From Lifespan to Healthspan

By Zhiyi Qiang, Ph.D., NRCC; Patrick Rainey, Ph.D., DABT

How often have you met two people of the same age, but one looks much younger than the other? Does the younger looking one have young genes? Less stress? Or maybe secret access to the fountain of youth?

More than half a century ago, Harman presented a theory of aging based on free radical induced oxidative stress which paved the way for the most modern principles of aging.1 These theories suggest that the cumulative burden of oxidative stress is a major determinant of lifespan, age-related diseases and ultimately mortality.2

On the other hand, inflammation, which is usually associated with oxidative stress, is also an important “culprit” of aging and age-related diseases. It’s still a bit controversial whether oxidative stress or inflammatory response is the initiator, just like chicken or the egg dilemma, however, these two underlying mechanisms are responsible for 7 out of 10 leading causes of death (heart disease, cancer, chronic lower respiratory disease, stroke and cerebrovascular disease, Alzheimer’s, diabetes, and kidney disease).

Geroscience is the study of the genetic, molecular, and cellular mechanisms that make aging a major risk factor of common chronic conditions and diseases of older people. There have been two new terms coined from geroscience research: healthspan and diseasespan. Healthspan is the number of years of our healthy life whereas diseasespan is the years we live with noticeable disease that interferes with our quality of living.

Because ~75% of all deaths will predictably occur between age 65 and 95 years and only a small proportion of all humans are capable of living to 115 years of age, the principal outcome and most important metric of success should be the extension of healthspan.3 Variations in our healthspan vs. diseasespan ultimately may be linked to the lifelong oxidative stress and inflammation of which the cumulative burden might be a genuine indicator of “biological age”.

Healthspan is considered to be more important than lifespan but how to measure healthspan? Unlike the average lifespan, which was 78.7 years in the US in 2016, we don’t have a statistic to quantify the average healthspan. One simple way is to use the average age of the 1st occurrence of the top 10 causes of death due to chronic diseases which is 62.7 years. This means that we, on average, live up to 20% of our lives unhealthy!4

Aging is closely related to the activity inside each person’s cells. The person who appears older may have prematurely aging cells which are predisposed to various age-related diseases and disorders such as cardiovascular disease, diabetes, cancer, Alzheimer’s and others.

The genetic heart of the cell resides in our chromosomes, which are made up of tightly wound DNA strands. Telomeres (tee-lo-meres) are repeating DNA segments that live at the ends of our chromosomes. Telomeres make up less than 1/10000 of the total DNA of our cells. For comparison, the length of a common ant is about 1/1200 the length of a giraffe. The length of a telomere compared to the chromosome is EIGHT times smaller than that! They are small and they naturally shorten every time a cell divides.

The central function of telomeres is to protect the ends of our chromosomes and provide genetic stability of the cell. Telomere length and the rate at which they shorten have been shown to act as a biomarker of “biological age”.5,6 This means the longer your telomere length, the more years of healthy living or longer healthspan, conversely, the shorter the telomere length, the more accelerated aging, increased incidence of diseases and longer diseasespan.

Oxidative stress leading to DNA damage is thought to be a major factor responsible for telomere shortening. One example is pesticide exposure induced oxidative stress. Environmental pesticide exposure is known to produce an oxidative stress environment and in this environment, telomeres are progressively shortened. Agricultural workers who are exposed to a mixture of pesticides while working in tobacco fields have been found to have shorter telomeres.7 Various oxidative stress biomarkers have been found to be correlated with telomere length such as F2-isoprostane (the gold standard for measuring oxidative stress in our body)2 and total antioxidant capacity (measuring our body’s capacity to fight against oxidative stress).8

Additionally, chronic inflammation, which usually co-exists with oxidative stress, can aggressively shorten telomere length. This is supported by the findings that various types of inflammatory and anti-inflammatory biomarkers are associated with telomere length. For example: higher plasma homocysteine (an inflammatory amino acid in your blood) was associated with shorter telomere length, which was exacerbated by lower folate and higher C-reactive protein (an inflammatory protein in our blood) levels.9,10 Among patients with coronary artery disease, there was an inverse relationship between baseline blood levels of omega-3 fatty acids (DHA + EPA, the major constituents in fish oil) and the rate of telomere shortening. Increased DHA+EPA levels was found to be associated with a 32% reduction in the odds of telomere shortening.11

The answer to the question of why two people of the same age can appear to be years apart becomes obvious once we understand the correlation between telomere length and cellular age. That’s why it’s important to routinely monitor your levels of oxidative stress and chronic inflammation through Prevé program’s advanced biomarker testing like CellCheck Ultra.

If we actively manage a healthy lifestyle that keeps oxidative stress and inflammation in check, we may be the ones asked if we’ve found the fountain of youth.

A Prevé membership includes tools to assist you in your wellness journey:

Community Support Groups: Connect with the MyPrevé community to reinforce the healthy lifestyle you’re cultivating with social support along your journey.

Educational Resources: Read material from our experts to continually learn more about nutrition, fitness, and lifestyle management and make the most informed choices about your health.

Lifestyle Management Tools: You can’t manage what you don’t measure. Our lifestyle management tools are integrated with smart technology to track your fitness, vitals, weight, nutrition and behavior.

Personalized Lab Result Discussions: Our lab result specialists will schedule time with you to help you make sense of what your results mean and to develop a strategy to further discuss these results and how to improve them with your physician.

Preve Wellness
11115 S W 93rd Court Rd.
Ocala, FL 34481
www.prevewellness.com | 352-389-8088

References
1. Harman, D., Aging: a theory based on free radical and radiation chemistry. J Gerontol, 1956. 11(3): p. 298-300.
2. Demissie, S., et al., Insulin resistance, oxidative stress, hypertension, and leukocyte telomere length in men from the Framingham Heart Study. Aging Cell, 2006. 5(4): p. 325-30.
3. Olshansky, S.J., From Lifespan to Healthspan. JAMA, 2018. 320(13): p. 1323-1324.
4. https://publichealth.wustl.edu/heatlhspan-is-more-important-than-lifespan-
so-why-dont-more-people-know-about-it/.
5. Cawthon, R.M., et al., Association between telomere length in blood and mortality in people aged 60 years or older. Lancet, 2003. 361(9355): p. 393-5.
6. Reichert, S. and A. Stier, Does oxidative stress shorten telomeres in vivo? A review. Biol Lett, 2017. 13(12).
7. Kahl, V.F., et al., Telomere measurement in individuals occupationally exposed to pesticide mixtures in tobacco fields. Environ Mol Mutagen, 2016. 57(1): p. 74-84.
8. Salpea, K.D., et al., Association of telomere length with type 2 diabetes, oxidative stress and UCP2 gene variation. Atherosclerosis, 2010. 209(1): p. 42-50.
9. Richards, J.B., et al., Homocysteine levels and leukocyte telomere length. Atherosclerosis, 2008. 200(2): p. 271-7.
10. Rode, L., et al., Increased body mass index, elevated C-reactive protein, and short telomere length. J Clin Endocrinol Metab, 2014. 99(9): p. E1671-5.
11. Farzaneh-Far, R., et al., Association of marine omega-3 fatty acid levels with telomeric aging in patients with coronary heart disease. JAMA, 2010. 303(3): p. 250-7.