Excellent advice given what we really know about SHBG:T interaction! I can dig that.
Related topic that also bears fruitful discussion:
For some years now, reduced testosterone levels have been related to obesity, insulin resistance, type 2 diabetes, heart disease, benign prostatic hypertrophy and even prostate cancer – often considered guilty more by association, than actual cause – with little attention paid to the important role of increased intracellular oestrogen, in the pathogenesis of these chronic diseases.
In the final stage of the steroidogenic cascade, testosterone is metabolised to oestradiol by P450 aromatase, in the cytoplasm of adipocytes, breast cells, endothelial cells and prostate cells, to increase intracellular oestradiol concentration at the expense of testosterone.
It follows therefore, that any compound that up-regulates aromatase, or any molecule that mimics oestrogen, will not only increase the activation of the mainly proliferative, classic ER-α, oestrogen receptors to induce adipogenesis and growth disorders in oestrogen-sensitive tissues, but also activate the recently identified transmembrane G protein-coupled oestrogen receptors (GPER), and deleteriously alter important intracellular signalling sequences, that promote mitogenic growth and endothelial damage.
This paper simplifies how stress, xeno-oestrogens, poor dietary choices and reactive toxins up-regulate aromatase to increase intracellular oestradiol production; how oestradiol in combination with leptin and insulin cause insulin resistance and leptin resistance through aberrant serine phosphorylation; how the increased oestradiol, insulin and leptin stimulate rapid, non-genomic G protein-coupled phosphorylation cascades, to increase fat deposition and create the vasoconstrictive, dyslipidemic features of metabolic syndrome; how aberrant GPER signalling induces benign prostatic hypertrophy; and how increased intracellular oestradiol stimulates mitogenic change and tumour-cell activators, to cause prostate cancer.
In essence, the up-regulation of aromatase produces increased intracellular oestradiol, increases ER-α activation and increases GPER activation, in combination with insulin, to cause aberrant downstream transduction signaling, and thus induce metabolic syndrome and mitogenic prostate growth.
To understand this fact, that raised intracellular oestradiol levels in men, induce and promote obesity, gynecomastia, metabolic syndrome, type two diabetes, benign prostatic hypertrophy and prostate cancer, rather than low testosterone, represents a shift in medical thinking, a new awareness, that will reduce the rising incidence of obesity, metabolic syndrome and prostate disease, and significantly improve the health of men worldwide.
► Do raised intracellular oestrogens in men contribute to adversely affect men’s health? ► Aromatase in oestrogen-sensitive tissues converts testosterone to oestradiol. ► Stress, poor dietary habits and xeno-oestrogens up-regulate aromatase. ► The resultant raised intracellular oestrogens activate proliferative ER-α and GPER’s. ► Aberrant signaling by oestrogens and insulin induce metabolic syndrome and prostate disease in men.
If SHGB’s job is to regulate your T level so you don’t overwhelm your receptors. I wonder why it drops so low when we inject a T overload with cycling or blasting? One would think the body would see all this T and make a ton of SHGB to prevent a receptor overload.
On my last blast my SHGB which has been running about 16 for the last two years dropped to 6.
The blast was 500/w for 12 weeks, Anavar for 4 weeks then winny for 4 weeks.
March 2021 SHGB
May 2021 SHGB post cycle bloods.
Just a hypothesis on it, but lower SHBG results in a faster clearance of testosterone. Perhaps that is the bodies way of saying, wow, this is a lot of Test, let’s flush it out a bit quicker. Again, just a hypothesis.
I’ve seen lower. Saw SHBG of 2nmol/l on a guys bloods once.
Can anyone on here beat that?
I’ve speculated in the past, though not online, that free hormones are especially important for mediating the fast effects of sex hormones via GPCR receptors like the GPER while SHBG bound sex hormones are especially important for intercellular action.
Mike Matarazzo at 0 nmol/L, but his word from his own interview.
This was gonna be my guess as well
I am not sure a super low SHGB is something you brag about. In fact, My recent post cycle bloods scared the shit out of me. I am now on 80mg Tcyp/wk for the next 6 months. It is time I clean up my bloods. Get my lipids back on track, SHGB above 20 and see if I can finely stop needing anastrozole. Look at my march 2021 bloods TT/FT/E2 that is on 125mg/w Tcyp. I am a E2 generating machine and I don’t know why. An honest assessment I am 25% body fat. I don’t have a 6pack I have a 2 pack, haha
The SHBG of 2nmol wasn’t mine. The lowest I’ve ever tested is 9nmol, highest is 27nmol
I’m sure I could get it down to 2nmol if I took GH/anything that causes insulin resistance + taking strong androgens. But I wouldn’t do that
I don’t know how much I aromatise, I rarely check E2 nowdays
What is your TRT regiment?
100-125mg/wk test E
Taken 1x/wk via 19 gauge needle or insulin syringe. Fluctuates depending on how much effort I feel like putting into it
Mine as well for the last 3 years. But for some reason I can’t keep my E2 in check at that dose. I have to take a 0.125mg of anastrozole with every shot. M/T to keep my E2 in range. I experience water weight and mood swings if I don’t. It blows me away that some guys here do 250-300/w with no AI as their self prescribed TRT protocol and have gotten away with it for years. No way could I do that.
EDIT: Ever get a warning from the forum AI you are talking to one person too much? I just did. So I guess I am done on this thread. I enjoyed our chat unreal.
So either a harpoon, or a slin pin? Maybe you meant 29 gauge?
No, 19 gauge
Primoteston comes pre-packaged with a 19 gauge syringe
I would inject it into a slin pin then. That is a big needle.
Fun fact, prior to bodybuilding Matarazzo was a boxer
I made a comment on mpmd video when he was talking about genetics and some people blowing up on low dosages. I said basically what my opening post on this thread said, that it is blood levels, not dose that impacts results and sides, and that we shouldn’t conclude that someone has bad genetics because of a poor response to a dose.
He found a research paper, which showed that the lower end blood results from a dose would be about 3x less blood concentration, than the upper end. I feel that alone is a giant factor in ones response in regards to muscle gains / sides.
This video, may or may not be in response to that, but he did go over the topic on point Imo.
Your approach is better than dose because it includes one of two factors that determines response.
The two factors are pharmacokinetics (which is essentially your blood levels after a dose and the changes of them) and pharmacodynamics.
The problem is that (at least in my opinion) individual response differs largely because of individual differences in dynamics. Binding affinities, down-stream molecules like transcription factors, tissue-density of ARs and so on.
It’s the same reason why some get gyno while others get bloating and still others get nothing side effect-wise from testosterone.
Nuclear receptors and their drugs are way more complicated than just a binding and an effect. You just have to look how the opinions on the free hormone hypothesis start to change to realize that it’s a complex process and therefore a crap-shoot how you’ll respond.
New approaches in the scientific community are tracking response and looking at genotypes. This will likely not happen for illegal substances as you need HUGE cohorts. The approach is way better than anything of the past but it is likely still not the end of the road.
All in all, your idea is better than just looking at dose but it misses a key element which is the biggest determinant.