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  1. Below paper citations and full text links or availability include a short excerpt or my synopsis in square brackets. The email list system is broken. Posts cannot be searched. Many of the posts do not make it to the messages I receive individually and via the daily mailings. Therefore, I am sending this message, comprised of citations papers that seem to be appropriate to the room of the Forum. I will try to also provide full-text links and a very brief excerpt or within brackets my synopsis of the paper. I apologize for the fact some papers discuss results of studies on the overweight or obese, but feel that some benefits seen in such subjects bears on a continuum of benefits accrued by CR and provide incentive to folks who are overweight or obese. Below are today's papers.. The Lancet Volume 388, Issue 10045, 13–19 August 2016, Pages 640–642 Comment Air pollution and heart disease Bert Brunekreef, Barbara Hoffmann doi:10.1016/S0140-6736(16)30375-0 http://www.sciencedirect.com.qe2a-proxy.mun.ca/science/article/pii/S0140673616303750 Joel D Kaufman, Sara D Adar, R Graham Barr, Matthew Budoff, Gregory L Burke, Cynthia L Curl, Martha L Daviglus, Ana V Diez Roux, Amanda J Gassett, David R Jacobs Jr, Richard Kronmal, Timothy V Larson, Ana Navas-Acien, Casey Olives, Paul D Sampson, Lianne Sheppard, David S Siscovick, James H Stein, Adam A Szpiro, Karol E Watson Association between air pollution and coronary artery calcification within six metropolitan areas in the USA (the Multi-Ethnic Study of Atherosclerosis and Air Pollution): a longitudinal cohort study The Lancet, Volume 388, Issue 10045, 13–19 August 2016, Pages 696-704 http://sci-hub.cc/10.1016/s0140-6736(16)00378-0 Summary Background Long-term exposure to fine particulate matter less than 2·5 μm in diameter (PM2·5) and traffic-related air pollutant concentrations are associated with cardiovascular risk. The disease process underlying these associations remains uncertain. We aim to assess association between long-term exposure to ambient air pollution and progression of coronary artery calcium and common carotid artery intima-media thickness. Methods In this prospective 10-year cohort study, we repeatedly measured coronary artery calcium by CT in 6795 participants aged 45–84 years enrolled in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) in six metropolitan areas in the USA. Repeated scans were done for nearly all participants between 2002 and 2005, for a subset of participants between 2005 and 2007, and for half of all participants between 2010 and 2012. Common carotid artery intima-media thickness was measured by ultrasound in all participants at baseline and in 2010–12 for 3459 participants. Residence-specific spatio-temporal pollution concentration models, incorporating community-specific measurements, agency monitoring data, and geographical predictors, estimated concentrations of PM2·5 and nitrogen oxides (NOX) between 1999 and 2012. The primary aim was to examine the association between both progression of coronary artery calcium and mean carotid artery intima-media thickness and long-term exposure to ambient air pollutant concentrations (PM2·5, NOX, and black carbon) between examinations and within the six metropolitan areas, adjusting for baseline age, sex, ethnicity, socioeconomic characteristics, cardiovascular risk factors, site, and CT scanner technology. Findings In this population, coronary calcium increased on average by 24 Agatston units per year (SD 58), and intima-media thickness by 12 μm per year (10), before adjusting for risk factors or air pollutant exposures. Participant-specific pollutant concentrations averaged over the years 2000–10 ranged from 9·2–22·6 μg PM2·5/m3 and 7·2–139·2 parts per billion (ppb) NOX. For each 5 μg PM2·5/m3 increase, coronary calcium progressed by 4·1 Agatston units per year (95% CI 1·4–6·8) and for each 40 ppb NOX coronary calcium progressed by 4·8 Agatston units per year (0·9–8·7). Pollutant exposures were not associated with intima-media thickness change. The estimate for the effect of a 5 μg/m3 higher long-term exposure to PM2·5 in intima-media thickness was −0·9 μm per year (95% CI −3·0 to 1·3). For 40 ppb higher NOX, the estimate was 0·2 μm per year (−1·9 to 2·4). Interpretation Increased concentrations of PM2·5 and traffic-related air pollution within metropolitan areas, in ranges commonly encountered worldwide, are associated with progression in coronary calcification, consistent with acceleration of atherosclerosis. This study supports the case for global efforts of pollution reduction in prevention of cardiovascular diseases. Graham A Colditz, Karen M Emmons The role of universal health coverage in reducing cancer deaths and disparities The Lancet, Volume 388, Issue 10045, 13–19 August 2016, Pages 638-640 http://sci-hub.cc/10.1016/s0140-6736(16)30376-2 KME is employed by Kaiser Permanente, a US managed care consortium. Mahiben Maruthappu, Johnathan Watkins, Aisyah Mohd Noor, Callum Williams, Raghib Ali, Richard Sullivan, Thomas Zeltner, Rifat Atun Economic downturns, universal health coverage, and cancer mortality in high-income and middle-income countries, 1990–2010: a longitudinal analysis The Lancet, Volume 388, Issue 10045, 13–19 August 2016, Pages 684-695 http://sci-hub.cc/10.1016/s0140-6736(16)00577-8 Summary Background The global economic crisis has been associated with increased unemployment and reduced public-sector expenditure on health care (PEH). We estimated the effects of changes in unemployment and PEH on cancer mortality, and identified how universal health coverage (UHC) affected these relationships. Methods For this longitudinal analysis, we obtained data from the World Bank and WHO (1990–2010). We aggregated mortality data for breast cancer in women, prostate cancer in men, and colorectal cancers in men and women, which are associated with survival rates that exceed 50%, into a treatable cancer class. We likewise aggregated data for lung and pancreatic cancers, which have 5 year survival rates of less than 10%, into an untreatable cancer class. We used multivariable regression analysis, controlling for country-specific demographics and infrastructure, with time-lag analyses and robustness checks to investigate the relationship between unemployment, PEH, and cancer mortality, with and without UHC. We used trend analysis to project mortality rates, on the basis of trends before the sharp unemployment rise that occurred in many countries from 2008 to 2010, and compared them with observed rates. Results Data were available for 75 countries, representing 2·106 billion people, for the unemployment analysis and for 79 countries, representing 2·156 billion people, for the PEH analysis. Unemployment rises were significantly associated with an increase in all-cancer mortality and all specific cancers except lung cancer in women. By contrast, untreatable cancer mortality was not significantly linked with changes in unemployment. Lag analyses showed significant associations remained 5 years after unemployment increases for the treatable cancer class. Rerunning analyses, while accounting for UHC status, removed the significant associations. All-cancer, treatable cancer, and specific cancer mortalities significantly decreased as PEH increased. Time-series analysis provided an estimate of more than 40 000 excess deaths due to a subset of treatable cancers from 2008 to 2010, on the basis of 2000–07 trends. Most of these deaths were in non-UHC countries. Interpretation Unemployment increases are associated with rises in cancer mortality; UHC seems to protect against this effect. PEH increases are associated with reduced cancer mortality. Access to health care could underlie these associations. We estimate that the 2008–10 economic crisis was associated with about 260 000 excess cancer-related deaths in the Organisation for Economic Co-operation and Development alone. [OP.2A.09] SYSTOLIC BLOOD PRESSURE VARIATION DURING 6 YEARS AND MORTALITY: THE AGE AMPLIFIES THE IMPACT OF A SPONTANEOUS INCREASE OR REDUCTION OF PRESSURE AMONG HYPERTENSIVE: IPC COHORT. Thomas-Jean F, Pannier B, Hanon O, Czernichow S, Lemogne C, Simon T, Simon J, Danchin N. J Hypertens. 2016 Sep;34 Suppl 2:e18. doi: 10.1097/01.hjh.0000491374.01833.d7. PMID: 27508617 [The abstract is pdf-availed.] Among normotensives, increase SBP has a deleterious effect only among subjects before 55 years old [OP.LB.02.09] WHAT ANGIOTENSIN CONVERTING ENZYME GENOTYPE AND HIGH BLOOD PRESSURE HAVE IN COMMON IN PORTUGUESE CENTENARIANS? Pereira Da Silva A, Ramos Marques N, Matos A, Gil A, Gorjão Clara J, Bicho M. J Hypertens. 2016 Sep;34 Suppl 2:e80-1. doi: 10.1097/01.hjh.0000491545.64127.b0. PMID: 27508809 [The abstract is pdf-availed.] [Not a prospective study but they compared centenarians with those unlikely to get that old and found that it was but was not only genes that seem to get them there -- hypertension is a risk for the oldest old too.] Association between body mass index and mortality in a prospective cohort of Chinese adults. Sun H, Ren X, Chen Z, Li C, Chen S, Wu S, Chen Y, Yang X. Medicine (Baltimore). 2016 Aug;95(32):e4327. PMID: 27512844 http://journals.lww.com/md-journal/Fulltext/2016/08090/Association_between_body_mass_index_and_mortality.10.aspx lowest risk of all-cause mortality was seen among persons with a BMI of 24 to 28 kg/m in male ... in female, a high BMI was associated with increased mortality, and a BMI of <18.5 kg/m was associated with the lowest risk. Personalized risk prediction for type 2 diabetes: the potential of genetic risk scores. Läll K, Mägi R, Morris A, Metspalu A, Fischer K. Genet Med. 2016 Aug 11. doi: 10.1038/gim.2016.103. [Epub ahead of print] PMID: 27513194 http://biorxiv.org/content/biorxiv/early/2016/02/29/041731.full.pdf genetic risk score (GRS) that has the strongest association with type 2 diabetes (T2D) ... Adding GRS to the prediction model for 5-year T2D risk resulted in continuous net reclassification improvement of 0.324 (95% CI: 0.211-0.444). In addition, a significant effect of the GRS on all-cause and cardiovascular mortality was observed. [OP.1C.09] REPRODUCTIVE HISTORY OF WOMEN AS A DETERMINANT OF ARTERIAL STIFFNESS - THE MALMÖ DIET CANCER STUDY. Nilsson PM, Carlqvist E, Gottsäter M. J Hypertens. 2016 Sep;34 Suppl 2:e10. doi: 10.1097/01.hjh.0000491354.79923.fb. PMID: 27508557 carotid femoral pulse wave velocity (c-f PWV) ... Reproductive Risk Index (RRI) was created to capture the combined effect of separate reproductive variables (age at menarche, parity, and age at menopause). ... Age at menarche (beta = -0.040, p < 0.05) was inversely associated with logarithmic c-f PWV ... RRI was significantly associated (beta = 0.050, p < 0.05) with non-logarithm (supposedly non-linear) c-f PWV. Subjective mood and energy levels of healthy weight and overweight/obese healthy adults on high-and low-glycemic load experimental diets. Breymeyer KL, Lampe JW, McGregor BA, Neuhouser ML. Appetite. 2016 Aug 6. pii: S0195-6663(16)30322-1. doi: 10.1016/j.appet.2016.08.008. [Epub ahead of print] PMID: 27507131 http://sci-hub.cc/10.1016/j.appet.2016.08.008 In conclusion, a high-glycemic load diet was associated with higher depression symptoms, total mood disturbance, and fatigue compared to a low-glycemic load diet especially in overweight/obese, but otherwise healthy, adults. Lifetime grain consumption and breast cancer risk. Farvid MS, Cho E, Eliassen AH, Chen WY, Willett WC. Breast Cancer Res Treat. 2016 Aug 10. [Epub ahead of print] PMID: 27510186 http://sci-hub.cc/10.1007/s10549-016-3910-0 adult brown rice which was associated with lower risk of overall and premenopausal breast cancer (for each 2 servings/week: RR 0.94; 95 % CI 0.89-0.99 and RR 0.91; 95 % CI 0.85-0.99, respectively) and adult white bread intake which was associated with increased overall breast cancer risk (for each 2 servings/week: RR 1.02; 95 % CI 1.01-1.04), as well as breast cancer before and after menopause. Further, pasta intake was inversely associated with overall breast cancer risk. Vegetarian diet reduces the risk of hypertension independent of abdominal obesity and inflammation: a prospective study. Chuang SY, Chiu TH, Lee CY, Liu TT, Tsao CK, Hsiung CA, Chiu YF. J Hypertens. 2016 Aug 10. [Epub ahead of print] PMID: 27512965 [The below paper is pdf-availed.] Taiwanese vegetarians had lower incidence of hypertension than nonvegetarians. [OP.1B.04] ASSOCIATIONS OF 15-YEAR AVERAGE POTASSIUM INTAKE WITH LONG-TERM CARDIOVASCULAR AND RENAL OUTCOME IN THE OUTPATIENT CLINICAL SETTING. Van Noordenne N, Olde Engberink RH, Van Den Hoek TC, Van Den Born BJ, Vogt L. J Hypertens. 2016 Sep;34 Suppl 2:e6. doi: 10.1097/01.hjh.0000491339.74085.91. PMID: 27508744 [The abstract is pdf-availed.] high potassium intake is associated with renoprotection ... not ... CV disease and mortality. xx Blood pressure variability and cardiovascular disease: systematic review and meta-analysis. Stevens SL, Wood S, Koshiaris C, Law K, Glasziou P, Stevens RJ, McManus RJ. BMJ. 2016 Aug 9;354:i4098. doi: 10.1136/bmj.i4098. PMID: 27511067 http://www.bmj.com/content/354/bmj.i4098 http://www.bmj.com/content/bmj/354/bmj.i4098.full.pdf Increased long term variability in systolic blood pressure was associated with risk of all cause mortality (hazard ratio 1.15, 95% confidence interval 1.09 to 1.22), cardiovascular disease mortality (1.18, 1.09 to 1.28), cardiovascular disease events (1.18, 1.07 to 1.30), coronary heart disease (1.10, 1.04 to 1.16), and stroke (1.15, 1.04 to 1.27). Increased mid-term and short term variability in daytime systolic blood pressure were also associated with all cause mortality (1.15, 1.06 to 1.26 and 1.10, 1.04 to 1.16, respectively). Effects of the Mediterranean Diet on Cardiovascular Outcomes-A Systematic Review and Meta-Analysis. Liyanage T, Ninomiya T, Wang A, Neal B, Jun M, Wong MG, Jardine M, Hillis GS, Perkovic V. PLoS One. 2016 Aug 10;11(8):e0159252. doi: 10.1371/journal.pone.0159252. eCollection 2016. PMID: 27509006 Free Article http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0159252 http://journals.plos.org/plosone/article/asset?id=10.1371%2Fjournal.pone.0159252.PDF evidence is limited and highly variable. Results must be interpreted with caution. https://www.crsociety.org/topic/11225-metabolism-aging-cr-exercise/?hl=%2Bpeak+%2Boxygen+%2Bconsumption Circadian Characteristics of Older Adults and Aerobic Capacity. Dupont Rocher S, Bessot N, Sesboüé B, Bulla J, Davenne D. J Gerontol A Biol Sci Med Sci. 2016 Jun;71(6):817-22. doi: 10.1093/gerona/glv195. Epub 2015 Nov 23. PMID: 26602866 http://sci-hub.cc/10.1093/gerona/glv195 Abstract BACKGROUND: Alteration of circadian rhythmicity with aging might depend on physical aerobic capacity. METHODS: Three groups of participants were established based on their peak oxygen consumption (Group 1 < 20mL/min/kg; Group 2 > 20mL/min/kg and <30mL/min/kg; Group 3 > 30mL/min/kg). Each participant had an individual evaluation of their circadian rhythmicity characteristics through two well-known circadian rhythms: core temperature and rest/activity cycles. Nocturnal sleep was also recorded using actimetry and diurnal vigilance tested in a car driving simulator. RESULTS: The amplitude of the oral temperature fluctuations for Group 1 is significantly lower (p < .05) than that of Group 3. Group 2 (p < .01) and Group 3 (p < .05) were significantly more active during the day than Group 1. The index of inactivity during the night for Groups 2 (p < .05) and 3 (p < .01) was higher than Group 1. Results of the car driving simulation showed that for Group 1, the number of lane crossings was significantly higher than Groups 2 (p < .01) and 3 (p < .01). In addition, diurnal vigilance was lower in Group 1. CONCLUSIONS: The biological clock seems to be enhanced in older participants with a higher level of physical capacity. KEYWORDS: Exercise; Physical activity; Physical performance
  2. I'm going to layout all my issues as i'm looking for hope/help starting a CR diet. I'm morbidly obese at 335 lbs and my body is falling apart. Recently I've had a cardiac stent inserted, I've got major back problems, fatigue, stomach problems, and now I have nerve damage (peripheral neuropathy) that's causing pain (pins needles) in my legs/arms. To say the least i'm not in great shape. Sometimes it's hard to find the will to go to work. It's a struggle just to do the basic things in my life like cooking, cleaning, and hanging out with kids and friends. Recently I've been reading a lot about following a CR diet to help repair the body in various ways, lose weight and extend your life. Mostly I just want to get healthy again, lose the weight and repair my nerve damage. I think a CR diet is the way to go because in my late 20's I went on a CR diet and lost 150 lbs.... for a period of time (about 2 years) I never felt better in my entire life. Unfortunately it didn't last and I put weight back on over the next several years. Fast forward 24 years and my body is a complete mess... I need to recapture my youth. Has anyone had experience rejuvenating their bodies using a CR diet?
  3. Dear colleagues, A very interesting conference will be held July 26-27 at the George Washington University Medical Center: https://PCRM.org/ICNM Among the many presenters is Dr. Dean Ornish, the well-known vegan guru (who is often cited by our own mikeccolella). Looks interesting, and, IMO, worth attending. -- Saul
  4. Been thinking about this ever since I read Kurzweil’s book ‘Transcend’. Many people might already be familiar with his ideas and his theory of exponential growth and how that will affect our health and longevity. Here’s the latest interview with him where he succintly summarizes his predictions about the future of health, aging and biotechnology: [media]https://www.youtube.com/watch?v=lpzXWGrngTw[/media] Thoughts? What do you think are the holes/blind spots in his arguments?
  5. Hi all, I'm creating a monthly newsletter that describes the latest advances in longevity sciences. The newsletter is intended for a non-technical audience without a formal background in chemistry and biology. Content Includes: Summaries of the latest research Basic overview of the science behind longevity Tests for personalized diagnostics of age-related diseases Database of the latest FDA drug and device submissions If you're interested, click on this landing page link http://www.mylanderpages.com/filez/LongevityDigest it enter your email. I will email you the newsletter once it's ready.
  6. Hello, I have a medical background and created an app to help you understand which of 10 habits could reduce your mortality risk (based on scientific research) and develop them using gamification. I'm looking for testers, so let me know if this could be useful to you. Thanks.
  7. All, I'm often critical in my posts about how badly the popular media butchers studies of diet, health and nutrition - and it often only becomes apparent how badly the media distorts and exaggerates research when you read the actual text of the study with a critical eye. For example, the bogus data low-fat gurus use to criticize olive oil. Even Dr. Greger, whose perspective and analysis I'm generally very impressed with, is guilty of spinning the evidence (also discussed here) in favor of a plant-based diet on occasion. That's why I was pleased and amused to see this new segment from late-night talk show host John Oliver in which he humorously tears to shreds the typical coverage we see of diet/nutrition/health studies in the mainstream media. It's a rather long segment (20min) embedded below, but I highly recommend it. If you're just in it for the laughs, I suggest jumping ahead to 15:45 (here is a direct link to that spot), featuring "TODD Talks - where the format of TED Talks meets the intellectual rigor of morning news shows". It is extremely amusing, while effectively driving home the point that you should believe very little of what you hear about "new research" on TV or via online news sources (except this one of course☺). --Dean
  8. There is a really interesting new meta-analysis [1] in this week's issue of The Lancet on the association between height and health/longevity. Here is a popular press article on the study, with the title Big And Tall: Nutritious Meals May Make Us Taller But They Could Also Increase Our Cancer Risk. The researchers looked at 121 epidemiological studies of over a million people that assessed the association of height with health and lifespan. The heart of the paper are these two graphs: showing how in both men and women, being taller reduces risk of coronary heart disease, but increases risk of cancer. Here is a graphical representation of the over/undernutrition-based mechanisms the authors postulate to explain the observations: The link to cancer via higher insulin in people who eat a lot (and hence grow taller) is familiar. What was a bit surprising was their suggestion that increased levels of grow factors like IGF-1 in taller people may actually improve insulin sensitivity and hence reduce diabetes and cardiovascular disease. --Dean ------------- [1] The Lancet Diabetes & Endocrinology Available online 28 January 2016 DOI: http://dx.doi.org/10.1016/S2213-8587(15)00474-X| Divergent associations of height with cardiometabolic disease and cancer: epidemiology, pathophysiology, and global implications Norbert Stefan, MD, Hans-Ulrich Häring, MD, Frank B Hu, MD, Dr Matthias B Schulze, DrPHcorrespondenceemail Full text: http://dx.doi.org.sci-hub.io/10.1016/S2213-8587(15)00474-X Summary Among chronic non-communicable diseases, cardiometabolic diseases and cancer are the most important causes of morbidity and mortality worldwide. Although high BMI and waist circumference, as estimates of total and abdominal fat mass, are now accepted as predictors of the increasing incidence of these diseases, adult height, which also predicts mortality, has been neglected. Interestingly, increasing evidence suggests that height is associated with lower cardiometabolic risk, but higher cancer risk, associations supported by mendelian randomisation studies. Understanding the complex epidemiology, biology, and pathophysiology related to height, and its association with cardiometabolic diseases and cancer, is becoming even more important because average adult height has increased substantially in many countries during recent generations. Among the mechanisms driving the increase in height and linking height with cardiometabolic diseases and cancer are insulin and insulin-like growth factor signalling pathways. These pathways are thought to be activated by overnutrition, especially increased intake of milk, dairy products, and other animal proteins during different stages of child development. Limiting overnutrition during pregnancy, early childhood, and puberty would avoid not only obesity, but also accelerated growth in children—and thus might reduce risk of cancer in adulthood.
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