Genetics Unzipped is the podcast from the Genetics Society - one of the oldest learned societies dedicated to promoting research, training, teaching and public engagement in all areas of genetics. Find out more and apply to join at genetics.org.uk

026 - The future is now: Curing HIV, advancing CRISPR therapies, predatory phages for superbug infections and advice for a healthy life

026 - The future is now: Curing HIV, advancing CRISPR therapies, predatory phages for superbug infections and advice for a healthy life

Kat: Hello, and welcome to Genetics Unzipped - the Genetics Society podcast with me, Dr Kat Arney. In this episode we’re reporting back from the Manova Global Health Summit, exploring the latest advances in health technology such as CRISPR-based gene therapies, infection-fighting viruses and a potential cure for HIV.

Plus veteran health columnist Jane Brody’s advice for a healthy life, and reflections on progress in cancer from US journalist and advocate Katie Couric. 

As the saying goes, get to know the future - it’s where you’re going to spend the rest of your life. Last month I headed out to Minneapolis for the Manova Global Summit on the Future of Health - three jam-packed days listening to some of the leading thinkers talking about how to change the future of healthcare. 

The sessions covered everything from a pair of very perky teens who’ve developed a mental health app to a project using drones to deliver blood supplies in rural Rwanda, elderly care robots to AI pandemic prediction, topped off with an appearance from actor, activist and icon Jane Fonda. Alas, I didn’t get to interview her, sorry.

The Perfect Predator

Perhaps my favourite talk of the summit came from Steffanie Strathdee, associate dean of global health sciences at UC San Diego, who’s taking an unusual approach to treating antibiotic-resistant superbug infections, using tiny bacteria-busting viruses called phage.

But she only started working on phage therapy by accident, when her husband fell ill while they were on holiday in Egypt back in 2015. 

Steffanie: My husband acquired a superbug infection which is a bacterium that's resistant to multiple antibiotics. He was dying. The doctor said, "There's nothing else we can do." I thought to myself, well, if he's going to die I want to know that I did everything I could to save him. So I hit the internet and I did my research on my own and I found a hundred-year-old forgotten cure; bacteriophage.

Phage are viruses that have naturally evolved to attack bacteria and they were discovered a hundred years ago. They even had a heyday in the 1920's and 1930's when they were used to treat bacterial infections but then when penicillin came along they were forgotten and left on the shelf, except in some parts of the former Soviet Union where they are still used today.

This was experimental treatment and we needed to see whether or not it was even going to get approved by the FDA.

Kat: So how do you go about turning a bacteria phage, this little virus, into an appropriate treatment for someone's infection?

Steffanie: Well first you have to find the right phage that match the bacteria that you're trying to kill. So it's both an advantage and a disadvantage that phage are very specific; they only match a certain bacterium and they leave the rest alone.

That means that you need to find the phage that will kill the bacteria that is the one that's causing your illness and there's 10 million trillion phages on the planet. That's ten to the power of 31, so they are the oldest and most populous organism on the planet, so you need to go on a phage hunt.

 Kat: That is a big screen. I wouldn't want that to be my PhD project.

Steffanie: Well, I was horrified when I realised that this was going to be a daunting task. After the doctors that were treating my husband agreed to treat him with this, they said, "You have to go out and find the phages that match his infection, if we're going to do this. Then the FDA has to agree to it."

 So I went back to the internet and then I made a list of doctors that were studying phage that attack his type of superbug and it was a mighty short list, at least in North America. I knew we didn't have much time so I wrote total strangers and sent them a picture of my husband lying in a coma. I said, "Please, please help me."

Surprisingly, within 24 hours a researcher, a total stranger from Texas A & M University, Doctor Ry Young responded and said, "I'm the same age as your husband, I'm about to retire. I've been working on phage for a long time and I'd like to see it actually do some good someday and if this case works, it would be a game-changer in the field."

Kat: So then what happened? Do you get a little vial of phage coming through the post? What happened next?

Steffanie: You won't believe where they found the phages that matched the bacteria.

Kat: OK. Do I want to know? Is it going to be somewhere really gross, like in a septic tank?

Steffanie: Uh huh.

Kat: Oh no!

Steffanie: When you're trying to kill bacteria, especially the bacteria that are in your gut, the best place to go is in sewage because that's where you'll find the perfect predator that will kill it.

So Doctor Young's lab turned their whole place into a command centre and a PhD student, Adriana, slept in the laboratory for a couple of weeks, found four phages that matched and we were over the moon.

Kat: The grossest project. So you get loads of poop, you get the bacteria, you grow the phage, you get loads of phage, you put them in the person and then the big plot point - what happened to your husband?

Steffanie: Well, first of all we actually had to purify the phage. That turned out to be the hardest part because essentially, you're taking something that was in sewage and you're also adding lots of bacteria to it. The bacteria die and there's all this debris from the bacterial  cell wall etcetera.

So we had to involve a number of laboratories, but we also had the Navy step in. The US Navy also had a phage library because this organism that my husband was infected with; its nickname is ‘Iraqibacter’ because so many Americans come back from the Middle East with it.

It's really important that you have multiple phage that match the bacteria you are trying to kill because if there's a hidden reservoir of bacteria that the phage don't reach, then the phage are useless because the bacteria becomes resistant.

Kat: This seems like an incredible amount of work to call in the lab, to call in the Navy, to find the phage, to grow it up and then to purify it. How long did that actually take?

Steffanie: Believe it or not, it only took three weeks. I wrote Doctor Young on February 21st and the day that we first administered phage therapy was March 15th. So people had worked around the clock - total strangers - to save the life of one man. It was just an incredible effort. I get shivers even thinking about it to this day.

Tom was so sick though, he was in a coma, he didn't know what was going on. I had signed the consent form for kidney dialysis the day we started phage therapy. That's because they said, "His lungs are failing, his heart is failing and now if his kidneys fail, that's game over."

So he was considered to be within hours of dying. We injected these phages first into these catheters or drains in his abdomen because that was closest to where his infection was and he lived through that.

The next day he seemed no better but no worse, and then the Navy phages were ready next. We knew these were more virulent and more powerful. We injected those, a billion viruses, a billion phages per dose, into his bloodstream.

Three days later, he woke up. He lifted his head up off the pillow and kissed his daughter's hand. Everybody in the ICU freaked out.

The day that he got off the ventilator was only a couple of weeks later and he had to learn how to swallow, how to talk, everything. He said to me, "What did I miss?".

I said, "Well, you've been in a coma two months. It's now end of March 2016 and Donald Trump is the presumptive nominee to be president of the United States for the Republican party. And we  saved your life with purified sewage from Texas."

He went, "Oh my god, I'm hallucinating again."

Kat: That is something to wake up to! So then, having done this incredible miracle, how do you actually then start to make that viable? Because presumably not everyone can commandeer a whole lab for three weeks just to make their personal phage?

Steffanie: Absolutely. This is personalised phage therapy. It can occur much more easily without having to go through sewage every single time. Imagine having a phage bank, essentially a library of phages that are already characterised; they're sequenced, we know what combination to add them with antibiotics etcetera.

You keep expanding it to match a superbug library. If these existed on every continent then you could actually find phage to match bacterial infections within a couple of days.

Now, compare that to an antibiotic that takes ten to fifteen years to develop and about a billion dollars, there's no comparison.

Kat: Steffanie has written a book about her experience, The Perfect Predator, together with Thomas Patterson and she’s working on bringing these antibacterial viruses to the world through IPATH, the Innovative Centre for Phage Therapy at UCSD. She’d be happy to hear from anyone who needs her help - visit the IPATH website for more information.

The London Patient

From good viruses to bad - the Manova Summit heard about another incredible medical miracle from Cambridge University’s Professor Ravi Gupta, who hit the headlines earlier this year after apparently completely curing a man of HIV through a stem cell transplant.

Known as The London Patient, because of where he was treated, this patient was the second in the world to have ever been successfully cured in this way. The first, more than a decade ago, was a man called Timothy Brown, or the Berlin Patient, as he used to be known.

I asked Ravi to explain what had made his cure successful, and what he and the London Patient could teach us about a potential cure for HIV. 

Ravi: Over ten years ago a case was reported called the Berlin Patient. This was an individual who was actually an American, who had HIV and then developed a quite severe blood cancer called AML. This cancer needed a bone marrow transport in order to cure it.

So the Berlin Patient who was HIV positive underwent this stem cell transplant, but his doctors in Germany managed to find a donor whose cells were resistant to HIV.

This is something that we'd known about for some time, that certain individuals - less than 1% - are immune to HIV. In that case they used these resistant cells to transport into the  Berlin Patient combined with quite heavy chemotherapy and radiation. This resulted in a cure.

Kat: So this means that he has none of the virus left, he's completely cured of HIV?

Ravi: In the Berlin case, we think yes because it was almost a decade without any anti-HIV treatment and the patient had no sign of HIV detected. That was documented as the first cure of HIV.

Kat: What made those immune cells so special that they couldn't be infected by HIV and so this person could no longer harbour the virus?

Ravi: So around 20 years ago, people realised that there were certain individuals who couldn't be infected with HIV despite repeated exposure and high-risk behaviour. When the genetics was done it was found that they had a mutation in a particular protein that sits on the surface of your white blood cells.

That mutation prevents HIV from getting inside the cells to infect them in the first place, so that renders you immune essentially.

Kat: So like, the door is locked, you're not coming in?

Ravi: That’s exactly right. There are a number of theories as to why this mutation arose in individuals. It's exclusively found in Europeans and so it's been suggested that this enabled people to survive certain diseases such as smallpox.

Kat: Let's jump forward and talk about another patient, the London Patient. Who is that?

Ravi: This is an individual who was diagnosed with HIV in 2003 who developed a different type of blood cancer from the Berlin Patient. This blood cancer was something called Hodgkin Lymphoma and is related to HIV and its effects on the immune system.

This individual was not responsive to standard chemotherapy for Hodgkin Lymphoma and so the last resort in that case is a transplant using cells from another matched individual, an unrelated individual.

We managed to find cells that were suitable but also had this mutation that was demonstrated in the Berlin Patient, and so the London Patient underwent this stem cell transplant procedure.

Kat: And the result was…?

Ravi: Well, immediately after the transplant we did a number of tests for HIV to see if we could detect it, and it seemed that there wasn't any detectable HIV after this transplant procedure.

We then had to gain ethical approval to stop his anti-viral medication, his HIV treatment. So we did that and then stopped the anti-HIV drugs a further 16 months after the transplant. After that period we have had two years now of no sign of HIV.

Kat: Fingers crossed, this looks like another complete cure?

Ravi: I think it is now highly likely that this is a complete cure because we've had no sign after two years.

Kat: So that's two patients, Berlin and London. There are an awful lot of people living with HIV in the world. How can we take those almost miracle cures and actually make that something that could benefit the many people living with HIV today.

Ravi: Part of the answer to that lies in the fact that we wanted to do it a second time. Partly because we weren't sure what we required to gain a cure. In the Berlin Patient's case, he had two rounds of chemotherapy and two rounds of radiation to the whole body.

Kat: That's quite hardcore.

Ravi: That's right. That's a very severe form of treatment and it was needed for the cancer. Of course a number of questions were raised such as, do you need such severe chemotherapy?

In our individual, we used much milder chemotherapy and there was no radiation involved. So we now know that you don't need radiation, you don't need certain chemotherapy. We are on a learning curve of what the requirements may be to achieve a cure.

Kat: Ravi Gupta, from Cambridge University. Although the transplant treatment is exciting - and can be curative - it’s not without risk, and using chemo drugs to take out the immune system isn’t a viable option for everyone.

Instead, Ravi and his team are starting to look at using CRISPR to genetically modify patients’ immune cells so they can’t be infected with HIV. It’s early days, but a potentially exciting and game-changing application of this gene editing technology.

Pack It In

Another person I spoke to who’s hoping to use CRISPR to cure disease is Vinod Jaskula-Ranga, the founder and CEO of Hunterian Medicine.

He’s found a new way to package up the molecular components of CRISPR so that they can be delivered effectively into cells in the body - that’s the molecular scissors that snip DNA, known as Cas9, and the guide RNA that acts as a map telling the scissors exactly where to cut.

While CRISPR works fine in cells growing in the lab, getting these tools into cells inside a living human body is the final hurdle in turning this incredible technology into effective treatments, and it’s turning out to be remarkably hard.

Vinny: If we have cells growing in a dish, it's very easy to do things, bombard it, create little pores in the membranes, zap it with electricity. We can get that stuff into the cells when we're dealing with cells in a culture. We can't do that for people. We can't hook them up --

 Kat: They don’t like being zapped.

Vinny: Yeah, right. There's all kinds of issues around that. So when we're doing the things with people, we need to ensure that we have something that is extremely safe and also effective. This is an incredibly difficult problem.

Kat: Because I guess when you're thinking about -- say if you were trying to repair a gene in muscle cells, you can't just do one muscle cell, you've got to do all the muscle cells in a person. What are the kinds of challenges that we're facing, in trying to get the stuff into different types of tissue in the body?

Vinny: If you think about the premise that it's easier to do it in culture, that actually tells us something. There are cells of the body that we can take out, we can edit in culture and put it back in. As we were talking about, bone marrow cells, blood cells, those are the kinds of things that are amenable to those types of manipulation.

For the vast majority of diseases we're going to have to get CRISPR to those tissues or those cells in the body. If you have an eye disease, for example, we need to get CRISPR into those eye cells and we don't need to get it to the rest. In fact it would be better not to get it into the rest of the cells of the body where it doesn't matter.

From the standard of safety, it's always going to be much better to target your treatments to the cells that are going to need it.

Kat: You're looking at this technology, you're looking at the scissors, you're looking at the guides, you're looking at disease cells - how did you start thinking about; how do we get these into there?

Vinny: Well, to be honest it was totally serendipitous.

Kat: I love stories like this. Go on.

Vinny: I was working on a specific aspect of it. In fact, I was working on the RNA component and how to turn it on. We can't just stick genes into cells and expect them to turn on and be expressed. We need to provide the instructions so the cell knows - okay, here is a gene, let's turn this on and make this in the cell.

I happened to be working on one specific example of this. I was cloning this region out of the genome cells, taking it out of the human genome, then I was going to stick the RNA  component or CRISPR on there, to express in its cells. When I did that, I ran into another gene.

It happened to be a gene that was oriented in the other direction. That gene happened to be a protein coding gene. When one looks at it, it's a very small region in the human genome and what it does is it produces a protein on one side and an RNA on the other side.

So if you work on CRISPR and you see this little region that can express the two types of biological entities that make up this CRISPR system; an RNA and a protein, you'll immediately be able to do the math and see that it falls under the packaging capacity for the gold standard delivery which is AAV.

Kat: Just to unpack that a little bit, what you did, you found that there's a little region of DNA, effectively a switch, that will turn on both a protein going one way on the piece of DNA, and an RNA going the other way. And CRISPR is the protein scissors and the RNA guide, so you're like, bingo!

Tell me a little bit more about why getting that size down was so important. AAV is a virus, what's the connection there?

Vinny: AAV is a fascinating virus. AAV is generally assumed to be the gold standard way of delivering cargo into cells. It has an incredible track record. It's been used in over 230 trials worldwide, largely without any toxicity or any known side effects.

This is the reason why the field has essentially converged on AAV as the gold standard for  getting things into people. Now, the one problem though for AAV - and this is something that people have known for a long time - is that it's very small. It's physically small. So there's only a set amount of DNA that we can put in there.

Kat: So we've got the two components together. You've got your AAV, your little modified virus, your delivery vehicle. You've got this wonderful two-way switch that enables you to get the CRISPR scissors and the guide into this tiny space and package them together.

What I still want to know is, how do you get that into the right tissues, into the right part of the body to have an effect? What sort of diseases do you have in your sights for this technology?

Vinny: Yes, I think there are two answers to that. One is; there are several different flavours, if you will, of AAV and the nice thing about that is those have a specificity for different tissues.

That means we can inject all the same stuff but use a different flavour of AAV into the blood stream. Some of them will hit muscle cells. With other ones we may hit lung cells or neurons or whatever. So that gives us a tool chest to pick and choose how we get things to specific cells and tissues.

Kat: Which diseases are you starting to tackle first?

Vinny: We are most interested in diseases of the eye and brain. We think that the field in a lot of these newer technologies will demonstrate that in those tissues first, genes that are related to vision, vision loss, that's certainly an area that we're looking at.

We are also interested in the vasculature of the eye and in the brain as well. For the eye a common disease or something that people may be aware of would be age-related macular degeneration. The current standard of treatment is to go in for either monthly or every other month injections in the eye. I don't know anybody that would enjoy getting --

Kat: Eew.

Vinny: Yeah, right. The benefit of CRISPR, what the promise is, is one-time treatment, one-time cures. If we can do that, if we can succeed in doing that and getting the number of treatments down to one, we think that would be just such an enormous benefit.

Kat: That’s Vinny Jaskula-Ranga, from Hunterian Medicine, speaking to me at the Manova Global Summit.

Where The Sun Don’t Shine

Kat: For all this exciting talk about CRISPR and cures, it’s important to remember that there’s a lot that we can do to protect and maintain our own health, especially when it comes to cancer.

One of the most inspiring speakers at the Manova Summit was journalist and cancer advocate Katie Couric - the first person to reveal her colon on national television, nearly twenty years ago.

It may seem tame by today’s show-and-tell standards, but she set the benchmark for cancer awareness. I asked her why she decided to bare her insides to the public in the first place. 

Katie: This was in 2000, and two years before that my husband Jay had died of colorectal cancer at 42. He'd just turned 42. During the course of his illness I learned so much about this very deadly form of cancer - the second leading cancer killer of men and women in the United States.

I decided that given my perch as a morning show anchor, that I could do a huge public service by educating people about the screening technique that can prevent colon cancer, can stop it in its tracks and leads to a 92 percent cure rate when the disease is detected early.

I felt a real obligation to demystify and destigmatise a procedure that people really didn't understand, could barely pronounce –

Kat: It's kind of like, butt stuff, as well --

Katie: Yes, exactly. It's interesting because I think there's no reason to get squeamish about it, because we all, if we are lucky, have colons. They serve a very important purpose.

If you look at the evolution of breast cancer awareness in the 1950s, the New York Times would have adverts for support groups and they'd call it, "cancer of the chest wall", because people didn't say the word "breast" in polite conversation.

So, similarly, I think there was a discomfort about talking about colons and rectums and bowels. But it's sort of silly when you think about it. I had no hesitation. I was so happy and grateful that I had a platform from which I could educate people and prevent them from getting this disease.

And as a result of my on-air colonoscopy - which was not live - a lot of people say it was live and I say that I'm not that brave - but colon cancer screening, colonoscopies in particular, increased 20 percent. If you think about that compliance rate, that translates to many, many lives saved as a result.

On television, we did it tastefully, we did it with a sense of humour. We didn't show - and I got a little sick to my stomach with my final glass of the inappropriately named, "GoLytely" which was the prep - I was like, is this a joke, that they named this Go Lightly?

I got a little sick to my stomach. I didn't show that because I didn't want to discourage people, but yes, I just went for it.

People came up to me and said, "I believe your advice saved my life. I got screened and it prevented me from -- I didn't get full out colon cancer." So I really got such positive feedback I'm really glad I did it. I'm afraid that I started a whole trend of TV anchors oversharing a bit.

Kat: Oh god. What's the worst that someone has got out on the telly?

Katie: I think I saw someone getting a prostate exam on television and I was like, um, maybe it's bad that I started this.

But I think overall this intersected with people taking care of their own health and feeling more responsible and becoming their own best health advocates. So I think on balance it's a really positive development in the discourse and for overall health in general.

Kat: You are continuing to use your media platform to reach people, to investigate challenging issues. When you're talking about something like cancer - and I know you're very involved in Stand Up to Cancer, which is a massive programme of research and communication - how do you make sure that the messages you're telling people are accurate?

Katie: Well, we rely on science and on scientists. I think we're very careful and conservative and we want to be a legitimate, respected and trusted source for information for people on all things cancer.

I think the internet is a very scary place when you're diagnosed with any disease but particularly cancer. If you read things that aren't necessarily true or vetted.

I talked to a very renowned clinician at Memorial Sloane Kettering. He said the people who should be writing about cancer are too busy treating it. And the people who are writing about it don't know the latest information because they've never treated it.

So I think you just have to take it with a grain of salt, but we're very, very careful about the information that we put out. I think Stand Up to Cancer has done an incredible job. Certainly as a journalist, I want to make sure that I don't give people false hope.

Particularly, public figures have to be careful about what they're communicating in terms of finding the right treatment because not all people have access to it.

Cancer is a million different diseases and a million different biologies and sometimes, as you know, what works for one person may not work for someone else because of all kinds of reasons.

Kat: What excites you most about the current crop of cancer research, and the treatments that are starting to come through?

Katie: Well I think immunotherapy is incredibly exciting. I think what I'm excited about is we have this convergence of all kinds of things that are happening that will move the ball forward.

Data science is so important to really measure the efficacy of certain treatments and drugs. You have mapping the human genome, so obviously genetics and our better understanding of cancer-causing genes is really an exciting area as well.

I think we have all kinds of different doctors getting involved and scientists and chemists and engineers. It's just a much more multidimensional approach to cancer and that I think is really, really exciting.

Kat: The other thing I think is exciting is the opportunity as journalists to be telling these stories. To work out, okay, how do we communicate them to the public authentically, ethically, accurately?

What do you see are the opportunities and the frontiers in communicating with people about the kinds of progress and the kinds of issues and the information that they should be aware of?

Katie: I think that the media writ large could do a much better job of explaining cancer in general. There was a recent documentary about Jim Allison who won the Nobel Prize, called "Breakthrough", which helped illustrate how he found the checkpoint inhibitor that was preventing immunotherapy from actually working on some cancer cells. Because cancer is a very, very clever disease.

I think that we could do an even better job of helping people understand. I think if you ask the average person, "What is immunotherapy and how does it work?", it's very hard to understand it. So first and foremost, the basics could be better explained.

It's very challenging because you don't want to give people false hope but you also want to le t them know the latest science, and when something is actually working.

But we have more opportunities than ever before through the various platforms to tell these stories and to keep the movement going. As always, with any good storytelling, it has to have a personal narrative and you have to hit an emotional note for people, so they can relate and connect with the person you're describing.

Kat: And for someone like you, you never asked for the role that you found yourself in. When you look back at what you have achieved through using your voice to tell the stories of your family, to share this kind of information, how does that make you feel?

Katie: Obviously I feel very proud of the work I've done vis a vis cancer research. Doctors have said to me, "Katie, you've probably saved more lives than we have in our whole lifetime." Which is an incredibly gratifying feeling.

To think that people are walking around and living their lives with people they love, because they actually took action because of something I helped them understand.

Then the idea that we're supporting all of these scientists and making sure they can do this life-saving work. That makes me feel just so great, because they are all brilliant and they're so hard working and they care so deeply, that to be able to be the wind beneath their wings - to sound really super-cheesy - is a really exciting and wonderful and gratifying thing.

Kat: If you want to hear more from Katie Couric and her journalism on health and many other important topics, you can follow her on Instagram, subscribe to her daily email newsletter, Wake Up Call, and even listen to her podcast - after you’ve finished listening to this one of course - by heading to her website, that’s katiecouric.com 

Gee-whizz or good health?

Finally, I managed to catch up with Jane Brody, personal health columnist for the New York Times, who distilled 50 years of writing about good health into a searingly insightful talk.

It was a breath of fresh-air - and a shot of realism - among a lot of more “gee-whizz” stories that we heard on stage, so I wanted to dig a bit deeper into what she believes should be the goal of medical research.

Jane: The truth is, when I started in the 1960s it was all gee-whizz medicine. The newest drug, the newest operation. That's closing the barn door after the horse has escaped. We want to close the barn door whilst the horse is still inside it.

So what I see happening now is an attempt at least to get people on a trajectory that keeps them healthy as long as humanly possible. I don't see the gee-whizz stuff as being very profitable for people. Maybe profitable for some company that's making it - their stock prices will go up or whatever - but in fact what individuals need is a prescription for keeping the God-given health that they were born with.

Kat: Some of this stuff doesn't seem very cool and sexy. Don't smoke, don't eat too much, take exercise. You've presumably been writing this kind of stuff for many years now.

Jane: And part of the problem is that because it doesn't sound sexy and it's the same message over and over again, the media - and I'm a member of the media and I have fought this battle for many, many decades - don't regard it as something that they want to put in the paper or put on the air.

We cannot stop repeating the message that the quality of your life is in your hands, and if you don't take advantage of it, no one is going to pick up the pieces for you.

Kat: I always think that if the newspapers reported the number of casualties from smoking-related diseases in the same way that they cover accidental atrocities or freak accidents, it should be on the front page every single day.

Jane: Yeah. And you have to remember that I started writing in 1963, the January 1964, I wasn't even working for six months, was the First Surgeon General's report on smoking and health.

That report really nailed the relationship between cigarette smoking and lung cancer. That was all they were talking about in those days, pretty much. Yet people did not want to buy into that.

Well, tobacco companies were using doctors to endorse their products. It was an outrage when you think about it. But we can't let go of the importance of repeating the message over and over again.

Kat: We do hear a lot now about the role of genetics in personal health. What are your views there?

Jane: Well it turns out that genetics determines how healthy you are in maybe at most 20 percent of your health quotient is genetically determined. 80 percent is determined by how you live your life. So to just say, "I can't help it, it's my genetics", is a very flimsy excuse and not an accurate one, and not going to help you live better.

My personal family history is very high on heart disease. My father, his father, his father's brother and my brother all have had serious heart conditions. I took that under advisement. I said, "This is not going to happen to me, I'm going to take good care of my heart."

And therefore I was physically active all the time, I try to eat a healthy diet. I'm not so great about minimising stress but I do my best. I think exercise does help you minimise your stress. But in fact, people who rely upon or use their genetics as their excuse are barking up the wrong tree.

Kat: So what would be your prescription for a good life?

Jane: Let's start with the most important things. That is; take advantage of your God-given qualities. If you can move, move. You can eat - eat healthily. You can sleep, get enough of it. Because we now know that sleep deficiency is a real problem in modern life.

Not only is it a psychological problem, it's a physical problem and it's an emotional problem. People are not as pleasant when they are sleep deprived.

Kat: And then more broadly, your advice for the healthcare community, people who really do care about people's health and developing new ways of improving health. What's your message there?

Jane: My message is that we have to get that message out to the public front and centre. Instead of talking about this new drug, that new treatment and that new this and that new that, let's put our money where our mouths should be.

And that's to tell people that they are in charge of their own well being and if they don't take charge of their own wellbeing, it's going to fall apart. And it does in too many cases.   

Kat: New York Times columnist Jane Brody, speaking to me at the Manova Global Health Summit last month. Thanks to the team at Manova and Tunheim for making me so welcome and for all their help.

That’s all for now. We’ll be back next time, delving into the past for some more of our 100 Ideas in Genetics - including finding out if Jurassic Park could really happen after all.

You can find us on Twitter @geneticsunzip and please do take a moment to rate and review us on Apple podcasts - it really makes a difference and helps more people discover the show.

Genetics Unzipped is presented by me, Kat Arney, and produced by First Create the Media for The Genetics Society - one of the oldest learned societies in the world dedicated to supporting and promoting the research, teaching and application of genetics.

You can find out more and apply to join at genetics.org.uk  Our theme music was composed by Dan Pollard, and the logo was designed by James Mayall, transcription is by Viv Andrews and production was by Hannah Varrall. Thanks for listening, and until next time, goodbye. 

027 - Uprooting the tree of life: Darwin, DNA and de-extinction

027 - Uprooting the tree of life: Darwin, DNA and de-extinction

025 - When 'Becky' met Bateson: Edith Rebecca Saunders, the mother of British plant genetics

025 - When 'Becky' met Bateson: Edith Rebecca Saunders, the mother of British plant genetics

0