4.+Impact+of+Cannabis+Use+on+Psychosis

 The amount of research on the relationship between cannabis and psychosis is quite extensive. Marijuana’s ever-growing popularity in the general population may be one of the reasons why research on cannabis, and its effects on the user, is so abundant. The formal research on marijuana and its effects on health dates back to at least since the British government concluded, in their Indian Hemp Commission of 1893, that the moderate use of cannabis had no detrimental effects on either mental or moral faculties (Parakh & Basu, 2013).
 * Impact of Cannabis Use on Psychosis **



(photo retrieved from: http://saalg.blogspot.ca/2010/09/indian-hemp-drugs-commission.html)  Plenty of research since the nineteenth century, however, contradicts the findings of the Indian Hemp Commission. Accordingly, the general public’s perception of marijuana has been mixed and inconsistent at best. Despite the fact that marijuana and its effects on the individual are a fairly controversial, nearly subjective topic in the media and to the layperson, the scientific evidence is quite clear. There is hardly any statistical doubt as to the relationship between cannabis use and the development of psychosis. There is strong evidence that cannabis use leads to psychosis.

 It can, however, be argued that cannabis use is merely correlated to the development of psychosis. In other words, the relationship between cannabis use and psychosis may only by correlational, not causal. In order to conduct experimental research (that is, in order to prove causation), the researchers need to be able to manipulate the independent variables. In most studies, the independent variable (specifically, whether the participants used cannabis or not) was not manipulated. The researchers simply took participants as they already were. The results they found, namely the strong relationship between cannabis use and later psychosis, were therefore only correlational. They could not prove, for example, that cannabis was used in order to alleviate early, already present prodromal symptoms of psychosis. In other words, perhaps the participants already had early symptoms of psychosis, and they were using cannabis to relieve those early symptoms. Because most research designs only demonstrated correlations, they could not ignore the possibility of this hypothesis.

 Despite these arguments, evidence from a recent meta-analysis supports the claim that the relationship between cannabis use and the early development of psychosis may in fact be causal (Large, Sharma, Compton, Slade, & Nielssen, 2011). The meta-analysis found that alcohol (y = -0.28 years), non-specified substances (y = -2 years), and especially cannabis (y = -2.7 years) each induce psychosis at an earlier age (“earlier”, compared to individuals with psychosis who did not report likewise substance use). This indicates that individuals who used cannabis developed psychosis 2.7 years earlier than individuals who did not use cannabis. Perhaps unsurprisingly, it was also found that heavy substance use (y = -2.72 years) had a greater, though ultimately non-significant effect on earlier onset of psychosis as compared to light substance use (y = -2.07 years). This may indicate that the amount, or the extent to which one uses substances may not be as important as using the substances in the first place.

 Despite this possible causal relationship between cannabis use and the age of onset of psychosis, there are certain individuals for which the cannabis’ catalytic properties are especially relevant. This warrants the question:


 * Who Develops Psychosis From Cannabis Use? **

 Again, while there is ample evidence to support the claim that the use of cannabis is associated with an increased risk of developing psychosis, the majority of individuals who use cannabis do not develop psychosis (Parakh & Basu, 2013). In other words, the average individual who uses cannabis will not likely go on to develop psychosis. Essentially, there are several other factors and medical conditions which interact with the use of cannabis that, combined in some way, additively increase the risk factor of developing psychosis. Using the diathesis-stress model as a principle guide, some of those factors are discussed below.

 Historically, psychologists and psychiatrists alike have spent an incredible amount of time and energy on developing and defending various etiological accounts of mental health issues. Realistically, however, mental health issues and psychiatric disorders are of such a highly complex nature that they usually cannot be explained completely by only one, exclusive paradigm (e.g., biological, behaviourism, psychoanalytic, etc.). Therefore, the best approach would include partial recognition on behalf of a variety of etiological accounts. The diathesis-stress model does just that by taking an integrative approach to illness origin, specifically by focusing on the interaction between genetic predisposition – the diathesis component – and environmental stressors, which constitute the stress component (Davison, Blankstein, Flett, & Neale, 2008).
 * Diathesis-stress model. **

According to the diathesis-stress model, even if an individual is genetically predisposed to developing psychosis, they will not necessarily develop it. The individuals who are at the highest risk for developing psychosis, according to the diathesis-stress model, are those who are both genetically vulnerable, and who are surrounded by a multitude of environmental stressors. In other words, the environmental stressors trigger the development of the underlying, biological potential for psychotic symptoms. The current literature supports this idea because, again, only a small percentage of individuals who uses cannabis will develop psychosis (Parakh & Basu, 2013). Much like an environmental stressor, the use of cannabis is best seen as a catalyst, an inducer or trigger, towards developing psychosis for those who are already genetically predisposed to develop it.



(modified photo retrieved from: http://picsbox.biz/key/diathesis%20stress%20model%20bipolar%20disorder)  Some significant, specific genetic predispositions and environmental factors that are relevant to the development of psychosis are discussed below.

An individual’s genetic predisposition for developing psychosis can be as broad and generic as simply having a relative who has psychotic symptoms. Accordingly, it is thought that individuals who have a greater genetic predisposition (e.g., those who have a higher prevalence of schizophrenia in their family) are more likely to develop psychosis from cannabis use (Parakh & Basu, 2013).
 * //<span style="font-family: 'Times New Roman',serif; font-size: 12pt;"> Genetic predispositions. //**

<span style="font-family: 'Times New Roman',serif; font-size: 12pt;"> There has been an extensive amount of research on the particular genes that are relevant in the relationship between cannabis and psychosis. Caspi et al. (2005) have identified the valine (Val) and methionine (Met) alleles of the catechol-O-methyltransferase gene to be important predictors of whether an individual is more or less likely to develop psychosis from cannabis use. Specifically, it was found that individuals homozygous for the Val allele (i.e., a Val-Val combination) were nearly 10 times more likely to develop psychosis after adolescent cannabis use than individuals homozygous for the Met allele (i.e., a Met-Met combination).

<span style="font-family: 'Times New Roman',serif; font-size: 12pt;">There are also certain environmental and social factors which add to the likelihood of developing psychosis. Urbanicity – living in highly urbanized, highly populated, central areas – has been shown to consistently yield more individuals with psychosis per capita than rural areas do (Parakh & Basu, 2013). Also, childhood trauma, especially in terms of sexual abuse, is another factor which has been consistently found to increase the risk factor for developing psychosis (Vinkers et al., 2013). In terms of social factors, individuals who have consistently tumultuous relationships, especially in the form of familial dysfunction, are at an increased risk of developing psychosis (Vinkers et al., 2013). Given these environmental factors, an individual who consistently lives in highly urbanized areas, who has experienced childhood trauma, and who consistently experiences difficulties in relationships, is at a heightened risk of developing psychosis.
 * //<span style="font-family: 'Times New Roman',serif; font-size: 12pt;"> Environmental factors. //**

<span style="font-family: 'Times New Roman',serif; font-size: 12pt;"> When looking at the etiology of psychotic disorders, there are a number of medical conditions that are thought to increase the risk factor for developing psychosis. The following illnesses and diseases are thought to increase the likelihood of developing psychosis, especially for individuals who also use cannabis: <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">(Sinacola & Peters-Strickland, 2012).
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;"> Medical conditions. **
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">brain tumours
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">dementia (e.g., Alzheimer’s disease)
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">epilepsy
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">multiple sclerosis
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">stroke
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">traumatic brain injuries

<span style="font-family: 'Times New Roman',serif; font-size: 12pt;"> **Medications and substances.** <span style="font-family: 'Times New Roman',serif; font-size: 12pt;"> In addition to comorbid medical conditions, there are certain medications and substances that, if consumed by an individual, may further increase their risk factor for developing psychosis. These medications and substances include, but are not limited to: <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">(Sinacola & Peters-Strickland, 2012).
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">alcohol
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">appetite suppressants
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">barbiturates
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">benzodiazepines
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">other drugs of abuse, such as amphetamines, cocaine, heroin, etc.
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;">narcotic medications, such as morphine, hydrocodone, oxycodone, etc.

<span style="font-family: 'Times New Roman',serif; font-size: 12pt;">There are also other factors, specifically related to the use of cannabis, which further increase the psychosis risk factor. For example, the age of initial exposure is an important factor. In a longitudinal study of nearly 50,000 Swedish conscripts, Andréasson, Engström, Allebeck, and Rydberg (1995) found that individuals who consumed cannabis for the first time at or before the age of 18, were 2.4 times more likely to develop psychotic (specifically schizophrenic) symptoms than those who had not. That risk factor increased to as high as 6 times increased probability, if cannabis use was frequent, or heavy. In cases where heavy cannabis use began before the age of 16, the chances of developing psychotic symptoms were quadrupled. It seems that the age of initial exposure is a very strong predictor of whether an individual will go on to develop psychosis. Specifically, the younger the individual is, the more likely they will develop psychosis. A possible explanation for this may be that the cannabis use essentially interrupts neurogenesis and neuro-remodelling. The brain continues to shape and develop well into adolescence, and early, heavy cannabis use may interrupt or distort that process (Parakh & Basu, 2013).
 * <span style="font-family: 'Times New Roman',serif; font-size: 12pt;"> Other factors. **

<span style="font-family: 'Times New Roman',serif; font-size: 12pt;">The factors that have been discussed, which additively increase the risk of developing psychosis, are presented in a simplified chart below.




 * <span style="font-family: 'Times New Roman',Times,serif; font-size: 14pt;">Antipsychotic Effects of Cannabis **

<span style="font-family: 'Times New Roman',serif; font-size: 12pt;"> Despite the various adverse effects that cannabis has on the user, there are also thought to be positive, possibly even therapeutic effects that it can have. Essentially, it seems that different chemical components of cannabis induce different effects on the user. Two major components of cannabis are delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD). The psychoactive effects (and their levels of intensity) of cannabis increases with the relative amount of THC present. In other words (and as was stated in the **A Brief Overview of Marijuana** page), THC is the principal psychoactive agent in cannabis (Hart, Ksir, Hebb, Gilbert, & Black, 2012). It is also thought to be the chief ingredient responsible for the increased risk in developing schizophrenia and other psychotic disorders following chronic, regular use of cannabis. CBD, on the other hand, has been shown to have anxiolytic, even antipsychotic effects on the user (Parakh & Basu, 2013). Accordingly, marijuana strains that are high in THC and low in CBD can be potentially harmful by increasing the risk factor of developing psychosis. Conversely, marijuana strains that are low in THC and high in CBD may in fact be therapeutic, since the CBD combats the risk factor of developing psychosis; the relatively high levels of CBD would at least offset the negative effects of the THC. Unfortunately, however, the general trend across regions indicates that marijuana potency is increasing (Davison et al., 2008; Hart et al., 2012). This increase in potency is due to a proportional increase in the cannabis’ underlying THC content. This THC increase would likely be accompanied by a decrease in CBD content. This trend may lead to an increased prevalence of drug-induced, specifically cannabis-induced, psychosis.

<span style="font-family: 'Times New Roman',serif; font-size: 12pt;">The attached video demonstrates other therapeutic effects, specifically anticonvulsant effects, that high-CBD marijuana strains can provide. The entire documentary is interesting, but a particularly fascinating component occurs between (mm:ss) 09:30 and 14:11.

<span style="display: block; font-family: 'Times New Roman',serif; font-size: 12pt; text-align: center;">http://youtu.be/Z3IMfIQ_K6U?t=9m30s <span style="font-family: 'Times New Roman',Times,serif; font-size: 120%;">It seems pretty ironic that the least dangerous drug that can be prescribed for epilepsy (which, in Chaz's case, took the form of myoclonus diaphragmatic flutter) is the most difficult to obtain. Chaz had been prescribed substances like diazepam and morphine, which could be dangerous, even deadly. The use of high-CBD cannabis, however, seemed to be incredibly effective and hardly deleterious to his health. Indeed, it was suggested that marijuana significantly increased the quality of Chaz's life. And yet, the medicinal use of cannabis continues to be surrounded by a plethora of red tape.