cambridge University Press, Cambridge.

23 -Verdoux, H (2004). Cannabis and psychosis proneness, In D Castle and R Murray (eds) Marijuana and Madness. Cambridge University. Cambridge.

24 - Huttenlocher, P R (1979). Synaptic density in human frontal cortex – developmental changes and effects of aging. Brain Research, 163, 195–205.

25 - Griffin, J. and Tyrrell, I (2005). Freedom from Addiction. HG Publishing, East Sussex.

26 - Meltzer, H Y and Stahl, S M (1976). The dopamine hypothesis of schizophrenia: a review. Schizophrenia Bulletin, 2, 19–76.

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