48 h ambulatory BP monitoring would be needed to see the true impact on BP.
Would not get too caught up on just elevated hematocrit when it comes to use of exogenous T and BP.
Although many tend to blame estradiol when it comes to bloat/water retention keep in mind that androgens increase sodium/water.
Androgens increase the retention of electrolytes.
The use of exogenous androgens will result in the retention of sodium, chloride, water, potassium, calcium, and inorganic phosphates.
Bloating/edema can be common in some and to what degree depends on many factors.
This can easily drive up ones blood pressure.
Inhibition of corticosteroid 11β-hydroxysteroid dehydrogenase enzymes plays a role.
Most of the initial increases in weight gain on trt are water-related whether extracellular/intracellular.
Many men on trt can gain 5-15 lbs of water weight within the first month.
The majority of gains when first starting trt are due to extracellular water (between the muscle and skin) which shows up as bloat/puffiness and intracellular water (inside the muscle cell) which will make the muscle look fuller and harder due to increased glycogen stores.
Even then once the body adjusts or measures have been taken to minimize the bloat/puffiness you are always going to hold more water when using androgens as the muscle cells will retain more water (intracellular).
When coming off androgens, especially high doses you are always going to be pissing out the water weight (extra/intracellular).
Part of the reason why men who abuse androgens mainly the so-called wet compounds deflate when they come off is because they are holding a shit load of excess water weight which is always going to be pissed away.
Does Patient-Applied Testosterone Replacement Therapy Pose Risk for Blood Pressure Elevation? Circadian Medicine Perspectives (2022) Michael H. Smolensky, Ramon C. Hermida, Linda Sackett-Lundeen, *Ramon G. Hermida-Ayala, and Yong-Jian Geng ABSTRACT We reviewed medication package inserts, US...
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Some take home points here!
• Complications of TRTs are elevated blood pressure (BP) and hypertension. Further investigation is required to determine if these and other adverse effects, like altered lipids and hematocrit and risk of major acute cardiovascular events (MACE), result from the produced T nonphysiologic 24 h patterning
• Determination of the true risk of elevated BP per unique TRT requires 48 h ambulatory BP monitoring and the correct choice of outcome measures, that is, asleep systolic BP mean and amount of asleep systolic BP dipping, most indicative of risk for MACE
Testosterone Replacement Therapy and Blood Pressure
Elevation of BP and new-onset and worsened HTN are adverse effects of TRTs; they are of major concern because they are predisposing to MACE, especially when accompanied by a treatment-induced increase of low-density lipoprotein cholesterol, a decrease of high-density lipoprotein cholesterol, and polycythemia. The package insert of each PA-TRT reports by type and frequency of the likely medication-caused adverse effects recorded in company-sponsored safety trials. There is a great disparity between the 10 unique PA-TRTs in the reported effects upon BP. BP safety trials conducted prior to 2018 entailed only daytime OBPM; nonetheless, in most package inserts the actual mean numerical change in diastolic (D) and systolic (S) BP (DBP, SBP) from baseline and scheduled clinical patient visits during treatment is not specified. Furthermore, the exact incidence of new-onset and progressed HTN is not always conveyed; instead, their incidence is categorized along with other adverse effects as proportions, for example, less than 1% or less than 3%, of trialed participants so affected. With these limitations in mind, the incidence based on OBPM of new-onset HTN of five of the six gel and solution PA-TRTs, that is, of Axiron® (https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/ 022504s013lbl.pdf),Fortesta®(https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/021463s020lbl.pdf), Natesto® (https://www.accessdata.fda.gov/drugsatfda_docs/label/ 2014/205488s000lbl.pdf), Testim® (https://www.accessdata .fda.gov/drug/satfda_docs/label/2009/021454s008lbl.pdf) [and its biosimilar Vogelxo® (https://www.accessdata.fda .gov/drugsatfda_docs/label/2019/204399s010lbl.pdf)], and Striant® (https://www.accessdata.fda.gov/drugsatfda_docs/ label/2004/21543s002lbl.pdf), is reported to be less than 1%. Even though the package insert of the other PA-TRTs warns of BP elevation and HTN as adverse effects, as later discussed few list specific incidences.
Accurate determination of the actual effect of the individual PA-TRTs on BP and induced incidence of HTN in hypogonadal men is difficult because of the inherent limitations of OBPM to ascertain representative DBP and SBP values, even though it is the recommended method of assessing BP and diagnosing HTN.
Discussion
Reports of animal model and human studies concerning the mechanisms mediating T-induced effects on BP are inconsistent (30, 37, 58, 72, 80, 82, 83, 90, 121, 157, 158, 178). According to Dubey et al. (37), T acts as a pro-hypertension hormone by stimulating catecholamine synthesis, modulating the renin-angiotensin-aldosterone system, altering endothelin-1 level, inducing endothelial damage to further atherosclerosis, and injuring glomerular endothelial cells to negatively affect renal function. Although some of the cited reports assert T constricts blood vessels and raises BP, some others assert T dilates blood vessels and lessens arterial stiffness and thus reduces BP.
The major focus of this article has been to compare the PK and achieved 24 h patterning of T concentration in relation to the adverse effects of BP elevation and HTN, known risk factors for MACE, of the different FDA-approved nonbiosimilar PA-TRTs. Serum TT, FT, and DHT concentrations in young adult men exhibit pronounced predictable-in-time 24 h variation. However, in men with an androgen hormone deficiency, these T concentrations are not only abnormally low but lack prominent circadian patterning. Accordingly, we characterized each PA-TRT according to its ability to simulate the normal TT circadian rhythm (Figure 1A). We developed five criteria for this purpose: (i) elevated and near peak TT level during nighttime sleep, (ii) peak TT level around the time of morning awakening, (iii) moderately elevated TT level during the initial hours of wakefulness, (iv) reduced TT level in the late afternoon, and (v) lowest TT level in the evening. Because at this time it is unknown whether any one of these criteria, for example, circadian time of highest or lowest TT level, is of greater biological importance than the others, we weighted each one of them equally.
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Given all that I know now and how I manage to control my BP I think I will give TRT(or HRT) another go in the future just not sure when as I still have more then 20ml of Sustanon, 20ml of Deca, 10ml of Prop and 10ml of Primobolan left in my cupboard 
