Bloods post - (readable?) what to do about CRP and lipids?

[Ghoul]

I think the goal is just to keep LDL as low as possible.
Going around chasing HDL is not beneficial.

Products that apparently improve higher quality HDL measured by CEC has been shown to not be beneficial.

Post in thread 'Chronic low HDL but good LDL (need advice)'

Aug 3, 2025

No.

Hundreds of studies after that 2014 paper went on to establish that cardiovascular risk is lowered by quality, not only quantity of HDL. HDL's ability to remove cholesterol, measured by CEC (cholesterol efflux capacity) and anti-inflammatory properties are what matters most.

The 2014 studies looks at the following, all of which i believe improve CEC, with CETP providing the strongest improvements.







In a different post i believe you ranked Niacin and Fibrates as well, right after Pita, both of which were also evaluated in the 2014 study...

• Photon

Some products which drastically improve HDL, CEC and Apoa-I actually even cause more harm.

Post in thread 'Chronic low HDL but good LDL (need advice)'

Aug 3, 2025

The 2014 studies looks at the following, all of which i believe improve CEC, with CETP providing the strongest improvements.

View attachment 339122

View attachment 339130

View attachment 339131

In a different post i believe you ranked Niacin and Fibrates as well, right after Pita, both of which were also evaluated in the 2014 study as not being beneficial.
Edit, found it

Interesting read about CETP. I havnt heard of it before, but it looks like it does boost apoA1...

• Photon

• 

The main suspect with those compounds is that they don't raise ApoA-I enough, compared to the massive increase in HDL (75%+) so the end result is a large quantity of low quality "more harm than benefit HDL".

Pita only raises HDL slightly, 5-10%, and ApoA-I modestly, but enough to ensure the HDL produced is high quality. So when HDL function (aka 'HDL efflux capacity') is measured post Pitavastatin, it's confirmed that it's improved. Obviously you wouldn't switch to Pita for a big increase in HDL, it's more of a nice bonus if you're deciding between statins, and reassuring to know it's producing "good HDL".

Pitavastatin increases HDL particles functionally preserved with cholesterol efflux capacity and antioxidative actions in dyslipidemic patients - PubMed

In addition to its LDL-C-lowering effects, pitavastatin elevates the HDL-C level and enhances the cholesterol efflux capacity and antioxidative properties of HDL. Pitavastatin therefore increases the amount of functional HDL without attenuating HDL quality.

pubmed.ncbi.nlm.nih.gov

 

[Photon]

The main suspect with those compounds is that they don't raise ApoA-I enough, compared to the massive increase in HDL (75%+) so the end result is a large quantity of low quality "more harm than benefit HDL".

Pita only raises HDL slightly, 5-10%, and ApoA-I modestly, but enough to ensure the HDL produced is high quality. So when HDL function (aka 'HDL efflux capacity') is measured post Pitavastatin, it's confirmed that it's improved. Obviously you wouldn't switch to Pita for a big increase in HDL, it's more of a nice bonus if you're deciding between statins, and reassuring to know it's producing "good HDL".

View attachment 340474

Pitavastatin increases HDL particles functionally preserved with cholesterol efflux capacity and antioxidative actions in dyslipidemic patients - PubMed

In addition to its LDL-C-lowering effects, pitavastatin elevates the HDL-C level and enhances the cholesterol efflux capacity and antioxidative properties of HDL. Pitavastatin therefore increases the amount of functional HDL without attenuating HDL quality.

pubmed.ncbi.nlm.nih.gov

Statins in general improve outcomes, I have nothing against statins.

Torcetrapid for instance, improves HDL/apoA1 by 29/25%.
I'd say it's pretty close.
Sadly, seems to produce poorer outcomes.

 

[Raiders789]

So the TLDR is you're not accumulating plaque, you're removing it to some degree, and theres no urgent need to increase your HDL, though it would be beneficial to reducing existing soft plaque.

So you're saying it's time to bust out the 100mg var tabs?

Most compounds that raise HDL don't raise ApoA-I. This results in low quality HDL being produced. Not only is it not able to remove plaque, it's inflammatory so does more harm than good despite pushing the HDL count higher.

This is really interesting. I did not know this, I've been spamming 1-2g flush niacin for the past few months but I guess I'll pull that out. My ApoA1 came in at 80 last blast, so just below the reference range but I figure with the low ApoB that isn't a problem.

If you switch from Rosu 10mg to Pitavastatin 4mg, you'll raise HDL slightly, raise ApoA-I moderately, so the HDL you produce will be of higher quality, and unlike every other statin, Pita has a neutral or improving effect on insulin sensitivity, which is always good. It's also better for muscles, mitochondrial function, and doesn't deplete CoQ10.

Also very cool - I had never heard of pitavastatin before reading this. Unfortunately no prescription but I'm sitting on like a 2 year supply of rosuvastatin, so I'll ride that out and then invest in some indian pharma pita.

Thanks for all the info Ghoul! With this and the thyroid help I might as well just hire you as my concierge doc . I really appreciate all the good info you spread on these forums.

 

[Photon]

So you're saying it's time to bust out the 100mg var tabs?

With that Cystatin value, might want to switch to a different oral instead.
Var seems to hit the kidneys more in general.

 

[Ghoul]

So you're saying it's time to bust out the 100mg var tabs?

This is really interesting. I did not know this, I've been spamming 1-2g flush niacin for the past few months but I guess I'll pull that out. My ApoA1 came in at 80 last blast, so just below the reference range but I figure with the low ApoB that isn't a problem.

Also very cool - I had never heard of pitavastatin before reading this. Unfortunately no prescription but I'm sitting on like a 2 year supply of rosuvastatin, so I'll ride that out and then invest in some indian pharma pita.

Thanks for all the info Ghoul! With this and the thyroid help I might as well just hire you as my concierge doc . I really appreciate all the good info you spread on these forums.

It's a two way street for sure. For instance, MESO got me wondering why Telmisartan was the "go to" BP med here. My first encounter with collective bro science wisdom got me questioning the BP meds that I had been prescribed to me (chosen via clinical inertia and prioritizing cost effectiveness as it turns out), starting me on a quest to find the best way to manage my own.

Once that was nailed, the next lowest hanging fruit on the longevity tree was lipids. I've crushed LDL from 160 to 30ish without sides of any kind (Pita/Eze/Repatha). LDL is far and away the most important factor for long term lipid based risk reduction. I had to lighten my stack to avoid going lower (it's probobly not necessary, but there's a tiny bit of uncertainty and no significant benefit so I'll keep it from going lower as a little insurance).

 

[Raiders789]

With that Cystatin value, might want to switch to a different oral instead.
Var seems to hit the kidneys more in general.

Luckily for me, my Cystatin C is sitting at 0.8(eGFR of 120). I think my kidneys are asking to be pounded by a ridiculous amount of anavar

 

[Photon]

Luckily for me, my Cystatin C is sitting at 0.8(eGFR of 120). I think my kidneys are asking to be pounded by a ridiculous amount of anavar

I mistook you for the OP lol

 

[TRTSCOUT]

Hey bro, came across this and wanted to share my experience because I came off a pretty similar cycle a few months ago -

Was running 300 test 300 primo 4IU growth; was using Beligas 200mg/ml primo which would give me horrible PIP/knots even when doing EOD injections. Had a CRP of 11 which is definitely not ideal, but was on ezetimibe so my LDL was 50 and HDL was 25. From my understanding, having a CRP > ~3 isn't idea long term but is ok short term, and is really only threatening if your lipids are out of place too so I just pushed on. Once I pulled the primo my CRP dropped to 0.7.

Your lipids look pretty good so if I were you I wouldn't be concerned, at the least you're doing better than I was. You could look into niacin to raise HDL, but honestly I don't think the transient bump will do you much, or at least isn't worth the flushing from it. I think you'd be better off potentially looking into ezetimibe/statin - I'm currently doing 10mg ezetimibe + 5mg rosuvastatin and that keeps my ApoB at 40 and LDL at 25, so I'm not even really worried about low HDL.

Also, as long as you are on trt/cycle your FSH/LH will always be bottomed out because your HPTA is shut off and you aren't producing any natural test. From my understanding it's not a problem at all, but it means your testes aren't functioning, so I take a little HCG to maintain testicular function because I'm younger and want to have kids someday. Although if thats not a concern you could save some money.

One other thing; your iron looks pretty low. I'm currently going through the same thing and have been supping 75mg iron twice a day because I've been getting bad low iron sides. It looks like your hematocrit/hemoglobin are good so its probably not a big deal but it might be worth keeping an eye on, and if you start getting consistent fatigue you might want to consider getting your ferritin checked also.

great response, and experience share, thank you. What are low iron sides? i have some ferritin or iron supp will get on that right now!

 

[TRTSCOUT]

w $1 h. n

In short, plaque accumulation and therefore heart disease risk potential is overwhelmingly determined by total atherogenic particles, ie, LDL, VLDL. Lp(a), represented cumulatively by ApoB.

Yours is very low. Well below the lowest levels advocated by guidelines for the highest risk patients. You're in "regression" territory, where soft plaque can be removed from arteries.

And that's where HDL comes in. It's the vehicle that transports lipids from the arteries back to the liver. The lower HDL is the less reverse transport can take place. Even more important is ApoA-I, which defines how well HDL can carry out this reverse transport function. In other words, it determines the quality of the HDL you do have.

So the TLDR is you're not accumulating plaque, you're removing it to some degree, and theres no urgent need to increase your HDL, though it would be beneficial to reducing existing soft plaque.

Some technical nuance:

Most compounds that raise HDL don't raise ApoA-I. This results in low quality HDL being produced. Not only is it not able to remove plaque, it's inflammatory so does more harm than good despite pushing the HDL count higher.

Low HDL is often an indicator of insulin resistance or inflammation. So keep an eye on those.

If you switch from Rosu 10mg to Pitavastatin 4mg, you'll raise HDL slightly, raise ApoA-I moderately, so the HDL you produce will be of higher quality, and unlike every other statin, Pita has a neutral or improving effect on insulin sensitivity, which is always good. It's also better for muscles, mitochondrial function, and doesn't deplete CoQ10.

If you want to switch, and Rosu is prescribed, you could just tell your doctor you've been getting some muscle aches and would like to try Pitavastatin because you heard that has the lowest side effect profile of all statins.

thx for your time on this, good rundown

 

[BamaCrazy]

great response, and experience share, thank you. What are low iron sides? i have some ferritin or iron supp will get on that right now!

Fatigue, weakness and shortness of breath are common symptoms of low ferritin. Personally I never have any symptoms when my ferritin is very low and out of range.

 

[Photon]

great response, and experience share, thank you. What are low iron sides? i have some ferritin or iron supp will get on that right now!

With that HCT value i would not supplement any iron without further testing..