Creatine Intake Research Articles

Impact of Dietary Protein intake, Lean Body Mass percentage, Body Mass Index, Physical activity on Urinary Creatine and Urinary Creatinine excretion in a TeamSport

Background: Creatine and Creatinine plays a role in muscle function. Urinary creatine and urinary creatinine concentration was measured in order to see significance in monitoring athlete and athlete’s performance. Objective: Evaluate association of dietary protein intake, Lean Body Mass (LBM) percentage, Body Mass Index (BMI) and physical activity on urinary creatine, urinary creatinine concentration in different team sports [cricket players (C), basketball players (B) and football players (F)]. Methodology: A total of 62 players from different team sports - C (n-20), B (n-17) and F (n-25) age of 18-30 years participated. Post training urine samples was analyzed. Using Jaffe's reaction, urinary creatinine was obtained and Urinary creatine is obtained by difference in the creatinine present before and after heating with acid solution. 24 hour dietary recall was taken to find athletes protein intake. LBM were taken using Body Impedence Analysis (BIA machine). Data were analysed using SPSS (Statistical Package for Social Sciences Version 16.0). Findings: Pearson bivariate correlation (2-tailed) was used to find the relationship between BMI, LBM, total dietary protein intake per day, dietary protein, duration of practice with urine creatinine and creatine level. Positive correlation between urinary creatine and total dietary protein intake per day, dietary protein according to body weight per day was found (p<0.001), (p<0.005) respectively. Negative correlation between urinary creatinine and dietary protein according to body weight per day and duration of practice per day was found (p<0.001), (p<0.005) respectively. Urinary creatine mean (SD) values- C group 78.63 ± 27.17, B group 102.65 ± 38 and F group 169.60±41.58. Urinary creatinine mean (SD) values- C group 46.60 ± 37.23,B group 84.88 ± 48.27 and F group 70.40±44.083. Conclusion & Significance: Significant increase was seen in urinary creatine excretion with respect to dietary protein per day, dietary protein according to body weight per day. Urinary creatine excretion is more in football players followed by basketball players. Significant decline was seen in urinary creatinine excretion with respect to increase dietary protein according to body weight per day and increase duration of practice. Urinary Creatine excretion is more in basketball players followed by football players Urinary creatine and urinary creatinine excretion depends on sports-type, duration of sports and protein consumption.

UNICORN Babies: Understanding Circulating and Cerebral Creatine Levels of the Preterm Infant. An Observational Study Protocol.

Creatine is an essential metabolite for brain function, with a fundamental role in cellular (ATP) energy homeostasis. It is hypothesized that preterm infants will become creatine deplete in the early postnatal period, due to premature delivery from a maternal source of creatine and a limited supply of creatine in newborn nutrition. This potential alteration to brain metabolism may contribute to, or compound, poor neurological outcomes in this high-risk population. Understanding Creatine for Neurological Health in Babies (UNICORN) is an observational study of circulating and cerebral creatine levels in preterm infants. We will recruit preterm infants at gestational ages 23+0–26+6, 27+0–29+6, 30+0–32+6, 33+0–36+6, and a term reference group at 39+0–40+6 weeks of gestation, with 20 infants in each gestational age group. At birth, a maternal capillary blood sample, as well as a venous cord blood sample, will be collected. For preterm infants, serial infant plasma (heel prick), urine, and nutrition samples [total parenteral nutrition (TPN), breast milk, or formula] will be collected between birth and term “due date.” Key fetomaternal information, including demographics, smoking status, and maternal diet, will also be collected. At term corrected postnatal age (CPA), each infant will undergo an MRI/1H-MRS scan to evaluate brain structure and measure cerebral creatine content. A general movements assessment (GMA) will also be conducted. At 3 months of CPA, infants will undergo a second GMA as well as further neurodevelopmental evaluation using the Developmental Assessment of Young Children – Second Edition (DAYC-2) assessment tool. The primary outcome measures for this study are cerebral creatine content at CPA and plasma and urine creatine and guanidinoacetate (creatine precursor) concentrations in the early postnatal period. We will also determine associations between (1) creatine levels at term CPA and neurodevelopmental outcomes (MRI, GMA, and DAY-C); (2) dietary creatine intake and circulating and cerebral creatine content; and (3) creatine levels and maternal characteristics. Novel approaches are needed to try and improve preterm-associated brain injury. Inclusion of creatine in preterm nutrition may better support ex utero brain development through improved cerebral cellular energy availability during a period of significant brain growth and development.Ethics Ref: HDEC 18/CEN/7 New Zealand.ACTRN: ACTRN12618000871246.

Creatine supplementation in Walker-256 tumor-bearing rats prevents skeletal muscle atrophy by attenuating systemic inflammation and protein degradation signaling.

The aim of this study was to investigate the effects of creatine supplementation on muscle wasting in Walker-256 tumor-bearing rats. Wistar rats were randomly assigned into three groups (n = 10/group): control (C), tumor bearing (T), and tumor bearing supplemented with creatine (TCr). Creatine was provided in drinking water for a total of 21days. After 11days of supplementation, tumor cells were implanted subcutaneously into T and TCr groups. The animals' weight, food and water intake were evaluated along the experimental protocol. After 10days of tumor implantation (21 total), animals were euthanized for inflammatory state and skeletal muscle cross-sectional area measurements. Skeletal muscle components of ubiquitin-proteasome pathways were also evaluated using real-time PCR and immunoblotting. The results showed that creatine supplementation protected tumor-bearing rats against body weight loss and skeletal muscle atrophy. Creatine intake promoted lower levels of plasma TNF-α and IL-6 and smaller spleen morphology changes such as reduced size of white pulp and lymphoid follicle compared to tumor-bearing rats. In addition, creatine prevented increased levels of skeletal muscle Atrogin-1 and MuRF-1, key regulators of muscle atrophy. Creatine supplementation prevents skeletal muscle atrophy by attenuating tumor-induced pro-inflammatory environment, a condition that minimizes Atrogin-1 and MuRF-1-dependent proteolysis.

Creatine and creatine forms intended for sports nutrition.

Creatine is a popular ergogenic supplement in sports nutrition. Yet, supplementation of creatine occasionally caused adverse effects such as gastrointestinal complaints, muscle cramps and an increase in body weight. Creatine monohydrate has already been evaluated by different competent authorities and several have come to the conclusion that a daily intake of 3g creatine per person is unlikely to pose safety concerns, focusing on healthy adults with exclusion of pregnant and breastfeeding women. Possible vulnerable subgroups were also discussed in relation to the safety of creatine. The present review provides an up-to-date overview of the relevant information with special focus on human studies regarding the safety of creatine monohydrate and other marketed creatine forms, in particular creatine pyruvate, creatine citrate, creatine malate, creatine taurinate, creatine phosphate, creatine orotate, creatine ethyl ester, creatine pyroglutamate, creatine gluconate, and magnesium creatine chelate. Limited data are available with regard to the safety of the latter creatine forms. Considering an acceptable creatine intake of 3g per day, most of the evaluated creatine forms are unlikely to pose safety concerns, however some safety concerns regarding a supplementary intake of creatine orotate, creatine phosphate, and magnesium creatine chelate are discussed here.

Does brain creatine content rely on exogenous creatine in healthy youth? A proof-of-principle study.

It has been hypothesized that dietary creatine could influence cognitive performance by increasing brain creatine in developing individuals. This double-blind, randomized, placebo-controlled, proof-of-principle study aimed to investigate the effects of creatine supplementation on cognitive function and brain creatine content in healthy youth. The sample comprised 67 healthy participants aged 10 to 12 years. The participants were given creatine or placebo supplementation for 7 days. At baseline and after the intervention, participants undertook a battery of cognitive tests. In a random subsample of participants, brain creatine content was also assessed in the regions of left dorsolateral prefrontal cortex, left hippocampus, and occipital lobe by proton magnetic resonance spectroscopy (1H-MRS) technique. The scores obtained from verbal learning and executive functions tests did not significantly differ between groups at baseline or after the intervention (all p > 0.05). Creatine content was not significantly different between groups in left dorsolateral prefrontal cortex, left hippocampus, and occipital lobe (all p > 0.05). In conclusion, a 7-day creatine supplementation protocol did not elicit improvements in brain creatine content or cognitive performance in healthy youth, suggesting that this population mainly relies on brain creatine synthesis rather than exogenous creatine intake to maintain brain creatine homeostasis.

Effects of creatine monohydrate supplementation and exercise on depression-like behaviors and raphe 5-HT neurons in mice

[Purpose]The effects of creatine and exercise on chronic stress-induced depression are unclear. In the present study, we identified the effects of 4-week supplementation of creatine monohydrate and/or exercise on antidepressant behavior and raphe 5-HT expression in a chronic mild stress-induced depressed mouse model. [Methods]Seven-week-old male C57BL/6 mice (n=48) were divided randomly into 5 groups: (1) non-stress control (CON, n=10), (2) stress control (ST-CON, n=10), (3) stress and creatine intake (ST-Cr, n=10), (4) stress and exercise (ST-Ex, n=9), and (5) combined stress, exercise, and creatine intake (ST-Cr+Ex, n=9). After five weeks’ treatment, we investigated using both anti-behavior tests (the Tail Suspension Test (TST) and the Forced Swimming Test (FST)), and 5-HT expression in the raphe nuclei (the dorsal raphe (DR) and median raphe (MnR)). [Results]Stress for 4 weeks significantly increased depressive behaviors in the mice. Treatment with creatine supplementation combined with exercise significantly decreased depressive behaviors as compared with the CON-ST group in both the TST and FST tests. With stress, 5-HT expression in the raphe nuclei decreased significantly. With combined creatine and exercise, 5-HT positive cells increased significantly and had a synergic effect on both DR and MnR. [Conclusion]The present study found that even a single treatment of creatine or exercise has partial effects as an antidepressant in mice with chronic mild stress-induced depression. Furthermore, combined creatine and exercise has synergic effects and is a more effective prescription than a single treatment.

The role of dietary creatine.

The daily requirement of a 70-kg male for creatine is about 2g; up to half of this may be obtained from a typical omnivorous diet, with the remainder being synthesized in the body Creatine is a carninutrient, which means that it is only available to adults via animal foodstuffs, principally skeletal muscle, or via supplements. Infants receive creatine in mother's milk or in milk-based formulas. Vegans and infants fed on soy-based formulas receive no dietary creatine. Plasma and muscle creatine levels are usually somewhat lower in vegetarians than in omnivores. Human intake of creatine was probably much higher in Paleolithic times than today; some groups with extreme diets, such as Greenland and Alaskan Inuit, ingest much more than is currently typical. Creatine is synthesized from three amino acids: arginine, glycine and methionine (as S-adenosylmethionine). Humans can synthesize sufficient creatine for normal function unless they have an inborn error in a creatine-synthetic enzyme or a problem with the supply of substrate amino acids. Carnivorous animals, such as lions and wolves, ingest much larger amounts of creatine than humans would. The gastrointestinal tract and the liver are exposed to dietary creatine in higher concentrations before it is assimilated by other tissues. In this regard, our observations that creatine supplementation can prevent hepatic steatosis (Deminice et al. J Nutr 141:1799-1804, 2011) in a rodent model may be a function of the route of dietary assimilation. Creatine supplementation has also been reported to improve the intestinal barrier function of the rodent suffering from inflammatory bowel disease.

Dietary creatine supplementation during pregnancy: a study on the effects of creatine supplementation on creatine homeostasis and renal excretory function in spiny mice.

Recent evidence obtained from a rodent model of birth asphyxia shows that supplementation of the maternal diet with creatine during pregnancy protects the neonate from multi-organ damage. However, the effect of increasing creatine intake on creatine homeostasis and biosynthesis in females, particularly during pregnancy, is unknown. This study assessed the impact of creatine supplementation on creatine homeostasis, body composition, capacity for de novo creatine synthesis and renal excretory function in non-pregnant and pregnant spiny mice. Mid-gestation pregnant and virgin spiny mice were fed normal chow or chow supplemented with 5% w/w creatine for 18days. Weight gain, urinary creatine and electrolyte excretion were assessed during supplementation. At post mortem, body composition was assessed by Dual-energy X-ray absorptiometry, or tissues were collected to assess creatine content and mRNA expression of the creatine synthesising enzymes arginine:glycine amidinotransferase (AGAT) and guanidinoacetate methyltransferase (GAMT) and the creatine transporter (CrT1). Protein expression of AGAT and GAMT was also assessed by Western blot. Key findings of this study include no changes in body weight or composition with creatine supplementation; increased urinary creatine excretion in supplemented spiny mice, with increased sodium (P<0.001) and chloride (P<0.05) excretion in pregnant dams after 3days of supplementation; lowered renal AGAT mRNA (P<0.001) and protein (P<0.001) expressions, and lowered CrT1 mRNA expression in the kidney (P<0.01) and brain (P<0.001). Creatine supplementation had minimal impact on creatine homeostasis in either non-pregnant or pregnant spiny mice. Increasing maternal dietary creatine consumption could be a useful treatment for birth asphyxia.

Maternal creatine supplementation affects the morpho-functional development of hippocampal neurons in rat offspring

Creatine supplementation has been shown to protect neurons from oxidative damage due to its antioxidant and ergogenic functions. These features have led to the hypothesis of creatine supplementation use during pregnancy as prophylactic treatment to prevent CNS damage, such as hypoxic–ischemic encephalopathy. Unfortunately, very little is known on the effects of creatine supplementation during neuron differentiation, while in vitro studies revealed an influence on neuron excitability, leaving the possibility of creatine supplementation during the CNS development an open question. Using a multiple approach, we studied the hippocampal neuron morphological and functional development in neonatal rats born by dams supplemented with 1% creatine in drinking water during pregnancy.CA1 pyramidal neurons of supplemented newborn rats showed enhanced dendritic tree development, increased LTP maintenance, larger evoked-synaptic responses, and higher intrinsic excitability in comparison to controls. Moreover, a faster repolarizing phase of action potential with the appearance of a hyperpolarization were recorded in neurons of the creatine-treated group. Consistently, CA1 neurons of creatine exposed pups exhibited a higher maximum firing frequency than controls.In summary, we found that creatine supplementation during pregnancy positively affects morphological and electrophysiological development of CA1 neurons in offspring rats, increasing neuronal excitability. Altogether, these findings emphasize the need to evaluate the benefits and the safety of maternal intake of creatine in humans.

Creatine and creatinine contents in different diet types for dogs - effects of source and processing.

The concentrations of creatine and its degradation product creatinine were determined in a variety of unprocessed as well as processed feedstuffs suitable for dogs. Unprocessed feedstuffs were categorised as single feedstuffs, bone and raw food diets (BARF), and small vertebrates, for example prey animals. Processed feedstuffs were categorised as meat/meat and bone meals, complete wet diets and complete dry diets. The feedstuffs were chosen to cover a broad range of each of the three defined processed and unprocessed feed categories available on the market without further subclustering. The creatine content of the samples was compared on a dry matter, protein and energy basis. The relation of creatine to crude protein permitted a rating of the meat quality in terms of muscle tissue. We found no difference in creatine concentrations between the three categories of unprocessed feedstuffs (raw single feedstuffs, prey and BARF diets), neither on a dry matter basis nor when expressed relative to crude protein and metabolisable energy respectively. Significantly lower levels were determined in meat/meat and bone meal and commercial dry diets (e.g. 303 mg creatine/MJ ME in unprocessed vs. 6 mg/MJ ME in processed feedstuffs; p < 0.001). We conclude that in relation to ME, the exclusive use of conventionally processed diets for dogs, especially dry diets, leads to considerably lower intake of creatine which is a natural compound of the diet of this carnivorous and omnivorous species.

The influence of maternal dietary creatine intake on placental nutrient transfer in the spiny mouse

The influence of maternal dietary creatine intake on placental nutrient transfer in the spiny mouse

Creatine is a scavenger for methylglyoxal under physiological conditions via formation of N-(4-methyl-5-oxo-1-imidazolin-2-yl)sarcosine (MG-HCr).

Following incubation of methylglyoxal and creatine under physiological conditions, N-(4-methyl-5-oxo-1-imidazolin-2-yl)sarcosine (MG-HCr) was isolated and identified by NMR and mass spectrometry. Due to its rapid formation, MG-HCr represents a specific product following "scavenging" of methylglyoxal by creatine. Using hydrophilic interaction chromatography coupled to mass spectrometry, MG-HCr was analyzed in urine samples of healthy volunteers. Daily MG-HCr excretion of nonvegetarians ranged from 0.35 to 3.84 μmol/24 h urine (median: 0.90 μmol/24 h urine) and of vegetarians from 0.11 to 0.31 μmol/24 h urine (median: 0.19 μmol/24 h urine), indicating that formation of MG-HCr in vivo is influenced by the dietary intake of creatine. The trapping of methylglyoxal by creatine may delay the formation of advanced glycation compounds in vivo and, therefore, could be of special importance in situations in which the body has to deal with pathophysiologically increased amounts of dicarbonyl compounds ("carbonyl stress"), for instance in diabetic patients.

Creatine and guanidinoacetate content of human milk and infant formulas: implications for creatine deficiency syndromes and amino acid metabolism

Creatine is essential for normal neural development; children with inborn errors of creatine synthesis or transport exhibit neurological symptoms such as mental retardation, speech delay and epilepsy. Creatine accretion may occur through dietary intake or de novo creatine synthesis. The objective of the present study was to determine how much creatine an infant must synthesise de novo. We have calculated how much creatine an infant needs to account for urinary creatinine excretion (creatine's breakdown product) and new muscle lay-down. To measure an infant's dietary creatine intake, we measured creatine in mother's milk and in various commercially available infant formulas. Knowing the amount of milk/formula ingested, we calculated the amount of creatine ingested. We have found that a breast-fed infant receives about 9 % of the creatine needed in the diet and that infants fed cows' milk-based formula receive up to 36 % of the creatine needed. However, infants fed a soya-based infant formula receive negligible dietary creatine and must rely solely on de novo creatine synthesis. This is the first time that it has been shown that neonatal creatine accretion is largely due to de novo synthesis and not through dietary intake of creatine. This has important implications both for infants suffering from creatine deficiency syndromes and for neonatal amino acid metabolism.

Disturbed energy metabolism and muscular dystrophy caused by pure creatine deficiency are reversible by creatine intake

Creatine (Cr) plays an important role in muscle energy homeostasis by its participation in the ATP-phosphocreatine phosphoryl exchange reaction mediated by creatine kinase. Given that the consequences of Cr depletion are incompletely understood, we assessed the morphological, metabolic and functional consequences of systemic depletion on skeletal muscle in a mouse model with deficiency of l-arginine:glycine amidinotransferase (AGAT(-/-)), which catalyses the first step of Cr biosynthesis. In vivo magnetic resonance spectroscopy showed a near-complete absence of Cr and phosphocreatine in resting hindlimb muscle of AGAT(-/-) mice. Compared with wild-type, the inorganic phosphate/β-ATP ratio was increased fourfold, while ATP levels were reduced by nearly half. Activities of proton-pumping respiratory chain enzymes were reduced, whereas F(1)F(0)-ATPase activity and overall mitochondrial content were increased. The Cr-deficient AGAT(-/-) mice had a reduced grip strength and suffered from severe muscle atrophy. Electron microscopy revealed increased amounts of intramyocellular lipid droplets and crystal formation within mitochondria of AGAT(-/-) muscle fibres. Ischaemia resulted in exacerbation of the decrease of pH and increased glycolytic ATP synthesis. Oral Cr administration led to rapid accumulation in skeletal muscle (faster than in brain) and reversed all the muscle abnormalities, revealing that the condition of the AGAT(-/-) mice can be switched between Cr deficient and normal simply by dietary manipulation. Systemic creatine depletion results in mitochondrial dysfunction and intracellular energy deficiency, as well as structural and physiological abnormalities. The consequences of AGAT deficiency are more pronounced than those of muscle-specific creatine kinase deficiency, which suggests a multifaceted involvement of creatine in muscle energy homeostasis in addition to its role in the phosphocreatine-creatine kinase system.

The effects of supplementation of creatine on total homocysteine

Background Small increases in homocysteine are associated with increased risk for cardiovascular events patients with end-stage renal disease (ESRD). Endogenous creatine intake may decrease homocysteine via negative feedback inhibition, as creatine is a by-product of methionine and homocysteine metabolism. Therefore, this study was conducted to examine whether oral supplementation of creatine would affect levels of plasma homocysteine in ESRD patients. Methods: 16 ESRD patients with hyperhomocysteinemia completed the study. Patients supplemented 5 g/day of creatine monohydrate for 30 days. Results: Homocysteine levels significantly increased (t=-2.315, p=0.035) in ESRD patients (pre-test 18.9±14.0 mg/dlitre, 139.80±103.56 μmol/litre; post-test 28.8±11.2 mg/dlitre, 213.03±82.85 μmol/litre). Conclusions: The current study suggests that ingestion of 5 g/day of creatine monohydrate in ESRD patients results in an increase in homocysteine. Combined with previous studies it appears that dosages ≥ 5 g/day of creatine increase homocysteine in patients with decreased renal function.

The behavioral actions of creatine vary with duration of intake

Dietary creatine has been promoted for its positive health effects, and is best known for its use by athletes to boost physical performance. Creatine also has protective effects on the brain in models of neuronal damage, and improves cognitive performance on stressful tasks. However, there is little research examining how soon behavioral effects are seen after supplementation with creatine. To further explore the behavioral actions of creatine in rats, we used the forced‐swim test (FST) as a stressor, and assessed anxiety‐like behavior using the Elevated Plus Maze (EPM), and spatial learning using the Morris Water Maze (MWM). Female rats were fed chow alone or chow mixed with 4% w/w creatine for 1, 3, or 5 wks prior to the FST. Rats were tested in the EPM 24h after the FST and in the MWM 48h after the FST. There were no differences in any measures after 1 wk of creatine. At 3 wks, rats given creatine showed improved performance on the MWM relative to controls, but tended to show more anxiety‐like behavior in the EPM. At 5 wks, rats given creatine showed worse performance on the MWM and more anxiety‐like behavior in the EPM relative to controls. These findings indicate that there are time‐related differences in the behavioral effects of creatine supplementation, and suggest that continuous chronic intake of creatine may not be the most advantageous use of the supplement. Supported by internal research funds from Tufts University.

Relationship of Creatinine and Nutrition with Arsenic Metabolism

Basu et al. (2011) reported the associations of both dietary and blood nutrient measures, as well as urinary creatinine (uCr), with arsenic (As) methylation capacity, as assessed by the proportions of urinary inorganic, monomethyl, and dimethyl As metabolites. One finding was that uCr was the strongest predictor of As methylation; participants with higher uCr concentrations had a higher percentage of total urinary As as dimethylarsinic acid (DMA) compared to those with lower uCr. This is consistent with what we have previously reported in Bangladeshi adults and children (Gamble et al. 2005; Ahsan et al. 2007; Hall et al. 2009), and is an interesting and potentially very important observation. Approximately 40% of S-adenosylmethionine (SAM)-derived methyl groups are devoted to the biosynthesis of creatine, the precursor of creatinine (Brosnan et al. 2011; Mudd and Poole 1975). At high levels of As exposure (500–1,000 µg/L), based on one-carbon kinetics (Schalinske and Steele 1989), we estimated that methylation of 80% of a daily dose of inorganic As (InAs) to DMA would require approximately 50 µmol SAM, thus consuming approximately 2–4% of the SAM normally turning over in a well-nourished adult per day. Low dietary creatine intake associated with low-protein or vegetarian diets places an increased demand for SAM for creatine biosynthesis (Brosnan 2011). This could potentially reduce the availability of SAM for As methylation, providing a plausible mechanism underlying this highly reproducible observation. This assumes that uCr reflects, to some extent, dietary creatine intake, as we have observed (Gamble M, unpublished data). Conversely, dietary creatine intake and/or creatine supplementation down-regulates endogenous creatine biosynthesis, potentially sparing SAM for methylation of other substrates such as As. We are currently testing this hypothesis in a randomized controlled trial of creatine supplementation. In addition, as Basu et al. (2011) noted, and as we have previously reported (Gamble and Liu 2005), one implication of the observed association between uCr and As methylation capacity is that urinary As should not be expressed per gram creatinine to correct for urine concentration. Rather, uCr should be included as a covariate in regression models. One concerning aspect of the study by Basu et al. (2011) is the handling of blood samples used for nutrient measurements. As noted by Basu et al. and in a previous publication on these same participants (Chung et al. 2006), the blood samples were stored in an ice chest in the field for up to 24 hr before processing. This 24-hr delay can be problematic for some nutrients, especially folate, which is extremely sensitive to oxidative degradation (Drammeh et al. 2008). Basu et al. (2011) reported that in univariate analyses, they observed higher urinary percentages of InAs in individuals with higher serum folate concentrations. This finding is contrary to our previous findings that folate facilitates As methylation (Gamble et al. 2005, 2006, 2007; Hall et al. 2007, 2009). This discrepancy might be explained by differences in sample processing. Basu et al. (2011) also reported associations between dietary intake of several nutrients (assessed using a modified 24-hr recall) and As methylation capacity. One of the most critical and widely discussed issues in nutritional epidemiology is the method used to adjust for total energy intake (TEI) (Willett et al. 1997). The main reasons to adjust for TEI are to a) adjust for potential confounding by TEI, b) remove extraneous variation in nutrient intakes that is due only to their correlation with TEI, and c) simulate a dietary intervention. What is often most relevant is diet composition, or nutrient intake in relation to TEI (Willett et al. 1997). Several methods are available to adjust for TEI, and the best approach can vary depending on the nutrient and question of interest. Basu et al. (2011) adjusted for TEI by dividing each nutrient intake by TEI (nutrient density method). While this approach is appealing because of its simplicity, in reality it can create a complex variable (Willett and Stampfer 1998). For example, when TEI is related to the outcome of interest, the use of nutrient densities can actually induce confounding in the opposite direction. Although we cannot determine from Basu et al.’s article whether TEI measured by the 24-hr recall was associated with As methylation, in theory, an association seems plausible. Also, because their statistical analysis tested for associations between multiple nutrients and urinary As metabolites, it is best to acknowledge that some of the statistically significant associations might be due to chance alone.

Effects of creatine supplementation on muscle wasting and glucose homeostasis in rats treated with dexamethasone

We aimed to investigate the possible role of creatine (CR) supplementation in counteracting dexamethasone-induced muscle wasting and insulin resistance in rats. Also, we examined whether CR intake would modulate molecular pathways involved in muscle remodeling and insulin signaling. Animals were randomly divided into four groups: (1) dexamethasone (DEX); (2) control pair-fed (CON-PF); (3) dexamethasone plus CR (DEX-CR); and (4) CR pair-fed (CR-PF). Dexamethasone (5 mg/kg/day) and CR (5 g/kg/day) were given via drinking water for 7 days. Plantaris and extensor digitorum longus (EDL) muscles were removed for analysis. Plantaris and EDL muscle mass were significantly reduced in the DEX-CR and DEX groups when compared with the CON-PF and CR-PF groups (P<0.05). Dexamethasone significantly decreased phospho-Ser473-Akt protein levels compared to the CON-PF group (P<0.05) and CR supplementation aggravated this response (P<0.001). Serum glucose was significantly increased in the DEX group when compared with the CON-PF group (DEX 7.8±0.6 vs. CON-PF 5.2±0.5 mmol/l; P<0.05). CR supplementation significantly exacerbated hyperglycemia in the dexamethasone-treated animals (DEX-CR 15.1±2.4 mmol/l; P<0.05 vs. others). Dexamethasone reduced GLUT-4 translocation when compared with the CON-PF and CR-PF (P<0.05) groups and this response was aggravated by CR supplementation (P<0.05 vs. others). In conclusion, supplementation with CR resulted in increased insulin resistance and did not attenuate muscle wasting in rats treated with dexamethasone. Given the contrast with the results of human studies that have shown benefits of CR supplementation on muscle atrophy and insulin sensitivity, we suggest caution when extrapolating this animal data to human subjects.

Creatine supplementation does not impair kidney function in type 2 diabetic patients: a randomized, double-blind, placebo-controlled, clinical trial

Creatine supplementation may have a therapeutic role in diabetes, but it is uncertain whether this supplement is safe for kidney function. The aim of this study was to investigate the effects of creatine supplementation on kidney function in type 2 diabetic patients. A randomized, double-blind, placebo-controlled trial was performed. The patients were randomly allocated to receive either creatine or placebo for 12weeks. All the patients underwent exercise training throughout the trial. Subjects were assessed at baseline and after the intervention. Blood samples and 24-h urine samples were obtained for kidney function assessments. Additionally, (51)Cr-EDTA clearance was performed. To ensure the compliance with creatine intake, we also assessed muscle phosphorylcreatine content. The creatine group presented higher muscle phosphorylcreatine content when compared to placebo group (CR Pre 44±10, Post 70±18mmol/kg/wt; PL Pre 52±13, Post 46±13mmol/kg/wt; p=0.03; estimated difference between means 23.6; 95% confidence interval 1.42-45.8). No significant differences were observed for (51)Cr-EDTA clearance (CR Pre 90.4±16.9, Post 96.1±15.0mL/min/1.73m(2); PL Pre 97.9±21.6, Post 96.4±26.8mL/min/1.73m(2); p=0.58; estimated difference between means -0.3; 95% confidence interval -24.9 to 24.2). Creatinine clearance, serum and urinary urea, electrolytes, proteinuria, and albuminuria were unchanged. CR supplementation does not affect kidney function in type 2 diabetic patients, opening a window of opportunities to explore its promising therapeutic role in this population. ClinicalTrials.gov registration number: NCT00992043.

탄수화물과 크레아틴 섭취가 남성무용수의 운동수행력 및 혈중피로변인에 미치는 영향

탄수화물과 크레아틴 섭취가 남성무용수의 운동수행력 및 혈중피로변인에 미치는 영향