Thoughts on Nick Hiebert on Mark Bell's Power Project

Introduction

Here’s the prior installment in what I hope will not become a series: “Thoughts on Nick Hiebert's “A Comprehensive Rebuttal of Seed Oil Sophistry” (Goodrich, 2021b)

I concluded that post with this quote:

“Falsus in uno, falsus in omnibus” is a Latin term which means "false in one thing, false in everything." It in fact is a legal principle in common law that a witness who testifies falsely about one matter is not at all credible to testify about any other matter” (Bansal, 2018)

Nevertheless, Mark Bell had Nick on his podcast (Bell,2022a, 2022b), which I had appeared on previously (Bell,2021; Goodrich, 2021a).

Nick at one point calls me a “pathological liar”, and makes a bunch of claims about positions I have taken or claims I have made. As with the prior post, I don’t have enough time to go through all of Nick’s claims*, so here are a few highlights and as in the prior post:

“I am doing this in the manner of an audit. I’m not going to go through the whole thing, but until I have a feeling that I can assess the quality of the argument to my satisfaction, and hopefully to that of the reader.”

(I think it’s Chris Bell on the left, Mark Bell in the middle, Nsima Inyang on the right, and Andrew Zaragoza behind the screens. Nick is at the bottom. If I’m not correct, I apologize, but that’s how I am attributing the quotes.)

Heated oils and health

Mark Bell: “But when they are heated up, because that’s the complaint… when they’re heated up and we use them for cooking, they’re a shitty fat and they’re bad for us.”

Nick: “Well with the limited data that we have on the subject, would largely suggest that the benefits survive heating. It’s only really been robustly investigated, like a few times. There is one systematic review on the results and the results seem to suggest that the benefits survive heating.”

The International Agency for Research on Cancer says:

“Since the 1970s, a total of 17 case–control studies have explored the relationship between exposure to cooking fumes and the risk for lung cancer.”

“Mechanistic data show the probable involvement of peroxidation products of polyunsaturated fatty acids [PUFA: of which seed oils are primarily comprised]; however, the involvement of polycyclic aromatic hydrocarbons, which have also been detected in cooking oil emissions, cannot be discounted.”

“On the basis of limited evidence in humans and sufficient evidence in experimental animals, the Working Group concluded that emissions from high-temperature frying are ‘probably carcinogenic to humans (Group 2A)’”. (IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; Straif et al., 2006)

The section of the IARC monograph on cooking oils and cancer (“High-temperature frying”) is 95 pages long (IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010), so it’s hardly been looked at only “a few times”, as Nick claims.

The type of cancer that is thought to be caused by cooking oils is increasing world-wide, as (Fidler-Benaoudia et al., 2020) found in a study of 40 countries:

“In this international study, the authors found that, while lung-cancer rates have declined among younger men, they are rising among younger women, despite the fact that these women are not smoking more than men. Adenocarcinoma appears to account for much of this increase.”

So other than lung cancer, they’re fine. Just don’t use cooking oils for cooking.

Nick: “I don’t see any persuasive evidence that heating the oil significantly reduces the health value.”

Red meat and disease risk: do we need evidence?

Chris Bell: “How does read meat influence disease risk? What is the mechanism there?”

Nick: Goes on for a bit, then: “We don’t really need a mechanism for causal inference.”

At some point you do, of course.

0 out of 52 claims from epidemiological studies replicated.
100% failure rate. (Young & Karr, 2011)

But if you are trying to impress with observational (observational = epidemiological) studies, this is a handy claim to make. Unfortunately, it’s not supported by the evidence: “Any claim coming from an observational study is most likely to be wrong” (Young & Karr, 2011). In that particular paper, they examined 52 different claims of causation based on observational studies, which were then tested to determine if the inferred mechanism actually worked—the point of causal inference is to infer a mechanism that might cause the effect observed, hence the name.

“The 12 clinical trials tested 52 observational claims. They all confirmed no claims in the direction of the observational claims. We repeat that figure: 0 out of 52. To put it another way, 100% of the observational claims failed to replicate. In fact, five claims (9.6%) are statistically significant in the clinical trials in the opposite direction to the observational claim” (Young & Karr, 2011)

Lest you think I’m citing an irrelevant finding, here are two of the foremost epidemiologists in the world (Walter Willett and John Ioannidis) discussing this paper (Swiss Re, 2018 Starts at 23:41), which was co-authored by the Director of the National Institute of Statistical Sciences.

Given such a success rate, who would believe “causal inference” without a confirmatory, mechanistic study?

Chris Bell: “Were these randomized, controlled trials, or are these epidemiological trials…?”

Nick: “They’re epidemiological studies, but I don’t think there’s anything persuasive that disqualifies epidemiological evidence—of a certain quality—from being able to inform a causal inference.”

Only the epidemiological studies of the highest quality ever merit a confirmatory RCT. Still looking at a 0% success rate.

So Nick claims epidemiology is enough, but the scientific literature contradicts him. Epidemiology is clearly never enough.

Debate with Alan Flanagan

Nick: “…He dodged pretty much every single point that Alan made, in fact there was one primary point that Alan made at the very beginning of the debate that Tucker dodged and they never got back to it…” Nick goes on with some attacks against Alan.

So I went back to identify this moment in the debate. I’m now 45 minutes into it, and still haven’t come to this moment.

Nick: “Almost every single point that Tucker brought up was completely and utterly tangential to the debate proposition that Alan had laid out at the beginning of the debate.”

Nick still hasn’t identified what that proposition was, exactly.

As I review the debate, Mark introduced our discussion, “I think probably the most appropriate way to kick off the show, is maybe just get a little bit of background, and then if one of you guys doesn’t mind sharing how we got to this point…” Alan introduced himself and his argument, then I introduced myself and went through Alan’s argument from the article he wrote that started this whole debate.

I can’t find any proposition, in fact the debate starts off with a question from Mark: “Wouldn’t these metabolic diseases be more spawned from simply overeating?...” I let Alan answer first. This was 26 minutes into the video. He continues for 6 minutes without any interruption, from me or the hosts. (In reviewing this, btw, let me compliment Alan: he did a great job of presenting his position, I think, even if I don’t agree with some of it.) Alan then lets me go on until 37 minutes (“Words, words, words,” as my wife would put it). At this point we get into a more back-and-forth part of the debate, where we discuss part of my introductory statement. But don’t take my word for it, watch it.

At 45 minutes into the video, we were still discussing the change in dietary behavior and what might have caused that, and I was discussing Rimonabant, gastric bypass surgery, and the relevance to the change in food intake that Alan had highlighted. When are we out of the “beginning of the debate”?

Rather than “dodging” as Nick claims, I was providing an explanation for a phenomenon that Alan had correctly highlighted as being crucial: overconsumption of calories.

So after inventing this moment, Nick goes on to call me a “pathological liar”.

“I contacted primary researchers…”

Nick: “Many of his claims were straight-up false. Absolutely false. False to the point where I contacted primary researchers that he was citing, and they told me that Tucker was out to lunch.”

Chris Bell: “One of the things that he did bring up, kind of the only thing that got me, was when he brought up, I think it was soybean oil, using soybean oil as a medication and a bunch of people got sick, was that bullshit?

Nick: “I could go into that…”

In reviewing this, it’s interesting that Chris happened to bring up exactly the anecdote that Nick had alluded to, without Nick having been specific enough for anyone not already familiar with Nick’s claim to know what he was referring to.

Chris Bell: “I’d love to. I’d love to hear it.”

Nick: “I could go into that. See, that is one of the cases where Tucker made something up… But what he said about Intralipid [(Sigma-Aldrich, Inc., 2020)] which was the soybean-oil-based lipid emulsion that was used on those children, what he said about it was false, utterly false. I contacted the primary researcher that he credits with the discovery of linoleic acid as a hepatotoxin? She told me that he needs to read the publications again, because he got it wrong. [He goes on for a bit in this vein], and why he was spreading misinformation about her publications…

The researcher in question (not the primary researcher on these papers, that was Mark Puder) is Kathleen Gura. She’s part of a team from Boston Children's Hospital that identified the cause of liver failure in children put on Intralipid for Parenteral Nutrition (PN). These are often children who have an intestinal problem that prevents them from eating normally, so Intralipid is infused into their veins to bypass the intestinal tract. Liver disease is an unfortunate consequence of this procedure, in from 74 to 85% of the patients, and 27% go on to die from liver failure (Nandivada et al., 2015).

Gura figured out how to prevent this from happening, and the means to do that was by switching from soybean-oil-based Intralipid to fish-oil-based Omegaven (Diamond et al., 2009). One of the differences between these two products is the linoleic acid content. Intralipid has a high amount, Omegaven has almost none.

In 2017 Gura gave a talk to parents of patients on PN (Gura, 2017), in which she explained the history of PN and pros and cons of each formula. Here she discussed the reason for switching away from Intralipid:

Kathleen Gura: “So why do we want to reduce the soybean oil when we give IV therapy? Well, we have learned over time that too much omega-6 fatty acids, too much of the pro-inflammatory fatty acids may not be good in many different patient populations, so we want to decrease it in our diet.”

I'm not wasting more time on this guy. He claims I'm making up the Intralipid claim, apparently. Here's the woman who did the research, in her own words.

Nick, you need a new hobby.https://t.co/CJAsvf9Rbt pic.twitter.com/pyEQGE3XM7

— Tucker Goodrich (@TuckerGoodrich) August 25, 2021

Of course the primary omega-6 fat in our diet and in Intralipid is linoleic acid, as you can see it the slide  from her presentation, above. Note, she doesn’t give any other reason for getting rid of Intralipid, which causes liver failure in human children, except for “decreases linoleic acid load”. She goes on to explain that a high omega-6 to omega-3 ratio, like that found in Intralipid, is “very unhealthy”.

Some folks weren’t convinced that a formula like Omegaven was a good idea, due to the extremely low levels of linoleic acid (Klek et al., 2018). So Puder’s group went on to show that linoleic acid was not required in humans (de Meijer et al., 2010), or in animals(Carlson et al., 2019), thus overturning a scientific mistake that has persisted from the 1930s (Burr & Burr, 1930).

“Altogether, these findings question the notion of the true essentiality of ALA and [linoleic acid] for cognitive development and growth.” (Carlson et al., 2019)

Gura convinced the FDA of the benefit of Omegaven, getting it approved (Gura et al., 2020; Gura & Puder, 2018), and additionally convinced the FDA that the harm from other formulas did not occur with Omegaven, thus getting the mortality warning removed (Nussbaum et al., 2018).

Extraordinary claims require extraordinary evidence. Nick says he has an email from Gura claiming that she now disavows her claims of causation in the above video, and the subsequent years of work they did on convincing the world that it's OK to reduce linoleic acid.

Or it maybe the email doesn’t exist. We’ve been waiting since August.

Priceless.

Call up Harvard's PR department. This should be good.

Correctly, she disagrees with Nick's misrepresentation of me, since all I did was post her speech. https://t.co/tzdMPw0VGx pic.twitter.com/gnuzWKteQi

— Tucker Goodrich (@TuckerGoodrich) August 26, 2021

P.S. 2022/02/09: Nick (thanks to JR in the comments—Nick still blocks me), has released the email exchange with Gura. See below.

“It’s a plant oil thing, it’s not a linoleic acid thing…”

Nick: “Here’s the thing, they actually know why vegetable oil, or plant oil—it’s a plant oil thing, it’s not a linoleic acid thing—they know why this happens to the children, it’s because of the phytosterol content. Because when you… actually inject people with phytosterols, it does fucking things to their livers…

“There is a rodent study where they take soybean-oil-based lipid emulsion and then fish-oil-based lipid emulsions which don’t have phytosterols, they add the phytosterols to the fish-oil emulsions, and you see the exact same pathology.”

“It’s not a function of linoleic acid, they have causality here.”

(Fell et al., 2019)

The paper Nick seems to be referring to is another Puder/Gura effort, this one from 2019 (Fell et al., 2019). What do they find? From the abstract:

“Phytosterols do not appear to compromise the hepatoprotective effects of fish oil.”

In direct contradiction to Nick’s claim:

“A fish oil emulsion (FO) and an emulsion of fish oil containing phytosterols (FO+P) protected from steatosis [liver damage] in this model.”

So no difference. Fish oil with phytosterols did not harm the liver.

Nick got it entirely wrong.

Soybean oil, unsurprisingly, had the expected negative effect on the liver.

Conclusion: “Falsus in uno, falsus in omnibus”

Nick kind of goes off the rails after this, it’s consistent personal attacks, and not just on me.

It’s pretty clear from this and the previous post of mine that he’s not a reliable source of information. The only way to explain the misrepresentation of the two studies above is that he’s obviously using them to attack me, facts be damned.

I keep hoping to stop wasting time on him, maybe after this I will get my wish.

P.S. 2022/02/09

Here’s the email exchange:

From (Hiebert, 2022).

So in the falsus in uno vein, I’ll note that Nick asks her for permission to reproduce this, doesn’t receive it, and does so anyway. His “redaction” is a joke, it’s obvious who it is from, she includes her paper “The Power of Networking and Lessons Learned From Omegaven”, of which she is the sole author (Gura, 2020), and the title is clearly visible.

Reminds me of a line from the movie Animal House…

As she concludes, “Direct your audience to the published literature.” For that, see above.

Nick asks her:

“An individual with a very large following [Thanks, Nick!] is using your publications to make a… claim… that lipid emulsions containing linoleic acid uniquely cause liver dysfunction and fatty liver disease…”

Her answer is non-responsive to the liver aspect, but carefully worded:

“All lipid emulsions contain some linoleic acid or its downstream metabolite, arachidonic acid. Whoever said otherwise is misunderstanding something.”

Emphasis mine. Well, it certainly wasn’t me that said it, and it’s not the question Nick was asking her. I covered her 2019 paper, as quoted above:

“Altogether, these findings question the notion of the true essentiality of ALA and [linoleic acid] for cognitive development and growth.” (Carlson et al., 2019)

In my 2020 blog post (Goodrich, 2020), noting that this disproves the requirement for LA, but the requirement for AA remains (hence her “or”).

Nick tries to redirect her (“He doesn’t claim that LA is not essential”—but I do!), but she avoids the question (“He claims it took you 14 years…”), saying what took 14 years was getting Omegaven approved (Gura, 2020).

She obviously doesn’t want to get in the middle of a dispute between two strangers about linoleic acid, or harms.

Why do I say that?

Serendipity is God’s gift, and while looking for something completely different this morning, I came across (Dockser Marcus, 2006), a Wall Street Journal article about Puder, Gura, and Omegaven:

"Early on, Dr. Puder alienated some colleagues, especially with his inflammatory words that the standard IV nutrition product given to babies may be one of the causes of the liver damage. Fresenius Kabi also makes that product. The company says it has no concerns about its safety.

“Dr. Puder says colleagues who, unlike him, had worked for years in the field, flat out told him he was wrong in thinking the standard lipid solution was the cause of the liver damage.

“He even started calling Intralipid, the standard formula, ‘the white poison,’ a term that he says didn't go over well with the other doctors. ‘It caused a firestorm at the hospital,’ he recalls.

“In Nov. 2003, at a weekly clinic of those in the short bowel syndrome program, Dr. Gura says colleagues told her Dr. Puder needed to be more judicious in how he presented his findings. Intralipid had been used in patients for decades. His mouse data wasn't even published yet.

“She noted that he seemed angry when he left the hospital the previous day. In her email, she reminded him, 'politics always plays into things.'”

So Nick’s smoking gun turns out to be a damp squib, once again, it doesn’t say what he claims it said.

He can keep pushing the white poison if he would like.

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*(This means I have to listen to it again, so please pray for me. When I started listening to this, I had no intention of responding to it, but since Nick slanders me (IMHO) I don’t feel that I have a choice.)

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