Episode 24 - Tucker and Gabor on Seed Oils vs Refined Carbs – Part 2

by Break Nutrition | Podcast

Show notes:

  • You can find Tucker Goodrich at http://yelling-stop.blogspot.com and on Twitter @tuckergoodrich
    • Oxidative stress is the inevitable result of metabolism and basic chemistry, resulting from reactive oxygen species (ROS) like “slow” reacting hydrogen peroxide and “fast” reacting peroxyl radicals. Omega-6 and omega-3 PUFAs form peroxidation products like malondialdehyde, 4-hydroxynonenal (HNE) , isoprostanes or 9- and 13-hydroxyoctadecadienoic acids. Here’s a study from 2015 for more on PUFA chemistry.

  •  PUFAs are not stable at the physiological temperature of ~37°C. When anti-oxidant action is lacking and the clearance of oxidation products is impaired this is either a result of or cause of disease.
  • Chronic inflammation is in part a result these oxidative processes. Chronic inflammation is common on high-sugar and brain functions regulating energy intake and expenditure can be diminished from it (in rodents). An inflamed hypothalamus can result, which I wrote about here
  • Marty Kendall of Optimising Nutrition shared an interview of Dr.Kyle Mamounis who researches fatty acids.
  • Dr.Mamounis published “Linoleic acid causes greater weight gain than saturated fat without hypothalamic inflammation in the male mouse
    • 1%, 15% and 22.5% LA rich diets (from soybean oil) were given to rats with macros, fiber and micronutrients controlled for across diets ⇒ the percentages were representative of modern industrialized intakes.
      • Results
        • “In conclusion, SFA- and LA-rich HFDs induced obesity and disturbed metabolic profiles in the mouse compared to a low-fat diet. However, LA produced greater body weight gain and insulin resistance, and suppressed activity more than the SFA […] although the effect is not as large as the results obtained previously by other groups”
        • Glucose disposal lower in all 3 HFD groups ⇒ consistent with Randle Cycle whereby mitochondrial fat oxidation inhibits glucose oxidation and thus its cellular uptake
          • “This suggests fatty acids are not equal in their participation in the Randle Cycle”
            • There’s support for the idea that increased HNE levels, acting through the Randle Cycle, increases malonyl-CoA and thus fatty acid synthesis, leading to apportioning of energy towards fat storage ⇒ study in C. elegans “Fat accumulation in Caenorhabditis elegans triggered by the electrophilic lipid peroxidation product 4-Hydroxynonenal (4-HNE)”
    • “An example of non-respiratory O2 consumption is lipid peroxidation, such as oxidation of PUFA-rich LDL. As previously mentioned, only PUFA oxidize non-enzymatically at physiological temperatures, with greater chain length and number of double bonds increasing oxidative risk”
    • “[although insulin was not measured] these results suggest that the 22.5% group would require more insulin in order to achieve a rate of glucose disposal equal to [control], 1% and 15%”
    • “The effects of LA compared to other FAs should be a focus of DIO research”
    • Lard high-SFA diet

  • Study (2017) “Omega-3 deficiency impairs honey bee learning” (article)
  • Study (2017) “Breastmilk with a high omega-6 to omega-3 fatty acid ratio induced cellular events similar to insulin resistance and obesity in 3T3-L1 adipocytes”
    • “increased exposure to n-6 PUFA during critical period in the development of adipocytes could result in a permanent increase in the number and size of adipocytes
    • Methods
      • non-overweight women 2 weeks post-delivery (n = 47)
      • Measures
        • In vitro measures made in pre-adipocytes cells (3T3-L1)
        • total n-6 to n-3 PUFA ratio [namely low (between 1 and 7), medium (between 7 and 8) and high (between 9 and 11)] via gas chromatography
        • Soluble cytokines IL-2/4/6/10,TNF and IFN-γ
        • Adipogenic enzymes diacylglycerol acyltransferase-2 (DGAT2), stearoyl-CoA desaturase (SCD-1), RPLPO (large ribosomal protein) and leptin
          • SCD-1 = catalyzes the rate-limiting step in the formation of monounsaturated fatty acids (MUFAs), specifically oleate and palmitoleate from stearoyl-CoA and palmitoyl-CoA
          • DGAT = catalyzes the formation of triglycerides from diacylglycerol and Acyl-CoA. The reaction catalyzed by DGAT is considered the terminal and only committed step in triglyceride synthesis and to be essential for the formation of adipose tissue
          • RPLPO = located in the cytoplasm it catalyzes protein synthesis
    • Results
      • high n-6 to n-3 PUFA ratio showed higher amounts of soluble pro-inflammatory cytokines, IL-6 (22.45 pg/ml) and TNF (3.74 pg/ml)”
      • “The n-6 to n-3 PUFA ratio in the low group was 2.28 (ɷ3 5.68%), in the medium group was 6.02 (ɷ3 2.61%) and in the high group was 8.79 (ɷ3 1.79%)”
      • no significant correlation between AA and total n-6 PUFA with any of the measured soluble cytokines
      • “a significant negative correlation was observed between DHA concentration with major pro-inflammatory cytokines, namely IL-6 and TNF
      • “Whey from breast milk with high n-6 to n-3 polyunsaturated fatty acid ratio increased lipogenesis
        • “[breast milk] samples with medium and high n-6 to n-3 PUFA ratio showed a significantly lower mRNA expression of leptin” vs low PUFA ratio
        • higher n-6 PUFA is the driving force for the detrimental health effects” ⇒ health effects not about increasing n-3 PUFA
    • Finally I ask Gabor and Tucker about the big picture, to give a statement (and a percentage if they dare) on how responsible refined carbs and seed oils are for the diseases of civilization
      • Gabor sees refined carbs (and possibly combinations of the latter with fructose) as the major etiological agent. Nevertheless, he doesn’t consume seed oils himself nor does he advise any else to. Same for refined flours. He leaves the door open to seed oils having a larger role than previously thought
      • Tucker sees seed oils as the major etiological agent, possibly accounting for ~80% of the damage. He also agrees that novel combinations, not only novel agents, can be to blame as well. Tucker does not consume refined carbs nor does he advise any else to. Same for seed oils.
      • As for myself, I’m somewhere in the middle but currently lean more towards refined carbs as carrying most of the blame. However, the deeper I dive into the research on seed oils the more ground I cede to them. I do not consume seed oils or refined carbs and do not advise anyone consume them.

*correction: I said PUFAs are very sensitive to oxygen and that this enables them to mediate cell-to-cell communication. I should have said that they mediate cell-wall reinforcement (after a microbial attack for example).

Want more actionable episodes ? Subscribe to our podcast !


If you’d like to receive the new Break Nutrition podcast episodes on your favorite devices, subscribe with your preferred method below:


[Total: 0    Average: 0/5]

Well, Since you are here why you don't take the Challenge ?