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Go Back Ā  Anabolic Steroids Discussion and Bodybuilding Forum > Anabolic Science Section > Anabolic Science Forum

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Jiujitsu7
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❗️Helpppppp needed❗️ - 12-11-2013, 12:06 PM

I'm new to this obviously...my situation is slightly complicated but here it is...I was on suboxone ( opiate ) for about 5 years during that time I used anavar ...then a few months later deca with dbol ..the idiot that I am I never did a post cycle. That was about 2 years ago. About one year ago I started feeling the symptoms of low test..pain in my balls no energy..all of that good stuff..had blood work done, testosterone came back 430.. Which is considered normal but mayb for a 60 year old guy but I'm 28. I am now off the suboxone for about a month and was hoping I would recover from this but I have not. Iv been offered advice from many different people. Most of all I'm told to run test followed by hcg . I would go to the doctor but I have no insurance and simply can't afford it...I should mention also I def have atrophy. Any help at all would be awesome and greatly appreciated thanks.
   
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12-11-2013, 12:19 PM

You've only been off suboxone one month, why not train naturally for a couple months and then get retested.
   
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12-11-2013, 12:22 PM

Thanks for the reply brother...Iv come off opiates before and it was before I messed around with juice...things got better within a week...this time I'm positive it's the result of not running a pct..I try to train but I literally have no energy to even get out of bed and my nuts hurt and r shrinking so I'm kinda in a rush lol
   
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amateurmale
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12-11-2013, 12:29 PM

Why are you on opiates?
   
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joshck
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12-11-2013, 12:31 PM

Suboxone is prescribed to people that are addicted to pain pills...its just trading one drug for another..
   
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12-11-2013, 12:33 PM

I'm not on opiates..I was
   
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12-11-2013, 12:39 PM

Your test levels are well within range... depending on the lab, the general range on the low end is about 300ng/dL. You do not have low testosterone. There could be number of factors at play and honestly, unless you WANT TRT, there is no need for it. To put it in perspective, I had a totat test level of 20ng/dL at 24 years old... never did any drugs either. That is low.

If you want to find out hat the issue is you will need more than just total T levels. Is your LH and FSH off? Do you have excess cortisol contributing to low T? Are you eating a healthy diet/ How is your vitamin D level? What are your sleep patterns? How is your thyroid functioning? How is you blood pressure? What about cholesterol? What time of day did you have your test done?

If you need anything, i would simply suggest running some HCG, clomid, nolvadex and possibly DAA to upregulate the HPTA.

Post by Hawkmoon from pro muscle:

Suppression of the HPTA (Hypothalamus, Pituitary, Testicular Axis) is seemingly unavoidable during a steroid cycle. What I will be presenting in this article is a new idea to the world of AAS users. This exciting new concept addresses the possibility of limiting and possibly preventing suppression of the (HPTA) during cycle. More specifically, I will show you how to actively modulate the hypothalamus & pituitary pulse generator during cycle and how this can prime our endocrine system for a quicker, smarter, and healthier recovery from anabolic androgenic steroids (AAS).

For a moment, let’s forget the concept of “post cycle therapy”, and embrace the idea of “on cycle therapy” – active therapy throughout a steroid cycle. The HPTA involves a constant biological interplay of responses and feedback loops that can ultimately become shutdown and degraded during AAS administration. However, research suggests suppression of the hypothalamus and pituitary may be preventable during steroid use. Before we delve into the details, lets first take a quick recap on the HTPA and how it responses to AAS.

HPTA – The basics

When the hypothalamus senses low hormone levels, it secretes gonandotropin releasing hormone (GnRH). This GnRH then travels a short distance to the nearby pituitary gland to stimulate the release of the gonadotrophins -- luteinizing hormone (LH) and follicle stimulating hormone (FSH). These gonadotrophins travel all the way down to the testes, to activate their respective leydig and seritoli cells. LH initiates testosterone production by stimulating the leydig cell receptor (steroidogenesis), while FSH initiates sperm production by stimulating the sertoli cell receptor (spermatogenesis).

AAS’s inhibit hormone production just as your body’s own hormones do. Testosterone interacts with the androgen receptor (AR) and estrogen interacts with the estrogen receptor (ER). When these hormones are in high concentration, they cause the hypothalamus to decrease its release of GnRH, which decreases LH and FSH production from the pituitary. (1) This cuts off the signal to the testis and halts all hormone production. This process is a daily event for the rhythmic endocrine system. Spikes in LH & FSH are followed by spikes in testosterone, and spikes in testosterone result in a reduction of LH & FSH release until testosterone levels decline and LH & FSH is released again. The caveat with most steroids, is that hormone levels remain chronically high (24/7) and do not allow release of LH or FSH, thus leaving the pituitary and testis in a dormant state for as long as the steroids are administered.

While low-dose on-cycle hCG is a good protocol to mimic LH and keep the testes from atrophy, (discussed here) it won’t help prevent pituitary atrophy. We forget that the pituitary is susceptible to the same degradation and atrophy as the testes. That is, when the GnRH secretion from the hypothalamus stops (during a steroid cycle), the pituitary reduces its number of GnRH receptors and becomes less and less responsive to GnRH stimulation as time goes on. (11) This is analogous to atrophy of the testis, during absence of an LH or FSH signal. On the other hand, both the pituitary and testis will decrease receptor concentration during over stimulation as well, as its been found from too much hCG use or too much GnRH stimulation.(12,13) The point here, is that only minor stimulus is required for the preservation of sensitivity in the endocrine organs. Perhaps a completely neglected and suppressed pituitary (or testes) may explain the lack of full and prompt recovery for many steroid users, despite adherence to a “tried and true” PCT regimen. So the question is – How can we prevent suppression of the testes, and better yet, how can we prevent suppression of the pituitary?



A closer look –

There are several ways that steroids can inhibit LH & FSH release from the pituitary based on the receptors they occupy, and this is important to understand if you plan on blocking AAS induced suppression. For instance, it appears that AAS which bind strictly to the AR only inhibit LH & FSH release by suppressing GnRH release from the hypothalamus (ie Primobolan, Proviron, Anavar or Masteron). (34,37,39) However, AAS which possess estrogenic (ER) or progestogenic (PR) activity inhibit LH & FSH by directly down-regulating the GnRH receptors on the pituitary, while also reducing GnRH release from the hypothalamus. (35,38) Therefore, progestin based AAS such as trenbolone and nandrolone are “double suppressive” because they are binding to the AR and PR and suppressing LH & FSH by two different mechanisms. (36) The same can be said for steroids that aromatize, such as testosterone or methandrostenolone since they can activate both AR and ER receptors.

Evidence suggests that estradiol is about 200x more suppressive than testosterone on a molar basis (37), and that administration of Arimidex can greatly reduce testosterone’s suppression of LH release. (42) However, since progesterone based AAS’s such as nandrolone and trenbolone are inherently progestogenic based on their hormone structure, there is no way to prevent them from activating the PR. Therefore, it’s virtually pointless to try to block the suppression from progestin based anabolics. However, we can block suppression from the ER by using either non-aromatizing AAS’s or aromatase inhibitors. So this now leaves us with suppression of LH & FSH via the AR, but this suppression can be blocked, and that’s exactly what I’m going to show you.

When it comes to suppression of the hypothalamus, there is more than a simple on/off switch for the hypothalamus control center. Evidence suggests that there isn’t even a direct AR or ER receptor on GnRH secreting neurons. (2-6) Meaning, steroid hormones do not directly influence GnRH release from the hypothalamus, but actually communicate through an intermediary. (7)

It was well summarized here by A. J Tilbrook et al,

“It follows, that the actions of testicular steroids on GnRH neurons must be mediated via neuronal systems that are responsive to steroids and influence the activity of GnRH neurons.”

And again here by FJ Hayes et al,

“It was thus postulated that estrogen-receptive neurons were acting as intermediaries in the non-genomic regulation of GnRH by estrogen”

There is a network of neurogenic intermediaries in the hypothalamus governing GnRH release from steroid hormone influence. More specifically, it is the combined efforts of neuro-active peptides and catecholamines which send the message of “suppression” to the GnRH neurons once activated by steroid hormones. (16) These primary messengers are known as a group of neuro-active peptides called endogenous opioid peptides (EOP’s). (7,16) The EOP’s consist of the three main peptides -- b-endorphin, dynorphin, and enkephalins, which act upon their respective u-opioid, k-opioid, and s-opioid receptors. It appears that the most influential EOP in GnRH modulation is b-endorphin, acting upon the u-opioid receptor. (8-10) For this reason, b-endorphin will be the main focus of the article (although there are other minor intermediates involved.)

When steroid hormones reach the hypophysial portal, they activate the EOP’s, which suppress GnRH and consequently suppress LH & FSH. We know that steroid hormones must communicate with these opioid receptors in order for them to inhibit the release of GnRH from the GnRH neurons, since the GnRH neurons do not have their own AR or ER receptors. What’s most interesting here is that the suppression on GnRH neurons can actually be intercepted by a u-opioid receptor antagonist – such as naloxone, and the orally active congers naltrexone, and nalmefene.

This is accomplished by blocking the u-opioid receptor and preventing the inhibitory effects of b-endorphin upon the GnRH releasing neuron. It should be noted that this “antagonism” of suppression is not due to antagonism of the AR or ER itself, since u-opioid antagonists to not bind to hormone receptors. (15,32)

The effect of a u-opioid receptor antagonist on the HPTA is demonstrated here --



Essentially, a u-opioid antagonist such as naloxone takes the brakes off of GnRH release and allows pulses of GnRH to occur as if no steroid hormones are present. (17) Naloxone, and related u-opioid antagonists have consistently proven to block the suppressive effects of testosterone, DHT, and estrogen administration in both animals and humans. (18-25) It also appears that these drugs have the ability to increase pituitary sensitivity to GnRH. (26,27)

U-opioid antagonists have long been used for treatment of opioid dependence; not only to control cravings of narcotics, but to restore a suppressed endocrine system. (28,29) It’s well known that strong opioid based drugs such as methadone, cocaine, heroin and alcohol can suppress GnRH and therefore suppress LH & FSH. It seems that this decease of GnRH, LH & FSH is due to the same EOP mechanisms seen with AAS induced suppression. (33) In alcoholics, cocaine and heroin users, naltrexone and naloxone have been used to restore LH and testosterone levels. (28,29) Naltrexone has even been proposed as a treatment for male impotence and erectile dysfunction. (30,31)

Naloxone, naltrexone and nalmefene seem progressively more powerful in their potency to block b-endorphin, respectively. (14,18) Naloxone lacks oral bioavailability therefore injection is required. An injectable preparation could easily be made with ba water due to the water solubility of the compound. A 40mg subcutaneous injection would be a typical dose of naloxone. Naltrexone is orally active, with a safe and effective oral dose being about 100mg for a 220lb male. (18) While a lower dose of about 25-50mg of nalmefene would seemingly have the same benefit. (20,24) Increasing the dose of these drugs will surely increase the likelihood of side-effects without notably increasing the benefit. A twice a week dosing protocol would seem appropriate with these drugs, as only to increase GnRH and LH release enough to prevent pituitary and testicular shutdown – Just enough to keep them in the “ball game” so to speak. Also, a twice a week dosing protocol would most likely limit the increased opioid sensitivity induced by the long-term use of the drugs.

A word of caution: The opioid antagonists mentioned in this article are recognized as safe and non-toxic at the given dosages; however they can cause severe withdrawal symptoms in opiate users (methadone, morphine, cocaine, and heroin addicts.) Caution is also advised when using opioid antagonists prior to sedation or surgery as they can reduce effectiveness of anesthetics. Temporary nausea, headache or fatigue, are occasional side-effects associated with the use of these drugs. Naltrexone has been reported to heighten liver enzymes, while naloxone and nalmefene do not appear to have this issue. At any rate, a twice a week protocol for 4-16 weeks is unlikely to cause any liver issues that may be associated with naltrexone. Contrary to popular believe, opioid antagonists do NOT have any addictive properties.

A few point to consider -

For those who choose to embark on an opioid antagonist protocol several things should be considered.



Remember, progestin based anabolics such as trenbolone and nandrolone are “double suppressive” because they desensitize the pituitary directly by PR activation. It also appears that no opioid receptor antagonist or aromatase inhibitor can prevent suppression via the PR. Therefore, trenbolone or nandrolone are going to cause unavoidable inhibition of HTPA function by causing suppression via the ER, AR and PR. (40,41) If one hopes for a prompt and full recovery post cycle, perhaps progestin based anabolics are better avoided, or at least limited in duration of use.
As it was pointed out earlier in this article, estrogen has a markedly stronger effect on suppression of LH release compared to androgens since estrogen suppresses the hypothalamus and pituitary. Usage of an AI such as anastrozole, letrozole, or exemestane (Aromasin) can reduce estrogen and greatly reduce suppression on GnRH, LH and FSH release by preventing excessive ER activation in the hypothalamus and desensitization of the pituitary GnRH receptors. (35,37,38) Anastrozole has ~50% maximal total estrogen suppression at 1mg/day. Exemestane has ~50% maximal total estrogen suppression at 25mg/day. While letrozole has ~60% at 1mg/day. These are averages based on compiled data from several studies. Similar estrogen suppression can also been seen from only twice a week administration of these AI’s. (43-47)


References

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9. Do gonadotropin-releasing hormone, tyrosine hydroxylase-, and ß-endorphin-immunoreactive neurons contain oestrogen receptors? A double-label immunocytochemical study in the Suffolk ewe
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13. Chronic administration of the luteinizing hormone-releasing hormone (LHRH) antagonist cetrorelix decreases gonadotrope responsiveness and pituitary LHRH receptor messenger ribonucleic acid levels in rats.
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CICERO, T. J., et al.
Endocrinology 104: 1286-1291, (1979)

17. Opiatergic control of LH secretion is eliminated by gonadectomy.
BHANOT, R. et al.
Endocrinology 112: 399-401, (1983)

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23. Effect of naloxone on the plasma levels of LH, FSH, prolactin and testosterone in Beetal bucks.
Singh B, et al.
Department of Animal Production Physiology, CCS Haryana Agricultural University, 125004, Hisar, India

24. Endocrinology: The effect of nalmefene on pulsatile secretion of luteinizing hormone and prolactin in men
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25. Effects of the novel opiate antagonist, SDZ 210-096, on luteinizing hormone secretion in the rat
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26. Effect of antagonists of dopamine and opiates on the basal and GnRH-induced secretion of luteinizing hormone, follicle stimulating hormone and prolactin during lactational amenorrhoea in breastfeeding women
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27. Naltrexone administration modulates the neuroendocrine control of luteinizing hormone secretion in hypothalamic amenorrhoea
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30. Erectile function and naltrexone
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31. Opiate antagonists in erectile dysfunction: a possible new treatment option? Results of a pilot study with naltrexone
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33. Morphine exerts testosterone-like effects in the hypothalamus of the castrated
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34. Studies of gonadotropin-releasing hormone (GnRH) action using GnRH receptor-expressing pituitary cell lines.
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35. Patterns of LH secretion in castrated bulls during intravenous infusion of androgenic and estrogenic steroids: Pituitary response to exogenous luteinizing hormone-releasing hormone
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36. Demonstration of progesterone receptor mediated gonadotrophin suppression in men.
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37. The direct pituitary effect of testosterone to inhibit gonadotropin secretion in men is partially mediated by aromatization to estradiol.
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38. Studies on the role of sex steroids in the feedback control of FSH concentrations in men.
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39. Is aromatization of testosterone to estradiol required for inhibition of luteinizing hormone secretion in men?
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40. Influence of nandrolondecanoate on the pituitary-gonadal axis in males.
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42. Aromatization Mediates Testosterone's Short-Term Feedback Restraint of 24-Hour Endogenously Driven and Acute Exogenous Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone and Follicle-Stimulating Hormone Secretion in Young Men
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43. Short-Term Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and Testosterone Secretion in Older Men
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44. Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels
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46. Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Males
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2jz_calgary is offline

Post by Doggcrapp on Pro muscle

I think the worst thing someone can do is be continuously on year round in high amounts......but regardless...a great many of the top competitors and (hell) ran*** Joe Blow gym rats are on year round.

So here is the thing....the decisions you need to make

1) do you want to have kids some day? if the answer is yes, then I would be as sure as hell to send signals to the HPTA at predetermined intervals
2) do you want to be healthy? Im talking hematocrit, kidney health, cardiomyopathy, etc etc etc then you better as sure as hell take being on "year round" into account as it pertains to your health.
3) do you want to suffer muscle/tendon tears (low endo testosterone), low sex drive, lethargy, and disintegrate muscle size wise when you do FINALLY GET OFF......then you better sure as hell send signals to the HPTA at predetermined intervals.

Do you want to do one cycle a year and then be clean the rest of the year? Well that changes everything doesnt it? And my "supposed" 'HPTA upregulation whateverthingamajiggy above really wouldnt make sense now would it? Again it drives me absolutely bonkers when things I say get taken out of a context and I have no idea what that context was.

Do you want to do 2 eight week cycles this year and be off the other 36 weeks? Well that changes the whole equation totally also doesnt it?

This is all about personal choices. And when i comment on this stuff its in regarding the personal choice someone has made concerning their own BEING ON usage.

My opinion?

You tell me.......

Some of you guys hit every show as fans.....YOU TELL ME!

February = Ironman Pro bodybuilding championships
Did any pro's or top ams you saw at this show look alot smaller or soft to you?
March = Arnold classic
Did any pro's or top ams you saw at this show look alot smaller or soft to you?
May = NY pro show
Did any pro's or top ams you saw at this show look alot smaller or soft to you?
July = USA championships
Did any pro's or top ams you saw at this show look alot smaller or soft to you?
September = Olympia
Did any pro's or top ams you saw at this show look alot smaller or soft to you?
November = Nationals
Did any pro's or top ams you saw at this show look alot smaller or soft to you?

Throw in the Europa, Houston pro, all the guest posings year round, all the appearances, all the photo shoots, all the boothwork at expos!!!!!
Did any pro's or top ams you saw at this appearance look alot smaller or soft to you?

They aint getting off.

So you want my opinion....I'll give it to you below

Whats better?

Stay on year round and drive your HPTA into dormancy so fargone that you destroy any chances of having kids, drive your endo testosterone levels so low that you go into andropause at 32 years of age (when you TRY to maybe clean out for a little bit but panic because you feel so g'damn shitty so you go back on)......and if you do get off you disintegrate and muscle mass falls off you like its dead skin?!?!?!

or

(and ive caught more shit for this over the last decade than anything Ive ever talked about.....but ohhhhh I kind of proved my points over time and it actually DID WORK DIDN'T IT!).....Yes I will be the first to tell you I have a bug up my ass at the arguments i used to get into with this stuff with people telling me I was full of shit below

(sorry rant there) or

Is it better to send intermittent signals to the HPTA so there isnt a gigantic dormancy period?

Trust me on this......intermittent signals is the way to go. Every single one of my former trainee's can, will and/or have kids......including myself. My wife got pregnant in our 2nd month of trying when we decided to have kids and i have yet another one on the way in 2 months.

Now i had these huge huge huge arguments with people online many years back saying sending signals to the HPTA while on or having any tiny bit of outside source of testosterone in your body would do absolutely nothing.

I knew better. And I couldnt prove it until.....

---------------------------------------------------------------

The effects of aging in normal men on bioavailable testosterone and luteinizing hormone secretion: response to clomiphene citrate.

Tenover JS, Matsumoto AM, Plymate SR, Bremner WJ.

Geriatric Research, Education, and Clinical Center, Veterans Administration Medical Center, Seattle, Washington.

Serum testosterone (T) levels in men decline with age while serum LH levels, as measured by RIA, increase. To assess if the decline in serum T levels in healthy aging men is paralleled by an age-related decline in the bioavailable non-sex hormone-binding globulin (SHBG)-bound fraction of T and to determine whether there are age-related changes in LH secretion or LH control of T production, we studied 29 young (aged 22-35 yr) and 26 elderly (aged 65-84 yr) healthy men. All men had single ran*** blood samples drawn, and 14 men in each age group underwent frequent blood sampling for 24 h, both before and after 7 days of clomiphene citrate (CC) administration. Both mean 24-h serum total T levels and non-SHBG-bound T were reduced in elderly men compared to those in young men (P less than 0.05), while estradiol and SHBG levels were similar in the 2 age groups. Serum FSH determined by RIA and LH by RIA and bioassay were higher in the elderly men compared to those in young men (P less than 0.05), but the ratios of LH bioactivity to immunoreactivity and the LH pulse frequency and amplitude were similar. After CC administration, mean serum total T and non-SHBG-bound levels in young men increased by 100% and 304%, respectively, while in older men these values increased by only 32% and 8%, respectively. However, CC-stimulated LH pulse characteristics and serum levels of estradiol, SHBG, FSH, and bioactive and immunoreactive LH were similar in the 2 groups. Thus, both at baseline and after CC stimulation, elderly men had significantly lower serum total T and non-SHBG-bound (bioavailable) T levels than did young men, despite similar or increased levels of bioactive LH and similar bioactive to immunoreactive LH ratios and LH pulse characteristics. These results suggest that major age-related changes in the hypothalamic-pituitary-testicular axis occur at the level of the testes and are manifested by decreased responsiveness to bioactive LH. Administration of CC to young and elderly men resulted in similar changes in LH pulse characteristics and LH bioactivity and immunoreactivity, suggesting preserved hypothalamic-pituitary responsiveness in the elderly.

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Look at the bold=normal healthy men with normal testosterone levels. So there isnt a need for an increase in total T and non-SHBG-bound levels but it happens anyway with the administration of clomid. That told me alot....and I knew i was on the right path with this stuff years ago. So all those people for all these years who have argued vociferously with me that PCT does absolutely nothing if testosterone is present whether endogenous or exogenous, got a big foot in the mouth with this study.

You dont need a total test level of 75 to 180 ng for clomiphene to work....it works regardless....and increased normal testosterone levels above by 100 to 304%.........signals to the HPTA Work!

So let me run thru some of my opinions here on all this and again this all comes down to choices.

1) I believe in 250-500IUS of HCG done 2x a week, done on the day before shots.....and believe this is one of the most important things any bodybuilder can do for himself to keep himself as "normalized as possible"....this is Swales recommendation and kudo's go to his work.....dont credit me in the least on this...because its 100% Swale
2)Clomid is a very hard compound for people to take, it makes alot of guys depressed, anxious and absolutely irritable....want to know what its like for your girlfriend/wife on her period? Thats clomid by 5x. It also works very well if you can hack it (alot of people cant)
3)This is just personal opinion and nothing more than that. I believe Letrozole is just too powerful. You need some estrogen for health reasons. Always remember homeostatis......if you drive your estrogen levels down to nothing, guess where your endo testosterone is going to go. And there is nothing more dangerous in my opinion than having seriously low testosterone levels, especially for endothelial/cardiac health. I would probably pick something like exemestane and use the least amount you can of it for an anti arom.
4) Nolvadex/tamoxifen i go back and forth on opinionwise as an anti est. Ive kind of soured on it again....
a) raises HDL
b) can raise LH, FSH and testosterone in some/most
c) can cause blood clots
d) can cause some retinal damage maybe in some (thats for you killerstack)
e) can potentially reduce IGF liberation

(yes Ive started to get to the opinion that steroids and testosterone are pretty safe but its all the ancillary stuff that people are using in large amounts that they think is like pez candy (but are in actuality pretty darn powerful) might be a big culprit in alot of the side effects (especially cardiovascular/lipid/clot wise) we are seeing.

so my opinions would be the following

while on, use the lowest amount of juice you can to make gains so you can always have something to go up to later. Ive seen LATS say this, Ive seen Evan C say this, and ive said this alot of the years......if you do 2 grams of test now when you are 205 pounds......what the hell are you going to have to use when you are 225 pounds and stuck? 4000-5000mg of test a week? What?!?!, till you get past your plateau or have a cardiovascular event?

while on

1) HCG 2x a week
2) if you must use an anti arom...then use exemestane at its lowest dose you can and maybe every 2nd or 3rd day.

always go 4 to 8 (maybe 12 weeks tops if you are still gaining) and then send signals to the HPTA.

Signals-

If i was someone who rarely or sporadically was on.....as I got off i would keep using HCG and exemestane (in the lowest dose possible).....along with clomid if i could hack it either cycled back and forth 2-3 weeks at a time with DAA (very excited by this compound, I think its going to be the one FINALLY EVERYONE HAS BEEN WAITING FOR) or with DAA concurrently (I dont know on that one...DAA is so new).....until the point I felt somewhat normalized....that might mean 1 month, 2 months, maybe even 3 months....depends on the individual......I would also use the lowest dose of clomid I could in that case also. Its all about getting back to normal endogenous testosterone wise. Getting back to normal solves everything....including longterm muscle mass retainment.
(If more people thought in the terms of "how can i get back to normal as quickly as possible after this cycle to keep all this muscle mass" instead of "how can i get get huge during this cycle, fuck what happens after"......there would be so many more happy and content bodybuilders around.....I digress

If I was someone who used year round, I would do everything in my power to keep my endo test levels as normalized as possible.

Every 4-12 weeks, I would try my best to either get completely off or very low dose testosterone (again depending on the individual and his own personal choices)......and use HCG, clom, exemestane and DAA to the best of my ability for 10 days to 3 weeks before getting back on again or raising the low dose testosterone back up...(but hey my opinion on low dose testosterone seems to be alot different than alot of people in this forum).....I am talking either completely off or pyramiding downward during the 10 days to 21 days or using a very low dose amount (25mg to 50mg every 4th day or so) during the 10 to 21 days......before going back up. Again my opinion of going back up means 500-750mg (maybe 1000mg for the big boys) and not the 2000mg and upwards of testosterone that it seems alot of 220 pounders use in this forum. Thats what I would do if I was using year round.

There I commented on something I didnt want to comment on because I felt I had to....LOL


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Jiujitsu7
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12-11-2013, 01:08 PM

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Yeah... A little respect goes a long way. With that, I shall bail on this thread.
I appreciate your help thank u...I'm always respectful, but not to people who call me a loser because I was in a car accident
   
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joshck
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12-11-2013, 01:24 PM

I lost a friend from addiction. ..and I have learned that they always have an excuse for their addiction.u got off pills and then got off suboxone...good job...but I think someone with a addictive personality shouldnt do steroids...
   
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Jiujitsu7
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12-11-2013, 01:27 PM

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I lost a friend from addiction. ..and I have learned that they always have an excuse for their addiction.u got off pills and then got off suboxone...good job...but I think someone with a addictive personality shouldnt do steroids...
Good try...but after my surgery my doctor put me on suboxone for pain management. Not sure what any of this has to do with what this site is about but I'm done explaining myself to obviously bored people
   
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LastChance
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12-11-2013, 02:00 PM

I have struggled with addiction in my own life. I overcame and so can anyone else. The first step is to admit its a problem as cliche as that sounds. I have an addictive personality of that there is no doubt. I have turned that to the gym and it is working out for me. I am not the only person that owes their sobriety or even their life to the gym and a few guys that helped me get started and steered me.

It sounds to me like this guy is about in the place that he is looking for help.

It's easy to say he is a dick, but if I posted on a forum and got called a loser I doubt I would respond well myself.

We shouldn't be about shunning and ridiculing people. Just what I think.

I don't know this guy and have no idea what is really going on, but I think everyone deserves some respect.

JiuJitsu7 feel free to PM me and I will answer your questions as best I can. I am not an expert on anything, but I will do my best to help you get answers.
   
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AtomAnt
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12-11-2013, 02:11 PM

Guys, and I mean everyone... On this site, we are not about belittling people and making them feel like shit. That is what I love about this site. Yes, the OP was disrespectful, that does not give anyone free reign to light him up like a christmas tree. Just ignore it and move on. Bid them farewell and good luck and just don't respond. There is no need for hostility here.

OP, as you saw from my post, it seems you are having issues with the HPTA... I would research that and get your HPTA to rebound. Adding in more aanabolics will further suppress your HPTA... think long term recovery and health first. Good luck


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joshck
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12-11-2013, 02:18 PM

I have helped people in need as well. But they were nice and sincere. I feel like he not being 100% honest here. People with an addiction do seem to go a bit overboard. He just got off suboxone and want to jump right in doing something else. I could see a cycle going bad here meaning over doing it. Some people do recover lastchance..im glad u did...but u know as much as I do...most people dont . Drug r a big epidemic here where I live..
   
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12-11-2013, 02:36 PM

The thing about it is ...suboxone has a blocker in it so if u take other meds with it ...it wont do anything...like a high...or some people get sick...I will help a brother in need but not when I think its just gonna set someone up for failure.
   
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12-11-2013, 07:27 PM

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Originally Posted by AtomAnt View Post
Guys, and I mean everyone... On this site, we are not about belittling people and making them feel like shit. That is what I love about this site. Yes, the OP was disrespectful, that does not give anyone free reign to light him up like a christmas tree. Just ignore it and move on. Bid them farewell and good luck and just don't respond. There is no need for hostility here.

OP, as you saw from my post, it seems you are having issues with the HPTA... I would research that and get your HPTA to rebound. Adding in more aanabolics will further suppress your HPTA... think long term recovery and health first. Good luck
Great post mental, that's why I came over from another site. Much respect.
   
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BIGAINS
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01-01-2014, 12:52 AM

Long term opiate use supresses the HPTA and will lower test levels. I am glad to hear you have been able to get off of the sublaxone. Certin people will be more likely to become addicted to things like pain meds than others if they use them, it is in the genes and they have to stay away from addictive substances for life. A persons genetics doesn't tell the whole story or make them a loser. Everyone has their own story but for an addict it can be a living hell until they get sober and stay that way, and oversimplifying it ranges from ignorance to stupidity. This guy came here for help after succesfully getting off the sublaxone, with some prior cycle history a while back, and wonders why his levels are low and feels the way he does... Either way a good PCT will likely help.
   
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01-01-2014, 02:18 AM

just saw this thread tonight omg... Just want to say to jitsu is that u have stressed your liver and other organ it seems for quite sometime... therefore jumping on gear is the last thing u want to do because your body, joints ,and heart are so out of tune you need to give it a rest so u will live a long healthy life. Whats your rush? Pick your priorities if u have nut atrophy its obvious you need to get hpta fixed by hcg and hmg
.test will dig u deeper into bad health with your situation..
Best a luck to be sober for life ..ib
   
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01-01-2014, 02:53 AM

I would try everything everyone has suggested drug wise...If you really wanna pull out all the stops then try juicing organic vegetable/fruit juice to try and freshen up your nervous/endocrine system...worth a try
   
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Jello
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01-01-2014, 03:05 AM

Why the fuck you guys jumped this guys shit right out the gate is beyond me. AM you for sure had no reason to go at this guy like that. There is a couple good posts on this thread, let's take it from there and just give the guy some advice to help him.




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01-01-2014, 03:28 AM

Sorry jello I was in a bad mood. My apologies OP.
   
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