sethroberts
Active member
Reasonable cardio should definitely be included. The danger arises for those athletes that have extreme cardiovascular fitness (sprinters, etc) who have a chance of dropping dead from sudden cardiac death.
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- Thread starter sethroberts
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Reasonable cardio should definitely be included. The danger arises for those athletes that have extreme cardiovascular fitness (sprinters, etc) who have a chance of dropping dead from sudden cardiac death.
Smiley
Member
Could you elaborate on that for me please? Would it become much worse if that athlete is taking EQ with other AAS? I have heard that the increase in RBC count increases the chance for heart attack.
sethroberts
Active member
You are assuming that EQ raises RBC count higher than any other AAS -- no evidence of this -- just bro-lore. An increase in RBC count will not necessarily increase the chance for a heart attack while an increase in blood viscosity could theoretically increase the risk.
tyler4
Active member
Seth, almost done with the book. It is extremely well written and contained lots of useful information, most of which I haven't previously came accross in my own research. I had a couple questions and would be greatly appreciative if you could help me out.
1) In you book you explain two different types of edema, one being extracellular and the other being inracellular. I may have missed this but Pheraplex causes edema via 11BHSD2. Is this type intra or extracellular? Either way, since it is not from estrogen, what would be a good way to combat this? Low sodium intake I suppose?
2) I also see where 11BHSD can cause gyno from increased DHEA levels. That combined with lowering SHBG can increase gyno chances for sure. I am planning on running a P-Plex/Epi cycle very soon. I think I know your answer to this one, but what would you run to combat gyno on this particular cycle? (length/Doses?)
3) One more, what do you think makes someone "gyno sensitive?" If someone has a small case of it do you think that automatically makes then more prone to it? Or is it something that you just have to find out through your cycle experience? I would suspect males with slightly above average breast tissue means they have higher numbers of estrogen receptors in that area, thus making them "prone."
1) In you book you explain two different types of edema, one being extracellular and the other being inracellular. I may have missed this but Pheraplex causes edema via 11BHSD2. Is this type intra or extracellular? Either way, since it is not from estrogen, what would be a good way to combat this? Low sodium intake I suppose?
2) I also see where 11BHSD can cause gyno from increased DHEA levels. That combined with lowering SHBG can increase gyno chances for sure. I am planning on running a P-Plex/Epi cycle very soon. I think I know your answer to this one, but what would you run to combat gyno on this particular cycle? (length/Doses?)
3) One more, what do you think makes someone "gyno sensitive?" If someone has a small case of it do you think that automatically makes then more prone to it? Or is it something that you just have to find out through your cycle experience? I would suspect males with slightly above average breast tissue means they have higher numbers of estrogen receptors in that area, thus making them "prone."
RoadBlocK
Well-known member
I musta missed it, but nonetheless congrats to those that won, Im sure you will find a wealth of info to absorb.
Steveoph
NutraPlanet NinjaMonkey Rep
sethroberts
Active member
I have narrowed it down -- I have been busy but I will announce shortly.
sethroberts
Active member
Just to clarify, inhibition of 11BHSD2 will cause sodium and water retention, but it is different from inhibition of 11-beta hydroxylase. Inhibition of 11BHSD2 allows cortisol to act as a mineralocorticoid while inhibition of 11-beta hydroxylase decreases the formation of cortisol and increases the production of deoxycorticosterone which is a mineralocorticoid. This may seem like the end result is the same, but it is not. In any case, Pheraplex likely causes water retention through inhibition of 11-beta hydroxylase -- and this is intracellular edema (mostly but there can be some subcutaneous edema through the action of DHEA or other semipotent estrogens). The best way to combat this is probably through reduced sodium intake. The answer to number 2 would probably be nolvadex at 20 mg per day.
As far as gyno sensitivity, there are many factors: 1) size of breast tissue -- some men have none some men have a lot. 2) adiposity -- more fat means more estrogen 3) subtle differences in the enzyme systems that I outline in my book could make a big difference in whether someone experiences gyno while others do not.
tyler4
Active member
Thanks a lot Seth. Would you recomend an AI while on a Epi/P-Plex cycle? I know that most of the gyno risk will come from lowered SHBG levels so I would guess an AI would not suffice.
As for the Nolva, I may just wait until I notice signs before I start it. Unless you think that would be a crazy idea.
sethroberts
Active member
I don't think that would be too crazy. You don't want to take an additional substance if there is no need but understand that you ma not be able to totally reverse any growth that does occur if you catch it too late -- that is the catch-22
tyler4
Active member
Yea, I'm kinda torn here. So an AI would not do any good while on cycle in your opinion?
Zero V
Well-known member
I have always wondered this. Wouldn't estro induced gyno be preventable this way? At least thats what 1+1=2 logic says. Then again steroids works like 1+2=13
EasyEJL
Never enough
an AI can do good, but the idea is "the less different **** you have to put in your mouth, the better". So if you can do ok without the AI, its better to not take the AI.
The other problem Zero V is that taking estrogen too low for too long and having a sudden rebound is as likely to cause gyno as getting estrogen high in the first place. Rapid high changes are more likely to create problems than slow changes to the same levels. I had E2 at over 65 for 5 years without gyno.
tyler4
Active member
I typed out a long answer to this but then I thought I would let Seth give the real answer. I dont want to butcher it. But in his book he states that it will not help when the gyno cause is lowered SHBG levels.
tyler4
Active member
EasyEJL
Never enough
Yeah, see you can start following the trail of infinite supplements at some point, as you are taking a to avoid side effects of b, and c to avoid side effects of b, etc. Like using test enan, so you take arimidex to control estrogen. But then you take statins and igf-1 LR3 to counteract the changes to choleserol and igf levels from the arimidex, and finasteride to block DHT conversion as with less test converting to estrogen there is more to convert to dht. Then you are taking something to avoid hypoglycemia from the IGF, etc etc
sethroberts
Active member
An AI may help or it may make things worse -- I am still mulling it over. An AI will further reduce SHBG and may result in estrogen sensitization so long lived estrone sulfate or DHEA may have an easier time.
tyler4
Active member
What you do is get daily blood tests, and adjust ai to get your estrogen levels at just middle of range of normal for men
I wish that was possible! I will be seeing a new doc before I start my cycle, so I may see if a couple during cycle tests would be possible.
EasyEJL
Never enough
it really is the only way to get that "right" and even then it changes as you age, and as your bodyfat levels change. Its part of why to me cycles with low testosterone to preserve libido with shutdown, but higher doses of other items like deca that have don't aromatise as the major anabolic are intriguing.
sethroberts
Active member
It depends on which 1 steroid and which 4 to 5 different steroids you are talking about.
sethroberts
Active member
Stacking AAS is really about taking adbvantage of different properties of different molecules -- if you don;t know their properties, it is hard to do that.
wood23
Member
I suppose if i bought your book i would know their properties.....
sethroberts
Active member
Of the more common steroids where some research has been done, yes. On designers and more obscure steroids where little or no research has been done, probably not. I can speculate on some of the properties, but some things are not knowable without tests. Fo instance, I have seen blood test results that lead me to believe that epi is an inhibitor of TBG like many oral AAS, superdorl is likely a very potent inhbitor of 11-beta hydroxylase etc..
Zero V
Well-known member
So technically if there was alot more testing done on most of these "PH/DS" types then we could possibly counteract some of their harsher side effects?
Sub7
Member
Hi Seth,
What can be done to burn the visceral belly fat, which as you discussed in another thread, anavar targets effectively. If someone does not wish to go the DS, PH route, what other legal substances can work? Phosp. Serine may work at high doses (at commonly recommended affordable doses it does not) but for most people, the common "cortisol blockers" do not.
If one were OK going the PH, DS route, is there anything out there than can at least partially provide anavar''s fat burning properties?
Superdrol maybe?
What can be done to burn the visceral belly fat, which as you discussed in another thread, anavar targets effectively. If someone does not wish to go the DS, PH route, what other legal substances can work? Phosp. Serine may work at high doses (at commonly recommended affordable doses it does not) but for most people, the common "cortisol blockers" do not.
If one were OK going the PH, DS route, is there anything out there than can at least partially provide anavar''s fat burning properties?
Superdrol maybe?
sethroberts
Active member
There were a lot of great questions and here are the winners -- I actually chose three:
Zero V : For this question: "Based off of the ability to manipulate the chemistry of steroids, and the ability to predict conversion of one hormone into another what can we expect in the future. I mean can we say every steroid ever is already drawn into a book, or based off of the understanding of anabolic androgenic steroids can we expect new creations in the future. As in a another way to tickle our androgen receptors maybe through advancements from current steroids into a chemical compound that can work like a steroids, but have less or side effects. "and for his comment regarding your stomach getting roid rage and that's why you get heartburn -- It still breaks me up.
Roadblock : For this question; "Why, since the tail end years of the heyday era of Duchaine and Philips, have the generally accepted and/or "published" dosage recommendations of aas steadily and consistently increased over previously considered very effective, safe and accepted amounts, now that we are in the present era of folks like Llewellyn and Rea? "
Cord195148 : For these two questions: "In reality, how similar is the final compound of a PH or DS to the targeted or advertised AAS? Both in structure, binding affinity, and effect? " and "How similar are the effects of a SARM to AAS on any given AR? How different? "
You guys have 1 week to email your shipping issue information to [email protected]. If you fail to do so I will pick alternates.
Zero V : For this question: "Based off of the ability to manipulate the chemistry of steroids, and the ability to predict conversion of one hormone into another what can we expect in the future. I mean can we say every steroid ever is already drawn into a book, or based off of the understanding of anabolic androgenic steroids can we expect new creations in the future. As in a another way to tickle our androgen receptors maybe through advancements from current steroids into a chemical compound that can work like a steroids, but have less or side effects. "and for his comment regarding your stomach getting roid rage and that's why you get heartburn -- It still breaks me up.
Roadblock : For this question; "Why, since the tail end years of the heyday era of Duchaine and Philips, have the generally accepted and/or "published" dosage recommendations of aas steadily and consistently increased over previously considered very effective, safe and accepted amounts, now that we are in the present era of folks like Llewellyn and Rea? "
Cord195148 : For these two questions: "In reality, how similar is the final compound of a PH or DS to the targeted or advertised AAS? Both in structure, binding affinity, and effect? " and "How similar are the effects of a SARM to AAS on any given AR? How different? "
You guys have 1 week to email your shipping issue information to [email protected]. If you fail to do so I will pick alternates.
sethroberts
Active member
Don't worry, I got your email.
sethroberts
Active member
Very cool thread. I've put your book in my shopping cart to go along my next order.
Got some questions too, maybe your book covers it already then i'll read it in the near future
A) How do you feel about newer serms like raloxifene and toremifene? Everybody is always talking nolva but the newer serms seem more "safe" / "effective".
B) How do you feel about the companies stating to everybody who wants to hear it that their product CANNOT possibly cause gyno because it doesnt aromatise when there are different routes like lowering of shbg or estro rebound post cycle that cause gyno issues in lots of people.
C) Could you guesstimate how many actually do develop gyno because of cycling? I seen an increasing amount of "help gyno" threads/posts popping up the past years. Might be because of all the ds/phs being pushed by supplement companies and ease of access for the uneducated? Do you think the sermless pct advocates have a hand in this maybe? I think many go on cycle without a serm on hand because they read allover the plaxe that you can pct without serm just as effectively. Then gyno hits and they have to order nolva and wait for 2 weeks till it gets there..
Thanks a lot!
a) toremifene is better but more expensive. Not sure yet about raloxifene.
b) I think a lot of company owners don't know **** about the products they produce but they have to sound like they know everything or people will lose confidence and not buy their products.
c) That could be part of it but I think there is a good deal of gyno paranoia out there and a lot of people think they have gyno when they have a random inch in their nipple region. I do suspect that the use of AI's might also be responsible.
Zero V
Well-known member
OK thanks lol. I was just doing the math in my head. New email account+my luck+deadline=My life, which is usually not bueno :lol:
RoadBlocK
Well-known member
Now thats funny and true at the very same time:lol:
RoadBlocK
Well-known member
Ive got another question, while anxiously awaiting the arrival of your book. Whats your opinion/suggestion for or against the use of thyroid drugs, tricana, cytomel, levothyroxine, t3,t4,etc. on cycle with aas. Ofcourse theres lots of brolore about these drugs, but theoretically wouldn't one or more of these be truly beneficial or is the risk really more than what the benefits would/could be. Some guys will take anything, regardless of risk, and some are more cautious when considering the "known" warnings. Obviously, Im not asking you for prescribing information, and I know what Ive read, just wanted to see what your feeling were on the subject.
sethroberts
Active member
My apologies. I have been crushed by work lately but the books should be to you guys this week.
I am not a big fan of messing around with the thyroid system. It is just too important. If you mess up your nuts you will be unhappy but you will be alive and endogenous tests can more or less replicate natural production. The same is not necessarily true for the thyroid.
That being said, AAS do manipulate the throid system to some degree (as you will read in my book). Early on, many AAS will increase T3 uptake but over longer cycles, thyroid hormone production will be reduced. So, it might be worthwhile to supplement with small doses once this transition occurs. The big probem is that it might be difficult to determine.
RoadBlocK
Well-known member
Good points, I appreciate it.
One more if you have the time. Whats you take on formestane, topical or the oral currently out. Im more interested in side effects, and Im curious what the risk/benefit ratio might actually be, any toxicity, any effect on lipids, as well as so many of the purported uses, ie: on cycle, pct, stand alone high dose cycle, daily staple, trt cycles, etc. And what happens upon cessation, does your system crash, is there a viscous rebound, etc. Any thoughts would be appreciated.
One more if you have the time. Whats you take on formestane, topical or the oral currently out. Im more interested in side effects, and Im curious what the risk/benefit ratio might actually be, any toxicity, any effect on lipids, as well as so many of the purported uses, ie: on cycle, pct, stand alone high dose cycle, daily staple, trt cycles, etc. And what happens upon cessation, does your system crash, is there a viscous rebound, etc. Any thoughts would be appreciated.
Zero V
Well-known member
From my use of it, I love the fact it is a hell of a mood elevator for me. Currently playing with TD form made with penetrate.
Zero V
Well-known member
Heres more of an entertainment question
2 questions easy.
1: you can make a nasal spray for hormone absorption?
2: can you make a sublinqual test?
Also I remember people talking about old school andro poppers. Any one remember them?
Zero V
Well-known member
yes to both questions.
So technically you could make sublingual test tabs, carry around a dispenser of em, and take it as often as needed each day to make it equal to 400-500mg of Test a week?
aranoid: