Are you aware of our genes response to cannabis? Cannabis has its potent effects on the brain and body, primarily when the protein-made receptors that are created inside our cells reside or the CB1 and CB2 receptors (which blueprints for building them are found in our DNA). But the fact that the striking similarity of the human genome across people also shows common mutations in these blueprints can also be the source of inherited diseases, which is also responsible for people’s differences in cannabis reaction.
Scientists have acknowledged 15 variations of CB1 receptor mutations in humans hitherto. These mutations are the central spot of cannabis intoxication and target for THC, and the differences in the blueprints of the protein almost always affect its function.
This explains an individual’s greater or lesser sensitivity to cannabis intoxication. Due to these 15 different mutations of the CB1 receptor protein, some may be more susceptible to diseases like Crohn’s disease, anorexia, or addiction, and some can dramatically modify one’s sensitivity to molecules that comes with it (e.g., THC).
Likewise, there are also no less than 11 mutations of an enzyme that cut into the naturally produced cannabinoid molecules or the FAAH gene, and at least seven mutations of the CB2 receptors. However, the genetic mutations that are responsible for our cannabis experience are not only limited to our endogenous cannabinoid system and some hold mutation in the Akt gene, the Protein kinase B (not specifically an endocannabinoid gene) which keeps the cells from dying and inhibit tissue growth associated with many types of cancer. Individuals who have Akt mutation changes how cannabinoids affect them, and their genes’ response to cannabis is likely to make error judgments and inadequate motor responses.
Another vital variation is found in the liver. When cannabis is ingested, it passes through a different system compared to smoking. It will go through your digestive system and liver before it reaches the bloodstream and brain. Similarly, the liver also has many enzymes that process different kinds of medications and substances. One of its proteins is known for converting delta-9-THC into 11-hydroxy-THC, which is more potent than activating the CB1 receptor and advancing intoxication.
CYP2C9: Destroyer of THC
CYP2C9, a part of the Cytochrome P-450 family of enzymes, is a gene that instructs the building of protein, which is made by the liver and GI tract. The Cytochrome P-450 family of enzymes is considered phase I detoxification molecules, meaning they act on the “first pass” of metabolizing different substances, from prescription drugs to inhale the smoke that comes into our body and even mass-produced hormones like estrogen.
CYP2C9 is ideal because its chemical structure matches the primary psychoactive molecule in marijuana or the THC. That is to say, when the circulation of THC comes into contact with CYP2C9, it chemically transforms THC into its resulting molecules, which are called the metabolite. It is safe to say that CYP2C9 also changes the amount of THC in your body.
We do not have an identical “version” of the CYP2C9 gene. In reality, an individual has their variation of CYP2C9 gene that is accountable for our uniquely different metabolism, the same concept as to how we differ in eye color. These distinctions can be called Single Nucleotide Polymorphisms or SNPs.
The following briefly defines SNPs;
- SNPs are not mutations; they are variations that commonly occur in genes.
- SNPs are identified with an “rs” number, which tells us precisely the specific location of an SNP in our DNA.
- An SNP varies from person to person, meaning, one letter of your DNA sequence is unique only to you.
- Your allele type serves as evidence of the version of SNP you have. They are indicated using two letters, for example AA, AT, or TT.
Cytochrome P-450 is known to have many variations of SNPs that change the function of each enzyme. Specific SNPs such as the CYP2D6 gene causes poor reactions to SSRI antidepressant drugs. In contrast, the CYP1A2 gene has a significant effect on the breaking down of caffeine, which is related to the 4-fold risk of high blood pressure and heart attack due to caffeine consumption.
Findings From Studies
The first study regarding pharmacogenetics of THC and CYP2C9 was conducted in 2005. This was carried out through the use of the enzymes in a petri dish and found that despite not being a human subject, the CYP2C9*3 version, a C allele carriers-produced protein, found that it metabolized 30% less THC than CYP2C9*1 version, an A allele carriers-produced enzyme. In other words, breaking down THC in one version is 30% less useful than the different versions.
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The different reactions a person has when consuming cannabis accounts for the complexity and uniqueness of one’s genes. The genes’ response to cannabis differs based on what you are made of as a person. The level of tolerance to cannabis does not mean that a person is physically weak or strong; it only implies the difference of people from one another. It is not also a subject for worry because this genetic mutation has always been present since birth; it is not something you can control. Genes respond to many stimuli such as viruses, diet stress, and such. At some point, the DNA tests might be done to determine what it looks like, identify genetic diseases, and counter them and what you expect from consuming cannabis.