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.

Thursday, November 18, 2021

Does Linoleic Acid Induce Obesity? Part 2—RYGB and HNE

Part 2: Roux-en-Y Gastric Bypass and 4-Hydroxynonenal

Roux-en-Y Gastric Bypass (RYGB)

Post moved to Substack.

Does Linoleic Acid Induce Obesity? Part 1

[P.S. Part 2: Roux-en-Y Gastric Bypass and 4-Hydroxynonenal]

Introduction

OK folks, into the wayback machine.

In 2010 I stopped eating seed oils, and saw a chronic inflammatory bowel disease resolve in days:

“So a few months ago, I stopped eating industrial seed oils (veggie oils). In two days the diarrhea stopped. Eat the oils, it started again. I no longer craved starch or sugar, so I didn't eat any wheat for a week, without meaning to….  So now I could turn the symptoms of the last 16 years on or off, based on eating veggie oils or wheat. Wow!” (Goodrich, 2010)

Post moved to Substack.

Tuesday, October 19, 2021

What Is The Most Fattening Food?

I came across this paper recently:


"Changes in Diet and Lifestyle and Long Term Weight Gain in Women and Men” (Mozaffarian et al., 2011)

From the illustrious New England Journal of Medicine.

The most notable authors (apologies to the rest!) are F. B. Hu—Frank Hu, the current Frederick J. Stare Professor of Nutrition and Epidemiology at the Harvard T. H. Chan School of Public Health (Harvard University, 2021a); D. Mozaffarian—Dariush Mozaffarian, Dean of Tufts Friedman School of Nutrition Science and Policy (Tufts University, 2021); and W. C. Willett—Walter Willett, the previous Frederick J. Stare Professor of Nutrition and Epidemiology at the aforementioned Harvard School  (Harvard University, 2021b), and until 2017 the chair of the department of nutrition—per Wikipedia as of this writing.

The three are the Holy Trinity of the Nutrition Establishment of the United States, and, by extension, the world. Combined, the three have written countless papers, editorials, and opinion pieces on the subject of health and nutrition.

This post has been moved to Substack. Please follow me there!

Tuesday, September 21, 2021

Good Keto vs. Bad Keto

This is what passes for a keto diet in the rodent literature.
From (Li et al., 2021)

It's Envigo's TD.96355, from a paper finding negative effects of a keto diet. 
"Ketogenic diet aggravates colitis, impairs intestinal barrier and alters gut microbiota and metabolism in DSS-induced mice" (Li et al., 2021)
F3666 is another rodent keto diet, (Lecker, 2011). It's also high in seed oils, and it's also commonly used. 

Virta Health explicitly advises patients to limit seed oil consumption (Phinney et al., 2020), based on Phinney's labratory experience and self-experimentation, in which he found seed oils to be acutely, albeit mildly, toxic: 

Monday, September 20, 2021

Interview: "Tucker Goodrich & Dr Berry Question the Safety of Canola & Soybean Oil"


Really nice discussion with Ken Berry with a live audience, so we got some good questions.

I don't think he has a podcast, but this is on YouTube now:


Friday, August 27, 2021

Interview: Tucker Goodrich Challenges Failed Experts with David Gornoski on A Neighbor's Choice

"Tucker Goodrich Challenges Failed Experts"
My part starts at 00:24:00.
"Also in the show, Tucker Goodrich joins David to comment on the censorship of information, the Diet Doctor podcast on vegetable oils, intralipid , the horrible dietary guidelines of hospitals, whether salt is harmful to our bodies, burning excess PUFAs, and more."
Radio, so no video for this one. Here's a link to the podcast, and here's an embedded player:


Thursday, August 26, 2021

AHS21 Presentation: "Why Did We All Get Sick? The Nutritional Transition & How Seed Oils Drove It"

"Why Did We All Get Sick? The Nutritional Transition & How Seed Oils Drove It", my presentation at the 10th Ancestral Health Symposium

I discuss the nutritional transitions that led to man being man, and the chronic diseases that were introduced along the way, along with mechanisms for causation, both known and proposed.



References for Ancestral Health Symposium 2021 talk, "Why Did We All Get Sick?"

This is slide-by-slide, some slides don't have any refs or no new refs, so they are skipped.

Health fallout from a visit to LA and a stay in a hotel: "How Much Seed Oil Is Too Much? Short-term Consequences of Going Off The Wagon"

Notes from the last one I attended, in 2012. (Pictures are mostly missing, as they were links.) 


Thanks to Tess Falor, Naomi Norwood, and of course Aaron Blaisdell and all the rest of the folks that put this fine event together. And to Chris Knobbe for getting me on the program!

Wednesday, August 25, 2021

How Much Seed Oil Is Too Much? Short-term Consequences of Going Off The Wagon

A cold day in Hell's Canyon
Have I mentioned I got married?

So this post is going to be a joint effort with my wife, Jen.

We went to high school together in Connecticut, and reconnected after many years and found ourselves to be a very good fit.

Unbeknownst to me, she had been suffering from a chronic auto-immune disease, fibromyalgia, for decades, since shortly after we graduated high school.
"Fibromyalgia affects about 4 million US adults, about 2% of the adult population."
When we reconnected in 2019, she was a Greger-style near-vegan, running her own organic farm in upstate New York, and producing most of her own food. She was also quite ill, overweight, and on a number of medications.

So at our first dinner together, after negotiating with the waitress about what food I could eat and winding up with a plate of sausages and a hard cider, I mentioned why I eat the way I do, and told her what to eat:
"Avoid seed oils, refined carbohydrates, refined sugars, and make sure to eat animal protein and animal fats."
Just a sentence. While we were friends, I didn't want to get into a diet debate with a vegan.

A few weeks later she let me know that she had fixed her diet, and was down 17 lbs already (for a total of 56 lbs over the next few months, back to beauty-queen weight).

What she didn't mention until much later was the fibromyalgia. What a near-vegan diet, a physician's care, and drugs hadn't accomplished was fixed with a paleo diet in a few months: the pain went away, for the first time in decades.

She had also suffered from cracks in her heels. I first learned about this from the Barefoot Sisters (podcast at the link), who were also vegetarians. I've long had a suspicion that heel cracks were a function of a low animal-fat diet, and along with the fibromyalgia, the heel cracks resolved.

So two years into this process, we went to LA for a few days for the Ancestral Health Symposium 2021, where I spoke. Since we were staying in a (very nice!) hotel where the conference was held, it was unavoidable that we were going to have to eat out in restaurants, something we do very rarely at home.

We are always careful when we eat out, since I am ridiculously gluten-intolerant. I have no choice. But seed oils are much harder to manage when eating in restaurant. We went to an In-N-Out Burger joint, for instance, and ordered burgers without buns or sauce, telling them I had a wheat allergy. But it's not possible to determine in what they are cooking the burgers. What do they use to lubricate the grill? Obviously we skipped the fries!

Same problem with the restaurant at the hotel: what are the vegetables cooked in? Given that they wouldn't put butter on the table even when they served gluten-free toast (what was in the toast?), I doubt they were using butter for the bread or the sautéed vegetables.

My general assumption is that since I don't have an acute reaction to seed oils, a little bit when I rarely eat out isn't going to harm me.

So when we get home, Jen reveals that her fibromyalgia is back. So are the cracks in her heels. She also had a rather severe intestinal distress which she'd rather not detail here! 

All three are improving, but that's a pretty severe reaction to a few days of not rigorously controlling her diet! The intestinal distress required a fast and a period of carnivory to resolve.

When fibromyalgia was full-on she describes it as having a "whole-body sprain", but now it's just in a few locations, like her hips.  Now the connection between fibromyalgia and seed oils is pretty clear (Albrecht et al., 2019; Cordero et al., 2011; Meeus et al., 2013), and I've helped others put it into remission via a low n-6 diet, but I've never heard of it coming back from just a few days of not-so-careless eating!

Luckily she's improving already.

So this raises a number of questions: 
  1. What is the amount of n-6 fats that causes these illnesses?
  2. What is the  amount stored in adipose tissue, and how does this interact with dietary intake?
  3. How long does it take to clear these fats out of the body, until one can tolerate a small intake?
Jen's only been eating this way for 2 years, after years of being on a high n-6 diet. It took me 5 years to really start feeling totally well, and the last odd health improvement happened after 7 years.

Five years is about how long it should take adipose tissue to lose stored n-6, based on the half-life of fats in adipose tissue. Some tissues with a high turnover, like the skin or gut, appear to happen quickly, some, like cartilage, likely take years, if ever.

In celiac it is recognized that a lack of exposure builds tolerance, and that symptoms also may take a while to return. This was my experience, and my tolerance to small, accidental exposures has grown. Not sure if this will directly apply to Jen's auto-immune condition, however.

In talking to Aaron Blaisdell, the founder and director of AHS, he described how he put his 'genetic' porphyria into remission, he said he suspects it was the seed oils that caused it (an update from his previous position.) For a guy who used to blister under the sun and had to wear denim and canvas when outside, he's looking quite tan!

But a lot of the answers to the above conditions are going to have to be addressed individually, since, as in Aaron's case, there are genetic factors driving individual responses to environmental triggers, and they're not always well understood.



Albrecht, D. S., Forsberg, A., Sandström, A., Bergan, C., Kadetoff, D., Protsenko, E., Lampa, J., Lee, Y. C., Höglund, C. O., Catana, C., Cervenka, S., Akeju, O., Lekander, M., Cohen, G., Halldin, C., Taylor, N., Kim, M., Hooker, J. M., Edwards, R. R., … Loggia, M. L. (2019). Brain glial activation in fibromyalgia – A multi-site positron emission tomography investigation. Brain, Behavior, and Immunity, 75, 72–83. https://doi.org/10.1016/j.bbi.2018.09.018
Cordero, M. D., Alcocer-Gómez, E., Cano-García, F. J., De Miguel, M., Carrión, A. M., Navas, P., & Sánchez Alcázar, J. A. (2011). Clinical Symptoms in Fibromyalgia Are Better Associated to Lipid Peroxidation Levels in Blood Mononuclear Cells Rather than in Plasma. PLoS ONE, 6(10), e26915. https://doi.org/10.1371/journal.pone.0026915
Meeus, M., Nijs, J., Hermans, L., Goubert, D., & Calders, P. (2013). The role of mitochondrial dysfunctions due to oxidative and nitrosative stress in the chronic pain or chronic fatigue syndromes and fibromyalgia patients: Peripheral and central mechanisms as therapeutic targets? Expert Opinion on Therapeutic Targets, 17(9), 1081–1089. https://doi.org/10.1517/14728222.2013.818657

Tuesday, August 17, 2021

Wednesday, August 11, 2021

Show notes for Flanagan and Goodrich on Mark Bell's Power Project Podcast

Here it is.

These are notes for things I referenced in the discussion. I didn't try to represent Alan Flanagan's research.

This post moved to Substack.

Monday, August 9, 2021

References for Ancestral Health Symposium 2021 talk, "Why Did We All Get Sick?"

Slide 11:

“Thus, as modern food preparation techniques spread throughout the world during the 19th century, so did dental crowding [malocclusion].” (Rose & Roblee, 2009)

Slide 18:

“Between 1900 and 1920… the death rate from diabetes, despite improved treatment of the disease, had increased by as much as 400 percent... It had increased fifteen-fold since the end of the Civil War.” (Taubes, 2008)

Slide 20:

“Sesame seed first cultivated ~5 Kya, in India, oil extracted by crushing” (Fuller, 2003)

Sesame seed oil spread into Egypt, the Mediterranean, and Africa

Safflower was cultivated in Egypt, use was common in Ptolemaic period, but references begin 3.5 Kya

Used as food and for lamps

Animal fat illegal in Ptolemaic Egypt (!) (Sandy, 1989)

Slide 21

Modern mass-production of seed oils started in 19th century, 200 ya

“By the early 19th century, Russian farmers were growing over 2 million acres of sunflower”

(The National Sunflower Association)

American production was mostly cottonseed oil, first a toxic waste product

Generally the manufacturers in the United States make no pretence [sic] of exporting pure lard….

“The chief adulterant found is cotton seed oil”

(Dominion of Canada, 1890)

Hydrogenated cottonseed oil (Crisco) introduced in 1911, taking vegetable fats mainstream

Slide 22

Cottonseed ruled until soybean oil introduced

Biggest change in diet in modern era is increase in seed oils

(Blasbalg et al., 2011)

Slide 23

“The Nutrition Transition: New Trends in the Global Diet”

“By the 1990s,soybean oil accounted for about 70% of… edible oils and fats in the [US]… soybeans now account for the bulk of vegetable oil consumption worldwide

“This dramatic difference was largely accounted for by a major increase in the consumption of vegetable fats by poor and rich nations alike

“Although meat consumption declined in high-income countries (by 6-9%), there was little overall reduction in fat intakes, as animal fats were replaced by a greater proportion of vegetable oils and products”

(Drewnowski & Popkin, 1997)

Slide 24

“Fifty years later, I still cannot cite a definite mechanism or mediator by which saturated fat is shown to kill people.”

(Lands, 2008)

Slide 27

HNE is involved in every aspect of Chronic Disease

Marker/mediator of Oxidative Stress
(Tsimikas, 2006; Žarković et al., 1999)

Induces

Atherosclerosis (Willeit et al., 2020; Witztum & Steinberg, 1991)

Insulin resistance (Ingram et al., 2012; Pillon et al., 2012)

DNA damage (Chung et al., 2003; Hu et al., 2002)

Inflammation (Poli & Schaur, 2000; Trevisani et al., 2007)

Mitochondrial Dysfunction (Gomes et al., 2014)

Fibrosis (Chiarpotto et al., 2005; Gomes et al., 2014)

Pain (C. Li et al., 2018; Trevisani et al., 2007) (Mis-cited as Trevisani et al., 2017; Chen et al., 2018)

Etc (Poli & Schaur, 2000; Shoeb et al., 2014; Sottero et al., 2019)

HNE is derived exclusively from n-6 fats (Ayala et al., 2014)

Slide 28

“So few subjects in the present survey were found to have any of the conventional signs of coronary disease that it would be futile to analyze the data with any hope of defining the existence of risk factors for this disease within this population. ” (Sinnett & Whyte, 1973b)

Slide 29

Cardiovascular Disease (CVD) is a modern disease

While it existed in Ancient Egypt… (Finch, 2011)

“Heart disease was an uncommon cause of death… at the beginning of the 20th century. By midcentury it had become the commonest cause” (Dalen et al., 2014)

And when heart attack was unknown, some ate lots of animal fat (Michaels, 1966)

CVD is still unknown in populations eating ancestrally—no industrially-produced food (Kaplan et al., 2017)

Slide 30

In the 1960s, researchers looked at CVD in different countries. (Lee et al., 1964)

They used heart attack determined by autopsy, an extremely reliable method

Was CVD genetic, or environmental?

They used thousands of autopsies, even bringing some hearts back to the US to confirm diagnosis

What they found confirms the earlier studies…

Slide 32

So what could the environmental factor be?

In the 1970s, Brown and Goldstein attempted to induce the first step of atherosclerosis (Goldstein et al., 1979)

It failed

LDL would not convert macrophages to foam cells

They discovered the LDL must be modified

Slide 33

Steinberg and Witztum demonstrated the nature of the modification (Witztum & Steinberg, 1991)

Fats in the LDL must be oxidized, when they are sufficently oxidized, foam cells (poisoned macrophages) will form

OxLDL is cytotoxic: toxic to cells.

The toxins in oxLDL are oxidized n-6 fats, such as HNE

Slide 34

Human studies show that dietary seed oils lead to LDL oxidation (Reaven et al., 1993; Witztum & Steinberg, 1991)

Several human RCTs demonstrate higher CVD events with seed oil feeding (Ramsden et al., 2016 Appendix part 2)

One RCT reduced n-6 intake to an evolutionarily-appropriate level, saw a 70% decline in CVD events (de Lorgeril et al., 1994)

“…if you… remove [oxLDL] from "LDL-C" to derive a corrected LDL-C, corrected LDL-C is NO LONGER predictive of events.” (Willeit et al., 2020)

Tsimikas tweet thread.

Slide 36

Chart (Hiraga, 2014)

Slide 38

“The diet consisted almost entirely of sweet potato, carbohydrate providing over 90% of the calories.”

“No clinical evidence of diabetes mellitus was found in this survey.” (Sinnett & Whyte, 1973a, 1973b)

Slide 39

And since you’re wondering… (Lai et al., 2013)

They do eat less sucrose, but compare to Chinese children (Afeiche et al., 2018)

Data in graphs from sources cited above.

Slide 41

Lots of populations ate/eat traditional diets w/out T2DM

“…their mean two-hour post-glucose level of 121 mg/ 100 ml could be regarded as falling within the "diabetic" range.”

“…the relative carbohydrate intolerance of our primitive Bushmen subjects is at first glance rather surprising.” (Joffe et al., 1971)

“…the prolonged increase after two hours in both San series certainly suggested a diabetes-like condition in the San…” (T. Jenkins et al., 1974)

Slide 42

!Kung eat lots of mongongo fruit and nuts

As much as 1/3 of their calories. (Bindon, 2009)

Mongongo nut season is when the diabetic OGTT was taken (Bindon, 2009; Guyenet, 2010; Joffe et al., 1971)

One other non-diabetic OGTT was taken of HG !Kung, not stated when. (Wilmsen, 1982)

!Kung eating non-HG diet did not test diabetic. (H. C. Jenkins et al., 2010)

Mongongo nuts are high in n-6 (Gwatidzo et al., 2017)

Slide 43

1961: soybean oil introduced as an IV food supplement—Intralipid (Gura, 2020)

1964: Noted that Intralipid induces insulin resistance and hyperglycemia (Felber & Vannotti, 1964)

2014: “Infusion of Intralipid, comprised predominantly of polyunsaturated fatty acids [linoleic (44–62%)…]… is an established model for producing lipid-induced insulin resistance.” In humans (Chow et al., 2014; Jensen et al., 2003)

Slide 44

“The lack of… gluconeogenesis in the Clinoleic vs. the Intralipid group suggests that different classes of fatty acids exert different effects on glucose kinetics in preterm infants.”

Proposed mechanism is IR (van Kempen et al., 2006)

Clinoleic is an olive-oil infusion, low in n-6

Of course eating something is vastly different from injecting something

Slide 45

In humans, IR precedes T2DM by years (Martin et al., 1992)

OxLDL is associated with IR, and precedes it by years (Carantoni et al., 1998; Park et al., 2009)

As discussed, seed oils lead to LDL oxidation

Other sources of oxLDL (smoking, sepsis) also induce IR (Attvall et al., 1993; Behnes et al., 2008; Carlson, 2003; Lymperaki et al., 2015)

Unexpectedly,… targeting oxidized LDL [via antibodies] improves insulin sensitivity…” in monkeys (S. Li et al., 2013)

Slide 46

Switching from high to low n-6 oils lowers insulin resistance (Nigam et al., 2014)

Dose-dependent relationship to n-6 content of seed oils

Liver fat also improved—NAFLD patients

“… 15–21% protein… 55–70% carbohydrates, and 20% fats.”

Slide 48

Lowering n-6:n-3 ratio lowers insulin resistance (Van Name et al., 2020)

“The intervention diet consisted of a low n–6 to n–3 PUFA ratio of 4:1…”

“…macronutrient content was 50%–55%... carb., 20% from protein, and 25%–30% from fat…”

Diet monitored by blood biomarkers, including oxLAMs

No control, performed at Yale

Slide 51

“In 1616, Ieyasu Tokugawa, the founder of the Edo government died. It is said he had been overeating fish fried in sesame oil.”

From “Tempura... Another Usage of Lamp Oil”

(Walker, 2003 quoting Ishige, 1980)



References:

Afeiche, M. C., Koyratty, B. N. S., Wang, D., Jacquier, E. F., & Lê, K.-A. (2018). Intakes and sources of total and added sugars among 4 to 13-year-old children in China, Mexico and the United States. Pediatric Obesity, 13(4), 204–212. https://doi.org/10.1111/ijpo.12234

Attvall, S., Fowelin, J., Lager, I., Schenck, H. V., & Smith, U. (1993). Smoking induces insulin resistance—A potential link with the insulin resistance syndrome. Journal of Internal Medicine, 233(4), 327–332. https://doi.org/10.1111/j.1365-2796.1993.tb00680.x

Ayala, A., Muñoz, M. F., & Argüelles, S. (2014, May 8). Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal [Review Article]. Oxidative Medicine and Cellular Longevity; Hindawi. https://doi.org/10.1155/2014/360438

Behnes, M., Brueckmann, M., Liebe, V., Liebetrau, C., Lang, S., Putensen, C., Borggrefe, M., & Hoffmann, U. (2008). Levels of oxidized low-density lipoproteins are increased in patients with severe sepsis. Journal of Critical Care, 23(4), 537–541. https://doi.org/10.1016/j.jcrc.2008.09.002

Bindon, J. R. (2009). Foraging with the !Kung [Educational]. University of Iowa, Anthropology Dept., Unknown. https://anthropology.ua.edu/bindon/ant476/topics/Foragers.pdf

Blasbalg, T. L., Hibbeln, J. R., Ramsden, C. E., Majchrzak, S. F., & Rawlings, R. R. (2011). Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. The American Journal of Clinical Nutrition, 93(5), 950–962. https://doi.org/10.3945/ajcn.110.006643

Carantoni, M., Abbasi, F., Warmerdam, F., Klebanov, M., Wang, P.-W., Chen, Y.-D. I., Azhar, S., & Reaven, G. M. (1998). Relationship Between Insulin Resistance and Partially Oxidized LDL Particles in Healthy, Nondiabetic Volunteers. Arteriosclerosis, Thrombosis, and Vascular Biology, 18(5), 762–767. https://doi.org/10.1161/01.ATV.18.5.762

Carlson, G. L. (2003). Insulin resistance in sepsis. BJS, 90(3), 259–260. https://doi.org/10.1002/bjs.4081

Chiarpotto, E., Castello, L., Leonarduzzi, G., Biasi, F., & Poli, G. (2005). Role of 4-hydroxy-2,3-nonenal in the pathogenesis of fibrosis. BioFactors, 24(1–4), 229–236. https://doi.org/10.1002/biof.5520240127

Chow, L. S., Mashek, D. G., Austin, E., Eberly, L. E., Persson, X.-M., Mashek, M. T., Seaquist, E. R., & Jensen, M. D. (2014). Training status diverges muscle diacylglycerol accumulation during free fatty acid elevation. American Journal of Physiology-Endocrinology and Metabolism, 307(1), E124–E131. https://doi.org/10.1152/ajpendo.00166.2014

Chung, F.-L., Pan, J., Choudhury, S., Roy, R., Hu, W., & Tang, M. (2003). Formation of trans-4-hydroxy-2-nonenal- and other enal-derived cyclic DNA adducts from ω-3 and ω-6 polyunsaturated fatty acids and their roles in DNA repair and human p53 gene mutation. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 531(1), 25–36. https://doi.org/10.1016/j.mrfmmm.2003.07.001

Dalen, J. E., Alpert, J. S., Goldberg, R. J., & Weinstein, R. S. (2014). The Epidemic of the 20th Century: Coronary Heart Disease. The American Journal of Medicine, 127(9), 807–812. https://doi.org/10.1016/j.amjmed.2014.04.015

de Lorgeril, M., Renaud, S., Mamelle, N., Salen, P., Martin, J. L., Monjaud, I., Guidollet, J., Touboul, P., & Delaye, J. (1994). Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet (London, England), 343(8911), 1454–1459. https://doi.org/10.1016/s0140-6736(94)92580-1

Dominion of Canada. (1890). Sessional Papers of the Dominion of Canada (Vol. 1). Dominion of Canada. https://books.google.com/books?id=JA0xAQAAMAAJ&printsec=frontcover&source=gbs_ge_summary_r&cad=0#v=onepage&q=cotton%20seed&f=false

Drewnowski, A., & Popkin, B. M. (1997). The nutrition transition: New trends in the global diet. Nutrition Reviews, 55(2), 31–43. https://doi.org/10.1111/j.1753-4887.1997.tb01593.x

Felber, J. P., & Vannotti, A. (1964). EFFECTS OF FAT INFUSION ON GLUCOSE TOLERANCE AND INSULIN PLASMA LEVELS. Medicina Experimentalis: International Journal of Experimental Medicine, 10, 153–156. https://doi.org/10.1159/000135410

Finch, C. E. (2011). Atherosclerosis is an old disease: Summary of the Ruffer Centenary Symposium, The Paleocardiology of Ancient Egypt, a meeting report of the Horus Study team. Experimental Gerontology, 46(11), 843–846. https://doi.org/10.1016/j.exger.2011.08.011

Fuller, D. Q. (2003). Further evidence on the Prehistory of sesame. Asian Agri-History(India). https://agris.fao.org/agris-search/search.do?recordID=IN2003000892

Goldstein, J. L., Ho, Y. K., Basu, S. K., & Brown, M. S. (1979). Binding site on macrophages that mediates uptake and degradation of acetylated low density lipoprotein, producing massive cholesterol deposition. Proceedings of the National Academy of Sciences of the United States of America, 76(1), 333–337. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC382933/

Gomes, K. M. S., Campos, J. C., Bechara, L. R. G., Queliconi, B., Lima, V. M., Disatnik, M.-H., Magno, P., Chen, C.-H., Brum, P. C., Kowaltowski, A. J., Mochly-Rosen, D., & Ferreira, J. C. B. (2014). Aldehyde dehydrogenase 2 activation in heart failure restores mitochondrial function and improves ventricular function and remodelling. Cardiovascular Research, 103(4), 498–508. https://doi.org/10.1093/cvr/cvu125

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

Guyenet, S. (2010, November 20). Whole Health Source: Glucose Tolerance in Non-industrial Cultures. Whole Health Source. http://wholehealthsource.blogspot.com/2010/11/glucose-tolerance-in-non-industrial.html

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AHS21

Thursday, August 5, 2021

Interview: Ray Peat, with David Gornoski on A Neighbor's Choice

"Ray Peat Interview with Tucker Goodrich, David Gornoski on PUFAs, Seed Oils, Benefits of Sugar, Milk"
"In this fascinating interview, David Gornoski and Tucker Goodrich are joined by Dr. Ray Peat, researcher of aging, nutrition, and hormones. Dr. Ray Peat talks about how his interest in nutrition science started; how changes in diet affected health in Mexico and Israel; whether sugar is harmful to our bodies; the connection between PUFAs, cancer, and diabetes; how ketogenic diets can be harmful; how avoiding PUFAs lowers the skin’s susceptibility to sunburn; what kind of milk is beneficial to our health; and more.

"Subscribe to Dr. Peat’s newsletter by emailing raypeatsnewsletter@gmail.com


Here's a link to the podcast, and here's an embedded player:


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.