Hacking Healthspan: Gene Therapy and Your Telomeres

Liz Parrish, CEO of BioViva Science, is the world’s most genetically modified person. She took a telomere-restoring gene therapy in 2015 alongside follistatin, making her the first person to take gene therapy to treat biological aging.

But why telomeres?

While there are other ways to measure and address the aging process, lengthening telomeres is an especially promising avenue.

Telomeres are the protective caps at the ends of our chromosomes. They safeguard the integrity of our genetic information during cell division. When they become critically short, genomic instability ensues, contributing to the aging process on several fronts.

A path paved by three pioneers

Research by Elizabeth Blackburn, Jack W. Szostak, and Carol Greider culminated in a Nobel Prize for the discovery of an enzyme called telomerase. Telomerase lengthens DNA before cellular division, acting as a buffer to telomere attrition (Corey, 2009).

Telomeres are more than the guardians of genetic integrity; they are portentous biomarkers of cellular health — pointing to favorable or unfavorable healthspan outcomes.

Their erosion is a harbinger of cellular aging and the onset of its accompanying ailments. When telomeres become critically short, the risk of sickness and all-cause mortality sharply rises (Cawthorn, 2003; Marioni, 2018).

When telomeres become critically short, cells stop dividing

This was observed decades ago by Leonard Hayflick (Hayflick, 1965).

Although telomere length is partially genetically determined, we are not powerless. There are low-tech ways to maintain, or even restore, our telomeres — for a while.

Physical activity is one. Of all readily available methods, moderate to robust exercise seems to be best. In a meta-analysis of 11 studies, exercise and telomere lengths were positively correlated.

This is an ongoing area of inquiry, as there are inconsistencies in recommended exercise intensity, likely owing to range of ages and genetic diversity of participants (Lin, 2019).

Greenspace in one’s surroundings is correlated with telomeres longer than those with minimal exposure. However, the correlation became non-significant when known abrasive factors, like air pollution and poverty, were taken into account (Ogletree, 2023).

There is no reason to become disheartened: telomere shortening is reversible–up to a point and for a time. In fact, some unexpected methods have yielded remarkable results.

Blackburn co-authored a book called The Telomere Effect with psychologist Elissa Epel. In a paper titled How “Reversible” is Telomeric Aging?, Epel cites several studies, including one where dementia caregivers taught to meditate showed a 43% increase in telomerase activity compared with a relaxation control group (Epel, 2012; Lavretsky, 2012).

While yoga and meditation are helpful, aging eventually forces us to call in the heavy artillery.

Because no matter how carefully or consciously we live, telomeres deteriorate for reasons beyond our control–without the therapeutics of tomorrow, this will not change.

However, we can no longer allow–or afford–to let this humanitarian and economic crisis proceed unabated.

Telomeres in the Twenty-First Century

Liz Parrish is a tireless advocate for patient rights through BioViva and Best Choice Medicine. As the world’s most genetically modified person, she has walked the walk from the beginning. She is a living testament to gene therapy’s power to lengthen telomeres, combat the ravages of aging, and more.

Parrish’s age-associated telomere length went from 66 to 44 according to multiple independent laboratories. As of 2022, based on her telomere length, her biological age is now less than 25 (Chace, 2022).

While there are other ways to measure biological aging, these results are still stupendous. All the hallmarks of aging are intertwined. By addressing one, many can be alleviated.

In an interview with Forbes, Parrish stated, “41 million people are dying this year of aging-associated, non-communicable diseases. We could save them. We need to get on the right side of history.”

And BioViva continues to take action.

A New Beginning

Gene therapies like BioViva’s BV-702, delivered with a vector like BioViva’s CMV platform, could be ideal for preventing or reversing neurodegeneration caused by issues like telomere shortening and mitochondrial dysfunction (Whittemore, 2019).

This could completely overhaul treatment of Alzheimer’s and other forms of dementia.

Senior mice given telomerase experience improvements in metabolic and mitochondrial fitness. This translates to benefits for multiple biomarkers of aging and an astounding increase in median lifespan of 24 and 13 percent (de Jesus, 2012).

This was again confirmed in a study with BioViva’s CMV vector, which extended median lifespans by over 41% (Jaiyan, 2022). Once again, the veritas group was, by all measures, younger and healthier.

But what about cancer?

To quote a widely cited research paper: “Cancers are caused by mutations that may be inherited, induced by environmental factors, or result from DNA replication errors.”

The same paper swiftly debunks the popular idea that cancer can be blamed exclusively on environmental factors, noting that roughly three mutations are observed every time a cell divides and, as Shay reminds us, malignant cells generally have shorter telomeres (Tomasetti, 2021; Shay, 2011).

Pediatric cancers are the result of rare mutations, and this is why it is uncommon in children. By and large, the “emperor of all maladies” is the result of aging, making it just one vassal to the real king.

Telomeres preemptively clamp down on genomic instability, one of the hallmarks of aging; they are one of the first defenders against harmful mutations. For this reason, telomere restoring gene therapies could be among the most potent preventative precautions in our arsenal.

Mice with hyper-long telomeres lived nearly 13% longer. They were leaner, had less white fat tissue, and better metabolic health. Hyper-long telomere mice exhibited nearly a 50% reduction in tumor development. This is likely due to less accrued DNA damage. The mice were also lean, with low cholesterol and LDL levels, as well as improved glucose and insulin tolerance (Munoz-Lorente, 2019).

By warding off genomic instability, telomere-lengthening interventions for cancer prevention could become commonplace.

AAV is fine, but there is plenty of room for innovation…

Mostly because AAV doesn’t have enough room!

Recently published research has underscored the superiority of CMV vectors. AAV, though effective, has a smaller carrying capacity (Zeng, 2023). It is too cramped to solve complex problems and treat multifactorial diseases.

Bigger and better vectors are needed, and that’s what makes them indispensable to the future of gene therapy.

CMV more effectively induces CD8+ T cell responses for immune support. It is both safe and well-tolerated in humans, with a remarkable adeptness at delivering therapeutic genes (Zeng, 2023).

BioViva’s CMV gene delivery platform has three times the payload of AAV therapies

CMV can be delivered non-invasively (intranasally), has a solid safety profile, and may be redosable. CMV’s payload may eclipse AAV’s by over 10 times (Parrish, 2023).

Liz Parrish embodies the perennial quest to transcend our limitations. Through ongoing research and continued public engagement, BioViva is on the cusp of redefining human potential in the twenty-first century through gene therapy.

Authored by Adam Alonzi and Ryan Hall

Adam is a writer, independent researcher, award-winning author, and video maker. He is the Marketing Director for BioViva Science.

Ryan is an independent writer, and an avid enthusiast of emerging technologies. He was a history major at Northern Michigan University, where he was inducted into the Phi Beta Kappa Society for academic excellence.

References and Works Cited

• Bär, C., et al. (2016). Telomerase gene therapy rescues telomere length, bone marrow aplasia, and survival in mice with aplastic anemia. Blood. 127(14), 1770–1779.
• Bernardes de Jesus, B., et al. (2012). Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer. EMBO Mol Med. 4(8), 691–704.
• Cawthon, Richard M., et al. (2003). Association between telomere length in blood and mortality in people aged 60 years or older. The Lancet 361.9355, 393–395.
• Chace, Calum. (2022). Extending Health Spans by Extending Telomeres: Profile of Liz Parrish. Forbes.
• Corey, DR (2009). Telomeres and telomerase: from discovery to clinical trials. Chem Biol. 16(12), 1219–1223.
• Dai, W., et al. (2019). Cancer therapy with a CRISPR-assisted telomerase-activating gene expression system. Oncogene 38, 4110–4124.
• Epel, ES, et al. (2004). Accelerated telomere shortening in response to life stress. Proc Natl Acad Sci U S A. 101(49), 17312–17315.
• Hong, J., & Yun, CO. (2019). Telomere Gene Therapy: Polarizing Therapeutic Goals for Treatment of Various Diseases. Cells. 8(5), 392.
• Jafri, MA, et al. (2016). Roles of telomeres and telomerase in cancer, and advances in telomerase-targeted therapies. Genome Med. 8(1), 69.
• Jaijyan, DK, et al. (2022). New intranasal and injectable gene therapy for healthy life extension. Proc Natl Acad Sci U S A. 119(20), e2121499119.
• Lin, X., et al. (2019). Effect of different levels of exercise on telomere length: A systematic review and meta-analysis. J Rehabil Med. 51(7), 473–478.
• Marioni, RE, et al. (2018). The epigenetic clock and telomere length are independently associated with chronological age and mortality. Int J Epidemiol. 45(2), 424–432.
• Ogletree, SS, et al. (2023). The relationship between greenspace exposure and telomere length in the National Health and Nutrition Examination Survey. Sci Total Environ. 905, 167452.
• Parrish, Liz. [Nature News]. Nature Publishing Group.
• Tomasetti, C., et al. (2017). Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention. Science. 355(6331), 1330–1334.
• Vyas, Chirag M, et al. (2021). Telomere length and its relationships with lifestyle and behavioural factors: variations by sex and race/ethnicity. Age and Ageing. 50(3), 838–846.
• Whittemore, K., et al. (2019). Telomerase gene therapy ameliorates the effects of neurodegeneration associated to short telomeres in mice. Aging (Albany NY). 11(10), 2916–2948.
• Zeng, J., et al. (2023). Exploring the Potential of Cytomegalovirus-Based Vectors: A Review. Viruses. 15(10), 2043.