CoSci Debate Cromwell, Nadir, Scher: 90 minutes

cholesterol
(Mark Rhodes) #1

This is a must see video if heart disease and lipids plagues your life. Nadir is a friend and my former cardiologist. He actively challenges Dr. William Cromwell, leading lipidologist researcher. This was an active debate and readily moderated by Dave Feldman.

(Robin) #2

Ooh, will watch for sure. Thanks.

#3

Worth listening to. All of the doctors brought up valid points. Including the importance of metobolic health and the importance of an individual patient needing help. There are tools that a doctor can stack with other tools to access the risk or benefit of a certain protocol to employ. It’s not one thing that is suitable for all. Neiter Nadir or Scher questioned Cromwell’s assertion that ‘plaques get smaller if we markedly decrease LDL. Or that lowering LDL and ApoB will stabilize and degrade the formation of new plaque. It effects the natural history of the disease.’ He went further and said, “Does that transfer to a specific outcome benefit or to a morality benefit?”

(Mark Rhodes) #4

I think by that time Nadir felt like he was bullying Cromwell plus Nadir had a presentation to give on his own mental health in less than an hour

(Bob M) #5

The only way to do this would be to use a drug…which could have benefits unrelated to LDL lowering. For instance, if statins benefit mitochondria, maybe that’s what causes “degradation of the formulation of new plaque” and not the lowering of LDL?

#6

So I just finished watching the entire video and I loved it. I loved seeing both perspectives presented respectfully and fairly. Thank you for posting this video. Please post more as they become available.

I couldn’t help being bothered by a silly observation though: that Ali and Scher were sitting twice the distance from each other as Cromwell and Scher yet not once did I see Cromwell make a single attempt to share his mic with Scher so that Dr Ali wouldn’t have to stretch so far every time he wished to speak. Where were his mind and thoughts that he wouldn’t make equal considerations that the other two were making? I didn’t want to let this bother me because I wanted to keep my mind open to all Dr Cromwell was sharing, but it stood out so strongly the entire time.

As always every video that I watch with Dr Ali he makes a wonderful comical comment that cuts through the science and speaks truth: “…you see that the emperor really does not have any clothes.” :rofl: (In regards to actually seeing the real data of these drug trials.)

Some people accuse others of lazy thinking and evasive tactics by overusing metaphors and figures of speech to win followers, and they would be right for a lot of speakers, because that’s really all they do. But Dr Ali has no financial gain to be had like any of them and he first presents sound science, then summarizes the main point the science shows with a comical analogy or metaphor. That’s why I love him.

One very big concern I had that was addressed is the use of AI in our diagnostic futures. I am a victim of poorly outdated diagnostic criteria for hyperparathyroidism that left me with the worst quality of life for over six years until I found doctors out of state that knew the truth, were the world experts on the condition, and whose surgeons literally saved my life by fully curing me. But as I sit here and write this all the hospitals and clinics around me in the Chicago area are still applying the faulty diagnostic criteria and defending it fiercely for God only knows what reasons. Pride? Ego? Fear of Lawsuits? The top surgeons at the top hospital near me (Northwestern Medicine) attacked my choice of clinic for treatment and tried to scare me away from using them with really unprofessional and underhanded comments about them, yet that FL clinic remained gracious in return, telling me the Chicago surgeons didn’t know any better and not to blame them, and that they really were acting in my best interests given the data and experience that they have. I disagree wholeheartedly because the surgeons in FL have long been publishing and communicating their findings for way too long now. This is about egos. How many people are dying 5-10 years earlier because of this disease not being properly diagnosed? It’s more dangerous and critical than high blood pressure or high cholesterol, yet no effort is spent catching it early before it leads to countless other health problems, which it does. The diagnostic criteria were first drafted at a conference where the actual minutes of the meeting show that they had admitted to having no idea what markers were truly accurate to diagnose hyperparathyroidism and that they needed to gather data and reconvene to set proper diagnostic criteria. In the interim they set criteria that they admitted may not be accurate at all but they had to start somewhere. Well they never gathered the data or reconvened and the criteria set became canon that to this date is thought to be sound medical science. The clinic in Tampa FL that I went to DID gather that data over a 30 year period with over 55,000 surgeries and it showed just how wrong the diagnostic criteria being used is, which is why I was left to suffer. An AI system today would plug in that faulty criteria just like the doctors do in person. But because of the faith they will have in AI it stands much less chance of ever being corrected. Garbage in garbage out. And in the present landscape, it is not a far stretch to believe that it would quickly become a tool to benefit pharma and government. If they have the ability to hijack the medical journals, societies, and RCTs in the way that they already have, AI software is going to be a breeze for them to corrupt to their benefit. God help us all.

(Mark Rhodes) #7

I would love to see a seperate post concerning hyperparathyroidism. I have suspected my wife has some issue here and can see no really great resource without falling into the whirlpool. Having a personal experience helps me erect gurdrails. When you have time I am sur eit would benefit others.

Nadir is too gracious to make a big deal abou the mic and it was obvious to the audience that Cromwell’s body posture was very dismissive of Nadir and to a lesser extent Scher.

#8

I am not sure what is going on. You may be correct. There are studies that show statins can have positive effects on mitochondria, as well as other studies that show statins have negative effects on mitochondria.

#9

I would happily create a post, but most of what I would share I got from the website of the Norman Parathyroid Clinic and I’d just be copying and pasting from there, because once something is articulated so well it’s hard to restate it and easier to just link to it.

But I will be more than happy to share my personal experiences in a post. I’ll work on that today for you. I read personal experiences from others that greatly helped me and combined with the NPC information fueled my tenacious desire to take back control of my health. My hyperparathyroidism experience is what led to my searching for the best way to change my diet and that led me to Keto.

(Bob M) #10

Well, I’m not a fan of statins or any LDL-lowering medication solely because of their LDL lowering. I just think that all drugs have multiple effects, and I think that statins in particularly work because of effects other then LDL lowering. (I can’t find the study now, but two dosages of the same statin had basically the same results, though LDL levels were lowered more on the higher dosage.)

But I did find this from Zoe Harcombe, talking about a study:

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https://www.zoeharcombe.com/2022/05/a-new-look-at-statins-ldl-cholesterol-cvd/

So, to the extent that statins “work” for heart disease, it’s likely not because of LDL reduction.

#11

I was asked this question recently. "You were 30 years old, and you had a family history of CVD, heart attacks, strokes, T2D, and obesity running on the male side of your family. Would you be precautionary or preemptive and go on a low-dose statin or a PCSK9 inhibitor? Even though his risk of an event (10 years) is low now? His CAC score was 125 and ApoB 180.

(Mark Rhodes) #12

@ffskier This seems to be the stance of David Diamond. His talk(out soon) was really informative and focused on how LDL really cannot be the issue but Lp(a) and ApoB are more than likely detrimental. Especially with co-morbidities. AND ALMOST certainly if you have a genetic mutation which he did not name. In these case by case scenarios he would consider a statin. After his presentation I asked him would the genetic mutation be Lieden Factor V and he siad no, Factor VIII and I was like “Dammit, I have both!”

(Bob M) #13

@ffskier That’s a tough one. Statins increase CAC score, supposedly making the calcification more “stable” though. Do you know if the person has FH or did the people with heart disease in his family have FH? What type of CVD was it?

@marklifestyle Ugh, it seems like you got some of the worst combinations. I’d guess that statins – to the extent they work – do something with inflammation. I wonder if they also help with coagulation (make it better/less likely to coagulate)?

It’s like with FH and potentially Lp(a), part of the issue could be coagulation. But since all people have is a hammer (drugs that lower LDL), everything is a nail (lowering LDL). No one considers coagulation, other than maybe telling you to take a daily aspirin.

#14

The insulin paradox. The same cholesterol molecule inside HDL is also in LDL. What’s bad is that LDL traffics that cholesterol into the artery wall, where it gets retained and oxidized, and leads to the process of atherosclerosis. HDL does not.

(Bacon is a many-splendoured thing) #15

They may reduce inflammation to some extent, but statins are useless for primary prevention of cardiovascular disease, and have a very small clinical effect in secondary-prevention studies. This according even to studies performed by the manufacturers themselves.

Statins work marvelously to lower LDL, but as you say, that is not an effect that confers any benefit.

(Bacon is a many-splendoured thing) #16

He is referring to such genetic variants as the alleles found in about 50% of people with familial hypercholesterolaemia that make their blood far more likely to clot (mostly variants of fibrinogen and clotting factor VIII, in their case).

Diamond and Ravnskov have asserted in a couple of papers that it is hypercoagulopathy that is at the root of cardiovascular disease, which is why quite a few factors seem to be relevant, since they all promote coagulopathy in one way or another. Kendrick’s thinking seems to be leaning that way, as well.

However, LDL is not one of those relevant factors, and all the science that has actually been done contradicts the hypothesis that cholesterol in any form is a cause of cardiovascular disease.

(Bacon is a many-splendoured thing) #17

In the case of a high-glucose (carbohydrate) diet, the greatly increased glycation of haemoglobin is what promotes coagulopathy, whereas air pollution particulates promote coagulopathy by damaging the glycocalyx of the arterial walls.

(KM) #18

If it were really that simple, wouldn’t an anticoagulant / blood thinner be enough to stop cvd in its tracks? I realize this Is a therapy used, but is it that significantly effective?

(Bacon is a many-splendoured thing) #19

Good point, but anti-coagulant drugs have other, less desirable effects. Even a baby aspirin a day is not without its serious side effects.

Diet is the best treatment, because reducing mitochondrial damage and lowering insulin have many positive long-term benefits and no side effects. No sugar, starches, or grains, and real whole foods are the way to go.

(KM) #20

In English … Sugar makes your blood sticky. :grin: