Lipoprotein (a) & endothelial dysfunction
HTML-код
- Опубликовано: 8 сен 2024
- Paul talks about the relationship between PUFAs/seed oils and LDL/apoB. Michael Twyman weighs in, as a cardiologist, on lipoprotein (a) levels versus LDL and how they may contribute to endothelial dysfunction.
![Megan Thee Stallion - Neva Play (feat. RM) [Official Video]](http://i.ytimg.com/vi/TpYTyAaTRts/mqdefault.jpg)
I’m slowly eating what I have and easing into a carnivore diet. I have been using honey, local raw honey on pineapple and blue berries. So good. So far at 54 I have lost 100 pounds eating healthy and caloric Deficit.
I still want drop 40 more pounds
Please review the work done by Dr. Nadir Ali, Houston Texas cardiologist, regarding Lp(a). Dr. Ali opines that Lp(a) is NOT causal when it comes to cardiovascular disease and that this lipoprotein is critical for human tissue healing. It would be quite enlightening for us heart patients if you would interview Dr. Ali and discuss his view that Lp(a), much like LDL, is a "firefighter" and NOT an "arsonist."
Have you looked at Linus pauling's research on LP (a)?
I hope so, my LP(a) is 233% above the benchmark for 'high'.
@@jackoconnor21are you on carnivore?
Can someone give me the “cliff’s notes” on Pauling’s findings?
@@user-fl3ez3cr9e
Take lysine supplements and proline supplement. They believe that those bind to the same areas that LPA does so if you flood your body with those the theory is that LPA won’t be able to buy into the vessel wall.
Take vitamin C. The theory is that LPA came into being from an evolutionary standpoint because there was famine or something which caused low vitamin C intake which caused vessels to have micro cracks, and then the first person was born with high lipoprotein a to heal those cracks and be able to live long enough to procreate and continue the species
But my levels are still high because none of those are shown to reduce LPA levels
Saturated fat reduces it compared to the same amount of calories of protein or unsaturated fats, alcohol has been shown to reduce, and recently that protein reduces it
It looks like kind of whack tends to lower it like a factory that’s overproducing this product
Hope that helps
It's the 9 and 13 HODE and the 4-HNE that's responsible for plaque build-up. Here is the mechanism for the 13 HODE.
In atherosclerosis, an underlying cause of Coronary artery disease and strokes, atheromatous plaques accumulate in the vascular tunica intima thereby narrowing blood vessel size and decreasing blood flow. In an animal model and in humans 13-HODE (primarily esterified to cholesterol, phospholipids, and possibly other lipids) is a dominant component of these plaques.[51][52][53][54] Since these studies found that early into the progression of the plaques, 13-HODE consisted primarily of the S stereoisomer while more mature plaques contained equal amounts of S and R stereoisomers, it was suggested that 15-LOX-1 contributes to early accumulation while cytochrome and/or free radical pathways contributes to the later accumulation of the plaques. Further studies suggest that 13(S)-HODE contributes to plaque formation by activating the transcription factor, PPARγ (13(R)-HODE lacks this ability[55]), which in turn stimulates the production of two receptors on the surface of macrophages resident in the plaques, 1) CD36, a scavenger receptor for oxidized low density lipoproteins, native lipoproteins, oxidized phospholipids, and long-chain fatty acids, and 2) adipocyte protein 2 (aP2), a fatty acid binding protein; this may cause macrophages to increase their uptake of these lipids, transition to lipid-laden foam cells, and thereby increase plaque size.[56] The 13(S)-HODE/PPARγ axis also causes macrophages to self-destruct by activating apoptosis-inducing pathways;, this effect may also contribute to increases in plaque size.[57] These studies suggest that 13-HODE-producing metabolic pathways,[56] PPARγ,[56][57] CD36,[58] and aP2[59] may be therapeutic targets for treating atherosclerosis-related diseases. Indeed, Statins, which are known to suppress cholesterol synthesis by inhibiting an enzyme in the cholesterol synthesis pathway, 3-hydroxy-3-methyl-glutaryl-CoA reductase HMG-CoA reductase, are widely used to prevent atherosclerosis and atherosclerosis-related diseases. Statins also inhibit PPARγ in human macrophages, vascular endothelial cells, and smooth muscle cells; this action may contribute to their anti-atherogenic effect.[60]
en.wikipedia.org/wiki/13-Hydroxyoctadecadienoic_acid
Nailed it
Boy, I wish my Dr was this smart. All he thinks about is LDL, CRESTOR, and more pills...
Too many doctors, lack critical thinking and problem solving abilities. *Doctors are just people*
Those that have the ability, then dig deeper into root causes and mechanisms, not allowing the status quo bias to affect their understanding, are quite rare.
Protocol is why he does that. It protects him from law suits. That's why if your LDL is high, they push the statins to indemnify themselves.
@@MK-ft3qt it's true, standard of care IS a good defense that you acted properly in a situation, should you be accused otherwise.
Is it also protocol to be ignorant of the research and data available to treat otherwise, *to the point one can question your oaths taken as a physician?*
If all physicians did this, we'd still be blood letting and measuring people's humors.
Fun fact, blood letting, aka therapeutic phlebotomy, is still a medical treatment, though only for a few specific conditions.
Linus pauling's research on LPa is very extensive.
I’m a survivor of an MI in which I had 100% blockage of my LAD back in 2016. LPa now is
That's exactly correct...you educated yourself and now you're healing your body because doctors are not in that business.
It is very sad that it is so, I am in Europe, and it is the same, I collected many illnesses and after many visits to doctors you very quickly see that you must do your own research and your own experimentation and be your own doctor, in all my cases they would do wrong stuff or say you can't do nothing. For example, GERB, tinnitus, psoriasis, leaky gut. With this stuff you are on your own. After a year of studying these you know more than your doctor. Even after one week ;-)
@@samcohanun my LPa is
@@samcohanun 100%
@@samcohanun never had my LPa checked in the past. Wasn’t worried about heart disease being that I was young. I was 39 when I had my MI, btw.
"Remarkably, one-quarter of the centenarians had high Lp(a) serum levels even though they never suffered from atherosclerosis-related diseases." 1998 G. Baggio.
lp(a) without oxidized LDL is just like a native LDL particle (it just floats right by and helps elsewhere). targeting any particular molecule that may be elevated is missing the point of the lipoprotein system. each piece has a role, and removing pieces to the puzzle has negative consequences. addressing the root cause (diet) is the real answer
@@joerandom157 That does make some sense but maybe some pharma company is trying to create a problem so then they can at a later time sell you a solution?
Do you have a link to this full article or site where this was written?
@@IlIKRATOSIlI The name of the study has the title: Lipoprotein(a) and lipoprotein profile in healthy centenarians: a reappraisal of vascular risk factors.
I think because their vascular system is in declined by the time they’re that old, but they’re LPA levels are higher. I imagine they were not higher when they were younger.
I use Magnesium Glycinate and Liposomal Vitamin C to help heal my artery walls
Yet again I hear that niacin doesn’t change it much. It’s just not true as a blanket statement. I’ve lowered mine from 256 to 156 with 1000mg of niacin a day. I even lowered it to 45 with 1500 but my liver enzymes were then raised so it probably wasn’t worth it. But don’t believe things like ‘niacin only lowers it 10%.
Have been eating carnivore for 2 years.
Labs showed:
Total Cholesterol-350
LDL-C-247
HDL-97
TG-50
Apo B-130
LP(a)-25
So while my total and LDL-C and ApoB up, my HDL also high, TG super low, and LP(a) low.
My LDL was pattern A.
LP(a) seems to correlate to oxidized LDL
So the question then becomes, how do you interpret all of this mishmash? I would think that my overall risk is low given my HDL, triglyceride, and LP levels. I’m also relatively fit and lean. Resting heart rate in 40s.
But a cardiologist would see my cholesterol numbers and immediately recommend a statin
@Bladerunner2049 Is that a question or a statement?
@Bladerunner2049 That’s potentially going to get us down a rabbit hole! Lol. I’m not one who believes in statins. There really are no compelling data to support primary prevention with statins. Some data that maybe they help a little with folks who have already had an event.
I would say focus on healthy diet alone. Exercise. Don’t smoke. Etc
My LPa is high, im 56, calcium score of 3. Its all pure speculatory and doctors are largely clueless.
Hi
I'm perplexed because my LP(a) is 28(optimal), and my LpPLA2 Activity is 290 (increased risk)? Thanks for the video/info!
@ Paul saladino - what do you think about emotional stress / low self esteem & stress causing skin issues? Like rosacea I suffer from im currently doing animal based & i find it’s not going away could this be due to obsessing over the skin issue? More a psychological symptom rather than just diet alone?
Thunderbirds are go
Did he borrow Elton John's glasses
Looks like blue light filter glasses to me, hence the yellow appearance.
No he got those off of Hunter S. Thompson
Mine swings from 300 to almost 600 and I check it about once a month.!
How can anybody tell me that it doesn’t vary????????
Hi
Hi , my last labs this month were 1025mg/L , will taking lysine bind to the Lp(a)?
That’s really high. I thought mine was high at 380 nmol/L. What are your particle counts? They should be under 1000, and have you tested Lp-Pla2?
@@plants_and_wellness1574 1025mg/L translates to 102mg/dl
This dude is Terry tibbs right
Amazing lack of info in this video. Didn't even say what high/dangerous level of lipoprotein (a) is.
Com on guys! Little a is the fire fighter not the fire. Centurians they found at autopsy had high little a.
I don’t care how high your LDL-C is, whether you are diabetic or metabolically unhealthy. You will have a zero CAC score at age 43. At age 45 (earliest age we have numbers) 93% of the women and 75% of the men will have a zero CAC score. So it is a meaningless test at that age unless it is positive, which is very rare.
Paul is clueless as always. Unless you are in the 20% of the population with elevated lp(a), then it is not a risk factor. If you are in the 20% with high lp(a), lowering it by 8-11% is meaningless. They predict that it will need to be 80% lowering for a drug to pass a trial. The last thing you want to do is eat a diet that will raise your LDL-C. You have 10 times as many LDL-C particles. So anyone with very high lp(a is trying to reduce their LDL-C to below 50.
My Lipoprotein (a) is 700mg/L (175 nmol/L) - uh oh
Are you on a keto diet of some sort ?
@@bethjohnson8719 I actually am this month (jan). But that result was from December, when I wasn't. Supposedly it's a fixed marker though, for the most part.
I bet that markers improves on keto ! Good luck! Make sure to post any changes.
Lp(a) can be reduced by Vit C, cysteine and glycine..
Can you please share the source? I would love to read about it since I already take Vitamin C, NAC, and Glycine.
and lysine
@@sonarcher I have heard it's genetic and cannot be changed through diet or lifestyle.
Vitamin c and lysine doesn't reduce lp 'a'....
@@AK-qo6tx thats wrong..
lipoprotrin a es rising because people are deficient in magnesium, vit.c and lysine
Not true. I upped all those things after reading Linus Pauling's books and working with a holistic doctor. My Lpa went up almost 100 points.
hey doc nice specs
This guy is Fkn Dahmer bro
I hav e bizarrely low lp(a).
Fancy seeing you here 🌱🌿
The Lp(a) levels were inversely correlated with the CIMT in this population, suggesting that subjects with a low Lp(a) level may have a predisposition to carotid atherosclerosis. This finding was preliminary and should be investigated further in larger studies and in additional settings. 2012 article CIMT thickness in asymptomatic subject with low Lp(a).
@@StanDupp6371 Again, another fly in the ointment . At the end of the day, how do you interpret any of this stuff in terms of the massive amounts of discordance?
@@keywestfan2503 It's up to you to interpret it for what you want to believe but these Japanese scientists who wrote it are living in the country with the highest life expectancy but it did say the findings are preliminary at this time.
This guys shooting range glasses are such a huge distraction…I can’t watch this
Lipoprotein. a is genic grandparents older generation died younger why they ate animal base diet the study has been done for years