Productive Member
Hey, fellas. I really feel like posting tonight, so here's another question that I've always pondered: Generally, how long does it take for someone's androgen receptors to clear? And does the amount of time that you were on gear/the dosages you took on your cycle have anything to do with clearance time?
Member
the best way to do it is time on=time off, but people who are hardcore about it (which im not reccomending), do pct then wait for the blood levels to go back to normal then jump back on.
Productive Member
Ok, but that really didn't answer my question. I've heard that there is no real way by taking blood tests to see if your receptors are cleared; I was just wondering if anyone here knew a general amount of time it takes for them to clear? Few weeks? Months?
Member
if theres no way to find out through blood test then how would anyone know
?
Banned
As you stated it would depend on several things. How long your cycle was. How much you were doing and what you were doing. Then the only real way to know is through blood work.Originally Posted by musclestack
AR-Hall of Famer ~ Cocky motherF*cker!
Tough to say bro.Blood work will show what your Test levels are,but won't give any indication of whether your receptors are clear.It appears to take a good three months "off" (given the cycle was 12-15 weeks)before you'll respond well to an anabolic cycle.
~Pinnacle~
VET Retired
It's a myth androgen receptors do not get blocked up so no need to "clear" them out. In fact receptors increase in number when androgens concentrations increase. Other factors are involved estrogen and shbg levels etc.
Anabolic Member
AR-Hall of Famer ~ Cocky motherF*cker!
Could you elaborate in detail please.
Reason I ask is,well,for two reasons.
1).In the past I've ran cycles far to close together and didn't respond well at all on the second go around,even upping the dose.If what you state is fact/true.Why did/does this happen?
2).I'm on year round.I cruise in between cycles at 250 mgs.I really need to bump my dose heavily(when on cycle) in order to see anything substanical.That tells me my receptors are somewhat flooded/saturated.
~Pinnacle~
~Pinnacle~
Anabolic Member
Actually, it indicates that your SHBG level has increased...not that your receptors are saturated.
AR Biggerologist
Yep, bumpin Nark and K.I.G. on this one-don't believe in receptor saturation myself.
AR-Hall of Famer ~ Cocky motherF*cker!
HAHA...so I'm doomed to run ultra high doses forever...great.
~Pinnacle~
VET Retired
Well Pinnacle as I said other factors are involved. SHBG will bind to the AAS in you blood reducing the cycles effectiveness. Eating to accommodate all this new muscle can be a challenge to some as well. Remember your body wants to keep homeostasis adding new muscle tissue will get harder over time. I'll go into more detail later but i really don't feel like right now. Really though the AR does not get blocked up it's a myth.
Anabolic Member
Not necessarily.
There're differing schools of thought on this...and different approaches to the same end.
Proviron is noted to reduce shbg levels.
AR Biggerologist
The corresponding raise in SHGB is one of the best reasons to take proviron or winnie toward the end of a long cycle. Tongkat ali might also be beneficial, but not sure exactly how much it inhibits SHGB.
VET Retired
Use low amounts of letro during your cruse period and on cycle.
VET Retired
Insulin as well. God dammit man think! Man think!
Anabolic Member
Or Aromasin at 20-25 mgs ED
Anabolic Member
duh plucky....
AR-Hall of Famer ~ Cocky motherF*cker!
Coupled with cycling slin as well?I can do that.Wasn't sure on the long term effects of running a anti for lengthy periods of time.
Good info guys!
~Pinnacle~
VET Retired
I would not advise you to run an A.I for lenghly periods due to cholesterol issues. Best bet would be to get blood work and use it as your guide.
AR-Hall of Famer ~ Cocky motherF*cker!
Yes..Cholestrol was on my mind as well as it having some effects of bone density or something of that nature.
I'm due for blood work in about 2 weeks.So I'll specify I'm concerned with my SHBG levels.As I sometimes just get tested for specifics.ie: cholesterol/liver values that sort of thing.
THX much!
~Pinnacle~
Associate Member
Pinn,
Here is a link to check out:
http://forums.steroid.com/showthread...highlight=shgb
Scroll down for Hooker's response to lower SHBG.
Anabolic Member
I don't think Anadrol would fit here.
imo, anadrol would increase SHBG.
Big K. ...take over i'm going to bed
AR-Hall of Famer ~ Cocky motherF*cker!
Nice thread!First decent conversation I had on this board in quite some time.
I'm leaning more towards Prov than letro(as I'm not a fan of it).
~Pinnacle~
VET Retired
I don't have a facking clue. I guess Hook is right. Anadrol is a DHT derived drug and it does not aromatize yet it has direct estrogenic activity. I'm stuck. Ummmmmmmmm Hooker take over.
Anabolic Member
I take that back.
The jury's out on Anadrol
Hooker's profile notes: Schroeder et al. Am J Physiol Endocrinol Metab 284:E 120-28
Whereas Anadrol lowered SHBG... still, his profile also noted that mechanism tru which anadrol manifests estrogenic properties is unknown.
Anabolic Member
lol... and here i was thinking you had my back.
You're fired.
Anabolic Member
good discussion guys! One question : is this the only reason that causes too early cycle to be non-responsive? I do believe that ppl were right about the receptor thing so that is not the answer. But does the SHBG levels explain all? Are there other factors at play we still dont know about. Is the SHBG really all covering: If some would be able to downgrade SHBG levels would he be able to avaoid the eventual plateau in a cycle, I am doubting it..
According to Bill Roberts there is no such thing as receptor down-regulation.
http://www.mesomorphosis.com/article...regulation.htm
Obviously there is some underlying factor that causes a 2nd cycle in quick succession to be less effective, but I don't think shbg is to blame either.
Now this doesn't directly relate to AAS obviously. But if there is a surge of shbg before a rise in testosterone, we can assume that the body would actually reduce shbg in response to the use of exogenous androgens.Conclusion: In contrast to general belief, SHBG levels barely influence levels of non-SHBG-bound testosterone both in male newborns and healthy adult men: the influence, if any, is positive. Consequently the age related increase of SHBG does not account for the age related decline in non-SHBG-T in healthy adult men.
Anabolic Member
where do u base that latter statement because I have read completely opposite statements.. It says the same in all my books also..
Productive Member
Do SHBG levels decrease after coming off of a cycle? I'm trying to figure out why we all plateau at some point in our cycle, and if the saturation of androgen receptors is a myth, and instead the reason is because our SHBG (I'm still researching on this subject) levels have increased, what exactly allows us to gain again on our next upcoming cycle?
Simply put, if our SHBG levels were the same as they were on our last cycle, and we couldn't gain then (after we've plateaued), why is it that with a certain amount of time off, we can start to gain again?
AR-Hall of Famer ~ Cocky motherF*cker!
I feel there's more to it than SHBG levels as well.I've had this happen,and my dose was significantly higher,diet and training in perfect order.
I will say this about my current cycle.When I discontinued the masteron at week 8,my growth practically halted.My nutritionist,trainer and myself all thought in old school fashion(receptor saturation).It does make sense that once the masteron was discontinued(being a DHT derivative) that my SHGB levels sky rocketed deadening my cycle.
I'm going to spend some time on "cuttingedge" today and research some of the late,great Nandi's thoughts on this topic.
~Pinnacle~
AR-Hall of Famer ~ Cocky motherF*cker!
Posted by Big Cat on cuttingedge muscle.
I'm still looking arounf for info.This is interesting in regards to SHGB levels.
[QUOTE]Originally posted by Big Cat
[B]Ok, I recently had a debate with some guy who designed a supplement for PCT and part of its action is to lower SHBG. I pointed out the ludicracy of this, but I wanted to open it up for debate, get some input from everyone here.
First of all, the amount of SHBG seems to be fairly irrelevant in terms of the amount of free testosterone. I present you this abstract :
My guess previous to the debate would have been that you may want to increase SHBG for PCT purposes, to expedite clearance of androgens. Sadly most used androgens don't have much affinity for SHBG, and given the length of PCT, it would be pretty much moot factor. So I'm back to the conclusion there is no point in manipulating SHBG in PCT either way, but definotely not for lowering it.
A second point that came to my attention was that SHBG is needed for the conversion of androstenedione.
Of course this only deals with erythrocytes, but I think everyone can follow me in the assumption that a similar process takes place in most cells and for most enzymes. Now, one common problem I have seen with people who haven't run proper PCT is that they often have low but normal LH/FSH as well as test, prior to full recovery, but their androstenedione is off the charts. That indicates that one of the slowest mechanisms to repair in a depressed HPTA is androstenedione to testosterone conversion.
i'd like to point out at this time that androgen use decreases SHBG and the use of an estrogen blocker in PCT further decreases that amount. It seems to me that one of the problems when coming off a cycle is actually lowered SHBG. So again, I not only couldn't see a use for decreasing SHBG, from the look of it low SHBG is a contributring factor in slow recovery and muscle loss.
Another study, originally done to test the influence of thyroid hormones (1), demonstrates that a surge in SHBG is seen prior to an expected surge in testosterone. This confirms the fact that SHBG is needed for testosterone synthesis, most likely via the aforementioned mechanism for increasing androstenedione conversion.
AR-Hall of Famer ~ Cocky motherF*cker!
More...
Originally posted by jboldman
Talking about shbg is something that you want to make sure your bood sugar is not low when doing. I find it a very complex subject to wrap yourself around. In many ways it seems to be contradictory since common bbr lore would have us believe that increased levels of shbg are a bad thing because they preferentially bind testosterone leading to an increased level of estrogen (ala swales theory of estrogen imbalance) and a decreased T/E ratio. We even have some promoting proviron to free up testosterone for anabolic effect. The first abstract BC posted is exteremly reve****g (btw, what is the study ref for that so i can add it to my lib.) since we now have a contradictory notion that increased levels of shbg, as expected, are positively correlated with increased total T but surprisingly are either slightly positivelly correlated with non-bound T or free T remains unchanged. In another study that i posted sometime ago here, a similar conclusion was reached whre contrary to prevailing opinion. " we conclude that in eugonadal men, higher SHBG levels are associated with lower levels of non-SHBG-E2 but slightly higher levels of non-SHBG-T. This means that SHBG cannot be regarded as an estrogen amplifier in eugonadal men.". So we may have another reason to wish shbg not to be lower in pct since increased levels of E could lead to continued suppression of the hpta, just a thought.
jb
The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 1 157-162
Copyright © 2005 by The Endocrine Society
Associations of Sex-Hormone-Binding Globulin (SHBG) with Non-SHBG-Bound Levels of Testosterone and Estradiol in Independently Living Men
Willem de Ronde, Yvonne T. van der Schouw, Majon Muller, Diederick E. Grobbee, Louis J. G. Gooren, Huibert A. P. Pols and Frank H. de Jong
Department of Internal Medicine (W.d.R., H.A.P.P., F.H.d.J.), Erasmus Medical Center, 3000 DR Rotterdam, The Netherlands; Julius Center for Health Sciences and Primary Care (Y.T.v.d.S., M.M., D.E.G.), University Medical Center 3508 GA Utrecht, The Netherlands; Department of Endocrinology (W.d.R., L.J.G.G.), Vrije Universiteit Medical Center, 1007 MB Amsterdam, The Netherlands; and Department of Epidemiology and Biostatistics (H.A.P.P.), Erasmus Medical Center, 3000 DR Rotterdam, Netherlands
Address all correspondence and requests for reprints to: Frank H. de Jong, Ph.D., Endocrine Laboratory, Room Ee 516, Department of Internal Medicine, Erasmus MC, PO Box 1738, 3000 DR Rotterdam, The Netherlands. E-mail: [email protected].
Results of in vitro experiments indicate that with increasing concentrations of SHBG, testosterone (T) is preferentially bound to SHBG in comparison with estradiol (E2). In these studies, the ratio of non-SHBG-bound E2 (non-SHBG-E2) to non-SHBG-T increased with increasing levels of SHBG. SHBG has consequently been regarded as an estrogen amplifier. In this cross-sectional study in 399 men aged between 40 and 80 yr we tested whether higher levels of SHBG are associated with a higher estrogen/androgen ratio in vivo. The mean T level of these men was in the eugonadal range [536 ± 152 ng/dl (18.6 ± 5.26 nmol/liter), mean ± SD]. With increasing SHBG levels the non-SHBG-bound fraction of T decreased from 80 to 36% and that of E2 from 89 to 53%. Higher levels of SHBG were associated with higher levels of both total T [regression coefficient (ßafter adjustment for age and body mass index, 286 ± 15.8; P < 0.001] and total E2 (ß = 4.47 ± 0.90; P < 0.001). However, SHBG levels were negatively related with levels of non-SHBG-E2 (ß = –1.78 ± 0.69; P < 0.001), whereas there was a positive association between levels of SHBG and non-SHBG-T (ß = 32.0 ± 9.78; P = 0.001). Furthermore, we observed a negative relationship between SHBG levels and the E2/T ratio of either total (ß = –0.016 ± 0.002; P < 0.001) or non-SHBG-bound (ß = –0.011 ± 0.002; P < 0.001) hormone. Therefore, we conclude that in eugonadal men, higher SHBG levels are associated with lower levels of non-SHBG-E2 but slightly higher levels of non-SHBG-T. This means that SHBG cannot be regarded as an estrogen amplifier in eugonadal men.
AR-Hall of Famer ~ Cocky motherF*cker!
OBJECTIVE: It is generally accepted that SHBG decreases the bioavailability and activity of testosterone (T). In in vitro experiments increased levels of SHBG will be associated with decreased levels of non-SHBG bound testosterone (non-SHBG-T). However, in vivo SHBG can alter both production and clearance rates and thus plasma levels of T. DESIGN AND PATIENTS: In order to study the effect of SHBG on the levels of non-SHBG-T in vivo in the presence of an active hypothalamo-pituitary-gonadal (HPG) axis we conducted a cross sectional study in 400 healthy adult men with an age range of 40-80 years and in 106 newborn boys. MEASUREMENTS: In both groups, regression coefficients (beta) and partial correlation coefficients (r) were calculated for the relationship between SHBG and T or non-SHBG-T. Adult men were divided into age groups per decade (40-50 years, 51-60 years, 61-70 years and 71-80 years) to study possible differences in the impact of SHBG on the level of non-SHBG-T throughout ageing. RESULTS: Higher levels of SHBG were associated with higher levels of total testosterone in neonates (beta = 0.02 +/- 0.004, r = 0.44, P < 0.001) but not with non-SHBG-T (beta = -0.001 +/- 0.001, r = 0.05, P = 0.52). In adult men there was a significant age related increase in levels of SHBG and an age-related decrease of both total and non-SHBG-T. Higher SHBG was strongly associated with higher total testosterone in all age groups (beta = 0.26, 0.26, 0.26 and 0.23 for 40-50 years, 51-60 years, 61-70 years and 71-80 years, respectively, P < 0.001 for all age groups). Higher SHBG was not or only slightly associated with higher non-SHBG-T beta = 0.02 (P = 0.32), beta = 0.04 (P = 0.03), beta = 0.04 (P = 0.02) and beta = 0.02 (P = 0.16) for 40-50 years, 51-60 years, 61-70 years and 71-80 years, respectively. CONCLUSIONS: In contrast to general belief, SHBG levels barely influence levels of non-SHBG-bound testosterone both in male newborns and healthy adult men: the influence, if any, is positive. Consequently the age related increase of SHBG does not account for the age related decline in non-SHBG-T in healthy adult men.
AR-Hall of Famer ~ Cocky motherF*cker!
Acta Endocrinol (Copenh). 1981 Jan;96(1):136-40. Related Articles, Links
Influence of sex hormone binding globulin and serum albumin on the conversion of androstenedione to testosterone by human erythrocytes.
Egloff M, Savoure N, Tardivel-Lacombe J, Massart C, Nicol M, Degrelle H.
The influence of human serum albumin and sex hormone binding globulin (SHBG) on the enzymic conversion of androstenedione to testosterone in human erythrocytes was investigated in vitro. Total plasma and albumin delayed the conversion rate of androstenedione, while SHBG increased it markedly. The effect of SHBG was largely abolished by heating to 60 degrees C for 1 h and by saturating its binding sites by DHT. The effect of both proteins was found to be related to their concentration. It appears that the binding sites of albumin provide a mechanism for retarding androstenedione uptake by the erythrocytes and that the high binding affinity of SHBG for testosterone facilitates the diffusion of this steroid out of the cell and thus, displaces the chemical equilibrium within the cell.
VET Retired
Good finds but what about other anabolics? SHBG is just one factor involved that slow muscle gains. Hell if we know exectly what is was that slowed muscle gains we would has overcome it by now. This is something we just don't have the answer to....................yet.
Associate Member
Lucky that we're men and we see upregulation of AR's when androgen blood levels increase. Women do not see this trend as much. Also, new research indicates that the binding globulins may not decrease effectiveness of exogenous testosterone as concentrations of globulins increase. Remember there is an equilibrium system in the blood, and a certain percentage of testosterone in the blood is bound to the globulin (where it is ineffective). Only when free (unbound) test levels get depleted will the testosterone dissociate from the globulin. Thus if you're training hard and your cells are demanding nutrients (and recieving them) it shouldn't matter how many globulins you have, your body will be able to use the same amount of test via the constant shift of the equilibrium system. What has been found is that the increased globulin levels are only correlates to the real reason for decreased effectiveness of a given level of test in experienced lifters, which is yet to be determined. I speculate that as telomere length decreases as cells age their sensetivity to testosterone decreases (by various mechanisms in the transduction pathway). Also, as cells age they become less efficient and require more energy do do the same things than they used to. Insulin is required for importing sugar (energy) and aa's etc into the cells, and high levels or androgens decrease sensetivity of myocytes to insulin (see a study I posted earlier in November).
I guess this is confusing, sorry.
Montgomery
AR-Hall of Famer ~ Cocky motherF*cker!
You sparked an interest my friend.
The search continues forward.
~Pinnacle~
There are currently 1 users browsing this thread. (0 members and 1 guests)
Posting Permissions
Reply With Quote