Are we talking about an ApoB in the 95th percentile? (above 140) Stacked with an equally high, small LDL particle count, I would agree it’s a concern.
How old are you?
If it were me, I would be on a statin and a PCSK9 inhibitor. Yes, about 5% of the population has intractable muscle soreness, regardless of the statin chosen.
I would start here: rosuvastatin or pravastatin; if you have an issue, then move to Livalo (pitavastatin); if you are still having issues with statins, you could try ezetimibe or mefenamic acid.
Have a look at the work of Dr. Allan Sniderman. (Cardiologist McGill U)
Please keep in mind that I am not a medical doctor. (I am married to a doctor) Any advice I have offered above should not be taken as medical advice but rather as a starting point for a conversation with your doctor.
Are you thin? You’re most likely a lean mass hyper-responder (LMHR).
If you want something to tell you your actual risk, get a coronary arterial calcification scan (measures calcified plaque). There are better tests that measure both calcified and non-calcified plaque, but the CAC scan tends to be very good in terms of risk calculation and is usually relatively cheap.
Reducing saturated fat is meaningless. There is no known mechanism for saturated fat to raise LDL. If you’re an LMHR, the type of fat you eat is meaningless. Nick Norwitz is an LMHR, and he eats low saturated fat, high olive oil diet.
I suspect you also have a family history of CVD. Have you done a CAC?
Why? It could save your life. The sooner you reduce your extremely high levels, the sooner you reduce your risk. Also, if looking at studies online, be aware that 99.9% of risk models are only for a 10-year period. Your risk of having a cardiac event in 10 years may be low at your age, but the risk is completely different 20–30 years down the road. Treat now and reduce your risk, or treat later, when you will have a harder time trying to reduce and your risk level will be much higher.
Statins, based on their relative usefulness (not absolute, relative) and horrifying side effects, are some of the last drugs I would ever consider taking.
I recommend reading my thread on oxLDL: Discussion of dietary cholesterol and cardiovascular disease
“small, dense LDL” is generally a generic term for oxLDL. If yours correlates to truly high levels of oxLDL I believe you should be concerned. I believe you should be able to get an oxLDL test from Quest labs. In a nut shell, generally the reason for very high small, dense LDL is because they have become oxidized and are not getting recycled by the liver. This actually causes the oxLDL particle to gain a negative charge, which is part of its danger, as it is more prone to sticking to the artery walls.
If you are interested, I will post you a link to an explanation of how I lowered my oxLDL score to optimal levels.
Yes, I would love to see an explanation of how you lowered oxidized LDL.
From what I have been learning, the CAC test, being an indicator of hard plaque, ie mature and not soft plaque, means that disease has already been present for a number of years/decades. A CT angiogram would be a better test, since it can see soft (less mature) plaque.
There seems to be a war between cardiologists and lipidologists (the “you need a statin” crowd) and keto/carnivore types (both lay and doctors). My issue is that, as I dive deeper and learn more, I become less concerned with one marker (LDL) but then suddenly learn about another that is less possible to ignore (ApoB). Just when I think that ribeyes 3x/day is doing me some good, along comes what appears to be a credible and educated scientist or doctor who dives deeper and uncovers yet another concern.
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I was just reading a different thread where we were discussing, basically, hedging one’s bets and thereby not achieving ketosis at all. (keto, with plenty of “healthy fruit” added in, for example.) I find the whole question of plaque and cdv similar, just more complicated, because we don’t have a nice simple biochemical reaction to strive for.
Typically true. The angiogram is considered the gold standard of diagnosis because it positively confirms the presence or not of blockages from plaques. The CAC is a good indicator in comparison. However, there still seems to be debate in the scientific community about why calcium deposits occur, and it doesn’t seem to occur in all cases of plaque.
There is def a war with the old crowd which has been indoctrinated into the use of statins, but the actual science doesn’t ever seem to find any actual life extension benefits to their use. I personally plan never to use them, but in the case of hypercholesterolemia, they may save lives. The LDL has a very weak correlation to CVD, but I believe it is the quality of the LDL that matters and not the quantity. I believe people going around with high levels of native LDL have little to worry about, while those with “normal” levels but high oxLDL can end up on the operating table. I personally believe the new emphasis on apoB is a red herring. It is basically the same as counting small, dense LDL. Having lots of those will raise apoB relative to cholesterol numbers, because small, dense LDL have relatively little cholesterol. So, in that sense it is probably a more accurate marker than the old LDL-C marker, but still very flawed IMHO.
In my own case by the time I found out about oxLDL tests, I had already changed my diet, so when I got tested in Dec of 2022, I was somewhat confident that I would have a low oxLDL score, but in Dec 2022 my oxLDL was 91. That is still a moderate range for CVD risk, so I changed my diet more: the way you buy, prepare and store foods is also relevant to their oxidation rates, and I believe ultimately, the amount of oxidation which occurs in the LDL.
In 2023 I took a more stringent strategy to see if I could lower my oxLDL score more - into the low/optimal range. Did I stop eating my meat? No. I still ate about a half pound of some kind of animal flesh per day - whether that was lamb or salmon. However, instead of buying pre-frozen salmon, I also began buying vacuum-packed Sockeye salmon from Costco’s refrigerated meat section, which although it has been briefly frozen for shipping has minimal oxidation due to its essentially vacuum-packed packaging. I would take this home for use that same week. I stopped consuming tuna salad. Canned tuna is a heavily oxidized meat product. For a much healthier quick meal, I bought Wild Planet canned sardines for days when I had little or no time to prepare a meal. These are canned whole with skin in virgin olive oil - again minimizing oxidative exposure - while getting the benefit of their collagen and omega 3 fats. The leg of lamb I also get from Costco, and it is imported from Australia - where probably 95% of lamb is grass-fed. Sam’s Club has a similar product from New Zealand. I also consumed somewhat less grain-fed beef. All my ground beef is now grass-fed beef packed with minimal exposure to air. I also gave up the cheaper cured bacon for uncured, sugarless bacon I get at a Kroger grocery-affiliate. Also my egg breakfasts became strictly pasture-raised eggs instead of “cage-free” etc - hopefully less omega 6s. Towards the end of the year I joined a food distributorship which allowed me to get A2 cheddar cheese, which I use on my morning eggs when not having bacon. Shrimp is an issue, and I began buying uncooked, raw wild shrimp, often still fully in the shell - figuring that the meat in the shell would be more protected from oxidation in the freezing process. Shelled, farm-raised shrimp is a common product these days. I also finally gave up my daily pocessed dessert habit. No more daily pie or cookies, etc. Instead, I usually have a whole fruit for dessert. Barring that, I have a less processed dessert of guava shells and crackers or goat cheese with blueberry sauce and crackers. That is probably my biggest remaining vice because the wheat thins and crackers still have some vegetable oil, and some sugar is still involved - but that is far less than the usual daily, fully processed desserts I was having. High blood sugar glycates LDL apoB protein, which is 6 times more prone to oxidation than native LDL. An additional positive effect was an additional 2 pound fat loss down to the 17% body fat level. In 2022 I still had the occassional salad dressing with some vegetable oil because the kale salad mix I bought at Costco came with a very delicious poppy seed dressing. However, in 2023 I stopped using this salad dressing altogether in favor of my home-made MCT and balsamic vinegar dressing. Lastly, I even gave up my store bought goat yogurt in favor of home-made yogurt I made from either raw, A2 cow milk or raw goat milk. I do not pasteurize this milk, which does involve some risk of culturing a malevolent bacterium, so care is taken. I typically start the yogurt the same day I purchase the raw milk, and I add a probiotic which has Lactobacillus salivarius and Lactobacillus reuteri, which are good bacterium hostile to many dangerous bacterium. Dairy can be a major source of oxidized cholesterol, and I believe my new approach would minimize my exposure from my morning breakfast yogurts.
What did all this effort yield me? In December 2023 I tested my oxLDL again, and the test result was a 47, which is within the lowest risk range of <60 for minimal heart disease risk. I enjoy the way I am eating, but unfortunately do not know which of the measures I took made “the” impact I was looking for - probably a mix of all of them - utilizing what I have learned about oxidized cholesterol and heart disease. Also, I was preparing meals for one of my sons, so ate very little in the way of refrigerated leftovers in the latter half of 2023, which can double oxidation rates. Nevertheless, I believe my results prove I do not have to become a vegetarian to minimize my cardiovascular disease risks. I can still eat a substantial amount of animal products with the appropriate care taken, and get the benefits of protein and collagen from them with minimal risk of heart disease. All that is needed is the appropriate knowledge. In the interest of full disclosure, I also recalled that about a month or two before getting this oxLDL test, I began taking Ubiquinol in my morning supplements. Subsequent research revealed that Ubiquinol is perhaps the most efficient anti-oxidant the body uses in its LDL to prevent its oxidation.
I have a link here to a video which indicates why I believe young people are getting CVD. Here is a thin, very healthy looking young woman who volunteered for Bryan Johnson’s program, and found she had an oxLDL of 222! I don’t know her history, but it seems from what is available that she ate out a lot: https://youtu.be/QkQenoT-MzA?si=JS82frhF-2XYDZQk&t=357 Clearly, some kind of change in eating habits is called for in young people, if they want to avoid surgical intervention in their mid-life.
There is a crowd which discounts oxLDL as a causative factor, but even though there may be issues with the accuracy of oxLDL tests, I believe they probably are more prone to undermeasuring oxLDL than anything else, because there are lots of different forms of oxidation oxLDL can go through which must be accounted for. The science is fairly settled that oxLDL gets taken up by monocytes/macrophages rather than native LDL, and that is the beginning of CVD. Native LDL cannot start the plaque process.
Super interesting, wow. Thank you for sharing all of that.
I just finished putting 8 years worth of blood test results (26 markers tracked in total) into excel, and can now very clearly see trend data quite easily.
When I was earing “clean paleo” with a few cheats per week, my oxLDL was at its lowest, along with hsCRP, A1c, and my hdl:trig ratio was at its best. My LDL was “high” as per modern standards, but not terribly so. T was 810 and Free T was 81.
As soon as I did strict carnivore, I felt better, but all numbers changed. T went to 1042, but Free T at that time was 18 (!). oxLDL at its peak was 98 during this time (red meat, eggs, chicken, butter, bacon). Trigs was also lower than HDL, but the numbers moved around a bit as one might expect.
Since now adding back some fruits, veggies, and oats, my numbers are now on the decline, including ApoB. Although I have only two years’ worth of particle count numbers, and I need to research how to fully interpret those, as I am not familiar with what they mean. oxLDL is going down, however particle count is going up.
I am still leaning towards membership in the LMHR phenotype, given that I can reduce lipid levels substantially with carbs, and that no carbs at all zooms my LDL into the 250+ range quite quickly, with total C being well above 300.
I have an appt with a lipidologist in a few weeks, and I will be clear that I am interested in lifestyle intervention ONLY, insofar as I need intervention at all (and I’m not yet convinced), but more importantly I want him to help me understand each marker independently and then in relation to the others. Specifically particle size as that’s the area I’ve done the least research and have the least knowledge.
I am not carni, so would personally encourage your “clean” carbs like vegetables since those seem to improve your numbers.
I believe the best new science on oxLDL is getting ignored - probably because to eat the way I do would destroy the food industry which controls lots of advertising dollars. It would also destroy big pharma which is now built around “managing” metabolic disease. And it involves preparing your own food - something many are no longer willing to do. Anyway, I believe there is lots and lots of money out there that doesn’t want this science to be known… so, consequently, no one hears about it. Nevertheless, the science has advanced far beyond correlation studies or Bro science. There’s many, many studies on it now - which have shown that oxLDL is what gets taken up by monocytes which become foam cells starting the CVD process. So, somewhat predictably in my view the debate has shifted to where the oxidation occurs - does it occur once native LDL gets embedded in the artery walls? Or before? Or both? There is still much to learn, but in my view, it is safest to avoid unnecessarily high oxLDL. There is too much science for me to ignore showing it is the trouble-maker.
The endothelial cells have receptors. It seems they suck in the oxLDL and then emit cytokines which call monocytes to come consume the oxLDL. The valence of oxLDL changes. It seems they become more negatively charged, and evidence also indicates that these receptors have at least a large component of electrostatic operation.
I don’t think the science here is established. But once BP starts going up, the glycocalix can become damaged - allowing more oxLDL to penetrate into the intima. The endothelium is only one cell thick, and is fairly easily damaged. I think you are hitting on less well established issues.
I’m familiar with the lipid energy hypothesis and Feldman’s work, again to a lay extent, and do believe I fit the LMHR phenotype. I still wonder if, when I am eating exclusively meat, although I am using fat for energy, the small dense count is dangerous.
Has Feldman or his team posted data on super-nuanced lipid levels of the trial’s participants? I’m aware that CT angiograms demonstrated zero soft plaque accumulation over the given period of time, but I don’t believe I’ve seen ApoB, particle size or count, etc. levels for these participants.
I definitely don’t want to be on a statin, and I wouldn’t take a SARM for all the money in the world. I’m not anti-medication, but I don’t want to be on anything long term, or for life, and I don’t want to be on anything with horrifying side effects like diabetes, muscle wasting, body aches, and dementia.
