That would be something I would advise against. In fact, higher cholesterol - all else equal - at your age of 75 is more likely to be protective than harmful.
Sure, your total cholesterol dropped, but at the expense of a less favorable HDL/Trig ratio. You were clearly better off at 0.9 than you are at 0.6. Most all reliable research agrees on that point. Ideally, you want to lower your trigs and raise your HDL - not the other way around.
In any event, while your CAC increased, this may not really be of such a grave concern anyhow. Your Agatston score is moderate, not highly elevated for your age. But itās not stabilizing, and that is also less than ideal.
But most importantly, since restricting fat, how do you feel? Is the vegan eating with some salmon/chicken making you feel better than you did on keto (presumably, it had been high fat with minimal carbs)?
Appreciate the update. Outside of sickle cell anemia, the greatest risk factor to getting CVD is ā¦ age. At your age, your CAC score is average http://www.newportbodyscan.com/ebt-coronary-calcium-scoring-guide/ . While obviously you would want it to be lower, it certainly seems that your vegan trial was a failure as compared to before as noted, since your CVD markers have gotten worse, and your CAC score still increased. Having said this, it takes a while for soft plaque to become hard plaque, so your increased number may not have been from your current diet, and as mentioned by @SomeGuy , it is also possible that your risk fell despite the increased CAC score. I recently had a CCTA done to look at soft plaque - and while expensive and you need to take a radioactive isotope, it is the best way to determine your true current risk. If you really want to go all out (and live in the States), you can get a CCTA that comes with computer analyzing to determine the exact amount of necrotic, soft and hard plaques. This would give a better indication of the effects of your diet on your risk.
If premature CAD is detected, this can lead to a search for less ātraditionalā risk factors, such as homocysteine levels, Lp(a), and wider screening of family members for these and other treatable cardiac risk factors.
I have āhighā homosysteine levels and extremely high Lp(a), yet a zero score on CAC. These might not be the CAD-causing problems that people think they are.
Most avocado oil is refined. Use virgin oil if you can find it. Otherwise switch to virgin olive oil or maybe even non-gmo pressed canola oil. If I were you, I would insist on getting an oxLDL test on your next blood panel. You may have to pay $50 or so for it. If it is above 100, you can probably lower it by cooking at 300 F or less, and not eating much leftover animal foods. Also avoid processed and most canned meats - esp canned tuna. Any frozen meats should be essentially vacuum packed. Avoid soybean oil based mayo, etc. Sounds to me like you are doing everything else right. If your CAC is athlerosclerotic plaque based, these suggestions should help.
Calcification is a feature of advanced atherosclerosis. There is very strong evidence that people who have coronary Calcification are at higher risk of a heart attack or stroke than people who do not have coronary calcification. As we age, our coronary calcium does go up, as does our risk for the disease. After about age 60, the CAC test really isnāt helpful. Current guidelines show that most American men by age 60 are at high risk. Woman are about 5-10 years later. Have a look at Dr. Allan Sniderman. He is recognized as one of the worldās leading cardiologists and researchers and a professor of medicine at McGill.
No, they are not. They literally have nothing to do with heart disease. Back when I was on Twitter, I was following a guy who accumulated a massive list of the MANY times ApoB failed at CHD prediction. I canāt remember where he kept the list though.
Not sure what such guidelines indicate other than the fact that most Americans eat the S.A.D.?
I fully agree that the CAC-based Agatston score is a flawed metric. Yet, to be clear, Iād prefer to have a zero score than a positive one. But thatās not entirely rational on my partā¦
It remains unclear to me why calcified plaque - i.e., the scabbed-over protection kind that is the only type that can be detected through the CT scan upon which an Agatston CAC score is based - is more concerning than a zero score that could well have missed plenty of undetected soft plaque - i.e., the kind which has not been scabbed by calcification and is therefore prone to detach and produce the dangerous/fatal outcomes of concern in the first place?
The Agatston scores are deficient both in that respect and the fact that they do not properly address the density of detected calcified plaque - shown to be inversely associated with CVD events (see study links provided on related threads).
That test measures oxidized ldl in the bloodstream which is not where oxldl is believed to cause issues ( as opposed to oxldl in the intima, which is when it is of concern).
How does it get into the intima? The ONLY way it can get there is from the blood - so you measure the levels in the blood. I agree it is not a problem until it gets in the intimaā¦ but it does. That is the problem. Normal LDL not so much. When it becomes oxidized, it is more likely to get lodged into the artery wall. I donāt know if science understands why that it is. It may be partially because HDL is less effective at unsticking oxLDL from artery walls than native LDL. Once it gets lodged, the cell seems to call a macrophage to eat it. If more oxLDL is lodged, the macrophage will keep eating it until it becomes a foam cell, and you are on your way to a plaque. Once the plaque forms, if it ruptures, it will form a blood clot - a very dangerous condition, and the cause of strokes. To prevent this, the next step the body seems to take is to calcify the plaque - one of the main causes of high CAC scores. I believe oxLDL to be the primary cause of heart disease. High blood sugar will glycate the LDL, and glyLDL oxidizes much faster than native LDL. Hence diabetics are more prone to heart disease. The science is finally getting there to show the real cause of heart disease.
This is part of my recent study. (Dr Lustig) says something along the lines of 2 types of LDL, the larger less dense and more buoyant that make up 80% of LDL are no problem, but the smaller dense LDL burrow into the cell wallā¦ Iām still working on this btw
My understanding is It gets into the intima as regular ldl and oxidized within the intima as way to help clear out oxidation that would not otherwise be cleared by macrophages. In other words the ldl helps to clear unwanted oxidation within the intima. If the oxidation therein can be handled in such a way that the macrophages can process and clear the ldl faster than it accumulated, then no signs of atherosclerosis is present, if not the macrophages become overly inflamed and convert to foam cells. The idea is that ldl oxidized within the intima is a natural mechanism, as are macrophages. What is not natural is too heavy a burden for the macrophages to clear on a clean way. At least this is how it makes sense to me and joins theories together.
Science? I have seen no studies supporting this. And it does not comport with your very assertion that blood oxLDL test is not useful. If LDL gets oxidized within the intima, then there should be no oxLDL in the blood. Yet, the blood oxLDL tests are finding oxLDL in the blood, and it does correspond to heart disease. Most people with heart disease have oxLDL in the 200 range. There are other causes. There are people who genetically have small cholesterol particles which are known to become easily lodged. It is ashame that this new science is being resisted. People are still so married to the old, misinformed models. I will add that LDL is not designed to leave the blood stream. It is supposed to stay inside the blood vessels, and is merely a delivery vessel to deliver triglycerides and cholesterol ester to the cells - much like the red blood cells are delivering oxygen, but are not supposed to leave the blood vessels. I really donāt see another way for oxLDL to get into the intima.
They really arenāt two different types of LDL. When the liver makes LDL, it starts out as VLDL or Very Low Density Lipoprotein. This is the less dense ābuoyantā LDL he is talking about. It is a lipoprotein shell full of triglycerides and cholesterol ester put there by the liver to deliver to the body through the blood stream. The cells throughout your body have receptor sites designed to receive these lipoproteins, which they will when they need cholesterol or triglycerides. They then offload the contents they need and release the lipoprotein particle, which becomes a little smaller. By the time the particle gets into the veins, it usually is going to be smaller and more dense or LDL. However, the science is showing that if the protein layer has become oxidized, at this point when it gets back to the liver, the receptors there are less likely to grasp it, because the surface has lost its recognizable protein nature - it is now more oxidized or glycated. So, then rather than getting recycled and refilled with protective antioxidants by the liver, it ends up just circulating around into the arteries again in its oxidized state. In the meantime it continues to either get drained of its contents or slowly leaks them out, and gets smaller yet - until it gets lodged in the artery wall. When there is a lot of this going on, ApoB is going to be higher, and ācholesterolā is going to be higher, but these are weak correlations because the native LDL count can be naturally higher. In the case of oxLDL, because its native protein layer has become ācorruptedā, I believe HDL no longer works to dislodge it either. Sometimes it works its way into folds in the endothelium of the artery walls, and there you have the start of the plaque process. As BP increases, it only becomes more likey to become lodged I believe. I am not saying Dr Lustig is wrong, but there are different stages to understand what is going on.
The last stage of the bodyās defense system are the macrophages, but in heart disease, I believe there is so much oxLDL, that they just get overwhelmed, and become part of the disease process. In our native diet, there is not enough oxLDL to overwhelm them, and we continue on heathily. In the SAD, the glycation and other oxidation processes simply overwhelm the native defenses of the body, which isnāt designed to eat the SAD or to address all the issues it causes. The powers that advertise on the big networks arenāt interested in our understanding the new actual science vs the old correlation studies, because they make all their money on the SAD. Hence, no one has heard about the new, dependable science it seems. I have shown studies on this site, and it seems to be new to most everybody.
