Cannabidiolic acid (CBDA) is the acidic precursor to cannabidiol (CBD) and is most abundantly found in the glandular trichomes in the raw cannabis and hemp plant. Through the process of decarboxylation, CBDA converts to CBD. On its own CBDA has demonstrated a host of potential therapeutic benefits such as anti-nausea, anti-seizure, and anti-inflammatory activity. Let’s take a deeper dive into what research has to say about CBDA and its anti-hyperalgesia and anti-inflammatory effects.
In a 2018 study, CBDA was given to a rodent model of carrageenan induced acute inflammation and hyperalgesia in the rat hind paw. Hyperalgesia occurs when there is damage to the nerves or chemical changes to the nerve pathways, increasing sensitivity to pain. This can occur from nerve and tissue injuries, as well as long term opioid use. When CBDA was given to the rodent model 60 minutes prior to carrageenan, the cannabinoid produced dose dependent anti-hyperalgesia and anti-inflammatory effects. In addition, when ineffective doses of CBDA and Delta 9 THC alone were combined, the low doses showed effective in preventing inflammation and hyperalgesia. To compare CBDA and CBD an equivalent dose of CBD was administered in the rodent model and did not reduce hyperalgesia nor inflammation, suggesting CBDA is more potent than CBD in this indication. (Rock, et al, 2018)
CBDA may also produce anti-inflammatory effects via its role as a COX-2 (cyclooxygenase 2) enzyme inhibitor. COX-2 has an anti-inflammatory effect that non-steroidal anti-inflammatory drugs, such as aspirin, also inhibit. However, these drugs also inhibit COX-1, which with long term use can cause gastrointestinal complications. Because of this there is great therapeutic interest in finding a COX-2 inhibitor that bypasses COX-1. As a COX-2 inhibitor, studies have demonstrated CBDA as a safer option for anti-inflammatory effects. (Ruhaak, et al, 2011)
A 2008 study demonstrated CBDA inhibits the COX-2 enzyme in vitro. CBDA selectivity inhibited COX-2 activity with a 50% inhibition concentration (IC⁵⁰) of around 2 microM, having a 9-fold greater selectivity in inhibiting the COX-2 enzyme over COX-1. When the structural requirement for the CBDA mediated COX-2 inhibition was studied, it showed the inhibition was dependent on the presence of the carboxylic acid moiety in the CBDA molecule. (Takeda, et al, 2008)
These studies demonstrate CBDA as a potential therapeutic for those with inflammation and hyperalgesia and shows the need for continued research. As new research is concluded, will it show CBDA as a therapeutic option for those with arthritis, fibromyalgia, peripheral neuropathy, spinal injuries, and a host of other diseases that would benefit from the reduction of inflammation and hyperalgesia in the body? Only time and research will tell.
Rock, et al, 2018
Ruhaak, et al, 2011
Takeda, et al, 2008