Indigo-3GTM Repartitions Nutrients into
Muscle Instead of Fat

"Everything I eat seems to turn to muscle.

"When I started taking the dark-indigo capsules I weighed 221. Eight days later I had dumped fat and excess water and dropped down to 211. At first I thought I was taking a fat-burner. But after six days of adding carbs (like you suggested) I'm up to a lean 224, and I'm just as lean (if not leaner) as I was at 211!

"I hate to be 'that guy' who keeps on raving about something, but I honestly would take up a second mortgage to make sure that I never run out of this stuff. It keeps getting better and better. The only downside is that I'm changing too fast and people are starting to 'talk.'"

– Christian Thibaudeau

Medical research has given us something special, something that has the potential to make building muscle and losing fat a whole lot easier. Scientists have discovered a naturally occurring compound that has the ability to precisely control nutrients so that what you eat literally turns to muscle instead of fat.

No more bulking up and then dieting down, only to find that you lost as much muscle as fat. No more ketogenic starvation diets. No more haunting thoughts about the carbohydrate-dense foods you eat in moments of "weakness" destroying your hard work in the gym. And no more depriving yourself of the optimal nutrition for building muscle because "your body can't handle the calories and carbs" – because now it can.

All of this might seem hard to believe, but this compound really can override your body's often dysfunctional nutrient uptake signals and drive anabolic nutrition right into muscle cells, while at the same time starving fat cells.

The compound is called cyanidin 3-glucoside, or simply C3G. C3G is an anthocyanidin that's found mostly in certain berries. It's technically classified as a "pigment" – it's what gives blueberries their deep indigo-blue color.

Research has proven that C3G has a powerful effect on insulin signaling and glucose management. Furthermore, research has also shown that C3G is highly beneficial in regulating a variety of important cellular functions, including cell growth. C3G has even been shown to enhance night vision.

These are all incredible findings, but it's the research on glucose management that's grabbed the attention of the muscle-building world. To be able to precisely control nutrient uptake – shutting it down in fat and ramping it up in muscle – has been the ultimate desire of every advanced bodybuilder for the last 30 years.

C3G's effects on insulin signaling, selective insulin sensitivity, glucose and nutrient repartitioning, as well as its direct effect on fat and muscle cells, is extremely elaborate and precise. It literally makes your body function perfectly for building muscle mass without the fear of gaining fat, even while on a bulking diet.

C3G makes the body-building process a whole new ballgame, and here's how it performs its body-composition magic.

How C3G Works

Here's an interesting fact that you might not know. The fat cell (not the muscle cell) is a major regulator of how easily you gain muscle. It's the fat cell that sends all of the molecular signals for glucose and nutrient uptake in both fat and lean tissue. This is especially important because it's the nutrient uptake that has the most impact (not androgens) on gaining muscle.

As most advanced bodybuilders know, the most anabolic hormone in the body is insulin, not testosterone. Unfortunately, insulin is anabolic in both muscle and fat. But by decreasing the effects of insulin on fat and increasing the effects of insulin on muscle, you can achieve what no one thought was possible and turn the common man into a bodybuilding genetic freak.

As always, there are genetic limitations to how much muscle an individual can gain – C3G can't turn short muscle bellies into long muscle bellies. But I think we all understand that. The real issue at hand isn't the genetic limits on overall muscle size. The sad fact is, most people will never attain but a fraction of the gains they could – both in terms of muscle gains and overall leanness – due to their dysfunctional nutrient uptake.

"I Want to Get Big... I Want to Get Shredded... No, I Want to Get Big..."

Dysfunctional nutrient uptake results in what amounts to a bodybuilding identity crisis, where you go back and forth between trying to get big and trying to get shredded – but never truly achieving either goal.

You get bigger, alright, but it's mostly fat. You tend to rationalize it until the day you see some guy in the gym with razor-sharp etched muscle who has your look – at least, the one you've decided you want now. You're sick about what you've done to yourself, and with renewed vigor you're off to shredded-land. Except, at the end of that jaunt, you haven't etched anything and you're now "skinny," which totally ticks you off and sends you back the other direction.

This is obviously an irrational approach to achieving a lean and muscular body. But what's not so obvious is the cause of this dysfunction. It's due to a condition that's tantamount to "inflammatory fat disease."

Inflammatory Fat Disease

Most diseases of modern living have been linked to inflammation. So it's no wonder that researchers have found that inflammatory signaling has also caused fat cells to become dysfunctional, resulting in high circulating glucose levels, out of control appetite, fat cells that love to get "fatter," and lazy muscle cells that prefer to leave most of the fuel for the fat cells to gobble up and store.

This is where C3G comes in. The consensus among researchers is that C3G acts primarily (through the Glut4-RBP4 system) to optimize molecular crosstalk between fat cells, which directly decreases adipocyte inflammatory signals. The overall effect causes the body to repartition nutrients so that what you eat literally turns to muscle instead of fat.

In other words, your body resists storing fat, releases and oxidizes fat-cell content (fatty acids), and preferentially pulls glucose and nutrients into muscle cells.

The Effects of C3G on Target Tissues

Fat Cells – C3G actually up-regulates gene expression for fat oxidation (fat burning) and down-regulates gene expression for fat storage. The oxidation of fatty acids increases further directly through the release of adiponectin. The overall effect is that fat cells begin to shrink in size. The reduced inflammation also decreases the size of fat cells and disgorges the excess water associated with the inflammatory process (less bloated and squishy feeling to the fat under the skin).

Muscle Cells – Insulin sensitivity of muscle cells increases, thereby enhancing insulin signaling and glucose uptake, along with enhancing glycogen synthesis, which drives glucose and nutrients preferentially into muscle.

Liver Cells – Liver cells decrease gluconeogenesis via downregulation of glucose-6-phosphatase, preventing the liver from increasing circulating glucose levels.

GI Tract – Taken prior to meals, C3G decreases amylase and glucosidase, effectively decreasing the speed and extent of carbohydrate digestion.

A Permanent Solution?

This is "educated speculation" on our part, but if you're one of the many who can't handle carbs, your carb intolerance might not be a "life sentence." In fact, you could find that after being on C3G for a while (maybe 12 weeks or so), you might not need to continue taking it. In other words, we're thinking that fixing the fat cell really does fix the fat cell, and hopefully you'll eventually be handling carbs like a "normal" person even without taking C3G.

On the other hand, if, after going off C3G, you were to throw caution to the wind and begin eating like a carb junkie, you'd eventually go right back to your carb-intolerant old self with the added bonus of carrying around extra kilos of jiggly body fat. But if you followed reasonable dietary guidelines, it's perfectly plausible that you'd continue handling carbohydrates well.

Of course, you'd probably want to still use C3G from time to time as a preventative measure tune-up. You'd for sure want to use C3G during mass-gaining programs and, due to the highly anabolic nutrient-uptake effect C3G provides in muscle, advanced lifters would especially want to use C3G every time they trained.

Effective C3G Dosing

It's simple. Find raspberries or blueberries that actually contain high levels of C3G and then eat 12 pounds of them per day.

Too bad that's not really feasible. Besides, blueberries (and the other berries and their extracts) that contain C3G also contain quercetin and other compounds (anthocyanins and anthocyanidins) that can either inhibit or diminish the effects of C3G.

So, even if you had a bottomless pit of a stomach, it's literally impossible to eat enough blueberries or raspberries or berry extract to achieve any repartitioning effects from C3G.

And lastly, to make C3G even workable as a super-repartitioning compound, it needs to be formulated with enhanced bioavailability. So in summary, to be highly effective, you need a pure C3G compound that's bioengineered with enhanced bioavailability.

The only problem is, at the time we started this project, no one had produced C3G in a purified state and in quantities suitable for drug or supplement applications. The only pure C3G being sold was intended for research and it cost $1,200 for 100 mg. That means it would've cost more than $60,000 just to manufacture a single bottle of C3G!

So if we wanted pure C3G, we had no other choice but to make it ourselves.

This may come as a surprise, but we started this project a little more than six years ago. In January, 2005, Biotest began working with a drug-development group to produce a pure C3G compound. This past January (2011) – exactly six years later – Biotest finally received its first bulk shipment of C3G. It's a good thing we stuck with the project, too, because other than the material we produced, there's currently no production quantities of C3G available anywhere in the world.

Still, there is a small handful of supplements on the market formulated with crude extracts that claim to contain C3G. But just as the case with fresh berries and berry extracts, none of these products contain the purified form of C3G or anywhere close to the amount of C3G required to be effective for nutrient repartitioning. Furthermore, none are designed to enhance the absorption of C3G.

Indigo-3GTM – Bio-enhanced C3G

As soon as we received the material, we immediately began engineering a delivery system that would yield the enhanced bioavailability required to get the full effect we were after. Based on the chemical structure, we designed a self-microemulsifying gel matrix that, due to the dense color of C3G, produced a cool-looking dark indigo blue gel that we're calling Indigo-3GTM.

The Indigo-3GTM gel matrix was injected into capsules, each dosed with 125 milligrams of bioavailability enhanced C3G.

Next, we conducted a dosing time-course study in humans to see if we could achieve the blood levels of C3G we were hoping for. We also wanted to map the pharmacokinetics of the compound to determine optimal dose amounts and timing. Here are the findings thus far:

Indigo-3GTM Delivers High Levels of C3G

1.  Indigo-3GTM substantially enhances the bioavailability of C3G and produces much higher levels in circulating blood than any of the previous research indicated was possible.

2.  Indio-3GTM easily achieves the blood levels of C3G that we believe are required for maximum results.

3.  Indigo-3GTM dosing is optimal at three times per day, taken on an empty stomach, 30 - 60 minutes prior to a main meal or prior to starting peri-workout nutrition.

On to Phase 2

The next step is releasing Indigo-3GTM to a limited number of consumers, which will begin sometime next week. It's not because we need more people to "try" it to convince us it really works as well as it's working on our test subjects. We're far beyond that phase. Our test protocol was designed to see if it were possible to make Indigo-3GTM fail. It was pretty simple, really. We gave Indigo-3GTM to a variety of individuals and told them to follow only three rules:

We've been monitoring subjects for as long as three months, and the results we're seeing are so consistently profound among all subjects, we don't need any more convincing. It's simply time to begin letting the rest of the world in on our little secret.

Hopefully you'll be one of the fortunate few who are able to get your hands on Indigo-3GTM.

C3G Research

Cyanidin 3-glucoside ameliorates hyperglycemia and insulin sensitivity due to downregulation of retinol binding protein 4 expression in diabetic mice.

Adipocyte dysfunction is strongly associated with the development of obesity and insulin resistance. It is accepted that the regulation of adipocytokine expression is one of the most important targets for the prevention of obesity and improvement of insulin sensitivity. In this study, we have demonstrated that anthocyanin (cyanidin 3-glucoside; C3G) which is a pigment widespread in the plant kingdom, ameliorates hyperglycemia and insulin sensitivity due to the reduction of retinol binding protein 4 (RBP4) expression in type 2 diabetic mice. KK-A(y) mice were fed control or control +0.2% of a C3G diet for 5 weeks. Dietary C3G significantly reduced blood glucose concentration and enhanced insulin sensitivity. The adiponectin and its receptors expression were not responsible for this amelioration. C3G significantly upregulated the glucose transporter 4 (Glut4) and downregulated RBP4 in the white adipose tissue, which is accompanied by downregulation of the inflammatory adipocytokines (monocyte chemoattractant protein-1 and tumor necrosis factor-alpha) in the white adipose tissue of the C3G group. These findings indicate that C3G has significant potency in an anti-diabetic effect through the regulation of Glut4-RBP4 system and the related inflammatory adipocytokines.

Biochem Pharmacol. 2007 Dec 3;74(11):1619-27. Epub 2007 Aug 10.

Anthocyanin enhances adipocytokine secretion and adipocyte-specific gene expression in isolated rat adipocytes.

Adipocyte dysfunction is strongly associated with the development of obesity and insulin resistance. It is accepted that the regulation of adipocytokine secretion or the adipocyte-specific gene expression is one of the most important targets for the prevention of obesity and amelioration of insulin sensitivity. In this study, we demonstrated that anthocyanins (cyanidin or cyanidin 3-glucoside) have the potency of a unique pharmacological function in isolated rat adipocytes. Treated adipocytes with anthocyanins enhanced adipocytokine (adiponectin and leptin) secretion and up-regulated the adipocyte specific gene expression without activation of PPARgamma in isolated rat adipocytes. The gene expression of adiponectin was also up-regulated in white adipose tissue in mice fed an anthocyanin supplemented diet. As one of the possible mechanisms, AMP-activated protein kinase activation would be associated with these changes, nevertheless, the AMP:ATP ratio was significantly decreased by administration of the anthocyanins. These data suggest that anthocyanins have a potency of unique therapeutic advantage and also have important implications for preventing obesity and diabetes.

Biochem Biophys Res Commun. 2004 Mar 26;316(1):149-57.

Cyanidin 3-glucoside protects 3T3-L1 adipocytes against H2O2- or TNF-alpha-induced insulin resistance by inhibiting c-Jun NH2-terminal kinase activation.

Anthocyanins are naturally occurring plant pigments and exhibit an array of pharmacological properties. Our previous study showed that black rice pigment extract rich in anthocyanin prevents and ameliorates high-fructose-induced insulin resistance in rats. In present study, cyanidin 3-glucoside (Cy-3-G), a typical anthocyanin most abundant in black rice was used to examine its protective effect on insulin sensitivity in 3T3-L1 adipocytes exposed to H(2)O(2) (generated by adding glucose oxidase to the medium) or tumor necrosis factor alpha (TNF-alpha). Twelve-hour exposure of 3T3-L1 adipocytes to H(2)O(2) or TNF-alpha resulted in the increase of c-Jun NH(2)-terminal kinase (JNK) activation and insulin receptor substrate 1 (IRS1) serine 307 phosphorylation, concomitantly with the decrease in insulin-stimulated IRS1 tyrosine phosphorylation and cellular glucose uptake. Blocking JNK expression using RNA interference efficiently prevented the H(2)O(2)- or TNF-alpha-induced defects in insulin action. Pretreatment of cells with Cy-3-G reduced the intracellular production of reactive oxygen species, the activation of JNK, and attenuated H(2)O(2)- or TNF-alpha-induced insulin resistance in a dose-dependent manner. In parallel, N-acetyl-cysteine, an antioxidant compound, did not exhibit an attenuation of TNF-alpha-induced insulin resistance. Taken together, these results indicated that Cy-3-G exerts a protective role against H(2)O(2)- or TNF-alpha-induced insulin resistance in 3T3-L1 adipocytes by inhibiting the JNK signal pathway.

Biochem Pharmacol. 2008 Mar 15;75(6):1393-401. Epub 2007 Dec 3.

Microarray profiling of gene expression in human adipocytes in response to anthocyanins.

Adipocyte dysfunction is strongly associated with the development of obesity and insulin resistance. It is accepted that the regulation of adipocytokine secretion or the adipocyte specific gene expression is one of the most important targets for the prevention of obesity and amelioration of insulin sensitivity. Recently, we demonstrated that anthocyanins, which are pigments widespread in the plant kingdom, have the potency of anti-obesity in mice and the enhancement adipocytokine secretion and its gene expression in adipocytes. In this study, we have shown the gene expression profile in human adipocytes treated with anthocyanins (cyanidin 3-glucoside; C3G or cyanidin; Cy). The human adipocytes were treated with 100 microM C3G, Cy or vehicle for 24 h. The total RNA from the adipocytes was isolated and carried out GeneChip microarray analysis. Based on the gene expression profile, we demonstrated the significant changes of adipocytokine expression (up-regulation of adiponectin and down-regulation of plasminogen activator inhibitor-1 and interleukin-6). Some of lipid metabolism related genes (uncoupling protein2, acylCoA oxidase1 and perilipin) also significantly induced in both common the C3G or Cy treatment groups. These studies have provided an overview of the gene expression profiles in human adipocytes treated with anthocyanins and demonstrated that anthocyanins can regulate adipocytokine gene expression to ameliorate adipocyte function related with obesity and diabetes that merit further investigation.

Biochem Pharmacol. 2006 Apr 14;71(8):1184-97. Epub 2006 Feb 17.

Gene expression profile of isolated rat adipocytes treated with anthocyanins.

Adipocyte dysfunction is strongly associated with the development of obesity and insulin resistance. It is accepted that the regulation of adipocytokine secretion or the adipocyte specific gene expression is one of the most important targets for the prevention of obesity and amelioration of insulin sensitivity. Recently, we demonstrated that anthocyanins, which are pigments widespread in the plant kingdom, have the potency of anti-obesity in mice and the enhancement adipocytokine secretion and adipocyte gene expression in adipocytes. In this study, we have shown for the first time the gene expression profile in isolated rat adipocytes treated with anthocyanins (cyanidin 3-glucoside; C3G or cyanidin; Cy). The rat adipocytes were treated with 100 muM C3G, Cy or vehicle for 24 h. The total RNA from the adipocytes was isolated and carried out GeneChip microarray analysis. A total of 633 or 427 genes was up-regulated (>1.5-fold) by the treatment of adipocytes with C3G or Cy, respectively. The up-regulated genes include lipid metabolism and signal transduction-related genes, however, the altered genes were partly different between the C3G- and Cy-treated groups. Based on the gene expression profile, we demonstrated the up-regulation of hormone sensitive lipase and enhancement of the lipolytic activity by the treatment of adipocytes with C3G or Cy. These data have provided an overview of the gene expression profiles in adipocytes treated with anthocyanins and identified new responsive genes with potentially important functions in adipocytes related with obesity and diabetes that merit further investigation.

Biochim Biophys Acta. 2005 Apr 15;1733(2-3):137-47. Epub 2005 Jan 12.

Hypoglycemic activity of a novel anthocyanin-rich formulation from lowbush blueberry, Vaccinium angustifolium Aiton.

Blueberry fruits are known as a rich source of anthocyanin components. In this study we demonstrate that anthocyanins from blueberry have the potency to alleviate symptoms of hyperglycemia in diabetic C57b1/6J mice. The anti-diabetic activity of different anthocyanin-related extracts was evaluated using the pharmaceutically acceptable self-microemulsifying drug delivery system: Labrasol. Treatment by gavage (500 mg/kg body wt) with a phenolic-rich extract and an anthocyanin-enriched fraction formulated with Labrasol lowered elevated blood glucose levels by 33 and 51%, respectively. The hypoglycemic activities of these formulae were comparable to that of the known anti-diabetic drug metformin (27% at 300 mg/kg). The extracts were not significantly hypoglycemic when administered without Labrasol, demonstrating its bio-enhancing effect, most likely due to increasing the bioavailability of the administered preparations. The phenolic-rich extract contained 287.0+/-9.7 mg/g anthocyanins, while the anthocyanin-enriched fraction contained 595+/-20.0 mg/g (cyanidin-3-glucoside equivalents), as measured by HPLC and pH differential analysis methods. The greater hypoglycemic activity of the anthocyanin-enriched fraction compared to the initial phenolic-rich extract suggested that the activity was due to the anthocyanin components. Treatment by gavage (300 mg/kg) with the pure anthocyanins, delphinidin-3-O-glucoside and malvidin-3-O-glucoside, formulated with Labrasol, showed that malvidin-3-O-glucoside was significantly hypoglycemic while delphinidin-3-O-glucoside was not.

Phytomedicine. 2009 May;16(5):406-15. Epub 2009 Mar 20.

Dietary cyanidin 3-O-beta-D-glucoside-rich purple corn color prevents obesity and ameliorates hyperglycemia in mice.

Anthocyanins, which are used as a food coloring, are widely distributed in human diets, suggesting that we ingest large amounts of anthocyanins from plant-based foods. Mice were fed control, cyanidin 3-glucoside-rich purple corn color (PCC), high fat (HF) or HF + PCC diet for 12 wk. Dietary PCC significantly suppressed the HF diet-induced increase in body weight gain, and white and brown adipose tissue weights. Feeding the HF diet markedly induced hypertrophy of the adipocytes in the epididymal white adipose tissue compared with the control group. In contrast, the induction did not occur in the HF + PCC group. The HF diet induced hyperglycemia, hyperinsulinemia and hyperleptinemia. These perturbations were completely normalized in rats fed HF + PCC. An increase in the tumor necrosis factor (TNF)-alpha mRNA level occurred in the HF group and was normalized by dietary PCC. These results suggest that dietary PCC may ameliorate HF diet-induced insulin resistance in mice. PCC suppressed the mRNA levels of enzymes involved in fatty acid and triacylglycerol synthesis and lowered the sterol regulatory element binding protein-1 mRNA level in white adipose tissue. These down-regulations may contribute to triacylglycerol accumulation in white adipose tissue. Our findings provide a biochemical and nutritional basis for the use of PCC or anthocyanins as a functional food factor that may have benefits for the prevention of obesity and diabetes.

J Nutr. 2003 Jul;133(7):2125-30.

Cyanidin 3-glucoside protects 3T3-L1 adipocytes against H2O2- or TNF-alpha-induced insulin resistance by inhibiting c-Jun NH2-terminal kinase activation.

Anthocyanins are naturally occurring plant pigments and exhibit an array of pharmacological properties. Our previous study showed that black rice pigment extract rich in anthocyanin prevents and ameliorates high-fructose-induced insulin resistance in rats. In present study, cyanidin 3-glucoside (Cy-3-G), a typical anthocyanin most abundant in black rice was used to examine its protective effect on insulin sensitivity in 3T3-L1 adipocytes exposed to H(2)O(2) (generated by adding glucose oxidase to the medium) or tumor necrosis factor alpha (TNF-alpha). Twelve-hour exposure of 3T3-L1 adipocytes to H(2)O(2) or TNF-alpha resulted in the increase of c-Jun NH(2)-terminal kinase (JNK) activation and insulin receptor substrate 1 (IRS1) serine 307 phosphorylation, concomitantly with the decrease in insulin-stimulated IRS1 tyrosine phosphorylation and cellular glucose uptake. Blocking JNK expression using RNA interference efficiently prevented the H(2)O(2)- or TNF-alpha-induced defects in insulin action. Pretreatment of cells with Cy-3-G reduced the intracellular production of reactive oxygen species, the activation of JNK, and attenuated H(2)O(2)- or TNF-alpha-induced insulin resistance in a dose-dependent manner. In parallel, N-acetyl-cysteine, an antioxidant compound, did not exhibit an attenuation of TNF-alpha-induced insulin resistance. Taken together, these results indicated that Cy-3-G exerts a protective role against H(2)O(2)- or TNF-alpha-induced insulin resistance in 3T3-L1 adipocytes by inhibiting the JNK signal pathway.

Biochem Pharmacol. 2008 Mar 15;75(6):1393-401. Epub 2007 Dec 3.

Indigo-3G™

Selective Nutrient Repartitioning Agent™

180 capsules

Info Label + Favorites

$160