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These people with genetically low cholesterol, however, have other issues. Familial hypobetalipoproteinemia (FHBL) is a disorder that impairs the body's ability
by FollowingTheDao 1y ago
These people with genetically low cholesterol, however, have other issues. Familial hypobetalipoproteinemia (FHBL) is a disorder that impairs the body's ability to absorb and transport fats. Many individuals with FHBL develop an abnormal buildup of fats in the livercalled hepatic steatosis or fatty liver.
You have to understand the point which you’re not yet able to put in your head. Yes it is true that lowering cholesterol lowers cardiovascular disease. No one here is disagreeing with that. What we are explaining is that cholesterol alone does not cause heart disease. It is cholesterol plus inflammation that causes heart disease. I don’t know why this is so hard to understand. Lowering inflammation not only would reduce cardiovascular disease, but also cancer, arthritis and a multitude of other diseases.
- llm_nerd 1y ago>These people with genetically low cholesterol, however, have other issues Neat. >You have to understand the point which you’re not yet able to put in your head Nowhere did I ever dismiss other causative inputs. All I did was reply to some probably-listen-to-chiropractor people who sure are trying incredibly hard to downplay cholesterol.
- FollowingTheDao 1y agoIf one person with high cholesterol does not get heart disease then cholesterol is not the problem. Fact. Logic. Why don’t you stop your appeal to authority arguments and focus on the facts. It’s not that I haven’t died yet either. My calcium artery score was zero. I have no plaque in my arteries and I’ve had high cholesterol for probably 30 years of my life because of my genetics. If that is not interesting to you then you have an odd bias. I merely saying that inflammation is the risk factor that matters more than high cholesterol. You can lower cholesterol for someone who has high inflammation and reduce heart disease, but reducing inflammation is more important overall.
- array_key_first 1y ago> If one person with high cholesterol does not get heart disease then cholesterol is not the problem. Fact. Logic. This is the stupidest thing I've ever heard in my life. If one person doesn't die from cancer than cancer is not the problem. Fact. Logic. Not sure if this is your first day on Earth or what, but YES, there's variances in outcomes. Welcome to Earth and being a human. My grandfather smoked for 70 years and died peacefully. And what?
- FollowingTheDao 1y ago[flagged]
- array_key_first 1y ago> The body does not need cancer, but it does need LDL to transport fats around the body. Of course the body needs cancer. Cancer is your own bodies cells. They're essential for you being alive. And, cells with damaged DNA train and hone your immune system. You have millions of cancer cells in your body right now. Your immune system is killing them as we speak. If a few happen to slip through, then that's we would say you have cancer. Why might they slip through? Your immune system makes mistakes. Because everything makes mistakes. > What was it that he did that proved him immune to the ravages of smoking? Um, nothing? Is this your first day on Earth? Life is not an algorithm. Everything is risk, everything is probability. Smoking increases your risk. It doesn't give you anything. Your HIV and AIDS argument is just fucking stupid. Sorry to be blunt. Yes, SOME things are A -> B. That is an extremely rare exception to the rule. Extremely. That almost never happens. Like, if I drive fast, I might die. Might. Its not a garuantee. I can drive 150 every day and live, or drive 10 and die immediately. That's life. Welcome to risk and probability. That's just how things work. Having LDL and no heart disease doesn't prove anything to anyone. That doesn't prove LDL doesn't cause heart disease.
- cthalupa 1y ago>If one person with high cholesterol does not get heart disease then cholesterol is not the problem. Fact. Logic. This is such a silly statement I'm not sure where to begin. Plenty of people smoke and drink and don't die of issues related to smoking or drinking, but smoking and drinking are bad for you. Individual response to things varies. No one reasonable is going to say that because such and such person did X, Y, Z things that we know are bad and didn't have a negative outcome that we must flip the script on if those things are bad are not. Exceptions exist for a wide variety of reasons. > It’s not that I haven’t died yet either. My calcium artery score was zero. I have no plaque in my arteries and I’ve had high cholesterol for probably 30 years of my life because of my genetics. Calcium score does not tell you how much plaque you have in your arteries - it tells you how much calcified plaque you have in your arteries. This is NOT the same thing. You need a CCTA to tell if you have soft plaque or not. I'm sorry, but you're just severely misinformed here and spreading all sorts of dangerous misinformation all over the comments here.
- bluGill 1y ago> What we are explaining is that cholesterol alone does not cause heart disease. It is cholesterol plus inflammation that causes heart disease. interesting idea which I have heard before. However so far as I can tell we don't know if it is true. It seems to fit the evidence that the two are independantly causes of heart attack, when combined it is worse. maybe someday science will figure this out but it is not easy and so will take a while. Until we do I avoid saying things with high confidence.
- mac-mc 1y agoCholesterol is more of a proxy "smoke" or "firefighter" measure than a measurement of the actual fire. It's very much a wet streets cause rain kind of thing. Artificially eliminating the firefighters doesn't necessarily mean you've solved most of the problem. Heart disease is a far more complicated problem than "cholesterol" or "cholesterol + inflammation", but humans and patients mentally gravitate to silver bullet thinking, which makes it really hard to work with. One interesting measure I've encountered is the lipid clearance rate, but it costs something like +$20k to measure and is not something a doctor can order from a lab; it's typically only performed in research settings.
- cthalupa 1y agoComments like these just aren't based in reality. LDL levels are not a proxy or a wet streets cause rain. We even have a strong understanding of the mechanisms in which cholesterol causes things like heart attacks, strokes, peripheral arterial disease, etc. etc. etc. Something has to deposit plaque in your arteries. Yes, from a mechanistic standpoint, inflammation is also an important causal factor. Lp(a) is also an important factor for people that are genetically predisposed to high levels - it also deposits plaque, and is one of the reasons ApoB is recommended. Most people don't have worrisome Lp(a) levels but enough do that we've been missing them, and we now also have good treatments for them - PCKS9 inhibitors reduce it by ~1/3rd, and we have Lp(a) specific medications in phase 3 trials that are even stronger. But we know that statins work. This is some of the most established science in health. I keep seeing claims in these comments from people stating otherwise, but it just doesn't match reality. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60367-5/fulltext https://www.thelancet.com/journals/lancet/article/PIIS0140-6... We have MR studies on genetics that further reinforce this idea to a huge degree https://pubmed.ncbi.nlm.nih.gov/28444290/ https://pubmed.ncbi.nlm.nih.gov/28444290/ We also know that lowering LDL in and of itself lowers inflammation within the arterial wall, though this isn't necessarily reflected in hsCRP. We know that foam cell activation and cytokine signaling increase inflammation at the site of the plaque, which results in further deposition, and these require ApoB particles be depositing plaque there to begin with. Some PCSK9 inhibitors show zero change in hsCRP results yet still show less localized inflammation - due to the significant reduction in LDL-C and Lp(a) particles. https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2022.763516/full https://www.frontiersin.org/journals/cardiovascular-medicine... Lowering inflammation also works for reducing events independent of lowering ApoB particles - colchicine works even though it does nothing there - but if we're really trying to stretch the fire analogy, it's more like LDL and Lp(a) are the years of unmaintained brush and flammable debris in a forest, and inflammation is the strong winds. Both can lead to the spread of fire even without the other, fire can still spread even in the absence of both, but having either and especially having both will greatly increase the risk of the fire continuing to spread.
- CAPSLOCKSSTUCK 1y ago[flagged]