Blood work and Estrogen

[AE1079]

Ok I need to point out that Drostanolone is not a SERM class drug as its unable to bind to estrogen sites which is what the literature says and ive never seen anything regarding its metabolites in the literature being of a SERM class. If there is literature on please post it as ive never seen it. It was through its mechanism of action via gene transcription and effect on certain proteins that it was used as treatment along with its ability to slow or even prevent the estrogen receptor growth in estrogen-mediated breast cancer. But there's certainly no binding to the ER.

Im assuming the definition high estradiol is above reference range. So 10-50 picograms. Let's take just testosterone first. The aromatase pool is finite. Once saturated, there can be no more conversion of T to E. This is why men can experience gyno or ED at 400mg T but don't suffer from it at 1500mg T. How high would estrogen be at 1500mg T? Probably maxed out as the literature shows 600mg of T yeilding 2-3 times normal estrogen range. Yet there will be no high estrogen side effects as the A:E ratio is sorted. We can do this with any AAS.

The point is that we can have high estrogen on paper, have an imbalance of A:E and symptoms there of, introduce non ARO androgens like anavar or masteron or jack T through the roof and see symptoms leave while blood serum estrogen is in the high range.

If that’s the case I think you should update your knowledge as of 2024, the literature is based off from mid 1990s, as the drug was produced in 1959. The original use was to prevent mast cells from proliferating.

Do you understand what you have just said?
You said you haven’t seen any metabolites cause E2BR activity, yet you say that its affects are through gene transcription. I am not here to give you a biology lesson brother, but have a look at how gene transcription actually works inside a cell. Have you studied any kind of human biology?
Or are you quickly reading off pubmed? Metabolism of a drug occurs way before it gets to gene transcription. Gene transcription occurs in the nucleus of a cell right? Before this, the drug is broken down through many different process through the organelles within a cell to get to the nucleus allowing gene transcription.. basic shit.
I’m sorry but your information seems really vague and not fully understood. Saying even its ability to slow estrogen or prevent estrogen related growth.. you do realise what you have said right? For this to happen, the drug needs to bind to receptor. In this case it’s the E2BR, things don’t magically just happen out of no where. There are different processes for all of these mechanisms to occur at a cellular level. Do you understand this basic biological function? I’m not trying to be rude but your argument isn’t adding up and seems like you’re pulling information from different sources without fully understanding or have stuided human biology at some point? I have literally sat down with books, as part of my curriculum and been examined on this topic.. I’m sorry man but it seems to me what your presenting is basic top line internet found information as it’s not adding up. I could be wrong, there’s just so many holes in your argument.

Now you have admitted then men suffer from Gyno and ED at higher levels of T.. which was the initial argument you are against.

“Im assuming the definition high estradiol is above reference range. So 10-50 picograms. Let's take just testosterone first. The aromatase pool is finite. Once saturated, there can be no more conversion of T to E. This is why men can experience gyno or ED at 400mg T but don't suffer from it at 1500mg T”

Whether maxing out T or E, Gyno is a causation of having high androgen load - particularly testosterone, which you respectfully disagreed with and now saying it happens at even levels of 400mg.


“The point is that we can have high estrogen on paper, have an imbalance of A:E and symptoms there of, introduce non ARO androgens like anavar or masteron or jack T through the roof and see symptoms leave while blood serum estrogen is in the high range”

Well you have now swayed the argument to a different topic all together, how to mitigate E2 sides by keeping a lid on it with extra drugs. We can talk about this to if you want? Not that I disagree with the use of Masteron, anavar though? No one will use Anavar for use to stabilise E2, it may help with lowering SHBG with people using lower doses of test? But e2 control?

Yeah we can have a Imbalance of T:E and people will get side effects based of individual response, but the intial cause of getting ED or Gyno is simple? Higher test = Higher E2 = Higher Prolactin = Aromatase activation = Gyno in predisposed genetic individuals. You have disagreed with this, it’s been proven above. What more evidence do you need ?

 

[AE1079]

Ok I need to point out that Drostanolone is not a SERM class drug as its unable to bind to estrogen sites which is what the literature says and ive never seen anything regarding its metabolites in the literature being of a SERM class. If there is literature on please post it as ive never seen it. It was through its mechanism of action via gene transcription and effect on certain proteins that it was used as treatment along with its ability to slow or even prevent the estrogen receptor growth in estrogen-mediated breast cancer. But there's certainly no binding to the ER.

Im assuming the definition high estradiol is above reference range. So 10-50 picograms. Let's take just testosterone first. The aromatase pool is finite. Once saturated, there can be no more conversion of T to E. This is why men can experience gyno or ED at 400mg T but don't suffer from it at 1500mg T. How high would estrogen be at 1500mg T? Probably maxed out as the literature shows 600mg of T yeilding 2-3 times normal estrogen range. Yet there will be no high estrogen side effects as the A:E ratio is sorted. We can do this with any AAS.

The point is that we can have high estrogen on paper, have an imbalance of A:E and symptoms there of, introduce non ARO androgens like anavar or masteron or jack T through the roof and see symptoms leave while blood serum estrogen is in the high range.

Apologies also if I have come across rude or condescending but there is no room for error when it comes to this information. I don’t claim to know everything but we are taking Extremely Basic Pharmacology and Biology. I have been in many group discussions around similar topics, there is way to many holes in your argument for me to consider your points. I can see a lack of basic understanding of basic human cell structure and the different processes that a drug goes through for it to reach its nucleus, let alone talk about transcription. I’m not trying to be rude, and I’m sure you’re a great bloke. I just think this argument is now pointless

 

[Jimboslice117]

Apologies also if I have come across rude or condescending but there is no room for error when it comes to this information. I don’t claim to know everything but we are taking Extremely Basic Pharmacology and Biology. I have been in many group discussions around similar topics, there is way to many holes in your argument for me to consider your points. I can see a lack of basic understanding of basic human cell structure and the different processes that a drug goes through for it to reach its nucleus, let alone talk about transcription. I’m not trying to be rude, and I’m sure you’re a great bloke. I just think this argument is now pointless

Not taking it as rude mate. I just don't see the hole where if we keep estrogen over the references range/high and we take androgens up to rebalance the A:E ratio to correct those effects. Like the cross section of an erection from the study that discusses the need to address the ratio rather than focus on one part of it. We can clearly see that high estrogen (over normal) combined with high T or androgens is the best outcome. Once one of those things is to low or to high relative to the other we see ED.

Prehaps i didnt make my position clear because I'm not blaming high/low T or high/low E. I'm blaming the cause on the imbalance of A:E ratio. I don't recall saying you can't have gyno with high a T level? You can have gyno if T level 2X physiological. All thay means is that the androgen to estrogen ratio is unbalanced and we can fix that with adding more androgens, which I know includes T or masteron or anavar. Anavar doesnt control estrogen here, it just contributes to the balancing of androgens to estrogens. Going through posts I don't see where I disagree that gyno can present with high T levels? I may not be stating my position clearly. I said initially "I would have to respectfully disagree on there being such a thing as high estrogen side effects such gynecomastia, erectile dysfunction etc based on the evidence at hand".
Gynecomastia is not a side effect of high estrogen because we can have estrogen 2x above the normal range, 100+, and have zero gyno if androgens are raised to match it, i.e if the A:E ratio is in check for that individual. I'm fine with the disagreement and a better way to to spend the time is what you said about using more drugs. I agree, if there's no need to ise more drugs then don't. Thats why I don't think AI or SERMs have a place while using AAS.

 

[AE1079]

This seems very Victor Black like. I get what you’re saying but you need to understand basic biological functions here. Im speaking from an indepth biological perspective, your claims are very top line and general. Which shows a lack of understanding in biology, again I’m not dissing you, but if you want to come to the table with this type of conversation I feel like you need to explain more then just spit out what a balance of e2 and T looks like in xzy setting. It’s too vague. If you can A. Explain to me why Masteron is not a SERM and explain its chemistry with its function and metabolism at a cellular level, I’m here for it.

Sure the variance of scale differs, and increase of E2 wether it’s 20-pmol or 100, someone may get gyno at the increase of 20 and others may get it further up the scale, which I explained before it’s based of individual responses, there is no argument here. But an increase can induce gyno, doesn’t matter how big or small, once you slide the scale to higher androgens, biological intervention shows in different ways. Honestly where else does gyno come from in the scenario of bodybuilding? Injecting air?

High E2 in males isn’t best, it needs to be in range. The function of Estrogen differs between male and female, sexually Bi-morphic. More isn’t better, but it needs to be in range, as the effects of high(er) E2 is not a great outcome we want. I can go through this in detail in another post and will post another write up on estrogen. Please don’t spew out to people that high e2 is preferable, not saying you are, but it’s not correct. We do need some for its protective actions against varied conditions, such as high ROS as an example. But we don’t need this out of range as it can be problematic in most males.

AIs were not invented for the use with steroids, they were prescribed to breast cancer patients. Not bodybuilders with estrogen problems. Can agree here. However it’s all we have, and it’s our best chance to mitigate side effects of increased E2 in the presence of androgens. There are many ways of going about this and using harm reduction techniques. There is no evidence of bodybuilders using these drugs in bodybuilding scenarios. There are too many variances. Hence we rely on information anecdotally, but a clear explanation and reasoning of use should be clearly explained and understood from a cellular level. As a coach it is your responsibility to balance a clients health. If you are raising androgens to counteract gyno, then how will that affect their health and serum markers? You can’t just increase dosages on dosages. Hence why we use different routes of treatment so we mitigate unwanted side effects. There’s an art of balance within the sport.

Your approach is a little reckless. I suggest rethinking it. Do some more research and learn. Don’t just listen to Victor Black or Boderick Chavez, literally get into the weeds of it. Understand biology and science, marry it with anecdotes and form a better solution. Because I can guarantee you, increasing androgens in certain individuals will create more problems down the line, when you could’ve resolved the issue with something less harmful and intended for use..

Again I apologise if I’m coming across rude but I need to remain objective with these conversations, you are mucking around with peoples hormones. You need to learn more.

 

[Jimboslice117]

This seems very Victor Black like. I get what you’re saying but you need to understand basic biological functions here. Im speaking from an indepth biological perspective, your claims are very top line and general. Which shows a lack of understanding in biology, again I’m not dissing you, but if you want to come to the table with this type of conversation I feel like you need to explain more then just spit out what a balance of e2 and T looks like in xzy setting. It’s too vague. If you can A. Explain to me why Masteron is not a SERM and explain its chemistry with its function and metabolism at a cellular level, I’m here for it.

Sure the variance of scale differs, and increase of E2 wether it’s 20-pmol or 100, someone may get gyno at the increase of 20 and others may get it further up the scale, which I explained before it’s based of individual responses, there is no argument here. But an increase can induce gyno, doesn’t matter how big or small, once you slide the scale to higher androgens, biological intervention shows in different ways. Honestly where else does gyno come from in the scenario of bodybuilding? Injecting air?

High E2 in males isn’t best, it needs to be in range. The function of Estrogen differs between male and female, sexually Bi-morphic. More isn’t better, but it needs to be in range, as the effects of high(er) E2 is not a great outcome we want. I can go through this in detail in another post and will post another write up on estrogen. Please don’t spew out to people that high e2 is preferable, not saying you are, but it’s not correct. We do need some for its protective actions against varied conditions, such as high ROS as an example. But we don’t need this out of range as it can be problematic in most males.

AIs were not invented for the use with steroids, they were prescribed to breast cancer patients. Not bodybuilders with estrogen problems. Can agree here. However it’s all we have, and it’s our best chance to mitigate side effects of increased E2 in the presence of androgens. There are many ways of going about this and using harm reduction techniques. There is no evidence of bodybuilders using these drugs in bodybuilding scenarios. There are too many variances. Hence we rely on information anecdotally, but a clear explanation and reasoning of use should be clearly explained and understood from a cellular level. As a coach it is your responsibility to balance a clients health. If you are raising androgens to counteract gyno, then how will that affect their health and serum markers? You can’t just increase dosages on dosages. Hence why we use different routes of treatment so we mitigate unwanted side effects. There’s an art of balance within the sport.

Your approach is a little reckless. I suggest rethinking it. Do some more research and learn. Don’t just listen to Victor Black or Boderick Chavez, literally get into the weeds of it. Understand biology and science, marry it with anecdotes and form a better solution. Because I can guarantee you, increasing androgens in certain individuals will create more problems down the line, when you could’ve resolved the issue with something less harmful and intended for use..

Again I apologise if I’m coming across rude but I need to remain objective with these conversations, you are mucking around with peoples hormones. You need to learn more.

No offence taken in any of this. To clarify where most of my thinking on the matter comes from, it comes from Dr Scott Howell, Dr Keith Nicholes and Dr Neil Rouzier. Dr Scott directed me to Victor Black as another credible source of this information although Dr Scott is the world's leader in androgen toxicity and has recently mapped out new forms of toxicity previously unknown. He's also used heavy doses before becoming an academic. So that should give some insight on the origin of my thoughts. My personal study has been on Evolutionary Endocrinology.

So I agree with you that as androgens raise, so does estrogen. This is theorised to have happened in vertebrae where androgen receptors and esteogen receptors co-evolved. This has to happen for the survival of the animal. As androgens increase, so does estrogen and this helps protect the organism from the harmful effects that an androgen dominant environment brings (heart enlargement for example). So yes we agree here that as androgens increase, so do estrogens...it simply has too.

However we now have androgens that do not aromatise or 5 alpha reduce, Masteron for example. Therefore we can artificially raise the androgen load without a corresponding estrogen rise. Now I understand your point of adding drugs to offset problems which end up creating more problems. However I need to frame the context of what I'm saying by raising androgens and leaving SERM and AI out of long term responsibile PED use being the better option, in my opinion.
Let's say we have a guy who needs 1000mg to grow. He can only tolerate 300mg of T until the A:E ratio becomes imbalanced. There are 2 options we have before us.

1. We take his testosterone up to 750mg or whatever higher number you want. We then add an AI (very standard practice) and we add in 250mg of masteron or Nadrolone or Primobolan and life is good and he grows.

2nd option is we leave testosterone at 300mg (where he can longer tolerate more without AI) and we add in 700mg masteron and life is good and he grows just the same. This option negates the need for AI or SERMs.

This is where we probably disconnect now. I'd say the second option is safer. The use of AI and SERMs brings health risks on their own, separate to the androgens. For one thing, we only need look at the autopsy reports of passed bodybuilders to see the effect AI and SERMs have had on the cardiac system. We see collagen infiltration of the myocardium and the purkinje fibers. This isn't from the Androgens, but rather, not enough estrogen binding to those areas to counteract. Lowering of estrogen artificially is also going to make lipid profile worse when paired with androgens. AIs also lower bone mineral density substantially. We see the effects of this without drugs in the rare aromatase deficiency disorder in men, the mutation in the CYP19A1 gene where men suffer loss in bone density, heart disease, bad lipids etc.

SERMs bring a substantial risk of thrombosis and pulmonary embolism. Layer these drugs on top androgen use where we already see lowering of LDL, a risk factor for thrombosis/stroke, high BMI, moderate to high blood pressure etc and were entering some dicey territory now.

Therefore I have to say that when total weekly dose is the same, adding in masteron is a lower risk option rather than adding another class of drug brining extra risks separate to the androgens.

 

[AE1079]

No offence taken in any of this. To clarify where most of my thinking on the matter comes from, it comes from Dr Scott Howell, Dr Keith Nicholes and Dr Neil Rouzier. Dr Scott directed me to Victor Black as another credible source of this information although Dr Scott is the world's leader in androgen toxicity and has recently mapped out new forms of toxicity previously unknown. He's also used heavy doses before becoming an academic. So that should give some insight on the origin of my thoughts. My personal study has been on Evolutionary Endocrinology.

So I agree with you that as androgens raise, so does estrogen. This is theorised to have happened in vertebrae where androgen receptors and esteogen receptors co-evolved. This has to happen for the survival of the animal. As androgens increase, so does estrogen and this helps protect the organism from the harmful effects that an androgen dominant environment brings (heart enlargement for example). So yes we agree here that as androgens increase, so do estrogens...it simply has too.

However we now have androgens that do not aromatise or 5 alpha reduce, Masteron for example. Therefore we can artificially raise the androgen load without a corresponding estrogen rise. Now I understand your point of adding drugs to offset problems which end up creating more problems. However I need to frame the context of what I'm saying by raising androgens and leaving SERM and AI out of long term responsibile PED use being the better option, in my opinion.
Let's say we have a guy who needs 1000mg to grow. He can only tolerate 300mg of T until the A:E ratio becomes imbalanced. There are 2 options we have before us.

1. We take his testosterone up to 750mg or whatever higher number you want. We then add an AI (very standard practice) and we add in 250mg of masteron or Nadrolone or Primobolan and life is good and he grows.

2nd option is we leave testosterone at 300mg (where he can longer tolerate more without AI) and we add in 700mg masteron and life is good and he grows just the same. This option negates the need for AI or SERMs.

This is where we probably disconnect now. I'd say the second option is safer. The use of AI and SERMs brings health risks on their own, separate to the androgens. For one thing, we only need look at the autopsy reports of passed bodybuilders to see the effect AI and SERMs have had on the cardiac system. We see collagen infiltration of the myocardium and the purkinje fibers. This isn't from the Androgens, but rather, not enough estrogen binding to those areas to counteract. Lowering of estrogen artificially is also going to make lipid profile worse when paired with androgens. AIs also lower bone mineral density substantially. We see the effects of this without drugs in the rare aromatase deficiency disorder in men, the mutation in the CYP19A1 gene where men suffer loss in bone density, heart disease, bad lipids etc.

SERMs bring a substantial risk of thrombosis and pulmonary embolism. Layer these drugs on top androgen use where we already see lowering of LDL, a risk factor for thrombosis/stroke, high BMI, moderate to high blood pressure etc and were entering some dicey territory now.

Therefore I have to say that when total weekly dose is the same, adding in masteron is a lower risk option rather than adding another class of drug brining extra risks separate to the androgens.

Pretty much is how people should plan their cycles out, this is the approach I use with health markers and tolerance in mind, you obviously won’t give Primobolan to someone I has high liver enzymes, or deca to someone with high BP so there’s careful considerations before filling out the load with different compounds. We use Test for a E2 base to allow IGF-1 to convert from HGH, we supplement this with anabolics to allow new tissue to grow which was created from donated Nuclei. I just feel that as a coach it’s important to go into more in depth. Then I suppose copy from base models and practises. Learning Biology, Pharmacology and even Organic Chemistry helps with this understanding, which I think is important to the bigger picture.

With masteron yes, it’s a good way to fill out the load, all of this is Victor Black J3U methodology. It’s becoming more common as people are getting into the know of harm reduction.

Yes this is all correct bro nothing new in relation to AIs, Serms ect, not disagreeing with the methodology of building cycles. The cascading effects mentioned from high E2 levels is men is all correct and it’s what J3U, Victor Black all teach. I have gone into their material as I went through the entire courses and what you are saying correlates to what they say in the courses and videos and dare say referenced.

We have completely strayed away from the initial argument of what the initial discussion of High E2 is not the cause of Gyno or ED now, whether you feel like you still stand correct on this is your prerogative

 

[LevButlerov]

Pretty much is how people should plan their cycles out, this is the approach I use with health markers and tolerance in mind, you obviously won’t give Primobolan to someone I has high liver enzymes, or deca to someone with high BP so there’s careful considerations before filling out the load with different compounds. We use Test for a E2 base to allow IGF-1 to convert from HGH, we supplement this with anabolics to allow new tissue to grow which was created from donated Nuclei. I just feel that as a coach it’s important to go into more in depth. Then I suppose copy from base models and practises. Learning Biology, Pharmacology and even Organic Chemistry helps with this understanding, which I think is important to the bigger picture.

With masteron yes, it’s a good way to fill out the load, all of this is Victor Black J3U methodology. It’s becoming more common as people are getting into the know of harm reduction.

Yes this is all correct bro nothing new in relation to AIs, Serms ect, not disagreeing with the methodology of building cycles. The cascading effects mentioned from high E2 levels is men is all correct and it’s what J3U, Victor Black all teach. I have gone into their material as I went through the entire courses and what you are saying correlates to what they say in the courses and videos and dare say referenced.

We have completely strayed away from the initial argument of what the initial discussion of High E2 is not the cause of Gyno or ED now, whether you feel like you still stand correct on this is your prerogative

@Jimboslice117 To be fair I think this conversation has gone away from the argument.
"high estrogen doesn't cause gyno" was the topic here. I think @AE1079 laid his case out perfect.

 

[Jimboslice117]

@Jimboslice117 To be fair I think this conversation has gone away from the argument.
"high estrogen doesn't cause gyno" was the topic here. I think @AE1079 laid his case out perfect.

@Jimboslice117 To be fair I think this conversation has gone away from the argument.
"high estrogen doesn't cause gyno" was the topic here. I think @AE1079 laid his case out perfect.

I think we just agree to disagree on it as I still firmly believe the imbalance of A: E ratio is the cause, as an individual can still have high E (out of normal range) and not have any of the blamed side effects of it, like gyno *IF* androgens are also increased accordingly.



The important thing which should overshadow the disagreement is how we modulate that ratio/manipulate estrogen for safer use reasons. That's to say, remove AI and SERM use (for the already stated dangers they bring to the enhanced men above) and work with whatever total androgen load you need by using the right amount of testosterone that you as an individual can tolerate without blocking aromatase or estrogen and fill in the rest with another non aromatising androgen or one that converts very little like nandrolone, dependant on the individuals response of course to compound selection.



I'm totally happy for someone to believe that gyno, ED and high blood pressure are directly caused by an above normal estrogen range, so long as they avoid the unnecessary risk of using AI and SERMs. We already engage is risky behaviours and we don't need to be adding extra drugs that offer no therapeutic benefits while adding to bad lipid profile, increasing likelihood of thrombosis/stroke, heart disease, loss of bone mineral density and lessening the protective effects of estrogen on the tissues of the heart, brain and kidneys

 

[AE1079]

You just said it your self, the imbalanced ratio of A:E is the cause, most of the time it’s the imbalance of E2 being higher then it was pre-gyno.. IN predisposed men.
Have High E and not get gyno, as I said before bro, if you are lacking a aromatase gene and do not have a high binding to E2 Receptors you will not get gyno. You’re still talking top line explanations? Everyone is different and are going to react to different treatments.

Yes your second line is now what a lot of people are doing now thanks to Victor Black and J3U who mainstreamed the safer use. But mate, when you have symptoms of gyno, they need to be treated. Whether you use a lower androgen load, more frequent dosing, SERM use or a AI. Something needs to happen. You can’t copy and paste Victor Blacks models to every individual, this where Experience and anecdote comes in. We as coaches need to be fluid and not rigid in our approach, however have a sound knowledge of basic biology and pharmacology at the very least.

And you do know bro we can mitigate the effects of the following diseases with simply manipulating diet, cardio and other lifestyle factors and not rely on pharmaceuticals..

 

[Jimboslice117]

You just said it your self, the imbalanced ratio of A:E is the cause, most of the time it’s the imbalance of E2 being higher then it was pre-gyno.. IN predisposed men.
Have High E and not get gyno, as I said before bro, if you are lacking a aromatase gene and do not have a high binding to E2 Receptors you will not get gyno. You’re still talking top line explanations? Everyone is different and are going to react to different treatments.

Yes your second line is now what a lot of people are doing now thanks to Victor Black and J3U who mainstreamed the safer use. But mate, when you have symptoms of gyno, they need to be treated. Whether you use a lower androgen load, more frequent dosing, SERM use or a AI. Something needs to happen. You can’t copy and paste Victor Blacks models to every individual, this where Experience and anecdote comes in. We as coaches need to be fluid and not rigid in our approach, however have a sound knowledge of basic biology and pharmacology at the very least.

And you do know bro we can mitigate the effects of the following diseases with simply manipulating diet, cardio and other lifestyle factors and not rely on pharmaceuticals..

No i agree here. Nothing wrong with attacking existing gyno with AI and SERM if it hasn't become fibrotic. A treatment like that isn't going give you a stroke or heart disease and the user can make the adjustments to testosterone knowing what dose skews the A:E ratio for him. Rather I don't like to see men take AI and SERMs in their weekly protocol in the expectation or fear of gyno. My experience as a coach over 17 years has taught me that the only time to bring out the AI and SERMs is for gyno treatment and for planned pregnancy although not always the case. But they're never there in the cycle design. As for Victor's model, it simply appealed to what I already felt to be true and Dr Scott has assured me I'm on the right path as far as client safety is concerned.



As for your rigidity concerns, I feel like there's plenty of flexibility for client preferences regarding compound selection.

 

[AE1079]

No i agree here. Nothing wrong with attacking existing gyno with AI and SERM if it hasn't become fibrotic. A treatment like that isn't going give you a stroke or heart disease and the user can make the adjustments to testosterone knowing what dose skews the A:E ratio for him. Rather I don't like to see men take AI and SERMs in their weekly protocol in the expectation or fear of gyno. My experience as a coach over 17 years has taught me that the only time to bring out the AI and SERMs is for gyno treatment and for planned pregnancy although not always the case. But they're never there in the cycle design. As for Victor's model, it simply appealed to what I already felt to be true and Dr Scott has assured me I'm on the right path as far as client safety is concerned.



As for your rigidity concerns, I feel like there's plenty of flexibility for client preferences regarding compound selection.

Good stuff mate. Keep learning