Sierra Acai Company
Sierra Acai Company
Open 7 Days a Week
MonaVie Independent Distributor
Distributor Training
Shop Online
Enroll Now
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
Friends
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
22-AUGUST-2008 06:13:22 - Free-radical theory The free-radical theory of aging states that organisms age because cells accumulate free radical damage over time. In general, a free radical is any molecule that has a single unpaired electron in an outer shell. While a few free radicals such as melanin are not chemically reactive, this is not true of most biologically-relevant free radicals. For most biological structures, free radical damage is closely associated with oxidative damage. Oxidative damage is familiar by analogy with the process of rust formation of iron exposed to oxygen. As the name suggests, antioxidants like vitamin C prevent oxidation, because they are reducing agents. In biochemistry, the free radicals of interest are often referred to as reactive oxygen species ROS because the most biologically significant free radicals are oxygen-centered. But not all free radicals are ROS and not all ROS are free radicals. For example, the free radicals superoxide and hydroxyl radical are ROS, but the ROS hydrogen peroxide H2O2 is not a free radical. The free-radical theory of aging also encompasses damage due to these compounds, however. Denham Harman first proposed the FRTA in the 1950s 1 and extended the idea to implicate mitochondrial production of ROS in the 1970s2. Of all the theories of aging, Harman's has the most consistent experimental support. However models exist i.e. Sod2+/- mice that demonstrate increased oxidative stress without any effect on lifespan. Hence, more data is needed to identify the role of free radicals/oxidative stress in aging. Contents 1 The Free Radical Theory of Aging 2 Evidence For and Against 2.1 Mitohormesis 2.2 Calorie restriction 3 Antioxidant therapy 4 See also 5 References 6 External links 6.1 Calorie restriction 6.2 Biology of Aging The Free Radical Theory of Aging The free radical theory of aging was conceived by Harman at a time when most scientists still believed that free radicals were too unstable to exist in biological systems and before anybody had invoked them as a cause of degenerative diseases. Harman drew inspiration from two sources: 1 the rate of living theory, which held that lifespan was an inverse function of metabolic rate, oxygen consumption. 2 Rebbeca Gershman's observation that hyperbaric oxygen toxicity and radiation toxicity could be explained by the same underlying phenomenon: oxygen free radicals. Noting that radiation causes mutation, cancer and aging Harman argued that oxygen free radicals produced during normal respiration would cause cumulative damage which would eventually lead to organismal loss of functionality, and ultimately, death. In later years, the free radical theory was expanded to not only include aging per se, but also age related diseases. Free radical damage within cells has been linked to a range of disorders including cancer, arthritis, atherosclerosis, Alzheimer's disease, and diabetes. This involvement is not at all surprising as free radical chemistry is an important aspect of phagocytosis, inflammation, and apoptosis. Cell suicide, or apoptosis, is the body's way of controlling cell death and involves free radicals and redox signalling. Redox factors play an even greater part in other forms of cell death such as necrosis or autoschizis. More recently, the relationship between disease and free radicals has led to the formulation of a greater generalization about the relationship between aging and free radicals. In its strong form, the hypothesis states that aging per se is a free radical process. The weak hypothesis holds that the degenerative diseases associated with aging generally involve free radical processes and that, cumulatively, these make you age. The latter is generally accepted, but the strong hypothesis awaits further proof. Both models trace back to Harman's work. Evidence For and Against Results have demonstrated that the overexpression of catalase, an enzyme involved in the decomposition of hydrogen peroxide, increased both the average lifespan and maximum lifespan of mice by 20%3. However, the authors of that paper also indicated that the lifespan extension effect had apparently lessened in new generations of these mice. Making a well-studied roundworm, Caenorhabditis elegans, more susceptible to free radicals has led to shortened lifespan 4. However, increasing atmospheric oxygen tension above the normal 21% O2, does not meaningfully decrease lifespan of C. elegans. On the other hand, consistent with the free radical theory, it does shorten lifespan of the fruit fly Drosophila. Drosophila that have mutations in enzymes relating to ROS metabolism have also been shown to have dramatically reduced life-spans, increased susceptibility to oxidative stress and ionizing radiation, partial female and complete male sterility, and a general enfeebled phenotype characterized by deformed wings and abdomen.5 While genetic manipulations that increase the levels of oxidative damage generally do shorten lifespan in mice, there is as yet very limited evidence that decreasing free radicals below their normal levels, actually extends lifespan see above. Feeding of antioxidants, which should increase lifespan if the theory is correct, can extend average but not maximum lifespan in mice, even so, this effect is weak when it is observed and overall inconsistent. One possible strike against the FRT of Aging but not necessarily the FRT of certain diseases is that antioxidant supplementation has not yet been convincingly shown to produce a mammalian extension of lifespan. A possible exception is PBN phenybutylnitrone, which was shown to produce about a 10% extension of maximum lifespan in experimental animals 6 in one laboratory, however, this finding has not been reproduced by other laboratories. Mitohormesis While there is good evidence to support the idea of FRTA in model organisms such as Drosophila melanogaster7 and Caenorhabditis elegans,8 recent evidence suggests that oxidative stress may also promote life expectancy of Caenorhabditis elegans by inducing a secondary response to initially increased levels of reactive oxygen species.9 This process was previously named mitohormesis or mitochondrial hormesis on a purely hypothetical basis.10. The situation in mammals is even less clear.111213 Recent epidemiological findings support the process of mitohormesis, and even suggest that antioxidants may increase disease prevalence in humans although this meta-analysis included large studies on smokers, for whom it was already known that beta-carotene supplements are harmful.14 Calorie restriction See main article: Calorie restriction Calorie restriction, or severely cutting the intake of energy, has been found to reduce ROS and to increase the life-span of rodents possibly by promoting mitohormesis. Studies have shown that both calorie restriction and reduced meal frequency/intermittent fasting can suppress the development of various diseases and can increase life span in rodents by 30-40% by mechanisms involving stress resistance and reduced oxidative damage. Severe calorie restriction over 50% resulted in increased mortality 159 One of the most popular proponents of calorie restriction as a way to longer life was the late Dr. Roy Walford 1924-2004, formerly Professor of Pathology at the University of California, Los Angeles School of Medicine. Dr. Walford died of Amyotrophic Lateral Sclerosis ALS. Antioxidant therapy This theory implies that antioxidants e.g. Vitamin A, vitamin C, vitamin E and Superoxide dismutase - which prevent free radicals from oxidizing sensitive biological molecules, or reduce the formation of free radicals - will slow the aging process and prevent disease. The antioxidant chemicals found in many food-stuffs such as the well known vitamins A, C and E are frequently cited as the basis of claims for the benefits of a high intake of vegetables and fruits in the diet. In particular, antioxidant therapy forms the basis of many basic pharmacological interventions and particularly orthomolecular medicine. See also American Aging Association Antioxidant Life extension List of life extension-related topics Senescence Mitohormesis References ^ Harman, D 1956. Aging: a theory based on free radical and radiation chemistry. Journal of Gerontology 11 3: 298-300. PMID 13332224. ^ Harman, D 1972. A biologic clock: the mitochondria?. Journal of the American Geriatrics Society 20 4: 145-147. PMID 5016631. ^ Schriner SE, Linford NJ, Martin GM, Treuting P, Ogburn CE, Emond M, Coskun PE, Ladiges W, Wolf N, Van Remmen H, Wallace DC, Rabinovitch PS 2005. Extension of murine life span by overexpression of catalase targeted to mitochondria. Science 308 5730: 1909-11. doi:10.1126/science.1106653. PMID 15879174. ^ Ishii N 2000. Oxidative stress and aging in Caenorhabditis elegans. Free Radical Research 33 6: 857-64. doi:10.1080/10715760000301371. PMID 11237107. ^ T Parkes, K Kirby, J Phillips, A Hilliker. 1998. Transgenic analysis of the cSOD-null phenotypic syndrome in Drosophila. Genome 41: 642-651. ^ Saito K, Yoshioka H, Cutler RG 1998. A Spin Trap, N-tert-Butyl-α-phenylnitrone Extends the Life Span of Mice. Bioscience, Biotechnology, and Biochemistry 62 4: 792-794. doi:10.1271/bbb.62.792. PMID 9614711. ^ Helfand S, Rogina B 2003. Genetics of aging in the fruit fly, Drosophila melanogaster. Annu Rev Genet 37: 329-48. doi:10.1146/annurev.genet.37.040103.095211. PMID 14616064. ^ Larsen P 1993. Aging and resistance to oxidative damage in Caenorhabditis elegans. Proc Natl Acad Sci U S A 90 19: 8905-9. doi:10.1073/pnas.90.19.8905. PMID 8415630. ^ a b Schulz TJ, Zarse K, Voigt A, Urban N, Birringer M, Ristow M 2007. Glucose restriction extends Caenorhabditis elegans life span by inducing mitochondrial respiration and increasing oxidative stress. Cell Metabolism 6 4: 280-93. doi:10.1016/j.cmet.2007.08.011. PMID 17908557. ^ Tapia PC 2006/2005epub. Sublethal mitochondrial stress with an attendant stoichiometric augmentation of reactive oxygen species may precipitate many of the beneficial alterations in cellular physiology produced by caloric restriction, intermittent fasting, exercise and dietary phytonutrients: Mitohormesis for health and vitality. Medical Hypotheses 66 4: 832-43. PMID 16242247. ^ Sohal R, Mockett R, Orr W 2002. Mechanisms of aging: an appraisal of the oxidative stress hypothesis. Free Radic Biol Med 33 5: 575-86. doi:10.1016/S0891-58490200886-9. PMID 12208343. ^ Sohal R 2002. Role of oxidative stress and protein oxidation in the aging process. Free Radic Biol Med 33 1: 37-44. doi:10.1016/S0891-58490200856-0. PMID 12086680. ^ Rattan S 2006. Theories of biological aging: genes, proteins, and free radicals. Free Radic Res 40 12: 1230-8. doi:10.1080/10715760600911303. PMID 17090411. ^ Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C 2007. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis. The Journal of the American Medical Association 297 8: 842-57. PMID 17327526. . See also the letter to JAMA by Philip Taylor and Sanford Dawsey and the reply by the authors of the original paper. ^ Mattson MP 2005. Energy intake, meal frequency, and health: a neurobiological perspective. Annual Review of Nutrition 25 25: 237-60. doi:10.1146/annurev.nutr.25.050304.092526. PMID 16011467. Muller, F. L., Lustgarten, M. S., Jang, Y., Richardson, A. and Van Remmen, H. 2007. Trends in oxidative aging theories. Free Radical Biology Medicine 43 4: 477-503. doi:10.1016/j.freeradbiomed.2007.03.034. PMID 17640558. External links Calorie restriction Calorie Restriction Society. Biology of Aging Damage-Based Theories of Aging Includes a discussion of the free radical theory of aging. The Free Radical Theory of Aging Free Radicals and Human Disease--a Review Retrieved from http://en..org/wiki/Free-radical_theory Categories: Aging | Free radicals | Gerontology Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page This page was last modified on 20 July 2008, at 16:26. of the GNU Free Documentation License. ® , Inc., a U.S.
39 Reasons to Drink Acai Juice Every Day
What is MonaVie - Watch the 8-minute video
Discovering MonaVie video
The Power of You video
Log into your Wholesale MonaVie Account
So many of us do not eat a balanced diet, get enough sleep, have too much stress, or are impacted with toxins and pollutants. Drinking 2 ounces of MonaVie twice a day will help your body detoxify as well as build your immune system. Its the smartest thing you can do for yourself, so start today. Buying MonaVie through our company guarantees you support 7 days a week and, if you would like to share MonaVie with your family and friends we will guide you from start to finish.
1. Click on Enroll Now (30 - 55% off retail price)
2. Pay $39 for your Wholesale ID number.
3. NO minimum order required.
4. MonaVie is delivered to your door in 3 to 5 days.