Lp(a): What We Should Know; Need to Know; and Hope to Know - CME
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- Опубликовано: 23 авг 2024
- Join Dr. Stephanie Saucier and Dr. Benjamin Hirsh as they discuss the role of lipoprotein(a) and its therapeutic options for patients with cardiovascular disease and review the science of Lp(a) and its role in the management and prevention of cardiovascular risk. Emerging therapeutics to reduce Lp(a) will be examined as well as how to apply currently available therapies. The material of this lecture will provide crucial information for healthcare providers to improve outcomes in patients.
How about Triglycerides over HDL and give her D3 and K2-MK7 and Nattokinase and Nitric Oxide?
Interesting - but pls start with the bottom line up front. A complex case study with no clear direction of where we are going puts a huge burden on the audience to synthesize all of this, somewhat aimlessly.
thank you. fabulous presentation
SLN360 is now entering Phase 3! SLN360 showed up ton99% knockdown of LP(a) expression in the Phase 2 trial!! 👌👌👌
How about Magnesium Glycinate and Liposomal Vitamin C at dosage above 10 grams per day? Works for me - no drugs.
Best treatment for atherosclerosis: Vitamin C
Why do only coronary arteries clog with cholesterol and not veins or small capillaries?
Scurvy = No vitamin C in your diet.
Symptom: Your blood vessels break and you bleed to death. Think of the sailor of the past.
Scurvy of the heart = Just enough vitamin C from food.
Symptom: Arteries around the heart are not strong enough to resist high blood pressure. Damage is repaired with cholesterol LP(a) to prevent worse. After years of repair, your arteries become clogged.
Enough vitamin C supplement of at least 3000 mg. per day gives strong and flexible arteries. Cholesterol is not needed as a repair agent. Cholesterol in your coronary arteries is broken down and burned in your liver.
Source RUclips: Cardiovascular disease and vitamin C (Dr. Rath Foundation)
or
Breakthrough Towards The Natural Control Of Cardiovascular Disease - Dr. Rath's 2018 Cyprus Lecture
My Lp(a) was 246 nmol/L in June of last year, by September it was 293 nmol/L, and got it checked again in April because it was part of a package I bought and it came back at 380 nmol/L. So, in one year my Lp(a) went from 246 to 380 🙃 it was lower when I was eating lots of meat and butter and higher now that I am plantbased…on the other hand my particle count has come DOWN exponentially as well as my LDL-small particles. My LDL is actually higher now though and I don’t know why 😢 it was 117 last June and now it’s 132.
Who CARES? the last thing you should worry about is LDL!
Hello - i read study paper from 10 plus yrs ago indicating significant reduction of lpa with oral l-carnitine supplementation. And slight reduction with 40mg daily flax seed. Any more can add to this with maybe newer studies or newer thinking on exactly why these of true benefit?
Let’s see if I have this right. Statins didn’t do a thing for this patient ( because they actually don’t work since LDL-C is just a marker for metabolic disfunction), and LP(a) is the better predictor but don’t give niacin to reduce LP(a) even though you showed that a lower level of LP(a) worked and instead go ever lower with LDL lowering by adding PCSk9 inhibitors? Hmmm
How would you treat TC: 240, LDL: 157, TG:65, HDL: 68, LP(a): 81, apoB: 105? Thx, Tim
With a doctor and not on RUclips...
Were you taking statins to lower your LDLs - I thought I saw that statins can raise LPa
Yes, statins can raise LP(a).
The thinking around LDL levels is changing. Cholesterol is critical to your body functioning properly.
I’m pretty shocked at the treatment decisions these two doctors are choosing - they treat LDLs and try to get results below 70 and they say that statin treatment can elevate LPa which causes increased risk of ASCD BUT they don’t check after initiating statin therapy because they don’t want to make their patients nervous because their therapy is elevating the LPa - to me it is recipe for malpractice - except it probably is the standard of care. How disturbing!
No no no. They're being cautious about eliminating LDL therapy in favor of minimal interventions available for LP(a). Once the LP(a) therapies are available in ~2026, we might see less focus on LDL. That said, you would need to have head-to-headbstudies for LP(a) therapy with and without LDL drugs, once the LP(a) drugs are available.
Is it just me, or have these lipoproteins(a) and other heart issues suddenly started to come to the surface? 🤔
I think it's because the tests have become easily available and cheap
Yes, and new astronomically priced treatments....@@themekfrommars
LP(a) finally has some therapies for addressing the issue in Phase 2/3 studies