Frankincense, also called, olibanum, is an aromatic resin obtained by tapping the Boswellia tree. These trees grow primarily in the horn of Africa and the Arabian Peninsula; we source our resins from producers who use sustainable harvesting and fair-trade labor practices (because frankincense is so prized in perfumery, there’s a lot of overharvesting). We also use the whole resin versus the distilled oil because some of the heavier components are retained, which imbues the finished product with more therapeutic value and a rounder scent.

So what are those therapeutic properties? Primarily, anti-inflammatory,[1] meaning its great for muscle pain and sore joints. There have been a number studies investigating the precise mechanism of this action. One found that the triterpene acids help counteract inflammation,[2] another found that “Boswellic acids inhibit the leukotriene synthesis via 5-lipoxygenase.”[3] A third found that frankincense “exhibits anti-inflammatory property in human PBMCs and mouse macrophages through inhibition of TNFα, IL-1β, NO and MAP kinases.”[4]  Since we don’t really understand what any of that means, we’ll take their word for it.

Citations

[1] Singh, G.B. & Atal, C.K. Pharmacology of an extract of salai guggal ex-Boswellia serrata, a new non-steroidal anti-inflammatory agent. Agents and Actions (1986) 18: 407. doi:10.1007/BF01965005

[2] Banno, N., Akihisa, T., Yasukawa, K., Tokuda, H., Tabata, K., Nakamura, Y., . . . Suzuki, T. (2006). Anti-inflammatory activities of the triterpene acids from the resin of Boswellia carteri. Journal of Ethnopharmacology, 107(2), 249-253. doi:10.1016/j.jep.2006.03.006

[3] Ammon, H., Safayhi, H., Mack, T., & Sabieraj, J. (1993). Mechanism of antiinflammatory actions of curcumine and boswellic acids. Journal of Ethnopharmacology, 38(2-3), 105-112. doi:10.1016/0378-8741(93)90005-p

[4] Gayathri, B., Manjula, N., Vinaykumar, K., Lakshmi, B., & Balakrishnan, A. (2007). Pure compound from Boswellia serrata extract exhibits anti-inflammatory property in human PBMCs and mouse macrophages through inhibition of TNFα, IL-1β, NO and MAP kinases. International Immunopharmacology, 7(4), 473-482. doi:10.1016/j.intimp.2006.12.003