Increased risk of stroke/clotting has never been the primary or even secondary driver over concern with elevated Hct.
As I shared with Danny Bossa a few years ago: The primary concern with elevated blood viscosity is hypertension, increased shear stress to the lumen (I’m sure you are familiar with what that does), and risk of ischemia and reduced perfusion for compromised patients / older patients. Also, what’s the concern with young person running high blood viscosity for years? Ask AAS abusers what the long term implications of elevated Hct are? Integrate out over 20 years the cost of making your heart do extra, measurably more work. Combine that with a patient who has limited vasodilation ability.
Hct + inflammation status in the individual can lead to two very different whole blood viscosities in two patients with the same Hct.
@enackers / @yeti308 I am posting these here so you have the opportunity to read again or maybe the first time if you didn’t read it last time. @enackers from your posts above it doesn’t appear you did read it since you are still spouting the elevated Hct is harmless mantra from Rouzier and his folks. As I state over and over and over and over, this is a dangerous message for people with autoimmune/inflammation issues and cardio-compromised/older patients. It may also be a bad plan for younger patients when integrated out over time.
@enackers I do give you credit for making room for the possibility that elevated Hct may be problematic in some people. Thank you for adding this:
No informed person or provider confuses PCV for erythrocytosis although it is unfortunate that the term polycythemia and erythrocytosis get used interchangeably in the literature.
Erythrocytosis increases blood viscosity (it’s not just PCV that increases blood viscosity).
That’s a valuable perspective too, brother — I really appreciate the time you put into compiling all your responses. Lots of data and nuance to sort through!
For someone like me — young, plans to be on TRT forever, no autoimmune issues or other symptoms — what do you think is a good (or fine, at least) HCT range?
Edit: I should add I recently had an EKG and my doctor said it was flawless and he has no concerns about my heart at this point. Granted that can only tell you so much (limited data), but figured it might be relevant.
IMO, look at HCT and BP. If BP is high, and so is HCT, I would look at lowering HCT as a means to lower BP. BP is a good indicator of how hard the heart is working. If HCT is somewhat high, but BP is good, I think your body handles the HCT well (it isn’t causing a lot more stress on the heart).
Here was my experience (HCT dose response to TRT):
I was just about to invoke @mnben87 's advice from post above to cut through all my technical jargon and crap. Monitor your blood pressure as I don’t have the ability to determine what your dose response profile (HCT/BP vs weekly TRT dosage) looks like. In your particular case with high SHBG, you are running high TT/fT levels to resolve symptoms and the typical way to reduce Hct is to reduce T dose. In your case that may prove difficult so you’ll have to balance BP vs other symptom resolution (or maybe you won’t and your BP will be 110/70 with Hct of 55).
I have no idea the long term ramifications of running supra T for you and short term BP monitoring is great advice. How running elevated T for years will affect your endothelium and NO production capability is state of the art and an individual response. Just want you to go in informed.
Some additional implications for TRT patients to ponder (tall vs short):
Abstract
Bigger animals live longer. The scaling exponent for the relationship between lifespan and body mass is between 0.15 and 0.3. Bigger animals also expend more energy, and the scaling exponent for the relationship of resting metabolic rate (RMR) to body mass lies somewhere between 0.66 and 0.8. Mass-specific RMR therefore scales with a corresponding exponent between -0.2 and -0.33. Because the exponents for mass-specific RMR are close to the exponents for lifespan, but have opposite signs, their product (the mass-specific expenditure of energy per lifespan) is independent of body mass (exponent between -0.08 and 0.08). This means that across species a gram of tissue on average expends about the same amount of energy before it dies regardless of whether that tissue is located in a shrew, a cow, an elephant or a whale. This fact led to the notion that ageing and lifespan are processes regulated by energy metabolism rates and that elevating metabolism will be associated with premature mortality–the rate of living theory. The free-radical theory of ageing provides a potential mechanism that links metabolism to ageing phenomena, since oxygen free radicals are formed as a by-product of oxidative phosphorylation. Despite this potential synergy in these theoretical approaches, the free-radical theory has grown in stature while the rate of living theory has fallen into disrepute. This is primarily because comparisons made across classes (for example, between birds and mammals) do not conform to the expectations, and even within classes there is substantial interspecific variability in the mass-specific expenditure of energy per lifespan. Using interspecific data to test the rate of living hypothesis is, however, confused by several major problems. For example, appeals that the resultant lifetime expenditure of energy per gram of tissue is ‘too variable’ depend on the biological significance rather than the statistical significance of the variation observed. Moreover, maximum lifespan is not a good marker of ageing and RMR is not a good measure of total energy metabolism. Analysis of residual lifespan against residual RMR reveals no significant relationship. However, this is still based on RMR. A novel comparison using daily energy expenditure (DEE), rather than BMR, suggests that lifetime expenditure of energy per gram of tissue is NOT independent of body mass, and that tissue in smaller animals expends more energy before expiring than tissue in larger animals. Some of the residual variation in this relationship in mammals is explained by ambient temperature. In addition there is a significant negative relationship between residual lifespan and residual daily energy expenditure in mammals. A potentially much better model to explore the links of body size, metabolism and ageing is to examine the intraspecific links. These studies have generated some data that support the original rate of living theory and other data that conflict. In particular several studies have shown that manipulating animals to expend more or less energy generate the expected effects on lifespan (particularly when the subjects are ectotherms). However, smaller individuals with higher rates of metabolism live longer than their slower, larger conspecifics. An addition to these confused observations has been the recent suggestion that under some circumstances we might expect mitochondria to produce fewer free radicals when metabolism is higher–particularly when they are uncoupled. These new ideas concerning the manner in which mitochondria generate free radicals as a function of metabolism shed some light on the complexity of observations linking body size, metabolism and lifespan.
I don’t have the scientific rigor of @readalot (too lazy for that), but I am able to understand mechanical things in a practical way. Readalot and I had a discussion on this a while back, and concluded a great tool to assess heart work load is BP and heart rate (BPM). Higher pressure = more stress on a lot of tissues in the body (including some things most wouldn’t think of like kidneys, but also artery walls). I wouldn’t advocate a super high HCT if BP is normal, but I wouldn’t be worried about borderline HCT if BP is normal.
That’s what I’m thinking for right now. I will have another HCT value on file soon, as I just had it retested, but my BP has always been very normal – so I’m not overly concerned, though I’ll certainly keep an eye on it!
I dont know much about cholesterol because i never had any issues, and did not have to look into it. I bet someone here knows way more about that than i ever will.
Whatever your genetics say. I mean when we get low t, obviously our HCT will drop some, maybe a ton. When we take TRT it increases. That’s my educated guess. Some folks on huge doses of TRT are in the high 40s. Others take little and sky rocket into the 50s. I dont think there is a one size fits all standard.
I see the other guys posts and it is a bit perplexing.
There is a rare fucking chance this or that could be the problem. They are very quick to jump on anyone who does not account for the 1 out of 1 million chances. Reference a group of people who will inherently have morbidity issues because old people are morbid. They are close to death. haha. comparisons of the ages. literally.
I know my information comes from two doctors who practice hormone therapy. The info the guy above is posting, is from an armchair expert. He refers to anabolic abusers / body builders and says ask them about their HCT and blood. Last i recall we are both on TRT.
The amount of folks who used to give blood on TRT was massive just 3 years ago. Today i rarely see anyone giving blood.
Im saying this to just as a response, but im also saying it because it is reality. I mean the guys around here aren’t popping up like flies and telling us "be careful guys. "My friend, husband, dad, brother just had a stroke/heart attack on TRT. He had a 54 HCT and now hes dead ". We would hear about it and i am sure of it.
Shit we would see this all over the place, but we don’t.
Doctor Rouzier and Nichols and others have been practicing for a very loooong time now and they are not having patients who have had these issues. I say this in response to "These guys should stop making these suggestions because they are going to hurt someone "…
Mind boggling how experience and education can be thrown out the window by a nobody.
Good luck man. I bet your HCT levels are lower this time around.
I agree that the line has been blurred, as folks like me take TRT to high doses, but I still think there is an important difference. BBers often take astronomical doses these days.
Amen, that’s why I highlighted the term “anabolic abusers” and not BBs. Whether running a free T of 40 ng/dL and TT above 2000 ng/dL is anabolic abuse has been continually up for debate and I’m sure very dependent on the individual. Hence, I posted way up above that I understood what you were trying to accomplish at the time. I hope you can find a good sweet spot that balances how you feel with longevity!
Many start on TRT and decide to throw in a blast. Then it is an annual blast. Maybe the blasts are moderate. Do we call this a TRT guy or Blast and Cruise? Does it matter if he has a script? Some of the guys with a script are abusing more than the UGL guys.
I think a majority here are on because of wanting to feel and look younger and perhaps be more muscular / more powerful. I think one can do things safely (or moderately safely), or not. I think one can even Blast and Cruise moderately safely if the blast isn’t extreme and neither is the cruise. One can perma blast (not safe in my book, but probably won’t kill you for at least a decade).
One thing we have in common is most of us are using T for it’s benefits. We fall on different points on the risk scale though.
Additionally, I would not call @readalot an armchair expert. HIs info could be a bit more practical in some cases, but he knows his stuff. There aren’t a lot of people who I would trust to read medical literature and take their word on conclusions, but I would with him.
Hmm, great point. I hadn’t thought of that. I think if someone doesn’t ever blast, though, but just takes TRT to high doses for legitimate medical purposes, we can fairly call him a TRT guy. Maybe performance TRT.
Edit: I don’t care if someone says I’m a steroid user. I am. But I do think, when we’re talking about long-term health outcomes, there is some difference between TRT (at high doses) and even higher-dose AAS usage.
My PCP gave it extremely slim odds of success, but insurance approved our request for an echocardiogram! So I’ll have more data soon. I don’t expect to see anything too troubling at this point (on TRT for a little over 2 years), but at least it will give me a good reference point for down the road.
With it getting warm out, I’m starting to face the usual temptation to cut. Beach season approaching.
I’ve gotten peeled the past two summers but am not this year. Making a list for myself of the reasons not to get shredded — maybe it’ll help someone else, too:
It’s not ideal for your long-term health. It’s fine to be lean (like 12%, as I am now), but I’m convinced sub-10% BF stresses your system.
For me, it leads to excessive food focus and body-image issues. This would set a bad example for my son. I don’t want him to think life revolves around food. That’s a silly POV.
It impedes socialization and relationship-building. It makes you less present. Plus: as long as you’re within a certain BF range, truly no one gives a shit how lean you are.
It’s not at all conducive to muscle-building, and I’d like to gain 20-30 lbs more of LBM to achieve my ideal physique. I need to focus on gaining, not losing. And given my high TRT dose, my body should be primed for it! Time to take advantage.
It’s the weak way out (for me). My psychological struggle has always been feeling overweight, because I was a chubby kid. We all veer to one direction or the other based on our insecurities. I’ll grow more as a person by not cutting.
Let me know if anyone thinks of something I missed
That definitely includes