Who here is on a statin?

[nullandvoid]

Free AI is garbage. You’re the product on those not the other way around.

New England Journal of Medicine keeps a leaderboard of best models for medicine.

View attachment 370548

Open AI advanced models are consistently at the top, but you need a paid subscription to access the correct ones.

Rather than spending a few hundred bucks a month, you can “rent” a seat in a corporate multi user account for a tiny fraction of the cost to get the same type of pro account as an individual. It’s all a bit “shady” but more grey area than illegal. Be prepared to pay with crypto and follow some convoluted account set up instructions.

https://www.g2g.com/categories/chatgpt-accounts

Yea I kept your recommendation stashed aside for one you mentioned on you.com. I keep cycling through the major players... paying for the one a month or two I finally land on that is pissing me off the least at that moment. Maybe I should just give a good look at the you.com one. It seemed more complicated to set up.

Edit: So not really sure why I found it so "daunting." I think because they don't have a free version you can try first. Anyway, I signed up to check it out.

 

[trtchin]

Just got my most recent labs back.

Ldl was 60 with 5 mg rosuvaststin. Added in 10 mg ezetimibe and now at LDL 30. Pretty happy. Hoping for plaque regression as I have a small 2 mm buildup in my carotid artery which isnt fully calcified. But my hdl continues to drop now at 33 (week 18 of my first cycle).

 

[Ghoul]

Just got my most recent labs back.

Ldl was 60 with 5 mg rosuvaststin. Added in 10 mg ezetimibe and now at LDL 30. Pretty happy. Hoping for plaque regression as I have a small 2 mm buildup in my carotid artery which isnt fully calcified. But my hdl continues to drop now at 33 (week 18 of my first cycle).

At that low LDL, some plaque regression will occur just from lipids “equalizing” with low cholesterol blood. You really can’t maintain very high HDL with 30 LDL.

HDL function matters more than quantity.

Divide triglycerides / HDL. If it’s below 1.5 HDL function is likely good.

HS-CRP: below 1, another sign HDL well functioning.

Check ApoI for the best check of HDL function you can get in a regular lab.

 

[trtchin]

At that low LDL, some plaque regression will occur just from lipids “equalizing” with low cholesterol blood. You really can’t maintain very high HDL with 30 LDL.

HDL function matters more than quantity.

Divide triglycerides / HDL. If it’s below 1.5 HDL function is likely good.

HS-CRP: below 1, another sign HDL well functioning.

Check ApoI for the best check of HDL function you can get in a regular lab.

What is that did u mean ApoB? Just fyi ApoB is now 49.

 

[Ghoul]

What is that did u mean ApoB? Just fyi ApoB is now 49.

No ApoI (or Apo-I).

It’s the molecule that makes HDL “good” or “bad”. The reason things like Niacin, which boosts HDL numbers stopped being recommended is because producing more HDL without an increase in Apo-I, gives you a great looking HDL number, but it’s the result of making highly oxidative HDL which harms blood vessels and doesn’t help regression at all.

 

[trtchin]

No ApoI (or Apo-I).

It’s the molecule that makes HDL “good” or “bad”. The reason things like Niacin, which boosts HDL numbers stopped being recommended is because producing more HDL without an increase in Apo-I, results in a great looking HDL number, that’s the result of making highly oxidative HDL which harms blood vessels and doesn’t help regression at all.

Thanks never heard about it. Is it a common blood markers that most labs can check?

 

[trtchin]

This one?

Apo A-I - Testing.com

Describes how the Apo A-I test is used, when the Apo A-I test is ordered, and what the results of an Apo A-I test might mean

www.testing.com

 

[Ghoul]

This one?

Apo A-I - Testing.com

Describes how the Apo A-I test is used, when the Apo A-I test is ordered, and what the results of an Apo A-I test might mean

www.testing.com

That’s it.

Get Lp(a), aka Lipoprotein A, if you haven’t already, HS-CRP, and A1C.

With LDL as low as yours, we’re now addressing what are known in preventative cardiology as “residual risk factors”. Only a fraction of the significance of LDL, and they become even less important when you’re at <30, but you didn’t come this far to let other controllable factors chip away at your cardiovascular health if they’re easily correctable. You also want to prevent the less catastrophic, but more “aging” damage that occurs to microvasculature throughout your body and brain. Controlling these residual risk factors are more important for microvasculature protection and damage reversal than LDL is (they don’t build plaque like arteries do, inflammation is the main source of damage). In many ways these are even more important for quality of life, and get little attention because they only chip away at function, rather than threatening death.

What you’re trying to ensure is nothing causes a chunk of the existing soft plaque from sloughing off your arterial wall, leaving a wound, then clotting factors come in creating a blockage.

The longer you maintain this low LDL, the more that existing soft plaque will shrink, then develop a thick fibrous “cap”, that stabilizes it, and finally calcifies and takes on its final, fossilized, safe and stable form. A process that will take approximately a decade on average, but most of the benefit occurs within the first two years.

 

[trtchin]

My LPa is 35.9 but didnt test since going on statin and ezetimibe. I understand most likely it wont change greatly but its possible

A1c is 5.2.

Given my current markers what do you think about occasionally running orals at medium dose for max 6 weeks?

 

[Ghoul]

My LPa is 35.9 but didnt test since going on statin and ezetimibe. I understand most likely it wont change greatly but its possible

A1c is 5.2.

Given my current markers what do you think about occasionally running orals at medium dose for max 6 weeks?

I just saw someone’s numbers taking Orals with Pitavastatin and they barely budged, which was astonishing.

Rosu 5 should have a similar effect on LDL, but HDL is going to be crushed by orals. While on Pita, insane as it sounds, HDL (good type) can go up when on orals. As far as I know, this is unique to Pitavastatin.

Also, don’t test Lp(a) on orals, or for a month after any cycle. AAS lowers Lp(a) significantly (a good thing but doesn’t offset the other damage to lipids, and will give you a deceptively low number).

It’s good anyway, even by more recent guidelines that lowered the amount of Lp(a) considered desirable.

 

[trtchin]

Thanks that LPa figure was 1 month into my cycle.

Last question. If I got Pita just to run on oral cycles since Rousva is free for me, how to switch between do I need to take a break before changing over?

 

[Ghoul]

Thanks that LPa figure was 1 month into my cycle.

Last question. If I got Pita just to run on oral cycles since Rousva is free for me, how to switch between do I need to take a break before changing over?

It’s perfectly fine, even ideal, to stop one and start the other the next day. The half lives overlap, LDL reduction stays steady as Rosu wears off and Pita builds up. There’s no contraindication between them, and the Pita replacement lowers stress on the liver as Rosu levels drop. This would actually keep lipids even better while on cycle, since you’re reducing the total load on your liver Rosu+AAS would cause. (Rosu is metabolized by the same CYP450 enzyme family as AAS and a ton of other substances, while Pita is metabolized by a liver enzyme that’s far less crowded).

 

[BendigoShafter]

I'm currently on atorvastatin but it sounds like pita might be the way to go. Any reason not to prefer pita?

 

[Ghoul]

I'm currently on atorvastatin but it sounds like pita might be the way to go. Any reason not to prefer pita?

Lower cost and a slightly higher max LDL reduction are the only advantages, everything else is much better with Pitavastatin, including the emerging anti-cancer properties.

In a study of 200 million patient’s medical records, Pitavastatin users have a ~20% lower risk of pancreatic cancer, for instance.

 

[a1b2c3]

I had bloodwork done yesterday (I've tried searching this up, but couldn't find any info) - my HDL is at a high risk (so, basically, this lab that I went to has some strange reference ranges ), according the lab - 0,86 mmol/L. It is stated that high risk is <90.

My total cholesterol is 3.8 mmol/L, which is in range - <5.2.

LDL - 2,71 mmol/L - in range - >4.92.

And the triglycerides are okay as well.

I'm very curious about the high HDL. Is that okay, is it not? I'll be visiting my GP next week, but I was curious what you guys on here would say as well.