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adidas32
(@adidas32)
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Hello,

I just finished my first bottle of Lipoderm-Y and I was happy with the results. BAsed on feedback from friends I have decided to try Ab-Solved. With Lipoderm-Y the labels reads that you should not combine with ephedra. I do not see that same warning on Ab-Solved so I can take ephedra based supplements while using ab-solved?

I was using Lipoderm-Y twice a day. CAn I use Ab-SOvled in the morning and evenings as well?

THANKS!


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Twin Peak
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Yes, to all of that.

And welcome to the board.


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Par Deus
(@par-deus)
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Yes, can take with ephedra.

Yes, use 2X per day, as with LipoDerm

par deus

Juggernaut, bitch!!


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George
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hmm... i am using Lipoderm-Y with both oral E and oral Y however, i think my receptors are fried already as i barely feel 50 mg of ephedra lately (as in single dose).


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nightop
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Posted by: @George
hmm... i am using Lipoderm-Y with both oral E and oral Y   however, i think my receptors are fried already as i barely feel 50 mg of ephedra lately (as in single dose).

E's effectiveness at fat loss has been shown to increase over time for the most part, just because you can't feel its effect anymore is not really an indicator of its efficacy, I believe. This is why it has been recommended to cycle use if one wishes to use it for its stimulant/alertness and pre-workout purposes, and to not cycle if body comp is the goal.

READ MIND & MUSCLE ARTICLES FROM PAST ISSUES.


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ergoman500
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Posted by: @nightop
hmm... i am using Lipoderm-Y with both oral E and oral Y   however, i think my receptors are fried already as i barely feel 50 mg of ephedra lately (as in single dose).

E's effectiveness at fat loss has been shown to increase over time for the most part, just because you can't feel its effect anymore is not really an indicator of its efficacy, I believe. This is why it has been recommended to cycle use if one wishes to use it for its stimulant/alertness and pre-workout purposes, and to not cycle if body comp is the goal.

E has this property only when combined with C or N or Y.
E use all by itself, causes for fat-loss cycled 10 weeks on, followed by 1 week off -- only if it is the only lipolytic agent being used. -- At least in this context, not cycling E use will decrease its effectiveness over time...


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Par Deus
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Do you have a study or mechanism on that??

par deus

Juggernaut, bitch!!


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shpongled
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Posted by: @ergoman500
hmm... i am using Lipoderm-Y with both oral E and oral Y   however, i think my receptors are fried already as i barely feel 50 mg of ephedra lately (as in single dose).

E's effectiveness at fat loss has been shown to increase over time for the most part, just because you can't feel its effect anymore is not really an indicator of its efficacy, I believe. This is why it has been recommended to cycle use if one wishes to use it for its stimulant/alertness and pre-workout purposes, and to not cycle if body comp is the goal.

E has this property only when combined with C or N or Y.
E use all by itself, causes for fat-loss cycled 10 weeks on, followed by 1 week off -- only if it is the only lipolytic agent being used. -- At least in this context, not cycling E use will decrease its effectiveness over time...

The mechanism for long-term fat loss with ephedrine is upregulation of BAT, which isn't dependant on caffeine or anything else.

-David Tolson


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Spook
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The mechanism for long-term fat loss with ephedrine is upregulation of BAT, which isn't dependant on caffeine or anything else.

except humans have allmost no BAT. and BAT induced thermogenesis in humans amounts to about nothing in terms of energy expenditure.

I definantly think cyclic use superior.

Normal Person + Anonymity + Audience = Total Fuckwad.
If you meet the bodybuilding guru on the information super-highway, kill the bodybuilding guru.
trust != truth


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George
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too bad i can't stop. i just can't survive my workouts without E


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shpongled
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Posted by: @Spook
It is well established that  3-adrenoceptor mRNA is expressed in rodent adipocytes and that  3-adrenoceptors play a functional role. The existence and role of  3-adrenoceptors in human adipocytes is more controversial, however. Most,10,11,12,13,14 although not all15,16 workers have detected  3-adrenoceptor mRNA in human adipose tissue, but expression is some 50-fold lower than in rodent adipose tissue13,14 and  3-adrenoceptor transcripts represent less than 20% of total  -adrenoceptor transcripts compared with more than 90% in rodents.12 Studies in transgenic mice indicate that the promoter for the human  3-adrenoceptor drives expression mainly in brown adipose tissue, of which there is relatively little in adult humans.

17Functional evidence for  3-adrenoceptors in white adipocytes was largely based upon the lipolytic activity of CGP-12177, which was believed to be a potent  1/2-adrenoceptor antagonist and a  3-adrenoceptor agonist at somewhat higher concentrations. CGP-12177 has now, however, been shown also to activate a conformation of the  1-adrenoceptor (previously called the  4-adrenoceptor).18,19 The activation of  1-adrenoceptors by CGP-12177 is less sensitive than activation by standard agonists to  1-adrenoceptor antagonists. The pharmacology of the  1-adrenoceptor when stimulated by CGP-12177 therefore resembles that of the  3-adrenoceptor. Nevertheless, there are selective  3-adrenoceptor agonists (SB-226552; SB-251023) which do not activate  1- (or ' 4-') adrenoceptors and which stimulate lipolysis in human white adipocytes.19,20,21 Thus the low levels of  3-adrenoceptor mRNA in human white adipocytes appear to produce sufficient  3-adrenoceptors to mediate functional responses to highly selective  3-adrenoceptor agonists.

In the present study we provide direct evidence for the existence of  3-adrenoceptor protein in white adipocytes from both lean and obese subjects and in brown adipocytes from phaeochromocytoma patients using immunohistochemistry coupled with light microscopy. A previous study demonstrated the selectivity of the antibody that we have used for the human cloned  3-adrenoceptor over  1- and  2-adrenoceptors, and detected the  3-adrenoceptor in adipocyte membranes by time-resolved fluorescence.8 The authors were unable, however, to detect the  3-adrenoceptor in intact adipocytes. Our success in this respect may be due to our experience in fixing and embedding adipose tissue samples.22 We also demonstrate the presence of the  3-adrenoceptor in some other human tissues, notably myocardium.

Staining was often localized to the periphery of cells (eg Figure 3d), as would be expected of a 7-transmembrane receptor. Moreover, the tissue distribution of immunoreactivity stongly supports the evidence of the previous paper.8 that the antibody selectively detects the  3-adrenoceptor rather than  1- or  2-adrenoceptors. First, no immunoreactivity was detected in lung, skeletal muscle or arterioles, which are known to express high numbers of  2-adrenoceptors. Secondly, staining of cardiac tissues and intestine was far less pronounced than would be expected of an antibody that reacts with  1-adrenoceptors. Thirdly, staining was especially pronounced in multilocular adipocytes of perirenal tissue from phaeochromocytoma patients, consistent with the higher expression of  3-adrenoceptor mRNA in brown compared to white adipocytes.10,16 In contrast, expression of the  1-adrenoceptor is lower in brown than in white adipocytes, at least during the transformation of bovine perirenal adipose tissue from brown into white fat.23 Lastly, staining was less in obese than in lean subjects but was restored to the level in lean subjects by treatment with ephedrine and caffeine. Since ephedrine promotes noradrenaline release as well as causing some direct stimulation of adrenoceptors, and with caffeine it enhances sympathetic activity, it is to be expected that it would have a similar effect to phaeochromocytoma on  3-adrenoceptor expression. Indeed there is evidence that the thermogenic effect of ephedrine in humans is in part mediated by  3-adrenoceptors24 and that the  3-adrenoceptor-mediated component of this effect is enhanced by repeated administration of ephedrine or ephedrine plus caffeine.25,26 This latter finding also accords with the expectation that the thermogenic response to a  3-adrenoceptor agonist should increase during chronic therapy, at least in part because it leads to increases in brown adipocyte and therefore  3-adrenoceptor numbers. Indeed, clinical data from the obese subjects of the present study on body composition, resting energy expenditure and lipid metabolism are overall compatible with a more pronounced thermogenic and lipolytic effect by ephedrine plus caffeine plus energy restriction as compared to energy restriction alone (manuscript in preparation).

There is also the Dulloo review ( http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8384178&dopt=Abstract). From the full text: "Single dose studies indicate that skeletal muscle and viscera contribute most of the thermogenic effects of ephedrine, with a minor contribution from brown adipose tissue (BAT). However, this tissue can be reactivated and indeed proliferate in response to chronic catecholaminergic activation, and may therefore assume a greater importance than that reported in acute studies. This contention may also explain the findings that long-term ephedrine therapy in obese women results in enhancement of its thermogenic effects."

So, in sum, these are my reasons for favoring chronic use:

(1) The longest studies indicate that with chronic use of EC, the effects on energy expenditure remain and may become stronger, and there is increased thermogenic response to acute doses as well.

(2) Additionally, negative side effects are greatly reduced with chronic use, and reach placebo levels after 8-12 weeks.

(3) We know that a large part of thermogenesis induced by ephedrine is due to beta(3) activation (here's another reference on this): http://www.ncbi.nlm.nih.gov/entrez/query.f...&dopt;=Abstract).

(4) We also know that there is a large amount of beta(3) adrenoreceptors in BAT and that chronic stimulation upregulates the amount of BAT. This is in agreement with the clinical findings.

(5) Finally, it should be noted that the weight loss from EC is much more modest than is commonly thought - in the 1-2 kg per month range - and this could be fully accounted for by BAT.

David

-David Tolson


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Labrat
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Posted by: @Spook
The mechanism for long-term fat loss with ephedrine is upregulation of BAT, which isn't dependant on caffeine or anything else.

except humans have allmost no BAT. and BAT induced thermogenesis in humans amounts to about nothing in terms of energy expenditure.

I definantly think cyclic use superior.

Although studies suggest that long-term use is more efficacious than cycling it.

I agree that BAT association is not relevant for humans, unless you are an Eskimo. However, the hypothesized mechanism of long term efficacy is related to chronic stimulation of the beta3-AR. This adrenoceptor does not downregulate as quickly as the other two beta-ARs, and it exists in other adipose tissue than just BAT, such as WAT (albeit in smaller density than beta2-ARs). It also exists in muscle tissue.

It has also been suggested that the long-term efficacy may be related to increased metabolic rate during sleep. Although the increase in energy expenditure is not significant, the cumulative EE may account for its long-term efficacy.

The other reason may be sustained appetite suppression.


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Labrat
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Posted by: @shpongled
Regarding BAT, did you ever look at the article I posted? Here is the discussion section which I was referring to, the last paragraph being most important.

Thanks for posting the excerpt. It supports my previous post in this thread. I missed your post that you reference. Could you email me the full citation? It has been awhile since I read any of the recent adrenoceptor studies. The last one I read was with a primate model, which was quite interesting. The article from which this excerpt is derived peaks my interest.


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Spook
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I am sorry. I should have been clear in my original post. My opinion is that as follows.

1) Those who are significantly overweight should use E continually.
2) Those who are only slightly over weight should not use E as a fat burner and should only use it as a pre-workout stimulant if at all.
3) Those who are extremely lean should use it in a cyclic and high dose fashion.

My reasoning is as follows:

In the obese group studies have shown continual usage is superior. Now we must ask the question, why is this so? It is my opinion that the ECA stack was a rather remarkable accident. The three ingredients were obviously stacked to enhance lipolysis. However I do not think its effects on weight loss have all that much to do with enhanced lipolysis. We know that most obese people suffer from attenuated SNS outflow. We also know that most overweight people show an attenuated response to B-AR induced lioplysis. Mostly because of reduced Testosterone and thyroid hormone. Testosterone is the primary mediator of AR density and isoform distribution. Thyroid hormone is the primary regulator of AR regulation by enhancing migration to the cell membrane. The obese more often than not already poses elevated levels of serum FFA. So lipolysis is not much of a concern. In the obese the rate limiting step is oxidation not lipolysis. B1/2-AR activation in skeletal muscle enhances AMPK activation and CPT transcription increases fat oxidation capacity and enhancing glucose disposal.

So lets break this down in to two time periods. The initial response (about the first 6 weeks at 60mg/day) and the adapted response (anything after about 6 weeks).

So during the first six weeks or so we get all the normal effects. Increased heart rate, increased lipolysis, elevated thyroid hormone, increased fat oxidation at rest, decreased insulin secretion, and enhanced glucose disposal. So the decrease in plasma leptin and insulin in this phase reset the VMH-PVN system correcting part of the obese persons physiological abnormalities. This should also help reset the BBB glut1 content making there brains sensing of glucose more normal. The activation of B-AR in skeletal muscle will enhance lipolytic enzymes in said muscle and aid in eliminating intra-myocellular lipids (IML). IML being the other big problem the obese must have. So in my opinion this period of time acts as a corrective measure. Resting numerous systems so that they appear more like a healthy persons.

Then we enter the adaptation stage where the side effects disappear. Now either the SNS is depleted or the receptors have down regulated. It looks like it’s the later as weight loss continues. So during this time B3 which I agree is expressed all over the place plays the primary role. Still in an obese person lipolysis is not the rate limiting step. B3 is not that lipolytic anyway in human adipose tissue as is evidenced by the in vitro studies of human WAT utilizing very specific B3 agonists. So what is enhancing weight loss in vivo? My opinion B3 activation in skeletal muscle is what is regulating it. All though not very potent at enhancing oxidation on its own B3 activation in skeletal muscle has been tied to glucose disposal. Thus such an individual spends more hours each day in the hypoglycemic state and the VMH-PVN responds accordingly enhancing weight loss. It probably also continues to enhance fat oxidation but I think this benefit is minimal compared to the glucose disposal mechanism. So all of this looks ideal. First you get correction then you get maintenance.

First let me define normal people to be those who are not significantly over weight but not in great shape either. I tend to think this group should only use E as a pre work out stimulant or cyclicly as a diet aid if they really feel the need. Of course pre-workout E has many benefits so I wont even go in to that. The reason why I think it would be best to back off in this group is that for these people E is not going to be much more than an appetite suppressant. These folks already show good lipolysis and good oxidation. They could probably get better results with E but E use also caries some negatives along with it. Continual use shows receptor down regulation so your messing with your bodies natural partitioning system by doing so. Also it has negative effects in the PVN. There are sympathetic nerve projections running form the CNS in to the PVN. These can be activated by psychological or physiological stress. They can also be activated by stimulants. Activation of these sympathetic neurons causes NE release and by binding to the A2-AR in the PVN alters its normal mode of operation. It makes the PVN super sensitive to activation of the hypothalamic-pituitary-adrenal axis (HPA). Thus it makes one more prone to increased CRF production and decreased TRH production. So for this group that loses weight just fine on their own would be better off with an appetite suppressant instead of E.

Now in the very lean exercise trained type you have a different set of problems. These folks like you and me have no problem oxidizing fat. However riding our selves of that last little bit is increasingly difficult because of reduced lipolysis. So heavy short cyclic usage would seem to be the best as that is the usage pattern that would promote lipolysis the most.

Thoughts?

Normal Person + Anonymity + Audience = Total Fuckwad.
If you meet the bodybuilding guru on the information super-highway, kill the bodybuilding guru.
trust != truth


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shpongled
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Posted by: @Spook
Thoughts?

That will take me a while to digest, many things were brought up that hadn't occured to me or that I hadn't thought about much. But aren't lipolysis and increased fat oxidation synonymous?

-David Tolson


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