Dr. Joseph I. Miller, MD discusses Lp(a) Basics, Emerging therapies and Guidelines at Napa Cardiology Conference. Learn more at Piedmont.org/heartlearning
My Lp(a) is 315 nmol. Supposedly this is a genetic inheritance. Yet my parents lived into their 90s with no CVD and I (age 78) have had no symptoms of CVD or aortic stenosis. Clearly, there must be protective factors that mitigate the risks of elevated LP(a). As a scientist, it is obvious to me that our understanding of the role of this lipid in disease is still in its infancy.
I'm a little higher than you in Lp(a) but in my low 50's. My PCP recently tested for Lp(a) and it is genetic, my cholesterol has always been at the normal / tad high LDL (131 or 132). HDL 80, Tg 90. I started Repatha a few weeks ago and LDL is half what it was. Went from Lipitor to Crestor a year prior and happy to leave the achy muscles behind. Like any genetic predisposition, I'm doing what I can control. Low carb diet, 4-5 days pf cardio and resistance work, supplements like Lysine, chondroitin sulfate, fish oil and so on.
@@sheddkkhan6758 Yes I did in 2012 and it was 81 nmol/L. after I discovered online that it could be a possible cause for my mini strokes. At least the Dr was willing to go along with my request. There wasn't really any treatment though except to be placed on a statin. Have you been tested?
Inflammation as the mechanism is more important than lpa which is the effect not cause. You stated yourself events continued with lowered lpa, reinforcing my point
Can you please clarify your comment? Everything I have read since finding out I have very elevated Lp(a) has indicated that our Lp(a) measurement is pretty much set for life by age 5, with very little change as we age other than a slight bump for women after menopause, and the Lp(a) number itself is not affected by lifestyle, nutrition, or activity. If that is so, how can Lp(a) be an effect of anything other than genetics?
A very detailed explanation of the physiology is done by dr. Robert cywes , on his youtube channel in one of his newer videos. The lpa from my understanding can fluctuate but that is not the cause of atherosclerosis and isn’t even an accurate proxy for atherosclerosis anyway. Cardiologists recommend getting a cimt score and cac score to more accurately and directly measure atherosclerosis
Atherosclerosis is caused only by inflammation. Lpa is just an observer. APOB must be measured to know your inflammation. Even CRP doesn't show the inflammation in the arteries. Lpa
Everyone should have their Lp(a) tested once. As a primary patient with no other obvious risk factors, I was surprised that my ApoB was 120. My primary was not even sure I needed a statin because my LDL-C (tested three months later) was 107. Fortunately, I tested my Lp(a) which was 280 nmol. The statin dropped my LDL-C to 79 and ApoB to 80. Without the Lp(a) I would’ve been satisfied. But with this knowledge, I started a PCSK-9 inhibitor.
I keep reading that MANY lipidologists opine that a person's Lp(a) is very static during one's lifetime. Researcher, Siobhan Huggins, has shown that Lp(a) is far from static and that DIET AND LIFESTYLE can cause very large fluctuations in that lipoprotein's blood level.📈🩸📉 @@adithyavikram7
There's some evidence that plavix+aspirin is helpful long-term in people who have had a coronary stent already and also have a high Lp(a). There is no evidence in the general population with high Lp(a) that other anticoagulants have benefit
If Lp(a) is such a "BAD" lipoprotein, why is it that there are a significant number of elderly humans who have lifelong elevated Lp(a) blood levels, yet their coronary angiograms show pristine coronary arteries-ZERO plaque? Please see Dr. Nadir Ali's RUclips presentation on Lp(a).
@@sheddkkhan6758 Please take a look at Dr. Nadir Ali's RUclips video on Lp(a) from September 14, 2021. Dr. Nadir Ali believes that Lp(a), just like LDL, is a FIREFIGHTER. Lp(a) and LDL particles are part of the repair proces of arteries that have been inflamed and damaged.
??? From a molecular structure perspective, do you know if the cholesterol found in animal based products, like say ground beef, or different types of steak, is the exact chemcial nature and structure produced organically by our internal organs, (namely the liver) I find it very curious that ''cholesterol'' from diet sources, got so much negative attention the past 50 years, while the public remained largely ignorant that 75 to 80% of cholesterol in the body is made organically, but I think we need to be first asking how human liver made cholesterol our body's have been making is potentially different dietary cholesterol from cattle and eggs? (maybe it's time to zoom out and question first the chemical nature of each, than move on to any mechanical differences, rather than just assume ''cholesterol is cholesterol'' (maybe that assumption all along should be re-analyzed) P.S. 10% apx of our brain matter is cholesterol.
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
Terriblely undisciplined chaotic presentation. It a very rough draft that says everything that comes to mind. This guy should have edited this down. There is way too much unnecessary verbiage.
Mine is
My Lp(a) is 315 nmol. Supposedly this is a genetic inheritance. Yet my parents lived into their 90s with no CVD and I (age 78) have had no symptoms of CVD or aortic stenosis. Clearly, there must be protective factors that mitigate the risks of elevated LP(a). As a scientist, it is obvious to me that our understanding of the role of this lipid in disease is still in its infancy.
I'm a little higher than you in Lp(a) but in my low 50's. My PCP recently tested for Lp(a) and it is genetic, my cholesterol has always been at the normal / tad high LDL (131 or 132). HDL 80, Tg 90. I started Repatha a few weeks ago and LDL is half what it was. Went from Lipitor to Crestor a year prior and happy to leave the achy muscles behind. Like any genetic predisposition, I'm doing what I can control. Low carb diet, 4-5 days pf cardio and resistance work, supplements like Lysine, chondroitin sulfate, fish oil and so on.
I have a much lower LPa of 81 and have had 3 strokes!
Did you go for any test?
@@sheddkkhan6758 Yes I did in 2012 and it was 81 nmol/L. after I discovered online that it could be a possible cause for my mini strokes. At least the Dr was willing to go along with my request. There wasn't really any treatment though except to be placed on a statin. Have you been tested?
Hi
My Lipoprotein-a is 31 nmol. I'm a 63-year old female who eats 80 percent animal based. No inflammation.
Why are you commenting about your level when you are in the normal range?
Inflammation as the mechanism is more important than lpa which is the effect not cause. You stated yourself events continued with lowered lpa, reinforcing my point
Can you please clarify your comment? Everything I have read since finding out I have very elevated Lp(a) has indicated that our Lp(a) measurement is pretty much set for life by age 5, with very little change as we age other than a slight bump for women after menopause, and the Lp(a) number itself is not affected by lifestyle, nutrition, or activity. If that is so, how can Lp(a) be an effect of anything other than genetics?
A very detailed explanation of the physiology is done by dr. Robert cywes , on his youtube channel in one of his newer videos. The lpa from my understanding can fluctuate but that is not the cause of atherosclerosis and isn’t even an accurate proxy for atherosclerosis anyway. Cardiologists recommend getting a cimt score and cac score to more accurately and directly measure atherosclerosis
Atherosclerosis is caused only by inflammation. Lpa is just an observer. APOB must be measured to know your inflammation. Even CRP doesn't show the inflammation in the arteries. Lpa
Everyone should have their Lp(a) tested once. As a primary patient with no other obvious risk factors, I was surprised that my ApoB was 120. My primary was not even sure I needed a statin because my LDL-C (tested three months later) was 107. Fortunately, I tested my Lp(a) which was 280 nmol. The statin dropped my LDL-C to 79 and ApoB to 80. Without the Lp(a) I would’ve been satisfied. But with this knowledge, I started a PCSK-9 inhibitor.
Which PCKS9i did you start with? Did insurance approve paying for it?
@@dwtubeyou repatha. Insurance did cover, but I would have gone forward without insurance.
Cool and good luck with the results!
Role of diet on LP[a].
I keep reading that MANY lipidologists opine that a person's Lp(a) is very static during one's lifetime. Researcher, Siobhan Huggins, has shown that Lp(a) is far from static and that DIET AND LIFESTYLE can cause very large fluctuations in that lipoprotein's blood level.📈🩸📉 @@adithyavikram7
Do true anticoagulants (not just aspirin) offer any protection since Lp(a) promotes blood clotting?
There's some evidence that plavix+aspirin is helpful long-term in people who have had a coronary stent already and also have a high Lp(a). There is no evidence in the general population with high Lp(a) that other anticoagulants have benefit
Would blood thinners reduce the chance of stroke for those with elevated LPa?
If Lp(a) is such a "BAD" lipoprotein, why is it that there are a significant number of elderly humans who have lifelong elevated Lp(a) blood levels, yet their coronary angiograms show pristine coronary arteries-ZERO plaque? Please see Dr. Nadir Ali's RUclips presentation on Lp(a).
When dr nadir said it
@@sheddkkhan6758 Please take a look at Dr. Nadir Ali's RUclips video on Lp(a) from September 14, 2021. Dr. Nadir Ali believes that Lp(a), just like LDL, is a FIREFIGHTER. Lp(a) and LDL particles are part of the repair proces of arteries that have been inflamed and damaged.
If smoking causes lung cancer, why are there a significant number of elderly humans who have smoked their entire lives with no lung cancer?
??? From a molecular structure perspective, do you know if the cholesterol found in animal based products, like say ground beef, or different types of steak, is the exact
chemcial nature and structure produced organically by our internal organs, (namely the liver) I find it very curious that ''cholesterol'' from diet sources, got so much negative
attention the past 50 years, while the public remained largely ignorant that 75 to 80% of cholesterol in the body is made organically, but I think we need to be first asking
how human liver made cholesterol our body's have been making is potentially different dietary cholesterol from cattle and eggs? (maybe it's time to zoom out and question first the chemical nature of each, than move on to any mechanical differences, rather than just assume ''cholesterol is cholesterol'' (maybe that assumption all along should be re-analyzed) P.S. 10% apx of our brain matter is cholesterol.
Role of diet in lipoprotein a
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
Terriblely undisciplined chaotic presentation. It a very rough draft that says everything that comes to mind.
This guy should have edited this down. There is way too much unnecessary verbiage.