First Cycle Questions for 46Y/O

I think so.

Anavar doesn’t always increase FT though. If TT drops enough, FT may not go up, or even could go down. It is kinda individual what will happen to your FT numbers. IIRC, @tareload had almost the same FT numbers, but TT dropped.

I wouldn’t say that one of the benefits of Anavar is higher FT values, because it may or may not happen. Some guys say this like it is gospel though (that FT will go up on anavar).

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As I understand it, a normal short (6 plus weeks?) of oxandrolone will cause your LH to drop very low, obviously not ideal but possibly easier to start recovering from than a reading of zero?
This isn’t the same as a testosterone cycle where the figures will go to zero.
Regarding semantics, yep it could be seen I am just picking up on something that doesn’t actually make much of a difference, so I may be totally wrong on some or all of this!
I’ll tag a couple of people who may be able to put me right.
@lordgains @unreal24278

TL/DR
I thought oxandrolone lowered your LH and FSH to very low levels which can be quicker to get going again when you stop taking it against testosterone (and many AAS) which cause a total “shutdown”.

So should i dump using the Anavar then? I have paid for blood tests from Optimale so i get an idea where im at currently.

I will say with regards to using Test etc, id rather go above natural levels, but im not bothered about getting huge, but would like to keep a decent build.

I appreciate all the replies guys, im learning and would rather do it this way than jump in using to much and get ill.

The most concise way I can explain it:

The fundamental roles of fT and TT are typically explained backwards.

Dose sets fT (your body eliminates fT not TT). fT + SHBG then set your TT on a very rapidly attained chemical equilibrium between fT and SHBG. Reaction of fT + SHBG —> TT much faster than apparent elimination rate of fT with injectable testosterone ester.

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This isn’t semantics. Suppression by literal definition would be a reduction of FSH/LH without reducing them to ZERO. Definitively, exogenous hormones shuts them down… not reduces them. If somebody has labs showing Var only suppressing FSH/LH after a reasonable use period I would be interested to see that.

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I won’t link to EM anymore but there are lots of good analogies over there if you take a look @Andrewgen_Receptors

The idea of SHBG as a sponge that sucks up large amounts of testosterone and leaves your free T low doesn’t seem to be how it really works. The way I understand it, high SHBG makes your meager production (revealed by the free T) look like it’s normal or even high when it isn’t. The SHBG is basically extending the half-life of the testosterone you’ve produced and the relationship seems to me alot like ferritin and iron.

An SHBG sponge analogy is compatible with your other points. I’ve used a similar reservoir analogy. Think of testosterone as like water being dripped onto the sponge. The important feature is that the sponge saturates, at which point it doesn’t interfere with the “flow” of free testosterone—free testosterone being driven exclusively by endogenous production or exogenous dosing. If you double the size of the sponge then the flow is temporarily impaired until the sponge is again saturated. Then free testosterone flows the same as before. A larger sponge means more total testosterone is held, but at steady state this is independent of the flow of free testosterone.

Also compounding the issue is accurate measurement of fT vs calculated or direct RIA methods. Historically only TT gets measured. If measuring your fT accurately, oxandrolone use will not increase your fT unless it changes you fundamental elimination rate of fT (sometimes correlated but not caused by SHBG). What oxandrolone will do is drop liver production of SHBG and TT (for a given level of fT).

For a fixed dose of exogenous T, at steady state your fT is fixed. Adding oxandrolone drops SHBG. Fixed fT (based on dose via law of mass action) + lowered SHBG ====> lowered TT.

Hence, absolute fT does not increase but %fT (fT/TT) does increase on oxandrolone.

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Sorry if I’ve dragged up something, it’s what I thought I’d seen on Tnation and when I had bloods done after a course (4 weeks) of var my LH was at 1.0 (scale of 1.7 - 8.6 IU/L) after 4 weeks with no PCT. (L 1.5 scale of 1.5 - 12.4 IU/L)
I assumed this was because it hadn’t shut down totally, only lowered. One of the papers I remember looking at was this

where shutdown wasn’t seen, but this was in a study of young boys, not dodgy old blokes doing illegal substances…

Big difference between endogenous T production with an intact HPTGA vs using exogenous T where one uncouples negative feedback loop between T/E2 and hypothalamus/pituitary.

With endogenous T production there is typically strong correlation between TT and SHBG. With exogenous T use you see SHBG decrease over time with TRT/AAS usage [usually dose dependent].

Also usually misunderstood…your T dose sets your free T level and then SHBG sets your Total T. That is fT level set by mass action (how much T you inject) then SHBG binds some fT to TT by dynamic equilibrium (storage). At steady state for same injection amount per unit time, the amount of fT leaving body is proportional to amount entering body. At steady state there is no accumulation hence SHBG can’t change fT level for a constant T dosage per unit time (only the storage amount). Also ignoring downstream conversion, E2, etc.

You can try this experiment yourself by keeping your TRT dose constant and drop SHBG with another medication like oxandrolone/etc. Now compare your pre and post TT/ fT levels using accurate TT/fT methods.

I’d argue (if SHBG does play a role) that more realistically the honeymoon period fades for many due to T/AAS abuse which erodes SHBG over time (there’s probably a bunch of factors in the erosion of that honeymoon phase). You don’t see SHBG increase over time with with exogenous T use. We still don’t understand the full roles of fT/TT and relative impacts which are coupled with SHBG.

@Andrewgen_Receptors

As I may be totally wrong on the info I’ve given soo far, please take this with a pinch of salt until others have chipped in!
Doing blood tests now will show very low levels as the anavar will have changed things so not a representation of what you had 3 weeks ago.
If you are seriously thinking of going on TRT (or B+C longer term when all dialed in) then this isn’t such a consideration unless you may want to stop TRT at a later date, the normal reason for this is to help conceive where its good to know where you were before starting.
However your possible provider (Optimale) may need to see clear results before they can go ahead and treat you, being honest with what you’ve done soo far will help speed things up.
If you plan on just getting bloods and doing it yourself then it doesn’t matter soo much (IMO).
Did I mention I’m not a med pro?

@cataceous nice analogy at EM:

Perhaps we make the concept less clear by thinking about discrete doses instead of continuous flows: we give ourselves an injection; we apply a dose of cream, etc. But these still translate to fairly continuous flows of testosterone into circulation. Consider an analogy in which the body is represented as a bathtub with an open drain, into which we’re pouring water, which represents testosterone. Total water in the tub is like total testosterone in the body. At steady state the flow out of the tub matches the flow in. The key assumption is that the flow rate out of the tub, governed in this model by the drain size and the water depth, corresponds to the metabolism and excretion of testosterone governed by a proportionality to free testosterone. Now what happens if we increase the drain size, which is equivalent to lowering SHBG? Initially the flow rate out of the drain increases, but over time the water level lowers and the flow decreases to again match the flow rate into the tub. Therefore lowering SHBG while keeping dose and underlying metabolism constant results in lower total testosterone and the same free testosterone. The tub analogy isn’t perfect, but I think it’s close enough to give us a feel for what’s happening.

On your specific points: In this theory, TRT dosing drives the total rate of metabolism and excretion, which in turn forces free testosterone to the required level for the rate of use to equal rate of input. This makes total testosterone a dependent variable, just as the water level in the tub analogy can be controlled by the flow rate into the tub. And it is true that men with higher SHBG do not need more testosterone, at least to achieve identical free testosterone to their twins with lower SHBG.

@Andrewgen_Receptors

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I look at this from a controls engineering approach, as in a PID control system. Much of my employment at an electric generation plant was boiler controls. If the feedback signal is high enough and stays there, the controller output will eventually become zero in this feedback system for testosterone control. This is proper operation of the feedback system. I would never call the situation as “shutdown”, for that would be a misleading description.

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@tareload
can you please shed light on the LH question? Does oxandolone totally shut you down like testosterone does or will it lower it (at least during short courses?)

Enquiring minds need to know!

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Methods:

Randomized, double-blind, placebo-controlled trial. Two hundred sixty-two HIV-infected men with documented 10% to 20% weight loss or body mass index ≤20 kg/m2 were randomized to placebo or to 20, 40, or 80 mg of oxandrolone daily. After 12 weeks, subjects were allowed to receive open-label oxandrolone at a dose of 20 mg for another 12 weeks.

Gonadal-Pituitary Function

Baseline total testosterone levels averaged close to the lower limits of normal (270 ng/dL; [Table 5]. At 12 weeks, serum LH and FSH concentrations decreased significantly from baseline in all oxandrolone-treated groups, consistent with an androgenic action. Serum SHBG concentrations also decreased with increasing doses of oxandrolone, which also suggests an androgenic effect of oxandrolone (SHBG was determined in a subset of patients, and total testosterone levels in the subset were similar to those in the larger cohort; data not shown).

Total and free testosterone concentrations measured bydirect RIA did not show a dose-related change. We used celite chromatography to separate testosterone from oxandrolone before RIA and found that serum total testosterone concentrations were significantly decreased from baseline at all doses of oxandrolone but not with placebo treatment (see [Table 5]).

Remember these guys aren’t injecting T.

RIA TT useless (interference). Accurate fT measurement (equilibrium dialysis). Bottom TT numbers in Table 5 more accurate.

SHBG crushed. Endogeneous fT production after 12 weeks significantly suppressed and still some measured LH and FSH. Lowered fT plus lowered SHBG ===> lower TT.

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Both will drop test levels very low, however I’ve seen blockwork where people on var only drop down to like 80ng/dl, and LH/FSH isn’t TOTALLY shutdown… but like 80-90% of the way there.

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There you have it. Suppression without shut down. Now does this lead to a faster recovery which is the question from inquiring minds?

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Beautiful tandem post almost at same time. We should be figure skating pair.

You get 10/10 for conciseness. I get 0/10 since I bore the crap out of everyone putting literature reference behind every post (when I can). Kind of a wasteful gimmick.

Compared to test ester? I would argue yes. Plenty of literature out there on suppression dose response where between 25-100 mg/week will drop LH to 0 (I won’t look it up right now :slight_smile: ). Then you got to wait a few weeks, blah blah based on ester.

Oxandrolone doesn’t shut you down all the way and out in a week looking at liver values (duration of effect once it’s removed).

I always figured shutdown was just enough suppression over long enough time. Oral AAS and SARMs are suppressive (dose dependent) and if taken over a long enough time frame would lead to shutdown.

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Yes, and that’s what I figured this meant as well. My issue was the phrasing of this

like we’re talking suppression so strong it could be mistaken for being shut down… are we still considering this suppression? or should we be calling this ‘shut down’?

It’s semantics, but accuracy is important in some situations - this one feels important to be accurate in our terminology.

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@Andrewgen_Receptors

More posts from @cataceous over on my What is TRT… thread at EM regarding paper above. You’d do well to study this if you want to understand.

The issue with this study is that they are basing MCR on total T rather than free T. The standard equation used is:

Production_rate = MCR * Hormone_concentration

But as I argued above, the proportionality applies to free testosterone, not total. So the equation should be:

Production_rate = MCR * Hormone_concentration = MCR * FT = MCR * f(SHBG, T)

The reason it might appear to work anyway is because at constant SHBG, free T is nearly proportional to total T. So you get:

Production_rate = MCR * f(SHBG, T) ~= MCR * f1(SHBG) * T = MCRx * T

The problem is that their measured clearance rate, MCRx, is actually dependent on both the underlying metabolism (MCR) and SHBG. Unfortunately they don’t separate out the two, which potentially weakens their conclusions. The results are further muddied by the drop in SHBG—mainly in younger men—over the course of the experiment. It’s frustrating, because they did measure free testosterone, apparently by an accurate method, along with baseline and final SHBG values—so they did have the raw data needed to separate out the various effects.

So people know what we’re talking about I’ll insert my earlier criticism of the MCR definition in this same study. I think it shows where SHBG fits in, and I also think SHBG is pretty independent of true MCR. I’ve noted before that with SHBG varying from low 40s nMol/L to low 20s, my free testosterone appeared to stay linear with dose.

The issue with this study is that they are basing MCR on total T rather than free T. The standard equation used is:

Production_rate = MCR * Hormone_concentration

But as I argued above, the proportionality applies to free testosterone, not total. So the equation should be:

Production_rate = MCR * Hormone_concentration = MCR * FT = MCR * f(SHBG, T)

The reason it might appear to work anyway is because at constant SHBG, free T is nearly proportional to total T. So you get:

Production_rate = MCR * f(SHBG, T) ~= MCR * f1(SHBG) * T = MCRx * T

The problem is that their measured clearance rate, MCRx, is actually dependent on both the underlying metabolism (MCR) and SHBG.