excellent study on pheraplex

[sethroberts]

i have perscription beta blocker that I do not use...this could be used for the BP if it gets too high? So is it the BP increase from phera that could cause heart enlargement?

In otherwords if I keep BP low I should not have any enlargement?

It is doubtful that the cardiomyopathy seen with AAS use is solely a result of the hypertensive effects, so I would say no. On the other hand, keeping blood pressure in check would definitely help -- although I am not sure I would self medicate with beta-blockers.

 

[hardknock]

If you took my statement to mean that people popping them like candy shows that they are safe then you misunderstood. I was pointing out that people should be concerned with the health ramification of AAS AND stimulants as well as any other supplements or drugs they are taking -- there is no free ride.

Indeed, that was not my intentions. The statement I made was for the stevie wonders of AM in accordance with your statement ...

 

[sethroberts]

Indeed, that was not my intentions. The statement I made was for the stevie wonders of AM in accordance with your statement ...

Stevie Wonders -- lol. Sad, but true.

 

[nattydisaster]

i have perscription beta blocker that I do not use...this could be used for the BP if it gets too high? So is it the BP increase from phera that could cause heart enlargement?

In otherwords if I keep BP low I should not have any enlargement?

See the story of the guy I posted: http://scienceofmuscle.com/forum/steroids/203-high-blood-pressure-silent-killer-true-story.html

He was having BP issues.

I agree with seth, I would not self medicate with Beta-Blockers. They are not something you mess around with.

 

[LakeMountD]

I agree with everything you've said about cardiac output. It is the primary equation when determining the adequacy of overall cardiac function. I brought up ejection fraction specifically because it's vital in the diagnosis, as well as the long term prognosis of those people who are affected by either a dilated, hypertrophic, or restrictive cardiomyopathy pathology.

The kidneys are most definitely overlooked in their role of fluid and blood pressure management. ACE inhibitors have come a long way in hypertensive management.....especially those with a prior cardiac histroy.


BTW - Great convo, lake.

I really do enjoy threads of this nature. Not only are the informative and interesting for all involved and observing, but they provide a great intellectual stimulus environment.

Exactly, and I completely agree on the ACE inhibitors. Being on the pharmaceutical side of things I have seen how much more interest they have in them with the discovery of ang1-7 and other mechanisms behind controlling blood pressure. There is a crazy feedback system in the RAAS. AngII can upregulate angiotensinogen but decrease renin, etc. it is strange. That is why I am intrigued with the kidneys though .

 

[Trauma1]

i have perscription beta blocker that I do not use...this could be used for the BP if it gets too high? So is it the BP increase from phera that could cause heart enlargement?

In otherwords if I keep BP low I should not have any enlargement?

Hypertension is not nearly the sole cause of heart enlargement or cardiomegaly. Other factor such as Valvular Heart Disorders (mitral valve prolapse, aortic valve stenosis), Cardiac Congenital Anomaly, Hyperthyroid (Graves Disease), Hypothyroid (Myxedema), Recreational Drug Use (Cocaine in particular) Hormonal Pharmacology Use, Chronic Anemia, or even heredity can play crucial roles in its development.

Were you actually prescribed this beta blocker, or is this a self medication issue? I strongly DO NOT advise you to be self medicating with beta blockers to control situational hypertension. It can be VERY dangerous and life threatening.

 

[LakeMountD]

Hypertension is not nearly the sole cause of heart enlargement or cardiomegaly. Other factor such as Valvular Heart Disorders (mitral valve prolapse, aortic valve stenosis), Cardiac Congenital Anomaly, Hyperthyroid (Graves Disease), Hypothyroid (Myxedema), Recreational Drug Use (Cocaine in particular) Hormonal Pharmacology Use, Chronic Anemia, or even heredity can play crucial roles in its development.

Were you actually prescribed this beta blocker, or is this a self medication issue? I strongly DO NOT advise you to be self medicating with beta blockers to control situational hypertension. It can be VERY dangerous and life threatening.

Although stenosis is typically caused from hypertension. But yes you are exactly right, there is an enormous list of causes including secondary disorders such as pheochromocytoma, primary and secondary aldosteronism, and Cushings disease.

For those of you that don't know there are two main types of hypertension: primary and secondary. Primary is basically idiopathic as we don't truly know what causes it, but they are subtle and chronic changes. Secondary can be caused by other factors such as the disease states listed above. ~90% of all hypertensive causes are primary.

It is actually interesting to note that not only does high salt intake increase BP over the long run, but so does major salt restriction. Salt restriction actually causes a release in angiontensin via the macula densa pathway.

 

[hardknock]

i have perscription beta blocker that I do not use...this could be used for the BP if it gets too high? So is it the BP increase from phera that could cause heart enlargement?

In otherwords if I keep BP low I should not have any enlargement?

You have occasional high BP, brought on by exogenous substances, which you normally do not take...

That's easy math. Do not take the beta blockers unless you have been prescribed them for a reason, not situational BP.

 

[Trauma1]

Although stenosis is typically caused from hypertension. But yes you are exactly right, there is an enormous list of causes including secondary disorders such as pheochromocytoma, primary and secondary aldosteronism, and Cushings disease.

For those of you that don't know there are two main types of hypertension: primary and secondary. Primary is basically idiopathic as we don't truly know what causes it, but they are subtle and chronic changes. Secondary can be caused by other factors such as the disease states listed above. ~90% of all hypertensive causes are primary.

It is actually interesting to note that not only does high salt intake increase BP over the long run, but so does major salt restriction. Salt restriction actually causes a release in angiontensin via the macula densa pathway.

You're absolutely right, hypertensive etiology can certainly be a factor in its development. Aortic valve stenosis is typically the result of either a congenital or acquired (Rheumatic fever, Fibrosis, atherosclerosis or Calcification issues) cause.

Pheochromocytoma is one nasty, yet very interesting tumor of the adrenal medulla. It was one of my favorite reads in nursing school.

 

[LakeMountD]

You're absolutely right, hypertensive etiology can certainly be a factor in its development. Aortic valve stenosis is typically the result of either a congenital or acquired (Rheumatic fever, Fibrosis, atherosclerosis or Calcification issues) cause.

Pheochromocytoma is one nasty, yet very interesting tumor of the adrenal medulla. It was one of my favorite reads in nursing school.

I just liked saying it when I learned about it lol. You don't sound any smarter than when you say pheochromocytoma or diffuse proliferative glomerulonephritis, acute peylonephritis (honeymoon nephritis lol), or chronic nephrosclerosis.

And yes I forgot to mention the pathogenic causes of stenosis such as rheumatic fever. I had a lot of fun when we did the heart, such as how to diagnose things like a coarctation of the aorta via feeling for bruits (or a lack their of) and such.

 

[sethroberts]

I just liked saying it when I learned about it lol. You don't sound any smarter than when you say pheochromocytoma or diffuse proliferative glomerulonephritis, acute peylonephritis (honeymoon nephritis lol), or chronic nephrosclerosis.

And yes I forgot to mention the pathogenic causes of stenosis such as rheumatic fever. I had a lot of fun when we did the heart, such as how to diagnose things like a coarctation of the aorta via feeling for bruits (or a lack their of) and such.

Psuedohyperaldosteronism was one of the big words I liked saying and probably plays a role in the pathologic mechanims of AAS in the heart.

 

[Trauma1]

I just liked saying it when I learned about it lol. You don't sound any smarter than when you say pheochromocytoma or diffuse proliferative glomerulonephritis, acute peylonephritis (honeymoon nephritis lol), or chronic nephrosclerosis.

And yes I forgot to mention the pathogenic causes of stenosis such as rheumatic fever. I had a lot of fun when we did the heart, such as how to diagnose things like a coarctation of the aorta via feeling for bruits (or a lack their of) and such.

Lol, so true. :lol:

 

[LakeMountD]

Lol, so true. :lol:

Yeah I had as my away message for the last week, "Nobody worry! I didn't get acute pyelonephritis ." because I just got married lol.

 

[nattydisaster]

Yeah I had as my away message for the last week, "Nobody worry! I didn't get acute pyelonephritis ." because I just got married lol.

Congrats!

 

[nattydisaster]

Anyone find any studies about this with other androgens/Anabolic steroids?

 

[LakeMountD]

Anyone find any studies about this with other androgens/Anabolic steroids?

Steroids and the Heart - Science of Muscle Forums

Those are all on the heart, although pretty disturbing. There are two cases in point here:

1) Yes, any anabolic steroid will have an effect on the heart, not just Pherplex.

2) The case in point is not that steroids hurt the heart but that large doses of it are ultimately responsible for a lot of it. Most people I have seen abuse steroids. Why? Impatience, no one wants to wait 10 weeks when they can wait 5, but there is a cost. Be smart, keep your doses lower, fix your diet, train hard, and relax.

:food:izza:

 

[nattydisaster]

Wow...surprised this isn't discussed more often. Those are serious cases

 

[LakeMountD]

Wow...surprised this isn't discussed more often. Those are serious cases

I know, it was definitely a good read, but most just disregard them.

 

[thesinner]

wow

and test prop causes heart enlargement too?

Any AAS can cause heart hypertrophy

 

[Sldge]

yeah,my only comments goes to the fact that in the study they say that phera is less anabolic than test prop and I thought the opposite and the problem of the heart weight, maybe its better not to overdose it cause the heart enlargement was greater than with test prop.

It is stronger then test prop, well the anabolic value is the androgenic value is lower.

 

[nunes]

It is stronger then test prop, well the anabolic value is the androgenic value is lower.

I think that for muscle growth, the anabolic value its the first to be consider, or am I wrong?

 

[Dr Packenwood]

I ran a great cycle of PP last summer. Gained some strength, but put on literally 0 lbs.

 

[bigred869]

Ok now the possibility of having hypetrophic cardiomyopathy is scaring the sh!t out of me because sudden death would suck. I have included anadrol in one previous cycle and phera in two. I notice palpitations when I stand up too fast sometimes, which I'm hoping is common. I read a study on how exercise might prevent it so I'm going to cut back on lifting and pick up on some cardio. Also get an echo asap. Any other suggestions for prevention or treatment?

 

[Cordeen]

Would Ergomax fall into this category?

 

[thesinner]

Would Ergomax fall into this category?

ergomax is desoxymethyltestosterone, just with a little more isomerization than pheraplex or madol.

Phera is 99.9% DMT as 2-ene

Ergomax is something like 70% as 2-ene and 30% as 3-ene

 

[dude]

If you read the dosage used the rats were taking 1mg/kg. That would mean 100mg/day for a 220lb person. Aren't the normal daily dosages of PP 10-40mg/day? I can't remember if this is correct but that is something to take into consideration.

 

[sethroberts]

If you read the dosage used the rats were taking 1mg/kg. That would mean 100mg/day for a 220lb person. Aren't the normal daily dosages of PP 10-40mg/day? I can't remember if this is correct but that is something to take into consideration.

It is inappropriate to do a one to one conversion of doses from rats to humans. A more proper conversion would be based on body surface area and is generally accepted to be about 5:1 for rats to humans. Therefore, a comparable dose of 1 mg/kg in rat to a 100 mg human would be about 20 mg in humans. This is only a general conversion and does not hold true for every compound or every class of compounds.

 

[dude]

It is inappropriate to do a one to one conversion of doses from rats to humans. A more proper conversion would be based on body surface area and is generally accepted to be about 5:1 for rats to humans. Therefore, a comparable dose of 1 mg/kg in rat to a 100 mg human would be about 20 mg in humans. This is only a general conversion and does not hold true for every compound or every class of compounds.

I'm not sure I understand. Why does it matter what the body surface area is? If a rat weighs say 1kg they would be taking 1mg while a human weighs 100kg so there dose is 100mg. These are proportional to the size of the species. Is there a different conversion through the liver?

 

[conwict]

im defiantly not going to use pp

Shake your fist, that'll make you even more defiant!

 

[sethroberts]

I'm not sure I understand. Why does it matter what the body surface area is? If a rat weighs say 1kg they would be taking 1mg while a human weighs 100kg so there dose is 100mg. These are proportional to the size of the species. Is there a different conversion through the liver?

There are alot of differences but body surface area was found to correlate well as a comparitor between species when trying to find a human equivalent dose (HED) particularly when going from preclinical, animal studies into human clinical testing. This is accepted practice by the FDA and pharmaceutical companies. You can see a big write up on the FDA web site here:

http://www.fda.gov/cber/gdlns/dose.htm

with the dose conversions appearing in table 1 about a third of the way down.

 

[citystreets]

include Coq10 in all your cycles, and even when your off, all the studies on it have shown it to be incredibly beneficial to the heart even more so than hawthorne berry. I even heard from 1 pharmacist that it make reverse some types of heart damage.

 

[dude]

There are alot of differences but body surface area was found to correlate well as a comparitor between species when trying to find a human equivalent dose (HED) particularly when going from preclinical, animal studies into human clinical testing. This is accepted practice by the FDA and pharmaceutical companies. You can see a big write up on the FDA web site here:


with the dose conversions appearing in table 1 about a third of the way down.

Thanks, the conversion table is and will be very helpful.

 

[sethroberts]

Thanks, the conversion table is and will be very helpful.

No problem.

 

[jmh80]

include Coq10 in all your cycles, and even when your off, all the studies on it have shown it to be incredibly beneficial to the heart even more so than hawthorne berry. I even heard from 1 pharmacist that it make reverse some types of heart damage.

Resveratrol too, I think. Will have to re-read PubMed but I think it can correct some of the heart enlargement (maybe not all).

Someone else that knows please chime in on res.

 

[Trauma1]

include Coq10 in all your cycles, and even when your off, all the studies on it have shown it to be incredibly beneficial to the heart even more so than hawthorne berry. I even heard from 1 pharmacist that it make reverse some types of heart damage.

What types of heart damage, infarction? That's not possible if that's what you're pertaining to.

It definitely demonstrates fantastic coenzyme properties that are vital to the maintenance of adequate cardiac function, as well as the rest of the body. I've seen it used as an adjunct in the treatment of CHF (congested heart failure) patients to maximize their cardiac output potential.