As you may recall from our many “Nrf2-activating” discussions over the years, certain botanical compounds like sulforaphane glucosinolate, curcumin, resveratrol and green tea function to increase intracellular signaling of a key transcription factor, Nrf2. When activated, this master antioxidant switches functions to increase the production of many detoxification, antioxidant-SOD, and catalase- and anti-inflammatory proteins (See image above).
Before we discuss Abbott Pharmaceutical’s announcement to invest $400 million in the development of Nrf2 activators (see below), we should note that since 2006 we have been teaching functional practitioners about the incredible science and health benefits surrounding sulforaphane mediated activation of the Nrf2 pathway.
As such, it’s not surprising that many other nutrient lines and now big pharma have recently tried to picky-back on this innovation by jumping on the Nrf2-sulforaphane bandwagon. Unfortunately, most of these companies are providing sub-therapeutic levels of sulforaphane (e.g. 5 mg VS 30 mg and 100 mg) and/or don’t use 100% of the true Johns Hopkins high-yield, 13% sulforaphane material, as found in products produced by reputable nutrition companies. If your shopping for sulforaphane product, make sure you have an assay from industry leading 3rd party groups to verify the amount of sulforaphane in your raw material.
To learn more about increasing sales, and other great tips, sign up for our exclusive Blog Marketing Academy newsletter.
Just today, Abbott announced that they are going to spend $400 million in R&D in collaboration with Reata Pharmaceuticals to create “oral antioxidant inflammation modulators” or AIMs for short. The press release notes: “AIMs are potent activators of the transcription factor Nrf2. Activation of Nrf2 promotes the production of a wide range of antioxidant, detoxification and anti-inflammatory genes.”
Also highlighted is something we’ve been teaching to clinicians about Nrf2 activation for years: Nrf2 activators like sulforaphane crank the gas pedal on anti-inflammatory gene networks while at the same time slam the brakes on the pro-inflammatory gene networks, also known as NFKB. Abbott notes:
“Activation of Nrf2 also inhibits NF-KB, a transcription factor that regulates many pro-inflammatory enzymes. Suppression of Nrf2 and activation of NF-KB have been associated with numerous chronic diseases, including multiple sclerosis, rheumatoid arthritis, chronic kidney disease, neurodegenerative disease and COPD.”