lowest LDL without using a PCSK9 inhibitor?

[Ghoul]

no i calculated it from 92 but still thought it was a great response

It is a strong response even from 92. Perhaps @Raww was on TRT or cruise, or had residual AAS in his system at time of the 92 baseline. The same disproportionate anti-AAS induced lipid rise applies to injectables, but they don’t have anything close to oral’s level of cholesterol trashing capacity on the liver.

Another possible explanation is he’s one of those who absorbs more dietary cholesterol than average, and ezetimibe, which directly counteracts that, has a bigger impact than usual. In some genetic outliers, eze alone can reduce LDL by 80%+.

 

[just some dude]

statin safety profiles

 

[Raww]

It is a strong response even from 92. Perhaps @Raww was on TRT or cruise, or had residual AAS in his system at time of the 92 baseline. The same disproportionate anti-AAS induced lipid rise applies to injectables, but they don’t have anything close to oral’s level of cholesterol trashing capacity on the liver.

Another possible explanation is he’s one of those who absorbs more dietary cholesterol than average, and ezetimibe, which directly counteracts that, has a bigger impact than usual. In some genetic outliers, eze alone can reduce LDL by 80%+.

Yes - TRT for 6+ years.

 

[Ghoul]

Yes - TRT for 6+ years.

Until I learned about the disproportionate impact of Pita on AAS driven lipids, I was starting to think everyone’s tabs might be overdosed, since nearly every report here has been a “stronger than average” LDL reduction.

 

[Ivan221106]

Докато не научих за непропорционалното въздействие на Пита върху липидите, причинени от анаболни стероиди (ААС), започвах да си мисля, че таблетките на всички може да са предозирани, тъй като почти всеки доклад тук е за „по-силно от средното“ намаление на LDL.

How long can the combination of rosuvastatin and ezetimibe be used without interruption?

 

[Ghoul]

How long can the combination of rosuvastatin and ezetimibe be used without interruption?

For most people, forever.

Both have been used for 20+ years without side effects.

Ezetimibe is extremely safe, side effects are almost unheard of.

Rosu does cause side effects in a very small percentage of people. If you don’t get side effects within the first month or two, you will probably never get them. If you do get side effects, stopping the medicine will reverse them.

The only long term effects with Rosu you need to watch are 1) check liver enzymes at least once a year (extremely rare to have a serious problem) and 2) watch out for prediabetes / diabetes. It makes you a little more insulin resistant. It doesn’t really “cause” diabetes, but if you’re close to getting it, this could push you over the edge.

Pitavastatin has a much lower rate of the already low risk of muscle problems, and in most people, it doesn’t increase the chance of diabetes. In fact, it improves insulin sensitivity in many, reducing the risk,

 

[BP_6]

what’s the lowest you’ve managed to get your LDL without using a PCSK9 inhibitor?

20. About 4-5 months ago. Time for another check. With a statin and zetia combo.

 

[just some dude]

Imagine LDL cholesterol as a giant mountain of snow sitting in a river, threatening to flood the valley below. You want to clear the river.

• Along come the trio combo — Pitavastatin, Bempedoic Acid, and Ezetimibe. They’re massive bulldozers. They roar into action, pushing 82% of the snow off the river in a single, unstoppable wave. The river is mostly clear, flowing smoothly.
• Meanwhile, the world stack — Berberine, Retatrutide, Citrus Bergamot, Metformin, and exercise — are like a team of gardeners with shovels and brooms. They chip away carefully, clearing the remaining 18%. Their work is important for finesse, fine-tuning, and maintaining the flow, but by themselves, they wouldn’t move the mountain.
• The story here: the heavy machinery does the heavy lifting, but the small helpers polish the work. Together, they leave the river not just cleared, but optimally flowing.

 

[nullandvoid]

I just want to go straight to being polished.

 

[BigChungusRX]

I’ll just mention here if anyone in US does want Repatha, get a prescription from your doctor or telehealth, and get a coupon code from goodRx for your pharmacy.

Amgen lowered the price for cash payers from $700/mo to $239 (lowest in the world). If you DO go through your insurance policy get a “copay card” from Repatha.com and your price will be $15/mo with Repatha picking up the rest. If you’re uninsured, and your household income is less than 3x the poverty level (ie $50k for 1 person, higher for multiple), you can get Repatha for free.

They had been selling direct but decided to work through GoodRx instead.


View attachment 367312

As someone pointed out, even if you only use 1, instead of 2 pens a month, you’ll still get most of the benefit at half the cost.

Finally, this is the only way at the moment to put a big dent in Lp(a), dropping it by ~30%.

Is it worth going through all that to reduce LPA?

 

[Ghoul]

Is it worth going through all that to reduce LPA?

Depends on your Lp(a).

< 30 mg/dL (<75 nmol/L) then no.

Also depends on LDL. Because Lp(a) is a risk enhancer, a “multiplier”, the lower LDL is the less significant Lp(a) is. 100 mg/ Lp(a) with 20 LDL isn’t particularly dangerous. But 50 mg / Lp(a) with 100 LDL is.

When LDL (or ApoB) is extremely low, other lipid markers (HDL, Triglycerides, particle size etc) really don’t mean anything significant in terms of cardiovascular risk. That’s why knocking that down as low as possible is the easiest, most effective strategy to follow.

 

[shcidheuddvv]

Depends on your Lp(a).

< 30 mg/dL (<75 nmol/L) then no.

Also depends on LDL. Because Lp(a) is a risk enhancer, a “multiplier”, the lower LDL is the less significant Lp(a) is. 100 mg/ Lp(a) with 20 LDL isn’t particularly dangerous. But 50 mg / Lp(a) with 100 LDL is.

When LDL (or ApoB) is extremely low, other lipid markers (HDL, Triglycerides, particle size etc) really don’t mean anything significant in terms of cardiovascular risk. That’s why knocking that down as low as possible is the easiest, most effective strategy to follow.

LDL is currently at 69 mg/dL on TRT (175mg weekly) and ezetimibe, although I plan to get my Apo(b) checked again in Jan. I followed your advice on Repatha through telehealth, greatly appreciate your contributions btw, and got the prescription. Willing to cough up the 240$ if it's a vaccination against ASCVD, but wondering if there is any potential issues crushing Apo(b) so low given how young I am (20 yrs old). Any advice?

 

[Ateam2023]

I have my LDL creeping up over the last couple years nothing extreme but it's going in the wrong direction so I have some PITA coming, looking forward to trying that to see how far I can get a reduction in ldl

 

[BigChungusRX]

Depends on your Lp(a).

< 30 mg/dL (<75 nmol/L) then no.

Also depends on LDL. Because Lp(a) is a risk enhancer, a “multiplier”, the lower LDL is the less significant Lp(a) is. 100 mg/ Lp(a) with 20 LDL isn’t particularly dangerous. But 50 mg / Lp(a) with 100 LDL is.

When LDL (or ApoB) is extremely low, other lipid markers (HDL, Triglycerides, particle size etc) really don’t mean anything significant in terms of cardiovascular risk. That’s why knocking that down as low as possible is the easiest, most effective strategy to follow.

My LPA is 140. If I keep LDL under 100 am I chilling? Should I just run ezetimibe with all cycles?
Also will it be harder to drop LDL because LPA makes it sticky?

 

[Ghoul]

My LPA is 140. If I keep LDL under 100 am I chilling? Should I just run ezetimibe with all cycles?
Also will it be harder to drop LDL because LPA makes it sticky?

I assume (hope) you mean nmol not mg.

That’s elevated under all guidelines, and as a rule of thumb, it acts as a 2x multiplier of risk.

So if by LDL “under 100” you mean 25, x2=50, that’s fine.

But if you mean 90, X2 = LDL 180, very high risk (esp with AAS use). If you have any other risk factors like elevated BP those are doubled as well. Chillin in that case would be horizontally in a cooler, decades earlier than necessary.

LDL is no more difficult to lower because of high Lp(a). The stickiness means a greater proportion of passing particles penetrates arterial walls and contributes to plaque, as if your cholesterol was twice as high as the levels they are.

 

[just some dude]

I assume (hope) you mean nmol not mg.

That’s elevated under all guidelines, and as a rule of thumb, it acts as a 2x multiplier of risk.

So if by LDL “under 100” you mean 25, x2=50, that’s fine.

But if you mean 90, X2 = LDL 180, very high risk (esp with AAS use). If you have any other risk factors like elevated BP those are doubled as well. Chillin in that case would be horizontally in a cooler, decades earlier than necessary.

LDL is no more difficult to lower because of high Lp(a). The stickiness means a greater proportion of passing particles penetrates arterial walls and contributes to plaque, as if your cholesterol was twice as high as the levels they are.

Godsend, brother.

 

[explodingHeart]

31 taking test and primo, on no chol lowering drugs, cuz of my genes

 

[deadbeef]

My LPA is 140. If I keep LDL under 100 am I chilling?

Lp(a) additive risk is linear with Lp(a) level (higher levels = higher risk). The hazard ratio at 140 nmol/L is 1.3-1.5 (30-50% increased risk) depending on what study we're looking at. The researchers gave us a handy dandy table to tell us how much we need to lower LDL to mitigate the risk of elevated Lp(a):

Lp(a) (nmol/L)	Δ Lp(a) vs median (nmol/L)	Lp(a) percentile	HR for MCVE due to ↑Lp(a)	LDL‑C reduction starting age 30 y (mg/dL)	40 y (mg/dL)	50 y (mg/dL)	60 y (mg/dL)
320	300	99	2.56	≈46	≈54	≈66	≈89
270	250	97.5	2.19	≈39	≈46	≈58	≈73
220	200	93.5	1.87	≈31	≈35	≈46	≈58
170	150	90	1.60	≈23	≈27	≈35	≈43
120	100	82.5	1.37	≈15	≈19	≈23	≈31
70	50	75	1.17	≈8	≈8	≈12	≈15
20	ref.	50	ref.	ref.	ref.	ref.	ref.