This is just my opinion, I have learnt from people on here far more knowledgable than me, and I’m perfectly open to being corrected if anyone disagrees with me.
A decent Endo should be able to help you with this and go thru the options with you. I would just pay and go privately, things will happen far more quickly. As soon as you mention AAS NHS GPS/Endos aren’t interested (just my experience).
It’s seems that you are suffering secondary hypogonadism, and we can tell this because you have low free & total T but inappropriately normal Gonadotropins (LH/FSH)
Personally, for an attempt at recovery, I would try a power PCT, consisting of:
2000iu HCG EOD 16 days
50mg clomid 30 days
20mg Nolvadex 45 days
Then you’d have to just give it time, have blood tests monthly to see if it’s working.
The alternative would be to run a cruise dose test, aiming for a total T of between 20-30 nmol/ml. I have achieved this before with 125mg test E every 10 days, but we are all different, it’s something you’d have to keep track of closely and alter if required.
There will be a kind of threshold T level which will resolve your symptoms, and below this (or above) will cause problems. For me, it’s about 23 nmol/ml, but like before, we are all different.
The drawbacks of a cruise would be reduced fertility (which may or may not be important to you) and increased RBC count & haematocrit. These would both need to be monitored carefully with Full Blood Count (FBC) blood tests, as if they get too high and left unchecked can increase risk of heart attack and stroke.
Before doing your next cycle, I’d have a read of swoll trolls guide to PCT on here, it certainly helped me a lot. I couldn’t help but notice that you were running Eq, a long acting ester with an active life of 21 days, but starting PCT immediately as your cycle ended. Each compound is different, but it’s important that PCT does not before the active life has ended, so for Eq, PCT should start no sooner than 21 days after the last shot (while running HCG until 3 days before PCT start)
Again, it’s just my humble opinion, and I’m perfectly happy to learn from others if they feel I’m wrong! All the best mate
In bold is the crucial information although i advise reading entire post
This has been done and stickied before by far more knowledgeable posters than I but even so i get asked on a near enough daily basis by those planning their first cycle or more worryingly those who have already started their first cycle "what should i do for pct?" or "does this PCT look ok?"
so without further ado i'll try to keep things short n sweet
the cycle itself is what's shutting you down so where better to start than to do our best to minimize suppresion
HCG 500iu pinned on mondays and thursday (1000iu per week total) from your first shot of gear until 3 days prior to starting clomid
video on preparing your hcg which must be stored in the fridge once mixed: https://www.youtube.com/watch?v=JBcRZte98-g
oestrogen is far more suppresive than testosterone yet many will preach to only use an aromatase inhibitor if you start getting itchy nipples (signs of gyno) this is a ridiculous indicator of when to use an AI imo as high oestrogen doesnt always present in the form of gyno and if allowed to run rampant will definitely make recovery that much harder not to mention all the other health risks associated with elevated oestrogen
you should use an AI from day one of your cycle, preferably aromasin as it has little effects on lipids unlike arimidex and letrozole plus it's a suicide inhibitor so there is much less risk of rebound
I generally advise people to run either 12.5mg aromasin or 0.5mg arimidex ED from the start of their cycle and adjust from there, the chances of driving oestrogen too low whilst on 5 times the normal amount of test that a male produces is relatively slim as the body likes to maintain homoeostasis between oestrogen and testosterone, test rises = oestrogen rises *Please note first time steroid users who do not understand how their body responds to steroids and aromatase inhibitors it is a lot easier to rectify mistakes with anastrazole (arimidex) than it is exemestane (aromasin)
if you push your e2 too low with anastrazole you can rebound it back up fairly quickly and adjust as needed, with exemestane you get no such privilege and you can end up spending a long time waiting for your e2 to rise again which will have a negative impact on lipid profile, joint integrity, mental health, libido and overall gains*
here's a good guide for how to gauge where abouts your oestrogen is - http://www.superiormuscle.com/forums/steroid-articles/59096-estrogen-handbook
ideally we'd all be getting bloods done but if you've overlooked PCT then id be surprised if blood tests were high on your list of priorities
here is a rough guide of the start times for PCT after your final shot:
"Below you'll find starting times for your PCT based on the active life of each compound. The active life is the duration of time it takes for the exogenous hormone to be absorbed, utilized, and expelled; no longer being bioavailable. Keep in mind that active life is an approximation which is dependant on dose, ester, as well as the individuals metabolization of the compound ; but for the moderate user, these are as close to precise as you'll find.
Anadrol /Anapolan: 24 hours after last administration Deca : 21 days after last injection Dianabol : 24 hours after last administration Equipoise : 21 days after last injection Fina: 3 days after last injection Primobolan depot: 14 days after last injection Sustanon : 18 days after last injection Testosterone Cypionate : 18 days after last injection Testosterone Enanthate : 14 days after last injection Testosterone Propionate : 3 days after last injection Testosterone Suspension : 24 hours after last administration Winstrol : 24 hours after last administration"
the above chart has loose estimates at best as it doesn't take into consideration how long you've been on or what dosages you've used but assuming you've ran test enth at 500mg every week for 12-15 weeks id advise leaving 21 days after your final shot before starting PCT
during this time you continue to run your HCG at 500iu twice per week until the last 3 days prior to starting PCT when you cease HCG usage
you then run
Clomid 100/100/100/50/50 5 weeks total
Nolva 40/20/20/20/20/20/20 7 weeks total
Aromasin 25/ followed by 12.5 EOD 2 weeks total
/100/ represents 100mg ED for a week
OTC supplements that assist in PCT -
Vitamin d3 5000iu Vitamin c 500mg twice a day AM/PM (1000mg total)
mix up 30 grams of EAA powder in a litre bottle of water and drink throughout the day in between meals, do this every day for the duration of your pct and also sip a EAA drink during training
and if you havnt already been using it on cycle now would be a good time to start using creatine
during pct your body will happily dispose of all that hard earned muscle if you don't make the environment perfect for it to justify holding onto it, do this by keeping intensity high but sessions slightly shorter, train no more than 4 days per week ideally 3 with a days rest in between each session, drop cardio for the duration of pct, eat in a very slight surplus, keep your protein high and get plenty of sleep (ideally sleep without setting an alarm and wake up naturally)
Dave Crosland's take on PCT - https://www.youtube.com/watch?v=HEOfjebN1qs
Dr Michael Scally radio talk - http://www.rxmuscle.com/2013-01-11-01-57-36/blue-collar-muscle/10119-blue-collar-radio-with-shelby-starnes-john-meadows-01-31-14-this-week-john-and-shelby-talk-to-michael-scally-an-expert-on-anabolic-steroid-side-effects.html
if you are are unsure on how to run your first cycle (dosages, compounds, timing ect) then please see my "first steroid cycle... it's not that difficult" thread -
This one is far from clear cut, all I'm providing with this thread is some information for you to go off and experiment with the amount of AI / aromatase inhibitor you require on cycle, I will also loosely cover SERM's or selective estrogen receptor modulators for use in gynecomastia prevention
Ok so what are aromatase inhibitors and why do we need them?
"Aromatase inhibitors (AIs) are a class of drugs used in the treatment of breast cancer and ovarian cancer in postmenopausal women and gynecomastia in men. They may also be used off-label to reduce increase of estrogen conversion during cycle with external testosterone. They may also be used for chemoprevention in high risk women.
Aromatase is the enzyme that synthesizes estrogen. As breast and ovarian cancers require estrogen to grow, AIs are taken to either block the production of estrogen or block the action of estrogen on receptors."
a healthy male between the ages of 20-30 will produce on average 7mg of testosterone per day or 50mg per week
there is obviously variation to this figure for a whole host of reasons such as genetics, drug or alcohol use, certain diseases and conditions, stress... the list goes on, but on average most males will produce somewhere around the above figure
now at this amount of testosterone a certain percentage aromatizes into oestrogen (ive heard the figure 10% but i've found no exact data)
"Aromatization is a process that occurs naturally in the body to convert testosterone into estrogen. The reason for the name is because the enzyme aromatase performs the conversion. "
the balance between T / E is called homoeostasis and the body is tuned in a manner that in healthy males just the right amount of each is present, so what happens when we decide we want 10x the amount of testosterone our body produces naturally? the body fights to maintain that T / E ratio and as a result oestrogen shoots right up outside of the healthy range along with the exogenous testosterone (the body has no mechanism to decipher the difference between endogenous and exogenous so reacts accordingly as if it were your body producing that amount)
so we implement an aromatase inhibitor in order to keep the E2 within healthy range even whilst testosterone is at supra physiological levels
there is a whole host of side effects that elevated E2 can bring in males:
1. Gynecomastia/Male breast growth
The growth of male breasts is called gynecomastia. When estrogen is present in high levels in men, the cells in breasts change their behavior. They begin to grow and this leads to the breasts becoming larger and more firm instead of the distinct pectoral fat deposits most men have. This condition can occur in around half of boys in puberty, but if it continues into adulthood, there may be an underlying reason.
2. Low sex drive
Men who have high levels of estrogen may have a problem known as erectile dysfunction. This means he is unable to maintain an erection. Any man who is experiencing sexual problems should talk to his doctor about a possible hormone imbalance.
A man’s fertility is determined by the number of sperm he has, the movement of the sperm and whether they can survive long enough to reach and fertilize an egg. Men who are exposed to high levels of estrogen have a higher rate of infertility than men who are not. This is because estrogen lowers the sperm’s mobility.
4. Stroke risk
Because excess estrogen may cause blood clots, if a man has too much estrogen in his system, he may be at a higher risk of having a stroke.
5. Heart attack
The bodies of older men produce less testosterone. This causes a hormonal imbalance with estrogen becoming more dominant. An imbalance like this is often overlooked as a possible cause of cardio disease.
6. Prostate problems
High levels of estrogen in men can cause differing results. Some studies show that excess estrogen may cause prostate cancer, but once the cancer occurs, the estrogen may have some anticancer effects.
7. Weight gain
High estrogen levels in men can cause weight gain and that weight gain may cause higher levels of estrogen. It is a cycle that is not easily broken.
so since we are looking for the benefits of raised testosterone whilst avoiding the negatives of raised oestrogen we use an aromatase inhibitor, so what are the most commonly used (3rd generation) aromatase inhibitors and what are the therapeutic doses?
PMC full text:
Int J Clin Pract. 2007 Dec; 61(12): 2051–2063.
Copyright/License ►Request permission to reuse
Efficacy of aromatase suppression by three generations of AIs
AIs, aromatase in
"Although aromatase inhibition by anastrozole and letrozole is reported to be close to 100%, administration of these inhibitors to men will not suppress plasma estradiol levels completely. In men third-generation aromatase inhibitors will decrease the mean plasma estradiol/testosterone ratio by 77%"
NOTE - they say "third-generation aromatase inhibitors will decrease the mean plasma estrdiol/testosterone ration by 77%" they didnt specify which AI as theyre all of such similar strengths of aromatase inhibition and makes little overall difference to plasma estrodiol levels
source - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3143915/
with all of the above said my real life experience of all of the 3rd gen AI's has noted a noticeable increase of E2 inhibition whilst using letrozole over arimidex or aromasin once it has reached peak plasma levels
what are the external side effects of elevated oestrogen?
High estrogen sides
Acne, water retention (Bloat), moon face, very small testicles, scrotum hanging too high, soft testicles, extreme oiliness all over, soft erections, sensitive nipples (sore, itchy, burning, enlarged aerola)
Low estrogen sides
Dry skin, dry lips, good morning wood no wood when its time for sex, loss of wood while having sex, loss of sensitivity, dry gland (penis), white gland, hesitation just before urinating, night sweats
bear in mind these are only some of the external side effects and people can still suffer from a wide array of negative effects of elevated E2 without displaying any apparent ones, this is why blood work is highly advisable at the very least when first starting out to get a baseline of how much you aromtase and how much AI is needed to keep you within range
why in some cases is there a need for selective estrogen receptor modulator on cycle?
" Selective estrogen receptor modulators (SERMs) are a class of drugs that act on the estrogen receptor (ER). A characteristic that distinguishes these substances from pure ER agonists and antagonists (that is, full agonists and silent antagonists) is that their action is different in various tissues, thereby granting the possibility to selectively inhibit or stimulate estrogen-like action in various tissues. "
there are certain scenarios where someone may opt to implement a SERM into their cycle namely raloxifene and tamoxifen alongside their AI
the reason the two (aI and serm) are used concurrently is because SERM's do not actually prevent any of the circulating E2 but rather block its effects on certain parts of the body
generally a SERM will be used as a safety net for those that have previously developed glandular growth (gyno) which will be more susceptible to elevated E2 or with certain compounds where the user hopes to keep an elevated level of oestrogen such as with metandienone commonly known as dianabol which is often tooted as yielding greater strength gain via excessive water retention from elevated e2 although I do not agree with or condone this ideology as the same could be said for all aromatasing compounds
with only a serm on board we are merely protecting the breast site whilst allowing massively elevated E2 levels to still cause all of their negative health effects around the body (listed above)
it is for this reason that your first plan of attack should always be an AI, you implement a SERM when you are struggling to control glandular growth (gyno)
i've heard the interaction between SERM's and AI's renders AI's useless?
this is a common fallacy thrown around forums, the interaction between tamoxifen and anastrazole and femara causes a blood plasma reduction of 27% in anastrazole and 38% in femara
the reason this happens is because tamoxifen speeds up the process at which your liver processes the arimidex and letrozole
all you need to do is merely adjust your dosage as needed to allow for the slight reduction in potency.
It is also worth noting that there is no interaction with raloxifene or any of the 3rd gen AI's
Also there is no interaction between tamoxifen and exemestane (aromasin)
Doesn't nolvadex inhibit your gains?
tamoxifen does have a slight impact on IGF-1 that is overstated on internet forums, the overall reduction in IGF-1 is massively trumped by the use of exogenous hormones and will result in no notable decrease in overall gains
which AI do you recommend?
aromasin for the following reasons
* zero impact on lipids
* suicide inhibitor
* no interaction with tamoxifen
* no oestrogen rebound
note - first time steroid users who do not understand how their body responds to steroids and aromatase inhibitors it is a lot easier to rectify mistakes with anastrazole (arimidex) than it is exemestane (aromasin)
if you push your e2 too low with anastrazole you can rebound it back up fairly quickly and adjust as needed, with exemestane you get no such privilege and you can end up spending a long time waiting for your e2 to rise again which will have a negative impact on lipid profile, joint integrity, mental health, libido and overall gains
it is for this reason that i advise new steroid users to use anastrazole (arimidex) in order to get a feel for how much overall AI they require and then switch to aromasin in future cycles (use table below to decipher the equivalent doses)
I've been using X compound, what is the equivalent dose of the other common AI's?
for a rough guide think of 2.5mg of letrozole as 2mg of arimidex or 50mg of aromasin
Oestrogen control is the most individual need of a male using AAS, we can safely assume that 500mg of testosterone for a newer steroid user is ample however the percentage at which that testosterone aromatases we cannot predict
i for example need to take 1mg of anastrazole ED for anything over 500mg of testosterone, some guys this would completely crush their E2 but others require even more AI or sometimes the inclusion of a SERM
you basically need to trial and error your dosages ideally with blood work but its fairly easy to 'feel out' your required dose if you know the signs of both high and low oestrogen
this guide is pretty accurate for sussing out where your levels are at if youre not willing to pay for bloods - https://www.anabolicarchitect.com/topic/5530-estrogen-handbook/
I wrote this entire thread out this morning and for me to write out all of the relevant information I felt necessary in determining your approach to on cycle E2 control it took me the best part of 2 hours only for me to delete the entire thread with a keyboard shortcut i was unable to reverse
after going through somewhat of an outburst that wasn't helped by the fact I'm 4 weeks deep into a TTM blast and a heavy caloric deficit, I managed to get majority of my thoughts back on 'paper' for you
so apologies if some sections appear rushed (copy and pastes of previous info I've put out) or I've missed certain points
please feel free to fire any questions below as I have an overwhelming feeling I've missed some of the information I had written out this morning
(i was literally on the last line of text when I deleted the entire page by mistake)