T Nation

Does Low SHBG Mean a Shorter Half Life to Testosterone?

T Nation,
Glad to be a part of it. This is my 1st post. I know I cant believe everything I read so I’m asking:

I’ve read that the half life of T cypionate is 6-8 days, so that means it takes about 30-40 days to reach stable levels.

I’ve also read that low SHBG guys piss out T quicker, with more frequent injections being a solution. But someone mentioned low SHBG guys have a shorter half life with cypionate, so they reach stable levels quicker. Is that true?

This will help me set up my protocol. I have low SHBG (16 nmol/L), low T (200 ng/dL) and due to that, low estradiol. Could be wrong but from what I’ve gathered, an average daily dose is anywhere from 8mg-20mg. I think I’ll start low around 8mg, but I’m wondering how long I should stay there until I analyze my symptoms and decide if I should slowly increase dosage.

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no, shbg has nothing to do with the half life of testosterone. About 1-2% of testosterone, IF THAT is excreted in urine.

Conjucation, Reduction (in liver), metabolism by 5a and 5b reductase, 3HSD etc all play pivotal roles with regard to the metabolisation rate of T, furthermore esterified testosterone has a HALF LIFE (of which individual metabolism will differentiate between) but there is a generalised bell curve as to what the HL should be (aside from genetic outliers). an ED shot for someone with test C (provided they have a normal rate of metabolism towards said drug) will produce inconsequential, insignificant differences in hormonal status, as would EOD, with a half life of 7ish days, it takes 7 days to reach a 50% fluctuation within hormonal levels. Male’s natural circadian rhythm is about 30% differentiation in T levels.

My SHBG (on tests, SHBG is known to fluctuate a LOOOOT) ranges from 8-26, on 200mg test/wk 5 days in I clock out at about 500ng/dl (according to last test), I feel fine injecting every 3-5-7 and even 9 days.

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Not all low SHBG guys excrete testosterone at the same rate, I’ve seen high SHBG guys excrete testosterone like wouldn’t believe. Low SHBG guys need to keep levels in a tight range to ward off symptoms of either low or high levels, this is why very frequent dosing is needed.

My SHBG is low (14-22) and once weekly injections didn’t see much loss, if T levels fluctuated 100 ng/dL, free T fluctuated by a larger degree and TRT became less effective because my body doesn’t like big changes in levels.

When I was injecting moderate doses twice weekly, my trough was 679 ng/dL, free T 29 pg/mL and levels were sliding too much and it felt like I was barely on TRT. I feel amazing on 7-10mg daily, a fraction of the previous dose.

You may be able (if you’re interested) to get an import permit for unesterified testosterone for therapeutic purposes. (It’s still produced, but sparingly and only in certain countries).

I’ve tried unesterified testosterone, it isn’t painful like testosterone propionate (of which propanoic acid is an irritant to skeletal muscle).

Have you ever tried sustanon? I’m on sustanon at the moment, it hurts more than testosterone propionate or ANY other testosterone preparation I’ve ever used (even testosterone with extra solvents added to suit a 450mg/ml concentration), I believe there’s something in the carrier that my body rejects and/or has an overt immune response to

Seriously, I get massive, MASSIVE swelling anywhere I inject the stuff. I shoot it in my left deltoid as I have a structural abnormality within my left deltoid related to my body not forming fully (born very premature), so both my shoulders, whilst roughly the same size give or take a couple millimetres, are shaped drastically differently, especially visible from the front view, a shot to the right portion of my deltoid evens that out for like 6 days (swelling lasts a long time)… #vanity.

I’ve been offered plastic surgery for it, however building enough muscle around the area has greatly amoreliated how strange it looks. Furthermore ultrasounds found “significant structural abnormalities” around the area, and said area of my shoulder is one of the area’s I get a lot of pain, clicking and cracking from. Given it’s a structural deformity, not much I can do but simply work with it or shell out like 10K for plastic surgery.

Dam bro. I am amazed at your knowledge. I have a degree in Pharmacology and you still put me to shame haha.

did you enjoy the course? I’m considering going into pharmacy (it opens me up to other avenues after I have the degree and allows me to go into med post-grad, also I sometimes think it’d be cool to be a pharmacist, likely owning my own independent pharmacy).

I’m a bit lost at the moment, my previous goal of an endocrinologist isn’t as cut and dry as it used to be… There’s so many possibilities… How can I possibly know which pathway is the best for me both in terms of income and happiness and wellbeing?

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Man I loved pharmacology. I did several modules as part of the 3 year degree: molecular pharmacology, neuropharmacology, synaptic pharmacology etc. All great stuff.

Really comes in handy in my opinion.

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I used testosterone suspension (aka aqueous test) back in the day. It hit you fast, you’re looking for a gym or a woman quickly after injecting. It burned a little, not bad.

:rofl::rofl::rofl:

I’ve used it too, never used higher than 20mg at a time (in one day), was great for when I had to deal with shots of T e3w and needed something to keep me going while my T was bottomed out. The HL was so short I could use it right up until bloods

@weightliftingwithoutlimits @unreal24278 I would love your take on im v subq for TRT.

I already gave my opinion on sub Q hormonal injections in another thread today??

These compounds (with regard to solvents used, particle size and whatnot) aren’t designed for sub Q administration, and thus adverse site reactions are def on the table. However androgens are highly lipophilic and thus bioavailability may be increased (as may mean residence time/duration of action) when injected sub Q. Literature backs this up when comparing the pharmacokinetics of test/deca with regard to sub q vs IM shots, lower peaks and valleys, longer half life, seemingly higher bioavailability, however adipose tissue, being a major endocrine organ contains aromatase, thus if you are overweight or have a high amt of visceral fat sub Q test shots (or any aromatising hormone) may actually lead to excess aromatisation, and I don’t usually say this, as this is almost never a problem.

Other issues such as long term development of scar tissue (as the compounds are not formatted for sub Q inj) do exist, I have long lasting scar tissue on my stomach from experimenting with sub Q shots of primoteston and sustanon.

Formulations do exist (in America, FDA approved) of test for sub Q shots, maximum weekly prescribable dose is 100mg/wk (which wouldn’t be adequate for an individual such as myself) but besides the point, it’s a non generic product of which seemed merely like a futile attempt to make more money, the whole “you need to go to the doctors office so the doc can administer the shot” rhetoric is retarded, how stupid do they think the general populace is… anyone CAN administer a shot if taught how to, hell… I administer my own flu shots and various other vaccinations.

Thanks for this. You may have heard the thinking that 80mg of test injected subq is equal to 100mg injected im. From my experimentation I believe the opposite.

Any thoughts on this?

For me I think (not completely confident) that I need to inject more subq to get my e2 high enough than when I tried im

Btw I estimate my BF at 16-19%

obviously it’s individualistic in nature, there will obvious be a wide variability with regard to effectiveness, we just don’t have enough research to gauge the effectiveness of sub Q test administration (or generalised sub q androgen administration).

With you’re 80mg sub q vs 100mg IM, did you use pharm grade both times? Say you inject 100mg test E IM vs 100mg test E sub Q, the peak from a dose of both (with equivalent oral bioavailability) should, in theory be lower for the sub q formulation/shot, that being said the HL is also longer, thus the Cavg would remain about the same.

I’m unsure as to whether you’re subQ experimentation affected (in a deleterious fashion) you’re ability to raise E2, maybe it did, maybe it didn’t, bloods are generally a good way to gauge the effectiveness of a routine, did you acquire bloods of peak and nadir on sub Q?

On trough my e2 on subq is low 20s on im closer to 30 where I like it.

Not sure if I should inject more subq or switch to im. That’s my dilemma. I also want to keep my hct and hgb reasonable and those numbers look better on subq. But either way my CBC numbers were always within range just near the Top on im.

I would like your analysis on 1 more think if I may. My LVEF is low at 45%. No wall thickness . Heart cavity’s all normal size. Everything else with heart normal. Even had a CT angiogram that showed no plaque buildup.
What would cause this mild cardiomyopathy? I take daily cialis, allopurinol

I can paste the cardio report if u would like.

@unreal24278

Here’s the report
IndI C A T I O N S

Palpitations

P R O C E D U R E

Cardiac MRI

MRI CONTRAST AND MEDICATIONS

Contrast Agent Contrast Dosage Creatinine

Dotarem 0.15 Mmol/kg , 25ml

T E C H N I Q U E

The study was performed on a 3T scanner.SSFP Cine for Cardiac Function;Phase contrast for large

vessels;Phase contrast for valves;Delayed Enhancement with Gad 0.15;Pre-contrast T1 mapping;

Post-contrast T1 mapping;T2 mapping

I N T E R P R E T A T I O N

Impressions:

Non-ischemic, dilated cardiomyopathy.

No evidence of inflammation or edema. No delayed enhancement.

Findings:

  1. Mildly dilated left ventricle. Mild left ventricular global hypokinesis with mildly reduced

systolic function(EF 45%).

  1. Normal right ventricular size. Mildly reduced right ventricular systolic function (EF 46%).

  2. Normal right and left atrial size.

  3. No evidence of inflammation or edema. No delayed enhancement.

A S S E S S M E N T

Left Ventricle:

The left ventricle is mildly dilated. There is no evidence of left ventricular hypertrophy.

There is no left ventricular regional hypertrophy. Left ventricular global systolic function is

mildly reduced. The ejection fraction is 45%. Left ventricular regional systolic function is

showing diffuse hypokinesis. Mild global hypokinesis.

Right Ventricle:

The right ventricle is normal in size. There is no evidence of right ventricular hypertrophy.

Right ventricular global systolic function is mildly reduced. The ejection fraction is 46%.

Left Atrium:

The left atrium is normal in size. Left atrium area in 4 chamber view is 22 cm2. Left atrium

volume is 97.10 ml. and Left atrium volume indexed with BSA is 46.68 ml/m2.

Right Atrium:

The right atrium is normal in size. Right atrium area in 4 chamber view is 16 cm2.

Aortic Valve:

The aortic valve is tri-leaflet. The aortic valve has no significant abnormalities noted.

Mitral Valve:

The mitral valve has no significant abnormalities noted.

Tricuspid Valve:

The tricuspid valve has no significant abnormalities noted.

Pulmonic Valve:

The pulmonic valve has no significant abnormalities noted.

Aorta:

There are no abnormalities in the visualized portions of the thoracic aorta.

Pulmonary Artery:

There are no abnormalities noted in the visualized portions of the pulmonary artery.

Pericardium:

There are no abnormalities in the pericardium.

Pericardial effusion:

There is no evidence of pericardial effusion.

Delayed Enhancement Imaging:

Normal LGE

Q U A N T I T A T I O N S

MEASUREMENT LEFT VENTRICLE RIGHT VENTRICLE

End Diastolic Volume 207 ml 197 ml

End Diastolic Volume indexed by BSA 100 ml/m2 95 ml/m2

End Systolic Volume 114 ml 107 ml

End Systolic Volume indexed by BSA 55 ml/m2 51 ml/m2

Ejection Fraction % 45% 46%

Myocardial Mass 142 g 38 g

Myocardial Mass indexed by BSA 68 g/m2 18 g/m2

Stroke Volume 94 ml 91 ml

I doubt it’s the allopurinol, in rodent/animal models said drug increases cardiac function and capacity… Why are you on allopurinol though, do you have gout or something? Hypothyroidism, kidney disease??? Thinking of various mechanisms as to why you might have said issue and that’s. I could make a joke about you potentially having metabolic abnormalities leading to high uric acid however that occurs in individuals with cancer, and that wouldn’t be funny…

Look… 45% is low, what amount of exercise do you participate in weekly? Do you blast gear by any chance? Athletes heart is a known phenomenon stemming from adaptations related to intense exercise, a large majority of tour de France cyclists (doped or undoped) have extremely enlarged hearts meeting the criteria for development for hypertrophic and/or dilated cardiomyopathy (usually a combination of concentric + eccentric LVH and RVH sometimes), the ejection fractions of many of these athletes are low to low normal. To see whether you’re heart is able to meet the demands required with regard to oxygen transportation I’d say potentially (not giving advice as I’m NOT a doctor) get a stress echo, with athletes heart (provided no other maldaptation and or damage has occurred) ejection fractions will generally go right back into normality when intense exercise is initiated and the demand for oxygen and/or blood to be pumped around the body increases.

I’ll give you a more detailed response tomorrow, you see I’m supposed to be studying for a maths test but I’m fucking around instead…

What’s you’re TT and FT like on TRT? Do you drink and/or use recreational drugs (totally fine, I promise no judgement from me, some people use drugs, I have many friends/family/acquaintances that enjoy the occasional (or frequent) line (or lines) of coke, ketamine or whatever… so long as they know the risks and don’t push it on anyone else it’s all fine by me) to clarify I don’t use drugs… aside from cannabis…

Back to you’re topic, do you experience shortness of breath, presyncope during exercise, how about while not exercising, do you notice frequent arrhythmias (PVC’s and PAC’s are normal, but if they make up a large portion of you’re daily beats, say 10%+ it could be a symptom of underlying cardiovascular disease and. Do you have a familial history of cardiovascular disease, what about prior endocrine pathology, adrenal, thyroid?

There’s simply too many variables for me too deal with here, while I’m not a doctor I may be able to point something out if I had a detailed history of you’re prior medical history, however that’d likely make you uncomfortable, that and like I said I’m not a doctor thus I REALLY shouldn’t be playing doctor, it’d be innapropiate and reckless behaviour on my behalf.

Potentially contact Dr Sir through email? Otherwise I will help to the best of my abilities if it’s required.

Good luck on ur math test.

I am not looking for medical advice just trying to get as informed as I can when I talk with cardiologists.

Never did cycles. No recreational drugs. I don’t smoke anything.

What I do notice is after I exercise even for 20 minutes on treadmill that involves a couple of 2-3 minutes sprints after stopping exercise my HR goes from 160 to about 115 in less than a minute which I read is a good thing. BUT my HR stays near 100 for hours after exercise. My waking up HR is 65-70. During day near 80.
I also notice a lower blood pressure reading during these hours that my hr is near 100.

I did have a Holter monitor on for 7 days about 8 months ago. It showed occasional PVC. Burden was 1%.

Recent ekg was totally normal.

I exercise 2-3 x a week. I am not a athlete. I do not get short of breathe

Thanks @unreal24278

My HR stays elevated for prolonged periods of exercise depending on how intense the exercise is. For instance say I do a phat workout, exhausting my back, chest, biceps and triceps.

Then I get on the treadmill and run (steady pace) at 10km/hr for 25-30 mins (run 4-5k) then go on the cycling machine and crank out 10ks or so (I don’t typically go this hard, but sometimes when I’m wound up I’ll go in for an intense workout like this), having kept my HR up at 150-190 (peak) for SUCH a long time + induced catecholamic surge causes HR to remain elevated for quite a while after exercise, other variables such as eating large meals post workout don’t help either. The surge of catecholamines and individualistic sensitivity to said surge (androgens potentiate this greatly) can lead to elevated HR for a while after exercise.

BP is typically lower post-exercise, I sometimes get dizzy due to absurd hypotension (like 80/45) as exercise induced vasodilation causes a tremendous drop in BP post exercise, furthermore excess vasodialation/low BP can cause an increase in HR. If you’re highly uncomfortable (yet cardiologist says you’re fine) and the palpitations make you anxious, just do what I do and take beta blockers (I originally took them for palpitations, now I take them for social anxiety and anxiety in general), with them I never experience the physiologic side effects of increased adrenaline related to anxiety, and without the physiological effects taking place, the psychological effects are greatly blunted (and thus the vicious cycle of the two potentiating one another doesn’t occur)

BB will further lower BP further though and may decrease glucose tolerance, I take such a low dose that it doesn’t matter and has negligible impact on my BP

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Thanks for clearing confusion guys. Knowing SHBG doesn’t effect half-life, that helps clear up how much time one should give treatment. I know understanding half lives can make or break a successful protocol.

I like to start low and slow. Starting today, I’m going to follow:
10-30IU HCG daily (drop/increase depending on size of ballz)
+
-6-9mg daily of T cyp for a month. Maybe do a blooddraw. Should be close to a stable level by then, so I’ll evaluate symptoms and if needed, increase to…
-10-13mg for 2nd month
-14-17mg for 3rd month. Maybe do another blooddraw.

Btw, this thread sounds like conversations I have. Talk about 1 topic, and then 2-4 other completely different topics lol.

@unreal24278 On that topic of what to be when you grow up, I don’t think you can ever go wrong doing what interests you and making money while at it. I was actually talking to myself a few days ago saying:
“Hmm…I’m already make decent money doing a job that’s boring… but if TRT successfully works for me, I know I’ll get excited about it. If I get excited about something, I know I want to learn more to help others/myself. To make as money off that, maybe I’ll study to be a TRT/endo/primary doc too.” Didnt think of the pharmacist route at the time, but that’s definitely something to look into too.

WISHFUL thinking right now, but I have been known on occasion to make big moves :slight_smile:

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