Showing posts with label Whinging. Show all posts
Showing posts with label Whinging. Show all posts

Monday, October 16, 2023

Podcast Ep 9: Dave Feldman, Citizen Scientist—What Causes Heart Disease

 


Trying something new, thanks to the many issues with Blogger, and Google, in general.

New posts are going to be at the Substack I have set up, I'll make a more complete notice once I figure it out a bit better.

First one is the shownotes for this podcast, and links to the files.

Ep 9: Dave Feldman, Citizen Scientist—What Causes Heart Disease

Monday, November 7, 2022

"A Clue to Rheumatoid Arthritis"

Yeesh. Are there any known endogenous antigens that mimic bacterial infection? And that are *already* known to be involved in Rheumatoid Arthritis? Beuller... Beuller...

Link via AAAS: Keyword search for query

Here's the clue:

Friday, October 21, 2022

Should the FDA Exist? and Heart Disease Linked to Seed Oils—A Neighbor's Choice with David Gornoski

Nice Friday evening discussion. Thank you David!

"David Gornoski is joined by Tucker Goodrich and the two comment on the CDC’s unscientific pushing of the vaccines; the legitimacy of the VAERS system; the legitimacy of the FDA and the CDC; EcoHealth Alliance receiving more grants; seed oil consumption and the rise of coronary heart disease; whether sugar contributes to cardiovascular disease; and more."
Visit A Neighbor's Choice website at https://aneighborschoice.com"

Radio, so no video this time. Podcast:
 

Tuesday, June 28, 2022

Regarding the last three posts...

IFTTT is a social media automation product.

It works, occasionally; it's what auto-posts my Instagram posts to Twitter, and what auto-posts my blog posts to Twitter.

This was an automation I set up years ago, to do I can't remember what.

But the posts I linked to are all dated 2017, so I'm guessing something woke up after five years asleep, and decided to finish auto-posting that stuff.

Too funny.

Thursday, February 3, 2022

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.”

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.)



References

Bansal, D. R. P. (2018). The Doctrine of FALSUS IN UNO, FALSUS IN OMNIBUS & Its Applicability in India. International Journal of Law Management & Humanities, 1(2), 3.

Bell, M. (2021, August 17). Are PUFAs Killing You? Debate Between Alan Flanagan & Tucker Goodrich (No. 575) [Mp3]. https://markbellspowerproject.libsyn.com/ep-575-are-pufas-killing-you-debate-between-alan-flanagan-tucker-goodrich

Bell, M. (2022a, February 1). Nick Heibert: Seed Oils Aren’t As Bad As You May Think ft. Guest Host Chris Bell (No. 670) [Mp3]. https://markbellspowerproject.libsyn.com/mbpp-ep-670-nick-heibert-seed-oils-arent-as-bad-as-you-may-think-ft-guest-host-chris-bell

Bell, M. (2022b, February 1). Nick Hiebert: Seed Oils Aren’t As Bad As You May Think ft. Guest Host Chris Bell (Vol. 670) [Mp4]. https://www.youtube.com/watch?v=omzCi2CGoxo

Burr, G. O., & Burr, M. M. (1930). On the Nature and Rôle of the Fatty Acids Essential in Nutrition. Journal of Biological Chemistry, 86(2), 587–621. https://doi.org/10.1016/S0021-9258(20)78929-5

Carlson, S. J., O’Loughlin, A. A., Anez-Bustillos, L., Baker, M. A., Andrews, N. A., Gunner, G., Dao, D. T., Pan, A., Nandivada, P., Chang, M., Cowan, E., Mitchell, P. D., Gura, K. M., Fagiolini, M., & Puder, M. (2019). A Diet With Docosahexaenoic and Arachidonic Acids as the Sole Source of Polyunsaturated Fatty Acids Is Sufficient to Support Visual, Cognitive, Motor, and Social Development in Mice. Frontiers in Neuroscience, 13, 72. https://doi.org/10.3389/fnins.2019.00072

de Meijer, V. E., Le, H. D., Meisel, J. A., Gura, K. M., & Puder, M. (2010). Parenteral Fish Oil as Monotherapy Prevents Essential Fatty Acid Deficiency in Parenteral Nutrition Dependent Patients. Journal of Pediatric Gastroenterology and Nutrition, 50(2), 212–218. https://doi.org/10.1097/MPG.0b013e3181bbf51e

Diamond, I. R., Sterescu, A., Pencharz, P. B., Kim, J. H., & Wales, P. W. (2009). Changing the paradigm: Omegaven for the treatment of liver failure in pediatric short bowel syndrome. Journal of Pediatric Gastroenterology and Nutrition, 48(2), 209–215. https://doi.org/10.1097/MPG.0b013e318182c8f6

Dockser Marcus, A. (2006, November 13). A Doctor’s Push For Drug Pits Him Against Its Maker. Wall Street Journal. https://www.wsj.com/articles/SB116338867216321332

Fell, G. L., Anez-Bustillos, L., Dao, D. T., Baker, M. A., Nandivada, P., Cho, B. S., Pan, A., O’Loughlin, A. A., Nose, V., Gura, K. M., & Puder, M. (2019). Alpha-tocopherol in intravenous lipid emulsions imparts hepatic protection in a murine model of hepatosteatosis induced by the enteral administration of a parenteral nutrition solution. PLOS ONE, 14(7), e0217155. https://doi.org/10.1371/journal.pone.0217155

Fidler-Benaoudia, M. M., Torre, L. A., Bray, F., Ferlay, J., & Jemal, A. (2020). Lung cancer incidence in young women vs. young men: A systematic analysis in 40 countries. International Journal of Cancer, 147(3), 811–819. https://doi.org/10.1002/ijc.32809

Goodrich, T. D. (2020, September 28). Fat and Weight Gain (a Note to Peter) and the Essentiality of Linoleic Acid [Blog]. Yelling Stop. http://yelling-stop.blogspot.com/2020/09/fat-and-weight-gain-note-to-peter-and.html

Goodrich, T. D. (2021a, August 17). Interview/Debate: PUFAs Killing You? Debate Between Alan Flanagan & Tucker Goodrich on Mark Bell’s Power Project [Blog]. Yelling Stop. https://yelling-stop.blogspot.com/2021/08/interviewdebate-pufas-killing-you.html

Goodrich, T. D. (2021b, December 10). Thoughts on Nick Hiebert’s “A Comprehensive Rebuttal of Seed Oil Sophistry” [Blog]. Yelling Stop. http://yelling-stop.blogspot.com/2021/12/thoughts-on-nick-hieberts-comprehensive.html

Gura, K. M. (2017, August 1). Oils Well That Ends Well (Lipids That Is!) [Video]. 2017 Oley Foundation Annual Conference. https://www.youtube.com/watch?v=RJFxh6GKHZQ

Gura, K. M. (2020). The Power of Networking and Lessons Learned From Omegaven. The Journal of Pediatric Pharmacology and Therapeutics : JPPT, 25(8), 663–674. https://doi.org/10.5863/1551-6776-25.8.663

Gura, K. M., Calkins, K. L., & Puder, M. (2020). Use of Fish Oil Intravenous Lipid Emulsions as Monotherapy in the Pediatric Intestinal Failure Patient: Beyond the Package Insert. Nutrition in Clinical Practice, 35(1), 108–118. https://doi.org/10.1002/ncp.10413

Gura, K. M., & Puder, M. (2018, July). Omegaven Receives FDA Approval [Informational]. Oley Foundation. https://oley.org/page/Omegaven

Hiebert, N. (2022, February 5). Gura email exchange. https://twitter.com/The_Nutrivore/status/1489863311155810304

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. (2010). Household Use of Solid Fuels and High-temperature Frying (Vol. 95). International Agency for Research on Cancer. https://publications.iarc.fr/Book-And-Report-Series/Iarc-Monographs-On-The-Identification-Of-Carcinogenic-Hazards-To-Humans/Household-Use-Of-Solid-Fuels-And-High-temperature-Frying-2010

Klek, S., Szczepanek, K., Scislo, L., Walewska, E., Pietka, M., Pisarska, M., & Pedziwiatr, M. (2018). Intravenous lipid emulsions and liver function in adult chronic intestinal failure patients: Results from a randomized clinical trial. Nutrition, 55–56, 45–50. https://doi.org/10.1016/j.nut.2018.03.008

Nandivada, P., Chang, M. I., Potemkin, A. K., Carlson, S. J., Cowan, E., O’loughlin, A. A., Mitchell, P. D., Gura, K. M., & Puder, M. (2015). The natural history of cirrhosis from parenteral nutrition-associated liver disease after resolution of cholestasis with parenteral fish oil therapy. Annals of Surgery, 261(1), 172. https://doi.org/10.1097/SLA.0000000000000445

Nussbaum, B. B., Spoelhof, B., Galli, K., Health, L., & Golenia, P. (2018). Massachusetts Society of Health-System Pharmacists Newsbriefs. 11.

Sigma-Aldrich, Inc. (2020, November 11). Intralipid I141 [Advertisement]. Sigma-Aldrich, Inc. https://www.sigmaaldrich.com/catalog/product/sigma/i141

Straif, K., Baan, R., Grosse, Y., Secretan, B., El Ghissassi, F., Cogliano, V., & WHO International Agency for Research on Cancer Monograph Working Group. (2006). Carcinogenicity of household solid fuel combustion and of high-temperature frying. The Lancet Oncology, 7(12), 977–978. https://doi.org/10.1016/s1470-2045(06)70969-x

Swiss Re. (2018, June 14). John Ioannidis: The role of bias in nutritional research [Mp4]. https://www.youtube.com/watch?v=KTAbx4i8Dyg

Young, S. S., & Karr, A. (2011). Deming, data and observational studies. Significance, 8(3), 116–120. https://doi.org/10.1111/j.1740-9713.2011.00506.x

Friday, January 7, 2022

I Caught A Cold

No, not "the" cold. Two COVID-19 antigen tests were negative, the second in the thick of the symptoms.



It started as a simple head cold, which nevertheless was able to quite knock me out for a bunch of days.

Lack of sleep due to a flight from Idaho to Newark, NJ through Seattle in the thick of the recent Seattle snow apocalypse was likely the cause of it. 

Getting this message in the middle of taking off while flying to Seattle probably kicked off some stress, and the combination of that and lack of sleep is not good for one's immune system!

It's then progressed to bronchitis, and has put me quite behind on some projects I am working on.

So if you are wondering where I've been, and why I won't be around much for the next few weeks. that's the answer.

The COVID tests were done for the friends and family we were visiting. My parents-in-law are both 80, and while quite healthy, are obviously concerned about the ill effects of that particular virus on older people.

Friday, December 10, 2021

Thoughts on Nick Hiebert's “A Comprehensive Rebuttal of Seed Oil Sophistry”

Introduction

Consider this a follow-up of sorts to my post and debate with Alan Flanagan (Goodrich, 2021a, 2021b), if you want some background.


Nick Hiebert (Hiebert, 2021a), whom I have been interacting with for several years on Twitter, thought he could do a better job than Alan did, and challenged me to a debate. After going through a little back-and-forth on format, it became clear that Nick wanted to debate me only if he could have a moderator that would take his side in his view of the facts and the logic. I proposed a standard Oxford-style debate, where such matters are handled by the debaters, and the moderator simply enforces the rules (time, taking turns, etc.).

Nick refused, and blocked me. And then apparently wrote this, “A Comprehensive Rebuttal of Seed Oil Sophistry” (Hiebert, 2021b). And then challenged me again to a debate (I’ve been told), which I couldn’t see, as he has continued to block me. Which is most amusing, but…

After several requests, I’ve decided to take a look at his post. I’m responding as I read it, as it’s 60-odd pages long*. 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.

This post moved to Substack.

Tuesday, July 20, 2021

Katherine Eban on COVID-19 Origin

Peter Attia interviewed Katherine Eban about the origin of the COVID-19 disease (link to podcast), an investigative reporter who's done some amazing work on generic drugs in the past.


While I have a few issues with her argument about the COVID-19 disease's origins (hence this short post) let me say that I think this is in general an excellent interview, and a very good introduction to the issue if you are not familiar with it already. Eban and Attia go through the key points, and a number of rather uncomfortable points are included. So I recommend it, but with the caveats addressed below (which is not comprehensive).

Attia sells the transcript to these podcasts to subscribers, and I do not subscribe, so I did these brief snippets myself. Timestamps are mine, as are any errors.

00:05:47: "One might say [the origin] was settled a while ago, or seemingly settled..."

So, a little bit of my background on looking into this:
So over a year before Vanity Fair published Eban's article, it was pretty obvious that the Wuhan Institute of Virology lab (WIV) was a possible, if not likely source of the disease.
"“The idea that it was just a totally natural occurrence is circumstantial. The evidence it leaked from the lab is circumstantial. Right now, the ledger on the side of it leaking from the lab is packed with bullet points and there’s almost nothing on the other side,” the [Trump administration] official said."

That quote was from an OpEd in the Washington Post published on April 14, 2020. This podcast contains nothing that adds to or subtracts from that conclusion.

So, disagreements.

The Moratorium

The Asian Times article from April 22, 2020 makes a mistake that Eban repeats in her own analysis:

"Back in October 2014, the US government had placed a federal moratorium on gain-of-function (GOF) research – altering natural pathogens to make them more deadly and infectious – as a result of rising fears about a possible pandemic caused by an accidental or deliberate release of these genetically engineered monster germs."

Lin, the author, links to an article that says: 

"[The White House] is halting all federal funding for so-called gain-of-function (GOF) studies that alter a pathogen to make it more transmissible or deadly so that experts can work out a U.S. government-wide policy for weighing the risks. Federal officials are also asking the handful of researchers doing ongoing work in this area to agree to a voluntary moratorium."

Eban's Vanity Fair article states:

"In October 2014, the Obama administration imposed a moratorium on new funding for gain-of-function research projects that could make influenza, MERS, or SARS viruses more virulent or transmissible. But a footnote to the statement announcing the moratorium carved out an exception for cases deemed “urgently necessary to protect the public health or national security.”
Eban sent me an article similar to Lin's source via twitter: 

Which stated (correctly) that:

"...the US government is temporarily halting funding for new studies aiming to give novel functions to influenza, SARS, and MERS viruses."

Despite it's erroneous title: "Moratorium on Gain-of-Function Research".

NIAID funding of EcoHealth, including WIV.
The relevant definition of "moratorium" here is "a suspension of activity". As the 2014 White House order makes clear, this was not a moratorium, as all existing research projects were grandfathered, only "new" projects were prohibited. Further, there's no evidence whatsoever that anyone asked or that Ecohealth refused to "voluntarily" halt its gain-of-function (GoF) research project. (As I discussed in this twitter thread, based on NIAID and HHS documents, the WIV research was clearly GoF.)

It's clear from the language of the White House order that someone from NIAID should have asked EcoHealth to pause its research!

And indeed, as HHS documents make clear, the research project, which was not "new", continued to receive funding.

Even NIAID Director Fauci states that funding continued:

""About $600,000 was spent over a five-year period," Fauci said during a congressional budget hearing. "That comes to anywhere between $125 (thousand) and $150,000 per year that went to collaboration with Wuhan."
So there was never a moratorium that applied to or was followed by the NIAID and the WIV.

Further evidence that there was no moratorium for WIV is that the "pause" was lifted on December 13, 2017, while on November 30, 2017, Zheng-Li Shi (the 'bat woman') published a paper that listed the NIAID grant as a funding source:
"Funding: This work was jointly funded... the National Institutes of Health (NIAID R01AI110964)..."
And it was GoF, using the "reverse genetic" technique:
"Recombinant viruses with the S gene of the novel bat SARSr-CoVs and the backbone of the infectious clone of SARSr-CoV WIV1 were constructed using the reverse genetic system..."
As Eban had noted, in the VF article: "The grant was not halted under the moratorium or the P3CO framework." Which is quite obvious, as it was never subject to the "pause", however none of this nuance is discussed in the podcast.
00:31:53: "...led the US Government to impose a moratorium on funding of any kind of gain of function research of SARS and MERS pathogens."
This is clearly not accurate.
00:32:10: "Interestingly, in the very beginning of the Trump Administration, in January of 2017, that moratorium was lifted. But it was replaced by this [P3CO] framework..."
Obviously since the pause never applied to WIV, and was never followed by WIV, it is incorrect to imply, as she does here, that it was lifted by the Trump Admin. There was nothing to lift.

Her discussion of the P3CO framework is well worth reading, as NIAID Director Anthony Fauci had apparently decided to ignore it, just as he had ignored the Obama-administration request to voluntarily halt the SARS research conducted by WIV. However she never makes this connection, despite (inaccurately) quoting part of the footnote noting who at NIAID had the authority to waive the pause for WIV funding: 
"An exception from the research pause may be obtained if the head of the USG funding agency determines that the research is urgently necessary to protect the public health or national security."

Did NIAID Fund Gain-of-Function Research? 

Attia then asks her (00:32:47) about NIH Director Collins and NIAID Director Fauci denying they funded GoF work (in at least one case for Fauci, under oath). "Can you evaluate the veracity of those statements?"

00:33:44, Eban: "So here is where we enter this true semantic marshland, because the feeling of, and I'm not talking about wingnuts who want to fire Fauci, credible people who have evaluated this say that there is some sort of rhetorical grey area here. First of all... well the Government hasn't funded research at the [WIV] directly, they have funded, basically, an intermediary non-profit called EcoHealth Alliance, which in turn has given sub-grants to the [WIV]. So, yeah, no direct funding, but yeah, indirect funding. 
"Now, part of the obligation of EcoHealth Alliance was to report back to the NIH [actually, the NIAID] and say, here's our progress reports, here is what the [WIV] was doing with some of your grant money, and we ensure that they have been doing this safely. We don't know what's in those progress reports, because NIH [again, NIAID] has not released them. 
Attia: "That sounds like a FOIA waiting to happen..."

Well, we really don't need a FOIA to come to a conclusion about this, and it's not a semantic marshland, because sufficient information to draw a conclusion is already available.

For starters as I detailed here, NIAID defines GoF research as: 

"...any selection process involving an alteration of genotypes and their resulting phenotypes is considered a type of Gain-of-Function (GoF) research, even if the U.S. policy is intended to apply to only a small subset of such work.

"...To answer these questions, virologists use gain- and loss-of-function experiments to understand the genetic makeup of viruses and the specifics of virus-host interaction. For instance, researchers now have advanced molecular technologies, such as reverse genetics, which allow them to produce de novo recombinant viruses from cloned cDNA, and deep sequencing that are critical for studying how viruses escape the host immune system and antiviral controls. Researchers also use targeted host or viral genome modification using small interfering RNA or the bacterial CRISPR-associated protein-9 nuclease as an editing tool."

WIV was clearly doing reverse genetics research, a type of GoF, per the NIAID definition, as detailed above and reported in a publicly-available, peer reviewed paper, or, as the State Department put it recently:

"The WIV has a published record of conducting “gain-of-function” research to engineer chimeric viruses."

Second, NIAID monitors what award grantees and sub-award grantees are doing:

"The work was a collaboration among scientists from EcoHealth Alliance, Duke-NUS Medical School, Wuhan Institute of Virology and other organizations, and was funded by the National Institute of Allergy and Infectious Diseases [NIAID], part of the National Institutes of Health. The research is published in the journal Nature."

Third, NIAID requires that sub-award grantees be approved:

"While principal investigators (PIs) can perform a range of grant actions under the NIH standard terms of award, they must get prior approval from NIAID for the following things: ...Addition of a new foreign site or foreign subaward."

Fourth, the Government was notified that the WIV was not meeting standards:

"Two years before the novel coronavirus pandemic upended the world, U.S. Embassy officials visited a Chinese research facility in the city of Wuhan several times and sent two official warnings back to Washington about inadequate safety at the lab, which was conducting risky studies on coronaviruses from bats."

Eban seems to be paltering here: the distinction that she attempts to present as a justification for Fauci's and Collins' statements falls apart simply when looking at the NIAID documents about their supervisory role in sub-award grants.

"“I can’t guarantee everything that’s going on in the Wuhan lab, we can’t do that,” Dr. Fauci said..."
It's the NIAID's self-declared responsibility to ensure basic protocols are followed, and he is the Director. If he has doubts (as he should have) about the WIV, he should have pulled the grant. He could also have implemented the pause and the protocols outlined above, which he failed (or declined) to do. Collins is similarly culpable.

In light of the evidence, it's simply impossible to answer Attia's question in any other way than to acknowledge they were likely being dishonest.

Bias

00:06:11 Eban: "...with Trump out of office... it was a good time to begin to look into..."

Why is the fact that Trump is out of office relevant to where a disease that has killed millions come from? It shouldn't be, unless you are putting politics ahead of people's health.

Identifying the cause of this disease, if it was human-caused, as seemed likely even a year ago (and as Eban notes, even the Chinese came to the conclusion that the labs in Wuhan were likely the cause of it), is rather crucial if we're going to avoid another apparently iatrogenic pandemic.

From Vanity Fair:

"As the pandemic raged, the collaboration between EcoHealth Alliance and the WIV wound up in the crosshairs of the Trump administration. At a White House COVID-19 press briefing on April 17, 2020, a reporter from the conspiratorial right-wing media outlet Newsmax asked Trump a factually inaccurate question about a $3.7 million NIH grant to a level-four lab in China. “Why would the U.S. give a grant like that to China?” the reporter asked.

Eban in the podcast:

00:35:45: "In my investigation there are credible questions about that funding. Why were we allowing taxpayer dollars to a high-level Chinese laboratory, where we now believe there were was actually military scientists working in there. They're obviously an adversary..."

The Newsmax question was not "factually inaccurate", the grant did indeed go to China and the NIAID oversight process makes it clear that they would have known where it was going. It's actually a damn good question, and had it come from "the mainstream media" which had "studiously avoided" the topic, as she noted, Eban would doubtless have approved of it. 

Eban did excellent work, as far as she went, but it appears her political bias prevented her from drawing the obvious conclusions above—comments about conspiracy theories are used repeatedly, even as her reporting demonstrates that the 'conspiracy theorists' were working off the known facts most effectively in this particular case.

Conclusion

From the Vanity Fair article:

""Inside the NIH, which funded such research, the P3CO framework was largely met with shrugs and eye rolls, said a longtime agency official: “If you ban gain-of-function research, you ban all of virology.” He added, “Ever since the moratorium, everyone’s gone wink-wink and just done gain-of-function research anyway.”"

From Fauci's FOIA'ed emails:

"Auchincloss replied to Fauci, saying, “The paper you sent me says the experiments were performed before the gain of function pause but have since been reviewed and approved by NIH. Not sure what that means since Emily is sure that no Coronavirus work has gone through the P3 framework ... She will try to determine if we have any distant ties to this work abroad.”"

Concluding that a manager who presides over what seems likely to be a gross violation of safety protocols, ignores policies designed to enhance safety, and then attempts to hide his culpability should be fired isn't a "wing nut" response, it's management 101. 

00:35:07 Eban: "The NIH now is being buried up to their eyeballs in FOIAs, absolutely. People want to know, what did they know about this research."

This is what happens when you're not forthrightly trying to find out what went wrong. It's a red flag.

The conclusion I have gotten to, which she provides a good bit of evidence to support, is that the fellow who has been leading our response to COVID-19 likely financed its creation, and the fellow who was tasked with finding out where it came from likely created it. Both are doing their very best to distract us from those conclusions. And there's little chance either will pay a price.

That's a pretty grim conclusion to come to.

Hopefully Eban will continue this line of research, but put the bias to the side.

Thursday, June 24, 2021

Thoughts on 'Of Rats and Sidney Diet Heart...', Alan Flanagan's Post Defending Seed Oils

Apologies to Stan Efferding, who asked me last year to look at this blog post. I really don’t like doing this kind of post, especially when it’s a soft target, but as it keeps coming up, I guess I have no choice.

So here we go.

Introduction

Alan Flanagan
Alan Flanagan
(Flanagan, 2020a)
The blog post in question is titled “Of Rats and Sydney Diet-Heart: Drawing a Line Under Polyunsaturated Pseudoscience” (Flanagan, 2020b), the author is Alan Flanagan, who “…has an MSc in Nutritional Medicine, is currently pursuing his PhD, and a [sic] former practicing Lawyer (Barrister) from Dublin, Ireland.” He states, “The core values behind Alinea Nutrition are critical thinking that is clear, objective, rational, free from dogma, and informed by evidence” (Flanagan, 2020a). Alinea being his website’s name.

He commences his post:

“To say that hysteria about the health effects of polyunsaturated fats [PUFA] has reached fever pitch may be an understatement.

“It can be interesting watch [sic] a trend of thought gain traction when that train of thought is inconsistent with a substantial total body of evidence, from multiple converging lines of inquiry.

“It speaks to something at play beyond scientific discourse, and frankly much of the “debate” regarding PUFA is steeped in a mix of narratives, from fantasies about our evolutionary past to conspiracy theories about governments, scientists, the food industry, and ‘BigPharma’.

“I have a few thoughts as to why the PUFA-hysteria appears to have exponentially increased in recent years. It’s likely not an exhaustive list, but these are some of the more common narratives I’ve observed….”

Well, I’ve been told I’m in a good part responsible for the “PUFA-hysteria”, so I guess I have an interest in defending it.

Post has moved to Substack.

Friday, April 23, 2021

Experts: Do As We Say, Not As We Do.

This is a little off-topic, but relevant.

I live in Idaho now, and since I'm still into getting out into the wilderness to hike, trail run, backpack, etc., I'm getting up to speed on Idaho issues with being in the wilderness.

One of the issues is predators. Like in the East, there are ticks, snakes (more rattlers than back East, where they are very rare), and black bears; but there are also mountain lions, wolves, and grizzly bears.

Grizzly bears are a particular issue in certain parts of the state. Montana is adjacent, and since grizzlies don't know about state lines, they have a habit of crossing back and forth, especially around Yellowstone National Park.

"Angler Killed by Grizzly in First Attack of 2021":
"The first responders transported Mock... to the Eastern Idaho Regional Medical Center in Idaho Falls. Mock passed away Saturday morning in Idaho Falls following a massive stroke."

A very sad incident, the fellow was only 40 years old, with a family. It's relevant because of what he was doing to mitigate his risk:

"According to Montana Fish, Wildlife and Parks, Mock was carrying bear spray when he was attacked. Although the safety tab was found off, it’s unclear whether he was able to deploy the canister."

Well that's just idiotic. It doesn't take an "expert" to figure out if a can full of fluid is full or empty. If it's full, he didn't deploy it, if it's empty, he did. (It's exceedingly unlikely that he was carrying an empty can of bear spray into grizzly country. We can dismiss that possibility.) 

Given the dishonesty our expert and journalist classes seem prone to, it's safe to assume he used the bear spray and it was ineffective. If he hadn't used it they would have just said so, as there are reasons why he may not have been able to use the bear spray.

So then the experts come in, to see what's going on with this bear: 

"Investigators later found a moose carcass cached within 50 yards of the original attack site, indicating that the bear was defending the food during both incidents."

Well, that's a fine reason to attack a person from a bear's perspective, but not from ours.

The experts, needless to say, didn't rely on bear spray to deter the bear.

"The group attempted to haze the bear away but were unsuccessful. Members of the team were ultimately forced to shoot the bear dead at only 20 yards."
So what is the advice the Montana Fish, Wildlife and Parks gives after a careful analysis of this incident?
"Carry bear spray. Know how to use it and be prepared to deploy it immediately."
And don't worry, if the bear spray doesn't work, as it didn't in this case, the "experts" will come in with proper tools and dispatch the bear.

Guns aren't the only way to deal with a bear. Pepper spray certainly can be effective.

But it would be nice if our experts would be honest with us about the risks and benefits.

Eckel's Creek Trail:
There's bears up there!
P.S. So after posting this I went camping in the Hell's Canyon area, which is spread across several national forests, national recreation areas, and private land on the border of Idaho and Oregon.

We decided to go for a long trail run, but since there are only black bears in the area, we didn't bother with bear spray or anything else.

Three-quarters of the way through the run, we see a mother black bear with two cubs running down the slope. They were across a steep and rugged ravine, so we stopped to see if we could get a picture of them when they came out of of the copse of trees they had run into. They never did come out, but a very large, light brown bear did appear, running in the opposite direction. Sadly the dash from one copse to the next was too quick to allow for photography!

"That looks like a grizzly...", we said. It was still quite far away, so there was no immediate risk, but we proceeded to high-tail it down the trail back to the car, which was a couple of miles away.

Some of the locals explained to us that there aren't grizzlies in the area, but there are some blond black bears (which do exist) and some bears that might be hybrids of black and grizzly bears (which are rare, but also do exist). Apparently a large blond bear had come down and availed himself of a sprinkler system a couple days prior!

I don't think it was a blond black bear, as it was much bigger than the black bear sow we had seen moments before.

Note to self: The experts may say there are no bears in an area, but the bears don't know where they are supposed to be. 





Bear spray, like a gun, are both useful tools to deal with the threat of a bear. This isn't an either-or case.

And gun control is rather beside the point here. Norway has strict gun control laws, and has a lot of polar bears, which are even more aggressive than grizzlies.
"The use, trade and import of bear repellent spray and pepper-balls for protection against polar bears in Svalbard is prohibited."

So what are your choices?

"Due to the polar bear threat in Svalbard, anyone travelling outside the settlements must be equipped with appropriate means of frightening and chasing off polar bears. The Governor of Svalbard also recommends having firearms with you."

Pity our "experts" aren't quite so forthright.


Sunday, January 24, 2021

Comments

 After marveling that almost no-one ever comments on my blog, I've just noticed that there are loads "pending moderation".

Not quite sure what is going on, as I've not been receiving notifications for these, but I'll go through them.

Of course some junk spam comments have gotten through.

Typical Google software.

Tuesday, October 27, 2020

Comments on "The Cause of Metabolic Syndrome: Excess Omega-6 Fats (Linoleic Acid) in Your Mitochondria"

 It's a post from 2016, seems like yesterday. Yesterday someone asked about it, so I retweeted it:


Mark Sisson retweeted it, and commented: 


Professor Tim Noakes also saw fit to retweet it:


Ivor Cummins, aka "Fat Emperor", also had some kinds words:
Rogue Scholar Press seemed to like it too, as he commented:
Thanks to you all, it's heartening to think I've produced something meaningful!

Saturday, February 23, 2019

Malfunction

Apparently IFTTT (If This Then That), the web app. that I use to copy content from my RSS reader Newsblur to this blog, lost its mind yesterday.

Sorry for the deluge of posts.

Tuesday, August 7, 2018

Review: Jane Brody of the "New York Times" on the Paleo Diet

Ms. Brody (I presume it's Ms., since she does work at the Times) is the Times' august "personal health columnist, a position she has held since 1976," and as such, one would think she'd be well-suited to examine the details of a diet.

So let us see what she has to say about my own personal diet.
"Is the Paleo Diet Right for You?"
"In the Paleo era, people ran around all day and rarely lived past 40, so their risk of developing the so-called diseases of civilization is unknown."
That's not even the article, it's just the starting blurb, which ought to entice us to read further, not induce wincing, as is the case here.
  1. "...people ran around all day..."
This no doubt refers to the debunked calories-in, calories-out model, oft summarized as "east less, move more".  We now know that human movement appears to be largely constant, and the fact that paleo man ran around more doesn't per se have an impact on their weight, obesity being the primary current manifestation of the Diseases of Civilization. See here:
"Energy expenditure and activity among Hadza hunter-gatherers." [1]
  1. "...rarely lived past 40..."
This is a familiar trope, and indicates that Ms. Brody does not understand arithmetic. Forty would represent (assuming her number is correct) an average, not a max lifespan for a paleolithic person.
"Life expectancy is an average, and it fluctuates with age as the risks we face change throughout our lifetimes. Both those facts make it a frequently misunderstood statistic. High infant-mortality rates depress the figure substantially. This can lead contemporary observers to the false conclusion that most humans died quite young, even in the not-so-distant past."
That's from this article, "Who Lives Longest?" that appeared in the NYT in 2013. It includes a discussion of paleolithic lifespans. The max was higher than 40. Ms. Brody should read it.
  1. "...their risk of developing the so-called disease of civilization is unknown..."
Hard to know, but not unknown. Paleopathology is the field of determining ancient health, and what it tells us is clear: the diseases of civilization appeared at the end of the Paleolithic, and people got sick, fast. From Jared Diamonds 1987 article, "The Worst Mistake in the History of the Human Race":
"Skeletons from Greece and Turkey show that the average height of hunter-gatherers toward the end of the ice ages was a generous 5' 9'' for men, 5' 5'' for women. With the adoption of agriculture, height crashed, and by 3000 B. C. had reached a low of only 5' 3'' for men, 5' for women. By classical times heights were very slowly on the rise again, but modern Greeks and Turks have still not regained the average height of their distant ancestors... 
"...Compared to the hunter-gatherers who preceded them, the farmers had a nearly 50 per cent increase in enamel defects indicative of malnutrition, a fourfold increase in iron-deficiency anemia (evidenced by a bone condition called porotic hyperostosis), a theefold rise in bone lesions reflecting infectious disease in general, and an increase in degenerative conditions of the spine, probably reflecting a lot of hard physical labor. "Life expectancy at birth in the pre-agricultural community was about twenty-six years," says Armelagos, "but in the post-agricultural community it was nineteen years. So these episodes of nutritional stress and infectious disease were seriously affecting their ability to survive.""
I haven't even gotten out of the blurb yet, and we've discovered 81% of the words in the blurb are untrue or at least grossly questionable statements.

Welcome to the New York Times! And thus you see the problem with fake news. It takes me 469 words to debunk 21 bogus ones.

The article doesn't get any better from there, but having demonstrated the general tone (most of these points are repeated in the body) I'll just hit a couple of high points.

Ms. Brody observes:
"There have been no studies of large groups of people who have followed the currently popular versions of the Paleo diet for decades to assess their long-term health effects."
This is a nonsensical criticism, as there are no such long-term studies of ANY DIETS for their health effects, with the exception of the Dietary Guidelines we are all forced to follow. The Dietary Guidelines failed to show any benefits for the health problems they were purported to ameliorate. The few paleo diet studies (as she mentions at the very end) have shown greater benefits than almost every other diet studied, including the ability to reverse many of the diseases of civilization.
"Several short-term studies among small groups of people (often with no control groups) suggest that the Paleo diet is more effective than the Mediterranean approach..."
She nevertheless endorses the Mediterranean diet, while ignoring the fact that it also has no studies to assess its long-term health effects. Note the double standard.

She seems to be using the Paleo Diet as espoused by Loren Cordain, which is fine, although not my personal choice. It's rather odd that she doesn't look into other versions of the paleo diet, which address some of her criticisms. Some of them are fair, but couched in language that demonstrates a lack of basic knowledge of food and physiology. No, dairy is not a great source of Vitamin D, Ms. Brody, the sun is. "There is no such thing as “a” Paleo diet" she says. Which is true, and every single paleo diet book tells you that. It's a strawman argument, and could have been rectified in a few moments online.

She does go talk to one "expert", Dr. Marlene Zuk, who wrote a book called Paleofantasy [2], from which Ms. Brody apparently got the substance of her article. Dr. Zuk is an evolutionary biologist, but she studies insects, not people. Hence she's not familiar with the subject she criticizes. But don't take my word for it, here's a review, from the academic journal Evolutionary Psychology: "Throwing Out the Mismatch Baby with the Paleo-Bathwater" [3]:
"In sum, Zuk has written a wide-ranging, accessible, and stimulating book, but one that mainly triumphs in dispatching paleo-hucksters, anonymous bloggers, and scholarly straw men. In failing to acknowledge the successes of the mismatch perspective, Zuk has reached the wrong conclusion: The mismatch perspective has not been a failure; it has been tremendously fruitful."
Now what you need to understand is that Dr. Zuk's book was published in 2012, and Ms. Brody's NYT article was published on August 6, 2018. So it's six years out of date.

In the interim Prof. Daniel Lieberman, Chairman of the Department of Human Evolutionary Biology at Harvard wrote the masterful The Story of the Human Body: Evolution, Health, and Disease [4]. If there hadn't been a paleo diet already, this book would have spurred it. And if Ms. Brody had based her criticism on the paleo diet on that book, she might have realized there is much less to criticize. (Prof. Lieberman is not a fan of the paleo diet per se, but cites some of the early papers from the founders, and makes the same argument.)

What's entirely missing, of course, is any defense of the paleo diet from a supporter.

So the Times turns out to be not even news, just fake; simple fear, uncertainty, and doubt. This article is basically a tarted-up book review of a book six years old combined with a snarl.




[1] Pontzer, H. , Raichlen, D. A., Wood, B. M., Emery Thompson, M. , Racette, S. B., Mabulla, A. Z. and Marlowe, F. W. (2015), Energy expenditure and activity among Hadza hunter‐gatherers. Am. J. Hum. Biol., 27: 628-637. doi:10.1002/ajhb.22711

[2] Paleofantasy: What Evolution Really Tells Us about Sex, Diet,and How We Live. W. W. Norton & Company: NY. 2013. 255 pp., ISBN #978- 0393081374 (hardcover).

[3]  Robert O. Deaner and Benjamin M. Winegard; 2013; Book Review: Throwing Out the Mismatch Baby with the Paleo-Bathwater; Evolutionary Psychology; doi: 10.1177/147470491301100123

[4] The Story of the Human Body: Evolution, Health & Disease By Daniel Lieberman
Publishers: Pantheon Books, Random House, USA (2013) and Allen Lane (UK) 2013 ISBN: 978-1-846-14393-9

Friday, April 27, 2018

LDL Cholesterol: You Aren't Always What You Eat, or Roundabout Ways to Improve Your Diet

Sometimes you read these papers and shake your head.

"Lowering Dietary Saturated Fat and Total Fat Reduces the Oxidative Susceptibility of LDL in Healthy Men and Women"

The troll who pointed me to this was trying to argue that this invalidated the claim that omega-6 polyunsaturated (n-6) fats are important in cardiovascular disease (I gather), since lowering saturated fat (see the title) lowered oxidation.

Oddly enough, he was almost right, but not quite.

Fat components
The intervention was to have fixed protein (15%), but a variable rate of saturated fat (SFA), to be replaced by carbohydrate (CHO), and fixed rates of monounsaturated and polyunsaturated fats (MUFA and PUFA, respectively). And they did a good job of detailing what the diet included, right down to the individual fats.

However you have to go to a different study to find all the details ("Effects of Reducing Dietary Saturated Fatty Acids on Plasma Lipids and Lipoproteins in Healthy Subjects")

To sum the variation, SFAs were 16%, 9%, and 5%; and CHO was therefore 48%, 55%, and 59%. MUFA was 14%, and PUFA was 7%.

The diet part of it seems to have been very well done, indeed. If you want some idea from where the food may have come, may I introduce you to their sponsors?
"The DELTA Investigators express thanks to the following contributors: AARHUS, Bertolli, USA., Best Foods, Campbell Soup Company, Del Monte Foods, General Mills, Hershey Foods Corp., Institute of Edible Oils and Shortenings, Kraft General Foods, Land O'Lakes, McCormick Incorporated, Nabisco Foods Group, Neomonde Baking Company, Palm Oil Research Institute, Park Corporation, Procter & Gamble, Quaker Oats, Ross Products Division/Abbott Laboratories, Swift-Armour and Eckrick, Van Den Bergh Foods, Cholestech, Lifelines Technology Incorporated."
Wow.

The troll was almost right because LDL oxidation did indeed go down in this study. But it went down for a reason that I wouldn't have expected, and which leaves me somewhat perplexed to explain mechanistically. 

The paper goes on ad nauseum along these lines:
"Convincing evidence suggests that oxidative modification of LDL plays an important role in the pathophysiology of atherogenesis (Steinberg 1997). In recent years, numerous molecular mechanisms have been proposed to explain the different oxidation pathways that lead to modification of LDL (Steinberg 1997). 
"One of the earliest steps in the generation of oxidatively modified LDL is the peroxidation of its polyunsaturated fatty acids (PUFA).3 The oxidative breakdown products of these fatty acids, such as malondialdehyde [MDA] and 4-hydroxynonenal [HNE], form covalent bonds with apolipoprotein B (apo B)..."
Yeah, yeah. Old news (the paper is from 2000), but here's where it gets odd:
"The results of the present study also show that LDL composition (LDL quality) affects susceptibility to oxidation. [It] was inversely correlated with the quantity of LDL oleic acid (r = −0.29, P < 0.01), and positively correlated with the quantity of LDL linoleic acid (r = 0.23, P = 0.04) and the 18:2-to-18:1 ratio (r = 0.52, P < 0.001). The oxidation rate was positively correlated with the 18:2-to-18:1 ratio (r = 0.24, P = 0.03)."
To lower n-6, cut SFA?

What?

So lowering SFA indeed made the LDL more resistant to oxidation. But it did so by lowering n-6 and raising MUFA in the LDL! SFA was basically unchanged.

A little Lipidology 101, MDA and HNE, mentioned above, aren't made from SFA, they're made from PUFA, and HNE is made exclusively from n-6. MDA and HNE pretty much are oxidized LDL. So you're not getting oxidized LDL from SFA in the body. It just won't happen.

Of course the authors don't mention that little fact. More below.

For some reason I am unable to explain, lowering SFA (16:0, palmitate in the chart) in the diet lowered n-6 (18:2, linoleate) in the LDL, and increased MUFA (18:2, oleate), protecting LDL from oxidation. SFA stayed  the same, basically.

My best guess is that it was the increased CHO in the diet (is this what's behind the Japanese diet, which is low in SFA and high in CHO?) but it is just a guess.
"In the present study, the ratios of 18:2 to 18:1 and PUFA to MUFA in the LDL from subjects when they consumed the Step-1 and Low-Sat diets were significantly lower than they were in the LDL from subjects when they consumed the AAD. Linoleic acid (n-6) in LDL from subjects when they consumed the Low-Sat diet also was significantly lower compared with those from subjects when they consumed the AAD. "
The first citation for this paper is:

"Oxidation of low-density lipoproteins: intraindividual variability and the effect of dietary linoleate supplementation"
"LDL oxidized faster after the linoleate diet than after the oleate diet... and produced more conjugated diene [that's bad] in proportion to the increase in LDL linoleate."
Here's where we get to the shaking my head part.

Why in blazes wouldn't you reduce the thing that is actually capable of causing the harm, as your first cite shows, and as your own study shows, is the source of the problem? Why keep n-6 flat and reduce something else, which through some round-about effect, lowers what you need to lower, the n-6?

Just lower the n-6 and you reduce the susceptibility for oxidation! They cite other papers that have done exactly that!

This study was done in 2000, did I mention that?

Think of the progress we would have made if they'd actually done what any engineer reading this paper would have told them to do. 
"N-6 converts to these toxins? You're proved that? Why not reduce the n-6?"
Let's not get too into conspiracies here, but on the face of it this study is clearly little more than a misleading advertisement for the sponsors listed above, who are forced to follow the United States Dietary Guidelines and replace saturated fats with the n-6 fat that their own research claims is harmful.




This post started with a twitter troll who cited the first-mentioned study: