Dr. David Diamond: Exposing the cholesterol myth

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I have an LAD stent after angina with exertion at age 54, no MI, 95-98% occlusion.

LPa 6, ref range <30mg/dl

No other significant risks in Cleveland Heart labs/lipidology, Previous heart scan showed tiny-minimal calcification way downstream in a R side artery, not considered a risk.

Not overweight, active, no diabetic troubles or insulin resistance, etc.

Only ongoing marker not ideal, low-ish HDL

Shit happens regardless of your numbers.

Did the 95-98% occlusion show up on the previous heart scan?
 
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I have had high cholesterol, according to every MD who ever tested me, since I was 35. I decided recently (age 63), as my LDL was twice the maximum, to do something about it. I follow a ketogenic diet and so 80% of my diet is fat. I cut down saturated fat by removing coconut oil (!) from my diet and reducing my beef intake to 50% of previous, whilst making up the caloric shortfall with chicken (gristle, skin etc not just the white meat), thereby increasing my intake of polyunsaturated fat. Within one month, my LDL is just at the top of the maximum range (i.e. it halved) and my total cholesterol is just a tad over the maximum. I am doing another lipid profile next week (end of month 2). I think there are some truths to the bigGovt positions on the effects of SFA/PFA etc, but it is almost certainly depends on individual susceptibility. Hope this helps someone. Namaste.
 
I have an LAD stent after angina with exertion at age 54, no MI, 95-98% occlusion.

LPa 6, ref range <30mg/dl

No other significant risks in Cleveland Heart labs/lipidology, Previous heart scan showed tiny-minimal calcification way downstream in a R side artery, not considered a risk.

Not overweight, active, no diabetic troubles or insulin resistance, etc.

Only ongoing marker not ideal, low-ish HDL

Shit happens regardless of your numbers.

whats your diet like?
 
whats your diet like?

Immaculate, organic, grass fed, free range no packaged/processed food etc. No junk. Plants, meat, fish, some dairy, Prior to Cardiac event probably ate more fruit and PUFA than desired, used canola andolive oil for cooking. Since dropped PUFA oils and only cook in cocnut oil and butter. Save the olive oil for drizzle over food. I also ate a lot of grains including gluten. Have shifted to less grains, mostly gluten free, less fruit in favor of more greens and veggies, and more soaked/pressure cooked legumes, somewhat lower carb, added more sat fat, shifted to more meat fish and eggs over dairy. Only eat a little bit of cheese, no milk or yogurt any longer.
 
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Immaculate, organic, grass fed, free range no packaged/processed food etc. No junk. Plants, meat, fish, some dairy, Prior to Cardiac event probably ate more fruit and PUFA than desired, used canola andolive oil for cooking. Since dropped PUFA oils and only cook in cocnut oil and butter. Save the olive oil for drizzle over food. I also ate a lot of grains including gluten. Have shifted to less grains, mostly gluten free, less fruit in favor of more greens and veggies, and more soaked/pressure cooked legumes, somewhat lower carb, added more sat fat, shifted to more meat fish and eggs over dairy. Only eat a little bit of cheese, no milk or yogurt any longer.

I would say more like Paleo, even though I don't like to label diet. I'm shifting to this Diet as well, the only grains I use are Brown Rice and Oats, but I'm actually limiting my Oatmeal now at 2/3 times per week. All grains seem to trigger inflammation, I have to say the evidence I saw just pertains to Gluten, but I do believe Paleo expert such as Loren Cordain about other grains as well being bad, whether whole Grain or not. PUFA is well know to be inflammatory but I think your diet overall was ok, go figure, although I know that there is always an answer to everything.
 
Seems like he is stating cholesterol does not cause heart damage. I have not checked the markers he stated, so I can not answer those things, YET! I will try to get the items he mentioned checked. My total chol was 180 is and ldl was top of range and occasionally over. Still had a heart attack while being in really good shape overall.
Not sure what that means, but I do not think cholesterol can be ruled out completely.
I do agree that big pharma is funding the statin and all other drugs. I also appreciate his breaking down of published stats. All numbers can be made what you want them to say.
SO i heard him and will check other indicators he spoke about, just not sure he is 100%, maybe he is and I am wrong.
After having a surprise heart attack I am checking out a lot of things. What I have found is for everything one side says, I can back it up with another study from the other side!
@Moose, Have you even done an oral glucose tolerance test? Everything about your numbers looks good, except that you could have insulin resistance. I am your age and have 8% body fat. Exersize well, good diet, my HDL is 112, LDL is 76, Tri's 48. BP is 117/76. Perfect right? Except I have extensive calcification in my arterial tree. I had no idea why until I started checking my blood glucose after meals. Turns out that I regularly go over well 140 on my glucose meter. These blood sugar excursions cause damage to the arterial walls. Note well, that my fasting glucose is 92. Not great but no cause for alarm. I thought I was fine until I started checking my - after meal glucose.
 
@Moose, Have you even done an oral glucose tolerance test? Everything about your numbers looks good, except that you could have insulin resistance. I am your age and have 8% body fat. Exersize well, good diet, my HDL is 112, LDL is 76, Tri's 48. BP is 117/76. Perfect right? Except I have extensive calcification in my arterial tree. I had no idea why until I started checking my blood glucose after meals. Turns out that I regularly go over well 140 on my glucose meter. These blood sugar excursions cause damage to the arterial walls. Note well, that my fasting glucose is 92. Not great but no cause for alarm. I thought I was fine until I started checking my - after meal glucose.
So, what is your strategy to deal with this? What is your carb intake like?
 
So, what is your strategy to deal with this? What is your carb intake like?
Sorry it took so long to reply @JimBob.
I went very low carb starting 1/1/2019. I eat less than 50 total grams carb / day. On a net carb basis it is usually 35 or less. Many days I am at 30 grams of net carb.

The low carb diet has been a real pain in the rear to get right. My physical performance suffered immensely and I was always very tired.

I have recently discovered that I was doing 2 things wrong. #1, I was getting around 300g of protein/day. Way too much for me. I need to be below 200g. #2, I was not getting enough salt. I need to consume 3 teaspoons a day in order to feel right. My gym performance has gotten much better since making these 2 changes.

I have noticed that since I have lowered my protein intake, that my blood sugar has been behaving much better. With the higher protein, even while being super low carb, my blood sugar would climb into the 120's after eating. Now it stays under 110.
 
I have an LAD stent after angina with exertion at age 54, no MI, 95-98% occlusion.

LPa 6, ref range <30mg/dl

No other significant risks in Cleveland Heart labs/lipidology, Previous heart scan showed tiny-minimal calcification way downstream in a R side artery, not considered a risk.

Not overweight, active, no diabetic troubles or insulin resistance, etc.

Only ongoing marker not ideal, low-ish HDL

Shit happens regardless of your numbers.

I'm curious: did you have Apo B / Apo A-1 or an NMR lipid panel done? MPO, hs-CRP, and/or LP-PLA2?
 
2 years after the stent and after discontinuing Lipitor I had Cleveland heart labs dome which included NMR (attached).

And LP-PLA2 77 range <75

You can imagine I was concerned for any numbers out of range, and I grilled the cardiologist and functional med docs about it. Both said they were unconcerned since the rest of the numbers were so good. And this was with both knowing the stent history

I have also had CRP tested though I don't know about the "hs" aspect. CRP has never been high.

I am interested in any observations/comments on this.
 

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2 years after the stent and after discontinuing Lipitor I had Cleveland heart labs dome which included NMR (attached).

And LP-PLA2 77 range <75

You can imagine I was concerned for any numbers out of range, and I grilled the cardiologist and functional med docs about it. Both said they were unconcerned since the rest of the numbers were so good. And this was with both knowing the stent history

I have also had CRP tested though I don't know about the "hs" aspect. CRP has never been high.

I am interested in any observations/comments on this.

Thank you for sharing, this is very interesting. I'm by no means an expert - I just have a family history of cardiovascular disease so I've been researching it for a long time now in an attempt to stay on top of my health.

My understanding is that LDL particle count is an independent predictor of atherosclerosis development, and maybe the most important single predictor. Dr. Peter Attia has an excellent blog series on this, and says "If you want to stop atherosclerosis, you must lower the LDL particle number". The whole series is worth a read - highly recommended.
 
Thank you for sharing, this is very interesting. I'm by no means an expert - I just have a family history of cardiovascular disease so I've been researching it for a long time now in an attempt to stay on top of my health.

My understanding is that LDL particle count is an independent predictor of atherosclerosis development, and maybe the most important single predictor. Dr. Peter Attia has an excellent blog series on this, and says "If you want to stop atherosclerosis, you must lower the LDL particle number". The whole series is worth a read - highly recommended.

I read that article, but just drove 1900 miles and am a bit foggy. The one thing that stood out for me is that his argument cites relative risk figures, which typically drastically amplifies actual comparative statistics... exactly the same kind of mathematical manipulation that touted lipitor as reducing cardiac risk by 36% based on closer to 2% vs 3% actual comparative data (and some decimals, my grey matter hasn't kept the decimals stored). The 2% vs 3% would be 33% relative risk reduction... i.e. without lipitor 3 out of a hundred people have events, and those taking taking lipitor 2 out of 100 have cardiac events. That's 1% comparatively, but 33% RRR. So seeing 6.2 relative risk tells me that potentially the actual comparative data is very possibly in the decimal point range. This is rampant in medical research and drug marketing. Will be interesting to see actual comparative data.
 
I read that article, but just drove 1900 miles and am a bit foggy. The one thing that stood out for me is that his argument cites relative risk figures, which typically drastically amplifies actual comparative statistics... exactly the same kind of mathematical manipulation that touted lipitor as reducing cardiac risk by 36% based on closer to 2% vs 3% actual comparative data (and some decimals, my grey matter hasn't kept the decimals stored). The 2% vs 3% would be 33% relative risk reduction... i.e. without lipitor 3 out of a hundred people have events, and those taking taking lipitor 2 out of 100 have cardiac events. That's 1% comparatively, but 33% RRR. So seeing 6.2 relative risk tells me that potentially the actual comparative data is very possibly in the decimal point range. This is rampant in medical research and drug marketing. Will be interesting to see actual comparative data.

I think the way I'd think about it: what could the causal agent be for your event? Not being an expert but looking at what you've shown here, my best guess is your LDL particle count. In some people, maybe that particle count with that HDL never leads to any kind of event. But there are factors that can't be easily measured (in particular, HDL function -- not count). So I would think that reducing your particle count will likely reduce your future risk.

There are some very promising new, non-statin drugs -- PCSK9 inhibitors (a bit pricey, but depending on your budget may be very worth it) and bempedoic acid (coming soon) come to mind.
 
I think the way I'd think about it: what could the causal agent be for your event? Not being an expert but looking at what you've shown here, my best guess is your LDL particle count. In some people, maybe that particle count with that HDL never leads to any kind of event. But there are factors that can't be easily measured (in particular, HDL function -- not count). So I would think that reducing your particle count will likely reduce your future risk.

There are some very promising new, non-statin drugs -- PCSK9 inhibitors (a bit pricey, but depending on your budget may be very worth it) and bempedoic acid (coming soon) come to mind.

I am absolutely not interested in cholesterol lowering meds. No way. Been there, done that. nearly killed me. Lipitor and lowered cholesterol was not a solution. These novel drugs also reduce total cholesterol. I am not going to do that... period.
 
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I am absolutely not interested in cholesterol lowering meds. No way. Been there, done that. nearly killed me. Lipitor and lowered cholesterol was not a solution. These novel drugs also reduce total cholesterol. I am not going to do that... period.

I'd highly encourage you to read more about these new drugs with an open mind.

PCSK9 inhibitors work using an entirely different mechanism than statins, and do not have the associated side effects.

Statins slow the body's own production of cholesterol at the cell level, and do so in every cell in the body. This has the effect of lowering LDL particle count, but it also means that if the statin is inappropriately dosed (or the individual is just susceptible to the side effects), some cells may not get enough cholesterol (that's my layman's understanding). There are also side effects of the inhibition of the enzyme directly, e.g. needing to supplement with Coq10, etc.

PCSK9 inhibitors do something totally different: they up-regulate the number of LDL receptors inside your cells. So the LDL particles can still fly around inside the body, and when a cell wants some cholesterol, it can get it. But it means there's less free-floating LDL that's /not/ being used by a cell at a given time, so it reduces the LDL particle count. It's like adding a bunch of lanes to a freeway, and statins are like slowing the freeway (sort of).

Total cholesterol decreases but that has no effect on a cell's ability to get cholesterol when needed. Total cholesterol is just a measure of how much cholesterol (sum) is in the blood, not a measure of how well cells can get or create cholesterol.
 
Thank you for sharing, this is very interesting. I'm by no means an expert - I just have a family history of cardiovascular disease so I've been researching it for a long time now in an attempt to stay on top of my health.

My understanding is that LDL particle count is an independent predictor of atherosclerosis development, and maybe the most important single predictor. Dr. Peter Attia has an excellent blog series on this, and says "If you want to stop atherosclerosis, you must lower the LDL particle number". The whole series is worth a read - highly recommended.
Of course, there is much debate over the significance of the LDL-P number...much. As an aside, I see that Dr. Attia blocked Dr. David Diamond from his Twitter account very recently.

 
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