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Maintaining heart health while on AAS

MyNameIsJeff

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I came across this paper:

While acute administration of testosterone seems to decrease vascular tone, the long-term net effect of androgens appears to be vasoconstriction via upregulation of thromboxane A2 expression, norepinephrine synthesis, angiotensin II expression, and endothelin-1 action. Furthermore, androgens cause cardiac hypertrophy, promote atherosclerosis, vascular remodelling and stimulate renal prohypertensive processes involving the renin-angiotensin-aldosterone system. Androgens seem to promote oxidative stress in the kidney and may also play a role in the differentiation of brain areas involved in blood pressure regulation.
https://www.ncbi.nlm.nih.gov/pubmed/18319594

We have 4 channels through which AAS exert negative effects on the cardiovascular system, causing damage to blood vessels, heart, and kidneys. Let's look at each in turn:

1) thromboxane A2

- Thromboxane A2 (TXA2) is a type of thromboxane that is produced by activated platelets and has prothrombotic properties: it stimulates activation of new platelets as well as increases platelet aggregation.
- Thromboxane A2 is also a known vasoconstrictor[1][2][3][4] and is especially important during tissue injury and inflammation. It is also regarded as responsible for Prinzmetal's angina.
-TXA2 is generated from prostaglandin H2 by thromboxane-A synthase in a metabolic reaction which generates approximately equal amounts of 12-Hydroxyheptadecatrienoic acid (12-HHT). Aspirin irreversibly inhibits platelet cyclooxygenase 1 preventing the formation of prostaglandin H2, and therefore thromboxane A2.


So how can we remedy the AAS induced upregulation of Thromboxane A2? Based on the information above, a baby aspirin every day should suffice. There are cardiovascular health benefits of aspirin in non-enhanced people, but it seems that for AAS users it is even more important.

2)norepinephrine
-In the rest of the body (i.e not the brain), norepinephrine increases heart rate and blood pressure
- Beta blockers, which counter some of the effects of norepinephrine, are frequently used to treat glaucoma, migraine, and a range of cardiovascular problems.
How do we counter the negative health consequences of AAs induced norepinephrine synthesis? Again, quite easy. just take a cardioselective beta blocker like Nebivolol.

3) angiotensin II

-Angiotensin is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure. It is part of the renin-angiotensin system, which is a major target for drugs that raises blood pressure. Angiotensin also stimulates the release of aldosterone, another hormone, from the adrenal cortex. Aldosterone promotes sodium retention in the distal nephron, in the kidney, which also drives blood pressure up.

Conclusions: Collectively, these results indicate that androgens potentiate Ang II-induced renal vascular responses, an effect mediated at
least partly via up-regulation of the Rho kinase signaling pathway.
https://academic.oup.com/cardiovascres/article-pdf/72/3/456/934304/72-3-456.pdf

Myocardial hypertrophy and extended cardiac fibrosis are independent risk factors for congestive heart failure and sudden cardiac death. Before age 50, men are at greater risk for cardiovascular disease than age-matched women. In the current studies, we found that cardiac hypertrophy and fibrosis were significantly more pronounced in males compared with females of guanylyl cyclase-A knockout (GC-A KO) mice at 16 wk of age. These gender-related differences were not seen in wild-type mice. In the further studies, either castration (at 10 wk of age) or flutamide, an androgen receptor antagonist, markedly attenuated cardiac hypertrophy and fibrosis in male GC-A KO mice without blood pressure change. In contrast, ovariectomy (at 10 wk of age) had little effect. Also, chronic testosterone infusion increased cardiac mass and fibrosis in ovariectomized GC-A mice. None of the treatments affected cardiac mass or the extent of fibrosis in wild-type mice. Overexpression of mRNAs encoding atrial natriuretic peptide, brain natriuretic peptide, collagens I and III, TGF-β1, TGF-β3, angiotensinogen, and angiotensin converting enzyme in the ventricles of male GC-A KO mice was substantially decreased by castration. The gender differences were virtually abolished by targeted deletion of the angiotensin II type 1A receptor gene (AT1A). Neither castration nor testosterone administration induced any change in the cardiac phenotypes of double-KO mice for GC-A and AT1A. Thus, we suggest that androgens contribute to gender-related differences in cardiac hypertrophy and fibrosis by a mechanism involving AT1A receptors and GC-A.
https://academic.oup.com/endo/article/145/2/951/2500799

The second study in particular shows that AAS induced changes in Angiotensin are probably the biggest contributing factor to cardiac hypertrophy and fibrosis. The first study suggests that the mechanism of action is an potentiation of Angiotensin II action in the heart and kidneys.
Luckily, the 'fix' for this is fairly easy as well. An Angiotensin receptor blocker such as Telmisartan should be able to bring Angiotensin activity back to normal. Of course, ARBs/ACEs are also beneficial in hypertensive people who do not use AAS. It's just that for AAS users with or without pathological hypertension it is even more crucial.

4) endothelin-1
-Endothelin 1 (ET-1), also known as preproendothelin-1 (PPET1), is a potent vasoconstrictor
-Endothelins are the most potent vasoconstrictors known.[5] In a healthy individual, a delicate balance between vasoconstriction and vasodilation is maintained by endothelin and other vasoconstrictors on the one hand and nitric oxide, prostacyclin and other vasodilators on the other.

-Overproduction of endothelin in the lungs may cause pulmonary hypertension, which can sometimes be treated by the use of an endothelin receptor antagonist, such as bosentan, sitaxentan or ambrisentan. The latter drug selectively blocks endothelin A receptors, decreasing the vasoconstrictive actions and allowing for increased beneficial effects of endothelin B stimulation, such as nitric oxide production. The precise effects of endothelin B receptor activation depends on the type of cells involved.
So in principle using a low dose of an endothelin 1 receptor blocker could be beneficial to counteract the increased vasoconstriction resulting from AAS-induced increases in endthelin 1. Unfortunately, all drugs that do so appear to be highly liver toxic and have a host of other side effects. One of the more promising drugs IMO is Macitentan. As with the other drugs, AAS users who want to take the drugs preventatively and off-label would probably need to take a lower dose than used in most of the clinical trials. In that case, the liver toxicity may be less of a concern.
Another very interesting 'side effect' of endothelin 1 receptor blocker is a reduction in red blood cell count. So potentially, this class of drugs could be used to counteract pathological increases in RBC due to AAS use. Just speculation though.
here some more information about the side effects of Macitentan:
-Some medicines that are like OPSUMIT can cause liver problems. Your doctor should do blood tests to check your liver before you start OPSUMIT

-Fluid retention could happen during the first weeks after starting OPSUMIT. Tell your doctor right away if you notice unusual weight gain or swelling in your ankles or legs. Your doctor will look for the cause

-Low red blood cell levels (anemia) can happen while taking OPSUMIT, usually during the first weeks after starting OPSUMIT. In some cases a blood transfusion may be needed, but this is not common. Your doctor will do blood tests to check for anemia before you start OPSUMIT. You may also need to do these blood tests while taking OPSUMIT

-Reduced sperm counts. This has been seen in some men taking a medicine similar to OPSUMIT. If fathering a child is important to you, tell your doctor

The most common side effects are:

-Stuffy nose or sore throat
-Irritation of the airways (bronchitis)
-Headache
-Flu
-Urinary tract infection
https://opsumit.com/


DISCLAIMER: I am not a doctor, and the above is not medical advice. I have just started researching this topic and plan to add much more info later on in this thread. Constructive feedback and criticism is very welcome. BTW the first 3 points are basically the recommendation of gotgame, I just tried to gather some more info to see why these drugs make sense. The 4th one is pure speculation though.
 

[email protected]

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good info.
however, i would not take aspirin and beta blockers even if i were on cycle.
both have a host of negative sides.
ARBs/ACEs okay, both are rly safe and negledible side effects imo (plus many other benefits)
 

MyNameIsJeff

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good info.
however, i would not take aspirin and beta blockers even if i were on cycle.
both have a host of negative sides.
ARBs/ACEs okay, both are rly safe and negledible side effects imo (plus many other benefits)
New generation cardioselective beta blockers such as Nebivolol have barely any side effects if you are not already hypotensive.
Also, I believe that the cost/benefit ratio of daily low dose aspirin is favorable in anyone with high cardiovascular risk, and unfortunately that includes heavy AAS users. As pointed out above, AAS use increases thromboxane A2 expression, which increases the risk for thrombosis (Coronary thrombosis =heart attack). Taking low dose Aspirin in principle would merely bring thromboxane activity back to normal.
 

2swole79

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Greatly informative post! I recently started both telmisartan as well as the beta blocker inderall. I can 100% notice that the inderall made me feel “better”. However after reading about their actions, I came to question whether or not beta blockers would render typicall fat burners such as eca or Clen innefective. Don’t they block the hormones realesed that are responsible for its fat burning properties? I’d love some clarification on that. And I plan to switch to bystolic very soon as it seems the better choice than inderall for a couple reasons, correct?
 

prodaf

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nebivolol could be safe
 

tommyguns2

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Extremely interesting information. Will be following this thread closely. I presently take one baby aspirin daily, and have done so for years. My BP is still on the high side of normal (140/100), and would like to see it "normal."
 
D

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so to counter act all my drugs, I need to take more drugs, which then give other unwanted side effects? I`ll stick with a more responsible protocol
 

buck

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so to counter act all my drugs, I need to take more drugs, which then give other unwanted side effects? I`ll stick with a more responsible protocol

And the interactions of these drugs with each other has probably never been tested. But we can just hope for the best, I guess.
 

MyNameIsJeff

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so to counter act all my drugs, I need to take more drugs, which then give other unwanted side effects? I`ll stick with a more responsible protocol
How is it 'responsible' to just let your heart continuously get destroyed until you end up with heart failure at 40 years old? There are only 2 responsible courses of action: 1) Don't take steroids at all, or don't go above a real TRT level of say 150mg per week. 2) take large amounts of steroids and do what you can to mitigate the negative health effects.

The way to mitigate the negative health effects is to take additional drugs, yes. And it is true that in doing so we might exchange one side effect with another one, or end up with several more. But side effects are not created equal. For example, I would always choose to trade a high risk of heart failure for low risk of intestinal bleeding.

Furthermore, the drugs I outlined above have barely any side effects in healthy people. And as I already explained, we use very selective drugs to bring very specific health variables back to normal levels. In the case of Aspirin, we seek to bring thromboxane A2 levels back to what they are normally, so that blood clotting levels should also be back to normal, resulting in theory in no additional risk of intestinal bleeding.

That is not to say that the new side effects introduced are always harmless. In my first post, I explicitly say that the side effects of endothelin-1 receptor blockers are most likely not worth the positive effects it might have. Similarly, I would not recommend bodybuilders to take statins (Many threads on this) even though this would have a positive effect on cardiovascular health.

But to make the blanket statement that taking an additional drug to control the side effects of a drug is irresponsible is frankly retarded. It's the kind of dumb folklore that gets people killed.
 

MyNameIsJeff

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And the interactions of these drugs with each other has probably never been tested. But we can just hope for the best, I guess.
Telmisartan combined with Nebivolol is one of the most common treatments of essential hypertension nowadays :banghead: Millions of people take Aspirin in combination with these classes of drugs. Given that we have a pretty good understanding of how these compounds work, we can anticipate undesirable interactions without needing to run a trial for each possible combination. In this case there are no concerns, there are databases where you
can look this up.
 

MyNameIsJeff

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In cardiac fibroblasts, Angiotensin-II induces expression of TGF-β1 through angiotensin type-I receptor [28]. It also induces expression of collagen through TGF-β/Smad pathway and extracellular signal-regulated kinase by IL-6 dependent mechanism [29, 30]. Angiotensin receptor inhibitors like losartan have been shown to reduce cardiac fibrosis in animal and human trials [31, 32]. Inflammation plays a role in the formation and progression of cardiac fibrosis. The cytokines released from macrophages and T cells, such as IL-1β and TNF-α, can promote the proliferation of cardiac fibroblasts and upregulate the expression of tissue inhibitor of matrix metalloproteinase (TIMP)-1, leading to cardiac fibrosis [33]. Use of drugs to suppress inflammation in the heart has shown benefits in reducing cardiac fibrosis. For example the administration of the selective p38 MAPK inhibitor blocked the secretion of TNFα and decreased cardiac fibrosis [34]. The drugs inhibiting cardiac fibroblast growth can also be used to inhibit cardiac fibrosis, such as β-blockers, relaxin, and statins
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4879750/

Inflammation is another factor in the development of cardiac fibrosis, whether caused by AAS use or not. There is a number of supplements that help in reducing inflammation. Four of the most popular ones are Curcumin, EGCG, CoQ10, and Lutein. Inflammation also plays an important role in atherosclerosis, but more on that later.

1) Curcumin
TNFs are major mediators of inflammation and inflammation-related diseases, hence, the United States Food and Drug Administration (FDA) has approved the use of blockers of the cytokine, TNF-α, for the treatment of osteoarthritis, inflammatory bowel disease, psoriasis and ankylosis. These drugs include the chimeric TNF antibody (infliximab), humanized TNF-α antibody (Humira) and soluble TNF receptor-II (Enbrel) and are associated with a total cumulative market value of more than $20 billion a year. As well as being expensive ($15 000-20 000 per person per year), these drugs have to be injected and have enough adverse effects to be given a black label warning by the FDA. In the current report, we describe an alternative, curcumin (diferuloylmethane), a component of turmeric (Curcuma longa) that is very inexpensive, orally bioavailable and highly safe in humans, yet can block TNF-α action and production in in vitro models, in animal models and in humans. In addition, we provide evidence for curcumin's activities against all of the diseases for which TNF blockers are currently being used. Mechanisms by which curcumin inhibits the production and the cell signalling pathways activated by this cytokine are also discussed. With health-care costs and safety being major issues today, this golden spice may help provide the solution.
https://www.ncbi.nlm.nih.gov/pubmed/23425071

CONCLUSION:
This meta-analysis of RCTs suggested a significant effect of curcumin in lowering circulating TNF-α concentration
https://www.ncbi.nlm.nih.gov/pubmed/27025786

2)EGCG
RESULTS:
EGCG significantly suppressed the TNF-α-induced protein and mRNA expression of MCP-1. Investigation of the mechanism suggested that EGCG suppressed the TNF-α-mediated NF-κB activation. In addition, the 67-kD laminin receptor (67LR) was involved in EGCG-mediated suppression of MCP-1 generation. Furthermore, EGCG potently inhibited monocyte adhesion to activated HUVECs.
CONCLUSION:
EGCG suppresses TNF-α-induced MCP-1 expression in HUVECs. This effect was mediated by 67LR and was via the inhibition of NF-κB activation. Our results demonstrated that EGCG might be a possible medicine for CVD prevention and treatment.
https://www.ncbi.nlm.nih.gov/pubmed/24852948

3) CoQ10
The aims of this meta-analysis were to evaluate the effects of coenzyme Q10 (CoQ10) supplementation on inflammatory mediators including C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) by analyzing published randomized controlled trials (RCTs). A systematic search in PubMed, Cochrane Library and Clinicaltrials.gov was performed to identify eligible RCTs. Data synthesis was performed using a random- or a fixed-effects model depending on the results of heterogeneity tests, and pooled data were displayed as weighed mean difference (WMD) and 95% confidence interval (CI). Seventeen RCTs were selected for the meta-analysis. CoQ10 supplementation significantly reduced the levels of circulating CRP (WMD: -0.35mg/L, 95% CI: -0.64 to -0.05, P=0.022), IL-6 (WMD: -1.61pg/mL, 95% CI: -2.64 to -0.58, P=0.002) and TNF-α (WMD: -0.49pg/mL, 95% CI: -0.93 to -0.06, P=0.027). The results of meta-regression showed that the changes of CRP were independent of baseline CRP, treatment duration, dosage, and patients characteristics. In the meta-regression analyses, a higher baseline IL-6 level was significantly associated with greater effects of CoQ10 on IL-6 levels (P for interaction=0.006). In conclusion, this meta-analysis of RCTs suggests significant lowering effects of CoQ10 on CRP, IL-6 and TNF-α. However, results should be interpreted with caution because of the evidence of heterogeneity and limited number of studies.
https://www.ncbi.nlm.nih.gov/pubmed/28179205

4) Lutein
The researchers extracted immune cells from the participants' blood and exposed them to lutein. The higher the concentration of lutein, the less interleukin-6, interleukin-1-beta and TNF-alpha the cells produced.
http://www.ergo-log.com/lutein-arteries-inhibiting-inflammatory-factors.html

next up: The role of VEGF and cardio exercise.
 

nothuman

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Great thread man. Keep going. I'm researching Nebivolol right now for lowering heart rate for when I'm on gh or something that raises it.
 

bieberhole69

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Great thread man. Keep going. I'm researching Nebivolol right now for lowering heart rate for when I'm on gh or something that raises it.

FWIW, the three B-blockers that show reduced mortality in HF patients are:

bisoprolol
carvedilol
metoprolol succinate (the tartrate version was not shown to improve mortality)

If I was going to get on a beta-blocker, it'd be one of these three as they seem to offer the most benefits, clinically. Granted we aren't HF patients, but it makes sense to use these over others, IMO.

But on a side note, nebiviolol MAY have vasodilating properties, so may be slightly more beneficial depending on your needs.
 
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VinnyG

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what do you think about the impact aspirin has on the synthesis of prostacyclin??

seems like it is 1 step forward 1 step back if you block your own body's mechanism of reducing platelets

I just did bloodwork and my platelets were high, gonna do the aspirin protocol and do bloods again in 10 days

Regards.
 
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adpolice

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Low dose cialis also looks very promising for cardiovascular health.I'm on carvepen 3 years now and i talked to my doctor about nebivolol he insists that carvedilol is the best option among beta blockers,especially for those who train frequently
 

ALLEX

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Low dose cialis also looks very promising for cardiovascular health.I'm on carvepen 3 years now and i talked to my doctor about nebivolol he insists that carvedilol is the best option among beta blockers,especially for those who train frequently

I go a lot by how I feel and low dose daily cialis didn't make me feel any healthier.
 

MyNameIsJeff

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Why Nebivolol?

It's important no note that the recommendation of a beta blocker is tailored here to the preventative use in AAS using athletes. For this purpose, I would argue that Nebivolol is ideal. Someone who is already in heart failure is a different story of course, and those people shouldn't be taking more than replacement doses anyways. It might be that for them, another beta blocker is superior. But let's focus on the preventative use in AAS users who don't have extensive heart damage yet:

Why Nebivolol and not another cardioselective beta blocker like atenolol? As it turns out, Nebivolol has powerful vasodilating effects which among other things contributes to its ability to lower blood pressure. Thus, for a given level of blood pressure reduction, Nebivolol will require less beta blockage in the heart, thereby maintaining exercise capacity:

Patients treated with beta-blocking agents often complain of fatigue during exercise. Exercise capacity is decreased under this condition. Nebivolol is a new beta 1-adrenoceptor antagonist with a particular hemodynamic profile, which might be due to an ancillary property. Five milligrams once daily seems the optimal dose for antihypertensive treatment. In a double-blind, placebo-controlled crossover study, the effects of nebivolol on maximal and endurance exercise capacity are compared with those of atenolol in healthy volunteers. The hemodynamic and metabolic effects during exercise are also studied. Nebivolol 5 mg once daily and atenolol 100 mg once daily decrease blood pressure at rest similarly. At these dosages nebivolol shows a smaller decrease in heart rate than atenolol. During exercise, the rise in systolic blood pressure and heart rate is less depressed with nebivolol than with atenolol. In contrast to atenolol, nebivolol does not decrease maximal and endurance exercise capacity, and does not increase perceived exertion significantly. Changes in hemodynamics influence maximal exercise capacity. Since nebivolol has less effect on exercise hemodynamics than atenolol, this might explain why maximal work capacity is not changed during nebivolol. During endurance exercise metabolic effects are thought to be more important. Under nebivolol glycerol and NEFA production is less depressed during exercise and might explain the preserved endurance capacity. These data suggest less beta blockade during nebivolol than during atenolol at the dosages used in this study. In conclusion, at a dose known to be antihypertensive, nebivolol does not alter exercise capacity significantly in healthy volunteers.
https://www.ncbi.nlm.nih.gov/pubmed/1353367

Now, why not use carvedilol instead? After all, it has similar vasodilating effects. Unfortunately, this drug is a non-selective beta blocker, meaning that besides blocking beta 1 receptors (which are mainly found in the heart and kidneys), it also blocks beta 2 receptors. The latter action may lead to the typical side effects of beta blockers such as erectile dysfunction and have negative metabolic effects. Though it would appear that in the case of carvedilol, insulin sensitivity is not negatively impacted. In fact, a recent study found carvedilol and nebivolol to have almost identical effects on blood pressure and metabolic markers:

Results:
Blood pressure and heart rate were significantly and similarly reduced in the carvedilol and nebivolol groups after treatment compared to those before treatment (both P < .001). Serum glucose (P < .001), insulin (P < .01), HOMA-IR (P < .01), HDL (P < .001), LDL (P < .001), total cholesterol (P < .001), and apolipoprotein B (P < .05) levels decreased in a similar manner in the carvedilol and nebivolol groups after treatment compared to those before treatment. Serum triglyceride and apolipoprotein AI levels did not change after treatment with both drugs.

Conclusion:
New generation beta-blockers, carvedilol and nebivolol, efficiently and similarly decrease blood pressure. They have similar favorable effects on glucose, insulin, IR, and the lipid profile
SAGE Journals: Your gateway to world-class journal research

So I would agree that carvedilol is a good option for preventative use as well, but the presence of side effects such as erectile dysfunction might be a reason to avoid it for some.

The aim of this study was to compare the effect of antihypertensive treatment with valsartan or cavedilol on sexual activity in hypertensive men who were never treated for hypertension. A total of 160 newly diagnosed hypertensive men (diastolic blood pressure [DBP] > or = 95 mm Hg and < 110 mm Hg), aged 40 to 49 years, all married and without any previous sexual disfunction, were enrolled. After a 4-week placebo period, the patients were divided into two groups: a) 120 patients were randomized to receive carvedilol 50 mg once daily or valsartan 80 mg once daily for 16 weeks according to a double-blind, cross-over design; after another 4-week placebo period, patients were crossed over to the alternative regimen for a further 16 weeks; b) 40 patients were treated with placebo according to a single-blind design for 16 weeks. At the screening visit and every 4 weeks thereafter, blood pressure (BP) was evaluated and patients were interviewed by a questionnaire about their sexual activity. Blood pressure was significantly lowered by both treatments, with a 48% of normalization with valsartan and 45% with carvedilol. During the first month of therapy, sexual activity (assessed as number of sexual intercourse episodes per month) declined with both drugs as compared with baseline, although the decrease was statistically significant in the carvedilol (from 8.2 to 4.4 sexual intercourse episodes, P < .01) but not in the valsartan-treated patients (from 8.3 to 6.6 sexual intercourse episodes, not significant). Ongoing with the treatment the sexual activity further worsened with carvedilol (3.7 sexual intercourse episodes per month) while fully recovered and also improved with valsartan (10.2 sexual intercourse episodes per month). The results were confirmed by the cross-over. Erectile dysfunction was a complaint of 15 patients with carvedilol (13.5%), one patient with valsartan (0.9%), and one patient in the placebo group. These findings suggest that carvedilol induces a chronic worsening of sexual activity, whereas valsartan not only does not significantly worsen sexual activity but may even improve it.
https://www.ncbi.nlm.nih.gov/pubmed/11206674
 

Dog-Slime

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Cbd lowers blood pressure for people having problems. I stay on a moderately high dose for my neuropathy and a brain injury. Been on a decent amount of gear including orals and ran some clen and it’s still kept mine in check (got out of range on clen but was much better than expected) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5470879/
 

pickapeck

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Well it could be that I will be dead in 10 minutes but I am 56 and have been using on and off for 28 years. I think the major problem here is that use today by even regular gym rats is far in excess of the average user 30 years ago and cycling is something that has pretty much gone out the window so there is little or no normalization time between cycles. So now we have hypothesizers that look to the pharmacy to mitigate PED polypharmacy with ancillary polypharmacy.

I think it is getting a little bit silly and, more importantly, dangerous. There is probably 1/100,000 that really has the gifts to be a high level national competitor or professional BBer. For the rest of us I just don't see why one would really push the envelope to the point to justify the unproven protocols that we are seeing here.
We are seeing gym rats on 52 weeks out of the year with a cruise dose of 500 test 300 some anabolic and 2-3 iu GH with some insulin in the mix. Then we are seeing blast periods where everything is in but the kitchen sink. Do we really think that's necessary?

I guess I should pop up an avaitar so my old wrinkled big ass delts can speak since all the young guys only listen to guys that are built even though, in my experience, most of the really big guys are jut gifted and could probably take all the wrong direction and still blow 90% of us away.

So how about some reason and responsibility in all of our game playing. Let's face it, we are all men. Men take risks. Men push to be superior to ither men. We compete pretty much with every step and every breath. But that doesn't mean we do 4 grams a week until the head pops off. Doing a true TRT (one that puts you at 800 ng/dL) or HRT with Test and a little GH modulation (like 2 iu 5/7 or a peptide or 2) is probably something all of us PED addicts should do for at least 2 periods of 8-12 weeks a year or PCT and get off if under 30 since you guys should be able to recover well if you don't abuse this shit.

If you actually cycle: that is use your PEDs for 8-16 weeks and then TRT or come off for 8-16 weeks; you can stay healthy... more than average guy healthy because the true BBer eats suoer clean 90% of the time, does cardio and caries around 20-70 lbs of extra calorie burning lean mass compared to the average Westerner. If one cycles he should be able to make great improvements with moderate dosed cycles of AAS, GH, peptides and a few ancillaries.

Once this becomes an endless cycle where the body is tossed into disarray with high dose PEDs and a dozen ancillaries the game is lost. What performance are you enhancing at that point where you cannot even run up 4 flights of stairs without turning blue and stopping to catch your breath for 5 minutes?
 

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