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BRITE™ Enhanced Write-up
Intro
In 2013, Evolutionary Muse rocked the industry by releasing the first product designed to cause white adipocytes to convert into BRITE adipocytes. Aptly named BRITE, these adipocytes are named for being BROWN IN WHITE cells—white adipocytes which behave like brown adipocytes. Brown adipocytes are metabolically active cells which, unlike white adipocytes, use their fat stores to generate body heat. Long thought to be non-existent or very rare in humans, brown adipocytes were discovered to be quite active, though through evolution, environmental mastery (i.e., comfortable living via climate control), and more than adequate dietary satisfaction (leading to its own hormonal milieu), brown fat activation became almost dormant. This brown fat:white fat reduction has instead led to massive insulin resistance, leptin chaos, and major obesity.
With years more painstaking research, Evolutionary Muse has once again taken huge leaps forward, finally perfecting a formula that is easily encapsulated in a powdered version, while delivering a powerhouse formula that triggers a huge shift in damaging white fat towards metabolically hyperactive BRITE fat.
Difference between WAT and BAT
Brown Adipose Tissue (BAT) is abundant in small mammals like rodents, as well as newborn humans, and is thought to offer an evolutionary protection against cold temperatures to increase survival rate. BAT works quite differently, if not opposite, to White Adipose Tissue (WAT). BAT is dense in mitochondria and considered a highly thermogenic fat cell, responsible for creating heat through a process called “non-shivering thermogenesis”. This process burns calories through a futile cycle of shuttling protons to the mitochondria to generate heat. WAT, however, is what we all think of when we hear the term “body fat”. It stores calories so they can be used later during periods of hunger or famine, and secretes various adipokines. This is a crucial part of our physiology, and we would not exist today without it. But these WAT cells can become dysfunctional (for genetic reasons, poor diet, lack of exercise, etc.) and get too good at storing fat.
It was previously thought that adult humans have an inconsequential amount of BAT. In recent years, however, it has been determined that we have more than originally thought. We have also learned that we don’t need a large volume of these cells to have a significant impact.
Even more recently, we have discovered another player in the adipocyte story—Brown-In-White cells, or “BRITE”. At a microscopic level, these cells display a color between brown and white, and behave in a similar thermogenic fashion to BAT cells. They are also known as beige, inducible, recruitable-brown, and brown adipocyte-like cells, but we will refer to them as beige/brite moving forward.
The research on brite cells is still in early stages, but we now know enough about how they are formed and the metabolic advantage they are capable of providing that we can target them as a viable and important angle in weight management and metabolic optimization. UCP1 expressing adipocytes are lower in obese and older subjects. While we don’t know yet if reduced thermogenic activity is a cause or consequence of obesity, we do know that an increase in BAT and/or brite cells improves glucose tolerance and insulin sensitivity.
Two distinct pathways exist towards increasing brite cells in adult humans, (1) triggering precursor cells into becoming brite cells, and (2) turning mature WAT cells into brite cells. We want to target these pathways directly so that we can increase the ratio of brite cells to WAT cells, allowing your body to constantly burn more calories.
Let’s dive into some of the known methods of brite cell creation and activation.
Irisin and PGC-1alpha
Exercise causes increased expression in muscle of PPARg coactivator 1-alpha (PGC-1a), which downstream results in a hormone/myokine called irisin. This irisin contributes to a browning of WAT cells. So not only does exercise burn calories directly, but also secondarily through triggering the browning process with irisin. Fortunately, this is an exploitable angle independent of exercise by triggering the PPARg cascade.
Cold Therapy, B3 adrenergic activators
Cold exposure triggers macrophages in BAT to produce catecholamines like norepinephrine (NE). NE agonizes b-adrenergic receptors on fat cells. Cold also activates beige cell development and function. The effect can be mimicked with b3 adrenergic activators, which also trigger PGC-1a and brite cell development. It can also be mimicked with TRPM, or cold-sensor activators.
PRDM16, BMP-7
Prdm16 is a transcriptional cofactor, substantially enriched in human BAT compared to adjacent WAT. It acts by binding to and modulating other factors like C/EBPb, PPARy, PPARa, and the aforementioned PGC-1a. Knocking out Prdm16 negates the thermogenic effect of brown cells, and increases WAT. Considered a key driver of brown fat cell fate, this cofactor is quite important. Bone Morphogenetic Protein-7 (BMP-7) increases expression of Prdm16 in precursor cells, and is essential for brown fat development. BMP-7 is fortunately something we can target with supplementation.
Adenylyl Cyclase (AC) and Alpha-1 adrenergic activation
AC is an enzyme that catalyzes the conversion of ATP to cyclic AMP. We mentioned beta-adrenergic receptor agonism, but it turns out this is greatly enhanced with simultaneous AC upregulation and alpha-1 activation. So targeting AC, alpha-1, and beta-adrenergic agonism together causes enhanced brite cell creation.
UCP1
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. Multiple ingredients in the BRITE™ formula will encourage WAT cells to upregulate UCP1 levels.
Some of you may be familiar with a somewhat popular drug in the bodybuilding community years ago called DNP (which actually has roots in the 1930s as a weight loss drug). DNP was meant to mimic activated UCP1, which drastically elevated thermogenesis. While extremely effective, unregulated uncoupling can (and did) cause hyperthermia and death. Fortunately, we now have effective ways of targeting UCP1 safely.
Intro
In 2013, Evolutionary Muse rocked the industry by releasing the first product designed to cause white adipocytes to convert into BRITE adipocytes. Aptly named BRITE, these adipocytes are named for being BROWN IN WHITE cells—white adipocytes which behave like brown adipocytes. Brown adipocytes are metabolically active cells which, unlike white adipocytes, use their fat stores to generate body heat. Long thought to be non-existent or very rare in humans, brown adipocytes were discovered to be quite active, though through evolution, environmental mastery (i.e., comfortable living via climate control), and more than adequate dietary satisfaction (leading to its own hormonal milieu), brown fat activation became almost dormant. This brown fat:white fat reduction has instead led to massive insulin resistance, leptin chaos, and major obesity.
With years more painstaking research, Evolutionary Muse has once again taken huge leaps forward, finally perfecting a formula that is easily encapsulated in a powdered version, while delivering a powerhouse formula that triggers a huge shift in damaging white fat towards metabolically hyperactive BRITE fat.
Difference between WAT and BAT
Brown Adipose Tissue (BAT) is abundant in small mammals like rodents, as well as newborn humans, and is thought to offer an evolutionary protection against cold temperatures to increase survival rate. BAT works quite differently, if not opposite, to White Adipose Tissue (WAT). BAT is dense in mitochondria and considered a highly thermogenic fat cell, responsible for creating heat through a process called “non-shivering thermogenesis”. This process burns calories through a futile cycle of shuttling protons to the mitochondria to generate heat. WAT, however, is what we all think of when we hear the term “body fat”. It stores calories so they can be used later during periods of hunger or famine, and secretes various adipokines. This is a crucial part of our physiology, and we would not exist today without it. But these WAT cells can become dysfunctional (for genetic reasons, poor diet, lack of exercise, etc.) and get too good at storing fat.
It was previously thought that adult humans have an inconsequential amount of BAT. In recent years, however, it has been determined that we have more than originally thought. We have also learned that we don’t need a large volume of these cells to have a significant impact.
Even more recently, we have discovered another player in the adipocyte story—Brown-In-White cells, or “BRITE”. At a microscopic level, these cells display a color between brown and white, and behave in a similar thermogenic fashion to BAT cells. They are also known as beige, inducible, recruitable-brown, and brown adipocyte-like cells, but we will refer to them as beige/brite moving forward.
The research on brite cells is still in early stages, but we now know enough about how they are formed and the metabolic advantage they are capable of providing that we can target them as a viable and important angle in weight management and metabolic optimization. UCP1 expressing adipocytes are lower in obese and older subjects. While we don’t know yet if reduced thermogenic activity is a cause or consequence of obesity, we do know that an increase in BAT and/or brite cells improves glucose tolerance and insulin sensitivity.
Two distinct pathways exist towards increasing brite cells in adult humans, (1) triggering precursor cells into becoming brite cells, and (2) turning mature WAT cells into brite cells. We want to target these pathways directly so that we can increase the ratio of brite cells to WAT cells, allowing your body to constantly burn more calories.
Let’s dive into some of the known methods of brite cell creation and activation.
Irisin and PGC-1alpha
Exercise causes increased expression in muscle of PPARg coactivator 1-alpha (PGC-1a), which downstream results in a hormone/myokine called irisin. This irisin contributes to a browning of WAT cells. So not only does exercise burn calories directly, but also secondarily through triggering the browning process with irisin. Fortunately, this is an exploitable angle independent of exercise by triggering the PPARg cascade.
Cold Therapy, B3 adrenergic activators
Cold exposure triggers macrophages in BAT to produce catecholamines like norepinephrine (NE). NE agonizes b-adrenergic receptors on fat cells. Cold also activates beige cell development and function. The effect can be mimicked with b3 adrenergic activators, which also trigger PGC-1a and brite cell development. It can also be mimicked with TRPM, or cold-sensor activators.
PRDM16, BMP-7
Prdm16 is a transcriptional cofactor, substantially enriched in human BAT compared to adjacent WAT. It acts by binding to and modulating other factors like C/EBPb, PPARy, PPARa, and the aforementioned PGC-1a. Knocking out Prdm16 negates the thermogenic effect of brown cells, and increases WAT. Considered a key driver of brown fat cell fate, this cofactor is quite important. Bone Morphogenetic Protein-7 (BMP-7) increases expression of Prdm16 in precursor cells, and is essential for brown fat development. BMP-7 is fortunately something we can target with supplementation.
Adenylyl Cyclase (AC) and Alpha-1 adrenergic activation
AC is an enzyme that catalyzes the conversion of ATP to cyclic AMP. We mentioned beta-adrenergic receptor agonism, but it turns out this is greatly enhanced with simultaneous AC upregulation and alpha-1 activation. So targeting AC, alpha-1, and beta-adrenergic agonism together causes enhanced brite cell creation.
UCP1
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. Multiple ingredients in the BRITE™ formula will encourage WAT cells to upregulate UCP1 levels.
Some of you may be familiar with a somewhat popular drug in the bodybuilding community years ago called DNP (which actually has roots in the 1930s as a weight loss drug). DNP was meant to mimic activated UCP1, which drastically elevated thermogenesis. While extremely effective, unregulated uncoupling can (and did) cause hyperthermia and death. Fortunately, we now have effective ways of targeting UCP1 safely.
-GP inhibition and Physical contact enhancement with enterocytes.
is finishing up production today, and will be ready to ship to customers early next week.
