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Michael R

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  1. This seems pretty strong evidence against BAT being an important driver of retardation of aging by CR, since (despite one odd one-off study) it's well-established that more severe (in some cases up to ≈55%) CR is dose-dependently more effective than less severe CR. This certainly makes sense. It's also a reminder of something I've said before and should get more care in this thread: that mere induction of genes is an inadequate indicator of fat browning. There should be data on the target proteins, and preferably on the actual phenotype of the fat and/or experimental subject. Dean, it would help if you would tare down your list to things that at least meet this criterion, and preferably tag off those shown effective in humans. That's certainly one possibility, although there are many others. And anecdotally, I'm of course extremely slim, doubt I have more than a tiny shred of BAT on my skinny ass (or subscapula ;)), but when actually put to OGTT rather than surrogate markers, I have excellent glucose tolerance — and that, when there's a rationale for which I probably ought to be tested with a lower dose of glucose to be metabolically meaningful. [1] Aging Cell [28 Mar 2019, 18(3):e12948] DOI: 10.1111/acel.12948 Long-term caloric restriction ameliorates deleterious effects of aging on white and brown adipose tissue plasticity. Corrales P 1 , Vivas Y 1 , Izquierdo-Lahuerta A 1 , Horrillo D 1 , Seoane-Collazo P 2 , Velasco I 1 , Torres L 1 , Lopez Y 1 , Martínez C 1 , López M 2 , Ros M 1 , Obregon MJ 3 , Medina-Gomez G 1 (PMID:30920127 PMCID:PMC6516146) --------- [2] Aging Cell. 2012 Dec;11(6):1074-83. doi: 10.1111/acel.12010. Epub 2012 Oct 24. Aging leads to a programmed loss of brown adipocytes in murine subcutaneous white adipose tissue. Rogers NH(1), Landa A, Park S, Smith RG. DOI: 10.1111/acel.12010 PMCID: PMC3839316 PMID: 23020201 [Indexed for MEDLINE] -------- [3] Age (Dordr). 2010 Mar;32(1):97-108. doi: 10.1007/s11357-009-9118-z. Epub 2009 Nov11. Effects of long-term calorie restriction and endurance exercise on glucose tolerance, insulin action, and adipokine production. Fontana L(1), Klein S, Holloszy JO. DOI: 10.1007/s11357-009-9118-z PMCID: PMC2829643 PMID: 19904628 [Indexed for MEDLINE]
  2. If you spend a moment looking at the thread subject and the line of discussion, you'll see that these interventions are intended to increase brown adipose tissue mass and/or activity, "for increased health and longevity" — not strength and muscle mass gain.strength and muscle mass gain. I'm aware of no evidence that testosterone injection will affect any of this. Can you point to any? Indeed, barring any other changes, effective interventions on this front might well modestly decrease strength and muscle mass, simply because of energy balance. Your post might giv epeople the impression that you're here to sell steroids; if so, you need to revise your marketing analysis 😉 .
  3. I've been meaning to get back to this for some time. I would agree to a point that "You can't make yourself live longer by forcing yourself to sleep more," if by "force" you mean an individual who (hypothetically) is perfectly well-rested with just 6 h of sleep opportunity time (actually a vanishingly small number of people) somehow willing hirself to sleep an extra hour just to make an epidemiologically-determined cutpoint. But as is I think widely recognized, most people have adopted habits that restrict their sleep to less than what is actually needed to meet their physiological needs staying up late (relative to a set wake time) to complete work or study projects, or to go out for entertainment, or to watch TV, or to keep up with the Kardashians on Instagram, or to address the unending problem that someone on the internet is wrong. Very few people are actually getting recommended amounts of sleep (meaning, actually, sleep-opportunity time, not PSG-measured sleep), as study after study documents, and multiple studies show that when taken away from other stimuli and from clocks — or even just blue light from devices — they sleep more and better than they habitually allow themselves to. Studies also show that people are very poor judges of whether they're getting enough sleep, or how sleep-deprived they are. In PMID 12683469, "48 healthy adults (ages 21-38)" were randomized to " 8 h, 6 h or 4 h [of sleep] per day for 14 days, or to 0 h for 3 days". "Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days." "Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks" — that is, the longer you suffered these very mild sleep deprivations, and the shorter your sleep, the worse your cognitive performance got: Despite the fact that these deficits (PVT, DSST, SAST) got worse and worse over time and with lower and lower amounts of sleep, "Sleepiness ratings suggest that subjects were largely unaware of these increasing cognitive deficits": the subjects' self-reported sleepiness ratings flattened after the first 3-4 days (SSS in the Figure above), "and did not significantly differentiate the 6 h and 4 h conditions." "[C]hronic restriction of sleep to 6 h or less per night produced cognitive performance deficits equivalent to up to 2 nights of total sleep deprivation, [so] it appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults." The disconnect between self-reported sleepiness and objective deficits "may explain why the impact of chronic sleep restriction on waking cognitive functions is often assumed to be benign." Here are a couple of trials of "forcing" people to sleep more, by simply making them go to bed earlier than they normally do and not waking them up until they had achieved the target sleep time: In PMID 21731144, In PMID: 31166059, the authors identified "Seven studies that aimed to increase sleep duration in adults by any sleep extension intervention and described at least one cardiometabolic risk factor ... These studies had a combined sample size of 138 participants who were either healthy (n = 14), healthy short‐sleeping (n = 92), overweight short‐sleeping (n = 10), or pre‐ or hypertensive short‐sleeping (n = 22) individuals. The durations of the sleep extension interventions ranged from 3 days to 6 weeks, and all successfully increased total sleep time by between 21 and 177 min. Sleep extension was associated with improved direct and indirect measures of insulin sensitivity, decreased leptin and peptide tyrosine‐tyrosine, and reductions in overall appetite, desire for sweet and salty foods, intake of daily free sugar, and percentage of daily caloric intake from protein." It appears that there are benefits to sleep extension in children, too. So, yes: most people can "force" themselves to get more sleep, by forcing themselves to go to bed early enough to get adequate sleep — a hard thing, with all the opportunities or entertainment and procrastination presented by our modern world. The act of going to bed is more likely to lead to more and better sleep when enabled by good sleep hygiene (compare the CDC , the American Academy of Sleep Medicine, and the National Sleep Foundation) and some more high-tech tools, like good blue-blocking glasses — and for those that need it, cognitive-behavioral therapy for insomnia (CBT-I). And the evidence is that even in the very short term, "forcing" yourself to get more sleep is good for your performance and health.
  4. Michael R

    Inspiratory Muscle Strength Training

    What makes you believe that this device "was developed with the help of the foremost reasearcher in this area"? The product info in the listing is minimal, and the reviews look fake, which doesn't inspire (ha ha — "inspire," get it?) confidence.
  5. Michael R

    Romaine Lettuce vs. Cabbage Slaw

    Your best resource is good nutrition software, most especially CRON-O-meter, which you should really be using for your entire diet in addition to helping you choose amongst foods. Its "Oracle" function is designed to help with the latter. I'd agree with Thomas that when eating cabbage, there may be an advantage to going red or the anthocyanidins, tho' it's slightly higher in Calories so you can't just switch one-to-one.
  6. Sirtuin, you're short on Ca and protein, and evidently not vegan since you eat meat; is the mind-numbingly obvious solution not milk or its fermented products?
  7. Michael R

    Dean's Current Diet

    I don't think anyone ever suggested that dilute vinegar or peroxide was any good for either microbes or pesticides: I use these less than I used to, but I use them at full off-the-shelf potency, with a misting spray bottle or (rarely) by swishing during immersion. (I don't do this with things like berries, however, as it's hard to get the taste out and they sometimes exacerbate damage to the fruit).
  8. Michael R

    Hong Kong beats the blue zones

    The Blue Zones are not about life expectancy (average lifespan calculated from birth), but about cohort incidence of "exceptional longevity" — in the best cases, centenarians, or at least what is currently "exceptional longevity" (age >85 in most studies).
  9. Michael R

    Exercise optimization

    Good God, McCoy! You're a beast!
  10. 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.
  11. 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):
  12. 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.
  13. 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)?
  14. 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.
  15. 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 ...?
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