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.”
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.
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.
*(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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