Cardiovascular Health

#414

Really good question here, thanks.

I’m probably considered to be an LDL skeptic by many here. I understand getting rid of LDL will get rid of ApoB and reduce heart disease. Also I understand LDL is an important part of the immune system and it hauls around fats, which is also important. I think getting rid of it is throwing out the baby with the bath water. Also it’s unnecessary.

First I would get rid of heavy metals, they’re like sand in a bearing. This problem can be solved easily (over time). Do a chelation challenge, by far the best way.

I think the cyclodextrins are a good solution to reduce inflammation. Alpha is easy to take orally and really no side effects. Beta is taken rectally and takes serious commitment, but I think it works. The idea is to subtract out the sLDL, it is damaged and causes damage, without throwing out all the other LDL’s

I have an order in for Colchicine and am looking forward to trying it.

I think low carb or keto is good if you can maintain a well rounded diet. Vitamins, minerals, polyphenols and polysaccharides. I’m not strict keto any more because I eat berries and veg.

#415

What evidence is there for this other than mechanistic speculation? Do people who have genetically low apoB/LDL or suppress it via medications have increases mortality rates from infections? With the recent pandemic, such data shouldn’t be difficult to find.

Do a chelation challenge, by far the best way.

Chelation is a mixed bag.

I think low carb or keto is good if you can maintain a well rounded diet.

The low carb diet did not result in decreased mortality rates in mice, unlike the low protein diet.

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#416

What evidence is there for this other than mechanistic speculation?

Lustgarten talks about it in his book. It’s a carrier for LPS and is involved in breaking it down. LPS causes T2D, which causes everything else. Cardiovascular disease is related to microbial burden.

There are people that agree with you on chelation, but it depends on how bad you are. Also EDTA is roundly put down by many, but DMSA if your problem is mostly lead, not so much. It really helps my sleep. You don’t know if you have a problem without checking.

I wouldn’t go by mice on diet questions. I agree the most important thing is to take all essentials. I think keeping sugar, or BG, low is essential. I’ve tried everything and find low carb works for me. Gotta keep body fat low too and it works for that.

#417

By that logic, shouldn’t we see higher mortality rates in people from cardiovascular causes in people who take statins/PCSK9i instead? We see the opposite in pretty much all clinical trials.

I wouldn’t go by mice on diet questions.

In regards to diabetes, mice data is somewhat valuable. If low carb diets didn’t increase lifespan like acarbose or SGLT2i did, then we can, at the very least, conclude that low carb diets don’t provide any benefit for blood sugar control.

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#418

I agree for primary prevention there doesn’t seem to be any rct evidence to go lower. If i had risk factors i’d be tempted to edge lower though. But i don’t think id be evidence based.

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#419

I may not count because I’m only an “apob skeptic” to the extent that I haven’t seen any rct evidence to show unequivocal benefit in primary prevention from lowering it below 60 with pharma.
But…
Apob below 70
Bp systolic below 120
Hba1c below 6%
CRP below 0.9 mg/dL

Hit all those targets long term and your cvd risk is probably lower than having a naturally sub 20 apob (eg thanks to a psk9 mutation).

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#420

0 for both :smiley:
The only reason I would argue for an even lower apoB count and HbA1c value is because cancer loves both cholesterol and sugar.

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#421

Thanks. “You can’t improve what you don’t measure.” What are the metric(s)/indicator(s) you would follow in your protocol? What are the thresholds that determine when to start treatment/intervention? What’s the optimal/low risk threshold?

#422

Mendelian randomization studies have shown that people with low LDL do not have higher rates of infections, RCT’s aside.

This is why you need double blind, placebo-controlled trials, these effects can be due to placebo and as you say we don’t know whether neurological side effects are things like headaches. Besides, it was not statistically significant which they say in the study there was no difference.

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#423

Ok but the average patient was 64yo in this study. If ezetimibe is so good on CVD, what did they die from instead to make ACM not significantly lower in the sim+eze group?

They write: “The benefit appeared to be particularly pronounced in patients with diabetes mellitus and in patients 75 years of age or older.” but don’t give more details. Was ACM lower in these subgroups?

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#424

From one who has been on keto and low-carb diets in the past, my experience is that keto does nothing for blood sugar control except to raise fasting glucose levels in the morning. Though, it had little effect on my A1c levels.

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#425

I think your quote is from IMPROVE-IT, my comments were about the other study. No statistical significant difference in side effects there and it was for the primary endpoint not ACM. I don’t know what to think of a non-statistical significant effect.

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#426

Really good question. For years everybody has known their cholesterol numbers, then they go buy drugs to lower them. Yet heart disease continues to rise. I would like the pleiotropic effects only please, forget the cholesterol lowering.

CAC is what got me on to this journey, but now if I use chelation and it gets rid of the calcium it is probably meaningless.

After I read Lustgarten’s book I thought everybody should know their microbial burden. I wanted to go to the doc and find out my LPS level. I still think this plays a big part in longevity but no idea how to get it measured. It’s called microbial burden for a reason. It isn’t microbial boost. It is like weeds in a field or homeless on the street or criminals in the general store. Burden. And we don’t know the level.

I just take all the cyclodextrin I can. Too much alpha and you get gas, it turns into SCFA in the colon. I used to take a lot of the SGLT2’s and then I took it when I took beta cyclodextrin and got kidney pain. So didn’t do it again. I should try it again and see if it was a fluke.

I did a second chelation challenge this week and when the heavy metals are gone I’ll quit that. My doctor does a yearly stress test and does all my numbers and estimates my time of death. I know it’s BS, but I go by that too. I don’t have good answers here.

#427

Uh, 5mg is not the “lowest possible dose,” at all. Take a 10mg and with a razor cut it into quarters. Or, crush one 10mg tablet and carefully mix it with some crushed calcium carbonate, then divide into 10 capsules and you’ll have 1mg.

Even a 1mg dose can drop LDL-C close to 20%. Some meds cannot be crushed and some are critical dosages, Rosuvastatin is neither, but of course, rely or your Practitioner.

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#428

Bigoz, have you looked into K2 supplementation and its effect on plaque?

Effects of vitamins K2 and D3 supplementation in patients with severe coronary artery calcification: a study protocol for a randomized controlled trial.

I have no idea if k2 helps remove plaque. Further, there is soft plaque and hardened calcified plaque and from a MI point of view the soft plaque seems more dangerous.

I wish that I had a CAC score from a decade ago, but then, I wish I had one right now, I’ll have to look into getting one.

Keeping plaque from developing w/in arteries in the first place and attempts to remove or stabilize it are two very different things.

Still, I take Rosuvastatin and have for more than a decade. From https://health.clevelandclinic.org/can-statins-actually-reverse-plaque-buildup:

Q: Can statins actually reverse plaque buildup?

A: Yes. There have been several clinical studies — many of them done here at Cleveland Clinic — that show statins can reverse plaque buildup.

Two statins in particular, atorvastatin, which is sold under the brand name Lipitor, and rosuvastatin, which is sold under the brand name Crestor, are the strongest statins.

Clinical studies using ultrasound in the coronary arteries have shown that when you are on high doses of these medicines, even if you have plaque buildup already, you can stabilize the plaque on statin therapy.

If your LDL cholesterol is lowered below 70 mg/dL, you can even see a regression in the plaque by up to 24%. So having really a low LDL cholesterol level can help stabilize any plaque buildup you have, and prevent further plaque progression.

— Cardiologist Steven Nissen, MD

I used to have access to a CholestTek and chose Rosuvastatin and asked my doc to prescribe 20mg and w/ his permission to “play with dosage.” I started at 2.5mg, then 5, then 7.5 and so on. The response was classical and I settled on 6.7mg (1/3 of a 20mg tablet) though lately being on keto I’ve dropped to 5mg, my numbers are currently LDL 83, a bit higher than a usual ~43 due to being on keto/omad.

I’m a USDOL field nurse (RN) and I oversee care for about 40 injured federal workers at a time, about 200 a year (they come and go). In many cases injured workers w/ ruptured or torn tendons (a very common injury) I often see pretty high-dose statins. Often I find myself wondering, was it the accident that caused the rupture/tear, or was it the statin?

I do wonder if statins are in fact a “wonder drug,” but one that is often prescribed at levels far higher than is necessary. Were I a Practitioner I’d start a patient on a low or very-low dose, test a few months later, then move higher. The pharmacodynamic curve is quite straight, so then choose the dose to obtain necessary changes but not to overshoot, risking adverse effects.

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#429

Do you feel that Bempedoic Acid would avoid the muscle side effects from statins? (i.e. torn tendons)

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#430

Are there any apob - cancer studies that you rate. I’d be interested to take a look.

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#431

It’s mostly speculation on my part based on the JUPITER trial’s cancer death rates and mechanistic studies regarding cancer and apoB.

#432

I should have found this sooner but have been busy:

So it turns out that if you inject LPS (for those who don’t know, LPS is the broken pieces of your microbial burden that have been killed by your AMP’s. So it’s a little like if fingernails and toes and eyelids are floating around in your bloodstream. All the time. The levels of this are used as a signal to your body.) into 26 year old healthy subjects they get T2D.

This is a study that demonstrates how LDL and HDL inactivate LPS:

https://www.ahajournals.org/doi/abs/10.1161/01.atv.12.3.341

And this is a short article and discussion about how the lipoproteins are part of the immune system:

People may wonder what part of the statin it is that increases the odds of getting T2D. It’s the fact that they reduce lipids. Lipids are important. Your body is not stupid. Some of the lipids are bad, some are good. Just take out the bad. Cyclodextrins.

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#433

HDL is increased by statins. Is there a role that LDL-p fulfill that HDL-p can’t?

People may wonder what part of the statin it is that increases the odds of getting T2D. It’s the fact that they reduce lipids. Lipids are important.

Then why do some statins have a higher or lower risks for developing T2D even at dose-equivalents if the LDL decrease is the same?

Your body is not stupid.

Your body is (supposed to be) locally optimized to help you survive in the environment you find yourself in. It is not optimized to help a bunch of individuals survive past their “expiration rate”. If the body was truly “smart”, it wouldn’t allow itself to develop t2d either, would it?

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