Which Steroids are the easiest on YOUR Lipids? (Poll)

[RockyP]

We all know that it is highly idiosyncratic (aside from orals) which side effects we get from gear. I've done a search of the board and wasn't able to find anything specific on this topic. I want to hear from members what injectables (orals are bad for most everyone's lipids), keeping in mind this is all dosage dependent, were easiest on you lipids. At the end of the day we all need to try and find out, hopefully at low dosages, but for me personally, my LDL is fine but I have a genetically low HDL, so i need to be very careful what I use. My ApoB / A1 ratio came in at 0.9, which is 2x average risk. ApB was ok 77 but the A1 was low (genetic). Anecdotally you'll hear all sorts of things from different folks about different compounds. I'm hoping to get an actual Poll of what gear you all have run that was easiest on lipids (will exclude test for now).

 

[readalot]

We all know that it is highly idiosyncratic (aside from orals) which side effects we get from gear. I've done a search of the board and wasn't able to find anything specific on this topic. I want to hear from members what injectables (orals are bad for most everyone's lipids), keeping in mind this is all dosage dependent, were easiest on you lipids. At the end of the day we all need to try and find out, hopefully at low dosages, but for me personally, my LDL is fine but I have a genetically low HDL, so i need to be very careful what I use. My ApoB / A1 ratio came in at 0.9, which is 2x average risk. ApB was ok 77 but the A1 was low (genetic). Anecdotally you'll hear all sorts of things from different folks about different compounds. I'm hoping to get an actual Poll of what gear you all have run that was easiest on lipids (will exclude test for now).

Nandrolone. Easy. Doesn't touch lipids at reasonable loadings for me.

Stay away from primo/mast if you value endothelium. Estradiol is important.

Looking forward to trying tren A....

 

[RockyP]

Nandrolone. Easy. Doesn't touch lipids at reasonable loadings.

That was my vote also. I dont run it more than 150 - 200 / week.

 

[Trades]

Looking forward to trying tren A....

I bet you'll like it, at least for the first few weeks. While nand is instant depression for me, turns out tren A is a much smoother ride until sleep starts to get seriously disturbed and night sweats creep in around week 3-4.

 

[RockyP]

I've had Low-ish HDL (37-39) for as long as I can remember but being on Arimidex 1.5 mg weekly with an E2 of 35 has brought it down to 30, which it hasn't been before. I'm wondering if I should drop down to 0.5 mg weekly of Adex and see how the HDL loots at a slightly higher E2. Or would that be a waste?

 

[readalot]

While nand is instant depression for me

About week 6 to 8 I always wish I was using NPP. But now that I put on my big boy pants that can be a reality.

 

[readalot]

I've had Low-ish HDL (37-39) for as long as I can remember but being on Arimidex 1.5 mg weekly with an E2 of 35 has brought it down to 30, which it hasn't been before. I'm wondering if I should drop down to 0.5 mg weekly of Adex and see how the HDL loots at a slightly higher E2. Or would that be a waste?

That ain't helping things any. Long term I would shoot for minimizing AI usage if you use it regularly or switch up your protocol.

 

[RockyP]

That ain't helping things any. Long term I would shoot for minimizing AI usage if you use it regularly or switch up your protocol.

It's a remnant from my HRT doc who I no longer see due to my lack of confidence in his expertise. I will taper to 1 mg and then 0.5 mg weekly and re-check Test, E2, and lipids.

I say this with utmost sincerity and without any sarcasm. There is far more expertise on this board than there is in any medical clinic I have ever seen when it comes to this sort of thing. You can't get a straight answer from MD's about lipids (they blow off the utility of AboB / A1 / Lp(a)), they all have different ideas about phlebotomy for secondary erythrocytosis, and just when you think you may have found one that knows what they're doing, like Patrice O'Neal would say, "they put marbles in their ass."

 

[readalot]

It's a remnant from my HRT doc who I no longer see due to my lack of confidence in his expertise.

I could quote you Dr. Saya if you haven't already read some of his stuff. Most reasonable dude I have met when it comes to E2 and Hct.

Don't assume you are an outlier unless you can prove it or something like that.


View: https://youtu.be/mH9NzJwldok

 

[watchtymeflyyy]

Tren only slightly lowers HDL… Nandrolone doesn’t lower it at all. But it does raise my HCT. Tren does not.

 

[RockyP]

Tren only slightly lowers HDL… Nandrolone doesn’t lower it at all. But it does raise my HCT. Tren does not.

I do like me some LOW dose tren, like 60 mg weekly low.

 

[readalot]

Tren only slightly lowers HDL…

trigs?
cRP?

 

[RockyP]

Who the F voted for Primo!? Make yourself known and explain.

 

[readalot]

Who the F voted for Primo!? Make yourself known and explain.

You should have made the polling public so we could shame them.

 

[Ghoul]

You can't get a straight answer from MD's about lipids (they blow off the utility of AboB / A1 / Lp(a)),

The way I'd explain it to a buddy:

ApoB: drive your LDL-C down low enough and ApoB will follow to the point of becoming irrelevant (with very rare genetic exceptions).

ApoA1: puts the "good" in good cholesterol. It determines the ability of HDL to remove fatty plaque from your arteries. Above 140 is ideal. Below 120 HDL becomes inflammatory and harms blood vessels.

Lp(a): Completely independent risk marker for cardiovascular disease. It's genetic, generally only needing a single test after 18. Since widespread testing and treatment isn't considered "cost effective" unless you have a family member who you know had high Lp(a) and a heart attack its an uphill battle with insurance to even get tested. Above 75 is high risk. Niacin can bring it down 30% but doesn't seem to actually reduce risk. PCSK9 inhibitors also lower by about 30%, but only partially lower risk. Right now. if you have high risk LP(a) levels it mostly means you should do everything possible to lower other risks (ahem, LDL-C). Effective drugs are coming soon for this.

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If you have an LDL-C below 55, you've essentially stopped plaque accumulation. If ApoA1 is above 120, regardless of HDL numbers, you're reversing it.

Keep BP below 130/80 and CRP below 1mg and you've pretty much minimized cardiovascular disease risk and even turning back the clock on it. (with ApoA1 and HDL levels determining how fast and deep the reversal of soft plaque is).

 

[RockyP]

The way I'd explain it to a buddy:

ApoB: drive your LDL-C down low enough and ApoB will follow to the point of becoming irrelevant (with very rare genetic exceptions).

ApoA1: puts the "good" in good cholesterol. It determines the ability of HDL to remove fatty plaque from your arteries. This is mostly relevant if LDL is below 60 and you're beyond stopping plaque buildup, and trying to reverse it. Above 140 is ideal. Below 120 HDL becomes inflammatory and harms your blood vessels.

Lp(a): Completely independent risk marker for cardiovascular disease. It's genetic, generally only needing a single test after 18. Since widespread testing and treatment isn't considered "cost effective" unless you have a family member who you know had high Lp(a) and a heart attack its an uphill battle with insurance to even get tested. Above 75 is high risk. Niacin can bring it down 30% but doesn't seem to actually reduce risk. PCSK9 inhibitors also lower by about 30%, but only partially lower risk. Right now. if you have high risk LP(a) levels it mostly means you should do everything possible to lower other risks (ahem, LDL-C). Effective drugs are coming soon for this.

------
If you have an LDL-C below 55, you've essentially stopped plaque accumulation. If ApoA1 is above 120, regardless of HDL numbers, you're reversing it.

Keep BP below 130/80 and CRP below 1mg and you've pretty much minimized cardiovascular disease risk and even turning back the clock on it.

Thank you very much. Bookmarked!

 

[RockyP]

The way I'd explain it to a buddy:

ApoB: drive your LDL-C down low enough and ApoB will follow to the point of becoming irrelevant (with very rare genetic exceptions).

ApoA1: puts the "good" in good cholesterol. It determines the ability of HDL to remove fatty plaque from your arteries. Above 140 is ideal. Below 120 HDL becomes inflammatory and harms blood vessels.

Lp(a): Completely independent risk marker for cardiovascular disease. It's genetic, generally only needing a single test after 18. Since widespread testing and treatment isn't considered "cost effective" unless you have a family member who you know had high Lp(a) and a heart attack its an uphill battle with insurance to even get tested. Above 75 is high risk. Niacin can bring it down 30% but doesn't seem to actually reduce risk. PCSK9 inhibitors also lower by about 30%, but only partially lower risk. Right now. if you have high risk LP(a) levels it mostly means you should do everything possible to lower other risks (ahem, LDL-C). Effective drugs are coming soon for this.

------
If you have an LDL-C below 55, you've essentially stopped plaque accumulation. If ApoA1 is above 120, regardless of HDL numbers, you're reversing it.

Keep BP below 130/80 and CRP below 1mg and you've pretty much minimized cardiovascular disease risk and even turning back the clock on it.

Unfortunately my Apo A1 is 87, AboB is 77, LDL is 65, HDL ranges from 30 - 39. CRP 0.56, BP 129/74. LDL(a) hasn't come back yet. So a mixed bag. I'm cutting right now so hoping that shaving an extra 30 lbs off the frame will help. Other supports are citrus bergamot, fish oil, statin. Diet is very clean, mostly chicken / rice with EFA's. No alcohol. No oral AAS. My cardiologist advised me to get the LDL as low as humanly possible given my Apo A-1 and HDL levels.

 

[Ghoul]

Unfortunately my Apo A1 is 87, AboB is 77, LDL is 65, HDL ranges from 30 - 39. CRP 0.56, BP 129/74. LDL(a) hasn't come back yet. So a mixed bag. I'm cutting right now so hoping that shaving an extra 30 lbs off the frame will help. Other supports are citrus bergamot, fish oil, statin. Diet is very clean, mostly chicken / rice with EFA's. No alcohol. No oral AAS. My cardiologist advised me to get the LDL as low as humanly possible given my Apo A-1 and HDL levels.

It's not as bad as it seems. The good news is get ApoA1 up, the other markers will improve in the process, and you're good to go. There's no single thing that would get it above 120.

ApoA1 is largely insulin sensitivity related.

30lbs of weight loss is likely to get ApoA1 up by ~15%. Visceral fat loss would be exceptionally effective. rHGH or Tesa would make things worse in the near term (insulin resistance) but using those to blast stubborn visceral fat would do more to help lipids over the long term than any other lifestyle change.

Tirz would give you another 10-15%. boost and help with visceral fat lipolysis and insulin sensitivity (especially useful if on GH).

Which statin are you using? Pitavastatin is by far the best at raising ApoA1, raising it by 10%, though it's the least used.

I'm sure you know cardio is the best exercise for ApoA1 as well,

Weight loss, a GLP, switch to Pita, and some cardio will almost certainly get you over 120. Since the statin isn't dropping LDL enough, ezetimibe is very safe as a statin add on for another 10-15% drop, and widely used in the BB community as you probobly know.

 

[RockyP]

It's not as bad as it seems. The good news is get ApoA1 up, the other markers will improve in the process, and you're good to go. There's no single thing that would get it above 120.

ApoA1 is largely insulin sensitivity related.

30lbs of weight loss is likely to get ApoA1 up by ~15%. Visceral fat loss would be exceptionally effective. rHGH or Tesa would make things worse in the near term (insulin resistance) but using those to blast stubborn visceral fat would do more to help lipids over the long term than any other lifestyle change.

Tirz would give you another 10-15%. boost and help with visceral fat lipolysis and insulin sensitivity (especially useful if on GH).

Which statin are you using? Pitavastatin is by far the best at raising ApoA1, raising it by 10%, though it's the least used.

I'm sure you know cardio is the best exercise for ApoA1 as well,

Weight loss, a GLP, switch to Pita, and some cardio will almost certainly get you over 120. Since the statin isn't dropping LDL enough, ezetimibe is very safe as a statin add on for another 10-15% drop, and widely used in the BB community as you probobly know.

Thank you again for your thoughtful response. I’m on crestor only 5 mg currently. Doing 75-90 mins LISS cardio daily. Fasting sugar was 87 and A1C was 5 on 4 iu HGH with only 2.5 tirz (started 5 mg today. Labs were Monday). My cardiologist said LDL < 65 with a 30 lb weight loss should do it. Also taking a high quality Berbarine supplement. I can tell my insulin sensitivity is way up. I can tolerate 250 g of white rice with 180 g chicken very easily with no post prandial fatigue. Prior to tirz I would get sleepy above 150 g rice per meal. I’m hopeful that when this cut is over the HdL will bounce into the 40’s. Thanks again for all your insight!

 

[Ghoul]

Thank you again for your thoughtful response. I’m on crestor only 5 mg currently. Doing 75-90 mins LISS cardio daily. Fasting sugar was 87 and A1C was 5 on 4 iu HGH with only 2.5 tirz (started 5 mg today. Labs were Monday). My cardiologist said LDL < 65 with a 30 lb weight loss should do it. Also taking a high quality Berbarine supplement. I can tell my insulin sensitivity is way up. I can tolerate 250 g of white rice with 180 g chicken very easily with no post prandial fatigue. Prior to tirz I would get sleepy above 150 g rice per meal. I’m hopeful that when this cut is over the HdL will bounce into the 40’s. Thanks again for all your insight!

I think he's probably right and you'll be good on the other side of the weight loss. Even though Pita boosts ApoA-I and HDL quite a bit more, Crestor lowers LDL more, so it's not worth bothering to switch if you're not having muscle related sides, which is that main reason Pitavastatin exists, for statin intolerant patients.