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  3. Influence of genetic polymorphisms and habitual caffeine intake on the changes in blood pressure, pulse rate, and calculation speed after caffeine intake: A prospective, double blind, randomized trial in healthy volunteers. Yoshihara T, Zaitsu M, Shiraishi F, Arima H, Takahashi-Yanaga F, Arioka M, Kajioka S, Sasaguri T. J Pharmacol Sci. 2019 Feb 1. pii: S1347-8613(19)30011-8. doi: 10.1016/j.jphs.2019.01.006. [Epub ahead of print] PMID: 30773300 https://reader.elsevier.com/reader/sd/pii/S1347861319300118?token=186FBFAA7DE77CAE70F8110EF18B9BB41E8DB1583DDB42B5439CB6D1A3BBE6FC8DE780979B1B0DA274292395896C2BA2 Abstract The aim of this study was to investigate the contribution of gene polymorphisms, in combination with habitual caffeine consumption, to the effect of caffeine intake on hemodynamic and psychoactive parameters. A double-blind, prospective study was conducted with 201 healthy volunteers randomly allocated 2:1 to the caffeinated group (150 mL decaffeinated coffee with additional 200 mg caffeine) or decaffeinated group (150 mL decaffeinated coffee). We measured the changes in blood pressure (BP) and calculation speed upon coffee intake, stratifying with gene polymorphisms, e.g., those in adenosine A2A receptor (ADORA2A) and cytochrome P450 (CYP) 1A2, and daily caffeine consumption (≤90 mg/day and >90 mg/day). Overall, caffeine intake independently increased BP and calculation speed (p-values < 0.05), irrespective of the polymorphisms. In stratified analysis, a statistical significance within the caffeinated group was observed for the change in systolic BP in the stratum of CYP1A2 polymorphism with daily caffeine consumption ≤90 mg/day: change in systolic BP in the CYP1A2 rs762551 CC group (mean ± SD = 11.8 ± 5.9) was higher than that in the AA/CA group (4.1 ± 5.5). Gene polymorphisms may limitedly modify the effect of caffeine intake on hemodynamic parameters in combination with habitual caffeine consumption. KEYWORDS: ADORA2A; Blood pressure; CYP1A2; Caffeine; Polymorphism Dietary exposure to polychlorinated biphenyls and risk of heart failure - A population-based prospective cohort study. Åkesson A, Donat-Vargas C, Berglund M, Glynn A, Wolk A, Kippler M. Environ Int. 2019 Feb 15;126:1-6. doi: 10.1016/j.envint.2019.01.069. [Epub ahead of print] PMID: 30776745 Abstract BACKGROUND: Beneficial effects of fish consumption on heart failure (HF) may be modified by contaminants in fish. Polychlorinated biphenyls (PCBs) are of particular concern as they have been associated with well-established risk factors of HF, but current data are limited. OBJECTIVES: We aimed to assess the association between dietary PCB exposure and risk of HF, accounting for dietary intake of long-chain omega-3 fish fatty acids. DESIGN: We used the prospective population-based research structure SIMPLER (previously the Swedish Mammography Cohort and Cohort of Swedish Men) comprising 32,952 women and 36,546 men, free from cancer, cardiovascular disease and diabetes at baseline in 1997. Validated estimates of dietary PCBs and long-chain omega-3 fish fatty acids [eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA)] were obtained via a food frequency questionnaire at baseline. Incident cases of HF were ascertained through register linkage. RESULTS: During an average of 12 years of follow-up, we ascertained 2736 and 3128 incident cases of HF in women and men, respectively. In multivariable-adjusted models, mutually adjusted for PCBs and EPA-DHA, the relative risk (RR) for dietary PCB exposure was 1.48 (95% CI 1.12-1.96) in women and 1.42 (95% CI 1.08-1.86) in men, comparing extreme quintiles. Corresponding RRs for EPA-DHA intake were 0.71 (95% CI 0.54-0.93) and 0.82 (95% CI 0.63-1.07), respectively. CONCLUSIONS: Dietary exposure to PCBs was associated with an increased risk of HF in both women and men. EPA-DHA intake was associated with a lower risk of HF in women, with a similar tendency in men. KEYWORDS: Fish; Heart failure; Long-chain omega-3 fish fatty acids; Polychlorinated biphenyls Primary and secondary prevention of preterm birth: a review of systematic reviews and ongoing randomized controlled trials. Matei A, Saccone G, Vogel JP, Armson AB. Eur J Obstet Gynecol Reprod Biol. 2019 Jan 25. pii: S0301-2115(18)31153-9. doi: 10.1016/j.ejogrb.2018.12.022. [Epub ahead of print] Review. PMID: 30772047 Abstract BACKGROUND: Preterm birth (PTB) is a leading cause of perinatal morbidity and mortality. Interventions aimed at preventing PTB can be classified as primary, secondary, or tertiary prevention. OBJECTIVE: To conduct a review of systematic reviews on the effectiveness and safety of primary and secondary preterm birth prevention interventions. SEARCH STRATEGY: A systematic literature search of the Cochrane, PubMed/Medline, EMBASE and CINAHL databases was conducted on 2 September 2015, and updated on 21 November 2016. SELECTION CRITERIA: We included any published systematic review of randomized controlled trials (RCTs) or individual patient data (IPD) of RCTs related to primary or secondary prevention of PTB, published between 2005-2016 where gestational age at birth (of any interval) was a pre-specified outcome. Individual trials and non-systematic reviews were not eligible. DATA COLLECTION AND ANALYSIS: The population of interest was all pregnant women, regardless of PTB risk. The primary outcome was PTB < 37 weeks. MAIN RESULTS: In total, 112 reviews were included in this study. Overall there were 49 Cochrane and 63 non-Cochrane reviews. Eight were individual participant data (IPD) reviews. Sixty reviews assessed the effect of primary prevention interventions on risk of PTB. Positive effects were reported for lifestyle and behavioural changes (including diet and exercise); nutritional supplements (including calcium and zinc supplementation); nutritional education; screening for lower genital tract infections. Eighty-three systematic reviews were identified relating to secondary PTB prevention interventions. Positive effects were found for low dose aspirin among women at risk of preeclampsia; clindamycin for treatment of bacterial vaginosis; treatment of vaginal candidiasis; progesterone in women with prior spontaneous PTB and in those with short midtrimester cervical length; L-arginine in women at risk for preeclampsia; levothyroxine among women with tyroid disease; calcium supplementation in women at risk of hypertensive disorders; smoking cessation; cervical length screening in women with history of PTB with placement of cerclage in those with short cervix; cervical pessary in singleton gestations with short cervix; and treatment of periodontal disease. CONCLUSION: The overview serves as a guide to current evidence relevant to PTB prevention. Only a few interventions have been demononstrated to be effective, including cerclage, progesterone, low dose aspirin, and lifestyle and behavioural changes. For several of the interventions evaluated, there was insufficient evidence to assess whether they were effective or not. KEYWORDS: Neonatal; Obstetrics; Prematurity; Preterm birth; Prevention
  4. AlPater

    Al's CR updates

    HSF1/HSP pathway in the hippocampus is involved in SIRT1-mediated caloric restriction-induced neuroprotection after surgery in aged mice. Yao M, Zhao Z, Wei L, Zhou D, Xue Z, Ge S. Exp Gerontol. 2019 Feb 14. pii: S0531-5565(18)30537-0. doi: 10.1016/j.exger.2019.02.011. [Epub ahead of print] PMID: 30772489 Abstract Postoperative cognitive dysfunction is common in the elderly. Endoplasmic reticulum stress (ER-stress) increases neuronal apoptosis after surgery, and chaperone molecules, such as heat shock proteins (HSPs), help reduce unfolded protein reactions, thereby promoting protein homeostasis. Mammal sirtuin1 (SIRT1)-mediated deacetylation of heat shock factor 1 (HSF1) upregulates HSF1 binding to the HSP70 promoter. Caloric restriction (CR) improves cognition in many neurodegenerative models. In this study, we evaluated whether CR improves impaired learning and memory after surgery by attenuating ER-stress in an SIRT1-dependent manner. Male 18-month-old C57BL/6J mice receiving a 12-week CR or an ad libitum (AL) diet pre-intervention were challenged with tibial open fracture surgery and anesthesia or no treatment. We found a significant protective effect of CR on memory in contextual fear conditioning test after surgery compared with the AL group. CR alleviated ER-stress and neuronal apoptosis in the hippocampus induced by surgery. CR increased HSP70 expression through the HSF1/HSP pathway in a SIRT1-mediated manner, and inhibition of SIRT1 in the hippocampus by lentivirus injection partially reduced the benefits of CR (increased HSP70, deacetylated HSF1, reduced ER-stress, and improved memory). Taken together, our results showed that CR alleviates memory impairment postoperatively via attenuation of ER-stress in the hippocampus in an SIRT1-dependent manner, and the SIRT1/HSF1/HSP70 pathway is involved in this process. KEYWORDS: Caloric restriction; HSF1; HSP70; Neuroprotection; SIRT1 SAHMRI research reveals why high-protein diets are bad for you Clare Peddie, Science Reporter, The Advertiser February 14, 2019 https://www.adelaidenow.com.au/news/south-australia/sahmri-research-reveals-why-highprotein-diets-are-bad-for-you/news-story/9277b39a4ad84b5f1ce38b6ddfaf001f?nk=db94ec9b47b2d84b4dda8cee105fbb26-1550338206 >>>>>>>> Regulation of the Elongation Phase of Protein Synthesis Enhances Translation Accuracy and Modulates Lifespan. Xie J, de Souza Alves V, von der Haar T, O'Keefe L, Lenchine RV, Jensen KB, Liu R, Coldwell MJ, Wang X, Proud CG. Curr Biol. 2019 Feb 4. pii: S0960-9822(19)30031-4. doi: 10.1016/j.cub.2019.01.029. [Epub ahead of print] PMID: 30773367 https://www.cell.com/action/showPdf?pii=S0960-9822(19)30031-4 Xie et al. report that eukaryotic elongation factor 2 kinase (eEF2K), which impairs the rate of elongation, decreases misreading or termination readthrough errors and promotes the correct recognition of start codons in mRNAs. Depletion of the eEF2K ortholog or other factors implicated in translation fidelity in C. elegans decreases lifespan. Highlights •eEF2 kinase enhances the accuracy of protein synthesis under a range of conditions •mTORC1 inhibition improves translation accuracy by activating eEF2K •eEF2K assists correct start codon selection during translation initiation •Impairing translation fidelity reduces lifespan in C. elegans Summary Maintaining accuracy during protein synthesis is crucial to avoid producing misfolded and/or non-functional proteins. The target of rapamycin complex 1 (TORC1) pathway and the activity of the protein synthesis machinery are known to negatively regulate lifespan in many organisms, although the precise mechanisms involved remain unclear. Mammalian TORC1 signaling accelerates the elongation stage of protein synthesis by inactivating eukaryotic elongation factor 2 kinase (eEF2K), which, when active, phosphorylates and inhibits eEF2, which mediates the movement of ribosomes along mRNAs, thereby slowing down the rate of elongation. We show that eEF2K enhances the accuracy of protein synthesis under a range of conditions and in several cell types. For example, our data reveal it links mammalian (m)TORC1 signaling to the accuracy of translation. Activation of eEF2K decreases misreading or termination readthrough errors during elongation, whereas knocking down or knocking out eEF2K increases their frequency. eEF2K also promotes the correct recognition of start codons in mRNAs. Reduced translational fidelity is known to correlate with shorter lifespan. Consistent with this, deletion of the eEF2K ortholog or other factors implicated in translation fidelity in Caenorhabditis elegans decreases lifespan, and eEF2K is required for lifespan extension induced by nutrient restriction. Our data uncover a novel mechanism linking nutrient supply, mTORC1 signaling, and the elongation stage of protein synthesis, which enhances the accuracy of protein synthesis. Our data also indicate that modulating translation elongation and its fidelity affects lifespan. KEYWORDS: Caenorhabditis elegans; caloric restriction; eEF2; eEF2K; elongation; lifespan; mTOR; tRNA; translation fidelity ROLE of IGF-1 System in the Modulation of Longevity: Controversies and New Insights From a Centenarians' Perspective. Vitale G, Pellegrino G, Vollery M, Hofland LJ. Front Endocrinol (Lausanne). 2019 Feb 1;10:27. doi: 10.3389/fendo.2019.00027. eCollection 2019. Review. PMID: 30774624 https://www.frontiersin.org/articles/10.3389/fendo.2019.00027/full Abstract Human aging is currently defined as a physiological decline of biological functions in the body with a continual adaptation to internal and external damaging. The endocrine system plays a major role in orchestrating cellular interactions, metabolism, growth, and aging. Several in vivo studies from worms to mice showed that downregulated activity of the GH/IGF-1/insulin pathway could be beneficial for the extension of human life span, whereas results are contradictory in humans. In the present review, we discuss the potential role of the IGF-1 system in modulation of longevity, hypothesizing that the endocrine and metabolic adaptation observed in centenarians and in mammals during caloric restriction may be a physiological strategy for extending lifespan through a slower cell growing/metabolism, a better physiologic reserve capacity, a shift of cellular metabolism from cell proliferation to repair activities and a decrease in accumulation of senescent cells. Therefore, understanding of the link between IGF-1/insulin system and longevity may have future clinical applications in promoting healthy aging and in Rehabilitation Medicine. KEYWORDS: IGF-1; aging; caloric restriction; centenarians; insulin; longevity; rehabilitation medicine
  5. Almost all ketogenic diets increase the ratio of protein to carbs. This increases IGF1, the opposite. -- Saul
  6. Some aspects of the NIH study would suggest that the beneficial effecgts of a KD in rats is correlated to the dietary restrictio inherent in those. The control group, as far as I understood, is fed ad-libitum, so there is no isocaloric state: Apparently, the KD group was fed an hypocaloric diet, which is the same as traditional CR, barring the different macronutrients ratios. ttwo more differences, one negative (glucose intolerance) the other positive (lesser weight loss) of KD: But I expect that there was a weight reduction, although not at the same levels of CR. Some outputs of the mTORC cascade are the same in both traditional CR and KD regimens. My take as related to humans is that KD (traditional KD with low protein) takes to bottom the insulin signal, and that's not always a good thing. IGF-1 is decreased as well, testosterone is bound by higher SHBG so free T drops down, muscular development is thwarted, bodyweight drops. That's good in overweight people who also accept a loss of musculoskeletal tissue. Bodybuilders also loose weight and muscle mass while on a strict KD, that's why it's prevalently used to shred before contests. The only way to ensure preservation of muscle tissue during KD is use of androgens (and exercise). I'm aware of people like Dom d'Agostino, who are absolute exceptions, researchers who experiment on themselves and also make anple use of costly exogenous ketones. Bottom line, the research is still at its inception and there is apparently no definite proof that KD may extend longevity in humans. It may also be dangerous, if lipids and inflammation parameters are not checked. Barring particular conditions, I find it a very unconvenient way to hypothetically gain better longevity and healthspan, unless we desire to practice stoicism and eliminate many foods from our table...Also, if we pursue celibacy that's a good method, considering the absolute crash in free testosterone. N:B: I tried a KD diet and experienced unwanted weight loss and total loss of libido. Advantage was a more controlled fasting blood glucose. I appreciated though the mental discipline inherent in avoiding simple sugars.
  7. Yesterday
  8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609489/ After reading the article I linked and what Dr.Peter Attia presents, there is some very strong evidence that KD increases Healthspan significantly (not sure about Kraft Dinner though). However people doing CRON or even Time Restricted Feeding should have similar or higher ketone levels - so already getting these health benefits.
  9. That study to me appears too far-fetched. Untrained grip strenght is a function among other things of genetic hand size and pattern of muscle and tendons insertions, plus the neurological genetic pattern (innervation and neurological recruitment of fibers), quantity and ratios of various muscle fibers.... How can the above genetic factors iunfluence CVD hazard? I can really find no logical answer to that.
  10. Yes, the push-ups proficiency level seems to have been adopted as a general qualitative proxy for a combination of aerobic plus resistance exercise. Obviously, the conclusions are valid insofar as the proxy reflects accurtely the underliyng mechanistic principles. Which are????? Proxy: Ability to keep the body rigid while doing brisk arm resistance exercise which imply some level of previous training and no upper-limb related injuries or inflammations.... Mechanistic principle: max VO2? tolerance to lactic acid? slow twitch fibers in upper arms? Are they really the fundamental elements of CVD hazard?
  11. Last week
  12. mccoy

    Vegan specimens and protein

    Guys, next time around that I'll have my blood drawn I'm going to request an IGF-1 value, so that we know for sure if systemic IGF-1 is overly increased in my case. By the way, we all know that IGF-1 like so many other parameters seems to have an optimum, too low is bad too high likewise. My reasoned feeling is that, if bodybuilding is done giving priority to an healthy balanced diet, no drugs, no supplements, no caloric nor proteic abuse, no overtraining, then it's not going to be detrimental to longevity. Whereas if done competitively, like many other sports in today's world, it may have deleterious effects.
  13. Yes. For example, I do vigorous aerobic exercise 30 minutes 6 days a week; my CVD health is great. But I can't do a single pushup (rotator cuff sports injuries). -- Saul
  14. TomBAvoider

    Hype Hucksters and Life Extension

    Man, oh man! Does this article check off all the boxes for me - holy Moses! It exposes the hucksters such as David Sinclair, whom I've denounced as a huckster for years and years now. It exposes how the hype machine works inflating claims for dubious supplements for the sole benefit of the wallets of the promoters and sellers. HYPE, HYPE, HYPE - something I've been combatting every chance I get, often to the irritation of even people on this board. I despise hype in all its forms, whether it pertains to AI or anything else in science. It's everywhere, wasting resources and taking people in. And yeah, always at the bottom of the outrageous claims and shameless hype of these money grabs - studies in mice. I can't say enough about never extrapolating from mice to humans - my response to some "great result" is always "good for the mice". This is really good: https://www.nbcnews.com/health/health-news/pill-reverse-aging-enthusiasm-outpaces-reality-n971616
  15. Todd Allen

    Push-up Exercise Capacity and Future Cardiovascular Events

    Although it wasn't explicitly stated my expectation would be a metronome beat per movement up or down and thus a rate of 40 pushups per minute. Seems much more reasonable to me. Clearly the test is imperfect, one can imagine a wide range of things that could impact pushup performance with minimal impact on cvd health such as injuries to wrists, elbows, shoulders or back. My expectation is accurate measures of body fat %, resting pulse and blood pressure could better predict cvd risk. The pushup test is appealing for not needing much in the way of equipment or expense. But consumer grade pulse and blood pressure monitoring is very affordable and one can get a fair estimate of body fat % with a tape measure and scale weight. I'd be interested to see how that stacks up against the pushup test and against the best measures of pulse, blood pressure and body fat. I also expect for the roughly half of US adults that are prediabetic or diabetic that monitoring post prandial blood sugar could be a potent indicator of cvd risk and achieving stable moderate blood sugar is an important element of reducing cvd risk.
  16. Influence of Eating Schedule on the Postprandial Response: Gender Differences. Masihy M, Monrroy H, Borghi G, Pribic T, Galan C, Nieto A, Accarino A, Azpiroz F. Nutrients. 2019 Feb 14;11(2). pii: E401. doi: 10.3390/nu11020401. PMID: 30769861 https://www.mdpi.com/2072-6643/11/2/401/htm Abstract Ingestion of a meal induces conscious sensations depending of the characteristics of the meal and the predisposition of the eater. We hypothesized that the eating schedule plays a conditioning role, specifically, that an extemporaneous meal is less rewarding than when eaten at the habitual schedule. We conducted a randomized parallel trial in 10 women and 10 men comparing the responses to a consistent savoury lunch-type meal (stewed beans) eaten at the habitual afternoon schedule or at an unconventional time in the morning. Schedule and gender differences were analyzed by repeated measures analysis of covariance. In women, the sensory experience induced by the probe meal, particularly postprandial satisfaction, was weaker when eaten at an unconventional time for breakfast. Men were resilient to the schedule effect and experienced the same sensations regardless of the timing of ingestion; the effect of the eating schedule was significantly more pronounced in women for fullness (F(1,55) = 14.9; p < 0.001), digestive well-being (F(1,36.8) = 22.3; p < 0.001), mood (F(1,12.4) = 13.8; p < 0.001), and anxiety (F(1,11.9) = 10.9; p = 0.001). No differences in the physiological responses induced by the afternoon and morning meals were detected either in women or men. Our data indicate that women are more susceptible to changes in meal schedule than men. KEYWORDS: eating habits; gender differences; hedonic response; homeostatic responses; meal ingestion; meal schedule; postprandial sensations Searching Tardigrades for Lifesaving Secrets Researchers are drawing inspiration from the proteins that they think let hearty water bears cheat time by decelerating their biology. Tardigrades have special proteins that scientists believe help them achieve suspended animation. By Steph Yin Feb. 15, 2019 https://www.nytimes.com/2019/02/15/health/tardigrades-suspended-animation.html
  17. The true purpose of meditation is to let go of your constant stream of thoughts that you go through daily like your fears, desires, anxieties, etc., and experience stillness so that you can have glimpse of your soul.And about Foods with high water content, such as fruits and vegetables, moisturize the skin and keep you hydrated. They also contain antioxidants to protect against cell damage for younger-looking skin. Omega-3 fatty acids found in fish, such as salmon, nourish the skin and may help reduce the appearance of wrinkles.
  18. TomBAvoider

    New Drug to Rejuvenate Brain

    Caveat: in old mice. New experimental drug rapidly repairs age-related memory loss and improves mood "In animal tests the drug has been found to be remarkably effective, with old mice displaying rapid improvements in memory tests within an hour of administration, resulting in performance similar to that of young mice. Daily administration of the drug over two months was also seen to result in an actual structural regrowth of brain cells, returning their brains to a state that resembles a young animal. "The aged cells regrew to appear the same as young brain cells, showing that our novel molecules can modify the brain in addition to improving symptoms," says Sibille."
  19. This addresses itself to psychology, but there's also a big replication crisis in medical studies, thus probably quite relevant: The replication crisis may also be a theory crisis
  20. This is a link to the full study, and it's interesting from many points of view. A few comments Association Between Push-up Exercise Capacity and Future Cardiovascular Events Among Active Adult Men "Abstract Importance Cardiovascular disease (CVD) remains the leading cause of mortality worldwide. Robust evidence indicates an association of increased physical fitness with a lower risk of CVD events and improved longevity; however, few have studied simple, low-cost measures of functional status. Objective To evaluate the association between push-up capacity and subsequent CVD event incidence in a cohort of active adult men. Design, Setting, and Participants Retrospective longitudinal cohort study conducted between January 1, 2000, and December 31, 2010, in 1 outpatient clinics in Indiana of male firefighters aged 18 years or older. Baseline and periodic physical examinations, including tests of push-up capacity and exercise tolerance, were performed between February 2, 2000, and November 12, 2007. Participants were stratified into 5 groups based on number of push-ups completed and were followed up for 10 years. Final statistical analyses were completed on August 11, 2018. Main Outcomes and Measures Cardiovascular disease–related outcomes through 2010 included incident diagnoses of coronary artery disease and other major CVD events. Incidence rate ratios (IRRs) were computed, and logistic regression models were used to model the time to each outcome from baseline, adjusting for age and body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared). Kaplan-Meier estimates for cumulative risk were computed for the push-up categories. Results A total of 1562 participants underwent baseline examination, and 1104 with available push-up data were included in the final analyses. Mean (SD) age of the cohort at baseline was 39.6 (9.2) years, and mean (SD) BMI was 28.7 (4.3). During the 10-year follow up, 37 CVD-related outcomes (8601 person-years) were reported in participants with available push-up data. Significant negative associations were found between increasing push-up capacity and CVD events. Participants able to complete more than 40 push-ups were associated with a significantly lower risk of incident CVD event risk compared with those completing fewer than 10 push-ups (IRR, 0.04; 95% CI, 0.01-0.36). Conclusions and Relevance The findings suggest that higher baseline push-up capacity is associated with a lower incidence of CVD events. Although larger studies in more diverse cohorts are needed, push-up capacity may be a simple, no-cost measure to estimate functional status." In the methodology section we have this for push-ups: "For push-ups, the firefighter was instructed to begin push-ups in time with a metronome set at 80 beats per minute. Clinic staff counted the number of push-ups completed until the participant reached 80, missed 3 or more beats of the metronome, or stopped owing to exhaustion or other symptoms (dizziness, lightheadedness, chest pain, or shortness of breath)." To me, this is somewhat unclear. It reads - to me - as if the idea was to complete 40 push-ups in 30 seconds. That means less than a second per push-up - that's a pretty brisk pace for a full push-up - a full push up would incorporate two stages, the move UP and the drop DOWN before you can move UP again; all this in less than a second? Btw., very quick push-ups are not the most challenging. It is much harder if you have to SLOWLY push up than if you push up explosively using momentum, and further, if you then have to use your muscles to SLOWLY get down controlling the rate of descent rather than using gravity. Meanwhile, with super fast push-ups, it is not really possible to control the rate of descent, and you are using gravity to just drop - much less exertion that way. The other thing that's unclear to me is the sensitivity of this test. What exactly are you measuring? If you take someone who is not used to doing push-ups, it is unlikely that the person in question will be able to deliver 40 chest-to-the-ground push-ups without training; in effect you are selecting for those who regularly do anaerobic exercise and training and incorporate push-ups into their regular exercise. Well, DUH. I mean, aren't you just saying "those who do anaerobic exercise/training regularly have better CVD health than those who don't"? In this case, the push-up test is merely a proxy or marker for a specific exercise status. But the sensitivity seems to me low. What if you have someone who does a lot of aerobic exercise, but not much in the way of push-ups - their CVD status is probably very good, even thought they'd fail this test. Meanwhile, you can have someone who constantly works out like many bodybuilders who could pass this test with flying colors who nonetheless have terrible CVD status (as many bodybuilders paradoxically have - see any number of them dropping dead from heart attacks). In other words, there is nothing that's particular to training your push-up muscles wrt. CVD health - it's all a marker, and a pretty fuzzy one at that. What is a more interesting question is whether there is an effect similar to what has been said about grip strength - what matters is your *un*trained grip strength, as that is a more accurate gauge of your physiological potential/health than a trained state that merely obscures the underlying condition. Now I suppose these being firefighters, they are not exercise naive - isn't doing a set number of push-ups a requirement to get or stay on the job as a firefighter? Any thoughts here? Can YOU do 40 push-ups in 30 seconds?
  21. Saul

    Vegan specimens and protein

    Hi McCoy! I agree with Gordo. True, you need to do a CERTAIN AMOUNT of "pumping" to prevent sarcopenia -- but bulging muscles are a huge calorie burner; and the higher IGF1 numbers are likewise undesirable, likely increasing the rate of aging. That said: AEROBIC EXERCISE is a pure plus; and one should additionally do adequate strengthening exercises to prevent sarcopenia. Other useful things: meditation, yoga. Yoga is good for preserving -- and extending -- flexibility. -- Saul
  22. The exceptional longevity of the naked mole-rat may be explained by mitochondrial antioxidant defenses. Munro D, Baldy C, Pamenter ME, Treberg JR. Aging Cell. 2019 Feb 15:e12916. doi: 10.1111/acel.12916. [Epub ahead of print] PMID: 30768748 Abstract Naked mole-rats (NMRs) are mouse-sized mammals that exhibit an exceptionally long lifespan (>30 vs. <4 years for mice), and resist aging-related pathologies such as cardiovascular and pulmonary diseases, cancer, and neurodegeneration. However, the mechanisms underlying this exceptional longevity and disease resistance remain poorly understood. The oxidative stress theory of aging posits that (a) senescence results from the accumulation of oxidative damage inflicted by reactive oxygen species (ROS) of mitochondrial origin, and (b) mitochondria of long-lived species produce less ROS than do mitochondria of short-lived species. However, comparative studies over the past 28 years have produced equivocal results supporting this latter prediction. We hypothesized that, rather than differences in ROS generation, the capacity of mitochondria to consume ROS might distinguish long-lived species from short-lived species. To test this hypothesis, we compared mitochondrial production and consumption of hydrogen peroxide (H2 O2 ; as a proxy of overall ROS metabolism) between NMR and mouse skeletal muscle and heart. We found that the two species had comparable rates of mitochondrial H2 O2 generation in both tissues; however, the capacity of mitochondria to consume ROS was markedly greater in NMRs. Specifically, maximal observed consumption rates were approximately two and fivefold greater in NMRs than in mice, for skeletal muscle and heart, respectively. Our results indicate that differences in matrix ROS detoxification capacity between species may contribute to their divergence in lifespan. KEYWORDS: Heterocephalus glaber ; antioxidants; mitochondria; reactive oxygen species; skeletal muscle heart
  23. AlPater

    Al's CR updates

    FEBRUARY 14, 2019 Uncovering a 'smoking gun' of biological aging clocks by Harvard T.H. Chan School of Public Health https://medicalxpress.com/news/2019-02-uncovering-gun-biological-aging-clocks.html >>>>>>>>>>>>>>>> Ribosomal DNA harbors an evolutionarily conserved clock of biological aging. Wang M, Lemos B. Genome Res. 2019 Feb 14. doi: 10.1101/gr.241745.118. [Epub ahead of print] PMID: 30765617 https://sci-hub.tw/10.1101/gr.241745.118 Abstract The ribosomal DNA (rDNA) is the most evolutionarily conserved segment of the genome and gives origin to the nucleolus, an energy intensive nuclear organelle and major hub influencing myriad molecular processes from cellular metabolism to epigenetic states of the genome. The rDNA/nucleolus has been directly and mechanistically implicated in aging and longevity in organisms as diverse as yeasts, Drosophila, and humans. The rDNA is also a significant target of DNA methylation that silences supernumerary rDNA units and regulates nucleolar activity. Here, we introduce an age clock built exclusively with CpG methylation within the rDNA. The ribosomal clock is sufficient to accurately estimate individual age within species, is responsive to genetic and environmental interventions that modulate life-span, and operates across species as distant as humans, mice, and dogs. Further analyses revealed a significant excess of age-associated hypermethylation in the rDNA relative to other segments of the genome, and which forms the basis of the rDNA clock. Our observations identified an evolutionarily conserved marker of aging that is easily ascertained, grounded on nucleolar biology, and could serve as a universal marker to gauge individual age and response to interventions in humans as well as laboratory and wild organisms across a wide diversity of species. [Calorie restriction (CR) has long been reported to extend lifespan and retard aging. For the C57BL/6 mice subjected to CR starting at 14 wk old, we observed lower rDNAm age compared to their ad libitum (AL) controls (one-tailed t-test of the differences between rDNAm age and chronological age, P = 1.17 × 10−9) (Fig. 3A). The CR effect remained obvious when instead examining the B6D2F1 strain mice (P = 0.002) (Supplemental Fig. S7A).]
  24. mccoy

    Vegan specimens and protein

    Gordo, I believe that Todd's arguments are valid. By pumping muscles, I'm opposing the natural trend towards myopenia with increasing age. Plus the glucose sink. Plus the hormetic stress. Plus the enhanced digestive function. Plus enhanced cognitive function. How much is too much pumping? In natural bodybuilding, there is a defined threshold by which overwhelming muscularity is avoided. Drug induced superphysiological hypertrophy may actual be of detriment to health and longevity, whereas the natural resistance-induced muscularity provides usually benefits. The higher exercise-induced IGF-1 appears to be local rather than systemic, and we know that local IGF-1 in muscle and nervous tissue is beneficial. Higher T is also notoriously provided by sun exposure. Such natural boosters may be beneficial in opposing the natural decline in physiological androgens. Diet wise, I keep eating an healthy diet and presently am avoiding all the usual supplements like protein isolates, BCCAs and others because in my case they just do not work. There are flip sides, like the increased hunger causing an increased intake of carbs and a consequent higher fasting blood glucose. Since I feel very good with lifting weight and hypertrophic muscles, I'm going to make this specific gamble, trying my best not to get injured (first and foremost rule). After all, I remember you described doing things contrary to longevity, like taking Aya or going canoeing in perilous waters. Dean also described engaging in parachuting, which is an highly hazardous activity.
  25. Todd Allen

    Vegan specimens and protein

    I can't speak for mccoy but I believe it. At least I believe the opposite, the loss of ones muscle is a cause of death. There are many, many studies linking muscular frailty to morbidity and mortality. I don't believe having larger muscle mass protects one from precipitous decline in advanced age but it probably reduces the risk of frailty induced premature death. And those with well developed musculature tend to have less incidence of other degenerations of aging such as osteoporosis, alzheimer's, etc. And I expect it provides one with a bit more reserve to survive other problems. For example a significant percentage of people with cancer die during treatment due to cachexia or weakness induced accidents such as falling and breaking a hip.
  26. Todd Allen

    CR might increase number of cancers

    Tom, yes I am familiar with Sabatini's work and respect his scientific contributions. Gordo didn't elaborate on what he disagreed with but there were a few statements by Sabatini I thought questionable. His description of CR seemed a bit extreme as if it were an all or nothing dietary approach - 30 to 40% caloric restriction and a focus on some of the worst things that occur at the extremes of restriction such as lethargy and food obsession. He also suggested there might be 1000 people practicing CR. I'd be surprised if there are that many doing his described extreme CR long term with health and longevity as the motivation. But there are undoubtedly far more doing moderate CR or extreme CR for other reasons such as anorexia. As for the science, he is talking about an increase in tumors found in lab mice. Perhaps this is relevant to us, but I don't know enough to reach that conclusion. I could imagine many factors impact the relevance: free living humans voluntarily restricting diet seeking optimal nutrition vs food deprived caged mice of questionable genetics in an unnatural environment with artificial lighting, processed foods and in semi-sterile housing isolated from typical mouse biota. People find imprisonment punishing and stressful and chronic stress is considered a risk factor for cancer. Perhaps a semi-starvation diet exacerbates whatever chronic stresses imprisonment causes for a mouse? The number of people doing involuntary CR likely falls in the range of millions to billions depending on the threshhold of deprivation one uses. Their limited control of environment, difficulty obtaining a balanced diet of clean high quality foods and water and the other stresses of poverty and disempowerment may make the mouse studies statistically relevant for humanity but still largely irrelevant for those of us more privileged to be doing voluntary CR for longevity.
  27. AlPater

    Al's CR updates

    The association between dietary protein intake, energy intake and physical frailty- results from the Rotterdam Study. Schoufour JD, Franco OH, Kiefte-de Jong JC, Trajanoska K, Stricker B, Brusselle G, Rivadeneira F, Lahousse L, Voortman T. Br J Nutr. 2018 Nov 13:1-23. doi: 10.1017/S0007114518003367. [Epub ahead of print] No abstract available. PMID: 30419973 https://sci-hub.tw/10.1017/S0007114518003367 Interaction of growth hormone and calorie restriction. Masternak MM, Bartke A. Expert Rev Endocrinol Metab. 2006 Nov;1(6):775-781. doi: 10.1586/17446651.1.6.775. PMID: 30754151 https://sci-hub.tw/https://www.tandfonline.com/doi/full/10.1586/17446651.1.6.775 Abstract Sustaining health and extending longevity have been perpetual goals of all human societies. For almost as long, there has been an ongoing effort to develop treatments that could prevent aging and, more importantly, make us live longer and more healthily. At present, there is one known intervention that delays aging, increases lifespan and prevents diseases in many animal species: calorie restriction. There are other physiological factors that are believed to have corresponding impacts on longevity and aging, including growth hormone and the insulin/insulin-like growth factor 1 signaling pathway. However, there is still much debate regarding the complex action of growth hormone on lifespan and aging. KEYWORDS: Ames dwarf; GHR-KO; calorie restriction; growth hormone; growth hormone receptor; knockout; longevity
  28. Sibiriak

    CR might increase number of cancers

    Thanks Tom. I did find the clip interesting, although way too brief and superficial. Sabatini makes the following points (among others): There is substantial evidence that extended CR will likely increase human health and lifespan (there is contradictory evidence, though, as well.) Although extended CR retards the growth of tumors, it appears to increase the number of tumors through increased stem cell activation. If CR is halted and followed by a diet high in mutagenic foods, the CR-increased number of tumors could then become the basis for increased cancer. Stem cells + mutation --> transformed cells --> cancerous tumor growth. There are two possible solutions to this problem: a) remain calorie-restricted indefinitely; b) don’t eat a highly mutagenic diet But since CR influences many different physiological systems and affects many different disease processes apart from cancer, simply reducing mutagenic food intake alone would not be expected have the same broad anti-aging effects as extended CR. Alternate day fasting is bad because CR benefits require at least two weeks to materialize, so all you get with A/D fasting is a boom and bust cycle. I did not hear Sabatini claim that CR per se might increase number of cancers. Rather, he repeatedly stresses that it is the alternation of CR with an ad lib mutagenic diet which is problematic. I also did not hear Sabatini claim directly that alternate day fasting "likely strongly generates cancer." What he says is that the A/D fasting period would be way too short to have the same positive effects as extended CR, so it’s just a “boom and bust cycle”. But if A/D fasting is too short to produce the positive effects of CR, wouldn't it also be too short to produce the negative tumor-initiation effects? In any case, his remarks on A/D fasting are too brief to be of much interest.
  29. TomBAvoider

    CR might increase number of cancers

    Btw., for those who are into podcasts, here's a very interesting longevity/aging podcast by Peter Attia interviewing David Sabatini: https://peterattiamd.com/davidsabatini/ I listen to such podcasts when doing cardio exercise 🙂
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