SupraBiotic™The Slimming Probiotic™Beyond the cutting edge of probiotic research and development, SupraBiotic™ combines 6 probiotic strains, 100 billion colony forming units, with an unrivalled auxillary formula, optimized to turn the bacterial milieu of your gut into a mean, lean body machine. It does not stop at fat loss, though, fighting and fixing inflammatory pathways that wreak havoc on insulin sensitivity, cardiovascular and digestive health, the immune system, and even your skin.

Currently, probiotics are mostly thought of and used in relation to a healthy digestive system (reducing upset stomach, gas and bloating, diarrhea, and IBS type symptoms) and the immune system (coughs, colds, and general sinus and respiratory health). While they certainly are indeed useful for such applications, the ramifications of an unhealthy gut and microbiota go far, far beyond that.

The gut and its microbiome are essentially a massive endocrine organ, controlling and influencing basically your entire body and brain. And, given that all of the trillions of bacteria that call it home originally came from outside your body – and entered without your permission – it is by far the most important organ in which we can take steps to manipulate and take back control.

We will first look at some basic science and data on how this all works. Then, we will look at studies that have shown alterations in the microbiotic make-up of the gut, and the correlations they display in health and disease, suboptimal and optimal fitness, and just general things that everyone would consider part of good or bad life outcomes.

It is a massive subject, far too much to discuss in complete depth, here, so we’ll do our best to keep it as short and sweet as possible while still giving you enough background in this field to understand the shocking reality, scope, and importance of this microscopic invasion.

Subsequently, we will get down to business and specifically get into the science of Shock Treatment™, the first step in the process of making yourself king or queen of your own castle, again. We’ll show you how it can immediately ameliorate symptoms, while preparing the gut for a permanent fix, with special emphasis on a lean, healthy body.

Deus Vult!

The BasicsIt basically works like this. The Western lifestyle, including diet, lack of exercise, and alcohol use (and, in all likelihood, genetics, though the data just isn’t there, yet) leads to an imbalance of the bacterial composition of the gut (1, 2). This results in the excess production and release of inflammatory signals, such as Lipopolysaccharide, TNF-alpha, interleukins, and prostaglandins, which subsequently escape the gut and enter the rest of your body (3).

Though, they all contribute to the pathologies we will cover in various ways, it is Lipopolysaccharide (LPS) that we will focus on the most. Within the gut, this leads to the general digestive issues and inflammatory bowel syndromes like IBS and colitis that you have commonly known probiotics as being used to alleviate (4).

While fixing digestive disorders will come along for the ride, our primary focus is going to be on body composition and metabolic health. In other words, we want to make you leaner, protect against diabetes, and help keep you from having a heart attack or stroke. However, there really is so much more to it than that, as a few quotes from the literature aptly demonstrate:

“Changes in the composition of the gut microbiota (dysbiosis) may be associated with several clinical conditions, including obesity and metabolic diseases, autoimmune diseases and allergy, acute and chronic intestinal inflammation, irritable bowel syndrome (IBS)…” (5)

“In this milieu… disturbance of the gut microbiota balance and the intestinal barrier permeability is a potential triggering factor for systemic inflammation in the onset and progression of obesity, type 2 diabetes and metabolic syndrome.” (6)

“Through these varied mechanisms, gut microbes shape the architecture of sleep and stress reactivity of the hypothalamic-pituitary-adrenal axis. They influence memory, mood, and cognition and are clinically and therapeutically relevant to a range of disorders, including alcoholism, chronic fatigue syndrome, fibromyalgia, and restless legs syndrome… Nutritional tools for altering the gut microbiome therapeutically include changes in diet, probiotics, and prebiotics.” (7)

As you can see, alterations in the microbiota can affect basically everything, but that there is also hope for change.

Getting back to the gut and body composition, the aforementioned Lipopolysaccharide (LPS) leads to overactivation of cannabinoid receptor 1 (CB1) within the gut, which causes an increase in intestinal motility (speed of food going through) in the proximal parts of the intestine. This leads to less absorption of nutrient feedback signals that tell the brain you are well fed, and that it is time to stop eating (8). Concurrent with this is an increase in transit time in the colon, which results in a greater total harvest of caloric energy from your food (9, 10).

In other words, the signal your brain is getting is that you are not getting enough food, while you are actually extracting more calories from what you eat. This not only directly leads to more fat accumulation from harvesting more calories, it lends itself to over-eating. This aggravates the cycle further, as overeating and increased adiposity are themselves inflammatory. So, what you have is more inflammation, more dysfunction, greater food intake, greater extraction of food, more fat accumulation, then REPEAT!

The carnage does not even end here. Along with this inflammatory state is a disruption in the intestinal barrier. Intestinal permeability is increased and these inflammatory agents spill out systemically. This is often called a “leaky gut”. This results in a low-level inflammatory state in the entire body. The biggest culprit here is, once again, LPS (11).

LPS activates CB1 receptors in the body and brain, just as in the intestine. In the fat tissue, this leads to activation of PPAR-gamma, and an upregulation of triglyceride synthesis, fat cell formation, and fat storage (12). In the brain, activation of CB1 increases orexegenic pathways, thus increasing appetite, hunger, and ultimately, food intake (13). This should not much as much of a surprise considering “the munchies” that accompany intake of famous cannabinoid receptor agonist, marijuana.

And, LPS is not done yet, not at all. It also activates Toll-like Receptor 4 which, along with other inflammatory signals (TNF-alpha, interleukins), promotes both insulin and leptin insensitivity, peripherally and centrally (14, 15). At this point, your adipostat (the thermostat for your body fat level) is wrecked. Your ability to control food intake is gone, and you are a fat storing machine. Obviously, this is not what you want your body doing to itself. It is not what you want it doing to you. It is not what you want it doing to your life.

Oh, and to top it off, atherosclerosis, heart disease, and stroke are promoted by these same inflammatory pathways. Combined with the increased body fat and insulin resistance, you officially have all of the perfect ingredients for the dreaded Metabolic Syndrome (16, 17).

And, it is just a bunch of microscopic bacteria that call your gut “home” causing all of this devastation.

General DataThe most well-known genera of bacteria in commercial probiotics are Lactobacillus and Bifidobacterium. They are also among the most common in the body, along with several other ones which are not commercially available, but which we can manipulate with supplementation. We will talk about these in length in a bit, as well as in the Primer™ write-up.

Unfortunately, Lactobacillus belong to the Firmicutes phylum which has been found to be associated with weight gain and obesity (18-20). Just a 20% increase in Firmicutes (which Lactobacillus is usually the primary genus) with an equal decrease in Bacteroides results in an increased energy harvest of 150 calories per day in humans (21). That is equal to 15lbs of fat per year! The Western style diet promotes these negative changes in microbial proportions (22). Thus, one can plainly see why it can be so difficult to get lean, as well as how easily obesity has become an epidemic.

Interestingly, smoking cessation produces the same negative changes in bacterial composition, while gastric bypass surgery improves it (23-24). The well-known effects on weight with both of these further highlights the negative body compositional effects of this intestinal dysbiosis.

In addition, probiotic treatment with several Lactobacillus species that are in a great number of commercial formulations, including Lactobacillus acidophilus, Lactobacillus fermentum, and Lactobacillus ingluviei , have been directly associated with weight gain and obesity (25). Type-2 diabetics had significantly more Lactobacillus, with L. acidophilus being particularly bad in this regard (26). Further, L. Reuteria and L. Sakei have been found to be positively associated with obesity and body mass index (27-29). They probably don’t tell you that on the label.

More powerful evidence of the profound effect of the microbiota on body weight and metabolism come from studies on “fecal transfer”. And, yes, that is exactly what it sounds like – transferring poop from one subject’s intestine to another’s.

In twins, transfer of an obese microbiota to lean mice was accompanied by an increase in bodyweight, fat mass, and a dysbiotic alteration of the Firmicutes:Bacteroides ratio to reflect that of the obese model (30). A similar transfer replicated the obese phenotype with increased weight gain, lipogenesis, adipogenesis, overeating, and lower satiety, as well as inflammation and hyperglycemia in formerly lean, healthy subjects (31, 32).

On the other side of the coin, transferring the intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome, as well as reversing obesity and gastrointestinal issues (33). It also reduced markers of metabolic syndrome, inflammation, and oxidative stress in animals challenged with high-fructose diets (34).

Obviously, while it highlights the science, doing a fecal transfer is not terribly practical, appetizing, or readily available -- unless maybe you are in California.

Fortunately, there is good news. While several species and strains of lactobacillus have been found to promote weight gain, several have also been found to protect against it. And, of course, we only used the good ones. Furthermore, Bifidobacterium have shown only positive effects to a remarkable extent.

SupraBiotic™ IngredientsBifidobacterium are anti-obesity and lipid lowering, decreasing fat weight, blood glucose, cholesterol, and triglyceride levels (35). They are higher in lean subjects, as well as being lower in obese (36, 37). They are significantly lower in type-II diabetics and have been shown to improve glucose tolerance as well to decrease inflammatory signaling (38-40). In addition, they increase levels of fish oils EPA and DHA, as well as conjugated linoleic acid (CLA), in fat tissue and the brain (40). They have also been found to be reduced with aging (41).

We can also readily manipulate levels of the good bacteria that are not commercially available such as Bacteroides species, Roseburia species, Akkermansia Muciniphilia, and Facealbacterium Prausnitzii via supplementation of ingredients that ARE available.

You may have noticed that almost no probiotic formulas contain just a single species of bacteria, nowadays. And, if you did not, I will just say that it is for a good reason. They work better in combination.

First of all, microbial diversity seems to be good, in and of itself. Essentially, a diverse gut is a healthy gut (42). Obesity has been associated with a lack of microbial diversity and, as you might expect, lean subjects have greater microbial diversity in the gut (43-45). Insulin sensitivity is also improved along with diversity increases (46). Finally, in the interesting but not terribly shocking category, exercise increases

microbial diversity (47, 48).

Combinations also work to specifically create an environment where probiotic bacteria can thrive, thus enhancing their ultimate performance (49). Compared to individual strains alone, it greatly increases adhesion to intestinal mucus, which is necessary for most survival, growth, and activity (50, 51). Conversely, they inhibit adhesion of pathogenic bacteria better when in combination (52, 53).

However, you do not want to just throw every single commercially available species and strain into a product as so many companies do. They need to be rationally combined. If not, they can interfere with each other’s actions and compete for space and resources (54-56).

But, the most interesting benefit of probiotic combinations is through cross-feeding. This is when one bacterial strain produces metabolites the others use for fuel (57).

We will get into this in detail, in a bit. Right now, let’s get to the SupraBiotic™ probiotic combination.

Bifidobacterium breveB. breve supplementation significantly suppressed the accumulation of body weight and fat mass, while improving serum levels of total cholesterol, fasting glucose, and insulin (58). The expression of genes related to fat metabolism and insulin sensitivity in both the gut and fat tissue was upregulated by its administration (59). It also improved lipid levels and insulin resistance while lowering bodyweight (60).

In addition, B. breve combats the cycle of LPS inflammation, leaky gut, and insulin/leptin resistance. It reduced LPS activity 60% and quelled general colonic inflammation, particularly TNF-alpha, a downstream signal of LPS (61-63). It also upregulated anti-inflammatory pathways such as interleukin-8 and Toll-like Receptor-2 (64, 65). The latter having the opposite effect as TLR-4. Ultimately, it is reinforcing on intestinal epithelial cells and mucosa, improving the physical barrier of the intestine (66, 67).

Bifidobacterium animalis subsp. lactisB. animalis subsp. lactis ferments a wide range of oligosaccharides quite extensively, so it is very versatile, being viable under numerous different conditions (68). It increased short chain fatty acid (SCFA) production to distal parts of the colon, meaning it has a long acting mechanism of action (69). We will discuss SCFAs a good bit more below, but they provide fuel for intestinal barrier repair, as well as having other metabolic benefits – and, their production is one of the main ways probiotics exert their positive effects.

This species is negatively associated with body mass index in humans, and increased levels are associated with resistance to obesity (70-71). It prevents weight gain, reduces fat mass accumulation and LPS levels, while preserving glucose tolerance in the face of a high-fat diet (72, 73). Administration shifts the microbiota toward that of a lean phenotype while reducing inflammatory activity (73). Interestingly, it also improved the efficacy of diabetic drug and AMPK agonist metformin, suggesting

potentiation with that pathway (74). Other direct metabolic improvements were enhanced energy and lipid metabolism, as well as an increase in markers of satiety (75).

Switching to complementary mechanisms, B. animalis subsp. lactis limits increases of pro-inflammatory signals, supporting mucosal recovery to stress (76). It increases tight junction proteins, restoring normal intestinal permeability and preserving gut barrier function in the face of inflammation (77). Finally, it prevents translocation of pathogenic bacteria from intestine to body tissue, reversing inflammation induced insulin resistance (77).

Lactobacillis PlantarumL. plantarum has a great deal of good data. Levels are higher in lean subjects than in the overfat (78). It lowered plasma glucose, insulin, triglycerides, and oxidative stress levels (78b). Further, it reduced lipogenesis and increased fatty acid oxidation via up-regulation of PPARalpha (79). It inhibits the formation of fat cells while decreasing adipose size as well as white adipose tissue mass (80, 81). L. plantarum also reduced weight gain and fat accumulation, upregulated fatty acid oxidation, while improving insulin and leptin sensitivity against an obesity promoting diet (82, 83).

In addition to reducing weight gain and fat mass, it also lowered blood triglyceride levels, while improving leptin sensitivity and intestinal permeability (83). Remarkably, it led to a significant increase in leptin levels, concurrent with weight loss (84). Weight loss typically results in augmented leptin sensitivity, but decreased leptin levels, which is one of the primary causes of hitting the wall on fat loss with prolonged dieting. L. plantarum also improved glucose levels and insulin sensitivity – and, continuing with its remarkable effects, it increased weight with same body fat (85). This means it seemingly helped direct calories toward muscle formation instead of fat.

It was more potent in combination with other probiotics as well as with polyphenols in reducing fat accumulation and improving metabolic alterations (86, 87). Another nice perk, in a comprehensive formula like SupraBiotic™, is that it increased levels of the genus Bacteroides while reducing the Firmicutes:Bacteroides ratio that is associated with obesity (88, 89).

L. plantarum also displays potent anti-inflammatory actions, attenuating signaling of LPS and TLR-4, as well as COX-2, TNF-alpha, and inflammatory interleukins (90, 91). The reduction in inflammatory responses downstream of the LPS signaling pathway was consistently found in several studies (92, 93). Improvements of inflammatory colitis were also seen with L. plantarum (94, 95). Finally, it increased tight junction protein formation and improved intestinal barrier function (96-98).

Lactobacillis gasseriL. gasseri is consistently associated with weight loss in both animals and humans in the literature (99). It mitigates bodyweight and fat mass increases in obesity promoting diets (100). It decreases body fat in both in visceral and subcutaneous adipose, while also increasing insulin and leptin sensitizing peptide

adiponectin (100-101). This loss of visceral adipose tissue was associated with attenuation in inflammatory gene expression (102).

This species elevated total energy expenditure, while diminishing body weight gain and improving glucose tolerance (103). It reduced bodyweight, triglycerides, and lipogenic genes, while augmenting insulin and leptin sensitivity (104, 105).

Finally, L. gasseri increases tight-junction protein expression and improves intestinal barrier function (106). It elevated levels of the short chain fatty acid, butyrate, relieving inflammatory signaling (103). And, in kind, it inhibits intestinal permeability, LPS production, and adipose tissue inflammation (107, 108).

Lactobacillis RhamnosumL. rhamnosum reduces fat mass, fat synthesis, and improves the obesity associated Firmicutes:Bacteroides ratio (109). It prevented weight gain in diet induced obesity (110). In women, it decreased fat mass, increased weight loss, and improved leptin sensitivity (111). Perhaps most notably, it reduced bodyweight and increased insulin and leptin sensitizing peptide adiponectin while also increasing leptin levels (112). As previously mentioned, leptin normally decreases along with metabolism and appetite control during weight loss, so this is a really nice effect.

Administration of L. rhamnosum resulted in decreased weight gain, with enhanced fatty acid oxidation, insulin sensitivity, and adiponectin via activation of AMPK in both adipose and skeletal muscle tissue (113). It has also been shown to reduce bodyweight and adipose tissue, with increased conjugated linoleic acid (CLA) formation and upregulation of thermogenic protein UCP2 and leptin sensitivity (114, 115).

On the inflammation and gut barrier side of things, L. rhamnosum decreased LPS and LPS induced systemic inflammatory markers including IL-6, COX-2, and TNF-alpha (116-118). Relatedly, it also reduces TLR-4 expression (119). Further, it increases tight junction proteins and restores intestinal barrier function, while inhibiting inflammation downstream of LPS (120-122). A novel action of this species is the production of soluble proteins, p40 and p75, which protect against tight junction and barrier function disruption (123). In addition, it raised Bacteroide levels, tight junction proteins, reduced inflammation, and protected barrier function against a high fructose diet (124).

While this very likely goes for our other probiotic bacteria to some extent, L. rhamnosum has a good bit of data in regard to alcohol consumption. It protects against ethanol induced microbiomal changes, inflammation, and pathology (125). It is also protective against ethanol stimulated inflammation and damage via AMPK (126). Finally, it prevented not just inflammation but also gut barrier disruption in response to ethanol (127). Somewhat related, given alcohol’s use as self-medication, it increased GABA activity and was anxiolytic in response to stress (128).

Bifidobacterium adolescentisB. adolescentis does not have a lot of direct data on body composition. It is higher in lean than obese populations and levels predict leanness, in general (129, 130). Administration resulted in reduction in bodyweight, visceral adipose tissue, and fat mass, while improving insulin resistance (131). It also is synergistic with polyphenols as an anti-inflammatory (132).

However, it is probably the most interesting and important species that is commercially available. That is because it functions as THE archetypal cross-feeder of several of the most important and impressive strains of bacteria. And, those strains are not commercially available.

As a reminder, cross-feeding is production of metabolic substrates by one bacterial species which other species and strains can utilize (133). B. adolescentis produces acetate and oligosacharrides which are then consumed by acetate utilizing, butyrate and propionate producing bacteria (134).

The Best Probiotics That Money Can’t Buy.Unfortunately, several species of bacteria with some of the very best data are not available commercially, due to regulatory issues and well as practical challenges such as stability and viability of the bacteria themselves. We are working on these, as are several other groups, but it will happen later rather than sooner, at best.

Fortunately, there are a myriad of ways to specifically target and increase these strains using methods that ARE available. And, that is exactly what we have done. So, let’s take a look at these novel wonder-bacteria, and then we will get to the data on B. adolescentis as the ultimate cross-feeding probiotic.

Genus Bacteroides

Bacteroides are butyrate and propionate producing. Levels were 6-fold higher in lean vs. obese subjects, as well as being reduced in obese patients, in general, compared to control populations (135-138). The Firmicutes:Bacteroides ratio was also significantly worse in obese patients, even in comparison with the merely overweight (137, 138). It has a negative correlation with fat mass and waist circumference (139, 140). It was also 60% lower in obese pigs – yeah, apparently that is a thing (141).

Bacteroides levels in Type-2 diabetes were only half that of the those with normal glucose tolerance (142). Lower Bacteroides was correlated with increased energy intake (143). Additionally, it was decreased after smoking cessation similar to differences in obese compared to lean subjects suggesting a link between Bacteroides and the weight gain of smoking cessation (144).

Among various species in the Bacteroides genus, B. uniformis reduced bodyweight gain, triglycerides, and adipocyte volume while improving insulin and leptin sensitivity. It also lowered LPS and other inflammatory signals (145). Bacteroides acidifaciens decreased bodyweight and fat gain, while increasing

fatty acid oxidation via PPAR-alpha (146). In addition to an elevated Firmicutes:Bacteroides ratio, B. vulgatus levels were found to be lower in the obese (147).

B. fragilis releases a symbiotic immunomodulatory anti-inflammatory factor called Polysacharride A (148). This activates TLR-2, which releases anti-inflammatory interleukins. PSA is basically the opposite of LPS, and TLR-2 the opposite of TLR-4 (149). This has been shown not just to prevent but to cure experimental colitis, an extreme version of a leaky, inflammatory gut (150). It has also been shown to prevent demyelination of neurons in the central nervous system, indicative of protection against inflammation well outside of the gut (151).

Finally, a few tidbits that will make more sense after reading the Primer™ write-up. A few of the Bacteroides species bind to mucins for colonization and consume these mucin polysaccharides (152, 152b). Bacteroides species also have greater glycan degrading capability than Firmicutes, thus they are preferentially increased by polyphenols (153). Hint: Primer™ contains both mucin and polyphenols.

Faecalibacterium prausnitzii

Faecalibacterium prausnitzii is butyrate producing and is considered a physiological sensor and marker of human health (154). It does not get much more important than that. It is lower in the obese and type-2 diabetics (155-157). Conversely, it is higher in normal glucose tolerance vs. prediabetic subjects (158).

Faecalibacterium prausnitzii is also negatively correlated with inflammatory markers and sharply decreased in inflammatory bowel diseases (157, 159). It is greatly reduced in ulcerative colitis and less abundant in Crohn’s disease (160, 161). As would be expected from the above, it improves intestinal barrier function (162).

Akkermansia muciniphilia

Akkermansia muciniphilia is mucin degrading, meaning it feeds on mucins (163). Levels are higher in lean subjects than the general population (164). It is also decreased in obesity and type-2 diabetes. Its administration reduced fat mass, adipose tissue inflammation, and enhanced insulin sensitivity. Along with this, improved gut barrier function and increased intestinal endocannabinoid levels were seen (165).

This species is also inversely related to fasting glucose, waist-to-hip ratio, subcutaneous adipocyte diameter, plasma triglyceride levels, visceral adipose tissue mass, and insulin resistance (166). Along with enhanced glucose tolerance, it reduced adipose tissue inflammation (167). Akkermansia levels are higher in normal glucose tolerance vs. pre-diabetic subjects (168). It decreased inflammatory cytokine production and protected intestinal barrier function in experimental colitis (169). Finally, its levels are reduced in ulcerative colitis (170).

Roseburia Species

Roseburia species are butyrate producing (171). An increase in this species is associated with decreased body weight, fat mass, insulin sensitivity, and triglycerides -- independent of calorie intake (172). Increased Roseburia correlated with reduced body weight, improved profile of lipid and obesity related gene expression, along with a normalized inflammatory status (173). It is also lower in type-2 diabetes (174). Levels are increased by a Mediterranean diet, as is insulin sensitivity (175). Roseburia is enriched in healthy populations vs. those with atherosclerosis (176). And, its levels display an inverse correlation with disease activity in ulcerative colitis (177).

High protein/low carbohydrate diets, which are so effective and popular, reduce Roseburia and SCFA levels (178, 179). This does not mean don’t use them, it just means make sure you make a point to get fiber/prebiotics to feed your good bacteria that produce SCFAs. Butyrate is especially important amongst the SCFAs, as it the preferred energy source, along with Glutamine, for epithelial cells in the colon (180). Butyrate is basically the fat to Glutamine’s protein and carbohydrate as far as feeding these cells. We will talk more on Glutamine in the Primer™ write-up.

Bifidobacterium adolescentis as Cross-Feeder

As mentioned, the most important contribution of B. adolescentis is to feed other bacteria, specifically the really good ones that we just talked about and which we cannot get commercially.

B. adolescentis is superior to other potential cross-feeding Bifidobacterium in that it provides a slow, steady degradation of oligosaccharides for a long, continuous release of substrate for these various bacteria to feed on. It is essentially time-released, allowing acetate feeding, butyrate producing bacteria to grow and thrive throughout the entire length of the gut (181).

Faecalibacterium prausnitzii is almost fully dependent on acetate, which B. adolescentis supplies. F. prausnitzii converts it to butyrate with 85% efficiency, and its growth is enhanced by co-culture with B. adolescentis (182, 183).

Roseburia is also an acetate user (184). It is, in fact, generally required for growth (185). In addition to acetate production, B. adolescentis increases Roseburia via partial breakdown of oligosaccharides, which it can then utilize (186).

Cross-feeding with Bifidobacterium modulates the prebiotic effect of inulin and arabinoxylan-oligosaccharides on Roseburia and F. prausnitzii by making acetate available (187). Roseburia was able to grow in pure complex carbohydrate cultures, which it cannot metabolize on its own, owing to cross-feeders (188).

Short Chain Fatty Acids (SCFAs)

One of the primary ways that probiotic bacteria work their magic is by fermenting prebiotics and producing SCFAs (primarily acetate, butyrate, and propionate), so we are going to talk about those, and how they work.

They primarily work through two mechanisms: 1) activation of free fatty acid receptors, FFA2 and FFA3. 2) Decreasing inflammation and permeability in the gut.

SCFAs protect against obesity and insulin resistance. Butyrate and propionate induce anorectic gut hormones, while acetate does so without reducing food intake (Supplementary 1). FFAR2 deficiency results in obesity on a normal diet, whereas with overexpression, subjects remain lean, even on an obesity promoting high-fat diet. Activation of FFAR2 suppresses insulin signaling in adipocytes, which inhibits fat accumulation in adipose tissue and promotes the metabolism of lipids and glucose in other tissues such as muscle (S2).

Propionate and butyrate activate intestinal gluconeogenesis. Butyrate does so through AMPK, while propionate works through a gut-brain neural circuit involving FFAR3 (S3). Propionate is sensed in the portal vein walls via FFAR3, initiating intestinal gluconeogenesis. This glucose then triggers a signal to the brain to modulate hunger sensations and normalize whole body glucose homeostasis (S4). In a fasting state, as much as 62% of infused propionate is converted to glucose, accounting for 69% of total glucose production (S5). This is quite applicable to lower carb diets. Basically, it makes your brain think you are plenty fed with carbs/glucose, so it signals not to eat more, as well as not to produce or pump out more glucose into the blood.

SCFAs also stimulate the release of anorectic and satiey inducing peptides like GLP-1 and PYY via FFAR2/3 (S6, S7). Activation of FFAR3 by SCFAs inhibits insulin secretion and increases sympathetic outflow. This raises energy expenditure and help to protect against obesity (S8, S9). Acetate has been found to increase brown adipose tissue, UCP1, and mitochondrial biogenesis via FFAR2 (S10).

Short-chain fatty acids also improve intestinal barrier function via activation of AMPK (S11). Sodium butyrate has been specifically found to be an AMPK agonist (S12). And, butyrate increase tight junction assembly, thus improving barrier function, specifically through AMPK (S13, S14).

This seems like as good of a place as any to add a bit more about AMPK, as it is one of the major targets in all of this.

AMPK

AMPK is a primary signaler in the maintenance of tight junction integrity and intestinal barrier function. It is one of the most important pathways in preventing the “leaky gut” we have spoken of earlier in regard to LPS and other inflammatory and infectious molecules escaping into the body to wreak havoc (S15, S16). Modern food processing and the Western diet is a particularly egregious malefactor in this (S17).

In addition to its involvement in barrier function, AMPK activation is extremely positive for the great bacteria that we can’t get commercially.

Metformin increased Akkermansia 18-fold through AMPK activation. Also, against a high-fat diet, it restored Bacteroides levels and the Firmicutes:Bacteroides ratio to that of lean subjects (S18-S20). It inhibited LPS induced inflammation and gut permeability increases, while improving glucose uptake and insulin sensitivity (S19). Akkermansia increases are likely at least partially due to greatly elevated production of its favorite food, mucin, which is stimulated by AMPK. It also reduces insulin resistance and adipose tissue inflammation in a high-fat diet (S20).

Pomegranate ExtractPomegranate Extract is an extremely rich source of polyphenols. Polyphenols are generally prebiotic for good bacteria (Bifidobacterium, Akkermansia, Bacteroides, and Roseburia), and antibacterial for less favorable and pathogenic ones (189-191). Fruit/berry based polyphenols seem to be particularly favorable toward Bacteroides, the Firmicutes:Bacteroides ratio, and Akkermansia compared to other polyphenol sources. Lactobacillus (Firmicute) lack glycan degrading enzymes, thus do not grow on them particularly well compared to the others (192).

Strawberry polyphenols elevate Bifidobacterium and Bacteroides, butyrate and propionate, as well as decreasing Firmicutes (193). Red wine polyphenols raise Bifidobacterium and Bacteroides as well (194, 195). Polyphenols improve the Firmicutes:Bacteroides ratio, while also increasing Roseburia (196, 197).

Akkermansia REALLY loves polyphenols (198). Grape polyphenols gave a 10-fold increase in Akkermansia and decreased the Firmicutes:Bacteroides ratio, while also reducing weight gain, triglyceride storage, insulin resistance, LPS, and inflammation (199). Cranberry polyphenols produced a 30-fold increase in Akkermansia and decreased weight gain, visceral adipose tissue, triglyceride synthesis, insulin resistance, LPS, and inflammation (200).

Finally, Pomegranate Extract, itself, produced a massive 33 to 47 fold increase in Akkermansia (201). Caffeic acid, a component of Pomegranate Extract, increased Akkermansia 15-fold vs control and several hundred fold vs. subjects with induced colitis! It also improved the Firmicutes:Bacteroides ratio (202).

Polyphenols activate AMPK, enhancing intestinal barrier function (203). They increase tight junction proteins, decrease tight junction pore formation, and ameliorate inflammatory bowel disease (204). Pomegranate Extract activates AMPK at 2 times the potency of metformin (205). It also displayed extremely potent alpha-glucosidase inhibitory activity (this is an ezyme that metabolizes carbohydrates to glucose), being 10 times as potent as acarbose, lowering blood glucose after sucrose intake, but not after glucose (206, 207). It consistently decreases glucose levels, as well as being anti-inflammatory (208, 209).

Fermented Herbs

Fermentation of herbs results in much higher concentrations of active compounds compared to unfermented (210). This same fermentation is done in the body, but it is highly dependent upon the microbial make-up of the individual’s gut, so it can vary widely from person to person (211, 212). As just one example, a fermented herb preparation inhibited LPS mediated inflammatory damage, while the unfermented was ineffective (213, 214)

Fermented KudzuKudzu is a group of polyphenol rich plants belonging to the pea family. Its administration reduced body weight, fat mass, and lipogenesis while stimulating lipolysis and thermogenesis (215). It also lowers body mass index and visceral fat (216). Kudzu increased fatty acid oxidation, and decreased weight gain, triglyceride levels, and visceral adipose tissue on a high-fat diet (217). In addition, it improves insulin sensitivity and lipid metabolism (218).

Kudzu is anti-inflammatory, with components inhibiting LPS, TNF-alpha, and ROS induced inflammation (219, 220). It is also a potent inhibitor of COX-2 (221). In addition, Kudzu reduced intestinal permeability and improved intestinal barrier function (222, 223). Finally, it reduces expression of the dreaded TLR-4 (224, 225).

Fermented GinsengThe anti-obesity effect of unfermented ginseng was shown to be dependent on bacterial make-up of the microbiota (226). It increased mucins (the Akkermansia and Bacteroides food) by 50% (227). It is metabolized by Bifidobacterium as well as Bacteroides. There is a dramatic difference in levels of those bacteria between metabolizers and non-metabolizers, suggesting strong prebiotic specificity toward them (228). And, it was indeed found to enhance growth of Bacteroides (229).

Absorption of one of its main active ingredients, Compound K, is increases by prebiotics (230). And, there are plenty of those in Primer™. Fermented Ginseng decreased bodyweight, fat mass, and food efficiency, while improving insulin and leptin sensitivity (231, 232). In addition to reduced body weight, decreases in fat mass, adipocyte size, and glucose uptake were also observed. And, all of these effects were superior with fermented vs. regular ginseng (233, 234). Finally, it decreases inflammatory cytokines and protects the intestinal barrier (235, 235b).

Mulberry Extract SupraBiotic™ contains an industry-best Mulberry Extract, standardized to over 5% 1-Deoxynojirimycin (1-DNJ) and containing relevant amounts of d-Fagomine, as well. Like all berries, it also has high polyphenol content, the benefits of which we have already talked about.

1-DNJ1-DNJ is a naturally occurring carbohydrate mimic. Its use significantly lowered body weight, blood glucose, and serum insulin levels, and it conversely improved glucose tolerance and insulin sensitivity (236). It increased the insulin and leptin sensitizing peptide adiponectin (which activates AMPK),

reduced visceral adipose tissue, adipose mass, triglycerides, lipid accumulation, and increased fatty acid oxidation (237).

It is remarkably potent, elevating adiponectin, GLUT4, and AMPK at just .5uM (238). This is 1000 times as potent as metformin. Along with increasing AMPK, it improved mitochondrial function and lipid metabolism (239). Finally, it is a more potent alpha-glucosidase inhibitor than acarbose, which futher helps with glucose and insulin (240).

D-fagomine D-fagomine is also a naturally occurring sugar mimic. It reduced weight gain, plasma triglycerides, glucose, and enhanced leptin and insulin sensitivity (241). It attentuated fat gain on high-fat diet (242). D-fagomine was also found to inhibit intestinal sucrase, lowering post-prandial glucose levels (with either sucrose or starch), as well as modulating bacterial adhesion, inhibiting pathogenic ones without effecting Bifidobacterium or Lactobacillus (243).

Selenium Selenium increases microbial diversity, and it is synergistic with probiotics for this gut bacteria modulation (244, 245). It works by enhancing the fermentation activity of gut bacteria resulting in better bacteria growth as well as output of SCFAs (246).

Queen’s Bee Acid (10-hydroxy-2-decenoic acid) QBA is a medium chain fatty acid from Royal Jelly. It is a very potent AMPK agonist, being effective at just 20uM. This is 25 times as potent as research standard AICAR and the pharmaceutical metformin. (247)

We have mentioned it over and over, but it bears repeating more about the machinations that result in the vicious cycle of gut dysbiosis. Inflammation in the gut, followed by low-level but constant systemic inflammation, PRECEDES obesity and insulin/leptin resistance. It is what gets them started. If you are not either quite lean, or have been on a diet long enough that fat loss has basically stopped, insulin and leptin resistance are already at work, particularly in the brain/adipostat (248). This is bad news for appetite control, metabolism, and body weight regulation.

LPS levels of just 2 to 3-fold above normal, which occur during a Western-style/high-fat diet, initiate the low level inflammatory response that leads to reduced insulin and leptin senstivity, and ultimately type-2 diabetes and Metabolic Syndrome. And, again, this happens before the weight gain starts (249). It sets you up for it to begin in earnest.

AMPK is one of the primary brakes on this ride. It inhibits the LPS induced inflammatory response, as well as the leaky gut. Super potent AMPK agonist, like 1-DNJ and QBA, are basically airbrakes on a runaway train.

QBA inhibits LPS induced cytokine production (250). It increases GLUT4, glucose uptake, and insulin signaling (247). It enhances intestinal barrier function and tight junction assembly in an AMPK dependent manner (251-253). AMPK activation also improves LPS induced blood-brain-barrier disruption much as it does with the intestinal barrier (254). This improves central insulin and leptin signaling, keeping your adipostat functioning properly.

Palmitoylethanolamide (PEA)PEA is a naturally occurring cannabinoid-like lipid, from a class called acylethanolamides. It is a competitive FAAH inhibitor (this is the enzyme that breaks down endocannabinoids). Decreased levels of endocannabinoids lead to upregulation of cannabinoid receptors, which leads to the increased activity at CB1 via LPS that gets the increased fat storage and over-eating part of the vicious cycle really going into overdrive.

Endocannabinoid activation of CB2, along with PEA/acylethanolamide activation of PPAR-alpha, normally keeps this inflammatory response balanced and in check, but when it gets out of whack, LPS CB1 reigns supreme.

Let’s take a closer look at all of this and what PEA does to fix it.

Intake of dietary fat stimulates production of PEA, and the other acylethanolamides (255, 256). They increase satiety, and reduce food intake and body weight (257, 258). It creates satiety via activation of PPAR-alpha in the intestine followed by direct vagal signal to brain -- i.e. immediate, no gene transcription needed (259, 260). This is one of the steps in which fast transit times in the proximal small intestine become problematic. You get less PEA, thus less satiety signaling to the brain.

In addition, PEA specifically decreases this intestinal transit rate, so it is double plus good on appetite and satiety signaling (261). It both directly makes you feel full and prolongs its own duration of activity in doing so. PEA does, in fact, ultimately reach the brain, where it is active in nM concentrations through gene transcription (258). But, you would have already finished eating too much at that sitting, and each of your other meals, before it did anything, centrally.

In addition to the appetite side of things, PEA decreases intestinal inflammation and permeability. It does so through CB2 and PPAR-alpha as this is blocked by antagonists of either one (262, 263). It is also anti-inflammatory in the intestine via selective targeting of TLR-4 (263).

All sounds great, right? Well, the problem is that with a Western-style or chronic high-fat diet, the PEA release trigger becomes desensitized, ultimately resulting in reduced levels (256, 259, 265). This disrupts normal functioning of the whole system, leading to LPS induction of CB1 becoming dominant. And, this is on top of losing its direct beneficial effects on satiety and food intake.

An increase in inflammation happens in parallel with decreases in PEA, endocannabinoids, and FAAH – and, an upregulation of the cannabinoid receptors (266). It all happens together, at the same time,

because they are all connected. And, FAAH inhibitors restore levels of all of these and suppress this inflammation (266). FAAH inhibitors also decrease intestinal motility, as we would expect (267). They do so by restoring PEA and the endocannabinoids, thus normalizing the system.

The final bit of evidence on how this operates is that chronic administration of tetrahydrocannabinol (THC), the main active ingredient in marijuana, reduces weight gain, fat mass gain, and energy intake in obese but not lean mice, despite an initial increase in food consumption (268). This is because it is both a CB1 and CB2 agonist. So, you have anti-inflammatory CB2 activation by THC snuffing out the inflammatory LPS pathway, as well as it down-regulating and competing for CB1, such that LPS cannot act on it to wreak its havoc, unchallenged.

This THC administration even improved select gut microbiota profiles. It increased Akkermansia by 4-fold, and improved the Firmicutes:Bacteroides ratio by 6-fold (268). It did not have these same effects in lean subjects because these pathways were not messed up to begin with for them.

So, you can see that PEA helps correct the system at basically all levels that we have been talking about.

One more thing of note is that, as we mentioned with high protein diets negatively altering the bacterial make-up of the microbiota if one does not make a point to get plenty of fiber/prebiotics, the high-fat side of such diets will negatively affect PEA levels, long-term, thus the entire system will be functioning sub-optimally.

Again, I am not bashing these diets at all, they are quite effective. Consuming an excess of glucose and/or fructose is the worst thing you can do to your body as far as inflammation and insulin and everything we have been talking about, just to be clear. But, we want to be optimal, and we can be, quite easily with supplementation.

Ginger Extract (20% Gingerols)Ginger is well known as a digestive aid. The extract is an all-around nice ingredient, aiding through several pathways, and it is particularly effective as an anti-inflammatory and protector of barrier function. The primary component of the extract is 6-gingerol, though 8-, and 10-gingerol, as well as 6-, 8, and 10-shogaol are present in significant, pharmacologically relevant numbers. They all pretty much do the same thing, just at different potencies.

Mechanistically, it is primarily an anti-inflammatory and antioxidant. It decreases basically all inflammatory cytokines (269, 275, 276). It inhibits LPS induced inflammation as well as TNF-alpha (270). It reduced interleukins 3-fold at just 50uM, and its COX inhibition is comparable to aspirin (271-273). It also displays extremely potent anti-oxidant activity, being effective against various radicals at just 1-25uM (274).

Gingerols activate PPAR-alpha, as well as AMPK, with 5 times the potency of metformin and AICAR in suppression of inflammatory cytokines (275, 276). They increase tight junction proteins and integrity via protection against inflammatory assault (277, 278). They suppress colitis via anti-inflammatory and anti-oxidant activity (279). Gingerols enhanced the survival and proliferation of intestinal epithelial cells via reductions in pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β), while also elevating anti-inflammatory

cytokines (IL-10 and IL-22) in colitis models (280). They also reduce spasms of smooth muscle in the digestive tract (281).

In addition, gingerols displayed some modest inhibitory activity on α-glucosidase and α-amylase, being about 1/6 as potent as acarbose (282). Finally, it increased uptake of Calcium (100+%) and Glutamic acid (60%), both of which we will talk in detail about in the Primer™ write-up (283).

CONCLUSIONAs you can see, SupraBiotic™ takes the concept of probiotic far beyond where anyone has previously taken it before. It starts with bacterial species carefully and purposefully selected to protect against dysfunction of the gut and microbiota to promote better health, better appetite control, better metabolism, and better fat loss. On top of this, SupraBiotic™ addresses and supports novel probiotic bacterial species that you cannot attain, anywhere. And, it does so in a way that no other product is even close to doing. Finally, its supporting ingredients crush inflammation and repair your leaky gut, leaving your body functioning in the optimal way it is intended to.

SupraBiotic™ is a one of a kind product that fits in perfectly with and enhances any diet and exercise program, any supplement regimine, any lifestyle.

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