Hope Science

Simply put, Esterified oils are natural lubricants that work at the cellular level. Inflammation can occur or be made worse when dryness or a lack of lubrication occurs.

As an example, when a car is low on oil it can overheat or “inflame” resulting in damage to the engine. When we are inflamed damage to our cells can also occur.

It has been said that “We are not aging, rather we are inflaming.” Inflammation is a natural and necessary process that is always occurring in our bodies, but it is excess inflammation that is a concern.

Esterified oils are unique in that a high percentage of them are found in the cell membranes of our white blood cells or WBCs. White blood cells are known as the mediators of inflammation or in other words, WBCs play a key role in the process of inflammation.

In short, by targeting WBCs these lubricating oils travel to where they need to be in order to impact inflammation.

In Technical Language . . .

The cellular pathway instrumental in the efficacy of EFAC or Esterified Fatty Acid Complex

The clinical efficacy of EFAC has been documented in such esteemed journals as the Journal of Rheumatology and the Journal of Strength Conditioning and Research. It has been shown that EFAC reduces joint and muscular discomfort within 30 minutes of topical application and within 14 days of oral consumption.

Radio tracer label data and ligand binding assays support the hypothesis that EFAC interacts with membrane receptors involved with the inflammatory cascade. To support this hypothesis dual-label tracer data show the appearance of the labeled components of EFAC in the phospholipid fractions.

The greatest amount of the label was found in the phospholipid fractions of liver homogenates (e.g. microsomes) and white blood cell microsomes.

Binding assay studies have been conducted. In these in vitro studies, EFAC was shown to inhibit the thromboxane synthase enzyme using prostaglandin G2 (PGG2) and prostaglandin H2 (PGH2) as substrates.

Thromboxane is a very strong facilitator of inflammation and local tissue damage through a variety of mechanisms.

To further elucidate the mechanism of action on thromboxane production, receptor binding assays were carried out on the thromboxane A2 membrane receptor. EFAC was found to exert strong receptor binding inhibition using a standard radio binding assay.

The appearance of labeled EFAC within cellular membranes, especially those of the white blood cells, coupled with inhibition of thromboxane production or receptor inhibition suggests that EFAC influences the prostaglandin cascade and resulting inflammation.