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Michael R

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  1. This is from the "Discussion" from a recent Meta‐Analysis of Self‐Reported Sleep Duration and Quality and Cardiovascular Disease and Mortality (PMID 30371228): The meta-analysis itself finds: ... but long self-reported sleep duration may reflect COPD, sleep disturbed by stress, noise, and light, etc.
  2. Michael R

    Olive oil? Healthy or not?!

    All: in a post in another thread, I noted: Certainly, both the epidemiological evidence within Mediterranean countries where olive oil is used in meaningful quantities, as well as now large-scale clinical trials, demonstrate that plant-based MUFA, and especially real extra-virgin olive oil (or, though less celebrated, canola) reduces cardiovascular events and mortality, likely total mortality, and mortality from some cancers. A recent report supports this specifically for CVD risk, without even narrowly specifying olive oil (let alone high-phenolic EVOO):
  3. Michael R

    Systemic mTOR activation

    No, this really doesn't work: adipose tissue "grows" primarily by socking more TG into existing adipocytes, not by adipocyte proliferation or hypertrophy sensu stricto, and is driven by simple energy excess. (This is even more so in insulin-resistant states and with age). By contrast, mTOR drives cell hypertrophy and proliferation, is decoupled from TG storage in adipocytes, and while it is certainly downregulated by energy deficit, it has a much more complex regulatory regime, including importantly a 'leucine threshold' as a necessary and almost-sufficient condition, as well as a role for methionine. This decoupling is readily apparent in sarcopenic obesity, and in aging, where body composition gradually shifts to more and more adipose and less and less lean tissue — initially in the face of misleadingly-stable weight, and increasingly with age and in the last 9 years of life one becomes more adipose (and less lean tissue) even in the face of involuntary weight loss.
  4. Michael R

    Coratina EVOO

    First: McCoy, would you please link the source for the Servili article? I couldn't find it via Google; is it maybe actually in Italian, with the above being your translation? In any case: I suspect that the reason for the discrepancy you're seeing is that in 2017, the IOC adopted a new HPLC method for the measurement of 'biophenols;' as I've pointed out a couple of times, HPLC- (or NMR-) based methods give numbers that are on their face several times higher than you get from the colorimetric Folin–Ciocalteu reagent, which has been used in the vast majority of health and nutrition research on EVOO (as opposed to the analytical chemistry literature). HPLC- (or NMR-) based methods are certainly more accurate than colorimetric methods, but unfortunately there is no way to simply convert from one to the other (I have seen oils with data on both, and it really varies pretty wildly — it really is like apples and oranges), which is very annoying in the near term as it makes nearly all the existing nutrition research hard to 'translate.' VF/Amphora have historically reported F-C data and have been responsible in reporting uniformly using caffeic-equivalents, which minimized a similar but much less severe problem even within colorimetric methods; they have for the last while been gathering data using both methods, but putting F-C numbers on their website to avoid unintentionally misleading customers — though I expect they will eventually convert over to the IOC HPLC method. Because of the EU health claim requirements and the publication of an official IOC methodology, EU producers are now increasingly measuring phenolics and are doing so using the IOC method. Servilli is presumably quoting such numbers, as is the producer in tea's first post (I don't see numbers for the oils in your other posts, tea — were they just made to give McCoy people to call and inquire)?
  5. All: Features me, Matthew "Oki" O'Connor (VP for Research at SENS Research Foundation) and Tristan Bettencourt, a CR practitioner who was active on the old CRS Listserv from the 1990s to the early 2000s. Also has Dr. Roz Andersen, who heads up the WNPRC nonhuman primate CR study. Not bad, albeit a bit lightweight, aside from the git doctor at the end who said CR works by slowing one's metabolic rate, which it most certainly does not.
  6. Michael R

    New to this site

    Hi Ladygirl, Welcome! Glad you're having good results. Is CR affecting your lipids? (I'm assuming you're on some kind of drug therapy, though there's no need to divulge that if you don't want to). Was the news story on NBC ...?
  7. You're being unreasonable here in all kinds of ways, including notably foregoing a well-established benefit for a purely hypothetical risk (which is like a caricature of the precautionary principle, which is to be cautious in the face of preliminary evidence of risk). But as regards the above: again, in a typical year the vaccine is roughly 59% effective. How "dramatically" could it improve? I suspect that Karl has already dug much of this up, but on the subject of vaccine effectiveness: I've posted separately about the Dreem headband, an auditory closed-loop system for enhancing slow-wave sleep (SWS):
  8. Michael R

    5:2 or daily -10%

    It's quite clear that what matters for aging is the overall decrease in Calorie consumption, not the pattern of eating.
  9. Yeah, I actually got a free beta-test of the latter: it did a similar but qualitatively different job of subjectively improving the degree to which I felt refreshed by my sleep, but it was somewhat more of a PITA to use, as it has a wet electrode with partially-reusable pads, and it would now and then crap out on me in the middle of the night; also, it was a poor sleep tracker. I don't see any reason why they would address such an issue. Actually the most important things it has clearly done for me are (a) to show me clearly that I wasn't going to bed when I tell myself I'm going to bed , thereby pushing me to actually go to bed on time (which probably even mickey-mouse trackers could've told me if I'd taken them as seriously — see (b)), and (b) to give me extremely satisfying sleep-tracking results in the morning. It seems to increase the degree to which my sleep mentally refreshes me, tho' of course that's exactly the kind of thing most susceptible to placebo effects. Of course, I have no real way to know if it's improving my glymphatic system's functioning. NOTA. Despite saying quite some time ago that it was in the cards, they haven't even integrated with Apple Health — my biggest annoyance. It has some audible sound, but most of the sound and as I understand it all of the "pink noise" sounds that amplify your NREM slow waves use bone conduction. When I was expressing optimism about eg. LA (which I certainly never said was a sure thing), it was based on very preliminary research, in animals, and some very indirectly-relevant human work (diabetic neuropathy). Here we have multiple peer-reviewed human studies on the tech in general and two on the Dreem specifically. Do you have any evidence of a scam? If so, please post it; if not, please don't post unsubstantiated assertions.
  10. Michael R

    Clinton's Stack

    Well, yes — but he's saying that with those tools, his sleep is good. So we should (ha ha) put that to rest, right?
  11. Michael R

    Clinton's Stack

    It would indeed turn common wisdom upside down that lower LDL is always better — particularly LDL-P rather than LDL-C — but one study does not overturn the massive body of evidence underlying the common wisdom. It's well-established that lower LDL-P is always better, at least as far down as 70 mg/dL LDL-C/700 nmol/L LDL-P , with suggestions that 50/500 is safe (provided, of course, that you aren't doing it via something that is itself bad for you, like giving someone Alzheimer's disease): it's the very driver of atherosclerosis — everything else is modification of that core effect. We also have strong evidence that replacing SaFA with plant-based MUFA or mixed (and likely even omega-6 PUFA) lowers your risk, and that raising either apoB or TC:HDL is bad for you.
  12. Michael R

    Clinton's Stack

    Why does this seem like a possible red flag? A red flag of what? This is a graph risk of CHD per TC:HDL vs. apoB count in a single study, not a graph of CHD risk per saturated fat intake, with or without insulin — let alone as part of a well-done meta-analysis of such findings. It's also not by itself very generalizable, even for what it says, since it has the highest apoB tertile (with low TC:HDL) having lower risk than those with lower apoB and the same TC:HDL. You also seem to be assuming (as is often said) that increasing SaFA will improve TC:HDL , which is an oft-repeated claim — but isn't true. TC:HDL improves when SaFA is replaced with MUFA or PUFA— though it is either worsened or held neutral by replacement with carbohydrate,(1,2) which latter doubtless will depend at the margins on the specific carbohydrate food, the specific mix of saturated fatty acids, the rest of the diet, and the immediate metabolic state. It's also not true that increasing SaFA intake with improve the "LDL profile" (by which you mean particle size): particle size is a distraction, being a crude surrogate for discordance between LDL particle number and LDL cholesterol, as eplained here. It tells you nothing in itself about risk of atherosclerosis, and certainly nothing mechanistic. Saturated fat really is bad for you; additional evidence on saturated fat. References 1: Sacks FM, Katan M. Randomized clinical trials on the effects of dietary fat and carbohydrate on plasma lipoproteins and cardiovascular disease. Am J Med. 2002 Dec 30;113 Suppl 9B:13S-24S. Review. PubMed PMID: 12566134. 2. Mensink RP, World Health Organization. Effects of saturated fatty acids on serum lipids and lipoproteins: a systematic review and regression analysis. World Health Organization.
  13. Michael R

    Clinton's Stack

    Certainly there would be no difference in that respect between blending and just plain eating. However, I would counsel against smoothies as such for a different reason: smoothies increase the glycemic index of foods, which is unlikely to be good for you.
  14. Do you have any actual scientific basis for this assertion, or just the usual intuitive incredulity?
  15. Another Reminder that BMI is a Shitty Measure of Anthropometry Another problem with the BMI epidemiology is that it poorly captures the actual anthropometry of individuals: is this BMI 23 person lean and fit, or is s/he loaded with visceral fat related to South Asian heritage? Is this BMI 27.5 person bearing fat inside and out, or is he Lebron James? This study is one of several to instead look at measures of (or more directly linked to) body fat than simple body weight, and one of the few that does so while also having genuinely long-term followup (eliminating the problem of the long period of weight loss preceding death from diseases of aging) and looking at true never-smokers (rather than ex-). Lo and behold, less and less fat is good, all the way down: ... and here are the data for men for BMI in lifelong nonsmokers and in people without pre-existing comorbidities: References 1: Iliodromiti S, Celis-Morales CA, Lyall DM, Anderson J, Gray SR, Mackay DF, Nelson SM, Welsh P, Pell JP, Gill JMR, Sattar N. The impact of confounding on the associations of different adiposity measures with the incidence of cardiovascular disease: a cohort study of 296 535 adults of white European descent. Eur Heart J. 2018 May 1;39(17):1514-1520. doi: 10.1093/eurheartj/ehy057. PubMed PMID: 29718151; PubMed Central PMCID: PMC5930252. https://academic.oup.com/eurheartj/article/39/17/1514/4937957