extending health and life by cleaning the body of dead cells

[joachim]

not hair-related, but found this interesting for overall health and life extension:

http://nextbigfuture.com/2016/02/scientists-extend-life-of-mice-by-35.html?m=1

[Swooping]

Well it could be hair related actually. Senescence is (way) more multi-faceted than the article explains in your link though.

I have written a article about this recently in relation to AGA, enjoy;

Randall et al. cultured dermal papilla cells from balding and non-balding scalp (1). They showed that balding dermal papilla cells are harder to culture and grow way slower in vitro than non-balding dermal papilla cells. In 2008 Philpott et al. confirmed these findings (2). More importantly however they showed that this loss of proliferate capacity is associated with the onset of premature senescence. Balding dermal papilla cells in comparison to non-balding dermal papilla cells also expressed a number of markers of oxidative stress and DNA damage.

In 2009 another study highlighted the role of proliferation, DNA damage and apoptosis in the pathogenesis of Androgenetic Alopecia (AGA) (3). In this study instead of looking how the cells behaved in vitro they compared several factors in balding scalp to non-balding scalp (occipital). P53 was overexpressed in balding scalp while there was a low expression of APE1.

The study called “androgen receptor accelerates premature senescence of human dermal papilla cells in association with DNA damage” took it one step further (4). While it had already been shown that balding dermal papilla cells undergo premature senescence in vitro with expression of DNA damage markers they investigated whether androgen/AR signaling would have influence on this phenomenon. As the study name suggests they did find that androgen/AR signaling accelerates the phenomenon of premature senescence of balding DPC in vitro. They also showed that androgen/AR action leads to DNA damage in DPC.

Lee et al. analysed the microRNA expression profile of normal human dermal papilla cells treated with DHT (5). Interestingly they found out that the target genes of these downregulated and upregulated microRNA were involved in cell growth, cell cycle arrest, cell death, production of ROS and senescence. Another study investigated the difference between balding and non-balding DPC in relation to microRNA expression and found out that four microRNA’s were significantly upregulated in balding DPC in comparison to non-balding DPC. In the study they refer to these microRNA’s and show what possible factors they might influence. Interestingly these factors have been shown to participate in senescence or cell cycle arrest.

If we take all these studies we could definitely say that there seems to be indicative evidence for the role of senescence or cell cycle arrest and the likes of ROS and DNA damage in AGA. If you want to know more about senescence or cell cycle arrest I would suggest to start reading about it, it’s actually very interesting and there is too much to say to be covered in this article. Anyway, in my opinion something like senescence could very well have a central role in AGA. Why? Well the observations made in AGA would correlate very well with senescence. If we look at a unified of model of senescence;



We find that the “damage” would eventually lead to senescent cells. The damage in AGA could be DNA damage or ROS for instance which are known to induce senescence. Here is a study that shows for example how the androgen receptor can drive cellular senescence. This is very interesting, as we all know that the androgen receptor plays a huge role in AGA. AGA is dependent on the androgen receptor (AR). Androgens simply need to exert their biological action through the androgen receptor. The observations on people suffering from androgen insensitivity syndrome are also important. The condition results when the AR is impaired. As expected, these people never display any sign of AGA. Studies have furthermore also shown that the AR gene seems to play a huge role in AGA.

The second thing that would correlate is the SASP response that is often seen in senescence. SASP stands for senescence-associated secretory phenotype and a hallmark of SASP is the secretion of inflammatory factors which as you can see in the picture can lead to chronic inflammation. Several studies have shown the link between micro-inflammation and AGA. Not only that, in later stages even fibrosis has been shown in AGA that can even lead to permanent destruction of the hair follicle. Again, something that is seen in senescence and in the model here above. Senescence would also very well explain how miniaturization happens gradually and why it is so hard to reverse...

Well, the complexity of AGA is definitely very intriguing. I will probably do another article later that goes more in depth cause there are more definitely correlations and interesting things to say about this in relation to AGA.

[champpy]

I wonder how much ridding the body of old blood cells (bloodletting) or nowadays donating blood would help make way for new younger cells to form. Thats the only natural way i can think that we could remove portions of old dead cells from our body

[hope777]

very interesting

[pixels]

Pay for a blood transfusion from a young persons blood? Is that what you're thinking?

[burtandernie]

So in short the solution or treatment we should all be on to prevent or reverse these things is....what?

[jamesst11]

I hear PRP, or LLLT is a viable option... or extracting the Femur from a fetal cow and just sucking out the bone marrow. haha