BRITE Supplement Write-up

Supplement Write-Up Disclaimer:

In addition to running Depasi Fitness, I am also a freelance writer. Supplement companies hire me to do science write-ups for their new products, which are then published on the websites of retailers, the company itself, and various fitness forums. I only write for companies whose products I believe in, and I do not receive any financial compensation for the sale of their products, only payment for the writing itself. So when I post a write-up here, it's a product that I like, have probably used myself, and I make exactly zero dollars if you buy it.

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 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), can trigger brite cell formation, as well as cold therapy. 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

Tung Oil has been included in Brite as a major source of CLnA, as well as the 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, 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

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

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).


OxyMatrine has been shown to reduce fatty acid synthase (FAS, a fat storing enzyme) and Srebf1, increase CPT1A (an essential component of beta oxidation), and activate PPAR-a (27).

An exciting recent study looking at OxyMatrine's potential effect on non-alchoholic fatty liver disease (NAFLD) found some impressive results. These included reduced body fat, lower triglycerides, lower cholesterol, lower fasting insulin, improved insulin sensitivity, and PPAR-a activation (28).

Further investigation showed that OxyMatrine was able to combat the majority of the effects typically seen when overfeeding diabetic rats. It was able to decrease fasting glucose, glycosylated hemoglobin, triglycerides and LDL levels, while boosting insulin sensitivity, HDL and muscle cell GLUT-4 content (29).


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

Trans-Retinoic Acid 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).

Product Usage

Brite comes in a liquid suspension, and should be consumed three times daily (preferably with meals). While acute fat loss effects can and should be expected, the most pronounced benefits will likely be achieved over continued use due to the gradual conversion of WAT to Brite cells, helping those that are typically efficient at fat storage adopt a more naturally lean, fat burning phenotype.


1. Rosenwald M, Wolfrum C. The origin and definition of brite versus white and classical brown adipocytes. Adipocyte [Internet]. 2014 Jan 1 [cited 2014 Apr 19];3(1):4–9. Available from:

2. Nakamura Y, Sato T, Shiimura Y, Miura Y, Kojima M. FABP3 and brown adipocyte-characteristic mitochondrial fatty acid oxidation enzymes are induced in beige cells in a different pathway from UCP1. Biochem Biophys Res Commun [Internet]. 2013 Nov 8 [cited 2014 Apr 19];441(1):42–6. Available from:

3. Harms M, Seale P. Brown and beige fat: development, function and therapeutic potential. Nat Med [Internet]. 2013 Oct [cited 2014 Mar 20];19(10):1252–63. Available from:

4. Hennessy AA, Ross RP, Devery R, Stanton C. The health promoting properties of the conjugated isomers of α-linolenic acid. Lipids [Internet]. 2011 Feb [cited 2014 Apr 18];46(2):105–19. Available from:

5. Saha SS, Ghosh M. Antioxidant and anti-inflammatory effect of conjugated linolenic acid isomers against streptozotocin-induced diabetes. Br J Nutr [Internet]. 2012 Sep 28 [cited 2014 Apr 18];108(6):974–83. Available from:

6. Dhar P, Bhattacharyya D, Bhattacharyya DK, Ghosh S. Dietary comparison of conjugated linolenic acid (9 cis, 11 trans, 13 trans) and alpha-tocopherol effects on blood lipids and lipid peroxidation in alloxan-induced diabetes mellitus in rats. Lipids [Internet]. 2006 Jan [cited 2014 Apr 18];41(1):49–54. Available from:

7. Koba K, Akahoshi A, Yamasaki M, Tanaka K, Yamada K, Iwata T, et al. Dietary conjugated linolenic acid in relation to CLA differently modifies body fat mass and serum and liver lipid levels in rats. Lipids [Internet]. 2002 Apr [cited 2014 Apr 18];37(4):343–50. Available from:

8. Chou Y-C, Su H-M, Lai T-W, Chyuan J-H, Chao P-M. cis-9, trans-11, trans-13-Conjugated linolenic acid induces apoptosis and sustained ERK phosphorylation in 3T3-L1 preadipocytes. Nutrition [Internet]. 2012 Jul [cited 2014 Apr 14];28(7-8):803–11. Available from:

9. Dhar P, Chattopadhyay K, Bhattacharyya D, Roychoudhury A, Biswas A, Ghosh S. Antioxidative effect of conjugated linolenic acid in diabetic and non-diabetic blood: an in vitro study. J Oleo Sci [Internet]. 2006 Jan [cited 2014 Apr 18];56(1):19–24. Available from:

10. Lee J-S, Takai J, Takahasi K, Endo Y, Fujimoto K, Koike S, et al. Effect of dietary tung oil on the growth and lipid metabolism of laying hens. J Nutr Sci Vitaminol (Tokyo) [Internet]. 2002 Apr [cited 2014 Apr 14];48(2):142–8. Available from:

11. Tsuzuki T, Tokuyama Y, Igarashi M, Nakagawa K, Ohsaki Y, Komai M, et al. Alpha-eleostearic acid (9Z11E13E-18:3) is quickly converted to conjugated linoleic acid (9Z11E-18:2) in rats. J Nutr [Internet]. 2004 Oct [cited 2014 Apr 24];134(10):2634–9. Available from:

12. Kim Y, Kelly OJ, Ilich JZ. Synergism of α-linolenic acid, conjugated linoleic acid and calcium in decreasing adipocyte and increasing osteoblast cell growth. Lipids [Internet]. 2013 Aug [cited 2014 Mar 31];48(8):787–802. Available from:

13. Tran HNA, Bae S-Y, Song B-H, Lee B-H, Bae Y-S, Kim Y-H, et al. Pomegranate (Punica granatum) seed linolenic acid isomers: concentration-dependent modulation of estrogen receptor activity. Endocr Res [Internet]. 2010 Jan [cited 2014 Mar 26];35(1):1–16. Available from:

14. Chuang C-Y, Hsu C, Chao C-Y, Wein Y-S, Kuo Y-H, Huang C. Fractionation and identification of 9c, 11t, 13t-conjugated linolenic acid as an activator of PPARalpha in bitter gourd (Momordica charantia L.). J Biomed Sci [Internet]. 2006 Nov [cited 2013 Nov 7];13(6):763–72. Available from:

15. Nishimura K, Tsumagari H, Morioka A, Yamauchi Y, Miyashita K, Lu S, et al. Regulation of apoptosis through arachidonate cascade in mammalian cells. Appl Biochem Biotechnol [Internet]. [cited 2014 May 12];102-103(1-6):239–50. Available from:

16. Chan LLY, Chen Q, Go AGG, Lam EKY, Li ETS. Reduced adiposity in bitter melon (Momordica charantia)-fed rats is associated with increased lipid oxidative enzyme activities and uncoupling protein expression. J Nutr [Internet]. 2005 Nov [cited 2014 Apr 26];135(11):2517–23. Available from:

17. Hsieh C-H, Chen G-C, Chen P-H, Wu T-F, Chao P-M. Altered White Adipose Tissue Protein Profile in C57BL/6J Mice Displaying Delipidative, Inflammatory, and Browning Characteristics after Bitter Melon Seed Oil Treatment. PLoS One [Internet]. 2013 Jan [cited 2013 Oct 16];8(9):e72917. Available from:

18. Le NH, Shin S, Tu TH, Kim C-S, Kang J-H, Tsuyoshi G, et al. Diet enriched with korean pine nut oil improves mitochondrial oxidative metabolism in skeletal muscle and brown adipose tissue in diet-induced obesity. J Agric Food Chem [Internet]. 2012 Dec 5 [cited 2014 Apr 14];60(48):11935–41. Available from:

19. Park S, Lim Y, Shin S, Han SN. Impact of Korean pine nut oil on weight gain and immune responses in high-fat diet-induced obese mice. Nutr Res Pract [Internet]. 2013 Oct [cited 2014 Apr 14];7(5):352–8. Available from:

20. Takahashi Y, Ide T. Dietary n-3 fatty acids affect mRNA level of brown adipose tissue uncoupling protein 1, and white adipose tissue leptin and glucose transporter 4 in the rat. Br J Nutr [Internet]. 2000 Aug [cited 2014 Apr 14];84(2):175–84. Available from:

21. Okuno M, Kajiwara K, Imai S, Kobayashi T, Honma N, Maki T, et al. Perilla oil prevents the excessive growth of visceral adipose tissue in rats by down-regulating adipocyte differentiation. J Nutr [Internet]. 1997 Sep [cited 2014 Apr 14];127(9):1752–7. Available from:

22. Kim H-K, Choi H. Stimulation of acyl-CoA oxidase by alpha-linolenic acid-rich perilla oil lowers plasma triacylglycerol level in rats. Life Sci [Internet]. 2005 Aug 5 [cited 2014 Apr 14];77(12):1293–306. Available from:

23. Fukumitsu S, Villareal MO, Onaga S, Aida K, Han J, Isoda H. α-Linolenic acid suppresses cholesterol and triacylglycerol biosynthesis pathway by suppressing SREBP-2, SREBP-1a and -1c expression. Cytotechnology [Internet]. 2013 Dec [cited 2014 Mar 23];65(6):899–907. Available from:

24. Kim S-H, Nam J-H, Park E-J, Kim B-J, Kim S-J, So I, et al. Menthol regulates TRPM8-independent processes in PC-3 prostate cancer cells. Biochim Biophys Acta [Internet]. 2009 Jan [cited 2014 May 12];1792(1):33–8. Available from:

25. Rossato M, Granzotto M, Macchi V, Porzionato A, Petrelli L, Calcagno A, et al. Human white adipocytes express the cold receptor TRPM8 which activation induces UCP1 expression, mitochondrial activation and heat production. Mol Cell Endocrinol [Internet]. 2014 Mar 5 [cited 2014 May 1];383(1-2):137–46. Available from:

26. Takahashi Y, Ide T, Fujita H. Dietary gamma-linolenic acid in the form of borage oil causes less body fat accumulation accompanying an increase in uncoupling protein 1 mRNA level in brown adipose tissue. Comp Biochem Physiol B Biochem Mol Biol [Internet]. 2000 Oct [cited 2013 Oct 16];127(2):213–22. Available from:

27. Shi L, Shi L, Song G, Zhang H, Hu Z, Wang C, et al. Oxymatrine attenuates hepatic steatosis in non-alcoholic fatty liver disease rats fed with high fructose diet through inhibition of sterol regulatory element binding transcription factor 1 (Srebf1) and activation of peroxisome proliferator activated recep. Eur J Pharmacol [Internet]. 2013 Aug 15 [cited 2014 Apr 14];714(1-3):89–95. Available from:

28. Shi L, Shi L, Zhang H, Hu Z, Wang C, Zhang D, et al. Oxymatrine ameliorates non-alcoholic fatty liver disease in rats through peroxisome proliferator-activated receptor-α activation. Mol Med Rep [Internet]. 2013 Aug [cited 2014 Apr 14];8(2):439–45. Available from:

29. Guo C, Zhang C, Li L, Wang Z, Xiao W, Yang Z. Hypoglycemic and hypolipidemic effects of oxymatrine in high-fat diet and streptozotocin-induced diabetic rats. Phytomedicine [Internet]. 2014 Mar 25 [cited 2014 Apr 18]; Available from:

30. Couturier A, Ringseis R, Mooren F-C, Krüger K, Most E, Eder K. Carnitine supplementation to obese Zucker rats prevents obesity-induced type II to type I muscle fiber transition and favors an oxidative phenotype of skeletal muscle. Nutr Metab (Lond) [Internet]. 2013 Jul 10 [cited 2014 May 12];10(1):48. Available from:

31. Hahn P, Skala J. Carnitine and brown adipose tissue metabolism in the rat during development. Biochem J [Internet]. 1972 Mar [cited 2014 May 12];127(1):107–11. Available from:

32. Schlüter A, Barberá MJ, Iglesias R, Giralt M, Villarroya F. Phytanic acid, a novel activator of uncoupling protein-1 gene transcription and brown adipocyte differentiation. Biochem J [Internet]. 2002 Feb 15 [cited 2014 May 12];362(Pt 1):61–9. Available from:

33. Schluter A, Giralt M, Iglesias R, Villarroya F. Phytanic acid, but not pristanic acid, mediates the positive effects of phytol derivatives on brown adipocyte differentiation. FEBS Lett [Internet]. 2002 Apr 24 [cited 2014 May 12];517(1-3):83–6. Available from:

34. Kiefer FW, Vernochet C, O’Brien P, Spoerl S, Brown JD, Nallamshetty S, et al. Retinaldehyde dehydrogenase 1 regulates a thermogenic program in white adipose tissue. Nat Med [Internet]. 2012 Jun [cited 2014 Mar 20];18(6):918–25. Available from:

35. Mercader J, Palou A, Bonet ML. Induction of uncoupling protein-1 in mouse embryonic fibroblast-derived adipocytes by retinoic acid. Obesity (Silver Spring) [Internet]. 2010 Apr [cited 2014 Apr 18];18(4):655–62. Available from:

36. Del Mar Gonzalez-Barroso M, Pecqueur C, Gelly C, Sanchis D, Alves-Guerra MC, Bouillaud F, et al. Transcriptional activation of the human ucp1 gene in a rodent cell line. Synergism of retinoids, isoproterenol, and thiazolidinedione is mediated by a multipartite response element. J Biol Chem [Internet]. 2000 Oct 13 [cited 2014 Mar 23];275(41):31722–32. Available from:

37. Mercader J, Madsen L, Felipe F, Palou A, Kristiansen K, Bonet ML. All-trans retinoic acid increases oxidative metabolism in mature adipocytes. Cell Physiol Biochem [Internet]. 2007 Jan [cited 2014 Apr 18];20(6):1061–72. Available from:


Ingredients For Homemade Guacamole_ Avocado, Lemon, Salt And Pepper.jpg
Table Settings.jpg

Follow Us:

  • Grey YouTube Icon
  • Grey Pinterest Icon
  • Grey Twitter Icon
  • Grey Instagram Icon
  • Grey Facebook Icon