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Way back when we talked about SCFAs positive effects on inflammation and permeability of the gut, we said we would get back to its actions outside of the gut, and here we are.
In addition to butyrate’s peripheral anti-inflammatory effects via keeping LPS contained inside the gut, it also directly inhibits TNF-alpha and the inflammatory response to LPS (460, 461). Elimination of the gut microbiome (thus SCFA production) with antibiotics decreases IGF-1, which is restored with SCFA administration (462). Dietary administration of fellow SCFA, propionate, up-regulated the expression of GH, IGF1 and down-regulated myostatin (463). Butyrate improves insulin-resistance in skeletal muscle, along with its induction of Akt (464, 465). And, it increased muscle fiber cross-sectional area along with improving glucose metabolism in aged subjects (466).
Let’s take a closer look at some of the several mechanisms through which it works.
Activation of Free Fatty Acid Receptors (FFAR2 & FFAR3) in the gut by butyrate stimulates the release glucagon-like peptide-1 (GLP-1) which then enters the blood stream (467, 468). Much like insulin, GLP-1 activates the anabolic Akt/mTOR pathway (469, 470, 471, 472). It also promotes dilation of muscle microvascular (473, 474). This enhances nutrient uptake in the muscle cell and is dependent on Akt/mTOR upregulation of nitric oxide production (475, 476). Its effects in this regard were both independent of, and additive to, insulin (477, 478). Recall also the positive effects of NO on satellite cell activation, muscle regeneration, and repair discussed earlier. In addition to skeletal muscle microvasculature, GLP-1 also significantly increases vasodilation and blood flow in large vessels like the brachial and radial arteries and femoral vein (479, 480). Treatment with GLP-1 improves exercise capacity and mitochondrial function, as well as skeletal muscle mass and strength (481, 482).
While GLP-1’s positive effects in muscle begin with butyrate activity in the gut, butyrate, itself, is also taken up from the gut and enters the systemic circulation producing direct actions that support muscle growth. One of the primary mechanisms is its function as a Histone De-Acetylase (HDAC) inhibitor. This is epigenetic stuff. To put it simply, epigenetics involves (heritable) changes in without change to the DNA sequence, itself. It basically changes how the DNA is interpreted, similar to translating a foreign language book. The original book (DNA) stays the same, but a different author (epigenetics) is going to translate it differently. Negative epigenetic changes are a huge part of the build-up of dysfunction with aging in everything from metabolism, to muscle mass, to the brain, with inflammation being a particular culprit (483, 484, 485).
Propionate and acetate also augment histone acetylation, but the bulk of the data is on butyrate (486, 487). HDAC inhibition amplifies Akt/mTOR signaling, as well as preventing induction of atrophy genes (488). Increased histone acetylation blocks downstream activity of glucocorticoids, including FoxO (489, 490). Inhibition of HDAC during muscle disuse significantly attenuated both disuse muscle fiber atrophy and contractile dysfunction via FoxO (491). The effects of acetylation on FoxO, and other targets such as mTOR, appear to be quite similar to phosphorylation with Akt, though data is still new and scarce (492, 493). But, that will definitely be something to keep an eye on. Finally, inhibition of HDAC activity significantly enhanced androgen receptor mediated protein synthesis (494).
You have likely heard the term “muscle memory”, but you may not know that skeletal muscle stem cells do indeed have a memory that is created epigenetically. Stem cells from muscles of young, aged, physically active, and diabetic subjects carry on their altered metabolic characteristics when isolated and cultured (495). In other words, the bad (or good) epigenetic build-up semi-permanently alters them to such an extent that it is maintained when they are taken out of subjects and grown in a lab. HDAC inhibitors promote muscle regeneration through epigenetic regulation of both satellite stem cells and differentiated muscle cells (496). Via upregulation of follistatin (basically the anti-myostatin), HDAC inhibition also blocks the adipogenic potential of stem cells, pushing them toward the formation of muscle cells rather than adipocytes (497, 498). The importance of HDAC inhibition reversing long-term damage from inflammation and aging basically cannot be understated.
Heat Shock Proteins
Butyrate also induces Heat Shock Proteins (499, 500). Heat Shock Proteins (HSPs) are called such because they were initially discovered in cells subjected to hyperthermia, but they function as a protective and subsequent regenerative and repair mechanism against all kinds of cellular stressors (501). Other HDAC inhibitors induce HSPs as well, suggesting this as butyrate’s mechanism in this regard (502, 503). Induction of HSPs protects intestinal epithelial tight junction barriers, decreasing LPS leakage, and reducing the inflammatory response (504). Increased HSP levels also reduce TLR-4, and the subsequent production of TNF-alpha and NF-κB (505).
HSPs strongly blunt increases of cortisol to stressors (506, 507). The synthetic glucocorticoid dexamethasone decreased myotube diameter and protein content, and heat stress prevented this along with recovering Akt signaling (508). HSPs directly bind to and protect Akt, and HSP induction defends against glucocorticoid induction of catabolic FoxO via Akt (509, 510). Silencing of HSP genes decreases Akt and myotube diameter while increasing FoxO, and treatment with an HSP inducer reverses this (511).
Exercise also increases HSPs, along with Akt and downstream anabolic signaling (512). Aged subjects have a blunted HSP response to exercise, along with decreased muscle repair, which is reversed with HSP overexpression (513). HSPs’ positive effects on muscle repair and regeneration seems to be to some extent from protection of satellite cells (514). Androgens and Clenbuterol also strongly upregulate HSP expression, with this likely being particularly important for Clen’s anabolic effects (515, 516, 517, 518).
Last but not least, butyrate protects against the negative effects of Angiotensin II (Ang II). Like butyrate, itself, Ang II produces effects both inside and outside the gut. But, its effects are negative. It is kind of a wingman of LPS in that regard. It also displays bi-directional communication between the gut and brain in hypertension, much like cortisol with stress (519). In addition to its effects on blood pressure, it is strongly induced by LPS and mediates some of the inflammatory response to it (520, 521, 522). LPS induction of Ang II may be through TNF-alpha, but it is also a direct ligand for TLR-4, just as LPS is (533, 534, 535). It is a really interesting molecule, and Renin-Angiotensin a really interesting system, as it ties high blood pressure in with inflammation, insulin resistance, and the cardiovascular system in Metabolic Syndrome. You will likely hear a lot more about it over the next 5-10 years, but parts of the understanding are still relatively in their infancy, so we are going to keep it fairly brief.
There is a decrease in microbial richness and diversity in hypertension and with Ang II infusion, as well as decreases in acetate and butyrate producing bacteria (536). This is accompanied by increased intestinal permeability and decreased tight junction proteins (537). Butyrate administration elevated Akkermansia levels, with significant positive effects on inflammation and ROS, and led to improvement of hypertension (538).
Butyrate significant reduces blood pressure, as well as TNF-alpha, in response to Ang II infusion (539, 540). Data on other HDAC inhibitors indicate that this may be a primary mechanism for butyrate’s antagonism of Ang II’s actions. HDAC inhibitors prevented inflammation and ROS from Angiotensin II (541). They also protected against Ang II induced hypertension and vasoconstriction (542). And, again, the semi-permanent nature of epigenetics makes this especially important.
Outside of the gut, Ang II basically does all of the same bad stuff as LPS because, as we mentioned, it mediates some of LPS signaling, plus shares signaling downstream from TLR-4. It shares the same link between inflammation and insulin resistance, and ACE inhibitors or Ang II receptor blockade reverses these (543, 544, 545). It reduces protein synthesis and increases catabolism, leading to muscle atrophy (546). Ang II inhibits the insulin and IGF-1 signaling pathways via Akt inhibition (547, 548). It impairs insulin stimulated nitric oxide and vasodilation (549). This is, once again, via the Akt/mTOR pathway (550, 551). As a result, Ang II also reduces muscle regeneration and satellite cell differentiation into muscle fibers (552). Finally, it increases the glucorticoid/myostatin catabolic pathways (553, 554).
Will it work for me and what to expect
With the science out of the way, the obvious question is “How much do you need and/or should you want pro- and prebiotics to fix your gut and your body?”
Because the gut and systemic inflammation affect every system, and basically every cell, in your body, a good probiotic/prebiotic combo kind of stands apart from any other category of supplement. It is most analogous to going from a shitty diet to a good diet or from an okay diet to a perfect one.
We briefly mentioned hardgainers and the “skinny fat” phenotype, earlier. You definitely want to fix your gut. I would expect around an extra 10 lbs of muscle in a year, as your body starts living up to its genetic potential. For significantly fat people (and, even moreso, if showing signs of glucose intolerance), you absolutely need to fix your gut. I would expect very noticeable body composition changes in 1-3 months, and borderline miraculous ones in a year. This article has been about muscle mass, but as we alluded to with the mention of Metabolic Syndrome, the gut and inflammation play a huge role in health, as well.
Other general parameters pointing toward its usefulness for you are being over 30, the fatter you are, the worse your diet is, being in a calorie surplus, and having a (personal or family) history of inflammatory related conditions (heart disease, blood pressure, auto-immune, IBS/IBD, etc.).
On other hand, if you are 19, quite lean, on great diet with low-moderate carbs including fruits and veggies, with an iron stomach, and in a calorie deficit, it is not going to noticeably do a lot for you. It would be much more of a preventative measure to keep your cells young as you get older, to keep you still being awesome 5-10+ years from now. A big exception would be during bulking phases – and, the dirtier the bulk, the more it would help. Likewise, if you tend to go off the rails during holidays or vacations, it is damage control.
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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.
DERFDude, 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.
DERFI'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.
DERFThanks, 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.
DERFBullshit. 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 nods. Dan pulls out another.
He injects it and pulls out another.
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.
Did that chubby bitch just cut in front of us?
Does she think we're just standing here to greet people as they walk in the door?
She doesn't need to be getting seconds anyway.
How much do you think she weighs?
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?
Like the height requirements for rollercoasters?
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.
"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.
She needs some EC.
Fuck EC, she needs DNP and some meth.
Maybe she just has low leptin levels.
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.
She's just got more to love, that's all.
Derf walks up closer to her back. He pretends to spank her.
Big is beautiful. Ain't it baby.
(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.
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.
Things like Nicole Bass, and pimples, and warts, and melted flesh from third degree burns... And well-fed bitches like her.
You make a good argument.
Don't kid yourself, Derf. I'm not finished. I haven't yet begun to ridicule.
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?
It's a sick thought.
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.
I did read on MFW about a study linking obesity to a virus.
Well, then the CDC needs to come out here and quarantine this bitch.
If it was a virus, what do you think they'd call it.
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 following was a fictional skit. Any resemblance to actual people, be they from your local gym or alt.support.fat-acceptance, is purely coincidental.
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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]
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