My hematologist had strong opinions on these journalistic presentations. Said it was the fact that the immune system sees LDL as an allergen, forming inflammation responses and glutting on the LDL. White blood cells glutting themselves on LDL kills them; and if you've seen the animations of white blood cell transport in vascular system you'll note they distinctly stick to the arteries and veins and roll down the surface, when they die from over eating LDL THAT is where they stay, while also causing inflammation which complicates things. That's why, when biopsied they're called "foam cells" because they look like foam under the microscope, and when micro pipettes are inserted into their internal vacuoles the goo they're full of is LDL. The reason a surgeon can't just vacuum them out, or a drug "release them" or "dissolve them" is because the endometrial cells that line the arteries and veins grow over these dead white blood cells as part of the inflammation response, so you not only have to get rid of the bags of LDL inside the dead white blood cells, the dead white blood cells but also layers and layers of lining cells trying to help opening up the arteries and veins deeper layers creating new nucleation sites for clotting events. So no, no rotor-rooter for the heart will work, if anything is to work it'll be one hell of a complicated dance that works with the autoimmune system, circulatory system and perhaps surgical system choreographed perfectly... Frankly the "plumbing example" of grease bergs and "build up" is actively holding up informed discussion on this subject with patients, it's not like Calcium build up in copper pipes of a house.
Wow! For a non-physician, that is actually an excellent explanation, though you get the minute details wrong (like, it’s not technically an allergic reaction but it is another type of immune reaction, and it’s ‘endothelial’ not ‘endometrial-‘ those are the cells that line the uterus during menses). You must have a great hematologist to explain all that to you and also you must be in a field like engineering or something to have understood it that well!
Your hematologist does a pretty great job explaining it all! Many folks forget that the pathogenesis of atherosclerosis is in fact an inflammatory process, so the allergy analogy, while not 100% on point, is still a great way to think about it. That being said, the "plumbing example" is sort of helpful to explain things to the general public - after all, there's a reason percutaneous coronary interventions work - while they don't remove plaque, they do "buy" some time back for the patient by opening the vessel lumen. The rest is as the hematologist said - a complicated dance of more factors involved. In the world of cardiology, we call this residual risk - and we aim to reduce it through other means, like medications and improving modifiable risk factors.
@MandrakeFernflower Well, unfortunately, the receptors involved in said binding are not specifically unique to foam cells, and targeting them would cause some degree of immune suppression or other very generalized side effects.. So in effect the best thing turns out to be reducing LDL directly, or as some folks pointed, ApoB
There is exactly only one type of cholesterol, it’s called cholesterol, and it’s essential. The lipoproteins are the vehicles moving the cholesterol around. It’s never ever the problem of cholesterol itself. Ancel Keys got F as a scientist, and SciShow got another F on nutrition.
As a physician I can say that lipid metabolism and cholesterol levels are a constant source of concern and skepticism. Thank you for helping to explain this.
My mum was put on a low-fat diet to reduce her slightly too high cholesterol. Except she apparently belongs to the group of people whose body will go into overdrive and produce even more of it, so it made her cholesterol levels sky-rocket. And because the doctors would just give her statins, which completely knock her metabolism out of balance, she quietly stopped the diet again and didn't tell them. She's short and thin anyway, so it's not like they'd notice.
@@Hi_Im_Akward Great question. As they said, there is a lot of nuance when it comes to cholesterol/lipids, much like your overall health in general. Some people process cholesterol vastly different than others so they require some sort of lipid controlling medication (familial hypertriglyceridemia for example). We always like to start with lifestyle changes with diet and exercise, but for some that's not enough. We are always learning more about what is healthy and what might need some improvement. If nothing else, if you want to do your own research...I'd recommend just avoiding pretty much any "influencer" or anybody like that as they generally don't have your best interest/health at heart. Find good peer-reviewed studies on the subject, preferably double blinded studies or meta-analyses of multiple studies. If you start to get into the Krebs cycle or gluconeogenesis...you've gone too far. ;)
@@SinisterMDas a fellow physician I giggled intensely when you mentioned Krebs cycle. But besides this, the reason we do not routinely check for LP(a) is our lack of ability to do anything about it. It could do a lot more nocebo harm to know a risk than to just keep on living with the individual background risk. This is actually a key element in determining which diseases to create large screening programmes to catch, but this is a whole different story.
They won’t find more kinds. It’s one only one kind and it’s just called cholesterol. The vehicles cholesterol attached to are lipoproteins, obviously those are proteins.
There's many more infact. Look at the classic "Sugar: The bitter truth" lecture on youtube. Not sure how it held up to the test of time but will inform you of other cholesterol types.
LDL and HDL are NOT forms of cholesterol. They are lipoproteins that transport cholesterol. Moreover, these proteins are necessary for lipid metabolism and are not inherently good or bad. Persistent high or low levels of LDL and HDL are signs of dyslipidemia and faulty lipid regulation; moreover, some studies show some correlation between high/low levels with coronary artery disease and other illnesses. However, this is not the same as proof of causation - I.e., LDL causes heart disease. Referring to “good” and “bad” is an oversimplification and does a disservice to patients, causing them to misunderstand cholesterol and lipid metabolism and the effect on health.
Plus, statins, which are proven to reduce risk are also proven to increase Lpa leves. So what gives? Right? The story of atherosclerosis is a lot more complicated than good/bad cholesterol. Oversymplification in the name of education is problematic.
Nice that you mention this. I missed the fact that the level of LDL and HDL in reference to eachother is key in keeping a healthy blood vessel. Too much HDL while simultaneously low LDL is just as bad as the other way around. Some peoples metabolism is just more sensitive to high HDL levels. Mine suddenly spiked one day, and I still have no clue why. Cos when it was discovered, I was highly active, doing workouts multiple times a week. As to never doing any workout on a regular basis ever before.😅 So... I thought I was healthier, but my blood said differently.
This is outdated, in the medical literature of cardiology since 2017 with a meta analysis and mandelian randomization, LDL has been proven, outside of any other variable as causation for athelosclerosis. In fact, current "normal" numbers are too high, people with 100 LDL, 60% already have developed soft plaque. its only in the
@@wojciechkurdzielewicz7781 statin doesn’t reduce risk, not a single bit. Statin is the greatest con in medicine history. And cholesterol doesn’t cause heart disease or anything. Cholesterol has essential functions in our body, not just some random functions. One function is to patch the broken things. It’s why we see cholesterol in arteries, because it is deliberately transported there to patch whatever the damage there. It’s like blaming firemen for causing fires while the real arsonists are free to go.
I worked as a lab tech in the Veterans Affairs for three years and i can day LPAs is a common test when patients come in with 250+ LDL cholesterols. I've pulled dozens of tubes on patients as young as 25. Its good to see many VA docs order more diagnostic tests
Excellently done! I've been tested for LP(a) by a Cardiologist after a heart-attack and was put on an additional medication to help bring my overall numbers down even more than they were on just the statin alone. Apparently I've got some eastern European genes in me that are really good at making extra cholesterol.
Maybe you should look into reducing carbohydrates intake and sugars and fructose. At least don't mix them in the same meal. And start fasting. Then after 30 days review the tests again. Our bodies like one or the other (protein+fat or carbs) but it reacts badly when mixing all of this together. Eating fat doesn't translate directly in high cholesterol. Carbs are responsible for inhibiting the fat utilisation and breakdown. Apo(a) and other types of no so good lipoproteins appear in the blood stream when they get distorted or glycated because they are forced to stay too much time in circulation because the body is using glucose instead. So the problem is not so simple.
I've been diagnosed with high amounts of Lipoprotein a. I had a massive heart attack when I was only 34 because of it. Not overweight or anything, just out of the blue BOOM. I've had a small stroke and a second less sever heart attack since then. I now have 5 stents in my heart and it's been really crappy to say the least. I have loads of pills and 2 injections (Alirocumab) I need to take each month. I'd sure like to just get that normal lifespan. Oh and the real sucky thing is it seems to be inherited. :(
@@vituperator9603 I like that you've made a wild assumption that OP hasn't thought of literally everything under the sun already. But also what the other person said. Unless you've gone through this exact same scenario, or are a medical professional, maybe don't give out unsolicited advice.
@@vituperator9603 my dad has also inherited something very similar and when its inherited (ie genetic) diet makes little to no difference. he stayed in a hospital for some time eating his meal plan they provided for him in hopes it could lower is cholesterol and it did not make a difference at all
We really need to be discussing a transition to chronic and preventative care for these life ending conditions since we're getting to the end of what acute care responses can accomplish. Getting a blood test for LDL if nothing else at the age of 18 y/o for every adult just to see if they "want to feel old one day" or if they want a preventative Statin R/x would go a long way towards this. The Japanese and Koreans get such wonderful outcomes and longevity primarily because your average Japanese or Korean's primary health care provider is a pharmacist. It's a system betting on strategic / preventative responses by the medical field instead of tactical / acute responses. Look up a Japanese Manga: "Other world Pharmacist" for an excellent ... high school level primer on how pharmacists act as front line agents of the health care system to affect excellent results; it's a paradigm shift of thought for average people who's best source of medical information is House MD. :)
Glad Lp(a) is getting mentioned more. But because of lack of studies it is still commonly reported that diet and exercise don’t make a difference. Both my mom and I HAVE LOWERED our results with Niacin. I also lost 30 lbs. just got lab results back yesterday and my score is way down, still out of range but way better.
TedEd had a video going over HDL and LDL just yesterday, and it gave me the background knowledge I needed for this video. Is it cholesterol week? Or was this just a coincidence, lol.
They must have some kind of partnered media sources. The info is nearly identical, especially the way they bring up different impacts like food, exercise, and statins.
Would those really have an effect here? I am subscribed to both channels, and I was only watching whatever videos popped up in my notification section.
Not mentioned in the video, but it's important to know that it has been shown that eating cholesterol does not affect your blood cholesterol levels. Egg yolks for instance are extremely high in cholesterol, but they have no negative effects when consumed. Only saturated fats are problematic.
@@robertgossett6228 Saturated fat is solid at room temperature. While yolks do contain some, most of their fat is unsaturated, which is why they remain liquid even in the fridge.
Buried on page 91 of this 572 page report: “Previously, the Dietary Guidelines for Americans recommended that cholesterol intake be limited to no more than 300 mg/day. The 2015 DGAC will not bring forward this recommendation because available evidence shows no appreciable relationship between consumption of dietary cholesterol and serum (blood) cholesterol, consistent with the AHA/ACC (American Heart Association / American College of Cardiology) report. Cholesterol is not a nutrient of concern for overconsumption.” (Quote from the Scientific Report of the 2015 Dietary Guidelines Advisory Committee).p 91.
I have, doctor diagnosed hypercholesterolemia type II. I inherited it (thanks, Dad). And yes, I went on a 5% fat diet, lost 20 lbs. and raised my cholesterol 45 points! And found out it's typical for people with this condition. I then went on statins. I didn't know about this third type and I would love to hear about the way triglycerides relate with these 3 substances. Especially since the NIH and CDC will be run by RFK, Jr. We need dependable info.
@@ladyeowyn42 Once they found one that I didn't react to, that was fine. I've been on them since 1992. My brother & sister had jobs that didn't include health insurance. Sis died at 44 of "broken heart" syndrome and my brother eventually got health insurance and started treatment about 10 years after. He's still living, but had a heart attack at 63. He's 74 now. Best of luck to you!
Ugh, I think I may be in the same boat. Uncontrolled high cholesterol and triglycerides run in the family and my tests are starting to creep up into the danger zone now that I'm in menopause despite virtually no changes to diet and exercise. And I did the sensible thing and spent the time between my first high reading and my last screening going HAMM on lifting weights, taking fiber supplements, eating more veg-heavy, etc...and my scores went up. *le sigh* My mom once came of a check-in with triglycerides in the high 300s, despite being a near vegan. We may be in the "turn carbs into lipid-based death" category. I may have to go antithetical and try low-carb to see if it helps.
My highest total cholesterol was never higher than 240, but I had too low HDL and high LDL; I had a stent at 39 and 42 years old, and I had to have a triple bypass heart surgery at 55 years old. Then, I tested my Lp(a), which was a very high 86. Men with this level can have heart attacks and strokes in their 40s. Yes, I take my meds and cycle 5 times a week, do intermittent fasting, and eat low-carb.
I like that they say nobody is the same. You really do have to find what works for you. For me, sugar will raise my LDL and eating more saturated fat raises my HDL but does nothing to my LDL. Thus a lower sugar diet that includes butter and bacon is just fine for me. Not the case for everybody though. I think people kind of knows this now and are really looking for more personalized diet advice. I would start with doing your best to eat what your ancestors ate.
Two years ago I got the diagnosis that and I quote "I have too much good cholesterol and too little bad cholesterol" which makes you wonder how good the names are...
chronic inflammation, often caused by factors like smoking, high sugar intake, and processed foods, is a significant contributor to cardiovascular disease (CVD). These inflammatory triggers can lead to oxidative stress, damage blood vessels, and promote the buildup of arterial plaques. Regarding saturated fat, recent research challenges earlier claims that it directly causes CVD. Evidence suggests that saturated fat has neutral or even anti-inflammatory effects in the context of whole, unprocessed foods like fatty cuts of meat and dairy. However, its role in inflammation and heart health can depend on the overall diet composition and whether the fats are consumed alongside inflammatory foods like refined sugars and seed oils. This aligns with the idea that context is crucial, and an anti-inflammatory diet likely minimizes sugar and processed foods while emphasizing nutrient-dense, whole foods.
I wonder how many more people will die bc of the blatantly wrong narrative that eating meat and saturated fats will kill you. This video was released in 2025😭
Always hate when peopel write "processed food", that's just stupid. Processed in what way? You can process food and make it 100 times more healthy or you could make it 100 times worse. A lot of food would just rott before it can reach you without being "processed." It's like peopel who come up with "chemicals". EVERYTHING is "chemicals".
Interesting stuff....not too keen on a new RNA treatment though....Also can SciShow do a video on how cholesterol goes up during (peri)menopause in which case HRT is first line treatment. Maybe just do a video on (peri)menopause, for those who do not follow menopause specialists on social media. It's important to know for men too, to understand and support the (peri)menopausal family and friends in their lives.
It's likely to hit the market somewhere in '26 or '27,the phase 3 trial is almost finished,and judging by phase 2 results you can expect up to 90 percent reduction in Lp(a).
@@RoxanneRichardson Might have been too optimistic . It ends Dec 29,2026. Then data collection, unblinding, preprint , peer-review, publication and then FDA registration. More like summer of '28 .
A 2014 review of people who took statins showed that they extended life expectancy by 3-4 days. "The effect of statins on average survival in randomised trials, an analysis of end point postponement"
I read the paper. It says, “There are a number of caveats that need to be considered. First, this analysis only estimates the survival gain achieved within the trials’ running time (2-6 years). After termination of the trials, the treated would continue to accrue survival gain as long as there was a difference in cumulative mortality between the treatment arms. There are a few studies with long-term follow-up after cardiovascular intervention trials showing that this survival might be substantial,17 but there are also studies showing that mortality becomes similar in the two groups after the trial's termination.” When used as preventative treatment over many years, there’s good reason to expect significant improvements.
I'm one of the few with catastrophically high Lp(a) levels. Medications and activity levels and diet don't affect it, and my levels are at over 30x normal. As a result, I've had six heart attacks, and six stents placed into my arteries. I'm only 38. I'm expected to die before I am 45. My systemic atherosclerosis (artery narrowing) is so bad that I am permanently disabled, and I can barely function. It's genetic, and there's currently nothing that can be done about it.
There's still some hope for you. Olpasiran is on it's way. While it's not there atherectomy and/or quadruple bypass may be your only options besides stents( discuss with your doctor), exceptional diet and all the apoB and blood pressure lowering medications you can get.
I have high LP(a), without treatment; I'm like at a minimum of 40% more likely for heart attack and stroke over my lifetime. Thankfully I found out this year, so I can try and do the not die.
Because it is an essential part of our biological Nature. We tend to forget that no more than one generation ago (only) we were used to physically working much more and longer along the day and eating completely differently and in a way that today would be categorized as "scarcity" Plus, add all the pollution in which we live and is part of our nowadays industrialized society.
Might be the answer but most do not know what is to "eat well" or properly exercise for therapuetic effect. They think that eating brown instead of white bread its eating healthy or something. this is so incredibly ignorant from the general population, nutrition its 80% nonsense, 10% conspiracies and the other 10% actual factual data in the general population, and this is why people even who try to get healthy end up like bad regardless
Great! Like I don't have enough to worry about already as a heart patient. I appreciate your help in keeping me informed. This is one of the few channels that I hold in high and trusted esteem.
Love the video just like all the others…. Only wish is that I wasnt being hit with a flashbang when you show things. I watched this WAY too late and it hurt to watch. Can you change the white to a bit of gray to help ease the eye strain. Many thanks for all you guys do
There's also the argument that if we don't know exactly what LP(a) is supposed to do in the body, efforts to reduce it might cause unintended negative side effects.
A lot of studies and experts now say the large sugar consumption of modern diets is worse than saturated fat when it comes to bad cholesterol. Then why does red meat keep getting the majority of the blame and no mention of limiting sugar? Also not all sugars are the same and many types exist which use different enzymes and metabolic pathways. For instance fructose is a major cause of fatty liver disease due to how much we consume now and the majority has to get broken down by the liver. Non-alcoholic liver disease has been at a higher rate than alcoholic for years now. Why do science shows like this continue to avoid the talk around sugar and even support it through generalization of sugars as if they are all glucose?
Peopel simply eat and especially drink way more sugar than fat. Overall it's absurd how people focus on fat vs sugar vs protein, while ingoring how many people DRINK 2l+ of sugary drinks or alcohol per day. 2l of non-diet soda got over 200g sugar - and fruit juices tend to have even more! And that before you eat a single gramm of food. That's the same as FOUR FULL 100g bars of chocolat! You can see how many peope, drink non diet soda, juice and alcohol when you look at a grocery shop. The majority of drinks wouldn't be just that if no one would buy them. Alcohol is just pure poison anyway.
Our so called acceptable levels of LDL is actually about 2 times higher than is found in indigenous tribes and babies. So it might be difficult to assess LipoA actual evolutionary use as it's sadly a bit rare to see people with actually evolutionarily normal cholesterol numbers. I can't remember seeing any (without medication) in my day-to-day work as a doctor for over 10 years that are quite that low. Just as a point of curiosity, we also regularly check for triglycerides when looking at cholesterol levels. These are also a significant risk factor for cardiovascular disease, but much less than LDL and low HDL. But the sad fact is that all our medications that lower triglycerides doesn't actually lower the cardiovascular risk. We don't know why this is. Lowering LDL leads to a significant risk reduction, especially for those with other diseases contributing to cardiovascular diseases.
Since it wasn't ever mentioned Lp(a) is almost exclusively affected by genetics rather than diet. That's what makes it hard to test for in blood tests and even if its high there isn't much the doctor can tell you to do. In a more rational healthcare system these are types of things to put investment into screening tests and so on to know who should be testing for it regularly.
Let's appreciate the fact that a finding from 1977 is still thought of as true today. How much other stuff in science is basically rewritten 3 times in the same amount of time?
Something that I was hoping you would touch on in this video and missed are the sub-types of LDL. There is an increasing body of evidence that shows high levels of LDL, by itself, is not actually a good indicator of CHD risk. There is a type of LDL called small dense LDL (sdLDL), and this is the "bad" portion of LDL. High ratios of sdLDL to LDL is a much more reliable marker for CHD risk (even among individuals with nominally acceptable levels of LDL), and appears to have a strong association with other risk factors such as insulin resistance and elevated blood triglycerides.
There are different lipoproteins that trasnsport cholesterol, BUT there is only one kind of cholesterol, it is called cholesterol. Stop referring to lipoproteins as cholesterol.
This is such a useless criticism. In common parlance we call them the difference "types" of cholesterol because cholesterol is their job. So it's two different cholesterol workers. You don't get angry when people call microwave ovens "microwaves" so this is such a useless thing to get uppity about. Chill out
@@chettlar212 it's wrong because it's a gross simplication. Lipoproteins are so much more than just cholesterol. They also have triglycerides and phospholipids which are as critical to their functions as cholesterol.
Good point, if we clarified that then understanding our health would be just that much easier! Also don't listen to nutters that get mad when other people put in the effort to change the world for the better! 😂
@@williamt2700 you may be unaware but that is a common comment people use to promote fringe dieting practices, that may be why you're sensing hostility
There is no such thing as "bad cholesterol". Your body makes hormones from the LDL cholesterol. Yes, if your cholesterol numbers are out of a healthy ratio, that can be a bad thing. But it is not inherently "bad cholesterol"
LP(a) is a nasty one but that’s still not the whole picture. Next video should cover Apolipoprotein B. Its heavily influenced by genetics and doesn’t change from diet. Due to this, u only need to get it checked once. Sort of a genetic screening if u will.
I love that even with all these advances in science there is a molecule we can pin point to having evolved TWICE in our ancestry, but are not clear on what it even does. Nature is amazing!
I wish people would talk about the fact that we need LDL. We don't have it for no reason. I have a friend with almost none and when they get it higher, they feel less sick. I know this is anecdotal, but nobody talks about it being necessary in the first place.
So now I know that there is no such thing as bad cholesterol, just a poor balance between LDL and HDL that transport cholesterol back and forth to the liver. And LP carrier may be used to reach small capillaries areas where cholesterol is needed for cell membranes, hormones and vitamin D production.
that 3rd kind actually sound like it could be good if it destabilizes plaque might help the body remove it, and we only made it bad because of how much LDL and triglycerides and plaque people get from eating junk and by making plaque break in bigger chunks then the body can manage. maybe increasing LP(a) instead of decreasing it would be good if done before too much plaque is formed.
I would have liked at least a mention of triglycerides, since they are part of the lipid panel. My family has ongoing challenges with cholesterol, since apparently our bodies make it out of anything and everything (my slim, active grandmother who ate whole grains, fruits and veggies with minimal animal products clocked in at 400 total cholesterol.)
I have had two seperate doctors see my lipid levels and be stumped. I am pescetarian, and consume not a lot of dietary cholesterol, nor high amounts of saturated fats, i am physically active and eat a solid amount of fiber a day. My HDL is like 12. And my LDL is about 60. This left them confused as to what to do about my HDL and say, "you're LDL and total cholesterol are good, and your Triglycerides and blood pressure are good." So they both came to the same final conclusions. "I just genetically dont produce much HDL"
The last time I checked, scientist were saying that everyone has a base level of cholesterol depending on their genes and the problem arised when that cholesterol increased. For example, if you eat too much refined carbohydrates, they damage the blood vessels inner lining, so your body generates more cholesterol to fix those problems. Actually they said that blaming cholesterol for heart diseases was like blaming firefighters for the fires. Cholesterol is a marker, not the cause of problems with the circulatory system. If you want to lower the cholesterol, stop eating refined carbohydrates, stop drinking alcohol, and have a healthy diet. Everyone knows what a healthy diet is. Buy raw ingredientes and cook your own food, while reducing ultra processed foods to a minimum.
^^^ This. Refined carbohydrates cause your body to make more cholesterol as a reaction to the inflammation. IOW, it's not so much about fats as we've been led to believe.
Lots of (probably most) people have no idea what a healthy diet is for them... It's not always very easy to figure out (let alone follow). I agree with your last sentence though (well I buy cooked food too but I eat those in moderation and I choose well what kind), it works with many different diets.
Santa Claus comes by with special big presents for the Good Cholesterol, who Santa's been finding out if he's naughty, about, you know, sort of like that.
Don’t you mean ApoB is bad? It’s the key component in LDL that contributes to plaque. ApoA is the component that promotes reverse cholesterol transport and is anti-inflammatory. A high ApoB to ApoA ratio correlates to increased risk of heart attack and stroke. So I think you may have it backwards
100% correct, but to be honest, the way SciShow explains it here is generally considered to be more digestible to folks who are less scientifically literate (i.e. most of the general public). You are correct, the culprit here is ApoB because it's the "docking" mechanism for these lipoproteins. However, just like when we learn biology, chemistry, or physics through middle school, high school, and college by continuously backtracking on more rudimentary ideas and replacing them with more advanced concepts (e.g. the electron "ball" model in high school being replaced by electron clouds in college), the same applies here. While LDL isn't the exact problem, the truth is that measuring blood levels of LDL and ApoB shows a pretty linear relationship. After all, the normal or desirable blood levels of ApoB are just about 30 units above LDL targets. Most labs don't have the equipment to check ApoB, so approximating it with LDL is "accurate enough" to implement healthy changes. Hope you agree!
No such thing as good/ bad cholesterol, just high, very high, or low, very low density lipoprotein (HDL, VHDL, LDL, VLDL) each chemical having a specific role in metabolic processes.
Not sure ethically how but needs be a study on LPa on how it would function if it act as a limiting factor in clothing if the body suffered frequent lacerations. That may have be a frequent situation getting scrapped up and cuts running away from things trying to eat you back then.
A huge number of people have a genetic predisposition to high LpA; some studies estimate as high as 2% of Americans. If your family has a history of heart disease, ask your doctor for an LpA test, they don't do it normally! High LpA is really dangerous even if you eat very healthily and exercise, the best treatment is intervention before serious damage is done!
It's even more complicated than that. There are two types of LDL cholesterol, one of which is bad for you, and the other not so much. Plus, the cholesterol doesn't just 'stick' as it's going, you have an inflammatory response in the lining of the arteries (perhaps LP(a), perhaps other things) and the immune cells that react to that inflammation recruit the cholesterol from the blood, which makes the inflammation worse. Reducing through use of drugs seems to help, but may have unknown side effects (attempt to reduce amyloid beta plaques in the brain caused inflammation rather than helping, as an example of a treatment that has unexpected side effects) particularly as cholesterol increases with age. There may be pieces to the puzzle that are still unknown. A hundred years from now, doctors may be asking why 20th century doctors were reducing cholesterol instead of interfering in the chemical signaling that the immune system uses to recruit the cholesterol to the plaques in the first place. Only time and research will tell.
There's little to no point in testing for something if the only thing they can do is recommend that you update your will. Statins lower cholesterol but it just masks the problem -- people on statins die at almost the same rates as people not on them with caveats -- statins do appear to extend the life of people who've had an ischemic event and are over a certain age (aka don't have some crazy genetics for dying at 50). We way overprescribe them to make people *feel* better by making the scary *number* go down. If you have the scary number, you'll probably die early. But even that isn't certain, with plenty of people with massive cholesterol numbers dying at the usual ages while others die younger.
The hidden fact is the SIZE of the molecules. You can have many of the "bad" ones, without problems when the size is right. Tests for this are expensive, but there are 2. And lower amounts of wrong size can issue serious problems if they are small. I ask a KI told me that. Just the view of the TYPES is insufficient, it depends on the SIZE, too.
So is the third kind called vldl on my readout? That was the only other cholesterol reading I saw and I was waiting to hear that designation and I didn’t
Re: LDL cholesterol - I thought that the real problem was a subset, VLDL, and that also is not tested for. So people are given statins which lower LDL overall but may not be taking care of the real problem. I am not a doctor but try to read good sources about this.
I just learned of vldl because I just got a blood test that tested for it and came out high. But my hdl and ldl have always been low and still is. This video had such good timing for me.
So, wait... This is a different kind of cholesterol? So there is 4 types? I thought I had learned about the third type, but this is not the same thing.
eventually we'll need to figure out a viable protocol for determining an individuals response to different cholesterol ratios. that way we don't blanket peoples treatment when it may in fact not be the treatment they need.
Doctor is a level of 50 mg/dl of Lp(a) of concern. My LDL is 65, HDL is 46, Triglycerides is 50 and APO B is 80. Are these levels considered optimal. I have had an angioplasty with 1 stent 2 years ago.
Just got my blood drawn a few days ago to test my blood sugar, liver, and lipids. I doubt that third cholesterol type was tested though. Maybe I should look into that as well as I have genetically high lipids. I went to my primary care doctor because of pain in the upper right side above my belly a year ago, and even though an ultrasound was negative my doctor suspected gallbladder stones. I've been living with that pain for a year as I was told to just take pain meds whenever it flares up. I learned a month ago from youtube (Mama Doctor Jones) that PCOS can cause problems with the liver. Both my PCOS and my hereditary high blood fat levels should be in my patient files and yet my doctor ruled out the liver as the source from the beginning.
Recently, the doctors in Greece started to prescribe the check of the LPa levels. But if you have high levels, are you doomed? What are the chances? What can you do?
My cholesterol issue is that I would like my cholesterol to be higher. lol my total is always under 100. My ratios are always perfect but that super skews recommendations based on pure levels alone. I try to eat fattier foods but it stays low, would like a lil boost to help promote better hormone health.
correct, it's genetic and you can't change it with diet, exercise, or medication. Women with lower estrogen levels can increase their estrogen levels to put it lower, to where it would be if their estrogen was normal, but not to bring it so low that it is in a safe range. For example before HRT mine was 650, on HRT it's 290, normal levels are 10-30. LDL and HDL don't affect Lp(a) numbers at all.
My hematologist had strong opinions on these journalistic presentations. Said it was the fact that the immune system sees LDL as an allergen, forming inflammation responses and glutting on the LDL. White blood cells glutting themselves on LDL kills them; and if you've seen the animations of white blood cell transport in vascular system you'll note they distinctly stick to the arteries and veins and roll down the surface, when they die from over eating LDL THAT is where they stay, while also causing inflammation which complicates things. That's why, when biopsied they're called "foam cells" because they look like foam under the microscope, and when micro pipettes are inserted into their internal vacuoles the goo they're full of is LDL. The reason a surgeon can't just vacuum them out, or a drug "release them" or "dissolve them" is because the endometrial cells that line the arteries and veins grow over these dead white blood cells as part of the inflammation response, so you not only have to get rid of the bags of LDL inside the dead white blood cells, the dead white blood cells but also layers and layers of lining cells trying to help opening up the arteries and veins deeper layers creating new nucleation sites for clotting events. So no, no rotor-rooter for the heart will work, if anything is to work it'll be one hell of a complicated dance that works with the autoimmune system, circulatory system and perhaps surgical system choreographed perfectly... Frankly the "plumbing example" of grease bergs and "build up" is actively holding up informed discussion on this subject with patients, it's not like Calcium build up in copper pipes of a house.
Wow! For a non-physician, that is actually an excellent explanation, though you get the minute details wrong (like, it’s not technically an allergic reaction but it is another type of immune reaction, and it’s ‘endothelial’ not ‘endometrial-‘ those are the cells that line the uterus during menses). You must have a great hematologist to explain all that to you and also you must be in a field like engineering or something to have understood it that well!
@@VyvienneEauxendometrial made me laugh
Your hematologist does a pretty great job explaining it all! Many folks forget that the pathogenesis of atherosclerosis is in fact an inflammatory process, so the allergy analogy, while not 100% on point, is still a great way to think about it. That being said, the "plumbing example" is sort of helpful to explain things to the general public - after all, there's a reason percutaneous coronary interventions work - while they don't remove plaque, they do "buy" some time back for the patient by opening the vessel lumen. The rest is as the hematologist said - a complicated dance of more factors involved. In the world of cardiology, we call this residual risk - and we aim to reduce it through other means, like medications and improving modifiable risk factors.
I feel like the best thing to do would be to block whatever protein the foam cells use to adhere to other cells
@MandrakeFernflower Well, unfortunately, the receptors involved in said binding are not specifically unique to foam cells, and targeting them would cause some degree of immune suppression or other very generalized side effects.. So in effect the best thing turns out to be reducing LDL directly, or as some folks pointed, ApoB
They could be named good cholesterol, bad cholesterol and worst cholesterol.
No, the good, the bad and the ugly...
badder cholesterol
The good cholesterol would be "mostly good" cholesterol.
Even water will kill you if you drink too much at once.
Or, Clint Eastwood cholesterol. (CEC)
There is exactly only one type of cholesterol, it’s called cholesterol, and it’s essential. The lipoproteins are the vehicles moving the cholesterol around. It’s never ever the problem of cholesterol itself. Ancel Keys got F as a scientist, and SciShow got another F on nutrition.
As a physician I can say that lipid metabolism and cholesterol levels are a constant source of concern and skepticism. Thank you for helping to explain this.
Seeing comments that this has misinformation. I know attitudes and understanding of cholesterol has changed a bit. Any insight?
My mum was put on a low-fat diet to reduce her slightly too high cholesterol. Except she apparently belongs to the group of people whose body will go into overdrive and produce even more of it, so it made her cholesterol levels sky-rocket. And because the doctors would just give her statins, which completely knock her metabolism out of balance, she quietly stopped the diet again and didn't tell them. She's short and thin anyway, so it's not like they'd notice.
@@Hi_Im_Akward Great question. As they said, there is a lot of nuance when it comes to cholesterol/lipids, much like your overall health in general. Some people process cholesterol vastly different than others so they require some sort of lipid controlling medication (familial hypertriglyceridemia for example). We always like to start with lifestyle changes with diet and exercise, but for some that's not enough. We are always learning more about what is healthy and what might need some improvement. If nothing else, if you want to do your own research...I'd recommend just avoiding pretty much any "influencer" or anybody like that as they generally don't have your best interest/health at heart. Find good peer-reviewed studies on the subject, preferably double blinded studies or meta-analyses of multiple studies. If you start to get into the Krebs cycle or gluconeogenesis...you've gone too far. ;)
@@SinisterMDas a fellow physician I giggled intensely when you mentioned Krebs cycle.
But besides this, the reason we do not routinely check for LP(a) is our lack of ability to do anything about it. It could do a lot more nocebo harm to know a risk than to just keep on living with the individual background risk. This is actually a key element in determining which diseases to create large screening programmes to catch, but this is a whole different story.
@@mtdnspirit Are there any lifestyle or dietary changes that effect LP(a) at all? Or is it just not well known AT ALL what causes or prevents it?
They are going to need an alignment chart for cholesterol if they find any more kinds.
My cholesterol is definitely chaotic-good in nature.
They won’t find more kinds. It’s one only one kind and it’s just called cholesterol. The vehicles cholesterol attached to are lipoproteins, obviously those are proteins.
😂😂 my cholesterol is lawful evil
Actually, that’s a great idea! A chart of the different combination possibilities of apolipoproteins!
There's many more infact.
Look at the classic "Sugar: The bitter truth" lecture on youtube.
Not sure how it held up to the test of time but will inform you of other cholesterol types.
Contrary to popular belief, an ApoA day does not keep the doctor away.
boooooooo
Go to your room! And don't you come out until you think about what you have done!
LDL and HDL are NOT forms of cholesterol. They are lipoproteins that transport cholesterol. Moreover, these proteins are necessary for lipid metabolism and are not inherently good or bad. Persistent high or low levels of LDL and HDL are signs of dyslipidemia and faulty lipid regulation; moreover, some studies show some correlation between high/low levels with coronary artery disease and other illnesses. However, this is not the same as proof of causation - I.e., LDL causes heart disease. Referring to “good” and “bad” is an oversimplification and does a disservice to patients, causing them to misunderstand cholesterol and lipid metabolism and the effect on health.
Plus, statins, which are proven to reduce risk are also proven to increase Lpa leves. So what gives? Right? The story of atherosclerosis is a lot more complicated than good/bad cholesterol. Oversymplification in the name of education is problematic.
Nice that you mention this. I missed the fact that the level of LDL and HDL in reference to eachother is key in keeping a healthy blood vessel.
Too much HDL while simultaneously low LDL is just as bad as the other way around.
Some peoples metabolism is just more sensitive to high HDL levels. Mine suddenly spiked one day, and I still have no clue why. Cos when it was discovered, I was highly active, doing workouts multiple times a week. As to never doing any workout on a regular basis ever before.😅 So... I thought I was healthier, but my blood said differently.
This is outdated, in the medical literature of cardiology since 2017 with a meta analysis and mandelian randomization, LDL has been proven, outside of any other variable as causation for athelosclerosis.
In fact, current "normal" numbers are too high, people with 100 LDL, 60% already have developed soft plaque. its only in the
maybe watch the video first, then make a comment.
@@wojciechkurdzielewicz7781 statin doesn’t reduce risk, not a single bit. Statin is the greatest con in medicine history. And cholesterol doesn’t cause heart disease or anything. Cholesterol has essential functions in our body, not just some random functions. One function is to patch the broken things. It’s why we see cholesterol in arteries, because it is deliberately transported there to patch whatever the damage there. It’s like blaming firemen for causing fires while the real arsonists are free to go.
I worked as a lab tech in the Veterans Affairs for three years and i can day LPAs is a common test when patients come in with 250+ LDL cholesterols. I've pulled dozens of tubes on patients as young as 25. Its good to see many VA docs order more diagnostic tests
Excellently done! I've been tested for LP(a) by a Cardiologist after a heart-attack and was put on an additional medication to help bring my overall numbers down even more than they were on just the statin alone. Apparently I've got some eastern European genes in me that are really good at making extra cholesterol.
Maybe you should look into reducing carbohydrates intake and sugars and fructose. At least don't mix them in the same meal. And start fasting. Then after 30 days review the tests again. Our bodies like one or the other (protein+fat or carbs) but it reacts badly when mixing all of this together. Eating fat doesn't translate directly in high cholesterol. Carbs are responsible for inhibiting the fat utilisation and breakdown. Apo(a) and other types of no so good lipoproteins appear in the blood stream when they get distorted or glycated because they are forced to stay too much time in circulation because the body is using glucose instead. So the problem is not so simple.
_Doctors report a sudden increase in appointment requests_
I've been diagnosed with high amounts of Lipoprotein a. I had a massive heart attack when I was only 34 because of it. Not overweight or anything, just out of the blue BOOM. I've had a small stroke and a second less sever heart attack since then. I now have 5 stents in my heart and it's been really crappy to say the least. I have loads of pills and 2 injections (Alirocumab) I need to take each month. I'd sure like to just get that normal lifespan. Oh and the real sucky thing is it seems to be inherited. :(
Have you considered a plant-based diet for your heart health?
@@vituperator9603 As the video said your body creates the cholesterol. People assume it's from diet but it's not.
@@vituperator9603 I like that you've made a wild assumption that OP hasn't thought of literally everything under the sun already. But also what the other person said. Unless you've gone through this exact same scenario, or are a medical professional, maybe don't give out unsolicited advice.
@@vituperator9603 my dad has also inherited something very similar and when its inherited (ie genetic) diet makes little to no difference. he stayed in a hospital for some time eating his meal plan they provided for him in hopes it could lower is cholesterol and it did not make a difference at all
We really need to be discussing a transition to chronic and preventative care for these life ending conditions since we're getting to the end of what acute care responses can accomplish. Getting a blood test for LDL if nothing else at the age of 18 y/o for every adult just to see if they "want to feel old one day" or if they want a preventative Statin R/x would go a long way towards this. The Japanese and Koreans get such wonderful outcomes and longevity primarily because your average Japanese or Korean's primary health care provider is a pharmacist. It's a system betting on strategic / preventative responses by the medical field instead of tactical / acute responses. Look up a Japanese Manga: "Other world Pharmacist" for an excellent ... high school level primer on how pharmacists act as front line agents of the health care system to affect excellent results; it's a paradigm shift of thought for average people who's best source of medical information is House MD. :)
Glad Lp(a) is getting mentioned more. But because of lack of studies it is still commonly reported that diet and exercise don’t make a difference. Both my mom and I HAVE LOWERED our results with Niacin. I also lost 30 lbs. just got lab results back yesterday and my score is way down, still out of range but way better.
Diet and exercise don't make a difference to your lp(a) levels because it's determined entirely by your genetics
The fact that nobody talks about book called Health Secrets Industry Hides really gets to me. Always loved doctors that opens our eyes.
TedEd had a video going over HDL and LDL just yesterday, and it gave me the background knowledge I needed for this video. Is it cholesterol week? Or was this just a coincidence, lol.
Because this video is nonsense, so you can skip it.
They must have some kind of partnered media sources. The info is nearly identical, especially the way they bring up different impacts like food, exercise, and statins.
@ yeah, that makes sense.
Cookies, my guy. (The tracking kind.)
Would those really have an effect here? I am subscribed to both channels, and I was only watching whatever videos popped up in my notification section.
Not mentioned in the video, but it's important to know that it has been shown that eating cholesterol does not affect your blood cholesterol levels. Egg yolks for instance are extremely high in cholesterol, but they have no negative effects when consumed. Only saturated fats are problematic.
I thought egg yolks are saturated fat?
@@robertgossett6228 Saturated fat is solid at room temperature. While yolks do contain some, most of their fat is unsaturated, which is why they remain liquid even in the fridge.
@@gab.lab.martins that’s good to know because I eat lots of em. Boiled scrambled fried Love em
Buried on page 91 of this 572 page report:
“Previously, the Dietary Guidelines for Americans recommended that cholesterol intake be limited to no more than 300 mg/day. The 2015 DGAC will not bring forward this recommendation because available evidence shows no appreciable relationship between consumption of dietary cholesterol and serum (blood) cholesterol, consistent with the AHA/ACC (American Heart Association / American College of Cardiology) report. Cholesterol is not a nutrient of concern for overconsumption.” (Quote from the Scientific Report of the 2015 Dietary Guidelines Advisory Committee).p 91.
AHA told you to eat trans fat to lower your saturated fat intake.
I know AHA is the worst. Weird history.
@@LittleRadicalThinker Almost like science evolves in response to new information, huh?
@@alexisdougherty2652 it’s pseudoscience evolves in response to new information, such as the pseudoscientists from AHA.
@@LittleRadicalThinker You might want to review the scientific method or indeed read it for the first time if you think that. Our schools failed you.
Neither good cholesterol nor bad cholesterol, but a secret third thing
Bravo. We're to start a CT for RNA LP-a modulator in EU. Wish us luck and good results!
lpa was on my blood test i had done recently. glad all 3 were in healthy levels.
I have, doctor diagnosed hypercholesterolemia type II. I inherited it (thanks, Dad). And yes, I went on a 5% fat diet, lost 20 lbs. and raised my cholesterol 45 points! And found out it's typical for people with this condition. I then went on statins. I didn't know about this third type and I would love to hear about the way triglycerides relate with these 3 substances. Especially since the NIH and CDC will be run by RFK, Jr. We need dependable info.
SAME I lost 45lbs and my metabolic panel got much worse. My dad died of a heart attack last year. I’m 36 and am on a statin and have a cardiologist.
@@ladyeowyn42 Once they found one that I didn't react to, that was fine. I've been on them since 1992. My brother & sister had jobs that didn't include health insurance. Sis died at 44 of "broken heart" syndrome and my brother eventually got health insurance and started treatment about 10 years after. He's still living, but had a heart attack at 63. He's 74 now. Best of luck to you!
Ugh, I think I may be in the same boat. Uncontrolled high cholesterol and triglycerides run in the family and my tests are starting to creep up into the danger zone now that I'm in menopause despite virtually no changes to diet and exercise. And I did the sensible thing and spent the time between my first high reading and my last screening going HAMM on lifting weights, taking fiber supplements, eating more veg-heavy, etc...and my scores went up. *le sigh*
My mom once came of a check-in with triglycerides in the high 300s, despite being a near vegan. We may be in the "turn carbs into lipid-based death" category. I may have to go antithetical and try low-carb to see if it helps.
Wfpb diet 🌱
casts a dubious look at the pack of chicken nuggets on the table
Yeah I guess they feel that they can't mention meat vs. vegetables; too contentious for Americans to deal with
My highest total cholesterol was never higher than 240, but I had too low HDL and high LDL; I had a stent at 39 and 42 years old, and I had to have a triple bypass heart surgery at 55 years old. Then, I tested my Lp(a), which was a very high 86. Men with this level can have heart attacks and strokes in their 40s. Yes, I take my meds and cycle 5 times a week, do intermittent fasting, and eat low-carb.
Bart Kay. Zone 2.
Do you do weight training too? I'm not suggesting it. Just wanna know what works for people and what doesnt
I like that they say nobody is the same. You really do have to find what works for you. For me, sugar will raise my LDL and eating more saturated fat raises my HDL but does nothing to my LDL. Thus a lower sugar diet that includes butter and bacon is just fine for me. Not the case for everybody though. I think people kind of knows this now and are really looking for more personalized diet advice. I would start with doing your best to eat what your ancestors ate.
Two years ago I got the diagnosis that and I quote "I have too much good cholesterol and too little bad cholesterol" which makes you wonder how good the names are...
Somehow it’s a bit like the “humors” all over again 🤣
Excellent video of a very complicated topic! BTW, LP(a) is more commonly referred to as LP little (a).
chronic inflammation, often caused by factors like smoking, high sugar intake, and processed foods, is a significant contributor to cardiovascular disease (CVD). These inflammatory triggers can lead to oxidative stress, damage blood vessels, and promote the buildup of arterial plaques.
Regarding saturated fat, recent research challenges earlier claims that it directly causes CVD. Evidence suggests that saturated fat has neutral or even anti-inflammatory effects in the context of whole, unprocessed foods like fatty cuts of meat and dairy. However, its role in inflammation and heart health can depend on the overall diet composition and whether the fats are consumed alongside inflammatory foods like refined sugars and seed oils.
This aligns with the idea that context is crucial, and an anti-inflammatory diet likely minimizes sugar and processed foods while emphasizing nutrient-dense, whole foods.
I wonder how many more people will die bc of the blatantly wrong narrative that eating meat and saturated fats will kill you. This video was released in 2025😭
Say it louder fir people in the back.
Always hate when peopel write "processed food", that's just stupid. Processed in what way? You can process food and make it 100 times more healthy or you could make it 100 times worse.
A lot of food would just rott before it can reach you without being "processed."
It's like peopel who come up with "chemicals". EVERYTHING is "chemicals".
Interesting stuff....not too keen on a new RNA treatment though....Also can SciShow do a video on how cholesterol goes up during (peri)menopause in which case HRT is first line treatment. Maybe just do a video on (peri)menopause, for those who do not follow menopause specialists on social media. It's important to know for men too, to understand and support the (peri)menopausal family and friends in their lives.
Dear lord. no more "DNA" treatments.
I beg of thee.
This seems incomplete without also talking about bile acids and their cycle and production from cholesterol.
I can't wait for a treatment that can lower my Lp(a).
It's likely to hit the market somewhere in '26 or '27,the phase 3 trial is almost finished,and judging by phase 2 results you can expect up to 90 percent reduction in Lp(a).
@@RoxanneRichardson Might have been too optimistic . It ends Dec 29,2026. Then data collection, unblinding, preprint , peer-review, publication and then FDA registration. More like summer of '28 .
A 2014 review of people who took statins showed that they extended life expectancy by 3-4 days.
"The effect of statins on average survival in randomised trials, an analysis of end point postponement"
I read the paper. It says, “There are a number of caveats that need to be considered. First, this analysis only estimates the survival gain achieved within the trials’ running time (2-6 years). After termination of the trials, the treated would continue to accrue survival gain as long as there was a difference in cumulative mortality between the treatment arms. There are a few studies with long-term follow-up after cardiovascular intervention trials showing that this survival might be substantial,17 but there are also studies showing that mortality becomes similar in the two groups after the trial's termination.”
When used as preventative treatment over many years, there’s good reason to expect significant improvements.
I'm one of the few with catastrophically high Lp(a) levels. Medications and activity levels and diet don't affect it, and my levels are at over 30x normal. As a result, I've had six heart attacks, and six stents placed into my arteries. I'm only 38. I'm expected to die before I am 45. My systemic atherosclerosis (artery narrowing) is so bad that I am permanently disabled, and I can barely function. It's genetic, and there's currently nothing that can be done about it.
There's still some hope for you. Olpasiran is on it's way. While it's not there atherectomy and/or quadruple bypass may be your only options besides stents( discuss with your doctor), exceptional diet and all the apoB and blood pressure lowering medications you can get.
I'm so sorry to hear this.
I have high LP(a), without treatment; I'm like at a minimum of 40% more likely for heart attack and stroke over my lifetime. Thankfully I found out this year, so I can try and do the not die.
Wfpb diet 🌱
Best to minimize your inflammation. Read The Clot Thickens.
Eat well and exercise. Damn, why is that always the answer!
Because it is an essential part of our biological Nature. We tend to forget that no more than one generation ago (only) we were used to physically working much more and longer along the day and eating completely differently and in a way that today would be categorized as "scarcity"
Plus, add all the pollution in which we live and is part of our nowadays industrialized society.
@@GooogleGogleewell done. Perfect example of the naturalistic fallacy.
Might be the answer but most do not know what is to "eat well" or properly exercise for therapuetic effect.
They think that eating brown instead of white bread its eating healthy or something. this is so incredibly ignorant from the general population, nutrition its 80% nonsense, 10% conspiracies and the other 10% actual factual data in the general population, and this is why people even who try to get healthy end up like bad regardless
@@GooogleGoglee #ItWasAJokeMyGuy
Because high lp(a) is a genetic issue. Diet and exercise do not affect your lp(a) levels.
My cardiologist tested me for Lp(a) this September. First time I heard about it. Now this video is the second
Amazing and educational. You explained incredibly well. Thank you! 👏🏼👏🏼👏🏼👏🏼
Thought you were gonna talk about triglycerides. Glad those aren't what you were talking about bc I just found out mine are high.
The brightside is your doc might be able to get you on Lovazza. I really wish it was an option without a perscription.
Right, off to modify the conditional formatting on the HDL column of my bloods excel sheet. Didn't realise there was a top end.
Great! Like I don't have enough to worry about already as a heart patient. I appreciate your help in keeping me informed. This is one of the few channels that I hold in high and trusted esteem.
It sort of makes sense not to test for LP(a) if there is no treatment for it yet.
Agrée. Although having statistics about it could assist in getting research
Love the video just like all the others…. Only wish is that I wasnt being hit with a flashbang when you show things. I watched this WAY too late and it hurt to watch. Can you change the white to a bit of gray to help ease the eye strain. Many thanks for all you guys do
2:15 "This figure was brought to you by uwu"
Heart attack, brought to you by a catgirl.
There's also the argument that if we don't know exactly what LP(a) is supposed to do in the body, efforts to reduce it might cause unintended negative side effects.
I like the explanation in the book "The Clot Thickens".
A lot of studies and experts now say the large sugar consumption of modern diets is worse than saturated fat when it comes to bad cholesterol. Then why does red meat keep getting the majority of the blame and no mention of limiting sugar? Also not all sugars are the same and many types exist which use different enzymes and metabolic pathways. For instance fructose is a major cause of fatty liver disease due to how much we consume now and the majority has to get broken down by the liver. Non-alcoholic liver disease has been at a higher rate than alcoholic for years now. Why do science shows like this continue to avoid the talk around sugar and even support it through generalization of sugars as if they are all glucose?
Peopel simply eat and especially drink way more sugar than fat.
Overall it's absurd how people focus on fat vs sugar vs protein, while ingoring how many people DRINK 2l+ of sugary drinks or alcohol per day. 2l of non-diet soda got over 200g sugar - and fruit juices tend to have even more! And that before you eat a single gramm of food. That's the same as FOUR FULL 100g bars of chocolat!
You can see how many peope, drink non diet soda, juice and alcohol when you look at a grocery shop. The majority of drinks wouldn't be just that if no one would buy them.
Alcohol is just pure poison anyway.
You should see the bad rap of sugar
Wonder why your dentists never told you not to eat sugar.
More about these topics pleaseee!!
I literally had my gaming computer’s screensaver folding APOa for 4 months and I didn’t know what it was until now. 😅
may our healthcare system never stop improving
Our so called acceptable levels of LDL is actually about 2 times higher than is found in indigenous tribes and babies.
So it might be difficult to assess LipoA actual evolutionary use as it's sadly a bit rare to see people with actually evolutionarily normal cholesterol numbers. I can't remember seeing any (without medication) in my day-to-day work as a doctor for over 10 years that are quite that low.
Just as a point of curiosity, we also regularly check for triglycerides when looking at cholesterol levels. These are also a significant risk factor for cardiovascular disease, but much less than LDL and low HDL. But the sad fact is that all our medications that lower triglycerides doesn't actually lower the cardiovascular risk. We don't know why this is. Lowering LDL leads to a significant risk reduction, especially for those with other diseases contributing to cardiovascular diseases.
Since it wasn't ever mentioned Lp(a) is almost exclusively affected by genetics rather than diet. That's what makes it hard to test for in blood tests and even if its high there isn't much the doctor can tell you to do. In a more rational healthcare system these are types of things to put investment into screening tests and so on to know who should be testing for it regularly.
My Boss thinks cholesterol doesn’t exist, he thinks the insurance companies made it up.
Sorry, but unfortunately you can't fix stupid...
Find out how it got discovered in the first place
Why did this video pops up when I just went for a cholesterol check ? 😂
After 5 heart attacks, this is the first I have heard of this. Interesting.
Better late than never
Let's appreciate the fact that a finding from 1977 is still thought of as true today. How much other stuff in science is basically rewritten 3 times in the same amount of time?
I have elevated Lp(a) about 4x times normal and have a family history of heart attacks and strokes in their 40s
Let me guess, small/short chain low density lipoprotein?
Something that I was hoping you would touch on in this video and missed are the sub-types of LDL. There is an increasing body of evidence that shows high levels of LDL, by itself, is not actually a good indicator of CHD risk. There is a type of LDL called small dense LDL (sdLDL), and this is the "bad" portion of LDL. High ratios of sdLDL to LDL is a much more reliable marker for CHD risk (even among individuals with nominally acceptable levels of LDL), and appears to have a strong association with other risk factors such as insulin resistance and elevated blood triglycerides.
There are different lipoproteins that trasnsport cholesterol, BUT there is only one kind of cholesterol, it is called cholesterol. Stop referring to lipoproteins as cholesterol.
This is such a useless criticism. In common parlance we call them the difference "types" of cholesterol because cholesterol is their job. So it's two different cholesterol workers. You don't get angry when people call microwave ovens "microwaves" so this is such a useless thing to get uppity about. Chill out
@@chettlar212 it's wrong because it's a gross simplication. Lipoproteins are so much more than just cholesterol. They also have triglycerides and phospholipids which are as critical to their functions as cholesterol.
Good point, if we clarified that then understanding our health would be just that much easier!
Also don't listen to nutters that get mad when other people put in the effort to change the world for the better! 😂
@@williamt2700 criticizing pedantry is good actually
@@williamt2700 you may be unaware but that is a common comment people use to promote fringe dieting practices, that may be why you're sensing hostility
There is no such thing as "bad cholesterol". Your body makes hormones from the LDL cholesterol. Yes, if your cholesterol numbers are out of a healthy ratio, that can be a bad thing. But it is not inherently "bad cholesterol"
Much like becoming an adult. You know about the good and the bad. But nothing can prepare you for the worst.
Fish Oil with large amounts of EPA and DHA increase average LDL particle size. So LP(a) is small dense LDL, fish oil will help.
My doc has me on extended release Niacin to combat high Lp(a) levels.
LPA sounds like a gamer term representing one of the bad guys.
LP(a) is a nasty one but that’s still not the whole picture. Next video should cover Apolipoprotein B. Its heavily influenced by genetics and doesn’t change from diet. Due to this, u only need to get it checked once. Sort of a genetic screening if u will.
I love that even with all these advances in science there is a molecule we can pin point to having evolved TWICE in our ancestry, but are not clear on what it even does. Nature is amazing!
Thanks dude i can use ur advice for my grandma who has high cholesterol thx ❤
Edit: i just like and subscribe ❤
Ngl, I kinda expected Enio Moriconi's to play when you said "the good, the bad and the ugly".
So its the good, the bad and the ugly?
beat me to it!
Science has a lot of work to do in implementing the dimensional model approach and getting away from the old levels model
Thanks!
I wish people would talk about the fact that we need LDL. We don't have it for no reason. I have a friend with almost none and when they get it higher, they feel less sick. I know this is anecdotal, but nobody talks about it being necessary in the first place.
They talked about that in this video though
So now I know that there is no such thing as bad cholesterol, just a poor balance between LDL and HDL that transport cholesterol back and forth to the liver. And LP carrier may be used to reach small capillaries areas where cholesterol is needed for cell membranes, hormones and vitamin D production.
that 3rd kind actually sound like it could be good if it destabilizes plaque might help the body remove it, and we only made it bad because of how much LDL and triglycerides and plaque people get from eating junk and by making plaque break in bigger chunks then the body can manage. maybe increasing LP(a) instead of decreasing it would be good if done before too much plaque is formed.
I would have liked at least a mention of triglycerides, since they are part of the lipid panel. My family has ongoing challenges with cholesterol, since apparently our bodies make it out of anything and everything (my slim, active grandmother who ate whole grains, fruits and veggies with minimal animal products clocked in at 400 total cholesterol.)
I have had two seperate doctors see my lipid levels and be stumped. I am pescetarian, and consume not a lot of dietary cholesterol, nor high amounts of saturated fats, i am physically active and eat a solid amount of fiber a day. My HDL is like 12. And my LDL is about 60. This left them confused as to what to do about my HDL and say, "you're LDL and total cholesterol are good, and your Triglycerides and blood pressure are good." So they both came to the same final conclusions. "I just genetically dont produce much HDL"
The last time I checked, scientist were saying that everyone has a base level of cholesterol depending on their genes and the problem arised when that cholesterol increased. For example, if you eat too much refined carbohydrates, they damage the blood vessels inner lining, so your body generates more cholesterol to fix those problems. Actually they said that blaming cholesterol for heart diseases was like blaming firefighters for the fires. Cholesterol is a marker, not the cause of problems with the circulatory system. If you want to lower the cholesterol, stop eating refined carbohydrates, stop drinking alcohol, and have a healthy diet. Everyone knows what a healthy diet is. Buy raw ingredientes and cook your own food, while reducing ultra processed foods to a minimum.
^^^ This. Refined carbohydrates cause your body to make more cholesterol as a reaction to the inflammation. IOW, it's not so much about fats as we've been led to believe.
Also seed and vegetal oils!
@@User-w7ckl yes! Those oils/fats cause more inflammation than (some) saturated fats!
Lots of (probably most) people have no idea what a healthy diet is for them... It's not always very easy to figure out (let alone follow).
I agree with your last sentence though (well I buy cooked food too but I eat those in moderation and I choose well what kind), it works with many different diets.
@@User-w7cklAre seed oils really that bad when they're not refined though? i mean, non-oxidised PUFAs aren't somehow inherently harmful.
Santa Claus comes by with special big presents for the Good Cholesterol, who Santa's been finding out if he's naughty, about, you know, sort of like that.
Never knew there was a second kind.
Chaotic Neutral , Righteous Evil, Neutral Good.
Don’t you mean ApoB is bad? It’s the key component in LDL that contributes to plaque. ApoA is the component that promotes reverse cholesterol transport and is anti-inflammatory. A high ApoB to ApoA ratio correlates to increased risk of heart attack and stroke. So I think you may have it backwards
100% correct, but to be honest, the way SciShow explains it here is generally considered to be more digestible to folks who are less scientifically literate (i.e. most of the general public). You are correct, the culprit here is ApoB because it's the "docking" mechanism for these lipoproteins. However, just like when we learn biology, chemistry, or physics through middle school, high school, and college by continuously backtracking on more rudimentary ideas and replacing them with more advanced concepts (e.g. the electron "ball" model in high school being replaced by electron clouds in college), the same applies here. While LDL isn't the exact problem, the truth is that measuring blood levels of LDL and ApoB shows a pretty linear relationship. After all, the normal or desirable blood levels of ApoB are just about 30 units above LDL targets. Most labs don't have the equipment to check ApoB, so approximating it with LDL is "accurate enough" to implement healthy changes. Hope you agree!
No such thing as good/ bad cholesterol, just high, very high, or low, very low density lipoprotein (HDL, VHDL, LDL, VLDL) each chemical having a specific role in metabolic processes.
I wonder why they aren't calling it VLDL here...
Not sure ethically how but needs be a study on LPa on how it would function if it act as a limiting factor in clothing if the body suffered frequent lacerations. That may have be a frequent situation getting scrapped up and cuts running away from things trying to eat you back then.
A huge number of people have a genetic predisposition to high LpA; some studies estimate as high as 2% of Americans. If your family has a history of heart disease, ask your doctor for an LpA test, they don't do it normally! High LpA is really dangerous even if you eat very healthily and exercise, the best treatment is intervention before serious damage is done!
It's even more complicated than that. There are two types of LDL cholesterol, one of which is bad for you, and the other not so much. Plus, the cholesterol doesn't just 'stick' as it's going, you have an inflammatory response in the lining of the arteries (perhaps LP(a), perhaps other things) and the immune cells that react to that inflammation recruit the cholesterol from the blood, which makes the inflammation worse. Reducing through use of drugs seems to help, but may have unknown side effects (attempt to reduce amyloid beta plaques in the brain caused inflammation rather than helping, as an example of a treatment that has unexpected side effects) particularly as cholesterol increases with age. There may be pieces to the puzzle that are still unknown. A hundred years from now, doctors may be asking why 20th century doctors were reducing cholesterol instead of interfering in the chemical signaling that the immune system uses to recruit the cholesterol to the plaques in the first place. Only time and research will tell.
I felt like raymond reddington was giving me a lecture about colesterol.
There's little to no point in testing for something if the only thing they can do is recommend that you update your will. Statins lower cholesterol but it just masks the problem -- people on statins die at almost the same rates as people not on them with caveats -- statins do appear to extend the life of people who've had an ischemic event and are over a certain age (aka don't have some crazy genetics for dying at 50). We way overprescribe them to make people *feel* better by making the scary *number* go down. If you have the scary number, you'll probably die early. But even that isn't certain, with plenty of people with massive cholesterol numbers dying at the usual ages while others die younger.
The hidden fact is the SIZE of the molecules. You can have many of the "bad" ones, without problems when the size is right. Tests for this are expensive, but there are 2. And lower amounts of wrong size can issue serious problems if they are small. I ask a KI told me that. Just the view of the TYPES is insufficient, it depends on the SIZE, too.
I'm a physician. You seem to have a limited understanding of the issue. Good day!
Nonsense
@@bobdog90how is this helpful? Why are you announcing your credentials and then just insulting someone? Do better.
So is the third kind called vldl on my readout? That was the only other cholesterol reading I saw and I was waiting to hear that designation and I didn’t
Re: LDL cholesterol - I thought that the real problem was a subset, VLDL, and that also is not tested for. So people are given statins which lower LDL overall but may not be taking care of the real problem. I am not a doctor but try to read good sources about this.
YEs. This. LP(a).
Would definitely watch a western based around cholesterol.
I just learned of vldl because I just got a blood test that tested for it and came out high. But my hdl and ldl have always been low and still is. This video had such good timing for me.
So, wait... This is a different kind of cholesterol? So there is 4 types? I thought I had learned about the third type, but this is not the same thing.
Vldl sounds like a typo.
Very Low Density Lipoprotein
That means you have high triglycerides. triglycerides divided by 5 equals your vldl.
eventually we'll need to figure out a viable protocol for determining an individuals response to different cholesterol ratios. that way we don't blanket peoples treatment when it may in fact not be the treatment they need.
Doctor is a level of 50 mg/dl of Lp(a) of concern. My LDL is 65, HDL is 46, Triglycerides is 50 and APO B is 80.
Are these levels considered optimal. I have had an angioplasty with 1 stent 2 years ago.
Just got my blood drawn a few days ago to test my blood sugar, liver, and lipids. I doubt that third cholesterol type was tested though. Maybe I should look into that as well as I have genetically high lipids.
I went to my primary care doctor because of pain in the upper right side above my belly a year ago, and even though an ultrasound was negative my doctor suspected gallbladder stones. I've been living with that pain for a year as I was told to just take pain meds whenever it flares up. I learned a month ago from youtube (Mama Doctor Jones) that PCOS can cause problems with the liver. Both my PCOS and my hereditary high blood fat levels should be in my patient files and yet my doctor ruled out the liver as the source from the beginning.
Hey, forewarned is forearmed.
Recently, the doctors in Greece started to prescribe the check of the LPa levels.
But if you have high levels, are you doomed? What are the chances? What can you do?
Thank god I got checked for this for free and even got paid for it.
My cholesterol issue is that I would like my cholesterol to be higher. lol my total is always under 100. My ratios are always perfect but that super skews recommendations based on pure levels alone. I try to eat fattier foods but it stays low, would like a lil boost to help promote better hormone health.
Title should have been “The good the bad and the ugly cholesterol “
So is lp(a) not affected by diet and exercise like ldl & hdl?
correct, it's genetic and you can't change it with diet, exercise, or medication. Women with lower estrogen levels can increase their estrogen levels to put it lower, to where it would be if their estrogen was normal, but not to bring it so low that it is in a safe range. For example before HRT mine was 650, on HRT it's 290, normal levels are 10-30. LDL and HDL don't affect Lp(a) numbers at all.