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Cabergoline and Pre-Existing Low Resting Heart Rate

So 3 days ago i started taking cabergoline, only one dose of 0.25mg so far and plan to take 0.25mg e5d until prolactin normalizes.
Prolactin is 50% above the top of the reference and i am tired of being impotent.
the very next day after my caber dose i started feeling horny again and woke up with morning wood after many days.

it is also helping me with anxiety, i am much calmer and panic is subsiding.

however, my resting heart rate is normally very low, it gets to 40s when i lay in bed and minimum measured during sleep was 39 bpm.

this single dose of caber definitely lowered my blood pressure a bit (dyastolic was in the high 50s yesterday) but i managed to bring it up a bit by superhydrating myself and increasing sodium intake.

but i am worried that caber is going to drop my sleeping heart rate too low. that coupled with my not so thin blood (hct of 0.51) could be a recipe for disaster, remember cyclists dying in their sleep?

and i cant donate since i am already anemic from frequent phlebotomies. my damn hct doesnt want to go down, hcg (i am off test) is driving it up.

soo, should i be concerned about caber further lowering my heart rate. I would really hate to stop it since it has brought my libido back and is cutting down on my anxiety.
As i said, i am not worried during daytime. i get little drowsy and that is about it. i am scared of what happens at night.
My daytime sitting resting heart rate dropped from like 60 to 50.

What do you fellas think?

Should i maybe go with 0.125mg 2x per week? But i am not sure whether it works at such a low dose. i mean, 0.25 is usually recommended starting dose.

ok so today it seems that my bpm are a bit higher, where they were prior to caber. Maybe 0.125 twice per week is the answer.

50 during the day is fine, esp if employing regular cardiovascular exercise. Unless you’re having frequent, palpable arrythmias (bradycardia notwithstanding) arrythmias related to a slow heart rate I wouldn’t worry.

A lowerish RHR is a byproduct of athletes heart. When my autonomic dysfunction isn’t acting up at all my HR can reach as low as mid 40s, I’ve had it at 38 on one occasion, otherwise it’s typically low-mid 60s when resting. Currently 63, but can go as high as 75 (but I feel uncomfortable when it’s in the range of 72+)

Nothing to worry about unless you’re symptomatic

I had a thorough cardiological exam 2 weeks ago, ecg, ultrasound and 24h monitor that i went to the gym with.
They said my heart was fine.

Granted, i do feel nervous taking a drug (dostinex) that is known to cause cardiac issues. But that is why i am keeping dose and duration of use to a minimum.

Hi @crolifter any idea why your prolactin is so high? Is it just because you were on too much T causing high E2/ prolactin and had to donate blood for HCT reasons?

I had high E2 and prolactin from a T mono protocol given to me by my PCP. I ended up going to Defy to fix my issues. In 5 weeks my TT was higher and E2 and prolactin were back in range. For me it only took .125mg of anastrozole twice a week. If I keep my E2 in check my prolactin follows.

So i am on hcg currently and my e2 is still crashed.
Recently i started cabergoline for high ptolactin, 0.125 3x per week. Took 0.375mg so far.

I am worried as i am constantly having high pulse pressure, like 135/65 and 125/60.
And at first when starting caber my blood pressure dropped to like 110/55 and now it is higher, like 135/65.

I talked to my doc about this, they didnt even seem to pay attention to my caber use. When i said the dose i am taking, they were like “that cant cause problems, you are fine”. But i am worried about this high pulse pressure as it is a risk factor for cardiovascular disease.

What do you think?

I also want to add that my hematocrit is 50.3 %. Not terribly high but not ideal. And i cant do a phlebotomy since my ferritin is crashed, i am barely starting to feel better, 2 weeks ago i was so light headed, out of breath and nauseous from the lack of iron (frequrnt phlebotomies, drained 1500ml of blood in a span of 7 weeks to keep my hct under 50%).

I wish the high side of my blood pressure was 135/65…I don’t think you have much to worry about.

You are nowhere near high pressure, on either number. 110/55 is actually low. If mine came in that low they’d treat me for shock

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I meant pulse pressure, the difference between systolic and dyastolic.

So it seems i cannot eat grapefruit to try to lower my hematocrit since it interacts badly with cabergoline,

Eating grapefruit to reduce HCT is bro-science and does not work.
I eat pink grapefruit everyday for the last 4 years. My HCT is always above 50%
I have to donate blood twice a year just before my 6 month blood test for TRT consult.

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Actually there is literature demonstrating grapefruit may have an effect on normalising hematocrit

In vitro studies demonstrate nargarin, a flavonoid present in grapefruit (and responsible for the bitter taste) to remove excess RBC’s via phagocytosis. Furthermore a couple studies have demonstrated naringin extract to have a statistically significant effect on RBC counts.

I sure does not work for me.

Why does hematocrit climb so high for us even on replacement doses? Are we actually using more than we need (100mg per week split into 2 shots puts me at 7,1 ng/ml, most recent bloodwork, a little above middle of the reference range)?

Or is it the “unnatural” nature of much more constant levels compared to daily fluctuations in endogenous production?

Just found this study https://www.auajournals.org/doi/full/10.1016/j.juro.2016.02.1856
More frequent smaller dosing increases the risk of polycythemia?

Androgens stimulate erythrocytosis, mechanism as to why exactly is unknown. It’s hypothesized to be related to androgen receptor interaction within the kidney (bone marrow also contains androgen receptors) however increased erythropoietin output and sensitivity to said output likely hints at an action both directly at the kidney and bone marrow.

Typically excess erythrocytosis indicates pharmacology is being created, as in, more androgen is being dumped into you’re body at one point or another than what you’re genetic set-point dictates. However this theory is somewhat flawed as some dudes don’t notice high HCT even when blasting high doses, thus it’s likely (to some extent) based on genetic factors within androgen receptor expression and individualistic response to synthetic androgens.

Typically in the absence of high clotting factors, a high HCT in itself isn’t particularly worrying unless you’re approaching 60% or RBC count is a over or at 6.5 x10^12/L. However the older you get, the narrower the point of cutoff should become (in my opinion) as you do become more prone to clotting, esp if you have heart disease, atherosclerosis becomes more prevelant as we age, also individuals who use higher doses of AAS such as myself may develop cardiomyopathy and/of premature CAD thus the concern would set in at a younger age

This can further be said for individuals with clotting factor disorders such as polycythemia (unrelated to AAS), familial hypercholesterolemia or high trigs, or connenital defects related to the myocardium.

Shots in general due to higher peaks and ability to reach high T concentrations in general have a higher risk of causing excess erythrocytosis compared to other methods of trt such as gels, patches etc

But you see, once per week equivalent dose compared to biweekly dosing even though once per week dose obviously creates a higher peak, causes erythrocytosis to a lesser amount than biweekly dosing which causes 2 smaller peaks, as the study shows.

Basically, maximizing time off or cruising phases of true replacement doses and minimizing exposure to super pharmacological doses is the only thing we can do to minimize the erythrochtosis, apart from blood donations and staying hydrated.

Since yet science has not come up with a substance which would inhibit erythropoetin release.
For sure someday such a substance wilo be created.

@crolifter I sure hope you are right. I have battled high HCT since I started TRT.
Donating blood is not the fix do to the ferritin issues it causes.

I wish more people would try things for themselves and do blood test to prove if something worked or not over posting studies. This is the Internet. You can find a study to support any position. A study does not mean it works for all. We should have a rule here on the forum. If you haven’t tested it yourself it ain’t worth posting unless it is to backup your testing on yourself.

Well you’d need to make a drug that causes apoptosis in red blood cells specifically. You see there are drugs that lower RBC counts and cause anaemia, but these are typically cytotoxic chemotherapy medications which kill many, MANY types of cells. Secondly you’d have to somehow make the drug kill off the cells in a dose dependent manner. As in not cause a drastic decrease of RBC count causing anaemia. Even then with such a diverse population doses would differ from person to person depending on individualistic drug metabolism (of however the drug is metabolised/processed), wouldn’t want to risk crashing someone’s RBC count.