Something like this…How can we extend sex appeal?

Gyms and beauty salons are in charge of this question now. There is some success, but it’s mostly superficial. Plastic surgery only masks, but doesn’t delay the processes of aging.

Expanding sex appeal is a complex task. Its aspects include both beauty and the activity of the brain. To be sexually attractive we have to be smart and fun. One cannot solve the problem of dementia with makeup.

We have to be in an excellent physical shape to be sexually attractive, but also things should be running smoothly with our hormonal regulation.

The task of extending the period of sex appeal is extremely science-intensive. It is not only the Viagra, but a complex impact on the whole organism. It is obvious that molecular biology is responsible for sex in the modern world.

I’m guessing you’d be like: surprised .

So, here’s the deal. My biohacker friends led by Peter Fedichev and Sergey Filonov in collaboration with my old friend and the longevity record holder Robert Shmookler Reis published a very cool paper. They proposed a way to quantitatively describe the two types of aging – negligible senescence and normal aging. We all know that some animals just don’t care about time passing by. Their mortality doesn’t increase with age. Such negligibly senescent species include the notorious naked mole rat and a bunch of other critters like certain turtles and clams to name a few. So the paper explains what it is exactly that makes these animals age so slowly – it’s the stability of their gene networks.

What does network stability mean then? Well, it’s actually pretty straightforward – if the DNA repair mechanisms are very efficient and the connectivity of the network is low enough, then this network is stable. So, normally aging species, such as ourselves, have unstable networks. This is a major bummer by all means. But! There is a way to overcome this problem, according to the proposed math model.

The model very generally describes what happens with a gene network over time – the majority of the genes are actually working perfectly, but a small number doesn’t. There are repair mechanisms that take care of that. Also, there are mechanisms that take care of defected proteins like heat shock proteins, etc. Put together all of this in an equasion and solve it, and bam! here’s an equasion that gives you the Gompertz law for all species that have normal aging, and a time independent constant for the negligibly senescent ones.

What’s the difference between those two aging regimes? The model suggests it’s the right combination of DNA repair efficiency and the combined efficiency of proteolysis and heat shock response systems, mediating degradation and refolding of misfolded proteins. So, it’s not the accumulation of damages that is responsible for aging, but rather the properties of the gene network itself. The good news is that even we are playing with a terrible hand at first, there is a chance we can still win by changing the features of our network and making it stable. For example, by optimizing misfolded protein response or DNA repair.

Let’s formulate the task of life extension slightly differently. Something like this…How can we extend sex appeal?

Gyms and beauty salons are in charge of this question now. There is some success, but it’s mostly superficial. Plastic surgery only masks, but doesn’t delay the processes of aging.

Expanding sex appeal is a complex task. Its aspects include both beauty and the activity of the brain. To be sexually attractive we have to be smart and fun. One cannot solve the problem of dementia with makeup.

We have to be in an excellent physical shape to be sexually attractive, but also things should be running smoothly with our hormonal regulation.

The task of extending the period of sex appeal is extremely science-intensive. It is not only the Viagra, but a complex impact on the whole organism. It is obvious that molecular biology is responsible for sex in the modern world.

What would you say if I told you that aging happens not because of accumulation of stresses, but rather because of the intrinsic properties of the gene network of the organism? I’m guessing you’d be like: surprised .

So, here’s the deal. My biohacker friends led by Peter Fedichev and Sergey Filonov in collaboration with my old friend and the longevity record holder Robert Shmookler Reis published a very cool paper. They proposed a way to quantitatively describe the two types of aging – negligible senescence and normal aging. We all know that some animals just don’t care about time passing by. Their mortality doesn’t increase with age. Such negligibly senescent species include the notorious naked mole rat and a bunch of other critters like certain turtles and clams to name a few. So the paper explains what it is exactly that makes these animals age so slowly – it’s the stability of their gene networks.

What does network stability mean then? Well, it’s actually pretty straightforward – if the DNA repair mechanisms are very efficient and the connectivity of the network is low enough, then this network is stable. So, normally aging species, such as ourselves, have unstable networks. This is a major bummer by all means. But! There is a way to overcome this problem, according to the proposed math model.

The model very generally describes what happens with a gene network over time – the majority of the genes are actually working perfectly, but a small number doesn’t. There are repair mechanisms that take care of that. Also, there are mechanisms that take care of defected proteins like heat shock proteins, etc. Put together all of this in an equasion and solve it, and bam! here’s an equasion that gives you the Gompertz law for all species that have normal aging, and a time independent constant for the negligibly senescent ones.

What’s the difference between those two aging regimes? The model suggests it’s the right combination of DNA repair efficiency and the combined efficiency of proteolysis and heat shock response systems, mediating degradation and refolding of misfolded proteins. So, it’s not the accumulation of damages that is responsible for aging, but rather the properties of the gene network itself. The good news is that even we are playing with a terrible hand at first, there is a chance we can still win by changing the features of our network and making it stable. For example, by optimizing misfolded protein response or DNA repair.

Meanwhile there is something important going on in the fight against baldness.

As in the majority of tissues, the hair follicle has stem cells. There are two types of stem cells that are responsible for the continuous renewal of the follicles. The first type is called active stem cells and they start dividing quite easily. Stem cells of the second type are called quiescent and in case of the new hair growth they don’t start dividing as easily. At the same time, the new hair is based primarily on quiescent cells, which attracted close attention of researchers to these cells. At first people thought that baldness was due to this type of cells.

However, recent studies showed that bald men did have those quiescent cells in their follicles. The problem was that they didn’t divide at all and didn’t contribute to forming new hairs.

This means that even a bald person still has the potential to grow new hair, but because of lack of some regulatory factors quiescent cells can’t start replicating.

Elaine Fuchs was able to identify these regulatory factors in her study published in Cell. Apparently, it’s all about the transit-amplifying cells that are the progeny of the active stem cells.

Read more

What would you say if I told you that aging happens not because of accumulation of stresses, but rather because of the intrinsic properties of the gene network of the organism? I’m guessing you’d be like: surprised .

So, here’s the deal. My biohacker friends led by Peter Fedichev and Sergey Filonov in collaboration with my old friend and the longevity record holder Robert Shmookler Reis published a very cool paper. They proposed a way to quantitatively describe the two types of aging – negligible senescence and normal aging. We all know that some animals just don’t care about time passing by. Their mortality doesn’t increase with age. Such negligibly senescent species include the notorious naked mole rat and a bunch of other critters like certain turtles and clams to name a few. So the paper explains what it is exactly that makes these animals age so slowly – it’s the stability of their gene networks.

What does network stability mean then? Well, it’s actually pretty straightforward – if the DNA repair mechanisms are very efficient and the connectivity of the network is low enough, then this network is stable. So, normally aging species, such as ourselves, have unstable networks. This is a major bummer by all means. But! There is a way to overcome this problem, according to the proposed math model.

The model very generally describes what happens with a gene network over time – the majority of the genes are actually working perfectly, but a small number doesn’t. There are repair mechanisms that take care of that. Also, there are mechanisms that take care of defected proteins like heat shock proteins, etc. Put together all of this in an equasion and solve it, and bam! here’s an equasion that gives you the Gompertz law for all species that have normal aging, and a time independent constant for the negligibly senescent ones.

What’s the difference between those two aging regimes? The model suggests it’s the right combination of DNA repair efficiency and the combined efficiency of proteolysis and heat shock response systems, mediating degradation and refolding of misfolded proteins. So, it’s not the the accumulation of damages that is responsible for aging, but rather the properties of the gene network itself. The good news is that even we are playing with a terrible hand at first, there is a chance we can still win by changing the features of our network and making it stable. For example, by optimizing misfolded protein response or DNA repair.

Read more

Meanwhile there is something important going on in the fight against baldness.

As in the majority of tissues, the hair follicle has stem cells. There are two types of stem cells that are responsible for the continuous renewal of the follicles. The first type is called active stem cells and they start dividing quite easily. Stem cells of the second type are called quiescent and in case of the new hair growth they don’t start dividing as easily. At the same time, the new hair is based primarily on quiescent cells, which attracted close attention of researchers to these cells. At first people thought that baldness was due to this type of cells.

However, recent studies showed that bald men did have those quiescent cells in their follicles. The problem was that they didn’t divide at all and didn’t contribute to forming new hairs.

This means that even a bald person still has the potential to grow new hair, but because of lack of some regulatory factors quiescent cells can’t start replicating.

Elaine Fuchs was able to identify these regulatory factors in her study published in Cell. Apparently, it’s all about the transit-amplifying cells that are the progeny of the active stem cells.

Read more

Let’s formulate the task of life extension slightly differently. Something like this…How can we extend sex appeal?

Gyms and beauty salons are in charge of this question now. There is some success, but it’s mostly superficial. Plastic surgery only masks, but doesn’t delay the processes of aging.

Expanding sex appeal is a complex task. Its aspects include both beauty and the activity of the brain. To be sexually attractive we have to be smart and fun. One cannot solve the problem of dementia with makeup.

We have to be in an excellent physical shape to be sexually attractive, but also things should be running smoothly with our hormonal regulation.

The task of extending the period of sex appeal is extremely science-intensive. It is not only the Viagra, but a complex impact on the whole organism. It is obvious that molecular biology is responsible for sex in the modern world.

Read more

I have mentioned mTOR as one of the main aging genes on multiple occasions. It’s about time I tell you what it is, what it does and why it is so important in aging.

mTOR has a little m in front of TOR, which means I am speaking about mammals. It technically means «mechanistic» TOR, but think of it as the molecule that mice and all of us have, whereas in worms is it just TOR.

mTOR gene produces one mTOR protein that can act in two pretty different ways. mTOR does so, because it forms two complexes with other molecules. These complexes are called mTORC1 and mTORC2. Yeah, I know, it’s a lot of letters, but C1 and C2 stand for «complex 1» and «complex 2», so it kinda makes sense.

So, how are these complexes different? For starters, they have different proteins that are part of the complexes, and these differences define the drastic variance in functions.

mTOR is one of the most studied genes that the scientists have known about for decades, however we still don’t know much about how those complexes react to different signals in the cells, especially mTORC2. We know much more about what the first complex does, but not really a lot about the second complex. This is not good, because both of them play a huge, enormous role in aging and in age-related disease like cancer and metabolic disorders like diabetes.

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When I hear that the conversation is about an ethical problem I anticipate that right now the people are going to put everything upside down and end with common sense. Appealing to ethics has always been the weapon of conservatism, the last resort of imbecility.

How does it work? At the beginning you have some ideas, but in the end it’s always a “no”. The person speaking on the behalf of ethics or bioethics is always against the progress, because he or she is being based on their own conjectures. What if the GMO foods will crawl out of the garden beds and eat us all? What if there will be inequality when some will use genetic engineering for their kids and some won’t? Let’s then close down the schools and universities – the main source of inequality. What if some will get the education and other won’t?

That’s exactly the position that ‪Elon Musk took by fearing the advances in genetic engineering. Well, first of all, there already is plenty of inequality. It is mediated by social system, limited resources and genetic diversity. First of all, why should we strive for total equality? More precisely, why does the plank of equality has to be based on a low intellectual level? How bad is a world where the majority of people are scientists? How bad is a world where people live thousands of years and explore deep space? It’s actually genetic engineering that gives us these chances. From the ‪#‎ethics‬ point of view things are visa versa. It’s refusing the very possibility of helping people is a terrible deed. Let’s not improve a person, because if we do what if this person becomes better than everybody else? Let’s not treat this person, because if we do he might live longer than everybody else? Isn’t this complete nonsense?

There’s another aspect of ‪#‎geneticengineering‬ – people always talk about improving the children, however genetic engineering first and foremost gives the opportunity to improve the already living people. Gene therapies already exist and it would be wonderful if we could live to see the moment when they are able to improve our health and intellect many fold. It is obvious that these technologies have to be safe. So, if we can help a child or a grown up, let’s do it immediately. This is the real ethic position.

I will also allow myself to speculate that genetic engineering is the fastest track towards the Artificial Intelligence. The majority thinks that AI will arise in a computer, but I think it might be easier to grow the superbrain and train it. And yes, with the help of genetic engineering.

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