From owner-ageing@net.bio.net Wed Feb 10 22:00:00 1993 Path: biosci!bcm!cs.utexas.edu!usc!howland.reston.ans.net!spool.mu.edu!sgiblab!munnari.oz.au!ariel.ucs.unimelb.EDU.AU!ucsvc.ucs.unimelb.edu.au!lugb!lure.latrobe.edu.au!demo16 From: demo16@lure.latrobe.edu.au Newsgroups: bionet.molbio.ageing Subject: senility Message-ID: <1993Feb11.141855.1@lure.latrobe.edu.au> Date: 11 Feb 93 04:18:55 GMT Sender: news@lugb.latrobe.edu.au (USENET News System) Organization: VAX Cluster, Computer Centre, La Trobe University Lines: 6 Why is this newsgroup empty??? I would have thought that with all of the information upon ageing that there would be 1000's of bits of info in here!! Anyway, to start the discussion: I am studying the mitochondrial theroy of ageing in Drosophila at LaTrobe in Australia, if anyone out there has any relevant info, I would much appriciate it!! B. Romberg (yet to obtain his final computer account!) From owner-ageing@net.bio.net Thu Feb 11 22:00:00 1993 Path: biosci!daresbury!doc.ic.ac.uk!agate!spool.mu.edu!sgiblab!news.kpc.com!kpc!hollasch From: hollasch@kpc.com (Steve Hollasch) Newsgroups: bionet.molbio.ageing Subject: Re: senility Summary: Why is this newsgroup empty? Message-ID: <1993Feb11.225553.10194@kpc.com> Date: 11 Feb 93 22:55:53 GMT References: <1993Feb11.141855.1@lure.latrobe.edu.au> Sender: usenet@kpc.com Organization: Kubota Pacific Computer, Inc. Lines: 36 demo16@lure.latrobe.edu.au writes: | Why is this newsgroup empty??? I would have thought that with all of the | information upon ageing that there would be 1000's of bits of info in here!! | Anyway, to start the discussion: I am studying the mitochondrial theroy of | ageing in Drosophila at LaTrobe in Australia, if anyone out there has any | relevant info, I would much appriciate it!! Well, I'll respond, though I have nothing to offer you with respect to your study. As far as I know, this is the best group for discussion of dementia and related disorders brought on (or triggered?) by aging, esp. Alzheimer's. My father, while not clinically diagnosed with Alzheimer's, is beginning to show indications of the disease. My main reason for subscribing to this newsgroup is to watch for any additional information that might pass this way with respect to Alzheimer's. With regard to Alzheimer's-related discussion (caregiving, coping strategies, getting diagnoses), I'm not sure that the appropriate group would be. This group (as a subgroup of bionet) _appears_ to be dedicated to the clinical studies, diagnoses and treatments of age-related disorders or processes. So I'm interested in seeing discussion of current theory, experimentation, drug development/use/studies and the like, with respect to Alzheimer's. Anyway, with that out of the way, I'm afraid that there are only a handful of posts to this newsgroup in a month, sometimes none in a month. Not sure why, but I suspect that the net is still limited to folks that have an affinity for and access to computers. For what it's worth, I'd certainly be interested in any information about your research, whether it's discoveries or questions. ______________________________________________________________________________ Steve Hollasch Kubota Pacific Computer, Inc. hollasch@kpc.com Santa Clara, California From owner-ageing@net.bio.net Thu Feb 11 22:00:00 1993 Path: biosci!bcm!cs.utexas.edu!sdd.hp.com!caen!uwm.edu!psuvax1!psuvm!bll102 From: BLL102@psuvm.psu.edu Newsgroups: bionet.molbio.ageing Subject: Re: senility Message-ID: <93043.111154BLL102@psuvm.psu.edu> Date: 12 Feb 93 16:11:54 GMT References: <1993Feb11.141855.1@lure.latrobe.edu.au> Organization: Penn State University Lines: 16 In article <1993Feb11.141855.1@lure.latrobe.edu.au>, demo16@lure.latrobe.edu.au says: >Anyway, to start the discussion: I am studying the mitochondrial theroy of >ageing in Drosophila at LaTrobe in Australia, if anyone out there has any >relevant info, I would much appriciate it!! I believe it was the January issue of Nature Genetics that contained several articles about aging and mitochondrial DNA. You might try there for some recent information. ================ Belinda LeFor (bll102@psuvm.psu.edu) Department of Anthropology Penn State University From owner-ageing@net.bio.net Fri Feb 12 22:00:00 1993 Path: biosci!daresbury!buzz.bmc.uu.se!corax.udac.uu.se!sunic!isgate!krafla!einararn From: einararn@rhi.hi.is (Einar Arnason) Newsgroups: bionet.molbio.ageing Subject: age in theory Keywords: age,sex and death Message-ID: <6286@krafla.rhi.hi.is> Date: 13 Feb 93 16:40:05 GMT Sender: usenet@rhi.hi.is Lines: 18 Nntp-Posting-Host: hengill.rhi.hi.is I am currently trying to write a paper for the anual biology magazine of the University of Iceland. I chose to write about agening. I have read G.C.Williams article (1957) and alson some of teh literature such as Stearns on the evolution of life histories and so on. What i would like to know is wheter there is some newer summary of agetheory available somewhere ( I mean something like G.C.W.). I would also really like if people could share their opinion of what such an article should include and maybe explain where ageing theory is going to day. Is it going molecular still or is evoltion still ther? I anyone has any info on death-genes in drosophila or other organisms that would be nice to... Pitur Henry Petersen php@lif.hi.is Deptm. Biology. University of Iceland. From owner-ageing@net.bio.net Fri Feb 12 22:00:00 1993 Path: biosci!uwm.edu!zaphod.mps.ohio-state.edu!saimiri.primate.wisc.edu!usenet.coe.montana.edu!news.u.washington.edu!news.u.washington.edu!news From: bishopj@botany.washington.edu Newsgroups: bionet.molbio.ageing Subject: Re: ageing theory Message-ID: <1ljeamINNjqm@shelley.u.washington.edu> Date: 13 Feb 93 18:23:18 GMT References: <6286@krafla.rhi.hi.is> Organization: University of Washington Lines: 20 NNTP-Posting-Host: lupine.botany.washington.edu In article <6286@krafla.rhi.hi.is> einararn@rhi.hi.is (Einar Arnason) writes: .. > What i would like to know is wheter there is some newer > summary of agetheory available somewhere ( I mean something like G.C.W.). > I would also really like if people could share their opinion of what such > an article should include and maybe explain where ageing theory is going > to day. Is it going molecular still or is evoltion still ther? I anyone > has any info on death-genes in drosophila or other organisms that would > be nice to... Yes, check out Michael Rose's book, "Evolutionary Biology of Ageing" (Oxford Univ. Press, 1990). After reading Stearns and Williams, you probably will be well-prepared to read this book. To paraphrase from reviews in Nature and Science, Rose surveys and synthesizes the literature on ageing in the light evolutionary theory. -- John Bishop Department of Botany University of Washington, Seattle bishopj@botany.washington.edu From owner-ageing@net.bio.net Sat Feb 13 22:00:00 1993 Path: biosci!daresbury!daresbury!news From: bafa1@central.sussex.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: Recent Reviews on Cell Ageing Message-ID: <1993Feb14.203914.7664@gserv1.dl.ac.uk> Date: 14 Feb 93 20:31:13 GMT Sender: list-admin@daresbury.ac.uk Distribution: bionet Lines: 77 Original-To: AGEING@uk.ac.Daresbury X-Mailer: ELM [version 2.3 PL11] Recently, several people have enquired for reviews on ageing. There has appeared in the January issue of Physiological Reviews a review on; Cellular and Molecular Mechanisms of Aging. By J. Fred Rice, of the Department of Physiology, Tufts University School of Medicine, Boston, massachusetts, U.S.A. In this review he covers the following arteas; 1. Evolution of Ageing, 2. Life-Prolonginh effects of caloric restriction. 3. long-lived mutants. 4. Cellular Senescence. 5. Cellular senescence and organismal ageing. 6. Senescent phenotype in cultured cells is dominant. 7. Causes of cellular ageing. A. Error theories. B. Program theories. I think some people might find this review a useful introduction to the field; others might find it thought-provoking. Sydney SHALL. ------------------------------------------------------------------------------ Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Telephone: +44.273.67.83.03 FAX: +44.273.67.83.33 E-Mail: Janet: BAFA1@uk.ac.sussex.central Elsewhere: BAFA1@central.sussex.ac.uk EARN/BITNET: BAFA1%sussex.central@ukacrl ------------------------------------------------------------------------------- From owner-ageing@net.bio.net Sun Feb 14 22:00:00 1993 Path: biosci!agate!doc.ic.ac.uk!daresbury!bioftp.unibas.ch!rc1!pespmc1.vub.ac.be!fheyligh From: fheyligh@vnet3.vub.ac.be (Francis Heylighen) Newsgroups: bionet.molbio.ageing,bionet.molbio.evolution Subject: Evolutionary necessity of senescence? Message-ID: <1219@rc1.vub.ac.be> Date: 15 Feb 93 10:10:20 GMT Sender: news@rc1.vub.ac.be Organization: Free University of Brussels Lines: 142 Xref: biosci bionet.molbio.ageing:384 bionet.molbio.evolution:756 X-UserAgent: Nuntius v1.1.1d17 X-XXMessage-ID: X-XXDate: Mon, 15 Feb 93 09:55:04 GMT It is sometimes said that mortality through senescence is "necessary" in genetic evolution. For example, V. Turchin and C. Joslyn in their "Cybernetic Manifesto" (published in Kybernetes, Vol. 19, Nos. 2-3, p. 63-65) state the following: "16. Evolution and immortality [...] In natural selection, the source of change is the mutation of the gene; nature creates by experimenting on genes and seeing what kind of a body they produce. Therefore, nature HAS TO destroy older creations in order to make room for the newer ones. The mortality of multicellular organisms is an evolutionary NECESSITY. [...]" [EMPHASIS added] The statement that individual mortality is necessary for evolution is rather strong. Therefore, in a later text, I have reformulated this idea in a somewhat more prudent way: "Natural selection entails survival and development as the essential values. Although the death of individual organisms MAY BE USEFUL for genetic evolution (genes themselves being immortal), it is no longer necessary for cultural evolution. Hence the maximisation of survival leads to the striving toward immortality." [emphasis added] This view was influenced by my study of Dawkins's "Selfish Gene" picture of evolution, where the fundamental unit to be maintained by natural selection is not the individual, nor the group or the species, but the gene. Individuals are merely disposable vehicles for the replicating information contained in the genes. As long as the genes survive (that is, are replicated in offspring before the individual dies), the survival or death of the individual is not very important. A paper in a recent "Scientific American" issue (I don't have the reference at hand), summarizing the most recent theories of aging, leads me to an even more skeptical view. Though some theories seem to assume that aging (and hence death) are preprogrammed in the genes, thus implying some kind of evolutionary necessity of individual mortality, more recent theories explain aging without such special assumptions. The main idea is that every evolutionary adaptation has a cost: using genes for one specific activity or function implies that resources (matter, energy, time, neguentropy) are wasted, which thus can no longer be invested in another function. In practice there is always a trade-off, and it is impossible to simultaneously maximize two different functions (e.g. reproduction and survival). For a gene, the main criterion that must be fulfilled or maximized in order to be naturally selected, is that its vehicle (individual organism) should survive long enough to be able to produce (numerous) offspring. Now, one might argue that the longer the organism lives, the more offspring it can produce, and the more copies of its genes will be made. Hence, the genes of organisms that do not age, and thus live longer, would be naturally selected. However, mortality depends on at least two different factors: (internal) aging, and (external) perturbations (accidents, diseases, predation, starvation, ...). Though a gene can make its vehicle or carrier stronger, smarter and more resistent, it can never completely eliminate all possible perturbations causing death. On the other hand, we might imagine genes stopping the process of aging (there are enough examples of self-repair mechanisms in cells and organisms, and the fact that genes themselves are immortal should be sufficient to counter any arguments based on uncontrollable deterioration because of the second law of thermodynamics). But the question is whether it is worthwhile for a gene to invest lots of resources in counteracting the effects of aging. The factor of death because of external perturbations could be measured as some kind of average probability for an individual to be killed in a given lapse of time due to external causes. This would make it possible to compute an average life expectancy, not taking into account internal aging. The normal life expectancy for primitive people living in a natural environment (unlike our own highly protective environment) seems to be about 30-40 years. Now, if you are likely to die around the age of 35 by external causes, there is little advantage in spending a lot of resources on combating the effects of aging, so that you might theoretically live for 1000 years. That is why we might expect that in the trade-off between early reproduction and long-time survival the genes would tend towards the former pole, making sure that sufficient off-spring is generated by the age of 35, rather than trying to extend the maximal age beyond 120 years (the apparent maximum for humans). This implies that if our present environment, where the probability of being killed by predators, starvation or diseases before reaching old age is much smaller than in the original human environment, would continue to exist for a million year or so, natural selection would promote genes that would make us live longer. As to the process of aging, there seems to be a multitude of effects involved, so that we should not expect any single genetic mutation to solve the problem. One of those is the production of "free radicals" (a type of oxidyzing agents, damaging proteins necessary for the functioning of the cell) during energy production. Another one is an apparently inbuilt limit on the number of times a cell can divide (mitosis). This limit (of the order of 50 divisions) is well beyond the one that is reached during normal life, and should thus not be interpreted as a preprogrammed death. The hypothesis is that it functions to limit the risks for the development of cancer or tumors (characterized by unrestricted reproduction of cancerous cells). The mechanism seems to be that during each splitting of a cell, the chromosomes are copied incompletely, with a small stretch of DNA on the outer extremum being cut off during the split. The outer stretches of DNA for a young cell are not functional, so that losing them does not impair function. But after a sufficient number of divisions, the process would start to cut off functional DNA, thus making it impossible for the cell to survive. The cutting off does not happen during cell divisions (meiosis) producing sex cells (sperm or egg cells). Otherwise each subsequent generation would have less DNA than the previous one. This reminds us of the fact that the loss of DNA is not an unavoidable effect of increase of entropy or a similar physical principle leading to aging. In conclusions, those genetic models of aging seem to imply that death is not necessary for evolution, as Turchin and Joslyn originally stated: it is only a side-effect of the fact that a gene can spread more quickly by early reproduction than by long-term survival of its carrier, depending on the average life-expectancy (and reproduction expectancy) in the given environment. From the point of view of the selfish gene, there is no reason whatsoever why it should destroy older copies of itself in order "to make room for the newer ones". This is merely an anthropomorphization of "Nature" as an intelligent agent, looking ahead and concluding that the new generation should be promoted at the expense of the older generation. All genes are selfishly striving for survival, and the only thing that would make one of them give up the fight is because it is less fit than its rivals, not because it is "older". From that point of view, I would even reject the more careful formulation that mortality "may be useful for genetic evolution". The only reason for mortality would be that not having it (i.e. maintaining the necessary apparatus for unlimited self-repair of cells and organisms) would take away many resources from reproduction, for a very small return in terms of reproductive fitness. But I would hardly call that "being useful". Of course, these theories of aging are still very hypothetical. But the "selfish gene" view seems to preclude any argument that would make mortality necessary. Or did I overlook something? Please comment! _______________________________________________________________________ Dr. Francis Heylighen Systems Researcher PO, Free University of Brussels, Pleinlaan 2, B -1050 Brussels, Belgium Phone:+32-2-6412525; Fax:+32-2-6412489; Email: fheyligh@vnet3.vub.ac.be _______________________________________________________________________ From owner-ageing@net.bio.net Sun Feb 14 22:00:00 1993 Path: biosci!daresbury!daresbury!news From: bafa1@central.sussex.ac.uk (Sydney Shall) Newsgroups: bionet.molbio.ageing Subject: Free radical Damage as a contribution to cell ageing? Message-ID: <1993Feb15.111414.12770@gserv1.dl.ac.uk> Date: 15 Feb 93 11:06:32 GMT Sender: list-admin@daresbury.ac.uk Distribution: bionet Lines: 88 Original-To: AGEING@UK.AC.DARESBURY X-Mailer: ELM [version 2.3 PL11] Question? Do free radicals and superoxide species contribute to cell ageing? It is necessary to divide up the discussion into two parts; one should, I think, first separate out non-dividing cells from normal proliferating cells. There is abundant evidence that in fact free radicals and superoxide species can and do damage living cells. There is also much data that shows that living cells are able to repair much of the damage that these agents cause. The situation with non-dividing cells is unclear in my view; it is highly probable that free radicals and superoxide species do in fact contribute to damage and perhaps death of these cells eventually. However, even here one must take into account the state of the mitochondria. For the moment, I will leave this discussion in this unsatisfactoryu state, for other contributions. Now I can offer my views on the situation regarding proliferating cells in in vitro culture. In this case it is almost certain to me that damage of any sort is not part of the mechanism, because it has become clearly established that the cessation of growth is not due to celling killing, but is due to a process whic I have long-ago call cellular mortalization; which is in contrast to the immortralization of cultures one sees when the cells are derived from tumours, or when the normal cells had been exposed to DNA viruses, radiation or mutagenic chemicals. What actually happens during the "ageing" of normal cells in culture is that at each generation a fraction of the new-born cells become mortalized, that means reproductively sterile, but otherwise metabolically active. In very old-fashioned words, these cells become post-mitotic, or if you prefer, terminally differentiated. For the case of cells in culture, both human and rodent this is a statement of experimental results, and not an hypothesis. Thus, we now know that duringm cellular senescence in vitro the phenomenon is due to a progressive and continual increase in the fraction of cells that cannot divide. There is no significant fraction of cell death in these cultures. This statement has been experimentally documented. Therefore, in this specific case we cannot look for an explanation for the limited lifespan in terms of damage to the cell and cell death. There is a more subtle view which proposes that while cell death is not involved, DNA damge is the cause of the cessation of proliferation. This is then attributed to very specific DNA damage which inactivates those specific genes which cause the limited life-span or which are required to achieve cell proliferation. This more sophisticated theory is more difficult to disprove, but is highly unlikely; the kinetics of mortalization are totally different from what one would expect. For example, mortalization of the culture actually starts from the beginning of the culture and increases progressively; this is precisely contrary to what the mutation theory (Which I have just deswcribed) would predict. In summary then, it is clear that cell death is not part of the phenomenon of cell ageing in in vitro culture. Whether it plays a significant part in ageing in intact bodies is less clear, but I would guess from the available evidence that this is highly likely. Sydney SHALL. ************************************************************************** ************************************************************************** Sydney SHALL, Laboratory of Cell and Molecular Biology, Biology Building, University of Sussex, Brighton, East Sussex BN1 9QG, ENGLAND. Telephone: +44.273.67.83.03 FAX: +44.273.67.83.33 E-Mail: Janet: BAFA1@uk.ac.sussex.central Elsewhere: BAFA1@central.sussex.ac.uk EARN/BITNET: BAFA1%sussex.central@ukacrl ******************************************************************************* ******************************************************************************* From owner-ageing@net.bio.net Sun Feb 14 22:00:00 1993 Path: biosci!lhc!darwin.sura.net!sgiblab!munnari.oz.au!ariel.ucs.unimelb.EDU.AU!ucsvc.ucs.unimelb.edu.au!lugb!lure.latrobe.edu.au!genbdr From: genbdr@lure.latrobe.edu.au Newsgroups: bionet.molbio.ageing Subject: Free Radicals Message-ID: <1993Feb15.094745.1@lure.latrobe.edu.au> Date: 14 Feb 93 23:47:45 GMT Sender: news@lugb.latrobe.edu.au (USENET News System) Organization: VAX Cluster, Computer Centre, La Trobe University Lines: 5 Thanks for the info, guys! But I would not mind some serious discussion. For a start, who would agree that super oxides do have a major effect when it comes to cellular ageing? I believe that the increase of free radicals within the cell may be some style of pre-programmed cell death, as the cell is usually detroyed by the increase in these radicals. Any comments? From owner-ageing@net.bio.net Sun Feb 14 22:00:00 1993 Path: biosci!uwm.edu!wupost!howland.reston.ans.net!zaphod.mps.ohio-state.edu!cis.ohio-state.edu!news.sei.cmu.edu!bb3.andrew.cmu.edu!crabapple.srv.cs.cmu.edu!tsf From: tsf@CS.CMU.EDU (Timothy Freeman) Newsgroups: bionet.molbio.ageing,bionet.molbio.evolution Subject: Re: Evolutionary necessity of senescence? Summary: Natural evolution of humans only matters in the short run. Message-ID: Date: 15 Feb 93 20:19:22 GMT References: <1219@rc1.vub.ac.be> Sender: news@cs.cmu.edu (Usenet News System) Organization: Carnegie Mellon University Lines: 25 Xref: biosci bionet.molbio.ageing:385 bionet.molbio.evolution:759 In-Reply-To: Francis Heylighen's message of 15 Feb 93 10:10:20 GMT Originator: tsf@U.ERGO.CS.CMU.EDU Nntp-Posting-Host: u.ergo.cs.cmu.edu In article <1219@rc1.vub.ac.be> Francis Heylighen writes: Of course, these theories of aging are still very hypothetical. But the "selfish gene" view seems to preclude any argument that would make mortality necessary. I believe that arguments about biological evolution are useful to explain our present situation, but I don't think that they are useful for reasoning about the long term consequences of our actions. The "selfish gene" view will only be meaningful for as long as radical genetic engineering is not popular. Once it becomes popular, culture will be driving the genetic evolution in a very straightforward way. I can't imagine that happening later than three or four human generations from now. Thus the amount of human genetic evolution by natural selection that will happen in the future is very limited. The present human genome is only important insofar as it allows us to get from here to place where we can rewrite the genome. -- Tim Freeman When they took the fourth amendment, I was silent because I don't deal drugs. When they took the sixth amendment, I kept quiet because I know I'm innocent. When they took the second amendment, I said nothing because I don't own a gun. Now they've come for the first amendment, and I can't say anything at all. From owner-ageing@net.bio.net Mon Feb 15 22:00:00 1993 Path: biosci!uwm.edu!cs.utexas.edu!uunet!bounce-back From: bmdelane@midway.uchicago.edu (Brian Manning Delaney) Newsgroups: news.announce.newgroups,news.groups,sci.med,sci.med.nutrition,sci.bio,sci.cryonics,sci.nanotech,alt.psychoactives,rec.arts.sf.science,bionet.molbio.ageing Subject: 2nd RFD: sci.life-extension Message-ID: <1lpeu9INNkag@rodan.UU.NET> Date: 16 Feb 93 01:10:33 GMT Sender: tale@rodan.UU.NET Followup-To: news.groups Organization: uchicago.edu Lines: 51 Approved: tale@uunet.uu.net Xref: biosci news.announce.newgroups:489 news.groups:9965 sci.med:8554 sci.med.nutrition:1772 sci.bio:2077 sci.cryonics:246 sci.nanotech:301 rec.arts.sf.science:1545 bionet.molbio.ageing:386 NNTP-Posting-Host: rodan.uu.net This is a formal Request for Discussion regarding the establishment of an unmoderated sci.life-extension newsgroup. My original proposal for this group was edited by news administrators. They changed the name to sci.bio.life-extension, which seemed not to make sense to many people, so now I am proposing the group again under the original name. (The Rationale section has been revised.) <> Purpose of the Newsgroup. The newsgroup would be primarily for the discussion of techniques of slowing, stopping, and reversing the aging process, from a practical as well as theoretical standpoint. This includes, as life-extensionists say, "adding life to years as well as years to life;" i.e., we'll discuss not just techniques of "extending" what in some cases might be a state of already senescent decrepitude, but also ways of restoring and maintaining youth. (The name of the group implies no stance on the merits of the book, "Life Extension," by Pearson and Shaw.) <> Rationale. This topic has received increasing attention in recent years as research gerontologists have begun to understand the mechanisms of aging. As interest in this topic has grown, so has discussion on the Net. The discussion has been scattered across a variety of newsgroups, including bionet.molbio.aging, sci.cryonics, sci.med.nutrition, and alt.psychoactives. None of these newsgroups is appropriate to a broad discussion of life-extension: The "bionet" groups are not carried by many sites. In addition, they are designed as a medium of exchange for professional researchers, whose professional needs should be respected by other (mostly amateur) scientists. Moreover, the proposed group would be a forum for the discussion of life-extension from a variety of scientific perspectives -- some falling within the sphere of molecular biology, some within other areas of biology, and some not in biology at all (but rather in psychology, cryonics, etc.). Sci.cryonics specializes in only one technique of life extension. Sci.med.nutrition and alt.psychoactives allow only the limited discussion of life-extension that falls within the spheres of nutrition and psychoactive drugs, respectively, and the emphasis of each is not on life-extension *per se*. A new group would consolidate the discussion, and would provide a more appropriate forum for the more general issues related to longevity, which do not fall under the purview of any current newsgroup. <> Note All discussion should be posted to news.groups. -Brian From owner-ageing@net.bio.net Mon Feb 15 22:00:00 1993 Path: biosci!daresbury!daresbury!news From: SUNDARAM@cmu.unige.ch (Ganesh) Newsgroups: bionet.molbio.ageing Subject: cancel subscription Message-ID: <1993Feb16.220711.20346@gserv1.dl.ac.uk> Date: 16 Feb 93 23:05:50 GMT Sender: list-admin@daresbury.ac.uk Distribution: bionet Lines: 1 X-Envelope-To: ageing@daresbury.ac.uk Content-Identifier: cancel subscr... X-Vms-Cc: SUNDARAM Original-To: ageing@uk.ac.daresbury Content-Transfer-Encoding: 7BIT Mime-Version: 1.0 X-Vms-To: IN%"ageing@daresbury.ac.uk" Please cancel subscription. Thanks From owner-ageing@net.bio.net Tue Feb 16 22:00:00 1993 Path: biosci!uwm.edu!cs.utexas.edu!usc!howland.reston.ans.net!agate!toxic!tyersome From: tyersome@toxic (Randall Tyers) Newsgroups: bionet.molbio.ageing,bionet.molbio.evolution Subject: Re: Evolutionary necessity of senescence? Summary: Ageing as wear Message-ID: <1ludla$2c6@agate.berkeley.edu> Date: 17 Feb 93 22:19:22 GMT References: <1219@rc1.vub.ac.be> Sender: tyersome@insect.berkeley.edu (Randall Tyers) Organization: Plant Biology Lines: 13 Xref: biosci bionet.molbio.ageing:388 bionet.molbio.evolution:771 NNTP-Posting-Host: toxic.berkeley.edu With respect to the original posting which mentioned free-radicals as a by-product of metabolism and leading to unavoidable deterioration: I recently saw a ?Dec'92? issue of Science on NO (nitrous oxide). In one of the articles it discussed NO (a free radical) as an essential signalling molecule within ?vertebrates? and also mentioned the possibility that CO and other gasses may be involved in signal transduction. This would indicate that there is a constant and essential (without a heroic {maybe impossible} engineering effort) production of toxins within our bodies. This seems to reinforce the general idea that we die because it is more advantageous to put energy into reproduction than a (futile) attempt to reverse 'ageing' processes. Randall Tyers From owner-ageing@net.bio.net Wed Feb 17 22:00:00 1993 Path: biosci!agate!howland.reston.ans.net!usc!sdd.hp.com!network.ucsd.edu!sdcc12!jeeves!wsun From: wsun@jeeves.ucsd.edu (Fiberman) Newsgroups: bionet.molbio.ageing,bionet.molbio.evolution Subject: Re: Evolutionary necessity of senescence? Message-ID: <45258@sdcc12.ucsd.edu> Date: 18 Feb 93 22:16:31 GMT References: <1219@rc1.vub.ac.be> <1ludla$2c6@agate.berkeley.edu> Sender: news@sdcc12.ucsd.edu Followup-To: bionet.molbio.ageing Organization: University of California, San Diego Lines: 18 Xref: biosci bionet.molbio.ageing:389 bionet.molbio.evolution:772 Nntp-Posting-Host: jeeves.ucsd.edu In article <1ludla$2c6@agate.berkeley.edu> tyersome@toxic (Randall Tyers) writes: > [stuff deleted] >production of toxins within our bodies. This seems to reinforce the >general idea that we die because it is more advantageous to put energy >into reproduction than a (futile) attempt to reverse 'ageing' processes. > >Randall Tyers Why is it more advantages to put energy into reproduction? It seems to me that theres less energy requirement to keep an organism at homeostasis. Growth requires more energy than homeostasis. Reversing aging may be futile, but I think stopping aging is definitely possible, and more economical than reproduction. -fm From owner-ageing@net.bio.net Thu Feb 18 22:00:00 1993 Path: biosci!uwm.edu!wupost!howland.reston.ans.net!sol.ctr.columbia.edu!usenet.ucs.indiana.edu!sunflower.bio.indiana.edu!adpeters From: adpeters@sunflower.bio.indiana.edu (Andy Peters) Newsgroups: bionet.molbio.ageing Subject: Re: Evolutionary necessity of senescence? Message-ID: Date: 19 Feb 93 00:20:21 GMT References: <1219@rc1.vub.ac.be> <1ludla$2c6@agate.berkeley.edu> <45258@sdcc12.ucsd.edu> Sender: news@usenet.ucs.indiana.edu (USENET News System) Organization: Program in Evolution, Ecology, and Behavior, Indiana University Lines: 45 Nntp-Posting-Host: sunflower.bio.indiana.edu In article <45258@sdcc12.ucsd.edu> wsun@jeeves.ucsd.edu (Fiberman) writes: >In article <1ludla$2c6@agate.berkeley.edu> tyersome@toxic (Randall Tyers) writes: >> [stuff deleted] > >>production of toxins within our bodies. This seems to reinforce the >>general idea that we die because it is more advantageous to put energy >>into reproduction than a (futile) attempt to reverse 'ageing' processes. >> >>Randall Tyers > >Why is it more advantages to put energy into reproduction? It >seems to me that theres less energy requirement to keep an >organism at homeostasis. Growth requires more energy than >homeostasis. Reversing aging may be futile, but I think >stopping aging is definitely possible, and more economical than >reproduction. While stopping aging (through somatic repair) is certainly possible, stopping _death_ isn't. Even if there's no senescence (i.e. decrease in fitness components of an individual with increasing age), there's still a given probability of death from stochastic environmental factors each season. So, as age increases, the strength of selection decreases, because there's a lower probability that the individual has survived to that season. Hence, one (or both) of two things can occur: (1) Deleterious mutations which act later in life can build up (since selection against them is weak, they reach mutation-selection balance at a higher frequency than those acting early in life). (2) Phenotypes involving a tradeoff between early and late survival or reproduction can be selected for. So energy use that leads to later free-radical buildup, the use of certain proteins which are limited in quantity, etc., can increase early fitness, and the decrease in late fitness they cause isn't selected against strongly enough to counteract the early benefit. In a nutshell, the individual organism is going to die one way or the other. The only way to achieve immortality is through reproduction. >-fm -- --Andy "God is a real estate developer / with offices around the nation They say one day he'll liquidate / his holdings on High I say it's all speculation." -- Michelle Shocked From owner-ageing@net.bio.net Sun Feb 21 22:00:00 1993 Path: biosci!agate!howland.reston.ans.net!usc!sdd.hp.com!decwrl!pa.dec.com!oct17.dfe.dec.com!ryn.mro4.dec.com!dedeye.mro4.dec.com!gvt From: gvt@dedeye.mro4.dec.com (George VanTreeck) Newsgroups: bionet.molbio.ageing Subject: RE: Do free radicals and superoxide species contribute to cell ageing? Message-ID: <1993Feb17.220744.4348@ryn.mro4.dec.com> Date: 17 Feb 93 22:07:44 GMT Sender: news@ryn.mro4.dec.com (USENET News System) Reply-To: gvt@dedeye.mro4.dec.com (George VanTreeck) Organization: Digital Equipment Corporation Lines: 44 Free radicals may have something to do with aging. Please be patient, the first part of what follows might not seem like it's related to aging. But the connection will become very obvious. It's been hypothesized since the 1970s that damage to chloraphyll by ultraviolet light is an impetus to some species of trees to replace their leaves or needles. Some think that carotnoids may inhibit the amount of free radical reactions, protecting the chrolaphyll. Some pine trees, like the Ponderosa pine, shed about half their needles every year. A species of Bristlecone pine, Pinus Longeava, sheds less than one twentieth of their needles every year. And the Bristlecone pine grows at higher elevations than any other species of tree, where the intensity of ultraviolet light is much stronger! Thus, one might ask what protects the Bristlecone's chloraphyll so much better? And one might also ask if this is related to the fact that Bristlecone pine are the oldest living plants on this planet? For example, there are specimens about 5,000 years old and still alive. The vitamin A derivative used for treating acne and thought to reverse skin aging is a carotnoid, as are vitamin A, D, E, and K. I'm attempting to grow Bristlecone pine, Pinus Longeava, (the oldest growing species of Bristlecone) in my house in the NE of the US. I'd someday like to do a chemical analysis of the carotnoids and evaluate their quenching capability. I have a plant about a 20cm high. I've had hundreds of seedlings die. And the one plant doesn't seem to be extremely healthy. The roots seem to be very suspectable to mold -- yet they like a lot of water. And they seem to lack resistance to bugs. Perhaps, that is why there are no specimens of this plant in the arboretums on the East coast. I also have a similar sized specimen of Giant Seqouia, which grow to ages over 2,000 years old. My Giant Redwood seeds also failed to grow. But it will probably be years before any of my plants are big enough to take large enough samples for chemical analysis. I'll probably pay some graduate student to do the analysis for me, as I now work in the computer industry and getting very rusty at chemistry. George Van Treeck Digital Equipment Corporation vantreeck@mr4dec.enet.dec.com From owner-ageing@net.bio.net Mon Feb 22 22:00:00 1993 Path: biosci!agate!dog.ee.lbl.gov!network.ucsd.edu!sdcc12!jeeves!wsun From: wsun@jeeves.ucsd.edu (Fiberman) Newsgroups: bionet.molbio.ageing Subject: Re: Evolutionary necessity of senescence? Message-ID: <45465@sdcc12.ucsd.edu> Date: 23 Feb 93 01:13:23 GMT References: <1ludla$2c6@agate.berkeley.edu> <45258@sdcc12.ucsd.edu> Sender: news@sdcc12.ucsd.edu Organization: University of California, San Diego Lines: 41 Nntp-Posting-Host: jeeves.ucsd.edu In article adpeters@sunflower.bio.indiana.edu (Andy Peters) writes: > (1) Deleterious mutations which act later in life can build up >(since selection against them is weak, they reach mutation-selection >balance at a higher frequency than those acting early in life). > (2) Phenotypes involving a tradeoff between early and late survival >or reproduction can be selected for. So energy use that leads to >later free-radical buildup, the use of certain proteins which are >limited in quantity, etc., can increase early fitness, and the >decrease in late fitness they cause isn't selected against strongly >enough to counteract the early benefit. > >-- >--Andy > "God is a real estate developer / with offices around the nation > They say one day he'll liquidate / his holdings on High > I say it's all speculation." -- Michelle Shocked These are descriptions of phenomena that are occurring at the moment when man is not doing anything to affect his aging process. For instance, the first argument considers the affect of deleterious mutations. But theoretically, it is possible to make the effect of mutations close to negligible. This may require genetic engineering to make a better DNA repair system. Or, it may involve controlling the cell cycle such that cells can survive for much longer time without division (or DNA replication). The second argument above considers the effect of free-radical buildup. Again, this phenomenon can also be controlled. We don't have the understanding or knowledge to control these events yet. But already we can see how diet can affect this phenomenon and decrease the chance of cancer. In short, stopping aging is possible as long as there's input of energy. Aging can be thought of as an increase in the entropy of an organism. As long as there's energy input, a system can be maintained at a steady state, and hence, aging can be eliminated. -fm From owner-ageing@net.bio.net Sun Feb 28 22:00:00 1993 Path: biosci!NET.BIO.NET!kristoff From: kristoff@NET.BIO.NET (David Kristofferson) Newsgroups: bionet.molbio.ageing Subject: BIOSCI/bionet Frequently Asked Questions Message-ID: <9303011000.AA25151@net.bio.net> Date: 1 Mar 93 10:00:02 GMT Sender: kristoff@net.bio.net Distribution: bionet Lines: 16 New users of BIOSCI/bionet may want to read the "Frequently Asked Questions" or "FAQ" sheet for BIOSCI. The FAQ provides details on how to participate in these forums and is available for anonymous FTP from net.bio.net [134.172.2.69] in pub/BIOSCI/biosci.FAQ. It may also be requested by sending e-mail to biosci@net.bio.net (use plain English for your request). The FAQ is also posted on the first of each month to the newsgroup BIONEWS/bionet.announce immediately following the posting of the BIOSCI information sheet. Sincerely, Dave Kristofferson BIOSCI/bionet Manager kristoff@net.bio.net