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  1. Mechanism

    Puzzling over approach and calorie paramaters

    It is a nice thread, but easy to get bogged down in controversies. This review may interest. Both authors are well known to this community. With regard to resolving the controversies, not much has changed since 2014. Optimal body weight for health and longevity: bridging basic, clinical, and population research. Aging Cell. 2014 Jun;13(3):391-400. doi: 10.1111/acel.12207. Epub 2014 Mar 14. doi: 10.1111/acel.12207 https://onlinelibrary.wiley.com/doi/10.1111/acel.12207.
  2. Mechanism

    Nuts and Mortality

    Similar experiences, and agree with all your comments above. Thanks for sharing.
  3. Mechanism

    Nuts and Mortality

    Regarding the deletion of my content- My motivation at the time was primarily to prevent potential harm from poor information rendered prior to my getting up-to-speed on the health & CR literature. I really was quite naive and it took years to get reasonably up to speed. I don't remember the details but I think I came across an old post that was off the mark and my instinct was to "do no harm" and it was simply easier at the time to systematically purge my posts to create a clean slate following achieved nutritional competency than to screen all the hundreds of posts individually. Though the intention behind it was good (I figured my comments were dated and of so-so quality at best up to that point anyway, so what good would even my better comments be in this vibrant community with new updated information coming every day), I should have given the decision more thought than I did at the time. I had not realized it would have adversely affected the group like it apparently did, but I should have. That was a major oversight and poor judgement on my part. I'm sorry and extend my sincere apology to everyone here who was affected. If it makes any difference, I'm also happy to put in my 2 cents on a subject previously discussed if it helps. There is no comparison of course Dean, but I am curious what went in your own semi-departure and then return? I realize removing your personal labs ( which I never shared) is very different. Moreover if frustration over the potential risks of deep CR & overappraisal of its benefits played some role in your leaving (based on your posts), how then did you decide to re-engage? I sense there is more to the story though entirely up to you what to share if that is the case. Was the break from the forum a good transition (you deliberately increased your BMI again about that time if memory serves), and if so, what do you get from the forum these days that brought you back? I find this forum is less about CR these days than our own unique conceptions of optimal health. Michael's posts are direly missed (though to his credit all his old ones are still online!). I agree with your 2nd set of comments re: the study. It was an interesting one and I wish there were more metabolic ward controlled feeding studies in persons these days.
  4. Mechanism

    Nuts and Mortality

    Nice find Dean. I love Luigi's work and appreciated the reference. This particular diet does not narrowly focus on the matter of %fat macros. Other reasonable and valuable conclusions can be made however. First, as you noted, the differences in weight can account for the results. The weight loss observed in the macro diet does however dispel the myth that high carbohydrate diets can't lead to high compliance weight loss and improvement in biomarkers in out of control diabetics. It would be easy to stop there but I think it is worth looking at other differences. The authors indeed compared "macrobiotic Ma-Pi 2 diet" vs. the "recommended diet." If this was indeed the recommended diet, yes it absolutely stinks. Sure it has whole grains and fruit, etc. but the high meat (veal specifically) content and associated high saturated fat content with the particular meat/cheese selection have well-established relationships (at certain doses) with insulin resistance, elevated LDL, and metabolic dysfunction all variables equal. Even the carbohydrates selected in the control group (notwithstanding that they had less carbohydrate overall) including substantial whole wheat is associated with a high glycemic index (though whole wheat is not quite as bad as refined - exceptions apply such as sourdough), and even worse for the breakfast whole wheat crispbread. By contrast the macro diet was quite lovely: though it had a little brown rice (high GI but reasonable portions) and most of the carbs came from low GI millet, millet balls, barley, legumes and and assortment of high fiber starchy below ground & "chunky" whole vegetables. Yum. It is an interesting study and thank you Dean for bringing attention to it. The author title conclusions focusing an macro vs. that version of recommended was appropriate. But to make further inferences regarding what aspects of the differences accounted for the observations requires additional study and indeed is the focus of ongoing investigation. But reasonable, more narrow conclusion can be made: 1) Macro diet is superior to diet the standard diet for the biomarkers in question & 2) Macro diet (including the associated whole foods based starchy vegetables) implemented as they did is compatible with and may result significant improvement in a population of out-of-control diabetics. Would you agree?
  5. Mechanism

    Nuts and Mortality

    PS- If it's the micronutrients you are interested in, see Table 2 for %RDA (many are below). http://www.hsph.jp/JT2009/documents/Caloric Restriction, the Traditional Okinawan Diet, and Healthy Aging.pdf
  6. Mechanism

    Nuts and Mortality

    This is very crude (I'm using population rather than individual data - this is statistical blasphemy and can be way off; furthermore we are interested in a probability distribution rather than mean. We really need individual-level data) but if you take a 50 kg Okinawan from 1949 (http://www.hsph.jp/JT2009/documents/Caloric Restriction, the Traditional Okinawan Diet, and Healthy Aging.pdf) 0.8 mg/kg RDA = 40 grams protein vs the 39 g reported here (lots of assumptions here, right or wrong). The EAR is of course much lower at ~ 0.66 mg/kg https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4997405/. Apologies for my laziness, I'm sure there are much better figures are out there, or even in this same study, relative to my flawed back-of-the envelope approximation.
  7. Mechanism

    Sci Fi Movie and Book Recommendations

    Not a book, but somehow fits: https://www.inputmag.com/tech/deepfake-videos-of-tom-cruise-show-just-fast-its-improving/amp
  8. Mechanism

    Sci Fi Movie and Book Recommendations

    Hi Dean, I just saw the theory... I mean history... of time travel. It was a good recommendation, I love cerebral cinema. Thanks.
  9. Doctors get rare diseases... and statisticians get rare odds! May your next improbability drive event be a good one!
  10. Saul, I'm glad you stayed healthy on placebo- congratulations on your apt to get the real thing!
  11. Thank you Gordo. I heard good things about it. Reason also had mentioned it here: https://www.fightaging.org/archives/2021/01/ageless-the-new-science-of-getting-older-without-getting-old/ , referring to the story about it at The Guardian: https://www.theguardian.com/science/2021/jan/03/observer-magazine-do-we-have-to-age-biologist-andrew-steele
  12. Mechanism

    Lost your marbles yet??

    Wow, now that’s a wonderful turn of events! Happy New Year... and live long and prosper!🖖
  13. Mechanism

    LDL: What's Optimal For Health And Longevity?

    This point is often confused. What the research supports is that “changes in HDL cholesterol caused by diet or drug treatments can no longer be directly linked to changes in CVD, and therefore, the LDL cholesterol–raising effect should be considered on its own.” (1) The context here is caution in the context of coconut oil until more research is done, since coconut raises HDL as well as LDL. (There are many other arguments pertaining to coconut oil on both sides of the debate, but this is not the focus of this post). But in that context the Presidential Advisory from the AHA was essentially taking the position that we cannot be as confident that raising HDL via diet will compensate for the increase in LDL. In contrast, elevated HDL achieved via weight loss and exercise does have a consistent favorable profile. [“because coconut oil increases LDL cholesterol, a cause of CVD, and has no known offsetting favorable effects, we advise against the use of coconut oil.”]. The basis of this skepticism of a rise in HDL outside of established benefit via lifestyle intervention was described earlier in (1): “However, unlike LDL cholesterol, genetic variation that affects HDL cholesterol is not associated with expected differences in CVD unless LDL cholesterol or triglyceride is also affected by the genetic variants84 or reverse cholesterol transport is impaired.85 Still, these genetic studies, often called mendelian randomization, may not be capturing important loci for the protective effect of HDL that may be reflective in HDL cholesterol raising by dietary fats compared with carbohydrates. Although increases in HDL cholesterol by some pharmacological treatments have not decreased CVD,86,87 this does not directly pertain to the effects of dietary fat because the underlying mechanisms of effects of drugs such as a cholesterylester transfer protein inhibitor and nicotinic acid are probably not the same as those affected by dietary fats and carbohydrates. The HDL field is working toward a functional approach to CVD risk prediction and treatment. For example, a small experimental study showed that consumption of saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat.” An editorial in Circulation by Frank Sacks (2) subsequently reaffirmed this position, ie, “Although coconut oil increases plasma HDL cholesterol, it is impossible to know if this is a beneficial mechanism in cardiovascular disease.7 Although HDL cholesterol is a robust risk marker for cardiovascular disease, genetic studies and HDL-raising drugs have not so far supported a causal relationship between HDL cholesterol and cardiovascular disease. HDL, the lipoprotein, is composed of a huge array of subparticles that may have adverse or beneficial actions.7,8 It is unknown which, if any, foods or nutrients that raise HDL cholesterol do so in a way that reduces atherosclerosis and coronary events. Thus, effects on cardiovascular disease of foods or nutrients cannot be judged from changes in HDL cholesterol.” As the Harvard Heart letter noted (3) , the track record for HDL raising drugs is particularly dismal with “To date, five major clinical trials that sought to raise HDL levels with drugs have failed to lower heart disease risk” Lipidologist Dr. Thomas Dayspring & others have speculated it is more of an HDL function story, still poorly characterized as of now. (1) https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000000510 (2) https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.119.044687 (3) https://www.health.harvard.edu/heart-health/rethinking-good-cholesterol Further reading (primary sources of said publications): Sacks FM, Jensen MK. From high-density lipoprotein cholesterol to measurements of function: prospects for the development of tests for high-density lipoprotein functionality in cardiovascular disease.Arterioscler Thromb Vasc Biol. 2018; 38:487–499. doi: 10.1161/ATVBAHA.117.307025LinkGoogle Scholar & Furtado JD, Yamamoto R, Melchior JT, Andraski AB, Gamez-Guerrero M, Mulcahy P, He Z, Cai T, Davidson WS, Sacks FM. Distinct proteomic signatures in 16 HDL (high-density lipoprotein) subspecies.Arterioscler Thromb Vasc Biol. 2018; 38:2827–2842. doi: 10.1161/ATVBAHA.118.311607LinkGoogle Scholar
  14. Sad to hear the news. While death is inevitable, our daily choices do much to impact the quality of our lives while we are here.