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SupraBiotic(tm) Ingredients -- Part 1

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Par Deus


SupraBiotic™ Ingredients

Bifidobacterium 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 breve
B. 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. lactis
B. 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 Plantarum
L. 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 gasseri
L. 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 decreases intestinal permeability, LPS production, and adipose tissue inflammation (107, 108).


Lactobacillis Rhamnosum
L. 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 adolescentis
B. 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).

See "Full Science Write-up" here http://neobium.org/product-line/suprabiotic/ for references.

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