Chemical processing—or metabolism—within the body isn’t just a linear or two-dimensional process. It can be exponential. It can be logarithmic. It can be three- or four-dimensional. Somewhere along the educational timeline thinking of every correlation as linear became the norm, but it probably lies within the lower quartile of observed phenomena. Pharmaceutical products are no exception.
Supplements, prescriptions, and even certain foods react with and work variably within the human body based upon genetic composition; especially significant for target systems, such as the endocannabinoid system, whose expression and function are solely dependent upon genetic programming. There is a multiplicity of responses to these kinds of products. The emerging field of pharmacogenomics seeks to merge the dimensions of pharmacology and genetics.
It has already revealed to us how an individual’s genetic makeup can affect pharmacokinetic and pharmacodynamic response (1). Pharmacogenetic knowledge is the key to true treatment customization. In the 1950s doctors observed varying responses to succinylcholine due to a genetic variation in plasma cholinesterase enzymes (1). The volume of evidence grew exponentially in the following five decades thanks to the emergence of genomic sequencing technology.
The Human Genome Project gave us an unprecedented look within our bodies. We learned that we possess 30,000-40,000 genes which code for approximately 100,000 proteins (1). (We later discovered that only 1-3% of our DNA actually code for proteins, but that’s another blog post). This knowledge coincided with the elucidation of ribosome function and gene transcription. Discovery of a status quo sequence opened the door to discovering a phenomenon known as single nucleotide polymorphisms (SNP), which occur in at least 1% of the population (1). They exist within the domain of approximately 60,000 protein coding regions (1).
The most common SNPs affect pharmacokinetics. Pharmacokinetics encompasses: extent of absorption from administration site; how the drug is distributed after absorption; the extent and means by which the chemical is metabolized; and mode of excretion (kidney, liver, etc.)(1). With all that said, different individuals respond to chemicals, foods, and supplements differently. For instance, a hemp extract product will affect you differently than another individual. You might be either a fast, medium, or slow metabolizer of a product; this is all dictated by genetic instructions of the target metabolism sites of that product.
One common SNP region and corresponding metabolizing enzyme is CYP2C19. CYP2C19 activity affects warfarin, proton pump inhibitors, certain benzodiazepines, and the common cannabinoid CBD found in hemp extract. This enzyme’s activity is one of the variables that dictates how long the previously stated compounds stay active in the body; other variables include site of administration, speed of absorption, and metabolism bypassing, but these are topics for future blog posts. In the case of a fast metabolizer, if that enzyme metabolizes the product too quickly then the desired effects will wear away just as fast. The converse is true for a slow metabolizer. Furthermore, the presence of multiple chemicals which are to be processed by the same metabolizing enzyme (e.g. concurrent proton pump inhibitors and benzodiazepines) can potentially lead to an increase of one of the chemicals in body.
This knowledge becomes vital as healthcare and nutritional treatments become more advanced. A precise treatment regimen that is tailor made to an individual’s pharmacogenomics would be the ideal.
 Zdanowicz, M. M. (2010). Pharmacogenomics: Past, Present, and Future. In Concepts in Pharmacogenomics
(pp. 3-18). Bethesda, MD: American Society of Health-System Pharmacists.