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Interview with George Church - Is the End of Aging Near?



Preface by Gregory Fahey


Being a biogerontologist, I have been attending scientific meetings on aging since the early 1980s and have seen and heard many amazing things. But when I attended the George Church lecture at a conference organized by the SENS Aubrey de Gray Foundation at the end of 2014, I realized that I had just heard the most wonderful lecture in my life.

Why? For three very simple reasons.

First, as Dr. Church emphasized in his lecture, aging seems to be largely controlled by the action of a small subset of your genes and, mainly, by the master genes controlling a large number of other genes. Your genes are areas of your DNA that determine your eye color, hair color, gender, height and other characteristics of your body. But it is becoming more and more obvious that genes also determine how you age , and maybe you even age.
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Secondly, Dr. Church spoke about how technology has progressed to such an extent that the activity of your genes, whether it is "on" (expressed) or "off" (not expressed), becomes more and more controlled. And this is possible not only in a test tube, but also in the whole body, and even in the brain.

Dr. Church focuses on CRISPR ( clustered regular intermediate short palindromic repeats ), which is a relatively new and very powerful method for regulating gene activity.

CRISPR can “edit” or alter genes to correct harmful mutations or create intentional mutations that can have a positive effect (for example, turn off genes that affect aging). Thus, the relationship is very clear: if aging is controlled by master genes, and if the activity of such genes can now be intentionally controlled, then we begin to approach aging control at a fundamental level. And the same technology can be applied to the correction of many diseases, no matter whether they are age-related or not.

Finally, our ability to control aging would be completely useless if we had no desire to use it in real medicine. Fortunately, Dr. Church wants his achievements to be quickly in clinics. He intends to make aging control a practical reality - and very soon. And Dr. Church, as an eminent professor of genetics and a major figure at Harvard Medical School, is well placed to translate his desires into reality.

In an interview with the Washington Post in early December 2015, Dr. Church said that his laboratory had already reversed aging in mice, and tests on humans could take place in a few years. Dr. Church stated:

“One of our biggest economic disasters now is our aging population.”

“If all these gray-haired guys could go back to work and feel healthy and young, then we would have prevented one of the greatest economic disasters in history.”

He said he sees:

“The scenario [in which] everyone gets gene therapy, not only for treating rare diseases such as cystic fibrosis, but diseases that everyone has, including aging.”

Dr. Church also mentioned his personal interest in reversing an aging person when he stated:

“I want to become younger, I still try to do something new every few years.”

CRISPR technology can change the world and our lives as we know them.

CRISPR is a technology originally developed in nature to fight viruses by cutting their DNA. Fortunately, now it has been modified by scientists, and can make specific controlled changes in the right places of the genome. As soon as doctors can adjust or “edit” DNA, they will begin work on restoring youth in the elderly.

How serious is the promise of scientists? Consider the following:


In general, in my estimation, the CRISPR revolution is a turning point in science with overwhelming consequences. If everything works out, our world will never be the same. The prospects are as impressive - to say the least - as with the appearance of electric lighting, telephones, personal cars, airplanes, personal computers, the Internet, and cell phones. Only this time it is not only about how you live, but also about whether you will live at all and for how long: your health, longevity and their impact on the quality of your life.

Will it work? We'll see. Opinions vary. Of course, there will be a lot of problems, sudden turns and pits on our way. Even the famous scientist Craig Venter says it will take 100 years to fix everything. But the George Church lab is already reversing aging in experiments. So the process looks very promising, incredibly rapid and based on the solid scientific foundation of our knowledge of aging. I bet on Church, and almost everyone has a similar opinion. The end of at least some critical aspects of aging can be very close.

The Life Extension Foundation participates in this innovative and future-oriented project. The Life Extension Foundation assisted Dr. Church by providing data from a research project dedicated to super-long-timers. As Dr. Church notes in his interview, the study of super-dutymen can provide a new insight into how to reverse human aging when we get the necessary gene editing tools and apply them.

We hope that you appreciate what, in our opinion, could be the coming revolution that will change your life.

Managing Human Aging with Genome Editing


Interview with George Church


Attempting to delay aging is already an outdated concept. A new goal is to convert it not only in animals, but also in humans. Rejuvenation is very important, since significant age-related disorders have already occurred in most people due to changes in gene expression profiles.

The profile of gene expression changes with age. This affects the speed with which a person ages, and also determines what age-related diseases he will have. But innovative gene editing methods based on the unique CRISPR technology (clustered regular intermediate short palindromic repeats) are currently being successfully tested as age therapy for humans.

In response to these breakthroughs, Life Extension sent a biogerontologist, Dr. Gregory M. Fei, to Harvard University for an interview with Dr. George Church , who is a leading developer of advanced CRISPR technologies. In it, Dr. Church explains the incredible possibilities for reversing an aging person who can reach their potential earlier than many have suggested.

An interview with Dr. Church begins with a discussion of the issue of reversing the aging of cells by restoring the expression of youth genes.

Fahey : If aging is caused by changes in gene expression, the ability to control it using CRISPR technology can have enormous implications for an aging person. Why do you think aging can be at least partly due to changes in gene expression?

Church : We know that there are cells that work worse with age, and that we have the opportunity to turn them into young cells again. This means that we can reset their biological clock to zero and keep them in this form as much as we want. For example, we can take old skin cells that have a limited lifespan, and turn them into stem cells (stem cells are cells that can turn into other types of cells), and then back into skin cells. This transformation leads to the fact that they look like cells of children's skin. It seems as if my 60-year-old cells become the cells of a one-year-old child. There are many markers associated with aging, and they all return to a young age.

Fahey : It's fantastic. Does this mean that the treatment of aging skin on your face will allow you to rejuvenate your entire face?

Church : If you rejuvenate at the molecular level, it will not necessarily lead to external rejuvenation. So, for example, if I have a scar on my face, it does not have to disappear (although theoretically I do not exclude this). But we can change the tendency of your cells (and, therefore, your entire body) to decay over time.

Technology: how genes and their expression can be changed


Fahey : So CRISPR allowed you to reverse the aging of human cells. CRISPR is a unique technology. The CRISPR molecular machine, consisting of protein and some associated RNA, can now be made in the laboratory or in our own cells and can change the genes and their expression. This is an incredibly powerful method. Please tell us more about him.

Church : CRISPR is the newest method for genome editing (editing the entire set of genes). Its advantage lies in the fact that it is much easier to create a specific CRISPR construct than other tools for editing genes, and CRISPR is about 5 times more accurate than other methods. The combination of ease of design, high efficiency and great flexibility makes it the most powerful tool for editing genes to date.

Fahey : Right now, with the help of CRISPR, you can change, delete, insert, activate and reduce the influence or completely turn off any gene with high accuracy - both temporarily and permanently. Now let's talk about what this new fantastic opportunity can bring.

Specific Opportunities for Reversing Human Aging TFAM: Keeping Eternal Youth


Fahey : Nowadays, a lot of very interesting things happen in the study of aging. In 2013, the Sinclair Laboratory at Harvard came up with the news that the aging of mitochondria (which are energy producers inside cells) is largely due to a decrease in the levels of one specific molecule in the cell nucleus: oxidized NAD (NAD +).

The team showed that they can reverse the aging of mitochondria, just for one week, giving old mice nicotinamide mononucleotide (NMN), which is a vitamin-like substance and can be converted to NAD +. This has led to a phenomenal overall rejuvenation, including the disappearance of signs of muscle atrophy, inflammation and insulin resistance. Now your lab has shown that there is a very interesting alternative in the form of genetic engineering, including TFAM (Transcription Factor A, Mitochondrial). Why is TFAM important and what have you done with it?

Church : TFAM is a key protein regulating the production of NMN and NAD +. It allows cells to independently receive their predecessor NMN, so you do not need to produce it outside the cell, and then try to deliver it to it from the outside. Ideally, you do not want to take the NMN for the rest of your life, you want to allow the body to create its own NMN and get rejuvenation for at least several decades before you have to worry about NMN again. To achieve this at the cellular level, we used CRISPR to activate TFAM and made it semi-permanent.

Fahey : With this technology, you were able to increase the level of TFAM in the cell 47 times. This has led to the restoration of ATP levels, an increase in NAD + and an increase in the NAD + / NADH ratio. She also increased the total mass of mitochondria and reversed several other age-related changes.

Church : Yes. We have several ways to measure mitochondrial function and their age-related changes. When we activated TFAM, mitochondrial functions returned to what you expect from a younger cell. We have built in the ability to rejuvenate the cell, allowed it to self-renew and eliminated the need to take pills or injections.

GDF11: Towards a General Rejuvenation


Fahey : Now let's move on to GDF11 (growth differentiation factor 11), which is a protein and a type of adolescent that is present in the blood of young organisms, but declining with time.

Church : Yes, my lab is related to GDF11. We are working with Amy Wagers, a Harvard biologist who is known for her work on heterochronic parabiosis, and her group, one of the first to tackle this problem.

Fahey : It is reported that GDF11 rejuvenates the heart, muscles and brain. It restores strength, muscle regeneration, memory, the formation of new brain cells, the formation of blood vessels in the brain, the ability to smell and the function of mitochondria. All this is done by only one molecule. Infusion of young plasma containing GDF11 in older animals also has a good effect on other tissues, such as the liver and spinal cord, and improves the ability of old brain cells to form connections with each other.

How would you use CRISPR to make sure that the level of GDF11 in the blood never drops?

Church : CRISPR-regulated GDF11 can be delivered in adulthood, just when you need it. If you want to install it at a certain level, you can use the GDF11 sensor to provide feedback so that you can automatically control the production of GDF11. If necessary, you can recalibrate and fine-tune it, perhaps once in several decades with a different dose of CRISPR. This is a great molecule, and we work with it.

We have a number of other projects with Amy, we deal with muscular diseases, such as muscular dystrophy. We are working on possible treatments that include proteins such as myostatin and follistatin.

Strong bones and strong muscles


Fahey : Speaking of myostatin, the absence of which causes increased muscle development, you mentioned in your talk of SENS 2014 that you are interested in the possibility of improving muscles and bones. Is this another treatment for aging?

Church : Muscle atrophy and osteoporosis are symptoms of aging. The key to fighting them is to eliminate the underlying causes, even if they are complex. Known genes involved in muscle atrophy, and genes that can reverse it. We are interested in such powerful tools as growth hormone, myostatin, and a target for new drugs for the treatment of osteoporosis, RANKL (activator of the nuclear factor receptor kappa-B ligand).

Fahey : What about going beyond aging and really improving people by making them stronger bones and strong muscles?

Church : Instead of waiting for the muscles to atrophy, and then trying to fix the problem or wait until someone breaks the bone and casts plaster, we suggest making them stronger and stronger initially. Think of it as preventive medicine. We must act carefully, but there are quite a few people around us who have much stronger bones and strong muscles, and we see nothing wrong, so we know that such things are possible.

Fei : Is it possible to stop osteoporosis?

Church : I would say that osteoporosis can definitely be addressed. The process of bone formation and destruction is a regulated process that responds to conditions such as stress on standing or running. So yes, this is an example of what is reversible.

IKKβ: Treatment of a possible full body aging program


Fahey : Let's move on to another manifestation of the aging process, which is of great importance. According to Nature’s article, body weight, body aging, and longevity are largely controlled by increased expression of one specific IKKβ protein in one particularly specific place, microglial cells in the hypothalamus in the brain. When this overexpression is prevented in mice, the average and maximum lifespan is increased by 20% and 23% , learning is improved, physical activity is improved, as well as skin thickness and bone density. In addition, collagen cross-links decrease, and gonadotropin production increases. If these improvements could be combined with improvements brought about by other interventions that we discussed, the consequences would be overwhelming.

Church : Yes. What you are talking about is the direction of a certain scientific school - aging, programmed by the neuroendocrine system, the brain. The reason why mice die for two and a half years, and whales after 160.

Fahey : Yes. And this is a particularly interesting problem, because it is not only important in itself, but also offers us practical ways to stop the changes that occur in the brain. This part of the brain is protected from most molecules placed in the bloodstream through the blood-brain barrier. Is it possible to use CRISPR technology across the blood-brain barrier and target it to this biochemical pathway or other pathways in the brain?

Church : The blood-brain barrier is highly overvalued, there are so many things that cross it, for example, various drugs, viruses, and even whole cells. So the answer is yes, we can deliver CRISPR through the blood-brain barrier.

Telomerase: brain aging and cancer?


Fei : Telomerase is widely known as an enzyme that can prevent aging at the cellular level. But the absence of telomerase can also lead to brain aging and cancer. Can CRISPR be used to increase telomeres?

Church : Yes, it is certainly possible.

The gene expression profile is a measure of aging in humans.


Fahey : Could you explain epigenetics and comment on the evidence that there are epigenetic hours of aging?

Church : Epigenetic - is all that controls gene expression. One of the components of epigenetics is DNA methylation, which consists of adding chemical objects, called methyl groups, to DNA in certain places. DNA methylation is important in part because it is easy to measure as a component of the epigenome (the totality of all epigenetic conditions). It turns out that DNA methylation changes over time. In fact, a DNA methylation profile can predict a person’s age with an accuracy of about three years.

In principle, if you could change the biological age of a cell or organism to a younger one, and if these methylation sites (the total amount of which is called "methyl)" really reflect the biological age, then methyl should change to a profile corresponding to an earlier age. In other words, if aging itself changes, then this aging biomarker should change in the same way. We use methylation sites as a measure of how well we have advanced in our research on the treatment of aging, and it works great.

DNA methylation is very useful for assessing a person’s age, and it can also be changed. Although in normal life it is always associated with chronological age, in the world of reversed aging and epigenetic intervention, you can change it, and such a change will be significant.

Fahey : Not all 50-year-old people are biologically 50. Some are biologically older and some are biologically younger. People age at different speeds. All of these differences can be found in the state of methyloma. If methyl indicates a different age from your chronological age, you are really older or younger than your chronological age, and this is confirmed by a number of other measurements.

Church : Yes, that's right. Scientists who discovered the epigenetic clock of aging, studied their variations and found interesting correlations with them. There are many ways to measure aging at the molecular level, and they tend to confirm each other. We do not know enough about the correlation between such indicators as methyl and aging factors, for example, GDF11, IKKβ and TFAM, but if you do something to reverse aging, you should also expect reverse changes in the methylme.

Fahey : Apparently, the DNA methylation model becomes increasingly chaotic as it ages. For example, the methylation patterns of identical twins begin to diverge over time, more modified profiles are associated with greater pathology. This is consistent with the recent theory linking the lack of aging in some species (“negligible aging”) with a relatively stable model of gene expression over time, and conventional aging with unstable and increasingly chaotic models of gene expression. If you change the expression of the genes back to the one that should be, all this instability should be reversible, right?

Church : Right. The spread of various parameters in any biological system increases when you move away from a physiologically normal state. You can think of the difference in methylation as another risk factor for aging and disease.

How to quickly detect and begin to correct the still unknown causes of aging at the gene level



Fahey : If aging is caused by changes in gene expression, and these changes can be reversed, then we need to find all the important age-related changes in gene expression as soon as possible. How can this be done?

Church : The result of gene expression in a cell is the presence of specific RNA and proteins, and they can be studied. You are not required to identify each individual RNA in a cell to determine changes in it, but you can, and we have just developed a new method that allows us to see all tens of thousands of RNA in one cell at once, as well as in neighboring cells. So now we can see how different cells interact with each other. This new method, called in situ fluorescence sequencing or FISSEQ, allows all RNAs in a cell to be counted, at the same time counting all RNAs in adjacent cells. In addition, we obtain three-dimensional coordinates for each RNA molecule in each cell.

Fahey : This is incredible. How can you use this method to look for changes related to aging?

Church : Suppose there are two different types of cells, and we want to know which gene expression distinguishes them from each other. We can first compare two cells using FISSEQ to determine differences in gene expression between them. We can then select specific differences that we believe will cause the cells to be different, and change the expression of specific genes in either or both of the cells, using, for example, CRISPR, and see if we can turn one cell type to another. Even if we don’t succeed for the first time, we can make a lot of assumptions about which RNAs are important and how we change them so that we can succeed.

The same principle can be applied to any pair of cells. Comparing old cells with young ones, we can find out what makes an old cell old and how to turn it into a young one.

Fahey : Fantastic.

Church : One of the problems in studying the development and aging of the body is that it takes a long time. But if we know the epigenetic state of all these different cells, it doesn't matter what their age difference is, in just a few days you can reprogram the cell and reproduce the effects of decades of slow changes in the body or reverse them altogether.Therefore, in principle, we could turn a young cell into an old or old cell into a young one, because the only difference between them is epigenetics or gene expression.

Fahey : What other ways are there to identify important gene targets that can interfere with human aging?

Church : There are four basic ways to find key genes.

First, we can look at the genes that underlie individual variability in such things as the low risk of viral infections, diabetes, osteoporosis, etc. The most extreme example here is to compare normal people with super-long-livers, with those who live 110 years and more. In a small group or even in one person, you can find unique useful genes.

There are hundreds of genes that have small effects, but then something like a double zero mutant for myostatin or over / underproduction of human growth hormone appears at the end of the Gaussian curve. Genes that have enormous influence and completely overlap the effects of small environmental and genetic factors - this is the right type of gene to look for.

The second way to find gene targets is to take them from basic research, such as GDF11 and TFAM, which we talked about earlier.

The third way is to use a special genomic strategy, for example, mutations of thousands of genes one by one, and see if any of them blocks aging, or using the FISSEQ method that we discussed earlier.

The fourth way to determine gene targets is to compare closely related species, one of which is aging much slower than the other (for example, naked excavators and rats).

No matter where you get your results, you don’t need to worry that you have too many hypotheses. Just use CRISPR to activate or inhibit this candidate gene and look for biomarkers of aging reversal, which we talked about earlier. The idea is to see if your change affects or not, and whether it enhances other techniques successfully tested in the past.

Fahey : So, if we saw something unusual in superdilineurs, we could create the same change, for example, in the normal human cell line and see if the correct longevity pattern appeared.

Church: Yes.

Fahey : James Clement, funded by the Life Extension Foundation, told me that they were doing a joint work with you on the genetics of superdolongers, you could even take their gene expression models, put them in mice and see if the mice will age more slowly.

Church: Right. Our protocol will probably collect results from four different sources and first test them on human cells. Working directly with human cells, we will not spend many years on mice, which is quite expensive, only to find out that reception does not work in humans. We can do cheaper and more relevant research on human cells, confirm it in mice, then test for larger animals, and then in humans. I think that the transition from human cells to mice and back to humans is likely to save us time and money. Many systems of cellular blood testing are becoming better and better, such as "organs on the chip" or organelles that are becoming more and more attractive in in vivo studies.

Elimination of problems with aging


Fahey : Can the high specificity of CRISPR eliminate the side effects of some anti-aging interventions? For example, I am working on regenerating the thymus in humans and restoring T-cell production using growth hormone. Although growth hormone does not cause cancer in adult animals or humans, it slows down DNA repair in animals — an effect unrelated to its beneficial effect on thymus regeneration.

Church : So you want to get rid of its effect on DNA repair, while maintaining good effects.

Fahey : Yes. If CRISPR can be used to work directly on genes of interest and not follow normal biochemical pathways, we could avoid unwanted effects, right?

Church: Exactly. You can list all the growth hormone targets and either select the targets you need and activate them selectively, or select the targets you don’t need and block them so that you can use the growth hormone as usual, but without inhibiting DNA repair .

The appropriateness of the use of CRISPR in the adult body


Fahey : In order to reverse the aging process of people, CRISPR technology must ultimately be applied throughout the body, and not just in cells in a test tube. How appropriate is it to use CRISPR technology in vivo?

Church : Gene therapy can be based on ex vivo manipulations in which cells are removed from the body, genetically modified, and then returned to the body or in vivo methods (inside the body), in which, for example, the modified virus can be used to transfer the genome of a cassette in different cells of the body. Each of these methods has pros and cons.

There are viral and non-viral systems that can be used to deliver CRISPR constructs; they will leave the blood vessels and enter the tissues. The delivery system may contain CRISPR, guide RNA and donor DNA, or it may contain CRISPR, guide RNA and protein activator, and so on. But regardless of whether it is viral or non-viral, the total weight of the constructs for editing the genes to be delivered must be significant. But this is not a problem, you can not rush and deliver them in batches.

Fortunately, there are cheap ways to produce biological products. The price of wood and even food and fuel is about the dollar per kilogram range. If we could make a kilogram of a viral delivery system and load it with CRISPR, then it could be inexpensive enough to apply it to the whole body.

Fahey : Yes, a kilogram would be enough! Thus, the viral delivery system contains a gene for CRISPR, a separate gene for targeting RNA, and so on. When it delivers these genes into a cell, it produces proteins and nucleic acids, and all components simply assemble themselves in it, right?

Church : Yes.

Fahey : What is the best CRISPR delivery system?

Church: Adeno-associated viruses (AAV) are nowadays one of the best delivery systems, because they can be targeted to tissues other than the liver (where many other delivery systems end their way). This is an active area of ​​research. It is booming, and the CRISPR revolution has made it even more attractive.

Security


Fahey : How specific can a virus be designed to deliver CRISPR to only one type of body cell?

Church : For every thousand cells of a certain type, there is usually one wrong delivery to a cell of another type that was not targeted. This is quite good. In addition, if you have something necessary for all cells, it must be delivered to all cells. Even if you have something specific, it usually does not matter which cells it is delivered to. But in those cases where it is important, you can get the correct delivery about 999 times out of 1000.

Faey : Can there be problems with one incorrect delivery out of 1000? In general, it would still be a lot of mistakes.

ChurchA: It must be remembered that most drugs actually enter all the cells in your body. It would be superfluous to say that CRISPR should be more specific than any previous drug.

Safety also depends on what brand of “explosives” you are dealing with. Like nitroglycerin or trotyl. If you make security one of your top priorities, you will not use the technique if it can work incorrectly until you are sure of very high cellular specificity.

Fahey : It is also very important for the safe use of CRISPR - this is not only what cell it got into, but whether it is editing the correct gene. How accurately can you target CRISPR in the genome?

ChurchA: In practice, when we presented our first CRISPR in 2013, its error rate was about 5%. In other words, CRISPR would incorrectly edit 5 cells out of 100. Now we get about one error per 6 trillion cells.

Fahey : This means that the probability of a serious error is now so low that it is very difficult to measure, it is much less than the rate of spontaneous mutations.

Church : Yes. In addition, small molecules can be used as conditional activators to ensure that the intended changes occur only in the desired cells. The combination of a fully safe small molecule activator and programmable targeting is unprecedented.

Other checks can also be entered for even more security. For example, when a virus enters the cell, it may make further decisions. He may essentially ask: "Am I in the right place?" - before acting. There is a whole range of molecular logic schemes that can be used to avoid errors.

Availability


Fahey : Will aging treatment be affordable with this approach?

Church : If you look at the current price, it looks huge and inaccessible. About 2,000 gene therapies are involved in clinical trials, but the only one approved for use is worth more than one million dollars per dose. You need only one dose, but at this price it is clearly not available for most people. As far as I know, this is the most expensive medicine in history.

Fahey : What is this medicine?

Church: It is called Glybera. It treats pancreatitis, a rare genetic disease. But the first sequencing of the human genome cost $ 3 billion per genome, and now its price is only $ 1,000, so I think that reducing the price from one million to thousands will not be problematic.

Fahey : Another cost savings to intervene in the aging process would arise if we could significantly slow down aging simply by changing 5-10 genes. This could lead to a reduction in the total cost to an acceptable one.

Church : Right. The combination needed to change, say, a trillion cells in the whole body and 10,000 genes would be difficult. But if you could only change a part of the cells and genes, you would make it more accessible.

Feyi : You said that CRISPR therapy has the potential to replace conventional drugs. Why?

Church : A big advantage of CRISPR is that it is much better than normal procedures, it has excellent opportunities for “placing control buttons” where there are currently no buttons. Now you need to be very lucky to get a good preparation that will do exactly what you want and nothing else. With CRISPR, we can be much more accurate.

How much can you fix at once?


Fei : If we know what to do and we can afford to do it, how quickly can we reverse aging? How about the simultaneous modification of, say, 10 different cell types in the body that cause most senile changes? Can they all be changed at the same time?

Church: “Everything” is a big word, but I think a lot can be changed right away. This can be done using what we call multiplexing, using a mixture of viruses or delivery vectors, which allows you to make many changes at once. But you can go a slow way, starting with the highest priority fabrics, and then move on to lower priorities. Determining which tissues are the highest priority may vary depending on the heredity of the patient, it is possible that a particular tissue will be at a higher risk of aging.

The road to the clinic: how long will it take?


Fahey : Using your best method, how long does it take to test a person?

Church : I think it can happen very quickly. It may take years to get full approval, but it may take just a year to get permission to test the first phase. Tests of GDF11, myostatin, and others have already been conducted on animals, like a large number of CRISPR studies. I think that in a year or two we will see the first human trials.

Fahey : Can you tell what these tests might be?

ChurchA: I helped create a company called Editas, which deals with genome-based CRISPR-based treatments. Some of them are aimed at rare childhood diseases, while others, I hope, will be aimed at aging. We also have an aging treatment company that will test these treatments on animals and humans.

Aging treatment, FDA and nutritional supplement model


Fei : Is it a fact that the FDA does not recognize aging as a disease?

Church : The FDA deals with many of the symptoms of aging, such as osteoporosis, muscular dystrophy, heart disease, cognitive dysfunction, etc. As a rule, it is more difficult to prove a preventive approach than the effectiveness of a drug that treats a fast and very dangerous disease. And because the FDA does not want you to make any unsubstantiated claims about your health, they had to take responsibility for regulating any health related condition that could be claimed. In fact, aging does not have to be officially a disease.

Fahey : It has been suggested that the FDA simply evaluates safety, not efficacy. What do you think about it?

Church: I love it. The Internet is likely to save us from ineffective drugs. The market for nutritional supplements is an excellent example of the fact that safety is all that is necessary for resolution. You can supply a dietary supplement to the market only on the basis of its safety, but you cannot supply a prescription drug only on the basis of its safety. There should be a general rule.

Fahey : Freedom of innovation and the creation of food additives is what the Life Extension Foundation is. They finance all my research in the field of cryobiology, and their nutritional supplements are based on research. Good results of freedom and free work.

Church: It's true. I'm just saying that there is a double standard in the FDA. Standards for nutritional supplements differ from standards for new prescription drugs.

Fei : Perhaps, if this were changed in favor of standards for supplements, we would have much more drugs, and everything would be much better.

Church : Yes. Focusing on security is probably the right model.

Fei : Thank you, doctor, for an amazing excursion in the near future!

About the authors


George M. Church, PhD - American geneticist, molecular engineer and chemist. Professor at Harvard Medical School and Professor of Health Sciences at Harvard and MIT. He founded the Wyss Institute for Biologically Inspired Engineering and 9 bioengineering companies.

Gregory M. Fahy, PhD - Cryobiologist and Bioherologist, Vice President and Chief Researcher at Twenty-First Century Medicine, Inc. The world's best expert on cryopreservation and vitrification of organs.

Source: https://habr.com/ru/post/373659/

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