0:26 Peter’s background and history with lipid research
Term used: Familial Hypercholesterolemia (“FH”) is a cluster of genetic abnormalities that result in high total or LDL cholesterol. If someone has Heterozygous Familial Hypercholesterolemia it means they got a copy of an FH gene from one parent only. If they have Homozygous Familial Hypercholesterolemia, they have a copy from both parents. Homozygous FH is considered more severe of the two.
6:20 For people who see their cholesterol rise on low carb, can Peter provide information on whether they should be concerned?
7:00 How big of a problem is heart disease in general?[
9:35 The physical progression of atherosclerosis[
11:54 Are the steps of atherosclerosis necessarily progressive? Can they be stopped or reversed?
16:15 The complexity of the lipid system – a long way to go to full understanding.[
17:20 The work of the Russian researcher Nikolai Anitschkow and what his rabbit study showed about the development of atherosclerosis
21:21 What does the research show regarding cholesterol level and heart disease outcomes/risk?
23:47 What does Peter say to the criticism that there can be possible cherry-picking for studies on cholesterol lowering and cardiovascular disease?
25:00 Thoughts on CETP Inhibitor trials – why did they fail? What does it mean?
Term used: CETP stands for Cholesterol Ester Transfer Protein. It is a protein which transfers cholesterol and triglycerides between the lipoproteins. There is a class of drugs which inhibits the actions of this protein, ultimately resulting in higher HDL-C and lower LDL-C.
29:30 Is LDL-C a causal factor in atherosclerosis?
33:05 Could there be other underlying problems with Familial Hypercholesterolemia other than high LDL?
Term used: CIMT stands for Carotid Intima-Media Thickness, it is an ultrasound that looks at the thickness of certain layers of the artery in the neck (the carotid). It is used as a measure of risk of heart disease, with thicker IMT being higher risk.
40:54 Caveat: The problems with CIMT measurements
43:16 Dave’s CIMT results – are they significant, and is there a danger of confirmation bias?
47:45 Comparing risk and context.
50:45 Could Lean Mass Hyper-responders be an example of paradoxical responders?
51:26 Case study – “Miss K.”[
57:04 Comparing treated versus untreated people who have Familial Hypercholesterolemia
1:04:03 Devil’s Advocate Intro
1:04:23 Are LDL particles, like macrophages, a part of the immune response? In addition is it possible that some of the association between LDL and atherosclerosis is due to this immune response?
Study mentioned: Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California: prevalence of coronary and hypertensive heart disease and associated risk factors.
1:10:47 As more evidence emerges to stratify for this triad (high LDL-C, high HDL-C, and low triglycerides), do you likewise predict it will show lower risk for cardiovascular disease?
1:23:45 Many studies tout changes in risk for cardiovascular disease mortality, yet show no difference in all-cause mortality. Doesn’t this run the risk of misleading people to assume overall benefit where there is none?
1:32:30 Audience questions
1:32:42 Are there any CAC scan studies on people from before and after statin therapy?
Term used: CAC stands for Coronary Artery Calcification. It is a CT scan which looks for calcium in the arteries, the score is used as a risk marker for things like heart attack or all-cause mortality, with lower scores being better risk.
1:34:37 Does Peter know how to access databases to test the triad?
1:38:47 Does Peter have any thoughts on how young to start statin treatment in children with Familial Hypercholesterolemia? Is there any information on it interfering with growth, or adverse side effects?
1:44:04 Side effects and statins – is there a problem with using run ins?
1:49:42 Is the increase in residence time of LDL due to modification of the LDL (e.g. glycation, oxidation, etc).
1:50:40 Can LDL be present and not cause plaque?
1:51:31 What does Peter think about Vladimir Subbotin’s work, wherein he disputes that lipid deposition is the initiating factor for atherosclerosis, rather he states that excessive intimal hyperplasia is the initiating factor?
Study mentioned: Excessive intimal hyperplasia in human coronary arteries before intimal lipid depositions is the initiation of coronary atherosclerosis and constitutes a therapeutic target.
1:53:11 What about the impact on heart disease risk of genetic mutations which result in high LDL without affecting the cells ability to uptake lipids/lipoproteins (e.g. glycogen storage disease)?
2:01:18 Credits and Outro
So the success with Miss ‘K’ on statins resulted in her sudden death?? Not an example I’d have chosen.
Hi could I ask a quick question unrelated to the video.
I’m vegetarian and have cholesterol which is a little high LDL4.8 HDL1.1 but when I cut down fat it spiked higher and then when I thought to try eating cheese and peanut butter again it dropped…..seems consistent with some of the things I have read on here even though I am not on a keto diet. Any quick thoughts on how to keep it down and particularly keep LDL down. Thanks
This not only relates to the ketogenic diet, but diets as a whole it seems (high carb, low carb, etc) as it relates to energy distribution (from what we understand so far).
When you cut fat, were you simply removing fat, or did you *swap* the fat for carbs or protein? This is important, as if you accidentally put yourself in a caloric deficit, it can raise LDL (as the VLDL transports more fat from storage to make up the difference).
There are also other things that could have impacted as well – including the length of the fast before the blood draw, etc.
Thanks I didn’t deliberately add more carbs or protein if I remember I was just cutting fat out of my diet.
Like you I wonder about the factors that affect cholesterol – time of day, time of year, weight, exercise, illness apart from if body isn’t getting enough fat from the diet does it produce more of its own and yes whether if you’re like me and don’t eat late in the evening so the fast is more like 15 hours as opposed to someone who may have a snack before bed and have only 8-10 hours fasting……
As aside the nurse told me last time that even chewing gum can have an affect on the test as anything that stimulates digestive enzymes will affect the test……
I suppose the question is whether its harmful to have higher LDL I’m sure there must be a paper out there somewhere with figures for cholesterol of those shown to have atherosclerosis through imaging.
Then that makes perfect sense as to why LDL is going up when you lowered fat – it may be because you’re creating a situation where you need to get more energy from your “cupboards”, which can be transported by lipoproteins like VLDL.
And yes, length of the fast can definitely impact as well – over 14 hours, and again, you’re likely needing to rely more on fat from storage. As opposed to the middle ground of 12-14 hours where chylomicrons (which transport fat you just ate) being cleared but probably no large upregulation of VLDL yet. Hopefully that makes sense.
As for your other question, I don’t think there’s a solid answer on that yet. There is some research to indicate that context does seem to matter, such as HDL and triglyceride level, and I do think there can be benign or detrimental situations that can cause high LDL – such as some sort of damage causing inflammation and an upregulation of LDL as part of the immune or repair process, but this is usually paired with other signs of trouble like high fasting triglycerides, low HDL, high insulin, high inflammation markers, and others. Perhaps why context changes the risk.
Could I ask for what advice you would give – my sense from reading your website would be to up my fat – maybe a couple of spoons of olive oil, an extra avacado and see what happens at my next cholesterol test scheduled for April and make sure on the full 14 hour fast….does that sound about right.
Definitely make sure only 12-14 hours fasted, and you are not restricting calories during the week leading into the test (just eat normally).
The answer to the other question depends on the context of the higher LDL – what were your triglycerides? If they are high, that could be another reason which might require a different approach. (Just my opinion – not medical advice!)
Thanks I’ll get back to you when I get my triglycerides …….sounds like you are very educated more than most doctors in this field so advice at least worth a try.
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Ferty9 Hospital & Research Center [FHRC] is a hospital set up by highly experienced doctors & gynecologists with more than 25 years of experience to serve those with infertility issues, nationally and globally.
I appreciate Dave all day long but this guest was a mistake. Following people like this, heart patients start their downward slide to a miserable death shortly after diagnosis. Statins are NOT the answer. I have tried to take statins at my cardiologist’s demand. One made me sick, another made me suicidal. They are poison, I don’t care what this guy who makes his living pushing the status quo says about them.