BioViva

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BioViva is a Bainbridge Island, Washington-based biotechnology company researching treatments to interfere the ageing process in humans.

BioViva
Founded2015; 6 years ago (2015)
HeadquartersBainbridge Island, Washington,

History[edit]

BioViva was founded in 2015.[1] CEO Elizabeth Parrish appeared at WIRED Health 2017 in London to discuss BioViva's testing of gene therapies targeting hallmarks of the ageing process. She stated, "The company was built essentially to prove these therapies work or not. Remember BioViva is not a research organisation. We are taking things like gene therapies and using them like technology."[2]

Responses to Parrish using herself as first experimental subject[edit]

Parrish's decision to be 'patient zero' and test the company's technology on herself in a personalized N=1 study has been both criticized and lauded. Dr. Lawrence Altman, author of Who Goes First? The Story of Self-Experimentation in Medicine has said, "N's of 1 have had their value through history, and will. But you're not going to license a drug based on an N-of-1."[3] Her treatment, labelled as self-experimentation, was highly controversial. As the requirements to progress to human trials had not started, the US Food and Drug Administration did not authorize Parrish's experiments. Parrish traveled to Colombia for the treatments.[4]

Some have criticized BioViva's release of data claiming an extension of Parrish's leukocyte telomeres following her therapy, stating that the aforementioned extension is within the error change for telomere measurements. Dr. Bradley Johnson, Associate Professor of Pathology and Lab Medicine at the University of Pennsylvania said, "Telomere length measurements typically have low precision, with variation in measurements of around 10 percent, which is in the range of the reported telomere lengthening apparently experienced by Elizabeth Parrish."[5]

Altering the genetic makeup of humans, or gene therapy, by lengthening telomeres has been described as dangerous, as the ageing process is poorly understood. The telomeres' function is to restrict the number of times a cell can divide (thereby multiplying) to suppress cancer. Duncan Baird, a professor of Cancer and Genetics at Cardiff University's School of Medicine states, "Meddling with a fundamentally important tumor-suppressive mechanism that has evolved in long-lived species like ours doesn't strike me as a particularly good idea."[4]

Timothy Caulfield, a professor in the Faculty of Law and the School of Public Health at the University of Alberta, characterized BioViva's work as 'pseudoscience' and lacking scientific rigor.[citation needed] George M. Martin, Professor of Pathology at the University of Washington had agreed to be an adviser to the company but resigned upon hearing about Parrish's self-experiments.[4]

Antonio Regalado, a reporter for the MIT Technology Review states, "The experiment seems likely to be remembered as either a new low in medical quackery or, perhaps, the unlikely start of an era in which naive people receive genetic modifications not just to treat disease, but to reverse aging."[6]

Research[edit]

BioViva's research interests are based on preclinical research of both the enzyme telomerase and inhibition of myostatin.[7]

Telomerase gene therapy utilizing an adeno-associated virus at the Spanish National Cancer Research Centre (CNIO), has demonstrated several beneficial effects and an increase in median lifespan of up to 24% in mice.[8][9][10][11] Discussing her team's research, María Blasco stated in discussion with The Scientist, "We demonstrated that AAV9-Tert gene therapy was sufficient to delay age-related pathologies and extend both median and maximum longevity in mice. Many pathologies were delayed, including cancer. Translating these results to human diseases (telomere syndromes or certain age-related diseases without effective treatments) may be of interest in the context of clinical trials approved by the corresponding regulatory agencies."[7] However, some experts draw attention that the results of studies in mice cannot always be directly transferred to humans.[12]

References[edit]

  1. ^ "Company Overview of BioViva USA Inc". Bloomberg. Archived from the original on 2019-04-02. Retrieved November 14, 2016.
  2. ^ Medeiros, João. "Ageing is a disease. Gene therapy could be the 'cure'". Wired UK. Retrieved 31 March 2017.
  3. ^ "Biotech executives using themselves as human guinea pigs". STAT. 7 July 2016. Retrieved 2017-03-31.
  4. ^ a b c Nicola Davis; Dara Mohammadi (24 July 2016). "Can this woman cure ageing with gene therapy?". The Guardian. Retrieved 1 August 2016.
  5. ^ "Liz Parrish Is Patient Zero in Her Own Anti-Aging Experiment - The Crux". The Crux. 2016-04-29. Retrieved 2017-03-31.
  6. ^ Regalado, Antonio (14 October 2015). "A Tale of Do-It-Yourself Gene Therapy". MIT Technology Review. Retrieved 25 July 2016.
  7. ^ a b Kerry Grens (25 April 2016). "First Data from Anti-Aging Gene Therapy". The Scientist.
  8. ^ "Telomeres and Telomerase Group". Spanish National Cancer Research Centre. 19 May 2008. Archived from the original on 3 December 2008. Retrieved 24 August 2019.
  9. ^ Bernardes de Jesus, Bruno; Vera, Elsa; Schneeberger, Kerstin; Tejera, Agueda M.; Ayuso, Eduard; Bosch, Fatima; Blasco, Maria A. (15 May 2012). "Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer". EMBO Molecular Medicine. 4 (8): 691–704. doi:10.1002/emmm.201200245. PMC 3494070. PMID 22585399.
  10. ^ Muñoz-Lorente, Miguel A.; Cano-Martin, Alba C.; Blasco, Maria A. (2019-10-17). "Mice with hyper-long telomeres show less metabolic aging and longer lifespans". Nature Communications. 10: 4723. doi:10.1038/s41467-019-12664-x.
  11. ^ "Hyper-Long Telomeres Give Non-Genetically Modified Mice Longer, Healthier Lives". Genetic Engineering and Biotechnology News. 2019-10-18.
  12. ^ "Telomere Dynamics with Age are Very Different Between Mammalian Species". Fight Aging!. 2019-07-11. It is well known that mouse telomere dynamics and telomerase expression are quite different from that of humans. This might make us suspect that positive results from telomerase gene therapies in mice, where life span is extended and health improved, without raising the risk of cancer, may not hold up in humans. There is no particular reason why increased cancer risk through putting damaged cells back to work will be balanced in the same way by improved tissue function and improved immune function, from species to species. The research and development community will find out in the years ahead by trying telomerase gene therapies in primates and then humans.

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