Let's cure aging ASAP!
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L Kilgoi

Anti-Aging  - 
Geoffrey Dodd's profile photoL Kilgoi's profile photo
+Geoffrey Dodd This community is about the science of fighting aging and death. If one food or another extends lifespan then let us see the science behind it. As a moderator, I get barraged with bogus claims of "miracle" pills, "wonder" foods and anti-aging "breakthroughs". Some may even seem authentic with scientific studies to back their claims. However, when I see the study was published in a fake journal, it raises serious doubts.

To sum it up, the multi- billion dollar anti-aging industry is by and large BS. While "Anti-Aging" is a legitimate scientific term, many activists in this area prefer the term "Regenerative Medicine" to differentiate serious scientific study of aging and death from the myriad bromides that saturate the market.

I believe that if the billions spent on bromides and frauds had been channeled instead into legitimate research, we would have 120 year lifespans right now.
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Anca Ioviţă

Anti-Aging  - 
The biology of aging is traditionally studied in fast-living organisms such as mice, C. elegans worms and fruit flies.
It is time for gerontology to focus on negligible senescence species as well such as the ocean quahog, several turtles, the red sea urchin, the naked mole rat, rockfish and many more.
Species mainly prolong their lifespan by decreasing their metabolism and/or by undergoing regeneration of their somatic tissues.
Join our Facebook group 'Comparative gerontology' on how species rate at different speeds and what could be the mechanisms underlining this differences!

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Zoltan Istvan

Anti-Aging  - 
It's not just religious terrorism that is killing people. A religious anti-science culture--which most of us live amongst--also cuts short everyone's lives. People simply don't care much about longevity if they believe in an afterlife. http://www.huffingtonpost.com/entry/atheist-presidential-candidate-religion-is-literally_us_578a5f62e4b0b107a2411aa1
Don Peterson's profile photo
being in a body is nice =)) but not an end in and of itself……
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Michael Weiner

Anti-Aging  - 
This is important information on helping those with Alzheimer's, and I can use help getting the information out.

Science has made great strides, and the opportunity and evidence are not being adequately engaged.


Alzheimer's therapy working in humans needs more trials. There is a therapy for Alzheimer's that helps slow degeneration, and has has been shown in human studies as safe, with no contraindications. Lumineu (.com) will start a pilot study in 2017, which is anticipated to improve over the previous...
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Ferez Nallaseth

Anti-Aging  - 
'BBC - Will we ever win the "war on cancer"?' Huxley & the Mendel Darwin Genetic Basis of Evolution! All the more reason for NHZ/SHFSSCB! Redux!
Jun 24, 2016

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How cancer was created by evolution!
The cells inside a tumour change and evolve just like animals in the wild. Understanding how this works could help us stop cancer in its tracks
Will we ever win the "war on cancer"? Huxley & the Mendel Darwin Genetic Basis of Evolution! All the more reasons for NHZ/SHFSSCB!Redux!

The latest figures show just how distant a prospect victory is right now. In the US, the lifetime risk of developing cancer is 42% in men and 38% in women, according to the American Cancer Society. The figures are even worse in the UK. According to Cancer Research UK, 54% of men and 48% of women will get cancer at some point in their lives.

And cases are on the rise. As of 2015 there are 2.5 million people in the UK living with the disease, according to Macmillan Cancer Support. This is an increase of 3% each year, or 400,000 extra cases in five years.

Cancer is not only extremely pervasive, but also becoming more and more common

Figures like this show that cancer is not only extremely pervasive, but also becoming more and more common. But why will so many people develop the disease at some point in their lives?

To get to the answer, we must understand that cancer is an unfortunate by-product of the way evolution works. Large and complicated animals like humans are vulnerable to cancer precisely because they are large and complicated.

But even though it is evolutionary processes that have made cancer such a problem, it is also evolutionary thinking that is now leading to pioneering treatments that could stack the odds against cancer and in favour of our health.

The better a cell is at dividing, the more successful it will be (Credit: Alamy)

The better a cell is at dividing, the more successful it will be (Credit: Sebastian Kaulitzki/Alamy)

To understand how cancer exists at all, we need to go back to a fundamental process that occurs in our bodies: cell division.contd...

(1) http://www.bbc.com/earth/story/20160601-is-cancer-inevitable

(2) https://www.linkedin.com/pulse/what-lost-confronting-global-health-economic-ratios-ferez-soli?trk=mp-reader-card
(3) https://www.linkedin.com/pulse/upcoming-posts-classical-passe-vs-contemporary-ii-ferez-soli?trk=mp-reader-card
The cells inside a tumour change and evolve just like animals in the wild. Understanding how this works could help us stop cancer in its tracks
Michael Yaremchuk, Craniofacial & Cosmetic Plastic Surgeon's profile photo
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Zoltan Istvan

Anti-Aging  - 
Transhumanist Party candidate Zoltan Istvan wants to conquer death. Not personally, that is. He’s leaving that up to the researchers. But Istvan predicts that within 10 to 15 years, artificial intelligence will advance to the point of solving all of civilization’s most vexing problems – including, among other things, how to slow or halt the aging process by integrating our human selves with technology.
Tim Goodwin's profile photo
Let's hope they conquer stupidity, racism and arrogant nationalism first.
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Alex Alaniz

Anti-Aging  - 
Ultrasound method allowing drugs to pass blood-brain barrier.
The brain’s built-in protection system also prevents potentially lifesaving drugs from getting in, but maybe not for much longer.
Michael Yaremchuk, Craniofacial & Cosmetic Plastic Surgeon's profile photo
interesting article to read..and a must...additional information and thanks for sharing
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About this community

The #SemanticWeb is the crucible in which #Anti-Aging #Medicine, #Science and #Engineering will forge a profound healing and relief from the scourge of #aging. This community welcomes all to contribute to the advancement of this cause. Dr. Aubrey D. N. J. de Grey, the noted Biomedical Gerontologist, has developed an engineering approach to curing the diseases of aging called Strategies for Engineered Negligible Senescence (SENS). Simply, he states that there are 7 deadly things that cause aging: Nuclear Mutations, Mitochondrial Mutations, Intracellular Aggregates, Extracellular Junk, Death-Resistant Cells, Cell Loss and Atrophy, and Extracellular Crosslinks. His SENS Foundation's research project can be divided into strands that correspond to the 7 areas above: OncoSENS, MitoSENS, LysoSENS, AmyloSENS, ApoptoSENS, RepleniSENS and GlycoSENS. In addition, there is the Delivery Systems strand researching ways to introduce regenerative therapies into the human body. This community is interested in SENS because it is a comprehensive program to directly solve the problem of aging. However, we are interested in aging research from other points of view. GUIDELINES Foreign language posts are welcome if they are translated with Google Translate. If your post did not get displayed, it was probably arrested by the Google Spam Bot. Spam Posts will be removed and repeat abusers will also be banned. Your posts should be informative, descriptive and present knowledge and value, not just a way to promote your biz or site or blog. Blog posts are okay if they are on topic. While techniques like cosmetic surgery, Botox injections or sheep placenta facials have their value to society, this community focuses on real anti-aging therapies to extend lifespan. Finally, decisions on which posts to include or reject are totally arbitrary. There are no clear-cut borders to the anti-aging domain.
Phoenix AZ USA

Will Blesch

Anti-Aging  - 
Today I'll point out a great open access paper on the evolution of human telomere dynamics: telomere length, how that length changes over time, and especially how it changes with aging. This makes a good companion piece to another paper from last week that covered the differences in telomere dynamics between mice and humans.

This is quite important, since most of the work on this topic involves mouse studies, not human studies. As telomerase gene therapies continue to extend average telomere length and - in mice at least - also extend healthy life span, this is becoming a hot topic in the aging research community.

It is increasingly a good idea to have a grounding of the basics and current scientific thinking on this portion of our biochemistry. Sooner or later someone will be selling telomerase gene therapies to the public as an alleged method to slow the progression of aging, and most likely selling these treatments well in advance of any comprehensive human studies or definitive answers as to their effectiveness. You will find yourself in the position of deciding whether or not to pay the price and undertake the therapies. Better to figure out your position and what would change your mind today rather than later.

Telomeres are repeating sequences of DNA that cap the ends of chromosomes. Their purpose is primarily to act as a part of the limiting mechanisms on cell replication: a little of the length is lost with each cell division, and when they become too short the cell self-destructs or becomes senescent, ceasing replication. For any given tissue the distribution of telomere length among cells is a function of how often new cells with long telomeres are created by stem cells, and how often cells divide.

Stem cells maintain long telomeres through the use of telomerase, which adds more repeating sections to replace those lost to cell division. In humans only stem cells use telomerase, but in mice it has a much more widespread activity. Mice also have much longer telomeres than humans. All of this has everything to do with cancer, of course. The whole complicated arrangement of cells that are limited coupled to a much smaller number of cells that are privileged has evolved because it limits uncontrolled growth sufficiently well for evolutionary success. Without it highly structured and comparatively long-lived species such as our own couldn't exist.

Since stem cell activity declines with aging, it isn't surprising to see that measures of average telomere length also tend to do so - but this is a very poor measure of aging, and really only shows up in statistical studies across populations. There are too many other influences over the most commonly measured types of cell, such as immune cells. So average telomere length, much discussed this past decade, looks a lot like a measure of age-related damage, far removed from root causes.

Given that, why does increased telomerase activity extend life in mice? Most likely for the same reasons that any method of spurring greater stem cell activity improves matters in an old individual: greater tissue repair and maintenance, a net benefit even if it is old and damaged cells that do the work. There are also other, less well explored activities undertaken by telomerase that might be beneficial, such as improvements in mitochondrial function. In mice at least it seems that these benefits come with no greater risk of cancer.

It may be that improved immune function destroys more potential cancers than are created through greater activity in age-damaged cell populations, but that is pure speculation at this point. For humans the effects on cancer risk are much more of a question mark, though it is worth noting that stem cell therapies to date have exhibited far less risk of cancer than was expected at the outset.

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L Kilgoi's profile photoMichael Yaremchuk, Craniofacial & Cosmetic Plastic Surgeon's profile photo
good to have a healthy heart..
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Anca Ioviţă

Anti-Aging  - 
Short-lived and fast aging species are great choices to screen anti-aging interventions: chemical substances, physical factors, biological additions. Once an effect is noticed on short-lived species, gradual-aging ones can be used to test what you screened. And where do you start when you want to screen interventions? You start from those species that ‘know’ what they’re doing: negligibly senescent and long-lived ones.
The secret sauce here is big data.

Anthony Loera's profile photoAnca Ioviţă's profile photo
Hi Anthony, thanks for the invite. Guess we could talk it in private. 
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