האם יש קשר בין שימוש בקנאביס לבין סכיזופרניה?

בסרטון הבא מרואיין פרופסור משולם ומספר איך נוצר הקשר כביכול בין קנביס לפסיכוזה, בדקה 4:30 של הסרטון פרופ' משולם מתייחס לנושא הפסיכוזות:
http://www.youtube.com/watch?v=ycmz4jUcFbM

התייחסות נוספת לנושא:
http://www.youtube.com/watch?v=PVBxNsTDjDM

הבה נבדוק את הטענות שמנגד:
להלן דוגמא למחקר שהרשות למלחמה בסמים מרבה לצטט:
http://www.bmj.com/content/342/bmj.d738#ref-17

Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study,

Conclusion: Cannabis use is a risk factor for the development of incident psychotic symptoms. Continued cannabis use might increase the risk for psychotic disorder by impacting on the persistence of symptoms.

ואולם, לאחר עיון באותיות הקטנות של המחקר, מתברר שישנם פקטורים רבים שלא נלקחו בחשבון ואשר מטים את המחקר ומוצאים ממנו את העוקץ:
קיראו בעצמכם:

Cougnard and co-workers provided evidence that childhood trauma, urban environment, and cannabis act additively in increasing the risk of persistence of psychotic experiences.17
Methodological issues
The results should be interpreted in the light of several limitations.
Firstly, information on substance use and psychosis outcome was acquired with the DIA-X/M-CIDI, which essentially provides self reported information.
The interview was conducted face to face by clinical psychologists, however, who were allowed to follow up with clinical questioning to ensure systematic and valid assessment of outcomes and can therefore be assumed to yield better and more valid results than a self report questionnaire.

Secondly, the analyses were not directly adjusted for the possible confounding effects of a family history of psychosis as this information was not available in the EDSP data.

Previous research has shown that associations between cannabis use and psychotic symptoms are not reducible to family history of psychosis41 42 and that genetic liability for psychotic disorder does not predict cannabis use.43 In addition, individuals with a family history of psychosis report more positive symptoms than individuals without such predisposition.44 45 As we excluded all individuals with at least one T2 lifetime psychotic symptom from the analysis, the possible confounding effect of family history for psychosis was indirectly adjusted for to a degree. Furthermore, we used a rather broad outcome measure, defined as a minimum of one positive rating on a G section item, representing psychotic experiences rather than clinically relevant psychotic disorder. It has been shown, however, that psychotic experiences show continuity with psychotic disorders such as schizophrenia.18 46 In addition, given that fact transient psychotic experiences might, under certain circumstances, become abnormally persistent, giving rise to clinical psychotic disorder,15 17 19 psychotic experiences represent an important phenotype for the investigation of mechanisms and pathways by which environmental risk factors such as cannabis impact on psychosis risk.

A further limitation concerns the use of the G section of the DIA-X/M-CIDI. This section was administered at T2 to assess lifetime occurrence of symptoms, which represents a long period for retrospective assessment of psychotic phenomena, possibly resulting in false negative results.

As we excluded participants with T2 lifetime experience of psychotic symptoms from the analyses, under-reporting would have resulted in false negative results being incorrectly retained in the analyses. It is unlikely that under-reporting would have occurred as a function of cannabis use, which could have resulted in biased estimates.

In addition, 23% of participants reported lifetime subclinical psychotic symptoms at T2, which is in keeping with the estimated 15-28% rate of subclinical psychotic symptoms in the general population.47

Therefore, the influence of under-reporting is probably limited. Finally, as the time between follow-up visits was four years on average, selective recall could have influenced the results. Spurious findings could have arisen if those with psychotic symptoms had better recall of earlier cannabis use. Given the well known link between psychosis liability and cognitive alterations, including impaired memory, any influence of selective recall would probably have been conservative rather than anti-conservative.



לסיכום, המציאות עצמה מפריכה את הטענה ששימוש בקנביס עשוי להוות טריגר לסכיזופרניה: הנה יש לנו בארץ מעל ל- 10,000 חולים בעלי אישור שימוש בקנאביס רפואי:
-כמה מהם היו מעורבים בתאונות דרכים קשות?
-כמה מהם פיתחו פסיכוזה? (ד"ר משיח, תקן אותי אם אני טועה - אנו מדברים על פחות מ- 0.2% מהחולים שפיתחו פסיכוזה קלה שחלפה כעבור מספר שעות.)
-כמה מהם עברו לשימוש בסמים קשים, כפי שמתנגדי הקנאביס איימו עלינו שיקרה?
המציאות מוכיחה כי קנאביס הוא אחת התרופות היעילות, הזולות והבטוחות ביותר לשימוש!