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  1. In the last episode of The CKD Files, Derf and Dan Jr. had just returned home from the gym following their two hour glycogen depletion workout and had subsequently commenced preparations for the ensuing carb-up. 

    Setting: Daytime in a living room

    DERF: Typical musclehead, 240+ lbs, sub 6% bodyfat, head shaved to hide the consequences of years of 5-alpha reductase activity, rummages through a tackle box full of pills, vials, and syringes.

    DAN JR: who couldn't grow on a gram of tren a day, sits, rolling a joint.
     
     
    DERF
    Dude, I'm low on gear.

     
     DAN JR. 
    Yeah, me too. We should go back by the gym and see BigWill after we smoke this.
     
    He takes a puff and hands it to Derf, who does the same.

     
    DERF 
    I'm gonna need to eat first.

     
    DAN JR.
    (annoyed) 
    Did you take your shot already??
     
    He nods, a bit woozy. Dan just shakes his head, grabsa syringe, and stands up. 
     
    Derf passes out. 
     
    Dan heads to the kitchen and returns with a bottle of glucose. He draws some into the syringe and injects it into one of the giant veins on Derf's arm.
     
    He comes to.

     
    DERF 
    Thanks, dude. Let's hit McDonald's.

     
    DAN JR.
    (shakes his head)
    That's far too high in fat. Glycogen storage and amino acid uptake are optimal right now -- We need high Glycemic Index carbohydrates. A post workout drink of dextrose and whey is ideal.

     
    DERF 
    Bullshit. I haven't had anything except whey and flaxfor the last two weeks. I want some food.

     
    DAN JR. 
    Fine. But, we're not eating McDonald's -- we'll go toan all you can eat place.
     
    Dan takes out a syringe and injects himself in thethigh. 

     
    DERF 
    Nubain?

     
    DAN JR. 
    Insulin.
     
    Derf nods. Dan pulls out another.


    DERF 
    Nubain?


    DAN JR. 
    GH.
     
    He injects it and pulls out another.


    DERF 
    Nubain?


    DAN JR. 
    Yep.
     
     
    Setting: Daytime at all All-You-Can-Eat Restaurant

    They walk into the restaurant, anxious to begin refilling of glycogen stores and raising leptin levels. There are a couple of people in line in front of them, so they step back. 

    They stand there for a moment, already impatient, when an OBESE WOMAN waddles up and cuts in front of them in line. 

    They give each other a "What the fuck?!" look, then stare at her back, in a rage fueled by low blood sugar, serotonin depletion, and supraphysiological androgen levels.


    DAN JR.
    Did that chubby bitch just cut in front of us? 


    DERF 
    Yeah. 


    DAN JR. 
    Does she think we're just standing here to greet people as they walk in the door?
     
    Derf shrugs.


    DAN JR. 
    She doesn't need to be getting seconds anyway. 


    DERF
    Nope. 


    DAN JR. 
    How much do you think she weighs?


    DERF 
    Three hundred? 


    DAN JR.
    I'm thinking maybe as much as four bills. But it's pretty hard to tell when they get that big... I'd say she's definitely pushing at least three and somechange... You'd think they'd have some kind of width limit to eat at all-you-can-eatrestaurants. You know? 


    DERF
    (laughs) 
    Like the height requirements for rollercoasters? 


    DAN JR.
    Yeah. They should have a sign when you first walk in the door with a guy holding his arms out that says: 
     
    Dan holds his arms out really wide. 


    DAN JR. 
    "You must not be this wide to eat at this restaurant." -- 'Cause if you are, you damn sure don't need to be eating at an all-you-can-eat restaurant.
     

    DERF 
    She needs some EC.


    DAN JR. 
    Fuck EC, she needs DNP and some meth. 


    DERF 
    Maybe she just has low leptin levels. 


    DAN JR. 
    Yeah, and maybe she swallowed a guy who swallowed a fly, but I fucking seriously doubt it. It takes a concerted effort to get that fat. You don't go to sleep one night looking like a normal human being and wake up the next day with 54% bodyfat. That doesn't happen. It takes years of determination and willpower. To look like that, there can be no skipping meals, no going to bed hungry, no exercise. Shit, just walking from the couch to the kitchen must burn more than a hundred calories when you weigh that much... I bet she keeps a crate of Krispy Kremes, in her fucking living room, so she can grab a box whenever the urge should strike... Low leptin levels my ass. I guarantee you that bitch gets three tiers of food on her tray. 


    DERF
    (smiles) 
    She's just got more to love, that's all.
     
    Derf walks up closer to her back. He pretends to spank her.


    DERF 
    Big is beautiful. Ain't it baby. 


    DAN JR.
    (shaking his head) 
    Fat is not beautiful unless you're a sick, deviant motherfucker with a fetish for that shit. It just isn't aesthetically pleasing.
     
    The Obese Woman continues piling food on her tray.


    DAN JR.
    I mean, granted, culture and normal personal preferences play a role incertain aspects of what is considered beautiful at different times. For example: Hairstyles and fashion change -- certain trends are hip for a while, but fiveyears later are atrocious -- the 1980's come to mind.

    But some things are universally beautiful. And certain things are universally not beautiful in any way, shape, or form. 


    DERF 
    Like what? 


    DAN JR. 
    Things like Nicole Bass, and pimples, and warts, and melted flesh from third degree burns... And well-fed bitches like her.


    DERF 
    You make a good argument.


    DAN JR. 
    Don't kid yourself, Derf. I'm not finished. I haven't yet begun to ridicule.


    DERF 
    Oh. 


    DAN JR. 
    You know it's gotta be unsanitary. I mean, can you imagine what kind ofbacteria and yeast and STD's and shit are spawning and fermenting betweeneach and every fucking chub roll on that immense body? 


    DERF 
    It's a sick thought. 


    DAN JR. 
    Of course, it is. And the other day I heard on Oprah something about "foodaholism". Like it's a fucking disease, like cancer. Like they can't help. Like it's not their fault. 


    DERF 
    I did read on MFW about a study linking obesity to a virus. 


    DAN JR. 
    Well, then the CDC needs to come out here and quarantine this bitch. 


    DERF 
    (laughing) 
    If it was a virus, what do you think they'd call it. 


    DAN JR. 
    There's already a name for what she has. It's called "gluttony". 
     
    The Obese Woman turns around with two trays full of food, each with plates piled one on top of the other like a pyramid.


     DAN JR .
    (as she walks by) 
    How now, brown cow. 
     
    She doesn't respond. Derf laughs, and they finally approach the windowto order their long-awaited food.

    The End.
     
     
    The following was a fictional skit. Any resemblance to actual people, be they from your local gym or alt.support.fat-acceptance, is purely coincidental.

  2. You ever go to take a shit and realize you are right in the middle of a marathon? You ever cross the finish line only to see a competitor drop dead of heat stroke or a heart attack? Have you ever just felt tired and run down, for days after an event or during peak levels of training -- or gotten a respiratory infection? Well, it is not because you didn’t drink enough Gatorade, or carb load, or get the right running shoes. It is because of trillions of shitty little bacteria in your gut pumping out inflammatory agents which attack testosterone production, increase toxic ammonia, and biochemically overheat your muscles and brain. Neobium™ Sport™ delivers an inexhaustible probiotic blend and friends that fortify your gut, reverses the pro-inflammatory milieu, increase mitochondrial density and function, and protects against the catabolic pathways that hinder recovery and health.

    Run your shit, don’t let it run you.


     

    Temperature (Austin). 2016 Apr 28;3(2):240-251. eCollection 2016 Apr-Jun.
    Heat stress, gastrointestinal permeability and interleukin-6 signaling -
    Implications for exercise performance and fatigue.
    Vargas N(1), Marino F(1).
    
    Exercise in heat stress exacerbates performance decrements compared to
    normothermic environments. It has been documented that the performance decrements
    are associated with reduced efferent drive from the central nervous system (CNS),
    however, specific factors that contribute to the decrements are not completely
    understood. During exertional heat stress, blood flow is preferentially
    distributed away from the intestinal area to supply the muscles and brain with
    oxygen. Consequently, the gastrointestinal barrier becomes increasingly
    permeable, resulting in the release of lipopolysaccharides (LPS, endotoxin) into 
    the circulation. LPS leakage stimulates an acute-phase inflammatory response,
    including the release of interleukin (IL)-6 in response to an increasingly
    endotoxic environment. If LPS translocation is too great, heat shock,
    neurological dysfunction, or death may ensue. IL-6 acts initially in a
    pro-inflammatory manner during endotoxemia, but can attenuate the response
    through signaling the hypothalamic pituitary adrenal (HPA)-axis. Likewise, IL-6
    is believed to be a thermoregulatory sensor in the gut during the febrile
    response, hence highlighting its role in periphery - to - brain communication.
    Recently, IL-6 has been implicated in signaling the CNS and influencing
    perceptions of fatigue and performance during exercise. Therefore, due to the
    cascade of events that occur during exertional heat stress, it is possible that
    the release of LPS and exacerbated response of IL-6 contributes to CNS modulation
    during exertional heat stress. The purpose of this review is to evaluate previous
    literature and discuss the potential role for IL-6 during exertional heat stress 
    to modulate performance in favor of whole body preservation.
    
    DOI: 10.1080/23328940.2016.1179380 
    PMCID: PMC4964994
    PMID: 27857954 

     

     

    Compr Physiol. 2011 Oct;1(4):1883-928. doi: 10.1002/cphy.c100082.
    Integrated physiological mechanisms of exercise performance, adaptation, and
    maladaptation to heat stress.
    Sawka MN(1), Leon LR, Montain SJ, Sonna LA.
    
    This article emphasizes significant recent advances regarding heat stress and its
    impact on exercise performance, adaptations, fluid electrolyte imbalances, and
    pathophysiology. During exercise-heat stress, the physiological burden of
    supporting high skin blood flow and high sweating rates can impose considerable
    cardiovascular strain and initiate a cascade of pathophysiological events leading
    to heat stroke. We examine the association between heat stress, particularly high
    skin temperature, on diminishing cardiovascular/aerobic reserves as well as
    increasing relative intensity and perceptual cues that degrade aerobic exercise
    performance. We discuss novel systemic (heat acclimation) and cellular (acquired 
    thermal tolerance) adaptations that improve performance in hot and temperate
    environments and protect organs from heat stroke as well as other dissimilar
    stresses. We delineate how heat stroke evolves from gut underperfusion/ischemia
    causing endotoxin release or the release of mitochondrial DNA fragments in
    response to cell necrosis, to mediate a systemic inflammatory syndrome inducing
    coagulopathies, immune dysfunction, cytokine modulation, and multiorgan damage
    and failure. We discuss how an inflammatory response that induces simultaneous
    fever and/or prior exposure to a pathogen (e.g., viral infection) that
    deactivates molecular protective mechanisms interacts synergistically with the
    hyperthermia of exercise to perhaps explain heat stroke cases reported in
    low-risk populations performing routine activities. Importantly, we question the 
    "traditional" notion that high core temperature is the critical mediator of
    exercise performance degradation and heat stroke. Published 2011. This article is
    a U.S. Government work and is in the public domain in the USA.
    
    DOI: 10.1002/cphy.c100082 
    PMID: 23733692  [Indexed for MEDLINE]

     

     

    Tissue Barriers. 2015 May 29;3(3):e1039691. doi: 10.1080/21688370.2015.1039691.
    eCollection 2015 Jul-Sep.
    Microbiota and the control of blood-tissue barriers.
    Al-Asmakh M(1), Hedin L(2).
    
    The gastro-intestinal tract is an ecosystem containing trillions of commensal
    bacteria living in symbiosis with the host. These microbiota modulate a variety
    of our physiological processes, including production of vitamins, absorption of
    nutrients and development of the immune system. One of their major functions is
    to fortify the intestinal barrier, thereby helping to prevent pathogens and
    harmful substances from crossing into the general circulation. Recently, effects 
    of these microbiota on other blood-tissue barriers have also been reported. Here,
    we review the evidence indicating that gut bacteria play a role in regulating the
    blood-brain and blood-testis barriers. The underlying mechanisms include control 
    of the expression of tight junction proteins by fermentation products such as
    butyrate, which also influences the activity of histone deacetylase.
    
    DOI: 10.1080/21688370.2015.1039691 
    PMCID: PMC4574894
    PMID: 26451344 
    

     

    Acta Physiol Hung. 2005;92(2):121-37.
    Testosterone and endurance exercise: development of the "exercise-hypogonadal
    male condition".
    Hackney AC(1), Moore AW, Brownlee KK.
    
    During the last 30 years a large number of research studies have been conducted
    examining reproductive endocrine dysfunction in exercising women. The number of
    similar studies examining men is still relatively small. Nevertheless, an
    increasing amount of research studies in men indicate endurance exercise training
    has significant effects upon the major male reproductive hormone, testosterone,
    and the hypothalamic-pituitary-testicular axis that regulates reproductive
    hormones. This review article addresses one reproductive endocrine dysfunction
    found in exercising men, what has been deemed the "exercise-hypogonadal male
    condition". Specifically, men with this condition exhibit basal (resting-state)
    free and total testosterone levels that are significantly and persistently
    reduced. The exact physiological mechanism inducing the reduction of testosterone
    is currently unclear, but is postulated to be a dysfunction (or perhaps a
    readjustment) within the hypothalamic-pituitary-testicular regulatory axis. The
    time course for the development of the "exercise-hypogonadal condition" or the
    threshold of exercise training necessary to induce the condition remains
    unresolved. The potential exists for these reduced testosterone levels within the
    exercise-hypogonadal male to disrupt and be detrimental to some anabolic or
    androgenic testosterone-dependent physiological processes. Unfortunately,
    extremely few research studies have addressed whether such processes are
    affected, and thus findings are inconclusive. Conversely, the alterations in
    testosterone levels brought about by endurance exercise training have the
    potential for cardiovascular protective effects and thus could be beneficial to
    the health of these men. Current evidence suggests this condition is limited to
    men who have been persistently involved in chronic endurance exercise training
    for extended periods of time (i.e., years). Many questions, however, regarding
    the male reproductive endocrine adaptive process to exercise and exercise
    training remain unanswered, necessitating the need for further research on this
    topic.
    
    DOI: 10.1556/APhysiol.92.2005.2.3 
    PMID: 16268050  [Indexed for MEDLINE]
    

     

     

    Eur J Appl Physiol. 2004 Apr;91(4):382-91. Epub 2003 Nov 8.
    New aspects of the hormone and cytokine response to training.
    Steinacker JM(1), Lormes W, Reissnecker S, Liu Y.
    
    Exercise training is associated with peripheral-cellular and central-cerebral
    processes, hormonal-neuronal regulation and transmission mechanisms. During the
    acute training response, peripheral cellular mechanisms are mainly metabolostatic
    to achieve energy supply and involve associated cytokine and hormonal reactions. 
    Glycogen deficiency is associated with increased expression of local cytokines
    (interleukin-6, IL-6), decreased expression of glucose transporters, increased
    cortisol and decreased insulin secretion and beta-adrenergic stimulation. A
    nutrient-sensing signal of adipose tissue may be represented by leptin which, as 
    for insulin, IL-6 and insulin-like growth-factor I (IGF-I), has profound effects 
    on the hypothalamus and is involved in the metabolic hormonal regulation of
    exercise and training. Muscle damage and repair processes may involve the
    expression of inflammatory cytokines (e.g. tumour necrosis factor-alpha,
    TNF-alpha) and of stress proteins (e.g. heat shock protein 72). During
    overreaching and overtraining, a myopathy-like state is observed in skeletal
    muscle with depressed turnover of contractile proteins (e.g. in fast-type
    glycolytic fibres with a concomitant increase in slow type myosins). These
    alterations are influenced by exercise-induced hypercortisolism, and by decreased
    somatotropic hormones (e.g. IGF-I). The hypothalamus integrates various error
    signals (metabolic, hormonal, sensory afferents and central stimuli) and
    therefore pituitary releasing hormones represent the functional status of an
    athlete and long-term hypothalamic hormonal and sympathoadrenal downregulation
    are some of the prominent hormonal signs of prolonged overtraining and
    performance incompetence syndrome.
    
    DOI: 10.1007/s00421-003-0960-x 
    PMID: 14608461  [Indexed for MEDLINE]

     

     

    Br J Nutr. 2011 Jun 28;105(12):1729-33. doi: 10.1017/S000711451000557X. Epub 2011
    Feb 16.
    Keto analogue and amino acid supplementation affects the ammonaemia response
    during exercise under ketogenic conditions.
    Prado ES(1), de Rezende Neto JM(2), de Almeida RD(1), Dória de Melo MG(3),
    Cameron LC(1).
    
    Hyperammonaemia is related to both central and peripheral fatigue during
    exercise. Hyperammonaemia in response to exercise can be reduced through
    supplementation with either amino acids or combined keto analogues and amino
    acids (KAAA). In the present study, we determined the effect of short-term KAAA
    supplementation on ammonia production in subjects eating a low-carbohydrate diet 
    who exercise. A total of thirteen male cyclists eating a ketogenic diet for 3 d
    were divided into two groups receiving either KAAA (KEx) or lactose (control
    group; LEx) supplements. Athletes cycled indoors for 2 h, and blood samples were 
    obtained at rest, during exercise and over the course of 1 h during the recovery 
    period. Exercise-induced ammonaemia increased to a maximum of 35 % in the control
    group, but no significant increase was observed in the supplemented group. Both
    groups had a significant increase (approximately 35 %) in uraemia in response to 
    exercise. The resting urate levels of the two groups were equivalent and remained
    statistically unchanged in the KEx group after 90 min of exercise; an earlier
    increase was observed in the LEx group. Glucose levels did not change, either
    during the trial time or between the groups. An increase in lactate levels was
    observed during the first 30 min of exercise in both groups, but there was no
    difference between the groups. The present results suggest that the acute use of 
    KAAA diminishes exercise-induced hyperammonaemia.
    
    DOI: 10.1017/S000711451000557X 
    PMID: 21324213  [Indexed for MEDLINE]

     

     

    J Clin Gastroenterol. 2017 Apr;51(4):312-323. doi: 10.1097/MCG.0000000000000789.
    The Effects of Probiotics and Symbiotics on Risk Factors for Hepatic
    Encephalopathy: A Systematic Review.
    Viramontes Hörner D(1), Avery A, Stow R.
    
    Alterations in the levels of intestinal microbiota, endotoxemia, and inflammation
    are novel areas of interest in the pathogenesis of hepatic encephalopathy (HE).
    Probiotics and symbiotics are a promising treatment option for HE due to possible
    beneficial effects in modulating gut microflora and might be better tolerated and
    more cost-effective than the traditional treatment with lactulose, rifaximin or
    L-ornithine-L-aspartate. A systematic search of the electronic databases PubMed, 
    ISI Web of Science, EMBASE, and Cochrane Library was conducted for randomized
    controlled clinical trials in adult patients with cirrhosis, evaluating the
    effect of probiotics and symbiotics in changes on intestinal microflora,
    reduction of endotoxemia, inflammation, and ammonia, reversal of minimal hepatic 
    encephalopathy (MHE), prevention of overt hepatic encephalopathy (OHE), and
    improvement of quality of life. Nineteen trials met the inclusion criteria.
    Probiotics and symbiotics increased beneficial microflora and decreased
    pathogenic bacteria and endotoxemia compared with placebo/no treatment, but no
    effect was observed on inflammation. Probiotics significantly reversed MHE [risk 
    ratio, 1.53; 95% confidence interval (CI): 1.14, 2.05; P=0.005] and reduced OHE
    development (risk ratio, 0.62; 95% CI: 0.48, 0.80; P=0.0002) compared with
    placebo/no treatment. Symbiotics significantly decreased ammonia levels compared 
    with placebo (15.24; 95% CI: -26.01, -4.47; P=0.006). Probiotics did not show any
    additional benefit on reversal of MHE and prevention of OHE development when
    compared with lactulose, rifaximin, and L-ornithine-L-aspartate. Only 5 trials
    considered tolerance with minimal side effects reported. Although further
    research is warranted, probiotics and symbiotics should be considered as an
    alternative therapy for the treatment and management of HE given the results
    reported in this systematic review.
    
    DOI: 10.1097/MCG.0000000000000789 
    PMID: 28059938  [Indexed for MEDLINE]

     

     

  3. Primer™ Ingredients

    As Primer™ is primarily a prebiotic, let’s start with those. Prebiotics have come a long way since oat bran and psyllium husks. Beginning with inulin, a huge array of oligosaccharide and glycan type compounds have been found to be fermented and fed on by intestinal bacteria. These newer prebiotics tend to be basically tasteless and dissolve effortlessly, which is quite handy.

    With the importance of microbial diversity for optimal gut and body health, we want a number of different prebiotics for them to feed on. Likewise, we want to choose the ones that best increase the bacteria we want to increase, rather than just randomly feeding all of them.

     

    Galacto-oligosaccharides (GOS)

    GOS reduced fat mass, food intake by 14%, and elevated expression of pro-satiety peptides. Combining them with Calcium increased propionate formation (116). In addition to reductions in food intake, appetite, bodyweight, and inflammation are also decreased (117). GOS increase beneficial bacteria, particularly Bifidobacterium, with 5-10 fold increases in some subjects being noted (118-121). They also raise Bacteroides levels (121). They are long-acting, providing prebiotic effect throughout the entire length of the colon, while strongly inhibiting pathogenic bacteria (122). This owes to high resistance to conditions early in gut digestion (123).

    GOS provide direct enhancement of intestinal barrier function through interaction with goblet cells, separate from SCFA or anti-inflammatory mediated mechanisms. They also showed a 2-4 fold mucin elevation, which would create a positive environment for mucin feeders such as Akkermansia and Bacteroides (124). They inhibited inflammatory responses, augmented protein junction assembly by 85%, and prevented loss of barrier function (125). GOS displayed a microbiota independent increase in tight junction assembly and improved barrier function (126). Finally, they mitigate LPS induced inflammation and protect against stress induced LPS activity (127, 128).

     

    Arabinoxylan-oligosaccharides (AXOS)
    AXOS are strongly Bifidogenic. They increase satiety inducing peptides, while decreasing weight gain, fat mass, and insulin resistance (129). They raise butyrate levels along with Bifidobacterium suggestive of subsequent cross-feeding to butyrate producing bacteria (130).  They also reduce protein fermentation in the gut (130, 131). This spares amino acids for more useful purposes as well as preventing toxic breakdown products.

    AXOS are long-acting, with bacterial fermentation occurring throughout length of colon.  They significantly promote Bacteroides as well as Lactobacillus (132). They are even better than inulin at providing fermentation products to the distal portions of the colon (133). AXOS elevated Roseburia and butyrate levels, with total SCFA increases as high as 2-3 fold (134, 135).  Finally, they increase tight junction proteins, improve barrier function, and inhibit inflammation in adipose tissue (129).

     

    Xylo-oligosaccharides (XOS)
    XOS increased Bifidobacterium along with acetate and butyrate. Combining with inulin further augmented butyrate formation, as well as increasing propionate, suggesting cross-feeding to butyrate and propionate producing bacteria like Roseburia and Bacteroides (136, 137). And, XOS have indeed been found to promote both Roseburia and Bacteroides, as well as improving the Firmicutes:Bacteroides ratio (138, 139). Bacteroides possess special xylan degrading enzymes, making them a preferred fermenter of XOS (140). Elevated Bacteroides and butyrate from XOS protected against genotoxicity in a colonic simulator (141). They also decreased LPS and increased epithelial cell proliferation (137, 142).

     

    Lactulose
    Lactulose inhibits adipogenesis and fat accumulation, down-regulates adipogenic genes, and reduces caloric extraction efficiency, while increasing energy expenditure and lipolysis (143). It also improves post-prandial blood glucose and insulin levels (144, 145). Lactulose raises Bifidobacterium counts, particularly of the ideal cross-feeder B. adolescentis, as well as Akkermansia (146-148). Finally, it decreases intestinal permeability and proteolysis of amino acids in the gut (147, 149).

     

    Inulin
    Inulin improved glucose uptake in insulin resistant cells, and activated AMPK (150). It increases Bifidobacterium and butyrate, while reducing protein fermentation (151, 152). It has a prolonged Bifidogenic effect, with more distal fermentation and SCFA production vs. fructo-oligosaccharides, particularly of butyrate and propionate – again, suggestive of cross-feeding (153, 154). In fact, it was found to increase B. adolescentis more than 4-fold and F. Prausnitzii by 50% (155). It also increased Roseburia, while augmenting mucin production 6-fold, leading to large elevations in Akkermansia and propionate, distally (156).

     

    Resistant Starch 3 (RS3)
    Resistant Starch 3 is formed when starchy foods such as potatoes and rice are cooked and then cooled. This turns formerly digestible starches into resistant starches via a process called retrogradation.  RS3 is particularly, and somewhat uniquely, highly prebiotic for Ruminococcus bromii, with increases up to 4-fold (157-159). R. bromii has superior ability to degrade this resistant starch, which is the most prevalent fermentable carbohydrate in the average diet, making it a “keystone species” by acting as a cross-feeder for other species (160, 161).

    It was also found to be readily consumed by Bacteroides, elevating faecal propionate, rather than butyrate as is often observed following resistant starch feeding of other types. This propionate formation reflects a gut community dominated by the Bacteroides, and it actually became the primary lineage in this study (162).

     

    Amylopectin
    Amylopectin was found to be superior to several other prebiotics for increasing butyrate, as well as butyrate producers F. prausnitzii and Roseburia (163). It also raises Bacteroides, with increases in Roseburia and Bacteroides being found to be proportional to the amylopectin content of barley and oats (164, 165).

     

    Mucin
    Mucin is the glycoprotein constituent of the mucus which lines the wall of the intestines and protects it. Several species of bacteria, including some of the really good ones, feed off of it. Akkermansia is the most well characterized mucin consumer (166, 167). Verrucomicrobia, of which Akkermansia is the primary genus, was increased from .03% to 5.25% by mucin, and in combination with inulin, Bacteroides was raised as well (168).

    Bacteroides thetaiotamicron is a known mucin degrading specialist (169-171). Bacteroides fragillis consumes mucins as well (172, 173). Roseburia intestinalis also colonizes the mucosal layer and feeds on mucins (174).

    With these bacteria colonizing the mucus and being close to the epithelium, particularly with the butyrate producers, bioavailability for epithelial cell regeneration and barrier function is enhanced.

     

    Rhamnose
    Rhamnose is a preferred sugar for the propanediol pathway of propionate production by Roseburia inulinivorans (175, 176). It is quite selectively metabolized to propionate (177, 178). It is much more selective for propionate formation than lactulose or glucose, which utilize different, less selective pathways, resulting in 4 times more propionate than with lactulose or glucose (179). Rhamnose was also found to decrease triglyceride synthesis and serum triglyceride levels, likely due to propionates effects on the SCFA receptors FFAR 2/3 (180).

     

    Glutamine  
    Glutamine is the primary substrate of rapidly diving cells, a category to which the epithelial cells of the digestive tract belong. It increases tight junction protein production (181). It does so by activating the mammalian target of rapamycin (mTOR) cell signaling in enterocytes.   It enhances intestinal growth, enterocyte proliferation and survival, and regulates intestinal barrier function in injury, infection, stress, inflammation, and other catabolic conditions (182). It is basically both the leucine (protein) and the glucose (carbohydrate), to go along with butyrate as the fat, for the fueling of survival, growth, and reproduction of the enterocyte. This makes it quite possibly the most important nutrient for intestinal barrier health and function.

    Glutamine also reduces utilization of other amino acids (asparagine, aspartate, serine, lysine, leucine, valine, ornithine, and arginine) in the gut, preserving them for more useful things while reducing toxic metabolites (183, 184). It decreases intestinal permeability and enhances intestinal mucosa and barrier function (185). Glutamine improves intestinal barrier impairment and quells the LPS mediated inflammatory cascade (186). It also prevents mucosal injury and promotes recovery from LPS induced inflammatory damage, as well as downregulating TLR-4 expression (187, 188).

    Inflammatory conditions increase the requirements for Glutamine to maintain the intestinal barrier (189). It has specifically been shown to protect the intestinal barrier against processed, Western diet style foods (190). AMPK mediates its enhancement of tight junction integrity and barrier preservation (191).

    Conversion to glutamate and subsequent cellular uptake is a pivotal step in its protective effects (192). Monosodium Glutamate has been found to promote the colonization of F. prausnitzii and Roseburia (193). And, finally, L-glutamate enhances barrier function (194).

     

    Calcium Phosphate
    Increasing dietary Calcium produced a reduction in weight gain and fat pad mass of 26-39% with a 51% inhibition of adipocyte fatty acid synthase expression and activity, while stimulating lipolysis by 3 to 5-fold (195). In another study, an almost 50% increase in weight loss was found (196). A high-Calcium diet decreased fat gain by 55%, stimulated adipose tissue uncoupling protein (UCP2) and skeletal muscle UCP3 expression, increased thermogenesis and lipolysis,  while lowering fatty acid synthase expression and activity (197, 198). Calcium also elevated peptides GLP-1 and GLP-2, which increase satiety and decrease food intake (199, 200).

    Calcium improves intestinal permeability, strengthens the mucosal barrier, reduces inflammation, and alleviates colitis (201). Prebiotics have actually been found to have negative effects on intestinal permeability and inflammation without Calcium Phosphate rather than the positive effects produced when it is present (202, 203). This protection is dependent on Phosphate, thus Calcium likely pulls it into the colon, improving luminal buffering capability (204). This is because SCFAs produced by prebiotic fermentation could lower pH too much in its absence.

    Finally, Calcium is necessary for the Calcium/Calmodulin-dependent Protein Kinase Kinase 2 (CaMKK2) mediated AMPK signaling and barrier maintenance produced by Glutamine (205).

     

    Multi-Berry Powder

    Multi-berry powder has the power of berries!! A day’s worth of Primer™ is equal to ¼ cup of mixed berries. It has the polyphenols and fiber and such that berries have, but it is mostly in here because it gives it a nice, subtle berry flavor.

     

    Conclusion

    Primer™ takes the concept of prebiotic far beyond where anyone has previously taken it before. It starts by carefully and selectively feeding the most beneficial bacterial species, including novel probiotic species that you cannot attain, anywhere. It does so in a way that no other product comes even close to doing. It protects against dysfunction of the gut and microbiota to promote better health, better appetite control, better metabolism, and better fat loss. Finally, its supporting ingredients go to work on making your inflamed and leaky gut as good as new, leaving your body functioning in the optimal way it is intended to.

    Primer™ is a gourmet meal for your microbiota and a happy-ending massage for your gut. It is a one of a kind product that fits in perfectly with and enhances any diet and exercise program, any supplement regimine, any lifestyle.

     

    For references, see "View Full Science Write-Up" here: http://neobium.org/product-line/primer/

  4. Dr. Gonzo's Hour of Power

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