Additional Clinical Studies

Professional Commentary. Ribose: An Additive for Caffeine

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Does caffeine offer a health hazard or a performance benefit? This debate rages even though caffeine continues to be one of the most commonly consumed ingredients in beverages. Approximately 90 % of people in the United States consume caffeine daily.1 Caffeine, which takes hours to be completely eliminated from our body, is found in coffee, tea, and increasingly in energy beverages, most often combined with a sugar. The increasing consumption of energy beverages is primarily due to its promoted “energy” benefit, providing a perceived edge to our stressful daily pace. In reality, we know that caffeine does not produce energy, but acts as a stimulant.

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Bioenergy Ribose & Caffeine

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There seems to be a logical synergy for combining ribose and reasonable doses of caffeine. Caffeine has been proven to decreased fatigue, increased alertness and elevated mood while ribose helps make the energy and higher sport performance. As a result, combination of caffeine and ribose should show combination of these effects and possibly improved cognitive and mental health.

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Effect of D-Ribose on Insulin and Blood Glucose: A Chronological Examination (2003)

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Summary

The effect of D-ribose (ribose) on insulin secretion and plasma glucose has been investigated since 1957, when the effect of insulin on the transport of various sugars, including ribose, across cell membranes was first studied. Over the decades, research has consistently shown that oral or intravenous ribose administration produces a transient, asymptomatic, and dose dependant decrease in plasma blood glucose to a nadir that is reached 30- to 75-minutes post-administration, before returning to baseline levels in approximately 60- to 120-minutes once administration is discontinued. The mechanism of this blood glucose lowering effect has not been fully elucidated, but several have been studied and more than one appear to contribute to the effect. Suggested mechanisms include direct stimulation of insulin secretion by the pancreas, indirect stimulation of insulin secretion by the liver and other tissues, a saturation of carbohydrate receptors in the liver and various tissues affecting insulin release, increased glucose utilization or decreased glucose production resulting from rising levels of blood ribose, and the competition in the liver for the enzyme phosphoglucomutase responsible for glycogen recruitment. Increased glucose utilization does not appear to materially contribute to the mechanism. Instead, the blood glucose lowering effect of ribose appears to result from a combination of factors including indirect stimulation of pancreatic insulin secretion, stimulation of humoral effectors causing secretion of minor, but important, amounts of insulin from tissues in the hepatic-portal pathway, and delayed glucose recruitment in the liver, likely due to competition for phosphoglucomutase activity.

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Purine Salvage to Adenine Nucleotides in Different Skeletal Muscle Fiber Types (J. Appl. Physiol.91: 231-238, 2001)

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Jeffrey J. Brault and Ronald L. Terjung.

Physiology. College of Medicine Biomedical Sciences, College of Veterinary Medicine, and Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211

The rates of purine salvage of adenine and hypoxanthine into the adenine nucleotide (AdN) pool of the different skeletal muscle phenotype sections of the rat were measured using an isolated perfused hindlimb preparation. Tissue adenine and hypoxanthine concentrations and specific activities were controlled over a broad range of purine concentrations, ranging from 3-100 fold normal, by employing an isolated rat hindlimb preparation perfused at a high flow rate. Incorporation of H-adenine or 3H-hypoxanthine into the AdN pool was not meaningfully influenced by tissue purine concentration over the range evaluated (-0.10 to 1.6 µmol/g). Purine salvage rates were greater (p<0.05) for adenine (35-55 nmol/h/g), compared to hypoxanthine (20-30 nmol/h/g), and moderately different (p<0.05) among fiber types. The low oxidative fasttwitch white muscle section exhibited relatively low rates of purine salvage that were -65% of the rates in the high-oxidative fast twitch red section of the gastrocnemius.  The soleus muscle, characterized by slowtwitch red fibers, exhibited a high rate of adenine salvage, but a low rate of hypoxanthine salvage. Addition of ribose to the perfusion medium increased salvage of adenine (up to 3-6 fold; p<0.00 1) and hypoxanthine (up to 6-8 fold; p<0.001), depending upon the fiber type, over a range of concentrations up to 10 mM. This is consistent with tissue 5-phosphoribosyl-1-pyrophosphate being rate limiting for purine salvage. Purine salvage is favored over de novo synthesis, as delivery of adenine to the muscle decreased (p<O.OOS) de novo synthesis of AdN. Providing ribose did not alter this preference of purine salvage pathway over de novo synthesis of adenine nucleotides. In the absence of ribose supplementation purine salvage rates are relatively low, especially compared the AdN pool size in skeletal muscle.

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Metabolism of D-Ribose Administered Continuously to Healthy Persons and to Patients with Myoadenylate Deaminase Deficiency (Klinische Wochenschrift, 1989)

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M. Gross, S. Reiter and N. Zollner

Medizinische Poliklinik der Universitat Munchen

Summary. D-ribose was administered orally or intravenously over at least 5 h to eight healthy volunteers and five patients with myoadenylate deaminC~ se deficiency. Intravenous administration rates were 83, 167, and 222 mg/kg/h, which were well tolerated but oral administration of more than 200 mg/kg/h caused diarrhea. The average steady state serum ribose level ranged between 4.8 mg/100 ml (83 mg/kg/h, oral administration) and 81.7 mg/100 ml (222 mg/kg/h, intravenous administration). Serum glucose level decreased during ribose administration. The intestinal absorption rate of orally administered ribose was 87.8%-99.8% or the intake at doses up to 200 mg/kg/h without first pass effect. Urinary losses were 23% of the intravenously administered dose at 222 mg/kg/h. Ribose appeared to be excreted by glomerular filtration without active reabsorption; a renal threshold could not be demonstrated. The amount of ribose transported back from the tubular lumen depended on the serum ribose level. There was no difference in ribose turnover in healthy subjects and patients with MAD deficiency.

D-ribose and xylitol are the only substances known to prevent the symptoms of patients with myoadenylate deaminase (MAD) deficiency. An oral administration of 15-20 g ribose per hour can prevent pain and stiffness of the muscles [33, 34].

In experiments with rats, Zimmer [31] showed that after temporary ischemia the myocardium loses its purine nucleotides; their pool has to be recompleted by purine synthesis de novo. The initial cellular purine concentration is regained after 72 h. If ribose is administered, the restoration of cardiac ATP pool takes only 12 h. These results may become important in the therapy of human coronary infarction or chronic coronary heart disease.

The first experiment with ribose in man were done in 1946 [30] but up to today, no investigations were done with long-lasting administration of ribose in man. These early experiments did not show whether a steady state concentration of serum ribose concentration after administering ribose for several hours is obtained.

A hypoglycemic effect of ribose has repeatedly been described [1, 2, 6-8, 21, 22, 24, 25] after short-term administrations. It is not known whether the hypoglycemia induced by ribose will persist during a continuous administration over several hours -an important question for the therapy of patients with MAD deficiency.

Experiments with human lymphocyte cultures revealed cytotoxic effects of ribose after an incubation in concentrations of 20-50 mmol/1 after 24 h [15, 23, 28, 35]. It is important to know whether such concentrations may be reached during therapy with this sugar.

The aim of the study was the investigation of basic pharmacological data of D-ribose for the treatment of patients with MAD deficiency. The main topics were intestinal resorption and urinary excretion after oral administration, serum ribose concentration after long-term administration, disappearance of ribose from blood, and side-effects including the known hypoglycemic effect.  

 

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