Pharmacokinetic vs Pharmacodynamic interactions.
Hello kava lovers, today’s topic will be in regards to the different types of interactions we speak of. There are two distinct types of interaction that we should note. These two are pharmacodynamic, and pharmacokinetic. Pharmacokinetics and pharmacodynamics are spoken of quite a bit in terms of kava consumption. It is a good idea for us to understand the basics of both.
Pharmacokinetics: This is defined as the study of absorption, distribution, metabolism and excretion of drugs and compounds in the human body and other compartmental systems (Spruill 2013). We’ll be addressing this word in the context of kava interactions in the realm of focusing on the metabolizing CYP enzymes.
Pharmacodynamics: This word refers to the relationship between drug concentration at the site of action and the resulting effect of the compound at this site. This includes intensity of effects and adverse effects (Spruill 2013). We’ll be arriving at this location based on the effects we see of pharmaceutical drugs and alcohol causing differences in perceived effects related to kava consumption.
An example of a pharmacokinetic interaction would be how kava may extend the half-life and consequently raise the serum concentration of drugs that specifically use the CYP2E1 metabolic pathway to metabolize. Kava seems to have an inhibitory effect on this pharmacogene based on a study in 2005 in which it was found that kava inhibited, in vivo, CYP2E1 to a ~40% reduction in healthy volunteers (Gurley et al. 2005). CYP2E1 participates in the metabolism of anesthetics, ethanol (in chronic consumption), nicotine, APAP (acetaminophen/Tylenol), and chlorzoxazone among others. CYP2E1 also plays a role in the activation of toxic precarcinogens in tobacco smoke and nitrosamine compounds (García-Suástegui et al. 2017). On a personal note, this reduction in 2E1 could explain why people suddenly begin smoking less cigarettes after starting to drink kava on a regular basis. This reduction in metabolism enzyme due to kava may be extending the half-live and therefore effects profile of nicotine. Effects on CYP2E1 may also explain a portion of kava’s anti-cancerous profile, seeing as 2E1 plays a part in activating precancerous compounds. Kava’s inhibitory effect may be reducing the amounts of these chemicals that make it to systemic circulation, therefore reducing the cancerous effects of tobacco consumption.
One example of pharmacodynamic interactions would be that of alcohol. It was reported that the combination of alcohol and kava further decreased cognition, coordination, and attention, and increased general levels of intoxication. (Foo and Lemon 1997). Another example would be with ADHD medications. Kava was shown to reduce amphetamine-related hyperactivity and conditioned place avoidance in rodents, indicating it likely will counteract some of the stimulating properties seen in these types of medications (Volgin et al. 2020). Pharmacodynamic effects will also extend to that of antidepressants based on their method of action, and certainly anxiolytics such as benzodiazepines. These interactions may increase or blunt the physiological and/or psychological effects of kava.
In summary, pharmacodynamic interactions are those that occur between the main effects of two or more substances. Pharmacokinetic interactions occur when changes are incurred in the process of metabolization and excretion by one or more compounds, affecting the elimination or activation of others.
Foo, H., and J. Lemon. 1997. “Acute Effects of Kava, Alone or in Combination with Alcohol, on Subjective Measures of Impairment and Intoxication and on Cognitive Performance.” Drug and Alcohol Review 16 (2): 147–55. https://doi.org/10.1080/09595239700186441.
García-Suástegui, W. A., L. A. Ramos-Chávez, M. Rubio-Osornio, M. Calvillo-Velasco, J. A. Atzin-Méndez, J. Guevara, and D. Silva-Adaya. 2017. “The Role of CYP2E1 in the Drug Metabolism or Bioactivation in the Brain.” Oxidative Medicine and Cellular Longevity 2017 (January): 4680732. https://doi.org/10.1155/2017/4680732.
Gurley, Bill J., Stephanie F. Gardner, Martha A. Hubbard, D. Keith Williams, W. Brooks Gentry, Ikhlas A. Khan, and Amit Shah. 2005. “In Vivo Effects of Goldenseal, Kava Kava, Black Cohosh, and Valerian on Human Cytochrome P450 1A2, 2D6, 2E1, and 3A4/5 Phenotypes.” Clinical Pharmacology and Therapeutics 77 (5): 415–26. https://doi.org/10.1016/j.clpt.2005.01.009.
Spruill, William J. 2013. “Introduction to Pharmacokinetics and Pharmacodynamics.” In Concepts in Clinical Pharmacokinetics, 18.
Volgin, Andrey, Longen Yang, Tamara Amstislavskaya, Konstantin Demin, Dongmei Wang, Dongni Yan, Jingtao Wang, et al. 2020. “DARK Classics in Chemical Neuroscience: Kava.” ACS Chemical Neuroscience, January. https://doi.org/10.1021/acschemneuro.9b00587.
Hello kava lovers, today’s topic will be in regards to the different types of interactions we speak of. There are two distinct types of interaction that we should note. These two are pharmacodynamic, and pharmacokinetic. Pharmacokinetics and pharmacodynamics are spoken of quite a bit in terms of kava consumption. It is a good idea for us to understand the basics of both.
Pharmacokinetics: This is defined as the study of absorption, distribution, metabolism and excretion of drugs and compounds in the human body and other compartmental systems (Spruill 2013). We’ll be addressing this word in the context of kava interactions in the realm of focusing on the metabolizing CYP enzymes.
Pharmacodynamics: This word refers to the relationship between drug concentration at the site of action and the resulting effect of the compound at this site. This includes intensity of effects and adverse effects (Spruill 2013). We’ll be arriving at this location based on the effects we see of pharmaceutical drugs and alcohol causing differences in perceived effects related to kava consumption.
An example of a pharmacokinetic interaction would be how kava may extend the half-life and consequently raise the serum concentration of drugs that specifically use the CYP2E1 metabolic pathway to metabolize. Kava seems to have an inhibitory effect on this pharmacogene based on a study in 2005 in which it was found that kava inhibited, in vivo, CYP2E1 to a ~40% reduction in healthy volunteers (Gurley et al. 2005). CYP2E1 participates in the metabolism of anesthetics, ethanol (in chronic consumption), nicotine, APAP (acetaminophen/Tylenol), and chlorzoxazone among others. CYP2E1 also plays a role in the activation of toxic precarcinogens in tobacco smoke and nitrosamine compounds (García-Suástegui et al. 2017). On a personal note, this reduction in 2E1 could explain why people suddenly begin smoking less cigarettes after starting to drink kava on a regular basis. This reduction in metabolism enzyme due to kava may be extending the half-live and therefore effects profile of nicotine. Effects on CYP2E1 may also explain a portion of kava’s anti-cancerous profile, seeing as 2E1 plays a part in activating precancerous compounds. Kava’s inhibitory effect may be reducing the amounts of these chemicals that make it to systemic circulation, therefore reducing the cancerous effects of tobacco consumption.
One example of pharmacodynamic interactions would be that of alcohol. It was reported that the combination of alcohol and kava further decreased cognition, coordination, and attention, and increased general levels of intoxication. (Foo and Lemon 1997). Another example would be with ADHD medications. Kava was shown to reduce amphetamine-related hyperactivity and conditioned place avoidance in rodents, indicating it likely will counteract some of the stimulating properties seen in these types of medications (Volgin et al. 2020). Pharmacodynamic effects will also extend to that of antidepressants based on their method of action, and certainly anxiolytics such as benzodiazepines. These interactions may increase or blunt the physiological and/or psychological effects of kava.
In summary, pharmacodynamic interactions are those that occur between the main effects of two or more substances. Pharmacokinetic interactions occur when changes are incurred in the process of metabolization and excretion by one or more compounds, affecting the elimination or activation of others.
Foo, H., and J. Lemon. 1997. “Acute Effects of Kava, Alone or in Combination with Alcohol, on Subjective Measures of Impairment and Intoxication and on Cognitive Performance.” Drug and Alcohol Review 16 (2): 147–55. https://doi.org/10.1080/09595239700186441.
García-Suástegui, W. A., L. A. Ramos-Chávez, M. Rubio-Osornio, M. Calvillo-Velasco, J. A. Atzin-Méndez, J. Guevara, and D. Silva-Adaya. 2017. “The Role of CYP2E1 in the Drug Metabolism or Bioactivation in the Brain.” Oxidative Medicine and Cellular Longevity 2017 (January): 4680732. https://doi.org/10.1155/2017/4680732.
Gurley, Bill J., Stephanie F. Gardner, Martha A. Hubbard, D. Keith Williams, W. Brooks Gentry, Ikhlas A. Khan, and Amit Shah. 2005. “In Vivo Effects of Goldenseal, Kava Kava, Black Cohosh, and Valerian on Human Cytochrome P450 1A2, 2D6, 2E1, and 3A4/5 Phenotypes.” Clinical Pharmacology and Therapeutics 77 (5): 415–26. https://doi.org/10.1016/j.clpt.2005.01.009.
Spruill, William J. 2013. “Introduction to Pharmacokinetics and Pharmacodynamics.” In Concepts in Clinical Pharmacokinetics, 18.
Volgin, Andrey, Longen Yang, Tamara Amstislavskaya, Konstantin Demin, Dongmei Wang, Dongni Yan, Jingtao Wang, et al. 2020. “DARK Classics in Chemical Neuroscience: Kava.” ACS Chemical Neuroscience, January. https://doi.org/10.1021/acschemneuro.9b00587.