I’ve seen that argument used over and over and over and over on several forums, Facebook groups and YouTube videos… you bringing up the real reason is the first time I had ever heard of it not being an issue with a decimal being off one place
Well it’s been about 13 months now since my AFIB incident and this thread is as good a place as any to put a brief update given the big round-and-round I did with our favorite TOT ambassador.
After switching back to T4 monotherapy and keeping my TRT dosage at 70 mg/week (once weekly injection) with intermittent hCG usage last summer, the panic attacks and heart racing at night have subsided and no noticeable PVCs/PVAs anymore. Libido and performance are back to pre-nandrolone and AAS-use level. Doesn’t appear to be any lasting damage and my cardiovascular system, weights are doing well and bodyfat hasn’t budged.
Using moderate to high-ish dosages of T3 (I ended up at 50 mcg/day along with 125-150 mcg/day of T4) for a while was a dumb thing to do in retrospect and one can easily fall for all this high rT3 rubbish you read on the internet and from “optimization” providers. Especially dumb to combine with even very modest dosages of Test and some AAS. I tried it and paid.
Be careful before you take advice that you need to “optimize” your thyroid even though you have numbers in range. Be even more careful if you are hypo as you may have less thyroid reserve and less room for error. My multi-year experiment with T3 and T3/T4 hybrid treatment taught me a lot. For those that may be interested in decent case studies on how to properly dose titrate with T4, here’s a nice treatment (albeit some cherry-picking). It’s backed by reasonable process control theory and would be supported by those mainstream board-certified Endos that get bashed on here all the time:
If there’s some genuine interest in how to use this approach, I may post a brief summary of key equations and how you would use this approach in practice. It’s a little more satisfying for those trying to nail down an “optimum” TSH when their Endo tells them they are in range and they are left wanting a little more. The approach also employs a physiologic approach to managing the thyroid. This treatment lays out a process to target “optimum” TSH and why it is where it is (it’s a model and all models are wrong, but this one seems useful).
Enjoy the nice literature summary. Still no concrete causation between clotting and AAS use and reinforces the YMMV principle. It’s great to not have any issues with long-term use of high dosages of AAS until it isn’t. I like the highlighted summary statement below:
In summary, the evidence presented herein leads to the conclusion that AAS excess may generate a prothrombotic state based on elevated platelet count, platelet agonists reactivity, and platelet activation with subsequent enhanced platelet aggregation. As noted, most of the reviewed human and animal studies revealed a stimulatory action of exogenous androgens on platelet function and count, whereas only a few others indicated a neutral, or even an inhibitory, effect. Regarding the influence of androgens in physiological doses on platelet function, researchers agreed on them having a beneficial effect. The heterogeneity of the findings results from imponderable factors, such as the various types of androgens used, the large variability in doses, time of intake, way of administration, or cycle of drug-use in athletes, as well as the variable number of subjects included in studies, the hemostatic status of the human subjects prior to treatment, or even their individual susceptibility to androgen intake or therapy.
Even if there is a comprehensive body of evidence suggesting the existence of a pro-aggregant effect of exogenous androgens, the link between AAS abuse and thrombosis remains to be more clearly established. This causal relationship must also refer to the influence of androgen excess over the humoral system of coagulation and fibrinolysis, another subject of debate. The gathered data in this area suggest that AAS abuse induces an overactivation of the hemostatic system, with both procoagulant and fibrinolytic effects . Depending on various exogenous or endogenous factors, at a certain moment the procoagulant action probably overcomes the fibrinolytic one. The coagulation abnormalities, especially when associated with increased platelet activity, may therefore lead to a thrombotic diathesis, which could explain the multitude of thromboembolic events reported so far in the AAS-abusing population.
Despite over fifty years of research on the thrombotic risk of androgens, the current state of knowledge in this regard is still scarce. Taking into account the fact that the prospective longitudinal studies in humans have unavoidable limitations, because of obvious ethical considerations, it is a certainty that at least more epidemiological studies with thrombosis outcome, and animal experiments with “real-life” AAS dosages are warranted, in order to elucidate the overall effect of supraphysiological androgens on hemostasis and to provide new compelling evidence for their claimed thrombogenic potential.
Hi @readalot. Can you please post a short summary on how to use this TSH titrating approach in practice?
On my list, thanks for asking. I’ll try to keep it practical as it’s quite the topic.
A reference range for TT from 1984.
So much for 1500 ng/dL upper limits in the good ole days.
They have decreased though.
Heres UK medichecks reference ranges - notice the difference in SHBG and T ranges.
Especially at the bottom end of T and upper SHBG.
Basically you could have a Free T level way lower now if you were upper end SHBG and lower end T with those changes combined than back then.
Interestingly the NHS SHBG range goes up to 94!!! I had SHBG in the 70s and my GP said it was in range. I felt like crap despite “normal” testosterone levels
1980…still looking for those 1500 ng/dL natty beasts.
I looked hard a year or so back and couldn’t find anything to substantiate a significant generational decline in T levels. There was evidence of modest decline but certainly no 1500 ng/dl levels for average joes walking around.
I reckon the top ofnthat reference range isn’t to be sniffed at.
Not far off a 15% drop in top end healthy levels!
The FSH reference range puzzles me… whats happened there?
Still… you very, very rarely see a ref range that goes up to 36 nowadays. I’ve seen ref ranges cut off below 20nmol/l
There actually is a moderate body of evidence suggestive of generational decline. It isn’t particularly significant (i.e 1500ng/dl to 500ng/dl) it’s closer to 650ng/dl - 450/500ng/dl.
We are basically saying the same thing.
Good point, one lab I use now has 700 ng/dL as the top of range. However, we do have data from 50 years ago (reasonably accurate RIA data) and 300-1100 ng/dL is still a decent reference range just like it was 50 years ago. Just don’t want guys believing their granddads were walking around routinely with 1200 ng/dL TT levels which I’ve read on here plenty of times. Ok maybe the granddads of T-Nation members were :-).
Anyone able to answer my question about the change in FSH ref range?
Good question and that would be a fun project (with associated time) to see if there was systematic shift in ref ranges, sampling bias, or initial inaccuracies from then till now. I cannot currently answer your question and look forward to hearing/reading more about this.
Scope of my post was around TT and evolution in its ref range over last 50 years. I have looked enough to satisfy my curiosity. Will let you know if I find an answer for you.
That’s more than “up there”, that’s suspicious as hell… Even women with PCOS have a TT below 150ng/dl, above 200ng/dl is indicative of a tumour or something. A woman with a TT of almost 1000ng/dl tis probably doping.
A TT of 40 1154ng/dl within a man is possible, but such a number is rare, esp for an elite athlete wherein overtraining prior to competition may adversely alter endocrine parameters. I’d argue many can get away with using testosterone in competitive sports as the standardised test to look at testosterone/epitestosterone ratio, if you fail a carbon isotope ratio test is typically conducted, but the test is expensive to perform. There is a genetic mutation (I’d have to look it up again) regarding this ratio that could theoretically allow a subset of athletes to seriously abuse testosterone (like 400mg/wk) and not get popped.
The cutoff criteria for T/ET rato is 4:1, very few have such a ratio naturally. One study I’ve looked at indicates a fair portion of me can use a decent amount of testosterone (enough to statistically enhance performance) without getting popped.
I happen to personally know one individual who competed in the Olympics within a predominantly anaerobic sport. If you look at pictures of him before/after his competitive days he goes into professional athletics as a relatively skinny guy with a full head of hair, comes out looking like a brick shithouse with no hair. Might have been natty… but I’ll suspend my disbelief