Comments by Jayy
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    Thanks for the wonderful podcasts. I am curious about the use of glycerol in Dr. Longo’s FMD. Dr. Longo has explained, elsewhere, that glycerol extends the life of yeast when used as an alternate carbon source (alternate to glucose or ethanol) ie glycerol shifts metabolism away from glycolysis towards oxidative phosphorylation thereby mimicking calorie restriction. Other researchers have found similar benefits in some organisms. In the recent Eric Verdin podcast, Dr. Verdin explains (~39 minutes in) the importance of mitochondrial health and hints at a positive role for oxidative phosphorylation. I am hoping the use/role of glycerol and its impact on longevity can be explored somewhere along the line.

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      I’m interested in trying a Ketogenic diet but my genetics report found 3 negative markers related to saturated fat intake:

      FTO - rs17817449(G;T): “Saturated fat may have a negative effect on blood glucose and insulin levels and increases type 2 diabetes risk in individuals with this genotype.”

      FTO - rs9939609(A;T): “This genotype has also been associated with obesity particularly in the context of a high saturated fat and low polyunsaturated fat intake.”

      FTO - rs1121980(C;T): “This genotype, rs1121980(C;T), is associated with a roughly 1.67-fold increased risk for obesity, particularly in the context of a high saturated fat and low polyunsaturated fat intake.”

      Knowing the above issues I may have with saturated fat, I’m having a hard time finding any Ketogenic diets that would work. It seems that most of the Ketogenic diets are heavy in saturated fats, and I’m unsure if this will push me towards obesity, diabetes, or both?

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        I have the same genetic makeup and started a keto diet 3 years ago. While eating saturated fat from dairy, my lipid profile got very bad (400+LDL, high TG/HDL ratio, low particle size).

        After moderating the SF and cutting out most dairy, it got better. It seems more people have this issue. Rhonda and Peter Attia recently discussed it on his podcast.

        Feel free to get in touch for any details or data.

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          I also have the same FTO profile as brywatson. I have been on a keto diet for a few years - very high saturated fat. Last year I found my LDL had gone through the roof (~ 400 mg/dL or ~ 10 mmol/L). I purchased a chlorestech LDX in order to closely monitor my lipid profile. I do time-restricted feeding (just water for 14 hours a day). I have done 2 five day fasts and one three day fast in the past 8 months and multiple one-day fasts. I am a 65-year-old male Caucasian. My PPAR alpha and gamma indicate “normal fat metabolism”. My triglycerides average about 60 mg/dL or .7 mmol/L after an overnight fast. My HDL typically averages 77 mg/dL or ~ 2 mmol/L. My 4 foxo3 and APOC3 genotypes all “may increase lifespan”. Not so for IL6 (rs1800795(C;G)). I swim ~12 km per week. My LDL and lipid profile are unchanged in the last year. As per manuel8849, I am entering this info in response to the Attia/Patrick podcast. After listening to the podcast and reading manuel8849’s comments I will eliminate saturated fat moving to good quality olive oil and fatty fish for a month or two (or longer?) - my lipidologist has also recommended this. I had a recent CAC. I am on no meds. My LDL increased slightly during a water and salt only 5-day fast. My glucose dropped from ~85 mg/dL or 4.7 mmol/L (overnight fast) pre-fast to 50 mg/ dL or 2.8 mmol/L at end of the fast (and after a pool workout). PS. I don’t mind natto at all.

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            Refreshing to see more cases like this. Numbers are similar to mine. Kudos for a clean CAC at 65. Some pointers on your observations and high LDL on low-carb diets in general.

            • Fasting increases LDL. Possibly because the body releases and transports fat from stored body fat.

            “Fasting increased total serum cholesterol from 4.90 ± 0.23 to 6.73 ± 0.41 mmol/L (37.3 ± 5.0%; P < 0.0001) and LDL cholesterol from 2.95 ± 0.21 to 4.90 ± 0.36 mmol/L (66.1 ± 6.6%; P < 0.0001). ” (R)

            • Eating saturated fat (especially from dairy) allows some bacteria toxins from the intestines to pass through. Those endotoxins are cleared by LDL. The genetic adaption discussed here may be a response to farming. (R)

            “In rats, LPS [the toxin from bacteria] significantly inhibits the clearance of LDL from the circulation by posttranscriptional down-regulation of LDLR during inflammation; ” (R)

            • Also look at Dave Feldman’s work on “lean mass hyper responders”, if you haven’t yet (you likely have). His theory is that lean and active people on a low carb diet will require more LDL particles to meet their energy demands.

            “So think about it — (1) lower adipose fuel tank, (2) lower glycogen fuel tank, yet (3) higher energy demands. It makes perfect sense for the body to want to mobilize more fat-based energy to meet the need. And yes, that will ultimately mean more VLDL particles (VLDL-P) delivering more triglycerides to the cells, ultimately remodeling to LDL particles (LDL-P). Likewise, this means more of the cholesterol in those boats (LDL-C) being circulated along with them.” (R and R)

            He also uses some alternative lipid measures, like remnant cholesterol and atherogenic index, which seem to be more precise than LDL alone. Also look into the CIMT ultrasound he talks about. It should measure something similar as CAC at a lower cost.

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              Thank you very much, that information is very useful. I have read various blogs by Dave Feldman, as you suspected, and watched several of his videos. I have done the cholesterol calculations and read papers on remnants through links at Feldman’s site and many more (I am retired so I have the time).
              Regarding LPS, I have been circling around the literature since listening to Tommy Wood at NBT discuss LPS in relation to Dave Feldman’s LMHR’s. The links you provided have taken me straight to the heart of what I want to learn about/understand.
              It seems that a great deal of thought by all of these various bloggers is focused on inflammation, which seems to be a worthy focus no matter what the individual/personal theories are. By extension, I am trying to understand how to keep epithelium tissues healthy no matter where they reside in the body. Thanks again, I am currently plowing through the links you provided and beyond.

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          As you mentioned, these FTO-related SNPs can be harmful in the context of a high saturated fat and low monounsaturated and polyunsaturated fat ratio. The best way to know if saturated fat has a negative effect on your health would be to measure blood biomarkers including a LDL/HDL lipid particle and size test, triglycerides, HbA1c, high sensitivity CRP etc. Also, eating a time-restricted diet has been shown to improve all of these biomarkers.

          Foods that are high in monounsaturated fat and polyunsaturated fat include avocados, nuts, salmon, olives and olive oil and avocado oil. These foods actually make up a significant proportion of the Mediterranean diet. I’m not sure how feasible it is to try a ketogenic diet using these foods but they are healthy foods to eat in general.

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            In some of the public discussion regarding FTO only polyunsaturated fats are mentioned as counterbalances to saturated fat. Will eating monounsaturated fat help me counterbalance saturated fat if I have FTO?