A Masterclass on Cardiovascular Risk: Decoding Lipoprotein(a) | Dr Dayspring | The Proof EP
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- Опубліковано 25 лип 2024
- Are you part of the 20% of people with this dangerous gene? There’s a cheap, simple test you can do just once in your life to find out. Join me in Episode #320 as I sit down with renowned lipidologist Dr Thomas Dayspring to help you understand Lipoprotein(a) and the test that might change your life.
Specifically, we discuss:
00:00 - Introduction
00:13 - Demystifying Lipoprotein(a): An Overview of its Role in Cardiovascular Health
06:32 - Genetic Inheritance Patterns and Variability of Lipoprotein(a)
11:11 - Drug Development Strategies for Reducing Lipoprotein(a) Levels
16:49 - Exploring the Functional Role and Genetic Variations of Lipoprotein(a)
28:57 - Inside the Artery Walls: Mechanisms and Structure of Lipoprotein(a)
38:54 - A Deep Dive in Production to Measurement of Lipoprotein(a)
56:21 - Identifying High-Risk Indicators for Lipoprotein(a)
01:09:07 - Statins and Elevated Lipoprotein(a): Understanding the Relationship
01:17:53 - Exploring PCSK9 Inhibitors in Lipoprotein(a) Management
01:28:48 - Emerging Treatments and Future Therapies for Lowering Lipoprotein(a)
01:32:06 - Exploring Lifestyle Considerations and Alternative Therapies
01:40:41 - Oxidized Phospholipids and Their Role in Cardiovascular Health
01:49:25 - Relationship Between Oxidized Phospholipids and Lipoprotein(a)
01:57:06 - Understanding Aortic Valve Calcification and Its Link to Lipoprotein(a)
02:04:17 - Key Takeaways and Future Landscape of Lipoprotein(a) Treatments
02:10:57 - Conclusion and Final Remarks
👇 Visit The Proof website for the full show notes and supporting studies. 👇 theproof.com/podcast/
Dr Thomas Dayspring is a Fellow of both the American College of Physicians and the National Lipid Association and is certified in internal medicine and clinical lipidology. He is currently a virtual cardiovascular educational research assistant and clinical lipidologist at a prestigious national practice and has given over 4000 domestic and international lectures among many other notable achievements. As we saw in the Dr Dayspring’s lipid series on The Proof, he is adept at communicating complex science in an accessible way and brings this skill to today’s episode.
Connect with Dr Thomas Dayspring:
- Twitter/X: / drlipid
- Previous lipid series and cheat sheet: theproof.com/lipid-series/
If you have any additional questions you would like answered in the future, let me know in the comments.
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Enjoy, friends.
Simon
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Thank you for having Dr. Dayspring on again! I really enjoyed the ApoB series!
Thank you so much Simon Hill for this enlightening podcast
Thanks for listening
@ Simon, thank you for having Dr. Tom Dayspring on again. He is a gift to everyone's lives:
- He fights to get the medical community educated on the latest/best info;
- He doesn't BS about things that aren't known, he just states that they aren't yet known;
- He fights misinformation on social media; and,
- His only goal is to help people have longer, healthier lives.
Love the enthusiasm and wealth of leading edge knowledge Dr Dayspring brings to the proof podcasts and kudos Simon for translating it into bite side bits for non-experts in the field
This discussion is orders of magnitude more complex and nuanced than anything I have ever heard on any topic including apoB. Phenomenal complexity and I believe you barely scraped the surface.
Almost halfway through this and never get tired of listening to both of you, you ask incredible questions Simon, so sharp; Dr. Dayspring you amaze me how well you know lipidology and giving a casual talk like this with so much depth and accuracy just tells me how well your brain functions, these talks along with many more are your legacy , I listened to ApoB series several times and learned so much , and now release how much more there is to APo A, apo (a), clearly no other professor can explain lipids better than Dr. Dayspring, long live you Dr. Dayspring, this is my wish for you. Thanks for all your teachings.
Fascinating! I could listen to Dr. Dayspring all day, even if some of the science goes (still) a bit over my head. I appreciate that you don't dumb down the science and trusts your audience to reach higher for a greater ultimate benefit.
Well, I did the tests for APO-B and Lp(a) last year and came up 1800+ Apo-B and 534 Lp(a), triglycerides 77. I had been ignoring my high total cholesterol (ranged from 220-280) for years since everyone in my family has high cholesterol and there is no history of heart or artery disease. Rounded up a heart doctor cause I have had a functional heart murmur since I was a teenager and I wanted to get the skinny on the condition of that valve, which is now 74 years old. Had a consultation last month. I was delighted that his first part of his lecture was "become a vegan." Beat him to that 8 years ago, and I was never much of a junk food consumer prior to that. He mentioned we might have to go to a statin. Anyway, he ran me thru the ultrasounds to determine the condition of my arteries as well as an echocardiogram. Arteries clean as a whistle and no issue with my heart. He wants to see me in 2 years. YEAH!!!! So glad I am an outlier on the curve!
Yeah, presumably you have some kind of protective effect in your body as apoB of 1800+ and 534 lp(a) is just so unfathomably high risk to the point where if you didn’t have some protective effect in your body, you’d have been likely to have already had a heart attack or some other event a while ago if you’re 74 years old now.
@@meltedsnowman9637 You are oh so right. I was bowled over when I saw those numbers. I don't do doctors willingly but I found a heart doc very quickly. I had watched a video by David Attia so I bought the Apo-B blood test and the Lp(a) report came with it. I had to do research to learn what that was. All I can say is that my family has elevated cholesterol , nobody gets it treated, and so far no history of heart disease in the women; we die of cancer, late in life. Both my granddads had killer heart attacks but both were wealthy, would have laughed if you suggested exercising just because, were overweight, and were tobacco chain-smokers. I have never been much of a junk-food consumer, have had to deal with reactive hypoglycemia all my life so sweets were kept to a minimum, I have always eaten a large amount of produce, not very much starch, and mostly pork and dark meat poultry. I am 50 lbs overweight (eat too many veggies), and exercise quite a bit (I can hold my max heart rate for 1 minute while on my treadmill, once a week). I have never smoked anything, have had alcohol a couple of times a year, and learned to avoid transfats when in my 20s, and lived what was, for the most part, a stress-free life, with the freedom to change employers at will, doing what I loved, for enough money. I do hope people who read my message will understand that high numbers are not the point of panic. Wait for the damage assessment.
Would like to know the units for those measurements as well! 🙂
But anyhow, sounds like you and the family members with same genes, might be of great interest to lipid researchers, who tries to find out in more detail, who's at risk and who's not, despite of elevated levels! 😉
However, as mentioned in the video, there currently is a challenge regarding the accuracy of Lipoprotein(a) blood tests. So that's one issue. Fingers crossed a near perfect assay shows up and gets to be the standard for measuring lp(a) in all countries. So we can compare results in a more meaningful way! 😉
And genes aside, inflammation caused by unhealthy diet or lifestyle, I suspect plays a huge role as well...as too how soon the raised levels start to really show the nasty side effects.
But just being a woman, seems to delay the deleterious effect by up to 15-20 years compared to males, according to the current available statistics I've seen.
So being 74, might just mean your at the edge/limit, for the positive effect/protection your hormones has provided so far! 😉
But very interesting field of research, in my opinion! 🙂
@@danieljrgensen133 units were nanomoles per (? I forget) I had a very physical high-paying job with lots of "good" stress (the consequences of my failure meant someone got hurt), little "bad" stress in my life, and was raised on a very good diet. I continued that. I exercise quite a bit even though I am quite fat at 50 lbs too much (too much rice and beans).
Wow, that is great news considering your numbers!
Thank you for this one. Measured my APoB and LP(a) in the context of the Proof Challenge and was disappointed to see them both high (despite an in-range total cholesterol). I think what is missing from the conversation (or maybe this is the next super-important conversation) at this point is how to fully optimize *everything* we can when we are one of the unlucky ones with high LP(a) and are resistant to or unable to take a statin (honestly my doc suggested she *could* send me to a preventative cardiologist, but it would undoubtedly be out of pocket and she didn't think it was really warranted given all my other stellar numbers and apparent health). I think that so many people/doctors under-estimate what individual/patients are willing to do in terms of lifestyle and I now feel the urgency of doing everything I can and doing it optimally. I'm already WFPB vegan with very limited oil, salt, sugar but now I wonder should I forgo nuts/seeds (Esselstyn?) or simply limit them (Ornish?) or focus on nutritional-density (Fuhrman?) or anti-inflammation (Goldner). How reassured should I be that my HbAic, hs-CRP, triglycerides, etc are good and my VO2 max, resting HR are good? How much benefit might I get from adding foods on the Portfolio diet? Ground flax? Switching from my french press to drip coffee (that one was new to me, Simon thanks). It's a really weird place to be knowing you have this risk factor which is apparently causal and yet I also feel like "we" are just on the front end of understanding it. I remember all the conversation had about people trying to raise HDL cholesterol and I wonder if in 5 years the conversation around LP(a) will be very different. Anyway - thanks so much for this deep dive, Simon! Would you consider getting Esselstyn and Joel Kahn on next?
I’m right there with you on the high Lp(a) train. Mine was 380 nmol/L and unlike you, my other numbers I just can’t seem to get down. My LDL was 115 last I checked but my LDL-P was over 1600, LDL-small over 400, pretty much every cardiovascular number was in red. It’s all improved so much since I went WFPB in summer of 2022 but still not where it should be. I also do eat salmon 3-4 times a week. I use Function Health instead of inside tracker because you get double the amount of test for the same price. I just order my own labs through them to keep track of everything. For $499 you can get 112 biomarkers checked and that includes 60 biomarkers rechecked 6 months later. Highly recommend if you want to keep track of your numbers.
When you say you are the unlucky ones with high Lp(a) do you mean these centenarians? "Remarkably, one-quarter of the centenarians had high Lp(a) serum levels even though they never suffered from atherosclerosis-related diseases." 1998 G. Baggio.
Or do you mean the unlucky ones who wrecked their health by having low levels of Lipoprotein(a) in their genetics? 2012 article title: Low Lipoprotein(a) Concentration Is Associated with Cancer and All-Cause Deaths: A Population-Based Cohort Study (The JMS Cohort Study).
Are you working on a pill that can raise Lp(a) levels high enough to be optimal for all of humanity? "Nonetheless, the apo(a) size distribution in centenarians did not entirely explain the high Lp(a) levels observed in this population. Factors other than apo(a) size, and which may be either genetic or environmental in nature, appear to contribute to the elevated plasma Lp(a) levels of our centenarian population. We conclude therefore that high plasma Lp(a) levels are compatible with longevity." 1998 article by J Thillet
I do think this is the main question healthy vegans have: how low fat should we go? I'm on the Fuhrmann/Dr. Greger train: limited consumption of nuts and seeds is better than eliminating them completely. I think the evidence is pretty clear.
You didn't specify "high numbers"??
But I've seen a lot of people in the comments section, who is scared, just because their numbers is outside the current estimated "ideal range" between 0-75 nmols/L. 125 nmols/L is a agreed upon threshold, where we begin to detect a risk of significance(albeit still small) starts to happen. So, unless your significantly above this, I would recommend not to lose sleep over your lp(a) value! 😉
It's important to realize, that there is still uncertainty as to how well these lp(a) numbers reflect risk on a individual level.
If you don't have a family history of heart disease, then I would use that as your most precise indicator for risk assessment, regardless of your lp(a) number.
I'm currently at 650nmol/L and was initially scared. Until I looked around in my family, and realized nobody had died in early age of heart disease. So, as Dayspring mentioned, there is still research needed to be done in this field, as there are "outliers" who don't seem affected by high numbers....and the answer to that, still needs investigation.
But on a population level, the data clearly shows an increased risk with increasing higher numbers.
Thank you. I found the Pelicarson trial. We're at 2024. Hoping for good outcomes and additional clinical trials.
You’re welcome
To be honest I am personally more excited about the currently ongoing phase 3 olpasiran trial( siRNA injectable drug), since in phase 2 they established it's safe and reduces Lp(a) up to 90 percent.
@@demonfedor3748Yeah, that's the one I'm mostly interested in as well.
But the sad part is...if it really turns out to be a "wonder drug", nobody will be able to afford it and insurance won't cover it as well.
It's only tested for secondary prevention and thus will only be approved for those patients. So you have be a survivor of your first heart attack, in order to even be considered a candidate for the drug.
But on the more bright side, 10 years from now or whenever the patent runs out....we all(hopefully) can get it for a lot more accessible price! 🙂
In June 2020, right after the first series of interviews with Tom on ApoB, I had my Lp(a) checked and it was 10, so I thought I was good. But in Nov 2023, my doctor accidentally re-tested me while doing a other re-tests of three liver enzymes were "out of normal range" for almost a year. And that time my LPa was 25, a jump of 15 points. I found one website that said that Lp(a) can change when there is disease of the liver and/or kidney. I kept pressing my doctor for why my Lp(a) value, which is never supposed to change had jumped 15 points. So a month later, at the end of Dec 2023, we re-tested again and my third Lp(a) value was 25. My liver enzymes values resolved on their own 2 months later in February 2024. My Kaiser Permanente doctor consulted with an cardiologist and lipidologist and their combined conclusion was that the first reading must have been a lab error. They could not explain the change in the third test. I promised my doctor that I would not "chase" Lp(a) and worry about it because all readings were under 30. But........ its a cheap test and I plan to fight for it again at my annual physical in March 2025, and thereafter until I'm convinced it's stabilized. You have to lookout for yourself. I've just started watching this video. I'm hoping it includes some insight about value variability.
Check your units. Sounds like first test was mg/dl and the rest were nmol
@@ericmw9340 Thanks for the suggestion. All were mg/dl on a scale where, as Simon mentioned,
Thanks for this. It's very timely; just found out I have an Lp (a) of 141 nmol/L.
Mines 179nmol and Incant lower it
@@SJC-nz7ix I believe you'd basically be limited to pharmaceuticals to lower it. Presently, PCSK9 inhibitors often lower it 20-30% (which may not be great enough to significantly impact outcomes). It's not indicated for primary prevention (if that's your situation), but if you have the money to pay out of pocket, that's probably the treatment I'd go with. I'm looking into repatha myself.
Interestingly, watching a presentation on youtube from the University of Colorado School of Medicine, they noted that individuals with higher Lp(a) are less likely to develop diabetes / metabolic syndrome. In the Odyssey trial, reduction in Lp(a) resulted in statistically significant increase in the development of the condition in people with the highest levels (exceeding ~175 nmol/L). So, once better pharmaceuticals are available to lower Lp(a), ensuring body fat is maintained at a lower level may help offset the risk.
This was an interesting discussion. Dr. Dayspring was giving very assured analysis about the threat of Lp(a) from the start of the discussion, all the way up to the question that gets raised after 1:40:43. But at this point he is suddenly not so assured about the threat of Lp(a) and theorizes that there could be benefit to Lp(a); i.e. reducing Lp(a) levels could be detrimental.
FWIW, I have high levels of Lp(a) that vary anywhere from 160 nmol/L to 205 nmol/L.
Wow, what a tour de force on lp(a). Excellent conversation. I am going to revisit daily low dose aspirin therapy (already on a statin) as my lp(a) is 200 nmol/L. I definitely do not have the money for off label use of some of the upcoming niche drugs, and don't want to wait around to have a heart attack so my insurance will pay for them either.
Thanks for insight
Our pleasure!
When I finally tested, my ApoB was 120 and my lp(a) was 280 nmol. I have always had high LDL-C. Now my ApoB is 57, LDL-P is 326 and LDL-C is 37. Nothing to be done about the lp(a) unfortunately.
Thank you for this episode, Simon! Dr. Dayspring is such an amazing teacher. Just to be clear, when I have my apoB levels measured (in mg/dL), does that also include the Lp(a) too? Or does it not? I'll need to rewatch it, like I have other Dr. Dayspring episodes to understand this better!
To make my question clearer: Is the following true?
Total apoB = non-Lp(a) containing apoB + Lp(a) containing apoB ?
They are separate tests. Lp(a) is only tested once in your lifetime.
Yes LP(a) is included in an ApoB test but because it makes up just a fraction of ApoB containing lipoproteins you need to test LP(a) at least once per lifetime to know your LP(a)-driven risk
@@TheProofWithSimonHill Thank you, Simon!
What about cobtributung to strokes ?
I found the discussion on aspirin interesting. I’m 47 with a LP(a) of 164. Would I benefit from aspirin? No other risk factors, healthy weight and blood sugar levels
If you listened closely, Dayspring said it's only recommended for secondary prevention patients. Meaning, people already with established heart disease and thus with a risk that is greater than the risk of internal bleeding, which comes as a side effects of using aspirin.
Dayspring only briefly mentioned, that if you are one of those few people with severely elevated lp(a), like +300 nmol/L...then the bleeding risk from aspirin, may possibly be lower than the heart disease risk and could make sense to use in a primary prevention session. He forgot to mention such a call should only be done by a qualified doctor! 😉
But in other words, from your description, your not a candidate for using aspirin! 😉
Thank you for the great review. I had a Lp(a) of 82 nmol with low TG of 36 and ApoB of 80. With a retest 6 months later everything when down little , HDL went up but LP(a) jumped 50% to 122 nmol. Would this be a testing error. I will get a retest I believe but was wondering about frequency of testing errors
Did you use the same lab? Some labs use nmol/L, other labs use mg/dl. The same lp(a) level will look very different when measured using different units. Check your units. Good luck.
@@Mimulus2717 Thank you for the reply, I did use the same lab and both are in nmols. If genetic 50% swings in LP (a) with only 5% in any other bio markers seems erroneous. I will use another lab and try again. Thanks
@@David-bn6el Agreed, good to have some certainty around these numbers as such a big difference changes risk. My PCP knew nothing about lp(a) so I went out and educated myself (mine is 200 nmol/L) and got a carotid intima media thinkness ultrasound and discovered, that at age 58, despite lifelong low LDL, I had the carotids of a 85 year old (asymptomatic). That got my attention. I am on a statin now, (ApoB 60-65) and considering adding low dose aspirin therapy too. FWIW, my 86 year old mother has the same LPA mutation and level, and even as a T2DM she has no heart symptoms (but will probably die of a MI or stroke some day soon). So, my other familial CVD genetics must be pretty good. Hopefully yours are too. Good luck.
@@David-bn6elmine bounces around too. I was told that may mean it’s due to something other than genetics.
What about high Apob and low LPa? It seems that high apob would indicate heart issues even if the lpa is low? I'm trying to learn about all of this.
Covered in our previous lipid series. Want to always get ApoB to goal irrespective of LP(a) level
So much of this is like listening to a foreign language! I get so confused with all of the medical terms. But I'm really trying to learn and put together why my results don't make sense. Low Lpa, trigly, blood pressure, non diabetic but high apob and cholesterol. None of that makes sense to me.
@@TheProofWithSimonHill In your 6x Brown belt vs 1x lack belt analogy LDL was compared to LP(a). Could we equally look at ApoB as being the 6x brown belts? And hence ApoB is the dominant risk factor?
So what is the optimal Lpa range?
0 - 75 nmol/L
@@danielj.1402 thanks. I'm good then. 👍
“God forbid your Lp(a) is 200-300” 😅 mine is 380 nmol/L
Very good analysis but you missed your own conclusion that externally reducing Ap(a) might actually make things worse. Reducing the oxidation is ultimately the cure if not by saturated fat by other means or at least the main cure should be to reduce that oxidation not Ap(a) reduction.
Didn’t miss that. It remains to be seen
@@TheProofWithSimonHillTo me you already explained a viable mechanism for impact of inflammation but omitting so far its impact because it is difficult to prove at this point. It is interesting to listen to Dr Dayspring explaining all mechanisms but on the solution to problem he fails to see beyond trials done by big pharmaceutical companies developing statins. It is hard to believe majorly of stroke incidence that is now rising every year depends on high Lp(a) which comes from our genes that existed for centuries. Also that the only solution is not by diet rather by a medicine has been around for 20-30 years and still incident of heart track is rising. The bigger picture doesn’t add up and suggests our current trials are missing the fundamental cause.
So I notice there has been no uptake of providing proof of no conflict of interest. I guess I’ll assume that there is. If scientific papers need to state conflicts then so should guests on podcasts. We as humans are all bias in some way whether we think we do or not but when money is involved the bias has a multiplier effect.
Dr Dayspring describes the birth of LP(a), but not its catabolism. Comment?
Why talking about 'drugs' only and not also 'nutraceuticals' able to lower Lp(a)?
" Several foods and decreases in saturated fat and ethanol intake, especially red wine intake, may lower Lp(a) concentration, but limits are necessary. Coffee and tea intake may decrease Lp(a) level; further investigation is crucial before they can be considered potent Lp(a)-lowering agents. Among supplementation strategies, only l-carnitine and coenzyme Q10 are promising clinical candidates to lower Lp(a) level. Since both l-carnitine and coenzyme Q10 supplementation are commonly used for CV support, they deserve further exploration regarding clinical applicability" Lipoprotein(a)". Current Evidence for a Physiologic Role and the Effects of Nutraceutical Strategies. I read about curcumin and flaxseed as well in Lifestyle and Lipoprotein(a) Levels: Does a Specific Counseling Make Sense?
@@jft8994 It's my understanding that Pycnogenol could help.
@@ukispargitus970 I take some.
@@ukispargitus970 Taking some.
@@ukispargitus970 Using it.
Ai will soon take the guess work out of it and all gurus and snake oil salesmen will soon be gone. I challenge everything this man says ❤. Send me the research pappers and studys ! Don't die ! Decentralization.
Please state any conflicts of interest that dayspring has. He appears to be a salesman for statins so please prove me wrong by stating that he does not receive money directly or indirectly from pharma. The studies that show niacin has no benefit aren’t comparing niacin to nothing they are comparing niacin to statins. Have a look at physionic for details. I personally have lowered my Lp(a) from 254 nmol/L to 150 with 1000 mg niacin. Better than a PCSK9 inhibitor.
What form of niacin do u use?
Niacin, niacinamide or something else
It’s from Life Extension and the bottle simply says ‘Vitamin B3 Niacin . I believe it’s Nicotinic acid. And just for you info, I was able to lower my Lp(a) to 45 by using 1500mg but unfortunately that was the point that my liver enzymes started to rise so I’ve dropped back to 1000 and I’ll live with the 150 reading. I’m only small (63kg male) which might be relevant to others who could handle more than I can.
The current worry/unknown with using niacin/nicotinic acid, is the lower numbers could be caused by it inhibiting certain liver functions.
The study data has not shown any meaningful risk reduction from using niacin. But there where cases with liver damages instead.
Playing the devils advocate here....what if the decreased numbers, stems from inducing liver damage?
Just like the cancer patients in a large LDL cholesterol study, sqewed the results by showing increased mortality in the really low LDL data....confusing certain people into thinking low LDL is bad.
Like wise, if niacin/nicotinic acid is simply "beating up" the liver, and this makes it to spit out lower numbers for the duration of time it's trying to recover? That could explain why no risk reduction is seen, and because the liver is the only organ who can repair itself, to an extent....it could explain why people can get away with doing this for years, as long as the dose stays below a certain level.
Curious as to what you(or anybody reading this) think of that angle! 😉
Yeah that’s all possible I suppose but as I have mentioned in one metanalysis (I think that’s what is was from memory so stand to be corrected if it was just a single study) there was no meaningful advantage of niacin but that wasn’t up against a placebo, it was up against a statin. So working backwards that would bring down any statin effect to meaningless. And who knows, perhaps both are true. I guess it’s all a gamble but as someone living in Australia with very very high Lp(a) I don’t have many options. Take niacin and lower it (whilst watching liver enzymes) or take nothing and live with 254nmol/L until that kills me. Pick your poison. Believe me I’m not happy about needing to make this decision.
@@stevemc2626I would choose a low dose statin(5 mg rosuvastatin) and combine it with Ezetimibe. Lp(a) is an LDL and travels together with the others in the blood vessels. Lowering your total amount of Ldl's will make the damage the lp (a) particles can do, significantly less! 😉
You can still take niacin if you choose, but I would recommend lowering the dose, until you got an ALT measurement, so you don't risk inflicting self damage.
Btw. my lp(a) is more than twice your number.....and yes, I am impatiently waiting for a new lp(a) lowering drug, that is safe to use! 😉
If LDL causes atherosclerosis, why do we not see it forming in the walls of veins?? I would love a detailed explanation of this. The veins carry the same blood and LDL as the arteries, for some reason nobody, not even the so called experts can explain this for certain....it's the one fact that debunks the theory that LDL is the root cause of heart disease, endothelial dysfunction is the root cause of heart disease, not LDL, LDL is there doing it's job to rectify the damage. If LDL is the root cause of atherosclerosis then we're all doomed from birth obviously. What a joke the modern world of health and nutrition is. All this BS isn't helping anybody make better health choices, just confusing them. Just eat real food people, stay active and get on with enjoying your life.
If you put veins into the arterial system they can get atherosclerosis. The veins actually begin to act as arteries (adapting to local environment)
@@TheProofWithSimonHill exactly, so why do they not get atherosclerosis when on the venous side of the circulation system? You have not answered the question, just confirmed that arterial plaque only occurs in the arteries. You need to explain why plaque does not form in veins when the same blood containing the same levels of LDL is circulating....to prove beyond doubt that LDL is causal. This fact clearly debunks the LDL heart hypothesis but everybody just conveniently overlooks it, and can't give a logical explanation.
@@Richleisa "In conclusion, we have demonstrated that arterial blood has a substantially higher percentage of lymphocytes, but a lower percentage of neutrophils, compared with venous blood. This is potentially responsible for the more frequent occurrence of vascular sclerosis in arteries than veins. This hypothesis needs to be further examined in more mechanistic studies, both in vitro and in vivo."
Effects of arterial blood on the venous blood vessel wall and differences in percentages of lymphocytes and neutrophils between arterial and venous blood
@@jft8994 This is "POTENTIALLY" responsible....not certainly. This "HYPOTHESIS" needs to be FURTHER EXAMINED
@@Richleisa Could not find better.
My mother akmost 94 took no meds fainted at Ymca in steam room sent to hospital . The quack doc immobised her ( sibling had power of attorney) and of course woukd not comminicate witth me. Mom stated if they would let her out of bed she would get rid of the phlegm on lungs caused by no mobility. They gave her statins iv which reduced her heat energy ( they have no co q 10 ) no opportunities to wheel her in sun and killed her by not allowing mobility nor allowing any alterntive treatnent. Thr problem with chloedterol is not chloredterol. Its the oxidation of chloredterol. Trumps proposed commission investgstinh big pharma if for no OTHER reason is a reason to vote Trump
Wow. That is the worst reason to vote Trump since it is the Dems who are fighting to improve healthcare. Biden has done so much already including expanding services and decreasing drug costs. Trump says things but doesn't actually do them. After his covid response he would be the last person to trust for justice for your poor mother (I'm so sorry). Big Pharma are donors to Trump's campaign so there's no way he will do what's right.