Talk:Senescence/Archive 1

Archive 1

Simple species that do not age

I have read somewhere that some worms (like tapeworm) never get old and all of their cells keep dividing without limit. Where can I find scientific references about it?

Senescence manifests

Althought It might seem stupid to ask it's not, what is characteristic of senescence? I mean, anyone knows senescent people have wrinkles... But... Ia that all? I mean, are there any other indications of old age? Most people see the wrinkles and make the decision, if they do not see wrinkles then there is no old age... But this... It's not accurate... There are more... Mmmm... To say so "symptoms" of old age... Aren't they? _____________

Theories of aging taken from http://jap.physiology.org/cgi/content/full/95/4/1706

Biological Level/Theory -- Description

Evolutionary

• Mutation accumulation -- Mutations that affect health at older ages are not selected against.
• Disposable soma -- Somatic cells are maintained only to ensure continued reproductive success; after reproduction, soma becomes disposable.
• Antagonistic pleiotropy -- Genes beneficial at younger age become deleterious at older ages.

Molecular

• Gene regulation -- Aging is caused by changes in the expression of genes regulating both development and aging.
• Codon restriction -- Fidelity/accuracy of mRNA translation is impaired due to inability to decode codons in mRNA.
• Error catastrophe -- Decline in fidelity of gene expression with aging results in increased fraction of abnormal proteins.
• Somatic mutation -- Molecular damage accumulates, primarily to DNA/genetic material.
• Dysdifferentiation -- Gradual accumulation of random molecular damage impairs regulation of gene expression.

Cellular

• Cellular senescence-Telomere theory -- Phenotypes of aging are caused by an increase in frequency of senescent cells. Senescence may result from telomere loss (replicative senescence) or cell stress (cellular senescence).
• Free radical -- Oxidative metabolism produces highly reactive free radicals that subsequently damage lipids, protein and DNA.
• Wear-and-tear -- Accumulation of normal injury.
• Apoptosis -- Programmed cell death from genetic events or genome crisis.

System

• Neuroendocrine -- Alterations in neuroendocrine control of homeostasis results in aging-related physiological changes.
• Immunologic -- Decline of immune function with aging results in decreased incidence of infectious diseases but increased incidence of autoimmunity.
• Rate-of-living -- Assumes a fixed amount of metabolic potential for every living organism (live fast, die young).

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Shouldn't this be at Ageing? (currenty a redirect) That is by far the more common name. - SimonP 17:10, Jun 11, 2004 (UTC)

Ageing is spelled aging in the US. Let's keep it senescence. Speciate 07:31, 13 January 2007 (UTC)

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I watched a show on the Science Channel on TV. It mentioned that scientists had observed that ageing stops after age 95. Theoretically if they can find out how it is switched off at age 95, then they can find a way to switch it off at an earlier age, such as at a man's prime. Is this claim true? Can someone research it deeper and add the findings in the article. Kowloonese 10:54, 12 Nov 2004 (UTC)

Link between stress and aging

Should this study be noted in the biological causes, or should we wait for confirmation? (Obviously it is required, eventually.) —Daelin 04:15, 30 Nov 2004 (UTC)

The text below should be merged with the article

1. Careful studies of health statistics support a systems approach to aging. When enough systems are damaged, a catastrophic failure occurs.
2. Dr. Leonard Hayflick discovered that mammalian cells divide only a fixed number of times. This "Hayflick limit" was later proven to be caused by telomeres on the ends of chromosomes that shorten with each cell-division. When the telomeres are gone, the DNA can no longer be copied, and cell division ceases. In 2001, experimenters at Geron Corp. lengthened the telomeres of senescent mammalian cells by introducing telomerase to them. They then became youthful cells. Sex and some stem cells regenerate the telomeres by two mechanisms: Telomerase, and alternative lengthening of telomeres (ALT). At least one form of progeria (atypical accelerated aging) is caused by premature telomeric shortening. Also in 2001, research showed that naturally occurring stem cells must sometimes extend their telomeres, because some stem cells in middle-aged humans had anomalously long telomeres.
3. Experimenters discovered that mice whose pituitary glands were removed lived half again as long as unmodified mice, though with terrible side-effects. Therefore, mammals are believed to have a hormonal system that triggers some age-related disease. However, humans with their pituitary glands removed do not live longer.
4. In 2002, genetic modification of a small worm (Caenorhabditis elegans) increased its lifespan sixfold. Related experiments have increased maximum life-span in mice and fruit flies. These experiments prove that there is a genetically-coded death clock that triggers some part of aging. This may be related to the hormonal death clock.
5. A number of research programs have proven that mutations in body cells occur and accumulate as an organism ages, and degrade its function. In 1999, researchers discovered that naturally occurring stem cells recolonize organ systems, countering this effect by reintroducing cells from a reduced number of cellular lineages. The number of cellular lineages is further decreased because the older half of the reproduced DNA is far more likely to remain in a stem cell. The mechanism of old-strand conservation is still being researched.
6. Latest researches and theories consider senescence as a programmed mechanism rather than a result of some error or accumulation of cross linkages and hence believes in the telomere theory of aging. - himanshu grover
7. A number of clinicians noted that the cumulative damage in diabetic patients strongly resembled accelerated aging. This was generalized into a theory that some aging is caused when sugar chemically combines with proteins and other bodily chemicals. It is known that feeding adolescent mice a fully-nutritive diet with minimal food energy can extend their maximum life-spans by half. It is also known that feeding mice small amounts of chromium picolinate can extend their maximum life span about 15%. Chromium is an integral part of active insulin, and insulin is cleaved, to excrete chromium in normal metabolism. Most adult nonvegetarians have large amounts of inactive insulin, which may indicate a chronic deficiency of dietary chromium. Veterinarians routinely treat middle-aged animals for diabetes with chromium supplementation.
8. Studies of patients with Alzheimer's disease patients and age-spotting discovered that the body builds deposits of waste within and without cells. The deposits inside cells are called lipofuscin (Latin for "fat dirt"). These deposits may decrease metabolic efficiencies, causing some age-related symptoms. Mammalian cells have enzymes to cleave and digest proteins. The most common such clean-up enzyme is triggered by a three-element chain of Ubiquinone (CoQ10) attached to the elderly protein.
9. Dr. Denham Harman theorized that some aging damage might be caused by oxidative damage to the body. Experiments discovered that the body has substantial amounts of enzymes and chemicals to reverse oxidative changes. Studies also showed that longer-lived animals have larger amounts, per weight of animal of these mechanisms, in a linear relation to life-span. The experiments also found an internal mechanism, respiration in mitochondria, that creates free radicals that would cause oxidative damage. Feeding of antioxidants to mice increased average life-spans, but not maximum life spans. It is now believed that oxidative damage depletes self-repair mechanisms, whose limits are controlled by other systems.
10. The failures of natural stem cells are now an active area of research. In many cases of damaged organ systems, stem cells do not migrate to the damaged area.
11. Experimenters discovered that mice fed extra melatonin lived 20 percent longer than control mice.

BEFORE YOU ADD TO THIS ARTICLE....

...read WP:AWW. This article presents a myriad of scientific theories and hardly cites any of them. Most theories are preceded by "some gerontologists blieve" or "research has shown" .....you get the idea. These forms of claims are unreputable and require citations. There is a ton of good information in this article, but it needs to be appropriately cited.

If you have the information to add, it shouldn't be that much trouble to cite it. And remember, citing it does not just (or even necessarily) mean putting the title of a book at the bottom of the page. In-line citations are great, and describing the history of a development of a theory adds legitimacy as well.

Keep up the good work guys, and keep being bold. Just remember to cite as you go. Shaggorama 05:45, 27 April 2006 (UTC)

Proposed merge

Also see discussion here. - Samsara (talk • contribs) 14:41, 13 June 2006 (UTC)

Propose renaming to biology of ageing

While I acknowledge that senescence is a term typically applied to a wider range of taxa than "ageing" (e.g. plants typically "senesce" rather than "age"), I think the article would become more approachable (yes, because the links would be labelled with something intelligible for the average Joe) by renaming it to "biology of ageing". - Samsara (talk • contribs) 14:45, 13 June 2006 (UTC)

There is always #redirect for the average Joe. Encyclopedia should use more formal terminologies instead of everyday English. Kowloonese 17:12, 13 June 2006 (UTC)

Well, that's exactly my point. "Biology of ageing" in my experience is more commonly used to refer to the study of senescence in humans, which presumably is of interest to most people coming to read this kind of article; secondly, it would much simplify what's being done here. Just because it's latinised doesn't mean it's right. The best books in science were written in prose that a layperson could follow. - Samsara (talk • contribs) 17:22, 13 June 2006 (UTC)

Ageing is spelled aging in the US. Let's keep it senescence Speciate 07:28, 13 January 2007 (UTC)

The article for Aging states the following: “This article is about all aspects of ageing. For the biological aspect of ageing specifically, see Senescence.” Also, this article begins with the words “Senescence or biological aging,” implying that both have the same meaning. This may or may not be a sufficient measure for clarification. Everything Is Numbers (talk) 10:59, 26 September 2012 (UTC)

Merging Aging DNA into this article and/or mentioning it

The article on Aging DNA seems to be a bit orphaned, but it merits some mention, if not inclusion, in both this article and the one on DNA repair. IMHO, it should remain its own article, and we could have this article make a mention of it in one or two paragraphs. However, I am not a professional geneticist, so I would like the input of some experts on where this should be mentioned/merged. The ikiroid (talk·desk·Advise me) 15:56, 4 August 2006 (UTC)

PNC1 is a Nicotinamidase, PBEF is NOT a Nicotinamidase

The protein PNC1 has been shown to play a key role in yeast aging. Mammals do not have a PNC1 homolog. Instead, we use a Nicotinamide phosphoribosyltransferase (Nampt or PBEF or visfatin, same protein, different names) enzyme to recycle NAD from nicotinamide. Even though they both play functional similar roles, they are, in fact, different enzymes, and it is therefore improper to call Nampt/PBEF/visfatin a nicotinamidase.

Re: Evolutionary theories

Why do not man live longer than women since they can reproduce up to a very old age and women cannot leading to a higher selection. —The preceding unsigned comment was added by 128.197.42.60 (talk) 22:10, 25 January 2007 (UTC).

Evolutionary theory is a bit more complicated than that; specifically, when determining whether a particular trait would have been subject to evolutionary selection, it is important to keep in mind the historical context of that trait. For the vast majority of human history, an individual's lifespan was on the order of 30 years. Disease, predators, and harsh living conditions prevented most individuals from reaching their maximum reproductive age, thus there was little evolutionary pressure for selecting individuals that could reproduce for the longest time. This is a specific case of the general maxim "the force of natural selection declines with age".

de Grey and SENS

I recently read the book "Ending Aging" by Aubrey de Grey about his Engineered negligible senescence. There is a lot of historic (and thus outdated) information in this article and the structure of it also conforms to older theories. While I am not sure how objective de Grey's book is, I am quite sure that a complete overhaul of the article would be a good thing to point out the currently leading theories. --84.178.118.140 13:34, 13 October 2007 (UTC)

Just to blow the telomerase dreamers' bubble, ...

... I added a long-overdue mention of the fact that cancers are immortals. Yes, (parts of) humans can become immortal!. In fact, there are probably a few cells in your body that are acquiring this ghastly property right now. You and I hope they will remain few.

All available science points to the fact that, if some crazy scientist can reactivate your telomerases at age 60, you will not have enough time to see your new youth before your body fills with tumors. Your life will thus be shortened, not lengthened, and you will die with the excruciating pain of bone metastases.

Pop goes the bubble. Emmanuelm (talk) 21:47, 19 November 2007 (UTC)

The majority of cancers, but not all, express telomerase. On the other hand, all embryonic stem cells express telomerase, and some other cells in the human body do, as well, e.g., some keratinocytes. Just as "inhibiting telomerase = curing cancer" is too simplistic, "activating telomerase = causing cancer" is, as well. --SierraSciSPA (talk) 18:08, 23 January 2008 (UTC)

Red Links (Wikipedians don't know bout this article's useless links)

If a link goes nowhere (commonly called by us trolls as "that red word"), please delink it. Or unlink it. Or non-link-ify it. Or some other of your high-learning vocab that means "Clean up this article." SgtHydra 71.111.76.124 (talk) 03:03, 26 January 2008 (UTC)

Red links are often considered useful reminders that an article on the subject should exist, and somebody needs to write it. I agree, though, that this article needs cleanup - certainly, no phrase needs to be red-linked more than once. --SierraSciSPA (talk) 00:07, 28 January 2008 (UTC)

higher organisms

This page frequently uses the expression "higher organisms" without explanation of what this might refer to. The term is ambiguous, obsolete and makes it impossible to understand which organisms are beig described. It would be great if an expert in this area could clarify by refering to specific evolutionary clades, rather than to outdated and nebulous concepts such as higher and lower organisms.Spamburgler (talk) 05:40, 7 August 2008 (UTC)

Cures for Cellular Senescence

Following the theory of the Hayflick Limit, replicative senescence may be cured by the [1] cyclic application of telomerase activators such as those found in astragalus extracts prepared with ethanol and water. For instance, see TA Sciences TA-65. The first work on telomerase activators that people can readily obtain was done by Geron Corporation (2005) and Hong Kong University in their twin patents "Compositions and Methods for Increasing Telomerase Activity" and "Formulations Containing Astragalus Extracts and Uses Thereof". TA Sciences announced TA-65 in 2007. In October of 2010 Intertek/AAC Labs, an ISO 17025 internationally recognized lab, found the largest component of TA-65 to be Cycloastragenol. One may alternate the application of telomerase activators with the application of telomerase inhibitors, making sure not to take both at the same time, since they interfere with each other. Lenthening telomeres cures cellular senescence by causing telomere t-loops to close, silencing the DNA damage signal that causes cellular senescence, modifying gene expression from that of the immortal phenotype. Lengthening telomeres provides more genomic stability, restores the immortal phenotype of mitotically dividing cells, and provides protection against forms of cancer originating in telomeric fusions in old senescent cells. However, telomere remodeling is time-consuming, so that today we typically achieve rejuvenation rates of about 0.667 to 0.75 years per month, or 8 to 9 years per year based on telomerase activation, as reported by TA Sciences based on their measurements of telomere length. In addition to lengthening telomeres to restore youthful patterns of gene expression to cells, a program of modern treatment includes DNA and lipid membrane protective antioxidants such as cocoa powder in water, treatment for mitochondrial senescence with alpha lipoic acid and acetyl L-carnitine, 2000-3000 mg/day vitamin C for collagen synthesis, homocystiene blockers featuring vitamins B6, B12, and folic acid with trimethylglycine to prevent artherosclerosis leading to heart attack and stroke, 3 grams per day arginine with exercise to produce nitric oxide for endothelial cell rejuvenation and restoration of thymic hormone levels, and other options, such as Cat's Claw extract for improved DNA repair. For additional details and options for advanced treatment, see [2] Greenwood Research on Anti-Aging Medicine and Longevity. JamesAGreen (talk) 16:34, 2 October 2008 (UTC) —(talk • contribs) 15:21, 2 October 2008 (UTC)

Why seemingly subtle punctuation matters

Consider this difference:

Senescence encompasses all of the biological processes of a living organism approaching an advanced age

Senescence encompasses all of the biological processes of a living organism's approaching an advanced age

Does senescence include all of the processes of an organism that happens to be approaching an advanced age? No: some of the processes in such an organism may happen the same was as when it was young, and may not be part of the aging process.

Does senescence include all of the processes of an organism's approach toward an advanced age? Sure—why not?

In the pair of sentences above, the difference is all in that one apostrophe. That's why I added it to the article. Michael Hardy (talk) 23:19, 16 January 2009 (UTC)

Gene regulation

Seriously, this section is way ahead of me...I can't understand a bit of it, could anyone try to make it easier on the mind for those of us without a PhD? 213.67.62.172 (talk) 21:00, 19 March 2009 (UTC)

Evolutionary Theories

"The explanation for the long lifespans of primates (such as humans, monkeys and apes) relative to body size is that their rage intelligence and often sociality helps them avoid becoming prey."

Is "rage intelligence" a biological concept? If this is supposed to be "rage, intelligence" then is rage really a technical term whose relation to "being a predator" is analogous to the relationship between intelligence and "being smart," as the subsequent sentence in the article suggests? --anon 76.97.209.44 (talk) 19:48, 9 August 2009 (UTC)

Turtles

Is it true that turtles are not affected by senescence?--80.141.225.9 (talk) 15:15, 8 May 2010 (UTC)

Y Indeed, some genera of the order are negligibly senescent. It is already mentioned in this article that negligible senescence is present in some groups of animal organisms, and the main article on the phenomenon specifies the types of animals, so I don't see any need for doing the same in this article. Everything Is Numbers (talk) 14:25, 25 September 2012 (UTC)

Gotta die of somethin!

Article talk page is not a forum
The following discussion has been closed. Please do not modify it.
Look, everything we know of other than God dies of some cause - even whole planets, stars and galaxies. (Perhaps even God could die of loneliness at the end of the universe). Immortality is a theory at best and more likely a fantasy. Let's separate wishful thinking from reality. --71.245.164.83 (talk) 03:37, 2 October 2010 (UTC) As pedantic as this may sound, these remarks must be made: first of all, this talk page is not a forum for general philosophical inquiries; secondly, I'm afraid your invocation of theism into this discussion is inappropriate. Your statements are out of context: this article is strictly about biology, not philosophy, astronomy, mythology or theology. Perhaps, you believe that the age of the world is 6 millennia; there are trees that have lived nearly as long, there are life forms that have lived almost 6 times as much, and still kickin'! Now, even if your reasoning was sound, it would still have no authority in commanding that we should not have a Wikipedia article on this extremely important and most solemn biological process. Everything Is Numbers (talk) 13:54, 25 September 2012 (UTC) Anyway, WP:NOTFORUM. EIN (talk) 17:40, 25 June 2013 (UTC)

Cellular senescence

Greetings, The section "Cellular senescence" could be significantly improved. Here are some relevant excerpts from a scientific book, which may help to those who will do such improvement: http://longevity-science.org/pdf/Biology-of-Lifespan-5.6.pdf Good luck! Gavrilov (talk) 02:49, 21 August 2011 (UTC)

Y Good idea. I know there's enough room for expansion. In fact, I've been thinking about splitting the section into an article in its own right, as the topic probably deserves. I suppose that it's not the best time for me to immerse into all of this, but if no-else will, I intend to take up the task eventually. And thank you for the link! Everything Is Numbers (talk) 14:07, 25 September 2012 (UTC)

drug eliminates senescent cells, old mice show retained health

http://www.nytimes.com/2011/11/03/science/senescent-cells-hasten-aging-but-can-be-purged-mouse-study-suggests.html — Preceding unsigned comment added by 75.85.14.106 (talk) 00:11, 3 November 2011 (UTC)

any follow up on this? looks very interesting. — Preceding unsigned comment added by 76.172.122.94 (talk) 01:39, 27 July 2012 (UTC)

It's been all over the news last year. I suppose we can cite the study in this article. I heard they had decided to halt funding for the research, on undue grounds. How very regrettable! Everything Is Numbers (talk) 14:14, 25 September 2012 (UTC)

Y By now, the study is mentioned in two different parts of this article. Everything Is Numbers (talk) 07:40, 28 September 2012 (UTC)

Adding a picture to the lead section

It's typical for an article as important as this to have a picture placed in its lead section—which, at least to me, often makes the impression of a credential—and I imagine it to be desirable. Now, the next step, as I see it, is to reach a consensus on whether it should be done and, if the result will be affirmative, proceed to choose a picture optimally fitting the requirements. Everything Is Numbers (talk) 21:56, 26 September 2012 (UTC)

N I have reconsidered this proposal and concluded that no additional pictures are needed. Everything Is Numbers (talk) 07:37, 28 September 2012 (UTC)

Giving a different definition

The current definition has three flaws: (1) first, it doesn't sit well with the existence of negligibly senescent organisms, which experience changes in metabolism after maturity despite their lack of senescence; (2) then also, it ignores the fact that some aging processes may be at work even before maturity; (3) finally, it fails to acknowledge that not all changes in an organism's biology occurring after maturity are necessarily senescent in nature. This is unsatisfactory. For nomination of a more precise definition, I suggest the following candidates:

• accumulated damage to macromolecules, cells, tissues and organs with the passage of time;
• collection of cumulative changes to the molecular and cellular structure of an adult organism, which result in essential metabolic processes but which also, once they progress far enough, increasingly disrupt metabolism, resulting in pathology and death;
• gradual deterioration in function that, over time, leads to increased mortality risk, and declining fertility;
• gradual build-up of genetic and cellular error, resulting in deterioration of basic biological functions;
• a progressive deterioration of physiological function, an intrinsic age-related process of loss of viability and increase in vulnerability;
• condition resulting from the transitions and accumulations of the deleterious aging processes.

The last one is out of my favor because it uses the synonymous word “aging,” thereby creating the loophole of cyclical reasoning. Everything Is Numbers (talk) 22:43, 26 September 2012 (UTC)

Y Done. Everything Is Numbers (talk) 11:55, 28 September 2012 (UTC)

Why do we have 2 sections bearing the same title (“Cellular senescence”)?

Everything Is Numbers (talk) 13:50, 27 September 2012 (UTC)

Borrowing from the Ukrainian and Russian versions, if needed

There's plenty of extensive information there. If we wish to keep expanding this topic, they could undoubtedly be of aid. I am in a position to translate the material. Everything Is Numbers (talk) 07:51, 28 September 2012 (UTC)

To-do list: “Add a proper lead section”

Y I should like to think I have fulfilled the requirement. I will now cross the item off the list. Everything Is Numbers (talk) 11:05, 28 September 2012 (UTC)

Sources

If I've read the links correctly on my personal discussion page, things have to be sourced and neutral.

To quote: "The above categorisation of theories of aging is generally considered obsolete by biogerontologists."

End quote.

If the statement is included, it looks like it would need multiple reliable citations. Otherwise, it is opinion, stated as fact. I looked for a reference, but could not find one. If you reinsert it, can you add the sources? WordMachine (talk) 13:10, 23 January 2008 (UTC)

I'll look for a source. In the meantime, you might want to reconsider trying to link the two paragraphs together with a simple "conversely," since its meaning is not very clear at all. Information does have to be sourced on Wikipedia, but I notice that the programmed and stochastic theories of aging are presented without any source whatsoever to indicate that they have scientific merit, or even that they were considered to have had scientific merit in the past. I'll try to get an expert opinion on this. --SierraSciSPA (talk) 18:18, 23 January 2008 (UTC)

While we're on the topic of sources, we're all aware Aubrey de Grey and the SENS Foundation have basically been denounced to pseudo-science, right? They're being cited here, and I don't know much about citation rules, but that seems like it would be a problem... Those are more like movements with transhumanism and such than legitimate sciences, at least according to the Technology Review and a few other respected scientist who made the point. 76.78.30.85 (talk) 06:34, 10 October 2014 (UTC)

Expansion, structure reform

I'm considering adopting the following as the base arrangement:

1. Cellular senescence

2. Organismal senescence

3. Effects

4. Hypotheses

5. Treatment

6. Differences between taxa

7. Evolution

8. Accelerated aging-disorders

9. Cloning

Everything Is Numbers (talk) 11:33, 28 September 2012 (UTC)

Senescence / Senesce

Can anyone explain the difference between Senescence & Senesce. Is senesce an actual word. It is mentioned once in the article and can be found else where on the net. Are they used interchangeably? Ctbolt (talk) 04:49, 9 August 2013 (UTC)

Protein Misfolding Theory of Aging

I would like to add the following section to this page. As a biochemistry professor who has studied human aging for 35 years, I am currently beginning a clinical trial on this cause of aging. I have previously worked on slowing the other processes, and think this practical information is likely to greatly reduce human suffering by reducing the development of chronic disease. OR ELSe it could be entered as a separate new article, just linked on the senescence page as 3.7 Rocordman (talk) 20:36, 23 November 2014 (UTC)

Extended content

Contents [hide] 3.7 Protein Misfolding or Translational Error Theory of Aging 3.7.1 The free radical theory of aging 3.7.2 Inflammation 3.7.3 Telomere shortening 3.7.4 Translational infidelity error theory of aging 3.7.5 Teaberry Trial References Protein Misfolding or Translational Error Theory of Aging[edit] The Translational Error Theory of human aging –“Lost in Translation” There are many theories about why humans age, what causes chronic diseases to develop, and why we eventually die. Below four are highlighted which one can clearly do something about. Understanding the rationale and evidence for each of these theories provides guidance on actions one can take that help increase healthspan. Healthspan is the term used to distinguish lifespan or years of being alive, from years of aging in a pleasant state of health. Most people want their years to be enjoyable, and not a burden for those who care about them. Below are theories of aging for which specific actions can be taken easily. The free radical theory of aging[edit] This theory is well documented. To lessen free radical damage, I consume vitamin C 500 mg twice a day, vitamin E 400IU twice a week, and eat a diet of colorful fruits and vegetables that contain a variety of antioxidants. Inflammation[edit] Also called “Inflammaging” by researchers, this is a cause of chronic disease, including plaque in the arteries, cancer, etc. To reduce inflammation, I consume fish oil, avoid 4-legged meat, reduce stress by exercising and avoiding the media, by treasuring friends, meditating and doing yoga. Telomere shortening[edit] The length of telomeres, which are caps on the end of the DNA in our cells, preserve our genetic information to allow longevity. Actions that shorten telomeres include stress and high metabolic rate. Consuming antioxidants, staying fit, and relaxing are all useful to keep long telomeres. Note that EGCG and quercetin help maintain telomere length [1]. Translational infidelity error theory of aging[edit] The basic mechanism is that mRNA is translated incorrectly, incorporating the wrong amino acids into proteins that then fold improperly (based on the AA error theory of Wolfgang Freist). These proteins are either destroyed, causing a shortage of needed proteins, or worse, remain malfunctioning and accumulating as hazardous waste such as plaque in Alzheimer’s. Processes that will lessen functional proteins being lost in translation include: 1) increasing the availability of needed amino acids, 2) slowing the rate of translation to increase accuracy, 3) providing time for better proofreading, 4) increasing degradation of misfolded proteins, or 5) diluting the accumulated damage by half through cell division. Helpful actions include getting exercise, eating blueberries, drinking green tea, and adjusting the diet to include beneficial foods, such as tomatoes, onions, strawberries, and cabbage. Protein misfolding and translation errors have been documented as a cause of human aging [2]. One hypothesis of a major cause of aging is errors in translation. One source of such errors is caused by incorrect binding of amino acids of similar structure to tRNA that are then misincorporated into proteins, which subsequently do not function properly. Another possibility is when translation occurs so rapidly that proteins are not properly proofread or do not fold into the proper three dimensional structure. The first place errors can occur is when the amino acid (AA) is bound to the transfer RNA. Briefly, deficiency of three AAs (PHE, SER, and GLN) (PSG) and excess of 2 AAs (CYS and MET) (CM) increase the occurrence of errors, so correct protein sequences are lost in translation. For human evidence, a metabolomics study was done of 100 yr old Italians. They had high levels of PSG in their blood, which may have reflected that they ate foods containing high levels of PSG. One can search for foods that are particularly rich in PSG, and have less CM. A group of Italians living past 100 were probably eating a Mediterranean diet, which is known to be far superior to the Western diet, and also is high in PSG and low in CM This paragraph explains why those 5 AAs are so important. For instance, phenylalanine (PHE), an essential aromatic AA, is similar in structure to tyrosine and tryptophan, and when the PHE-tRNA should bind PHE, the wrong AA might be incorporated. So by ensuring there is enough PHE available, this mistake is less likely to occur. The Italian centenarian results suggest this type of error is especially likely for three AAs, PSG, so eating a diet with foods containing more of these is likely to reduce such errors. CYS and MET are 2 AAs that contain highly reactive –SH groups that are likely to crosslink and be oxidized by free radicals. –SH is also likely to bind Al, Cu, and Fe. Those metal atoms generate lots of free radicals, and are suspected to contribute to Alzheimer’s and Parkinson’s diseases. The second likely source of protein errors is when protein synthesis is too rapid. There are proofreading mechanisms that will catch mistakes as the protein is being synthesized, if translation is going slowly enough. One way to slow the process is by exercising. This depletes the supply of ATP, which is necessary to synthesize proteins. After exercise, your proteins are more likely to be synthesized slowly, allowing proper proofreading so mistakes can be corrected. Another molecule that slows translation is EGCG EGCG inhibits protein synthesis, lipogenesis, and cell cycle progression through activation of AMPK in p53 positive and negative human hepatoma cells [3]. Green tea has much higher levels of EGCG than black tea or other foods. The abundant polyphenols from blueberries such as quercetin help prevent the degradation of EGCG. So eating blueberries, and drinking a single cup of green tea will raise EGCG levels 4 to 8 fold [4]. The EGCG inhibits myosin motors running the cell, slowing key processes that might otherwisse cut short effective proofreading. This may be a key reason that green tea is well known to increase longevity. Healthspan has been shown to increase regularly up to 5 cups of green tea daily [5]. Combined with eating blueberries, only one or two cups of green tea may be needed. Finally, after the protein is made, there may be further checkpoints. Chaperone proteins exist in our bodies to ensure that proteins fold into the proper shape. If they do not fold properly, usually they are degraded by a structure known as the proteasome. However, some mistakes escape this process, especially ones that act as prions. After bacteria and then viruses were discovered, the next disease-causing contagious particles to be discovered were infectious proteins, known as prions. These proteins are improperly folded, and they cause other proteins to misfold as well. An example is the degenerative brain disease scrapie. There is concern that eating brain material from animals that had this disease will cause the disease in other animals, and probably even humans. It is possible Alzheimer’s is a disease of this nature, where plaque in the brain may be caused by beta-amyloid, a misfolded protein that coagulates and then cannot be degraded by proteasomes. Once we are adults, cell division is rare, so misfolded proteins that are not degraded will accumulate. It is likely this is especially damaging for proteins that adhere to chromosomal DNA causing errors in gene expression that can cause cancer. Those proteins on chromosomes are often not repaired. However, during mitosis the cell divides so faulty proteins are diluted from one cell to two. So newly divided cells, including stem cells, stay much healthier than “senescent” cells that no longer divide. Dr. Martin is arranging internet-based studies that can be completed at home to determine whether food choices, including consumption of blueberries and green tea, may be able to partially reverse damage caused by the accumulation of misfolded proteins and deficiency of proper folding. Senescent cells with adequate levels of polyphenols and EGCG may continue to degrade misfolded proteins and produce functional ones, and such recovery may be measurable by tests of abilities like memory that can be conducted online. To receive email notices when such trials have been authorized, please email Roc Ordman at ordman@beloit.edu, SUBJ: Healthspan trial. Here is an index of healthspan activities[6]. Teaberry Trial[edit] The Teaberry Trial is a clinical trial to develop a nutraceutical method to reduce the risk for what may be a major cause of human aging, or senecense, and the development of chronic disease. For other efforts, see Strategies for Engineered Negligible Senescence. The trial has been approved by the Beloit College IRB, is being managed by Roc Ordman, and analyzed by Rolf Martin. Professor Ordman, nicknamed Nutrition Investigator , is interested in extending human healthspan. The goal of Nutrition Investigator is to help people achieve the maximum healthspan based on current nutrition research. Here is current information to extend healthspan with convenient actions. The first key to the Teaberry Trial is the health benefits of blueberries. This is based on results of a clinical trial since 2002. The benefits found from this trial for which Rolf Martin has been responsible for analysis, has resulted in the popularity of blueberries. The emails which indicate and reference the potential benefits of consuming blueberries and green tea appropriately are shown [1]. Our new trial extends the benefits of the polyphenols in blueberries by combining their action with the active ingredient in green tea, EGCG. If you are interested in further information about the trial, here is the announcement that has been authorized: Drs. Rolf Martin and Alfred “Roc” Ordman plan to conduct a clinical trial to determine whether consuming blueberries and/or green tea on a daily basis may affect cognitive functions of decision making, memory, and hearing. This is the first part of our investigation of a new theory of why people develop chronic diseases associated with aging. If you are interested in further information about the study, please email teaberrystudy@gmail.com, SUBJ: clinical trial. References[edit] Jump up ^ Nutr Cancer. 2012;64(4):580-7. doi: 10.1080/01635581.2012.661514. Epub 2012 Mar 27. Quercetin increased the antiproliferative activity of green tea polyphenol (-)-epigallocatechin gallate in prostate cancer cells. Wang P1, Heber D, Henning SM Jump up ^ Ribosome rescue and neurodegeneration Jennifer C. Darnell Science 25 July 2014: 378-379 Jump up ^ Huang C et al, Molecular Nutrition & Food Research Volume 53, Issue 9, pages 1156–1165, September 2009 Jump up ^ Nutr Cancer. 2012;64(4):580-7. doi: 10.1080/01635581.2012.661514. Epub 2012 Mar 27. Quercetin increased the antiproliferative activity of green tea polyphenol (-)-epigallocatechin gallate in prostate cancer cells. Wang P1, Heber D, Henning SM Jump up ^ Green Tea Consumption and Mortality Due to Cardiovascular Disease, Cancer, and All Causes in Japan, The Ohsaki Study, S. Kuriyama et al, JAMA. 2006;296(10):1255-1265 Jump up ^ http://chemistry.beloit.edu/Ordman/nutrition/indices/ihealthspan.htm Rocordman (talk) 20:36, 23 November 2014 (UTC)

Hi Rocordman! Thanks for your suggestions - it's always great when I see a professor taking the time to edit Wikipedia. This is very interesting, but unfortunately I think a lot of it is probably too detailed for this article. Since Wikipedia's organization is closer to traditional encylopedias than to scientific literature, the idea of an article on a topic as large as senescence is to give the reader a broad overview of the subject and put more specific details in more specific articles.

Also, not all of the proposed content is cited. Since the reader won't know who wrote any particular sentence, they need to know how to confirm that it's correct. Ideally the majority of the content should be cited to secondary sources (that is, review papers).

There are also a couple of other things but those are the most important points I would emphasize. Let me know if I can help. Cheers, Sunrise (talk) 07:29, 24 November 2014 (UTC)

PS. To help make the page easier to navigate, I've made a small formatting change to put your writing in a drop-down box. Also, Since I see that you've been writing this in your sandbox, you could have also left a link to it (like this: [[User:Rocordman/sandbox]]) and then you wouldn't have had to copy it over. :-) Sunrise (talk) 07:33, 24 November 2014 (UTC)

Less human-focused pictures

Since this is the article on the general biological/cellular phenomenon of senescence, rather than about human aging specifically, it feels unbalanced to devote the bulk of the accompanying pictures (including the lead one) to pictures of elderly people. At very least, showing some diversity of organisms in some ways would be better (including the lead, I think, to show the focus of the article).

I realize that readers are readily familiar with what aging looks like in humans, and less so with what it looks like in other organisms (although probably more with other mammals than with animals less closely related). I realize I don't really know what an "old jellyfish" looks like, or an "old fern", per se. But the captions and/or text could provide some explanatory context. — Preceding unsigned comment added by Memories of lost time (talk • contribs) 20:26, 1 March 2015 (UTC)

I propose changing the main photo for this article. It does not seem adequate to use an image of a nursing home for this biological phenomenon. Somerandomuser (talk) 16:26, 13 June 2017 (UTC)

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The origin of senescence

The great majority of species in the phylum, chordata, are subject to death from aging-associated disease. Single cell organisms are not. The section on "Theories of aging" suggests that some instances of senescence occurring within a species evolved as a preventative for cancer, but gives no reference. Is this as much as can be had in Wikipedia on the origin of senescence? - Fartherred (talk) 18:31, 4 March 2016 (UTC)

* Suggesting that death can be "natural" suggests that science cannot be involved.  I am bothered by the current definition of senescence/.  In today's modern science world, we all die of "something".  I'm not asking for an autopsy with every death - but just saying every death has a cause, despite what is published in obituaries.  — Preceding unsigned comment added by 2600:6C48:7006:200:B056:6066:1296:EF0B (talk) 04:16, 5 March 2019 (UTC) 

Too technical/too much jargon

Much of this article is greatly informative but I also found myself skipping large swaths and entire sections that were too technical and filled with abbreviated jargon. Geeks On Hugs (talk) 01:55, 28 December 2016 (UTC)

Wiki Education Foundation-supported course assignment

This article was the subject of a Wiki Education Foundation-supported course assignment, between 27 January 2020 and 8 May 2020. Further details are available on the course page. Student editor(s): 291653ABC.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 08:57, 17 January 2022 (UTC)