How Does Decarboxylation Effect Cannabinoids?

CANNABIS CULTURE-  Marco Troiani is a lab scientist with with cannabis research firm, Digamma Consulting. In the following piece, Troiani explains how the decarboxylation process helps create safe, potent, quality cannabis extracts.


Decarboxylation is a process by which carbon dioxide (CO2) leaves a stable molecule and floats off as a gas. Atoms in a molecule can be thought of like billiard balls, with each one having a size, weight, and exact position. As these atoms float away, the substance left behind will become lighter, like a dry towel being lighter than that same towel soaking wet. The idea is that as the CO2 leaves, the weight left behind is a process in which carbon dioxide (CO2) leaves a stable molecule and floats off as a gas. Atoms in a molecule can be thought of like billiard balls, with each one having a size, weight, and exact position. As these atoms float away, the substance left behind will become lighter, like a dry towel being lighter than that same towel soaking wet. The idea is that as the CO2 leaves, the weight left behind is reduced.



As we can see in the illustration, the weight of the CO2 is lost as it floats away, leaving less mass and weight of substance than before decarboxylation occurred. Decarboxylation typically occurs when a substance is heated, but it can also be caused by exposure to certain frequencies of light, and catalyzed by certain substances like molecular oxygen in the air.

If the weight of the molecule before and after its decarboxylation is known, then a percent of mass lost in decarboxylation can be calculated. If the CO2 contributes 10% of the weight of a molecule, than 90% of the mass remains after decarboxylation. This would mean that continuously heating 100 g of this substance would eventually yield 90 g of the decarboxylated substance, as the remaining 10 g represent the weight of CO2 which gassed off.

Cannabis only has the ability to produce cannabinoid acids, like THCA and CBDA. THC is only created when the buds are decarboxylatedized outside the plant. This decarboxylation is usually achieved by the heat of fire when smoked, or from the heat of baking in edibles. Most cannabinoids lose approximately 12.3% of their mass upon decarboxylation. That means that if you had 100g of crystalline isolate of a cannabinoid acid, such as THCA, after decarboxylation you would have 87.7 grams left of THC.

This knowledge is important for people decarboxylating cannabinoids by themselves, particularly producers of cannabis-infused edible products and hash oil producers that wish to sell decarboxylated oil. This is also important for brokers of raw cannabis products such as cured cannabis flower, who must either report the value of the cannabinoid acid directly observed by the testing lab, use the theoretical conversion, or display both.

The labeling issue with raw flower is not as easy as it seems at first glance. Let’s consider a typical example of THC-dominant cannabis. A lab will test the flower and find 26% THCA and 3% THC. 3% THC occurs because a small amount of the cannabinoid acids are decarboxylated by air and sun before harvesting and curing. The smaller amount of THC observed directly by the lab typically indicates that the cultivator has submitted fresh cannabis that has been protected from light and exposure. A higher THC content indicates that the cannabis flower has undergone more exposure and is therefore not as fresh as flower with a low THC content.

Now a broker or dispensary has a choice to advertise certain numbers: 26% and 3% from lab testing, a theoretically calculated number of 25.8% THC, or both sets of numbers. Providing the patient with both sets of numbers gives them the greatest amount of information, while also reducing liability on the cannabis business involved in label making. Sample calculations are provided below:

26% THCAobserved x 0.877 = 22.8% THCtheoretical [decarboxylation of THCA]

22.8% THCtheoretical + 3% THCobserved = 25.8% THCmaximum [summing of THC]

(26% THCAobserved x 0.877) + 3% THCobserved = 25.8% THCmaximum [compound formula]

It is important to note that the mass loss is not a conversion rate. Mass loss assumes that all of a substance will decarboxylate and calculates how the mass will change. An accurate answer must account for how much of the cannabinoid will decarboxylate. Studies indicate that 30-70% of cannabinoids undergo decarboxylation under standard smoking conditions34. This is why our calculations at Digamma are only a theoretical maximum, and are not a result with the same standing as those directly observed in the plant. This is also why it can be very important to label your theoretical calculations as such, and provide all original values provided by lab results, as a means of reducing liability upon your business.

Common naming systems used in California, Colorado, Massachusetts, Nevada, Oregon, and Washington for the maximum calculated THC are “total THC” “potential THC” and “maximum THC”, though one naming scheme has not emerged as the industry standard yet.

Part 2

Decarboxylation of cannabinoids is crucial to understanding cannabis as medicine. Each cannabinoid acid decarboxylates into its corresponding free cannabinoid, such as THCA decarboxylating to THC and CBDA decarboxylating to CBD. Although the body is capable of converting cannabinoids into a variety of metabolites, once a cannabinoid acid enters the body it is generally not converted to its free cannabinoid form. This means that administering THCA and THC will have different effects on the human mind and body, and this essential difference can be found among all cannabinoids. Below is an overview of the major cannabinoids and the pharmacological and medical differences between their acids and their free forms.


Tetrahydrocannabinol (THC) is a well-known cannabinoid that acts as the primary intoxicant and euphoriant of cannabis. THC is also one of the most practical and safe treatments for neuropathic, chronic, and other types of pain1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12. THC is effective in addressing both the immunological and symptom component of Multiple Sclerosis (MS)5, 6, 13, 14, 15, 16.



Despite the fact that THCA is not an intoxicant, it is a powerful medicine. THCA is one of the strongest anti-inflammatory agents in cannabis7, 17, 18. Smokers receive very little to none of this cannabinoid, due to its decomposition in the smoking process. THCA is an anti-inflammatory agent, and according to one study, a more powerful neuroprotective agent than THC19. THCA is a powerful COX-1 and COX-2 antagonist, similar to aspirin and ibuprofen, but with far less toxicity to the liver17.

The effects of THCA and THC reflect the diversity of action on the human body a cannabinoid and its precursor acid can have. The other cannabinoids, CBD, CBG, CBC, and THCV all have acid forms which have distinct effects on human health.


Cannabidiol (CBD) has been shown to be an effective medicine for people suffering from anxiety5, 7, 18, 20, 21, 22, 23, 24, 25, 26, 27, 28. CBD has also been shown to be effective at fighting is breast cancer cells29, 30. Many studies find that CBD promotes apoptosis, or cell suicide, in breast cancer cells while leaving the healthy cells unaffected.


Cannabidiolic acid (CBDA) is CBD’s acid precursor from raw cannabis flower. CBDA has also been shown to fight human breast cancer, but in a different way. Whereas CBD causes apoptosis in breast cancer cells, CBDA has been shown to slow or stop metastasis of breast cancer cells by arresting their motility, or ability to move throughout the body31. This evidence would indicate that a breast cancer patient may want to talk to their doctor about dual CBD/CBDA therapy, taking both decarboxylated CBD and raw CBDA together.


Cannabigerol (CBG) has been shown to have some potent anti-inflammatory properties that are particularly applicable in inflammatory bowel disease (IBS)32. Additionally, CBG has been shown to have some properties not known among many other cannabinoids, such as an ability to interact with human adrenal receptors and serotonin receptors33. Currently, more studies need to be done on Cannabigerolic Acid (CBGA) in isolation from CBG to learn what, if any, difference there are between the cannabinoid and its precursor acid on human health.



Featured Image of Marco Troiani provided by Digamma Consulting



  1. Burns, Tammy L., and Joseph R. Ineck. “Cannabinoid analgesia as a potential new therapeutic option in the treatment of chronic pain.” Annals of Pharmacotherapy 40.2 (2006): 251-260.
  2. De Petrocellis, Luciano, et al. “Plant-derived cannabinoids modulate the activity of transient receptor potential channels of ankyrin type-1 and melastatin type-8.” Journal of Pharmacology and Experimental Therapeutics 325.3 (2008): 1007-1015.
  3. Fine, Perry G., and Mark J. Rosenfeld. “The endocannabinoid system, cannabinoids, and pain.” Rambam Maimonides medical journal 4.4 (2013).
  4. Fine, Perry G., and Mark J. Rosenfeld. “Cannabinoids for neuropathic pain.” Current pain and headache reports 18.10 (2014): 451.
  5. Kogan, Natalya M., and Raphael Mechoulam. “Cannabinoids in health and disease.” Dialogues in clinical neuroscience 9.4 (2007): 413.
  6. Russo, Ethan B. “Cannabinoids in the management of difficult to treat pain.” Therapeutics and Clinical Risk Management 4.1 (2008): 245.
  7. Russo, Ethan B. “Taming THC: potential cannabis synergy and phytocannabinoid‐terpenoid entourage effects.” British journal of pharmacology 163.7 (2011): 1344-1364.
  8. Mechoulam, Raphael, and Shimon Ben-Shabat. “From gan-zi-gun-nu to anandamide and 2-arachidonoylglycerol: the ongoing story of cannabis.” Natural product reports 16.2 (1999): 131-143.
  9. Wilson-Poe, Adrianne R., et al. “The periaqueductal gray contributes to bidirectional enhancement of antinociception between morphine and cannabinoids.” Pharmacology Biochemistry and Behavior 103.3 (2013): 444-449.
  10. Ware, Mark A., et al. “Smoked cannabis for chronic neuropathic pain: a randomized controlled trial.” Canadian Medical Association Journal 182.14 (2010): E694-E701.
  11. Nurmikko, Turo J., et al. “Sativex successfully treats neuropathic pain characterised by allodynia: a randomised, double-blind, placebo-controlled clinical trial.” Pain® 133.1 (2007): 210-220.
  12. Johnson, Jeremy R., et al. “Multicenter, double-blind, randomized, placebo-controlled, parallel-group study of the efficacy, safety, and tolerability of THC: CBD extract and THC extract in patients with intractable cancer-related pain.” Journal of pain and symptom management 39.2 (2010): 167-179.
  13. Koppel, Barbara S., et al. “Systematic review: Efficacy and safety of medical marijuana in selected neurologic disorders Report of the Guideline Development Subcommittee of the American Academy of Neurology.” Neurology 82.17 (2014): 1556-1563.
  14. M Saito, Viviane, Rafael M Rezende, and Antonio L Teixeira. “Cannabinoid modulation of neuroinflammatory disorders.” Current neuropharmacology 10.2 (2012): 159-166.
  15. Russo, Ethan, et al. “Chronic cannabis use in the Compassionate Investigational New Drug Program: An examination of benefits and adverse effects of legal clinical cannabis.” Journal of Cannabis Therapeutics 2.1 (2002): 3-57.
  16. Zajicek, J. P., et al. “Cannabinoids in multiple sclerosis (CAMS) study: safety and efficacy data for 12 months follow up.” Journal of Neurology, Neurosurgery & Psychiatry 76.12 (2005): 1664-1669.
  17. Ruhaak, Lucia Renee, et al. “Evaluation of the cyclooxygenase inhibiting effects of six major cannabinoids isolated from Cannabis sativa.” Biological and Pharmaceutical Bulletin 34.5 (2011): 774-778.
  18. Izzo, Angelo A., et al. “Non-psychotropic plant cannabinoids: new therapeutic opportunities from an ancient herb.” Trends in pharmacological sciences 30.10 (2009): 515-527.
  19. Moldzio, Rudolf, et al. “Effects of cannabinoids Δ (9)-tetrahydrocannabinol, Δ (9)-tetrahydrocannabinolic acid and cannabidiol in MPP+ affected murine mesencephalic cultures.” Phytomedicine 19.8 (2012): 819-824.
  20. Bergamaschi, Mateus M., et al. “Cannabidiol reduces the anxiety induced by simulated public speaking in treatment-naive social phobia patients.” Neuropsychopharmacology 36.6 (2011): 1219-1226.
  21. Bergamaschi, Mateus Machado. Subjecffve effects of cannabidiol in anxiety disorder and canabinoid excretion in chronic daily cannabis smokers during sustained abstinence. Diss. Universidade de São Paulo.
  22. Campos, Alline Cristina, et al. “Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders.” Phil. Trans. R. Soc. B 367.1607 (2012): 3364-3378.
  23. Gururajan, Anand. “Comment on:“Anxiogenic-like effects of chronic cannabidiol administration in rats”(Elbatsh MM, Assareh N, Marsden CA, Kendall DA, Psychopharmacology 2012).” Psychopharmacology (2012): 1-2.
  24. Malone, Daniel Thomas, Dennis Jongejan, and David Alan Taylor. “Cannabidiol reverses the reduction in social interaction produced by low dose Δ 9-tetrahydrocannabinol in rats.” Pharmacology Biochemistry and Behavior 93.2 (2009): 91-96.
  25. Hill, Andrew J., et al. “Phytocannabinoids as novel therapeutic agents in CNS disorders.” Pharmacology & therapeutics 133.1 (2012): 79-97.
  26. Sarris, Jerome, Erica McIntyre, and David A. Camfield. “Plant-based medicines for anxiety disorders, part 2: a review of clinical studies with supporting preclinical evidence.” CNS drugs 27.4 (2013): 301-319.
  27. Khanum, Farhath, and Sakina Razack. “Anxiety–Herbal treatment: A review.” Res Rev Biomed Biotech 1.2 (2010): 83-89.
  28. Fusar-Poli, Paolo, et al. “Modulation of effective connectivity during emotional processing by Δ9-tetrahydrocannabinol and cannabidiol.” International journal of neuropsychopharmacology 13.4 (2010): 421-432.
  29. Ligresti, Alessia, et al. “Antitumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma.” Journal of Pharmacology and Experimental Therapeutics 318.3 (2006): 1375-1387.
  30. Caffarel, María M., et al. “Cannabinoids: a new hope for breast cancer therapy?.” Cancer treatment reviews 38.7 (2012): 911-918.
  31. Takeda, Shuso, et al. “Cannabidiolic acid, a major cannabinoid in fiber-type cannabis, is an inhibitor of MDA-MB-231 breast cancer cell migration.” Toxicology letters 214.3 (2012): 314-319.
  32. Borrelli, Francesca, et al. “Beneficial effect of the non-psychotropic plant cannabinoid cannabigerol on experimental inflammatory bowel disease.” Biochemical pharmacology 85.9 (2013): 1306-1316.
  33. Cascio, M. G., et al. “Evidence that the plant cannabinoid cannabigerol is a highly potent α2‐adrenoceptor agonist and moderately potent 5HT1A receptor antagonist.” British journal of pharmacology 159.1 (2010): 129-141.
  34. Dussy, Franz E., et al. “Isolation of Δ 9-THCA-A from hemp and analytical aspects concerning the determination of Δ 9-THC in cannabis products.” Forensic science international 149.1 (2005): 3-10.