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  1. An argument against prolonged fasting (>24 hours): In their book “the perfect health diet” by Paul Jaminet Ph.D. and Shou-Ching Jaminet Ph.D., the authors note that “Long fasts do not upregulate autophagy more than short fasts do. In mice, autophagy peaks within the first twenty-four hours of a fast and then drops back to normal levels within forty-eight hours of fasting.” While this is in mice, since they published their work similar findings have come out in humans too. Further, they note that “Although long fasts do not upregulate autophagy, they do lead to a more exaggerated drop in autophagy upon resumption of feeding. Mice starved for forty-eight hours experience complete suppression of autophagy when feeding is resumed. [1] In rats starved for five days, autophagy is completely eliminated throughout the first day of refeeding and takes several more days to return to normal. [2] Regarding this delay in resumption of autophagy, they cite “a study of famine victims who had lost 25 percent of body weight during a famine and then were given unlimited food found that only 4.9 percent had detectable infections when refeeding began, but 29.1 percent had overt infections two weeks later. […] the infections that flared up were all intracellular infections—the kind that are fought by autophagy.” [3].Those authors, who saw increased malaria following fasting, concluded “Severe undernutrition can suppress certain infections, mostly those due to intracellular pathogens and especially P. falciparum. Refeeding reactivates suppressed infection and can increase vulnerability to certain new infections especially of viral origin. Based on this, they argue that, “with autophagy suppressed [ by prolonged fasts ] pathogens are free to multiply,” and therefore: “in order to maximize immunity, we want our fasts to be shorter than twenty-four hours. Such short fasts are long enough to induce the highest rates of autophagy—thus maximizing immunity. Longer fasts would not increase autophagy, but would increase the period of immune suppression after the fast ends. Long fasts make infections worse, not better.” They did endorse shorter fasts [4] in the 16-24 hour range, citing the work in alternate day fasts. They also noted a couple of healthy population that practice some version of least partial intermittent fasting, Orthodox Christians following a Mediterranean diet [5] and the Kitavans, [6] “who are noted for their absence of disease […] where the “main and only cooked meal is at sunset, after the gardening has been completed, and generally consists of yams, taro, and occasionally fish, wild fowl, pork, or sea fowl eggs. During the day mangoes, breadfruit, bananas, and green coconuts and their milk may be eaten while working.” [5] We should probably acknowledge here that besides not quite practicing complete intermittent fasting, these populations may be healthy for other reasons. But I think their basic point here is that we have pretty good empirical data on safety of practicing a lifetime of shorter <24 hour fasts in real populations. In contrast, we have less empirical data for the long-term health impact - including any cumulative metabolic damage from the hypothetical proliferation of intracellular parasitic and opportunistic infection -- of practicing lifelong regular prolonged complete fasts >24 hours. Has delayed resumption of autophagy with prolonged fasts been raised as a concern here in the past? Interested in thoughts and perspectives on their arguments for keeping fasts <24 hours. References* * Link to their book via Amazon provided above, repaginated references obtained from http://perfecthealthdiet.com/notes/#Ch40 [1] Mortimore GE et al. Quantitative correlation between proteolysis and macro- and microautophagy in mouse hepatocytes during starvation and refeeding. Proceedings of the National Academy of Sciences of the United States of America 1983 Apr;80(8):2179–83, http://pmid.us/6340116. [2] Pfeifer U, Bertling J. A morphometric study of the inhibition of autophagic degradation during restorative growth of liver cells in rats re-fed after starvation. Virchows Archive B: Cell Pathology 1977 Jun 24;24(2):109–20, http://pmid.us/407706. [3] Murray MJ et al. Infections during severe primary undernutrition and subsequent refeeding: paradoxical findings. Australian and New Zealand Journal of Medicine 1995 Oct;25(5):507–11, http://pmid.us/8588773. [4] Carlson AJ, Hoelzel F. Apparent prolongation of the life span of rats by intermittent fasting. Journal of Nutrition 1946 Mar;31:363–75, http://pmid.us/21021020. Hat tip to Mark Sisson: The myriad benefits of intermittent fasting, February 16, 2011, www.marksdailyapple.com/health-benefits-of-intermittent-fasting/. [5] Sarri KO et al. Greek Orthodox fasting rituals: a hidden characteristic of the Mediterranean diet of Crete. British Journal of Nutrition 2004 Aug;92(2):277–84, http://pmid.us/15333159. Trepanowski JF, Bloomer RJ. The impact of religious fasting on human health. Nutrition Journal 2010 Nov 22;9:57, http://pmid.us/21092212. [6] Malone MJ. Society—Trobriands, http://lucy.ukc.ac.uk/ethnoatlas/hmar/cult_dir/culture.7877 [link does not work but is the citation provided at http://perfecthealthdiet.com/notes/#Ch40 ]
  2. All, Over on the thread Common Chronic Viral Infections Linked to Cognitive Decline we've seen how cytomegalovirus (CMV) is associated with immunosenescence, atherosclerotic plaques, and cognitive decline. It appear the body's immune system gets worn out (i.e. immune system stem cells get depleted) by trying in vain to eliminate chronic CMV infection. This heighted immune response results in systemic inflammation, increased plaque formation in arteries and reduced blood flow to the brain, triggering cognitive decline. Overall bad news. The news is made even worse by the fact that between 50 and 80% of people are infected with cytomegalovirus by age 40! And in the elderly, the typical infection rate can be upwards of 95%... But the real kicker, and the reason for this new thread devoted to CMV, is this study [1], ominously titled Cytomegalovirus infection accelerates epigenetic aging, which was covered this week in a blog post by Reason over at FightAging! In the study, they looked at the CMV status of two sets of people - some their 20s and some in their 90+ and correlated CMV status with "epigenetic age" as measured by "clock like" changes in DNA methylation that appear to happen as people age. This epigenetic age metric has been shown in several studies to correlated with both physical and mental fitness [2], and with mortality rate [3]. For example Marioni et al. [3] observed that 69–79 year old individuals had a 16% increased mortality during a 4–10 year follow-up if the epigenetic age was 5 years higher than the calendar age. What they found first was that 57% of the 20-somethings tested positive for CMV, and 95% of the nonagenarians tested positive - once again showing CMV infection is extremely common in the general population. Further, they found that in the younger cohort, being CMV-positive as associated with a 2.5 year increase in epigenetic age, and in the older folks, testing positive for CMV was associated with a 7 year increase in epigenetic age. But it gets worse. This 2011 study [4] found that in 14,000+ people age ≥25 from the NHANES III cohort, being CMV-positive was associated with an 20% increase in all-cause mortality over a ~16 year follow-up period. People who were both CMV-positive and had elevated C-reactive protein (> 3.0 mg/L) had it even worse - they were at a 30% higher risk of mortality relative to the (already mortality-challenged) CMV-positive folks with low CRP. Here is the graph of the data for all-cause mortality as a function of CMV status and CRP level ("high" CRP means ≥ 3.0 mg/L): Notice how simply being CMV-positive (even with low CRP) was dramatically worse for all-cause mortality risk than if you have a CRP of > 3.0 mg/L, but are free from CMV infection. How sucky is that? We try so hard to make sure our level of systemic inflammation (as measured by C-reative protein) is low. But it turns out having high CRP isn't nearly as bad for longevity as simply having a chronic CMV infection, which almost everyone has. In short, having what has long been thought to be a (relatively) harmless chronic infection with CMV appears associated with dramatic speeding up of the aging process and an increase in mortality risk. More bad news - once you've got CMV, you've got it for life. There are antiviral drugs to fight CMV given to people who have compromised immune systems and solid organ recipients, but they don't cure it and have nasty side effects like immune system suppression and kidney damage to boot. LEF offers tests for chronic CMV infection or acute CMV infection for $59 and $99 respectively (member pricing), but for those who've recently donated blood, you should be able to call your blood bank like I did to find out your CMV status for free. What can someone do to avoid contracting CMV if they are lucky enough not to have it already? It's passed via bodily fluids, so the best way to avoid contracting it is through practicing good hygiene, including: Wash your hands often. Use soap and water for 15 to 20 seconds, especially if you have contact with young children or their diapers, drool or other oral secretions. This is especially important if the children attend child care. Avoid contact with tears and saliva when you kiss. Instead of kissing on the lips, for instance, kiss on the forehead. This is especially important if you're pregnant. Avoid sharing food or drinking out of the same glass as others. Sharing glasses and kitchen utensils can spread the CMV virus. Be careful with disposable items. When disposing of diapers, tissues and other items that have been contaminated with bodily fluids, be careful not to touch your hands to your face until after thoroughly washing your hands. Clean toys and countertops. Clean any surfaces that come into contact with children's urine or saliva. Practice safe sex. Wear a condom during sexual contact to prevent spreading the CMV virus through semen and vaginal fluids. Given the serious apparent downsides of CMV infection, protecting my current CMV-negative status seems to me the most compelling reason to diligently adhering to this admittedly rather burdensome set of hygiene practices. --Dean ------- [1] Exp Gerontol. 2015 Dec;72:227-9. doi: 10.1016/j.exger.2015.10.008. Epub 2015 Oct 17. Cytomegalovirus infection accelerates epigenetic aging. Kananen L(1), Nevalainen T(2), Jylhävä J(3), Marttila S(4), Hervonen A(5), Jylhä M(6), Hurme M(7). Full text: http://sci-hub.cc/10.1016/j.exger.2015.10.008 Epigenetic mechanisms such as DNA methylation (DNAm) have a central role in the regulation of gene expression and thereby in cellular differentiation and tissue homeostasis. It has recently been shown that aging is associated with profound changes in DNAm. Several of these methylation changes take place in a clock-like fashion, i.e. correlating with the calendar age of an individual. Thus, the epigenetic clock based on these kind of DNAm changes could provide a new biomarker for human aging process, i.e. being able to separate the calendar and biological age. Information about the correlation of the time indicated by this clock to the various aspects of immunosenescence is still missing. As chronic cytomegalovirus (CMV) infection is probably one of the major driving forces of immunosenescence, we now have analyzed the correlation of CMV seropositivity with the epigenetic age in the Vitality 90+cohort 1920 (122 nonagenarians and 21 young controls, CMV seropositivity rates 95% and 57%, respectively). The data showed that CMV seropositivity was associated with a higher epigenetic age in both of these age groups (median 26.5 vs. 24.0 (p < 0.02,Mann–Whitney U-test) in the young controls and 76.0 vs. 70.0 (p < 0.01) in the nonagenarians). Thus, these data provide a new aspect to the CMV associated pathological processes. DOI: 10.1016/j.exger.2015.10.008 PMID: 26485162 ------ [2] Marioni, R.E., Shah, S., McRae, A.F., Ritchie, S.J., Muniz-Terrera, G., Harris, S.E., et al., 2015b. The epigenetic clock is correlated with physical and cognitive fitness in the Lothian birth cohort 1936. Int. J. Epidemiol. (doi:dyu277 [pii]) ------- [3] Marioni, R.E., Shah, S., McRae, A.F., Chen, B.H., Colicino, E., Harris, S.E., et al., 2015a. DNA methylation age of blood predicts all-cause mortality in later life. Genome Biol. 16 (1), 25 (doi:s13059-015-0584-6 [pii]). ------- [4] PLoS One. 2011 Feb 17;6(2):e16103. doi: 10.1371/journal.pone.0016103. Seropositivity to cytomegalovirus, inflammation, all-cause and cardiovascular disease-related mortality in the United States. Simanek AM(1), Dowd JB, Pawelec G, Melzer D, Dutta A, Aiello AE. Free full text: http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21379581/ BACKGROUND: Studies have suggested that CMV infection may influence cardiovascular disease (CVD) risk and mortality. However, there have been no large-scale examinations of these relationships among demographically diverse populations. The inflammatory marker C-reactive protein (CRP) is also linked with CVD outcomes and mortality and may play an important role in the pathway between CMV and mortality. We utilized a U.S. nationally representative study to examine whether CMV infection is associated with all-cause and CVD-related mortality. We also assessed whether CRP level mediated or modified these relationships. METHODOLOGY/PRINCIPAL FINDINGS: Data come from subjects ≥ 25 years of age who were tested for CMV and CRP level and were eligible for mortality follow-up on December 31(st), 2006 (N = 14153) in the National Health and Nutrition Examination Survey (NHANES) III (1988-1994). Cox proportional hazard models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for all-cause and CVD-related mortality by CMV serostatus. After adjusting for multiple confounders, CMV seropositivity remained statistically significantly associated with all-cause mortality (HR 1.19, 95% CI: 1.01, 1.41). The association between CMV and CVD-related mortality did not achieve statistical significance after confounder adjustment. CRP did not mediate these associations. However, CMV seropositive individuals with high CRP levels showed a 30.1% higher risk for all-cause mortality and 29.5% higher risk for CVD-related mortality compared to CMV seropositive individuals with low CRP levels. CONCLUSIONS/SIGNIFICANCE: CMV was associated with a significant increased risk for all-cause mortality and CMV seropositive subjects who also had high CRP levels were at substantially higher risk for both for all-cause and CVD-related mortality than subjects with low CRP levels. Future work should target the mechanisms by which CMV infection and low-level inflammation interact to yield significant impact on mortality. DOI: 10.1371/journal.pone.0016103 PMCID: PMC3040745 PMID: 21379581
  3. Dean Pomerleau

    CR and Cold / Flu Survey Results

    Hey Everybody, The CR Cold & Flu survey has been active for about a week, and we got 14 responses, with no more coming in lately, so I figured I'd summarize the results. I've screen captured the entire results as an image below so you can see the details, but here are the highlights: We got half of our respondents from the CR Forums, and half from the Facebook CRS group. We got a pretty good split of genders (9 male / 5 female) A pretty wide distribution of ages and time practicing CR, with quite a few veterans. A good number of low-BMI, apparently serious CR practitioners, so it was a pretty good sample. 80% of people reported getting a single cold / flu or less per year on average. This seems a lot lower than the general population. Nearly 80% say they get fewer colds / flu now than they did before starting CR. 54% say they get colds / flu less frequently than others in their household. 85% said they have low or low-normal white blood cell counts. 57% percent never get the flu shot. Overall, I think this confirms our hypothesis - that CR folks have a less inflammable body (reflected in low WBC count), but if anything possess a more competent immune system, as reflected in contracting fewer colds and flu than before they started CR, than others in their household, and than is average in the general population. --Dean
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