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SIED Moderators: Genetic Freak | Serotonin101
HPTA recovery: Time off or PCT?
- Thread starter hazukiguy
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Pct drugs will help boost production while they're active, but once they're removed, bye bye production. It's a bandaid for symptoms without actually doing anything with the problem. Using drugs to counteract drugs just doesn't seem logical to me. Honestly everyone I know who goes on, I make sure to beat it into their head that they may have permanent effects and the more cycling they do with higher doses, more drugs, and longer time on you're pushing it that much more towards the possibility of needing trt for life.
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Not from short cycle, low dose anavar..
From my personal oral only runs and PCT (one without for 6 months and one immediately after) I definitely think it helped. My test levels landed (roughly based on about 6 blood work averages) at 250 6 months post cycle with no PCT and 400 several months after PCT for the one I did PCT immediately after for.
Wouldnt trust it as a fix and would expect to need HRT for life at some point following AAS use but that was my experience in the short term post cycle. Realistically though, HCG on cycle is going to be more effective than anything
Wouldnt trust it as a fix and would expect to need HRT for life at some point following AAS use but that was my experience in the short term post cycle. Realistically though, HCG on cycle is going to be more effective than anything
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CFC
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On top of what's already been mentioned:
If the reason guys took time to recover from a cycle of AAS was simply HPTA shutdown (negative feedback) from a decrease in LH/FSH, then the mildly supraphysiological levels you can get from using SERMs may arguably accelerate that process, though natural LH/FSH levels recover very rapidly as it is, and cell (if not receptor) regrowth is inherently rate-limited.
However, since most men suffer from longer-term effects and a failure to fully recover after various cycles of AAS, some worse than others, this is generally regarded as proof that the AAS themselves - rather than merely the decline in LH/FSH levels as a result of that negative feedback and shrinkage of the testes - cause long-term harm to cells in the testes, and probably the hypothalamus and pituitary as well.
And there is weak evidence for transiently elevated LH/FSH from SERMs undoing that damage. Most will enjoy a temporary boost to test levels, only to see them decline back to a lower baseline once off. In fact, you could speculate their use and the transient boost to test may actually hamper underlying recovery, since most SERMs diminish growth hormone levels, and there is a mechanism via elevated GH and local IGF-1 for the recovery of leydig cell number and density in testes.
Some of the known harms from AAS cycles include direct oxidative damage to various cells in the testes and brain. And there is some experimental evidence that various free radical scavengers can attenuate these oxidative harms or balance natural recuperative systems. So in terms of cost/benefit it's likely very worthwhile to take some additional supplements on cycle that may help, like taurine, NAC, astralagus, raw cacao, royal jelly, bioavailable curcumin, etc.
Either way, as already said, low dose anavar is one of those compounds that appears to do less harm to the HPTA than many others. So by all means do a PCT if you want, but bear in mind it's probably not really going to do much.
I?m going to also throw in that I have a few clients (the only ones that cycle) that I have cruise on a low dose SERM (personally recommend clomid) between cycles and all of them have given me extremely positive feedback as compared to the past where they did a PCT and then discontinued SERM use.
My typical rec is clomid @ 12.5-25mg three times weekly and has always given good blood work
My typical rec is clomid @ 12.5-25mg three times weekly and has always given good blood work
CFC
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Ok, but bear in mind there may be some unpleasant long-term risks to persistently elevating LH/FSH levels through SERM treatment.
Interesting note. I do think it would just be an incredible stretch to jump from rodents to humans when it comes to potential cognitive implications though...and things like tren have been linked to Alzheimer?s but we don?t see bodybuilders coming down left and right with the disease. Definitely something to follow but if I had to choose between low T symptoms and these implications, I?d take the risk although the endocrinologist I saw suggested and discussed the safety of long term clomid use with me.
Not sure if it would be possible to dial the dose down low enough to keep LH/FSH in range but I would think it would be. At the end of the day though, everything has the potential for risk
Not sure if it would be possible to dial the dose down low enough to keep LH/FSH in range but I would think it would be. At the end of the day though, everything has the potential for risk
CFC
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I'm not saying it's guaranteed, hence my use of "may" - I tend to couch most things I say like this. But it's certainly not 'incredible' to make the jump from rodents to humans - most preliminary in vivo research is based on doing just that - you can't just chop up humans to see what's going on, you see
In this instance, it was observed in the late '90s and early '00s that Alzheimer's and dementia patients had chronically elevated LH/FSH levels. Having observed a correlation, researchers then began performing research on rodents to test hypotheses and come up with theories.
Some of their findings you can read below:
An association of elevated serum gonadotropin concentrations and Alzheimer disease? (2000)
Alzheimer disease affects almost 4 million Americans and costs $65 billion annually. The disease is more common in women than in men, and studies suggest that oestrogen may have a protective effect. Oestrogen replacement lowers circulating concentrations of gonadotropins. When gonadotropins are added to rat granulosa cells in culture, the number of low density lipoprotein (LDL) receptors and the rate of uptake of low density lipoprotein increases. Many proteins found in Alzheimer disease plaques are ligands for low density lipoprotein receptors (LDLR) on central nervous system (CNS) neurones. This study evaluated whether gonadotropins may be associated with Alzheimer disease. Circulating concentrations of follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels in 40 male residents of long-term care facilities with the primary diagnosis of dementia were compared to 29 age-matched controls. Serum concentrations of FSH and LH were significantly higher in dementia patients. We speculate they may play an aetiologic role in the deposition of abnormal proteins, particularly those associated with low density lipoprotein receptors, in CNS neurones.
https://europepmc.org/abstract/med/10718932
Elevated Gonadotropin Levels in Patients With Alzheimer Disease (2001)
Gonadotropin levels are elevated in some patients with AD, ie, women not taking estrogen. Elevated gonadotropin levels may have a role in the production of amyloid-β protein, which is related to formation of senile plaques. Therefore, elevated gonadotropin levels may be involved in the pathogenesis of AD.
https://www.sciencedirect.com/science/article/pii/S0025619611621095
The Contribution of Luteinizing Hormone to Alzheimer Disease Pathogenesis (2007)
Several hypotheses have been proposed that attempt to explain the pathogenesis of Alzheimer Disease (AD) including theories involving senile plaque and neurofibrillary tangle formation, increased oxidative stress, and cell cycle abnormalities, since evidence for each of these pathological phenomena have been well documented in AD. Recent epidemiological and experimental data also support a role for the gonadotropin luteinizing hormone in AD. Paralleling the female predominance for developing AD, luteinizing hormone levels are significantly higher in females as compared to males, and furthermore, luteinizing hormone levels are higher still in individuals who succumb to AD. Luteinizing hormone, which is capable of modulating cognitive behavior, is not only present in the brain, but also has the highest receptor levels in the hippocampus, a key processor of cognition that is severely deteriorated in AD. Furthermore, we recently examined cognitive performance in a well-characterized transgenic mouse that over-expresses luteinizing hormone and found that these animals show decreased cognitive performance when compared to controls. We have also found that abolishing luteinizing hormone in amyloid-β protein precursor transgenic mice (Tg2576) using a potent gonadotropin-lowering gonadotropin-releasing hormone agonist, leuprolide acetate, resulted in improved hippocampally-related cognitive performance and decreased amyloid-β deposition. These findings, together with data indicating that luteinizing hormone modulates amyloid-β protein precursor processing in vivo and in vitro, suggest that luteinizing hormone may contribute to AD pathology through an amyloid-dependent mechanism. These promising findings support the importance of luteinizing hormone in AD and bring to the forefront an alternative, and much needed, therapeutic avenue for the treatment of this insidious disease.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2111407/
A recent review of the research (open access) can be read here:
Luteinizing Hormone: Evidence for direct action in the CNS (2015)
Hormonal dysfunction due to aging, especially during menopause, plays a substantial role in cognitive decline as well as the progression and development of neurodegenerative diseases. The hypothalamic-pituitary-gonadal (HPG) axis has long been implicated in changes in behavior and neuronal morphology. Most notably, estrogens have proven beneficial in the healthy brain through a host of different mechanisms. Recently, luteinizing hormone (LH) has emerged as a candidate for further investigation for its role in the CNS. The basis of this is that both LH and the LH receptor are expressed in the brain, and serum levels of LH correlate with cognitive deficits and Alzheimer's disease (AD) incidence. The study of LH in cognition and AD primarily focuses on evaluating the effects of downregulation of this peptide. This literature has shown that decreasing peripheral LH, through a variety of pharmacological interventions, reduces cognitive deficits in ovariectomy and AD models. However, few studies have researched the direct actions of LH on neurons and glial cells. Here we summarize the role of luteinizing hormone in modulating cognition, and we propose a mechanism that underlies a role for brain LH in this process.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741372/
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So would me being shut down and not producing LH be beneficial or at least a possible preventative measure?
CFC
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From this POV, it would appear to not be harmful to have below "average" LH levels. We are talking about something that typically develops later in life though.
So while it could potentially be 'preventative' to have lower levels now, we still don't really understand at what point the body struggles to clear the faulty proteins from the brain that cause tangles and plaques that kill neurons, or if there's a threshold of build-up after which the clean-up system starts to fail and symptoms gradually develop.
It has made me nervous about the two years I've been off-cycle, after years of abuse, with relatively low test and high LH/FSH levels though. Clomid would not be an option since that would make it worse. I could try some triptorelin or may just go on TRT and drop LH/FSH back down again that way.
So while it could potentially be 'preventative' to have lower levels now, we still don't really understand at what point the body struggles to clear the faulty proteins from the brain that cause tangles and plaques that kill neurons, or if there's a threshold of build-up after which the clean-up system starts to fail and symptoms gradually develop.
It has made me nervous about the two years I've been off-cycle, after years of abuse, with relatively low test and high LH/FSH levels though. Clomid would not be an option since that would make it worse. I could try some triptorelin or may just go on TRT and drop LH/FSH back down again that way.
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Well for me being young, this would pertain to later in life lol. Even if the risk of elevated LH isn't apparent for 20-30 years I'll only be in my 40s-50s at that point where quality of life is still really important to me. I guess I can be a case study here and update everyone when I start losing my mind... That's if the alzheimers doesn't cause me to forget to report back here lmao
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Why more effective than reducing oxidative free radical stress on cycle with the use of previously discussed supplementation..?
Not sure which youre referring to? If its taurine and royal jelly, mostly because there arent any human studies showing that its effective while there are lots showing the efficacy of HCG. You actually agreed in a post about a month or so ago when I asked about it. If it comes to really wanting to protect the HTPA then it makes sense to use something we know works as opposed to something we hope would work imo
All for natural supplementation over pharma when possible but Id also rather not take a chance when things like HCG are low risk and proven to work
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Honestly if you have the money, why not PCT? It helps with feeling shitty from shutdown. Yeah it may not take you back to normal levels but atleast it makes it smoother?
That?s what I?m getting out of most the research I?ve done.
As for HCG, what?s the difference between on cycle and off cycle??
The 45 day PCT that?s pretty popular does it after cycle.
That?s what I?m getting out of most the research I?ve done.
As for HCG, what?s the difference between on cycle and off cycle??
The 45 day PCT that?s pretty popular does it after cycle.
CFC
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Well, we know that's not true, and it's disingenuous (and irresponsible) of you to claim this. Countless bodybuilders have used hCG and still not recovered. I'm waving at you from here. So we know it does not protect the HPG axis, and if it did we wouldn't even be discussing this subject since it would be a fait accompli.
CFC
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By all means do a PCT if you want to. Can I suggest you read your last log, as we had all these discussions back then and there was a lot of information given to you.
I shall!! It?s always good to look back at the info given to me. If I remember correctly though, I had no idea what it was like to come off cycle and I?m all for testing out a PCT on my next cycle. I won?t do one for my current as I?m sure to get back to my normal levels of 375 soon enough
How do we know that its not true? Studies I've seen, as well as the endocrinologist I've seen, have said that HCG is the most effective protector against damage to leydig cells induced by exogenous hormone administration since it keeps them active by mimicking LH signaling. I definitely wouldn't call it irresponsible given that its probably the most comprehensive information we have available in humans. In fact I can't recall any studies showing otherwise although there may be for all I know.
As far as bodybuilders not recovering, it would need to be a clinical study where they were using HCG the entire time any hormones were administered which I don't think has been effectively evaluated. Genetic Freak commented a reply to a post of mine a few weeks ago in the thread below that seemed to confirm my thoughts although supplementation of multiple protective substances would be ideal as he stated.
http://www.bluelight.org/vb/threads/851363-Ostarine-Dosage-and-PCT?p=14398158#post14398158
CFC
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So do us the courtesy of posting them up, and also explain your theory of how LH mimetics protect Leydig cells from oxidative harm.
I have a few which I'm going to write up into a sticky. So having your proof of hCG's proven effectiveness will be a handy balance to that.