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Michael R

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  1. There's quite a bit on this, specifically on AD, including multiple studies in transgenic AD mouse models and reductions in Abeta in nonhuman primates (PMID 17183154). That's certainly true in some cases, like the Morris water maze, but there are plenty of other studies that don't involve physical condition at all — the extreme case being a standard contextual memory test that measures whether the mice freeze up when exposed to a stimulus they (should) have learned to associate with a coming shock. Your memory of the literature is failing you — perhaps because you quit CR 😉 . Steven Spindler proved that this wasn't true if CR was done properly in 2004: https://www.pnas.org/doi/full/10.1073/pnas.0305300101 ... and has subsequently been independently confirmed in numerous other studies by other groups, such as: https://doi.org/10.1016/j.cell.2020.02.008 https://doi.org/10.1109/IEMBS.2007.4352809 https://doi.org/10.1093/cvr/cvq273 https://doi.org/10.1038/s42255-019-0121-0 I certainly agree that CR is much riskier when started in older adults, and granted that CR is already an experimental and risky intervention when started in young people, starting it at advanced ages would have to be considered very carefully indeed. Additionally, today there are numerous pharmacological options with a lower level evidence than CR but still good evidence as potential anti-aging interventions that don't have as many known risks to older adults.
  2. Obviously, this was a high-risk, older group; however, there's room for improvement by further reducing sodium intake and starting younger.
  3. 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.
  4. 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.
  5. 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.
  6. 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.
  7. 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.
  8. 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).
  9. 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!
  10. 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.
  11. ... an 'objection' covered in my original post, of course ...
  12. 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.
  13. 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.
  14. 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]
  15. 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 😉 .
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