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  1. All, Dr. Greger has an interesting video out today on "Paleo-Poop", discussing the evidence from fossilized human feces that our ancestors ate a very high fiber diet, > 100g of fiber per day vs. < 20g for most people today eating a standard American diet. This wasn't particularly new news to me, or to anyone reading this I suspect. But what I found most interesting about the video was at 2:30, where he discusses what was the likely source of all that fiber. In particular, whether ancestral humans were folivores (foliage / vegetable eaters), frugivores (fruit eaters) or faunivores (meat eaters). Its pretty clear from lots of evidence that we're not primarily meat eaters, and it has only been relatively recently in our evolutionary heritage that meat and other animal products became a large part of our diet. So we can knock faunivores out of the running - at least when considering deep evolutionary time. What was most interesting was the distinction between the other two categories - folivores vs. frugivores. The evidence he shows in the video is from [1], and it is a plot of organism body size (x-axis) vs. density of gut mucosa (y-axis). Apparently the three categories (folivores, frugivores and faunivores) fall into distinct clusters. Here is the graph, with the range at which humans fall as the intersection of the horizontal and vertical lines with the label "Homo Sapiens": As you can see, humans of today fall squarely in the cluster of frugivores, which the authors interpret to indicate that our distant ancestors were primarily fruit eaters. Obviously we're omnivorous now, and have been for quite a while, especially since we expanded out of Africa into environments where fruit isn't readily available in large quantities or year-round, and since we develop cooking and other processing techniques to make meat (as well as other parts of plants) more digestible, and more palatable! But being a fruit-lover myself, I thought it interesting to know that at least our distant ancestors appear to have been heavy fruit eaters like orangutan (who apparently also love durian!), rather than folivores like gorillas. --Dean --------- [1] Claude Marcel Hladik, Patrick Pasquet. The human adaptations to meat eating: a reappraisal. Human Evolution, Springer Verlag, 2002, 17, pp.199-206. Free full text Abstract In this paper we discuss the hypothesis, proposed by some authors, that man is a habitual meat-eater. Gut measurements of primate species do not support the contention that human digestive tract is specialized for meat-eating, especially when taking into account allometric factors and their variations between folivores, frugivores and meat-eaters. The dietary status of the human species is that of an unspecialized frugivore, having a flexible diet that includes seeds and meat (omnivorous diet). Throughout the various time periods, our human ancestors could have mostly consumed either vegetable, or large amounts of animal matter (with fat and/or carbohydrate as a supplement), depending on the availability and nutrient content of food resources. Some formerly adaptive traits (e. g. the “thrifty genotype”) could have resulted from selective pressure during transitory variations of feeding behavior linked to environmental constraints existing in the past. Key Words: meat eating, hominids, gut allometry, thrifty genotype
  2. Here is an interesting short blog post by our friend and evolutionary biologists, Josh Mitteldorf which he titles Aging is a Military Coup. In it he suggests two things, which I paraphrase thusly: Aging is not the passive process we used to think it was. Instead, aging is programmed into the body, and it is often a result of the body actively attacking itself in one way or another - commonly a result of the immune system response to inflammation. From a multi-level natural selection perspective, this self-destruction by individuals may be the way a community/society clears out its weaker members to make way for a new generation, and thereby promote the flourishing of the group. I don't think anyone can argue with #1 - aging, at least in the manifest forms Josh enumerates, does appear to be a very active, programmed response. But I'm much more skeptical about #2. It seems plausible, but far from proven. Here is how Josh describes it: If evolution found it necessary to regulate the individual’s life span for the larger good of the community or the ecosystem, there would be no need to invent a new and specialized death program. It would be far easier to coopt the body’s existing armies, and redirect them in a suicide mission. You can see where Josh gets the "military coup" metaphor in his title. But I think a better analogy is apoptosis. In Josh's model, the individual person is "self destructing" when they get old for the good of the community/society, in the same way an individual cell "self destructs" when it is damaged (via the process called apoptosis) for the good of body. Perhaps resources have been scarce enough in human history that it benefitted the group if older members died off to avoid consuming resources "unproductively". But it's not clear to me that there were enough long-lived, "parasitic" elders in our deep evolutionary history (when our ancestors rarely lived beyond age 30-40) to generate the kind of selection pressure in favor of "human apoptosis" that Josh postulates. Plus there is the "grandmother effect" which suggests older people (particularly women) may have been productive caregivers in a community even after their reproductive years. Regardless of whether his model is right or not, I don't believe that Josh thinks this human apoptosis is a good thing! --Dean
  3. All, Dr. Greger had another fascinating video out today on the link between inflammation and depression, and why an anti-inflammatory diet might be effective for treating depression. Apparently, it has long been known that systemic inflammation and depression are pretty highly correlated. And apparently, based on several studies cited in the video, you can induce depression in people by increasing the inflammation level in their bodies. Researchers have made an argument for why evolution might have set it up this way. Throughout our evolutionary history, systemic inflammation has been almost exclusively associated with infections of some sort, many of which are contagious. When we develop an infection, and our body responds with an inflammatory response, it would have been 'good' for our kin (and therefore our genes, which they share), if we felt crappy, and all we wanted to do is curl up in a corner and avoid contact with other people - in order not to infect them. So, the evolutionary theorists say, we developed a mechanism by which systemic inflammation triggers a depressed mood. Fast forward to today. We've pretty much defeated pathogenic infections, but still feel like curling up and dying when we get an infection - not much we can do about that. But in addition, despite few pathogenic infections, the bodies of most people are still inflamed continuously these days, largely as a result of the crappy diet most people eat. So the same depressive response to inflammation that used to provide a survival advantage, now simply makes us depressed, as a result of the food we're eating. Not surprisingly, Dr. Greger goes on to advocate an anti-inflammatory diet centered around whole plant foods. He says meats in general, and even fatty fish, are proinflammatory for a variety of reasons, including endotoxins. He says that may be why the early hopes for fish and fish oil as a treatment for depression haven't seemed to pan out in larger studies. I thought the most interesting graphs in the whole video are shown below, taken from [1]. In this study, researchers injected into human subjects an endotoxin derived from E. Coli, and then measured both their blood markers of inflammation and their mood over the next few hours. As their bodies mounted an inflammatory response to the endotoxin (as indicated by the IL-6 and TNF-a markers of inflammation), subjects reported a depressed mood. As the inflammation subsided, so did the depressed mood. The correlation between the inflammation and the depressed mood was high, and wasn't observed in the subjects injected with a placebo. I thought it was a really thought provoking video, and a reasonable explanation for the mystery of why depression might have evolved and persisted in our highly social species. Maybe the fact that CR practitioners generally eat a highly anti-inflammatory diet, and have low levels of inflammation as measured by blood tests like C-reactive protein (CRP), may explain why, after the initial weight loss period when toxins may be released from the fat we're losing, triggering inflammation and therefore depressed mood, CR practitioners generally report being in very good moods - quite in contrast to the expectation most people have that CR would make you permanently irritable. Finally, I don't want to oversimplify true clinical depression - which is an incredibly complex and debilitating condition. The kind of "depression" Dr. Greger is talking about in this video and that may be associated with chronic inflammation might be better characterized as "depressed mood", as opposed to true clinical depression. For more info on some of the complexities of clinical depression, including its genetic component, check out this short video on the science of depression. --Dean ------------ [1] Brain Behav Immun. 2010 May;24(4):558-63. doi: 10.1016/j.bbi.2009.12.009. Epub 2010 Jan 4. Inflammation and social experience: an inflammatory challenge induces feelings of social disconnection in addition to depressed mood. Eisenberger NI(1), Inagaki TK, Mashal NM, Irwin MR. Free full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856755/ Although research has established links between feelings of social isolation and inflammation, the direction of these effects is unclear. Based on the role that proinflammatory cytokines play in initiating "sickness behavior," which includes symptoms such as social withdrawal, it is possible that inflammatory processes heighten feelings of 'social disconnection.' Here, we examined whether exposure to an inflammatory challenge increased self-reported feelings of social disconnection. In addition, because both inflammatory processes and feelings of social disconnection contribute to depressive symptoms, we also explored whether increases in feelings of social disconnection played a role in the link between inflammation and depressed mood. Participants were randomly assigned to either receive endotoxin, an inflammatory challenge, or placebo. Proinflammatory cytokines (IL-6, TNF-alpha) were collected at baseline and then hourly for 6h. Participants completed self-reports of sickness symptoms ("fatigue"), social disconnection ("I feel disconnected from others"), and depressed mood ("unhappy") hourly. Results revealed that endotoxin led to significant increases (from baseline) in IL-6 and TNF-alpha levels as well as feelings of social disconnection and depressed mood. Moreover, controlling for increases in social disconnection eliminated the relationship between exposure to inflammatory challenge and depressed mood. This study demonstrates that inflammation can have social psychological consequences, which may play a role in cytokine-related depressive symptoms. Copyright 2009 Elsevier Inc. All rights reserved. PMCID: PMC2856755 PMID: 20043983
  4. Dean Pomerleau

    Epigenetics and "Intelligent Design"

    [Note: I really hate to put this post on the "Chit-Chat" forum, since it is science heavy. It would fit much better on a (longed-for) "Non-CR Health and Longevity" forum. But its too far from CR to justify posting it to "CR Science", so here goes...] I'm reading philosopher Thomas Nagel's most recent book, Mind and Cosmos in which he argues that the "neo-Darwinian conception of nature is almost certainly false" - in fact, that is the subtitle of the book. Key to his argument is that it doesn't appear that the cornerstone of neo-Darwinism, namely random mutation to genes that turn out to be fitness enhancing, could ever come up with the vast variety of large scale variations in body morphology and physiological systems we see in the world, many of which are argued to be "irreducibly complex" (i.e. all-or-nothing from an evolutionary fitness perspective). The architecture of the eye, and the molecular motor that powers flagellum in bacteria are examples of these complex biological structures that would seem (to some) impossible to evolve through simple random mutation. Nagel, and others (and not just intelligent design (ID) folks, some of whom think God orchestrates evolution) see the need for some more directed form of evolution to explain the diversity and complexity of life on our planet. Nagel seems to think mind / consciousness, and not God in the traditional conception of the term, might fit the bill. But to me that seems rather extreme, and goes against "reductive materialism / naturalism" that has been so successful at explaining how the world works over the last few hundred years. One wonders if a less drastic solution that tweaks the mechanism of neo-Darwinian evolution, might be invoked to save the day for materialism / naturalism. As discussed elsewhere (see this post for details), I've recently been studying epigenetics, where gene expression can be modulated by methylation (among other mechanisms). In methylation, a methyl groups can attach to a particular DNA base pair, causing the gene to "wrap up" around a histone, preventing it from being transcribed into RNA, thereby suppressing expression of the protein that the gene codes for. This methylation can be driven by environmental factors, is quite localized, specific, and repeatable, and can occur not only in somatic cells, but also in germ-line cells (eggs and sperm), and thereby get passed down to several subsequent generations. While the epigenetic changes can be adaptive both for the organism in which they first occur, as well as their progeny, they aren't permanent changes to the base-pair sequence of genes, so they aren't heritable variations over thousands or millions of years, like we see across species in the world. So they are "Lamarkian" to a point, but not in the true sense of the world - giraffe necks could get longer for a generation or two after (hypothetical) epigenetic changes occurred as a result of a giraffe stretching to reach the high leaves on a tree, but eventually the epigenetic changes would "wear off" and subsequent generations would go back to having short necks. But what if epigenetic changes via methylation not only silences genes, but also made those silenced genes more prone to mutation? The methylation would not only be a signal that "this gene isn't worth expressing in the current environment", it would also be signaling "this gene is not very useful in is current form in the current environment, so target it for mutation". With an elevated mutation rate specific to maladaptive genes lasting several generations, new variations should more readily arise in subsequent generations, accelerating experimentation with parts of the genome where changes would be mostly likely to be beneficial in a rapidly changing environment. This sort of elevated mutation rate in parts of genes that have been methylated (silenced) is exactly what this study [1] found. To quote the abstract: Our results ... provid[e] the first supporting evidence of mutation rate variation at human methylated CpG sites using the genome-wide sing-base resolution methylation data. It's not clear that this targeting of random mutations to specific maladaptive genes could result in the type of big changes Nagel and others point to when criticizing neo-Darwinian evolution. But it seems like a way to facilitate a sort of "semi-Intelligent Design", without an explicit designer, by focusing "random tinkering" with the genome in places where genetic changes could do the most good in the current environment. Anyway, while not (directly) related to CR, I thought it was interesting nonetheless. Comments appreciated. --Dean ---------- [1] Full text: http://www.biomedcentral.com/1471-2164/13/S8/S7 BMC Genomics. 2012;13 Suppl 8:S7. doi: 10.1186/1471-2164-13-S8-S7. Epub 2012 Dec 17.Investigating the relationship of DNA methylation with mutation rate and allele frequency in the human genome. Xia J1, Han L, Zhao Z. Author information AbstractBACKGROUND:DNA methylation, which mainly occurs at CpG dinucleotides, is a dynamic epigenetic regulation mechanism in most eukaryotic genomes. It is already known that methylated CpG dinucleotides can lead to a high rate of C to T mutation at these sites. However, less is known about whether and how the methylation level causes a different mutation rate, especially at the single-base resolution. RESULTS:In this study, we used genome-wide single-base resolution methylation data to perform a comprehensive analysis of the mutation rate of methylated cytosines from human embryonic stem cell. Through the analysis of the density of single nucleotide polymorphisms, we first confirmed that the mutation rate in methylated CpG sites is greater than that in unmethylated CpG sites. Then, we showed that among methylated CpG sites, the mutation rate is markedly increased in low-intermediately (20-40% methylation level) to intermediately methylated CpG sites (40-60% methylation level) of the human genome. This mutation pattern was observed regardless of DNA strand direction and the sequence coverage over the site on which the methylation level was calculated. Moreover, this highly non-random mutation pattern was found more apparent in intergenic and intronic regions than in promoter regions and CpG islands. Our investigation suggested this pattern appears primarily in autosomes rather than sex chromosomes. Further analysis based on human-chimpanzee divergence confirmed these observations. Finally, we observed a significant correlation between the methylation level and cytosine allele frequency. CONCLUSIONS:Our results showed a high mutation rate in low-intermediately to intermediately methylated CpG sites at different scales, from the categorized genomic region, whole chromosome, to the whole genome level, thereby providing the first supporting evidence of mutation rate variation at human methylated CpG sites using the genome-wide sing-base resolution methylation data. PMID: 23281708