Free Shipping on orders over $99

Biological Age - Current research trends of age related biomarkers

Age related illnesses, General | July 16, 2014 | Author: The Super Pharmacist

age related, general, biological age

Biological Age - Current research trends of age related biomarkers

Your “chronological age” is the number of years you have been alive. Your “biological age,” which is related to your health, can differ greatly from your chronological age. Because the best treatment option often depends on your health rather than your age, calculating biological age can help doctors better tailor their treatments to individual patients.

In recent years, research has vastly improved our understanding of aging and the biology associated with getting older. As a result, it has been suggested that we may be able to develop biomarkers for aging that can help determine biological age, particularly when used to complement other pre-existing clinical techniques. 

The idea of a biomarker for aging was introduced in 1988 and was described as a factor that allowed for better predictions about functional abilities than chronological age. Since the introduction of the idea of a biomarker for aging, several candidates have been explored.

Telomere Length

Cellular aging appears to be a result of telomere length.

Telomeres are DNA-protein complexes that cap chromosome ends. Telomeres shorten with each cellular division, so their length can be used as an indicator of biological age.

Once telomeres lose a certain amount of their length, the likely lose certain functions. Shorter telomeres are associated with an increased risk for several conditions including diabetes, hypertension, atherosclerosis, heart attack, Alzheimer’s disease, and cancer. 

Influencing Factors

Several factors influence the rate at which our telomeres shorten, including heredity and environmental factors. Males’ telomeres shorten faster than females’telomeres, which has been hypothesised to contribute to the longer lifespan observed in women. It has even been shown that people who are unmarried have shorter telomeres compared to married people of the same chronological age. 

Obesity, lack of exercise, and smoking all increase the rate of telomere shortening. 

Pro-Inflammatory Markers

Inflammation has become implicated with the aging process. Inflammation results from immune system activity. Cellular markers of inflammation are popular candidates for biomarkers of aging and functional decline. 

Specific markers that may indicate that biological age is higher include high levels of interleukin-6 or C-reactive protein and low levels of serum cholesterol or albumin. Such changes may result from chronic inflammation, which is likely a sign of dysregulated immune processes. Studies have shown that people with elevated interleukin-6 levels were more likely to suffer disabilities in their mobility. Similarly, people with raised C-reactive protein were at higher risk for cardiovascular and non-cardiovascular death.              

Advanced Glycation End Product

Advanced glycation end products (AGEs) are macromolecules that can be identified in blood and urine tests and are practical candidates for biomarkers of aging. AGE accumulation appears to increase biological age by damaging tissue and activation of the immune system. 

AGEs may be consumed or may be produced by the body when breaking down sugars.

Highly processed foods are more likely to contain AGEs.

Laboratory studies on the link between AGEs and aging have shown that elevated AGE levels are associated with functional decline, cardiovascular problems, and earlier death.  

 

Patients with diabetes are known to have enhanced AGE levels, and elevated AGE levels have been observed in plaques in the brains of Alzheimer disease patients. 

Sirtuin Proteins

A family of proteins called sirtuins appear to regulate aging and the development of diseases associated with aging. These proteins are involved in stress-response pathways, and reduced levels of sirtuins increase risk for diabetes, cancer, neurodegeneration, and osteoporosis, all of which are age-related conditions. In animal models, depletion of the gene that encodes sirtuin proteins has been shown to increase the risk for tumor development and age-related hearing loss.

Summary

In clinical practice, physicians often base decisions based on chronological age. For example, treatment of prostate and breast cancer tend to depend on the chronological age of the patient. 

Biological age, however, often tells us more about the health of a patient than chronological age, so biomarkers of aging are likely to become an influential factor in decision making processes.

Further research is needed to help define the most useful biomarkers for aging as well as the conditions for which treatment success depends on biological age.

www.superpharmacy.com.au Australia's best online pharmacy

Reference

Anisimov V.N.: Biology of aging and cancer. Cancer Control 2007; 14: 23-31

Simm A., Nass N., Bartling B.: Potential biomarkers of ageing. Biol Chem 2008; 389: 257-265

Baker G.T., Sprott R.L.: Biomarkers of aging. Exp Gerontol 1988; 23: 223-239

Shammas M.A.: Telomeres, lifestyle, cancer, and aging. Curr Opin Clin Nutr Metab Care 2011; 14: 28-34

de Lange T.: Protection of mammalian telomeres. Oncogene 2002; 21: 532-540

Samani N.J., Boultby R., Butler R.: Telomere shortening in atherosclerosis. Lancet 2001; 358: 472-473

Obana N., Takagi S., Kinouchi Y.: Telomere shortening of peripheral blood mononuclear cells in coronary disease patients with metabolic disorders. Intern Med 2003; 42: 150-153

Benetos A., Okuda K., Lajemi M.: Telomere length as an indicator of biological aging: The gender effect and relation with pulse pressure and pulse wave velocity. Hypertension 2001; 37: 381-385

Jeanclos E., Schork N.J., Kyvik K.O.: Telomere length inversely correlates with pulse pressure and is highly familial. Hypertension 2000; 36: 195-200

Panossian L.A., Porter V.R., Valenzuela H.F.: Telomere shortening in T cells correlates with Alzheimer's disease status. Neurobiol Aging 2003; 24: 77-84

Willeit P., Willeit J., Kloss-Brandstätter A.: Fifteen year follow-up of association between telomere length and incident cancer and cancer mortality. JAMA 2011; 306: 42-44.

Bekaert S., De Meyer T., Van Oostveldt P.: Telomere attrition as ageing biomarker. Anticancer Res 2005; 25: 3011-3021

Barrett E.L., Richardson D.S.: Sex differences in telomeres and lifespan. Aging Cell 2011; 10: 913-921

Song Z., von Figura G., Liu Y.: Lifestyle impacts on the aging-associated expression of biomarkers of DNA damage and telomere dysfunction in human blood. Aging Cell 2010; 9: 607-615

Mainous A.G., Everett C.J., Diaz V.A.: Leukocyte telomere length and marital status among middle-aged adults. Age Ageing 2011; 40: 73-78

Reuben D.B., Cheh A.I., Harris T.B.: Peripheral blood markers of inflammation predict mortality and functional decline in high-functioning community-dwelling older persons. J Am Geriatr Soc 2002; 50: 638-644

Ershler W.B.: Interleukin-6: A cytokine for gerontologists. J Am Geriatr Soc 1993; 41: 176-181

Harris T.B., Ferrucci L., Tracy R.P.: Associations of elevated interleukin-6 and C-reactive protein levels with mortality in the elderly. Am J Med 1999; 106: 506-512

Semba R.D., Nicklett E.J., Ferrucci L.: Does accumulation of advanced glycation end products contribute to the aging phenotype?. J Gerontol A Biol Sci Med Sci 2010; 65: 963-975

Johnson T.E.: Recent results: Biomarkers of aging. Exp Gerontol 2006; 41: 1243-1246

Semba R.D., Bandinelli S., Sun K.: Plasma carboxymethyl-lysine, an advanced glycation end product, and all-cause and cardiovascular disease mortality in Older Community-Dwelling Adults. J Am Geriatr Soc 2009; 57: 1874-1880

Aso Y., Inukai T., Tayama K.: Serum concentrations of advanced glycation endproducts are associated with the development of atherosclerosis as well as diabetic microangiopathy in patients with type 2 diabetes. Acta Diabetol 2000; 37: 87-92

Valente T., Gella A., Fernàndez-Busquets X.: Immunohistochemical analysis of human brain suggests pathological synergism of Alzheimer's disease and diabetes mellitus. Neurobiol Dis 2010; 37: 67-76

Park S.H., Ozden O., Jiang H.: Sirt3, mitochondrial ROS, ageing, and carcinogenesis. Int J Mol Sci 2011; 12: 6226-6239

Guarente L., Franklin H.: Epstein Lecture: Sirtuins, aging, and medicine. N Engl J Med 2011; 364: 2235-2244

Kim H.S., Patel K., Muldoon-Jacobs K.: SIRT3 is a mitochondria-localized tumor suppressor required for maintenance of mitochondrial integrity and metabolism during stress. Cancer Cell 2010; 17: 41-52

Someya S., Yu W., Hallows W.C.: Sirt3 mediates reduction of oxidative damage and prevention of age-related hearing loss under caloric restriction. Cell 2010; 143: 802-812

NCCN clinical practice guidelines in oncology: Prostate cancer, Version 3.2012. Fort Washington, PA: National Comprehensive Cancer Network, 2012

Hughes K.S., Schnaper L.A., Berry D: Lumpectomy plus tamoxifen with or without irradiation in women 70 years of age or older with early breast cancer. N Engl J Med 2004; 351: 971-977

backBack to Blog Home