# Yohimbe HCL vs. Aspirin



## the nut (Jun 15, 2006)

Most posts say to use either 5 mg yohimbe hcl or 200 mg aspirin with 25 mg epherdine and 200 mg caffiene. What's the difference between the 2?


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## ag-guys (Jun 15, 2006)

the nut said:
			
		

> Most posts say to use either 5 mg yohimbe hcl or 200 mg aspirin with 25 mg epherdine and 200 mg caffiene. What's the difference between the 2?



Not sure with the aspirin, but Yohimbine is supposed to work on the fat cells in the lower parts (particularly the midsection) of the body to encourage the cells to open....at least I think that is the case.  It's been quite some time since I've looked up the information.

AG
www.ag-guys.com


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## the nut (Jun 15, 2006)

ag-guys said:
			
		

> Not sure with the aspirin, but Yohimbine is supposed to work on the fat cells in the lower parts (particularly the midsection) of the body to encourage the cells to open....at least I think that is the case.  It's been quite some time since I've looked up the information.
> 
> AG
> www.ag-guys.com



That sounds good to me. Ive heard that the aspirin thins out the blood. I didn't know if I should take both or pick one.


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## sawastea (Jun 18, 2006)

Please do not combine yohimbine HCL with ephedrine HCL. 

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The addition of the 2-adrenolytic drug, yohimbine, to caffeine and ephedrine is an attractive support to obesity treatment. However, administration of three drugs influencing the cardiovascular system could have some undesirable effects, especially in obese subjects.

We tried to determine if the supporting pharmacological treatment of obese women composed of ephedrine, caffeine and yohimbine could modify the cardiovascular state at rest and during static (handgrip) or dynamic (cycloergometer) exercise. We found that loss of body mass did not differ between groups receiving only diet and groups with two or three drugs administration together with diet. We supposed that 10 days is too short a time to define real weight loss after treatment. Further study is needed to define the influence of these doses of drugs on metabolic effects and weight loss during a longer period of treatment.

However, the aim of our study was to determine if caffeine and ephedrine used together or these two drugs in combination with yohimbine were safe for the cardiovascular system. Ten days of observation is a sufficient period to detect some cardiovascular reactions. A very low caloric diet is usually associated with a decrease in adrenergic system activity. The aim of ephedrine, caffeine and yohimbine administration was to diminish this phenomenon and to increase the effect of a low caloric diet. We did not observe significant changes in most haemodynamic parameters after 10 days of diet only administration. However, the ejection fraction decreased. It is possible that this drop is one of the symptoms indicating this phenomenon.

We found that the therapy composed of ephedrine (2 25 mg) and caffeine (2 200 mg) did not modify the haemodynamic parameters at rest and during the handgrip exercise. Only during cycloergometer exercise was ejection fraction increased. This fact suggests that the combination of the drugs we used did not exert undesirable effects on the cardiovascular system. The increased in ejection fraction even has a profitable significance. It is also an indirect proof that ephedrine and caffeine in the doses we used could weakly activate the adrenergic system. For this reason the charge in the cardiovascular system in our obese subjects during static or dynamic exercise at the time of ephedrine and caffeine administration was not very large and seemed safe.We observed different reactions of the cardiovascular system when three drugs were used. Application of three drugs produced a depression of the cardiovascular system at rest, which was expressed by a decrease in stroke index and ejection fraction. This was probably the result of diastolic pressure and heart rate increase. In these circumstances, the systole of the heart is less efficient. We could speculate that these effects of yohimbine were due to an increase in noradrenaline concentration in the plasma ( Hedner et al., 1992; Tavernier et al., 1992). If this was the case, noradrenaline could increase the afterload, and thereby cardiac performance would be decreased. This could be an undesirable effect of yohimbine treatment. The same drug regimen during the handgrip test led to a decrease in ejection fraction only. Diastolic pressure, heart rate and ejection fraction tended in a similar direction during the handgrip test, but did not show significant changes between groups. We suppose that activation of the adrenergic system and following cardiovascular system during exercise is much stronger than after pharmacological stimulation. For this reason, the pharmacological influence of drugs is proportionally attenuated.

When cycloergometer exercise was performed, not only ejection fraction, but also cardiac load increased in the group receiving three drugs. The last effect was not observed during the handgrip test. However, cycloergometer exercise and handgrip are quite different types of effort. During dynamic exercise, heart rate reached higher values than during the handgrip test. Systolic pressure was inversely higher during the handgrip test. It could be speculated that, during the handgrip test, -activation predominated but during the cycloergometer exercise -activation predominated. End-diastolic index observed during dynamic exercise reached greater values than during the handgrip test. Central translocation of blood volume from the lower part of the body during exercise on the cycloergometer could have cardinal meaning. This centralization of circulation was probably in part due to the work of the leg muscles. Stroke index during cycloergometer exercise was also greater than during the handgrip test. Increased volume of heart and circulating blood, augmented heart rate together with the influence of the three drugs evoked an increase in cardiac load. The influence of yohimbine in these circumstances is very important, because we did not observe an increase in cardiac load when only two drugs were administered. This fact has significant clinical implications, because it suggests that yohimbine evokes some dangerous changes in the cardiovascular system. For this reason, this drug could only be used in some persons with caution.

Our results indicate that the pharmacological support of a low caloric diet by ephedrine and caffeine during obesity treatment induces only minimal changes in the cardiovascular system, but the addition of yohimbine to this regimen may lessen the cardiac performance at rest and during the handgrip test. Using three drugs during the cycloergometer exercise leads to an increase in cardiac work. Therefore, these findings demonstrate that chronic administration of ephedrine and caffeine has no undesirable effects on cardiovascular state in obese patients. The addition of yohimbine should be treated with caution and must be excluded in particular obese individuals with cardiovascular complications.


Waluga M, Janusz M, Karpel E, Hartleb M, Nowak A. Cardiovascular effects of ephedrine, caffeine and yohimbine measured by thoracic electrical bioimpedance in obese women. Clin Physiol. 1998 Jan;18(1):69-76





Int J Mol Med. 2001 Jul;8(1):103-9. Related Articles, Links


Divergent effects of an alpha2-adrenergic antagonist on lipolysis and thermogenesis: interactions with a beta3-adrenergic agonist in rats.

Gomez-Ambrosi J, Fruhbeck G, Aguado M, Milagro FI, Margareto J, Martinez AJ.

Department of Physiology and Nutrition, University of Navarra, 31008 Pamplona, Spain.

This study was undertaken in order to test the hypothesis that selective beta3-AR stimulation and simultaneous blockade of alpha2-AR would result in an increase of lipolysis and thermogenesis in rats. Incubation of isolated white adipocytes with the alpha2-AR antagonist yohimbine produced a concentration-dependent increase in glycerol release (P<0.001) for all assayed concentrations (10-12-10-6 M) and potentiated the lipolytic effect of the beta3-AR agonist Trecadrine. However, in vivo administration of yohimbine produced a marked decrease in body temperature (1.3-1.5 degrees C, P<0.001) and blocked the thermogenic effect of Trecadrine when simultaneously administered. A similar response was observed for whole body oxygen consumption. Furthermore, yohimbine did not modify brown adipose tissue oxygen consumption, but blocked the beta3-AR-mediated increase triggered by Trecadrine. Brown adipose tissue UCP-2 and -3 mRNA expression was not changed by yohimbine. In conclusion, the present work indicates that in vitro alpha2-AR blockade by yohimbine potentiates the beta3-AR-mediated stimulation of lipolysis. On the other hand, in vivo alpha2-AR antagonism blocks the thermogenic effects mediated by beta3-AR stimulation, suggesting a possible interplay between the receptors.



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As for aspirin:



This is from an article written by Stephen Schmitz, MD, MPH and Bruce Kneller, BSN-RN.

Aspirin

"Aspirin {salicyclic acid acetate} and it's naturally occurring methyl ester (methyl salicylate)-- found in the leaves of Gaultheria procumbrens and on the bark of Betula lenta-- have long been used as analgesics, anti-inflammatories, antipyretics and recently as anti-coagulants. The "A" portion of ECA, aspirin has been thought of potentiating the thermogenic and lipolytic properties of both ephedrine and caffeine. Recent research seems to contradict this however. At a study at The University of London's Department of Nutrition and Dietetics, 40 women (20 non-obese and 20 obese) were given either ephedrine and caffeine (30 mg and 100 mg) or ephedrine, caffeine and aspirin (30 mg, 100 mg, and 300 mg) post prandially (1050 kJ liquid meal). Using indirect calorimetry, observations were made in all groups every 30 minutes for 160 minutes. There was no significant differences between the groups that received aspirin and the groups that did not. We conclude that aspirin does not potentiate the acute thermic effect of ephedrine and caffeine.6

In another study conducted at King's College in London, it was demonstrated that aspirin does not potentiate the thermogenic response to ephedrine in lean women and only slightly so in obese women.7 The increase seen in this study represented a 1.2 kcal per hour increase in metabolism for lean women and a 2.4 kcal per hour increase in metabolism in obese women over use of ephedrine alone, which over an entire week, would represent less than one ounce of bodyweight. We feel that this is insignificant.7

Based on these two studies, we feel that aspirin and its analogs do not play a substantial role in inducing or increasing thermogenesis and/or lipolysis but they do have the potential to induce SAEs when consumed over long periods of time (e.g. ulceration of the stomach and increases in bleeding times). Therefore, we feel that aspirin and it's analogs should not be used in any thermogenic/lipolytic stack."

6) Horton TJ, Geissler CA. Post-prandial Thermogenesis with Ephedrine, Caffeine and Aspirin in Lean, Predisposed Obese and Non-obese women. Int J Obes Relat Metab Disorder, 1996 Feb;20(2):91-95.
7) Horton TJ, Geissler CA. Aspirin Potentiates the Effect of Ephedrine on the Thermogenic Response to a Meal in Obese but not Lean Women. Int J Obes, 1991 May;15(5):359-366.






Most of the arguements that people make for aspirin state that aspirin extends the thermogenic effects of ephedrine by inhibiting the enzyme cyclooxygenase and therefore decreasing prostaglandin synthesis (why aspirin is an anti-inflammatory). This helps combat one of ephedrine's effects. Ephedrine stimulates the release of norepinephrine, which stimulates the release of adenosine and the synthesis of prostaglandins by the activated tissue. Since aspirin inhibits the synthesis of prostaglandins (1), it is believed it enhances the effect of norepinephrine (the reason why caffeine is included in the stack to combat adenosine). By increasing the amount of norepinephrine one would expect to increase lipolysis. Caffeine achieves this, however in actual studies aspirin as yet to prove the same. One can only hypothesize on why aspirin's effect on prostaglandins does not effect lipolysis.


There have been no studies that I am aware of that show that an ECA stack is more effective than an EC stack. The only studies that have been proven to work are when an ECA stack has been done in a study against a placebo. Couple this information with the effects aspirin has on the stomach (nausea, heartburn, and sometimes bleeding ulcers) one could conclude that the most effective stack would be just Ephedrine and Caffeine.

1. Rawson ES, Clarkson PA. Ephedrine as an ergogenic aid. Performance-enhancing Substances in Sport and Exercise. Ed Bahrke MS, Yesalis CE. Human Kinetics. 2002.


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