• Short-term inflammation is a protective response, but chronic inflammation can have a negative effect on the human body.
• Palmitoylethanolamide (PEA), Terminalia chebula, grape seed extract and magnolia are among the options for formulators.
• The anti-inflammatory market is projected to reach US$130.6 billion by 2026 with a CAGR of 8.5 percent from 2018 to 2026.
Inflammation is one of the body’s natural defense mechanisms, addressing hazardous stimuli such as tissue damage or allergens. On a short-term basis, inflammation can help the body return to a healthy state. However, according to a 2016 review, “Uncontrolled inflammatory response is the main cause of a vast continuum of disorders including allergies, cardiovascular dysfunctions, metabolic syndrome, cancer and autoimmune diseases.”1
While various pharmaceuticals are available to help control and suppress inflammatory crisis, the potential for side effects and the desire for a natural course of action lead many consumers to seek alternative solutions. The review noted several herbs with anti-inflammatory effects that have been evaluated in clinical and experimental studies, including Curcuma longa (curcumin), Zingiber officinale (ginger), Rosmarinus officinalis (rosemary), Borago officinalis (borage), evening primrose and devil’s claw. It also mentioned, “the treatment of inflammation is not a one-dimensional remedy,” and therefore, suggested “a multidimensional therapeutic approach to inflammation with the help of herbal medicine and modification in lifestyle.”
Blake Ebersole, president of NaturPro Scientific, pointed to palmitoylethanolamide (PEA) as an emerging anti-inflammatory ingredient that’s been studied in large trials in Europe. It’s a peroxisome proliferator-activated receptor-alpha (PPAR-α) ligand that exerts anti-inflammatory, analgesic and neuroprotective actions.2 A 2014 review noted PEA was first identified as an anti-inflammatory compound more than half a century ago, but greater exploration didn’t occur until the mid-1990s. PEA was shown to reduce tumor necrosis factor (TNF)-α in lipopolysaccharide (LPS, a pro-inflammatory endotoxin)-induced pulmonary inflammation in mice, as well as mast cell degranulation and edema formation in various inflammatory models.3
The review mentioned more recent investigation of the anti-inflammatory mechanisms. PEA inhibited phosphorylation of kinases involved in activation of pro-inflammatory pathways, and the nuclear translocation of nuclear factor-kappa beta (NF-κβ) and activator protein 1 (AP-1), as well as preventing degradation of the inhibitory IκB-α, which when associated to NF-κβ prevents its nuclear translocation.4,5