SHE zei:
vorruit dan maar weer; al ga ik pas op BC reageren als ik meer tijd heb, want ik moet helaas ook nog werken enzo tussendoor.
Gebleken is(J.L. Zenk, M.D., Internal Medicine pub. 2002
Certified American Board of Internal Medicine, red. ) dat 20 mg efedrine ongeveer 12 extra calorieën verbrandt in een periode van 3 uur. (die hoeveelheid calorieën verbrand je zelfs wanneer je een kop koffie neemt) Daar bovenop is minimaal 75% van het gewichtsverlies door efedrine een direct resultaat van de onderdrukking van de eetlust. Dat is werkelijk de slechtste manier om gewicht te verliezen, het remt de stofwisseling enorm.
Los daarvan zijn zulke temperatuursstijgingen echt niet bevordelijk voor je lichamelijke gezondheid.
( zie RIVM Nederland voor recente onderzoeksresultaten )
Bovendien heeft dit goedje geen blijvend effect.
Int J Obes Relat Metab Disord. 1993 Feb;17 Suppl 1:S69-72. Related Articles, Links
Safety and efficacy of long-term treatment with ephedrine, caffeine and an ephedrine/caffeine mixture.
Toubro S, Astrup AV, Breum L, Quaade F.
Research Department of Human Nutrition, Royal Veterinary and Agricultural University, Fredriksberg, Copenhagen, Denmark.
In a randomized, placebo-controlled, double blind study, 180 obese patients were treated by diet (4.2 MJ/day) and either an ephedrine/caffeine combination (20mg/200mg), ephedrine (20mg), caffeine (200mg) or placebo 3 times a day for 24 weeks. 141 patients completed this part of the study. All medication was stopped between week 24-26 in order to catch any withdrawal symptoms. From week 26 to 50, 99 patients completed treatment with the ephedrine/caffeine compound in an open trial design, resulting in a statistically significant (p = 0.02) weight loss of 1.1kg. In another randomized, double-blind, placebo-controlled 8 week study on obese subjects we found the mentioned compound showed lean body mass conserving properties. We conclude that the ephedrine/caffeine combination is effective in improving and maintaining weight loss, further it has lean body mass saving properties. The side effects are minor and transient and no withdrawal symptoms have been found.
Int J Obes Relat Metab Disord. 1993 Feb;17 Suppl 1:S41-3. Related Articles, Links
Thermogenic, metabolic, and cardiovascular responses to ephedrine and caffeine in man.
Astrup A, Toubro S.
Research Department of Human Nutrition, Royal Veterinary and Agricultural University, Copenhagen, Denmark.
To develop an appropriate combination of ephedrine and caffeine consisting of clinically relevant doses, we examined the acute thermogenic, metabolic, and cardiovascular effects of different doses of caffeine (C) and ephedrine (E) given separately and in combination to normal subjects. The thermogenic effect after E+C (20 mg/200mg) was larger than that of any other combinations, and E and C exerted a supra-additive synergism on thermogenesis and systolic blood pressure, while being without effect on diastolic blood pressure. The combination also had pronounced effects on glucose metabolism by increasing plasma glucose, insulin and C-peptide concentrations. During chronic treatment the effect of E+C on energy expenditure is maintained, while side effects subside because tolerance develops to its hemodynamic and metabolic effects. During dietary energy restriction E+C promotes fat loss and preserves fat-free mass, which may contribute to its chronic effect on energy balance. In conclusion, the hemodynamic and side effects to E+C are transient during chronic treatment, while the effect on energy expenditure persists. The compound also possesses repartitioning properties, which may be useful in the treatment of obesity.
Int J Obes Relat Metab Disord. 1993 Feb;17 Suppl 1:S73-8. Related Articles, Links
Ephedrine, caffeine and aspirin: safety and efficacy for treatment of human obesity.
Daly PA, Krieger DR, Dulloo AG, Young JB, Landsberg L.
Dept of Medicine, Harvard Medical School, Boston.
The safety and efficacy of a mixture of ephedrine (75-150mg), caffeine (150mg) and aspirin (330mg), in divided premeal doses, were investigated in 24 obese humans (mean BMI 37.0) in a randomized double blind placebo-controlled trial. Energy intake was not restricted. Overall weight loss over 8 weeks was 2.2kg for ECA vs. 0.7 kg for placebo (p < 0.05). 8 of 13 placebo subjects returned 5 months later and received ECA in an unblinded crossover. After 8 weeks, mean weight loss with ECA was 3.2 kg vs 1.3 kg for placebo (p = 0.036). 6 subjects continued on ECA for 7 to 26 months. After 5 months on ECA, average weight loss in 5 of these was 5.2 kg compared to 0.03 kg gained during 5 months between studies with no intervention (p = 0.03). The sixth subject lost 66 kg over 13 months by self-imposed caloric restriction. In all studies, no significant changes in heart rate, blood pressure, blood glucose, insulin, and cholesterol levels, and no differences in the frequency of side effects were found. ECA in these doses is thus well tolerated in otherwise healthy obese subjects, and supports modest, sustained weight loss even without prescribed caloric restriction, and may be more effective in conjunction with restriction of energy intake.
Am J Physiol Endocrinol Metab. 2004 Jan 13 [Epub ahead of print] Related Articles, Links
Epinephrine Stimulates Interleukin-6 (IL-6) Expresssion in Skeletal Muscle and C2C12 Myoblasts: Role of Jun NH2-Terminal Kinase and Histone Deacetylase Activity.
Frost RA, Nystrom GJ, Lang CH.
Departments of Cellular and Molecular Physiology, The Pennsylvania State University College of Medicine, Hershey, PA, USA.
Although an individual's genetic makeup is a major determinant of their muscle mass, other influences, such as hormones, cytokines, nutrition, and exercise can also modulate muscle size. Interleukin-6 is an important inflammatory cytokine. Mice that over-express IL-6 fail to thrive and/or have reduced skeletal muscle mass. The purpose of the present study was to determine whether the stress hormone epinephrine increases inflammatory cytokine expression in skeletal muscle and muscle cells. Infusion of epinephrine in vivo for 2 h increased IL-6 protein (15-fold) and mRNA (40- fold) in skeletal muscle, but not in liver. Epinephrine had a similar effect in C2C12 muscle cells where the hormone increased IL-6 protein and mRNA in a dose- and time-dependent manner. Epinephrine-stimulated IL-6 expression was attenuated by the alpha-adrenergic receptor antagonist phentolamine and completely blocked by either the beta1/2 adrenergic receptor antagonist propranalol or the beta2 antagonist ICI118551. The transcriptional inhibitor DRB and the synthetic glucocorticoid dexamethasone also blocked epinephrine-induced IL-6. SP600125 (a Jun-N-terminal kinase inhibitor) and SB202190 (a p38 MAP kinase inhibitor) completely blocked epinephrine-induced IL-6 synthesis. Endotoxin and epinephrine given together had a synergistic affect on IL-6 mRNA and protein expression. Trichostatin A (a histone deacetylase inhibitor) blocked both endotoxin- and epinephrine- induced IL-6 expression. These data suggest that epinephrine induces IL-6 synthesis in skeletal muscle in vivo and myocytes in vitro. Epinephrine utilizes predominantly B2-adrenergic receptors to stimulate IL-6 synthesis. Endotoxin and epinephrine synergize to increase IL-6 mRNA expression. Optimal IL-6 synthesis may require both stress kinase and histone deacetylase activity.
Adv Exp Med Biol. 2003;543:223-36. Related Articles, Links
Hypoxic regulation of blood flow in humans. Skeletal muscle circulation and the role of epinephrine.
Halliwill JR.
University of Oregon, Eugene 97403-1240, USA.
halliwil@uoregon.edu
Vascular tone represents the balance between local vasodilator mechanisms which attempt to secure adequate blood flow for metabolic demand and neural vasoconstrictor reflexes attempting to maintain arterial pressure. Hypoxia alters vascular tone, shifting this balance in complex ways. Hypoxic vascular responses are not uniform across vascular beds and the mechanisms of hypoxic vasodilation appear to be tissue specific. In healthy humans, skeletal muscle vascular beds exhibit a graded vasodilation in response to hypoxia despite increases in sympathetic vasoconstrictor nerve activity. Previous studies have documented a number of vasodilator substances or systems that appear to be involved in this hypoxic vasodilation. My colleagues and I have conducted studies on the extent to which sympathetic vasoconstriction can mask hypoxic vasodilation, and how sympathetic vasoconstrictor activity interacts with local factors that mediate hypoxic vasodilation in humans. We have focused largely on beta-adrenergic mediated vasodilation, noting that it produces some of its effects via a nitric oxide (NO) pathway. This review will explore the role of epinephrine in generating skeletal muscle vasodilation. How the many factors that determine vascular tone during hypoxic stress impact on the regulation of arterial pressure and how hypoxic vasodilation is altered in several pathophysiological conditions will be discussed.
Int J Obes. 1991 May;15(5):317-26. Related Articles, Links
Peripheral mechanisms of thermogenesis induced by ephedrine and caffeine in brown adipose tissue.
Dulloo AG, Seydoux J, Girardier L.
Centre Medical Universitaire, Department of Physiology, University of Geneva, Switzerland.
The peripheral mechanisms by which ephedrine and caffeine influence thermogenesis were investigated in innervated rat interscapular brown adipose tissue (IBAT) by assessing its rate of oxygen consumption (MO2) in vitro. Dose-response measurements with tissues from intact or sympathectomized (6-OHDA) animals indicate that the thermogenic effects of low concentrations of ephedrine and also of caffeine are entirely dependent upon the presence of intact sympathetic nerve endings, and thus depend on presynaptic mechanisms. Direct postsynaptic stimulation of thermogenesis is only apparent at much higher concentrations, namely greater than 1 microM for ephedrine and greater than 2mM for caffeine. At subminimal concentrations that neither ephedrine nor caffeine influenced basal tissue respiration, they induced a 4-5-fold increase in basal MO2 when administered in combination, a synergistic response prevented by pre-treatment of the rat with 6-OHDA. Synergistic increases in IBAT respiration were also obtained when subminimal concentration of ephedrine was added to 3-propylxanthine (a specific inhibitor of phosphodiesterase), to 8-phenyltheophylline (a potent adenosine receptor antagonist) or to adenosine deaminase (for enzymatic inactivation of endogenous adenosine). Conversely, the marked synergism in thermogenic response with ephedrine + caffeine was reduced in the presence of 2-chloroadenosine (an adenosine analogue). In tissues from fasted rats, the ephedrine + caffeine synergism in thermogenic response, although attenuated, was nevertheless present. These studies therefore demonstrate that ephedrine, at doses comparable with therapeutic use, stimulates thermogenesis in BAT via sympathetically released NA. In addition, a synergistic interaction between caffeine and ephedrine on BAT thermogenesis is explained by ephedrine's enhancement of sympathetic neuronal release of NA, together with caffeine's dual ability to antagonize adenosine and to inhibit cellular phosphodiesterase activity.
Begin maar al te lezen
ze mag de dingen nog wat meer met voor anderen na te zoeken studies onderbouwen, maar ik vind die frisse wind wel leuk 
