HOT-ROX vs. ECA Stack

[quote]big69penisman wrote:
garethhe wrote:
Cy Willson wrote:
g
HOT-ROX should never be used concurrently with ephedrine and caffeine or any other fat loss supplements. Either use one or the other.

Doing so could result in very serious adverse effects.

thank you Cy, i’m taking your advice. i do see how it is a good idea to take one fat loss supplement at a time, and also that prolonged exposure to any particular supplement can be ineffective and/or dangerous.

it sounds to me like cycling ECA and HOT-ROX is a solid plan. does anybody have any suggestions on how long one should be on each? and is there a third fat loss option that is relatively effective, safe, and not overpriced?

I know nothing of cycling HOT-ROX but there is at least one study that shows extended use of EC only gets better, so no need to cycle off.

A third option? Consistency to a reduced cal diet. Nicotine works well for me and has been shown to work well in studies. Phentermine has worked for some but you’ll need a prescription. DNP but most people are too stupid to use it properly (again, this goes back to the MORE IS BETTER!!! mentality).[/quote]

I’d be interested in seeing the study which demonstrated a greater effect with continued use.

what is DNP by the way?

Dinitrophenol

[quote]Cy Willson wrote:

I’d be interested in seeing the study which demonstrated a greater effect with continued use.[/quote]

Let me see if I can find it again.

[quote]big69penisman wrote:
Cy Willson wrote:

I’d be interested in seeing the study which demonstrated a greater effect with continued use.

Let me see if I can find it again.[/quote]

Here’s one.

The effect of chronic ephedrine treatment on substrate utilization, the sympathoadrenal activity, and energy expenditure during glucose-induced thermogenesis in man.

Astrup A, Madsen J, Holst JJ, Christensen NJ.

Chronic ephedrine treatment of man has recently been found to enhance the thermogenic response to an acute dose of ephedrine. Conceivably, this sensitization to beta-adrenergic stimulation might also affect the facultative component of diet-induced thermogenesis. The glucose-induced thermogenesis (GIT) was studied in five healthy female subjects after 3 months of chronic peroral ephedrine treatment. Similar experiments 3 months after cessation of treatment served as controls. During chronic ephedrine treatment a sustained 10% elevation of the metabolic rate was found compared to that in the control study. Plasma epinephrine levels were increased 87% during treatment. These increases tended to be positively correlated (r = 0.54, P less than 0.07). GIT expressed as a percentage of the ingested energy load was unaltered during chronic ephedrine treatment compared with that in the control study (9.0% v 8.9%). The respiratory quotient (RQ) indicate that relatively more lipid was oxidized during chronic ephedrine treatment than in the control study. This change was observed in the fasting state as well as after glucose administration. Certain effects of ephedrine seems to be appropriate to a thermogenic drug for the treatment of obesity: A single dose of ephedrine stimulates thermogenesis, an effect that is enhanced during chronic treatment; Chronic treatment elevates the metabolic rate; and The substrate utilization is changed in favor of lipid oxidation.

PMID: 3512957 [PubMed - indexed for MEDLINE]

[quote]big69penisman wrote:
Cy Willson wrote:

I’d be interested in seeing the study which demonstrated a greater effect with continued use.

Let me see if I can find it again.[/quote]

Here’s one.

The effect of chronic ephedrine treatment on substrate utilization, the sympathoadrenal activity, and energy expenditure during glucose-induced thermogenesis in man.

Astrup A, Madsen J, Holst JJ, Christensen NJ.

Chronic ephedrine treatment of man has recently been found to enhance the thermogenic response to an acute dose of ephedrine. Conceivably, this sensitization to beta-adrenergic stimulation might also affect the facultative component of diet-induced thermogenesis. The glucose-induced thermogenesis (GIT) was studied in five healthy female subjects after 3 months of chronic peroral ephedrine treatment. Similar experiments 3 months after cessation of treatment served as controls. During chronic ephedrine treatment a sustained 10% elevation of the metabolic rate was found compared to that in the control study. Plasma epinephrine levels were increased 87% during treatment. These increases tended to be positively correlated (r = 0.54, P less than 0.07). GIT expressed as a percentage of the ingested energy load was unaltered during chronic ephedrine treatment compared with that in the control study (9.0% v 8.9%). The respiratory quotient (RQ) indicate that relatively more lipid was oxidized during chronic ephedrine treatment than in the control study. This change was observed in the fasting state as well as after glucose administration. Certain effects of ephedrine seems to be appropriate to a thermogenic drug for the treatment of obesity: A single dose of ephedrine stimulates thermogenesis, an effect that is enhanced during chronic treatment; Chronic treatment elevates the metabolic rate; and The substrate utilization is changed in favor of lipid oxidation.

PMID: 3512957 [PubMed - indexed for MEDLINE]

Here’s the earlier study. This one was in overweight women where things are screwy, but the previous one was in healthy men which should mean something (this type of research is not my first hand thing, so I may be wrong).

Enhanced thermogenic responsiveness during chronic ephedrine treatment in man.

Astrup A, Lundsgaard C, Madsen J, Christensen NJ.

The thermogenic effect of a single oral dose of ephedrine (1 mg/kg body weight) was studied by indirect calorimetry in five women with 14% overweight before, during and 2 mo after 3 mo of chronic ephedrine treatment (20 mg, perorally, three times daily). Before treatment and 2 mo after its cessation a similar thermogenic response to ephedrine was observed. The total extra consumption of oxygen was 1.3 1 before and 1.2 1 after cessation of the chronic treatment. After 4 and 12 wk of treatment ephedrine elicited a more sustained response, the extra oxygen consumption in the 3 h following ephedrine intake being 7.0 and 6.9 1, respectively. The ratio of serum T3 to T4 increased significantly after 4 wk of treatment (15.6 +/- 1.3 vs 19.4 +/- 2.4; p less than 0.05), but decreased below the initial value after 12 wk treatment. The mean body weight was significantly reduced after 4 and 12 wk of treatment (2.5 and 5.5 kg, respectively). An improved capacity for beta-adrenergic induced thermogenesis may be useful in the treatment of obesity.

PMID: 4014068 [PubMed - indexed for MEDLINE]

[quote]jsbrook wrote:
K-Narf wrote:
dvv wrote:
jsbrook wrote:
Are actual pre-formulated ECA stacks being sold again?

I’ve seen a few on various websites, however they are very expensive and use a small dose of ephedra (I believe 10mg or so)…

Personally, I think your better off just getting some Ephedrine Hcl, and making your own E/C stack, its done wonders for me for preworkout and best of all its very cost effective :slight_smile:

Agreed. I found this to be the best way to go.

Interesting. I might look into that. I’ve never used Ephedrine. I’d be interested in a personal test of how it compares to HOT-ROX

[/quote]

If you do decide to use it, start small. Not saying you won’t as I don’t know you, but a lot of people just jump right in and don’t assess tolerance.

Actually, neither study was using men. Both were using 5 overweight women.

However, I have to argue that it’s not accurate to assume that research in women can’t be applied to men. I see people make that mistake quite often when looking at abstracts. Unless you’re talking about an effect that is directly and significantly dependent upon sex hormones, it’s not unreasonable to assume that on a qualitative level, something similar will happen in males. If one takes a look at available weight loss drugs, or really, the vast majority of drugs in general, they’ll see that they are not sex-dependent.

So, the study you found still has value.

As for the study evaluating a thermogenic response (the other was a continuation of the first study, this time evaluating the effect upon glucose induced thermogenesis), it’s not that it was actually demonstrated that the ephedrine became more effective in terms of reducing fat mass. This is not what they found.

Rather, they were measuring metabolic rate via oxygen consumption. They first administered ephedrine on a single day (prior to initiating the 12 week study) and measured oxygen consumption.

Each subject then began taking 20 mg, three times daily.

At weeks 4 and 12, they repeated the ephedrine load and again measured metabolic rate via oxygen consumption. They then compared oxygen consumption from their pre-trial measurement to weeks 4 and 12, and as one would expect, found a much larger increase. However, one major flaw is that the author never considers the half-life (never makes any mention about it) of ephedrine. Well, considering that one had just been taking 60 mg/day for 4 and 12 previous weeks, it should be a no brainer that one is going to have higher blood levels after an oral load of ephedrine than they would when they were administered ephedrine prior to the study beginning. In fact, if oxygen consumption truly were increasing with continual use, you’d expect to see an increase going from week 4 to week 12, yet there was no significant difference (week 12 had a decrease in fact, though not significant).

Actual measured fat loss did not persist at the same rate, nor increase in this study. As one would expect, it decreased over time.

In any event, the reason I asked to see such a study is simply because it’s as close to being dogmatic as possible in molecular/cell biology that chronic administration of a beta adrenergic agonist will produce down-regulation (not to be confused with desensitization which is much more acute) and hence a diminished biological response. In fact, that’s what is demonstrated over and over. Now, that of course doesn’t mean there aren’t other mechanisms through which an effect upon metabolism couldn’t be maintained, but to have such a powerful effect that one continues to reduce fat mass at a greater rate than when starting administration would be nothing short of amazing. This study simply did not demonstrate that.

[quote]big69penisman wrote:
Here’s the earlier study. This one was in overweight women where things are screwy, but the previous one was in healthy men which should mean something (this type of research is not my first hand thing, so I may be wrong).

Enhanced thermogenic responsiveness during chronic ephedrine treatment in man.

Astrup A, Lundsgaard C, Madsen J, Christensen NJ.

The thermogenic effect of a single oral dose of ephedrine (1 mg/kg body weight) was studied by indirect calorimetry in five women with 14% overweight before, during and 2 mo after 3 mo of chronic ephedrine treatment (20 mg, perorally, three times daily). Before treatment and 2 mo after its cessation a similar thermogenic response to ephedrine was observed. The total extra consumption of oxygen was 1.3 1 before and 1.2 1 after cessation of the chronic treatment. After 4 and 12 wk of treatment ephedrine elicited a more sustained response, the extra oxygen consumption in the 3 h following ephedrine intake being 7.0 and 6.9 1, respectively. The ratio of serum T3 to T4 increased significantly after 4 wk of treatment (15.6 +/- 1.3 vs 19.4 +/- 2.4; p less than 0.05), but decreased below the initial value after 12 wk treatment. The mean body weight was significantly reduced after 4 and 12 wk of treatment (2.5 and 5.5 kg, respectively). An improved capacity for beta-adrenergic induced thermogenesis may be useful in the treatment of obesity.

PMID: 4014068 [PubMed - indexed for MEDLINE]
[/quote]

[quote]Cy Willson wrote:
Actually, neither study was using men. Both were using 5 overweight women.

However, I have to argue that it’s not accurate to assume that research in women can’t be applied to men. I see people make that mistake quite often when looking at abstracts. Unless you’re talking about an effect that is directly and significantly dependent upon sex hormones, it’s not unreasonable to assume that on a qualitative level, something similar will happen in males. If one takes a look at available weight loss drugs, or really, the vast majority of drugs in general, they’ll see that they are not sex-dependent.

So, the study you found still has value.

As for the study evaluating a thermogenic response (the other was a continuation of the first study, this time evaluating the effect upon glucose induced thermogenesis), it’s not that it was actually demonstrated that the ephedrine became more effective in terms of reducing fat mass. This is not what they found.

Rather, they were measuring metabolic rate via oxygen consumption. They first administered ephedrine on a single day (prior to initiating the 12 week study) and measured oxygen consumption.

Each subject then began taking 20 mg, three times daily.

At weeks 4 and 12, they repeated the ephedrine load and again measured metabolic rate via oxygen consumption. They then compared oxygen consumption from their pre-trial measurement to weeks 4 and 12, and as one would expect, found a much larger increase. However, one major flaw is that the author never considers the half-life (never makes any mention about it) of ephedrine. Well, considering that one had just been taking 60 mg/day for 4 and 12 previous weeks, it should be a no brainer that one is going to have higher blood levels after an oral load of ephedrine than they would when they were administered ephedrine prior to the study beginning. In fact, if oxygen consumption truly were increasing with continual use, you’d expect to see an increase going from week 4 to week 12, yet there was no significant difference (week 12 had a decrease in fact, though not significant).

Actual measured fat loss did not persist at the same rate, nor increase in this study. As one would expect, it decreased over time.

In any event, the reason I asked to see such a study is simply because it’s as close to being dogmatic as possible in molecular/cell biology that chronic administration of a beta adrenergic agonist will produce down-regulation (not to be confused with desensitization which is much more acute) and hence a diminished biological response. In fact, that’s what is demonstrated over and over. Now, that of course doesn’t mean there aren’t other mechanisms through which an effect upon metabolism couldn’t be maintained, but to have such a powerful effect that one continues to reduce fat mass at a greater rate than when starting administration would be nothing short of amazing. This study simply did not demonstrate that.

big69penisman wrote:
Here’s the earlier study. This one was in overweight women where things are screwy, but the previous one was in healthy men which should mean something (this type of research is not my first hand thing, so I may be wrong).

Enhanced thermogenic responsiveness during chronic ephedrine treatment in man.

Astrup A, Lundsgaard C, Madsen J, Christensen NJ.

The thermogenic effect of a single oral dose of ephedrine (1 mg/kg body weight) was studied by indirect calorimetry in five women with 14% overweight before, during and 2 mo after 3 mo of chronic ephedrine treatment (20 mg, perorally, three times daily). Before treatment and 2 mo after its cessation a similar thermogenic response to ephedrine was observed. The total extra consumption of oxygen was 1.3 1 before and 1.2 1 after cessation of the chronic treatment. After 4 and 12 wk of treatment ephedrine elicited a more sustained response, the extra oxygen consumption in the 3 h following ephedrine intake being 7.0 and 6.9 1, respectively. The ratio of serum T3 to T4 increased significantly after 4 wk of treatment (15.6 +/- 1.3 vs 19.4 +/- 2.4; p less than 0.05), but decreased below the initial value after 12 wk treatment. The mean body weight was significantly reduced after 4 and 12 wk of treatment (2.5 and 5.5 kg, respectively). An improved capacity for beta-adrenergic induced thermogenesis may be useful in the treatment of obesity.

PMID: 4014068 [PubMed - indexed for MEDLINE]

[/quote]

Thanks for the reply. I mistyped that, meant females. The only other long study I found was this one that had a 50 week study. Didn’t show increased Thermogenesis, but it continued to work.

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.

[quote]big69penisman wrote:
Cy Willson wrote:
Actually, neither study was using men. Both were using 5 overweight women.

However, I have to argue that it’s not accurate to assume that research in women can’t be applied to men. I see people make that mistake quite often when looking at abstracts. Unless you’re talking about an effect that is directly and significantly dependent upon sex hormones, it’s not unreasonable to assume that on a qualitative level, something similar will happen in males. If one takes a look at available weight loss drugs, or really, the vast majority of drugs in general, they’ll see that they are not sex-dependent.

So, the study you found still has value.

As for the study evaluating a thermogenic response (the other was a continuation of the first study, this time evaluating the effect upon glucose induced thermogenesis), it’s not that it was actually demonstrated that the ephedrine became more effective in terms of reducing fat mass. This is not what they found.

Rather, they were measuring metabolic rate via oxygen consumption. They first administered ephedrine on a single day (prior to initiating the 12 week study) and measured oxygen consumption.

Each subject then began taking 20 mg, three times daily.

At weeks 4 and 12, they repeated the ephedrine load and again measured metabolic rate via oxygen consumption. They then compared oxygen consumption from their pre-trial measurement to weeks 4 and 12, and as one would expect, found a much larger increase. However, one major flaw is that the author never considers the half-life (never makes any mention about it) of ephedrine. Well, considering that one had just been taking 60 mg/day for 4 and 12 previous weeks, it should be a no brainer that one is going to have higher blood levels after an oral load of ephedrine than they would when they were administered ephedrine prior to the study beginning. In fact, if oxygen consumption truly were increasing with continual use, you’d expect to see an increase going from week 4 to week 12, yet there was no significant difference (week 12 had a decrease in fact, though not significant).

Actual measured fat loss did not persist at the same rate, nor increase in this study. As one would expect, it decreased over time.

In any event, the reason I asked to see such a study is simply because it’s as close to being dogmatic as possible in molecular/cell biology that chronic administration of a beta adrenergic agonist will produce down-regulation (not to be confused with desensitization which is much more acute) and hence a diminished biological response. In fact, that’s what is demonstrated over and over. Now, that of course doesn’t mean there aren’t other mechanisms through which an effect upon metabolism couldn’t be maintained, but to have such a powerful effect that one continues to reduce fat mass at a greater rate than when starting administration would be nothing short of amazing. This study simply did not demonstrate that.

big69penisman wrote:
Here’s the earlier study. This one was in overweight women where things are screwy, but the previous one was in healthy men which should mean something (this type of research is not my first hand thing, so I may be wrong).

Enhanced thermogenic responsiveness during chronic ephedrine treatment in man.

Astrup A, Lundsgaard C, Madsen J, Christensen NJ.

The thermogenic effect of a single oral dose of ephedrine (1 mg/kg body weight) was studied by indirect calorimetry in five women with 14% overweight before, during and 2 mo after 3 mo of chronic ephedrine treatment (20 mg, perorally, three times daily). Before treatment and 2 mo after its cessation a similar thermogenic response to ephedrine was observed. The total extra consumption of oxygen was 1.3 1 before and 1.2 1 after cessation of the chronic treatment. After 4 and 12 wk of treatment ephedrine elicited a more sustained response, the extra oxygen consumption in the 3 h following ephedrine intake being 7.0 and 6.9 1, respectively. The ratio of serum T3 to T4 increased significantly after 4 wk of treatment (15.6 +/- 1.3 vs 19.4 +/- 2.4; p less than 0.05), but decreased below the initial value after 12 wk treatment. The mean body weight was significantly reduced after 4 and 12 wk of treatment (2.5 and 5.5 kg, respectively). An improved capacity for beta-adrenergic induced thermogenesis may be useful in the treatment of obesity.

PMID: 4014068 [PubMed - indexed for MEDLINE]

Thanks for the reply. I mistyped that, meant females. The only other long study I found was this one that had a 50 week study. Didn’t show increased Thermogenesis, but it continued to work.

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.
[/quote]

No problem!

Well, let’s take a look at this. This was 24 weeks of administration (double-blinded) followed by a 2 week break and then another 24 weeks followed that, this time as an open trial (not blinded-subjects knew what they were taking).

So, just to be anal about it, it was 24 weeks followed by a 2 week break, then treatment continued in a different study design for 24 weeks. So, 48 weeks of treatment, split in half by a 2 week break. Again though, only half of that 48 was using the “gold standard” trial design…though a psychologist friend always makes me question how “golden” it truly is.

That aside, this doesn’t demonstrate an increase in effectiveness nor a maintenance of initial effectiveness.

I’m not arguing one iota that ephedrine and caffeine will become completely ineffective with continual use. Rather, I’m saying that it doesn’t become more effective with continual use nor will initial effectiveness be maintained. If one takes a look at the effects across time, they’ll see just that. Again, going back to what is considered an expected and documented response, beta adrenergic receptors will down-regulate in response to continued agonism, resulting in a diminished biological response.

[quote]ChrisKing wrote:
ThisIsMyRifle wrote:
How does HOT-ROX compare to a ECA Stack? Has anyone tried both. I got decent results from the ECA. Although I take out the asprin but interested in the HOT-ROX. Can anyone give me any input… I also plan to stack that with Methoxy-7… Thanks

As stated previously, I get significantly better fat-loss results with HOT-ROX. Plus, HOT-ROX doesn’t make me feel like my heart is going to blow out of my chest.[/quote]

You don’t like that feeling? That’s the fun part!

[quote]ipjunkie wrote:
jsbrook wrote:
Are actual pre-formulated ECA stacks being sold again?

Yes, although the dosage is only 10mg of ephedra. But I’m not sure how or if they are playing with the dosages of the rest of the stack.[/quote]

Yes, each pill will contain 10/100.

I am currently taking a product that has 120 capsules per bottle and I take 2 capsules 3X a day. Each bottle cost me $19.95.

[quote]Cy Willson wrote:
I’d be interested in seeing the study which demonstrated a greater effect with continued use.[/quote]

Enhanced thermogenic responsiveness during chronic ephedrine treatment in man.

Ephedrine works by stimulating the release of the bodies own noradrenaline, which stimulates ALL the adrenergic receptors. The stimulant side effects subside because they are primarily mediated by the beta-1 and beta-2 receptors, which downregulate during chronic use. Thus, the scientists were startled when they found that the thermogenic effect actually INCREASED with chronic use.

This phenomena led scientists to believe that there must be an undiscovered receptor involved in noradrenaline-induced thermogenesis. Then the scientists found that – even after blocking all the known adrenergic receptors – non-selective drugs like ephedrine still caused a significant thermogenic effect. The evidence supporting the existence of an undiscovered receptor that is stimulated by noradrenaline continued to increase.

Eventually, this led to the discovery of the beta 3 receptor, which is more resistant to desensitization (see links below) than the other beta receptors – and that is why the thermogenic effect of ECA is maintained so well during chronic use. Now you know why it is not necessary to “cycle” ECA.

[quote]Marmadogg wrote:
Cy Willson wrote:
I’d be interested in seeing the study which demonstrated a greater effect with continued use.

Enhanced thermogenic responsiveness during chronic ephedrine treatment in man.

Ephedrine works by stimulating the release of the bodies own noradrenaline, which stimulates ALL the adrenergic receptors. The stimulant side effects subside because they are primarily mediated by the beta-1 and beta-2 receptors, which downregulate during chronic use. Thus, the scientists were startled when they found that the thermogenic effect actually INCREASED with chronic use.

This phenomena led scientists to believe that there must be an undiscovered receptor involved in noradrenaline-induced thermogenesis. Then the scientists found that – even after blocking all the known adrenergic receptors – non-selective drugs like ephedrine still caused a significant thermogenic effect. The evidence supporting the existence of an undiscovered receptor that is stimulated by noradrenaline continued to increase.

Eventually, this led to the discovery of the beta 3 receptor, which is more resistant to desensitization (see links below) than the other beta receptors – and that is why the thermogenic effect of ECA is maintained so well during chronic use. Now you know why it is not necessary to “cycle” ECA.

[/quote]

I addressed the first abstract linked in my previous post. It’s a good illustration as to why I cringe a bit when I see the copying and pasting of abstracts from medline because words seem to fit to support a statement. I don’t mean that in a negative way, I just think one shouldn’t reference or cite the abstract without having read the full paper as the abstract is never providing sufficient information. That’s what I was taught at least.

As for the other statements, a quick look in to the literature will reveal that beta 2-adrenergic agonism (and to a lesser extent beta 1) is primarily responsible for the effects. Even if we were to ignore the fact that selective beta 3-adrenergic agonists have been developed quite a number of years ago and have failed in clinical trials (at least in terms of fat loss…at least two reasons for the discrepancy between human and rodent efficacy were difference in receptor type and the fact that adult humans have very little BAT) and give in to the idea that the beta 3-adrenergic agonism plays a role, they’ve only hypothesized that it would perhaps contribute 40-43% to the overall effect. Since the fans of medline probably want to know what I’m talking about:

And yes, while beta 3-adrenergic receptors are more resistant to down-regulation, that still leaves 57-60% available for down-regulation, being mediated via the other adrenoreceptors.

Last but certainly not least, as I said, if you look at the actual measured fat loss, it does not persist at the same rate, nor increase. As one would expect, it decreases over time.

Also, again, not to be anal, but desensitization and down-regulation are two different things.

[quote]Cy Willson wrote:
I addressed the first abstract linked in my previous post. It’s a good illustration as to why I cringe a bit when I see the copying and pasting of abstracts from medline because words seem to fit to support a statement. I don’t mean that in a negative way, I just think one shouldn’t reference or cite the abstract without having read the full paper as the abstract is never providing sufficient information. That’s what I was taught at least.

As for the other statements, a quick look in to the literature will reveal that beta 2-adrenergic agonism (and to a lesser extent beta 1) is primarily responsible for the effects. Even if we were to ignore the fact that selective beta 3-adrenergic agonists have been developed quite a number of years ago and have failed in clinical trials (at least in terms of fat loss…at least two reasons for the discrepancy between human and rodent efficacy were difference in receptor type and the fact that adult humans have very little BAT) and give in to the idea that the beta 3-adrenergic agonism plays a role, they’ve only hypothesized that it would perhaps contribute 40-43% to the overall effect. Since the fans of medline probably want to know what I’m talking about:

And yes, while beta 3-adrenergic receptors are more resistant to down-regulation, that still leaves 57-60% available for down-regulation, being mediated via the other adrenoreceptors.

Last but certainly not least, as I said, if you look at the actual measured fat loss, it does not persist at the same rate, nor increase. As one would expect, it decreases over time.

Also, again, not to be anal, but desensitization and down-regulation are two different things.[/quote]

I am the first to admit that I hardly have the experience on these topics that you do.

I did read the abstracts.

You should sponsor a head to head long term trial with human patients that compares HOT-ROX to EC.

I would compare this argument to the argument that steroid use increases your risk of developing cancer. The medical industry likes to claim this to be fact.

We will never be able to scientifically prove or disprove this until a long term double blind study is conducted on human patients.

I have found that I loose body fat more efficiently on an EC stack than on HOT-ROX.

I get a much greater dopamine increase from EC than HOT-ROX.

Cy-
I appreciate your thorough response to my post. I know you are very busy.
Thank you!

No problem, Marmadogg!

As for the comparison study, there will be something available in the near-future that should provide at least some answers in that respect.

Though, I’d prefer terms “supportive data” or “evidence”, as we have to be careful with the use of words like “proof” and “fact” as they can imply that all possible variables have been taken in to account.

In any event, I think one should use what works best for them. For you, it appears obvious that it’s the E&C.

Thanks for the discussion!

[quote]Marmadogg wrote:
Cy Willson wrote:
I addressed the first abstract linked in my previous post. It’s a good illustration as to why I cringe a bit when I see the copying and pasting of abstracts from medline because words seem to fit to support a statement. I don’t mean that in a negative way, I just think one shouldn’t reference or cite the abstract without having read the full paper as the abstract is never providing sufficient information. That’s what I was taught at least.

As for the other statements, a quick look in to the literature will reveal that beta 2-adrenergic agonism (and to a lesser extent beta 1) is primarily responsible for the effects. Even if we were to ignore the fact that selective beta 3-adrenergic agonists have been developed quite a number of years ago and have failed in clinical trials (at least in terms of fat loss…at least two reasons for the discrepancy between human and rodent efficacy were difference in receptor type and the fact that adult humans have very little BAT) and give in to the idea that the beta 3-adrenergic agonism plays a role, they’ve only hypothesized that it would perhaps contribute 40-43% to the overall effect. Since the fans of medline probably want to know what I’m talking about:

And yes, while beta 3-adrenergic receptors are more resistant to down-regulation, that still leaves 57-60% available for down-regulation, being mediated via the other adrenoreceptors.

Last but certainly not least, as I said, if you look at the actual measured fat loss, it does not persist at the same rate, nor increase. As one would expect, it decreases over time.

Also, again, not to be anal, but desensitization and down-regulation are two different things.

I am the first to admit that I hardly have the experience on these topics that you do.

I did read the abstracts.

You should sponsor a head to head long term trial with human patients that compares HOT-ROX to EC.

I would compare this argument to the argument that steroid use increases your risk of developing cancer. The medical industry likes to claim this to be fact.

We will never be able to scientifically prove or disprove this until a long term double blind study is conducted on human patients.

I have found that I loose body fat more efficiently on an EC stack than on HOT-ROX.

I get a much greater dopamine increase from EC than HOT-ROX.

Cy-
I appreciate your thorough response to my post. I know you are very busy.
Thank you!
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