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Michael R

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  1. Michael R

    How much salt?

    Obviously, this was a high-risk, older group; however, there's room for improvement by further reducing sodium intake and starting younger.
  2. Michael R

    How much salt?

    That's a reasonable question. However, there's evidence that high-salt diets not only increase BP in the near term, but are major drivers of the age-related increase in BP — so even if your BP is low now, eating a lot of salt might set you up for higher (thus, more damaging ) BP later on. There's additionally some evidence for direct negative effects on angiotensin II signaling etc, but that's a bit too mechanistic to hang hats on. Yes — and that high sodium intake is thought to be the reason for their disproportionately high risk of stroke (granted otherwise-low CVD risk factors, high fish intake, and expectedly-low MI risk), and for their higher contribution of vascular dementia vs. AD in the West.
  3. Michael R

    Olive oil? Healthy or not?!

    The subjects increased their energy intake from baseline by 79 Cal on the Med diet, but decreased it by 500 Calories on the vegan diet. Consistent with that, the subjects were weight-stable on Med, but lost 6 kd (13.2 lbs) on the vegan diet. The metabolic changes are consistent with weight loss. It's not clear that there was any specific effect of the diet being either low-fat or vegan, let alone the specific presence or absence of EVOO. Also, "Participants were asked to use extra virgin olive oil instead of other fats or oils" on Med, but no food was provided or specific brands endorsed in the study: presumably they thought they were buying EVOO, but who knows what they were actually consuming (or if, were it EVOO, it contained decent levels of phenolics). And most importantly, there were no hard outcomes in this study, whose presence is a major strength of PREDIMED.
  4. Michael R

    Olive oil? Healthy or not?!

    It's indeed a high bar to clear (though, in fact, few foods can meet it and it's arguably too high: what's your justification for eating zucchini, for instance?), but EVOO has quite successfully passed it, as documented earlier.not just from risk factors but from actual events, as documented near the beginning of this thread.
  5. Michael R

    How late to start CR?

    Edward has put the issue well: assuming it translates, you enter into a slower-aging mode on CR, so the earlier you start, the biologically younger you'll be at any age going forward. If CR slows your aging rate 20% and you start at 36, then at age 86 chronologically you'll be 76 biologically; if you wait until age 50, you'll be biological 79 at chronological 86 — three years older, and three years closer to age-related death (and have 3 years less to benefit from any real anti-aging therapies that are developed late in the game). This figure is now rather old and thus omits some of the newer and better studies, but: Merry BJ. Molecular mechanisms linking calorie restriction and longevity. Int J Biochem Cell Biol. 2002 Nov;34(11):1340-54. Review. PMID: 12200030 [PubMed - indexed for MEDLINE]. Data are derived from 24 rodent lifespan studies.
  6. Michael R

    No wonder SCIENCE is scorned!

    No wonder SCIENCE is scorned! Otherwise-intelligent people believe what they read in highly-slanted, dishonest low-fat vegan blogs instead of actually reading the scientific papers those blogs falsely claim to summarize. I addressed this "crappy control diet" nonsense in my major post on extra-virgin olive oil and health, including PREDIMED: begin at "And the results can't be argued to be the result of a crappy control diet" etc.
  7. Michael R

    CRON vitamin and mineral levels

    Hi Tom, First, this appears to be your first post: welcome. Yeah, I have the same problem with copper. I've had no real success lowering it, and I do think this is an issue — see my thread on supplementation for vegetarians/vegans. I use the quite imperfect solution of supplementing a full RDA of zinc (as picolinate, which appears to be superior tho' it's not clear; citrate may also be a very good choice). I also get close to 3x RDA of iron, but I don't worry about that too much: it's all 'vegan' iron, its bioavailability is low, and I get blood tests to ensure that my iron stores are low-normal. The latter is the main thing (which everyone should be doing anyway): get tested annually for (at least) ferritin, and at least once and occasionally thereafter do Transferrin and Iron-binding Capacity (TIBC, UIBC), to make sure your iron stores are low-normal. (If you've been genetically tested, you may know about Wilson's disease and hemochromatosis, respectively).
  8. Dean, I've just come across this thorough and masterful demolition job, following a link I've just seen today via Iporuru. Very good work; thanks!
  9. Michael R

    Olive oil? Healthy or not?!

    Meanwhile, you evidently are "satisfied" by tiny, non-randomized and sometimes non-controlled studies involving low-fat diets with no hard outcomes and often confounded by things like smoking (Ornish, Esselstyn (sp) etc). It is a puzzlement.
  10. Michael R

    Olive oil? Healthy or not?!

    ... an 'objection' covered in my original post, of course ...
  11. Michael R

    Olive oil? Healthy or not?!

    A narrow metabolic study involving a single administration of , ~1.18 g/kg oil (=88.5 g of oil in a 75 kg adult person, ≈6.6 tablespoons) of a canola oil (not even refined olive oil, let alone high-phenolic fresh EVOO) can't be held up against a mountain of high-quality prospective epidemiology and two large-scale randomized controlled clinical trials — particularly when that body of evidence specifically shows the benefit of EVOO in preventing and ameliorating the course of diabetes. Please stop wasting time with this shite.
  12. Michael R

    Problems with Olive Oil

    This reasonably narrow question got spun off into a whole discussion about the healthfulness of EVOO per se, with a bunch of random half-relevant assertions and data points ... please see here on EVOO as supreme health food (my post of July 3 — I would expect the main thing Gordo originally had in mind when linking the thread) and stop making assertions on lower-grade evidence. Closer to the core question, see my post on EVOO freshness, storage, and cooking.
  13. 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]
  14. 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 😉 .
  15. 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.