Have you ever stopped to think there might be a difference between aging and getting old? Some ancient texts declare old age a virtue and a blessing, commanding the elderly to be respected for their wisdom, regardless of their scholarship. When your cheese gets old, it’s time to dump it; but when it ages, it reaches perfection, right? When things get old, they might no longer be useful or in style. Aging is a managed process through which a thing gains value or desirability. Do we perceive ourselves the same way as cheese or steak? The way you live your life as you age just might dictate how others see you. Do you constantly complain about things outside your control, or do you roll with the punches and build on your strengths? You may balk at being reminded by your spouse to write things down. Make yourself look good; write them down. And try not to forget where you put the list.
Is there anything to be done to arrest the process of aging? There are scores of ads in magazines and on the web that proclaim the virtues of this or that herb or secret concoction to inhibit Mother Nature’s treacherous design. The only science that supports many of those claims is ringed by dollar bills. Really now, is there something, anything, that can take thirty years off my wrinkled brow, my flabby arms and other parts, my sagging skin, and shrinking self-concept? Instead of saying “No,” let’s take a look at science.
Inside the nucleus of a cell, our genes sit on double-twisted strands of molecules called chromosomes. At the ends of the chromosomes are protective caps called telomeres, which act just like the little plastic things at the end of your shoelaces (aglets) that keep them from raveling…or unraveling. Telomeres also keep the ends of the chromosomes from sticking to each other, which would not only make a big mess but could also scramble genetic information and cause diseases. But every time a cell divides, its telomeres shorten. After a while the telomeres get too short to duplicate and the cells kick out—they become old or they die. If enough of these die at the same time, so do we.
We’ll try not to get too complicated, but we need to explain that telomeres are sequences of DNA chemical codes that are made from the same stuff as the rest of the chromosomes and genes, called nucleic acid bases, that repeat. A neonatal telomere might have as many as eight thousand bases, about half that at middle age, and only fifteen hundred as an old timer. Each time a cell divides, we lose between 30 and 200 base pairs. Cells normally divide fewer than a hundred times before they die. Now—pay attention here—there is an enzyme called telomerase that keeps the telomere from shrinking. Short telomeres set the stage for disease (Armanios, 2009) (Shen, 2007) (Serrano, 2004). Remember that. One thing science has yet to determine is whether telomeres start the aging process or are a sign that it has already begun. Still, the major cause of aging is believed to be oxidative stress, the state that results from simple things like breathing and from more complex activities that include infections, inflammation, smoking and booze, and the glycation that accompanies poor dietary choices (which is addressed in the AGE’s newsletter).
A very recent Ohio state study has discovered that omega-3 (n-3) fatty acids might slow aging. This work focused on overweight but healthy middle-aged and older adults who took n-3 supplements for four months and were later found to have altered the ratio of fatty acids in such a way as to preserve tiny segments of DNA in their white blood cells. Guess what those tiny segments are…Yep, telomeres. Omega-3 supplementation also reduced signs of oxidative stress caused by excessive free radicals in the blood by almost fifteen percent compared to the controls (Kiecolt-Glaser, Sept 2012). The bottom line is that changing the omega-6 to omega-3 ratio from the common 15:1—up to 30:1 in some cases—to the tenable 4:1 is a prudent endeavor. However, don’t hurry to give the n-6’s short shrift. The American Heart Association announced in 2009 that a considerable body of research supports the use of omega-6 fatty acids as a means to reduce the incidence of coronary heart disease (Harris, 2009). Many of us have heard only negative things about omega-6 fats, never learning that they are precursors to many anti-inflammatory metabolites, including prostacyclins (vasodilators) and lipoxins (anti-inflammatory mediators). The findings of Harris and colleagues recommend that n-6 fatty acids make up 5% to 10% of daily energy intake. Given this, the 4:1 ratio of 6’s to 3’s is not so hard to handle (Simopoulos, 2002).
In a five-year study done at San Francisco General Hospital, patients with coronary heart disease, who also took omega-3 fatty acids as EPA and DHA, demonstrated prolonged survival by virtue of extended telomere length, in contrast to those whose telomeres were shortened by the absence or deficiency of omega-3 fatty acids (Farzaneh-Far, 2010). If maintaining telomere length is a positive step in deceleration of aging, we need to examine the elements that influence the opposite. Historical factors cannot be changed: genetics, early insults, prenatal conditions, and the like. But current factors can be altered and their results even reversed with behavioral interventions (Epel, 2012). One recommendation, then, is the faithful intake of n-3 fats, at least as a limiting agent for inflammation that relates to middle-aged torpid lifestyle and weight management (Kiecolt-Glaser, Aug 2010) and at most as an extender of telomere viability.
Telomeres maintain chromosome stability by repeating the sequence of the nucleic acid bases, TTAGGG on one strand of DNA bound to AATCCC on the other strand, where T is thymine, A is adenine, C is cytosine and G is guanine. In studies of human sisters with differing telomere lengths, investigators found that the women with shorter telomeres were at a moderately higher risk for breast cancer at premenopause than their siblings (Shen, 2007). Yes, short telomeres are acquired with aging, and yes, they need more study, and yes, they can mediate the degenerative effects of old age.Inflammation is not a totally bad thing. Without it, wounds and infections wouldnot heal. Pro-inflammatory chemicals start the attack against invaders,and then the real healing begins after the inflammation is shut off. The post-inflammatorysubstances clean up the dead and dying tissues and get rid of the inflammatorywaste products (Serhan, 2008) (Schwab, 2007) (Serhan, 2004). Those post-inflammatorymolecules—resolvins and protectins--are provided courtesy of n-3 fatty acids,and have proven themselves functional in telomere protection.
Adler N, Pantell M, O'Donovan A, Blackburn E, Cawthon R, Koster A, Opresko P, Newman A, Harris TB, Epel E.
Educational attainment and late life telomere length in the Health, Aging and Body Composition Study.
Brain Behav Immun. 2012 Sep 5. pii: S08810.1016/j.bbi.2012.08.014.
Armanios M, Alder JK, Parry EM, Karim B, Strong MA, Greider CW. Short telomeres are sufficient to cause the degenerative defects associated with aging. Am J Hum Genet. 2009 Dec;85(6):823-32.
Burghardt PR, Kemmerer ES, Buck BJ, Osetek AJ, Yan C, Koch LG, Britton SL, Evans SJ. Dietary n-3:n-6 fatty acid ratios differentially influence hormonal signature in a rodent model of metabolic syndrome relative to healthy controls. Nutr Metab (Lond). 2010 Jun 28;7:53.
Epel E. How "reversible" is telomeric aging? Cancer Prev Res (Phila). 2012 Oct;5(10):1163-8. doi: 10.1158/1940-6207.CAPR-12-0370.
Farzaneh-Far R, Lin J, Epel ES, Harris WS, Blackburn EH, Whooley MA. Association of marine omega-3 fatty acid levels with telomeric aging in patients with coronary heart disease. JAMA. 2010 Jan 20;303(3):250-7.
Harris WS, Mozaffarian D, Rimm E, Kris-Etherton P, Rudel LL, Appel LJ, Engler MM, Engler MB, Sacks F. Omega-6 fatty acids and risk for cardiovascular disease: a science advisory from the American Heart Association Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention. Circulation. 2009 Feb 17;119(6):902-7. Epub 2009 Jan 26.
Kay-Tee Khaw, Marlin D. Friesen, Elio Riboli, Robert Luben, Nicholas Wareham The EPIC-Norfolk Prospective Study Plasma Phospholipid Fatty Acid Concentration and Incident Coronary Heart Disease in Men and Women:
Kiecolt-Glaser JK, Belury MA, Andridge R, Malarkey WB, Hwang BS, Glaser R. Omega-3 supplementation lowers inflammation in healthy middle-aged and older adults: a randomized controlled trial. Brain Behav Immun. 2012 Aug;26(6):988-95. Epub 2012 May 26.
Kiecolt-Glaser JK, Epel ES, Belury MA, Andridge R, Lin J, Glaser R, Malarkey WB, Hwang BS, Blackburn E. Omega-3 fatty acids, oxidative stress, and leukocyte telomere length: A randomized controlled trial. Brain Behav Immun. 2012 Sep 23. pii: S0889-1591(12)00431-X. doi: 10.1016/j.bbi.2012.09.004.
Sanders TA, Lewis F, Slaughter S, Griffin BA, Griffin M, Davies I, Millward DJ, Cooper JA, Miller GJ. Effect of varying the ratio of n-6 to n-3 fatty acids by increasing the dietary intake of alpha-linolenic acid, eicosapentaenoic and docosahexaenoic acid, or both on fibrinogen and clotting factors VII and XII in persons aged 45-70 y: the OPTILIP study. Am J Clin Nutr. 2006 Sep;84(3):513-22.
Schwab JM, Chiang N, Arita M, Serhan CN. Resolvin E1 and protectin D1 activate inflammation-resolution programmes. Nature. 2007 Jun 14;447(7146):869-74.
Serhan CN, Chiang N. Novel endogenous small molecules as the checkpoint controllers in inflammation and resolution: entrée for resoleomics. Rheum Dis Clin North Am. 2004 Feb;30(1):69-95.
Serhan CN, Chiang N, Van Dyke TE. Resolving inflammation: dual anti-inflammatory and pro-resolution lipid mediators. Nat Rev Immunol. 2008 May;8(5):349-61.
Antonio L. Serrano, Vicente Andrés Telomeres and Cardiovascular Disease: Does Size Matter? Circulation Research. 2004; 94: 575-584
Shen J, Terry MB, Gurvich I, Liao Y, Senie RT, Santella RM. Short telomere length and breast cancer risk: a study in sister sets. Cancer Res. 2007 Jun 1;67(11):5538-44.
Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother. 2002 Oct;56(8):365-79.
Simopoulos AP. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002 Dec;21(6):495-505.
Xia SH, Wang J, Kang JX. Decreased n-6/n-3 fatty acid ratio reduces the invasive potential of human lung cancer cells by downregulation of cell adhesion/invasion-related genes. Carcinogenesis. 2005 Apr;26(4):779-84. Epub 2005 Jan 20.
*These statements have not been evaluated by the FDA. These products are not intended to treat, diagnose, cure, or prevent any disease.