Stacking too many from the same "family"

[Deleted member 123722]

A few things I began practicing in regards to gear was no orals, and making sure I cover every "angle" during my cycles; taking a test, 19-nor, and a DHT drug.; it's why I do my Test/Deca/Primo to bulk, and now I'm currently on Test/Tren E/ Primo to cut.

Is it stupid or overkill to take, lets say, several DHTs at once: Suppose I dropped the Tren E, and made my cycle Test/Primo/Winny or Test/Primo/Var? Is having two DHT's just unnecessary?

Or if I went really nuts and did test/tren/primo/winny or var.

Not saying that I will, but I want to understand logic behind covering all the "families" of gear, and debunk any myths in regards of taking too much of one type.

Thanks.

 

[Cohiba]

I'm interested to hear from some more knowledgeable people on this topic as well.

I kind of do the same thing, test+dht+19-nor. So for example if I'm running anavar, I'll drop the mast I usually run while on it.

I plan to try tren one day, and I won't do it while on deca. I've read some stuff about androgen receptor binding affinity, and from what I remember it seems like there is not much use in running things that bind weaker when you have a stronger binging compound?

 

[T&H]

A few things I began practicing in regards to gear was no orals, and making sure I cover every "angle" during my cycles; taking a test, 19-nor, and a DHT drug.; it's why I do my Test/Deca/Primo to bulk, and now I'm currently on Test/Tren E/ Primo to cut.

Is it stupid or overkill to take, lets say, several DHTs at once: Suppose I dropped the Tren E, and made my cycle Test/Primo/Winny or Test/Primo/Var? Is having two DHT's just unnecessary?

Or if I went really nuts and did test/tren/primo/winny or var.

Not saying that I will, but I want to understand logic behind covering all the "families" of gear, and debunk any myths in regards of taking too much of one type.

Thanks.

Where Is your "logic" of covering every angle regarding AAS use even coming from? Please don't say some video found on YouTube. Would also love to hear some of these myths from too much of one type as well.

I mean, I don't read a lot but this is the first I'm hearing. I stick to what many would call DHT AAS such as Primo, Mast, Anavar, and Anadrol. And I've had no issues putting on size when I was specifically using high enough doses, eating, and training to gain size.

 

[Deleted member 123722]

Where Is your "logic" of covering every angle regarding AAS use even coming from? Please don't say some video found on YouTube. Would also love to hear some of these myths from too much of one type as well.

I mean, I don't read a lot but this is the first I'm hearing. I stick to what many would call DHT AAS such as Primo, Mast, Anavar, and Anadrol. And I've had no issues putting on size when I was specifically using high enough doses, eating, and training to gain size.

I picked it up from Broderick Chavez; not that he recommended it, per se, but when he explained what each does, it made sense to combine them all, as they all do different things.

 

[Nolij]

Every AAS does the same thing, increase protein synthesis.

they do it in different mechanism but same pathway.

Even though a DHT is similar, it doesn’t mean they don't work differently in your body.

Take tren for an example, is it the same as deca?

So yes, you can stack the same compounds.

Test Deca and primo is one of my fav cycles

 

[Cohiba]

I stick to what many would call DHT AAS such as Primo, Mast, Anavar, and Anadrol.

Can you elaborate on that? In other words, what do these cycles look like for you in terms of dosages/lengths/drug combinations?

Is there a reason you avoid 19-nors?

 

[Deleted member 123722]

Every AAS does the same thing, increase protein synthesis.

they do it in different mechanism but same pathway.

Even though a DHT is similar, it doesn’t mean they don't work differently in your body.

Take tren for an example, is it the same as deca?

So yes, you can stack the same compounds.

Test Deca and primo is one of my fav cycles

Right, but if IIRC, the pathways cause different effects: some "volumize" with those "wet gains" other give those "dry gains"; others "harden"; others increase strength.

If they all did exactly the same thing, then why wouldn't we just take one?

 

[narta]

Total aas burden is much more important than individual AAS that are being used. That said, every steroid has its unique effects.

There are the test/eq/deca cycles as there are test/deca/tren.

It all comes down to individual response to the compounds used

 

[Nolij]

Right, but if IIRC, the pathways cause different effects: some "volumize" with those "wet gains" other give those "dry gains"; others "harden"; others increase strength.

If they all did exactly the s thing, then why wouldn't we just take one?

Exactly, so I think what you’re doing is a good idea.. that’s my opinion.

I wouldn’t add more to your cycle though. I would find what my body likes and go with it
For example, my body loves Deca and NPP, doesn’t like tren E recently, hates EQ.. so I’d stick to whatever is giving you the best gains with minimal sides

What would John Jewett do?
Increase food, then increase intensity and weights, then increase dose..

 

[Deleted member 123722]

Exactly, so I think what you’re doing is a good idea.. that’s my opinion.

I wouldn’t add more to your cycle though. I would find what my body likes and go with it
For example, my body loves Deca and NPP, doesn’t like tren E recently, hates EQ.. so I’d stick to whatever is giving you the best gains with minimal sides

What would John Jewett do?
Increase food, then increase intensity and weights, then increase dose..

Yep.

I get no sides, so I can't complain.

Right now I'm in a cut, so I'm just maintaining.

 

[Type-IIx]

The broscience "DHT derivative-testosterone derivative--19-nor-testosterone derivative" model is replete with misclassifications, and does not hold up under basic scrutiny.

My impression is that it's a well-intentioned, but inadequately informed, attempt at classification by biological effects (aesthetics) or a qualitative grouping for practical bodybuilding use.

If it is correct, then we should straightforwardly be able to choose exactly one compound from each group and end up with a perfectly fine cycle, right?

So, select the following from each group:

1. MENT

2. Dianabol

3. Anadrol

Good cycle?

Or, let's go through and think about the following items:

1. Trenbolone, from the 19-nortestosterone group (bulking compounds, presumably). Is trenbolone qualitatively like Deca, with respect to aesthetic results? I think not. Trenbolone is a potently androgenic hardening/drying compound that does not aromatize. Deca is a bulking compound that does aromatize. It doesn't belong in this group.

2. Turinabol, from the testosterone group (base compounds, presumably). Turinabol is a nonaromatizable, non-5α-reducible, attenuated (very weak) androgen, quite unlike testosterone. Turinabol is great for women; what about Halotestin? It doesn't belong in this group.

3. Anadrol, from the DHT derivative group (dry compounds, presumably), is itself virtually inactive as an AR ligand and likely acts primarily as a prohormone to 17α-methyl-5α-androstane-3α,17β-diol. This active drug, 17α-methyl-5α-androstane-3α,17β-diol, is a good ligand for not only the AR, but also ER -α (associated with fluid retention, lipid, bone metabolism) & -β (involved in muscle remodeling, and is the primary mechanism by which ecdysterone & turkesterone induce muscle anabolism when they are continuously infused). Is Anadrol a dry compound like any of the others? It doesn't belong in this group.

Since this framework breaks down so readily under any scrutiny whatsoever, it should be confined to the dustbin of bad broscience.

 

[Deleted member 123722]

The broscience "DHT derivative-testosterone derivative--19-nor-testosterone derivative" model is replete with misclassifications, and does not hold up under basic scrutiny.

My impression is that it's a well-intentioned, but inadequately informed, attempt at classification by biological effects (aesthetics) or a qualitative grouping for practical bodybuilding use.

If it is correct, then we should straightforwardly be able to choose exactly one compound from each group and end up with a perfectly fine cycle, right?

So, select the following from each group:

1. MENT

2. Dianabol

3. Anadrol

Good cycle?

Or, let's go through and think about the following items:

1. Trenbolone, from the 19-nortestosterone group (bulking compounds, presumably). Is trenbolone qualitatively like Deca, with respect to aesthetic results? I think not. Trenbolone is a potently androgenic hardening/drying compound that does not aromatize. Deca is a bulking compound that does aromatize. It doesn't belong in this group.

2. Turinabol, from the testosterone group (base compounds, presumably). Turinabol is a nonaromatizable, non-5α-reducible, attenuated (very weak) androgen, quite unlike testosterone. Turinabol is great for women; what about Halotestin? It doesn't belong in this group.

3. Anadrol, from the DHT derivative group (dry compounds, presumably), is itself virtually inactive as an AR ligand and likely acts primarily as a prohormone to 17α-methyl-5α-androstane-3α,17β-diol. This active drug, 17α-methyl-5α-androstane-3α,17β-diol, is a good ligand for not only the AR, but also ER -α (associated with fluid retention, lipid, bone metabolism) & -β (involved in muscle remodeling, and is the primary mechanism by which ecdysterone & turkesterone induce muscle anabolism when they are continuously infused). Is Anadrol a dry compound like any of the others? It doesn't belong in this group.

Since this framework breaks down so readily under any scrutiny whatsoever, it should be confined to the dustbin of bad broscience.

Suppose we put them in categories "wet gains" (aromatizing) and "dry gains" (non-aromatizing) then would it be unnecessary to run Test, Primo, Var, since both Var and Primo are the same "dry gain" group? Or does it just make more sense to take more of one drug with the effect you want?

This is assuming of course, these drugs don't affect you negatively. Obvious, if drug X from the same group causes negative sides and drug Y doesn't, then you wouldn't take X.

But here I'm trying to see if it is just people stacking things based on a drugs reputation, but are just doing more of the same thing. One guy at the gym told me he was taking Test, Tren, Winny and Var, and I'm like why both var and winny?

Like even with training, I'll see someone do Bench, incline, then do the same movements with dumbbells or machines, and its jus redundant in my view.

Do you see what I mean?

 

[GuerillaPete]

Suppose we put them in categories "wet gains" (aromatizing) and "dry gains" (non-aromatizing) then would it be unnecessary to run Test, Primo, Var, since both Var and Primo are the same "dry gain" group? Or does it just make more sense to take more of one drug with the effect you want?

This is assuming of course, these drugs don't affect you negatively. Obvious, if drug X from the same group causes negative sides and drug Y doesn't, then you wouldn't take X.

But here I'm trying to see if it is just people stacking things based on a drugs reputation, but are just doing more of the same thing. One guy at the gym told me he was taking Test, Tren, Winny and Var, and I'm like why both var and winny?

Like even with training, I'll see someone do Bench, incline, then do the same movements with dumbbells or machines, and its jus redundant in my view.

Do you see what I mean?

What about someone taking primo/mast with testosterone for the reason that Primo kills his estrogen so he goes 50/50 primo mast so that he is in the right place estrogen and and anabolic wise .
In this case it would make sense .
Adding winstrol a couple of weeks at the end of a cut to sharpen the edges lose some water.
I think this also makes sense.
Running two orals full dose a whole cycle that does not make much sense to me.
So i think it depends on the situation if its good to mix them or not.
Also test/deca/mast or primo this are combinations that work and have worked so i think that is why we use them.
More steroids with less sides than just Testosterone for must guys at least.

 

[lukiss96]

What about someone taking primo/mast with testosterone for the reason that Primo kills his estrogen so he goes 50/50 primo mast so that he is in the right place estrogen and and anabolic wise .
In this case it would make sense .
Adding winstrol a couple of weeks at the end of a cut to sharpen the edges lose some water.
I think this also makes sense.
Running two orals full dose a whole cycle that does not make much sense to me.
So i think it depends on the situation if its good to mix them or not.
Also test/deca/mast or primo this are combinations that work and have worked so i think that is why we use them.
More steroids with less sides than just Testosterone for must guys at least.

Isn't it about what you as an individual can tolerate the best? While I can agree that most would probably love such cycle you mentioned, some would be just fine without mast or primo, but rather add in something else for more horsepower and using adex. I know you prefer a bit of an AI rather than dhts to try and bring down estrogen, or at least you used to prefer that.

Two oral stacking is pretty interesting, I have tried doing so, because I'm the type of person who loves to experiment. I find some stacks like dbol and anadrol really work together and make each other shine more. Annother one I quite liked is anavar/winstrol combo, the look you get is quite cool. Although, for a full cycle length not really, I usually only do it for 3 or 4 weeks towards the end of cycle.

More steroids with less sides than just Testosterone for must guys at least.

Interesting thing here is that when Testosterone is used solo, side effects of very high dosages seem easily manageable. So of course individual tolerance, but for me at least taking it solo at above 1g mark I actually feel even better than stacking, blood work is actually pretty damn good considering the amount. Only things to control are blood pressure and of course estrogen, but the latter is not as difficult as it seems at such dosages.

 

[GuerillaPete]

Isn't it about what you as an individual can tolerate the best? While I can agree that most would probably love such cycle you mentioned, some would be just fine without mast or primo, but rather add in something else for more horsepower and using adex. I know you prefer a bit of an AI rather than dhts to try and bring down estrogen, or at least you used to prefer that.

Two oral stacking is pretty interesting, I have tried doing so, because I'm the type of person who loves to experiment. I find some stacks like dbol and anadrol really work together and make each other shine more. Annother one I quite liked is anavar/winstrol combo, the look you get is quite cool. Although, for a full cycle length not really, I usually only do it for 3 or 4 weeks towards the end of cycle.


Interesting thing here is that when Testosterone is used solo, side effects of very high dosages seem easily manageable. So of course individual tolerance, but for me at least taking it solo at above 1g mark I actually feel even better than stacking, blood work is actually pretty damn good considering the amount. Only things to control are blood pressure and of course estrogen, but the latter is not as difficult as it seems at such dosages.

I know what you mean and i also feel good on higher test!
I was entertaining a imaginary scenario where it would make sense to combine two DHT derivates and get a possitive and productive result.
As others have said all steroids do basically the same thing but they also have unique effects that can be used in some scenarios that are in your advantage .
And there are occasions when staking two of the same class would be a good idea.
There are guys running just Test and make good progress .
Most guys swear by the 3grams+ test cycle and i believe them.
But its 3 grams you would grow on Test/deca/mast at 1 gram each also .
Anyways with all the deaths recently and the vaX maybe using lower dosages for non competitors seems like a better road to follow.

 

[lukiss96]

I know what you mean and i also feel good on higher test!
I was entertaining a imaginary scenario where it would make sense to combine two DHT derivates and get a possitive and productive result.
As others have said all steroids do basically the same thing but they also have unique effects that can be used in some scenarios that are in your advantage .
And there are occasions when staking two of the same class would be a good idea.
There are guys running just Test and make good progress .
Most guys swear by the 3grams+ test cycle and i believe them.
But its 3 grams you would grow on Test/deca/mast at 1 gram each also .
Anyways with all the deaths recently and the vaX maybe using lower dosages for non competitors seems like a better road to follow.

Totally agree man

 

[Type-IIx]

Suppose we put them in categories "wet gains" (aromatizing) and "dry gains" (non-aromatizing) then would it be unnecessary to run Test, Primo, Var, since both Var and Primo are the same "dry gain" group? Or does it just make more sense to take more of one drug with the effect you want?

This is assuming of course, these drugs don't affect you negatively. Obvious, if drug X from the same group causes negative sides and drug Y doesn't, then you wouldn't take X.

But here I'm trying to see if it is just people stacking things based on a drugs reputation, but are just doing more of the same thing. One guy at the gym told me he was taking Test, Tren, Winny and Var, and I'm like why both var and winny?

Like even with training, I'll see someone do Bench, incline, then do the same movements with dumbbells or machines, and its jus redundant in my view.

Do you see what I mean?

Yes, I know what you mean about these redundancies.

Certainly, I think that it's more useful to group AAS into aromatizable vs. nonaromatizable than this broscience model.

It's even more useful to learn the unique biological effects particular to each AAS to understand which features can combine favorably. Favorable combinations can be grouped into those that are synergistic (greater than additive; 1 + 1 > 2), complementary (opposite, such that combination yields a "middling out" of behavior; 1 + -1 = 0), or merely additive (everything else; 1 + 1 = 2).

Synergistic combinations are those that bring about a biological effect (e.g., muscle accrual) that is the result of multiple mechanisms (e.g., anticatabolism & protein synthesis, etc.) and/or pathways (e.g., MuRF1 & atrogin-1 vs. GR expression, WISP-2 vs. IGF-IEb activity, etc.) by different mechanisms and/or pathways, resulting in a greater than additive effects.
* Total AAS dose does not reflect effects where synergistic combinations are used.
* A higher # of AAS used, if synergistic, would be expected to be less harmful & healthier than just ramping up total AAS dose of merely additive AAS combinations where it is used to reduce total AAS dose.
* Indeed, that is borne out by the HAARLEM trial data. There was a positive correlation between AAS weekly dose & LV mass, intraventricular end-diastolic septal thickness, and left ventricular end-diastolic posterior wall thickness & AAS dose was negatively correlated with E/e' septal. The # of AAS used was negatively associated (so more compounds means lower values of) left ventricular end-diastolic volume 3D & left ventricular end-systolic volume 3D (mL) post-cycle. Conversely, combination of rhGH & AAS resulted in higher eft ventricular end-diastolic volume 3D & left ventricular end-systolic volume 3D (mL) post-cycle.

Complementary combinations are those for which each effect acts in opposition to the other, such that their combination results in a "middling out" of behavior. For example, aromatizable & nonaromatizable androgen, combined appropriately, will result in neither net antiestrogenic nor estrogenic effects, such that tolerability is maintained. For example, combination of AAS to modulate the comfort of joints ("dry" + "wet" = robust).

Additive combinations are the remainder - everything else. These are the result of similar effects between AAS, acting via the same mechanisms and/or pathways. Total dose (mg/week) reflects biological effects of combinations of AAS whose features are basically identical or functionally equivalent, and is a rough proxy for systemic effects after factoring in AR potency.

Important Factors that Affect Total AAS Dose (mg/week) as a Proxy for Systemic or Tissue-Level Effects

Appropriateness of mg/week as a unit of measure
Rather than weekly dose as mg/week, dose as time × fAUC, e.g., in units 168 h fAUC (nmol h/L), more adequately describes biological effects.

The dose/response curve (total AAS dose vs. LBM)


If AR is the sole mode of AAS action, AAS logarithmic dose/response curve should be S-shaped meaning that this dose/response would be plotted as a curve flat at both high & low doses & approximately linear at moderate doses... but for doses 100 - 1,000 mg/wk, the graph remains linear (the assumed nonlinear portion indicated by an asterisk in the above graph was indicated by a comment that this was not actually shown by the results).

AR Regulation
In skeletal muscle, AR density is ~ 3 nM/kg. A mere 2.5 mg oxandrolone tablet provides ~ 8,000 nM androgen. Since the AR must form dimers (before translation of AR-associated mRNA) & together bind 1 mol AAS, then if, hypothetically, 100 mg T binds 71% AR, then the square of the % reflects AR activation (i.e., 50% activation).

But this is still insufficient to explain the difference between this AAS vs. LBM dose/response curve vis-à-vis different combinations ("stacks") of AAS.

Factors that regulate AR include:
* AAS dose (increasing doses of AAS increases the # of AR in skeletal muscle)
* Increased translational capacity (increased AR mRNA synthesis by increased ribosomal biogenesis)

Non-AR Mechanisms
These include, nonexhaustively:
* tethering to other transcription factors thereby influencing expression of genes without response elements in their promoters
* engaging signal transduction pathways (e.g., PI3K/Akt, IGF-I, etc.) including activation of protein kinases, thereby modulating cellular responses to androgens
* cell surface membrane-bound receptors (e.g., GPCRs) that typically modulate, e.g., Ca²⁺ uptake
* non-ligand-dependent mechanisms

Illustration of IGF-I-mediated anabolism (a non-ligand-dependent mechanism)
Consider the non-ligand-dependent IGF-I-mediated anabolism of androgen (e.g., Testosterone), due in (small) part to aromatization and in (large) part to local muscle activity of IGF-I isoforms.

Mediated centrally (lack of AR in CNS reduces serum IGF-I) & by aromatization, Testosterone increases GH secretion, thereby increasing sytemic/circulating IGF-I (liver-secreted). This circulating GH & IGF-I plays only a minor role in AAS anabolism. Local IGF-I activity in skeletal muscle (mIGF-I) is more important.
* Testosterone increases muscle IGF-I activity more than Trenbolone, but Trenbolone increases satellite cell responsiveness to muscle IGF-I dramatically (doing more with less).
Human skeletal muscle expresses 2 IGF-I splice variants:
* IGF-IEa (similar to systemic/circulating IGF-I, liver-secreted); increases myoblast differentiation to myotubes (lesser effect on proliferation)
* IGF-IEc (MGF): mechanosensitive muscular IGF-I isoform; stimulates proliferation and inhibits terminal differentiation.

IGF-I stimulation of muscle mass relies on increased MPS (muscle protein synthesis) & myogenesis (muscle regeneration, as opposed to remodeling) & decreased proteolysis (protein breakdown) & apoptosis (cell death).
________________
Can you see how this post describes briefly, but sufficiently, some reasons that combinations of testosterone, trenbolone, and resistance training, are predictably synergistic (greater than additive) in muscle anabolism?

 

[Deleted member 123722]

Yes, I know what you mean about these redundancies.

Certainly, I think that it's more useful to group AAS into aromatizable vs. nonaromatizable than this broscience model.

It's even more useful to learn the unique biological effects particular to each AAS to understand which features can combine favorably. Favorable combinations can be grouped into those that are synergistic (greater than additive; 1 + 1 > 2), complementary (opposite, such that combination yields a "middling out" of behavior; 1 + -1 = 0), or merely additive (everything else; 1 + 1 = 2).

Synergistic combinations are those that bring about a biological effect (e.g., muscle accrual) that is the result of multiple mechanisms (e.g., anticatabolism & protein synthesis, etc.) and/or pathways (e.g., MuRF1 & atrogin-1 vs. GR expression, WISP-2 vs. IGF-IEb activity, etc.) by different mechanisms and/or pathways, resulting in a greater than additive effects.
* Total AAS dose does not reflect effects where synergistic combinations are used.
* A higher # of AAS used, if synergistic, would be expected to be less harmful & healthier than just ramping up total AAS dose of merely additive AAS combinations where it is used to reduce total AAS dose.
* Indeed, that is borne out by the HAARLEM trial data. There was a positive correlation between AAS weekly dose & LV mass, intraventricular end-diastolic septal thickness, and left ventricular end-diastolic posterior wall thickness & AAS dose was negatively correlated with E/e' septal. The # of AAS used was negatively associated (so more compounds means lower values of) left ventricular end-diastolic volume 3D & left ventricular end-systolic volume 3D (mL) post-cycle. Conversely, combination of rhGH & AAS resulted in higher eft ventricular end-diastolic volume 3D & left ventricular end-systolic volume 3D (mL) post-cycle.

Complementary combinations are those for which each effect acts in opposition to the other, such that their combination results in a "middling out" of behavior. For example, aromatizable & nonaromatizable androgen, combined appropriately, will result in neither net antiestrogenic nor estrogenic effects, such that tolerability is maintained. For example, combination of AAS to modulate the comfort of joints ("dry" + "wet" = robust).

Additive combinations are the remainder - everything else. These are the result of similar effects between AAS, acting via the same mechanisms and/or pathways. Total dose (mg/week) reflects biological effects of combinations of AAS whose features are basically identical or functionally equivalent, and is a rough proxy for systemic effects after factoring in AR potency.

Important Factors that Affect Total AAS Dose (mg/week) as a Proxy for Systemic or Tissue-Level Effects

Appropriateness of mg/week as a unit of measure
Rather than weekly dose as mg/week, dose as time × fAUC, e.g., in units 168 h fAUC (nmol h/L), more adequately describes biological effects.

The dose/response curve (total AAS dose vs. LBM)
View attachment 261067

If AR is the sole mode of AAS action, AAS logarithmic dose/response curve should be S-shaped meaning that this dose/response would be plotted as a curve flat at both high & low doses & approximately linear at moderate doses... but for doses 100 - 1,000 mg/wk, the graph remains linear (the assumed nonlinear portion indicated by an asterisk in the above graph was indicated by a comment that this was not actually shown by the results).

AR Regulation
In skeletal muscle, AR density is ~ 3 nM/kg. A mere 2.5 mg oxandrolone tablet provides ~ 8,000 nM androgen. Since the AR must form dimers (before translation of AR-associated mRNA) & together bind 1 mol AAS, then if, hypothetically, 100 mg T binds 71% AR, then the square of the % reflects AR activation (i.e., 50% activation).

But this is still insufficient to explain the difference between this AAS vs. LBM dose/response curve vis-à-vis different combinations ("stacks") of AAS.

Factors that regulate AR include:
* AAS dose (increasing doses of AAS increases the # of AR in skeletal muscle)
* Increased translational capacity (increased AR mRNA synthesis by increased ribosomal biogenesis)

Non-AR Mechanisms
These include, nonexhaustively:
* tethering to other transcription factors thereby influencing expression of genes without response elements in their promoters
* engaging signal transduction pathways (e.g., PI3K/Akt, IGF-I, etc.) including activation of protein kinases, thereby modulating cellular responses to androgens
* cell surface membrane-bound receptors (e.g., GPCRs) that typically modulate, e.g., Ca²⁺ uptake
* non-ligand-dependent mechanisms

Illustration of IGF-I-mediated anabolism (a non-ligand-dependent mechanism)
Consider the non-ligand-dependent IGF-I-mediated anabolism of androgen (e.g., Testosterone), due in (small) part to aromatization and in (large) part to local muscle activity of IGF-I isoforms.

Mediated centrally (lack of AR in CNS reduces serum IGF-I) & by aromatization, Testosterone increases GH secretion, thereby increasing sytemic/circulating IGF-I (liver-secreted). This circulating GH & IGF-I plays only a minor role in AAS anabolism. Local IGF-I activity in skeletal muscle (mIGF-I) is more important.
* Testosterone increases muscle IGF-I activity more than Trenbolone, but Trenbolone increases satellite cell responsiveness to muscle IGF-I dramatically (doing more with less).
Human skeletal muscle expresses 2 IGF-I splice variants:
* IGF-IEa (similar to systemic/circulating IGF-I, liver-secreted); increases myoblast differentiation to myotubes (lesser effect on proliferation)
* IGF-IEc (MGF): mechanosensitive muscular IGF-I isoform; stimulates proliferation and inhibits terminal differentiation.

IGF-I stimulation of muscle mass relies on increased MPS (muscle protein synthesis) & myogenesis (muscle regeneration, as opposed to remodeling) & decreased proteolysis (protein breakdown) & apoptosis (cell death).
________________
Can you see how this post describes briefly, but sufficiently, some reasons that combinations of testosterone, trenbolone, and resistance training, are predictably synergistic (greater than additive) in muscle anabolism?

Yes.

I appreciate the response, as usual my friend.

See in my case, I'm loving the stack I use: cyp/tren e/primo; I assume this stack is synergistic, according to what you posted above, that test and tren are, but I'm sure primo has its role as well, lowering estrogen a bit and other positives of it being very safe, along with other I don't know of.

So essentially, you're answer is to add drugs (despite their "family") based on effects desired, which are based on whatever goal.

I just want to avoid stacking things that would be considered overkill. But I think three drugs at a time is sufficient anyway; If I were to add var or winstrol, I would drop either tren e or primo to make room for it.

But I haven't been taking oral anymore, as I find injectables sufficient and essentially, less harsh on bloods.

 

[Type-IIx]

Yes.

I appreciate the response, as usual my friend.

See in my case, I'm loving the stack I use: cyp/tren e/primo; I assume this stack is synergistic, according to what you posted above, that test and tren are, but I'm sure primo has its role as well, lowering estrogen a bit and other positives of it being very safe, along with other I don't know of.

So essentially, you're answer is to add drugs (despite their "family") based on effects desired, which are based on whatever goal.

I just want to avoid stacking things that would be considered overkill. But I think three drugs at a time is sufficient anyway; If I were to add var or winstrol, I would drop either tren e or primo to make room for it.

But I haven't been taking oral anymore, as I find injectables sufficient and essentially, less harsh on bloods.

Test/Tren/Primo is highly synergistic, it's functionally equivalent to TMT which I have written a worked example for here: Maximally Synergistic Stacks.

Correct, my approach is generally to rely first on synergy in order to reduce total doses (including of AAS) and to do more with less. Synergy between compounds is a lever, that pressing on can elicit gains of great magnitude vs. titrating dose, that is more of a blunt instrument. I basically view the PEDs as one of 3 levers (and fundamental pillars), the linchpin that ties together the other levers, training & nutrition.

 

[T&H]

Can you elaborate on that? In other words, what do these cycles look like for you in terms of dosages/lengths/drug combinations?

Is there a reason you avoid 19-nors?

I've personally avoided 19nors only because of the sides experienced and posted by some. And while my cycles are light compared to many, I'm not against combining 19 nors with dhts. I only asked the OP about where he heard his claims from.

I have stacked primo, mast, and test a few years ago. I certainly haven't stacked every one I posted at the same time. The info that came out here is great, glad he asked what he did.