S-VV
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Your alive!
Thought you died of a NaCl overdose. Just kidding. I thoroughly enjoy different perspectives.
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Creatine
- Thread starter gretchen
- Start date
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- Tags
- creatine supplemental
Thought you died of a NaCl overdose. Just kidding. I thoroughly enjoy different perspectives.
Tristan Loscha
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- Dec 18, 2018
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Amazoniac
Member
- Creatine is a Conditionally Essential Nutrient in Chronic Kidney Disease: A Hypothesis and Narrative Literature Review
"[..]observations strongly suggest that the capacity for synthesis of guanidinoacetate by kidneys progressively decreases with increasing stages of CKD, to become absent or virtually absent in dialysis patients. However, even if kidneys would only contribute 20% to total endogenous guanidinoacetate synthesis, incomplete compensation for this loss of function by extra-renal sites of synthesis would pose patients at risk of negative creatine balance if exposed to a low-protein diet, particularly if that low-protein diet would be mainly plant-based [27]. Although this phenomenon might play a role over the continuum of stages of CKD, it should be present in patients that soon will start with dialysis and the most extreme situation should be present in patients on dialysis."
"CKD—particularly in its advanced stages—is [] associated with fatigue, poor cognition, depression and low quality of life [19,57,65,69,70,71,72]. Interestingly, these symptoms are similar to those observed in patients with a genetic deficiency of AGAT [73]. Importantly, in this genetic condition, the muscle symptoms are entirely reversible by creatine supplementation [73]. If creatine supplementation starts at a young age, the occurrence of cognitive dysfunction is reversible and even preventable [74,75,76]."
"[..]no causal links have been established between creatine levels and CKD symptoms, or sarcopenia, muscle weakness, fatigue or impaired cognition. As these symptoms are multifaceted, other factors likely contribute. These other factors include low physical inactivity, inflammation, metabolic acidosis, activation of the ubiquitin–proteasome system and defective insulin signaling, which have all been implicated in the loss of muscle and weakness related to CKD [19,109,110,111,112]."
"We hypothesize that with increasing stages of CKD, creatine coming from meat and dairy in food increasingly becomes an essential nutrient (Figure 3). This phenomenon will be most pronouncedly present in patients with dialysis-dependent CKD, because of the combination of low endogenous production of creatine and the unopposed losses of creatine and its precursor guanidinoacetate into the dialysate. With an increasing focus on a plant-based intake, it is likely that these increased demands for dietary creatine are not sufficiently met. This would result in a creatine deficiency, with important contributions to sarcopenia, fatigue, impaired quality of life, impaired cognition, and premature mortality seen in CKD. It is also important to consider that levels of phosphocreatine concentrations in muscle have been reported to be as high as over 30 mmol/L [26]. So, if a patient with dialysis-dependent CKD would swing back and forth between creatine sufficiency and insufficiency, or even be in a continuous state of creatine insufficiency, periods of muscle catabolism due to creatine insufficiency could possibly: Explain episodes of spurious hyperphosphatemia, which frequently occur; lead to false suspicion of non-adherence to diet or phosphate binder regimens; and most importantly, impair the quality of life of patients [80,81,82]."
"CKD—particularly in its advanced stages—is [] associated with fatigue, poor cognition, depression and low quality of life [19,57,65,69,70,71,72]. Interestingly, these symptoms are similar to those observed in patients with a genetic deficiency of AGAT [73]. Importantly, in this genetic condition, the muscle symptoms are entirely reversible by creatine supplementation [73]. If creatine supplementation starts at a young age, the occurrence of cognitive dysfunction is reversible and even preventable [74,75,76]."
"[..]no causal links have been established between creatine levels and CKD symptoms, or sarcopenia, muscle weakness, fatigue or impaired cognition. As these symptoms are multifaceted, other factors likely contribute. These other factors include low physical inactivity, inflammation, metabolic acidosis, activation of the ubiquitin–proteasome system and defective insulin signaling, which have all been implicated in the loss of muscle and weakness related to CKD [19,109,110,111,112]."
"We hypothesize that with increasing stages of CKD, creatine coming from meat and dairy in food increasingly becomes an essential nutrient (Figure 3). This phenomenon will be most pronouncedly present in patients with dialysis-dependent CKD, because of the combination of low endogenous production of creatine and the unopposed losses of creatine and its precursor guanidinoacetate into the dialysate. With an increasing focus on a plant-based intake, it is likely that these increased demands for dietary creatine are not sufficiently met. This would result in a creatine deficiency, with important contributions to sarcopenia, fatigue, impaired quality of life, impaired cognition, and premature mortality seen in CKD. It is also important to consider that levels of phosphocreatine concentrations in muscle have been reported to be as high as over 30 mmol/L [26]. So, if a patient with dialysis-dependent CKD would swing back and forth between creatine sufficiency and insufficiency, or even be in a continuous state of creatine insufficiency, periods of muscle catabolism due to creatine insufficiency could possibly: Explain episodes of spurious hyperphosphatemia, which frequently occur; lead to false suspicion of non-adherence to diet or phosphate binder regimens; and most importantly, impair the quality of life of patients [80,81,82]."
Zpol
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Sounds like a good combo for people with MTHFR and protein assimilation issues. What brand of phosphatidylcholine do you take?
BioPure Liposorb seems to be the best and possibly lowest in PUFA, plus it's in tocopheral but it's $75 for 24 servings, very pricey.
Jib
Member
- Joined
- Mar 20, 2013
- Messages
- 591
Double Wood brand. As I remember it was pretty affordable. I got the bottle with 250 softgels.
Actually have been forgetting to take it. Been keeping up with creatine and beta alanine but forgot about that one.
Amazoniac
Member
Sathan* said:
- Creatine Supplementation for Patients with Inflammatory Bowel Diseases: A Scientific Rationale for a Clinical Trial
"Cr may be a good candidate for an adjuvant treatment of IBD, since it has been shown to generally improve the energy state of cells, to enhance resilience of cells against several cell stressors, to modulate the immune system, to display anti-inflammatory influences and to dampen nociceptive pain, as will be elucidated below."
"The creatine kinase (CK)/phospho-creatine (PCr) system, with Cr as an energy precursor, plays a crucial physiological role for cells and tissues with high and fluctuating energy requirements, including skeletal, heart and smooth muscles, brain and nervous tissues, as well as other tissues and cells [3,8,9]. This also holds true for intestinal smooth muscle and intestinal epithelial cells, where cytosolic brain-type BB-CK and mitochondrial mtCK isoenzymes are prominently co-expressed [10] (see Figure 1)."
"Intestinal epithelial cells themselves also depend on the CK/PCr system for optimal physiological function. In these cells, PCr works in a similar way, as has been shown to be the case in other cells with high energy requirements [3], as an immediate high-energy buffer and as an energy transport vehicle to guarantee the maintenance of locally high PCr/ATP and ATP/ADP ratios in the vicinity of ATP-dependent processes, such as ion pumps and metabolite transporters [3,8,9], thus increasing the thermodynamic efficiency of intestinal epithelial cells [17] in a similar way as had been shown with other cells [3,8,10]."
"Experimental and clinical data strongly support profound cell-protective properties of creatine in neuronal cells and tissues in vitro and in vivo [18,19,20]. Similar beneficial effects have also been observed with direct intra-venous phospho-creatine (PCr) injections against hypoxic cardiovascular stress [21]. Hypoxia also seems to play a key role in the pathogenesis of intestinal mucosal epithelial diseases [22], compromising cellular energy metabolism by lowering the cellular energy charge, i.e., the PCr/ATP ratio. Hypoxia renders cells more vulnerable to cellular stressors, such as ROS, inflammation and toxins [20,23,24]. In addition, hypoxia has been shown to diminish Cr uptake into cardiac cells [25]. Although the above positive influences of Cr on cell metabolism and cell integrity have largely been studied in other tissues and cells compared to in intestinal epithelial cells, the physiological workings of the CK/PCr system, the CrT and of creatine as such turned out to be very similar in the different cells and, thus, they are likely to also hold true for intestinal epithelial cells. Indeed, it was recently shown that hypoxia profoundly decreases levels of Cr, PCr and total available energy (PCr + ATP + (0.5 × ADP) in intestinal epithelial cells [26]. Thus, creatine supplementation is likely to normalize the intracellular Cr and PCr levels and thus also the energy charge, exemplified as the PCr/ATP ratio, in intestinal epithelial cells. At the same time, creatine supplementation is also highly cytoprotective against oxidative stress by ROS [23,27]. Creatine also leads to a significant increase in cell survival after hypoxic insult in vivo [19,20,28]."
"Given the cytoprotective role of creatine in the setting of hypoxia and ischemia referenced above and the evidence that hypoxia occurs in the setting of IBD [31] with associated intestinal cell barrier dysfunction [32], it follows that creatine is likely to provide a protective influence on the concomitant hypoxia observed in IBD."
"Finally, as acidosis promotes lipid peroxidation and other manifestations of oxidant-mediated damage in various cell types, this condition is also relevant for intestinal epithelium. Acidosis, associated with inflammatory conditions, produces oxidative stress and amplifies these effects, e.g., at an acidotic pH, the response of the intestine to an oxidative insult is magnified [33]. In a rat model of chronic acidosis, creatine supplementation was shown to exert direct anti-oxidant properties by directly scavenging ROS and creatine abolished the chronic reduction in the expression levels of glucose transporter (GLUT2) [34]. Moreover, the administration of creatine under chronic acidosis led to functional strengthening of this jejunal acidotic phenotype, making the tissue more resistant to acidosis [34]. Thus, the beneficial influence and alleviation by creatine with respect to ischemic, oxidative and acidotic insults is certainly relevant for intestinal epithelial tissue, as well as for the entire intestine."
"Mitochondrial creatine kinase (mtCK) and creatine stimulate mitochondrial respiration [35] and thus contribute significantly to maintain a healthy energy state of cells, especially under metabolic stress or toxic insults. Within this context, MtCK and creatine also play a crucial role in an early event of apoptosis; that is, in controlling the opening of the so-called mitochondrial permeability transition pore (mPTP) [36] that is sensitive to cyclosporine A. The addition of creatine to liver mitochondria from transgenic mice expressing mtCK in their livers, after a challenge by 40 mM calcium plus 5 mM atractyloside, prevents swelling of mitochondria and the release of apoptotic factors and reactive oxygen species (ROS) in a similar fashion as the bona fide anti-apoptotic agent cyclosporine A. In liver mitochondria from normal mice, which do not express mtCK in their liver, no effect of creatine on mitochondrial swelling could be seen, indicating that the action of mtCK, located in the mitochondrial inter-membrane space and present in all cells except for liver, is necessary together with creatine to prevent challenged mitochondria from swelling and mitochondrial permeability transition pore (mPTP) from opening [37]. Similar anti-apoptotic protection by creatine or phospho-creatine could be observed with intact cardiomyocytes [38], or with human umbilical vein endothelial cells that both were protected by creatine from lipopolysaccharide (LPS)-induced apoptosis [39]. This anti-apoptotic effect of creatine could also be demonstrated in vivo in hyper-cholesterolemic mice, where pravastatin-induced mitochondrial mPTP opening in skeletal muscles was minimized by creatine [40]. A significant factor for cell protection by creatine is mediated by the action of octameric mtCK that stabilizes mitochondrial contact sites and protects mitochondrial and cell integrity [41]. Thus, creatine, together with mtCK, regulate mitochondrial oxidative phosphorylation and exert a significant anti-apoptotic effect on a variety of cells by protecting them from different cytotoxic insults (for review [42]). In line with this notion, the anti-apoptotic effects and preservation of the function and structural integrity of mitochondria under metabolic stress was demonstrated directly in vivo in murine cardiac muscle [30]. Intestinal epithelial cell apoptosis significantly contributes to the development of ulcerative colitis and IBD in humans and mice, and therapies that target the inflammatory cytokine TNF, as well as the p53-upregulated modulator of apoptosis (PUMA) that are both upregulated in colitis tissues, have been found to inhibit apoptosis in intestinal epithelial cells and to promote mucosal healing [43]. Taking the evidence for the role of creatine in inhibition of apoptosis in other tissues and the finding that apoptosis contributes to disease activity in IBD [44], it is thus very reasonable to postulate that creatine would be anti-apoptotic in the mucosa of IBD patients as well."
"There is solid evidence in sports medicine, e.g., from ironman competitions, that creatine supplementation reduces the plasma levels of pro-inflammatory cytokines and prostaglandin E2 (PGE2) [45]. Very recent data have provided evidence that creatine may also have the potential to lower pain sensitivity associated with inflammation by antagonizing the acid-sensing ion channel (ASIC3) [46]. This effect is most likely based on the structural similarity of creatine, itself a guanidino compound, to other guanidino compound ligands of the ASIC3 pain receptor, such as GMQ and amiloride, that modulated this ion sensing channel [46]. Thus, one may expect from creatine supplementation, as an additional beneficial effect, an improvement of the abdominal pain associated with intestinal inflammation. This is an important determinant of quality of life for patients with IBD both in the setting of active inflammation as well as in IBD patients with irritable bowel syndrome symptoms in the absence of inflammation [47]."
"Immune cells themselves express CK and seem to depend on the CK/PCr system in a similar way to muscle and brain cells [3,10], as pointed out in a recent review [48]. For example, leucocytes express the CRT-1 transporter for the import of extracellular creatine [49]. Additionally, in macrophages, CK has a functional impact on these cells by supporting the formation of actin-based protrusions needed for macrophage motility and phagocytosis [50]. In addition, the uptake and accumulation of creatine into macrophages leads to the reprogramming and polarization of macrophages by modulating cellular responses to cytokines, such as IFN-γ and Il-4, thus enhancing the ability of macrophages to sense viral and bacterial antigens [51]."
"With regard to T cells, creatine kinase is involved in T cell development and activation [52] and creatine uptake regulates CD8 T cell immunity [53]. Thus, it seems obvious that the CK/PCr system has a profound impact both on the innate and adaptive immune response, exhibiting significant immune modulatory effects [54] and, therefore, it may be inferred that patients with IBD, who often suffer from intestinal infections, may benefit by creatine supplementation as a general activator of immune responses [54]."
"Fully charged cellular energy batteries are a prerequisite for optimal body function not only for muscle and brain cells, but also for intestinal smooth muscle and epithelial cells. Long-term decay or failure of cellular energetics, e.g., by chronic ischemia, inflammation and progressive dysfunction of mitochondria, as well as deterioration of mucosal barrier functions, are important aspects of IBD that are accompanied by a state of chronic inflammation [17]. Mucosal surfaces of the lower gastrointestinal tract are subject to pronounced fluctuations in oxygen (O2) tension, particularly during inflammation(Figure 2). As an adaptive response to hypoxia, the hypoxia-induced transcription factors (HIF-1 and HIF-2) become stabilized [62]. An unbiased analysis of HIF target genes identified creatine kinases (both cytosolic BB-CK and mtCK) and the major Cr transporter SLC6A8 that are all coordinately regulated by HIF [16]. Further analysis revealed that cytosolic BB-CK is expressed in a HIF-2 dependent manner and that this enzyme localizes to apical intestinal epithelium cell adherence junctions, where it is critically involved in the ATP-dependent junction assembly, epithelial integrity and mucosal barrier function (see Figure 1). This same study revealed that tissue transcripts from 30 IBD patients (including both Crohn’s disease and ulcerative colitis) showed a marked reduction in the expression of all three isoforms of CK compared to non-IBD controls. In light of this observation, it is notable that the interaction of epithelial junctions with the actin cytoskeleton is a significant energy sink within the mucosa. Energy deficiencies associated with IBD, including those associated with microbial dysbiosis, likely contribute to barrier dysfunction during active inflammation [63]."
"Patients with IBD present with intestinal barrier dysfunction that is likely related to disturbed cellular energetics and dysbiosis. Since the CK/PCr system, as well as the creatine transporter (CrT1) are involved in a plethora of processes that are important for cellular energetics [3,8], also in intestinal epithelial cells [16,17,62] it is interesting that the investigation of mucosal biopsied from 30 patients with Crohn’s disease and 27 patients with ulcerative colitis both showed lower expression levels of CrT1, which might contribute to the reduced barrier function of intestinal epithelium [14](see Figure 3). Notably, in intestinal epithelial cells (IECs), CrT1 localized specifically around tight junctions and knockdown or overexpression of CrT1 in these cells corroborated the idea that CrT1, besides regulating the intracellular creatine concentration in IECs, was also modulating epithelial barrier formation and wound healing [14]. In CrT1 knockdown IECs—that is, in the absence of adequate creatine transport—these cells transformed to a stressed, glycolysis-predominant energy metabolism, resulting in leaky tight junctions and mislocalization of actin and tight junction proteins [14]. Despite the significant impacts of CrT1 loss, proliferation was not altered in CrT1 knockdown intestinal epithelial cells [14]. It is noteworthy that metabolomic analysis has revealed that the actin cytoskeleton demands nearly 20% of total available energy within the epithelium [26]. Taken together, these data support the fact that CrT1, together with CK, phosphocreatine (PCr) and creatine, regulates the energy balance of IECs and enforces the structural and functional integrity of the tight-junction-actin cytoskeleton. These are excellent arguments that speak for a clinical trial, using creatine supplementation directly on patients with IBD."
"Fully in line with these pioneering data is a first single case study with a 33-year-old patient with a two-year history of Crohn’s ileitis, who responded very well to creatine supplementation (1.5 g per day, given as monotherapy for a time period of 6 months) with both symptomatic and endoscopic improvement in disease activity [75]. Specifically, before creatine supplementation, the colonoscopy of the patient showed large ulcers of 0.5–2.0 cm in diameter with >30% ulcerative surface, 50–70% affected surface and no narrowing (SDS-CD:7), whereas after creatine supplementation, the same patient presented with aphthous ulcers <0.5 cm in diameter, <10% ulcerated surface, <50% affected surface and no-narrowing (SES-CD:3) (see Figures 1–3 in [75])."
"Almost certainly, since IBDs are multifactorial diseases with phenotypical and genetic subtypes, Cr is unlikely solving all the problems associated with these serious diseases, but if Cr should indeed turn out to be helpful in inducing such favorable responses or even the remission of the ulcerative pathology in colitis patients, an inclusion of creatine supplementation [..] as standard adjuvant therapeutic intervention for ulcerative colitis and/or Crohn’s disease, could be envisaged, preferably together with established medical treatment options."
"Intestinal epithelial cells themselves also depend on the CK/PCr system for optimal physiological function. In these cells, PCr works in a similar way, as has been shown to be the case in other cells with high energy requirements [3], as an immediate high-energy buffer and as an energy transport vehicle to guarantee the maintenance of locally high PCr/ATP and ATP/ADP ratios in the vicinity of ATP-dependent processes, such as ion pumps and metabolite transporters [3,8,9], thus increasing the thermodynamic efficiency of intestinal epithelial cells [17] in a similar way as had been shown with other cells [3,8,10]."
"Experimental and clinical data strongly support profound cell-protective properties of creatine in neuronal cells and tissues in vitro and in vivo [18,19,20]. Similar beneficial effects have also been observed with direct intra-venous phospho-creatine (PCr) injections against hypoxic cardiovascular stress [21]. Hypoxia also seems to play a key role in the pathogenesis of intestinal mucosal epithelial diseases [22], compromising cellular energy metabolism by lowering the cellular energy charge, i.e., the PCr/ATP ratio. Hypoxia renders cells more vulnerable to cellular stressors, such as ROS, inflammation and toxins [20,23,24]. In addition, hypoxia has been shown to diminish Cr uptake into cardiac cells [25]. Although the above positive influences of Cr on cell metabolism and cell integrity have largely been studied in other tissues and cells compared to in intestinal epithelial cells, the physiological workings of the CK/PCr system, the CrT and of creatine as such turned out to be very similar in the different cells and, thus, they are likely to also hold true for intestinal epithelial cells. Indeed, it was recently shown that hypoxia profoundly decreases levels of Cr, PCr and total available energy (PCr + ATP + (0.5 × ADP) in intestinal epithelial cells [26]. Thus, creatine supplementation is likely to normalize the intracellular Cr and PCr levels and thus also the energy charge, exemplified as the PCr/ATP ratio, in intestinal epithelial cells. At the same time, creatine supplementation is also highly cytoprotective against oxidative stress by ROS [23,27]. Creatine also leads to a significant increase in cell survival after hypoxic insult in vivo [19,20,28]."
"Given the cytoprotective role of creatine in the setting of hypoxia and ischemia referenced above and the evidence that hypoxia occurs in the setting of IBD [31] with associated intestinal cell barrier dysfunction [32], it follows that creatine is likely to provide a protective influence on the concomitant hypoxia observed in IBD."
"Finally, as acidosis promotes lipid peroxidation and other manifestations of oxidant-mediated damage in various cell types, this condition is also relevant for intestinal epithelium. Acidosis, associated with inflammatory conditions, produces oxidative stress and amplifies these effects, e.g., at an acidotic pH, the response of the intestine to an oxidative insult is magnified [33]. In a rat model of chronic acidosis, creatine supplementation was shown to exert direct anti-oxidant properties by directly scavenging ROS and creatine abolished the chronic reduction in the expression levels of glucose transporter (GLUT2) [34]. Moreover, the administration of creatine under chronic acidosis led to functional strengthening of this jejunal acidotic phenotype, making the tissue more resistant to acidosis [34]. Thus, the beneficial influence and alleviation by creatine with respect to ischemic, oxidative and acidotic insults is certainly relevant for intestinal epithelial tissue, as well as for the entire intestine."
"Mitochondrial creatine kinase (mtCK) and creatine stimulate mitochondrial respiration [35] and thus contribute significantly to maintain a healthy energy state of cells, especially under metabolic stress or toxic insults. Within this context, MtCK and creatine also play a crucial role in an early event of apoptosis; that is, in controlling the opening of the so-called mitochondrial permeability transition pore (mPTP) [36] that is sensitive to cyclosporine A. The addition of creatine to liver mitochondria from transgenic mice expressing mtCK in their livers, after a challenge by 40 mM calcium plus 5 mM atractyloside, prevents swelling of mitochondria and the release of apoptotic factors and reactive oxygen species (ROS) in a similar fashion as the bona fide anti-apoptotic agent cyclosporine A. In liver mitochondria from normal mice, which do not express mtCK in their liver, no effect of creatine on mitochondrial swelling could be seen, indicating that the action of mtCK, located in the mitochondrial inter-membrane space and present in all cells except for liver, is necessary together with creatine to prevent challenged mitochondria from swelling and mitochondrial permeability transition pore (mPTP) from opening [37]. Similar anti-apoptotic protection by creatine or phospho-creatine could be observed with intact cardiomyocytes [38], or with human umbilical vein endothelial cells that both were protected by creatine from lipopolysaccharide (LPS)-induced apoptosis [39]. This anti-apoptotic effect of creatine could also be demonstrated in vivo in hyper-cholesterolemic mice, where pravastatin-induced mitochondrial mPTP opening in skeletal muscles was minimized by creatine [40]. A significant factor for cell protection by creatine is mediated by the action of octameric mtCK that stabilizes mitochondrial contact sites and protects mitochondrial and cell integrity [41]. Thus, creatine, together with mtCK, regulate mitochondrial oxidative phosphorylation and exert a significant anti-apoptotic effect on a variety of cells by protecting them from different cytotoxic insults (for review [42]). In line with this notion, the anti-apoptotic effects and preservation of the function and structural integrity of mitochondria under metabolic stress was demonstrated directly in vivo in murine cardiac muscle [30]. Intestinal epithelial cell apoptosis significantly contributes to the development of ulcerative colitis and IBD in humans and mice, and therapies that target the inflammatory cytokine TNF, as well as the p53-upregulated modulator of apoptosis (PUMA) that are both upregulated in colitis tissues, have been found to inhibit apoptosis in intestinal epithelial cells and to promote mucosal healing [43]. Taking the evidence for the role of creatine in inhibition of apoptosis in other tissues and the finding that apoptosis contributes to disease activity in IBD [44], it is thus very reasonable to postulate that creatine would be anti-apoptotic in the mucosa of IBD patients as well."
"There is solid evidence in sports medicine, e.g., from ironman competitions, that creatine supplementation reduces the plasma levels of pro-inflammatory cytokines and prostaglandin E2 (PGE2) [45]. Very recent data have provided evidence that creatine may also have the potential to lower pain sensitivity associated with inflammation by antagonizing the acid-sensing ion channel (ASIC3) [46]. This effect is most likely based on the structural similarity of creatine, itself a guanidino compound, to other guanidino compound ligands of the ASIC3 pain receptor, such as GMQ and amiloride, that modulated this ion sensing channel [46]. Thus, one may expect from creatine supplementation, as an additional beneficial effect, an improvement of the abdominal pain associated with intestinal inflammation. This is an important determinant of quality of life for patients with IBD both in the setting of active inflammation as well as in IBD patients with irritable bowel syndrome symptoms in the absence of inflammation [47]."
"Immune cells themselves express CK and seem to depend on the CK/PCr system in a similar way to muscle and brain cells [3,10], as pointed out in a recent review [48]. For example, leucocytes express the CRT-1 transporter for the import of extracellular creatine [49]. Additionally, in macrophages, CK has a functional impact on these cells by supporting the formation of actin-based protrusions needed for macrophage motility and phagocytosis [50]. In addition, the uptake and accumulation of creatine into macrophages leads to the reprogramming and polarization of macrophages by modulating cellular responses to cytokines, such as IFN-γ and Il-4, thus enhancing the ability of macrophages to sense viral and bacterial antigens [51]."
"With regard to T cells, creatine kinase is involved in T cell development and activation [52] and creatine uptake regulates CD8 T cell immunity [53]. Thus, it seems obvious that the CK/PCr system has a profound impact both on the innate and adaptive immune response, exhibiting significant immune modulatory effects [54] and, therefore, it may be inferred that patients with IBD, who often suffer from intestinal infections, may benefit by creatine supplementation as a general activator of immune responses [54]."
"Fully charged cellular energy batteries are a prerequisite for optimal body function not only for muscle and brain cells, but also for intestinal smooth muscle and epithelial cells. Long-term decay or failure of cellular energetics, e.g., by chronic ischemia, inflammation and progressive dysfunction of mitochondria, as well as deterioration of mucosal barrier functions, are important aspects of IBD that are accompanied by a state of chronic inflammation [17]. Mucosal surfaces of the lower gastrointestinal tract are subject to pronounced fluctuations in oxygen (O2) tension, particularly during inflammation
"Patients with IBD present with intestinal barrier dysfunction that is likely related to disturbed cellular energetics and dysbiosis. Since the CK/PCr system, as well as the creatine transporter (CrT1) are involved in a plethora of processes that are important for cellular energetics [3,8], also in intestinal epithelial cells [16,17,62] it is interesting that the investigation of mucosal biopsied from 30 patients with Crohn’s disease and 27 patients with ulcerative colitis both showed lower expression levels of CrT1, which might contribute to the reduced barrier function of intestinal epithelium [14]
"Fully in line with these pioneering data is a first single case study with a 33-year-old patient with a two-year history of Crohn’s ileitis, who responded very well to creatine supplementation (1.5 g per day, given as monotherapy for a time period of 6 months) with both symptomatic and endoscopic improvement in disease activity [75]. Specifically, before creatine supplementation, the colonoscopy of the patient showed large ulcers of 0.5–2.0 cm in diameter with >30% ulcerative surface, 50–70% affected surface and no narrowing (SDS-CD:7), whereas after creatine supplementation, the same patient presented with aphthous ulcers <0.5 cm in diameter, <10% ulcerated surface, <50% affected surface and no-narrowing (SES-CD:3) (see Figures 1–3 in [75])."
"Almost certainly, since IBDs are multifactorial diseases with phenotypical and genetic subtypes, Cr is unlikely solving all the problems associated with these serious diseases, but if Cr should indeed turn out to be helpful in inducing such favorable responses or even the remission of the ulcerative pathology in colitis patients, an inclusion of creatine supplementation [..] as standard adjuvant therapeutic intervention for ulcerative colitis and/or Crohn’s disease, could be envisaged, preferably together with established medical treatment options."
*Reformulating Raj's words: a little stupid and unconsciously evil.
Amazoniac
Member
GorillaHead
Member
Does creatine deplete any other vitamins?
T
TheBeard
Guest
All I know is creatine supplementation gives me kidney pain.
Every single time, like clockwork, whether I supplement with 1 gram or 5 grams, all at once or sipped on throughout the day.
GorillaHead
Member
This is why i asked my question. Every-time i get a gram in u develop like uti like symptoms.
Rafael Lao Wai
Member
- Joined
- Jun 16, 2017
- Messages
- 1,790
How much protein are you eating at a time? I ask because creatine used to make my kindeys hurt, even in small amounts( 500mg to 1 gram), but now that I restrict my protein intake to about 30 grams per meal, I can take that same creatine dose without any kidney pain. Before, I was easily getting 50 to 60 grams of protein in one single meal. I think it's related to ammonia.
Amazoniac
Member
Amazoniac
Member
Lejeboca
Member
- Joined
- Jun 19, 2017
- Messages
- 1,039
Putting to rest the myth of creatine supplementation leading to muscle cramps and dehydration
Abstract
Creatine is one of the most popular athletic supplements with sales surpassing 400 million dollars in 2004. Due to the popularity and efficacy of creatine supplementation over 200 studies have examined the effects of creatine on athletic performance. Despite the abundance of research suggesting the effectiveness and safety of creatine, a fallacy appears to exist among the general public, driven by media claims and anecdotal reports, that creatine supplementation can result in muscle cramps and dehydration. Although a number of published studies have refuted these claims, a recent position statement by the American College of Sports Medicine (ACSM) in 2000 advised individuals who are managing their weight and exercising intensely or in hot environments to avoid creatine supplementation. Recent reports now suggest that creatine may enhance performance in hot and/or humid conditions by maintaining haematocrit, aiding thermoregulation and reducing exercising heart rate and sweat rate. Creatine may also positively influence plasma volume during the onset of dehydration. Considering these new published findings, little evidence exists that creatine supplementation in the heat presents additional risk, and this should be taken into consideration as position statements and other related documents are published.
ChetnikPeater
Member
CreaPure is exactly this, free from impurities.
Dave Clark
Member
- Joined
- Jun 2, 2017
- Messages
- 1,995
There was a 4 day Creatine Conference 2022 that had professors from various universities covering different topics. You can find them on YT.
DaveFoster
Member
I’ll need a source with lab testing results.
ChetnikPeater
Member
Check their site, they have third party testing
DaveFoster
Member
Great. I like the look of the website and its focus on informing the reader.
EMF Mitigation - Flush Niacin - Big 5 Minerals
