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Nathan Goodyear

http://ajcn.nutrition.org/content/76/5/1151S.full.pdf - 0 views

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    Great review article on SAMe.
Nathan Goodyear

JISSN | Full text | International Society of Sports Nutrition position stand: creatine ... - 0 views

  • the energy supplied to rephosphorylate adenosine diphosphate (ADP) to adenosine triphosphate (ATP) during and following intense exercise is largely dependent on the amount of phosphocreatine (PCr) stored in the muscle
  • Creatine is chemically known as a non-protein nitrogen
  • It is synthesized in the liver and pancreas from the amino acids arginine, glycine, and methionine
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  • Approximately 95% of the body's creatine is stored in skeletal muscle
  • About two thirds of the creatine found in skeletal muscle is stored as phosphocreatine (PCr) while the remaining amount of creatine is stored as free creatine
  • The body breaks down about 1 – 2% of the creatine pool per day (about 1–2 grams/day) into creatinine in the skeletal muscle
  • The magnitude of the increase in skeletal muscle creatine content is important because studies have reported performance changes to be correlated to this increase
  • "loading" protocol. This protocol is characterized by ingesting approximately 0.3 grams/kg/day of CM for 5 – 7 days (e.g., ≃5 grams taken four times per day) and 3–5 grams/day thereafter [18,22]. Research has shown a 10–40% increase in muscle creatine and PCr stores using this protocol
  • Additional research has reported that the loading protocol may only need to be 2–3 days in length to be beneficial, particularly if the ingestion coincides with protein and/or carbohydrate
  • A few studies have reported protocols with no loading period to be sufficient for increasing muscle creatine (3 g/d for 28 days)
  • Cycling protocols involve the consumption of "loading" doses for 3–5 days every 3 to 4 weeks
  • Most of these forms of creatine have been reported to be no better than traditional CM in terms of increasing strength or performance
  • Recent studies do suggest, however, that adding β-alanine to CM may produce greater effects than CM alone
  • These investigations indicate that the combination may have greater effects on strength, lean mass, and body fat percentage; in addition to delaying neuromuscular fatigue
  • creatine phosphate has been reported to be as effective as CM at improving LBM and strength
  • Green et al. [24] reported that adding 93 g of carbohydrate to 5 g of CM increased total muscle creatine by 60%
  • Steenge et al. [23] reported that adding 47 g of carbohydrate and 50 g of protein to CM was as effective at promoting muscle retention of creatine as adding 96 g of carbohydrate.
  • It appears that combining CM with carbohydrate or carbohydrate and protein produces optimal results
  • Studies suggest that increasing skeletal muscle creatine uptake may enhance the benefits of training
  • Nearly 70% of these studies have reported a significant improvement in exercise capacity,
  • Long-term CM supplementation appears to enhance the overall quality of training, leading to 5 to 15% greater gains in strength and performance
  • Nearly all studies indicate that "proper" CM supplementation increases body mass by about 1 to 2 kg in the first week of loading
  • short-term adaptations reported from CM supplementation include increased cycling power, total work performed on the bench press and jump squat, as well as improved sport performance in sprinting, swimming, and soccer
  • Long-term adaptations when combining CM supplementation with training include increased muscle creatine and PCr content, lean body mass, strength, sprint performance, power, rate of force development, and muscle diameter
  • subjects taking CM typically gain about twice as much body mass and/or fat free mass (i.e., an extra 2 to 4 pounds of muscle mass during 4 to 12 weeks of training) than subjects taking a placebo
  • The gains in muscle mass appear to be a result of an improved ability to perform high-intensity exercise via increased PCr availability and enhanced ATP synthesis, thereby enabling an athlete to train harder
  • there is no evidence to support the notion that normal creatine intakes (< 25 g/d) in healthy adults cause renal dysfunction
  • no long-term side effects have been observed in athletes (up to 5 years),
  • One cohort of patients taking 1.5 – 3 grams/day of CM has been monitored since 1981 with no significant side effects
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    Nice review of the data, up to the publication date, on creatine.
Nathan Goodyear

Is administrating branched-chain amino acid-enriched nutrition achieved symptom-free in... - 0 views

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    BCAA improve NH3 metabolism.  This is via muscle metabolism as reported in other studies.  This study highlighted the differences in BCAA supplementation.  One caveat is that high glutamine is the result from glutamate and this can increase hepatic encephalopathy.
Nathan Goodyear

Nutrition & Metabolism | Full text | Utilization of dietary glucose in the metabolic sy... - 0 views

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    Good review of the impact of a High Fat diet (HFD) and glucose dysregulation.
Nathan Goodyear

Caloric restriction modulates Mcl-1 expression and sensitizes lymphomas to BH3 mimetic ... - 0 views

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    Calorie restriction aids fight against cancer on several fronts.  Granted this is a mouse study, but Cancer should be attacked through nutrition just as through surgery and chemo/radiation.
Nathan Goodyear

Nutrition Journal | Full text | The emerging role of dietary fructose in obesity and co... - 0 views

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    Article links Fructose, to obesity and cognitive decline.
Nathan Goodyear

Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the met... - 0 views

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    Fructose implicated in just about every chronic disease of aging through obesity.
Nathan Goodyear

Cambridge Journals Online - British Journal of Nutrition - Abstract - Post-exercise whe... - 0 views

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    Whey protein hydrolysate shown to be superior to amino acids in recovery phase of exercise.  
Nathan Goodyear

Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslip... - 0 views

  • For thousands of years humans consumed fructose amounting to 16–20 grams per day
  • daily consumptions amounting to 85–100 grams of fructose per day
  • Of key importance is the ability of fructose to by-pass the main regulatory step of glycolysis, the conversion of glucose-6-phosphate to fructose 1,6-bisphosphate, controlled by phosphofructokinase
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  • Thus, while glucose metabolism is negatively regulated by phosphofructokinase, fructose can continuously enter the glycolytic pathway. Therefore, fructose can uncontrollably produce glucose, glycogen, lactate, and pyruvate, providing both the glycerol and acyl portions of acyl-glycerol molecules. These particular substrates, and the resultant excess energy flux due to unregulated fructose metabolism, will promote the over-production of TG (reviewed in [53]).
  • Glycemic excursions and insulin responses were reduced by 66% and 65%, respectively, in the fructose-consuming subjects
  • reduction in circulating leptin both in the short and long-term as well as a 30% reduction in ghrelin (an orexigenic gastroenteric hormone) in the fructose group compared to the glucose group.
  • A prolonged elevation of TG was also seen in the high fructose subjects
  • Both fat and fructose consumption usually results in low leptin concentrations which, in turn, leads to overeating in populations consuming energy from these particular macronutrients
  • Chronic fructose consumption reduces adiponectin responses, contributing to insulin resistance
  • A definite relationship has also been found between metabolic syndrome and hyperhomocysteinemia
  • the liver takes up dietary fructose rapidly where it can be converted to glycerol-3-phosphate. This substrate favours esterification of unbound FFA to form the TG
  • Fructose stimulates TG production, but impairs removal, creating the known dyslipidemic profile
  • the effects of fructose in promoting TG synthesis are independent of insulinemia
  • Although fructose does not appear to acutely increase insulin levels, chronic exposure seems to indirectly cause hyperinsulinemia and obesity through other mechanisms. One proposed mechanism involves GLUT5
  • If FFA are not removed from tissues, as occurs in fructose fed insulin resistant models, there is an increased energy and FFA flux that leads to the increased secretion of TG
  • In these scenarios, where there is excess hepatic fatty acid uptake, synthesis and secretion, 'input' of fats in the liver exceed 'outputs', and hepatic steatosis occurs
  • Carbohydrate induced hypertriglycerolemia results from a combination of both TG overproduction, and inadequate TG clearance
  • fructose-induced metabolic dyslipidemia is usually accompanied by whole body insulin resistance [100] and reduced hepatic insulin sensitivity
  • Excess VLDL secretion has been shown to deliver increased fatty acids and TG to muscle and other tissues, further inducing insulin resistance
  • the metabolic effects of fructose occur through rapid utilization in the liver due to the bypassing of the regulatory phosphofructokinase step in glycolysis. This in turn causes activation of pyruvate dehydrogenase, and subsequent modifications favoring esterification of fatty acids, again leading to increased VLDL secretion
  • High fructose diets can have a hypertriglyceridemic and pro-oxidant effect
  • Oxidative stress has often been implicated in the pathology of insulin resistance induced by fructose feeding
  • Administration of alpha-lipoic acid (LA) has been shown to prevent these changes, and improve insulin sensitivity
  • LA treatment also prevents several deleterious effects of fructose feeding: the increases in cholesterol, TG, activity of lipogenic enzymes, and VLDL secretion
  • Fructose has also been implicated in reducing PPARα levels
  • PPARα is a ligand activated nuclear hormone receptor that is responsible for inducing mitochondrial and peroxisomal β-oxidation
  • decreased PPARα expression can result in reduced oxidation, leading to cellular lipid accumulation
  • fructose diets altered the structure and function of VLDL particles causing and increase in the TG: protein ratio
  • LDL particle size has been found to be inversely related to TG concentration
  • therefore the higher TG results in a smaller, denser, more atherogenic LDL particle, which contributes to the morbidity of the metabolic disorders associated with insulin resistance
  • High fructose, which stimulates VLDL secretion, may initiate the cycle that results in metabolic syndrome long before type 2 diabetes and obesity develop
  • A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, disturbs normal hepatic carbohydrate metabolism leading to two major consequences (Figure 2): perturbations in glucose metabolism and glucose uptake pathways, and a significantly enhanced rate of de novo lipogenesis and TG synthesis, driven by the high flux of glycerol and acyl portions of TG molecules coming from fructose catabolism
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    Fructose and metabolic syndrome.  Good discussion of the impact of high fructose intake and metabolic dysfunction.  This study also does a great job of highlighting the historical change of fructose intake.
Nathan Goodyear

Nutrition Journal | Abstract | A daily glass of red wine associated with lifestyle chan... - 0 views

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    lifestyle changes, including red wine, shown to improve lipids.
Nathan Goodyear

Nutrition Journal | Full text | A daily glass of red wine associated with lifestyle cha... - 0 views

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    tools for health are all around us.  red wine reduced the LDL/HDL ratio by 13% in patients with carotid arteriosclerosis.  This occurred  independently from dietary changes and exercise.
Nathan Goodyear

Cambridge Journals Online - Proceedings of the Nutrition Society - Fulltext -... - 0 views

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    Peripheral 11Beta-HSD1 plays critical role in fat metabolism and energy utilization.  Good discussion on the role that extra-adrenal 11Beta-HSD1 plays in metabolism
Nathan Goodyear

Association of fructose consumption and components... [Nutrition. 2014] - PubMed - NCBI - 0 views

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    Fructose intake associate with increased fasting blood sugar, elevated triglycerides, and elevated systolic blood pressure--all parameters of metabolic syndrome.
Nathan Goodyear

Use of amino acids as growth hormone-relea... [Nutrition. 2002 Jul-Aug] - PubMed - NCBI - 0 views

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    Study finds that amino acid supplementation does not increase GH release.
Nathan Goodyear

Nutrition & Diabetes - Evidence for metabolic endotoxemia in obese and diabetic Gambian... - 0 views

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    altered gut microbiota lead to systemic inflammation, obesity and diabetes.
Nathan Goodyear

A High-Protein Breakfast Induces Greater Insulin and Glucose-Dependent Insulinotropic P... - 0 views

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    Study finds a high protein breakfast blunts and better controls glucose levels throughout the day when compared to a high carbohydrate breakfast.  The impact was seen, not just following breakfast, but at the following meal as well.
Nathan Goodyear

Polyphenols: food sources and bioavailability - 0 views

  • Fruit and beverages such as tea and red wine constitute the main sources of polyphenols
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    polyphenols
Nathan Goodyear

Exercise and the brain: something to chew on - 0 views

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    The absolute best way to promote neurogenesis is through exercise.  This is through an increase in BDNF.  There are ways to augment this: curcumin, n-3, nutrition...  The concept that the brain doesn't heal is out the window.
Nathan Goodyear

Saturated fat, carbohydrate, and cardiovascular disease - 0 views

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    simple sugars, not saturated fats linke to increased CVD.
Nathan Goodyear

Metabolic Effects of Dietary Fiber Consumption and Prevention of Diabetes - 0 views

  • DF are highly complex substances that can be described as any nondigestible carbohydrates and lignins not degraded in the upper gut
  • Commonly, DF are classified according to their solubility in water, even though grading according to viscosity, gel-forming capabilities, or fermentation rate by the gut microbiota might be physiologically more relevant
  • Main sources of soluble DF are fruits and vegetables
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  • n increased intake of total DF was inversely associated with markers of insulin resistance in several studies
  • consumption of insoluble DF increased whole body glucose disposal independent of changes in body weight in both short-term and more prolonged studies
  • Short-chain fatty acids (SCFA) such as acetate, propionate, and butyrate are produced by bacterial fermentation of indigestible DF polysaccharides in the colon
  • increased production of SCFA is assumed to be beneficial by reducing hepatic glucose output and improving lipid homeostasis
  • a high DF diet (oligofructose) reduced gram-negative bacterial content and body weight, whereas a high fat diet increased the proportion of a gram-negative bacterial lipopolysaccharides (LPS) containing microbiota in humans
  • Prospective cohort studies indicate that diets high in insoluble cereal DF and whole grains might reduce diabetes risk
  • soluble DF (i.e., pectin, inulin, and β-glucans)
  • cereal DF (i.e., cellulose and hemicelluloses)
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    Good discussion of dietary fiber intake and Diabetes.  
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