Podcast Interview: "Linoleic Acid- Interview with Tucker Goodrich" with Dr. Joseph Mercola

Welcome to Dr. Mercola listeners and subscribers, if any of you make it here!

For existing readers, the Youtube version of this interview has been released. Here's the podcast version, on Apple Podcasts.

Here's Dr. Mercola's article on this topic:

How Linoleic Acid Wrecks Your Health

They did a transcript of the interview, also! (PDF, I'm impressed!)

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P.S. The censors came after Mercola, and he took much of his content off-line, including my video.

I found another link to the video, and it's embedded below, but I have no idea who is hosting this, or how long it will last.

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For new visitors, here are a few of my key posts, some of which are mentioned in the interview.

What’s Worse—Carbs or Seed Oils? Understanding a High-PUFA Diet.

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

What Effect Does Linoleic Acid Have On Mitochondria?

Does Consumption of Omega-6 Seed Oils Worsen ARDS and COVID-19?

Below are the extremely rough notes that Dr. Mercola and I worked off in the interview, including a bibliography.

Questions are welcome in the comments.

I'm on twitter here, and am active.

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Why this is likely the major reason contributing to metabolic dysfunction and the epidemic of chronic disease

Criteria that I concluded had to be true for the cause (whatever it was) of chronic disease.

1.      Trans-Species
This is a problem that we see in all human populations, and the animal species that associate with them, which includes pets but also feral animals like rats, pigeons, and racoons.
This eliminates genetic causes, and many pathogens, which do not cross species lines easily.

2.      Diet-based
Several crucial books (Price, 1938; Stefansson, 1960; Trowell & Burkitt, 1981) looked at healthy, traditional cultures compared to sick ones, and made a clear suggestion that it was diet based T&B made it clear that it affected diseases seemingly unrelated to diet, like auto-immunity.
This eliminates other proposed mechanisms, like pollution (fattest country on earth is in the South Pacific: what is the pollution?).

3.      Novel
Must be a food that was recently introduced, contemporaneously with the emerging pandemics of T2DM and obesity. (Taubes, 2008) looked at diabetes emergence in the 1800s, (Lee et al., 1964) looked at emergence of ischaemic heart disease in the 20^th century vs traditional cultures.

4.      Mechanistic confirmation
Too easy to be fooled by epidemiology without some mechanistic confirmation, as happened to Ancel Keys. (Ramsden et al., 2016)

5.      Contained in D12492
This is the diet used to induce chronic diseases in lab animals. It seems silly, but no-one went through this diet to figure out what ingredient actually had the measured effect until 2012!

How you figured this out so early

Jen’s explanation (more complimentary): "Always open-minded and not biased as to what other people were believing and the trends. Simply were assessing evidence-based research and making decisions according to that."

My version: "Dumb luck and stubborn."

Had dramatic personal experience that couldn’t be explained by physicians, so looked into why it had happened. Stuck with exploration even when mentor in topic abandoned it.

Some seminal studies that provide irrefutable evidence of the hypothesis

“Irrefutable” is hard, if such a study had been done you wouldn’t be talking to me, this would be old news. Must follow Bill Lands, a pioneer in PUFA research, and “connect the dots”.

(Alvheim et al., 2012) shows what induces obesity, explains mechanism behind human-approved drug that treated multiple aspects of chronic diseases. Compare to D12492.

“Large randomized trials with rimonabant have demonstrated efficacy in treatment of overweight and obese individuals with weight loss significantly greater than a reduced calorie diet alone. In addition, multiple other cardiometabolic parameters were improved in the treatment groups including increased levels of [HDL], reduced triglycerides, reduced waist circumference, improved insulin sensitivity, decreased insulin levels, and in diabetic patients improvement in [HbA1c].” (Bronander & Bloch, 2007)

(Medina-Navarro et al., 2003) showing a physiological level of glucose and PUFA produced a poison in vitro. My tweet: “Etiology of metsym & chronic disease, in one chart. At physiologic lvls. God...”

(Singh et al., 2008) “Fat accumulation in Caenorhabditis elegans triggered by the electrophilic lipid peroxidation product 4-hydroxynonenal (4-HNE). Tweet: “N-6 metab 4-HNE induces obesity across species, "the process is conserved and thus likely to be universal."”

(Liu et al., 2011) “Formation Of 4-Hydroxynonenal From Cardiolipin Oxidation: Intramolecular Peroxyl Radical Addition And Decomposition”

(Witztum & Steinberg, 1991)

(Ghosh et al., 2004) “Brief episode of STZ-induced hyperglycemia produces cardiac abnormalities in rats fed a diet rich in n-6 PUFA” (Goodrich, 2018)

(Skulachev et al., 2009) “An attempt to prevent senescence: A mitochondrial approach”

(Bethancourt et al., 2019) “Household use of cooking oil increased and was positively associated with female BMI. Consumption of domesticated animal products did not change significantly but was positively associated with female BMI and male waist circumference. Conclusions Even small increases in energy-dense market-based foods can contribute to adiposity gains among a moderately active, subsistence-based population.”

(Maciejewska et al., 2015) “Following the six-month dietary intervention, hepatic steatosis resolved completely in all patients. This resulted in a significant decrease in the concentrations of all eicosanoids (LX4, 16-HETE, 13-HODE, 9-HODE, 15-HETE, 12-HETE, 5-oxoETE, 5-HETE) and key biochemical parameters (BMI, insulin, HOMA-IR, liver enzymes).”

(Goodrich, 2016) “The Cause of Metabolic Syndrome: Excess Omega-6 Fats (Linoleic Acid) in Your Mitochondria”

Will dive a bit into cardiolipin as I believe that is a major reason to explain the dilemma

Yes, covered in links above, plenty of material for discussion

Your best guess as to ideal LA consumption for optimal health and how to do that

LA is not essential, despite what was thought over last 90 years. Consumption should be minimal, discuss what should be avoided. (Alvheim et al., 2013; Blasbalg et al., 2011; Carlson et al., 2019)

Can tangent a bit to carnosine as a way to supply a sacrificial scavenger for reactive carbonyl species (RCS) or in LA context better known as OXLAMs or oxylipids

(Nègre-Salvayre et al., 2017) “A recent study by Colzani and colleagues analyzed and compared the ability of several classical carbonyl scavengers to prevent the carbonylation of proteins, and concluded that carnosine is the most effective scavenger for HNE...”
(Zhao et al., 2015) “Carnosic Acid as a Major Bioactive Component in Rosemary Extract Ameliorates High-Fat-Diet-Induced Obesity and Metabolic Syndrome in Mice”

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References

Alvheim, A. R., Malde, M. K., Osei‐Hyiaman, D., Hong, Y. H., Pawlosky, R. J., Madsen, L., Kristiansen, K., Frøyland, L., & Hibbeln, J. R. (2012). Dietary Linoleic Acid Elevates Endogenous 2-AG and Anandamide and Induces Obesity. Obesity, 20(10), 1984–1994. https://doi.org/10.1038/oby.2012.38

Alvheim, A. R., Torstensen, B. E., Lin, Y. H., Lillefosse, H. H., Lock, E.-J., Madsen, L., Hibbeln, J. R., & Malde, M. K. (2013). Dietary linoleic acid elevates endogenous 2-arachidonoylglycerol and anandamide in Atlantic salmon (Salmo salar L.) and mice, and induces weight gain and inflammation in mice. The British Journal of Nutrition, 109(8), 1508–1517. https://doi.org/10.1017/S0007114512003364

Bethancourt, H. J., Leonard, W. R., Tanner, S., Schultz, A. F., & Rosinger, A. Y. (2019). Longitudinal Changes in Measures of Body Fat and Diet Among Adult Tsimane’ Forager-Horticulturalists of Bolivia, 2002-2010. Obesity, 27(8), 1347–1359. https://doi.org/10.1002/oby.22556

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

Bronander, K. A., & Bloch, M. J. (2007). Potential role of the endocannabinoid receptor antagonist rimonabant in the management of cardiometabolic risk: A narrative review of available data. Vascular Health and Risk Management, 3(2), 181–190. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1994026/

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

Ghosh, S., Qi, D., An, D., Pulinilkunnil, T., Abrahani, A., Kuo, K.-H., Wambolt, R. B., Allard, M., Innis, S. M., & Rodrigues, B. (2004). Brief episode of STZ-induced hyperglycemia produces cardiac abnormalities in rats fed a diet rich in n-6 PUFA. American Journal of Physiology. Heart and Circulatory Physiology, 287(6), H2518-2527. https://doi.org/10.1152/ajpheart.00480.2004

Goodrich, T. (2016, February 5). The Cause of Metabolic Syndrome: Excess Omega-6 Fats (Linoleic Acid) in Your Mitochondria. Yelling Stop. http://yelling-stop.blogspot.com/2016/02/the-cause-of-metabolic-syndrome-excess.html

Goodrich, T. (2018, June 28). What’s Worse—Carbs or Seed Oils? Understanding a High-PUFA Diet. Yelling Stop. http://yelling-stop.blogspot.com/2018/06/whats-worsecarbs-or-seed-oils.html

Lee, K. T., Nail, R., Sherman, L. A., Milano, M., Lee, K. T., Deden, C., Imai, H., Goodale, F., Nam, S. C., Lee, K. T., Goodale, F., Scott, R. F., Snell, E. S., Lee, K. T., Daoud, A. S., Jarmolych, J., Jakovic, L., & Florentin, R. (1964). Geographic Pathology of Myocardial Infarction: Part I. Myocardial infarction in orientals and whites in the United States; Part II. Myocardial infarction in orientals in Korea and Japan; Part III. Myocardial infarction in Africans in Africa and negroes and whites in the United States; Part IV. Measurement of amount of coronary arteriosclerosis in Africans, Koreans, Japanese and New Yorkers. The American Journal of Cardiology, 13(1), 30–40. https://doi.org/10.1016/0002-9149(64)90219-X

Liu, W., Porter, N. A., Schneider, C., Brash, A. R., & Yin, H. (2011). Formation Of 4-Hydroxynonenal From Cardiolipin Oxidation: Intramolecular Peroxyl Radical Addition And Decomposition. Free Radical Biology & Medicine, 50(1), 166–178. https://doi.org/10.1016/j.freeradbiomed.2010.10.709

Maciejewska, D., Ossowski, P., Drozd, A., Ryterska, K., Jamioł-Milc, D., Banaszczak, M., Kaczorowska, M., Sabinicz, A., Raszeja-Wyszomirska, J., & Stachowska, E. (2015). Metabolites of arachidonic acid and linoleic acid in early stages of non-alcoholic fatty liver disease—A pilot study. Prostaglandins & Other Lipid Mediators, 121, 184–189. https://doi.org/10.1016/j.prostaglandins.2015.09.003

Medina-Navarro, R., Durán-Reyes, G., Díaz-Flores, M., Kumate Rodríguez, J., & Hicks, J. J. (2003). Glucose autoxidation produces acrolein from lipid peroxidation in vitro. Clinica Chimica Acta; International Journal of Clinical Chemistry, 337(1–2), 183–185. https://doi.org/10.1016/j.cccn.2003.07.005

Nègre-Salvayre, A., Garoby-Salom, S., Swiader, A., Rouahi, M., Pucelle, M., & Salvayre, R. (2017). Proatherogenic effects of 4-hydroxynonenal. Free Radical Biology and Medicine, 111, 127–139. https://doi.org/10.1016/j.freeradbiomed.2016.12.038

Price, W. (1938). Nutrition and Physical Degeneration. A Project Gutenberg of Australia EBook. http://gutenberg.net.au/ebooks02/0200251h.html

Ramsden, C. E., Zamora, D., Majchrzak-Hong, S., Faurot, K. R., Broste, S. K., Frantz, R. P., Davis, J. M., Ringel, A., Suchindran, C. M., & Hibbeln, J. R. (2016). Re-evaluation of the traditional diet-heart hypothesis: Analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ, 353. https://doi.org/10.1136/bmj.i1246

Singh, S. P., Niemczyk, M., Zimniak, L., & Zimniak, P. (2008). Fat accumulation in Caenorhabditis elegans triggeredby the electrophilic lipid peroxidation product 4-Hydroxynonenal (4-HNE)—Full Text. Aging, 1(1), 68–80. https://doi.org/10.18632/aging.100005

Skulachev, V. P., Anisimov, V. N., Antonenko, Y. N., Bakeeva, L. E., Chernyak, B. V., Erichev, V. P., Filenko, O. F., Kalinina, N. I., Kapelko, V. I., Kolosova, N. G., Kopnin, B. P., Korshunova, G. A., Lichinitser, M. R., Obukhova, L. A., Pasyukova, E. G., Pisarenko, O. I., Roginsky, V. A., Ruuge, E. K., Senin, I. I., … Zorov, D. B. (2009). An attempt to prevent senescence: A mitochondrial approach. Biochimica et Biophysica Acta (BBA) - Bioenergetics, 1787(5), 437–461. https://doi.org/10.1016/j.bbabio.2008.12.008

Stefansson, V. (1960). Cancer: Disease of Civilization?: An Anthropological and Historical Study. Hill and Wang.

Taubes, G. (2008). Good Calories, Bad Calories. Penguin RandomHouse. https://www.penguinrandomhouse.com/books/176680/good-calories-bad-calories-by-gary-taubes/9781400033461

Trowell, H. C., & Burkitt, D. P. (1981). Western Diseases, Their Emergence and Prevention. Harvard University Press.

Witztum, J. L., & Steinberg, D. (1991). Role of oxidized low density lipoprotein in atherogenesis. Journal of Clinical Investigation, 88(6), 1785–1792. https://doi.org/10.1172/JCI115499

Zhao, Y., Sedighi, R., Wang, P., Chen, H., Zhu, Y., & Sang, S. (2015). Carnosic Acid as a Major Bioactive Component in Rosemary Extract Ameliorates High-Fat-Diet-Induced Obesity and Metabolic Syndrome in Mice. Journal of Agricultural and Food Chemistry, 63(19), 4843–4852. https://doi.org/10.1021/acs.jafc.5b01246