Cannabis use causes genetic changes, increasing cancer risks and hereditary disruptions.
A new study highlights serious genetic changes caused by cannabis use, with findings that link its use to various forms of internal cellular damage, some of which may carry over to future generations. By examining the molecular effects of cannabis on cell structure, the study shows how exposure can contribute to cancer risks, congenital abnormalities, accelerated aging, and even hereditary genetic disruptions. This research, recently published in Addiction Biology, dives into the pathways through which cannabinoids, the active compounds in cannabis, can disrupt mitochondrial function and increase the formation of micronuclei—small, extra-nuclear bodies containing fragmented DNA. These disruptions create an environment conducive to genetic instability, ultimately leading to greater risks of mutations, and possibly impacting generational health outcomes.
Cannabis’s increasing potency and widespread use only deepens these risks, with higher levels of THC, the primary psychoactive compound, causing oxidative stress in cells. When THC and other, related cannabinoids disrupt mitochondrial activity, the cell’s energy production is stunted, leading to the production of reactive oxygen species (ROS). ROS can cause cellular stress, damaging not only cell structures but also genetic material. This high oxidative environment has been shown to lead to chromothripsis, a process of chaotic chromosome shattering and reassembly that is strongly associated with cancer development.
In examining specific proteins under stress, such as Charged Multivesicular Body Protein 7 (CHMP7) and components of the Endosomal Sorting Complex Required for Transport III (ESCRT-III), researchers discovered that these proteins lose their functionality due to oxidation. When deactivated, this process plays a role in the wearing of membrane, leading to cellular collapse. When applied to germline cells, such stress can cause not only immediate genetic damage but also mutations that carry through to subsequent generations.
Several types of cancer, including cancers of the testicles, pancreas, thyroid, and breasts, have been associated with cannabis use. Testicular cancer, in particular, shows nearly a 2.6-fold increase in risk among regular users, and the prevalence of congenital abnormalities such as cardiovascular and limb issues are substantially elevates in areas with high cannabis cultivation. Mis-segregation of chromosomes during meiosis has been observed in affected populations, which has been linked to birth defects such as amelia (absence of limbs) and phocomelia (shortened limbs).
Beyond structural defects, the genetic changes also include epigenetic effects, meaning cannabis can influence which genes are turned on or off without altering the DNA sequence itself. This results in an “epigenetic aging” effect where cellular age is accelerated. Cannabis users as young as 30 have shown increased cellular aging, with long-term use disrupting the regulation of gene expression and cellular equilibrium. Studies show that cannabis use impacts reproductive cells, including sperm and egg cells, leading to more rapid aging and structural changes. This shift not only affects the user but can also be transmitted to their children.
Researchers have also documented evidence of genetic changes including alterations in DNA methylation patterns. Altering these patterns have been associated with an increased likelihood of developmental conditions like autism spectrum disorder (ASD), which has been on the rise in recent years, in general. This draws attention to a need for more research targeting the connection between cannabis use and ASD.
Overall, more research will need to be done to determine safe versus toxic levels of cannabis use in those who are planning to conceive. Future studies might also focus on whether some strands and/or THC levels are safer than others.
Sources:
Study links cannabis use to genotoxicity and transgenerational health impacts
Key insights into cannabis‐cancer pathobiology and genotoxicity
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