And not being patient when first going on trt.
Like I did, we just don’t give our body enough time to adjust to the new found liquid gold. So what do we do we throw an AI at it that puts you on a never ending Rollercoaster. And blame everything in e2.
I also think it’s not useful to start a guy that’s been low t for many years with a dose greater than 120 MG. It will create to many symptoms on the onset
He will advise you to supplement both dhea start 25mg preg - 100mg sustained
And this has what to do with men having Caridac issues while on testosterone? Nothing.
I was replying to your comments on my 3 points. You trashed all 3 by lashing out and also misread my comments regarding point 2.
Point 1, vast majority of young males are not walking around with estradiol levels of 75-100. That’s it. Would be easy to just come out and educate folks on that in a podcast. Assuming patient is doing a good job with body composition, I can see where most would do fine without an AI.
Point 2 has to do with risk of CVD with Hct (Hct exhibits a typical U-shape with morbidity). I didn’t mention testosterone in point 2. You misread it. I am bringing up the concern of erythrocytosis secondary to the use of TRT. You immediately jump to accusing me of saying testosterone causes cardiac issues. It takes work to identify and discuss primary, secondary, tertiary effects.
Point 3 has to do with use of minimum effective dose of hCG for TRT induced organ failure.
I really struggle on these forums as reading comprehension seems to be a challenge on here for many. But, these are important topics that have significant health implications for men. Feel free to correct my facts on blood viscosity.
Men having their Hb and Hct Raised by testosterone for over 80 years but yet No heart attack strokes or blood clots. Your theory is just that. A theory that sounds reasonable but doesn’t pan out in reality or medical studies.
Optimize all your hormones as they all have their own beneficial effects
Never seen it. Really I’ve never had anyone complain of it. My response if I did would be to give it time. Let me tell you this though. Look at every study you can find on testosterone. Seriously no joke. I can send you as many as you would like as well. You won’t read that in any of the articles. In none of the studies showing the benefits of testosterone in over 80 years did they use testosterone except to preserve fertility. Hcg is not bioidentical. The beta unit is different than LH.
@readalot there is still a statement of yours from way up above that I will address (ranges). I believe @yeti308 has probably clarified several things.
There is no better individual on this entire forum to teach you this stuff. None. I’ll bet my life on it.
Heading back to my office now and I’ll reply there.
I didn’t say it was bioidentical but thanks for clarifying. I am very familiar with the chemical structure and therapeutic utility of hCG. Your clinical experience seems to differ from those of your peers. You’ve never had a patient complain of testicle pain while on TRT, especially a patient who is secondary? Wow. Thanks for weighing in.
@roscoe88 - yes, it is. In one or two if his posts he had info at the bottom with his name and contact info.
Feel free to correct my errors on blood viscosity. It’s not my theory, just relevant physics and clinical experience. I actually listened to a podcast a few months ago where suggestion was made to shoot for Hct of 55. Insanity, patient beware.
The implications of the systemic vascular resistance response for the treatment of several anemias have been discussed above. It is also worthwhile mentioning that increased blood viscosity is easily treated with therapeutic phlebotomy [Holsworth et al. 2014]. This intervention has great potential because increased blood viscosity is seen in association with all major risk factors for atherosclerotic cardiovascular disease [Sloop et al. 2015]. Therapeutic phlebotomy is not an obsolete modality from medieval times. Sir William Osler used it in treating pneumonia at Johns Hopkins Hospital. This quote is from the 1921 edition of his classic textbook, The Principles and Practice of Medicine :
We employ [therapeutic phlebotomy] much more than we did a few years ago, but more often late in the disease than early. To bleed at the very onset in robust, healthy individuals in whom the disease sets in with great intensity and high fever is good practice. Late in the course marked dilatation of the right heart is the common indication [Osler and McCrae, 1921, p. 102].
The benefit observed by this eminent clinician was probably due to a decrease in elevated blood viscosity caused by the acute phase reactant fibrinogen, which would improve vascular congestion as well as decrease pulmonary vascular resistance in cor pulmonale. Therapeutic phlebotomy was used for angina pectoris at Charity Hospital in New Orleans in the 1960s [Burch and Depasquale, 1965]. Those patients reported a general feeling of improvement in wellbeing after phlebotomy. Additional reports of the efficacy of therapeutic phlebotomy in angina pectoris were published in 1970 [Parker et al. 1970] and 1994 [Piccirillo et al. 1994]. Most recently, a prospective, randomized trial of therapeutic phlebotomy in metabolic syndrome resulted in significant decreases in serum glucose and blood pressure [Houschyar et al. 2012]. Systolic blood pressure decreased from 148 ± 12.3 mmHg to 130 ± 11.9 mmHg in subjects and from 144.7 ± 14.4 mmHg to 143.8 ± 11.9 in controls. Serum glucose decreased from 110.7 ± 29.4 to 98.5 ± 24.0 mg/dl in subjects and from 109.1 ± 39.4 to 107.3 ± 33.6 mg/dl in controls. Furthermore, blood donation is also associated with a reduced risk of myocardial infarction [Salonen et al. 1998]. Although prospective data on therapeutic phlebotomy, blood donation and blood viscosity on the risk of atherosclerotic cardiovascular disease are still either limited or not widely appreciated, hemodynamics must obey the laws of physics: perfusion is inversely proportional to blood viscosity, and without a response to maintain homeostasis, blood viscosity will increase systemic vascular resistance. Reduced blood viscosity will increase blood flow to skeletal muscle, increase glucose utilization, and improve hyperglycemia. Therapeutic phlebotomy will decrease systemic vascular resistance and blood pressure, whatever the cause.
Let me just address the important one. The erythrocytosis from testosterone is not dangerous (it’s beneficial) and has never caused a problem in the
History of testosterones use. The physiologic erythrocytosis has never caused a problem. That’s my point.
The underlying physics, easily accessible literature, and clinical experience of physicians would disagree with that reckless statement. So no intervention from you when a patient’s Hct increases to 55 on TRT? No concern for LVH with long term elevated Hct? Where’s the standard of care?
Testosterone use causing erythrocytosis
The implications of the systemic vascular resistance response for the treatment of several anemias have been discussed above. It is also worthwhile mentioning that increased blood viscosity is easily treated with therapeutic phlebotomy [Holsworth et al. 2014]. This intervention has great potential because increased blood viscosity is seen in association with all major risk factors for atherosclerotic cardiovascular disease [Sloop et al. 2015]. Therapeutic phlebotomy is not an obsolete modality from medieval times. Sir William Osler used it in treating pneumonia at Johns Hopkins Hospital. This quote is from the 1921 edition of his classic textbook, The Principles and Practice of Medicine :
We employ [therapeutic phlebotomy] much more than we did a few years ago, but more often late in the disease than early. To bleed at the very onset in robust, healthy individuals in whom the disease sets in with great intensity and high fever is good practice. Late in the course marked dilatation of the right heart is the common indication [Osler and McCrae, 1921, p. 102].
The benefit observed by this eminent clinician was probably due to a decrease in elevated blood viscosity caused by the acute phase reactant fibrinogen, which would improve vascular congestion as well as decrease pulmonary vascular resistance in cor pulmonale. Therapeutic phlebotomy was used for angina pectoris at Charity Hospital in New Orleans in the 1960s [Burch and Depasquale, 1965]. Those patients reported a general feeling of improvement in wellbeing after phlebotomy. Additional reports of the efficacy of therapeutic phlebotomy in angina pectoris were published in 1970 [Parker et al. 1970] and 1994 [Piccirillo et al. 1994]. Most recently, a prospective, randomized trial of therapeutic phlebotomy in metabolic syndrome resulted in significant decreases in serum glucose and blood pressure [Houschyar et al. 2012]. Systolic blood pressure decreased from 148 ± 12.3 mmHg to 130 ± 11.9 mmHg in subjects and from 144.7 ± 14.4 mmHg to 143.8 ± 11.9 in controls. Serum glucose decreased from 110.7 ± 29.4 to 98.5 ± 24.0 mg/dl in subjects and from 109.1 ± 39.4 to 107.3 ± 33.6 mg/dl in controls. Furthermore, blood donation is also associated with a reduced risk of myocardial infarction [Salonen et al. 1998]. Although prospective data on therapeutic phlebotomy, blood donation and blood viscosity on the risk of atherosclerotic cardiovascular disease are still either limited or not widely appreciated, hemodynamics must obey the laws of physics: perfusion is inversely proportional to blood viscosity, and without a response to maintain homeostasis, blood viscosity will increase systemic vascular resistance. Reduced blood viscosity will increase blood flow to skeletal muscle, increase glucose utilization, and improve hyperglycemia. Therapeutic phlebotomy will decrease systemic vascular resistance and blood pressure, whatever the cause.
The role of chronic hyperviscosity in vascular disease
Cardiovascular disease is still the leading cause of deaths for both men and women worldwide. Many risk factors have been identified and current therapeutic efforts have been centered on addressing these risk factors. However, as of today, the role that blood viscosity plays in this disease has not yet received its due attention. Viscosity is a fundamental property of any fluid. Its important role in both normal individuals and patients afflicted with cardiovascular disease has been underestimated. Past and current research has reported the benefits in addressing this important factor; however, mainstream medicine has not appreciated or fully accepted this important measurement. With continued research and published, peer-reviewed studies pertaining to the importance of blood viscosity in cardiovascular diseases, this relationship will be recognized, appreciated and will no doubt reveal the positive aspects of hemorheology, which will save lives.
You haven’t read these papers or spoken with even the most reasonably competent cardiologist about these topics?
Once again a great theory and concept but hasn’t played out in any study when we raise he hb and hct in any study including men with cardiac disease. So much more involved such as the pliability of the rbcs etc. So with regard to TRT the erythrocytosis has never caused harm
@readalot you need to differentiate erythrocytosis (harmless) which is normal and to be expected, to a certain degree, with TRT use vs polycythemia vera (harmful) which involved a clotting issue. Men with erythrocytosis have no need to donate. Guys at altitude wind up with higher levels. Elite athletes using depo etc wind up with higher levels. None of them are dropping dead. Guys at altitude are not lining up at the blood bank. We monitor levels if they start getting high to simply ensure it is erythrocytosis and not something else.
@yeti308 - do you have any thoughts about deceased ejaculate and taking forever to finish in relation to higher levels of E2?
I’ve had a vasectomy too…seems when I’ve increased my dose (assuming an increase of E2 as well since there is more test to convert) I always have a decrease in volume and there are times I have a hard time finishing.
I think this has also happen to @alldayeveryday and @NH_Watts too. Curious if there is some link to E2 and decreased volume/increased duration to finishing?
Thanks
Hcg doesn’t work for many and adding HCG to a protocol complicates things. If a man is having that much pain I’m sure Dr. Yeti would give the man HCG. Actually I know he would.
Simplicity is the key. Not the nonsense that goes on with “inject Monday and thursday and then add HCG on Tuesday and friday. At the same time apply part of this cream to the inside leg, just in case you have estrogen issues take an ai. .
Guys, and @readalot, as you may have heard, I do some very simple English podcasts on the subject these days. I’m going to post the links to two of them I’ve done which are on YouTube (doubt the mods here will mind). Watch these, then send me your questions. This will prevent me from having to repeat a lot of it. Yes, I made some mistakes of saying ‘estrogen’ instead of ‘testosterone’ (and vice versa), as public speaking is harder than you’d think if you’ve never done it. I await your questions.
Do I need an AI with TRT?
Hormone optimization mistakes:
Respectfully, you aren’t getting it. I am differentiating the two. With your logic, you call erythrocytosis harmless, therefore it must be harmless. What’s scary is you don’t seem to understand that. Go read my posts. I outline all of this. Here’s one verbatim from ExcelMale:
THE DETERMINATION OF BLOOD VISCOSITY IN MAN BY A METHOD BASED ON POISEUILLE’S LAW
So the formula that does a very nice job fitting all that pretty data in mammals is referred to as Hatschek’s formula (hat tip). That is viscosity is equal to viscosity of plasma divided by the quantity of (1-hematocrit raised to the 1/3 power).
So if you take this formula and manipulate to take the derivative of the viscosity with respect to hematocrit (I’ll spare you), you can plot out how quickly the function is increasing (rate aka slope) at any point on the curve of hematocrit vs apparent viscosity:
Here I am using a plasma viscosity (eta zero in equation above) of 1.3 cP. The line in blue is viscosity (goes with the left ordinate) and the orange line is the slope of the blue line (goes with the right ordinate or secondary y-axis). You can see blue line goes up pretty linearly but really starts to take off after about 45-50% hematocrit. So going from 50 to 55% hematocrit doesn’t result in the same absolute increase in viscosity as going from 40-45% or 45-50% (it’s more!).
So what about that plasma viscosity term since the equation above isn’t just dependent on hematocrit. Why all that variability in people’s experiences with BP, symptoms and hematocrit?
Why must a practitioner be cautious? When was the last time you had your plasma viscosity measured? I haven’t done it 
. Ah, finally a test I haven’t run.
So plasma behaves as a Newtonian fluid but its viscosity is a strong function of the proteins within. Take a look at these papers. Guess what really jacks with plasma viscosity, yep you guessed it, inflammation.
Plasma viscosity: a forgotten variable.
Plasma viscosity in inflammatory bowel disease
So let’s review an instructive example with two guys, Joe and Bill. Joe has a plasma viscosity of 1.3 cP and Bill (who’s got some immune issues) has a plasma viscosity of 1.5 cP (could be much worse). They both present with hematocrit of 55%. Let’s plot it:
Looking at the graphical construction above, Joe (at a Hct of 55%) has a blood viscosity of 7.2 cP. Bill at same Hct has a blood viscosity of 8.3 cP. Guess where Joe’s Hct would have to be to give the same blood viscosity as Bill? Just a little north of 60%! So Bill’s blood at 55% Hct is behaving the same way Joe’s blood would behave at 60%. An equivalent hematocrit reading in two persons does not necessarily indicate the same blood viscosity. Can you see now why a blanket suggestion that hematocrit levels above reference range are not a big deal is flawed practice? Individual mileage may vary.
But hold on, isn’t this example quite extreme. Are you exaggerating for effect readalot?
Well, if you substitute 1.1 and 1.3 cP (the normal range endpoints given in paper provided above) for Joe and Bill’s plasma viscosity, you draw the exact same conclusions. Modest (10% variation) in plasma viscosity combined with non-linear relationship of serum viscosity vs. Hct can result in very different serum viscosities for two individual’s with the same Hct.
Want even more fun…Here’s the plot for Joe, Bill, and their buddy Jay who all have Hct of 55%. Remember, Joe’s plasma viscosity is 1.3 cP and Bill’s is 1.5 cP. They’re jealous of their super stud buddy Jay who has a very low serum viscosity of 1.1 cP. How do they compare? Jay would need a hematocrit of 65% to match Bill’s serum viscosity even though Bill and Jay have the same hematocrit of 55%.
@readalot I will send this to Dr Scott Howell and I’ll let you know what he says about it.
