#2034

It is still only the author’s hypothesis, not fact.

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#2035

There is at least a fact that Lp(a) is an independent cause of ASCVD. There are numerous pathophysiological processes that contribute to ASCVD besides apoB. You can find plaque pathology reports that contain only marginally apoB… there are people with high apoB that are protected at least to some extent against apoB damage etc.

#2036

Which is genetically predetermined and even for that, therapies exist.

There are numerous pathophysiological processes that contribute to ASCVD besides apoB.

Diabetes, high blood pressure and smoking. All those risk factors can be mitigated by either other medication or better lifestyle choices.

You can find plaque pathology reports that contain only marginally apoB…

Afaik the people who genetically have low apoB never develop ASVCD.

there are people with high apoB that are protected at least to some extent against apoB damage etc.

Sure, but they are a minority and you are not likely to be part of them. I don’t believe I’d naturally get over the age of 100.

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#2037

My cardiologist would disagree here probably. Family history is a part of risk assessment and my parents at 78 and 80 have no ASCVD, my grandparents lived well into their nineties and no one died of ASCVD, all my great grandparents to my knowledge did not die of ASCVD, they lived till late eighties early nineties, my great grandmother lived to 98. One of my great grandfathers died at 78 but his cause of death was lifestyle cancer. If genetics play a role there is a chance I might be protected. But as probably ASCVD to some extent is not avoidable the goal is not to die of ASCVD, but with ASCD.

#2038

But as probably ASCVD to some extent is not avoidable the goal is not to die of ASCVD, but with ASCD.

Dr. Attia disagrees. Having very low levels of LDL will not only prevent ASVCD but possibly even reverse built-up of plaque according to some studies.

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#2039

This statement is purely speculative.

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#2040

If you watch the first link from Eades above, an Australian woman explains that the small dense LDL, which is the only part causing trouble, is actually not recycled because it is glycated. Meaning that a sugar has bonded to it over the site where it is supposed to dock on the liver and get recycled.

My question for anybody is how we ever get rid of these small LDL that are glycated. Do the 'flozens get them into the urine? My doctor was always telling me that Niacin helps get rid of the small dense LDL. How does it do that? Also they say that the PCSK9 can do it, but how if there is a sugar bonded over the docking site?

Just the questions popping into my head.

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#2041

Do those glycated LDLs go hand in hand with elevated glucose? If it’s connected, then regulating glucose could be the answer. Or it’s not that simple?

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#2042

It does seem to be that simple. You notice an earlier graph she showed how heart attacks are more closely related to glucose control by far than LDL.

I’ve had trouble controlling my fasting glucose since starting Rapa. I finally started a low dose of Pioglitazone and it doesn’t seem to do anything. My doctor said it would make me gain weight, which I’m not worried about. I use acarbose if I have carbs, but really I don’t. The only thing that seems to work is empagliflozen and if I take the low dose it is around 85 or 95, the high dose I woke up at 65. So I’ve been using the low dose.

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#2043

I’d be careful of observational trials. That said, keeping your HbA1c below 5.0 would be ideal.

#2044

Sure, happy to. Hubris. You are not medically trained and you think you know more than people that are. Just listen to any podcast by Peter Attia where he brings on experts and count the number of times they correct his errors, mistakes and incomplete understandings of the subject area. He learns from them. You would not. That’s your blind spot. And his base level of understanding is magnitudes above yours. You are floundering in shallow waters.

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#2045

That’s vague and not specific what argument I have that’s wrong or data that is wrong.

#2046

This question you should ask Sandra Kaufmann.

She replies her emails herself.

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#2047

What is the relationship between glyNac and pulmonary hypertension? I have seen nothing in the literature about it. Please explain.

#2048

That came from studies on Rats as I recall, it was mentioned in an old Life Extension article. They were debunking it. It’s probably nothing. There was another article on that and I can’t remember where I read it. Maybe I need another supp for memory.

I did get afib after taking NAC for the 12 weeks. It did improve my strength. I stopped and never had more afib until I gave it another short trial of just a few days at a lower dose. Got afib again. I take just glycine now and maybe one pill of NAC weekly.

#2049

A fib carries with it a significant stroke risk. Not to be viewed lightly and I’d stop it if I were you. I also get heart palpitations from it, though not A fib. I’ve totally stopped taking it.

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#2050

Shouldn’t you take anticoagulants if you have afib, even once?

#2051

I can not give you more guidance than that AnUser. But yes, you know nothing other than what you read in a paper that you partially understand. Any expert in the field would know 1000 times more than you, and would not be as confident as you in any of their answers. It would be better if you preface everything you said with [Thomas Dayspring, insert your expert] says. Because you’re just parroting what you read. Not that there is anything wrong with that.

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#2052

Everyone is parroting from somewhere, that’s how science is.
“Standing on the shoulders of giants”
“All of Western philosophy is but a footnote to Plato.”

But you’re free to say what argument I’ve said that is wrong or data that is wrong.

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#2053

As I have posted several times on this forum, In my view it is more like;

“It is very difficult to find a black cat in a dark room, especially when there no cat” ~Stuart Firestein