Anybody interested in a lipid chat with Dave Feldman?

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Re: Anybody interested in a lipid chat with Dave Feldman?

Postby DaveKeto » Thu Dec 13, 2018 5:04 pm

cdamaden wrote:
floramaria wrote:... I find everyone’s explanations convincing, though mutually exclusive!

I agree. The thing frustrating to me, and was at the root of the question I asked Dave, was whether they are even looking at the same evidence. (Dave focused on how bias affects us all, which is true, but doesn't get to the heart of the question.) I would like to see a dialogue on what team A says is their most compelling evidence, then team B says what theirs is, and then require each team to discuss why the other team's evidence doesn't convince them to change their views. I feel like there is a lot of discussion on why team A (or B)'s model is flawed but less on debating the implications of experiments X, Y, and Z.

I would also add that Dave is very gracious and a model of humility and civility. It seems that many of the other members debating these points are too quick to be dismissive of other perspectives (those low carb people, those establishment lipidologist, those people who dismiss HDL, chortle chortle), which I guess is a bit of human nature and tribal but disappointing nonetheless. I lose a lot of respect for those who use ad hominem justifications.


-- It's a very fair point with regard to looking at different data, coming to different conclusions and so forth. We see this especially with nutrition science.

This is why I specify a distinctive model by which I'm coming to these conclusions. Thus, my assertion is falsifiable -- hence the "#LCCholesterolChallenge" ( https://twitter.com/DaveKeto/status/963437664199352322 ). Something being falsifiable is at the heart of science. And I wouldn't be surprised if I have some things wrong. Indeed, I'm looking for it.

In other words, instead of grabbing studies A, B, and C that make a case while ignoring X, Y, and Z that dispute it, you make a hypothesis that *any* study (of merit, of course) can nullify. This is what I was getting at the end of the podcast with Peter. I was explaining how I'd like to get a very large dataset to test my hypothesis and test his counter-hypothesis as well.

This exchange toward the very end is where I sought to identify this:

Dave Feldman
The thing we’re dancing around here is, obviously when you have high HDLC and you have low triglycerides, it suggests a number of different things. But, more broadly, it’s suggesting a properly functioning lipid energy system, and probably not being in a state of challenge-

Peter Attia
HDLC tells us absolutely nothing. If we’ve seen enough from Mendelian randomizations and in other, how many more CTEP failures do we need to see? HDL cholesterol tells us nothing about HDL function. In fact, any time you increase HDL cholesterol pharmacologically, you seem to make patients worse.

Dave Feldman
I know, but these are modifications to the existing lipid system. If you block cholesterol-

Peter Attia
I get that, Dave. But, boy, if you’re gonna hang your hat on it’s all about HDLC triglyceride, I mean, wow, we are so far beyond that in the lipid world at this point. If you’re gonna go through this brain damage, make it for something worthwhile.

Dave Feldman
But, wouldn’t you predict right now, that if I did hang my hat on those two things, on those two markers, against LDLC or ApoB or LDLP, that it would fail. That if I were to say, “Hey, I wanna get a stratification just of high HDLC and low triglycerides.” That you’d say, “Sure, Dave.” I’ll bet you $10,000, I’ll give you 100 to 1 odds, those people with high LDL, even if you stratify for those two, will still have high rates of cardiovascular disease.

Peter Attia
Again, I’d have to completely see the patient population before I could even hazard a guess.

Dave Feldman
But, right now, you would assume that. Right?

Peter Attia
I am going to assume that LDLP is going to be a stronger maker of prediction than HDLC.

Dave Feldman
And that’s not what I’m making the case on. What I’m making the case on is, whether or not there’s a properly functioning lipid metabolism, which would be indicated by all three of those.

Peter Attia
No, you have absolutely no understanding of the lipid metabolism by looking at HDLC and triglyceride.

Dave Feldman
I think-

Peter Attia
Not even close. No, no, no, we can disagree on things that are nebulous. This is not nebulous, Dave. I mean, you do need … Again, I hate that I’m saying this, because I sound like a jerk and I don’t mean to. You’ve got to spend more time with lipid people, you really do. . . . You’re not dealing with your peers at this. You have to go and figure out … I mean, HDLC is just categorically not a useful metric. It is like a first order term on a … No, it’s not even that. In engineer-speak, it’s the fourth order term on a fifth order polynomial.


The larger point I was emphasizing is that I'd be willing to make the bet on HDLc+TG being more relevant (it's falsifiable), and I'd suspect one who believed in the Lipid Hypothesis would take the other side of that bet. It would have been enjoyable if we could both agree on this fundamental, testable assertion before I succeed at getting these data sets queried (a project now in progress).
Last edited by DaveKeto on Thu Dec 13, 2018 5:09 pm, edited 1 time in total.

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Re: Anybody interested in a lipid chat with Dave Feldman?

Postby DaveKeto » Thu Dec 13, 2018 5:06 pm

mike wrote:One thing that I was a bit surprised by during the podcast - the folks who asked questions had their name mentioned. I don't particularly care, but some might. If this is going to be the way of it going forward, you might want to put a disclaimer in there some place. :?


Fair point, Mike. I assumed the opposite, that people would want to be identified for the question they had asked.

But it would be a lot more private and less time consuming to just read the questions directly. Excellent suggestion. :)

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Re: Anybody interested in a lipid chat with Dave Feldman?

Postby slacker » Thu Dec 13, 2018 5:11 pm

Perhaps I'm not the only one who didn't know what falsifiable means...

Falsifiability is the capacity for some proposition, statement, theory or hypothesis to be proven wrong. That capacity is an essential component of the scientific method and hypothesis testing. In a scientific context, falsifiability is sometimes considered synonymous with testability.


More on this here.
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Re: Anybody interested in a lipid chat with Dave Feldman?

Postby Julie G » Thu Dec 13, 2018 6:31 pm

I would also add that Dave is very gracious and a model of humility and civility. It seems that many of the other members debating these points are too quick to be dismissive of other perspectives (those low carb people, those establishment lipidologist, those people who dismiss HDL, chortle chortle), which I guess is a bit of human nature and tribal but disappointing nonetheless. I lose a lot of respect for those who use ad hominem justifications.

Amen! Deep bow, Dave. Thank you for both for your generosity to us and your ongoing work. In many ways you epitomize the spirit of our project, using your N=1 to elucidate science.
I would like to see a dialogue on what team A says is their most compelling evidence, then team B says what theirs is, and then require each team to discuss why the other team's evidence doesn't convince them to change their views.

Agree. I feel like this is the missing component for those of us who’ve “survived” the Dayspring/Attia series, then listened to the Feldman/Attia interview. I think we did a good job of giving Dave a platform to rebut Peter’s arguments… but it felt a bit hollow without Peter responding. One of my problems with the entire Daysping/Attia interview is that they started from a place of (paraphrasing) “people used to die in droves from myocardial infarctions and now they’re not” implying that this somehow proves the lipid hypothesis. I wish Dayspring had started by providing his top five studies that reducing LDL-P is paramount to preventing heart disease. It was just accepted as fact throughout the interview likely because the interviewee was in agreement; a bit of an echo chamber.

I think Dave did a great job of defending his hypothesis yesterday. The fact that nobody can find a study that shows LDL-C to be an issue in the presence of high HDL-C and low TGs is strongly corroborative. I’m less convinced that arbitrarily raising TC to prevent mortality is a safe strategy for everyone. While Dave’s evidence on all cause mortality was compelling, TC, by itself, tells us very little and could encompass low HDL-C and high TGs at the same time which could prove dangerous for some, especially for those with a strong family or personal history of heart disease. IMHO, ratios matter a lot with a low TG/HDL being paramount. Additionally pursuing a low particle count, may be a smart bet, especially if you have any other risk factors, like insulin resistance, smoking, excessive stress, etc.
One thing that I was a bit surprised by during the podcast - the folks who asked questions had their name mentioned. I don't particularly care, but some might. If this is going to be the way of it going forward, you might want to put a disclaimer in there some place.

Agree, apologies! We didn’t think about privacy issues and will be more careful next time, just using first names. We could even encourage people to sign up with just first names or even pseudonyms.
Julie, you mentioned at one point that folks who are IR can't fast. I've done three extended water fasts, so does that mean that I'm NOT IR? My glucose levels are very high...

Yes, Mike, that was my experience, shared by many. I’m very impressed with the fact that you can do multi-day extended fasts and suspect that you’re on the right path as evidenced by your progress. I’ve previously mentioned that I thought you might benefit from slowly replacing some of your protein (160 g a day?) with high quality fat to see if that promotes continued healing. I’m not qualified to comment on whether or not you have IR, especially given your ongoing diabetes. What do you think?

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Re: Anybody interested in a lipid chat with Dave Feldman?

Postby MarcR » Thu Dec 13, 2018 9:13 pm

Julie G wrote:
One thing that I was a bit surprised by during the podcast - the folks who asked questions had their name mentioned. I don't particularly care, but some might. If this is going to be the way of it going forward, you might want to put a disclaimer in there some place.

Agree, apologies! We didn’t think about privacy issues and will be more careful next time, just using first names. We could even encourage people to sign up with just first names or even pseudonyms.
I actually did think about this. That's why I made Last Name optional in the registration - the default Zoom Webinar registration setting is required. I figured those for whom anonymity is important would use their forum handles, their real first names, or something else in the required field and leave Last Name blank.

Generally, the webinar model is patterned after the seminar, which is a professional event attended in person by people whose real life identities are usually known to one another. I think that's the right default approach as long as we continue to enable those for whom anonymity is important to protect their identities.

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Re: Anybody interested in a lipid chat with Dave Feldman?

Postby MarcR » Thu Dec 13, 2018 9:58 pm

Julie G wrote:I’m less convinced that arbitrarily raising TC to prevent mortality is a safe strategy
I didn't perceive anyone to be espousing that point of view at the webinar, but my own views are close enough that I feel the need to clarify.

This is what I think:

1. Using drugs that interfere with lipid biochemistry probably increases all cause mortality (ACM).
2. Using lifestyle to reduce or increase LDL or LDL-P may reduce or increase ACM.
3. Using lifestyle to optimize the biomarkers in the metabolic syndrome definition while trusting one's body to manage LDL and LDL-P almost certainly reduces ACM.

"Arbitrarily raising TC" would fall under item 2.

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Re: Anybody interested in a lipid chat with Dave Feldman?

Postby mike » Fri Dec 14, 2018 10:21 am

MarcR wrote:Agree, apologies! We didn’t think about privacy issues and will be more careful next time, just using first names. We could even encourage people to sign up with just first names or even pseudonyms.

I actually did think about this. That's why I made Last Name optional in the registration - the default Zoom Webinar registration setting is required. I figured those for whom anonymity is important would use their forum handles, their real first names, or something else in the required field and leave Last Name blank.


As I said, I didn't really care, but I was also surprised, so obviously didn't pick up the required/optional fields. You just might want to put in a clarification so it is more clear to us folks who can't read ;)
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Re: Anybody interested in a lipid chat with Dave Feldman?

Postby mike » Fri Dec 14, 2018 11:00 am

Julie G wrote:Agree. I feel like this is the missing component for those of us who’ve “survived” the Dayspring/Attia series, then listened to the Feldman/Attia interview. I think we did a good job of giving Dave a platform to rebut Peter’s arguments… but it felt a bit hollow without Peter responding.

And Attia starting his podcast with the reasons why he doesn't agree with Feldman, without Feldman being able to respond was better!? You let Dave rebut those three points in our podcast - I think that is just continuing the dialog. It will be these guys that will battle it out, trying to prove their own theories, and likely falsify someone else's. This is science. I had a year of Biochem in college, but that was 35 years ago. I can look at this stuff, but it takes numerous viewings to even feel like I'm approaching some understanding. We can push and prod, but ultimately, it will be these guys, in their back and forth, that hopefully figure this out.

I’m not qualified to comment on whether or not you have IR, especially given your ongoing diabetes. What do you think?

Julie, I'm rather confused myself. I need to get testing done. It has been about 5 weeks since I ended my last fast, so I will do in about a week. I had a c-peptide test done about 15 months ago, between my first two fasts, and it was in low normal range at 1.2 ng/ml. So I'm still making some insulin. From experience, my sugars climb quickly with only small amount of carbs - I certainly have no phase 1 insulin response, and it takes blood sugar a long time to come back down. The wiki discusses causes of IR, but not how to test for it... Do you, or anyone else know of good tests to have done to determine IR?
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Re: Anybody interested in a lipid chat with Dave Feldman?

Postby Ski » Fri Dec 14, 2018 11:41 am

What I find puzzling is the "need" for someone to be 100% right or the tone against certain strategies, especially a topic as complex as lipids. I can certainly see some frustration when one ultimately doesn't have any risk factors and is trying to choose the right path, but if you do have identified risk factors, you owe it to yourself to pick a path and experiment.

I see folks in the forum who may follow a practitioner and their theories, which are based a lot on association, with no clear evidence, but it works for them.

I certainly have shown to have completely different results to Dave Feldmans experiment as well as Dr Masons theory. So because anyone says this is how it works, doesn't mean that it will work that way with you. Does it make their theory wrong? No, Im sure it is substantiated in many patients. There are so many caveats (genetics) and ways to tweak these different strategies in a way to make them work for you versus taking a blanketed approach to it. People need to have an open mind versus a mentality of "this is how it works for 100% of the population" attitude, especially in this forum where we see so many different N=1 outcomes.

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Re: Anybody interested in a lipid chat with Dave Feldman?

Postby mike » Fri Dec 14, 2018 12:24 pm

MarcR wrote:I'm no doctor, but I would guess that you are hypo- rather than hyper-insulinemic. Perhaps your pancreas was damaged by a prior period of insulin resistance and hyperinsulinemia and no longer has enough functional beta cells to produce sufficient insulin?


Marc, hypoinsulinemic does seem to be a condition that they are researching: http://www.diabetesincontrol.com/intern ... us-part-4/

Apparently most often seen in earlier onset T2D, and less than 1% of adult onset T2D like me. Might be more common in African Americans.

Still seems like exogenous insulin would've helped me if I couldn't produce enough of my own, and I had normal IR. How do I measure IR?
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