Growers Network Staff

November 1, 2017 9 min read
November 1, 2017
9 min read

Smoking vs. Eating Cannabis: The Effects on Patient Health Pt. 3

Do you want to be part of our private, professional community?
Join Now

In the third article of this series, Marco Troiani of Digamma Consulting analyzes how the human body is affected by cannabinoids. If you would like to read the previous article, please click here!

Part 1
Part 2

The following is an article produced by a contributing author. Growers Network does not endorse nor evaluate the claims of our contributors, nor do they influence our editorial process. We thank our contributors for their time and effort so we can continue our exclusive Growers Spotlight service.

Short on time? You can listen to our harvest Podcast Episode on this article here.


Cannabis is becoming a popular medicine in the United States for patients wanting to fight a wide variety of diseases and disorders. Cannabis and derived products are used to treat conditions such as multiple sclerosis (MS), cancer, inflammatory disorders, autoimmune disorders, and a wide variety of psychological disorders, ranging from depression and anxiety to schizophrenia. The majority of medical benefits cannabis consumption provides are due to the presence of cannabinoids that interact with the human endocannabinoid system.


To get a good picture of the differences in effects between inhaled and orally-ingested cannabinoids, it is useful to monitor cannabinoid and metabolite concentrations in the blood of a patient over time. Oral ingestion of cannabis leads to higher levels of OH-THC found in the blood instead of the much lower levels of OH-THC found following inhalation. We first examine blood serum levels after inhalation in figure 6.

Figure 6: This graph illustrates the amount of THC and two primary metabolites in a patient's blood over time during inhalation.

We can see that immediately after smoking, the patient has the highest THC levels and very few metabolites. As time elapses, the body converts THC to OH-THC gradually, and THC levels begin to fall. A small amount of OH-THC accumulates in the blood. After sufficient time passes, the THC and OH-THC are fully converted into the inactive COOH-THC which becomes the predominant metabolite in the patient's blood.

Notice the very low levels OH-THC relative to THC. Only a small portion of blood exposed to THC is sent to the liver, resulting in the body converting THC to OH-THC very slowly. This leads to lower blood serum levels of OH-THC following inhalation. OH-THC peaks around the time that THC levels begin to decline. This pattern coincides with the cessation of initial symptoms of cannabinoid intoxication; in colloquial terms, this is the end of the “high” and the beginning of a “burn out” or “coming down” phase. The onset of these delayed symptoms, or “after effects” coincide with a OH-THC blood serum peak, which strongly implies that OH-THC plays a role in this phenomenon.

Now that we are familiar with the general pattern of THC/metabolite concentrations in blood after inhalation, we can examine empirical evidence from a published study, conducted by Huestis et al in 20095, from which figure 7 is taken.

Figure 7: Here we see three lines representing THC and its metabolites over time. Vertical arrows indicate when the test subject inhaled cannabinoids.

Because this is an experimental study, researchers first had to document blood levels before the introduction of any cannabinoids. Ten minutes after first inhalation, the graph mirrors figure 6, with decreasing THC levels, increasing COOH-THC levels, and a small bump of OH-THC in between the two.

The next scenario examines the oral ingestion of cannabinoids and how the resulting blood serum levels of THC, OH-THC, and COOH-THC change over time. Feel free to revisit our first article to review anatomical path of orally-ingested cannabinoids.

Figure 8: This graph illustrates the amount of THC and two primary metabolites in a patient's blood over time during ingestion.

In figure 8, at time=0, we see that the patient’s blood serum contains THC and OH-THC at approximately equal levels. THC must pass through the liver before reaching the brain, accounting for the high levels of OH-THC. However, some THC passes through the liver without being metabolized. For this reason, we do not see a complete absence of THC in the patient's blood.

As time progresses, THC continues its conversion into OH-THC, leading to an increased accumulation of OH-THC in the blood. As time passes though, all active THC metabolites are eventually converted to COOH-THC and rendered inactive. If OH-THC is higher potency than THC, it is clear how small doses of ingested THC have strong effects on patients relative to the same dose of inhaled THC.

Now that we are familiar with ingested cannabinoid pharmacokinetics, let’s examine the empirical data from Huestis5.

Figure 9: Lines represent blood concentration levels of THC and its metabolites over time. Note that the concentration of COOH-THC is plotted on a different scale than the other THC metabolites. This is due to COOH-THC's tendency to accumulate in the blood as an inactive product with a slow half-life, yielding higher concentrations than the transient concentrations of THC and OH-THC.

At beginning of the experiment, absorption rates in the blood are high, with OH-THC absorbing at slightly higher levels than THC. Between 5 and 15 hours, THC levels fall off while OH-THC continues to accumulate from THC metabolism. Around 15-25 hours, OH-THC levels fall to zero as it converts into COOH-THC, which also begins to decrease.

The scale covered in this experiment is between 0-2 parts per billion (ppb) in the blood. The concentration of THC-COOH was the only cannabinoid that exceeded 30 ppb. The previous experiment on inhalation was done over a much shorter time interval (minutes), but displayed concentrations ranging from 0-150 ppb. The difference in scales supports the hypothesis that OH-THC has increased potency over THC. However, further studies are needed to validate this hypothesis.


One important factor for patients who choose oral ingestion is the decarboxylation of THCA into THC. THCA does not have the psychoactive properties of THC, but it provides medical benefits that THC does not, such as anti-inflammatory effects (via inhibition of inflammatory cyclooxygenase (COX-1 and -2) enzymes)6. This distinction is less important for patients who choose inhalation, because the the process of smoking or vaporizing THCA automatically decarboxylates it into THC. An open flame (>300 C or >500F) or red hot nail (approximately 400 C or 750 F) will convert THCA to THC, as will an oven at baking temperature (approximately 177 C or 350 F) with 30-70% efficiency7.

THCA can be decarboxylated with relatively gentle heat outside the body, but once THCA enters the body it follows a different metabolic pathway than THC, and leads to no psychoactive effects. Studies have shown that it is not possible to decarboxylate THCA to THC in vivo8. Once THCA is introduced to the body, it is metabolized and excreted by the body as a metabolite of THCA, not THC or any of its metabolites. The following diagram, figure 10, outlines the relationship between THC and THCA as metabolites in the human body.

Figure 10: If THCA is not decarboxylated, it remains non-psychoactive throughout metabolism. The blue carboxylic acid (COOH) group remains attached to both THCA and its metabolite.

It is important for patients to understand their specific needs from cannabis therapy. If a patient chooses to ingest edible cannabis for their psychoactive effects, it is important that they read the lab testing results of any products they purchase in a dispensary. They should examine the levels of THC, THCA, and other cannabinoids that are relevant to their health. In general, patients looking for psychoactive effects should seek out products with high THC levels and almost no THCA. Conversely, a patient who does not desire the psychoactive effects from cannabis but instead seeks treatment for an inflammation-based or autoimmune-based dysfunction will need to orally ingest THCA, since absorption of THCA through inhalation is not known to be possible. The patient will want to check lab results for products purchased at dispensaries to make sure the level of THC present is low enough to be acceptable, and the level of THCA is adequate.

In Conclusion...

A firm grasp of the science behind cannabinoids and their interactions with the body can help a medical patient, prescribing doctor, or industry professional understand the effects that different routes of administration will have on health, function, and experience. As accidental oral ingestion “overdoses” become more frequent in recreational states, it is important for a patient or recreational user to be aware of how this route of administration will affect their body and mind.

Author’s Note: The term “overdose” appears in quotes because cannabinoids can cause a mentally unpleasant state, but have no known lethal dose associated with them.

As the cannabis industry becomes more aware of the chemistry of both the plant and biochemistry of the human body, it will be better able to serve, and more importantly meet, the needs of all patients and users.


  1. Huestis MA (June 2009) “Human Cannabinoid Pharmacokinetics”. Chem Biodivers. 2007 August ; 4(8): 1770–1804. doi:10.1002/cbdv.200790152.
  2. Ruhaak LR, Felth J, Karlsson PC, Rafter JJ, Verpoorte R, Bohlin L (2011), "Evaluation of the cyclooxygenase inhibiting effects of six major cannabinoids isolated from Cannabis sativa", Biological and Pharmaceutical Bulletin, 34 (5): 774– 8,doi:10.1248/bpb.34.774, PMID 21532172
  3. Dussy F, et al “Isolation of delta9-THCA-A from hemp and analytical aspects concerning the determination of delta9-THC in cannabis products”. Forensic Science Interanational, Volume 149, Issue 1, 3-10
  4. Jung J, Meyer MR, Maurer HH, Neusüss C, Weinmann W, Auwärter V (Oct 2009), "Studies on the metabolism of the Delta-9-tetrahydrocannabinol precursor delta-9-tetrahydrocannabinolic acid A (Delta9-THCA-A) in rat using LC-MS/MS, LC-QTOF MS and GC-MS techniques", Journal of Mass Spectrometry, 44 (10): 1423–33, doi:10.1002/jms.1624, PMID 19728318
  5. Pacher, Pál, Sándor Bátkai, and George Kunos. "The endocannabinoid system as an emerging target of pharmacotherapy." Pharmacological reviews 58.3 (2006): 389-462.
  6. Röhrich, J., et al. "Concentrations of Δ9-tetrahydrocannabinol and 11-nor-9-carboxytetrahydrocannabinol in blood and urine after passive exposure to cannabis smoke in a coffee shop." Journal of analytical toxicology 34.4 (2010): 196-203.
  7. Schwilke, Eugene W., et al. "Δ9-tetrahydrocannabinol (THC), 11-hydroxy-THC, and 11-nor-9-carboxy-THC plasma pharmacokinetics during and after continuous high-dose oral THC." Clinical chemistry 55.12 (2009): 2180-2189.
  8. Takahashi, Harumi, et al. "Population differences in S‐warfarin metabolism between CYP2C9 genotype‐matched Caucasian and Japanese patients." Clinical Pharmacology & Therapeutics 73.3 (2003): 253-263.
  9. Wang, Su-Lan, et al. "Detection of CYP2C9 polymorphism based on the polymerase chain reaction in Chinese." Pharmacogenetics and Genomics 5.1 (1995): 37-42.
  10. Imai, Jun, et al. "Polymorphism of the cytochrome P450 (CYP) 2C9 gene in Japanese epileptic patients: genetic analysis of the CYP2C9 locus." Pharmacogenetics and Genomics 10.1 (2000): 85-89.
  11. Niwa, Toshiro, Toshifumi Shiraga, and Akira Takagi. "Effect of antifungal drugs on cytochrome P450 (CYP) 2C9, CYP2C19, and CYP3A4 activities in human liver microsomes." Biological and Pharmaceutical Bulletin 28.9 (2005): 1805-1808.
  12. Fouts, James R. "Factors influencing the metabolism of drugs in liver microsomes." Annals of the New York Academy of Sciences 104.1 (1963): 875-880.
  13. Kato, Ryuichi, and James R. Gillette. "Sex differences in the effects of abnormal physiological states on the metabolism of drugs by rat liver microsomes." Journal of Pharmacology and Experimental Therapeutics 150.2 (1965): 285-291.
  14. Fouts, James R. "Factors influencing the metabolism of drugs in liver microsomes." Annals of the New York Academy of Sciences 104.1 (1963): 875-880.
  15. Forrester, L. M., et al. "Relative expression of cytochrome P450 isoenzymes in human liver and association with the metabolism of drugs and xenobiotics." Biochemical Journal 281.2 (1992): 359-368.
  16. Kuntzman, R., et al. "Metabolism of drugs and carcinogens by human liver enzymes." Journal of Pharmacology and Experimental Therapeutics 152.1 (1966): 151-156.
  17. Kuntzman, R., et al. "Metabolism of drugs and carcinogens by human liver enzymes." Journal of Pharmacology and Experimental Therapeutics 152.1 (1966): 151-156.
  18. Pirola, R. C., and C. S. Lieber. "The energy cost of the metabolism of drugs, including ethanol." Pharmacology 7.3 (1972): 185-196.
  19. Fouts, James R. "The metabolism of drugs by subfractions of hepatic microsomes." Biochemical and biophysical research communications 6.5 (1961): 373-378.
  20. Dixon, Robert L., Larry G. Hart, and James R. Fouts. "The metabolism of drugs by liver microsomes from alloxan-diabetic rats." Journal of Pharmacology and Experimental Therapeutics 133.1 (1961): 7-11.

Enjoyed the article? Want to continue the conversation?
Join Now

Do you want to receive the next Grower's Spotlight as soon as it's available? Sign up below!


Want to get in touch with Marco? He can be reached via the following methods:

  1. Email:

Do you have any questions or comments?

Feel free to post below!

About the Author

Marco Troiani is one of the founding members of Digamma Consulting and the laboratory manager. He was also the laboratory manager of DB Labs from its founding 2015-2016. His responsibilities included developing detection methods for terpenes and solvents (GC-MS), metals (ICP-MS), pesticides (GC-MS-MS), and Total Yeast and Mold, Total Aerobic Bacteria, Total Coliform Bacteria, and Salmonella spp. in cannabis and associated products.