tag:blogger.com,1999:blog-36840063.post2025928040625927411..comments2024-03-29T06:45:45.894+00:00Comments on Hyperlipid: On Stephen Phinney and an RQ of 0.62Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger23125tag:blogger.com,1999:blog-36840063.post-78111646148410462342020-02-09T05:38:42.737+00:002020-02-09T05:38:42.737+00:00That is an excellent link James, thank you.
I don...That is an excellent link James, thank you.<br /><br />I don't know how long you have been reading LC blogs for but back in the early years of this century one of the active bloggers/forum contributors was a girl with chronic lung disease who had specifically adopted a high (saturated) fat diet specifically to reduce CO2 production. I would suspect that basing your high fat diet on hearthealthypolyunsaturates might not be too helpful in the presence of a serious inflammatory response to a virus so I'll stick with beef fat plus a little butter... No idea what happened to the young lady, people come and go on the LC blogosphere over the decades.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-54786256367998385922020-02-08T14:56:18.503+00:002020-02-08T14:56:18.503+00:00With coronovirus on the horizon, and potentially l...With coronovirus on the horizon, and potentially limited resources. Now may be a good time to rekindle this discussion . Pharma has not seen to funding any direct pneumonia studies in regards to the diet but O2/CO2 complications seem the same as for COPD .<br /><br />https://pubmed.ncbi.nlm.nih.gov/8325067-the-effects-of-high-fat-and-high-carbohydrate-diet-loads-on-gas-exchange-and-ventilation-in-copd-patients-and-normal-subjects/Jameshttps://www.blogger.com/profile/13248972486404443499noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-49099032256916439182016-05-12T05:19:17.766+00:002016-05-12T05:19:17.766+00:00Converged on similar understanding through my own ...Converged on similar understanding through my own metabolic discovery. Discovered Krebs Cycle and the glucose and fat substrates. Find out more ATP from fat than glucose. Deduced from my own scientific training that Nature was not ever going to waste or misuse a better fuel. Lipophobia lies somewhere between religion and propaganda.js290https://www.blogger.com/profile/08157385596237909630noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-69044430505174771672016-05-11T21:41:35.555+00:002016-05-11T21:41:35.555+00:00Hi Peter,
Excellent analysis and very interesting...Hi Peter,<br /><br />Excellent analysis and very interesting!<br /><br />You've previously stated that one should eat some protein, not too little. <br /><br />Approximately how much protein do you find optimal on a mostly fat and severely CHO restricted diet?<br /><br />Recently Ron Rosedale has been pushing 0.7g / kg LBM, while Attia seems to be pushing about the same. Many others hover around 1.0 g / kg LBM, and yet others are in the range of 1.5 to 2.0. <br /><br />Cheers,<br />~Bruce<br /><br />GoBearshttps://www.blogger.com/profile/17845361020662059226noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-39650915911068071972016-05-10T15:44:44.821+00:002016-05-10T15:44:44.821+00:00@George Henderson
Triglyceride levels (different b...@George Henderson<br />Triglyceride levels (different but related to liver Trigly) are an associated risk factor for CAD. What most people don't seem to get is 'normal reference range' mean average - not really normal as in healthy. <br /><br />If you look at young, healthy kids or athletes or primitive peoples not eating western crops - they have trgly around 50 - similar to low-carb dieters. (Some low-carb MDs use Trygly levels as a test for diet compliance).<br /><br />So my take is that a normal trygly level probably is around 50. It is quite possible that the correlation with CAD is due to confounding variables, say sucrose consumption? The fructose in sucrose spikes trygly levels ( Something that was published and ignored from back in the 1960's).<br /><br />I don't think our bodies evolved to handle average levels ( 150 or more) - I'm not a palo nut (I would have a hard time eating all those insects), but I think it is prudent to try to go with what we have evolved with. <br /><br />Tyrgly is a confounded variable in it self as it can be made up of different fatty-acids - so is it really a independent risk-factor or not? - don't think we know.karlhttps://www.blogger.com/profile/13490274388549702613noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-15914244312123929892016-05-08T18:24:37.488+00:002016-05-08T18:24:37.488+00:00George, nice negative feedback!
Woo, I have a bit...George, nice negative feedback!<br /><br />Woo, I have a bit to say about Hall but Mike has covered the psychiatry and a lot of the biochemistry. I'm more interested in UCPs, FFAs, ketones and ATP as applies to the set up in Hall's project, to Phinney's 1980 paper and to a paper I found on acute fasting and ETC function (it's f*cked). There's a lot going on at the moment so not sure when it will pan out. MOT on the MX5 tmrw and some paddling with friends coming up. And the kids seem to have lost 2/3 of their PE kit and that's an evening trip to ASDA. All takes time...<br /><br />Peter<br /><br />Peterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-65856506418070651552016-05-08T08:17:31.034+00:002016-05-08T08:17:31.034+00:00Interesting series of posts as usual!
I hope you...Interesting series of posts as usual! <br /><br />I hope you comment on hall's study, eades early rebuttle to his media propaganda is quite great however.ItsTheWooohttps://www.blogger.com/profile/12057537399918684119noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-51328412490985982342016-05-08T01:56:18.652+00:002016-05-08T01:56:18.652+00:00@ Zachary,
someone commenting on Hall's last ...@ Zachary,<br /><br />someone commenting on Hall's last study parsed macros at 20% LA. Seems a little hard to swallow but even Jeff Browning's low carb NAFLD study used 15% E PUFA. <br /><br />https://www.researchgate.net/profile/Santhosh_Satapati/publication/50266937_Short-term_weight_loss_and_hepatic_triglyceride_reduction_Evidence_of_a_metabolic_advantage_with_dietary_carbohydrate_restriction/links/0912f510718fa1ea4d000000.pdf<br /><br />So maybe the 20% LA is 20% of fat, which would make 16%E.<br />Whereas Browning's NAFLD case study had fat of 57% SFA, 35% MUFA, and 8% PUFA, supposedly based on Dr Atkins Diet Revolution (which I would expect to give more MUFA than SFA, but anyway, good call).<br /><br />http://onlinelibrary.wiley.com/doi/10.1002/hep.21264/pdfPuddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-54092628923583236152016-05-08T01:41:43.798+00:002016-05-08T01:41:43.798+00:00The other side of this is, that the conversion of ...The other side of this is, that the conversion of acetoacetate to glucose via pyruvate and oxaloacetate is supplying a metabolic regulatory mechanism for inhibiting ketogenesis itself. When glucose can be made from ketones, the risk of ketoacidosis at times of high glucose demand is lessened.Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-82224898524969858282016-05-07T19:09:15.693+00:002016-05-07T19:09:15.693+00:00"Despite this "waste" of oxygen you...<br />"Despite this "waste" of oxygen you still use less O2 per ATP from fat oxidation, even if doing some gluconeogenesis"<br /><br />I can also think of further waste of oxygen/ATP from fat adaptation (not a complaint on my part, far from it): heat produced from uncoupling activities.<br /><br />IMO, despite this apparent drawback on paper physical activities performed in reduced oxygen environment, high altitude, fat metabolism still provides a net benefit. I'm thinking of better use of uncoupling heat, reduced dehydration, less AMS... JohnNhttps://www.blogger.com/profile/07639308289155393659noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-37286040352012096342016-05-07T08:00:46.971+00:002016-05-07T08:00:46.971+00:00karl, that's disturbing....
Peterkarl, that's disturbing....<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-77548812574909652942016-05-06T22:49:34.790+00:002016-05-06T22:49:34.790+00:00The type of fat may also control the lipogenesis h...The type of fat may also control the lipogenesis here via T3:<br /><br /><a rel="nofollow"> Inhibition of triiodothyronine's induction of rat liver lipogenic enzymes by dietary fat.</a><br /><br />So what happens if LA blocks lipogenesis ? My guess is BG goes up.karlhttps://www.blogger.com/profile/13490274388549702613noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-89630500452942058842016-05-05T18:09:15.003+00:002016-05-05T18:09:15.003+00:00LA update - Stephan has a new post about his paper...LA update - Stephan has a new post about his paper:<br /><br />https://wholehealthsource.blogspot.com/2016/05/my-recent-paper-on-linoleic-acid-in.html<br /><br />Should add a line to the graph for obesity.. At some point this is going to get hard to ignore..karlhttps://www.blogger.com/profile/13490274388549702613noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-14161032359137739872016-05-04T07:05:18.292+00:002016-05-04T07:05:18.292+00:00There are way to many papers that ignore the adapt...There are way to many papers that ignore the adaption effect - Not sure if this was the first paper to talk about it. <br /><br />I looked at this paper when I was trying to understand T4 => T3 . This is of interest to heart patients - there is a correlation of low T3 and heart disease. <br /><br />There were also a number of papers looking at effects of LA changing the effect of T3 (the active form of thyroid) apparently blocking activity of lipogenic enzymes. Seems that this would screw with BG levels as well. <br /><br />There is a certain amount of T4 => T3 conversion that happens in the liver as well - I'm not sure if it is for internal use or body wide.. Really hard to see the whole system. Or as they used to say "It will never sell; it has too many moving parts."karlhttps://www.blogger.com/profile/13490274388549702613noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-56085582444365002252016-05-03T08:34:11.515+00:002016-05-03T08:34:11.515+00:00@peter,
Yes, that's correct as far as i can t...@peter,<br /><br />Yes, that's correct as far as i can tell. I dug around a bit and found Stringer et al "The VCO2/V02 relationship during heavy, constant work rate exercise reflects the rate of lactic acid accumulation" (http://sci-hub.bz/10.1007/BF00964110). They say..."Underestimates or overestimates of the metabolic production of CO2 during non-steady state exercise conditions may occur when: (1) tissue PaCO2 increases at the start of exercise, (2) bicarbonate decreases in response lactic acid buffering, and (3) hyperventilation of pulmonary capillary blood occurs".<br />They've got interesting graphs plotting VCO2, VO2, lactate and HCO3- during and after moderate, heavy & very heavy exercise intensities.<br /><br />Overall, it seems that lactate accumulates exponentially upon reaching the lactate threshold, lots of HCO3- gets used up there & thus 'liberates' CO2; this is the origin of the increase in CO2 you point to.<br /><br />Figure 5.12 from "Exercise & Sport Physiology 5th Ed (2011)" shows how muscle pH quickly decreases from a baseline of 7.1 to 6.5 during a sprint, and returns smoothly to baseline within 30-35min. They go on to note that "even when normal pH is restored, blood and muscle lactate levels can remain quite elevated. However, experience has shown that an athlete can continue to exercise at relatively high intensities even with a muscle pH below 7.0 and a blood lactate level above 6 or 7 mmol/L, 4 to 5 times the resting value".<br /><br />Given how some level of glycogen breakdown is needed for the producing NADH used to maintain the ETC, might that fat=>oxaloacetate=>glucose be geared towards ETC maintenance? This is totally speculative so please squash the idea if you think it silly.<br /><br />Nutrition will always take 1st place for least scientific field of biology given its religious components, but exercise physiology is a close second (it's flooded with "broscience" after all).raphihttps://www.blogger.com/profile/08992252569979714724noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-62318365226202260422016-05-03T08:23:44.808+00:002016-05-03T08:23:44.808+00:00@Unknown:
I would guess switching mankind to lipi...@Unknown:<br /><br />I would guess switching mankind to lipids would also mean switching agriculture to fat-producing crops instead of the grains, and I suspect the former is a bit less efficient at extracting CO2 from the atmosphere and into complex organic chemistry than the latter. So it would be mostly a wash.<br /><br />See: http://www.majordifferences.com/2013/05/difference-between-c3-and-c4-cycle.htmlE-Shttps://www.blogger.com/profile/11618396250935467279noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-66550790035971772892016-05-03T02:55:24.969+00:002016-05-03T02:55:24.969+00:00Peter,
I'm thinking out of the box here. If mi...Peter,<br />I'm thinking out of the box here. If millions of people became fat-adapted, would that make a huge impact on atmospheric CO2 levels? That could possibly help with global climates?Anonymoushttps://www.blogger.com/profile/11654099265227567605noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-78901641317287697842016-05-02T18:01:32.712+00:002016-05-02T18:01:32.712+00:00raphi, am I correct that the elevated CO2 from bic...raphi, am I correct that the elevated CO2 from bicarbonate loss during lactic acidosis would occur at as the threshold in to lactic acidaemia was crossed and would cease once a steady state was achieved? It's a change in the buffering which liberates CO2, there is no extra CO2 being produced per se. We only have lactate post exhaustion here and RQ 10 mins in to exercise averaged with just before cessation, so a bit wooly data. I'm struggling to get a handle on how big this lactate/HCO3-/CO2 effect might be. 0.69 to 0.62 seems enormous to me. BTW Exercise physiology reminds me of nutrition research when you try to read the papers! "ketogenic" diets generating 0.15mmol/l BHB, 4 times the value on a mixed diet!!!!<br /><br />Zachary, yes, had vaguely heard. Might have a think about it at some stage.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-21391720338699517612016-05-02T16:33:09.587+00:002016-05-02T16:33:09.587+00:00Kevin Hall at it again..
https://www.youtube.com/...Kevin Hall at it again..<br /><br />https://www.youtube.com/watch?v=MiUyjMjuLl0<br /><br />I looked over his previous paper and can't figure out WTF the participants were actually eating. The diets were designed by dietitians (cough) using ProNutra software. Bet you $5 they weren't feeding them lard and butter... Zacharyhttps://www.blogger.com/profile/15765341233390228928noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-45431857865972836962016-05-02T15:21:52.815+00:002016-05-02T15:21:52.815+00:00@peter,
right, glycolysis is certainly well in pl...@peter,<br /><br />right, glycolysis is certainly well in play then. I wonder if that Carbon-14 4-11% estimate is meaningful in terms of contribution to glycolytic performance on a ketogenic diet...maybe this is where 'individuality' comes in.raphihttps://www.blogger.com/profile/08992252569979714724noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-72911004242871193492016-05-02T13:32:01.850+00:002016-05-02T13:32:01.850+00:00raphi, Phinney measure plasma lactate and it more ...raphi, Phinney measure plasma lactate and it more than doubled. Has to be a consideration...<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-68820402427123335852016-05-02T09:41:47.424+00:002016-05-02T09:41:47.424+00:00So many things are whizzing through my head after ...So many things are whizzing through my head after reading this post...Ok, 2 things in particular jumps to mind:<br /><br />1) in the paper <>, Hetlelid et al say "During increased glycolytic flux, lactate accumulation in the contracting muscle moves to the extracellular fluid and increases [H+], which is buffered by [HCO3−]. This excess (non-oxidative) CO2 is excreted through hyperpnoea, elevating the VCO2. As a result, indirect calorimetry overestimates CHOox and underestimates FATox during high-intensity exercise". So this is 1 reason why FATox's contribution to ATP during 'glycolytic levels of activity' may be underestimated.<br /><br />2) might this underestimate of FATox also partially stem from humans "performing a significant conversion of fat to glucose"?, i.e., because glucose is the substrate 'counted' as being oxidized, despite the starting substrate being fat?<br /><br />And down the rabbit hole we go.... :)raphihttps://www.blogger.com/profile/08992252569979714724noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-88625846473760410032016-05-02T08:49:31.347+00:002016-05-02T08:49:31.347+00:00I could see a very successful future for any subst...I could see a very successful future for any substrate that could drop a human's need for O2 to zero for a few hours, in the diving industry as well as aerospatial exploration.E-Shttps://www.blogger.com/profile/11618396250935467279noreply@blogger.com