Friday, December 11, 2020

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!)

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.

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

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.

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 20th 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”


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.

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.

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.

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.

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.

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.

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.

Goodrich, T. (2016, February 5). The Cause of Metabolic Syndrome: Excess Omega-6 Fats (Linoleic Acid) in Your Mitochondria. Yelling Stop.

Goodrich, T. (2018, June 28). What’s Worse—Carbs or Seed Oils? Understanding a High-PUFA Diet. Yelling Stop.

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.

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.

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.

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.

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.

Price, W. (1938). Nutrition and Physical Degeneration. A Project Gutenberg of Australia EBook.

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.

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.

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.

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

Taubes, G. (2008). Good Calories, Bad Calories. Penguin RandomHouse.

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.

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.



  1. Avoiding chicken and pork will make me sad. 😢

  2. In the podcast you make mention about olive oil fraud. Would you consider the list of olive oil put out by NAOOA Certified Olive Oils to be a valid list? I am skeptical!

    1. That's basically the list that I use, for lack of anything better.

      It's certainly partly a marketing effort on behalf of California olive oils, but since they seem to be the only ones testing, we'll just have to assume the competitors don't want to test.

  3. This interview was my introduction to this topic and it’s been life changing. I immediately cut out seed oils from my diet and have already begun losing weight and feeling more energetic throughout each day (it’s been a week only). Two questions:
    1.) do seed oils used topically (many seed oils in skin care products) have the same negative effect as when they are consumed in the diet? If so, this is alarming considering the number of “anti-aging “ skin care products which contain seed oils.

    2.) eliminating seed oils seems simple enough, but when it comes to limiting omega-6 consumption to 2-3grams per day, it’s taking some work to come up with new meal plans for myself and my family.... will you he including a list of Low LA foods in your book or blog? This would be so helpful!

    Thank you!

    1. The topical seed oil questions keeps coming up, and unfortunately I haven't seen a good answer. They can be beneficial in small amounts, it seems, but one starts getting into a huge number of questions and confounders.

      Personally, I don't really see any need for topical skin care creams, so I resolve the issue that way.

      I've found it's more effective to eat your skin care than apply it as a band-aid for a poor diet!

  4. This interview was my introduction to this issue of linoleic acid and it has been life changing for me. It’s only been a week and I’ve lost weight and feel more energetic throughout the day. Two questions :

    1.) topical use of seed oils (ie. seed oils found in skin care products) - does this have the same negative effect as when we ingest via our foods? It would be alarming If this is the case being that I’ve found seed oils in every “Aint-aging” product on my shelf.

    2.) navigating a whole new meal plan for myself and my family that falls within a 2-3g of omega 6 per day is a bit challenging. It was easy to eliminate all of the freezer foods / highly processed foods, but it’s choosing which grains (if any) are okay and if cheese is ok and so on. Will you be including a list of foods suggestions in your book or blog? This would be sooo helpful and appreciated!

    Thank you!

    1. Oops! You can ignore this comment.... it looked like my first comment hadn’t gone through so I rewrote it and now I see they have both posted.

  5. I understand the point that consuming excess polyunsaturated fat leads to more polyunsaturated fat in cardiolipin—which is a bad thing because it oxidizes easily, but then why would the heart prefer to use polyunsaturated fat for its mitochondrial cardiolipin?

    1. I have actually been digging into this myself since I posted, and one possible, simple answer may be 'diet.'

    2. Linoleic acid seems to allow mitochondria to operate at high efficiency. So yes, diet does play a large role in heart cardiolipin composition, but the heart does seem to like LA, probably because of increased efficiency.

      The heart also seems to have compensatory mechanisms, like a robust antioxidant system, avoidance of glucose as fuel, and perhaps other things we're not aware of.

      In noting the relationship of oxidative stress to cancer, it's interesting that heart cancers are exceedingly rare. The heart is protected, somehow.

  6. Very eye opening, thank you so much for your research and efforts in making this knowledge public. I've used coconut oil, but I also use avocado oil. I've started asking eateries what they are use for cooking and don't always get a straight forward answer. Sometimes I get "clear frying oil". What could that be? I wanted your opinion on peanut oil and avocado oil because I don't completely understand how these are extracted and if these are safe to use. Please advise. Thanks so much.

    1. First, extraction method isn't important. What is important is the n-6 level of the fat.

      A "clear frying oil" is almost certainly a high n-6 oil. I'd avoid.

      There are supposedly some high-oleic peanut oil on market, but peanut is in general a high-n-6 oil.

      Avocado oil is a better option, but ~80% of it is adulterated, similar to olive oil. If you can be sure you're actually getting olive or avocado oil, then it's not the worst option.

  7. Thank you for all the great info on linoleic acid! I've been keto for almost 5 years, I don't eat any vegetable fats. 90% pasture raised meats, only wild seafood. You didnt mention avocado oil, I'm very curious if you think its "safe"?

    I hope you can find lots of happy in the New Year!

    Cecily Reading

    1. Avocado oil is OK, unfortunately, like olive oil, a lot of it is adulterated with cheap seed oils. So it's hard to know what you are getting.

    2. FWIW a test of several avocado oils by UC Davis showed that Chosen Foods (available at Costco) tested well.

  8. Hi Tucker,

    Appreciate your work. I was wondering if you've ever come across the following study:

    Basically they fed mice a diet where they got 15% calories from fat. They varied the fat between coconut oil and corn oil. Corn oil ranged from .8% to 8.4% of diet. They looked at skin cancer and Mammary Tumors. They found that lower Linoleic acid was more protective against mammary tumors.

    For skin cancer they found that the worst outcomes came when the amount of linoleic acid was somewhere in the middle (2.2%-4.5% total calories). the best outcomes were at the max levels of linoleic acid, although the lowest levels were also good.

    Found this a bit confusing. Given that the outcomes are not linear (8.4% and 5.6% LA give better outcomes than 7% LA) perhaps the sample isn't big enough. There were 30 mice per group. Or perhaps there were other differences that we don't know about (something about the light they were exposed to maybe...)

    Either way, this is challenging the enjoyable certainty I had about what is and isn't healthy :)

    1. I hadn't seen this paper yet. Added it to the to-do list!