Reversing Biological Aging with Gene Therapy. Exclusive Interview with Liz Parrish, CEO of BioViva
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Reversing Biological Aging with Gene Therapy: Ines O’Donovan Interviews Liz Parrish, CEO of BioViva

Have you ever wondered about the future of aging? What if I told you that we're on the brink of a revolution that could redefine what it means to grow old … with gene therapy.

Today, I want to introduce you to a woman who is not just imagining this future, but actively creating it.

Meet Liz Parrish, the trailblazing CEO of BioViva, a biotech company that's pushing the boundaries of what's possible with gene therapies.

Liz isn't just talking the talk, she's walking the walk, having undergone several gene therapies herself to combat biological aging.

This year, she's bringing her expertise and insights to RAADFest, the world's largest conference on radical life extension.

Ready to meet the future face-to-face? Let's dive into the interview and see what Liz has to share about this exciting field.

Reversing Biological Aging with Gene Therapy. Exclusive Interview with Liz Parrish, CEO of BioViva

Liz, can you please start by introducing yourself and telling us a little bit about your role in the field of super-longevity?

My name is Liz Parrish and I'm the CEO of a company called BioViva. We work on gene therapies that regenerate cells. Our goal is to find the perfect combination that will reverse biological aging, therefore helping you live much longer.

The benefits of gene therapy is that it would be an injection that might last for 10 to 15 or more years.

We aim to shift this sickcare system to a healthcare system and use proactive medicine that keeps you from getting sick long before you would start to accumulate the damage associated with aging.

You're an expert in gene therapy. What are the most exciting developments and innovations you have seen over the last 12 months that will change the field? And how do you think will it impact super-longevity?

The most exciting thing that I've seen in the last 12 months in my space, actually just in the last few weeks, are two approvals of gene therapy, one for the use of Duchenne's muscular dystrophy and one for hemophilia A. And then within the last 12 months, I believe hemophilia B was also approved.

These are curative gene therapies for critical diseases. They're great proof of concepts that we'll be able to treat complex disorders like aging.

I think that now there are about 12 approvals in gene therapy for monogenic or single gene mutations. And that gives us the strength and purpose to start working on complex disorders.

Next gen longevity is personal and so is RAADfest

The most critical element in your super-longevity equation is not just cutting-edge longevity strategies shared by pioneering practitioners. Or visionary knowledge from thought leaders. It’s the human connection with people creating this future with you.

Meet your future face-to-face at RAADfest

Use the code ‘jeunessima’ at checkout to get 10% off any RAADFest registration. Click here to register. We're looking forward to meeting you face-to-face

The theme for this year's RAADFest is ‘Meet your future face-to-face.’ What does the theme mean to you, for your work and why do you think it's important for RAADFest attendees?

It has everything to do with meeting the people who are bringing in this proactive regenerative medicine to help you live longer. You're going to meet people who have partaken in these types of technologies and are trailblazing the future of these innovative medicines.

You will be talking about gene therapy to address cell damage due to aging. Can you give us a sneak preview of your talk already?

One of the things that RAADFest would like me to do is to educate the audience on what's happening in gene therapy. I want to walk you through the process of gene therapy, what it is, how it works, and where it's been and where it's going.

And then I will finish off by talking about several people's data and what has happened after they have taken a gene therapy called telomerase reverse transcriptase. It's a gene therapy that lengthens the caps of the ends of the chromosomes, and that gives you more cellular divisions. And your cellular divisions are historically in 25 species, tied in directly with how long the species can live. So the hope is, is that with longer telomeres, you'll be able to live healthier and longer.

My data is one of the several of the data points on the graph since I have been the patient with the longest amount of data collection on how my telomere length has been progressing.

Let's look at the next five years. What developments, innovations do you see happening and how might this change the way we address aging in the future?

What you're going to see is the slow move into the regulatory systems of new and innovative drugs that target aging rather than a symptom of the disease.

Historically, we have a reactionary healthcare system in which you wait until someone is sick. Then that someone goes to the doctor. And then they might have a condition such as Parkinson's. And then there are cognitive issues associated with Parkinson's. There might be tremor issues, difficulty with coordination. What medicine would then do is try to treat some of those symptoms. They might try to reduce your tremors or increase your coordination or your cognition.

But with the new medicine, what we'll be doing is actually reversing cellular aging and then reversing your propensity for the disease as it would be for a younger biological age.

For instance, it happens, but it's highly unlikely that you would get cancer, dementia, Parkinson's disease, or heart disease at the age of 20. So, your risk level is super low at that age. It's super high at the age of 65.

By biologically reversing the age of cells, we want to take them back to your risk factor of disease and keep you from getting sick.

You are going to see the slow progression of these therapies entering the regulatory system. It is way too slow, so I'm working on a regulatory path called Best Choice Medicine that would give terminally ill patients the access to these innovative medicines that current legislation doesn't allow them to have.

Hopefully we will also see a much faster adoption of known human data in these therapies, which will actually get them through the regulatory system even faster.

How do you see the measurement of biological age changing?

You can affect something without measuring it, but the best thing to do is to be able to measure it. So there's two sort of aging clocks that I generally describe. There's chronological aging, and that's getting older by years, and we want you to get older by many years. And then there's your biological aging clock, and that's your biological risk for death and disease. Disease first and then death.

And we want to reverse the biological clock. It turns out that there are 12 hallmarks of aging. That means there are a multitude of clocks of aging. So when we look at therapeutics, we are trying to reverse the biological clock on a specific marker of aging. We used to hope that you could just use one gene and reverse all of the biological markers of aging, but that probably is not going to happen.

So when we lengthen telomeres, your telomere length is a biological clock. It's a complicated clock because your telomeres can stay in a shortened state at the end of life for quite a while. Your cells go senescent and stop reproducing, but it is a biological clock. So reversing the telomere damage and lengthening telomeres adds biological age to your life.

Now it's not the whole story. There are also other clocks. There is the DNA methylation clock. A lot of people have heard about that and that changes as you age. There are therapies that reverse the epigenetic age, but that doesn't extend lifespan that much. It makes a healthier organism. You have to merge all of these clocks.

So what you're going to be seeing over time is the merging of several biological clocks in order to reverse aging. I know it sounds a little bit complicated and it is. But as we find these clocks or these measurements of cellular age and we pinpoint therapies at them, we will reverse the cellular age specifically of that hallmark.

That is how we will eventually cure all of aging … by targeting all of them. And some therapies, just to put your mind at ease, actually will reverse several of the aging mechanisms. They might reverse mitochondrial dysfunction, telomere attrition, and senescent cell buildup all in one swoop.

Is there any gene or gene therapy that already stands out, that addresses quite a large variety of different diseases … or hallmarks?

Yes. Lengthening telomeres helps with mitochondrial dysfunction, which is one of the hallmarks of aging. Telomere attrition is one of the hallmarks of aging, and it directly affects that. And senescent cell buildup is also one, and lengthening telomeres helps clear senescent cells to an extent. So that is a really promising therapy.

And then we also look at other genes. We have five other gene candidates that also have an effect on aging.

And then you probably heard about epigenetic reprogramming of cells. There are companies that are working on both the gene therapy and the small molecule approach to reprogramming the cell's epigenetic age. So, slowly we're gathering the genes associated with reversing this damage. Getting them all together in one or two therapies that you might take every 5 to 10 years is the goal.

In summary, the future of aging is on the brink of a revolution, with gene therapies being a critical component. As we move from a reactive sickcare to a proactive healthcare model, the potential to prevent and reverse diseases associated with aging becomes a tangible reality. With pioneers like Liz Parrish at the helm, we are not just imagining this future, but actively creating it. As we continue to explore the possibilities of gene therapy, we're not just looking at a future where we live longer, but where we live better, healthier, and more vibrant lives.

The future is arriving quicker than ever before. Let's meet it face-to-face.

Ines O'Donovan, PhD
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