Beta Blockers Stims and T3

[whacked]

Heart is healthy. No issues other than mild BP issues that I control well with 40mg Telmisartan.

I ‘electively’ take a small dose of 2.5mg Nebivolol to assist w the 15-20pt uptick in HR I got from GH use (2-3 IU’s/day TP grays) for years.

*It helped me return to 70 BMP resting.

Wanting to add either 30-50mcg of T3 OR stims (DMAA or ECA) assist w cutting cycle.

My question:
Will the Nebivolol inhibit the effects of either with respect to fat loss?
Thanks in advance

 

[nothuman]

I don't see how Nebivolol will inhibit fat loss effects. I've on occasion used them together (T3 early and Nebivolol night) and didn't notice anything on that front.

 

[whacked]

Thanks. My very limited understanding based-thought-process is…

Beta-blockers lower HR and I would assume, metabolism as well (?).

T3 and stims exert “some” of their effects by way of an increased metabolism.

Wouldn’t a beta-blocker inhibit / antagonize some of the intended effects then of T3 and stims?

Thanks

 

[maldorf]

I think one of the side effects of beta blockers is weight gain. Thing is, you're probably taking a low dose, so it shouldn't be very noticeable. I'm on a large dose and I can tell, but it's still not terrible.

 

[GreenTLB6]

I’ve seen a couple people say they feel Nebivolol didn’t inhibit fat loss like some other beta blockers.

 

[maldorf]

I’ve seen a couple people say they feel Nebivolol didn’t inhibit fat loss like some other beta blockers.

Yeah, I think the ones that are more beta 1 specific are better in that respect.

 

[Type-IIx]

Heart is healthy. No issues other than mild BP issues that I control well with 40mg Telmisartan.

I ‘electively’ take a small dose of 2.5mg Nebivolol to assist w the 15-20pt uptick in HR I got from GH use (2-3 IU’s/day TP grays) for years.

*It helped me return to 70 BMP resting.

Wanting to add either 30-50mcg of T3 OR stims (DMAA or ECA) assist w cutting cycle.

My question:
Will the Nebivolol inhibit the effects of either with respect to fat loss?
Thanks in advance

So, the increased pulse pressure from rhGH would have been better addressed with sodium intake reduction, switching to nighttime admininstration if taking early, starting lower and titrating up, and understanding that increased pulse pressure tends to stabilize or diminish and is generally NOT serious... so now you're probably accustomed/dependent on taking Nebivolol (already for years) unnecessarily.

To your question, it's the classic confusion of side-effects with effectiveness. I have not looked specifically at Nebivolol and this, but beta blockers + stims to treat the side-effects of the stims generally do not inhibit the efficacy (i.e., fat loss) of the stims (or T3).

Having a beta blocker on hand for stimulant sides would have made more sense than taking a beta blocker to address short-term systolic increases from rhGH. Now you're already on something that could have helped, and it's kind of been expended as a useful med you could have used.

Generally DMAA and ECA increase RMR but especially NEAT (fidgeting, expending nervous energy, etc.) that will not be altered by a beta blocker.

T3 is already increased by rhGH, and is responsible for some of its lipolysis. Since the rhGH dysregulates thyroid function substantially, I wouldn't use this.

 

[whacked]

Thanks Type-II! Could of used you a year ago when I began the Nebivolol. Lol.

 

[nothuman]

I think one of the side effects of beta blockers is weight gain. Thing is, you're probably taking a low dose, so it shouldn't be very noticeable. I'm on a large dose and I can tell, but it's still not terrible.

It is for most beta blockers but Nebivolol is a newer generation cardioselective beta blocker so it doesn't have this side effect

 

[nothuman]

Thanks. My very limited understanding based-thought-process is…

Beta-blockers lower HR and I would assume, metabolism as well (?).

T3 and stims exert “some” of their effects by way of an increased metabolism.

Wouldn’t a beta-blocker inhibit / antagonize some of the intended effects then of T3 and stims?

Thanks

If you took Metoprolol, then this is possible. With Nebivolol, it is unlikely.

 

[maldorf]

It is for most beta blockers but Nebivolol is a newer generation cardioselective beta blocker so it doesn't have this side effect

Yeah, thats what Im talking about when I refer to beta 1 specific. I take Bisoprolol, which is much the same. For many years I took Carvedilol and it wasnt so selective. I got off of that because it was lowering my BP too much. i feel like it also made my metabolism more sluggish. Carvedilol though is one of the mainstay heart failure meds.

 

[cmryan]

Heart is healthy. No issues other than mild BP issues that I control well with 40mg Telmisartan.

I ‘electively’ take a small dose of 2.5mg Nebivolol to assist w the 15-20pt uptick in HR I got from GH use (2-3 IU’s/day TP grays) for years.

*It helped me return to 70 BMP resting.

Wanting to add either 30-50mcg of T3 OR stims (DMAA or ECA) assist w cutting cycle.

My question:
Will the Nebivolol inhibit the effects of either with respect to fat loss?
Thanks in advance

I think Lyle McDonald posited that the use of beta blockers (specifically B1 selective ones) could improve lipolysis by increasing ANP. Well, he did say if used in isloation they're a net negative but the increase in ANP made it less of a net negative than one would think. And if used in concert with a stimulant that's a strong beta agonist like ephedrine or clen then it improves the overall effectiveness.

 

[bigsonbitch]

I’m on low dose T3 (12.5mcg) and my heart rate was constantly in the mid 90s. Fat was melting but the high HR had me concerned to I started 40mg propopanol at night
Brought to mid to high 60’s low 70s
Fat loss still coming off and I’ve been on for about 4 weeks
So for me it hasn’t been an issue

 

[whacked]

I think Lyle McDonald posited that the use of beta blockers (specifically B1 selective ones) could improve lipolysis by increasing ANP. Well, he did say if used in isloation they're a net negative but the increase in ANP made it less of a net negative than one would think. And if used in concert with a stimulant that's a strong beta agonist like ephedrine or clen then it improves the overall effectiveness.

Embarrassed to ask but what is ANP?

 

[whacked]

I’m on low dose T3 (12.5mcg) and my heart rate was constantly in the mid 90s. Fat was melting but the high HR had me concerned to I started 40mg propopanol at night
Brought to mid to high 60’s low 70s
Fat loss still coming off and I’ve been on for about 4 weeks
So for me it hasn’t been an issue

Nice! Thanks for the feedback.
Ps. That’s crazy that you’re getting such great results at just 12.5mcg. Good for you!

 

[bigsonbitch]

Nice! Thanks for the feedback.
Ps. That’s crazy that you’re getting such great results at just 12.5mcg. Good for you!

Yea I don’t believe in T3 of more than 25mcg for me. My body is sensitive to it I suppose. Even with clen I don’t do more than 20mcg

 

[cmryan]

Embarrassed to ask but what is ANP?

No embarrassment mate. I’d never heard of it before reading his book. It’s atrial natriuretic peptide. It’s a peptide that’s released from cardiac tissue apparently with the main intent of causing uresis. It’s seen in higher levels naturally in people with congestive heart failure. I forgot when but it was discovered that anp also causes some lipolysis, and that the beta 1 antagonism caused by beta blockers can raise anp.

 

[BigNJ]

Beta blockers block epinephrine/adrenaline, so it's fucking pointless to take stimulants on Beta blockers at the same. They lower heart rate and they do improve blood flow.
That's why people on a decent dose of Beta blockers feel more tired.
I'd take a beta blocker before bed instead of in the morning.

 

[nothuman]

Yea I don’t believe in T3 of more than 25mcg for me. My body is sensitive to it I suppose. Even with clen I don’t do more than 20mcg

My hypothyroid symptoms get worse if I go above 12.5mcg per day. I make sure to take just enough to boost my Free T3 levels without suppressing my TSH too much.

 

[whacked]

No embarrassment mate. I’d never heard of it before reading his book. It’s atrial natriuretic peptide. It’s a peptide that’s released from cardiac tissue apparently with the main intent of causing uresis. It’s seen in higher levels naturally in people with congestive heart failure. I forgot when but it was discovered that anp also causes some lipolysis, and that the beta 1 antagonism caused by beta blockers can raise anp.

Thank you!