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- Smoking cannabis boosts brains' sensitivity to cocaine, US researchers report
- Young rats exposed to cannabis had 'enhanced reaction' to cocaine exposure
- In young humans cannabis abuse can enhance experiences with a different drug
Cannabis is a gateway drug that gives users a heightened sensitivity to harder illegal substances like cocaine, a new study suggests.
US researchers found adolescent rats that had been pre-exposed to cannabis had an enhanced reaction to their first exposure to cocaine.
Exposure to psychoactive cannabinoids during adolescence was found to 'prime' the animal's prefrontal cortex in the brain.
If applied to humans, the study suggests smoking a lot of weed as a teenager makes people more sensitive to cocaine and can lead to continued use and addiction.
Cannabis abuse during adolescence can enhance a person's initial positive experience with a different drug, such as cocaine, leading to sustained use.
Cannabinoid exposure in rat adolescence reprograms the initial behavioral, molecular, and epigenetic response to cocaine
The Science – Significance - The endocannabinoid system has a modulatory role in brain reward and cognitive processes. It has been hypothesized that repeated interference with endocannabinoid signaling (e.g., through abuse of cannabis or synthetic cannabinoids) can remodel the adolescent brain and make it respond differently to more addictive substances, such as cocaine. In the present study, we demonstrate that a history of synthetic cannabinoid exposure in adolescent animals results in distinct molecular and epigenetic changes following initial exposure to cocaine. These changes were pronounced in the prefrontal cortex and associated with an enhanced response to cocaine’s stimulatory effects. The prefrontal cortex is a brain region that still undergoes maturation in adolescence and its dysfunction contributes to the development of addictions.
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Scientific Reports volume 11, Article number: 13892 (2021) Cite this article
Abstract: Cannabis and cannabinoids are implicated in multiple genotoxic, epigenotoxic and chromosomal-toxic mechanisms and interact with several morphogenic pathways, likely underpinning previous reports of links between cannabis and congenital anomalies and heritable tumours. However the effects of cannabinoid genotoxicity have not been assessed on whole populations and formal consideration of effects as a broadly acting genotoxin remain unexplored. Our study addressed these knowledge gaps in USA datasets. Cancer data from CDC, drug exposure data from National Survey of Drug Use and Health 2003–2017 and congenital anomaly data from National Birth Defects Prevention Network were used. We show that cannabis, THC cannabigerol and cannabichromene exposure fulfill causal criteria towards first Principal Components of both: (A) Down syndrome, Trisomies 18 and 13, Turner syndrome, Deletion 22q11.2, and (B) thyroid, liver, breast and pancreatic cancers and acute myeloid leukaemia, have mostly medium to large effect sizes, are robust to adjustment for ethnicity, other drugs and income in inverse probability-weighted models, show prominent non-linear effects, have 55/56 e-Values > 1.25, and are exacerbated by cannabis liberalization (P = 9.67 × 10–43, 2.66 × 10–15). The results confirm experimental studies showing that cannabinoids are an important cause of community-wide genotoxicity impacting both birth defect and cancer epidemiology at the chromosomal hundred-megabase level.
For more go to | Scientific Reports (nature.com)
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Cannabis in ALL FORMS takes a Weed Whacker to Your Chromosomes
with Professor, Dr. Stuart Reece