Brite Cell Overview
In order to fully understand the concept of EvoMuse Brite, a bit of background science will be beneficial before we get into the specific ingredients.
Many years ago, it was thought that adult mammalian fat cells (adipocytes) were all basically the same. Under a microscope, they appeared white (white adipose tissue, or WAT), and they did a great job at storing fat in case it needed to be used later during periods of hunger or famine. While much maligned by fitness enthusiasts, WAT is essential to our functioning and survival, and is actually quite beneficial when it works as intended. However, sometimes WAT becomes dysfunctional, and gets too good at storing fat, for various genetic and/or dietary reasons, leading to conditions of overweight and obesity.
Then came the discovery of brown fat (BAT) it rodents, which appeared to act quite differently from traditional WAT. Behaving in a contradictory fashion, BAT was actually shown to be dense in mitochondria, and therefore thermogenic. It was determined that these cells primary function was something called “non-shivering thermogenesis”, involving a futile cycle of shuttling protons to the mitochondria to generate heat (1).
This got researchers excited, and they began to study BAT for anti-obesity purposes. Several years later, this was all but abandoned, due to the initial apparent lack of BAT cells in humans past infancy.
Fast forward to recent years, and it was discovered that adult humans actually do have a significant amount of BAT cells. The quantity is small in comparison to WAT cells, but as it turns out, you don’t need a large volume of these fat-burning cells to instigate a significant metabolic effect. So researchers revisited BAT upregulation as an avenue to treat obesity.
Based on the most current research, we have now discovered another player in the adipocyte continuum. These are called “Brite” cells. At a microscopic level, brite cells display a color in-between BAT and WAT cells, although they behave similar if not almost the same as BAT. And unlike BAT, they are actually created within WAT cells.
These cells are currently referred to in the research by several names; brite, beige, inducible, recruitable-brown, and brown adipocyte-like cells. For the purpose of this write up, we will be referring to them as “brite”; a name derived from a combination of the words “brown-in-white”.
While the research on brite cells is in its infancy, we do know enough about these fascinating metabolically active fat depots to take steps to encourage their activation and therefore fat burning potential. EvoMuse Brite has been developed with the goal of shifting those with the unfortunate fat storing phenotype to a more genetically lean, fat burning phenotype.
The goal is to convince the WAT cells currently in your body, to trigger the intracellular production of brite cells, so that instead of just being fat storage depots and adipokine factories, they will also actually burn fat.
Research has shown that the hormone irisin (endogenous or exogenous), might trigger brite cell formation, as well as cold therapy, but the evidence is quite often contradictory as far as effectiveness. One of the current lines of thought is that not all white cells have this potential to turn brite, but those that do are located in specific places in humans, particularly along the spine and around the collarbone. But like BAT cells, we don’t need many of them to have a big effect. And it turns out; people genetically prone to fatness are likely to express less of these cells.
BAT mitochondria respond to something called UCP1 (uncoupling protein 1) to burn fat and generate heat, while brite cells seem to express lower levels of UCP1. However, brite cells potentially burn fat independently of UCP1 signaling, and furthermore, with the proper triggers, brite fat can actually turn on high levels of UCP1 (2). Multiple ingredients in the Brite formula will encourage WAT cells to upregulate UCP1 levels.
The research shows that once developed, these brite cells directly correlate with leanness and can likely reduce metabolic disease and obesity in humans (3).
With that background in mind, the next thing we want to look at is a fatty acid called CLnA.
Conjugated Linolenic Acid (CLnA)
By now most people are well aware of conjugated linoleic acid (CLA), and while a similar fatty acid, conjugated linolenic acid (CLnA) functions quite differently. CLnA is found naturally in several seed oils, but can also be produced in small amounts endogenously by gut bacteria.
Current research has demonstrated CLnA’s unique potential for fat loss from multiple angles. We have multiple sources of CLnA in the Brite formula, but first lets look at a little background on the overall CLnA research.
In a recent review published in the journal Lipids, CLnA was found to exhibit anti-obeseogenic properties, as well as reducing inflammation, boosting immune function, and improving overall cardiovascular health (4).
The worst thing a WAT cell can do is become dysfunctional, which will reduce it’s ability to become a brite cell and cause it to become highly efficient at excessive fat storage and poor at releasing stored fatty acids to be oxidized. Normal cellular functioning involves low oxidative stress, low lipid peroxidation, and low inflammation, with optimal levels of superoxide dismutase (SOD). CLnA administration has been shown to support all of these (5,6).
In a study comparing CLnA to CLA, animals had a higher beta-oxidation rate and lost more fat in the CLnA group (7). Another study showed that CLnA had an apoptotic effect on proliferating pre-adipocytes (8). From a general health perspective, CLnA has also been shown to protect LDL cholesterol from oxidation (9).
TUNG OIL HAS BEEN REMOVED. THE DOSAGE OF BMSO HAS BEEN INCREASED TO COVER THE AEA REQUIREMENT.
has been included in Brite as a major source of CLnA, as well as the specific isomer a-Eleostearic Acid (AEA). Aside from all of the above cellular browning benefits from CLnA, researchers looking directly at the effects of Tung Oil found that when they added it to the diet of hens, they demonstrated a remarkably small amount of adipose tissue weight compared to non-Tung fed counterparts. They also noted reduced tryglyceride levels in heart and adipose tissue (10).
Also another point of interest, research shows that a portion of ingested AEA converts to CLA in the body (11). And while the body of research supporting the fat loss potential of CLA has been inconclusive, a 2013 study published in the journal Lipids found that a combination of CLA and alpha linoleic acid (see Perilla Oil below) blocked adipogenesis (12).
Additionally, AEA has been shown to act as a Selective Estrogen Receptor Modulator (SERM), thereby potentially reducing some of the negative effects of excess estrogen (13).
Bitter Melon Seed Oil
Bitter Melon Seed Oil (BMSO) is a another source of CLnA as well as AEA. In addition to the previously stated benefits of CLnA and AEA, Bitter Melon has also been shown to be a direct PPAR-a activator, which is one of the most important players in all three stages of fat burning (14). It has also been shown to cause apoptosis in undifferentiated adipocytes, thereby inhibiting the creation of new fat cells (15).
BMSO has also been shown in multiple studies to upregulate mitochondrial biogenesis and UCP1 (16),(27). And in an exciting study published in 2013, BMSO was shown to have a direct browning effect on WAT cells (17).
Korean Pine Nut Oil
Korean Pine Nut Oil (PNO) has been shown to upregulate UCP1 levels via its Pinolenic Acid content, as well as activate PPAR alpha and delta. Based on these findings, the researchers concluded PNO may have potential to counteract obesity (18).
In addition, a recent study showed that mice supplemented with PNO, when overfed, gained significantly less weight vs. the control group, demonstrating potential as an anti-obesity agent (19).
Perilla Seed Oil
Perilla Seed Oil (PO) is rich in Alpha Linoleic Acid (ALA), which has been shown to upregulate UCP1 levels and improve glucose metabolism (20). As discussed above, it also has an anti-adipogenic effect when coupled with CLA, for which Tung Oil is a precursor.
In comparison to feeding of olive oil or beef fat, Perilla Seed Oil (PO) was shown to reduce body fat and lower serum triglycerides, as well as suppress the late phase of adipocyte differentiation (21,22).
ALA has also been shown to decrease several fat storing enzymes and upregulate fatty acid oxidation (23).
Peppermint oil activates a cellular protein called TRPM8, also known as the cold and menthol receptor (24). Upon activation we see an increased expression of UCP1 in WAT cells, causing a direct browning effect (25).
Borage Oil is a rich source of Gamma Linoleic Acid (GLA), a fatty acid with a long list of benefits. For our purposes, GLA has been shown to increase expression of UCP1, decrease body fat storage, and increase fat oxidation (26).
Carnitine has been shown to increase UCP1 levels in rats (30). Acetyl-l-Carnitine also plays an important role in optimizing fat oxidation in browned adipocytes (31).
Phytol is an organic alcohol that converts to phytanic acid during metabolism. Phytanic acid has been shown to cause a browning effect in pre-adipocytes as well as activate UCP1 in existing brown fat cells, enhancing their fat burning function (32,33).
Trans-Retinoic Acid, from botanicals such as Rosehip Oil, has been included in the formula due to its potential ability to encourage adipocyte browning, again through UCP1 activation (34–36). It has also been shown to decrease cellular triglyceride content, while upregulating lipolysis and fatty acid oxidation, therefore shifting WAT to behave in a more metabolically oxidative fashion (37).