Ivor Destroying the Cholesterol LDL Theory on the Big Stage - March 2020!
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- เผยแพร่เมื่อ 11 ก.พ. 2025
- Well guys lots of interest in my last Subbotin interview, so here's me blasting out the FULL story, with no accent to complain about!
Super testimonials flowing from my new workshop attendees, listed some on my homepage - you can join the fun and learning here: ivorcumminswor...
Super testimonials flowing from my new workshop attendees, listed some on my homepage - you can join the fun and learning here: ivorcumminsworkshops.com/
Thanks for all your hard work Ivor🙏
Love you Ivor ♥️. Thank you for all you hard work and truth 🙏🏼.
It's a theory not truth
Thanks for this edited version 🙏🏻❤️🙏🏻
The release of free radicals from the oxidation of dietary omega 6 fatty acids that become incorporated into the walls of cells and mitochondria are most likely the primary source of the chronic inflammation that leads to the damage of endothelial cells, clotting, and cardiovascular disease, peripheral artery disease, dementia, chronic renal disease,and hypertension. Dr Chis Knobbe’s book on the ancestral diet explains this in detail.
It's an interesting theory but in reality vegetable oils lower risk. There's a linear increase in risk with LDL-C not vegetable oils.
@@micaineseeley5339 Evidence?
@@micaineseeley5339 Seed oils are extremely harmful. Things like olive oil are much more healthy.
@kengraves6425 that's not what the studies show.
@@micaineseeley5339 studies sponsored by big harma? Lmao
Thank you so much. I have high LDL I have many "causes" to have it. Yet they did the scope on my arteries and the surgeon told me they're spectacular his words not mine
Do a CIMT test, it's more medically accurate.
LOVE YOUR PROGRAMS THANK YOU
Beyond my comprehension. Just one question, do the pharmaceutical companies come up with a drug first and then look for something they don't properly understand which the drug might or might not have an effect on which they then claim could be a potential benefit depending on your point of view. All I am beginning to understand about the biology of the human body is that it is more closely linked to financial balance sheets than patient health.
If you actually understand the science, the meat, dairy and eggs industry work extremely hard to make their products appear healthy, when they are the primary drivers of disease (which is well documented in their own Journals), then came the big sugar blame game, which focused on a symptom of the bigger issue - that being high fat, high cholesterol diets reducing your insulin sensitivity, driving the pancreas to produce more insulin (as insulin acts as a key to allow glucose to enter cells) when your body processes sugars, eventually your pancreas gives up and you're up shit creek.
But hey, let's ignore the ACTUAL science... and go with the charlatan on TH-cam.. the stupidity of American's never ceases to amaze me.
@@cjpartridge Big harma is not interested in cures...they are only interested in patenting harmful drugs to treat symptoms and not cure.
How would a "high fat" diet effect insulin sensitivity?
My cardiologist should watch this. He's old school and still believes cholesterol is serious and recommends statins. I always decline.
Your cardiologist probably took one look at you and knew even mentioning changing your diet would be impossible task, so they always go for the next best thing (statins) so you can squeeze a couple extra years in.
But the question is, will you decline the bypass surgery when the inevitable stroke or heart attack comes?
But go right ahead, confirm your biases with a charlatan charging you $50 to tell you to eat more foods that cause heart disease 😂
Statins are pure poison. The discoverer of Statins Akira Endo wouldn’t take them. Cell killers. Stops the Mevolanate pathway stone dead.
@@cjpartridge oops. Biochemistry not your strong suit is it?
@@Mark-hu9tf that's because the data shows that...look it up
@@micaineseeley5339 I did and it doesn't. Dr Aseem Malhotra talks about this a lot. Check it out.
Hm, so any serious person ( professional or not ) should at least be asking questions...
Thinking that LDL is the root cause is like driving at a tree at 300 km/h and hoping that your up-to-date NCT will save you...
@@declanmcardle that a terrible comparison. We know it's the root driver because the only group that doesn't get ASCVD in our cohort has a lifetime LDL-C below 65 mg/dl, there's a linear increase in risk from there, and when one lowers LDL-C below 70 mg/dl there's a linear reduction in plaque...
Thanks for that, The accent of Mr Subbotin was VERY thick.
Glad you are back on health. Would be interesting if you would follow efforts of RFK and report back to us to see if he is on the right track. I hear a lot of talk about food additves but not much about the harm the recommended macros are responsible for.
I don't give a shit about additives really - that focus misses the elephant in the room - possibly he is being misled on purpose?
Thank you my exact question. Vital info but hard to decipher accent. Much thanks.
When the Irishman mentions someone with a "Tick Accent" 😂
Very interesting and a great presentation. The only part I’m missing in this is LDL and sdLDL (previously thought of as the firefighter and the cause of the fire) - does this viewpoint of LDL still hold in this new model? You talk about LDL leaking from VV from the outside in, but is it primarily small dense particles leaking from the VV causing the problems? If so, I imagine the initial creation of sdLDL ties in with your list of root causes.
sdLDL is just a proxy for hyperinsulinemia really - LDL particles get very SLIGHTLY smaller when insulin is an issue - so a bit of a distraction
@@jimw6659 sdLDL is a proxy for insulin resistance. When you account for insulin resistance sdLDL is meaningless. All LDL particles are atherogenic. VLDL & ILDL are the most atherogenic and they're large particles. Small particles deposit less and larger particles deposit more so they equal out. There's many publications showing this.
Great presentation Ivor. I have a question about the outside in hypothesis. Dr Davis has evidence that fixing the metabolic syndrome and a lot of Vit D can reduce calcification. I always assumed that the mechanism for this was inside out. Let’s assume that the outside in hypothesis is true. Can this co-exist with the inside out mitigation of arterial plaques?
Yep all the stuff on what insults the intima is cool - fits either way!
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So, as an ageing person with presumably damaged intima from lifelong bad diet, high ldl wold at this stage still be undesirable, right?
Depends if you independently, currently have a clotting issue, IR etc....
My cholesterol levels have actually dropped since I stopped taking statins and cut seed oils out of my diet. Go figure.
In the end it doesn't really matter what theory it is. Elevated ApoB leads to ASCVD regardless, and if a persons ApoB is low enough across their lifetime they won't develop heart disease.
It's just a proxy for IR essentially
@IvorCumminsScience the problem is that with multi factorial analysis it's been determined that ApoB is an independent risk factor independent of insulin resistance, so a person can have a low HOMA-IR but still have advanced ASCVD. Young people with familial hypercholesterolemia only have elevated ApoB, not IR, and have advanced ASCVD. The theory doesn't explain FH.
@micaineseeley5339 FH people with serious disease at a given age have same levels of cholesterol as those with none. The diff with FH is higher genetic clotting propensity. See David Diamond lectures
@@IvorCumminsScience they have advanced heart disease from high ApoB. Clotting conditions do not have similar cardiovascular risks as FH. FH have genetic defect in cholesterol production only. It's not the clotting issues driving the condition.
@@IvorCumminsScienceI watched his lectures, he cherry picks. There's different forms of FH. Monogenic homozygous is the worst presentation of hypercholesterolemia they can have a heart attack or stroke by age 5. Monogenic heterogenous is less risk making it to 25-30 years of age before an event. The Polygenic homozygous by age 35 has had their first event and the polygenic heterogenous could make it up to 50-55 years of age before their first event depending on their sex. The severity of the condition is directly related to their altered ApoB clearance, not clotting. The clotting polymorphism does not occur in everyone with FH, it will impart extra risk in the people that have it, but the risk of FH is independent of that polymorphism. The reason FH is harmful is due to ApoB, that's why the different phenotypes have increased risk.
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