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    Hi Rhonda,

    I noticed that at the 24 min mark there are discussions about high protein consumption on a keto diet that could lead to unhealthy results. During the discussion you shortly mentioned that

      "And, you know, so do you think that the ketogenic diet you used you hadn’t have done a 
       10% protein if they had done a little bit more? I’m not sure if maybe that technically 
       wouldn’t have even been a ketogenic diet. But would it have changed the IGF-1 mTOR 
       axis as much..." (Quoted from the transcript)

    Does the above quote mean that a traditional ketogenic diet sticks to 10% and less protein as daily calorie intake, and if the protein daily consumption is increased over that ratio, then the said unhealthy conditions will happen?

    I am very concerned about that bit because I am on a “keto-ish” diet for almost a year, with restricted carb intake (20-25g per day), however my protein intake ratio is usually 15-25% of daily calorie intake.

    Thank you in advance if you reply.


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      Hi! I havent been able to use your tool as yet because I did my DNA through ancestry. But I am interested in these that I got from another tool - Your genotypes are; rs662-(TC) and rs1800588-(CT). Both of these genotypes are associated with a reduced ability to process fat following exercise [34][35]. Does that mean perhaps keto may not be great for me? I do seem to have high ish blood lipids ^ do exercise alot.

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        What could cause kidney pain during ketosis?

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          Interesting but I hope folks don’t take this to imply a ketogenic diet is healthy. Don’t confuse longevity with a life of reduced disease. These rats live for only a year without the opportunity to suffer the ill effects of a high fat diet such as stroke, heart disease, diabetes, etc. A lot can happen in 60 years as opposed to 6 months. On a ketogenic diet you won’t get a chance to die of “old age”.

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            I’m definitely a layman, but I would have to say every single indicator of good health has improved dramatically since I began the ketogenic diet. My bouts of Afib have ceased, even with an increased intake of caffeine. I’m wondering what it is that’s supposed to increase heart disease, and I’m certainly curious how a low-carb diet contributes to diabetes… it is literally used as a cure for type 2 diabetes. If you have links to good research, I’d be very much interested in seeing them. I searched for a long time and found no reliable research condemning an intelligently engaged ketogenic diet.

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            While I will watch the rest of the video, the fact that Verdin points to the PURE study is troubling. That has been thoroughly critiqued to reveal that the it only actually shows the obvious: negative impacts on health are due to poor socio-economic conditions, not diet. It found that higher consumption of low-quality carbohydrates in poor countries without access to decent medical care led to worse outcomes than those in advanced and developed countries with higher fat diets. Surprise, surprise!

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              Hello Dr. Patrick,

              I started the keto diet about 2 and a half weeks ago. I’ve lost around 10 pounds, but I’m not sure I can do it anymore. I’ve had diarrhea about 4x per day everyday since I started. And it’s pretty bad. Besides the diarrhea, I was able to maintain the diet. I of course like the amount of weight I lost, though most of it may be due to water weight, but I wanted to know what kind of diet you would recommend? I’m 26 years old, about 220 lbs. I would like to get back to about 190 lbs. I’m working out about 3x a week. Mostly cardio. I also intermittent fast from 9pm till 11am. I would love to hear your recommendations.


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                What foods are you consuming on your keto diet? My experience has been the opposite but I am consuming a lot of fibre (70-90g daily) from vegetables, on 15% carbs, 10-15% protein, 70-75% fat.

                Ketone levels are usually in the 4-8mmol/L even at this level of carbs.

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                Rhonda Somewhat confusing to me. Explain dichotomy, if you will, regarding the all cause mortality reduction of strength training…..requiring anabolic upregulation and the decreased all cause mortality of fasting and unregulated autophagy/catabolism…….

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                  FMF, similar to Garymlong’s comment below, I’m interested in the systems diagram of fasting and ketogenesis at 18:18. Perhaps there’s a way to make these images available? They could quite easily be branded with FMF logo’s and become marketing materials.

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                    Does anyone know the source of the diagram at 43:40 in the video, the diagram that shows fasting and ketogenic diet signaling pathways to decrease aging? It is a great overview and really puts different eating programs into into context.

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                      Gary, it was created just for this episode. We’ll post it as an extra resource on this page as part of the notes soon.

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                      Hi same here, using your genetic tool Rhonda I have the same gene polymorphisms as brywatson, in the beginning of the podcast you said that although ppar-alpha will be mentioned it will only be briefly, I was excited to listen to this podcast until I heard that, I really wish you would dedicate a whole podcast or article or video on PPAR-ALPHA and the other genetic polymorphisms that make a ketogenic diet as you said dangerous for some people, and more specifically how can someone in my position still do a ketogenic diet effectively I would say that would be hugely helpful, when I was on keto I didn’t feel well and I had ldl-p and cholesterol through the roof, you are actually the only one that talked about my genes issue when I was trying to find answers, but now I feel like ok I have these gene markers but where do I go from here, please Rhonda any help on how our types can move forward with respects to diet and aging would be so awesome

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                        I do plan on diving in an doing short videos on specific SNPs, particularly ones related to fat metabolism since low-carb, high-fat and ketogenic diets have become popular. The PPAR-alpha SNP is one that is most concerning when it comes to ketogenic diets since that gene is essential for the process of ketogenesis. It is good that you measured a variety of blood biomarkers since that is really the only way to test whether a diet works for you.

                        What you’re saying might suggest that a ketogenic diet may not work for you. At least that’s one way to interpret it. (Note: I don’t mean that as medical advice!)

                        With respect to PPAR-alpha, other factors that can activate are polyunsaturated fatty acids particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), which are the fatty acids abundant in fish oil. DHA and EPA have been shown to be agonists for PPAR-genes. PPAR-alpha is under circadian regulation, so time-restricted eating may be even more important. If you really want to try a monounsaturated and polyunsaturated fat-based ketogenic diet see my comment to @brywatson. Of course, you would have to measure your blood biomarkers again to monitor how the diet affects those markers of health status. It would be appropriate to monitor these under the trained guidance of a physician.

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                          Hi Dr. Patrick. I really enjoy your podcast when I get the chance to listen. I also have a question about the PPARA. Your analyzer showed I have the rs1800206 SNP, but I also have a normal PPARG rs1801282, so do these perhaps balance each other out? I’ve been experimenting with a ketogenic diet, but have been hesitant to overdo the saturated fats based on my abnormal PPARA. I’m curious if there’s a recommended ratio of PUFAs to SFAs for people with this SNP. Would appreciate your take on this. Thanks for all you do!

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                            Thanks Rhonda I will be looking out for those, I feel a bit boxed in because I have other Polymorphisms that indicate the other fats I respond bad as well I guess I am destined for a low fat high carb diet but the that seems to go against what was covered in your latest podcast with regards to longevity

                            ADIPOQ | rs17300539 | MAF: 0.027 GG LEPR | rs8179183 | MAF: 0.142 CG You have a worse response to monounsaturated fat

                            PPARA | rs1800206 | MAF: 0.023 GC G = higher fat in blood (risk for blood clots) after eating polyunsaturated fats ®

                            Thanks so much again, I think this topic is much overlooked in the Keto Community

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                              I’m not sure I have seen any convincing data that rs17300539 causes a bad response to monounsaturated fat or rs1800206 leads to clots after polyunsaturated fat, particular the omega-3 fatty acids which have a positive effect on PPARA, not a negative effect, but I could be convinced… with sufficient references.

                              Also, longevity has been associated with a diet high in vegetables and fruits in many, many observational studies. Not all carbs are created equal! You’ll notice that even in this interview, Dr. Verdin himself mentions he doesn’t always adhere strictly to a ketogenic diet. If the case could be made that he’s dramatically shortening his lifespan by not doing so, we might hear differently!

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                                I’m using selfdecode.com as well which sometimes gets a little too deep for me so far your tool is the simplest to understand and yes I agree Blue Zones always seem to confirm longevity pillars as you mention

                                References from selfcode again I don’t understand it all I was going to try ketogenic PUFA/MUFA but was not sure

                                PUFA: http://m.jn.nutrition.org/content/135/3/397.long

                                MUFA: https://www.ncbi.nlm.nih.gov/m/pubmed/19238139

                                Thanks again Rhonda!

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                                  With respect to the PPAR-alpha and PUFA study you linked, it shows that omega-6 fatty acids may specifically decrease plasma triglyceride concentrations in carriers of the 162L allele, whereas dietary omega-3 fatty acids may lower triglycerides independent of the PPARA-L162V polymorphism.

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                                    Awesome so PUFA’s are fine for my genotype it seems thanks for taking the time to look at that Rhonda and clarifying that

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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?