My Perspective on ApoB, LDL and Lpa PT 2

[@jon0604]

Take a look at the meta analysis from southern Denmark where they calculated longevity based on 11 major statin studies including the Jupiter study and other major studies. This along with various others will convince anyone that statin use does absolutely nothing or may hurt when it considering all cause mortality. Keep in mind and make the adjustment knowing that these studies were done by the pharmaceutical companies and in the case of Jupiter, the co- inventor of the c reactive protein test. Also, many of these studies are done before 2006 where they didn’t have to register the study. It is one thing to read the results of a study using relative risk , but it’s another to dig into it.

[@KevinSmith-4Liberty]

I have had 4 CAC Score scans. On and off statins. Off statins I had a 25% annual increase in my score. On statins I had a 45% annual increase in my score. Statins stabilize plaque by accelerating the calcification of your arteries.

[@ldx1793]

Interesting, I've had 1 cac, 523 at age 52, went whole foods and mostly meat. Hoping to stop the inflammation /soft plaques that come b4 the calcium "patching". Hoping to cease arterial damage as well.

[@AATN_2019]

Sounds like pharma is trying to kill us 😳 CAC score of 400 and at my first annual after Doc placed me on a statin he didn’t even run a lipid panel. Said that was more for my family Doc to run. I stoped going to this Doc

[@rentner1762]

My lp(a) is 54, fibrogene around 200, cholesterol under 150, HDL 45, Ldl under 90. 2 stents, a lot of sports, 250watt on bike no problem. And still my arteriosclerosis (only in the heart) does not seem to improve. So far no insulin resistence has been detected. As you can see, it's not all cut and dried.

[@ldx1793]

Does not improve how? What was your base? Cac score or soft plaque assessment before and after ?

[@jamescalifornia2964]

It appears that we have much to learn about vascular disease ... 🤔💭 ( I like the idea of low dose Crestor as prophylactic to stabilize soft plaque ) ✔️

[@jna9888]

Agree. And it's a continuing process for those who are willing to continue. For the others, well, your drug rep will tell you what you need to know. Ask me how I know. I have a cardiologist who told me to get a voodoo to help me, and a PCP who says fractionated lipid tests aren't worth anything.

[@glauberborges5820]

Could you let me know what do you think about I-P6

[@jeff911rn99]

Do you really care what your Lpa is if you are not insulin resistant, fasting insulin less than 4, and metabolically healthy?

[@MyFatAdaptedLife]

My body fat is 9.8%, HDL 90 mg/dL, triglyceride 71 mg/dL, LDL 559 mg/dL, total cholesterol 663 mg/dL, remnant cholesterol 14, triglyceride:HDL 0.79, CT Calcium score zero, C Reactive Protein (cardio) 0.7 mg/L, NMR LP+Lipids Small LDL-P

[@naijaman6639]

Brilliant results. Well done.

[@MyFatAdaptedLife]

@@naijaman6639 Thank you

[@jimmatzek5895]

You are a definitely an outlier and your blood should be studied. Fascinating

[@MyFatAdaptedLife]

@jimmatzek5895 These numbers are typical of a lean mass hyper-responder. I'm waiting to hear from Dave Feldman to find out if I made it into his study.

[@MJ-gg3zq]

Wow! Thank you for sharing.

[@stevemc2626]

I keep hearing that an increasing calcium score from a statin is good but an increasing calcium score if you aren’t on a statin is bad. Please tell me the difference. It feels like twisted big pharma logic. But maybe I’m wrong.

[@bartrobinson2103]

That's a great question

[@efanjul5768]

There is hard plaque (calcified and stable) and soft plaque (unstable and dangerous). Calcified plaque is kind of like scar tissue; it shows there has been inflammation happening for a while. Statins calcify soft plaque, rendering it more stable, that's why your CAC score goes up with statins, but at the same time, your soft, dangerous plaque diminishes. You can achieve much better results with lifestyle than with statins, without the bad side effects.

[@stevemc2626]

@@efanjul5768 That sounds all correct to me so thanks for that. But I have heard many times that increasing calcium is a bad thing if you aren’t on a statin. So , for example, if I completely changed my lifestyle and reduced all inflammation then hopefully the formation of new soft plaque would not occur but my old soft plaque would slowly be stabilised by calcium deposits. So in this scenario how is it still a bad thing just because a statin isn’t used. That’s seems to be the message I hear over and over. Like I said it seems very ‘pharma-centric’.

[@user-fl5lr1nm5v]

@@stevemc2626 Calcification of existing soft plaque is a good thing, because once calcified it is stable and harmless and won't progress any more, but new lesions may develop elsewhere along the arterial tree. Stabilisation/calcification is achieved via lifestyle or medication or both. However, the goal is to stop more plaque from forming. This is where meds and lifestyle come in. If successful then NO new plague should form but calcium score can still increase for a while until the pre-existing soft plaque has finished calcifying or regressing. BUT at some point this should all stabilise and the calcium score should stop increasing eventually, assuming that the interventions have been successful. It is worth noting that it is almost impossible for plaque to form without LDL. Ergo driving LDL through the floor will stop plaque formation. No LDL, no plaque. It's quite simple. Unfortunatel KZbin is full of arguments about statins and other meds - they literallv can't see the forest for the trees. If you don't want coronarv artery plaque then simblv annihilate LDL, either via lifestyle, meds or both. If you want to know whether you have soft plaque as well as calcified plaque then you will need a CTCA rather than just a calcium score. The latter involves the injection of some dye but otherwise is just as quick as a CAC score. Good luck.

[@richardmoeller3143]

My Aunt was metabolically unhealthy lived to 99 no heart disease but had dementia starting at 88

[@PrevMedHealth]

thank you for sharing

[@222ouch]

what if we have normal LIPa and moderate ApoB?!! I am confused on proper treatment. LDL high HDL high Trigs low LDL pattern type A... Supplements or statins.

[@stacisterling5680]

You state in this video that 30-40 is not a significant risk and that even 3-4 times that is not a significant risk. Is that mg/dl or nmol/l?

[@richardmoeller3143]

Hey doc what about the 90 year olds that have 350 and up LDL and have no heart disease my doctor told me about one of his patients who is this way.

[@PrevMedHealth]

Very likely a Lean Mass HyperResponder, we have videos on that

[@sheddkkhan6758]

How much liproprotein (a) you have

[@abdulazizsen7372]

Türkçe ceviri yaparsaniz sevinirim

[@glendaguilott3765]

Yahusha bless you !!!

[@UnknownUser-sc6jx]

My total cholesterol before low carb was 177. Now it's 360. The doctors in Australia think I have FH but my brothers have normal cholesterol and so does my father but my mother has elevated cholesterol but I think because of medicine she takes for depression 🤔

[@tommydinob]

Begin using immediate release niacin. I’m a pharmacist. I eat keto the last 2 years. My cholesterol shot up. Niacin normalized it. 750-1000mg twice daily.

[@dmmcmah1]

@@tommydinob is niacin safe if you’re on losartan? A nurse friend recommended slo-niacin. It had an additive effect with the BP med. I got flushing and my BP dropped to 80/50 and I couldn’t stand up. The effect was very short lived and passed after 2 minutes but that was pretty scary and I haven’t taken niacin since. My LDL/ApoB go up fairly high on keto, I can lower it dramatically with RYR but that gives me muscle fatigue.

[@efanjul5768]

@@dmmcmah1 Sorry, what does RYR stand for?

[@ldx1793]

​@@efanjul5768red yeast rice. It's what statins were based on I believe

[@efanjul5768]

@@ldx1793 Red Rice Yeast.

[@jeremyking3986]

Just got my results for my CAC score, 210. What do I do now?

[@faethsnowowl5982]

Carnivore diet

[@lloydhlavac6807]

My LDL is over 300, but I believe I am a LMHR. My most recent blood test showed a Lp-PLA2 of 196 nmol/min/mL supposedly showing reduced risk (under 224). Didn't get my Apo B done this time, but my MPO was 294 pmol/L with low risk under470, and my oxidized LDL was 73 ng/mL (normal range) and (hs)C-reactive protein of 0.19 mg/L, low risk.

[@dmmcmah1]

According to my recent quest results Lp-PLA2 activity should be less than 125 nmol/min/mL.

[@lloydhlavac6807]

@@dmmcmah1 I got my tests done at Quest also, but they then actually went through Life Extension, so the parameters are theirs.

[@directajith]

i have high triglycerides. when I reduce it through excercise, ldl sky rockets. can you please give an explanation? my ldl is 208, triglycerides is 276. previous it was 160 and 321 respectively.

[@jpdoc5722]

me too😞, but my Triglycerides to HDL ratio is only 0.31

[@TheShumoby]

Lmhr here lp(a) is less than 8. Cac=0

[@lotembenatar7163]

Thanks, Dr. But this video goes against the Mendelian randomization studies on LDL-C. People with genetically high LDL-C seem to be at a higher risk independently of insulin resistance

[@glauberborges5820]

IP-6

[@jaqueitch]

How could a practicing doctor NOT know about LP(a) and that it is a big risk factor for cardiac health??? That is scary

[@timsmith6100]

If my triglyceride/HDL are 1:1 but my lp(a) is 141, should I be concerned? A1c is 5.4. CRP is 3.44. BMI is around 21.